Maternal air pollution exposure and congenital heart defects in offspring: A systematic review and meta-analysis

Hu, Chengyang; Huang, Kai; Fang, Yuan; Yang, Xiao-Jing; Ding, Kan; Jiang, Wen Qi; Hua, Xiao-Guo; Da-yan, Huang; Jiang, Zhengxuan; Zhang, Xiujun

doi:10.1016/j.chemosphere.2020.126668

Cited by 70 publications

(34 citation statements)

References 60 publications

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“…In our initial examination of air pollution exposure and risk of these selected birth defects, we did not find consistent associations for any air pollutants (Padula, Tager, Carmichael, Hammond, Lurmann, et al, 2013a, Padula, Tager, Carmichael, Hammond, Yang, et al, 2013b. Additional studies have found mixed results between air pollution and orofacial clefts, gastroschisis and congenital heart defects (Hu et al, 2020).…”

Section: Introductioncontrasting

confidence: 59%

“…Birth defects are a leading cause of infant morbidity and mortality and affect approximately 3% of births and causes of most birth defects are largely unknown. Ambient air pollution has been associated with risk of several birth defect phenotypes, though results have not been consistent across different study populations (Hu et al, 2020). Such inconsistencies may be due to environmental or methodologic differences between studies or study populations having different susceptibilities to air pollution based on genetic variation.…”

Section: Introductionmentioning

confidence: 98%

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Gene–environment interactions between air pollution and biotransformation enzymes and risk of birth defects

Padula

Yang

Schultz

et al. 2021

Birth Defects Research

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Genetic and environmental factors have been observed to influence risks for birth defects, though few studies have investigated gene-environment interactions. Our aim was to examine the interaction terms of gene variants in biotransformation enzyme pathways and air pollution exposures in relation to risk of several structural birth defects. We evaluated the role of ambient air pollutant exposure (nitrogen dioxide [NO 2 ], nitrogen oxide, carbon monoxide, particulate matter <10 [PM 10 ] and <2.5 [PM 2.5 ] microns) during pregnancy and 104 gene variants of biotransformation enzymes from infant bloodspots or buccal cells in a California population-based case-control study in 1997-2006. Cases included cleft lip with or without cleft palate (N = 206), gastroschisis (N = 94), tetralogy of Fallot (N = 69), and dextro-transposition of the great arteries (d-TGA; N = 40) and were compared to 208 nonmalformed controls.Overall, the results were not consistent, though did highlight some associations for further investigation as indicated by Wald chi-square test p value <.1.Increased risk of cleft lip was associated with exposure to high PM 10 and two CYP gene variants. High PM 2.5 and the variant of SLCO1B1 was associated with increased risk of teratology of Fallot. Higher NO 2 and two gene variants, CYP2A6 and SLC01B1, were associated with increased risk of d-TGA. Results for gastroschisis were inconsistent in direction and across pollutants. These exploratory results suggest that some individuals based on their genetic background may be more susceptible to the adverse effects of air pollution.

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Section: Introductioncontrasting

confidence: 59%

Section: Introductionmentioning

confidence: 98%

Gene–environment interactions between air pollution and biotransformation enzymes and risk of birth defects

Padula

Yang

Schultz

et al. 2021

Birth Defects Research

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“…Additionally, there are several studies showing association with various PMs and CKD (56)(57)(58). Despite the association between maternal air pollution exposure and birth defects has been addressed (68,69), how early exposure to particulate matters may increase the risk of adverse renal outcome in offspring is still largely unknown.…”

Section: Air Pollutionmentioning

confidence: 99%

Adverse Impact of Environmental Chemicals on Developmental Origins of Kidney Disease and Hypertension

Hsu

Tain

2021

Front. Endocrinol.

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Chronic kidney disease (CKD) and hypertension are becoming a global health challenge, despite developments in pharmacotherapy. Both diseases can begin in early life by so-called “developmental origins of health and disease” (DOHaD). Environmental chemical exposure during pregnancy can affect kidney development, resulting in renal programming. Here, we focus on environmental chemicals that pregnant mothers are likely to be exposed, including dioxins, bisphenol A (BPA), phthalates, per- and polyfluoroalkyl substances (PFAS), polycyclic aromatic hydrocarbons (PAH), heavy metals, and air pollution. We summarize current human evidence and animal models that supports the link between prenatal exposure to environmental chemicals and developmental origins of kidney disease and hypertension, with an emphasis on common mechanisms. These include oxidative stress, renin-angiotensin system, reduced nephron numbers, and aryl hydrocarbon receptor signaling pathway. Urgent action is required to identify toxic chemicals in the environment, avoid harmful chemicals exposure during pregnancy and lactation, and continue to discover other potentially harmful chemicals. Innovation is also needed to identify kidney disease and hypertension in the earliest stage, as well as translating effective reprogramming interventions from animal studies into clinical practice. Toward DOHaD approach, prohibiting toxic chemical exposure and better understanding of underlying mechanisms, we have the potential to reduce global burden of kidney disease and hypertension.

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“…A number of epidemiological studies have also demonstrated positive associations between maternal PM exposure during pregnancy and adverse birth outcomes, such as preterm birth ( 9 ), low birth weight ( 10 ), and birth defects ( 11 ). A recent meta-analysis ( 12 ) on ambient air pollution and cardiac anomalies reported that each 10 μg/m 3 increment in PM 10 is associated with increased risk of atrial septal defects. However, there has been conflicting evidence of the effect of maternal PM 10 exposure during pregnancy on certain types of birth defects because of great variability in the study populations, sample sizes, exposure assessments, ascertainment methods, and statistical adjustments.…”

Section: Introductionmentioning

confidence: 99%

Maternal PM10 Exposure Increases Risk for Spina Bifida: A Population-Based Case-Control Study

Huang

et al. 2021

Front. Public Health

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Limited studies have focused on the impact of ambient air pollution on spina bifida. A population-based case-control study was conducted in Liaoning Province, China to assess the associations between maternal PM10 exposures in various exposure windows and spina bifida risk. Data on spina bifida cases born between 2010 and 2015 were available from the Maternal and Child Health Certificate Registry of Liaoning Province. Controls were a random sample of healthy livebirths without any birth defects delivered in the selected five cities during 2010–2015. Ambient air monitoring data for PM10 were obtained from 75 monitoring stations in Liaoning Province. The multivariable logistic regression models were established to calculate adjusted odds ratios (OR) and 95% confidence intervals (CI). We further performed sensitivity analyses by using three propensity score methods. A total of 749 spina bifida cases and 7,950 controls were included. After adjusting for potential confounders, spina bifida was associated with a 10 μg/m3 increment in PM10 during the first trimester of pregnancy (adjusted OR = 1.06, 95% CI: 1.00–1.12) and the 3 months before pregnancy (adjusted OR = 1.12, 95% CI: 1.06–1.19). The adjusted ORs in the final model for the highest vs. the lowest quartile were 1.51 (95% CI: 1.04–2.19) for PM10 during the first trimester of pregnancy and 2.01 (95% CI: 1.43–2.81) for PM10 during the 3 months before pregnancy. Positive associations were found between PM10 exposures during the single month exposure windows and spina bifida. Sensitivity analyses based on two propensity score methods largely reported similar positive associations. Our findings support the evidence that maternal PM10 exposure increases the risk of spina bifida in offspring. Further, validation with a prospective design and a more accurate exposure assessment is warranted.

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Maternal air pollution exposure and congenital heart defects in offspring: A systematic review and meta-analysis

Cited by 70 publications

References 60 publications

Gene–environment interactions between air pollution and biotransformation enzymes and risk of birth defects

Gene–environment interactions between air pollution and biotransformation enzymes and risk of birth defects

Adverse Impact of Environmental Chemicals on Developmental Origins of Kidney Disease and Hypertension

Maternal PM10 Exposure Increases Risk for Spina Bifida: A Population-Based Case-Control Study

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