The thyroid gland is a large, butterfly-shaped gland located at the base of the neck. Although it may seem insignificant in nature, this ductless gland is fundamental for the human body’s overall function. The thyroid gland secretes an essential collection of thyroid hormones which aid in the growth and development of the systems through the rate of metabolism.
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The continuous release of thyroid hormones activate numerous bodily functions, including proper heart and digestive function, muscle control, brain growth and development, bone maintenance and even body temperature.
As important as the thyroid gland is, however, the human body’s own immune system can sometimes attack and damage a healthy thyroid gland, a condition medically referred to as autoimmune thyroid disease. Autoimmune thyroid diseases, or AITD’s, such as Hashimoto’s thyroid disease and Graves’ disease can ultimately alter the overall function of the body. Autoimmune thyroid disease is believed to have no apparent cause, but, research studies have hypothesized that exposure to environmental pollutants and toxins can bring an onset of AITD’s.
The exposure to environmental pollutants and toxins have been previously implicated in the induction of autoimmune thyroid diseases throughout various research studies. Similar studies have also linked AITD’s to other environmental factors, such as iodine intake and selenium deficiency. However, in cases where autoimmune thyroid disease cannot be attributed to diet and nutrition, healthcare professionals have suspected the influence of other environmental factors.
Polyhalogenated biphenyls are commonly used compounds with a variety of applications. Polybrominated biphenyls are flame retardant, and polychlorinated biphenyls, or PCB’s, are used as lubricants, adhesives, inks, and plasticizers. PCB’s are known to accumulate in rivers and lakes and then in the adipose tissue of fish and humans. AITD’s might be triggered by these compounds by interfering with iodide transport, causing oxidative stress. There is proof that thyroid hormone levels in rat pups decrease with exposure to perinatal PCB’s. In adults, adolescents, and children from such areas, the concentration of PCB’s in blood samples negatively correlated with levels of circulating thyroid hormones.
Populations with long-term exposure to PCB’s have increased prevalences of antibodies, which can be linked to the increased effects of these compounds in the environment. Pollutants and toxins from heavy industry and auto emissions, in addition to coal pollution and agricultural fungicides, are also implicated in development of AITD’s.
Smoking is associated with an increased risk of developing Graves’ disease, an autoimmune thyroid disease which causes hyperthyroidism, an overactive thyroid gland, as well as a remission rate after thionamide treatment. Even more striking is the impact of smoking on Graves’ orbitopathy, which tends to become more serious in smokers. Smoking might contribute to the pathogenesis of Graves’ disease by altering the structure of the thyrotropin receptor, making it more immunogenic and causing the creation of thyrotropin antibodies that react with retroorbital tissue.
Smoking increases antigens by cells that are damaged and induces the polyclonal activation of T and B cells. Hypoxia can play a part in Graves’ orbitopathy when cultured under hypoxic conditions because retrobulbar fibroblasts show a significant increase in proliferation and glycosaminoglycan production. The impacts of smoking on thyroid function in fetuses or infants that are 1-year-old offer insight into the interrelationship between smoking and autoimmune thyroid disease. The latter study found that the mothers and fathers of babies whose had higher cord serum levels of Tg and thiocyanate than did infants whose parents did not smoke. The result observed in adolescents exposed to passive smoking could be due to direct stimulation of sympathetic nervous activity from smoking in addition to the increase in thyroid hormone secretion. The association of smoking with chronic autoimmune thyroiditis is less well-defined.
In conclusion, various research studies have demonstrated that exposure to environmental pollutants and toxins, including smoking, may have a connection with autoimmune thyroid diseases. While the thyroid gland is virtually an essential part of the function of the human body, it can no doubt be sensitive to environmental factors.
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By Dr. Alex Jimenez
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