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HomePollutionAir PollutionRisk of Acute IPF Flares Seen to Rise With Air Pollutant Exposure

Risk of Acute IPF Flares Seen to Rise With Air Pollutant Exposure


Long-term exposure to air pollutants — nitrogen dioxide, ozone, and fine particle matter — appears to greatly raise the risk of acute exacerbations, or sudden bouts of symptom worsening, in people with idiopathic pulmonary fibrosis (IPF), a study of patients in Greece reported.

“Our findings show consistent positive associations” between previous year mean exposure and a flare risk, “suggesting that ambient air pollution may represent one of a series of factors that could trigger acute exacerbation in IPF,” the researchers wrote.

The study, “Long-term personal air pollution exposure and risk for acute exacerbation of idiopathic pulmonary fibrosis” was published in the journal Environmental Health.

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Acute IPF exacerbations, characterized by rapid disease worsening, diminish lung function and can be deadly. Urban air pollution is increasingly recognized to play a role in lung diseases that include IPF, but its role in acute IPF exacerbations remains unclear.

“Although it is widely accepted that air pollution deteriorates diverse chronic respiratory diseases such as asthma and chronic obstructive pulmonary disease, there is lack of evidence on its potential role on the course of IPF and particularly on the devastating event” of an acute IPF exacerbation, the research team wrote.

Led by researchers at National and Kapodistrian University of Athens, the team investigated the link between long-term air pollution exposure and acute exacerbation risk.

Research recently suggested that air pollution is associated with the shortening of telomeres — structures located at the tip of chromosomes that protect them from damage, much like the plastic tips of shoelaces. Telomere shortening occurs as part of the aging process, but it has also been linked with an increased susceptibility to IPF.

As such, the researchers took into account the potential confounding effects of telomeres in their analysis.

Their study enrolled 118 IPF patients (88 men, mean age of 72), of whom 55 (47.4%) had at least one acute exacerbation. All had been treated with broad-spectrum antibiotics, but not immunosuppressive therapies.

Each person’s exposure to outdoor air pollutants was estimated retrospectively, based on their residential addresses in 2012. Pollutants considered included ozone, nitrogen dioxide (NO2), particulate matter measuring 10 micrometers or less in diameter (PM10) and fine particulate matter measuring 2.5 micrometers or less in diameter (PM2.5).

Particulate matter is of importance because this airborne matter contains microscopic solids or liquid droplets that, at 10 or 2.5 micrometers, are so small they can be inhaled and drawn deep into the lungs. A human hair, in comparison, is about 100 micrometers.

Nitrogen dixoide largely enters the air through the burning of fuel by cars, trucks and other vehicles, and by power plants; ozone is a highly reactive gas that, at ground level, largely results from photochemical reactions between two major classes of air pollutants, volatile organic compounds and nitrogen oxides. Ozone is a major contributor to the haze known as “smog.”

People living in the Greater Athens area, which accounted for more than half (56%) of this study’s population, were exposed to significantly higher mean levels of NO2, as well as PM10 and PM2.5. Those residing outside Greater Athens were exposed to higher ozone concentrations.

A significant link was found between acute exacerbations and a mean increase of 10 micrograms per cubic meter (mcg/m3) of NO2, PM10, and PM2.5 levels in the previous year.

Notably, this association was “independent of age, gender, smoking, lung function and antifibrotic treatment,” the researchers wrote. This link was maintained even after taking into account the length of telomeres, which was determined in a subgroup of 36 patients.

Researchers also assessed the potential link between exposure to air pollutants and certain inflammatory mediators known to be involved in acute IPF exacerbations, including interleukin-4 (IL-4), IL-3, and the protein osteopontin.

A 10 mcg/m3 increase in ozone levels in the previous year was associated with changes in IL-4 and, to a lesser extent, in IL-3 and osteopontin, analyses found.

Overall, “long term personal exposure to increased concentrations of air pollutants is associated with increased risk of [acute exacerbations] in IPF patients,” they wrote.

“Identifying potential modifiable risk factors, such as air pollution exposure, could represent a critical preventive tool against IPF progression and morbidity,” the team added, recommending further study into this area.





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