Effects Of Exposure Research Articles

Associations between co-exposure to per- and polyfluoroalkyl substances and metabolic diseases: The mediating roles of inflammation and oxidative stress

BackgroundPer- and polyfluoroalkyl substances (PFAS) pose potential risks to human health. In real-world settings, humans are exposed to various PFAS through numerous pathways. ObjectivesThis study evaluated the associations between co-exposure to PFAS and obesity and its comorbidities, along with the mediating roles of inflammation and oxidative stress. MethodsWe analyzed 11,090 participants from National Health and Nutrition Examination Survey (NHANES), 2003–2018. Linear regression, logistic regression, and generalized additive models were used to assess the individual effects of PFAS exposure on obesity and its comorbidities. The environmental risk score (ERS) was calculated using the adaptive elastic-net model to assess the co-exposure effects. Linear and logistic regression models explored the associations between ERS, obesity, and comorbidities. Mediation analyses explored the roles of inflammatory (neutrophils, lymphocytes, and alkaline phosphatase) and oxidative stress (gamma-glutamyl transferase, total bilirubin, and uric acid) markers in the associations between ERS and obesity and its comorbidities. ResultsFor each unit increase in ERS, the odds of obesity and type 2 diabetes mellitus (T2DM) increased 3.60-fold (95 % CI: 2.03, 6.38) and 1.91-fold (95 % CI: 1.28, 2.86), respectively. For each unit increase in ERS, BMI increased by 2.36 (95 % CI: 1.24, 3.48) kg/m2, waist circumference increased by 6.47 (95 % CI: 3.56, 9.37) cm, and waist-to-height ratio increased by 0.04 (95 % CI: 0.02, 0.06). Lymphocytes, alkaline phosphatase, and total bilirubin were significantly associated with both ERS and obesity, with mediation proportions of 4.17 %, 3.62 %, and 7.37 %, respectively. Lymphocytes, alkaline phosphatase, total bilirubin, and uric acid were significantly associated with both ERS and T2DM, with the mediation proportions of 8.90 %, 8.74 %, 29.73 %, and 38.19 %, respectively. ConclusionsCo-exposure to PFAS was associated with obesity and T2DM, and these associations may be mediated by inflammation and oxidative stress. Further mechanistic and prospective studies are required to verify these associations.

Long-term effects of an early-life exposure of fathead minnows to sediments containing bitumen. Part II: Behaviour, reproduction, and gonad histopathology

The oil sands area of northern Alberta has river sediments that contain natural bitumen. Eggs and fish in these rivers may be exposed to bitumen-related chemicals early in life. This paper assesses a short embryo-larval fish exposure to oil sands sediment and follows the fish behaviour as they mature in clean water and examines their breeding success as adults (5 months afterwards). The three different oil sands river sediments tested were: a sediment collected outside of the bitumen deposit (tested at 3 g/L, Reference sediment from upstream Steepbank River site), and two sediments collected within the deposit (each tested at low (1 g/L) and high (3 g/L) concentrations). The sediments within the bitumen deposit were from the Ells and Steepbank (Stp) Rivers, and both contained significant total PAHs (>170 ng/g wet weight sediment) and alkylated PAHs (>4480 ng/g). Fish were exposed to these sediments for 21 days (as eggs and larval fish), and then transferred permanently to clean water to mature and breed. There was a significant decrease in the number of egg clutches produced by fish exposed early in life to Stp downstream high sediment (compared to Reference sediment). There was also a decrease in overall cumulative egg production, with fish from Stp downstream high sediment producing just over 1000 eggs in total while fish exposed to Ref sediment produced nearly 6900 eggs. The fish with reduced egg production were also less social than expected as they matured, and they had a lower % of early vitellogenic eggs in their ovaries. Overall, the exposure shows that a single, brief exposure during early life stages to natural bitumen can affect fish in adulthood. Naturally occurring bitumen-derived PAHs can reduce fish reproductive output by complex mechanisms, measurable as lower ovary maturity and changes in social behaviour.

Higher maternal bread and thiamine intakes are associated with increased infant allergic disease.

A mother's diet during pregnancy may influence her infant's immune development. However, as potential interactions between components of our dietary intakes can make any nutritional analysis complex, here we took a multi-component dietary analysis approach. Nutritional intake data was collected from 639 pregnant women using a validated semi-quantitative food frequency questionnaire to reflect their dietary intakes during 32-36 weeks of gestation. To investigate their dietary intake pattern, we calculated Dietary Inflammatory Index scores. Maternal consumption of 12 food groups, 20 individual whole foods, and 18 specific nutrient intakes, along with any vitamin and mineral supplementation, were determined. Infant outcomes included eczema, allergen sensitization, and IgE-mediated food allergy. Regression-based analyses with covariates adjustment were applied. Women with higher white bread consumption were more likely to have an infant with doctor-diagnosed eczema (adjusted relative risk [aRR] 1.16; 95% CI 1.08, 1.24; p < .001) and IgE-mediated food allergy (aRR 1.14; 95% CI 1.02, 1.28; p = .02). Higher maternal intakes of fiber-rich bread (aRR 1.14; 95% CI 1.04, 1.25; p = .01) and legumes (aRR 1.11; 95% CI 1.02, 1.21; p = .02) were also associated with infant doctor-diagnosed eczema. Higher maternal thiamine intakes were associated with increased parent-reported infant eczema (aRR 1.08; 95% CI 1.03, 1.12; p < .001). In Australia, where bread flour is fortified with thiamine, we identified consistent links between higher maternal thiamine-rich diets and increased risk of infant eczema and food allergy. Our results highlight a need for further investigation of potential effects of high thiamine exposures on immune development, especially in-utero.

The long-term effects of norgestrel on the reproductive and thyroid systems in adult zebrafish at environmentally relevant concentrations

Progestins are crucial steroid hormones that have attracted wide attention due to their endocrine disrupting effects in fish. The aim of this study is to investigate the effects of long-term exposure to low concentrations of norgestrel (NGT) on the reproductive and thyroid endocrine systems of adult zebrafish. Adult zebrafish were exposed to 7 and 39 ng/L NGT for a duration of 90 days. The results revealed that exposure to 39 ng/L NGT led to a significant up-regulation of 3β-hydroxysteroid dehydrogenase (hsd3b) and 20β-hydroxysteroid dehydrogenase (hsd20b) genes in the ovary of female zebrafish. Additionally, there was a significant up-regulation of 11β-hydroxysteroid dehydrogenase 2 (hsd11b2) gene in the testis of male zebrafish. Furthermore, egg production decreased significantly, accompanied by notable alterations in the proportion of ovarian development stages, as well as reductions of sex hormone levels (E2, 11-KT, and T) in both females and males. However, long-term exposure to low concentrations of NGT did not lead to changes in thyroid hormone levels and thyroid histopathology in adult zebrafish. The overall results imply that environmental concentrations of NGT have a strong endocrine disrupting effect on the reproductive system of zebrafish, while the thyroid system is not sensitive to NGT exposure. The present study underscores the reproductive endocrine impacts of NGT and emphasizes the necessity for prolonged exposure at environmental concentrations.

Sex Differences in Impacts of Early Gestational and Peri-Adolescent Ozone Exposure on Lung Development in Rats: Implications for Later Life Disease in Humans

Air pollution exposure during pregnancy may affect fetal growth. Fetal growth restriction (FGR) is associated with reduced lung function in children that can persist into adulthood. Using an established model of asymmetrical FGR in Long-Evans rats, this study investigated sex differences in effects of early life ozone exposure on lung development and maturation. Adverse health effects for i) gestational exposure (with impacts on primary alveolarization), ii) peri-adolescent exposure (with impacts on secondary alveolarization), and iii) cumulative exposure across both periods were evaluated. Notably, female offspring were most affected by gestational ozone exposure, likely because of impaired angiogenesis and corresponding decreases in primary alveolarization. Females had diminished lung capacity, fewer mature alveoli, and medial hypertrophy of small and large pulmonary arteries. Males, especially FGR-prone offspring, were more affected by peri-adolescent ozone exposure. Males had increased ductal areas, likely due to disrupted secondary alveolarization. Altered lung development may increase risk of developing diseases, such as pulmonary arterial hypertension or chronic obstructive pulmonary disease. Pulmonary arterial hypertension disproportionately affects women. In the United States, chronic obstructive pulmonary disease prevalence is increasing, especially in women; and prevalence for both men and women is highest in urbanized areas. This investigation underlines the importance of evaluating results separately by sex, and provides biologic plausibility for later consequences of early-life exposure to ozone, a ubiquitous urban air pollutant.

Chronic UVB exposure induces hepatic injury in mice: Mechanistic insights from integrated multi-omics

Chronic UVB exposure poses a significant threat to both skin and visceral health. In recent years, the adverse role of chronic UVB exposure in liver health has been suggested but not fully elucidated. This study aims to comprehensively investigate the effects of chronic UVB exposure on liver health in male SKH-1 hairless mice and clarify potential mechanisms through multi-omics approaches. The findings suggested that 10-week chronic skin exposure to UVB not only triggers hepatic inflammation and oxidative stress but also, more importantly, results in lipid metabolism abnormalities in the liver. Hepatic transcriptomic analysis revealed significant alterations in various signaling pathways and physiological processes associated with inflammation, oxidative stress, and lipid metabolism. Further lipidomic analysis illustrated significant changes in the metabolism of glycerolipids, sphingolipids, and glycerophospholipids in the liver following chronic UVB exposure. The 16S rRNA sequencing analysis indicated that chronic UVB exposure disrupts the structure and function of the microbiota. In search of potential mechanisms used by the microbiome to regulate the hepatic disease morphology, we filtered mouse fecal supernatants and cultured the supernatants with HepG2 cells. Fecal supernatant from UVB-exposed mice induced increased secretion of the inflammatory cytokine IL-8, accumulation of MDA, reduced SOD activity, and decreased lipid content in normal hepatic cells. In summary, skin chronic exposure to UVB induces multiple liver injuries and gut microbiota dysbiosis in mice and gut microbiota metabolites may be one of the contributing factors to hepatic injury caused by chronic UVB exposure. These discoveries deepen the comprehension of the health risks associated with chronic UVB exposure.

NMR-based metabolomics analysis reveals the effect of environmental contamination exposure on fishermen living around the Mundaú lagoon in Maceió (Alagoas, Brazil)

The Mundaú lagoon in Maceió (Alagoas, Brazil) is a crucial resource for the local population, particularly fishing communities. Recent studies have revealed potential toxic metal contamination in the lagoon, particularly with mercury (Hg) levels exceeding the maximum regulated values. This inorganic contaminant may be impacting the health of fishermen and the local population. In this context, metabolomics, a study of small-molecule metabolites, can offer insights into the physiological impact of environmental contamination on humans. Thus, volunteers from the control and exposed groups were selected, considering the main exposure criteria primarily defined by their proximity and interaction with the lagoon. Blood and urine samples were collected from the volunteers and subjected to analysis using NMR spectroscopy. The data underwent Principal Component Analysis (PCA) and Orthogonal Partial Least-Squares Discriminant Analysis (OPLS-DA) based on metabolic patterns to establish group discrimination or identification. Metabolic pathways were assessed through enrichment analysis. The study revealed several metabolic disturbances in the exposed group's urine and plasma samples compared to control group. Noteworthy findings included arginine and proline metabolism disruptions, indicative of ammonia recycling and urea cycle impairment. These changes suggest compromised ammonia detoxification in the exposed group. Disturbances in the tricarboxylic acid (TCA) cycle and the transfer of acetyl groups into mitochondria suggested systemic metabolic stress in energy metabolism. Furthermore, elevated carnitine and ketone levels may indicate compensatory responses to low TCA cycle activity. Alterations in glutamate and glutathione metabolism and imbalances in glutathione levels indicate oxidative stress and impaired detoxification. This study highlights significant metabolic changes in fishermen exposed to contaminated environments, which can affect various metabolic pathways, including energy metabolism and antioxidant processes, potentially making individuals more vulnerable to the adverse effects of environmental contaminants. Finally, this work highlights insights into the relationship between environmental contamination and metabolic pathways, particularly in regions with limited studies.

Genetic Patterning in Hippocampus of Rat Undergoing Impaired Spatial Memory Induced by Long-term Heat Stress

The organism's normal physiological function is greatly impacted in a febrile environment, leading to the manifestation of pathological conditions including elevated body temperature, dehydration, gastric bleeding, and spermatogenic dysfunction. Numerous lines of evidence indicate that heat stress significantly impacts the brain's structure and function. Previous studies have demonstrated that both animals and humans experience cognitive impairment as a result of exposure to high temperatures. However, there is a lack of research on the effects of prolonged exposure to high-temperature environments on learning and memory function, as well as the underlying molecular regulatory mechanisms. In this study, we examined the impact of long-term heat stress exposure on spatial memory function in rats and conducted transcriptome sequencing analysis of rat hippocampal tissues to identify the crucial molecular targets affected by prolonged heat stress exposure. It was found that the long-term heat stress impaired rats’ spatial memory function due to the pathological damages and apoptosis of hippocampal neurons at the CA3 region, which is accompanied with the decrease of growth hormone level in peripheral blood. RNA sequencing analysis revealed the signaling pathways related to positive regulation of external stimulation response and innate immune response were dramatically affected by heat stress. Among the verified differentially expressed genes, the knockdown of Arhgap36 in neuronal cell line HT22 significantly enhances the cell apoptosis, suggesting the impaired spatial memory induced by long-term heat stress may at least partially be mediated by the dysregulation of Arhgap36 in hippocampal neurons. The uncovered relationship between molecular changes in the hippocampus and behavioral alterations induced by long-term heat stress may offer valuable insights for the development of therapeutic targets and protective drugs to enhance memory function in heat-exposed individuals.

Tobacco use, secondhand exposure and knowledge of secondhand and third-hand smoke among medical college students in Western Nepal: a cross-sectional study

ObjectivesThis study was conducted to assess the prevalence of tobacco use, secondhand smoke (SHS) exposure and knowledge about SHS and third-hand smoke (THS) exposure among students in a medical college...

Evaluating the Effects of Perinatal Exposures to BPSIP on Hepatic Cholesterol Metabolism in Female and Male Offspring ICR Mice

Evaluating the Effects of Perinatal Exposures to BPSIP on Hepatic Cholesterol Metabolism in Female and Male Offspring ICR Mice

Gender Differences in the Effects of Cadmium Exposure on Hematological Parameters in Wistar Rats

This study aims to investigate the gender dimorphism in cadmium exposure on hematological parameters in male and female Wistar rats. Twenty Wistar rats (120g-150g) were divided into four groups: male control, male cadmium-treated, female control, and female cadmium-treated. Cadmium chloride (50 mg/kg) was administered orally to the experimental groups for 45 days. Hematological parameters were analyzed using an auto hematological analyzer. Data were statistically evaluated using two-way ANOVA with significance set at p &lt; 0.05. Cadmium exposure significantly increased white blood cell (WBC) counts in male rats compared to controls, with notable decrease in neutrophils and an increase in lymphocytes. Female rats showed significant increase in monocyte and basophil levels. Furthermore, red blood cell (RBC) parameters showed significant reductions in hemoglobin concentration, mean corpuscular volume (MCV), and mean corpuscular hemoglobin (MCH) in female cadmium-treated rats. No significant effects were observed on platelet count or distribution width in both male and female rats. The study concluded there are gender-specific hematological alterations due to cadmium exposure in Wistar rats. These findings underscore the need for gender-specific approach in the understanding and amelioration of cadmium toxicity.

Influence of Combat Experience on Psychophysiological and Fine Motor Skill Responses in Air Force Warfighters under Acute Stress

This study investigates the influence of experience on stress responses and fine motor skills among professional male military parachutists. We analyzed 132 paratroopers, divided into a non-experienced group (NEG; ≤6 parachute jumps) and an experienced group (EG; &gt;50 jumps). Baseline samples were collected 2.5 hours before participants performed a 500 m jump, with post-jump evaluations conducted immediately after landing. Results indicated that experience significantly influences fine motor skills and stress responses. Non-experienced jumpers showed greater degradation in fine motor skills and higher cortical arousal pre-jump levels, suggesting an increased anticipatory state. In contrast, experienced parachutists maintained more consistent fine motor skills and exhibited a ceiling effect in stress response. Leg strength was higher in non-experienced jumpers, reflecting youth and greater muscle mass, with no significant difference in hand strength. These findings highlight the role of experience in managing stress and maintaining motor skills under pressure. The study suggests further exploration into psychological aspects like motivation and resilience, along with the long-term effects of stress exposure. The importance of experience in high-stress military operations emphasizes the need for targeted training interventions to enhance stress-coping mechanisms in less experienced individuals.

Exposure to volatile organic compounds and growth indicators in adolescents: Unveiling the association and potential intervention strategies

Environmental pollutant is considered to be one of the important factors affecting adolescent growth. However, the effects of volatile organic compounds (VOCs) exposure on adolescent growth have not been assessed. Data from the National Health and Nutrition Examination Survey (NHANES) 2011-2018 was used to examine the associations between VOCs exposure and adolescent growth indicators through three statistical models. The mediating effect of bone mineral density (BMD) on these associations was examined. The potential pathways and key targets were identified by the network pharmacology analysis methods. This study included 746 adolescents. Three statistical methods consistently showed a negative correlation between VOCs exposure and adolescents growth indicators. Furthermore, BMD mediated the relationship between VOCs exposure and adolescent growth indicators, with mediated proportion ranging from 4.3% to 53.4%. Network pharmacology analysis found a significant enrichment in IL-17 signaling pathway. Moreover, the adverse effects of VOCs exposure on adolescent growth were observed to significantly attenuate in adolescents with high serum vitamin D levels. Our results suggested that VOCs exposure was an adverse factor affecting adolescent growth, with BMD playing a significant regulatory role, and IL-17 signaling pathway was the underlying mechanism. Vitamin D supplementation may be a viable strategy to prevent VOCs exposure from affecting adolescent growth. Environmental implicationVolatile organic compounds (VOCs), a group of pollutants pervasive in daily life, are absorbed by the human body in various ways, resulting in the occurrence of various diseases. The results of this study suggested that VOCs exposure may affect adolescent growth, with bone mineral density playing an important mediating role, and IL-17 signaling pathway was the potential mechanism. Vitamin D may be a potential intervention strategy to prevent the adverse effects of VOCs on adolescent growth. Our results not only revealed the potential relationship and mechanism between VOCs exposure and adolescent growth, but also provided a potential intervention strategy.

Intergenerational metabolism-disrupting effects of maternal exposure to plasticizer acetyl tributyl citrate (ATBC)

Environmental chemicals and pollutants are increasingly recognized for their potential transgenerational effects. Acetyl tributyl citrate (ATBC), a widely used plasticizer substituting di-(2-ethylhexyl) phthalate (DEHP), was identified as an inducer of lipogenesis in male mice by our previous research. This study aimed to investigate the impact of ATBC exposure on the metabolic homeostasis of female mice and simultaneously evaluate its intergenerational effects.Female C57BL/6J mice were orally exposed to ATBC (0.01 or 1 μg/kg/day) for 10 weeks before mating with unexposed male mice. The resulting F1 female mice were bred with unexposed males to generate F2 offspring. Our results indicated that 10-week ATBC exposure disrupted glucose metabolism homeostasis and the reproductive system in F0 female mice. In F1 female mice, elevated liver lipid levels and mild insulin resistance were observed. In the F2 generation, maternal ATBC exposure resulted in increased weight gain, elevated liver triglycerides, and higher fasting blood glucose levels, primarily in F2 male mice. These findings suggest that maternal ATBC exposure may exert intergenerational disturbing effects on glucose metabolism across generations of mice. Further investigation is needed to evaluate the health risks associated with ATBC exposure.

Benzo(a)pyrene exposure during pregnancy leads to germ cell apoptosis in male mice offspring via affecting histone modifications and oxidative stress levels

Infertility has gradually become a global health concern, and evidence suggests that exposure to environmental endocrine-disrupting chemicals (EDCs) represent one of the key causes of infertility. Benzo(a)pyrene (BaP) is a typical EDC that is widespread in the environment. Previous studies have detected BaP in human urine, semen, cervical mucus, oocytes and follicular fluid, resulting in reduced fertility and irreversible reproductive damage. However, the mechanisms underlying the effects of gestational BaP exposure on offspring fertility in male mice have not been fully explored. In this study, pregnant mice were administered BaP at doses of 0, 5, 10 and 20 mg/kg/day via gavage from Days 7.5 to 12.5 of gestation. The results revealed that BaP exposure during pregnancy disrupted the structural integrity of testicular tissue, causing a disorganized arrangement of spermatogenic cells, compromised sperm quality, elevated levels of histone modifications and increased apoptosis in the testicular tissue of F1 male mice. Furthermore, oxidative stress was also increased in the testicular tissue of F1 male mice. BaP activates the AhR/ERα signaling pathway, affects H3K4me3 expression and induces apoptosis in testicular tissue. AhR and Cyp1a1 are overexpressed, and the expression of key molecules in the antioxidant pathway, including Keap1 and Nrf2, is reduced. The combined effects of these molecules lead to apoptosis in testicular tissues, damaging and compromising sperm quality. This impairment in testicular cells further contributes to compromised testicular tissues, ultimately impacting the reproductive health of F1 male mice.

Evaluating Physiological Responses of Microalgae towards Environmentally Coexisting Microplastics: A Meta-Analysis

Microplastics (MPs) are abundantly present in aquatic environments, where the phytoplankton—microalgae, are now inevitably bound to a long-term coexistence with them. While numerous studies have focused on the toxicological effects of high-concentration MPs exposure, there remains controversy over whether and how MPs affect microalgae at environmentally relevant concentrations. This study aims to draw conclusions that narrow the gap from 52 studies with varying results. Overall, MPs can inhibit growth and photosynthesis, induce oxidative damage, from which microalgae can recover after an appropriate period. Cyanobacteria exhibit greater vulnerability than chlorophyta. The relative size of MPs to algal cells potentially governs their coexistence behavior, thereby altering the mechanisms of impact. Pristine MPs may increase the production of extracellular polymeric substances (EPS) and microcystins (MCs), while aged MPs have the opposite effect. Additionally, relevant factors are systematically discussed, offering insights for future research.

Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.

Microplastics (MPs) have become a global environmental problem, emerging as contaminants with potentially alarming consequences. However, long-term exposure to polystyrene microspheres (PS-MS) and its effects on diet-induced obesity are not yet fully understood. We aimed to investigate the effect of PS-MS exposure on high-fat diet (HFD)-induced obesity and underlying mechanisms. In the present study, C57BL/6J mice were fed a normal diet (ND) or a HFD in the absence or presence of PS-MS via oral administration for 8 wk. Antibiotic depletion of the microbiota and fecal microbiota transplantation (FMT) were performed to assess the influence of PS-MS on intestinal microbial ecology. We performed 16S rRNA sequencing to dissect microbial discrepancies and investigated the dysbiosis-associated intestinal integrity and inflammation in serum. Compared with HFD mice, mice fed the HFD with PS-MS exhibited higher body weight, liver weight, metabolic dysfunction-associated steatotic liver disease (MASLD) activity scores, and mass of white adipose tissue, as well as higher blood glucose and serum lipid concentrations. Furthermore, 16S rRNA sequencing of the fecal microbiota revealed that mice fed the HFD with PS-MS had greater -diversity and greater relative abundances of Lachnospiraceae, Oscillospiraceae, Bacteroidaceae, Akkermansiaceae, Marinifilaceae, Deferribacteres, and Desulfovibrio, but lower relative abundances of Atopobiaceae, Bifidobacterium, and Parabacteroides. Mice fed the HFD with PS-MS exhibited lower expression of MUC2 mucin and higher levels of lipopolysaccharide and inflammatory cytokines [tumor necrosis factor- (TNF-), interleukin-6 (IL-6), IL-1, and IL-17A] in serum. Correlation analyses revealed that differences in the microbial flora of mice exposed to PS-MS were associated with obesity. Interestingly, microbiota-depleted mice did not show the same PS-MS-associated differences in Muc2 and Tjp1 expression in the distal colon, expression of inflammatory cytokines in serum, or obesity outcomes between HFD and HFD + PS-MS. Importantly, transplantation of feces from HFD + PS-MS mice to microbiota-depleted HFD-fed mice resulted in a lower expression of mucus proteins, higher expression of inflammatory cytokines, and obesity outcomes, similar to the findings in HFD + PS-MS mice. Our findings provide a new gut microbiota-driven mechanism for PS-MS-induced obesity in HFD-fed mice, suggesting the need to reevaluate the adverse health effects of MPs commonly found in daily life, particularly in susceptible populations. https://doi.org/10.1289/EHP13913.

P21-35 Cardiorespiratory effects of indoor ozone exposure during sleep and the influencing factors: a prospective study among adults in China

P21-35 Cardiorespiratory effects of indoor ozone exposure during sleep and the influencing factors: a prospective study among adults in China

The effect of larval exposure to acids and detergents on the life history of the major malaria vector Anopheles arabiensis Patton (Diptera: Culicidae).

Anopheles arabiensis, a highly adaptable member of the Anopheles gambiae complex, poses a challenge for control efforts due to its outdoor biting and resting behaviour. Consequently, indoor insecticide-based control methodsare ineffective against An. arabiensis. Furthermore, An. arabiensis are adapting to breeding in polluted waters, and may be contributing to residual malaria and malaria in urban areas. There have been some advances in understanding the effect of rural pollutants on Anopheles mosquitoes, but the effect of urban pollutants is poorly understood. Thus, in this study, the effect of acidic pollutants [nitric acid (HNO3) and hydrochloric acid (HCl)] and alkaline pollutants (phosphate-free and phosphate-containing detergent) on two laboratory-reared An. arabiensis strains - an insecticide susceptible strain (SENN) and an insecticide-resistant strain selected from SENN (SENN-DDT) - were determined. The median lethal concentration (LC50) and larval exposure on larval development, adult longevity and insecticide tolerance were evaluated. Nitric acid and phosphate-containing detergent were found to be more toxic than HCl and phosphate-free detergent in terms of LC50 values. Detergent exposure (both phosphate-containing and phosphate-free) increased adult longevity of both strains. Nitric acid reduced larval development time in both SENN and SENN-DDT, whereas HCl reduced larval development time in SENN only. By contrast, both phosphate-containing and phosphate-free detergents increased larval development time of both strains. Furthermore, HNO3 and phosphate-containing detergent increased insecticide tolerance the most. The two An. arabiensis strains responded to urban pollutants differently. Thus, this study provides insight into the adaptation of An. arabiensis to acidic and alkaline urban pollutants. © 2024 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Significant Metabolic Alterations in Mouse Dams Exposed to an Environmental Mixture of Polychlorinated Biphenyls (PCBs) During Gestation and Lactation: Insights into PCB and Metabolite Profiles

Polychlorinated biphenyls (PCBs) and metabolites are linked to developmental neurotoxicity, but their levels in the gestational and lactational environment remain unexplored. This study investigated the effects of dietary exposure to the Fox River Mixture (FRM) on serum levels of PCBs and their metabolites in female C57BL/6J mice. Mice were exposed to 0.1, 1.0, or 6.0mg/kg body weight/day of FRM beginning two weeks before mating and throughout gestation and lactation. Serum samples collected from the dams at weaning were analyzed using gas chromatograph-mass spectrometry and nontarget liquid chromatography-high resolution mass spectrometry. Results showed complex and dose-dependent differences in PCB and metabolite profiles. Untargeted metabolomics revealed alterations in metabolites involved in glucuronidation. Network analysis suggested disturbances in heme and amino acid metabolism associated with higher chlorinated PCBs. These findings suggested that PCBs and metabolites present in the gestational and lactation environment of mice may contribute to developmental neurotoxicity in rodents.