Background Air pollution in cities has been linked to increasedrates of mortality and morbidity in developed and developingcountries. Although these findings have helped lead to a tighteningof air-quality standards, their validity with respect to publichealth has been questioned.
Methods We assessed the effects of five major outdoor-air pollutantson daily mortality rates in 20 of the largest cities and metropolitanareas in the United States from 1987 to 1994. The pollutantswere particulate matter that is less than 10 µm in aerodynamicdiameter (PM10), ozone, carbon monoxide, sulfur dioxide, andnitrogen dioxide. We used a two-stage analytic approach thatpooled data from multiple locations.
Results After taking into account potential confounding by otherpollutants, we found consistent evidence that the level of PM10is associated with the rate of death from all causes and fromcardiovascular and respiratory illnesses. The estimated increasein the relative rate of death from all causes was 0.51 percent(95 percent posterior interval, 0.07 to 0.93 percent) for eachincrease in the PM10 level of 10 µg per cubic meter. Theestimated increase in the relative rate of death from cardiovascularand respiratory causes was 0.68 percent (95 percent posteriorinterval, 0.20 to 1.16 percent) for each increase in the PM10level of 10 µg per cubic meter. There was weaker evidencethat increases in ozone levels increased the relative ratesof death during the summer, when ozone levels are highest, butnot during the winter. Levels of the other pollutants were notsignificantly related to the mortality rate.
Conclusions There is consistent evidence that the levels offine particulate matter in the air are associated with the riskof death from all causes and from cardiovascular and respiratoryillnesses. These findings strengthen the rationale for controllingthe levels of respirable particles in outdoor air.
Studies showing that current levels of air pollution in thecities of many developed and developing countries are associatedwith increased rates of mortality and morbidity have heightenedconcern that air pollution continues to pose a threat to publichealth.1,2,3 The evidence suggests that small airborne particlesare a toxic component of urban air pollution. Using this interpretationof the evidence as a rationale, the Environmental ProtectionAgency implemented a new standard for fine particulate matter.4The existing standard, promulgated in 1987, specified the maximallevels allowable in a 24-hour period and on an annual basisfor particulate matter with an aerodynamic diameter (the diameterof a unit-density sphere that has the same settling velocityin gas as the particle of interest) that was less than 10 µm(PM10). In 1997, the agency added standards for particulatematter that is less than 2.5 µm in aerodynamic diameter(PM2.5), since the size of such particles better correspondsto the size of particles that can penetrate to the airways andalveoli of the lung. This decision has been controversial; criticsquestion whether the scientific evidence is strong enough totake regulatory action.5,6,7,8 A more detailed version of ourmethods and findings is available elsewhere.9
Key findings on particulate air pollution have come from time-seriesanalyses of the association of air-pollution levels with thenumber of deaths per day.3 With the exception of a few studies,such as the multi-city Air Pollution and Health: a EuropeanApproach (APHEA) project10 and an analysis of data from sixU.S. cities,11 most of these studies have been based on singlelocations selected without a defined sampling plan. Consequently,the generalizability of the findings is uncertain, and analyticstrategies have differed among studies. Citing these limitations,critics have questioned whether the findings indicate an effectof air pollution generally or of particles specifically.7,12,13
To address these limitations, we combined information on theassociations of levels of the five major outdoor-air pollutants— PM10, ozone, sulfur dioxide, carbon monoxide, and nitrogendioxide — with daily mortality rates from 20 of the largestU.S. cities.14 Our estimates are based on a defined sample ofthe cities; statistical precision was enhanced by combininginformation from multiple locations.
Methods
Data Collection
Data were collected from 1987 through 1994. We began with the20 counties deemed the largest in the 1990 U.S. Census on thebasis of population (or with logical groupings of counties),and for the analysis, we used data for the counties that includedthe associated cities, thus encompassing a population of morethan 50 million. Analysis was carried out at the county levelbecause the county was the common coding unit for the variousdata sets. In this article, we refer to cities and metropolitanareas rather than counties. Daily mortality rates were obtainedfrom the National Center for Health Statistics (Table 1). Afterexcluding deaths from external causes (e.g., accidents, suicide,and homicide) and deaths of nonresidents, we classified thedeaths according to age group (<65 years, 65 to 74 years,and 75 years) and cause (cardiovascular and respiratory andother).15 Data on selected demographic characteristics wereobtained from the 1990 U.S. Census.16
Table 1. Rates of Death from All Causes and from Cardiovascular and Respiratory Causes in 20 U.S. Cities and Metropolitan Areas, According to Various Socioeconomic Characteristics, 1987–1994.
Hourly temperature and dew-point data were available from theEarthInfo compact-disk17 data base of the National ClimaticData Center. For analysis we used the 24-hour mean value foreach day. The air-pollution data were obtained from the database of the Aerometric Information Retrieval System,18 whichis maintained by the Environmental Protection Agency. For population-orientedmonitoring variables, we downloaded all available data for PM10,ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide.For the pollutants measured on an hourly basis, we calculatedthe 24-hour average. If the levels of pollutants were monitoredat multiple locations in a metropolitan area, we averaged thedata. To avoid the potential consequences of outlying values,we excluded the highest and lowest 10 percent of values (10percent trimmed mean) and then averaged the values for eachset of monitors, after the value for each monitor had been correctedfor its yearly average.
Statistical Analysis
We used a two-stage log-linear regression model.19,20,21 Inthe first stage, a separate log-linear regression of the dailymortality rate on air-pollution measures and other confounderswas fitted to obtain estimates of the relative rate of mortalityassociated with the pollution variable and the degree of statisticaluncertainty for each of the 20 cities. In the second stage,the estimates of the relative rates were combined for all cities(after adjustment for the various levels of uncertainty) toobtain an overall estimate and to assess whether city-specificcharacteristics modified the estimated effect of air pollutionon the relative rate of death.
In the first-stage log-linear regressions, we controlled forpossible confounding by longer-term trends resulting from changesin the size and characteristics of the population, health status,and health care and from shorter-term effects of seasonalityand the presence or absence of influenza epidemics. To do this,we used a flexible function that took into account the variationin the mortality rate over periods of several months (a smoothingfunction with respect to calendar time with 7 degrees of freedomper year per city, which was allowed to differ in the threeage groups). We also adjusted for the short-term effect of weatheron the risk of death by including similar smoothing functionswith respect to a specific day's temperature and the averagetemperature for the three days preceding it (6 degrees of freedom)and to dew point (3 degrees of freedom). Finally, we includedindicator variables for the day of the week. This model specificationwas based on extensive, previously reported exploratory analyses.15,22,23In this article, our results do not reflect the degrees of freedomused. We have found that the relative rates of air pollutionwere not sensitive to the number of degrees of freedom selectedfor the smoothing functions of time, temperature, and dew point.14,15,22,23
In the first-stage analysis, we analyzed the effect of the dayon which the pollution data were obtained (the current day,the day before, or two days before) on the association withmortality rates. The overall effect did not vary with the laginterval selected. Consequently, we report data for a one-daylag between pollution variables and mortality.
We considered the effects of multiple pollutants on the relativerate of mortality. We initially conducted univariate analysesthat included PM10 alone and ozone alone. We then consideredthe effects of these two pollutants in a bivariate model anddeveloped trivariate models that also included sulfur dioxide,nitrogen dioxide, or carbon monoxide. The trivariate modelsprovided estimates of the individual effects of carbon monoxide,sulfur dioxide, and nitrogen dioxide on the risk of death afteradjustment for PM10 and ozone levels.
The second stage of the analysis provided pooled estimates ofthe relative rates of mortality associated with specific pollutantsand a characterization of the effects of air pollutants amongthe cities. We also examined factors determining heterogeneityin the effect of air pollution on mortality. With respect todeterminants of heterogeneity in the second stage of the analysis,we assumed that first-stage estimates of the relative mortalityrates associated with specific pollutants followed a linearregression with the selected city-specific demographic characteristics(Table 1) as predictor variables. The second-stage analysisprovided an estimate of the effect of each predictor variableon the relative rate of mortality associated with PM10.
Model fitting was performed with use of a Bayesian statisticalapproach,24 which provides an estimate of the posterior distributionof the variable of interest. We carried out this analysis withoutmaking a strong prior assumption as to the value of the relativerate. The posterior distribution is used to determine the probabilitythat the relative rate of mortality associated with PM10 hasa particular value — that is, it is a measure of the strengthof the evidence. One important calculation is the posteriorprobability that the relative rate of mortality associated withPM10 is greater than zero. The posterior distribution can alsobe used to determine the 95 percent posterior intervals. The95 percent posterior interval encompasses 95 percent of theposterior distribution, a Bayesian formulation similar to the95 percent confidence interval. All analyses were performedwith use of S-Plus statistical software.25
Results
The 20 cities and metropolitan areas broadly represented theUnited States. The number of days for which pollution data wereavailable varied (Table 2). Since the Environmental ProtectionAgency requires levels of PM10 to be measured only every sixdays, data for ozone and other pollutants were generally availableon more days. The mean daily values for PM10 ranged from about20 µg per cubic meter to nearly 50 µg per cubicmeter; the present maximal allowable level of PM10 in a 24-hourperiod is 150 µg per cubic meter. The average numbersof deaths per day were substantial, ranging from less than 20to nearly 200 (Table 1). The correlation coefficients of allcorrelations between pollutants for all 20 cities and metropolitanareas are provided in Table 3. The correlation structure generallyreflects the common sources of the primary combustion-relatedgases (sulfur dioxide, nitrogen dioxide, and carbon monoxide)and of PM10. The level of ozone was only slightly correlatedwith that of PM10 and was not correlated with the levels ofother gaseous pollutants.
Table 3. Correlation Coefficients of All Pairwise Correlations between Pollutants for the 20 Cities and Metropolitan Areas.
In initial univariate analyses, the level of PM10 was positivelyassociated with the rate of death from all causes in most ofthe 20 cities and metropolitan areas (Figure 1). Adjustmentfor the effect of ozone levels had little effect on the association,whereas the effects of the ozone level, before and after adjustmentfor PM10 levels, tended to be more variable. The analysis ofeach pollutant was also stratified according to the cause ofdeath. The city-specific associations between PM10 levels andthe rate of death from cardiovascular and respiratory causeswere similar to those for the rate of death from all causes.A previous univariate analysis stratified according to age showedno age-associated trend.14
Figure 1. Regression Coefficients for the Changes in the Rate of Death from All Causes for Each Increase in the PM10 Level of 10 µg per Cubic Meter, before and after Adjustment for Ozone Levels, and for Each Increase in the Ozone Level of 10 ppb, before and after Adjustment for PM10 Levels in 20 Cities and Metropolitan Areas.
PM10 denotes particulate matter that is less than 10 µm in aerodynamic diameter. Bars indicate 95 percent confidence intervals. No data on ozone were available for Minneapolis.
The combined analysis for all 20 cities and metropolitan areasconfirmed the association between PM10 levels and the rate ofdeath from all causes (Figure 2) and of death from cardiovascularand respiratory causes. Figure 2 shows the posterior distributionsof the estimated increases in the relative rates of death fromall causes associated with each increase in the PM10 level of10 µg per cubic meter before and after adjustment forlevels of ozone, nitrogen dioxide, sulfur dioxide, and carbonmonoxide, as well as the probability that overall effects aregreater than zero for each model. With respect to death fromall causes, the distributions are shifted toward the right,with the respective mean increases in the number of deaths perday for each increase in the PM10 level of 10 µg per cubicmeter (i.e., estimated relative rates) ranging between approximately0.3 percent and 0.6 percent. An increase in the relative rateof 0.3 percent corresponds to a relative risk of death of 1.003.In the model that included PM10 alone, the estimated increasein the relative rate of death from all causes was 0.51 percentfor each increase in the PM10 level of 10 µg per cubicmeter (95 percent posterior interval, 0.07 to 0.93 percent).The posterior distributions of the PM10 levels did not changesubstantially after adjustment for the other pollutants, suggestingthat the univariate findings were not affected by confoundingby other pollutants (Figure 2).
Figure 2. Posterior Distributions of the Overall Relative Rate of Increase in Death from All Causes for Each Increase in the PM10 Level of 10 µg per Cubic Meter, before and after Adjustment for the Levels of Ozone (O3), Nitrogen Dioxide (NO2), Sulfur Dioxide (SO2), and Carbon Monoxide (CO).
Values in parentheses are the posterior probabilities that the overall effects are greater than zero. PM10 denotes particulate matter that is less than 10 µm in aerodynamic diameter.
The PM10 level had a somewhat greater effect on the rate ofdeath from cardiovascular and respiratory causes than on therate of death from all causes and was associated with a correspondinglylarger probability that the effect was greater than zero. Theestimated increase in the relative rate of death from cardiovascularand respiratory causes was 0.68 percent for each increase of10 µg per cubic meter in the PM10 level (95 percent posteriorinterval, 0.20 to 1.16 percent).
The univariate effects of ozone levels were examined duringa one-year period and according to season. Overall, the posteriordistributions of the effects of ozone were concentrated nearzero, and there was only an even chance that the effect waslarger than zero when death from all causes and death from cardiovascularand respiratory causes were considered separately. Because ozonelevels vary strongly with the season, we compared the effectsof ozone levels during the three hottest summer months (June,July, and August), when levels are highest, and three cold months(November, December, and January), when levels tend to be lowest.With the use of this stratification, the estimated relativerates of death from all causes with each increase in the ozonelevel of 10 ppb were 0.41 percent (95 percent posterior interval,–0.20 to 1.01 percent) during the summer months and –1.83percent (95 percent posterior interval, –2.69 to –0.96percent) during the cold months.
The differences between cities in the relative rates did notdepend on average PM10 or ozone levels in a city or on city-specificdemographic characteristics; for these variables, all associated95 percent posterior intervals included zero. Consequently,the analyses and results for PM10 were not adjusted for thesecity-specific characteristics.
We also analyzed the effects of levels of carbon monoxide, sulfurdioxide, and nitrogen dioxide in a fashion similar to that ofthe analysis of PM10 levels. After adjustment for PM10 and ozonelevels, we found little evidence that these pollutants had asignificant effect on the relative rate of death.
Discussion
We found consistent evidence that the level of PM10 is associatedwith the rates of death from all causes and from cardiovascularand respiratory causes. The association of PM10 was not affectedby the inclusion of other pollutants in the statistical modelor by the time at which data were collected. Our findings stronglysupport the findings of prior studies of particulate matterand mortality.26 These studies, which were largely based ondata from single cities, used a variety of measures of particulatematter, including levels of total suspended particles, blacksmoke (a measure of soiling of a filter that provides an indexof particle levels), PM10, and PM2.5. The statistical methodsused to assess the relations between levels of pollution andthe risk of death were also heterogeneous; for example, therewas no uniformity in the approaches used to control for factorsthat varied over time or for other pollutants. Nonetheless,using a weight-of-evidence approach, the Environmental ProtectionAgency interpreted the results of the studies as indicatinga possibly causal association between levels of particulatematter and adverse effects on health.3
In a meta-analysis of U.S. studies of particulate air pollutionpublished between 1990 and 1993, Dockery and Pope2 estimatedthat each increase in the PM10 level of 10 µg per cubicmeter increased the relative rate of death from all causes by1 percent. In a subsequent update that included data from reportspublished through 1995, Dockery and Pope found little changein this estimate.27 Schwartz28 also performed a meta-analysisof studies published between 1990 and 1993 but included datafrom London and Minneapolis in addition to the data on the eightcities considered by Dockery and Pope. The resulting estimatedincrease in the relative rate of death from all causes was 0.7percent for each increase in the PM10 level of 10 µg percubic meter. The APHEA project analyzed data from 12 Europeancities and then estimated summary measures. For the six westernEuropean cities in the study, the mortality rate was estimatedto increase by 0.4 percent for each increase in the PM10 levelof 10 µg per cubic meter. In our 20-city analysis, ourestimate of an increase of approximately 0.5 percent in therate of death from all causes for each increase in the PM10level of 10 µg per cubic meter is very similar to theestimate of the APHEA project.10 The fact that our estimatewas lower than those of Dockery and Pope2 and Schwartz28 mayreflect differences in analytic techniques and the cities selected.The initial reports included in the meta-analyses may have beenbiased by the fact that studies with positive findings are morelikely to be selected for publication than those with negativefindings. Our 20-city estimate is not subject to such bias andour results should thus be more applicable to the United Statesin general.
We did not find an effect of ozone levels on the overall rateof death from all causes or from cardiovascular and respiratorycauses during the full year period. Ozone levels were positivelyassociated with mortality rates during the summer months whenozone levels were highest, although the 95 percent posteriorinterval extended into the range indicating no effect of ozonelevels on mortality. The finding of an effect of ozone levelsonly during the summer may reflect the higher levels of ozoneduring these months or, possibly, differences in the characteristicsof photochemical pollution during the various seasons. Otherrecent studies have generally found an association between ozonelevels and the risk of death.29 In the APHEA project, the maximalozone levels during a one-hour period were associated with thenumbers of deaths per day in four cities (London; Athens, Greece;Barcelona, Spain; and Paris), and a quantitatively similar effectwas found with additional data from three cities (Amsterdam;and Basel and Zurich, Switzerland) that were not part of theAPHEA project.30 For each increase of 50 µg per cubicmeter in the one-hour maximal level, the estimated relativerisk of death was 1.029 (i.e., a 1.1 percent increase in therate of death for each increase in the ozone level of 10 ppb),with the use of a random-effects model for combining the city-specificdata. Thurston and Ito29 pooled data from 15 studies and estimatedthat the relative risk of death was 1.036 for each increaseof 100 ppb in the daily one-hour maximal level of ozone (i.e.,a 0.36 percent increase in the rate of death for each increasein the ozone level of 10 ppb). For the summer months, our estimate(a 0.41 percent increase in the rate of death for each increasein the ozone level of 10 ppb) was similar to those of Thurstonand Ito. Taken together, the results of these three studiesprovide consistent evidence that exposure to ozone also increasesthe risk of death.
The limitations of our analyses should be considered. Data onlevels of PM2.5 are not yet available nationally, since a monitoringnetwork for particles in this size range is currently beingimplemented. We used PM10 levels because they have been monitoredsince 1987; there is variation across the United States in theproportion of PM10 mass that is made up of PM2.5, so that thePM10 level is an imperfect surrogate for the PM2.5 level.3 Inaddition, for regulatory purposes, PM10 levels must only bemeasured every six days, limiting the extent of available data.
Our analyses also did not address the extent to which life isshortened in association with daily exposure to the variouspollutants. The finding that the association between PM10 levelsand the risk of death was strongest for cardiovascular and respiratorycauses of death is consistent with the hypothesis that personsmade frail by advanced heart and lung disease are more susceptibleto the adverse effects of air pollution. The findings from severalepidemiologic studies of the longer-term effects of air pollutionon the risk of death suggest that exposure to air pollutionmay do more than simply shorten life by a few days.31,32 Severalanalyses of daily mortality data also indicate that the effectof air pollution may go beyond shortening life by a few days.33,34
We found no evidence that key socioeconomic factors such aslow socioeconomic status affect the association between PM10levels and the risk of death in linear regression models. Themedical conditions and poor health that increase the risk ofdeath may not be adequately reflected by the socioeconomic indicatorsrecorded by the U.S. Census. Thus, more specific informationon health status, rather than on social factors, may be neededto explore this issue, particularly in relation to the susceptibilityof particular groups of people. Finally, we used county-leveldata for these social factors because most of our data werecategorized according to county. The variation in socioeconomicstatus in a typical urban county, however, is usually considerablylarger than the variation among counties. Thus, the demographicfactors considered in the second stages of the models may betoo broad to be informative.
The epidemiologic evidence that levels of particulate matterare associated with the risk of mortality and morbidity hasprompted the promulgation of a new standard for PM2.5 in theUnited States and a rethinking of guidelines for particulatematter in Europe. Our analyses provide evidence that particulateair pollution continues to have an adverse effect on the public'shealth and strengthen the rationale for limiting levels of respirableparticles in outdoor air.
Supported by a contract with the Health Effects Institute, anorganization jointly funded by the Environmental ProtectionAgency (EPA R824835) and automotive manufacturers. The contentsof this article do not necessarily reflect the views and policiesof the Health Effects Institute, the Environmental ProtectionAgency, or manufacturers of motor vehicles or engines. Alsosupported by a grant from the National Institute of EnvironmentalHealth Sciences (P30 ES0 3819-12, to Johns Hopkins Center inUrban Environmental Health). Dr. Dominici is the recipient ofa Rosenblith Young Investigator Award from the Health EffectsInstitute.
Source Information
From the Departments of Epidemiology (J.M.S.) and Biostatistics (F.D., F.C.C., I.C., S.L.Z.), School of Hygiene and Public Health, Johns Hopkins University, Baltimore.
Address reprint requests to Dr. Samet at Johns Hopkins University, School of Public Health, 615 N. Wolfe St., Suite 6041, Baltimore, MD 21205, or at jsamet{at}jhsph.edu.
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75 years) and cause (cardiovascular and respiratory and other).15 Data on selected demographic characteristics were obtained from the 1990 U.S. Census.16 
