A Meta-Analysis of Time-Series Studies of Ozone and Mortality With Comparison to the National Morbidity, Mortality, and Air Pollution Study

School of Forestry and Environmental Studies, Yale University, New Haven, Connecticut, United States
Epidemiology (Impact Factor: 6.2). 08/2005; 16(4):436-45. DOI: 10.1097/01.ede.0000165817.40152.85
Source: PubMed


Although many time-series studies of ozone and mortality have identified positive associations, others have yielded null or inconclusive results, making the results of these studies difficult to interpret.
We performed a meta-analysis of 144 effect estimates from 39 time-series studies, and estimated pooled effects by lags, age groups, cause-specific mortality, and concentration metrics. We compared results with pooled estimates from the National Morbidity, Mortality, and Air Pollution Study (NMMAPS), a time-series study of 95 large U.S. urban centers from 1987 to 2000.
Both meta-analysis and NMMAPS results provided strong evidence of a short-term association between ozone and mortality, with larger effects for cardiovascular and respiratory mortality, the elderly, and current-day ozone exposure. In both analyses, results were insensitive to adjustment for particulate matter and model specifications. In the meta-analysis, a 10-ppb increase in daily ozone at single-day or 2-day average of lags 0, 1, or 2 days was associated with an 0.87% increase in total mortality (95% posterior interval = 0.55% to 1.18%), whereas the lag 0 NMMAPS estimate is 0.25% (0.12% to 0.39%). Several findings indicate possible publication bias: meta-analysis results were consistently larger than those from NMMAPS; meta-analysis pooled estimates at lags 0 or 1 were larger when only a single lag was reported than when estimates for multiple lags were reported; and heterogeneity of city-specific estimates in the meta-analysis were larger than with NMMAPS.
This study provides evidence of short-term associations between ozone and mortality as well as evidence of publication bias.

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    • "Long-term exposure to high levels of ozone (O 3 ) has been linked to increased risk of respiratory illness, while chronic exposure to elevated fine particulate matter (PM 2.5 ) is associated with lung cancer, respiratory disease, and cardiovascular disease (e.g., Dockery et al., 1993; Jerrett et al., 2009; Krewski et al., 2009; Pope III et al., 2009). In addition to these consistently documented risks of chronic exposure, there is some evidence that acute exposures to pollution may themselves carry risks to human health above and beyond those of the long-term mean exposures (Bell et al., 2005). Thus, high pollution events may be responsible for a larger fraction of annual acute mortality. "
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    Atmospheric Chemistry and Physics 05/2015; 15(10):14075-14109. DOI:10.5194/acpd-15-14075-2015 · 4.88 Impact Factor
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    • "Sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ) and ground-level ozone (O 3 ) are important criteria air pollutants. A number of epidemiological studies suggest an association between short-and long-term exposure to SO 2 , NO 2 and O 3 and increased morbidity, mortality, and hospital admissions for cardiovascular and pulmonary diseases including acute myocardial infarction and arrhythmias (Künzli et al., 1997; Burnett et al., 1998, 1999, 2004; Stieb et al., 2002; Bell et al., 2005; Ruidavets et al., 2005; Dockery et al., 2005; Neuberger et al., 2007; Latza et al., 2009). They are also associated with acid deposition and photochemical smog (Cooper and Alley, 2002; Cox, 2003). "
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    • "Short-term risk factors such as stress from high-pressure work deadlines, episodes of physical or sexual activity, and acute anger had relative risks well over 2.0. In contrast, a meta-analysis of 39 studies evaluating the association between short-term exposure to ozone and CVD mortality found a central tendency relative risk ratio of 1.0111, which was not statistically signifi cant (Bell et al. 2005). Overall, Petito Boyce et al. (2015) did not fi nd evidence for a causal role of ozone in CVD mortality, in stark contrast to validation of the causal role of well-known risk factors. "
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