Absence of lung tumor promotion with reduced tumor size in mice after inhalation of copper welding fumes.

Welding fumes are a Group 1 (carcinogenic to humans) carcinogen as classified by the International Agency for Research on Cancer. The process of welding creates inhalable fumes rich in iron (Fe) that may also contain known carcinogenic metals such as chromium (Cr) and nickel (Ni). Epidemiological evidence has shown that both mild steel (Fe-rich) and stainless steel (Fe-rich + Cr + Ni) welding fume exposure increases lung cancer risk, and experimental animal data support these findings. Copper-nickel (CuNi) welding processes have not been investigated in the context of lung cancer. Cu is intriguing, however, given the role of Cu in carcinogenesis and cancer therapeutics. This study examines the potential for a CuNi fume to induce mechanistic key characteristics of carcinogenesis in vitro and to promote lung tumorigenesis, using a two-stage mouse bioassay, in vivo. Male A/J mice, initiated with 3-methylcholanthrene (MCA; 10 µg/g), were exposed to CuNi fumes or air by whole-body inhalation for 9 weeks (low deposition-LD and high deposition-HD) and then sacrificed at 30 weeks. In BEAS-2B cells, the CuNi fume-induced micronuclei and caused DNA damage as measured by γ-H2AX. The fume exhibited high reactivity and a dose-response in cytotoxicity and oxidative stress. In vivo, MCA/CuNi HD and LD significantly decreased lung tumor size and adenomas. MCA/CuNi HD exposure significantly decreased gross-evaluated tumor number. In summary, the CuNi fume in vitro exhibited characteristics of a carcinogen, but in vivo, the exposure resulted in smaller tumors, fewer adenomas, less hyperplasia severity, and with HD exposure, less overall lung lesions/tumors.

Bioaerosol Exposures and Respiratory Diseases in Cannabis Workers.

PURPOSE OF REVIEW: This review investigates occupational inhalation hazards associated with biologically derived airborne particles (bioaerosols) generated in indoor cannabis cultivation and manufacturing facilities. RECENT FINDINGS: Indoor cannabis production is growing across the US as are recent reports of respiratory diseases among cannabis workers, including occupational asthma morbidity and mortality. More information is needed to understand how bioaerosol exposure in cannabis facilities impacts worker health and occupational disease risk. Preliminary studies demonstrate a significant fraction of airborne particles in cannabis facilities are comprised of fungal spores, bacteria, and plant material, which may also contain hazardous microbial metabolites and allergens. These bioaerosols may pose pathogenic, allergenic, toxigenic, and pro-inflammatory risks to workers. The absence of multi-level, holistic bioaerosol research in cannabis work environments necessitates further characterization of the potential respiratory hazards and effective risk prevention methods to safeguard occupational health as the cannabis industry continues to expand across the US and beyond.

Occupational particle exposure and chronic kidney disease: a cohort study in Swedish construction workers.

OBJECTIVES: Increasing epidemiological and experimental evidence suggests that particle exposure is an environmental risk factor for chronic kidney disease (CKD). However, only a few case-control studies have investigated this association in an occupational setting. Hence, our objective was to investigate associations between particle exposure and CKD in a large cohort of Swedish construction workers. METHODS: We performed a retrospective cohort study in the Swedish Construction Workers' Cohort, recruited 1971-1993 (n=286 089). A job-exposure matrix was used to identify workers exposed to nine different particulate exposures, which were combined into three main categories (inorganic dust and fumes, wood dust and fibres). Incident CKD and start of renal replacement therapy (RRT) were obtained from validated national registries until 2021 and analysed using adjusted Cox proportional hazards models. RESULTS: Exposure to inorganic dust and fumes was associated with an increased risk of CKD and RRT during working age (adjusted HR for CKD at age <65 years 1.15, 95% CI 1.05 to 1.26). The elevated risk did not persist after retirement age. Exposure to cement dust, concrete dust and diesel exhaust was associated with CKD. Elevated HRs were also found for quartz dust and welding fumes. CONCLUSIONS: Workers exposed to inorganic particles seem to be at elevated risk of CKD and RRT. Our results are in line with previous evidence of renal effects of ambient air pollution and warrant further efforts to reduce occupational and ambient particle exposure.

Enhancement of keratinocyte survival and migration elicited by interleukin 24 upregulation in dermal microvascular endothelium upon welding-fume exposure.

Occupational exposure to welding fumes constitutes a serious health concern. Although the effects of fumes on the respiratory tract have been investigated, few apparent reports were published on their effects on the skin. The purpose of this study was to investigate the effects of exposure to welding fumes on skin cells, focusing on interleukin-24 (IL-24), a cytokine involved in the pathophysiology of skin conditions, such as atopic dermatitis and psoriasis. Treatment with welding fumes increased IL-24 expression and production levels in human dermal microvascular endothelial cells (HDMEC) which were higher than that in normal human epidermal keratinocytes. IL-24 levels in Trolox and deferoxamine markedly suppressed welding fume-induced IL-24 expression in HDMEC, indicating that oxidative stress may be involved in this cytokine expression. IL-24 released from HDMEC protected keratinocytes from welding fume-induced damage and enhanced keratinocyte migration. Serum IL-24 was higher in welding workers than in general subjects and was positively correlated with elevated serum levels of 8-hydroxy-2'-deoxyguanosine, an oxidative stress marker. In summary, welding fumes enhanced IL-24 expression in HDMEC, stimulating keratinocyte survival and migration. IL-24 expression in endothelial cells may act as an adaptive response to welding-fume exposure in the skin.

Welding fume exposure and prevalence of chronic respiratory symptoms among welders in micro- and small-scale enterprise in Akaki Kality sub-city, Addis Ababa, Ethiopia: a comparative cross-sectional study.

BACKGROUND: Exposure to welding fumes can lead to different respiratory health disorders, including lung cancer, due to long-term exposures. In Ethiopia, large numbers of people are engaged in the welding sector. Often, these workers are exposed to welding fumes at their workplaces, however, the level of exposure and its health effects have never been studied. OBJECTIVE: To measure the level of personal welding fume exposure and assess chronic respiratory symptoms and associated factors, among micro and small-scale enterprise metal workshop workers, in Akaki Kality Sub city, Ethiopia. METHODS: A comparative cross-sectional study involving 226 welders and 217 controls. Chronic respiratory symptoms were assessed using a standardized questionnaire adopted from the American Thoracic Society (ATS). Welding fumes were collected from the welder's breathing zone using 37 mm close-faced plastic cassettes fitted with Polyvinyl Chloride (PVC) filters connected to Casella pumps at an airflow rate of 2 L/min. RESULT: The overall prevalence of chronic respiratory symptoms among welders and controls were 54 (23.9%) and 20 (9.2%) respectively. The geometric mean and geometric standard deviation (GSD) of personal welding fume exposure, among welders was 5.98 mg/m3 (± GSD = 1.54). In this study, 53.3% of the samples exceeded the Occupational Exposure Limit defined by the American Conference of Governmental Industrial Hygiene. Chronic respiratory symptoms were significantly associated with educational status (Adjusted Odds Ratio (AOR): 5.11, 95% CI: 1.35, 19.33), respiratory protective equipment use (AOR: 3.33, 95% CI: 1.52, 7.31), safety training (AOR: 2.41, 95% CI: 1.10, 5.28), smoking (AOR:3.57, 95% CI: 1.54, 8.23), welding machine maintenance (AOR: 1.87, 95% CI: 1.01, 3.59) and welding site (i.e. indoors vs. outdoor) (AOR: 6.85. 95% CI: 2.36, 19.89). CONCLUSIONS: The prevalence of chronic respiratory symptoms among welding workers was significantly higher than controls. More than half of the samples exceeded the Occupational Exposure Limit. Educational status, implementation of safety training, and welding sites were significantly associated with chronic respiratory symptoms. The results suggested a need to reduce welding fume exposure to improve the respiratory health of the workers.

Impact of welding occupation on serum aluminium level and its association with physical health, cognitive function, and quality of life: a cross-sectional study.

OBJECTIVE: There is an occupational health concern about welders' inhalation of toxic aluminium fumes. We investigated whether serum aluminium level (SAL) and demographic variables can significantly predict physical health parameters, cognition, and quality of life (QoL) among welders. METHODS: The cross-sectional study involved 100 age- and location-matched men (50 welders and 50 non-welders). SAL obtained using a graphite furnace atomic absorption spectrometer, and data collected using blood pressure and body mass index (BMI) apparatuses, biodata form, pain rating scale, General Practitioner Assessment of Cognition, WHOQoL-BREF, and Nordic musculoskeletal symptoms (MSS) questionnaire were analysed using independent samples t test, chi-square, Pearson's correlation, and hierarchical linear regression. RESULTS: Welders had significantly higher SAL (mean difference [MD] = 1.77 µg/L, p < 0.001), lower QoL (MD = 3.92, p = 0.039), and higher prevalence of MSS on the neck (χ2 = 10.187, p = 0.001), shoulder (χ2 = 9.007, p = 0.003), upper back (χ2 = 6.832, p = 0.009), and knee (χ2 = 12.190, p < 0.001) than non-welders. There was a significant bivariate association between SAL, systolic blood pressure (ß = 0.313, p = 0.002), and BMI (ß = 0.279, p = 0.005), but not pain intensity, cognition, or QoL. SAL remained a significant predictor of systolic blood pressure after adjustment for physical health and QoL parameters (ß = 0.191, p = 0.044). The association between SAL and social QoL became significant after adjustment for physical health and other QoL domains (ß = - 0.210, p = 0.032) and demographic variables (ß = - 0.233, p = 0.046). CONCLUSION: Welders had significantly higher SAL, musculoskeletal symptoms, blood pressure, and lower QoL than non-welders. SAL was associated with adverse physical health parameters and social-related QoL, not cognition. We recommend routine aluminium bioavailability and physical health checks among welders.

Risk of bladder, kidney and prostate cancer from occupational exposure to welding fumes: a systematic review and meta-analysis.

BACKGROUND: Our aimed to conduct a meta-analysis of cohort studies on risk of genitourinary (GU) cancers in workers exposed to welding fumes (WF). METHODS: We performed a systematic review of studies published on Pubmed, Scopus and Embase following PRISMA criteria. Two researchers selected cohort studies on WF exposure. From 2582 articles, 7 non-overlapping studies were included. Quality of studies was scored according to CASP. We run a random effects meta-analysis to calculate the relative risk (RR) and 95% confidence intervals (CI) of GU cancer, overall and stratified by cancer, country, and quality score. RESULTS: We included seven studies reporting results on GU cancers, including prostate, bladder and kidney cancer (PC, BC, and KC). The RR was 1.19 (95% CI = 1.07-1.32, 16 risk estimates) for GU cancer; 1.13 (95% CI = 0.90-1.42, 4 risk estimates) for PC; 1.26 (95% CI = 0.98-1.60, 7 risk estimates) for BC and 1.28 (95% CI = 1.12-1.47, 5 risk estimates) for KC. Heterogeneity was present in all meta-analyses (p < 0.001). The increased risk was more pronounced in North American than in European studies (respectively, OR = 1.35, 95% CI = 1.18-1.55; OR = 1.13, 95% CI = 1.01-1.27 p heterogeneity = 0.03). There was no heterogeneity according to quality score (p = 0.4). Data were insufficient to investigate associations by industry or welding type. Publication bias for each cancer was excluded. CONCLUSION: This meta-analysis suggests increased risk of KC and BC, but not of PC, in workers exposed to WF. Confounding by other occupational and non-occupational risk factors could not be excluded. Data were not adequate to address the risk of specific exposure circumstances.

Longitudinal changes in cardiovascular disease-related proteins in welders.

OBJECTIVE: Occupational exposure to welding fumes is linked to a higher risk of cardiovascular disease; however, the threshold exposure level is unknown. Here, we aimed to identify changes in proteins associated with cardiovascular disease in relation to exposure to welding fumes. METHODS: Data were obtained from two timepoints six years apart for 338 non-smoking men (171 welders, 167 controls); of these, 174 (78 welders, 96 controls) had measurements available at both timepoints. Exposure was measured as personal respirable dust (adjusted for personal protective equipment), welding years, and cumulative exposure. Proximity extension assays were used to measure a panel of 92 proteins involved in cardiovascular processes in serum samples. Linear mixed models were used for longitudinal analysis. The biological functions and diseases related to the identified proteins were explored using the Ingenuity Pathway Analysis software. RESULTS: At both timepoints, the median respirable dust exposure was 0.7 mg/m3 for the welders. Seven proteins were differentially abundant between the welders and controls and increased incrementally with respirable dust: FGF23, CEACAM8, CD40L, PGF, CXCL1, CD84, and HO1. CD84 was significant after adjusting for multiple comparisons. These proteins have been linked to disorders of blood pressure, damage related to clogged blood vessels, and chronic inflammatory disorders. CONCLUSION: Exposure to mild steel welding fumes below current occupational exposure limits for respirable particles and welding fumes in Europe and the US (1-5 mg/m3) was associated with changes in the abundance of proteins related to cardiovascular disease. Further research should evaluate the utility of these proteins as prospective biomarkers of occupational cardiovascular disease.

Neurological and neurobehavioral effects of welders in Egypt exposed to manganese containing welding fumes.

PURPOSE: Welders are more likely to develop neurobehavioral disorders because of their exposure to neurotoxic metals such as manganese. This study aimed to measure the neurobehavioral performance of welders occupationally exposed to manganese at welding enterprises and its relationship with the workplace environment. METHODS: It is a comparative cross-sectional study carried out on 130 welders working at 50 welding enterprises in Menoufia governorate, Egypt, compared to 130 non-occupationally exposed controls. RESULTS: It was found that the environments of the studied welding enterprises had levels of respirable dust, manganese, and total welding fumes that exceeded internationally permissible limits. In addition, the mean blood manganese levels were significantly higher among welders (4.16 ± 0.61) than the controls (1.72 ± 0.41). Welders had a significantly higher prevalence of neurological manifestations and lower performance of neurobehavioral tests. Lower neurobehavioral performance among welders was significantly correlated with increased work duration and blood levels in some tests. CONCLUSION: To lessen the fumes in the breathing zone of workers, it is therefore strongly recommended to regularly wear high-quality personal protective equipment, especially masks, and to ensure proper ventilation.

Association between exposure to metalworking fluid aerosols, occupational noise and chronic kidney disease: a cross-sectional study in China.

BACKGROUND: Chronic kidney disease (CKD) carries a high public health burden yet little is known about the relationship between metalworking fluid (MWF) aerosols, occupational noise and CKD. We aimed to explore the relationship between occupational MWF aerosols, occupational noise and CKD. METHODS: A total of 2,738 machinists were sampled from three machining companies in Wuxi, China, in 2022. We used the National Institute for Occupational Safety and Health (NIOSH) method 5524 to collect individual samples for MWF aerosols exposure, and the Chinese national standard (GBZ/T 189.8-2007) method to test individual occupational noise exposure. The diagnostic criteria for CKD were urinary albumin/creatinine ratio (UACR) of ≥ 30 mg/g and reduced renal function (eGFR < 60 mL.min- 1. 1.73 m- 2) lasting longer than 3 months. Smooth curve fitting was conducted to analyze the associations of MWF aerosols and occupational noise with CKD. A segmented regression model was used to analyze the threshold effects. RESULTS: Workers exposed to MWF aerosols (odds ratio [OR] = 2.03, 95% confidence interval [CI]: 1.21-3.41) and occupational noise (OR = 1.77, 95%CI: 1.06-2.96) had higher prevalence of CKD than nonexposed workers. A nonlinear and positive association was found between increasing MWF aerosols and occupational noise dose and the risk of CKD. When daily cumulative exposure dose of MWF aerosols exceeded 8.03 mg/m3, the OR was 1.24 (95%CI: 1.03-1.58), and when occupational noise exceeded 87.22 dB(A), the OR was 1.16 (95%CI: 1.04-1.20). In the interactive analysis between MWF aerosols and occupational noise, the workers exposed to both MWF aerosols (cumulative exposure ≥ 8.03 mg/m3-day) and occupational noise (LEX,8 h ≥ 87.22 dB(A)) had an increased prevalence of CKD (OR = 2.71, 95%CI: 1.48-4.96). MWF aerosols and occupational noise had a positive interaction in prevalence of CKD. CONCLUSIONS: Occupational MWF aerosols and noise were positively and nonlinearly associated with CKD, and cumulative MWF aerosols and noise exposure showed a positive interaction with CKD. These findings emphasize the importance of assessing kidney function of workers exposed to MWF aerosols and occupational noise. Prospective and longitudinal cohort studies are necessary to elucidate the causality of these associations.

A study of inflammatory biomarkers in crystalline silica exposed rock drillers.

BACKGROUND: Crystalline silica (CS) exposure can cause serious lung disease in humans, but mechanisms of pulmonary toxicity have not been completely elucidated. AIMS: To assess pro-inflammatory and anti-inflammatory biomarkers and biomarkers related to the development of chronic obstructive pulmonary disease and fibrosis in serum of rock drillers exposed to CS. METHODS: Rock drillers (N = 123) exposed to CS and non-specified particulate matter (PM) were compared to 48 referents without current or past exposure to PM in a cross-sectional study. RESULTS: The rock drillers had been exposed to CS for 10.7 years on average. Geometric mean (GM) current exposure was estimated to 36 µg/m3. Their GM concentration of matrix metalloproteinase 12 (MMP-12) was significantly higher (16 vs. 13 ng/L; p = 0.04), while interleukin (IL) 6 and IL-8 were significantly lower compared to the referents. Also pentraxin 3 was significantly lower (3558 vs. 4592 ng/L; p = 0.01) in the rock drillers. A dose-response relationship was observed between cumulative exposure to CS and MMP-12, the highest exposed subgroup having significantly higher MMP-12 concentrations than the referents. CONCLUSION: Exposure to CS may increase circulating MMP-12 concentrations in a dose-response related fashion. The results may also suggest a down-regulation of pro-inflammatory pathways.

Exposure to occupational air pollution and vascular endothelial dysfunction in workers of the steel industry in Iran.

Air pollution is recognized as a risk factor for cardiovascular diseases; however, the precise underlying mechanisms remain unclear. This study investigated the impact of occupational air pollution exposure on endothelial function in workers within the steel industry. Specifically, we examined male employees in the coke-making division of the Isfahan Steel Company in Iran, as well as those in administrative roles with no known history of cardiovascular risk. Data on age, body mass index, duration of employment, blood pressure, fasting blood sugar, and lipid profile were collected. To assess endothelial function, flow-mediated dilation (FMD) was measured. The baseline brachial artery diameter was greater (mean difference [95% CI] = 0.068 mm [0.008 to 0.128]), while the FMD was lower (mean difference [95% CI] = -0.908 % [-1.740 to -0.075]) in the coke-making group than in the control group. After controlling for potential confounding variables, it was observed that working in the coke-making sector of the industry was associated with lower FMD (F = 3.954, p = .049). These findings indicated that occupational air pollution exposure among workers in the steel industry is linked to impaired endothelium-dependent vasodilation.

Assessing lifetime occupational chrysotile inhalation exposure, respiratory symptoms, and lung cancer risk among brake maintenance workers in Malaysia.

This study aimed to estimate workers' occupational lifetime exposure to chrysotile and examine the respiratory symptoms and lung cancer risk. A total of 112 workers were interviewed about their occupational histories. Exposure modeling using information on the determinants of exposure was used to estimate chrysotile emissions. The cumulative lifetime exposure was then assessed for each worker. Respiratory symptoms were obtained using a validated questionnaire. Lung cancer mortality rate was also predicted using a model. Almost all the workers were male and young (mean age = 30 years, SD = 7). The estimated lifetime occupational chrysotile inhalation exposure ranged from 0.0001 to 0.0486 f/mL.years (median = 0.0018 f/mL.years, IQR = 0.486). A high prevalence of cough symptom (11.7%), and low estimated cancer risk (<1%) were reported. In conclusion, the lung cancer risk among our cohort of workers was at a low level because of lower cumulative lifetime occupational chrysotile exposure.

Alterations to biomarkers related to long-term exposure to diesel exhaust at concentrations below occupational exposure limits in the European Union and the USA.

BACKGROUND: We previously found that occupational exposure to diesel engine exhaust (DEE) was associated with alterations to 19 biomarkers that potentially reflect the mechanisms of carcinogenesis. Whether DEE is associated with biological alterations at concentrations under existing or recommended occupational exposure limits (OELs) is unclear. METHODS: In a cross-sectional study of 54 factory workers exposed long-term to DEE and 55 unexposed controls, we reanalysed the 19 previously identified biomarkers. Multivariable linear regression was used to compare biomarker levels between DEE-exposed versus unexposed subjects and to assess elemental carbon (EC) exposure-response relationships, adjusted for age and smoking status. We analysed each biomarker at EC concentrations below the US Mine Safety and Health Administration (MSHA) OEL (<106 µg/m3), below the European Union (EU) OEL (<50 µg/m3) and below the American Conference of Governmental Industrial Hygienists (ACGIH) recommendation (<20 µg/m3). RESULTS: Below the MSHA OEL, 17 biomarkers were altered between DEE-exposed workers and unexposed controls. Below the EU OEL, DEE-exposed workers had elevated lymphocytes (p=9E-03, false discovery rate (FDR)=0.04), CD4+ count (p=0.02, FDR=0.05), CD8+ count (p=5E-03, FDR=0.03) and miR-92a-3p (p=0.02, FDR=0.05), and nasal turbinate gene expression (first principal component: p=1E-06, FDR=2E-05), as well as decreased C-reactive protein (p=0.02, FDR=0.05), macrophage inflammatory protein-1ß (p=0.04, FDR=0.09), miR-423-3p (p=0.04, FDR=0.09) and miR-122-5p (p=2E-03, FDR=0.02). Even at EC concentrations under the ACGIH recommendation, we found some evidence of exposure-response relationships for miR-423-3p (ptrend=0.01, FDR=0.19) and gene expression (ptrend=0.02, FDR=0.19). CONCLUSIONS: DEE exposure under existing or recommended OELs may be associated with biomarkers reflective of cancer-related processes, including inflammatory/immune response.

[Current status and research progress of occupational health monitoring in welding fume operations].

Welding operations are widely present in the manufacturing production process, involving a large number of occupational groups, and are the key occupations where work injuries and occupational diseases occur in China. For different welding processes and welding materials, the content and focus of occupational health monitoring are different. At present, the item of occupational health examination in welding operation is in poor consistency with the on-site exposure of occupational hazard factors, and it is mainly concentrated in the stage of disease development, which can not reflect the early health damage caused by welding dust exposure in time. The emergence of biomarkers of welding dust can make up for this defect. Therefore, it is of great significance to describe the current situation of occupational health monitoring of welding dust and summarize the research progress of related biomarkers for the early prevention of diseases caused by welding dust and the practice of occupational health monitoring.

Lifetime Exposure to Welding Fumes and Risk of Some Rare Cancers.

We investigated the association between exposure to welding fumes and the risk of biliary tract, male breast, bone, and thymus cancer, as well as cancer of the small intestine, eye melanoma, and mycosis fungoides, among men in a European, multicenter case-control study. From 1995-1997, 644 cases and 1,959 control subjects from 7 countries were studied with respect to information on welding and potential confounders. We linked the welding histories of the participants with a measurement-based exposure matrix to calculate lifetime exposure to welding fumes. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression models, conditional on country and 5-year age groups, and adjusted for education and relevant confounders. Regular welding was associated with an increased risk of cancer of the small intestine (OR = 2.30, 95% CI: 1.17, 4.50). Lifetime exposure to welding fumes above the median of exposed controls was associated with an increased risk of cancer of the small intestine (OR = 2.00, 95% CI: 1.07, 3.72) and male breast (OR = 2.07, 95% CI: 1.14, 3.77), and some elevation in risk was apparent for bone cancer (OR = 1.92, 95% CI: 0.85, 4.34) with increasing lifetime exposure to welding fumes. Welding fumes could contribute to an increased risk of some rare cancers.

Genotoxicity biomarkers in car repair workers from Barranquilla, a Colombian Caribbean City.

Exposure to chemicals and particles generated in automotive repair shops is a common and underestimated problem. The objective of this study was to assess the genotoxic status of auto repair workers with (1) a questionnaire to gather sociodemographic information and self-reported exposure to hazardous chemicals and (2) measurement of various biochemical parameters. Blood and oral mucosa samples were collected from 174 male volunteers from Barranquilla, Colombia, aged 18-55 years: 87 were active car repairmen and 87 were individuals with no known exposure to hazardous chemicals. Peripheral blood lymphocytes were collected for the comet and cytokinesis-blocking micronucleus (CBMN) assays, while oral mucosal epithelium extracted to quantify micronucleated cells (MNC). DNA was extracted to assess polymorphisms in the DNA repair (XRCC1) and metabolism-related genes (GSTT1 and GSTM1) using PCR-RFLP. DNA damage and frequency of micronuclei (MN) in lymphocytes and oral mucosa were significantly higher in exposed compared to control group. In both groups genotypes and allelic variants for XRCC1 and GSTT1 met the Hardy-Weinberg equilibrium (HWE). In contrast, GSTM1 deviated from HWE. In the exposed group genotypic variants were not correlated with DNA damage or MN presence in cells. DNA damage and occurrence of MN in mucosa and lymphocytes correlated with age and time of service (occupational exposure ≥ 3 years). In summary, workers in car repair shops exhibited genotoxic effects depending upon exposure duration in the workplace which occurred independent of DNA repair XRCC1 gene and metabolism genes GSTT1 and GSTM1. Date demonstrate that health authorities improve air quality in auto repair facilities to avoid occupational DNA damage.

Endotyping asthma related to 3 different work exposures.

BACKGROUND: Work exposures play a significant role in adult-onset asthma, but the mechanisms of work-related asthma are not fully elucidated. OBJECTIVE: We aimed to reveal the molecular mechanisms of work-related asthma associated with exposure to flour (flour asthma), isocyanate (isocyanate asthma), or welding fumes (welding asthma) and identify potential biomarkers that distinguish these groups from each other. METHODS: We used a combination of clinical tests, transcriptomic analysis, and associated pathway analyses to investigate the underlying disease mechanisms of the blood immune cells and the airway epithelium of 61 men. RESULTS: Compared with the healthy controls, the welding asthma patients had more differentially expressed genes than the flour asthma and isocyanate asthma patients, both in the airway epithelia and in the blood immune cells. In the airway epithelia, active inflammation was detected only in welding asthma patients. In contrast, many differentially expressed genes were detected in blood cells in all 3 asthma groups. Disease-related immune functions in blood cells, including leukocyte migration and inflammatory responses, and decreased expression of upstream cytokines such as TNF and IFN-γ were suppressed in all the asthma groups. In transcriptome-phenotype correlations, hyperresponsiveness (R ∼ |0.6|) had the highest clinical relevance and was associated with a set of exposure group-specific genes. Finally, biomarker subsets of only 5 genes specifically distinguished each of the asthma exposure groups. CONCLUSIONS: This study provides novel data on the molecular mechanisms underlying work-related asthma. We identified a set of 5 promising biomarkers in asthma related to flour, isocyanate, and welding fume exposure to be tested and clinically validated in future studies.

Bisphenol A at a human exposed level can promote epithelial-mesenchymal transition in papillary thyroid carcinoma harbouring BRAFV600E mutation.

Bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical, alters the function of endocrine system and enhances the susceptibility to tumorigenesis in several hormone-dependent tumours as thyroid carcinoma. About 50% of papillary thyroid cancers (PTC), the most common type of thyroid malignancy, harbours the BRAFV600E mutation. This study aimed to investigate a potential combined effect of BPA exposure and BRAFV600E mutation on epithelial-mesenchymal transition (EMT) in PTC. Firstly, the level of BPA in plasma, the evaluation of BRAFV600E mutation and the level of EMT-related proteins in PTC samples were individually determined. Additionally, the migration, invasion, colony formation capacity and the expression of EMT-related proteins after exposure to BPA were precisely analysed in vitro thyroid cells genetically modified by the introduction of BRAFV600E mutation. Moreover, ERK-Cox2 signalling pathway was also introduced to explore the possible mechanism in PTC development. As expected, whether the clinical investigation or cultured thyroid cells demonstrated that BPA at a concentration compatible with human exposed levels (10-7  M) synergized with the BRAFV600E mutation promoted EMT via the activation of ERK-Cox2 signalling pathway. Our findings offer some evidence that BPA as an environmental risk factor can facilitate the progression of PTC harbouring BRAFV600E mutation.

Aerosols, airflow, and airspace contamination during laparoscopy.

Laparoscopic surgery has been undermined throughout the COVID-19 pandemic by concerns that it may generate an infectious risk to the operating team through aerosolization of peritoneal particles. There is anyway a need for increased awareness and understanding of the occupational hazard for surgical teams regarding unfiltered escape of pollutants generated by surgical smoke and other microbials. Here, the aerosol-generating nature of this access modality was confirmed through repeatable real-time methodology both qualitatively and quantitively to inform best practice and additional engineering solutions to optimize the operating room environment.

Laparoscopic surgery has been undermined throughout the COVID-19 pandemic by concerns that it may generate an infectious risk to the operating team through aerosolization of peritoneal particles. There is anyway a need for increased awareness and understanding of the occupational hazard for surgical teams regarding unfiltered escape of pollutants generated by surgical smoke and other microbials. Here, the aerosol-generating nature of this access modality was confirmed through repeatable real-time methodology both qualitatively and quantitively to inform best practice and additional engineering solutions to optimize the operating room environment.