Dataset Information

Infant Mortality Related to NO2 and PM Exposure: Systematic Review and Meta-Analysis.

ABSTRACT: Background: We conducted this systematic review and meta-analysis to address the crucial public health issue of the suspected association between air pollution exposure during pregnancy and the risk of infant mortality. Methods: We searched on MEDLINE ® databases among articles published until February, 2019 for case-control, cohort, and ecological studies assessing the association between maternal exposure to Nitrogen Dioxide (NO2) or Particular matter (PM) and the risk of infant mortality including infant, neonatal, and post-neonatal mortality for all-and specific-causes as well. Study-specific risk estimates were pooled according to random-effect and fixed-effect models. Results: Twenty-four articles were included in the systematic review and 14 of the studies were taken into account in the meta-analysis. We conducted the meta-analysis for six combinations of air pollutants and infant death when at least four studies were available for the same combination. Our systematic review has revealed that the majority of studies concluded that death risk increased with increased exposure to air pollution including PM10, PM2.5, and NO2. Our meta-analysis confirms that the risk of post-neonatal mortality all-causes for short-term exposure to PM10 increased significantly (pooled-OR = 1.013, 95% CI (1.002, 1.025). When focusing on respiratory-causes, the risk of post-neonatal death related to long-term exposure to PM10 reached a pooled-OR = 1.134, 95% CI (1.011, 1.271). Regarding Sudden Infant Death Syndrome (SIDS), the risk also increased significantly: pooled-OR = 1.045, 95% CI (1.01, 1.08) per 10 µg/m3), but no specific gestational windows of exposure were identified. Conclusion: In spite of a few number of epidemiological studies selected in the present literature review, our finding is in favor of a significant increase of infant death with the increase of air pollution exposure during either the pregnancy period or the first year of a newborn's life. Our findings have to be interpreted with caution due to weaknesses that could affect the strength of the associations and then the formulation of accurate conclusions. Future studies are called to overcome these limitations; in particular, (i) the definition of infant adverse outcome, (ii) exposure assessment, and (iii) critical windows of exposure, which could affect the strength of association.

SUBMITTER: Kihal-Talantikite W

PROVIDER: S-EPMC7215927 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundExposure to triclosan, an antimicrobial chemical used in some personal care and cleaning products, has been associated with reduced birth weight in some, but not all epidemiological studies.ObjectivesWe conducted a systematic review and meta-analysis to characterize the relation of gestational triclosan exposure with infant birth weight and identify sources of heterogeneity between studies.MethodsWe identified original studies measuring urinary triclosan concentrations during pregnancy and reporting their association with infant birth weight, gestational age (GA) adjusted birth weight (g), or GA-standardized birth weight z-scores. Using a random effects model, we estimated differences in these outcomes per 10-fold increase in triclosan concentrations and considered triclosan levels and infant sex as sources of heterogeneity. Using Navigation Guide Methods, we evaluated risk of bias within individual studies and across the body of evidence.ResultsAmong thirteen studies, median triclosan concentrations varied by almost 2-orders of magnitude (0.6-29 ng/mL), with higher concentrations in North American and some European studies compared to Asian ones. Associations between triclosan and birth weight (β:-20 g; 95% CI:-65, 26; n = 6) were stronger than those for GA-adjusted birth weight (β:-12 g; 95% CI:-29, 5; n = 9). Triclosan was not associated with GA-standardized birth weight z-scores (β:-0.04; 95% CI:-0.16, 0.07; n = 5). The association between triclosan and GA-adjusted birth weight was stronger in studies with median triclosan values ≥10 ng/mL compared to studies with median values < 10 ng/mL (β:-27 g; 95% CI:-61, 7; n = 4 vs. β:6g; 95% CI:-20, 31; n = 5). With a limited number of studies, we observed suggestive evidence that inverse associations were more apparent in studies with ≥ 2 prospective triclosan measures compared to those with one measure.DiscussionAvailable evidence, with "low" risk of bias, provides limited evidence that triclosan exposure and reduces infant birth weight. We observed stronger inverse associations between triclosan concentrations and birth weight in populations with higher triclosan exposure.

Project description:ObjectivesA systematic review was conducted in high-income country settings to analyse: (i) spina bifida neonatal and IMRs over time, and (ii) clinical and socio-demographic factors associated with mortality in the first year after birth in infants affected by spina bifida.Data sourcesPubMed, Embase, Ovid, Web of Science, CINAHL, Scopus and the Cochrane Library were searched from 1st January, 1990 to 31st August, 2020 to review evidence.Study selectionPopulation-based studies that provided data for spina bifida infant mortality and case fatality according to clinical and socio-demographical characteristics were included. Studies were excluded if they were conducted solely in tertiary centres. Spina bifida occulta or syndromal spina bifida were excluded where possible.Data extraction and synthesisIndependent reviewers extracted data and assessed their quality using MOOSE guideline. Pooled mortality estimates were calculated using random-effects (+/- fixed effects) models meta-analyses. Heterogeneity between studies was assessed using the Cochrane Q test and I2 statistics. Meta-regression was performed to examine the impact of year of birth cohort on spina bifida infant mortality.ResultsTwenty studies met the full inclusion criteria with a total study population of over 30 million liveborn infants and approximately 12,000 spina bifida-affected infants. Significant declines in spina bifida associated infant and neonatal mortality rates (e.g. 4.76% decrease in IMR per 100, 000 live births per year) and case fatality (e.g. 2.70% decrease in infant case fatality per year) were consistently observed over time. Preterm birth (RR 4.45; 2.30-8.60) and low birthweight (RR 4.77; 2.67-8.55) are the strongest risk factors associated with increased spina bifida infant case fatality.SignificanceSignificant declines in spina bifida associated infant/neonatal mortality and case fatality were consistently observed, advances in treatment and mandatory folic acid food fortification both likely play an important role. Particular attention is warranted from clinicians caring for preterm and low birthweight babies affected by spina bifida.

Project description:Prenatal exposure to air pollution is considered to be associated with adverse effects on child health. This may partly be mediated by mechanisms related to DNA methylation.We investigated associations between exposure to air pollution, using nitrogen dioxide (NO2) as marker, and epigenome-wide cord blood DNA methylation.We meta-analyzed the associations between NO2 exposure at residential addresses during pregnancy and cord blood DNA methylation (Illumina 450K) in four European and North American studies (n = 1,508) with subsequent look-up analyses in children ages 4 (n = 733) and 8 (n = 786) years. Additionally, we applied a literature-based candidate approach for antioxidant and anti-inflammatory genes. To assess influence of exposure at the transcriptomics level, we related mRNA expression in blood cells to NO2 exposure in 4- (n = 111) and 16-year-olds (n = 239).We found epigenome-wide significant associations [false discovery rate (FDR) p < 0.05] between maternal NO2 exposure during pregnancy and DNA methylation in newborns for 3 CpG sites in mitochondria-related genes: cg12283362 (LONP1), cg24172570 (3.8 kbp upstream of HIBADH), and cg08973675 (SLC25A28). The associations with cg08973675 methylation were also significant in the older children. Further analysis of antioxidant and anti-inflammatory genes revealed differentially methylated CpGs in CAT and TPO in newborns (FDR p < 0.05). NO2 exposure at the time of biosampling in childhood had a significant impact on CAT and TPO expression.NO2 exposure during pregnancy was associated with differential offspring DNA methylation in mitochondria-related genes. Exposure to NO2 was also linked to differential methylation as well as expression of genes involved in antioxidant defense pathways. Citation: Gruzieva O, Xu CJ, Breton CV, Annesi-Maesano I, Antó JM, Auffray C, Ballereau S, Bellander T, Bousquet J, Bustamante M, Charles MA, de Kluizenaar Y, den Dekker HT, Duijts L, Felix JF, Gehring U, Guxens M, Jaddoe VV, Jankipersadsing SA, Merid SK, Kere J, Kumar A, Lemonnier N, Lepeule J, Nystad W, Page CM, Panasevich S, Postma D, Slama R, Sunyer J, Söderhäll C, Yao J, London SJ, Pershagen G, Koppelman GH, Melén E. 2017. Epigenome-wide meta-analysis of methylation in children related to prenatal NO2 air pollution exposure. Environ Health Perspect 125:104-110;?http://dx.doi.org/10.1289/EHP36.

Project description:BackgroundAmbient air pollution is among the greatest environmental risks to human health. However, little is known about the health effects of nitrogen dioxide (NO2), a traffic-related air pollutant. Herein, we aimed to conduct a meta-analysis to investigate the long-term effects of NO2 on mortality.MethodsWe conducted a systematic search for studies that were published up to February 2020 and performed a meta-analysis of all available epidemiologic studies evaluating the associations between long-term exposure to NO2 with all-cause, cardiovascular, and respiratory mortality. Overall pooled effect estimates as well as subgroup-specific pooled estimates (e.g. location, exposure assessment method, exposure metric, study population, age at recruitment, and key confounder adjustment) and 95% confidence intervals were calculated using random-effects models. Risk of bias assessment was accessed by following WHO global air quality guidelines. Publication bias was accessed by visually inspecting funnel plot and Egger's liner regression was used to test of asymmetry.ResultsOur search initially retrieved 1349 unique studies, of which 34 studies met the inclusion criteria. The pooled hazard ratio (HR) for all-cause mortality was 1.06 (95%CI: 1.04-1.08, n = 28 studies, I2 = 98.6%) per 10 ppb increase in annual NO2 concentrations. The pooled HRs for cardiovascular and respiratory mortality per 10 ppb increment were 1.11 (95%CI: 1.07-1.16, n = 20 studies, I2 = 99.2%) and 1.05 (95%CI: 1.02-1.08, n = 17 studies, I2 = 94.6%), respectively. The sensitivity analysis pooling estimates from multi-pollutant models suggest an independent effect of NO2 on mortality. Funnel plots indicate that there is no evidence for publication bias in our study.ConclusionWe provide robust epidemiological evidence that long-term exposure to NO2, a proxy for traffic-sourced air pollutants, is associated with a higher risk of all-cause, cardiovascular, and respiratory mortality that might be independent of other common air pollutants.

Dataset Information

Infant Mortality Related to NO2 and PM Exposure: Systematic Review and Meta-Analysis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets