Suchergebnisse

Rationale: Areas near parks may present active travelers with higher risks than in other areas due to the confluence of more pedestrians and bicyclists, younger travelers, and the potential for increased numbers of motor vehicles. These risks may be amplified in low-income and minority neighborhoods due to generally higher rates of walking or lack of safety infrastructure. Objectives: We pursued three research objectives: (1) to determine if pedestrian and bicycle crashes occur at higher rates in park-adjacent neighborhoods compared to the rest of the study area; (2) to identify if demographic characteristics predict active crash risk after controlling for population and the rate of active trips; and (3) to assess if there is an amplified effect of park proximity for active crash risk in low-income and minority neighborhoods after controlling for population and the rate of active trips. Methods: With negative binomial regression modeling techniques, we used ten years of geolocated pedestrian and bicyclist crash data and a quarter mile (~400 meter) buffer around public parks to assess the risk of active travel near parks. We controlled for differential exposures to active travel risks using travel survey data. Measurements: Quarter-mile network buffers were designated around parks from the Green Visions Plan for 21st Century California in 2249 census tracts. Crashes came from the 90,846 pedestrian and bicyclist injuries and fatalities from the Statewide Integrated Traffic Reporting System, and active travel was predicted using travel data from 9135 households that participated in the Southern California Association of Governments 2001 Travel and Congestion Survey. These data were combined with demographic and income data from the U.S. Census and traffic density predictions. Results: The ratio of active crashes per 100,000 population within the quarter-mile park buffer to those outside is 1.52. The increased risk of crash for active travelers near parks remained after adjusting for varying rates of active travel in different census tracts. Minority and low-income residents of the study area are more likely to walk or bicycle than White and higher-income residents. This higher risk near parks is amplified in neighborhoods with high proportions of minority and low-income people. Higher traffic levels are highly predictive of active crashes. Conclusions: Active travelers accessing parks may lack a safe route to places for play. The socioeconomic modification of active crashes near parks found in this study is supported by existing research showing disparities in park access and higher active travel risks in low-income and minority neighborhoods.

BackgroundNumerous studies have linked criteria air pollutants with adverse birth outcomes, but there is less information on the importance of specific emission sources, such as traffic, and air toxics.ObjectivesWe used three exposure data sources to examine odds of term low birth weight (LBW) in Los Angeles, California, women when exposed to high levels of traffic-related air pollutants during pregnancy.MethodsWe identified term births during 1 June 2004 to 30 March 2006 to women residing within 5 miles of a South Coast Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. Pregnancy period average exposures were estimated for air toxics, including polycyclic aromatic hydrocarbons (PAHs), source-specific particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) based on a chemical mass balance model, criteria air pollutants from government monitoring data, and land use regression (LUR) model estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of term LBW (< 2,500 g) were examined using logistic regression.ResultsOdds of term LBW increased approximately 5% per interquartile range increase in entire pregnancy exposures to several correlated traffic pollutants: LUR measures of NO, NO2, and NOx, elemental carbon, and PM2.5 from diesel and gasoline combustion and paved road dust (geological PM2.5).ConclusionsThese analyses provide additional evidence of the potential impact of traffic-related air pollution on fetal growth. Particles from traffic sources should be a focus of future studies.

Abstract Background Numerous studies have associated air pollutant exposures with adverse birth outcomes, but there is still relatively little information to attribute effects to specific emission sources or air toxics. We used three exposure data sources to examine risks of preterm birth in Los Angeles women when exposed to high levels of traffic-related air pollutants - including specific toxics - during pregnancy. Methods We identified births during 6/1/04-3/31/06 to women residing within five miles of a Southern California Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. We identified preterm cases and, using a risk set approach, matched cases to controls based on gestational age at birth. Pregnancy period exposure averages were estimated for a number of air toxics including polycyclic aromatic hydrocarbons (PAHs), source-specific PM2.5 (fine particulates with aerodynamic diameter less than 2.5 μm) based on a Chemical Mass Balance model, criteria air pollutants based on government monitoring data, and land use regression (LUR) estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of preterm birth were estimated using conditional logistic regression. Results Odds of preterm birth increased 6-21% per inter-quartile range increase in entire pregnancy exposures to organic carbon (OC), elemental carbon (EC), benzene, and diesel, biomass burning and ammonium nitrate PM2.5, and 30% per inter-quartile increase in PAHs; these pollutants were positively correlated and clustered together in a factor analysis. Associations with LUR exposure metrics were weaker (3-4% per inter-quartile range increase). Conclusions These latest analyses provide additional evidence of traffic-related air pollution's impact on preterm birth for women living in Southern California and indicate PAHs as a pollutant of concern that should be a focus of future studies. Other PAH sources besides traffic were also associated with higher odds of preterm birth, as was ammonium nitrate PM2.5, the latter suggesting potential importance of secondary pollutants. Future studies should focus on accurate modeling of both local and regional spatial and temporal distributions, and incorporation of source information.

RATIONALE: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive. OBJECTIVES: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults. METHODS: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 μm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates. MEASUREMENTS AND MAIN RESULTS: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models. CONCLUSIONS: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations. ; M.C.T. was funded by a Government of Canada Banting Postdoctoral Fellowship. D.K. is the McLaughlin Chair in Risk Science at the University of Ottawa. Health Canada, the Centers for Disease Control and Prevention, and the National Institutes of Health funded the development of the PM2.5 exposure model. The American Cancer Society funded the creation, maintenance, and follow-up of the Cancer Prevention Study II cohort.