Fertility-sparing surgery in children and adolescents with borderline ovarian tumors: a retrospective study.

OBJECTIVE: To describe the characteristics of children and adolescents with borderline ovarian tumors (BOTs) and evaluate the efficacy and safety of fertility-sparing surgery (FSS) in these patients. METHODS: Patients with BOTs younger than 20 years who underwent FSS were included in this study. RESULTS: A total of 34 patients were included, with a median patient age of 17 (range, 3-19) years; 97.1% (33/34) of cases occurred after menarche. Of the patients, 82.4% had mucinous borderline tumors (MBOTs), 14.7% had serous borderline tumors (SBOTs), and 2.9% had seromucinous borderline tumor (SMBOT). The median tumor size was 20.4 (range, 8-40)cm. All patients were at International Federation of Gynecology and Obstetrics stage I and all underwent FSS: cystectomy (unilateral ovarian cystectomy, UC, 14/34, 41.2% and bilateral ovarian cystectomy, BC, 1/34, 2.9%), unilateral salpingo-oophorectomy (USO; 18/34; 52.9%), or USO + contralateral ovarian cystectomy (1/34; 2.9%). The median follow-up time was 65 (range, 10-148) months. Recurrence was experienced by 10 of the 34 patients (29.4%). One patient with SBOT experienced progression to low-grade serous carcinoma after the third relapse. Two patients had a total of four pregnancies, resulting in three live births. The recurrence rate of UC was significantly higher in MBOTs than in USO (p = 0.005). The 5-year disease-free survival rate was 67.1%, and the 5-year overall survival rate was 100%. CONCLUSIONS: Fertility-sparing surgery is feasible and safe for children and adolescents with BOTs. For patients with MBOTs, USO is recommended to lower the risk of recurrence.

Toxic effect and mechanism of ß-cypermethrin and its chiral isomers on HTR-8/SVneo cells.

Beta-cypermethrin (ß-CYP) consists of four chiral isomers, acting as an environmental estrogen and causing reproductive toxicity, neurotoxicity, and dysfunctions in multiple organ systems. This study investigated the toxic effects of ß-CYP, its isomers, metabolite 3-phenoxybenzoic acid (3-PBA), and 17ß-estradiol (E2) on HTR-8/SVneo cells. We focused on the toxic mechanisms of ß-CYP and its specific isomers. Our results showed that ß-CYP and its isomers inhibit HTR-8/SVneo cell proliferation similarly to E2, with 100 µM 1S-trans-αR displaying significant toxicity after 48 h. Notably, 1S-trans-αR, 1R-trans-αS, and ß-CYP were more potent in inducing apoptosis and cell cycle arrest than 1R-cis-αS and 1S-cis-αR at 48 h. AO/EB staining and flow cytometry indicated dose-dependent apoptosis in HTR-8/SVneo cells, particularly at 100 µM 1R-trans-αS. Scratch assays revealed that ß-CYP and its isomers variably reduced cell migration. Receptor inhibition assays demonstrated that post-ICI 182780 treatment, which inhibits estrogen receptor α (ERα) or estrogen receptor ß (ERß), ß-CYP, its isomers, and E2 reduced HTR-8/SVneo cell viability, whereas milrinone, a phosphodiesterase 3 A (PDE3A) inhibitor, increased viability. Molecular docking studies indicated a higher affinity of ß-CYP, its isomers, and E2 for PDE3A than for ERα or ERß. Consequently, ß-CYP, its isomers, and E2 consistently led to decreased cell viability. Transcriptomics and RT-qPCR analyses showed differential expression in treated cells: up-regulation of Il24 and Ptgs2, and down-regulation of Myo7a and Pdgfrb, suggesting the PI3K-AKT signaling pathway as a potential route for toxicity. This study aims to provide a comprehensive evaluation of the cytotoxicity of chiral pesticides and their mechanisms.

Antioxidants improve ß-cypermethrin degradation by alleviating oxidative damage and increasing bioavailability by Bacillus cereus GW-01.

Microbial degradation of pesticide residues has the potential to reduce their hazards to human and environmental health. However, in some cases, degradation can activate pesticides, making them more toxic to microbes. Here we report on the ß-cypermethrin (ß-CY) toxicity to Bacillus cereus GW-01, a recently described ß-CY degrader, and effects of antioxidants on ß-CY degradation. GW-01 exposed to ß-CY negatively affected the growth rate. The highest maximum specific growth rate (µm) appeared at 25 mg/L ß-CY. ß-CY induced the oxidative stress in GW-01. The activities of superoxide dismutase (SOD), catalyse (CAT), and glutathione-S-transferase (GST) were significantly higher than that in control (p < 0.01); but they are decreased as growth phase pronged, which is contrary to the ß-CY degradation by GW-01 cells obtaining from various growth phase. Ascorbic acid (Vc), tea polyphenols (TP), and adenosine monophosphate (AMP) improved the degradation through changing the physiological property of GW-01. TP and AMP prompted the expression of gene encoding ß-CY degradation in GW-01, while Vc does the opposite. Biofilm formation was significantly inhibited by ß-CY, while was significantly enhanced by certain concentrations of TP and AMP (p < 0.05); while cell surface hydrophobicity (CSH) was negatively associated with ß-CY concentrations from 25 to 100 mg/L, and these 4 antioxidants all boosted the CSH. Cells grown with ß-CY had lower levels of saturated fatty acids but increased levels of some unsaturated and branched fatty acids, and these antioxidants alleviated the FA composition changes and gene expression related with FA metabolism. We also mined transcriptome analyses at lag, logarithmic, and stationary phases, and found that ß-CY induced oxidative stress. The objective of this study was to elaborate characteristics in relation to the microbial resistance of pesticide poisoning and the efficiency of pesticide degradation, and to provide a promising method for improving pesticide degradation by microbes.

The research landscape of the quality of life or psychological impact on gynecological cancer patients: A bibliometric analysis.

Background: Gynecological cancer is one of the most common cancers in women. The quality of life (QoL) or psychological impact has emerged as an outcome indicator in many clinical trials of gynecological cancer and gained much concern in the clinical setting at the start of the 21st century. Our paper conducted a bibliometric analysis of QoL or psychological impact on gynecological cancer patients to show the status and hotspots. Methods: Related publications from 2000 to 2022 were included by screening from the Web of Science Core Collection (WOSCC) on 26 June 2022. The bibliometrics was analyzed and visualized by bibliometrix R-package, VOSviewer, and CiteSpace V. Results: A total of 6,479 publications were included in our study. The publications in this field were increased annually. The United States (n = 2,075) was the country with the most published papers. Sydney University (n = 167) was the most productive affiliation. Gynecologic Oncology and Journal of Clinical Oncology were the most relevant and most cited sources, respectively. The article written by Bray F et al. has the highest citation. Kim J and Aaronson NK ranked first in most productive author and most co-cited author, respectively. The keywords "mortality", "fertility preservation", and "palliative care" have bursts till 2022, which represented the frontiers of this field. Conclusion: Our study provides an overall analysis of QoL or psychological impact on gynecological cancer patients, which can serve as a reference in future research.

Possible Mechanism of Dysphania ambrosioides (L.) Mosyakin & Clemants Seed Extract Suppresses the Migration and Invasion of Human Hepatocellular Carcinoma Cells SMMC-7721.

Mexican tea (Dysphania ambrosioides (L.) Mosyakin & Clemants) is rich in phenolic acids and flavonoids and could be a potential medicinal herb that can be used for prevention of human hepatocellular carcinoma. The objective of this study was to elaborate the possible mechanism for the prevention or treatment of hepatocellular carcinoma using Mexican tea, and to provide new avenues for the utilization of the invasive plant. In this study, the D. ambrosioides seed extracts (CSE) were analyzed by gas chromatography-mass spectrometry, and the effects of CSE on proliferation, migration, invasion, and gene expression of SMMC-7721 cells were investigated. Eight compounds were identified in CSE, and the compound with the highest content was ascaridole (25.82 %). The proliferation was significantly inhibited by CSE (p<0.05), and IC50 values were 0.587 g/L, 0.360 g/L, and 0.361 g/L at 24 h, 36 h, and 48 h, respectively. Migration and invasion were significantly inhibited (p<0.05). The network pharmacology and transcriptome analysis indicated that 2-hydroxy-2,6,6-trimethylbicyclo[3.1.1]heptan-3-one, cis-11-eicosenoic acid and 2-ethylcyclohexanone might be the active compounds. Transcriptome analysis indicated that the Wnt signaling pathway, which is related to migration and invasion, was significantly altered; this was verified by western blot assay. The expression of wnt11, lef1 and mmp7 genes in SMMC-7721 cells was significantly down-regulated (p<0.05), while gsk-3ß was significantly up-regulated (p<0.05). These results indicate that CSE inhibits the invasion and migration of SMMC-7721 cells in hepatocellular carcinoma through the Wnt signaling pathway.

The efficacy of cell-assisted versus conventional lipotransfer: A systematic review and meta-analysis.

Autologous lipotransfer is an essential component of soft tissue reconstruction. However, it is not widely applied or accepted by surgeons due to its unstable survival rate and uncertain efficacy. The cell-assisted fat transfer (CAL) is a promising technique that increases the fat survival rate. However, it is controversial based on various clinical studies. Here, we assessed the fat survival and complication rates of CAL, compared to the conventional autologous lipotransfer. To conduct our research, two reviewers independently screened related articles published in Medicine (via PubMed), EMBASE, Cochrane Library, and Web of Science. The combined effect estimates for efficacy evaluation was performed by the Review Manager software (RevMan 5.4.1). In total, 14 articles were included in our analysis (n = 722). Based on our analysis, the survival rate of the fat graft in CAL was significantly higher than the conventional fat grafting group (non-CAL group) (SMD = 2.81, 95%CI [1.54, 4.08], P < 0.01). In the subgroup, the fat retention of CAL in the facial filling was higher than the conventional one (SMD = 3.01, 95%CI [1.68, 4.33], P < 0.01). After breast augmentation, however, the difference between the experimental and control group was not statistically significant (SMD = 1.80, 95%CI [-0.31, 3.91], P = 0.09). Moreover, the CAL group exhibited comparable complications as the non-CAL group. Based on our analysis, the CAL group was significantly better than the conventional lipotransfer in terms of fat survival, particularly, during facial filling. However, it failed to reduce the complication rate, compared to the non-CAL group.

Cytotoxic Effect of the Essential oils from Erigeron Canadensis L. on Human Cervical Cancer HeLa Cells in Vitro.

Erigeron Canadensis L. (E. canadensis) is a widely distributed invasive weed species in China. Potentially anti-cancer qualities may exist in its essential oils (EOs). The purpose of this study was to analyze the components of the EOs of E. canadensis and their effects on the normal liver cell lines L02 and the human cervical cancer cell lines HeLa. The EOs from the upper region of E. canadensis were prepared, its components were identified by GC/MS. Cell viability, cell morphology observation, AO/EB dual fluorescence staining assay, flow cytometry, mitochondrial membrane potential, western blot, caspase inhibitor test, and oxidative stress tests were used to investigate the impact of the EOs on HeLa cells. Network pharmacological analysis was employed to study the potential mechanism of the EOs in the treatment of cervical cancer. According to the findings, the EOs had 21 chemical components, of which limonene made up 65.68 %. After being exposed to the EOs, the cell viability of HeLa and L02 dramatically declined. The inhibition of EOs was more effective than that of limonene when used in an amount equivalent to that in the EOs. L02 cells were less susceptible to the cytotoxicity of EOs than HeLa cells were. Furthermore, EOs altered the cell cycle in HeLa cells and caused oxidative stress and apoptosis. Compared with the control group, the reactive oxygen species (ROS) levels increased in HeLa cells at first and then decreased, total superoxide dismutase (SOD) and catalase (CAT) activities in HeLa cells significantly decreased. G1 phase cells decreased whereas G2/M phase cells increased. The rate of apoptosis rose. Reduced mitochondrial membrane potential and Caspase-3, -9, and -12 protein expression were both observed. Nerolidol, dextroparaffinone, and α-pinene were shown to be the primary components for the suppression of HeLa cells, according to the results of the prediction of pharmacologic targets. In conclusion, findings of this study indicated the EOs may have the potential to curb the growth of cervical cancer cells. Further research is needed to explore the in vivo effect of EOs.

A Potential Synbiotic Strategy for the Prevention of Type 2 Diabetes: Lactobacillus paracasei JY062 and Exopolysaccharide Isolated from Lactobacillus plantarum JY039.

The disturbance of intestinal microorganisms and the exacerbation of type 2 diabetes (T2D) are mutually influenced. In this study, the effect of exopolysaccharides (EPS) from Lactobacillus plantarum JY039 on the adhesion of Lactobacillus paracasei JY062 was investigated, as well as their preventive efficacy against T2D. The results showed that the EPS isolated from L. plantarum JY039 effectively improved the adhesion rate of L. paracasei JY062 to Caco-2 cells (1.8 times) and promoted the proliferation of L. paracasei JY062. In the mice experiment, EPS, L. paracasei JY062 and their complex altered the structure of the intestinal microbiota, which elevated the proportion of Bifidobacterium, Faecalibaculum, while inversely decreasing the proportion of Firmicutes, Muribaculaceae, Lachnospiraceae and other bacteria involved in energy metabolism (p < 0.01; p < 0.05); enhanced the intestinal barrier function; promoted secretion of the gut hormone peptide YY (PYY) and glucagon-like peptide-1 (GLP-1); and reduced inflammation by balancing pro-inflammatory factors IL-6, TNF-α and anti-inflammatory factor IL-10 (p < 0.01; p < 0.05). These results illustrate that EPS and L. paracasei JY062 have the synbiotic potential to prevent and alleviate T2D.

Cadmium cytotoxicity and possible mechanisms in human trophoblast HTR-8/SVneo cells.

The accumulation of cadmium (Cd) in the human body through food chain can lead to adverse pregnancy outcomes. In this study, Cd cytotoxicity and its mechanisms in HTR-8/SVneo cells were investigated. Cd disrupted the cellular submicrostructure and inhibited the cell viability in a time- and dose-dependent manner. The levels of reactive oxygen species, malondialdehyde content, and the activities of glutathione peroxidase (GSH-Px) and total superoxode dismutase (T-SOD) were concentration-dependently increased by Cd. In addition, Cd dose-dependently inducedcell apoptosis and decreased cell migration and invasion capacities. Finally, Cd significantly upregulated all the genes related to oxidative stress (SOD1, ROS1, and HSPA6), inflammatory response, cell cycle, apoptosis, and migration and invasion. This study will provide insights into the prevention and treatment of pregnancy-related diseases caused by Cd intoxication.

Substrate regulation on co-metabolic degradation of ß-cypermethrin by Bacillus licheniformis B-1.

Beta-cypermethrin (ß-CY) residues are a serious threat to food safety and human health. However, the residues are not efficiently biodegraded because microorganisms preferentially use the nutrients found in food and the environment for growth. In this study, the mechanisms underlying nutrient regulation during co-metabolic degradation of ß-CY by Bacillus licheniformis B-1 were investigated. The strain B-1 resting cells and the suspension containing NaN3 showed no significant differences in ß-CY degradation. The co-metabolic degradation and strain B-1 growth could be separately inhibited by iodoacetic acid and sodium fluoride. Adenosine monophosphate (AMP), fructose 1-6 bisphosphate (F1-6BP), Mg2+, and Mn2+ could improve the degradation, whereas adenosine triphosphate (ATP), alanine (Ala), phenylalanine (Phe), and phosphoenolpyruvate (PEP) were found to exert the opposite effect, indicating that ß-CY degradation was positively associated with pyruvate kinase activity. Furthermore, glycerol, urea, ammonium chloride and peptone improved ß-CY degradation in corn flour. The results provided a promising approach for nutrient regulation of pyrethroids biodegradation in food and the environment.

Gene regulation analysis of the effects of evodiamine on tongue squamous cell carcinoma.

OBJECTIVE: To use gene chip technology to study the effects of evodiamine (EVO) on the gene expression profile of tongue squamous cell carcinoma (TSCC) CAL-27 cell line, for the purpose of analyzing the mechanisms underlying the effects of EVO on gene expression and functional regulation of TSCC cells at the gene level. METHOD: Differentially expressed genes in CAL-27 cells treated with EVO were detected using gene chip technology and analyzed using ingenuity pathway analysis. RESULTS: Microarray results showed that there were 1243 differentially expressed genes following treatment with CAL-27 cells; 684 genes were upregulated and 559 were downregulated. Classical pathway analysis revealed a total of 89 signal transduction pathways with upregulated gene set enrichment, including lipopolysaccharide/interleukin (IL)-1-mediated inhibition of retinoid X receptor (RXR) function, agrin interactions at neuromuscular junctions, cholecystokinin/gastrin-mediated signaling, toll-like receptor signaling, and IL-6 signaling. A total of 39 signal transduction pathways were enriched for the downregulated genes, including interferon signals, liver X receptor/RXR activation signals, and RhoGDI signals. In the disease and function analysis, the upregulated genes were enriched in viral infection, RNA virus replication, viral replication, cancer cell invasion, cell invasion, and other related functions, while downregulated genes were enriched in neuromuscular diseases, and leukocyte differentiation, antiviral response, connective tissue cell death and other functions. CONCLUSIONS: Gene chip analysis offers an effective means of screening differential gene expression between EVO-treated TSCCs and controls, thus providing a sound basis for further research.

Evodiamine inactivates NF-κB and potentiates the antitumor effects of gemcitabine on tongue cancer both in vitro and in vivo.

OBJECTIVE: The aim of this study was to investigate whether evodiamine (EVO) could potentiate the antitumor activity of gemcitabine (GEM) in tongue cancer cells and determine its potential underlying mechanisms. MATERIALS AND METHODS: Human Tca8113 and CAL-27 tongue squamous carcinoma cell lines were treated with EVO and GEM in different sequences and doses, after which cell proliferation was measured. Drug interactions were analyzed using the Chou-Talalay method with CompuSyn software. Clonality, apoptosis, and migration were measured using the plate clone formation assay, annexin V/propidium iodide (PI) staining, Hoechst 33342 staining, and the wound-healing test. The activity of the nuclear factor kappa light-chain enhancer of activated B cell (NF-κB) p65 subunit and its downstream proteins was quantified by Western blotting. The effects of the drug combination in vivo were assessed using a CAL-27 heterotopic xenograft model. RESULTS: EVO and GEM had synergistic effects on CAL-27 and Tca8113 cell lines in time- and concentration-dependent manners. Combination of drugs inhibited cell proliferation and migration and reduced the expression of NF-κB p65, B cell lymphoma 2 (Bcl-2), and B cell lymphoma extra large (Bcl-xl) compared with the control and either drug alone. In vivo, combination treatment of the xenograft model with EVO and GEM led to a significant reduction in tumor volume growth and inhibited the activation of NF-κB p65 with no obvious adverse reactions. CONCLUSION: The results of this study showed that EVO may inhibit cancer cells by suppressing NF-κB activity, and in combination with GEM, it may increase the chemosensitivity of tongue squamous cancer cells, thereby improving the treatment response.

Assessing electronic cigarette emissions: linking physico-chemical properties to product brand, e-liquid flavoring additives, operational voltage and user puffing patterns.

Users of electronic cigarettes (e-cigs) are exposed to particles and other gaseous pollutants. However, major knowledge gaps on the physico-chemical properties of such exposures and contradictory data in published literature prohibit health risk assessment. Here, the effects of product brand, type, e-liquid flavoring additives, operational voltage, and user puffing patterns on emissions were systematically assessed using a recently developed, versatile, e-cig exposure generation platform and state-of-the-art analytical methods. Parameters of interest in this systematic evaluation included two brands (A and B), three flavors (tobacco, menthol, and fruit), three types of e-cigs (disposable, pre-filled, and refillable tanks), two puffing protocols (4 and 2 s/puff), and four operational voltages (2.2-5.7 V). Particles were generated at a high number concentration (106-107 particles/cm3). The particle size distribution was bi-modal (∼200 nm and 1 µm). Furthermore, organic species (humectants propylene glycol and glycerin, nicotine) that were present in e-liquid and trace metals (potassium and sodium) that were present on e-cig heating coil were also released into the emission. In addition, combustion-related byproducts, such as benzene and toluene, were also detected in the range of 100-38,000 ppbv/puff. Parametric analyzes performed in this study show the importance of e-cig brand, type, flavor additives, user puffing pattern (duration and frequency), and voltage on physico-chemical properties of emissions. This observed influence is indicative of the complexity associated with the toxicological screening of emissions from e-cigs and needs to be taken into consideration.

Assessment of reactive oxygen species generated by electronic cigarettes using acellular and cellular approaches.

Electronic cigarettes (e-cigs) have fast increased in popularity but the physico-chemical properties and toxicity of the generated emission remain unclear. Reactive oxygen species (ROS) are likely present in e-cig emission and can play an important role in e-cig toxicity. However, e-cig ROS generation is poorly documented. Here, we generated e-cig exposures using a recently developed versatile exposure platform and performed systematic ROS characterization on e-cig emissions using complementary acellular and cellular techniques: 1) a novel acellular Trolox-based mass spectrometry method for total ROS and hydrogen peroxide (H2O2) detection, 2) electron spin resonance (ESR) for hydroxyl radical detection in an acellular and cellular systems and 3) in vitro ROS detection in small airway epithelial cells (SAEC) using the dihydroethidium (DHE) assay. Findings confirm ROS generation in cellular and acellular systems and is highly dependent on the e-cig brand, flavor, puffing pattern and voltage. Trolox method detected a total of 1.2-8.9nmol H2O2eq./puff; H2O2 accounted for 12-68% of total ROS. SAEC cells exposed to e-cig emissions generated up to eight times more ROS compared to control. The dependency of e-cig emission profile on e-cig features and operational parameters should be taken into consideration in toxicological studies.

Development and characterization of electronic-cigarette exposure generation system (Ecig-EGS) for the physico-chemical and toxicological assessment of electronic cigarette emissions.

Electronic cigarettes (e-cig) have been introduced as a nicotine replacement therapy and have gained increasing attention and popularity. However, while findings on possible toxicological implications continue to grow, major knowledge gaps on both the complex chemistry of the exposure and toxicity exist, prohibiting public health assessors from assessing risks. Here, a versatile electronic cigarette exposure generation system (Ecig-EGS) has been developed and characterized. Ecig-EGS allows generation of real world e-cig emission profiles under controlled operational conditions, real time monitoring and time-integrated particle/gas sampling for physico-chemical characterization, and toxicological assessment (both in vitro and in vivo). The platform is highly versatile and can be used with all e-cig types. It enables generation of precisely controlled e-cig exposure while critical operational parameters and environmental mixing conditions can be adjusted in a systematic manner to assess their impact on complex chemistry and toxicity of emissions. Results proved the versatility and reproducibility of Ecig-EGS. E-cig emission was found to contain 106-107 particles/cm3 with the mode diameter around 200 nm, under air change rate of 60/h. Elevated CO2 and volatile organic specie generation was also observed. Furthermore, environmental mixing conditions also influenced e-cig emission profile. The versatility of Ecig-EGS will enable linking of operational and environmental parameters with exposure chemistry and toxicology and help in assessing health risks.

Increase in oxidative stress levels following welding fume inhalation: a controlled human exposure study.

BACKGROUND: Tungsten inert gas (TIG) welding represents one of the most widely used metal joining processes in industry. It has been shown to generate a large majority of particles at the nanoscale and to have low mass emission rates when compared to other types of welding. Despite evidence that TIG fume particles may produce reactive oxygen species (ROS), limited data is available for the time course changes of particle-associated oxidative stress in exposed TIG welders. METHODS: Twenty non-smoking male welding apprentices were exposed to TIG welding fumes for 60 min under controlled, well-ventilated settings. Exhaled breathe condensate (EBC), blood and urine were collected before exposure, immediately after exposure, 1 h and 3 h post exposure. Volunteers participated in a control day to account for oxidative stress fluctuations due to circadian rhythm. Biological liquids were assessed for total reducing capacity, hydrogen peroxide (H2O2), malondialdehyde (MDA), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentrations at each time point. A linear mixed model was used to assess within day and between day differences. RESULTS: Significant increases in the measured biomarkers were found at 3 h post exposure. At 3 h post exposure, we found a 24 % increase in plasma-H2O2 concentrations ([95%CI: 4 % to 46 %], p = 0.01); a 91 % increase in urinary-H2O2 ([2 % to 258 %], p = 0.04); a 14 % increase in plasma-8-OHdG ([0 % to 31 %], p = 0.049); and a 45 % increase in urinary-8-OHdG ([3 % to 105 %], p = 0.03). Doubling particle number concentration (PNC) exposure was associated with a 22 % increase of plasma-8-OHdG at 3 h post exposure (p = 0.01). CONCLUSION: A 60-min exposure to TIG welding fume in a controlled, well-ventilated setting induced acute oxidative stress at 3 h post exposure in healthy, non-smoking apprentice welders not chronically exposed to welding fumes. As mass concentration of TIG welding fume particles is very low when compared to other types of welding, it is recommended that additional exposure metrics such as PNC are considered for occupational risk assessments. Our findings highlight the importance of increasing awareness of TIG welding fume toxicity, especially given the realities of welding workplaces that may lack ventilation; and beliefs among interviewed welders that TIG represents a cleaner and safer welding process.

Characterization of Tungsten Inert Gas (TIG) Welding Fume Generated by Apprentice Welders.

Tungsten inert gas welding (TIG) represents one of the most widely used metal joining processes in industry. Its propensity to generate a greater portion of welding fume particles at the nanoscale poses a potential occupational health hazard for workers. However, current literature lacks comprehensive characterization of TIG welding fume particles. Even less is known about welding fumes generated by welding apprentices with little experience in welding. We characterized TIG welding fume generated by apprentice welders (N = 20) in a ventilated exposure cabin. Exposure assessment was conducted for each apprentice welder at the breathing zone (BZ) inside of the welding helmet and at a near-field (NF) location, 60cm away from the welding task. We characterized particulate matter (PM4), particle number concentration and particle size, particle morphology, chemical composition, reactive oxygen species (ROS) production potential, and gaseous components. The mean particle number concentration at the BZ was 1.69E+06 particles cm(-3), with a mean geometric mean diameter of 45nm. On average across all subjects, 92% of the particle counts at the BZ were below 100nm. We observed elevated concentrations of tungsten, which was most likely due to electrode consumption. Mean ROS production potential of TIG welding fumes at the BZ exceeded average concentrations previously found in traffic-polluted air. Furthermore, ROS production potential was significantly higher for apprentices that burned their metal during their welding task. We recommend that future exposure assessments take into consideration welding performance as a potential exposure modifier for apprentice welders or welders with minimal training.

The oxidative potential of differently charged silver and gold nanoparticles on three human lung epithelial cell types.

BACKGROUND: Nanoparticle (NPs) functionalization has been shown to affect their cellular toxicity. To study this, differently functionalized silver (Ag) and gold (Au) NPs were synthesised, characterised and tested using lung epithelial cell systems. METHODS: Monodispersed Ag and Au NPs with a size range of 7 to 10 nm were coated with either sodium citrate or chitosan resulting in surface charges from -50 mV to +70 mV. NP-induced cytotoxicity and oxidative stress were determined using A549 cells, BEAS-2B cells and primary lung epithelial cells (NHBE cells). TEER measurements and immunofluorescence staining of tight junctions were performed to test the growth characteristics of the cells. Cytotoxicity was measured by means of the CellTiter-Blue ® and the lactate dehydrogenase assay and cellular and cell-free reactive oxygen species (ROS) production was measured using the DCFH-DA assay. RESULTS: Different growth characteristics were shown in the three cell types used. A549 cells grew into a confluent mono-layer, BEAS-2B cells grew into a multilayer and NHBE cells did not form a confluent layer. A549 cells were least susceptible towards NPs, irrespective of the NP functionalization. Cytotoxicity in BEAS-2B cells increased when exposed to high positive charged (+65-75 mV) Au NPs. The greatest cytotoxicity was observed in NHBE cells, where both Ag and Au NPs with a charge above +40 mV induced cytotoxicity. ROS production was most prominent in A549 cells where Au NPs (+65-75 mV) induced the highest amount of ROS. In addition, cell-free ROS measurements showed a significant increase in ROS production with an increase in chitosan coating. CONCLUSIONS: Chitosan functionalization of NPs, with resultant high surface charges plays an important role in NP-toxicity. Au NPs, which have been shown to be inert and often non-cytotoxic, can become toxic upon coating with certain charged molecules. Notably, these effects are dependent on the core material of the particle, the cell type used for testing and the growth characteristics of these cell culture model systems.