Dataset Information

Exposure to Ambient Fine Particulate Air Pollution in Utero as a Risk Factor for Child Stunting in Bangladesh.

ABSTRACT: Pregnant mothers in Bangladesh are exposed to very high and worsening levels of ambient air pollution. Maternal exposure to fine particulate matter has been associated with low birth weight at much lower levels of exposure, leading us to suspect the potentially large effects of air pollution on stunting in children in Bangladesh. We estimate the relationship between exposure to air pollution in utero and child stunting by pooling outcome data from four waves of the nationally representative Bangladesh Demographic and Health Survey conducted between 2004 and 2014, and calculating children's exposure to ambient fine particulate matter in utero using high resolution satellite data. We find significant increases in the relative risk of child stunting, wasting, and underweight with higher levels of in utero exposure to air pollution, after controlling for other factors that have been found to contribute to child anthropometric failure. We estimate the relative risk of stunting in the second, third, and fourth quartiles of exposure as 1.074 (95% confidence interval: 1.014-1.138), 1.150 (95% confidence interval: 1.069-1.237, and 1.132 (95% confidence interval: 1.031-1.243), respectively. Over half of all children in Bangladesh in our sample were exposed to an annual ambient fine particulate matter level in excess of 46 µg/m³; these children had a relative risk of stunting over 1.13 times that of children in the lowest quartile of exposure. Reducing air pollution in Bangladesh could significantly contribute to the Sustainable Development Goal of reducing child stunting.

SUBMITTER: Goyal N

PROVIDER: S-EPMC5800122 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Exposure to Ambient Fine Particulate Air Pollution in Utero as a Risk Factor for Child Stunting in Bangladesh.

Goyal Nihit N Canning David D

International journal of environmental research and public health 20171223 1

Pregnant mothers in Bangladesh are exposed to very high and worsening levels of ambient air pollution. Maternal exposure to fine particulate matter has been associated with low birth weight at much lower levels of exposure, leading us to suspect the potentially large effects of air pollution on stunting in children in Bangladesh. We estimate the relationship between exposure to air pollution in utero and child stunting by pooling outcome data from four waves of the nationally representative Bang ...[more]

PMID: 29295507

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Project description:ImportanceIncreased levels of ambient fine particulate matter (PM2.5) air pollution are associated with increased risks for detrimental health outcomes, but risks for patients with kidney transplants (KTs) remain unknown.ObjectiveTo investigate the association of PM2.5 exposure with KT outcomes.Design, setting, and participantsThis retrospective cohort study was conducted using data on patients who received KTs from 2004 to 2016 who were identified in the national US transplant registry and followed up through March 2021. Multiple databases were linked to obtain data on PM2.5 concentration, KT outcomes, and patient clinical, transplant, and contextual factors. Data were analyzed from April 2020 through July 2021.ExposuresExposures included post-KT time-dependent annual mean PM2.5 level (in 10 μg/m3) and mean PM2.5 level in the year before KT (ie, baseline levels) in quartiles, as well as baseline annual mean PM2.5 level (in 10 μg/m3).Main outcomes and measuresAcute kidney rejection (ie, rejection within 1 year after KT), time to death-censored graft failure, and time to all-cause death. Multivariable logistic regression for kidney rejection and Cox analyses with nonlinear assessment of exposure-response for death-censored graft failure and all-cause death were performed. The national burden of graft failure associated with PM2.5 levels greater than the Environmental Protection Agency recommended level of 12 μg/m3 was estimated.ResultsAmong 112 098 patients with KTs, 70 522 individuals (62.9%) were older than age 50 years at the time of KT, 68 117 (60.8%) were men, and the median (IQR) follow-up was 6.0 (3.9-8.9) years. There were 37 265 Black patients (33.2%), 17 047 Hispanic patients (15.2%), 48 581 White patients [43.3%]), and 9205 patients (8.2%) of other race or ethnicity. The median (IQR) baseline PM2.5 level was 9.8 (8.3-11.9) μg/m3. Increased baseline PM2.5 level, compared with quartile 1 baseline PM2.5 level, was not associated with higher odds of acute kidney rejection for quartile 2 (adjusted odds ratio [aOR], 0.99; 95% CI, 0.92-1.06) but was associated with increased odds for quartile 3 (aOR, 1.11; 95% CI, 1.04-1.20) and quartile 4 (aOR, 1.13; 95% CI, 1.05-1.23). Nonlinear assessment of exposure-response for graft failure and death showed no evidence for nonlinearity. Increased PM2.5 levels were associated with increased risk of death-censored graft failure (adjusted hazard ratio [aHR] per 10 μg/m3 increase, 1.17; 95% CI, 1.09-1.25) and all-cause death (aHR per 10 μg/m3 increase, 1.21; 95% CI, 1.14-1.28). The national burden of death-censored graft failure associated with PM2.5 above 12 μg/m3 was 57 failures (95% uncertainty interval, 48-67 failures) per year among patients with KTs.Conclusions and relevanceThis cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with KTs. These findings suggest that efforts toward decreasing levels of PM2.5 concentration may be associated with improved outcomes after KT.

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.

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.

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.

Dataset Information

Exposure to Ambient Fine Particulate Air Pollution in Utero as a Risk Factor for Child Stunting in Bangladesh.

Publications

Exposure to Ambient Fine Particulate Air Pollution in Utero as a Risk Factor for Child Stunting in Bangladesh.

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