Exposure to air pollution – even short term – may play a role in triggering psoriasis flares, according to new research from Italy, which found a significant association between exposure to higher levels of air pollution prior to patients presenting for psoriasis flares at medical visits, compared with visits unrelated to flares.
“We found that higher concentration of different air pollutants was associated with psoriasis flares in patients living in an industrialized city of the Po Valley” in Verona, Italy, report the authors of the study, published in JAMA Dermatology.
The findings underscore the need for clinicians to “consider environmental/external triggers in patients with chronic inflammatory diseases experiencing flares,” first author Francesco Bellinato, MD, of the Section of Dermatology and Venereology, University of Verona, Italy, told this news organization.
He and his coauthors conducted a case-crossover and cross-sectional longitudinal study that involved a retrospective analysis of data in 957 patients in Verona with chronic plaque psoriasis, who were evaluated every 3-4 months at an outpatient dermatology clinic for a median of 2.7 years.
Over the study period, disease flares, defined as an increase in the Psoriasis Area and Severity Index (PASI) of 5 or more points from the previous visit, occurred in 369 patients (38.6%), consistent with known flare rates in psoriasis. Participants in the study (mean age, 61) had median PASI scores of 12 during visits for psoriatic flares compared with PASI scores of 1 during control (no flare) visits (P < .001).
Evaluations of mean concentrations of several air pollutants within 10 miles of the patients over 4,398 visits showed that concentrations were significantly higher in the 60 days prior to the psoriasis flare, compared with control visits that were not related to flares (P < .05), after adjusting for factors including seasonality (by trimester, to adjust for weather conditions and UV/sunlight exposure) and the type of systemic psoriasis treatments patients were receiving (conventional or biological).
Increases in air pollutant levels prior to flares were observed among the 35.8% of patients who had a flare of at least a 50% increase in the PASI score, as well among the 47.2% of patients who had at least a 100% increase in PASI, compared with control visits not involving flares. In addition, mean and area-under-the-curve concentrations of air pollutants were higher in the 60 days before the visits among those with PASI 5 or greater, compared with those with PASI scores below 5, the authors add.
Dr. Bellinato noted that the associations were not limited to any particular subgroup. “The associations with air pollution and flares were observed in the entire population,” he said in an interview.
Vehicle, industry emissions
The pollutants that were measured were those mainly associated with fossil fuel combustion from vehicle and industry emissions, including carbon monoxide, nitrogen dioxide, other nitrogen oxides, benzene, coarse particulate matter (2.5-10.0 μm in diameter) and fine particulate matter (less than 2.5 μm in diameter).
They note that the risk of having a PASI score of 5 or greater was elevated even at thresholds of exposure that are largely considered safe. “Indeed, the risk for having a PASI score of 5 or greater was 40% to 50% higher at exposures as low as 20 μg/m3” of coarse particulate matter and 15 μg/m3 of fine particulate matter in the 60-day period prior to the visits, they write.
The authors referred to evidence linking air pollution with a worsening of a variety of inflammatory cutaneous diseases, including atopic dermatitis and acne, as well as photoaging. Psoriasis flares are known to be triggered by a variety of environmental factors, including infections or certain drugs; however, evidence of a role of air pollution has been lacking. Potential mechanisms linking the exposures to flares include the possibility that exhaust particles can activate skin resident T-cells, “resulting in abnormal production of proinflammatory cytokines including tumor necrosis factor α (TNF-α) and interleukins (ILs), including IL-1α, IL-1β, IL-6, and IL-8.8,” the authors write.
Their results, though inferring a causal relationship, fall short of showing a clear dose–response relationship between higher pollutant levels and an increased risk of psoriasis flares, possibly the result of a smaller sample size of subjects exposed to higher levels of pollution, they add.
Limitations of the study included the definition of flare, which used a clinical score that could be affected by other measurements, they point out, while strengths of the study included the large cohort of patients followed for over 7 years and the availability of daily measurements of air pollutants.
While the study suggests that environmental air pollutant fluctuations may affect psoriasis course,” the authors concluded, “further study is needed to examine whether these findings generalize to other populations and to better understand the mechanisms by which air pollution may affect psoriasis disease activity.”
Dr. Bellinato and four coauthors had no disclosures; the remaining authors had disclosures that included receiving personal fees from pharmaceutical companies that were outside of the submitted work.
A version of this article first appeared on Medscape.com.