EFFECTS OF LONG‑TERM AIR POLLUTION EXPOSURE ON THE DEVELOPMENT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Abstract

COPD is a significant contributor of morbidity and mortality in the world and an emerging body of literature is mainstreaming air pollution in the ambient air as one of the key etiological factors that cannot be linked to tobacco smoking. Nonetheless, the relationships between the exposure and the response, the pollutant-specific effects and mechanisms have not been completely defined. In this systematic review and meta-analysis 147 studies (with more than 12.8 million participants) were synthesized in 27 countries. These were random-effects-combination risk models of the incidence of COPD of various types of pollutants and stratified by subgroup analysis, by smoking status, geographic area and genetic predisposition. Two stage multivariate meta-analytical models with spline functions were used to model the non-linear exposure-response relationships. Standardized mean difference was used to mix the key biomarkers of oxidative stress, inflammation and cellular injury of the mechanistic data. The PM 2.5 had become the most significant one as it was related to COPD incidence by that time compared to black carbon. The risk estimates among the non-smokers were much higher as opposed to the current smokers. There was supra-linearity in exposure-response relationships with a critical threshold of 7.2 µg.m -1 of PM.5. Mechanistic analyses showed that the level of IL-6 (SMD = 0.84, 1.87-fold increase), 8-hydroxy-2'-deoxyguanosine (SMD = 0.93, 2.12-fold increase) and TNF-alpha were significantly increased after chronic exposure. The gene-environment interaction susceptibility was found to be significant in AGER ( 0.112 = 0.038) where the gene is the gene of interest. Also, it was found that the black carbon and PM 2.5 were synergistic to guarantee that they were supra-additive effects (synergy index = 1.47). Time-lagged analyses determined that, there was a critical exposure period of 610 years before diagnosis (HR = 1.124 per IQR) and urban residents were 7.5% more at risk compared to rural residents. The attributable risk studies revealed that exposure to the environment was a cumulative risk factor resulting in an approximate 50.7% COPD among the non-smokers. Exposure to chronic air pollution, especially that of a combustion-derived particulate matter, is a major contributor to COPD risk with mechanisms that include oxidative stress, chronic inflammation, as well as genetic susceptibility interactions. The results reveal the importance of implementing a comprehensive population health intervention that includes air quality management with customary tobacco control interventions to curtail the COPD burden in the world.