• Journal of Preventive Medicine and Public Health
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• v.10 no.1
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• pp.166-175
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• 1977

The author have performed an epidemiological study on the accidental deaths at industry from 1970 to 1975, in order to seek for the preventive measures of industrial accident with the under-standing of its cause and characteristics of the accidental deaths. The obtained results were as follows; 1. Total number of deaths for 6 years were 361 (350 males, 11 females). and the mean death rate was 33.8 per 100,000 industrial workers during 6 years. By the highest as 52.9 was in 1974 and the lowest as 13.7 in 1970. By the industry group, the death rate of Electricity, Gas and Water was 149.3, Construction 83.9 and the lowest was Manufacturing as 18.3. 2. Standardized mortality rate of the cases by the age group showed that 20-29 years old group was 43.0, 40-49 years old group 38.1, 30-39 years old group 32.0, and the lowest as 17.9 was under 19 years old group. 3. The cumulative percentage of the cases by years of service showed that under 6 months was 60.4%, under 1 year 72.9%, under 2 years 83.1%. 4. By the month of occurrence, the highest was 15.8% which occurred in August and the lowest was 5.8% in February. The highest as 19.1% was on Friday and the lowest as 11.9% on Monday by the day of a week. 5. By the causes of accident, car accidents was 28.3%, fall accidents 19.1%, accidents by a crash 9.1% in that order. By the location of injury, head was 44.6%, multiple injuries 33.0%, chest 10.5%, and back was the lowest as 1.9%. The distribution of the cases by nature of injury shelved that cerebral contusion and hemorrhage was 39.4%, fracture and dislocation 33.2%, asphyxia 8.0% in that order. 6. The cumulative percentage of the cases by the duration from injury to death showed that the injuried day was 74.2%, within 3 days after injury 88.5%, within 7 days 96.1%. Therefore most of the cases were occurred within 7 days after injury. 7. Byythe daily mean wages, most of the cases as 91.7% were under 2,000 won, and more 4,000 won was 1.6% merely.

• Journal of Chest Surgery
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• v.35 no.5
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• pp.343-349
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• 2002

background: In an attempt to investigate the role of oxidants in the activation of phospholipase $A_2$(PLA$_2$) and endogenous oxidative stress in the lung. acute inflammatory lung injury was induced by the instillation of hydrogen peroxide into the trachea of Sprague-Dawley rats. Material and Method: To prove the hypothesis thats released oxidants from neutrophils activate the PLA$_2$ retrogradely, activities of PLA$_2$ and lysoplatelet activating factor acetyltransferase(lysoPAF AT) were assayed i hours after instillation of hydrogen peroxide. In addition, to confirm the impairing effects of the activation of PLA$_2$ associated with endogenous oxidative stress, lung weight/body weight ratio(L$\times$10$^{-3}$ B), protein contents(mg/two lungs) in bronchoalveolar lavage(BAL) were measured. As neutrophilic respiratory burst has been known to play a pivotal role in the genesis of endogenous oxidative stress associated with acute inflammatory lung injury, BAL neutrophils counts and level of lung myelperoxidase(MPO) were measured after hydorgen peroxide insult. Morphological and histochemical studies were also performed to identify the effect of the endogenous oxidative stress. Result: Five hours after hydrogen peroxide instillation, lungs showed marked infiltration of neutrophils and increased weight. Protein contents in BAL increased significantly compared to those of normal rats. PLA$_2$ activity was enhanced in the hydrogen peroxide instilled group. Interestingly, the accelerated production of platelet activating factor(PAF) was confirmed by the increased activity of lysoPAF AT in the $H_2O$$_2$ employed lung. Morphologically, light microscopic findings of lungs after instillation of hydrogen peroxide showed atelectasis and infiltration of inflammatory cells, which was thought to be caused by lipid mediators produced by PLA$_2$ activation. In cerium chloride cytochemical electron microscopy, dense deposits of cerrous perhydroxide were identified. In contrast, no deposit of cerrous perhydroxide was found in the normal lung.

• Journal of Chest Surgery
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• v.36 no.8
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• pp.545-558
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• 2003

Adult respiratory distress syndrome (ARDS) is of particular interest because of its severity of the associated lung injury and its high mortality. However, the pathophysiologies of ARDS in infant and childhood groups are still not well clarified inspite of many previous investigations. To investigate the time course of pathophysiology of ARDS in infant and childhood groups, this study was designed with experimental endotoxin-induced ARDS model using young rabbits (8 week-old). Material and Method: Rabbits were divided into the control group (n=8) and the endotoxin-treated group (n=32). The endotoxin group was subdivided into 4 groups by the sampling times as 3, 6, 12 and 24 hr-groups (G- $E_{3,6,12,24,}$ each n=8). The experimental ARDS was made by a bolus injection of endotoxin (Escherichia coli serotype 055 : B5, 0.50 mg/kg) via rabbit ear vein. For evaluation of the hematologic and inflammatory markers, and superoxide dismutase (SOD) concentrations, the blood samples were taken from the heart. The bronchoalveolar lavage fluid (BALF) were obtained for analysis of the leukocytes and protein concentration. With biopsy of the lung, histopathologic changes of the lung were also evaluated. Result: In the endotoxin groups, significant leukopenia (owing to pancytopenia) occurred in 3 and 6-hr groups, which was followed by significant leukocytosis (owing to neutrophilia) in the 12 and 24-hr groups (p<0.05). Serum levels of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-1 $\beta$ (IL-1 $\beta$) in the endotoxin groups were higher than those of control group (p<0.05). Serum levels of superoxide dismutase (SOD) of G- $E_{3}$ and G- $E_{6}$ were higher than those of control group, whereas those of G- $E_{12}$ were lower than those of control groups (p<0.05). Total leukocyte counts and protein con-centrations in BALF were significantly elevated in the endotoxin groups compared to the control group (p < 0.05). The hemorrhagic pattern of BALF showed occurred in the endotoxin groups. The endotoxin groups (in G- $E_{6}$) had severe infiltration of inflammatory cells (lymphocyte and monocyte) in the pulmonary interstitium and parenchyma, migrations of neutrophil and eosinophil into alveolar spaces and interstitial widening, which are the evidences of acute lung injury. In the endotoxin groups, there were significant positive correlations between the BALF findings and the immunologic markers (TNF-$\alpha$, IL-1$\beta$, SOD) (p<0.05). Conclusion: Severe acute lung injury occurred in all the endotoxin-treated rabbits. The pathophysiologic findings were so progressive until 6-hr by time dependant pattern, and then recovered slowly, Variable hematologic, immuno-logic, and pathologic factors were well correlated in the development and progression of endoxin-induced lung injury. The pathophysiologic responses were sensitive and rapid in young rabbit Young rabbit seemed to be a useful experimental animal model for infant and childhood groups.roups.