Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report

Abstract

Although it is well accepted that air pollution exposure exacerbates preexisting airway disease, it has not been firmly established that long-term pollution exposure increases the risk of new-onset asthma or chronic obstruction pulmonary disease (COPD). This Workshop brought together experts on mechanistic, epidemiological, and clinical aspects of airway disease to review current knowledge regarding whether air pollution is a causal factor in the development of asthma and/or COPD. Speakers presented recent evidence in their respective areas of expertise related to air pollution and new airway disease incidence, followed by interactive discussions. A writing committee summarized their collective findings. The Epidemiology Group found that long-term exposure to air pollution, especially metrics of traffic-related air pollution such as nitrogen dioxide and black carbon, is associated with onset of childhood asthma. However, the evidence for a causal role in adult-onset asthma or COPD remains insufficient. The Mechanistic Group concluded that air pollution exposure can cause airway remodeling, which can lead to asthma or COPD, as well as asthma-like phenotypes that worsen with long-term exposure to air pollution, especially fine particulate matter and ozone. The Clinical Group concluded that air pollution is a plausible contributor to the onset of both asthma and COPD. Available evidence indicates that long-term exposure to air pollution is a cause of childhood asthma, but the evidence for a similar determination for adult asthma or COPD remains insufficient. Further research is needed to elucidate the exact biological mechanism underlying incident childhood asthma, and the specific air pollutant that causes it.

Keywords: COPD; air pollution; asthma; new-onset airway disease.

Figure 1.

Meta-analysis of studies of nitrogen dioxide and new-onset asthma in children. Reprinted by permission from Reference . CI = confidence interval; I² = percentage of variation across studies due to heterogeneity; IV = instrumental variable; SE = standard error.

Figure 2.

Meta-analysis of black carbon soot associations with new-onset asthma. Reprinted by permission from Reference . CI = confidence interval; I² = percentage of variation across studies due to heterogeneity; IV = instrumental variable; SE = standard error.

Figure 3.

Long-term ozone exposure effects consistent with a role for air pollution in airway inflammation and remodeling leading to asthma development. IL-5 = interleukin-5; IL-13 = interleukin-13; ILC = innate lymphoid cells. Image by Jack R. Harkema.

Figure 4.

Workshop findings and conclusions. BC = black carbon; COPD = chronic obstructive pulmonary disease; NO₂ = nitrogen dioxide; PM_2.5 = particulate matter less than or equal to 2.5 μm in aerodynamic diameter; TRAP = traffic-related air pollution.