Academic journal article Environmental Health Perspectives

Thyroid Hormones in Relation to Lead, Mercury, and Cadmium Exposure in the National Health and Nutrition Examination Survey, 2007-2008

Academic journal article Environmental Health Perspectives

Thyroid Hormones in Relation to Lead, Mercury, and Cadmium Exposure in the National Health and Nutrition Examination Survey, 2007-2008

Article excerpt

Thyroid hormones (THs) play a critical role in the functions of nervous, reproductive, and cardiovascular systems in both children and adults (Danzi and Klein 2012; Williams 2008; Yazbeck and Sullivan 2012). The hypothalamus-pituitary-thyroid (HPT) axis regulates thyroid function through thyrotropin releasing hormone, thyroid-stimulating hormone (TSH), and the THs [thyroxine ([T.sub.4]) and triiodothyronine ([T.sub.3])]. Circulating [T.sub.4] and [T.sub.3] are mostly bound to thyroxine-binding globulin, transthyretin, and albumin; < 1% is unbound and biologically active. In peripheral tissues, [T.sub.4] is converted to [T.sub.3] by type 1 and type 2 deiodinases; [T.sub.3] in turn binds thyroid receptors [alpha] and [beta] and initiates target gene expression (Stathatos 2012). Disruption of TH synthesis, transport, deiodination, and metabolism can result in clinical or subclinical thyroid diseases (Cooper and Biondi 2012). Circulating TSH and THs, even at levels within reference ranges, are significantly associated with effects in neurodevelopment (Ghassabian et al. 2011; Pop et al. 2003), blood pressure (Asvold et al. 2007), cholesterol, triglycerides, and insulin resistance (Roos et al. 2007).

Environmental chemicals might alter TH levels via several mechanisms, including disruption of iodine (I) transport, thyroid peroxidase, TH-binding proteins, hepatic catabolism, deiodinases, and receptor binding (Miller et al. 2009). Studies of human populations have focused primarily on chemicals that are structurally similar to [T.sub.4], such as polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers, and bisphenol A (BPA), with little attention on heavy metals (Boas et al. 2006; Pearce and Braverman 2009). Lead (Pb), mercury (Hg), and cadmium (Cd) are known environmental toxicants, but only a few studies have examined associations with total and free [T.sub.4] (T[T.sub.4], F[T.sub.4]), total and free [T.sub.3] (T[T.sub.3], F[T.sub.3]), or TSH (Dundar et al. 2006; Jin et al. 2006; Lamb et al. 2008; Pearce and Braverman 2009; Robins et al. 1983; Schell et al. 2008).

Pb is known to have adverse neurological, hematological, renal, and gastrointestinal effects (Bellinger 2004; Gurer-Orhan et al. 2004); however, associations with THs have been inconsistent (Meeker et al. 2009). Pb exposure [mean 15 [micro]g/dL blood Pb (BPb) level] was negatively correlated with transthyretin levels in cerebrospinal fluid samples from human patients (Zheng et al. 2001). Previous studies of populations with high exposure to Pb (indicated by BPb levels of > 20 [micro]g/dL) suggested negative associations with circulating [T.sub.4], F[T.sub.4], or [T.sub.3] (Lopez et al. 2000; Robins et al. 1983; Singh et al. 2000; Tuppurainen et al. 1988); however, associations were not evident in other similar study populations (Erfurth et al. 2001; Schumacher et al. 1998; Siegel et al. 1989). Fewer studies have investigated associations of BPb levels of < 10 [micro]g/dL with THs. Dundar and colleagues reported a negative association between BPb and F [T.sub.4] levels in adolescents with mean BPb of 7 [micro]g/dL (Dundar et al. 2006). A recent study (Meeker et al. 2009) has suggested an inverse association between BPb (median, 1.5 [micro]g/dL) and TSH levels in men of the couples presenting at infertility clinics. Another study, in the lakeside communities of Quebec, Canada, found no association between BPb (median, 3.1 [micro]g/dL) and THs in men, but identified a positive association with [T.sub.3] and an inverse association with TSH in females with median BPb of 1.7 [micro]g/dL (Abdelouahab et al. 2008).

Hg has adverse effects on a variety of systems that vary with the level, length of exposure, and time window of exposure (Tan et al. 2009). Proposed mechanisms of Hg-related TH disruption involve selective binding to sulfhydryl (SH)-containing ligands in the thyroid, reduced TSH production, and inhibition of deiodination (Soldin et al. …

Search by... Author
Show... All Results Primary Sources Peer-reviewed

Oops!

An unknown error has occurred. Please click the button below to reload the page. If the problem persists, please try again in a little while.