General Description
White to off-white crystalline powder.
Reactivity Profile
SIMAZINE(122-34-9) is hydrolyzed by strong acids and alkalis .
Air & Water Reactions
Insoluble in water.
Potential Exposure
A potential danger to those involved in the manufacture, formulation, and application of this preemergence herbicide. Pesticide not in use; TRI and/or IUR indicates importers or manufacturers are unlikely. Banned for use in the EU.
Fire Hazard
Literature sources indicate that this chemical is nonflammable.
First aid
If this chemical gets into the eyes, remove any contact lenses at once and irrigate immediately for at least 15 minutes, occasionally lifting upper and lower lids. Seek medical attention immediately. If this chemical contacts the skin, remove contaminated clothing and wash immediately with soap and water. Seek medical attention immediately. If this chemical has been inhaled, remove from exposure, begin rescue breathing (using universal precautions, including resuscitation mask) if breathing has stopped and CPR if heart action has stopped. Transfer promptly to a medical facility. When this chemical has been swallowed, get medical attention. Give large quantities of water and induce vomiting. Do not make an unconscious person vomit.
Shipping
UN3077 Environmentally hazardous substances, solid, n.o.s., Hazard class: 9; Labels: 9-Miscellaneous hazardous material, Technical Name Required. UN2763 Triazine pesticides, solid, toxic, Hazard Class: 6.1; Labels: 6.1-Poisonous materials.
Incompatibilities
Powder may form explosive mixture with air. Incompatible with strong oxidizers (chlorates, nitrates, peroxides, permanganates, perchlorates, chlorine, bromine, fluorine, etc.); contact may cause fires or explosions. Keep away from alkaline materials, strong bases, strong acids, oxoacids, epoxides.
Description
While compounds exhibiting estrogen mimicry are structurally
diverse, they share common properties such as retention in
body fat deposits (highly lipophilic), ability to cross the
placental barrier, transport in blood usually unbound to
specialized serum proteins (e.g., steroid hormone binding
globulin, SHBG/TeBG), and their affinity for the estrogenreceptor
protein. If the environmental compound impersonates
estrogen sufficiently, it associates with the estrogen-receptor
protein and either disrupts the action of the native hormone or
communicates activities similar to estrogen (i.e., antagonistic or
agonistic activities). Association between a xenoestrogen and
the estrogen receptor (ER), characterized by a wide range of
affinities, is reversible and saturable. No metabolism of the ligand occurs when it is bound to the receptor protein. In
addition to the phenotypic expression of gender, estrogens and
their mimics may influence development and physiological
processes in many organs of the body, particularly the reproductive
tract, as well as the central nervous system and skeleton.
It is obvious that fragile, biological events occurring during
ovulation, pregnancy, fetal development, and lactation could
easily be influenced by xenoestrogens with endocrine disruptor
compound (EDC) activities, which mimic naturally occurring
hormones.
With a variety of sensitive, rapid assays, xenoestrogens now
may be detected and activities assessed by ER proteins. The
range of techniques available includes both cell-free and
whole-cell-based assays:
1. Rat uterine cytosol preparations containing ERs (a cell-free
assay using radiolabeled ligand);
2. Recombinant human ER proteins produced by a bacteria,
yeast, or baculovirus-infected insect cell system (cell-free
assays using radiolabeled ligand);
3. A yeast cell system containing recombinant human ER and
a reporter gene (yeast whole-cell assay);
4. The LUMI-CELL ER transcriptional activation assay
(BG1Luc ER TA, a mammalian whole-cell assay); and
5. MCF7 cell proliferation assay (E-SCREEN assay) and modifications
of this method (mammalian whole-cell assay).
Additionally, certain investigations are focused on differential
recognition of EDCs by ER isoforms separated by highperformance
liquid chromatography.
Waste Disposal
Strong acid or alkaline hydrolysis leads to complete degradation of simazine. However,large quantities of simazine should be incinerated in a unit operating @ 850℃ equipped with off-gas scrubbing equipment. In accordance with 40CFR165, follow recommendations for the disposal of pesticides and pesticide containers. Must be disposed properly by following package label directions or by contacting your local or federal environmental control agency, or by contacting your regional EPA office.
Definition
ChEBI: A diamino-1,3,5-triazine that is N,N'-diethyl-1,3,5-triazine-2,4-diamine substituted by a chloro group at position 6.
Production Methods
Simazine is prepared by reacting two equivalents of ethylamine
in the presence of an acid acceptor. It is stable in neutral
and slightly basic or acidic media, but is hydrolyzed by
stronger acids and bases especially at higher temperatures.
Primary exposures occur during application, not during
production, and include both inhalation and dermal components.
Health Hazard
Inconsistent data in the literature; oral LD50values in rats reported as 970 and 5000 mg/L,showing a wide difference; toxicity is of loworder.
Agricultural Uses
Pre-emergence herbicide, Algaecide: and ornamental crops, turf grass, orchards, and vineyards. At higher rates, it is used for non-selective weed control in industrial areas. Before 1992, simazine was used to control submerged weeds and algae in large aquariums, farm ponds, fish hatcheries, swimming pools, ornamental ponds, and cooling towers. Simazine is available in wettable powder, waterdispersible granule, liquid, and granular formulations. It may be soil-applied. Not approved for use in EU countries. A U.S. EPA restricted Use Pesticide (RUP) for all land uses because of its potential to contaminate ground water
Trade name
AKTINIT S®; ALCO® Simizine; AQUAZINE®; ATLAS SIMAZINE®; BATAZINA®; BITEMOL®; CALIBER®; CDT®; CEKUSAN®; CEKUZINA-S®; FRAMED®; G 27692®; GEIGY 27692®; GESARAN®; GESATOP®; GESATOP-50®; H 1803®; HARLEQUIN®; HERBAZIN® 500 BR; HERBAZIN® 50; HERBEX®; HERBOXY®; HUNGAZIN DT®; OXON ITALIA SIM-TROL®; PREMAZINE®; PRIMATEL S®; PRIMATOL S®; PRINCEP®; PRINCEP® 80W; SIMADEX®; SIMANEX®; SIMAZINE® 80W; SIMAZAT®; SIM-TROL®; TAFAZINE®; TAFAZINE® 50-W; TANZINE®; TAPHAZINE®; TOTAZINE®; TRIAZINE A 384®; W 6658®; WEEDEX®; ZEAPUR®
Carcinogenicity
No tumorigenic response was
seen in mice treated orally at doses ranging from 75 to
215mg/kg. In a 2-year feeding study in rats, 100 ppm
produced mammary tumors. Sarcomas at the injection
sitewere produced in another study ofboth rats and mice.
Simazinewas fedtoratsatdoselevelsequivalent to 0,0.5,5,and
50mg/kg for 2 years.Bodyweight and hematological changes
were seen primarily at the highest dose. After 24 months at
50mg/kg, an increase in ovarian atrophy and Sertoli cell
hyperplasia were seen. Increases in mammary gland tumors
were seen in females at 50mg/kg.
Environmental Fate
Soil. The reported half-life in soil is 75 days (Alva and Singh, 1991). Under laboratory
conditions, the half-lives of simazine in a Hatzenbühl soil (pH 4.8) and Neuhofen soil (pH
6.5) at 22°C were 45 and 100 days, respectively (Burkhard and Guth, 1981).
The half-lives for simazine in soil incubated in the laboratory under aerobic conditions
ranged from 27 to 231 days (Zimdahl et al., 1970; Beynon et al., 1972; Walker, 1976,
1976a). In field soils, the disappearance half-lives were lower and ranged from 11 to 91
days (Roadhouse and Birk, 1961; Clay, 1973; Joshi and Datta, 1975; Marriage et al., 1975).
Groundwater. According to the U.S. EPA (1986) simazine has a high potential to leach
to groundwater.
Plant. Simazine is metabolized by plants to the herbicidally inactive 6-hydroxysimazine which is further degraded via dealkylation of the side chains and hydrolysis of
the amino group releasing carbon dioxide (Castelfranco et al., 1961; Humburg et al., 1989).
Photolytic. Pelizzetti et al. (1990) studied the aqueous photocatalytic degradation of
simazine and other s-triazines (ppb level) using simulated sunlight (λ >340 nm) and
titanium dioxide as a photocatalyst. Simazine rapidly degraded forming cyanuric acid,
nitrates and other intermediate compounds similar to those found for atrazine. Mineralization of cyanuric acid to carbon dioxide was not observed (Pelizzetti et al., 1990). In
aqueous solutions, simazine is converted exclusively to hydroxysimazine by UV light (λ
= 253.7 nm). The UV irradiation of methanolic solutions of simazine afforded simetone
(2-methoxy-4,6-bis(ethylamino-s-triazine). Photodegradation of simazine in methyl alcohol did not occur when irradiated at wavelengths >300 nm (Pape and Zabik, 1970).
Chemical/Physical. Emits toxic fumes of nitrogen oxides and chlorine when heated
to decomposition (Sax and Lewis, 1987). In the presence of hydroxy or perhydroxy radicals
generated from Fenton’s reagent, simazine undergoes dealkylation to give 2-chloro-4,6-
diamino-s-triazine as the major product (Kaufman and Kearney, 1970).
Toxicity evaluation
With regard to estrogen-associated toxicity, the primary
mechanism appears to be via association with the estrogen receptor proteins (ERa and ERb) and subsequent alteration in
the signal transduction pathway. While largely acting as
estrogen antagonists, some xenoestrogens (e.g., diethylstilbestrol
(DES)) may act as agonists at low doses and antagonists at
elevated doses. Furthermore, compounds such as DES are
classified as an EDC since it may promote transgenerational
effects, including development of clear cell adenocarcinoma of
the vagina in daughters of mothers administered DES as
a therapeutic.
Many studies of toxicokinetics suggest the difficulty in
extrapolating quantitative structure–activity relationships
(QSARs) of particular compounds with their influence on
biological responses (e.g., reproduction, neuroendocrine behavior).
Several compounds classified as xenoestrogens (BPA
and BBP) are reported to have estrogenic activity, although the
concentrations required in vitro for the effects and those doses
given in vivo to animal models are significantly higher than the
estimated doses observed in human exposure. The variety of ERbased
tests for assessing QSARs of diverse xenoestrogens cannot
address the effects of long-term exposure to low doses of these
compounds. In addition, factors such as age at exposure and
mixtures of compounds influence latent effects of chronic
exposure. However, QSAR models using results from ER-based
tests are used for chemical risk management and development
of regulatory practices.
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