Endocrine Abstracts

Objectives: Recent evidence suggest that environmental pollution may be involved in the worldwide increase of thyroid cancer (TC) incidence occurred over the last few decades. Indeed, some environmental pollutants, namely endocrine disruptive chemicals (EDCs), have been linked to endocrine system disruption, including thyroid dysfunction, and increased risk of TC. Several EDCs are known to be Persistent Organic Pollutants (POPs) due to their long half-life in the environment, such as Per-Fluoroalkyl Substances (PFAS), poly-chlorinated biphenyls (PCBs), and the pesticide dichlorodiphenyltrichloroethane (4,4’-DDT, and its metabolite 4,4’-DDE). Threatening ecosystems and human health, POPs have raised global concern, but to date few studies explored their association with TC and none considered the possible correlation with TC clinical and molecular features. The present case-control study aimed to evaluate the possible association between serum PFAS, PCBs and 4,4’-DDE concentrations, TC, and its clinical and molecular characteristics.

Materials and methods: We recruited 224 participants, of which 112 patients with a diagnosis of TC in the last five years and 112 sex and age-matched controls with no known history of thyroid diseases, primitive gonadic diseases, or other malignancies. Blood samples were taken from all participants and serum concentrations of some PFAS and PCBs, and 4,4’-DDE were measured using liquid chromatography or gas chromatography coupled to mass spectrometry. BRAF V600E mutation was assessed by standard methods. Logistic regression models were used to evaluate the association between TC, its clinical and molecular features, and POPs serums levels.

Results: The detection of perfluorodecanoic acid (PFDA) was positively correlated to TC (OR=2.03), while a negative association was found with perfluorohexanesulfonic acid (PFHxS) levels (OR=0.63). Worthy, perfluorononanoic acid (PFNA) was positively associated with the presence of thyroiditis, while PFHxS and perfluorooctane sulfonic acid (PFOS) with higher levels of pre-surgical TSH. PFHxS, PFOS, PFNA and PFDA were associated with less aggressive TC, while two poly-chlorinated biphenyls (PCB-105 and PCB-118) with larger and more aggressive tumours. Lastly, the presence of BRAF V600E mutation resulted associated with PCB-153, PCB-138 and PCB-180.

Conclusions: Our case-control study evaluate the impact of some POPs on TC, and it is the first to investigate their association with clinical and molecular features of the tumour. Beside the already known association between TC and PFDA, we found interesting correlations between some POPs and tumour aggressiveness, and between BRAF V600E mutation and PCBs. On the other hand, an inverse association was found with PFHxS, already reported in TC, but the underlying biochemical mechanisms are still unclear.