Thyroid Troubles: Pollutants To Watch Out For

Thyroid problems are common, with an estimated 20 million people in the United States suffering from some form of thyroid disorder. Thyroid issues can range from harmless goiters (enlarged glands) to life-threatening cancer. The most common thyroid problems involve abnormal hormone production, with too much thyroid hormone resulting in hyperthyroidism, and too little leading to hypothyroidism. Several pollutants are known to cause thyroid problems, including cigarette smoke, radiation exposure, increased iodine intake, and various environmental chemicals and pesticides. These pollutants can interfere with iodine concentration, disrupt thyroid function, and increase the risk of autoimmune thyroid diseases such as hypothyroidism and hyperthyroidism.

Perchlorate, nitrate, and thiocyanate

Perchlorate is a strong oxidizing anion used in rocket fuels, explosives, fireworks, and missile fuels. It is also naturally formed in the atmosphere and accumulates in arid climate regions. Thiocyanate is found in foods such as milk, vegetables, cassava, bamboo shoots, sweet potatoes, Brussels sprouts, cauliflower, corn, broccoli, apricots, and almonds. It is also the main metabolite of cyanide exposure from tobacco smoke and certain foods. Nitrates can occur naturally in food, such as green leafy vegetables, or can be added as preservatives in meat and fish.

Several studies have reported that exposure to these contaminants was not associated with alterations in TSH or T4 serum levels in humans. However, other studies have shown significant alterations in the function of the pituitary-thyroid axis in humans co-exposed to perchlorate and other NIS-inhibitory anions, especially in iodine-deficient areas. A recent study indicated that humans co-exposed to perchlorate, nitrate, and thiocyanate presented an increased central thyroid hormone sensitivity, which seems to be more precise than single parameters such as TSH or T4 serum levels in evaluating the homeostasis of the pituitary-thyroid axis.

The impact of human exposure to these anions is highly controversial, and future studies are needed to fully understand their effects on thyroid function and human health. However, it is clear that perchlorate, nitrate, and thiocyanate are environmental contaminants that can interfere with thyroid function and have potential health consequences, especially for individuals living in iodine-deficient areas.

Polychlorinated biphenyls

Thyroid problems are common, with around 20 million people in the United States alone suffering from some form of thyroid disorder. Thyroid diseases are split into two types: primary and secondary. In primary thyroid disease, the disease originates in the thyroid gland, whereas in secondary thyroid disease, the disease originates in the pituitary gland.

PCBs have been shown to affect thyroid function, particularly in people exposed during childhood. Studies have found inverse associations between total thyroxine (T4) and thyroid-stimulating hormone (TSH) with exposure to PCBs. Higher levels of exposure to PCBs have been linked to a decrease in fT4 and an increase in TSHRab levels over time. PCBs have also been associated with the onset of cardiovascular, endocrine, and metabolic diseases, although no conclusive evidence has been provided.

The effects of PCBs on the thyroid gland have been studied, but the findings are inconsistent. Some studies have found negative correlations between higher chlorinated biphenyls and fT3, while others have shown no clear results. The discrepancies in the findings may be due to the cross-sectional design of the studies, which limits the ability to evaluate the temporal association between organochlorine exposure and thyroid hormone changes.

It is important to note that the impact of PCBs on thyroid function may depend on the age of exposure. A study on Michigan residents who were exposed to PCBs as children found an association between PCB exposure and thyroid function. The study used linear regression models to analyze the relationship between serum measures of thyroid function and serum PCB levels in 715 participants.

Radiation exposure

The risk of thyroid cancer from radiation exposure is influenced by two main factors: the radiation dose delivered to the thyroid gland and the age at exposure. Higher radiation doses increase the risk, and exposure during childhood carries a higher risk than exposure during adulthood. The minimum latency period for the development of thyroid cancer after radiation exposure is 5 to 10 years, with papillary carcinoma being the most frequently diagnosed type.

In addition to cancer, radiation exposure can also induce hypothyroidism, a condition where the thyroid gland does not produce enough thyroid hormones. This can lead to a slowdown in metabolism. Radiation exposure can cause cellular death and trigger autoimmune processes, resulting in the production of autoantibodies that attack the thyroid gland. While the exact mechanism is not fully understood, studies have indicated a possible association between low doses of radiation and an increased prevalence of anti-thyroid antibodies.

The effects of radiation exposure on the thyroid vary depending on factors such as age, radiation dose, and individual susceptibility. While radiation-induced thyroid cancer has been well-documented, the link between radiation exposure and hypothyroidism is less extensively studied. However, evidence from medically-irradiated patients, atomic bombing survivors, and those affected by nuclear accidents suggests a potential connection between radiation exposure and thyroid dysfunction.

Furthermore, radiation exposure is not limited to nuclear incidents or medical radiation therapy. Environmental exposures to radiation, including nuclear fallout, can also impact thyroid function. The combination of radiation exposure with other environmental factors, such as iodine intake and other environmental toxicants, may further contribute to thyroid-related issues.

Cigarette smoke

The effects of cigarette smoke on thyroid function are evident in the changes observed in thyroid hormone levels. Smoking is associated with lower thyroid-stimulating hormone (TSH) levels and higher levels of free thyroxine (FT4) and free triiodothyronine (FT3). These hormonal alterations can have significant implications for overall thyroid health and function.

Additionally, cigarette smoke has been linked to the onset of autoimmune thyroid disease, even during pregnancy. The presence of cyanide in cigarette smoke can interfere with iodine concentration in the thyroid, affecting thyroid function. Furthermore, the act of quitting smoking has also been associated with an increased risk of autoimmune thyroid disease, possibly due to weight gain and the subsequent development of hypothyroidism.

While the relationship between cigarette smoke and thyroid cancer is less established, some studies suggest that smoking may reduce the risk of differentiated thyroid cancer. However, the impact of cigarette alternatives, such as vaping, on the thyroid is still largely unknown and requires further investigation.

Selenium and vitamin D deficiency

Selenium is a non-metallic mineral that is essential for human health. It is important for thyroid hormone metabolism and plays a key role in the thyroid gland's ability to produce thyroid hormones. Selenium is not produced by the body and can only be obtained through food and/or supplements.

Selenium deficiency is associated with a higher prevalence of thyroid disease. Studies have shown that selenium deficiency decreases the synthesis of thyroid hormones by reducing the function of selenoproteins, specifically iodothyronine deiodinases (DIOs), which are responsible for converting T4 to T3. This decreased production of thyroid hormones leads to the overstimulation of the hypothalamic-pituitary axis and increased production of TSH, which further stimulates DIOs. This results in the production of hydrogen peroxide, which can damage thyroid cells if not adequately removed. Selenium deficiency can also lead to a higher risk of an enlarged thyroid gland and the development of thyroid nodules.

People at risk of selenium deficiency include those with intestinal, digestive, or absorption issues, such as Crohn's disease, those living in regions with selenium-deficient soil or crops, those undergoing kidney dialysis, and people living with HIV.

Selenium supplementation has been found to have a positive impact on thyroid health. It can reduce thyroid antibodies, improve symptoms, and enhance overall well-being. Studies have shown that selenium supplementation can improve the quality of life and outcomes for those with thyroid eye disease (Graves' orbitopathy) and slow the progression of symptoms.

Vitamin D, on the other hand, is a steroid molecule mainly produced in the skin through exposure to ultraviolet B (UVB) radiation. It can also be obtained from dietary sources, such as fatty fish, or plants and fungi, which produce vitamin D2. Vitamin D plays a crucial role in regulating bone metabolism and calcium and phosphorus homeostasis.

Vitamin D deficiency is common worldwide and has been associated with autoimmune diseases, cancers, metabolic syndromes, cardiovascular disease, and infection. Low levels of vitamin D have been specifically linked to autoimmune thyroid diseases (AITD), such as Hashimoto's thyroiditis (HT) and Graves' disease (GD). Impaired vitamin D signaling has been implicated in the development of thyroid tumours.

In summary, both selenium and vitamin D deficiencies have been associated with thyroid problems. Selenium deficiency can lead to a higher prevalence of thyroid diseases, including hypothyroidism and Graves' disease, while vitamin D deficiency has been linked to autoimmune thyroid diseases, thyroid cancer, and other health issues.

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