Dataset Information

Household Air Pollution and Under-Five Mortality in Bangladesh (2004-2011).

ABSTRACT: Household air pollution (HAP) is one of the leading causes of respiratory illness and deaths among children under five years in Bangladesh. This study investigates the association between HAP from cooking fuel and under-five mortality using Bangladesh Demographic and Health Survey (BDHS) datasets over the period 2004-2011 (n = 18,308 children), and the extent to which this association differed by environmental and behavioral factors affecting level of exposure. The association between HAP and neonatal (age between 0-28 days), infant (age between 0 and 11 months) and under-five (age between 0 and 59 months) mortality was examined using multilevel logistic regression models. HAP was not strongly associated with overall neonatal (OR = 1.49, 95% CI = 1.01-2.22, p = 0.043), infant (OR = 1.27, 95% CI = 0.91-1.77, p = 0.157) or under-five mortality (OR = 1.14, 95% CI = 0.83-1.55, p = 0.422) in the context of overall decreasing trends in under-five mortality. The association was stronger for households with an indoor kitchen using polluting fuels, and in women who had never breastfed. Reductions in exposure to pollution from cooking fuel, given it is a ubiquitous and modifiable risk factor, can result in further declines in under-five mortality with household design and behavioural interventions.

SUBMITTER: Naz S

PROVIDER: S-EPMC4627003 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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Household Air Pollution and Under-Five Mortality in Bangladesh (2004-2011).

Naz Sabrina S Page Andrew A Agho Kingsley Emwinyore KE

International journal of environmental research and public health 20151015 10

Household air pollution (HAP) is one of the leading causes of respiratory illness and deaths among children under five years in Bangladesh. This study investigates the association between HAP from cooking fuel and under-five mortality using Bangladesh Demographic and Health Survey (BDHS) datasets over the period 2004-2011 (n = 18,308 children), and the extent to which this association differed by environmental and behavioral factors affecting level of exposure. The association between HAP and ne ...[more]

PMID: 26501296

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Project description:Household air pollution (HAP) arising from combustion of biomass fuel (BMF) is a leading cause of morbidity and mortality in low-income countries. Air pollution may stimulate pro-inflammatory responses by activating diverse immune cells and cyto/chemokine expression, thereby contributing to diseases. We aimed to study cellular immune responses among women chronically exposed to HAP through use of BMF for domestic cooking. Among 200 healthy, non-smoking women in rural Bangladesh, we assessed exposure to HAP by measuring particulate matter 2.5 (PM2.5), black carbon (BC) and carbon monoxide (CO), through use of personal monitors RTI MicroPEM™ and Lascar CO logger respectively, for 48 h. Blood samples were collected following HAP exposure assessment and were analyzed for immunoprofiling by flow cytometry, plasma IgE by immunoassay analyzer and cyto/chemokine response from monocyte-derived-macrophages (MDM) and -dendritic cells (MDDC) by multiplex immunoassay. In multivariate linear regression model, a doubling of PM2.5 was associated with small increments in immature/early B cells (CD19+CD38+) and plasmablasts (CD19+CD38+CD27+). In contrast, a doubling of CO was associated with 1.20% reduction in CD19+ B lymphocytes (95% confidence interval (CI) = -2.36, -0.01). A doubling of PM2.5 and BC each was associated with 3.12% (95%CI = -5.85, -0.38) and 4.07% (95%CI = -7.96, -0.17) decrements in memory B cells (CD19+CD27+), respectively. Exposure to CO was associated with increased plasma IgE levels (beta(β) = 240.4, 95%CI = 3.06, 477.8). PM2.5 and CO exposure was associated with increased MDM production of CXCL10 (β = 12287, 95%CI = 1038, 23536) and CCL5 (β = 835.7, 95%CI = 95.5, 1576), respectively. Conversely, BC exposure was associated with reduction in MDDC-produced CCL5 (β = -3583, 95%CI = -6358, -807.8) and TNF-α (β = -15521, 95%CI = -28968, -2074). Our findings suggest that chronic HAP exposure through BMF use adversely affects proportions of B lymphocytes, particularly memory B cells, plasma IgE levels and functions of antigen presenting cells in rural women.

Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 Âµg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.

Dataset Information

Household Air Pollution and Under-Five Mortality in Bangladesh (2004-2011).

Publications

Household Air Pollution and Under-Five Mortality in Bangladesh (2004-2011).

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