Douglas W. Dockery

An association between air pollution and mortality in six U.S. cities

BACKGROUND Recent studies have reported associations between particulate air pollution and daily mortality rates. Population-based, cross-sectional studies of metropolitan areas in the United States have also found associations between particulate air pollution and annual mortality rates, but these studies have been criticized, in part because they did not directly control for cigarette smoking and other health risks. METHODS In this prospective cohort study, we estimated the effects of air pollution on mortality, while controlling for individual risk factors. Survival analysis, including Cox proportional-hazards regression modeling, was conducted with data from a 14-to-16-year mortality follow-up of 8111 adults in six U.S. cities. RESULTS Mortality rates were most strongly associated with cigarette smoking. After adjusting for smoking and other risk factors, we observed statistically significant and robust associations between air pollution and mortality. The adjusted mortality-rate ratio for the most polluted of the cities as compared with the least polluted was 1.26 (95 percent confidence interval, 1.08 to 1.47). Air pollution was positively associated with death from lung cancer and cardiopulmonary disease but not with death from other causes considered together. Mortality was most strongly associated with air pollution with fine particulates, including sulfates. CONCLUSIONS Although the effects of other, unmeasured risk factors cannot be excluded with certainty, these results suggest that fine-particulate air pollution, or a more complex pollution mixture associated with fine particulate matter, contributes to excess mortality in certain U.S. cities.

Health Effects of Fine Particulate Air Pollution: Lines that Connect

INTRODUCTION Herein is the discussion of the 2006 A&WMA Critical Review1,2 on “Health Effects of Fine Particulate Air Pollution: Lines that Connect.” In the review, Drs. C. Arden Pope III and Douglas Dockery addressed the epidemiological evidence for the effects of particulate matter (PM) on human health indicators. The review documents substantial progress since the 1997 Critical Review3 in the areas of: (1) short-term exposure and mortality; (2) long-term exposure and mortality; (3) time scales of exposure; (4) the shape of the concentration-response function; (5) cardiovascular disease; and (6) biological plausibility. Invited and contributing discussants agree and disagree with points made in the review. Each discussion is self-contained and adds information relevant to the topic. Joint authorship of this article does not imply that a discussant subscribes to the opinions expressed by others. Commentaries are the opinions of the author only and do not necessarily reflect the positions of their respective organizations. In particular, Dr. Costa’s comments have not been reviewed by U.S. Environmental Protection Agency (EPA) and do not reflect official positions or policies of the agency. CRITICAL REVIEW DISCUSSION ISSN 1047-3289 J. Air & Waste Manage. Assoc. 56:1368–1380

Is Daily Mortality Associated Specifically with Fine Particles

Recent epidemiologic studies have consistently reported increased daily mortality associated with exposures to particulate air pollution. Currently, particulate mass is measured as particles smaller than 10 \im (PM10). Fine (PM2 s) and coarse (PM10 - PM2 s) mass and sulfate particle concentrations were measured in six eastern U.S. cities for eight years, and aerosol acidity concentrations were measured for approximately one year. Daily mortality for these metropolitan areas was combined with particulate air pollution and weather measurements. City-specific associations with each measure of particle pollution were estimated by Poisson regression, adjusting for time trends and weather by nonparametric methods. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. PM10, PM2 5, and SO4= were each significantly associated with increased daily mortality, while no associations were found with coarse mass nor with aerosol acidity (H+) concentrations. The strongest association was found with PM2 5. A10 (ig/m3 increase in two-day mean PM2S was associated with a 1.5% (95% CI 1.1% to 1.9%) increase in total daily mortality. Somewhat larger increases were found for deaths caused by chronic obstructive pulmonary disease (+3.3%) and by ischemic heart disease (+2.1%). These data suggest that increased daily mortality is specifically associated with particle mass constituents found in the aerodynamic diameter size range under 2.5 urn, that is, with combustion-related particles.

Fine-Particulate Air Pollution and Life Expectancy in the United States

BACKGROUND Exposure to fine-particulate air pollution has been associated with increased morbidity and mortality, suggesting that sustained reductions in pollution exposure should result in improved life expectancy. This study directly evaluated the changes in life expectancy associated with differential changes in fine particulate air pollution that occurred in the United States during the 1980s and 1990s. METHODS We compiled data on life expectancy, socioeconomic status, and demographic characteristics for 211 county units in the 51 U.S. metropolitan areas with matching data on fine-particulate air pollution for the late 1970s and early 1980s and the late 1990s and early 2000s. Regression models were used to estimate the association between reductions in pollution and changes in life expectancy, with adjustment for changes in socioeconomic and demographic variables and in proxy indicators for the prevalence of cigarette smoking. RESULTS A decrease of 10 microg per cubic meter in the concentration of fine particulate matter was associated with an estimated increase in mean (+/-SE) life expectancy of 0.61+/-0.20 year (P=0.004). The estimated effect of reduced exposure to pollution on life expectancy was not highly sensitive to adjustment for changes in socioeconomic, demographic, or proxy variables for the prevalence of smoking or to the restriction of observations to relatively large counties. Reductions in air pollution accounted for as much as 15% of the overall increase in life expectancy in the study areas. CONCLUSIONS A reduction in exposure to ambient fine-particulate air pollution contributed to significant and measurable improvements in life expectancy in the United States.

Increased Particulate Air Pollution and the Triggering of Myocardial Infarction

Background—Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown. Methods and Results—We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 &mgr;m (PM2.5), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 &mgr;g/m3 PM2.5 during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 &mgr;g/m3 PM2.5 in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively). Conclusions—The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.

REVIEW OF EPIDEMIOLOGICAL EVIDENCE OF HEALTH EFFECTS OF PARTICULATE AIR POLLUTION

AbstractThis article summarizes epidemiological evidence of health effects of particulate air pollution. Acute exposure to elevated levels of particulate air pollution has been associated with increased cardiopulmonary mortality, increased hospitalization for respiratory disease, exacerbation of asthma, increased incidence and duration of respiratory symptoms, declines in lung function, and restricted activity. Small deficits in lung function, higher risk of chronic respiratory disease and symptoms, and increased mortality have also been associated with chronic exposure to respirable particulate air pollution. Health effects have been observed at levels common to many U.S. cites and at levels below current US. National Ambient Air Quality Standards. Although the biological mechanisms involved are poorly understood, recent epidemiological evidence supports the hypothesis that respirable particulate air pollution is an important risk factor for respiratory disease and cardiopulmonary mortality.

Air pollution and incidence of cardiac arrhythmia.

Air pollution episodes have been associated with increased cardiovascular hospital admissions and mortality in time-series studies. We tested the hypothesis that patients with implanted cardioverter defibrillators experience potentially life-threatening arrhythmias after such air pollution episodes. We compared defibrillator discharge interventions among 100 patients with such devices in eastern Massachusetts, according to variations in concentrations of particulate matter, black carbon, and gaseous air pollutants that were measured daily for the years 1995 through 1997. A 26-ppb increase in nitrogen dioxide was associated with increased defibrillator interventions 2 days later (odds ratio = 1.8; 95% confidence interval = 1.1-2.9). Patients with ten or more interventions experienced increased arrhythmias in association with nitrogen dioxide, carbon monoxide, black carbon, and fine particle mass. These results suggest that elevated levels air pollutants are associated with potentially life-threatening arrhythmia leading to therapeutic interventions by an implanted cardioverter defibrillator.

Heart rate variability associated with particulate air pollution

BACKGROUND Epidemiologic studies have linked fine particulate air pollution with cardiopulmonary mortality, yet underlying biologic mechanisms remain unknown. Changes in heart rate variability (HRV) may reflect changes in cardiac autonomic function and risk of sudden cardiac death. This study evaluated changes in mean heart rate and HRV in human beings associated with changes in exposure to particulate air pollution. METHODS Repeated ambulatory electrocardiographic monitoring was conducted on 7 subjects for a total of 29 person-days before, during, and after episodes of elevated pollution. Mean HR, the standard deviation of normal-to-normal (NN) intervals (SDNN), the standard deviation of the averages of NN intervals in all 5-minute segments of the recording (SDANN), and the square root of the mean of squared differences between adjacent NN intervals (r-MSSD) were calculated for 24-hour and 6-hour time segments. Associations of HRV with particulate pollution levels were evaluated with fixed-effects regression models. RESULTS After controlling for differences across patients, elevated particulate levels were associated with (1) increased mean HR, (2) decreased SDNN, a measure of overall HRV, (3) decreased SDANN, a measure that corresponds to ultralow frequency variability, and (4) increased r-MSSD, a measure that corresponds to high-frequency variability. The associations between HRV and particulates were small but persisted even after controlling for mean HR. CONCLUSIONS This study suggests that changes in cardiac autonomic function reflected by changes in mean HR and HRV may be part of the pathophysiologic mechanisms or pathways linking cardiovascular mortality and particulate air pollution.

Effects of Cigarette Smoking on Lung Function in Adolescent Boys and Girls

BACKGROUND Little is known about the sex-specific effects of cigarette smoking on the level and growth of lung function in adolescence, when 71 percent of people in the United States who smoke tried their first cigarette. METHODS We studied the effects of cigarette smoking on the level and rate of growth of pulmonary function in a cohort of 5158 boys and 4902 girls 10 to 18 years of age, examined annually between 1974 and 1989 in six cities in the United States. RESULTS We found a dose-response relation between smoking and lower levels of both the ratio of forced expiratory volume in one second to forced vital capacity (FEB1/FVC) and the forced expiratory flow between 25 and 75 percent of FVC (FEF25-75). Each pack per day of smoking was associated with a 3.2 percent reduction in FEF25-75 for girls (P=0.01) and a 3.5 percent reduction in FEF25-75 for boys (P=0.007). Whereas the FVC level was elevated in smokers, the rate of growth of FVC and FEV1 was reduced. Among adolescents of the same sex, smoking five or more cigarettes a day, as compared with never smoking, was associated with 1.09 percent slower growth of FEV1 per year in girls (95 percent confidence interval 0.70 to 1.47) and 0.20 percent slower growth in boys (95 percent confidence interval, -0.16 to 0.56), and with 1.25 percent slower growth of FEF25-75 per year in girls (95 percent confidence interval 0.38 to 2.13) and 0.93 percent slower growth in boys (95 percent confidence interval, 0.21 to 1.65). Whereas girls who did not smoke reached a plateau of lung function at 17 to 18 years of age, girls of the same age who smoked had a decline of FEV1 and FEF25-75. CONCLUSION Cigarette smoking is associated with evidence of mild airway obstruction and slowed growth of lung function in adolescents. Adolescent girls may be more vulnerable than boys to the effects of smoking on the growth of lung function.

Air pollution and daily mortality: Associations with particulates and acid aerosols

The association between total daily mortality and air pollution was investigated for a 1-year period (September 1985 through August 1986) in St. Louis and in the counties in eastern Tennessee surrounding Kingston/Harriman. The purpose of this study was to evaluate the relative importance of various measures of particulate and gaseous air pollution as predictors of daily mortality. Concentrations of inhalable particles (PM10), fine particles (PM2.5), the elemental composition of these particles, and aerosols acidity were measured daily during the period of study. The effect of each air pollutant on daily mortality was estimated after controlling for meteorologic and seasonal influences. Total mortality in St. Louis was found to increase 16% (95% CI-1 to 33%) for each 100 micrograms/m3 increase in PM10, and by 17% (95% CI-12 to 57%) in eastern Tennessee. Positive but progressively weaker associations were found with PM2.5, sulfate, and aerosol acidity concentrations in both communities. Associations with gaseous pollutants--sulfur dioxide, nitrogen dioxide, and ozone--were all far from statistical significance. Because of the short monitoring period for daily particulate air pollution, the power of this study to detect associations was limited. Nevertheless, statistically significant associations with PM10 were found in St. Louis, and, more importantly, the estimated effects were consistent between the two communities studied and with other reported analyses of the effects of particles on daily mortality. These data suggest that the acidity of particles is not as important in associations with daily mortality as the mass concentrations of particles.