Pregnant women and their fetuses represent susceptible populations to environmental contaminants. Exposure to polycyclic aromatic hydrocarbons (PAHs) among pregnant women may contribute to adverse birth outcomes such as preterm birth. Multiple previous studies have assessed airborne sources of PAHs among pregnant women but few have measured urinary PAH metabolites which can capture total exposure through multiple routes. The aim of this study was to bridge this knowledge gap by assessing longitudinal urinary PAH metabolite concentrations over two time points in pregnancy cohorts in Boston (N = 200) and Puerto Rico (N = 50) to better understand exposure distributions throughout pregnancy and how they relate to demographic factors. Urine samples were analyzed for 1-NAP, 2-NAP, 2-FLU, 1-PHE, 2,3-PHE, 4-PHE, 9-PHE, and 1-PYR. Concentrations of 2-NAP, 1-PYR, and 4-PHE were higher in Puerto Rico, while all other metabolites were present in higher concentrations in Boston. In Puerto Rico, intraclass correlation coefficients (ICC) were weak to moderate, ranging from 0.06 to 0.42. PAH metabolite concentrations were significantly higher among younger, heavier (except 1-NAP and 9-PHE), and less educated individuals in Boston only. Consistent significant associations between PAH concentrations and measured covariates were not found in Puerto Rico. Our results suggest that potentially important differences in PAH exposure exist between these two populations. Additionally, our results indicate that multiple urinary measurements are required to accurately assess PAH exposure throughout pregnancy.

Prenatal disinfection by-products (DBPs) exposure is linked with adverse birth outcomes. Genetic susceptibility to DBP metabolism may modify the exposure-outcome associations.To investigate whether CYP2E1 and GSTZ1 genetic polymorphisms modified the associations of prenatal DBP exposures with adverse birth outcomes.Two biomarkers of DBP exposures including trihalomethanes (THMs) in blood and trichloroacetic acid (TCAA) in urine were determined among 426 pregnant women from a Chinese cohort study. CYP2E1 (rs2031920, rs3813867, and rs915906) and GSTZ1 (rs7975) polymorphisms in cord blood were genotyped. Statistical interactions between prenatal DBP exposures and newborns CYP2E1 and GSTZ1 polymorphisms on birth outcomes (birth weight, birth length, and gestational age) were examined by multivariable linear regression with adjustment for potential confounders.We found that newborns CYP2E1 genetic polymorphisms (rs2031920 and rs3813867) modified the associations of maternal blood THMs or urinary TCAA levels with birth outcomes. However, these interactions were nonsignificant after Bonferroni correction for multiple comparisons, except for the interaction between maternal blood BrTHMs [sum of dibromochloromethane (DBCM), bromodichloromethane (BDCM), and bromoform (TBM)] and newborns CYP2E1 gene rs2031920 polymorphisms on birth weight (P for interaction = 0.003).Newborns genetic variations of CYP2E1 rs2031920 may modify the impacts of prenatal BrTHM exposure on birth weight. This finding needs to be further confirmed.

An increasing number of studies have been conducted to determine a possible linkage between maternal exposure to ambient fine particulate matter and effects on the developing human fetus that can lead to adverse birth outcomes, but, the present results are not consistent. A total of 23 studies published before July 2016 were collected and analyzed and the mean value of reported exposure to fine particulate matter (PM2.5) ranged from 1.82 to 22.11 We found a significantly increased risk of preterm birth with interquartile range increase in PM2.5 exposure throughout pregnancy (odds ratio (OR) = 1.03; 95% conditional independence (CI): 1.01–1.05). The pooled OR for the association between PM2.5 exposure, per interquartile range increment, and term low birth weight throughout pregnancy was 1.03 (95% CI: 1.02–1.03). The pooled ORs for the association between PM2.5 exposure per 10 increment, and term low birth weight and preterm birth were 1.05 (95% CI: 0.98–1.12) and 1.02 (95% CI: 0.93–1.12), respectively throughout pregnancy. There is a significant heterogeneity in most meta-analyses, except for pooled OR per interquartile range increase for term low birth weight throughout pregnancy. We here show that maternal exposure to fine particulate air pollution increases the risk of preterm birth and term low birth weight. However, the effect of exposure time needs to be further explored. In the future, prospective cohort studies and personal exposure measurements needs to be more widely utilized to better characterize the relationship between ambient fine particulate exposure and adverse birth outcomes.

Low birth weight (<2500 g) (LBW), premature birth (<37 weeks of gestation) (PB), and late foetal death (<24 h of life) (LFD) are causes of perinatal morbi-mortality, with short- and long-term social and economic health impacts. This study sought to identify gestational windows of susceptibility during pregnancy and to analyse and quantify the impact of different air pollutants, noise and temperature on the adverse birth outcomes.Time-series study to assess the impact of mean daily PM2.5, NO2 and O3 (μg/m3), mean daily diurnal (Leqd) and nocturnal (Leqn) noise levels (dB(A)), maximum and minimum daily temperatures (°C) on the number of births with LBW, PB or LFD in Madrid across the period 2001–2009. We controlled for linear trend, seasonality and autoregression. Poisson regression models were fitted for quantification of the results. The final models were expressed as relative risk (RR) and population attributable risk (PAR).Leqd was observed to have the following impacts in LBW: at onset of gestation, in the second trimester and in the week of birth itself. NO2 had an impact in the second trimester. In the case of PB, the following: Leqd in the second trimester, Leqn in the week before birth and PM2.5 in the second trimester. In the case of LFD, impacts were observed for both PM2.5 in the third trimester, and minimum temperature. O3 proved significant in the first trimester for LBW and PB, and in the second trimester for LFD.Pollutants concentrations, noise and temperature influenced the weekly average of new-borns with LBW, PB and LFD in Madrid. Special note should be taken of the effect of diurnal noise on LBW across the entire pregnancy. The exposure of pregnant population to the environmental factors analysed should therefore be controlled with a view to reducing perinatal morbi-mortality.

Chromium exposure from increasing industrial releases has become a threat for pregnant women due to the potential health effects on vulnerable embryos. Previous studies have suggested that maternal chromium exposure is associated with adverse birth outcomes, but no epidemiological research has been conducted to examine the relationship between chromium exposure and premature rupture of membranes (PROM). This study aimed at investigating the association of maternal urinary chromium exposure levels with PROM and was performed with 5408 pregnant women recruited from 2012 to 2014 in the city of Wuhan, China. Maternal urinary chromium collected before labor was adjusted with creatinine, and its association with PROM was evaluated using logistic regression. Each one unit increase in the natural logarithm transformed maternal urinary chromium concentration (μg/g creatinine), an odds ratio (OR) of 1.47 [95% confidence interval (CI): 1.36, 1.58] for PROM was observed. Compared to the lowest tertile of maternal urinary chromium, PROM was positively correlated with increased urinary levels of chromium (adjusted OR = 1.42; 95% CI: 1.09, 1.84 for the medium tertile; adjusted OR = 2.77; 95% CI: 2.18, 3.52 for the highest tertile). Additionally, the association of chromium with PROM appeared to be more significant among male infants (adjusted OR = 3.52; 95% CI: 2.51, 4.94 for the highest tertile) than female infants (adjusted OR = 2.16; 95% CI: 1.52, 3.06 for the highest tertile) (p for interaction = 0.05). Our large birth cohort showed an association between maternal urinary chromium levels and PROM, and the association may differ by infant gender. Further studies from different populations are needed to confirm the observed association.

Maternal arsenic exposure leads to adverse birth outcomes, but the critical window of this susceptibility keeps unclear. To determine whether the associations between maternal arsenic exposure and birth outcomes were trimester-specific, we conducted a birth cohort study of 1390 women from 2014 to 2016 in Wuhan, China. We examined associations between total urinary arsenic concentrations in three trimesters and birth weight, birth length and the risk of small for gestational age (SGA), and the differences of these associations across trimesters using generalized estimating equations. Maternal urinary arsenic concentrations varied across trimesters and were weakly correlated. Arsenic concentrations in the 3rd trimester, but not in the 1st and 2nd trimesters, were associated with birth outcomes. For each doubling of arsenic levels in the 3rd trimester, birth weight was decreased 24.27 g (95% confidence interval (CI): −46.99, −1.55), birth length was decreased 0.13 cm (95% CI: −0.22, −0.04), and the risk for SGA birth was increased 25% (95% CI: 1.03, 1.49). Further, stratified analyses indicated that these associations were only observed in female infants. Our findings indicate maternal arsenic levels in the 3rd trimester seemed to have significant impacts on birth outcomes, and also emphasize the public health interventions relevance to arsenic exposure in late pregnancy.

Exposures to chlorophenols (CPs) have been linked with adverse health effects on wildlife and humans. This study aimed to evaluate prenatal exposure to five CP compounds using maternal urinary concentrations during pregnancy and the potential associations with birth outcomes of their infants at birth. A total of 1100 mother-newborn pairs were recruited during June 2009 to January 2010 in an agricultural region, China. Urinary concentrations of five CPs from dichlorophenol (DCP) to pentachlorophenol (PCP), namely, 2,5-DCP, 2,4-DCP, 2,4,5-trichlorophenol (2,4,5-TCP), 2,4,6-TCP and PCP, were measured using large-volume-injection gas chromatography-tandem mass spectrometry (LVI-GC-MS-MS), and associations between CP levels and weight, length as well as head circumference at birth were examined. Median urinary creatinine-adjusted concentrations of 2,5-DCP, 2,4-DCP, 2,4,5-TCP, 2,4,6-TCP and PCP were 3.34 μg/g, 1.03 μg/g, < LOD, 1.78 μg/g and 0.39 μg/g creatinine, respectively. We found lower birth weight 30 g [95% confidence interval (CI): −57, −3; p = 0.03] for per SD increase in log10-transformed concentrations of 2,4,6-TCP and lower birth weight 37 g (95% CI: −64, −10; p = 0.04) for PCP, respectively. Similarly, head circumference decrease in associations with creatinine-corrected 2,4,6-TCP and PCP concentrations were also achieved. Considering sex difference, the associations of lower birth weight were only found among male neonates, while head circumference was associated with 2,4-DCP and 2,5-DCP only found among female neonates. This study showed significant negative associations between CPs exposure and reduction in neonatal anthropometric measures. The biological mechanisms concerning CPs exposure on fetal growth deserved further investigations.

Reduced birth weight (RBW) and reduced head circumference (RHC) are adverse birth outcomes (ABOs), often linked to environmental exposures. However, spatial identification of specific health hazards, associated with these ABOs, is not always straightforward due to presence of multiple health hazards and sources of air pollution in urban areas. In this study, we test a novel empirical approach to the spatial identification of environmental health hazards potentially associated with the observed RHC and RBW patterns. The proposed approach is implemented as a systematic search, according to which alternative candidate locations are ranked based on the strength of association with the observed birth outcome patterns. For empirical validation, we apply this approach to the Haifa Bay Area (HBA) in Israel, which is characterized by multiple health hazards and numerous sources of air pollution. We identified a spot in the local industrial zone as the main risk source associated with the observed RHC and RBW patterns. Multivariate regressions, controlling for personal, neighborhood, and geographic factors, revealed that the relative risks of RHC and RBW tend to decline, other things being equal, as a function of distance from the identified industrial spot. We recommend the proposed identification approach as a preliminary risk assessment tool for environmental health studies, in which detailed information on specific sources of air pollution and air pollution dispersion patterns is unavailable due to limited reporting or insufficient monitoring.

Exposure to ambient air pollutants during pregnancy may be associated with numerous side health effects and adverse birth outcomes. Growing numbers of studies have explored a possible linkage between prenatal exposure to PM₂.₅ (particulate matter with aerodynamic diameter ≤ 2.5 μm) and impacts on fetal development. We aimed to conduct a systematic review based on published cohort studies to summarize evidence regarding the association between maternal PM₂.₅ exposure and birth outcomes, including birth weight, low birth weight (LBW), preterm birth (PTB), and small for gestational age (SGA). Eligible studies meeting the following criterion were selected: PM₂.₅ exposure during pregnancy and live birth singletons, certain presentation of sample sizes, and quantitative evaluation of the associations between exposure and outcomes. Among the 42 selected studies, 23 evaluated the impact of prenatal PM₂.₅ exposure on birth weight of infants while 12 of them provided a significantly negative association for exposure and birth weight. Twenty-one studies aimed to identify the possible relationship between maternal exposure and LBW and 8 studies proved significant associations. Among 18 studies that explored the correlation between prenatal exposure and PTB, 9 reached a consistent conclusion that gestational exposure would add to the risk of PTB. Nine studies assessed the impact of PM₂.₅ on SGA and 5 of them demonstrated a significant effect. So far, linkages between maternal PM₂.₅ exposure during varied gestational stages and multiple adverse birth outcomes have been observed in many studies. A summary of them will be meaningful for further research on maternal exposure and adverse birth outcomes.

Chlordecone (CLD) is a chlorinated hydrocarbon insecticide, now classified as a persistent organic pollutant. Several studies have previously reported that chronic exposure to CLD leads to hepatotoxicity, neurotoxicity, raises early child development and pregnancy complications, and increases the risk of liver and prostate cancer. In situ chemical reduction (ISCR) has been identified as a possible way for the remediation of soils contaminated by CLD. In the present study, the objectives were (i) to evaluate the genotoxicity and the mutagenicity of two CLD metabolites formed by ISCR, CLD-5a-hydro, or CLD-5-hydro (5a- or 5- according to CAS nomenclature; CLD-1Cl) and tri-hydroCLD (CLD-3Cl), and (ii) to explore the angiogenic properties of these molecules. Mutagenicity and genotoxicity were investigated using the Ames’s technique on Salmonella typhimurium and the in vitro micronucleus micromethod with TK6 human lymphoblastoid cells. The proangiogenic properties were evaluated on the in vitro capillary network formation of human primary endothelial cells. Like CLD, the dechlorinated derivatives of CLD studied were devoid of genotoxic and mutagenic activity. In the assay targeting angiogenic properties, significantly lower microvessel lengths formed by endothelial cells were observed for the CLD-3Cl-treated cells compared to the CLD-treated cells for two of the three tested concentrations. These results suggest that dechlorinated CLD derivatives are devoid of mutagenicity and genotoxicity and have lower proangiogenic properties than CLD.