Association of In Utero Persistent Organic Pollutant Exposure With Placental Thyroid Hormones

Abstract

In utero exposure to persistent organic pollutants (POPs) can result in thyroid function disorder, leading to concerns about their impact on fetal and neonatal development. The associations between placental levels of various POPs and thyroid hormones (THs) were investigated. In a prospective Danish study initially established for assessing congenital cryptorchidism, 58 placenta samples were collected from mothers of boys born with (n = 28) and without (n = 30) cryptorchidism. The concentrations of polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs), organotin chemicals (OTCs), organochlorine pesticides (OCPs), T 4 , T 3 , and rT 3 were measured. The associations between placental THs and various POPs were analyzed using multiple linear regression. Five PBDEs, 35 PCBs, 14 PCDD/Fs, 3 OTCs, 25 OCPs, T 4 , T 3 , and rT 3 were measured. No correlation between THs and the odds of cryptorchidism was found. Several POPs were significantly associated with THs: (1) T 4 was inversely associated with BDEs 99, 100, SPBDE, and 2378-TeCDD, and positively associated with 1234678-HpCDF; (2) T 3 was positively associated with 2378-TeCDF and 12378-PeCDF; and (3) rT 3 was positively associated with PCB 81, 12378-PeCDF, and 234678-HxCDF, and inversely associated with tributyltin, SOTC, and methoxychlor. These results revealed that POP exposures were associated with TH levels in placenta, which may be a possible mechanism for the impacts of POP exposures on children's growth and development. This study provides new insight into the complexity of thyroid-disrupting properties of POPs. More research is needed to elucidate the biological consequences of POP exposures. (Endocrinology 159: 3473-3481, 2018) T hyroid hormones (THs) are a group of tyrosine-based hormones that act on cells of almost all tissues and therefore are involved in important physiological processes during a life span (1, 2). The human thyroid system is susceptible to disruption by endogenous (e.g., autoantibodies) or exogenous (e.g., iodine) factors via interference with the sodium-iodide symporter, TH metabolism, receptors, and TH transport (3). Consequently, there are concerns regarding the chronic background exposure to persistent organic pollutants (POPs), which