Maternal atmospheric particulate matter exposure and risk of adverse pregnancy outcomes: A meta-analysis of cohort studies.

Ambient air particulate exposure not only capable of elevating the risks of adverse pregnancy outcomes, but also has profound implications for human health, but the results are discrepant. This meta-analysis aimed to provide higher grade evidence on the impacts of air particulate on specific pregnancy outcomes. A total of 81 eligible cohort studies were included in this meta-analysis, of which the outcomes included preterm birth (PTB), moderate PTB, very PTB, extreme PTB, term low birth weight (TLBW), term birth weight (TBW), stillbirth (SB) and small for gestational age (SGA). The results showed that every 10 µg/m3 increase of PM2.5 exposure associated with 2.7%-9.3% increase of PTB risk in entire pregnancy, 2nd and 3rd trimesters; 10.5%-19.3% increase of very PTB risk in entire pregnancy, 1st and 2nd trimesters; 8.3% and 10.1% increase of TLBW and SGA risk in entire pregnancy; 25.6% and 10.1% increase of SB in entire pregnancy and 3rd trimester; and -13.274 g and -4.916 g reduce of TBW during entire pregnancy and 2nd trimester, respectively. Every 10 µg/m3 increase of PM10 exposure associated with 12.1% and 2.6% increase of PTB risk in entire pregnancy and 3rd trimester; 48.9% and 5.0% increase of moderate PTB risk in entire pregnancy and 2nd trimester; 14.4% and 10.3% increase of very PTB risk in 1st and 3rd trimesters; 2.9% increase of extremely PTB risk in 2nd trimester; 1.5%-3.8% and 2.9%-3.7% increase of TLBW and SGA risk in entire pregnancy, 1st and 2nd trimesters; 7.0% increase of SB risk in 3rd trimesters; and -4.537 g and -5.263 g reduce of TBW in 1st and 2nd trimesters, respectively. High mean annual PM concentrations were associated with more extreme adverse pregnancy outcomes (PTBs, SGA and SB), while low mean annual PM concentrations were associated with decreased TBW and increased risk of TLBW.

Outdoor air pollution exposure and the risk of asthma and wheezing in the offspring.

According to the "fetal origin of disease" hypothesis, air pollution exposure in pregnancy may play an important role in stimulating the early programming of asthma and allergies. However, previous studies reported inconsistent findings. The aim of this meta-analysis was to provide higher grade evidence and quantitatively analyze the link between prenatal exposure to outdoor air pollutants and childhood asthma and wheezing. Databases (Web of Science and PubMed) were extensively searched for articles published from the start of the database to September 15, 2021. Either random-effect model or fixed-effect model was used to estimate the disease-specific relative risks (RR) with the corresponding 95% confidence intervals (CIs) to estimate the association. Newcastle-Ottawa Quality Score (NOS) was used to assess the quality of studies. This study finally included 13 cohort studies, and the findings showed that NO2 and SO2 exposure during entire pregnancy was significantly associated with wheezing (RR = 1.032, 95% CI: 1.000, 1.066) and asthma (RR = 1.114, 95% CI: 1.066, 1.164), respectively. Further analyses showed that PM2.5 were positively associated with asthma in the second (RR = 1.194, 95% CI: 1.143, 1.247) and third trimester (RR = 1.050, 95% CI: 1.007, 1.094), while NO2 (RR = 1.060, 95% CI: 1.021, 1.101) and SO2 (RR = 1.067, 95% CI: 1.013, 1.123) were shown positively associated with asthma only in the second trimester. The relationship between wheezing and outdoor air pollutants was not significant in any of the pregnancy subgroups. This study suggests that prenatal exposure of outdoor air pollution may increase the asthma and wheezing risk in the offspring and that the second trimester may be a sensitive period for air pollution exposure. But the interpretation of the causal association is hampered by limited number of studies on dose response.

Uterine decidual stromal cell-derived exosomes mediate the indirect effects of 1-nitropyrene on trophoblast biological behaviors.

1-nitropyrene (1-NP) is representative nitropolycyclic aromatic hydrocarbon pollutant widely present in exhaust particles of internal combustion engine, which is known for its carcinogenicity and mutagenicity. Previous studies have demonstrated that 1-NP has reproductive toxicity, but the specific mechanism is unknown. In this study, Human decidual stromal cells (HDSCs) were treated by 1-NP, exosomes were extracted from the conditioned medium of HDSCs, which were then used to treat human chorionic trophoblast cells (HTR8/SVneo) for 24 h. The findings showed that human decidual stromal cell-derived exosomes (HDSC-EXOs) can promote the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT; Vimentin and N-cadherin) of HTR8/SVneo by about 64%, 17%, 23%, 81% and 13%. The process of regulating the biological behaviors of embryonic trophoblast cells by maternal decidual stromal cells during pregnancy was simulated. Further investigations showed that HDSC-EXOs treatment activated the Wnt/ß-catenin signaling pathway in HTR8/SVneo. Co-treatment by dickkopf-1 (DKK-1) significantly suppressed the activation of Wnt/ß-catenin signaling pathway in HTR8/SVneo, and inhibited the proliferation, migration, invasion and EMT (N-cadherin and E-cadherin) of HTR8/SVneo by about 60%, 22%, 42%, 25%, 55% and 21%. These findings indicated that 1-NP exposure could induce the secretion of HDSC-EXOs from HDSCs, which in turn activate the Wnt/ß-catenin signaling pathway and enhance the proliferation, migration, invasion and EMT of HTR8/SVneo.

Prenatal air pollution exposure increases the risk of macrosomia: evidence from a prospective cohort study in the coastal area of China.

Effects of prenatal ambient air pollution exposure could increase the risk of adverse pregnancy outcomes, which have been well documented by various studies. However, only very few studies investigated the effects on macrosomia. This study investigated the effects of prenatal air pollution exposure on the risk of macrosomia in a coastal city of China. Data of birth outcomes and air pollution in a coastal city in China between November 1, 2013, and December 31, 2017, were collected. Finally, 58,713 eligible births, including 8159 (13.9%) macrosomia and 50554 (86.1%) normal birth weight (NBW) infants, were included in the analysis. Logistic regression analyses were used to evaluate the effects of prenatal air pollution exposure on macrosomia. In the single-pollutant models, each 10 µg/m3 increase of PM2.5, PM10, and SO2 exposures, during the entire pregnancy or three trimesters, were related to elevated risk of macrosomia (adjusted RR, 95% CI) ranging from 1.018 (1.001, 1.035) to 1.314 (1.188, 1.454). In addition, O3 exposure in the first trimester (adjusted RR =1.034, 95% CI 1.009, 1.059) also increased the macrosomia risk. Prenatal PM2.5, PM10, and SO2 exposure could significantly increase the risk of macrosomia. These findings need to be further verified in more studies with multiple coastal cities included.

MiR-582-3p participates in the regulation of biological behaviors of A549 cells by ambient PM2.5 exposure.

Ambient fine particulate matter (PM2.5) is one of the main environmental air pollutants that is closely related to the development of lung cancer, but the mechanisms are unclear. In this study, A549 cells were exposed to ambient PM2.5 to investigate the alterations of biological behaviors, and the possible role of miR-582-3p in the effects was further explored. The findings showed that PM2.5 exposure could significantly enhance the biological behaviors of A549 cells, and promote their epithelial-mesenchymal transition (EMT) transformation, especially at relatively low doses. Over-activation of Wnt/ß-catenin signaling pathway and increased expression of miR-582-3p were also found in A549 cells after PM2.5 exposure. After the knockdown of miR-582-3p in A549 cells, the effects of PM2.5 on malignant biological behavior changes, EMT, and the activation of Wnt/ß-catenin signaling pathway were all significantly alleviated. Furthermore, the inhibition of Wnt/ß-catenin signaling pathway also inhibited the EMT process of A549 cells, which was rescued by the overexpression of miR-582-3p. Therefore, this study showed that ambient PM2.5 can upregulate the expression of miR-582-3p, consequently activate the Wnt/ß-catenin signaling pathway, and thereby enhance EMT transformation and promote the malignant biological behaviors of A549 cells. These findings provide evidence for further research into the mechanisms by which exposure to PM2.5 in the environment promotes lung cancer.

Maternal air pollution exposure increases the risk of preterm birth: Evidence from the meta-analysis of cohort studies.

Preterm birth (PTB), a major public health impact, has been shown to be associated with prenatal air pollution exposure, but the results are still inconsistent. This meta-analysis was performed to quantitatively evaluate the correlation between maternal air pollutant exposure and PTB, and provide evidence of higher grade to help improving the pregnancy outcomes. Databases including Web of Science and PubMed were searched to retrieve eligible studies published up to October 2020. The quality of the articles was assessed by the Newcastle-Ottawa Quality Score (NOS), after which the pooled estimate of the effect was calculated. The robustness of the joint estimates was confirmed by sensitivity analysis of excluded studies one by one, and the sources of heterogeneity were discussed by stratification analysis. Egger's and Begg's tests were performed to examine publication bias. Sixty studies that met the eligible criteria were finally included in this study. The findings showed combined relative risks of 1.032-1.070 for PTB, 0.859-1.081 for moderate PTB, 1.119-1.194 for very PTB and 1.128-1.259 for extremely PTB when mothers were exposed to PM2.5, PM10, NO2, O3, SO2, CO and NOx during pregnancy, while the sensitive windows varied for different air pollutants. Notably, PM2.5 exposure in only the 2nd trimester, NO2 exposure in only the 3rd trimester, and O3 exposure in all three trimesters were positively associated with PTB, while NO2 exposure in the 1st trimester was negatively associated with PTB. In addition, exposure of PM2.5 and PM10 in the 2nd trimester was positively associated with moderate PTB, and in the 1st and 2nd trimesters were positively associated with very PTB. These findings demonstrated that PM2.5, PM10, O3, NO2 were associated with PTB (including moderate PTB, very PTB, and/or extremely PTB), while NOx was not, and the relationship between CO and SO2 and PTB was not stable.

Association between preconceptional air pollution exposure and medical purposes for selective termination of pregnancy.

BACKGROUND: Exposure to air pollutants is associated with adverse pregnancy outcomes. But evidence on the effects of preconceptional air pollution exposure on the risk of termination of pregnancy (TOP) caused by pregnancy losses and congenital malformations is lacking. METHODS: The distributed lag nonlinear model (DLNM) was used to evaluate the impact of short-term air pollutants exposure on the risk of TOP. Stratified analyses by age (<35 years old, ≥ 35 years old) and season (warm season, cold season) were further conducted. Relative risk (RR) and 95 % confidential interval (95 % CI) were calculated for per interquartile range (IQR) increment in air pollutants during the study period. RESULTS: PM2.5, PM10, and O3 exposure were significantly associated with elevated risk of TOP. The risk of TOP was associated with PM2.5 exposure from lag11 to lag15 in the single-pollutant model, and the strongest association was observed at lag13 (RR = 1.021, 95%CI:1.002-1.040). PM10 exposure from lag10 to lag15 was associated with increased TOP risk, with the corresponding peak association being at lag13 (RR = 1.020, 95%CI: 1.004-1.037). For O3, the single-day lag association appeared to be statistically significant from lag26 to lag27, with the highest RR of TOP cases being at lag27 (RR = 1.044, 95%CI: 1.005-1.084). Similar results were observed for pregnancy losses (PL). However, no significantly association between air pollution exposure and the risk of congenital malformations (CM) was found in this study. Stratified analyses showed that pregnant women with more advanced ages were more susceptible to PM2.5, PM10, and O3 exposure. The effect of PM2.5 exposure was statistically significant in cold season subgroups. CONCLUSION: The findings suggest that exposure to PM2.5, PM10, and O3 before pregnancy are associated with the risk of TOP in Lu'an, China, reflecting the significance of preconceptional environmental exposure in the development of adverse pregnancy outcomes.

Structural organization and functional divergence of high isoelectric point α-amylase genes in bread wheat (Triticum aestivum L.) and barley (Hordeum vulgare L.).

BACKGROUND: High isoelectric point α-amylase genes (Amy1) play major roles during cereal seed germination, and are associated with unacceptable high residual α-amylase activities in ripe wheat grains. However, in wheat and barley, due to extremely high homology of duplicated copies, and large and complex genome background, the knowledge on this multigene family is limited. RESULTS: In the present work, we identified a total of 41 Amy1 genes among 13 investigated grasses. By using genomic resources and experimental validation, the exact copy numbers and chromosomal locations in wheat and barley were determined. Phylogenetic and syntenic analyses revealed tandem gene duplication and chromosomal rearrangement leading to separation of Amy1 into two distinct loci, Amy1θ and Amy1λ. The divergence of Amy1λ from Amy1θ was driven by adaptive selection pressures performed on two amino acids, Arg97 and Asn233 (P > 0.95*). The predicted protein structural alteration caused by substitution of Asp233Asn in the conserved starch binding surface site, and significantly expressional differentiation during seed germination and grain development provided evidence of functional divergence between Amy1θ and Amy1λ genes. We screened out candidate copies (TaAmy1-A1/A2 and TaAmy1-D1) associated with high residual α-amylase activities in ripe grains. Furthermore, we proposed an evolutionary model for expansion dynamics of Amy1 genes. CONCLUSIONS: Our study provides comprehensive analyses of the Amy1 multigene family, and defines the fixation of two spatially structural Amy1 loci in wheat and barley. Potential functional divergence between them is reflected by their sequence features and expressional patterns, and driven by gene duplication, chromosome rearrangement and natural selections during gene family evolution. Furthermore, the discrimination of differentially effective copies during seed germination and/or grain development will provide guidance to manipulation of α-amylase activity in wheat and barley breeding for better yield and processing properties.

New insights into the origin and evolution of α-amylase genes in green plants.

Gene duplication is a source of genetic materials and evolutionary changes, and has been associated with gene family expansion. Functional divergence of duplicated genes is strongly directed by natural selections such as organism diversification and novel feature acquisition. We show that, plant α-amylase gene family (AMY) is comprised of six subfamilies (AMY1-AMY6) that fell into two ancient phylogenetic lineages (AMY3 and AMY4). Both AMY1 and AMY2 are grass-specific and share a single-copy ancestor, which is derived from grass AMY3 genes that have undergone massive tandem and whole-genome duplications during evolution. Ancestral features of AMY4 and AMY5/AMY6 genes have been retained among four green algal sequences (Chrein_08.g362450, Vocart_0021s0194, Dusali_0430s00012 and Monegl_16464), suggesting a gene duplication event following Chlorophyceae diversification. The observed horizontal gene transfers between plant and bacterial AMYs, and chromosomal locations of AMY3 and AMY4 genes in the most ancestral green body (C. reinhardtii), provide evidences for the monophyletic origin of plant AMYs. Despite subfamily-specific sequence divergence driven by natural selections, the active site and SBS1 are well-conserved across different AMY isoforms. The differentiated electrostatic potentials and hydrogen bands-forming residue polymorphisms, further imply variable digestive abilities for a broad substrates in particular tissues or subcellular localizations.