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The Italian Interministerial Decree of February 11, 2021, introduces the diesel engine exhaust (DDE) among the carcinogenic occupational compounds, also establishing an occupational exposure limit. Elemental carbon (EC), improperly called black carbon, has been proposed as a tracer of DDE exposure; EC is the carbon that is quantified in the ambient matrixes after all the organic carbon has been removed; traditionally, EC is measured with a thermo-optical analytical technique. EC determination and relative interpretation are challenging for the following reasons: (i) the scarce availability of equipped laboratories hampers EC analysis, (ii) EC interpretation is not easy due to the lack of reference values. Finally, (iii) the limit value of 0.050 mg/m³ of EC in the workplace appears too high compared to recently published exposure data. All these aspects stimulate a reflection on the significance of EC data in the context of both occupational hygiene and occupational medicine. [ABSTRACT FROM AUTHOR]

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.

Copyright of Low-Carbon Chemistry & Chemical Engineering is the property of Low-Carbon Chemistry & Chemical Engineering Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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. [ABSTRACT FROM AUTHOR]

Abstract 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.

Abstracts: 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.

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.

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. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study investigated time trends in occupational exposure to various chemicals in Sweden and the distribution across demographic and labor market sectors. METHODS: Exposure to six chemicals was investigated from 1980 to 2013 by application of a job exposure matrix to national population registers. Respirable crystalline silica (RCS), diesel engine exhaust, welding fumes, wood dust, chlorinated hydrocarbon solvents, and lead were selected to represent different groups of chemicals. Trends in exposure prevalence were investigated by linear regression and compared to the occupationally active population. Confidence intervals for the rate of change over time were obtained by bootstrapping. RESULTS: The proportion of workers born outside the Nordic countries increased over time in those exposed to RCS, diesel exhaust and wood dust. There was a shift of exposed jobs to small companies (

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. [ABSTRACT FROM AUTHOR]

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. [Display omitted] • High levels of PAH exposure were associated with elevated FBG, and three key OH-PAHs (1-OHNa, 2-OHPh, and 9-OHPh) were identified. • The sirtuin signaling, asparagine metabolism, and proline metabolism pathways were related to PAHs induced dysglycemia. • 2-Aminooctanoic acid as a novel biomarker mediated the association between different structural OH-PAHs and elevated FBG concentrations. [ABSTRACT FROM AUTHOR]

Objective This study investigated time trends in occupational exposure to various chemicals in Sweden and the distribution across demographic and labor market sectors. Methods Exposure to six chemicals was investigated from 1980 to 2013 by application of a job exposure matrix to national population registers. Respirable crystalline silica (RCS), diesel engine exhaust, welding fumes, wood dust, chlorinated hydrocarbon solvents, and lead were selected to represent different groups of chemicals. Trends in exposure prevalence were investigated by linear regression and compared to the occupationally active population. Confidence intervals for the rate of change over time were obtained by bootstrapping. Results The proportion of workers born outside the Nordic countries increased over time in those exposed to RCS, diesel exhaust and wood dust. There was a shift of exposed jobs to small companies (<50 employees), especially for RCS, welding fumes, wood dust, and chlorinated hydrocarbon solvents. For RCS and welding fumes, there was a marked drop in exposure levels from 1980 to 1990 but small changes thereafter. Exposure to lead diminished, both in terms of prevalence and intensity. Conclusions Over time, several exposures tended to shift to small companies, the construction sector, and migrant workers, all factors being indicative of less well-controlled working conditions. Occupational exposure to chlorinated organic solvents and lead diminished, while exposure levels to RCS and welding fumes have changed little since 1990. In view of the serious and well-established negative health effects, increased efforts to reduce exposure to RCS and welding fumes are needed. [ABSTRACT FROM AUTHOR]

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/cm 3 to 8×104 p/cm 3 , 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 m 2 /cm 3 ) 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

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.

Respirable crystalline silica in mineral dust, wood dust, diesel engine exhaust emissions and welding fumes are among the most common process‐generated substances to which millions of workers are exposed daily. The composition of process‐generated substances can vary substantially, depending on the parameters of the underlying processes; for example, the composition and intensity of diesel motor emissions differs among the various generations of diesel engines and working environments (e.g. surface or underground mining). We illustrate how common these occupational exposures are and discuss challenges in estimating their global prevalence and their contribution to the burden of occupational cancer. Estimates of the number and proportion of workers exposed in most countries and on a global scale are generally scarce. A remarkable exception is based on the proactive bottom‐up estimates generated within the European Network for Silica. Actions to reduce exposures and research to fill gaps in knowledge adapted to local settings are warranted to mitigate the occupational cancer burden, especially in under‐researched settings including low‐ and middle‐income countries.

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 (β = −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. [ABSTRACT FROM AUTHOR]

Diesel engine exhaust (DEE) and crystalline silica exposures occur simultaneously in the mining industry, and occupational sampling campaigns can be time- and cost-consuming. The authors evaluated a dual-port system for simultaneous sampling of DEE and crystalline silica in laboratory and field conditions. Laboratory tests evaluated the operation of pumps during 8 h sampling and the intensity of the flow variation for various filter loading conditions and for different modes of operation. Field validation was performed in an underground mine. Pumps operated in constant flow or constant pressure modes. Tests in constant flow mode showed that when the flowrate increased on one side of the system, it decreased on the opposite side according to the loading intensity. Tests in constant pressure mode showed that flowrates systematically decreased when using loaded cassettes. However, the higher the backpressure setting, the lower the flow variation was. Flow variations during field tests were generally within the acceptable ±5% range. However, significant flow variations were identified in higher concentrations. A significant negative correlation was found between flowrate variation and total carbon concentration. While the majority of tests support the use of the dual-port for evaluating concomitant exposures, results highlight the possibility of filter overloading as a cause of flowrate changes.

The rising rate of pollution in urban areas has become a worldwide concern in recent years. Diesel engines are considered one of the largest contributors to environmental pollution caused by exhaust emissions, and they are responsible for several health problems as well. Diesel engines contain carbon monoxide, carbon dioxide, unburned hydrocarbons, and oxides of nitrogen. The reduction of Nitric oxides (NOx) emission from diesel engine exhaust is currently being researched by automotive manufacturers. After much research, selective catalytic reduction (SCR) technology was discovered to be effective in reducing nitrogen oxide emission from diesel engine exhaust. This paper is an attempt to explore the problems associated with the use of selective catalytic reduction (SCR) and compares selective catalytic reduction (SCR) with the latest technology named solid selective catalytic reduction (SSCR) for efficient reduction of NOx emission from the exhaust of diesel engines. The issue of contamination, malfunctioning, and freezing of diesel exhaust fluid (DEF) at low temperatures are the major problems associated with the application of SCR. It is observed that by controlling the quantity of ammonia slip, SSCR can give better performance in the reduction of NOx emission from the exhaust of diesel engines. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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. This study aims to investigate the airway inflammation and hyperresponsiveness and its relationship with ILC after DEE exposure. 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. 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. 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. [Display omitted] • Long-term DEE exposure can initiate asthmatic characteristic including AHR and airway inflammation in mice. • The airway inflammation is feature as mix Th2/Th17 response. • The functional proportions of IL-5+ILC2 and IL-17+ILC were higher than that of Th2 and Th17 cells. • Lung-resident ILCs can induce a mixed Th2/Th17 response and AHR after CD4 depletion. • Inhibition of ILCs may be a potential strategy for DEE induced-respiratory disease. [ABSTRACT FROM AUTHOR]

The synchronous removal of soot particles and NO x using high-performance catalysts is a research hotspot in the catalytic purification of diesel engine exhaust. In this paper, glucose is used as a complexing agent to successfully prepare a series of praseodymium and/or potassium doped La–Ni-based perovskite catalysts. The La 0.9 Pr 0.05 K 0. 05 NiO 3 catalyst exhibits the best catalytic performance when NO 2 is present in the environment, with values of T 10 , T 50 , and T 90 at 287, 331, and 361 °C, respectively. The CO 2 selectivity reaches over 98% and has good thermal stability. Through characterization experiments, it was found that the co-doping of Pr and K can lead to the formation of oxygen vacancies by changing the valence state of Ni atoms, thereby increasing the adsorption and activation centers of reactive oxygen species, and enhancing the oxygen storage capacity of the catalyst through the redox cycle between Pr3+ and Pr4+. • A novel porous soot catalytic material was prepared using bimetallic doped perovskite. • Bimetal doping increases the active oxygen and oxygen vacancy contents of perovskite. • Conduct comprehensive tests on the characterization and properties of materials. • The prepared materials exhibit excellent catalytic and thermal stability performance. • The required materials for preparation are cheap and green. [ABSTRACT FROM AUTHOR]

Due to the way occupational exposure limits (OELs) are set in Canada, workers across the country are not equally and adequately protected from harmful workplace exposures. This disparity is illustrated in the case of exposure to diesel engine exhaust (DEE). Based on the findings of a recent pan-Canadian and international scan of OELs for DEE, we recommend that Canada overcome these current disparities by moving towards harmonized, evidence-based OELs. To achieve this, Canada should adopt a centralized framework for setting OELs that considers the most recent scientific evidence as well as feasibility of implementation in the Canadian context. We assert that harmonizing OELs across Canada would allow for expertise and resources to be consolidated and is a crucial step to ensuring that all workers are consistently protected from harmful workplace exposures. [ABSTRACT FROM AUTHOR]

Respirable crystalline silica in mineral dust, wood dust, diesel engine exhaust emissions and welding fumes are among the most common process‐generated substances to which millions of workers are exposed daily. The composition of process‐generated substances can vary substantially, depending on the parameters of the underlying processes; for example, the composition and intensity of diesel motor emissions differs among the various generations of diesel engines and working environments (e.g. surface or underground mining). We illustrate how common these occupational exposures are and discuss challenges in estimating their global prevalence and their contribution to the burden of occupational cancer. Estimates of the number and proportion of workers exposed in most countries and on a global scale are generally scarce. A remarkable exception is based on the proactive bottom‐up estimates generated within the European Network for Silica. Actions to reduce exposures and research to fill gaps in knowledge adapted to local settings are warranted to mitigate the occupational cancer burden, especially in under‐researched settings including low‐ and middle‐income countries. [ABSTRACT FROM AUTHOR]

Objectives: This study provides a detailed analysis of the global and regional burden of cancer due to occupational carcinogens from the Global Burden of Disease 2016 study.Methods: The burden of cancer due to 14 International Agency for Research on Cancer Group 1 occupational carcinogens was estimated using the population attributable fraction, based on past population exposure prevalence and relative risks from the literature. The results were used to calculate attributable deaths and disability-adjusted life years (DALYs).Results: There were an estimated 349 000 (95% Uncertainty Interval 269 000 to 427 000) deaths and 7.2 (5.8 to 8.6) million DALYs in 2016 due to exposure to the included occupational carcinogens-3.9% (3.2% to 4.6%) of all cancer deaths and 3.4% (2.7% to 4.0%) of all cancer DALYs; 79% of deaths were of males and 88% were of people aged 55 -79 years. Lung cancer accounted for 86% of the deaths, mesothelioma for 7.9% and laryngeal cancer for 2.1%. Asbestos was responsible for the largest number of deaths due to occupational carcinogens (63%); other important risk factors were secondhand smoke (14%), silica (14%) and diesel engine exhaust (5%). The highest mortality rates were in high-income regions, largely due to asbestos-related cancers, whereas in other regions cancer deaths from secondhand smoke, silica and diesel engine exhaust were more prominent. From 1990 to 2016, there was a decrease in the rate for deaths (-10%) and DALYs (-15%) due to exposure to occupational carcinogens.Conclusions: Work-related carcinogens are responsible for considerable disease burden worldwide. The results provide guidance for prevention and control initiatives. [ABSTRACT FROM AUTHOR]

Abstract Background Increasing evidence from toxicological and epidemiological studies indicates that the central nervous system is an important target for ambient air pollutants. We have investigated whether long-term inhalation exposure to diesel engine exhaust (DEE), a dominant contributor to particulate air pollution in urban environments, can aggravate Alzheimer’s Disease (AD)-like effects in female 5X Familial AD (5XFAD) mice and their wild-type female littermates. Following 3 and 13 weeks exposures to diluted DEE (0.95 mg/m3, 6 h/day, 5 days/week) or clean air (controls) behaviour tests were performed and amyloid-β (Aβ) plaque formation, pulmonary histopathology and systemic inflammation were evaluated. Results In a string suspension task, assessing for grip strength and motor coordination, 13 weeks exposed 5XFAD mice performed significantly less than the 5XFAD controls. Spatial working memory deficits, assessed by Y-maze and X-maze tasks, were not observed in association with the DEE exposures. Brains of the 3 weeks DEE-exposed 5XFAD mice showed significantly higher cortical Aβ plaque load and higher whole brain homogenate Aβ42 levels than the clean air-exposed 5XFAD littermate controls. After the 13 weeks exposures, with increasing age and progression of the AD-phenotype of the 5XFAD mice, DEE-related differences in amyloid pathology were no longer present. Immunohistochemical evaluation of lungs of the mice revealed no obvious genetic background-related differences in tissue structure, and the DEE exposure did not cause histopathological changes in the mice of both backgrounds. Luminex analysis of plasma cytokines demonstrated absence of sustained systemic inflammation upon DEE exposure. Conclusions Inhalation exposure to DEE causes accelerated plaque formation and motor function impairment in 5XFAD transgenic mice. Our study provides further support that the brain is a relevant target for the effects of inhaled DEE and suggests that long-term exposure to this ubiquitous air pollution mixture may promote the development of Alzheimer’s disease.

Objectives: Using nationwide register data, we investigated the association between maternal and paternal perinatal employment in industries with exposure to diesel engine exhaust and risk of leukaemia and central nervous system (CNS) cancers, including certain subtypes.Methods: Children aged≤19 years and diagnosed with childhood cancer from 1968 to 2016 were identified in the Danish Cancer Registry and 25 randomly selected cancer-free controls per case were matched by age and sex. Parents were identified in the Danish Civil Registration System and employment histories were retrieved from a nationwide mandatory pension fund. The probability of exposure to diesel engine exhaust was assessed using a validated job exposure matrix. Conditional logistic regression was used for estimation of ORs, including their 95% CIs.Results: Maternal employment in industries with diesel engine exhaust exposure was associated with an increased risk of CNS cancers (OR 1.31, 95% CI 0.99 to 1.74) and of astrocytoma (OR 1.49, 95% CI 1.04 to 2.14) in offspring. The highest OR for these cancers were seen for mothers with highest probability of exposure to diesel engine exhaust. For fathers, ORs for cancers under study were close to one. No increased risks of leukaemias were found for either mothers or fathers employed in diesel industries.Conclusions: Risks were increased for CNS and astrocytoma for maternal employment in industries with diesel engine exhaust. [ABSTRACT FROM AUTHOR]

Metabolites of polycyclic aromatic hydrocarbons measured in human samples are often used as biomarkers of exposure to diesel engine exhaust (DEE). The aim of this study was to assess the changes in urinary levels of 1-aminopyrene (1-AP) and 1-hydroxypyrene (1-OHP) and their relationship with Elemental Carbon (EC), as a component of diesel engine exhaust exposure, among a hard-rock gold-mining population. Urine samples were collected at the beginning and end of a 12-hour work shift from 100 underground and above ground gold miners. Miners were fitted with personal exposure monitoring equipment to quantify exposure to DEE, measured as Elemental Carbon (EC), across their 12-hour work shift. General linear regression assessed associations of the post-shift urinary 1-AP and 1-OHP concentrations with EC, controlling for age, gender, the pre-shift biomarker level, Body Mass Index (BMI), days on current shift, time in mining, smoking status and second-hand smoke exposure. The concentrations of 1-AP and 1-OHP increased significantly across a 12-hour mining work shift. Moreover, consistent with the sensitivity analysis, the concentration of 1-AP was significantly associated with EC after adjustments. Urinary 1-OHP, but not 1-AP was significantly associated with current smoking. Urinary 1-AP may be a more robust and specific biomarker of DEE than 1-OHP. Unlabelled Image • Elemental carbon measured as a surrogate of diesel exhaust by personal monitors • Urinary 1-AP and 1-OHP increased significantly across a 12-hour work shift. • 1-AP showed a robust and significant association with elemental carbon. [ABSTRACT FROM AUTHOR]

Emissions of NOX from automobile causes various environmental impacts. In order to satisfy the emission norms and standards, it is necessary to reduce the toxic gases from emission. This paper concentrates on designing a packed column and analysis on the selection of an effective absorbent to reduce NOX emission from diesel engines. NOX emission is taken from the exhaust of diesel engine (Kirloskar TV1 Diesel engine). Flue gas inlet to the packed column and the treated gas at the outlet of the packed column are measured using NOX inlet and outlet gas sensors, respectively. Absorbent flow is carried out in a lab-scale packed column experimental setup. Various parameters of the packed column such as liquid: gas ratio, diameter, total height and packing height are determined based on the mathematical modeling. The NOX emission was experimentally measured with various combinations of different absorbents with different flow rate. Based on the experiments, effective absorbents are chosen as NaClO2 and NaOH. Experimental results show chemical absorbent combination with 0.5 M concentration of sodium chlorite and 0.3 M concentration of sodium hydroxide at 80% data acquisition card opening condition is absorbing NOX effectively. [ABSTRACT FROM AUTHOR]

Abstract Diesel engine exhaust (DEE), which is the product of diesel combustion, is considered carcinogenic in humans. It comprises toxic gases, polycyclic aromatic hydrocarbons (PAHs) and particulate matter which can reach the pulmonary parenchyma and trigger various diseases, including cancer. The aim of the present study was to evaluate the potential cytotoxic and genotoxic effects of DEE exposure on peripheral blood and buccal epithelial cells in mechanics occupationally exposed to DEE. We recruited 120 exposed mechanics and 100 non-exposed control individuals. Significant differences were observed between the two groups in terms of percentage of tail DNA and damage index (DI) in the alkaline comet assay; levels of biomarkers by cytokinesis-block micronucleus cytome (CBMN-Cyt) assay; frequency of micronucleus (MN), nucleoplasmic bridge (NPB), nuclear bud (NBUD) and apoptotic cells (APOP) and levels of biomarkers for micronucleus, karyorrhexis (KRX), karyolysis (KRL) and condensed chromatin (CC) by the buccal micronucleus cytome (BM-Cyt) assay. A significant and positive correlation was found between the frequency of MN in lymphocytes and buccal cells in the exposed group. Also, there was a significant correlation between age and percentage of tail DNA and DI in the comet assay, APOP and MN in the CBMN-Cyt assay and NBUD and MN in the BM-Cyt assay. Additionally, we found a positive and significant correlation of MN frequency in lymphocytes and buccal cells and age and MN frequency in lymphocytes with the time of service (years). Regarding lifestyle-related factors, a significant correlation was observed between meat and vitamin consumption and NBUD formation on CBMN-Cyt and between meat consumption and MN formation on CBMN-Cyt. Of the BM-Cyt biomarkers, there was a correlation between alcohol consumption and NBUD formation and between binucleated cell (BN), pyknosis (PYC), CC and KRL occurrence and family cancer history. These results are the first data in Colombia on the cytotoxic and genotoxic effects induced by continuous exposure to DEE and thus showed the usefulness of biomarkers of the comet, CBMN-Cyt and BM-Cyt assays for human biomonitoring and evaluation of cancer risk in the exposed populations. Graphical abstract fx1 Highlights • Significant differences in biomarkers evaluated between exposed and control group. • A significant correlation between age and percentage tail DNA and DI in comet assay. • A significant correlation between age and APOP and MN in the CBMN-Cyt assay. • A significant correlation between age and NBUD and MN in the BM-Cyt assay. • A significant correlation between meat consumption and MN occurrence on CBMN-Cyt. [ABSTRACT FROM AUTHOR]

Abstract NTP based Ozone injection cascaded with catalysts/adsorbents for diesel exhaust treatment has been demonstrated by various researchers as a competent method for mitigation of nitrogen oxides. In this present study, one more NTP reactor is cascaded instead of catalysts/adsorbents to treat the ozone mixed diesel exhaust. While most of the laboratory studies were carried out using expensive dry air cylinders for ozone generation, in the present study, ozone has been generated from atmospheric air only. The nitrogen oxides removal/conversion efficiency of this process depends on various electrical and physical parameters. A dimensionless relation has been obtained between the ratio of summation of NO and NO 2 concentrations after treatment to that before treatment and other parameters affecting nitrogen oxides removal using dimensional analysis. Prediction of sum of NO and NO 2 concentrations with the variation in six dominant parameters have been done using nonlinear regression technique. Six parameters, i.e. ozone concentration, voltage, frequency, flow rate, temperature and discharge gap have been varied to collect the experimental data required to train and test this model. The predicted sum of NO and NO 2 concentrations are found to be well matching with the experimental results. The RMS error is found to be 3.7 % and 5.9 % respectively for training and test data. [ABSTRACT FROM AUTHOR]

Abstract Non-thermal plasma technique (NTP) for mitigation of NO X from diesel engine exhaust is a laboratory proven technique with a good number of experimental studies. However, there are constraints which are preventing this technique to appear in practical applications. Prior prediction of exhaust characteristics with the NTP treatment according to the variations in its operating parameters can be a step ahead to make this technique applicable in real time. In this present study, experiments are conducted by varying parameters voltage, flow rate, temperature, discharge gap and initial sum of NO and NO 2 concentrations. Six hundred number of datasets are collected to train and test the predictive models which are made using multilayer perceptrons (MLP). The objective of these models is to predict the sum of NO and NO 2 concentrations at the downstream of the reactor during NTP based diesel exhaust treatment. As a part of the study, optimum number of neurons in the hidden layers is also found out. The root mean square error (RMSE) of an MLP with two hidden layers, each of 20 neurons, is found to be 3.29 ppm. Results assure that the prediction of sum of NO and NO 2 concentrations can be achieved with a good accuracy using MLP. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to estimate the number of workers exposed to diesel engine exhaust (DEE) by industry and year in the Republic of Korea. Method: The estimates of workers potentially exposed to DEE in the Republic of Korea were calculated by industry on the basis of the carcinogen exposure (CAREX) surveillance system. The data on the labor force employed in DEE exposure industries were obtained from the Census on Establishments conducted by the Korea National Statistical Office from 1993 to 2013. The mean values of prevalence rates adopted by EU15 countries were used as the primary exposure prevalence rates. We also investigated the exposure prevalence rates and exposure characteristics of DEE in 359 workplaces representing 11 industries. Results: The total number of workers exposed to DEE were estimated as 270,014 in 1993 and 417,034 in 2013 (2.2% of the total labor force). As of 2013, the industry categorized as “Land transport” showed the highest number of workers exposed to DEE with 174,359, followed by “Personal and household services” with 70,298, “Construction” with 45,555, “Wholesale and retail trade and restaurants and hotels” with 44,005, and “Sanitation and similar services” with 12,584. These five industries, with more than 10,000 workers exposed to DEE, accounted for 83% of the total DEE-exposed workers. Comparing primary prevalence rates used for preliminary estimation among 49 industries, “Metal ore mining” had the highest rate at 52.6%, followed by “Other mining” with 50.0%, and “Land transport” with 23.6%. Conclusion: The DEE prevalence rates we surveyed (1.3–19.8%) were higher than the primary prevalence rates. The most common emission sources of DEE were diesel engine vehicles such as forklifts, trucks, and vans. Our estimated numbers of workers exposed to DEE can be used to identify industries with workers requiring protection from potential exposure to DEE in the Republic of Korea.

Objectives: Diesel exhaust fumes emission is a significant source of ultrafine particles, the size of which is expressed in nanometers. People occupationally exposed to diesel exhaust particles include mainly workers servicing vehicles with engines of this type. This article presents the analysis of measurements of ultrafine particle concentrations occurring in the bus depot premises during the work connected with everyday technical servicing of buses. Material and Methods: The measurements were carried out in the everyday servicing (ES) room of the bus depot before, during and after the work connected with bus servicing. Determinations included: particle concentrations in terms of particle number and particle surface area, and mass concentrations of aerosol. Results: Mean value of number concentration of 10- to 1000-nm particles increased almost 20-fold, from 7600 particles/cm3 before starting bus servicing procedures to 130 000 particles/cm3 during the bus servicing procedures in the room. During the procedures, the mean surface area concentration of particles potentially deposited in the alveolar (A) region was almost 3 times higher than that of the particles depositing in the tracheo-bronchial (TB) region: 356.46 μm2/cm3 vs. 95.97 μm2/cm3, respectively. The mass concentration of the fraction of particulate matter with aerodynamic diameter 0.02–1 μm (PM1) increased 5-fold during the analyzed procedures and was 0.042 mg/m3 before, and 0.298 mg/m3 while the procedures continued. Conclusions: At the time when bus servicing procedures continued in the ES room, a very high increase in all parameters of the analyzed particles was observed. The diesel exhaust particles exhibit a very high degree of fragmentation and, while their number is very high and their surface area is very large, their mass concentration is relatively low. The above findings confirm that ultrafine particles found in diesel exhaust fumes may be harmful to the health of the exposed people, and to their respiratory tract in particular.

The Diesel Exhaust in Miners Study is unquestionably the most suitable data material to date to examine a possible link between diesel engine emissions and lung cancer risk. But the results do not appear to be consistent in themselves. The crucial methodological problem in this study, however, has yet to be discovered, to which the lack of any description of age related information (year of birth, year of hire, year of first exposure, year of death) for the cohort as well as for the cases might have contributed. This information is important to understand the flaws in the analysis. It turns out that the year of birth is associated with the exposure, i.e. with the chance to be exposed over a certain period of time as well as with the chance to be an ever-smoker. A further important issue for the interpretation of the results is the validity of the data on smoking, which are mainly obtained from next of kin for decedents up to 50 years after death. Taking all these aspects into account, it can be concluded that only the SMR-analysis can be considered from all published results. [ABSTRACT FROM AUTHOR]

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The International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross‐sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)‐1, IL‐6, IL‐8, tumor necrosis factor (TNF)‐α, macrophage inflammatory protein (MIP)‐1β, and monocyte chemotactic protein (MCP)‐1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP‐1β were significantly reduced by ∼37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM2.5 concentrations in all subjects (Ptrend < 0.001) as well as in exposed subjects only (Ptrend = 0.001). Levels of IL‐8 and MIP‐1β were significantly lower in workers in the highest exposure tertile of PM2.5 (>397 µg/m3) compared to unexposed controls. Further, significant inverse exposure‐response relationships for IL‐8 and MCP‐1 were also found in relation to increasing PM2.5 levels among the DEE exposed workers. Given that IL‐8, MIP‐1β, and MCP‐1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144–150, 2018. © 2017 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]