Environmental Health Criteria 67
TETRADIFON
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INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
ENVIRONMENTAL HEALTH CRITERIA 67
TETRADIFON
This report contains the collective views of an international group of experts and does not necessarily represent the decisions or the stated policy of the United Nations Environment Programme, the International Labour Organisation, or the World Health Organization.
Published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization
World Health Orgnization Geneva, 1986
The International Programme on Chemical Safety (IPCS) is a joint venture of the United Nations Environment Programme, the International Labour Organisation, and the World Health Organization. The main objective of the IPCS is to carry out and disseminate evaluations of the effects of chemicals on human health and the quality of the environment. Supporting activities include the development of epidemiological, experimental laboratory, and risk-assessment methods that could produce internationally comparable results, and the development of manpower in the field of toxicology. Other activities carried out by the IPCS include the development of know-how for coping with chemical accidents, coordination of laboratory testing and epidemiological studies, and promotion of research on the mechanisms of the biological action of chemicals.
ISBN 92 4 154267 5
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CONTENTS
ENVIRONMENTAL HEALTH CRITERIA FOR TETRADIFON
1. SUMMARY AND CONCLUSIONS
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1. Identity 2.2. Physical and chemical properties 2.3. Analytical methods
3. SOURCES, ENVIRONMENTAL TRANSPORT AND DISTRIBUTION
4. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
4.1. Environmental levels 4.1.1. Air 4.1.2. Water 4.1.3. Soil 4.1.4. Food 4.1.5. Other products 4.1.6. Terrestrial and aquatic organisms 4.2. General population exposure 4.3. Occupational exposure
5. KINETICS AND METABOLISM
6. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
6.1. Aquatic organisms 6.2. Terrestrial organisms 6.3. Microorganisms 6.4. Bioaccumulation
7. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS
7.1. Single exposure 7.1.1. Toxicity 7.1.2. Skin Irritation 7.1.3. Eye irritation
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7.2. Short-term exposures 7.3. Long-term exposures 7.4. Effects on reproduction 7.5. Mutagenicity 7.6. Carcinogenicity
8. EFFECTS ON MAN
9. EVALUATION OF RISKS FOR HUMAN HEALTH AND EFFECTS ON THE ENVIRONMENT
9.1. Evaluation of health risks for man 9.2. Evaluation of effects on the environment 9.3. Conclusions
10. RECOMMENDATIONS
11. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
REFERENCES
ANNEX EXTRACT FROM HEALTH AND SAFETY GUIDE INCLUDING INTERNATIONAL CHEMICAL SAFETY CARD
TASK GROUP MEETING ON ENVIRONMENTAL HEALTH CRITERIA FOR ORGANOCHLORINE PESTICIDES
Members
Dr L. Albert, Environmental Pollution Programme, National Institute of Biological Resource Research, Xalapa, Mexico (Vice- Chairman)b
Dr E. Astolfi, Faculty of Medicine of Buenos Aires, Buenos Aires, Argentinaa
Dr I. Desi, Department of Environmental Hygienic Toxicology, National Institute of Hygiene, Budapest, Hungary (Vice- Chairman)a
Dr R. Drew, Department of Clinical Pharmacology, Flinders University of South Australia, Bedford Park, South Australiaa
Dr Y. Hayashi, Pathology Division, National Institute of Hygienic Sciences, Tokyo, Japanb
Dr S.K. Kashyap, National Institute of Occupational Health, Ahmedabad, Indiaa
Dr R. Kimbrough, Center for Environmental Health, Centers for Disease Control, Atlanta, Georgia, USA (Rapporteur)b
Dr A.N. Mohammed, University of Calabar, Calabar, Nigeriaa
Mr Y.T. Mosuro, Federal Ministry of Health, Food, and Drug Administration and Laboratory Services, Oshodi, Nigeriab
Dr Y. Osman, Occupational Health Department, Ministry of Health, Khartoum, Sudanb
Dr O.E. Paynter, Office of Pesticide Programs, US Environmental
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Protection Agency, Washington DC, USAa
Dr W.O. Phoon, Department of Social Medicine and Public Health, Faculty of Medicine, University of Singapore, Singapore (Chairman)a
Dr L. Rosival, Centre of Hygiene, Research, Institute of Preventive Medicine, Bratislava, Czechoslovakia (Chairman)b
Dr Sakdiprayoon Deema, Ministry of Agriculture and Cooperatives, Bangkok, Thailandb
Dr F.W. van der Kreek, Ministry of Welfare, Health, and Culture, Leidschendam, Netherlandsb
Dr D. Wassermann, Department of Occupational Health, The Hebrew University, Hadassah Medical School, Jerusalem, Israela
Dr Xue Shou Zheng, School of Public Health, Shanghai Medical University, Shanghai, Chinab
Representatives of Other Organizations
Dr A. Berlin, Health and Safety Directorate, Commission of the European Communities, Luxembourgb
Dr V.E.F. Solman, International Union for Conservation of Nature and Natural Resources (IUCN), Ottawa, Ontario, Canadaa
Observers
Dr H. Kaufmann, International Group of National Associations of Agrochemical Manufacturers (GIFAP), Brussels, Belgiuma
Dr A.A. van Kolfschoten, International Group of National Associations of Agrochemical Manufacturers (GIFAP), Brussels, Belgiumb
Secretariat
Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood Experimental Station, Huntingdon, United Kingdom (Temporary Advisor)a,b
Dr M. Gilbert, International Register for Potentially Toxic Chemicals, United Nations Environment Programme, Geneva, Switzerlanda,b
Dr K.W. Jager, Division of Environmental Health, International Programme on Chemical Safety, World Health Organization, Geneva, Switzerland (Secretary)a,b
Dr A. Pelfrene, Vector Biology and Control, Insecticides Development and Safe Use, World Health Organization, Geneva, Switzerlandb
Dr T. Vermeire, National Institute for Public Health and Environmental Hygiene, Bilthoven, Netherlands (Temporary Adviser)b
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Dr D.C. Villeneuve, Health Protection Branch, Department of National Health and Welfare, Tunney's Pasture, Ottawa, Ontario, Canada (Temporary Advisor) (Rapporteur)a
Mr J.D. Wilbourn, International Agency for Research on Cancer, Lyons, Francea
------a Present at first Task Group meeting. b Present at second Task Group meeting.
NOTE TO READERS OF THE CRITERIA DOCUMENTS
Every effort has been made to present information in the criteria documents as accurately as possible without unduly delaying their publication. In the interest of all users of the environmental health criteria documents, readers are kindly requested to communicate any errors that may have occurred to the Manager of the International Programme on Chemical Safety, World Health Organization, Geneva, Switzerland, in order that they may be included in corrigenda, which will appear in subsequent volumes.
* * *
A detailed data profile and a legal file can be obtained from the International Register of Potentially Toxic Chemicals, Palais des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 - 985850).
ENVIRONMENTAL HEALTH CRITERIA FOR TETRADIFON
A WHO Task Group on Environmental Health Criteria for Organochlorine Pesticides other than DDT (Endosulfan, Quintozene, Tecnazene, Tetradifon) was held at the Health Protection Branch, Department of National Health and Welfare Ottawa from 28 May - 1 June, 1984. The meeting was opened by Dr E. Somers, Director- General, Environmental Health Directorate, and Dr K.W. Jager welcomed the participants on behalf of the three co-sponsoring organizations of the IPCS (UNEP/ILO/WHO). The Task Group reviewed and revised the draft criteria document and concluded that the data available were so sparse that no proper evaluation could be made of the potential hazard of tetradifon for the general population, exposed workers, or the environment. The Task Group recommended that a preliminary hazard assessment should be circulated to all IPCS and IRPTC national focal points with a request for further information.
A second WHO Task Group was convened in Geneva 9-13 December 1985 to review and revise an amended draft and to make an evaluation of the risks of tetradifon on human health and the environment.
The initial drafts of the tetradifon document were prepared by DR D.C. VILLENEUVE of Canada and DR S. DOBSON of the United Kingdom.
The proprietary data mentioned in this document were made available to the Central Unit by Duphar BV for use at the Task
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Group.
The present draft was prepared by the IPCS Secretariat, updating the preliminary hazard assessment with new information received in more than 50 replies.
Selected sections from the Health and Safety Guide on Tetradifon, published by the World Health Organization, are included as an Annex.
The efforts of all who helped in the preparation and finalization of the document are gratefully acknowledged.
* * *
Partial financial support for the publication of this criteria document was kindly provided by the United States Department of Health and Human Services, through a contract from the National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA - a WHO Collaborating Centre for Environmental Health Effects. The United Kingdom Department of Health and Social Security generously supported the costs of printing.
1. SUMMARY AND CONCLUSIONS
Technical tetradifon (1,2,4-trichloro-5-(4-chlorophenyl)- sulfonyl benzene) is a white crystalline solid that is more than 94% pure. It is used in formulation as an acaricide. The method of choice for its determination is gas-liquid chromatography with electron capture detection.
Tetradifon is persistent and only slightly mobile in soils. The compound degrades more rapidly with increasingly aerobic conditions. Both the parent compound and its initial degradation product in soil, adsorb on soil particles and resist leaching.
The short-term toxicity of tetradifon is low for birds, moderate for fish, and moderate to high for aquatic crustacea. It is relatively non-toxic for bees. Long-term studies are not available for these organisms. Tetradifon does not bioaccumulate significantly in fish, which metabolize and eliminate the compound rapidly. No adverse effects on terrestrial plants have been reported and tetradifon did not have any effects on cultures of an aquatic unicellular alga (Chlorella pyrenoidova).
Exposure of the general population is mainly through food, but, with recommended application rates, residues in food are virtually absent. Occupational exposure levels for workers spraying crops at recommended use levels have been estimated to be far below toxic levels, based on oral and dermal LD50s for rats.
In the rat, most (70%) of a single, orally-administered dose of tetradifon was excreted via the bile in the faeces within 48 h. Part of the remainder was distributed in all organs and tissues. The results of one study suggest that tetradifon and its metabolites are rapidly excreted from the body. On continued dosing in beef cattle, tetradifon was detected in adipose tissue. It is not known whether tetradifon is excreted in milk.
The oral LD50 for technical tetradifon in the rat ranges from 5000 to 14 700 mg/kg body weight. Tetradifon has been classified in the category of technical products that are unlikely to present acute hazards if used as recommended. The formulated product may
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be more toxic, depending on the other components of the formulation. The toxicity may also vary with the purity of the product. In the past, both chlorinated dibenzodioxins and 2,4,5-T have been identified in samples of tetradifon. It has been shown that, with regular strict quality control procedures, levels of these contaminants are below the limits of detection.
In a 90-day study on rats, 50 mg/kg tetradifon in the diet was a no-observed-adverse-effect level. At higher dose levels, induction of microsomal liver enzymes occurred, with increased liver weight and increased endoplasmic reticulum. At 200 mg/kg diet, histological changes were noted in the thyroid. In a 2-year study on rats, induction of microsomal enzymes and increased liver weight were noted at a dietary level of 1200 mg/kg.
No effects on reproduction were found in a 2-generation reproduction study on rats administered tetradifon at 0, 40, 200, or 1000 mg/kg diet. In a 90-day study on the F2b generation, the only effects of dietary tetradifon were a lower body weight gain and an increased dose-related incidence of dilated renal pelvis.
In a 1-year study on dogs, enlarged livers were seen at dietary concentrations of 5000 mg technical tetradifon/kg. Small infarct-like spots in the outer cortical layer of the kidneys were reported at a dietary level of 5000 mg/kg and in one of 4 dogs administered 1000 mg/kg diet. Serum-alkaline phosphatase values were slightly elevated at 5000 mg/kg diet. The no-observed-adverse- effect level in this study was suggested to be in the range of 500 - 1000 mg/kg diet, which is roughly equivalent to a daily intake of 12.5 - 25 mg/kg body weight.
Tetradifon was negative in short-term in vitro tests for mutagenicity.
Negative results were obtained in a screening test for carcinogenicity in mice, but the test was considered to be inadequate for the evaluation of the carcinogenicity of this compound.
No adverse health effects from exposure to tetradifon have been reported in man.
Although the information available for this evaluation of tetradifon is incomplete and not always up to present-day standards, there are no indications, at present, that the normal recommended use of tested tetradifon products as an acaricide causes any health or safety hazards for the general population, exposed workers, or the environment.
2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS
2.1. Identity
Chemical structure:
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Molecular formula: C12H6C14O2S
CAS chemical name: 1,2,4-trichloro-5-[(4-chlorophenyl)- sulfonyl]-benzene
Synonyms: 4-chlorophenyl-2,4,5-trichlorophenyl sulfone, 2,4,4',5-tetrachlorodiphenyl sulfone
Common trade names: Akaritox, Aredion, Duphar 23737, ENT 23737, FMC 5488, Mition, NIA 5488, Polacaritox, Roztoczol, Roztozol, Tedion V18, Tetradichlone (a complete list of trade names is available from IRPTC)
CAS registry number: 116-29-0
2.2. Physical and Chemical Properties
Some physical and chemical properties of tetradifon are given in Table 1. The solubility of tetradifon in different organic solvents at room temperature varies from 10 g/litre (in kerosene and methanol) to 255 g/litre (in chloroform) (Van Rossum et al., 1978).
Tetradifon is manufactured by a Friedel-Craft's reaction between 2,4,5-trichlorophenylsulfonyl chloride and monochlorobenzene in the presence of anhydrous aluminium chloride or ferric chloride (Van Rossum et al., 1978), or by Sandmeyer diazotization (Windholz et al., 1983). The technical product is more than 94% pure, but since production processes may vary, the type and quality of impurities present may differ in commercial products from different companies. In addition, the limits of detection for different chlorinated dibenzodioxins, in commercial products vary. In a study by Woolson et. al. (1972), the limit of detection for chlorinated dibenzodioxins was equal to or less than 0.5 mg/kg. The di-, tri-, tetra-, and hexachlorinated dibenzodioxins were not separated from each other; the authors stated that higher chlorinated dibenzodioxins were found in some samples of tetradifon, but no specific information was given.
Table 1. Some physical and chemical properties of tetradifona ------Physical state crystalline solid
Colour slightly yellow
Relative molecular mass 356.04
Melting point 148 - 149 °C
Vapour pressure (20 °C) 0.32 x 10-10 kPa
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Octanol/water partition 4.61 coefficient
Solubility in water (10 °C) 0.05 % (20 °C) 0.08 % (50 °C) 0.34 % ------a From: Van Rossum et al. (1978) and Duphar BV, personal communication (1982).
Impurities including 2-chlorophenyl-2,4,5-trichlorophenyl sulfone up to a maximum level of 5 g/kg and 2,4,5-trichloro- phenoxyacetic acid (2,4,5-T) have been reported by Matano et al. (1971) and trace amounts of highly-chlorinated dibenzodioxins, but not 2,3,7,8-TCDD by Woolson et al. (1972). It has been shown that regular strict quality control procedures maintain the total sum of all isomeric tetrachlorodibenzofurans in technical tetradifon at less than 10 µg/kg (detection limit) (Duphar BV, 1985). Furthermore, analysis of concentrated mother liquids revealed that the concentrations of 2,3,7,8-tetrachlorodibenzofuran, the sum of all isomeric tetrachlorodibenzo- p -dioxins, and 2,3,7,8-tetra- chlorodibenzo- p -dioxin were all lower than 1 µg/kg, and that 2,4,5-tri-chlorophenoxyacetic acid (2,4,5-T) was not present as an impurity (Duphar BV, 1985).
Tetradifon is resistant to hydrolysis by acid and alkali and is non-corrosive (Worthing, 1979). Particle size has a strong influence on its biological effectiveness in that small particles show a better rain resistance than larger ones (Maas, 1979). In 1954, tetradifon was introduced in the Netherlands as a non- systemic acaricide, which was toxic for the eggs (ovicide) and all non-adult stages of a wide range of phytophagous mites. It is used, particularly in mixtures, in horticulture, including domestic greenhouses, mainly on top-fruit, vegetables, ornamentals, hops, cotton, and sugarcane, and forestry.
Tetradifon remained stable to ultraviolet radiation (UVR) for 12 h at 50 - 60 °C (Duphar BV, 1985).
2.3. Analytical Methods
Several methods have been used for the extraction of tetradifon residues from different tissues. Burke & Mills (1963) introduced a method involving microcoulometric gas-liquid chromatography (GLC). Mitchell (1976) used GLC with electron capture detection to study the tetradifon contents of apple and cucumber samples. According to Van Rossum et al. (1978), the recovery of tetradifon from crop samples using the GLC method was 85 - 100%. They also reported that tetradifon could be extracted from soil samples with ether and then detected directly by GLC with electron capture detection. The limit of detection in soil samples was 0.02 mg/kg.
Analytical methods are based on total organic chlorine, column chromatography, and UV spectrophotometric detection (Zweig & Sherma, 1972; Suzuki et al., 1973, 1974; Burke, 1976; Bontoyan, 1979). Zweig & Sherma (1972) mentioned a recovery of 95 - 102% from vegetables. Gas chromatography is recommended by CIPAC (Henriet et al., 1983) for the analysis of formulations and technical material.
3. SOURCES, ENVIRONMENTAL TRANSPORT AND DISTRIBUTION
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Tetradifon is manufactured in the Netherlands and in Italy and formulated in several countries. The uses of tetradifon in selected countries are shown in Table 2.
Table 2. The uses of tetradifon in selected countriesa ------Country Quantity Year Uses ------Colombia 2786 kg 1982 agricultural acaricide 2073 kg 1981 recommended in the growth 2343 kg 1980 of cotton, fruits, and other products
Mexico 1000 kg 1981 on strawberries, tomatoes, grapes, cucumber, apples, and citrus fruits
Sweden 400 kg 1981 agricultural and horticultural use
Thailand 42 100 kg 1984 14 600 kg 1983 14 175 kg 1982 acaricide 12 237 kg 1981 acaricide 1620 kg 1980 acaricide 216 kg 1979 acaricide 1000 kg 1978 acaricide 208 kg 1977 acaricide 272 kg 1976 acaricide
United Kingdom 320 kg/year 1975-79 acaricide
USA 1983 used prior to 1983; registration voluntarily cancelled in 1983 by producers ------a Information received from national contact points of IRPTC (1984).
Responses to a questionnaire received from 49 countries around the world indicated the continuing registration and use of tetradifon in 37 countries. Nine developing countries stated that tetradifon was not used, and 3 countries (China, the Federal Republic of Germany, and the USA) stated that registration of tetradifon had been discontinued for reasons other than its toxicity. Thirteen of these countries taken together used approximately 200 tonnes of tetradifon per year during the years 1982-84 (information received from national contact points of the IPCS and IRPTC, 1985).
4. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE
Only limited information is available on tetradifon as an environmental pollutant. Its water solubility is low, and a study by Yaron et al. (1974) showed that there was only restricted leaching from soil by rain.
4.1. Environmental Levels
4.1.1. Air
No data are available on tetradifon levels in air.
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4.1.2. Water
No data are available on tetradifon levels in water.
4.1.3. Soil
Only minute amounts of tetradifon were found in the deep layers of soil from an irrigated potato field sprayed at a rate of 10 kg/ha. Tetradifon persisted throughout the irrigation season. Transport of tetradifon into the soil was not affected by the amount of water applied (Yaron et al., 1974).
In a degradation experiment, sandy loam soil was incubated aerobically for 106 weeks. Approximately 70% of the added tetradifon was recovered unchanged and 20% was recovered as extractable metabolites (Borst et al., 1983). Four metabolite fractions were identified. One chlorine atom appeared to be substituted by more polar groups (-SOCH3, -SO2CH3, -SO3H, -SCH3) (Borst et al., 1983; Willems et al., 1983). In a water/sandy loam hydro-soil system, tetradifon had a half-life of 36 weeks. Almost all of the tetradifon was retained in the soil phase. Under more aerobic conditions, degradation was more rapid, 31% of the added tetradifon being recovered after 32 weeks (Willems & Nimmo, 1981). The movement of tetradifon and partially degraded tetradifon in overlying loam soil was also investigated. The results showed that neither tetradifon nor its degradation products are leachable compounds (Willems & Smit, 1982).
4.1.4. Food
In a study on the fate of insecticides in an irrigated field, Yaron et al. (1974) found a tetradifon concentration of 250 mg/kg (wet weight) in the peel of potato tubers. This was due to the direct contact of the pesticide with the tuber. No tetradifon was found in the tuber pulp or in the leaves of the potato plant; the amounts of pesticide applied in this study were much greater (2 applications of 10 kg pesticide/ha soil) than those normally used.
Radioactive tetradifon in a solution prepared from either a wettable powder (WP) or a miscible oil (MO) was sprayed on 2 apple trees. Changes in radioactivity in and on the leaves were followed for 4 months. Externally, the greater part of the activity was lost from the leaves within the first few days. Uptake into the leaves reached a maximum in approximately 1 day equalling 8% of initial activity with the WP and 30% with the MO. More than a month after spraying, intact tetradifon could still be found on and in the leaves. The level in the ripe apples was less than 0.2 mg/kg (Halberstadt, 1958).
Cassil & Fullmer (1958) sprayed fruit-bearing apple, pear, peach, lemon, and orange trees with either 500 or 1500 g of 25% tedion wettable powder per 455 litres of water, 32 days before harvest. Pears and peaches were sprayed at 0.56 litre/m2, oranges and lemons at 1.16 litres/m2, and apples were sprayed manually to runoff. Maximum residue levels on the surface of the fruits sprayed at 500 and 1500 g varied from 1.5 to 3.6 and from 3.4 to 7.0 mg/kg, respectively. Tetradifon residues diminished largely as a result of fruit growth and not through decomposition.
In a second study, Cassil & Fullmer (1958) followed tetradifon residue levels on similarly-sprayed oranges for 100 days. As in the first study, they concluded that tetradifon is very stable when exposed to weathering at high summer temperatures.
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For many years, the US Food and Drug Administration has examined more than 10 000 food samples yearly using methods with which it is possible to determine residues of tetradifon. Residues have been found infrequently and have been limited primarily to fresh fruits. From 1964 to 1969, 1607 fruit samples were examined and tetradifon residues ranging from trace to 2 mg/kg were found in only 2.05% of the fruits; from 1970 to 1976, 1201 fruit samples were examined and similar tetradifon residues were found in only 1.42% of the samples. On the basis of the total number of fruit samples examined, the average residue of tetradifon in fruits was 0.007 mg/kg for 1964-69 and 0.004 mg/kg for 1970-76. The only other foods in which tetradifon residues were found during these years were one sample of cereal by-products, one sample of fish, and one sample of leafy vegetables. Findings have been less frequent in recent years and have primarily been found in produce imported from Mexico (US FDA, personal communication, 1984).
In New Zealand, apples from 32 growers were checked for tetradifon residues. The maximum level found was 0.7 mg/kg (average 0.11 mg/kg) (Department of Health, Wellington, personal communication, 1984).
No studies are available from other countries.
4.1.5. Other products
When tetradifon was sprayed on a tea plantation at 0.5 g/litre and 750 - 1000 litres/ha, initial deposits on leaves were in the range of 12.6 - 13.6 mg/kg. After 10 days, residues were < 5 mg/kg (Rajukkannu et al., 1981). No other studies were available for review.
4.1.6. Terrestrial and aquatic organisms
In pregnant beef cattle fed apple pomace containing about 0.07 - 0.53 mg tetradifon/kg and 0.53 - 8.33 mg total DDT/kg, for 160 days, tetradifon accumulated in depot fat at a rate similar to those of DDT and DDD, but only 29% as fast as DDE. On day 160, the concentrations in the extracted fat were 0.16 mg tetradifon/kg and 2.56 mg total DDT/kg (Rumsey et al., 1977). The depletion of these two compounds following cessation of exposure was not investigated. Thus, this study does not give any information on the persistence of tetradifon in cattle.
Tetradifon was not detected (detection level: 0.05 mg/kg) in the tissues of 750 fish samples collected from 11 major lakes and rivers in Alberta, Canada (Chovelon et al., 1984).
4.2. General Population Exposure
In a market-monitoring programme conducted in California and Arizona, during 1967, the maximum tetradifon residue found on citrus fruits (whole fruit) was 0.3 mg/kg (Gunther, 1969). The results of market-basket studies in the USA during 1966-67, which included both domestic and imported food, showed that tetradifon was virtually absent (USDA, 1968). In a market-basket study in Spain in 1971-72, tetradifon was not detected in 97% of fruit samples and in 87% of vegetable samples (Carrasco et al., 1976).
In the USA in the years 1975-76, tetradifon was not detected in foods including unfortified infant and toddler total diet samples from 10 cities in the USA sampled between August 1975 and July 1976 (Johnson et al., 1981a,b). Furthermore, there have been
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no findings of tetradifon in FDA total diet ("market basket") studies from 1976 to the present time (US FDA, personal communication, 1984).
While most measurements in food were negative, no information was available on the use patterns in the countries where the food was monitored.
4.3. Occupational Exposure
Following the analyses of dermal exposure pads or hand rinses and of respirator pads, an estimate of the levels of dermal and respiratory exposure that sprayers would potentially incur was made by Wolfe et al. (1967, 1972). The values derived were 36.4 mg/h for dermal exposure and 0.07 mg/h for inhalation (Durham & Wolfe, 1962; Wolfe et al., 1967). No information on the risks of combined dermal and inhalation exposure is available for formulators or workers manufacturing the product.
5. KINETICS AND METABOLISM
In a preliminary study, a few rats were fed 10 mg 35S- tetradifon/rat per day for 10 days and then examined. The highest percentages of radioactivity during the 10 days were found in the faeces and urine, followed by fat, gastrointestinal tissue, liver, and muscles (Halberstadt, 1958). One rat was given 10 mg 35S- tetradifon suspended in peanut oil/water, by stomach tube, and killed 48 h later. Seventy-one percent of the dose was eliminated with the faeces, 4% with urine, and 7% was recovered from the gastrointestinal tract. The remaining 18% was present in very small quantities in all organs and tissues. Only 20 - 40% of the activity in organs was associated with unchanged tetradifon (Halberstadt, 1958). The Task Group realized that results from single animals are difficult to interpret, however, no other data were available.
In another study (De Lange et al., 1975), rats received a single oral dose of approximately 1 mg labelled tetradifon. The elimination of radioactivity in urine and faeces was measured in 6 rats, for 96 h. Collection of urine and faeces was continued for 168 h in 3 more rats. The elimination of radioactivity in these rats was low in urine (2 - 4%) and high in faeces. Total recoveries were about 75% of the dose after 96 h and 87% after 168 h; the carcass contained about 11% at 96 h. When the bile duct was ligated in 3 rats, excretion via the urine increased and was equal to about two-thirds of the dose. By cannulating the bile duct in 3 rats, the biliary excretion of 1 mg tetradifon was determined to be 30 - 60% of the dose. This means that up to two-thirds of the dose was absorbed.
The distribution of tetradifon in intact rats was studied (De Lange et al., 1975). The radioactivity in the fatty tissues was found to exceed the plasma level by a factor of 50 at 96 h; the level in the lung was about 15 times higher than the plasma level. The continuing excretion of radioactive material after 96 h suggests depletion of these depots.
Unchanged tetradifon was not detected in any of the urine and bile samples. The chromatographic determination of metabolite patterns in urine suggested that the principal metabolites could be chlorinated benzenesulfonic acids. However, another pattern seems to be present in the bile.
6. EFFECTS ON ORGANISMS IN THE ENVIRONMENT
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6.1. Aquatic Organisms
The LC50s for tetradifon in 2 species of crustacea and 3 species of fish are summarized in Table 3. The compound is moderately toxic for fish, and moderately to highly toxic for crustacea. The guppy (Lebistes reticulatus) showed signs of intoxication when exposed to tetradifon at 1 mg/litre for 5 h but recovered completely after being transferred to untreated water (Adlung, 1957). Guppies, 3-4 weeks old, did not show any signs of intoxication when exposed to suspensions containing 2 mg technical tetradifon/litre for 96 h (Gijswijt, 1984a).
Waterfleas (Daphnia magna) were exposed to water suspensions of tetradifon of 0.2 or 2.0 mg/litre for 48 h (both concentrations exceed the water solubility of tetradifon). No toxic effects were observed (Gijswijt, 1984b).
6.2. Terrestrial Organisms
Sherman & Sanchez (1968) did not find any toxic effects on plant growth or gross leaf pathology, when tetradifon was sprayed on papaya plants, once a week for 3 weeks, at a concentration of 1.97 g/litre.
Tetradifon is relatively non-toxic for birds. Hill et al. (1975) studied its toxicity for 4 species: bobwhite quail, ring- necked pheasant, mallard (all at 10 days of age), and 12-day-old Japanese quail. Tetradifon was included in food at concentrations of up to 5000 mg/kg and fed to the birds for 5 days. The mortality rate was estimated at 8 days. Bobwhite quail showed a 10% mortality rate at 5000 mg tetradifon/kg diet, but no deaths occurred in any other species. The LC50 for birds is therefore greater than 5000 mg/kg diet. No long-term studies on birds were available for review. Beran (1970) reported an oral LD50 for bees of 1600 µg/bee and an LD50 of 160 µg/bee for tetradifon when applied topically. This second LD50, expressed as a surface deposit, was stated to be equivalent to an application rate of 25 kg tetradifon active ingredient/ha. Tetradifon, at aqueous concentrations of 0.2 - 1.6%, applied externally to bees was not toxic over a 24-h period (Roger, 1968). A topical LD50 of > 1250 µg/bee was reported by Lippold (1960). Roger (1968) fed Tedion V18 emulsifiable concentrate in honey syrup to honey bees and reported an oral LD50 of 176 µg/bee (of the formulation). Müeller (1959) reported the oral LD50 of tetradifon for bees to be between 50 and 100 µg/bee. No contact activity of tetradifon was detected. A field trial with a spray concentration of up to 4 g/litre did not produce any effects in honey bees. Tetradifon was classified by Anderson & Atkins (1968) as "relatively non-toxic" for bees (LD50 greater than 11 µg/bee). A higher toxicity of tetradifon for bees, with an oral LD100 over 12 h of 1.01 µg/bee, several orders of magnitude below other reported values was reported in a series of studies by Arzone & Vidano (1974) and Vidano & Arzone (1975). No explanation for this discrepancy is given.
Table 3. Toxicity of tetradifon for aquatic organisms ------Organism Age/ Grade Temp pH Parameter Concentration weight (°C) (µg/litre) ------Scud 2 months technical 23.8 7.1 24-h LC50 370 (280-500) (Gammarus lacustris) 2 months technical 23.8 7.1 48-h LC50 140 (100-200) 2 months technical 23.8 7.1 96-h LC50 110 (80-150)
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21 96-h LC50 111 (82-150) (Gammarus fasciatus)
Rainbow trout 1.1 g technical 12 96-h LC50 1200 (Salmo gairdneri) (949-1600)
Rainbow trout 96 h LCO 10 (Salmo gairdneri)
Channel catfish 0.3 g technical 18 96-h LC50 2100 (Ictalurus punctatus) (1150-3830)
Bluegill 0.8 g technical 24 96-h LC50 880 (664-1166) (Lepomis macrochirus) ------Addition of tetradifon to insecticides increases their toxicity for bees (synergism) (Johansen, 1983).
In studies on other insects, Lippold (1960) reported LD50 values for topically applied tetradifon (acetone solution) as > 9000 µg/insect for the Mexican bean beetle (Epilachna varivertis); > 4300 µg/insect for the milkweed bug (Oncopeltus fasciatus), and > 6900 µg/insect for plum curculio (Conotrachelus nenuphar).
6.3. Microorganisms
The growth of cultures of the fresh water green alga Chlorella pyrenoidova in a suspension of tetradifon at 2 mg/litre for 96 h did not differ significantly from that of controls (Gijswijt, 1984c).
6.4. Bioaccumulation
In a study to examine uptake and loss of tetradifon, guppies (Lebistes reticulatus) were exposed to water containing 15 µg 14C- labelled tetradifon/litre, for 14 days, and then transferred to clean water for a further 7 days. Fish were sampled at regular intervals throughout the study and whole body extracts (acetonitrile and methanol under reflux) were made. Tetradifon was determined in these extracts using high-performance liquid chromatography (HPLC). Maximum tetradifon residues were found on the third day and represented a bioconcentration factor of 200 times the water concentration. The residues declined over the remainder of the study, in spite of continued exposure to tetradifon. The decline was rapid and stabilized at between 15 and 45X water concentrations between days 7 and 14. Seventeen, 21, and 28 days after transfer to clear water, tetradifon could not be detected in fish extracts. The results are explained by rapid metabolism and excretion of tetradifon after an initial lag period (Willems & de Winter, 1985). These results confirm that tetradifon does not bioaccumulate significantly in fish.
7. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS
7.1. Single Exposure
7.1.1. Toxicity
Data on the acute toxicity of tetradifon in experimental animals are summarized in Table 4.
Table 4. Acute toxicity of tetradifon ------Animal Route LD50 (mg/kg Reference
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body weight) ------rat oral 5000 - 14 700 Bordas (1968); Jones et al. (1968) rat oral 566a Ben-Dyke et al. (1970) dog oral 2000 Hendriksen (1956) rabbit dermal > 10 000 Ben-Dyke et al. (1970); US NIOSH (1977) mouse intraperitoneal 75 Ishida & Shirakawa (1969) mouse subcutaneous 1953 (TDLo)b Bionetics (1973) ------a Tedion V18 emulsifiable concentrate, containing 8% tetradifon (weight/volume) was tested. LD50 only in part related to tetradifon. b TDLo = lowest toxic dose.
Ishikawa et al. (1978) examined the effects of tetradifon on plasma-alpha-lipoprotein cholesterol in male Sprague Dawley rats following an intraperitoneal injection of 40 mg/kg body weight. No effects were observed with regard to alpha-lipoprotein cholesterol, plasma-triglycerides, and weight gain. Treatment with tetradifon resulted in slightly elevated levels of total plasma-cholesterol, 7 days after treatment, with a return to threshold levels by day 21.
7.1.2. Skin irritation
A total of 0.5 g technical tetradifon was applied to the back of the rabbit under an occlusive dressing. No skin irritation was noted (Koopman 1985a). However, the tetradifon formulation Tedion EC-8 was slightly irritating to rabbit skin (0.5 ml of the concentrate, which contains 80 g/litre in xylene) (Koopman 1985b).
7.1.3. Eye irritation
Application of 100 mg technical tetradifon in the rabbit's eye produced slight irritation (Koopman, (1985c); Tedion EC-8 was moderately irritating at a dose of 0.1 ml of the concentrate containing 80 g tetradifon/litre in xylene (Koopman 1985d).
7.2. Short-Term Exposures
Street et al. (1971) reported tetradifon to be fairly effective in rats in reducing dieldrin storage and hexobarbital sleeping time, and increasing the oxidative metabolism of O - ethyl- O -( p -nitrophenyl)-phenylphosphonothioate (EPN). The compound was added to the diet at a concentration of 50 mg/kg and, depending on the enzymatic test, exposures ranged from 10 to 15 days.
When tetradifon was tested in rats (7 days at 200 mg/kg body weight) and fish (7 days at 2 mg/litre water), no clinical changes were seen. The main biochemical alterations were increased values for some enzymes (Zamfir et al., 1972).
A good correlation was found between no-observed-adverse- effect levels based on the induction of liver microsomal enzymes in male rats and no-observed-adverse-effect levels based on histopathological changes, for 13 organochlorine pesticides.
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Tetradifon was one of the least active substances in this series. The lowest dose level that induced an effect was 50 mg/kg diet for 2 weeks (Den Tonkelaar & Van Esch 1974).
Verschuuren et al. (1973) conducted a study on rats in which 5 structurally-related acaricides were compared. Groups of 10 male and 10 female rats were fed these substances in the diet at 0, 50, 200, 1000, or 3000 mg/kg for 90 days. In the case of tetradifon, a dietary level of 50 mg/kg was a no-observed-adverse-effect level. There was no growth retardation at any level. Histological changes in the thyroid were noted at 200 mg/kg diet; liver weight was increased at 1000 mg/kg with the appearance of SER whorls, consisting of smooth endoplasmic reticulum.
Niepolomski et al. (1972) administered doses of 0, 30, 90, 270, 810, or 2430 mg tetradifon/kg body weight, by gavage, to groups of 10 male and 10 female Wistar rats, for 90 days. Only the 30 mg/kg level did not produce any effects. From 90 mg/kg onwards, dose-related pathomorphological changes in liver, kidney, and lung and impairment of lipid metabolism were seen.
Technical tetradifon was administered to groups of 4 dogs at dietary levels of 0, 500, 1000, and 5000 mg/kg, for 1 year (Keller, 1959). No effects of tetradifon treatment were seen on behaviour, general health, and haematological and most biochemical parameters. Serum-alkaline phosphatase values were slightly elevated at 5000 mg/kg diet. Gross autopsy at the end of the study revealed enlarged livers at 5000 mg/kg diet and small grey infarct-like spots in the outer cortical layer of the kidneys in one dog at the dietary level 1000 mg/kg and 2 dogs at the 5000 mg/kg dietary level. The gross findings were not described at the microscopic level. Histopathology did not reveal any compound-related changes. The no-observed-adverse-effect level was suggested to be in the range of 500 - 1000 mg/kg feed.
7.3. Long-Term Exposures
Two 2-year studies were conducted with tetradifon as long ago as 1955 (Duphar BV, 1960). Both chemically pure and commercial grade tetradifon were tested in groups of 15 male and 15 female rats at concentrations of 0, 30, 100, 300, 1200, 5000, or 20 000 mg/kg in the diet. No dose-related changes were found in body weight, haemoglobin, white blood cell and red blood cell concentrations, or differential blood count.
Pathology and histological examination of liver, kidney, spleen, heart, lung, stomach, small intestine, colon, thyroid, adrenal, testis/ovary, and bone marrow after 24 months did not show any dose-related effects at levels of 300 mg/kg or less in either groups. At 1200 mg/kg upwards, degenerative changes developed in the liver and kidney in both groups.
In the studies available for review, the numbers of animals used, the tests, and the reports were limited compared with present-day standards. However, review of these studies suggests a no-observed-adverse-effect level for short-term and long-term exposure of rats of between 2.5 and 15 mg/kg body weight.
7.4. Effects on Reproduction
A 2-generation reproduction study with tetradifon (98.4% pure) was carried out on Charles River Sprague Dawley rats (25 per sex per group) at dose levels 0, 40, 200, or 1000 mg/kg diet. The parents in both generations were fed the appropriate diets for at
Page 17 of 30 Tetradifon (EHC 67, 1986)
least 9 weeks and then subjected to 2 subsequent matings. No differences attributable to tetradifon administration were noted in parental body weight, food or water consumption data, survival rates, pregnancy rates, implantation efficiencies, or parturition indices. The first F1 generation offspring were killed and examined at weaning. One-fifth of the second F1 litters was evaluated for teratogenic effects after Caesarian section, one fifth was born naturally and examined 3 weeks postnatally, and three-fifths of the litters were used to produce the F2 litters. The first F2 litters were killed and examined at weaning. Half of the second set of F2 litters (F2a) were delivered by Caesarian section and used for teratological evaluation. The other half of the second set of F2 litters (F2b) was evaluated after 3 months of postnatal treatment at dietary levels of 40, 200, and 1000 mg tetradifon/kg, after weaning. Evaluation of the survival indices, sex ratios, and body weights of the fetuses taken by Caesarian section, and the offspring examined at 3 weeks postnatally, did not reveal any compound-related differences between the control and treated groups. In the F2b litters examined 3 months postnatally, body weight gains were lower than control values in all treated groups; there was no correlation with dose. However, in the same set of litters, there was a dose-dependent increase in the incidence of dilated renal pelvis (7.8%, 11.9%, and 26.7%, respectively, in 37.5, 42.9, and 87.5% of the litters) compared with the control value (6.6% in 40.0% of the litters). The difference was statistically significant only at the highest dose.
These phenomena were not seen in the offspring examined at weaning. Moreover, in the F1 offspring evaluated at weaning, dilated renal pelvis was seen in 10.8% of the control pups and 19.4% of the low- dose group but not in the middle- and high-dose groups. The significance of the findings is not clear.
7.5. Mutagenicity
Tetradifon was not among the compounds that responded positively in tests using two strains of Bacillus subtilis, two strains of Escherichia coli, and four strains of Salmonella typhimurium. However, it must be noted that no metabolic activation was attempted with tetradifon and also that Salmonella TA 98 and TA 100, two of the most sensitive strains, were not included in the early studies of this group (Shirasu et al., 1976). The same group (Moriya et al., 1983) reported negative results for tetradifon in a bacterial reversion assay with S. typhimurium TA 100, TA 98, TA 1535, TA 1537, TA 1538 and E. coli WP2 hcm.
Tetradifon was weakly positive in a sister chromatid exchange assay in human lymphocyte cultures at a 10-4 molar concentration, but inactive at 10-5 or 10-6 molar concentration (Sobti et al., 1983).
Cultures of human lymphocytes treated with tetradifon did not show any significant increase in the proportion of metaphase figures containing chromosome abberrations, compared with the concurrent solvent controls. Thus, tetradifon did not show any evidence of mutagenic potential in this in vitro cytogenetic assay (Allen, 1985).
7.6. Carcinogenicity
Innes et al. (1969) tested many pesticides in a special screening test. Small groups of mice were given tetradifon at 100 mg/kg body weight by intubation on the 7th - 28th day of age, followed by 260 mg/kg diet for approximately 18 months. Tetradifon
Page 18 of 30 Tetradifon (EHC 67, 1986)
was reported not to produce a significant increase in the incidence of tumours. No further details were given and this study was not considered adequate for the evaluation of the carcinogenicity of tetradifon. No other studies were available for review.
8. EFFECTS ON MAN
No adverse health effects on human beings from exposure to tetradifon have been reported.
In photo-patch tests on 51 patients, Horiuchi & Ando (1978) found tetradifon to be one of the least active compounds of 29 pesticides tested.
9. EVALUATION OF RISKS FOR HUMAN HEALTH AND EFFECTS ON THE ENVIRONMENT
9.1. Evaluation of Health Risks For Man
The oral LD50 in rats ranged from 5000 - 14 700 mg/kg body weight. In the WHO Classification of Pesticides by Hazard, tetradifon was included in the category of technical products unlikely to present acute hazards in normal use (WHO, 1984). The formulated product may be more toxic, depending on other components of the formulation.
In experimental animals, most orally administered tetradifon is eliminated rapidly with the faeces.
A no-observed-adverse-effect level of 50 mg/kg diet was reported in a 90-day study on rats. At higher dose levels, the liver increased in weight, and induction of microsomal liver enzymes occurred. At levels exceeding 200 mg/kg, there was an increase in thyroid weight with histological changes. In 2-year studies on rats, dietary levels of 1200 mg/kg or more caused degenerative changes in the liver and kidneys.
No reproductive or teratogenic effects were found in a 2- generation reproduction study on rats. However, in a 90-day dietary study on the F2b offspring, there was a dose-related increased incidence of dilated renal pelvis.
In several short-term in vitro tests adopted to detect somatic mutagenicity, tetradifon showed a negative response. No information on the mutagenic effects on germ cells is available at present.
Adequate carcinogenicity studies are not available.
The general population is mainly exposed through food, but market-basket studies have shown that, at normal application rates of tetradifon as an acaricide, residues are virtually absent from food.
Under normal application conditions, it has been estimated that occupational exposure levels would be less than 0.01% of the dermal toxic dose per hour. No adverse health effects from exposure to tetradifon have been reported in man.
9.2. Evaluation of Effects on the Environment
Tetradifon is not toxic for Chlorella pyrenoidova. A single study reported the absence of toxic effects on papaya plants. The short-term toxicity of the compound is low for birds, moderate for fish, and moderate to high for aquatic crustacea. Tetradifon is
Page 19 of 30 Tetradifon (EHC 67, 1986)
relatively non-toxic for honey bees and its toxicity for other insects is low. However, it may synergize with insecticides to increase their insecticidal potency. Tetradifon does not bioaccumulate significantly in fish. No long-term toxicity data are available and, therefore, more subtle hazards cannot be adequately evaluated. On the basis of the data available, tetradifon does not present a short-term threat for the environment.
9.3. Conclusions
Notwithstanding the fact that the information available for this evaluation of tetradifon is incomplete and not always up to present-day standards, there are no indications, at present, that the normal recommended use of tested tetradifon products as an acaricide causes any health or safety hazards for the general population, exposed workers, or the environment.
10. RECOMMENDATIONS
1. More information is needed on metabolism, on the effects on reproduction, and on long-term toxic effects including carcinogenicity.
2. It is advised that the purity of the products registered and used be ascertained, since the contamination of the product by some chlorinated compounds may increase its toxicity.
11. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES
In the "Guidelines to the Use of the WHO Recommended Classification of Pesticides by Hazard" (WHO, 1984), tetradifon is classified in the list of technical products unlikely to present an acute hazard in normal use.
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RUTTER, H.A. (1982) A two-generation reproduction study on rats. Tedion. Addendum to final report, Vienna, Virginia, Hazleton Laboratories (Project No. 681-110) (Proprietary data for product registration purposes made available by Duphar BV to the IPCS).
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ANNEX EXTRACT FROM HEALTH AND SAFETY GUIDE INCLUDING INTERNATIONAL CHEMICAL SAFETY CARD
A1. HEALTH HAZARDS FOR MAN; PREVENTION AND PROTECTION; EMERGENCY ACTION
A1.1 Main Hazards for Man; Prevention and Protection; First Aid
The toxicity of technical tetradifon for man is thought to be low, and no adverse health effects from exposure to tetradifon have been reported. The toxicity and hazard of a formulation may largely depend on the vehicle used.
A1.1.1 Prevention and Protection
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In spite of the low toxicity and hazard of tetradifon, the following precautions should be observed during handling and use in order to reduce the risk of accidental contamination:
(a) Avoid contact with the skin and eyes. If eyes become contaminated, flush with water. If irritation persists, obtain medical attention.
(b) Wash hands and any exposed skin before eating, drinking, smoking, and after work.
(c) Avoid raising a dust cloud when handling wettable powder formulations.
(d) Avoid breathing dust from powder products.
(e) When unloading and handling containers, wear protective PVC or neoprene gloves.
(f) When handling leaking containers or when dealing with leaks and spills, wear overalls and PVC or neoprene gloves and boots. If overalls become contaminated, change and wash them thoroughly before re-use.
(g) Store products in original containers out of reach of children and away from food and feeding stuffs.
A1.1.2 First aid
Poisoning by tetradifon is unlikely unless there has been gross (negligent) exposure or intentional ingestion. In cases of overexposure, apply routine first aid measures.
If material has been spilled on the skin, immediately remove the patient from the source of the contamination, remove all contaminated clothing, and wash affected areas with soap and running water. If material is in the eyes, flush with clean water for at least 15 min. Keep patient prone and quiet. Start artificial respiration immediately if patient is not breathing.
Never give anything by mouth to an unconscious person.
In serious cases, medical attention should be sought.
A1.2 Advice to Physicians
The human toxicity of tetradifon is believed to be low. There is no specific antidote. Treat symptomatically when required. In cases of ingestion, gastric lavage may be indicated.
A1.3 Explosion and Fire Hazards and Precautions
Technical tetradifon is not highly flammable, but liquid formulations may be, depending on the solvent used.
Fight small fires with CO2, dry powder, or alcohol resistant foam. Confine the use of water spray to cooling of unaffected stock only, thus avoiding the accumulation of polluted run-off from the site.
Fire service personnel should be advised that self-contained breathing apparatus may be required, because noxious fumes may be generated through a fire.
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A1.4 Storage and Transport Precautions
All products should be stored in secure buildings, out of reach of children and animals, and also comply with any local transport regulations. Containers should be sound and well labelled.
A1.5 Spillage/Disposal Procedures
Keep spectators away from any leakage. Prevent contamination of other goods or cargo, or nearby vegetation and waterways.
Absorb spillage of liquid products with sawdust or sand, sweep up and place in separate container.
Empty any product remaining in damaged or leaking containers into a clean empty container, which should be suitably labelled.
Sweep up any spilt powder with damp sawdust taking care not to raise a dust cloud. Place in separate container for subsequent disposal.
Contaminated absorbents, used containers, surplus product, etc., should be burnt in an incinerator designed for pesticide disposal. When no incinerator is available, bury in an approved dump or in an area where there is no risk of contamination of ground or surface water. Comply with any local legislation applying to waste disposal.
A1.6 International Chemical Safety Card
This card should be easily available to all health workers concerned and to all users of tetradifon. It should be displayed at, or near, entrances to areas with potential exposure to tetradifon, on processing equipment, and on containers. The sheet should be translated into the appropriate language(s). All persons potentially exposed to the chemical should also have the instructions on the chemical safety card clearly explained.
A2. HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION
No effects on the environment have been reported for tetradifon.
A2.1 Precautionary Measures to Protect the Environment
Do not contaminate ponds, waterways, and ditches with product or used containers. Puncture empty containers.
A3. CURRENT REGULATIONS, GUIDELINES, AND STANDARDS
The information given in this section has been extracted from the International Register of Potentially Toxic Chemicals (IRPTC) legal file.
The file contains regulatory data on chemicals from 12 countries and recommendations issued by 6 international organizations.
The reader must be aware that regulatory decisions about chemicals taken in a certain country can only be fully understood in the framework of the legislation of that country. A full
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reference to the original national document from which the information was extracted can be obtained from the IRPTC.
When no effective date appears in the IRPTC legal file, the publication year of the national document from which the data are taken is mentioned; where appropriate, this is indicated by (r).
Sample International Chemical Safety Card for Tetradifon (technical) (2,4,5,4'-tetrachlorodiphenylsulfone; C12H6Cl4O2S) ------Physical properties Other charact ------Relative molecular mass 356.04 slightly yell Melting point 148 - 149 °C very stable n Water solubility (20 °C) 0.08% may emit toxi Density (20 °C) 1.515 to decomposit Octanol/water partition coefficient 4.61 Vapour pressure (20 °C) 0.32 x 10-10 kPa ------Hazard/symptom Prevention and protection First aid ------Skin: mild irritation neoprene gloves, face shield remove contami wash with ple Eyes: marginal irritant safety goggles, face shield flush with cle at least 15 m Inhalation: irritation of upper local exhaust ventilation; fresh air respiratory tract wear a dust mask
Ingestion: none observed unlikely professional hazard gastric lavage ------Spillage Storage Fire and expl ------Collect spillage in closed container store cool and dry in Fire: not flam or dust bin bag; in the case of original packing conditio liquid, first use absorbant material; Explosion: non clean up with water Fire extinguis
------Waste disposal ------Should be burnt in an incinerator designed for pesticide disposal ------A3.1 Exposure Limit Values
Some exposure limit values are given in Table A.1.
A3.2 Specific Regulatory Actions
In Czechoslovakia (effective date: 1981) and the United Kingdom (1983 (r)), the substance is approved as a pesticide or acaricide, and specified uses, limitations, and safety precautions are listed. In the USSR, the substance is approved as an insecticide for agricultural use and application; dose, mode, and treatment frequency are specified (effective date: 1982). In Sweden, the substance is an active ingredient in pesticide formulations that are registered at the products control board and therefore may be marketed and used. The formulations may be sold only to persons authorized to use such formulations (1984 (r)).
A3.3 Transport and Labelling
The United Nations Committee of Experts on the Transportation
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of Dangerous Goods classifies tetradifon as a poisonous substance (Class 6.1) presenting minor danger for packing purposes when the active ingredient constitutes 25 - 100% of the formulation (1982 (r)). The recommended label is:
Table A.1. Some exposure limit values ------Medium Specification Country Exposure limit description
------Food plant Argentina maximum residue limit meat, milk mint hops dried hops
Food plant (specified) Brazil acceptable limit (safety interval: 14 days)
Food plant (specified) Germany, Federal maximum residue limit Republic of
plant (general) maximum residue limit
Food food products Kenya maximum limit
Food fruit, vegetables Sweden maximum acceptable concentration
Food food products USA residue tolerance (specified)
raw agricultural acceptable residue limit products
Food food products USSR maximum residue limit (specified) ------
See Also: Toxicological Abbreviations Tetradifon (HSG 11, 1987) Tetradifon (ICSC)
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