Bart Ostro

The Global Burden of Disease Due to Outdoor Air Pollution

As part of the World Health Organization (WHO) Global Burden of Disease Comparative Risk Assessment, the burden of disease attributable to urban ambient air pollution was estimated in terms of deaths and disability-adjusted life years (DALYs). Air pollution is associated with a broad spectrum of acute and chronic health effects, the nature of which may vary with the pollutant constituents. Particulate air pollution is consistently and independently related to the most serious effects, including lung cancer and other cardiopulmonary mortality. The analyses on which this report is based estimate that ambient air pollution, in terms of fine particulate air pollution (PM2.5), causes about 3% of mortality from cardiopulmonary disease, about 5% of mortality from cancer of the trachea, bronchus, and lung, and about 1% of mortality from acute respiratory infections in children under 5 yr, worldwide. This amounts to about 0.8 million (1.2%) premature deaths and 6.4 million (0.5%) years of life lost (YLL). This burden occurs predominantly in developing countries; 65% in Asia alone. These estimates consider only the impact of air pollution on mortality (i.e., years of life lost) and not morbidity (i.e., years lived with disability), due to limitations in the epidemiologic database. If air pollution multiplies both incidence and mortality to the same extent (i.e., the same relative risk), then the DALYs for cardiopulmonary disease increase by 20% worldwide.

Fine Particulate Air Pollution and Mortality in Nine California Counties: Results from CALFINE

Many epidemiologic studies provide evidence of an association between daily counts of mortality and ambient particulate matter < 10 μm in diameter (PM10). Relatively few studies, however, have investigated the relationship of mortality with fine particles [PM < 2.5 μm in diameter (PM2.5)], especially in a multicity setting. We examined associations between PM2.5 and daily mortality in nine heavily populated California counties using data from 1999 through 2002. We considered daily counts of all-cause mortality and several cause-specific subcategories (respiratory, cardiovascular, ischemic heart disease, and diabetes). We also examined these associations among several subpopulations, including the elderly (> 65 years of age), males, females, non-high school graduates, whites, and Hispanics. We used Poisson multiple regression models incorporating natural or penalized splines to control for covariates that could affect daily counts of mortality, including time, seasonality, temperature, humidity, and day of the week. We used meta-analyses using random-effects models to pool the observations in all nine counties. The analysis revealed associations of PM2.5 levels with several mortality categories. Specifically, a 10-μg/m3 change in 2-day average PM2.5 concentration corresponded to a 0.6% (95% confidence interval, 0.2–1.0%) increase in all-cause mortality, with similar or greater effect estimates for several other subpopulations and mortality subcategories, including respiratory disease, cardiovascular disease, diabetes, age > 65 years, females, deaths out of the hospital, and non-high school graduates. Results were generally insensitive to model specification and the type of spline model used. This analysis adds to the growing body of evidence linking PM2.5 with daily mortality.

Air pollution and exacerbation of asthma in African-American children in Los Angeles.

Significant increases in asthma morbidity and mortality in the United States have occurred since the 1970s, particularly among African-Americans. Exposure to various environmental factors, including air pollutants and allergens, has been suggested as a partial explanation of these trends. To examine relations between several air pollutants and asthma exacerbation in African-Americans, we recruited a panel of 138 children in central Los Angeles. We recorded daily data on respiratory symptoms and medication use for 13 weeks and examined these data in conjunction with data on ozone (O3) nitrogen dioxide (NO2), particulate matter (PM10 and PM2.5), meteorological variables, pollens, and molds. Using generalized estimating equations, we found associations between respiratory symptom occurrence and several environmental factors. For example, new episodes of cough were associated with exposure to PM10 (OR = 1.25; 95% CI = 1.12–1.39; interquartile range [IQR] = 17 &mgr;g/m3, 24-hour average), PM2.5 (OR = 1.10; 95% CI = 1.03–1.18; IQR = 30 &mgr;g/m3, 12-hour average), NO2, and the molds Cladosporium and Alternaria, but not with exposure to O3 or pollen. The factors PM10 and O3 were associated with the use of extra asthma medication. For this population several bioaerosols and air pollutants had effects that may be clinically significant.

Long-Term Exposure to Constituents of Fine Particulate Air Pollution and Mortality: Results from the California Teachers Study

Background Several studies have reported associations between long-term exposure to ambient fine particulate matter (PM) and cardiovascular mortality. However, the health impacts of long-term exposure to specific constituents of PM2.5 (PM with aerodynamic diameter ≤ 2.5 μm) have not been explored. Methods We used data from the California Teachers Study, a prospective cohort of active and former female public school professionals. We developed estimates of long-term exposures to PM2.5 and several of its constituents, including elemental carbon, organic carbon (OC), sulfates, nitrates, iron, potassium, silicon, and zinc. Monthly averages of exposure were created using pollution data from June 2002 through July 2007. We included participants whose residential addresses were within 8 and 30 km of a monitor collecting PM2.5 constituent data. Hazard ratios (HRs) were estimated for long-term exposure for mortality from all nontraumatic causes, cardiopulmonary disease, ischemic heart disease (IHD), and pulmonary disease. Results Approximately 45,000 women with 2,600 deaths lived within 30 km of a monitor. We observed associations of all-cause, cardiopulmonary, and IHD mortality with PM2.5 mass and each of its measured constituents, and between pulmonary mortality and several constituents. For example, for cardiopulmonary mortality, HRs for interquartile ranges of PM2.5, OC, and sulfates were 1.55 [95% confidence interval (CI), 1.43–1.69], 1.80 (95% CI, 1.68–1.93), and 1.79 (95% CI, 1.58–2.03), respectively. Subsequent analyses indicated that, of the constituents analyzed, OC and sulfates had the strongest associations with all four outcomes. Conclusions Long-term exposures to PM2.5 and several of its constituents were associated with increased risks of all-cause and cardiopulmonary mortality in this cohort. Constituents derived from combustion of fossil fuel (including diesel), as well as those of crustal origin, were associated with some of the greatest risks. These results provide additional evidence that reduction of ambient PM2.5 may provide significant public health benefits.

The relationship of respiratory and cardiovascular hospital admissions to the southern California wildfires of 2003

Objective: There is limited information on the public health impact of wildfires. The relationship of cardiorespiratory hospital admissions (n = 40 856) to wildfire-related particulate matter (PM2.5) during catastrophic wildfires in southern California in October 2003 was evaluated. Methods: Zip code level PM2.5 concentrations were estimated using spatial interpolations from measured PM2.5, light extinction, meteorological conditions, and smoke information from MODIS satellite images at 250 m resolution. Generalised estimating equations for Poisson data were used to assess the relationship between daily admissions and PM2.5, adjusted for weather, fungal spores (associated with asthma), weekend, zip code-level population and sociodemographics. Results: Associations of 2-day average PM2.5 with respiratory admissions were stronger during than before or after the fires. Average increases of 70 μg/m3 PM2.5 during heavy smoke conditions compared with PM2.5 in the pre-wildfire period were associated with 34% increases in asthma admissions. The strongest wildfire-related PM2.5 associations were for people ages 65–99 years (10.1% increase per 10 μg/m3 PM2.5, 95% CI 3.0% to 17.8%) and ages 0–4 years (8.3%, 95% CI 2.2% to 14.9%) followed by ages 20–64 years (4.1%, 95% CI −0.5% to 9.0%). There were no PM2.5–asthma associations in children ages 5–18 years, although their admission rates significantly increased after the fires. Per 10 μg/m3 wildfire-related PM2.5, acute bronchitis admissions across all ages increased by 9.6% (95% CI 1.8% to 17.9%), chronic obstructive pulmonary disease admissions for ages 20–64 years by 6.9% (95% CI 0.9% to 13.1%), and pneumonia admissions for ages 5–18 years by 6.4% (95% CI −1.0% to 14.2%). Acute bronchitis and pneumonia admissions also increased after the fires. There was limited evidence of a small impact of wildfire-related PM2.5 on cardiovascular admissions. Conclusions: Wildfire-related PM2.5 led to increased respiratory hospital admissions, especially asthma, suggesting that better preventive measures are required to reduce morbidity among vulnerable populations.

The effects of fine particle components on respiratory hospital admissions in children.

Background Epidemiologic studies have demonstrated an association between acute exposure to ambient fine particles and both mortality and morbidity. Less is known about the relative impacts of the specific chemical constituents of particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) on hospital admissions. Objective This study was designed to estimate the risks of exposure to PM2.5 and several species on hospital admissions for respiratory diseases among children. Data and Methods We obtained data on daily counts of hospitalizations for children < 19 and < 5 years of age for total respiratory diseases and several subcategories including pneumonia, acute bronchitis, and asthma for six California counties from 2000 through 2003, as well as ambient concentrations of PM2.5 and its constituents, including elemental carbon (EC), organic carbon (OC), and nitrates (NO3). We used Poisson regression to estimate risks while controlling for important covariates. Results We observed associations between several components of PM2.5 and hospitalization for all of the respiratory outcomes examined. For example, for total respiratory admissions for children < 19 years of age, the interquartile range for a 3-day lag of PM2.5, EC, OC, NO3, and sulfates was associated with an excess risk of 4.1% [95% confidence interval (CI), 1.8–6.4], 5.4% (95% CI, 0.8–10.3), 3.4% (95% CI, 1.1–5.7), 3.3% (95% CI, 1.1–5.5), and 3.0% (95% CI, 0.4–5.7), respectively. We also observed associations for several metals. Additional associations with several of the species, including potassium, were observed in the cool season. Conclusion Components of PM2.5 were associated with hospitalization for several childhood respiratory diseases including pneumonia, bronchitis, and asthma. Because exposure to components (e.g., EC, OC, NO3, and K) and their related sources, including diesel and gasoline exhaust, wood smoke, and other combustion sources, are ubiquitous in the urban environment, it likely represents an identifiable and preventable risk factor for hospitalization for children.

Long-Term Exposure to Air Pollution and Cardiorespiratory Disease in the California Teachers Study Cohort

RATIONALE Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause specific mortality. METHODS We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals.We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5), scaled to an increment of 10 μg/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02-1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02-1.38). Long-term exposure to particulate matter less than 10 μm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99-1.14) and incident stroke (1.06; 95% CI, 1.00-1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality. CONCLUSIONS This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.

Characterizing temperature and mortality in nine California counties.

Background: Elevated temperature has been associated with increased mortality. Few epidemiologic studies, however, have considered air pollutants as potential confounders or effect modifiers. None has focused on California, where the climate is generally mild and pollution levels tend to be high—an ideal setting to examine the independent effect of temperature from air pollution. Methods: We examined the association between mean daily apparent temperature and nonaccidental mortality in 9 counties throughout California from May to September 1999–2003. Data were obtained from the National Climatic Data Center (temperature and relative humidity), the California Department of Health Services (mortality), and the California Air Resources Board (particulate matter, ozone, carbon monoxide, and nitrogen dioxide). We conducted a time-stratified case-crossover study, with a time-series analysis as a sensitivity analysis, adjusting for day of the week using both methods and adjusting for time trend in the time-series analysis. We first obtained county-specific estimates and then combined them using meta-analytic methods. Results: A total of 248,019 deaths were included. Each 10° (Fahrenheit) increase in same-day mean apparent temperature corresponded to a 2.3% increase in mortality (95% confidence interval = 1.0%–3.6%) in the case-crossover analysis for all 9 counties combined, with nearly identical results produced from the time-series analysis. No air pollutant examined was found to be a significant confounder or effect modifier. Conclusions: Even without extremes in apparent temperature, we observed an association between temperature and mortality in California that was independent of air pollution.

The Association of Air Pollution and Mortality: Examining the Case for Inference

An association between air pollution measured as particulate matter, and mortality has been reported in several different locations. These studies have been conducted over a wide range of climates and populations. The time-series studies, which examine the joint occurrence of daily fluctuations in air pollution and mortality, provide the strongest evidence of a true association. However, several criteria, including the consistency of the results, need to be explored before causality is inferred from these studies. A striking consistency in the results was observed, after the different studies were converted into a common metric. The mean effect of an 10 micrograms/m3 change in PM10 implied by these studies varies between 0.64 and 1.49%. The fulfillment of other criteria, including specificity, presence of a dose-response relationship, and coherence of results, lend strong support to the existence of an actual association between particulate matter and mortality. However, the biologic mechanism is not well understood at this time. In addition, the precise measure of the pollutant responsible for the health effect--total suspended particles, PM10, fine particles, sulfates, acidic aerosols, sulfur dioxide, or some as yet unmeasured pollutant--is unclear, based on current available evidence.

Coarse and fine particles and daily mortality in the Coachella Valley, California: a follow-up study.

Many epidemiological studies provide evidence of an association between ambient particles, measured as PM10, and daily mortality. Most of these studies have been conducted in urban areas where PM10 is highly correlated with and dominated by fine particles less than 2.5 μm in diameter (PM2.5). Fewer studies have investigated impacts associated with the fraction of coarse mode particles (between 2.5 and 10 μm in diameter). In a previous study using data from 1989 through 1992 in the Coachella Valley, a desert resort and retirement area east of Los Angeles, we reported associations between PM10 and several different measures of mortality [Ostro B.D., Hurley S., and Lipsett M.J. Air pollution and daily mortality in the Coachella Valley, California: a study of PM10 dominated by coarse particles. Environ. Res. 1999: 81: 231–238]. In this arid environment, coarse particles of geologic origin are highly correlated with and comprise approximately 60% of PM10, increasing to >90% during wind events. This study was intended to repeat the earlier investigation using 10 years (1989–1998) of daily data on mortality and PM10. The last 2.5 years of data also included daily measures of PM2.5, allowing examination of size-specific impacts. To ensure adequate statistical power, we attempted to develop predictive models for both fine and coarse particles to use in analyses of the full 10-year period. An acceptable fit was found only for coarse particles, which were found to be a cubic function of PM10 (R2=0.95). Outcome variables included several measures of daily mortality, including all-cause (minus accidents and homicides), cardiovascular and respiratory mortality. Multivariate Poisson regression analyses using generalized additive models were employed to explain the variation in these endpoints, controlling for temperature, humidity, day of the week, season, and time, using locally weighted smoothing techniques. Pollution lags of up to 4 days were examined. Several pollutants were associated with all-cause mortality, including PM2.5, carbon monoxide and nitrogen dioxide. More consistent results were found for cardiovascular-specific mortality, for which associations were found for coarse particles (RR=1.02; 95% C.I., 1.01–1.04), PM10 (RR=1.03; 95% C.I., 1.01–1.05). None of the pollutants was associated with respiratory-specific mortality. Ozone was not associated with any of the mortality outcomes. These findings are generally consistent with those we previously reported for the Coachella Valley for the period 1989–1992, demonstrating associations between several measures of particulate matter and daily mortality in an environment in which particulate concentrations are dominated by the coarse fraction.