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Background: Emerging evidence suggests that the systemic vasculature may be a target of inhaled pollutants of vehicular origin. We have identified several murine markers of vascular toxicity that appear sensitive to inhalation exposures to combustion emissions. Objective: We sought to examine the relative impact of various pollutant atmospheres and specific individual components on these markers of altered vascular transcription and lipid peroxidation. Methods: Apolipoprotein E knockout (ApoE-/-) mice were exposed to whole combustion emissions (gasoline, diesel, coal, hardwood), biogenically derived secondary organic aerosols (SOAs), or prominent combustion-source gases [nitric oxide (NO), NO2, carbon monoxide (CO)] for 6 hr/day for 7 days. Aortas were assayed for transcriptional alterations of endothelin-1 (ET-1), matrix metalloproteinase- 9 (MMP-9), tissue inhibitor of metalloproteinase-2 (TIMP-2), and heme oxygenase-1 (HO-1), along with measures of vascular lipid peroxides (LPOs) and gelatinase activity. Results: We noted transcriptional alterations with exposures to gasoline and diesel emissions. Interestingly, ET-1 and MMP-9 transcriptional effects could be recreated by exposure to CO and NO, but not NO2 or SOAs. Gelatinase activity aligned with levels of volatile hydrocarbons and also monoxide gases. Neither gases nor particles induced vascular LPO despite potent effects from whole vehicular emissions. Conclusions: In this head-to-head comparison of the effects of several pollutants and pollutant mixtures, we found an important contribution to vascular toxicity from readily bioavailable monoxide gases and possibly from volatile hydrocarbons. These data support a role for traffic-related pollutants in driving cardiopulmonary morbidity and mortality. [ABSTRACT FROM AUTHOR]

Background: Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. However, there has been little study of effects of traffic exposure at school on new-onset asthma. Objectives: We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools. Methods: Parent-reported physician diagnosis of new-onset asthma (n = 120) was identified during 3 years of follow-up of a cohort of 2,497 kindergarten and first-grade children who were asthmaand wheezing-free at study entry into the Southern California Children's Health Study. We assessed traffic-related pollution exposure based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO2), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. Hazard ratios (HRs) for new-onset asthma were scaled to the range of ambient central site pollutants and to the residential interquartile range for each traffic exposure metric. Results: Asthma risk increased with modeled traffic-related pollution exposure from roadways nearhomes [HR 1.51; 95% confidence interval (CI), 1.25-1.82] and near schools (HR 1.45; 95% CI, 1.06-1.98). Ambient NO2 measured at a central site in each community was also associated with increased risk (HR 2.18; 95% CI, 1.18-4.01). In models with both NO2 and modeled traffic exposures, there were independent associations of asthma with traffic-related pollution at school and home, whereas the estimate for NO2 was attenuated (HR 1.37; 95% CI, 0.69-2.71). Conclusions: Traffic-related pollution exposure at school and homes may both contribute to the development of asthma. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to combustion-derived fine particulate matter (PM) is associated with increased cardiovascular morbidity and mortality especially in individuals with cardiovascular disease, including hypertension. PM inhalation causes several adverse changes in cardiac function that are reflected in the electrocardiogram (ECG), including altered cardiac rhythm, myocardial ischemia, and reduced heart rate variability (HRV). The sensitivity and reliability of ECG-derived parameters as indicators of the cardiovascular toxicity of PM in rats are unclear. OBJECTIVE: We hypothesized that spontaneously hypertensive (SH) rats are more susceptible to the development of PM-induced arrhythmia, altered ECG morphology, and reduced HRV than are Wistar Kyoto (WKY) rats, a related strain with normal blood pressure. METHODS: We exposed rats once by nose-only inhalation for 4 hr to residual oil fly ash (ROFA), an emission source particle rich in transition metals, or to air and then sacrificed them 1 or 48 hr later. RESULTS: ROFA-exposed SH rats developed nonconducted P-wave arrhythmias but no changes in ECG morphology or HRV. We found no ECG effects in ROFA-exposed WKY rats. ROFA-exposed SH rats also had greater pulmonary injury, neutrophil infiltration, and serum C-reactive protein than did ROFA-exposed WKY rats. CONCLUSIONS: These results suggest that cardiac arrhythmias may be an early sensitive indicator of the propensity for PM inhalation to modify cardiovascular function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Long-term human exposure to ambient pollutants can be an important contributing or etiologic factor of many chronic diseases. Spatiotemporal estimation (mapping) of long-term exposure at residential areas based on field observations recorded in the U.S. Environmental Protection Agency's Air Quality System often suffer from missing data issues due to the scarce monitoring network across space and the inconsistent recording periods at different monitors. OBJECTIVE: We developed and compared two upscaling methods: UM1 (data aggregation followed by exposure estimation) and UM2 (exposure estimation followed by data aggregation) for the long-term PM10 (particulate matter with aerodynamic diameter ≤ 10 µm) and ozone exposure estimations and applied them in multiple time scales to estimate PM and ozone exposures for the residential areas of the Health Effects of Air Pollution on Lupus (HEAPL) study. METHOD: We used Bayesian maximum entropy (BME) analysis for the two upscaling methods. We performed spatiotemporal cross-validations at multiple time scales by UM1 and UM2 to assess the estimation accuracy across space and time. RESULTS: Compared with the kriging method, the integration of soft information by the BME method can effectively increase the estimation accuracy for both pollutants. The spatiotemporal distributions of estimation errors from UM1 and UM2 were similar. The cross-validation results indicated that UM2 is generally better than UM1 in exposure estimations at multiple time scales in terms of predictive accuracy and lack of bias. For yearly PM10 estimations, both approaches have comparable performance, but the implementation of UM1 is associated with much lower computation burden. CONCLUSION: BME-based upscaling methods UM1 and UM2 can assimilate core and site-specific knowledge bases of different formats for long-term exposure estimation. This study shows that UM1 can perform reasonably well when the aggregation process does not alter the spatiotemporal structure of the original data set; otherwise, UM2 is preferable. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Climate change is likely to affect the nature of pathogens and chemicals in the environment and their fate and transport. Future risks of pathogens and chemicals could therefore be very different from those of today. In this review, we assess the implications of climate change for changes in human exposures to pathogens and chemicals in agricultural systems in the United Kingdom and discuss the subsequent effects on health impacts. DATA SOURCES: In this review, we used expert input and considered literature on climate change; health effects resulting from exposure to pathogens and chemicals arising from agriculture; inputs of chemicals and pathogens to agricultural systems; and human exposure pathways for pathogens and chemicals in agricultural systems. DATA SYNTHESIS: We established the current evidence base for health effects of chemicals and pathogens in the agricultural environment; determined the potential implications of climate change on chemical and pathogen inputs in agricultural systems; and explored the effects of climate change on environmental transport and fate of different contaminant types. We combined these data to assess the implications of climate change in terms of indirect human exposure to pathogens and chemicals in agricultural systems. We then developed recommendations on future research and policy changes to manage any adverse increases in risks. CONCLUSIONS: Overall, climate change is likely to increase human exposures to agricultural contaminants. The magnitude of the increases will be highly dependent on the contaminant type. Risks from many pathogens and particulate and particle-associated contaminants could increase significantly. These increases in exposure can, however, be managed for the most part through targeted research and policy changes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Particulate matter, especially ultrafine particles (UFPs), may cause health effects through generation of oxidative stress, with resulting damage to DNA and other macromolecules. OBJECTIVES: Wc investigated oxidative damagc to DNA and related repair capacity in peripheral blood mononuclear cells (PBMCs) during controlled exposure to urban air particles with assignment of numher concentration (NC) to four size modes with average diameters of 12, 23, 57, and 212 nm. DESIGN. Twenty-nine healthy adults participated in a randomized, two-factor cross-ovcr study with or without biking excrcise for 180 min and with exposure to particles (NC 6169-15362/cm³) or filtered air (NC 91-542/cm³) for 24 hr. METHODS: The levels of DNA strand breaks (SBs), oxidized purines as formamidopyrimidine DNA glycolase (FPG) sites, and activity of 7,8-dihydro-8-oxoguanine-DNA glycosylase (OGGI) in PBMCs were measured by the Comet assay. mRNA levels of OGGI, nucleoside diphosphate linked moiety X-type motif I (NUDTI), and heme oxygenase-1 (HOl) were determined by real-time reverse transcriptase-polymerase chain reaction. RESULTS: Exposure to UFPs for 6 and 24 hr significantly increased the levels of SBs and FPG sites, with a further insignificant increase after physical exercise. The OGGI activity and expression of OGGI, NUDl, and HOl were unaltered. There was a significant dose-response relationship between NC and DNA damage, with the 57-nm mode as the major contributor to effects. Concomitant exposure to ozone, nitrogen oxides, and carbon monoxide had no influence. CONCLUSION: Our results indicate that UFPs, especially the 57-nm soot fraction from vehicle emissions, causes systemic oxidative stress with damage to DNA and no apparent compensatory up-regulation of DNA repair within 24 hr. [ABSTRACT FROM AUTHOR]

BACKGROUND: Otitis media is one of the most common infections in young children. Although exposure to environmental tobacco smoke is a known risk factor associated with otitis media, little information is available regarding the potential association with air pollution. OBJECTIVE: We set out to study the relationship between exposure to traffic-related air pollution and otitis media in two birth cohorts. METHODS: Individual estimates of outdoor concentrations of traffic-related air pollutants—nitrogen dioxide, fine particles [particulate matter with aerodynamic diameters ≤ 2.5 μm (PM2.5)], and elemental carbon—were calculated for home addresses of approximately 3,700 and 650 infants from birth cohort studies in the Netherlands and Germany, respectively. Air pollution exposure was analyzed in relation to physician diagnosis of otitis media in the first 2 years of life. RESULTS: Odds ratios (adjusted for known major risk factors) for otitis media indicated positive associations with traffic-related air pollutants. An increase in 3 μg/m3 PM2.5, 0.5 μg/m3 elemental carbon, and 10 μg/m3 NO2 was associated with odds ratios of 1.13 (95% confidence interval, 1.00–1.27), 1.10 (1.00–1.22), and 1.14 (1.03–1.27) in the Netherlands and 1.24 (0.84–1.83), 1.10 (0.86–1.41), and 1.14 (0.87–1.49) in Germany, respectively. CONCLUSIONS: These findings indicate an association between exposure to traffic-related air pollutants and the incidence of otitis media. Given the ubiquitous nature of air pollution exposure and the importance of otitis media to children's health, these findings have significant public health implications. [ABSTRACT FROM AUTHOR]

The article presents a letter to the editor in which the author discusses research conducted by Joseph W. Green and Paul A. Zandbergen that evaluates positional errors of geocoded addresses and proxies for traffic-related exposures.

The article discusses the autumn-season wildfires in Southern California and the particulate emissions they generate, referring to a January 6, 2009 online report by engineering professor Constantinos Sioutas in advance of the associated print version of "Environmental Science & Technology." Compared to vehicular particulate emissions, wildfire particles are larger and contain more water-soluble organic compounds that are readily absorbed by the human body. Wildfire particles evoked more oxidative stress than traffic-related particles using the standard dithiothreitol (DDT) assay and the macrophage reactive oxygen species (ROS) assay.

This article explains that children who grow up in impoverished, urban communities, in close proximity to the highway, are at greater risk for developing asthma and other breathing disorders. Also, children in these areas often witness violent acts, and the resulting stress weakens their immune system, therefore making symptoms worse. Air pollutants that contribute to asthma include nitrogen dioxide found in car exhaust. The details of the study that pertains to these issues, the Maternal-Infant Smoking Study of East Boston, are discussed.