麻豆果冻传媒影音

Is there any disease with an inflammatory aspect that isn't triggered or exacerbated by air pollution? It's certainly getting harder to name one with any certainty, as a new study has now identified a link between new-onset psoriasis and exposure to four major pollutants in Great Britain.

Prospectively collected data from the U.K. Biobank program, with median follow-up of 11.9 years, showed that average annual exposure to these pollutants -- PM_2.5 and PM₁₀ (particulate matter 2.5 μm or less and 10 μm or less, respectively), nitrogen dioxide (NO₂₎, and any nitrogen oxide species (NO_x) -- 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.

But 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, according to the group's .

Although the researchers acknowledged that these data can't prove causality, they nevertheless believed their findings warrant action. "[T]here 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.

Last week, Yang and colleagues 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. Previous studies have exposure to .

For the psoriasis study, Yang's group drew on the U.K. 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 over 4,000 new cases of psoriasis were recorded for participants after enrollment in the Biobank. Based solely on pollutant exposures, psoriasis development correlated with pollution level, per increase in quartile of exposure, as follows:

• PM_2.5: 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)
• NO_x: 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 PM_2.5 and PM₁₀, respectively, and 1.64 and 1.34 for NO₂ and NO_x, 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 NO_x, respectively, again with respect to low genetic risk and low exposure.

An 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 moisturizers 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."

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