Several studies indicate pyrethroids disrupt the endocrine system by mimicking the effects of the female hormone estrogen. This in turn can cause breast cancer in women and lowered sperm counts in men. When estrogen levels are elevated, old cells are not removed from the body and cell proliferation occurs, whether benign or malignant.
Mount Sinai School of Medicine: This study examined four pyrethroid pesticides, including sumithrin. It concludes "Overall, our studies imply that each pyrethroid compound is unique in its ability to influence several cellular pathways. These findings suggest that pyrethroids should be considered to be hormone disruptors, and their potential to affect endocrine function in humans and wildlife should be investigated." [Environmental Health Perspectives, vol. 107, no. 3, March 1999, pages 173-177.]
The Roger Williams General Hospital, Brown University: This study on pyrethroids concludes "Chronic exposure of humans or animals to pesticides containing these compounds may result in disturbances in endocrine effects." [Journal of Steroid Biochemistry, March 1990, volume 35, issue 3-4, pages 409-414.]
Cambridge University: A report issued in June 2000 by the Royal Society in England and written by a group from Cambridge University called for international cooperation to deal with the dangers posed by endocrine-disrupting chemicals, including pyrethroids, and recommends reducing human exposure to these chemicals.
University of Greifswald: Several pesticides used as herbicides, insecticides and fungicides known to be endocrine disrupting chemicals were examined in this series of German studies. Acute and chronic pesticide exposure led to changes in sex hormone concentrations, with concentrations of testosterone decreasing one day after acute exposure. These studies found "a hormonal and immune suppression after acute exposure." ["Disruption of male sex hormones with regard to pesticides," Toxicology Letters, June 30, 1999;107(1-3):225-31 ]
A study of pesticides and childhood brain cancers has revealed a strong relationship between brain cancers and compounds used to kill fleas and ticks, according to a report published in Environmental Health Perspectives. The study concludes "The specific chemicals associated with children's brain cancers were pyrethrins and pyrethroids (which are synthetic pyrethrins, such as permethrin, tetramethrin, allethrin, resmethrin and fenvalerate) and chlorpyrifos (trade name: Dursban)." [Janice M. Pogoda and Susan Preston-Martin, "Household Pesticides and Risk of Pediatric Brain Tumors," Environmental Health Perspectives, vol. 105, no. 11 (November 1997), pages 1214-1220.] The EPA, in June 2000, halted sales of Dursban.
Several studies have indicated neurological damage resulting from exposure to pyrethroids, and some of the damages have been found to be long term.
Ludwig Maximilians University: This study, conducted by the Physiological Institute at Ludwig Maximilians University in Munich, Germany, found that although "a majority of complaints following an acute pyrethroid intoxication disappeared after the end of exposure," several effects were still seen in patients after more than two years. Among these long-term symptoms were "(1) cerebro-organic disorders (reduced intellectual performance with 20%-30% reduction of endurance during mental work, personality disorder), visual disturbances, dysacousia, tinnitus; (2) sensomotor-polyneuropathy, most frequently in the lower legs; (3) vegetative nervous disorders," including increased heat-sensitivity and reduced exercise tolerance due to circulatory disorder. The study concludes "Many of these patients exhibit pathological autoimmune diagnostical findings and developed autoimmune diseases." [Toxicology Letters, 1999 June 30;107(1-3):161-76.]
Uppsala University: This study, conducted by the Department of Environmental Toxicology at Uppsala University in Sweden studied mice, not humans, but found that "low-dose exposure" to pyrethroids "resulted in ³irreversible changes in adult brain function in the mouse" when exposed during the growth period. This occurred at levels of exposure less than what was found to affect adult mice. The study also found "neonatal exposure to a low dose of a neurotoxic agent can lead to an increased susceptibility in adults to an agent having a similar neurotoxic action, resulting in additional behavioral disturbances and learning disabilities." [Neurotoxicology, 1997;18(3):719-26.]
Northwestern University Medical School: A series of investigations conducted at Northwestern's Department of Molecular Pharmacology and Biological Chemistry in Chicago, has found neurological damage from pyrethroids. One study, conducted by international expert Toshio Narahashi, finds nervous-system damage from pyrethroids to be comparable to DDT. This study found that "Detailed voltage clamp and patch clamp analyses have revealed that pyrethroids and DDT modify the sodium channel to remain open for an extended period of time." The result of this damage is "potent effects on the nervous system." ["Nerve membrane ion channels as the target site of environmental toxicants," Environmental Health Perspectives,1987 April;71:25-9.]. A separate study found that pyrethroids cause "membrane depolarization, repetitive discharges and synaptic disturbances leading to hyperexcitatory symptoms of poisoning in animals." This study found that only 1% "of sodium channel population is required to be modified by pyrethroids to produce severe hyperexcitatory symptoms." ["Neuronal ion channels as the target sites of insecticides," Pharmacol Toxicology, 1996 July;79(1):1-14.]
A study conducted by four scientists on a variety of pesticides found a connection to thyroid damage, although this study was conducted on rats and not on humans. The study concludes "exposure to organochlorine, organophosphorus, and pyrethroid insecticides for a relatively short time can suppress thyroid secretory activity in young adult rats." The study also said a decrease in body weight seen "suggests that pyrethroid insecticides can inhibit growth rate." [Journal of Applied Toxicology, vol. 16, no. 5, pages 397-400, 26 references, 1996.]
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