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. 2009 Mar 12;360(11):1085-95.
doi: 10.1056/NEJMoa0803894.

Long-term ozone exposure and mortality

Michael Jerrett  1 , Richard T Burnett, C Arden Pope 3rd, Kazuhiko Ito, George Thurston, Daniel Krewski, Yuanli Shi, Eugenia Calle, Michael Thun
Affiliations

Long-term ozone exposure and mortality

Michael Jerrett et al. N Engl J Med. .

Abstract

Background: Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.

Methods: Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.

Results: In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.

Conclusions: In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.

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Conflict of interest statement

No other potential conflict of interest relevant to this article was reported.

Figures

Figure 1
Figure 1. Ozone Concentrations in the 96 Metropolitan Statistical Areas in Which Members of the American Cancer Society Cohort Resided in 1982
The average exposures were estimated from 1 to 57 monitoring sites within each metropolitan area from April 1 to September 30 for the years 1977 through 2000.
Figure 2
Figure 2. Exposure–Response Curve for the Relation between Exposure to Ozone and the Risk of Death from Respiratory Causes
The curve is based on a natural spline with 2 df estimated from the residual relative risk of death within a metropolitan statistical area (MSA) according to a random-effects survival model. The dashed lines indicate the 95% confidence interval of fit, and the hash marks indicate the ozone levels of each of the 96 MSAs.
See this image and copyright information in PMC

Comment in

  • Ozone exposure and mortality.
    Semple JL, Moore GW. Semple JL, et al. N Engl J Med. 2009 Jun 25;360(26):2786-7; author reply 2788-9. doi: 10.1056/NEJMc090738. N Engl J Med. 2009. PMID: 19553654 No abstract available.
  • Ozone exposure and mortality.
    Tong DQ, Yu S, Kan H. Tong DQ, et al. N Engl J Med. 2009 Jun 25;360(26):2788; author reply 2788-9. N Engl J Med. 2009. PMID: 19557887 No abstract available.

References

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    1. Krewski D, Burnett RT, Goldberg MS, et al. Reanalysis of the Harvard Six Cities Study and the American Cancer Society Study of Particulate Air Pollution and Mortality: a special report of the institute’s Particle Epidemiology Reanalysis Project. Part II. Sensitivity analyses. Cambridge, MA: Health Effects Institute; 2000.
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