<unk>  is alleged to be responsible for many fatal pesticide poisoning incidents around the world by NGOs opposing pesticide usage.<unk>  is also a xenoestrogen—a synthetic substance that imitates or enhances the effect of estrogens—and it can act as an endocrine disruptor, causing reproductive and developmental damage in both animals and humans. It has also been found to act as an aromatase inhibitor. Whether<unk>  can cause cancer is debated. With regard to consumers' intake of<unk>  from residues on food, the Food and Agriculture Organization of United Nations has concluded that long-term exposure from food is unlikely to present a public health concern, but short-term exposure can exceed acute reference doses. Toxicity<unk>  is acutely neurotoxic to both insects and mammals, including humans. The US EPA classifies it as Category I: "Highly Acutely Toxic" based on a LD50 value of 30 mg/kg for female rats, while the World Health Organization classifies it as Class II "Moderately Hazardous" based on a rat LD50 of 80 mg/kg. It is a GABA-gated chloride channel antagonist, and a Ca2+, Mg2+ ATPase inhibitor. Both of these enzymes are involved in the transfer of nerve impulses. Symptoms of acute poisoning include hyperactivity, tremors, convulsions, lack of coordination, staggering, difficulty breathing, nausea and vomiting, diarrhea, and in severe cases, unconsciousness. Doses as low as 35 mg/kg have been documented to cause death in humans, and many cases of sublethal poisoning have resulted in permanent brain damage. Farm workers with chronic<unk>  exposure are at risk of rashes and skin irritation. EPA's acute reference dose for dietary exposure to<unk>  is 0.015 mg/kg for adults and 0.0015 mg/kg for children. For chronic dietary expsoure, the EPA references doses are 0.006 mg/(kg·day) and 0.0006 mg/(kg·day) for adults and children, respectively. Endocrine disruption Theo Colborn, an expert on endocrine disruption, lists<unk>  as a known endocrine disruptor, and both the EPA and the Agency for Toxic Substances and Disease Registry consider<unk>  to be a potential endocrine disruptor. Numerous in vitro studies have documented its potential to disrupt hormones and animal studies have demonstrated its reproductive and developmental toxicity, especially among males. A number of studies have documented that it acts as an antiandrogen in animals.<unk>  has shown to affect crustacean molt cycles, which are important biological and endocrine-controlled physiological processes essential for the crustacean growth and reproduction. Environmentally relevant doses of<unk>  equal to the EPA's safe dose of 0.006 mg/kg/day have been found to affect gene expression in female rats similarly to the effects of estrogen. It is not known whether<unk>  is a human teratogen (an agent that causes birth defects), though it has significant teratogenic effects in laboratory rats. A 2009 assessment concluded the endocrine disruption in rats occurs only at<unk>  doses that cause neurotoxicity. Reproductive and developmental effects Some studies have documented that<unk>  can also affect human development. Researchers studying children from many villages in Kasargod District, Kerala, India, have linked<unk>  exposure to delays in sexual maturity among boys.<unk>  was the only pesticide applied to cashew plantations in the villages for 20 years, and had contaminated the village environment. The researchers compared the villagers to a control group of boys from a demographically similar village that lacked a history of<unk>  pollution. Relative to the control group, the exposed boys had high levels of<unk>  in their bodies, lower levels of testosterone, and delays in reaching sexual maturity. Birth defects of the male reproductive system, including cryptorchidism, were also more prevalent in the study group. The researchers concluded, "our study results suggest that<unk>  exposure in male children may delay sexual maturity and interfere with sex hormone synthesis." Increased incidences of cryptorchidism have been observed in other studies of<unk>  exposed populations. A 2007 study by the California Department of Public Health found that women who lived near farm fields sprayed with<unk>  and the related organochloride pesticide dicofol during the first eight weeks of pregnancy are several times more likely to give birth to children with autism. However a 2009 assessment concluded that epidemiology and rodent studies that suggest male reproductive and autism effects are open to other interpretations, and that developmental or reproductive toxicity in rats occurs only at<unk>  doses that cause neurotoxicity. Cancer<unk>  is not listed as known, probable, or possible carcinogen by the EPA, IARC, or other agencies. No epidemiological studies link exposure to<unk>  specifically to cancer in humans, but in vitro assays have shown that<unk>  can promote proliferation of human breast cancer cells. Evidence of carcinogenicity in animals is mixed. In a 2016 study by the Department of Biochemistry, Indian Institute of Science, Bangalore published in Carcinogenesis,<unk>  was found to induce reactive oxygen species (ROS) in a concentration and time-dependent manner leading to double-stranded breaks in the DNA and also found to favour subsequent erroneous DNA repair.
Endosulfan
Palifermin
Povidone-iodine
Aquamid
Mecasermin
Treosulfan
Amylmetacresol
Lisocabtagene maraleucel