Dataset Information

The association of early-life exposure to ambient PM_2.5 and later-childhood height-for-age in India: an observational study.

ABSTRACT:

Background

Children in India are exposed to high levels of ambient fine particulate matter (PM_2.5). However, population-level evidence of associations with adverse health outcomes from within the country is limited. The aim of our study is to estimate the association of early-life exposure to ambient PM_2.5 with child health outcomes (height-for-age) in India.

Methods

We linked nationally-representative anthropometric data from India's 2015-2016 Demographic and Health Survey (n?=?218,152 children under five across 640 districts of India) with satellite-based PM_2.5 exposure (concentration) data. We then applied fixed effects regression to assess the association between early-life ambient PM_2.5 and subsequent height-for-age, analyzing whether deviations in air pollution from the seasonal average for a particular place are associated with deviations in child height from the average for that season in that place, controlling for trends over time, temperature, and birth, mother, and household characteristics. We also explored the timing of exposure and potential non-linearities in the concentration-response relationship.

Results

Children in the sample were exposed to an average of 55 ? g/m³ of PM_2.5 in their birth month. After controlling for potential confounders, a 100??g/m³ increase in PM_2.5 in the month of birth was associated with a 0.05 [0.01-0.09] standard deviation reduction in child height. For an average 5 year old girl, this represents a height deficit of 0.24 [0.05-0.43] cm. We also found that exposure to PM_2.5 in the last trimester in utero and in the first few months of life are significantly (p?ConclusionsIndia experiences some of the worst air pollution in the world. To our knowledge, this is the first study to estimate the association of early-life exposure to ambient PM_2.5 on child height-for-age at the range of ambient pollution exposures observed in India. Because average exposure to ambient PM_2.5 is high in India, where child height-for-age is a critical challenge in human development, our results highlight ambient air pollution as a public health policy priority.

SUBMITTER: Spears D

PROVIDER: S-EPMC6617650 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Publications

The association of early-life exposure to ambient PM<sub>2.5</sub> and later-childhood height-for-age in India: an observational study.

Spears Dean D Dey Sagnik S Chowdhury Sourangsu S Scovronick Noah N Vyas Sangita S Apte Joshua J

Environmental health : a global access science source 20190709 1

<h4>Background</h4>Children in India are exposed to high levels of ambient fine particulate matter (PM<sub>2.5</sub>). However, population-level evidence of associations with adverse health outcomes from within the country is limited. The aim of our study is to estimate the association of early-life exposure to ambient PM<sub>2.5</sub> with child health outcomes (height-for-age) in India.<h4>Methods</h4>We linked nationally-representative anthropometric data from India's 2015-2016 Demographic an ...[more]

PMID: 31288809

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Project description:BackgroundStudies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.MethodsA total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β HSD), 17β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).ResultsExposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.ConclusionConcentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.

Project description:Anemia is highly prevalent in India, especially in children. Exposure to ambient fine particulate matter (PM2.5) is a potential risk factor for anemia via. systemic inflammation. Using health data from the National Family and Health Survey 2015-2016, we examined the association between ambient PM2.5 exposure and anemia in children under five across India through district-level ecological and individual-level analyses.MethodsThe ecological analysis assessed average hemoglobin levels and anemia prevalence (hemoglobin < 11 g/dL considered anemic) by district using multiple linear regression models. The individual-level analysis assessed average individual hemoglobin level and anemia status (yes/no) using generalized linear mixed models to account for clustering by district. Ambient PM2.5 exposure data were derived from the Multiangle Imaging SpectroRadiometer (MISR) level 2 aerosol optical depth (AOD) data and averaged from birth date to date of interview.ResultsThe district-level ecological analysis found that, for every 10 μg m-3 increase in ambient PM2.5 exposure, average anemia prevalence increased by 1.90% (95% CI = 1.43, 2.36) and average hemoglobin decreased by 0.07 g/dL (95% CI = 0.09, 0.05). At the individual level, for every 10 μg m-3 increase in ambient PM2.5 exposure, average hemoglobin decreased by 0.14 g/dL (95% CI = 0.12, 0.16). The odds ratio associated with a 10-μg m-3 increase in ambient PM2.5 exposure was 1.09 (95% CI = 1.06, 1.11). There was evidence of effect modification by wealth index, maternal anemia status, and child BMI.ConclusionOur results suggest that ambient PM2.5 exposure could be linked to anemia in Indian children, although additional research on the underlying biologic mechanisms is needed. Future studies on this association should specifically consider interactions with dietary iron deficiency, maternal anemia status, and child BMI.Keywords: Anemia; Children; Ambient PM2.5 exposure; India; Association.

Project description:India is currently experiencing degraded air quality, and future economic development will lead to challenges for air quality management. Scenarios of sectoral emissions of fine particulate matter and its precursors were developed and evaluated for 2015-2050, under specific pathways of diffusion of cleaner and more energy-efficient technologies. The impacts of individual source sectors on PM2.5 concentrations were assessed through systematic simulations of spatially and temporally resolved particulate matter concentrations, using the GEOS-Chem model, followed by population-weighted aggregation to national and state levels. We find that PM2.5 pollution is a pan-India problem, with a regional character, and is not limited to urban areas or megacities. Under present-day emissions, levels in most states exceeded the national PM2.5 annual standard (40 μg m-3). Sources related to human activities were responsible for the largest proportion of the present-day population exposure to PM2.5 in India. About 60 % of India's mean population-weighted PM2.5 concentrations come from anthropogenic source sectors, while the remainder are from "other" sources, windblown dust and extra-regional sources. Leading contributors are residential biomass combustion, power plant and industrial coal combustion and anthropogenic dust (including coal fly ash, fugitive road dust and waste burning). Transportation, brick production and distributed diesel were other contributors to PM2.5. Future evolution of emissions under regulations set at current levels and promulgated levels caused further deterioration of air quality in 2030 and 2050. Under an ambitious prospective policy scenario, promoting very large shifts away from traditional biomass technologies and coal-based electricity generation, significant reductions in PM2.5 levels are achievable in 2030 and 2050. Effective mitigation of future air pollution in India requires adoption of aggressive prospective regulation, currently not formulated, for a three-pronged switch away from (i) biomass-fuelled traditional technologies, (ii) industrial coal-burning and (iii) open burning of agricultural residue. Future air pollution is dominated by industrial process emissions, reflecting larger expansion in industrial, rather than residential energy demand. However, even under the most active reductions envisioned, the 2050 mean exposure, excluding any impact from windblown mineral dust, is estimated to be nearly 3 times higher than the WHO Air Quality Guideline.

Project description:BackgroundThe metabolomic signatures of short- and long-term exposure to PM2.5 have been reported and linked to inflammation and oxidative stress. However, little is known about the relative contribution of the specific PM2.5 species (hence sources) that drive these metabolomic signatures.ObjectivesWe aimed to determine the relative contribution of the different species of PM2.5 exposure to the perturbed metabolic pathways related to changes in the plasma metabolome.MethodsWe performed mass-spectrometry based metabolomic profiling of plasma samples among men from the Normative Aging Study to identify metabolic pathways associated with PM2.5 species. The exposure windows included short-term (one, seven-, and thirty-day moving average) and long-term (one year moving average). We used linear mixed-effect regression with subject-specific intercepts while simultaneously adjusting for PM2.5, NO2, O3, temperature, relative humidity, and covariates and correcting for multiple testing. We also used independent component analysis (ICA) to examine the relative contribution of patterns of PM2.5 species.ResultsBetween 2000 and 2016, 456 men provided 648 blood samples, in which 1158 metabolites were quantified. We chose 305 metabolites for the short-term and 288 metabolites for the long-term exposure in this analysis that were significantly associated (p-value < 0.01) with PM2.5 to include in our PM2.5 species analysis. On average, men were 75.0 years old and their body mass index was 27.7 kg/m2. Only 3% were current smokers. In the adjusted models, ultrafine particles (UFPs) were the most significant species of short-term PM2.5 exposure followed by nickel, vanadium, potassium, silicon, and aluminum. Black carbon, vanadium, zinc, nickel, iron, copper, and selenium were the significant species of long-term PM2.5 exposure. We identified several metabolic pathways perturbed with PM2.5 species including glycerophospholipid, sphingolipid, and glutathione. These pathways are involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair. Results were overlapped with the ICA.ConclusionsWe identified several significant perturbed plasma metabolites and metabolic pathways associated with exposure to PM2.5 species. These species are associated with traffic, fuel oil, and wood smoke. This is the largest study to report a metabolomic signature of PM2.5 species' exposure and the first to use ICA.

Project description:Previous studies have shown that long-term exposure to fine particulate matter (PM2.5) increases the morbidity and mortality of pulmonary diseases such as asthma, chronic obstructive pulmonary disease and pulmonary emphysema. Oxidative stress and inflammation play key roles in pulmonary damage caused by PM2.5. Nuclear factor erythroid 2-related factor 2 (Nrf2) could regulate the expression of antioxidant and anti-inflammatory genes and is pivotal for protection against PM2.5-induced oxidative stress. In this study, a real-ambient exposure system was constructed with the outdoor ambient air in north China. Wild-type (WT) and Nrf2-/- (KO) mice were exposed to the real-ambient system for six weeks. After PM2.5 exposure, our data showed that the levels of inflammatory factors and malondialdehyde were significantly increased in WT and KO mice. Moreover, the lung function and pathological phenotype of the WT mice were altered but there was no obvious change in the Nrf2-/- mice. To further explore the potential molecular mechanisms, we performed RNA-sequencing. The RNA-sequence analysis results showed that the CYP450 pathway in the first ten pathways of KEGG was related to the metabolism of PM2.5. In WT and KO mice, the expression of CYP2E1 in the CYP450 pathway showed opposite trends after PM2.5 exposure. The data showed that the expression of the CYP2E1 gene in WT-PM mice increased while it decreased in KO-PM; the expression of the CYP2E1 protein showed a similar trend. CYP2E1 is primarily distributed in the endoplasmic reticulum (ER) where it could metabolize various exogenous substances attached to PM2.5 and produce highly toxic oxidation products closely related to ER stress. Consistently, the expression level of GRP94, a biomarker of ER stress, was increased in WT mice and reduced in KO mice under PM2.5 exposure. Persistent ER stress is a mechanism that causes lung damage under PM2.5 exposure. Nrf2 facilitates lung injury during PM2.5 exposure and CYP2E1 metabolism is involved in this process.

Dataset Information

The association of early-life exposure to ambient PM_2.5 and later-childhood height-for-age in India: an observational study.

Background

Methods

Results

Publications

The association of early-life exposure to ambient PM<sub>2.5</sub> and later-childhood height-for-age in India: an observational study.

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Dataset Information

The association of early-life exposure to ambient PM2.5 and later-childhood height-for-age in India: an observational study.

Background

Methods

Results

Publications

The association of early-life exposure to ambient PM<sub>2.5</sub> and later-childhood height-for-age in India: an observational study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

The association of early-life exposure to ambient PM_2.5 and later-childhood height-for-age in India: an observational study.