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 PM10, CO, SO2, NO2, and O3. In Los Angeles, monitoring information on PM2.5 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 SO2 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 PM10 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 PM10. Exposure-response analyses using flexible smoothers showed significant departures from linearity, particularly for PM effects.

Abstract  The United States is making the transition from the 1979 1 hr maximum ozone standard to the newly adopted 8 hr ozone standard (3 yr average of the 4th highest maximum 8 hr ozone concentration). Consequently, we analyzed and compared ozone concentrations under both standards from a variety of monitoring sites throughout the central Appalachian region of Kentucky (KY), West Virginia (WV), and Virginia (VA). Data from 1988-1999 were used to determine how ozone exposure between the two metrics compared for remote sites. Most sites exceeded the 1 hr standard in 1988-1990 due to the 3 yr averaging and multiple high ozone concentrations that occurred over the region in 1988. All sites were in compliance with the 1 hr standard every year after 1991. It was much more common for the ozone exposure to exceed the 8 hr standard, particularly from 1997-1999. Many sites showed exceedences beginning in 1995; Big Meadows (VA) exceeded the 8 hr standard all years except 1994 and 1996. Response of vegetation to ozone in these areas was determined using the combination of W126 values (sigmoidally weighted exposure index), the number of hours that average concentrations >O. 10 ppm (N100), and the presence of moderate or more extreme droughts. In general, W126 and Nl00 values suggested that negative vegetation growth responses over most of the 12 yr would have been minimal for most sites, even for those exceeding ozone standards. Drought-induced stomata1 closures would have overridden more extreme negative growth responses at all but the Big Meadows site in 1988.

Abstract  Endothelial cells play important roles in anticoagulant and fibrinolytic systems. Recent studies suggest that increases in ambient particulate matter (PM) levels have been associated with an increase in mortality rate from cardiovascular diseases. We examined the production of heme oxygenase-1 (HO-1) and factors related to the fibrinolytic function by rat heart microvessel endothelial cells exposed to organic extracts of diesel exhaust particles (OE-DEP) and urban fine particles (OE-UFP) to investigate the direct effects of these soluble organic fractions in these PM on the fibrinolytic function of endothelial cells. The cell monolayer exposed to 10 μg/ml OE-DEP produced a larger amount of HO- 1 than cells exposed to 10 μg/ml OE-UFP. OE-DEP and OE-UFP exposure reduced plasminogen activator inhibitor-1 (PAI-1) production by the cells but did not affect the production of thrombomodulin, tissue-type plasminogen activator, or urokinase-type plasminogen activator. Increased PAI-1 synthesis in response to treatment with 1.0 ng/ml tumor necrosis factor-α or 0.5 ng/ml transforming growth factor-β1 was reduced by OE-DEP exposure. Suppression of PAI-1 production by OE-DEP exposure was mediated through oxidative stress and was independent of HO-1 activity. These results suggest that exposure to the soluble organic fraction of PM and DEP induced oxidative stress and reduced the PAI-1 production of endothelial cells.

Abstract  The application of newly developed semi-continuous aerosol monitors allows for the measurement of all the major species Of PM2.5 on a 1-h time basis. Temporal resolution of both non-volatile and semi-volatile species is possible. A suite of instruments to measure the major chemical species of PM2.5 allows for semi-continuous mass closure. A newly developed dual-oven Sunset carbon monitor is used to measure non-volatile organic carbon, semi-volatile organic carbon and elemental carbon. Inorganic species, including sulfate and nitrate, can be measured with an ion chromatograph based sampler. Comparison of the sum of the major chemical species in an urban aerosol with mass measured by an FDMS resulted in excellent agreement. Linear regression analysis resulted in a zero-intercept slope of 0.98 +/- 0.01 with an R-2 = 0.86. One-hour temporal resolution of the major species Of PM2.5 may reduce the uncertainty in receptor based source apportionment modeling, will allow for better forecasting Of PM2.5 episodes, and may lead to increased understanding of related health effects. (c) 2007 Elsevier Ltd. All rights reserved.

Abstract  Residence in urban areas with much traffic has been associated with various negative health effects. However, the contribution of traffic emissions to these adverse health effects has not been fully determined. Therefore, the objective of this in vivo study is to compare the pulmonary and systemic responses of rats exposed to particulate matter (PM) obtained from various locations with contrasting traffic profiles. Samples of coarse (2.5 microm-10 microm) and fine (0.1 microm-2.5 microm) PM were simultaneously collected at nine sites across Europe with a high-volume cascade impactor. Six PM samples from various locations were selected on the basis of contrast in in vitro analysis, chemical composition, and traffic profiles. We exposed spontaneously hypertensive (SH) rats to a single dose (3 mg PM/kg body weight or 10 mg PM/kg body weight) of either coarse or fine PM by intratracheal instillation. We assessed changes in biochemical markers, cell differentials, and histopathological changes in the lungs and blood 24 h postexposure. The dose-related adverse effects that both coarse and fine PM induced in the lungs and vascular system were mainly related to cytotoxicity, inflammation, and blood viscosity. We observed clear differences in the extent of these responses to PM from the various locations at equivalent dose levels. There was a trend that suggests that samples from high-traffic sites were the most toxic. It is likely that the toxicological responses of SH rats were associated with specific PM components derived from brake wear (copper and barium), tire wear (zinc), and wood smoke (potassium).

Abstract  Three multivariate receptor algorithms were applied to seven years of chemical speciation data to apportion fine particulate matter to various sources in Spokane, Washington. Source marker compounds were used to assess the associations between atmospheric concentration of these compounds and daily cardiac hospital admissions and/or respiratory emergency department visits. Total carbon and arsenic had high correlations with two different vegetative burning sources and were selected as vegetative burning markers, while zinc and silicon were selected as markers for the motor vehicle and airborne soil sources, respectively. The rate of respiratory emergency department visits increased 2% for a 3.0 ?g/m3 interquartile range change in a vegetative burning source marker (1.023, 95% CI 1.009-1.038) at a lag of one day. The other source markers studied were not associated with the health outcomes investigated. Results suggest vegetative burning is associated with acute respiratory events.

Abstract  Size-fractionated particulate matter (PM) samples were collected from six U.S. cities and chemically analyzed as part of the Multiple Air Pollutant Study. Particles were administered to cultured lung cells and the production of three different proinflammatory markers was measured to explore the association between the health effect markers and PM. Ultrafine, fine, and coarse PM samples were collected between December 2003 and May 2004 over a 4-wk period in each city. Filters were pooled for each city and the PM samples were extracted then analyzed for trace metals, ions, and elemental carbon. Particle extracts were applied to cultured human primary airway epithelial cells, and the secreted levels of interleukin-8 (IL-8), heme oxygenase-1, and cyclooxygenase-2 were measured 1 and 24 h following exposure. Fine PM sources were quantified by the chemical mass balance (CMB) model. The relationship between toxicological measures, PM sources, and individual species were evaluated using linear regression. Ultrafine and fine PM mass were associated with increases in IL-8 (r2 = .80 for ultrafine and r2 =.52 for fine). Sources of fine PM and their relative contributions varied across the sampling sites and a strong linear association was observed between IL-8 and secondary sulfate from coal combustion (r2 =.79). Ultrafine vanadium, lead, copper, and sulfate were also associated with increases in IL-8. Increases in inflammatory markers were not observed for coarse PM mass and source markers. These findings suggest that certain PM size fractions and sources are associated with markers of lung injury or inflammation.

Abstract  BACKGROUND: Interest in the health effects of particulate matter (PM) has focused on identifying sources of PM, including biomass burning, power plants, and gasoline and diesel emissions that may be associated with adverse health risks. Few epidemiologic studies, however, have included source-apportionment estimates in their examinations of PM health effects. We analyzed a time-series of chemically speciated PM measurements in Atlanta, Georgia, and conducted an epidemiologic analysis using data from three distinct source-apportionment methods. OBJECTIVE: The key objective of this analysis was to compare epidemiologic findings generated using both factor analysis and mass balance source-apportionment methods. METHODS: We analyzed data collected between November 1998 and December 2002 using positive-matrix factorization (PMF), modified chemical mass balance (CMB-LGO), and a tracer approach. Emergency department (ED) visits for a combined cardiovascular (CVD) and respiratory disease (RD) group were assessed as end points. We estimated the risk ratio (RR) associated with same day PM concentrations using Poisson generalized linear models. RESULTS: There were significant, positive associations between same-day PM(2.5) (PM with aero-dynamic diameter

Abstract  BACKGROUND: The effects of environmental factors and ambient concentrations of grass pollen on allergic asthma are yet to be established. OBJECTIVE: We sought to estimate the independent effects of grass pollen concentrations in the air over Melbourne on asthma hospital admissions for the 1992-1993 pollen season. METHODS: Daily grass pollen concentrations were monitored over a 24-h period at three stations in Melbourne. The outcome variable was defined as all-age asthma hospital admissions with ICD9-493 codes. The ambient air pollutants were average daily measures of ozone, nitrogen dioxide and sulphur dioxide, and the airborne particle index representing fine particulate pollution. Semi-parametric Poisson regression models were used to estimate these effects, adjusted for air temperature, humidity, wind speed, rainfall, day-of-the-week effects and seasonal variation. RESULTS: Grass pollen was a strong independent non-linear predictor of asthma hospital admissions in a multi-pollutant model (P=0.01). Our data suggest that grass pollen had an increasing effect on asthma hospital admissions up to a threshold of 30 grains/m3, and that the effect remains stable thereafter. CONCLUSION: Our findings suggest that grass pollen levels influence asthma hospital admissions. High grass pollen days, currently defined as more than 50 grains/m3, are days when most sensitive individuals will experience allergic symptoms. However, some asthmatic patients may be at a significant risk even when airborne grass pollen levels are below this level. Patients with pollen allergies and asthma would be advised to take additional preventive medication at lower ambient concentrations.

Abstract  OBJECTIVE: To review the roles of viral respiratory tract infections, environmental tobacco smoke and air pollution in asthma.

DATA SOURCES: MEDLINE (1992-1995) searches were conducted for publications on asthma, environmental tobacco smoke, ozone, nitrogen dioxide and particulates.

STUDY SELECTION: Representative original experimental and epidemiological studies and reviews of viral infections in asthma.

DATA SYNTHESIS: Respiratory virus infections are the most common and important trigger of asthma attacks in children and probably also in adults. Their role in promoting development of asthma is not so clear. Exposure to environmental tobacco smoke is almost certainly responsible for some cases of childhood asthma, and can also trigger symptoms of bronchoconstriction in adults with asthma. Exposure to ozone or nitrogen dioxide is associated with symptoms, impaired lung function, bronchial hyperresponsiveness and hospital presentations for asthma. These pollutants may also act as cofactors in the development of allergen-specific bronchial hyperresponsiveness.

CONCLUSIONS: Research on preventing upper respiratory viral infections may reduce asthma morbidity. The move to non-smoking workplaces is welcome, but new interventions are needed to prevent young women taking up smoking and subsequently exposing their children. The ambient air quality guideline for ozone should be revised and a health-based guideline for respirable particulates introduced.

Abstract  Ozone and several polar volatile organic compounds (VOCs) including organic acids and carbonyls (aldehydes and ketones) were measured over an aroximately 24 hour period in four residences during the winter of 1993 and in nine residences during the summer of 1993. All residences were in the greater Boston, Massachusetts area. The relation of the polar VOCs to the ozone concentration was examined. Indoor carbonyl concentrations were similar between the summer and winter, with the total mean winter concentration being 31.7 ppb and the total mean summer concentration being 36.6 ppb. However, the average air exchange rate was 0.9 hr(-1) during the winter and 2.6 hr(-1) during the summer. Therefore, the estimated carbonyl emission rates were significantly higher during the summer. Indoor organic acid concentrations were about twice as high during the summer as during the winter. For formic acid, the indoor winter mean was 9.8 ppb, and the summer indoor mean was 17.8 ppb. For acetic acid, the indoor winter mean was 15.5 ppb, and the summer indoor mean was 28.7 ppb. The concentrations of the polar VOCs were found to be significantly correlated with one another. Also, the emission rates of the polar VOCs were found to be correlated with both the environmental variables such as temperature and relative humidity and the ozone removal rate; however, it was difficult to apportion the relative effects of the environmental variables and the ozone removal.

Abstract  Rates of atmospheric deposition of biologically active nitrogen (N) are two to seven times the pre-industrial rates in many developed nations because of combustion of fossil fuels and agricultural fertilization. They are expected to increase similarly over the next 50 years in industrializing nations of Asia and South America. Although the environmental impacts of high rates of nitrogen addition have been well studied, this is not so for the lower, chronic rates that characterize much of the globe. Here we present results of the first multi-decadal experiment to examine the impacts of chronic, experimental nitrogen addition as low as 10 kg N ha(-1) yr(-1) above ambient atmospheric nitrogen deposition (6 kg N ha(-1) yr(-1) at our site). This total input rate is comparable to terrestrial nitrogen deposition in many industrialized nations. We found that this chronic low-level nitrogen addition rate reduced plant species numbers by 17% relative to controls receiving ambient N deposition. Moreover, species numbers were reduced more per unit of added nitrogen at lower addition rates, suggesting that chronic but low-level nitrogen deposition may have a greater impact on diversity than previously thought. A second experiment showed that a decade after cessation of nitrogen addition, relative plant species number, although not species abundances, had recovered, demonstrating that some effects of nitrogen addition are reversible.

Abstract  Exacerbations of asthma have been associated with exposure to ozone or particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10). We postulated in this study that the association of summertime air pollution (i.e. ozone and PM10) with acute respiratory symptoms, medication use and peak expiratory flow differs among patients grouped according to asthma severity. During the summer of 1995, effects of ambient air pollution on these parameters were studied in a panel of 60 nonsmoking patients with intermittent to severe persistent asthma. These patients were recruited from our Pulmonary Out-patient Clinic. Subgroup analysis was performed on the degree of hyperresponsiveness and lung steroid use before the start of the study, as indictors for the severity of asthma. Associations of the parameters studied with ozone, PM10, nitrogen dioxide (NO2), sulphur dioxide (SO2) and black smoke were evaluated using time series analysis. Several episodes with increased summertime air pollution occurred during the 96 day study period. Eight hour average ozone concentrations exceeded the World Health Organization (WHO) Air Quality Guidelines (120 microg x m(-3)) on 16 occasions. Daily mean levels of PM10 were moderately elevated (range 16-98 microg x m(-3)). Levels of the other measured pollutants were low. There was a consistent, positive association of the prevalence of shortness of breath (maximal relative risk (RRmax) 1.18) with ozone, PM10, black smoke and NO2. In addition, bronchodilator use was associated with both ozone and PM10 levels (RRmax 1.16). Stratification by airway hyperresponsiveness and steroid use did not affect the magnitude of the observed associations. No associations with peak expiratory flow measurements were found. We conclude that the severity of asthma is not an indicator for the sensitivity to air pollution.

Abstract  As part of an EPA-sponsored workshop to investigate the use of source apportionment in health effects analyses, the associations between the participant's estimated source contributions of PM(2.5) for Phoenix, AZ for the period from 1995-1997 and cardiovascular and total nonaccidental mortality were analyzed using Poisson generalized linear models (GLM). The base model controlled for extreme temperatures, relative humidity, day of week, and time trends using natural spline smoothers. The same mortality model was applied to all of the apportionment results to provide a consistent comparison across source components and investigators/methods. Of the apportioned anthropogenic PM(2.5) source categories, secondary sulfate, traffic, and copper smelter-derived particles were most consistently associated with cardiovascular mortality. The sources with the largest cardiovascular mortality effect size were secondary sulfate (median estimate=16.0% per 5th-to-95th percentile increment at lag 0 day among eight investigators/methods) and traffic (median estimate=13.2% per 5th-to-95th percentile increment at lag 1 day among nine investigators/methods). For total mortality, the associations were weaker. Sea salt was also found to be associated with both total and cardiovascular mortality, but at 5 days lag. Fine particle soil and biomass burning factors were not associated with increased risks. Variations in the maximum effect lag varied by source category suggesting that past analyses considering only single lags of PM(2.5) may have underestimated health impact contributions at different lags. Further research is needed on the possibility that different PM(2.5) source components may have different effect lag structure. There was considerable consistency in the health effects results across source apportionments in their effect estimates and their lag structures. Variations in results across investigators/methods were small compared to the variations across source categories. These results indicate reproducibility of source apportionment results across investigative groups and support applicability of these methods to effects studies. However, future research will also need to investigate a number of other important issues including accuracy of results.

Abstract  Traffic- and urban-influenced areas are prone to enhanced pollution with products of incomplete combustion of fossil fuels and biomass such as black carbon or polycyclic aromatic hydrocarbons (PAHs). Black carbon is composed of aromatic and graphitic structures and may act as a carrier for pollutants such as PAHs and heavy metals. However, little is known about possible contributions of traffic-derived black carbon to the black carbon inventory in soils. Similar uncertainties exist regarding the contribution of different pollutant sources to total PAH and black carbon contents. Therefore, the objective of this study was to quantify the importance of traffic pollution to black carbon and PAH inventories in soils. PAH contamination of soils adjacent to a major German highway in the urban area of Bayreuth with about 50 000 vehicles per day was in the same order of magnitude compared to highway-close soils reported in other studies. Using molecular (black carbon and PAHs) and compound-specific stable carbon isotope evidence (PAHs) it was demonstrated that this contamination originated not only from automobile exhausts, here primarily diesel, but also from tire abrasion and tailpipe soot which significantly contributed to the traffic-caused black carbon and PAH contamination. Low molecular weight PAHs were more widely transported than their heavy molecular counterparts (local distillation), whereas highway-traffic-caused black carbon contamination was distributed to at least 30 m from the highway. On the other hand, urban fire exhausts were distributed more homogeneously among the urban area.

Abstract  Little is known about particulate elemental carbon (EC) personal exposure levels, a key component of diesel exhaust, specifically in transport microenvironments. A method utilizing the optical properties of EC particles has been applied to personal exposure measurement filter samples. In a series of field studies carried out in London, UK, during 19992000 over 400 fine particle (PM2.5) personal exposure level measurements were taken for journeys in bicycle, bus, car and underground rail transport microenvironments, along three main fixed routes. The particulate EC contribution to the PM2.5 personal exposure was assessed indirectly by means of an optical technique and with the development and use of a size fraction specific and site-specific calibration curve. In this first EC personal exposure study of transport users geometric mean exposure levels in the summer field campaign were 11.2 mug m(- 3) (GSD=2.7) for cyclists, 13.6 mug m(-3) (GSD = 1.9) for bus passengers and 21.6 mug m(-3) (GSD = 2. 1) for car drivers; corresponding exposure levels in the winter ;were 16.4 mug m(-3) (GSD= 1.8), 18.6 mug m(-3) (GSD=2.3) and 27.3 mug m(-3) (GSD=2.0), respectively. EC/PM2.5 ratios were approximately 0.5-0.6 for bicycle and bus modes and 0.7-0.8 for the car mode. EC/PM2.5 ratios for different routes ranged from approximately 0.7 for Route 1 to 0.4 for Route 3. Cyclists had the lowest exposure to EC, and car occupants the highest exposure. A large difference in exposure levels between a central high traffic density route and the other less central routes was observed. Particulate EC was a very significant proportion of the total PM2.5 personal exposure and EC personal exposure levels were considerably higher than reported fixed site monitor EC concentrations. (C) 2002 Elsevier Science Ltd. All rights reserved.

Abstract  In 2003, a bus strike paralyzed the fleet of buses in SÒo Paulo, Brazil during 3 days, from 6 to 8 of April, the complete interruption of services being achieved on the 7th. We evaluated the effect of the absence of this source of pollution on the composition, mutagenicity, and toxicity of the fine particulate material collected during this period. Particles were sampled in glass fiber filters on days 7 and 15 of April of 2003 (strike and nonstrike days, respectively), using a high-volume sampler. Trace element determinations (As, Br, Co, Cl, Fe, La, Mn, Sb, Sc, and Th) of particulate material samples were carried out by neutron activation analysis. Sulfur determination was done by X-ray fluorescence analysis. The ratio between nonstrike/strike concentrations of hydrocarbons associated with automotive emissions (benzene, toluene, ethyl-benzene, and xylenes; BTEX) was determined by gas chromatography/mass spectrometry. Mutagenesis of testing solutions was determined by means of the Tradescantia micronucleus assay in early tetrads of Tradescantia pallida. The inhibition of mitosis of the cells of the primary meristema of the root tips of Allium cepa was used as an index of the toxicity. Fine particle trace element contents were lower during the strike. The concentrations of sulfur and BTEX were 50% and 39.3% lower, respectively, on the strike day. A significant (P=0.038) reduction of micronuclei induced by fine particles sampled during the strike was observed. No effect of the strike on toxicity was detected. These results indicate that a program aiming to reduce emissions of the bus fleet in our town may impact positively the air quality by reducing the mutagenic potential of ambient particles.

Abstract  Environmental quality standards (EQSs) have been established as desirable levels to be maintained for protection of human health and the conservation of the living environment by Basic Environment Law. EQSs in ambient air had been set for 10 substances (sulfur dioxide (SO(2)), carbon monoxide (CO), suspended particulate matter (SPM), nitrogen dioxide (NO(2)) and photochemical oxidants (Ox), benzene, tetrachloroethylene, trichloroethylene, dioxins and dichloromethane) and guideline values for 7 (acrylonitorile, vinyl chloride monomer, mercury, nickel compounds, 1,3-butadiene, chloroform and 1,2-dichloromethane) in Japan by 2009. EQSs for the classical (or traditional) air pollutants, SO(2), CO, SPM, NO(2) and Ox, were set according to the minimal requirement to protect human health, based on evidence from epidemiological studies conducted before the 1970s. In 1996, the Central Environment Council designated substances which may be hazardous air pollutants and substances requiring priority action, and adopted the concept of risk assessment to set EQSs and guideline values. A life-long risk level (virtually safe dose) of 10(-5) was used to set EQS for benzene, and guideline values for vinyl chloride monomer, nickel compounds, and 1,3-butadiene. EQSs for trichloroethylene, tetrachloroethylene and dichloromethane, and guideline values for acrylonitorile and mercury were set using uncertain factors and lowest observed adverse effect (LOAEL)/no observed adverse effect level (NOAEL). The results of animal experiments were utilized to set guideline values for chloroform and 1,2-dichloroethane. The benchmark approach and human equivalent concentration (HEC) were adopted for 1,2-dichloroethane. The history of setting EQSs and guideline values for hazardous air pollutants is one of adopting new concepts into risk assessment.

Abstract  The impact of air pollution on asthma in children in different age group has not been well defined. Objective: This study aimed to evaluate the association between seasonal variations in air pollution and asthma hospitalization of children within a two-year period.

Using the National Health Insurance database, seasonal variations in hospitalization trends in children with a primary diagnosis of asthma (International Classification of Disease 9th revision, code 493) for patients aged < 18 years from 2001 to 2002 were investigated. Data on the average concentration of nitrogen dioxide (NO(2)), carbon monoxide (CO), ozone(O(3)), sulphur dioxide (SO(2)), and particles with aerodynamic diameter < 10 microm (PM(10)) for each month were obtained from the Environmental Protection Department through 71 stations of air quality monitor distributed nationwide. PSI value (pollutants standard index)> 100 was considered poor air quality. Seasonal variations in asthma admissions were compared to the air pollution quality data using Spearman's rank correlation.

Asthma hospitalization was not related to the number of days when the PSI was > 100 during the 24-months period (r = -0.361; p = 0.083). However, it was significantly associated with seasonal changes in the concentration of each pollutant. The most strongly related air pollutant variable was PM(10) (standardized coefficients 0.384), followed by 0(3) (standardized coefficients 0.255) and SO(2) (standardized coefficients 0.162) concentrations. The association of seasonal changes in asthma hospitalization with these pollutants was greater in pre-school and school age children. Temperature and rainfall in all seasons were not related to asthma hospitalization. None of the pollutants were associated with seasonal variations in admission rate for adolescents.

Seasonal variations of asthma hospitalization among preschool children are associated with concentration of air pollutants.

Abstract  Traffic-related particulate matter (PM) may play an important role in the development of adverse health effects, as documented extensively in acute toxicity studies. However, rather little is known about the impacts of prolonged exposure to PM. We hypothesized that long-term exposure to PM from traffic adversely affects the pulmonary and cardiovascular system through exacerbation of an inflammatory response. To examine this hypothesis, Fisher F344 rats, with a mild pulmonary inflammation at the onset of exposure, were exposed for 4 weeks, 5 days/week for 6 h a day to: (a) diluted diesel engine exhaust (PM(DEE)), or: (b) near roadside PM (PM(2.5)). Ultrafine particulates, which are largely present in diesel soot, may enter the systemic circulation and directly or indirectly trigger cardiovascular effects. Hence, we assessed the effects of traffic-related PM on pulmonary inflammation and activity of procoagulants, vascular function in arteries, and cytokine levels in the heart 24 h after termination of the exposures. No major adverse health effects of prolonged exposure to traffic-related PM were detected. However, some systemic effects due to PM(DEE) exposure occurred including decreased numbers of white blood cells and reduced von Willebrand factor protein in the circulation. In addition, lung tissue factor activity is reduced in conjunction with reduced lung tissue thrombin generation. To what extent these alterations contribute to thrombotic effects and vascular diseases remains to be established. In conclusion, prolonged exposure to traffic-related PM in healthy animals may not be detrimental due to various biological adaptive response mechanisms.

Abstract  BACKGROUND: Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes. OBJECTIVES: To identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making. METHODS: This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles (aerodynamic diameter ≤2.5 µm; PM2.5), NO2, and NO were estimated at subjects' residences using land use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records. RESULTS: An interquartile range elevation in the average concentration of black carbon (0.94×10-5/m filter absorbance, equivalent to approximately 0.75 µg/m3 elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1-5%) and a 6% increase in CHD mortality (3-9%) after adjustment for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and co-pollutants (PM2.5 and NO2). There were clear linear exposure-response relationships between black carbon and coronary events. CONCLUSIONS: Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.

Abstract  Following the meteorological evaluation in Part I, this Part II paper presents the statistical evaluation of air quality predictions by the U.S. Environmental Protection Agency (U.S. EPA)'s Community Multi-Scale Air Quality (Models-3/CMAQ) model for the four simulated months in the base year 2005. The surface predictions were evaluated using the Air Pollution Index (API) data published by the China Ministry of Environmental Protection (MEP) for 31 capital cities and daily fine particulate matter (PM(2.5), particles with aerodiameter less than or equal to 2.5 mu m) observations of an individual site in Tsinghua University (THU). To overcome the shortage in surface observations, satellite data are used to assess the column predictions including tropospheric nitrogen dioxide (NO(2)) column abundance and aerosol optical depth (AOD). The result shows that CMAQ gives reasonably good predictions for the air quality. The air quality improvement that would result from the targeted sulfur dioxide (SO(2)) and nitrogen oxides (NO(x)) emission controls in China were assessed for the objective year 2010. The results show that the emission controls can lead to significant air quality benefits. SO(2) concentrations in highly polluted areas of East China in 2010 are estimated to be decreased by 30-60% compared to the levels in the 2010 Business-As-Usual (BAU) case. The annual PM(2.5) can also decline by 3-15 mu g m(-3) (4-25%) due to the lower SO(2) and sulfate concentrations. If similar controls are implemented for NO(x) emissions, NO(x) concentrations are estimated to decrease by 30-60% as compared with the 2010 BAU scenario. The annual mean PM(2.5) concentrations will also decline by 2-14 mu g m(-3) (3-12%). In addition, the number of ozone (O(3)) non-attainment areas in the northern China is projected to be much lower, with the maximum 1-h average O(3) concentrations in the summer reduced by 8-30 ppb. (C) 2010 Elsevier Ltd. All rights reserved.

Abstract  An impact related daily air quality index (DAQx), calculated for 15 air quality monitoring stations (traffic, background, and industry) in Belgium, France, Germany and Luxembourg, was compared to mesoscale atmospheric patterns between 2001 and 2007. Meteorological conditions were described by the Hess and Brezowsky synoptic weather classification system and gridded data of the EU FP6 ENSEMBLES project of total precipitation and mean surface temperature. DAQx values indicate sufficient to poor air quality in the urban area of Brussels and at urban traffic stations, as well as satisfactory air quality at the background stations. The air quality index refers to more than 90% to the presence of high PM10, O-3 and NO2 concentrations. SO2 and CO play only a minor role. The investigation of weather regimes indicates that zonal and mixed cyclonic circulation regimes are associated with better air quality than meridional and anticyclonic weather regimes. In general, weather regimes with high daily precipitation lead to better air quality than dryer air masses because of lower contribution of PM10 to the air quality index. A trend analysis of weather regimes from 1978 to 2007 shows significant (alpha = 0.05) positive trends for weather classes associated with lower PM10 concentrations. The results of a case study at a German station examining the relationship between PM10 concentrations and local meteorological quantities (wind speed and precipitation) confirm the results of the regional analysis. (C) 2010 Elsevier Ltd. All rights reserved.

Abstract  Examining global effects of toxic metals on gene expression can be useful for elucidating patterns of biological response, discovering underlying mechanisms of toxicity, and identifying candidate metal-specific genetic markers of exposure and response. Using a 1,200 gene nylon array, we examined changes in gene expression following low-dose, acute exposures of cadmium, chromium, arsenic, nickel, or mitomycin C (MMC) in BEAS-2B human bronchial epithelial cells. Total RNA was isolated from cells exposed to 3 M Cd(II) (as cadmium chloride), 10 M Cr(VI) (as sodium dichromate), 3 g/cm2 Ni(II) (as nickel subsulfide), 5 M or 50 M As(III) (as sodium arsenite), or 1 M MMC for 4 hr. Expression changes were verified at the protein level for several genes. Only a small subset of genes was differentially expressed in response to each agent: Cd, Cr, Ni, As (5 M), As (50 M), and MMC each differentially altered the expression of 25, 44, 31, 110, 65, and 16 individual genes, respectively. Few genes were commonly expressed among the various treatments. Only one gene was altered in response to all four metals (hsp90), and no gene overlapped among all five treatments. We also compared low-dose (5 M, noncytotoxic) and high-dose (50 M, cytotoxic) arsenic treatments, which surprisingly, affected expression of almost completely nonoverlapping subsets of genes, suggesting a threshold switch from a survival-based biological response at low doses to a death response at high doses.