Folic Acid Supplementation and the Association between Maternal Airborne Particulate Matter Exposure and Preterm Delivery: A National Birth Cohort Study in China
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ABSTRACT: Background:
Potential modification of the association between maternal particulate matter (PM) exposure and preterm delivery (PTD) by folic acid (FA) supplementation has not been studied. Objective:
We examined whether FA supplementation could reduce the risk of PTD associated with maternal exposure to PM in ambient air during pregnancy. Method:
In a cohort study covering 30 of the 31 provinces of mainland China in 2014, 1,229,556 primiparas of Han ethnicity were followed until labor. We collected information on their FA supplementation and pregnancy outcomes and estimated each participant’s exposure to PM with diameters of Results:
Participants who initiated FA Conclusion:
Our findings require confirmation in other populations, but they suggest that initiating FA supplementation
SUBMITTER: Li Q
PROVIDER: S-EPMC7747880 | biostudies-literature | 2020 Dec
REPOSITORIES: biostudies-literature
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Project description:Importance:Airborne particulate matter pollution has been associated with preterm birth (PTB) in some studies. However, most of these studies assessed only populations living near monitoring stations, and the association of airborne particulate matter having a median diameter of 1 μm or less (PM1) with PTB has not been studied. Objective:To evaluate whether PM1 concentrations are associated with the risk of PTB. Design, Setting, and Participants:This national cohort study used National Free Preconception Health Examination Project data collected in 324 of 344 prefecture-level cities from 30 provinces of mainland China. In total, 1 300 342 healthy singleton pregnancies were included from women who were in labor from December 1, 2013, through November 30, 2014. Data analysis was conducted between December 1, 2016, and April 1, 2017. Exposures:Predicted weekly PM1 concentration data collected using satellite remote sensing, meteorologic, and land use information matched with the home addresses of pregnant women. Main Outcomes and Measures:Preterm birth (<37 gestational weeks). Gestational age was assessed using the time since the first day of the last menstrual period. Cox proportional hazards regression analysis was used to examine the associations between trimester-specific PM1 concentrations and PTB after controlling for temperature, seasonality, spatial variation, and individual covariates. Results:Of the 1 300 342 singleton live births at the gestational age of 20 to 45 weeks included in this study, 104 585 (8.0%) were preterm. In fully adjusted models, a PM1 concentration increase of 10 μg/m3 over the entire pregnancy was significantly associated with increased risk of PTB (hazard ratio [HR], 1.09; 95% CI, 1.09-1.10), very PTB as defined as gestational age from 28 through 31 weeks (HR, 1.20; 95% CI, 1.18-1.23), and extremely PTB as defined as 20 through 27 weeks' gestation (HR, 1.29; 95% CI, 1.25-1.34). Pregnant women who were older (30-50 years) at conception (HR, 1.13; 95% CI, 1.11-1.14), were overweight before pregnancy (HR, 1.13; 95% CI, 1.11-1.15), had a rural household registration (HR, 1.09; 95% CI, 1.09-1.10), worked as farmers (HR, 1.10; 95% CI, 1.09-1.11), and conceived in autumn (HR, 1.48; 95% CI, 1.46-1.50) appeared to be more sensitive to PM1 exposure than their counterparts. Conclusions and Relevance:Results from this national cohort study examining more than 1.3 million births indicated that exposure to PM1 air pollution was associated with an increased risk of PTB in China. These findings will provide evidence to inform future research studies, public health interventions, and environmental policies.
| S-EPMC5885853 | biostudies-literature
Project description:This study uses machine learning and population data to analyze major determinants of preterm birth including depression and particulate matter. Retrospective cohort data came from Korea National Health Insurance Service claims data for 405,586 women who were aged 25-40 years and gave births for the first time after a singleton pregnancy during 2015-2017. The dependent variable was preterm birth during 2015-2017 and 90 independent variables were included (demographic/socioeconomic information, particulate matter, disease information, medication history, obstetric information). Random forest variable importance was used to identify major determinants of preterm birth including depression and particulate matter. Based on random forest variable importance, the top 40 determinants of preterm birth during 2015-2017 included socioeconomic status, age, proton pump inhibitor, benzodiazepine, tricyclic antidepressant, sleeping pills, progesterone, gastroesophageal reflux disease (GERD) for the years 2002-2014, particulate matter for the months January-December 2014, region, myoma uteri, diabetes for the years 2013-2014 and depression for the years 2011-2014. In conclusion, preterm birth has strong associations with depression and particulate matter. What is really needed for effective prenatal care is strong intervention for particulate matters together with active counseling and medication for common depressive symptoms (neglected by pregnant women).
| S-EPMC8003604 | biostudies-literature
Project description:BackgroundParticulate matter ≤10 μm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts.ObjectivesTo evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks.MethodsPM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines.ResultsIn adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 μg/m3) during the second trimester, while negative associations were seen during the second (≥74 μg/m3) and third trimesters (55-65 μg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth.DiscussionAssociations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.
| S-EPMC7525039 | biostudies-literature
Project description:Background: In classrooms high concentrations of particulate matter PM10 were measured. It is unknown whether the hazard of indoor particles is similar to that of the better studied outdoor particles. This study therefore analyzed adverse biological effects of classroom in comparison to outdoor PM10. Methods: Samples were taken from six schools during teaching hours. Genome-wide gene expression in human bronchial BEAS-2B epithelial cells was analyzed, and regulated genes were verified by quantitative PCR. Polycyclic aromatic hydrocarbons (PAH), endotoxin, and cat allergen Fel d 1 were analyzed with standard methods. Enhancement of allergic reactivity by PM10 was confirmed with CD63 upregulation in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Results: Indoor PM10 induced SERPINB2 (involved in blood coagulation) and inflammatory genes (like CXCL6, CXCL1, IL6, IL8, all p<0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (CYP1A1, CYP1B1, TIPARP, all p<0.001). The induction of inflammatory genes by indoor PM10 could be explained by endotoxin (indoor 128.5±42.2EU/mg versus outdoor 13.4±21.5EU/mg, p<0.001), the induction of CYP by outdoor PAH (indoor 8.3±4.9ng/mg versus outdoor 16.7±15.2ng/mg, p<0.01). The induction of SERPINB2 was confirmed by a more rapid human blood coagulation (p<0.05). Indoor PM10 had no effect on the allergic reactivity from human primary basophils, except in cat allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (p<0.001). Conclusions: Indoor PM10, compared to outdoor PM10, was 6 times higher, had a different composition, and on an equal weight basis induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps by intensified ventilation.
2012-12-21 | GSE34607 | GEO
Project description:Background: In classrooms high concentrations of particulate matter PM10 were measured. It is unknown whether the hazard of indoor particles is similar to that of the better studied outdoor particles. This study therefore analyzed adverse biological effects of classroom in comparison to outdoor PM10. Methods: Samples were taken from six schools during teaching hours. Genome-wide gene expression in human bronchial BEAS-2B epithelial cells was analyzed, and regulated genes were verified by quantitative PCR. Polycyclic aromatic hydrocarbons (PAH), endotoxin, and cat allergen Fel d 1 were analyzed with standard methods. Enhancement of allergic reactivity by PM10 was confirmed with CD63 upregulation in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM10-exposed human peripheral blood monocytes. Results: Indoor PM10 induced SERPINB2 (involved in blood coagulation) and inflammatory genes (like CXCL6, CXCL1, IL6, IL8, all p<0.001). Outdoor PM10 induced xenobiotic metabolizing enzymes (CYP1A1, CYP1B1, TIPARP, all p<0.001). The induction of inflammatory genes by indoor PM10 could be explained by endotoxin (indoor 128.5M-BM-142.2EU/mg versus outdoor 13.4M-BM-121.5EU/mg, p<0.001), the induction of CYP by outdoor PAH (indoor 8.3M-BM-14.9ng/mg versus outdoor 16.7M-BM-115.2ng/mg, p<0.01). The induction of SERPINB2 was confirmed by a more rapid human blood coagulation (p<0.05). Indoor PM10 had no effect on the allergic reactivity from human primary basophils, except in cat allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM10 (p<0.001). Conclusions: Indoor PM10, compared to outdoor PM10, was 6 times higher, had a different composition, and on an equal weight basis induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM10 had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM10 seem reasonable, perhaps by intensified ventilation. For genome-wide gene expression analysis, BEAS-2B cells (passage 41) were incubated with 10M-BM-5g/ml PM10 (school 4 indoor and outdoor) for 4, 10 or 24h, all in triplicate. experiment type : time course
2012-12-21 | E-GEOD-34607 | biostudies-arrayexpress
Project description:Bacterial Communities on Airborne Particulate Matter Raw sequence reads
| PRJNA753552 | ENA
Project description:Objectives: To explore the molecular mechanisms of PM2.5-induced dysfunction in human corneal epithelial cells (HCECs). Methods: RNA-Seq was performed to identify the differentially expressed genes (DEGs) in PM2.5-exposed HCECs compared to unexposed condition, which was followed by validation via real-time PCR (qRT-PCR). Results: A total of 434 DEGs—240 up-regulated and 194 down-regulated—were identified in PM2.5-exposed HCECs rather than unexposed HCECs. The expression of a few genes related to proliferation, inflammation, and aryl hydrocarbon stimulation were significantly altered by PM2.5 exposure, which may contribute to PM2.5-related corneal diseases. Conclusion: The present study identified the altered expression of hundreds of genes in HCECs exposed to PM2.5, which suggests the importance of PM2.5 for cornea health.
2022-08-01 | GSE135262 | GEO
Project description:Several studies have examined associations between particulate matter with aerodynamic diameter of 2.5 µm or less (PM2.5) and preterm birth, but it is uncertain whether results were affected by individual predispositions (e.g., genetic factors, social conditions) that might vary considerably between women. We tested the hypothesis that a woman is at greater risk of preterm delivery when she has had elevated exposure to ambient PM2.5 during a pregnancy than when she has not by comparing pregnancies in the same woman. From 271,204 births, we selected 29,175 women who had vaginal singleton livebirths at least twice in Connecticut in 2000-2006 (n = 61,688 births). Analyses matched pregnancies to the same woman. Adjusted odds ratios per interquartile range (2.33-µg/m(3)) increase in PM2.5 in the first trimester, second trimester, third trimester, and whole pregnancy were 1.07 (95% confidence interval (CI): 1.00, 1.15), 0.96 (95% CI: 0.90, 1.03), 1.03 (95% CI: 0.97, 1.08), and 1.13 (95% CI: 1.01, 1.28), respectively. Among Hispanic women, the odds ratio per interquartile range increase in whole-pregnancy exposure was 1.31 (95% CI: 1.00, 1.73). Pregnancies with elevated PM2.5 exposure were more likely to result in preterm birth than were other pregnancies to the same woman at lower exposure. Associations were most pronounced in the first trimester and among Hispanic women.
| S-EPMC3864709 | biostudies-literature
Project description:Most research to date has focused on epigenetic modifications in the nuclear genome, with little attention devoted to mitochondrial DNA (mtDNA). Placental mtDNA content has been shown to respond to environmental exposures that induce oxidative stress, including airborne particulate matter (PM). Damaged or non-functioning mitochondria are specifically degraded through mitophagy, exemplified by lower mtDNA content, and could be primed by epigenetic modifications in the mtDNA. We studied placental mtDNA methylation in the context of the early life exposome. We investigated placental tissue from 381 mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mtDNA methylation by bisulfite-pyrosequencing in 2 regions, i.e., the D-loop control region and 12S rRNA (MT-RNR1), and measured mtDNA content by qPCR. PM2.5 exposure was calculated for each participant's home address using a dispersion model. An interquartile range (IQR) increment in PM2.5 exposure over the entire pregnancy was positively associated with mtDNA methylation (MT-RNR1: +0.91%, P = 0.01 and D-loop: +0.21%, P = 0.05) and inversely associated with mtDNA content (relative change of -15.60%, P = 0.001) in placental tissue. mtDNA methylation was estimated to mediate 54% [P = 0.01 (MT-RNR1)] and 27% [P = 0.06 (D-loop)] of the inverse association between PM2.5 exposure and mtDNA content. This study provides new insight into the mechanisms of altered mitochondrial function in the early life environment. Epigenetic modifications in the mitochondrial genome, especially in the MT-RNR1 region, substantially mediate the association between PM2.5 exposure during gestation and placental mtDNA content, which could reflect signs of mitophagy and mitochondrial death.
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Project description:Emissions from indoor biomass burning are a major public health concern in developing areas of the world. Less is known about indoor air quality, particularly airborne endotoxin, in homes burning biomass fuel in residential wood stoves in higher income countries. A filter-based sampler was used to evaluate wintertime indoor coarse particulate matter (PM₁₀₋₂.₅) and airborne endotoxin (EU/m³, EU/mg) concentrations in 50 homes using wood stoves as their primary source of heat in western Montana. We investigated number of residents, number of pets, dampness (humidity), and frequency of wood stove usage as potential predictors of indoor airborne endotoxin concentrations. Two 48-h sampling events per home revealed a mean winter PM₁₀₋₂.₅ concentration (± s.d.) of 12.9 (± 8.6) μg/m³, while PM₂.₅ concentrations averaged 32.3 (± 32.6) μg/m³. Endotoxin concentrations measured from PM₁₀₋₂.₅ filter samples were 9.2 (± 12.4) EU/m³ and 1010 (± 1524) EU/mg. PM₁₀₋₂.₅ and PM₂.₅ were significantly correlated in wood stove homes (r = 0.36, P < 0.05). The presence of pets in the homes was associated with PM₁₀₋₂.₅ but not with endotoxin concentrations. Importantly, none of the other measured home characteristics was a strong predictor of airborne endotoxin, including frequency of residential wood stove usage.
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