Search

Background: We sought to replicate our 2015 findings linking chemical intolerance in parents with the risk of their children developing autism and/or ADHD. Drawing upon our 2021 discovery of a strong association between chemical intolerance and mast cells, we propose an explanation for this link. Methods: In a population-based survey of U.S. adults, we used the internationally validated Quick Environmental Exposure and Sensitivity Inventory (QEESI) to assess symptom severity and chemical intolerance. Parents were asked how many of their biological children had been diagnosed with autism and/or ADHD. Results: Parents with chemical intolerance scores in the top versus bottom tenth percentile had 5.7 times the risk of reporting a child with autism and 2.1 times for ADHD. Conclusions: High chemical intolerance scores among parents of children with autism, coupled with our 2021 discovery of mast cell activation as a plausible biomechanism for chemical intolerance, suggest that (1) the QEESI can identify individuals at increased risk, (2) environmental counseling may reduce personal exposures and risk, and (3) the global rise in autism and ADHD may be due to fossil-fuel-derived and biogenic toxicants epigenetically “turning on” or “turning off” critical mast cell genes that can be transmitted transgenerationally. It is important to note that this study was observational in nature; as such, further research is needed using controlled trials to confirm causality and explore the proposed mechanism.

The migration of heavy metals and radionuclides is interrelated, and this study focusses on the interaction and complex influence of various toxicants. The rehabilitation of radioactively contaminated territories has a complex character and is based on scientifically supported measures to restore industrial, economic, and sociopsychological relations. We aim for the achievement of pre-emergency levels of hygienic norms of radioactive contamination of output products. This, in its sum, allows for further economic activity in these territories without restrictions on the basis of natural actions of autoremediation. Biosorption technologies based on bacterial biomass remain a promising direction for the remediation of soils contaminated with radionuclides and heavy metals that help immobilise and consolidate contaminants. A comprehensive understanding of the biosorption capacity of various preparations allows for the selection of more effective techniques for the elimination of contaminants, as well as the overcoming of differences between laboratory results and industrial use. Observation and monitoring make it possible to evaluate the migration process of heavy metals and radionuclides and identify regions with a disturbed balance of harmful substances. The promising direction of the soil application of phosphogypsum, a by-product of the chemical industry, in bioremediation processes is considered.

Monitoring data from several European countries indicate that European hedgehog (Erinaceus europaeus) populations are declining, and research exploring the causes of the decline, including exposure to potentially harmful xenobiotics and metals, may inform conservation initiatives to protect this species in the wild. Hedgehogs are ground-dwelling mammals, feeding on a range of insects, slugs, snails, and earthworms, as well as eggs, live vertebrates, and carrion, including carcasses of apex predator species representing higher levels of the food chain. Consequently, hedgehogs come into close contact with contaminants present in their habitats and prey. This review investigated the studies available on the subject of the occurrence of metals and organic xenobiotics in hedgehogs. This study found that a vast range of different pesticides; persistent organic pollutants (POPs), including organochlorine compounds and brominated flame retardants (BFRs); as well as toxic heavy metals could be detected. Some compounds occurred in lethal concentrations, and some were associated with a potential adverse effect on hedgehog health and survival. Due to their ecology, combined with the opportunity to apply non-invasive sampling techniques using spines as sampling material, we suggest that the European hedgehog is a relevant bioindicator species for monitoring the exposure of terrestrial wildlife to potential toxicants in urban and rural environments.

Matricaria chamomilla flower essential oils (EOs) blue Egyptian (EO-1), chamomile German CO2 (EO-2), and chamomile German (EO-3) and the pure compound α-bisabolol were evaluated against red imported fire ants (RIFA), Solenopsis invicta Buren, black imported fire ants, S. richteri Forel (BIFA), and hybrid imported fire ants (HIFA) for their repellency and toxicity. A series of serial dilutions were tested starting from 125 µg/g until the failure of the treatment. Based on the amount of sand removed, EO-1 showed significant repellency at dosages of 7.8, 7.8, and 31.25 µg/g against RIFA, BIFA, and HIFA, respectively. EO-3 was repellent at 3.9, 7.8, and 31.25 µg/g against BIFA, RIFA, and HIFA, whereas α-bisabolol was active at 7.8, 7.8, and 31.25 µg/g against BIFA, HIFA, and RIFA, respectively. DEET (N, N-diethyl-meta-toluamide) was active at 31.25 µg/g. Toxicity of EOs and α-bisabolol was mild to moderate. For EO-1, LC50 values were 93.6 and 188.11 µg/g against RIFA and BIFA; 98.11 and 138.4 µg/g for EO-2; and 142.92 and 202.49 µg/g for EO-3, respectively. The LC50 of α-bisabolol was 159.23 µg/g against RIFA. In conclusion, M. chamomilla EOs and α-bisabolol offer great potential to be developed as imported fire ant repellents.

Poly- and perfluoroalkyl substances (PFASs) are a group of anthropogenic chemicals with an aliphatic fluorinated carbon chain. Due to their durability, bioaccumulation potential, and negative impacts on living organisms, these compounds have drawn lots of attention across the world. The negative impacts of PFASs on aquatic ecosystems are becoming a major concern due to their widespread use in increasing concentrations and constant leakage into the aquatic environment. Furthermore, by acting as agonists or antagonists, PFASs may alter the bioaccumulation and toxicity of certain substances. In many species, particularly aquatic organisms, PFASs can stay in the body and induce a variety of negative consequences, such as reproductive toxicity, oxidative stress, metabolic disruption, immunological toxicity, developmental toxicity, cellular damage and necrosis. PFAS bioaccumulation plays a significant role and has an impact on the composition of the intestinal microbiota, which is influenced by the kind of diet and is directly related to the host’s well-being. PFASs also act as endocrine disruptor chemicals (EDCs) which can change the endocrine system and result in dysbiosis of gut microbes and other health repercussions. In silico investigation and analysis also shows that PFASs are incorporated into the maturing oocytes during vitellogenesis and are bound to vitellogenin and other yolk proteins. The present review reveals that aquatic species, especially fishes, are negatively affected by exposure to emerging PFASs. Additionally, the effects of PFAS pollution on aquatic ecosystems were investigated by evaluating a number of characteristics, including extracellular polymeric substances (EPSs) and chlorophyll content as well as the diversity of the microorganisms in the biofilms. Therefore, this review will provide crucial information on the possible adverse effects of PFASs on fish growth, reproduction, gut microbial dysbiosis, and its potential endocrine disruption. This information aims to help the researchers and academicians work and come up with possible remedial measures to protect aquatic ecosystems as future works need to be focus on techno-economic assessment, life cycle assessment, and multi criteria decision analysis systems that screen PFAS-containing samples. New innovative methods requires further development to reach detection at the permissible regulatory limits.

The purpose of this article is to examine the current literature regarding the relationship between adverse childhood experiences (ACEs) and environmental exposures. Specifically, the paper will focus on how this relationship between ACEs and physical environmental factors impacts the neurocognitive development of children. With a comprehensive literary search focusing on ACEs, inclusive of socioeconomic status (SES), and environmental toxins common in urban environments, the paper explores how these factors contribute to cognitive outcomes that are associated with the environment and childhood nurturing. The relationship between ACEs and environmental exposures reveals adverse outcomes in children’s neurocognitive development. These cognitive outcomes include learning disabilities, lowered IQ, memory and attention problems, and overall poor educational outcomes. Additionally, potential mechanisms of environmental exposures and children’s neurocognitive outcomes are explored, referencing data from animal studies and evidence from brain imaging studies. This study further analyzes the current gaps in the literature, such as the lack of data focusing on exposure to environmental toxicants resulting from experiencing ACEs and discusses the research and social policy implications of ACEs and environmental exposure in the neurocognitive development of children.

New bronchopulmonary dysplasia (BPD) is a neonatal disease that is theorized to begin in utero and manifests as reduced alveolarization due to inflammation of the lung. Risk factors for new BPD in human infants include intrauterine growth restriction (IUGR), premature birth (PTB) and formula feeding. Using a mouse model, our group recently reported that a paternal history of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure increased his offspring’s risk of IUGR, PTB, and new BPD. Additionally, formula supplementation of these neonates worsened the severity of pulmonary disease. In a separate study, we reported that a paternal preconception fish oil diet prevented TCDD-driven IUGR and PTB. Not surprisingly, eliminating these two major risk factors for new BPD also significantly reduced development of neonatal lung disease. However, this prior study did not examine the potential mechanism for fish oil’s protective effect. Herein, we sought to determine whether a paternal preconception fish oil diet attenuated toxicant-associated lung inflammation, which is an important contributor to the pathogenesis of new BPD. Compared to offspring of standard diet TCDD-exposed males, offspring of TCDD-exposed males provided a fish oil diet prior to conception exhibited a significant reduction in pulmonary expression of multiple pro-inflammatory mediators (Tlr4, Cxcr2, Il-1 alpha). Additionally, neonatal lungs of pups born to fish oil treated fathers exhibited minimal hemorrhaging or edema. Currently, prevention of BPD is largely focused on maternal strategies to improve health (e.g., smoking cessation) or reduce risk of PTB (e.g., progesterone supplementation). Our studies in mice support a role for also targeting paternal factors to improve pregnancy outcomes and child health.

The presence of large sources of environmental pollution due to persistent organic pollutants (POPs), in particular, polychlorinated biphenyls (PCBs), in Kazakhstan necessitates the assessment of pollution as a result of these toxicants. For this purpose, we chose snow cover as an indicator for assessing pollution status in the study area. An assessment of the PCB accumulation level included in the list of POPs was carried out for a snow cover (SC) study in south-east Kazakhstan. The content of PCBs with a wide congener composition was determined using the chromatographic analysis method. During the winter periods of 2014, 2015, 2018–2020 and 2021, the SC pollution of the study area from up to 25 individual PCB congeners was identified. These congeners included highly toxic dioxin-like congener PCBs 105; 108; 114; 118 and “marker” PCBs 52; 101; 138; 153. These congeners were mainly found in snow samples with a wide range of PCB congener compositions. The main PCB pollution sources were indicated. The analysis of the obtained results and structure of the congener composition of PCBs show that the SC contamination in this territory occurs under the influence of local and regional sources.

Epidemiology and animal studies suggest that a paternal history of toxicant exposure contributes to the developmental origins of health and disease. Using a mouse model, our laboratory previously reported that a paternal history of in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased his offspring’s risk of developing necrotizing enterocolitis (NEC). Additionally, our group and others have found that formula supplementation also increases the risk of NEC in both humans and mice. Our murine studies revealed that intervening with a paternal fish oil diet preconception eliminated the TCDD-associated outcomes that are risk factors for NEC (e.g., intrauterine growth restriction, delayed postnatal growth, and preterm birth). However, the efficacy of a paternal fish oil diet in eliminating the risk of disease development in his offspring was not investigated. Herein, reproductive-age male mice exposed to TCDD in utero were weaned to a standard or fish oil diet for one full cycle of spermatogenesis, then mated to age-matched unexposed females. Their offspring were randomized to a strict maternal milk diet or a supplemental formula diet from postnatal days 7–10. Offspring colon contents and intestines were collected to determine the onset of gut dysbiosis and NEC. We found that a paternal fish oil diet preconception reduced his offspring’s risk of toxicant-driven NEC, which was associated with a decrease in the relative abundance of the Firmicutes phylum, but an increase in the relative abundance of the Negativicutes class.

Transmission Electron Microscopic (TEM) assessments were performed on the renal cells of common carp Cyprinus carpio to observe the deleterious effects of two organophosphate insecticides, Phorate and Dimethoate. Pesticides such as Phorate and Dimethoate often pollute aquatic systems where they may negatively impact fish, but so far, the ultrastructural toxicity of these pesticides remains poorly understood. Here, we use Transmission Electron Microscopy (TEM) to determine how acute exposure to sublethal concentrations of these two pesticides may affect the renal cells of common carp Cyprinus carpio. For each insecticide, the fish were divided in four experimental conditions: a control and three different exposure concentrations of the pesticide. The Phorate treated fish were exposed to three sublethal concentrations of 0.2 mg/L, 0.4 mg/L, 0.6 mg/L for a duration of 24, 48 & 72 h. The dimethoate treated fish were exposed to three sublethal concentrations of 0.005 mL/L, 0.01 mL/L, 0.015 mL/L for a duration of 24, 48 and 72 h. The two-dimensional transmission electron microscopy revealed ultrastructural abnormalities in the treated fish renal cells when exposed to two toxicants including deformation in the glomerulus, vacuolization of cytoplasm, degenerative nucleus and damaged mitochondria. Furthermore, the ultrastructural abnormalities were more prominent with the increase in the concentrations of both the insecticides and also with their exposure period. Overall, these results provide important baseline data on the ultrastructural toxicity of Phorate and Dimethoate and will allow important follow-up studies to further elucidate the underlying cellular mechanisms of pesticide toxicity in wildlife.

Emerging evidence has shown that cell-cell interactions between testicular cells, in particular at the Sertoli cell-cell and Sertoli-germ cell interface, are crucial to support spermatogenesis. The unique ultrastructures that support cell-cell interactions in the testis are the basal ES (ectoplasmic specialization) and the apical ES. The basal ES is found between adjacent Sertoli cells near the basement membrane that also constitute the blood-testis barrier (BTB). The apical ES is restrictively expressed at the Sertoli-spermatid contact site in the apical (adluminal) compartment of the seminiferous epithelium. These ultrastructures are present in both rodent and human testes, but the majority of studies found in the literature were done in rodent testes. As such, our discussion herein, unless otherwise specified, is focused on studies in testes of adult rats. Studies have shown that the testicular cell-cell interactions crucial to support spermatogenesis are mediated through distinctive signaling proteins and pathways, most notably involving FAK, Akt1/2 and Cdc42 GTPase. Thus, manipulation of some of these signaling proteins, such as FAK, through the use of phosphomimetic mutants for overexpression in Sertoli cell epithelium in vitro or in the testis in vivo, making FAK either constitutively active or inactive, we can modify the outcome of spermatogenesis. For instance, using the toxicant-induced Sertoli cell or testis injury in rats as study models, we can either block or rescue toxicant-induced infertility through overexpression of p-FAK-Y397 or p-FAK-Y407 (and their mutants), including the use of specific activator(s) of the involved signaling proteins against pAkt1/2. These findings thus illustrate that a potential therapeutic approach can be developed to manage toxicant-induced male reproductive dysfunction. In this review, we critically evaluate these recent findings, highlighting the direction for future investigations by bringing the laboratory-based research through a translation path to clinical investigations.

New bronchopulmonary dysplasia is a developmental lung disease associated with placental dysfunction and impaired alveolarization. Risk factors for new BPD include prematurity, delayed postnatal growth, the dysregulation of epithelial-to-mesenchymal transition (EMT), and parental exposure to toxicants. Our group previously reported that a history of paternal toxicant exposure increased the risk of prematurity and low birth weight in offspring. A history of paternal toxicant exposure also increased the offspring’s risk of new BPD and disease severity was increased in offspring who additionally received a supplemental formula diet, which has also been linked to poor lung development. Risk factors associated with new BPD are well-defined, but it is unclear whether the disease can be prevented. Herein, we assessed whether a paternal fish oil diet could attenuate the development of new BPD in the offspring of toxicant exposed mice, with and without neonatal formula feeding. We investigated the impact of a paternal fish oil diet preconception because we previously reported that this intervention reduces the risk of TCDD associated placental dysfunction, prematurity, and low birth weight. We found that a paternal fish oil diet significantly reduced the risk of new BPD in neonatal mice with a history of paternal toxicant exposure regardless of neonatal diet. Furthermore, our evidence suggests that the protective effects of a paternal fish oil diet are mediated in part by the modulation of small molecules involved in EMT.

This paper aims to form a unified concept of the integrated use of different wastewater treatment methods to form a resistant biological treatment stage of technological systems under the influence of such toxic factors as antibiotics and surfactants. The processes of mechanical treatment, ozonation, UV irradiation, and electrolytic anodic oxidation were implemented in an electrotechnological wastewater treatment facility. Wastewater treatment quality was determined by the concentration of nitrogen compounds in aqueous solutions according to the method of Lurie. Biodiagnostics of the investigated activated sludge via surfactant action was carried out at polyethylene oxide concentrations of 10, 30, and 50 mg/dm3. As a result of experiments on wastewater treatment after aquaculture, an improvement in the reduction of pollutants only by the indicator “nitrate concentration” was determined: by 20% after anodic oxidation, and by 15% after photolysis. At almost all surfactant concentrations studied, the activated sludge was not completely recovered, which was expressed in a decrease in its quantity and in the inability to aggregate flakes of activated sludge. The diameter of the growth retardation of the standard disk with antibiotic (amoxiclav) by the accumulative culture of activated sludge was 17.3 ± 2 mm at a concentration of 4 mg/dm3 and 31.3 ± 3 mm at a concentration of 6 mg/dm3. In the process of studying the state of the activated sludge’s biocenosis under the influence of such toxicants, several regularities were revealed. The directions of using combined approaches of water treatment and wastewater treatment were defined. The structural model of treatment facilities using aerobic and anaerobic bioprocesses together with advanced oxidative technologies was substantiated.

Background: We sought to replicate our 2015 findings linking chemical intolerance in parents with the risk of their children developing autism and/or ADHD. Drawing upon our 2021 discovery of a strong association between chemical intolerance and mast cells, we propose an explanation for this link., Methods: In a population-based survey of U.S. adults, we used the internationally validated Quick Environmental Exposure and Sensitivity Inventory (QEESI) to assess symptom severity and chemical intolerance. Parents were asked how many of their biological children had been diagnosed with autism and/or ADHD., Results: Parents with chemical intolerance scores in the top versus bottom tenth percentile had 5.7 times the risk of reporting a child with autism and 2.1 times for ADHD., Conclusions: High chemical intolerance scores among parents of children with autism, coupled with our 2021 discovery of mast cell activation as a plausible biomechanism for chemical intolerance, suggest that (1) the QEESI can identify individuals at increased risk, (2) environmental counseling may reduce personal exposures and risk, and (3) the global rise in autism and ADHD may be due to fossil-fuel-derived and biogenic toxicants epigenetically "turning on" or "turning off" critical mast cell genes that can be transmitted transgenerationally. It is important to note that this study was observational in nature; as such, further research is needed using controlled trials to confirm causality and explore the proposed mechanism.

Country-level differences in nicotine vaping products used and biomarkers of exposure among long-term e-cigarette users and dual users remain understudied. This cross-sectional study was conducted in 2014 in the United States (n = 166), United Kingdom (n = 129), and Poland (n = 161). We compared patterns of tobacco product use and nicotine and toxicant exposure among cigarette-only smokers (n = 127); e-cigarette-only users (n = 124); dual users of tobacco cigarettes and e-cigarettes (n = 95); and non-users (control group, n = 110) across three countries using mixed-effects linear regression. Compared with cigarette smokers, e-cigarette-only users had lower levels of toxicant biomarkers, but higher levels of nicotine biomarkers. Dual users had higher levels of toxicant biomarkers than e-cigarette-only users but similar levels to cigarette-only smokers. E-cigarette users in Poland, who overwhelmingly used refillable tank devices, exhibited greater levels of nicotine, and toxicant biomarkers relative to e-cigarette users in US/UK. Despite smoking fewer cigarettes, dual users from Poland exhibited similar levels of nicotine biomarkers compared with UK dual users, but higher than US dual users. Country-level differences in e-cigarette devices used and smoking behaviors (e.g., intensity) may contribute to differences in biomarker levels among users of the same products residing in different countries.

This paper postulates that water structure is altered by biomolecules as well as by disease-enabling entities such as certain solvated ions, and in turn water dynamics and structure affect the function of biomolecular interactions. Although the structural and dynamical alterations are subtle, they perturb a well-balanced system sufficiently to facilitate disease. We propose that the disruption of water dynamics between and within cells underlies many disease conditions. We survey recent advances in magnetobiology, nanobiology, and colloid and interface science that point compellingly to the crucial role played by the unique physical properties of quantum coherent nanomolecular clusters of magnetized water in enabling life at the cellular level by solving the “problems” of thermal diffusion, intracellular crowding, and molecular self-assembly. Interphase water and cellular surface tension, normally maintained by biological sulfates at membrane surfaces, are compromised by exogenous interfacial water stressors such as cationic aluminum, with consequences that include greater local water hydrophobicity, increased water tension, and interphase stretching. The ultimate result is greater “stiffness” in the extracellular matrix and either the “soft” cancerous state or the “soft” neurodegenerative state within cells. Our hypothesis provides a basis for understanding why so many idiopathic diseases of today are highly stereotyped and pluricausal.

Recently, there is a growing interest in fortifying food products with flavonoids to enhance health benefits. Naringenin, naringin, hesperetin, and dihydromyricetin are four typical flavonoids constituting a natural part of our diet. In the present work, they were fortified into a chia oil cookie model to evaluate their thermal stability during baking as well as their impact on antioxidant capacity and toxicant formation. Among them dihydromyricetin was the most unstable one (only 36.1% of which was left after baking at 180 °C for 20 min) and led to a loss of brightness in cookie. However, the antioxidant capacity of cookie fortified with dihydromyricetin was significantly enhanced compared with untreated cookie; on the other hand, dihydromyricetin showed the strongest effect to attenuate lipid and protein oxidation as well as decrease the level of fluorescent advanced glycation endproducts and carboxymethyl lysine in cookie model. Overall, among the four selected flavonoids, dihydromyricetin might be the most promising functional bakery additive enhancing the antioxidant capacity while decreasing the formation of toxicants.

Indoor fire detection using gas chemical sensing has been a subject of investigation since the early nineties. This approach leverages the fact that, for certain types of fire, chemical volatiles appear before smoke particles do. Hence, systems based on chemical sensing can provide faster fire alarm responses than conventional smoke-based fire detectors. Moreover, since it is known that most casualties in fires are produced from toxic emissions rather than actual burns, gas-based fire detection could provide an additional level of safety to building occupants. In this line, since the 2000s, electrochemical cells for carbon monoxide sensing have been incorporated into fire detectors. Even systems relying exclusively on gas sensors have been explored as fire detectors. However, gas sensors respond to a large variety of volatiles beyond combustion products. As a result, chemical-based fire detectors require multivariate data processing techniques to ensure high sensitivity to fires and false alarm immunity. In this paper, we the survey toxic emissions produced in fires and defined standards for fire detection systems. We also review the state of the art of chemical sensor systems for fire detection and the associated signal and data processing algorithms. We also examine the experimental protocols used for the validation of the different approaches, as the complexity of the test measurements also impacts on reported sensitivity and specificity measures. All in all, further research and extensive test under different fire and nuisance scenarios are still required before gas-based fire detectors penetrate largely into the market. Nevertheless, the use of dynamic features and multivariate models that exploit sensor correlations seems imperative.

Poly- and perfluoroalkyl substances (PFASs) are a group of anthropogenic chemicals with an aliphatic fluorinated carbon chain. Due to their durability, bioaccumulation potential, and negative impacts on living organisms, these compounds have drawn lots of attention across the world. The negative impacts of PFASs on aquatic ecosystems are becoming a major concern due to their widespread use in increasing concentrations and constant leakage into the aquatic environment. Furthermore, by acting as agonists or antagonists, PFASs may alter the bioaccumulation and toxicity of certain substances. In many species, particularly aquatic organisms, PFASs can stay in the body and induce a variety of negative consequences, such as reproductive toxicity, oxidative stress, metabolic disruption, immunological toxicity, developmental toxicity, cellular damage and necrosis. PFAS bioaccumulation plays a significant role and has an impact on the composition of the intestinal microbiota, which is influenced by the kind of diet and is directly related to the host's well-being. PFASs also act as endocrine disruptor chemicals (EDCs) which can change the endocrine system and result in dysbiosis of gut microbes and other health repercussions. In silico investigation and analysis also shows that PFASs are incorporated into the maturing oocytes during vitellogenesis and are bound to vitellogenin and other yolk proteins. The present review reveals that aquatic species, especially fishes, are negatively affected by exposure to emerging PFASs. Additionally, the effects of PFAS pollution on aquatic ecosystems were investigated by evaluating a number of characteristics, including extracellular polymeric substances (EPSs) and chlorophyll content as well as the diversity of the microorganisms in the biofilms. Therefore, this review will provide crucial information on the possible adverse effects of PFASs on fish growth, reproduction, gut microbial dysbiosis, and its potential endocrine disruption. This information aims to help the researchers and academicians work and come up with possible remedial measures to protect aquatic ecosystems as future works need to be focus on techno-economic assessment, life cycle assessment, and multi criteria decision analysis systems that screen PFAS-containing samples. New innovative methods requires further development to reach detection at the permissible regulatory limits.

The purpose of this article is to examine the current literature regarding the relationship between adverse childhood experiences (ACEs) and environmental exposures. Specifically, the paper will focus on how this relationship between ACEs and physical environmental factors impacts the neurocognitive development of children. With a comprehensive literary search focusing on ACEs, inclusive of socioeconomic status (SES), and environmental toxins common in urban environments, the paper explores how these factors contribute to cognitive outcomes that are associated with the environment and childhood nurturing. The relationship between ACEs and environmental exposures reveals adverse outcomes in children's neurocognitive development. These cognitive outcomes include learning disabilities, lowered IQ, memory and attention problems, and overall poor educational outcomes. Additionally, potential mechanisms of environmental exposures and children's neurocognitive outcomes are explored, referencing data from animal studies and evidence from brain imaging studies. This study further analyzes the current gaps in the literature, such as the lack of data focusing on exposure to environmental toxicants resulting from experiencing ACEs and discusses the research and social policy implications of ACEs and environmental exposure in the neurocognitive development of children.

Transmission Electron Microscopic (TEM) assessments were performed on the renal cells of common carp Cyprinus carpio to observe the deleterious effects of two organophosphate insecticides, Phorate and Dimethoate. Pesticides such as Phorate and Dimethoate often pollute aquatic systems where they may negatively impact fish, but so far, the ultrastructural toxicity of these pesticides remains poorly understood. Here, we use Transmission Electron Microscopy (TEM) to determine how acute exposure to sublethal concentrations of these two pesticides may affect the renal cells of common carp Cyprinus carpio . For each insecticide, the fish were divided in four experimental conditions: a control and three different exposure concentrations of the pesticide. The Phorate treated fish were exposed to three sublethal concentrations of 0.2 mg/L, 0.4 mg/L, 0.6 mg/L for a duration of 24, 48 & 72 h. The dimethoate treated fish were exposed to three sublethal concentrations of 0.005 mL/L, 0.01 mL/L, 0.015 mL/L for a duration of 24, 48 and 72 h. The two-dimensional transmission electron microscopy revealed ultrastructural abnormalities in the treated fish renal cells when exposed to two toxicants including deformation in the glomerulus, vacuolization of cytoplasm, degenerative nucleus and damaged mitochondria. Furthermore, the ultrastructural abnormalities were more prominent with the increase in the concentrations of both the insecticides and also with their exposure period. Overall, these results provide important baseline data on the ultrastructural toxicity of Phorate and Dimethoate and will allow important follow-up studies to further elucidate the underlying cellular mechanisms of pesticide toxicity in wildlife.

New bronchopulmonary dysplasia is a developmental lung disease associated with placental dysfunction and impaired alveolarization. Risk factors for new BPD include prematurity, delayed postnatal growth, the dysregulation of epithelial-to-mesenchymal transition (EMT), and parental exposure to toxicants. Our group previously reported that a history of paternal toxicant exposure increased the risk of prematurity and low birth weight in offspring. A history of paternal toxicant exposure also increased the offspring's risk of new BPD and disease severity was increased in offspring who additionally received a supplemental formula diet, which has also been linked to poor lung development. Risk factors associated with new BPD are well-defined, but it is unclear whether the disease can be prevented. Herein, we assessed whether a paternal fish oil diet could attenuate the development of new BPD in the offspring of toxicant exposed mice, with and without neonatal formula feeding. We investigated the impact of a paternal fish oil diet preconception because we previously reported that this intervention reduces the risk of TCDD associated placental dysfunction, prematurity, and low birth weight. We found that a paternal fish oil diet significantly reduced the risk of new BPD in neonatal mice with a history of paternal toxicant exposure regardless of neonatal diet. Furthermore, our evidence suggests that the protective effects of a paternal fish oil diet are mediated in part by the modulation of small molecules involved in EMT.

This paper elaborates on the potential toxicants detected in inland water, freshwater crustaceans, and tilapia in an island that experienced mining disasters in 1993 and 1996. Specimen samples were collected in six municipalities of the island province in 2019 and presence of metals (Cd, Cr, Cu, Fe, Mn, Ni, Pb, and Zn) were analyzed using Inductively Coupled Plasma-Optical Emission Spectrometer (ICP-OES). Potential ecological risks analysis followed the Hakanson approach. Canonical correspondence analysis PAST Version 3.22, IBM SPSS 25.0, and Pearson correlation were employed for statistical analysis, and GIS Pro 2.5 for mapping of sampling locations and spatial distribution. Results showed that Mn and Zn concentration was highest in surface water (SW) and groundwater (GW), respectively. All metal concentration values exceeded the maximum permissible limit by regulatory international organizations. Elevated concentration of Cr, Cu, Fe, Mn, and Zn was detected in both crustaceans and tilapia. The calculated health hazard indices were greater than one, which means potential high adverse effects on public health when ingested. The municipality of Sta. Cruz and Torrijos recorded higher potential ecological risk among the six municipalities. Results of the correlation analysis suggested that metals in SW and GW have a similar origin, mutual dependence, and identical behavior during transport.

Country-level differences in nicotine vaping products used and biomarkers of exposure among long-term e-cigarette users and dual users remain understudied. This cross-sectional study was conducted in 2014 in the United States ( n = 166), United Kingdom ( n = 129), and Poland ( n = 161). We compared patterns of tobacco product use and nicotine and toxicant exposure among cigarette-only smokers ( n = 127); e-cigarette-only users ( n = 124); dual users of tobacco cigarettes and e-cigarettes ( n = 95); and non-users (control group, n = 110) across three countries using mixed-effects linear regression. Compared with cigarette smokers, e-cigarette-only users had lower levels of toxicant biomarkers, but higher levels of nicotine biomarkers. Dual users had higher levels of toxicant biomarkers than e-cigarette-only users but similar levels to cigarette-only smokers. E-cigarette users in Poland, who overwhelmingly used refillable tank devices, exhibited greater levels of nicotine, and toxicant biomarkers relative to e-cigarette users in US/UK. Despite smoking fewer cigarettes, dual users from Poland exhibited similar levels of nicotine biomarkers compared with UK dual users, but higher than US dual users. Country-level differences in e-cigarette devices used and smoking behaviors (e.g., intensity) may contribute to differences in biomarker levels among users of the same products residing in different countries.

Autism Spectrum Disorder (ASD) is a complex condition with early childhood onset, characterized by a set of common behavioral features. The etiology of ASD is not yet fully understood; however, it reflects the interaction between genetics and environment. While genetics is now a well-established risk factor, several data support a contribution of the environment as well. This paper summarizes the conclusions of a consensus conference focused on the potential pathogenetic role of environmental factors and on their interactions with genetics. Several environmental factors have been discussed in terms of ASD risk, namely advanced parental age, assisted reproductive technologies, nutritional factors, maternal infections and diseases, environmental chemicals and toxicants, and medications, as well as some other conditions. The analysis focused on their specific impact on three biologically relevant time windows for brain development: the periconception, prenatal, and early postnatal periods. Possible protective factors that might prevent or modify an ASD trajectory have been explored as well. Recommendations for clinicians to reduce ASD risk or its severity have been proposed. Developments in molecular biology and big data approaches, which are able to assess a large number of coexisting factors, are offering new opportunities to disentangle the gene⁻environment interplay that can lead to the development of ASD., Competing Interests: The authors declare no conflicts of interest.