Browsing by Subject "Particulate Matter"
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Item Open Access A method of assessing air toxics concentrations in urban areas using mobile platform measurements.(J Air Waste Manag Assoc, 2007-11) Isakov, Vlad; Touma, Jawad S; Khlystov, AndreyThe objective of this paper is to demonstrate an approach to characterize the spatial variability in ambient air concentrations using mobile platform measurements. This approach may be useful for air toxics assessments in Environmental Justice applications, epidemiological studies, and environmental health risk assessments. In this study, we developed and applied a method to characterize air toxics concentrations in urban areas using results of the recently conducted field study in Wilmington, DE. Mobile measurements were collected over a 4- x 4-km area of downtown Wilmington for three components: formaldehyde (representative of volatile organic compounds and also photochemically reactive pollutants), aerosol size distribution (representing fine particulate matter), and water-soluble hexavalent chromium (representative of toxic metals). These measurements were,used to construct spatial and temporal distributions of air toxics in the area that show a very strong temporal variability, both diurnally and seasonally. An analysis of spatial variability indicates that all pollutants varied significantly by location, which suggests potential impact of local sources. From the comparison with measurements at the central monitoring site, we conclude that formaldehyde and fine particulates show a positive correlation with temperature, which could also be the reason that photochemically generated formaldehyde and fine particulates over the study area correlate well with the fine particulate matter measured at the central site.Item Open Access Controlled human exposures to ambient pollutant particles in susceptible populations.(Environmental health : a global access science source, 2009-01) Huang, Yuh-Chin T; Ghio, Andrew JEpidemiologic studies have established an association between exposures to air pollution particles and human mortality and morbidity at concentrations of particles currently found in major metropolitan areas. The adverse effects of pollution particles are most prominent in susceptible subjects, including the elderly and patients with cardiopulmonary diseases. Controlled human exposure studies have been used to confirm the causal relationship between pollution particle exposure and adverse health effects. Earlier studies enrolled mostly young healthy subjects and have largely confirmed the capability of particles to cause adverse health effects shown in epidemiological studies. In the last few years, more studies involving susceptible populations have been published. These recent studies in susceptible populations, however, have shown that the adverse responses to particles appear diminished in these susceptible subjects compared to those in healthy subjects. The present paper reviewed and compared control human exposure studies to particles and sought to explain the "unexpected" response to particle exposure in these susceptible populations and make recommendations for future studies. We found that the causes for the discrepant results are likely multifactorial. Factors such as medications, the disease itself, genetic susceptibility, subject selection bias that is intrinsic to many controlled exposure studies and nonspecificity of study endpoints may explain part of the results. Future controlled exposure studies should select endpoints that are more closely related to the pathogenesis of the disease and reflect the severity of particle-induced health effects in the specific populations under investigation. Future studies should also attempt to control for medications and genetic susceptibility. Using a different study design, such as exposing subjects to filtered air and ambient levels of particles, and assessing the improvement in biological endpoints during filtered air exposure, may allow the inclusion of higher risk patients who are likely the main contributors to the increased particle-induced health effects in epidemiological studies.Item Open Access Environmental Impacts of the Coal Ash Spill in Kingston, Tennessee: An 18-Month Survey(2010) Ruhl; L; Vengosh, A; Dwyer; G, S; Hsu-Kim; H; DeonarineAn 18 month investigation of the environmental impacts of the Tennessee Valley Authority (TVA) coal ash spill in Kingston, Tennessee combined with leaching experiments on the spilled TVA coal ash have revealed that leachable coal ash contaminants (LCACs), particularly arsenic, selenium, boron, strontium, and barium, have different effects on the quality of impacted environments. While LCACs levels in the downstream river water are relatively low and below the EPA drinking water and ecological thresholds, elevated levels were found in surface water with restricted water exchange and in pore water extracted from the river sediments downstream from the spill. The high concentration of arsenic (up to 2000 mu g/L) is associated with some degree of anoxic conditions and predominance of the reduced arsenic species (arsenite) in the pore waters. Laboratory leaching simulations show that the pH and ash/water ratio control the LCACs' abundance and geochemical composition of the impacted water. These results have important implications for the prediction of the fate and migration of LCACs in the environment, particularly for the storage of coal combustion residues (CCRs) in holding ponds and landfills, and any potential CCRs effluents leakage into lakes, rivers, and other aquatic systems.Item Open Access Exposure to concentrated coarse air pollution particles causes mild cardiopulmonary effects in healthy young adults.(Environmental health perspectives, 2009-07) Graff, Donald W; Cascio, Wayne E; Rappold, Ana; Zhou, Haibo; Huang, Yuh-Chin T; Devlin, Robert BBACKGROUND: There is ample epidemiologic and toxicologic evidence that exposure to fine particulate matter (PM) air pollution [aerodynamic diameter < or = 2.5 microm (PM(2.5))], which derives primarily from combustion processes, can result in increased mortality and morbidity. There is less certainty as to the contribution of coarse PM (PM(2.5-10)), which derives from crustal materials and from mechanical processes, to mortality and morbidity. OBJECTIVE: To determine whether coarse PM causes cardiopulmonary effects, we exposed 14 healthy young volunteers to coarse concentrated ambient particles (CAPs) and filtered air. Coarse PM concentration averaged 89.0 microg/m(3) (range, 23.7-159.6 microg/m(3)). Volunteers were exposed to coarse CAPs and filtered air for 2 hr while they underwent intermittent exercise in a single-blind, crossover study. We measured pulmonary, cardiac, and hematologic end points before exposure, immediately after exposure, and again 20 hr after exposure. RESULTS: Compared with filtered air exposure, coarse CAP exposure produced a small increase in polymorphonuclear neutrophils in the bronchoalveolar lavage fluid 20 hr postexposure, indicating mild pulmonary inflammation. We observed no changes in pulmonary function. Blood tissue plasminogen activator, which is involved in fibrinolysis, was decreased 20 hr after exposure. The standard deviation of normal-to-normal intervals (SDNN), a measure of overall heart rate variability, also decreased 20 hr after exposure to CAPs. CONCLUSIONS: Coarse CAP exposure produces a mild physiologic response in healthy young volunteers approximately 20 hr postexposure. These changes are similar in scope and magnitude to changes we and others have previously reported for volunteers exposed to fine CAPs, suggesting that both size fractions are comparable at inducing cardiopulmonary changes in acute exposure settings.Item Open Access Gestational age modifies the association between exposure to fine particles and fetal death: findings from a nationwide epidemiological study in the contiguous United States.(Environmental health : a global access science source, 2023-09) Tong, Mingkun; Lin, Weiwei; Liu, Hengyi; Gong, Jicheng; Zhang, Junfeng Jim; Xue, TaoBackgrounds
The vulnerability of fetuses differs at different developmental stages, in response to environmental stressors such as fine particulate matter (PM2.5), a ubiquitous air pollutant. Whether gestational age (GA) modifies the association between prenatal fine particulate matter (PM2.5) exposure and fetal death remains unclear.Methods
We selected approximately 47.8 million eligible United States (US) livebirth and fetal death (defined as a termination at a GA of 20-43 weeks) records from 1989 to 2004. For each record, we took the level of prenatal exposure to PM2.5 as the average concentration in the mother's residential county during the entire gestational period, or a specific trimester (i.e., GA-specific exposure), according to well-established estimates of monthly levels across the contiguous US. First, we evaluated the associations between PM2.5 exposure and fetal death at a specific GA (i.e., GA-specific outcome) using five different logit models (unadjusted, covariate-adjusted, propensity-score, double robust, and diagnostic-score models). Double robust model was selected as the main model due to its advantages in causal inference. Then, we conducted meta-analyses to pool the estimated GA-specific associations, and explored how the pooled estimates varied with GA.Results
According to the meta-analysis, all models suggested gestational PM2.5 exposure was associated with fetal death. However, there was slight heterogeneity in the estimated effects, as different models revealed a range of 3.6-10.7% increase in the odds of fetal death per 5-µg/m3 increment of PM2.5. Each 5-µg/m3 increase in PM2.5 exposure during the entire gestation period significantly increased the odds of fetal death, by 8.1% (95% confidence interval [CI]: 5.1-11.2%). In terms of GA-specific outcomes, the odds of fetal death at a GA of 20-27, 28-36, or ≥ 37 weeks increased by 11.0% (5.9-16.4%), 5.2% (0.4-10.1%), and 8.3% (2.5-14.5%), respectively. In terms of GA-specific exposure, the odds of fetal death increased by 6.0% (3.9-8.2%), 4.1% (3.9-8.2%), and 4.3% (0.5-8.2%) with 5-µg/m3 increases in PM2.5 exposure during the first, second, and third trimester, respectively. The association had the largest effect size (odds ratio = 1.098, 95% CI: 1.061-1.137) between PM2.5 exposure during early gestation (i.e., first trimester) and early fetal death (i.e., 20-27 weeks).Conclusions
Prenatal exposure to PM2.5 was significantly associated with an increased risk of fetal death. The association was varied by gestational-age-specific exposures or outcomes, suggesting gestation age as a potential modifier on the effect of PM2.5. The fetus was most vulnerable during the early stage of development to death associated with PM2.5 exposure.Item Open Access Global air quality and health co-benefits of mitigating near-term climate change through methane and black carbon emission controls.(Environ Health Perspect, 2012-06) Anenberg, Susan C; Schwartz, Joel; Shindell, Drew; Amann, Markus; Faluvegi, Greg; Klimont, Zbigniew; Janssens-Maenhout, Greet; Pozzoli, Luca; Van Dingenen, Rita; Vignati, Elisabetta; Emberson, Lisa; Muller, Nicholas Z; West, J Jason; Williams, Martin; Demkine, Volodymyr; Hicks, W Kevin; Kuylenstierna, Johan; Raes, Frank; Ramanathan, VeerabhadranBACKGROUND: Tropospheric ozone and black carbon (BC), a component of fine particulate matter (PM ≤ 2.5 µm in aerodynamic diameter; PM(2.5)), are associated with premature mortality and they disrupt global and regional climate. OBJECTIVES: We examined the air quality and health benefits of 14 specific emission control measures targeting BC and methane, an ozone precursor, that were selected because of their potential to reduce the rate of climate change over the next 20-40 years. METHODS: We simulated the impacts of mitigation measures on outdoor concentrations of PM(2.5) and ozone using two composition-climate models, and calculated associated changes in premature PM(2.5)- and ozone-related deaths using epidemiologically derived concentration-response functions. RESULTS: We estimated that, for PM(2.5) and ozone, respectively, fully implementing these measures could reduce global population-weighted average surface concentrations by 23-34% and 7-17% and avoid 0.6-4.4 and 0.04-0.52 million annual premature deaths globally in 2030. More than 80% of the health benefits are estimated to occur in Asia. We estimated that BC mitigation measures would achieve approximately 98% of the deaths that would be avoided if all BC and methane mitigation measures were implemented, due to reduced BC and associated reductions of nonmethane ozone precursor and organic carbon emissions as well as stronger mortality relationships for PM(2.5) relative to ozone. Although subject to large uncertainty, these estimates and conclusions are not strongly dependent on assumptions for the concentration-response function. CONCLUSIONS: In addition to climate benefits, our findings indicate that the methane and BC emission control measures would have substantial co-benefits for air quality and public health worldwide, potentially reversing trends of increasing air pollution concentrations and mortality in Africa and South, West, and Central Asia. These projected benefits are independent of carbon dioxide mitigation measures. Benefits of BC measures are underestimated because we did not account for benefits from reduced indoor exposures and because outdoor exposure estimates were limited by model spatial resolution.Item Open Access Long-term dynamics of death rates of emphysema, asthma, and pneumonia and improving air quality.(Int J Chron Obstruct Pulmon Dis, 2014) Kravchenko, J; Akushevich, I; Abernathy, AP; Holman, S; Ross, WG; Lyerly, HKBACKGROUND: The respiratory tract is a major target of exposure to air pollutants, and respiratory diseases are associated with both short- and long-term exposures. We hypothesized that improved air quality in North Carolina was associated with reduced rates of death from respiratory diseases in local populations. MATERIALS AND METHODS: We analyzed the trends of emphysema, asthma, and pneumonia mortality and changes of the levels of ozone, sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and particulate matters (PM2.5 and PM10) using monthly data measurements from air-monitoring stations in North Carolina in 1993-2010. The log-linear model was used to evaluate associations between air-pollutant levels and age-adjusted death rates (per 100,000 of population) calculated for 5-year age-groups and for standard 2000 North Carolina population. The studied associations were adjusted by age group-specific smoking prevalence and seasonal fluctuations of disease-specific respiratory deaths. RESULTS: Decline in emphysema deaths was associated with decreasing levels of SO2 and CO in the air, decline in asthma deaths-with lower SO2, CO, and PM10 levels, and decline in pneumonia deaths-with lower levels of SO2. Sensitivity analyses were performed to study potential effects of the change from International Classification of Diseases (ICD)-9 to ICD-10 codes, the effects of air pollutants on mortality during summer and winter, the impact of approach when only the underlying causes of deaths were used, and when mortality and air-quality data were analyzed on the county level. In each case, the results of sensitivity analyses demonstrated stability. The importance of analysis of pneumonia as an underlying cause of death was also highlighted. CONCLUSION: Significant associations were observed between decreasing death rates of emphysema, asthma, and pneumonia and decreases in levels of ambient air pollutants in North Carolina.Item Open Access Plastic Dominates Developmental Toxicity Responses to Burn pit related Smoke in Zebrafish: Role for Polycyclic Aromatic Hydrocarbons(2023-04-27) Smoot, JacobCombustion of mixed materials during open air burning of refuse or housefires produces emissions that worsen air quality and may cause adverse health effects. Although previous studies have linked air pollution exposure from other sources to congenital defects, the potential developmental toxicity of mixed material combustion emissions remains uncertain. The purpose of this study was to compare the developmental toxicity of smoke derived from the combustion of 5 different material types (plywood, cardboard, plastic, mixture, and mixture plus diesel) in zebrafish larvae, a model often used to assess the behavioral and developmental effects of chemicals. Zebrafish have been shown to have similar physiological and biochemical responses to smoke exposure as other vertebrates and absorb chemicals (such as PAHs) through their epidermis from their surroundings. Larvae were exposed to organic extracts of each smoke at various concentrations and assessed for morphological and behavioral toxicity at 5 days post fertilization. All extracts caused concentration-dependent effects, including mortality, impaired swim bladder inflation, pericardial edema, spinal curvature tail kinks, or craniofacial deformities, although plastic and the mixture caused the most pronounced effects. Plastic also altered locomotor responsiveness to light changes to the greatest extent. Interestingly, some morphological and behavioral responses correlated strongly with total and specific polycyclic aromatic hydrocarbons concentrations in the smoke extracts. Overall, the findings suggest that material type and combustion chemistry impact the severity of developmental toxicity of mixed material smoke in zebrafish.Item Open Access Survey of the potential environmental and health impacts in the immediate aftermath of the coal ash spill in Kingston, Tennessee.(Environ Sci Technol, 2009-08-15) Ruhl, L; Vengosh, A; Dwyer, GS; Hsu Kim, H; Deonarine, A; Bergin, M; Kravchenko, JAn investigation of the potential environmental and health impacts in the immediate aftermath of one of the largest coal ash spills in U.S. history at the Tennessee Valley Authority (TVA) Kingston coal-burning power plant has revealed three major findings. First the surface release of coal ash with high levels of toxic elements (As = 75 mg/kg; Hg = 150 microg/kg) and radioactivity (226Ra + 228Ra = 8 pCi/g) to the environment has the potential to generate resuspended ambient fine particles (< 10 microm) containing these toxics into the atmosphere that may pose a health risk to local communities. Second, leaching of contaminants from the coal ash caused contamination of surface waters in areas of restricted water exchange, but only trace levels were found in the downstream Emory and Clinch Rivers due to river dilution. Third, the accumulation of Hg- and As-rich coal ash in river sediments has the potential to have an impact on the ecological system in the downstream rivers by fish poisoning and methylmercury formation in anaerobic river sediments.Item Open Access Temporal and spatial distribution of health, labor, and crop benefits of climate change mitigation in the United States.(Proceedings of the National Academy of Sciences of the United States of America, 2021-11) Shindell, Drew; Ru, Muye; Zhang, Yuqiang; Seltzer, Karl; Faluvegi, Greg; Nazarenko, Larissa; Schmidt, Gavin A; Parsons, Luke; Challapalli, Ariyani; Yang, Longyi; Glick, AlexSocietal benefits from climate change mitigation accrue via multiple pathways. We examine the US impacts of emission changes on several factors that are affected by both climate and air quality responses. Nationwide benefits through midcentury stem primarily from air quality improvements, which are realized rapidly, and include human health, labor productivity, and crop yield benefits. Benefits from reduced heat exposure become large around 2060, thereafter often dominating over those from improved air quality. Monetized benefits are in the tens of trillions of dollars for avoided deaths and tens of billions for labor productivity and crop yield increases and reduced hospital expenditures. Total monetized benefits this century are dominated by health and are much larger than in previous analyses due to improved understanding of the human health impacts of exposure to both heat and air pollution. Benefit-cost ratios are therefore much larger than in prior studies, especially those that neglected clean air benefits. Specifically, benefits from clean air exceed costs in the first decade, whereas benefits from climate alone exceed costs in the latter half of the century. Furthermore, monetized US benefits largely stem from US emissions reductions. Increased emphasis on the localized, near-term air quality-related impacts would better align policies with societal benefits and, by reducing the mismatch between perception of climate as a risk distant in space and time and the need for rapid action to mitigate long-term climate change, might help increase acceptance of mitigation policies.Item Open Access The toxicology of climate change: environmental contaminants in a warming world.(Environ Int, 2009-08) Noyes, Pamela D; McElwee, Matthew K; Miller, Hilary D; Clark, Bryan W; Van Tiem, Lindsey A; Walcott, Kia C; Erwin, Kyle N; Levin, Edward DClimate change induced by anthropogenic warming of the earth's atmosphere is a daunting problem. This review examines one of the consequences of climate change that has only recently attracted attention: namely, the effects of climate change on the environmental distribution and toxicity of chemical pollutants. A review was undertaken of the scientific literature (original research articles, reviews, government and intergovernmental reports) focusing on the interactions of toxicants with the environmental parameters, temperature, precipitation, and salinity, as altered by climate change. Three broad classes of chemical toxicants of global significance were the focus: air pollutants, persistent organic pollutants (POPs), including some organochlorine pesticides, and other classes of pesticides. Generally, increases in temperature will enhance the toxicity of contaminants and increase concentrations of tropospheric ozone regionally, but will also likely increase rates of chemical degradation. While further research is needed, climate change coupled with air pollutant exposures may have potentially serious adverse consequences for human health in urban and polluted regions. Climate change producing alterations in: food webs, lipid dynamics, ice and snow melt, and organic carbon cycling could result in increased POP levels in water, soil, and biota. There is also compelling evidence that increasing temperatures could be deleterious to pollutant-exposed wildlife. For example, elevated water temperatures may alter the biotransformation of contaminants to more bioactive metabolites and impair homeostasis. The complex interactions between climate change and pollutants may be particularly problematic for species living at the edge of their physiological tolerance range where acclimation capacity may be limited. In addition to temperature increases, regional precipitation patterns are projected to be altered with climate change. Regions subject to decreases in precipitation may experience enhanced volatilization of POPs and pesticides to the atmosphere. Reduced precipitation will also increase air pollution in urbanized regions resulting in negative health effects, which may be exacerbated by temperature increases. Regions subject to increased precipitation will have lower levels of air pollution, but will likely experience enhanced surface deposition of airborne POPs and increased run-off of pesticides. Moreover, increases in the intensity and frequency of storm events linked to climate change could lead to more severe episodes of chemical contamination of water bodies and surrounding watersheds. Changes in salinity may affect aquatic organisms as an independent stressor as well as by altering the bioavailability and in some instances increasing the toxicity of chemicals. A paramount issue will be to identify species and populations especially vulnerable to climate-pollutant interactions, in the context of the many other physical, chemical, and biological stressors that will be altered with climate change. Moreover, it will be important to predict tipping points that might trigger or accelerate synergistic interactions between climate change and contaminant exposures.Item Open Access TRPV4-mediated calcium influx into human bronchial epithelia upon exposure to diesel exhaust particles.(Environ Health Perspect, 2011-06) Li, Jinju; Kanju, Patrick; Patterson, Michael; Chew, Wei-Leong; Cho, Seung-Hyun; Gilmour, Ian; Oliver, Tim; Yasuda, Ryohei; Ghio, Andrew; Simon, Sidney A; Liedtke, WolfgangBACKGROUND: Human respiratory epithelia function in airway mucociliary clearance and barrier function and have recently been implicated in sensory functions. OBJECTIVE: We investigated a link between chronic obstructive pulmonary disease (COPD) pathogenesis and molecular mechanisms underlying Ca2+ influx into human airway epithelia elicited by diesel exhaust particles (DEP). METHODS AND RESULTS: Using primary cultures of human respiratory epithelial (HRE) cells, we determined that these cells possess proteolytic signaling machinery, whereby proteinase-activated receptor-2 (PAR-2) activates Ca2+-permeable TRPV4, which leads to activation of human respiratory disease-enhancing matrix metalloproteinase-1 (MMP-1), a signaling cascade initiated by diesel exhaust particles (DEP), a globally relevant air pollutant. Moreover, we observed ciliary expression of PAR-2, TRPV4, and phospholipase-Cβ3 in human airway epithelia and their DEP-enhanced protein-protein complex formation. We also found that the chronic obstructive pulmonary disease (COPD)-predisposing TRPV4P19S variant enhances Ca2+ influx and MMP 1 activation, providing mechanistic linkage between man-made air pollution and human airway disease. CONCLUSION: DEP evoked protracted Ca2+ influx via TRPV4, enhanced by the COPD-predisposing human genetic polymorphism TRPV4P19S. This mechanism reprograms maladaptive inflammatory and extracellular-matrix-remodeling responses in human airways. The novel concept of air pollution-responsive ciliary signal transduction from PAR-2 to TRPV4 in human respiratory epithelia will accelerate rationally targeted therapies, possibly via the inhalatory route.