Ozone exposure, antioxidant genes, and lung function in an elderly cohort: VA normative aging study
- S E Alexeeff1,
- A A Litonjua2,
- R O Wright1,2,
- A Baccarelli1,4,
- H Suh1,
- D Sparrow3,
- P S Vokonas3,
- J Schwartz1,2
- 1 Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
- 2 Channing Laboratory, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
- 3 VA Normative Aging Study, VA Boston, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA
- 4 Department of Environmental and Occupational Health, IRCCS Maggiore Hospital, Milan, Italy
- Stacey E Alexeeff, Exposure, Epidemiology and Risk Program, Harvard School of Public Health, Landmark Center West, 415, 401 Park Dr., Boston, Massachusetts 02215, USA;
- Accepted 4 April 2008
- Published Online First 4 June 2008
Background: Ozone (O3) exposure is known to cause oxidative stress. This study investigated the acute effects of O3 on lung function in the elderly, a suspected risk group. It then investigated whether genetic polymorphisms of antioxidant genes (heme oxygenase-1 (HMOX1) and glutathione S-transferase pi (GSTP1)) modified these associations.
Methods: 1100 elderly men from the Normative Aging Study were examined whose lung function (forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1)) was measured every 3 years from 1995 to 2005. The study genotyped the GSTP1 Ile105Val and Ala114Val polymorphisms and the (GT)n repeat polymorphism in the HMOX1 promoter, classifying repeats as short (n<25) or long (n⩾25). Ambient O3 was measured continuously at locations in the Greater Boston area. Mixed linear models were used, adjusting for known confounders.
Results: A 15 ppb increase in O3 during the previous 48 h was associated with a 1.25% decrease in FEV1 (95% CI: −1.96% to −0.54%). This estimated effect was worsened with either the presence of a long (GT)n repeat in HMOX1 (−1.38%, 95% CI: −2.11% to −0.65%) or the presence of an allele coding for Val105 in GSTP1 (−1.69%, 95% CI: −2.63% to −0.75%). A stronger estimated effect of O3 on FEV1 was found in subjects carrying both the GSTP1 105Val variant and the HMOX1 long (GT)n repeat (−1.94%, 95% CI: −2.89% to −0.98%). Similar associations were also found between FVC and O3 exposure.
Conclusions: Our results suggest that O3 has an acute effect on lung function in the elderly, and the effects may be modified by the presence of specific polymorphisms in antioxidant genes.
Competing interests: None declared.