Effects of Secondhand Smoke on Thyroid Function
Growing evidence suggests that the effects of second hand smoke (SHS) exposure contribute to disruptions in thyroid function. Toxic elements contained in cigarette smoke, such as thiocyanate, may be partially responsible for impaired thyroid hormonogenesis. SHS-induced inflammatory stress, namely interleukin 1β (IL-1β), impairs thyroid hormonogenesis and iodine uptake; initiates interleukin 6 (IL-6) production from thyroid epithelial cells and stimulates the expression of molecules that exacerbate thyroid autoimmunity. The link between SHS exposure and thyroid autoimmune disease is not well documented and thus, remains to be fully understood. Elevated inflammatory stress and thyroid hormone secretion in response to SHS exposure initiates catabolic processes that alter body composition via lean body mass breakdown; translating to an elevation in resting energy expenditure of ∼10%. The combination of certain biological factors, such as sex and/or existing thyroid disease may stimulate differential SHS-induced effects on thyroid function. Nevertheless, exposure to SHS disturbs vital human processes via thyroid disruption.
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Document Type: Research Article
Publication date: 01 December 2009
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- Inflammation & Allergy - Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular targets involved in inflammation and allergy e.g. disease specific proteins, receptors, enzymes, genes. Each issue of the journal contains a series of timely in-depth reviews written by leaders in the field covering a range of current topics on drug targets involved in inflammation and allergy. As the discovery, identification, characterization and validation of novel human drug targets for anti-inflammation and allergy drug discovery continues to grow, this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.