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.

The knowledge about the effects of environmental temperature on human epigenome is a potential key to understand the health impacts of temperature and to guide acclimation under climate change. We performed a systematic review on the epidemiological studies that have evaluated the association between environmental temperature and human epigenetic modifications. We identified seven original articles on this topic published between 2009 and 2019, including six cohort studies and one cross-sectional study. They focused on DNA methylation in elderly people (blood sample) or infants (placenta sample), with sample size ranging from 306 to 1798. These studies were conducted in relatively low temperature setting (median/mean temperature: 0.8–13 °C), and linear models were used to evaluate temperature-DNA methylation association over short period (≤28 days). It has been reported that short-term ambient temperature could affect global human DNA methylation. A total of 15 candidate genes (ICAM-1, CRAT, F3, TLR-2, iNOS, ZKSCAN4, ZNF227, ZNF595, ZNF597, ZNF668, CACNA1H, AIRE, MYEOV2, NKX1-2 and CCDC15) with methylation status associated with ambient temperature have been identified. DNA methylation on ZKSCAN4, ICAM-1 partly mediated the effect of short-term cold temperature on high blood pressure and ICAM-1 protein (related to cardiovascular events), respectively. In summary, epidemiological evidence about the impacts of environment temperature on human epigenetics remains scarce and limited to short-term linear effect of cold temperature on DNA methylation in elderly people and infants. More studies are needed to broaden our understanding of temperature related epigenetic changes, especially under a changing climate.

Lead (Pb) contaminated soil is of particular concern for infants and children due to their susceptibility to exposure, fast metabolic rates and rapidly developing neuronal systems. Determining the bioaccessibility of Pb in soils is critical in human health risk assessments, which can vary due to different soil properties and sources of Pb contamination. In this study, the potential relationships between soil properties and Pb bioaccessibility from various Pb sources including Pb contamination from mining (specifically, Broken Hill), three shooting ranges, a smelter and two industry sites (pottery and battery), were investigated using the Relative Bioavailability Leaching Procedure (RBALP). We found the following: (1) CEC, TOC, sand and silt content, and total Pb were significantly different (p < 0.05) between the two particle size fractions of < 2 mm and < 250 μm; (2) EC, CEC and total Pb were significantly correlated to Pb bioaccessibility (p < 0.05); and (3) soil analyses based on source of Pb demonstrated a strongly significant relationship between Pb bioaccessibility and soil properties (CEC, EC, clay content and total Pb) for mining soils from Broken Hill (r² = 0.86, p < 0.05, n = 18). These results demonstrated the influences of Pb contamination sources, soil properties and particle size fractions on Pb bioaccessibility as well as the prediction of Pb bioaccessibility using soil properties. The findings documented here will help in developing a predictive tool for human health risk assessment and the remediation of Pb contaminated soils.

While infants are developing, they are easily affected by toxic chemicals existing in their environments, such as semi-volatile organic compounds (SVOCs): phthalates, polycyclic aromatic hydrocarbons (PAHs), polybrominated diphenyl ethers (PBDEs), and organophosphate esters (OPEs). However, the specific living environment of infants, including increased plastic products and foam floor mats, may increase the presence of these chemicals. In this study, 68 air, dust, and window film samples were collected from homes, with 3- to 6-month-old infant occupants, to analyze phthalates, PAHs, PBDEs, and OPEs. High detection rates and concentrations suggest that these SVOCs are widespread in infant environments and are associated with cooking methods, smoking habits, the period of time after decoration, and room floors. The partitioning behavior of SVOCs indicates that the logarithms of the dust/gas-phase air partition coefficient (logKD) and the window film/gas-phase air partition coefficient (logKF) in homes are not at an equilibrium state when the logarithm of the octanol/air partition coefficient (logKOA) is less than 8 or greater than 11. Considering the 3 exposure routes, ingestion and dermal absorption have become the main routes of infant exposure to phthalates and OPEs, and ingestion and inhalation have become the dominant routes of exposure to PAHs and PBDEs. The total carcinogenic risk of SVOCs, which have carcinogenic toxicities, via ingestion and dermal absorption for infants in homes exceeds the acceptable value, suggesting that the current levels of these SVOCs in homes might pose a risk to infant health.

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.

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.

Hexabromocyclododecanes (HBCDs) are the subject of recent interest and potential risk assessment particularly in China due to its ubiquitous existence in a variety of environmental media. This paper reviews the recent studies conducted on HBCDs in different environmental media (air, soil, water, river sediment, sewage sludge, biota and daily food) in China. At the same time, human health risks via food and occupational exposure of HBCDs in production plants, expanded polystyrene (EPS) and extruded polystyrene (XPS) plants were assessed. The review reveals that HBCDs levels of air, soil, sediment, sewage sludge, biota and food presented a geographical variation in the eastern coastal regions of China. There were many factors resulting in the variation, such as sampling sites, climate and analytical method. In terms of diastereoisomer, α-HBCD and γ-HBCD were the predominant diastereoisomers in air, soil, sediment, and sewage sludge. In the water, α-HBCD and γ-HBCD shared the major proportion to the total HBCDs. However, only α-HBCD was the predominant diastereoisomer in biota. With regard to human exposure pathway to HBCDs, food was the major route for human exposure to HBCDs, especially meat. In addition, soil and road dust were also important exposure pathways. Furthermore, workers and residents, especially infants in and around waste dumping sites and industrial areas are exposed to the highest HBCDs levels among all the populations studied thus far. HBCDs posed a potential threat to the environment and human health. Therefore, risk assessment and management have an important role to play in preventing and mitigating HBCDs risks.

Triclosan (TCS) is an organic compound with a wide range of antibiotic activity and has been widely used in items ranging from hygiene products to cosmetics; however, recent studies suggest that it has several adverse effects. In particular, TCS can be passed to both fetus and infants, and while some evidence suggests in vitro neurotoxicity, there are currently few studies concerning the mechanisms of TCS-induced developmental neurotoxicity. Therefore, this study aimed to clarify the effect of TCS on neural development using zebrafish models, by analyzing the morphological changes, the alterations observed in fluorescence using HuC-GFP and Olig2-dsRED transgenic zebrafish models, and neurodevelopmental gene expression. TCS exposure decreased the body length, head size, and eye size in a concentration-dependent manner in zebrafish embryos. It increased apoptosis in the central nervous system (CNS) and particularly affected the structure of the CNS, resulting in decreased synaptic density and shortened axon length. In addition, it significantly up-regulated the expression of genes related to axon extension and synapse formation such as α1-Tubulin and Gap43, while decreasing Gfap and Mbp related to axon guidance, myelination and maintenance. Collectively, these changes indicate that exposure to TCS during neurodevelopment, especially during axonogenesis, is toxic. This is the first study to demonstrate the toxicity of TCS during neurogenesis, and suggests a possible mechanism underlying the neurotoxic effects of TCS in developing vertebrates.

The health risk of triadimefon (TF) to cardiovascular system of human is still unclear, especially to pesticide suicides population, occupational population (farmers, retailers and pharmaceutical workers), and special population (young children and infants, pregnant women, older people, and those with compromised immune systems) who are at a greater risk. Therefore, firstly we explored the toxic effects and possible mechanism of cardiovascular toxicity induced by TF using zebrafish model. Zebrafish at stage of 48 h post fertilization (hpf) exposed to TF for 24 h exhibited morphological malformations which were further confirmed by histopathologic examination, including pericardial edema, circulation abnormalities, serious venous thrombosis and increased distance between the sinus venosus (SV) and bulbus arteriosus (BA) regions of the heart. In addition to morphological changes, TF induced functional deficits in the heart of zebrafish, including bradycardia and a significant reduced cardiac output that became more serious at higher concentrations. To better understand the possible molecular mechanisms underlying cardiovascular toxicity in zebrafish, we investigated the transcriptional level of genes related to calcium signaling pathway and cardiac muscle contraction. Q-PCR (quantitative real-time polymerase chain reaction) results demonstrated that the expression level of genes related to ATPase (atp2a1l, atp1b2b, atp1a3b), calcium channel (cacna1ab, cacna1da) and cardiac troponin C (tnnc1a) were significantly decreased after TF exposure. For the first time, the present study revealed that TF exposure had observable morphological and functional negative impacts on cardiovascular system of zebrafish. Mechanistically, this toxicity might result from the pressure of down-regulation of genes associated with calcium signaling pathway and cardiac muscle contraction following TF exposure. These findings generated here can provide information for better pesticide poisoning treatments, occupational disease prevention, and providing theoretical foundation for risk management measures.

In-pram babies are more susceptible to air pollution effects, yet studies assessing their exposure are limited. We measured size-resolved particle mass (PMC; 0.25–32 μm) and number (PNC; 0.2–1 μm) concentrations on a 2.7 km route. The instruments were placed inside a baby pram. The route passed through 4 traffic intersections (TIs) and a bus stand. A total of ∼87 km road length was covered through 64 trips, made during school drop-in (morning) and pick-up (afternoon) hours. The objectives were to assess PMC and PNC exposure to in-pram babies at different route segments, understand their physicochemical characteristics and exposure differences between in-pram babies and adults carrying them. Over 5-fold variability (14.1–78.2 μg m⁻³) was observed in PMCs. Small-sized particles, including ultrafine particles, were always higher by 66% (PM1), 29% (PM2.5) and 31% (PNC) during the morning than afternoon. Coarse particles (PM2.5-10) showed an opposite trend with 70% higher concentration during afternoon than morning. TIs emerged as pollution hotspots for all the particle types. For example, PM2.5, PM2.5-10 and PNCs during the morning (afternoon) at TIs were 7 (10)%, 19 (10)% and 68 (62)% higher, respectively, compared with the rest of the route. Bus stand was also a section of enhanced exposure to PNC and PM2.5, although not so much for PM2.5-10. EDX analyses revealed Cl, Na and Fe as dominant elements. Road salt might be a source of NaCl due to de-icing during the measurements while Fe contributed by non-exhaust emissions from brake abrasion. The respiratory deposition rates imitated the trend of PMC, with higher doses of coarse and fine particles during the afternoon and morning runs, respectively. Special protection measures during conveyance of in-pram babies, especially at pollution hotspots such as traffic intersections and bus stands, could help to limit their exposure.