Effects of weather, time, and pollution level on the amount of particulate matter deposited on leaves of Ligustrum lucidum.
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ABSTRACT:
SUBMITTER: Wang H
PROVIDER: S-EPMC4313054 | biostudies-other | 2015
REPOSITORIES: biostudies-other
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Project description:Trees play a pivotal role in improving urban environmental quality and provide several ecosystem services including the removal of pollutants from the air, such as particular matter (PM) and potentially toxic elements (PTE). Therefore, understanding the tree PM and PTE capturing potential, also in connection with plant species, is of great concern, especially in urban areas. This study aims to reveal the link between the elemental composition of PM deposited on tree leaves and soils PTE contents, as well as to rank the PM capturing efficiency of 10 different tree species growing under the impact of urban environments. This also allowed us to test the efficiency of PM deposited on tree leaves as a PTE biomonitoring and pollution source identification tool, in the two biggest urban areas of Armenia. Indeed, high contents of PTE are detected in both soil- and leaf-deposited PM from sites characterized by the presence of localized and active pollution sources (i.e., industrial unites, high traffic, etc.), which are identified by specific tracers (such as Mo, Cu, Zn, Pb, and Cd). Among the studied tree species, the highest PM amount per unit leaf area is observed for Platanus orientalis, but elm species are also identified as promising canditates to be considered for their PM removing potential, and need to be included in future more details studies.
| S-EPMC8508361 | biostudies-literature
Project description:Airborne particulate matter is a serious threat to human health, especially in fast-growing cities. In this study, we carried out a magnetic and elemental study on tree leaves used as passive captors and urban dust from various sites in the city of Santiago, Chile, to assess the reliability of magnetic and elemental measurements to characterize particulate matter pollution from vehicular origin. We found that the magnetic susceptibility and saturation isothermal remanent magnetization measured on urban tree leaves is a good proxy for tracing anthropogenic metallic particles and allow controlling the exposure time for particulate matter collection, in agreement with other studies carried out in large cities. Similar measurements on urban soil can be influenced by particles of detritic (natural) origin, and therefore, magnetic measurements on tree leaves can help to identify hotspots where fine particles are more abundant. Elemental particle-induced X-ray emission analysis of tree leaves showed the presence of a number of elements associated with vehicular emissions, in particular Cu, Zn, Fe, K and S which are present at every site, and As, Se, V, Ni, Sr, Zr, Mo and Pb identified at some sites. We observed a correlation between magnetic parameters and the concentrations of S and Br as well as Cu to a smaller extent. Moreover, this study shows the importance of selecting carefully the tree species as well as the location of trees in order to optimize phytoremediation.
| S-EPMC10140104 | 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:Particulate matter (PM) air pollution exposure has been associated with cancer incidence and mortality especially with lung cancer. The liver is another organ possibly affected by PM due to its role in detoxifying xenobiotics absorbed from PM. Various studies have investigated the mechanistic pathways between inhaled pollutants and liver damage, cancer incidence, and tumor progression. However, little is known about the effects of PM on liver cancer survival. Twenty thousand, two hundred and twenty-one California Cancer Registry patients with hepatocellular carcinoma (HCC) diagnosed between 2000 and 2009 were used to examine the effect of exposure to ambient PM with diameter <2.5 μm (PM2.5 ) on HCC survival. Cox proportional hazards models were used to estimate hazard ratios (HRs) relating PM2.5 to all-cause and liver cancer-specific mortality linearly and nonlinearly-overall and stratified by stage at diagnosis (local, regional and distant)-adjusting for potential individual and geospatial confounders.PM2.5 exposure after diagnosis was statistically significantly associated with HCC survival. After adjustment for potential confounders, the all-cause mortality HR associated with a 1 standard deviation (5.0 µg/m3 ) increase in PM2.5 was 1.18 (95% CI: 1.16-1.20); 1.31 (95% CI:1.26-1.35) for local stage, 1.19 (95% CI:1.14-1.23) for regional stage, and 1.05 (95% CI:1.01-1.10) for distant stage. These associations were nonlinear, with substantially larger HRs at higher exposures. The associations between liver cancer-specific mortality and PM2.5 were slightly attenuated compared to all-cause mortality, but with the same patterns.Exposure to elevated PM2.5 after the diagnosis of HCC may shorten survival, with larger effects at higher concentrations.
| S-EPMC5505313 | biostudies-literature
Project description:BackgroundIn the last decades, marathon running has become a popular form of physical activity among people around the world. It should be noticed that the main marathon races are performed in large cities, where air quality varies considerably. It is well established that breathing polluted air results in a number of harmful effects to the human body. However, there have been no studies to show the impact of marathon run performance on the amount of the deposition of varied fractions of airborne particulate matter (PM) in the respiratory tract of runners. This is why the present study sought to determine the impact of marathon run performance in the air of varying quality on the deposition of the PM1, PM2.5, PM10 in the respiratory tract in humans.MethodsThe PM1, PM2.5 and PM10 deposition was determined in an "average runner" (with marathon performance time 4 h: 30 min) and in an "elite marathon runner" (with marathon performance time 2 h: 00 min) at rest, and during a marathon race, based on own measurements of the PM content in the air and the size-resolved DF(d) profile concept.ResultsWe have shown that breathing air containing 50 µg m-3 PM10 (a borderline value according to the 2006 WHO standard - still valid) at minute ventilation (VE) equal to 8 L min-1 when at rest, resulted in PM10deposition rate of approximately 9 µg h-1, but a marathon run of an average marathon runner with the VE = 62 L min-1 increased the deposition rate up to 45 µg h-1. In the elite runner, marathon run with the VE= 115 L min-1 increased PM10 deposition rate to 83 µg h-1. Interestingly, breathing the air containing 50 µg m-3of PM10 at the VE = 115 L min-1by the elite marathon runner during the race resulted in the same PM10deposition rate as the breathing highly polluted air containing as much as 466 µg m-3 of PM10 when at rest. Furthermore, the total PM10 deposition in the respiratory tract during a marathon race in average runners is about 22% greater (203 / 166 = 1.22) than in elite runners. According to our calculations, the concentration of PM10in the air during a marathon race that would allow one not to exceed the PM10 deposition rate of 9 µg h-1should be lower than 10 µg m-3 in the case of an average runner, and it should be lower than 5.5 µg m-3 in the case of an elite runner.ConclusionsWe conclude that a marathon run drastically increases the rate of deposition of the airborne PM in the respiratory tract of the runners, as a consequence of the huge VE generated during the race. A decrease of the PM content in the air attenuates this rate. Based on our calculations, we postulate that the PM10 content in the air during a "clean air marathon run", involving elite marathon runners, should be below 5.5 µg m-3.
| S-EPMC8214849 | biostudies-literature
Project description:In order to examine associations between asthma morbidity and local ambient air pollution in an area with relatively low levels of pollution, we conducted a time-series analysis of asthma hospital admissions and fine particulate matter pollution (PM2.5) in and around Jackson, MS, for the period 2003 to 2011. Daily patient-level records were obtained from the Mississippi State Department of Health (MSDH) Asthma Surveillance System. Patient geolocations were aggregated into a grid with 0.1° × 0.1° resolution within the Jackson Metropolitan Statistical Area. Daily PM2.5 concentrations were estimated via machine-learning algorithms with remotely sensed aerosol optical depth and other associated parameters as inputs. Controlling for long-term temporal trends and meteorology, we estimated a 7.2% (95% confidence interval 1.7-13.1%) increase in daily all-age asthma emergency room admissions per 10 μg/m3 increase in the 3-day average of PM2.5 levels (current day and two prior days). Stratified analyses reveal significant associations between asthma and 3-day average PM2.5 for males and blacks. Our results contribute to the current epidemiologic evidence on the association between acute ambient air pollution exposure and asthma morbidity, even in an area characterized by relatively good air quality.
| S-EPMC10072932 | biostudies-literature
Project description:Air pollution is a complex mixture of gaseous and particulate components, each of which has detrimental effects on human health. While the composition of air pollution varies greatly depending on the source, studies from across the world have consistently shown that air pollution is an important modifiable risk factor for significantly increased morbidity and mortality. Moreover, clinical studies have generally shown a greater impact of particulate matter (PM) air pollution on health than the gaseous components. PM has wide-ranging deleterious effects on human health, particularly on the cardiovascular system. Both acute and chronic exposure to PM air pollution is associated with increased risk of death from cardiovascular diseases including ischemic heart disease, heart failure, and ischemic/thrombotic stroke. Particulate matter has also been shown to be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus, which themselves are risk factors for cardiovascular disease. While the epidemiological evidence for the deleterious effects of PM air pollution on health is increasingly accepted, newer studies are shedding light on the mechanisms by which PM exerts its toxic effects. A greater understanding of how PM exerts toxic effects on human health is required in order to prevent and minimize the deleterious health effects of this ubiquitous environmental hazard. Air pollution is a growing public health problem and mortality due to air pollution is expected to double by 2050. Here, we review the epidemiological evidence for the cardiovascular effects of PM exposure and discuss current understanding about the biological mechanisms, by which PM exerts toxic effects on cardiovascular system to induce cardiovascular disease.
| S-EPMC6250783 | biostudies-literature
Project description:Size fractionated particulate matter (PM) samples (including PM2.5 and PM10) were collected at Peking University in Northwestern Beijing, China for a 2 week period prior to the Olympics, during the 2 week period of the Olympics, and for a 4 week period following the 2008 Olympics, during both source control and nonsource control periods. PM10 concentrations in this study were high correlated with, but a factor of 1.3 times higher than, the Beijing Environmental Protection Bureau's PM10 concentrations at near-by sites because of differences in the measurement methods used. The mean PM2.5 and PM10 concentrations were statistically different, and lower by 31 and 35%, during the Olympic period compared to the non-Olympic period. However, the PM concentrations were not statistically different between the source control and nonsource control periods. While meteorological parameters (air masses from the south and precipitation) accounted for 40% of the total variation in PM10 concentration, source control accounted for 16%, suggesting that meteorology accounted for more of the variation in PM concentration than source control measures. The PM10 concentrations in Beijing during the Olympic period were 2.9, 3.5, and 1.9 times higher than those in Atlanta, Sydney, and Athens. In addition, the PM2.5 and PM10 concentrations during the Olympic period exceeded the WHO 24-h guideline 100% and 81% of the time, respectively. Finally, the PM10 concentrations in October, November, and December 2008 were reduced by 9-27% compared to the same months in 2007, suggesting that the Olympic source control efforts (and possibly a down turn in the economy) have resulted in lower PM10 concentrations in Beijing.
| S-EPMC2739612 | biostudies-literature
Project description:Using daily fine particulate matter (PM2.5) composition data from the 2000-2005 U.S. EPA Chemical Speciation Network (CSN) for over 200 sites, we applied multivariate methods to identify and quantify the major fine particulate matter (PM2.5) source components in the U.S. Novel aspects of this work were: (1) the application of factor analysis (FA) to multi-city daily data, drawing upon both spatial and temporal variations of chemical species; and, (2) the exclusion of secondary components (sulfates, nitrates and organic carbon) from the source identification FA to more clearly discern and apportion the PM2.5 mass to primary emission source categories. For the quantification of source-related mass, we considered two approaches based upon the FA results: 1) using single key tracers for sources identified by FA in a mass regression; and, 2) applying Absolute Principal Component Analysis (APCA). In each case, we followed a two-stage mass regression approach, in which secondary components were first apportioned among the identified sources, and then mass was apportioned to the sources and to other secondary mass not explained by the individual sources. The major U.S. PM2.5 source categories identified via FA (and their key elements) were: Metals Industry (Pb, Zn); Crustal/Soil Particles (Ca, Si); Motor Vehicle Traffic (EC, NO2); Steel Industry (Fe, Mn); Coal Combustion (As, Se); Oil Combustion (V, Ni); Salt Particles (Na, Cl) and Biomass Burning (K). Nationwide spatial plots of the source-related PM2.5 impacts were confirmatory of the factor interpretations: ubiquitous sources, such as Traffic and Soil, were found to be spread across the nation, more unique sources (such as Steel and Metals Processing) being highest in select industrialized cities, Biomass Burning was highest in the U.S. Northwest, while Residual Oil combustion was highest in cities in the Northeastern U.S. and in cities with major seaports. The sum of these source contributions and the secondary PM2.5 components agreed well with the U.S. PM2.5 observed during the study period (mean=14.3 ug/m3; R2= 0.91). Apportionment regression analyses using single-element tracers for each source category gave results consistent with the APCA estimates. Comparisons of nearby sites indicated that the PM2.5 mass and the secondary aerosols were most homogenous spatially, while traffic PM2.5 and its tracer, EC, were among the most spatially representative of the source-related components. Comparison of apportionment results to a previous analysis of the 1979-1982 IP Network revealed similar and correlated major U.S. source category factors, albeit at lower levels than in the earlier period, suggesting a consistency in the U.S. spatial patterns of these source-related exposures over time, as well. These results indicate that applying source apportionment methods to the nationwide CSN can be an informative avenue for identifying and quantifying source components for the subsequent estimation of source-specific health effects, potentially contributing to more efficient regulation of PM2.5.
| S-EPMC3951912 | biostudies-literature
Project description:BackgroundEpigenetic age, as defined by DNA methylation, may be influenced by air pollution exposure.ObjectiveTo evaluate the relationship between NO2, particulate matter (PM), PM components and accelerated epigenetic age.MethodsIn a sample of non-Hispanic white women living in the contiguous U.S. (n = 2747), we estimated residential exposure to PM2.5, PM10 and NO2 using a model incorporating land-use regression and kriging. Predictive k-means was used to assign participants to clusters representing different PM2.5 component profiles. We measured DNA methylation (DNAm) in blood using the Illumina's Infinium HumanMethylation450 BeadChip and calculated DNAm age using the Hannum, Horvath and Levine epigenetic clocks. Age acceleration was defined based on residuals after regressing DNAm age on chronological age. We estimated associations between interquartile range (IQR) increases in pollutants and age acceleration using linear regression. For PM2.5, we stratified by cluster membership. We examined epigenome-wide associations using robust linear regression models corrected with false discovery rate q-values.ResultsNO2 was inversely associated with age acceleration using the Hannum clock (β = -0.24, 95% CI: -0.47, -0.02). No associations were observed for PM10. For PM2.5, the association with age acceleration varied by PM2.5 component cluster. For example, with the Levine clock, an IQR increase in PM2.5 was associated with an over 6-year age acceleration in a cluster that has relatively high fractions of crustal elements relative to overall PM2.5 (β = 6.57, 95% CI: 2.68, 10.47), and an almost 2-year acceleration in a cluster characterized by relatively low sulfur fractions (β = 1.88, 95% CI: 0.51, 3.25). In a cluster distinguished by lower relative nitrate concentrations, PM2.5 was inversely associated with age acceleration (β = -1.33, 95% CI: -2.43, -0.23). Across the epigenome, NO2 was associated with methylation at 2 CpG sites.ConclusionAir pollution was associated with epigenetic age, a marker of mortality and disease risk, among certain PM2.5 component profiles.
| S-EPMC6754788 | biostudies-literature