Environmental Pollution Exposure Research Articles

Environmental noise exposure is associated with one-year survival after a first myocardial infarction

Abstract Introduction Although several studies have shown a link between environmental noise exposure and risk of acute Myocardial Infarction (MI), only few studies have investigated its association with prognosis after MI. We aimed was to analyze the relationship between residential environmental noise exposure and one-year prognosis after a first MI. Methods This observational, longitudinal study was conducted from data collected by a French observatory (RICO) from 2004 to 2009. The outcome was defined by Major Adverse Cardiovascular Events (MACE). Medical data were collected from patients hospitalized for an acute MI from patients registered in the database between January 1st, 2004, and December 31st, 2008, with the following criteria: first MI, aged 18 years or older, with a valid home address and residing in a French urban unit, and who survived at least 28 days after the acute MI were included in the present study. Environmental noise and air pollutants exposure were considered at the residence of the patients. Noise exposure was quantified for two time periods: daily (LAeq,24h) and at night (Lnight) with an annual average. Two outdoor air pollutants were considered: nitrogen dioxide (NO2) and particulate matter with an aerodynamic diameter ≤ 10 µm (PM10). Air pollution exposure levels within the 30 days preceding a major cardiac event (MACE) were estimated. MACE were defined as cardiac death, re-hospitalisation for heart failure, recurrent MI, emergency revascularization, stroke, angina and or unstable angina Results Among the 864 subjects included, most were male (64%), the median age was at 69 y. Nineteen percent (N = 164) presented a MACE during the one year follow-up, and the most frequent were cardiac death (32%). For each 10 dB(A) increase during Lnight , the hazard ratio (HR) of MACE was 1.25 (95% IC 1.09 to 1.43), independently of air pollutants and other confounding. This effect was modified by age and gender. Conclusion and relevance: Our findings suggest for the first time a strong association between noise exposure, in particular during the night, and prognosis at one year after a first MI. If confirmed by larger prospective studies, our study could help to identify original opportunities for environment-based secondary prevention strategies.

EV-miRNA associated with environmental air pollution exposures in the MADRES cohort

ABSTRACT Air pollution is a hazardous contaminant, exposure to which has substantial consequences for health during critical periods, such as pregnancy. MicroRNA (miRNA) are an epigenetic mechanism that modulates transcriptome responses to the environment and have been found to change in reaction to air pollution exposure. The data are limited regarding extracellular-vesicle (EV) miRNA variation associated with air pollution exposure during pregnancy and in susceptible populations who may be disproportionately exposed. This study aimed to identify EV-miRNA expression associated with ambient, residential exposure to PM2.5, PM10, NO2, O3 and with traffic-related NOx in 461 participants of the MADRES cohort, a low income, predominantly Hispanic pregnancy cohort based in Los Angeles, CA. This study used residence-based modeled air pollution data as well as Nanostring panels for EVmiRNA extracted with Qiagen exoRNeasy kits to evaluate 483 miRNA in plasma in early and late pregnancy. Average air pollution exposures were considered separately for 1-day, 1-week and 8-week windows before blood collection in both early and late pregnancy. This study identified 63 and 66 EV-miRNA significantly associated with PM2.5 and PM10, respectively, and 2 miRNA associated with traffic-related NOX (FDR-adjusted p-value<0.05). Of 103 unique EV-miRNA associated with PM, 92% were associated with lung conditions according to HMDD (Human miRNA Disease Database) evidence. In particular, EV-miRNA previously identified with air pollution exposure also associated with PM2.5 and PM10 in this study were: miR-126, miR-16-5p, miR-187-3p, miR200b-3p, miR486-3p, and miR-582-3p. There were no significant differences in average exposures in early vs late pregnancy. Significant EV-miRNA were only identified in late pregnancy with an eight-week exposure window, suggesting a vulnerable timeframe of exposure, rather than an acute response. These results describe a wide array of EV-miRNA for which expression is affected by PM exposure and may be in part mediating the biological response to ambient air pollution, with potential for health implications in pregnant women and their children.

Studying the Effects of Inhaled Environmental Pollutants on Olfactory Function in Mice.

Olfactory impairment is a significant public health problem and independently predicts the risk of neurodegenerative diseases. Inhaled environmental pollutants exposure may impair olfaction; thereby, there is an urgent need for methods to evaluate the effects of inhaled environmental pollutants exposure on olfaction. Mice are ideal models for olfactory experiments because of their highly developed olfactory system and behavioral characteristics. To assess the effects of inhaled environmental pollutants exposure on olfactory function in mice, a detailed buried food test and social odor discrimination experiment is provided, including the experiment preparation, the selection and construction of experimental facilities, the testing process, and indexes of time. Meanwhile, timekeeping equipment, operational details, and the experimental environment are discussed to ensure the success of the assay. Zinc sulfate is used as the treatment to demonstrate the feasibility of the experimental approach. The protocol provides a simple and clear operational process for assessing the effects of inhaled environmental pollutants on olfactory function in mice.

Developmental neurotoxicity evaluation of acrylamide based on in vitro to in vivo extrapolation by pregnancy PBTK modelling

Acrylamide (ACR) is a known neurotoxicant that can pass the placenta and has been detected in breast milk. Some in vivo and in vitro studies indicate that ACR exposure might lead to developmental neurotoxicity (DNT). Here, we have developed a physiologically-based toxicokinetic model for a pregnant human population using PK-Sim. We performed an in vitro to in vivo extrapolation (IVIVE) of data collected from human neuroblastoma SH-SY5Y cells exposed during differentiation to ACR. The developed PBTK model was successfully evaluated and predicted fetal plasma concentrations in the low nM range after exposing the model to an estimated average daily intake for pregnant women. The IVIVE showed that low concentrations of ACR (fM-nM) that induced attenuated differentiation of the SH-SY5Y neuronal cell model, were relevant for human exposure to ACR from oral intake. However, doses estimated in the IVIVE from concentrations in the µM range, were found to be unrealistic by exposure through food intake for an average daily intake. However, in case of exposure due to environmental pollution or occupational exposure, these concentrations may be reached in fetal plasma. The findings in this study raise the concern regarding ACR exposure during pregnancy as well as the relevance of testing concentrations in vitro that are several orders of magnitude higher than the predicted fetal plasma concentrations.

Neuroinflammation and Brain Health Risks in Veterans Exposed to Burn Pit Toxins.

Military burn pits, used for waste disposal in combat zones, involve the open-air burning of waste materials, including plastics, metals, chemicals, and medical waste. The pits release a complex mixture of occupational toxic substances, including particulate matter (PM), volatile organic compounds (VOCs), heavy metals, dioxins, and polycyclic aromatic hydrocarbons (PAHs). Air pollution significantly impacts brain health through mechanisms involving neuroinflammation. Pollutants penetrate the respiratory system, enter the bloodstream, and cross the blood-brain barrier (BBB), triggering inflammatory responses in the central nervous system (CNS). Chronic environmental exposures result in sustained inflammation, oxidative stress, and neuronal damage, contributing to neurodegenerative diseases and cognitive impairment. Veterans exposed to burn pit toxins are particularly at risk, reporting higher rates of respiratory issues, neurological conditions, cognitive impairments, and mental health disorders. Studies demonstrate that Veterans exposed to these toxins have higher rates of neuroinflammatory markers, accelerated cognitive decline, and increased risks of neurodegenerative diseases. This narrative review synthesizes the research linking airborne pollutants such as PM, VOCs, and heavy metals to neuroinflammatory processes and cognitive effects. There is a need for targeted interventions to mitigate the harmful and escalating effects of environmental air pollution exposures on the CNS, improving public health outcomes for vulnerable populations, especially for Veterans exposed to military burn pit toxins.

Exposure range matters: considering non-linear associations in the meta-analysis of environmental pollutant exposure using examples of per- and polyfluoroalkyl substances and birth outcomes.

Meta-analysis is a powerful analytic method for summarizing effect estimates across studies. However, conventional meta-analysis often assumes a linear exposure-outcome relationship and does not account for variability over the exposure ranges. In this work, we first used simulation techniques to illustrate that the linear-based meta-analytical approach may result in oversimplistic effect estimation based on three plausible non-linear exposure-outcome curves (S-shape, inverted U-shape, and M-shape). We showed that subgroup meta-analysis that stratifies on exposure levels can investigate non-linearity and identify the consistency of effect magnitudes in these simulated examples. Next, we examined the heterogeneity of effect estimates across exposure ranges in two published linear-based meta-analyses of prenatal exposure to per- and polyfluoroalkyl substances (PFAS) on changes in mean birth weight or risk of preterm birth. The re-analysis found some varying effect sizes and potential heterogeneity when restricting to different PFAS exposure ranges, but findings were sensitive to the cut-off choices used to rank the exposure levels. Finally, we discussed methodological challenges and recommendations for detecting and interpreting potential non-linear associations in meta-analysis. Using meta-analysis without accounting for exposure range could contribute to literature inconsistency for exposure-induced health effects and impede evidence-based policymaking. Therefore, investigating result heterogeneity by exposure range is recommended.

Environmental pollutant exposures and children’s cognitive, academic and mental health outcomes in India

Environmental pollutant exposures and children’s cognitive, academic and mental health outcomes in India

Adenosine protects cardiomyocytes against acrolein-induced cardiotoxicity by enhancing mitochondrial homeostasis, antioxidant defense, and autophagic flux via ERK-activated FoxO1 upregulation

Acrolein is a ubiquitous gaseous air pollutant and endogenous toxicant, which poses strong risk for oxidative stress-related diseases such as cardiovascular disease. Adenosine has been identified as potential therapeutic agent for age-related cardiovascular disease, while the molecular mechanisms underlying its cardioprotection remain elusive. In the present study, we investigated the myocardial protective effects and the mechanism of adenosine on acrolein-induced toxicity in H9c2 cells and primary neonatal rat cardiomyocytes. We found that acrolein caused apoptosis of cardiomyocytes resulting from oxidative damage, autophagy defect, and mitochondrial dysfunction, as evidenced by loss of mitochondrial membrane potential, impairment of mitochondrial biogenesis, dynamics, and oxidative phosphorylation, decrease of mitochondrial deoxyribonucleic acid (mtDNA) copy number and adenosine 5’-triphosphate (ATP) production. Adenosine pretreatment protected against acrolein-induced cardiotoxicity by maintaining mitochondrial homeostasis, activating the phase II detoxifying enzyme system, promoting autophagic flux, and alleviating mitochondrial-dependent apoptosis. We further demonstrated that the up-regulation of forkhead box protein O1 (FoxO1) mediated by extracellular regulated protein kinases (ERK) activation contributes to the cardioprotection of adenosine. These results expand the application of adenosine in cardioprotection to preventing myocardial damages induced by environmental pollutant acrolein exposure, and uncover the adenosine-ERK-FoxO1 axis as the underlying mechanism mediating the protection of mitochondrial homeostasis, Nrf2-mediated antioxidant defense and autophagic flux, shedding light on the better understanding about the pathological mechanism of cardiovascular disease caused by environmental pollutants and applications of adenosine in cardioprotection.

Correlation between environmental pollutant exposure and cardiopulmonary health by serum biomarker analysis in the Swedish elderly population

ABSTRACT Persistent organic pollutants (POPs) affect human health through the aryl hydrocarbon receptor (AhR) pathway and are implicated in mitochondrial dysfunction. Using data from the PIVUS study, we investigated the associations of serum AhR ligand (POP)-mediated luciferase activity (AhRL), mitochondrial ATP production inhibiting substances (MIS-ATP), and those affecting reactive oxygen species (MIS-ROS) with several metabolic syndrome (MetS) and cardiopulmonary function parameters. These include insulin resistance (HOMA-IR), inflammation, oxidative stress, and cardiopulmonary variables (FVC, FEV1, LV-EF, CCA distensibility). MIS-ATP showed significant correlations with HOMA-IR and pulmonary functions, indicating its direct impact of MIS-ATP on metabolic and pulmonary health. MIS-ROS correlated with oxidative stress markers and CCA distensibility, suggesting a role in systemic inflammatory responses. This study highlights the intricate relationships between environmental pollutant mixture and cardiopulmonary health in MetS as indicated by biomarkers of POP exposure in the elderly population, suggesting POP exposure may influence MetS onset and progression through mitochondrial dysfunction.

Evaluating the Impact of Airborne Fine Particulate Matter and Heavy Metals on Oxidative Stress via Vitamin Supplementation.

This cross-sectional study aimed to assess the interrelationships between PM2.5 exposure, heavy metal concentrations, and oxidative stress indicators, while evaluating the impact of antioxidant intake, such as vitamins, on these associations. PM2.5 exposure assessments were conducted using portable sensor-based monitors; biomarker analyses for heavy metals and oxidative stress were performed in 114 non-smoking adults. We observed that personal or ambient PM2.5 exposure levels were not associated with increased levels of heavy metals in blood and urine, nor with oxidative stress levels in urine. However, the concentrations of cadmium and lead in blood, and those of chromium and nickel in urine, were significantly associated with the urinary malondialdehyde (MDA) concentration. Additionally, increases in blood cadmium, urinary chromium, and nickel levels were significantly associated with higher urinary MDA concentrations in the non-vitamin-supplement group, but this trend was not observed in the regular vitamin supplement group. Our findings suggest that a regular intake of vitamin supplements might modulate the relationship between heavy metal exposure and oxidative stress, indicating potential protective effects against oxidative damage induced by PM2.5 and heavy metals. This study highlights the complexity of environmental pollutant exposure and its impact on human health, emphasizing the need for further research to elucidate the underlying mechanisms and explore potential protective strategies.

Heterocyclic Amines Disrupt Lipid Homeostasis in Cryopreserved Human Hepatocytes.

Metabolic dysfunction associated-steatotic liver disease (MASLD)/metabolic dysfunction-associated steatohepatitis (MASH) is the liver manifestation of metabolic syndrome, which is characterized by insulin resistance, hyperglycemia, hypertension, dyslipidemia, and/or obesity. Environmental pollutant exposure has been recently identified as a risk factor for developing MASH. Heterocyclic amines (HCAs) are mutagens generated when cooking meat at high temperatures or until well-done. Recent epidemiological studies reported that dietary HCA exposure may be linked to insulin resistance and type II diabetes, and we recently reported that HCAs induce insulin resistance and glucose production in human hepatocytes. However, no previous studies have examined the effects of HCAs on hepatic lipid homeostasis. In the present study, we assessed the effects of two common HCAs, MeIQx (2-amino-3, 8-dimethylimidazo [4, 5-f] quinoxaline) and PhIP (2-amino-1-methyl-6-phenylimidazo[4, 5-b] pyridine), on lipid homeostasis in cryopreserved human hepatocytes. Exposure to a single concentration of 25μM MeIQx or PhIP in human hepatocytes led to dysregulation of lipid homeostasis, typified by significant increases in lipid droplets and triglycerides. PhIP significantly increased expression of lipid droplet-associated genes, PNPLA3 and HSD17B13, and both HCAs significantly increased PLIN2. Exposure to MeIQx or PhIP also significantly increased expression of several key genes involved in lipid synthesis, transport and metabolism, including FASN, DGAT2, CPT1A, SCD, and CD36. Furthermore, both MeIQx and PhIP significantly increased intracellular cholesterol and decreased expression of PON1 which is involved in cholesterol efflux. Taken together, these results suggest that HCAs dysregulate lipid production, metabolism, and storage. The current study demonstrates, for the first time, that HCA exposure may lead to fat accumulation in hepatocytes, which may contribute to hepatic insulin resistance and MASH.

Reproductive toxicology of environmental endocrine-disrupting chemicals in women: a cohort study protocol.

Introduction: Epidemiological evidence over the last few decades has consistently shown that exposure to endocrine-disrupting chemicals (EDCs) is associated with adverse reproductive health outcomes, including male and female infertility, poor-pregnancy outcomes, and increased risk of diseases in childhood and beyond. To investigate the effects of EDCs and lifestyle on all aspects of reproduction (including early oocyte development, fertilization, embryo development, embryo implantation, abortion, and preterm birth). Methods: We performed this cohort study on patients receiving in vitro fertilization (IVF) treatment. Biological samples including urine, serum, follicular fluid, semen, fetal tissue, decidua, and placenta, were obtained. Results: By studying the correlations between reproductive outcomes and environmental pollutant exposure and lifestyle, we determined the toxicological mechanisms and health effects of EDCs on female reproductive health. We found that higher concentrations of per- and polyfluoroalkyl substances were correlated with polycystic ovary syndrome (PCOS). Using specific biomarkers, we also detected the concentrations of organophosphorus flame retardants (OPFRs) in urine and found that OPFRs may disrupt hormone homeostasis. Discussion: All of these results reveal EDCs may disrupt female reproduction.

Environmental pollution and extreme weather conditions: insights into the effect on mental health.

Environmental pollution exposures, including air, soil, water, light, and noise pollution, are critical issues that may implicate adverse mental health outcomes. Extreme weather conditions, such as hurricanes, floods, wildfires, and droughts, may also cause long-term severe concerns. However, the knowledge about possible psychiatric disorders associated with these exposures is currently not well disseminated. In this review, we aim to summarize the current knowledge on the impact of environmental pollution and extreme weather conditions on mental health, focusing on anxiety spectrum disorders, autism spectrum disorders, schizophrenia, and depression. In air pollution studies, increased concentrations of PM2.5, NO2, and SO2 were the most strongly associated with the exacerbation of anxiety, schizophrenia, and depression symptoms. We provide an overview of the suggested underlying pathomechanisms involved. We highlight that the pathogenesis of environmental pollution-related diseases is multifactorial, including increased oxidative stress, systematic inflammation, disruption of the blood-brain barrier, and epigenetic dysregulation. Light pollution and noise pollution were correlated with an increased risk of neurodegenerative disorders, particularly Alzheimer's disease. Moreover, the impact of soil and water pollution is discussed. Such compounds as crude oil, heavy metals, natural gas, agro-chemicals (pesticides, herbicides, and fertilizers), polycyclic or polynuclear aromatic hydrocarbons (PAH), solvents, lead (Pb), and asbestos were associated with detrimental impact on mental health. Extreme weather conditions were linked to depression and anxiety spectrum disorders, namely PTSD. Several policy recommendations and awareness campaigns should be implemented, advocating for the advancement of high-quality urbanization, the mitigation of environmental pollution, and, consequently, the enhancement of residents' mental health.

Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis.

The objective of the present study was to review the molecular mechanisms of the adverse effects of environmental pollutants on chondrocytes and extracellular matrix (ECM). Existing data demonstrate that both heavy metals, including cadmium (Cd), lead (Pb), and arsenic (As), as well as organic pollutants, including polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCB), bisphenol A, phthalates, polycyclic aromatic hydrocarbons (PAH), pesticides, and certain other organic pollutants that target cartilage ontogeny and functioning. Overall, environmental pollutants reduce chondrocyte viability through the induction apoptosis, senescence, and inflammatory response, resulting in cell death and impaired ECM production. The effects of organic pollutants on chondrocyte development and viability were shown to be mediated by binding to the aryl hydrocarbon receptor (AhR) signaling and modulation of non-coding RNA expression. Adverse effects of pollutant exposures were observed in articular and growth plate chondrocytes. These mechanisms also damage chondrocyte precursors and subsequently hinder cartilage development. In addition, pollutant exposure was shown to impair chondrogenesis by inhibiting the expression of Sox9 and other regulators. Along with altered Runx2 signaling, these effects also contribute to impaired chondrocyte hypertrophy and chondrocyte-to-osteoblast trans-differentiation, resulting in altered endochondral ossification. Several organic pollutants including PCDD/Fs, PCBs and PAHs, were shown to induce transgenerational adverse effects on cartilage development and the resulting skeletal deformities. Despite of epidemiological evidence linking human environmental pollutant exposure to osteoarthritis or other cartilage pathologies, the data on the molecular mechanisms of adverse effects of environmental pollutant exposure on cartilage tissue were obtained from studies in laboratory rodents, fish, or cell cultures and should be carefully extrapolated to humans, although they clearly demonstrate that cartilage should be considered a putative target for environmental pollutant toxicity.

Early and late onset childhood eczema: Role of preconceptional, pre-natal and post-natal environmental exposures

BackgroundDespite mounting evidence linking indoor and outdoor environments to eczema, the role of indoor and outdoor environmental pollutant(s) exposure during critical time window(s) on eczema remains unknown. ObjectiveTo investigate the correlations between childhood eczema and itchy rashes and exposure to outdoor air pollution and the home environment. MethodsA combined cross-sectional and retrospective cohort study of 8689 kindergarten students was conducted. We collected information about each child's health outcomes and home environment, as well as calculated individual exposure to air pollutants. Multiple logistic regression models were used to investigate the links between indoor and outdoor environments and childhood eczema and itchy rashes. ResultsChildhood ever doctor-diagnosed eczema (DDE) was linked to NO2, CO, PM2.5, PM2.5-10 and PM10 exposure during the preconceptional, pregnant, and postnatal periods, with ORs (95 % CI) ranging from 1.06 (1.00–1.13) to 1.21 (1.08–1.37). Ever doctor-diagnosed itchy rash (DDIR) was associated with SO2, CO, PM2.5, PM2.5-10 and PM10 exposure during preconceptional and postnatal periods, with ORs (95 % CI) ranging from 1.11 (1.02–1.20) to 1.31 (1.13–1.52). Preconceptional outdoor air pollution was associated with a higher risk of ever, early, and late DDE and DDIR. Indoor smoke, renovation, and dampness were all associated with DDE and DDIR. Postnatal exposure to plants has been linked to both ever and early DDE. There was no link between indoor environments and late DDE. Furthermore, pregnancy has been identified as a critical indoor exposure time window for DDE and DDIR. ConclusionsEarly-life exposure to outdoor air pollutants and indoor environments, particularly before birth, played important roles in childhood eczema.

Cumulative Exposures to Environmental and Socioeconomic Risk Factors in Milwaukee County, Wisconsin.

The environmental justice literature demonstrates consistently that low-income and minority communities are disproportionately exposed to environmental hazards. In this case study, we examined cumulative multipollutant, multidomain, and multimatrix environmental exposures in Milwaukee County, Wisconsin for the year 2015. We identified spatial hot spots in Milwaukee County both individually (using local Moran's I) and through clusters (using K-means clustering) across a profile of environmental pollutants that span regulatory domains and matrices of exposure, as well as socioeconomic indicators. The cluster with the highest exposures within the urban area was largely characterized by low socioeconomic status and an overrepresentation of the Non-Hispanic Black population relative to the county as a whole. In this cluster, average pollutant concentrations were equivalent to the 78th percentile in county-level blood lead levels, 67th percentile in county-level NO2, 79th percentile in county-level CO, and 78th percentile in county-level air toxics. Simultaneously, this cluster had an average equivalent to the 62nd percentile in county-level unemployment, 70th percentile in county-level population rate lacking a high school diploma, 73rd percentile in county-level poverty rate, and 28th percentile in county-level median household income. The spatial patterns of pollutant exposure and SES indicators suggested that these disparities were not random but were instead structured by socioeconomic and racial factors. Our case study, which combines environmental pollutant exposures, sociodemographic data, and clustering analysis, provides a roadmap to identify and target overburdened communities for interventions that reduce environmental exposures and consequently improve public health.

Association of air pollution with incidence of late-onset seborrhoeic dermatitis: a prospective cohort study in UKBiobank.

Late-onset seborrhoeic dermatitis seriously affects patients' quality of life. Studies have shown an association between air pollution and other inflammatory skin diseases. However, associations between air pollution exposures and the incidence of late-onset seborrhoeic dermatitis have not been elucidated. To investigate air pollution's role in the incidence of late-onset seborrhoeic dermatitis. We engaged a prospective cohort analysis utilizing the UK Biobank database. Exposure data spanning various years for specific air pollutants, namely particulate matter [PM; with an aerodynamic diameter of ≤ 2.5 µm (PM2.5), between 2.5 and 10 μm (PM2.5-10), ≤ 10 μm (PM10)] along with nitrogen oxides (NO plus NO2, denoted NOx) and NO2, were incorporated. Through a composite air pollution score constructed from five pollutants and employing Cox proportional hazards models, the relationship between air pollution and seborrhoeic dermatitis was delineated. Our examination of 193 995 participants identified 3363 cases of seborrhoeic dermatitis. Higher concentrations of specific pollutants, particularly in the upper quartile (Q4), were significantly linked to an elevated risk of seborrhoeic dermatitis. Notably, PM2.5, PM10, NO2 and NOx exhibited hazard ratios of 1.11, 1.15, 1.22 and 1.15, respectively. The correlation was further solidified with a positive association between air pollution score increments and onset of seborrhoeic dermatitis. Intriguingly, this association was accentuated in certain demographics, including younger men, socioeconomically deprived people, smokers, daily alcohol consumers, and those engaging in regular physical activity. Our findings revealed that air pollution exposures were associated with incidence of late-onset seborrhoeic dermatitis. These results emphasize the importance of preventing environmental air pollution exposures to mitigate the risk of developing the condition.

Innovative explorations: unveiling the potential of organoids for investigating environmental pollutant exposure.

As the economy rapidly develops, chemicals are widely produced and used. This has exacerbated the problems associated with environmental pollution, raising the need for efficient toxicological evaluation techniques to investigate the toxic effects and mechanisms of toxicity of environmental pollutants. The progress in the techniques of cell culture in three dimensions has resulted in the creation of models that are more relevant in terms of biology and physiology. This enables researchers to study organ development, toxicology, and drug screening. Adult stem cells (ASCs) and induced pluripotent stem cells (iPSCs) can be obtained from various mammalian tissues, including cancerous and healthy tissues. Such stem cells exhibit a significant level of tissue memory and ability to self-assemble. When cultivated in 3D in vitro environments, the resulting organoids demonstrate a remarkable capacity to recapitulate the cellular composition and function of organs in vivo. Recently, many tumors' tissue-derived organoids have been widely used in research on tumor pathogenesis, drug development, precision medicine, and other fields, including those derived from colon cancer, cholangiocarcinoma, liver cancer, and gastric cancer. However, the application of organoid models for evaluating the toxicity of environmental pollutants is still in its infancy. This review introduces the characteristics of the toxicity responses of organoid models upon exposure to pollutants from the perspectives of organoid characteristics, tissue types, and their applications in toxicology; discusses the feasibility of using organoid models in evaluating the toxicity of pollutants; and provides a reference for future toxicological studies on environmental pollutants based on organoid models.

A high-affinity fluorescent probe for human uridine-disphosphate glucuronosyltransferase 1A9 function monitoring under environmental pollutant exposure

Uridine-disphosphate glucuronosyltransferase 1A9 (UGT1A9), an important detoxification and inactivation enzyme for toxicants, regulates the exposure level of environmental pollutants in the human body and induces various toxicological consequences. However, an effective tool for high-throughput monitoring of UGT1A9 function under exposure to environmental pollutants is still lacking. In this study, 1,3-dichloro-7-hydroxy-9,9-dimethylacridin-2(9H)-one (DDAO) was found to exhibit excellent specificity and high affinity towards human UGT1A9. Remarkable changes in absorption and fluorescence signals after reacting with UGT1A9 were observed, due to the intramolecular charge transfer (ICT) mechanism. Importantly, DDAO was successfully applied to monitor the biological functions of UGT1A9 in response to environmental pollutant exposure not only in microsome samples, but also in living cells by using a high-throughput screening method. Meanwhile, the identified pollutants that disturb UGT1A9 functions were found to significantly influence the exposure level and retention time of bisphenol S/bisphenol A in living cells. Furthermore, the molecular mechanism underlying the inhibition of UGT1A9 by these pollutant-derived disruptors was elucidated by molecular docking and molecular dynamics simulations. Collectively, a fluorescent probe to characterize the responses of UGT1A9 towards environmental pollutants was developed, which was beneficial for elucidating the health hazards of environmental pollutants from a new perspective.

Identification of biological indicators for human exposure toxicology in smart cities based on public health data and deep learning.

With the acceleration of urbanization, the risk of urban population exposure to environmental pollutants is increasing. Protecting public health is the top priority in the construction of smart cities. The purpose of this study is to propose a method for identifying toxicological biological indicators of human exposure in smart cities based on public health data and deep learning to achieve accurate assessment and management of exposure risks. Initially, the study used a network of sensors within the smart city infrastructure to collect environmental monitoring data, including indicators such as air quality, water quality, and soil pollution. Using public health data, a database containing information on types and concentrations of environmental pollutants has been established. Convolutional neural network was used to recognize the pattern of environmental monitoring data, identify the relationship between different indicators, and build the correlation model between health indicators and environmental indicators. Identify biological indicators associated with environmental pollution exposure through training optimization. Experimental analysis showed that the prediction accuracy of the model reached 93.45%, which could provide decision support for the government and the health sector. In the recognition of the association pattern between respiratory diseases, cardiovascular diseases and environmental exposure factors such as PM2.5 and SO2, the fitting degree between the model and the simulation value reached more than 0.90. The research design model can play a positive role in public health and provide new decision-making ideas for protecting public health.