How renal toxins respond to renal function deterioration and oral toxic adsorbent in pH-controlled releasing capsule.

The number of patients with chronic kidney disease (CKD) is increasing. Oral toxin adsorbents may provide some value. Several uremic toxins, including indoxyl sulfate (IS), p-cresol (PCS), acrolein, per- and poly-fluoroalkyl substances (PFAS), and inflammation markers (interleukin 6 [IL-6] and tumor necrosis factor [TNF]-alpha) have been shown to be related to CKD progression. A total of 81 patients taking oral activated charcoal toxin adsorbents (AC-134), which were embedded in capsules that dissolved in the terminal ileum, three times a day for 1 month, were recruited. The renal function, hemoglobulin (Hb), inflammation markers, three PFAS (PFOA, PFOS, and PFNA), and acrolein were quantified. Compared with the baseline, an improved glomerular filtration rate (GFR) and significantly lower acrolein were noted. Furthermore, the CKD stage 4 and 5 group had significantly higher concentrations of IS, PCS, IL-6, and TNF but lower levels of Hb and PFAS compared with the CKD Stage 3 group at baseline and after the intervention. Hb was increased only in the CKD Stage 3 group after the trial (p = .032). Acrolein did not differ between the different CKD stage groups. Patients with improved GFR (responders) (about 77%) and nonresponders had similar baseline GFR. Responders had higher acrolein and PFOA levels throughout the study and a more significant reduction in acrolein, indicating a better digestion function. Both the higher PFOA and lower acrolein may be related to improved eGFR (and possibly to improvements in proteinuria, which we did not measure. Proteinuria is associated with PFAS loss in the urine), AC-134 showed the potential to improve the GFR and decrease acrolein, which might better indicate renal function change. Future studies are needed with longer follow-ups.

Areca nut procyanidins prevent ultraviolet light B-induced photoaging via suppression of cyclooxygenase-2 and matrix metalloproteinases in mouse skin.

Chronic exposure to solar ultraviolet (UV) light induces photoaging in human skin. Our previous results have shown that areca nut procyanidins (ANPs) have antioxidant capacity and possess potential anti-inflammatory effects. Here, we aimed to investigate the effect of ANPs on UVB-induced photoaging. In the present study, dorsal skin of CD-1 mice was exposed to UVB at a minimal erythema dose (130 mJ/cm2) throughout a 3-week period. The effects of ANPs and epigallocatechin-3-gallate (EGCG), a polyphenolic constituent of green tea, on UVB-induced photoaging were compared. The results show that oral administration of ANP prevented UVB-induced photoaging, indicated by epidermal thickness and collagen disorientation, and inhibited UVB-induced expression of cyclooxygenase-2 and matrix metalloproteinases (MMPs), such as MMP-2, MMP-9, and TIMP1. The protective potential of ANP on UVB-induced photodamage was comparable to that of EGCG. These data suggest that ANP could be useful as a dietary supplement to attenuate solar UVB-induced premature skin aging.

Uncovering the microbiome landscape in sashimi delicacies.

It is widely believed that a significant portion of the gut microbiota, which play crucial roles in overall health and disease, originates from the food we consume. Sashimi is a type of popular raw seafood cuisine. Its microbiome, however, remained to be thoroughly explored. The objective of this study is to explore the microbiome composition in sashimi at the time when it is served and ready to be eaten. Specifically, our tasks include investigating the diversity and characteristics of microbial profiles in sashimi with respect to the fish types. We utilized the Sanger-sequencing based DNA barcoding technology for fish species authentication and next-generation sequencing for sashimi microbiome profiling. We investigated the microbiome profiles of amberjack, cobia, salmon, tuna and tilapia sashimi, which were all identified using the MT-CO1 DNA sequences regardless of their menu offering names. Chao1 and Shannon indexes, as well as Bray-Curtis dissimilarity index were used to evaluate the alpha and beta diversities of sashimi microbiome. We successfully validated our previous observation that tilapia sashimi has a significantly higher proportions of Pseudomonas compared to other fish sashimi, using independent samples (P = 0.0010). Salmon sashimi exhibited a notably higher Chao1 index in its microbiome in contrast to other fish species (P = 0.0031), indicating a richer and more diverse microbial ecosystem. Non-Metric Multidimensional Scaling (NMDS) based on Bray-Curtis dissimilarity index revealed distinct clusters of microbiome profiles with respect to fish types. Microbiome similarity was notably observed between amberjack and tuna, as well as cobia and salmon. The relationship of microbiome similarity can be depicted as a tree which resembles partly the phylogenetic tree of host species, emphasizing the close relationship between host evolution and microbial composition. Moreover, salmon exhibited a pronounced relative abundance of the Photobacterium genus, significantly surpassing tuna (P = 0.0079), observed consistently across various restaurant sources. In conclusion, microbiome composition of Pseudomonas is significantly higher in tilapia sashimi than in other fish sashimi. Salmon sashimi has the highest diversity of microbiome among all fish sashimi that we analyzed. The level of Photobacterium is significantly higher in salmon than in tuna across all the restaurants we surveyed. These findings provide critical insights into the intricate relationship between the host evolution and the microbial composition. These discoveries deepen our understanding of sashimi microbiota, facilitating our decision in selecting raw seafood.

Double Filtration Plasmapheresis with Polyvinyl Alcohol-Based Membrane Lowers Serum Inflammation and Toxins in Patients with Hyperlipidemia.

Hyperlipidemia is increasing in prevalence and is highly correlated with cardiovascular disease (CVD). Lipid-lowering medications prevent CVD but may not be suitable when the side effects are intolerable or hypercholesterolemia is too severe. Double-filtration plasmapheresis (DF) has shown its therapeutic effect on hyperlipidemia, but its side effects are not yet known. We enrolled 45 adults with hyperlipidemia in our study. The sera before and two weeks after DF were evaluated, and we also analyzed perfluorochemicals to see if DF could remove these lipophilic toxins. After DF, all lipid profile components (total cholesterol, triglycerides, high-density lipoprotein [HDL], and low-density lipoprotein [LDL]) had significantly decreased. Leukocyte counts increased while platelet levels decreased, which may have been caused by the puncture wound from DF and consumption of platelets during the process. As for uremic toxins and inflammation, levels of C-reactive protein, uric acid, and alanine transaminase (ALT) all decreased, which may be related to the removal of serum perfluorooctane sulfonate (PFOS) and improvement of renal function. The total cholesterol/HDL ratio and triglycerides were significantly higher in the diabetes mellitus (DM) group at baseline but did not significantly differ after DF. In conclusion, DF showed potential for improving inflammation and removing serum lipids and PFOS in adults with hyperlipidemia.

The Effects of Yoga Exercise on Blood Pressure and Hand Grip Strength in Chronic Stroke Patients: A Pilot Controlled Study.

BACKGROUND: We investigated the beneficial effect of add-on yoga with rehabilitation on blood pressure (BP) and hand grip strength in patients with chronic stroke (more than 90 days). METHODS: The study included patients 30-80 years of age who could stand independently for 1 min. Patients with psychiatric diseases or undergoing other therapies (like acupuncture) were excluded. The yoga group received training (1 h session twice weekly) with standard rehabilitation for 8 weeks. The control group received standard rehabilitation only. There were no differences in age, gender, hand grip strength, or BP between the two groups (16 subjects in each group) at baseline. RESULTS: The systolic BP (p = 0.01) decreased significantly, and the diastolic BP also decreased but not significantly in the yoga group (p = 0.11). For hand grip strength, both the unaffected hand (p = 0.00025) and the affected hand (p = 0.027) improved significantly. The control group showed no significant change in systolic or diastolic BP, nor did the grip strength change in both hands. Gender and age also affected the results of overall rehabilitation in that women benefited more from a decrease in BP, while men and young people (lower than the mean age of 60) benefited from hand grip strength improvement. CONCLUSIONS: Combining yoga with rehabilitation in chronic stroke patients can improve hand grip strength and decrease systolic BP.

The Associations between Erythropoietic Response with Inflammation Markers and Perfluorinated Chemicals in Hemodialysis Patients.

Erythropoiesis-stimulating agents (ESA) are used to treat anemia in hemodialysis (HD) patients. We investigated the role of inflammation and accumulation of environmental toxins (perfluorinated chemicals (PFCs), such as perfluorooctanoic acid and perfluorooctane sulfonate) in the erythropoietic response of HD patients who receive a fixed monthly continuous erythropoietin receptor activator (CERA) dosage. Forty-five patients underwent three successive phases of ESA treatment for two months each (phase one: 100 µg CERA once monthly; phase two: 50 µg CERA twice monthly; phase three: 100 µg CERA once monthly). Patient data were collected to determine the association of various factors with erythropoietic response (change in hematocrit). Liquid chromatography-tandem mass spectrometry was used to analyze perfluorinated chemicals. Twenty-eight patients exhibited a poor erythropoietic response that was significantly associated with: age > 80 years, initial hematocrit > 36%, glucose > 200 mg/dL, alanine aminotransferase > 21 U/L, c-reactive protein > 1 mg/dL, interleukin-6 > 10 ng/mL, lactate dehydrogenase ≤ 190 U/L, and chloride ≤ 93 mEq/L. There was also a borderline significant association between inflammation and PFCs, although PFCs failed to show any impact on ESA response. Age, glucose, chloride, liver function, and inflammation may be associated with cost-effective fixed CERA dosage administered at an increased frequency.

Effect of heated tobacco products and traditional cigarettes on pulmonary toxicity and SARS-CoV-2-induced lung injury.

Cigarette smoke (CS) significantly contributes to the development of chronic obstructive pulmonary disease (COPD). Heated tobacco products (HTPs), newly developed cigarette products, have been proposed as an alternative for safe cigarette smoking. Although it is plausible to think that replacing traditional cigarettes with HTPs would lower the risks of COPD, this notion requires confirmation by further investigations from sources independent of the tobacco industry. COPD is characterized by an ongoing inflammatory process in the lungs, and the renin-angiotensin system (RAS) has been implicated in the pathogenesis of COPD. Angiotensin-converting enzyme-2 (ACE2) functions as a negative regulator of RAS and has been suggested as a cellular receptor for the causative agent of SARS-CoV-2. It has been shown that smoking is most likely associated with the negative progression and adverse outcomes of SARS-CoV-2. In this study, we found that cigarette smoke extracts from traditional cigarettes (CSE) caused higher cytotoxicity and higher oxidative stress levels than extracts from HTPs (HTPE) in two lung cell lines (Calu-3 and Beas-2B). CSE and HTPE induced RAS activation, MAPK activation, and NF-kB inflammatory pathway activation, resulting in the production of inflammatory cytokines. Furthermore, CSE and a high dose of HTPE reduced tight junction proteins, including claudin 1, E-cadherin, and ZO-1, and disrupted lung epidermal tight junctions at the air-liquid interface (ALI). Finally, CSE and HTPE enhanced the spike protein S1-induced lung injury response. Together, these results suggest that HTPE induced similar lung pathogenesis relevant to COPD and SARS-CoV-2-induced lung injury caused by CSE.

Perfluorooctanesulfonate Can Cause Negative Bias in Creatinine Measurement in Hemodialysis Patients Using Polysulfone Dialysis Membranes.

Serum creatinine is an important clinical marker for renal clearance. However, two conventional methods (Jaffe and enzymatic) are prone to interferences with organic compounds as compared to the standard method (isotope dilution-liquid chromatography-mass spectrometry) and can cause a significant negative bias. Perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA) are two common perfluorochemicals (PFCs) that can easily be accumulated in humans. We aimed to verify whether this bias is the result of an accumulation of PFCs. The serum creatinine values of 124 hemodialysis patients were analyzed using the three methods. We also aimed to evaluate which biochemical parameters will influence the difference between the conventional methods and the standard method. We found that a significant underestimation occurred when using the conventional methods. Albumin is an independent factor associated with negative bias, but it loses this correlation after dialysis, likely due to the removal of protein-bound uremic toxins. PFOS can cause negative bias when using the enzymatic method. Furthermore, this linear correlation is more significant in patients who used polysulfone-based dialysis membranes, possibly due to the better clearance of other uremic toxins. The serum creatinine of uremic patients can be significantly underestimated when using conventional methods. PFCs, as well the type of dialysis membrane being used, can be influencing factors.

Acrolein plays a culprit role in the pathogenesis of diabetic nephropathy in vitro and in vivo.

Objective: Diabetic nephropathy (DN), also known as diabetic kidney disease (DKD), is a major chronic complication of diabetes and is the most frequent cause of kidney failure globally. A better understanding of the pathophysiology of DN would lead to the development of novel therapeutic options. Acrolein, an α,ß-unsaturated aldehyde, is a common dietary and environmental pollutant. Design: The role of acrolein and the potential protective action of acrolein scavengers in DN were investigated using high-fat diet/ streptozotocin-induced DN mice and in vitro DN cellular models. Methods: Acrolein-protein conjugates (Acr-PCs) in kidney tissues were examined using immunohistochemistry. Renin-angiotensin system (RAS) and downstream signaling pathways were analyzed using quantitative RT-PCR and Western blot analyses. Acr-PCs in DN patients were analyzed using an established Acr-PC ELISA system. Results: We found an increase in Acr-PCs in kidney cells using in vivo and in vitro DN models. Hyperglycemia activated the RAS and downstream MAPK pathways, increasing inflammatory cytokines and cellular apoptosis in two human kidney cell lines (HK2 and HEK293). A similar effect was induced by acrolein. Furthermore, acrolein scavengers such as N-acetylcysteine, hydralazine, and carnosine could ameliorate diabetes-induced kidney injury. Clinically, we also found increased Acr-PCs in serum samples or kidney tissues of DKD patients compared to normal volunteers, and the Acr-PCs were negatively correlated with kidney function. Conclusions: These results together suggest that acrolein plays a role in the pathogenesis of DN and could be a diagnostic marker and effective therapeutic target to ameliorate the development of DN.

Cigarette Smoke Containing Acrolein Upregulates EGFR Signaling Contributing to Oral Tumorigenesis In Vitro and In Vivo.

Oral squamous cell carcinoma (OSCC) accounts for 80-90% of all intraoral malignant neoplasms. The single greatest risk factor for oral cancer is tobacco use, including cigarettes, cigars, chewing tobacco, and snuff. Aberrations of the epidermal growth factor receptor (EGFR) pathway features prominently in oral tumorigenesis and progression. It was shown that cigarette smoking (CS) is associated with worse prognosis in OSCC patients and overexpression of EGFR in tumor tissue. However, the mechanism by which cigarette smoking induced EGFR pathway activation remains to be fully elucidated. Acrolein, an IARC group 2A carcinogen, is a highly reactive aldehyde found in CS. Here we report that acrolein is capable of inducing tumorigenic transformation in normal human oral keratinocytes (NOK). The acrolein-transformed NOK cells showed EGFR copy number amplification, increased EGFR expression, and activation of downstream ERK and AKT signaling pathway. No p53 mutations were observed in acrolein-transformed NOK cells. Inhibiting EGFR pathway using an anti-EGFR antibody, cetuximab, inhibits tumor growth. Furthermore, by examining tissue sample from patients, we found an increased EGFR copy number was positively associated with acrolein-induced DNA damages in OSCC patients. Taken together, our results indicate that acrolein is important in tumorigenic transformation through amplification of EGFR and activating the downstream signaling pathway, contributing to oral carcinogenesis. This is the first study to provide molecular evidence showing that CS containing acrolein contributes to EGFR amplification in OSCC.

Acrolein contributes to human colorectal tumorigenesis through the activation of RAS-MAPK pathway.

Colorectal cancer (CRC) is one of the most well-known malignancies with high prevalence and poor 5-year survival. Previous studies have demonstrated that a high-fat diet (HFD) is capable of increasing the odds of developing CRC. Acrolein, an IARC group 2A carcinogen, can be formed from carbohydrates, vegetable oils, animal fats, and amino acids through the Maillard reaction during the preparation of foods. Consequently, humans are at risk of acrolein exposure through the consumption of foods rich in fat. However, whether acrolein contributes to HFD-induced CRC has not been determined. In this study, we found that acrolein induced oncogenic transformation, including faster cell cycling, proliferation, soft agar formation, sphere formation and cell migration, in NIH/3T3 cells. Using xenograft tumorigenicity assays, the acrolein-transformed NIH/3T3 clone formed tumors. In addition, cDNA microarray and bioinformatics studies by Ingenuity Pathway Analysis pointed to the fact that RAS/MAPK pathway was activated in acrolein-transformed clones that contributed to colon tumorigenesis. Furthermore, acrolein-induced DNA damages (Acr-dG adducts) were higher in CRC tumor tissues than in normal epithelial cells in CRC patients. Notably, CRC patients with higher levels of Acr-dG adducts appeared to have better prognosis. The results of this study demonstrate for the first time that acrolein is important in oncogenic transformation through activation of the RAS/MAPK signaling pathway, contributing to colon tumorigenesis.

Acute and Chronic Exposure of Toluene Induces Genotoxicity in Different Regions of the Brain in Normal and Allergic Mouse Models.

Toluene is a widely used industrial organic solvent and is ubiquitous in our environment. The neurobehavioral and neurotoxic effects of toluene are well recognized; however, its genotoxicity is still under discussion. Toluene biotransformation leads to the generation of reactive oxygen species that cause oxidative stress and DNA damages. Individuals with different immunogenetic backgrounds have different sensitivities to toxic chemical exposure. Previous studies have suggested that allergic stimulation may influence the threshold for toluene sensitivity due to the modulation of neurotrophin-related genes. Therefore, we aimed to investigate toluene-induced genotoxicity in different brain regions following acute and chronic exposure in vivo and to further examine whether allergic stimulation may influence the sensitivity to toluene-induced genotoxicity. In this present study, we found that exposure of toluene induced oxidative DNA damages resulting in genotoxicity in different brain regions including cortex, cerebellum, and hippocampus using comet assay. Higher genotoxicity induced by toluene was observed in the hippocampus of control mice compared to OVA-immunized mice. These results provide evidence that toluene-induced genotoxicity may contribute to its neurotoxicity in different immunogenetic individuals.

Identification of acrolein metabolites in human buccal cells, blood, and urine after consumption of commercial fried food.

SCOPE: Acrolein is a highly electrophilic α,ß-unsaturated aldehyde and is associated with human diseases. It is formed by Maillard reaction during food processing and could be detected in the emissions of overheated cooking oils. Consequently, humans are at risk of acrolein exposure through consumption of such prepared food. METHODS AND RESULTS: We conducted three human studies that healthy subjects (21-30 years) were served fried foods including fried chicken and French fries from three commercial fast food restaurants. Acrolein-related metabolites including urinary 3-hydroxypropyl mercapturic acid (3-HPMA), serum acrolein-protein conjugates (Acr-FDP), and buccal acrolein-induced DNA damages (Acr-dG adducts) along with GSH levels in serum or buccal cells were investigated for different times after consumption. CONCLUSION: Urinary 3-HPMA levels were increased after 2-hr consumption of fried food with an elimination half-life of 10 hr. In addition, increased Acr-dG adducts in oral cavity were inversely correlated to buccal glutathione (GSH) levels after consumption. However, there was no significant change in systemic GSH levels or Acr-FDP adducts in serum. These results indicate that exposure of acrolein from consuming fried food affects local oral cavity homeostasis. This may provide a possible link between intake of fried food and increased risk of upper aerodigestive tract cancers.

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking- and Betel Quid Chewing-Related Human Oral Cancer.

BACKGROUND: Cigarette smoking (CS) and betel quid (BQ) chewing are two known risk factors and have synergistic potential for the development of oral squamous cell carcinoma (OSCC) in Taiwan. The p53 mutation characteristics in OSCC (G to A or G to T mutations) are similar to that of acrolein-induced DNA damage. Acrolein is a major cigarette-related carcinogen that preferentially causes p53 mutations and inhibits DNA repair function in lung cancer. We hypothesize that acrolein is associated with OSCC carcinogenesis. METHODS: A total of 97 patients with OSCC and 230 healthy subjects with CS and/or BQ chewing histories were recruited. Slot blot analysis of Acr-dG adducts, an indicator of acrolein-induced DNA damage in buccal DNA, and LC/MS-MS analysis of 3-HPMA levels, urinary Acr metabolites, were performed. RESULTS: Our results showed that the level of Acr-dG adducts in buccal cells was 1.4-fold higher in patients with OSCC than in healthy subjects with CS and/or BQ chewing histories (P < 0.001). In addition, in healthy subjects, CS and BQ chewing were associated with significantly higher levels of 3-HPMA, indicating that CS and BQ chewing promotes acrolein absorption. However, 3-HPMA levels in patients with OSCC were significantly lower than those in healthy subjects, indicating impaired acrolein metabolism. CONCLUSIONS: In this study, we provide a novel mechanism by which increased acrolein uptake and impaired metabolism may contribute to the synergistic potential of CS and BQ-induced OSCC. IMPACT: Elevated acrolein-induced DNA damage (Acr-dG adducts) detected in buccal swabs may serve as an early indicator to identify patients at risk of developing OSCC.

Betel quid containing safrole enhances metabolic activation of tobacco specific 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).

Cigarette smoking (CS) and betel quid (BQ) chewing are two known risk factors that have synergistic potential for the enhancing the development of oral squamous cell carcinoma (OSCC) in Taiwan. Most mutagens and carcinogens are metabolically activated by cytochrome P450 (CYP450) to exert their mutagenicity or carcinogenicity. Previous studies have shown that metabolic activation of the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), by CYP2A6 activity determines NNK-induced carcinogenesis. In addition, safrole affects cytochrome P450 activity in rodents. However, the effect of BQ safrole on the metabolism of tobacco-specific NNK and its carcinogenicity remains elusive. This study demonstrates that safrole (1 mg/kg/d) induced CYP2A6 activity, reduced urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) levels, and increased NNK-induced DNA damage, including N7-methylguanine, 8-OH-deoxyguanosine and DNA strand breaks in a Syrian golden hamster model. Furthermore, altered NNK metabolism and increased NNK-induced DNA damage were also observed in healthy subjects with CS and BQ chewing histories compared to healthy subjects with CS histories. In conclusion, BQ containing safrole induced tobacco-specific NNK metabolic activation, resulting in higher NNK-induced genotoxicity. This study provides valuable insight into the synergistic mechanisms of CS- and BQ-induced OSCC.

Alterations in Acrolein Metabolism Contribute to Alzheimer's Disease.

Alzheimer's disease (AD) is a detrimental neurodegenerative disease, and early diagnosis appears to be the key to successful treatment. Acrolein, a byproduct of lipid peroxidation, has been shown to contribute to the pathological process of AD. This study recruited 118 elderly subjects consisting of 58 non-demented control subjects and 62 AD patients. We analyzed the acrolein-related metabolites in the plasma, cerebrospinal fluid (CSF), and urine of all subjects. We found that the levels of acrolein-conjugated protein (Acr-PC) in the plasma (p = 0.00012) and CSF (p = 0.00161) of AD patients were significantly higher than those of control subjects, whereas the levels of a urinary acrolein metabolite, 3-hydroxypropyl mercapturic acid (3-HPMA), were markedly decreased (p = 0.00882) in AD patients. These data suggest that deregulated acrolein metabolism may be correlated with neuronal damage in AD patients, which might provide further insights into the disease progression and early diagnosis of AD.

Sources identification of PCDD/Fs in soil and atmospheric deposition in Taiwan.

PCDD/Fs are among pollutants, which gain major concern from Taiwan government and citizens during industrialization. PCDD/Fs can be emitted into the atmosphere, soil, and water environment in either vapor or solid forms. Atmospheric deposition is the main pathways for atmospheric PCDD/Fs to precipitate on surface soil. In this study, a simultaneous analysis of both soil and deposition PCDD/Fs was done to investigate the relationship between in-soil and deposited PCDD/Fs in Taiwan. Soil samples (n = 84) and atmospheric deposition samples (n = 57) were collected within overlapped periods of time. Geometric mean of 10.4 pg WHO-TEQ/g was found in the soil samples when the geometric mean of atmospheric deposited PCDD/F concentrations was found to be 7.39 pg WHO-TEQ/m2/day. Concentration of PCDD/Fs in samples collected in industrial location were higher than those collected in other locations in all sampling areas. OCDD, OCDF, HpCDD, HpCDF, were the predominant congeners in PCDD/F profile in both soil and atmospheric deposited samples, when 1,2,3,7,8-PeCDD and 2,3,4,7,8-PeCDF were major contributors for PCDD/F fingerprint with WHO-TEQ transformation. Positive Matrix Factorization (PMF) analysis showed that 83% of soil PCDD/Fs correlate with atmospheric deposition process originated from industrial activities (44%) and long range transport activities (39%). Furthermore, the PMF analysis found long range transport, municipal solid water incinerators (MSWIs), industrial waste incinerators (IWIs), electric arc furnace, recycling process of aluminum, sintering plants to be the main sources contributing to atmospheric deposited PCDD/Fs.

Associations between perfluorinated chemicals and serum biochemical markers and performance status in uremic patients under hemodialysis.

Perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA) are commonly used perfluorinated chemicals (PFCs). PFCs are mainly excreted by urine. Uremic patients tend to accumulate toxins in their body and have poor functional status. We investigated the associations between PFCs and the clinical profile of uremic patients under hemodialysis (HD). Liquid chromatography tandem mass spectrometry coupled with isotope dilution was used to quantify PFOA and PFOS. We enrolled 126 patients under regular HD. Compared with previous research, the concentration of PFOA was lower, but that of PFOS was higher in uremic patients than in the general population. The levels of PFOA and PFOS in uremic patients before dialysis were 0.52 (ng/ml) and 21.84 (ng/ml) respectively. The PFOA level remained unchanged but that of PFOS decreased to1.85 ng/mL after dialysis. PFOS can be removed by HD. Patients using hypertensive medication had a lower PFOS then those who did not. The PFOS level was negatively correlated with the duration of the HD session and patient performance status, but positively correlated with levels of cholesterol, chloride (an indicator of acidemia), ferritin, and total protein. (p<0.05). The association with serum protein may explain the long half-life of PFCs in humans. This is the first study which investigated PFCs in uremic patients and showed PFCs are associated with adverse effects in this population.

Dialysis Membranes Influence Perfluorochemical Concentrations and Liver Function in Patients on Hemodialysis.

Introduction: Perfluoro-octanesulfonate (PFOS) and perfluoro-octanoic acid (PFOA) are two toxic perfluorochemicals (PFCs) commonly used as surfactants. PFCs are difficult to be eliminated from the body. We investigated the influence of different dialysis membranes on the concentrations of PFCs in patients under hemodialysis. Method: We enrolled 98 patients. Of these, 58 patients used hydrophobic polysulfone (PS) dialysis membranes, and the other 40 had hydrophilic membranes made by poly-methyl methacrylate (PMMA) or cellulose triacetate (CTA). Liquid chromatography tandem mass spectrometry coupled was used with isotope dilution to quantify PFOA and PFOS. Results: The predialysis concentrations of PFOA and PFOS in patients with hydrophobic PS dialysis membranes were 0.50 and 15.77 ng/mL, respectively, lower than the concentrations of 0.81 and 22.70 ng/mL, respectively, in those who used hydrophilic membranes (such as CTA or PMMA). Older patients have higher PFOS and poorer body function, with lower Karnofsky Performance Status Scale (KPSS) scores. The demographic data of the two groups were similar. However, patients with hydrophobic PS dialysis membranes had lower predialysis aspartate transaminase (AST) (p = 0.036), lower glucose levels (p = 0.017), and better body function (nonsignificantly higher KPSS scores, p = 0.091) compared with patients who used other membranes. These differences may be associated with the effects of different membranes, because PFOA positively correlated with AST, while PFOS negatively correlated with body function. Conclusions: This is the first study comparing PFC levels in uremic patients with different dialysis membrane. PS membrane may provide better clearance of PFCs and may, therefore, be beneficial for patients.