Inferring Atmospheric Particulate Matter Concentrations from Chinese Social Media Data.
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ABSTRACT:
SUBMITTER: Tao Z
PROVIDER: S-EPMC5029919 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background: Particulate matter pollution has become a growing health concern over the past few decades globally. The problem is especially evident in China, where particulate matter levels prior to 2013 are publically unavailable. We conducted a systematic review of scientific literature that reported fine particulate matter (PM2.5) concentrations in different regions of China from 2005 to 2016. Methods: We searched for English articles in PubMed and Embase and for Chinese articles in the China National Knowledge Infrastructure (CNKI). We evaluated the studies overall and categorized the collected data into six geographical regions and three economic regions. Results: The mean (SD) PM2.5 concentration, weighted by the number of sampling days, was 60.64 (33.27) ?g/m³ for all geographic regions and 71.99 (30.20) ?g/m³ for all economic regions. A one-way ANOVA shows statistically significant differences in PM2.5 concentrations between the various geographic regions (F = 14.91, p < 0.0001) and the three economic regions (F = 4.55, p = 0.01). Conclusions: This review identifies quantifiable differences in fine particulate matter concentrations across regions of China. The highest levels of fine particulate matter were found in the northern and northwestern regions and especially Beijing. The high percentage of data points exceeding current federal regulation standards suggests that fine particulate matter pollution remains a huge problem for China. As pre-2013 emissions data remain largely unavailable, we hope that the data aggregated from this systematic review can be incorporated into current and future models for more accurate historical PM2.5 estimates.
| S-EPMC5334745 | 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:Initially transparent organic particulate matter (PM) can become shades of light-absorbing brown via atmospheric particle-phase chemical reactions. The production of nitrogen-containing compounds is one important pathway for browning. Semisolid or solid physical states of organic PM might, however, have sufficiently slow diffusion of reactant molecules to inhibit browning reactions. Herein, organic PM of secondary organic material (SOM) derived from toluene, a common SOM precursor in anthropogenically affected environments, was exposed to ammonia at different values of relative humidity (RH). The production of light-absorbing organonitrogen imines from ammonia exposure, detected by mass spectrometry and ultraviolet-visible spectrophotometry, was kinetically inhibited for RH < 20% for exposure times of 6 min to 24 h. By comparison, from 20% to 60% RH organonitrogen production took place, implying ammonia uptake and reaction. Correspondingly, the absorption index k across 280 to 320 nm increased from 0.012 to 0.02, indicative of PM browning. The k value across 380 to 420 nm increased from 0.001 to 0.004. The observed RH-dependent behavior of ammonia uptake and browning was well captured by a model that considered the diffusivities of both the large organic molecules that made up the PM and the small reactant molecules taken up from the gas phase into the PM. Within the model, large-molecule diffusivity was calculated based on observed SOM viscosity and evaporation. Small-molecule diffusivity was represented by the water diffusivity measured by a quartz-crystal microbalance. The model showed that the browning reaction rates at RH < 60% could be controlled by the low diffusivity of the large organic molecules from the interior region of the particle to the reactive surface region. The results of this study have implications for accurate modeling of atmospheric brown carbon production and associated influences on energy balance.
| S-EPMC5832997 | biostudies-literature
Project description:BackgroundAmbient air pollution has been linked to the development of gestational diabetes mellitus (GDM). However, evidence of the association is very limited, and no study has estimated the effects of ozone.ObjectiveOur aim was to determine the association of prenatal exposures to particulate matter ≤ 2.5 μm (PM2.5) and ozone (O3) with GDM.MethodsWe used Florida birth vital statistics records to investigate the association between the risk of GDM and two air pollutants (PM2.5 and O3) among 410,267 women who gave birth in Florida between 2004 and 2005. Individual air pollution exposure was assessed at the woman's home address at time of delivery using the hierarchical Bayesian space-time statistical model. We further estimated associations between air pollution exposures during different trimesters and GDM.ResultsAfter controlling for nine covariates, we observed increased odds of GDM with per 5-μg/m3 increase in PM2.5 (ORTrimester1 = 1.16; 95% CI: 1.11, 1.21; ORTrimester2 = 1.15; 95% CI: 1.10, 1.20; ORPregnancy = 1.20; 95% CI: 1.13, 1.26) and per 5-ppb increase in O3 (ORTrimester1 = 1.09; 95% CI: 1.07, 1.11; ORTrimester2 = 1.12; 95% CI: 1.10, 1.14; ORPregnancy = 1.18; 95% CI: 1.15, 1.21) during both the first trimester and second trimester as well as the full pregnancy in single-pollutant models. Compared with the single-pollutant model, the ORs for O3 were almost identical in the co-pollutant model. However, the ORs for PM2.5 during the first trimester and the full pregnancy were attenuated, and no association was observed for PM2.5 during the second trimester in the co-pollutant model (OR = 1.02; 95% CI: 0.98, 1.07).ConclusionThis population-based study suggests that exposure to air pollution during pregnancy is associated with increased risk of GDM in Florida, USA.CitationHu H, Ha S, Henderson BH, Warner TD, Roth J, Kan H, Xu X. 2015. Association of atmospheric particulate matter and ozone with gestational diabetes mellitus. Environ Health Perspect 123:853-859; http://dx.doi.org/10.1289/ehp.1408456.
| S-EPMC4559952 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-02-23 | GSE183099 | GEO
Project description:Antimony (Sb), a priority pollutant listed by the U.S. Environmental Protection Agency (USEPA), can cause adverse effects on human health, with particular impacts on skin, eyes, gastrointestinal tract, and respiratory system. In this study, a database of Sb concentrations in the global atmosphere was developed through a survey of measurements published in more than 600 articles, which was then used to assess the health risks of Sb exposure based on a USEPA assessment model. Most measurements showed Sb concentrations of less than ∼10 ng m-3, but those at several contaminated sites exhibited Sb concentrations of more than 100 ng m-3. For measurements conducted in urban environments, Sb concentrations in the total suspended particles (TSP) and particles of less than 10 (PM10) or 2.5 μm (PM2.5) were the highest in Asia, followed by Europe, South America, and North America. Sb concentrations were generally higher in winter and fall than during other seasons in TSP and PM10 samples. A significant correlation was observed between Sb and As in TSP and PM2.5 on a global scale. Sb was mainly derived from anthropogenic sources, especially traffic emission, industrial emission, and fossil combustion. Hazard quotients (HQ) of Sb in TSP, PM10, and PM2.5 were higher for children than adults because of their lighter body weight, inferior physical resistance, and higher ingestion probability. The global database for atmospheric Sb concentrations demonstrates a relatively low noncarcinogenic risk in most regions. Long-term monitoring is still required to identify the sources and growth potentials of Sb so that effective control policies can be established.
| S-EPMC8047740 | biostudies-literature
Project description:Lung diseases, including asthma, COPD, and other autoimmune lung pathologies are aggravated by exposure to particulate matter (PM) found in air pollution. IL-17 has been shown to exacerbate airway disease in animal models. As PM is known to contain aryl hydrocarbon receptor (AHR) ligands and the AHR has recently been shown to play a role in differentiation of Th17 T cells, the aim of this study was to determine whether exposure to PM could impact Th17 polarization in an AHR-dependent manner. This study used both cell culture techniques and in vivo exposure in mice to examine the response of T cells to PM. Initially experiments were conducted with urban dust particles from a standard reference material, and ultimately repeated with freshly collected samples of diesel exhaust and cigarette smoke. The readout for the assays was increased T cell differentiation as indicated by increased generation of IL-17A in culture, and increased populations of IL-17 producing cells by intracellular flow cytometry. The data illustrate that Th17 polarization was significantly enhanced by addition of urban dust in a dose dependent fashion in cultures of wild-type but not AHR(-/-) mice. The data further suggest that polycyclic aromatic hydrocarbons played a primary role in this enhancement. There was both an increase of Th17 cell differentiation, and also an increase in the amount of IL-17 secreted by the cells. In summary, this paper identifies a novel mechanism whereby PM can directly act on the AHR in T cells, leading to enhanced Th17 differentiation. Further understanding of the molecular mechanisms responsible for pathologic Th17 differentiation and autoimmunity seen after exposure to pollution will allow direct targeting of proteins involved in AHR activation and function for treatment of PM exposures.
| S-EPMC3859609 | biostudies-literature
Project description:Epidemiological studies have shown that air pollution is associated with the morbidity and mortality from cardiopulmonary diseases. Currently, limited experimental models are available to evaluate the physiological and cellular pathways activated by chronic multi-pollutant exposures. This manuscript describes an atmospheric simulation reactor (ASR) that was developed to investigate the health effects of air pollutants by permitting controlled chronic in vivo exposure of mice to combined particulate and gaseous pollutants. BALB/c mice were exposed for 1 hr/day for 3 consecutive days to secondary organic aerosol (SOA, a common particulate air pollutant) at 10-150 μg/m3, SOA (30 μg/m3) + ozone (65 ppb) or SOA + ozone (65 ppb) + nitrogen dioxide (NO2; 100 ppb). Daily exposure to SOA alone led to increased airway hyperresponsiveness (AHR) to methacholine with increasing SOA concentrations. Multi-pollutant exposure with ozone and/or NO2 in conjunction with a sub-toxic concentration of SOA resulted in additive effects on AHR to methacholine. Inflammatory cell recruitment to the airways was not observed in any of the exposure conditions. The ASR developed in this study allows us to evaluate the chronic health effects of relevant multi-pollutant exposures at 'real-life' levels under controlled conditions and permits repeated-exposure studies.
| S-EPMC5294446 | biostudies-literature
Project description:Atmospheric Particulate Matter (PM) is one of the leading environmental risk factors for the global burden of disease. Increasing epidemiological studies demonstrated that PM plays a significant role in CNS demyelinating disorders; however, there is no direct testimony of this, and yet the molecular mechanism by which the occurrence remains unclear. Using multiple in vivo and in vitro strategies, in the present study we demonstrate that PM exposure aggravates neuroinflammation, myelin injury, and dysfunction of movement coordination ability via boosting microglial pro-inflammatory activities, in both the pathological demyelination and physiological myelinogenesis animal models. Indeed, pharmacological disturbance combined with RNA-seq and ChIP-seq suggests that TLR-4/NF-κB signaling mediated a core network of genes that control PM-triggered microglia pathogenicity. In summary, our study defines a novel atmospheric environmental mechanism that mediates PM-aggravated microglia pathogenic activities, and establishes a systematic approach for the investigation of the effects of environmental exposure in neurologic disorders.
2022-02-23 | GSE183098 | GEO
Project description:Atmospheric Particulate Matter (PM) is one of the leading environmental risk factors for the global burden of disease. Increasing epidemiological studies demonstrated that PM plays a significant role in CNS demyelinating disorders; however, there is no direct testimony of this, and yet the molecular mechanism by which the occurrence remains unclear. Using multiple in vivo and in vitro strategies, in the present study we demonstrate that PM exposure aggravates neuroinflammation, myelin injury, and dysfunction of movement coordination ability via boosting microglial pro-inflammatory activities, in both the pathological demyelination and physiological myelinogenesis animal models. Indeed, pharmacological disturbance combined with RNA-seq and ChIP-seq suggests that TLR-4/NF-κB signaling mediated a core network of genes that control PM-triggered microglia pathogenicity. In summary, our study defines a novel atmospheric environmental mechanism that mediates PM-aggravated microglia pathogenic activities, and establishes a systematic approach for the investigation of the effects of environmental exposure in neurologic disorders.
2022-02-23 | GSE183097 | GEO