Nexus between perfluoroalkyl compounds (PFCs) and human thyroid dysfunction: A systematic review evidenced from laboratory investigations and epidemiological studies

Perfluoroalkyl compounds (PFCs) have attracted massive attention in recent years for their endocrine-disrupting potential. This review summarizes the underlying evidence on the primary fate andin vitro/vivotoxic effects of PFCs and their interactions and relationships with thyroid dysfunction and cancer induction in exposed groups, including the general population, occupationally exposed groups, highly exposed individuals, and prone subjects (pregnant women and neonates). The potential endocrine-disrupting mechanism of PFCs may include multiple processes of thyroid malfunction or hormonal imbalance. The increased level of thyroid stimulating hormone (TSH) was observed as the most consistent outcome of PFC exposure among generally exposed populations. Specifically, the levels of perfluorooctane sulfonate (PFOS) and TSH were significantly correlated among pregnant women. In some instances, the maternal PFC level was negatively correlated with the neonatal thyroxine (T4) level in serum. The PFCs and thyroid malfunction or thyroid hormone (TH) levels also revealed a potential association among the population under high-level environmental exposure, albeit not always following a strict exposure-response relationship. Moreover, occupational exposure to perfluorooctanoic acid (PFOA) showed a probable link with TH (excluding TSH) alterations in serum. Importantly, no concrete and statistically significant evidence highlighted the risk of thyroid cancer in humans exposed to PFCs.