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Pesticide-Induced Diseases: Endocrine Disruption

Common household products –detergents, disinfectants, plastics, and pesticides– contain chemical ingredients that enter the body, disrupt hormones and cause adverse developmental, disease, and reproductive problems. Known as endocrine disruptors, these chemicals, which interact with the endocrine system, wreak havoc in humans and wildlife. The endocrine system consists of a set of glands (thyroid, gonads, adrenal and pituitary) and the hormones they produce (thyroxine, estrogen, testosterone and adrenaline), which help guide the development, growth, reproduction, and behavior of animals, including humans. Hormones are signaling molecules, which travel through the bloodstream and elicit responses in other parts of the body.

Download Beyond Pesticides' Endocrine Disruption brochure (bi-fold), or read Beyond Pesticides article, "Pesticides That Disrupt Endocrine System Still Unregulated by EPA."

Endocrine disruptors function by: (i) Mimicking the action of a naturally-produced hormone, such as estrogen or testosterone, thereby setting off similar chemical reactions in the body; (ii) Blocking hormone receptors in cells, thereby preventing the action of normal hormones; or (iii) Affecting the synthesis, transport, metabolism and excretion of hormones, thus altering the concentrations of natural hormones. Endocrine disruptors have been linked to attention deficit hyperactivity disorder (ADHD), Parkinson’s and Alzheimer’s diseases, diabetes, cardiovascular disease, obesity, early puberty, infertility and other reproductive disorders, and childhood and adult cancers.

More than 50 pesticide active ingredients have been identified as endocrine disruptors by the European Union and endocrine disruptor expert Theo Colborn, PhD. Endocrine disruption is the mechanism for several health effect endpoints. See the related sections (Cancer, Developmental and Learning Disorders, Parkinson’s disease, Reproductive Health) for more information.

 

  • Hormones and endocrine-disrupting chemicals: low-dose effects and nonmonotonic dose responses.
    Here, a team of researchers review two major concepts in EDC studies: low dose and nonmonotonicity. Low-dose effects were defined by the National Toxicology Program as those that occur in the range of human exposures or effects observed at doses below those used for traditional toxicological studies. They review the mechanistic data for low-dose effects and use a weight-of-evidence approach to analyze five examples from the EDC literature. Additionally, they explore nonmonotonic dose-response curves, defined as a nonlinear relationship between dose and effect where the slope of the curve changes sign somewhere within the range of doses examined. Authors illustrate that nonmonotonic responses and low-dose effects are remarkably common in studies of natural hormones and EDCs. Whether low doses of EDCs influence certain human disorders is no longer conjecture, because epidemiological studies show that environmental exposures to EDCs are associated with human diseases and disabilities. Authors conclude that when nonmonotonic dose-response curves occur, the effects of low doses cannot be predicted by the effects observed at high doses. Thus, fundamental changes in chemical testing and safety determination are needed to protect human health.
    [Vandenberg LN, Colborn T, Hayes TB, Heindel JJ, Jacobs DR Jr, et al. 2012. Endocr Rev.33(3):378-455.]