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Effect of Particulate Matter 2.5 on Fetal Growth in Male and Preterm Infants through Oxidative Stress.

ABSTRACT: Particulate matter 2.5 (PM_2.5) levels are associated with adverse pregnancy outcomes. In this retrospective cohort study, we examined whether the concentration of indoor PM_2.5 affected pregnancy outcomes. Additionally, we evaluated biomarkers of pregnancy-related complications caused by fine dust. We collected clinical information and data based on residential addresses from the Air Korea database to assess PM_2.5 exposure levels. As a multicenter prospective cohort study, we measured the indoor PM_2.5 concentration and inflammatory and oxidative stress markers. The PM_2.5 concentration of the low-birth-weight (LBW) delivery group was 27.21 μg/m³, which was significantly higher than that of the normal-birth-weight (NBW) group (26.23 μg/m³) (p = 0.02). When the newborns were divided by sex, the PM_2.5 concentration of the LBW group was 27.89 μg/m³ in male infants, which was significantly higher than that of the NBW group (26.26 μg/m³) (p = 0.01). In the prospective study, 8-hydroxy-2-deoxyguanosine significantly increased in the high-concentration group (113.55 ng/mL, compared with 92.20 ng/mL in the low-concentration group); in the high-concentration group, the rates of preterm birth (PTB) and small size for gestational age significantly increased (p < 0.01, p = 0.01). This study showed an association between PM_2.5, oxidative stress, and fetal growth, with the PTB group being more vulnerable.

SUBMITTER: Park S

PROVIDER: S-EPMC10669397 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature

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Effect of Particulate Matter 2.5 on Fetal Growth in Male and Preterm Infants through Oxidative Stress.

Park Sunwha S Kwon Eunjin E Lee Gain G You Young-Ah YA Kim Soo Min SM Hur Young Min YM Jung Sooyoung S Jee Yongho Y Park Mi Hye MH Na Sung Hun SH Kim Young-Han YH Cho Geum Joon GJ Bae Jin-Gon JG Lee Soo-Jeong SJ Lee Sun Hwa SH Kim Young Ju YJ

Antioxidants (Basel, Switzerland) 20231026 11

Particulate matter 2.5 (PM2.5) levels are associated with adverse pregnancy outcomes. In this retrospective cohort study, we examined whether the concentration of indoor PM2.5 affected pregnancy outcomes. Additionally, we evaluated biomarkers of pregnancy-related complications caused by fine dust. We collected clinical information and data based on residential addresses from the Air Korea database to assess PM2.5 exposure levels. As a multicenter prospective coho ...[more]

PMID: 38001768

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Project description:BackgroundFetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.MethodsA total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).ResultsThe full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, - 1.91), 5.57 (- 6.66, - 4.47), and 5.47 (- 6.39, - 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, - 13.49) grams by Hadlock's third formula and 13.56 (- 14.71, - 12.50) grams by Shepard's formula with each 10 μg/m3 increase in PM2.5 exposure.ConclusionsA negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Project description:Numerous toxicological studies have highlighted the association between urban particulate matter (PM) and increased respiratory infections and lung diseases. The adverse impact on the lungs is directly linked to the complex composition of particulate matter, initiating reactive oxygen species (ROS) production and consequent lipid peroxidation. Excessive ROS, particularly within mitochondria, can destroy subcellular organelles through various pathways. In this study, we confirmed the induction of ferroptosis, an iron-dependent cell death, upon exposure to an urban PM using RT-qPCR and signaling pathway analysis. We used KRISS CRM 109-02-004, the certified reference material for the analysis of particulate matter, produced by the Korea Research Institute of Standards and Science (KRISS). To validate that ferroptosis causes lung endothelial toxicity, we assessed intracellular mitochondrial potential, ROS overproduction, lipid peroxidation, and specific ferroptosis biomarkers. Following exposure to the urban PM, a significant increase in ROS generation and a decrease in mitochondrial potential were observed. Furthermore, it induced hallmarks of ferroptosis, including the accumulation of lipid peroxidation, the loss of antioxidant defenses, and cellular iron accumulation. In addition, the occurrence of oxidative stress as a key feature of ferroptosis was confirmed by increased expression levels of specific oxidative stress markers such as NQO1, CYP1B1, FTH1, SOD2, and NRF. Finally, a significant increase in key ferroptosis markers was observed, including xCT/SLC7A11, NQO1, TRIM16, HMOX-1, FTL, FTH1, CYP1B1, CHAC1, and GPX4. This provides evidence that elevated ROS levels induce oxidative stress, which ultimately triggers ferroptosis. In conclusion, our results show that the urban PM, KRISS CRM, induces cellular and mitochondrial ROS production, leading to oxidative stress and subsequent ferroptosis. These results suggest that it may induce ferroptosis through ROS generation and may offer potential strategies for the treatment of lung diseases.

Project description:The main objective of this study was chemical characterization and source apportionment of the oxidative potential of ambient PM2.5 samples collected in an urban background area in Athens, Greece. Ambient PM2.5 samples were collected during the summer (June-September) of 2017 and winter (February-March) of 2018 at a residential, urban background site in the outlying neighborhood of the Demokritos National Laboratory in Athens, Greece. The collected PM samples were analyzed for their chemical constituents including metals and trace elements, water-soluble organic carbon (WSOC), elemental and organic carbon (EC/OC), and marker of biomass burning (i.e., levoglucosan). In addition, the DCFH in vitro assay was performed to determine the oxidative potential of the PM2.5 samples. We performed a series of statistical analyses, including Spearman rank-order correlation analysis, principal component analysis (PCA), and multi linear regression (MLR) to determine the most significant species (as source tracers) contributing to the oxidative potential of PM2.5. Our findings revealed that the intrinsic (per PM mass) and extrinsic (per m3 of air volume) oxidative potentials of the collected ambient PM2.5 samples were significantly higher than those measured in many urban areas around the world. The results of the MLR analyses indicated that the major pollution sources contributing to the oxidative potential of ambient PM2.5 were vehicular emissions (characterized by EC) (44%), followed by secondary organic aerosol (SOA) formation (characterized by WSOC) (16%), and biomass burning (characterized by levoglucosan) (9%). The oxidative potential of the collected ambient PM2.5 samples was also higher in summer compared to the winter, mainly due to higher concentrations of EC and WSOC during this season. Results from this study corroborate the impact of traffic and SOA on the oxidative potential of ambient PM2.5 in greater Athens area, and can be helpful in adopting appropriate public health policies regarding detrimental outcomes of exposure to PM2.5.

Project description:BackgroundFetal growth has been known to be associated with particulate matter (PM) air pollution during gestation. Given that regular working may deviate outdoor air pollution exposure, the association between air pollution and fetal growth restriction can be different across maternal working status. This study was to assess possible effect modification by maternal employment in the association between exposure to PM during pregnancy and fetal growth restriction.MethodsUsing hourly PM less than or equal to 10 and 2.5 μm in diameter (PM10 and PM2.5) regulatory monitoring data for 2001-2012 and 2008-2012, respectively, and birth certificate data for 2002-2012, we computed maternal exposures with district-level averages of PM10 and PM2.5 during one year before birth, entire pregnancy, and the 1st, 2nd and 3rd trimesters. The outcomes of fetal growth restriction were assessed by small for gestational age (SGA, weighted <10th percentile in the same gestational age) as well as low birth weight (LBW, < 2.5 kg) at term. We performed logistic regression to examine the association between PM and each of fetal growth restriction outcomes adjusting for individual risk factors. For effect modification by maternal employment, we estimated adjusted odds ratio (OR) of SGA or LBW for interquartile (IQR) increases in PM10 or PM2.5 stratified by employed and non-employed mothers. We also computed relative excess risk due to interaction (RERI) to investigate additive interaction.ResultsAmong 824,011 singleton term births, 34.0% (279,856) were employed and 66.0% (544,155) were non-employed mothers. Proportions of LBW were 1.5% in employed and 1.6% in non-employed (P < 0.001). SGA occurred in 12.7% of employed and 12.8% of non- employed (P = 0.124) mothers. For non-employed mothers, we observed increased odds of SGA per IQR increase in PM10 for one year before birth (OR = 1.02, 95% confidence intervals (CI): 1.00-1.04, P = 0.028). ORs of SGA for full pregnancy period and the 3rd trimester were also positive but did not reach statistical significance. We did not observe positive association for PM2.5. RERI was not significant both for PM10 and PM2.5.ConclusionsWe did not observe evidence of effect modification by maternal employment in the association between ambient PM and fetal growth restriction. Future studies using more refined exposure measures should confirm this finding.

Dataset Information

Effect of Particulate Matter 2.5 on Fetal Growth in Male and Preterm Infants through Oxidative Stress.

Publications

Effect of Particulate Matter 2.5 on Fetal Growth in Male and Preterm Infants through Oxidative Stress.

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