Per- and polyfluoroalkyl substances (PFASs) are persistent environmental pollutants linked to adverse health outcomes, notably kidney disease. This study examines the effects of hemodialysis and dialysis membrane characteristics on the clearance of eight specific PFASs in patients undergoing hemodialysis. A cohort of 301 chronic hemodialysis patients, each treated for a minimum of 90 days, was analyzed. Automated column-switching ultra-performance liquid chromatography-tandem mass spectrometry was utilized to detect the PFASs, and multivariable linear regression models assessed the association between PFAS levels and clinical nutritional biochemistry markers. Results revealed significantly lower PFAS concentrations in the FILTRYZER dialyzer membrane compared to Polyamix, with no notable differences across varying membrane surface areas. Moreover, significant correlations were observed between nutritional markers-such as albumin, uric acid, and the normalized protein catabolic rate-and the levels of perfluoroheptanoic acid (PFHpA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroundecanoic acid (PFUnDA). The findings indicate that PFAS levels in hemodialysis patients are influenced by the membrane composition and properties but are unaffected by the surface area of the membranes.

Ultramafic outcrop settings are characterized by long-term heavy metal (HM) stress and nutrient imbalances, making plant resilience highly challenging. This study investigated that how native plant types in the serpentine environment influence the variation of synergistic interactions between rhizosphere arbuscular mycorrhizal fungi (AMF) and mycorrhizal helper bacteria (MHB) communities under HM stress and nutrient-deficient conditions, which support native plant endemism and their HM accumulation potential. The results displayed significant enrichment of key MHB (Rhizobium_tropici, Bacillus_subtilis, Pseudomonas_parafulva, Pseudomonas_akapagensis) and AMF species (Glomus_constrictum, Glomus_aggregatum, Rhizophagus_intraradices, Rhizophagus_irregularis) in rhizosphere soils (q < 0.05). Pseudomonas_chlororaphis and Burkholderia_cepacia were strongly associated with Rhizophagus_irregularis and Glomus_mosseae in Panicum maximum Jacq (PMJ) and Bidens pilosa (BP) under chromium (Cr), and cadmium (Cd) and arsenic (As) stress. Pseudomonas_fluorescens and Bacillus_pabuli were linked to Geosiphon_pyriformis and Glomus_aggregatum in Pueraria montana (PM) under nickel (Ni), lead (Pb), and cobalt (Co) stress, while Arthrobacter_globiformis and Rhizobium_leguminosarum were associated with Glomus_intraradices under copper (Cu) stress in Leucaena leucocephala (LL). Pathways related to nitrogen, phosphorous and potassium (NPK) cycling, HM detoxification, and resistance were enriched, with AMF predominantly symbiotrophic root-endophytic, except for one as lichenized nostoc endosymbiont. Canonical correspondence analysis (CCA) showed HM stress and nutrients influence MHB-AMF symbiosis, while pH moisture content (MC) and electric conductivity (EC) significantly regulate their distribution. Rhizobium_leguminosarum, Rhizobium_tropici, Nitrospira_japonica, and Rhizobium_cauense with Glomus_mosseae and Rhizophagus_irregularis drive NPK cycling in HM-stressed rhizosphere soils. This finding suggested that association between plants type and their functional rhizosphere microbiome promote an eco-friendly strategy for HM recovery from serpentine soil.

The global production and use of polybrominated diphenyl ethers, including 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), have been substantially curtailed in recent decades. However, BDE-47 remains ubiquitously detectable in environmental matrices and human tissues worldwide. In this study, we investigated whether prenatal exposure to BDE-47 disrupts sperm function and DNA methylation in rat offspring. Pregnant rats were treated with BDE-47 from gestational day 0 to parturition. Sperm count, motility, morphology, mitochondrial membrane potential (MMP), reactive oxygen species (ROS) production, sperm chromatin DNA fragmentation index (DFI), serum testosterone, and histopathology were evaluated across generations. Testicular DNA methyltransferase expression and whole-genome bisulfite sequencing were performed to determine the DNA methylation in the F3 generation. BDE-47 exposure altered anogenital distance (AGD), sperm count, motility, morphology, MMP, ROS production, mean DFI, and %DFI in the F1 generation; AGD, morphology, and ROS production in the F2 generation; and AGD, motility, morphology, MMP, ROS production, mean DFI, %DFI, and testicular DNA methyltransferase expression in the F3 generation. Gene ontology analysis revealed that SYCP2, ASMT, and MSH4 were associated with sex differentiation and reproductive development. Our findings indicate that prenatal exposure to BDE-47 exerts transgenerational epigenetic effects, inducing phenotypic changes in the male reproductive system.

OBJECTIVE:This study investigated the associations of lifestyle, work environment, and health status with subacute COVID-19 symptoms or postacute sequelae of COVID-19 (PASC). METHODS:The questionnaire was used to collect data on lifestyles, work environment, health status, and coronavirus infection history and sequelae symptoms in a semiconductor packaging plant workers in Taiwan. Univariate and multiple logistic regression analyses were performed to identify the factors associated with the risks of subacute COVID-19 and PASC. RESULTS:This study included 333 subjects, with an average age of 37.6 years. Multivariate logistic regression analysis indicated that night shift work, exercise habit, and prolonged treatment were significant independent predictors of PASC. CONCLUSIONS:Night shift work and prolonged medical treatment were positively associated with PASC, and exercise was negatively associated with PASC. Optimizing work environments and shift schedules can reduce PASC risk.

Fine particulate matter (PM2.5) negatively impacts the reproductive system. Yet, the impact of water-insoluble PM2.5 (WI-PM2.5) particles and water-soluble PM2.5 (WS-PM2.5) extracts on male fertility is not fully elucidated. The current research is aimed to identify and analyze individual toxic effect patterns of WI-PM2.5 and WS-PM2.5 exposures. This investigation involved the intratracheal instillation of both low (20 μg) and high (200 μg) doses of WS-PM2.5 and WI-PM2.5 in male C57BL/6 mice (n = 6 in each group). PM2.5 samples were collected adjacent to polluted industrial complex in southern Taiwan in 2020–21. To elucidate the influence of PM2.5 composition on reproductive toxicity, a comprehensive range of health measures was analyzed (body and gonadal organ weights, sperm count, motility, morphology, mitochondrial membrane potential [MMP], reactive oxygen species generation, sperm chromatin DNA fragmentation index [DFI], testicular DNA content during spermatogenesis, and testicular histopathology). Exposure to WS-PM2.5 and WI-PM2.5 reduced rates of normal sperm morphology, with each also presenting unique toxic effects. WI-PM2.5 exposure can cause reduction in the cauda epididymis weight, while raising the percentage of abnormal sperm heads, MMP, and DFI in both low- and high-dose groups. Also, it increased the rate of tetraploid cells in the low-dose group. Conversely, exposure to WS-PM2.5 resulted in a decline in the weight of the cauda epididymis, coupled with elevated levels of elongating spermatids, round spermatids, and diploid cells at both doses. The testicular histopathological alterations were observed in both dose groups. Our study unequivocally demonstrated that being exposed to PM2.5, even at modest levels of air contaminants, can negatively impact the male reproductive system through causing biological impairments and cellular dysfunctions, including disturbances in sperm MMP, among other testicular effects. With separate hazard profiles associated with WI-PM2.5 and WP-PM2.5 exposures, it is imperative to consider the distinct features of PM2.5 when examining its toxic hazards.

Phthalates are common environmental pollutants known to disrupt various regulatory systems and are associated with several health issues, such as impaired immune response, developmental toxicity, hormonal disruption, and type 2 diabetes. Epigenetic modifications, such as DNA methylation, can serve as early indicators of environmental toxicant exposure due to their rapid alteration in response to varying environmental factors without altering the underlying DNA sequence. To investigate the impact of phthalate exposure on human health and the affected regulatory mechanisms, this study analysed a DNA methylation dataset generated using the Illumina Infinium MethylationEPIC BeadChip (EPIC BeadChip) array, along with the concentrations of 15 urinary phthalate metabolites from 389 participants. The results revealed sex-specific differences in phthalate concentrations, with females exhibiting relatively higher levels than males. These differences may reflect a combination of factors, including lifestyle behaviours and potential differences in exposure sources. Furthermore, differentially methylated CpG sites (DMCs) were identified only in the mono-ethylhexyl phthalate (MEHP) dataset, where a total of 53 DMCs were detected, including 11 that were consistently detected across multiple MEHP concentration comparisons. Additionally, the functional analysis showed that these DMCs are primarily involved in protein and nucleotide binding, immune response, ion channel regulation, and membrane-associated pathways. This study provides high-potential phthalate-related methylation markers, their associated genes, and the functions they are involved in. These findings offer valuable insights for the research on environmental toxicants and epigenetics, while supporting clinical applications related to phthalates.

Persistent organic pollutants (POPs) are chemicals that persist in the environment, bioaccumulate through the food chain, and exhibit toxic effects that threaten the health of humans and animals alike. The potential influence of POP-related air pollution on male reproductive outcomes has attracted increasing interest in the scientific community and among policymakers and the public. Therefore, epidemiological studies on fertility should examine the impact of chronic exposure to POPs via inhalation. The objective of this review is to present and discuss the available evidence linking the exposure to airborne POPs to male reproductive health problems. This study focuses on the air concentrations, biomarkers, and potential effects on the male reproductive health of two classes of POPs: the industrial polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs). Although the association between atmospheric pollutants and male reproductive health has been extensively investigated, particularly in relation to semen quality and endocrine outcomes, the molecular mechanisms of action, the adverse effects, and the dose-response relationships for many of these chemicals remain poorly understood. No systematic screening of common chemicals for negative endocrine effects is currently underway, and many questions remain regarding the impact on male reproductive health of exposures to these POPs. This review presents the air concentrations, biomarkers, and adverse male reproductive effects of PCBs and PBDEs pollutants. Given the dearth of information on this topic in the literature, studies are clearly needed to assess how pre-and post-natal exposure to airborne PCBs and PBDEs affects the male reproductive system. Future studies must also identify aerosols and airborne POPs that have a significant impact on male reproductive health and the pathways responsible for those effects.

Pneumonia is an inflammatory condition of the lungs caused by infection, which may be triggered and exacerbated by particulate matter (PM) exposure. We aimed to estimate the effect of PM on emergency department (ED) visits in pneumonia patients with septicemia after controlling for gaseous pollutants. Measurements on PM2.5, PM10, and other air pollutants at each of the 11 air-quality monitoring stations in Kaohsiung City, Taiwan, were collected between 2007 and 2013. The medical records of non-trauma patients who were over 17 years old and had visited the ED with a principal diagnosis of pneumonia were extracted. Poisson models were used to examine the relationship between air pollutants and daily ED visits for pneumonia with septicemia. Interquartile increments in the levels of PM2.5, PM10, and NO2 at lag 0 were associated with increments of 25.5%, 21.61%, and 21.97%, respectively, in the number of ED visits for pneumonia with septicemia during the warm season. The effect estimates of PM2.5 were robust after adjusting for PM10 and NO2 in the two-pollutant model. PM2.5 had stronger associations with ED visits in the cases of pneumonia with septicemia in relatively healthy patients, such as those without comorbid hypertension, diabetes, stroke, liver cirrhosis, respiratory disease, or malignancy. In conclusion, although the existing evidence already supports a causal relationship between PM2.5 and pulmonary dysfunction, we propose that PM2.5 may also play an important role in emergency visits for pneumonia with septicemia during the warm season in southern Taiwan after adjusting for PM10 and NO2, especially among relatively healthy residents.

Perfluoroalkyl substances (PFAS) have been reported to be harmful to multiple organs in the human body. Based on a previous study suggesting that hemodialysis (HD) may be a means of eliminating PFAS from the human body, we aimed to compare the serum PFAS concentrations of patients undergoing regular HD, patients with chronic kidney disease (CKD) and controls. Additionally, we also investigated the correlation between PFAS and biochemical data, as well as concurrent comorbidities. We recruited 301 participants who had been on maintenance dialysis for >90 days, 20 participants with stage 5 non-dialysis CKD, and 55 control participants who did not have a diagnosis of kidney disease, with a mean creatinine level of 0.77 mg/dl. Eight different PFAS, namely perfluorooctanoic acid (PFOA), total and linear perfluorooctanesulfonic acid (PFOS), perfluoroheptanoic acid (PFHpA), perfluorohexanesulfonic acid (PFHxS), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluoroundecanoic acid (PFUnDA), were measured using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Spearman correlation and multivariable linear regression with 5 % false discovery rate were used to evaluate the relationships between PFAS and clinical parameters in HD patients and controls. Circulating concentrations of seven PFAS, including total and linear PFOS (T-PFOS and L-PFOS) PFDA, PFNA, PFHxS, PFOA, and PFUnDA, were significantly lower in the HD group compared to the CKD and control group. For the interplay between biochemical data and PFAS, all of the studied PFAS were positively correlated with aspartate aminotransferase, alanine aminotransferase, glucose, blood urea nitrogen, ferritin, and vitamin D in the controls, while in HD patients, the PFAS were all positively correlated with albumin, uric acid, iron, and vitamin D. These findings may offer valuable insights for future studies seeking to eliminate PFAS.

BACKGROUND AND AIM: Fine atmospheric particles, which are particulate matter (PM) with a diameter ≤ 2.5 μm in total suspended atmospheric particles, can enter the terminal alveoli and even blood circulation along with human respiratory movement; insoluble PM2.5 particles can attach to various toxic entities and could threaten human health, and result in a variety of human dysfunctions and diseases. Knowledge about the effects of prenatal insoluble PM2.5 particle particles on male reproduction and whether transgenerational effects occur in subsequent generations are scant. METHOD: Therefore, in this study, we tested the hypothesis that prenatal exposure to insoluble PM2.5 particles disrupted sperm function in the F1, F2, and F3 generations of male mice. Pregnant Balb/c mice were treated by intratracheal instillation in gestation day 7, 11, and 15 with 10 mg insoluble PM2.5 particles/kg/day. On postnatal day 105 for all generations, epididymal sperm counts, motility, morphology, mitochondrial membrane potential (MMP), reactive oxygen species (ROS) generation, sperm chromatin DNA structure integrity, testicular DNA content in spermatogenesis, serum testosterone, and testicular DNA methyltransferases (Dnmts) levels were assessed. RESULTS: In the F1 generation, prenatal exposure to insoluble PM2.5 particles decreased anogenital distance (AGD) and normal sperm morphology, disrupted body weight, testis, and caput epididymal weight, and significant differences in ROS generation, MMP, and Dnmt1. In the F2 generation, insoluble PM2.5 particles decreased AGD, sperm motility, and normal sperm morphology, with significant differences in ROS generation and MMP. In the F3 generation, disrupted body weight, testis weight, and normal sperm morphology showed significant differences in ROS generation. CONCLUSIONS: Prenatal exposure to insoluble PM2.5 particles might induce the transgenerational effects on male reproductive toxicity in F3.

During respiration, particulate matter with a diameter of 2.5 µm or less (PM2.5) suspended in the atmosphere enters the terminal alveoli and blood. PM2.5 particles can attach to toxic substances, resulting in health problems. Limited information is available regarding the effects of prenatal exposure to water-soluble PM2.5 (WS-PM2.5) and water-insoluble PM2.5 (WI-PM2.5) on male reproduction. In addition, whether exposure to these particles has transgenerational effects remains unknown. We investigated whether prenatal exposure to WS-PM2.5 and WI-PM2.5 disrupts sperm function in generations F1, F2, and F3 of male mice. Pregnant BALB/c mice were treated using intratracheal instillation on gestation days 7, 11, and 15 with 10 mg of a water extract or insoluble PM2.5. On postnatal day 105, epididymal sperm count, motility, morphology, mitochondrial membrane potential (MMP), reactive oxygen species (ROS) production, the sperm chromatin DNA fragmentation index (DFI), and testicular DNA methyltransferase (Dnmt) levels were evaluated in all generations. Whole-genome bisulfite sequencing was used to analyze the DNA methylation status of generation F3. According to the results, exposure to WS-PM2.5 affected sperm morphology, ROS production, and mean DFI in generation F1; ROS production and mean DFI in generation F2; and sperm morphology and MMP in generation F3. Similarly, exposure to WI-PM2.5 affected sperm morphology, ROS production, mean DFI, %DFI, and Dnmt1 expression in generation F1; sperm morphology, MMP, and ROS production in generation F2; and sperm morphology, ROS, and %DFI in generation F3. Two hypermethylated genes, PRR16 and TJP2, were observed in the WS-PM2.5 and WI-PM2.5 groups, two hypomethylated genes, NFATC1 and APOA5, were observed in the WS-PM2.5 group, and two hypomethylated genes, ZFP945 and GSE1, were observed in the WI-PM2.5 group. Hence, prenatal exposure to PM2.5 resulted in transgenerational epigenetic effects, which may explain certain phenotypic changes in male reproduction.

Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer that is widely used to enhance the flexibility and durability of various products. As an endocrine disruptor, DEHP can interfere with normal hormonal functions, posing substantial health risks to organisms. Given the critical role of the liver in DEHP metabolism, we investigated potential liver damage in offspring induced by prenatal exposure to low doses of DEHP in Sprague Dawley rats. Pregnant rats were divided into three groups and administered 20 or 200 μg/kg/day of DEHP or corn oil vehicle control via oral gavage from gestation days 0–20. Male rat offspring were euthanized on postnatal day 84, and blood and liver specimens were collected for analysis. We observed fibrotic changes in the livers of the exposed groups, accompanied by the proliferation and activation of hepatic stellate cells and upregulated expression of TGF-B and collagen 1A1. Additionally, an inflammatory response, characterized by increased macrophage infiltration and elevated levels of pro-inflammatory cytokines, was evident. Third, hepatic and serum triglyceride and serum cholesterol were notably increased, along with upregulated expression of lipid metabolism-related proteins, such as sterol regulatory element-binding protein-1c, acetyl-CoA carboxylase, fatty acid synthase, and diacylglycerol O-acyltransferase 1, particularly in the low-dose group. These results suggest that prenatal exposure to DEHP can disrupt lipid metabolism, resulting in hepatic lipid accumulation in the offspring. This exposure may also induce an inflammatory response that contributes to the development of liver fibrosis. Thus, even at relatively low doses, such exposure can precipitate latent liver damage in offspring.

Tris(2-butoxyethyl) phosphate (TBEP) is one of the most abundant organophosphate flame retardants in the environment. This study aimed to evaluate the effect of TBEP exposure during adolescence on male reproductive function in adult rats. Male Sprague-Dawley rats were treated with 20 and 200 mg/kg body weight of TBEP or corn oil from postnatal day (PND) 42 to PND 105. A significant increase in the proportion of sperm with abnormal morphology (flattened head and bent tail) and superoxide anion (O2-.) production in the sperm of the 200 mg/kg treated group was observed (p < 0.05). Excessive production of sperm hydrogen peroxide (H2O2) was found in both the 20 and 200 mg/kg treatment groups (p < 0.05). Disruption of testicular structure was observed in the 20 and 200 mg/kg treated groups and seminiferous tubule degeneration was observed in the 200 mg/kg treated group. Our study demonstrated the adverse effects of TBEP on male reproductive function in rats.

Decabromodiphenyl ether (BDE-209), a congener of polybrominated diphenyl ethers, is a commonly used brominated flame retardant and a known endocrine disrupting chemical (EDC). Knowledge about the effects of prenatal BDE-209 exposure on male reproduction and whether transgenerational effects occur in subsequent generations are scant. Therefore, in this study, we tested the hypothesis that prenatal exposure to BDE-209 disrupted sperm function in the F1, F2, and F3 generations of male rats. Pregnant Sprague-Dawley rats were treated by gavage from gestation day 0 to birth with 5 mg BDE-209/kg/day. This treatment was based on the lowest-observed-adverse-effect level for DNA damage to sperm in male offspring. On postnatal day 84 for all generations, epididymal sperm counts, motility, morphology, reactive oxygen species generation, sperm chromatin DNA structure integrity, testicular DNA content in spermatogenesis, and serum testosterone levels were assessed. DNA methyltransferase (Dnmts) mRNA expression and methyl-CpG binding domain sequencing were also examined to analyze DNA methylation status in the F3 generation. In the F1 generation, prenatal exposure to BDE-209 disrupted body weight, decreased anogenital distance (AGD), sperm count, and motility; and increased bent tail rates of sperm. In the F2 generation, exposure to BDE-209 decreased AGD, sperm count, normal morphology rates, Dnmt1 expression, and increased Dnmt3a expression. In the F3 generation, BDE-209 exposure decreased AGD and normal sperm morphology, disrupted testicular elongated spermatid and round spermatid rates, reduced serum testosterone levels, and inhibited the mRNA expression of Dnmt1 and Dnmt3b. Compared with the control group, there existed 215 differentially hyper-methylated and 83 hypo-methylated genes in the BDE-209 group. BDE-209 is an EDC to disrupt the male reproduction from F1 to F3. BDE-209-induced changes in sperm function and hyper- or hypo-DNA methylation in the F3 generation might therefore explain the possible mechanism underlying BDE-209-mediated epigenetic transgenerational effects on the male reproductive system.

Di(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer in the manufacture of polyvinylchloride plastics and has been associated with concerns regarding male reproductive toxicity. In this study, we hypothesized that maternal exposure to DEHP induces transgenerational inheritance of adult-onset adverse reproductive outcomes through the male germline in the F1, F2, and F3 generations of male offspring. Pregnant rats were treated with 5 or 500 mg of DEHP/kg/day through gavage from gestation day 0 to birth. The offspring body weight, anogenital distance (AGD), anogenital index (AGI), sperm count, motility, and DNA fragmentation index (DFI) were measured for all generations. Methyl-CpG binding domain sequencing was performed to analyze sperm DNA methylation status in the F3. DEHP exposure at 500 mg/kg affected AGD, AGI, sperm count, mean DFI, and %DFI in the F1; AGD, sperm count, and mean DFI in the F2; and AGD, AGI, mean DFI, and %DFI in the F3. DEHP exposure at 5 mg/kg affected AGD, AGI, sperm count, and %DFI in the F1; sperm count in the F2; and AGD and AGI in F3. Compared with the control group, 15 and 45 differentially hypermethylated genes were identified in the groups administered 5 mg/kg and 500 mg/kg DEHP, respectively. Moreover, 130 and 6 differentially hypomethylated genes were observed in the groups administered 5 mg/kg and 500 mg/kg DEHP. Overall, these results demonstrated that prenatal exposure to DEHP caused transgenerational epigenetic effects, which may explain the observed phenotypic changes in the male reproductive system.

Background: Fine particulate matter (particulate matter with aerodynamic diameter of <= 2.5 mu m, PM2.5) exposure cause adverse health effects, including lung inflammation. Through intra-tracheal instillation of PM2.5 compo-nents, the study aimed to evaluate the inflammatory and proliferative effects on mice liver. PM2.5 samples were collected near an industrial complex at southern Taiwan. Mice were exposed to water extracts or insoluble particles by intra-tracheal instillation. Male C57BL/6 mice were divided into five groups: control, low dose insoluble particle exposure (LP), high dose insoluble particle exposure (HP), low dose water extract exposure (LW), and high dose water extract exposure (HW). Biochemical analysis, western blotting, histological exami-nation, and immunohistochemistry were employed to evaluate the results. Result: Enrichment factor (EF) of metallic elements showed that the EFs of trace elements (Ti, V, Ni, Zn, Pb, Cr, and Cu) in PM2.5 were above 10. Hematoxylin and Eosin (H&E) staining of the liver tissue showed inflammatory infiltration in particle exposure group; hepatocyte ballooning degeneration and karyomegaly were seen in the water extract exposure group. Upregulation of inflammatory signaling, p65 and p50, and caspase-3 (an impor-tant effector involved in apoptosis) positive hepatocytes was significantly increased in the HP group, followed by an elevation in protein levels of growth arrest and DNA damage-inducible protein 153 (GADD153). Increased protein expression of proliferating cell nuclear antigen (PCNA) was noted in the LW and HW groups. An increase in phosphorylation of regulators of cell proliferation, Akt and extracellular signal-regulated kinase (ERK) 1/2, were detected in the LW and HW groups. Conclusion: The present study shows that the insoluble particle composition of PM2.5 induced inflammatory signaling and cytokines upregulation in the liver, accompanied with inflammatory cell and macrophage infil-tration and an abnormal liver function. Exposure of water extract to PM2.5 induced signals of upregulated cellular proliferation, elevated markers of cell proliferation in liver, hepatocyte ballooning degeneration and karyomegaly.

This study aimed to examine the association between air pollution and out-of-hospital cardiac arrest (OHCA), and the effects of underlying diseases. Between January 2015 and December 2016, data on particulate matter (PM)2.5 and other air pollutants in Kaohsiung City were collected, and an emergency medical service database was used for information on patients who experienced OHCA. Overall, 3566 patients were analyzed and subgroup analyses by sex, age, and preexisting morbidities were performed. Interquartile increments in PM2.5, PM10, and O3 levels on lag 1 and NO2 level on lag 3 were associated with increments of 10.8%, 11.3%, 6.2%, and 1.7% in OHCA incidence, respectively. Subgroup analyses showed that patients with diabetes (1.363; interaction p = 0.009), heart disease (1.612; interaction p = 0.001), and advanced age (≥70 years, 1.297; interaction p = 0.003) were more susceptible to NO2 on lag 3. Moreover, patients were more susceptible to O3 during the cold season (1.194; interaction p = 0.001). We found that PM2.5, PM10, NO2, and O3 may play an important role in OHCA events, and the effects vary by underlying condition, age and season.

Di(2-ethylhexyl)phthalate (DEHP) may cause carcinogenicity in the liver; however, few have detailed on the potential effects of DEHP exposure on colorectal cancer. Male Sprague-Dawley rats received i.p. injections of 1,2-dimethylhydrazine (DMH) once-a-week for the first 4 weeks, and rats in each group were treated with DEHP through oral gavage daily for either 7, 10 or 15 weeks; after which, all rats were euthanized and their colons were assessed (a) morphologically for aberrant crypt foci (ACF) or tumors, (b) cytologically for mitotic index (MI), and (c) immunohistochemically for the expression of β-catenin, cyclooygenase (COX)-2, vascular endothelial growth factor (VEGF), proliferating cell nuclear antigen (PCNA), cyclin D1, and c-myc. Our results indicated that the mean total ACF, tumor incidence, and MI were significantly higher in the DEHP-treated DMH compared to control and the DEHP-alone groups. The level of β-catenin and cyclin D1 was increased in DEHP-exposed rats. Expression of β-catenin, COX-2, VEGF, and cyclin D1 was significantly higher in the combined DMH and DEHP-treated rats by comparison to that of the DMH group. In conclusion, this study indicates that exposure to DEHP may exacerbate DMH-induced colon tumorigenesis and provides impetus to evaluate the effect of DEHP in conjunction with other carcinogens.