SP1002 Appendix 4

SP1002 Appendix 4

Objective 4: Quantification of other sources of exposure to the case study contaminants

1. Introduction 2. Benzene 3. Benzo[a]pyrene 4. Arsenic 5. Cadmium 6. Conclusions 7. References

1. Introduction Arsenic, benzene, benzo[a]pyrene and cadmium were used as case studies during work for Objective 2 to characterise uncertainties in assessment of risk from . Information on sources of exposure to contaminants other than from contaminated land provides important context for the assessment of potentially contaminated land. The Environment Agency of England and Wales have recently reviewed background intakes of benzene, arsenic, and cadmium (Environment Agency 2009a;b;c), drawing on previous work by the Health Protection Agency and for the UK Total Dietary Study (TDS; this study has been undertaken in the UK since the mid-1970s; data have been used to estimate dietary exposure to various contaminants and how exposures have changed over time). Review of these various documents found general agreement on magnitude of exposure from other sources and these three contaminants are only briefly reviewed within the current document. Benzo[a]pyrene has not been reviewed by the Environment Agency to date and is thus considered in more detail within the current review. The case studies presented under Objective 2 use measurements for contaminant concentrations in . To create a standardised comparison point, the case studies were re-run within the CLEA model for calculating exposure from contaminated land, but with contaminant concentrations in re-set to the (SGV) for the respective scenario. In those instances that a SGV is not available for the scenario, a scenario-specific concentration was back-calculated from the respective Health Criteria Value and this is described in the text. Table 4.1 summarises the receptor characteristics and exposure calculations with soil concentration set to the SGV.

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Table 4.1. Details of calculations of exposure to the four case-study contaminants when soil concentration is set to the respective SGV. These data are used for comparison with other sources of exposure.

Scenario1 Age groups Receptor Soil guideline Exposure estimate for SGV (years) weights value level (kg) (mg/kg DW) (μg/kg BW/day) (μg/day) CS1a: Benzene 0-1, 1-2, 2-3, 3- 5.6, 9.8, 12.7, 0.33 1.67 22.2 in residential 4, 4-5, and 5-6 15.1, 16.9, and 19.7 CS1b: Benzene 16-65 83.2 95 0.87 72.4 in commercial CS2: 1-2, 2-3, 3-4, 9.8, 12.7, 15.1, 2.082 0.0172 0.255 Benzo[a]pyrene 4-5, and 5-6 16.9, and 19.7 in allotments CS3: Arsenic in 16-65, 16-70 83.2 and 82.7 11802 0.29 24.1 public space CS4: Cadmium 1-2, 2-3, and 3- 9.8, 12.7 and 10 0.083 1.04 in residential 4 15.1 1 CS = case study 2 No SGV available; value derived via back-calculation from health criteria value

2. Benzene

Vehicular emissions accounted for 60% of total emissions in the UK in 1990, but the reduction of benzene content in engine fuels and compulsory introduction of catalytic convertors has greatly reduced this emission source (HPA, 2007). Vehicular emissions were 20% of UK total emissions in 2004, whereas domestic sources from fuel combustion for cooking and heating and operation of garden appliances such as lawn mowers and patio heaters contributed the largest proportion (33%; HPA, 2007). Benzene exposure from different sources and routes has been estimated by IEH (1999). The predominant route of exposure is inhalation, with exposure to road traffic and smoking giving the largest exposures (Figure 4.1). Indoor air concentrations are generally larger than those outdoor, generally by a factor of about 2 to 2.5. Factors implicated in this finding are indoor sources of benzene (e.g. smoking), lower levels of ventilation (particularly during winter) and the presence of an attached garage which greatly increases concentrations in household air. Dietary exposure to benzene and that from drinking water are minor components (<2% of the total).

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Figure 4.1. Indicative concentrations of benzene in ambient air (source: HPA, 2007); S = smoker, NS = non-smoker.

The Environment Agency (2009a) used the analysis of IEH (1999) as a basis in calculating background intakes of benzene that were estimated assuming 50% adsorption of inhaled benzene. Table 4.2 compares environmental exposures to benzene (i.e. those unrelated to contaminated land) with those calculated for a child aged 0-6 exposed via residence on potentially contaminated land (case study 1a) and for an adult worker exposed in a contaminated commercial setting; in both cases, the concentration of benzene has been reset to the respective SGV. Table 4.2 shows that the exposure of the child to benzene from potentially contaminated land is smaller than background exposure via air in a rural setting. The exposure to the commercial worker is equivalent to background exposure via air in a rural setting and smaller than background exposure via air in an urban environment.

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Table 4.2. Comparison between environmental exposure to benzene in the general population and potential exposure from contaminated land (values are intake for an adult; occupational exposures excluded). Source: IEH (1999).

Source Mean daily intake (ng/person) Dietary intake 1.5 Drinking water <0.2 Air in a rural environment 73 (adult) 29 (child 1-10yr) 15 (infant 0-1yr)

Air in an urban environment 95 (adult) 38 (child 1-10yr) 20 (infant 0-1yr) Smoking (20 cigarettes/day) 400 Passive smoking (sharing room with smokers for 27 (adult) 11 (child 1-10yr) 6 (infant 0-1yr) 5 hours per day) Exposure to a resident (female child aged 0-6) 22 calculated using CLEA default parameters and with benzene concentration set to the respective SGV (case study 1a) Exposure to a commercial worker calculated 72 using CLEA default parameters and with benzene concentration set to the respective SGV (case study 1b)

3. Benzo[a]pyrene Benzo[a]pyrene (BaP) is a product of incomplete combustion of fossil fuels and plant matter such as wood. As such, it occurs very widely within the environment and has been identified in ambient air, drinking water and foodstuffs. Primary sources of non-occupational exposure to BaP are outdoor air, indoor air, contaminated food, drinking water and smoking. Estimates for exposure via each of these routes are discussed below. The main emission sources causing contamination of ambient outdoor air are industrial plants and production processes, domestic combustion of coal, oil and wood and traffic emissions (Vincent et al., 2007). Data presented by Vincent et al. (2007) show a ca. 80% reduction in the UK’s emissions of BaP over the last 15 years and a proportionate decrease in ambient air concentrations (Figure 4.2). Most studies of intake from ambient air date back to the 1990s, so are likely to over-estimate current intakes; a range of European and USA studies give an estimate of between 4.0 and 43.5 ng d-1 (WHO, 1998). Vincent et al. (2007) estimate that the number of people in the UK exposed to ambient air with BaP concentration ≥0.25 ng m-3 threshold from the National Air Quality Strategy has decreased from 2.4 million to 1.0 million between studies undertaken in 2006 and 2007. However, they estimate that future decreases in this number will be smaller (estimated 0.88 million by 2010).

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Figure 4.2. BaP concentration in air measured at sampling sites in Hazelrigg and London compared with the national BaP emission total (source: Vincent et al., 2007)

Human exposure to BaP from inhalation of contaminated indoor air has been estimated to range between 10 and 50 ng/d in the USA (Waldman et al., 1991). Loh et al. (2007) assigned mean air concentrations for exposure to BaP in the USA to be 0.06, 0.09 and 2 ng/m3 for indoor air, outdoor air and air during commuting, respectively. Thus whilst generates <5% of UK national emissions of BaP (Vincent et al., 2007), proximity to source means that exposure during commuting is on average likely to be the largest component of inhalation exposure to the general population (Loh et al., 2007). The European Food Safety Authority undertook a detailed review of risks associated with dietary intake of PAHs (EFSA, 2008). Surveys across 16 member states including the UK estimated mean and high-level dietary intake of BaP across the EU to be 235 and 389 ng/d, respectively. The mean and high-level dietary intake for the UK was 189 and 315 ng/d, respectively (EFSA, 2008). UK total dietary surveys based on 1986-87 consumption data and analysis of food items collected in 2000 estimated mean exposure to be 40 to 110 ng/d and high level exposure to be 70-190 ng d-1 (COT, 2002). These values for dietary items collected in 2000 were 4- to 5-fold smaller than equivalent values based on a 1979 survey. COT (2002) estimated that average dose from dietary intake of BaP increased with decreasing age from 1.6 ng/kg body weight (bw)/d in adults to 3.8 ng/kg bw/d in toddlers aged 1.5-2.5 years (equivalent high level intake values were 2.7 ng/kg bw/d in adults to 6.2 ng/kg bw/d in toddlers aged 1.5-2.5 years. EFSA (2008) report that the major dietary sources of BaP in the UK are oils and fats (ca. 50%), cereals (ca. 30%) and vegetables (<10%). Smoked meat and fish were a relatively minor contributor and barbequed food provided a very small part of the dietary intake assuming that barbecuing is an infrequent activity. Exposure via drinking water was relatively insignificant (0.2-2 ng/d), presumably because BaP tends to sorb to solid matrices in the environment (EFSA, 2008). Based on surveys of the BaP content of cigarettes (2-20 ng/cigarette; mean delivery assumed to be 6.5 ng/cigarette) and 80% deposition of inhaled particle-bound BaP in the respiratory tract, EFSA (2008) calculate a daily intake based on 20 cigarettes per day of 105 ng. Sidestream smoke (that emitted directly to air from a burning cigarette) is found to contain almost 10 times more BaP than mainstream (inhaled) smoke and EFSA (2008)

Page 5 of 11 SP1002 Appendix 4 calculate exposure of 40 ng/day based on mid-range air concentrations and sharing a room with smokers for 5 hours per day. Table 4.3 compares environmental exposures to BaP with that calculated for a child aged 1- 6 exposed via a potentially contaminated allotment (case study 2). As there is no SGV for this situation, the soil concentration was back-calculated using CLEA and the appropriate Health Criteria Value. Table 4.3 shows that the exposure to BaP within the allotment scenario is six times larger than mean dietery intake for a toddler aged 1.5 to 2.5 years (COT, 2002) and in the same range as dietary exposure for an adult (EFSA, 2008).

Table 4.3. Comparison between environmental exposure to benzo[a]pyrene in the general population and potential exposure from contaminated land (values are intake for an adult except where stated; occupational exposures excluded) [source: EFSA, 2008; COT, 2002].

Source Mean daily intake (ng/person) Dietary intake for an adult (body weight assumed 189 (mean) at 83.2 kg to match CLEA assumptions) 315 (high-level) Dietary intake for a toddler aged 1.5-2.5 years 43 (mean) (body weight assumed at 11.25 kg to match 70 (high level) CLEA assumptions) Drinking water 0.2-2 Air 20 Smoking (20 cigarettes/day) 105 Passive smoking (sharing room with smokers for 40 5 hours per day) Exposure to a child aged 1-6 based on exposure 255 to soil and contaminated food from an allotment and with BaP concentration back-calculated from the Health Criteria Value (case study 2)

4. Arsenic Non-occupational human exposure to arsenic in the environment is primarily through the ingestion of food and water. Of these, food is generally the principal contributor to the daily intake of total arsenic. WHO (2001) calculate a total daily intake of arsenic from food and beverages of between 20 and 300 µg/day. The Total Dietary Study (TDS) has been undertaken in the UK since the mid-1970s. Data have been used to estimate dietary exposure to arsenic and how exposures have changed over time. Figure 4.3 shows that population dietary exposure to total arsenic decreased between 1977 and 2000 from 100 µg/day to 55 µg/day before increasing slightly to 61-64 µg/day in 2006. The 2006 TDS estimates dietary exposure to total arsenic to be greatest for toddlers (1.5-4.5 years) with mean and high-level exposure of 2.71-2.80 and 12.27-12.34 µg/kg bw/day, respectively. Dietary exposure is smaller for adults with mean exposure in the range 1.65-1.68 µg/kg bw/day and high-level exposure in the range 6.83-6.85 µg/kg bw/day. WHO (2001) estimated that ca. 25% of arsenic present in food is in inorganic form but this varies greatly with food type (for example, organic arsenic dominates in fish and shellfish). Organic arsenic is much less toxic than inorganic arsenic (HPA, 2008) and organic arsenic is excluded from the derivation of the Health Criteria Value for arsenic (Environment Agency, 2009b). The

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2006 TDS contains separate information on inorganic arsenic for the first time. Population dietary exposure is estimated at 1.4-7.0 µg/day (i.e. ca. 2-11% of dietary exposure to total arsenic). The Environment Agency (2009b) used the 2006 TDS to estimate the adult mean daily intake of inorganic arsenic from food and drinking-water to be 5 μg/day.

Figure 4.3. Changes in population dietary exposure to arsenic and cadmium in the UK over time (FSA, 2009)

In some parts of the world, including areas in Bangladesh, Vietnam and China, arsenic in drinking-water is a significant source of exposure to inorganic arsenic and may constitute the main component of daily arsenic intake. This is not the case in the UK. Farmer et al. (1989) calculated inorganic arsenic intake of a Glasgow adult who was not occupationally exposed to be 11.0-16.5 µg/day. They further calculated that the additional intake for adults in Cornwall where there is much greater background contamination with arsenic (due to historic and metal-working activities) was 4.25-6.40 µg/day. All other routes of intake of arsenic (inhalation and dermal) are of minor importance in comparison to the oral route (ATSDR, 2007). For example, inhalation would add about 1 µg/day from airborne and approximately 6 µg/day may be inhaled from 20 cigarettes (WHO, 2001). Environment Agency (2009b) estimate that the adult mean daily intake of inorganic arsenic from inhalation of ambient air is much smaller at 0.014 μg/day. Table 4.4 compares environmental exposures to arsenic with that calculated for exposure to potentially contaminated land based on case study 3 and resetting the concentration of arsenic in soil to a value similar to a SGV for recreational use (this was back-calculated within CLEA using the open space scenario with specification of limited use; the resulting soil concentration was 1180 mg/kg dry weight). Table 4.4 shows that the exposure to inorganic arsenic back-calculated within CLEA to match the Health Criteria Value (Environment Agency, 2009d) is nearly five times larger than the mean dietary intake for an adult and more than twice as large as the combined average intake from diet and smoking for an adult smoker.

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Table 4.4. Comparison between environmental exposure to inorganic arsenic in the general population and potential exposure from contaminated land (values are intake for an adult; occupational exposures excluded).

Source Mean daily intake (µg/person) Dietary intake 5 Drinking water Not known Air (background exposure) 0.014 Smoking (20 cigarettes/day) 6 Recreational exposure calculated using CLEA 24.1 default parameters and with inorganic arsenic concentration set to a value similar to a SGV for recreational use (case study 3)

5. Cadmium Human exposure to cadmium is dominated by dietary exposure with minimal contribution from inhalation, consumption of water and dermal exposure. Smoking provides an additional source of exposure. Natural levels of cadmium in UK soils generally have concentrations in the range 0.1-0.5 mg/kg (HPA, 2006) compared to current SGVs for different land uses and soil pH in the range 1-1400 mg/kg. In Derbyshire, soils derived from the Carboniferous black shales have been shown to have natural cadmium levels as high as 24 mg/kg (Defra/EA, 2002). A strict separation of exposure to cadmium attributable to contaminated land and other sources is difficult because much of the cadmium present in soil arises from a range of anthropogenic activities including fossil fuel combustion, metal smelting and metal-working, waste and use of phosphate fertiliser. Natural sources include bedrock, volcanic eruptions and forest fires. The Total Dietary Study (TDS) has been undertaken in the UK since the mid-1970s. Data have been used to estimate dietary exposure to cadmium and how exposures have changed over time. Figure 4.3 shows that population dietary exposure decreased between 1976 and 2000 from 20 µg/day to 9 µg/day before increasingly slightly to 11-13 µg/day in 2006. The 2006 TDS estimates dietary exposure to be greatest for toddlers (1.5-4.5 years) with mean and high-level exposure of 0.37-0.45 and 0.65-0.75 µg/kg bw/day, respectively, and smaller for adults with mean and high-level exposure of 0.14-0.17 and 0.25-0.29 µg/kg bw/day, respectively (FSA, 2009). The Environment Agency (2009c) estimate average daily exposure from drinking water of 0.4 µg/day based on average concentrations in drinking water in England and Wales and consumption by an adult of 2 L/day. The WHO (1992) estimated that smoking 20 cigarettes per day contributes 2-4 µg/day to exposure to cadmium. Cadmium is primarily present as cadmium oxide in the air. Background exposure via inhalation in a rural, urban and industrialised environment is estimated to be less than 0.01, 0.2 and 0.4 µg/day, respectively (WHO, 2000). Table 4.5 compares environmental exposures to cadmium with that calculated for a child aged 1-4 exposed via a potentially contaminated residential situation (case study 4) and

Page 8 of 11 SP1002 Appendix 4 resetting the concentration of cadmium in soil to the SGV for residential use. Table 4.5 shows that the exposure to cadmium for the residential scenario is five to six times smaller than mean dietary exposure for a toddler of the same age (FSA, 2009). Case study 4 excludes exposure via consumption of home produce grown on contaminated soil and this pathway of exposure accounts for 45% of total exposure within CLEA calculations of the SGV (Environment Agency, 2009e).

Table 4.5. Comparison between environmental exposure to cadmium in the general population and potential exposure from contaminated land (values are intake for an adult except where stated; occupational exposures excluded).

Source Mean daily intake (µg/person) Dietary intake for an adult 11-13 Dietary intake for a toddler aged 1.5-4.5 years 5.1-6.2 (mean) (body weight assumed at 13.7 kg to match CLEA 8.9-10.3 (high assumptions) level) Drinking water <0.2 Air (background exposure in rural environment) <0.01 Air (background exposure in urban environment) <0.2 Smoking (20 cigarettes/day) 2-4 Exposure to a child aged 1-4 based on exposure 1.0 to soil and dust but not home-grown food within a residential scenario and with cadmium concentration set to the SGV for residential use (case study 4)

6. Conclusions An alternative approach to the analysis that has been undertaken would be to compare directly exposures from sources other than contaminated land with Health Criteria Values (HCVs) developed to underpin the derivation of Soil Guideline Values (SGVs). The current analysis takes site-specific characteristics from the case study situations, but resets the contaminant concentration in soil to either the respective SGV or a concentration that yields the HCV where an SGV is not available. It should be noted that most contaminated land will have concentrations of contaminants in soil that are larger than the SGV. The comparison between potential exposure from contaminated land and from other sources varies markedly with contaminant. Exposure from land potentially contaminated with benzene is smaller than or similar to background exposure via air in a rural environment. In this instance, the Intake Dose for inhalation is reset based on the current Air Quality Objective for benzene in England and Wales. Similarly, the residential estimate for a child exposed to cadmium at a soil concentration equivalent to the SGV is smaller than mean dietary exposure estimates by a factor of five to six. Inclusion of exposure via home-grown produce within this case study would narrow the gap between contaminated land exposure and exposure from other environmental sources. Potential contaminated land exposure for benzo[a]pyrene is more than twice as large as dietary exposure to the substance for the child considered in the case study. Similarly, adult exposure to arsenic from potentially contaminated land exceeds environmental exposure estimates by almost a factor of five.

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7. References ATSDR (2007). Toxicological profile for arsenic (update). PB/2008/1000002. Atlanta, Georgia: US Department of Health and Human Services, Agency for Toxic Substances and Disease Registry. Available at: http://www.atsdr.cdc.gov/toxprofiles/tp2.htmlCOT (2002). Polycyclic Aromatic Hydrocarbons in the 2000 Total Diet Study. Committee on of Chemicals in Food, Consumer Products and the Environment Report TOX/2002/26. http://www.food.gov.uk/multimedia/pdfs/TOX-2002-26.PDF. Defra/EA (2002). Soil guideline values for cadmium contamination. R&D Publication SGV3, Environment Agency, Almondsbury, UK, 15p. EFSA (2008). Polycyclic aromatic hydrocarbons in food. Scientific opinion of the panel on Contaminants in the Food Chain. The EFSA Journal (2008) 724, 64-114. Environment Agency (2009a). Contaminants in soil: updated collation of toxicological data and intake values for humans. Benzene. Science Report SC050021, Almondsbury, UK, 39p. Environment Agency (2009b). Contaminants in soil: updated collation of toxicological data and intake values for humans. Inorganic arsenic. Science Report SC050021/TOX1, Almondsbury, UK, 40p. Environment Agency (2009c). Contaminants in soil: updated collation of toxicological data and intake values for humans. Cadmium. Science Report SC050021/TOX3, Almondsbury, UK, 43p. Environment Agency (2009d). Soil guideline values for inorganic arsenic in soil. Science Report SC050021/arsenic SGV, Almondsbury, UK, 11p. Environment Agency (2009e). Soil guideline values for cadmium in soil. Science Report SC050021/Cadmium SGV, Almondsbury, UK, 11p. Farmer JG, Johnson LR, Lovell MA (1989). Urinary arsenic speciation and the assessment of UK dietary, environmental and occupational exposures to arsenic. Environmental Geochemistry and Health 11:93-95. FSA, 2009. Measurement of the concentrations of metals and other elements from the 2006 UK total diet study. London: Food Standards Agency. HPA (2006). Health Protection Agency, Compendium of chemical hazards: cadmium. http://www.hpa.org.uk/chemicals/compendium/cadmium/default.htm. HPA (2007). Health Protection Agency, Compendium of chemical hazards: benzene. http://www.hpa.org.uk/chemicals/compendium/benzene/default.htm. HPA (2008b). Health Protection Agency, Compendium of chemical hazards: arsenic v3. http://www.hpa.org.uk/HPA/Topics/ChemicalsAndPoisons/CompendiumOfChemicalHazards/ 1158313434454/. IEH (1999). IEH report on benzene in the environment. MRC Institute for Environmental Health, Report R12, Leicester, UK. Loh MM, Levy JI, Spengler JD, Houseman EA, Bennett DH (2007). Ranking cancer risks of organic hazardous air in the United States. Environmental Health Perspectives 115: 1160-1168. Vincent KJ, Bush T, Coleman P (2007). Assessment of benzo[a]pyrene concentrations in the UK in 2005, 2015 and 2020. AEA Group report AEA/ENV/R/2373. Waldman JM, Lioy PJ, Greenberg A, Butler JP (1991). Analysis of human exposure to benzo[a]pyrene via inhalation and food ingestion in the Total Human Environmental Exposure Study (THEES). Journal of Exposure Analysis and Environmental Epidemiology 1:193-225.

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WHO (1992). Environmental Health Criteria 134 - Cadmium International Programme on Chemical Safety (IPCS) Monograph, World Health Organisation. WHO (1998). Environmental Health Criteria 202 – Selected non-heterocyclic polycyclic aromatic hydrocarbons. International Programme on Chemical Safety of the World Health Organisation. WHO (2000). Air quality guidelines – second edition. Chapter 6.3 – cadmium. World Health Organisation Regional Publications, European Series No. 91. Copenhagen, Denmark. WHO (2001). Environmental Health Criteria 224 – arsenic and arsenic compounds. International Programme on Chemical Safety of the World Health Organisation.

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