• Environmental Analysis Health and Toxicology
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• v.29
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• pp.9.1-9.3
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• 2014

Diesel exhaust particles (DEP) contain elemental carbon, organic compounds including Polyaromatic hydrocarbons (PAHs), metals, and other trace compounds. Diesel exhaust is complex mixture of thousands of chemicals. Over forty air contaminants are recognized as toxicants, such as carcinogens. Most diesel exhaust particles have aerodynamic diameters falling within a range of 0.1 to $0.25{\mu}m$. DEP was classified as a definite human carcinogen (group 1) by the International Agency for Research on Cancer at 2012 based on recently sufficient epidemiological evidence for lung cancer. Significant decreases in DEP and other diesel exhaust constituents will not be evident immediately, and outworn diesel car having longer mileage still threatens health of people in spite of recent remarkable development in diesel engine technology. Policy change in South Korea, such as introduction of diesel taxi, may raise health risk of air pollution in metropolitan area with these limitations of diesel engine. To protect people against DEP in South Korea, progressive strategies are needed, including disallowance of diesel taxi, more strict regulation of diesel engine emission, obligatory diesel particulate filter attachment in outworn diesel car, and close monitoring about health effects of DEP.

• Environmental Analysis Health and Toxicology
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• v.19 no.1
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• pp.59-64
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• 2004

Metallothionein gene expression of diesel exhaust particles (DEP) was investigated in human lung epithelial cell line. DEP was collected from diesel motor bus and soluble fraction in water was obtained. Cells, grown to near confluence, were exposed to 5-50 ppm DEP for 6 hours. Regarding the metallothionein gene expressions, MT-1 and MT-2 were induced in the DEP-treated cell by using RT-PCR and real-time PCR. However, MT-3 which is known to be brain specific, and another isoform MT-4 were not expressed in cadmium-treated groups as well as control group. Heavy metal of DEP was also analyzed and Zn was found as the major component of heavy metals in DEP used in this study.

• Asian Journal of Atmospheric Environment
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• v.1 no.1
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• pp.28-35
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• 2007

Accumulated epidemiological and animal studies have suggested that prolonged exposure to ambient particulate matter (PM) is associated with an increased risk of cardiovascular disease and pulmonary dysfunction. While diesel exhaust particles (DEP) contain large variety of compounds, polycyclic aromatic hydrocarbons (PAHs) are a dominant component contaminated in DEP. This article reviews effects of two PAH quinones, 9,10-phenanthraquinone (9,10-PQ) and l,2-naphthoquinone (l,2-NQ), on vascular and respiratory systems.

• Environmental Analysis Health and Toxicology
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• v.19 no.1
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• pp.109-117
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• 2004

The purpose of the present study was to examine the effect of diesel exhaust particles on human aortic vascular smooth muscle cells (VSMCs). DNA synthesis, cell viability and morphology of VSMCs after treatment of diesel exhaust particles (DEP) and fine particulate matter (PM$_{2.5}$) were assayed. PM$_{2.5}$ inhibited the DNA synthesis of VSMCs in a concentration -dependent manner, whereat DEP did not affect VSMCs up to 50$\mu\textrm{g}$/mL. These results were confirmed by morphological examination of VSMCs. PM$_{2.5}$ showed a dose-dependent cytotoxicity of VSMCs by MTT assay. Fraction 4 (organic acids) and fraction 8 (moderately polar compounds) showed the most potent inhibition of DNA synthesis of VSMCs, and fraction 7 (slightly polar compounds), fraction 9 (higher polar compounds), and fraction 6 (aromatic compounds) were next order. These results were confirmed by morphological examination of VSMCs. These results suggest that PM$_{2.5}$ inhibits the DNA synthesis of VSMCs through the cytotoxicity.oxicity.

• Journal of Korean Society for Atmospheric Environment
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• v.18 no.E2
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• pp.121-128
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• 2002

This study was carried out to investigate if nitric oxide synthase (NOS) inhibitors modulate airway inflammation induced by diesel exhaust particles (DEP). N$\^$G/-nitro-L-arginine methyl ester (L-NAME), a potent constitutive NOS (cNOS) inhibitor, and aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, were administered to mice in their drinking water for 7 weeks. Airway inflammation was elicited by the repeated intratracheal administration of DEP. The results showed that macrophages, inflammatory eosinophils and neutrophils in bronchoalveolar lavage (BAL) fluids by intratracheal DEP instillation were significantly suppressed in the mice treated with two NOS inhibitors toghther with DEP. The suppression of these cells was more effective in AG treated groups than in L -NAME treated groups. NOS inhibitor treatment also reduced interleukin -5 (IL-5 in the BAL fluids and lung homogenates. Additionally, it was found that eosinophil peroxidase (EPO) activity in the BAL fluids was also decreased by NOS inhibitor treatment. These results suggest that nitric oxide (NO) is produced in airway inflammation by repeated DEP instillation, and that iNOS inhibition as well as cNOS inhibition can play a modulating role in this airway inflammation by DEP.

• Korean Journal of Medicinal Crop Science
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• v.17 no.2
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• pp.90-96
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• 2009

The objective of this study was to investigate the effect of crude ginseng total saponins (CGS) against airway inflammation (AI) and airway hyperresponsiveness (AH) induced by diesel exhaust particles (DEP) in mice. AI and AH were induced by the intratracheal instillation with 0.1 $mg/m{\ell}$ of DEP suspension once a week for 10 weeks combined with ovalbumin (OVA) sensitization. Mice were also treated orally with 75 $mg/m{\ell}$ of CGS, 5 days a week for 10 weeks. Oral CGS treatment decreased in the level of serum immunoglobulin (IgE) and histamine increased by DEP and OVA, and declined respiratory resistance. It also dropped an enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF) of mice, and an increased T helper type 2 cell derived cytokine levels such as of interleukin (IL)-4, IL-13 and IL-5 in the BALF. However, it did not influence T helper type 1 cytokine such as interferon-gamma in the BALF. These results indicate that CGS may alleviate allergen-related AI and AH in mice and may play an important role in the modulation of asthmatic inflammation.

• Environmental Analysis Health and Toxicology
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• v.21 no.2 s.53
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• pp.127-138
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• 2006

In urban areas, diesel exhaust particles (DEP) are probably a major component of particulate matters, especially in Korea where drive many diesel vehicles. The aim of this study was to investigate genotoxic effects of DEP using single ceil gel electrophoresis. In order to evaluate the mechanisms of DEP genotoxicity, the rat microsome mediated and DNA repair enzyme treated comet assays together with conventional comet assay were performed. Total diesel particles (DEPT) was collected without site fractionation from diesel engine bus and dichloromethane extract was obtained. The organic extract of DEPT revealed DNA damage itself in NIH/3T3 cells. The level of DNA breaks plus oxidative DNA lesions and microsome mediated DNA damage was assessed by modified single cell gel eletrophoresis. DEPT was able to induce oxidative DNA damage as well as microsome mediated DNA damage. Vitamin C as an model antioxidant reduced DNA damage in endonuclase III treated comet assay. One of flavonoid, galangin as a CYP1A1 inhibitor. reduced DNA damage in the presence of S-9 mixture. $DEP_T$ is the sources of oxidative stress, but antioxidants can significantly reduce oxidative DNA dmage. And $DEP_T$ may contain indirect mutagens which can be inhibited by CYP1A1 inhibitors. The ethanol extracts of the mixed vegetables (BV) or the mixed fruits (BF) were evaluated for their in vitro antigenotoxic effects. BV and BF showed potent Inhibitory effects against DEPT induced DNA damage with oxidative DNA lesions and in the prescence of S-9 mixture. These results indicate that BV and BF could prevent cellular DNA damage by inhibiting oxidative stress and suppressing cytochrome P4501A1 in cell culture.

• Journal of Life Science
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• v.16 no.2 s.75
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• pp.192-198
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• 2006

Epidemiological studies have demonstrated an association between exposure to diesel exhaust particles (DEP) and adverse cardiopulmonary effects. Despite the epidemiological proof, the pathogenesis of DEP-related pulmonary diseases remain poorly understood. So, comprehensive in vivo and in vitro researches are required to know the effects of DEP on diverse lung diseases. Alveolar macrophages (AM) and airway epithelial cells are known as important cellular targets in DEP-induced lung diseases. Other studies have shown that nitric oxide (NO) is involved in particle matter induced lung injury. The present study was undertaken to determine whether DEP has an synergistic effects on lipopolysaccharide (LPS)-induced NO formation and inducible nitric oxide synthase (iNOS) with nitrotyrosilated-protein formation in cultured primary alveolar macrophages. The formation of NO was determined through the Griess reaction in the cultured medium and iNOS with nitrotyrosilated-proteins are analyzed by immunohistochemical staining and Western analysis. The results indicate that DEP exposure does not induce NO formation by itself, however DEP showed significant synergistic effects on LPS-induced NO formation. So, our results suggest that DEP inhalation could aggravate inflammatory lung disease through NO formation.

• Toxicological Research
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• v.22 no.1
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• pp.9-13
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• 2006

Diesel exhausted particles (DEP), a kind of fine particles with aerodynamic diameters less than $2.5{\mu}m$ (PM2.5), is of great concern to human health because they remain in atmosphere for long periods, invade an indoor air environment, and can be breathed most deeply into lung and reached the alveoli because of their small size ($0.1{\sim}0.4\;{\mu}m$ in diameter). Epidemiological and experimental studies suggested that DEP may play an active role in the increased respiratory mortality and morbidity. In addition to their physical characteristics, the chemical components including polyaromatic hydrocarbon (PAH) are regarded as a carcinogen causing pulmonary tumors. PLD plays an important role in cell proliferation with various physiological phenomena and affects other enzymes by activating signal transduction pathway. We investigated the cytotoxic mechanism of DEP on RAW 264.7 cells focusing on the role in activation of PLD. Our results suggested DEP induced PLD activity through a specific signaling pathway involving phospholipase $A_2$, PLC, PKC and $Ca^{2+}$ mobilization.

• Korean Journal of Medicinal Crop Science
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• v.20 no.2
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• pp.129-135
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• 2012

The feature of asthma are airway inflammation (AI), reversible airway obstruction, and an increased sensitivity to bronchoconstricting agents, elevated airway hyperresponsiveness (AHR), excess production of Th2 cytokines, and eosinophil accumulation in the lungs. This study was performed to investigate if oral administration of $Scutellaria$ $baicalensis$ Georgi water extracts (SBG) have the antiasthmatic potential for the treatment of asthma. Asthmatic HI and AHR were induced by systemic sensitization to ovalbumin (OVA) with intratracheal instillation with 0.1 mg/mL of diesel exhaust particles (DEP) suspension once a week for 10 weeks in BALB/c mice. SBG was orally administered with the concentraion of 200 mg/kg 5 days a week for 10 weeks. Long-term SBG treatment suppressed the eosinophil infiltration into airways from blood, the asthmatic AI and AHR by attenuating the production of cytokine IL-4, IL-5 and IL-13, histamine and OVA-specific IgE. Our data suggest that SBG has inhibitory effects on AI and AHR in a mouse model of asthma, may act as a potential Th2 cytokine antagonist, and may have a therapeutic effect on allergic asthma.