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Psychosocial job stress has been shown to be associated with the development of cardiovascular disease. However, the pathophysiological mechanisms underlying this relationship remain unclear. The aim of the present study was to elucidate whether marked job stress affects the parameters of blood coagulation and fibrinolysis, such as plasma fibrinogen concentration, tissue plasminogen activator (t-PA), and plasminogen activator inhibitor 1 (PAI-1) activities, in 213 middleaged male workers in a computer-producing factory. Job stress was measured using a Japanese version of the Job Content Questionnaire (JCQ) developed by Karasek. The mean t-PA activity in workers with lower and higher job demands was 0.23 and 0.18 IU/ml respectively, and this difference was significant (P < 0.05). The mean plasma fibrinogen in workers with lower and higher job decision latitude was 224.8 and 236.3 mg/dl respectively, and the mean PAI-1 activity in workers with lower and higher job strain was 14.9 and 17.7 U/ml respectively, though these differences remained at a borderline level of significance (0.05 < P < 0.10). Multiple regression analyses showed that the parameters of blood coagulation and fibrinolysis were closely associated with the cardiovascular risk factors of age, obesity, blood pressure, elevated serum lipids, and smoking, but that high job demands were significantly related to decreases in t-PA activity, independently of the traditional risk factors. These results suggest that psychosocial job stress may be related, at least partly, to the development of cardiovascular disease via changes in plasma fibrinolytic activity.

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alcohol consumption, increase in serum GGT and development of the metabolic syndrome. Prevention of the metabolic syndrome [1][2][3] , a complex of multiple coronary risk factors, such as hypertension (HYT), impaired glucose tolerance (IGT) and dyslipidemia, should be targeted by health promotion activities for people living in modern society including occupational fields, where coronary heart disease is a leading cause of death and obesity, the most powerful promoter of the metabolic syndrome, is epidemic 4) . Meanwhile, moderate alcohol consumption has been shown to protect against the development of coronary heart disease and death [5][6][7] , and it may even protect against the development of non-insulin dependent diabetes mellitus (NIDDM) 8,9) although this is still disputed 10) . The protective effects of moderate alcohol consumption on coronary heart disease have been attributed to high serum HDL-cholesterol levels, suppressed coagulation capacity of platelets, or the suspected role of anti-oxidant substances contained in alcoholic beverages 11,12) . More recently, beneficial effects on insulin resistance, the core pathology of the metabolic syndrome, have been proposed as another possible mechanism 13) , implying that improved insulin resistance in moderate alcohol consumers may suppress the development of the metabolic syndrome, and thus coronary heart disease, but there have also been contradictory studies suggesting increases in insulin resistance after alcohol consumption [14][15][16][17] . In addition, high serum gamma-glutamyltransferase (GGT), a wellknown biological indicator of alcohol consumption 18,19) , has been shown to be associated with the metabolic syndrome [20][21][22] . The aim of the present study is to clarify The relationships between alcohol consumption, serum gammaglutamyltransferase (GGT) levels, and the prevalence of major coronary risk factors were analyzed crosssectionally in 2,399 male and 1,402 female middle-aged workers, to clarify the effects of moderate alcohol consumption on the development of the metabolic syndrome. Male moderate drinkers, consuming less than 60 ml of alcohol per day, had a lower prevalence of upper body obesity and low serum HDL-cholesterolemia (LHDLC) in comparison with nondrinkers, but not of hypertension, impaired glucose tolerance or hypertriglyceridemia (HTG). In women, alcohol consumption did not show any significant associations with the coronary risk factors. Men with an elevated serum GGT (EGGT) of 40 U/l or above had a significantly higher odds ratio for all the coronary risk factors as compared with those with normal GGT, even after adjusting for alcohol consumption, together with age, body mass index, cigarette consumption and physical activity. Women with an EGGT of 25 U/l or above had similar findings, although significance was found only in HTG. Nearly 80% and 55% of the appearance of EGGT in men and women were attributable to alcohol consumption, and 20% and 10% of the male and female moderate drinkers had EGGT. These results suggest tha...

Objectives To clarify the renal effects of cigarette smoking in a middle-aged occupational population because the effects have previously been demonstrated mainly in community populations that included many elderly people who are thought to be vulnerable to such effects. Methods In 990 middle-aged men recruited from a chemical plant, proteinuria was measured by a dipstick method and the glomerular filtration rate was estimated (eGFR) using a formula proposed by the Japanese Society of Nephrology. Results Proteinuria was found in 4.6% of the current smokers and 1.5% of the never-smokers. It was found in 4.8% of the subjects having a Brinkman index (BI) of 400-599 and 6.3% of those having a BI of 600 or above. The odds ratio for proteinuria in them was 2.94 (CI: 1.01-8.55) and 3.61 (CI: 1.29-10.1), respectively, adjusting for possible confounders. The mean eGFR was higher in smokers than in nonsmokers throughout middle age up to 64 years. Normal but high eGFR was found in 6.7% of the current heavy smokers and subnormal eGFR in 5.7% of the largest cumulative cigarette consumers in contrast to 3.0% or less of the never-smokers. Proteinuria was found in 13.3% of the subjects showing subnormal eGFR, specifically in 16.7% of the smokers and 8.3% of the nonsmokers. Conclusions Smoking causes proteinuria in working middle-aged men. Smokers tend to have a high eGFR, but those with subnormal eGFR showed proteinuria most frequently. Whether the high eGFR in smokers will eventually decrease and cause proteinuria remains an important focus for further studies.

Objectives The strength of the association between smoking and the development of chronic kidney disease (CKD) in the healthy middle-aged working age population has not been established. Methods This was a retrospective 6-year observational study involving 4,121 male and 2,877 female workers who were free of primary kidney disease, diabetes mellitus, severe hypertension, and the signs and symptoms of CKD. Proteinuria was detected by a dipstick method, and glomerular filtration rate (GFR) was estimated by the equation of the Japan Society of Nephrology. Results Sixty men (1.5 %) and 21 women (0.7 %) developed proteinuria over the 6 years of the study. Irrespective of sex, in comparison with non-smokers, those who continued smoking showed an odds ratio (OR) of 2.52 with a 95 % confidence interval (CI) of 1.50-4.25 for developing proteinuria while those who quit smoking showed an OR of 1.29 (95 % CI 0.48-3.42), following adjustment for confounders. Among the study population, 443 men (10.7 %) and 356 women (12.4 %) developed a GFR of \60 mL/min/1.73 m 2 , corresponding to stage III CKD. Continuing smokers had a low OR (0.74, 95 % CI 0.60-0.90) for developing a low GFR, as well as a higher mean GFR than non-smokers. The reduction in GFR during the 6-year study period was not different between smokers and non-smokers, but it was larger in those who developed proteinuria than in those who did not, irrespective of smoking.Conclusions Continuing smokers showed a twofold or more higher risk of developing proteinuria. Discontinuation of smoking substantially reduced the risk. A longer observational period may be required to detect the smoking-induced risk of developing stage III CKD in the middle-aged working population.