Chronic estradiol exposure suppresses luteinizing hormone surge without affecting kisspeptin neurons and estrogen receptor alpha in anteroventral periventricular nucleus†.

Mammalian ovulation is induced by a luteinizing hormone surge, which is triggered by elevated plasma estrogen levels; however, chronic exposure to high levels of estradiol is known to inhibit luteinizing hormone secretion. In the present study, we hypothesized that the inhibition of the luteinizing hormone surge by chronic estradiol exposure is due to the downregulation of the estrogen receptor alpha in kisspeptin neurons at hypothalamic anteroventral periventricular nucleus, which is known as the gonadotropin-releasing hormone/luteinizing hormone surge generator. Animals exposed to estradiol for 2 days showed an luteinizing hormone surge, whereas those exposed for 14 days showed a significant suppression of luteinizing hormone. Chronic estradiol exposure did not affect the number of kisspeptin neurons and the percentage of kisspeptin neurons with estrogen receptor alpha or c-Fos in anteroventral periventricular nucleus, but it did affect the number of kisspeptin neurons in arcuate nucleus. Furthermore, chronic estradiol exposure did not affect gonadotropin-releasing hormone neurons. In the pituitary, 14-day estradiol exposure significantly reduced the expression of Lhb mRNA and LHß-immunoreactive areas. Gonadotropin-releasing hormone-induced luteinizing hormone release was also reduced significantly by 14-day estradiol exposure. We revealed that the suppression of an luteinizing hormone surge by chronic estradiol exposure was induced in association with the significant reduction in kisspeptin neurons in arcuate nucleus, luteinizing hormone expression in the pituitary, and pituitary responsiveness to gonadotropin-releasing hormone, and this was not caused by changes in the estrogen receptor alpha-expressing kisspeptin neurons in anteroventral periventricular nucleus and gonadotropin-releasing hormone neurons, which are responsible for estradiol positive feedback.

Sulfuric acid-induced skin neoplasms in immunocompetent mice.

This study investigates the carcinogenic potential of chronic dermal exposure (16 weeks) to sulfuric acid (SA) in immunocompetent mice. Clinical assessments, histopathological analyses, immunohistochemical analyses and biochemical assays were conducted to evaluate skin irritation, oxidative stress biomarkers and the potential carcinogenic effect of SA. Results indicated that prolonged exposure to SA leads to various alterations in skin structure, notably inflammation, preneoplastic and neoplastic proliferation in hair follicles, as well as hyperkeratosis and acanthosis, resulting in an increased epidermal thickness of 98.50 ± 21.6 µm. Immunohistochemistry analysis further corroborates these observations, showcasing elevated nuclear expression of p53 and Ki-67, with a significant mitotic index of (57.5% ± 2.5%). Moreover, biochemical analyses demonstrate that SA induces lipid peroxidation in the skin, evidenced by a high level of Malondialdehyde and a consequential reduction in catalase activity. These findings suggest that prolonged exposure to SA can induce skin neoplasms, highlighting the need for stringent safety measures in environments where SA is frequently used. This study underscores the potential occupational health risks associated with SA exposure.

Long-term exposure to PM2.5 species and all-cause mortality among Medicare patients using mixtures analyses.

BACKGROUND: The relationship between long-term exposure to PM2.5 and mortality is well-established; however, the role of individual species is less understood. OBJECTIVES: In this study, we assess the overall effect of long-term exposure to PM2.5 as a mixture of species and identify the most harmful of those species while controlling for the others. METHODS: We looked at changes in mortality among Medicare participants 65 years of age or older from 2000 to 2018 in response to changes in annual levels of 15 PM2.5 components, namely: organic carbon, elemental carbon, nickel, lead, zinc, sulfate, potassium, vanadium, nitrate, silicon, copper, iron, ammonium, calcium, and bromine. Data on exposure were derived from high-resolution, spatio-temporal models which were then aggregated to ZIP code. We used the rate of deaths in each ZIP code per year as the outcome of interest. Covariates included demographic, temperature, socioeconomic, and access-to-care variables. We used a mixtures approach, a weighted quantile sum, to analyze the joint effects of PM2.5 species on mortality. We further looked at the effects of the components when PM2.5 mass levels were at concentrations below 8 µg/m3, and effect modification by sex, race, Medicaid status, and Census division. RESULTS: We found that for each decile increase in the levels of the PM2.5 mixture, the rate of all-cause mortality increased by 1.4% (95% CI: 1.3%-1.4%), the rate of cardiovascular mortality increased by 2.1% (95% CI: 2.0%-2.2%), and the rate of respiratory mortality increased by 1.7% (95% CI: 1.5%-1.9%). These effects estimates remained significant and slightly higher when we restricted to lower concentrations. The highest weights for harmful effects were due to organic carbon, nickel, zinc, sulfate, and vanadium. CONCLUSIONS: Long-term exposure to PM2.5 species, as a mixture, increased the risk of all-cause, cardiovascular, and respiratory mortality.

Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice.

Microplastics (MPs) have attracted significant attention due to their global distribution in living environments. Although some studies have reported MP-induced hepatotoxicity in mouse models, a systematic approach to MP-mediated liver toxicity was still lacking. Therefore, we used a mouse model to study the sub-chronic effects of MP exposure on the liver. Female C57BL/6 mice, aged 6 weeks, received an oral administration of 0.3 mg of Nile Red-labeled polystyrene (PS) microplastics, with particle sizes of 0.5 µm (submicron) and 5 µm (micron), via gavage, while control mice received vehicle only. Each mouse was exposed to MPs twice a week for 12 weeks. After sacrifice, the levels of MP accumulation, oxidative stress, inflammation, and pathological changes were measured in the mouse liver, and blood samples were collected for serum biochemistry analysis. Our results demonstrated that 0.5 µm PS-MPs were accumulated in mouse livers post-MP exposure, but not in the 5 µm MP exposure group. Simultaneously, increased levels of glucose, triglyceride, alanine transaminase (ALT), aspartate transaminase (AST), superoxide dismutase, 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA), interleukin-6, and lipid droplets were found in the 0.5 µm MP exposure group, while the fewer responses, including elevated liver weight index, glucose, high-density lipoprotein, AST, and decreased HNE-MA were observed in 5 µm MP exposure group. These results indicate that sub-chronic exposure to submicron MPs causes MP deposition in mouse livers, which further induces oxidative stress, increases inflammatory cytokines and perturbs glucose and lipid homeostasis, which might trigger more severe metabolic dysfunction or non-alcoholic steatohepatitis-like hepatotoxicity.

Association of ambient air pollution with hemoglobin levels and anemia in the general population of Korean adults.

BACKGROUND: Emerging evidence has suggested significant associations between ambient air pollution and changes in hemoglobin levels or anemia in specific vulnerable groups, but few studies have assessed this relationship in the general population. This study aimed to evaluate the association between long-term exposure to air pollution and hemoglobin concentrations or anemia in general adults in South Korea. METHODS: A total of 69,830 Korean adults from a large-scale nationwide survey were selected for our final analysis. Air pollutants included particulate matter with an aerodynamic diameter less than or equal to 10 micrometers (PM10), particulate matter with an aerodynamic diameter less than or equal to 2.5 micrometers, nitrogen dioxide, sulfur dioxide (SO2), and carbon monoxide (CO). We measured the serum hemoglobin concentration to assess anemia for each participant. RESULTS: In the fully adjusted model, exposure levels to PM10, SO2, and CO for one and two years were significantly associated with decreased hemoglobin concentrations (all p < 0.05), with effects ranging from 0.15 to 0.62% per increase in interquartile range (IQR) for each air pollutant. We also showed a significant association of annual exposure to PM10 with anemia (p = 0.0426); the odds ratio (OR) [95% confidence interval (CI)] for anemia per each increase in IQR in PM10 was estimated to be 1.039 (1.001-1.079). This association was also found in the 2-year duration of exposure (OR = 1.046; 95% CI = 1.009-1.083; adjusted Model 2). In addition, CO exposure during two years was closely related to anemia (OR = 1.046; 95% CI = 1.004-1.091; adjusted Model 2). CONCLUSIONS: This study provides the first evidence that long-term exposure to air pollution, especially PM10, is significantly associated with reduced hemoglobin levels and anemia in the general adult population.

Detrimental effects of amitraz exposure in honey bees (Apis mellifera) infected with Nosema ceranae.

In recent years, there has been growing concern on the potential weakening of honey bees and their increased susceptibility to pathogens due to chronic exposure to xenobiotics. The present work aimed to study the effects on bees undergoing an infection by Nosema ceranae and being exposed to a frequently used in-hive acaricide, amitraz. To achieve this, newly emerged bees were individually infected with N. ceranae spores and/or received a sublethal concentration of amitraz in their diets under laboratory conditions. Mortality, food intake, total volume excrement, body appearance, and parasite development were registered. Bees exposed to both stressors jointly had higher mortality rates compared to bees exposed separately, with no difference in the parasite development. An increase in sugar syrup consumption was observed for all treated bees while infected bees fed with amitraz also showed a diminishment in pollen intake. These results coupled with an increase in the total number of excretion events, alterations in behavior and body surface on individuals that received amitraz could evidence the detrimental action of this molecule. To corroborate these findings under semi-field conditions, worker bees were artificially infected, marked, and released into colonies. Then, they were exposed to a commercial amitraz-based product by contact. The recovered bees showed no differences in the parasite development due to amitraz exposure. This study provides evidence to which extent a honey bee infected with N. ceranae could potentially be weakened by chronic exposure to amitraz treatment.

Metabolome evidence of CKDu risks after chronic exposure to simulated Sri Lanka drinking water in zebrafish.

It is still a serious public health issue that chronic kidney disease of uncertain etiology (CKDu) in Sri Lanka poses challenges in identification, prevention, and treatment. What environmental factors in drinking water cause kidney damage remains unclear. This study aimed to investigate the risks of various environmental factors that may induce CKDu, including water hardness, fluoride (HF), heavy metals (HM), microcystin-LR (MC-LR), and their combined exposure (HFMM). The research focused on comprehensive metabolome analysis, and correlation with transcriptomic and gut microbiota changes. Results revealed that chronic exposure led to kidney damage and pancreatic toxicity in adult zebrafish. Metabolomics profiling showed significant alterations in biochemical processes, with enriched metabolic pathways of oxidative phosphorylation, folate biosynthesis, arachidonic acid metabolism, FoxO signaling pathway, lysosome, pyruvate metabolism, and purine metabolism. The network analysis revealed significant changes in metabolites associated with renal function and diseases, including 20-Hydroxy-LTE4, PS(18:0/22:2(13Z,16Z)), Neuromedin N, 20-Oxo-Leukotriene E4, and phenol sulfate, which are involved in the fatty acyls and glycerophospholipids class. These metabolites were closely associated with the disrupted gut bacteria of g_ZOR0006, g_Pseudomonas, g_Tsukamurella, g_Cetobacterium, g_Flavobacterium, which belonged to dominant phyla of Firmicutes and Proteobacteria, etc., and differentially expressed genes (DEGs) such as egln3, ca2, jun, slc2a1b, and gls2b in zebrafish. Exploratory omics analyses revealed the shared significantly changed pathways in transcriptome and metabolome like calcium signaling and necroptosis, suggesting potential biomarkers for assessing kidney disease.

Chronic polystyrene microplastics exposure-induced changes in thick-shell mussel (Mytilus coruscus) metaorganism: A holistic perspective.

Microplastics have emerged as a significant global concern, particularly in marine ecosystems. While extensive research has focused on the toxicological effects of microplastics on marine animals and/or their associated microorganisms as two separate entities, the holistic perspective of the adaptability and fitness of a marine animal metaorganism-comprising the animal host and its microbiome-remains largely unexplored. In this study, mussel metaorganisms subjected chronic PS-MPs exposure experienced acute mortality but rapidly adapted. We investigated the response of innate immunity, digestive enzymes and their associated microbiomes to chronic PS-MPs exposure. We found that PS-MPs directly and indirectly interacted with the host and microbe within the exposure system. The adaptation was a joint effort between the physiological adjustments of mussel host and genetic adaptation of its microbiome. The mussel hosts exhibited increased antioxidant activity, denser gill filaments and increased immune cells, enhancing their innate immunity. Concurrently, the gill microbiome and the digestive gland microbiome respective selectively enriched for plastic-degrading bacteria and particulate organic matter-utilizing bacteria, facilitating the microbiome's adaptation. The microbial adaptation to chronic PS-MPs exposure altered the ecological roles of mussel microbiome, as evidenced by alterations in microbial interactions and nutrient cycling functions. These findings provided new insights into the ecotoxicological impact of microplastics on marine organisms from a metaorganism perspective.

Chronic exposure to polystyrene nanoplastics induces intestinal mechanical and immune barrier dysfunction in mice.

Micro(nano)plastics are prevalent in the environment, and prolonged exposure to them represents a threat to human health. The goal of this study is to assess the health risk of long-term exposure to nanoplastics (NPs) at environmental concentrations on the intestinal mechanical and immune barrier in mice. In this study, mice were provided drinking water containing polystyrene NPs (PS-NPs; 0.1, 1, and 10 mg·L-1) for 32 consecutive weeks. The levels of endocytosis proteins caveolin and clathrin and of tight junctional proteins claudin-1, occludin, and ZO-1, and morphological changes, proportion of lymphocytes B in MLNs and lymphocytes T in IELs and LPLs were determined by immunohistochemistry, hematoxylin-eosin, and flow cytometry assays in the intestinal tissues of mice at 28 weeks. The activities or concentrations of ROS, SOD, MDA, and GSH-Px and inflammatory factors (IL-1ß, IL-6, and TNF-α) in the intestinal tissues of mice were measured by ELISA at 12, 16, 20, 24, and 32 weeks. Compared with the control group, oral ingested PS-NPs entered the intestinal tissues of mice and upregulated expression levels of the clathrin and caveolin. The intestinal tissue structure of mice in the PS-NPs (1 and 10 mg·L-1) exposure groups showed significant abnormalities, such as villus erosion, decreased of crypts numbers and large infiltration of inflammatory cells. Exposure to 0.1 mg·L-1 PS-NPs decreased occludin protein levels, but not claudin-1 and ZO-1 levels. The levels of these three tight junction proteins decreased significantly in the 1 and 10 mg·L-1 PS-NPs exposed groups. Exposure to PS-NPs led to a significant time- and dose-dependent increase in ROS and MDA levels, and concurrently decreased GSH-Px and SOD contents. Exposure to PS-NPs increased the proportion of B cells in MLNs, and decreased the proportion of CD8+ T cells in IELs and LPLs. The levels of pro-inflammatory cytokines IL-6, TNF-α and IL-1ß were markedly elevated after PS-NPs exposure. Long-term PS-NPs exposure impaired intestinal mechanical and immune barrier, and indicate a potentially significant threat to human health.

Evaluation of oxidative stress and genetic instability among residents near mobile phone base stations in Germany.

Human exposure to radiofrequency electromagnetic fields (RF-EMF) is restricted to prevent thermal effects in the tissue. However, at very low intensity exposure "non-thermal" biological effects, like oxidative stress, DNA or chromosomal aberrations, etc. collectively termed genomic-instability can occur after few hours. Little is known about chronic (years long) exposure with non-thermal RF-EMF. We identified two neighboring housing estates in a rural region with residents exposed to either relatively low (control-group) or relatively high (exposed-group) RF-EMF emitted from nearby mobile phone base stations (MPBS). 24 healthy adults that lived in their homes at least for 5 years volunteered. The homes were surveyed for common types of EMF, blood samples were tested for oxidative status, transient DNA alterations, permanent chromosomal damage, and specific cancer related genetic markers, like MLL gene rearrangements. We documented possible confounders, like age, sex, nutrition, life-exposure to ionizing radiation (X-rays), occupational exposures, etc. The groups matched well, age, sex, lifestyle and occupational risk factors were similar. The years long exposure had no measurable effect on MLL gene rearrangements and c-Abl-gene transcription modification. Associated with higher exposure, we found higher levels of lipid oxidation and oxidative DNA-lesions, though not statistically significant. DNA double strand breaks, micronuclei, ring chromosomes, and acentric chromosomes were not significantly different between the groups. Chromosomal aberrations like dicentric chromosomes (p=0.007), chromatid gaps (p=0.019), chromosomal fragments (p<0.001) and the total of chromosomal aberrations (p<0.001) were significantly higher in the exposed group. No potential confounder interfered with these findings. Increased rates of chromosomal aberrations as linked to excess exposure with ionizing radiation may also occur with non-ionizing radiation exposure. Biological endpoints can be informative for designing exposure limitation strategies. Further research is warranted to investigate the dose-effect-relationship between both, exposure intensity and exposure time, to account for endpoint accumulations after years of exposure. As established for ionizing radiation, chromosomal aberrations could contribute to the definition of protection thresholds, as their rate reflects exposure intensity and exposure time.

Hepatic histopathological and morphometric changes in male mice exposed to rosuvastatin from pre-puberty to adulthood: a possible adaptive hepatic response.

Lifestyle changes, such as poor eating habits and a reduction in physical exercise, have impaired human lipid profiles. Statins are widely used to treat dyslipidemias, of which rosuvastatin shows greater improvement in the lipid profile and may be used since childhood. This study aimed to assess the hepatic effects when male mice were given 0.9% saline solution or doses of rosuvastatin of 1.5 or 5.5 mg/kg/day from postnatal day (PND) 23 until PND 80. Body mass gain and water and food consumption were monitored during the treatment. Mice were euthanized on PND 80 when blood was collected for serum obtainment, and several organs were collected and weighed. Serum was used for evaluating lipid profiles and markers of hepatic injuries. The liver was assessed for histopathological, morphometric, and stereological changes. There was a temporary reduction in body mass gain and water and food consumption in the rosuvastatin-exposed groups. Both rosuvastatin-treated groups exhibited reduced total cholesterol levels and showed signs of hepatic tissue adaptation in response to prolonged exposure, such as sinusoidal dilation, inflammatory infiltrates, and cell death of hepatocytes. These results are considered side effects of the treatment and may indicate a hepatic adaptation to the chronic exposure.

Population transcriptogenomics highlights impaired metabolism and small population sizes in tree frogs living in the Chernobyl Exclusion Zone.

BACKGROUND: Individual functional modifications shape the ability of wildlife populations to cope with anthropogenic environmental changes. But instead of adaptive response, human-altered environments can generate a succession of deleterious functional changes leading to the extinction of the population. To study how persistent anthropogenic changes impacted local species' population status, we characterised population structure, genetic diversity and individual response of gene expression in the tree frog Hyla orientalis along a gradient of radioactive contamination around the Chernobyl nuclear power plant. RESULTS: We detected lower effective population size in populations most exposed to ionizing radiation in the Chernobyl Exclusion Zone that is not compensated by migrations from surrounding areas. We also highlighted a decreased body condition of frogs living in the most contaminated area, a distinctive transcriptomics signature and stop-gained mutations in genes involved in energy metabolism. While the association with dose will remain correlational until further experiments, a body of evidence suggests the direct or indirect involvement of radiation exposure in these changes. CONCLUSIONS: Despite ongoing migration and lower total dose rates absorbed than at the time of the accident, our results demonstrate that Hyla orientalis specimens living in the Chernobyl Exclusion Zone are still undergoing deleterious changes, emphasizing the long-term impacts of the nuclear disaster.

The Respiratory Effects of Chronic Exposure to Gas Faring Among Residents of Some Communities in the Niger Delta Region of Nigeria.

BACKGROUND: This study presents the pattern of respiratory effects seen among residents chronically exposed to gas flaring in some communities in the Niger Delta Region, Nigeria. The other health challenges associated with this chronic exposure to gas were also evaluated in the study. METHODS: A total of three hundred and eighty-six 386 adult residents in Ibeno, Niger Delta Region who have been residents for at least two years. Four hundred and fourteen (414) age, sex, and height-matched control unexposed residents in Etinan were recruited for a cross-sectional survey study comparing their respiratory symptoms and other related health challenges. Past and current smokers were excluded from the study in both groups. The study was conducted using a questionnaire as the investigative tool. Both descriptive and inferential statistics were used to analyze the data. RESULTS: Most of the respondents in both exposed and control communities were aged 18-30 years, with a height range of 161-170 cm. Both exposed and control subjects experienced similar symptoms suggestive of respiratory disorders, however, the prevalence was significantly higher among exposed subjects than controls: Cough 57(14.8%) vs. 39(10.1%); breathlessness 58(15%) vs. 28(7.3); wheezing 22(5.7) vs. 12(3.1). The respondents from the exposed community were mostly traders and fishermen while the controls were predominantly farmers. CONCLUSION: There is substantial evidence from the data presented that prolonged exposure to air pollution from gas flaring has significant respiratory and other health implications on residents in these communities reflected as increased frequency of symptoms of cough, chest pain, difficulty in breathing, wheezing, chest tightness, Skin and eye irritation. There is therefore an urgent need for intensified efforts and commitment by the government to speed up the implementation of policies regarding the reduction of flaring of natural gas associated with oil production and the adoption of measures to mitigate the effect of the exposure on human health.

CONTEXTE: Cette étude présente les effets respiratoires observés chez les résidents chroniquement exposés au torchage de gaz dans certaines communautés de la région du delta du Niger, au Nigeria. Les autres problèmes de santé associés à cette exposition chronique au gaz ont également été évalués dans cette étude. MÉTHODES: Un total de 386 résidents adultes d'Ibeno, dans la région du delta du Niger, ayant résidé pendant au moins deux ans, ont été inclus dans l'étude. Quatre cent quatorze (414) résidents non exposés, appariés en fonction de l'âge, du sexe et de la taille, à Etinan ont été recrutés pour une étude transversale comparant leurs symptômes respiratoires et d'autres problèmes de santé associés. Les fumeurs passés et actuels ont été exclus de l'étude dans les deux groupes. L'étude a été menée à l'aide d'un questionnaire comme outil d'investigation. Des statistiques descriptives et inférentielles ont été utilisées pour analyser les données. RÉSULTATS: La plupart des répondants dans les communautés exposées et témoins avaient entre 18 et 30 ans, avec une taille allant de 161 à 170 cm. Les sujets exposés et témoins ont présenté des symptômes similaires suggérant des troubles respiratoires, cependant, la prévalence était significativement plus élevée chez les sujets exposés que chez les témoins : Toux - 57 (14,8 %) contre 39 (10,1 %) ; essoufflement 58 (15 %) contre 28 (7,3 %) ; sifflement 22 (5,7 %) contre 12 (3,1 %). Les répondants de la communauté exposée étaient principalement des commerçants et des pêcheurs, tandis que les témoins étaient principalement des agriculteurs. CONCLUSION: Les données présentées fournissent des preuves substantielles que l'exposition prolongée à la pollution de l'air due au torchage de gaz a des implications respiratoires et autres sur la santé des résidents de ces communautés, se traduisant par une fréquence accrue des symptômes de toux, douleur thoracique, difficulté à respirer, sifflement, oppression thoracique, irritation de la peau et des yeux. Il est donc urgent d'intensifier les efforts et l'engagement du gouvernement pour accélérer la mise en œuvre des politiques visant à réduire le torchage du gaz naturel associé à la production de pétrole et à adopter des mesures pour atténuer les effets de l'exposition sur la santé humaine. MOTS CLÉS: Effet respiratoire, Exposition chronique, Torchage de gaz, Delta du Niger.

Effects of chronic dichlorodiphenyldichloroethylene exposure on testosterone secretion and steroidogenic pathway in the male gonad.

Endocrine disrupting chemicals are present in the environment and/or in consumer products. These agents have the capacity to mimic and/or antagonize endogenous hormones and thus perturb the endocrine axis. The male reproductive tract expresses steroid hormone (androgen and estrogen) receptors at high levels and is a major target for endocrine disrupting chemicals. In this study, Long-Evans male rats were exposed to dichlorodiphenyldichloroethylene, a metabolite of dichlorodiphenyltrichloroethane and a chemical present in the environment, in drinking water at 0.1 and 10 µg/L for 4 weeks. At the end of exposure, we measured steroid hormone secretion and analyzed steroidogenic proteins, including 17ß-hydroxysteroid dehydrogenase, 3ß-hydroxysteroid dehydrogenase, steroidogenic acute regulatory protein, aromatase, and the LH receptor. We also analyzed Leydig cell apoptosis (poly-(ADP-ribose) polymerase) and caspase-3 in the testes. Testicular testosterone (T) and 17ß-estradiol (E2) were both affected by exposure to dichlorodiphenyldichloroethylene by displaying altered steroidogenic enzyme expression. Dichlorodiphenyldichloroethylene exposure also increased the expression of enzymes mediating the pathway for programmed cell death, including caspase 3, pro-caspase 3, PARP, and cleaved PARP. Altogether, the present results demonstrate that dichlorodiphenyldichloroethylene directly and/or indirectly can target specific proteins involved in steroid hormone production in the male gonad and suggest that exposure to environmentally relevant dichlorodiphenyldichloroethylene levels has implications for male reproductive development and function.

NMR metabolomics study of chronic low-dose exposure to a cocktail of persistent organic pollutants.

Nowadays, exposure to endocrine-disrupting chemicals (EDCs), including persistent organic pollutants (POPs), is one of the most critical threats to public health. EDCs are chemicals that mimic, block, or interfere with hormones in the body's endocrine system and have been associated with a wide range of health issues. This innovative, untargeted metabolomics study investigates chronic low-dose internal exposure to a cocktail of POPs on multiple tissues that are known to accumulate these lipophilic compounds. Interestingly, the metabolic response differs among selected tissues/organs in mice. In the liver, we observed a dynamic effect according to the exposure time and the doses of POPs. In the brain tissue, the situation is the opposite, leading to the conclusion that the presence of POPs immediately gives a saturated effect that is independent of the dose and the duration of exposure studied. By contrast, for the adipose tissues, nearly no effect is observed. This metabolic profiling leads to a holistic and dynamic overview of the main metabolic pathways impacted in lipophilic tissues by a cocktail of POPs.

Chronic Exposure to Environmental Pollutant Ammonia Causes Damage to the Olfactory System and Behavioral Abnormalities in Mice.

Ammonia (NH3) is a major air pollutant. However, few studies have been extended beyond the histopathological changes in the olfactory mucosa to the impact of NH3 exposure on other parts of the olfactory system and olfactory functioning. Therefore, we assessed the effects of exogenous NH3 (either 20 ppm for the low exposure group or 200 ppm for the high exposure group) on the various parts of the olfactory system by histological observation, gene expression, immunochemistry, and chemical analyses. A total of 140 Institute of Cancer Research mice (4 weeks old), 70 females and 70 males (average body weight at the start: 21.5 ± 1.9 g), were used. The exposure lasted for 4 weeks, and the mice were exposed to the NH3 for 4 h per day. Our results showed that chronic exposure to NH3 damaged the olfactory system, with consequences for changing the foraging behavior and anxiety behavior. Our results also suggest that it is plausible that NH3 recruited T cells and activated microglia cells and astrocytes, leading to inflammation in the olfactory system. Increased release of proinflammatory cytokines (TNF-α, IL-1ß, IL-6, and interferon-γ) and reduced release of anti-inflammatory cytokines (IL-4 and IFN-beta) led to tissue damage and compromised the functions of the olfactory system.

Small Butt Harmful: Individual- and Population-Level Impacts of Cigarette Filter Particles on the Deposit-Feeding Polychaete Capitella teleta.

In the marine environment, discarded cigarette filters (CFs) deteriorate and leach filter-associated chemicals. The study aim was to assess the effects of smoked CFs (SCFs) and non-smoked CFs (NCFs) particles on individual life-history traits in the deposit-feeding polychaete Capitella teleta and extrapolate these to possible population-level effects. C. teleta was exposed to sediment-spiked particles of NCFs and SCFs at an environmentally realistic concentration (0.1 mg particles g-1 dw sed) and a 100-fold higher (10 mg particles g-1 dw sed) concentration. Experimental setup incorporated 11 individual endpoints and lasted approximately 6 months. There were significant effects on all endpoints, except from adult body volume and egestion rate, in worms exposed to 10 mg SCF particles g-1 dw sed. Although not statistically significant, there was ≥50% impact on time between reproductive events and number of eggs per female at 0.1 mg SCF particles g-1 dw sed. None of the endpoints was significantly affected by NCFs. Results suggest that SCFs are likely to affect individual life-history traits of C. teleta, whereas the population model suggests that these effects might not transform into population-level effects. The results further indicate that chemicals associated with CFs are the main driver causing the effects rather than the CF particles.

Causal effects of prenatal and chronic PM2.5 exposures on cognitive function.

Growing evidence indicated an association between PM2.5 exposure and cognitive function, but the causal effect and the cognitive effect of prenatal PM2.5 exposure remain elusive. We obtained 15,099 subjects from a nationally representative sample of China and measured their cognitive performance. We ascertained subjects' prenatal PM2.5 exposure and chronic PM2.5 exposure of the recent two years. Using this national sample, we found that PM2.5 exposure during the mid- to late-pregnancy was significantly associated with declined cognition and income; chronic PM2.5 exposure was also independently associated with cognition and income measured at adulthood with greater magnitude. Negative effect modification was observed between prenatal and chronic PM2.5 exposure. Instrumental variable approach and difference-in-difference study verified causal effects: every 1 µg/m3 increase in prenatal and chronic PM2.5 exposures were causally associated with -0.22% (-0.38%, -0.06%) and -0.17% (-0.31%, -0.03%) changes in cognitive function, respectively. People with low cognition and low income were more vulnerable to PM2.5 exposure with greater cognitive and income decline. In the future, although China's improved air quality continues to benefit people and reduce cognitive decline induced by chronic PM2.5 exposure, high prenatal PM2.5 exposure will continue to hurt the overall cognition of Chinese population, since in total 360 million people were born during the 2000-2020 polluted era. Prenatal PM2.5-induced cognitive decline would remain largely unchanged before 2050 and gradually reduce after 2065, regardless of environmental policy scenarios. The long-lasting cognitive impact of PM2.5 is worth considering while enacting environmental policies.

E-waste management, treatment options and the impact of heavy metal extraction from e-waste on human health: Scenario in Vietnam and other countries.

Ho Chi Minh (HCM) City is the most important urban region of Vietnam, Southeast Asia. In recent times, the quantity of electronic waste (e-waste) has been growing by several thousand tonnes every year. In this research, some of the existing and developing technologies being employed for the recycling of e-waste have been reviewed. Accordingly, the paper has been divided into three sections namely, e-waste treatment technologies in Ho Chi Minh City, the effect of heavy metals on human health and the extraction of metals from e-waste using pyrolysis, hydrometallurgy, bioleaching, mechanical, and air classifier methods, respectively. The extraction of precious metals and heavy metals such as Cd, Cr, Pb, Hg, Cu, Se, and Zn from e-waste can be hazardous to human health. For example, lead causes hazards to the central and peripheral nervous systems, blood system and kidneys; copper causes liver damage; chronic exposure to cadmium ends up causing lung cancer and kidney damage, and mercury can cause brain damage. Thus, this study examines the key findings of many research and review articles published in the field of e-waste management and the health impacts of metal pollution.

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data.

Nowadays, more and more attention has been focused on the risk of the neurotoxic action of cadmium (Cd) under environmental exposure. Due to the growing incidence of nervous system diseases, including neurodegenerative changes, and suggested involvement of Cd in their aetiopathogenesis, this review aimed to discuss critically this element neurotoxicity. Attempts have been made to recognize at which concentrations in the blood and urine Cd may increase the risk of damage to the nervous system and compare it to the risk of injury of other organs and systems. The performed overview of the available literature shows that Cd may have an unfavourable impact on the human's nervous system at the concentration >0.8 µg Cd/L in the urine and >0.6 µg Cd/L in the blood. Because such concentrations are currently noted in the general population of industrialized countries, it can be concluded that environmental exposure to this xenobiotic may create a risk of damage to the nervous system and be involved in the aetiopathogenesis of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, as well as worsening cognitive and behavioural functions. The potential mechanism of Cd neurotoxicity consists in inducing oxidative stress, disrupting the activity of enzymes essential to the proper functioning of the nervous system and destroying the homoeostasis of bioelements in the brain. Thus, further studies are necessary to recognize accurately both the risk of nervous system damage in the general population due to environmental exposure to Cd and the mechanism of this action.