Chronic Exposure to Fine Particles and Mortality, 1974-2009
Chronic Exposure to Fine Particles and Mortality, 1974-2009
Background: Epidemiologic studies have reported associations between fine particles (aerodynamic diameter ≤ 2.5 μm; PM2.5) and mortality. However, concerns have been raised regarding the sensitivity of the results to model specifications, lower exposures, and averaging time.
Objective: We addressed these issues using 11 additional years of follow-up of the Harvard Six Cities study, incorporating recent lower exposures.
Methods: We replicated the previously applied Cox regression, and examined different time lags, the shape of the concentration–response relationship using penalized splines, and changes in the slope of the relation over time. We then conducted Poisson survival analysis with time-varying effects for smoking, sex, and education.
Results: Since 2001, average PM2.5 levels, for all six cities, were < 18 μg/m. Each increase in PM2.5 (10 μg/m) was associated with an adjusted increased risk of all-cause mortality (PM2.5 average on previous year) of 14% [95% confidence interval (CI): 7, 22], and with 26% (95% CI: 14, 40) and 37% (95% CI: 7, 75) increases in cardiovascular and lung-cancer mortality (PM2.5 average of three previous years), respectively. The concentration–response relationship was linear down to PM2.5 concentrations of 8 μg/m. Mortality rate ratios for PM2.5 fluctuated over time, but without clear trends despite a substantial drop in the sulfate fraction. Poisson models produced similar results.
Conclusions: These results suggest that further public policy efforts that reduce fine particulate matter air pollution are likely to have continuing public health benefits.
All-cause, cardiopulmonary, cardiovascular, and lung-cancer mortality have been associated with chronic air pollution exposure in prospective studies that controlled for individual covariates (Abbey et al. 1999; Beelen et al. 2008b; Beeson et al. 1998; Cao et al. 2011; Dockery et al. 1993; Eftim et al. 2008; Filleul et al. 2005; Gehring et al. 2006; Katanoda et al. 2011; Laden et al. 2006; Miller et al. 2007; Nafstad et al. 2004; Ostro et al. 2010; Pope et al. 2002; Puett et al. 2009; Yorifuji et al. 2011). The studies that specifically considered lung-cancer mortality associations with fine particles (aerodynamic diameter < 2.5 μm; PM2.5), all found positive associations (Beelen et al. 2008b; Dockery et al. 1993; Laden et al. 2006; McDonnell et al. 2000), although this association was only statistically significant (p < 0.05) in the American Cancer Society study (ACS) (Pope et al. 2002; Turner et al. 2011).
Although compelling evidence supports the harmful effects of PM2.5 on longevity, concerns have been raised regarding the sensitivity of the results to model specifications. In particular, Moolgavkar (2005, 2007) suggested that covariates may not be proportional and hence were not controlled for properly in proportional hazards models; that the concentration–response relation may not be linear; and that there are few observations at levels as low as or below the current World Health Organization and U.S. Environmental Protection Agency (EPA) air quality standards. In addition, the relative toxicity of particle elements is still controversial, and most of the recent reduction in PM2.5 concentrations in the United States has come from sulfate control. Hence it is of interest whether the concentration–response curve has changed over time as particle composition has changed. Health impact assessments in the United States assume that health benefits of reducing particles are only fully realized after 20 years (U.S. EPA 2010), so examination of the lag between exposure and mortality is also relevant for consideration of changes in the standard.
Our goal was to test the robustness of the association between chronic exposure to PM2.5 and mortality observed in the original study (Dockery et al. 1993), and the first extended follow-up of the Harvard Six Cities study (Laden et al. 2006) by replicating the analyses using 11 additional years of follow-up with exposures well below the U.S. annual standard (15 μg/m) (U.S. EPA 1997). We examined different lags of exposure, tested the shape of the PM2.5 concentration–mortality relationship, tested for changes in this slope over time, and relaxed the proportion assumption by allowing the effects of covariates to vary each year. We reexamined the association of PM2.5 with specific causes of death such as lung cancer and examined the effects of PM2.5 depending on participants' chronic conditions and smoking status.
Abstract and Introduction
Abstract
Background: Epidemiologic studies have reported associations between fine particles (aerodynamic diameter ≤ 2.5 μm; PM2.5) and mortality. However, concerns have been raised regarding the sensitivity of the results to model specifications, lower exposures, and averaging time.
Objective: We addressed these issues using 11 additional years of follow-up of the Harvard Six Cities study, incorporating recent lower exposures.
Methods: We replicated the previously applied Cox regression, and examined different time lags, the shape of the concentration–response relationship using penalized splines, and changes in the slope of the relation over time. We then conducted Poisson survival analysis with time-varying effects for smoking, sex, and education.
Results: Since 2001, average PM2.5 levels, for all six cities, were < 18 μg/m. Each increase in PM2.5 (10 μg/m) was associated with an adjusted increased risk of all-cause mortality (PM2.5 average on previous year) of 14% [95% confidence interval (CI): 7, 22], and with 26% (95% CI: 14, 40) and 37% (95% CI: 7, 75) increases in cardiovascular and lung-cancer mortality (PM2.5 average of three previous years), respectively. The concentration–response relationship was linear down to PM2.5 concentrations of 8 μg/m. Mortality rate ratios for PM2.5 fluctuated over time, but without clear trends despite a substantial drop in the sulfate fraction. Poisson models produced similar results.
Conclusions: These results suggest that further public policy efforts that reduce fine particulate matter air pollution are likely to have continuing public health benefits.
Introduction
All-cause, cardiopulmonary, cardiovascular, and lung-cancer mortality have been associated with chronic air pollution exposure in prospective studies that controlled for individual covariates (Abbey et al. 1999; Beelen et al. 2008b; Beeson et al. 1998; Cao et al. 2011; Dockery et al. 1993; Eftim et al. 2008; Filleul et al. 2005; Gehring et al. 2006; Katanoda et al. 2011; Laden et al. 2006; Miller et al. 2007; Nafstad et al. 2004; Ostro et al. 2010; Pope et al. 2002; Puett et al. 2009; Yorifuji et al. 2011). The studies that specifically considered lung-cancer mortality associations with fine particles (aerodynamic diameter < 2.5 μm; PM2.5), all found positive associations (Beelen et al. 2008b; Dockery et al. 1993; Laden et al. 2006; McDonnell et al. 2000), although this association was only statistically significant (p < 0.05) in the American Cancer Society study (ACS) (Pope et al. 2002; Turner et al. 2011).
Although compelling evidence supports the harmful effects of PM2.5 on longevity, concerns have been raised regarding the sensitivity of the results to model specifications. In particular, Moolgavkar (2005, 2007) suggested that covariates may not be proportional and hence were not controlled for properly in proportional hazards models; that the concentration–response relation may not be linear; and that there are few observations at levels as low as or below the current World Health Organization and U.S. Environmental Protection Agency (EPA) air quality standards. In addition, the relative toxicity of particle elements is still controversial, and most of the recent reduction in PM2.5 concentrations in the United States has come from sulfate control. Hence it is of interest whether the concentration–response curve has changed over time as particle composition has changed. Health impact assessments in the United States assume that health benefits of reducing particles are only fully realized after 20 years (U.S. EPA 2010), so examination of the lag between exposure and mortality is also relevant for consideration of changes in the standard.
Our goal was to test the robustness of the association between chronic exposure to PM2.5 and mortality observed in the original study (Dockery et al. 1993), and the first extended follow-up of the Harvard Six Cities study (Laden et al. 2006) by replicating the analyses using 11 additional years of follow-up with exposures well below the U.S. annual standard (15 μg/m) (U.S. EPA 1997). We examined different lags of exposure, tested the shape of the PM2.5 concentration–mortality relationship, tested for changes in this slope over time, and relaxed the proportion assumption by allowing the effects of covariates to vary each year. We reexamined the association of PM2.5 with specific causes of death such as lung cancer and examined the effects of PM2.5 depending on participants' chronic conditions and smoking status.
Source...