<unk>  is a moderately toxic compound, falling in EPA toxicity class II.<unk>  does not cause reproductive toxicity and it is not likely to cause teratogenic effects, but the available data is not sufficient to draw a firm conclusion about the carcinogenicity of<unk> . The primary target organ for<unk>  is the nervous system. Using the Margin of Exposure (MOE) approach to assess the risk of<unk> , the EPA deemed that there is little to no concern of<unk>  having an MOE at or above 100. The primary toxicological endpoint of concern to the EPA is cholinesterase inhibition; a common toxic effect of organophosphate poisoning. The table below shows the no observed adverse effect level (NOAEL) and lowest observed adverse effect level (LOAEL) of short and long-term exposure in rats. NOAEL LOAEL Short-term 15 mg/kg/day 22.5 mg/kg/day Long-term 1.1 mg/kg/day 1.8 mg/kg/day Fetal health Research on<unk> ’s (and other organophosphate/chlorine insecticides) effect on the placenta indicate that<unk>  has been found to enter the placenta and carryover to the fetus. In addition, the compound has been shown to decrease PI 4-kinase activity in the nucleus, but has no effect on membrane PI 4-kinase. Affecting PI 4-kinase activity suggests detrimental effects on different processes regulated by 4-phosphoinositides. However, more research is needed on the consequences of<unk>  and other organophosphates on placenta physiopathology. In vitro studies have shown<unk>  induces apoptosis in trophoblasts, through oxidative stress. Endocrine system Estrogens<unk>  has been found to give positive results in aromatase inhibition assays, indicating<unk>  decreases aromatase activity. Androgens<unk>  gives positive results in androgen receptor binding assays, this indicates that<unk>  binds to androgen receptors. More research is needed to find the physiological effects of aromatase inhibition and androgen receptor binding.
Phosmet
Cerate
Phosphate
Selenous acid
SeHCAT
Hydrogen fluoride
Biotin
Phosphine