Performance evaluation of air pollution control device at traffic intersections in Delhi.
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ABSTRACT: Supplementary information
The online version contains supplementary material available at 10.1007/s13762-021-03641-3.
SUBMITTER: Gulia S
PROVIDER: S-EPMC8447116 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Existing estimations of air pollution from automobile sources are based on either experiments or small-scale governmental interventions. China's nationwide traffic control during the coronavirus disease 2019 outbreak provided us a unique opportunity to assess the direct dose-effect relationship between vehicle density and air pollution. We found that, during the coronavirus disease 2019 outbreak, the nationwide reduced air pollution (except for O3) could be largely explained by traffic control measures. During the traffic control period, every doubling of vehicle density was associated with a decrease of 4.2 (2.0, 6.4) μg/m3 in PM2.5, 5.5 (2.9, 8.1) μg/m3 in PM10, 1.5 (0.9, 2.0) μg/m3 in NO2, and 0.04 (0.02, 0.07) mg/m3 in CO comparing cities with different vehicle densities. Similarly, for every 10% increase in the truck proportion, PM2.5 decreased by 12.3 (4.1, 20.6) μg/m3, PM10 decreased by 14.3 (4.6, 23.9) μg/m3, and CO decreased by 0.14 (0.05, 0.23) mg/m3. Moreover, the associations between vehicle density and reduction in PM2.5, PM10, and CO during the traffic control period were stronger and showed near-complete linearity in cities with low green coverage rate (All P < 0.05 for interaction). According to our estimation, PM2.5 emissions from every doubling of vehicle density can lead to over 8000 excess deaths per year, 66% of which were caused by cardiopulmonary diseases. This natural experiment study is the first to observe the dose-effect relationship between on-road traffic and traffic-generated air pollution, as well as the mitigating effect of urban greening. Findings provide key evidence to the assessment and control of traffic-generated air pollution and its public health impact.
| S-EPMC9671408 | biostudies-literature
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:Traffic-related air pollution has been linked to multiple adverse pregnancy outcomes. However, few studies have examined pregnancy loss, targeting losses identified by hospital records, a large limitation as it does not capture events not reported to the medical system. METHODS:We used a novel variation of the time-series design to determine the association, and identify the critical window of vulnerability, between week-to-week traffic-related air pollution and conceptions resulting in live births, using nitrogen dioxide (NO2) as a traffic emissions tracer. We used information from all live births recorded at Beth Israel Deaconess Medical Center in Boston, MA (2000-2013) and all live births in Tel Aviv District, Israel (2010-2013). RESULTS:In Boston (68,969 live births), the strongest association was during the 15th week of gestation; for every 10 ppb of NO2 increase during that week, we observed a lower rate of live births (rate ratio [RR] = 0.87; 95% confidence interval [CI], 0.78, 0.97), using live birth-identified conceptions to infer pregnancy losses. In the Tel Aviv District (95,053 live births), the strongest estimate was during the 16th gestational week gestation (RR = 0.82; 95% CI, 0.76, 0.90 per 10 ppb of NO2). CONCLUSIONS:Using weekly conceptions ending in live birth rather than identified pregnancy losses, we comprehensively analyzed the relationship between air pollution and all pregnancy loss throughout gestation. The observed results, with remarkable similarity in two independent locations, suggest that higher traffic-related air pollution levels are associated with pregnancy loss, with strongest estimates between the 10th and 20th gestational weeks.
| S-EPMC6269216 | biostudies-literature
Project description:Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments.To examine the relationship between traffic-related air pollution, air quality, and autism.This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development.Case-control study from California.A total of 279 children with autism and a total of 245 control children with typical development.Crude and multivariable adjusted odds ratios (AORs) for autism.Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 ?m in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates.Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal.
| S-EPMC4019010 | biostudies-literature
Project description:BackgroundA recent meta-analysis suggested evidence for an effect of exposure to ambient air pollutants on risk of certain congenital heart defects. However, few studies have investigated the effects of traffic-related air pollutants with sufficient spatial accuracy.ObjectivesWe estimated associations between congenital anomalies and exposure to traffic-related air pollution in Barcelona, Spain.MethodCases with nonchromosomal anomalies (n = 2,247) and controls (n = 2,991) were selected from the Barcelona congenital anomaly register during 1994-2006. Land use regression models from the European Study of Cohorts for Air Pollution Effects (ESCAPE), were applied to residential addresses at birth to estimate spatial exposure to nitrogen oxides and dioxide (NOx, NO2), particulate matter with diameter ? 10 ?m (PM10), 10-2.5 ?m (PMcoarse), ? 2.5 ?m (PM2.5), and PM2.5 absorbance. Spatial estimates were adjusted for temporal trends using data from routine monitoring stations for weeks 3-8 of each pregnancy. Logistic regression models were used to calculate odds ratios (ORs) for 18 congenital anomaly groups associated with an interquartile-range (IQR) increase in exposure estimates.ResultsIn spatial and spatiotemporal exposure models, we estimated statistically significant associations between an IQR increase in NO2 (12.2 ?g/m3) and coarctation of the aorta (ORspatiotemporal = 1.15; 95% CI: 1.01, 1.31) and digestive system defects (ORspatiotemporal = 1.11; 95% CI: 1.00, 1.23), and between an IQR increase in PMcoarse (3.6 ?g/m3) and abdominal wall defects (ORspatiotemporal = 1.93; 95% CI: 1.37, 2.73). Other statistically significant increased and decreased ORs were estimated based on the spatial model only or the spatiotemporal model only, but not both.ConclusionsOur results overall do not indicate an association between traffic-related air pollution and most groups of congenital anomalies. Findings for coarctation of the aorta are consistent with those of the previous meta-analysis.CitationSchembari A, Nieuwenhuijsen MJ, Salvador J, de Nazelle A, Cirach M, Dadvand P, Beelen R, Hoek G, Basagaña X, Vrijheid M. 2014. Traffic-related air pollution and congenital anomalies in Barcelona. Environ Health Perspect 122:317-323;?http://dx.doi.org/10.1289/ehp.1306802.
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Project description:Traffic congestion increases vehicle emissions and degrades ambient air quality, and recent studies have shown excess morbidity and mortality for drivers, commuters and individuals living near major roadways. Presently, our understanding of the air pollution impacts from congestion on roads is very limited. This study demonstrates an approach to characterize risks of traffic for on- and near-road populations. Simulation modeling was used to estimate on- and near-road NO2 concentrations and health risks for freeway and arterial scenarios attributable to traffic for different traffic volumes during rush hour periods. The modeling used emission factors from two different models (Comprehensive Modal Emissions Model and Motor Vehicle Emissions Factor Model version 6.2), an empirical traffic speed-volume relationship, the California Line Source Dispersion Model, an empirical NO2-NOx relationship, estimated travel time changes during congestion, and concentration-response relationships from the literature, which give emergency doctor visits, hospital admissions and mortality attributed to NO2 exposure. An incremental analysis, which expresses the change in health risks for small increases in traffic volume, showed non-linear effects. For a freeway, "U" shaped trends of incremental risks were predicted for on-road populations, and incremental risks are flat at low traffic volumes for near-road populations. For an arterial road, incremental risks increased sharply for both on- and near-road populations as traffic increased. These patterns result from changes in emission factors, the NO2-NOx relationship, the travel delay for the on-road population, and the extended duration of rush hour for the near-road population. This study suggests that health risks from congestion are potentially significant, and that additional traffic can significantly increase risks, depending on the type of road and other factors. Further, evaluations of risk associated with congestion must consider travel time, the duration of rush-hour, congestion-specific emission estimates, and uncertainties.
| S-EPMC4243514 | biostudies-literature
Project description:PurposeTo investigate the association between exposure to traffic-related air pollution and use of spectacles (as a surrogate measure for myopia) in schoolchildren.MethodsWe analyzed the impact of exposure to NO2 and PM2.5 light absorbance at home (predicted by land-use regression models) and exposure to NO2 and black carbon (BC) at school (measured by monitoring campaigns) on the use of spectacles in a cohort of 2727 schoolchildren (7-10 years old) in Barcelona (2012-2015). We conducted cross-sectional analyses based on lifelong exposure to air pollution and prevalent cases of spectacles at baseline data collection campaign as well as longitudinal analyses based on incident cases of spectacles use and exposure to air pollution during the three-year period between the baseline and last data collection campaigns. Logistic regression models were developed to quantify the association between spectacles use and each of air pollutants adjusted for relevant covariates.ResultsAn interquartile range increase in exposure to NO2 and PM2.5 absorbance at home was respectively associated with odds ratios (95% confidence intervals (CIs)) for spectacles use of 1.16 (1.03, 1.29) and 1.13 (0.99, 1.28) in cross-sectional analyses and 1.15 (1.00, 1.33) and 1.23 (1.03, 1.46) in longitudinal analyses. Similarly, odds ratio (95% CIs) of spectacles use associated with an interquartile range increase in exposures to NO2 and black carbon at school was respectively 1.32 (1.09, 1.59) and 1.13 (0.97, 1.32) in cross-sectional analyses and 1.12 (0.84, 1.50) and 1.27 (1.03, 1.56) in longitudinal analyses. These findings were robust to a range of sensitivity analyses that we conducted.ConclusionWe observed increased risk of spectacles use associated with exposure to traffic-related air pollution. These findings require further confirmation by future studies applying more refined outcome measures such as quantified visual acuity and separating different types of refractive errors.
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Project description:The Swedish Civil Air Traffic Control (SCAT) dataset consists of 13 weeks of data collected from the area control in Sweden flight information region. The dataset consists of detailed data from almost 170,000 flights as well as airspace data and weather forecasts. The flight data includes system updated flight plans, clearances from air traffic control, surveillance data and trajectory prediction data. Each week of data is continuous but the 13 weeks are spread over one year to provide variations in weather and seasonal traffic patterns. The dataset does only include scheduled flights not involved in any incident reports. Sensitive data such as military and private flight has been removed. The SCAT dataset can be useful for any research related to air traffic control, e.g. analysis of transportation patterns, environmental impact, optimization and automation/AI.
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Project description:The policymakers need research studies indicating the role of different pollutants with morbidity for polluted cities to install a strategic air quality management system. This study critically assessed the air pollution of Delhi for 2016-18 to found out the role of air pollutants in respiratory morbidity under the ICD-10, J00-J99. The critical assessment of Delhi air pollution was done using various approaches. The mean PM2.5 and PM10 concentrations during the measurement period exceeded both national and international standards by a wide margin. Time series charts indicated the interdependence of PM2.5 and PM10 and connection with hospital visits due to respiratory diseases. Violin plots showed that daily respiratory disease hospital visits increased during the winter and autumn seasons. The winter season was the worst from the city's air pollution point of view, as revealed by frequency analyses. The single and multi-pollutant GAM models indicated that short-term exposure to PM10 and SO2 led to increased hospital visits due to respiratory diseases. Per 10 units increase in concentrations of PM10 brought the highest increase in hospital visits of 0.21% (RR: 1.00, 95% CI: 1.001, 1.002) at lag0-6 days. This study found the robust effect of SO2 persisted in Delhi from lag0 to lag4 days and lag01 to lag06 days for single and cumulative lag day effects, respectively. While every 10 μg m-3 increase of SO2 concentrations on the same day (lag0) led to 32.59% (RR: 1.33, 95% CI: 1.09, 1.61) rise of hospital visits, the cumulative concentration of lag0-1 led to 37.21% (RR: 1.37, 95% CI:1.11, 1.70) rise in hospital visits which further increased to even 83.33% (RR: 1.83, 95% CI:1.35, 2.49) rise at a lag0-6 cumulative concentration in Delhi. The role of SO2 in inducing respiratory diseases is worrying as India is now the largest anthropogenic SO2 emitter in the world.
| S-EPMC9488831 | biostudies-literature
Project description:While many studies have evaluated the association between acute childhood leukemia and environmental factors, knowledge is limited. Ambient air pollution has been classified as a Group 1 carcinogen, but studies have not established whether traffic-related air pollution is associated with leukemia. The goal of our study was to determine if children with acute leukemia had higher odds of exposure to traffic-related air pollution at birth compared to controls.We conducted a case-control study using the Oklahoma Central Cancer Registry to identify cases of acute leukemia in children diagnosed before 20 years of age between 1997 and 2012 (n=307). Controls were selected from birth certificates and matched to cases on week of birth (n=1013). Using a novel satellite-based land-use regression model of nitrogen dioxide (NO2) and estimating road density based on the 2010 US Census, we evaluated the association between traffic-related air pollution and childhood leukemia using conditional logistic regression.The odds of exposure to the fourth quartile of NO2 (11.19-19.89ppb) were similar in cases compared to controls after adjustment for maternal education (OR: 1.08, 95% CI: 0.75, 1.55). These estimates were stronger among children with acute myeloid leukemia (AML) than acute lymphoid leukemia, with a positive association observed among urban children with AML (4th quartile odds ratio: 5.25, 95% confidence interval: 1.09, 25.26). While we observed no significant association with road density, male cases had an elevated odds of exposure to roads at 500m from the birth residence compared to controls (OR: 1.39, 95% CI: 0.93, 2.10), which was slightly attenuated at 750m.Although we observed no association overall between NO2 or road density, this was the first study to observe an elevated odds of exposure to NO2 among children with AML compared to controls suggesting further exploration of traffic-related air pollution and AML is warranted.
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