Operational evaluation of the RLINE dispersion model for studies of traffic-related air pollutants.
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ABSTRACT:
SUBMITTER: Milando CW
PROVIDER: S-EPMC8064696 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Human exposure to air pollution in many studies is represented by ambient concentrations from space-time kriging of observed values. Space-time kriging techniques based on a limited number of ambient monitors may fail to capture the concentration from local sources. Further, because people spend more time indoors, using ambient concentration to represent exposure may cause error. To quantify the associated exposure error, we computed a series of six different hourly-based exposure metrics at 16,095 Census blocks of three Counties in North Carolina for CO, NO(x), PM(2.5), and elemental carbon (EC) during 2012. These metrics include ambient background concentration from space-time ordinary kriging (STOK), ambient on-road concentration from the Research LINE source dispersion model (R-LINE), a hybrid concentration combining STOK and R-LINE, and their associated indoor concentrations from an indoor infiltration mass balance model. Using a hybrid-based indoor concentration as the standard, the comparison showed that outdoor STOK metrics yielded large error at both population (67% to 93%) and individual level (average bias between -10% to 95%). For pollutants with significant contribution from on-road emission (EC and NO(x)), the on-road based indoor metric performs the best at the population level (error less than 52%). At the individual level, however, the STOK-based indoor concentration performs the best (average bias below 30%). For PM(2.5), due to the relatively low contribution from on-road emission (7%), STOK-based indoor metric performs the best at both population (error below 40%) and individual level (error below 25%). The results of the study will help future epidemiology studies to select appropriate exposure metric and reduce potential bias in exposure characterization.
| S-EPMC4690943 | biostudies-literature
Project description:Traffic-related air pollution (TRAP) is increasing worldwide. Habitual physical activity is known to prevent cardiorespiratory diseases and mortality, but whether exposure to TRAP during exercise affects respiratory health is still uncertain. Exercise causes inflammatory changes in the airways, and its interaction with the effects of TRAP or ozone might be detrimental, for both athletes exercising outdoor and urban active commuters. In this Mini-Review, we summarize the literature on the effects of exposure to TRAP and/or ozone during exercise on lung function, respiratory symptoms, performance, and biomarkers. Ozone negatively affected pulmonary function after exercise, especially after combined exposure to ozone and diesel exhaust (DE). Spirometric changes after exercise during exposure to particulate matter and ultrafine particles suggest a decrease in lung function, especially in patients with chronic obstructive pulmonary disease. Ozone frequently caused respiratory symptoms during exercise. Women showed decreased exercise performance and higher symptom prevalence than men during TRAP exposure. However, performance was analyzed in few studies. To date, research has not identified reliable biomarkers of TRAP-related lung damage useful for monitoring athletes' health, except in scarce studies on airway cells obtained by induced sputum or bronchoalveolar lavage. In conclusion, despite partly counteracted by the positive effects of habitual exercise, the negative effects of TRAP exposure to pollutants during exercise are hard to assess: outdoor exercise is a complex model, for multiple and variable exposures to air pollutants and pollutant concentrations. Further studies are needed to identify pollutant and/or time thresholds for performing safe outdoor exercise in cities.
| S-EPMC7793908 | biostudies-literature
Project description:Vehicles are major sources of air pollutant emissions, and individuals living near large roads endure high exposures and health risks associated with traffic-related air pollutants. Air pollution epidemiology, health risk, environmental justice, and transportation planning studies would all benefit from an improved understanding of the key information and metrics needed to assess exposures, as well as the strengths and limitations of alternate exposure metrics. This study develops and evaluates several metrics for characterizing exposure to traffic-related air pollutants for the 218 residential locations of participants in the NEXUS epidemiology study conducted in Detroit (MI, USA). Exposure metrics included proximity to major roads, traffic volume, vehicle mix, traffic density, vehicle exhaust emissions density, and pollutant concentrations predicted by dispersion models. Results presented for each metric include comparisons of exposure distributions, spatial variability, intraclass correlation, concordance and discordance rates, and overall strengths and limitations. While showing some agreement, the simple categorical and proximity classifications (e.g., high diesel/low diesel traffic roads and distance from major roads) do not reflect the range and overlap of exposures seen in the other metrics. Information provided by the traffic density metric, defined as the number of kilometers traveled (VKT) per day within a 300 m buffer around each home, was reasonably consistent with the more sophisticated metrics. Dispersion modeling provided spatially- and temporally-resolved concentrations, along with apportionments that separated concentrations due to traffic emissions and other sources. While several of the exposure metrics showed broad agreement, including traffic density, emissions density and modeled concentrations, these alternatives still produced exposure classifications that differed for a substantial fraction of study participants, e.g., from 20% to 50% of homes, depending on the metric, would be incorrectly classified into "low", "medium" or "high" traffic exposure classes. These and other results suggest the potential for exposure misclassification and the need for refined and validated exposure metrics. While data and computational demands for dispersion modeling of traffic emissions are non-trivial concerns, once established, dispersion modeling systems can provide exposure information for both on- and near-road environments that would benefit future traffic-related assessments.
| S-EPMC4199035 | biostudies-literature
Project description:BACKGROUND:Communities need to efficiently estimate the burden from specific pollutants and identify those most at risk to make timely informed policy decisions. We developed a risk-based model to estimate the burden of black carbon (BC) and nitrogen dioxide (NO2) on coronary heart disease (CHD) across environmental justice (EJ) and non-EJ populations in Allegheny County, PA. METHODS:Exposure estimates in census tracts were modeled via land use regression and analyzed in relation to US Census data. Tracts were ranked into quartiles of exposure (Q1-Q4). A risk-based model for estimating the CHD burden attributed to BC and NO2 was developed using county health statistics, census tract level exposure estimates, and quantitative effect estimates available in the literature. RESULTS:For both pollutants, the relative occurrence of EJ tracts (> 20% poverty and/or > 30% non-white minority) in Q2 - Q4 compared to Q1 progressively increased and reached a maximum in Q4. EJ tracts were 4 to 25 times more likely to be in the highest quartile of exposure compared to the lowest quartile for BC and NO2, respectively. Pollutant-specific risk values (mean [95% CI]) for CHD mortality were higher in EJ tracts (5.49 × 10- 5 [5.05 × 10- 5 - 5.92 × 10- 5]; 5.72 × 10- 5 [5.44 × 10- 5 - 6.01 × 10- 5] for BC and NO2, respectively) compared to non-EJ tracts (3.94 × 10- 5 [3.66 × 10- 5 - 4.23 × 10- 5]; 3.49 × 10- 5 [3.27 × 10- 5 - 3.70 × 10- 5] for BC and NO2, respectively). While EJ tracts represented 28% of the county population, they accounted for about 40% of the CHD mortality attributed to each pollutant. EJ tracts are disproportionately skewed toward areas of high exposure and EJ residents bear a greater risk for air pollution-related disease compared to other county residents. CONCLUSIONS:We have combined a risk-based model with spatially resolved long-term exposure estimates to predict CHD burden from air pollution at the census tract level. It provides quantitative estimates of effects that can be used to assess possible health disparities, track temporal changes, and inform timely local community policy decisions. Such an approach can be further expanded to include other pollutants and adverse health endpoints.
| S-EPMC7075037 | biostudies-literature
Project description:Traffic-related air pollution particulate matter (TRAP-PM) is associated with increased risk of Alzheimer Disease (AD). Rodent models respond to nano-sized TRAP-PM (nPM) with increased production of amyloid Aβ peptides, concurrently with oxidative damage. Because pro-Aβ processing of the amyloid precursor protein (APP) occurs on subcellular lipid rafts, we hypothesized that oxidative stress from nPM exposure would alter lipid rafts to favor Aβ production. This hypothesis was tested with J20 mice and N2a cells transgenic for hAPPswe (familial AD). Exposure of J20-APPswe mice to nPM for 150 h caused increased lipid oxidation (4-HNE) and increased the pro-amyloidogenic processing of APP in lipid raft fractions in cerebral cortex; the absence of these changes in cerebellum parallels the AD brain region selectivity for Aβ deposits. In vitro, nPM induced similar oxidative responses in N2a-APPswe cells, with dose-dependent production of NO, oxidative damage (4-HNE, 3NT), and lipid raft alterations of APP with increased Aβ peptides. The antioxidant N-acetyl-cysteine (NAC) attenuated nPM-induced oxidative damage and lipid raft alterations of APP processing. These findings identify neuronal lipid rafts as novel targets of oxidative damage in the pro-amyloidogenic effects of air pollution.
| S-EPMC7075030 | biostudies-literature
Project description:Total RNA sequencing of olfactory mucosa (OM) cells derived from cognitively healthy individuals exposed to traffic-related ultrafine particles (UFPs) for 24h and 72h in submerged cultures. The UFPs used for exposures were: A0, A20 and Euro6. Exposures were compared to the corresponding blank samples.
| EGAS00001007528 | EGA
Project description:BackgroundTraffic-related air pollution (TRAP) is made up of complex mixtures of particulate matter, gases and volatile compounds. However, the effects of TRAP on the cardiopulmonary system in most animal studies have been tested using acute exposure to singular pollutants. The cardiopulmonary effects and molecular mechanisms in animals that are chronically exposed to unmodified air pollution as a whole have yet to be studied. Additionally, sex-dependent toxicity of TRAP exposure has rarely been evaluated.ObjectivesThis study sought to assess the cardiopulmonary effect of chronic exposure to unmodified, real-world TRAP in both female and male rats.MethodsFour-week-old male and female rats were exposed to TRAP or filtered air for 14 months in a novel facility drawing air from a major freeway tunnel system in Northern California. Inflammation and oxidative stress markers were examined in the lung, heart, spleen, and plasma, and TRAP deposits were quantified in the lungs of both male and female rats.ResultsElemental analysis showed higher levels of eight elements in the female lungs and one element in the male lungs. Expression of genes related to fibrosis, aging, oxidative stress, and inflammation were higher in the rat hearts exposed to TRAP, with female rats being more susceptible than males. Enhanced collagen accumulation was found only in the TRAP-exposed female hearts. Plasma cytokine secretion was higher in both female and male rats, but inflammatory macrophages were higher only in TRAP-exposed male spleens.DiscussionOur results in rats suggest pathological consequences from chronic TRAP exposure, including sex differences indicating females may be more susceptible to TRAP-induced cardiac fibrosis. https://doi.org/10.1289/EHP7045.
| S-EPMC7717845 | biostudies-literature
Project description:Background:Air pollution has become a major problem around the world and is increasingly an issue in Togo due to increased vehicular traffic. Gaseous pollutants are released by engines and are very harmful to human health and the environment. The fuels used on the major road in Togo, the N2, are adulterated with unknown contents and are of poor quality. Many of the vehicles come from neighboring countries, such as Benin, Ghana and Nigeria. Objectives:The present study aims to evaluate the pollution rate in Togo through the estimation of the concentrations of sulfur dioxide (SO2), nitrogen oxides (NOx), and particular matter (PM) on the international road, the National Road N2, in Lomé, compared to the World Health Organization's (WHO) standard limit. Methods:The simulations of pollutant concentration were performed using the Industrial Source Complex Short Term Version 3 model, which is included in the United States Environmental Protection Agency Regulatory Model (USEPA) AERMOD View software. The meteorological averages data were obtained from the local station near the National Road N2 in Togo in 2018. Hourly averages were calculated according to the European Monitoring Evaluation Programme/European Environmental Agency air pollutant emission inventory guidebook 2016 and were processed using AERMET View and a terrain pre-processor, AERMAP. For the model, the sources of pollution were the vehicles traveling on the road segment. The source was a line volume with 20 m of width and 2 m of height. The estimation methodology covered exhaust emissions of NOx, SO2 and PM contained in the fuel. Results:The simulations provided average hourly, daily and annual concentrations of the different pollutants: 71.91 ?g/m3, 42.41 ?g/m3,11.23 ?g/m3 for SO2; 16.78 ?g/m3, 9.89 ?g/m3, 2.46 ?g/m3 for NOx and below the detection limit, 0.62 ?g/m3, 0.15 ?g/m3 for PM, respectively. These results indicate that on the National Road N2 in Togo, the concentrations of SO2 were high compared to those of NOx and PM. The daily average concentration of SO2 was twice the permissible limits set by the WHO. Conclusions:Emissions obtained from the AERMOD for NOx and PM were less than the permissible limits set by the WHO, while the rate of SO2 was twice the permissible limit. The fuels used on this road were very rich in sulfur. The sulfur level in fuels must be monitored by stakeholders in Togo. Competing Interests:The authors declare no competing financial interests.
| S-EPMC7453808 | biostudies-literature
Project description:Exposures to ambient diesel exhaust particles have been associated with respiratory symptoms and asthma exacerbations in children; however, epidemiologic evidence linking short-term exposure to ambient diesel exhaust particles with airway inflammation is limited. We conducted a panel study with asthmatic and nonasthmatic adolescents to characterize associations between ambient diesel exhaust particle exposures and exhaled biological markers of airway inflammation and oxidative stress. Over four weeks, exhaled breath condensate was collected twice a week from 18 asthmatics and 18 nonasthmatics (ages 14-19 years) attending two New York City schools and analyzed for pH and 8-isoprostane as indicators of airway inflammation and oxidative stress, respectively. Air concentrations of black carbon, a diesel exhaust particle indicator, were measured outside schools. Air measurements of nitrogen dioxide, ozone, and fine particulate matter were obtained for the closest central monitoring sites. Relationships between ambient pollutants and exhaled biomarkers were characterized using mixed effects models. Among all subjects, increases in 1- to 5-day averages of black carbon were associated with decreases in exhaled breath condensate pH, indicating increased airway inflammation, and increases in 8-isoprostane, indicating increased oxidative stress. Increases in 1- to 5-day averages of nitrogen dioxide were associated with increases in 8-isoprostane. Ozone and fine particulate matter were inconsistently associated with exhaled biomarkers. Associations did not differ between asthmatics and nonasthmatics. The findings indicate that short-term exposure to traffic-related air pollutants may increase airway inflammation and/or oxidative stress in urban youth and provide mechanistic support for associations documented between traffic-related pollutant exposures and respiratory morbidity.
| S-EPMC3577992 | biostudies-literature
Project description:BackgroundPrevious studies have shown inconsistent results regarding the impact of traffic pollution on the prevalence of chronic obstructive pulmonary disease (COPD). Therefore, using frequency matching and propensity scores, we explored the association between traffic pollution and COPD in a cohort of 8284 residents in a major agricultural county in Taiwan.MethodsAll subjects completed a structured questionnaire interview and health checkups. Subjects with COPD were identified using Taiwan National Health Insurance Research Databases. A hybrid kriging/LUR model was used to identify levels of traffic-related air pollutants (PM2.5 and O3). Multiple logistic regression models were used to calculate the prevalence ratios (PRs) of COPD and evaluate the role played by traffic-related indices between air pollutants and COPD. The distributed lag nonlinear model was applied in the analysis; we excluded current or ever smokers to perform the sensitivity analysis.ResultsIncreased PRs of COPD per SD increment of PM2.5 were 1.10 (95% CI 1.05-1.15) and 1.25 (95% CI 1.13-1.40) in the population with age and sex matching as well as propensity-score matching, respectively. The results of the sensitivity analysis were similar between the single and two pollutant models. PM2.5 concentrations were significantly associated with traffic flow including sedans, buses, and trucks (p < 0.01). The higher road area and the higher PM2.5 concentrations near the subject's residence correlated with a greater risk of developing COPD (p for interaction < 0.01).ConclusionsOur results suggest that long-term exposure to traffic-related air pollution may be positively associated with the prevalence of COPD.
| S-EPMC8336021 | biostudies-literature