Inhalation Toxicology, 19(Suppl. 1):3338, 2007Copyright c Informa Healthcare USA, Inc.ISSN: 0895-8378 print / 1091-7691 onlineDOI: 10.1080/08958370701492961

Mortality Effects of Longer Term Exposures to FineParticulate Air Pollution: Review of RecentEpidemiological Evidence

C. Arden Pope IIIDepartment of Economics, Brigham Young University, Provo, Utah, USA

This article evaluates the dynamic exposure-response relationship between particulate matterair pollution (PM) and mortality risk by integrating epidemiological evidence from studies thatuse different time scales of exposure. The evidence suggests that short-term exposure studiesare observing more than just harvesting or mortality displacement. There is little evidence ofshort-term compensatory reduction in deaths, and estimated PM effects are generally largerfor intermediate and longer term time scales of exposure. Although proximity in time matters,with most recent exposure having the largest health impact, there is evidence that the short-term exposure studies capture only a small amount of the overall health effects of long-termrepeated exposure to PM. The overall epidemiological evidence suggests that adverse healtheffects are dependent on both exposure concentrations and length of exposure, and that long-term exposures have larger, more persistent cumulative effects than short-term exposures.

There are many epidemiological studies that link exposure ofambient particulate matter air pollution (PM) with increased riskof cardiopulmonary mortality. The majority of epidemiologicalstudies that evaluate PMmortality effects have been designedto exploit two obvious natural sources of exposure variability:(1) short-term temporal variability that reflects day-to-daychanges in ambient PM, and (2) spatial (or cross-sectional) vari-ability that reflect differences in longer term (years or decades)cumulative or average exposures between cities or other well-defined geographic areas. Fairly consistent PMmortality as-sociations have been observed with both short-term and long-term exposures, but the associations with long-term exposureshave generally been much larger than with short-term exposures.More detailed reviews and discussions of this literature are givenelsewhere (Pope & Dockery, 2006; U.S. EPA, 2004). The objec-tive of this article is to briefly review how the literature addressesthree related questions: (1) Are the excess deaths observed inthe short-term studies due primarily to short-term harvesting ormortality displacement? (2) Why are the PMmortality effectestimates from the long-term studies so much larger than fromthe short-term studies? (3) What can we learn about the dy-

Received 10 July 2006; accepted 9 October 2006.Supported in part by funds from the Mary Lou Fulton Professorship,

Brigham Young University, Provo, UT.Address correspondence to C. Arden Pope III, PhD, 142 FOB,

Brigham Young University, Provo, UT 84602-2363, USA. E-mail:cap3@byu.edu

namic exposure-response relationship by integrating evidencefrom long-term, intermediate, and short-term time scales?

EFFECT ESTIMATES FOR SHORT AND LONGTERM EXPOSURE

Examples of studies that use short-term temporal variabilityin PM exposure include studies of early well-documented ex-treme air pollution episodes that linked cardiopulmonary deathswith several days of abnormally high concentrations of air pollu-tion (Firket, 1931; Schrenk et al., 1949; Logan, 1953; Bell et al.,2004). Other examples include the daily time-series mortalitystudies (Anderson et al., 2005) and related case-crossover stud-ies (Schwartz, 2004) that evaluate effects of short-term temporalvariability by analyzing associations between changes in dailymortality counts with day-to-day changes in air pollution at rel-atively low, more common levels of pollution. Since 1990, therehave been over 100 studies that evaluated short-term PM expo-sure and mortality associations. There have also been quantita-tive reviews or meta-analyses of these studies (Anderson et al.,2005), many of which provide pooled effect estimates. Short-term PM exposure and mortality associations have more recentlybeen evaluated in several large multicity studies with less op-portunity for city selection or publication bias (Samet et al.,2000; Dominici et al., 2003a; Katsouyanni et al., 2003; Analitiset al., 2006). Table 1 presents a summary of pooled estimatesof the percent increase (and 95% confidence interval) in risk ofmortality estimated across selected meta-analyses and multic-ity studies of short-term (daily) changes in exposure to PM2.5

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34 C. A. POPE III

TABLE 1Estimates of percent increase (and 95% confidence intervals) in mortality risk across selected studies of short-term

and long-term exposure

Percent increases in mortality risk(95% CI)

Cardiovascular/Study areas and types Primary sources Exposureincrement All cause Cardiopulmonary

Short-term exposureMeta-estimate from single-city studies,

Adjusted for publication-biasAnderson et al. (2005) 20 g/m3 PM10 1.2 (1.0, 1.4)

1.0 (0.8, 1.2)

Meta-estimates from COMEAP COMEAP (2006) 20 g/m3 PM1010 g/m3 PM2.5

1.8 (1.4, 2.4)a1.4 (0.7, 2.2)a

U.S. 6 cities Klemm and Mason (2003) 10 g/m3 PM2.5 1.2 (0.8, 1.6) 1.3 (0.3, 2.4)cCalifornian 9 cities Ostro et al. (2006) 10 g/m3 PM2.5 0.6 (0.2, 1.0) 0.6 (0.0, 1.1)aU.S. 10-cities Schwartz (2000c, 2003b) 20 g/m3 PM10 1.3 (1.0, 1.6) U.S. 14-city case-crossover Schwartz (2004) 20 g/m3 PM10 0.7 (0.4, 1.0) NMMAPS 20100 U.S. cities Dominici et al. (2003a) 20 g/m3 PM10 0.4 (0.2, 0.8) 0.6 (0.3, 1.0)bAPHEA-2 1529 European cities Katsouyanni et al. (2003)

Analitis et al. (2006)20 g/m3 PM10 1.2 (0.8, 1.4) 1.5 (0.9, 2.1)a

Long-term exposureHarvard Six Cities cohort study Laden et al. (2006) 10 g/m3 PM2.5 16 (7, 26) 28 (13, 44)aACS, U.S. cohort Pope et al. (2002) 10 g/m3 PM2.5 6.2 (1.6, 11) 9.3 (3.3, 16)bACS, intra-metro Los Angeles cohort Jerrett et al. (2005) 10 g/m3 PM2.5 17 (5, 30) 12 (3, 30)b

aCardiovascular only.bCardiovascular and respiratory deaths combined.cIschemic heart disease deaths.

(the most common indicator of fine PM, consisting of particleswith an aerodynamic diameter less than or equal to a 2.5-m cutpoint) or PM10 (the most common indicator of inhalable or tho-racic PM, consisting of particles with an aerodynamic diameterless than or equal to a 10-m cut point). Incremental increasesin exposure of 10 g/m3 PM2.5 or 20 g/m3 PM10 are asso-ciated with approximately a 0.4% to 1.3% increase in relativerisk of mortality. These effect estimates are small but reasonablyconsistent across meta-analyses and multicity studies.

Examples of studies that have taken advantage of long-termspatial variability include studies that reported that average PMconcentrations of fine PM or sulfate are associated with annualmortality rates across U.S. metropolitan areas (Lave & Seskin,1970; Evans et al., 1984; Ozkaynak & Thurston, 1987). Otherexamples include prospective cohort studies (Dockery et al.,1993; Pope et al., 1995, 2002; Krewski et al., 2000; Jerrett et al.,2005; Laden et al., 2006) that control for individual differencesin age, sex, smoking history, and other risk factors, and haveprovided the most compelling evidence of mortality effects oflong-term PM exposure (Brunekreef, 2003). Pooled estimatesof the percent increase in risk of mortality from selected recentprospective cohort studies of long-term exposure are also pre-sented in Table 1. A more complete summary of effect estimates

for both short-term and long-term exposures is given elsewhere(Pope & Dockery, 2006; U.S. EPA, 2004). These results suggestthat an incremental elevation in long-term exposure of 10 g/m3PM2.5 is associated with approximately a 6% to 17% increase inrelative risk of mortality. These PMmortality effect estimatesfor long-term exposure are obviously much larger than thoseobserved in the studies of short-term exposure.

INTERMEDIATE TIME SCALES OF EXPOSUREAs part of an effort to explore the extent to which the stud-

ies of short-term exposure are just observing an effect of har-vesting or mortality displacement, several researchers developedapproaches to analyze daily time-series data for time scales ofexposure longer than just a few days. If deaths due to short-termPM exposure occur only among the very frail who would havedied in a few days anyway, then the excess deaths during andimmediately following days of high pollution would be followedby a short-term compensatory reduction in deaths. To explorethis phenomena, Zeger, Dominici, and colleagues (Zeger et al.,1999; Kelsall et al., 1999; Dominici et al., 2003b) conductedfrequency decompositions of both the mortality counts and airpollution data and applied frequency domain log-linear regres-sion using data from several cities. PMmortality associations

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MORTALITY AND LONGER TERM FINE PARTICLE EXPOSURE 35

were larger at longer time scales (10 days to 2 mo) than attime scales of one or a few days. A related approach, usingsmoothing techniques to decompose the data into different timescales, was employed by Schwartz using data from two cities(Schwartz, 2000a, 2001, 2003a). Again, PMmortality associa-tions were larger for longer time scales. Longer time scales ofexposure can also be evaluated by using extended distributedlags in time-series analyses. Extended distributed lag modelshave been used to evaluate associations for up to 60 days post-exposure using data from 10 U.S. cities (Schwartz, 2000b; Bragaet al., 2001), 10 European cities (Zanobetti et al., 2002, 2003),and Dublin, Ireland (Goodman et al., 2004). In all of these analy-ses, PMmortality effect estimates were larger when time scaleslonger than a few days were useda finding that is inconsis-tent with the supposition that mortality effects of short-term PMexposure are largely due to short-term harvesting or mortalitydisplacement.

Two natural intervention studies have provided opportunitiesto evaluate changes in mortality risk associated with changesin PM exposure at intermediate time scales. The first study in-volved the intermittent operation of a steel mill in Utah Valley(Pope, 1989, 1996; Pope et al., 1992). During the winter of19861987, a labor dispute and change in ownership of a lo-cal steel mill resulted in a 13-mo closure of the largest singlesource of PM in the valley. During the closure period, average

TABLE 2Comparison of estimated excess risk of mortality estimates for different time scales of exposure

Percent change in riskof mortality associated with an increment

of 10 g/m3 PM2.5 or 20 g/m3 PM10 or BS

Study areas and types Primary sourcesTime scaleof exposure All cause

Cardiovascular/cardiopulmonary Respiratory

10 U.S.cities, time-series,extended distributed lag

Schwartz (2000b) 1 day 1.3 2 days 2.1

2.6

5 days 10 European cities,

time-series, extendeddistributed lag

Zanobetti et al. (2002) 2 days40 days

1.43.3

10 European cities,time-series, extendeddistributed lag

Zanobetti et al. (2003) 2 days 1.4 1.520 days 2.7 3.430 days 3.5 5.340 days 4.0 8.6

Dublin daily time series,extended distributed lag,intervention

Goodman et al. (2004)Clancy et al. (2002)

1 day 0.8 0.8 1.840 days 2.2 2.2 7.2

Months to year 3.2 5.7 8.7Utah Valley, time series and

interventionPope et al. (1992) 5 days 3.1 3.6 7.5

13 mo 4.3 Harvard Six Cities, time

series and cohort extendedanalysis

Schwartz et al. (1996) 2 days 1.2 Klemm and Mason (2003) 1 yr 14.0 Laden et al. (2006) 18 yr 16.0

PM10 concentrations decreased by 15 g/m3 and mortality de-creased by 3.2%. A second natural intervention study occurredin Dublin, Ireland (Clancy et al., 2002). The primary source ofDublins ambient PM pollution was coal smoke from domesticfires, but in September of 1990 the sale of coal was banned. Av-erage ambient PM (as measured by BS [black smoke or Britishsmoke] measured by optical densities or light absorbance of PMfilters) decreased by 36 g/m3 and, after adjusting for tempera-ture, relative humidity, day of week, respiratory epidemics, andstandardized cause-specific death rate in the rest of Ireland, sta-tistically significant drops in all nontrauma, cardiovascular, andrespiratory deaths were observed.

A recent analysis of the Harvard Six Cities cohort (Ladenet al., 2006) extended the follow-up period by 8 years. Duringthese 8 years, fine PM concentrations were much lower thanduring the original analysis, especially for 2 of the most pol-luted cities. The reductions in PM2.5 in the extended follow-upcompared to the original study period were associated with im-proved survival, suggesting that mortality effects of long-termair pollution may be at least partially reversible over periodsof a decade (Laden et al., 2006). Furthermore, estimated PMmortality associations were nearly as large when estimated using1-yr average time scales. A stylized summary of estimated ex-cess risk of mortality for different studies with different timescales of exposure is presented in Table 2.

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36 C. A. POPE III

FIG. 1. Comparison of percent change in risk of mortality associated with an increment of 10 g/m3 PM2.5 or 20 /m3 PM10 orBS estimated for different time scales of exposure (approximate number of days, log scale).

DISCUSSIONAn attempt to illustrate the integrated evidence from different

time scales of exposure is presented in Figure 1. The estimatedpercent change in risk of mortality associated with an incrementof 10 g/m3 PM2.5 or 20 g/m3 PM10 or BS is plotted over theexposure period measure in approximate number of days (logscale). Although Figure 1 clearly does not provide the completepicture, it does illustrate increased estimates of PM effects withincreasing lengths of exposure. It also illustrates that proximityin time also matters. Most recent exposures have the largesteffects (thus the need for a log scale in time). Furthermore, withregards to the intervention studies (Utah Valley and Dublin), thefull expected reduction in mortality risks due to a reduction inexposure may not be realized during a period of just 6 to 13mo. However, based on the extended analysis of the HarvardSix Cities study, the reduction in mortality risks may be largelyrealized within 1 to 8 yr.

We can gain important insights about the dynamic exposure-response relationship between PM and mortality risk by integrat-

ing evidence from different time scales of exposure. Short-termexposure studies appear to be observing more than just short-term mortality displacement because there is little evidence ofshort-term compensatory reduction in deaths and there are gener-ally larger estimated PM effects for intermediate and longer termtime scales of exposure. The evidence suggests that the short-term exposure studies capture only a small amount of the over-all health effects of long-term repeated PM exposure. Adversehealth effects are dependent on both exposure concentrationsand length of exposure, and long-term exposures have largermore persistent cumulative effects than short-term exposures.

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