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Persistent organic pollutants (POPs) can disrupt the thyroid hormone system in humans. We assessed the associations of several POPs with serum thyroid hormones (T3 and T4) and thyroid-stimulating hormone, and investigated the modulating effects of sex, menopausal status, and age on these associations, in a subgroup of the adult population (n = 1250) from the Korean National Environmental Health Survey. PCB105 and PCB118 were negatively associated with total T4 in premenopausal females and males aged50, whereas the associations were insignificant in other groups. PCB180, p,p'-DDE, and p,p'-DDT showed positive associations with total T3 in postmenopausal females; however, among males aged ≥50, PCB118, PCB138, and p,p'-DDE showed negative associations with total T3. The effects of exposure to multiple POPs were examined in multi-factor analyses. Factor 2 comprised PCB52, hexachlorobenzene, and BDE-47 was associated with an increase in free T4 in premenopausal females (β = 0.015, p = 0.024), while Factor 1, which contained most POPs, was associated with a change in total T3 in postmenopausal females (β = 0.032, p = 0.040) and males aged ≥50 (β = -0.039, p = 0.023). Changes in total T4 or total T3 could be explained by differences in thyroxine-binding globulin (TBG) and peripheral deiodinase activity (G

Air pollution and fuel emissions are the common sources of human exposure to polycyclic aromatic hydrocarbons (PAHs) and heavy metals. Several studies have suggested potential associations between PAHs/heavy metals and thyroid hormones, however, reports have been inconsistent. In this study, we employed a subpopulation of the adults (n = 1254) who participated in the Korean National Environmental Health Survey 2015–2017, and investigated the association of PAHs and major heavy metals with thyroid hormones, and explored the underlying mechanisms of thyroid disruption. Four PAH metabolites and three heavy metals of lead (Pb), mercury (Hg), and cadmium (Cd) were measured either in urine or in total blood. In addition, thyroid hormones (T3 and T4), TSH, thyroxine-binding globulin (TBG), and thyroid autoantibodies were measured, and peripheral deiodinase activity (GD) and thyroid's secretory capacity (GT) were calculated. Urinary Hg was negatively associated with total T3 in both males and females, while it was positively associated with total T4 among females only. Urinary Hg was related to decreased GD and increased GT in both sexes. In contrast, urinary Cd was positively associated with total T3 and GD in both male and female populations. Urinary Cd also showed a positive association with thyroid autoantibodies, but only in males. A multi-factor model considering co-exposure to multiple chemicals also resulted in similar associations. Among the measured PAH metabolites, only urinary 1-hydroxypyrene showed a negative association with total T3 in males. However, this association was marginal, and disappeared in a multi-chemical model. The present observations are suggestive that exposures to Hg and Cd might disrupt thyroid hormones, possibly through an alteration of deiodinase activity. Association of PAH exposure with thyroid hormone appears to be insignificant.