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.
