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IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Occupational Exposures in Insecticide Application, and Some Pesticides. Lyon (FR): International Agency for Research on Cancer; 1991. (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 53.)

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Occupational Exposures in Insecticide Application, and Some Pesticides.

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Simazine

1. Exposure Data

1.1. Chemical and physical data

1.1.1. Synonyms, structural and molecular data

  • Chem. Abstr. Serv. Reg. No.: 122-34-9
  • Replaced CAS Reg. Nos: 11141-20-1; 12764-71-5; 39291-64-0; 119603-94-0 Chem Abstr. Name:6-Chloro-N,N′-diethyl-l,3,5-triazine-2,4-diamine
  • IUPAC Systematic Name: 6-Chloro-N2,N4-diethyl-l,3,5-triazine-2,4-diamine Synonyms: 4,6-Bis(ethylamino)-2-chlorotriazine; 2,4-bis(ethylamino)-6-chloro-s-tria-zine; 2-chloro-4,6-bis(ethylamino)-s-triazine
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1.1.2. Chemical and physical properties

1.1.3. Trade names, technical products and impurities

Some examples of trade names are: Aktinit S; Aquazine; Azotop; Bitemol S 50; CAT; CDT; CET; Geigy 27,692; Gesatop; H 1803; Herbazin; Herbex; Herbatoxol S; Herboxy; Hungazin DT; Premazine; Princep; Radocon; Radokor; Simanex; Simatsin-neste; Simazin; Symazine; Tafazine; Taphazine; Triazine A 384; W 6658; Yrodazin

Simazine is registered in the USA as a technical material with 95–99.9% active ingredient (US Environmental Protection Agency, 1984b). It is available there in wettable powder, granular, liquid, flowable concentrate, soluble concentrate and dry flowable forms. The usual carrier is water, oil or clay (US Environmental Protection Agency, 1984a). In Europe, it is available as dustable powders, emulsifiable concentrates, liquid creams, granules, microgranules, suspension concentrates, soluble concentrates, ultra-low volume suspensions, water-dispersible granules and wettable powders (Royal Society of Chemistry, 1986). In the USSR, simazine is manufactured as a wettable powder or dust (Izmerov, 1983).

Simazine can be formulated with most other herbicides and fertilizers (Royal Society of Chemistry, 1986,1989). It is formulated in the USA in combination with amitrole (see IARC, 1987a), atrazine (see monograph, p. 441), prometen, trietazine, sodium chlorate and sodium metaborate (Anon., 1989; Meister, 1990). It has also been formulated in various countries in combination with metoxuron, diquat, sodium trichloroacetate, secbumeton, MCPA (see IARC, 1987b), ametryne, paraquat dichloride, diquat dichloride, paraquat dibromide, sodium 2-(2,4-dichlorophenoxy)ethyl sulfate, 2,4-D (see IARC, 1987b), diuron, propyzamide, nonflurazon, dalapon sodium and picloram (Worthing & Walker, 1987).

1.1.4. Analysis

Selected methods for the analysis of simazine in various matrices are given in Table 1.

Table 1.. Methods for the analysis of simazine.

Table 1.

Methods for the analysis of simazine.

1.2. Production and use

1.2.1. Production

Simazine was first introduced in 1957 (US Environmental Protection Agency, 1984a). It is produced by the reaction of cyanuric chloride and monomethylamine in water or aqueous acetone (Izmerov, 1983).

It is produced currently by four companies in Israel, Switzerland and the USA (Meister, 1990). Estimated production in 1978–80 in the USA was approximately 5000 tonnes per annum, of which about 1000 tonnes were exported (Vlier Zygadlo, 1982). A major US producer reported producing an average of 4000 tonnes per annum in 1981–84 and an average of 8000 tonnes per annum in 1985–89.

1.2.2. Use

Simazine is a pre-emergent systemic herbicide that inhibits photosynthesis. It has been used for the control of germinating annual grasses and broad-leaved weeds in a variety of vegetables and fruit, turf and ornamental plants, and in forestry (Meister, 1990); its major use is on maize (US Environmental Protection Agency, 1984b). It is also used for total weed control on non-crop land and as an aquatic herbicide and algicide for control of algae and submerged weeds in ponds (Royal Society of Chemistry, 1989).

Methods of application include broadcast, band, soil incorporated and soil surface using ground or aerial equipment (US Environmental Protection Agency, 1984a). It is also registered for use in the USA in swimming pools, ponds and cooling towers (US Environmental Protection Agency, 1984b).

It was estimated that in the USA during the period 1978–80, yearly usage of simazine (active ingredient) was as follows: maize, 1000–1300 tonnes; aquatic uses, 700–900 tonnes industrial sites, 600–800 tonnes; grapes, 220–290 tonnes; oranges, 220–290 tonnes; apples, 100–120 tonnes; and various other fruits, 300 tonnes (Vlier Zygadlo, 1982).

In the USSR, simazine is used on vineyards, strawberries and winter wheat sowings; it is also used to suppress couchgrass, Bermuda grass and some other perennial weeds (Izmerov 1983).

1.3. Occurrence

1.3.1. Water

Simazine has been found in groundwater in California, Pennsylvania and Maryland, USA, at levels in the range of 0.2 to 3.0 µg/1. It was found in 922 of 5873 surface water samples and 202 of 2654 groundwater samples in the USA. The 85th percentile was 2.18 µg/1 in surface water and 1.60 ug/1 in groundwater; the maximal concentration in surface water was 1.3 mg/1 and that in groundwater, 0.8 mg/1. Simazine was found in surface water in 16 states and in groundwater in eight states (US Environmental Protection Agency, 1988a).

Simazine did not hydrolyse in sterile aqueous solutions buffered at pH 5, 7 or 9 at 20 °C, over a 28-day test period. Dissipation studies in pond and lake water with simazine gave variable results, with half-times ranging from 50 to 700 days. 2-Chloro-4-ethylamino-6-amino-s-triazine was identified in lake water but was no more persistent than simazine (US Environmental Protection Agency, 1988a).

1.3.2. Soil

The half-time of simazine varies depending on the soil microbial population, moisture, temperature and farming practice. Under aerobic conditions, the degradation of simazine in soil depends largely on the soil moisture and temperature (Walker, 1976). In a sandy loam soil, half-times ranged from 36 to 234 days. When applied to a loamy sand and silt loam soils and incubated (25–30 °C) for 48 weeks, simazine dissipated with half-times of 16.3 and 25 5 weeks, respectively. Under anaerobic conditions, 14C-simazine had a half-time of 8–12 weeks in a loamy sand soil. Degradation products included 2-chloro-4-ethylamino-6-amino-s-triazine, 2-chloro-4,6-bis(amino)-s-triazine, 2-hydroxy-4,6-bis(ethylamino)-s-triazine and 2-hydroxy-4-ethylamino-6-amino-s-triazine (US Environmental Protection Agency, 1988a).

Studies of column leaching and adsorption/desorption indicated that simazine would be expected to be slightly to very mobile in soils ranging in texture from clay to sandy loam. Its adsorption was correlated with the content of organic matter in the soil and to a lesser degree with the cation exchange capacity and clay content (US Environmental Protection Agency 1988a).

In field studies, simazine had a half-time of about 30–139 days in sandy loam and silt loam soils (US Environmental Protection Agency, 1988a). In a study with four New Zealand soils, with acid pH (5.4–5.5) and organic carbon levels of 4.6 and 9.4%, the half-times were 25 and 32 days, respectively (Rahman & Holland, 1985).

Field studies with simazine on Taichung (Taiwan) clay loam in different seasons and Taipei loam soils showed a significant effect of climate on degradation rate. Simazine had a half-time of 18 days in summer and 24 days in winter at Taichung; the more moderate temperature and precipitation of the autumn in Taipei resulted in a half-time of 14 days (Chen et al., 1983).

1.3.3. Food

In the national surveillence programme in Canada, 1664 samples were analysed for simazine during the period 1984/85 to 1988/89. No residue was detected in fruit, meat, vegetables or wine (Government of Canada, 1990). No simazine residue (< 0.05 ppm [mg/kg]) was reported in a survey of 19 851 samples of various foods and feeds in the USA over 1982–86 (Luke et al., 1988).

1.4. Regulations and guidelines

WHO (1987) recommended a drinking-water guideline of 17 µg/1 for simazine. The maximal allowable concentration of simazine in drinking-water in Canada is 10 µg/1 (Ritter & Wood, 1989). The US Environmental Protection Agency proposed to establish the ‘maximal contaminant level’ (feasible and enforceable limits to protect public health) and ‘maximal contaminant level goal’ (desirable but not enforceable) for simazine at 1 µg/l (Anon., 1990).

In the USSR, the maximal allowable concentration of simazine in workplace air is 2 mg/m3. The single and mean daily maximal allowable concentration in the atmosphere of residential areas is 0.02 mg/m3 (Izmerov, 1983).

National pesticide residue limits for simazine in food are presented in Table 2.

Table 2.. National pesticide residue limits for simazine in foods.

Table 2.

National pesticide residue limits for simazine in foods.

Tolerances are established for residues of simazine in sugar-cane byproducts (molasses and syrup and molasses intended for animal feed), resulting from application of the herbicide to growing sugar-cane, at 1 ppm (mg/kg); that for combined residues of simazine and its metabolites (2-amino-4-chloro-6-ethylamino-s-triazine and 2,4-diamino-6-chloro-s-triazine) in potable water when present therein as a result of application of the herbicide to growing aquatic weeds is 0.01 ppm (mg/kg) (US Environmental Protection Agency, 1989d,e).

2. Studies of Cancer in Humans

One case-control study that suggested an association between ovarian cancer and exposure to herbicides in Italy mentioned simazine among the triazine herbicides to which subjects were exposed (Donna et al., 1989) (see monograph on atrazine, p. 449).

3. Studies of Cancer in Experimental Animals1

The Working Group was aware of studies by the US National Technical Information Service (1968), Innes et al. (1969) and Pliss and Zabezhinsky (1970), in which simazine was tested in mice or rats by oral or subcutaneous administration and in mice by skin application. These studies were considered to be uninformative for an evaluation of carcinogenicity.

4. Other Relevant Data

4.1. Absorption, distribution, metabolism and excretion

4.1.1. Humans

No data were available to the Working Group.

4.1.2. Experimental systems

The primary route of metabolism of simazine in rats, rabbits and other species in vivo and in vitro is N-dealkylation (Böhme & Bär, 1967; Adams et al., 1990). [The Working Group noted that, while minor metabolites (other than some oxidation products of the alkyl side-chains) have not been identified, it is probable that the aromatic chlorine group is a site for glutathione conjugation, as occurs with atrazine (Timchalk et al., 1990).]

Simazine is readily nitrosated by nitrogen oxides at an air:solid interface (Janzowski et al., 1980).

4.2. Toxic effects

4.2.1. Humans

Simazine has been implicated as a cause of occupational contact dermatitis (Elizarov, 1972).

4.2.2. Experimental systems

The oral LD50 was reported to be > 5000 mg/kg bw in rats (Ben-Dyke et al., 1970) and 973, 971 and 2367 mg/kg bw in adult female, male and weanling male rats, respectively. The dermal LD50 was > 2500 mg/kg bw in rats of each sex (Gaines & Linder, 1986). The lethal single dose of simazine in sheep has been estimated at 500 mg/kg bw (Hapke, 1968).

The liver and biliary system were identified as the targets for toxicity in rats given simazine by gavage at 15 mg/kg bw per day for three or 28 days (Olędzka-Sfotwinska, 1974). Hypothyroidism was the most sensitive indicator of simazine toxicity in sheep at daily dose rates of 1.4–6 mg/kg bw; higher doses produced frank goitres and diffuse hepatic and cerebral damage. Necrotic and dystrophic changes of the testicular germinal epithelium were noted in rams given 6–25 mg/kg bw per day (Dshurov, 1979).

4.3. Reproductive and prenatal effects

4.3.1. Humans

No data were available to the Working Group.

4.3.2. Experimental systems

Simazine perturbed development of gonads in ovo and in vitro and reduced fertility in chicks and quail (Didier & Lutz-Ostertag, 1972). [The Working Group noted that doses and concentrations were not clearly defined.] It was reported in an abstract that simazine administered at 2.0 and 20 ppm (mg/kg) in the diet to laying mallard ducks throughout the egg production cycle caused no reproductive impairment (Fink, 1975).

Inhalation by rats of simazine at concentrations of up to 317 mg/m3 on days 7–14 of gestation resulted in no developmental toxicity (Dilley et al., 1977, abstract; Newell & Dilley, 1978). In contrast, a Bulgarian triazine herbicide (Polyzin 50) [impurities unspecified] was embryotoxic when pregnant rats were exposed by inhalation to 2 mg/m3 in air; it was teratogenic following exposure to 0.2 and 2 mg/m3 throughout pregnancy and to 2 mg/m3 during the first trimester of pregnancy. Postnatal liver insufficiency occurred in the offspring (Mirkova & Ivanov, 1981). [The Working Group noted that the apparent discrepancy in effects between these studies might be due to unspecified impurities in the latter study.]

Administration of simazine to rats during the organogenetic period (gestational days 6–15) caused embryolethality at > 312 mg/kg bw, decreased fetal body weight at 2500 mg/kg bw and retarded ossification at > 78 mg/kg bw. No teratogenic effect was observed (Chen et al., 1981).

4.4. Genetic and related effects (see also Table 3 and Appendices 1 and 2)

Table 3.. Genetic and related effects of simazine.

Table 3.

Genetic and related effects of simazine.

4.4.1. Humans

No data were available to the Working Group.

4.4.2. Experimental systems

Simazine did not induce gene mutation in bacteria or in Saccharomyces cerevisiae, whereas there were mixed responses in mutation assays with plants. Simazine induced sex-linked recessive lethal mutation in Drosophila melanogaster.

Mutations were induced at the tk locus in mouse lymphoma L5178Y cells, but DNA damage, as indicated by unscheduled DNA synthesis, was not induced in cultured human fibroblasts.

Neither gene conversion nor mitotic recombination was induced in S. cerevisiae or aneuploidy in Neurospora crassa. Chromosomal aberrations were induced consistently in plants.

Dominant lethal effects, but not aneuploidy, were induced in D. melanogaster in a single study.

In a single study with cultured human lymphocytes, simazine induced a small increase in the frequency of sister chromatid exchange, but it had no such effect in cultured Chinese hamster cells, even at very high concentrations.

It did not induce micronucleus formation in bone-marrow cells of mice in vivo.

5. Summary of Data Reported and Evaluation

5.1. Exposure data

Simazine was introduced in 1957 as a systemic herbicide for use on grasses and weeds in food crops, especially maize, and for general weed control. It is available in many types of formulation, including wettable powders, granules, concentrates, suspensions and liquids. Exposure can occur during its production and application and via contamination of ground-and surface water.

Exposure could also occur through consumption of foods containing residues. Simazine residues were not detected in large-scale surveys of food products in Canada and the USA.

5.2. Carcinogenicity in humans

No adequate data were available to the Working Group.

5.3. Experimental carcinogenicity data

No adequate data were available to the Working Group.

5.4. Other relevant data

No data on the genetic and related effects of simazine in humans were available to the Working Group.

Simazine did not induce micronucleus formation in mice. It induced a small increase in the frequency of sister chromatid exchange in human cells in vitro but not in rodent cells. Simazine did not induce genetic damage in any other tests, except in plants where chromosomal aberrations were induced and in Drosophila melanogaster where dominant lethal effects and gene mutation were induced.

5.5. Evaluation1

There is inadequate evidence in humans for the carcinogenicity of simazine.

There is inadequate evidence in experimental animals for the carcinogenicity of simazine.

Overall evaluation

Simazine is not classifiable as to its carcinogenicity to humans (Group 3).

6. References

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Footnotes

1

Calculated from: mg/m3= (molecular weight/24.45) × ppm, assuming standard temperature (25°C) and pressure (760 mm Hg [101.3 kPa])

1

The Working Group was aware of a study in progress in rats in which simazine was administered by oral administration (IARC, 1990).

1

For definition of the italicized terms, see Preamble, pp. 26–28.

©International Agency for Research on Cancer, 1991.
Bookshelf ID: NBK499646
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