Effects Of Particulate Air Pollution Research Articles

Investigating the geographical heterogeneity in PM10-mortality associations in the China Air Pollution and Health Effects Study (CAPES): A potential role of indoor exposure to PM10 of outdoor origin

This study gives the first-time evidence for China that the geographical heterogeneity of the acute effects of outdoor PM10 can be partially explained by differences in indoor exposure to PM10 of outdoor origin. We used data from the China Air Pollution and Health Effects Study (CAPES), which demonstrated a geographical heterogeneity of the acute effect of particulate air pollution (particulate matter with an aerodynamic diameter smaller than 10 μm, or PM10) on mortality in 16 Chinese cities. Given that a large fraction of the exposure to PM10 of outdoor origin occurs indoors, we made the hypothesis that this heterogeneity might be partially explained by inter-city differences in indoor exposure to PM10 of outdoor origin. In our analysis, we estimated PM10 exposure coefficients (the change in the estimated personal exposure to PM10 of outdoor origin per unit change in outdoor PM10 concentration) in these 16 Chinese cities and examined their correlation with PM10 mortality coefficients (the increase in mortality associated with a given increase in the concentrations of outdoor PM10). We showed that the PM10 mortality coefficients and the PM10 exposure coefficients were significantly correlated, with an R-squared (R2) value of 0.549 (95% confidence interval: 0.201, 0.771; p < 0.01) for the 16 cities. The correlation was robust with different values of the key input parameters, and close in value to estimations found in previous studies on similar subjects.

Seasonal variation in the acute effect of particulate air pollution on mortality in the China Air Pollution and Health Effects Study (CAPES)

Epidemiological findings concerning the seasonal variation in the acute effect of particulate matter (PM) are inconsistent. We investigated the seasonality in the association between PM with an aerodynamic diameter of less than 10μm (PM10) and daily mortality in 17 Chinese cities. We fitted the “main” time-series model after adjustment for time-varying confounders using smooth functions with natural splines. We established a “seasonal” model to obtain the season-specific effect estimates of PM10, and a “harmonic” model to show the seasonal pattern that allows PM10 effects to vary smoothly with the day in a year. At the national level, a 10μg/m3 increase in the two-day moving average concentrations (lag 01) of PM10 was associated with 0.45% [95% posterior interval (PI), 0.15% to 0.76%], 0.17% (95% PI, −0.09% to 0.43%), 0.55% (95% PI, 0.15% to 0.96%) and 0.25% (95%PI, −0.05% to 0.56%) increases in total mortality for winter, spring, summer and fall, respectively. For the smoothly-varying plots of seasonality, we identified a two-peak pattern in winter and summer. The observed seasonal pattern was generally insensitive to model specifications. Our analyses suggest that the acute effect of particulate air pollution could vary by seasons with the largest effect in winter and summer in China. To our knowledge, this is the first multicity study in developing countries to analyze the seasonal variations of PM-related health effects.

Air pollution in pristina, influence on cardiovascular hospital morbidity.

ABSTRACTIntroduction:Numerous studies observed health effects of particulate air pollution. Ambient air quality is particularly bad in Pristina. The principal sources of contaminants are sulfur dioxide (SO2), nitrogen oxides NO and NO2 (NOx), ozone (O3), lead (Pb), carbon dioxide (CO2), particulate matter (PM or dust).Objective:to investigate effects of concentrations of pollutants in ambient air on hospital admissions for cardiovascular disease in UCCK- Pristina.Methods:Retrospective ecological study. During the three year analytical research predict the potential benefit of decreasing for concentration of PM 2.5, PM 10 were measured in two station in Pristina. The study population consisted of all hospitalization patient in intern clinic for 2010,2011 and 2012 year. Air pollution measurements will be used by KHMI data for the year of 2010, 2011 and 2012 for the municipality ofPristina in the measurements point in:KHMI-MESP which is equipped with automatic analyzer- Air Compact Monitoring System (Version 2.2) recordum MESSTECHNIK GmbH. Statistical data processing will be done with SPSS 17.0 statistical package.Results:Based on the results obtained during the study period concentrated PM are higher level than standards value. The results showed that the number of hospital admissions for cardiovascular disease are positively correlated with concentration pollutants. Results show clear seasonal variation in the effects of PM on hospital admissions in Kosovo. The study period was short but the mean daily admissions for cardiovascular illnesses were quite large.Conclusion:The main source for air pollution was coal-burned power plant and traffic (old vehicles) in Kosovo.

Elemental concentrations of ambient particles and cause specific mortality in Santiago, Chile: a time series study

BackgroundThe health effects of particulate air pollution are widely recognized and there is some evidence that the magnitude of these effects vary by particle component. We studied the effects of ambient fine particles (aerodynamic diameter < 2.5μm, PM2.5) and their components on cause-specific mortality in Santiago, Chile, where particulate pollution is a major public health concern.MethodsAir pollution was collected in a residential area in the center of Santiago. Daily mortality counts were obtained from the National Institute of Statistic. The associations between PM2.5 and cause-specific mortality were studied by time series analysis controlling for time trends, day of the week, temperature and relative humidity. We then included an interaction term between PM2.5 and the monthly averages of the mean ratios of individual elements to PM2.5 mass.ResultsWe found significant effects of PM2.5 on all the causes analyzed, with a 1.33% increase (95% CI: 0.87-1.78) in cardiovascular mortality per 10μg/m3 increase in the two days average of PM2.5. We found that zinc was associated with higher cardiovascular mortality. Particles with high content of chromium, copper and sulfur showed stronger associations with respiratory and COPD mortality, while high zinc and sodium content of PM2.5 amplified the association with cerebrovascular disease.ConclusionsOur findings suggest that PM2.5 with high zinc, chromium, copper, sodium, and sulfur content have stronger associations with mortality than PM2.5 mass alone in Santiago, Chile. The sources of particles containing these elements need to be determined to better control their emissions.

Temperature modifies the acute effect of particulate air pollution on mortality in eight Chinese cities

BackgroundBoth temperature and particulate air pollution are associated with increased death risk. However, whether the effect of particulate air pollution on mortality is modified by temperature remains unsettled. MethodsA stratified time-series analysis was conducted to examine whether the effects of particulate matter less than 10μm in aerodynamic diameter (PM10) on mortality was modified by temperature in eight Chinese cities. Poisson regression models incorporating natural spline smoothing functions were used to adjust for long-term and seasonal trends of mortality, as well as other time-varying covariates. The bivariate response surface model was applied to visually examine the potential interacting effect. The associations between PM10 and mortality were stratified by temperature to examine effect modification. ResultsThe averaged daily concentrations of PM10 in the eight Chinese cities ranged from 65μg/m3 to 124μg/m3, which were much higher than in Western countries. We found evidence that the effects of PM10 on mortality may depend on temperature. The eight-city combined analysis showed that on “normal” (5th–95th percentile) temperature days, a 10-μg/m3 increment in PM10 corresponded to a 0.54% (95% CI, 0.39 to 0.69) increase of total mortality, 0.56% (95% CI, 0.36 to 0.76) increase of cardiovascular mortality, and 0.80% (95% CI, 0.64 to 0.96) increase of respiratory mortality. On high temperature (>95th percentile) days, the estimates increased to 1.35% (95% CI, 0.80 to 1.91) for total mortality, 1.57% (95% CI, 0.69 to 2.46) for cardiovascular mortality, and 1.79% (95% CI, 0.75 to 2.83) for respiratory mortality. We did not observe significant effect modification by extreme low temperature. ConclusionsExtreme high temperature increased the associations of PM10 with daily mortality. These findings may have implication for the health impact associated with both air pollution and global climate change.

Seasonal influences on CAPs exposures: differential responses in platelet activation, serum cytokines and xenobiotic gene expression

Increasing evidence suggests a role for a systemic pro-coagulant state in the pathogenesis of cardiac dysfunction subsequent to inhalation of airborne particulate matter (PM). We evaluated platelet activation, systemic cytokines and pulmonary gene expression in mice exposed to concentrated ambient particulate matter (CAPs) in the summer of 2008 (S08) and winter of 2009 (W09) from the San Joaquin Valley of California, a region with severe PM pollution episodes. Additionally, we characterized the PM from both exposures including organic compounds, metals, and polycyclic aromatic hydrocarbons. Mice were exposed to an average of 39.01 μg/m3 of CAPs in the winter and 21.7 μg/m3 CAPs in the summer, in a size range less than 2.5 μm for 6 h/day for 5 days per week for 2 weeks. Platelets were analyzed by flow cytometry for relative size, shape, CD41, P-selectin and lysosomal associated membrane protein-1 (LAMP-1) expression. Platelets from W09 CAPs-exposed animals had a greater response to thrombin stimulation than platelets from S08 CAPs-exposed animals. Serum cytokines were analyzed by bead based immunologic assays. W09 CAPs-exposed mice had elevations in IL-2, MIP-1α, and TNFα. Laser capture microdissection (LCM) of pulmonary vasculature, parenchyma and airways all showed increases in CYP1a1 gene expression. Pulmonary vasculature showed increased expression of ICAM-1 and Nox-2. Our findings demonstrate that W09 CAPs exposure generated a greater systemic pro-inflammatory and pro-coagulant response to inhalation of environmentally derived fine and ultrafine PM. Changes in platelet responsiveness to agonists, seen in both exposures, strongly suggests a role for platelet activation in the cardiovascular and respiratory effects of particulate air pollution.

Low-level exposure to ambient particulate matter is associated with systemic inflammation in ischemic heart disease patients

Short-term exposure to ambient air pollution is associated with increased cardiovascular mortality and morbidity. This adverse health effect is suggested to be mediated by inflammatory processes. The purpose of this study was to determine if low levels of particulate matter, typical for smaller cities, are associated with acute systemic inflammation.Fifty-two elderly individuals with ischemic heart disease were followed for six months with biweekly clinical visits in the city of Kotka, Finland. Blood samples were collected for the determination of inflammatory markers interleukin (IL)-1β, IL-6, IL-8, IL-12, interferon (IFN)γ, C-reactive protein (CRP), fibrinogen, myeloperoxidase and white blood cell count. Particle number concentration and fine particle (particles with aerodynamic diameters <2.5μm (PM2.5)) as well as thoracic particle (particles with aerodynamic diameters <10μm (PM10)) mass concentration were measured daily at a fixed outdoor measurement site. Light-absorbance of PM2.5 filter samples, an indicator of combustion derived particles, was measured with a smoke-stain reflectometer. In addition, personal exposure to PM2.5 was measured with portable photometers. During the study period, wildfires in Eastern Europe led to a 12-day air pollution episode, which was excluded from the main analyses.Average ambient PM2.5 concentration was 8.7μg/m3. Of the studied pollutants, PM2.5 and absorbance were most strongly associated with increased levels of inflammatory markers; most notably with C-reactive protein and IL-12 within a few days of exposure. There was also some evidence of an effect of particulate air pollution on fibrinogen and myeloperoxidase. The concentration of IL-12 was considerably (227%) higher during than before the forest fire episode. These findings show that even low levels of particulate air pollution from urban sources are associated with acute systemic inflammation. Also particles from wildfires may exhibit pro-inflammatory effects.

Effects of Particulate Air Pollution on Cardiovascular Health: A Population Health Risk Assessment

Particulate matter (PM) air pollution is increasingly recognized as an important and modifiable risk factor for adverse health outcomes including cardiovascular disease (CVD). However, there are still gaps regarding large population risk assessment. Results from the nationwide Behavioral Risk Factor Surveillance System (BRFSS) were used along with air quality monitoring measurements to implement a systematic evaluation of PM-related CVD risks at the national and regional scales. CVD status and individual-level risk factors were collected from more than 500,000 BRFSS respondents across 2,231 contiguous U.S. counties for 2007 and 2009. Chronic exposures to PM pollutants were estimated with spatial modeling from measurement data. CVD outcomes attributable to PM pollutants were assessed by mixed-effects logistic regression and latent class regression (LCR), with adjustment for multicausality. There were positive associations between CVD and PM after accounting for competing risk factors: the multivariable-adjusted odds for the multiplicity of CVD outcomes increased by 1.32 (95% confidence interval: 1.23–1.43) and 1.15 (1.07–1.22) times per 10 µg/m3 increase in PM2.5 and PM10 respectively in the LCR analyses. After controlling for spatial confounding, there were moderate estimated effects of PM exposure on multiple cardiovascular manifestations. These results suggest that chronic exposures to ambient particulates are important environmental risk factors for cardiovascular morbidity.

Short-term health effects of particulate air pollution with special reference to the needs of southern European countries

Exposure to air pollution, especially from particulate matter, is generally accepted to be one of the most important public health problems in Europe and worldwide. The effects caused in the general population are associated with relatively small relative risks, but if the ubiquity of exposure is considered, the attributable number of events is large. Furthermore, there is evidence that the effects in sensitive population subgroups (such as the elderly, those with chronic diseases and children) are stronger. Within large European Union funded collaborative projects (such as the Air Pollution and Health: a European Approach-APHEA), effect modification by geographical characteristics has been investigated and it was found that in warmer countries, in locations where particles come from traffic and where the proportion of the elderly is greater, particle toxicity is increased. These characteristics are particularly relevant to Southern European locations. From other projects we know that meteorological, climatic, environmental and socioeconomic factors are effect modifiers of the effects of specific air pollutants. In this presentation we will show the evidence on the short-term health effects of particulate and gaseous air pollutants and emphasize particularly results concerning southern Europe and potential effect modifiers. The gaps in knowledge and the need to study air pollution in Southern European countries more extensively will be demonstrated. To conduct useful research, good quality air pollution and health data are needed.

Effects of particulate air pollution on blood pressure in a highly exposed population in Beijing, China: a repeated-measure study

BackgroundParticulate Matter (PM) exposure is critical in Beijing due to high population density and rapid increase in vehicular traffic. PM effects on blood pressure (BP) have been investigated as a mechanism mediating cardiovascular risks, but results are still inconsistent. The purpose of our study is to determine the effects of ambient and personal PM exposure on BP.MethodsBefore the 2008 Olympic Games (June 15-July 27), we examined 60 truck drivers and 60 office workers on two days, 1-2 weeks apart (n = 240). We obtained standardized measures of post-work BP. Exposure assessment included personal PM2.5 and Elemental Carbon (EC, a tracer of traffic particles) measured using portable monitors during work hours; and ambient PM10 averaged over 1-8 days pre-examination. We examined associations of exposures (exposure group, personal PM2.5/EC, ambient PM10) with BP controlling for multiple covariates.ResultsMean personal PM2.5 was 94.6 μg/m3 (SD = 64.9) in office workers and 126.8 (SD = 68.8) in truck drivers (p-value < 0.001). In all participants combined, a 10 μg/m3 increase in 8-day ambient PM10 was associated with BP increments of 0.98 (95%CI 0.34; 1.61; p-value = 0.003), 0.71 (95%CI 0.18; 1.24; p-value = 0.01), and 0.81 (95%CI 0.31; 1.30; p-value = 0.002) mmHg for systolic, diastolic, and mean BP, respectively. BP was not significantly different between the two groups (p-value > 0.14). Personal PM2.5 and EC during work hours were not associated with increased BP.ConclusionsOur results indicate delayed effects of ambient PM10 on BP. Lack of associations with exposure groups and personal PM2.5/EC indicates that PM effects are related to background levels of pollution in Beijing, and not specifically to work-related exposure.

Comparative gene responses to collected ambient particles in vitro: endothelial responses

Epidemiologic studies associate exposure to ambient particulate matter (APM) with increased cardiovascular mortality. Since both pulmonary inflammation and systemic circulation of ultrafine particles are hypothesized as initiating cardiovascular effects, we examined responses of potential target cells in vitro. Human aortic endothelial cells (HAEC) were exposed to 10 μg/ml fine and ultrafine APM collected in an urban setting in summer 2006 or winter 2007 in the San Joaquin Valley, California. RNA isolated after 3 h was analyzed with high-density oligonucleotide arrays. Summer APM treatment affected genes involved in xenobiotic and oxidoreductase activity, transcription factors, and inflammatory responses in HAEC, while winter APM had a robust xenobiotic but lesser inflammatory response. Real-time polymerase chain reaction analysis confirmed that particulate matter (PM)-treated HAEC increased mRNA levels of xenobiotic response enzymes CYP1A1, ALDH1A3, and TIPARP and cellular stress response transcription factor ATF3. Inflammatory response genes included E-selectin, PTGS2, CXCL-2 (MIP-2α), and CCL-2 (MCP-1). Multiplex protein assays showed secretion of IL-6 and MCP-1 by HAEC. Since induction of CYP1A1 is mediated through the ligand-activated aryl hydrocarbon receptor (AhR), we demonstrated APM induced AhR nuclear translocation by immunofluorescence and Western blotting and activation of the AhR response element using a luciferase reporter construct. Inhibitor studies suggest differential influences of polycyclic aromatic hydrocarbon signaling, ROS-mediated responses and endotoxin alter stress and proinflammatory endothelial cell responses. Our findings demonstrate gene responses correlated with current concepts that systemic inflammation drives cardiovascular effects of particulate air pollution. We also demonstrate a unique pattern of gene responses related to xenobiotic metabolism in PM-exposed HAEC.

Comparative evaluation of the effects of short-term inhalation exposure to diesel engine exhaust on rat lung and brain

Combustion-derived nanoparticles, such as diesel engine exhaust particles, have been implicated in the adverse health effects of particulate air pollution. Recent studies suggest that inhaled nanoparticles may also reach and/or affect the brain. The aim of our study was to comparatively evaluate the effects of short-term diesel engine exhaust (DEE) inhalation exposure on rat brain and lung. After 4 or 18 h recovery from a 2 h nose-only exposure to DEE (1.9 mg/m3), the mRNA expressions of heme oxygenase-1 (HO-1), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and cytochrome P450 1A1 (CYP1A1) were investigated in lung as well as in pituitary gland, hypothalamus, olfactory bulb, olfactory tubercles, cerebral cortex, and cerebellum. HO-1 protein expression in brain was investigated by immunohistochemistry and ELISA. In the lung, 4 h post-exposure, CYP1A1 and iNOS mRNA levels were increased, while 18 h post-exposure HO-1 was increased. In the pituitary at 4 h post-exposure, both CYP1A1 and HO-1 were increased; HO-1 was also elevated in the olfactory tuberculum at this time point. At 18 h post-exposure, increased expression of HO-1 and COX-2 was observed in cerebral cortex and cerebellum, respectively. Induction of HO-1 protein was not observed after DEE exposure. Bronchoalveolar lavage analysis of inflammatory cell influx, TNF-α, and IL-6 indicated that the mRNA expression changes occurred in the absence of lung inflammation. Our study shows that a single, short-term inhalation exposure to DEE triggers region-specific gene expression changes in rat brain to an extent comparable to those observed in the lung.

Exposure of mice to concentrated ambient particulate matter results in platelet and systemic cytokine activation

Increasingly, evidence suggests a role for a systemic procoagulant state in the pathogenesis of cardiac dysfunction subsequent to inhalation of airborne particulate matter. The authors evaluated blood cell parameters and markers of platelet activation in mice exposed to concentrated ambient particulate matter (CAPs) from the San Joaquin Valley of California, a region with severe particulate matter (PM) pollution episodes. The authors exposed mice to an average of 88.5 μg/m3 of CAPs in a size range less than 2.5 μm for 6 h/day for 5 days per week for 2 weeks. Platelets were analyzed by flow cytometry for relative size, shape, aggregation, fibrinogen binding, P-selectin, and lysosomal-associated membrane protein-1 (LAMP-1) expression. Serum cytokines were analyzed by bead-based immunologic assays. CAPs-exposed mice had elevations in macrophage inflammatory protein (MIP)-1α, MIP-1β, interleukin (IL)-6, IL-10, tumor necrosis factor alpha (TNFα), macrophage colony-stimulating factor (M-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), platelet-derived growth factor (PDGF)-bb, and RANTES (regulated upon activation, normally T-expressed, and presumably secreted). Platelets were the only peripheral blood cells that were significantly elevated in number in CAPs-exposed mice. Flow cytometric analysis of unstimulated platelets from CAPs-exposed mice indicated size and shape changes, and platelets from CAPs-exposed animals had a 54% increase in fibrinogen binding indicative of platelet priming. Stimulation of platelets by thrombin resulted in up-regulation of LAMP-1 expression in CAPs-exposed animals and an increased microparticle population relative to control animals. These findings demonstrate a systemic proinflammatory and procoagulant response to inhalation of environmentally derived fine and ultrafine PM and suggests a role for platelet activation in the cardiovascular and respiratory effects of particulate air pollution.

Diabetes Mellitus Modifies the Association Between Particulate Air Pollution and Acute Ischemic Stroke: Results from the Registry of the Canadian Stroke Network

ISEE-0529 Background and Objective: Previous studies have reported an association between short-term exposure to ambient fine particulate matter (PM2.5) and the risk of hospitalization for ischemic stroke. Patients with diabetes mellitus have been shown to have enhanced sensitivity to the vascular effects of ambient particles and thus may be at increased risk of ischemic stroke, but this hypothesis has not been previously evaluated. Methods: We analyzed data from 8882 patients hospitalized between 2003 and 2008 with acute ischemic stroke, having a documented date and time of stroke symptom onset, and residing ≤50 km from a PM2.5 monitor in one of 8 major metropolitan regions in Ontario, Canada. All patients were admitted to a Regional Stroke Center participating in the Registry of the Canadian Stroke Network. We applied the time-stratified case-crossover design to estimate the effect of mean PM2.5 in each city 0–47 hr prior to time of stroke symptom onset, controlling for meteorological variables, and used random-effects meta-analytic techniques to combine the city-specific estimates. Separate analyses were performed according to the presence or absence of a history of diabetes mellitus, atrial fibrillation, and hypertension. Results: Overall, there was no consistent association between PM2.5 levels and risk of ischemic stroke 0–47 hr later. However, we found significant effect modification by diabetes mellitus (P = 0.033). Among patients with diabetes we observed a 9.5% (95% CI: −0.1%, 20.1%; P = 0.052) increased risk of ischemic stroke per 10 μg/m3 increase in PM2.5. We did not find evidence of statistically significant effect modification by a history of hypertension (P = 0.82) or atrial fibrillation (P = 0.73). Conclusion: Patients with diabetes mellitus may be especially susceptible to the cerebrovascular effects of particulate air pollution. This observation is consistent with prior studies suggesting that patients with diabetes may be at greater risk of particulate-related cardiac events.

Particulate Air Pollution and Cardiovascular Risk: Short-term and Long-term Effects

It is well known that exposure to particulate air pollutants is associated with the development of adverse health effects. In particular, there is growing evidence of a close relationship between increased levels of environmental pollutants and cardiovascular disease. Particle exposure may trigger acute cardiac events as well as promote the chronic development of cardiovascular disorders. Several biological mechanisms have been suggested to explain the important effect of air pollution on cardiovascular morbidity and mortality, although the exact pathways are not fully understood. The literature data on the short-term and long-term cardiovascular effects of particulate air pollutants are discussed in this review from a clinical and mechanistic point of view.

Adverse Health Effects of Particulate Air Pollution

The short-term effects of particulate matter (PM) on mortality and morbidity differ by geographic location and season. Several hypotheses have been proposed for this variation, including different exposures with air conditioning (AC) versus open windows. Bayesian hierarchical modeling was used to explore whether AC prevalence modified day-to-day associations between PM10 and mortality, and between PM2.5 and cardiovascular or respiratory hospitalizations, for those 65 years and older. We considered yearly, summer-only, and winter-only effect estimates and 2 types of AC (central and window units). Communities with higher AC prevalence had lower PM effects. Associations were observed for cardiovascular hospitalizations and central AC. Each additional 20% of households with central AC was associated with a 43% decrease in PM2.5 effects on cardiovascular hospitalization. Central AC prevalence explained 17% of between-community variability in PM2.5 effect estimates for cardiovascular hospitalizations. Higher AC prevalence was associated with lower health effect estimates for PM.

Health Effects of Particulate Air Pollution

In the 1980's it was generally felt that particulate air pollution concentrations in the United States were not a hazard to the public health. However, in the early 1990's the application of econometric time-series studies and prospective cohort studies suggested increased mortality associated with acute (daily) and chronic (decades) exposures to particulate air pollution commonly observed in the developed world. The epidemiologic evidence was not supported by evidence of causal associations from other disciplines. Nevertheless, the EPA moved to tighten controls on fine particulate air pollution. The debate over the science was played out in public hearings and the courts. The experience provides lessons on the use of epidemiologic data in setting public policy.

Direct Impairment of Vascular Function by Diesel Exhaust Particulate through Reduced Bioavailability of Endothelium-Derived Nitric Oxide Induced by Superoxide Free Radicals

BackgroundDiesel exhaust particulate (DEP) is a key arbiter of the adverse cardiovascular effects of air pollution.ObjectivesWe assessed the in vitro effects of DEP on vascular function, nitric oxide (NO) availability, and the generation of oxygen-centered free radicals.MethodsWe assessed the direct vascular effects of DEP (10–100 μg/mL) in isolated rat aortic rings using myography. We investigated NO scavenging and oxygen-centered free radical generation using an NO electrode and electron paramagnetic resonance (EPR) with the Tempone-H (1-hydroxyl-2,2,6,6-tetramethyl-4-oxo-piperidine) spin trap, respectively.ResultsAcetylcholine-induced relaxation was attenuated by DEP (maximum relaxation reduced from 91 ± 4% to 49 ± 6% with 100 μg/mL DEP; p < 0.001) but was restored by superoxide dismutase (SOD; maximum relaxation, 73 ± 6%; p < 0.001). DEP caused a modest inhibition of relaxation to NO donor drugs, an effect that could be reversed by SOD (p < 0.01). At 10 μg/mL, DEP did not affect verapamil-induced relaxation (p = 0.73), but at 100 μg/mL DEP inhibited relaxation (p < 0.001) by a mechanism independent of SOD. NO concentrations generated by 2-(N,N-diethylamino)-diazenolate-2-oxide (DEA/NO; 10 μM) were reduced by DEP (100 μg/mL; from 5.2 ± 0.4 to 3.3 ± 0.4 μM; p = 0.002). Free radical generation was increased by DEP (10 μg/mL; 9-fold increase in EPR spectra; p = 0.004) in a manner that could be attenuated by SOD (p = 0.015).ConclusionsDEP caused oxidative stress through the generation of oxygen-centered free radicals that reduced the bioavailability of endothelium-derived NO without prior interaction with the lung or vascular tissue. These findings provide a mechanism for the adverse cardiovascular effects of particulate air pollution.

The effect of ambient air pollution on respiratory health of school children: a panel study

BackgroundAdverse respiratory effects of particulate air pollution have been identified by epidemiological studies. We aimed to examine the health effects of ambient particulate air pollution from wood burning on school-age students in Christchurch, New Zealand, and to explore the utility of urine and exhaled breath condensate biomarkers of exposure in this population.MethodsA panel study of 93 male students (26 with asthma) living in the boarding house of a metropolitan school was undertaken in the winter of 2004. Indoor and outdoor pollution data was continuously monitored. Longitudinal assessment of lung function (FEV1 and peak flow) and symptoms were undertaken, with event studies of high pollution on biomarkers of exposure (urinary 1-hydroxypyrene) and effect (exhaled breath condensate (EBC) pH and hydrogen peroxide concentration).ResultsPeak levels of air pollution were associated with small but statistically significant effects on lung function in the asthmatic students, but not healthy students. No significant effect of pollution could be seen either on airway inflammation and oxidative stress either in healthy students or students with asthma. Minor increases in respiratory symptoms were associated with high pollution exposure. Urinary 1-hydroxypyrene levels were raised in association with pollution events by comparison with low pollution control days.ConclusionThere is no significant effect of ambient wood-smoke particulate air pollution on lung function of healthy school-aged students, but a small effect on respiratory symptoms. Asthmatic students show small effects of peak pollution levels on lung function. Urinary 1-hydroxypyrene shows potential as a biomarker of exposure to wood smoke in this population; however measurement of EBC pH and hydrogen peroxide appears not to be useful for assessment of population health effects of air pollution.Some of the data presented in this paper has previously been published in Kingham and co-workers Atmospheric Environment, 2006 Jan; 40: 338–347 (details of pollution exposure), and Cavanagh and co-workers Sci Total Environ. 2007 Mar 1;374(1):51-9 (urine hydroxypyrene data).

Potential Health Risks of Air Pollution Beyond Triggering Acute Cardiopulmonary Events

Andrea Baccarelli, MD; Ida Martinelli, MD; Antonella Zanobetti, PhD; Paolo Grillo, MD; Li-Fang Hou, PhD; Pier A. Bertazzi, MD; Pier Mannuccio Mannucci, MD; Joel Schwartz, PhD Background Particulate air pollution has been linked to heart disease and stroke, possibly resulting from enhanced coagulation and arterial thrombosis. Whether particulate air pollution exposure is related to venous thrombosis is unknown. Methods We examined the association of exposure to particulate matter of less than 10 μm in aerodynamic diameter (PM10) with deep vein thrombosis (DVT) risk in 870 patients and 1210 controls from the Lombardy region in Italy, who were examined between 1995 and 2005. We estimated exposure to PM10 in the year before DVT diagnosis (cases) or examination (controls) through area-specific mean levels obtained from ambient monitors. Results Higher mean PM10 level in the year before the examination was associated with shortened prothrombin time (PT) in DVT cases (standardized regression coefficient [β] = −0.12; 95% confidence interval [CI], −0.23 to 0.00) (P = .04) and controls (β = −0.06; 95% CI, −0.11 to 0.00) (P = .04). Each increase of 10 μg/m3 in PM10 was associated with a 70% increase in DVT risk (odds ratio [OR], 1.70; 95% CI, 1.30 to 2.23) (P < .001) in models adjusting for clinical and environmental covariates. The exposure-response relationship was approximately linear over the observed PM10 range. The association between PM10 level and DVT risk was weaker in women (OR, 1.40; 95% CI, 1.02 to 1.92) (P = .02 for the interaction between PM10 and sex), particularly in those using oral contraceptives or hormone therapy (OR, 0.97; 95% CI, 0.58 to 1.61) (P = .048 for the interaction between PM10 level and hormone use). Conclusions Long-term exposure to particulate air pollution is associated with altered coagulation function and DVT risk. Other risk factors for DVT may modulate the effect of particulate air pollution.