Abdominal adiposity intensifies the negative effects of ambient air pollution on lung function in Korean men.

Abstract

Some studies have provided the possibility that adipose tissue may mediate air pollution-induced lung dysfunction. Studies using quantified fat mass data are needed to understand the biological mechanisms between adipocyte and air pollution in lung function. We aimed to investigate whether abdominal adiposity measured by computed tomography (CT) modifies the effects of air pollution on lung function in Korean men. A total of 1876 men who visited one of two health checkup centers were recruited for this study. Adiposity traits such as visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and total adipose tissue (TAT) areas were measured by CT. We used the annual mean concentrations of ambient air pollutants including nitrogen dioxide (NO2) and particulate matter with an aerodynamic diameter ⩽10 μm (PM10). Interquartile range (IQR) increase in annual mean concentration of NO2 was significantly associated with a 2.5% lower forced expiratory volume in 1 s (FEV1) and 2.9% lower forced vital capacity (FVC) (both P<0.05). The decrease in lung function was more strongly associated with adiposity traits than with body mass index. In a stratified analysis of adiposity, compared with subjects with low-VAT area (VAT⩽200 cm2), those with high-VAT area (VAT>200 cm2) showed a rapid decrease in FEV1 with each IQR increase in PM10 (β=-0.0812; 95% confidence interval (CI) =-0.1590, -0.0035) and NO2 (β=-0.0979; 95% CI=-0.1611, -0.0346). In the high-VAT group, each IQR increase in NO2 content was significantly associated with a 10.6% decrease (β=-0.1056; 95% CI=-0.1770, -0.0343) in FVC. SAT and TAT areas showed similar patterns. We report the first finding that abdominal adiposity intensifies the inverse relationship between air pollution and lung function.