Fine Airborne Particulate Matter Research Articles

Therapeutic Effects of (+)-Afzelechin on Particulate Matter-Induced Pulmonary Injury.

Particulate matter (PM) constitutes a hazardous blend of organic and inorganic particles that poses health risks. Inhalation of fine airborne PM with a diameter of ≤ 2.5 μm (PM2.5) can lead to significant lung impairments. (+)-afzelechin (AZC), a natural compound sourced from Bergenia ligulata, boasts a range of attributes, including antioxidant, antimicrobial, anticancer, and cardiovascular effects. However, knowledge about the therapeutic potential of AZC for patients with PM2.5-induced lung injuries remains limited. Thus, in this study, we investigated the protective attributes of AZC against lung damage caused by PM2.5 exposure. AZC was administered to the mice 30 min after intratracheal instillation of PM2.5. Various parameters, such as changes in lung tissue wet/dry (W/D) weight ratio, total protein/total cell ratio, lymphocyte counts, levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF), vascular permeability, and histology, were evaluated in mice exposed to PM2.5. Data demonstrated that AZC mitigated lung damage, reduced W/D weight ratio, and curbed hyperpermeability induced by PM2.5 exposure. Furthermore, AZC effectively lowered plasma levels of inflammatory cytokines produced by PM2.5 exposure. It reduced the total protein concentration in BALF and successfully alleviated PM2.5-induced lymphocytosis. Additionally, AZC substantially diminished the expression levels of Toll-like receptors 4 (TLR4), MyD88, and autophagy-related proteins LC3 II and Beclin 1. In contrast, it elevated the protein phosphorylation of the mammalian target of rapamycin (mTOR). Consequently, the anti-inflammatory attribute of AZC positions it as a promising therapeutic agent for mitigating PM2.5-induced lung injuries by modulating the TLR4-MyD88 and mTOR-autophagy pathways.

PM2.5 pollution in Texas: a geospatial analysis of health impact functions.

Air pollution is the greatest environmental threat to human health in the world today and is responsible for an estimated 7-9 million deaths annually. One of the most damaging air pollutants is PM2.5 pollution, fine airborne particulate matter under 2.5 microns in diameter. Exposure to PM2.5 pollution can cause premature death, heart disease, lung cancer, stroke, diabetes, asthma, low birthweight, and IQ loss. To avoid these adverse health effects, the WHO recommends that PM2.5 levels not exceed 5 μg/m3. This study estimates the negative health impacts of PM2.5 pollution in Texas in 2016. Local exposure estimates were calculated at the census tract level using the EPA's BenMAP-CE software. In BenMAP, a variety of exposure-response functions combine air pollution exposure data with population data and county-level disease and death data to estimate the number of health effects attributable to PM2.5 pollution for each census tract. The health effects investigated were mortality, low birthweight, stroke, new onset asthma, new onset Alzheimer's, and non-fatal lung cancer. This study found that approximately 26.7 million (98.9%) of the 27.0 million people living in Texas in 2016 resided in areas where PM2.5 concentrations were above the WHO recommendation of 5 μg/m3, and that 2.6 million people (9.8%) lived in areas where the average PM2.5 concentration exceeded 10 μg/m3. This study estimates that there were 8,405 (confidence interval [CI], 5,674-11,033) premature deaths due to PM2.5 pollution in Texas in 2016, comprising 4.3% of all deaths. Statewide increases in air-pollution-related morbidity and mortality were seen for stroke (2,209 - CI: [576, 3,776]), low birthweight (2,841 - CI: [1,696, 3,925]), non-fatal lung cancers (636 - CI: [219, 980]), new onset Alzheimer's disease (24,575 - CI: [20,800, 27,540]), and new onset asthma (7,823 - CI: [7,557, 8,079]). This study found that air pollution poses significant risks to the health of Texans, despite the fact that pollution levels across most of the state comply with the EPA standard for PM2.5 pollution of 12 μg/m3. Improving air quality in Texas could save thousands of lives from disease, disability, and premature death.

Evidence for multi-decadal fuel buildup in a large California wildfire from smoke radiocarbon measurements

In recent decades, there has been a significant increase in annual area burned in California’s Sierra Nevada mountains. This rise in fire activity has prompted the need to understand how historical forest management practices affect fuel composition and emissions. Here we examined the total carbon (TC) concentration and radiocarbon abundance (Δ14C) of particulate matter (PM) emitted by the KNP Complex Fire, which occurred during California’s 2021 wildfire season and affected several groves of giant sequoia trees in the southern Sierra Nevada. During a 26 h sampling period, we measured concentrations of fine airborne PM (PM2.5), as well as dry air mole fractions of carbon monoxide (CO) and methane (CH4), using a ground-based mobile laboratory. We also collected filter samples of PM2.5 for analysis of TC concentration and Δ14C. High correlation among PM2.5, CO, and CH4 time series confirmed that our PM2.5 measurements captured variability in wildfire emissions. Using a Keeling plot approach, we determined that the mean Δ14C of PM2.5 was 111.6 ± 7.7‰ (n = 12), which was considerably enriched relative to atmospheric carbon dioxide in the northern hemisphere in 2021 (−3.2 ± 1.4‰). Combining these Δ14C data with a steady-state one-box ecosystem model, we estimated that the mean age of fuels combusted in the KNP Complex Fire was 40 years, with a range of 29–57 years. These results provide evidence for emissions originating from woody biomass, larger-diameter fine fuels, and coarse woody debris that have accumulated over multiple decades. This is consistent with independent field observations that indicate high fire intensity contributed to widespread giant sequoia mortality. With the expanded use of prescribed fires planned over the next decade in California to mitigate wildfire impacts, our measurement approach has the potential to provide regionally-integrated estimates of the effectiveness of fuel treatment programs.

Oxidative stress and activation of H2A.X in lung alveolar epithelial cells (A549) by nanoparticulate carbon black

Fine airborne particulate matter enter the respiratory system, induce oxidative stress and initiate DNA damage. The aim of our study was the estimation of cell viability, oxidative stress, DNA damage, cell cycle alterations and activation of histone H2A.X. Experiments were done on lung alveolar epithelial (A549) cells grown for 24 h with 200 µg mL−1 coarse carbon black (CB), or nanoparticulate CB (NPCB). Neither CB nor glutathione depletion altered cell viability, growth rates, and H2A.X expression while NPCB decreased cell viability, increased oxidative stress and DNA damage. The cell cycle was blocked at G0/G1. NPCB but not CB increased expression and activation of H2A.X at mRNA and protein levels. Co-expression data point to γH2A.X as a major NPCB target, and show the interdependence of γH2A.X and oxidative stress. We conclude, that NPCB increases γ-H2A.X expression in A549 cells at mRNA and protein levels and stimulates H2A.X (Ser139), phosphorylation, associated with oxidative stress, the DNA damage response and G1 cell cycle arrest.

Winter-time pollution in Central European cities shifts the 208Pb/207Pb isotope ratio of atmospheric PM2.5 to higher values: Implications for lead source apportionment

Atmospheric lead pollution has adverse health effects on humans. Identification of anthropogenic Pb sources is thus crucial for understanding of pollution-related risks and for formulation of efficient abatement strategies. We analyzed concentrations and isotope ratios of Pb in fine air-borne particulate matter (PM2.5) in three Central European cities. Aerosol sampling in 12-h intervals was performed during summer and winter in Hradec Králové, Olomouc and Brno, regional centers of highly industrialized Czech Republic, each with a population of more than 90 thousand. Lead analysis was complemented with concentration measurements of Zn, Cu, Cd, As, Sb, and S. Trace element and PM2.5 concentrations were higher in winter than in summer in all studied cities, on average by 47%. The overall mean concentration of PM2.5 in urban air was 21 μg m−3, similar to that in Bern (Switzerland) and Vienna (Austria). Across the sites, 206Pb/207Pb ratios ranged from 1.142 to 1.178 in summer and from 1.143 to 1.173 in winter. The mean 206Pb/207Pb ratios were statistically indistinguishable in all three studied cities (1.165 in Hradec Králové, 1.163 in Olomouc, and 1.160 in Brno). In the 206Pb/207Pb vs.208Pb/207Pb graph, Pb isotope composition of summer samples formed a straight line, whereas Pb isotope composition of winter samples was shifted toward higher 208Pb/207Pb ratios. A Pb isotope inventory of regional pollution sources indicated that winter-time Pb pollution was not caused solely by household heating and increased electricity production in coal-burning power plants. Recycling of industrial Pb originating from Variscan ores and waste incineration could have shifted the 208Pb/207Pb ratio of PM2.5 to higher values, however, such sources do not emit more Pb in winter than in summer. Remobilization of legacy alkyl-Pb from gasoline additives and Pb emissions from current unleaded gasoline and diesel could have shifted both Pb isotope ratios to lower values.

Long-term exposure to PM2.5 aggravates pulmonary fibrosis and acute lung injury by disrupting Nrf2-mediated antioxidant function

Epidemiological studies have indicated that exposure to ambient air-borne fine particulate matter (PM2.5) is associated with many cardiopulmonary diseases; however, the underlying pathological mechanisms of PM2.5-induced lung injury remain unknown. In this study, we aimed to assess the impact of acute or prolonged exposure to water-insoluble fractions of PM2.5 (PM2.5 particulate) on lung injury and its molecular mechanisms. Balb/c mice were randomly exposed to PM2.5 once (acute exposure) or once every three days for a total of 6 times (prolonged exposure). Lung, BALF and blood samples were collected, and pulmonary pathophysiological alterations were analyzed. Nrf2 knockout mice were adapted to assess the involvement of Nrf2 in lung injury, and transcriptomic analysis was performed to delineate the mechanisms. Through transcriptomic analysis and validation of Nrf2 knockout mice, we found that acute exposure to PM2.5 insoluble particulates induced neutrophil infiltration-mediated airway inflammation, whereas prolonged exposure to PM2.5 insoluble particulate triggered lung fibrosis by decreasing the transcriptional activity of Nrf2, which resulted in the downregulated expression of antioxidant-related genes. In response to secondary LPS exposure, prolonged PM2.5 exposure induced more severe lung injury, indicating that prolonged PM2.5 exposure induced Nrf2 inhibition weakened its antioxidative defense capacity against oxidative stress injury, leading to the formation of pulmonary fibrosis and increasing its susceptibility to secondary bacterial infection.

The links of fine airborne particulate matter exposure to occurrence of cardiovascular and metabolic diseases in Michigan, USA.

Air pollutants, particularly airborne particulate matter with aerodynamic diameter < 2.5μm (PM2.5), have been linked to the increase in mortality and morbidity associated with cardiovascular and metabolic diseases. In this study, we investigated the dose-risk relationships between PM2.5 concentrations and occurrences of cardiovascular and metabolic diseases as well as the confounding socioeconomic factors in Michigan, USA, where PM2.5 levels are generally considered acceptable. Multivariate linear regression analyses were performed to investigate the relationship between health outcome and annual ground-level PM2.5 concentrations of 82 counties in Michigan. The analyses revelated significant linear dose-response associations between PM2.5 concentrations and cardiovascular disease (CVD) hospitalization. A 10 μg/m3 increase in PM2.5 exposure was found to be associated with a 3.0% increase in total CVD, 0.45% increase in Stroke, and a 0.3% increase in Hypertension hospitalization rates in Medicare beneficiaries. While the hospitalization rates of Total Stroke, Hemorrhagic Stroke, and Hypertension in urbanized counties were significantly higher than those of rural counties, the death rates of coronary heart disease and ischemic stroke in urbanized counties were significantly lower than those of rural counties. These results were correlated with the facts that PM2.5 levels in urbanized counties were significantly higher than that in rural counties and that the percentage of the population with health insurance and the median household income in rural counties were significantly lower. While obesity prevalence showed evidence of a weak positive correlation (ρ = 0.20, p-value = 0.078) with PM2.5 levels, there was no significant dose-response association between county diabetes prevalence rates and PM2.5 exposure in Michigan. In summary, this study revealed strong dose-response associations between PM2.5 concentrations and CVD incidence in Michigan, USA. The socioeconomic factors, such as access to healthcare resources and median household income, represent important confounding factors that could override the impact of PM2.5 exposure on CVD mortality.

Air Pollution, Political Corruption, and Cardiovascular Disease in the Former Soviet Republics.

Background:Ambient air pollution is a serious problem in many Eastern European countries. Elevated levels of fine airborne particulate matter (PM2.5) pollution in the former Soviet republics relative to the rest of Europe contribute to elevated rates of disease, especially cardiovascular disease (CVD).Objective:Information on the underlying social and political causes of air pollution in Eastern Europe is important for pollution control and disease prevention.Methods:To quantify relationships between pollution, and air-pollution-related CVD, and political corruption throughout Europe and particularly in the former Soviet republics, we relied on the State of Global Air report for information on air pollution levels; on the 2019 Global Burden of Disease study (GBD) for estimates of the burden of air-pollution-related CVD; and on Transparency International (TI) for rankings of governmental corruption.Findings:Air-pollution-related CVD was responsible for an estimated 178,000 (UI: 112,000–251,000) premature deaths and for the loss of 4,010,000 (UI: 2,518,000–-5,611,000) productive years of life (DALYs) in 2019 in the former Soviet republics. A significant positive correlation (R = 0.72, p 1.7e–8) was found across Europe between air-pollution-related CVD mortality rates and national corruption rankings.Conclusions:We conclude that lack of governmental transparency, inadequate air pollution monitoring, and opposition by vested interests have hindered air pollution control and perpetuated high rates of pollution-related morbidity and mortality in the former Soviet republics. Ending corruption and modernizing industrial production will be key to air pollution and related diseases.

A protective role of autophagy in fine airborne particulate matter-induced apoptosis in LN-229 cells

Air pollution is a public health threat and global epidemiological studies have shown that ambient air pollutants are closely related to various poor health conditions, including neurodegenerative diseases. Here, we evaluated the toxic effects and the underlying mechanisms of fine airborne particulate matter (PM2.5) on human glioblastoma LN-229 cells. Our results showed that exposure of LN-229 cells to PM2.5 (≥ 200 μg/mL) significantly reduced cell viability. PM2.5 exposure increased autophagy, apoptosis, and ROS production in the cells. Pre-treatment with a ROS scavenger, catalase, or depletion of mtDNA (ρ0 cells) abolished PM2.5-induced autophagy and apoptosis. PM2.5 exposure also activated MAPK signals in cells, which were blocked by catalase pre-treatment or mtDNA depletion. Furthermore, inhibition of JNK, but not ERK1/2 or p38, attenuated PM2.5-induced autophagy and apoptosis in cells. Finally, suppression of autophagy with Bafilomycin A1 or Beclin 1 siRNA exacerbated PM2.5-induced apoptosis, indicating a protective role of autophagy against PM2.5-induced apoptosis. Our results demonstrated that exposure of LN-229 cells to PM2.5 caused autophagy and apoptosis through PM2.5-induced ROS generation, mainly by mitochondria, and JNK activation. Autophagy may have a transient protective response in PM2.5-induced apoptosis. These findings have important implications for understanding the potential neurotoxicity of PM2.5.

Sr-Nd-Hf isotopic analysis of reference materials and natural and anthropogenic particulate matter sources: Implications for accurately tracing North African dust in complex urban atmospheres.

We present novel chemical separation protocols for isotopic analysis of low mass aliquots (0.3mg and 25mg) of several reference materials and real-world samples of relevance to urban airborne particulate matter (PM) investigations. A high-yielding gravity flow column chromatography scheme was developed for facile and quantitative separation of Sr, Nd, and Hf prior to multi collector - inductively coupled plasma - mass spectrometry (MC-ICP-MS). Because we are interested in isolating and accurately quantitating individual anthropogenic and natural aerosol sources in complex industrial/metropolitan atmospheric environments, laboratory protocols were optimized using National Institute of Standards and Technology Standard Reference Material (SRM) 1648a (urban atmospheric PM), SRM 1633b (coal fly ash), and European Commission standards BCR-723 (vehicular road dust), and BCR-2 (basalt rock standard). Sr, Nd, and Hf procedural blanks from column chromatography were low (averaging only 37pg, 17pg, 11pg, respectively) and recoveries were high (averaging 95%, 82%, and 92%, respectively). A volume-adjustment protocol was established using isotope reference solutions SRM 987 (SrCO3), JNdi (Nd2O3), and in-house Hf standards to dilute the dried samples prior to MC-ICP-MS based on projected uncertainties for low sample masses. 87Sr/86Sr, 143Nd/144Nd, and 176Hf/177Hf isotopic ratios in SRM 1648a, BCR-723, and SRM 1633b are reported for the first time that can serve as provisional reference values. The novel method was used to characterize isotopic ratios and elemental abundances in two anthropogenic urban aerosol sources, namely motor vehicles and petroleum refining using airborne fine PM collected in a vehicular tunnel and fluidized-bed catalytic cracking catalysts, respectively. Two other important mineral-rich urban PM sources, namely soil (i.e., resuspended crustal material) and concrete/cement dust (i.e., construction activity) were also characterized. These are the first isotopic measurements in these environmental compartments and were compared with literature data for long-range transported North African dust, which is a prominent summertime PM source in urban regions in southeastern United States. We demonstrate the capability of coupled Sr-Nd-Hf isotopes to uniquely trace different mineral dust sources with overlapping elemental composition (Sahara-Sahel region, local soil, and concrete/cement) and accurately isolate various urban PM sources demonstrating the superiority of isotopic markers over elemental tracers.

A new on-line SPE LC-HRMS method for the analysis of Perfluoroalkyl and Polyfluoroalkyl Substances (PFAS) in PM2.5 and its application for screening atmospheric particulates from Dublin and Enniscorthy, Ireland

A sensitive analytical method has been developed and validated for the determination of 16 polyfluorinated alkyl substances (PFAS) in fine airborne particulate matter (PM2.5) using on-line solid phase extraction (SPE) coupled with liquid chromatography (LC) – negative electrospray ionisation high resolution mass spectrometry (−) ESI-HRMS. On-line SPE allows simultaneous sample clean-up from interfering matrices and lower limits of detection (LODs) by injecting a large volume of sample into the LC system without compromising chromatographic efficiency and resolution. The method provides LODs in the range 0.08–0.5 pg/mL of sample extract allowing detection of selected PFAS in aerosol particles at low fg/m3 level and showed good tolerance to the considered PM matrix. The validated method was applied for analysis of PFAS in ambient PM2.5 samples collected at two urban locations in Ireland, i.e., Enniscorthy and Dublin. Several PFAS were observed above the detection limit, including perfluorobutyrate (PFBA), perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorobutanesulfonic acid (L-PFBS) and perfluorononanoic acid (PFNA), as well as fluorotelomer sulfonates: 4:2 FTS, 6:2 FTS and 8:2 FTS. The results indicate that some toxic PFAS, such as PFOS and PFOA, are still detected in the environment despite being phased out from production and subject to restricted use in the EU and USA for more than two decades. Observation of fluorotelomer sulfonates (4:2 FTS, 6:2 FTS and 8:2 FTS, which are used as alternatives for legacy PFOA and PFOS) in ambient PM2.5 samples raises a concern about their persistence in the atmosphere and impact on human health considering emerging evidence that they could have similar health endpoints as PFOA and PFOS. To our knowledge, this is the first study to identify PFAS in ambient PM2.5 at urban locations in Ireland and also the first study to detect 4:2 and 8:2 fluorotelomer sulfonates in atmospheric aerosol particles.

Fine particulate matter-induced lung inflammation is mediated by pyroptosis in mice

BackgroundExposure to ambient air-borne fine particulate matter (PM2.5) increases respiratory morbidity and mortality. The mechanisms underlying PM2.5-induced adverse effects remain unclear. This study aimed to uncover the molecular mechanisms of PM2.5-induced lung toxicity using a mouse model. MethodsScanning electron microscopy and inductively coupled plasma mass spectrometry were used to examine and analyze PM2.5 morphology and element compositions, respectively. Twenty four male mice were randomly divided into three groups: control (PBS), PM2.5 (4.0 mg/kg b.w.), and PM2.5 + Z-YVAD-FMK. In the latter group, the pan-caspase inhibitor (Z-YVAD-FMK) was intraperitoneally injected into mice at a dose of 12.5 mg/kg body weight prior to intratracheal instillation of PM2.5 (4.0 mg/kg b.w.) every other day for a total of 3 times (n = 8 in each group). Bronchoalveolar lavage fluids (BALFs) were collected 24 h after the last instillation of PM2.5. Levels of total proteins (TP), lactate dehydrogenase (LDH), IL-1β and IL-18 were analyzed for biomarkers of cell injury and inflammation. Additionally, histological alterations of lung tissues were assessed by hematoxylin-eosin staining. mRNA and protein expression of Caspase1, NLRP3 and GSDMD were examined by real-time fluorescent quantitative PCR and immunohistochemical staining. ResultsExposure to PM2.5 increased levels of TP, LDH, IL-1β, IL-18 and inflammatory cell counts in lung. The mRNA and protein expression of Caspase1, NLRP3 and GSDMD were increased. Inhibition of the NALRP3/Caspase-1 signaling pathway ameliorated PM2.5-induced lung injury and inflammation, partially through suppressing pyroptosis in lung. ConclusionPM2.5 exposure induces lung injury and inflammation, which is mediated by the NALRP3/Caspase-1 signaling pathway.

Nuclear analytical techniques for identification of elemental composition of fine and coarse airborne particulate matter Collected in Bandung, Indonesia

Air pollution has received serious attention from both the government and the public in Bandung, Indonesia. Nuclear analytical techniques (NAT) such as X-ray fluorescence (XRF) have been implemented for the quantification of environmental pollutants, especially airborne particulate matter (APM). Sampling for fine APM (PM2.5) and coarse APM (PM2.5-10) have been conducted in Bandung using a GENT sampler, once a week for 24 hrs from 2015 to 2017. The samples were then analyzed for their mass, black carbon (BC), and elemental composition using gravimetric, smoke stain reflectometer, and ED-XRF, respectively. The results obtained indicate that the annual average of PM2.5 is in the range of 17.85-20.90 µg/m3 which has exceeded the Indonesian annual standard (15 µg/m3). While for PM10 it is still below the standard. Compared to PM2.5 and PM2.5-10 in 2002-2004, the concentration has increased by around 35% and 29%, respectively. This situation needs serious attention especially because of the adverse effects of PM2.5 on human health. The average BC fraction at PM2.5 is around 19%. In this paper, chemical composition, annual concentration trends, and correlations between elements will be discussed in detail including the advantages and disadvantages of the NATs method. For the next stage, this information can be used to identify sources of pollutants.

Pollution Characteristics of Particulate Matter (PM2.5 and PM10) and Constituent Carbonaceous Aerosols in a South Asian Future Megacity

The future megacity of Faisalabad is of prime interest when considering environmental health because of its bulky population and abundant industrial and anthropogenic sources of coarse particles (PM10) and fine airborne particulate matter (PM2.5). The current study was aimed to investigate the concentration level of PM2.5 and PM10, also the characterization of carbonaceous aerosols including organic carbon (OC), elemental carbon (EC) and total carbon (TC) in PM2.5 and PM10 samples collected from five different sectors (residential, health, commercial, industrial, and vehicular zone). The data presented here are the first of their kind in this sprawling city having industries and agricultural activities side by side. Results of the study revealed that the mass concentration of PM2.5 and PM10 is at an elevated level throughout Faisalabad, with ambient PM2.5 and PM10 points that constantly exceeded the 24-h standards of US-EPA, and National Environment Quality Standards (NEQS) which poses harmful effects on the quality of air and health. The total carbon concentration varied between 21.33 and 206.84 μg/m3, and 26.08 and 211.15 μg/m3 with an average of 119.16 ± 64.91 μg/m3 and 124.71 ± 64.38 μg/m3 for PM2.5 in summer and winter seasons, respectively. For PM10, the concentration of TC varied from 34.52 to 289.21 μg/m3 with an average of 181.50 ± 87.38 μg/m3 (for summer season) and it ranged between 44.04 and 300.02 μg/m3 with an average of 191.04 ± 87.98 μg/m3 (winter season), respectively. No significant difference between particulate concentration and weather parameters was observed. Similarly, results of air quality index (AQI) and pollution index (PI) stated that the air quality of Faisalabad ranges from poor to severely pollute. In terms of AQI, moderate pollution was recorded on sampling sites in the following order; Ittehad Welfare Dispensary &gt; Saleemi Chowk &gt; Kashmir Road &gt; Pepsi Factory, while at Nazria Pakistan Square and Allied Hospital, higher AQI values were recorded. The analysis and results presented in this study can be used by policy-makers to apply rigorous strategies that decrease air pollution and the associated health effects in Faisalabad.

Estimating the Effects of Fine Particulate Matter on 432 Cardiovascular Diseases Using Multi-Outcome Regression With Tree-Structured Shrinkage

The positive relationship between airborne fine particulate matter (PM2.5) and cardiovascular disease (CVD) is established. Little is known about effect size heterogeneity across distinct CVD outcomes. We conducted a multi-outcome case-crossover study of Medicare beneficiaries aged >65 years residing in the mainland USA from 2000 through 2012. The exposure was two-day average PM2.5 in each individual’s residential zipcode. The outcomes were hospitalization for 432 distinct CVDs defined by the International Classification of Diseases, Revision 9. Our dataset included almost 24 million CVD hospitalizations. We analyzed the data using multi-outcome regression with tree-structured shrinkage (MOReTreeS), a novel method that enables: (1) borrowing of strength across outcomes; (2) data-driven discovery of outcome groups that are similarly affected by the exposure; (3) estimation of a single effect for each group. MOReTreeS grouped 420 outcomes together; for this group, the odds ratio [OR] for hospitalization associated with a 10 μg m− 3 increase in PM2.5 was 1.011 (95% credible interval [CI] = 1.011–1.012). The model identified congestive heart failure as having the strongest positive association with PM2.5 (OR = 1.019; 95%CI = 1.017–1.022). Some outcomes exhibited negative associations with PM2.5, including aortic dissection, subarachnoid and intracerebral hemorrhage, abdominal aneurysm, and essential hypertension; further research is needed to understand these counterintuitive findings. Supplementary materials for this article, including a standardized description of the materials available for reproducing the work, are available as an online supplement.

A Distributed Low-Cost Pollution Monitoring Platform

Personal exposure to heightened levels of fine airborne particulate matter (PM) has been linked to numerous adverse health effects in sensitive groups. However, researchers investigating these correlations are struggling to find the spatio-temporal datasets that are sufficient for study. Current airborne PM monitoring solutions are highly accurate, but expensive. Therefore, they are not feasible candidates for spatially dense deployments, and cannot be used to analyze the effects of exposure to pollution microclimates. In this article, we present a low-cost pollution monitoring station that operates as a single node in a wireless network. Each node periodically collects airborne pollution and supporting meteorological data and uploads measurements to a central, open-source database. A total of 50 nodes were deployed across a large metropolitan area (roughly 100 km2) over a six-month campaign. The experimental results show good correlation ( $R^{2}=0.88$ ) between devices co-located with the federal equivalent methods, which have an accuracy traceable to the National Institute of Standards and Technology. By applying linear corrections derived from in situ field measurements to each PM sensor, we were able to demonstrate a $1.8\times $ decrease in root-mean-squared error over the raw measurements.

PIXE and statistical analysis of fine airborne particulate matter (PM2.5) in Damascus

Air particulate matter (PM) samples were collected over the period from May 2017 to January 2018 for determination of chemical elements. Sampling campaign is realized in Damascus, the capital of Syria, and conducted twice per week. PM samples were taken as two size fractions (PM2.5 and PM2.5-10) using ISAP air sampler. The results showed that the mass concentrations for PM2.5 were higher than those for PM10-2.5. The overall mean mass concentrations were 32.48 ± 14 μg/m3 and 18.9 ± 10 μg/m3 for PM2.5 and PM10-2.5, respectively. The PM2.5 samples were subjected to PIXE analysis in order to determine the major (Ca, S, Si, Fe, Al, K, Mg and Na) and trace elements (Cl, Pb, Zn, Ti, P, Mn, Cu, Sr, Zr, Br, V and Ni). Elemental composition data were modelled using cluster analysis and principal component analysis to determine particle source categories contributing to the air pollution. The identified sources of PM2.5 were (1) resuspended soil characterized by high concentrations of Si, Al, Fe and Mg; (2) traffic source identified by the presence of Pb, Br, and S; (3) heavy oil combustion characterized by association between Ni and V; (4) a mixed industrial source; and (5) agriculture activities (K, Ca and P). The concentrations of elements initiated from anthropogenic sources are much lower than those induced naturally from earth’s crust.

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

The association between airborne fine particulate matter (PM2.5) concentration and the risk of respiratory diseases has been well documented by epidemiological studies. However, the mechanism underlying the harmful effect of PM2.5 has not been fully understood. In this study, we exposed the C57BL/6J mice to airborne PM2.5 for 3 months (mean daily concentration ~50 or ~110 μg/m3, defined as PM2.5–3L or PM2.5–3H) or 6 months (mean daily concentration ~50 μg/m3, defined as PM2.5–6L) through a whole-body exposure system. Histological and biochemical analysis revealed that PM2.5–3H exposure caused more severe lung injury than did PM2.5–3L, and the difference was greater than that of PM2.5–6L vs PM2.5–3L exposure. With RNA-sequencing technique, we found that the lungs exposed with different concentration of PM2.5 have distinct transcriptional profiles. PM2.5–3H exposure caused more differentially expressed genes (DEGs) in lungs than did PM2.5–3L or PM2.5–6L. The DEGs induced by PM2.5–3L or PM2.5–6L exposure were mainly enriched in immune pathways, including Hematopoietic cell lineage and Cytokine-cytokine receptor interaction, while the DEGs induced by PM2.5–3H exposure were mainly enriched in cardiovascular disease pathways, including Hypertrophic cardiomyopathy and Dilated cardiomyopathy. In addition, we found that upregulation of Cd5l and reduction of Hspa1 and peroxiredoxin-4 was associated with PM2.5-induced pulmonary inflammation and oxidative stress. These results may provide new insight into the cytotoxicity mechanism of PM2.5 and help to development of new strategies to attenuate air pollution associated respiratory disease.

Chemiluminescence of Oleic Acid Capped Black Phosphorus Quantum Dots for Highly Selective Detection of Sulfite in PM2.5.

Quantum dots (QDs), especially metal-free QDs with their unique optoelectronic properties, environmental friendliness, and excellent biocompatibility, have opened a new avenue to explore novel chemiluminescence (CL) systems for analytical applications. However, the unknown CL properties, relatively weak emission, and instability of some of them in water (e.g., black phosphorus QDs) often seriously hinder their further practical applications. Chemical modification trends have offered new properties for materials and have been proved to be desirable ways to establish sensing platforms with improved sensitivity and stability. Herein, oleic acid capped black phosphorus QDs (OA-BP QDs) with improved stability and optical properties were successfully synthesized. More importantly, an extraordinary CL emission when OA-BP QDs reacted with SO32- was first observed. In the CL process, OA-BP QDs acted as the catalyst to trigger singlet oxygen (1O2) generation in NaHSO3, and then a chemiluminescence resonance energy transfer (CRET) between (1O2)2* (1O2 dimeric aggregate) and OA-BP QDs was produced. On this basis, a new CL system for directly monitoring SO32- in airborne fine particulate matter (PM2.5) was fabricated. The study opens attractive perspectives of modified metal-free QDs for the practice of CL in monitoring the chemical species in PM2.5.

Identification of Sources from Chemical Characterization of Fine Particulate Matter and Assessment of Ambient Air Quality in Dhaka, Bangladesh

ABSTRACT Air pollution in Dhaka has drawn the attention of the government and the public over the past several decades, especially upon the discovery of Pb in the air. As a result, several policy interventions have been implemented to improve the air quality. Sampling for fine airborne particulate matter (PM2.5, PM with an aerodynamic diameter < 2.5 µm) has been conducted at a semi-residential site (AECD) in Dhaka since December 1996 using a GENT sampler. The retrieved samples were analyzed for their mass, black carbon (BC), and elemental compositions, and the resulting data set was analyzed for source identification via the Positive Matrix Factorization (PMF) technique. The identified sources are wood burning, soil dust, brick kilns, fugitive Pb, road dust, Zn sources, motor vehicles, and sea salt. The Government of Bangladesh is considering various interventions to reduce the emissions from these sources by promoting the replacement of diesel/petrol automobiles with CNG vehicles, increasing traffic speed in the city, and introducing green technologies for brick production. However, reducing the effect of transboundary contributions on the local air quality will necessitate regional measures as well.