In Iraq, war contamination is the result of dispensed bombs, bullets, detonation of chemical and conventional weapons, and burn-pit emissions by US bases. Increases in congenital anomalies were reported from Iraqi cities post-2003. These cities were heavily bombed and encircled by US bases with burn-pits. Thorium is a radioactive compound and a direct depleted-uranium decay-product. Radioactive materials, including depleted uranium, are routinely stored in US bases and they have been shown to leak into the environment. We conducted a case-control study to investigate associations of residential proximity to Tallil Air Base, a US military base near Nasiriyah, as well as levels of uranium and thorium in hair and deciduous teeth with congenital anomalies. The study was based on a sample of 19 cases and 10 controls who were recruited during late Summer and early Fall of 2016. We developed mixed effects logistic regression models with village as the random effect, congenital anomaly as the outcome and distance to the US base and hair metal levels (one at a time) as the predictor variable, controlling for child's age, sex and paternal education. We also explored the mediation of the association between proximity to the base and congenital anomalies by hair metal levels. We found an inverse association between distance to Tallil Air Base and risk of congenital anomalies and hair levels of thorium and uranium. The results of our mediation analyses were less conclusive. Larger studies are necessary to understand the scope of war contamination and its impact on congenital anomalies in Iraq.

Per- and polyfluoroalkyl Substances (PFAS) are ubiquitous in the environmental matrix, and their eco-toxicity on wide life and health risks on humans arising concerns. Due to the information gap, current risk assessments of PFAS ignore the indoor exposure pathway such as indoor dust and the different sources of drinking water. We collected and analyzed 168 indoor dust and 27 drinking water samples (including tap water, filtered water and bottled water). The mean concentrations of six typical PFAS measured in indoor dust and drinking water are in the range of 15.13–491.07 ng g⁻¹ and 0.31–4.14 ng L⁻¹, respectively. For drinking water, PFOA and PFOS were the dominant compounds, while PFHxS was the most abundant in indoor dust. Short-chain PFAS concentrations were higher than long-chain PFAS in both drinking water and indoor dust. Higher concentration of PFAS was observed in tap water and filtered water than bottled water. The total daily intake (TDI) of six PFAS are 20.67–52.97 ng kg⁻¹ d⁻¹ for infants, children, teenagers, and adults. As to children, teenagers, and adults, perfluorooctanoate (PFOA) is the major compound, accounting for 72.9–74.7% of the total daily intake. And PFOA (38.7%) and perfluorooctane sulfonate (PFOS, 42.2%) are the dominant PFAS for infants. The quantitative proportions of exposure sources are firstly revealed in this study, which in the order of foodstuff > indoor dust > drinking water > indoor air. Although the contribution to the PFAS intake of drinking water and indoor dust was not predominant (<9%), the health risks caused by long-term exposure need our attention. The hazard quotient (HQ) values of total PFAS were in the range of 0.154–0.498, which suggesting the relatively lower exposure risk in Chinese population. This study provides important reference to understand PFAS exposure status other than foodstuff.

To monitor the body burden of persistent organic pollutants in mothers and infants living in proximity to a 10-year-old municipal waste incinerator (MWI), levels of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) in the breast milk of mothers were evaluated, and the estimated daily intake (EDI) level of these pollutants in infants was assessed. In total, 14 mothers from the exposure area and 18 mothers from a control area were recruited for this study. In addition, the levels of 17 PCDD/F congeners and 18 PCB congeners in the breast milk of the mothers were estimated, and risk assessment for their infants by calculating their EDI levels was performed. The mean levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs in the breast milk of the exposure group were significantly greater than those of the control group (3.36 vs. 1.47 pg/g wet weight; and 0.24 vs. 0.12 pg TEQ/g wet weight, respectively; p < 0.05). With respect to PCBs, the mean levels of the total PCBs (ΣPCBs) and non-dioxin like-PCBs (ΣNDL-PCBs) in the exposure group were significantly greater than those in the control group (269 vs. 141 pg/g wet weight; 230 vs. 115 pg/g wet weight, respectively; p < 0.05). The mean levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs were positively correlated with the inhabit time of the exposure group (r = 0.636, r = 0.629, p < 0.05, respectively). The mean EDI level of the exposure group in infants was significantly greater than that of the control group (22.0 vs. 13.0 pg TEQ/kg bw day; p < 0.05). In conclusion, mothers and their breast-fed infants living in proximity to the 10-year-old MWI located in the Zhejiang Province of China exhibited a significantly higher body burden of PCDD/Fs and PCBs compared to those living in the control area.

Maternal exposure to ambient air pollution has been related to oral clefts in offspring; however, the epidemiologic evidence is equivocal. Especially, the association between high levels of exposure to ambient air pollution during pregnancy and oral clefts remains unclear. The objective of this study was to evaluate whether high levels of maternal exposure to PM2.5, PM10, O3, CO and SO2 are related to increased risk of oral clefts in Wuhan, China. A population-based study was conducted using cohort of 105,927 live-born infants, fetal deaths, and stillbirths during a two-year period from 2011 to 2013. For each participant, weekly and monthly averages of daily mean concentrations for each pollutant were estimated. Multiple logistic regression analyses were constructed to quantify the adjusted odds ratios (aORs) for the relationship between each air pollutant and oral clefts while controlling for key covariates. Using monthly averages, a cleft lip with or without cleft palate (CLP) was associated with PM2.5 (aORs 2nd month = 1.34, CI:1.19–1.49; aORs 3rd month=1.14, CI:1.02–1.28), PM10 (aORs 2nd month = 1.11, CI:1.00–1.23) and CO (aORs 2nd month = 1.31, CI:1.14–1.51; aORs 3rd month = 1.17, CI:1.03–1.33). A cleft palate only (CPO) was associated with PM2.5 (aORs 2nd month = 1.24, CI: 1.03–1.48), and O3 (aORs 2nd month = 1.21, CI: 1.03–1.42; aORs 3rd month = 1.18, CI: 1.02–1.37). Our findings reveal an association between air pollutants exposure and the risk of oral clefts. Future studies are needed to confirm these associations, and clarify the causality related to specific pollutants during the most relevant vulnerable exposure time windows for oral clefts during pregnancy.

The widespread application of organophosphorous flame retardants (OPFRs) has led to considerable human exposure, with major concerns regarding their health risks. Herein, we investigate the effects of triphenyl phosphate (TPP), one of the most widely used OPFRs, and one of its main metabolite diphenyl phosphate (DPP) on the endocrine systems and metabolic profiles after neonatal exposure from postnatal days 1–10 at two dosages (2 and 200 μg per day). Both TPP and DPP had no negative effect on uterine weight, glucose tolerance, and estradiol. 1H-NMR-based metabolomics revealed a sex-specific metabolic disturbance of TPP. Specifically, low dose of TPP altered the metabolic profiles of male mice while exerting no significant effects on female ones. Furthermore, a dose-dependent effect of TPP in male mice was observed, where a low toxicity dose up-regulated lipid-related metabolites, while a high toxicity dose down-regulated the pyruvate metabolism and TCA cycles. These results highlight the importance of carefully assessing the health impact of TPP on infants.

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.

Polybrominated diphenyl ethers (PBDEs) are environmentally persistent chemicals that structurally resemble legacy pollutants, such as polychlorinated biphenyls (PCBs). PBDEs were added to consumer products for over 30 years, before being phased out due to evidence of toxicity. We examined temporal changes in prenatal exposure to PBDEs, as well as other sources of variation. We measured PBDEs in umbilical cord plasma from 327 minority infants born in New York City between 1998 and 2006. We used linear regression to examine changes in concentrations over time and in relation to lifestyle characteristics collected during pregnancy. We detected BDE-47 in 80% of samples with a geometric mean concentration of 14.1 ng/g lipid. Ethnicity was the major determinant of PBDE exposure; African American infants had 58% higher geometric mean cord plasma concentrations of BDE-47 (p < 0.01) compared to Dominican infants. Notably, African American mothers were more likely to be born in the United States, which itself was associated with 40% (p < 0.01) higher concentrations. We observed small decreases in PBDE concentrations by date of birth and no difference before and after their phase-out in 2004. Final multivariable models explained 8–12% of variability in PBDE concentrations depending on the congener. Our finding that prenatal exposure to PBDEs decreased only modestly between 1998 and 2006 is consistent with the persistent properties of PBDEs and their ongoing release from existing consumer products.

Evidence supporting an inverse association between maternal exposure to air pollutants and foetal growth has been accumulating. However, the findings from Asian populations are limited, and the question of critical windows of exposure remains unanswered. We examined whether maternal exposure to air pollutants, in particular exposure during the first trimester (an important period of placental development), was associated with foetal growth in Japanese term infants. From the Japan Perinatal Registry Network database, we received birth data for 29,177 term singleton births in western Japan (Kyushu-Okinawa Districts) between 2005 and 2010. Exposure was expressed in terms of average concentrations of air pollutants (ozone, suspended particulate matter, nitrogen dioxide, and sulphur dioxide), as measured at the nearest monitoring stations to the respective delivery hospitals of the pregnant women, during the entire pregnancy and each trimester. As proxy markers of foetal growth restriction, we used small for gestational age (SGA), and adverse birth weight (low birth weight in addition to SGA). For pollutant exposure during the entire pregnancy, we did not observe the association with SGA and adverse birth weight. In the single-trimester model for the first trimester, however, we found a positive association between ozone exposure, and SGA (odds ratio [OR] per 10 ppb increase = 1.07, 95% confidence interval [CI] = 1.01–1.12) and adverse birth weight (OR = 1.07; 95% CI = 1.01–1.14). This association persisted in the multi-trimester model, and no association for exposure during the second or third trimester was observed. Exposure to other pollutants during each trimester was not associated with these outcomes. In conclusion, maternal exposure to ozone during the first trimester was independently associated with an elevated risk of poor foetal growth.

Rare earth elements (REEs) have many applications in industry, agriculture, and medicine, resulting in occupational and environmental exposure and concerns regarding REE-associated health effects. However, few epidemiological studies have examined the adverse effects of REEs on pregnancy outcomes. Therefore, this study examined the relationship between the REE concentrations in maternal hair growing during early pregnancy and the risk of neural tube defects (NTDs) in offspring. We included 191 women with NTD-affected pregnancies (cases) and 261 women delivering healthy infants (controls). The cases were divided into three subtypes: anencephaly, spina bifida, and encephalocele. Four REEs in maternal hair were analyzed by inductively coupled plasma-mass spectrometry: lanthanum (La), cerium (Ce), praseodymium (Pr), and neodymium (Nd). A questionnaire was used to collect information about maternal sociodemographic characteristics and dietary habits. The median concentrations of Ce and Pr in the NTD group were higher than those in the control group, whereas there were no significant differences for La and Nd. The adjusted odds ratios (ORs) for the four REE concentrations above the median in the case groups were not significantly > 1. An increasing frequency of the consumption of beans or bean products and fresh fruit was negatively correlated with the four REE concentrations. Our results did not suggest that the concentrations of REEs in maternal hair were associated with the risk of NTDs or any subtype of NTDs in the general population.

Quantifying population exposure level to tobacco smoke is important for investigating its adverse effects on human health. We aimed to investigate the feasibility and application of using population hair concentrations of nicotine and cotinine to indicate their exposure level to tobacco smoke among pregnant women. Our study recruited 256 mothers who delivered healthy babies and collected their hair samples from scalp, of which 172 mothers were self-reported non-passive smokers and the other 84 mothers were self-reported passive smokers. We analyzed nicotine and cotinine concentrations of the hair section grown during the early pregnancy. The linear relationship between cotinine and nicotine was developed and validated by internal cross-validation method. Our results revealed that self-reported passive smokers had higher concentrations of nicotine [2.08 (1.00–4.46) ng/mg hair, i.e. median value (inter-quartile range)] and cotinine [0.063 (0.041–0.148) ng/mg hair] than non-passive smokers [1.35 (0.58–2.59) ng/mg hair of nicotine and 0.049 (0.022–0.087) ng/mg hair of cotinine, respectively]. There existed a linear regression model between hair cotinine and nicotine concentrations, i.e. [cotinine] = 0.024 × [nicotine]+0.0184 (R2 = 0.756) for this population. The internal cross-validation squared correlation coefficient slightly increased from 0.689 to 0.734 with the training subjects varying from 20% to 90%, suggesting that this regression model had high robustness and predictive accuracy. It was concluded that nicotine in maternal hair can evaluate the hair cotinine level and reflect maternal passive exposure level to ambient tobacco smoke with high sensitivity.