TERT-independent telomere elongation and shelterin dysregulation after pulmonary exposure to stainless-steel welding fume in-vivo.

Telomeres are inert DNA sequences (TTAGGG) at the end of chromosomes that protect genetic information and maintain DNA integrity. Emerging evidence has demonstrated that telomere alteration can be closely related to occupational exposure and the development of various disease conditions, including cancer. However, the functions and underlying molecular mechanisms of telomere alteration and shelterin dysregulation after welding fume exposures have not been broadly defined. In this study, we analyzed telomere length and shelterin complex proteins in peripheral blood mononuclear cells (PBMCs) and in lung tissue recovered from male Sprague-Dawley rats following exposure by intratracheal instillation (ITI) to 2 mg/rat of manual metal arc-stainless steel (MMA-SS) welding fume particulate or saline (vehicle control). PBMCs and lung tissue were harvested at 30 d after instillation. Our study identified telomere elongation and shelterin dysregulation in PBMCs and lung tissue after welding fume exposure. Mechanistically, telomere elongation was independent of telomerase reverse transcriptase (TERT) activation. Collectively, our findings demonstrated that welding fume-induced telomere elongation was (a) TERT-independent and (b) associated with shelterin complex dysregulation. It is possible that an alteration of telomere length and its regulatory proteins may be utilized as predictive biomarkers for various disease conditions after welding fume exposure. This needs further investigation.

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.

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.

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.

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.

In vitro evaluation of the toxicological effects of cooking oil fumes using a self-designed microfluidic chip.

Cooking oil fumes (COFs) are widely acknowledged as substantial contributors to indoor air pollution, having detrimental effects on human health. Despite the existence of commercialized in vitro aerosol exposure platforms, assessment risks of aerosol pollutants are primarily evaluated based on multiwell plate experiments by trapping and redissolving aerosols to conduct comprehensive in vitro immersion exposure manner. Therefore, an innovative real-time exposure system for COF aerosol was constructed, featuring a self-designed microfluidic chip as its focal component. The chip was used to assess toxicological effects of in vitro exposure to COF aerosol on cells cultured at the gas-liquid interface. Meanwhile, we used transcriptomics to analyze genes that exhibited differential expression in cells induced by COF aerosol. The findings indicated that the MAPK signaling pathway, known for its involvement in inflammatory response and oxidative stress, played a crucial role in the biological effects induced by COF aerosol. Biomarkers associated with inflammatory response and oxidative stress exhibited corresponding alterations. Furthermore, the concentration of COF aerosol exposure and post-exposure duration exert decisive effects on these biomarkers. Thus, the study suggests that COF can induce oxidative stress and inflammatory response in BEAS-2B cells, potentially exerting a discernible impact on human health.

Fishermen and the Risk of Toxic Fumes from the Fish Storage Tanks.

Haroon H, Naik SB. Fishermen and the Risk of Toxic Fumes from the Fish Storage Tanks. Indian J Crit Care Med 2024;28(3):307-308.

Where there are fumes, there may be lung cancer: a systematic review on the association between exposure to cooking fumes and the risk of lung cancer in never-smokers.

PURPOSE: Lung cancer in never-smokers (LCINS) is the seventh leading cause of cancer, and exposure to cooking fumes has recently emerged as a potential risk factor. This systematic review is the first to summarize and evaluate the relationship between exposure to cooking fumes and the risk of LCINS. METHODS: This study conducted an online literature search of PubMed, CINAHL, and PsychInfo databases. Inclusion criteria were original research articles published in English, that assessed the relationship between exposure to cooking fumes and the risk of lung cancer between 1 January 2012 and 6 December 2022, and that included never-smokers. RESULTS: Thirteen case-control studies and three prospective cohort studies, focusing mostly on women with LCINS, met the inclusion criteria. Seven case-control studies reported an association between exposure to cooking oil fumes and an increased risk of LCINS. Two case-control studies found that using a fume extractor was associated with a decreased risk of LCINS. In other case-control studies, coal use was linked to an increased risk of LCINS, and participants who did not use a ventilator in their kitchens had a higher risk for LCINS. Poor ventilation [Adjusted Hazard Ratio (AHR) = 1.49; 95% CI: 1.15, 1.95] and poor ventilation in combination with coal use (AHR = 2.03; 95% CI: 1.35, 3.05) were associated with an increased risk for LCINS in one prospective cohort study. CONCLUSION: The evidence reviewed underscores the need to develop culturally-tailored interventions that improve access to affordable and clean fuel through engaging relevant stakeholders.

Health consequences of exposure to aircraft contaminated air and fume events: a narrative review and medical protocol for the investigation of exposed aircrew and passengers.

Thermally degraded engine oil and hydraulic fluid fumes contaminating aircraft cabin air conditioning systems have been well documented since the 1950s. Whilst organophosphates have been the main subject of interest, oil and hydraulic fumes in the air supply also contain ultrafine particles, numerous volatile organic hydrocarbons and thermally degraded products. We review the literature on the effects of fume events on aircrew health. Inhalation of these potentially toxic fumes is increasingly recognised to cause acute and long-term neurological, respiratory, cardiological and other symptoms. Cumulative exposure to regular small doses of toxic fumes is potentially damaging to health and may be exacerbated by a single higher-level exposure. Assessment is complex because of the limitations of considering the toxicity of individual substances in complex heated mixtures.There is a need for a systematic and consistent approach to diagnosis and treatment of persons who have been exposed to toxic fumes in aircraft cabins. The medical protocol presented in this paper has been written by internationally recognised experts and presents a consensus approach to the recognition, investigation and management of persons suffering from the toxic effects of inhaling thermally degraded engine oil and other fluids contaminating the air conditioning systems in aircraft, and includes actions and investigations for in-flight, immediately post-flight and late subsequent follow up.

Compositional variations in metal nanoparticle components of welding fumes impact lung epithelial cell toxicity.

Welding fumes contain harmful metals and gas by-products associated with development of lung dysfunction, asthma, bronchitis, and lung cancer. Two prominent welding fume particulate metal components are nanosized iron (Fe) and manganese (Mn) which might induce oxidative stress and inflammation resulting in pulmonary injury. Welding fume toxicity may be dependent upon metal nanoparticle (NP) components. To examine toxicity of welding fume NP components, a system was constructed for controlled and continuous NP generation from commercial welding and customized electrodes with varying proportions of Fe and Mn. Aerosols generated consisted of nanosized particles and were compositionally consistent with each electrode. Human alveolar lung A459 epithelial cells were exposed to freshly generated metal NP mixtures at a target concentration of 100 µg/m3 for 6 hr and then harvested for assessment of cytotoxicity, generation of reactive oxygen species (ROS), and alterations in the expression of genes and proteins involved in metal regulation, inflammatory responses, and oxidative stress. Aerosol exposures decreased cell viability and induced increased ROS production. Assessment of gene expression demonstrated variable up-regulation in cellular mechanisms related to metal transport and storage, inflammation, and oxidative stress based upon aerosol composition. Specifically, interleukin-8 (IL-8) demonstrated the most robust changes in both transcriptional and protein levels after exposure. Interleukin-8 has been determined to serve as a primary cytokine mediating inflammatory responses induced by welding fume exposures in alveolar epithelial cells. Overall, this study demonstrated variations in cellular responses to metal NP mixtures suggesting compositional variations in NP content within welding fumes may influence inhalation toxicity.

Synergistic Effect of Reactive Oxygen Species in Photothermocatalytic Removal of VOCs from Cooking Oil Fumes over Pt/CeO2/TiO2.

The volatile organic compounds (VOCs) from cooking oil fumes are very complex and do harm to humans and the environment. Herein, we develop the high-efficiency and energy-saving synergistic photothermocatalytic oxidation approach to eliminate the mixture of heptane and hexanal, the representative VOCs with high concentrations in cooking oil fumes. The Pt/CeO2/TiO2 catalyst with nanosized Pt particles was prepared by the simple hydrothermal and impregnation methods, and the physicochemical properties of the catalyst were measured using numerous techniques. The Pt/CeO2/TiO2 catalyst eliminated the VOC mixture at low light intensity (100 mW cm-2) and low temperature (200 °C). In addition, it showed 25 h of catalytic stability and water resistance (water concentration up to 20 vol %) at 140 or 190 °C. It is concluded that O2 picked up the electrons from Pt to generate the •O2- species, which were transformed to the O22- and O- species after the rise in temperature. In the presence of water, the •OH species induced by light irradiation on the catalyst surface and the •OOH species formed via the thermal reaction were both supplementary oxygen species for VOC oxidation. The synergistic interaction of photo- and thermocatalysis was generated by the reactive oxygen species.

Oxidative stress and DNA damage resulting from welding fumes exposure among professional welders: A systematic review and meta-analysis.

The present systematic review aimed to evaluate the associations between welding fumes exposure and changes in oxidative stress [superoxide dismutase (SOD) and malondialdehyde (MDA)] and DNA damage [8-hydroxy-2'-deoxyguanosine (8-OHdG) and DNA-protein crosslink (DPC)] markers in professional welders (PROSPERO CRD42022298115). Six electronic bibliographic databases were searched from inception through September 2021 to identify observational epidemiological studies evaluating the association between welding fumes exposures and changes in oxidative stress and DNA damage in professional welders. Two reviewers independently assessed the risk of bias and certainty of the evidence. A narrative synthesis of results was conducted using the Synthesis Without Meta-analysis (SWiM) method. Pooled mean differences with 95% confidence intervals were calculated in a random-effects meta-analysis for the outcomes of interest in the review. From 450 studies identified through the search strategy, 14 observational epidemiological studies were included in the review. Most studies reported significantly higher welding fumes levels in welders than in controls. The narrative synthesis results of SOD showed a significant difference between welders and controls, while the meta-analysis results of MDA did not show a significant difference between the studied groups (MD = 0.26; 95% CI, -0.03, 0.55). The meta-analysis results of 8-OHdG (MD = 9.38; 95% CI, 0.55-18.21) and DPC (MD = 1.07; 95% CI, 0.14-2) revealed significantly differences between the studied groups. The included studies were at high risk of exclusion and confounding bias. The certainty of the evidence for oxidative stress and DNA damage results were very low and moderate, respectively. Exposure to welding fumes and metal particles is associated with DNA damage in professional welders, and 8-OHdG and DPC might be considered reliable markers to assess DNA damage resulting from exposure to welding fumes. We recommend, however, that the evaluation of oxidative stress resulting from welding fumes exposure not be solely based on MDA and SOD.

Short-term associations between barbecue fumes and respiratory health in young adults.

BACKGROUND: Epidemiological studies have associated biomass combustion with (respiratory) morbidity and mortality, primarily in indoor settings. Barbecuing results in high outdoor air pollution exposures, but the health effects are unknown. OBJECTIVE: The objective was to investigate short-term changes in respiratory health in healthy adults, associated with exposure to barbecue fumes. METHODS: 16 healthy, adult volunteers were exposed to barbecue smoke in outdoor air in rest during 1.5 h, using a repeated-measures design. Major air pollutants were monitored on-site, including particulate matter <2.5 µm (PM2.5), particle number concentrations (PNC) and black- and brown carbon. At the same place and time-of-day, subjects participated in a control session, during which they were not exposed to barbecue smoke. Before and immediately after all sessions lung function was measured. Before, immediately after, 4- and 18 h post-sessions nasal expression levels of interleukin (IL)-8, IL6 and Tumor Necrosis Factor alpha (TNFα) were determined in nasal swabs, using quantitative polymerase chain reaction. Associations between major air pollutants, lung function and inflammatory markers were assessed using mixed linear regression models. RESULTS: High PM2.5 levels and PNCs were observed during barbecue sessions, with averages ranging from 553 to 1062 µg/m3 and 109,000-463,000 pt/cm3, respectively. Average black- and brown carbon levels ranged between 4.1-13.0 and 5.0-16.2 µg/m3. A 1000 µg/m3 increase in PM2.5 was associated with 2.37 (0.97, 4.67) and 2.21 (0.98, 5.00) times higher expression of IL8, immediately- and 18 h after exposure. No associations were found between air pollutants and lung function, or the expression of IL6 or TNFα. DISCUSSION: Short-term exposure to air pollutants emitted from barbecuing was associated with a mild respiratory response in healthy young adults, including prolonged increase in nasal IL8 without a change in lung function and other measured inflammatory markers. The results might indicate prolonged respiratory inflammation, due to short-term exposure to barbecue fumes.

Organic pollutant exposure and health effects of cooking emissions on kitchen staff in food services.

This study was conducted to determine the exposure and health risk to cooking fumes of a total of 88 volunteer kitchen staff aged between 18 and 65 years working in five different kitchens in Ankara. Gas- and particle-phase polycyclic aromatic hydrocarbons (PAHs), and volatile organic compound (VOCs) concentrations were evaluated in the indoor air of 5 kitchens. Serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels were analyzed to determine the oxidative damage as a result of the exposure to cooking fumes among the cooks and waiters. Significant positive relationships were found between serum MDA levels of the hot kitchen workers and indoor chrysene (Chr), indeno(1,2,3-c,d)pyrene (Ind), and total VOC levels. Although the carcinogenic risks estimated for the exposed population were between the acceptable/tolerable levels, the hazard quotient (HQ) estimated for the exposure to indoor benzene exceeded the safe level. The results of the study revealed that exposure to organic pollutants in indoor air may be a risk factor for the development of oxidative stress, especially in hot kitchen workers. The importance of efficient ventilation in the kitchen has been pointed out to reduce health risks caused by cooking fumes.

Metformin antagonizes nickel-refining fumes-induced cell pyroptosis via Nrf2/GOLPH3 pathway in vitro and in vivo.

Nickel compounds, an international carcinogen in the industrial environment, increased the risk of lung inflammation even lung cancer in Ni refinery workers. Metformin has displayed the intense anti-inflammation and anti-cancer properties through regulating pyroptosis. This study was designed to explore whether Nickel-refining fumes (NiRF) can induce cell pyroptosis and how AMPK/CREB/Nrf2 mediated the protection afforded by metformin against Ni particles-induced lung impairment. Our results represented that Ni fumes exposure evoked pyroptosis via GOLPH3 and induced oxidative stress, while, metformin treatment alleviated Ni particles-mediated above changes. Moreover, nuclear factor erythroid 2-related factor 2 (Nrf2) involved in the protection of metformin, and the deficiency of Nrf2 attenuated the beneficial protection. We also determined that Nrf2 was a downstream molecule of AMPK/CREB pathway. Furthermore, male C57BL/6 mice were administered with Ni at a dose of 2 mg/kg by non-exposed endotracheal instillation and metformin (100, 200 and 300 mg/kg) via oral gavage for 4 weeks. The results indicated that NiRF promoted GOLPH3 and pyroptosis by stimulating NLRP3, caspase-1, N-GSDMD, IL-18 and IL-1ß expression. However, various doses of metformin reduced GOLPH3 and the above protein levels of pyroptosis, also improved AMPK/CREB/Nrf2 expression. In summary, we found that metformin suppressed NiRF-connected GOLPH3-prompted pyroptosis via AMPK/CREB/Nrf2 signaling pathway to confer pulmonary protection.

Metformin alleviates nickel-refining fumes-induced aerobic glycolysis via AMPK/GOLPH3 pathway in vitro and in vivo.

Nickel (Ni) compounds is recognized industrial carcinogen, which could increase the risk of lung cancer in Ni refineries workers. However, the underlying carcinogenic mechanism still remains to elucidate. Metformin has shown the anticancer properties through suppressing aerobic glycolysis. In the present study, we evaluated the effect of Ni-refining fumes exposure on aerobic glycolysis and the role of AMPK/GOLPH3, as well as how metformin alleviated nickel-induced aerobic glycolysis in vitro and vivo. Firstly, Beas-2B cells were exposed to different concentrations of Ni-refining fumes and pretreated with metformin (activation of AMPK), compound C (AMPK inhibitor) in vitro. Our findings indicated that Ni fumes expose evoked aerobic glycolysis by AMPK/GOLPH3, while metformin attenuated Ni particles-promoted GOLPH3-mediated aerobic glycolysis by p-AMPK expression increase. Then Mito-TEMPT (a mitochondria-targeted antioxidant) and lipopolysaccharide (LPS, ROS activator) were pretreated to affect ROS production in Beas-2B cells. Ni-induced ROS prevented AMPK activation. Moreover, C57BL/6 mice were exposed to 2 mg/kg Ni by non-exposed endotracheal instillation and metformin (100, 200 and 300 mg/kg) via oral gavage for 4 weeks. The effects of AMPK/GOLPH3 axis on Ni-induced aerobic glycolysis were assessed. The results indicated that metformin decreased the protein levels of GOLPH3, LDHA, HK2, MCT-4 and improved p-AMPK expression. Thus, our findings demonstrated metformin antagonized Ni-refining fumes-caused aerobic glycolysis via AMPK/GOLPH3.

The toxicity of cooking oil fumes on human bronchial epithelial cells through ROS-mediated MAPK, NF-κB signaling pathways and NLRP3 inflammasome.

Cooking oil fumes (COFs) are the main pollutants in kitchen and indoor air, which threaten human health. Exposure to COFs may lead to respiratory diseases and impair pulmonary function. To investigate the toxicity of COFs on human bronchial epithelial cells (Beas-2B) and explore the underlying mechanisms, MTT assay was conducted to detect the viability of Beas-2B. Intracellular reactive oxygen species (ROS) levels and nitric oxide (NO) levels were determined with DCFH-DA assay and DAF-FM assay. The expression of genes involved in inflammation were measured with quantitative real-time PCR (qRT-PCR). The phosphorylation and the expression of proteins related to Mitogen-activated protein kinase (MAPK), NF-κB signaling pathways were measured with western blot. Our results revealed that COFs decreased cell viability, increased the ROS levels and NO levels and induced apoptosis in Beas-2B cells. The results of qRT-PCR and western blot showed that the expression of NLRP3, p65, iNOS, IL-1ß, and the factors related to oxidative stress and inflammation increased, NF-κB signaling pathway and MAPK signaling pathway were activated. This study provided some useful information to evaluate the toxicity of COFs and revealed the possible mechanism for the damage on respiratory system induced by COFs.

Respiratory health disorders among workers in some Egyptian welding enterprises.

Welding fumes contain a complex mixture of metallic oxides that pose a risk to welders' respiratory systems. This study aimed to evaluate respiratory health disorders among workers in some Egyptian welding enterprises and their relationship to the workplace environment. This research was performed from January 1st, 2019 to February 28th, 2021 in welding enterprises in Birket El-Sabaa, a randomly selected district of Menoufia governorate, Egypt. A cross-sectional comparative study was conducted on 110 welders and 110 non-occupationally exposed subjects. Environmental studies were carried out for total welding fumes, respirable dust, and manganese air levels. Spirometric measures and manganese levels in whole blood were applied. Analysis of the personal air samples revealed that the mean values of welding fumes, respirable dust, and manganese air levels were higher than the international permissible levels. Welders had a higher significant prevalence of respiratory manifestations (rhinitis, cough, expectoration, wheezes, dyspnea, and chronic bronchitis) as well as decreased spirometric measures (FVC%, FEV1%, FEV1/FVC%, and FEF25-75%) than controls. The mean value of whole blood manganese level was statistically significantly higher among welders than that of the controls (3.35 ± 0.5 and 1.81 ± 0.79 ng/mL; respectively). A significant relationship was reported between longer work time and the prevalence of respiratory manifestations and decreased spirometric measurements. The use of masks/respirators was associated with a reduced prevalence of respiratory manifestations. Finally, welders that are exposed to welding fumes at concentrations higher than the permissible levels in welding establishments suffer from adverse respiratory problems, as shown by increased prevalence of respiratory manifestations and lower spirometric measurements. Regular use of high-quality personal protective equipment, especially masks, as well as periodic medical examinations for welders, is highly urged.

Welding Fume Instillation in Isolated Perfused Mouse Lungs-Effects of Zinc- and Copper-Containing Welding Fumes.

Zinc- and copper-containing welding fumes can cause systemic inflammation after exposure in humans. Recent ex vivo studies have shown that the observed inflammation originates from exposed immune cells. In vitro studies identified the soluble fraction of metal particles as the main effectors. Isolated perfused mouse lungs (IPLs) were perfused and ventilated for 270 min. Lungs were instilled with saline solution (control), welding fume particle suspension (WFs) or the soluble fraction of the welding fumes (SF-WFs). Bronchoalveolar lavage fluid (BALF) and perfusate samples were analyzed for cytokine levels and lung tissue mRNA expression levels were analyzed via RT-PCR. All lungs instilled with WFs did not complete the experiments due to a fatal reduction in tidal volume. Accordingly, IL-6 and MPO levels were significantly higher in BALF of WF lungs compared to the control. IL-6 and MPO mRNA expression levels were also increased for WFs. Lungs instilled with SF-WFs only showed mild reactions in tidal volume, with BALF and mRNA expression levels not significantly differing from the control. Zinc- and copper-containing welding fume particles adversely affect IPLs when instilled, as evidenced by the fatal loss in tidal volume and increased cytokine expression and secretion. The effects are mainly caused by the particles, not by the soluble fraction.

Sample Preparation and Analytical Methods for Identifying Organic Compounds in Bituminous Emissions.

Bitumen is a major construction material that can emit harmful fumes when heated. These fumes pose health risks to workers and communities near construction projects or asphalt mixing plants. The chemical complexity of bitumen fumes and the increasing use of additives add to the difficulty of analytically quantifying the harmful chemicals emitted using a single technique. Research on bitumen emissions consists of numerous sample preparation and analytical methods. There are a range of considerations to be made when deciding on an appropriate sample preparation method and instrumental configuration to optimise the analysis of specific organic contaminants in emissions. Researchers investigating emissions from bituminous materials may need to consider a range of analytical techniques to quantify harmful chemicals and assess the efficacy of new additives. This review summarises the primary methodologies for sample preparation and analytical techniques used in bitumen research and discusses future challenges and solutions.