Exposure to diesel exhaust may be more harmful to former smokers with chronic obstructive pulmonary disease (COPD) than to ex-smokers without COPD or healthy individuals who never smoked. Notably, the harm accrues via an inflammatory response. These were among findings of a Canadian study recently published in the American Journal of Respiratory Critical Care Medicine.

Because mounting evidence suggests that COPD can be caused and worsened by air pollution, the researchers sought to chronicle the impact of short-term air pollution exposure on inflammatory markers, proteases, and antiproteases in the lower airways of older adults with COPD and without. The COPA study, a randomized, double-blinded, controlled, human crossover, exposure clinical trial (ClinicalTrials.gov Identifier: NCT02236039) recruited 30 participants (aged 40 to 80 years; mean age 60), including 10 ex-smokers with mild to moderate COPD, 9 healthy ex-smokers, and 11 healthy individuals who never smoked.

At the Air Pollution Exposure Laboratory in Vancouver, Canada, the control group was exposed to filtered air without exhaust, whereas the other 2 randomly assigned groups were exposed to diesel exhaust in washout-separated 2-hour periods. Bronchoscopy was conducted 24 hours after exposure to gather lavage, and cell counts were performed on blood and airway samples. The researchers used enzyme-linked immunosorbent assays to measure acute inflammatory proteins, matrix proteinases, and antiproteases in the airway and in blood samples.


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In previous smokers with COPD, exposure to diesel exhaust raised serum amyloid A by 1.67 (95% CI, 1.21-2.30; P =.04) and matrix metalloproteinase 10 by 2.61 (95% CI, 1.38-4.91; P =.04) in bronchoalveolar lavage. Circulating lymphocytes rose following exhaust exposure by 0.14 cells x 109/L; (95% CI, 0.05-0.24; P =.03) regardless of COPD status. These increases were not observed in the other participants.

Limitations of the study include studying a small sample size compared with the number of phenotypic changes; having a COPD group that was older than the non-COPD groups; measuring the total abundance of proteases and antiproteases rather than measuring proteolytic activity in the bronchial samples; and working with COPD participants who were similar in age, limiting how much exposure-by-age interactions could have been evaluated. The study data nonetheless suggest that age alone bestows some susceptibility independent of patient COPD status, a finding that was not an original focus of the trial.

The investigators suggested that future studies attempt to recruit more participants with differing COPD endotypes and severities. “Moreover, future studies should include those with other cardiopulmonary disease to assess the relationship between air pollution and other chronic conditions,” they wrote. “It is important to note that factors such as genetics, sex, and age may modify one’s response to air pollution, and future studies, particularly those that use prospective observational study design or parallel study arm design, should consider these factors, and adjust for them in the analyses for generalizability,” they added.

Reference

Ryu MH, Afshar T, Li H, et al. Impact of exposure to diesel exhaust on inflammation markers and proteases in former smokers with COPD: a randomized, double-blinded, crossover study. Am J Respir Crit Care Med. Published online February 24, 2022. doi:10.1164/rccm.202104-1079OC