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Cigarette smoking is the strongest modifiable risk factor for developing GO. Despite various limitations and difficulties in comparing available studies, there is a strong evidence for a causal association between smoking and development of GO [28, 29].

A positive association between smoking and GO is found in 4 case-control studies in which control patients had Graves’ hyperthyroidism but no orbitopathy (odds ratio 1.94–10.1) and in 7 case-control studies in which control subjects did not have thyroid disease (odds ratio 1.22–20.2) [30].

About 40% of GO patients are smokers [10]. Among patients with orbitopathy, smokers are more likely to have severe disease than non-smokers. The severity of GO is related to the number of cigarettes smoked per day. The volume of intraorbital fat/connective tissue also correlates well with cumulative smoking [31]. Current smokers are also more likely to experience disease progression or poorer outcome of treatment [32, 33]. The effect of immunosuppressive treatment of GO may be attenuated in cigarette smokers [34]. Among patients with mild GO, eye disease progression after radioiodine treatment seems to be significantly higher in smokers than in non-smokers.