Occupational pesticide exposure and subclinical hypothyroidism among male pesticide applicators.

Abstract

Animal studies suggest that exposure to pesticides may alter thyroid function; however, few epidemiologic studies have examined this association. We evaluated the relationship between individual pesticides and thyroid function in 679 men enrolled in a substudy of the Agricultural Health Study, a cohort of licensed pesticide applicators. Self-reported lifetime pesticide use was obtained at cohort enrolment (1993-1997). Intensity-weighted lifetime days were computed for 33 pesticides, which adjusts cumulative days of pesticide use for factors that modify exposure (eg, use of personal protective equipment). Thyroid-stimulating hormone (TSH), thyroxine (T4), triiodothyronine (T3) and antithyroid peroxidase (anti-TPO) autoantibodies were measured in serum collected in 2010-2013. We used multivariate logistic regression to estimate ORs and 95% CIs for subclinical hypothyroidism (TSH >4.5 mIU/L) compared with normal TSH (0.4-<u><</u>4.5 mIU/L) and for anti-TPO positivity. We also examined pesticide associations with TSH, T4 and T3 in multivariate linear regression models. Higher exposure to the insecticide aldrin (third and fourth quartiles of intensity-weighted days vs no exposure) was positively associated with subclinical hypothyroidism (OR_Q3=4.15, 95% CI 1.56 to 11.01, OR_Q4=4.76, 95% CI 1.53 to 14.82, p_trend <0.01), higher TSH (p_trend=0.01) and lower T4 (p_trend=0.04). Higher exposure to the herbicide pendimethalin was associated with subclinical hypothyroidism (fourth quartile vs no exposure: OR_Q4=2.78, 95% CI 1.30 to 5.95, p_trend=0.02), higher TSH (p_trend=0.04) and anti-TPO positivity (p_trend=0.01). The fumigant methyl bromide was inversely associated with TSH (p_trend=0.02) and positively associated with T4 (p_trend=0.01). Our results suggest that long-term exposure to aldrin, pendimethalin and methyl bromide may alter thyroid function among male pesticide applicators.