A popular herbicide still being applied to conventional maize and other factory-farmed food crops by the tons annually has been thoroughly established in the scientific literature as a silent killer. This herbicide is known as atrazine, and researchers from across the world have found that it destroys the male prostate gland, interferes with normal human reproduction, disrupts healthy hormone balance and can even lead to early death.
First registered for commercial use in the U.S. back in 1959, atrazine quickly became one of the most widely used herbicides in the world, making its way onto factory farms growing corn, sorghum, sugar cane and various other commodity crops. But several decades after its initial approval, atrazine came under closer scrutiny by independent scientists who found that it was hardly the innocuous miracle chemical that its manufacturer made it out to be.
Research conducted in the late 1980s earned atrazine the designation of a class C carcinogen, meaning that it is “possible” for the chemical substance to cause cancer in humans. But nothing was done at this time to address the dangers associated with atrazine exposure, and the chemical has continued to remain in approved use ever since, polluting growing soils and water all across the country and throughout North America.
Atrazine has since been banned in Europe, but U.S. regulators continue to allow its use domestically despite mounting evidence that continued exposure to atrazine, primarily through contaminated drinking water, is causing widespread harm to human health. The U.S. Environmental Protection Agency (EPA), in fact, admits that it has conducted extensive research on over 150 published studies on atrazine since 2003, the findings of which are concerning.
“Reproductive effects are the most sensitive effects observed in atrazine toxicity tests and, as such, our efforts to regulate the pesticide to protect against these effects through drinking water exposure will protect against all other effects that occur at higher levels,” explains an information sheet released by the EPA on the latest science covering atrazine.
Atrazine causes gender malformation, organ failures, developmental disorders
And just what are these “other effects” of which the EPA speaks? According to a 2011 study out of the University of Illinois at Urbana-Champaign, atrazine causes a broad range of reproductive problems in creatures of all kinds, including amphibians, fish, reptiles and, of course, mammals. Male frogs exposed to the chemical were found to be so affected hormonally by atrazine that many of them actually turned into females.
Corresponding research out of Massachusetts conducted several years prior observed similar hormone-disrupting effects specifically in amphibians. Within just 12 to 24 hours of exposure to atrazine, tadpoles were observed to have major developmental failures, including failure of the heart to properly develop into normal size. Atrazine was also observed to cause cell death and tissue malformation.
A more recent study out of Texas linked atrazine exposure in humans to a rare congenital abnormality in the nasal cavity known as choanal atresia. This condition is marked by improper development of the nasal passage during fetal development, which results in nasal passage blockages that can leave a child unable to breathe properly without surgery.
As it turns out, the primary driver behind choanal atresia is endocrine disruption, a known adverse effect of atrazine exposure. And the vast majority of known cases of this condition occur in areas where atrazine exposure is the most pronounced, with virtually no incidences in areas where atrazine is not present.
“[A]trazine works through a number of different mechanisms,” stated Tyrone Hayes, a professor of integrative biology at the University of California at Berkeley and lead author of the study on frogs. “It’s been shown that [atrazine] increases production of (the stress hormone) cortisol. It’s been shown that it inhibits key enzymes in steroid hormone production while increasing others. It’s been shown that it somehow prevents androgen from binding to its receptor.”
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