Previous studies have tied air pollution exposure to cardiovascular disease, diabetes, Parkinson’s disease, even autism and obesity – and recent research has now identified a link between new-onset psoriasis and exposure to four major pollutants in Britain.
The Chinese researchers also suggested that having high degrees of genetic risk (as established from previous genome-wide association studies) roughly doubled the psoriasis risk for every degree of pollution exposure, reports Medpage Today.
Prospectively collected data from the UK Biobank programme, with median follow-up of 11.9 years, showed that average annual exposure to these pollutants – PM2.5 and PM10 (particulate matter 2.5 μm or less and 10 μm or less, respectively), nitrogen dioxide (NO2), and any nitrogen oxide species (NOx) – was associated with increases of 19% to 47% in risk for incident psoriasis for each step up in quartiles of exposure, reported Jian Yang, PhD, of China Three Gorges University in Yichang, China, and colleagues.
In their report, published in JAMA Network Open, the researchers acknowledged that while these data can't prove causality, they nevertheless believed their findings warrant action.
“There is a need to devise and implement effective interventions aimed at mitigating air pollution and safeguarding individuals from the effects associated with psoriasis,” they wrote.
Recently, Yang and colleagues also published a paper using the same data source and virtually identical methods to identify very similar associations between new-onset systemic lupus erythematosus and particulate matter and nitrogen oxide exposure.
Their rationale for looking for such connections was also nearly the same: particulate matter and nitrogen oxides promote systemic inflammation, which in turn raises risk for all manner of chronic diseases affecting organ systems throughout the body.
For the psoriasis study, Yang’s group drew on the UK Biobank, a prospective project that collects health records for some 500 000 individuals in Britain, enrolled from 2006 to 2010, and also administers periodic questionnaires and physical exams. Tissue samples are collected to allow for genetic analysis. Participants living in areas without regular air pollution monitoring were excluded, as were those with psoriasis at baseline, such that about 474 000 were included in the study.
Exposures for the four pollutants were derived from British environmental monitoring data and averaged annually for individual participants. Levels of each pollutant were stratified into quartiles. Adjustments were taken for a wide variety of potential confounders: age, sex, race-ethnicity, poverty level, education, employment, smoking and alcohol status, diet quality, physical activity, and certain comorbidities.
Just more than 4 000 new cases of psoriasis were recorded for participants after enrolment in the Biobank. Based solely on pollutant exposures, psoriasis development correlated with pollution level, per increase in quartile of exposure, as follows:
• 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)
Yang and colleagues also reported these associations as comparisons between quartile 1 (the reference) and quartile 4. Hazard ratios in this analysis were 2.01 and 2.21 for PM2.5 and PM10, respectively, and 1.64 and 1.34 for NO2 and NOx, respectively – all with P<0.001.
Adding in genetic risk, however, raised these increases markedly. Hazard ratios above 4.0 were found for individuals at high genetic risk who also had the greatest exposures to both types of particulate matter, relative to those with both low genetic risk and low exposures. The “high-high” combination for nitrogen oxides was associated with psoriasis risk with hazard ratios of 2.95 and 2.44 for NO2 and NOx, respectively, again with respect to low genetic risk and low exposure.
An accompanying commentary by three independent scholars also took as given that pollution plays some kind of causative role in psoriasis and other diseases, and agreed that risk mitigation is key.
The question is how, according to Katrina Abuabara, MD, MSCE, of the University of California San Francisco, and two colleagues.
Although lowering pollution levels would obviously be preferred, clinicians have little power in that sphere. But medical interventions for individual patients may be possible, the commentators said.
For example, other research has identified a certain pathway involving the aryl hydrocarbon receptor that, at least in animal models, reacts with air pollutants to worsen atopic dermatitis. Better understanding of this phenomenon might lead to novel preventive therapies, Abuabara and colleagues suggested.
“More generally, future research is needed on gene-environment interactions with air pollution and the potential role of treatments on the interaction between air pollution and inflammatory skin disease,” they wrote.
But in the short term, the commentators were pessimistic about practical approaches to prevention. “It is unclear whether topical moisturisers and treatments are likely to protect high-risk individuals or whether they may increase the penetration of air pollutants,” they wrote, adding, “While it may seem intuitive to counsel patients to use protective clothing, there are little data to support the efficacy of such a recommendation.”
Blocking sun exposure could even be counterproductive, as ultraviolet radiation can help in inflammatory skin diseases.
The upshot, they concluded, is that “(a)s climate change induces worldwide alterations in air quality, additional research to inform clinical recommendations on how best to protect patients from and treat pollution-sensitive inflammatory skin disease is urgently needed”.
Study details
Exposure to Air Pollution, Genetic Susceptibility, and Psoriasis Risk in the UK
Junhui Wu, Yudiyang Ma, Jian Yang, et al
Published in JAMA Network Open on 16 July 2024
Abstract
Importance
Psoriasis is a common auto-inflammatory disease influenced by complex interactions between environmental and genetic factors. The influence of long-term air pollution exposure on psoriasis remains underexplored.
Objective
To examine the association between long-term exposure to air pollution and psoriasis and the interaction between air pollution and genetic susceptibility for incident psoriasis.
Design, Setting, and Participants
This prospective cohort study used data from the UK Biobank. The analysis sample included individuals who were psoriasis free at baseline and had available data on air pollution exposure. Genetic analyses were restricted to white participants. Data were analysed between November 1 and December 10, 2023.
Exposures
Exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter with a diameter less than 2.5 µm (PM2.5), and particulate matter with a diameter less than 10 µm (PM10) and genetic susceptibility for psoriasis.
Main Outcomes and Measures
To ascertain the association of long-term exposure to NO2, NOx, PM2.5, and PM10 with the risk of psoriasis, a Cox proportional hazards model with time-varying air pollution exposure was used. Cox models were also used to explore the potential interplay between air pollutant exposure and genetic susceptibility for the risk of psoriasis incidence.
Results
A total of 474 055 individuals were included, with a mean (SD) age of 56.54 (8.09) years and 257 686 (54.36%) female participants. There were 9186 participants (1.94%) identified as Asian or Asian British, 7542 (1.59%) as black or black British, and 446 637 (94.22%) as white European. During a median (IQR) follow-up of 11.91 (11.21-12.59) years, 4031 incident psoriasis events were recorded. There was a positive association between the risk of psoriasis and air pollutant exposure. For every IQR increase in PM2.5, PM10, NO2, and NOx, the hazard ratios (HRs) were 1.41 (95% CI, 1.35-1.46), 1.47 (95% CI, 1.41-1.52), 1.28 (95% CI, 1.23-1.33), and 1.19 (95% CI, 1.14-1.24), respectively. When comparing individuals in the lowest exposure quartile (Q1) with those in the highest exposure quartile (Q4), the multivariate-adjusted HRs were 2.01 (95% CI, 1.83-2.20) for PM2.5, 2.21 (95% CI, 2.02-2.43) for PM10, 1.64 (95% CI, 1.49-1.80) for NO2, and 1.34 (95% CI, 1.22-1.47) for NOx. Moreover, significant interactions between air pollution and genetic predisposition for incident psoriasis were observed. In the subset of 446 637 white individuals, the findings indicated a substantial risk of psoriasis development in participants exposed to the highest quartile of air pollution levels concomitant with high genetic risk compared with those in the lowest quartile of air pollution levels with low genetic risk (PM2.5: HR, 4.11; 95% CI, 3.46-4.90; PM10: HR, 4.29; 95% CI, 3.61-5.08; NO2: HR, 2.95; 95% CI, 2.49-3.50; NOx: HR, 2.44; 95% CI, 2.08-2.87).
Conclusions and Relevance
In this prospective cohort study of the association between air pollution and psoriasis, long-term exposure to air pollution was associated with increased psoriasis risk. There was an interaction between air pollution and genetic susceptibility on psoriasis risk.
Medpage Today article – Psoriasis Joins List of Diseases Tied to Air Pollution (Open access)
See more from MedicalBrief archives:
Psoriasis tied to increased heart disease risk – Italian study
Pollution impact far-reaching from reduced sperm count to cancer: UK study
One in six people dying prematurely from air pollution
Study finds air-pollution's impact on health may be worse than thought