Smoking and thyroid

Summary Current smoking in population surveys is associated with a slight dose‐dependent fall of serum TSH , likely secondary to a rise of serum FT 4 and FT 3 induced by activation of the sympathetic nervous system; it is independent of iodine intake. In contrast, the slightly greater thyroid size in smokers is observed in iodine‐deficient but not in iodine‐sufficient areas and caused by competitive inhibition of thyroidal iodide uptake by thiocyanate. Smokers have an increased prevalence of nontoxic goitre and thyroid multinodularity, at least in iodine‐deficient areas. Current smoking reduces dose dependently the risk of thyroid cancer, which is more pronounced for papillary than for follicular types; the risk in former smokers approaches that of never smokers. The lower TSH and lower body mass index in smokers might contribute to this reduced risk. Current smoking lowers the risk of developing thyroid peroxidase and thyroglobulin antibodies and subclinical and overt autoimmune hypothyroidism; the effect is dose dependent, but disappears within 3 years after quitting smoking. There is evidence from an animal model of experimental autoimmune thyroiditis that anti‐inflammatory effects of nicotine are involved. In contrast, smoking is a dose‐dependent risk factor for Graves’ hyperthyroidism and especially for Graves’ ophthalmopathy. Smoking is related to a higher recurrence rate of Graves’ hyperthyroidism, a higher risk on Graves’ ophthalmopathy after 131I therapy and a less favourable outcome of GO treatment with steroids or retrobulbar irradiation. The observed associations with smoking likely indicate causal relationships in view of consistent associations across studies, the presence of dose–response effects and disappearance of associations after cessation of smoking.