Elastin Degradation and Lung Function Deterioration with Remote Secondhand Tobacco Smoke Exposure in Never-smokers.

Background Prolonged past exposure to secondhand tobacco smoke (SHS) in never-smokers is associated with abnormal lung function and reduced diffusing capacity suggestive of an associated lung tissue injury and damage. The mechanisms by which past SHS exposure may contribute to lung tissue damage are unknown. Elastin is a major constituent of extracellular matrix in lung parenchyma. Objective To determine whether past exposure to SHS is associated with ongoing lung tissue damage as indicated by elevated elastin degradation products that are linked to lung function. Methods We measured the plasma levels of elastin degradation markers (EDM) from 193 never-smoking flight attendants with history of remote SHS exposure in aircraft cabin and 103 nonsmoking flight attendants or sea-level control participants without such history of cabin SHS exposure, and examined those levels versus their lung function with adjustment for covariates. The cabin SHS exposure was estimated based on airline employment history and years of smoking ban enactment. Results The median [interquartile range] plasma EDM level for all participants was 0.30 [0.24-0.36] ng/mL with a total range of 0.16-0.65 ng/mL. Plasma EDM levels were elevated in those with history of exposure to cabin SHS compared to those not exposed (0.33±0.08 vs. 0.26±0.06 ng/mL; age- and sex-adjusted P<0.001). In those with history of cabin SHS-exposure, higher EDM levels were associated with lower diffusing capacity (parameter estimate (PE) [95%CI]=4.2 [0.4-8.0] %predicted decrease per 0.1 ng/mL increase in EDM; P=0.030). Furthermore, EDM levels were inversely associated with FEV1, FEV1/FVC, and FEF25-75 (PE [95%CI]=5.8 [2.1-9.4], 4.0 [2.2-5.7], and 12.5 [5.8-19.2] %predicted decrease per 0.1 ng/mL increase in EDM, respectively; P<0.001). Plasma EDM mediated a substantial fraction of the association of SHS with FEV1, FVC, and FEF25-75 (P<0.05). Conclusions Long after past exposure to SHS, there is ongoing elastin degradation beyond what is expected from the aging process, which likely contributes to lower lung function and reduced pulmonary capillary bed as seen in COPD.