Environmental and health factors are known to be associated with an increased risk of thyroid cancer in humans. Exposure to radiation, both from nuclear weapons and from radioactive or medical fallout, as well as to certain toxic organic and inorganic chemicals, represent a global public health problem due to their carcinogenic properties. Radiation exposure is a proven risk factor for thyroid cancer, with sources including medical treatments and accidents at power plants or nuclear weapons. Environmental factors are also determinants for the onset of autoimmune thyroid diseases (AITD) in susceptible individuals. Increased iodine intake, selenium and vitamin D deficiency, radiation exposure, nuclear rain or medical radiation are environmental factors that can increase AITD.
Smoking is associated with Graves' disease and Graves' ophthalmopathy, while it decreases the risk of hypothyroidism and thyroid autoimmunity. Viral infections are also important environmental factors in the pathogenesis of AITD, particularly human parvovirus B19 (EVB1) and hepatitis C virus. Among the many chemical pollutants, halogenated organochlorines and pesticides variably alter thyroid function. Polychlorinated biphenyls (PCBs) and their metabolites, as well as polybrominated diethyl ethers (PBDEs), bind to thyroid transport proteins such as transthyretin, displacing thyroxine and disrupting thyroid function. Drugs containing interferon and iodine have also been associated with AITD.
In addition, intestinal dysbiosis can cause autoimmune thyroiditis. To reduce the risk for populations and individuals alike, it is necessary to understand the association between environmental agents and thyroid dysfunction. One possible group of chemicals in the environment are flame retardants called PBDEs, which were commonly used in electronics and furniture manufacturing practices. While the use of PBDEs has been eliminated for the most part, these chemicals still persist in the environment, especially in household dust. It has been proposed that exposure to these and other endocrine-disrupting chemicals could increase the risk of thyroid cancer by altering thyroid hormone levels. This study was conducted to examine whether exposure to flame-retardant chemicals in the environment could be associated with increased thyroid cancer.
The issue of chemicals that affect the thyroid is extremely complex, and there are numerous reasons why thyroid cancer might be on the rise. However, this study is interesting at least to begin to examine how chemicals in the environment might be related to thyroid cancer. More studies are needed to better understand the role of endocrine-disrupting chemicals in the development of thyroid disease. Experiments in rats documented the role of vanadium in affecting iodine metabolism and thyroid function by decreasing thyroid peroxidase activity (Uthus & Nielsen 1990). Scientific advances such as synthetic and systems biology, the use of organoids grown in 3D in vitro to model the thyroid as an example, and large-scale prospective cohort studies combined with pre-trained deep learning algorithms would allow for the identification of key risk factors and better adaptation of strategies for the prevention of thyroid cancer. Even if no known hereditary syndrome has been identified, having a first-degree relative with thyroid cancer increases one's risk of developing it.
Parvovirus B19 infection has been linked to Hashimoto's thyroiditis, papillary thyroid carcinoma and anaplastic thyroid carcinoma. A 3-year epidemiological survey by the Sicilian Regional Register for Thyroid Cancer (SRRTC) recently collected data on all incident thyroid cancers in Sicily (the largest island in the Mediterranean) and their associations with different environmental factors. Nitrate can compete with iodine and inhibit iodine absorption, which affects the production of thyroid hormones, potentially leading to stimulation of thyroid growth and tumor formation (Tonacchera et al.). Stable iodine given shortly before, during or immediately after exposure may reduce the absorption of radioactive iodine by the thyroid gland, leading to a decrease in radiation dose delivered to it (Nauman & Wolff 1993; Zanzonico & Becker 2000).Amiodarone has a structure similar to that of thyroid hormones due to its internal benzene ring containing iodine residues; it can cause thyroid dysfunction. HCV infection positively regulates CXCL10 expression and thyroid cell secretion, recruiting other Th1 lymphocytes into the gland which can lead to AITD in predisposed individuals (99; 100).Risk factors for and prevalence of thyroid disorders were studied through a cross-sectional study among healthy female relatives of patients with autoimmune thyroid disease.
In addition, there may be an “overdiagnosis” where research tools detect subclinical lesions that may not adversely affect human health, leading to an apparent explosion of cases - such as seen in Korea. Thyroid cancer occurs when abnormal cells in the gland begin to divide and grow uncontrollably. To reduce its risk for populations as well as individuals it is necessary to understand how environmental agents affect its development. Experiments in rats have documented vanadium's role in affecting iodine metabolism and function by decreasing peroxidase activity (Uthus & Nielsen 1990). Scientific advances such as synthetic biology combined with large-scale prospective cohort studies combined with pre-trained deep learning algorithms would allow for better adaptation of strategies for its prevention.