Toxic Chemicals In Environment Research Articles

P05-19 Interpretable graph neural networks trained on OECD test guideline data for screening inhalation toxicity of environmental chemicals

P05-19 Interpretable graph neural networks trained on OECD test guideline data for screening inhalation toxicity of environmental chemicals

Can the microbiome mediate the toxicity of environmental chemicals?

Can the microbiome mediate the toxicity of environmental chemicals?

Systematic review on dietary exposure to toxic environmental chemicals and health outcomes

Systematic review on dietary exposure to toxic environmental chemicals and health outcomes

Highly sensitive response to the toxicity of environmental chemicals in transparent casper zebrafish

The response sensitivity to toxic substances is the most concerned performance of animal model in chemical risk assessment. Casper (mitfaw2/w2;mpv17a9/a9), a transparent zebrafish mutant, is a useful in vivo model for toxicological assessment. However, the ability of casper to respond to the toxicity of exogenous chemicals is unknown. In this study, zebrafish embryos were exposed to five environmental chemicals, chlorpyrifos, lindane, α-endosulfan, bisphenol A, tetrabromobisphenol A (TBBPA), and an antiepileptic drug valproic acid. The half-lethal concentration (LC50) values of these chemicals in casper embryos were 62–87 % of that in the wild-type. After TBBPA exposure, the occurrence of developmental defects in the posterior blood island of casper embryos was increased by 67–77 % in relative to the wild-type, and the half-maximal effective concentration (EC50) in casper was 73 % of that in the wild-type. Moreover, the casper genetic background significantly increased the hyperlocomotion caused by chlorpyrifos and lindane exposure compared with the wild-type. These results demonstrated that casper had greater susceptibility to toxicity than wild-type zebrafish in acute toxicity, developmental toxicity and neurobehavioral toxicity assessments. Our data will inform future toxicological studies in casper and accelerate the development of efficient approaches and strategies for toxicity assessment via the use of casper.

Gestational exposure to organochlorine compounds and metals and infant birth weight: effect modification by maternal hardships

BackgroundGestational exposure to toxic environmental chemicals and maternal social hardships are individually associated with impaired fetal growth, but it is unclear whether the effects of environmental chemical exposure on infant birth weight are modified by maternal hardships.MethodsWe used data from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, a pan-Canadian cohort of 1982 pregnant females enrolled between 2008 and 2011. We quantified eleven environmental chemical concentrations from two chemical classes – six organochlorine compounds (OCs) and five metals – that were detected in ≥ 70% of blood samples collected during the first trimester. We examined fetal growth using birth weight adjusted for gestational age and assessed nine maternal hardships by questionnaire. Each maternal hardship variable was dichotomized to indicate whether the females experienced the hardship. In our analysis, we used elastic net to select the environmental chemicals, maternal hardships, and 2-way interactions between maternal hardships and environmental chemicals that were most predictive of birth weight. Next, we obtained effect estimates using multiple linear regression, and plotted the relationships by hardship status for visual interpretation.ResultsElastic net selected trans-nonachlor, lead, low educational status, racially minoritized background, and low supplemental folic acid intake. All were inversely associated with birth weight. Elastic net also selected interaction terms. Among those with increasing environmental chemical exposures and reported hardships, we observed stronger negative associations and a few positive associations. For example, every two-fold increase in lead concentrations was more strongly associated with reduced infant birth weight among participants with low educational status (β = -100 g (g); 95% confidence interval (CI): -215, 16), than those with higher educational status (β = -34 g; 95% CI: -63, -3). In contrast, every two-fold increase in mercury concentrations was associated with slightly higher birth weight among participants with low educational status (β = 23 g; 95% CI: -25, 71) compared to those with higher educational status (β = -9 g; 95% CI: -24, 6).ConclusionsOur findings suggest that maternal hardships can modify the associations of gestational exposure to some OCs and metals with infant birth weight.

Crosstalk of MAP3K1 and EGFR signaling mediates gene-environment interactions that block developmental tissue closure

Aberrant regulation of signal transduction pathways can adversely derail biological processes for tissue development. One such process is the embryonic eyelid closure that is dependent on the Mitogen-Activated Protein Kinase Kinase Kinase 1 (MAP3K1). Map3k1 knockout in mice results in defective eyelid closure and an autosomal recessive eye-open at birth phenotype. We have shown that in utero exposure to dioxin, a persistent environmental toxicant, induces the same eye defect in Map3k1+/- heterozygous but not wild type pups. Here we explore the mechanisms of the Map3k1 (gene) and dioxin (environment) interactions (GxE) underlying defective eyelid closure. We show that, acting through the Aryl Hydrocarbon Receptor (AHR), dioxin activates Epidermal Growth Factor Receptor (EGFR) signaling, which in turn depresses MAP3K1-dependent Jun N-terminal Kinase (JNK) activity. The dioxin mediated JNK repression is moderate but is exacerbated by Map3k1 heterozygosity. Therefore, dioxin exposed Map3k1+/- embryonic eyelids have a marked reduction of JNK activity, accelerated differentiation and impeded polarization in the epithelial cells. Knocking out Ahr or Egfr in eyelid epithelium attenuates the open-eye defects in dioxin-treated Map3k1+/- pups, whereas knockout of Jnk1 and S1pr that encodes the Sphigosin-1-phosphate (S1P) receptors upstream of the MAP3K1-JNK pathway potentiates the dioxin toxicity. Our novel findings show that the crosstalk of AHR, EGFR and S1P-MAP3K1-JNK pathways determines the outcome of dioxin exposure. Thus, gene mutations targeting these pathways are potential risk factors for the toxicity of environmental chemicals.

Antagonistic interaction between caffeine and ketamine in zebrafish: Implications for aquatic toxicity

The coexistence of caffeine (CF) and ketamine (KET) in surface waters across Asia has been widely reported. Previous studies have implied that CF and KET may share a mechanism of action. However, the combined toxicity of these two chemicals on aquatic organisms remains unclear at environmental levels, and the underlying mechanisms are not well understood. Here we demonstrate that KET antagonizes the adverse effects of CF on zebrafish larvae by modulating the gamma-aminobutyric acid (GABA)ergic synapse pathway. Specifically, KET (10–250 ng L−1) ameliorates the locomotor hyperactivity and impaired circadian rhythms in zebrafish larvae induced by 2 mg L−1 of CF, showing a dose-dependent relationship. Additionally, the developmental abnormalities in zebrafish larvae exposed to CF are mitigated by KET, with an incidence rate reduced from 26.7% to 6.7%. The competition between CF and KET for binding sites on the GABA-A receptor (in situ and in silico) elucidates the antagonistic interactions between the two chemicals. Following a seven-day recovery period, the adverse outcomes of CF exposure persist in the fish, whereas the changes observed in the CF + KET groups are significantly alleviated, especially with KET at 10 ng L−1. Based on these results, it is imperative to further assess the environmental risks associated with CF and KET co-pollution. This pilot study underscores the utility of systems toxicology approaches in estimating the combined toxicity of environmental chemicals on aquatic organisms. Moreover, the nighttime behavioral functions of fish could serve as a sensitive biomarker for evaluating the toxicity of psychoactive substances.

Additive-free electroless deposition on graphene/copper foil: Photo-induced and defect-assisted approach for environmentally friendly plating

The environmental toxicity of chemicals used in electroless plating process is often overlooked. In fact, the wastewater from the electroless plating process contains metal complexes, reducing agents and stabilizers that can create hazard to our environment. To address this concern, an additive-free electroless deposition process on graphene/Cu foil is proposed. The defect structure of graphene plays a pivotal role by acting as a reservoir for concentrating photoelectrons generated from ultra-thin cuprous oxide (Cu2O) located at the interface of graphene and Cu foil upon exposure to light irradiation. In the Cu ion solution, Cu ions were anchored on the defect sites and formed a Cu-C4 structure with graphene. The Cu-C4 sites accumulate abundant photoelectrons and trigger the reduction of Cu ions to form island-like growth of Cu, which immediately was oxidized to Cu2O, leaving only a small portion of metallic Cu. Concurrently, the presence of Cu ions induces the generation of additional defect sites on graphene, providing further growth sites for Cu deposition. This process continues until the entire graphene surface is covered by the deposited Cu2O. Ultimately, the deposition of metallic oxides with lower redox potential can be achieved. The proposed deposition mechanism assisted by irradiation of photocatalyst and defect structure of graphene material provides a truly environmentally friendly electroless plating process. By eliminating the need for additives and significantly reducing the environmental hazards associated with electroless plating, this method holds great promise for sustainable materials manufacturing.

Production and Characterization of Pellets from Agricultural Residue: Cotton, Tur, and Soybean

Substituting biomass for conventional sources of fuel can help to provide cleaner energy. Woody biomass pellets are gaining popularity in the primary energy industry. Agricultural biomass is either burned on the farm or used as fodder for animals recently, which releases toxic chemicals in environment. Locally cultivated crop waste has potential to be more environmentally benign than imported biomass. As a result, residues of locally grown Cotton, Tur, and Soybean crops were used for pelleting in this study. The collected residues were sundried and shredded to particle sizes ranging between 2.36 mm to 4.75mm. The pellets were prepared without binder by using pelleting machine. The proximate and ultimate analysis of crop residue and pellet samples was carried out to check characteristics and applicability of pellets as bioenergy source. The thermogravimetric analysis was conducted to check thermal behaviour and SEM-EDS analysis was carried out to detect the inorganics present in ash sample. The obtained calorific values of cotton, tur, and soybean pellets are 3696.57, 3487.83, and 3281.65 Kcal/Kg respectively and moisture content is below 10% for all three types of pellets. The findings showed that crop residue pellets as an alternative to conventional fuel sources provide superior economic and environmental outcomes.

Decline in human sperm parameters: How to stop?

A large systematic review and meta-regression analysis found that sperm counts all over the world appeared to be declining rather than stabilizing. The decline in male sperm counts does not necessarily translate to a decline in male fertility. The cause of declining sperm counts remains unknown; however, several potential causative factors have been identified: 1. Chronic diseases: diabetes mellitus, hypertension; hyperlipidemia, hyperuricemia and skin Diseases & metabolic syndrome. 2. Environmental factors: bisphenol a; phthalates; heavy metals and heat. 3. Lifestyle: obesity, diet, tobacco, alcohol, marijuana, stress, reduced sleep & sedentary life. Addressing these causes is required to stop or decrease male fertility decline. Action to improve semen quality such as prevention & treatment of chronic disease, decreasing unhealthy lifestyle behaviors such as smoking, poor diet, or lack of physical activity & eliminating toxic environmental chemicals.

Exposure to Polycyclic Aromatic Hydrocarbons and adverse reproductive outcomes in women: current status and future perspectives.

Polycyclic Aromatic Hydrocarbons (PAHs) are ubiquitous, toxic environmental chemicals that can cause adverse reproductive health effects. The objectives of this mini-review are to highlight the adverse reproductive outcomes due to PAH exposure with the main focus on polycystic ovary syndrome (PCOS) and premature ovarian failure (POF) and to provide perspectives on future research needs. We reviewed studies that have reported the adverse reproductive outcomes associated with PAHs exposures in women through a comprehensive search of bibliographic databases and gray literature sources. In addition, potentially modifiable sources of exposure to PAHs and associated reproductive outcomes were also investigated. A total of 232 papers were retrieved through a comprehensive search of bibliographic databases, out of which three studies met the eligibility criteria and were included in the review. Results showed that exposure to PAHs is associated with adverse reproductive outcomes defined as PCOS, POF, and reproductive hormone imbalance. Sources of PAH exposure associated with adverse reproductive outcomes include active and passive tobacco smoking, specific cooking methods, and pesticides. Future studies are warranted to examine the mechanisms by which PAHs result in adverse reproductive endpoints in women. Further, environmental exposures that are potentially modifiable such as exposure to tobacco smoke, may contribute to PAH exposure, and these exposures should be targeted in future policies and interventions.

Disruption of the tumor suppressor-like activity of aryl hydrocarbon receptor by arsenic in epithelial cells and human lung cancer.

As the most classic and extensively studied transcription factor in response to environmental toxic chemicals, the human aryl hydrocarbon receptor (AHR) has been implicated in mediating some oncogenic responses also. Limited information is available, however, on whether arsenic, a widely presented environmental carcinogen, can regulate AHR to exert its carcinogenic activity. Through chromatin immunoprecipitation and sequencing (ChIP-seq), CRISPR-Cas9 gene editing, RNA-seq, and immunohistochemistry (IHC), in this report we provided evidence showing that arsenic enforces TGFβ and other oncogenic signaling pathways in bronchial epithelial cells through disrupting the tumor suppressor-like activity of AHR. AHR is normally enriched on a number of oncogenic genes in addition to the known phase I/II enzymes, such as genes in TGFβ and Nrf2 signaling pathways and several known oncogenes. Arsenic treatment substantially reduced the binding of AHR on these genes followed by an increased expression of these genes. CRISPR-Cas9-based knockout of AHR followed by RNA-seq further demonstrated increased expression of the TGFβ signaling and some oncogenic signaling pathway genes in the AHR knockout cells. IHC studies on human tissue samples revealed that normal human lung tissues expressed high level of AHR. In contrast, the AHR expression was diminished in the lung cancer tissues. Accordingly, the data from this study suggest that AHR has tumor suppressor-like activity for human lung cancer, and one of the carcinogenic mechanisms of arsenic is likely mediated by the inhibition of arsenic on the tumor suppressor-like activity of AHR.

Predicting Dose-Range Chemical Toxicity using Novel Hybrid Deep Machine-Learning Method.

Humans are exposed to thousands of chemicals, including environmental chemicals. Unfortunately, little is known about their potential toxicity, as determining the toxicity remains challenging due to the substantial resources required to assess a chemical in vivo. Here, we present a novel hybrid neural network (HNN) deep learning method, called HNN-Tox, to predict chemical toxicity at different doses. To develop a hybrid HNN-Tox method, we combined two neural network frameworks, the Convolutional Neural Network (CNN) and the multilayer perceptron (MLP)-type feed-forward neural network (FFNN). Combining the CNN and FCNN in the field of environmental chemical toxicity prediction is a novel approach. We developed several binary and multiclass classification models to assess dose-range chemical toxicity that is trained based on thousands of chemicals with known toxicity. The performance of the HNN-Tox was compared with other machine-learning methods, including Random Forest (RF), Bootstrap Aggregation (Bagging), and Adaptive Boosting (AdaBoost). We also analyzed the model performance dependency on varying features, descriptors, dataset size, route of exposure, and toxic dose. The HNN-Tox model, trained on 59,373 chemicals annotated with known LD50 and routes of exposure, maintained its predictive ability with an accuracy of 84.9% and 84.1%, even after reducing the descriptor size from 318 to 51, and the area under the ROC curve (AUC) was 0.89 and 0.88, respectively. Further, we validated the HNN-Tox with several external toxic chemical datasets on a large scale. The HNN-Tox performed optimally or better than the other machine-learning methods for diverse chemicals. This study is the first to report a large-scale prediction of dose-range chemical toxicity with varying features. The HNN-Tox has broad applicability in predicting toxicity for diverse chemicals and could serve as an alternative methodology approach to animal-based toxicity assessment.

Genotoxicity assessment of per- and polyfluoroalkyl substances mixtures in human liver cells (HepG2)

Per- and polyfluoroalkyl substances (PFAS) are ubiquitous, toxic, and persistent environmental chemicals of concern that have been widely detected in all environmental matrices including human biological fluids. Although humans are exposed to complex mixtures of PFAS, it remains uncertain whether the co-exposure to PFAS mixtures could induce genotoxic damage in humans. Hence, this study evaluated the combined genotoxicity of PFAS mixtures in a human cell line system. To assess the possible genotoxic damage caused by human exposure to PFAS and their mixtures, we investigated their potential to induce cytotoxicity (cell viability) and genotoxicity (DNA damage) in a human liver cell line (HepG2). The selected PFAS include perfluorononanoic acid (PFNA), perfluorooctane sulfonic acid (PFOS), perfluorodecanoic acid (PFDA), perfluorooctanoic acid (PFOA), and perfluorohexane sulfonic acid (PFHxS). The interaction toxicities of these PFAS in binary mixtures were also determined using the additive index approach. The results revealed that exposure to PFNA, PFOS, PFDA, PFOA, and PFHxS singly and in binary mixtures induced a concentration-dependent decrease in cell viability. The additive index values indicated that the binary mixtures of PFOS + PFNA, PFOS + PFDA, and PFOS + PFOA displayed synergistic interaction, whereas the binary mixtures of PFOS + PFHxS, PFOA + PFNA, PFOA + PFDA, and PFOA + PFHxS behaved additively. Using the alkaline Comet assay, the potential of PFAS and their mixtures to induce DNA damage was evaluated based on a 1:1 ratio of the concentration of respective compounds required to produce a 1/10th of effective concentrations causing 50 % inhibition in cell viability (EC50). The results revealed that exposure to PFNA, PFOS, PFDA, PFOA, and PFHxS singly and in binary mixtures (PFOS + PFNA, PFOS + PFDA, PFOS + PFOA, PFOS + PFHxS, PFOA + PFNA, PFOA + PFDA, and PFOA + PFHxS) caused a moderate increase in cellular DNA damage, but no dose-response relationship was observed. Overall, this study indicates that the tested PFAS causes a concentration-dependent decrease in cell viability and only a modest increase in cellular DNA damage under these conditions.

Serum levels of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans in a sample of Lebanese pregnant women: The role of dietary, anthropometric, and environmental factors

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) are unintentionally produced, toxic environmental chemicals that persist for long years and bioaccumulate along the food chain, contaminating humans through diet. A particularly critical population subgroup is pregnant women given the adverse health effects on fetuses and newborns. Several anthropogenic sources of exposure to PCDD/Fs exist in Lebanon. Therefore, the aim of the present cross-sectional study is to measure the levels of PCDD/Fs in a sample of pregnant women in Lebanon and to explore potential associated factors. In this study, we measured serum concentrations of seven dioxins and ten furans, among 423 pregnant women recruited at delivery, using gas chromatography MS/MS. Among 269 participants, maternal sociodemographic information was collected including vicinity to landfills, incineration, pesticide use, industrial activity, and smoking. Anthropometric data were registered regarding pre-pregnancy body mass index (BMI), pre-pregnancy weight loss from restrictive diet, and gestational weight gain. Intake of major food groups generally related to PCDD/Fs was reported (fish, red meat, poultry, and dairy). Bivariate and multivariate analyses were performed to identify associations. PCDD/Fs were detected in 0 to 56.1% of the sample. Geometric mean concentrations were 75.5 (2.35) pg/g lipid and 2.25 (1.39) TEQ2005 pg/g lipid for total dioxins, and 2.66 (1.76) pg/g lipid and 0.34 (1.78) TEQ2005 pg/g lipid for total furans. Levels were relatively lower than levels previously observed in France, Germany, Mexico, Ghana, and Japan. Red meat consumption was the most consistently associated factor with a 2.38–2.57 fold increase in PCDD/F levels. Pre-pregnancy weight loss showed inverse associations with PCDD/F congeners. Vicinity to illegal incineration was also associated with a 2.32–2.43 fold increase in PCDD/F levels. In conclusion, results showed the importance of dietary, anthropometric, and environmental factors in the present sample's exposure to PCDD/Fs, in a region that contains anthropogenic sources of contamination.

Promising effects of herbal compounds against strongyloidiasis: a systematic review.

Strongyloidiasis could be a significant global health issue undervalued in several countries, which is caused by Strongyloides spp. Challenges stemming from the use of anthelmintic chemotherapy, such as the development of resistance, the progressive cost of medicines, environmental toxicity of chemicals, and residuals in beast products have increased interest in promoting alternative means of control for the use of plant-based parasite control methods. A study on herbal extracts may offer a less expensive yet equally effective alternative for the prevention and treatment of helminthic multi-resistance. We systematically searched the Web of Sciences, PubMed/MEDLINE, and Scopus databases to explore original publications related to medicinal plants and Strongyloides in English on September 29, 2021. The keywords of medicinal plant, traditional medicine, plant extract, herbal medicine, herbal extract, natural drug, Strongyloides, strongyloidiasis, Strongyloides infection, and helminth were used in our search. Researchers can make use of this review as a quick reference. In this study, we have summarized recent advancements and published investigations on herbal and naturally derived medicines in treating strongyloidiasis undertaken by several researchers worldwide. These medicinal herbs, as well as the active and significant compounds they contain, such as alkaloids, phenolic derivatives, tannins, and terpenes, have been outlined in recent articles. Various studies on herbal remedies to treat strongyloidiasis have been undertaken to date, but further research is still required on moderately effective and low harmful substances.

Analysis of Nanomaterials on Biological and Environmental Systems and New Analytical Methods for Improved Detection.

The advancing field of nanoscience has produced lower mass, smaller size, and expanded chemical composition nanoparticles over recent years. These new nanoparticles have challenged traditional analytical methods of qualification and quantification. Such advancements in nanoparticles and nanomaterials have captured the attention of toxicologists with concerns regarding the environment and human health impacts. Given that nanoparticles are only limited by size (1–100 nm), their chemical and physical characteristics can drastically change and thus alter their overall nanotoxicity in unpredictable ways. A significant limitation to the development of nanomaterials is that traditional regulatory and scientific methods used to assess the biological and environmental toxicity of chemicals do not generally apply to the assessment of nanomaterials. Significant research effort has been initiated, but much more is still needed to develop new and improved analytical measurement methods for detecting and quantitating nanomaterials in biological and environmental systems.

A microengineered biomimetic model of the placental barrier to study environmental exposures during pregnancy

Exposure to toxic heavy metals contributes to the development of pregnancy complications that can adversely affect fetal development. Despite increasing evidence suggesting the negative health impact of heavy metals, investigating their adverse effects in the context of human pregnancy remains a major challenge due to the difficulty of human subject research and the limited capacity of animal models to properly represent the anatomy and function of the human reproductive system. Motivated by problem, here we describe a microengineered in vitro model designed to reverse engineer the maternal-fetal interface in the human placenta. This biomimetic system enables advanced capabilities to grow human trophoblast cells and fetal vascular endothelial cells in a physiological spatial arrangement and dynamic culture conditions to engineer the placental barrier in vitro that can emulate regulated material transport between maternal and fetal circulations. Using cadmium (CdCl2 ) as a representative example of heavy metals, we investigate whether and how this environmental chemical affects the human placental barrier and its physiological function as a gatekeeper. Our study also examines the role of membrane transporters in the maternal-to-fetal transfer of cadmium to provide insights into efflux transporter-medicated protection against environmental exposures during pregnancy.We used soft lithography to construct a compartmentalized elastomeric device consisting of two overlapping chambers separated by a thin semipermeable membrane. After sterilization and surface coating with extracellular matrix protein, the device was seeded with BeWo b30 human trophoblast cells and primary human villous endothelial cells on the opposite sides of the membrane. The bi-layer tissue was then cultured under perfusion conditions by using syringe pumps connected to each chamber. To mimic the physiological process of placental development, we treated the trophoblast cell layer in the maternal chamber with forskolin (50 µM) to induce syncytialization.Our microengineered model of the human placental barrier formed a tight barrier (evaluated by expression of E-cadherin and VE-cadherin), secreted the pregnancy hormone human chorionic gonadotropin beta (hCGβ), and supported physiological maternal-to-fetal transport of glucose. Following CdCl2 treatment (0.5-50 µM), we observed concentration-dependent deleterious responses of the maternal and fetal tissues as demonstrated by reduced cell viability and placental hormone secretion, compromised barrier function, and increased secretion of proinflammatory cytokines. The results also indicated upregulated expression of metallothioneins IA and IIA (MT-IA/IIA) metal binding proteins.The placenta-on-a-chip is an innovative and translational in vitro platform for the study of environmental chemical toxicity in the human placenta. With further improvements, this technology may advance our ability to model, interrogate, and predict the potential of xenobiotics to disrupt placentation and maintenance of human pregnancy.

Membrane Lipid Replacement with Glycerolphospholipids Slowly Reduces Self-Reported Symptom Severities in Chemically Exposed Gulf War Veterans

Background: Chemically exposed veterans of the 1991 Gulf War have few options for treatment of conditions and symptoms related to their chemical exposures. Membrane Lipid Replacement (MLR) with oral membrane glycerolphospholipids is a safe and effective method for slowly removing hydrophobic organic molecules from tissues, while enhancing mitochondrial function and decreasing the severity of certain signs and symptoms associated with multi-symptom illnesses. Methods: A preliminary open-label study utilizing 20 male veterans who were deployed to combat areas, exposed to environmental toxic chemicals and subsequently diagnosed with Gulf War Illnesses (GWI) were utilized. These subjects took 6 g per day oral glycerolphospholipids for 6 months, and the severities of over 100 signs and symptoms were self-reported at various times using illness survey forms. Results: In the sixteen patients that fully complied and completed the study, there were gradual and significant reductions of symptom severities in categories related to fatigue, pain, musculoskeletal, nasopharyngeal, breathing, vision, sleep, balance, and urinary, gastrointestinal and chemical sensitivities. There were no adverse incidents during the study, and the all-natural oral study supplement was extremely well tolerated. Conclusions: MLR with oral glycerolphospholipids appears to be a simple, safe and potentially effective method of slowly reducing the severities of multiple symptoms in chemically exposed veterans.

Sentinel animals for monitoring the environmental lead exposure: combination of traditional review and visualization analysis.

In nature, certain animals share a common living environment with humans, thus these animals have become biomonitors of health effects related to various environmental exposures. As one of the most toxic environmental chemicals, lead (Pb) can cause detriment health effects to animals, plants, and even humans through different exposure pathways such as atmosphere, soil, food, water, and dust, etc. Sentinel animals played an "indicative" role in the researches of environmental pollution monitoring and human health. In order to comprehend the usage of sentinel animals in the indication of environmental Pb pollution and human Pb exposure completely, a combination of traditional review and visualization analysis based on CiteSpace literature was used to review earlier researches in this study. In the first instance, present researches on exposure sources and exposure pathways of Pb were summarized briefly, and then the studies using sentinel animals to monitor environmental heavy metal pollution and human health were combed. Finally, visualization software CiteSpace 5.8.R3 was used to explore and analyze the hotspots and frontiers of lead exposure and sentinel animals researches at home and abroad. The results showed that certain mammals were good indicators for human lead exposure. Sentinel animals had been widely used to monitor the ecological environment and human lead exposure. Among them, the blood lead levels of small mammals, particularly for domestic dogs and cats, had a significant correlation with the blood lead levels of human living in the same environment. It indicated that certain biological indicators in animals can be used as surrogates to monitor human body exposure to heavy metals. This study also explored the challenges and perspectives that may be faced in sentinel animal research, in order to provide a certain theoretical basis and train of thought guidance for future research.