Impact de la pollution sur le vitiligo.

Does pollution play a role in the onset of vitiligo?

Vitiligo is an autoimmune disease that causes white patches on the skin. Although the mechanisms leading to its onset are partially understood today, several environmental factors are still suspected of being involved in the pathogenesis of vitiligo. Among them, pollution is considered a potential trigger or aggravator of this condition. Let's explore this together.

Summary
Published December 12, 2024, updated on December 12, 2024, by Pauline, Chemical Engineer — 5 min read

Is air pollution implicated in vitiligo?

Whether it originates from natural or anthropogenic sources, pollution has significant effects on human health, as well as on the skin. It is defined by the World Health Organisation (WHO) as follows: "a contamination of the indoor or outdoor environment by any chemical, physical or biological agent that modifies the natural characteristics of the atmosphere." There are numerous sources of pollutants, including marshes, biological decomposition, thermal power plants, and the incineration of household and industrial waste. Even though air pollution is particularly prevalent in urban areas and zones of activity, rural environments are by no means spared.

Pollution is now considered a potential trigger for certain autoimmune diseases, including the vitiligo. This hypothesis is particularly derived from the association between high oxidative stress and the onset of vitiligo. Several studies have indeed shown an increased sensitivity to oxidative stress in patients with vitiligo and the presence in these patients of 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 pollution 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 alter the cellular function of melanocytes. Moreover, oxidative stress promotes inflammation, an important 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.

Indeed, pollution, particularly that of anthropogenic origin, constitutes a major source of pro-oxidants. It includes fine particles (PM2.5 and PM10), nitrogen oxides (NOx), polycyclic aromatic hydrocarbons (PAHs) and free radicals resulting from the combustion of fossil fuels and industries. These agents are capable of penetrating the skin, where they generate exacerbated oxidative stress and where they can cause direct damage to skin cells, including melanocytes. Once inside the cells, pollution particles react with lipids, proteins and DNA, creating free radicals and triggering oxidation processes that disrupt cellular balance. These disruptions could be particularly significant in individuals predisposed to vitiligo, who are highly sensitive to oxidative stress.

A recent study has explored the connection between vitiligo and pollution, employing the so-called Mendelian randomisation method. This technique utilises the properties of genetics to better understand the cause-and-effect relationships between an external factor and a disease. To carry out this Mendelian randomisation, the researchers used information from several large genetic databases and examined the effect of two pollutants, fine particles (PM2.5) and nitrogen oxides (NOx), on certain autoimmune diseases such as vitiligo. The analysis concluded a potential link between fine particles and vitiligo, meaning it is possible but not certain that pollution could be a triggering or exacerbating factor for vitiligo.

Given the well-established role of oxidative stress in vitiligo and the impact of pollution on this mechanism, it would seem logical to consider pollution as a factor that could influence this disease. However, further work is needed to confirm this hypothesis and better understand the underlying mechanisms.

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