— Poor Air Quality Amplifies Risks from Genetic Predispositions

Are there any inflammatory diseases that aren’t aggravated by air pollution? As more research emerges, it's becoming increasingly difficult to identify any. A recent study has unveiled a new association between exposure to key air pollutants and the onset of psoriasis in Great Britain.

Leveraging data from the U.K. Biobank, with a median follow-up period of nearly 12 years, scientists identified that annual exposure to particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx) increased the likelihood of developing psoriasis by 19% to 47% for each rise in exposure quartile, according to a report led by Jian Yang, PhD, of China Three Gorges University in Yichang, China, and colleagues.

Moreover, the risk of psoriasis was nearly doubled for those with a high genetic susceptibility, in conjunction with increased pollution exposure, as indicated by the results published in JAMA Network Open.

While the researchers acknowledged that causality cannot be definitively proven, they emphasized that the findings call for action. “The need for effective interventions to combat air pollution and its effects on individuals susceptible to psoriasis is pressing,” they wrote.

Recently, Yang’s team also explored similar data to draw parallels between systemic lupus erythematosus (SLE) and exposure to the same pollutants, yielding comparable outcomes.

Their interest in such associations stems from the role that particulate matter and nitrogen compounds play in driving systemic inflammation, which raises risks for an array of chronic diseases. Prior studies have linked air pollution to conditions such as cardiovascular disease, diabetes, Parkinson's disease, autism, and obesity.

For the psoriasis study, the researchers drew data from the U.K. Biobank—a project tracking the health of approximately half a million participants enrolled from 2006 to 2010. Alongside health data, genetic materials are also collected for analysis. Individuals from areas lacking consistent air pollution monitoring, as well as those with pre-existing psoriasis, were excluded, leaving a final cohort of about 474,000 participants.

Pollutant levels were sourced from environmental data across Britain and averaged on an annual basis for each participant, stratified into quartiles. Adjustments were made for various potential confounders such as age, sex, ethnicity, socioeconomic factors, smoking habits, alcohol consumption, physical activity, diet, and medical comorbidities.

Over the course of the study, more than 4,000 participants were diagnosed with psoriasis. The correlation between pollutant exposure and psoriasis risk, reflected as hazard ratios (HR) for each quartile increase, was notable:

• PM2.5: HR 1.41 (95% CI 1.35-1.46)
• PM10: HR 1.47 (95% CI 1.41-1.52)
• NO2: HR 1.28 (95% CI 1.23-1.33)
• NOx: HR 1.19 (95% CI 1.14-1.24)

The risk differences between the highest (quartile 4) and lowest exposure levels (quartile 1, used as the reference) showed even more pronounced effects. Hazard ratios were 2.01 for PM2.5 and 2.21 for PM10. For NO2 and NOx, hazard ratios were 1.64 and 1.34, respectively, with all results statistically significant at P<0.001.

When genetic predisposition was factored in, the risks increased substantially. Those with both high genetic risk and elevated particulate matter exposure had hazard ratios exceeding 4.0 compared to those with low genetic risk and minimal exposure. For nitrogen oxides, the combination of high genetic risk and high exposure resulted in hazard ratios of 2.95 for NO2 and 2.44 for NOx.

In an accompanying commentary, three independent experts highlighted the growing recognition that pollutants likely play a causative role in psoriasis and other autoimmune diseases, emphasizing the importance of risk mitigation efforts.

The challenge, however, is in determining how, argued Katrina Abuabara, MD, MSCE, of the University of California San Francisco, along with her colleagues.

While reducing pollution levels would seem the obvious solution, clinicians have limited influence over environmental policies. Nonetheless, the commentators pointed out that medical interventions could be an option for some patients.

For example, research has identified pathways involving the aryl hydrocarbon receptor, which may worsen skin conditions like atopic dermatitis when triggered by pollutants. Understanding these mechanisms better could lead to preventive treatments, they proposed. “Further exploration into genetic-environment interactions and potential treatments is essential to address the interplay between air pollution and inflammatory skin conditions,” they wrote.

In the short term, however, the outlook for prevention strategies remains uncertain. “It is unclear whether topical treatments or moisturizers provide any protection for high-risk individuals, or if they might even increase pollutant penetration,” they cautioned. They also warned against fully blocking UV light, as sunlight can aid with inflammatory skin diseases, despite the instinct to suggest protective clothing.

Ultimately, they concluded that “as climate change continues to reshape air quality worldwide, there is a critical need for further research to establish clinical guidelines for safeguarding patients susceptible to pollution-related skin inflammation.”

Disclosures

This study was supported by the China Postdoctoral Science Foundation.

The study’s authors reported no relevant financial conflicts of interest. However, the accompanying editorialists disclosed relationships with companies including Pfizer, Bristol Myers Squibb, Sanofi, Incyte, and others, as well as ties to the National Eczema Association.

Primary Source:

JAMA Network Open

Source Reference: Wu J, et al. “Exposure to air pollution, genetic susceptibility, and psoriasis risk in the UK” JAMA Netw Open. 2024; DOI: 10.1001/jamanetworkopen.2024.21665.

Secondary Source:

JAMA Network Open

Source Reference: Kim RW, et al. “Air pollution and inflammatory skin diseases — Can clinicians recommend strategies to reduce risk?” JAMA Netw Open. 2024; DOI: 10.1001/jamanetworkopen.2024.21633.