For understanding the relationship between the increased incidence of sudden cardiac death and air pollution, we examined the effects of intratracheal instillation of diesel exhaust particles (DEP) on acute myocardial ischemia/reperfusion-induced arrhythmia in rats. The animals received 1 mg DEP 24-48 h before the ischemia/reperfusion (DEP-pretreated group, DEP-PRE), and were subjected to 3 successive brief ischemia/reperfusion (3 min ischemia followed by 5 min reperfusion) procedures. These were to make the animals tolerant to ischemia/reperfusion-related myocardial deterioration. Thereafter the animals were subjected to a 10-min ischemia followed by a 30-min reperfusion. In the experiments, an increased mortality was observed in the DEP-PRE group compared to the vehicle (0.05% Tween 80-PBS)-treated group. Forty-six percent of the animals in DEP-PRE died during the first 3-min reperfusion period. The animals of other groups were intratracheally instilled with DEP at the beginning of ischemia/reperfusion experiment, or were pretreated with polyethylene glycol-conjugated superoxide dismutase (1000 IU kg(-1), iv). In these animals, incidences of both arrhythmia and mortality were similar to those in the animals treated with the vehicle. In experiments to investigate the effects of DEP on the biochemical and hematological parameters, neutrophil count was elevated by a higher dose (5 mg) of DEP at 24 h after the intratracheal instillation, and oxygen radical production, which was induced by 12-O-tetradecanoylphorbol 13-acetate, was enhanced at 72 h. These results indicate that intratracheal DEP instillation exacerbates short-period ischemia/reperfusion-induced arrhythmia. Delivery and activation of peripheral neutrophils and oxygen radicals produced in neutrophils might participate in this exacerbation. This is the first article that demonstrates the arrhythmogenicity of DEP using intratracheal instillation in rats.

Short-term inhalation experiments were performed using Fischer 344 rats exposed to emission from the urea selective catalytic reduction (SCR) diesel engine system to identify health effects and compare them to those of the conventional diesel engine system. Rats were exposed to high-, middle-, or low-concentration emission (dilution ratio 1:29, 1:290, or 1:580) or clean air (control) for 1, 3, or 7 days (6 h/day), under driving conditions at a speed of 1320 rpm and a torque of 840 Nm. For the high-concentration group, the major components of the urea SCR emission were 0.04 mg/m(3) particulate matter (PM) and 0.78 ppm nitrogen dioxide (NO(2)); those of the conventional emission were 0.95 mg/m(3) PM and 0.31 ppm NO(2). The authors evaluated the respiratory effects of each emission on rats. Lymphocytes for 3-day exposure of both emissions significantly increased in bronchoalveolar lavage fluid, but there were slight differences. With an increase in potential antioxidant (PAO), 8-hydroxy-2'-deoxyguanosine for the urea SCR emission was significantly decreased, but that of the conventional emission was highest among all groups and did not show a response to PAO. In lungs, heme oxygenase (HO)-1 and tumor necrosis factor (TNF)-alpha mRNA expressions for the urea SCR emission showed a tendency to increase compared to those of the conventional emission. Thus, gene analysis results suggested that NO(2) from the urea SCR emission affected the expressions of mRNAs in lungs. However, as a whole, the results suggested that the health effects of the urea SCR emission might be less than the conventional emission on rats.

We examined the effect of polluted roadside air on the pathogenesis of chronic respiratory diseases, by exposing rats directly to roadside air in Kawasaki City. Five-week-old Wistar rats were assigned to be exposed to either roadside air (containing 55.7 ppb NO2 and 62.7 microg/m(3) suspended particulate matter [SPM]; roadside-air group) or filtered air (containing 5.1 ppb NO2 and 14.3 microg/m(3) SPM; filtered-air group), prepared by eliminating dust and emission gas from the polluted roadside air, for a period of 60 consecutive wk. The morphological changes over time in the respiratory tissue of these animals were observed by light microscopy and electron microscopy at 24, 48, and 60 wk of exposure. In addition to the general microscopic findings, other features observed for included the proliferation of goblet cells producing mucus in the airways, acidification of neutral mucous granules in these goblet cells, the behavior of inflammatory cells such as alveolar macrophages, mast cells, and plasma cells, and the number of alveolar holes, known to be a primary indicator of early alveolar destruction. Focal anthracosis, acidified mucus in the goblet cells, and infiltration to the submucosa by inflammatory cells were observed in the lungs of the animals after 60 wk of exposure to polluted roadside air. However, these inflammatory changes were weak. No remarkable differences in the number of alveolar holes were noted between the two experimental groups. These findings suggest that the effects of roadside air on the respiratory tissue in rats may not be as severe as would be expected under these experimental conditions.

Wistar rats were exposed for 24 mo to diesel emissions containing a low (0.2 ppm, 0.21 mg/m(3)), medium (1.04 ppm, 1.18 mg/m(3)), or high (2.96 ppm, 3.05 mg/m(3)) concentration of NO(2) and particles, or diesel emissions containing a medium (1.12 ppm, 0.01 mg/m(3)) concentration of NO(2) without particles. At 6-mo intervals during the exposure period, rats were autopsied, and their lungs were prepared for light- and electron-microscopic examination. Morphological evaluations included examination for hyperplasia of airway goblet cells, shift in the types of glycoprotein of intracellular mucus granules in goblet cells, infiltration of inflammatory cells in the airways, enlargement of the cross-sectional area of an alveolus as a parameter of air space enlargement, and development of alveolar holes, which is considered to be an early hallmark of alveolar destruction. The number of goblet cells with acid-form mucus granules increased with the exposure concentration and time; however, goblet cells did not show any hyperplastic changes. Furthermore, inflammatory cells such as alveolar macrophages, mast cells, plasma cells, neutrophils, and lymphocytes infiltrated the airways and the alveoli, and showed some cell-to-cell contact. Although no significant enlargement of the air space of the lungs was seen in any exposure group, the number of alveolar holes was significantly higher in the high-concentration group in comparison with the control group at each exposure time, and also increased in other exposure groups, even in the low-concentration group at certain exposure times. Morphological changes in the lungs were mild even in the animals exposed to the highest levels of diesel emissions for 24 mo. Elimination of particles from diesel emissions led to reduced morphological changes such as a decreased shift in the types of glycoprotein of mucus granules in goblet cells, decreased infiltration of inflammatory cells in the lungs, and reduced anthracosis.

We examined the effect of polluted roadside air on the pathogenesis of chronic respiratory diseases, by exposing rats directly to roadside air in Kawasaki City. Five-week-old Wistar rats were assigned to be exposed to either roadside air (containing 55.7 ppb NO2 and 62.7 microg/m(3) suspended particulate matter [SPM]; roadside-air group) or filtered air (containing 5.1 ppb NO2 and 14.3 microg/m(3) SPM; filtered-air group), prepared by eliminating dust and emission gas from the polluted roadside air, for a period of 60 consecutive wk. The morphological changes over time in the respiratory tissue of these animals were observed by light microscopy and electron microscopy at 24, 48, and 60 wk of exposure. In addition to the general microscopic findings, other features observed for included the proliferation of goblet cells producing mucus in the airways, acidification of neutral mucous granules in these goblet cells, the behavior of inflammatory cells such as alveolar macrophages, mast cells, and plasma cells, and the number of alveolar holes, known to be a primary indicator of early alveolar destruction. Focal anthracosis, acidified mucus in the goblet cells, and infiltration to the submucosa by inflammatory cells were observed in the lungs of the animals after 60 wk of exposure to polluted roadside air. However, these inflammatory changes were weak. No remarkable differences in the number of alveolar holes were noted between the two experimental groups. These findings suggest that the effects of roadside air on the respiratory tissue in rats may not be as severe as would be expected under these experimental conditions.