Chronic Exposure Research Articles

Insights into the Chemical Exposome during Pregnancy: A Non-Targeted Analysis of Preterm and Term Births.

Human-made chemicals are ubiquitous, leading to chronic exposure to complex mixtures of potentially harmful substances. We investigated chemical exposures in pregnant women in New York City by applying a non-targeted analysis (NTA) workflow to 95 paired prenatal urine and serum samples (35 pairs of preterm birth) collected as part of the New York University Children's Health and Environment Study. We analyzed all samples using liquid chromatography coupled with Orbitrap high-resolution mass spectrometry in both positive and negative electrospray ionization modes, employing full scan and data-dependent MS/MS fragmentation scans. We detected a total of 1524 chemical features for annotation, with 12 chemicals confirmed by authentic standards. Two confirmed chemicals dodecyltrimethylammonium and N,N-dimethyldecylamine N-oxide appear to not have been previously reported in human blood samples. We observed a statistically significant differential enrichment between urine and serum samples, as well as between preterm and term birth (p < 0.0001) in serum samples. When comparing between preterm and term births, an exogenous contaminant, 1,4-cyclohexanedicarboxylic acid (tentative), showed a statistical significance difference (p = 0.003) with more abundance in preterm birth in serum. An example of chemical associations (12 associations in total) observed was between surfactants (tertiary amines) and endogenous metabolites (fatty acid amides).

Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer's disease.

Astrocytes are crucial to brain homeostasis, yet their changes along the spatiotemporal progression of Alzheimer's disease (AD) neuropathology remain unexplored. Here we performed single-nucleus RNA sequencing of 628,943 astrocytes from five brain regions representing the stereotypical progression of AD pathology across 32 donors spanning the entire normal aging to severe AD continuum. We mapped out several unique astrocyte subclusters that exhibited varying responses to neuropathology across the AD-vulnerable neural network (spatial axis) or AD pathology stage (temporal axis). The proportion of homeostatic, intermediate and reactive astrocytes changed only along the spatial axis, whereas two other subclusters changed along the temporal axis. One of these, a trophic factor-rich subcluster, declined along pathology stages, whereas the other increased in the late stage but returned to baseline levels in the end stage, suggesting an exhausted response with chronic exposure to neuropathology. Our study underscores the complex dynamics of astrocytic responses in AD.

A Case Study of Air Quality in Kabul, Afghanistan

The air quality in Afghanistan is severely affected by various pollutant sources, the impacts of which often cause acute health problems, particularly among the old, young and those suffering from poor health. The impacts of chronic exposure to air pollutants are also likely to become apparent over time. The purpose of this air quality dissertation is to assist policy makers in the design and implementation of policies, and in the development of monitoring and management tools to restore air quality in Afghanistan. Since 2001, Kabul city’s population has grown from four hundred thousand to six million people. Estimates of various pollutant emissions indicate that vehicular traffic, windblown dust, brick kilns, residential heating during winter season, and domestic and commercial generators are the major sources of air pollution in Kabul. The estimated total annual emissions in Kabul are 17,363 tons of PM10, 16,183 tons of NOx, 2,484 tons of SO2, 97,068 tons of CO2, and 650,846 tons of CO2 .In the article “In Kabul, air pollution a bigger killer than war” that every year around 3,000 people die in Kabul city due to air pollution whereas the total mortality rate due to war across the country is 2,777 cases.

Analysis of G:C&gt;T:A, G:C&gt;A:T, and G:C&gt;C:G Mutations in the TP53 Gene in Women with and without Breast Cancer in the Long-Term Period after Chronic Radiation Exposure

Analysis of G:C&gt;T:A, G:C&gt;A:T, and G:C&gt;C:G Mutations in the TP53 Gene in Women with and without Breast Cancer in the Long-Term Period after Chronic Radiation Exposure

The Interaction of Apical Periodontitis, Cigarette Smoke, and Alcohol Consumption on Liver Antioxidant Status in Rats

This study aimed to investigate the impact of alcohol (A), secondhand cigarette smoking (ShS), and their combined effect on liver antioxidant activity and hepatic damage in rats with induced apical periodontitis (AP). Thirty-five female Wistar rats were randomly allocated into five groups (n = 7): (1) control (rats without ShS, alcoholic diet, or AP), (2) control-AP (induced AP only), (3) ShS-AP (ShS exposure and induced AP), (4) A-AP (alcoholic diet and induced AP), and (5) A+ShS-AP (alcoholic diet, ShS exposure, and induced AP). Alcohol was administered through semi-voluntary intake, while ShS exposure involved the daily inhalation of cigarette smoke. The experimental period lasted 8 weeks, with AP induction occurring in the 4th week following molar pulp exposure. Liver samples were collected post-euthanasia for histomorphometric and antioxidant marker analyses. All AP-induced groups exhibited increased liver sinusoidal dilation compared to the control group (p &lt; 0.05). AP significantly reduced total antioxidant capacity (FRAP) across all groups (p &lt; 0.05). In AP-induced groups, FRAP levels were further decreased in ShS-AP and A+ShS-AP compared to control-AP (p &lt; 0.05). AP also led to a decrease in the glutathione defense system (p &lt; 0.05). Rats with alcohol exposure (A-AP and A+ShS-AP) showed reduced glutathione peroxidase activity (p &lt; 0.05). Glutathione reductase activity was comparable in the control and control-AP groups (p &gt; 0.05), but significantly decreased in the alcohol and ShS-exposed groups (p &lt; 0.05). Apical periodontitis can relate to morphological changes in the liver’s sinusoidal spaces and impairment of liver’s antioxidant capacity of rats, particularly when combined with chronic alcohol consumption and exposure to cigarette smoke.

Decreased Brain pH Underlies Behavioral and Brain Abnormalities Induced by Chronic Exposure to Glucocorticoids in Mice.

Depressed patients may exhibit glucocorticoid hypersecretion, suggesting that elevated levels of glucocorticoids may play an important role in the pathophysiology of depression. Some postmortem brain studies have shown decreased pH and increased lactate levels in psychiatric patients, implying involvement of these factors in the pathogenesis. To investigate the effects of glucocorticoids on brain pH and lactate levels, and their roles in depressive symptoms, brain pH and lactate were examined in mice treated with corticosterone (CORT), the major bioactive glucocorticoid in rodents. A single administration of CORT decreased hippocampal pH after 24 h. Three weeks of CORT treatment decreased pH in the prefrontal cortex (PFC), striatum, and hippocampus (HC), whereas intake of pH 9.0 drinking water increased pH in these brain regions. pH and lactate levels were correlated in the PFC and HC of mice treated with CORT for 3 weeks. The suppression of body weight gain and decrease in adrenal weight observed after 3 weeks of CORT treatment were not alleviated by pH 9.0 water. However, an increase in immobility time in the forced swim test and a decrease in neurogenesis in the hippocampus were alleviated. The decrease in brain pH and increase in immobility time in the forced swim test and a decrease in neurogenesis in the hippocampus induced by CORT treatment were abolished by co-treatment with the glucocorticoid receptor (GR) antagonist mifepristone. These findings indicate that decreased brain pH via GRs may be related to glucocorticoid-induced depression-like behavior and decreased hippocampal neurogenesis.

Chronic corticosterone exposure causes anxiety- and depression-related behaviors with altered gut microbial and brain metabolomic profiles in adult male C57BL/6J mice

Chronic exposure to glucocorticoids in response to long-term stress is thought to be a risk factor for major depression. Depression is associated with disturbances in the gut microbiota composition and peripheral and central energy metabolism. However, the relationship between chronic glucocorticoid exposure, the gut microbiota, and brain metabolism remains largely unknown. In this study, we first investigated the effects of chronic corticosterone exposure on various domains of behavior in adult male C57BL/6J mice treated with the glucocorticoid corticosterone to evaluate them as an animal model of depression. We then examined the gut microbial composition and brain and plasma metabolome in corticosterone-treated mice. Chronic corticosterone treatment resulted in reduced locomotor activity, increased anxiety-like and depression-related behaviors, decreased rotarod latency, reduced acoustic startle response, decreased social behavior, working memory deficits, impaired contextual fear memory, and enhanced cued fear memory. Chronic corticosterone treatment also altered the composition of gut microbiota, which has been reported to be associated with depression, such as increased abundance of Bifidobacterium, Turicibacter, and Corynebacterium and decreased abundance of Barnesiella. Metabolomic data revealed that long-term exposure to corticosterone led to a decrease in brain neurotransmitter metabolites, such as serotonin, 5-hydroxyindoleacetic acid, acetylcholine, and gamma-aminobutyric acid, as well as changes in betaine and methionine metabolism, as indicated by decreased levels of adenosine, dimethylglycine, choline, and methionine in the brain. These results indicate that mice treated with corticosterone have good face and construct validity as an animal model for studying anxiety and depression with altered gut microbial composition and brain metabolism, offering new insights into the neurobiological basis of depression arising from gut-brain axis dysfunction caused by prolonged exposure to excessive glucocorticoids.

Impact of chronic opioid use on acute health care utilization in children with IBD and arthritis: a retrospective cohort study

BackgroundOpioid use is non-trivial in children with inflammatory bowel disease (IBD) and arthritis, and options are limited for pain management. We aimed to determine the impacts of chronic opioid use on acute care utilization in children with both IBD and arthritis in United States.MethodsParticipants less than 18 years of age with IBD and arthritis, with at least one year of continuous enrollment (no interruption of insurance for at least 1 year) and at least one pharmacy claim in the Truven Health MarketScan Claims and Encounter Database, were included in the study. The primary exposure was chronic opioid use. Chronic opioid users were matched to non-exposed controls. The primary outcome was acute healthcare utilization (total number of emergency department visits and hospitalizations within 12–24 months after the index date). The association between acute care utilization and chronic opioid use was assessed using a multivariable negative binomial regression model.Results480 children with IBD and arthritis met inclusion criteria, out of which 59 (12.3%) met the criteria for chronic opioid exposure, and 46 of them had at least one year of follow-up. IRR (incidence rate ratio) of acute healthcare use for patients exposed to chronic opioid use was 1.7 higher than controls. Additionally, public insurance and having a chronic pain condition were independently and significantly associated with greater acute healthcare use.ConclusionChronic opioid use was significantly associated with greater acute health care utilization in children with IBD and arthritis than matched unexposed controls. Future investigation is warranted to determine if preferential use of non-opioid therapy for pain control can reduce acute healthcare costs in this population.

The essential roles of memory B cells in the pathogenesis of systemic lupus erythematosus.

Emerging evidence indicates that memory B cells are dysfunctional in systemic lupus erythematosus (SLE). They are hyporesponsive to signalling through the B cell receptor (BCR) but retain responsiveness to Toll-like receptor (TLR) and type I interferon signalling, as well as to T cell-mediated activation via CD40-CD154. Chronic exposure to immune complexes of ribonucleoprotein (RNP)-specific autoantibodies and TLR-engaging or BCR-engaging cargo is likely to contribute to this partially anergic phenotype. TLR7 or TLR8 signalling and the resulting production of type I interferon, as well as the sustained activation by bystander T cells, fuel a positive feedforward loop in memory B cells that can evade negative selection and permit preferential expansion of anti-RNP autoantibodies. Clinical trials of autologous stem cell transplantation or of B cell-targeted monoclonal antibodies and chimeric antigen receptor (CAR) T cells have correlated replenishment of the memory B cell population with relapse of SLE. Moreover, the BCR hyporesponsiveness of memory B cells might explain the failure of non-depleting B cell-targeting approaches in SLE, including BTK inhibitors and anti-CD22 monoclonal antibodies. Thus, targeting of dysfunctional memory B cells might prove effective in SLE, while also avoiding the adverse events of broad-spectrum targeting of B celland plasma cell subsets that are not directly involved in disease pathogenesis.

Gut microbiota modulates depressive-like behaviors induced by chronic ethanol exposure through short-chain fatty acids

BackgroundChronic ethanol exposure (CEE) is recognized as an important risk factor for depression, and the gut-brain axis has emerged as a key mechanism underlying chronic ethanol exposure-induced anxiety and depression-like behaviors. Short-chain fatty acids (SCFAs), which are the key metabolites generated by gut microbiota from insoluble dietary fiber, exert protective roles on the central nervous system, including the reduction of neuroinflammation. However, the link between gut microbial disturbances caused by chronic ethanol exposure, production of SCFAs, and anxiety and depression-like behaviors remains unclear.MethodsInitially, a 90-day chronic ethanol exposure model was established, followed by fecal microbiota transplantation model, which was supplemented with SCFAs via gavage. Anxiety and depression-like behaviors were determined by open field test, forced swim test, and elevated plus-maze. Serum and intestinal SCFAs levels were quantified using GC-MS. Changes in related indicators, including the intestinal barrier, intestinal inflammation, neuroinflammation, neurotrophy, and nerve damage, were detected using Western blotting, immunofluorescence, and Nissl staining.ResultsChronic ethanol exposure disrupted with gut microbial homeostasis, reduced the production of SCFAs, and led to anxiety and depression-like behaviors. Recipient mice transplanted with fecal microbiota that had been affected by chronic ethanol exposure exhibited impaired intestinal structure and function, low levels of SCFAs, intestinal inflammation, activation of neuroinflammation, a compromised blood-brain barrier, neurotrophic defects, alterations in the GABA system, anxiety and depression-like behaviors. Notably, the negative effects observed in these recipient mice were significantly alleviated through the supplementation of SCFAs.ConclusionSCFAs not only mitigate damage to intestinal structure and function but also alleviate various lesions in the central nervous system, such as neuroinflammation, and reduce anxiety and depression-like behaviors, which were triggered by transplantation with fecal microbiota that had been affected by chronic ethanol exposure, adding more support that SCFAs serve as a bridge between the gut and the brain.

Establishment of a human 3D in vitro liver-bone model as a potential system for drug toxicity screening.

Drug toxicity is an important cause of chronic liver damage, which in the long term can lead to impaired bone homeostasis through an imbalance in the liver-bone axis. For instance, non-steroidal anti-inflammatory drugs (e.g., diclofenac), which are commonly used to control pain during orthopaedic interventions, are known to reduce bone quality and are the most prevalent causes of drug-induced liver damage. Therefore, we used human cell lines to produce a stable, reproducible, and reliable in vitro liver-bone co-culture model, which mimics the impaired bone homeostasis seen after diclofenac intake in vivo. To provide the best cell culture conditions for the two systems, we tested the effects of supplements contained in liver and bone cell culture medium on liver and bone cell lines, respectively. Additionally, different ratios of culture medium combinations on bone cell scaffolds and liver spheroids' viability and function were also analysed. Then, liver spheroids and bone scaffolds were daily exposed to 3-6µM diclofenac alone or in co-culture to compare and evaluate its effect on the liver and bone system. Our results demonstrated that a 50:50 liver:bone medium combination maintains the function of liver spheroids and bone scaffolds for up to 21days. Osteoclast-like cell activity was significantly upregulated after chronic exposure to diclofenac only in bone scaffolds co-cultured with liver spheroids. Consequently, the mineral content and stiffness of bone scaffolds treated with diclofenac in co-culture with liver spheroids were significantly reduced. Interestingly, our results show that the increase in osteoclastic activity in the system is not related to the main product of diclofenac metabolism. However, osteoclast activation correlated with the increase in oxidative stress and inflammation associated with chronic diclofenac exposure. In summary, we established a long-term stable liver-bone system that represents the interaction between the two organs, meanwhile, it is also an outstanding model for studying the toxicity of drugs on bone homeostasis.

Burnout: a comprehensive review

AbstractBurnout has been the focus of extensive scientific research. The World Health Organization officially recognized burnout as an occupational phenomenon, defined as a syndrome resulting from chronic workplace stress that remains unmanaged and characterized by three dimensions: exhaustion, cynicism, and inefficacy. Existing literature highlights limitations in current measurement instruments for diagnostic purposes. These tools often yield scores that overlap with other conditions such as fatigue, anxiety, and depression. Chronic exposure to high job demands and low job resources emerges as the primary trigger for burnout. While individual characteristics (such as neuroticism) may increase susceptibility, specific personality traits associated with higher risk remain unclear. Burnout has adverse effects on both individuals and organizations. Typical interventions focus on stress relief and coping strategies to manage high job demands, but their effectiveness diminishes over time. Evidence from organizational interventions suggests that improving employees’ working conditions can reduce burnout risk. Combined interventions offer promise by creating a healthy work environment while empowering employees to handle occasional stress. Social partners should advocate for support in researching burnout, aiming for a clear diagnosis, effective treatment, and preventive measures to mitigate psychosocial risks in the workplace.Practical Relevance: The findings of this article highlight the importance of addressing both job demands and job resources to mitigate burnout in organizational settings. Implementing interventions that improve working conditions and provide adequate support can significantly reduce burnout risk and enhance employee well-being. Organizations should prioritize creating a healthy work environment and empowering employees with the necessary resources to manage workload effectively.

Molecular Impact of Sublethal Spinetoram Exposure on Honeybee (Apis mellifera) Larval and Adult Transcriptomes

Pesticide toxicity is a global concern for honeybee populations, and understanding these effects at the molecular level is critical. This study analyzed the transcriptome of honeybees at larval and adult stages after chronic exposure to a sublethal dose (0.0017 µg a.i./larva) of spinetoram (SPI) during the larval phase. Four groups were used: acetone-treated honeybee larvae (ATL), acetone-treated honeybee adults (ATAs), SPI-treated honeybee larvae (STL), and SPI-treated honeybee adults (STAs). In total, 5719 differentially expressed genes (DEGs) were identified for ATL vs. ATAs, 5754 for STL vs. STAs, 273 for ATL vs. STL, and 203 for ATAs vs. STAs (FC ≤ 1.5, p &lt; 0.05). In response to SPI, 29 unique DEGs were identified in larvae and 42 in adults, with 23 overlapping between comparisons, suggesting genes linked to SPI toxicity. Gene ontology analysis showed that SPI affected metabolism-related genes in larvae and lipid-transport-associated genes in adults. KEGG pathway analysis revealed an enrichment of pathways predominantly associated with metabolism, hormone biosynthesis, and motor proteins in STL. The transcriptomic data were validated by qPCR. These findings demonstrated that SPI disrupts essential molecular processes, potentially harming honeybee development and behavior, underscoring the need for safer agricultural practices.

Changes in the content of dopamine, serotonin, their precurrents and derivatives in the prefrontal cortex of the brain of young male rats under chronic exposure to low-intense electromagnetic field

Changes in the content of dopamine, serotonin, their precurrents and derivatives in the prefrontal cortex of the brain of young male rats under chronic exposure to low-intense electromagnetic field

Chronic inhalation exposure to the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) alters cardiac collagen in Wistar rats.

2,4-dichlorophenoxyacetic acid (2,4-D) is one of the most used in the world and exposure to herbicides can affect animals and humans, causing toxic effects that include cardiotoxicity. This is the first study to evaluate cardiac remodeling after experimental simulation of environmental exposure by chronic inhalation (6months) to the herbicide 2,4-D. Thirty male Wistar rats were exposed to two different concentrations of the 2,4-D formulation (low - 187.17mg/m3; and high - 467.93mg/m3) and the control group exposed to nebulization of chloride solution 0.9% sodium. Inhalation exposure lasted 6months. Mice hearts were collected for histology. There was a difference between exposure concentrations in relation to the increase in cardiac collagen (P<0.0001). In mice exposed to a low dose of 2,4-D and a decrease in the fractal dimension of cardiac collagen in the high dose of 2, 4-D (P=0.010). This study shows that chronic inhalation exposure to 2,4-D induces cardiotoxicity in rats, characterized by extracellular matrix reorganization and changes in collagen levels, highlighting the impact of the exposure route on cardiac outcomes. There was no difference in relation to anatomical parameters, cardiomyocyte area, collagen types I and III and analysis of arteriole thickness. Chronic exposure at different doses to the 2,4D herbicide had the potential to cause damage to cardiac remodeling by altering cardiac collagen in rats.

The Efficacy of Nutritional Strategies and Ergogenic Aids on Acute Responses and Chronic Adaptations to Exertional-Heat Exposure: A Narrative Review

Global warming is attributed to an increased frequency of high ambient temperatures and humidity, elevating the prevalence of high-temperature-related illness and death. Evidence over recent decades highlights that tailored nutritional strategies are essential to improve performance and optimise health during acute and chronic exertional-heat exposure. Therefore, the purpose of this review is to discuss the efficacy of various nutritional strategies and ergogenic aids on responses during and following acute and chronic exertional-heat exposure. An outline is provided surrounding the application of various nutritional practices (e.g., carbohydrate loading, fluid replacement strategies) and ergogenic aids (e.g., caffeine, creatine, nitrate, tyrosine) to improve physiological, cognitive, and recovery responses to acute exertional-heat exposure. Additionally, this review will evaluate if the magnitude and time course of chronic heat adaptations can be modified with tailored supplementation practices. This review highlights that there is robust evidence for the use of certain ergogenic aids and nutritional strategies to improve performance and health outcomes during exertional-heat exposure. However, equivocal findings across studies appear dependent on factors such as exercise testing modality, duration, and intensity; outcome measures in relation to the ergogenic aid’s proposed mechanism of action; and sex-specific responses. Collectively, this review provides evidence-based recommendations and highlights areas for future research that have the potential to assist with prescribing specific nutritional strategies and ergogenic aids in populations frequently exercising in the heat. Future research is required to establish dose-, sex-, and exercise-modality-specific responses to various nutritional practices and ergogenic aid use for acute and chronic exertional-heat exposure.

Stress and Pregnancy Outcomes: A Review of the Literature.

The human body has the ability to adapt to changing circumstances, and mobilizes various biological systems in order to do so. When exposed to stressful conditions, the endocrine, nervous, and immune systems come together to aid in maintaining homeostasis; however, during periods of chronic stress, these systems can become maladaptive and lead to long-term detrimental health outcomes. Amongst the lingering effects associated with chronic stress exposure, increasingly, studies are identifying a link to adverse pregnancy and neonatal outcomes. This review explores what has been uncovered in the field to date, and examines the effects of stress on fertility and gestation. Establishing additional factors which put women at risk for adverse pregnancy outcomes can aid in identifying a vulnerable population who could benefit from early stress-reducing interventions.

Application of Integrated Optical Density in Evaluating Insulin Expression in the Endocrine Pancreas During Chronic Ethanol Exposure and β-Carotene Supplementation: A Novel Approach Utilizing Artificial Intelligence

Background: β-carotene is an essential antioxidant, providing protection against type 2 diabetes mellitus, cardiovascular illnesses, obesity, and metabolic syndrome. This study investigates the impact of β-carotene on biochemical parameters and pancreatic insulin expression in mice exposed to ethanol. Methods: Thirty-six C57BL/6 mice (Mus musculus) were divided into six groups: 1. C (control), 2. LA (3% alcohol dose), 3. MA (7% alcohol dose), 4. B (0.52 mg/kg body weight/day β-carotene), 5. LA+B (3% alcohol dose + 0.52 mg/kg body weight/day β-carotene), and 6. MA+B (7% alcohol dose plus 0.52 mg/kg body weight/day β-carotene). After 28 days, the animals were euthanized for serum and pancreatic tissue collection. Biochemical analysis and pancreatic insulin expression were performed. One-way ANOVA was used. Results: The B, LA+B, and MA+B groups improved insulin levels and decreased HOMA-β versus the C group, with the LA+B and MA+B groups also showing lower ADH and ALDH levels than their nonsupplemented counterparts (p &lt; 0.05). The B, LA+B, and MA+B groups showed a greater β-cell mass area compared to the unsupplemented groups. Additionally, the LA+B and MA+B groups demonstrated significantly increased β-cell area and integrated optical density compared to the LA and MA groups, respectively (p &lt; 0.001). Conclusions: In mice, β-cell loss led to increased glucose release due to decreased insulin levels. β-carotene appeared to mitigate ethanol’s impact on these cells, resulting in reduced insulin degradation when integrated optical density was used. These findings suggest that antioxidant supplementation may be beneficial in treating ethanol-induced type 2 diabetes in animal models.

Volatile Organic Compound (VOC) Contamination in Hotel Rooms: A Pilot Study to Understand Sources and Health Risks

The COVID-19 pandemic drove the use of cleaning products, causing organic solvent contamination in hospitality environments. This pilot study investigated the presence and concentrations of volatile organic compounds (VOCs) in selected hotels in four different US cities with varying star ratings at the end of the pandemic period. Targeting 139 VOCs, 57 were detected across eight groups: alcohols, halocarbons, aromatics, alkanes, terpenes, carbonyls, ethers, and esters, in the indoor air. Alcohols were the most prevalent, especially in lower-rated hotels, suggesting higher use of cleaning supplies. Elevated levels of aromatics were detected in hotels rated under three stars, with a notable disparity compared to higher-rated hotels. Additionally, alkanes and terpenes such as n-tetradecane and d-limonene were consistently detected. Health risk assessment showed concentrations of all VOCs remained below their health criteria for customers. The cumulative cancer risk was 2.25 × 10−6 for hotel workers from chronic occupational exposure to eight carcinogenic VOCs, representing 1/3 of the lifetime risk from these chemicals in the ambient air. Cancer risks from individual VOCs ranged from 0.001 × 10−6 to 1.07 × 10−6, with chloroform accounting for nearly half of the cumulative risk. The findings underscore the need for careful selection and use of furnishings and cleaning supplies and for effective indoor air pollution control and management in hotel indoor environments.

Toxicity of Low-Level Multiple-Mycotoxin Mixture in Nile Tilapia (Oreochromis niloticus) Is Prevented with Organically Modified Clinoptilolite Feed Additive

Organically modified clinoptilolite (member of the zeolite family of minerals; MinazelPlus®) feed additive, with an average weight of 30 ± 2 g, was used to prevent mycotoxicosis in Nile tilapia (Oreochromis niloticus) through its supplementation for 42 days to the diet contaminated with multiple mycotoxins: aflatoxin B1 (40 µg/kg), fumonisin B1 and B2 (600 µg/kg), zearalenone (50 µg/kg), and deoxynivalenol (150 µg/kg). The fish were divided randomly into four experimental groups (basal diet control—C; fed 2 g/kg MinazelPlus®—MZ; fed multiple mycotoxins—MT; and fed a combination of MinazelPlus® and multiple mycotoxins—MZ + MT). Each group consisted of triplicate aquarium setups, with six fish in each replicate. Sampling was performed in weeks 2, 4, and 6. The lymphocyte count was significantly higher in the MZ group compared with the MT group and the MT + MZ group in week 6. An overall decrease in the neutrophil count was observed in the experimental groups. Histopathological analysis was performed in weeks 2 and 6, revealing significant changes in the liver, intestines, kidney, and spleen of fish from the MT group, while the MT + MZ and MZ groups were similar to the control. The addition of 2 g/kg MinazelPlus® has the ability to prevent and reduce the adverse effects of chronic exposure to low concentrations of multiple mycotoxins in juvenile Nile tilapia.