Maternal Particulate Matter Exposure Research Articles

Ambient particulate matter, maternal thyroid function, and birth weight: A mediation analysis

BackgroundBirth weight (BW) is an indicator of fetal growth and development. Previous studies showed inconsistent results on the association of ambient particulate matter (PM) exposure with BW, and the role of maternal thyroid function has not been clarified. MethodsWe recruited 1711 gravidas between 2017 and 2019 in Henan, China. All participants were followed up until delivery. Daily concentrations of PM, including PM2.5 and PM10, were evaluated by using the spatial-temporal model. Maternal thyroid hormone (TH) levels were quantified by electrochemiluminescent microparticle immunoassay. Linear regression models were employed to examine the association among PM, BW, and maternal TH. Mediating effects of maternal TH interrelated with PM exposure on BW were investigated by causal mediation analyses. ResultsA total of 1049 gravidas were identified. We found that per 10 µg/m3 increase in PM2.5 and PM10 were associated with a decreased BW of 9.941 g, and 7.758 g (PM2.5: 95 %CI: −18.184, −1.698; PM10: 95 %CI: −14.436, −1.080). An inverse correlation of maternal FT4 levels with BW was found, with the pooled β of −319.983 g (95 %CI: −483.216, −156.750). We found a prominent positive correlation between gestational FT4 and PM exposure (PM2.5: β = 0.004, 95 %CI: 0.001, 0.007; PM10: β = 0.003, 95 %CI: 0.000, 0.006). Mediation analysis found that FT4 levels mediated the relationship between maternal PM exposure and BW, ranging from 5.55 % to 15.86 %. ConclusionsMaternal PM exposure may induce a reduction in newborn BW by affecting the maternal TH concentrations.

Maternal exposure to aircraft emitted ultrafine particles during pregnancy and likelihood of ASD in children

BackgroundThere is increasing evidence for adverse health effects associated with aircraft-emitted particulate matter (PM) exposures, which are largely in the ultrafine (PM0.1) size fraction, but no previous study has examined neurodevelopmental outcomes. ObjectiveTo assess associations between maternal exposure to aircraft ultrafine particles (UFP) during pregnancy and offspring autism spectrum disorder (ASD) diagnosis. MethodsThis large, representative cohort study included 370,723 singletons born in a single healthcare system. Demographic data, maternal health information, and child’s ASD diagnosis by age 5 were extracted from electronic medical records. Aircraft exposure estimates for PM0.1 were generated by the University of California Davis/California Institute of Technology Source Oriented Chemical Transport model. Cox proportional hazard models were used to assess associations between maternal exposure to aircraft PM0·1 in pregnancy and ASD diagnosis, controlling for covariates. ResultsOver the course of follow-up, 4,554 children (1.4 %) were diagnosed with ASD. Increased risk of ASD was associated with maternal exposure to aircraft PM0.1 [hazard ratio, HR: 1.02, (95 % confidence interval (CI): 1.01–1.03) per IQR = 0.02 µg/m3 increase during pregnancy. Associations were robust to adjustment for total PM0.1 and fine particulate matter (PM2.5), near-roadway air pollution, and other covariates. Noise adjustment modestly attenuated estimates of UFP effects, which remained statistically significant. DiscussionThe results strengthen the emerging evidence that maternal particulate matter exposure during pregnancy is associated with offspring ASD diagnosis and identify aircraft-derived PM0.1 as novel targets for further study and potential regulation.

Maternal particulate matter exposure and gestational diabetes mellitus: a population–based cohort study

Gestational diabetes mellitus (GDM) prevalence is steadily increasing worldwide, posing a significant threat to the short- and long-term health of both mother and offspring. As particulate matter (PM) air pollution has been reported to affect glucose metabolism, it was suggested that maternal PM exposure may be associated with the development of GDM; however, evidence is limited and inconsistent. To study the association between maternal exposure to PM2.5 and PM10 and the risk of GDM, to identify critical windows of susceptibility and to evaluate effect modification by ethnicity. A retrospective cohort study was conducted including pregnancies of women who delivered at a large tertiary medical center in Israel between the years 2003 and 2015. Residential PM levels were estimated by a hybrid spatiotemporally resolved satellite-based model at 1-km spatial resolution. Multivariable logistic analyses were applied to study the association between maternal PM exposure in different pregnancy periods and GDM risk, while adjusting for background, obstetrical and pregnancy characteristics. Analyses were also stratified by ethnicity (Jewish / Bedouin). The study included 89,150 pregnancies, 3,245 (3.6%) were diagnosed with GDM. First trimester exposure to both PM2.5 (adj. OR per 5 μg/m3 = 1.09; 95%CI: 1.02, 1.17) and PM10 (adj. OR per 10 μg/m3 = 1.11; 95%CI: 1.06, 1.17) was significantly associated with increased risk for GDM. In the stratified analyses, the association with first trimester PM10 exposure was consistent among pregnancies of both Jewish and Bedouin women, while the association with first trimester PM2.5 exposure was significant among pregnancies of Jewish women only (adj. OR per 5 μg/m3 = 1.09; 95%CI: 1.00, 1.19), as well as association with preconception PM10 exposure (adj. OR per 10 μg/m3 = 1.07; 95%CI: 1.01, 1.14). No association was found between second trimester PM exposure and GDM risk. Maternal exposure to both PM2.5 and PM10 during the first trimester of pregnancy is associated with GDM, suggesting the first trimester as a particular window of susceptibility to the effect of PM exposure on GDM risk. The effects found in this study differed by ethnic group, emphasizing the importance of addressing ethnic disparities when assessing environmental impacts on health.

Tenascin C in Lung Diseases.

Tenascin C (TNC) is a multifunctional large extracellular matrix protein involved in numerous cellular processes in embryonic development and can be increased in disease, or under conditions of trauma or cell stress in adults. However, the role of TNC in lung diseases remains unclear. In this study, we investigated the expression of TNC during development, in offspring following maternal particulate matter (PM) exposure, asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. TNC expression is increased during lung development in biopsy cells, endothelial cells, mesenchymal cells, and epithelial cells. Maternal PM exposure increased TNC and collagen deposition, which was not affected by the removal of PM exposure after pregnancy. TNC expression was also increased in basal epithelial cells and fibroblasts in patients with asthma and AT2 and endothelial cells in patients with COPD. Furthermore, there was an increase in the expression of TNC in stage II compared to stage IA lung cancer; however, overall survival analysis showed no correlation between levels of TNC and survival. In conclusion, TNC is increased during lung development, in offspring following maternal PM exposure, and in asthma, COPD, and lung cancer tissues. Therefore, targeting TNC may provide a novel therapeutic target for lung diseases.

Sex-Dependent Responses to Maternal Exposure to PM2.5 in the Offspring.

Objective: Particulate matter (PM) with a diameter of 2.5 μm or less (PM2.5) can cross the blood-placental barrier causing adverse foetal outcomes. However, the impact of maternal exposure to low-levels of PM2.5 on liver health and the metabolic profile is unclear. This study aimed to investigate hepatic responses to long-term gestational low-dose PM2.5 exposure, and whether the removal of PM after conception can prevent such effects. Method: Female Balb/c mice (8 weeks) were exposed to PM2.5 (5 μg/day) for 6 weeks prior to mating, during gestation and lactation to model living in a polluted environment (PM group). In a sub-group, PM2.5 exposure was stopped post-conception to model mothers moving to areas with clean air (pre-gestation, Pre) group. Livers were studied in 13-week old offspring. Results: Female offspring in both PM and Pre groups had increased liver triglyceride and glycogen levels, glucose intolerance, but reduced serum insulin and insulin resistance. Male offspring from only the Pre group had increased liver and serum triglycerides, increased liver glycogen, glucose intolerance and higher fasting glucose level. Markers of oxidative stress and inflammation were increased in females from PM and Pre groups. There was also a significant sex difference in the hepatic response to PM2.5 with differential changes in several metabolic markers identified by proteomic analysis. Conclusions: Maternal PM exposure exerted sex-dependent effects on liver health with more severe impacts on females. The removal of PM2.5 during gestation provided limited protection in the offspring's metabolism regardless of sex.

Adverse organogenesis and predisposed long-term metabolic syndrome from prenatal exposure to fine particulate matter.

Exposure to fine particulate matter (PM) during pregnancy is associated with high risks of birth defects/fatality and adverse long-term postnatal health. However, limited mechanistic data are available to assess the detailed impacts of prenatal PM exposure. Here we evaluate fine PM exposure during pregnancy on prenatal/postnatal organogenesis in offspring and in predisposing metabolic syndrome for adult life. Between days 0 and 18 of gestation, two groups of adult female rats (n = 10 for each) were placed in a dual-exposure chamber device, one with clean ambient air (∼3 µg·m-3) and the other with ambient air in the presence of 100 to 200 µg·m-3 of ultrafine aerosols of ammonium sulfate. At birth (postnatal day 0, PND0), four males and four females were selected randomly from each litter to be nursed by dams, whereas tissues were collected from the remaining pups. At PND21, tissues were collected from two males and two females, whereas the remaining pups were fed either a high- or low-fat diet until PND105, when tissues were obtained for biochemical and physiological analyses. Maternal exposure to fine PM increased stillbirths; reduced gestation length and birth weight; increased concentrations of glucose and free fatty acids in plasma; enhanced lipid accumulation in the liver; and decreased endothelium-dependent relaxation of aorta. This lead to altered organogenesis and predisposed progeny to long-term metabolic defects in an age-, organ-, and sex-specific manner. Our results highlight the necessity to develop therapeutic strategies to remedy adverse health effects of maternal PM exposure on conceptus/postnatal growth and development.

Effects of particulate matter exposure during pregnancy on birth weight: A retrospective cohort study in Suzhou, China

BackgroundRecent studies have identified that exposure to particulate matter during pregnancy could result in adverse birth outcomes, but the effects of exposure at trimester-specific intervals are inconsistent. ObjectiveOur primary goal was to investigate whether particulate matter exposure during pregnancy could affect birth weight and gestational age of neonates. MethodsA retrospective cohort study was conducted to examine the relationship between maternal particulate matter exposure and neonatal birth weight. We collected 14,455 births records linked to hospital admission records (delivery and antenatal) from January 2013 to December 2015 in Suzhou Municipal Hospital. Air monitoring data in the same timeframe were also collected from Suzhou Environmental Protection Agency. The risk of low birth weight due to the exposure to PM2.5 (with median aerodynamic diameter≤2.5μm) and PM10 (with median aerodynamic diameter≤10μm) at each trimester and throughout the entire pregnancy were assessed. Linear regression models were applied and potential confounding factors were adjusted for data analysis. Gestational age, which was another important birth outcome, and its association with maternal particulate matter exposure were also studied. ResultsThe final analysis included 10,915 singleton live births. Using multiple linear regression models, we found that gestational exposure to PM2.5 and PM10 at 10μg/m3 increments in the second trimester led to decreases in birth weight of 4.94g (95% confidence interval: −9.828, −0.046) and 5.65g (95% confidence interval: −10.110, −1.188), respectively. However, gestational age was not significantly associated with maternal particulate matter exposure in term neonates. ConclusionThese findings indicate that pregnant women might be more susceptible to particulate matter during the second trimester which may lead to decreased neonatal birth weight.