Dataset Information

Spatially and Temporally Resolved Ambient PM_2.5 in Relation to Preterm Birth.

ABSTRACT: Growing evidence suggests that maternal exposure to ambient fine particulate matter (PM_2.5) during pregnancy is associated with preterm birth; however, few studies have examined critical windows of exposure, which can help elucidate underlying biologic mechanisms and inform public health messaging for limiting exposure. Participants included 891 mother-newborn pairs enrolled in a U.S.-based pregnancy cohort study. Daily residential PM_2.5 concentrations at a 1 × 1 km² resolution were estimated using a satellite-based hybrid model. Gestational age at birth was abstracted from electronic medical records and preterm birth (PTB) was defined as <37 completed weeks of gestation. We used Critical Window Variable Selection to examine weekly PM_2.5 exposure in relation to the odds of PTB and examined sex-specific associations using stratified models. The mean ± standard deviation PM_2.5 level averaged across pregnancy was 8.13 ± 1.10 µg/m³. PM_2.5 exposure was not associated with an increased odds of PTB during any gestational week. In sex-stratified models, we observed a marginal increase in the odds of PTB with exposure occurring during gestational week 16 among female infants only. This study does not provide strong evidence supporting an association between weekly exposure to PM_2.5 and preterm birth.

SUBMITTER: Cowell W

PROVIDER: S-EPMC8708619 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Spatially and Temporally Resolved Ambient PM2.5 in Relation to Preterm Birth.

Cowell Whitney W Colicino Elena E Zhang Xueying X Ledyard Rachel R Burris Heather H HH Hacker Michele R MR Kloog Itai I Just Allan A Wright Robert O RO Wright Rosalind J RJ

Toxics 20211214 12

Growing evidence suggests that maternal exposure to ambient fine particulate matter (PM2.5) during pregnancy is associated with preterm birth; however, few studies have examined critical windows of exposure, which can help elucidate underlying biologic mechanisms and inform public health messaging for limiting exposure. Participants included 891 mother-newborn pairs enrolled in a U.S.-based pregnancy cohort study. Daily residential PM2.5 concentrations at a 1 × 1 km2</ ...[more]

PMID: 34941786

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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:Rapid urbanization and consuming lifestyles have intensified air pollution in urban areas. Air pollution in megacities has imposed severe environmental damages to human health. Proper management of the issue necessitates identification of the share of emission sources. Therefore, numerous research works have studied the apportionment of the total emissions and observed concentrations among different emissions sources. In this research, a comprehensive review is conducted to compare the source apportioning results for ambient air PM2.5 in the megacity of Tehran, the capital of Iran. One hundred seventy-seven pieces of scientific literatures, published between 2005 and 2021, were reviewed. The reviewed research are categorized according to the source apportioning methods: emission inventory (EI), source apportionment (SA), and sensitivity analysis of the concentration to the emission sources (SNA). The possible reasons for inconsistency among the results are discussed according to the scope of the studies and the implemented methods. Although 85% of the reviewed original estimates identify that mobile sources contribute to more thant 60% of Tehran air pollution, the distribution of vehicle types and modes are clearly inconsistent among the EI studies. Our review suggests that consistent results in the SA studies in different locations in central Tehran may indicate the reliability of this method for the identification of the type and share of the emission sources. In contrast, differences among the geographical and sectoral coverage of the EI studies and the disparities among the emission factors and activity data have caused significant deviations among the reviewed EI studies. Also, it is shown that the results of the SNA studies are highly dependent on the categorization type, model capabilities and EI presumptions and data input to the pollutant dispersion modelings. As a result, integrated source apportioning in which the three methods complement each other's results is necessary for consistent air pollution management in megacities.Supplementary informationThe online version contains supplementary material available at 10.1007/s40201-023-00855-0.

Project description:We quantify the contributions of long-range and regionally transported aerosols to ambient primary PM2.5 and PM10 in a representative United States industrialized/urban atmosphere via detailed elemental analysis and chemical mass balance (CMB) modeling after identifying their presence using a variety of publicly available satellite data/information, software products, and synoptic-scale aerosol models. A year-long study in Houston, Texas identified North African dust as the principal long-range global source of primary particulate matter (PM). CMB estimated transatlantic dust from the Sahara-Sahel region to be dominant in the summer months contributing an average of 3.5 μg m-3 to PM2.5 and 7.9 μg m-3 to PM10 during May-August, i.e., the active Saharan dust season. Biomass burning was the chief source of regionally transported PM impacting air quality on different occasions throughout the year depending on the fire location. Four major biomass combustion events affecting air quality in Texas were calculated to contribute an average of 1.3 μg m-3 to PM2.5 and 1.4 μg m-3 to PM10 in corresponding samples whose origins were tracked to Canada, southeastern states of USA, and Central America using fire maps, HYSPLIT back trajectories, and the Navy Aerosol Analysis and Prediction System global aerosol model. Elemental concentrations and signature ratios revealed significant mixing of potassium, rare earth metals, and vanadium from proximal and distal crustal (natural) sources with anthropogenically emitted PM. This demonstrates the need to isolate the non-mineral components of these metals to employ them as tracers for primary PM emitted by biomass burning, petroleum refineries, and oil combustion. Transboundary contributions to primary PM2.5 were 1.5 μg m-3 and 3.1 μg m-3 to PM10 adding 16% to annual average mass concentration of both size fractions demonstrating that local sources were primarily responsible for ambient air quality with non-trivial contributions from international and interstate sources. Rigorously identifying and quantifying aerosol sources assists in improving air quality management policies designed to protect public health and comply with ever-decreasing federal PM standards that allow state agencies to exclude contributions that are not reasonably controllable or preventable from regulatory decisions and actions.

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.

Dataset Information

Spatially and Temporally Resolved Ambient PM_2.5 in Relation to Preterm Birth.

Publications

Spatially and Temporally Resolved Ambient PM<sub>2.5</sub> in Relation to Preterm Birth.

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