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Teresa Chahine,¹ Andrea Baccarelli,^1,2 Augusto Litonjua,³ Robert O. Wright,^1,3 Helen Suh,¹ Diane R. Gold,^1,3 David Sparrow,⁴ Pantel Vokonas,⁴ and Joel Schwartz¹

¹Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA; ²Center of Molecular Epidemiology and Genetics; and EPOCA Epidemiology Research Center, University of Milan and IRCCS Maggiore Hospital, Mangiagalli and Regina Elena Foundation, Milan, Italy; ³Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA; ⁴VA Normative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA

Abstract
Background and objectives: We have previously shown that reduced defenses against oxidative stress due to glutathione S-transferase M1 (GSTM1) deletion modify the effects of PM_2.5 (fine-particulate air pollution of < 2.5 µm in aerodynamic diameter) on heart rate variability (HRV) in a cross-sectional analysis of the Normative Aging Study, an elderly cohort. We have extended this to include a longitudinal analysis with more subjects and examination of the GT short tandem repeat polymorphism in the heme oxygenase-1 (HMOX-1) promoter.

Methods: HRV measurements were taken on 539 subjects. Linear mixed effects models were fit for the logarithm of HRV metrics—including standard deviation of normal-to-normal intervals (SDNN) , high frequency (HF) , and low frequency (LF) —and PM_2.5 concentrations in the 48 hr preceding HRV measurement, controlling for confounders and a random subject effect.

Results: PM_2.5 was significantly associated with SDNN (p = 0.04) and HF (p = 0.03) in all subjects. There was no association in subjects with GSTM1, whereas there was a significant association with SDNN, HF, and LF in subjects with the deletion. Similarly, there was no association with any HRV measure in subjects with the short repeat variant of HMOX-1, and significant associations in subjects with any long repeat. We found a significant three-way interaction of PM_2.5 with GSTM1 and HMOX-1 determining SDNN (p = 0.008) , HF (p = 0.01) and LF (p = 0.04) . In subjects with the GSTM1 deletion and the HMOX-1 long repeat, SDNN decreased by 13% [95% confidence interval (CI) , –21% to –4%], HF decreased by 28% (95% CI, –43% to –9%) , and LF decreased by 20% (95% CI, –35% to –3%) per 10 µg/m³ increase in PM.

Conclusions: Oxidative stress is an important pathway for the autonomic effects of particles.

Key words: air particles, air pollution, cardiovascular health, genetic variation, GST, heart rate variability, HMOX-1, PM_2.5. Environ Health Perspect 115:1617–1622 (2007) . doi:10.1289/ehp.10318 available via http://dx.doi.org/ [Online 20 August 2007]

Address correspondence to J. Schwartz, Exposure, Epidemiology, and Risk Program, Harvard School of Public Health, 401 Park Dr., Suite 415 W, PO Box 15698, Boston, MA 02215 USA. Telephone: (617) 384-8752. Fax: (617) 384-8745. E-mail: jschwrtz@hsph.harvard.edu

This work was supported by National Institute of Environmental Health Sciences grants RO1ES00002, RO1ES015172-01, PO1ES009825, and U.S. Environmental Protection Agency grants EPAR827353 and R83241601. The VA Normative Aging Study, a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston, Massachusetts, is supported by the Cooperative Studies Program/Epidemiology Research and Information Center of the U.S. Department of Veterans Affairs.

The authors declare they have no competing financial interests.

Received 30 March 2007 ; accepted 11 August 2007.