Bisphenols (BPs), and especially bisphenol A (BPA), are known endocrine disruptors (EDCs), capable of interfering with estrogen and androgen activities, as well as being suspected of other health outcomes. Given the crucial role of thyroid hormones and the increasing incidence of thyroid carcinoma in the last few decades, this review analyzes the effects of BPS on the thyroid, considering original research in vitro, in vivo, and in humans published from January 2000 to October 2019. Both in vitro and in vivo studies reported the ability of BPs to disrupt thyroid function through multiple mechanisms. The antagonism with thyroid receptors (TRs), which affects TR-mediated transcriptional activity, the direct action of BPs on gene expression at the thyroid and the pituitary level, the competitive binding with thyroid transport proteins, and the induction of toxicity in several cell lines are likely the main mechanisms leading to thyroid dysfunction. In humans, results are more contradictory, though some evidence suggests the potential of BPs in increasing the risk of thyroid nodules. A standardized methodology in toxicological studies and prospective epidemiological studies with individual exposure assessments are warranted to evaluate the pathophysiology resulting in the damage and to establish the temporal relationship between markers of exposure and long-term effects.

Radon is the second leading cause of lung cancer after cigarette smoking, and research on individual risk perception of radon is crucial to prevent its health effects. In this work, we aimed to systematically review the scientific literature that has analyzed radon risk perception, awareness, and knowledge to provide insight on communication actions. For this purpose, following the PRISMA 2020 statement, we searched PubMed, Embase, and Web of Science, focusing on articles published since 2010. After the screening process, we included 40 articles, of which 5 explored only knowledge, 11 added risk perception, 11 further investigated the willingness to make radon measurements, and 13 examined the full cycle of prevention, including risk mitigation actions. Many articles performed a quantitative assessment of the relationship between knowledge/awareness/perception and actions such as radon testing and remediation, showing positive associations and providing interesting elements for evaluating interventions. Furthermore, citizen science actions described by some studies could be crucial for enhancing community self-sufficiency, responsibility, and the quality of preventive actions. To conclude, risk communication can play a key role in making risk prevention possible by reducing exposure, and a multidisciplinary approach, involving constant collaboration with different experts, is essential.

Arsenic-induced health effects may be associated with critically shortened telomeres. However, few data are available on the effects of arsenic exposure on telomere length. The aim of this study was to investigate the effects of chronic arsenic exposure on leukocyte telomere length (LTL) as well as the contribution of common polymorphisms in genes implicated in arsenic metabolism (GSTT1 and GSTM1) and DNA repair (hOGG1 and XRCC1). A group of 241 healthy subjects was enrolled from four areas of Italy known to be affected by natural or anthropogenic arsenic pollution. Urine samples were tested for inorganic As (iAs), monomethylarsinic (MMA) and dimethylarsinic acid (DMA). LTL was evaluated by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Genotyping was carried out by PCR-RFLP on leukocyte DNA. In multiple linear regression analysis, LTL was significantly and inversely correlated with age (β = −0.231, P = 0.006) and showed a certain trend toward significance with iAs urinary concentration (log ₁₀ iAs, β = −0.106, P = 0.08). The genotype distribution showed significant associations between GSTT1 and the As concentration (log ₁₀ iAs, P = 0.01) and metabolite patterns (log ₁₀ DMA, P = 0.05) in the urine. However, GST genes did not interact with arsenic exposure in the modulation of LTL. Conversely, the combined presence of a higher level of iAs + MMA + DMA ≥ 19.3 μg/l ( F = 6.0, P_interaction = 0.01), Asi ≥ 3.86 ( F = 3.9, P_interaction = 0.04) μg/l, iAs + MMA + DMA ≥ 15 μg/l ( F = 4.2, P_interaction = 0.04) and hOGG1 Cys allele was associated with a significantly lower LTL. An interaction between XRCC1 Arg399Gln and arsenic exposure was also observed (all P_interaction = 0.04). These findings suggest that telomere shortening may represent a mechanism that contributes to arsenic-related disease. The interaction of hOGG1 and XRCC1 DNA repair polymorphisms and exposure enhances telomeric DNA damage. Future studies are warranted to understand better the epidemiologic impact of arsenic on telomere function as well as to identify the subgroups of exposed subjects who need better health surveillance.