Diesel Exhaust Nanoparticles Research Articles

Lessons from nanosafety research for effective regulation and safer handling of nanomaterials at the workplace

At the turn of the twentieth century, nanotechnology was regarded as the new innovation potential. However, increased industrial use of nanomaterials raised concerns whether nanomaterial exposure could pose occupational health risks similar to asbestos. In 2012, the National Research Centre for the Working Environment (NFA) established the ‘Danish Centre for Nanosafety’ with the aim to provide evidence-based knowledge for policy advice on occupational handling of nanomaterials. Relevant stakeholders including the Danish Working Environment Authority (WEA), the Danish Environment Protection Agency, and the social partners were engaged. The project achieved societal impact in various ways: NFA produced documentation for health-based occupational exposure limits for three engineered nanomaterials and diesel exhaust nanoparticles at the request of WEA. Denmark adopted a national occupational exposure limit for diesel particles in 2021. WEA made a guidance document on safe handling of nanomaterials. The Working Environment Council published fact sheets based on knowledge from NFA aimed at both nanomaterial providers and enterprises using nanomaterials. A revised law made it compulsory to register the presence of nanomaterials in products in the Danish Product Registry. Finally, the Danish Centre for Nanosafety supported development of a free, web-based control-banding tool for occupational risk assessment and -management of nanomaterials (NanoSafer.org).

CARDIOPROTECTIVE POTENTIAL OF QUERCETIN AGAINST DIESEL OR PETROL EXHAUST NANOPARTICLE INDUCED TOXICITY: A PROSPECTIVE IN VITRO PHARMACOLOGICAL STUDY IN H9C2 CELLS

Objective: Phytochemicals are known to elicit potential antioxidant activity. This study examined the cardioprotective effects of quercetin against oxidative damage to rat cardiomyocyte cells (H9c2) after treatment with Diesel Exhaust Nanoparticles (DEPs) or Petrol Exhaust Nanoparticles (PEPs).
 Methods: Cardiomyocyte cells were exposed to DEPs or PEPs alone and in a combination with quercetin for 24 h.
 Results: Results showed that quercetin had no lethal effect on H9c2 cells up to a concentration of 1.0 μg/ml. Exposure to DEPs (4.0 μg/ml) or PEPs (10.0 μg/ml) induced cytotoxicity, oxidative stress, and inflammation (p<0.05). It also provoked lipid peroxidation by an increase in MDA and a decrease in SOD activity and glutathione activity (p<0.05). Simultaneous addition of quercetin restored these parameters to near normal.
 Conclusion: These results thus specify that quercetin plays a protective role in cardiac cells exposed to DEPs and PEPs.

Hippocampal inflammation and oxidative stress following exposure to diesel exhaust nanoparticles in male and female mice

Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are involved in the development and progression of central nervous system (CNS) diseases. Ultrafine particles (UFPs) plays an important role in global air pollution and the diesel exhaust particles (DEPs) are the most important component in this regard. There are more than 40 toxic air pollutants in diesel exhaust (DE), which is one of the main constituents of an environmental pollutant and including particulate matter (PM) especially UFPs. Thus, in this study, adult female and male NMRI mice were exposed to DEPs (350–400 μg/m3) for 14 weeks (6 h per day and 5 days per week). After 14 weeks of exposure, expression of pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, TNF-α), nNOS, HO1, NR2A, and NR2B and malondialdehyde (MDA) level were analyzed in various brain regions such as the hippocampus (HI) and olfactory bulb (OB). Exposure to DEPs caused neuroinflammation and oxidative stress in female and male mice. That these effects observed in females were less pronounced than in male mice. The male mice emerged to be more susceptible significantly than the female mice to induced neuroinflammation following DEPs exposure. Also, our findings indicate that long term exposure to DEPs results in altered expression of hippocampal NMDA receptor subunits, and suggests that gender can play important role in the modulating susceptibility to neurotoxicity induced by DEPs exposure.

Anxiety and Depression Following Diesel Exhaust Nano-Particles Exposure in Male and Female Mice

Anxiety and Depression Following Diesel Exhaust Nano-Particles Exposure in Male and Female Mice

Effects of Mesenchymal Stem Cells and Their Derived Microvesicles on Pulmonary Toxicity Induced by Petrol Exhaust Nanoparticle; Histological and Immuno-Histochemical Study

Background: Diesel vehicles exhaust contains toxic nanoparticles that drastically affect lung tissue due to their direct cytotoxic effects, induction of oxidative stress, inflammatory signaling pathways and DNA damage. Mesenchymal stem cells (MSCs) exhibit anti-inflammatory effects and efficient regenerative capacity in chronic lung diseases. 
 Objectives: Evaluation of the effects of MSCs and MSCs-derived micro vesicles (MSCs-MVs) on pulmonary toxicity induced by diesel exhaust nanoparticles (DENPs).
 Materials and Methods: Sixty male rats were equally divided into: Group I (Control rats), Group II (DENPs group) received repeated doses of DENPs (180μg/rat) intratracheally every other day for 6 days, Group III (MSCs group) received MSCs intravenously (3×106 cells) after the last dose of DENPs and Group IV (MSCs-MVs group) received MSCs-MVs (0.5 mg/mL) intravenously after the last dose of DENPs. Lung tissue were subjected to histological and immunohistochemical assessment. Inflammatory cytokines and bronchoalveolar lavage fluid (BALF) contents of inflammatory cells, albumin, LDH and total proteins were evaluated.
 Results: Histological picture of lung tissue in DENPs group showed numerous collapsed alveoli, thick interalveolar septa and marked cellular infiltration. Elastic fibers were markedly decreased by DENPs. Increased optical density of NF-κB/p65 immunoreactivity. Bronchoalveolar lavage fluid showed significant elevation of inflammatory cytokines (TNF-a, IL-6), polymorphonuclear leukocytes (PMN), neutrophils, macrophages, LDH, total proteins and albumin. Treatment with either MSCs or MSCs-MVs led to a significant amelioration of all of the aforementioned studied parameters.
 Conclusion: MSCs-MVs and MSCs showed significant therapeutic effects against DENPs damaging effects on the lung tissues via their regenerative capacity and anti-inflammatory effects.

Impact of quercetin on pulmonary toxicity induced by diesel exhaust nanoparticles in albino rat : Histological, immunohistochemical and biochemical study

Background: Diesel exhaust nanoparticles (DENPs) are one of the most prevalent environmental pollutants that adverselyaffect human health. DENPs are involved in the occurrence of chronic lung diseases such as COPD, bronchial asthma, chronicbronchitis and cancer.Objective: Evaluation of DENPs damaging effects on the pulmonary tissue and assessment of the possible protective effectsof Quercetin (QRT) on the lung tissue via histological, immunohistochemical and biochemical assessment.Materials and Methods: Forty-five albino male rats were divided into 3 groups: Group I (control rats), Group II (DENPsgroup) received repeated doses of DENPs (180μg/rat) intratracheally every other day for 6 days, Group III (DENPs + QRT)received quercetin orally (60 mg/kg B.Wt.) 1h before DENPs exposure. Examination of Lung tissues were conductedbyhistological and immunohistochemical techniques. Assessment of certain oxidative stress markers were also conducted.Results: Group II showedsignificant changes in the histological picture of the lung tissue with collapsed alveoli, thickinteralveolar septa and marked cellular infiltration. Collagen fibers were markedly increased by DENPs. Quercetin treatmentled to amelioration of the histological findings in the lung tissue with marked decrease in collagen fibers. QRT led to significantdecrease in iNOS immunoreactivity and increase in PCNA immunoreactivity.Conclusion: Quercetin has protective effects against pulmonary toxicity induced by DENPs via its anti-inflammatory effectsand anti-oxidant properties.

Diesel exhaust nanoparticles and their behaviour in the atmosphere.

Diesel engine emissions are by far the largest source of nanoparticles in many urban atmospheres, in which they dominate the particle number count, and may present a significant threat to public health. This paper reviews knowledge of the composition and atmospheric properties of diesel exhaust particles, and exemplifies research in this field through a description of the FASTER project (Fundamental Studies of the Sources, Properties and Environmental Behaviour of Exhaust Nanoparticles from Road Vehicles) which studied the size distribution-and, in unprecedented detail, the chemical composition-of nanoparticles sampled from diesel engine exhaust. This information has been systematized and used to inform the development of computational modules that simulate the behaviour of the largely semi-volatile content of the nucleation mode particles, including consequent effects on the particle size distribution, under typical atmospheric conditions. Large-eddy model studies have informed a simpler characterization of flow around the urban built environment, and include aerosol processes. This modelling and engine-laboratory work have been complemented by laboratory measurements of vapour pressures, and the execution of two field measurement campaigns in London. The result is a more robust description of the dynamical behaviour on the sub-kilometre scale of diesel exhaust nanoparticles and their importance as an urban air pollutant.

The possible protective role of quercetin on induced cardiac Oxidative DNA Damage by repeated exposure to diesel exhaust nanoparticles in rats (a histological and immunohistochemical study)

Abstract Diesel exhaust nanoparticles (DENPs) are gaseous exhaust and one component of particulate matter (PM) air pollution which is found to cause health hazards in humans. Quercetin is widely known for its antioxidant and antitoxic

Combined effects of diesel exhaust nanoparticles and high frequency electromagnetic fields on the permeability of an in vitro blood-brain barrier model

Air pollution-exposure is associated with detrimental outcomes in the central nervous system (CNS) such as cerebrovascular disorders, including stroke, and neurodegenerative diseases. While the mechanisms of these CNS-related outcomes involved have not been fully elucidated, exposure to traffic-generated air pollutants has been associated with altered blood brain barrier (BBB) integrity and permeability. The current study investigated whether inhalation exposure to mixed vehicle emissions (MVE) alters cerebral microvascular integrity in healthy 3 mo old C57BL/6 mice, as well as whether exposure-mediated effects were exacerbated by a high-fat (HF) vs. low-fat (LF) diet. Mice on each diet were randomly assigned to be exposed to either filtered air (FA) or MVE [100 PM/m3 vehicle emissions mixture: 30 µg PM/m3 gasoline engine + 70 µg PM/m3 diesel engine emissions; median size ~ 60 nm; particle mass size distribution median of ~ 1 µm (range: < 0.5–20 µm)] for 6 h/d, 7d/wk, for 30d. Using sodium fluorescein as a tracer, we observed a significant increase in BBB permeability in both HF + MVE exposed and HF + FA animals, compared to LF + FA controls. Exposure to HF + MVE also led to a significant increase plasma ox-LDL and ox-LDL scavenger receptors (LOX-1 and CD-36) expression in the cerebral vasculature. Histological analysis revealed decreased expression of TJ protein, claudin-5, associated with increased matrix metalloproteinase (MMP)−9 activity and oxidative stress in the cerebral vasculature of HF + MVE mice, compared to LF + MVE. Such findings indicate that inhalation exposure to traffic-generated pollutants, coupled with a HF diet, results in altered BBB integrity and increased ox-LDL signaling in the cerebral vasculature in a wildtype animal model.

Protein corona formation in bronchoalveolar fluid enhances diesel exhaust nanoparticle uptake and pro-inflammatory responses in macrophages

In biological fluids nanoparticles bind a range of molecules, particularly proteins, on their surface. The resulting protein corona influences biological activity and fate of nanoparticle in vivo. Corona composition is often determined by the biological milieu encountered at the entry portal into the body, and, can therefore, depend on the route of exposure to the nanoparticle. For environmental nanoparticles where exposure is by inhalation, this will be lung lining fluid.This study examined plasma and bronchoalveolar fluid (BALF) protein binding to engineered and environmental nanoparticles. We hypothesized that protein corona on nanoparticles would influence nanoparticle uptake and subsequent pro-inflammatory biological response in macrophages.All nanoparticles bound plasma and BALF proteins, but the profile of bound proteins varied between nanoparticles. Focusing on diesel exhaust nanoparticles (DENP), we identified proteins bound from plasma to include fibrinogen, and those bound from BALF to include albumin and surfactant proteins A and D. The presence on DENP of a plasma-derived corona or one of purified fibrinogen failed to evoke an inflammatory response in macrophages. However, coronae formed in BALF increased DENP uptake into macrophages two fold, and increased nanoparticulate carbon black (NanoCB) uptake fivefold. Furthermore, a BALF-derived corona increased IL-8 release from macrophages in response to DENP from 1720 ± 850 pg/mL to 5560 ± 1380 pg/mL (p = 0.014). These results demonstrate that the unique protein corona formed on nanoparticles plays an important role in determining biological reactivity and fate of nanoparticle in vivo. Importantly, these findings have implications for the mechanism of detrimental properties of environmental nanoparticles since the principle route of exposure to such particles is via the lung.

Evaporation of traffic-generated nanoparticles during advection from source

Abstract Earlier work has demonstrated the potential for volatilisation of nanoparticles emitted by road traffic as these are advected downwind from the source of emissions, but there have been few studies and the processes have yet to be elucidated in detail. Using a dataset collected at paired sampling sites located respectively in a street canyon and in a nearby park, an in depth analysis of particle number size distributions has been conducted in order to better understand the size reduction of the semi-volatile nanoparticles. By sorting the size distributions according to wind direction and fitting log normal modes, it can be seen that the mode peaking at around 22 nm at the street canyon site is on average shrinking to 6.2 nm diameter at the park site which indicates a mean shrinkage rate for these particles of 0.13 nm s−1 with temperatures within the range 12–18 °C. The diurnal variation of the shrunken mode in the park reflects the diurnal pattern of particle concentrations at the street canyon site taken as the main source area. An analysis of peak diameter for the smallest mode at the downwind park site shows an inverse relationship to wind speed suggesting that dilution rather than travel time is the main determinant of the particle shrinkage rate. An evaluation of previously collected C10 to C35 n-alkane data from a different urban location shows a good fit to Pankow partitioning theory reflecting the semi-volatility of compounds believed to be representative of the composition of diesel exhaust nanoparticles, hence confirming the feasibility of an evaporative mechanism for particle shrinkage.

Determination of LC50 and sub-chronic neurotoxicity of diesel exhaust nanoparticles

Air pollution is a major problem faced globally and is seen associated with central nervous system (CNS) disorders like neuropathology and neuro-inflammation. Here, we investigated the CNS disorders as a result of sub-chronic exposure (90 days) to diesel exhaust nanoparticles (DENPs) and explored the minimal levels of DENPs needed to exhibit the early mediators of neuro-inflammation and neuropathology. Male and female wistar rats (6 rats per group) were exposed to DENPs (1/5th, 1/10th and 1/15th LC50) by inhalation for 4h per day, 5 days per week over 90 days and neurotoxicity end-points were analyzed. DENP exposure caused elevation in levels of pro-inflammatory cytokines, amyloid beta 42 (Aβ 42), reactive oxygen species (ROS), hydrogen peroxide (H2O2), nitrate (NO3−), nitrite (NO2−) and apurinic/apyrimidinic sites (AP) at varying degrees at different sections of rat brain. Hence, exposure to DENPs resulted in dose-dependent toxicity and was closely correlated to increased inflammation, DNA damage and oxidative stress.

Brain suppression of AP-1 by inhaled diesel exhaust and reversal by cerium oxide nanoparticles

One of the uses of cerium oxide nanoparticles (nanoceria, CeO2) is as a diesel fuel additive to improve fuel efficiency. Gene/environment interactions are important determinants in the etiology of age-related disorders. Thus, it is possible that individuals on high-fat diet and genetic predisposition to vascular disease may be more vulnerable to the adverse health effects of particle exposure. The aim of this pilot study was to test the hypothesis that inhalation of diesel exhaust (DE) or diesel exhaust-containing cerium oxide nanoparticles (DCeE) induces stress in the brain of a susceptible animal model. Atherosclerotic prone, apolipoprotein E knockout (ApoE−/−) mice fed a high-fat diet, were exposed by inhalation to purified air (control), DE or DCeE. The stress-responsive transcription factor, activator protein-1 (AP-1), was significantly decreased in the cortical and subcortical fraction of the brain after DE exposure. The addition of nanoceria to the diesel fuel reversed this effect. The activation of another stress-related transcription factor (NF-κB) was not inhibited. AP-1 is composed of complexes of the Jun and/or Fos family of proteins. Exposure to DCeE caused c-Jun activation and this may be a mechanism by which addition of nanoceria to the fuel reversed the effect of DE exposure on AP-1 activation. This pilot study demonstrates that exposure to DE does impact the brain and addition of nanoceria may be protective. However, more extensive studies are necessary to determine how DE induced reduction of AP-1 activity and compensation by nanoceria impacts normal function of the brain.

Interactive effects of cerium oxide and diesel exhaust nanoparticles on inducing pulmonary fibrosis

Cerium compounds have been used as a fuel-borne catalyst to lower the generation of diesel exhaust particles (DEPs), but are emitted as cerium oxide nanoparticles (CeO2) along with DEP in the diesel exhaust. The present study investigates the effects of the combined exposure to DEP and CeO2 on the pulmonary system in a rat model. Specific pathogen-free male Sprague–Dawley rats were exposed to CeO2 and/or DEP via a single intratracheal instillation and were sacrificed at various time points post-exposure. This investigation demonstrated that CeO2 induces a sustained inflammatory response, whereas DEP elicits a switch of the pulmonary immune response from Th1 to Th2. Both CeO2 and DEP activated AM and lymphocyte secretion of the proinflammatory cytokines IL-12 and IFN-γ, respectively. However, only DEP enhanced the anti-inflammatory cytokine IL-10 production in response to ex vivo LPS or Concanavalin A challenge that was not affected by the presence of CeO2, suggesting that DEP suppresses host defense capability by inducing the Th2 immunity. The micrographs of lymph nodes show that the particle clumps in DEP+CeO2 were significantly larger than CeO2 or DEP, exhibiting dense clumps continuous throughout the lymph nodes. Morphometric analysis demonstrates that the localization of collagen in the lung tissue after DEP+CeO2 reflects the combination of DEP-exposure plus CeO2-exposure. At 4weeks post-exposure, the histological features demonstrated that CeO2 induced lung phospholipidosis and fibrosis. DEP induced lung granulomas that were not significantly affected by the presence of CeO2 in the combined exposure. Using CeO2 as diesel fuel catalyst may cause health concerns.

English

The environmental problems in India are growing rapidly. The increasing economic development and a rapidly growing population that has taken the country from 300 million people in 1947 to more than one billion people today, is putting a strain on the environment, infrastructure, and the country&rsquo;s natural resources. Industrial pollution, soil erosion, deforestation, rapid industrialization,&nbsp;urbanization, and land degradation are all worsening problems. Over-exploitation of the country&#39;s resources, be it land or water, and the industrialization process, has resulted in environmental&nbsp;degradation of&nbsp;resources. Environmental pollution is one of the most serious problems facing humanity and other life forms on our planet today. The rapid growth in motor vehicle activity and rapid industrialization is contributing to high levels of urban air pollution.&nbsp;The population is mainly exposed to high air pollution concentrations; where motor vehicle emissions constitute the main source of fine and ultrafine particles, having a serious impact on our urban air quality and public health.Studies showed that the composition of atmospheric particulate matter has a great impact on human health.&nbsp;In this study, we have reviewed the toxicity of vehicle exhaust, especially diesel exhaust nanoparticles and the associated health problems. &nbsp; Key words:&nbsp;Pollution, diesel exhaust, toxicity, air pollutants, nanoparticles.

Thermal desorption – comprehensive two-dimensional gas chromatography coupled with tandem mass spectrometry for determination of trace polycyclic aromatic hydrocarbons and their derivatives

We developed a highly sensitive method for determination of polycyclic aromatic hydrocarbons (PAHs) and their derivatives (oxygenated, nitrated, and methylated PAHs) in trace particulate samples by using thermal desorption followed by comprehensive two-dimensional gas chromatography coupled with tandem mass spectrometry (TD–GC×GC–MS/MS) with a selected reaction monitoring mode. The sensitivity of TD–GC×GC–MS/MS was greater than that of TD–GC–HRMS and TD–GC×GC–QMS by one or two orders of magnitude. The instrumental detection limits were 0.03–0.3pg (PAHs), 0.04–0.2pg (oxygenated PAHs), 0.03–0.1pg (nitrated PAHs), and 0.01–0.08pg (methylated PAHs). For small amounts (10–20μg) of standard reference materials (SRMs 1649a and 1650b, urban dust and diesel exhaust particles, respectively), the values measured by using TD–GC×GC–MS/MS agreed with the certified or reference values within a factor of two. Major analytes were quantified successfully by TD–GC×GC–MS/MS from diesel exhaust nanoparticles (18–32nm) and accumulation-mode particles (100–180nm) from an 8-L diesel engine with no exhaust after-treatment system. The PAH profiles differed among driving conditions but they did not differ markedly among the particle sizes.

Characterization of Dilution Conditions for Diesel Nanoparticle Inhalation Studies

Diesel exhaust nanoparticles easily coagulate during transportation from the engine to the inhalation chamber, depending on concentrations and residence times. Although dilution is effective in suppressing coagulation growth of nanoparticles, volatile organic carbon (OC) evaporates as a result of dilution. Thus, the design of an inhalation facility to investigate the health effects of nanoparticle-rich exhaust is important. In this study, we determined the optimum dilution conditions in consideration of coagulation growth and evaporation of OC for inhalation studies of nanoparticle-rich diesel exhaust. We found that a short residence time prevented coagulation growth in the primary dilution tunnel after the primary dilution or before the diluted exhaust reached the inhalation chamber after the secondary dilution. However, due to the longer residence time in the inhalation chamber, the coagulation growth occurred in the inhalation chamber depending on secondary dilution ratio which controlled exposure dose (particle concentration in the inhalation chamber). We determined that the secondary dilution ratio for the high-concentration chamber should be around 4.5 times to prevent coagulation growth and to obtain the desired exposure dose. We also found that the loss of OC was relatively independent of the secondary dilution ratio when the secondary dilution ratio was more than 10 times because it seemed to reach a gas–particle equilibrium in the inhalation chamber. We therefore set the secondary dilution ratios for the middle- and low-concentration chambers to 13.5 and 40.5 times, respectively.

Effects of eicosane, a component of nanoparticles in diesel exhaust, on surface activity of pulmonary surfactant monolayers

Recently, it has been reported that n-alkanes are principal components of diesel exhaust nanoparticles. We investigated the effects of n-alkanes on the surface activity of a pulmonary surfactant monolayer using both fresh surfactant isolated from mouse lungs, and 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC), a major component of lung surfactant. To examine the effect of n-alkanes on the surfactant, we compared surface pressure/trough area isotherm features and topographic images of DPPC in the presence and absence of a specific n-alkane (eicosane, C(20)H(42)) by Langmuir-Wilhelmy methods. The pure DPPC isotherm shows a typical plateau feature at a monolayer collapse pressure of 70 mN/m. The collapse pressure diminishes with increasing concentration of eicosane in DPPC. DPPC monolayers containing eicosane exhibit isotherms with one phase transition, but not the coexistence plateau of a liquid-expanded (LE) and liquid-condensed (LC) phase observed with a pure DPPC monolayer. Atomic force microscopy studies suggest that a DPPC monolayer containing eicosane has the phase transition from LE phase to LC phase and the protrusions are squeezed out from the monolayer, below the phase transition. On the other hand, eicosane changes the isotherm from mouse lung surfactant less dramatically than that of DPPC. The addition of increasing amounts of eicosane to mouse surfactant increases surface compressibility at 30 mN/m during the second compression, suggesting that the deposition of alkane-rich nanoparticles onto pulmonary surfactants may be related to dysfunction of surfactant activity during breathing.

Effect of Lubricant on the Formation of Heavy-Duty Diesel Exhaust Nanoparticles

The effect of lubricants on nanoparticle formation in heavy-duty diesel exhaust with and without a continuously regenerating diesel particulate filter (CRDPF) is studied. A partial flow sampling system with a particle size distribution measurement starting from 3 nm, approximately, is used. Tests are conducted using four different lubricant formulations, a very low sulfur content fuel, and four steady-state driving modes. A well-documented test procedure was followed for each test. Two different kinds of nanoparticle formation were observed, and both were found to be affected bythe lubricant but in differentway. Without CRDPF, nanoparticles were observed at low loads. No correlation between lubricant sulfur and these nanoparticles was found. These nanoparticles are suggested to form mainly from hydrocarbons. With CRDPF, installed nanoparticles were formed only at high load. The formation correlated positively with the lubricant (and fuel) sulfur level, suggesting that sulfuric compounds are the main nucleating species in this situation. Storage effects of CRDPF had an effect on nanoparticle concentration as the emissions of nanoparticles decreased over time.