Faculty Bibliography

Epidemiological studies have generally found fine particle metrics such as PM2.5 (PM mass less than 2.5 mun in aerodynamic diameter) to be more strongly related to adverse health effects than PM metrics that are not size-fractionated, such as total suspended particulate matter (TSP). The latency of long-term PM exposure effects on health could potentially be investigated using the American Cancer Society Cancer Prevention Study 11 cohort and other nationwide cohorts. Unfortunately, historical PM2.5 data are not available for many past years in most of the US. With the recent introduction of a PM2.5 National Ambient Air Quality Standard (NAAQS), fine particulate data is now available through the Environmental Protection Agency's (EAP's) Aerometric Information Retrieval System (AIRS) database from 1999 onwards. Using this nationwide PM2.5 data, we have estimated ratios Of PM2.5-PM10 (PM mass less than 10 mum in aerodynamic diameter) for more than 100 Metropolitan Statistical Areas (MSAs) in the US Similarly, using TSP and PM10 data from the late 1980's, when both metric were measured, we have derived PM10/TSP ratios for hundreds of US MSAs. These MSA-specific PM ratios allow the estimation of historical annual fine particulate concentrations, for as far back as 1972, using available annual TSP or PM 10 data. We found mean ratios Of PM2.5/ PM10= 0.54+/-0.14, and PM2.5/TSP = 0.30+/-0.11. The Inhalable Particle Network (IPN), a database independent of the AIRS database, monitored TSP and PM2.5 between 1979-1982. Using a subset of MSAs common to both databases, this dataset has been used to test our hypothesis that MSA-specific mass ratios could be used to estimate PM2.5 from PM10 and TSP. Raw IPN TSP-PM2.5 concentration correlations for MSAs were non-significant (R-2 = 0.00). Using the IPN TSP and our PM2.5/TSP ratios, mean PM2.5 estimates for 26 MSA were found to correlate with the measured IPN PM2.5 at R-2 = 0.43. These results indicate that it is possible to use MSA-specific PM mass ratios to predict historical annual mean PM2.5 exposure levels from past TSP and PM10 measurements. In addition, the MSA-specific ratios were used to estimate nationwide PM2.5 concentrations for 1972-2000. These results indicate that considerable progress has been made in reducing U.S. PM2.5 levels over the 30 years. (C) 2004 Elsevier Ltd. All rights reserved

Particulate matter (PM) is a chemically non-specific pollutant, and may originate or be derived from different emission source types. Thus, its toxicity may well vary depending on its chemical composition. If the PM toxicity could be determined based on source types, the regulation of PM may be implemented more effectively. A large number of monitors began collecting PM less than 2.5 mum in diameter (PM2.5) mass samples for subsequent chemical speciation starting 2000-2001 in the US. The data from this chemical speciation network can be useful for source-oriented evaluations of PM health effects. However, there are several issues that need to be considered in the analysis and interpretation of these data. One major issue is a monitor's representation of regional, sub-regional, and local air pollution exposures to the population in a city or metropolitan area. Because health outcomes in time-series air pollution epidemiological studies are aggregated over a wide geographical area, regional PM pollution may have smaller errors in exposure estimates than more spatially varying local pollution. However, the relative strength of association between source-apportioned PM and health outcomes may not be interpretable as the relative causal role of the source types. To our knowledge, there has not yet been a systematic and quantitative evaluation of this issue. In this study, we attempt to evaluate this issue by analyzing newly available PM2.5 speciation data from three monitors (a few miles apart) in New York City during 2001-2002. The strongest temporal correlations across the three monitors were found for the individual PM. components that are related to secondary aerosols (e.g., S, NH4). We also conducted source-apportionment of the data using absolute principal component analysis and positive matrix factorization. We identified four major source/pollution types: (1) secondary (largely regional) aerosols; (2) soil; (3) traffic-related; and (4) residual oil burning/incineration, in each of the three monitors. The estimated source-apportioned PM2.5 mass showed generally the highest monitor-to-monitor correlation for the secondary aerosol factor (r range: 0.72-0.93). The correlation for the more localized traffic-related factor was more variable (r range: 0.26-0.95). The estimated mean PM2.5 mass contributions by source/pollution type across the monitors varied least for the secondary aerosol factor. The extent of variability in the source-apportioned PM2.5 mass by the monitor was comparable to that from the difference due to the two source-apportionment techniques used. The implication of the results of our study is that a source-oriented evaluation of PM health effects needs to take into consideration the uncertainty associated with spatial representative of the species measured at a single monitor. (C) 2004 Elsevier Ltd. All rights reserved

The objective of this study is to characterize the ambient air quality of the South Bronx, New York City (NYC), having high concentrations of diesel trucks and waste transfer facilities. We employed a mobile laboratory for continuous measurements of concentrations of fine particulate matter (PM2.5), black carbon (BC), and gaseous pollutants at 6 locations for three-four weeks each during the period of April 2001-February 2003. Integrated 24-hr PM2.5 samples were also collected for elemental and PAHs analyses. South Bronx PM2.5 and BC levels were compared to those at Bronx PS 154 (NYSDEC site) and at Hunter College in the Lower Manhattan. Although the median daily PM2.5 concentrations agreed within 20%, the median hourly BC concentrations were higher at all South Bronx sites ranging from 2.2 to 3.8 mug m(-3), compared to 1.0-2.6 mug m(-3) at Hunter College. Continuous Aethelometer measurements at additional 27 sampling sites in the South Bronx were conducted along major highways. BC concentrations Varied within each site, depending on time-of-day, with a large spatial variability from site-to-site. Daily median BC concentrations varied from 1.7 to 12 mug m(-3) on the weekdays, and were lower (0.50-2.9 mug m(-3)) on the weekends; Elemental concentrations were higher at all South Bronx sites than those at Hunter College for all measured elements but Ni and V, and at the Hunts Point, an industrial location, were approximately 2.5-fold higher. The average sum of 35 PAHs was 225 ng m(-3), which is 4.5 times larger than representative regional concentrations in Jersey City, NJ. Among the individual PAHs, 3,6-dimethylphenanthrene had the highest concentrations, and the overall PAH fingerprint differed from signal for Jersey City. Our data indicates that highways encircling the South Bronx are having a measurable adverse influence on residents' exposure to pollutants compared to other NYC areas. (C) 2004 Elsevier Ltd. All rights reserved

BACKGROUND: Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. METHODS AND RESULTS: General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. CONCLUSIONS: Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking

Many time series studies have found that individuals with primary cardiac conditions were susceptible to the adverse effects associated with increased ambient particle levels. However, the mechanism(s) of these associations is not yet understood. In this study, we evaluate whether individuals with nonrespiratory primary causes of death who also had contributing respiratory causes listed on their death certificates were more affected by air pollution, as compared with those not having contributing respiratory conditions. Short-term associations between ambient particulate matter (10 microm or less in aerodynamic diameter) and mortality were modeled in New York City for the years 1985-1994. It was observed that among those 75 years or more, those with contributing respiratory disease had higher relative risks (95% confidence intervals) calculated per interquartile range, as compared with those without contributing respiratory disease for both circulatory deaths (relative risk = 1.066 [1.027-1.106] versus 1.022 [1.008-1.035]) and cancer deaths (relative risk = 1.129 [1.041-1.225] versus 1.025 [1.000-1.050]). However, this pattern of association was not observed for those who were less than 75 years old. The results of this study suggest that past studies may have underestimated the role of respiratory disease in pollution-mortality associations, especially among older adults