Thyroid disease is common with a prevalence of approximately
7.5% in the US population. This may be an underestimate because some
studies have reported an additional 9% of adults with unidentified
clinical or subclinical disease.1–3 Known risk factors for thyroid disease, such as age, genetic predisposition, and female sex,4
are nonmodifiable, making the identification of modifiable risk factors
for thyroid disease all the more important. Thyroid disease is less
common in men than in women and has been less studied, so there is a
paucity of data regarding risk factors in men.
Some pesticides have been reported to act as endocrine disruptors with effects on many systems, including the thyroid.5–7
Studies focusing on the effect of pesticides on the levels of
circulating thyroid-stimulating hormone (TSH) or thyroid hormone,
triiodothyronine (T3) and thyroxine (T4), have found conflicting results.8–10
Mechanisms for thyroid disruption may include interference at the level
of the hypothalamus–pituitary–thyroid axis, inhibition of iodine intake
in the thyroid gland by the sodium–iodide symporter, increased
synthesis of uridine diphosphate glucoronyltransferase, altered binding
of the transport proteins resulting in increased excretion of thyroid
hormone, decreased cellular uptake of thyroid hormone, alteration in the
expression of deiodinases, altered transcriptional activity of thyroid
hormone receptors, and up- or downregulated expression of thyroid
hormone–regulated genes.11–13
Nevertheless, not all pesticides have been classified as endocrine
disruptors, and those that have do not all have the same effect on
thyroid function or have the same mechanism of action.
READ MORE: http://journals.lww.com/joem/Fulltext/2013/10000/Hypothyroidism_and_Pesticide_Use_Among_Male.7.aspx?WT.mc_id=EMxALLx20100222xxFRIEND
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