Does tobacco cause vitiligo?

Recognizable by the white patches it causes on the skin, vitiligo is a dermatosis primarily mediated by the autoimmune system. More specifically, the immune system of individuals suffering from this disease erroneously targets certain melanocytes, the epidermal cells responsible for producing melanin, and destroys them. In the absence of this pigment, the skin turns white. All areas of the body can be affected by vitiligo, although the face, hands, and feet are usually the first to be affected. Non-contagious and not harmful to health, vitiligo is nonetheless not benign and can have a significant psychological impact due to its conspicuous nature. The selective loss of melanocytes observed in individuals affected by vitiligo is due to several, sometimes intertwined, factors. Among them, tobacco is sometimes cited, due to the significant oxidative stress it generates in skin cells.

Cigarette smoke contains approximately 1017 free radicals per puff.

Indeed, several studies have shown that patients suffering from vitiligo exhibit an increased sensitivity to oxidative stress, as well as a cellular imbalance between pro-oxidants and antioxidants. It has been suggested that this imbalance could be responsible for the increased sensitivity of melanocytes to external pro-oxidant stimuli , such as tobacco, and over time, the induction of a pre-senescence state. Subsequently, the generation and accumulation of free radicals in the cells could damage DNA and impair the proper functioning of melanocytes. Moreover, oxidative stress promotes inflammation, a significant factor in the progression of vitiligo. The activation of inflammatory cytokines, such as TNF-α, IL-1, and IFN-γ, can indeed increase the infiltration of immune cells into the skin and intensify the attack on melanocytes.

To verify this hypothesis, a retrospective study was conducted in Korea between 2009 and 2012, examining the data of 23,503,807 individuals who underwent a health examination during this period. 22,811 cases of vitiligo were identified. After data analysis, researchers noted that the risk ratio, or hazard ratio in English, was 0.69, indicating that smokers would have a 31% reduced risk of developing vitiligo compared to non-smokers. The confidence interval, ranging from 0.65 to 0.72, reflects the accuracy of this estimate, suggesting that the true risk ratio is very likely within this range.

These findings contradict the hypothesis that tobacco could be a trigger for vitiligo, a disease for which the impact of oxidative stress has been confirmed by numerous studies. This could be explained as follows: while tobacco generally has a pro-oxidant effect, it may also have some antioxidant effects. Indeed, it has been shown that tobacco contains compounds that inhibit the activity of monoamine oxidase (MAO), an enzyme that stimulates the production of free radicals. However, high activity of this enzyme has been observed in individuals affected by vitiligo. Therefore, it is possible that the inverse relationship between vitiligo and smoking can be explained by the inhibition of MAO by smoking. More research is nevertheless needed to determine the exact mechanism.

Furthermore, the authors acknowledge some limitations in their study. The genetic susceptibility of individuals or family history of vitiligo were not initially evaluated. Moreover, the causal links between smoking and vitiligo could not be formally identified using an epidemiological study. Lastly, the smoking status of the participants was obtained from self-reported questionnaires. A response bias due to the fact that the respondents may not have provided accurate information cannot be ruled out.

Given the damage caused by tobacco on health and the fragility of the study's conclusions, smoking should not be considered as a prevention or treatment option for vitiligo.