Environmental Exposures and Pediatric Cardiology: A Scientific Statement From the American Heart Association.

Environmental toxicants and pollutants are causes of adverse health consequences, including well-established associations between environmental exposures and cardiovascular diseases. Environmental degradation is widely prevalent and has a long latency period between exposure and health outcome, potentially placing a large number of individuals at risk of these health consequences. Emerging evidence suggests that environmental exposures in early life may be key risk factors for cardiovascular conditions across the life span. Children are a particularly sensitive population for the detrimental effects of environmental toxicants and pollutants given the long-term cumulative effects of early-life exposures on health outcomes, including congenital heart disease, acquired cardiac diseases, and accumulation of cardiovascular disease risk factors. This scientific statement highlights representative examples for each of these cardiovascular disease subtypes and their determinants, focusing specifically on the associations between climate change and congenital heart disease, airborne particulate matter and Kawasaki disease, blood lead levels and blood pressure, and endocrine-disrupting chemicals with cardiometabolic risk factors. Because children are particularly dependent on their caregivers to address their health concerns, this scientific statement highlights the need for clinicians, research scientists, and policymakers to focus more on the linkages of environmental exposures with cardiovascular conditions in children and adolescents.

Establishment and validation of a prediction model for gestational diabetes.

AIM: To develop a visual prediction model for gestational diabetes (GD) in pregnant women and to establish an effective and practical tool for clinical application. METHODS: To establish a prediction model, the modelling set included 1756 women enrolled in the Zunyi birth cohort, the internal validation set included 1234 enrolled women, and pregnant women in the Wuhan cohort were included in the external validation set. We established a demographic-lifestyle factor model (DLFM) and a demographic-lifestyle-environmental pollution factor model (DLEFM) based on whether the women were exposed to environmental pollutants. The least absolute shrinkage and selection lasso-logistic regression analyses were used to identify the independent predictors of GD and construct a nomogram for predicting its occurrence. RESULTS: The DLEFM regression analysis showed that a family history of diabetes (odd ratio [OR] 2.28; 95% confidence interval [CI] 1.05-4.71), a history of GD in pregnant women (OR 4.22; 95% CI 1.89-9.41), being overweight or obese before pregnancy (OR 1.71; 95% CI 1.27-2.29), a history of hypertension (OR 2.61; 95% CI 1.41-4.72), sedentary time (h/day) (OR 1.16; 95% CI 1.08-1.24), monobenzyl phthalate (OR 1.95; 95% CI 1.45-2.67) and Q4 mono-ethyl phthalate concentration (OR 1.85; 95% CI 1.26-2.73) were independent predictors. The area under the receiver operating curves for the internal validation of the DLEFM and the DLFM constructed using these seven factors was 0.827 and 0.783, respectively. The calibration curve of the DLEFM was close to the diagonal line. The DLEFM was thus the more optimal model, and the one which we chose. CONCLUSIONS: A nomogram based on preconception factors was constructed to predict the occurrence of GD in the second and third trimesters. It provided an effective tool for the early prediction and timely management of GD.

Investigation of the Link between Per- and Polyfluoroalkyl Substances and Stress Biomarkers in Bottlenose Dolphins (Tursiops truncatus).

Bottlenose dolphins (Tursiops truncatus) are keystone and sentinel species in the world's oceans. We studied correlations between per- and polyfluoroalkyl substances (PFAS) and their stress axis. We investigated associations between plasma biomarkers of 12 different PFAS variants and three cortisol pools (total, bound, and free) in wild T. truncatus from estuarine waters of Charleston, South Carolina (n = 115) and Indian River Lagoon, Florida (n = 178) from 2003 to 2006, 2010-2013, and 2015. All PFAS and total cortisol levels for these dolphins were previously reported; bound cortisol levels and free cortisol calculations have not been previously reported. We tested null hypotheses that levels of each PFAS were not correlated with those of each cortisol pool. Free cortisol levels were lower when PFOS, PFOA, and PFHxS biomarker levels were higher, but free cortisol levels were higher when PFTriA was higher. Bound cortisol levels were higher when there were higher PFDA, PFDoDA, PFDS, PFTeA, and PFUnDA biomarkers. Total cortisol was higher when PFOA was lower, but total cortisol was higher when PFDA, PFDoDA, PFTeA, and PFTriA were higher. Additional analyses indicated sex and age trends, as well as heterogeneity of effects from the covariates carbon chain length and PFAS class. Although this is a cross-sectional observational study and, therefore, could reflect cortisol impacts on PFAS toxicokinetics, these correlations are suggestive that PFAS impacts the stress axis in T. truncatus. However, if PFAS do impact the stress axis of dolphins, it is specific to the chemical structure, and could affect the individual pools of cortisol differently. It is critical to conduct long-term studies on these dolphins and to compare them to populations that have no or little expose to PFAS.

Exploring environmental exposomes and the gut-brain nexus: Unveiling the impact of pesticide exposure.

This review delves into the escalating concern of environmental pollutants and their profound impact on human health in the context of the modern surge in global diseases. The utilisation of chemicals in food production, which results in residues in food, has emerged as a major concern nowadays. By exploring the intricate relationship between environmental pollutants and gut microbiota, the study reveals a dynamic bidirectional interplay, as modifying microbiota profile influences metabolic pathways and subsequent brain functions. This review will first provide an overview of potential exposomes and their effect to gut health. This paper is then emphasis the connection of gut brain function by analysing microbiome markers with neurotoxicity responses. We then take pesticide as example of exposome to elucidate their influence to biomarkers biosynthesis pathways and subsequent brain functions. The interconnection between neuroendocrine and neuromodulators elements and the gut-brain axis emerges as a pivotal factor in regulating mental health and brain development. Thus, manipulation of gut microbiota function at the onset of stress may offer a potential avenue for the prevention and treatment for mental disorder and other neurodegenerative illness.

Gestational glyphosate exposure and early childhood neurodevelopment in a Puerto Rico birth cohort.

INTRODUCTION: N-(phosphonomethyl)glycine, or glyphosate, is a non-selective systemic herbicide widely used in agricultural, industrial, and residential settings since 1974. Glyphosate exposure has been inconsistently linked to neurotoxicity in animals, and studies of effects of gestational exposure among humans are scarce. In this study we investigated relationships between prenatal urinary glyphosate analytes and early childhood neurodevelopment. METHODS: Mother-child pairs from the PROTECT-CRECE birth cohort in Puerto Rico with measures for both maternal urinary glyphosate analytes and child neurodevelopment were included for analysis (n = 143). Spot urine samples were collected 1-3 times throughout pregnancy and analyzed for glyphosate and aminomethylphosphonic acid (AMPA), an environmental degradant of glyphosate. Child neurodevelopment was assessed at 6, 12, and 24 months using the Battelle Developmental Inventory, 2nd edition Spanish (BDI-2), which provides scores for adaptive, personal-social, communication, motor, and cognitive domains. We used multivariable linear regression to examine associations between the geometric mean of maternal urinary glyphosate analytes across pregnancy and BDI-2 scores at each follow-up. Results were expressed as percent change in BDI-2 score per interquartile range increase in exposure. RESULTS: Prenatal AMPA concentrations were negatively associated with communication domain at 12 months (%change = -5.32; 95%CI: 9.04, -1.61; p = 0.007), and communication subdomain scores at 12 and 24 months. At 24 months, four BDI-2 domains were associated with AMPA: adaptive (%change = -3.15; 95%CI: 6.05, -0.25; p = 0.038), personal-social (%change = -4.37; 95%CI: 7.48, -1.26; p = 0.008), communication (%change = -7.00; 95%CI: 11.75, -2.26; p = 0.005), and cognitive (%change = -4.02; 95%CI: 6.72, -1.32; p = 0.005). Similar trends were observed with GLY concentrations, but most confidence intervals include zero. We found no significant associations at 6 months. CONCLUSIONS: Our results suggest that gestational exposure to glyphosate is associated with adverse early neurodevelopment, with more pronounced delays at 24 months. Given glyphosate's wide usage, further investigation into the impact of gestational glyphosate exposure on neurodevelopment is warranted.

Decrypting the skeletal toxicity of vertebrates caused by environmental pollutants from an evolutionary perspective: From fish to mammals.

The rapid development of modern society has led to an increasing severity in the generation of new pollutants and the significant emission of old pollutants, exerting considerable pressure on the ecological environment and posing a serious threat to both biological survival and human health. The skeletal system, as a vital supportive structure and functional unit in organisms, is pivotal in maintaining body shape, safeguarding internal organs, storing minerals, and facilitating blood cell production. Although previous studies have uncovered the toxic effects of pollutants on vertebrate skeletal systems, there is a lack of comprehensive literature reviews in this field. Hence, this paper systematically summarizes the toxic effects and mechanisms of environmental pollutants on the skeletons of vertebrates based on the evolutionary context from fish to mammals. Our findings reveal that current research mainly focuses on fish and mammals, and the identified impact mechanisms mainly involve the regulation of bone signaling pathways, oxidative stress response, endocrine system disorders, and immune system dysfunction. This study aims to provide a comprehensive and systematic understanding of research on skeletal toxicity, while also promoting further research and development in related fields.

Unveiling carcinogenic pollutant levels in environmental water samples through facile fabrication of gold nanoparticles on sulfur-doped graphitic carbon nitride.

Extensive utilization of pesticides and herbicides to boost agricultural production increased the environmental health risks, which can be mitigate with the aid of highly sensitive detection systems. In this study, an electrochemical sensor for monitoring the carcinogenic pesticides in the environmental samples has been developed based on sulfur-doped graphitic-carbon nitride-gold nanoparticles (SCN-AuNPs) nanohybrid. Thermal polycondensation of melamine with thiourea followed by solvent exfoliation via ultrasonication leads to SCN formation and electroless deposition of AuNPs on SCN leads to SCN-AuNPs nanohybrid synthesis. The chemical composition, S-doping, and the morphology of the nanohybrid were confirmed by various microscopic and spectroscopic tools. The as-synthesized nanohybrid was fabricated with glassy carbon (GC) electrode for determining the carcinogenic hydrazine (HZ) and atrazine (ATZ) in field water samples. The present sensor exhibited superior electrocatalytic activity than GC/SCN and GC/AuNPs electrodes due to the synergism between SCN and AuNPs and the amperometric studies showed the good linear range of detection of 20 nM-0.5 mM and 500 nM-0.5 mM with the limit of detection of 0.22 and 69 nM (S/N = 3) and excellent sensitivity of 1173.5 and 13.96 µA mM-1 cm-2 towards HZ and ATZ, respectively. Ultimately, the present sensor is exploited in environmental samples for monitoring HZ and ATZ and the obtained results are validated with high-performance liquid chromatography (HPLC) technique. The excellent recovery percentage and close agreement with the results of HPLC analysis proved the practicability of the present sensor. In addition, the as-prepared materials were utilized for the photocatalytic degradation of ATZ and the SCN-AuNPs nanohybrid exhibited higher photocatalytic activity with the removal efficiency of 93.6% at 90 min. Finally, the degradation mechanism was investigated and discussed.

Unlocking the secrets: exploring the influence of the aryl hydrocarbon receptor and microbiome on cancer development.

Gut microbiota regulates various aspects of human physiology by producing metabolites, metabolizing enzymes, and toxins. Many studies have linked microbiota with human health and altered microbiome configurations with the occurrence of several diseases, including cancer. Accumulating evidence suggests that the microbiome can influence the initiation and progression of several cancers. Moreover, some microbiotas of the gut and oral cavity have been reported to infect tumors, initiate metastasis, and promote the spread of cancer to distant organs, thereby influencing the clinical outcome of cancer patients. The gut microbiome has recently been reported to interact with environmental factors such as diet and exposure to environmental toxicants. Exposure to environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs) induces a shift in the gut microbiome metabolic pathways, favoring a proinflammatory microenvironment. In addition, other studies have also correlated cancer incidence with exposure to PAHs. PAHs are known to induce organ carcinogenesis through activating a ligand-activated transcriptional factor termed the aryl hydrocarbon receptor (AhR), which metabolizes PAHs to highly reactive carcinogenic intermediates. However, the crosstalk between AhR and the microbiome in mediating carcinogenesis is poorly reviewed. This review aims to discuss the role of exposure to environmental pollutants and activation of AhR on microbiome-associated cancer progression and explore the underlying molecular mechanisms involved in cancer development.

Intestinal carcinogenicity screening of environmental pollutants using organoid-based cell transformation assay.

The high incidence of colorectal cancer (CRC) is closely associated with environmental pollutant exposure. To identify potential intestinal carcinogens, we developed a cell transformation assay (CTA) using mouse adult stem cell-derived intestinal organoids (mASC-IOs) and assessed the transformation potential on 14 representative chemicals, including Cd, iPb, Cr-VI, iAs-III, Zn, Cu, PFOS, BPA, MEHP, AOM, DMH, MNNG, aspirin, and metformin. We optimized the experimental protocol based on cytotoxicity, amplification, and colony formation of chemical-treated mASC-IOs. In addition, we assessed the accuracy of in vitro study and the human tumor relevance through characterizing interdependence between cell-cell and cell-matrix adhesions, tumorigenicity, pathological feature of subcutaneous tumors, and CRC-related molecular signatures. Remarkably, the results of cell transformation in 14 chemicals showed a strong concordance with epidemiological findings (8/10) and in vivo mouse studies (12/14). In addition, we found that the increase in anchorage-independent growth was positively correlated with the tumorigenicity of tested chemicals. Through analyzing the dose-response relationship of anchorage-independent growth by benchmark dose (BMD) modeling, the potent intestinal carcinogens were identified, with their carcinogenic potency ranked from high to low as AOM, Cd, MEHP, Cr-VI, iAs-III, and DMH. Importantly, the activity of chemical-transformed mASC-IOs was associated with the degree of cellular differentiation of subcutaneous tumors, altered transcription of oncogenic genes, and activated pathways related to CRC development, including Apc, Trp53, Kras, Pik3ca, Smad4 genes, as well as WNT and BMP signaling pathways. Taken together, we successfully developed a mASC-IO-based CTA, which might serve as a potential alternative for intestinal carcinogenicity screening of chemicals.

Legal and regulatory instruments for NCD prevention: a scoping review and descriptive analysis of evaluations in OECD countries.

CONTEXT: Public health law is an important tool in non-communicable disease (NCD) prevention. There are different approaches available for achieving policy objectives, including government, co-, quasi- and self-regulation. However, it is often unclear what legal design features drive successes or failures in particular contexts. This scoping review undertakes a descriptive analysis, exploring the design characteristics of legal instruments that have been used for NCD prevention and implemented and evaluated in OECD countries. METHODS: A scoping review was conducted across four health and legal databases (Scopus, EMBASE, MEDLINE, HeinOnline), identifying study characteristics, legal characteristics and regulatory approaches, and reported outcomes. Included studies focused on regulation of tobacco, alcohol, unhealthy foods and beverages, and environmental pollutants. FINDINGS: We identified 111 relevant studies evaluating 126 legal instruments. Evaluation measures most commonly assessed implementation, compliance and changes to the built and lived environment. Few studies evaluated health or economic outcomes. When examining the design and governance mechanisms of the included legal instruments, government regulation was most commonly evaluated (n = 90) and most likely to be reported effective (64%). Self-regulation (n = 27) and quasi-regulation (n = 5) were almost always reported to be ineffective (93% and 100% respectively). There were few co-regulated instruments evaluated (n = 4) with mixed effectiveness. When examining public health risks, food and beverages including alcohol were more likely to be self- or quasi-regulated and reported as ineffective more often. In comparison, tobacco and environmental pollutants were more likely to have government mandated regulation. Many evaluations lacked critical information on regulatory design. Monitoring and enforcement of regulations was inconsistently reported, making it difficult to draw linkages to outcomes and reported effectiveness. CONCLUSIONS: Food and alcohol regulation has tended to be less successful in part due to the strong reliance on self- and quasi-regulation. More work should be done in understanding how government regulation can be extended to these areas. Public health law evaluations are important for supporting government decision-making but must provide more detail of the design and implementation features of the instruments being evaluated - critical information for policy-makers.

POLICY POINTS: Government regulation is reported as more effective than co-regulation, quasi-regulation or self-regulation. Voluntary approaches, including voluntary government regulation, are reported less effective due to low uptake and limited accountability. In public health law mandated government regulation should be strived for.Food and alcohol sectors are more likely to adopt self- or quasi-regulation and are frequently reported as ineffective. More work should be done to support government regulation in these areas.Many public health law evaluations are lacking critical design information for policy makers. This may make it difficult to learn from successes or failures and replicate interventions in other jurisdictions.

High-quality models for assessing the effects of environmental pollutants on the nervous system: 3D brain organoids.

The prevalence of environmental problems and the increasing risk of human exposure to environmental pollutants have become a global concern. The increasing environmental pollution is one of the main reasons for the rising incidence of most neurological-related diseases in recent years. However, the ethical constraints of direct human research and the racial limitations of animal models have slowed the progress of research in this area. The purpose of this study is to review the neurotoxicity of different environmental pollutants on the brain using brain organoids as a new model and to conclude that brain organoids may play a key role in assessing the mechanisms by which environmental pollutants affect neurogenesis and cause neurological pathogenesis. To accurately determine the negative effects of environmental pollutants on the nervous system, self-organizing brain organoids that are highly similar to the developing brain have become a new model system for studying the effects of environmental pollutants on human brain development and disease. This study uses brain organoids as a model to summarize the neurotoxicity of different environmental pollutants on the nervous system, including structural changes in brain organoids, inhibition of neuronal differentiation and migration, impairment of mitochondrial function, damage to cellular cilia, and influence on signaling pathways. In conclusion, exposure to environmental pollutants may cause different neurotoxicity to the nervous system. Therefore, it is crucial to understand how to use brain organoids to ameliorate neurological disorders caused by environmental pollution.

Chlordane exposure impairs the growth and behavior of Drosophila.

Chlordane, a previously extensively utilized insecticidal pesticide, has since been prohibited, however, owing to its limited degradability, it continues to persist significantly in soil and water reservoirs, subsequently accumulating within plant and animal organisms, representing a substantial threat to human health. Despite extensive research conducted over the past few decades to investigate the toxic effects of chlordane, there remains a notable dearth of studies focusing on its impact on sleep activity. Therefore, in this study, the effects of short-term and long-term exposure to chlordane on the activity and sleep of Drosophila were investigated. When exposed to chlordane at a concentration of 1 µM, Drosophila lost body weight, decreased body size and resulted in lipid metabolism disorders. In addition, chlordane exposure altered the arousal and sleep behaviors of Drosophila. Short-term exposure to chlordane resulted in an increase in night-time sleep duration, while long-term exposure to chlordane resulted in an increase in activity and a decrease in sleep, as evidenced by a decrease in the duration of each sleep session and the appearance of sleep fragmentation. Under conditions of long-term chlordane exposure, reactive oxygen species levels were significantly up-regulated in Drosophila. Our results suggest that long-term chlordane exposure triggers oxidative stress damage in Drosophila, leading to sleep disruption. This study offers novel insights into the harmful impacts of environmental pollutants on human sleep patterns and proposes that mitigating the presence of chlordane in the environment could potentially contribute to the reduction of global sleep disorder prevalence.

The uses of zebrafish (Danio rerio) as an in vivo model for toxicological studies: A review based on bibliometrics.

An in vivo model is necessary for toxicology. This review analyzed the uses of zebrafish (Danio rerio) in toxicology based on bibliometrics. Totally 56,816 publications about zebrafish from 2002 to 2023 were found in Web of Science Core Collection, with Toxicology as the top 6 among all disciplines. Accordingly, the bibliometric map reveals that "toxicity" has become a hot keyword. It further reveals that the most common exposure types include acute, chronic, and combined exposure. The toxicological effects include behavioral, intestinal, cardiovascular, hepatic, endocrine toxicity, neurotoxicity, immunotoxicity, genotoxicity, and reproductive and transgenerational toxicity. The mechanisms include oxidative stress, inflammation, autophagy, and dysbiosis of gut microbiota. The toxicants commonly evaluated by using zebrafish model include nanomaterials, arsenic, metals, bisphenol, and dioxin. Overall, zebrafish provide a unique and well-accepted model to investigate the toxicological effects and mechanisms. We also discussed the possible ways to address some of the limitations of zebrafish model, such as the combination of human organoids to avoid species differences.

Lanthanum interferes with the fundamental rhythms of stomatal opening, expression of related genes, and evapotranspiration in Arabidopsis thaliana.

The accumulation of rare earth elements (REEs) in the global environment poses a threat to plant health and ecosystem stability. Stomata located on leaves serve as the primary site for plant responses to REE-related threats. This study focused on lanthanum [La(III)], a prevalent REE in the atmospheric environment. Using interdisciplinary techniques, it was found that La(III) (≤80 µM) interfered with the fundamental rhythms of stomatal opening, related gene expression, and evapotranspiration in plants. Specifically, when exposed to low concentrations of La(III) (15 and 30 µM), the expression levels of six genes were increased, stomatal opening was enhanced, and the evapotranspiration rate was accelerated. The interference on stomatal rhythms was enhanced with higher concentrations of La(III) (60 and 80 µM), increasing the expression levels of six genes, stomatal opening, and evapotranspiration rate. To counter the interference of low concentrations of La(III) (15 and 30 µM), plants accelerated nutrient replenishment through La(III)-induced endocytosis, which the redundant nutrients enhanced photosynthesis. However, replenished nutrients failed to counter the disruption of plant biological rhythms at higher concentrations of La(III) (60 and 80 µM), thus inhibiting photosynthesis due to nutrient deficit. The interference of La(III) on these biological rhythms negatively affected plant health and ecosystem stability.

Recent advances in the development and applications of luminescent bacteria-based biosensors.

Luminescent bacteria-based biosensors are widely used for fast and sensitive monitoring of food safety, water quality, and other environmental pollutions. Recent advancements in biomedical engineering technology have led to improved portability, integration, and intelligence of these biotoxicity assays. Moreover, genetic engineering has played a significant role in the development of recombinant luminescent bacterial biosensors, enhancing both detection accuracy and sensitivity. This review provides an overview of recent advances in the development and applications of novel luminescent bacteria-based biosensors, and future perspectives and challenges in the cutting-edge research, market translation, and practical applications of luminescent bacterial biosensing are discussed.

Recent Developments of Fluorescence Sensors Constructed from Pillar[n]arene-Based Supramolecular Architectures Containing Metal Coordination Sites.

The field of fluorescence sensing, leveraging various supramolecular self-assembled architectures constructed from macrocyclic pillar[n]arenes, has seen significant advancement in recent decades. This review comprehensively discusses, for the first time, the recent innovations in the synthesis and self-assembly of pillar[n]arene-based supramolecular architectures (PSAs) containing metal coordination sites, along with their practical applications and prospects in fluorescence sensing. Integrating hydrophobic and electron-rich cavities of pillar[n]arenes into these supramolecular structures endows the entire system with self-assembly behavior and stimulus responsiveness. Employing the host-guest interaction strategy and complementary coordination forces, PSAs exhibiting both intelligent and controllable properties are successfully constructed. This provides a broad horizon for advancing fluorescence sensors capable of detecting environmental pollutants. This review aims to establish a solid foundation for the future development of fluorescence sensing applications utilizing PSAs. Additionally, current challenges and future perspectives in this field are discussed.

STAT3 Pathways Contribute to ß-HCH Interference with Anticancer Tyrosine Kinase Inhibitors.

Organochlorine pesticides (OCPs) are a class of environmentally persistent and bioaccumulative pollutants. Among these, ß-hexachlorocyclohexane (ß-HCH) is a byproduct of lindane synthesis, one of the most worldwide widespread pesticides. ß-HCH cellular mechanisms inducing chemical carcinogenesis correspond to many of those inducing chemoresistance, in particular, by the activation of signal transducer and activator of transcription 3 (STAT3) signaling pathways. For this purpose, four cell lines, representative of breast, lung, prostate, and hepatocellular cancers, were treated with ß-HCH, specific tyrosine kinase inhibitors (TKIs), and a STAT3 inhibitor. All cell samples were analyzed by a viability assay, immunoblotting analysis, a wound-healing assay, and a colony formation assay. The results show that ß-HCH reduces the efficacy of TKIs. The STAT3 protein, in this context, plays a central role. In fact, by inhibiting its activity, the efficacy of the anticancer drug is restored. Furthermore, this manuscript aimed to draw the attention of the scientific and socio-healthcare community to the issue of prolonged exposure to contaminants and their impact on drug efficacy.

Kinetic Study of Coprinus cinereus Peroxidase-Catalyzed Oxidation of 2,2'-Dihydroxyazobenzene.

Azo dyes are of concern due to their harmful effects on the environment and human health. The oxidation of 2,2'-dihydroxyazobenzene (DHAB) catalyzed with recombinant Coprinus cinereus (rCiP) peroxidase was investigated. The kinetic measurements were performed using the spectrophotometric and fluorimetric methods. The dependences of the initial reaction rates on enzyme, substrate and hydrogen peroxide concentrations during DHAB oxidation were established, and bimolecular constants of enzyme interaction with DHAB were calculated. This research demonstrated that the initial biocatalytic oxidation rates of DHAB depend on the pH and the estimated pKa values of the active forms of rCip. This study's findings thus contribute to a more comprehensive understanding of the biocatalytic oxidation of DHAB, providing valuable data for assessing the long-term toxicity, carcinogenesis and epigenetic effects of azo dyes in the environment.

CIL-ExPMRM: An Ultrasensitive Chemical Isotope Labeling Assisted Pseudo-MRM Platform to Accelerate Exposomic Suspect Screening.

Exposome is the future of next-generation environmental health to establish the association between environmental exposure and diseases. However, due to low concentrations of exposure chemicals, exposome has been hampered by lacking an effective analytical platform to characterize its composition. In this study, by combining the benefit of chemical isotope labeling and pseudo-multiple reaction monitoring (CIL-pseudo-MRM), we have developed one highly sensitive and high-throughput platform (CIL-ExPMRM) by isotope labeling urinary exposure biomarkers. Dansyl chloride (DnsCl), N-methylphenylethylamine (MPEA), and their isotope-labeled forms were used to derivatize polar hydroxyl and carboxyl compounds, respectively. We have programmed a series of scripts to optimize MRM transition parameters, curate the MRM database (>70,000 compounds), predict accurate retention time (RT), and automize dynamic MRMs. This was followed by an automated MRM peak assignment, peak alignment, and statistical analysis. A computational pipeline was eventually incorporated into a user-friendly website interface, named CIL-ExPMRM (http://www.exposomemrm.com/). The performance of this platform has been validated with a relatively low false positive rate (10.7%) across instrumental platforms. CIL-ExPMRM has systematically overcome key bottlenecks of exposome studies to some extent and outperforms previous methods due to its independence of MS/MS availability, accurate RT prediction, and collision energy optimization, as well as the ultrasensitivity and automated robust intensity-based quantification. Overall, CIL-ExPMRM has great potential to advance the exposomic studies based on urinary biomarkers.

The role of environmental pollutants in body composition: Systematic review and meta-analysis.

The effects of environmental pollution are associated with higher rates of mortality, morbidity, and years of life lost. It is known that these produce alterations in the human body, including changes in body composition. Research has focused on the association between contaminants and BMI through cross-sectional studies. The objective of this study was to synthesize the evidence for the association of pollutants on different measures of body composition. The PECOS strategy was defined, in which "P": participants of any age, sex, or ethnicity, "E": a higher level of environmental pollution, "C": a lower level of environmental pollution, "O": body composition measurements and "S": longitudinal studies. Studies from the following databases were included: MEDLINE, EMBASE, SciELO, LILACS, Scopus, Web of Science, SPORTDiscus, and gray literature from inception to January 2023.3069 studies were identified, 18 were included in the systematic review, and 13 in the meta-analysis. These studies included 8.563 people, 47 environmental contaminants, and 16 measures of body composition. The meta-analysis by subgroup found that the association between dioxins, furans, PCBs, and waist circumference was ß = 1.0 (95% CI: 0.85 to 1.16; I2: 95%), and the sum of four skinfolds ß = 1.02 (95% CI: 0.88 to 1.16; I2: 24%). The association between pesticides and waist circumference was ß = 1.00 (95% CI: 0.68 to 1.32; I2: 98%), and the fat mass was ß = 0.99 (95% CI: 0.17 to 1.81; I2: 94%). Pollutants, especially endocrine-disrupting chemicals, among which dioxins, furans, PCBs, and pesticides, are associated with changes in body composition, mainly with waist circumference and the sum of four skinfolds.