Pesticides and Thyroid Function

Experimental evidence has shown the ability of multiple pesticides to affect thyroid homeostasis. The thyroid-disrupting effects of organochlorine (OC) pesticides are the most studied. OC pesticides can affect the deiodination of thyroid hormones (TH) leading to increased T3 degradation; can bind to TH-binding proteins altering circulating TH levels; may mimic TH action; and interfere with their binding to hormonal receptors, altering TH-mediated gene expression. Epidemiological studies have shown inverse relationships between exposure to OC pesticides and levels of T3 and T4, and positive associations with TSH among pregnant women, newborns and adults. Non-persistent contemporary pesticides such as organophosphates (OP), carbamate and pyrethroids may also interfere with thyroid function, as suggested by various animal studies. Evidence from human studies linking non-persistent pesticides to thyroid function is still limited and controversial. However, alterations compatible with hypothyroidism were observed in some studies, particularly in relation to OP pesticides. Overall, experimental and epidemiological studies indicate that hypothyroid effect are the general effects from pesticide exposure, supporting that pesticide exposure causes a decrease in TH, but also an increase in TSH. The varying methodological approaches used in epidemiological research particularly hamper drawing conclusions about the evidence on the topic. In addition, exposure levels, modes of action of individual substances, and genetic variability might be important sources of variation between studies. Given the important role of TH on metabolism and brain development, exposure to even low doses of thyroid-disrupting pesticides may contribute to increase the risk of thyroid disease and neurodevelopmental disorders.

Keywords: Non-persistent pesticide, organochlorine pesticides, thyroid disruption, thyroid gland, toxicity.