Particulate matter, fine (PM 2.5)

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Studies and Reports

  • Enstrom J, Relative risk of death from all causes (RR and 95% CI) associated with increase of 10 μg/m3 in PM2.5, ScientificIntegrityInstitute.org, December 15, 2010.
  • Enstrom J, Major Epidemiologic Studies of PM2.5 and Total Mortality in California, ScientificIntegrityInstitute.org, September 9. 2010.
  • Gallus S et al., European studies on long-term exposure to ambient particulate matter and lung cancer, Eur J Cancer Prev. 2008 Jun;17(3):191-4.
    • Abstract. "European epidemiological studies on ambient air pollution and cancer published before December 2006 are reviewed, with focus on five analytic studies providing data on the association between various measures of particulate matter (PM) and lung cancer. A case-control study of 755 men who died from lung cancer in Trieste, Italy, reported that, compared with less than 0.18 g/m/day of deposition of particulate, the relative risk (RR) was 1.1 [95% confidence interval (CI): 0.8-1.5] for 0.18-0.30 and 1.4 (95% CI: 1.1-1.8) for more than 0.30 g/m/day. In the Netherlands Cohort Study on Diet and Cancer with 60 deaths from lung cancer, the RR was 1.06 (95% CI: 0.43-2.63) for an increase of 10 mug/m in black smoke. In the French Pollution Atmospherique et Affections Respiratoires Chroniques study cohort based on 178 deaths from lung cancer, the RR associated with an increase in exposure to 10 mug/m of total suspended particulate was 0.97 (95% CI: 0.94-1.01). A nested case-control study within the European Prospective Investigation on Cancer and Nutrition included 113 nonsmokers or exsmokers diagnosed with lung cancer and 312 controls. The RRs were 0.91 (95% CI: 0.70-1.18) for an increase in PM with diameter </=10 mum (PM10) of 10 mug/m, and 0.98 (95% CI: 0.66-1.45) for exposure over 27 mug/m compared with less than 27 mug/m. In a Norwegian record linkage study, based on 1453 lung cancer deaths, no significant excess risk was found for men, and a modest association was observed for women. European studies of PM exposure and lung cancer do not show a clear association, but uncertainties remain for the measurement of exposure and latency."
  • Enstrom J, Fine particulate air pollution and total mortality among elderly Californians, 1973-2002, Inhal Toxicol. 2005 Dec 15;17(14):803-16.
    • Abstract. "Fine particulate air pollution has been associated with increases in long-term mortality in selected cohort studies, and this association has been influential in the establishment of air quality regulations for fine particles (PM(2.5)). However, this epidemiologic evidence has been questioned because of methodological issues, conflicting findings, and lack of an accepted causal mechanism. To further evaluate this association, the long-term relation between fine particulate air pollution and total mortality was examined in a cohort of 49, 975 elderly Californians, with a mean age of 65 yr as of 1973. These subjects, who resided in 25 California counties, were enrolled in 1959, recontacted in 1972, and followed from 1973 through 2002; 39, 846 deaths were identified. Proportional hazards regression models were used to determine their relative risk of death (RR) and 95% confidence interval (CI) during 1973-2002 by county of residence. The models adjusted for age, sex, cigarette smoking, race, education, marital status, body mass index, occupational exposure, exercise, and a dietary factor. For the 35, 789 subjects residing in 11 of these counties, county-wide exposure to fine particles was estimated from outdoor ambient concentrations measured during 1979-1983 and RRs were calculated as a function of these PM(2.5) levels (mean of 23.4 microg/m(3)). For the initial period, 1973-1982, a small positive risk was found: RR was 1.04 (1.01-1.07) for a 10-microg/m(3) increase in PM(2.5). For the subsequent period, 1983-2002, this risk was no longer present: RR was 1.00 (0.98-1.02). For the entire follow-up period, RR was 1.01 (0.99-1.03). The RRs varied somewhat among major subgroups defined by sex, age, education level, smoking status, and health status. None of the subgroups that had significantly elevated RRs during 1973-1982 had significantly elevated RRs during 1983-2002. The RRs showed no substantial variation by county of residence during any of the three follow-up periods. Subjects in the two counties with the highest PM(2.5) levels (mean of 36.1 microg/m(3)) had no greater risk of death than those in the two counties with the lowest PM(2.5) levels (mean of 13.1 microg/m(3)). These epidemiologic results do not support a current relationship between fine particulate pollution and total mortality in elderly Californians, but they do not rule out a small effect, particularly before 1983."
    • Author's response to critique
  • Moolgavkar S, A review and critique of the EPA's rationale for a fine particle standard, Regul Toxicol Pharmacol. 42(1):123-44, June 2005.
    • Abstract. "I review the rationale for the Environmental Protection Agency's 1996 fine particle standard, which was based almost entirely on the epidemiological data with neither support from Toxicology nor understanding of mechanism. While many epidemiological papers available in 1996 reported associations between ambient particles and adverse effects on human health, many others did not and the evidence fell far short of supporting a causal association between particle mass concentration and human health. The literature appearing after 1996 further complicates the picture. The large studies that have appeared after 1996, such as National Mortality Morbidity and Air Pollution Study, and the reanalyses of the American Cancer Society II study, report risks that are substantially smaller than the risks reported in the 1996 Criteria Document and Staff Paper. Moreover, concerns about confounding by weather, temporal trends and co-pollutants remain unresolved. Other issues having to do with model choice have resurfaced as a result of reanalyses of critical data to address a glitch in a widely used software package for time-series epidemiology studies of air pollution. Finally, contemporary examples show that the results of observational epidemiology studies can be seriously biased, particularly when estimated risks are small, as is the case with studies of air pollution. The Agency has largely ignored these issues. I conclude that a particle mass standard is not defensible on the basis of a causal association between ambient particle mass and adverse effects on human health. Such a standard may be justifiable on the basis of the precautionary principle, however. The Agency could argue that the Science raises concerns about current levels of air pollution, and that reduction of ambient fine particulate matter mass, if it could be achieved without an increase in the level of the ultrafines, could have positive effects on human health. If the Agency justifies a particulate matter mass standard on these grounds then the debate over the form and level of the standard will, for all practical purposes, belong strictly in the Policy arena."
  • Moolgavkar S, Air pollution and daily mortality in two U.S. counties: season-specific analyses and exposure-response relationships, Inhal Toxicol. 15(9):877-907, August 2003.
    • Abstract. "I used generalized additive models to analyze the time series of daily total nonaccidental deaths and deaths due to vascular disease over the period 1987-1995 in two major metropolitan areas, Cook County, Illinois, and Los Angeles County, California, in the United States. In both counties I had monitoring information on PM(10), CO, SO(2), NO(2), and O(3). In Los Angeles, monitoring information on PM(2.5) was available as well. In addition to full-year analyses, I performed season-specific analyses. I present the results of both single- and multipollutant analyses. Although components of air pollution were associated with total nonaccidental and vascular disease mortality in both counties, the results indicate considerable heterogeneity of these associations in the two locations and also from season to season. In Los Angeles County, the gases, particularly CO and SO(2) but not ozone, were more strongly associated with mortality than was particulate matter, which exhibited only weak and inconsistent associations with both mortality endpoints. Both PM(10) and the gases were associated with total and vascular disease mortality in Cook County. The association of the gases with both mortality endpoints appeared to be stronger and more robust than that of PM(10). Exposure-response analyses using flexible smoothers showed significant departures from linearity, particularly for PM effects."
  • Moolgavkar S, Air pollution and daily mortality in three U.S. counties, Environ Health Perspect. 108(8):777-84, August 2000.
    • Abstract. "I used generalized additive models to analyze the time-series of daily total nonaccidental and cause-specific (cardiovascular, cerebrovascular, and chronic obstructive pulmonary disease) deaths over the period 1987-1995 in three major U.S. metropolitan areas: Cook County, Los Angeles County, and Maricopa County. In all three counties I had monitoring information on particulate matter [less than/equal to] 10 microm (PM(10)), carbon monoxide, sulfur dioxide, nitrogen dioxide, and ozone. In Los Angeles, monitoring information on particulate matter [less than/equal to] 2.5 microm (PM(2.5)) was available as well. I present the results of both single and multi-pollutant analyses. Air pollution was associated with each of the mortality end points. With respect to the individual components of the pollution mix, the results indicate considerable heterogeneity of air pollution effects in the different geographic locations. In general, the gases, particularly CO, but not ozone, were much more strongly associated with mortality than was particulate matter. This association was particularly striking in Los Angeles County."
  • Moolgavkar S, Air pollution and hospital admissions for diseases of the circulatory system in three U.S. metropolitan areas, J Air Waste Manag Assoc. 50(7):1199-206, July 2000.
    • Abstract. " Generalized additive models were used to analyze the time series of daily hospital admissions for cardiovascular and cerebrovascular diseases over the period of 1987-1995 in three major metropolitan areas--Cook County, IL; Los Angeles County, CA; and Maricopa County, AZ--in the United States. In Cook and Maricopa Counties, admissions information was only available for the elderly (ages 65 and over), while in Los Angeles County, admissions information was available for all ages. In Cook County, daily monitoring information was available on PM10, CO, SO2, NO2, and O3. In Los Angeles and Maricopa Counties, monitoring information was available daily on the gases, and information on PM10 was available every sixth day. In Los Angeles County, information on PM2.5 was also available every sixth day. In Cook and Los Angeles Counties, associations were found between each pollutant, with the exception of O3, and admissions for cardiovascular disease, with the gases showing the strongest associations. In two-pollutant models with PM and one of the gases, the effect of the gases remained stable, while the effect of PM became unstable and insignificant. In Maricopa County, the gases, with the exception of O3, were weakly associated with hospital admissions for cardiovascular disease, while PM was not. In two-pollutant models with two of CO, SO2, and NO2, the pattern of results is heterogeneous in the three counties. In all three counties, only weak evidence of any association between air pollution and cerebrovascular admissions was found."
  • Moolgavkar S, http://www.ncbi.nlm.nih.gov/pubmed/12881887, Inhal Toxicol. 12 Suppl 4:75-90, 2000.
    • Abstract. "I used generalized additive models to analyze the time series of daily admissions for chronic obstructive pulmonary disease (COPD) over the period 1987-1995 in three major metropolitan areas, Cook County, Los Angeles County, and Maricopa County, in the United States. In Cook and Maricopa counties I had admissions information only for the elderly (ages 65 yr and over). In Los Angeles County I had admissions information for all ages. In all three counties I had monitoring information on PM10, CO, SO2, NO2, and O3. In Los Angeles County, I had information on PM2.5 in addition. In Cook and Maricopa counties there was weak evidence of an association between the gaseous pollutants other than ozone and admissions. There was no evidence of an association with PM. In Cook and Los Angeles counties, in single-pollutant models, ozone was associated with admissions during the period April-September but not in full-year analyses. In Los Angeles, the other gases were strongly associated with COPD admissions. PM was also associated with admissions in single-pollutant models. The coefficients for PM were greatly attenuated and became insignificant in joint analyses with any one of the gases (with the exception of ozone). Analyses in three broad age ranges (0-19, 20-64, and 65 yr and over) yielded similar results. The results indicate that the gases, other than ozone, were more strongly associated with COPD admissions than PM and that there was considerable heterogeneity in the effects of individual pollutants in different geographic areas of the country."
  • Moolgavkar S and Luebeck E, A critical review of the evidence on particulate air pollution and mortality, Epidemiology. 7(4):420-8, July 1996.
    • Abstract. "We review epidemiologic studies of particulate air pollution and mortality in U.S. cities with respect to important methodologic issues. Many of these studies suffer from serious deficiencies in their control of the confounding effects of other pollutants. As a consequence, the small risks reported to be associated with the particulate component of air pollution could easily be attributed to residual confounding by co-pollutants. Most studies, moreover, have not considered modification of air pollution effects by seasonal factors, making the interpretation of the estimated risks difficult. We use a new analysis of mortality in Philadelphia that considers four pollutants simultaneously as well as seasonal effects to illustrate the methodologic issues raised in this paper. Air pollution, which is a complex mixture, appears to be associated with mortality even at the generally low levels of pollution in U.S. cities, but currently neither the statistical tools nor the biological understanding of mechanisms exists to tease out the contribution made by each component of this mixture. We conclude that it is not possible with the present evidence to show a convincing correlation between particulate air pollution and mortality."

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