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.

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.

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.

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.

Air pollution is an important public health concern especially for children who are particularly susceptible. Latin America has a large children population, is highly urbanized and levels of pollution are substantially high, making the potential health impact of air pollution quite large. We evaluated the effect of air pollution on children respiratory mortality in four large urban centers: Mexico City, Santiago, Chile, and Sao Paulo and Rio de Janeiro in Brazil.Generalized Additive Models in Poisson regression was used to fit daily time-series of mortality due to respiratory diseases in infants and children, and levels of PM10 and O3. Single lag and constrained polynomial distributed lag models were explored. Analyses were carried out per cause for each age group and each city. Fixed- and random-effects meta-analysis was conducted in order to combine the city-specific results in a single summary estimate.These cities host nearly 43 million people and pollution levels were above the WHO guidelines. For PM10 the percentage increase in risk of death due to respiratory diseases in infants in a fixed effect model was 0.47% (0.09–0.85). For respiratory deaths in children 1–5 years old, the increase in risk was 0.58% (0.08–1.08) while a higher effect was observed for lower respiratory infections (LRI) in children 1–14 years old [1.38% (0.91–1.85)]. For O3, the only summarized estimate statistically significant was for LRI in infants. Analysis by season showed effects of O3 in the warm season for respiratory diseases in infants, while negative effects were observed for respiratory and LRI deaths in children.We provided comparable mortality impact estimates of air pollutants across these cities and age groups. This information is important because many public policies aimed at preventing the adverse effects of pollution on health consider children as the population group that deserves the highest protection.

Short-chain chlorinated paraffins (SCCPs) are widely used chemicals in household products and might cause adverse human health effects. However, limited information is available on the occurrence of SCCPs in indoor environments and their exposure risks on humans. In this study the concentrations, profiles and human exposure of SCCPs in indoor dust from five different indoor environments, including commercial stores, residential apartments, dormitories, offices and laboratories were characterized. The SCCPs levels ranged from 10.1 to 173.0 μg/g, with the median and mean concentration of 47.2 and 53.6 μg/g, respectively. No significant difference was found on concentrations among the five microenvironments. The most abundant compounds in indoor dust samples were homologues of C13 group, Cl7 group and N20 (N is the total number of C and Cl) group. In the five microenvironments, commercial stores were more frequently exposed to shorter carbon chained and higher chlorinated homologues. Three potential sources for SCCPs were identified by the multiple linear regression of factor score model and correspondence analysis. The major sources of SCCPs in indoor dust were technical mixtures of CP–42 (42% chlorine, w/w) and CP–52 b (52% chlorine, w/w). The total daily exposure doses and hazard quotients (HQ) were calculated by the human exposure models, and they were all below the reference doses and threshold values, respectively. Monte Carlo simulation was applied to predict the human exposure risk of SCCPs. Infants and toddlers were at risk of SCCPs based on predicted HQ values, which were exceeded the threshold for neoplastic effects in the worst case. Our results on the occurrences, sources and human exposures of SCCPs will be useful to provide a better understanding of SCCPs behaviors in indoor environment in China, and to support environmental risk evaluation and regulation of SCCPs in the world.

The Mesel gold mine in the Ratatotok Sub-district operated between 1996 and 2004 with tailings disposal via an engineered submarine tailings placement (STP) into Buyat Bay. This operation raised concerns of increased levels of arsenic (As) and mercury (Hg) associated disease in the local communities from consumption of seafood contaminated with anthropogenic As and Hg. This report uses the dietary exposure to As and Hg, from local fishermen and market-purchased Codex “as consumed” and environmental fish results from the pre-mining baseline (1990–1995), the mine operational (1996–2004) and post-closure monitoring (2007–2016) to examine the potential health effects. The Ratatotok Sub-district consumers total As average daily intake from fish was between 152 and 317 μg/day (adults) and 58 and 105 μg/day (infants). The average daily intake of inorganic arsenic (Asi) from the dietary staples fish and rice and drinking water consumption was 77 μg/day (adults) and 35 μg/day (infants) at Buyat Pantai and 39 μg/day (adults) and 19 μg/day (infants) at Ratatotok township. Fish consumption contributed 8.2% (adults) and 6.5% (infants) to total daily Asi intake. Average Hg intake from fish consumption, exceeded the FAO WHO PTWI for methylmercury (MeHg) for all age and gender groups at Buyat Pantai 4.6 μg/kg bw/wk (adults) and 7.3 μg/kg bw/wk (infants) and for the infants at Buyat village and Ratatotok township (2.5 and 2.8 μg/kg bw/wk respectively). The Manado City consumers had average intakes below the MeHg PTWI. The Hg exceedances resulted from the high fish consumption in coastal communities and not elevated levels of Hg in fish. Hg exposure levels from the pre-mining baseline, Mesel STP operation and post-closure monitoring, confirmed that exceedances were unrelated to the tailings deposited into Buyat Bay.

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.

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.