Abstract

Thyroid diseases are progressively increasing, mainly in terms of congenital hypothyroidism, thyroiditis, and childhood thyrotoxicosis. A rapid increase in the incidence of thyroid cancer in children and adolescents has also been observed in the last decades, mirroring the incidence trend observed in adults. This epidemiologic tendency is paralleled by a progressive increment in costs for diagnosis and treatment of thyroid disease. Thyroid diseases depend on both genetic and environmental factors. Growing evidence link both altered thyroid function and thyroid cancer with a number of widely diffused toxic chemicals of anthropogenic origin. These synthetic substances persistently contaminate the environmental matrices (i.e., air, soil, water) and the food chain, and bio-accumulate in humans, starting from in utero life. Environmental toxics as air pollutants, endocrine disruptors, and high-frequency electromagnetic fields can act through common pathways, on common targets, and with trans-generational effects, with combined mechanisms contributing to thyroid damage. As shown by experimental and epidemiologic observation, these mechanisms include modulation of hormone synthesis, transportation and metabolism, direct interference with thyroid hormone receptors, modulation of gene expression, and autoimmunity. Available evidences linking environmental pollutants and thyroid disease, including cancer, should not be underestimated in consideration of the wide, worldwide, and increasing spread of these toxic substances, and of the key role of thyroid hormones in maintaining the systemic metabolic homeostasis and during the development. Thus, primary prevention measures are urgently needed in particular to protect children, the most exposed and vulnerable subjects.

https://www.eurekaselect.com/196304/article

The post Thyroid Function: a Target for Endocrine Disruptors, Air Pollution, and Radiofrequencies appeared first on EMFSA.

Abstract

Emerging studies have provided evidence on the carcinogenicity of radiofrequency radiation (RFR) from cell phones. This study aims to test the genetic susceptibility on the association between cell phone use and thyroid cancer. Population-based case-control study was conducted in Connecticut between 2010 and 2011 including 440 thyroid cancer cases and 465 population-based controls with genotyping information for 823 single nucleotide polymorphisms (SNPs) in 176 DNA genes. We used multivariate unconditional logistic regression models to estimate the genotype-environment interaction between each SNP and cell phone use and to estimate the association with cell phone use in populations according to SNP variants. Ten SNPs had P < 0.01 for interaction in all thyroid cancers. In the common homozygote groups, no association with cell phone use was observed. In the variant group (heterozygotes and rare homozygotes), cell phone use was associated with an increased risk for rs11070256 (odds ratio (OR): 2.36, 95% confidence interval (CI): 1.30–4.30), rs1695147 (OR: 2.52, 95% CI: 1.30–4.90), rs6732673 (OR: 1.59, 95% CI: 1.01–2.49), rs396746 (OR: 2.53, 95% CI: 1.13–5.65), rs12204529 (OR: 2.62, 95% CI: 1.33–5.17), and rs3800537 (OR: 2.64, 95% CI: 1.30–5.36) with thyroid cancers. In small tumors, increased risk was observed for 5 SNPs (rs1063639, rs1695147, rs11070256, rs12204529 and rs3800537), In large tumors, increased risk was observed for 3 SNPs (rs11070256, rs1695147, and rs396746). Our result suggests that genetic susceptibilities modify the associations between cell phone use and risk of thyroid cancer. The findings provide more evidence for RFR carcinogenic group classification.

https://www.sciencedirect.com/science/article/abs/pii/S0013935119308102?via%3Dihub

The post Genetic susceptibility may modify the association between cell phone use and thyroid cancer: A population-based case-control study in Connecticut appeared first on EMFSA.