Exposure to Fine Particulate Matter Air Pollution Alters mRNA and miRNA Expression in Bone Marrow-Derived Endothelial Progenitor Cells from Mice.
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SUBMITTER: Li X
PROVIDER: S-EPMC8307414 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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:BackgroundExposure to ambient fine particulate matter air pollution (PM(2.5); < 2.5 µm in aerodynamic diameter) induces endothelial dysfunction and increases the risk for cardiovascular disease. Endothelial progenitor cells (EPCs) contribute to postnatal endothelial repair and regeneration. In humans and mice, EPC levels are decreased upon exposure to elevated levels of PM(2.5).ObjectiveWe examined the mechanism by which PM(2.5) exposure suppresses circulating levels of EPCs.MethodsMice were exposed to HEPA-filtered air or concentrated ambient fine particulate matter (CAP, 30-100 µg/m³) from downtown Louisville (Kentucky) air, and progenitor cells from peripheral blood or bone marrow were analyzed by flow cytometry or by culture ex vivo.ResultsExposure of the mice to CAP (6 hr/day) for 4-30 days progressively decreased circulating levels of EPCs positive for both Flk-1 and Sca-1 (Flk-1(+)/Sca-1(+)) without affecting stem cells positive for Sca-1 alone (Sca-1(+)). After 9 days of exposure, a 7-day exposure-free period led to complete recovery of the circulating levels of Flk-1(+)/Sca-1(+) cells. CAP exposure decreased circulating levels of EPCs independent of apoptosis while simultaneously increasing Flk-1(+)/Sca-1(+) cells in the bone marrow. We observed no change in tissue deposition of these cells. CAP exposure suppressed vascular endothelial growth factor (VEGF)-induced Akt and endothelial nitric oxide synthase (eNOS) phosphorylation in the aorta, and it prevented VEGF/AMD3100-induced mobilization of Flk-1(+)/Sca-1(+) cells into the peripheral blood. Treatment with stem cell factor/AMD3100 led to a greater increase in circulating Flk-1(+)/Sca-1(+) cells in CAP-exposed mice than in mice breathing filtered air.ConclusionExposure to PM(2.5) increases EPC levels in the bone marrow by preventing their mobilization to the peripheral blood via inhibition of signaling events triggered by VEGF-receptor stimulation that are upstream of c-kit activation. Suppression of EPC mobilization by PM(2.5) could induce deficits in vascular repair or regeneration.
| S-EPMC3385427 | biostudies-literature
Project description:Acute and chronic exposures to airborne particulate matter (PM) have been linked in epidemiological studies to a wide spectrum of cardiovascular disorders that are characterized by a dysfunctional endothelium. The pathophysiological mechanisms underlying these associations are unclear.To examine whether exposure to fine PM with an aerodynamic diameter of <2.5 microm (PM(2.5)) affects the circulating levels of endothelial progenitor cell (EPC) populations, systemic inflammation and coagulation.Phenotypically distinct EPC populations were quantified by flow cytometry in young (18 to 25 years) adult humans exposed to episodic increases in PM(2.5) along the Wasatch Mountain Front in Utah. In addition, Sca-1+/Flk-1+ cells were measured in the peripheral blood of mice exposed to concentrated particles from ambient air in Louisville, Ky. In both studies, PM exposure was negatively correlated with circulating EPC levels. In humans, statistically significant associations between PM(2.5) exposure and the plasma levels of platelet-monocyte aggregates, high-density lipoprotein, and nonalbumin protein were also observed. Episodic increases in PM(2.5) did not change plasma levels of C-reactive protein, interleukin-1beta, interleukin-6, fibrinogen, or serum amyloid A.Episodic exposure to PM(2.5) induces reversible vascular injury, reflected in part by depletion of circulating EPC levels, and increases in platelet activation and the plasma level of high-density lipoprotein. These changes were also accompanied by an increase in nonalbumin protein and may be related to mechanisms by which exposure to particulate air pollution increases the risk of cardiovascular disease and adverse cardiovascular events.
| S-EPMC2943671 | biostudies-literature
Project description:With 2.8 billion biomass users globally, household air pollution remains a public health threat in many low- and middle-income countries. However, little evidence on pollution levels and health effects exists in low-income settings, especially slums. This study assesses the levels and sources of household air pollution in the urban slums of Nairobi. This cross-sectional study was embedded in a prospective cohort of pregnant women living in two slum areas-Korogocho and Viwandani-in Nairobi. Data on fuel and stove types and ventilation use come from 1058 households, while air quality data based on the particulate matters (PM2.5) level were collected in a sub-sample of 72 households using the DustTrak™ II Model 8532 monitor. We measured PM2.5 levels mainly during daytime and using sources of indoor air pollutions. The majority of the households used kerosene (69.7%) as a cooking fuel. In households where air quality was monitored, the mean PM2.5 levels were high and varied widely, especially during the evenings (124.6 µg/m³ SD: 372.7 in Korogocho and 82.2 µg/m³ SD: 249.9 in Viwandani), and in households using charcoal (126.5 µg/m³ SD: 434.7 in Korogocho and 75.7 µg/m³ SD: 323.0 in Viwandani). Overall, the mean PM2.5 levels measured within homes at both sites (Korogocho = 108.9 µg/m³ SD: 371.2; Viwandani = 59.3 µg/m³ SD: 234.1) were high. Residents of the two slums are exposed to high levels of PM2.5 in their homes. We recommend interventions, especially those focusing on clean cookstoves and lighting fuels to mitigate indoor levels of fine particles.
| S-EPMC5606663 | biostudies-literature
Project description:BackgroundExposure to fine particulate matter (PM2.5) air pollution has been linked to increased risk of mortality, especially cardiopulmonary and lung cancer mortality. It is unknown if cancer patients and survivors are especially vulnerable to PM2.5 air pollution exposure. This study evaluates PM2.5 exposure and risk for cancer and cardiopulmonary mortality in cohorts of US cancer patients and survivors.MethodsA primary cohort of 5 591 168 of cancer patients and a 5-year survivor cohort of 2 318 068 was constructed using Surveillance, Epidemiology, and End Results Program data from 2000 to 2016, linked with county-level estimates of long-term average concentrations of PM2.5. Cox proportional hazards models were used to estimate PM2.5-mortality hazard ratios controlling for age-sex-race combinations and individual and county-level covariables.ResultsOf those who died, 26% died of noncancer causes, mostly from cardiopulmonary disease. Minimal PM2.5-mortality associations were observed for all-cause mortality (hazard ratio [HR] = 1.01, 95% confidence interval [CI] = 1.00 to 1.03) per 10 µg/m3 increase in PM2.5. Substantial adverse PM2.5-mortality associations were observed for cardiovascular (HR = 1.32, 95% CI = 1.26 to 1.39), chronic obstructive pulmonary disease (HR = 1.10, 95% CI = 1.01 to 1.20), influenza and pneumonia (HR = 1.55, 95% CI = 1.33 to 1.80), and cardiopulmonary mortality combined (HR = 1.25, 95% CI = 1.21 to 1.30). PM2.5-cardiopulmonary mortality hazard ratio was higher for cancer patients who received chemotherapy or radiation treatments.ConclusionsAir pollution is adversely associated with cardiopulmonary mortality for cancer patients and survivors, especially those who received chemotherapy or radiation treatment. Given ubiquitous and involuntary air pollution exposures and large numbers of cancer patients and survivors, these results are of substantial clinical and public health importance.
| S-EPMC7898081 | biostudies-literature
Project description:Recent studies suggest an association between particulate matter (PM) air pollution and gastrointestinal (GI) disease. In addition to direct deposition, PM can be indirectly deposited in oropharynx via mucociliary clearance and upon swallowing of saliva and mucus. Within the GI tract, PM may alter the GI epithelium and gut microbiome. Our goal was to determine the effect of PM on gut microbiota in a murine model of PM exposure via inhalation. C57BL/6 mice were exposed via inhalation to either concentrated ambient particles or filtered air for 8-h per day, 5-days a week, for a total of 3-weeks. At exposure's end, GI tract tissues and feces were harvested, and gut microbiota was analyzed. Alpha-diversity was modestly altered with increased richness in PM-exposed mice compared to air-exposed mice in some parts of the GI tract. Most importantly, PM-induced alterations in the microbiota were very apparent in beta-diversity comparisons throughout the GI tract and appeared to increase from the proximal to distal parts. Changes in some genera suggest that distinct bacteria may have the capacity to bloom with PM exposure. Exposure to PM alters the microbiota throughout the GI tract which maybe a potential mechanism that explains PM induced inflammation in the GI tract.
| S-EPMC6400491 | biostudies-literature
Project description:BACKGROUND:Air pollution is a carcinogen and causes pulmonary and cardiac complications. We examined the association of fine particulate matter pollution (PM2.5) and mortality from cancer and all causes among pediatric, adolescent, and young adult (AYA) patients with cancer in Utah, a state with considerable variation in PM2.5. METHODS:We followed 2,444 pediatric (diagnosed ages 0-14) and 13,459 AYA (diagnosed ages 15-39) patients diagnosed in 1986-2015 from diagnosis to 5 and 10 years postdiagnosis, death, or emigration. We measured average monthly PM2.5 by ZIP code during follow-up. Separate pediatric and AYA multivariable Cox models estimated the association of PM2.5 and mortality. Among AYAs, we examined effect modification of PM2.5 and mortality by stage while controlling for cancer type. RESULTS:Increases in PM2.5 per 5 μg/m3 were associated with cancer mortality in pediatric lymphomas and central nervous system (CNS) tumors at both time points, and all cause mortality in lymphoid leukemias [HR5-year = 1.32 (1.02-1.71)]. Among AYAs, PM2.5 per 5 μg/m3 was associated with cancer mortality in CNS tumors and carcinomas at both time points, and all cause mortality for all AYA cancer types [HR5-year = 1.06 (1.01-1.13)]. PM2.5 ≥12 μg/m3 was associated with cancer mortality among breast [HR5-year = 1.50 (1.29-1.74); HR10-year = 1.30 (1.13-1.50)] and colorectal cancers [HR5-year = 1.74 (1.29-2.35); HR10-year = 1.67 (1.20-2.31)] at both time points. Effect modification by stage was significant, with local tumors at highest risk. CONCLUSIONS:PM2.5 was associated with mortality in pediatric and AYA patients with specific cancers. IMPACT:Limiting PM2.5 exposure may be important for young cancer patients with certain cancers.See all articles in this CEBP Focus section, "Environmental Carcinogenesis: Pathways to Prevention."
| S-EPMC7541555 | 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 ?m (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:Exposure to fine particulate matter (PM2.5 ) air pollution increases blood pressure, induces vascular inflammation and dysfunction, and augments atherosclerosis in humans and rodents; however, the understanding of early changes that foster chronic vascular disease is incomplete. Because perivascular adipose tissue (PVAT) inflammation is implicated in chronic vascular diseases, we investigated changes in aortic PVAT following short-term air pollution exposure. Mice were exposed to HEPA-filtered or concentrated ambient PM2.5 (CAP) for 9 consecutive days, and the abundance of inflammatory, adipogenic, and adipokine gene mRNAs was measured by gene array and qRT-PCR in thoracic aortic PVAT. Responses of the isolated aorta with and without PVAT to contractile (phenylephrine, PE) and relaxant agonists (acetylcholine, ACh; sodium nitroprusside, SNP) were measured. Exposure to CAP significantly increased the urinary excretion of acrolein metabolite (3HPMA) as well as the abundance of protein-acrolein adducts (a marker of oxidative stress) in PVAT and aorta, upregulated PVAT leptin mRNA expression without changing mRNA levels of several proinflammatory genes, and induced PVAT insulin resistance. In control mice, PVAT significantly depressed PE-induced contractions-an effect that was dampened by CAP exposure. Pulmonary overexpression of extracellular dismutase (ecSOD-Tg) prevented CAP-induced effects on urinary 3HPMA levels, PVAT Lep mRNA, and alterations in PVAT and aortic function, reflecting a necessary role of pulmonary oxidative stress in all of these deleterious CAP-induced changes. More research is needed to address how exactly short-term exposure to PM2.5 perturbs PVAT and aortic function, and how these specific genes and functional changes in PVAT could lead over time to chronic inflammation, endothelial dysfunction, and atherosclerosis.
| S-EPMC8322754 | biostudies-literature