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Ozone exposure, antioxidant genes, and lung function in an elderly cohort: VA normative aging study
  1. S E Alexeeff1,
  2. A A Litonjua2,
  3. R O Wright1,2,
  4. A Baccarelli1,4,
  5. H Suh1,
  6. D Sparrow3,
  7. P S Vokonas3,
  8. J Schwartz1,2
  1. 1
    Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA
  2. 2
    Channing Laboratory, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
  3. 3
    VA Normative Aging Study, VA Boston, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA
  4. 4
    Department of Environmental and Occupational Health, IRCCS Maggiore Hospital, Milan, Italy
  1. Stacey E Alexeeff, Exposure, Epidemiology and Risk Program, Harvard School of Public Health, Landmark Center West, 415, 401 Park Dr., Boston, Massachusetts 02215, USA; staceyac{at}


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.

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  • Competing interests: None declared.