Schoolchildren's antioxidation genotypes are susceptible factors for reduced lung function and airway inflammation caused by air pollution

• Published in: Environmental research 2016-08, Vol.149, p.145-150
• Main Authors: Chen, Bing-Yu, Chen, Chi-Hsien, Chuang, Yu-Chen, Kim, Ho, Honda, Yasushi, Chiang, Hung-Che, Guo, Yue Leon
• Format: Article
• Language: English
• Subjects: Adolescent; Air Pollutants - toxicity; Airway inflammation; Antioxidants - metabolism; Child; Children; Cities; Environmental Monitoring; Female; Follow-Up Studies; Genotype; Glutathione S-transferase M1; Glutathione Transferase - genetics; Glutathione Transferase - metabolism; Humans; Inflammation - chemically induced; Inflammation - genetics; Inhalation Exposure; Longitudinal Studies; Lung function; Male; Oxidation-Reduction - drug effects; Ozone; Particulate matter of aerodynamic smaller than 2.5 µm; Respiratory Function Tests; Respiratory Tract Diseases - chemically induced; Respiratory Tract Diseases - genetics; Superoxide Dismutase - genetics; Superoxide Dismutase - metabolism; Superoxide dismutases 2; Taiwan
• ISSN: 0013-9351; 1096-0953
• DOI: 10.1016/j.envres.2016.05.007

We recently reported the relationship between exposure to ambient air pollutants and changes in lung function and nasal inflammation among schoolchildren. A study was conducted to investigate whether antioxidation genotypes influence these associations. A follow-up study of 97 schoolchildren was conducted in New Taipei City, Taiwan. A structured respiratory health questionnaire was administered in September 2007, followed by monthly spirometry and measurement of nasal inflammation from October 2007 to November 2009. During the study period, complete daily monitoring data for air pollutants were obtained from the Environmental Protection Administration monitoring station and Aerosol Supersite. The genotypes of glutathione S-transferase (GST) subunits M1, T1, P1 and superoxide dismutases subunit 2 (SOD2) were characterized. Mixed-effects models were used, adjusting for known confounders. GSTM1 null children had significant PM2.5-related increment in leukocyte (8.52%; 95% confidence interval (CI): 3.13–13.92%) and neutrophil (9.68%; 95% CI: 4.51–14.85%) in nasal lavage. Ozone levels were significantly and inversely associated with forced expiratory flow at 25% of forced vital capacity (FEF25%) (−0.43L/s; 95% CI: −0.58,−0.28L/s) in SOD2 Ala16 variant children. In this longitudinal study of schoolchildren. Our data provide evidence that antioxidation genotype modifies the airway inflammation caused by PM2.5. Antioxidation genotype also acts as an effect modifier, but not strong, in ozone-related small airway function response. •Children with null GSTM1 genotype were susceptible to PM2.5-enhanced airway inflammation.•Children with SOD2 Ala16 variant were susceptible to ozone-related decrement in FEF25%.•Ozone-related decrements in FEF50%, FEF75%, and FEF25–75% were observed, regardless of genotype.•Antioxidation genotype modifies the airway inflammation caused by PM2.5.•Antioxidation genotype acts as an effect modifier, but not strong, in ozone-related small airway function response.