Association between maternal exposure to particulate matter (PM2.5) and adverse pregnancy outcomes in Lima, Peru

Tapia, Vilma; Vasquez, Bertha; Vu, Bryan N.; Liu, Yang; Steenland, Kyle; Gonzáles, Gustavo F.

doi:10.1038/s41370-020-0223-5

Cited by 37 publications

(33 citation statements)

References 29 publications

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“…The studies were published over a 12-year period from 2009 to 2012. There were 14 studies from the USA [ 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 ]; eight studies from China [ 6 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ]; four studies from the European region [ 37 , 38 , 39 , 40 ]; two studies from Canada [ 41 , 42 ]; two studies from Australia [ 43 , 44 ]; and one study from Peru [ 45 ].…”

Section: Resultsmentioning

confidence: 99%

A Simple Method to Establish Sufficiency and Stability in Meta-Analyses: With Application to Fine Particulate Matter Air Pollution and Preterm Birth

Pereira

2022

IJERPH

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Fine particulate matter air pollution (PM2.5) is a potential cause of preterm birth. Inconsistent findings from observational studies have motivated researchers to conduct more studies, but some degree of study heterogeneity is inevitable. The consequence of this feedback is a burgeoning research effort that results in marginal gains. The aim of this study was to develop and apply a method to establish the sufficiency and stability of estimates of associations as they have been published over time. Cohort studies identified in a recent systematic review and meta-analysis on the association between preterm birth and whole-pregnancy exposure to PM2.5 were selected. The estimates of the cohort studies were pooled with cumulative meta-analysis, whereby a new meta-analysis was run for each new study published over time. The relative risks (RR) and 95% confidence interval (CI) limits needed for a new study to move the cumulative RR to 1.00 were calculated. Findings indicate that the cumulative relative risks (cRR) for PM2.5 (cRR 1.07, 95% CI 1.03, 1.12) converged in 2015 (RR 1.07, 95% CI 1.01, 1.14). To change conclusions to a null association, a new study would need to observe a protective RR of 0.93 (95% CI limit 1.02) with precision equivalent to that achieved by all past 24 cohort studies combined. Preterm birth is associated with elevated PM2.5, and it is highly unlikely that any new observational study will alter this conclusion. Consequently, establishing whether an observational association exists is now less relevant an objective for future studies than characterising risk (magnitude, impact, pathways, populations and potential bias) and interventions. Sufficiency and stability can be effectively applied in meta-analyses and have the potential to reduce research waste.

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Section: Resultsmentioning

confidence: 99%

A Simple Method to Establish Sufficiency and Stability in Meta-Analyses: With Application to Fine Particulate Matter Air Pollution and Preterm Birth

Pereira

2022

IJERPH

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“…Mostly, the primary effect of PM toxicity is related to oxidative stress, which contributes to transcription factor activation and further leads to local or systematic inflammation through the induction of proinflammatory responses such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), interleukin-1 (IL-1), IL-6, IL-8, cyclooxygenase-2 (COX-2), and granulocyte-macrophage colony-stimulating factor (GMCF) [2,[6][7][8]. Inhaled PM has the ability to enter terminal alveoli and blood circulation via the blood-air barrier, affecting the human respiratory system, central nervous system, reproductive systems, and cardiovascular system [9][10][11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

PM10 Alters Trophoblast Cell Function and Modulates miR-125b-5p Expression

Chaiwangyen

Pintha

Tantipaiboonwong

et al. 2022

BioMed Research International

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Air pollution is one of the largest global environmental health hazards that threaten premature mortality or morbidity. Particulate matter 10 (PM10) has been demonstrated to contribute to several human diseases via dysregulated miRNA expression. Trophoblast cells play a key role in implantation and placentation for a successful pregnancy. Nonetheless, the PM10 associated trophoblast cell functions during pregnancy and miRNA expression are still unknown. Our study showed that PM10 affected HTR-8/SVneo cell viability and also decreased cell proliferation, migration, and invasion. A high concentration of PM10 caused an increase in HTR-8/SVneo cell apoptosis. Treatment with PM10 induced inflammation through the upregulated IL-1β, IL-6, and TNF-α expression in trophoblast cells. In PM10-treated HTR-8/SVneo cells, miR-125b-5p expression was considerably increased and TXNRD1 was found to be negatively related to miR-125b-5p. Collectively, our findings revealed that PM10 could alter miR-125b-5p expression by targeting TXNRD1 and suppressing trophoblast cell functions. Additional investigations relating to the function of miR-125b-5p and its target on particulate pollution exposure in trophoblast are warranted for future biomarker or effective therapeutic approaches.

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“…Both air pollutants are mainly caused by human activities and are likely to be changed and avoided by taking some measures. Pregnant women exposed to PM 2.5 during pregnancy can lead to adverse pregnancy outcomes, such as fetal congenital malformation, premature delivery, abnormal birth weight of the fetus, and in severe cases, neonatal death ( 14 , 15 ). Gestational SHS exposure at work and/or at home increased the risk of fetal stillbirth, neonatal death, and perinatal death ( 16 ).…”

Section: Introductionmentioning

confidence: 99%

Maternal Secondhand Smoke Exposure Enhances Macrosomia Risk Among Pregnant Women Exposed to PM2.5: A New Interaction of Two Air Pollutants in a Nationwide Cohort

Luo

Zhang

Pan

et al. 2021

Front. Public Health

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Background: Fine particulate matter (PM2.5) is one of the most common outdoor air pollutants, and secondhand smoking (SHS) is an important source of inhalable indoor air pollution. Previous studies were controversial and inconsistent about PM2.5 and SHS air pollutants on neonatal birth weight outcomes, and no studies assessed the potential interactive effects between PM2.5 and SHS on birth weight outcomes.Purpose: To investigate the interaction between gestational PM2.5 and SHS air pollution exposure on the risk of macrosomia among pregnant women and examine the modifying effect of SHS exposure on the association of PM2.5 air pollution and birth weight outcomes during pregnancy.Methods: Research data were derived from the National Free Preconception Health Examination Project (NFPHEP), which lasted 3 years from January 1, 2010, to December 31, 2012. At least 240,000 Chinese women from 220 counties were enrolled in this project. PM2.5 exposure concentration was obtained using a hindcast model specific for historical PM2.5 estimation from satellite-retrieved aerosol optic depth. Different interaction models about air pollution exposure on birth weight outcomes were established, according to the adjustment of different confounding factors and different pregnancy stages. The establishment of interaction models was based on multivariable logistic regression, and the main confounding factors were maternal age at delivery and pre-pregnancy body mass index (BMI) of participants. SHS subgroups analysis was conducted to further confirm the results of interaction models.Results: In total, 197,877 participants were included in our study. In the full-adjusted interaction model, maternal exposure to PM2.5 was associated with an increased risk of macrosomia in whole, the first-, second-, and third trimesters of pregnancy (p < 0.001). The interactive effect was statistically significant between maternal exposure to PM2.5 and SHS on the risk of macrosomia in the whole (interaction p < 0.050) and the first-trimester pregnancy (interaction p < 0.050), not in the second (interaction p > 0.050) or third trimester (interaction p > 0.050) of pregnancy. The higher frequency of SHS exposure prompted the stronger interaction between the two air pollutants in the whole pregnancy and the first-trimester pregnancy.Conclusions: In the whole and first-trimester pregnancy, maternal exposure to SHS during pregnancy enhanced the risk of macrosomia among pregnant women exposed to PM2.5 air pollutants, and the interaction became stronger with the higher frequency of SHS exposure.

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Association between maternal exposure to particulate matter (PM2.5) and adverse pregnancy outcomes in Lima, Peru

Cited by 37 publications

References 29 publications

A Simple Method to Establish Sufficiency and Stability in Meta-Analyses: With Application to Fine Particulate Matter Air Pollution and Preterm Birth

A Simple Method to Establish Sufficiency and Stability in Meta-Analyses: With Application to Fine Particulate Matter Air Pollution and Preterm Birth

PM10 Alters Trophoblast Cell Function and Modulates miR-125b-5p Expression

Maternal Secondhand Smoke Exposure Enhances Macrosomia Risk Among Pregnant Women Exposed to PM2.5: A New Interaction of Two Air Pollutants in a Nationwide Cohort

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