Exposure to Ambient Fine Particulate Air Pollution in Utero as a Risk Factor for Child Stunting in Bangladesh.
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SUBMITTER: Goyal N
PROVIDER: S-EPMC5800122 | biostudies-literature | 2017 Dec
REPOSITORIES: biostudies-literature
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Project description:Little is known about the effect of air pollution on the gastrointestinal (GI) system. We investigated the association between long-term exposures to outdoor fine particles (PM2.5) and hospitalization for peptic ulcer diseases (PUDs) in a large cohort of Hong Kong Chinese elderly.A total of 66,820 subjects aged ?65 years who were enrolled in all 18 Government Elderly Health Service centers of Hong Kong participated in the study voluntarily between 1998 and 2001. They were prospectively followed up for more than 10 years. Annual mean exposures to PM2.5 at residence of individuals were estimated by satellite data through linkage with address details including floor level. All hospital admission records of the subjects up to December 31, 2010 were retrieved from the central database of Hospital Authority. We used Cox regression to estimate the hazard ratio (HR) for PUD hospitalization associated with PM2.5 exposure after adjustment for individual and ecological covariates.A total of 60,273 subjects had completed baseline information including medical, socio-demographic, lifestyle, and anthropometric data at recruitment. During the follow-up period, 1991 (3.3%) subjects had been hospitalized for PUD. The adjusted HR for PUD hospitalization per 10??g/m of PM2.5 was 1.18 (95% confidence interval: 1.02-1.36, P?=?0.02). Further analysis showed that the associations with PM2.5 were significant for gastric ulcers (HR 1.29; 1.09-1.53, P?=?0.003) but not for duodenal ulcers (HR 0.98; 0.78 to 1.22, P?=?0.81).Long-term exposures to PM2.5 were associated with PUD hospitalization in elder population. The mechanism underlying the PM2.5 in the development of gastric ulcers warrants further research.
| S-EPMC4863781 | biostudies-literature
Project description:PurposeLong-term exposure to ambient fine particle (PM2.5) concentrations has been associated with an increased rate or risk of neurodegenerative conditions, but individual PM sources have not been previously examined in relation to neurodegenerative diseases.MethodsUsing the Statewide Planning and Research Cooperative System database, we studied 63,287 hospital admissions with a primary diagnosis of either Alzheimer's disease, dementia, or Parkinson's disease for New York State residents living within 15 miles from six PM2.5 monitoring sites. In addition to PM2.5 concentrations, we studied seven specific PM2.5 sources: secondary sulfate, secondary nitrate, biomass burning, diesel, spark-ignition emissions, pyrolyzed organic rich, and road dust. We estimated the rate of neurodegenerative hospital admissions associated with increased concentration of PM2.5 and individual PM2.5 sources average concentrations in the previous 0-29, 0-179, and 0-364 days.ResultsIncreases in ambient PM2.5 concentrations were not consistently associated with increased hospital admissions rates. Increased source-specific PM2.5 concentrations were associated with both increased (e.g., secondary sulfates and diesel emissions) and decreased rates (e.g., secondary nitrate and spark-ignition vehicular emissions) of neurodegenerative admissions.ConclusionsWe did not observe clear associations between overall ambient PM2.5 concentrations or source-apportioned ambient PM2.5 contributions and rates of neurologic disease hospitalizations.
| S-EPMC7796937 | biostudies-literature
Project description:Ambient particulate matter (PM) has been associated with mortality and morbidity for cardiovascular disease. MicroRNAs control gene expression at a posttranscriptional level. Altered microRNA expression has been reported in processes related to cardiovascular disease and PM exposure, such as systemic inflammation, endothelial dysfunction, and atherosclerosis. Polymorphisms in microRNA-related genes could influence response to PM.We investigated the association of exposure to ambient particles in several time windows (4-hour to 28-day moving averages) and blood leukocyte expression changes in 14 candidate microRNAs in 153 elderly males from the Normative Aging Study (examined 2005-2009). Potential effect modification by six single nucleotide polymorphisms (SNPs) in three microRNA-related genes was investigated. Fine PM (PM2.5), black carbon, organic carbon, and sulfates were measured at a stationary ambient monitoring site. Linear regression models, adjusted for potential confounders, were used to assess effects of particles and SNP-by-pollutant interaction. An in silico pathway analysis was performed on target genes of microRNAs associated with the pollutants.We found a negative association for pollutants in all moving averages and miR-1, -126, -135a, -146a, -155, -21, -222, and -9. The strongest associations were observed with the 7-day moving averages for PM2.5 and black carbon and with the 48-hour moving averages for organic carbon. The association with sulfates was stable across the moving averages. The in silico pathway analysis identified 18 pathways related to immune response shared by at least two microRNAs; in particular, the "high-mobility group protein B1/advanced glycosylation end product-specific receptor signaling pathway" was shared by miR-126, -146a, -155, -21, and -222. No important associations were observed for miR-125a-5p, -125b, -128, -147, -218, and -96. We found significant SNP-by-pollutant interactions for rs7813, rs910925, and rs1062923 in GEMIN4 and black carbon and PM2.5 for miR-1, -126, -146a, -222, and -9, and for rs1640299 in DGCR8 and SO4 for miR-1 and -135a.Exposure to ambient particles could cause a downregulation of microRNAs involved in processes related to PM exposure. Polymorphisms in GEMIN4 and DGCR8 could modify these associations.
| S-EPMC3977338 | 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:Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GRO? [growth-regulated protein ?], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNF? [tumor necrosis factor ?], IP-10 [interferon ?-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1?/? [macrophage inflammatory protein 1?/?], IL-6 [interleukin 6], and IL-1? [interleukin 1?]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.
| S-EPMC5215745 | 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:Fine particulate matter (PM2.5) air pollution and environmental temperatures influence cardiovascular morbidity and mortality. Recent evidence suggests that several air pollutants can promote dyslipidemia; however, the impact of ambient PM2.5 and temperature on high-density lipoprotein (HDL) function remains unclear. We hypothesized that daily exposures to higher levels of ambient PM2.5 and colder outdoor temperatures would impair HDL functionality. Lipoproteins, serum cholesterol efflux capacity (CEC), and HDL oxidation markers were measured twice in 50 healthy adults (age 32.1 ± 9.6 years) living in southeast Michigan and associated with ambient and personal-level exposures using mixed models. Although previous 7-day mean outdoor temperature (4.4 ± 9.8°C) and PM2.5 levels (9.1 ± 1.8 µg/m3) were low, higher ambient PM2.5 exposures (per 10 µg/m3) were associated with significant increases in the total cholesterol-to-HDL-C ratio (rolling average lag days 1 and 2) as well as reductions in CEC by -1.93% (lag day 5, p?=?0.022) and -1.62% (lag day 6, p?=?0.032). Colder outdoor temperatures (per 10°C) were also associated with decreases in CEC from -0.62 to -0.63% (rolling average lag days 5 and 7, p?=?0.027 and 0.028). Previous 24-hour personal-level PM2.5 and temperature exposures did not impact outcomes, nor were any exposures associated with changes in HDL-oxidation metrics. In conclusion, we provide the first evidence that ambient PM2.5 (even at low levels) and outdoor temperatures may influence serum CEC, a critical antiatherosclerotic HDL function.
| S-EPMC6133768 | biostudies-literature
Project description:ObjectiveTo quantitate the 2016 global and national burden of chronic kidney disease (CKD) attributable to ambient fine particulate matter air pollution ≤ 2.5 μm in aerodynamic diameter (PM2.5).DesignWe used the Global Burden of Disease (GBD) study data and methodologies to estimate the 2016 burden of CKD attributable to PM2.5 in 194 countries and territories. Population-weighted PM2.5 levels and incident rates of CKD for each country were curated from the GBD study publicly available data sources.SettingGBD global and national data on PM2.5 and CKD.Participants194 countries and territories.Main outcome measuresWe estimated the attributable burden of disease (ABD), years living with disability (YLD), years of life lost (YLL) and disability-adjusted life-years (DALYs).ResultsThe 2016 global burden of incident CKD attributable to PM2.5 was 6 950 514 (95% uncertainty interval: 5 061 533-8 914 745). Global YLD, YLL and DALYs of CKD attributable to PM2.5 were 2 849 311 (1 875 219-3 983 941), 8 587 735 (6 355 784-10 772 239) and 11 445 397 (8 380 246-14 554 091), respectively. Age-standardised ABD, YLL, YLD and DALY rates varied substantially among geographies. Populations in Mesoamerica, Northern Africa, several countries in the Eastern Mediterranean region, Afghanistan, Pakistan, India and several countries in Southeast Asia were among those with highest age-standardised DALY rates. For example, age-standardised DALYs per 100 000 were 543.35 (391.16-707.96) in El Salvador, 455.29 (332.51-577.97) in Mexico, 408.41 (283.82-551.84) in Guatemala, 238.25 (173.90-303.98) in India and 178.26 (125.31-238.47) in Sri Lanka, compared with 5.52 (0.82-11.48) in Sweden, 6.46 (0.00-14.49) in Australia and 12.13 (4.95-21.82) in Canada. Frontier analyses showed that Mesoamerican countries had significantly higher CKD DALY rates relative to other countries with comparable sociodemographic development.ConclusionsOur results demonstrate that the global toll of CKD attributable to ambient air pollution is significant and identify several endemic geographies where air pollution may be a significant driver of CKD burden. Air pollution may need to be considered in the discussion of the global epidemiology of CKD.
| S-EPMC6528010 | biostudies-literature
Project description:Air pollution may increase cardiovascular and respiratory risk through inflammatory pathways, but evidence for acute effects has been weak and indirect. Between December 2014 and July 2015, we enrolled 36 healthy, nonsmoking college students for a panel study in Shanghai, China, a city with highly variable levels of air pollution. We measured personal exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 ?m (PM2.5) continuously for 72 hours preceding each of 4 clinical visits that included phlebotomy. We measured 4 inflammation proteins and DNA methylation at nearby regulatory cytosine-phosphate-guanine (CpG) loci. We applied linear mixed-effect models to examine associations over various lag times. When results suggested mediation, we evaluated methylation as mediator. Increased PM2.5 concentration was positively associated with all 4 inflammation proteins and negatively associated with DNA methylation at regulatory loci for tumor necrosis factor alpha (TNF-?) and soluble intercellular adhesion molecule-1. A 10-?g/m3 increase in average PM2.5 during the 24 hours preceding blood draw corresponded to a 4.4% increase in TNF-? and a statistically significant decrease in methylation at one of the two studied candidate CpG loci for TNF-?. Epigenetics may play an important role in mediating effects of PM2.5 on inflammatory pathways.
| S-EPMC5860518 | biostudies-literature
Project description:BackgroundEpidemiological evidence suggests that exposure to ambient air fine particulate matter (PM2.5) increases the risk of developing type 2 diabetes and cardiovascular disease. However, the mechanisms underlying these effects of PM2.5 remain unclear.ObjectivesWe tested the hypothesis that PM2.5 exposure decreases vascular insulin sensitivity by inducing pulmonary oxidative stress.MethodsMice fed control (10-13% kcal fat) and high-fat (60% kcal fat, HFD) diets, treated with 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL) or mice overexpressing lung-specific extracellular superoxide dismutase (ecSOD) were exposed to HEPA-filtered air or to concentrated PM2.5 (CAP) for 9 or 30 days, and changes in systemic and organ-specific insulin sensitivity and inflammation were measured.ResultsIn control diet-fed mice, exposure to CAP for 30 days decreased insulin-stimulated Akt phosphorylation in lung, heart, and aorta but not in skeletal muscle, adipose tissue, and liver and did not affect adiposity or systemic glucose tolerance. In HFD-fed mice, 30-day CAP exposure suppressed insulin-stimulated endothelial nitric oxide synthase (eNOS) phosphorylation in skeletal muscle and increased adipose tissue inflammation and systemic glucose intolerance. In control diet-fed mice, a 9-day CAP exposure was sufficient to suppress insulin-stimulated Akt and eNOS phosphorylation and to decrease I?B? (inhibitor of the transcription factor NF-?B levels in the aorta. Treatment with the antioxidant TEMPOL or lung-specific overexpression of ecSOD prevented CAP-induced vascular insulin resistance and inflammation.ConclusionsShort-term exposure to PM2.5 induces vascular insulin resistance and inflammation triggered by a mechanism involving pulmonary oxidative stress. Suppression of vascular insulin signaling by PM2.5 may accelerate the progression to systemic insulin resistance, particularly in the context of diet-induced obesity. Citation: Haberzettl P, O'Toole TE, Bhatnagar A, Conklin DJ. 2016. Exposure to fine particulate air pollution causes vascular insulin resistance by inducing pulmonary oxidative stress. Environ Health Perspect 124:1830-1839;?http://dx.doi.org/10.1289/EHP212.
| S-EPMC5132639 | biostudies-literature