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Due to the complexity of environmental exposure factors and the low levels of exposure in the general population, identifying the key environmental factors associated with diabetes and understanding their potential mechanisms present significant challenges. This study aimed to identify key polycyclic aromatic hydrocarbons (PAHs) contributing to increased fasting blood glucose (FBG) concentrations and to explore their potential metabolic mechanisms. We recruited a highly PAH-exposed diesel engine exhaust testing population and healthy controls. Our findings found a positive association between FBG concentrations and PAH metabolites, identifying 1-OHNa, 2-OHPh, and 9-OHPh as major contributors to the rise in FBG concentrations induced by PAH mixtures. Specifically, each 10 % increase in 1-OHNa, 2-OHPh, and 9-OHPh concentrations led to increases in FBG concentrations of 0.201 %, 0.261 %, and 0.268 %, respectively. Targeted metabolomics analysis revealed significant alterations in metabolic pathways among those exposed to high levels of PAHs, including sirtuin signaling, asparagine metabolism, and proline metabolism pathway. Toxic function analysis highlighted differential metabolites involved in various dysglycemia-related conditions, such as cardiac arrhythmia and renal damage. Mediation analysis revealed that 2-aminooctanoic acid mediated the FBG elevation induced by 2-OHPh, while 2-hydroxyphenylacetic acid and hypoxanthine acted as partial suppressors. Notably, 2-aminooctanoic acid was identified as a crucial intermediary metabolic biomarker, mediating significant portions of the associations between the multiple different structures of OH-PAHs and elevated FBG concentrations, accounting for 16.73 %, 10.84 %, 10.00 %, and 11.90 % of these effects for 1-OHPyr, 2-OHFlu, the sum concentrations of 2- and 9-OHPh, and the sum concentrations of total OH-PAHs, respectively. Overall, our study explored the potential metabolic mechanisms underlying the elevated FBG induced by PAHs and identified 2-aminooctanoic acid as a pivotal metabolic biomarker, presenting a potential target for intervention.

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Diesel engine exhaust (DEE) is carcinogenic and potentially hazardous for those working in close proximity to diesel-powered machines. This study characterizes workplace exposure to DEE and its associated particulate matter (PM) during outdoor construction activities. We sampled at 4 construction sites in the Copenhagen metropolitan area. We used portable constant-flow pumps and quartz-fiber filters to quantify personal exposure to elemental carbon (EC), and used real-time instruments to collect activity-based information about particle number and size distribution, as well as black carbon (BC) concentration. Full-shift measurements of EC concentration ranged from < 0.3 to 6.4 µg/m3. Geometric mean (GM) EC exposure was highest for ground workers (3.4 µg/m3 EC; geometric standard deviation, GSD = 1.3), followed by drilling rig operators (2.6 µg/m3 EC; GSD = 1.4). Exposure for non-drilling-rig machine operators (1.2 µg/m3 EC; GSD = 2.9) did not differ significantly from background (0.9 µg/m3 EC; GSD = 1.7). The maximum 15-min moving average concentration of BC was 17 µg/m3, and the highest recorded peak concentration was 44 µg/m3. In numbers, the particle size distributions were dominated by ultrafine particles ascribed to DEE and occasional welding activities at the sites. The average total particle number concentrations (PNCs) measured in near-field and far-field positions across all worksites were 10,600 (GSD = 3.0) and 6,000 (GSD = 2.8)/cm3, respectively. Sites with active drilling rigs saw significantly higher average total PNCs at their near-field stations (13,600, 32,000, and 9,700/cm3; GSD = 2.4, 3.4, and 2.4) than sites without (4,700/cm3; GSD = 1.6). Overall, the DEE exposures at these outdoor construction sites were below current occupational exposure limits for EC (10 µg/m3 in Denmark; 50 µg/m3 in the European Union), but extended durations of exposure to the observed DEE levels may still be a health risk.

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RATIONALE: Diesel engine exhaust (DEE) is associated with the development and exacerbation of asthma. Studies have shown that DEE can aggravate allergen-induced eosinophilic inflammation in lung. However, it remains not clear that whether DEE alone could initiate non-allergic eosinophilic inflammation and airway hyperresponsiveness (AHR) through innate lymphoid cells (ILCs) pathway. OBJECTIVE: This study aims to investigate the airway inflammation and hyperresponsiveness and its relationship with ILC after DEE exposure. METHOD: Non-sensitized BALB/c mice were exposed in the chamber of diesel exhaust or filtered air for 2, 4, and 6 weeks (4 h/day, 6 days/week). Anti-CD4 mAb or anti-Thy1.2 mAb was administered by intraperitoneal injection to inhibit CD4+T or ILCs respectively. AHR、airway inflammation and ILCs were assessed. RESULT: DEE exposure induced significantly elevated level of neutrophils, eosinophils, collagen content at 4, 6 weeks. Importantly, the airway AHR was only significant in the 4weeks-DEE exposure group. No difference of the functional proportions of Th2 cells was found between exposure group and control group. The proportions of IL-5+ILC2, IL-17+ILC significantly increased in 2, 4weeks-DEE exposure group. After depletion of CD4+T cells, both the proportion of IL-5+ILC2 and IL-17A ILCs was higher in the 4weeks-DEE exposure group which induced AHR, neutrophilic and eosinophilic inflammation accompanied by the IL-5, IL-17A levels. CONCLUSION: Diesel engine exhaust alone can imitate asthmatic characteristics in mice model. Lung-resident ILCs are one of the major effectors cells responsible for a mixed Th2/Th17 response and AHR.

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Intravenous injection of capsaicin produces vagal-mediated protective cardio-pulmonary (CP) reflexes manifesting as tachypnea, bradycardia, and triphasic blood pressure (BP) response in anesthetized rats. Particulate matter from diesel engine exhaust has been reported to attenuate these reflexes. However, the effects of gaseous constituents of diesel exhaust are not known. Therefore, the present study was designed to investigate the effects of gaseous pollutants in diesel exhaust, on capsaicin-induced CP reflexes in rat model. Adult male rats were randomly assigned to three groups: Non-exposed (NE) group, filtered diesel exhaust-exposed (FDE) group and N-acetyl cysteine (NAC)-treated FDE group. FDE group of rats (n = 6) were exposed to filtered diesel exhaust for 5 h a day for 5 days (D1-D5), and were taken for dissection on day 6 (D6), while NE group of rats (n = 6) remained unexposed. On D6, rats were anesthetized, following which jugular vein was cannulated for injection of chemicals, and femoral artery was cannulated to record the BP. Lead II electrocardiogram and respiratory movements were also recorded. Results show that intravenous injection of capsaicin (0.1 ml; 10 µg/kg) produced immediate tachypneic, hyperventilatory, hypotensive, and bradycardiac responses in both NE and FDE groups of rats. However, these capsaicin-induced CP responses were significantly attenuated in FDE group as compared to the NE group of rats. Further, FDE-induced attenuation of capsaicin-evoked CP responses were diminished in the N-acetyl cysteine-treated FDE rats. These findings demonstrate that oxidant stress mechanisms could possibly be involved in inhibition of CP reflexes by gaseous pollutants in diesel engine exhaust.

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BACKGROUND: Ambient fine particulate matter (PM2.5) is considered a plausible contributor to the onset of chronic obstructive pulmonary disease (COPD). Mechanistic studies are needed to augment the causality of epidemiologic findings. In this study, we aimed to test the hypothesis that repeated exposure to diesel exhaust particles (DEP), a model PM2.5, causes COPD-like pathophysiologic alterations, consequently leading to the development of specific disease phenotypes. Sprague Dawley rats, representing healthy lungs, were randomly assigned to inhale filtered clean air or DEP at a steady-state concentration of 1.03 mg/m3 (mass concentration), 4 h per day, consecutively for 2, 4, and 8 weeks, respectively. Pulmonary inflammation, morphologies and function were examined. RESULTS: Black carbon (a component of DEP) loading in bronchoalveolar lavage macrophages demonstrated a dose-dependent increase in rats following DEP exposures of different durations, indicating that DEP deposited and accumulated in the peripheral lung. Total wall areas (WAt) of small airways, but not of large airways, were significantly increased following DEP exposures, compared to those following filtered air exposures. Consistently, the expression of α-smooth muscle actin (α-SMA) in peripheral lung was elevated following DEP exposures. Fibrosis areas surrounding the small airways and content of hydroxyproline in lung tissue increased significantly following 4-week and 8-week DEP exposure as compared to the filtered air controls. In addition, goblet cell hyperplasia and mucus hypersecretions were evident in small airways following 4-week and 8-week DEP exposures. Lung resistance and total lung capacity were significantly increased following DEP exposures. Serum levels of two oxidative stress biomarkers (MDA and 8-OHdG) were significantly increased. A dramatical recruitment of eosinophils (14.0-fold increase over the control) and macrophages (3.2-fold increase) to the submucosa area of small airways was observed following DEP exposures. CONCLUSIONS: DEP exposures over the courses of 2 to 8 weeks induced COPD-like pathophysiology in rats, with characteristic small airway remodeling, mucus hypersecretion, and eosinophilic inflammation. The results provide insights on the pathophysiologic mechanisms by which PM2.5 exposures cause COPD especially the eosinophilic phenotype.

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Exposure to diesel exhaust emissions (DEE) is strongly linked to innate immune injury and lung injury, but the role of macrophage chemoattractant CXCL17 in the lung damage caused by DEE exposure remains unclear. In this study, whole-body plethysmography (WBP), inflammatory cell differential count, and histopathological analysis were performed to assess respiratory parameters, airway inflammation, and airway injury in C57BL/6 male mice exposed to DEE for 3 months. qRT-PCR, IHC (immunohistochemistry), and ELISA were performed to measure the CXCL17 expression in airway epithelium or BALF (bronchoalveolar lavage fluid) following DEE/Diesel exhaust particle (DEP) exposure. Respiratory parameters, airway inflammation, and airway injury were assessed in CXCL17-overexpressing mice through adeno-associated virus vector Type 5 (AAV5) infection. Additionally, an in vitro THP-1 and HBE co-culture system was constructed. Transwell assay was carried out to evaluate the effect of rh-CXCL17 (recombinant human protein-CXCL17) on THP-1 cell migration. Flow cytometry and qRT-PCR were conducted to assess the impacts of rh-CXCL17 on apoptosis and inflammation/remodeling of HBE cells. We found that the mice exposed to DEE showed abnormal respiratory parameters, accompanied by airway injury and remodeling (ciliary injury in airway epithelium, airway smooth muscle hyperplasia, and increased collagen deposition). Carbon content in airway macrophages (CCAM), but not the number of macrophages in BALF, increased significantly. CXCL17 expression significantly decreased in mice airways and HBE after DEE/DEP exposure. AAV5-CXCL17 enhanced macrophage recruitment and clearance of DEE in the lungs of mice, and it improved respiratory parameters, airway injury, and airway remodeling. In the THP-1/HBE co-culture system, rh-CXCL17 increased THP-1 cell migration while attenuating HBE cell apoptosis and inflammation/remodeling. Therefore, CXCL17 might attenuate DEE-induced lung damage by recruiting and activating pulmonary macrophages, which is expected to be a novel therapeutic target for DEE-associated lung diseases.

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Reducing the pollution of internal combustion engines is a very important problem that can be solved in various ways. However, the acoustic agglomeration method is not used in diesel engines. The study used a 1.9 TDI diesel internal combustion engine supplied with a mixture of diesel (D100) and a 90% of rapeseed methyl ester - 10% propanol fuel mixture (ROMEP). The study also changed the position of the exhaust gas recirculation (EGR) valve by adjusting the 20% EGR throughput limits and maintaining a constant engine load of 90 Nm. It should be noted that the use of biofuels produces less particulate matter, which reinforces the relevance of this study. Measurements were performed using Measurement System: The Testo 380 fine particle analyzer system was used to determine the mass concentration, and a six-channel Fluke 985 particle counter with an isokinetic sampling probe was used to determine the fractional numerical concentration of the particulates. Six particle size distribution regimes in the size range of 0.3 to 10 µm were observed, controlling the transmittance of the EGR system by 20%. The direction of the sound pressure throughout the flow and the excitation frequency 21400 Hz and 33800 Hz were also investigated and compared with the results without agglomeration. The article examines the possibility of using the developed acoustic chamber in the exhaust systems of various objects that uses diesel or various alternative fuel mixtures as fuel. The acoustic field reduces the number of particles by up to 92.5% for 10 µm and up to 44.5% for 0.3 µm at an excitation frequency of 21400 Hz.

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Post-combustion carbon capture is a direct and effective way for onboard carbon capture. Therefore, it is important to develop onboard carbon capture absorbent that can both ensure a high absorption rate and reduce the energy consumption of the desorption process. In this paper, a K2CO3 solution was first established using Aspen Plus to simulate CO2 capture from the exhaust gases of a marine dual-fuel engine in diesel mode. The lean and rich CO2 loading results from the simulation were used to guide the selection and optimization of the activators used in the experiment. During the experiment, five amino acid salt activators including SarK, GlyK, ProK, LysK, and AlaK and four organic amine activators including MEA, PZ, AEEA, and TEPA were used. Experiments only considered the activation effect of CO2 loading between lean and rich conditions. The results showed that after adding a small amount of activator, the absorption rate of CO2 by the absorbent was greatly improved, and the activation effect of organic amine activators was stronger than that of amino acid salts. Among the amino acid salts, the SarK-K2CO3 composite solution showed the best performance in both absorption and desorption. Among the amino acid salts and the organic amino activators, SarK-K2CO3 showed the best performance in strengthening the CO2 desorption while PZ-K2CO3 enhanced the CO2 absorption process the most. In the study of the concentration ratio, it was found that when the mass concentration ratio was 1:1 for SarK:K2CO3 and PZ:K2CO3, the CO2 absorption and desorption processes improved well.

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The differences in the traffic fuels have been shown to affect exhaust emissions and their toxicity. Especially, the aromatic content of diesel fuel is an important factor considering the emissions, notably particulate matter (PM) concentrations. The ultra-fine particles (UFP, particles with a diameter of <100 nm) are important components of engine emissions and connected to various health effects, such as pulmonary and systematic inflammation, and cardiovascular disorders. Studying the toxicity of the UFPs and how different fuel options can be used for mitigating the emissions and toxicity is crucial. In the present study, emissions from a heavy-duty diesel engine were used to assess the exhaust emission toxicity with a thermophoresis-based in vitro air-liquid interface (ALI) exposure system. The aim of the study was to evaluate the toxicity of engine exhaust and the potential effect of 20 % aromatic fossil diesel and 0 % aromatic renewable diesel fuel on emission toxicity. The results of the present study show that the aromatic content of the fuel increases emission toxicity, which was seen as an increase in genotoxicity, distinct inflammatory responses, and alterations in the cell cycle. The increase in genotoxicity was most likely due to the PM phase of the exhaust, as the exposures with high-efficiency particulate absorbing (HEPA)-filtered exhaust resulted in a negligible increase in genotoxicity. However, the solely gaseous exposures still elicited immunological responses. Overall, the present study shows that decreasing the aromatic content of the fuels could be a significant measure in mitigating traffic exhaust toxicity.

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Diesel engine exhaust (DEE) is an established lung carcinogen, but the biological mechanisms of diesel-induced lung carcinogenesis are not well understood. MicroRNAs (miRNAs) are small noncoding RNAs that play a potentially important role in regulating gene expression related to lung cancer. We conducted a cross-sectional molecular epidemiology study to evaluate whether serum levels of miRNAs are altered in healthy workers occupationally exposed to DEE compared to unexposed controls. We conducted a two-stage study, first measuring 405 miRNAs in a pilot study of six DEE-exposed workers exposed and six controls. In the second stage, 44 selected miRNAs were measured using the Fireplex circulating miRNA assay that profiles miRNAs directly from biofluids of 45 workers exposed to a range of DEE (Elemental Carbon (EC), median, range: 47.7, 6.1-79.7 µg/m3 ) and 46 controls. The relationship between exposure to DEE and EC with miRNA levels was analyzed using linear regression adjusted for potential confounders. Serum levels of four miRNAs were significantly lower (miR-191-5p, miR-93-5p, miR-423-3p, miR-122-5p) and one miRNA was significantly higher (miR-92a-3p) in DEE exposed workers compared to controls. Of these miRNAs, miR-191-5p (ptrend  = .001, FDR = 0.04) and miR-93-5p (ptrend  = .009, FDR = 0.18) showed evidence of an inverse exposure-response with increasing EC levels. Our findings suggest that occupational exposure to DEE may affect circulating miRNAs implicated in biological processes related to carcinogenesis, including immune function.

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Diesel exhaust (DE) can enter the organism body and cause multiple organ damage. DE contains particles that can be suspended in the air for a long time. Epigenetic regulation is a post transcriptional regulation change that does not involve DNA sequence changes. Many evidences showed that DE can affect the normal physiological functions of multiple organs and systems through epigenetic changes, thus regulating the occurrence and development of multiple diseases. This paper reviewed the research progress of DNA methylation and non-coding RNA in the biological harmful effects of DE. This will provide a basis for the safety evaluation, health risk assessment, and management of DE.

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We investigated whether exposure to carcinogenic diesel engine exhaust (DEE) was associated with altered adduct levels in human serum albumin (HSA) residues. Nano-liquid chromatography-high resolution mass spectrometry (nLC-HRMS) was used to measure adducts of Cys34 and Lys525 residues in plasma samples from 54 diesel engine factory workers and 55 unexposed controls. An untargeted adductomics and bioinformatics pipeline was used to find signatures of Cys34/Lys525 adductome modifications. To identify adducts that were altered between DEE-exposed and unexposed participants, we used an ensemble feature selection approach that ranks and combines findings from linear regression and penalized logistic regression, then aggregates the important findings with those determined by random forest. We detected 40 Cys34 and 9 Lys525 adducts. Among these findings, we found evidence that 6 Cys34 adducts were altered between DEE-exposed and unexposed participants (i.e., 841.75, 851.76, 856.10, 860.77, 870.43, and 913.45). These adducts were biologically related to antioxidant activity.

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Selective catalytic reduction (SCR) technology is currently the most effective deNOx technology and has broad application prospects. Moreover, there is a large NOx content in marine engine exhaust. However, the marine engine SCR catalyst will be affected by heavy metals, SO2, H2O(g), hydrocarbons (HC) and particulate matter (PM) in the exhaust, which will hinder the removal of NOx via SCR. Furthermore, due to the high loading operation of the marine engine and the regeneration of the diesel particulate filter (DPF), the exhaust temperature of the engine may exceed 600 °C, which leads to sintering of the SCR catalysts. Therefore, the development of new catalysts with good tolerances to the above emissions and process parameters is of great significance for further reducing NOx from marine engines. In this work, we first elaborate on the mechanism of the SCR catalyst poisoning caused by marine engine emissions, as well as the working mechanism of SCR catalysts affected by the engine exhaust temperature. Second, we also summarize the current technologies for improving the properties of SCR catalysts with the aim of enhancing the resistance and stability under complex working conditions. Finally, the challenges and perspectives associated with the performance optimization and technology popularization of marine SCR systems are discussed and proposed further. Consequently, this review may provide a valuable reference and inspiration for the development of catalysts and improvement in the denitration ability of SCR systems matched with marine engines.

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Health effects of particulate matter (PM) from aircraft engines have not been adequately studied since controlled laboratory studies reflecting realistic conditions regarding aerosols, target tissue, particle exposure and deposited particle dose are logistically challenging. Due to the important contributions of aircraft engine emissions to air pollution, we employed a unique experimental setup to deposit exhaust particles directly from an aircraft engine onto reconstituted human bronchial epithelia (HBE) at air-liquid interface under conditions similar to in vivo airways to mimic realistic human exposure. The toxicity of non-volatile PM (nvPM) from a CFM56-7B26 aircraft engine was evaluated under realistic engine conditions by sampling and exposing HBE derived from donors of normal and compromised health status to exhaust for 1 h followed by biomarker analysis 24 h post exposure. Particle deposition varied depending on the engine thrust levels with 85% thrust producing the highest nvPM mass and number emissions with estimated surface deposition of 3.17 × 109 particles cm-2 or 337.1 ng cm-2. Transient increase in cytotoxicity was observed after exposure to nvPM in epithelia derived from a normal donor as well as a decrease in the secretion of interleukin 6 and monocyte chemotactic protein 1. Non-replicated multiple exposures of epithelia derived from a normal donor to nvPM primarily led to a pro-inflammatory response, while both cytotoxicity and oxidative stress induction remained unaffected. This raises concerns for the long-term implications of aircraft nvPM for human pulmonary health, especially in occupational settings.

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Particulate matter (PM) causes several diseases, including cardiovascular diseases (CVDs). Previous studies compared the gene expression patterns in airway epithelial cells and keratinocytes exposed to PM. However, analysis of differentially expressed gene (DEGs) in endothelial cells exposed to PM2.5 (diameter less than 2.5 µm) from fossil fuel combustion has been limited. Here, we exposed human umbilical vein endothelial cells (HUVECs) to PM2.5 from combustion of gasoline, performed RNA-seq analysis, and identified DEGs. Exposure to the IC50 concentrations of gasoline engine exhaust PM2.5 (GPM) for 24 h yielded 1081 (up-regulation: 446, down-regulation: 635) DEGs. The most highly up-regulated gene is NGFR followed by ADM2 and NUPR1. The most highly down-regulated gene is TNFSF10 followed by GDF3 and EDN1. Gene Ontology enrichment analysis revealed that GPM regulated genes involved in cardiovascular system development, tube development and circulatory system development. Kyoto Encyclopedia of Genes and Genomes and Reactome pathway analyses showed that genes related to cytokine-cytokine receptor interactions and cytokine signaling in the immune system were significantly affected by GPM. We confirmed the RNA-seq data of some highly altered genes by qRT-PCR and showed the induction of NGFR, ADM2 and IL-11 at a protein level, indicating that the observed gene expression patterns were reliable. Given the adverse effects of PM2.5 on CVDs, our findings provide new insight into the importance of several DEGs and pathways in GPM-induced CVDs.

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Diesel engine exhaust (DEE) is classified as a Group 1 human carcinogen. Using a targeted proteomics approach, we aimed to identify proteins associated with DEE and characterize these markers to understand the mechanisms of DEE-induced carcinogenicity. In this cross-sectional molecular epidemiology study, we measured elemental carbon (EC) using a personal air monitor and quantified 1317 targeted proteins in the serum using the SOMAScan assay (SOMALogic) among 19 diesel exposed factory workers and 19 unexposed controls. We used linear regressions to identify proteins associated with DEE and examined their exposure-response relationship across levels of EC using linear trend tests. We further examined pathway enrichment of DEE-related proteins using MetaCore. Occupational exposure to DEE was associated with altered levels of 22 serum proteins (permutation p < .01). Of these, 13 proteins (CXCL11, HAPLN1, FLT4, CD40LG, PES1, IGHE.IGK..IGL, TNFSF9, PGD, NAGK, CCL25, CCL4L1, PDXK, and PLA2G1B) showed an exposure-response relationship with EC (p trend < .01), with serum levels of all but PLA2G1B declining with increasing air levels of EC. For instance, C-X-C Motif Chemokine Ligand 11 (CXCL11) showed the most significant association with DEE (ß = -0.25; permutation p = .00004), where mean serum levels were 4121.1, 2356.7, and 2298.8 relative fluorescent units among the unexposed, lower exposed (median, range : 56.9, 40.2-62.1 µg/m3 EC), and higher exposed (median, range of EC: 72.9, 66.9-107.7 µg/m3 EC) groups, respectively (p trend = .0005). Pathway analysis suggested that these proteins are enriched in pathways related to inflammation and immune regulation. Our study suggests that DEE exposure is associated with altered serum proteins, which play a role in inflammation and immune regulation.

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The use of renewable resources for powering self-ignition engines in European Union countries involves a high demand for renewable energy which is not accompanied by the development of its production infrastructure. The application of biofuel in vehicle powering is supposed to provide reductions in greenhouse gas emissions and an increase in the share of renewable energy resources in the total energy consumption. The study includes the analyses of power unit exhaust components, such as oxygen, carbon monoxide, nitric oxides, carbonizers, carbon dioxide and a quantity of exhaust particles contained in exhaust gases. Tests using an exhaust gas analyzer and a vapor analyzer were conducted. Three high-pressure engines, characterized by direct fuel injection, were tested. The vehicle computer software adjustments included increasing the fuel dose and the air load. Mixtures of diesel oil and fatty acid methyl esters were used in the tests. Based on the results, a statistical analysis was performed and an assessment model was developed to understand the functioning of the research objects fueled with these mixtures, with simultaneous software changes in the vehicle computers. On the basis of the conducted analysis, it was found that only 30% of fatty acid methyl ester additives to diesel oil reduced the performance parameters of the drive units.

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BACKGROUND: Exposure to fine and ultrafine particles from transport processes is a main consequence of emissions from engines, especially those with self-ignition. The particles released in these processes are a source of occupational and environmental particles exposure. The aim of this study was to assess the fine and nano-sized particles emission degree during work connected with transport and vehicle servicing. MATERIAL AND METHODS: The tests were carried out at 3 workplaces of vehicles service and maintenance (a car repair workshop, a truck service hall, and a bus depot) during 1 work day in each of them. Measurements were performed using the following devices: DISCmini meters, GRIMM 1.109 optical counter and the DustTrak monitor. The number, surface area and mass concentration, and the number size distribution were analyzed. RESULTS: The mean number concentration (DISCmini) increased during the analyzed processes, ranging from 4×104 p/cm3 to 8×104 p/cm3, and the highest concentration was found in the car repair workshop. The particles mean diameters during the processes ranged 31-47 nm, depending on the process. An increase in the surface area concentration value was observed in correlation with the particles number, and its highest concentration (198 m2/cm3) was found during work in the car repair workshop. The number size distribution analysis (GRIMM 1.109) showed the maximum value of the number concentration for particles sized 60 nm. The mean mass concentrations increased during the tested processes by approx. 40-70%, as compared to the background. CONCLUSIONS: According to the measurement results, all the workplaces under study constituted a source of an increase in all analyzed parameters characterizing emissions of nano-sized particles. Such working environment conditions can be harmful to the exposed workers; therefore, at such workplaces solutions for minimizing workers' exposure, such as fume hoods or respiratory protection, should be used. Med Pr. 2021;72(5):489-500.

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This study was conducted to evaluate the exposure of diesel engine exhaust (DEE) and oxidative stress among tank maintenance workers in the Republic of Korea Army. Airborne concentrations of elemental carbon (EC), polycyclic aromatic hydrocarbons (PAHs), and metals were measured at two units. Urine analysis for 1-hydroxypyrene and 8-hydroxy-2'-deoxyguanosine (8-OHdG) was performed for tank maintenance workers from one unit (n=17). To compare the level of 8-OHdG, the analysis was performed in 17 unexposed controls. The airborne EC concentration was 8.6-24.3 µg/m3 in indoor unit. EC was not detected in the outdoor unit. As for the PAHs, trace -0.0004 mg/m3 of naphthalene was detected. ITWA for 26 metals was calculated to be 0.009-0.027. The geometric mean urinary 1-hydroxypyrene was 0.08 µg/g creatinine. The geometric mean of 8-OHdG was 1.04 µg/g for the maintenance workers, while 0.45 µg/g for controls. The level of urinary 8-OHdG was significantly higher among maintenance workers in multivariate analysis. In conclusion, tank maintenance workers are exposed to various by-products from diesel engine combustion during work, and their level of oxidative stress marker was increased. Countermeasures for reducing hazardous substances in the military workplace are necessary.

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Recent technical developments brought negative side effects such as air pollution and large-scale fires, increasingly exposing people to diesel engine exhaust particles (DEP). Testing how DEP inhalation triggers pathophysiology in animal models could be useful in determining how it affects humans. To this end, the aim of this study was to investigate the effects of pulmonary exposure to DEP for seven consecutive days in experimental male C5BL6/N mice. Twenty-four C5BL6/N mice were treated with one of the three test materials: distilled water for control, a low DEP exposure (5 mg/kg), or a high DEP exposure (15 mg/kg). Exposure to DEP induced decreased body weight; however, it gradually increased pulmonary weight in a DEP-dose-dependent manner. DEP exposure significantly elevated soot accumulation in the lungs, with the alteration of pulmonary homeostasis. It also elevated infiltrated immune cells, thus significantly increasing inflammatory cytokine mRNA and protein production in the lungs and broncho-alveolar lavage fluid, respectively. Pulmonary DEP exposure also altered behavioral responses in the open field test (OFT). Low exposure elevated moving distance and speed, while significantly decreasing the number of trials to enter the central zone. Different concentrations of DEP resulted in different behavioral changes; however, while anxiety levels increased, their degree was independent of DEP concentrations. Results suggest that DEP exposure may possess pro-inflammatory responses in the lungs and trigger anxiety.

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