RESUMEN
Gaseous and semi-volatile organic compounds emitted by the transport sector contribute to air pollution and have adverse effects on human health. To reduce harmful effects to the environment as well as to humans, renewable and sustainable bio-hybrid fuels are explored and investigated in the cluster of excellence "The Fuel Science Center" at RWTH Aachen University. However, data on the effects of bio-hybrid fuels on human health is scarce, leaving a data gap regarding their hazard potential. To help close this data gap, this study investigates potential toxic effects of a Ketone-Ester-Alcohol-Alkane (KEAA) fuel blend on A549 human lung cells. Experiments were performed using a commercially available air-liquid interface exposure system which was optimized beforehand. Then, cells were exposed at the air-liquid interface to 50-2000 ppm C3.7 of gaseous KEAA for 1 h. After a 24 h recovery period in the incubator, cells treated with 500 ppm C3.7 KEAA showed significant lower metabolic activity and cells treated with 50, 250, 500 and 1000 ppm C3.7 KEAA showed significant higher cytotoxicity compared to controls. Our data support the international occupational exposure limits of the single KEAA constituents. This finding applies only to the exposure scenario tested in this study and is difficult to extrapolate to the complex in vivo situation.
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Pulmón , Humanos , Células A549 , Pulmón/citología , Pulmón/efectos de los fármacos , Pulmón/metabolismo , Biocombustibles , Supervivencia Celular/efectos de los fármacos , Gases/toxicidad , Compuestos Orgánicos Volátiles/toxicidad , Alcanos , Contaminantes Atmosféricos/toxicidadRESUMEN
Food waste is a routine and increasingly growing global concern that has drawn significant attention from policymakers, climate change activists and health practitioners. Amid the plurality of discourses on food waste-health linkages, however, the health risks from food waste induced emissions have remained under explored. This lack of evidence is partly because of the lack of complete understanding of the effects of food waste emissions from household food waste on human health either directly through physiological mechanisms or indirectly through environmental exposure effects. Thus, this systematic review contributes to the literature by synthesizing available evidence to highlight gaps and offers a comprehensive baseline inventory of food waste emissions and their associated impacts on human health to support public health decision-making. Four database searches: Web of Science, OVID(Medline), EMBASE, and Scopus, were searched from inception to 3 May 2023. Pairs of reviewers screened 2189 potentially eligible studies that addressed food waste emissions from consumers and how the emissions related to human health. Following PRISMA guidelines, 26 articles were eligible for data extraction for the systematic review. Findings indicate that emissions from food waste, such as hydrogen sulphide, ammonia, and volatile organic carbons, can affect human endocrine, respiratory, nervous, and olfactory systems. The severity of the human health effects depends on the gaseous concentration, but range from mild lung irritation to cancer and death. This study recommends emission capture technologies, food diversion programs, and biogas technologies to reduce food waste emissions.
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Alimento Perdido y Desperdiciado , Humanos , Exposición a Riesgos Ambientales/efectos adversos , Alimento Perdido y Desperdiciado/efectos adversos , Gases/toxicidadRESUMEN
Toxic gases can be fatal as they damage many living tissues, especially the nervous and respiratory systems. They can cause permanent damage for many years by harming environmental tissue and living organisms. They can also cause mass deaths when used as chemical weapons. These chemical agents consist of organophosphates, namely ester, amide, or thiol derivatives of phosphorus, phosphonic or phosphinic acids, or can be synthesized independently. In this study, machine learning models were used to predict the toxicity of chemical gases. Toxic and non-toxic gases, consisting of 144 gases, were identified according to the United States Environmental Protection Agency, Occupational Safety and Health Administration, and the Centers for Disease Control and Prevention. Six machine-learning models were used to predict the toxicity of these chemical gases. The performance of the models was verified through internal and external validation. The results showed that the model's internal validation accuracy was 86.96% with the Relief-J48 algorithm. The accuracy value of the model was 89.65% with the Bayes Net algorithm for external validation. Our results reveal that identifying the toxicity of existing and potential chemicals is essential for the early detection of these chemicals in nature.
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Gases , Aprendizaje Automático , Estados Unidos , Gases/toxicidad , Teorema de Bayes , Algoritmos , AmidasRESUMEN
Occupational health and safety hazards associated with confined places are mainly caused by exposure to toxic gases and oxygen deficiency. Lack of awareness, inappropriate monitoring, and improper evacuation methods can lead to worker fatalities. Although previous studies have attempted to develop systems to solve this issue, limited research is available on their application in confined places. In this study, a real-time helmet-mounted system was developed to monitor major toxic gases (methane (CH4), hydrogen sulfide (H2S), ammonia (NH3), and carbon monoxide (CO)), oxygen, temperature, and humidity. Workers outside and inside confined spaces receive alerts every second to immediately initiate the rescue operation in the event of a hazard. The test results of a confined environment (wastewater treatment unit) highlighted that concentrations of CH4 and H2S were predominant (13 ppm). Compared to normal atmosphere, CH4 concentration was 122- and 130-fold higher in the landfill and digestion tanks, respectively, while H2S was 36- and 19-fold higher in the primary and secondary clarifiers, respectively. The oxygen content (18.2%) and humidity (33%) were below the minimum required limits. This study will benefit future research to target appropriate toxic gas monitoring and alert workers by studying the existing issues and associated factors in confined places.
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Dispositivos de Protección de la Cabeza , Sulfuro de Hidrógeno , Humanos , Gases/toxicidad , Monóxido de Carbono , OxígenoRESUMEN
Metal fume pollutants of urban Kano, a city of over 10 million people, and widespread metal works have increased exposure with related health effects. Few data on metal fume toxicity and atmospheric levels have been documented in Nigeria and Kano in particular. Hence, the work was aimed at evaluating the metal fume toxicity to laboratory rat species for setting the permissible limit of exposure in urban Kano. The investigation involved the collection of metal welding fumes and subsequent laboratory analysis. Experimental animals were then exposed intratracheally to varying doses of the fumes which were equivalent to normal metal workers' daily routine of 2, 4, and 8 h for 3, 5, 10, and 20 years. Following euthanization, whole blood samples were collected and functions of liver and delta-aminolevunilic acid dehydratase were evaluated in the serum. Exposure to the fumes has caused significant mortality that was observed to be dose-dependent and statistically different (p < 0.05); moreover, the fumes had synergistically affected the functions of liver. In addition, the fumes had increased (statistically) the activity delta-aminolevinilic acid dehydratase. This has indicated that exposure to metal welding fumes being multi-elemental is toxic and had produced mortality at exposure to higher doses of metal welding fumes. It was therefore established from the study that no-observed-adverse-effect level (NOAEL) for metal welding fumes is 25.73 mg with LD50 of 270 mg which corresponds to the metal worker's 4-h shifts daily for 5 years under existing working conditions. It was recommended that regular monitoring should be put in place to limit exposure and extent of engagement in metal works beyond NOAEL levels.
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Contaminantes Ocupacionales del Aire , Enfermedad Hepática Inducida por Sustancias y Drogas , Soldadura , Animales , Ratas , Nivel sin Efectos Adversos Observados , Contaminantes Ocupacionales del Aire/toxicidad , Contaminantes Ocupacionales del Aire/análisis , Nigeria , Metales/análisis , Gases/análisis , Gases/toxicidad , Hidroliasas/análisisRESUMEN
Legal restrictions on vehicle engine exhaust gas emission control do not always go hand in hand with an actual reduction in the emissions of toxins into the atmosphere. Moreover, the methods currently used to measure exhaust gas emissions do not give unambiguous results on the impact of the tested gases on living organisms. The method used to assess the actual toxicity of gases, BAT-CELL Bio-Ambient-Tests using in vitro tests, takes into account synergistic interactions of individual components of a mixture of gases without the need to know its qualitative and quantitative composition and allows for determination of the actual toxicity of the gas composition. Using the BAT-CELL method, exhaust gases from passenger vehicles equipped with spark-ignition engines complying with the Euro 3 and Euro 6 emission standards were tested. The results of toxicological tests were correlated with the results of chromatographic analysis. It was shown that diverse qualitative composition of the mixture of hydrocarbons determining the exhaust gases toxicity may decrease the percentage value of cell survival. Additionally, it was proven that the average survival of cells after exposure to exhaust gases from tested vehicles meeting the more restrictive Euro 6 standard was lower than for vehicles meeting the Euro 3 standard thus indicating the higher toxicity of exhaust gases from newer vehicles.
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Contaminantes Atmosféricos , Emisiones de Vehículos , Emisiones de Vehículos/toxicidad , Emisiones de Vehículos/análisis , Gasolina/análisis , Gases/toxicidad , Gases/análisis , Hidrocarburos/toxicidad , Hidrocarburos/análisis , Técnicas In Vitro , Contaminantes Atmosféricos/toxicidad , Contaminantes Atmosféricos/análisis , Vehículos a MotorRESUMEN
BACKGROUND: Occupational welding fumes contain varieties of toxic metal particles and may affect cardiovascular system like the Particulate Matters (PM). Few studies have focused on the effects of toxic metals on the hemodynamic balance; however, the reporting results were not consistent. This study aimed to investigate the association between toxic metals exposure (Chromium (Cr), Manganese (Mn) and Lead (Pb)) and blood hemostatic parameters status after a 3-week exposure cessation among workers exposed to welding fumes. METHODOLOGY: Structured interviews and biological samplings were conducted for 86 male workers without a history of Anemia and Cardiovascular diseases (CVDs) and working in a confined space to construct crude oil tanks. Metal levels of Cr, Mn and Pb in urine were measured during the working days using Inductively Coupled Plasma Mass Spectrometer (ICP-MS) method. The concentrations of hemostatic proteins in blood (White blood cell counts (WBC), Lymphocytes, Monocyte, Eosinophil, Neutrophil, Hematocrit (Hct) were assessed after a 3 weeks exposure cessation. Workers were divided into groups based on occupation type (welder group and non-welder group), and based on metal levels (high and low exposure groups) for comparison. Linear regression models were used to explore the association between metal exposure and multiple blood hemostatic parameters adjusted for age, Body Mass Index (BMI), and smoking status. RESULTS: Urine Mn and Cr level of the welder group was significantly higher than the non-welder group (Mn: 0.96 VS 0.22 ug/g creatinine, p < 0.001; Cr: 0.63 VS 0.22 ug/g creatinine, p < 0.01). The mean value of Hct in the welder group was 44.58 ± 2.84 vol%, significantly higher than the non-welder group (43.07 ± 3.31 vol%, p = 0.026). The median value of WBC in the high Mn-exposed group (6.93 ± 1.59 X 106 Cell/ml) was significantly lower than the low Mn-exposed group (7.90 ± 2.13 X 106 Cell/ml, p = 0.018). The linear regression analyses showed that there was a significantly negative association between log transformed WBC value and the Mn exposure groups (high and low) after adjusting for age, BMI, and smoking status (ß = - 0.049, p = 0.045), but no significant result was found between WBC and occupation types (welder and non-welder) (p > 0.05). Multiple linear regression analysis also showed positive association between Hct and occupational types (welder and non-welders) (ß = 0.014, p = 0.055). The other hemostatic parameters were not different from controls when divided by occupation type or metal level groups. CONCLUSIONS: Our results showed that welders were exposed to about 3 to 4 times higher Mn and Cr concentrations than non-welders. Moreover, one third of the non-welders were exposed to high-exposure groups of Mn and Cr metals. Regression models revealed a significant association of the WBC counts with the Mn exposure group. Therefore, we infer that Mn exposure may play a significant role on the blood hemostatic parameters of workers in the confined space. Hazard identification for non-welders should also be conducted in the confined space.
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Intoxicación por Gas/epidemiología , Obreros Metalúrgicos , Exposición Profesional/estadística & datos numéricos , Cromo/sangre , Cromo/toxicidad , Espacios Confinados , Eosinófilos , Gases/toxicidad , Hematócrito , Hemodinámica , Hemostáticos/toxicidad , Humanos , Plomo/sangre , Plomo/toxicidad , Recuento de Leucocitos , Manganeso/sangre , Manganeso/toxicidad , Monocitos , Neutrófilos , Enfermedades Profesionales/epidemiología , Enfermedades Profesionales/etiología , Exposición Profesional/economía , Tailandia , SoldaduraRESUMEN
BACKGROUND: Exposure to air pollution exerts direct effects on respiratory organs; however, molecular alterations underlying air pollution-induced pulmonary injury remain unclear. In this study, we investigated the effect of air pollution on the lung tissues of Sprague-Dawley rats with whole-body exposure to traffic-related PM1 (particulate matter < 1 µm in aerodynamic diameter) pollutants and compared it with that in rats exposed to high-efficiency particulate air-filtered gaseous pollutants and clean air controls for 3 and 6 months. Lung function and histological examinations were performed along with quantitative proteomics analysis and functional validation. RESULTS: Rats in the 6-month PM1-exposed group exhibited a significant decline in lung function, as determined by decreased FEF25-75% and FEV20/FVC; however, histological analysis revealed earlier lung damage, as evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2673 proteins that highlighted the differential dysregulation of proteins involved in oxidative stress, cellular metabolism, calcium signalling, inflammatory responses, and actin dynamics under exposures to PM1 and gaseous pollutants. The presence of PM1 specifically enhanced oxidative stress and inflammatory reactions under subchronic exposure to traffic-related PM1 and suppressed glucose metabolism and actin cytoskeleton signalling. These factors might lead to repair failure and thus to lung function decline after chronic exposure to traffic-related PM1. A detailed pathogenic mechanism was proposed to depict temporal and dynamic molecular regulations associated with PM1- and gaseous pollutants-induced lung injury. CONCLUSION: This study explored several potential molecular features associated with early lung damage in response to traffic-related air pollution, which might be used to screen individuals more susceptible to air pollution.
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Contaminantes Atmosféricos , Contaminación del Aire , Lesión Pulmonar , Material Particulado/toxicidad , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/análisis , Animales , Exposición a Riesgos Ambientales/análisis , Contaminantes Ambientales , Gases/toxicidad , Lesión Pulmonar/inducido químicamente , Material Particulado/análisis , Ratas , Ratas Sprague-DawleyRESUMEN
To assess the toxicities of gas/aerosol, inhalation exposure model is necessary. Especially important is the inhalation exposure early in life. Traditional inhalation exposure method requires specific instruments and may have to imitate the exposure either days before or after birth. Here, a new inhalation exposure method is introduced, which may be performed without any specific instruments and effectively expose late stage chicken embryos to gas/aerosol very early-in-life by inhalation. This method may facilitate the risk assessment and mechanistic studies regarding the early-in-life effects of gas/aerosol exposure.
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Aerosoles/efectos adversos , Embrión de Pollo/efectos de los fármacos , Gases/efectos adversos , Exposición por Inhalación/efectos adversos , Aerosoles/toxicidad , Animales , Pollos , Gases/toxicidad , Pruebas de Toxicidad/métodosRESUMEN
Concerns have been raised as to whether gunshot fumes induce prolonged reduced lung capacity or even cancer due to inhalation. Gunshot fumes from three different types of ammunition calibre 5.56 mm × 45 NATO were investigated. SS109 has a soft lead (Pb) core, while NM255 and NM229 have a harder steel core. Emissions from ammunitions were characterized with respect to particle number- and mass-size, and mass distribution, heavy metal content, and different gases. Lung epithelial cells were exposed to the fumes at the air liquid interface to elucidate cytotoxicity and genotoxicity. Irrespectively of ammunition type, the largest mass fraction of generated particulate matter (PM) had a size between 1 and 3 µm. The highest number of particles generated was in the size range of 30 nm. Fumes from NM255 and NM229 induced cytotoxic effects of which the emission from NM229 induced the highest effect. Fumes from NM229 induced a dose-related increase in DNA-damage. Significant effects were only achieved at the highest exposure level, which led to approximately 40% reduced cell viability after 24 h. The effect probably relates to the mass of emitted particles where the size may be of importance, in addition to emission of Cu and Zn. A complex mixture of chemical substances and PM may increase the toxicity of the fumes and should encourage measures to reduce exposure.
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Contaminantes Atmosféricos/toxicidad , Armas de Fuego , Gases/toxicidad , Pulmón/citología , Metales/toxicidad , Material Particulado/toxicidad , Células A549 , Contaminantes Atmosféricos/análisis , Supervivencia Celular/efectos de los fármacos , Ensayo Cometa , Daño del ADN , Gases/análisis , Humanos , Metales/análisis , Tamaño de la Partícula , Material Particulado/análisisRESUMEN
The objective of this study was to evaluate the histopathological effect of gas explosion on rats, and to explore the metabolic alterations associated with gas explosion-induced acute blast lung injury (ABLI) in real roadway environment using metabolomics analyses. All rats were exposed to the gas explosion source at different distance points (160 m and 240 m) except the control group. Respiratory function indexes were monitored and lung tissue analysis was performed to correlate histopathological effect to serum metabolomics. Their sera samples were collected to measure the metabolic alterations by ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). HE staining in lung showed that the gas explosion caused obvious inflammatory pulmonary injury, which was consistent with respiratory function monitoring results and the serum metabolomics analysis results. The metabolomics identified 9 significantly metabolites different between the control- and ABLI rats. 2-aminoadipic acid, L-methionine, L-alanine, L-lysine, L-threonine, cholic acid and L-histidine were significantly increased in the exposed groups. Citric acid and aconitic acid were significantly decreased after exposure. Pathway analyses identified 8 perturbed metabolic pathways, which provided novel potential mechanisms for the gas explosion-induced ABLI. Therefore, metabolomics analysis identified both known and unknown alterations in circulating biomarkers, adding an integral mechanistic insight into the gas explosion-induced ABLI in real roadway environment.
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Lesión Pulmonar Aguda/sangre , Traumatismos por Explosión/sangre , Explosiones , Gases/toxicidad , Lesión Pulmonar Aguda/metabolismo , Lesión Pulmonar Aguda/patología , Animales , Biomarcadores/sangre , Biomarcadores/metabolismo , Traumatismos por Explosión/metabolismo , Traumatismos por Explosión/patología , Cromatografía Liquida , Pulmón/efectos de los fármacos , Pulmón/patología , Masculino , Espectrometría de Masas , Metaboloma/efectos de los fármacos , Metabolómica , Ratas Sprague-DawleyRESUMEN
The objective of this work is to present the key elements in the design of emergency management and response plans in scenarios where there has been loss of containment of chemical agents of acute effect focused in the protection of not routinely exposed in a determined occupational environment. To this purpose, a validation of the current criteria for the management of accidental releases is carried out, taking into account hypothetical risk scenarios. The essential elements of the emergency management system are stated, from a systemic perspective and the corresponding risk control actions; recommendations for their implementation are showed, taking as prototype hydrogen sulfide, a highly toxic gas. Non controlled emissions of toxic gases of acute effect from an occupational standpoint represents a priority because of their human and financial high toll. Design and implementation of an appropriate emergency plan for uncontrollable emissions of toxics chemical agents must be addressed.
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Gases/toxicidad , Exposición Profesional/prevención & control , Industria del Petróleo y Gas , Gestión de Riesgos/normas , Planificación en Desastres/normas , Humanos , Sulfuro de Hidrógeno/toxicidad , Exposición Profesional/efectos adversos , Exposición Profesional/normas , Factores de TiempoRESUMEN
Perfluoroisobutyronitrile (C4F7N) is a new eco-friendly gas insulation medium that has potential to replace the most greenhouse gas sulfur hexafluoride (SF6) used in power industry. In order to ensure the engineering application safety, an in-depth assessment of the acute inhalation toxicity of C4F7N gas mixture is required. This article revealed gender differences in male and female mice after exposure to C4F7N and the physiological recovery characteristics of surviving mice by means of 4 h acute inhalation toxicity tests, hematological determinations and histopathological examination. Comparative analysis on the toxicity of C4F7N on mice and rats is also evaluated. We find that the LC50 of C4F7N for male and female mice is 1175 ppm (4 h), 1380 ppm (4 h) and female ones are more tolerant to C4F7N. Mice that exposed to 1000 ppm C4F7N for 4 h could survive and return to their normal state after the 14-day observation period without irreversible damage. The toxic effect duration of C4F7N on rats is longer than that of mice. Relevant results revealed the acute inhalation toxicity of C4F7N systematically and provided fundamental reference for inhalation safety protection and engineering application.
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Contaminantes Atmosféricos/toxicidad , Gases/toxicidad , Exposición por Inhalación/efectos adversos , Nitrilos/toxicidad , Animales , Femenino , Gases de Efecto Invernadero , Dosificación Letal Mediana , Masculino , Ratones , Ratones Endogámicos BALB C , Ratas , Hexafluoruro de Azufre , Pruebas de Toxicidad AgudaRESUMEN
Total dissolved gas (TDG) supersaturation generated by discharged flood water may cause the death of fish downstream of dams and severely threaten their survival during the flood season. No study has performed to investigate the effects of TDG on fish dwelling in shallows in China. Furthermore, varied TDG levels are caused by the varied flow of flood water during the spill season. Fish may alternatingly experience intermittent TDG exposure from equilibrated water and TDG-supersaturated water. However, little research on the effects of intermittent TDG exposure on fish has been conducted. To evaluate the tolerance of fish to continuous acute TDG exposure, juvenile yellow catfish living in the shallows were exposed to TDG-supersaturated water at 125%, 130%, 135% and 140% TDG for 96 h. The results showed that the juvenile yellow catfish exhibited obvious gas bubble disease (GBD) and abnormal behaviours (e.g., exophthalmos and bubbles on fins). The survival probability declined with the arising TDG levels. The median survival time (ST50) of yellow catfish was 8.57, 18.1, 33.86 and 58.84 h at above TDG levels, respectively. To further investigate the effects of intermittent TDG exposure on juvenile yellow catfish, the fish were subjected to varied TDG levels (125%, 130%, 135% and 140%) for a specific duration (3 h and 6 h) and then underwent a period of recovery (3, 6 and 9 h) in equilibrated water. The results showed that an increase in recovery time (or decreasing exposure time) can prolong the survival time of yellow catfish and improve their survival probability at the same exposure time (or same recovery time). Compared with that under continuous acute exposure, the ST50 of juvenile yellow catfish increased significantly with intermittent exposure. Intermittent exposure can enhance the tolerance of juvenile yellow catfish to TDG. The application of the results may contribute to the protection of aquatic organisms and the formulation of the scheme of reservoir operation in the Yangtze River.
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Adaptación Fisiológica/efectos de los fármacos , Bagres/fisiología , Gases/toxicidad , Ríos/química , Contaminantes del Agua/toxicidad , Animales , Conducta Animal/efectos de los fármacos , China , Gases/análisis , Probabilidad , Análisis de Supervivencia , Movimientos del Agua , Contaminantes del Agua/análisis , Calidad del AguaRESUMEN
Silver is used in a wide range of products, and during their production and use, humans may be exposed through inhalation. Therefore, it is critical to know the concentration levels at which adverse effects may occur. In rodents, inhalation of silver nanoparticles has resulted in increased silver in the lungs, lymph nodes, liver, kidney, spleen, ovaries, and testes. Reported excretion pathways of pulmonary silver are urinary and faecal excretion. Acute effects in humans of the inhalation of silver include lung failure that involved increased heart rate and decreased arterial blood oxygen pressure. Argyria-a blue-grey discoloration of skin due to deposited silver-was observed after pulmonary exposure in 3 individuals; however, the presence of silver in the discolorations was not tested. Argyria after inhalation seems to be less likely than after oral or dermal exposure. Repeated inhalation findings in rodents have shown effects on lung function, pulmonary inflammation, bile duct hyperplasia, and genotoxicity. In our evaluation, the range of NOAEC values was 0.11-0.75 mg/m3. Silver in the ionic form is likely more toxic than in the nanoparticle form but that difference could reflect their different biokinetics. However, silver nanoparticles and ions have a similar pattern of toxicity, probably reflecting that the effect of silver nanoparticles is primarily mediated by released ions. Concerning genotoxicity studies, we evaluated silver to be positive based on studies in mammalian cells in vitro and in vivo when considering various exposure routes. Carcinogenicity data are absent; therefore, no conclusion can be provided on this endpoint.
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Polvo , Gases/toxicidad , Nanopartículas del Metal/toxicidad , Plata/toxicidad , Administración por Inhalación , Animales , Humanos , Exposición por Inhalación , Pulmón/efectos de los fármacos , Nanopartículas del Metal/análisis , Pruebas de Mutagenicidad , Plata/sangre , Plata/farmacocinéticaRESUMEN
Here, we present a specially designed modular in vitro exposure system that enables the homogenous exposure of cultivated human lung cells at the ALI to gases, particles or complex atmospheres (e.g., cigarette smoke), thus providing realistic physiological exposure of the apical surface of the human alveolar region to air. In contrast to sequential exposure models with linear aerosol guidance, the modular design of the radial flow system meets all requirements for the continuous generation and transport of the test atmosphere to the cells, a homogenous distribution and deposition of the particles and the continuous removal of the atmosphere. This exposure method is primarily designed for the exposure of cells to airborne particles, but can be adapted to the exposure of liquid aerosols and highly toxic and aggressive gases depending on the aerosol generation method and the material of the exposure modules. Within the framework of a recently completed validation study, this exposure system was proven as a transferable, reproducible and predictive screening method for the qualitative assessment of the acute pulmonary cytotoxicity of airborne particles, thereby potentially reducing or replacing animal experiments that would normally provide this toxicological assessment.
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Aire , Exposición por Inhalación/efectos adversos , Pulmón/citología , Material Particulado/toxicidad , Gases/toxicidad , Humanos , Humo/efectos adversosRESUMEN
Welding generates and releases fumes that are hazardous to human health. Welding fumes (WFs) are a complex mix of metallic oxides, fluorides and silicates that can cause or exacerbate health problems in exposed individuals. In particular, WF inhalation over an extended period carries an increased risk of cancer, but how WFs may influence cancer behaviour or growth is unclear. To address this issue we employed a quantitative analytical framework to identify the gene expression effects of WFs that may affect the subsequent behaviour of the cancers. We examined datasets of transcript analyses made using microarray studies of WF-exposed tissues and of cancers, including datasets from colorectal cancer (CC), prostate cancer (PC), lung cancer (LC) and gastric cancer (GC). We constructed gene-disease association networks, identified signaling and ontological pathways, clustered protein-protein interaction network using multilayer network topology, and analyzed survival function of the significant genes using Cox proportional hazards (Cox PH) model and product-limit (PL) estimator. We observed that WF exposure causes altered expression of many genes (36, 13, 25 and 17 respectively) whose expression are also altered in CC, PC, LC and GC. Gene-disease association networks, signaling and ontological pathways, protein-protein interaction network, and survival functions of the significant genes suggest ways that WFs may influence the progression of CC, PC, LC and GC. This quantitative analytical framework has identified potentially novel mechanisms by which tissue WF exposure may lead to gene expression changes in tissue gene expression that affect cancer behaviour and, thus, cancer progression, growth or establishment.
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Aprendizaje Automático , Redes y Vías Metabólicas/efectos de los fármacos , Neoplasias/genética , Soldadura , Contaminantes Ocupacionales del Aire/toxicidad , Biología Computacional , Gases/toxicidad , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Humanos , Exposición por Inhalación/efectos adversos , Redes y Vías Metabólicas/genética , Proteínas de Neoplasias/genética , Neoplasias/inducido químicamente , Neoplasias/patologíaRESUMEN
BACKGROUND: Epidemiological studies have reported associations between elevated air pollution and autism spectrum disorders (ASD). However, we hypothesized that exposure to air pollution that mimics real world scenarios, is a potential contributor to ASD. The exact etiology and molecular mechanisms underlying ASD are not well understood. Thus, we assessed whether changes in OXTR levels may be part of the mechanism linking PM2.5/gaseous pollutant exposure and ASD. The current in-vivo study investigated the effect of exposure to fine particulate matter (PM2.5) and gaseous pollutants on ASD using behavioral and molecular experiments. Four exposure groups of Wistar rats were included in this study: 1) particulate matter and gaseous pollutants exposed (PGE), 2) gaseous pollutants only exposed (GE), 3) autism-like model (ALM) with VPA induction, and 4) clean air exposed (CAE) as the control. Pregnant dams and male pups were exposed to air pollutants from embryonic day (E0) to postnatal day (PND21). RESULTS: The average ± SD concentrations of air pollutants were: PM2.5: 43.8 ± 21.1 µg/m3, CO: 13.5 ± 2.5 ppm, NO2: 0.341 ± 0.100 ppm, SO2: 0.275 ± 0.07 ppm, and O3: 0.135 ± 0.01 ppm. The OXTR protein level, catalase activity (CAT), and GSH concentrations in the ALM, PGE, and GE rats were lower than those in control group (CAE). However, the decrements in the GE rats were smaller than other groups. Also in behavioral assessments, the ALM, PGE, and GE rats demonstrated a repetitive /restricted behavior and poor social interaction, but the GE rats had weaker responses compared to other groups of rats. The PGE and GE rats showed similar trends in these tests compared to the VPA rats. CONCLUSIONS: This study suggested that exposure to ambient air pollution contributed to ASD and that OXTR protein may serve as part of the mechanism linking them.
Asunto(s)
Contaminantes Atmosféricos/toxicidad , Trastorno del Espectro Autista/inducido químicamente , Conducta Animal/efectos de los fármacos , Gases/toxicidad , Material Particulado/toxicidad , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Contaminantes Atmosféricos/química , Animales , Animales Recién Nacidos , Trastorno del Espectro Autista/psicología , Encéfalo/efectos de los fármacos , Encéfalo/embriología , Encéfalo/metabolismo , Modelos Animales de Enfermedad , Femenino , Gases/química , Exposición por Inhalación/efectos adversos , Exposición por Inhalación/análisis , Masculino , Estrés Oxidativo/efectos de los fármacos , Oxitocina/metabolismo , Material Particulado/química , Embarazo , Efectos Tardíos de la Exposición Prenatal/psicología , Ratas , Ratas Wistar , Receptores de Oxitocina/metabolismoRESUMEN
OBJECTIVE: To determine the concentration of fluctuating gaseous formaldehyde in an anatomy laboratory and to investigate its effects on the subjective symptoms and the lung functions of medical students working there. METHODS: To measure the levels of formaldehyde gas at different physical ventilation times at the center of the study laboratory by the gaseous formaldehyde detector. A total of 251 of second-year medical students were randomly selected from 1004 students participating in the anatomy operation as the survey subjects, 77 medical students were randomly selected for lung function assessment. The subjective symptoms of the medical students exposed to this gas were investigated via questionnaire surveys before, during and after the dissection operation. The probable lung function damages caused by the exposure before and after the operation were also measured using various parameters. RESULTS: The concentration of gaseous formaldehyde decreased with an increase in the ventilation time(P<0. 05), but it was always higher than the occupational health standard(0. 50 mg/m~3). The gas concentration above the dissecting table(0. 43-2. 89 mg/m~3) was significantly higher than that at the center of the laboratory(0. 34-2. 31 mg/m~3)(P<0. 05). The levels of the gas in the thoracic and abdominal cavities(0. 67-2. 89 mg/m~3) were significantly higher than those in the superficial fascia(0. 50-2. 13 mg/m~3) and deep layer of the back(0. 34-1. 48 mg/m~3)(P<0. 05). When compared with that at the pre-operative period, the prevalence of most subjective symptomssuch as itchy eyes, nasal congestion, runny nose, dyspnea, headache, and lack of energy increased significantly during the operation and decreased thereafter(P<0. 05). After the procedure, forced expiratory volume 1(FEV1)/forced vital capacity(FVC), FEV1, peak expiratory flow(PEF), FEF25%-75%, maximum expiratory flow 25%(MEF25%), and FEF50%-75% were found to be lower in comparison with the corresponding values recorded before the operation(P<0. 05). CONCLUSION: Existing physical ventilation facilities are difficult to reduce the concentration of gaseous formaldehyde below the safety threshold. Exposure to ultra-high concentrations of gaseous formaldehyde caused a significant increase in subjective symptoms of medical students with secondary pulmonary function impairment.
Asunto(s)
Estudiantes de Medicina , Formaldehído/toxicidad , Gases/toxicidad , Humanos , Pulmón , Capacidad VitalRESUMEN
In the present investigation, we have employed heme as a material for absorbing haloarenes due to its unique structural property, abundant availability, non-toxic nature and its dynamic nature in absorbing oxygen molecule. Haloarenes are toxic gases that are released into atmosphere as an aftermath of various refrigerants. Using first principle study, the absorption of haloarenes on heme molecule was systematically investigated. Fluorine, Chlorine, Bromine and Iodine substituted Haloarenes were allowed to interact with heme molecule with metal ion at +2, +3 and + 4 oxidation states of both low and high spin states. The TD-DFT analysis shows that the heme is a better absorbent at +3 and + 4 oxidation states of Fe ion at low spin state. Among the haloarenes, the interaction energy between IHA and Fe ion at +4 state is maximum with -1.877 eV. The HOMO-LUMO band gap decreases with increase in oxidation state and the orbital delocalization is maximum for high oxidation state. The delocalization of these electronic orbitals shows the active interaction between the heme molecule and haloarene which was confirmed by the DOS plot and the LP to LP* transition in NBO analysis. The absorbing nature of heme was further extended to hexahaloarenes, where heme still stand as a strong absorbing candidate for these toxic gases. The detailed study of the interaction between heme and haloarenes showed that heme at low spin state and with both +3 and + 4 oxidation states can be employed as an absorbent for Haloarenes. Graphical abstract.