cardiovascular admissions. Peng et al. (2009) reported statistically significant heterogeneity among effect estimates for different PM com- ponents, with the strongest estimated risk of cardiovascular admissions associated with EC concentrations. Cakmak et al. (2009a, 2009b) also reported that the 95% CI of the estimated effect of an IQR increase in EC did not over- lap the 95% CIs of the other elements, with the exception of OC and two or three of the other 16 elements, indicating that the effect per IQR for EC was significantly greater than estimated effects of most other single elements. Cohort studies on long-term exposure to BCP and PM and mortality and morbid- ity. Cohort studies on mortality. We iden- tified seven papers that presented results from four different cohort studies, two of which included effect estimates for BS and PM and two for EC and PM (Table 3). When using the average conversion factor of 10 gμ/m 3 BS = 1.1 gμ/m 3 EC, RRs for all-cause or natural-cause mortality per 1 μg/m 3 EC in the two European studies and in the study by Smith et al. (2009) ranged from 1.05 to 1.06. RRs for EC and all-cause mortality in the veterans study (Lipfert et al. 2006) were about three times larger than RRs for the same out- comes from the other studies, but because the standard error in the veterans study was two to four times higher compared with the other studies, this study contributes less to the pooled estimate [RR = 1.06 (95% CI: 1.04, 1.09) per μg/m 3 EC]. Pooled estimates for a 1-μg/m 3 increase in EC derived using high- and low-end conversion factors of 1.8 and 0.5 gμ/m 3 per 10 μg/m 3 BS were 1.05 and 1.11, respectively. When expressed per 1 gμ/m 3, the RR for EC is therefore 7–16 times higher than that of PM2.5 mass (pooled estimate = 1.007 per 1 gμ/m 3). However, ratios of IQRs for PM2.5:EC for the studies by Smith et al. (2009) and Beelen et al. (2008) were 14 and 9, respectively, and we estimated a ratio of about 5 based on graphi- cal data presented for the study by Filleul et al. (2005). For the study by Lipfert et al. (2006), IQRs were not available, but RRs expressed for the difference between the mean concentration and the minimum were 1.06 per 9.5 gμ/m 3 for PM2.5 and 1.09 per 0.5 gμ/m 3 for EC. Hence, Black carbon as additional indicator it appears that effect estimates for PM2.5 and EC from cohort studies also would be similar if expressed for an IQR increase in exposure instead of a 1-gμ/m 3 exposure contrast. Multipollutant modeling was applied in the studies by Lipfert et al. (2006) and Smith et al. (2009). Based on four-pollutant models that included EC, OC, sulfate, and nitrate, Lipfert et al. (2006) concluded that EC had the greatest estimated impact on all-cause mor- tality and that nitrate was the next important constituent. In the American Cancer Society (ACS) study, Smith et al. (2009) found that the EC estimate for all-cause mortality was reduced by about 50% and lost statistical sig- nificance after adjusting for sulfate and ozone. For cardiopulmonary mortality, EC decreased by about 33% and remained significantly associated after adjustment for sulfate but decreased by about 80% and lost significance after additional adjustment for ozone. Cohort studies on morbidity. The eight papers on respiratory health outcomes in chil- dren included six papers describing results from one Dutch and two German birth Table 2. Results from single- and two-pollutant models of time-series studies including PM10 or PM2.5a and BCP (measured as BS in all studies shown here). Reference (study location) Mortality Bremner et al. 1999 (London) Hoek et al. 2000 (the Netherlands) Admissions Anderson et al. 2001 (West Midlands) Atkinson et al. 1999a (London) Atkinson et al. 1999b (London)e Le Tertre et al. 2002 (APHEA)f Health end point Respiratory mortality CVD mortality Total mortality CVD mortality Respiratory admissions (all ages) A&E visits for asthma; children Cardiovascular admissions (> 65 years) Cardiac (all ages) Cardiac (> 65 years) IHD (> 65 years) Percent change per 10-μg/m3 increase (95% CI) PM BS Correlation (R ) Single-pollutant Two-pollutant Single-pollutant PM–BSb model modelc model 0.77 0.64 0.6–0.7 0.5–0.8 1.3 (0.3, 2.3) 0.6 (–0.1, 1.2) 0.3 (0.0, 0.5) 0.2 (–0.2, 0.5) 0.6 (–0.5, 1.7) 2.4 (0.7, 4.1) 0.5 (–0.0, 1.0) 0.5 (0.2, 0.8) 0.7 (0.4, 1.0) 0.8 (0.3, 1.2) 0.4 (–1.0, 1.8) 0.2 (–0.6, 1.0) 0.1 (–0.3, 0.6) –0.6 (–1.3, 0.1) “Considerably reduced”d 2.0 (–0.1, 4.2) –0.1 (–0.8, 0.5) –0.2 (–1.2, 0.8) 0.1 (–0.4, 0.7) 0.2 (–0.9, 1.4) 1.9 (0.2, 3.7) 1.2 (0.1, 2.2) 0.7 (0.4, 0.9) 0.8 (0.4, 1.2) 1.1 (–0.1, 2.2) 2.8 (–0.0, 5.7) 1.9 (0.9, 3.0) 1.1 (0.4, 1.8) 1.3 (0.4, 2.2) 1.1 (0.7, 1.5) NA, not available. aCoefficient of the correlation (R ) between PM and BCP. bRR for EC in European studies estimated from BS as 10 μg/m3 BS = 1.1 μg/m3. cRR for PM2.5 estimated from TSP as PM2.5 = 0.5 × TSP (Verhoeff et al. 1996; Van der Zee et al. 1998). dFor all 24 sites, whereas RR presented for 18 sites (nontraffic). eInternational Classification of Diseases, 9th Revision (World Health Organization 1975), codes < 800. fPooled effect when using 10 μg/m3 BS = 1.8 μg/m3: 1.05 (95% CI: 1.02, 1.07); when using 10 μg/m3 BS = 0.5 μg/m3: 1.11 (95% CI: 1.06, 1.16). Environmental Health Perspectives • volume 119 | number 12 | December 2011 Two-pollutant modelc 2.0 (–0.4, 4.4) 0.8 (–0.6, 2.2) 0.4 (–0.6, 1.4) 2.1 (0.5, 3.7) 2.0 (0.3, 2.8) 0.9 (–3.0, 5.1) 2.3 (0.8, 3.8) 1.6 (–0.3, 3.5) 1.5 (0.3, 2.7) 0.8 (–1.1, 2.7) EC 1.06 (1.03, 1.09) 1.05 (0.98, 1.11) 1.03 (0.93, 1.14) 1.18 (1.05, 1.33) 1.05 (1.00, 1.10) 1.20 (0.99, 1.45) 1.04 (0.95, 1.12) 1.03 (0.89, 1.18) 1.04 (0.97, 1.11) 1.06 (1.01, 1.11) 1.11 (1.03, 1.19) 1.06 (1.04, 1.09) 1695 Abbreviations: A&E, admission and emergency department; CVD, cardiovascular disease; IHD, ischemic heart disease; NA, not available. aPM2.5 for Anderson et al. (2001); PM10 for all other studies. bCoefficient of the correlation (R) between PM and BS. cTwo-pollutant models include both PM and BS. dQuantitative infor- mation not available; paper states that the effect of PM2.5 was considerably reduced when BS was included in the model. eResults only described qualitatively in the paper; quantitative estimates provided by the authors on request. f Study locations were Amsterdam, the Netherlands; Barcelona, Spain; Birmingham, UK; London, UK; and Paris, France. Table 3. RR for mortality related to long-term exposure to PM2.5 and EC per 1 μg/m3. Reference Filleul et al. 2005b,c Lipfert et al. 2006 Beelen et al. 2008b Smith et al. 2009 Pooled effect (random)f Cohort 14,284 adults; age 25–59 years; France 70,000 male U.S. veterans 120,852 adults; age 55–69 years; the Netherlands 500,000 adults; age 20–87 years; USA Correlation (R) PM–BCPa 0.87d 0.54 0.82 Cause Natural causese Cardiopulmonary Lung cancer All causes Natural causese Respiratory Cardiovascular Lung cancer Other All causes Cardiopulmonary All causes RR (95% CI) PM2.5 1.010 (1.004, 1.016) 1.012 (1.002, 1.023) 1.000 (0.983, 1.019) 1.006 (0.993, 1.020) 1.006 (0.997, 1.015) 1.007 (0.972, 1.043) 1.004 (0.990, 1.019) 1.006 (0.980, 1.033) 1.008 (0.996, 1.021) 1.006 (1.002, 1.010) 1.012 (1.008, 1.018) 1.007 (1.004, 1.009)