Search Results (101)

Air pollution, particularly from vehicular emissions, has emerged as a critical environmental health concern, contributing to a global estimated 7 million premature deaths annually. Diesel exhaust, a major component of urban air pollution, contains fine particulate matter and gases that evade respiratory filtration, penetrating deep into the lungs and triggering oxidative stress, inflammation, and immune dysregulation. Epidemiological and in vitro studies have linked diesel exhaust exposure to respiratory diseases such as asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and lung cancer, with immunological mechanisms playing a central role. Diesel exhaust particles induce oxidative stress, impair macrophage phagocytosis, and skew T-cell polarization toward pro-inflammatory Th2 and Th17 responses, exacerbating chronic inflammation and tissue damage. Despite these insights, significant gaps remain in understanding the precise immunomodulatory pathways and long-term systemic effects of diesel exhaust exposure. While animal models and in vitro studies provide valuable data, they often fail to capture the complexity of human exposure and immune responses. Further research is needed to elucidate the mechanisms underlying diesel exhaust-induced immune dysregulation, particularly in vulnerable populations with pre-existing respiratory conditions. This review focuses on summarizing the current knowledge and identifying gaps that are essential for developing targeted interventions and policies to mitigate the adverse health impacts of diesel exhaust and improve respiratory health outcomes globally. Full article

Background/Objectives: Inhalation of environmental particulate air pollution has been reported to cause pulmonary and systemic events including coagulation disturbances, systemic inflammation, and oxidative stress. Nerolidol, a naturally occurring sesquiterpene alcohol, has effective antioxidant and anti-inflammatory effects. Hence, the aim in the present investigation was to evaluate the potential ameliorative effects of nerolidol on the coagulation and systemic actions induced by pulmonary exposure to diesel exhaust particles (DEPs). Methods: Nerolidol (100 mg/kg) was given to mice by oral gavage one hour before the intratracheal instillation of DEPs (0.5 mg/kg), and 24 h later various markers of coagulation and systemic toxicity were evaluated. Results: Nerolidol treatment significantly abrogated DEP-induced platelet aggregation in vivo and in vitro. Nerolidol has also prevented the shortening of the prothrombin time and activated plasma thromboplastin time triggered by DEP exposure. Likewise, while the concentrations of fibrinogen and plasminogen activator inhibitor-1 were increased by DEP administration, that of tissue plasminogen activator was significantly decreased. These effects were abolished in the group of mice concomitantly treated with nerolidol and DEP. Moreover, plasma markers of inflammation, oxidative stress, and endothelial dysfunction which were significantly increased in the DEP-treated group, returned to control levels in the nerolidol + DEP group. Nerolidol treatment significantly ameliorated the increase in the concentrations of hypoxia-inducible factor 1α, galectin-3, and neutrophil gelatinase-associated lipocalin induced by pulmonary exposure to DEP. The co-administration of nerolidol + DEPs significantly mitigated the increase in markers of oxidative DNA damage, 8-hydroxy-2-deoxyguanosine, and apoptosis, cleaved-caspase-3, induced by DEP. Conclusions: Collectively, our data demonstrate that nerolidol exert significant ameliorative actions against DEP-induced thrombotic events, endothelial dysfunction, systemic inflammation, oxidative stress, DNA damage, and apoptosis. Pending further pharmacological and toxicological studies, nerolidol could be a promising agent to alleviate the toxicity of inhaled DEPs and other pollutant particles. Full article

Exposure to air pollution poses a risk to human respiratory health, and a preventive and therapeutic remedy against fine dust-induced respiratory disease is needed. Background/Objectives: The respiratory-protective effects of Lysimachia mauritiana (LM) against airway inflammation were evaluated in a mouse model exposed to a fine dust mixture of diesel exhaust particles and particulate matter with a diameter of less than 10 µm (PM10D). Methods: To induce airway inflammation, PM10D was intranasally injected into BALB/c mice three times a day for 12 days, and LM extracts were given orally once per day. The immune cell subtypes, histopathology, and expression of inflammatory mediators were analyzed from the bronchoalveolar lavage fluid (BALF) and lungs. Results: LM alleviated the accumulation of neutrophils and the number of inflammatory cells in the lungs and the BALF of the PM10D-exposed mice. LM also reduced the release of inflammatory mediators (MIP-2, IL-17, IL-1α, CXCL1, TNF-α, MUC5AC, and TRP receptor channels) in the BALF and lungs. Lung histopathology was used to examine airway inflammation and the accumulation of collagen fibers and inflammatory cells after PM10D exposure and showed that LM administration improved this inflammation. Furthermore, LM extract inhibited the MAPK and NF-κB signaling pathway in the lungs and improved expectoration activity through an increase in phenol red release from the trachea. Conclusions: LM alleviated PM10D-exposed neutrophilic airway inflammation by suppressing MAPK/NF-κB activation. This study indicates that LM extract may be an effective therapeutic agent against inflammatory respiratory diseases. Full article

To fill a research gap on firefighter exposures and breast cancer risk, and guide exposure reduction, we aimed to identify firefighter occupational exposures linked to breast cancer. We conducted a systematic search and review to identify firefighter chemical exposures and then identified the subset that was associated with breast cancer. To do this, we compared the firefighter exposures with chemicals that have been shown to increase breast cancer risk in epidemiological studies or increase mammary gland tumors in experimental toxicology studies. For each exposure, we assigned a strength of evidence for the association with firefighter occupation and for the association with breast cancer risk. We identified twelve chemicals or chemical groups that were both linked to breast cancer and were firefighter occupational exposures, including polycyclic aromatic hydrocarbons, volatile aromatics, per- and polyfluoroalkyl substances, persistent organohalogens, and halogenated organophosphate flame retardants. Many of these were found at elevated levels in firefighting environments and were statistically significantly higher in firefighters after firefighting or when compared to the general population. Common exposure sources included combustion byproducts, diesel fuel and exhaust, firefighting foams, and flame retardants. Our findings highlight breast-cancer-related chemical exposures in the firefighting profession to guide equitable worker’s compensation policies and exposure reduction. Full article

Introduction: Exposure to environmental pollutants such as diesel exhaust particles (DEP) increases the risk of respiratory disease exacerbation. However, the possible effects of these particles on the general population remain poorly understood. The present study aimed to assess the immunomodulatory and inflammatory effects of the inhalation of DEP in a model of healthy mice undergoing short-, mid- and long-term exposure. Materials and Methods: BALB/c ByJ mice were randomly divided into five experimental groups. The control group received three intranasal instillations of saline over 8 days while the other four groups received intranasal instillations of 150 µg of DEP 3 days per week for 8, 17, 26, and 53 days. Lung function assessment and flow cytometry were performed. Results: In lung tissue, intranasal exposure to DEP decreased total monocytes (p < 0.015 in all groups). At 26 days, a reduction in inflammatory monocytes and an increase in resident monocytes were observed, p = 0.001 and 0.0001, respectively. Eosinophils and neutrophils decreased at 26 days (p = 0.017 and p = 0.041, respectively). The intranasal challenges of DEP increased the total population of dendritic cells (DC) at 26 and 53 days (p = 0.017 and p = 0.022, respectively) and decreased the total and alveolar populations of macrophages (p < 0.003 for all groups compared to control), while interstitial macrophage populations increased over the time period (p = 0.0001 for all groups compared to control). Conclusions: Continuous DEP exposure triggers immune mechanisms that predispose healthy individuals to a pro-inflammatory and hyper-reactive microenvironment. This mouse model provides evidence of the capacity of DEP to increase DC, interstitial macrophages, and resident monocytes. Full article

This study assessed workers’ exposure to vehicle exhaust emissions and its health effects at the Lebombo Port of Entry. A quantitative cross-sectional design was adopted, and a structured questionnaire was administered on 209 adult workers to measure their knowledge on vehicle exhaust emissions exposures. Air samples were also collected from the participants using air sampling pumps. Data were analyzed using Statistical Package for Social Sciences, version 27. Logistic regression was performed to examine the association between dependent variables and some sociodemographic factors. Vocational certificates and associate degrees were attributed to workers in the South African Police Services and those in Agriculture: (Odds Ratio) = 2.83%, Confidence Interval (1.41–5.65) and (Odds Ratio) = 4.58%, Confidence Interval (2.10–9.99), respectively. Divorced males had a high level of knowledge and awareness of vehicle exhaust emission and their health effects: (Adjusted Odds Ratio) = 5.31%, Confidence Interval (1.08–26.14). Males had better knowledge of vehicle exhaust emission with carcinogenic effects: (Adjusted Odds Ratio) = 3.28%, Confidence Interval (1.11–9.67). Having an associate’s degree as the highest level of education and irritation of nose and eyes were associated with lower awareness of vehicle exhaust emissions: (Adjusted Odds Ratio) = 0.42%, Confidence Interval (0.19–0.97) and (Adjusted Odds Ratio) = 0.31%, Confidence Interval (0.13–0.76), respectively. The diesel particulate matter concentration was higher during day shifts (0.027 mg/m³) compared to night shifts (0.021 mg/m³), p = 0.001. Seventy-one workers (34%) reported experiencing acute headaches often, and fewer workers (n = 31, 14.8%) reported to have never suffered from an acute headache. A majority of workers (71 (34%)) experienced acute irritation of nose and eyes often compared to a few (33 (16%)) workers who experienced the same less often. In addition, a majority of workers (84 (40.2%)) experienced acute fatigue and nausea often, while fewer workers (37 (17.7%)) experienced fatigue and nausea very often. The majority of workers (n = 116, 55.5%) suffered cough and sneezing more often compared to others. There is an urgent need for improved and effective controls to reduce workers’ exposure to vehicle exhaust emissions. Full article

This research aimed to analyze the possibility of installing an ultrasonic emitter in an already manufactured car and to prove the possibility of cleaning the exhaust gases of an internal combustion engine through the action of an ultrasonic wave due to coagulation and examining the optimal regimes of its work. The existing theoretical solution to describe the proposed process was analyzed. A Mercedes-Benz M-Class ML 270 CDI MT car with the OM 612 DE 27 LA Diesel engine was used for the experiment. An ultrasound generator and an ultrasound emitter were connected to the muffler. The stand was connected to the car via the inlet with a rubber hose that directs the exhaust gases out of the car. The crankshaft speed of the engine was changed in the range of 750 to 1250 rpm, which corresponds to urban conditions when cars are moving in heavy traffic jams. The content of CH, CO, CO₂, and O₂ in the exhaust gas of the vehicle was determined as a function of the crankshaft speed without ultrasonic exposure and with ultrasonic exposure at an ultrasound frequency of 25, 28, and 40 kHz. The results of the experiment showed that the introduction of an ultrasonic emitter into the muffler reduced the smoke content of the gas, increased the oxygen content, and reduced the amount of carbon dioxide in the exhaust gases. With an increase in the ratio between the ultrasonic frequency and the angular velocity of the engine crankshaft (f/ω), the smoke content of the gas also decreased. At the maximum values of ultrasonic frequency and angular velocity of the engine crankshaft selected in the experimental studies, the minimum value of the ratio of gas smoke indicators was achieved, and the degree of purification was 10–13%. Such results correspond to the condition of optimal operation of the ultrasonic muffler, where the ratio of gas to smoke values should tend to a minimum. These results confirm the potential of using ultrasound as a method for cleaning exhaust gases and underline the need for further research in this area. Full article

Airborne particulate matter (PM) is of great concern in the modern-day atmosphere owing to its association with a variety of health impacts, such as respiratory and cardiovascular diseases. Of the various size fractions of PM, it is the finer fractions that are most harmful to health, in particular ultrafine particles (PM_0.1; UFPs), with an aerodynamic diameter ≤ 100 nm. The smaller size fractions, of ≤2.5 µm (PM_2.5; fine particles) and ≤0.1 µm (PM_0.1; ultrafine particles), have been shown to have numerous linkages to negative health effects; however, their collection/sampling remains challenging. This review paper employed a comprehensive literature review methodology; 200 studies were evaluated based on the rigor of their methodologies, including the validity of experimental designs, data collection methods, and statistical analyses. Studies with robust methodologies were prioritised for inclusion. This review paper critically assesses the health risks associated with fine and ultrafine particles, highlighting vehicular emissions as the most significant source of particulate-related health effects. While coal combustion, diesel exhaust, household wood combustors’ emissions, and Earth’s crust dust also pose health risks, evidence suggests that exposure to particulates from vehicular emissions has the greatest impact on human health due to their widespread distribution and contribution to air pollution-related diseases. This article comprehensively examines current sampling technologies, specifically focusing on the collection and sampling of ultrafine particles (UFP) from ambient air to facilitate toxicological and physiochemical characterisation efforts. This article discusses diverse approaches to collect fine and ultrafine particulates, along with experimental endeavours to assess ultrafine particle concentrations across various microenvironments. Following meticulous evaluation of sampling techniques, high-volume air samplers such as the Chem Vol Model 2400 High Volume Cascade Impactor and low-volume samplers like the Personal Cascade Impactor Sampler (PCIS) emerge as effective methods. These techniques offer advantages in particle size fractionation, collection efficiency, and adaptability to different sampling environments, positioning them as valuable tools for precise characterisation of particulate matter in air quality research and environmental monitoring. Full article

Limited knowledge exists regarding gasoline and diesel exhaust effects on lipid metabolism. This study collected gasoline and diesel exhaust under actual driving conditions and conducted inhalation exposure on male young and middle-aged C57BL/6J mice for 4 h/day for 5 days to simulate commuting exposure intensity. Additionally, PM_2.5 from actual roadways, representing gasoline and diesel vehicles, was generated for exposure to human umbilical vein endothelial cells (HUVECs) and normal liver cells (LO2) for 24, 48, and 72 h to further investigate exhaust particle toxicity. Results showed that diesel exhaust reduced total cholesterol and low-density lipoprotein cholesterol levels in young mice, indicating disrupted lipid metabolism. Aspartate aminotransferase and alanine aminotransferase levels increased by 53.7% and 21.7%, respectively, suggesting potential liver injury. Diesel exhaust exposure decreased superoxide dismutase and increased glutathione peroxidase levels. Cell viability decreased, and reactive oxygen species levels increased in HUVECs and LO2 following exposure to exhaust particles, with dose- and time-dependent effects. Diesel exhaust particles exhibited more severe inhibition of cell proliferation and oxidative damage compared to gasoline exhaust particles. These findings provide novel evidence of the risk of disrupted lipid metabolism due to gasoline and diesel exhaust, emphasizing the toxicity of diesel exhaust. Full article

Diesel exhaust particles (DEPs) contribute to air pollution exposure-related adverse health impacts. Here, we examined in vitro, and in vivo toxicities of DEPs from a Caterpillar C11 heavy-duty diesel engine emissions using ultra-low-sulfur diesel (ULSD) and biodiesel blends (20% v/v) of canola (B20C), soy (B20S), or tallow–waste fry oil (B20T) in ULSD. The in vitro effects of DEPs (DEP_ULSD, DEP_B20C, DEP_B20S, and DEP_B20T) in exposed mouse monocyte/macrophage cells (J774A.1) were examined by analyzing the cellular cytotoxicity endpoints (CTB, LDH, and ATP) and secreted proteins. The in vivo effects were assessed in BALB/c mice (n = 6/group) exposed to DEPs (250 µg), carbon black (CB), or saline via intratracheal instillation 24 h post-exposure. Bronchoalveolar lavage fluid (BALF) cell counts, cytokines, lung/heart mRNA, and plasma markers were examined. In vitro cytotoxic potencies (e.g., ATP) and secreted TNF-α were positively correlated (p < 0.05) with in vivo inflammatory potency (BALF cytokines, lung/heart mRNA, and plasma markers). Overall, DEP_ULSD and DEP_B20C appeared to be more potent compared to DEP_B20S and DEP_B20T. These findings suggested that biodiesel blend-derived DEP potencies can be influenced by biodiesel sources, and inflammatory process- was one of the potential underlying toxicity mechanisms. These observations were consistent across in vitro and in vivo exposures, and this work adds value to the health risk analysis of cleaner fuel alternatives. Full article

Air pollution poses a significant global health risk, with fine particulate matter (PM_2.5) such as diesel exhaust particles (DEPs) being of particular concern due to their potential to drive systemic toxicities through bloodstream infiltration. The association between PM_2.5 exposure and an increased prevalence of metabolic disorders, including obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), is evident against a backdrop of rising global obesity and poor metabolic health. This paper examines the role of adipose tissue in mediating the effects of PM_2.5 on metabolic health. Adipose tissue, beyond its energy storage function, is responsive to inhaled noxious stimuli, thus disrupting metabolic homeostasis and responding to particulate exposure with pro-inflammatory cytokine release, contributing to systemic inflammation. The purpose of this study was to characterize the metabolic response of adipose tissue in mice exposed to either DEPs or room air (RA), exploring both the adipokine profile and mitochondrial bioenergetics. In addition to a slight change in fat mass and a robust shift in adipocyte hypertrophy in the DEP-exposed animals, we found significant changes in adipose mitochondrial bioenergetics. Furthermore, the DEP-exposed animals had a significantly higher expression of adipose inflammatory markers compared with the adipose from RA-exposed mice. Despite the nearly exclusive focus on dietary factors in an effort to better understand metabolic health, these results highlight the novel role of environmental factors that may contribute to the growing global burden of poor metabolic health. Full article

3-methyl-4-nitrophenol (PNMC), a well-known constituent of diesel exhaust particles and degradation products of insecticide fenitrothion, is a widely distributed environmental contaminant. PNMC is toxic to the female reproductive system; however, how it affects meiosis progression in oocytes is unknown. In this study, in vitro maturation of mouse oocytes was applied to investigate the deleterious effects of PNMC. We found that exposure to PNMC significantly compromised oocyte maturation. PNMC disturbed the spindle stability; specifically, it decreased the spindle density and increased the spindle length. The weakened spindle pole location of microtubule-severing enzyme Fignl1 may result in a defective spindle apparatus in PNMC-exposed oocytes. PNMC exposure induced significant mitochondrial dysfunction, including mitochondria distribution, ATP production, mitochondrial membrane potential, and ROS accumulation. The mRNA levels of the mitochondria-related genes were also significantly impaired. Finally, the above-mentioned alterations triggered early apoptosis in the oocytes. In conclusion, PNMC exposure affected oocyte maturation and quality through the regulation of spindle stability and mitochondrial function. Full article

Over the past decade, our understanding of the impact of air pollution on short- and long-term population health has advanced considerably, focusing on adverse effects on cardiovascular and respiratory systems. There is, however, increasing evidence that air pollution exposures affect cognitive function, particularly in susceptible groups. Our study seeks to assess and hazard rank the cognitive effects of prevalent indoor and outdoor pollutants through a single-centre investigation on the cognitive functioning of healthy human volunteers aged 50 and above with a familial predisposition to dementia. Participants will all undertake five sequential controlled exposures. The sources of the air pollution exposures are wood smoke, diesel exhaust, cleaning products, and cooking emissions, with clean air serving as the control. Pre- and post-exposure spirometry, nasal lavage, blood sampling, and cognitive assessments will be performed. Repeated testing pre and post exposure to controlled levels of pollutants will allow for the identification of acute changes in functioning as well as the detection of peripheral markers of neuroinflammation and neuronal toxicity. This comprehensive approach enables the identification of the most hazardous components in indoor and outdoor air pollutants and further understanding of the pathways contributing to neurodegenerative diseases. The results of this project have the potential to facilitate greater refinement in policy, emphasizing health-relevant pollutants and providing details to aid mitigation against pollutant-associated health risks. Full article

Particulate matter (PM) in the context of underground mining results from various operations such as rock drilling and blasting, ore loading, hauling, crushing, dumping, and from diesel exhaust gases as well. These operations result in the formation of fine particles that can accumulate in the lungs of mineworkers. The lung deposited surface area (LDSA) concentration is a variant solution to evaluate potential health impacts. The aim of this study is to analyse PM and LDSA concentrations in the operational workings of the oil shale underground mine. Experimental measurements were carried out by a direct-reading real-time PM monitor, Dusttrak DRX, and a multimetric fine particle detector, Naneous Partector 2, during the loading and dumping processes using the diesel engine loader. Consequently, the analysis was conducted on PM, LDSA, particle surface area concentration (SA), average particle diameter (d), particle number concentration (PNC), and particle mass (PM_0.3), producing a few valuable correlation factors. Averaged LDSA was around 1433 μm²/cm³ and reached maximum peaks of 2140 μm²/cm³ during the loading, which was mostly related to diesel exhaust emissions, and within the dumping 730 μm²/cm³ and 1840 μm²/cm³, respectively. At the same time, average PM₁ was about 300 μg/ m³ during the loading, but within the dumping peaks, it reached up to 10,900 μg/ m³. During the loading phase, particle diameter ranged from 30 to 90 nm, while during the dumping phase peaks, it varied from 90 to 160 nm. On this basis, a relationship between PNC and particle diameter has been produced to demonstrate an approximate split between diesel particulate matter (DPM) and oil shale dust diameters. This study offers important data on PM and LDSA concentration that can be used for estimating potential exposure to miners at various working operations in the oil shale underground mines, and will be used for air quality control in accordance with establishing toxic aerosol health effects. Full article

Diesel particulate matter is one of the most dangerous environmental stressors affecting human health. Many plant-derived compounds with antioxidant and anti-inflammatory properties have been proposed to protect the skin from pollution damage. Curcumin (CUR) has a plethora of pharmacological activities, including anticancer, antimicrobial, anti-inflammatory and antioxidant. However, it has low bioavailability due to its difficult absorption and rapid metabolism and elimination. CUR encapsulation in nanotechnological systems and its combination with biopotentiators such as piperine (PIP) can improve its pharmacokinetics, stability and activity. In this study, ethosomes (ETs) were investigated for CUR and PIP delivery to protect the skin from damage induced by diesel particulate matter. ETs were produced by different strategies and characterized for their size distribution by photon correlation spectroscopy, for their morphology by transmission electron microscopy, and for their drug encapsulation efficiency by high-performance liquid chromatography. Franz cells enabled us to evaluate in vitro the drug diffusion from ETs. The results highlighted that ETs can promote the skin permeation of curcumin. The studies carried out on their antioxidant activity demonstrated an increase in the antioxidant power of CUR using a combination of CUR and PIP separately loaded in ETs, suggesting their possible application for the prevention of skin damage due to exogenous stressors. Ex vivo studies on human skin explants have shown the suitability of drug-loaded ETs to prevent the structural damage to the skin induced by diesel engine exhaust exposure. Full article