Evaluating Parental Knowledge and Behaviors Regarding Developmental Toxicants in Jazan, Saudi Arabia Using the Prevention of Toxic Chemicals in the Environment for Children Tool (PRoTECT).

This study evaluated the level of knowledge among parents in Jazan, Saudi Arabia, regarding substances that can harm child development. The Prevention of Toxic Chemicals in the Environment for Children Tool (PRoTECT) was used for this assessment. A cross-sectional survey using a multi-stage cluster random sampling approach was undertaken among 424 parents who were enlisted from eight primary healthcare centers (PHCCs). The PRoTECT score's median value was 72 out of 90, suggesting a generally high level of awareness. The study found that individuals with higher education, particularly those with postgraduate degrees, had greater awareness of protecting their children's health. Interestingly, unemployed individuals and those residing in mountainous areas also demonstrated higher awareness, possibly due to having more time to focus on their children's health and well-being. Most participants (68.2%) acknowledged the correlation between exposure to toxic chemicals during pregnancy and early childhood, and the subsequent development of neurodevelopmental disorders. The study found a solid foundation of knowledge, with 85.1% of participants interested in learning more about reducing children's exposure, but it also stressed the need for specific actions to turn awareness into prevention. These findings would help policymakers develop effective strategies, such as targeted educational campaigns, collaboration with healthcare providers, utilization of media channels, and encouragement of community-led initiatives, to reduce children's exposure to developmental toxicants in line with national and global environmental health initiatives. Future research should focus on longitudinal consciousness and behavior evaluations and regional environmental contaminants.

Beta-caryophyllene attenuates experimental hepatocellular carcinoma through downregulation of oxidative stress and inflammation.

Hepatocellular carcinoma (HCC) is caused by various factors including toxic substances and xenobiotics. Numerous treatment strategies are used to address toxicity to the liver and HCC, yet their adverse effects are drawbacks. This study aimed to assess the effect of DEN/CCl4 on morphological changes in the liver, body weight, tumor incidence, and hematological tumor incidence, hematological parameters, hepatic markers, and histopathological analysis in mice following a preventive measure by using ß-caryophyllene (BCP). Adult Balb/c mice were administered a single dose of DEN 1-mg/kg body weight and 0.2-mL CCl4/kg body weight intraperitoneal twice a week (i.p.) for 22 weeks. BCP was treated in one group of mice at 30-mg/kg body weight, intraperitoneal, for 7 weeks. BCP alone was treated in one group of mice at 300-mg/kg body weight intraperitoneal for 22 weeks. DEN/CCl4 caused a reduction in mice's body weight, which was significantly attenuated by BCP administration. BCP supplementation attenuated the tumor incidence DEN/CCl4 (100%) to about 25%. DEN/CCl4 caused alterations in the hematological parameters, serum total protein albumin globulin, A/G ratio, liver function markers (AST, ALT, ALP, GGT, ACP, and bilirubin), and lipid profile markers that were significantly reinstated by BCP administration. Oxidative stress markers (MDA, SOD, CAT, NO, LDH, and GST) were reduced by DEN/CCl4, which were significantly increased in BCP-treated groups. The liver histopathology alterations caused by DEN/CCl4 were amended considerably by BCP treatment. Immunohistochemical studies suggest that AFP, caspase-3, and COX-2 were chronically overexpressed in DEN/CCl4-exposed mice, notably attenuated by BCP administration. BCP suppressed tumor incidence by downregulating inflammation and inducing caspase-3-mediated apoptosis. Conclusively, BCP appears to be a potent natural supplement capable of repressing liver inflammation and carcinoma through the mitigation of oxidative stress and inflammation pathways.

Investigating the protective properties of Panax ginseng and its constituents against biotoxins and metal toxicity: a mechanistic review.

Natural toxins are toxic substances produced by living microorganisms and cause harmful effects to other creatures, but not the organisms themselves. Based on the sources, they are classified into fungal, microbial, herbal, algae, and animal biotoxins. Metals, the oldest toxicants, are not created or destroyed by human industry as elements, just concentrated in the biosphere. An antidote can counteract the toxic effects of a drug or toxin or mitigate the adverse effects of a harmful substance. The potential antidote effects of Panax ginseng in organ toxicity have been proved by many scientific research projects. Herein, we are going to gather a comprehensive mechanistic review of the antidotal effects of ginseng and its main constituents against natural toxins and metal toxicity. In this regard, a literate search has been done in PubMed/Medline, Science Direct, and Scopus from 2000 until 2024. The gathered data showed the protective impacts of this golden plant and its secondary metabolites against aflatoxin, deoxynivalenol, three-nitro propionic acid, ochratoxin A, lipopolysaccharide, nicotine, aconite, domoic acid, α-synuclein, amyloid ß, and glutamate as well as aluminum, cadmium, chrome, copper, iron, and lead. These antidotal effects occur by multi-functional mechanisms. It may be attributed to antioxidant, anti-inflammatory, and anti-apoptotic effects. Future research directions on the antidotal effects of ginseng against natural toxins and metal toxicity involve broadening the scope of studies to include a wider range of toxins and metals, exploring synergistic interactions with other natural compounds, and conducting more human clinical trials to validate the efficacy and safety of ginseng-based treatments.

Comparison of Health Complaints, Occupational Risks, and Occupational Health Practices of Healthcare Workers According to Professions and Departments in the Hospital.

BACKGROUND: It is essential to protect the health of healthcare workers who constitute a large part of the workforce worldwide and whose importance has become more evident after the recent pandemic. There are numerous occupational hazards for healthcare workers in hospitals. PURPOSE: The study aims to assess the exposure hazards of healthcare workers and their health complaints, as well as their awareness, knowledge, opinions, and attitudes towards occupational health and safety (OHS), considering workers' professions and departments in a public hospital. This cross-sectional study conducted a survey among healthcare workers (n=608) who worked at Yozgat City Hospital, Yozgat, Turkey. RESULTS: The majority of workers were nurses (43.4%, N=264/608). Latex exposure (63.7%, N=387/608) and noise (55.8%, N=339/608) were the most common exposed hazards, and the risk varies depending on their professions and job descriptions. However, the risk perception of workers was priorities of infectious diseases (48.5%, N=292/602) and violence (27.4%, N=165/602). Musculoskeletal system problems (71.9%, n=439/608) were observed very frequently in workers. Additionally, 9.2% (N=56/608) of workers were diagnosed with an occupational disease. The unit and profession most commonly diagnosed with occupational diseases were the laboratory (22.5%, N=9/40) and midwives (19.4%, N=14/72), respectively. The frequency of workers who stated that they had a work accident at least once in their lives was 31.9% (N=194/608), and higher frequencies belonged to nurses, health officers, and midwives. Additionally, the emergency department was the riskier unit. The study conducted relationship analyses between exposure to various occupational agents at different exposure frequencies and various health complaints. The relationships of occupational hazards such as chemotherapeutics, anesthetic gases, aerosol type drugs, sterilization and disinfection agents, xylene, toluene, formaldehyde, and surgical smoke with health complaints such as liver, dermal diseases, respiratory problems, and varicose veins have been determined. CONCLUSIONS: The hospital workers had a high rate of injuries to sharp objects and musculoskeletal systems. Remarkably, operating rooms and emergency rooms were found to be riskier in terms of work accidents. More than half of healthcare workers may delay using personal protective equipment (PPE) due to excessive workload. Further studies are needed on the effects of more specific occupational chemicals and diseases, such as varicose veins, fertility, and neurological problems. Frequent risk assessments, effective training, workload reduction, and biomarker monitoring are crucial for hospital workplace safety.

An Insight into Different Experimental Models used for Hepatoprotective Studies: A Review.

Numerous factors, including exposure to harmful substances, drinking too much alcohol, contracting certain hepatitis serotypes, and using specific medicines, contribute to the development of liver illnesses. Lipid peroxidation and other forms of oxidative stress are the main mechanisms by which hepatotoxic substances harm liver cells. Pathological changes in the liver include a rise in the levels of blood serum, a decrease in antioxidant enzymes, as well as the formation of free radical radicals. It is necessary to find pharmaceutical alternatives to treat liver diseases to increase their efficacy and decrease their toxicity. For the development of new therapeutic medications, a greater knowledge of primary mechanisms is required. In order to mimic human liver diseases, animal models are developed. Animal models have been used for several decades to study the pathogenesis of liver disorders and related toxicities. For many years, animal models have been utilized to investigate the pathophysiology of liver illness and associated toxicity. The animal models are created to imitate human hepatic disorders. This review enlisted numerous hepatic damage in vitro and in vivo models using various toxicants, their probable biochemical pathways and numerous metabolic pathways via oxidative stressors, different serum biomarkers enzymes are discussed, which will help to identify the most accurate and suitable model to test any plant preparations to check and evaluate their hepatoprotective properties.

Assessing prenatal and early childhood social and environmental determinants of health in the HEALthy Brain and Child Development Study (HBCD).

The HEALthy Brain and Child Development (HBCD) Study, a multi-site prospective longitudinal cohort study, will examine human brain, cognitive, behavioral, social, and emotional development beginning prenatally and planned through early childhood. The charge of the HBCD Social and Environmental Determinants (SED) working group is to develop and implement a battery of assessments to broadly characterize the social and physical environment during the prenatal period and early life to characterize risk and resilience exposures that can impact child growth and development. The SED battery consists largely of measures that will be repeated across the course of the HBCD Study with appropriate modifications for the age of the child and include participant demographics, indicators of socioeconomic status, stress and economic hardship, bias and discrimination (e.g., racism), acculturation, neighborhood safety, child and maternal exposures to adversity, environmental toxicants, social support, and other protective factors. Special considerations were paid to reducing participant burden, promoting diversity, equity, and inclusion, and adopting trauma-informed practices for the collection of sensitive information such as domestic violence exposure and adverse childhood experiences. Overall, the SED battery will provide essential data to advance understanding of child development and approaches to advance health equity across infant and child development.

Advances in immunology of male reproductive toxicity induced by common environmental pollutants.

Humans are exposed to an ever-increasing number of environmental toxicants, some of which have gradually been identified as major risk factors for male reproductive health, even associated with male infertility. Male infertility is usually due to the reproductive system damage, which may be influenced by the exposure to contaminants such as heavy metals, plasticizers, along with genetics and lifestyle. Testicular immune microenvironment (TIM) is important in maintaining normal physiological functions of the testis, whether disturbed TIM after exposure to environmental toxicants could induce reproductive toxicity remains to be explored. Therefore, the current review aims to contribute to the further understanding of exposure and male infertility by characterizing environmental exposures and the effect on TIM. We first summarized the male reproductive toxicity phenotypes induced by common environmental pollutants. Contaminants including heavy metals and plastic additives and fine particulate matter (PM2.5), have been repetitively associated with male infertility, whereas emerging contaminants such as perfluoroalkyl substances and micro(nano)plastics have also been found to disrupt TIM and lead to male reproductive toxicity. We further reviewed the importance of TIM and its homeostasis in maintaining the normal physiological functions of the testis. Most importantly, we discussed the advances in immunology of male reproductive toxicity induced by metals and metalloids, plastic additives, persistent organic pollutants (POPs), micro(nano)plastic and PM2.5 to suggest the importance of reproductive immunotoxicology in the future study of environmental toxicants, but also contribute to the development of effective prevention and treatment strategies for mitigating adverse effects of environmental pollutants on human health.

High-Resolution Mass Spectrometry for Human Exposomics: Expanding Chemical Space Coverage.

In the modern "omics" era, measurement of the human exposome is a critical missing link between genetic drivers and disease outcomes. High-resolution mass spectrometry (HRMS), routinely used in proteomics and metabolomics, has emerged as a leading technology to broadly profile chemical exposure agents and related biomolecules for accurate mass measurement, high sensitivity, rapid data acquisition, and increased resolution of chemical space. Non-targeted approaches are increasingly accessible, supporting a shift from conventional hypothesis-driven, quantitation-centric targeted analyses toward data-driven, hypothesis-generating chemical exposome-wide profiling. However, HRMS-based exposomics encounters unique challenges. New analytical and computational infrastructures are needed to expand the analysis coverage through streamlined, scalable, and harmonized workflows and data pipelines that permit longitudinal chemical exposome tracking, retrospective validation, and multi-omics integration for meaningful health-oriented inferences. In this article, we survey the literature on state-of-the-art HRMS-based technologies, review current analytical workflows and informatic pipelines, and provide an up-to-date reference on exposomic approaches for chemists, toxicologists, epidemiologists, care providers, and stakeholders in health sciences and medicine. We propose efforts to benchmark fit-for-purpose platforms for expanding coverage of chemical space, including gas/liquid chromatography-HRMS (GC-HRMS and LC-HRMS), and discuss opportunities, challenges, and strategies to advance the burgeoning field of the exposome.

Toxicants improve glycerol production in the fermentation of undetoxified hydrolysate by Candida glycerinogenes.

OBJECTIVES: Toxicants inhibit microbial fermentation and reduce product titres. This work investigated the glycerol production characteristics of Candida glycerinogenes in highly toxic unwashed undetoxified hydrolysate and provided new ideas for high glycerol production from hydrolysates. RESULTS: The unwashed hydrolysate contains higher concentrations of toxicants, such as furfural, acetic acid, phenols and NaCl than the washed alkali-treated bagasse hydrolysate. C. glycerinogenes fermented unwashed undetoxified hydrolysate yielded 36.1 g/L glycerol, 15.8% higher than the washed hydrolysate, suggesting that the toxicants stimulated glycerol synthesis. qRT-PCR analysis showed that toxicants of unwashed undetoxified hydrolysates greatly up-regulated the transcript levels of the genes GPD1, HXT4 and MSN4 et al. Overexpressing the above genes increased glycerol production by 27.9% to 46.1 g/L. And it was further increased by 8.8% to 50.1 g/L in a 5 L bioreactor. CONCLUSIONS: This result proves that toxicants in lignocellulosic hydrolysates can increase the titre of microbial glycerol production.

How Do Environmental Toxicants Affect Oocyte Maturation Via Oxidative Stress?

In mammals, oogenesis initiates before birth and pauses at the dictyate stage of meiotic prophase I until luteinizing hormone (LH) surges to resume meiosis. Oocyte maturation refers to the resumption of meiosis that directs oocytes to advance from prophase I to metaphase II of meiosis. This process is carefully modulated to ensure a normal ovulation and successful fertilization. By generating excessive amounts of oxidative stress, environmental toxicants can disrupt the oocyte maturation. In this review, we categorized these environmental toxicants that induce mitochondrial dysfunction and abnormal spindle formation. Further, we discussed the underlying mechanisms that hinder oocyte maturation, including mitochondrial function, spindle formation, and DNA damage response.

Protective effects of Panax ginseng as a medical food against chemical toxic agents: molecular and cellular mechanisms.

Humans are exposed to different types of toxic agents, which may directly induce organ malfunction or indirectly alter gene expression, leading to carcinogenic and teratogenic effects, and eventually death. Ginseng (Panax ginseng) is the most valuable of all medicinal herbs. Nevertheless, specific data on the antidotal mechanisms of this golden herb are currently unavailable. Based on the findings of in vitro, in vivo, and clinical studies, this review focused on the probable protective mechanisms of ginseng and its major components, such as protopanaxadiols, protopanaxatriols, and pentacyclic ginsenosides against various chemical toxic agents. Relevant articles from 2000 to 2023 were gathered from PubMed/Medline, Scopus, and Google Scholar. This literature review shows that P. ginseng and its main components have protective and antidotal effects against the deteriorative effects of pesticides, pharmaceutical agents, including acetaminophen, doxorubicin, isoproterenol, cyclosporine A, tacrolimus, and gentamicin, ethanol, and some chemical agents. These improvements occur through multi-functional mechanisms. They exhibit antioxidant activity, induce anti-inflammatory action, and block intrinsic and extrinsic apoptotic pathways. However, relevant clinical trials are necessary to validate the mentioned effects and translate the knowledge from basic science to human benefit, fulfilling the fundamental goal of all toxicologists.

Environmental, Metabolic, and Nutritional Factors Concerning Dementia in African American and Hispanic American Populations.

African Americans and Hispanic Americans experience a higher incidence and prevalence of dementia than white Americans while also experiencing more environmental, metabolic, and nutritional factors potentially promoting such disparities. Greater exposure to air, water, and soil pollutants, including toxic metals associated with neurodegeneration, accrues in both minorities, as does worse dental care than Whites exposing them to periodontitis, raising dementia risk. Hispanic Americans experience greater occupational exposure to herbicides and pesticides, and have a higher rate of developing non-alcoholic fatty liver disease (NAFLD), predisposing to dementia. African Americans have a greater likelihood of both vitamin D deficiency and magnesium deficiency, increasing neuroinflammation and dementia risk. Both have greater air pollution exposure, a known dementia risk. Nutritional changes, including greater nut consumption and reduced sugar drink consumption, improved dental care, and reduced toxicant exposure, may help reduce this higher risk of dementia among African Americans and Hispanic Americans.

Association of Prenatal Dietary Toxicants and Inorganic Arsenic Exposure with Children's Emotional and Behavioral Problems: ECLIPSES Study.

Prenatal exposure to dietary toxicants is linked to neurocognitive issues, but its effect on early emotional and behavioral development in children is less clear. To explore the relationship between prenatal intake of As, iAs, Cd, MeHg, Pb, PCDD/Fs, DL-PCBs, and NDL-PCBs and emotional and behavioral issues in four-year-old children. This study included 192 mother-child pairs from the ECLIPSES study, assessing prenatal dietary toxicant exposure through a food-frequency questionnaire and Catalan Food Safety Agency data. Children's emotional and behavioral scores were evaluated using the Child Behavior Checklist for ages 1.5-5 years. Multivariable regression and logistic models were used, focusing on iAs after finding significant preliminary associations. Increased prenatal dietary intake of iAs was associated with internalizing, externalizing, and attention-deficit/hyperactivity problems. Higher iAs levels (>4.16 µg/day) significantly increased the risk of total problems (OR = 2.94) and specific issues like anxious/depressed (OR = 4.88), anxiety (OR = 3.27), and oppositional defiant problems (OR = 4.30). High iAs consumption correlated with the intake of meat, eggs, cereals, tubers, fruits, and pulses Prenatal dietary iAs exposure is associated with various emotional and behavioral problems in children. Monitoring and reducing iAs levels in food are crucial for public health.

Insights into the early-life chemical exposome of Nigerian infants and potential correlations with the developing gut microbiome.

Early-life exposure to natural and synthetic chemicals can impact acute and chronic health conditions. Here, a suspect screening workflow anchored on high-resolution mass spectrometry was applied to elucidate xenobiotics in breast milk and matching stool samples collected from Nigerian mother-infant pairs (n = 11) at three time points. Potential correlations between xenobiotic exposure and the developing gut microbiome, as determined by 16S rRNA gene amplicon sequencing, were subsequently explored. Overall, 12,192 and 16,461 features were acquired in the breast milk and stool samples, respectively. Following quality control and suspect screening, 562 and 864 features remained, respectively, with 149 of these features present in both matrices. Taking advantage of 242 authentic reference standards measured for confirmatory purposes of food bio-actives and toxicants, 34 features in breast milk and 68 features in stool were identified and semi-quantified. Moreover, 51 and 78 features were annotated with spectral library matching, as well as 416 and 652 by in silico fragmentation tools in breast milk and stool, respectively. The analytical workflow proved its versatility to simultaneously determine a diverse panel of chemical classes including mycotoxins, endocrine-disrupting chemicals (EDCs), antibiotics, plasticizers, perfluorinated alkylated substances (PFAS), and pesticides, although it was originally optimized for polyphenols. Spearman rank correlation of the identified features revealed significant correlations between chemicals of the same classification such as polyphenols. One-way ANOVA and differential abundance analysis of the data obtained from stool samples revealed that molecules of plant-based origin elevated as complementary foods were introduced to the infants' diets. Annotated compounds in the stool, such as tricetin, positively correlated with the genus Blautia. Moreover, vulgaxanthin negatively correlated with Escherichia-Shigella. Despite the limited sample size, this exploratory study provides high-quality exposure data of matched biospecimens obtained from mother-infant pairs in sub-Saharan Africa and shows potential correlations between the chemical exposome and the gut microbiome.

What is driving the global decline of human fertility? Need for a multidisciplinary approach to the underlying mechanisms.

An intense period of human population expansion over the past 250 years is about to cease. Total fertility rates are falling dramatically all over the world such that highly industrialized nations, including China and the tiger economies of SE Asia, will see their populations decline significantly in the coming decades. The socioeconomic, geopolitical and environmental ramifications of this change are considerable and invite a multidisciplinary consideration of the underlying mechanisms. In the short-term, socioeconomic factors, particularly urbanization and delayed childbearing are powerful drivers of reduced fertility. In parallel, lifestyle factors such as obesity and the presence of numerous reproductive toxicants in the environment, including air-borne pollutants, nanoplastics and electromagnetic radiation, are seriously compromising reproductive health. In the longer term, it is hypothesized that the reduction in family size that accompanies the demographic transition will decrease selection pressure on high fertility genes leading to a progressive loss of human fecundity. Paradoxically, the uptake of assisted reproductive technologies at scale, may also contribute to such fecundity loss by encouraging the retention of poor fertility genotypes within the population. Since the decline in fertility rate that accompanies the demographic transition appears to be ubiquitous, the public health implications for our species are potentially devastating.

Association between Prenatal Dietary Toxicants and Infant Neurodevelopment: The Role of Fish.

More research is needed to understand how the maternal consumption of fish and fish-borne toxicants impacts infant neurodevelopment. The present analysis was conducted over 460 mother-infant pairs within the ECLIPSES study. Dietary intake of metals and persistent organic pollutants from fish (including white fish, blue fish, and seafood) was estimated in pregnant women. The infants underwent cognitive, language, and motor function assessments using the Bayley Scales of Infant Development-III at the 40-day postpartum. Associations between dietary toxicants and outcomes were assessed using multivariable linear regression models. Estimated prenatal exposure to fish-borne toxicants, such as arsenic, inorganic arsenic, methylmercury, dioxin-like polychlorinated biphenyls (DL-PCBs), and non-DL-PCBs, was associated with poorer language functions in infants, whereas no significant associations were found with motor or cognitive functions. Maternal fish consumption exceeding the Spanish recommendation of no more than 71 g per day was linked to these adverse effects on language abilities without affecting motor or cognitive development. This highlights the importance of vigilant monitoring of environmental toxicants and the provision of dietary guidance for pregnant women, with potential implications for public health and child development.

LRRK2 kinase inhibition protects against Parkinson's disease-associated environmental toxicants.

Idiopathic Parkinson's disease (PD) is epidemiologically linked with exposure to toxicants such as pesticides and solvents, which comprise a wide array of chemicals that pollute our environment. While most are structurally distinct, a common cellular target for their toxicity is mitochondrial dysfunction, a key pathological trigger involved in the selective vulnerability of dopaminergic neurons. We and others have shown that environmental mitochondrial toxicants such as the pesticides rotenone and paraquat, and the organic solvent trichloroethylene (TCE) appear to be influenced by the protein LRRK2, a genetic risk factor for PD. As LRRK2 mediates vesicular trafficking and influences endolysosomal function, we postulated that LRRK2 kinase activity may inhibit the autophagic removal of toxicant damaged mitochondria, resulting in elevated oxidative stress. Conversely, we suspected that inhibition of LRRK2, which has been shown to be protective against dopaminergic neurodegeneration caused by mitochondrial toxicants, would reduce the intracellular production of reactive oxygen species (ROS) and prevent mitochondrial toxicity from inducing cell death. To do this, we tested in vitro if genetic or pharmacologic inhibition of LRRK2 (MLi2) protected against ROS caused by four toxicants associated with PD risk - rotenone, paraquat, TCE, and tetrachloroethylene (PERC). In parallel, we assessed if LRRK2 inhibition with MLi2 could protect against TCE-induced toxicity in vivo, in a follow up study from our observation that TCE elevated LRRK2 kinase activity in the nigrostriatal tract of rats prior to dopaminergic neurodegeneration. We found that LRRK2 inhibition blocked toxicant-induced ROS and promoted mitophagy in vitro, and protected against dopaminergic neurodegeneration, neuroinflammation, and mitochondrial damage caused by TCE in vivo. We also found that cells with the LRRK2 G2019S mutation displayed exacerbated levels of toxicant induced ROS, but this was ameliorated by LRRK2 inhibition with MLi2. Collectively, these data support a role for LRRK2 in toxicant-induced mitochondrial dysfunction linked to PD risk through oxidative stress and the autophagic removal of damaged mitochondria.

Epidemiology of Parkinson's Disease: An Update.

PURPOSE OF REVIEW: In recent decades, epidemiological understanding of Parkinson disease (PD) has evolved significantly. Major discoveries in genetics and large epidemiological investigations have provided a better understanding of the genetic, behavioral, and environmental factors that play a role in the pathogenesis and progression of PD. In this review, we provide an epidemiological update of PD with a particular focus on advances in the last five years of published literature. RECENT FINDINGS: We include an overview of PD pathophysiology, followed by a detailed discussion of the known distribution of disease and varied determinants of disease. We describe investigations of risk factors for PD, and provide a critical summary of current knowledge, knowledge gaps, and both clinical and research implications. We emphasize the need to characterize the epidemiology of the disease in diverse populations. Despite increasing understanding of PD epidemiology, recent paradigm shifts in the conceptualization of PD as a biological entity will also impact epidemiological research moving forward and guide further work in this field.

The Role of Endocrine Disruption Chemical-Regulated Aryl Hydrocarbon Receptor Activity in the Pathogenesis of Pancreatic Diseases and Cancer.

The aryl hydrocarbon receptor (AHR) serves as a ligand-activated transcription factor crucial for regulating fundamental cellular and molecular processes, such as xenobiotic metabolism, immune responses, and cancer development. Notably, a spectrum of endocrine-disrupting chemicals (EDCs) act as agonists or antagonists of AHR, leading to the dysregulation of pivotal cellular and molecular processes and endocrine system disruption. Accumulating evidence suggests a correlation between EDC exposure and the onset of diverse pancreatic diseases, including diabetes, pancreatitis, and pancreatic cancer. Despite this association, the mechanistic role of AHR as a linchpin molecule in EDC exposure-related pathogenesis of pancreatic diseases and cancer remains unexplored. This review comprehensively examines the involvement of AHR in EDC exposure-mediated regulation of pancreatic pathogenesis, emphasizing AHR as a potential therapeutic target for the pathogenesis of pancreatic diseases and cancer.

Comparison of emissions across tobacco products: A slippery slope in tobacco control.

In this narrative review, we highlight the challenges of comparing emissions from different tobacco products under controlled laboratory settings (using smoking/vaping machines). We focus on tobacco products that generate inhalable smoke or aerosol, such as cigarettes, cigars, hookah, electronic cigarettes, and heated tobacco products. We discuss challenges associated with sample generation including variability of smoking/vaping machines, lack of standardized adaptors that connect smoking/vaping machines to different tobacco products, puffing protocols that are not representative of actual use, and sample generation session length (minutes or number of puffs) that depends on product characteristics. We also discuss the challenges of physically characterizing and trapping emissions from products with different aerosol characteristics. Challenges to analytical method development are also covered, highlighting matrix effects, order of magnitude differences in analyte levels, and the necessity of tailored quality control/quality assurance measures. The review highlights two approaches in selecting emissions to monitor across products, one focusing on toxicants that were detected and quantified with optimized methods for combustible cigarettes, and the other looking for product-specific toxicants using non-targeted analysis. The challenges of data reporting and statistical analysis that allow meaningful comparison across products are also discussed. We end the review by highlighting that even if the technical challenges are overcome, emission comparison may obscure the absolute exposure from novel products if we only focus on relative exposure compared to combustible products.