UNITED NATIONS RC
UNEP/FAO/RC/CRC.5/10/Add.1
Distr.: General 2 December 2008
United Nations English only Environment Programme
Food and Agriculture Organization of the United Nations
Rotterdam Convention on the Prior Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International Trade Chemical Review Committee Fifth meeting Rome, 23–27 March 2009 Item 4 (b) (vii) of the provisional agenda* Listing of chemicals in Annex III to the Rotterdam Convention: review of notifications of final regulatory actions to ban or severely restrict a chemical: hexachlorobenzene
Hexachlorobenzene
Note by the Secretariat
Addendum
Supporting documentation provided by Canada
The Secretariat has the honour to provide, in the annex to the present note, documentation received from Canada to support its notification of final regulatory action on hexachlorobenzene as an industrial chemical.
* UNEP/FAO/RC/CRC.5/1.
K0842870 161208
For reasons of economy, this document is printed in a limited number. Delegates are kindly requested to bring their copies to meetings and not to request additional copies.
UNEP/FAO/RC/CRC.5/10/Add.1
Annex
• Hexachlorobenzene: Priority Substances List Assessment Report, Environment Canada, Health Canada. • Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act, Guidance Manual, Version 1.0 — March 1997. Environment Canada. • SOR/2005-41; CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999; Prohibition of Certain Toxic Substances Regulations, 2005, Canada Government Gazette.
2 Canadian Environmental Protection Act
Priority Substances List Assessment Report
Hexachlorobenzene
Government Gouvernement of Canada du Canada Environment Environnement Canada Canada Health Santé Canada Canada
Canada CANADA'S GREEN PLAN Canadian Environmental Protection Act
PRIORITY SUBSTANCES LIST ASSESSMENT REPORT
HEXACHLOROBENZENE
Government of Canada Health and Welfare Canada Environment Canada
Also available in French under the title: Loi canadienne sur la protection de l’environnement Liste des substances d’intérêt prioritaire Rapport d’évaluation Hexachlorobenzène CANADIAN CATALOGUING IN PUBLICATION DATA
Main entry under title:
Hexachlorobenzene (Priority substances list assessment report) At head of title: Canadian Environmental Protection Act. Issued also in French under title: Hexachlorobenzène. Includes bibliographical references. ISBN 0-662-20291-0 DSS cat. no. En40-215/7E
1. Hexachlorobenzene. 2. Hexachlorobenzene – Toxicity testing. 3. Hexachlorobenzene – Environmental aspects. I. Canada. Environment Canada. II. Canada. Health and Welfare Canada. III. Series.
TD196.C5H5 1993 363.73'84 C93-099427-2
Canada Groupe Communication Communication Group Canada Publishing Édition
©Minister of Supply and Services Canada 1993 Available in Canada through your local bookseller or by mail from Canada Communication Group -- Publishing Ottawa, Canada K1A 0S9 Cat. No. En40-215/7E ISBN 0-662-20291-0
Printed on Recycled Paper Hexachlorobenzene
TABLE OF CONTENTS
Overview of Findings...... v
1.0 Introduction...... 1
2.0 Summary of Information Critical to Assessment of "Toxic"...... 4
2.1 Identity, Properties, Production and Uses...... 4 2.2 Entry into the Environment...... 4 2.3 Exposure-related Information...... 6 2.3.1 Fate ...... 6 2.3.2 Concentrations ...... 7 2.4 Effects-related Information...... 13 2.4.1 Experimental Animals and In Vitro...... 13 2.4.2 Humans ...... 19 2.4.3 Ecotoxicology...... 19
3.0 Assessment of "Toxic" under CEPA ...... 23
3.1 CEPA 11(a): Environment...... 23 3.2 CEPA 11(b): Environment on Which Human Life Depends ...... 24 3.3 CEPA 11(c): Human Life or Health...... 25 3.4 Overall Conclusion...... 30
4.0 Recommendations for Research and Evaluation...... 31
5.0 References ...... 32
iii Hexachlorobenzene
Overview of Findings
Between 1948 and 1972, hexachlorobenzene (HCB) was used as a seed dressing for several crops to prevent fungal disease. HCB has not been used commercially in Canada since 1972, although it is released to the Canadian environment in small quantities as a by-product from the manufacture and use of chlorinated solvents and pesticides, through long-range transport and deposition, and “in emissions” from incinerators and other industrial processes. HCB is a persistent substance that has been distributed to all regions of Canada, primarily through long-range transport and deposition. As a result, HCB has frequently been detected in the various media to which humans and other organisms in Canada may be exposed, particularly in sediments and fatty tissues, where it tends to accumulate.
The highest concentrations of HCB have been observed near point sources in the Great Lakes and connecting channels. Current levels in air, water and forage fish from this area have the potential to cause harmful effects to fish-eating mammals, such as mink. The available data on current levels further indicate that HCB has the potential to cause reproductive impairment to predatory bird species across Canada, including the endangered peregrine falcon.
HCB is removed from the troposphere by photolysis and deposition to soil and water. These processes, combined with the low levels of HCB currently in the troposphere, indicate that HCB is not likely to trap significant quantities of thermal radiation from the Earth's surface, nor is it expected to reach the stratosphere. HCB is not, therefore, likely to be associated with global warming or stratospheric ozone depletion.
In several studies, HCB has been shown to cause cancer consistently in experimental animals, although available data are inadequate to determine whether HCB causes cancer in humans. It is, therefore, considered to be a “non-threshold toxicant” (i.e., a substance for which there is believed to be some chance of adverse health effect at any level of exposure). For such substances, estimated exposure is compared to quantitative estimates of potency to cause cancer, in order to characterize risk and provide guidance in establishing priorities for further action (i.e., analysis of options to reduce exposure). For hexachlorobenzene, such a comparison suggests that the priority for analysis of options to reduce exposure would be moderate to high.
Based on these considerations, the ministers of the Environment and of National Health and Welfare have concluded that the concentrations of HCB present in the Canadian environment may constitute a danger to the environment and to human life and health. HCB is, therefore, considered to be "toxic" as interpreted under section 11 of the Canadian Environmental Protection Act (CEPA).
v Hexachlorobenzene
1.0 Introduction
CEPA requires the ministers of the Environment and of National Health and Welfare to prepare and publish a Priority Substances List that identifies substances, including chemicals, groups of chemicals, effluents and wastes that may be harmful to the environment or constitute a danger to human health. The Act also requires both ministers to assess these substances and determine whether they are "toxic” as interpreted in section 11 of the Act, which states:
“…a substance is toxic if it is entering or may enter the environment in a quantity or concentration or under conditions
(a) having or that may have an immediate or long-term harmful effect on the environment;
(b) constituting or that may constitute a danger to the environment on which human life depends; or
(c) constituting or that may constitute a danger in Canada to human life or health."
Substances assessed to be "toxic" according to this section may be placed on Schedule I of the Act and considered for possible development of regulations, guidelines or codes of practice to control any aspect of their life cycle, from the research and development stage through manufacture, use, storage, transport and ultimate disposal.
The assessment of whether hexachlorobenzene is "toxic," as interpreted in CEPA, was based on the determination of whether it enters or likely enters the Canadian environment in a concentration or quantities or under conditions that could lead to exposure of humans or other biota at levels that could cause adverse effects.
For the human health-related portion of the assessment, a background review was prepared under contract by SRI International, Menlo Park, California, in February of 1990. For the period from 1983 to 1989, a literature survey was conducted by the contractor by searching a number of on-line bibliographic data bases from the National Library of Medicine in the United States [including Toxline, Medline, the Hazardous Substances Data Bank (HSDB) and the Registry of Toxic Effects of Chemical Substances (RTECS)], and consulting SRI's in-house data bases, chemical toxicity files, and standard reference sources. To identify other toxicological data relevant to the preparation of this Assessment Report, this initial search was supplemented by literature searches in the following computerized databases: HSDB, RTECS, IRIS, CCRIS (July, 1990); Toxline (1981 to March, 1992); Toxlit (1981 to March, 1992); and EMBASE (1981 to March, 1992). To identify data relevant to the estimation of exposure of the general population to HCB, literature searches were conducted on the following computerized data bases: Environmental Bibliography, Enviroline, Pollution Abstracts, Elias, Aquaref, Microlog, CODOC/GDOC (1981 to March, 1992); and Commonwealth Agricultural Abstracts, Food Science and Technology Abstracts and Agricola (1985 to 1990). Information on exposure is also included in some of the sources of toxicological data noted above, especially HSDB and Toxline. These were supplemented with manual searches of Current Contents throughout 1991.
1 Assessment Report
Representatives of the Drinking Water Surveillance and of the Sport Fish Contaminant Monitoring Programs of Ontario were contacted for unpublished information. The Canadian Chemical Producers Association was consulted concerning relevant data for consideration.
Data relevant to the environmental portions of the assessment were identified through searches of commercial and government data bases, including: AQUALINE (1984 to 1990); AQUAREF (1984 to November, 1990); AQUIRE (1978 to 1989); ASFA (1984 to November, 1990); BIOSIS (1984 to October, 1991); CAB (1984 to November, 1990); CA Search (1984 to 1990); ENVIROFATE (1966 to 1983); Enviroline (1983 to 1990); Environmental Bibliography (1984 to 1990); Federal Register (1984 to 1990); Hazardous Substances Data Bank (1972 to 1987); IRPTC Legal Database (1971 to October, 1991); Life Sciences Collection (1984 to 1990); NTIS (1984 to November, 1990); Pollution Abstracts (1984 to 1990); Toxline (1984 to 1990); U.S. EPA Toxics Release Inventory (1987 to 1989); Water Resources Abstracts (1984 to 1990); and World Textiles (1984 to 1990). Additional information was identified in review documents. Relevant unpublished data were also acquired from the Canadian Wildlife Service. A background report on the fate and levels of HCB in the Canadian environment was prepared under contract by Diane Koniecki.
Data obtained after April, 1992 and relevant to the assessment of whether HCB is "toxic" to human health were not considered for inclusion. As well, data obtained after July, 1992 and relevant to the assessment of whether HCB is "toxic" to the environment have not been incorporated.
Although much of the research on HCB has been conducted outside of Canada, avail- able Canadian data on sources, fate, levels and effects of HCB on the Canadian environment and human population were emphasized.
Review articles were consulted where considered appropriate; however, all original studies that form the basis for the determination of "toxic" under CEPA have been critically evaluated by the following Health and Welfare Canada staff (human exposure and effects on human health) and Environment Canada staff (entry, environmental exposure and effects):
R.L. Breton (Environment Canada) R. Burnett (Health and Welfare Canada) K. Lloyd (Environment Canada) M.E. Meek (Health and Welfare Canada) D.R.J. Moore (Environment Canada) R. Newhook (Health and Welfare Canada) L. Shutt (Environment Canada)
Following circulation and external peer review of the draft health-related sections by Dr. Michel Charbonneau of the Université de Montréal, Dr. Richard Kociba of Dow Chemical, U.S.A. (Supporting Document only), and BIBRA Toxicology International, these sections were approved by the Rulings Committee of the Bureau of Chemical Hazards of Health and Welfare Canada on June 9, 1992. The environmental portions of the Assessment Report were reviewed
2 Hexachlorobenzene by Dr. Lynn McCarty (CanTox Inc.), Dr. Barry Oliver (Zenon Consultants), Dr. Mike Whittle (Department of Fisheries and Oceans) and Dr. Bob Lane (Atmospheric Environmental Service). The final Assessment Report was reviewed and approved by the Environment Canada/Health and Welfare Canada CEPA Management Committee.
In this report, an overview of the findings is presented that will appear in the Canada Gazette. In addition, an extended summary of technical information critical to the assessment is presented in Section 2. The assessment of whether HCB is "toxic" under CEPA is presented in Section 3. A Supporting Document, in which the technical information is presented in greater detail, has also been prepared and is available upon request.
Copies of this Assessment Report and the unpublished Supporting Document are available upon request from:
Environmental Health Centre Commercial Chemicals Branch Health and Welfare Canada Environment Canada Room 104 Place Vincent Massey, 14th Floor Tunney' s Pasture 351 Saint-Joseph Boulevard Ottawa, Ontario, Canada Hull, Quebec, Canada K1A 0L2 K1A 0H3
3 Assessment Report
2.0 Summary of Information Critical to Assessment of "Toxic"
2.1 Identity, Properties, Production and Uses
The chemical formula of hexachlorobenzene is C6C16, its Chemical Abstract Service (CAS) number is 118-74-1, and its molecular weight is 284.79. At ambient temperature, HCB is a white crystalline solid. It is virtually insoluble in water (0.005 mg/L at 250C), but is soluble in ether, benzene, chloroform and hot ethanol. HCB has a high octanol/water partition coefficient 0 (log Kow = 5.5), low vapour pressure (0.0023 Pa at 25 C), and low flammability. Its Henry's Law constant is 131 Pa/m3/mol (U.S. EPA, 1985; ATSDR, 1990; Mackay et al, 1992).
HCB was introduced in 1940 for use as a seed dressing for wheat, barley, oats and rye to prevent fungal disease. Between 1948 and 1972, 17 fungicidal formulations registered under the Canadian Pest Control Products Act contained HCB in amounts of up to 80% (Tuttle, 1979); however, the use of HCB in fungicides was discontinued in 1972, due to concerns about adverse effects on the environment and human health.
In industry, HCB has been used directly in the manufacture of pyrotechnics, tracer bullets and as a fluxing agent in the manufacture of aluminum. HCB has also been used as a wood preserving agent, a porosity control agent in the manufacture of graphite anodes, and as a peptizing agent in the production of nitroso and styrene rubber for tires (Mumma and Lawless, 1975).
Based on records available since 1980, HCB has not been produced as a commercial chemical in Canada (Statistics Canada, 1981; 1982; 1983; Camford Information Services, 1991). However, small quantities of HCB were imported and subsequently exported, either in pesticide formulations or as the parent compound. Five tonnes of HCB was imported into Canada in 1980, 7 tonnes in 1981, 8 tonnes in 1982 and 10 tonnes in 1983 (Statistics Canada, 1981; 1982; 1983). According to Camford Information Services (1991), HCB was not imported from 1984 to 1987, but was imported into Ontario in 1988 (36 tonnes), 1989 (27 tonnes) and 1990 (10 tonnes) from France and the United States. At this time, the identities of the supplier(s) and importer(s) and the use of the material imported between 1988 and 1990 are considered to be Confidential Business Information.
2.2 Entry into the Environment
Currently, the principal sources of hexachlorobenzene to the Canadian environment are estimated to be by-products from the manufacture and use of chlorinated solvents, application of HCB-contaminated pesticides, incineration of HCB-containing wastes, and long-range transport from other countries (Table 2.1).
4 Hexachlorobenzene
Table 2.1 - Major Sources of Hexachlorobenzene to the Canadian Environment
Source Release (kg/yr)
Manufacture of Chlorinated Solvents 24.0-69.7a Use of Chlorinated Solvents = 122b Manufacture of Pesticides 0 Application of Pesticides 300-525c Incineration of HCB-containing Wastes Unknown Long-range Transport and Deposition 510d Manufacture of Chlorine and Sodium Chlorate 0e Hazardous Waste Landfills Unknown Emissions from other Industries Unknown Effluents from Municipal Waste Water Treatment Plants Unknown
a Estimated using emission factors from Brooks and Hunt (1984) multiplied by 1990 production figures in Canada (CPI, 1990a; 1990b; 1990c), assumes all wastes are incinerated with HCB destruction efficiency of 99.99% (Environment Canada, 1991a) b Based on domestic demand in Canada multiplied by upper limit concentration of 5 mg/L; assumes 100% release to environment following solvent use c Based on Canadian sales data for HCB-contaminated pesticides multiplied by HCB concentrations in the pesticides d Based on annual HCB loading rate for the Great Lakes (Eisenreich and Strachan, 1992) multiplied by surface area of Canada e HCB may be present in landfilled wastes due to past practices
HCB can be formed as a reaction by-product in the manufacture of chlorinated solvents, particularly carbon tetrachloride and tri- and tetrachloroethylene (Quinlivan et al., 1975; Jacoff et al., 1986). In Canada, there are two plants that manufacture carbon tetrachloride, and one plant that manufactures tetrachloroethylene (SRI International, 1990). In addition to generating HCB as a waste by-product during the manufacture of chlorinated solvents, HCB can also be found as a contaminant in the final products, at concentrations of up to 5 mg/L (Dow Chemical Canada Inc., 1991). Chlorinated solvents are used primarily in the manufacture of chlorofluorocarbons, metal cleaning and in dry-cleaning (CPI, 1990a; 1990b; 1990c).
A variety of chlorinated pesticides, including pentachlorophenol, dacthal, chlorothalonil, picloram, simazine, atrazine and pentachloronitrobenzene, are known to contain HCB as an impurity (Tobin, 1986). HCB is also generated as a by-product in the manufacture of these
5 Assessment Report
pesticides, but there has been no manufacture in Canada of the pesticides suspected of generating HCB-containing wastes since the 1970s (Environment Canada, 1979; Gilbertson, 1979; Tuttle, 1979; Environment Canada and Agriculture Canada, 1990).
HCB can be emitted from incinerators as a result of incomplete thermal decomposition of a variety of substances, including Kepone, mirex, chlorobenzenes, polychlorinated biphenyls, pentachlorophenol, poly (vinyl chloride) and mixtures of chlorinated solvents (Ahling et al., 1978; Dellinger et al., 1991). In November, 1991, there were 16 large operational incineration facilities in Canada, excluding a plant that will come on-line in 1992 (Environment Canada, 199lb). The majority of these plants are located in Ontario and British Columbia and, except for the five plants in British Columbia, are equipped with air pollution control technology systems. In the only study available that quantified HCB emissions from a Canadian incinerator, Environment Canada (1987) estimated atmospheric HCB emissions of < 1 kg/year and HCB wastes in ash of < 1 kg/year from a Quebec City mass burner system.
Long-range transport plays a significant role as a continuing source and means of redistribution of HCB throughout the world and the Canadian environment. Wet deposition is the primary mechanism for transport of HCB from the atmosphere to aquatic and terrestrial systems in Canada (Eisenreich and Strachan, 1992).
Until the early 1970s, emissions from chlor-alkali and sodium chlorate plants using graphite anodes (which generate HCB as a by-product) were an important source of HCB (Quinlivan et al., 1975; Mumma and Lawless, 1975; Alves and Chevalier, 1980; Christensen et al, 1989). Although current HCB production from this source is negligible, due to conversion to dimensionally stabilized anodes that do not produce HCB (Brooks and Hunt, 1984), unknown quantities of HCB may continue to be released from sites where wastes from these industries were landfilled.
HCB has been detected in emissions from a number of industries, including paint manufacturers, coal and steel producers, pulp and paper mills, textile mills, pyrotechnics producers, aluminum smelters, soap producers and wood-preservation facilities (Quinlivan et al, 1975; Gilbertson, 1979; Alves and Chevalier, 1980), likely reflecting the use of products contaminated with HCB. Municipal and industrial waste water facilities also discharge HCB- contaminated effluents (Environment Canada/Ontario Ministry of the Environment, 1986; King and Sherbin, 1986; UGLCCSMC, 1988; RAP, 1989), probably due to inputs from industrial sources. Although most of the hazardous waste landfill sites in Canada no longer accept HCB- contaminated wastes, leaching from sites where these wastes were previously landfilled continues to release HCB to the environment.
2.3 Exposure-related Information
2.3.1 Fate
Hexachlorobenzene is widely distributed throughout the Canadian environment because it is mobile and resistant to degradation. Volatilization from water to air and sedimentation
6 Hexachlorobenzene following adsorption to suspended particulates are the major removal processes from water. For example, Oliver (1984a) and Oliver and Charlton (1984) estimated that 80% of the HCB loading into Lake Ontario in 1982 was lost through volatilization, with the remainder removed by sedimentation (15%) and outflow to the St. Lawrence River (5%). Once in the sediments, HCB will tend to accumulate and become trapped by overlying sediments (Oliver and Nicol, 1982). However, desorption from resuspended bottom sediments does occur and may be an important and continuous source of HCB to water, even if inputs to the system cease (Oliver, 1984a; Oliver et al., 1989). Chemical and biological degradation are not considered to be important removal processes of HCB from water or sediments (Callahan et al., 1979; Mansour et al., 1986; Mill and Haag, 1986; Oliver and Carey, 1986). In the troposphere, HCB is transported long distances by virtue of its persistence, but does undergo slow photolytic degradation (t1/2 ˜ 80 days; Mill and Haag, 1986), or is removed from the air phase via atmospheric deposition to water and soil (Bidleman et al., 1986; Ballschmiter and Wittlinger, 1991; Lane et al,. 1992a; 1992b). Volatilization is the major removal process for soil at the surface (Kilzer et al., 1979; Griffin and Chou, 1981; Schwarzenbach et al., 1983; Nash and Gish, 1989), while slow aerobic (t1/2 = 2.7- 5.7 years) and anaerobic biodegradation (t1/2 =10.6-22.9 years) are the major removal processes at lower depths (Beck and Hansen, 1974; Howard et al., 1991).
Organisms generally accumulate HCB from water and from food, although benthic organisms may accumulate HCB directly from sediment (Oliver, 1984b; Knezovich and Harrison, 1988; Gobas et al., 1989). The relative importance of the water and food uptake routes is not fully understood, but field studies indicate that exposure via food is important for organisms at higher trophic levels. Thus, several studies have shown that higher trophic level organisms in natural aquatic ecosystems accumulated HCB to levels greater than those at lower trophic levels (Oliver, 1987; Oliver and Niimi, 1988). In Lake Ontario, Oliver and Niimi (1988) observed that tissue residue concentrations increased from plankton (mean 1.6 ng/g wet weight) to mysids (mean = 4.0 ng/g wet weight) to alewives (mean = 20 ng/g wet weight) to salmonids (mean = 38 ng/g wet weight). Braune and Norstrom (1989) used field data on body burdens of HCB in the herring gull (Larus argentatus) and one of its principal food items, the alewife (Alosa pseudoharengus) in a Great Lakes food chain to calculate a biomagnification factor (whole body, wet weight basis) of 31.
2.3.2 Concentrations
Hexachlorobenzene is a widely distributed substance in the Canadian environment. It has been detected in air, water, sediment, soil and biota. In this section, concentrations of HCB in the Canadian environment are summarized, with particular emphasis on studies conducted between 1980 and 1992.
Air
Data on concentrations of HCB in ambient air in southwestern Ontario have been collected as part of the Detroit Incinerator Monitoring Program. On roughly 30 days during
7 Assessment Report
1988-1989, HCB levels at a downtown Windsor site and at a rural site on Walpole Island each averaged 0.15 ng/m3 [limit of detection (LOD) 0.03 ng/m3] (Environment Canada, 1990; 1991c). Similar levels were reported for other sites in southern and central Ontario between 1985 and 1989 (Lane et al., 1992a), and in surveys from the Canadian high Arctic in the summers of 1986 and 1987 (Patton et al., 1988), highlighting the global long-range transport of HCB. No reports of HCB concentrations in indoor air were identified.
Drinking Water
HCB has been detected infrequently, and at low concentrations, in Canadian drinking water supplies. The substance was present in drinking water samples collected in 1980 from three Lake Ontario municipalities, at a mean concentration of 0.1 ng/L [LOD 0.01 ng/L] (Oliver and Nicol, 1982). HCH was not detected in a federal-provincial survey of roughly 600 municipal raw water sources in the maritime provinces between 1985 and 1988 (LOD 2 ng/L) (Environment Canada, 1989), nor in 86 drinking water sources analyzed during 1988-1989 under the Ontario Drinking Water Surveillance Program [LOD 1 ng/L] (Lachmaniuk, personal communication).
Surface Water
Of 1 042 surface water samples collected from lakes, streams, reservoirs, estuaries and coastal waters in the Atlantic provinces between 1979 and 1989, only six had concentrations above the LOD of 2.0 ng/L [maximum = 2.2 ng/L] (Leger 1991). Leger (1991), however, expressed reservations about the validity of these positive findings, since quality control testing was not used in 1980 when the six samples with HCB levels above the LOD were collected.
In numerous studies, the levels of HCB in surface water samples from the Great Lakes, their connecting channels and the St. Lawrence River have been measured. Of 189 surface water samples collected from the Great Lakes between 1980 and 1986, the concentration in only one, from Hamilton Harbour (4.0 ng/L), was found to exceed 1.0 ng/L (Oliver and Nicol, 1982; Neilson et al., 1986; Poulton, 1987; Biberhofer and Stevens, 1987; Stevens and Neilson, 1989; IJC, 1989). Mean concentrations of HCB in 1986 for each of the Great Lakes were 0.026 ng/L for Lake Superior, 0.033 ng/L for Lake Huron, 0.041 ng/L for Georgian Bay, 0.078 ng/L for Lake Erie and 0.063 ng/L for lake Ontario (Stevens and Neilson, 1989). The levels observed in 1986 for lakes Huron and Ontario were similar to those observed in 1980.
In the connecting channels to the Great Lakes, HCB levels more frequently exceeded 1.0 ng/L, particularly near point sources. For example, in the St. Clair River near the Dow Chemical outfall, HCB concentrations as high as 87 ng/L in 1985 and 75 ng/L in 1986 were observed (Oliver and Kaiser, 1986; OME, 1987). In samples of suspended solids taken from this location in 1986, the mean concentration of HCB was 14 000 ng/g dry weight (Lau et al., 1989). In the Niagara River near Niagara-on-the-Lake, mean concentrations of HCB in surface waters were 1.1 ng/L in a 1981 to 1983 survey [maximum = 29 ng/L] (Oliver and Nicol, 1984), and 0.1 ng/L in a 1988/1989 survey [maximum = 0.2 ng/L] (DIG, 1990).
8 Hexachlorobenzene
No recent (1980-1992) data were available concerning HCB levels in surface waters for any province west of Ontario.
Industrial and Municipal Waste Water
In a long-term monitoring program of effluents from the Sarnia industrial complex in 1986, the mean level of HCB detected was 117 ng/L in the Dow 42-inch sewer and 28 ng/L in the Polysar Cole drain (OME, 1987). HCB concentrations as high as 2 800 ng/L were observed in the Dow sewer in a short-term effluent study in 1985 (King and Sherbin, 1986).
HCB has also been detected in effluents from the Welland Water Pollution Control Plant (OME, 1989), Stelpipe Welland Tube Works (OME, 1989), Rainy River bleached kraft pulp and paper mill (Merriman, 1988), Sarnia municipal waste water treatment plant (Marsalek, 1986), and chlor-alkali industries in British Columbia (Wilson and Wan, 1982). Mean HCB levels in these effluents were generally low, ranging from < 1 to 11.6 ng/L.
Sediment
In sediment samples collected from 1979 to 1989 in the Atlantic provinces, HCB was reported to be below the limit of detection of 0.2 ng/g (dry weight) in 140 of 152 samples (Leger, 1991). HCB levels ranged from 0.4 to 10 ng/g (dry weight) in 12 sediment samples from the Annapolis River (Nova Scotia), Restigouche River (New Brunswick), Scales Pond (Prince Edward Island) and Deer Lake (Newfoundland). All 12 samples in which HCB was detected were collected from 1980 to 1982. Higher HCB levels have been reported in studies conducted near point sources. For example, HCB levels ranged from 19 to 273 ng/g (dry weight) in 1979 in sediment samples from the East River (Nova Scotia) near a chlor-alkali plant discharge (MacLaren Marex Inc., 1979).
In surveys conducted from 1980 to 1983, HCB levels in sediments were much higher in lakes Ontario and Erie than in lakes Huron and Superior. The observed ranges were 0.02 to 4.1 ng/g for Lake Superior, 0.4 to 5.2 ng/g for Lake Huron, 0.7 to 63 ng/g for Lake Erie, and 7.6 to 840 ng/g for Lake Ontario [dry weight] (Oliver and Nicol, 1982; Fox et al., 1983; Kaminsky et al., 1983; Oliver and Bourbonniere, 1985; Bourbonniere et al., 1986; Oliver et al., 1989; IJC, 1989). Analyses of sediment cores from Lake Ontario indicated that HCB levels have declined from the peak levels observed in the mid-1960s (mean ˜ 60 to 80 ng/g dry weight) to the early 1980s [mean ˜ 30 to 50 ng/g dry weight] (Oliver and Nicol, 1982; Oliver et al., 1989). More recent data are not available to determine if this downward trend has continued.
The highest levels of HCB have been observed in samples of sediment from the St. Clair, Detroit and Niagara rivers, particularly near point sources. In the St. Clair River, HCB levels in the 5-km stretch downstream of the Dow Chemical sewer discharges were found to be as high as 24 000 ng/g in 1984 (mean ˜ 5 200 ng/g) and 280 000 ng/g in 1985 [dry weight] (Oliver and Pugsley, 1986). The mean HCB concentration in a 35-km stretch of the
9 Assessment Report
St. Clair River downstream of the industrial complex was found to be 370 ng/g (dry weight) in 1985 (Oliver and Pugsley, 1986). HCB levels in bottom sediment observed in the late 1970s and early 1980s ranged from below the limit of detection (LOD) [1.0 ng/g] to 360 ng/g (dry weight) for the Detroit River (Hamdy and Post, 1985; UGLCCSMC, 1988), below the LOD (1.0 ng/g) to 250 ng/g (dry weight) for the Niagara River (NRTC, 1984), below the LOD (1.0 ng/g) to 351 ng/g (dry weight) for the St. Lawrence River (Merriman, 1987; Kuntz, 1988; Kauss et al., 1988; OME, 1989; Kaiser et al., 1990), and 0.4 to 170 ng/g (dry weight) for Lake St. Clair (Oliver and Bourbonniere, 1985; UGLCCSMC, 1988).
No recent (1980-1992) data were available concerning HCB levels in sediments for any province west of Ontario.
Soil
Levels of HCB in soil from agricultural areas of British Columbia were determined. Of 24 samples from cereal seed treatment areas, where HCB seed treatment had last been applied between 10 and 15 years prior to the survey, six had detectable HCB residues (LOD 1 ng/g dry weight) of between 1.3 and 2.2 ng/g. Due to use of HCB-contaminated herbicides, mean HCB levels in soil at forest nurseries and vegetable-growing areas were 11.2 and 2.3 ng/g, respectively (Wilson and Wan, 1982).
Biota
HCB has been detected in invertebrates, fish, reptiles, birds and mammals across Canada since the 1960s, when monitoring of organochlorines began. Based on data from long-term monitoring studies in various species of birds, HCB levels peaked in the mid-1970s and then declined from the late 1970s through the 1980s and into the 1990s (CWS, unpublished data base; Noble and Elliott, 1986). This section will focus on recent and ongoing surveys (i.e., 1980 to present) of HCB levels in Canadian biota.
Data on levels of HCB in tissues of invertebrates in Canada are limited. In studies conducted since 1981 in the Great Lakes and connecting channels, HCB levels in freshwater mussels (Elliptio complanata) have ranged from 0.1 ng/g wet weight in Lake St. Clair to 24 ng/g wet weight in the St. Clair River near Sarnia (Kauss and Hamdy, 1985; Innes et al., 1988; Muncaster et al., 1989). A similar range (0.1 to 26 ng/g wet weight) was observed in marine invertebrates from the Beaufort Sea (Hargrave et al., 1989).
In a 1981-1982 survey of watersheds in New Brunswick and Nova Scotia, HCB levels in brook trout (Salvelinus fontinalis) and yellow perch (Perca flavescens) ranged from below the limit of detection (4.2 ng/g in 1981; 0.2 ng/g in 1982) to 54 ng/g for trout and 15 ng/g wet weight for perch (Peterson and Ray, 1987). Relatively high body burdens of HCB have been observed in fish in Lake Ontario and connecting channels. For example, HCB was not detected (ND) in juvenile spottail shiners (Notropis hudsonius) from lakes Superior and Erie [LOD = 1 ng/g wet weight] (Suns et al., 1983; Environment Canada/Department of Fisheries
10 Hexachlorobenzene
and Oceans/Health and Welfare Canada, 1991), while mean body burdens in shiners in Lake Ontario were between ND and 13 ng/g wet weight, and those in the Detroit and Niagara rivers averaged 5 ng/g wet weight and ND to 8 ng/g wet weight, respectively (Suns et al., 1985). The highest levels were reported in the St. Clair River, particularly near Sarnia where a mean of 231 ng/g wet weight was observed in 1983 (Suns et al., 1985). Mean concentrations in the muscle tissue of Lake Ontario salmonids were 37 ng/g wet weight for lake trout (S. namaycush), 10 ng/g for brown trout (Salmo trutta), 5 and 16 ng/g for small and, large rainbow trout (Oncorhynchus mykiss) respectively, and 10 and 13 ng/g for small and large coho salmon (O. kisutch) respectively (Niimi and Oliver, 1989). Similar values were reported for Lake Ontario fish species through the Ontario Sport Fish Contaminant Monitoring Program, while concentrations in the muscle tissue of species from the other Great Lakes were somewhat lower (mean across ail species 1.4 ng/g wet weight, assuming 0.5 ng/g [one half of LOD] for ND). HCB was rarely detected in the other Ontario lakes surveyed (Cox and Ralston, 1990, Cox, personal communication). Limited recent information exists on HCB levels in fish in other parts of Canada. In the only recent study found for marine fish species, the mean concentration of HCB in arctic char (S. alpinus) was 6.9 ng/g wet weight in a 1987 survey (Hargrave et al., 1989).
There are limited data on levels of HCB in reptiles in Canada. In snapping turtle (Chelydra s. serpentina) eggs collected since 1986, mean levels of HCB were found to range from 1.0 ng/g wet weight in Algonquin Park to 25 ng/g wet weight in Hamilton Harbour in 1988 (Bishop et al., 1991).
The levels of HCB in birds have been similar across the various regions of Canada since the 1980s, likely as a combined result of emission reductions and the long-range transport of HCB to remote locations. For example, concentrations of HCB in herring gull eggs in 1991 were relatively uniform in the Great Lakes (two colonies per lake): Lake Michigan (37 & 71 ng/g wet weight); Lake Superior (34 & 41 ng/g); Lake Ontario (28 & 39 ng/g); Lake Huron (28 & 28 ng/g); and Lake Erie (16 & 30 ng/g) [Environment Canada/Department of Fisheries and Oceans/Health and Welfare Canada, 1991; CWS, unpublished data base]. These levels are approximately two orders of magnitude lower than in 1971. Recent surveys have indicated similar HCB residue levels in eggs of five other predatory bird species (means range from 10 to 53 ng/g wet weight) [Noble and Elliott, 1986; Pearce et al., 1989; Noble et al., 1992; CWS, unpublished data base]; however, the mean level of HCB in peregrine falcon (Falco peregrinus anatum) eggs collected across Canada from 1980 to 1987 was 279 ng/g wet weight, and ranged as high as 1 060 ng/g wet weight (Peakall et al., 1990). In breast muscle tissue samples from various species of birds, HCB concentrations tend to be progressively greater at higher trophic levels [i.e., piscivores > molluscivores > omnivores > grazers] (CWS, unpublished data base).
In the blubber of marine mammals, observed mean levels of HCB were 19 ng/g wet weight for ringed seals (Phoca hispida) and 491 ng/g wet weight for beluga whales (Delphinapterus leucas) in the Canadian Arctic (Norstrom et al., 1990), while male belugas sampled in the Gulf of St. Lawrence contained up to 1 340 ng/g (Béland et al., 1991). Male and female white-beaked dolphin blubber (Lagerorhunchus albirostris) collected near the
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Newfoundland coast had 1110 ng/g and 880 ng/g HCB wet weight. Lower levels (290 ng/g and 100 ng/g wet weight) were observed in blubber from male and female pilot whales (Globicephala me/eana), also collected near the Newfoundland coast (Muir et al., 1988a). The higher levels observed in the dolphin may reflect greater exposure to HCB because of overwintering and feeding in the Gulf of St. Lawrence.
Limited data are available on HCB levels in terrestrial mammals. Mean concentrations of HCB in the livers of adult male river otters (Lutra canadensis) in Alberta in 1983 were 25 ng/g (lipid basis) and 4 ng/g wet weight (Somers, 1985). HCB levels in livers of adult mink (Mustela vison) and river otter collected in 1991 along the Columbia River in British Columbia, Washington and Oregon ranged from 0.2 ng/g to 9.8 ng/g wet weight (CWS, unpublished data base). Levels of HCB in mink carcasses collected in Ontario in the late 1970s and early 1980s ranged from < 0.5 to 10 ng/g (Proulx et al., 1987) while burdens in the fat of coyotes (Canis latrans) and grey wolves (Canis lupis) collected in Alberta in the early 1970s were <0.5 ng/g wet weight (CWS, unpublished data base). In the Canadian north, the mean level of HCB in the fat of polar bears (Ursus maritimus) hunted between 1982 and 1984 was 296 ng/g wet weight (Norstrom et al., 1990).
The results of some studies of the levels of HCB in human tissues and fluids, and in foods, indicate that exposure of the general population in Canada declined from the 1970s to the mid-1980s (Frank and Ripley, 1990; Mes, 1990), while there has been no clear trend in other studies (Frank et al., 1988). In the most recent available national survey of organochlorine compounds in the breast milk of Canadians, from 1982, the mean concentration of HCB was 2 ng/g of whole milk (54 ng/g fat). The substance was present in all 210 samples analysed (Mes et al., 1986). (The data from a more recent national breast milk survey were not available at the time of writing.)
Food
In a limited number of recent surveys, HCB levels in commercial foods available in Canada have been determined. Davies (1988) reported the levels of organochlorines in composites of foods purchased in Toronto in 1985 and combined in proportion to the amounts purchased by Ontario residents. A composite of fresh meat and eggs contained 0.17 ng/g wet weight of HCB, a root-vegetables and potatoes composite 0.04 ng/g, a leafy and other above ground vegetables composite 0.02 ng/g and a 2%-milk composite 0.16 ng/g. No HCB was detected in a composite of fresh fruit (LOD 0.01 ng/g). In a subsequent Ontario survey designed to verify these findings (OMAF/MOE, 1988), HCB was not found in supplies of peaches, tomatoes, potatoes, wheat, eggs, pork or chicken (LOD 0.2 ng/g), but was present in some samples of apples, hamburger and prime beef.
The results of the U.S. Total Diet Study indicate that HCB is detected in a small fraction of food items, most often dairy products, meats, and peanuts/peanut butter. Mean levels over all surveys from 1982-1986 were less than 1 ppb (ng/g) for all products except for peanuts (3.2 ng/g), peanut butter (3.0 ng/g), frankfurters (1.2 ng/g) and butter (2.4 ng/g) [Gunderson, undated].
12 Hexachlorobenzene
2.4 Effects-related Information
2.4.1 Experimental Animals and In Vitro
Exposure to hexachlorobenzene causes a wide range of effects in several species of mammals, with similar lowest-observed-effect levels (LOELs) and no-observed-effect levels (NOELs) for a number of end-points (Table 2.2). This section summarizes the extensive literature on the toxicity of HCB to laboratory mammals, with emphasis on the lowest reported effect levels.
Acute, Short-term and Subchronic Toxicity
The acute toxicity of HCB in experimental animals is low; reported oral LD50 values for various species range from > 1 000 mg/kg b.w. for the guinea pig to between 3 500 and > 10 000 mg/kg b.w. for the rat. Reported LC 50 values for inhalation exposures range from 1 600 mg/m3 for the cat to 4 000 mg/m3 for the mouse (IARC, 1979; Strik, 1986; Sax, 1989). It is important to note that because the volatility of HCB is not high (vapour pressure is only 0.0019 Pa at 250C) and its solubility in oil is limited (approximately 10 mg/mL in corn oil), it is unlikely that some of very high doses reported in acute and short-term toxicity studies were actually achieved (Charbonneau, personal communication).
The effects of short-term, repeated exposure to HCB are primarily hepatotoxic and neurologic. In a number of studies, the effects of HCB on rats exposed to oral doses in the range from 30-250 mg/kg b.w./day include altered body weight, cutaneous lesions, tremors and other neurological signs, hepatomegaly, liver damage and, in some cases, early alterations in porphyrin or heme metabolism (U.S. EPA, 1985; Courtney, 1979; Strik, 1986). Short-term exposures induce a variety of Phase I (both cytochrome P450 IIB and cytochrome P450 I, as well as other mixed-function oxidases) and Phase II enzymes (Wada et al, 1968; Courtney, 1979; Denomme et al., 1983; U.S. EPA, 1985; Linko et al., 1986; Strik, 1986; Vos et al., 1988; Green et al., 1989; Rizzardini et al., 1990; D'Amour and Charbonneau, 1992); reported effect levels for this end-point in rats have been as low as 50 mg/kg feed (approximately 2.5 mg/kg b.w./day) [den Tonkelaar and van Esch, 1974].
The effects produced by subchronic exposure to HCB are similar to those observed in short-term studies, but are generally evident at lower doses (Courtney, 1979; U.S. EPA, 1985; ATSDR, 1990). At relatively high doses (32 mg/kg b.w./day and higher for periods from several weeks to 90 days), reported effects include deaths, skin lesions, behavioural and neurological changes, reduced body weight gain, increased organ weights, and altered thyroid function and serum levels of thyroid hormones. At lower doses, hepatotoxic effects are commonly reported, including histological alterations, the induction of a variety of hepatic microsomal enzymes, and porphyria. The lowest doses producing effects on the liver in a subchronic study were reported by den Tonkelaar et al. (1978). Pigs exposed for 90 days to doses of 0.5 mg/kg b.w./day and up in diet were porphyric, and had altered liver histology and microsomal enzyme activities, while no effects were observed at 0.05 mg/kg b.w./day.
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Table 2.2 - Lowest No-Observed-Effect and Low-Observed-Effect Levels (NOELs and LOELs) in Mammals Exposed to HCB
NOEL LOEL Reference Effects (mg/kg b.w./day) (mg/kgb.w./day) Increased urinary coproporphyrin and microsomal liver Den Tonkelaar et enzyme activity in pigs with subchronic exposure to HCB in al. (1978) 0.05 0.5 diet
Alterations in Ca metabolism (increased serum 1,25- Andrews et al. dihydroxyvitamin D, levels, alterations in femur density, bone 0.07 0.7 (1988; 1989; 1990) morphometry and strength), increased liver weights, with subchronic gavage exposure to HCB
Babineau et al. Ultrastructural changes in ovarian surface epithelium and ( 1991); Sims et al, follicular cells, ovarian follicles and developing ovum in --- 0.1 (1991); Singh et al. monkeys with subchronic exposure to HCB in gelatin capsules (1990a)
Increased cell-mediated and humoral immune function, b Vos et al. (1983) intraalveolar macrophage accumulation, microsomal EROD --- 0.2a activity, in rats exposed to HCB in utero, via nursing and in the diet to five weeks of age
Depressed delayed-type hypersensitivity response to Barnett et al. oxazolone in mice exposed to HCB in peanut butter in utero --- 0.5a (1987) (throughout gestation) and via nursing to 45 days of age
Increased susceptibility to Leishmania infection, and Loose et al. reductions in resistance to a challenge with tumour cells and in (1981); Loose --- the cytotoxic macrophage activity of the spleen in mice with 0.6 (1982) subchronic exposure to HCB in diet
Nodular hyperplasia of gastric lymphoid tissue in beagles with Gralla et al. (1977) 0.12 chronic exposure to HCB in gelatin capsules ---
Arnold et al. Increased organ weights (heart, brain and liver) in F0 males, (1985);Arnold and compound-related histological changes in liver of both sexes a 0.05-0.07 0.27-0.35a Krewski (1988) of f1 rats with chronic exposure to HCB in diet Ultrastructural changes in livers (proliferation of SER, altered Mollenhauer et al. mitochrondria, increase in numbers of storage vesicles) of rats (1975;1976) 0.05-0.06 with chronic exposure to HCB in diet 0.25-0.30
Induction of in vivo mixed function oxidase activity in rats Grant et al. (1974) 0.5-0.6 with chronic exposure to HCB in diet ---
Increased serotonin concentrations in hypothalamus of mink Rush et al. (1983); dams with chronic dietary exposure to HCB, decreased dopamine levels in hypothalamus, reduced birth weights, --- Bleavins et al. 0.16a a b increased mortality to weaning, no significant hepatic or renal (1984 ;1984 ) damage, in mink kits with in utero plus lactational exposure to HCB a Doses reported are those received by dams; actual doses received in utero or via nursing are unknown b Ethoxyresorufin-O-deethylase
14 Hexachlorobenzene
Subchronic exposure to relatively low doses of HCB has also caused changes in calcium homeostasis and bone morphometry. Male Fischer 344 rats administered HCB by gavage in corn oil had elevated serum levels of 1,25-dihydroxy-vitamin D3 and reduced calcium excretion after 5 weeks, and increased femur density, weight and strength after 15 weeks. These effects were evident at 0.7 mg/kg b.w./day, but not at 0.07 mg/kg b.w./day (Andrews et al., 1989; 1990). While technical HCB is known to be contaminated with chlorinated dibenzo-p-dioxins, dibenzofurans and biphenyls (Villenueva et al., 1974; Goldstein et al., 1978), the effects of subchronic dietary exposure of rats to either pure or technical HCB were virtually identical, indicating that the effects observed in this study were due to the parent compound (Goldstein et al., 1978).
HCB-induced porphyria has been well-studied, and has been reported for all species examined except the dog. It is most often manifested as increased levels of porphyrins and/or porphyrin precursors in the liver, other tissues and excreta. Female rats exposed to doses of several mg/kg b.w./day in diet or by gavage for periods of three to four months developed a marked porphyria, which was absent or much reduced in males (Kuiper-Goodman et al., 1977; Rizzardini and Smith, 1982; Smith et al., 1985). This sex-related difference may be related to differences between male and female rats in the induction of specific cytochrome P-450 isoenzymes (Smith et al., 1990), in the importance of glutathione conjugation (Rizzardini and Smith, 1982; D'Amour and Charbonneau, 1992) or perhaps in steroid hormones (Grant et al, 1975).
Chronic Toxicity, Carcinogenicity, and Genotoxicity
The non-neoplastic effects reported from chronic exposure to HCB, which are primarily hepatotoxic, are observed at relatively low doses (Table 2.2). In a two-generation study with Sprague-Dawley rats, increased heart and liver weights and histopathological changes in the liver and kidney were seen in F1 animals exposed to a maternal dose of 0.27-0.35 mg HCB/kg b.w./day in diet in utero, through nursing, and then continued on the same diet as their parents for their lifetimes. The no-effect level in this study was 0.05-0.07 mg/kg b.w./day (Arnold et al., 1985; Arnold and Krewski, 1988). Dietary exposures of Sprague-Dawley rats to 10 ppm and above (roughly 0.5-0.6 mg/kg b.w./day; NIOSH, 1985) for 9-10 months induced in vivo mixed-function oxidase activity, as indicated by reductions in drug-induced sleeping times (Grant et al., 1974). Exposure of Sprague-Dawley rats to 5 ppm HCB in diet (roughly 0.25-0.30 mg/kg b.w./day; NIOSH, 1985) for 3-12 months caused proliferation of smooth endoplasmic reticulum, altered mitochondria, and increased numbers of storage vesicles; these effects were not evident at 1 ppm in diet [roughly 0.05-0.06 mg/kg b.w./day; NIOSH, 19851 (Mollenhauer et al., 1975; 1976). Bleavins et al. (1984a) reported that exposure of female mink to a dietary concentration of 1 ppm HCB (estimated to yield a dose of 0.16 mg/kg b.w./day) for 47 weeks significantly increased serotonin concentrations in the hypothalamus of dams, and depressed hypothalmic dopamine concentrations in kits exposed in utero and through nursing.
The carcinogenicity of HCB has been assessed in several bioassays in rats, mice and hamsters. The following discussion is limited principally to the four studies in which adequate numbers of animals of both sexes were exposed for a sufficient length of time to more than one dose level (Cabral et al., 1977; Cabral et al., 1979; Arnold et al., 1985; Lambrecht et al., 1983a; 1983b).
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Cabral et al. (1977; see also Cabral and Shubik, 1986) reported a statistically significant increase of "liver cell tumours (hepatomas)" in male and female Syrian golden hamsters fed 50, 100 or 200 ppm (4, 8 or 16 mg/kg b.w./day) HCB in their diets for life. Survival of both sexes and weight gain of males were reportedly reduced at 200 ppm. The incidence of "haemangioendotheliomas" of the liver was significantly increased in both sexes at 200 ppm and in males at 100 ppm, and of alveolar adenomas of the thyroid in males at 200 ppm. The authors reported that three of the hepatic "haemangioendotheliomas" (which are benign by definition) metastasized.
HCB was administered in the diet to outbred male and female Swiss mice at concentrations of 0, 50, 100 and 200 ppm (0, 6, 12 and 24 mg/kg b.w./day [U.S. EPA, 1985]) for 120 weeks (Cabral et al., 1979; Cabral and Shubik, 1986). At 90 weeks, 4% of the males and none of the females survived, compared to survival rates of 50% for control males and 48% for control females. The rate of body weight increase was reportedly reduced in dosed females (at 50 and 200 ppm) and males (at 100 and 200 ppm). In females exposed to 200 ppm, a statistically significant increase in the incidence of "liver cell tumours (hepatomas)" was noted. "Hepatomas" were also elevated, although not significantly, in males at this dose and in both sexes at 100 ppm. The incidence of "hepatomas" for both sexes showed a dose dependency not only in the number of tumour-bearing animals but also in the latent period, and in multiplicity and size of tumours.
Arnold et al. (1985; see also Arnold and Krewski, 1988) investigated the potential carcinogenicity to rats of in utero, lactational and oral exposure to analytical-grade HCB. Weanling male and female Sprague-Dawley rats were fed diets containing 0, 0.32, 1.6, 8 or 40 ppm HCB. (Mean doses for males 0, 0.01, 0.05, 0.27 and 1.39 mg/kg b.w./day and for females 0, 0.01, 0.07, 0.35 and 1.72 mg/kg b.w./day [California Department of Health Services, 1988]). After 3 months, the F0 rats were bred, and 50 F1 pups of each sex were randomly selected from each group. From weaning, the F1 animals were continued on the same diet for their lifetimes (up to 130 weeks). In exposed F1 females, increased incidences of neoplastic liver nodules and adrenal phaeochromocytomas were noted at the highest dose. A significantly increased incidence of parathyroid adenomas was noted in males receiving 40 ppm HCB in their diet.
In a study by Lambrecht et al. (1983a; 1983b; Peters et al., 1983, in U.S. EPA, 1985; Ertürk et al., 1986), weanling Sprague-Dawley rats were fed diets containing 0,75 or 150 ppm of HCB (4 and 8 mg/kg b.w./day for males and 5 and 9 mg/kg b.w./day for females, respectively) for up to 2 years. Body weights were reportedly not affected by treatment until the final stages of the study. Statistically significant increases in the incidence of "hepatomas/hemangiomas" and of renal cell adenomas were noted at both doses in animals of both sexes surviving beyond 12 months. Incidences of hepatocellular carcinomas and bile duct adenomas/carcinomas were also elevated in females at both doses. In female rats, significant increases in the incidences of adrenal cortical adenomas at 75 ppm and phaeochromocytomas at both doses were reported in reviews of this study (U.S. EPA, 1985; California Department of Health Services, 1988). Lambrecht et al. (1983b) reported a generalized leukemia involving the thymus, spleen, liver and kidney in rats exposed to HCB in this study, but did not present any quantitative data.
High incidences of liver tumours have also been reported in some more limited studies in which single dietary concentrations were administered to very small groups of females of
16 Hexachlorobenzene three strains of rats (Smith and Cabral, 1980; Smith et al, 1985); in one strain (Fischer 344), hepatocellular carcinomas were observed (Smith et al, 1985). HCB has not, however, been carcinogenic in several other bioassays (Theiss et al., 1977; Shirai et al., 1978; Arnold et al, 1985; Smith et al., 1989), perhaps as a results of limitations in the design of these studies, including the low doses and/or small group sizes employed.
Results from a number of studies have indicated that HCB is a cocarcinogen or promoter of cancer. Concomitant exposure to HCB in diet enhanced the induction of liver tumours by polychlorinated terphenyl in mice (Shirai et al., 1978). Dietary exposure of rats to HCB promoted the development of liver tumours from prior exposure to iron (Smith et al, 1989), and of hepatocellular carcinomas and/or hepatic gamma-glutamyltranspeptidase-positive foci initiated by diethylnitrosamine (Pereira et al., 1982; Herren-Freund and Pereira, 1986; Stewart et al, 1989). Short-term exposures (< 1 day) of Sprague -Dawley rats to sublethal doses of HCB produced a 1.3- fold increase in ornithine decarboxylase activity, a marker for promotion (Kitchin and Brown, 1989).
In the majority of a large number of studies in which various end-points have been examined both in vitro and in vivo, HCB has not been genotoxic (Khera, 1974; Simon et al., 1979; Haworth et al., 1983; Górski et al, 1986; Kuroda, 1986; Kitchin and Brown, 1989; Rizzardini et al., 1990; Siekel et al., 1991). A questionable positive response was reported by Gopalaswamy and Aiyar (1986) in the Ames test. There have been reports of mutagenic activity for HCB in eukaryotic cells in vitro, but these appear questionable because of the small magnitude of the observed increase (Guerzoni et al, 1976; Kuroda, 1986), and because of limitations in the design of the study by Guerzoni et al.
Reproductive and Developmental Toxicity
In recent studies conducted by Health and Welfare Canada, relatively low doses of HCB affected the reproductive tissues in female monkeys. Oral exposure of cynomolgus monkeys to 0.1 mg HCB/kg b.w./day for 90 days caused degenerative ultrastructural changes in the ovarian surface epithelium (Babineau et al, 1991), and in the follicular cells, ovarian follicles and the developing ovum (Singh et al., 1990a). In parallel light microscopic investigations, HCB-induced histological alterations in the surface epithelium were observed (Sims et al., 1991). Alterations were more severe in animals receiving 1 and 10 mg/kg b.w./day (Babineau et al., 1991; Singh et al, 1990b; 1991; Sims et al., 1991). Further studies are required to establish the effects of the damage observed at the low dose on reproductive performance, although the higher doses used in these studies have been shown to affect circulating levels of reproductive hormones (Foster et al., 1992a; 1992b).
In contrast, the results of studies on a variety of species have indicated that repeated exposure to HCB can affect male reproduction, but only at relatively high doses (between 30 and 221 mg/kg b.w./day) [den Tonkelaar et al., 1978; Elissalde and Clark, 1979; Simon et al, 1979; Borzelleca and Carchman, 1982].
Placental and lactational transfer of HCB, demonstrated in a number of species, can adversely affect both the foetus and nursing offspring. Maternal doses in the range from 1.4 to 4 mg/kg to rats and cats have been hepatotoxic and/or affected the survival or growth of nursing offspring. In some cases, these or higher doses have reduced litter sizes and/or
17 Assessment Report increased numbers of stillbirths (Grant et al., 1977; Mendoza et al., 1977; 1978; 1979; Hansen et al, 1979; Kitchin et al., 1982; Arnold et al. 1985). Mink are particularly sensitive to the effects of prenatal and perinatal exposure to HCB; the offspring of mink fed diets containing concentrations as low as 1 ppm of HCB (approximately 0.16 mg/kg b.w./day) for 47 weeks (prior to mating and throughout gestation and nursing) had reduced birth weights and increased mortality (Rush et al., 1983; Bleavins et al., 1984b; Table 2.2).
Adverse effects on suckling infants (most often on the liver or pup survival) have generally been observed more frequently, and at lower doses, than effects resulting from in utero exposure to HCB (Mendoza et al, 1977; 1978; 1979; Kitchin et al, 1982; Arnold et al., 1985). However, Bleavins et al. (1984b) reported the results of a cross-fostering study with mink in which mortality to weaning was higher in kits exposed to HCB in utero than in those exposed through nursing.
The available data, although limited, indicate that HCB is not a potent developmental toxicant. The skeletal and renal abnormalities that have been reported in rats and mice exposed to HCB during gestation were not clearly related to treatment, or occurred at doses that were also maternally toxic (Khera, 1974; Courtney et al., 1976; Andrews and Courtney, 1986).
Immunotoxicity
The results of a number of studies have indicated that HCB affects the immune system. In rats or monkeys exposed to several mg HCB/kg b.w./day or more, histopathological effects in the thymus, spleen, lymph nodes, and/or lymphoid tissues of the lung have been observed (Kimbrough and Linder, 1974; latropoulos et al., 1976; Goldstein et al., 1978; Vos et al., 1979; Kitchin et al., 1982). GralIa et al. (1977) observed that chronic exposure to as little as 1 mg/day of HCB (equivalent to a dose at the start of the experiment of roughly 0.12 mg/kg b.w./day [ATSDR, 1990J) caused nodular hyperplasia of the gastric lymphoid tissue in beagle dogs (Table 2.2).
In a series of studies with Wistar rats summarized by Vos (1986), humoral immunity, and to a lesser extent cell-mediated immunity, were enhanced by several weeks exposure to HCB in diet, while macrophage function was unaltered. In these studies, the developing immune system was particularly sensitive to the effects of HCB. Rat pups that were exposed to 4 mg/kg of HCB in the maternal diet (approximately 0.2 mg/kg b.w./day [NIOSH, 1985]) during gestation, through nursing, and then in their own diet to 5 weeks of age had significant increases in humoral and cell-mediated immune responses, and accumulated macrophages in lung tissue (Vos et al., 1983; Table 2.2).
In contrast, HCB has been immunosuppressive in most studies with mice (Vos, 1986). Balb/C mice exposed to 5 mg HCB/kg diet (roughly 0.6 mg/kg b.w./day [NIOSH, 1985]) were more susceptible to Leishmania infection (Loose, 1982) and had reductions in resistance to a challenge with tumour cells and in the cytotoxic macrophage activity of the spleen (Loose et al., 1981) [Table 2.2]. Barnett et al. (1987) reported that the delayed-type hypersensitivity response was depressed in Balb/C mice exposed to HCB in utero (maternal dose of 0.5 mg/kg b.w./day) and through nursing (Table 2.2).
18 Hexachlorobenzene
2.4.2 Humans
More than 600 cases of a condition called porphyria cutanea tarda (PCT) were identified, primarily in children, following an accidental poisoning incident in Turkey between 1955 and 1959. Hexachlorobenzene-treated grain had been ground into flour and made into bread (Cam and Nigogosyan, 1963; Courtney, 1979; Peters et al., 1982; U.S. EPA, 1985; Gocmen et al., 1989). Clinical manifestations (primarily dermal lesions) and disturbances in porphyrin metabolism were associated with an estimated dose of 50-200 mg/day for a number of months (Cam and Nigogosyan, 1963). In addition, the infants of mothers who either had PCT or had eaten HCB-contaminated bread had a disorder called pembe yara ("pink sore"), involving cutaneous lesions and clinical symptoms; at least 95% of these children died within a year of birth. In 20- to 30-year follow-ups of exposed individuals, neurological, dermatological and orthopaedic abnormalities persisted, and there were elevated levels of porphyrins in excreta of some individuals (Gocmen et al., 1989).
There have been case reports of workers developing PCT as a result of direct contact with HCB (Gombos et al., 1969, in Currier et al., 1980; Mazzei and Mazzei, 1972, in Courtney, 1979), although there was no association between exposure to HCB and PCT in three cross-sectional studies of very small populations of exposed workers (Morley et al., 1973; Burns et al., 1974; Currier et al., 1980). There was no evidence of cutaneous porphyria in a cross-sectional study of the general population in Louisiana exposed to HCB through the transport and disposal of "hex" waste; however, plasma concentrations of HCB were significantly correlated with levels of coproporphyrin in urine and of lactic dehydrogenase in blood (Burns and Miller, 1975). Enriquez de Salamanca et al. (1990) have speculated that exposure to HCB could be responsible for annual variations in the incidence of PCT in Spain between 1977 and 1988, based on an association between the levels of HCB in human milk fat and adipose tissue and the numbers of cases of PCT reported annually.
Available data on the carcinogenicity of HCB in humans are restricted to one study of a cohort of magnesium metal production workers in Norway. Although the incidence of lung cancer was significantly elevated compared to that of the general population, workers were exposed to numerous other agents in addition to HCB (Heldaas et al., 1989).
2.4.3 Ecotoxicology
Data on the acute and chronic toxicity of hexachlorobenzene are available for species from a number of trophic levels, including protozoans, algae, invertebrates and fish, for both the freshwater and marine environments. For the terrestrial environment, toxicity data are available only for birds and mammals.
Since HCB is nearly insoluble in water (Section 2.1), and tends to partition from water to the atmosphere (Section 2.3.1), the substance disappears rapidly from open-test solutions. Hence, it is difficult to maintain test concentrations for a sufficient time to establish concentration-effects profiles for aquatic organisms. Further, HCB tends to bind to suspended solids in the water column and thus may not be bioavailable to test organisms. The discussion of the toxicity of HCB to aquatic organisms will therefore focus on tests conducted under flow-through conditions, static renewal conditions, or using closed vessels with minimal
19 Assessment Report
headspace. As well, no consideration has been given to tests in which HCB concentrations were well above the solubility limit of HCB in water of 5 µg/L at 250C.
Acute
Aquatic Biota
Of four freshwater algal species tested, only one, Chlorella pyrenoidosa, was affected by concentrations of HCB in water at or below its limit of aqueous solubility. Reduced production of chlorophyll, dry matter, carbohydrate and nitrogen was observed for C. pyrenoidosa after exposure to 1 µg/L HCB (unmeasured) for 46 hours in a static-closed system (Geike and Parasher, 1976a). A no-effect concentration (NOEC) was not determined in this study.
At concentrations equal to its aqueous solubility in water (5 µg/L), HCB was not lethal to the freshwater water flea, Daphnia magna, in a flow-through test in which concentrations of HCB were measured (Nebecker et al., 1989). In 96-hour flow-through tests on marine invertebrates, exposure to HCB caused 13% mortality in pink shrimp (Penaeus duorarum) at a measured concentration of 7 µg/L HCB, and 10% mortality in grass shrimp (Palaemonetes pugio) at 17 µg/L. The NOECs in these species were 2.3 µg/L and 6.1 µg/L, respectively (Parrish et al, 1974). In a static-closed system, there was a 10% reduction in reproduction of the ciliate protozoan, Euplotes vannus, after an exposure to 10 µg/L HCB (unmeasured) for 48 hours (Persoone and Uyttersprot, 1975).
The available data on freshwater fish species indicated no harmful effects at concentrations at or near the limit of solubility of HCB in water during acute exposures (Call et al., 1983; Ahmad et al., 1984). In the only available study for marine fish species, there were no harmful effects to sheepshead minnow (Cyprinodon variegatus) after a flow-through exposure to a measured concentration of 13 µg/L HCB for 96 hours (Parrish et al., 1974).
Limited data are available concerning the toxic effects of HCB in sediment to freshwater and marine biota. In a 96-hour sediment toxicity test on the marine shrimp, Crangon septemspinosa, no mortality was observed at the highest concentration of HCB tested, 300 µg/L wet weight (McLeese and Metcalfe , 1980).
Several studies have confirmed that there is a relatively constant body residue associated with acute lethality in freshwater fish, invertebrates and algae exposed to mono-through pentachlorobenzene (McCarty et al., 1992a and citations therein; Ikemoto et al., 1992). The acute LC50 critical body residue for chlorobenzenes is 2 µM/g wet weight, or 569.6 µg/g wet weight for HCB, assuming that HCB has the same mode of action as the other chlorobenzenes (McCarty et al., 1992b).
Terrestrial Biota
The LD50 for HCB in herring gull (Larus argentatus) embryos injected on day 4 and tallied on day 25 was 4.3 µg/g b.w. (Boersma et al, 1986). At a dose of 1.5 µg/g b.w., there were significant reductions in embryonic weight. Five-day LC50 values (i.e., 5 days of HCB- containing diet followed by 3 days of untreated diet) were 617 µg/g diet for 10-day-old
20 Hexachlorobenzene ring-necked pheasants (Phasianus colchicus) and > 5 000 µg/g diet for 5-day-old mallards (Anas platyrhynchos) [Hill et al., 1975]. Induction of porphyria has been observed in several short-term studies of Japanese quail following administration of 500 µg/g b.w./day HCB either in food or via intraperitoneal injection (Buhler and Carpenter, 1986; Lambrecht et al., 1988). The significance of porphyria to potential effects at the population level (e.g., lethality, reproductive impairment) is unknown. The acute and short-term toxicity of HCB to mammals are discussed in Section 2.4.1.
Long-term Aquatic Biota The growth of sensitive freshwater algae and protozoa is affected by concentrations of 1 µg/L HCB, while slightly higher concentrations (near the aqueous solubility of the compound) had effects on sensitive fish and invertebrates. Cultures of the alga Chlorella pyrenoidosa exhibited increased growth compared to controls after having been incubated for 3 months with a nominal concentration of 1 µg/L HCB (Geike and Parasher, 1976b), while growth of the protozoan, Tetrahymena pyriformis, was decreased after a 10-day exposure to a nominal concentration of 1 µg/L HCB (Geike and Parasher, 1976b). After an exposure to 5 µg/L HCB for 10 days in a static-renewal system, crayfish (Procambarus clarki) experienced an increase in damage to the hepatopancreas (Laseter et al., 1976). The fertility of Daphnia magna was reduced by 50% after an exposure for 14 days to a measured concentration of 16 µg/L HCB in a static-closed system (Calamari et al., 1983). Significantly increased mortality was observed after the amphipod, Gammarus lacustris, was exposed to a measured concentration of 3.3 µg/L HCB for 28 days under flow-through conditions (Nebecker et al., 1989); however, the results of this study indicated a weak-dose response relationship. The results of two other flow-through studies indicated no observed effects to survival, growth and reproduction of the amphipod, Hyallela azteca, and the worm, Lumbriculus variegatus, at a measured concentration of 4.7 µg/L HCB (Nebecker et al., 1989). Fathead minnows (Pimephales promelas) and rainbow trout (Oncorhynchus mykiss) were not adversely affected by exposure to levels of HCB approaching its aqueous solubility (Ahmad et al., 1984; Carlson and Kosian, 1987; Nebecker et al., 1989; U.S. EPA, 1988). After an exposure for 10 days to 3.5 µg/L of HCB under flow-through conditions, however, large-mouth bass (Micropterus salmoides) had liver necrosis (Laseter et al, 1976). No acceptable long-term toxicity data for HCB were found for marine algae, invertebrates or fish. There are no data from sediment toxicity tests available for HCB. A number of jurisdictions have, however, developed approaches to estimate the levels at which HCB in sediment will have effects on benthic organisms, based on correlations between benthic community composition and HCB sediment concentrations in field samples. Persaud et al. (1991) applied the Ontario Screening Level Concentration Approach to data from the Great Lakes and estimated a lowest-effect level for HCB of 20 ng/g sediment (dry weight, normalized to 1% total organic carbon content). The authors also estimated that benthic communities would be seriously impacted at sediment concentrations of 240 ng/g HCB dry
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weight and higher. For marine sediments, a similar approach, known as the Apparent Effects Threshold (AET) approach, was used to estimate the sediment concentration of HCB above which significant effects to benthic community composition are expected (Tetra Tech Inc., 1986). The marine sediment AET for HCB was estimated to be 3.8 ng/g dry weight (normalized to 1% total organic carbon content) on the basis of co-occurrence data collected from Puget Sound, Washington (Washington State Department of Ecology, 1990).
Quantitative structure-activity relationships (QSAR) have also been used to determine the sediment HCB level at which 95% of species in the freshwater community are unlikely to be affected (Van Leeuwen et al., 1992). The QSAR-derived level for HCB was 5 814 ng/g dry weight (20.4 nM/g in the reference) for sediments with 5% total organic carbon content. The adjusted level for sediment with 1% total organic carbon content (i.e., ÷ 5) is 1 163 ng/g, which is 58 times higher than the estimated lowest-effect level, based on the co-occurrence data described above.
The critical body residue for aquatic biota after a chronic exposure to chlorobenzene substances is approximately 0.2 µM/g wet weight, based on a limited data set for mono-through pentachlorobenzene (McCarty, 1986). If these data are applicable to HCB, the critical body residue after a chronic exposure would be 57.0 µg/g wet weight.
Terrestrial Biota
In adult Japanese quail (Coturnix japonica) fed diets containing HCB for 90 days, mortality was increased at 100 µg/g wet weight HCB in diet, and hatchability of eggs was significantly reduced at 20 µg/g HCB (Vos et al., 1971; 1972). At 5 µg/g HCB, increased liver weight, slight liver damage and increased fecal excretion of coproporphyrin were observed. The significance of these effects to those at the population level in the field is unknown. Eurasian kestrels (Falco tinnunculus) fed 50 and 200 µg/g wet weight of HCB in contaminated mice for 65 days had significant weight loss, ruffling of feathers, tremors, increased liver weight and decreased heart weight at the higher dose (Vos et al., 1972). The available long-term toxicity data for mammals are discussed in Section 2.4.1.
22 Hexachlorobenzene
3.0 Assessment of "Toxic" under CEPA
Hexachlorobenzene is not used commercially in Canada, but is released to the Canadian environment as a by-product from the manufacture and use of chlorinated solvents and pesticides, through long-range transport and deposition, and in emissions from incinerators and other industrial processes. This entry results in measurable concentrations of HCB in the various media to which humans and other organisms may be exposed.
3.1 CEPA 11(a): Environment
HCB is a persistent substance that has been dispersed throughout the Canadian environment. HCB accumulates in aquatic sediments and also biomagnifies, suggesting that benthic biota and those at higher trophic levels (e.g., predatory birds and fish-eating mammals) are the most likely to be exposed to high concentrations of this substance.
Mink (Mustela vison) are opportunistic carnivores, with aquatic organisms comprising up to 100% of their diet. Based on the data presented in Table 3.1, the potential total daily intake of HCB by mink in the St. Clair River area is estimated to be 36 509 ng/kg b.w./day. Reproductive impairment of mink exposed to HCB in their diet was shown to occur at 210 000 ng/kg b.w./day (Bleavins et al, 1984b), assuming that a 1 kg mink eats 210 grams of food per day in the wild with an HCB content of 1 000 ng/g. This value was divided by 10 in order to convert this effect level to a no-effects level and to account for differences between laboratory and field conditions. This results in a tolerable daily intake (TDI) of 21 000 ng/kg b.w./day for mink. The total daily intake calculated for mink in the St. Clair River area (36 509 ng/kg b.w./day) exceeds the TDI and therefore HCB has the potential to cause harmful effects to mink and possibly other fish- eating mammals in the St. Clair River area.
Table 3.1 - Estimated Total Daily Intake of HCB for a 1 Kg Adult Mink in the St, Clair River Area
a b Medium Concentration Intake of Medium Daily Intake Air 0.15 ng HCB/m3 0.55 m3/day 0.0825 ng/kg b.w./day Water 87 ng/L 0.1 L/day 8.7 ng/kg b.w./day Fish 231 ng/g 158 g/day 36 500 ng/kg b.w./day
TOTAL ______36 509 ng/kg b.w./day
a Air concentration from Environment Canada (1990; 1991c), water concentration from Oliver and Kaiser (1986), and fish tissue concentration from Suns et al. (1983) b Rate of consumption data for air from Stahl (1967), for water from Calder and Braun (1983), and for fish from Nagy (1987), with additional assumption that fish comprise 75% of mink diet
Injection studies in eggs have shown that tissue levels of 1 500 ng/g HCB wet weight caused reduced embryo weights in herring gulls [Larus argentatus] (Boersma et al, 1986). For many bird species, reduced embryo weights are associated with lower survival of chicks,
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although the severity of this effect on populations in the field cannot be determined. The effects level was divided by a factor of 10 in order to derive a no-effects level and to account for potential differences in species sensitivity and laboratory versus field conditions. Therefore, the no-effects level for HCB in tissues of sensitive bird species is estimated to be 150 ng/g wet weight. HCB concentrations in peregrine falcon eggs (Falco peregrinus anatum) collected between 1980 and 1987 across Canada had a mean concentration of 279 ng/g wet weight. HCB has the potential, therefore, to cause harmful effects to egg embryos of peregrine falcons in Canada. The potential for effects to peregrine falcons from exposure to HCB is considered to be a serious threat to the long-term survival of this species, given its current status as an endangered species in Canada. The levels of HCB observed in eggs of most other bird species [e.g., herring gulls, common murre (Uria aalge), northern gannet (Sula bassana)] in Canada indicate that harmful effects to these species are less likely.
The available information suggests that the lowest-observed-effect level for HCB in freshwater sediments (normalized to 1% total organic carbon content) lies between 20 and 1 163 ng/g dry weight. No additional information is available to further refine this estimate. Similarly, the estimated LOEL for HCB in fish tissues (57 µg/g wet weight) is based on limited toxicity testing that did not include HCB. Therefore, the available data are considered inadequate to assess whether HCB is "toxic" to benthic organisms or bottom-feeding fish.
Conclusion
On the basis of the available data on levels of hexachlorobenzene in Canadian air, water and forage fish, and the potential effects of exposure at these levels on predatory birds and fish-eating mammals, HCB is considered to be "toxic" as interpreted under paragraph 11(a) of CEPA.
3.2 CEPA 11(b): Environment on Which Human Life Depends
Hexachlorobenzene absorbs infrared light at several wavelengths (7, 13 and 14 µm) characteristic of trace gases associated with global warming. Substances that absorb strongly between 7 and 13 µm act to absorb thermal radiation from the Earth's surface that would
otherwise escape into space. HCB is, however, removed from the troposphere by photolysis (t1/2 ˜ 80 days) and deposition to soil and water, and thus current levels of HCB in the atmosphere are low (< 0.2 ng/m3). HCB is, therefore, unlikely to have a significant impact on global warming.
In general, substances such as HCB with tropospheric sinks or removal processes (e.g., photolysis, deposition to soil or water) are not transported to the stratosphere. These processes, combined with the low levels of HCB in the troposphere, indicate that little, if any, HCB is expected to reach the stratosphere. HCB is, therefore, unlikely to be associated with stratospheric ozone depletion.
Conclusion
Therefore, on the basis of available data, hexachlorobenzene is not considered to be "toxic" as interpreted under paragraph 11(b) of CEPA.
24 Hexachlorobenzene
3.3 CEPA 11(c): Human Life or Health
Population Exposure
Based on the most representative concentrations of HCB in air, water, food and soil presented in Section 2, and standard values for body weights and intakes of these environmental media, the mean daily intakes of HCB have been estimated for various age classes of the general population (Table 3.2). In addition, estimates have been made for more highly exposed subgroups of the population, including recreational fishermen who consume salmonids from Lake Ontario, and Inuit from the high Arctic who consume large quantities of marine mammals. Exposure of populations in the vicinity of industrial sources may also be greater than that for the general population, but the available data were considered inadequate as a basis for quantitative estimation. Since intakes vary considerably during the course of the lifespan and the critical toxicological effect is associated with long-term exposure to HCB, estimates of the average daily intake of HCB over a lifetime have also been calculated based on these age-specific intakes.
Table 3.2 - Estimated Intakes of Hexachlorobenzene (ng/kg b.w./day) for the Canadian General Population
Medium 0-6 moa 7 mo-4 yrb 5-11 yrc 12-19 yrd 20+ yre Airf 0.04 0.06 0.07 0.06 0.05 Drinking waterg 0i 0.006 0.003 0.002 0.002 Soilh 0.004 0.003 0.001 0.0003 0.0002 Foodj 214.3 i 17.7 9.8 4.8 2.7 TOTALk 214.3 17.8 9.9 4.8 2.8
aAssumed to weigh 7 kg, breathe 2 m3 of air, and ingest 35 mg of soil per day (EHD, 1992) bAssumed to weigh 13 kg, breathe 5 m3 of air, drink 0.8 L of water and ingest 50 mg of soil per day (EHD. 1992) cAssumed to weigh 27 kg, breathe 12 m3 of air, drink 0.9 L of water and ingest 35 mg of soil per day (EHD, 1992) dAssumed to weigh 57 kg, breathe 21 m3 of air, drink 1.3 L of water and ingest 20 mg of soil per day (EHD, 1992) eAssumed to weigh 70 kg, breathe 23 m3 of air, drink 1.5 L of water and ingest 20 mg of toil per day (EHD, 1992) fIntakes via air based on mean airborne concentrations (0.15 ng/m3) reported by Environment Canada (1990; 1991c) for both Walpole Island and Windsor sites; in absence of data on indoor air, assumed equal to ambient gIntakes via drinking water based on mean concentration (0.1 ng/L) for three Lake Ontario cities reported by Oliver and Nicol (1982) hIntakes via soil based on levels in B.C. agricultural soils treated 10-15 years prior with HCB cereal seed treatments (Wilson and Wan, 1982). Estimated mean soil concentration is 0.8 ng/g (assume mean concentration in soils with detectable HCB (6/24) is as midpoint of reported range (1.75 ng/g), and sites with no detectable HCB had mean concentration of one-half of the EOD of 1 ng/g, or 0.5 ng/g) iAssumed that infant is exclusively breast-.fed for first six months. Drinking water intake is assumed to be zero. as "exclusively breast-fed infants do not require supplementary liquids". Estimated intake via breast milk based on mean HCB concentration from 1982 Health and Welfare Canada survey (2 ppb, whole milk basis; Mes et al., 1986), breast milk consumption of 750 ml per day and body weight of 7 kg jIntakes via food estimated based on the concentrations of HCB reported by Davis (1988) for 2% milk (0.16 ng/g), fresh meat and eggs (0.17 ng/g), leafy above-ground vegetables (0.02 ng/g), root vegetables (0.04 ng/g), and fruit (0.005 ng/g = one-half LOD); by Gunderson (undated) for cheese (0.90 ng/g), cottage cheese (0.10 ng/g), processed cheddar (0.70 ng/g), butter (2.40), marine fish (0.20 ng/g), peanuts and peanut butter (3.10 ng/g), canned fish, shellfish, soups, grain-based foods, foods primarily sugar, fats and oils (all ND, use 0.05 ng/g = one-.half LOD); data for freshwater fish (1.10 ng/g) are average for all species monitored by Sport Fish Contaminant Monitoring Program (Cox, personal communication) from Crest Lakes other than Lake Ontario, and from several other major recreational Ontario lakes, assuming that ND are 0.5 ng/g (= one-half LOD). The concentration of HCB in each food has been multiplied by its consumption in the Nutrition Canada Survey for each age class (EHD, 1992). kTotal may not equal sum of medium-specific intakes, because of rounding off
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Virtually all (>98%) of the estimated intake of HCB by members of the Canadian general population is via food (Table 3.2), primarily through such dairy products as milk, butter and ice cream, and to a lesser extent through fresh meat and eggs and peanuts/peanut butter. HCB accumulates in breast milk, and the estimated intake for breast-fed infants is greater than in other age groups of the general population. Mean intakes of HCB by the Canadian general population are estimated to range from 214 ng/kg b.w./day for breast-fed infants to 2.8 ng/kg b.w./day for adults. Assuming a 70-year lifespan, the daily intake of HCB for members of the general population averaged over a lifetime is estimated to be 6.2 ng/kg b.w./day.
Although judged to be the best available, the monitoring data on which the estimated intakes are based are relatively limited. In particular, the intakes through most dairy products have been derived from levels of HCB in milk from a single study, and data on the remainder of dairy products are from the U.S. Total Diet Study. In addition, no data on HCB concentrations in indoor air were identified. These estimated intakes are based on mean concentrations in the general environment. Elevated levels of HCB present in ground water, for example, as a result of leaching from landfill sites were not considered relevant to estimation of exposure for the general population.
Sport fishermen who consume their catch from Lake Ontario, the Great Lake with the highest concentrations of HCB in fish tissues (Section 2.3.2), would be expected to have some of the highest intakes among recreational anglers. The mean consumption of Lake Ontario salmonids by fishermen responding to a questionnaire circulated in conjunction with the Toronto Star Great Salmon Hunt was 14.24 g/person/day (Cox and Johnson, 1990). Based on the mean concentrations in muscle for salmonid species reported by Niimi and Oliver (1989) [12 ng/g for chinook salmon; assume same for coho; 11 ng/g for rainbow trout; 10 ng/g for brown trout; and 37 ng/g for lake trout], weighted by the frequency of consumption for these species reported by Cox and Johnson (1990) [71.0%; 64.9%; 90.5%; 50.0%; and 9.4%,. Respectively], the mean concentration of HCB in fish muscle consumed by these respondents is estimated to be 12.2 ng/g wet weight. Assuming a 70 kg body weight, the intake via these fish would be 25 ng/kg b.w./day. In combination with the 2.8 ng/kg b.w./day received on average from other sources (Table 3.2), the total calculated intake for people who consume salmonid species from Lake Ontario is estimated to be 5.3 ng/kg b.w./day. This is almost twice the intake of adults from the general population. Assuming that the intake of HCB for age classes other than adults is the same as for the general population, the total daily intake for these recreational fishermen averaged over a 70- year lifespan is estimated to be 8.0 ng/kg b.w./day.
Intakes of HCB by people consuming large quantities of Inuit food were estimated using data from a study of residents of an isolated island community on the east coast of Baffin Island (Kinloch et al, 1992; Muir et al, 1988b; Kuhnlein, 1989). The primary source of food in this community is subsistence hunting and fishing. Marine mammals, which accumulate relatively high body burdens of lipophilic contaminants such as HCB (Section 2.3.2), are consumed in large quantities. The calculated intake includes only those species that were consumed in the largest quantities (seal, caribou, narwhal and fish, which comprised 90% of Inuit food intake) and those food types that had greater than 1% frequency of mention across all surveys in the study (Kuhnlein, 1989). Based on the reported intake of Inuit food by all consumers (Kinloch et al., 1992), and assuming a 1:1 sex ratio, it is estimated that 320.3 g of meat, 53.1 g of mattak, 42.5 g of fish, 32.5 g of fat and 24.3 g of blubber were consumed on average per person/day. The mean concentrations of HCB in these food groups, derived from
26 Hexachlorobenzene
the individual food types determined by Muir et al. (1988b), are calculated to be 2.9 ng/g, 20.3 ng/g, 2.1 ng/g, 21.8 ng/g, and 119.5 ng/g, wet weight, respectively. Based on an assumed body weight of 62 kg for Inuit (calculated from values in NHW, 1980, assuming a 1:1 sex ratio), the mean intake for adult consumers of Inuit food in this community is calculated to be 92 ng/kg b.w./day. Roughly one-half of this intake is consumed in blubber, with significant contributions from meat, mattak (skin) and fat. Although this intake of HCB was calculated for adults, it has been assumed to approximate the exposure over the total lifespan. While younger study participants had a lower consumption of Inuit foods than adults, a number of other minor pathways of exposure are not included in this estimate, and adulthood comprises the majority of the lifespan.
Effects
Potentially, the most sensitive end-point for assessment of whether or not HCB is toxic" under paragraph 11(c) of CEPA is carcinogenicity. Hence, the initial step in evaluation of whether or not HCB is "toxic" under paragraph 11(c) of CEPA is an assessment of the weight of evidence for carcinogenicity, an effect for which it is generally believed there is no threshold.
The available information is inadequate to assess the carcinogenicity of HCB in humans. No neoplasms have been reported in long-term follow-up studies of a population accidentally poisoned in Turkey between 1955 and 1959 as a result of HCB-treated wheat grain being ground into flour and made into bread (Peters et al., 1982; Cripps et al., 1984; Gocmen et al., 1989). These follow-up studies included only small numbers of individuals, however, and were not designed specifically to assess neoplastic end-points. Other epidemiological studies relevant to the carcinogenicity of HCB are limited to a single report of an increased incidence of lung cancer in a cohort of magnesium workers exposed to HCB and numerous other substances (Heldaas et al, 1989).
In the four carcinogenesis bioassays of adequate design, HCB has been tumourigenic in three species of rodents, inducing several tumour types rarely observed in control animals. Thus, administration of HCB in the diet (the principal source of exposure of humans) produced hepatomas in hamsters (Cabral et al., 1977), mice (Cabral et al., 1979) and rats (Arnold et al., 1985; Lambrecht et a/., 1983a). (The incidence of hepatomas in the control groups in all of these studies was zero.) In addition, there were increases in adenomas of the thyroid in hamsters (Cabral et al., 1977) and tumours of the kidney, bile duct (Lambrecht et al., 1983a; 1983b; Ertürk et al., 1986), parathyroid (Arnold et al., 1985) and adrenal glands (Arnold et al., 1985; data from Lambrecht et al. study reported by Peters et al., 1983, in U.S. EPA, 1985) in rats. In two of the critical bioassays, there was a dose-response relationship between exposure to HCB and tumour incidence (Cabral et al., 1977; Lambrecht et al., 1983a; 1983b), and in the other two there was a significant increase at the highest dose (Cabral et al., 1979; Arnold et al., 1985). Moreover, in two of the studies, there were dose-related trends in tumour latency and multiplicity (Cabral et al., 1977; Cabral et al., 1979). In some of the studies, increases in tumour incidence were observed at doses that were not clearly toxic in other respects (Cabral et al., 1977; Lambrecht et al., 1983a; 1983b; Ertürk et al., 1986), although effects on body weight gain and survival were inadequately reported in two of the bioassays (Cabral et al, 1977; Cabral et al., 1979).
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Although the majority of neoplasms observed in these bioassays was benign, there were also excesses of some malignant tumours. Significant increases in hepatocellular carcinomas in rats were observed (Lambrecht et al., 1983a; Ertürk et al., 1986). In addition, there were other malignant tumours which, while evidently not significantly increased, were only observed in exposed animals, including bile duct carcinomas (Lambrecht et al., 1983a; Ertürk et al., 1986), and renal cell carcinomas (Lambrecht et al., 1983b; Ertürk et al., 1986). Lambrecht et al. (1983b) also reported a generalized leukemia involving the thymus, spleen, liver, and kidney in HCB-exposed rats, although they did not present any quantitative data. Cabral et al. (1977) also reported metastases of three of the "haemangioendotheliomas" (which are, by definition, benign) observed in hamsters. It seems likely, therefore, that these tumours were malignant, though misclassified.
The results of some more limited assays have confirmed the neoplastic effects of HCB. High incidences of liver tumours have been reported in studies in which single dietary concentrations were administered to very small groups of females of three strains of rats (Smith and Cabral, 1980; Smith et al., 1985); in one strain (Fischer 344), hepatocellular carcinomas were observed (Smith et al, 1985). Moreover, Lambrecht et al. (1982a; 1982b; Ertürk et al., 1982; 1986) reported that following dietary exposure to HCB for more limited periods (i.e., 90 days, with serial sacrifices every 6 weeks thereafter), mice, hamsters and rats developed tumours in the liver, bile duct, kidney, thymus, spleen and lymph nodes. Although the information provided in the summary accounts of these studies was inadequate for evaluation, results showing dose-related increases in thymic, splenic and nodal lymphosarcomas were reported for male and female mice (Ertürk et al., 1982). Lymphatic and renal neoplasms were observed as early as the end of the 90-day exposure period.
Bouthillier et al. (1991) presented the results of studies of Sprague-Dawley rats exposed to HCB by gavage for periods of several weeks, which indicated that the observed increase in renal tumours in male Sprague-Dawley rats following exposure to HCB (Lambrecht et al., 1983b; Ertürk et al., 1986) is related to protein droplet nephropathy. The mechanism by which structurally diverse hydrocarbons induce hyaline droplet nephropathy in male rats has been well documented and involves accumulation of alpha-2-u-globulin, resulting in necrosis, regeneration and, in some cases, tumours. This response is sex- and species-specific, and hence is unlikely to be relevant to humans. This mechanism does not, however, explain the increased (but lower) incidence of renal tumours in females also reported by Lambrecht et al (1983b). In addition, mechanistic studies that address the relevance to humans of the remaining tumour types induced in rodents by HCB have not been identified.
Thus, HCB has induced tumours, some of which were malignant and several of which occurred at dietary concentrations that were not overtly toxic in other respects, at multiple sites in three species of rodents following administration for a large proportion of the lifespan. In addition, although information in the published accounts was insufficient for evaluation, tumours (some of which were malignant) have been observed in rodents following exposures for much shorter periods (i.e., 90-day).
Based on these considerations, HCB is classified in Group II (probably carcinogenic to man) of the classification scheme developed by the Bureau of Chemical Hazards for use in the derivation of the "Guidelines for Canadian Drinking Water Quality" (NHW, 1989).
28 Hexachlorobenzene
Although data on the mechanism of induction of most tumours by HCB are lacking, it is possible that the compound may induce tumours through an epigenetic mechanism. HCB has not been genotoxic in in vitro and in vivo assays of a range of genetic end-points (Section 2.4.1), and acts as a promoter in in vivo assays (Smith et al., 1989; Stewart et al, 1989). (It should be noted, however, that the pattern of tumour development in carcinogenicity bioassays for HCB is not entirely similar to that of other epigenetic carcinogens.) Carcinogens that act by an epigenetic mechanism are generally classified in Group IIIB (possibly carcinogenic to humans) of the classification scheme developed for use in the derivation of the "Guidelines for Canadian Drinking Water Quality" (NHW, 1989). For substances in this group, a tolerable daily intake (TDI) is derived on the basis of a no- or lowest-observed-(adverse)-effect level (NO[A]EL or LO[A]EL) in humans or animal species divided by an uncertainty factor which, when considered appropriate, takes into account the evidence of carcinogenicity. Although available information on the mechanisms of induction of tumours by HCB is insufficient to classify it in this category, even if such an approach were adopted, the estimated mean lifetime exposure of some subgroups of the population would exceed a TDI derived on the basis of data on non-neoplastic effects.
For non-neoplastic effects, the lowest reported NOELs and LOELs for severaldifferent types of effects, such as those on the liver, calcium metabolism, ovarian morphology, immune function and perinatal survival, fall within a very small range (Table 2.2). The lowest NOELs compiled in this table range from 0.05 to 0.07 mg/kg b.w/day and the lowest LOELs range from 0.1 to 0.7 mg/kg b.w./day. Based on the lowest reported NOELs included in the table [0.05 mg/kg b.w./day based primarily on hepatic effects in two species observed at higher doses (den Tonkelaar et al., 1978; Arnold et al, 1985; Mollenhauer et al., 1975; 1976)], a TDI of 50 ng/kg b.w./day could be derived, based on incorporation of an uncertainty factor of 1 000 (x 10 for intraspecies variation; x 10 for interspecies variation; x 10 for evidence of carcinogenicity). This value is less than the estimated mean lifetime exposure of some subgroups in the population.
For substances classified in Group II, where data permit, quantitative estimates of carcinogenic potency, expressed as the dose that induces a 5% increase in the incidence of relevant tumours (TD0.05) are compared to the estimated total daily intake in order to characterize risk and provide guidance for further action (i.e., analysis of options to reduce exposure).
There are four carcinogenesis bioassays with HCB that are of adequate design. These are studies in which adequate numbers of hamsters (Cabral et al., 1977), mice (Cabral et al., 1979), and rats (Arnold et al., 1985; Lambrecht et al., 1983a; 1983b; Ertürk et al., 1986) were exposed for a large proportion of the lifespan to several concentrations of HCB in the diet. The study by Arnold et al. (1985) has been selected for the purpose of estimating the carcinogenic potency of HCB, owing to the increased sensitivity and relevance to the nature of exposure of humans of the design of this study, which involved dietary exposure to relatively low concentrations of HCB in diet over two generations (including in utero and lactational exposure). Moreover, tumour pathology was inadequately reported in the studies in hamsters and mice conducted by Cabral et al. (1977) and Cabral et al. (1979), respectively, and there is some concern that in the study conducted by Lambrecht et al. (1983a; 1983b; Ertürk et al., 1986), rats may also have been exposed to some HCB (which was incorporated in diet as a powder) by inhalation.
29 Assessment Report
The estimates of carcinogenic potency of HCB derived from the results of the study by Arnold et al. (1985) are based on the multistage model. The tumour incidences in the pups were analyzed in the same manner as data from a single-generation study, due to the lack of information on individual litters. Owing to the lack of information about the extent of metabolism to unidentified active metabolite(s) and the possible role of such metabolites in carcinogenicity, a surface area to body weight correction was incorporated. The TD0.05 values calculated in this manner from the results of the study in rats by Arnold et al. (1985) range from 0.06 mg/kg b.w./day for hepatic neoplastic nodules in females to 0.17 mg/kg b.w./day for parathyroid adenomas in males.
The exposure/carcinogenic potency indices (EPI) have been calculated on the basis of the results of the study by Arnold et al. (1985) and the estimated total daily intake, averaged over a lifetime, by the general population of Canada and by high-exposure subpopulations. The indices for the general population in Canada range from 3.6 x l0-5 to 1.0 x l0-4 (6.2 x l0-6 mg/kg b.w./day ÷ 0.06-0.17 mg/kg b.w./day). The corresponding values for recreational fishermen consuming salmonids from Lake Ontario range from 4.7 x 10-5 to 1.3 x 10-4 (8.0 x 10-6 mg/kg b.w./day ÷ 0.06-0.17 mg/kg b.w./day), and those for people consuming large quantities of Inuit food range from 5.4 x 10-4 to 1.5 x l0-3 (92 x 10-6 mg/kg b.w/day ÷ 0.06-0.17 mg/kg b.w./day). Based on these EPIs, the priority for further action (i.e., analysis of options to reduce exposure) is considered to be moderate to high.
Conclusion
Substances classified in Groups I and II on the basis of the weight of evidence of carcinogenicity are considered non-threshold toxicants, substances for which there is some probability of harm for the critical effect at any level of exposure. Hexachlorobenzene is, therefore, considered to be "toxic" as interpreted under paragraph 11(c) of CEPA.
This approach is consistent with the objective that exposure to non-threshold toxicants should be reduced wherever possible and obviates the need to establish an arbitrary de minimis level of risk for determination of "toxic" under the Act.
3.4 Overall Conclusion
The data presented in this section indicate that hexachlorobenzene, at the concentrations found in Canada, has potential to cause adverse effects on the environment and on human life or health. Therefore, HCB is considered to be "toxic" as interpreted under paragraphs 11(a) and 11(c) of CEPA.
30 Hexachlorobenzene
4.0 Recommendations for Research and Evaluation
Although several data gaps have been identified in conducting this assessment, these data are not considered to be critical to the determination of "toxic" under CEPA, and the priority for the research recommended below is considered to be low.
1. Since no sediment toxicity bioassays have been conducted for hexachlorobenzene, studies to determine the effects of HCB on benthic organisms at environmentally relevant concentrations in sediment are desirable.
2. Since limited data were available to estimate food chain biomagnification in the St. Clair River system, a modelling and field validation exercise to estimate tissue residue levels at each trophic level in this system is desirable. The results of this exercise would be useful in conducting a more rigorous assessment of the potential effects of HCB on piscivorous birds and mammals in the St. Clair River.
3. In order to ascertain the relevance of the neoplasms observed in animals exposed to HCB to humans, additional data on the mechanisms of induction of these tumours in animal species by HCB are desirable.
31 Assessment Report
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Theiss, J.C., G.D. Stoner, M.B. Shimkin, and E.K. Weisburger. 1977. Test for carcinogenicity of organic contaminants of United States drinking waters by pulmonary tumor response in Strain A mice. Cancer Res. 37: 2717-2720.
Tobin, P.1986. Known and potential sources of hexachlorobenzene. In: C.R. Morris, and J.R.P. Cabrai, eds. Hexachlorobenzene: Proceedings of an International Symposium. International Agency for Research on Cancer, IARC Scientific Publications No.77, Lyon, France. 3-11.
Tuttle, J.R. 1979. A survey of the sources, uses and environmental distribution of hexachlorobenzene in Alberta, Saskatchewan, Manitoba and the Northwest Territories. Environmental Protection Service, Environment Canada, Edmonton, Alberta.
UGLCCSMC (Upper Great Lakes Connecting Channels Study Management Committee). 1988. Upper Great Lakes Connecting Channels Study. Environment Canada, U.S. Environmental Protection Agency, Michigan Department of Natural Resources, and Ontario Ministry of the Environment.
50 Hexachlorobenzene
U.S. EPA (U.S. Environmental Protection Agency). 1985. Health Assessment Document for Chlorinated Benzenes. Office of Health and Environmental Assessment, Washington, D.C., U.S. Environmental Protection Agency (EPA/60018-8410 1 SF).
U.S. EPA (U.S. Environmental Protection Agency) 1988. Draft. Ambient Aquatic Life Water Quality Criteria for Hexachlorobenzene. Office of Research and Development, Duluth, Minnesota, U.S. Environmental Protection Agency.
Van Leeuwen, C.J., P.T.J. Van Der Zandt, T. Aldenberg, H.J.M. Verhaar, and J.L.M. Hermans. 1992. Application of QSARs, extrapolation and equilibrium partitioning in aquatic effects assessment. I. Narcotic industrial pollutants. Environ. Toxicol. Chem. 11: 267-282. van Ommen, B., and P.1. van Bladeren. 1989. Possible reactive intermediates in the oxidative biotransformation of hexachlorobenzene. Drug Metab. Drug Interact. 7: 213-243.
Villenueva, E.C., R.W. Jennings, V.W. Burse, and R.D. Kimbrough. 1974. Evidence of chlorodibenzo-p-dioxin and chlorodibenzofuran in hexachlorobenzene. J. Agr. Food Chem. 22: 916-917.
Vos, J.G. 1986. Immunotoxicity of hexachlorobenzene. In: C.R. Morris, and J.R.P. Cabral, eds. Hexachlorobenzene: Proceedings of an International Symposium. International Agency for Research on Cancer, IARC Scientific Publications No.77, Lyon, France. 347-356.
Vos, J.G., H.L. Van Der Maas, A. Musch, and E. Ram. 1971. Toxicity of hexachlorobenzene in Japanese quail with special reference to porphyria, liver damage, reproduction and tissue residues. Toxicol. Appl. Pharmacol. 18: 944-957.
Vos, J.G., P.F. Botterweg, J.J.T.W.A. Strik, and J.H. Koeman. 1972. Experimental studies with HCB in birds. TNO-Nieuws 27: 599-603.
Vos, J.G., M.J. van Logten, J.G. Kreeftenberg, and W. Kruizinga. 1979. Hexachlorobenzene- induced stimulation of the humoral immune response in rats. Ann. N.Y. Acad. Sci. 320: 535-550.
Vos, J.G., G.M.J. Brouwer, F.X.R. van Leeuwen, and Sj. Wagenaar. 1983. Toxicity of hexa- chlorobenzene in the rat following combined pre- and post-natal exposure: comparison of effects on the immune system, liver and lung. In: D.V. Parke, G.G. Gibson, and R.Hubbard, eds. Immunotoxicology, Academic Press, London, p.219-235.
Vos, R.M.E., M.C. Snoek, W.J.H. van Berkel, F. Müller, and P.1. van Bladeren. 1988. Differ- ential induction of rat hepatic glutathione 5-transferase isoenzymes by hexachlorobenzene and benzyl isothiocyanate: comparison with induction by phenobarbital and 3-methyl-cholanthrene. Biochem. Pharmacol. 37: 1077-1082.
Wada, O., Y. Yano, G. Urata, and K. Nakao. 1968. Behavior of hepatic microsomal cyto- chromes after treatment of mice with drugs known to disturb porphyrin metabolism in liver. Biochem. Pharmacol. 17: 595-603.
51 Assessment Report
Washington State Department of Ecology. 1990. Proposed sediment management standards rule (September 18, 1990). Washington State Register. Issue 90-19.
Wilson, D.M., and M.T.K. Wan. 1982. Hexachlorobenzene - Industrial and Agricultural Sources in British Columbia. Environmental Protection Service, Environment Canada, Vancouver. Regional Program Report: 82-07.
52 EPS 2/CC/3E Chemicals Evaluation Division Commercial Chemicals Evaluation Branch Environment Canada
ENVIRONMENTAL
PROTECTION
SERIES
Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act
Guidance Manual Version 1.0 — March 1997
Environment Environnement Canada Canada
Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act
Guidance Manual Version 1.0 March 1997
GuidanceGuidance 9797
EPS/2/CC/3E Chemicals Evaluation Division Commercial Chemicals Evaluation Branch Environment Canada Canadian Cataloguing in Publication DatDataa
Main entry under title :
Environmental assessments of priority substances under the Canadian Environmental Protection Act : guidance manual-interim
(Report ; EPS 2/CC/3E) Includes bibligraphical references. ISBN 0-662-25403-1 Cat. no. En49-2/2-3E
1. Environmental monitoring — Canada — Handbooks, manuals, etc. 2. Pollution — Canada — Measurement — Handbooks, manuals, etc. I. Canada. Chemicals Evaluation Division. II. Canada. Environment Canada. III. Series: Report (Canada. Environment Canada) ; EPS 2/CC/3E.
TD193.5E58 1997 363.7’063’0971 C97-980047-1 Readers Comments
Comments on the content of this report may be addressed to:
Ken Taylor Chemicals Evaluation Division Commercial Chemicals Evaluation Branch Environmental Protection Service Environment Canada Hull, Quebec K1A 0H3
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The contents of this report have been reviewed by the Chemicals Evaluation Division, Environment Canada and approved for publication. Mention of trade names or commercial products does not constitute recommendation or endorsement for use.
iii Preface
This manual provides guidance for conducting environmental assessments of priority substances in Canada. It was developed by the Chemicals Evaluation Division, Commercial Chemicals Evaluation Branch, Environment Canada, to update the unpublished document Draft Guidelines for Conducting Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act, April 1992. This revision is based on experience gained from assessing substances on the first Priority Substances List and also reflects recent advances in the field of ecological risk assessment. This guidance manual has been extensively reviewed by numerous experts from other government departments, industry, academia, and nongovernmental and international organizations.
The intended audience for this manual is the assessors leading the environmental assessments of priority substances and the groups of experts who will assist them. The secondary audience is those interested parties who wish to gain insight into how Environment Canada conducts environmental assessments of priority substances.
This guidance manual represents the experience gained by the Priority Substances Assessment Program at this time and the current scientific understanding of ecological risk assessment. As more experience is gained during application of the guidance in assessments of substances on the second Priority Substances List, and as the science of ecological risk assessment becomes more developed, the guidance manual will be updated to reflect that experience and knowledge. The manual is intended to provide guidance only, not strict rules, to allow for the flexibility required to assess different types of substances and for developments in experience and science.
This manual is published in both English and French and is available on Environment Canada’s Green Lane on the World Wide Web at http://www.ec.gc.ca.
A companion document (Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act — Resource Document) elaborates on the guidance provided in this manual and describes methods and approaches in more detail. The resource document is unpublished, but it is available from the Commercial Chemicals Evaluation Branch. Owing to resource constraints, it has not been as thoroughly updated following the review phases as was the guidance manual. A policy and process document that presents guidance on nonscientific issues related to the assessment of priority substances is also available on request from the Commercial Chemicals Evaluation Branch.
v Préface
Le présent guide fournit des conseils sur l’évaluation environnementale des substances d’intérêt prioritaire au Canada. Il a été rédigé par la Division de l’évaluation des produits chimiques, Direction de l’évaluation des produits chimiques commerciaux, Environnement Canada, afin de mettre à jour le document non publié Draft Guidelines for Conducting Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act, April 1992. Cette révision est fondée sur l’expérience acquise à la suite de l’évaluation des substances figurant sur la première liste d’intérêt prioritaire et tient également compte des récents progrès accomplis dans le domaine de l’évaluation des risques écologiques. Le guide a fait l’objet d’un examen approfondi par de nombreux experts d’autres ministères gouvernementaux, de l’industrie, du milieu universitaire ainsi que d’organisations non gouvernementales et internationales.
Le guide s’adresse tout d’abord aux évaluateurs qui dirigent l’évaluation environnementale des substances d’intérêt prioritaire ainsi qu’aux groupes d’experts qui les aident, puis, en deuxième lieu, aux parties intéressées qui désirent savoir comment Environnement Canada effectue l’évaluation environnementale de ces substances.
Le guide est provisoire parce qu’il reflète l’expérience acquise jusqu’à présent grâce au Programme d’évaluation des substances d’intérêt prioritaire et les connaissances scientifiques actuelles en matière d’évaluation des risques écologiques. Il sera mis à jour pour tenir compte de l’expérience accrue par les conseils qu’il fournit concernant l’évaluation des substances figurant sur la deuxième liste d’intérêt prioritaire et par le perfectionnement des connaissances scientifiques en matière d’évaluation des risques écologiques. Plutôt que d’énoncer des règles rigoureuses, le guide offre des conseils seulement afin d’accorder la souplesse nécessaire pour évaluer différents types de substances et de tenir compte de l’accroissement de l’expérience et des connaissances scientifiques.
Le guide est publié en français et en anglais; il peut aussi être consulté sur la Voie verte d’Environnement Canada qui se trouve sur le site Web et dont l’adresse est http://www.ec.gc.ca.
Un document d’accompagnement (Environmental Assessments of Priority Substances Under the Canadian Environmental Protection Act Resource Document) étoffe les conseils présentés dans le guide et décrit plus en détail les méthodes et les façons de procéder. Ce document n’a pas été publié, mais il est possible de l’obtenir à la Direction de l’évaluation des produits chimiques commerciaux. En raison de restrictions financières, sa mise à jour, à la suite des diverses étapes de l’examen, n’a pas été aussi complète que dans le cas du guide. La Direction de l’évaluation des produits chimiques commerciaux peut aussi fournir sur demande un document d’orientation et de marche à suivre qui donne des conseils sur les questions non scientifiques se rapportant à l’évaluation des substances d’intérêt prioritaire.
vi Table of Contents
List of Acronyms ...... xii Glossary ...... xiii
Chapter 1 Framework and Overview ...... 1-1 1.1 Legislative Framework ...... 1-1 1.2 What Are We Trying to Protect? ...... 1-2 1.2.1 Levels of Biological Organization...... 1-2 1.3 Beyond “Toxic”...... 1-4 1.4 Weight-of-Evidence Approach ...... 1-4 1.5 Framework for Ecological Risk Assessment of Priority Substances ...... 1-5 1.6 Some Points to Remember...... 1-7 1.7 References ...... 1-8
Chapter 2 Data Collection and Generation ...... 2-1 2.1 Introduction ...... 2-1 2.2 Stage One: Data Gathering Required for Problem Formulation ...... 2-1 2.2.1 Data Provided by the Priority Substances List (PSL) Secretariat...... 2-2 2.2.2 Existing International Assessments...... 2-2 2.2.3 Desk References ...... 2-2 2.2.4 Readily Available Databases/Catalogues ...... 2-2 2.2.5 Commercial Databases ...... 2-2 2.2.6 Specialty Resources ...... 2-2 2.2.7 Concluding Stage One ...... 2-2 2.3 Stage Two: Conceptual Model Refinement with Participation of Interested Parties ...... 2-2 2.3.1 Consultation with Interested Parties...... 2-3 2.4 Stage Three: CEPA Section 16 and Section 18 Notices...... 2-3 2.5 Stage Four: Generation of Data Through Research ...... 2-3 2.5.1 Recommendation of Research Activities ...... 2-3
Chapter 3 Problem Formulation ...... 3-1 3.1 Introduction ...... 3-1 3.1.1 Goals and Objectives ...... 3-1 3.1.2 Relationship with Other Phases ...... 3-1 3.2 Initial Scoping ...... 3-1 3.3 Pathways Analysis ...... 3-2 3.4 Receptor Sensitivity ...... 3-4 3.5 Ecological Relevance ...... 3-4 3.6 Choosing Assessment Endpoints ...... 3-4 3.7 Choosing Measurement Endpoints...... 3-5 3.8 The Conceptual Model ...... 3-5 3.9 Some Points to Remember...... 3-6 3.10 References ...... 3-6
vii Chapter 4 Entry Characterization ...... 4-1 4.1 Introduction ...... 4-1 4.1.1 Goals and Objectives ...... 4-1 4.1.2 Relationship with Other Phases ...... 4-1 4.2 Identification of Sources ...... 4-1 4.2.1 Natural Sources ...... 4-1 4.2.2 Anthropogenic Sources ...... 4-2 4.2.3 Transboundary Sources ...... 4-3 4.2.4 Indirect Sources ...... 4-3 4.3 Characterization of Releases ...... 4-3 4.3.1 Quantifying Releases...... 4-3 4.3.2 Frequency and Patterns of Releases ...... 4-4 4.3.3 Chemical and Physical Nature of the Substance Released into the Environment ...... 4-4 4.3.4 Recognition of Trends in Releases ...... 4-4 4.4 Some Points to Remember...... 4-5 4.5 References ...... 4-5
Chapter 5 Exposure Characterization ...... 5-1 5.1 Introduction ...... 5-1 5.1.1 Goals and Objectives ...... 5-1 5.1.2 Relationship with Other Phases ...... 5-1 5.2 Pathways Analysis ...... 5-1 5.2.1 Verifying Pathways Analyses ...... 5-3 5.2.2 Quantifying Fate Parameters ...... 5-3 5.3 Quantifying Exposure ...... 5-4 5.3.1 Approaches to Quantification ...... 5-4 5.3.2 Use of Field Data ...... 5-4 5.3.3 Use of Calculated Values...... 5-5 5.3.4 Determining Bioavailability ...... 5-7 5.3.5 Representation of Temporal and Spatial Variability ...... 5-9 5.4 Estimating Natural Background Concentrations ...... 5-11 5.5 Some Points to Remember...... 5-11 5.6 References ...... 5-11
Chapter 6 Effects Characterization ...... 6-1 6.1 Introduction ...... 6-1 6.1.1 Goals and Objectives ...... 6-1 6.1.2 Relationship with Other Phases ...... 6-1 6.1.3 Overview of Approach ...... 6-1 6.2 Types of Effects Information ...... 6-2 6.2.1 Single-Species Toxicity Tests ...... 6-3 6.2.2 Multispecies Toxicity Tests...... 6-3 6.2.3 Ecoepidemiology ...... 6-4 6.2.4 Estimating Effects of Naturally Occurring Substances ...... 6-5 6.2.5 Critical Body Burdens (CBBs) ...... 6-5 6.2.6 Quantitative Structure–Activity Relationships (QSARs) ...... 6-5
viii 6.2.7 Equilibrium Partitioning (EqP) ...... 6-6 6.3 Deriving Critical Toxicity Values (CTVs) ...... 6-6 6.3.1 Tiers 1 and 2 ...... 6-7 6.3.2 Tier 3...... 6-7 6.3.3 Procedure for Estimating Low Toxic Effects: Regression-Based Approach ...... 6-8 6.3.4 Procedure for Estimating Low Toxic Effects: Hypothesis-Testing Approach...... 6-9 6.3.5 Estimating Median Toxic Effects ...... 6-9 6.4 Aquatic Effects Characterization ...... 6-9 6.4.1 Pelagic Biota ...... 6-9 6.4.2 Benthic Biota ...... 6-10 6.4.3 Groundwater Biota ...... 6-11 6.5 Terrestrial Effects Characterization...... 6-13 6.5.1 Soil Biota ...... 6-13 6.5.2 Wildlife ...... 6-14 6.6 Effects Mediated Through the Atmosphere ...... 6-15 6.6.1 Stratospheric Ozone Depletion ...... 6-15 6.6.2 Ground-Level Ozone Formation...... 6-26 6.6.3 Global Warming...... 6-26 6.7 Some Points to Remember...... 6-17 6.8 References ...... 6-17
Chapter 7 Risk Characterization ...... 7-1 7.1 Introduction ...... 7-1 7.1.1 Goals and Objectives ...... 7-1 7.1.2 Relationship with Other Phases ...... 7-1 7.2 Overview ...... 7-1 7.3 Tier 1: Hyperconservative Quotients ...... 7-2 7.4 Tier 2: Conservative Quotients ...... 7-4 7.5 Tier 3: Analyses...... 7-4 7.5.1 Key Concepts ...... 7-5 7.5.2 General Mechanics of a Probabilistic Risk Analysis...... 7-5 7.5.3 Choosing an Appropriate Model ...... 7-6 7.5.4 Choosing Input Distributions ...... 7-7 7.5.5 Methods for Probabilistic Risk Analysis ...... 7-9 7.5.6 Best Practices...... 7-12 7.6 Estimating Risks Due to Anthropogenic Sources of Naturally Occurring Substances...... 7-13 7.6.1 Bounding the Estimated No-Effects Value (ENEV) ...... 7-14 7.6.2 Evaluating the Choice of Endpoints ...... 7-14 7.6.3 Evaluating the Relative Tolerance of Assessment and Measurement Endpoints...... 7-14 7.7 Estimating Ecological Consequences ...... 7-14 7.7.1 Population- and Community-Level Effects ...... 7-15 7.8 Some Points to Remember...... 7-16 7.9 References ...... 7-16
ix Chapter 8 Complex Substances ...... 8-1 8.1 Background and General Approaches ...... 8-1 8.2 Problem Formulation ...... 8-2 8.3 Entry Characterization...... 8-3 8.4 Exposure Characterization...... 8-3 8.5 Effects and Risk Characterizations ...... 8-4 8.5.1 Weight-of-Evidence Approach...... 8-5 8.5.2 Field Toxicity Tests ...... 8-5 8.5.3 Artificial System Tests (Mesocosms and Microcosms) ...... 8-7 8.5.4 Laboratory-Ambient Toxicity Testing...... 8-7 8.5.5 Laboratory Toxicity Testing Using Whole Effluent and Mixtures ...... 8-8 8.5.6 Other Methods ...... 8-8 8.6 References ...... 8-9
x List of Figures
1.1 Framework for ecological risk assessment of priority substances ...... 1-6 3.1 The problem formulation phase in the ecological risk assessment framework for priority substances ...... 3-2 4.1 Entry characterization in the ecological risk assessment framework for priority substances ...... 4-2 5.1 Exposure characterization in the ecological risk assessment framework for priority substances ...... 5-2 6.1 Effects characterization in the ecological risk assessment framework for priority substances ...... 6-2 7.1 Risk characterization in the ecological risk assessment framework for priority substances ...... 7-2 7.2 Commonly used input distributions in ecological risk assessments ...... 7-9 7.3 Percentage of genera affected versus copper concentration ...... 7-10 7.4 Total daily intake for female mink exposed to hexachlorobenzene in the St. Clair River area near Sarnia, Ontario ...... 7-12
List of Tables
5.1 Estimated maximum total daily intake of hexachlorobenzene for a 1-kg adult mink in the St. Clair River area...... 5-4 5.2 Guidance on application of tiered approach to quantifying exposure ...... 5-6 7.1 Recommended maximum application factors for converting critical toxicity values to estimated no-effects values in Tier 1 ...... 7-4 7.2 Useful input distributions for probabilistic risk assessments of priority substances ...... 7-8 8.1 Approaches and type of controls to conduct field toxicity studies of waste crankcase oils (WCOs) ...... 8-6
List of Boxes
1.1 Second Priority Substances List ...... 1-2 5.1 Example of Qualitative Pathways Analysis ...... 5-3 5.2 Empirical Relationships Between Uptake of Substances, Exposure Concentrations, and Properties of Exposure Media ...... 5-8
xi LIST OF ACRONYMS
ACR Acute/chronic ratio MOIR Maximum ozone incremental reactivity AET Apparent effects threshold mRNA Mitochondrial ribonucleic acid ANOVA Analysis of variance NOEC No-observed-effects concentration AOX Adsorbable organic halogen NOEL No-observed-effects level ASTM American Society for Testing and OC Organic carbon Materials ODP Ozone-depleting potential BACI Before–After–Control–Impact OECD Organisation for Economic BAF Bioaccumulation factor Co-operation and Development BCF Bioconcentration factor OFP Ozone-forming potential CAS Chemical Abstracts Service OM Organic matter CBB Critical body burden PAH Polycyclic aromatic hydrocarbon CCME Canadian Council of Ministers of the PCB Polychlorinated biphenyl Environment PDF Probability density function CDF Cumulative density function POCP Photochemical ozone creation CEARC Canadian Environmental Assessment potential Research Council PSL Priority Substances List CEPA Canadian Environmental Protection Act QA/QC Quality assurance/quality control CEU Commission of the European Union QSAR Quantitative structure–activity CFC Chlorofluorocarbon relationship CTV Critical toxicity value RBE Relative biological effectiveness DOC Dissolved organic carbon RIVM The Netherlands National Institute of Public Health and Environmental EC50 Median effective concentration ECETOC European Centre for Ecotoxicology Protection and Toxicology of Chemicals SETAC Society of Environmental Toxicology and Chemistry ECx Effective concentration for an x% effect EEV Estimated exposure value TEF Toxic equivalent factor ENEV Estimated no-effects value TIE Toxicity identification and evaluation EqP Equilibrium partitioning TU Toxic unit FETAX Frog embryo teratogenesis assay U.S. EPA United States Environmental Protection GIS Geographic information system Agency GWP Global warming potential VKI Water Quality Institute (Denmark) IBI Integrated Biotic Index VOC Volatile organic compound WCEM Wildlife Contaminant Exposure Model IC25 Inhibiting concentration for a 25% effect WCO Waste crankcase oil WERF Water Environmental Research ICp Inhibiting concentration for a p% effect IR Infrared Foundation IUPAC International Union of Pure and Applied Chemistry
Koc Organic carbon partitioning coefficient
Kow Octanol–water partition coefficient
LC50 Median lethal concentration
LD50 Median lethal dose LOEC Lowest-observed-effects concentration LOEL Lowest-observed-effects level MATC Maximum allowable toxicant concentration MIR Maximum incremental reactivity MMWG Metals and Minerals Working Group
xii Glossary
Absorption: The penetration of one substance Bioaccumulation factor (BAF): The ratio of the into the inner structure of another. steady-state concentration of a substance in an organism owing to uptake from all routes of Acute/chronic ratio: A species’ mean acute exposure to the concentration of the substance value divided by the chronic value for the same in the medium to which the organism was species. Such ratios can be used to convert the exposed. median lethal results of a short-term study to an estimated long-term no-effects concentration. Bioavailable substance: A substance that is present in a form that can be readily taken up by Acute toxicity test: A toxicity test of short exposed organisms. duration in relation to the life span of the test organism (e.g., usually ≤ 4 days for fish). Bioconcentration: The net accumulation of a substance directly from aqueous solution by an Adsorption: Adherence of the atoms, ions, or aquatic organism. molecules of a liquid or gas to the surface of another substance. Bioconcentration factor (BCF): The ratio of the steady-state concentration of a substance in an Alpha (α): The symbol for a Type I error in organism owing to uptake via contact with water hypothesis testing, expressed as a probability or to the concentration of the substance in the test proportion (e.g., 0.05 or 5%). A Type I error is water; and/or the ratio of the uptake rate the probability of rejecting the null hypothesis constant to the depuration constant, assuming when in fact the null hypothesis is true. In first-order kinetics. hypothesis testing, α is specified by the user prior to carrying out the analysis (see Beta). Biotransformation: A process mediated by microorganisms or other living organisms that Atmospheric lifetime (or natural lifetime, J): The chemically alters the structure of a chemical. time it takes for the reactant concentration to fall to 1/e of its initial value (e is the base of natural Body burden: The amount of a substance that logarithms, 2.718), or 36.7% of the original has accumulated in the tissue of an exposed concentration. The lifetime is related to the rate organism, usually expressed as the concentration constant and to the concentrations of any other of the substance in a particular organ or in the reactants involved in the reactions. whole organism.
Benthic organism: An organism that lives in or Carrier and noncarrier controls: Toxicity tests on the bottom of a body of water. for certain substances may use a carrier to aid in dispersing the test substance evenly in the test Beta (β): The symbol for a Type II error in medium. Carrier and noncarrier controls are hypothesis testing, expressed as a probability or conducted with and without the carrier, proportion. A Type II error is the probability of respectively, in order to determine the effects of accepting the null hypothesis when in fact the the carrier on the test organisms. null hypothesis is false. The magnitude of the Type II error is generally inversely related to the Chronic toxicity test: A toxicity test that spans a magnitude of the Type I error that will be significant portion of the life span of the test tolerated (see Alpha). organism (e.g., 10% or more) and examines effects on such parameters as metabolism, Bioaccumulation: The net accumulation of a growth, reproduction, and survival. substance by an organism as a result of uptake from all routes of exposure. Complex: Dissolved species formed from two or more simpler species, each of which can exist in aqueous solution.
xiii Complex substance: Consists of a Effluent: A liquid complex substance composed heterogeneous association of many substances of many constituents that are not necessarily (i.e., constituents) that are not necessarily related related, that emerge from a pipe or similar and either are released at a given time and outlet, and that are discharged primarily into place or occur at a given time and place; see aquatic systems (e.g., industrial discharge, definitions of Mixture and Effluent. sewage effluent).
Critical body burden (CBB): The minimum Elutriate: An aqueous solution obtained by concentration of a substance that causes an adding water to a solid substance (e.g., adverse effect on the measurement endpoint sediment, tailings, drilling mud, dredge spoil), (e.g., reproductive potential of Daphnia) of shaking the mixture, then centrifuging or filtering interest. it or decanting the supernatant.
Critical toxicity value (CTV): The quantitative Endocrine disrupter: A substance that interferes
expression (e.g., IC25) of low toxic effect on the with the production, release, transport, measurement endpoint. CTVs are used in risk metabolism, binding, action, or elimination of characterization for the calculation of an natural ligands in the body that are responsible estimated no-effects value (ENEV). for the maintenance of homeostasis and the regulation of developmental processes. Cumulative probability distribution: A curve or mathematical expression that quantifies Environmental resource group: A group of uncertainty over a variable. It associates a people drawn from government, the private probability with all values in the set of possible sector, and academia who will assist with the values. The probability associated with each conduct and review of the ecological risk value of the variable is that of the occurrence of assessment of a substance. a value less than or equal to the specified value. Equilibrium: A condition in which the ratio of the Depuration: Clearance of a chemical from an concentrations of a substance in two or more organism as a result of elimination and/or phases (e.g., pore water and particulate phases degradation. of bottom sediments) is constant.
Desorption: The removal of an adsorbed Food web structure: Consists of many material from the substance on which it is interlinked food chains (i.e., organisms forming adsorbed. a series through which energy is passed). A typical food chain structure consists of producer Detritivore: An organism that feeds primarily on (e.g., green plant)→ primary consumer (e.g., detritus (i.e., organic particulate matter from herbivore)→ secondary consumers (consisting of nonliving and decomposing organisms). smaller then, at subsequent trophic levels, larger carnivores). ECx: The concentration of a substance that is estimated to cause some toxic effect on x% of Fugacity: The thermodynamic or “escaping the test organisms. The duration of the exposure tendency” of a chemical in a particular phase must be specified. EC describes quantal effects, x (e.g., water, air), given in units of partial lethal or sublethal, and is not applicable to pressure or pascals (Pa). If the fugacity of a quantitative effects (see IC ). p chemical is higher in water than in air, the Ecological risk assessment review group: A chemical will evaporate until an equilibrium is group of risk assessors, risk managers, and established. other interested parties who will review the Genotoxicity: The ability of a substance to problem formulation stage and data gaps and damage the genetic material of an organism, recommend research priorities for PSL2 which is then passed on to the next generation. substances.
xiv Group parameter: Group parameters are based Mesocosm: A small-scale model ecosystem on analytical-chemical techniques and somewhat similar to a microcosm (see determine specific elements or chemically Microcosm), but larger. Mesocosms are often defined groups of constituents in complex artificially constructed outdoor ponds with a substances. Examples of group parameters are volume of 100–1000 m3. dissolved organic carbon (DOC) and Adsorbable Organic Halogen (AOX). Microcosm: A small-scale model ecosystem, often contained in a laboratory test chamber, to Hydrolysis reaction: For organic substances, a which the test chemical is added. A microcosm reaction involving the introduction of a water typically contains more than one phase (e.g., molecule or a hydroxyl ion into an organic water, sediment, and biota). molecule, resulting in the cleavage of a chemical bond in the organic molecule. For Mineralization: Breakdown of an organic inorganic substances, a reaction involving a substance to form carbon dioxide, water, nitrate, water molecule and an inorganic substance, and phosphate ions. resulting in the cleavage of the water molecule. Mixture: A liquid, solid, or gaseous complex substance composed of many constituents that ICp: The inhibiting concentration for a specified percent effect. A point estimate of the are not necessarily related and are released into concentration of a test substance that causes p% various environmental compartments, including reduction in a quantitative biological water, air, and land (e.g., waste crankcase oils, measurement such as growth rate. creosote-impregnated waste materials, landfill leachate, smelter emissions). Immune suppression: The suppression of the reaction of the immune system by a substance, Mode of action: The manner in which a which leaves the organism vulnerable to substance causes an adverse effect in an infection, disease, etc. organism (e.g., narcosis, acetylcholinesterase inhibition, central nervous system seizure). Interpolation: The process of estimating a value between two or more known values. Narcotic substance: Any substance that induces narcosis (i.e., a reversible state of stupor,
LC50: The concentration of a substance that is insensibility, or unconsciousness) in an estimated to be lethal to 50% of the test organism. The mechanism of narcosis is organisms over a specified period of time. nonspecific, and, consequently, a narcotic substance’s toxicity is entirely dependent on its LD : The dose that causes mortality in 50% of the 50 tendency to partition to the tissue of the organisms tested. organism.
LOEL: Lowest-observed-effect level. The lowest NOEL: No-observed-effect level. The highest concentration or dose in a toxicity test that concentration or dose in a toxicity test not causes a statistically significant effect in causing a statistically significant effect compared comparison to the controls. with the controls.
MATC: The maximum allowable toxicant Nutrient cycling: The dissipation of energy in concentration, generally presented as the range ecosystems through the transport, between the NOEL and LOEL or as the decomposition, and recycling of materials geometric mean of the two measures. bound up in the biomass, living or dead, of Mean: The arithmetic average of a set of system components. Nutrient cycling can often numerical observations, calculated as the sum of be constrained by the availability to primary the observations divided by the number of producers of essential raw materials, including observations. macronutrients (e.g., phosphorus, nitrogen, calcium) and trace nutrients (e.g., iron, manganese, molybdenum).
xv Pelagic biota: Aquatic organisms living in the Sediment: Natural particulate matter that has water column of a body of water, rather than been transported to, and deposited at, the along the shore or in the bottom sediments. bottom of a body of water. The term can also describe a substrate that has been Photolysis (direct): The decomposition or experimentally prepared and into which test reaction of a substance on exposure to light. organisms can burrow. Occurs when sunlight is absorbed by a substance and the energy is used to form excited Sensitivity analysis: The computation of an or radical species, which react further to form output distribution’s sensitivity with respect to the stable products. input probability distributions.
Photolysis (indirect, or photooxidation): The Solid-phase sediment: The whole, intact reaction of a substance with intermediate sediment rather than a derivative of the oxidants formed during photolysis of dissolved sediment, such as an elutriate or a resuspended organic matter in water or soil, or photolysis of sediment. ozone or nitrogen dioxide in the atmosphere. Sorption: A surface phenomenon that may be Photosynthesis: The elaboration of organic either absorption or adsorption, or a matter (carbohydrate) from carbon dioxide and combination of the two. water with the aid of light energy. Spiked sediment: A control, reference, or other Pore water: Water occupying the space between clean sediment to which a test substance (such sediment particles. The amount of pore water is as a chemical or mixture of chemicals) has been expressed as a percentage of the wet sediment, added, then mixed throughout the sediment. by weight. Spiked-sediment toxicity test: An assay using a Probability density function: A probability test organism that is exposed to specified distribution describing a continuous random concentrations of a substance-spiked sediment variable. It associates a relative likelihood to the over a specified time period to determine any continuum of possibilities. effects.
Radiative balance: The quasi-equilibrium Standard deviation: A measurement of the between the heat absorbed by the Earth from the variability of a distribution. The standard sun and the heat lost by the Earth through deviation is the square root of the variance. radiation. Steady-state concentration: A condition in Receptor: In this document, “receptor” refers to which the concentration of a substance in a any environmental entity that is exposed to, and particular medium is constant. could be adversely affected by, a PSL substance. A receptor is usually an organism or a Sublethal toxicity test: A toxicity test conducted population, but it could also be an abiotic entity, using concentrations or doses of a substance such as stratospheric ozone. below levels causing death within the test period. Common endpoints for sublethal toxicity tests Regression analysis: A statistical procedure include reduction in growth or number of young based on empirical data that determines the produced. coefficients in a linear or nonlinear combination of one or more independent variables that best Vapour pressure: The pressure exerted by the estimates the value of a dependent variable. vapour phase of a substance when it is in equilibrium with the liquid or solid form from Saprovore: An organism that feeds primarily on which it is derived. Vapour pressure may be dead or decaying organic matter. considered a measure of a pure substance’s tendency to volatilize.
xvi Variance: A measure of the dispersion, or Water hardness: The amount of calcium and spread, of a set of values about a mean. When magnesium carbonates, bicarbonates, values are close to the mean, the variance is sulphates, and chlorides contained in a given small. When values are widely scattered about amount of water. Water hardness is usually the mean, the variance is larger. Variance is the expressed as the equivalent quantity of calcium mean of the squares of the deviations from the carbonate. Water containing less than about mean of the distribution. 85 mg calcium carbonate per litre is considered to be soft, whereas water containing more than Volatilization: The transfer of a substance from a about 500 mg calcium carbonate per litre is liquid or solid to a vapour phase. considered to be very hard.
xvii CHAPTER 1 FRAMEWORK AND OVERVIEW
1.1 Legislative Framework If the assessment concludes that a priority substance is “toxic” under the Act, the substance The Canadian Environmental Protection Act enters the risk management phase. Management (CEPA), proclaimed by the Government of strategies for “toxic” substances are currently being Canada in 1988, provides a legislative framework developed through a multistakeholder Strategic to deal with toxic substances in the environment. Options Process that considers such things as the The Act, administered by Environment Canada sources, release rates, and potential effects; and Health Canada, emphasizes prevention and existing pollution control technologies; and target deals with all stages of a substance’s life cycle, markets and impact on competitiveness. Risk from research and development to manufacture, management options can include voluntary transportation, distribution, use, and disposal. controls, process changes, substitutions, economic measures, federal regulations, guidelines or codes The Priority Substances Assessment Program is of practice, control by other federal or provincial/ mandated under Section 12 of the Act. That territorial legislation, or a combination of these Section instructs the Ministers of Environment and measures. Health to develop a list of substances that should be given priority for assessment to determine The first Priority Substances List (PSL1), which whether they are “toxic”, as defined under Section appeared in the Canada Gazette in February 11 of the Act. Section 11 states: 1989, contained 44 substances, including organic compounds, metals, mixtures, effluents, and emissions. Assessments of these substances were “A substance is toxic if it is entering or may completed by February 1994. The Ministers of enter the environment in a quantity or a con- Environment and Health established a second centration or under conditions Expert Advisory Panel in December 1994 to recommend a new list of priority substances for (a) having or that may have an immediate or assessment under the Act. This Panel, drawn from long-term harmful effect on the environ- major stakeholder groups, recommended a list of ment; 25 substances (Ministers’ Expert Advisory Panel 1995). The Ministers accepted this list and (b) constituting or that may constitute a danger published the second Priority Substances List (PSL2) to the environment on which human life in the Canada Gazette on December 16, 1995 depends; or (Box 1.1).
(c) constituting or that may constitute a dan- ger in Canada to human life or health.”
1-1 Box 1.1 Second Priority Substances List*
Acetaldehyde N-Nitrosodimethylamine (NDMA) Acrolein Nonylphenol and its ethoxylates Acrylonitrile Phenol Aluminum chloride, aluminum nitrate, Releases from primary and secondary aluminum sulphate copper smelters and copper refineries Ammonium in the aquatic environment Releases from primary and secondary 1,3-Butadiene zinc smelters and zinc refineries Butylbenzylphthalate (BBP) Releases of radionuclides from nuclear Carbon disulphide facilities (impacts on nonhuman Chloramines species) Chloroform Respirable particulate matter less than N,N-Dimethylformamide (DMF) or equal to 10 micrometres in diameter Ethylene glycol Road salts Ethylene oxide Textile mill effluents Formaldehyde Hexachlorobutadiene (HCBD) 2-Methoxy ethanol, 2-Ethoxy ethanol, 2-Butoxy ethanol
*See Expert Advisory Panel report for details on how substances were selected (Ministers’ Expert Advisory Panel 1995).
1.2 What Are We Trying to 1.2.1 Levels of Biological Organization Protect? Effects in the environment resulting from exposure to chemical substances can occur at various levels The objective of the environmental assessment is of biological organization. Effects at lower levels, to determine whether the substance is “toxic” as such as biochemical effects, are not always defined in CEPA Section 11 and to provide transmitted to higher levels, such as ecosystems scientific support for the determination. To (Allen and Starr 1982; O’Neill et al. 1986). determine whether or not a substance is CEPA Conversely, in cases in which effects at higher “toxic,” the assessment estimates and describes levels have occurred, lower levels of organization risks to receptors (e.g., plants, animals) exposed in will also have been seriously affected (Allen and the Canadian environment. Starr 1982; O’Neill et al. 1986). Therefore, Environmental assessments can be complex. They effects observed at the population, community, or must consider numerous species that may be ecosystem level are generally considered more affected by a substance, either directly or indirectly environmentally harmful and are of more concern due to disruptions to ecosystem structure and than those observed only at lower levels. Effects function. Given our limited understanding of on the individual may be significant for threatened ecosystem structure and function and the scarcity or endangered species, where population levels of information typically available, assessors must are low. carefully consider which effects are potentially Few studies have directly tested priority substances ecologically significant. Several factors affecting for effects at the population, community, or this judgment are discussed in the following Section. 1-2 ecosystem level of organization. Most toxicity elsewhere, risks predicted by the laboratory studies are conducted in the laboratory using test results alone will overestimate true risk relatively small sample sizes relative to population (Underwood 1995). sizes in natural communities. However, many of the effects measured in laboratory and field studies • The assessment endpoint for chemical B is have implications for populations, communities, abundance of salmonids based on evidence and ecosystems. Effects such as endocrine that the chemical is water soluble and is disruption, lethality, and reproductive impairment released to water bodies inhabited by these are closely related to the viability of natural fish. Chemical B is an estrogen agonist that populations. A strong link between toxicity study persists in the environment. Laboratory results (e.g., reduction in reproductive fecundity) evidence shows that it competitively binds to and environmental parameters (e.g., population the estrogen receptor, thus blocking binding by age structure) can provide good evidence for endogenous 17ß-estradiol, estrone, and determining whether a substance is “toxic” as estriol; it causes estrogen-inducible responses defined in CEPA. It is impossible to specify a rigid in vitro in fish cells and in vivo in rats (example cutoff point at which effects are considered adapted from Kramer and Giesy 1995). sufficient to declare the substance “toxic”. Further, levels of the chemical are highest Professional judgment is required. The following during periods of low steroid biosynthesis in examples illustrate how such judgment may be salmonids, such as during male embryo applied. development. This increases the relative potency of exogenous chemical B relative to • Based on a pathways analysis for chemical A, the endogenous estrogens. Finally, there have richness and abundance of grain-eating birds been anecdotal observations of have been selected as the assessment hermaphroditic fish downstream of wastewater endpoints (see Section 3.6 for a discussion treatment plants releasing chemical B. Field about this term). No field surveys or tests have studies in areas heavily contaminated by other been conducted to determine whether estrogen agonists show that observed effects at community-level endpoints have been affected the biochemical and physiological levels can in areas where the chemical has been be translated into serious adverse effects at the released. Available information indicates that population level owing to declines in the chemical is acutely toxic to chickens in reproductive success (Fry et al. 1987). This laboratory tests at exposure levels similar to evidence indicates that chemical B is “toxic” as those predicted for wild birds, and, further, defined under CEPA. dead birds have been reported following releases of the chemical. Although these • The assessment endpoint for chemical C, measurement endpoints (see Section 3.7) are which is released periodically to trout streams, at the individual level, one can reasonably is abundance of salmonids. The chemical is argue that the evidence suggests a potential not considered to be persistent. At levels for adverse effects on the assessment found downstream from outfalls following its endpoint. This evidence could therefore release, induction of cytochrome P450 mRNA indicate that chemical A is “toxic” under CEPA. and P450 protein in rainbow trout has been It is not possible to prove that adverse effects observed within 18 hours of the initial will occur or to determine the ecological exposure. The levels of mRNA in chemical consequences of such effects. Many factors C-treated fish peaked at about two days and could enhance or mitigate the translation of decayed by five days; P450 protein levels effects from the individual to community level remained elevated somewhat longer but of organization. For example, if the birds are declined to control levels at about 10 days. undernourished in the field, adverse effects Corresponding acute and chronic toxicity predicted by laboratory studies on well-fed studies indicate that trout survival, growth, and birds may considerably underestimate true risk. reproduction were not affected at similar levels Conversely, if population size is regulated by of chemical C following a single-dose recruitment from uncontaminated populations treatment. Given that chemical C is released
1-3 only periodically, that it is not persistent, and The following should be considered in evaluating that its effects at the biochemical level do not each line of evidence (adapted from U.S. EPA appear to translate to effects at higher levels, 1992): the evidence suggests that this chemical would not be considered “toxic” as defined under • Relevance of the evidence to the exposure CEPA based on this particular biochemical scenario of interest. Lines of evidence that are level effect. most relevant to exposure scenarios in Canada are given the greatest weight. 1.3 Beyond “Toxic” • Relevance of the evidence to the assessment Although Section 11 of CEPA requires only a endpoint. Toxicity tests that closely mimic field determination of whether a substance is “toxic”, conditions and yield results that are directly Section 13 requires that a summary of the related to ecologically significant parameters assessment be published in the Canada Gazette, are given more weight than tests that are less including a statement of whether the Ministers pertinent to field conditions and environmental intend to recommend that regulations be made effects. with respect to the substance. This means that the • Confidence in the evidence or risk estimate. PSL assessment must include adequate information Confidence is a function of the sufficiency and for risk management decisions. Therefore, where quality of the data and estimation techniques, a substance is toxic, the risk assessment should, including adherence to protocols, appropriate when possible, include detailed characterization of experimental designs and associated estimates the substance’s entry into the Canadian of statistical power, and theoretical plausibility. environment and specify the probabilities and magnitudes of environmental effects at sites of • Likelihood of causality. Some lines of elevated exposure in Canada. Such information is evidence, such as observed field effects, may useful in determining the priority for risk include a variety of stressors in addition to the management actions and ensuring that mitigation priority substance of interest. Fox (1991) lists measures are cost-effective and directed at the seven principles that can guide assessors in most serious problems. assessing the relationship between a priority substance and an observed adverse 1.4 Weight-of-Evidence environmental effect: time order, strength of Approach association, specificity of association, consistency of the association, coherence of Traditionally, environmental assessments of the association, probability, and predictive chemicals have relied on the results of a few performance (see Chapter 6 for more details). relatively simple laboratory bioassays and measured or estimated concentrations in a single By using a weight-of-evidence approach, risk medium to predict effects in complex, poorly assessment can reduce, but not eliminate, the understood ecosystems (Suter and Loar 1992; biases and uncertainties associated with using only Chapman 1995). This approach is fraught with one approach to estimate risk. A weight-of- assumptions and uncertainties. Alternative evidence approach is also a useful tool for approaches, such as using batteries of tests, field identifying areas where research is most needed. observations, ecoepidemiology, and population and ecosystem modelling, can be used to estimate risk, but each has its own assumptions and associated uncertainties. Rather than relying on a single approach, assessors must evaluate each separate line of evidence, organize these in a coherent fashion, and then use a weight-of- evidence approach to estimate risk (Suter 1993a).
1-4 1.5 Framework for Ecological develop appropriate management strategies for Risk Assessment of Priority substances found to be CEPA “toxic”. The involvement of interested parties such as those Substances from other government departments, industry, nongovernmental groups and academia helps to The framework for ecological risk assessment of ensure that a broad range of viewpoints is priority substances uses a modification of the one considered. developed by the United States Environmental Protection Agency (U.S. EPA). It incorporates the The analysis phase consists of three major parts: characterization of entry, exposure and effects that entry, exposure, and effects characterization. The is required to determine whether a substance is objective of entry characterization is to identify the “toxic” as defined under Section 11 of CEPA. This natural and anthropogenic sources of the framework involves three major steps: problem substance and to determine the amounts entering formulation, analysis, and risk characterization the Canadian environment from the various (Figure 1.1; see also U.S. EPA 1992). To ensure sources (Chapter 4). Entry characterization that assessments proceed only to the level of includes all phases of the life cycle of the refinement required for effective decision-making, substance. Information gathered from the a tiered approach has been adopted. Tiers 1 and characterization of entry may be used to further 2 use, respectively, hyperconservative and refine the problem formulation, as input to the conservative point estimates of exposure and characterization of exposure, and in the effects to determine whether or not a substance development of strategic options during risk has the potential to cause harm in the management. environment. Tier 3, which is most realistic, compares exposure and effects distributions, rather The objective of exposure characterization is to than point estimates. A special analysis is used for determine the estimated exposure value (EEV) or naturally occurring substances. The tiered the exposure distribution for each assessment approach is discussed in detail in Chapter 7. endpoint (Chapter 5). Information must be Environmental assessments of priority substances critically evaluated for quality assurance and use ecological risk assessment techniques and quality control (QA/QC). For a Tier 1 tools whenever possible and appropriate, hyperconservative analysis, the EEV is usually the particularly in Tier 3 analyses. maximum measured or estimated concentration in Canada. For Tier 2, it may be possible to reduce Problem formulation focuses on scoping and the hyperconservative EEV — for example, planning (Chapter 3). Pathways analysis and the because bioavailability is expected to be limited — identification of sensitive receptors are used to to obtain a more realistic point estimate of select assessment endpoints (Suter 1993b). As maximal exposure. Tier 3 analysis considers the direct toxicity information is not always available distribution of exposure values, rather than a point for assessment endpoints, measurement endpoints estimate, for each assessment endpoint. For are used to estimate effects on assessment wildlife, exposure is usually expressed as a total endpoints (Suter 1993b). A conceptual model is daily intake or, less often, as an environmental then prepared that describes the substance’s entry concentration or tissue residue. For quantitative and fate in the environment and its possible uncertainty analysis using, for example, Monte environmental effects (Chapter 3). Data gaps that Carlo simulation, it is necessary to define the must be filled in order for the environmental distribution for each exposure parameter (e.g., assessment to be completed are identified during octanol–water partition coefficient Kow ± 95% problem formulation. The PSL framework involves confidence limits) used in the simulation. For Tier risk assessors, risk managers, and other interested 2 and 3 analyses for naturally occurring parties during the risk assessment, particularly in substances, natural background concentrations the problem formulation stage (see also Hope should be estimated as precisely as possible for 1995; Moore and Biddinger 1995). Involving risk each area of concern. managers in the risk assessment process helps to ensure that there is sufficient information to
1-5 Ecological Risk Assessment
Problem Formulation
Analysis
Entry Exposure Effects Characterization Characterization Characterization Data Collection and Generation Risk Managers and Stakeholders Risk Characterization
If CEPA "Toxic"
Risk Management
Figure 1.1 Framework for ecological risk assessment of priority substances (modified from U.S. EPA, 1992)
The objective of effects characterization is to chronic or sublethal toxicity test, determine the critical toxicity value (CTV) or the effects distribution for each assessment endpoint • a lowest-observed-effects level (LOEL) from a using results of toxicity tests or other studies chronic or sublethal toxicity test, (Chapter 6). Studies on single- or multispecies • a no-observed-effects level (NOEL) from a toxicity tests, field studies, or critical body burdens chronic or sublethal toxicity test, if the LOEL (CBBs) can all be used to determine effects. indicates severe effects (e.g., >40% mortality), Quantitative structure–activity relationships and (QSARs) and equilibrium partitioning (EqP) can be used to corroborate results of toxicity tests or field • a median effects concentration (e.g., LC50 or studies. Toxicity information must be critically EC50) from an acute toxicity test, if chronic or evaluated with regard to accepted practices or sublethal toxicity data are not available. protocols for QA/QC. The results of toxicity studies on the most sensitive measurement Tier 1 analysis uses the CTV for the most sensitive endpoint are used to derive the CTV. In species tested. Tier 2 refines the point estimate by decreasing order of preference, the CTV may considering, for example, only test results for be in the form of: sensitive species that are most relevant to the assessment endpoints. Tier 3 considers effects
• an IC25 (or lower, if the estimate is the distributions, rather than point estimates. For result of interpolation) calculated from the quantitative uncertainty analysis using, for concentration–response curve from a example, Monte Carlo simulation, it is necessary
1-6 to define the distribution of each effects parameter Complex substances such as mixtures and effluents
(e.g., IC25 ± 95% confidence limits) used in the are on the second PSL. The interactions of simulation. individual constituents in a complex substance can cause a harmful effect that is qualitatively or Risk characterization, the third step in ecological quantitatively different from that of the constituents risk assessment, uses a tiered approach. Tier 1 acting alone. Effects of two or more interacting involves dividing the EEV by the estimated no- substances may be additive, antagonistic (i.e., less effects value (ENEV) for each assessment endpoint. than additive), or synergistic (i.e., more than For Tier 1, the EEV is generally the maximum additive). Therefore, complex substances require measured or estimated concentration in the different methods for assessing environmental Canadian environment, whereas the ENEV is risks. Chapter 8 discusses such methods. The calculated by dividing the CTV by an application chapter focuses on the differences between factor to derive a value with a very low probability assessments of complex and individual substances, of causing adverse effects on the assessment with particular emphasis on effects and risk endpoint. If the quotient is <1, the substance is characterization. not considered to be “toxic” as defined in Section 11 of CEPA, based on the assessment of This guidance manual presents a number of that endpoint. If the quotient is ≥1 for an approaches and tools that can be used in assessment endpoint, the assessment should move environmental assessments of priority substances. to Tier 2. Tier 2 involves a further analysis of Assessors, in consultation with risk managers, must exposure and effects (see discussion above) to decide which approaches and tools to use for their calculate a quotient that is still conservative but particular assessments. In general, existing data more “realistic” than the hyperconservative should be used whenever possible. Uncertainty quotient calculated in Tier 1. If this quotient is and variability must be identified, quantitatively <1, the substance is not considered to be “toxic” whenever possible, and their effects on the based on that assessment endpoint. If the assessment discussed. Assessors must determine if quotient is ≥1 for an assessment endpoint, the further data are required to complete the assessment should move to Tier 3. Tier 3 involves assessment and arrange to have research carried comparison of exposure and effects distributions to out to generate these data. Because of the determine the likelihood of adverse effects in the expense and time required for toxicological tests environment. This approach facilitates a more and environmental monitoring, additional data explicit consideration of sources of variability and should be generated only when uncertainties uncertainty in the risk analysis. A special analysis around an assessment are unacceptable and is required for naturally occurring substances that hence do not allow for a conclusion concerning have the potential to cause harmful effects, as CEPA toxicity to be made. Assessors should determined by the Tier 1 analysis. This analysis reevaluate data requirements and availability as requires adjusting the effects characterization to they begin each successive tier of the assessments. take into account the tolerance of organisms normally found in naturally enriched areas. If the 1.6 Some Points to Remember analysis indicates that anthropogenic sources can cause harmful effects to organisms normally found • Explicitly state the scope and objectives of the in areas of interest, then the substance is declared assessment. “toxic”. A detailed discussion of the tiered • Set out the content impartially, with a well- approach is presented in Chapter 7. balanced treatment of the evidence bearing on In some assessments, it may be possible to the conclusions. estimate the ecological consequences of exposure • Convey uncertainty explicitly and fairly. State to a substance through the use of field studies, and justify all assumptions. Where possible, population models, or food web models. This include a discussion of the research that might information can be helpful to risk managers to decrease the degree of uncertainty. identify the various actions that could be taken to protect the environment.
1-7 1.7 References Moore, D.R.J. and G.R. Biddinger. 1995. The interaction between risk assessors and risk Allen, T.F.H. and T.B. Starr. 1982. Hierarchy. managers during the problem formulation Perspectives for ecological complexity. phase. Environ. Toxicol. Chem. 14: 2013– University of Chicago Press, Chicago, Illinois. 2014.
Chapman, P.M. 1995. Extrapolating laboratory O’Neill, R.V., D.L. DeAngelis, J.B. Waide, and toxicity results to the field. Environ. Toxicol. T.F.H. Allen. 1986. A hierarchical concept of Chem. 14(6): 927–930. ecosystems. Princeton University Press, Princeton, New Jersey. Fox, G.A. 1991. Practical causal inference for ecoepidemiologists. J. Toxicol. Environ. Health Suter, G.W. 1993a. Predictive risk assessments 33: 359–373. of chemicals. In G.W. Suter (ed.), Ecological risk assessment. Lewis Publishers, Chelsea, Fry, D.M., C.K. Toone, S.M. Speich, and R.J. Michigan. pp. 49–88. Peard. 1987. Sex ratio skew and breeding patterns of gulls: Demographic and toxicological Suter, G.W. 1993b. Defining the field. In G.W. considerations. Stud. Avian Biol. 10: 26–43. Suter (ed.), Ecological risk assessment. Lewis Publishers, Chelsea, Michigan. pp. 3–20. Hope, B.K. 1995. Ecological risk assessment in a project management context. Environ. Prof. 17: Suter, G.W. and J.M. Loar. 1992. Weighing the 9–19. ecological risk of hazardous waste sites: The Oak Ridge case. Environ. Sci. Technol. 26(3): Kramer, V.J. and J.P. Giesy. 1995. 432–438. Environmental estrogens: A significant risk? Hum. Ecol. Risk Assess. 1: 37–42. Underwood, A.J. 1995. Toxicological testing in laboratories is not ecological testing of Ministers’ Expert Advisory Panel. 1995. Report of toxicology. Hum. Ecol. Risk Assess. 1: 178– the Ministers’ Expert Advisory Panel on the 182. Second Priority Substances List under the Canadian Environmental Protection Act (CEPA). U.S. EPA (United States Environmental Protection Ottawa, Ontario. 26 pp. Agency). 1992. Framework for ecological risk assessment. EPA 630/R-92-001. Risk Assessment Forum, Washington, D.C. 41 pp.
1-8 CHAPTER 2 DATA COLLECTION AND GENERATION
2.1 Introduction decisions regarding the quantity and quality of data for the assessment. As with the problem This chapter provides an effective approach to formulation phase of an assessment, data collect and generate data required for collection is an iterative process, and many of the environmental assessments of priority substances following steps may need to be revisited under CEPA. Chapter 2 of the resource document throughout the assessment process as additional provides details about information sources keywords, data sources, or data needs are found. available to collect and generate these data, with Guidance on search strategies is provided in the emphasis on data collection. chapter. Data used when conducting assessments of priority 2.2 Stage One: Data Gathering substances must be of acceptable quality. All key Required for Problem data must be verified by consulting their primary source. Assessors should obtain original Formulation references to critically and scientifically evaluate The first stage of the data collection and the data. In cases where sources of information generation process involves gathering data are incomplete (e.g., information on detection required for problem formulation, from initial limits, sample sizes, measured concentrations, etc. scoping through to the development of a is not reported), assessors should contact conceptual model (Chapter 3). The aim of the individual authors to obtain the data necessary to first stage is to complete a thorough review of evaluate the study. Also, erroneous data may existing sources of information about the result from transcription or typographical errors substance and to identify as early as possible any during the process of publication or database data gaps. development. As both published and unpublished data vary in quality, assessors should become At an early stage in the data collection process, familiar with issues of data quality. Specific QA/ assessors should develop a set of keywords that QC issues are addressed where applicable will be used to search for information in throughout this manual and the accompanying databases. The chemical name, Chemical resource document. Abstracts Service (CAS) number, and synonyms are a good starting point for single chemicals. The data collection and generation process Keywords should be refined when necessary described below has been designed as a flexible during the data collection process to obtain all guideline for assessors. While this process is an available data. Assessors should always obtain effective approach for obtaining most types of references for important data cited in journal data required for assessments of priority articles, reports, and databases. These references substances, information gathering may need to be can verify that data had been correctly cited and customized on a substance-by-substance basis. may also lead assessors to new sources of The lead assessors, with input from their information. Additional guidance on search environmental resource groups, will make 2-1 strategies for mixtures and effluents is presented in available at low cost, including Environment Chapter 8. Data gathered during stage one are Canada information holdings and databases. then used to develop an initial conceptual model This first general search for data should be for the assessment. conducted with the keywords identified previously.
2.2.1 Data Provided by the Priority 2.2.5 Commercial Databases Substances List (PSL) Secretariat Assessors should review the data gathered thus Scientific dossiers prepared by the PSL Secretariat far. Once data gaps are identified, keywords are made available to assessors. These dossiers should be redefined and the search criteria include basic information about the substance’s tailored to target missing data. Assessors should chemical identity and physical and chemical use the information presented in Chapter 2 of the properties. They also provide an initial review of resource document to select commercial toxicological and entry data, international databases with the appropriate focus and scope assessments, and the rationale provided to the for the types of data required. The search strategy Ministers’ Expert Advisory Panel to recommend the for a particular substance may need to be substance for the PSL. For many substances, the changed depending on the focus of a given information provided by the PSL Secretariat may database. The retrieval of irrelevant or duplicate be sufficient to complete the initial scoping stage data can thus be minimized. of the assessment. These data may not be sufficient to conduct initial scoping of complex 2.2.6 Specialty Resources substances; thus, more extensive data collection In order to ensure that all existing data have been may be required (consult Chapter 8 on mixtures found to fill data gaps, assessors should conduct a and effluents for additional guidance). careful search of specialized inventories, 2.2.2 Existing International Assessments databases, or reports. Assessors should use their knowledge of the substance to identify individuals The objective of this step is to collect and review or groups that likely have specialized published or relevant ecological assessments that have been unpublished data. Industry associations, other conducted by organizations such as the U.S. EPA federal government departments, and provincial/ or the Chemicals Program of the Organisation for territorial governments will be important resources Economic Co-operation and Development in this process. (OECD). These assessments may provide valuable scientific data and references. They may also 2.2.7 Concluding Stage One provide assessors with an overall picture of the key The data collected are then reviewed, focusing on issues in the assessment. the most relevant publications and reviews to build 2.2.3 Desk References an initial conceptual model that can be discussed with interested parties and refined throughout the Desk references can provide valuable assessment. While additional data are being environmental information. Sources that should collected during stages two, three, and four, be consulted include chemical dictionaries, assessors should critically review the data used to encyclopedias, guideline reports, handbooks of develop their initial conceptual model to confirm physicochemical properties, texts summarizing that these data are valid. environmental fate and exposure data, etc. 2.3 Stage Two: Problem 2.2.4 Readily Available Databases/ Formulation Refinement with Catalogues Participation of Interested After reviewing PSL dossiers, international Parties assessments, and desk references, assessors should conduct an extensive literature review with In stage two, environmental resource groups and a focus on Canadian data. Assessors should interested parties are invited to help refine the begin with the variety of information sources problem formulation. As well, assessors identify
2-2 people and groups whose information or expertise Division of Environment Canada will work in could assist with the assessment. conjunction with assessors to prepare Section 16 and Section 18 notices. Before notices are sent 2.3.1 Consultation with Interested Parties out, assessors should identify the appropriate Assessors should consult with risk managers, industry sectors or companies to which they should Environment Canada regional offices, research be sent and clearly define the types of information institutes and other interested parties including required. This ensures that notices are read and other government departments, provinces and acted upon by people knowledgeable in the area territories, industry associations and and that replies will be useful to the assessment. representatives, environmental groups, and 2.5 Stage Four: Generation of academia. Such consultations provide an opportunity to tap into scientific and technical Data Through Research support and expertise. They also provide an Research activities will be coordinated from a effective approach to quickly obtain unpublished program perspective by the Chemicals Evaluation data. This step also provides a forum to develop Division of Environment Canada to ensure a partnerships required for research. consistent approach and efficient and cost- 2.4 Stage Three: CEPA Section effective use of resources. 16 and Section 18 Notices 2.5.1 Recommendation of Research Activities Sections 16 and 18 of CEPA may be used to obtain information from Canadian manufacturers, As part of problem formulation, assessors should importers, and users of PSL substances on a identify any research activities that are essential for compulsory basis. This approach allows for a reaching a conclusion about whether or not their consistency and completeness in data gathering. substances are CEPA “toxic”. An ecological risk assessment review group will review the proposed Section 16 of CEPA authorizes the Minister of the data generation needs and identify overall Environment to gather existing data for the priorities and the most efficient means of fulfilling purpose of assessing whether a substance is toxic those needs. The lead assessors will be or capable of becoming toxic. Assessors can responsible for overseeing the generation of data determine whether the required data exist, so that for their substances. Appropriate partners should data gaps critical to the assessment can be be involved in the conduct or sponsorship of this identified and filled. work. Section 18 of CEPA can be used when the Ministers of Environment and Health have reason to suspect that a substance is toxic or capable of becoming toxic. Section 18 provides three methods to gather data about a specified substance. A notice may require that those involved with the substance notify the Minister of the Environment of their involvement, provide specified information in their possession or to which they can reasonably be expected to have access, or perform toxicological and other tests specified by the Minister and submit the test results once completed.
Data gaps should be identified as early as possible in the problem formulation phase, as preparing and executing notices may take several months. The Use Patterns Section of the Chemicals Control
2-3 CHAPTER 3 PROBLEM FORMULATION
3.1 Introduction process, the initial problem formulation will be general and qualitative. As more information is 3.1.1 Goals and Objectives obtained and analyzed, the problem formulation will become more focused, become more explicit Problem formulation is the planning phase in the in its identification of assessment and ecological risk assessment framework. Here, the measurement endpoints, and present more goals and focus of the assessment are established, quantitative details. As the environmental data gaps are identified, and a strategy for assessment proceeds through the entry, exposure, proceeding with the assessment is devised. This and effects characterization phases, problem phase includes the development of an initial formulation should be updated to serve as a scoping and a pathways analysis, consideration of running summary of the assessment. receptor sensitivity, analysis of the ecological relevance of potential receptors, selection of 3.2 Initial Scoping assessment endpoints and associated measurement endpoints, and the development of Initial scoping begins by considering the rationale a conceptual model (Figure 3.1). that the Ministers’ Expert Advisory Panel on the Second Priority Substances List (Ministers’ Expert In the problem formulation phase, risk assessors Advisory Panel 1995) gave for selecting the begin working with risk managers in Environment substance and the expected focus of the Canada and with interested parties in other assessment. Additional preliminary information is governmental departments, industry, non- gathered at this stage (see Section 2.2). governmental organizations and academia to ensure that the environmental assessment will have Information about the identity of the substance is a firm scientific basis and will ultimately be useful presented in the initial scoping stage, including an for decision-making. internationally accepted chemical name, following rules established by the International Union of An example of a problem formulation is presented Pure and Applied Chemistry (IUPAC) or the CAS, in Section 3.3 of the resource document. other commonly used synonyms and trade names, 3.1.2 Relationship with Other Phases and the CAS Registry Number, when available. For elements, the relative abundances of isotopes, Information set out in the problem formulation oxidation states in the environment, and the phase is used as the starting point for more in- identities of common environmental forms should depth analyses that follow during the also be determined. This information is needed to characterization of entry, exposure, and effects. It permit an efficient literature search and other is thus important that an initial problem data-gathering activities. In addition, the formulation be completed as early as possible in molecular structure of organic chemicals should the assessment process. Problem formulation is be elucidated for possible use in models or QSARs an iterative process. When little information about for exposure or effects characterization (Chapters a substance is available at the beginning of the 5 and 6). 3-1 Problem Formulation Initial Pathways Receptor Ecological Scoping Analysis Sensitivity Relevance Verification/Data Generation
Constraints (e.g., Data Availability, Time, Costs)
Assessment Endpoints Subject Characteristics Numerical Expression
Measurement Endpoints
Conceptual Model
Entry, Exposure and Effects Characterization
Figure 3.1 The problem formulation phase in the ecological risk assessment framework for priority substances
Physical and chemical properties of the substance 3.3 Pathways Analysis should be determined for predicting its environmental fate and potential effects. For Pathways analysis considers a substance’s entry organic substances, these usually include into the environment and its probable molecular weight, molecular volume, water environmental fate. This analysis is used to predict solubility, vapour pressure, partition coefficients, a substance’s geographic distribution and fate in and dissociation constants. For inorganic the Canadian environment and to identify substances, relevant properties vary depending potential receptors that may be exposed to it. upon the chemical forms (e.g., atoms, compounds, or complexes). Important parameters Consideration must be given to the potential for for inorganic substances include atomic or environmental releases at any stage of a molecular weight, water solubility, equilibrium commercial substance’s life cycle, from constants, and vapour pressure. Values chosen manufacture through distribution and use to final for key parameters used in fate or exposure disposal. A substance may also enter the models may significantly affect model predictions. Canadian environment in other ways — for Therefore, values for key parameters should be example, from natural sources, by transboundary determined as accurately as possible and any transport, as a transformation product of another uncertainty clearly presented. Experimental substance, or as a component of a mixture. methods of quantification are preferred, but To characterize environmental releases, calculated values based on QSARs, for example, information is required on: may be acceptable at this stage.
3-2 • amounts manufactured, imported, and transformation products,1 and its bioavailability exported, and tendency to bioaccumulate in living tissue may be required for models that can help to • specific uses, including amounts used for characterize the environmental fate of a substance various applications, and to define sensitive parameters and data gaps • significant sites of release in Canada from when establishing research priorities. The human activities and from natural processes, characterization of the environmental fate of a substance is discussed in more detail in • amounts, forms, and conditions under which Section 5.3. the substance is released into the Canadian environment, Information about quantities of a substance released in specific regions within Canada can be • temporal patterns of releases (e.g., used to predict its concentration in various continuous, intermittent, seasonal), and environmental compartments in these regions. Models may be used to make such predictions • environmental compartments (e.g., air, water, (see Chapter 5). If Canadian environmental soil) receiving releases. monitoring data are not available, data from This information enables assessors to estimate how similar areas, such as the northern United States, much of the substance is being released into the may be used to support the plausibility of Canadian environment and where and how often predicted environmental concentrations. A these releases are occurring. This information discussion of the characterization of environmental also serves as a starting point for the next step — concentrations is presented in Section 5.6 of the characterization of the substance’s environmental resource document. fate. From the initial characterization of environmental A substance’s environmental fate may be partitioning and fate and predicted environmental characterized by: concentrations, it is possible to predict, in a general way, ecosystems that are at risk (e.g., • identifying its probable environmental aquatic ecosystems). When specific sites of partitioning to air, soil, surface water, release are known, it is then possible to identify the groundwater, sediment, and biota and ecosystems more precisely (e.g., a specific stretch estimating its persistence in these of a river). Within ecosystems, particular compartments, components may be exposed to the substance under investigation. For example, benthic • estimating its geographic distribution and organisms are likely to be exposed to substances concentration ranges in the Canadian that partition to sediments. When precise environment, ecosystems have been identified, it is then possible to more precisely identify the components of those • identifying ecosystems that may be exposed to ecosystems that may be exposed (e.g., benthic the substance, and organisms in a specific stretch of a river). • identifying living or nonliving components of Nonliving components of the environment upon the ecosystems that may be exposed. which human life depends may also be exposed Information about a substance’s physical and and considered in the environmental assessment. chemical properties, amounts released into various For example, stratospheric ozone may be exposed compartments of the environment and persistence to persistent substances that reach the stratosphere in these compartments, the identity of its when released into air.
1 A transformation product may itself have the potential to cause adverse effects in the environment. If such a product is present in the environment primarily because of the transformation of the parent substance, the potential risks of the transformation product could be assessed along with those of the parent. If there are other major sources of the transformation product, the product should be considered as a candidate for a separate assessment (see further discussion in Section 5.4 of this guidance manual and the resource document). 3-3 3.4 Receptor Sensitivity for all ecological levels of organization (U.S. EPA 1992a; ASTM 1994). Possible assessment Consideration of receptor sensitivity involves the endpoints at the ecosystem level include primary analysis of information about the substance’s productivity, energy flow, nutrient cycling, and mechanism of toxicity and effects data from decomposition of organic matter. At the laboratory or field studies. This information is community level, assessment endpoints could used to identify species or larger taxonomic groups include biodiversity, including species richness and that are particularly sensitive to the substance and evenness, and food web structure. Possible to determine concentrations or doses that cause assessment endpoints at the population2 level adverse effects. QSARs may also be used in the could include population abundance, reproductive initial identification of sensitive organisms. Often, success, and age and size structure. At the the identity of particularly sensitive organisms is individual level, assessment endpoints could unknown. It is therefore desirable to review effects include survival or physiological status, data from a battery of toxicity tests using reproductive capacity, growth rate and organisms from several taxonomic and trophic development, and behaviour. When expressing levels. Such organisms should be representative an assessment endpoint, assessors should identify of biota in the environmental compartment(s) to an ecological component, such as a trout which the substance of concern is believed to population, and a characteristic of that partition. component, such as reproductive success. 3.5 Ecological Relevance Assessment endpoints selected at the population level will probably be most common in PSL The environmental roles of highly exposed or assessments. In many cases, abundance of the sensitive receptors should be analyzed in order to most sensitive species in each environmental identify the receptors’ ecological relevance and to compartment of concern may be a practical predict possible indirect effects on other ecosystem assessment endpoint to consider first. components, such as predator or prey species. Consideration of the species’ role in the This can be accomplished by considering the environment may suggest that an assessment receptors’ life cycles and by determining any endpoint at a higher level in the ecological special functions that they may have in the hierarchy (i.e., ecosystem > community > environment. For example, microorganisms may population) may be more appropriate. For be vitally important in nutrient cycling, and example, an adverse effect on microorganisms earthworms are important for the aeration and that are important decomposers may indicate an conditioning of soil. ecosystem endpoint such as “the rate of nutrient cycling.” When it is not possible to select The results of the initial scoping exercise, pathways assessment endpoints above the population level, analysis, and consideration of receptor sensitivity it may still be useful to indicate potential direct or and ecological relevance are then used to select indirect effects at higher levels, recognizing that assessment and measurement endpoints. extrapolating up the ecological hierarchy 3.6 Choosing Assessment introduces additional uncertainty at each step. Endpoints Several assessment endpoints are needed to assess substances that partition to more than one An assessment endpoint is “a quantitative or environmental compartment or that occur in the quantifiable expression of the environmental value environment in a number of geographic areas. considered to be at risk in a risk assessment” Furthermore, selection of several assessment (Suter 1993). Potential assessment endpoints exist endpoints ensures that a range of ecosystem components is considered in the assessment.
2 A “population” may be defined as a collective group of organisms of the same species occupying a particular space and having the potential to reproduce. 3-4 3.7 Choosing Measurement mortality derived from toxicity test results or field Endpoints surveys (ASTM 1994). Lethality and reproductive impairment, measured in laboratory toxicity A measurement endpoint is “a quantitative studies, provide a strong link to the potential summary of the results of a toxicity test, a effects of the substance on the growth and survival biological monitoring study, or other activity of natural populations. intended to reveal the effects of a substance” (Suter 1993). Each assessment endpoint must 3.8 The Conceptual Model have one or more measurement endpoints. A conceptual model describes as explicitly as Measurement endpoints are needed because possible a substance’s predicted fate, the assessment endpoints often refer to characteristics mechanisms by which it could affect assessment of populations, communities, and ecosystems endpoints, and the likely ecological consequences defined over fairly large geographic areas and of these effects. The level of detail, the relatively long time periods. These factors make information needed, and the methods to be used the direct measurement of effects difficult or to complete the assessment, including any impossible. The relationships between assessment research needed to fill data gaps, should also be and measurement endpoints must be clearly specified. described. The conceptual model is developed by Unlike assessment endpoints, measurement constructing a series of qualitative exposure endpoints are commonly selected at the individual scenarios that describe how the priority substance level of the ecological hierarchy. If an assessment could affect the assessment endpoints. Each endpoint is the population abundance of a scenario defines the assessment and measurement particular species of fish, an appropriate endpoints, their relationship, and spatial, measurement endpoint could be the result of an geographic, and temporal scales (U.S. EPA acute or chronic toxicity test using the same 1992b). Each scenario should also describe the species or a related species. Similarly, if methods and analyses that will be used to estimate abundance of an endangered raptor were chosen risk. As there is no universal method for as an assessment endpoint, dietary LD values 50 quantifying environmental risk, several methods from studies with another bird species would be an that aid in the process should be specified (Suter appropriate measurement endpoint. For the and Barnthouse 1993). Possible methods include: protection of terrestrial plants, necrosis, chlorosis, or reduction in growth of legumes or conifer • field studies or fate models to estimate seedlings resulting from soil or atmospheric exposure, exposure to the substance could be used as the measurement endpoint. • statistical regression techniques to estimate effects levels for measurement endpoints, Acceptable measurement endpoints for ecosystem- level assessment endpoints include measurements • the quotient method to compare exposure and of total biomass, productivity, and nutrient effects estimates, dynamics derived from microcosm or mesocosm • use of empirical field data or Monte Carlo studies or from field surveys if a cause-and-effect analyses to estimate the probabilities of relationship can be established. Acceptable specified effects, and measurement endpoints for community-level assessment endpoints include number of species, • population models to estimate, for example, measures of species evenness, community quality risks of extinction over a given time period. indices, and changes in community type derived from microcosm studies or field surveys. The rationale for choosing a particular scenario or Acceptable measurement endpoints for method should be documented (U.S. EPA 1992b). population-level assessment endpoints include Assessors should consult with risk managers at abundance, age and size distributions, Environment Canada (e.g., Commercial reproductive performance, and frequency of mass
3-5 Chemicals Evaluation Branch, National Office of 3.10 References Pollution Prevention, or Air Pollution Prevention Directorate, depending on the type of substance) ASTM (American Society for Testing and to determine if the proposed conceptual model Materials). 1994. Standard guide for selecting will provide information to support any subsequent and using ecological endpoints for risk management decisions. Assessors should also contaminated sites. Draft. Philadelphia, discuss the conceptual model with interested Pennsylvania. parties and selected experts to refine the proposed model and to prepare plans to conduct new Hope, B.K. 1995. Ecological risk assessment in a studies if necessary. When the conceptual model project management context. Environ. Prof. 17: and the plan to carry out the assessment have 9–19. been determined, the detailed entry, exposure, Ministers’ Expert Advisory Panel. 1995. Report of and effects characterization phases of the the Ministers’ Expert Advisory Panel on the environmental assessment can begin. Second Priority Substances List under the An example of a conceptual model is included in Canadian Environmental Protection Act (CEPA). Section 3.3 of the resource document. Ottawa, Ontario. 26 pp. Suter, G.W. 1993. Glossary. In G.W. Suter 3.9 Some Points to Remember (ed.), Ecological risk assessment. Lewis • Consult other interested parties and involve Publishers, Chelsea, Michigan. pp. 497–505. them in the scoping process. Suter, G.W. and L.W. Barnthouse. 1993. • Identify and involve experts in the assessment. Assessment concepts. In G.W. Suter (ed.), Assessors often feel that opening up the Ecological risk assessment. Lewis Publishers, process leads to additional out-of-scope Chelsea, Michigan. pp. 21–47. requirements and could adversely influence U.S. EPA (United States Environmental Protection the scientific integrity of the assessment. Agency). 1992a. Peer review workshop report Although such concerns are sometimes on a framework for ecological risk assessment. warranted, the risk assessment is far more EPA/625/3-91/022. Risk Assessment Forum, likely to lead to effective risk management Washington, D.C. 100 pp. decisions if assessors and interested parties have a clear understanding of the assessment U.S. EPA (United States Environmental Protection objectives and methods at the outset (Hope Agency). 1992b1992b. Framework for ecological risk 1995). assessment. EPA/630/R-92/001. Risk Assessment Forum, Washington, D.C. 41 pp. • Present and review all relevant information.
• Present the rationale for choosing assessment and measurement endpoints.
• Present the conceptual model used for risk analysis and risk characterization.
3-6 CHAPTER 4 ENTRY CHARACTERIZATION
4.1 Introduction Figure 4.1 summarizes the main steps involved in entry characterization. 4.1.1 Goals and Objectives 4.2 Identification of Sources The entry characterization phase identifies the anthropogenic and natural sources of a substance The first step in entry characterization is to identify and estimates the amounts and frequencies of its a substance’s sources in Canada. This includes release into the Canadian environment. This natural and anthropogenic sources and information is then used to assess the relative transboundary sources. Although major sources significance of various sources and help define the should have been identified during the problem spatial and temporal scales for the assessment. formulation stage, some significant sources may have been missed, or data may have been 4.1.2 Relationship with Other Phases lacking.
In the entry characterization phase, the entry 4.2.1 Natural Sources portion of the pathways analysis developed during problem formulation is verified and refined. This Inorganic and organic substances may be is achieved by accurately identifying and produced by a wide variety of natural processes. quantifying the various sources and releases. All processes leading to a substance’s release into Entry characterization sets the stage for the the Canadian environment should be identified so characterization of exposure. For example, that effects due to anthropogenic versus natural information about sources and releases is required sources can be differentiated. as inputs to fate and transport models (Chapter 5). For substances declared “toxic” as defined in Natural sources of inorganic substances to the Section 11 of CEPA, entry characterization atmosphere include windblown dusts, sea spray, provides information essential for developing volcanic emissions, crustal degassing (Rasmussen strategic options. 1994), volatile exudates from plants, volatile compounds formed by soil microbial activity Access to current and accurate information is key (Cullen and Reimer 1989), and natural to completing an accurate and useful risk combustion events (Havas and Hutchinson 1983). assessment. Chapter 2 describes several For soil, bedrock or glacial deposits from which it mechanisms by which to obtain entry information. was derived are the primary natural sources. This information is often difficult to obtain because Inputs also occur from natural atmospheric fallout it is typically site-specific and is usually not and from sediment deposits in areas subjected to available in the published literature. To overcome periodic flooding. Primary natural sources of these difficulties, it is imperative to establish, as inputs to aquatic systems are weathering and early as possible, a forum for the efficient erosion of geological materials and natural exchange of information among risk assessors, risk atmospheric fallout. managers, and other interested parties.
4-1 Problem Formulation
Entry Characterization
Identification of Sources
Establish efficient communication channels between risk assessors, risk managers and other interested parties Identify natural and anthropogenic sources
Characterization of Releases
Quantify concentrations or environmental loadings for Exposure Characterization significant sources Determine the frequency and pattern of releases Describe the physical and chemical nature of releases
Risk Characterization
Figure 4.1 Entry characterization in the ecological risk assessment framework for priority substances
Many organic substances, including halogen- The amount of the substance imported annually containing chemicals, may be produced by natural into Canada should be determined, along with its processes. Many types of organisms, including destination by province/territory or city. terrestrial plants, fungi, microorganisms, and mammals, contain haloperoxidase enzymes that Expected modes of transportation, distribution, can halogenate organic compounds in the and storage should be identified, because presence of chloride, bromide, or iodide (Gribble environmental releases can result from accidents 1994). such as pipeline ruptures, train derailments, tank truck collisions, and leakage from storage tanks. 4.2.2 Anthropogenic Sources The specific uses and applications of the Environmental releases can occur at any time substance in Canada should be determined. during a substance’s life cycle, including When possible, this should include the identity and production, transportation, use, and disposal. locations of industrial, commercial, and institutional users of the substance. Information Manufacturing sites, which may include raw about the substance’s domestic or household uses material extraction and chemical syntheses, should should also be obtained. be identified along with estimates of annual production at each site. Releases at the Required information about the disposal of the manufacturing and processing stage may take a substance includes disposal sites and a general variety of forms, including liquid effluents, stack description of disposal methods. Different gases, and accidental or fugitive emissions. environmental compartments may be affected,
4-2 depending upon the treatment or disposal method • describe the substance’s physical and employed. For example, incineration can result in chemical nature. significant atmospheric emissions as a result of incomplete combustion or reactions of 4.3.1 Quantifying Releases components in stack gases. Landfills that are not Releases of a substance can be characterized in adequately sealed can release soluble substances several ways. Key quantitative parameters are to local soils and groundwater. Disposal of concentrations of the substance in effluents, municipal sewage sludge on agricultural land can stacks, or the receiving environment and result in releases of volatile substances to air and environmental loadings — amounts released per soluble substances to local soils and groundwater unit of time. (Webber and Shamess 1987; Webber 1990). In general, site-specific monitoring data provide 4.2.3 Transboundary Sources the most accurate means of estimating substance Substances can enter the Canadian environment concentrations and rates of release in stack gases, through long- and short-range transport. effluents, spills, etc. (Carpenter et al. 1990). Transboundary transport is a well-known source of However, monitoring data are often unavailable. persistent substances, but it can also be significant Even when such data exist, their quality can vary for less persistent substances if an important depending on the location of sample stations, the source is located near the Canadian border. An accuracy of monitoring techniques, and the timing example is smog and incinerator emissions of sampling and release events. Also, because of migrating from Detroit into the Windsor area. the nonpoint nature of many natural sources, it is Entry of substances into Canada by aquatic often difficult to obtain accurate empirical transboundary transport has been well estimates of natural release rates. In cases where documented. An example is the contamination of monitoring data are of insufficient quality or the Great Lakes and St. Lawrence River from quantity to allow the reliable quantification of landfill sites in the United States. releases from major sources, release estimates may be based on model calculations or emission 4.2.4 Indirect Sources factors.
In addition to the direct releases listed above, Models used to characterize releases may be some substances can be formed in the simple mass-balance types, requiring information environment from other synthetic substances as a on a few easily obtained parameters, or more result of natural biotic or abiotic transformation complex ones, requiring more extensive processes. Trichlorobenzenes, for example, can information on system processes, data from be formed in anaerobic sediments by reductive monitoring programs, historical records, or dechlorination of more highly chlorinated assumptions about probability distributions. Case benzenes (Hollinger et al. 1992). Such processes Study 4.1 in the resource document provides an should be identified and their contribution to example of a simple mass-balance model used to measured ambient exposures taken into account. quantify releases from municipal wastewater treatment plants. This type of model can also be 4.3 Characterization of Releases used to quantify releases from natural sources, if steady-state conditions in the receiving Once the key sources have been identified, entry compartment are assumed. Case Study 4.2 in the characterization should focus on a more refined resource document provides an example of the analysis of the specific characteristics of the use of a more complex model. releases. Data gathered during this step should, to the extent possible, be quantitative. The Emission factors are usually expressed as the mass objectives are to: of a substance emitted per unit of mass or volume of product or per unit of time during a production • quantify the substance’s releases in Canada, process. Factors may be generated using • identify the frequency and patterns of the monitoring data, models, or professional releases, and judgment. Lists of factors for predicting releases of
4-3 substances from industrial sources have been other hand, are usually consumed in chemical compiled by various national and international processes and are released in only limited agencies (e.g., CEU 1995). Care must be used quantities. Estimates of the amounts of a when applying such factors to ensure that they are substance used in different applications, combined based on conditions that are relevant to the with dispersivity data, can indicate the magnitude industrial processes and emissions control of releases in different areas. technology currently used in Canada. Release estimates based on emission factors are generally When comparing releases from different sources, less reliable than those based on monitoring or it is important to recognize that the magnitude and site-specific models. If the uncertainty surrounding spatial extent of environmental impacts may differ the estimates of releases is judged to be depending on whether releases are point or unacceptable, it will be necessary to confirm the nonpoint. For example, while the absolute estimates using empirical data. Case Study 4.3 in magnitude of releases from nonpoint sources may the resource document provides an example of be large, the environmental impact may be small how emission factors may be used to estimate if releases are spread over wide areas. releases of an organic chemical associated with Conversely, although releases from a point source different commercial applications. may be small in absolute terms, they may cause significant harm locally if they are confined within Release data pertaining to leakage from storage a limited area. facilities or to accidents during transportation are not always available. These data may be of 4.3.3 Chemical and Physical Nature of the limited use in estimating exposure, as the Substance Released into the magnitude and locations of such releases are Environment often not adequately reported. Material balances An analysis of a substance’s physical and chemical showing the volumes of substances being properties should be conducted for each transported, the principal modes of transportation, significant source. This is used during exposure the physical form of the substance during characterization to gain an understanding about transport, and the locations of shipping and how a substance is likely to partition in the receiving points may be useful in identifying areas receiving environment. that are most at risk of exposure from some of these inadvertent releases. Assessors should obtain site-specific information about a substance’s physical forms and chemical 4.3.2 Frequency and Patterns of Releases nature. This is especially important for metals and The frequency and patterns of releases from each other chemical elements that can be released in a major source should be determined whenever variety of forms, each with its own reactivity and possible. For example, a substance may be mobility properties. For organic substances, the released from a site continuously or intermittently. chemical form is usually defined, but physical The quantities that are released may vary with the phase association (e.g., aqueous solution or seasons. If releases are intermittent, monitoring suspended solid in an effluent) can vary. This may periods must be long enough to allow the be an important fate determinant. For solids distribution of their severity and the time interval released into air and water, properties of between releases to be ascertained. Seasonal particular importance include density, size and variations in release rates should be determined, shape (which determine their rates of removal by as variations can affect loading estimates, which gravitational settling), and solubility (which are needed to make meaningful exposure determines their persistence in the solid form and estimates. ultimately their bioavailability) (Webber and Shamess 1987; Webber 1990). The quantity of a substance released into the environment varies depending upon its use. 4.3.4 Recognition of Trends in Releases Solvents used for cleaning are highly dispersive; Changes in release quantities and patterns may much of the amount used is released into the occur because of changes in the quantity of a environment. Chemical intermediates, on the substance produced or used at a facility. They 4-4 can also occur as a result of changes in industrial Cullen, W.R. and K.J. Reimer. 1989. Arsenic processes or waste treatment technologies. speciation in the environment. Chem. Rev. 89: Therefore, it is necessary to note any recent trends 713–764. in environmental releases, so that possible exposure scenarios may be considered during the Gribble, G. 1994. The natural production of exposure characterization phase. For example, it chlorinated compounds. Environ. Sci. Technol. may take many years for a persistent substance to 28(7): 310A–319A. disappear from sediments, soil, or groundwater, Havas, M. and T.C. Hutchinson. 1983. The even if releases have been stopped or severely Smoking Hills: Natural acidification of an reduced. Less persistent chemicals would aquatic system. Nature 301: 23–27. disappear more quickly. In these cases, assessors may need to obtain sufficient data about past Hollinger, C., G. Schraa, A.J.M. Stams, and releases so that the relative contribution of recent A.J.B. Zehnder. 1992. Enrichment and loadings can be estimated. Any anticipated properties of an anaerobic mixed culture increases or decreases in releases or changes in reductively dechlorinating 1,2,3- release patterns should be noted so that future trichlorobenzene to 1,3-dichlorobenzene. Appl. exposure scenarios may be predicted and taken Environ. Microbiol. 48(4): 1636–1644. into account in the assessment. Rasmussen, P. 19941994. Current methods of 4.4 Some Points to Remember estimating atmospheric mercury fluxes in remote areas. Environ. Sci. Technol. 28(13): 2233– • Identify and quantify potential sources, levels 2241. in the environment, pathways, and routes of exposure, and acknowledge and estimate Webber, M.D. 1990. Municipal sludge, organic uncertainties in these values. contaminants and agricultural utilization. In R.H. Louie, A. Bomke, and H. Schreier (eds.), 4.5 References Soil pollution in British Columbia. Proceedings of the 13th Meeting of the British Columbia Soil Carpenter, C.E., C.R. Lewis, and W.C. Crenshaw. Science Workshop. Vancouver, B.C. pp. 146– 1990. Estimating emissions from the synthetic 163. organic chemical manufacturing industry: An overview. Toxic Subst. J. 10: 323–371. Webber, M.D. and A. Shamess. 1987. Heavy metal concentration in Halton region soils: An CEU (Commission of the European Union). 1995. assessment of future municipal sludge utilization. Draft technical guidance on risk assessment of Can. J. Soil Sci. 67: 893–903. existing substances. Appendix I. Brussels, Belgium. pp. AI-1–AI-26.
4-5 CHAPTER 5 EXPOSURE CHARACTERIZATION
5.1 Introduction 5.2 Pathways Analysis
5.1.1 Goals and Objectives Detailed pathways analysis for a substance should integrate data on: The purpose of this phase of the assessment is to quantify contact between a substance1 that has • its releases from identified anthropogenic been released from anthropogenic sources and sources, appropriate receptors.2 The primary outputs are • its physical and chemical properties and EEVs, expressed as concentrations or doses for those of the receiving environment, and identified receptors in areas of concern. Estimates • key transport and transformation pro- of natural contributions to EEVs may be required cesses. for natural substances. Figure 5.1 summarizes the principal steps involved in detailed exposure characterization. The objective is to refine the initial pathways analysis developed for problem formulation and to 5.1.2 Relationship with Other Phases verify the environmental media in which the substance accumulates, as well as the size and Exposure characterization builds upon the location of the areas likely to be affected. The pathways analysis portion of initial problem identity and main routes of exposure of the formulation (Chapter 3) and release information principal receptors should also be verified at this obtained from detailed entry characterization stage. A table listing the primary routes of (Chapter 4). A calculated or measured maximum exposure for different classes of organisms is EEV is used as the numerator in a risk quotient for provided in Chapter 5 of the resource document. Tiers 1 and 2; frequency distributions are used to characterize EEVs for Tier 3 (Chapter 7). Estimates of natural contributions to exposure may be used during risk characterization (Chapter 7), to set lower bounds on ENEVs for natural substances and to evaluate the potential for natural tolerance in receptor organisms.
1 Exposure characterization for complex mixtures and effluents is described in Chapter 8.
2 When receptors are wildlife species (birds, mammals, amphibians, or reptiles), assessors should contact the Canadian Wildlife Service of Environment Canada for additional guidance on exposure characterization.
5-1 Problem Formulation
Exposure Characterization Verification/Data Generation
Refine Initial Pathway Analysis
Determine Estimated Exposure Values (EEVs)
Estimate Natural Background (If Required) Entry Characterization
Risk Characterization
Figure 5.1 Exposure characterization in the ecological risk assessment framework for priority substances
Detailed pathways analysis may be qualitative, environmental distribution on more local scales.3 although quantitative analysis — using numerical Food chain bioaccumulation models (e.g., models — is preferred. Regional multimedia Thomann 1989) could be used to estimate transfer fugacity models (e.g., Mackay et al. 1991; Cowan of organic substances across several trophic levels. et al. 1995) could, for example, be used to predict Experts should be consulted when using complex the identity of environmental compartments in models. which organic substances accumulate. Single- medium models for air, surface water, groundwater, or soil (e.g., ECETOC 1992; Crowe and Mutch 1994) could also be used to predict
3 Guidance on the selection of such models may be found, for example, in U.S. EPA (1987, 1988, 1991).
5-2 Accepted experimental methods of quantifying such properties are preferred (e.g., OECD Box 5.1 Example of Qualitative Pathways 1993a); however, values calculated as described Analysis by Lyman et al. (1990) or OECD (1993b) may be A qualitative pathways analysis relating acceptable. leakage from an above ground storage tank Properties of the receiving media can also to exposure of organisms in a nearby stream influence the behaviour, chemical form, and could take the form of a statement that, environmental concentrations of a substance. because Parameters of possible importance include light • the concentration of a persistent substance intensity, pH, oxidation potential, temperature, in an aquifer below a leaking tank, used to intermedia partition coefficients, physical store the substance, was observed to dimensions, and bulk densities of environmental decrease with increasing distance from the compartments. When used in numerical models, tank, and values for key environmental properties and their • the groundwater is flowing relatively uncertainties should, whenever possible, be based rapidly towards the stream, and on field data from the area of concern. • the substance was detected in the stream, The nature and rates of key transport and below (but not above) the expected point transformation processes affect the environmental of entry of the contaminated groundwater persistence and possibly bioavailability of a plume, substance. Transformation processes of potential importance include complexation, precipitation release of the substance from the tank and its and dissolution, sorption and desorption, oxidation dispersion in groundwater have resulted in and reduction, hydrolysis, volatilization, photolysis, exposure of organisms in local surface water. and biotransformation (e.g., Mill 1993; Hamelink et al. 1994). Rate values determined empirically using acceptable laboratory or field test methods When numerical modelling methods cannot be (e.g., Knox et al. 1993; OECD 1993a) are applied or are not required — because there are preferred. If required, however, rates may be abundant field data, for example — pathways based on calculated values (e.g., OECD 1993b). analyses may be expressed in conceptual terms (e.g., Box 5.1). The extent to which a substance accumulates in organisms that serve as food sources for sensitive 5.2.1 Verifying Pathways Analyses predators should be determined as bioaccumulation or bioconcentration factors (BAFs Whenever possible, data on measured or BCFs). BAFs are the preferred measure of concentrations of the substance in areas and accumulation potential; however, BCFs are also media of concern should be used to verify acceptable, particularly when ingestion of food is accumulations predicted by pathways analyses. not expected to be an important exposure route. 5.2.2 Quantifying Fate Parameters BAFs are usually calculated from field data, whereas BCFs are normally determined Values assigned to key fate parameters may experimentally. BCF test durations should be significantly affect pathways analysis. Values for sufficient to achieve a steady-state concentration in such parameters, and their uncertainties (e.g., the test organism (ASTM 1993; OECD 1993a). 95% confidence intervals), should be determined For organic substances, BCFs may also be as accurately as possible, particularly when used estimated from QSARs or Kow values (e.g., OECD in numerical fate or exposure models. 1993b). Because of the complexity of uptake processes, BAFs and BCFs for metal cations — The physical and chemical properties of a especially for nutritionally essential elements — substance, such as vapour pressure, partition should be applied only to organisms and exposure coefficients, and aqueous solubility, can conditions similar to those for which they were significantly influence its environmental fate. measured (CEU 1995; MMWG 1996).
5-3 5.3 Quantifying Exposure of intake. When more than one medium could contribute significantly to external exposure, EEVs Generally, exposure should be quantified as a should be calculated as the sum of intakes of all distribution of empirically determined or calculated relevant media. In the case of radionuclides, the EEVs for each identified receptor in each area of EEV will be the total dose of radiation. Total dose concern. includes dose from radionuclides within the organisms (internal dose) and that received from 5.3.1 Approaches to Quantification radionuclides in the environment (external dose, EEVs may be based on concentrations of the e.g., in sediment and water). A computerized substance in tissues of exposed organisms or on exposure model for organic substances developed various measures of external exposure (Suter by the Canadian Wildlife Service can be used to 1993). For dermal contact, EEVs may be calculate multimedia exposures of birds, expressed as concentrations in external media such mammals, amphibians, and reptiles. Assessors as water or soil. In cases of exposure by ingestion should contact the Canadian Wildlife Service or inhalation, EEVs should be determined as rates regarding its use. An example of output from this model is illustrated in Table 5.1.
Table 5.1 Estimated maximum total daily intake of hexachlorobenzene for a 1-kg adult mink in the St. Clair River area.
Medium Maximum Concentrationa Intake of Mediumb Maximum Daily Intake (ng•kg-bw-1•d-1)
Air 0.29 ng•m-3 0.55 m3•d-1 0.16 Water 87 ng•L-1 0.1 L•d-1 8.7 Diet 1: 100% fish 283 ng•g-1 215 g•d-1 60 845 Diet 2: 100% birds or mammals 30 ng•g-1 158 g•d-1 4 740
Total Daily Intake — for Air, Water, and Diet 1 60 854
Total Daily Intake — for Air, Water, and Diet 2 4 749
a Concentration data were obtained from Health Canada and Environment Canada (1993), assuming that concentrations in birds and mammals are approximately equal. Note that bioavailability is not considered in this example. b Methods of estimating intake of each medium are described in Moore et al. (1996).
EEVs for complex routes of exposure may be 5.3.2 Use of Field Data estimated as an internal dose using toxicokinetic models (Suter 1993). As explained in Chapter 5 EEVs, particularly those used in Tiers 2 and 3, of the resource document, although biomarker should usually be based on results of monitoring data may be used qualitatively, as part of the studies undertaken in the areas of concern. weight-of-evidence approach for estimating Methods of sample collection, handling, storage, exposure to certain substances, biomarker and analysis used in key studies should be measurements should not be used as surrogates carefully evaluated. Methods should, ideally, for more conventional dose or concentration data. follow acceptable protocols, such as CCME 5-4 (1993). When chemical species are determined, 5.3.3 Use of Calculated Values changes in chemical form should be avoided. Methods should also avoid contamination or loss Although EEVs that are directly measured are of analyte prior to or during analysis. Data on preferred, Tier 2 and 3 EEVs may be calculated by accuracy, precision, and detection limits of key applying simple exposure conversion models to analyses should be reviewed. To demonstrate concentration data for key exposure media (Table accuracy, standard reference samples (e.g., 5.2). For example, Environment Canada 1995) may be analyzed; concentrations reported should be within the accepted range. Analytical precision or • equilibrium models (see Appendix II of the reproducibility is usually acceptable if results of resource document) may be used to repeated analyses of a typical sample are within calculate concentrations of bioavailable 20% of the average value for the sample, at forms of a substance, approximately the 95% confidence interval.4 Less • body burden values may be calculated as precise data may be acceptable in some the product of measured concentrations in circumstances, however. An analytical method is an exposure medium and a BAF, or usually not acceptable if concentrations in most • total rate of intake may be calculated as samples analyzed are below detection limits, and the sum of measured concentrations in a more sensitive method should be sought. exposure media, including food, water, However, if detection limits are significantly lower and air, multiplied by consumption rates than the ENEV, a “not detected” result may be (e.g., Table 5.1). useful.
Sampling and analytical strategies should ideally When concentration data for key exposure media permit the characterization of spatial and temporal are lacking, outputs from simple exposure models variations of exposure both in areas of concern that have been adequately validated may be used and in appropriate background or reference to determine EEVs for Tiers 2 and 3, but only if the locations. uncertainties associated with calculated exposure values are small (Table 5.2). An example would EEVs should, to the extent possible, reflect current be a dilution model, where a measured 5 exposure conditions. Therefore, exposure concentration in an effluent is divided by a dilution estimates are preferably based on data that are no factor. When there is significant uncertainty more than a few years old. Older data may be associated with model outputs (e.g., for more acceptable when releases have not changed complex fate and exposure models that have not significantly over time and when: been adequately fiel tested), results should be used • estimating exposure values for Tier 1, only to complement empirical data, as part of a • estimating levels of a persistent substance weight-of-evidence approach to quantifying in media expected to remain composition- exposure. Tier 1 is exceptional, however, in that ally stable for relatively long periods (e.g., EEVs may be based entirely on complex or some soils and sediments), or uncertain model predictions, but only models have • determining natural background concen- been properly validated and when conservative trations of a substance. assumptions are made about exposure parameters (Table 5.2).
4 Precision is sometimes also expressed as a coefficient of variation. The coefficient of variation that corresponds to a precision of 20%, at approximately the 95% confidence level, is 0.1.
5 It is not necessary, however, that EEVs reflect current environmental loadings. For example, EEVs based on concentrations of persistent substances in recent samples of soil and sediment may be more reflective of historic than of current emission rates.
5-5 bioavailability a Values b Montesimulations of or Exposure Bioavailability over Time Simulations Range Types of Parameter value models or best estimate Guidance on application of tiered approach to quantifying exposure. Empirical Data Monte Carlo Home Acceptable Conservatism value measuredmaximum value complex maximum For example, BCFs, rate constants, etc. Outputs from more complex exposure models may be used to support empirical data. a b 2 95th percentile possiblysimple only intermediate use Table 5.2 1 99.9th percentile noor simple highest assume Tier Representation of EEVs Average3 distribution of values Modelsof Treatment Carlo-type lowest bioavailability
5-6 As indicated in Chapter 7, Monte Carlo methods Tissue concentrations may be based on analysis of may be used to derive distributions of EEVs for Tier a whole body or individual organs. Information 3, when EEVs are calculated as a function of two on the mechanism of action and pharmacokinetic or more exposure variables represented as properties of the chemical/organism combination distributions (e.g., distributions of concentrations in is needed to determine whether specific organs or food and of food intake rates). whole-body burdens should be used (Norton 1996). 5.3.4 Determining Bioavailability It may be appropriate to normalize whole-body In order to compare critical exposure and effects burdens of hydrophobic substances, with relatively data, the bioavailability of the substance in both rapid excretion rates, to lipid contents (Gobas and data sets should be similar (CEU 1995). Mackay 1989).6 This is less appropriate for very Generally speaking, toxicity studies are conducted slowly excreted chemicals with depuration rates under conditions that maximize bioavailability. For lower than growth rates (e.g., Borgmann and example, studies with aquatic organisms are Whittle 1992). As whole-body data on the metal typically conducted using soluble forms of a content of organisms may not be indicative of substance (e.g., a soluble metal salt) in test water potential biological effects (Hare 1992; Cain et al. that is free of the dissolved organic matter and 1995), data on metal levels in specific tissues suspended solids that commonly reduce (e.g., bone or blood) or cell components (e.g., bioavailability in natural waters. cytosol) may be preferred.
Consequently, for Tiers 2 and 3, EEVs should When data on metal concentrations in tissues generally be based on concentrations of are lacking, values may be calculated using bioavailable forms of substances. For some empirically derived regression equations (e.g., substances, it may be appropriate to normalize Box 5.2). These typically relate concentrations of EEVs — and CTVs — to parameters that control a metal in organisms to levels in exposure media bioavailability, such as organic carbon or water and to those physical and chemical properties of hardness. Tier 1 is exceptional, however, in that the media that determine bioavailability, such as maximum bioavailability may be assumed pH and clay or organic matter content. Because (Table 5.2). For example, the total concentration of their empirical character, such regressions of a metal in soil may be used to determine an should not be applied to organisms or EEV for Tier 1, even though only a small fraction environmental conditions that differ significantly of the total may be available for uptake by soil from those for which they were developed. organisms. Furthermore, because of their large uncertainties, Body burden data are the preferred measure of they should generally be used only to estimate exposure to bioavailable forms of substances that exposure for Tier 1 or to complement empirical are not significantly metabolized, but only when body burden data for Tiers 2 and 3. complementary effects data are available When body burden data cannot be used, exposure (McCarty et al. 1992). This is because body to bioavailable forms of a substance may be burdens integrate the effects of differing exposure determined based on concentrations of dissolved conditions and assimilation processes (Landrum et or “soluble” forms of the substance in key al. 1992). Furthermore, it is the accumulation of exposure media — including pore waters of a substance at a sensitive target site within an sediments or soils. organism that is responsible for its harmful effects (McCarty 1987).
6 This is most appropriate when lipid contents are high and easy to measure (e.g., >3–5%). Otherwise, large experimental errors may be introduced into exposure measurements (Lanno 1996).
5-7 Bioavailable forms of Box 5.2 Empirical Relationships Between Uptake of Substances, substances should be Exposure Concentrations, and Properties of Exposure determined on a case-by- Media case basis, depending upon the nature of the substance Regression methods may be used to relate data on and the assessment concentrations of a substance in organisms to concentrations of endpoint(s). In the case of the substance in an exposure medium, as well as to physical organic and metallo-organic and/or chemical properties of the medium that determine compounds, un-ionized,7 bioavailability. For example, freely dissolved forms are • the metal content of plants (M ) may be related to the HCl- primarily available for plant extractable metal content of the supporting soil (M ), as well uptake (Suffet et al. 1994). soil as its pH and clay and organic matter (OM) content, as For metals, the follows: concentration of the freely dissolved “aquo ion” (e.g., M = a(M ) + b(pH) + Zn(H O) 2+) is often the best plant soil 2 6 c(%clay) + d(%OM) + e indicator of metal bioavailability (Benson et al. where a, b, c, d, and e are empirically derived coefficients, 1994; Campbell 1995). or However, oxyanions are also taken up by organisms • the metal content of molluscs (M ) may be related to the (Benson et al. 1994), and mollusc H O -extractable metal content (M ) and organic carbon there is evidence that some 2 2 sed (OC) content of host sediment as follows: dissolved organic and M = a[M @ (%OC)-1] inorganic metal complexes mollusc sed are bioavailable (Campbell 1995). where a is an empirically derived coefficient.
The above was adapted from Martens (1968) and Tessier et al. (1984), respectively.
Methods that can be used to directly measure from total concentrations in unfiltered water concentrations of various dissolved forms of both samples and data on the nature and amounts of organic and inorganic substances are described in other dissolved and solid phases.8 Similarly, the Suffet et al. (1994) and Pickering (1995) (see EqP model of Di Toro et al. (1991) may be used Appendix II of the resource document). When to estimate concentrations of the freely dissolved there are no empirical data on specific form of a neutral organic compound in the pore bioavailable forms, equilibrium models may be water of a sediment, if its concentration and that used to estimate concentrations of dissolved of organic carbon in the solid phase of the species (see Appendix II of the resource sediment are known. document). For example, MINEQL+ (Schecher and McAvoy 1994) could be used to calculate concentrations of different dissolved metal species
7 Ionized forms of organic compounds are not entirely unavailable for uptake by organisms. For example, organic cations can (to some extent) partition to lipid phases, especially for chemicals that have neutral forms that are strongly hydrophobic (Erickson et al. 1994).
8 Equilibrium modelling should be applied only to systems containing metal-complexing ligands with known thermodynamic stability constants (Turner 1995).
5-8 Exposure to “soluble” solid forms of metals and 5.3.5 Representation of Temporal and metalloids in solid phases can be measured using Spatial Variability chemical reagents that remove the more weakly bound forms of the substance (see Appendix II of EEV distributions may reflect both spatial and the resource document). Reagents should be temporal variability of exposure, as well as selected carefully, taking into account the nature uncertainties associated with exposure of the substance and the conditions of exposure. measurements and — when EEVs are calculated— Box 5.2 presents examples of two such reagents ignorance of true values for key parameters (e.g., K , BAF) used in calculations (Hoffman and used to estimate the fractions of bioavailable ow metal in soils and sediments. Hammonds 1994).
When exposure is estimated as rates of intake As indicated in Table 5.2, the measured maximum (e.g., Table 5.1), bioavailability factors (ranging EEVs should be used as numerators in risk from 0 to 1) may be applied to total intake values quotients for Tier 1 risk estimates. If EEVs are for individual exposure media. Bioavailability based on Monte Carlo analysis, the 99.9th factors for ingested and inhaled solids may be percentile EEV may be conservatively chosen as a estimated using weak acid extractions intended to “bounding estimate” of exposure (U.S. EPA 1992). simulate conditions in the gastrointestinal tract For Tier 2 risk analyses, a less conservative value, 10 (metals only) or using data from assimilation such as the 95th percentile, should be used. studies with laboratory organisms (e.g., Borgmann Tier 3 analyses make use of entire EEV and Whittle 1992; Stern 1994; Fisher and distributions. In some circumstances (see below), Reinfelder 1995). EEVs may represent averaged exposure values.
For some substances, bioavailability is controlled For Tier 3, spatial and temporal variations in by a specific chemical component of an exposure exposure values should be separated whenever medium. Concentrations of such substances may possible. In such instances, EEVs may take the be adjusted or normalized to the controlling form of frequency distributions that reflect the variable. For example, uptake of metal ions from variability of exposures at the same time but at solution may be reduced by competition for different locations or at different times at a adsorption sites on the surface of exposed particular monitoring station. If sample locations organisms from calcium and magnesium (i.e., are selected at random and organisms are hardness) ions (Campbell 1995). In this case, assumed to be uniformly distributed within the EEVs — and CTVs — could be adjusted to sampled area, EEV distributions representing hardness, as described by Parkhurst et al. (1994). spatial variability can be used to estimate the Similarly, the bioavailability of nonionic organic proportion of the population of receptors that are substances in sediment is often inversely related to exposed at levels above the ENEV (see Chapter 7). the abundance of organic carbon (Di Toro et al. If sampling times are selected appropriately, 1991). Differences between bioavailabilities in temporal EEV distributions may be used to sediment used for toxicity testing and field estimate the proportion of time that exposure sediments may therefore be minimized by values exceed the ENEV at a particular monitoring normalizing total concentrations of nonionic station. organic substances in sediments to their total organic carbon contents.9
9 Limitations of this approach have been discussed by Landrum and Robbins (1990).
10 As explained in U.S. EPA (1992), Monte Carlo simulations often include low-probability estimates at the upper end of the exposure range that are higher than those actually experienced in a population.
5-9 For discontinuous exposures, the timing, duration, If exposure values are based on infrequent and frequency of exposure are important. Timing sampling of mobile media such as air and river may be a key determinant of exposure for water, variations in intensity of sources and flow organisms with seasonal migration patterns or with and dilution characteristics must be considered sensitive life stages. In such cases, EEVs should be when determining if such data are representative. based on data for times when receptors are likely EEVs based on one-time or short-duration to be exposed to the substance or are particularly sampling of relatively immobile media, such as sensitive to the substance (e.g., during spawning). soils and sediments, may often be assumed to represent longer exposure periods, if a substance Temporal Variability is persistent.
Generally, exposure at a particular location is Spatial Variability characterized by estimating arithmetic average exposure values for a specified time interval, such Tier 3 EEV distributions reflecting spatial variations as a day or month.11 The selection of an in exposure are often intended to reflect the appropriate time interval depends upon whether variability of exposure of individual organisms exposure is episodic or continuous and upon the within a population (U.S. EPA 1992). To acute or chronic nature of the assessment determine the exposure of individuals when endpoint. Short exposure averaging periods are assessment endpoints are chronic, spatial used when exposure is episodic or assessment variations in exposure values may be averaged endpoints are acute. Longer periods should be over areas that correspond to the expected “home used with chronic assessment endpoints. range” of individual organisms. Home ranges of Whenever possible, time intervals should be fish and mammals, for example, can be estimated matched to exposure periods used for determining as an allometric function of body size (e.g., Minns effects (e.g., Solomon et al. 1996).12 For 1995). Areas involved could be as small as a few example, if the exposure period used in a critical square metres for small immobile organisms or as toxicity experiment was four weeks, individual large as hundreds of square kilometres for large exposure values should ideally represent four-week mammals. averages.13 When samples have been collected at many sites When samples have been collected frequently over over a large area, home range-size subareas may an extended time at the same site, the sampling be defined and concentrations in samples within period may be divided into appropriate time each subarea averaged. In such cases, the intervals, and concentrations in samples from each maximum concentration in a single sample is used time interval may be averaged (e.g., Solomon et as a Tier 1 EEV; for Tiers 2 and 3, on the other al. 1996). In such cases, the maximum hand, the maximum EEV and the EEV distribution concentration in a single sample is used as a may be based on spatially averaged Tier 1 EEV; for Tiers 2 and 3, however, the concentrations (Table 5.2). Spatial averaging may maximum EEV and the EEV distribution should be difficult, however, because of limited generally be based on moving-average or time- knowledge of the distribution of organisms within averaged concentrations (Table 5.2). specific areas of concern and the limited sample densities of most field surveys. Consequently, Tier 3 EEV distributions are often based on “raw” or spatially unaveraged exposure data. When
11 Although median or geometric mean concentrations may be better estimates of “typical” concentrations, these statistics may downplay the importance of the highest concentrations, which are probably the most toxicologically significant (Norton 1996).
12 Such matching would not be appropriate, however, when chronic effects levels are estimated from acute toxicity data.
13 If required for Tier 3 analysis, confidence limits may be estimated for average exposure values (e.g., Dixon and Massey 1969).
5-10 interpreting EEVs based on such “raw” data, it • Describe uncertainties in exposure esti- should be recognized that there will be a tendency mates, and highlight the relative to overestimate the proportion of a population that importance of key assumptions and data. is exposed at high concentrations (Hattis and Burmaster 1994). • Describe research or data necessary to improve the exposure assessment. 5.4 Estimating Natural Background Concentrations 5.6 References Information on natural contributions to EEVs may be required to establish lower bounds on ENEVs ASTM (American Society for Testing and for natural substances and to evaluate the Materials). 1993. Standard practice for potential for natural tolerance in receptor conducting bioconcentration tests with fishes and organisms (see Chapter 7). saltwater bivalve molluscs. In ASTM standards on aquatic toxicology and hazard evaluation. Methods that may be used to distinguish between Philadelphia, Pennsylvania. pp. 356–372. natural and anthropogenic components of measured EEVs are described in Section 5.7 of the Benson, W.H., J.J. Alberts, H.E. Allen, C.D. Hunt, resource document. Methods may be simple, and M.C. Newman. 1994. Synopsis of such as comparing concentrations of a substance discussion session on the bioavailability of in an exposure medium to distance from a point inorganic contaminants. In J.L Hamelink, P.F. source (e.g., Freedman and Hutchinson 1980). Landrum, H.L. Bergman, and W.H. Benson Alternatively, more complex receptor models (e.g., (eds.), Bioavailability: Physical, chemical and Gordon 1988) or specialized statistical or biological interactions. Proceedings of the 13th chemical methods (e.g., Forstner 1983; Maenhaut Pellston Workshop, Pellston, Michigan, August et al. 1989) may be used. Although quantitative 17–22, 1992. Lewis Publishers, Boca Raton, results are preferred, there are often large Florida. pp. 63–72. uncertainties associated with estimates of natural Borgmann, U. and D.M. Whittle. 1992. background concentrations for anthropogenically Bioenergetics and PCB, DDE and mercury contaminated areas. Consequently, several dynamics in Lake Ontario lake trout (Salvelinus methods should be applied whenever possible, namaycush): A model based on surveillance using a weight-of-evidence approach. data. Can. J. Fish. Aquat. Sci. 49: 1086–1096.
5.5 Some Points to Remember Cain, D.J., S.N. Luoma, and M.I. Hornberger. 1995. Assessing metal bioavailability from • Clearly describe the purpose and scope of cytosolic metal concentrations in natural the exposure characterization and underly- populations of aquatic insects (abstract). ing methodologies. Abstract Book, Society of Environmental Toxicology and Chemistry, 2nd World Congress, • Critically evaluate exposure data and November 5–9, 1995, Vancouver, B.C. express the degree of confidence in the data. Present the rationale for excluding Campbell, P.G.C. 1995. Interaction between data. trace metals and aquatic organisms: A critique of the free-ion activity model. In A. Tessier and • If exposure models are used, describe their D. Turner (eds.), Metal speciation and benefits, weaknesses, and limitations. bioavailability in aquatic systems. John Wiley & Sons, New York. pp. 45–102. • Describe the central estimates and upper and lower confidence limits on exposures; note and support the use of any preferred estimates.
5-11 CCME (Canadian Council of Ministers of the Erickson, R., T.D. Bills, J.R. Clark, D. Hansen, J.P. Environment). 1993. Guidance manual on Knezovich, F.L. Mayer, and A.E. McElroy. sampling, analysis, and data management for 1994. Synopsis of discussion session on contaminated sites. Vols. I and II. Reports physicochemical factors affecting toxicity. In J.L. CCME EPC-NCS62E and EPC-NCS66E. Hamelink, P.F. Landrum, H.L. Bergman, and Winnipeg, Manitoba. W.H. Benson (eds.), Bioavailability: Physical, chemical and biological interactions. CEU (Commission of the European Union). 1995. Proceedings of the 13th Pellston Workshop, Environmental risk assessment of metals and Pellston, Michigan, August 17–22, 1992. Lewis metal compounds. Appendix VIII, October Publishers, Boca Raton, Florida. pp. 31–38. 1995 Draft. In Technical guidance documents in support of the Commission directive 93/67/ Fisher, N.S. and J.R. Reinfelder. 1995. The EEC on risk assessment for new substances and trophic transfer of metals in marine systems. In the Commission regulation (EC) No. 1488/94 A. Tessier and D. Turner (eds.), Metal speciation on the risk assessment for existing substances. and bioavailability in aquatic systems. John Brussels, Belgium. 12 pp. Wiley & Sons, New York. pp. 363–406.
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Environment Canada. 1995. Quality assurance Hattis, D. and D.E. Burmaster. 1994. Assessment reference materials and services. National of variability and uncertainty distributions for Water Research Institute, Burlington, Ontario. practical risk analyses. Risk Anal. 14(5): 713– 9 pp. 730.
5-12 Health Canada and Environment Canada. 1993. Martens, D.C. 19681968. Plant availability of Canadian Environmental Protection Act. Priority extractable boron, copper, and zinc as related to Substances List. Supporting document. selected soil parameters. Soil Sci. 106(1): 23– Hexachlorobenzene. (unedited version). June. 28. Ottawa, Ontario. 199 pp. McCarty, L.S. 19871987. Relationship between Hoffman, F.O. and J.S. Hammonds. 1994. toxicity and bioconcentration for some organic Propagation of uncertainty in risk assessments: chemicals. II. Application of the relationship. The need to distinguish between uncertainty due In K.L.E. Kaiser (ed.), QSAR in environmental to lack of knowledge and uncertainty due to toxicology C II. D. Reidel Publ. Co., Dordrecht, variability. Risk Anal. 14: 707–712. The Netherlands. pp. 221–229.
Knox, R.C., D.A. Sabatini, and L.W. Canter. McCarty, L.S., D. Mackay, A.D. Smith, G.W. 1993. Subsurface transport and fate processes. Ozburn, and D.G. Dixon. 1992. Residue- Lewis Publishers, Boca Raton, Florida. 430 pp. based interpretation of toxicity and bioconcentration QSARs from aquatic bioassays: Landrum, P.F. and J.A. Robbins. 1990. Neutral narcotic organics. Environ. Toxicol. Bioavailability of sediment-associated Chem. 11: 917–930. contaminants to benthic invertebrates. In R. Baudo, J.P. Giesy, and H. Muntau (eds.), Mill, T. 1993. Environmental chemistry. In G.W. Sediments: Chemistry and toxicity of in-place Suter (ed.), Ecological risk assessment. Lewis pollutants. Lewis Publishers, Chelsea, Michigan. Publishers, Chelsea, Michigan. pp. 91–127. pp. 237–263. Minns, C.K. 1995. Allometry of home range size Landrum, P.F., H. Lee II, and M.J. Lydy. 19921992. in lake and river fishes. Can. J. Fish. Aquat. Sci. Toxicokinetics in aquatic systems: Model 52: 1499–1508. comparisons and use in hazard assessment. Environ. Toxicol. Chem. 11: 1709–1725. MMWG (Metals and Minerals Working Group). 1996. Biodegradation/persistence and Lanno, R. 1996. Comments submitted on bioaccumulation/biomagnification of metals and (June 4) Draft 2.0 of Ecological Risk metal compounds. Technical workshop held Assessments of Priority Substances Under the December 11–13, 1995, sponsored by Canadian Environmental Protection Act, Canada/European Union, Metals and Minerals Guidance Manual. Department of Zoology, Working Group, Brussels, Belgium. 48 pp. Oklahoma State University, Stillwater, Oklahoma. Moore, D.R.J., R.L. Breton, and K. Lloyd. 1996. The effects of hexachlorobenzene on mink in the Lyman, W.J., W.F. Reehl, and D.H. Rosenblatt Canadian environment: An ecological risk (eds.). 1990. Handbook of chemical property assessment. Environ. Toxicol. Chem. (in press). estimation methods. American Chemical Society, Washington, D.C. Norton, S. 1996. Comments submitted on (May 10) Draft 2.0 of Ecological Risk Mackay, D., S. Paterson, and D.D. Tam. 1991. Assessments of Priority Substances Under the Assessment of chemical fate in Canada: Canadian Environmental Protection Act, Continued development of a fugacity model. Guidance Manual. U.S. Environmental Report prepared for Health and Welfare Protection Agency, Washington, D.C. Canada, September. 67 pp. OECD (Organisation for Economic Co-operation Maenhaut, W., P. Cornille, J.M. Pacyna, and V. and Development). 1993a. Guidelines for the Vitols. 19891989. Trace element composition and testing of chemicals. Paris, France. origin of the atmospheric aerosol in the Norwegian arctic. Atmos. Environ. 23(11): 2551–2569.
5-13 OECD (Organisation for Economic Co-operation Suter, G.W. 1993. Exposure. In G.W. Suter and Development). 1993b. Application of (ed.), Ecological risk assessment. Lewis structure–activity relationships to the estimation Publishers, Chelsea, Michigan. pp. 153–172. of properties important in exposure assessment. Environment Monograph No. 67. Paris, France. Tessier, A., P.G.C. Campbell, J.C. Auclair, and 65 pp. M. Bisson. 1984. Relationships between the partitioning of trace metals in sediments and Parkhurst, B.R., W. Warren-Hicks, and R.D. their accumulation in the tissues of the Caldwell. 1994. Methodology for aquatic freshwater mollusc Elliptio complanata in a ecological risk assessment. Draft final report, mining area. Can. J. Fish. Aquat. Sci. 41: April. Prepared for Water Environmental 1463–1472. Research Foundation, Alexandria, Virginia. Thomann, R.V. 1989. Bioaccumulation model Pickering, W.F. 1995. General strategies for for organic chemical distribution in aquatic food speciation. In A.M. Ure and C.M. Davidson chains. Environ. Sci. Technol. 23(6): 699–707. (eds.), Chemical speciation in the environment. Blackie Academic and Professional, New York. Turner, D.R. 1995. Problems with trace metal pp. 9–32. speciation modeling. In A. Tessier and D. Turner (eds.), Metal speciation and Schecher, W.D. and D.C. McAvoy. 1994. bioavailability in aquatic systems. John Wiley & MINEQL+: A chemical equilibrium model for Sons, New York. pp. 149–203. personal computers. User’s manual, Version 3.0. Environmental Research Software, U.S. EPA (United States Environmental Protection Hallowell, Maine. Agency). 1987. Selection criteria for mathematical models used in exposure Solomon, K.R., D.B. Baker, R.P. Richards, K.R. assessments: Surface water models. EPA-600/ Dixon, S.J. Klaine, T.W. La Point, R.J. Kendall, 8-87/042. Office of Health and Environmental C.P. Weisskopf, J.M. Giddings, J.P. Giesy, L.W. Assessment, Office of Research and Hall, Jr., and M. Williams. 1996. Ecological Development, Washington, D.C. risk assessment of atrazine in North American surface waters. Environ. Toxicol. Chem. 15(1): U.S. EPA (United States Environmental Protection 31–76. Agency). 1988. Selection criteria for mathematical models used in exposure Stern, A.H. 1994. Derivation of a target level of assessments: Ground-water models. EPA-600/ lead in soil at residential sites corresponding to a 8-88/075. Office of Health and Environmental de minimis contribution to blood lead Assessment, Office of Research and concentration. Risk Anal. 14(6): 1049–1056. Development, Washington, D.C.
Suffet, I.H., C. Jafvert, J. Kukkonen, M. Servos, A. U.S. EPA (United States Environmental Protection Spacie, L. Williams, and J. Noblet. 1994. Agency). 1991. Selection criteria for Synopsis of discussion session: Influences of mathematical models used in exposure particulate and dissolved material on the assessment: Atmospheric dispersion models. bioavailability of organic compounds. In J.L. EPA-600/8-91/038. Office of Health and Hamelink, P.F. Landrum, H.L. Bergman, and Environmental Assessment, Office of Research W.H. Benson (eds.), Bioavailability: Physical, and Development, Washington, D.C. chemical and biological interactions. Proceedings of the 13th Pellston Workshop, U.S. EPA (United States Environmental Protection Pellston, Michigan, August 17–22, 1992. Lewis Agency). 1992. Guidelines for exposure Publishers, Boca Raton, Florida. pp. 93–108. assessment. Fed. Regist. 57(104): 22888– 22938.
5-14 CHAPTER 6 EFFECTS CHARACTERIZATION
6.1 Introduction Once CTVs for the appropriate assessment endpoints are determined, they are used as inputs 6.1.1 Goals and Objectives to the next phase of the risk assessment, the risk characterization phase (Figure 6.1). The objective of the effects characterization phase is to define a CTV for each assessment endpoint. 6.1.3 Overview of Approach The results of toxicity studies on the most sensitive measurement endpoint are used to derive a CTV. Toxicity information should include data from a A CTV is usually an estimate of low toxic effect, wide range of trophic levels. These help determine which populations, communities, and such as an IC25 or LOEL, and may be in the form of a point estimate for Tiers 1 and 2 or a ecosystem processes may be particularly susceptible to adverse effects, as well as the types distribution for Tier 3, such as IC25 ± 95% confidence limits. Section 6.3 provides guidance and magnitude of these effects. Assessors should on deriving CTVs. Chapter 7 describes the attempt to locate data pertaining to Canadian approaches to be used for deriving an ENEV from species and conditions whenever possible. a CTV. Available toxicity studies are critically evaluated, 6.1.2 Relationship with Other Phases and only studies of acceptable quality are given further consideration (Appendix III of the resource The effects of a substance on assessment and document; Environment Canada 1996). measurement endpoints identified during problem Assessors should be aware that the toxicity of formulation are determined during the effects substances can be modified by various characterization stage. It is important that effects environmental conditions (e.g., temperature, water on sensitive receptors be identified as assessment hardness, etc.) and by characteristics of the biota endpoints. This is particularly important for uptake (e.g., species, age, behaviour, interaction among models that require input parameters, such as species) (Environment Canada 1996). Assessors ingestion rates or inhalation rates, that differ for should consult standard protocols for guidance on each receptor. It may become apparent that the acceptable studies. If no acceptable studies are assessment and measurement endpoints originally available, research may need to be carried out to identified are not appropriate. This would be the supply the required information. case, for example, if the results of toxicity studies show that other types of organisms are more Where necessary, the results from acceptable sensitive than previously believed or if the results of studies are refined to yield the type of experimental detailed exposure characterization indicate that endpoint required. In order of preference, these the substance partitions to media other than those are IC25, LOEL, NOEL, EC50, or other measure of originally identified during problem formulation. central tendency (see Section 6.3). In such cases, problem formulation would have to be revised and different endpoints identified.
6-1 Assessors should identify sources of uncertainty, both qualitative Problem Formulation and quantitative, related to toxicological data (see Section Effects Characterization 6.3 of the resource document). This will be taken into account at Evaluation of Supporting Evidence the risk characterization phase in Studies QSARs Single species EqP selecting the appropriate Multi-species application factor or in a Ecoepidemiology quantitative uncertainty analysis. Body burdens Areas of concern include No Acceptable uncertainties regarding the Measurement Data Generation relationship between the Endpoint(s) substance and the assessment Yes endpoint, uncertainties associated Quantification with parameters in the studies, (e.g., EC25 ) and natural variations in relevant media and biological effects. In Critical Toxicity the case of radionuclides, areas Value (CTV) of concern include uncertainties regarding the relationship Risk Characterization between whole-body doses and doses to sensitive tissues and organs, uncertainty in dosimetry Figure 6.1 Effects characterization in the ecological risk models for nonhuman species, assessment framework for priority substances and uncertainty in the most appropriate factor to take into account for the relative biological effectiveness (RBE) of alpha emitters. continuously released into the environment or are persistent, chronic studies are preferred. All 6.2 Types of Effects Information acceptable studies contribute to an understanding of a substance’s effects. The most relevant studies Studies on single species, multiple species, contribute directly towards the determination of ecoepidemiology, body burdens, QSARs, and the CTVs. These studies should use species found in EqP method can all be used to characterize effects Canada or closely related species. They should on the assessment endpoints of concern. be from a range of trophic levels and represent a Depending on the substance being assessed, variety of exposure routes. several of these types of studies can be used. The limitations of each, however, should be Full life cycle studies that determine effects on considered. Types of effects data required for embryonic development, hatching success, survival each tier will depend on the exposure scenario of of juvenile stages, growth, reproduction, and the substance in the environment. In order to survival of adults are preferred. In their absence, minimize the degree of uncertainty involved in results may be employed from partial life cycle extrapolation, the measurement endpoints selected studies using the most sensitive stages of the life should be as relevant as possible to the exposure cycle (OECD 1993a). If there is only one study, scenarios. For example, if the substance is assessors will have to decide on a case-by-case introduced into the environment in a pulsed or basis whether it provides sufficient information to intermittent way and is not persistent, then short- establish that there are adverse effects on the duration (acute) tests should be used in deriving assessment endpoint. The purpose of these the CTV for each tier. For substances that are studies is to determine if there is sufficient
6-2 information to establish whether there is an effect and density may have an effect. Alterations in on the assessment endpoint based on data from ecosystem characteristics, such as changes in the measurement endpoint. community function, energy flow, and nutrient cycling, cannot be predicted from single-species 6.2.1 Single-Species Toxicity Tests tests (Cairns 1983). Unlike many microcosm and Single-species toxicity tests determine the effects of mesocosm tests, single-species toxicity tests are not substances on organisms of a single species under designed to integrate the simultaneous study of specified test conditions. Such tests are needed to toxicity and various chemical transformation and obtain information about the concentrations of partitioning processes. Behavioural and substances and durations of exposure that cause ecological parameters, such as competition and changes in the survival, reproduction, growth, seasonal changes in temperature, may affect a physiology, biochemistry, or behaviour of species’ sensitivity to a substance. Application individuals within particular species (Cairns 1983). factors may account for uncertainties, and Biochemical or physiological perturbations may quantitative uncertainty analyses may estimate also have implications for population effects many of these uncertainties (Chapter 7). Ideally, (Section 1.2). Such effects at lower organization risk assessors should rely on a number of single- levels include endocrine disruption (Colborn et al. species and multispecies toxicity tests. The two 1993), genotoxicity (Anderson et al. 1994), and types of tests complement each other and present immune suppression. Standard measurement a more accurate characterization of effects than endpoints are available for some of these either type used alone. examples (OECD 1993a; Kramer and Giesy 6.2.2 Multispecies Toxicity Tests 1995). Multispecies toxicity tests, including microcosm, The usefulness of single-species tests for predicting mesocosm, and field tests, incorporate ecological effects depends on the degree to which predictions components (species, functional groups, or habitat can be extrapolated to natural systems with types) that simulate processes as they occur in confidence and the tests’ replicability and nature (SETAC 1992). A microcosm can range reproducibility (Cairns 1992). Single-species from a small laboratory-scale simulation of a toxicity tests make it easier to determine the direct portion of an ecosystem to a large outdoor tank. effects of varying individual test conditions. These A mesocosm can range from laboratory effects may be masked by interactions among microcosms to large, complex ecosystems (Grice species or environmental components in and Reeve 1982; Odum 1984). Mesocosm tests, microcosm or mesocosm tests. Standardized test generally performed outdoors, more closely methods developed by agencies such as approximate natural ecosystems than do Environment Canada, the U.S. EPA, and the microcosm tests (Taub 1985). Field tests, once OECD have enhanced the likelihood of achieving considered as large mesocosms, normally involve reproducible results when single-species tests are the isolation of terrain or part of a body of water carried out by researchers in different laboratories. and include within their boundaries the normal If other test methods are used, the procedures flora and fauna found under unperturbed must be described in sufficient detail that the conditions. reliability of the results can be judged. There are few examples of protocols for When using single-species laboratory tests for standardized microcosm tests for aquatic and assessing risk, the following points should be kept terrestrial systems. Several aquatic mesocosm test in mind. Physiological or biochemical variations protocols have been described in the literature among species, such as uptake and metabolism, (Touart 1988), and terrestrial mesocosms have can alter the potential toxicity of a substance. been used for several decades (Barrett 1968). Inbred laboratory strains may be unusually Field tests can confirm whether predicted fate, sensitive or resistant to the test substance. Single- chronic effects, or bioaccumulation actually occur species tests are often unable to accurately predict under reasonably realistic field conditions. They effects at higher levels of ecological organization, can also reveal secondary effects that result from where population dynamics such as age structure species interactions (OECD 1995). 6-3 Multispecies tests may not be as useful at 6.2.3 Ecoepidemiology demonstrating ecosystem recovery processes following a spill or stress as suggested by Harrass Ecoepidemiology attempts to determine the causes and Sayre (1989). In fact, Power (1996) indicates of observed effects in the field by examining the that both Cairns (1990) and Detenbeck et al. spatial and temporal relationships between these (1992) have shown that recovery is very difficult to effects and suspected causal agents (e.g., PSL demonstrate in a model ecosystem. Following substances). Effects of concern include diseases in disturbances in the natural environment, there are individuals and populations, disturbances in site-specific factors affecting rates of recovery, communities, and disruptions of ecological such as immigration rates from undisturbed areas, systems. In most risk assessments, laboratory that are difficult or impossible to reproduce in a toxicity data are used to predict adverse effects on microcosm. Multispecies tests may be particularly the environment, whereas ecoepidemiology starts useful in the ecological assessment of complex with observed field effects and attempts to identify mixtures and effluents (Chapter 8). Harrass and causes. Epidemiological criteria may be used in Sayre (1989) suggest that acceptable multispecies conjunction with other laboratory-derived test data include three key features: credibility, information to determine the potential of applicability, and endpoint interpretability (Section substances to cause adverse effects. 6.2.2 of the resource document). Assessors Ecoepidemiology may prove especially useful in should ensure that these features are included in assessments of complex mixtures, where direct multispecies test protocols. cause-and-effect relationships are difficult to Microcosm experiments, like single-species tests, ascertain in the laboratory (Chapter 8). are not globally sensitive to all stresses. When Confidence in causal relationships can be microcosms lack appropriate target species for increased by selecting reference sites and substances with specific modes of action, little evaluating changes along a concentration effect will be detected (Pratt et al. 1993). Toxicity gradient where differences in other environmental to individuals, as measured by single-species tests, factors are minimized (U.S. EPA 1992b). is not always reflected in toxicity to populations, Statistical associations derived from well-controlled and population interactions tend to dampen experimental studies can aid in establishing causal responses at the community level (Koojiman relationships even when the causative agent has 1985). Complex interactions can vary from one not been demonstrated conclusively. system to another, so that meaningful differences Confounding factors that can obscure a are often obscured. Assessors should be cautious substance’s effects include differences in habitat in making projections to ecosystems based on quality between areas, natural variations in these tests (Odum 1984). Population dynamics, environmental parameters within areas, the such as compensatory mortality mechanisms, play occurrence of undetected stressors, and the a pivotal role in attenuating the impact of many movement of organisms into or out of the study stresses. This capacity is limited, and, thus, area (U.S. EPA 1992b). accurate effects assessment requires detailed knowledge of the suite of stresses acting on a Results of the ecoepidemiology method will often population (Power and Power 1995). Microcosms be inconclusive. The best that can be expected is require a period of stabilization for component to reach the most reasonable explanation based species, and microcosm tests are much more on the evidence at hand. In ecoepidemiology, costly than single-species toxicity tests (U.S. EPA most studies are observational, and experiments to 1992a). Natural communities are often difficult to confirm cause-and-effect relationships may be sustain in an artificial arrangement. There may be difficult or impossible to carry out. extinctions and changes in community structure irrespective of substance exposure (Buikema and Ecoepidemiology has the same basic principles as Voshell 1993). epidemiology. Fox (1991) has adapted criteria to help assess the relationship between a suspect substance and an adverse environmental effect (see Section 6.2.3 of the resource document for a
6-4 complete listing). Although these criteria do not Assessors should use body burden data and, provide proof of a cause-and-effect relationship, where possible, CBBs, along with more traditional they do provide a process and framework upon toxicity information, in characterizing effects in which to exercise judgment. both the aquatic and terrestrial compartments. If research is required to fill data gaps, CBBs should 6.2.4 Estimating Effects of Naturally be measured during standard toxicity bioassays. Occurring Substances This reduces uncertainties in comparing field and Organisms resident in areas where natural laboratory data relating to bioavailability, background concentrations of a naturally exposure routes, and intake rates. occurring substance are elevated are likely to have CBBs may be especially useful for assessing acquired a tolerance for that substance. Toxicity complex mixtures. Narcotic substances are tests using standard laboratory strains would essentially of equal strength on a molar residue therefore not be directly applicable to these basis, and, therefore, the toxicity of mixtures of organisms. CTVs should ideally be based on these substances is additive. Based on this single- or multispecies tests or on field tests using additivity theory, acute lethality occurs if the sum of organisms collected from the areas with naturally the chemical concentrations in the organism elevated background concentrations. When this is reaches a threshold (effects) level (McCarty and not practical, CTVs should be derived from tests Mackay 1993). with organisms with tolerances matched as closely as possible to those of risk receptors. 6.2.6 Quantitative Structure–Activity Relationships (QSARs) 6.2.5 Critical Body Burdens (CBBs) In the absence of empirical data, QSARs may be CBBs are the minimum tissue concentrations that used to predict effects of chemical substances. are associated with an adverse effect on a QSARs may also be used to determine the physical measurement endpoint C the reproductive and chemical properties of a substance. QSARs potential of Daphnia, for example. Traditionally, are developed for groups of substances that are results from acute and chronic toxicity tests are differentiated by mode of action, which varies with expressed in terms of the concentration in the the structure and physicochemical properties of the external medium in relation to the biological substances, or by chemical class (e.g., chlorinated response or measurement endpoint. The CBB phenols, nonionic surfactants, phosphate esters). method, which is based on whole-tissue QSARs are applicable only to substances within concentrations or the concentration in a particular that group. target organ, can be an effective surrogate for the target site(s) of action. It can provide a more QSARs can be used to make preliminary estimates direct measure of a predicted adverse effect than of toxicity in problem formulation, to corroborate can an external exposure concentration C such as empirical data, and to determine the need for single-species testing C as problems associated additional testing. QSARs are also used as with estimating bioavailability and accumulation supporting lines of evidence for estimating CTVs are essentially eliminated. and should not be the primary source of evidence.
When appropriate, CBBs should be summarized Two QSAR programs, ECOSAR and TOPKAT, are and compared with tissue residue or body burden widely used for health and environmental data collected in the field. This information may assessments. The CEU (1995) also uses QSARs be used as the basis for the risk assessment or to for aquatic toxicity tests (Section 6.2.5 of the support a weight-of-evidence approach for other resource document). analyses, such as the external concentration method. Although CBBs of organic substances ECOSAR, developed by the U.S. EPA, uses over have been linked to the acute toxicity of narcotics 100 QSARs for 40 chemical classes to predict in aquatic organisms, more research is required acute and chronic toxicity to fish, Daphnia, and green algae as well as 14-day LC s for before this concept can be generally applied to 50 other modes of toxic action (McCarty and Mackay earthworms in artificial soil (U.S. EPA 1994). 1993). Approximately 50% of the QSARs are for neutral 6-5 organic chemicals. The remainder are for (Koc) of the solid medium are known. However, ionizable organic chemicals such as amines, the uncertainties associated with this method’s phenols, or anilines. basic assumptions can often limit its usefulness (Chapman 1989). For example, the method TOPKAT, developed by Health Designs, Inc. (HDI assumes: 1990), uses structure–activity relationships and statistical techniques to estimate various effects, • that the concentration of the substance in including Daphnia magna EC50s and fathead biota resident in the medium (i.e., a minnow LC50s. contaminated sediment, soil, etc.) is in equilibrium with concentrations in the aqueous Other QSAR programs could also be used for and solid phases (Di Toro et al. 1991), assessment purposes. The OECD (1993b) recommends the following: • that water column organisms and organisms in the contaminated medium are equally sensitive • The substance under investigation and those to the substance (Di Toro et al. 1991), and used in the QSAR should be similar in terms of structure and mode of action. • that dermal contact is the primary route of exposure and that exposure via ingestion of • Only QSARs that have been verified in terms solid phases is not significant (Chapman of range of application and predictive 1989). capability should be used. Despite the uncertainties surrounding these • A detailed description of the domain of the assumptions, effects values derived from the EqP QSAR should be provided. This includes the method may be useful as screening values for structural rules defining the group of problem formulation. Such data can also substances and the ranges of the parameters contribute to a weight-of-evidence approach for for which the QSAR is valid. selecting a particular CTV for Tier 2 risk analysis. • The data used to develop the QSAR should be 6.3 Deriving Critical Toxicity described or referenced. Values (CTVs) QSARs that fail to meet these criteria may still be useful, but they should be applied with particular The concentration–response curve describes the caution. When the need for QSARs is identified, response of individuals, populations, or other assessors should consult with experts to verify the biological systems to a range of concentrations of predicted effects of these models. a substance. For most priority substances, concentration-response curves will be available for 6.2.7 Equilibrium Partitioning (EqP) a variety of endpoints and experimental conditions. Previous sections of this chapter The EqP method estimates effects levels for describe how to select and evaluate studies as part benthic, soil-dwelling, and groundwater organisms of an effects characterization. The next step is to exposed to hydrophobic, nonpolar, nonionic derive the CTV (see Appendix I for definition). A organic substances (Di Toro et al. 1991; van de CTV is usually an estimate of low toxic effect (e.g., Plassche and Bockting 1993). This method LOEL, IC ) and is a point estimate for Tiers 1 and defines the chemical activity of the substance to 25 2. For Tier 3, the objective is to derive a which the resident biota are exposed by assuming distribution for the CTV (e.g., IC ± 95% chemical equilibrium between pore water and 25 confidence limits, concentration-response curve organic carbon in solid phases. It also assumes with confidence limits). In stating the CTV, that water column organisms and those in the assessors should indicate the type of result, the contaminated medium are equally sensitive to the organism involved, and the duration of the test. In substance. The advantage of this method is that this manual, acute tests refer to tests with an effects values can be calculated quickly using exposure duration that is a small portion of the test effects data for water column organisms if the K ow organism’s life cycle. Chronic tests may be partial of the substance and the organic carbon content or full life cycle tests. Quantal effects are referred
6-6 to as lethal concentrations (e.g., LC50) or as to hypothesis-testing methods such as ANOVA effective concentrations if the effects are than to regression-based approaches. categorical but nonlethal (e.g., EC50 for Nevertheless, hypothesis testing as an approach immobilization of Daphnia). Quantitative effects for estimating low toxic effects has a number of (e.g., biomass, growth rate) are referred to as the shortcomings, including the following: (i) NOELs inhibiting concentration for a (specified) percent and LOELs are test concentrations that do not effect (i.e., ICp). This section outlines the preferred correspond to specified effects levels from one test approaches and methods for quantifying CTVs. to the next, (ii) poor experimental design will Detailed descriptions of preferred approaches and mistakenly indicate that a substance is less toxic methods are provided in Section 6.3 of the than it really is, and (iii) most information from the resource document. toxicity test is not used (Stephan and Rogers 1985; Pack 1993; Suter 1996). As a result, hypothesis 6.3.1 Tiers 1 and 2 testing is not the preferred method for estimating CTVs used in Tier 1 and 2 assessments may be low toxic effects, particularly for Tier 2 derived by several methods. In order of assessments. If a LOEL or NOEL is to be used as preference, they are: the CTV, information regarding the minimal difference required to give a significant result should be provided (number of replicates, test (1) LC25, EC25, or IC25 variance, α, β, test concentration intervals). This is Recent publications have strongly recommended important, given that conventional hypothesis the use of a regression-based approach for testing will usually determine a NOEL and LOEL, deriving estimates of low toxic effects (e.g., Pack even with poor concentration-response data 1993; Noppert et al. 1994; Chapman et al. (meaning that effects >25% may not be detected 1996; Environment Canada 1996; Suter 1996). as significant) (Stephan and Rogers 1985; Suter et Low toxic effects are preferentially determined from al. 1987; Moore and Caux 1997). LOELs are the results of chronic toxicity tests, except for preferred to NOELs in deriving a CTV, except substances that are present in the Canadian when the LOEL represents a severe effect (e.g., environment only for short durations. This >40% effect). In the latter case, NOELs are approach generally requires five or more preferred. Maximum allowable toxicant treatments and involves specifying a model and concentrations (MATCs) are not used to derive a estimating its parameters through regression CTV. analysis. The desired point estimate is then determined by interpolation or extrapolation (see (3) Median Toxic Effects Section 6.3.3). As point estimates of low toxic effects are likely to be model dependent when Tier 1 and 2 assessments may use estimates of toxicity results are extrapolated to the extremes of median toxic effects derived from acute toxicity the curve (e.g., ≤ 5% effect) (Sebaugh et al. tests as CTVs, although it is the least preferred 1991; Moore and Caux 1997), we recommend a approach. Larger application factors are required cutoff of 25% effect for Tiers 1 and 2; the estimate to convert a CTV derived from a median toxic effect to an ENEV than is the case with a CTV could be lower (e.g., IC10) if it is the result of interpolation. derived from a low toxic effect.
(2) LOEL or NOEL 6.3.2 Tier 3
Analysis of variance (ANOVA) has been the most The objective of a Tier 3 assessment is to estimate common method of estimating low toxic effects the probabilities of specified effects or a range of from chronic tests. There are several reasons for effects. If the objective of the assessment is to this, including wide availability of software capable estimate the probability of exceeding a specified of performing ANOVA and related nonparametric effect (e.g., 25%), then the CTV should include tests and familiarity with the technique in the both the point estimate and the fiducial confidence limits (e.g., IC ± 95% confidence limits) (see regulatory community. Also, most toxicity-testing 25 protocols specify experimental designs more suited Section 6.3.4 of the resource document). Note that this is possible only using a regression-based
6-7 approach (e.g., IC25), as it is not possible to Step 3 Transform the independent and dependent calculate confidence limits for a LOEL or NOEL. If variables as necessary to meet the the objective is to estimate the probabilities of a assumptions of the regression analysis. range of effects, then the CTV should include the Concentrations should be loge or log10 entire concentration-response curve with transformed depending on which confidence limits. transformation produces the most symmetrical concentration–response curve. In some cases, the objective of a Tier 3 With quantitative data (e.g., growth rate, assessment may be to estimate effects at the biomass), it is not advisable to standardize community level of organization. For such the data to controls, as this reduces the assessments, assessors may use the Water degrees of freedom available for the Environmental Research Foundation (WERF) analysis and eliminates treatment approach to derive a cumulative effects curve with replicates with responses greater than confidence limits for the entire community of those of the controls. With this type of interest (see Parkhurst et al. 1996). This approach data, it is preferable to handle controls as involves (i) calculating the effects level of interest a separate model parameter. If there is a for each species or genus (e.g., LC s, IC s), (ii) 50 25 relationship between variance and arranging the data in cumulative form for magnitude of observed responses, percentage of species or genera affected versus transformations such as the square root concentration, (iii) fitting a model to the effects transformation may be required to ensure data, and (iv) calculating confidence limits for the that the homogeneity of variances modelled curve. The WERF approach is described assumption is met. in more detail in Sections 6.3.6 and 8.6.5.5 of the resource document for single substances and Step 4 Perform the regression analysis using any complex substances, respectively. of a variety of statistical packages (e.g., SAS, Statgraphics, SPSS, ToxCalc). An 6.3.3 Procedure for Estimating Low Toxic EXCEL spreadsheet package is available Effects: Regression-Based Approach in the Chemicals Evaluation Division of Step 1 Prepare a graphical summary of the Environment Canada (Caux and Moore concentration–response curve. This is the 1997). The package at present includes simplest means of showing the five models (i.e., three models in the relationship, and, by including replicates, logistic family, probit, Weibull) and the degree of scatter may be examined goodness-of-fit statistics, and it and outliers identified. This information automatically calculates effects may then be used to choose an concentrations for effects ranging from appropriate statistical analysis or to 0.1 to 99.9% using nonlinear regression. evaluate the scientific validity of the A wider range of models is available with analysis reported by the author. nonlinear regression analysis. The trade- Step 2 Choose an appropriate regression model. off is that the calculation of confidence For quantal endpoints, the probit and limits is much more complicated. If the linear logistic models are usually data can be linearized (e.g., by means of appropriate choices. For quantitative a probit or logit transformation), a endpoints, there is a wide variety of weighted linear regression can be models to choose from, including the performed. With weighted linear Weibull model and others that have been regression, calculation of confidence limits adapted to include control responses as a is straightforward. separate parameter (e.g., logistic model Step 5 Test model adequacy with a goodness-of- described in Seefeldt et al. 1995). fit statistic (e.g., chi-square test or G-test U-shaped models may be required for for quantal data, F-test for quantitative endpoints exhibiting stimulation at low data), and, if model fit is adequate concentrations (see Downs 1992).
6-8 (p ≥ 0.05), the results can be used to comparison tests; the NOEL is the highest derive CTVs if all other assumptions of the concentration not producing a significant effect. regression analysis are met. Regression The MATC is generally reported as the range analysis assumes that the errors are between the NOEL and LOEL or as the geometric independent, have zero mean, have a mean of the two concentrations. A variety of constant variance, and follow a normal statistics textbooks describe ANOVA techniques, distribution (Draper and Smith 1981). To related techniques such as analysis of covariance confirm that these assumptions have been and two-way ANOVA, and nonparametric met, the residuals from the fitted techniques in much more detail (e.g., Snedecor concentration-response model should be and Cochran 1980; Sokal and Rohlf 1981; Zar examined or formally tested. 1984). ANOVA and related techniques are included in a wide variety of software packages, 6.3.4 Procedure for Estimating Low Toxic including Systat, SPSS, SAS, and Statgraphics. Effects: Hypothesis-Testing Approach 6.3.5 Estimating Median Toxic Effects ANOVA is the most common hypothesis-testing method for estimating LOELs and NOELs. From a practical point of view, rigid rules are not Generally, the first step is to transform the data to required for selecting among the available stabilize the variances between treatments. The graphical and statistical procedures available for transformation depends on the type of data but estimating median toxic effects. For most types of may include, for example, an arcsine square root data, the estimates of the median lethal or transformation for response data expressed as a effective concentration will not vary significantly proportion (e.g., percentage of normal larvae at (Stephan 1977). Commonly used methods hatch) (Draper and Smith 1981; Gelber et al. include regression analysis (see Section 6.3.3), 1985). Such a transformation is necessary moving-average interpolation, and the Spearman- because the ANOVA procedure assumes that the Karber and trimmed Spearman-Karber methods. treatments exhibit homogeneity of variance. This The crucial point for assessors is to ensure that, for assumption is routinely tested in most statistical any given method, the assumptions have been met software packages, using, for example, Bartlett’s (e.g., normality for parametric methods) and the test. ANOVA also assumes that the data are limitations understood (e.g., confidence limits normally distributed, although ANOVA is fairly cannot be calculated with graphical interpolation, robust to this assumption. If the assumptions of quartiles other than 50% lethal or effective the ANOVA are violated, nonparametric tests such concentration cannot be calculated with moving- as the Shapiro-Wilks and Kruskal-Wallis tests may average interpolation). A variety of statistical be used as alternatives. packages can be used to estimate median toxic effects. The next step is to test for equivalence of the solvent carrier and noncarrier control treatments 6.4 Aquatic Effects with a t-test. The ANOVA is then performed on Characterization the treatment groups, and, if the null hypothesis that all treatments have the same effect is rejected 6.4.1 Pelagic Biota1 (i.e., a significant F-score, usually at p < 0.05), multiple comparison tests (i.e., Dunnett’s The results of single-species or multispecies toxicity procedure or preferably William’s test) are tests have often been used to estimate no-effects performed between treatment groups to determine concentrations or to derive water quality objectives which treatments are different from the control or guidelines for substances. For the surface water treatment. The LOEL is the lowest concentration compartment, results from long-term toxicity tests producing a significant effect in the multiple
1 Pelagic biota are free-swimming or free-floating aquatic organisms that inhabit the water column.
6-9 for organisms from different trophic levels can help (Environment Canada 1992b). Environment determine which populations, communities, and Canada (1992c) has also published an acute test ecosystem processes may be particularly for sediment toxicity using marine or estuarine susceptible to adverse effects and to determine the amphipods. However, only a limited number of types and magnitude of these effects. From the set these spiked-sediment toxicity tests have been of acceptable studies, the test result indicating the standardized to examine an organism’s exposure lowest toxic effect (e.g., the lowest derived EC10) to sediment-associated substances such as whole should be used as the CTV for pelagic biota. sediment, pore waters, or elutriates. Despite the paucity of standardized tests, a number of For most substances, results from single-species approaches have been developed to evaluate the toxicity tests will probably be the most abundant toxicological significance of substances in source of effects data on pelagic biota. However, freshwater, marine, and estuarine sediments. results from multispecies tests and Overall, assessors should be flexible. They will ecoepidemiology studies can be extremely useful need to evaluate potentially relevant benthic in characterizing direct and indirect effects under toxicity information by applying sound scientific natural or near-natural conditions. Field test principles and basic QA/QC considerations.2 results are particularly valuable when Owing to the complexities of interpreting data in characterizing the effects of complex mixtures and the sediment compartment, assessors are advised effluents on pelagic biota. The CBB approach is to consult with sediment specialists when applying particularly relevant when it is difficult to determine the following approaches. the concentration of bioavailable forms of a substance in the environment (Section 6.2). Assessors should locate all acceptable sediment toxicological data on Canadian marine and 6.4.2 Benthic Biota freshwater species. Ideally, these data should Sediments are an important component of aquatic cover a range of feeding behaviours, substrate ecosystems. They provide habitat to organisms — preferences, locomotion, and degree of such as microorganisms, aquatic plants, annelids, association of benthic organisms with bottom insects, amphipods, and molluscs — that spend a sediments. Sediment toxicity tests must use the major portion of their life cycle living on or in appropriate sediment phases — such as pore aquatic sediments. Sediments act as sinks and, water — because benthic organisms may be subsequently, as sources of substances that have exposed to some or all of these phases during entered the aquatic environment. Substances their life cycle. Qualitative and quantitative found in sediments may adversely affect benthic sources of uncertainty with the toxicological data species or bioaccumulate in benthos and should be documented. These uncertainties will subsequently be transferred to higher trophic be taken into account in selecting application levels. factors or in conducting the uncertainty analysis during risk characterization. The Water Quality Institute and RIVM (1995) provide a compendium of available standardized Spiked-sediment toxicity tests establish cause-and- test methods. Environment Canada (1994, 1995) effect relationships between exposed organisms has a number of sediment toxicity guidance and spiked concentrations of individual substances documents for aspects that are not covered in the or mixtures (Water Quality Institute and RIVM standard methods and are of general application 1995). A spiked-sediment toxicity test is directly to any sediment test. Canada has produced a few analogous to a water column test, except the standard methods applicable to sediment toxicity substance and test species are added to solid- testing, including testing of pore water with phase sediments. Researchers can use sediment echinoids (Environment Canada 1992a) and a solid-phase bioluminescent bacteria test
2 See Important Considerations in Section 6.4.2 and Appendix III, respectively, of the resource document.
6-10 from a reference location to provide contaminated area. This allows assessors to interlaboratory comparability. Artificially prepared determine whether effects have occurred on sediments may also be used instead of field infaunal species and to identify spatial and sediments, thereby avoiding concerns that the temporal trends in sediment contamination.3 For sediments may have been contaminated with other example, this information can be used to substances. Assessors should be aware of determine if a mixture of substances has affected concerns regarding the viability of organisms in community dynamics downstream of an industry. artificial sediments. Data interpretation still relies This weight-of-evidence approach is a recognized on expert judgment. For example, sediment in situ method for determining sediment quality. It spiking may be strongly influenced by the can be applied to a wide variety of aquatic methodology, and this may affect the ecosystems and to a wide variety of chemical comparability of results. groups. However, this approach does not identify substances found in the mixture. As with pelagic biota, single-species toxicity tests may be used to determine CTVs for sediment- The EqP approach (Section 6.2.7) may be used for dwelling biota. Toxicity tests may be short-term organic substances when the sediment solid phase acute or longer-term chronic. contains more than 0.2% organic carbon (Di Toro et al. 1991). An analogous approach has been A weight-of-evidence approach can be used to proposed for cationic metals (Campbell and establish associations between a substance’s Tessier 1996). A key parameter, for both organic concentration in sediments and observed adverse contaminants and metals, is the free solute biological effects. For example, the EqP approach concentration in the sediment pore water. This is provides a link to effects on benthic organisms. true not because pore water is necessarily an These associations can be based on data from important medium for uptake, but rather because laboratory tests conducted on field-collected [solute]free is a good estimate of the solute’s sediments that contain mixtures of substances. chemical activity and overall bioavailability in the These are referred to as co-occurrence data. sediment matrix. The EqP approach yields Field data in the literature should be evaluated on estimates of this key parameter (Di Toro et al. a case-by-case basis to determine their usefulness. 1991; Campbell and Tessier 1996). Co-occurrence data are often site-specific. Caution must be used in extrapolating results to Sediment quality guidelines and standards from other sites. various jurisdictions should also be reviewed for possible information on priority substances (e.g., CCME (1995) provides a discussion of the co- CCME 1995). occurrence approach based on work by Long and Morgan (1990), Long (1992), and Long and 6.4.3 Groundwater Biota MacDonald (1992). Other types of co-occurrence approaches include the apparent effects threshold Groundwater occupies pores and crevices in rock (AET), sediment quality triad, and informal and soil in the phreatic or saturated zone. evaluations of chemistry and biological responses Traditionally, it has been a resource for drinking (U.S. EPA 1992c). Sediment specialists will be water, agriculture, and industry. However, recent identified for risk assessors to consult when investigations have shown that a biologically applying a co-occurrence approach. diverse ecosystem exists within groundwater. The groundwater ecosystem provides habitat, food, The benthic community structure assessment is and nutrients for microbes such as bacteria and another weight-of-evidence approach that may be protozoa (Chapelle 1993) and for micro- and used to compare a community living at a macroinvertebrates, especially crustaceans reference station with a community living in a (Botosaneanu 1986; Danielopol 1992;
3 Examples of this approach are given by Diaz (1992), La Point and Fairchild (1992), Persaud et al. (1992), Reynoldson and Zarull (1993), and Reynoldson et al. (1995).
6-11 Marmonier et al. 1993). Biochemical reactions Leaching potential is also affected by a (aerobic and anaerobic respiration, fermentation, substance’s transformation rate in the soil (Boesten etc.) performed by bacteria in the subsurface and van der Linden 1991). Generally, owing to influence the chemical composition of the low organic matter content of aquifers, there is groundwater. Protozoa and multicellular low sorption capacity and, consequently, relatively organisms operate more indirectly on water quality high bioavailability. Groundwater invertebrates because of their influence on bacterial biomass, generally require some measurable dissolved growth, and metabolic state. Also, the self- oxygen and therefore a more positive redox cleansing potential of aquifers is related to these potential. These parameters can be good processes (Chapelle 1993; Stanford and Vallett diagnostic variables (although sometimes difficult 1994). There is now more research into to measure easily in these habitats). The assessor groundwater ecosystem dynamics and function, should be aware of the physical and chemical the identification and distribution of groundwater properties of the substance and the material organisms, and the effects of contaminants on through which it is being transported. groundwater organisms. Simple exposure screening strategies and While there are many approaches to evaluate the laboratory toxicity tests are recommended for effects of priority substances in surface water, evaluating effects on groundwater organisms. Test research to determine the effects of substances on organisms should be representative of Canadian natural populations of groundwater ecosystems is species and of groundwater biota in terms of an emerging field. No standard toxicity test function, trophic level, and route of exposure. protocols exist for groundwater organisms, and When reviewing toxicity studies, assessors should only effects on bacterial mineralization rates4 (Van be aware of the influence of pH, oxygen content, Beelen et al. 1991) and acute toxicity tests with temperature, and other parameters on the groundwater invertebrates are described in the bioavailability of organic and inorganic substances literature (Notenboom et al. 1994). Assessors and hence on their toxicity. For more discussion, should use all available data as long as good see Important Considerations in Section 6.4.3 of general QA/QC practices and sound scientific the resource document. principles are followed. In addition, all available data from the approaches described below should In practice, groundwater toxicity data will probably be included in a weight-of-evidence approach. be unavailable. If, however, groundwater biota Owing to the difficulty in interpreting effects data have been identified as being exposed to elevated for groundwater and surrogate organisms, levels of a substance, surrogate species such as assessors are advised to consult with groundwater surface water crustaceans may be used to ecology experts. determine the CTV for functionally similar species (Notenboom et al. 1994). Other candidates for
Substances with low Kow and Koc values are of the surrogate species can be found among rotifers, most concern to groundwater biota, because they nematodes, protozoans, and oligochaetes. These travel the furthest distance and may create the taxa, in addition to crustaceans, are frequently largest plume (Lesage 1995). However, found in groundwater and are also used in substances with a high Kow may also be of concern ecotoxicology studies. It is also possible that by desorbing slowly from organic matter to which effects threshold data for groundwater organisms they had adsorbed in the saturated zone. The could be estimated from toxicity results from soil- organic matter may then be a source of dwelling organisms such as earthworms (van den contamination of substances for a long time. High Berg and Roels 1991). For Tier 1 assessments,
Koc and Kow values also favour substance transport toxicity data from surrogate species (aquatic on colloids (Lafrance et al. 1989; McCarthy and crustaceans, protozoans, nematodes, and Zachara 1989; Kan and Tomson 1990). oligochaetes) can be used. Again, assessors are advised to consult with groundwater ecology experts when approaching this type of assessment.
4 This refers to the measurement of the ability of the bacteria to mineralize a given substrate/substance.
6-12 Assessors should identify areas of qualitative and and terrestrial plants (U.S. EPA 1985; OECD quantitative uncertainty in the toxicological data. 1993a). However, the only internationally These may include uncertainties regarding the harmonized soil toxicity test using invertebrates is relationship between the substance and the the acute earthworm toxicity test (OECD 1984). groundwater ecosystem, the parameters of the See Section 6.6.1 in the resource document for a study, and natural variations in groundwater description of this test and other tests currently systems. When using toxicity data measured for undergoing research to standardize lethal and aquatic surface water species to derive, sublethal toxicity tests for a wider range of soil- extrapolate, or otherwise estimate toxicity data for dwelling organisms. species in groundwater, it is important that the uncertainty be characterized. Data should be evaluated based on good general QA/QC practices and sound scientific principles The CTV is obtained from a weight-of-evidence (see Appendix III in the resource document; approach that examines all appropriate data. Environment Canada 1996). Toxicity information Chronic, full life cycle studies measuring nonlethal should ideally include data from a wide range of effects such as growth and reproduction are trophic levels and from both above ground and preferred. The EqP method (Section 6.2.7) may soil-dwelling biota. Soil organisms can be also contribute to the weight-of-evidence exposed to substances in soil via three routes: approach. If only acute toxicity data are available (i) oral uptake of food, soil particles, or pore or if the acute toxicity data are more sensitive than water, (ii) dermal uptake from contact with pore the chronic information, the CTV may be based on water or soil particles, and (iii) inhalation of soil air an LC50, EC50, or other significant ECx. (see Table 5.6 of the resource document). Assessors should therefore consider the 6.5 Terrestrial Effects partitioning of the substance within soil Characterization compartments and the life habits of the soil biota to determine the relevance of toxicity test data. 6.5.1 Soil Biota Toxicity studies considered in assessments should use test organisms and soil with properties that are Substances found in soils may exist as distinct solid representative of the areas of concern in the or liquid phases or may be dissolved in the soil Canadian environment. water, vaporized in the soil air, or adsorbed or absorbed to mineral or organic particles. Soil Toxicity information should include data from properties play a key role in determining the important trophic levels and functions such as bioavailability of a substance to soil organisms. decomposition (microorganisms and detritivores), These properties include soil particle size primary production (plants), and herbivores and distribution (percentage of sand, silt, and clay), saprovores (invertebrate fauna). To compare moisture content, pH, total organic carbon these tests, standardized soil that has similar content, and redox potential (Section 5.3 in the textural composition, pH, organic matter content, resource document). water content, and density should be used (van Leeuven and Hermens 1995). For assessment purposes, soil biota are organisms that live at least part of their life cycle in the soil. Acute and chronic toxicity data for aquatic species They may live above ground, in the litter layer, in may be used as a screening tool to estimate the mineral soil, or in soil pore water. Soil biota effects on soil organisms that are exposed include microorganisms, fungi, invertebrates, and primarily to a substance via soil pore water. plants. Mammals, birds, reptiles, and amphibians Aquatic species that can be used as surrogates for are assessed separately as wildlife (see below). related terrestrial organisms include crustaceans, insect larvae, annelids, plants, and algae (VKI There are a variety of approaches to assess the 1994). Two modifying factors must be considered effects of priority substances on soil-dwelling biota, — namely, soil organic carbon content (foc) and including single-species and multispecies toxicity soil water content (f ), such that: tests and field studies. Toxicity test protocols have w been developed to assess effects on earthworms
6-13 CTVs = [(foc • Koc ) + fw ] • CTVd exposure routes. For a volatile substance that partitions to the air, an inhalation study is where preferred. For a hydrophobic substance that CTV = CTV for soil biota partitions to biota, an oral ingestion study is s preferred. The Canadian Wildlife Service is developing a computerized Wildlife Contaminant foc = mass fraction of organic carbon in the solid phase Exposure Model (WCEM) to estimate wildlife exposure to organic substances through inhalation Koc = organic carbon partitioning and ingestion of food and water in the Canadian ≈ coefficient (where Koc Kow, the environment (Brownlee et al. 1995). All of the octanol–water partition coefficient) major routes of substance exposure identified in this model should be assessed. fw = mass fraction of water content in soil Wildlife-testing protocols have been reviewed CTVd = CTV of the dissolved substance on an aquatic organism (modified from recently by Hoffman et al. (1995). Avian protocols include acute oral (LC ), short-term dietary (LD ), VKI 1994). 50 50 chronic reproduction, embryo toxicity/ teratogenicity, behavioural, and field toxicity tests. Mammalian wildlife assessments rely heavily on Predictive approaches, such as the EqP approach laboratory data (Hodgson and Levi 1987) and QSARs, can provide supporting information generated for human assessments, although U.S. as part of the weight-of-evidence determination EPA protocols are available for the mink (Mustela but should not be used alone to derive the CTV. vison) and European ferret (Mustela putorius furo) These approaches involve considerable (Ringer et al. 1991). A standardized frog embryo uncertainty. Assessors should consult Sections teratogenesis assay (FETAX) has been developed 6.2.6 and 6.2.5, respectively, of the resource by ASTM (1991). There are no terrestrial toxicity document for information on the EqP method and test protocols for amphibians. However, the QSARs. aquatic life stages appear to be the most sensitive to potentially harmful substances. Soil quality guidelines and standards from various jurisdictions should also be reviewed for possible The range of sensitivity to environmental information on priority substances (e.g., CCME substances depends on taxonomic class, age, size, 1996). and life history characteristics. For example, birds are generally considered more sensitive than 6.5.2 Wildlife mammals, amphibians, or reptiles. Smaller For assessment purposes, wildlife refers to wild species consume more substance per unit body mammals, birds, amphibians, and reptiles. weight. These generalizations should be applied Because of the complexities in predicting the with caution, as there are always exceptions effects of substances on wildlife, assessors should (Tucker and Leitzke 1979). Owing to differences consult with the Canadian Wildlife Service when in wildlife physiology and sensitivity between parameters related to wildlife are the assessment classes, interclass extrapolations of quantitative endpoints. data are not recommended. However, when physiological similarities between classes and the Wildlife may be exposed to substances through mechanism of action are known, data may be inhalation; dermal contact with soil, sediment, discussed qualitatively in relation to another class water, or air; oral intake of aquatic or terrestrial to provide supporting evidence for the assessment. prey and water; incidental ingestion of soil or sediment; or cleaning feathers or fur. Assessment and measurement endpoints should involve similar
6-14 For wildlife, measurement endpoints such as Global warming resulting from climate change is reproductive and developmental toxicity5 and assessed under Section 11(a) of CEPA, as it is reduced survival are preferred, as they can be considered to cause direct adverse effects on the directly related to potential population-level environment or because there is no clearly defined effects. A substance may also have an impact on link to specific human health effects. “Toxic” wildlife populations through behavioural determinations for all atmospheric effects may not alterations, decreased food supply, or habitat be straightforward because of the complexities in degradation. Chronic studies on organ-specific predicting potential atmospheric interactions. effects may be used if the effect can potentially However, assessors should consult with experts in reduce survival or reproduction in wildlife. the Atmospheric Environment Service of Biochemical or physiological perturbations such as Environment Canada or elsewhere for assistance. endocrine disruption, genotoxicity, and immune suppression may also have serious repercussions The following sections summarize the methods for wildlife population effects. However, there are available for estimating a first approximation of no standard measurement endpoints for identifying the various potentials of atmospheric effects. population-level effects for some of these 6.6.1 Stratospheric Ozone Depletion examples. Ozone-depleting potential (ODP) is the ratio of Field studies are preferred when cause-and-effect calculated ozone column change for each mass relationships can be clearly established to derive a unit of a gas emitted into the atmosphere relative CTV for wildlife. They can integrate many to the depletion calculated for an equal mass of environmental factors that cannot be replicated in reference gas, chlorofluorocarbon-11 (CFC-11) a laboratory study. When field studies are (ODP = 1). An example of a calculation is unavailable, laboratory studies may be used, with provided in Section 6.6.3 of the resource preference given to wildlife species. CBB studies document. In a first approximation, the ODP (Section 6.2.5) and other body burden studies may value can be calculated using the formula: also be relevant, particularly for metals. ODP = (T /T ) (M /M ) ([n + αn ]/3) 6.6 Effects Mediated Through the S CFC-11 CFC-11 S Cl Br Atmosphere where T = atmospheric lifetime of substance S Substances identified during problem formulation S (years) that are likely to partition to the atmosphere may be assessed under either Section 11(a) or Section TCFC-11 = atmospheric lifetime of CFC-11 11(b) of CEPA. Their behaviour should be (60 years) compared with that of substances known to cause stratospheric ozone depletion, ground-level ozone MCFC-11 = molecular mass of CFC-11 formation, or global warming using one or more (137.5g•mol-1 ) of the methods outlined below. These methods M = molecular mass of substance S provide a rough estimate for the potentials S (g•mol-1 ) described, and, although they can be calculated quickly, their real value may be for screening n = number of Cl atoms per molecule during problem formulation and as indicators for Cl more in-depth study. nBr = number of Br atoms per molecule Under Section 11(b), “toxic” determinations will α = a measure of the effectiveness of Br include effects due to stratospheric ozone in ozone depletion with respect to depletion and ground-level ozone formation. Cl; a reasonable parameter is α = 30.
5 Includes effects on spermatogenesis, fertility, pregnancy rate, number of live embryos, neonatal mortality, eggshell thinning, egg production, hatchability, and offspring survival. 6-15 In general, ODP values approach zero for species There is too much uncertainty associated with this with atmospheric lifetimes less than one year. In methodology to assign an ozone-forming potential accord with the Montreal Protocol on Ozone (OFP) threshold above which a VOC could be Depleting Substances, any substance with an ODP considered “toxic” under CEPA Section 11(b). may be considered “toxic” under Section 11(b) of However, with technical assistance, it may be CEPA and subject to regulation. possible to generate more accurate OFPs.
6.6.2 Ground-Level Ozone Formation Computer simulations can be used by appropriate experts to arrive at more precise estimates of the Substances that contribute to ground-level ozone ozone creation potential for individual organic formation are volatile, reactive hydrocarbon gases compounds (Carter 1994). These simulations (volatile organic compounds, or VOCs) at ambient produce reactivity scales that take into account tropospheric temperatures. Such substances kinetic and mechanistic reactivity. In general, possess a wide range of ozone-producing reactivity scales numerically rank each VOC, potentials. providing a measure of how its emissions affect The photochemical ozone creation potential ozone formation. (POCP) index measures the relative effect on Two sets of reactivity factors have been calculated: ozone of a unit mass of any organic compound the maximum incremental reactivity (MIR) scale compared with that of an equivalent mass of and the maximum ozone incremental reactivity ethene (CEU 1995). Ethene has a POCP value (MOIR) scale. Many substances already have of 100. A first indication of episodic ozone published values for their reactivity, or these values formation can be obtained from a reactivity scale can be generated, if necessary (Dann 1994). based on the rate constant for the reaction of substance S with hydroxyl radicals and the With more precision, it may be easier to determine molecular weight of substance S compared with the extent of the contribution of any given VOC to that of ethene. An example of the calculation is ground-level ozone formation. However, the shown in Section 6.6.3 of the resource document problem of defining a threshold for that using the equation below: contribution to be “toxic” under CEPA Section 11(b) remains. OH-scale = (kS/MS) (Methene/kethene) x 100 Consequently, until a consensus is reached about where what constitutes a “toxic” determination under k = rate constant at T = 298 K for the CEPA Section 11(b) for ground-level ozone reaction with hydroxyl radicals formation and about the magnitude of the (cm3•mol-1•s-1) associated threshold, evidence of ozone formation should be used only in combination with other data, such as direct effects on biota or human kS = rate constant for the reaction of substance S with hydroxyl radicals health. (cm3•mol-1•s-1) 6.6.3 Global Warming kethene = rate constant for the reaction of ethene with hydroxyl radicals Global warming potential (GWP) is the ratio of (8.5 x 10-12 cm3•mol-1•s-1) warming for each unit mass of a gas emitted into the atmosphere relative to the warming for a mass unit of the reference gas CFC-11. Assessors will MS = molecular mass of substance S (g•mol-1) be able to estimate the GWP of a substance S using the following formula. An example of a Methene = molecular mass of ethene calculation is given in Section 6.6.3 of the -1 (28 g•mol ). resource document using the equation below:
6-16 GWP = (TS/TCFC-11) (MCFC-11/MS) (SS/SCFC-11) preferred data sets, and indicate the scientific consensus or lack thereof for critical issues or where assumptions. T = atmospheric lifetime of substance S S 6.8 References (years) Anderson, S., W. Sadinski, L. Shugart, P. Brussard, T = atmospheric lifetime of CFC-11 Anderson, S., W. Sadinski, L. Shugart, P. Brussard, CFC-11 M. Depledge, T. Ford, J. Hose, J. Stegeman, W. (60 years) M. Depledge, T. Ford, J. Hose, J. Stegeman, W. Suk, I. Wirgin, and G. Wogan. 1994. Genetic and molecular ecotoxicology: A research MS = molecular mass of substance S (g•mol-1) framework. Environ. Health Perspect. 102(Suppl. 12): 3–8.
MCFC-11= molecular mass of CFC-11 (137.5 g•mol-1) ASTM (American Society for Testing and Materials). 1991. Standard guide for SS = IR absorption strength of substance S conducting the frog embryo teratogenesis assay in the interval 800–1200 cm-1 C Xenopus. E 1439. In Annual book of ASTM (cm-2•atm-1) standards. Vol. 11.04. Philadelphia, Pennsylvania. pp. 1260–1270. SCFC-11 = IR absorption strength of CFC-11 in the interval 800–1200 cm-1 Barrett, G.W. 1968. The effect of an acute (2389 cm-2•atm-1). insecticide stress on a semi-enclosed grassland ecosystem. Ecology 49: 1019–1035. Methods for deriving absorption strengths (SS) are described by Kagann et al. (1983), Rogers and Boesten, J.J.T.I. and A.M.A. van der Linden. Stephens (1988), and CEU (1995). Using this 1991. Modelling the influence of sorption and calculation, substances with an estimated GWP of transformation on pesticide leaching and 0.05 or greater would be a concern. persistence. J. Environ. Qual. 20: 425–435.
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6-22 CHAPTER 7 RISK CHARACTERIZATION
7.1 Introduction must then try to resolve the difference by reexamining each line of evidence and, if 7.1.1 Goals and Objectives necessary, generating new data. The objective of risk characterization is to 7.2 Overview determine the likelihood and magnitude of adverse effects on assessment endpoints as a A tiered approach is used for environmental result of exposure to the priority substance assessments of priority substances under CEPA. In (definition adapted from Suter 1993). To do this, Tiers 1 and 2, a quotient is calculated for each ecological risk assessment techniques and tools assessment endpoint by dividing a single EEV by are used when appropriate and when sufficient an ENEV. An ENEV is calculated by dividing the data are available. This chapter describes a tiered CTV by an appropriate application factor. approach for estimating risks of adverse effects of Application factors are used to account for the priority substances on assessment endpoints. uncertainties inherent in extrapolating between measurement and assessment endpoints. A Tier 1 7.1.2 Relationship with Other Phases assessment involves the calculation of deliberately Risk characterization combines the results of the hyperconservative quotients (Section 7.3). If such characterization of entry, exposure, and effects hyperconservative quotients are <1 for an (Figure 7.1). These results may be combined in a assessment endpoint, then the likelihood that the number of ways. The most common approach is substance is causing adverse effects in the to estimate exposure based on monitoring studies Canadian environment is very small, and the and toxicity based on laboratory bioassays and assessment for that endpoint would not lead to the then compare the two. Other information should conclusion that the substance is “toxic” as defined also be used in a weight-of-evidence approach in CEPA. For an assessment endpoint with a ≥ whenever possible. For example, if field Tier 1 quotient 1, a more refined Tier 2 observations indicate a correlation between the assessment is normally required. Section 7.4 absence of sensitive species and levels of the describes ways of refining Tier 1 quotients to be priority substance, this evidence should be used in less conservative. For an assessment endpoint ≥ characterizing risk. Similarly, if several toxicity with a Tier 2 quotient 1, a Tier 3 assessment studies or QSARs corroborate the CTV (see should be undertaken. Tier 3 assessments are Chapter 6) or if fate model predictions support the probabilistic, integrating distributions of exposure monitoring data, these lines of evidence should be and/or effects. This approach facilitates a more highlighted in the risk characterization. The use of explicit consideration of sources of variability and several lines of evidence can strengthen our uncertainty in the risk analysis. This analysis confidence in the risk assessment conclusions. considers not only the risk of exceeding the ENEV, Conversely, if the lines of evidence contradict one but also the entire relationship between exposure another, then our confidence in the risk and response, in order to estimate the assessment conclusions will decrease. Assessors probabilities of effects of differing magnitudes.
7-1 Ecological risk assessment techniques are • incomplete understanding of the temporal and particularly well suited for Tier 3 assessments. spatial scales of exposure and the matching of Section 7.5 describes the procedures for a Tier 3 those scales with the ecological scales of the probabilistic risk analysis. risk assessment,
For many naturally occurring substances, there are • incomplete knowledge of substance naturally enriched areas in Canada. In these transformation due to chemical, physical, and areas, resident organisms will have developed a biological actions, tolerance to the substance of interest. However, there is a potential for harmful effects to these • poor understanding of the heterogeneity of the resident organisms if exposure is further increased populations at risk, as a result of anthropogenic sources. Assessments • incomplete knowledge of how stressors act of naturally occurring substances therefore involve upon a population or community and the estimating background concentrations and interactions among multiple stressors, adjusting ENEVs to account for expected tolerances in naturally enriched areas. This is • inadequate reproducibility of laboratory and discussed in Section 7.6. field studies,
Risk analyses are usually based on assessment • incomplete knowledge of the extrapolation of endpoints at the population or community level of laboratory toxicity test results to field organization. Assessment endpoints at the conditions, and individual level may be appropriate for threatened or endangered species, where population sizes are • incomplete knowledge of the extrapolation of already reduced. The quantitative prediction of toxicity test results for measurement endpoints mid- to long-term effects at higher levels of to assessment endpoints. organization generally requires linking toxicity test In deciding whether these or other sources of results with population- or community-level uncertainty are critical to the assessment of simulation models or field studies. Section 7.7 whether or not a substance is CEPA “toxic” or for provides guidance on how models and field effective risk management decisions, assessors studies may be used to quantitatively estimate the should communicate regularly with Environment consequences of exposure to priority substances at Canada risk managers and interested parties higher levels of organization. Models and field throughout the risk characterization phase. studies may not be required for qualitative Assessors, managers, and interested parties will descriptions of potential consequences at higher need to consider which analyses will ultimately be levels of organization. the most useful during risk management. They will In carrying out a risk analysis at any tier, key also need to decide when the analyses have sources of uncertainty must be identified and proceeded far enough. Regular communications described either qualitatively or quantitatively. with risk managers and interested parties will help Smith and Shugart (1994) examined uncertainty in to ensure that the risk assessment plays a central relation to the three phases of ecological risk role whenever it is necessary to develop strategic assessment — problem formulation, analysis, and options for priority substances. risk characterization. Uncertainties in problem formulation include choice of appropriate 7.3 Tier 1: Hyperconservative endpoints, models, and scale. In the analysis and Quotients risk characterization phases, potential sources of uncertainty include: Tier 1 of an environmental assessment involves calculating a hyperconservative quotient (i.e., EEV/ • incomplete knowledge of the composition, ENEV) for each assessment endpoint. For a Tier 1 magnitude, frequency, and duration of quotient, the EEV is usually the maximum total releases and discharges, observed or predicted concentration or dose in the environment, and the application factor used in • incomplete knowledge of the physical and chemical properties of the substance, 7-2 Entry Exposure Effects Characterization Characterization Characterization
Risk Characterization Risk Analysis
<1 Tier 1: Hyperconservative Quotients >1
Tier 2: Risk Managers and <1 Interested Parties Conservative Quotients >1
Adverse Effects Tier 3: Unlikely Analysis to Estimate Risks of Effects Adverse Effects Likely Estimate or Describe Ecological Consequences
Not CEPA "Toxic" CEPA "Toxic"
Risk Management
Figure 7.1 Risk characterization in the ecological risk assessment framework for priority substances.
deriving the ENEV may be large. The endpoint, and there is little justification in recommended maximum application factors proceeding to more detailed analyses. The presented in Table 7.1 are similar to those used by substance is not declared “toxic” as defined in a number of other agencies (Environment Canada Section 11 of CEPA, based on the assessment of 1996). Typically, hyperconservative scenarios that endpoint. For an assessment endpoint with a overestimate the risk posed to assessment hyperconservative quotient ≥1, the assessment endpoints (Bogen 1994; Cullen 1994). If the proceeds to a less conservative, more realistic hyperconservative quotient is <1 for an Tier 2 analysis. assessment endpoint, there is a very low probability of adverse effects on the assessment
7-3 Table 7.1 Recommended maximum application factors for converting critical toxicity values to estimated no-effects values in Tier 1.
Available Information Maximum Factor
Threshold (e.g., IC25) of sublethal toxicity from a base data set (e.g., fish, daphnid, and algal species) 10
Lowest acute LC50 or EC50 from a base data set (e.g., fish, daphnid, and algal species) 100
Lowest acute LC50 or EC50 from a data set of one or two species 1000
7.4 Tier 2: Conservative 7.5 Tier 3 Analyses Quotients Tier 3 analyses consider distributions of exposure A Tier 2 environmental assessment of a priority and/or effects. This approach allows a more substance involves a further analysis of exposure thorough consideration of sources of variability and/or effects to calculate a quotient that is still and uncertainty in the risk analysis. These conservative, but more “realistic” than the distributions can be analyzed, and the results of hyperconservative quotient calculated in Tier 1. the analyses presented, in a variety of ways. The For example, the EEV should be based on more following guidance is provisional and will be recent data and on the bioavailable fraction, updated when further experience is gained in rather than on total concentrations. When applying Tier 3 methods to priority substances. possible, the CTV should be derived from studies In its simplest form, Tier 3 assesses the risk or using test organisms that are closely related to probability of exceeding the ENEV by comparing species resident in areas of concern, rather than the exposure distribution with the point estimate from results of studies using the most sensitive ENEV. Tier 3 may be more complex, using species, if they are not related to the assessment ecological risk assessment techniques and tools to endpoint. It may be possible to decrease the size compare distributions of both exposure and effects of the application factor used to derive the ENEV in order to estimate the probabilities of differing from the CTV (from, for example, 100 to 20) if the magnitudes of effects. Assessors should consult substance is nonpersistent and does not with risk managers to determine the appropriate bioaccumulate or if QSAR or EqP calculations approach. support the CTV. When available, empirically derived acute/chronic ratios (ACRs) should be Choosing appropriate models and methods of used to estimate long-term no-effects analyses for a Tier 3 assessment is more involved concentrations from the results of acute toxicity and difficult than in Tiers 1 and 2. The methods studies (Kenaga 1982). It may be necessary to used to estimate risks should be capable of carry out research to generate exposure and/or propagating variabilities and uncertainties through effects data in order to complete Tier 2. If the Tier the analysis and, if possible, estimating ecological 2 quotients are <1 for an assessment endpoint, consequences. This requires more emphasis on there is a low probability of adverse effects, and site characteristics to estimate exposure and on the the substance is not declared “toxic” on the basis sensitivities of resident biota to characterize effects. of that assessment endpoint. For quotients ≥1, assessments should proceed to Tier 3 to estimate the potential risks posed by the substance. 7-4 Tier 3 estimates of risk may be obtained by a Uncertainty about a variable that is fixed or variety methods, including first-order error deterministic is referred to as Type B uncertainty analysis, Monte Carlo simulation, Baye’s method, (Hoffman and Hammonds 1994). If, for example, and others. These methods produce a single we had only a limited number of sediment number that estimates the probability of a samples in the case above, then there would be specified effect or a distribution of output that much uncertainty concerning the values for the provides information on the probabilities of a true mean and variance and the shape of the range of effects (Covello and Merkhofer 1993; distribution. Type B uncertainty comprises several Smith and Shugart 1994). The method selected sources of uncertainty, including (i) model by the assessor will depend on the nature of the uncertainty, resulting from lack of understanding of problem and the available information. For the ecosystem or failure to capture the salient substances for which the determination of “toxic” features of risk, (ii) parameter uncertainty, owing to is not clear-cut, it is impossible to specify universal the imprecise estimates of model parameters probability cutoffs that are sufficient for a “toxic” made from limited data, (iii) judgmental determination, as issues of magnitude of effects, uncertainty, arising from the inability of experts to spatial and temporal scales of effects, and specify precise values for model inputs when data availability of supporting lines of evidence all play are lacking, and (iv) completeness uncertainty, a role in the decision. Professional judgment is resulting from the possible omission of important required, and the assumptions underlying the processes from the analysis (Covello and judgment must be clearly stated. Key concepts, Merkhofer 1993). model selection issues, and methods that assessors may use to conduct a probabilistic risk analysis are Probability estimates often include both Type A discussed below. and Type B sources of uncertainty. It may be possible to separate Type A and Type B sources of 7.5.1 Key Concepts uncertainty in some probabilistic risk analyses (see Hoffman and Hammonds 1994 for an example). The concept of probability can be difficult, The results of such an analysis can be thought of because there is no universally agreed-upon as a risk function with confidence limits. In definition (Power et al. 1994). When empirical practice, apportioning Type A and Type B sources data are plentiful and relevant to the variable of of uncertainty for individual inputs is difficult. interest, development of a probability estimate can proceed using standard statistical techniques 7.5.2 General Mechanics of a Probabilistic (Taylor 1993). For example, substance Risk Analysis concentration in sediment over a defined spatial area has a true mean, variance, and shape of Finkel (1990), Hammonds et al. (1994), and distribution. If a well-designed sampling and others have developed guidelines for quantifying analytical strategy has been employed, then it is uncertainty that include the following steps. Some possible to estimate values for the mean and of these steps are expanded upon in subsequent variance and the shape of the distribution that are sections. close to the true values and distribution shape. In • Identify the desired numerical expression and this case, the estimated variance of substance X characteristic of risk for each assessment concentration could be used to state, for example, endpoint (e.g., 25% mortality to pelagic fish that a sedentary benthic organism has a 95% species, 10% growth rate impairment in diving probability of being exposed to substance X in the ducks) (see resource document, Section 3.1). -1 concentration range 1.5–9.9 µg•L . Hoffman The remaining steps need to be followed and Hammonds (1994) refer to this type of separately for each measurement and/or statement as Type A uncertainty. That is, the assessment endpoint. distribution of possible exposures for organisms is known, but the actual exposure to specific • Specify the model equation that will estimate individuals is unknown. Type A uncertainty is akin risk (Section 7.5.3). to the objective or classical view of probability, in that the probability estimate is a well-defined, measurable number. 7-5 • List all variables that will be specified as pie charts, histograms, summary statistics, or distributions. In general, it is preferable to risk indices. The objective is to ensure that the keep this list as short as possible by specifying risk manager understands the results of the input distributions only for those variables that analysis and the impact of any uncertainties are likely to have an important influence on not captured in the analysis on the conclusions the output (Seiler and Alvarez 1996). of the risk assessment and subsequent risk management decisions. The manager should • Generate a distribution for each input variable also be informed of any unresolved scientific in the risk equation (Section 7.5.4). These are controversies (Finkel 1990; Covello and often referred to as probability density Merkhofer 1993). functions or PDFs. 7.5.3 Choosing an Appropriate Model • Determine and account for dependencies among input variables. An example of a As one of the objectives of a Tier 3 assessment is dependency would be a positive correlation to estimate probabilities of effects, in addition to between concentrations in water and simply identifying possible risks, models are concentrations in prey species in a required to account for spatial and temporal probabilistic analysis of exposure for a variation in substance concentrations and predatory fish species. bioavailability, characteristics of the receiving environment, indirect effects, etc. The • Generate the output variable distribution by consequences of selecting one model over another combining the uncertainty distributions of the should be analyzed (Smith and Shugart 1994). input variables as specified in the risk Assessors should consider issues such as equation. This step often involves Monte availability of data, the appropriate aggregation Carlo simulation, but there are a variety of level for model inputs, spatial and temporal other possible methods (Section 7.5.5). scaling, initial condition sensitivity, applicability to • Fine-tune the analysis. At this point, assessors the system of interest, and whether the model has may use the results of a sensitivity analysis to been appropriately calibrated and validated, in determine those input variables that had an order to minimize uncertainty about the resulting important influence on the output variable. risk estimates (Beck 1987; Oreskes et al. 1994). Such input variables should be reexamined to It is useful to break the process of choosing a ensure that the data and distributions are model into two steps: model identification and scientifically acceptable. Often the tails of the model selection. In the first step, the assessor input variable distributions need to be identifies those aspects of the substance and truncated to eliminate physically or logically receiving environment that must be included in the impossible values. Input distributions may also model (i.e., a conceptual model is constructed). have to be adjusted to account for In the second step, the assessor chooses an dependencies between important variables. existing analytical or computer model that Once the input distributions and, if necessary, expresses the conceptual model. Before the model equation have been fine-tuned, the proceeding with a model simulation, credibility of analysis is repeated and a refined output the model should be assessed (Suter 1993). The generated. Fine-tuning the risk analysis often assessment of credibility is different from model involves numerous iterations. calibration and validation, because it does not yet • Summarize the results, highlighting important consider the fully parameterized form of the implications for risk managers. The major model. The goal is to develop a qualitative output of the analysis is a quantitative or measure of the predictive accuracy of the model. graphical description of the probability of an The following are indications that the model of effect (see Appendix V of the resource interest is credible: experimental testing on other document for an example). Such outputs may systems (e.g., mesocosms) indicates that the model be summarized as PDFs, cumulative performs adequately, the model has been probability distributions, ranges and box plots, published in a peer-reviewed journal, the model
7-6 has a long history of use, the model has been • If the distribution is known for the input subjected to carefully designed validation studies, variable, choose it. Typically, these variables and the model is supported by governmental are defined by the nature of the physical agencies or outside experts. processes that lead to variability in interactions or measurements (Seiler and Alvarez 1996). Assuming that the model is found to be credible, An example is the binomial distribution for the next steps are model calibration and experiments that determine probabilities by validation. The purpose of model calibration is to counting certain events. Normal and take the generic model and, by specifying the lognormal distributions may be inferred from “correct” parameter values, turn it into a predictive the structure of the variations in the stochastic tool for the system of interest. Validation tests the variable. For example, if the variability arises adequacy of the calibration exercise on an from a sum of contributions with many independent set of data. There are numerous variations, each with a mean and variance, statistical and graphical techniques that may be the distribution of the sum is asymptotically used to assess how well model performance normal. If, instead, the variability arises from matches observations. These include lumped the product of contributions with many measures of average model goodness-of-fit, variations, each with a mean and variance, correlation measures, parametric and the distribution is asymptotically lognormal nonparametric statistical tests, spatial analysis of (Ott 1995; Seiler and Alvarez 1996). Ott goodness-of-fit, and Bayesian measures of (1995) and the chapter by Mitchell Sharp in estimation error. Discussion of these and other Morgan and Henrion (1989) discuss the theory quantitative methods for testing model validity can underlying several key distributions in much be found in Reckhow et al. (1990) and in a more detail. special volume of Advances in Water Resources (Vol. 15, 1992), which is dedicated to the • Use empirical data to fit a distribution. discussion of validation of computer models. Measurements of substances in the environment often have histograms and logit Once a calibrated and validated model has been plots compatible with a lognormal distribution. selected, the next step is to select and Other variables may have histograms and parameterize each of the input distributions. probit plots compatible with a normal 7.5.4 Choosing Input Distributions distribution. Any fitting of data to a distribution should be examined visually The choice of an input distribution generally (e.g., probit or logit plots should produce depends on (i) the form of the observed data, straight lines for variables with underlying which may be determined by graphical or normal and lognormal distributions, statistical regression techniques, and (ii) a basic respectively) and tested (e.g., the W test may understanding of the system, which allows be used to test whether the data were drawn assessors to theorize about the distributions that from an underlying normal distribution; will best describe the underlying reality (Table 7.2 conducting the test on logarithms of the data and Figure 7.2). For example, a lognormal will test whether the data are from an distribution is usually appropriate for any variable underlying lognormal distribution) (Gilbert that is the product of a large number of random 1987). variables, such as concentration in a particular medium (Hattis and Burmaster 1994). • Use surrogate data to fit a distribution. An example is the use of measured body weights The following is a list of approaches for choosing of a particular mammal in a location different input distributions, going from the highest degree from the location of interest in the risk analysis. of confidence to the lowest (adapted from Seiler In this case, an assessor would have to justify and Alvarez 1996 and Moore 1996): that the extrapolation from one location to another is reasonable.
7-7 • Use existing data to fit portions of the variable. example, implies that we know a minimum This situation is common in environmental and a maximum with absolute certainty (which assessment. The tendency when information is is rarely the case) and that all values in lacking is to use uniform and triangular between are equiprobable (which is almost distributions. Seiler and Alvarez (1996) are never the case). Often in these situations, the quite critical of the use of such distributions assessor can make better use of the available when information is lacking. The reason is information to choose a more appropriate that use of the uniform distribution, for distribution.
Table 7.2 Useful input distributions for probabilistic risk assessments of priority substances.
Distribution Example Applications
Beta Modelling environmental concentrations. Rough model in absence of data.
Binomial Number of malformations at a contaminated site.
Chi-square Sum of weights of objects, each following a normal distribution.
Exponential Time between events. Lifetime of organism with constant probability of mortality.
Gamma Time to complete task. Modelling environmental concentrations.
Geometric Number of trials until success is achieved.
Lognormal Product of a large number of other quantities. Modelling environmental concentrations. Modelling toxicity test results with quantal data. Distribution of physical quantities in nature.
Normal Size of quantities that are the sum of other quantities. Distribution of population characteristics.
Poisson Number of events in a given unit of time (e.g., accidental releases).
Triangular Distribution when minimum, maximum, and most likely values are known.
Uniform Distribution when minimum and maximum are known and all values between are equiprobable.
Weibull Modelling environmental concentrations. Modelling toxicity test results with continuous data. Lifetime of a device.
7-8 Choice of distribution becomes inherently more subjective as one moves Custom Uniform down the list. Thus, the approaches at the top of the list are recommended over those at the bottom. When there is doubt about the effect of Binomial Triangular different input distributions, try each plausible distribution and note the effect on the estimates of risk. Bukowski et al. (1995) found that the selection Normal Lognormal of a distribution for a given input variable can have a profound effect on the risk estimate, whereas the inclusion of correlations between Figure 7.2 Commonly used input distributions in ecological risk input variables is assessments. important only if the Similarly, the variance of the output distribution is correlations are high and the variances large (also the sum of the variances of the input variables. see Smith et al. 1992). That is: 7.5.5 Methods for Probabilistic Risk p Analysis µ ∑ µ R = i In many probabilistic risk analyses, risk curves or i=1 estimates can be derived simply by integrating an exposure and an effects distribution. Examples p include scenarios where there is one dominant σσ2 2 R = ∑i route of exposure (e.g., concentration in water) i=1 and a single response variable (e.g., Daphnia mortality; percentage of genera affected). In other analyses, risk estimates are based on more where p is the number of variables in the model. complex models (e.g., exposure from multiple The shape of the resulting output distribution will media, risk cascades through a food web). This tend to be normal even if the distributions section describes probabilistic methods that may assigned to the inputs are not normal. be used for both of these situations. A similar approach can be taken with a Estimating Risks: Analytical Methods multiplicative model after first converting the model to its additive form by logarithmically Analytical methods may be used to estimate risks transforming the input variables. with relatively simple model equations. The analytical method most commonly used is Y = a x b x c variance propagation (Morgan and Henrion 1989; Hammonds et al. 1994). If one has a ln(Y) = ln (a)+ ln (b)+ ln (c) simple additive model and the input variables are independent, the mean value of the output distribution is the sum of the input means.
7-9 For multiplicative models, the geometric mean is types of information. The first is a distribution the exponential of the sum of the mean values of relating substance concentration or dose to the the logarithms of each input variable. The percentage of species or genera affected (see geometric standard deviation is found by taking Figure 7.3 and Section 6.3.6 of the resource the square root of the sum of variances of the document). The second is a distribution of transformed variables and exponentiating. That is: chemical concentrations or other measure of exposure. The two distributions are then µ,R integrated to produce a joint probabilistic risk X g,R = e function. The result of this analysis is a risk curve showing the probabilities of effects of varying magnitudes (i.e., percentage of genera affected). σ2 R S g,R = e Such curves are an excellent quantitative means of describing and communicating risks. Note that the same approach may be used to estimate risks where to single populations. The only difference is that the effects distribution is a concentration-response X = the geometric mean of the resulting g, R curve for the species of interest. The above output distribution equations can also be expanded to estimate risks m,R = the sum of the means of the of multiple substances that have similar modes of logarithms of the input variables action. The software for the WERF approach is available upon request to the original authors.
Sg, R = the geometric standard deviation of the resulting output distribution Estimating Risks: Monte Carlo Simulation
2 One very commonly used probabilistic risk sR = the variance of the logarithms. assessment technique in ecological risk assessment is Monte Carlo simulation. The basis for a Monte The distribution of the output distribution for a multiplicative model will tend to be lognormal 100 even when the input distributions have 80 different shapes. Hammonds et al. (1994) describe variance 60 propagation in more detail. 40 Estimating Risks: The % of Genera Affected WERF Approach 20 An approach has been developed for estimating 0 community-level risks 1 10 100 1,000 10,000 100,000 based on the Concentration (µg/L) percentage of genera affected by acute or chronic substance Figure 7.3 Percentage of genera affected versus copper concentration. Each point is an acute LC . A log logistic exposures (Parkhurst et 50 al. 1996). The model has been fitted to the data (solid line), and 95% approach requires two confidence limits have been calculated (dashed lines).
7-10 Carlo analysis is straightforward. Point estimates Estimating Risks: Other Methods in a model equation are replaced with probability distributions, samples are randomly taken from In many cases, the paucity of empirical data will each distribution, and the results are tallied, make it difficult to properly specify the input usually in the form of a PDF or cumulative density distributions. In such cases, it is inappropriate to function (CDF). Several variations of the Monte use Monte Carlo analysis. An alternative Carlo technique for sampling from input technique is probability bounds analysis, which distributions are available. One variation is represents each uncertain input distribution within importance sampling, in which values of particular an entire class of probability distributions that importance (usually the tails of the input conform with the available empirical information distributions) are sampled more often and then about the variable (Ferson et al. 1997). When given reduced weight in order to improve large quantities of empirical data are available, resolution in the tails of the output distribution. In this class may be very small. Other times, the stratified sampling, the input distributions are class is very large, reflecting the poor state of divided into intervals and input values obtained by knowledge about the input variable. Ferson et al. random sampling from within each interval. The (1997) describe how to derive optimal bounds on most popular version of stratified sampling is latin the cumulative distribution functions in these hypercube sampling, which divides input classes for situations in which empirical distributions into equiprobable intervals. Latin information is limited. Once the bounds on each hypercube sampling is more precise than input distribution have been determined, it is conventional Monte Carlo sampling because the possible to compute the bounds for the output risk entire range of the input distributions is sampled in curve using RiskCalc. Figure 7.4 shows the results a more even, consistent manner (Iman and Helton of a risk analysis for female mink exposed to 1988). hexachlorobenzene in the St. Clair River area near Sarnia, Ontario. Input distributions for this Monte Carlo techniques excel when large analysis included concentrations in air, water, and quantities of data and theory exist to properly selected prey items, as well as their corresponding specify the model equation and the input inhalation, drinking, and ingestion rates. The distributions. Difficulties arise when there is figure includes the results for two estimation insufficient information to specify input distributions techniques: Monte Carlo analysis using or the relationships between them. Dependencies conventional or default distributions, and between input distributions can exaggerate or probability bounds analysis. According to the reduce the predicted probabilities of effects Monte Carlo analysis, there is a 19% probability compared with the uncorrelated case (Smith et al. ([1 - 0.81] x 100) of total daily intake exceeding 1992; Ferson and Long 1994; Bukowski et al. the 20% effect level for decline in reproductive 1995). In cases where the dependency fecundity of mink. When uncertainty concerning relationships are linear and the data exist to input distribution shapes is taken into account, specify the correlation coefficients, @Risk, Crystal however, the probability bounds analysis indicates Ball, and other software packages have the that the probability of total daily intake exceeding capability to induce the dependencies in the the 20% effect level could range from 0 to 66%. analyses. If important dependencies are suspected but insufficient data exist to specify the Other numerical methods for probabilistic risk relationships, then the analysis becomes analysis include (i) two-dimensional Monte Carlo problematic. In such cases, other techniques such analysis (Hoffman and Hammonds 1994) and as probability bounds analysis or fuzzy arithmetic (ii) various Bayesian methods, including Bayesian should be considered, because the results of such Monte Carlo (Warren-Hicks and Butcher 1996). analyses do not depend on knowledge about the Nonprobabilistic techniques for propagating covariance among input variables (Ferson and uncertainty include interval analysis and fuzzy Kuhn 1994; Ferson and Long 1994). arithmetic (Ferson and Kuhn 1994). The choice of which method to use depends on the complexity of the risk analysis, the available information, and the expertise of the assessor. The following are
7-11 1
0.8 Monte Carlo CDF Probability Bound 0.6 Probability Bound
0.4 Cumulative Probability 20% Effect Level for Decline 0.2 in Reproductive Fecundity
0 0 100 200 300 400 Total Daily Intake (µgkg bw-1day-1)
Figure 7.4 Total daily intake for female mink exposed to hexachlorobenzene in the St. Clair River area near Sarnia, Ontario. Exposure was estimated by two techniques: Monte Carlo analysis and probability bounds analysis.
general points of guidance to assist assessors in 7.5.6 Best Practices choosing an appropriate probabilistic risk analysis method: The following 14 principles were developed by Burmaster and Anderson (1994) for Monte Carlo • For simple additive and logarithmically analysis. They have been slightly adapted here to transformed multiplicative models where the make them applicable to probabilistic risk analyses variables are independent, an analytical in general. If adhered to, these principles will approach such as variance propagation is make probabilistic risk analyses easier to recommended. understand, will explicitly distinguish assumptions from data, and will consider and quantify effects • For more complex models, Monte Carlo that could lead to misinterpretation of the results. simulation methods are recommended, but As such, it is strongly recommended that assessors only if there is sufficient information to follow these principles when carrying out a Tier 3 adequately characterize the input distributions probabilistic risk analysis. and the relationships between them. (1) Show all model equation formulae. • For complex models with limited information, other methods with less restrictive requirements (2) Use point estimates as inputs before are recommended (e.g., probability bounds proceeding to the probabilistic risk analy- analysis, fuzzy arithmetic). sis. The choice of a probabilistic risk analysis method and subsequent analyses should be peer reviewed (3) From the results of the deterministic analy- by experts. sis, identify the input variables (i) that account for a dominant fraction of the predicted risks (e.g., ingestion of contami- 7-12 nated fish may be the dominant route of (11) Perform probabilistic sensitivity analyses on exposure for mink exposed to persistent key inputs in such a way as to distinguish organochlorines) and/or (ii) the ranges of the effects of variability from the effects of which account for the dominant fraction of uncertainty (e.g., change uncertain inputs the range of predicted risks. These input and rerun analyses to determine influence variables are the ones suitable for proba- of lack of knowledge on the outputs). bilistic treatment. Report the results of these computational experiments. (4) Restrict the use of probabilistic techniques to the pathways or sources that can poten- (12) Investigate the numerical stability of the tially influence the assessment of CEPA central moments and tails of the output toxicity or subsequent risk management distribution. Typically, the tails of the decisions, in order to save scarce re- output distribution are less stable and sources. For example, if conservative, more sensitive to changes in the tails of the deterministic calculations indicate that a input distributions. Because the tails of the quotient for a particular metal in a com- output distribution stabilize slowly, include plex mixture is <0.01, then do not include enough iterations to ensure stability this substance in a probabilistic analysis (≥10 000), or use latin hypercube sam- designed to estimate total risks from the pling to stabilize the tails as quickly as mixture. possible.
(5) Provide a graph showing the distribution (13) Present the name and statistical quality of and a table showing the mean, variance the random number generator. Some estimate, and range for each input distri- well-known generators have short recur- bution. rence times and are thus unsuitable for Monte Carlo analysis. (6) Show how each input distribution repre- sents variability and uncertainty. (14) Discuss the limitations of the methods and (7) Use measured data, whenever possible, to of the interpretation of the results. Discuss select and parameterize inputs. the possible consequences of sources of uncertainty not included in the analysis, (8) Discuss the methods and report goodness- and indicate where additional research will of-fit statistics for any fitted input distribu- improve the analysis. tion. For distributions chosen on theoreti- cal grounds, include a rationale justifying the chosen distribution. 7.6 Estimating Risks Due to Anthropogenic Sources of (9) Discuss the presence or absence of mod- Naturally Occurring erate (r > 0.6) to strong correlations, Substances particularly if the assessment of CEPA toxicity will be influenced by the tails of the Risk assessments of naturally occurring substances output distribution. Where such correla- must take into account naturally enriched areas tions exist, invoke the dependencies in the and the tolerance of organisms occupying these analysis using high and low estimates of areas to elevated concentrations. Such an the correlation coefficients to learn if the analysis is required only when a Tier 1 risk analysis correlations influence the analysis. indicates a potential for harmful effects and there is evidence of areas being naturally enriched in (10) Provide detailed graphs and summary Canada. The problem facing assessors is to statistics (e.g., mean, quartiles, range) for evaluate the potential impacts of further increasing each output variable. exposure in these areas through anthropogenic
7-13 inputs. In such cases, natural background exposure. Potential for tolerance in different concentrations should be estimated as precisely as strains of a species or in related types of species possible. may be evaluated by reviewing the literature to determine whether high effects thresholds have If the natural background concentration of been reported, particularly when test organisms bioavailable forms of the substance exceeds the were preexposed to a substance. When Tier 1 ENEV for sensitive endpoints, the ENEV assessment endpoints are found to pertain to a should be refined for Tiers 2 and 3. This involves: class of organisms that may be highly tolerant, • defining a lower bound for the ENEV, different endpoints may be chosen. For example, abundance of aquatic invertebrates might be • evaluating the choice of assessment and substituted for algae, if review of the literature measurement endpoints, and indicates that invertebrates are much less likely than algae to develop high tolerance. • evaluating the relative tolerance of assessment and measurement endpoints. 7.6.3 Evaluating the Relative Tolerance of Assessment and Measurement These steps arose from a workshop on effects on Endpoints organisms in naturally metal-enriched areas, held at Trent University in August 1995 (Hutchinson Measurement endpoints should exhibit tolerances 1996). that are similar to those of the corresponding assessment endpoints. When measurement 7.6.1 Bounding the Estimated No-Effects endpoints are likely to be less tolerant than the Value (ENEV) assessment endpoints, consideration should be In areas of elevated natural concentrations of a given to reducing or even eliminating the substance, resident organisms have acquired a application factors employed to derive the ENEV. tolerance for the substance, whereas organisms If this approach is inappropriate because of large that are sensitive to the substance are excluded uncertainties, new toxicity studies may be required. from the areas. In these areas, the ENEV should Ideally, area-specific organisms would be chosen not be set below the estimated natural background for testing. A bioassay protocol for obtaining concentration. Unfortunately, estimating natural toxicity data relevant to plants inhabiting naturally background concentrations in contaminated areas enriched areas has been proposed by Hutchinson can be difficult. When a natural background (1996). concentration can be estimated only as a single 7.7 Estimating Ecological mean value, that value may be used as the lower boundary of the ENEV. In cases where the natural Consequences background can be characterized as a Estimating the probabilities of exceeding an effects distribution, the lower boundary of the ENEV threshold or effects of differing magnitudes only should be the 90th percentile of the distribution for fulfils part of the information required for risk the area of concern.1 management decisions. This is because 7.6.2 Evaluating the Choice of Endpoints statistically obvious effects (e.g., high probability of a 20% decline in reproductive fecundity) may or Organisms residing in areas where a substance is may not be ecologically important. At the naturally enriched will have some tolerance of the community level, a stressor-induced change in substance, but the degree of tolerance may vary. microbial species composition is not ecologically Assessment endpoints should pertain to classes of significant if there is redundancy in the functions organisms that are the least likely to develop high performed by the species (Harwell et al. 1994). tolerance but are still relevant to the site of
1 Depending upon the shape of the natural background distribution, setting the minimum ENEV at the maximum value could result in an ENEV that is much higher than typical exposure values. Thus, using the maximum value would seem inappropriate. Alternatively, setting the minimum ENEV equal to the median natural background value would imply that assessment endpoints are adversely impacted by natural levels of the substance in up to half of the area of concern — an unlikely occurrence. 7-14 Conversely, effects on a few sensitive species Ferson et al. 1989). These models can be used to might be viewed as ecologically insignificant at assess risks of decreased survival or decreased first glance; however, if those species are key fecundity in relation to ecological stressors (Ferson predators or form the basis of the food chain, then et al. 1996). Demographics models have been the risks may cascade and lead to serious developed to characterize the dynamics of plants, community-level impacts. Thus, risk managers invertebrates, and mammals (see references in and other interested parties need to know the Caswell 1996 and Sibly 1996). Demographics consequences of continued exposure to the priority models can be used to address longer-term substance in order to better understand the projections of risk on future population sizes of the substance’s potential effects in the environment. species of interest. Risks may be characterized as Population- and community-level models and field the probability of different magnitudes of studies may be used to explore the consequences population decline in comparison to baseline of exposure to a priority substance. The following projections for nonstressed reference populations. section describes some of the available There are many programs currently available that population- and community-level field methods use demographics models to estimate risks to and models that may be used to estimate populations, including GAPPS (Harris et al. 1986), ecological consequences. RAMAS/age (Ferson and AkHakaya 1990), RAMAS/stage (Ferson 1994), RAMAS/space 7.7.1 Population- and Community-Level (AkHakaya and Ferson 1992), and ALEX Effects (Possingham et al. 1992). Each of these Assessments of potential risks posed to populations programs contains a large number of assumptions will focus on the probability of different degrees of and simplistically models the behaviour of population reduction. Methods used to organisms. Thus, caution should be used in characterize such reductions may include interpreting the results of any such analysis. In quantitative comparison of the distribution and addition, no one model is best suited for all abundance of populations in contaminated areas population modelling because of the diversity of with those in control or reference areas. In the life histories and population dynamics among absence of field data, population models may be species. used to predict ecological consequences. Population dynamics and risks can also be Individual-oriented models (DeAngelis et al. 1991) described using bioenergetics models (e.g., Bartell have been developed to assess ecological risks et al. 1986). Bioenergetics models can address posed to smaller populations of threatened or both direct and indirect ecological effects of endangered species (e.g., Atlantic salmon; Power stressors on the accumulation and allocation of and Power 1994). These models permit the energy inputs (i.e., photosynthesis, consumption) integration of animal behaviour, life history, by individual organisms from the populations of biology, and ecology with degrees of realism and interest. Bioenergetics models are more detail that cannot easily be achieved using more appropriately scaled to characterize risks conventional aggregated models (e.g., associated with chronic stress. These models also demographics or bioenergetics models) (Power characterize risk as the probability of observing the and Power 1994). The trade-off for more realism effects of interest in relation to the magnitude of is the additional demand for model parameters. A stress — for example, substance exposure particularly powerful and promising approach for concentrations (e.g., Bartell et al. 1992). assessing ecological risks in terrestrial systems lies Community and ecosystem models can be used to in the integration of individual-oriented models explore how substances could affect higher-order with spatially explicit representations of necessary endpoints such as community composition, ecological resources, as well as stressors, using productivity, and nutrient cycling. Suter and geographic information system (GIS) technology Bartell (1993) concluded that there are 15–20 as an operational framework. Population models aquatic and 5–10 terrestrial community and can take the form of age- or size-structured ecosystem models that could be used or slightly demographic models (Caswell 1989, 1996; modified to estimate higher-order effects.
7-15 Examples include SWACOM (Bartell et al. 1992) interest. Environmental quality guidelines or and AQUATOX (Park 1996) for estimating the other environmental benchmarks may be effects of stressors on aquatic ecosystems. Few of useful here to help focus risk management these models are easy to use, and few have efforts. At this point, risk assessors may wish received adequate field testing to validate model to indicate logical groupings of substances structure and predictions. and possible priority actions for best managing environmental risks. Notwithstanding the difficulties in using and evaluating models, population and community 7.9 References models can strengthen the weight-of-evidence determination for conclusions established by other AkHakaya, H.R. and S. Ferson. 1992. RAMAS/ means. They can also identify key functional and space: Spatially structured population models for structural aspects of the system under conservation biology, version 1.3. Applied consideration (Oreskes et al. 1994). For priority Biomathematics, Setauket, New York. substances already determined to be “toxic” under CEPA, and where adequate data exist, risk Bartell, S.M., J.E. Breck, R.H. Gardner, and A.L. assessors and managers may use appropriate Brenkert. 1986. Individual parameter population- and higher-level models to better perturbation and error analysis of fish understand the potential ecological consequences bioenergetics models. Can. J. Fish. Aquat. Sci. of exposure and to make effective risk 43: 160–168. management decisions. Because of the level of Bartell, S.M., R.H. Gardner, and R.V. O’Neill. expertise required, assessors should work with 1992. Ecological risk estimation. Lewis recognized experts to carry out such analyses. Publishers, Chelsea, Michigan.
7.8 Some Points to Remember Beck, M.B. 1987. Water quality modeling: A review of the analysis of uncertainty. Water • Present a summary statement for each of the Resour. Res. 23: 1393–1442. major components of the risk assessment, along with estimates of risk, to give a Bogen, K.T. 1994. A note on compounded combined and integrated view of the evidence. conservatism. Risk Anal. 14: 379–381.
• Clearly identify the key assumptions, their Bukowski, J., L. Korn, and D. Wartenburg. 1995. rationale, the extent of scientific consensus and Correlated inputs in quantitative risk assessment: uncertainties, and the effect of reasonable The effects of distributional shape. Risk Anal. alternative assumptions on conclusions and 15: 215–219. estimates. In quantitative assessments, also include the rationale for model selection and Burmaster, D.E. and P.D. Anderson. 1994. information about parameter sensitivities, Principles of good practice for the use of Monte stochasticity, and model uncertainty (Smith and Carlo techniques in human health and Shugart 1994). ecological risk assessment. Risk Anal. 14: 477– 481. • Outline ongoing or potential research projects that would significantly reduce uncertainty in Caswell, H. 1989. Matrix population models: the risk estimation. Construction, analysis and interpretation. Sinauer Assoc., Sunderland, Massachusetts. • Provide a sense of perspective about the risk. In doing so, avoid unrelated or inappropriate Caswell, H. 1996. Demography meets risk comparisons, such as risk of mortality due ecotoxicology: Untangling the population level to benzene exposure versus risk of mortality effects of toxic substances. In M.C. Newman due to natural causes (Freudenberg and and C.H. Jagoe (eds.), Ecotoxicology: A Rursch 1994; Shrader-Frechette 1995). hierarchical treatment. Lewis Publishers, Boca Instead, discuss effects in terms of ecological Raton, Florida. pp. 255–292. consequences for the assessment endpoint of
7-16 Covello, V.T. and M.W. Merkhofer. 1993. Risk Finkel, A.M. 1990. Confronting uncertainty in assessment methods: Approaches for assessing risk management: A guide for decision-makers. health and environmental risks. Plenum Press, Center for Risk Management, Resources for the New York. 309 pp. Future, Washington, D.C.
Cullen, A.C. 1994. Measures of compounding Freudenberg, W.R. and J.A. Rursch. 1994. The conservatism in probabilistic risk assessment. risks of “putting the numbers in context”: A Risk Anal. 14: 389–393. cautionary tale. Risk Anal. 14: 949–958.
DeAngelis, D.L., L. Godbout, and B.J. Shuter. Gilbert, R.O. 1987. Statistical methods for 1991. An individual-based approach to environmental pollution monitoring. Van predicting density-dependent compensation in Nostrand Reinhold Co., New York. smallmouth bass populations. Ecol. Model. 57: 91–115. Hammonds, J.S., F.O. Hoffman, and S.M. Bartell. 1994. An introductory guide to uncertainty Environment Canada. 1996. Guidance analysis in environmental and health risk document on the interpretation and application assessment. Oak Ridge National Laboratory, of data for environmental toxicology (draft U.S. Department of Energy, Oak Ridge, document). Environmental Protection, Ottawa, Tennessee. Ontario. 227 pp. Harris, R.B., L.H. Metzger, and C.D. Bevinf. Ferson, S. 1994. RAMAS/stage: Generalized 1986. GAPPS, version 3.0. Montana Co- stage-based modeling for population dynamics. operative Research Unit, University of Montana, Applied Biomathematics, Setauket, New York. Missoula, Montana.
Ferson, S. and H.R. AkHakaya. 1990. RAMAS/ Harwell, M., J. Gentile, B. Norton, and W. age: Modelling fluctuations in age-structured Cooper. 1994. Issue paper on ecological populations. Applied Biomathematics, Setauket, significance. In Ecological risk assessment issue New York. papers. EPA/630/R-94/009. Risk Assessment Forum, U.S. Environmental Protection Agency, Ferson, S. and R. Kuhn. 1994. Uncertainty Washington, D.C. pp. 2-1–2-49. analysis with fuzzy arithmetic. RiskCalc user manual. Applied Biomathematics, Setauket, Hattis, D. and D.E. Burmaster. 1994. Assessment New York. of variability and uncertainty distributions for practical risk analysis. Risk Anal. 14: 713–730. Ferson, S. and T.F. Long. 1994. Conservative uncertainty propagation in environmental risk Hoffman, F.O. and J.S. Hammonds. 1994. assessments. In J.S. Hughes, G.R. Biddinger, Propagation of uncertainty in risk assessments: and E. Mones (eds.), Environmental toxicology The need to distinguish between uncertainty due and risk assessment. Vol. 3. ASTM STP 1218. to lack of knowledge and uncertainty due to American Society for Testing and Materials, variability. Risk Anal. 14: 707–712. Philadelphia, Pennsylvania. pp. 97–110. Hutchinson, T.C. 1996. Report to the Priority Ferson, S., L. Ginzburg, and A. Silvers. 1989. Substances Assessment Program of Environment Extreme event risk analysis for age-structured Canada, including the findings of an Effects populations. Ecol. Model. 47: 175–187. Working Group for naturally metal-enriched areas, held August 28–29, 1995, at Trent Ferson, S., L.R. Ginzburg, and R.A. Goldstein. University, Peterborough, Ontario. Chemicals 1996. Inferring ecological risk from toxicity Evaluation Division, Environment Canada. bioassays. Water Air Soil Pollut. 90: 71–82. Iman, R.L. and J.C. Helton. 1988. An Ferson, S., L. Ginzburg, and R. AkHakaya. 1997. investigation of uncertainty and sensitivity Whereof one cannot speak: When input analysis techniques for computer models. Risk distributions are unknown. Risk Anal. (in press). Anal. 8: 71–90.
7-17 Kenaga, E.E. 1982. Predictability of chronic Seiler, F.A. and J.L. Alvarez. 1996. On the toxicity from acute toxicity of chemicals in fish selection of distributions for stochastic variables. and aquatic invertebrates. Environ. Toxicol. Risk Anal. 16: 5–18. Chem. 1: 347–358. Shrader-Frechette, K.S. 1995. Comparative risk Moore, D.R.J. 1996. Using Monte Carlo analysis assessment and the naturalistic fallacy. TREE to quantify uncertainty in ecological risk 10: 50. assessment: Are we gilding the lily or bronzing the dandelion? Hum. Ecol. Risk Assess. 2: 628– Sibly, R.M. 1996. Effects of pollutants on 633. individual life histories and population growth rates. In M.C. Newman and C.H. Jagoe (eds.), Morgan, M.G. and M. Henrion. 1990. Ecotoxicology: A hierarchical treatment. Lewis Uncertainty: A guide to dealing with uncertainty Publishers, Boca Raton, Florida. pp. 197–223. in quantitative risk and policy analysis. Cambridge, Cambridge University Press, U.K. Smith, A.E., P.B. Ryan, and J.S. Evans. 1992. The effect of neglecting correlations when Oreskes, N., K. Shrader-Frechette, and K. Belitz. propagating uncertainty and estimating the 1994. Verification, validation and confirmation population distribution of risk. Risk Anal. 12: of numerical models in the earth sciences. 467–474. Science 263: 641–646. Smith, E.P. and H.H. Shugart. 1994. Uncertainty Ott, W.R. 1995. Environmental statistics and in ecological risk assessment. In Ecological risk data analysis. Lewis Publishers, Boca Raton, assessment issue papers. EPA/630/R-94/009. Florida. Risk Assessment Forum, U.S. Environmental Protection Agency, Washington, D.C. pp. 8-1– Park, R.A. 1996. AQUATOX user’s manual. Eco 8-53. Modeling, Montgomery Village, Maryland. Suter, G.W. 1993. Ecological risk assessment. Parkhurst, B.R., W.J. Warren-Hicks, R.D. Lewis Publishers, Chelsea, Michigan. Cardwell, J. Volosin, T. Etchison, J.B. Butcher, and S.M. Covington. 1996. Methodology for Suter, G.W. and S.M. Bartell. 1993. Ecosystem- aquatic ecological risk assessment. Contract level effects. In G.W. Suter (ed.), Ecological risk No. RP91-AER-1, Water Environmental Research assessment. Lewis Publishers, Chelsea, Foundation, Alexandria, Virginia. Michigan. pp. 275–308.
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7-18 CHAPTER 8 COMPLEX SUBSTANCES
8.1 Background and General • Type 4: those commercially manufactured Approaches or formulated products that serve a spe- cific function (e.g., oil recovery mixtures, Most of the work in environmental toxicology and de-icing fluids, flame retardants, road environmental assessment has focused on salts), that have a defined and constant individual substances. In nature, however, biota composition, and that are composed of are often exposed to complex substances, such as unrelated substances (e.g., co-solvent mixtures or effluents.1 carriers, surfactants, stabilizers, anti- freezes, dyes), often enhancing or impart- There are four types of complex substances ing special properties to one or several (adapted from U.S. EPA 1986, 1988; Vouk et al. active ingredients.2 1987): The objective of this chapter is to provide • Type 1: those composed of related sub- guidance on how to conduct an environmental stances having similar physical and chemi- assessment of a complex substance. The chapter cal properties (e.g., polycyclic aromatic will focus on the differences between assessments hydrocarbons, or PAHs, PCBs, dioxins), of complex and individual substances, with particular emphasis on effects and risk • Type 2: those that are generated or re- characterization. Much of the guidance for leased at a given time and place (e.g., assessments of individual substances addressed in emissions from smelters, effluents), that other chapters of this manual also applies to have a relatively defined and constant assessments of complex substances. Some of this composition, but that are not necessarily guidance is repeated in this chapter in order to composed of related substances, present a complete overview of the assessment of complex substances. Assessors should refer to • Type 3: those that are commercially or appropriate chapters when clarification or chemically unrelated (i.e., having different additional information is needed on a particular physical and chemical properties) and that issue. Chapter 8 of the resource document occur by coincidence at a given time and provides additional information on the approaches place (e.g., landfill leachate), and and methods discussed in this chapter and guidance on the collection of data unique to complex substances.
1 See definition in Glossary (Appendix I).
2 Active ingredients have commercially desirable attributes and are not necessarily the harmful components in the formulation, as is the case for pesticide formulations.
8-1 This chapter presents a number of approaches take into account the spatial and temporal scales and methods that can be used in environmental of effects, and, whenever possible, uncertainties assessments of priority complex substances. should be quantified. A weight-of-evidence Methods for conducting the assessment are approach is recommended for complex substances outlined in order of preference but should not be (see Section 8.5.1). interpreted as prescriptive. Studies required to conduct environmental assessments of complex A tiered approach may not be appropriate for the substances are not always available. In such assessment of complex substances in all cases. cases, research may be required to generate the For example, when data for a Tier 3 assessment appropriate data. Research needs can be are available, the assessment could proceed identified using appropriate models. Models that directly to that tier. If there is a strong suspicion have been calibrated and validated for Canadian that a substance causes environmental harm and conditions can also be used to estimate risks. research is needed to conduct the assessment, When models are used, experts should be then assessors should proceed directly to higher consulted with regard to their advantages, tiers in order to determine the extent of the limitations, and assumptions. Costs of generating damage. data for preferred methods are often onerous, and data should be generated only when uncertainties 8.2 Problem Formulation around an assessment are unacceptable. Such In problem formulation, the goals, breadth, and decisions will be made on a case-by-case basis focus of the assessment are established, data gaps with the involvement of assessors, risk managers, are identified, and a strategy for proceeding with and other interested parties. Regular the assessment is devised. This phase includes communication between assessors and risk initial scoping, pathways analysis, consideration of managers is key to decision-making regarding receptor sensitivity, an analysis of the ecological data generation. relevance of potential receptors, selection of For relatively simple, well-characterized effluents assessment endpoints and associated and mixtures for which joint toxicity or independent measurement endpoints, and the development of toxic action (see Section 8.6 in the resource a conceptual model. document) can be assumed, an approach similar A complex substance must be thoroughly to that for individual substances may be used. For characterized in the problem formulation stage. more complex substances, the tiered approach The characterization is carried out in initial used for assessments of individual substances may scoping and pathways analysis, where entry and be modified as required. For example, in place of exposure are identified. Ongoing refinement of using EEVs and ENEVs, results of whole-effluent or this characterization may be necessary throughout whole-mixture toxicity tests with sensitive organisms the assessment process as additional data are may be used for Tier 1 screening. Similarly, in obtained. some cases, results of laboratory-ambient toxicity tests (see Section 8.5.4) using samples of During initial scoping, the characterization involves environmental media collected close to sources identifying various technical names of the could be used for Tier 2. For example, a substance and, on a qualitative basis, identifying comparison of the toxicity test results using an major constituents, potential constituents of ambient water sample taken upstream (i.e., concern (such as substances previously determined control) of an effluent discharge and 50 m to be CEPA “toxic”), group parameters,3 and downstream of the discharge can provide an predetermined sources of release. estimate of risk. Whenever possible, Tier 3 should
3 Group parameters are based on analytical-chemical techniques and determine specific elements or chemically defined groups of constituents in complex substances. Examples of group parameters are dissolved organic carbon (DOC) and Adsorbable Organic Halogen (AOX).
8-2 In pathways analysis, data needed to characterize contamination. Other factors that affect exposure, environmental releases for complex substances such as diet, mobility, and body size, should also include volumes, flow rates or quantities released, be considered when selecting assessment location of releases, receiving environment endpoint organisms. characteristics, temporal patterns of release, and other information on the life cycle of the complex 8.3 Entry Characterization substance released to the environment. Entry characterization identifies sources of release Once the substance and its release are sufficiently and quantifies the amounts released to the characterized, its environmental partitioning, fate, Canadian environment using a life cycle and geographic distribution should be determined. approach. To do this, data are needed on chemical monitoring of constituents and group parameters Sources can be identified by updating a obtained from field and laboratory studies substance’s life cycle and by identifying domestic involving chemical analysis (see Sections 8.4 and and transboundary sources of entry. A life cycle 8.5). Physical and chemical properties of approach may not be necessary for substances constituents and group parameters indicate with predetermined sources of release (e.g., air possible fate, transport, and composition of the emission from a specific smelter). Once the complex substance following release. Models can sources of release have been identified, entry also predict the environmental fate of complex characterization should focus on a quantitative substances. The behaviour of complex substances analysis of the release characteristics and on cannot necessarily be predicted based on the refining pathways analysis. behaviour of the individual constituents. Data on 8.4 Exposure Characterization physical and chemical properties, interactions between constituents, and interactions between Exposure characterization quantifies the constituents and the receiving environment are relationship between source inputs of a complex often unavailable. Such modelling approaches substance and its resulting geographic distribution may, therefore, be used only for a qualitative fate in space and time (spatial and temporal scale) assessment. and identifies and quantifies exposure for Understanding how constituents and group populations at risk. parameters in complex substances behave is For complex substances, measures of exposure essential in considering receptor sensitivity, include constituents and/or group parameters that identifying assessment and measurement determine the fate and spatial and temporal endpoints, and assembling a conceptual model. scales of the assessment. Such data are also used Examples of measurement endpoints that have in the effects and risk characterizations. been used in bioassays of complex substances (types 1–4) are presented in Table 8.1 of the Monitoring of major constituents and/or group resource document. parameters is the preferred approach to quantitatively determine the fate of the complex Organisms selected as the ecological component substance and the spatial and temporal scales of of assessment endpoints should be among those the assessment. Monitoring variables should most at risk because of high exposure to the include constituents and/or group parameters that complex substance. Potential for exposure should are potential causal agents of environmental be based, if possible, on the following factors: effects. When monitoring studies are unavailable, (i) knowledge about how the constituents are data may be obtained from field and laboratory- distributed in the environment, (ii) major routes of ambient toxicity tests involving chemical analysis. exposure for different types of organisms, and In the latter type of study, samples of media are (iii) the spatial and temporal distributions of taken from the receiving environment at various potentially exposed organisms in Canada. In distances from the point of release for chemical doing so, this will ensure that the organisms analysis and toxicity bioassays. Results from field selected are likely to have been present in the and laboratory-ambient toxicity tests can help areas of concern prior to the onset of 8-3 determine the potential for exposure at a given distance from the release point and can be used (3) laboratory-ambient toxicity tests, and directly in the effects and risk characterizations. (4) laboratory toxicity tests using whole- Models can be used to predict the environmental effluent or whole-mixture samples. fate of complex substances. The usefulness of their outputs is based on the same considerations Constituents of complex substances often partition noted previously. into different environmental compartments, such Exposure characterization should also focus on as soil, water, sediment, biota, and air, and refining/confirming the selection of assessment single-species tests are customarily conducted in endpoints. Factors to consider when assessing only one of these compartments. Field studies at potential for exposure are presented in Section the community and ecosystem levels generally 8.2. provide a more realistic assessment of effects (Vouk et al. 1987). Such studies are often 8.5 Effects and Risk unavailable, however, and other types of field Characterizations toxicity tests, including population-level studies and in situ bioassays, can be useful. The advantages Risk characterization determines whether complex of field toxicity tests, microcosm/mesocosm tests, substances are causing adverse effects on exposed laboratory-ambient toxicity tests, and whole- organisms. By chemically characterizing a effluent and whole-mixture tests are outlined in the complex substance in field toxicity testing, artificial resource document (Section 8.6). system testing, and laboratory-ambient toxicity In order to use such methods, assessors must tests, exposure and effects data can be used demonstrate that the observed effects are due to directly to conduct a risk characterization. Such the complex substance and not to substances methods minimize uncertainty of extrapolation. released from other sources. Assessors should The environmental assessment of complex always try to determine the constituents and group substances can have several complications, parameters responsible for environmental effects. including partitioning and persistence of Such data may not always be available using the constituents of complex substances after their above methods. Other methods that can identify release in the environment and additive versus and assess the potential adverse effects of interactive effects among constituents, such as constituents include: antagonistic or synergistic effects. The effects of • various effluent and mixture fractionation one constituent may influence the kinetics of methods (e.g., toxicity identification and uptake, metabolism, and excretion of other evaluation, or TIE), constituents. Because of these factors, complex substances may require different methods for • the individual substance method assessing ecological risks. – similar joint action or toxic unit (TU) The preferred methods for this phase of the approach assessment are presented below. These methods – independent joint action, are listed in decreasing order of preference. It is emphasized that the order is preferred for • the representative substance class method, assessing complex substances and should not be interpreted as the order in which data may need to • the WERF approach, and be generated when these are lacking: • the toxic equivalent factors (TEF) method. (1) field toxicity tests (e.g., in situ biological These methods are briefly presented in Section testing, community surveys), 8.5.6 of this manual. Additional information on these methods is described in Section 8.6.5 of the (2) artificial system tests: microcosm and resource document. mesocosm tests using spiking with complex substances, 8-4 8.5.1 Weight-of-Evidence Approach 8.5.2 Field Toxicity Tests
Although field toxicity tests, artificial system tests, The main difference in designing approaches to laboratory-ambient toxicity tests, and whole- assess the environmental risk of mixtures effluent and whole-mixture toxicity tests are useful compared with effluents is that effluents are usually methods to assess complex substances, assessors discharged to water systems, whereas mixtures can should, whenever possible, use a combination of be discharged to various environmental these methods to increase confidence in the risk compartments, including air, land, and water. assessment conclusions. Other methods (noted Therefore, the experimental design of the preferred above) can also be used in a weight-of-evidence methods will depend not only on the use, physical approach. Integrating or combining methods to and chemical properties, and ultimate fate of the assess adverse effects of complex substances has mixture, but also on the type of receiving been recommended elsewhere (U.S. EPA 1991; environmental compartment. Adriaanse et al. 1995; De Zwart 1995; Groot and Villars 1995; Tonkes et al. 1995; van Loon and Aquatic Ecosystems Hermens 1995). Factors to consider when evaluating the results of Methods for directly determining the effects of field tests are discussed in Section 8.7.1 of the complex substances on the structure and function resource document. of natural populations, communities, and The use of spatial and temporal controls is ecosystems are available but are not as necessary in the experimental design. The standardized as are the protocols for laboratory recommended field tests used to determine if a tests. A variety of methods and comprehensive complex substance is harmful to the environment frameworks are available to assess the impacts of are presented below: complex substances on the receiving environment. Examples are the Environmental Effects Monitoring • Spatial Controls Program and the Canadian Environmental Assessment Research Council (CEARC) approach – in situ toxicity studies using caged organ- (Peterson et al. 1987; Sonntag et al. 1987; isms located upstream (control) and CEARC 1988). These frameworks are not entirely downstream of the discharge. compatible with the assessment of priority substances under CEPA, but their underlying – upstream control locations and several concepts and methodologies should be downstream locations at different distances considered for complex substances. The sediment from the point source. If the measure of quality triad approach is an example of a effects increases at the point source and structured, integrative method of determining declines monotonically as distance from sediment contamination and assessing complex the point source increases, then there is substances in sediments (Chapman 1986, 1989). strong evidence that the effluent or mixture is causing an adverse effect. Integrated methods can be used at the population and community levels. The methods combine – surveys of community structure, population habitat quality and higher organizational level survival, or other biological endpoints indices. They can be used as part of a weight-of- upstream and at several sites downstream evidence determination, improving on decision- from the discharge. making and on the current understanding of higher-order ecological systems. An example is • Temporal Controls the Integrated Biotic Index (IBI), which can be used along with Habitat Suitability Indices as an – in situ toxicity studies (e.g., Before–After– ecological tool to evaluate biological conditions in Control–Impact, or BACI, design) using streams to which effluents are discharged (Karr caged organisms located upstream and 1981). The methods are described in Section 8.6 downstream of the discharge and con- and Appendix VII of the resource document. ducted before and after a process change (e.g., switching to discharges of nonchlorinated effluents). 8-5 – surveys of community structure, population When burning WCOs, emission particulates are survival, or other biological endpoints deposited on nearby soil and vegetation. Effects conducted before and after a process can be determined on a qualitative or quantitative change upstream and downstream of the basis using spatial and temporal controls. A discharge. qualitative assessment could involve observations on the colour and size of affected vegetation and The difference between complex substances comparison with those of background (control site) discharged to lentic systems (i.e., having vegetation. A quantitative analysis could involve a continuous water flow systems, such as rivers) and biological survey (e.g., species composition) of lotic systems (i.e., having little or no water flow, vegetation or invertebrates living in soil and such as lakes and harbours) is choosing a proper comparison of results with those of background control site for lotic systems (as there are no findings; in doing so, effects can be determined upstream sites) for both the in situ toxicity tests and when, for example, tolerant species have replaced community and population surveys. The control sensitive species. Another example of the use of sites must have characteristics — such as naturally spatial controls is to conduct in situ toxicity tests occurring biota, physical and chemical properties using caged organisms downwind of the emission of the sediments and water — similar to those of and comparing responses with those of a control the affected study sites. Table 8.1 Approaches and type of controls to conduct field toxicity studies of waste crankcase oils (WCOs).
Scenario Approach Control
Burning as fuel In situ tests using caged organisms Spatial and/or temporal in fields controls
Disposal to land In situ tests using vegetation and/or microorganisms
Terrestrial Ecosystems site. Choosing a control site for discharges or transportation of complex substances is likely to be As approaches used to determine the more difficult in terrestrial ecosystems than in environmental risks of mixtures are designed on a aquatic systems. To do this, analysis of wind case-by-case basis, examples using waste currents may be necessary. When there is no crankcase oils (WCOs) are presented below consistent wind current direction, a background or (Environment Canada and Health Canada 1994). control site should have physical, chemical, and During the WCO assessment, an attempt was biological characteristics similar to those of the made to follow its life cycle from the point of affected site. Examples of temporal controls using collection to ultimate disposal. Two scenarios the same scenario include (i) comparing in situ outline ways in which WCOs enter the Canadian toxicity results before and after a process change environment — burning and land disposal (Table (BACI method, see Section 8.6.3 of the resource 8.1). The examples are not meant to be an document) and (ii) comparing toxicity test results exhaustive list of approaches. Rather, they help using current levels of constituents in the vicinity of illustrate experimental design that can be used to the emission and background levels acquired assess the environmental risk of mixtures. Expert before the facility was constructed (BACI method). judgment must always be used when designing an Factors that can influence results in this scenario approach to assess a particular mixture. Factors are variability in emission rates and in composition to consider when evaluating the validity of the and wind currents. results of field tests are discussed in Section 8.7.1 of the resource document.
8-6 In the disposal to land scenario, temporal controls 8.5.4 Laboratory-Ambient Toxicity Testing can be used by conducting a biological survey of microorganisms or by monitoring functional Information on methods for measuring the acute aspects of the ecosystem before and after or chronic toxicity of effluents and receiving waters application of WCOs (BACI method). Spatial to freshwater or marine organisms is available controls can be used for volatile constituents and (Environment Canada 1990a, 1990b; Klemm et constituents transported by particulate matter to al. 1991; Lewis et al. 1991; Weber 1991; De nearby vegetation. In this scenario, an analysis of Zwart 1995). This information can be used when wind currents may also be necessary to determine evaluating the QA/QC of a study. Factors to an appropriate control site. Comparing species consider when evaluating the validity of results composition of the affected populations with that from laboratory-ambient tests are discussed in of the controls can determine if adverse effects Section 8.7.1 of the resource document. have occurred. Examples of adverse effects could Laboratory-ambient toxicity testing for effluents involve differences in growth or in reproduction involves taking samples of receiving water or between the populations of concern and the sediments upstream (controls) and at various controls. distances downstream of the point of discharge Whenever possible, uncertainties associated with and conducting laboratory toxicity tests on the each scenario should be quantified. samples. For mixtures, adverse effects can be determined by collecting air, soil, or water 8.5.3 Artificial System Tests (Mesocosms samples containing constituents of the mixture and Microcosms) from various sites near the release and conducting toxicity tests on the samples. Chemical analyses Artificial systems may be used for functional (e.g., extraction, fractionation) and laboratory (various rate processes) and structural (species toxicity tests on the elutriate fractions can further composition, richness, etc.) measurements and characterize the components of the complex simple toxicity test measurements (e.g., lethality). substance that is responsible for causing The systems can be used for assessing effects of environmental harm. Whenever possible, effluents and mixtures. Artificial system tests can uncertainties associated with determining risk to also contribute to the understanding of the effects the environment using these methods (e.g., of complex substances and constituent interactions variability in effluent or mixture composition and if chemical transformation and partition kinetics quantity, flow, and quality of the receiving water, are measured simultaneously with structural and leachate plumes, extrapolation from the functional responses of the system (Vouk et al. measurement to the assessment endpoint and to 1987). chronic exposure effects) should be quantified.
Artificial system tests are very useful when it can be Using the scenarios presented in Table 8.1, demonstrated that concentrations of harmful laboratory-ambient toxicity tests for complex constituents and group parameters measured in mixtures could involve the collection of particulates the test systems also exist in the field. In doing so, near facilities burning WCOs. Using these an estimation of risk can be determined. samples, deposition levels of WCO constituents It is recommended that these tests be verified for could be determined and applied to laboratory experimental QA/QC and for proper design in biota. In this example, deposition levels could be order for these to best reflect natural ecosystems. collected over a specified time period or per Refer to Section 6.2 of the guidance manual and volume of WCOs burned and applied to Section 6.2.2 of the resource document for vegetation living near the facility. Another additional information on mesocosm and possibility could involve the collection of microcosm tests. contaminated sediments from nearby streams where road runoff of WCOs has accumulated. Laboratory toxicity tests using these samples and local benthic invertebrates could determine the mixture’s potential adverse effects and risks and provide data on fate and exposure. 8-7 8.5.5 Laboratory Toxicity Testing Using 8.5.6 Other Methods Whole Effluent and Mixtures The following methods can be applied to both Whole-effluent or whole-mixture toxicity tests are effluents and mixtures. The methods discuss usually conducted in the laboratory and involve analytical identification and fractionation either short-term (acute) or long-term (chronic) procedures for complex substances and exposures. subsequent determination of fraction toxicities. Also discussed are methods that quantitatively Toxicity can be measured by using effluent characterize and communicate environmental risk samples obtained at the point of discharge and by at the population or community level. conducting toxicity tests on the samples. This approach can be used as a hyper conservative Fractionation procedures for a complex substance scenario to screen effluents for potential toxicity involve a separation of constituents that have (i.e., effects at 100% effluent concentration). If no similar physical and/or chemical properties. toxicity is observed, no adverse effects are These are referred to collectively as group expected to occur downstream of the discharge. parameters. Aqueous or organic solutions of When effects are observed, dilutions of the 100% organic constituents are separated into elutriates effluent can be used to estimate, for example, an using techniques such as high-performance liquid
LC50. The sources of uncertainty in this approach chromatography or ultrafiltration. These elutriates include the extrapolation from the measurement to contain defined groups of related constituents and the assessment endpoint and to chronic exposure can then undergo toxicological testing. Fractions effects. Whenever possible, these should be determined to cause adverse effects can be either quantified. Extrapolation to chronic exposure chemically analyzed to identify harmful effects may be unnecessary if the effluent constituents or further fractionated and tested to constituents or group parameters have a short more precisely identify harmful constituents. This half-life (e.g., total residual chlorine for method is often referred to as TIE. chlorinated wastewater effluents). When the chemistry and toxicology of the Characterizing risk involves linking the inherent constituents have been characterized, the toxicity of the effluent, as measured in the individual substance method can be used to laboratory, to concentrations in the environment calculate the total effect of the complex substance. and demonstrating that the assessment endpoint Consideration of the possible interactions between organisms are exposed or have the potential to be constituents and between their effects on the exposed to the effluent or its constituents. To do exposed organism is required. Constituent this, it must be demonstrated that concentrations interactions in complex substances can be of harmful constituents and group parameters determined by two types of noninteracting joint measured in the dilution samples also exist in the actions: (i) similar joint action or concentration field. addition, where constituents act independently to produce similar biological effects so that the In the case of mixtures, whole-mixture samples are concentration of one constituent can be expressed used directly in laboratory toxicity testing. in terms of another, and (ii) independent joint Examples include applying WCOs directly to the action, where constituents act on different organisms likely to be exposed (e.g., bird eggs), biological systems or affect the same biological feeding organisms diets containing WCOs, or system differently owing to different modes or sites applying WCOs to laboratory soil plots to observe of action (Mumtaz et al. 1994). With similar joint the response of organisms living in the soil. This action, the toxicity of a complex substance can be approach can be used as a worst-case scenario to determined by identifying constituents with similar determine potential adverse effects. If adverse modes of action and by calculating their joint effects are observed, assessors must demonstrate toxicity. To do so, the ratio of each constituent that the receptors of concern have the potential to concentration (EEV) and toxicity (ENEV) is be exposed to the whole mixture. Such data can calculated. Each ratio is termed the TU and can then be used in risk characterization. be summed. With independent joint action, the
8-8 model assumptions are that constituents have 8.6 References independent modes of action and the susceptibilities of organisms to different Adriaanse, M., H.A.G. Niederländer, and P.B.M. constituents are the same. By assuming no Stortelder. 1995. Monitoring water quality in combined effect, the toxicity is the highest TU the future. Vol. 1. Chemical monitoring. associated with the complex substance; the highest Institute for Inland Water Management and TU alone can be used to characterize the risk Waste Water Treatment (RIZA), Lelystad, The associated with exposure to the complex Netherlands. 100 pp. substance. CEARC (Canadian Environmental Assessment In the representative substance class method, a Research Council). 1988. The assessment of complex substance can be qualitatively analyzed cumulative effects: A research prospectus. Hull, and a representative constituent identified as being Quebec. of biological significance from each class of constituents. Toxicological testing is conducted Chapman, P.M. 1986. Sediment quality criteria with each representative constituent, and its effects from the sediment quality triad: An example. are assumed to represent the constituent class as a Environ. Toxicol. Chem. 5: 957–964. whole (Parkhurst 1986). Chapman, P.M. 1989. Current approaches to The WERF approach estimates community-level developing sediment quality criteria. Environ. risks based on the percentage of species (or Toxicol. Chem. 8: 589–599. genera) affected by acute or chronic chemical De Zwart, D. 1995. Monitoring water quality in exposures from multiple substance exposure the future. Vol. 3. Biomonitoring. The (Parkhurst et al. 1996). The approach assumes Netherlands National Institute of Public Health that two pieces of information are available. The and Environmental Protection (RIVM), Bilthoven, first is a distribution relating substance The Netherlands. concentration to the percentage of species (or genera) affected (i.e., concentration vs. Environment Canada. 1990a. Biological test percentage of species affected). The second piece method: Reference method for determining of information is a distribution of substance acute lethality of effluents to rainbow trout. EPS concentrations in the appropriate environmental 1/RM/13. Ottawa, Ontario. compartment. The two distributions are integrated algebraically to produce a joint probability Environment Canada. 1990b. Biological test function. The result of this analysis is a risk curve method: Reference method for determining showing the probabilities of effects of varying acute lethality of effluents to Daphnia magna. magnitudes (i.e., percentage of taxa affected). EPS 1/RM/14. Ottawa, Ontario. Such curves are an excellent quantitative means of Environment Canada and Health Canada. 1994. describing and communicating risks. Refer to Waste crankcase oils. Priority Substances List Section 6.3.2 of the guidance manual and Section Assessment Report PSL-36E. Ottawa, Ontario. 6.3.6 of the resource document for additional 39 pp. information on the WERF approach. Groot, S. and M.T. Villars. 1995. Monitoring Another method for interpreting interactions is the water quality in the future. Vol. 5. TEF method. Toxic equivalent factors make use of Organizational aspects. Delft Hydraulics, Delft, the dose addition and potentiation concept, where The Netherlands. constituent concentrations in a complex substance are simply added to each other (with an Karr, J.R. 1981. Assessment of biotic integrity appropriate potentiation factor) because they have using fish communities. Fisheries 6: 21–27. similar modes of action (U.S. EPA 1989). The approach can be used for dioxins and furans and other complex substances, such as PAHs and PCBs.
8-9 Klemm, D.J., G.E. Morrison, C.I. Weber, F. Fulk, Tonkes, M., C. van de Guchte, J. Botterweg, D. T.W. Neiheisel, P.A. Lewis, and J.M. Lazorchak. de Zwart, and M. Hof. 1995. Monitoring water 1991. Short-term methods for estimating the quality in the future. Vol. 4. Monitoring chronic toxicity of effluents and receiving waters strategies for complex mixtures. Research to marine and estuarine organisms. EPA/600/ Institute of Toxicology (RITOX), Utrecht, The 4-87/028. U.S. Environmental Protection Netherlands. 104 pp. Agency, Cincinnati, Ohio. 331 pp. U.S. EPA (United States Environmental Protection Lewis, P.A., D.J. Klemm, F. Fulk, C.I. Weber, Agency). 1986. Guidelines for the health risk W.H. Peltier, T.J. Norberg-King, T.W. Neiheisel, assessment of chemical mixtures. Fed. Regist. Q.H. Pickering, and J.M. Lazorchak. 1991. 51(185): 34014–34025. Short-term methods for estimating the chronic toxicity of effluents and receiving water to U.S. EPA (United States Environmental Protection freshwater organisms. EPA/600/4-89/001. Agency). 1988. Technical support document U.S. Environmental Protection Agency, on risk assessment of chemical mixtures. PB91- Cincinnati, Ohio. 207 pp. 103556. Environmental Criteria and Assessment Office, Office of Research and Mumtaz, M.M., C.T. DeRosa, and P.R. Durkin. Development, Cincinnati, Ohio. 1994. Approaches and challenges in risk assessments of chemical mixtures. In R.S.H. U.S. EPA (United States Environmental Protection Yang (ed.), Toxicology of chemical mixtures. Agency). 1989. Summary of ecological risk Academic Press, New York. pp. 565–597. assessment methods and risk management decisions in superfund and RCRA. EPA/230/03- Parkhurst, B.R. 1986. The role of fractionation in 89-048. Office of Planning and Evaluation, hazard assessments of complex materials. In Washington, D.C. H.L. Bergman, R.A. Kimerle, and A.W. Maki (eds.), Environmental hazard assessment of U.S. EPA (United States Environmental Protection effluents. Pergamon Press, Elmsford, New York. Agency). 1991. Technical support document pp. 92–106. for water quality-based toxics control. EPA/505/ 2-90-001. Office of Water, Washington, D.C. Parkhurst, B.R., W.J. Warren-Hicks, R.D. Cardwell, J. Volosin, T. Etchison, J.B. Butcher, van Loon, W.M.G.M. and J.L.M. Hermens. 1995. and S.M. Covington. 1996. Methodology for Monitoring water quality in the future. Vol. 2. aquatic ecological risk assessment. Contract Mixture toxicity parameters. AquaSense No. RP91-AER-1, Water Environmental Research Consultants, Amsterdam, The Netherlands, and Foundation, Alexandria, Virginia. Institute for Inland Water Management and Waste Water Treatment (RIZA), Lelystad, The Peterson, E.B., Y.-H. Chan, N.B. Peterson, G.A. Netherlands. 45 pp. Constable, R.B. Caton, C.S. Davis, R.R. Wallace, and Y.A. Yarronton. 1987. Vouk, V.B., G.C. Butler, A.C. Upton, D.V. Parke, Cumulative effects assessment in Canada: An and S.C. Asher (eds.). 1987. Methods for agenda for action and research. Canadian assessing the effects of mixtures of chemicals. Environmental Assessment Research Council, SCOPE 30, IPCS Joint Symposia 6, SGOMSEC Hull, Quebec. 3. John Wiley & Sons, Toronto, Ontario.
Sonntag, N.C., R.R. Everitt, L.P. Rattie, D.L. Weber, C.I. 1991. Methods for measuring the Colnett, C.P. Wolf, J.C. Truett, A.H.L. Dorcey, acute toxicity of effluents and receiving water to and C.S. Holling. 1987. Cumulative effects freshwater and marine organisms. EPA/600/4- assessment: A context for further research and 90/027. U.S. Environmental Protection Agency, development. Canadian Environmental Cincinnati, Ohio. 293 pp. Assessment Research Council, Hull, Quebec.
8-10 Vol. 139, No. 5 Vol. 139, no 5 Canada Gazette
Gazette du Canada
Part II Partie II
OTTAWA, WEDNESDAY, MARCH 9, 2005 OTTAWA, LE MERCREDI 9 MARS 2005
Statutory Instruments 2005 Textes réglementaires 2005 SOR/2005-38 to 47 and SI/2005-15 and 16 DORS/2005-38 à 47 et TR/2005-15 et 16 Pages 296 to 368 Pages 296 à 368
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2005-03-09 Canada Gazette Part II, Vol. 139, No. 5 Gazette du Canada Partie II, Vol. 139, no 5 SOR/DORS/2005-41
Registration Enregistrement SOR/2005-41 February 15, 2005 DORS/2005-41 Le 15 février 2005
CANADIAN ENVIRONMENTAL PROTECTION ACT, 1999 LOI CANADIENNE SUR LA PROTECTION DE L’ENVIRONNEMENT (1999)
Prohibition of Certain Toxic Substances Règlement sur certaines substances toxiques Regulations, 2005 interdites (2005)
P.C. 2005-187 February 15, 2005 C.P. 2005-187 Le 15 février 2005
Whereas, pursuant to subsection 332(1)a of the Canadian Envi- Attendu que, conformément au paragraphe 332(1)a de la Loi ronmental Protection Act, 1999b, the Minister of the Environment canadienne sur la protection de l’environnement (1999)b, le published in the Canada Gazette, Part I, on April 3, 2004, a copy ministre de l’Environnement a fait publier dans la Gazette du of the proposed Prohibition of Certain Toxic Substances Regula- Canada Partie I, le 3 avril 2004, sous le titre Règlement sur l’inter- tions, 2005 under the title Total, Partial or Conditional Prohibi- diction totale, partielle ou conditionnelle relative à certaines tion of Certain Toxic Substances Regulations, substantially in the substances toxiques, le projet de règlement intitulé Règlement sur annexed form, and persons were given an opportunity to file certaines substances toxiques interdites (2005), conforme en comments with respect to the proposed Regulations or to file a substance au texte ci-après, et que les intéressés ont ainsi eu la notice of objection requesting that a board of review be estab- possibilité de présenter leurs observations à cet égard ou un avis lished and stating the reasons for the objection; d’opposition motivé demandant la constitution d’une commission de révision; Whereas, pursuant to subsection 93(3) of that Act, the National Attendu que, conformément au paragraphe 93(3) de cette loi, le Advisory Committee has been given an opportunity to provide its comité consultatif national s’est vu accorder la possibilité de for- advice under section 6 of that Act; muler ses conseils dans le cadre de l’article 6 de celle-ci; And whereas, in the opinion of the Governor in Council, pur- Attendu que la gouverneure en conseil est d’avis que, aux ter- suant to subsection 93(4) of that Act, the proposed Regulations do mes du paragraphe 93(4) de cette loi, le projet de règlement ne not regulate an aspect of a substance that is regulated by or under vise pas un point déjà réglementé sous le régime d’une autre any other Act of Parliament in a manner that provides, in the loi fédérale de manière à offrir une protection suffisante pour opinion of the Governor in Council, sufficient protection to the l’environnement et la santé humaine, environment and human health; Therefore, Her Excellency the Governor General in Council, À ces causes, sur recommandation du ministre de l’Environ- pursuant to subsection 93(1) of the Canadian Environmental Pro- nement et du ministre de la Santé et en vertu du paragraphe 93(1) tection Act, 1999b, on the recommendation of the Minister of the de la Loi canadienne sur la protection de l’environne- Environment and the Minister of Health, hereby makes the an- ment (1999)b, Son Excellence la Gouverneure générale en conseil nexed Prohibition of Certain Toxic Substances Regulations, 2005. prend le Règlement sur certaines substances toxiques inter- dites (2005), ci-après.
PROHIBITION OF CERTAIN TOXIC RÈGLEMENT SUR CERTAINES SUBSTANCES SUBSTANCES REGULATIONS, 2005 TOXIQUES INTERDITES (2005)
APPLICATION APPLICATION 1. Subject to sections 2 and 3, these Regulations apply to sub- 1. Sous réserve des articles 2 et 3, le présent règlement stances that are both specified on the List of Toxic Substances in s’applique à l’égard des substances mentionnées aux annexes 1 Schedule 1 to the Canadian Environmental Protection Act, 1999 et 2, lesquelles substances sont inscrites sur la liste des substances and set out in either Schedule 1 or 2 to these Regulations, referred toxiques de l’annexe 1 de la Loi canadienne sur la protection de to in these Regulations as “toxic substances”. l’environnement (1999) et sont ci-après désignées « substances toxiques ».
EXCEPTIONS EXCEPTIONS 2. These Regulations do not apply to any toxic substance set 2. Le présent règlement ne s’applique pas à la substance toxi- out in either Schedule 1 or 2 that is que mentionnée aux annexes 1 ou 2 : (a) contained in a hazardous waste, hazardous recyclable mate- a) qui est contenue dans des déchets dangereux, des matières rial or non-hazardous waste to which Division 8 of Part 7 of the recyclables dangereuses ou des déchets non dangereux aux- Canadian Environmental Protection Act, 1999 applies; quels s’applique la section 8 de la partie 7 de la Loi canadienne sur la protection de l’environnement (1999);
——— ——— a S.C. 2004, c. 15, s. 31 a L.C. 2004, ch. 15, art. 31 b S.C. 1999, c. 33 b L.C. 1999, ch. 33
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(b) contained in a control product within the meaning of sec- b) qui est contenue dans un produit antiparasitaire au sens de tion 2 of the Pest Control Products Act; or l’article 2 de la Loi sur les produits antiparasitaires; (c) present as a contaminant in a chemical feedstock used in a c) qui est présente comme contaminant dans une matière pre- process from which there are no releases of the toxic substance mière chimique utilisée au cours d’un processus n’occasionnant and provided that the toxic substance is destroyed or com- aucun rejet de la substance toxique, pourvu que celle-ci soit dé- pletely converted in that process to a substance that is not a truite ou totalement convertie au cours de ce processus en une toxic substance set out in either Schedule 1 or 2. substance autre qu’une substance toxique mentionnée aux an- nexes 1 ou 2. 3. (1) These Regulations, except subsections (2), (3) and (4), do 3. (1) Le présent règlement, sauf les paragraphes (2) à (4), ne not apply to any toxic substance set out in either Schedule 1 or 2 s’applique pas à la substance toxique mentionnée aux annexes 1 or to any mixture or product containing any such toxic substance ou 2 ni au mélange ou au produit qui en contient, s’ils sont desti- that is for use nés à être utilisés : (a) in a laboratory for analysis; a) pour des analyses en laboratoire; (b) in scientific research; or b) pour la recherche scientifique; (c) as a laboratory analytical standard. c) en tant qu’étalon analytique de laboratoire. (2) Any person that intends to use a toxic substance, mixture or (2) La personne qui prévoit utiliser une substance toxique, un product referred to in subsection (1) for a use referred to in that mélange ou un produit visé au paragraphe (1) à l’une des fins subsection shall, if the quantity of the toxic substance will ex- visées à ce paragraphe doit, si la quantité de la substance toxique ceed 10 g in any calendar year, submit to the Minister, at least doit dépasser 10 g au cours d’une année civile, présenter au mi- 30 days before the day on which the person begins using the sub- nistre les renseignements prévus à l’annexe 3, au moins trente stance, mixture or product, the information set out in Schedule 3. jours avant le début de l’utilisation. (3) Any person that, at the time of coming into force of these (3) La personne qui, à la date d’entrée en vigueur du présent Regulations, is using a toxic substance, mixture or product re- règlement, utilise une substance toxique, un mélange ou un pro- ferred to in subsection (1) for a use referred to in that subsection duit visé au paragraphe (1) à l’une des fins visées à ce paragraphe shall, if the quantity of the toxic substance exceeded 10 g in the doit, si la quantité de la substance toxique utilisée au cours calendar year immediately preceding the coming into force of de l’année civile précédant cette date a dépassé 10 g, présenter these Regulations, submit to the Minister, within 60 days after the au ministre les renseignements prévus à l’annexe 3, dans les date of coming into force of these Regulations, the information soixante jours suivant cette date. set out in Schedule 3. (4) If, after the coming into force of these Regulations, a toxic (4) Si une substance toxique est ajoutée aux annexes 1 ou 2 substance is added to Schedule 1 or 2, any person that, at the time après l’entrée en vigueur du présent règlement, la personne qui, à of the coming into force of the Regulations adding the toxic sub- la date d’entrée en vigueur du règlement visant à ajouter la subs- stance, is using the toxic substance or a mixture or product con- tance, utilise la substance, ou un mélange ou produit qui en taining that toxic substance for a use referred to in subsection (1) contient, à l’une des fins visées au paragraphe (1) doit, si la quan- shall, if the quantity of the toxic substance exceeded 10 g in the tité de la substance toxique utilisée au cours de l’année civile calendar year immediately preceding the coming into force of the précédant la date d’entrée en vigueur de ce règlement a dépas- Regulations adding the toxic substance, submit to the Minister, sé 10 g, présenter au ministre les renseignements prévus à within 60 days after the date of coming into force of those Regu- l’annexe 3, dans les soixante jours suivant cette date. lations, the information set out in Schedule 3.
PROHIBITIONS INTERDICTIONS 4. Subject to section 6, no person shall manufacture, use, sell, 4. Sous réserve de l’article 6, il est interdit de fabriquer, offer for sale or import a toxic substance set out in Schedule 1 or d’utiliser, de vendre, de mettre en vente ou d’importer une subs- a mixture or product containing any such toxic substance unless tance toxique mentionnée à l’annexe 1, ou un mélange ou un pro- the substance is incidentally present. duit qui en contient, à moins que la substance toxique n’y soit présente fortuitement. 5. Subject to section 6, no person shall manufacture, use, sell, 5. Sous réserve de l’article 6, il est interdit de fabriquer, offer for sale or import d’utiliser, de vendre, de mettre en vente ou d’importer : (a) a toxic substance set out in column 1 of Part 1 of Sched- a) une substance toxique mentionnée à la colonne 1 de la par- ule 2 if it is present, incidentally or not, in a mixture or product tie 1 de l’annexe 2, si elle est présente — fortuitement ou non — set out in column 2 and if the concentration of the toxic sub- dans un mélange ou un produit mentionné à la colonne 2 et si stance in the mixture or product exceeds the limit set out in sa concentration dans ce mélange ou ce produit est supérieure à column 3; or celle prévue à la colonne 3; (b) a toxic substance set out in column 1 of Part 2 of Sched- b) une substance toxique mentionnée à la colonne 1 de la par- ule 2 or a mixture or product containing the toxic substance if tie 2 de l’annexe 2, ou un mélange ou un produit qui en the toxic substance, mixture or product is designed for uses contient — sauf si sa présence y est fortuite —, si la substance other than the uses set out in column 2 unless the substance is toxique, le mélange ou le produit n’est pas destiné à l’une des incidentally present. utilisations prévues à la colonne 2.
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PERMITS PERMIS 6. (1) Any person that, at the time of coming into force of these 6. (1) La personne qui, à la date d’entrée en vigueur du présent Regulations, is manufacturing, using, selling or offering for sale a règlement, fabrique, utilise, vend, met en vente ou importe une toxic substance referred to in either section 4 or 5 or a mixture or substance toxique visée aux articles 4 ou 5, ou un mélange ou un product containing such a substance or imports such a toxic sub- produit qui en contient, peut poursuivre son activité si elle y est stance, mixture or product may continue that activity if that per- autorisée en vertu d’un permis délivré aux termes du paragra- son has been issued a permit under subsection (4). phe (4). (2) In the case of a toxic substance added to Schedule 1 and re- (2) Dans le cas d’une substance toxique ajoutée à l’annexe 1 et ferred to in section 4, any person that, at the time of coming into qui est visée à l’article 4, la personne qui, à la date d’entrée en force of the Regulations adding the toxic substance, is carrying vigueur du règlement visant à ajouter la substance, exerce une out an activity referred to in subsection (1) requires a permit is- activité visée au paragraphe (1) doit, pour poursuivre son activité, sued under subsection (4) to continue that activity. This rule also obtenir un permis aux termes du paragraphe (4). La même règle applies to any such person in the case of a toxic substance added s’applique à une telle personne dans le cas d’une substance toxi- to Schedule 2 and referred to in section 5. que ajoutée à l’annexe 2 et qui est visée à l’article 5. (3) An application for a permit shall be submitted to the Minis- (3) La demande de permis est présentée au ministre et com- ter and contain the information set out in Schedule 4. porte les renseignements prévus à l’annexe 4. (4) Subject to subsection (5), the Minister shall issue the permit (4) Sous réserve du paragraphe (5), le ministre délivre le per- if the following conditions are met: mis si les conditions suivantes sont réunies : (a) there is no technically or economically feasible alternative a) il n’est techniquement ou économiquement pas viable pour or substitute available to the applicant, other than a substance le demandeur de substituer à la substance toxique une subs- regulated under these Regulations, for the toxic substance; tance qui n’est pas visée par le présent règlement; (b) the applicant has taken all necessary measures to minimize b) le demandeur a pris les mesures nécessaires pour éliminer ou or eliminate any harmful effect of the toxic substance on the atténuer les effets nocifs de la substance toxique sur l’environ- environment and human health; and nement et la santé humaine; (c) a plan has been prepared respecting the toxic substance, c) un plan a été dressé à l’égard de la substance toxique com- identifying the measures to be taken by the applicant so that the portant les mesures que le demandeur s’engage à prendre pour applicant’s continued activity will be in compliance with these que ses activités soient conformes au présent règlement et le Regulations, and the period within which the plan is to be fully délai prévu pour sa mise à exécution n’excède pas trois ans implemented does not exceed three years from the date on suivant la date à laquelle le permis est délivré pour la première which a permit is first issued to the applicant. fois. (5) The Minister shall refuse to issue a permit if the Minister (5) Le ministre refuse de délivrer un permis s’il a des motifs has reasonable grounds to believe that the applicant has provided raisonnables de croire que le demandeur a fourni des renseigne- false or misleading information in support of their application. ments faux ou trompeurs au soutien de sa demande. (6) A permit issued under this section expires 12 months after (6) Le permis expire douze mois après la date de sa délivrance the day on which it is issued and may, upon application, only be et peut, sur demande, être renouvelé au plus deux fois pour le renewed twice for the same purpose or use of the substance. même objet ou pour la même utilisation de la substance toxique. (7) The Minister shall revoke a permit if the conditions set out (7) Le ministre révoque le permis si les conditions prévues aux in paragraphs (4)(a) to (c) are no longer met or if the Minister has alinéas (4)a) à c) ne sont plus respectées ou s’il a des motifs rai- reasonable grounds to believe that the permit holder has provided sonnables de croire que le titulaire du permis lui a fourni des ren- false or misleading information to the Minister. seignements faux ou trompeurs. (8) The Minister shall not revoke a permit unless the Minister (8) Le ministre ne peut révoquer le permis qu’après : has provided the permit holder with a) avoir avisé par écrit le titulaire des motifs de la révocation; (a) written reasons for the revocation; and b) lui avoir donné la possibilité de présenter des observations (b) an opportunity to be heard, by written representation, in re- écrites au sujet de la révocation. spect of the revocation.
REPORTS RAPPORTS 7. Every person that manufactures or imports a toxic substance 7. La personne qui fabrique ou importe une substance toxique set out in column 1 of Part 3 of Schedule 2 or a mixture or prod- mentionnée à la colonne 1 de la partie 3 de l’annexe 2, ou un mé- uct containing, whether incidentally or not, any such toxic sub- lange ou un produit qui en contient — fortuitement ou non —, doit stance shall submit to the Minister the information set out in présenter au ministre les renseignements prévus à l’annexe 5 dans Schedule 5 within three months after the end of the calendar year les trois mois suivant la fin de l’année civile durant laquelle la during which the toxic substance, mixture or product was manu- substance toxique, le mélange ou le produit a été fabriqué ou im- factured or imported if, in that calendar year, porté si, au cours de cette année : (a) the quantity of the toxic substance was equal to or greater a) la quantité de la substance toxique était égale ou supérieure à than that set out in column 2 of that Part, if any; celle prévue à la colonne 2, le cas échéant; (b) the mixture or product contained the toxic substance in an b) la moyenne de concentration de la substance toxique dans le average concentration equal to or greater than that set out in mélange ou le produit était égale ou supérieure à celle prévue à column 3 of that Part, if any; or la colonne 3, le cas échéant;
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(c) the quantity of the toxic substance and its concentration in c) la quantité de la substance toxique et sa concentration dans the mixture or product were equal to or greater than those set le mélange ou le produit étaient toutes deux égales ou supérieu- out in column 4 of that Part, if any. res à celles prévues à la colonne 4, le cas échéant.
TESTING REQUIREMENTS DÉTERMINATION DES CONCENTRATIONS ET QUANTITÉS 8. Any concentration or quantity required to be determined un- 8. Pour l’application du présent règlement, la concentration et der these Regulations shall be determined, in accordance with la quantité sont déterminées, conformément aux exigences de generally accepted standards of scientific practice, by a laboratory pratiques scientifiques généralement reconnues, par un laboratoire that is accredited under the International Organization for Stan- qui est accrédité selon la norme de l’Organisation internationale dardization standard ISO/IEC 17025: 1999, entitled General re- de normalisation ISO/CEI 17025 : 1999, intitulée Prescriptions quirements for the competence of testing and calibration labora- générales concernant la compétence des laboratoires d’étalon- tories, as amended from time to time, or by a laboratory that nage et d’essais, avec ses modifications successives, ou par un meets an equivalent standard. laboratoire qui répond à une norme équivalente.
CERTIFICATION ATTESTATION 9. Any information required to be submitted to the Minister 9. Tout renseignement devant être fourni au ministre en appli- under these Regulations shall be submitted in a form determined cation du présent règlement est présenté en la forme fixée par lui by the Minister and accompanied by a certification, dated and et est accompagné d’une attestation, datée et signée par l’intéressé signed by the person referred to in those provisions, or the person ou par la personne autorisée à agir en son nom, portant que les authorized to act on their behalf, that the information is accurate renseignements sont complets et exacts. and complete.
RECORD KEEPING REGISTRES 10. (1) Every person that submits information to the Minister 10. (1) La personne qui présente au ministre des renseigne- under these Regulations shall keep a copy of that information, the ments en application du présent règlement en conserve copie dans certification and any documents supporting the information, in- un registre, avec l’attestation et les documents à l’appui, y com- cluding test data, if applicable, for a period of at least five years pris les données d’essai, s’il y a lieu, pendant au moins cinq ans à beginning on the date of the submission of the information. compter de la date de leur présentation. (2) The information, certification and supporting documents (2) Les renseignements, l’attestation et les documents à l’appui shall be kept at the person’s principal place of business in Canada sont conservés à l’établissement principal de la personne au or, on notification to the Minister, at any other place in Canada Canada ou en tout autre lieu au Canada dont le ministre a été avi- where the information, certification, documents and test data can sé et où ils peuvent être examinés. be inspected.
REPEAL ABROGATION 11. The Prohibition of Certain Toxic Substances Regulations, 11. Le Règlement sur certaines substances toxiques interdites 20031 are repealed. (2003)1 est abrogé.
COMING INTO FORCE ENTRÉE EN VIGUEUR 12. These Regulations come into force three months after 12. Le présent règlement entre en vigueur trois mois après the day on which they are registered. la date de son enregistrement.
SCHEDULE 1 ANNEXE 1 (Sections 1 to 4 and 6) (articles 1 à 4 et 6) PROHIBITED TOXIC SUBSTANCES SUBSTANCES TOXIQUES INTERDITES
Item Toxic Substances Article Substance toxique 1. Dodecachloropentacyclo [5.3.0.02,6.03,9.04,8] decane (Mirex) 1. Dodécachloropentacyclo [5.3.0.02,6.03,9.04,8] décane (mirex)
2. Polybrominated Biphenyls that have the molecular formula C12H(10-n)Brn 2. Les biphényles polybromés dont la formule moléculaire est C12H(10-n)Brn, in which “n” is greater than 2 où « n » est plus grand que 2
3. Polychlorinated Terphenyls that have the molecular formula C18H(14-n)Cln 3. Les triphényles polychlorés dont la formule moléculaire est C18H(14-n)Cln, in which “n” is greater than 2 où « n » est plus grand que 2
4. Bis(chloromethyl) ether that has the molecular formula C2H4Cl2O 4. Éther bis(chlorométhylique) dont la formule moléculaire est C2H4Cl2O
5. Chloromethyl methyl ether that has the molecular formula C2H5ClO 5. Oxyde de chlorométhyle et de méthyle dont la formule moléculaire est 6. (4-Chlorophenyl) cyclopropylmethanone, O-[(4-nitrophenyl)methyl] C2H5ClO oxime that has the molecular formula C17H15ClN2O3 6. Le (4-chlorophényle) cyclopropylméthanone, O-[(4- nitrophényle)méthyl]oxime dont la formule moléculaire est C17H15ClN2O3 ——— ——— 1 SOR/2003-99 1 DORS/2003-99
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SCHEDULE 1 — Continued ANNEXE 1 (suite) PROHIBITED TOXIC SUBSTANCES—Continued SUBSTANCES TOXIQUES INTERDITES (suite)
Item Toxic Substances Article Substance toxique
7. N-Nitrosodimethylamine, which has the molecular formula C2H6N2O 7. N-Nitrosodiméthylamine, dont la formule moléculaire est C2H6N2O
8. Hexachlorobutadiene, which has the molecular formula C4Cl6 8. Hexachlorobutadiène, dont la formule moléculaire est C4Cl6 9. Dichlorodiphenyltrichloroethane (DDT), which has the molecular 9. Dichlorodiphényltrichloroéthane (DDT), dont la formule moléculaire est formula C14H9Cl5 C14H9Cl5
SCHEDULE 2 ANNEXE 2 (Sections 1 to 3 and 5 to 7) (articles 1 à 3 et 5 à 7)
CONCENTRATION LIMITS, PERMITTED USES CONCENTRATIONS MAXIMALES, UTILISATIONS AND REPORTING THRESHOLDS PERMISES ET SEUILS POUR FINS DE RAPPORT
PART 1 PARTIE 1
CONCENTRATION LIMITS CONCENTRATIONS MAXIMALES
Column 1 Column 2 Column 3 Colonne 1 Colonne 2 Colonne 3
Concentration Concentration Mixture or Product Containing Limit of the Mélange ou produit contenant maximale de la Item Toxic Substance the Toxic Substance Toxic Substance Article Substance toxique la substance toxique substance toxique 1. Hexachlorobenzene (a) Trichloroethylene 20 ppb 1. Hexachlorobenzène a) Trichloroéthylène 20 ppb (b) Tetrachloroethylene 20 ppb b) tétrachloroéthylène 20 ppb (c) Tetrachloromethane 20 ppb c) tétrachlorométhane 20 ppb (d) Magnesium salt (by- 20 ppb d) sel de magnésium (sous- 20 ppb product from the magnesium produit de l’industrie du industry) magnésium) (e) Magnesium sludge (by- 20 ppb e) boue de magnésium 20 ppb product from the magnesium (sous-produit de l’industrie du industry) magnésium) (f) Hydrochloric acid 20 ppb f) acide chlorhydrique 20 ppb (by-product) (sous-produit) (g) Ferric chloride 20 ppb g) chlorure ferrique 20 ppb (h) Ferrous chloride 20 ppb h) chlorure ferreux 20 ppb
PART 2 PARTIE 2
PERMITTED USES UTILISATIONS PERMISES
Column 1 Column 2 Colonne 1 Colonne 2
Item Toxic Substances Permitted Uses Article Substance toxique Utilisations permises 1. Benzidine and benzidine (a) Staining for microscopic 1. La benzidine et le dichlorhydrate a) Coloration pour l’examen dihydrochloride, that have the examination, such as de benzidine, dont les formules microscopique, telle que la molecular formula C12H12N2 immunoperoxidase staining, moléculaires sont respectivement coloration immunoperoxydase, and C12H12N2·2HCl, respectively histochemical staining or C12H12N2 et C12H12N2·2HCl la coloration histochimique et cytochemical staining la coloration cytochimique (b) Reagent for detecting blood b) réactif pour détecter le sang in biological fluids dans les liquides biologiques (c) Niacin test to detect some c) test à la niacine pour détecter micro-organisms certains micro-organismes (d) Reagent for detecting d) réactif pour détecter l’hydrate chloralhydrate in biological de chloral dans les liquides fluids biologiques
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PART 3 PARTIE 3
REPORTING THRESHOLDS SEUILS POUR FINS DE RAPPORT
Column 1 Column 2 Column 3 Column 4 Colonne 1 Colonne 2 Colonne 3 Colonne 4
Annual Annual Quantity Moyenne de Quantité et moyenne Annual Average and Annual Average Quantité concentration de concentration Item Toxic Substance Quantity Concentration Concentration Article Substance toxique annuelle annuelle annuelles 1. Hexachlorobenzene 10 g and 10 ppb 1. Hexachlorobenzène 10 g et 10 ppb 2. Benzidine and 1 kg 2. La benzidine et le 1 kg benzidine dichlorhydrate de dihydrochloride, that benzidine, dont les have the molecular formules moléculaires formula C12H12N2 sont respectivement and C12H12N2·2HCl, C12H12N2 et respectively C H N ·2HCl 12 12 2
SCHEDULE 3 ANNEXE 3 (Subsections 3(2) to (4)) (paragraphes 3(2) à (4)) INFORMATION RELATED TO THE USE RENSEIGNEMENTS SUR L’UTILISATION DE OF CERTAIN TOXIC SUBSTANCES IN A CERTAINES SUBSTANCES TOXIQUES À DES LABORATORY FOR ANALYSIS, FOR FINS D’ANALYSE EN LABORATOIRE OU DE SCIENTIFIC RESEARCH OR AS A RECHERCHE SCIENTIFIQUE OU COMME LABORATORY ANALYTICAL STANDARD ÉTALON ANALYTIQUE DE LABORATOIRE 1. Information respecting the laboratory where a toxic sub- 1. Renseignements sur le laboratoire qui utilise ou utilisera la stance or a mixture or a product containing it will be or is being substance toxique ou le mélange ou produit qui en contient : used: a) nom, adresses municipale et postale, numéro de téléphone (a) the name, civic and postal addresses, e-mail address, if any, et, le cas échéant, numéro de télécopieur et adresse électroni- telephone number and fax number, if any, of the laboratory; que du laboratoire; and b) nom, titre, adresses municipale et postale, numéro de télé- (b) the name, title, civic and postal addresses, e-mail address, if phone et, le cas échéant, numéro de télécopieur et adresse élec- any, telephone number and fax number, if any, of the person tronique de la personne autorisée à agir au nom du laboratoire, authorized to act on behalf of the laboratory, if any. s’il y a lieu. 2. Information respecting each toxic substance set out in 2. Renseignements sur chacune des substances toxiques men- Schedule 1 or 2, and each mixture or product containing the toxic tionnées aux annexes 1 et 2 et sur chaque mélange ou produit qui substance: en contient : (a) the name of the toxic substance and the name of the mixture a) le nom de la substance toxique et, le cas échéant, le nom du or product containing the toxic substance, if applicable; mélange ou du produit qui en contient; (b) the anticipated period of its use; b) la période d’utilisation prévue; (c) the estimated quantity to be used in a calendar year and the c) la quantité que l’on prévoit utiliser au cours d’une année ci- unit of measurement; and vile ainsi que l’unité de mesure; (d) the identification of each proposed use and each actual use, d) une description de chaque utilisation réelle ou projetée, se- as the case may be. lon le cas.
SCHEDULE 4 ANNEXE 4 (Subsection 6(3)) (paragraphe 6(3)) INFORMATION TO BE CONTAINED IN AN RENSEIGNEMENTS À FOURNIR DANS APPLICATION FOR A PERMIT LA DEMANDE DE PERMIS 1. Information respecting the applicant: 1. Renseignements sur le demandeur : (a) their name, civic and postal addresses, e-mail address, if a) nom, adresses municipale et postale et numéro de téléphone any, telephone number and fax number, if any; and du demandeur et, le cas échéant, son numéro de télécopieur et (b) the name, title, civic and postal addresses, e-mail address, if son adresse électronique; any, telephone number and fax number, if any, of the person b) nom, titre, adresses municipale et postale, numéro de télé- authorized to act on behalf of the applicant, if any. phone et, le cas échéant, numéro de télécopieur et adresse élec- tronique de la personne autorisée à agir au nom du demandeur, s’il y a lieu.
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2. In the case of a toxic substance referred to in section 4 of 2. S’agissant d’une substance toxique visée à l’article 4 du pré- these Regulations or a mixture or product containing any such sent règlement, ou d’un mélange ou produit qui en contient, les toxic substance, the following information: renseignements suivants : (a) the name of each toxic substance and the name of each mix- a) le nom de la substance toxique et, le cas échéant, le nom du ture or product containing the toxic substance, if applicable; mélange ou du produit qui en contient; (b) the estimated quantity to be manufactured, used, sold, of- b) la quantité de substance toxique, de mélange ou de produit fered for sale or imported in a calendar year and the unit of que le demandeur prévoit fabriquer, utiliser, vendre, mettre en measurement; vente ou importer au cours d’une année civile, ainsi que l’unité (c) the identification of each proposed use, if known; and de mesure; (d) if the applicant is a manufacturer, seller or importer, the c) le détail de chaque utilisation projetée, si le demandeur dis- name, civic and postal addresses, e-mail address, if any, tele- pose de cette information; phone number and fax number, if any, of each person in d) si le demandeur est un fabricant, un vendeur ou un importa- Canada to whom the applicant intends to sell a toxic substance teur, les nom, adresses municipale et postale, numéro de télé- or a mixture or product containing such a toxic substance and phone et, le cas échéant, numéro de télécopieur et adresse élec- the identification of each toxic substance, mixture or product. tronique de chaque personne au Canada à qui il projette de vendre la substance toxique, le mélange ou le produit, ainsi que le nom de la substance, du mélange ou du produit en cause. 3. In the case of a toxic substance referred to in section 5 of 3. S’agissant d’une substance toxique visée à l’article 5 du pré- these Regulations or any mixture or product containing any such sent règlement, ou d’un mélange ou produit qui en contient, les toxic substance, the following information: renseignements suivants : (a) the name of the toxic substance and the name of the mixture a) le nom de la substance toxique et, le cas échéant, le nom du or product containing the toxic substance, if applicable; mélange ou du produit qui en contient; (b) in the case of a toxic substance set out in column 1 of Part 1 b) la concentration de la substance toxique dans le mélange ou of Schedule 2, the concentration of the toxic substance in the le produit, s’il s’agit d’une substance mentionnée à la colonne 1 mixture or product; de la partie 1 de l’annexe 2; (c) the estimated quantity to be manufactured, used, sold, of- c) la quantité de substance toxique, de mélange ou de produit fered for sale or imported in a calendar year and the unit of que le demandeur prévoit fabriquer, utiliser, vendre, mettre en measurement; vente ou importer au cours d’une année civile, ainsi que l’unité (d) the identification of each proposed use, if known; and de mesure; (e) if the applicant is a manufacturer, seller or importer, the d) le détail de chaque utilisation projetée, si le demandeur dis- name, civic and postal addresses, e-mail address, if any, tele- pose de cette information; phone number and fax number, if any, of each person in e) si le demandeur est un fabricant, un vendeur ou un importa- Canada to whom the applicant intends to sell a toxic substance teur, les nom, adresses municipale et postale, numéro de télé- or a mixture or product containing such a toxic substance and phone et, le cas échéant, numéro de télécopieur et adresse élec- the identification of each toxic substance, mixture or product. tronique de chaque personne au Canada à qui il projette de vendre la substance toxique, le mélange ou le produit, ainsi que le nom de la substance, du mélange ou du produit en cause. 4. Evidence that there is no technically or economically feasi- 4. Les renseignements qui établissent qu’il ne lui est techni- ble alternative or substitute available to the applicant, other than a quement ou économiquement pas viable de substituer à la subs- substance regulated under these Regulations, for the toxic sub- tance toxique une substance qui n’est pas visée par le présent stance. règlement. 5. Evidence that explains what measures have been taken to 5. Les renseignements qui établissent que les mesures ont été minimize or eliminate any harmful effect of the toxic substance prises pour éliminer ou atténuer les effets nocifs de la substance on the environment and human health. toxique sur l’environnement et la santé humaine. 6. A description of the plan prepared respecting the toxic sub- 6. Le détail du plan à l’égard de la substance toxique compor- stance identifying the measures to be taken so that the applicant’s tant les mesures à prendre pour que les activités du demandeur continued activity will be in compliance with these Regulations as soient conformes au présent règlement ainsi que le délai prévu well as the period within which the plan is to be implemented. pour sa mise à exécution.
SCHEDULE 5 ANNEXE 5 (Section 7) (article 7) INFORMATION RELATED TO THE MANUFACTURE RENSEIGNEMENTS SUR LA FABRICATION ET OR IMPORT OF TOXIC SUBSTANCES L’IMPORTATION DE SUBSTANCES TOXIQUES 1. Information respecting the manufacturer or importer: 1. Renseignements sur le fabricant ou l’importateur : (a) their name, civic and postal addresses of principal place of a) nom, adresses municipale et postale de l’établissement prin- business, e-mail address, if any, telephone number and fax cipal, numéro de téléphone et, le cas échéant, numéro de télé- number, if any; and copieur et adresse électronique du fabricant ou de l’importa- teur;
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(b) the name, title, civic and postal addresses, e-mail address, if b) nom, titre, adresses municipale et postale, numéro de télé- any, telephone number and fax number, if any, of the person phone et, le cas échéant, numéro de télécopieur et adresse élec- authorized to act on behalf of the manufacturer or importer, if tronique de la personne autorisée à agir au nom du fabricant ou any. de l’importateur, s’il y a lieu. 2. Information respecting each toxic substance set out in col- 2. Renseignements sur chacune des substances toxiques men- umn 1 of Part 3 of Schedule 2 and each mixture or product con- tionnées à la colonne 1 de la partie 3 de l’annexe 2 qui est fabri- taining the toxic substance manufactured or imported during a quée ou importée au cours de l’année civile et sur chaque mé- calendar year: lange ou produit qui en contient : (a) the name of the toxic substance and the name of the mixture a) le nom de la substance toxique et, le cas échéant, le nom du or the product containing the toxic substance, if applicable; mélange ou produit qui en contient; (b) the calendar year; b) l’année civile visée; (c) the total quantity manufactured, and the unit of measure- c) la quantité totale fabriquée, ainsi que l’unité de mesure; ment; d) la quantité totale importée, ainsi que l’unité de mesure; (d) the total quantity imported, and the unit of measurement; e) la quantité vendue au Canada, ainsi que l’unité de mesure; (e) the quantity sold in Canada, and the unit of measurement; f) le détail de l’utilisation projetée de la substance toxique et, le (f) the identification of each proposed use of the toxic sub- cas échéant, du mélange ou produit qui en contient; stance and the mixture or product containing the toxic sub- g) la moyenne de concentration annuelle, le cas échéant; stance, if applicable; h) la méthode analytique utilisée pour déterminer la concentra- (g) the annual average concentration, if applicable; tion de la substance toxique dans le mélange ou le produit, le (h) the analytical method used to determine the concentration cas échéant; of the toxic substance in the mixture or product, if applicable; i) la limite de détection de la méthode analytique utilisée pour and déterminer la concentration de la substance toxique dans le mé- (i) the analytical method detection limit used to determine the lange ou le produit, le cas échéant. concentration of the toxic substance in the mixture or product, if applicable. 3. The name, civic and postal addresses, e-mail address, if any, 3. Les nom, adresses municipale et postale, numéro de télé- telephone number and fax number, if any, of each person in phone et, le cas échéant, numéro de télécopieur et adresse élec- Canada to whom the manufacturer or importer sold a toxic sub- tronique de chaque personne au Canada à qui le fabricant ou stance set out in column 1 of Part 3 of Schedule 2 or a mixture or l’importateur a vendu une substance toxique mentionnée à la co- product containing such a toxic substance and the identification of lonne 1 de la partie 3 de l’annexe 2, ou un mélange ou un produit each toxic substance, mixture or product sold. qui en contenait, ainsi que le nom de la substance, du mélange ou du produit en cause. 4. The name, civic and postal addresses, e-mail address, if any, 4. Les nom, adresses municipale et postale, numéro de télé- telephone number and fax number, if any, of the laboratory that phone et, le cas échéant, numéro de télécopieur et adresse élec- determined the concentration of the toxic substance in the mixture tronique du laboratoire où la concentration de la substance toxi- or product, if applicable. que dans le mélange ou le produit a été déterminée, le cas échéant.
Published by the Queen’s Printer for Canada, 2005 Publié par l’Imprimeur de la Reine pour le Canada, 2005 323 2005-03-09 Canada Gazette Part II, Vol. 139, No. 5 Gazette du Canada Partie II, Vol. 139, no 5 SOR/DORS/2005-40
REGULATORY IMPACT RÉSUMÉ DE L’ÉTUDE D’IMPACT ANALYSIS STATEMENT DE LA RÉGLEMENTATION (This statement is not part of neither the Order nor the Regulations.) (Ce résumé ne fait pas partie ni du décret ni du règlement.) Description Description The Prohibition of Certain Toxic Substances Regulations, 2005 Le Règlement sur certaines substances toxiques interdites (hereafter referred to as the Regulations) are made pursuant (2005) (ci-après appelé le « règlement ») a été établi en vertu du
306 2005-03-09 Canada Gazette Part II, Vol. 139, No. 5 Gazette du Canada Partie II, Vol. 139, no 5 SOR/DORS/2005-40 to subsection 93(1) of the Canadian Environmental Protection paragraphe 93(1) de la Loi canadienne sur la protection de Act, 1999 (CEPA 1999). The Regulations repeal the Prohibition l’environnement (1999) [(LCPE (1999)]. Ce règlement abroge le of Certain Toxic Substances Regulations, 2003 (hereafter referred Règlement sur certaines substances toxiques interdites (2003) (ci- to as the 2003 Regulations). après appelé le « règlement 2003 »). The Regulations prohibit the manufacture, use, sale, offer for Le règlement interdit la fabrication, l’utilisation, la vente, la sale and import of the toxic substances listed in Schedules 1 and 2 mise en vente et l’importation des substances toxiques figurant to the Regulations. Schedule 1 lists prohibited toxic substances dans ses annexes 1 et 2. L’annexe 1 énumère les substances toxi- subject to total prohibition, with the exception of incidental pres- ques qui sont assujetties à une interdiction complète, à l’exception ence. Schedule 2 includes toxic substances that are subject to d’une présence fortuite. L’annexe 2 comprend les substances prohibitions related to concentration or use. The 2003 Regulations toxiques pour lesquelles l’interdiction est reliée à la concentration included only one schedule that subjected all listed toxic sub- ou l’utilisation de la substance. Le règlement 2003 comprenait stances to the same regulatory requirements. As such, the restruc- une seule annexe qui assujettissait toutes les substances toxiques tured Regulations facilitate more flexible management of the aux mêmes exigences réglementaires. Ainsi, la restructuration du scheduled toxic substances, by providing more targeted regula- règlement facilite la voie pour une gestion plus souple des subs- tory controls. They also facilitate the addition of new toxic sub- tances toxiques répertoriées en permettant des contrôles régle- stances to the two Schedules in the future. mentaires mieux ciblés. De plus, ce remaniement facilitera à l’avenir l’ajout de nouvelles substances toxiques aux deux an- nexes. In addition, the restructured Regulations: En outre, les modifications ont pour effet : • list hexachlorobutadiene (HCBD), N-nitrosodimethylamine • d’inscrire l’hexachlorobutadiène (HCBD), la N-nitro- (NDMA) and dichlorodiphenyltrichloroethane (DDT) in sodiméthylamine (NDMA) et le dichlorodiphényltrichloroé- Schedule 1; thane (DDT) à l’annexe 1 du règlement; • introduce new reporting and record-keeping requirements • d’introduire de nouvelles exigences en matière de soumission with respect to hexachlorobenzene (HCB), benzidine and ben- de rapports et de tenue de registres pour l’hexachloroben- zidine dihydrochloride; zène (HCB), la benzidine et le dihydrochlorate de benzidine; • introduce a notification requirement for the use of Schedule 1 • d’introduire une exigence de fournir un avis lorsqu’une subs- and 2 substances in a laboratory setting or for the purposes of tance énumérée à l’annexe 1 ou 2 est utilisée en laboratoire ou scientific research; pour des fins de recherche scientifique; • create a permit system for granting temporary exemptions to • de créer un régime de permis pour accorder des dérogations prohibitions, where it is identified that a transition period will temporaires aux interdictions lorsqu’une période de transition be required to find or implement alternatives to toxic sub- sera jugée nécessaire afin de trouver ou de mettre en œuvre stances; des solutions de rechange pour des substances toxiques; • more tightly associate the limit established for the incidental • d’associer plus étroitement la limite établie pour la présence presence of HCB to products or mixtures where its presence fortuite de HCB à des produits ou à des mélanges où sa pré- has been detected, and control decisions have been taken; sence a été détectée et des décisions ont été prises pour la • assist Canada in meeting its international obligations respect- contrôler; ing DDT under the Stockholm Convention on Persistent Or- • d’aider le Canada à respecter ses obligations internationales ganic Pollutants (POPs). relatives au DDT en vertu de la Convention de Stockholm sur les polluants organiques persistants. Prior to being listed on a Schedule of these Regulations, a Une condition préalable pour qu’une substance soit répertoriée substance must be added to the List of Toxic Substances dans l’annexe du règlement est son ajout à la Liste des substances under CEPA 1999. As such, an Order to add DDT to the List of toxiques de la LCPE (1999). Pour ce faire, un décret d’inscription Toxic Substances under CEPA 1999 is included with these Regu- du DDT à l’annexe 1 de la LCPE (1999) est inclus avec ce règle- lations. ment. The Regulations will come into force three months after the Le règlement entrera en vigueur trois mois après sa date day on which they are registered. The Order will come into force d’enregistrement. Quant au décret, il entrera en vigueur à la date the day on which it is registered. de son enregistrement. Addition of New Substances to the Regulations Ajout de nouvelles substances au règlement The addition of HCBD, NDMA, and DDT, currently not pre- L’ajout du HCBD, de la NDMA et du DDT, actuellement ab- sent in the Canadian marketplace, to the Prohibited Toxic Sub- sent du marché canadien, à la Liste de substances toxiques inter- stances List (Schedule 1) of the Regulations, is intended to pre- dites (annexe 1) du règlement préviendra la réintroduction de ces vent their re-introduction to the Canadian market. substances sur le marché canadien. Prior to being added to the Prohibited Toxic Substances List, a Avant son inscription à la liste de substances toxiques interdi- substance must be present in the List of Toxic Substances (Sched- tes, une substance doit être inscrite à la Liste des substances toxi- ule 1) of CEPA 1999. ques de l’annexe 1 de la LCPE (1999). HCBD was added to Schedule 1 of CEPA 1999 in July 2003. Le HCBD a été ajouté à l’annexe 1 de la LCPE (1999) en juil- The substance meets the criteria for persistence and bioaccumula- let 2003. Le HCBD remplit les critères de persistance et de bioac- tion, as established by the Persistence and Bioaccumulation cumulation comme cela est établi dans le Règlement sur la
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Regulations made under CEPA 1999. It is not naturally occurring, persistance et la bioaccumulation, en vertu de la LCPE (1999). Il and may be present in the environment only as a result of human n’existe pas de sources naturelles de cette substance dans activity. Therefore, the implementation of the virtual elimina- l’environnement et il peut être présent dans l’environnement sur- tion of HCBD was proposed pursuant to subsection 77(4) tout en raison de l’activité humaine. La quasi-élimination of CEPA 1999, in the publication of the summaries of the draft du HCBD a donc été proposée, en vertu du paragraphe 77(4) de and final Priority Substances Assessment Reports for HCBD. la LCPE (1999), dans la publication des résumés de l’ébauche et de la version finale des rapports d’évaluation des substances d’intérêt prioritaire pour le HCBD. An Order adding HCBD to the Virtual Elimination List Un décret visant à ajouter le HCBD à la liste de quasi- of CEPA 1999 was pre-published in the Canada Gazette, Part I élimination de la LCPE (1999) a été publié au préalable dans la for public comment, on August 16, 2003. Virtual elimination Gazette du Canada Partie I le 16 août 2003, pour commentaires. involves reducing releases of a substance below those levels that La quasi-élimination consiste à réduire les rejets d’une substance can be measured with routine but sensitive tests. To do so, it is à un niveau inférieur aux concentrations qui peuvent être mesu- necessary to prohibit the sale, manufacture, use, and import rées par des méthodes d’analyses courantes mais sensibles. Pour of HCBD. Not imposing such prohibitions on HCBD would un- ce faire, il est nécessaire que la vente, la fabrication, l’utilisation dermine the intent of virtual elimination. et l’importation du HCBD soient interdites. Ne pas imposer de telles interdictions sur le HCBD irait à l’encontre du but de la quasi-élimination. NDMA was added to Schedule 1 of CEPA 1999 in May 2003. La NDMA a été ajouté à l’annexe 1 de la LCPE (1999) en Although NDMA is not slated for virtual elimination, it is likely mai 2003. Bien que la NDMA ne soit pas désignée pour la quasi- carcinogenic to humans at low levels of exposure. élimination, elle est, selon toute probabilité, cancérogène pour les humains à des niveaux d’exposition relativement faibles. An Environment Canada review of the physical, chemical, and Au cours des années 1990, Environnement Canada a procédé toxicity properties of DDT was conducted in the 1990s. The min- à un examen des propriétés physiques, chimiques et toxiques isters of the Environment and Health used a summary of this re- du DDT. Le ministre de l’Environnement et le ministre de la San- view to justify a decision that DDT meets the criteria for man- té ont utilisé un résumé de cet examen pour décider que le DDT agement as a Track 11 substance under the federal Toxic Sub- remplit les critères pour être géré comme une substance de la stances Management Policy. Accordingly, an Order adding DDT voie 11 en vertu de la Politique sur la gestion des substances toxi- to Schedule 1 of CEPA 1999 was made with the Regulations. ques. Par conséquent, ce règlement comprend aussi un décret visant à ajouter le DDT à la Liste des substances toxiques de l’annexe 1 de la LCPE (1999). DDT was first registered as a pesticide in the 1940s, and al- C’est dans les années 1940 que le DDT a été enregistré pour la though it was never manufactured in Canada, it was widely used première fois comme un pesticide, et bien qu’il n’ait jamais été in pest control products until the 1960s. In response to increasing fabriqué au Canada, il a été largement utilisé dans les produits environmental and safety concerns, most uses of DDT in Canada antiparasitaires jusqu’aux années 1960. Pour donner suite aux were phased out by the mid-1970s. Registration of all uses préoccupations croissantes exprimées au sujet de l’environnement of DDT was discontinued in 1985, with the understanding that et de la sécurité, la plupart des utilisations canadiennes du DDT existing stocks would be sold, used or disposed of by Decem- ont été progressivement éliminées vers le milieu des années 1970. ber 31, 1990. The sale or use of DDT in Canada today constitutes L’enregistrement de toutes les utilisations du DDT a été supprimé a violation of the Pest Control Products Act. en 1985 à condition que les stocks existants soient vendus, utilisés ou éliminés au plus tard le 31 décembre 1990. Depuis lors, la vente ou l’utilisation du DDT au Canada constitue une infraction à la Loi sur les produits antiparasitaires. DDT is an internationally acknowledged POP that is covered Le DDT est un polluant organique persistant reconnu interna- by the Stockholm Convention on Persistent Organic Pollutants. tionalement qui est visé par la Convention de Stockholm sur les The Convention seeks to control, reduce, or eliminate discharges, polluants organiques persistants. Celle-ci vise essentiellement à emissions, and losses of POPs to the environment. The substance contrôler, à réduire ou à éliminer les rejets, les émissions et les is also subject to the Prior Informed Consent (PIC) procedure pertes de polluants organiques persistants dans l’environnement. under the Rotterdam Convention on the Prior Informed Consent Cette substance est aussi assujettie à la procédure de consente- Procedure for Certain Hazardous Chemicals and Pesticides in ment préalable en vertu de la Convention de Rotterdam sur la International Trade, which requires notification or the consent of procédure de consentement préalable en connaissance de cause the country of destination before the substance is exported from applicable dans le cas de certains produits chimiques et pesticides Canada. Due to its characteristics and effects, DDT has already dangereux qui font l’objet du commerce international. Cette been banned or severely restricted in several jurisdictions. convention exige l’avis ou le consentement du pays de destination avant que la substance soit exportée du Canada. En raison de ses caractéristiques et de ses effets, le DDT a déjà été interdit ou con- sidérablement restreint dans plusieurs compétences.
——— ——— 1 Track 1 substances are persistent, bioaccumulative, and result predominantly 1 Une substance de la voie 1 est persistante, bioaccumulative et sa présence dans from human activity. These substances are slated for virtual elimination from the l’environnement est due principalement à l’activité humaine. Ces substances sont environment. visées par la quasi-élimination de leur rejet dans l’environnement.
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The prohibition of DDT under the Regulations applies only to L’interdiction en vertu du règlement s’applique seulement à non-pesticidal uses, as the Pest Control Products Act continues to l’utilisation du DDT à des fins autres que la lutte antiparasitaire, regulate pesticidal uses. puisque la Loi sur les produits antiparasitaires continue à régle- menter l’utilisation de cette substance comme pesticide. New Reporting, Record-keeping, and Notification Requirements Nouvelles exigences en matière de soumission de rapports, de tenue de registres et d’avis New reporting and record-keeping requirements apply to ben- Les nouvelles exigences en matière de soumission de rapports zidine, benzidine dihydrochloride and hexachlorobenzene (HCB). et de tenue de registres s’appliquent à la benzidine, au dihydro- They are necessary to promote compliance and facilitate en- chlorate de benzidine ainsi qu’au HCB, et sont nécessaires pour forcement. In the case of HCB, these requirements will provide faciliter l’application du règlement et promouvoir la conformité à Environment Canada with information on the presence of HCB in ce dernier. En outre, ces exigences fourniront à Environnement products or mixtures used in the Canadian market, which is criti- Canada des données concernant l’utilisation du HCB sur le mar- cal to effectively implementing virtual elimination of this sub- ché, ce qui est essentiel à la mise en œuvre efficace de la quasi- stance. élimination de cette substance. With respect to benzidine and benzidine dihydrochloride, these Pour ce qui est de la benzidine et du dihydrochlorate de benzi- requirements will help Environment Canada monitor these sub- dine, les exigences en matière de soumission de rapports et de stances to ensure they are used for permitted uses only. Moreover, tenue de registres aideront Environnement Canada à surveiller ces it will ensure that the import, manufacture, and use of these sub- substances afin d’assurer qu’elles sont utilisées seulement aux stances are subject to strict life-cycle controls designed to pre- fins permises. De plus, cela assurera que leur importation, leur vent/minimize exposure to and/or the release of these substances fabrication et leur utilisation font l’objet de rigoureux contrôles into the environment. du cycle de vie afin de prévenir ou de réduire au minimum l’ex- position à ces substances et/ou leur rejet dans l’environnement. A quantity (e.g., concentration limit) trigger is now applied to Un seuil de déclenchement quantitatif pour fin de rapport (par all reporting and notification. This trigger limit will circumvent exemple, la limite de concentration) s’applique maintenant à tous having very small quantities notified or reported. les rapports soumis ainsi qu’aux avis. Ce seuil de déclenchement quantitatif permettra d’éviter la soumission de rapports ou de préavis pour de très faibles quantités à aviser ou à déclarer. The Regulations also specify a one-time notification require- Le règlement contient également une exigence de fournir un ment for all laboratory and scientific research users of scheduled avis unique lorsqu’une substance toxique interdite est utilisée en substances. This requirement will provide Environment Canada laboratoire ou pour des fins de recherche scientifique. Le règle- with data on the use of toxic substances for scientific research and ment permettra à Environnement Canada d’obtenir des données in laboratories. sur l’utilisation de substances toxiques en laboratoire et pour des fins de recherche scientifique. New Permit System Nouveau régime de permis The Regulations establish a permit system intended to provide Le règlement établit un régime de permis qui a pour but de a mechanism for temporarily exempting certain applications of a fournir un mécanisme permettant d’exempter temporairement prohibited substance. A permit may be granted only if the Minis- certaines applications d’une substance interdite. Un permis peut ter of the Environment is satisfied that there is no technically and être octroyé seulement si le ministre de l’Environnement juge economically feasible alternative or substitute available for the qu’il n’est pas techniquement ou économiquement viable prohibited substance. In addition, the Minister must be satisfied d’utiliser un produit de remplacement ou un substitut autre qu’une that measures have been taken to minimize or eliminate any substance toxique. De plus, le ministre doit s’assurer que des me- harmful effects of the toxic substance on the environment and sures ont aussi été prises afin d’éliminer ou de réduire au mini- human health. Finally, the applicant must provide an implementa- mum les effets nuisibles de la substance toxique sur l’environne- tion plan that identifies specific timelines for eliminating the toxic ment et la santé humaine. Enfin, le demandeur doit fournir un substance. Each permit lasts for 12 months, and can be renewed plan de mise en œuvre identifiant des délais précis pour only twice. This system is similar to the one used in the Ozone- l’élimination de la substance toxique en cause. La durée d’un depleting Substances Regulations, 1998. permis est de douze mois et il ne pourra être renouvelé que deux fois. Cette formule est semblable à celle utilisée dans le Règle- ment sur les substances appauvrissant la couche d’ozone (1998). This permit system will assist in achieving the prohibitions Ce régime de permis aidera à réaliser l’interdiction de certaines placed on toxic substances covered by the Regulations, while substances toxiques visées par le règlement tout en accordant à allowing industry time to identify and implement alternatives in a l’industrie le temps pour identifier et mettre en œuvre des solu- manner that is not excessively onerous or costly. tions de rechange qui ne sont pas excessivement onéreuses ou coûteuses.
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Alternatives Solutions envisagées Restructuring the Regulations Remaniement du règlement The restructuring of the 2003 Regulations was necessary to Le remaniement du règlement 2003 était nécessaire pour offrir provide greater flexibility in imposing prohibitions on the use, plus de flexibilité quant à l’imposition d’interdictions sur l’utilisa- sale, offer for sale, and import of toxic substances (e.g., ability to tion, la vente, la mise en vente et l’importation des substances impose partial bans). The restructuring simplifies the process of toxiques (p.ex., la capacité d’imposer des interdictions partielles) adding new substances to the Regulations. As these issues all et la simplification du processus de l’ajout de nouvelles substan- relate to the structure and language of the text itself, a regulatory ces au règlement. Puisque ces questions se rattachent toutes à la change was the only viable option. As such, the repeal and re- structure et à la terminologie du texte lui-même, un changement placement of the 2003 Regulations was considered to be the best réglementaire était la seule solution valable. Ainsi, la meilleure solution. solution consiste à abroger et à remplacer le règlement 2003. Addition of New Substances to the Regulations Ajout de nouvelles substances au règlement It was assessed that both HCBD and NDMA are toxic pursuant Le HCBD et la NDMA ont été évalués comme étant tous deux to CEPA 1999. Both substances pose risks either to the health or toxiques conformément à la LCPE (1999). Ces deux substances environment of Canadians. Currently, neither substance is used, posent de graves risques soit pour la santé des Canadiennes et des sold, produced, imported, or exported in Canada. The only way to Canadiens ou leur environnement. Actuellement, aucune de ces ensure that neither substance is introduced into the Canadian substances n’est utilisée, vendue, fabriquée, importée ou exportée market is through a ban, which can only be effected through these au Canada. L’unique moyen d’assurer que ces substances ne Regulations. soient pas introduites sur le marché canadien consiste à les inter- dire, ce que seul le règlement permet de faire. Furthermore, in the case of HCBD, the federal government has En outre, dans le cas du HCBD, le gouvernement a proposé que proposed that the substance be subject to virtual elimination pro- cette substance soit sujette aux dispositions de la quasi- visions of CEPA 1999. The prohibition on manufacture, use, sale, élimination sous la LCPE (1999). L’interdiction de fabrication, offer for sale, or import of the substance will work towards the d’utilisation, de vente, de mise en vente ou d’importation de cette objective of virtual elimination. substance œuvrera pour l’atteinte de l’objectif de la quasi- élimination. DDT is globally acknowledged to be a persistent organic pol- À l’échelle internationale, le DDT est reconnu comme un pol- lutant, and it is already the subject of severe restrictions in most luant organique persistant qui fait déjà l’objet d’importantes res- jurisdictions. The Pest Control Products Act bans pesticidal use trictions dans la plupart des juridictions. La Loi sur les produits of DDT, and these Regulations are the only manner in which a antiparasitaires interdit actuellement d’utiliser le DDT comme prohibition on industrial use of DDT can be implemented. pesticide, et le règlement est le seul moyen permettant d’interdire l’utilisation industrielle de cette substance. If prohibitions are not implemented through these Regulations, Si les interdictions ne sont pas mises en place à travers ce rè- these substances could be introduced to the Canadian marketplace glement, ces substances pourraient être introduites sur le marché as industrial chemicals. As Canadian industry does not currently canadien comme des produits chimiques industriels. Puisque trade in or deliberately use these substances, introduction of these l’industrie canadienne ne commercialise pas actuellement ces chemicals could represent an increase in risk to Canadians’ health substances ou ne les utilise pas délibérément, l’introduction de and environment, if these chemicals were released to the envi- ces produits chimiques représenterait une importante augmenta- ronment. Furthermore, in the case of HCBD and NDMA, such an tion du risque pour la santé des Canadiennes et des Canadiens introduction would undermine risk management measures aimed et pour leur environnement, si ces substances étaient rejetées at controlling domestic releases of these toxic substances. A regu- dans l’environnement. En outre, l’introduction du HCBD et de latory ban is the only way to ensure that these substances do not la NDMA sur le marché saperait les mesures de gestion des ris- enter the Canadian marketplace. ques visant à contrôler les rejets nationaux de ces substances toxiques. Une interdiction réglementaire est la seule façon d’assurer que ces substances ne soient pas réintroduites sur notre marché. Benefits and Costs Avantages et coûts Benefits Avantages HCBD and NDMA are included in Schedule 1 of CEPA 1999. Le HCBD et la NDMA sont répertoriés dans l’annexe 1 de Risk management strategies have been developed to manage the la LCPE (1999). Des stratégies concernant la gestion des risques risks associated with each substance. For these strategies to suc- pour chaque substance ont été élaborées afin de gérer les risques ceed, it is critical that these substances, which are not deliberately posés par ces substances. La réussite de ces stratégies assurerait used in Canada, do not enter widespread use which could increase que ces substances, qui ne sont pas utilisées délibérément au health and environmental risks to Canadians. The prohibitions in Canada, ne deviennent pas largement utilisées à l’avenir, ce qui the Regulations would fulfill that objective and maximize the augmenterait les risques pour la population canadienne. Les inter- benefits derived from risk management measures implemented by dictions du règlement permettraient d’atteindre cet objectif et de domestic industry. maximiser les avantages résultant des mesures de gestion des risques mises en œuvre par l’industrie nationale.
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Restructuring the 2003 Regulations to have greater variation in Le remaniement du règlement 2003, pour une plus grande va- the controls placed on individual substances allows for more riation des contrôles imposés sur chacune des substances, permet flexible management of toxic substances. In addition, the Regula- d’assouplir la gestion des substances toxiques et de faciliter tions facilitate the addition of new toxic substances in the future, l’ajout de nouvelles substances toxiques à l’avenir, ce qui réduira which will result in reduced costs to government. les coûts encourus par le gouvernement. Costs Coûts Given that the Regulations prohibit the manufacture, use, sale, Étant donné que le règlement interdit la fabrication, l’utilisa- offer for sale, and import of three additional substances that are tion, la vente, la mise en vente et l’importation de trois substances not currently manufactured, used, sold, offered for sale, or im- supplémentaires qui ne sont pas actuellement fabriquées, utilisées, ported, there should be no significant impact on industry and vendues, mises en vente ou importées, il ne devrait pas en résulter compliance costs are expected to be minimal. de conséquences importantes pour l’industrie. D’autre part, il est prévu que les coûts d’observation du règlement seront réduits au minimum. The annual reporting requirements for HCB, benzidine and Les exigences en matière de soumission de rapports annuels benzidine dihydrochloride, and the one-time notification require- du HCB, de la benzidine et du dihydrochlorate de benzidine et ment for laboratories and scientific research facilities, imply l’unique avis pour les utilisations en laboratoire et pour fins de minimal reporting and record-keeping costs. This is particularly recherche scientifique entraîneront des coûts minimums pour la true due to the new quantity trigger added for reporting. soumission de rapports et la tenue des registres. Ceci est particu- lièrement vrai dû au nouveau seuil de déclenchement quantitatif ajouté dans le cas de soumission de rapports. Incremental costs to government resulting from the Regu- Il est prévu que les coûts additionnels découlant de ce règle- lations, including administrative and enforcement costs, are ment pour le gouvernement, y compris les frais d’administration expected to be minimal. It is estimated that enforcement active- et les coûts d’application du règlement, seront réduits au mini- ties associated with the Regulations will require an annual budget mum. Les coûts de l’application du règlement, sont estimés à of $58,600. Inspections will verify, among other things, environ 58 600 dollars annuellement. Les inspections permettront that HCBD, NDMA, and DDT are not being imported or pro- de vérifier, entre autres, que le HCBD, la NDMA et le DDT ne duced and that reports submitted under the Regulations are true soient pas importés ou fabriqués et que les rapports soumis en and accurate. vertu du règlement soient vrais et exacts. The addition of the permit system to these Regulations will im- L’ajout du régime de permis au règlement entraînera des frais ply negligible administrative costs as the number of applications d’administration négligeables puisque le nombre de demandes is expected to be minimal (i.e. not more than one application per sera probablement minime, soit pas plus d’une demande par an- year per applicant). It is expected that the additional enforcement née par requérant. Il est prévu que les coûts additionnels d’appli- related to permits can be accommodated through existing re- cation du règlement reliés aux permis pourront être payés à même sources. les ressources existantes. On balance, it is expected that the benefits accruing from the Finalement, il est prévu que les avantages résultant des chan- regulatory changes will exceed the costs. gements réglementaires seront supérieurs aux coûts. Consultation Consultations Addition of HCBD Ajout du HCBD On December 9, 2002, a multi-stakeholder consultation was Le 9 décembre 2002, une consultation multilatérale a eu lieu à held, in Ottawa, to discuss a proposed management approach for Ottawa afin de discuter, d’une part, d’une proposition de mode de reducing and virtually eliminating releases of HCBD, and to dis- gestion visant à réduire et à quasi-éliminer les rejets de HCBD et, cuss analytical approaches for testing for HCBD contamination in d’autre part, des démarches analytiques à employer pour tester si various products. A second stakeholder consultation was also held divers produits sont contaminés par le HCBD. Une seconde con- in Ottawa, on September 29, 2003, to review and discuss the draft sultation a eu lieu à Ottawa le 29 septembre 2003 dans le but Regulations. In addition, all stakeholders were invited to provide d’examiner et de discuter de l’ébauche du règlement. En outre, written comments to Environment Canada by October 31, 2003. tous les intervenants ont été invités à formuler par écrit leurs commentaires à Environnement Canada au plus tard le 31 octo- bre 2003. Eleven written responses from industry, environmental non- Au cours de cette période, 11 réponses écrites provenant de governmental organizations (ENGOs) and government were re- l’industrie, d’organisations non gouvernementales environnemen- ceived during this period. The primary concern expressed by tales (ONGE) et du gouvernement ont été reçues. La principale stakeholders, throughout the consultation period, was related to préoccupation exprimée par les intervenants, durant la période de the proposed contamination limit for HCBD. Stakeholders asked consultation, avait trait à la limite de contamination proposée that the proposed contamination limit in the draft Regulations be pour le HCBD. Les intervenants ont demandé que la limite propo- recalculated. The ENGOs suggested that the proposed level was sée dans l’ébauche du règlement soit recalculée. Selon les ONGE, too high, while industry asked that some buffering be incorpo- cette limite était trop élevée, tandis que l’industrie a demandé rated in setting the concentration limit, because of naturally oc- d’incorporer un certain tamponnage dans la fixation de la limite curring fluctuations in industrial processes. de concentration en raison des fluctuations naturelles se produi- sant dans les procédés industriels.
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Some stakeholders also indicated that Environment Canada Certains intervenants ont aussi mentionné qu’Environnement should not unnecessarily burden commercial sectors where the Canada ne devrait pas imposer inutilement de fardeau aux sec- contamination level in products is very low and close to the teurs commerciaux lorsque le niveau de contamination dans les method detection limit, by requiring that these sectors monitor produits est très faible et près de la limite de détection de la mé- and report their level of contamination. thode, en exigeant que ces secteurs examinent et déclarent leur niveau de contamination. After a review of the risks, it was decided to remove the pro- Après une évaluation des risques, il a été décidé d’éliminer la posed contamination limit for HCBD from the draft Regulations. limite de contamination proposée pour le HCBD de l’ébauche du Instead, guidelines will be developed to complement these Regu- règlement. En revanche, des lignes directrices seront élaborées, en lations, where acceptable contamination levels of HCBD would complément au règlement, établissant des limites de contamina- be set. This approach would significantly reduce the administra- tions acceptables. Cette approche permettrait de réduire considé- tive burden of both industry and Environment Canada, without rablement le fardeau administratif imposé à la fois à l’industrie et compromising the environmental objective. à Environnement Canada sans pour autant compromettre l’objec- tif environnemental. A detailed review of public comments received during the con- Il est possible de prendre connaissance de tous les commen- sultation for the draft Regulations, and responses to these com- taires formulés par le public au cours de la consultation sur ments, as well as comments received for other consultations, may l’ébauche du règlement ainsi que des réponses à ces commentai- be obtained from Environment Canada’s National Office of Pol- res, de même que les commentaires reçus pour d’autres consulta- lution Prevention Web site at http://www.ec.gc.ca/NOPP/ tions, en visitant le site Internet du Bureau national de la préven- Consultations/en/consult.cfm. tion de la pollution d’Environnement Canada à l’adresse suivante : www.ec.gc.ca/NOPP/Consultations/FR/consult.cfm. Addition of NDMA Ajout de la NDMA Stakeholders were invited to review and provide written com- En octobre 2003, les intervenants ont été invités à examiner ments on the draft Regulations in October 2003. The following l’ébauche du projet de règlement et à formuler par écrit des com- documents were provided as additional sources of information, mentaires à ce sujet. Les documents suivants ont été envoyés par through a mail-out and Web site postings: a synopsis of the as- la poste et affichés sur le site Web dans le but de fournir des sour- sessment report for NDMA; and a fact sheet containing informa- ces supplémentaires d’information : un résumé du rapport tion regarding NDMA, its uses and potential exposure sources. d’évaluation de la NDMA et une fiche de renseignements conte- An electronic version of all consultation documents pertaining nant des informations sur la NDMA, ses utilisations et les sources to NDMA was posted on Environment Canada’s National Office possibles d’exposition à cette substance. Une version électronique of Pollution Prevention Web site at http://www.ec.gc.ca/NOPP/ de tous les documents de consultation se rapportant à la NDMA a Consultations/en/consult.cfm. été affichée sur le site Internet du Bureau national de la préven- tion de la pollution d’Environnement Canada, à www.ec.gc.ca/ NOPP/Consultations/FR/consult.cfm. One stakeholder questioned why NDMA, a substance identi- Un intervenant a demandé pourquoi il était proposé que fied for management through its life cycle, is added to the pro- la NDMA, une substance identifiée comme devant être gérée posed Regulations. NDMA is not currently used in commerce in durant tout son cycle de vie, soit ajoutée au règlement. Cette subs- Canada. Nevertheless, the addition of this substance to the Regu- tance n’est pas actuellement utilisée commercialement au Canada. lations will prevent its reintroduction in Canadian commerce. No Néanmoins, son ajout au règlement préviendra sa réintroduction other comments were received. dans le commerce canadien. Aucun autre commentaire n’a été reçu. Addition of DDT Ajout du DDT Stakeholders were invited to review and provide written com- En octobre 2003, les intervenants ont été invités à examiner ments on the draft Regulations in October 2003. A fact sheet con- l’ébauche du règlement et à formuler par écrit des observations à taining information related to DDT, its characteristics and poten- ce sujet. Une fiche de renseignements contenant des informations tial exposure sources, was provided as an additional source of sur le DDT, ses caractéristiques et les sources possibles information through a mail-out and Web site postings. An elec- d’exposition à cette substance a été envoyée par la poste et affi- tronic version of all consultation documents pertaining to DDT chée sur le site Web dans le but de fournir des sources supplé- was posted on Environment Canada’s National Office of Pollu- mentaires d’information. Une version électronique de tous les tion Prevention Web site at http://www.ec.gc.ca/NOPP/ documents de consultation se rapportant au DDT a été affichée Consultations/en/consult.cfm. sur le site Internet du Bureau national de la prévention de la pol- lution d’Environnement Canada à l’adresse suivante : www.ec. gc.ca/NOPP/Consultations/FR/consult.cfm. One stakeholder questioned whether some internationally rec- Un intervenant a demandé si certaines utilisations avantageuses ognized beneficial uses should be allowed in the draft Regula- reconnues internationalement ne devraient pas être permises dans tions. Under the Stockholm Convention on Persistent Organic l’ébauche du règlement. Conformément à la Convention de Pollutants, which Canada has ratified, continued use of DDT is Stockholm sur les polluants organiques persistants, ratifiée par allowed for vector control until safe, affordable and effective le Canada, l’utilisation continue du DDT est permise pour la alternatives are in place. These Regulations do not address the use lutte antivectorielle jusqu’à ce que des solutions de rechange
312 2005-03-09 Canada Gazette Part II, Vol. 139, No. 5 Gazette du Canada Partie II, Vol. 139, no 5 SOR/DORS/2005-40 of DDT if registered as a pesticide under the Pest Control Prod- sécuritaires, abordables et efficaces soient mises en place. ucts Act; therefore, an exemption is not necessary. The other Comme le règlement ne porte pas sur l’utilisation du DDT si cette comments received for DDT during the consultation period did substance est enregistrée comme pesticide en vertu de la Loi sur not result in changes to the text of the proposed Regulations. les produits antiparasitaires, une exemption n’est pas nécessaire. Les autres commentaires reçus au sujet du DDT, durant la période de consultation, n’ont pas occasionné de changements dans le texte du projet de règlement. Record-keeping and Reporting Requirements Exigences en matière de tenue de registres et de soumission de rapports Provisions for keeping records and reporting of certain infor- Des dispositions relatives à la tenue de registres et à la soumis- mation related to HCB, HCBD, benzidine and benzidine dihydro- sion de certains renseignements se rapportant à l’HCB, au HCBD, chloride were included in the proposed Regulations. Stakeholders à la benzidine et au dihydrochlorate de benzidine ont été incluses were invited to review and provide written comments on the draft dans le projet de règlement. En octobre 2003, les intervenants ont Regulations, in October 2003. An electronic version of all consul- été invités à examiner l’ébauche du règlement et à formuler tation documents pertaining to HCB, HCBD, benzidine and ben- par écrit des commentaires à ce sujet. Une version électronique zidine dihydrochloride was posted on Environment Canada’s de tous les documents de consultation se rapportant au HCB, National Office of Pollution Prevention Web site at http://www. au HCBD, à la benzidine et au dihydrochlorate de benzidine a été ec.gc.ca/NOPP/Consultations/en/consult.cfm. affichée sur le site Internet du Bureau national de prévention de la pollution d’Environnement Canada, à www.ec.gc.ca/NOPP/ Consultations/FR/consult.cfm. It was suggested that either National Pollutant Release Inven- Il a été proposé que soit l’Inventaire national des rejets de pol- tory or the draft Regulations be used for reporting purposes. Op- luants ou l’ébauche du règlement soit utilisé à des fins de soumis- posing views were expressed on whether a list of products for sion de rapports. Des opinions contradictoires ont été émises : si which reporting is required should be added in the draft Regula- une liste de produits exigeant une soumission de rapports devrait tions, or whether well-defined limits that trigger reporting re- être ajoutée dans l’ébauche du règlement ou si des limites bien quirements should be identified. A list of products or mixtures for définies déclenchant une déclaration obligatoire, devraient être which the contamination limit is required was added to Sched- établies. Pour régler cette question, une liste de produits ou mé- ule 2, Part 1 to address this issue. langes pour lesquelles une limite de concentration est requise, a été ajoutée à la partie 1 de l’annexe 2. CEPA 1999 National Advisory Committee Comité consultatif national de la LCPE Prior to pre-publication in the Canada Gazette, Part I, members Avant la publication dans la Gazette du Canada Partie I les of the CEPA National Advisory Committee were provided a for- membres du Comité consultatif national de la LCPE ont été offi- mal opportunity to advise on the draft Total, Partial or Condi- ciellement priés de donner leur avis sur l’ébauche du Règlement tional Prohibition of Certain Toxic Substances Regulations, as sur l’interdiction totale, partielle ou conditionnelle de certaines well as on the proposed addition of DDT to Schedule 1 of CEPA substances toxiques de même que sur l’ajout proposé du DDT à 1999. No objections were received, and comments were consid- l’annexe 1 de la LCPE (1999). Aucune objection n’a été reçue et ered during the drafting of the Regulations. les commentaires ont été pris en compte durant l’élaboration du règlement. Comments Following Pre-Publication in the Canada Gazette, Commentaires suivant la publication au préalable dans la Gazette Part I, on April 3, 2004 du Canada Partie I le 3 avril 2004 The Regulations were pre-published in the Canada Gazette, Le règlement a été publié au préalable dans la Gazette du Part I, under the title Total, Partial or Conditional Prohibition of Canada Partie I sous le titre Règlement sur l’interdiction totale, Certain Toxic Substances Regulations. During the 60-day com- partielle ou conditionnelle de certaines substances toxiques. Pen- ment period, a total of eleven representations were submitted dant la période de commentaires de 60 jours, un total de 11 repré- from stakeholders. The majority of comments received were of sentations a été soumis par les intervenants. La plupart de ces either a technical or administrative nature. commentaires étaient soit de nature technique ou soit de nature administrative. Nine submissions came from private industry, including one Neuf des soumissions provenaient du secteur privé, incluant industry association and five laboratories. Laboratories recom- une association industrielle et cinq laboratoires. Les laboratoires mended the addition of a quantity trigger reporting standard. In ont recommandé l’ajout d’un seuil de déclenchement quantitatif addition, the regulated community recommended the addition of pour la soumission des rapports. De plus, la communauté régle- quantity triggers for the reporting of HCB, benzidine, and ben- mentée a recommandé l’ajout d’un seuil de déclenchement quan- zidine dihydrochloride. After a review of these proposals, quan- titatif pour la soumission de rapports pour le HCB, la benzidine et tity triggers were added to the reporting requirements for labora- le dihydrochlorate de benzidine. À la suite de la révision de ces tories, as well as manufacturers and importers of the two toxic recommandations, des seuils de déclenchement quantitatif ont été substances in Schedule 2, Part 3. ajoutés aux exigences de soumission de rapports pour les labora- toires ainsi que pour les fabricants et les importateurs des deux substances toxiques énumérées dans l’annexe 2, partie 3.
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Private industry also recommended that Environment Canada Le secteur privé a également recommandé qu’Environnement consider exempting destructive or consumptive uses of toxic sub- Canada considère exempter les usages destructeurs et non ration- stances where there is no to minimal risk. After a review of the nels des substances toxiques où le risque est nul à minime. Après risks, an exemption has been added for non-emissive and destruc- un examen des risques, une exemption a été ajoutée lors de tive chemical feedstock uses, where the toxic substance is de- l’utilisation d’une matière première chimique qui contient la subs- stroyed or completely converted to another substance. tance toxique en tant que contaminant. Cette exemption s’appli- que au cours d’un processus n’occasionnant aucun rejet de la substance toxique, pourvu que celle-ci soit détruite ou totalement convertie au cours de ce processus en une autre substance. Concern was expressed that fertilizers being potentially con- Des préoccupations ont été exprimées à l’effet que certains en- taminated with a toxic substance will not be regulated for toxic grais pouvaient être potentiellement contaminés par une substance contaminants to the same degree as other products or mixtures, toxique. Dans ce cas, la substance toxique ne serait pas réglemen- including those regulated under other enforced Acts that will be tée au même degré qu’une substance toxique contenue dans tout subjected to these Regulations. Hence, the exemption for fertiliz- autre produit ou mélange, incluant celles réglementées par ers within the meaning of section 2 of the Fertilizers Act has been d’autres lois en vigueur qui seront assujetties à ce règlement. removed. D’où le retrait de l’exemption pour les engrais au sens de l’arti- cle 2 de la Loi sur les engrais. A detailed review of public comments received during the con- Il est possible de prendre connaissance de tous les commentai- sultation period for the proposed Regulations, and responses to res formulés par le public au cours de la période de commentaires these comments, as well as comments received for other consulta- pour le projet de règlement ainsi que les réponses à ces commen- tions, may be obtained from Environment Canada’s National taires, de même que les commentaires reçus pour d’autres consul- Office of Pollution Prevention Web site at http://www.ec.gc.ca/ tations, en visitant le site Internet du Bureau national de la pré- NOPP. vention de la pollution d’Environnement Canada à l’adresse suivante : www.ec.gc.ca/NOPP/Consultations/FR/consult.cfm. Compliance and Enforcement Respect et exécution As the Regulations will be promulgated under CEPA 1999, en- Puisque le règlement sera promulgué en vertu de forcement officers will, when verifying compliance with the la LCPE (1999), les agents de l’autorité appliqueront, lors de la Regulations, apply the Compliance and Enforcement Policy im- vérification de la conformité aux règlements, la Politique plemented under that Act. The Policy outlines measures designed d’observation et d’application mise en œuvre en vertu de cette loi. to promote compliance, including education, information, pro- La Politique indique les mesures à prendre pour promouvoir la moting of technology development and consultation on the devel- conformité, ce qui comprend l’éducation, l’information, la pro- opment of the Regulations. It also sets out the range of possible motion du développement de la technologie et la consultation sur responses to alleged violations: warnings, directions, environ- l’élaboration des règlements. La Politique décrit aussi toute une mental protection compliance orders, ticketing, ministerial orders, gamme de mesures à prendre en cas de violations alléguées : injunctions, prosecution, and environmental protection alternative avertissements, ordres en cas de rejet, ordres d’exécution en ma- measures (which are an alternative to a court trial after the laying tière de protection de l’environnement, contraventions, ordres of charges for a violation under the Act). In addition, the Policy ministériels, injonctions, poursuites pénales et mesures de re- explains when Environment Canada will resort to civil suits by change en matière de protection de l’environnement (qui peuvent the Crown for cost recovery. remplacer une poursuite pénale, une fois que des accusations ont été portées pour une infraction présumée à la Loi). De plus, la Politique explique quand Environnement Canada aura recours à des poursuites civiles intentées par la Couronne pour recouvrer ses frais. When, following an inspection or an investigation, an enforce- Lorsque, à la suite d’une inspection ou d’une enquête, un agent ment officer discovers an alleged violation, the officer will de l’autorité arrive à la conclusion qu’il y a eu violation alléguée, choose the appropriate enforcement action based on the following l’agent se basera sur les critères suivants pour décider de la me- criteria: sure à prendre : • Nature of the alleged violation: This includes consideration of • La nature de la violation alléguée : Il convient notamment de the seriousness of the harm or potential harm to the environ- déterminer la gravité des dommages réels ou potentiels causés ment, the intent of the alleged violator, whether it is a repeat à l’environnement, s’il y a eu action délibérée de la part du violation, and whether an attempt has been made to conceal contrevenant, s’il s’agit d’une récidive et s’il y a eu tentative information or otherwise subvert the objectives and require- de dissimuler de l’information ou de contourner, d’une façon ments of the Act. ou d’une autre, les objectifs ou exigences de la Loi. • Effectiveness in achieving the desired result with the alleged • L’efficacité du moyen employé pour obliger le contrevenant à violator: The desired result is compliance with the Act within obtempérer : Le but visé est de faire respecter la Loi dans les the shortest possible time and with no further repetition of the meilleurs délais tout en empêchant les récidives. Les facteurs violation. Factors to be considered include the violator’s his- à être considérés sont entre autres le dossier du contrevenant tory of compliance with the Act, willingness to co-operate pour l’observation de la Loi, sa volonté de coopérer avec les with enforcement officers, and evidence of corrective action agents de l’autorité et la preuve que des mesures correctives already taken. ont été apportées.
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• Consistency in enforcement: Enforcement officers will con- • La cohérence dans l’application : Les agents de l’autorité sider how similar situations have been handled in determining tiendront compte de ce qui a été fait dans des cas semblables the measures to be taken to enforce the Act. pour décider de la mesure à prendre pour appliquer la Loi. Contacts Personnes-ressources Josée Trudel Josée Trudel Head Chef Toxics Control Section Section du contrôle des substances toxiques Chemical Controls Branch Direction du contrôle des produits chimiques Environment Canada Environnement Canada Gatineau, Quebec Gatineau (Québec) K1A 0H3 K1A 0H3 Telephone: (819) 953-6118 Téléphone : (819) 953-6118 E-mail: [email protected] Courriel : [email protected] Céline Labossière Céline Labossière Policy Manager Gestionnaire des politiques Regulatory and Economic Analysis Direction des analyses réglementaires et économiques Economic and Regulatory Affairs Directorate Direction générale des affaires économiques et réglementaire Environment Canada Environnement Canada Gatineau, Quebec Gatineau (Québec) K1A 0H3 K1A 0H3 Telephone: (819) 997-2377 Téléphone : (819) 997-2377 E-mail: [email protected] Courriel : [email protected]
Published by the Queen’s Printer for Canada, 2005 Publié par l’Imprimeur de la Reine pour le Canada, 2005 315