Air Pollution May Be Causing Your Eczema

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Air Pollution May Be Causing Your Eczema

New research shows that chemicals from car exhaust, wildfires, and cigarette smoke impair our skin’s ability to make healthy oil, making it more likely to get eczema. 

The finding points scientists toward how to better treat the skin ailment. There are now more than three times as many eczema cases as there were in the 1970s, and it now affects as many as 20% of children and 10% of adults.

“I think these authors are spot-on in recognizing that the incidence of allergic conditions is increasing concurrently with how different pollutants are increasing in our environment,” said Denver-based pediatric allergist and immunologist Jessica Hui, MD, according to NBC News. “We’re finally understanding more about why people are getting eczema.”

Some people get eczema due to genetics, but the new research built on the previous understanding of how chemicals called diisocyanates can trigger the eczema symptoms of severe itching, skin redness, and oozing or painful rashes. An experiment on mice showed that exposure to a specific part of diisocyanates, called isocyanates, disrupted oil production that the skin needs to stay healthy.

Researchers at the National Institutes of Health “found that when bacteria that live on healthy skin are exposed to isocyanate, they must adapt to survive,” the agency summarized in a news release. “When they adapt, these bacteria shift their metabolism away from making the lipids, or oils, that skin needs to stay healthy. This finding suggests that eczema may be treatable by replacing the modified skin bacteria with healthy bacteria.”

The study was published earlier this year in the journal Science Advances.

Sources:

NBC News: “Eczema’s cause could be in the air we breathe.”

National Institute of Allergy and Infectious Diseases: “NIAID Researchers Identify Link Between Common Chemicals and Eczema.”

Science Advances: “Exposure to isocyanates predicts atopic dermatitis prevalence and disrupts therapeutic pathways in commensal bacteria.”

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