Research report (Health Effects Institute)
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Res Rep Health Eff Inst · Oct 2009
Air pollution and health: a European and North American approach (APHENA).
This report provides the methodology and findings from the project: Air Pollution and Health: a European and North American Approach (APHENA). The principal purpose of the project was to provide an understanding of the degree of consistency among findings of multicity time-series studies on the effects of air pollution on mortality and hospitalization in several North American and European cities. The project included parallel and combined analyses of existing data. The investigators sought to understand how methodological differences might contribute to variation in effect estimates from different studies, to characterize the extent of heterogeneity in effect estimates, and to evaluate determinants of heterogeneity. The APHENA project was based on data collected by three groups of investigators for three earlier studies: (1) Air Pollution and Health: A European Approach (APHEA), which comprised two multicity projects in Europe. (Phase 1 [APHEA1] involving 15 cities, and Phase 2 [APHEA2] involving 32 cities); (2) the National Morbidity, Mortality, and Air Pollution Study (NMMAPS), conducted in the 90 largest U.S. cities; and (3) multicity research on the health effects of air pollution in 12 Canadian cities. ⋯ APHENA has shown that mortality findings obtained with the new standardized analysis were generally comparable to those obtained in the earlier studies, and that they were relatively robust to the data analysis method used. For PM10, the effect-modification patterns observed were not entirely consistent between Europe and the United States. For O3, there was no indication of strong effect modification in any of the three data sets.
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Current risk assessments of 1,3-butadiene (BD*) are complicated by limited evidence of its carcinogenicity in humans. Hence, there is a critical need to identify early events and factors that account for the heightened sensitivity of mice to BD-induced carcinogenesis and to deter-mine which animal model, mouse or rat, is the more useful surrogate of potency for predicting health effects in BD-exposed humans. HEI sponsored an earlier investigation of mutagenic responses in mice and rats exposed to BD, or to the racemic mixture of 1,2-epoxy-3-butene (BDO) or of 1,2,3,4-diepoxybutane (BDO2; Walker and Meng 2000). ⋯ In rats, it appears that the BD-diol pathway might account for nearly all the mutagenicity at the hight-level BD exposures where significant increases in Hprt Mfs are found and cancers are induced. Additional exposure-response studies of hemoglobin and DNA adducts specifics to BDO2, BDO-diol, and other reactive intermediates are needed to determine more definitively the relative contribution of each metabolite to the DNA alkylation and mutation patterns induced by BD exposure in mice and rats. For the fifth hypothesis, a multiplex polymerase chain reaction (PCR) procedure for the analysis of genomic DNA mutations in the Hprt gene of mice was developed. (ABSTRACT TRUNCATED)
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Res Rep Health Eff Inst · Jun 2009
Measurement and modeling of exposure to selected air toxics for health effects studies and verification by biomarkers.
The overall aim of our investigation was to quantify the magnitude and range of individual personal exposures to a variety of air toxics and to develop models for exposure prediction on the basis of time-activity diaries. The specific research goals were (1) to use personal monitoring of non-smokers at a range of residential locations and exposures to non-traffic sources to assess daily exposures to a range of air toxics, especially volatile organic compounds (VOCs) including 1,3-butadiene and particulate polycyclic aromatic hydrocarbons (PAHs); (2) to determine microenvironmental concentrations of the same air toxics, taking account of spatial and temporal variations and hot spots; (3) to optimize a model of personal exposure using microenvironmental concentration data and time-activity diaries and to compare modeled exposures with exposures independently estimated from personal monitoring data; (4) to determine the relationships of urinary biomarkers with the environmental exposures to the corresponding air toxic. Personal exposure measurements were made using an actively pumped personal sampler enclosed in a briefcase. ⋯ The models developed for PAHs explain some of the variance in the independent data set and are good indicators of the sources affecting PAH concentrations but could not be validated statistically, with the exception of the model for pyrene. A proposal for categorizing personal exposures as low or high is also presented, according to exposure thresholds. For both VOCs and PAHs, low exposures are correctly classified for the concentrations predicted by the proposed models, but higher exposures were less successfully classified.
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Res Rep Health Eff Inst · May 2009
Extended follow-up and spatial analysis of the American Cancer Society study linking particulate air pollution and mortality.
We conducted an extended follow-up and spatial analysis of the American Cancer Society (ACS) Cancer Prevention Study II (CPS-II) cohort in order to further examine associations between long-term exposure to particulate air pollution and mortality in large U. S. cities. The current study sought to clarify outstanding scientific issues that arose from our earlier HEI-sponsored Reanalysis of the original ACS study data (the Particle Epidemiology Reanalysis Project). ⋯ This study provides additional support toward developing cost-effective air quality management policies and strategies. The epidemiologic results reported here are consistent with those from other population-based studies, which collectively have strongly supported the hypothesis that long-term exposure to PM2.5 increases mortality in the general population. Future research using the extended Cox-Poisson random effects methods, advanced geostatistical modeling techniques, and newer exposure assessment techniques will provide additional insight.
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We conducted a retrospective study of a set of previously published electrocardiographic data to investigate the possible direct association between levels of particulate air pollution and changes in ventricular repolarization -- the cardiac electrophysiologic process that manifests itself as the T wave* of the electrocardiogram (ECG) and that is definitively linked to and responsible for increased arrhythmogenesis. The published findings from this data set demonstrated a clear cardiac effect, namely, a reduction in heart rate variability (HRV) parameter values with increased levels of particulate air pollution (Pope et al. 2004), suggesting possible arrhythmogenic effects. Given this positive finding and the well-established sensitivity of cardiac repolarization to physiologic, pharmacologic, and neurologic interventions, and in light of emerging novel tools for assessing repolarization, we hypothesized that high levels of particulate air pollution would alter repolarization independent of changes in heart rate and, consequently, would increase arrhythmogenic risk. ⋯ In addition, the study may have been underpowered. The findings do not refute the possibility of the deleterious repolarization effects of PM, particularly over prolonged periods of exposure, but suggest the need for exposure studies that provide better controls. In light of recent studies, it is also likely that in an at-risk population -- for example, patients compromised with heart disease -- repolarization changes may be more apparent.