Individual exposure to urban air pollution and its correlation with placental angiogenic markers in the first trimester of pregnancy, in São Paulo, Brazil.

Pollution of the atmosphere is known that may lead to adverse obstetric outcomes, including fetal growth restriction, gestational hypertension, and preeclampsia. Such disorders are correlated with imbalances in angiogenic factors, which may also be involved in the pathological mechanism as the pollutants impact placental and maternal physiology. In the first trimester of gestation, this study assessed the outcomes of personal maternal short period exposure to air pollution on soluble fms-like tyrosine kinase 1 (sFlt1) and placental growth factor (PLGF) of pregnant women blood concentrations. This was a cross-sectional study, held in the city of São Paulo, Brazil, and conducted with low-risk pregnant women, who carried personal passive nitrogen dioxide (NO2) and ozone (O3) monitors for about a few days preceding the ultrasound evaluation, and on this day, the venous blood sample was collected to measure the angiogenic factors sFlt1 and PLGF and their ratio (sFlt1/PLGF) by enzyme-linked immunosorbent assay (ELISA). By means of multiple regression models, the effect of the studied pollutants on the log-transformed concentrations of the angiogenic factors was evaluated. One hundred thirty-one patients were included. The log of the sFlt1/PLGF ratio increased with rising NO2 levels (p = 0.021 and beta = 0.206), and the log of the PLGF concentration showed a negative correlation with NO2 (p = 0.008 and beta = - 0.234). NO2, an indicator of the levels of primary air pollutants, presented significant positive correlation with an increased sFlt1/PLGF ratio and diminished PLGF levels, which may reflect an antiangiogenic state generated by air pollution exposure.

Association between exposure to air pollution during intrauterine life and cephalic circumference of the newborn.

It has been observed that air pollution can affect newborn health due to the negative effects of pollutants on pregnancy development. However, few studies have evaluated the impact of maternal exposure to urban air pollution on head circumference (HC) at birth. Reduced head growth during pregnancy may be associated with neurocognitive deficits in childhood. The objectives of this study were to evaluate the association between maternal exposure to air pollution and HC at birth and to provide context with a systematic review to investigate this association. This was a prospective study of low-risk pregnant women living in São Paulo, Brazil. Exposure to pollutants, namely, nitrogen dioxide (NO2) and ozone (O3), was measured during each trimester using passive personal samplers. We measured newborn HC until 24 h after birth. We used multiple linear regression models to evaluate the association between pollutants and HC while controlling for known determinants of pregnancy. To perform the systematic review, four different electronic databases were searched through November 2018: CENTRAL, EMBASE, LILACS, and MEDLINE. We selected longitudinal or transversal designs associating air pollution and HC at birth. Two reviewers evaluated the inclusion criteria and risk of bias and extracted data from the included papers. Thirteen studies were selected for the systematic review. We evaluated 391 patients, and we did not observe a significant association between air pollution and HC. Regarding the systematic review, 13 studies were selected for the systematic review, 8 studies showed an inverse association between maternal exposure to pollutants and HC, 4 showed no association, and one observed a direct association. In the city of São Paulo, maternal exposure to pollutants was not significantly associated with HC at birth. The systematic review suggested an inverse association between air pollution and HC at birth.

Short-Term Exposure to Urban Air Pollution and Influences on Placental Vascularization Indexes.

BACKGROUND: It has been widely demonstrated that air pollution can affect human health and that certain pollutant gases lead to adverse obstetric outcomes, such as preeclampsia and fetal growth restriction. OBJECTIVES: We evaluated the influence of individual maternal exposure to air pollution on placental volume and vascularization evaluated in the first trimester of pregnancy. METHODS: This was a cross-sectional study on low-risk pregnant women living in São Paulo, Brazil. The women carried passive personal NO2 and O3 monitors in the week preceding evaluation. We employed the virtual organ computer-aided analysis (VOCAL) technique using three-dimensional power Doppler ultrasound to evaluate placental volume and placental vascular indexes [vascularization index (VI), flow index (FI), and vascularization flow index (VFI)]. We analyzed the influence of pollutant levels on log-transformed placental vascularization and volume using multiple regression models. RESULTS: We evaluated 229 patients. Increased NO2 levels had a significant negative association with log of VI (p = 0.020 and beta = -0.153) and VFI (p = 0.024 and beta = -0.151). NO2 and O3 had no influence on the log of placental volume or FI. CONCLUSIONS: NO2, an estimator of primary air pollutants, was significantly associated with diminished VI and VFI in the first trimester of pregnancy.

Associations of maternal personal exposure to air pollution on fetal weight and fetoplacental Doppler: A prospective cohort study.

We determined the influence of maternal air pollution exposure during each trimester of pregnancy on fetal and birth weight and fetoplacental hemodynamics. In total, 366 women with singleton pregnancies were prospectively followed in the city of São Paulo, Brazil. Nitrogen dioxide (NO2) and ozone (O3) were measured during each trimester using passive personal samplers. We evaluated fetal weight and Doppler velocimetry data from the umbilical, middle cerebral, and uterine arteries in the 3rd trimester, and birth weight. Multivariate analysis was performed, controlling for known determinants of fetal weight. Exposure to higher levels of O3 during the 2nd trimester was associated with higher umbilical artery pulsatility indices (PIs) [p=0.013; beta=0.017: standard error (SE)=0.007]. Exposure to higher levels of O3 during the 3rd trimester was associated with lower umbilical artery PIs (p=0.011; beta=-0.021; SE=0.008). Our results suggest that in the environment of São Paulo, O3 may affects placental vascular resistance.