Biomedical subjects

M Sagai

Publications and source records attributed to M Sagai.

At least 19 recordsLinked to original sources

PubMed2001

Exposure to diesel exhaust exacerbates allergen-induced airway responses in guinea pigs.

Diesel exhaust (DE) is a major air pollutant in urban areas. To clarify the effects of DE on the exacerbation of asthma, guinea pigs were exposed 12 h daily to 3 mg/m(3) DE or air for 8 wk with or without sensitization to ovalbumin (OVA). In the DE-exposed sensitized animals, both immediate (IAR) and late (LAR) airway responses were enhanced after the inhalation challenge by OVA, compared with the DE-unexposed sensitized animals. Mucus was greatly accumulated in the airways of DE-exposed sensitized animals during IAR. The number of eosinophils and level of sialic acid concentration in bronchial lavage fluids were also significantly higher in the DE-exposed sensitized animals than in the DE-unexposed control animals. During LAR, intercellular spaces of the bronchial epithelium became enlarged in the DE-exposed sensitized animals, showing infiltration by numerous eosinophils. Albumin concentration was significantly higher in the bronchial lavage fluids from the DE-exposed sensitized animals than in those from the DE-unexposed control animals. These results suggest that exposure to DE enhances mucus hypersecretion and eosinophilic inflammation during IAR. DE exposure also increases airway permeability and airway inflammation during LAR. Thus, DE exposure exacerbates allergen-induced airway responses in guinea pigs.

Allergens↗

PubMed2001

Quantitative changes in glycosaminoglycans in the lungs of rats exposed to diesel exhaust.

Exposure to diesel exhaust (DE) induces lesions in lung epithelium by generation of reactive oxygen species. Glycosaminoglycans (GAG), components of extracellar matrix, are thought to play important roles in cell proliferation and differentiation in the repair process of injured tissue. We investigated how GAG are related to the recovery of lung tissue from injury. Using high-performance liquid chromatography analysis, we determined the amounts of GAG, such as chondroitin sulfate (CS), dermatan sulfate (DS), and hyaluronan (HA) in the lungs of rats exposed to DE for 4 weeks at concentrations of 0.3 or 3 mg/m(3) as suspended particulate matter, or to filtered air. The contents of CS and HA in the surroundings of the bronchi were significantly increased after exposure to DE. In addition, immunohistochemical staining showed that the number of 8-hydroxydeoxyguanosine-positive cells as a marker of cell damage, and proliferating cell nuclear antigen-positive cells also increased in the same areas in which the levels of GAG were elevated in the lungs of rats exposed to 3 mg/m(3) DE. These results suggest that CS and HA in the lung contribute to cell proliferation and remodeling in the process of recovery from injury caused by exposure to DE.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

Effects of diesel exhaust particles on blood pressure in rats.

The effects of diesel exhaust particles (DEP) on pulmonary functions and consequent diseases are well known, but there have been few reports concerning involvement of the cardiovascular system. In order to assess a direct action of DEP on cardiac tissue, the effects on blood pressure of intravenous administration of 12 or 120 mg/kg DEP to anesthetized rats were studied for a 15-min period. DEP (120 mg/kg) significantly lowered blood pressure for 25 s with no signs of arrhythmia or mortality, a phenomenon seen in guinea pigs. After 25 s blood pressure gradually returned to control levels and was maintained for 15 min. The 12-mg/kg DEP concentration did not markedly affect rat blood pressure. Pretreatment with atropine (24 mg/kg) blocked the DEP-induced fall in blood pressure, while pretreatment with propranolol (48 mg/kg) proved ineffective against DEP, suggesting involvement of the parasympathetic system. Data show that the rat is less sensitive to DEP-induced effects on blood pressure and may be a poor model to reflect cardiovascular changes.

Adrenergic beta-Antagonists↗

PubMed2001

Diesel exhaust (DE) affects the regulation of testicular function in male Fischer 344 rats.

To investigate the effects of diesel exhaust (DE) particles on the reproductive system, male Fischer 344 rats at 13 mo of age were exposed to clean air or DE at particle concentrations of 0.3, 1, or 3 mg/m3 for 8 mo. DE did not markedly affect testicular and body weights. However, DE at 0.3 mg/m3 significantly decreased prostate and coagulating gland weights, accompanied by a reduction in thymus and adrenal gland weight. In contrast, there was a significant rise in the weights of prostate, seminal vesicles, and coagulating glands in the 3 mg/m3 DE group. In rats exposed to 0.3 or 1 mg/m3 DE, serum luteinizing hormone (LH) and testosterone increased significantly, while a rise in testicular testosterone was noted with 3 mg/m3 DE. The concentrations of follicle-stimulating hormone (FSH) and inhibin as well as the sperm head counts were not markedly altered in any treatment group. Positive staining with inhibin-alpha subunit and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) were observed in Sertoli cells and Leydig cells, respectively. Immunolocalization of inhibin-alpha subunit and 3beta-HSD was not changed by exposure to DE. In conclusion, DE appears to exert greater effects on accessory glands than on testes in Fischer 344 rats, and the responsiveness of rats is less than that found in mice.

3-Hydroxysteroid Dehydrogenases↗

PubMed2001

The cytotoxic effects of diesel exhaust particles on human pulmonary artery endothelial cells in vitro: role of active oxygen species.

Diesel exhaust particles (DEP) have been proved to induce serious pulmonary injury, among which lethal pulmonary edema has been assumed to be mediated by vascular endothelial cell damage. In the present study, we investigated the cytotoxic mechanism of DEP on human pulmonary artery endothelial cells focusing on the role of active oxygen species. Endothelial cell viability was assessed by WST-8, a novel tetrazolium salt. Nitric oxide (NO) production was measured by using a new fluorescence indicator, diaminofluorescein-2 (DAF-2). Organic compounds in DEP were extracted by dichloromethane and methanol. DEP-extracts damaged endothelial cells under both subconfluent and confluent conditions. The DEP-extract-induced cytotoxicity was markedly reduced by treatment with SOD, catalase, N-(2-mercaptopropionyl)-glycine (MPG), or ebselen (a selenium-containing compound with glutathione peroxidase-like activity). Thus superoxide, hydrogen peroxide, and other oxygen-derived free radicals are likely to be implicated in DEP-extract-induced endothelial cell damage. Moreover, L-NAME and L-NMA, inhibitors of NO synthase, also attenuated DEP-extract-induced cytotoxicity, while sepiapterin, the precursor of tetrahydrobiopterin (BH(4), a NO synthase cofactor) interestingly enhanced DEP-extract-induced cell damage. These findings suggest that NO is also involved in DEP-extract-mediated cytotoxicity, which was confirmed by direct measurement of NO production. These active oxygen species, including peroxynitrite, may explain the mechanism of endothelial cell damage upon DEP exposure during the early stage.

Antioxidants↗

PubMed2001

Benzene-extracted components are important for the major activity of diesel exhaust particles: effect on interleukin-8 gene expression in human bronchial epithelial cells.

Epidemiologic and experimental studies suggest that diesel exhaust particles (DEPs) may be related to increasing respiratory mortality and morbidity. We have shown that DEPs augmented the production of inflammatory cytokines by human airway epithelial cells in vitro. To better understand the mechanisms of their proinflammatory activities, we studied the effects of several components extracted from DEPs on interleukin (IL)-8 expression in human bronchial epithelial cell line BEAS-2B and normal human airway epithelial cells obtained from very peripheral airways by an ultrathin bronchoscope. We used several agents active on signal transduction pathways in cytokine expression, such as the protein kinase C inhibitor staurosporin, antioxidant agents including N-acetyl cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), and p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. Benzene-extracted components showed effects mimicking DEPs on IL-8 gene expression, release of several cytokines (IL-8; granulocyte macrophage colony-stimulating factor; and regulated on activation, normal T cells expressed and secreted) and nuclear factor (NF)-kappa B activation. We also found that NAC, PDTC, and SB203580 suppressed the activities of DEPs and their benzene extracts, suggesting the roles of oxidants-mediated NF-kappa B activation and p38MAPK pathways. Finally, benzo[a]pyrene, one of the important compounds included in the benzene component, replicated the activities shown by DEPs.

Acetylcysteine↗

PubMed2001

Diesel exhaust particle-induced cell death of human leukemic promyelocytic cells HL-60 and their variant cells HL-NR6.

The cytotoxicity of diesel exhaust particles (DEPs) toward human leukemic promyelocytic cells HL-60 was examined. DEPs were toxic and cytotoxicity increased in a dose-dependent manner. All cells died with 750 microg/ml DEPs in culture media. Apoptosis occurred in HL-60 cells exposed to DEPs. The cytotoxicity of DEP extracts with organic solvents was much lower than those of DEPs and organic solvent-washed residual DEPs. HL-NR6 cells, an HL-60 variant cell line, having higher superoxide dismutase and catalase activities than HL-60 cells, were more resistant to DEP cytotoxicity. When preincubated with the fluorescent probe diacetoxymethyl 6-carboxy-2',7'-dichlorodihydrofluorescinate diacetate and then exposed to DEPs, HL-60 cells emitted green fluorescence under blue illumination, indicating that reactive oxygen species were generated within the cells. The DEP cytotoxicity correlated inversely with the cellular concentration of reduced glutathione (GSH), which had been attenuated with L-buthionine-(R,S)-sulfoximine, a gamma-glutamylcysteine synthetase inhibitor, and was lowered with ethyl reduced glutathionate, a GSH carrier across biomembranes. Further, DEPs themselves decreased the cellular concentration of GSH in a dose-dependent manner. The alpha-tocopherol model compound 2,2,5,7,8-pentamethylchroman-6-ol decreased DEP cytotoxicity, while alpha-tocopherol had no effect. In addition, quinacrine, an endocytosis inhibitor, decreased DEP cytotoxicity. These results show that DEPs are cytotoxic and suggest that the cytotoxicity results from generation of reactive oxygen species by DEPs which have been incorporated into cells.

Antioxidants↗

PubMed2001

The effect of dietary carotenoids on lung tumorigenesis induced by intratracheally instillated diesel exhaust particles.

The purpose of this study is to examine the carotenoid effects on lung tumorigenesis induced by intratracheal instillation of diesel exhaust particles (DEP) into mice weekly for 20 wk. It was suggested that active oxygen radicals might play an important role in DEP-induced lung tumorigenesis. Mice were divided to 4 groups of diet containing 0.02% of palm oil carotene, 0.02% of beta-carotene, or no carotenoid with or without DEP. The BF group (4% fat) and the HF group (16% fat) were prepared for each diet group. The experimental period was 12 mo. By the administration of palm oil carotene, neither adenocarcinoma nor adenoma was found in the BF group. In the HF group with palm oil carotene, no adenocarcinoma was observed, and adenoma was reduced. Adenoma in the HF group was not greatly reduced by beta-carotene, but rather increased in the BF group. No adenocarcinoma was found in either the BF or the HF groups with beta-carotene. The 8-hydroxydeoxyguanosine/deoxyguanosine ratio in palm carotene groups was lower than in the other groups, while that in beta-carotene groups was not. From these results, palm oil carotene was suggested to prevent lung tumorigenesis by its protective effect on DNA from active oxygen. Beta-carotene was supposed to have different effects from palm oil carotene on lung tumorigenesis. Besides the chemopreventive effect, the growth of mice was inhibited by the administration of palm oil carotene. Further studies are necessary to elucidate the mechanisms of carotenoid effects.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2000

Early molecular and cellular events of oxidant-induced pulmonary fibrosis in rats.

To evaluate the early molecular events of oxidant-induced pulmonary fibrosis, rats were continuously exposed to 0.4 ppm ozone and 7 ppm nitrogen dioxide. The early responses to the combined gases could be divided into three phases. Acute pulmonary inflammation indicated by an increase in pulmonary edema as well as an influx of neutrophils into the airspaces first occurred on days 1 to 3 of the exposure. The pulmonary inflammation was reversed by day 8, and no biochemical or morphologic aspects of tissue responses were detected from days 15 to 45, suggesting that rats adapted to the stimuli during that period. Pulmonary fibrosis could be detected by an increase in the biomarker of lung collagen content at day 60 and by histopathologic evaluation by day 90. Enhanced expression of macrophage inflammatory protein-2 was observed only at day 1, whereas the pulmonary expression of transforming growth factor-beta was upregulated on days 60 and 90 of the exposure. Macrophage expressions of interleukin-1beta and interleukin-6 were enhanced during acute pulmonary inflammation; however, macrophage expression of tumor necrosis factor-alpha was elevated at both day 1 and days 60-90. Activation of nuclear factor-kappa B and increased expression of thioredoxin in the lungs was also observed at day 1 and days 60-90. The expression of antioxidant enzymes, such as manganeous superoxide dismutase and glutathione peroxidase, was not altered during exposure. These results indicate that macrophage activation and the expression of macrophage-derived cytokines may play an important role in the early pulmonary responses against the combined gases.

Administration, Inhalation↗

PubMed2000

Ebselen decreases ozone-induced pulmonary inflammation in rats.

We studied the effects of ebselen on rat lung inflammatory responses against ozone exposure. Rats were treated with ebselen every 12 h from 1 h before a single 4-h exposure to 2 ppm ozone. Treatment with ebselen (10 mg/kg) significantly decreased pulmonary inflammation as indicated by the albumin concentration and the number of neutrophils in the bronchoalveolar lavage fluid 18 h after the ozone exposure. Although treatment with ebselen did not alter the macrophage expression of inducible nitric oxide synthase after the ozone exposure, it did markedly inhibit the nitration reaction of tyrosine residues, suggesting that ebselen scavenges peroxynitrite during ozone-induced pulmonary inflammation. Treatment with ebselen also enhanced the pulmonary expression of both copper, zinc, and manganous superoxide dismutases at the same time point. These enzymes may also contribute to a decrease in the formation of peroxynitrite by lowering the concentration of superoxide. Thus, ebselen represents a useful compound for protecting against certain acute lung injuries by modulating the oxidant-related inflammatory process.

Acute Disease↗

PubMed2000

Peroxynitrite formation by diesel exhaust particles in alveolar cells: Links to pulmonary inflammation.

Diesel exhaust particles (DEP) are assumed to be a causal substance for pulmonary inflammation. As peroxynitrite is recently implicated in inflammation and cytotoxity, the hypothesis was tested that instillation of DEP induces formation of peroxynitrite in cells migrated in lung. Rats were intratracheally instilled with DEP suspension (2 mg/0.5 ml/kg) and killed 24 h later. Alveolar cells were collected by broncho-alveolar lavage. Population of alveolar cells increased more than twice by DEP exposure, mainly due to a large increase of neutrophils. Peroxynitrite formation (N(G)-nitro-L-arginine methylester and superoxide dismutase inhibitable chemiluminescence) was detected in alveolar cells from treated rats, and 12-O-tetradecanoylphorbol 13-acetate-stimulation enhanced it. In addition, DEP induced expression of inducible NO synthase mRNA in these cells. But peroxynitrite was not detectable in cells from control. These results indicate that DEP exposure results in peroxynitrite formation in migrated cells, which leads to pulmonary inflammation.

Journal Article↗

PubMed2000

Cytoprotection by metallothionein against gastroduodenal mucosal injury caused by ethanol in mice.

Metallothionein (MT) is a small, cysteine-rich protein that can act as a free radical scavenger at least in vitro. To test the hypothesis that MT participates in gastroduodenal cytoprotection, we studied sensitivity to gastroduodenal mucosal injury caused by ethanol in MT-null mice that have null mutations in MT-I and MT-II genes. MT-null mice and wild-type mice were orally treated with ethanol (60% or 99.5%, 0.2 ml/mouse). The macroscopic gastric lesion indices were significantly higher in MT-null mice than in wild-type mice 90 minutes after ethanol treatment. Histopathological examination in ethanol-treated MT-null mice showed vacuolar degeneration, necrosis of the epithelial cells, and hemorrhage throughout the tunica mucosa. Moreover, the duodenum also showed morphologic changes, including marked degeneration and coagulative necrosis of the entire villi, desquamation of the degenerated epithelial cells, and hemorrhage. In contrast, histopathologic changes were less prominent in the wild-type mice treated with ethanol. MT was not detected either in the stomach or duodenum of MT-null mice, whereas gastric and duodenal zinc contents were not significantly different between MT-null mice and wild-type mice. These results provide direct evidence that intrinsic MT plays a cytoprotective role in gastroduodenal mucosal injury caused by ethanol.

Animals↗

PubMed2000

Increase in mutation frequency in lung of Big Blue rat by exposure to diesel exhaust.

Exposure to diesel exhaust (DE) is known to cause lung tumors in rats. To clarify the mutagenicity of DE, we estimated mutant frequency (MF) and determined the mutation spectra in rat lung after exposure to DE using lambda/lacI transgenic rats (Big Blue system). Male Big Blue rats (6 weeks old) were exposed for 4 weeks to 1 or 6 mg/m(3) DE, which contains suspended particulate matter. Control rats were maintained in filtered clean air. After exposure to 6 mg/m(3) DE, MF in lung was 4.8-fold higher than in control rats (P < 0.01), but no increase in MF was observed in rats exposed to 1 mg/m(3) DE. Sixty-nine mutants were identified after exposure to 6 mg/m(3) DE. The major mutations were A:T-->G:C (18 mutations) and G:C-->A:T (19 mutations) transitions. Remarkably, G-->T transversion of the lacI gene at site 221 was a hot-spot induced by exposure to DE, and there were complex mutations in which multiple mutations occurred in a single mutant, especially in the rats exposed to 6 mg/m(3) DE. DNA adducts formed by DE were analyzed using a (32)P-post-label TLC method and the amount of 8-hydroxydeoxyguanosine (8-OHdG) was measured using HPLC. Relative adduct level and amount of 8-OHdG were significantly increased in the rats exposed to 6 mg/m(3) DE compared with the controls (3.0- and 2.2-fold, respectively; P < 0.01). The level of cytochrome P450 1A1 mRNA was shown by northern blot analysis to be significantly increased in the lungs of rats exposed to 6 mg/m(3) DE (5.5-fold; P < 0.01). These results indicate that DE causes lesions in genomic DNA and acts as a mutagen in rat lung.

Animals↗

PubMed2000

Anti-estrogenic activity of diesel exhaust particles.

Estrogenic and anti-estrogenic activities of diesel exhaust particles (DEP) were evaluated using yeast cells expressing the human estrogen receptor and the responsive element regulating the expression of the receptor gene for beta-galactosidase (Routledge and Sumpter, 1996). It was found that a suspension of whole DEP suspension is not estrogenic but that this preparation possesses the ability to reduce the estrogen-dependent reporter activity. DEP were serially extracted with hexane, benzene, dichloromethane, methanol, and 1 M ammonia, and the estrogenic and anti-estrogenic activities of these preparations were determined. None of the extracts of DEP were estrogenic, but the extracts of benzene, dichloromethane and methanol possessed anti-estrogenic activity, and the activity of estrogen in the presence of hexane extract was slightly decreased. These results indicated that DEP contain heterologous compounds having anti-estrogenic activity. It is thought that those compounds in DEP can modulate the activity of estrogen, leading to the distruption of balance between estrogen and androgen. In this paper, the environmental effects of DEP in relation to the endocrine disrupting effect of organic compounds in DEP are discussed.

Air Pollutants↗

PubMed1999

Manipulation of the L-arginine-nitric oxide pathway in airway inflammation induced by diesel exhaust particles in mice.

The role of the L-arginine-nitric oxide (NO) pathway in bronchial asthma that is characterized by eosinophilic airway inflammation has not yet been established. We investigated the effects of three different agents on eosinophilic airway inflammation induced by the intratracheal instillation of diesel exhaust particles (DEP) in mice: L-Arginine, the substrate for NO synthases; L-N(G)-nitro-L-arginine methyl ester (L-NAME), a relatively selective inhibitor of constitutive NO synthase; and aminoguanidine, a relatively selective inhibitor of inducible NO synthase. The mice received drinking water with or without added drug for a continuous period of 9 weeks plus 4 days. Lung histology showed that airway inflammation with goblet cell proliferation induced by DEP was aggravated by the administration of L-arginine or L-NAME, whereas it was reduced by aminoguanidine. The numbers of neutrophils around the airways in animals that received plain drinking water, L-arginine, L-NAME, and aminoguanidine were 0.98+/-0.26, 3.66+/-0.81, 1.64+/-0.31, and 0.12+/-0.04 (number/mm basement membrane), respectively. The numbers of eosinophils around the airways were 0.37+/-0.08, 16.1+/-6.47, 11.1+/-3.59, and 0.21+/-0.11, respectively. The numbers of goblet cells in the bronchial epithelium were 1.67+/-0.80, 16.5+/-7.33, 19.0+/-3.40, and 0.86+/-0.41, respectively. The cellular profiles of the bronchoalveolar lavage fluid also showed that airway inflammation induced by DEP was aggravated by the administration of L-arginine or L-NAME, whereas it was reduced by aminoguanidine. These results suggest that NO produced from inducible NO synthase may have a detrimental effect on the DEP-induced airway inflammation. A relatively selective inhibition of inducible NO synthase by aminoguanidine may have therapeutic value in the inhalant injury. NO derived from constitutive NO synthase may afford protection against the airway inflammation induced by DEP.

Animals↗

PubMed1999

Oral administration of lipopolysaccharide exacerbates collagen-induced arthritis in mice.

We investigated whether oral administration of LPS exacerbated collagen-induced arthritis (CIA) in mice, which was an experimental model of autoimmune disease. CIA was induced by s.c. injection of type II collagen emulsified with CFA into the base of the tail (day 0) followed by a booster injection on day 21. To examine the ability of LPS to exacerbate CIA, varying doses of LPS were orally administered on day 50. The results showed that administration of LPS was followed by reactivation of CIA in a dose-related fashion. Histologically, on day 55 there were marked edema of synovium proliferated by day 50, new formation of fibrin, and intense infiltration of neutrophils accompanied with a large number of mononuclear cells. Severe destruction of cartilage and subchondral bone was also observed on day 70. The reactivation of CIA by oral administration of LPS was associated with increase in anti-type II collagen IgG and IgG2a Abs as well as varying kinds of cytokines including IL-12, IFN-gamma, IL-1beta, and TNF-alpha. Polymyxin B sulfate given either orally or i.v. suppressed the recurrence of CIA. Increased amounts of LPS were found in sera of mice given the endotoxin orally. LPS from Salmonella enteritidis, Salmonella typhimurium, and Klebsiella pneumoniae and its component, lipid A from Escherichia coli, also reactivated the disease. These findings suggest that LPS from intestinal bacteria may play a role in the exacerbation of autoimmune joint inflammation.

Administration, Oral↗

PubMed1999

Induction of systemic Th1 and Th2 immune responses by oral administration of soluble antigen and diesel exhaust particles.

The present study was undertaken to examine whether oral administration of soluble antigen together with diesel exhaust particles (DEP) induced the systemic immune response in mice. Mice were orally given 1 mg of hen egg lysozyme (HEL) with varying doses of DEP every 3 days over a period of 15 days. The results showed that oral administration of HEL plus DEP produced anti-HEL IgG antibodies in serum in a dose-related fashion, while either HEL or DEP alone failed to show the antigen-specific IgG antibody production. Production of anti-HEL IgG2a and IgG1 antibodies, which are dependent on Th1 and Th2 CD4(+) T cells, respectively, was seen in mice fed with combined HEL and DEP, although anti-HEL IgG1 antibodies appeared to be more efficiently produced by lower doses of DEP than anti-HEL IgG2a antibodies. There was marked antigen-specific proliferation of spleen cells in mice treated with HEL and DEP. The anti-HEL antibody production and lymphoid cell proliferation to the antigen were associated with marked secretion of the Th1 cytokine IFN-gamma as well as the Th2 cytokine IL-4. These results suggest that DEP may act as a mucosal adjuvant in the gut enhancing systemic Th1 and Th2 immune responses and might play a role in oral immunization and food allergy.

Administration, Oral↗

PubMed1999

PCDDs and PCDFs in vehicle exhaust particles in Japan.

Vehicle exhaust particles from gasoline and diesel engine cars were analyzed for PCDDs and PCDFs. The congener patterns of PCDDs and PCDFs in exhaust particles were different between gasoline and diesel engine cars. Suspended particulate matter from electrostatic precipitator connected to a highway tunnel was also analyzed for PCDDs and PCDFs. The congener pattern of suspended particular matter was different from both of gasoline and diesel engine cars. Total amounts of PCDDs/PCDFs sum concentrations in gasoline, diesel and suspended particulate matter were 0.21, 0.87 and 26.0 ng/g, respectively. The I-TEQs levels in gasoline, diesel and suspended particulate matter were 4.2, 11 and 242 pg/g, respectively.

Air Pollutants↗