(Stroke. 1995;26:767-773.)
© 1995 American Heart Association, Inc.
Articles |
Alcohol Intake and the Risk of Cardiovascular Disease in Middle-Aged Japanese Men
From the Institute of Community Medicine, University of Tsukuba, Tsukuba (H.I., T. Shimamoto, T. Sankai); the Department of Epidemiology and Mass Examination, The Center for Adult Diseases, Osaka (A.K., Y.N., S.S., M.K., M.I.); and the Osaka Prefectural Institute of Public Health, Osaka (Y.K.); Japan.
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Abstract |
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Background and Purpose Understanding the effects of alcohol intake on stroke and other cardiovascular diseases is an important issue for public health.
Methods A 10.5-year prospective study of the relationship between alcohol intake and cardiovascular disease incidence was conducted in 2890 men, aged 40 to 69 years and free of a history of stroke and coronary heart disease, in three rural communities of Japan.
Results One hundred seventy-eight strokes (40 intracerebral
hemorrhages, 18 subarachnoid hemorrhages, 104 nonhemorrhagic strokes,
and 16 unclassified strokes), 34 coronary heart disease events, and 19
sudden unclassified deaths occurred. Drinkers of 
70 g/d ethanol had
an approximately 2.5 times higher age-adjusted risk of all stroke than
never-drinkers; the excess risk was more evident for hemorrhagic stroke
than nonhemorrhagic stroke. When hypertension category, serum total
cholesterol level, cigarette smoking, and diabetes mellitus were taken
into account, these excess risks were reduced but remained significant
for all stroke (2.0; 95% confidence interval, 1.3 to 3.1) and
hemorrhagic stroke (3.4; 95% confidence interval, 1.2 to 9.2). A
J-shaped relationship was suggested between
alcohol intake and risk of nonhemorrhagic stroke; drinkers of <42 g/d
ethanol had a slightly lower risk and heavy drinkers had a higher risk
than never-drinkers. Current drinkers had a slightly lower risk of
coronary heart disease than never-drinkers, although the risk
difference was not statistically significant. The age-adjusted risk of
sudden death was 10 times higher in heavy drinkers than never-drinkers,
and the excess risk did not change when the covariates were controlled
for. Total cardiovascular disease showed a similar pattern as did all
stroke.
Conclusions Heavy drinking appeared to increase the risk of hemorrhagic stroke, in part due to hypertension, and to increase the risk of sudden death, which was probably due to drinking per se. Light or moderate alcohol consumption seemed to protect against nonhemorrhagic stroke and coronary heart disease.
Key Words: alcohol drinking • coronary heart disease • Japan • risk factors
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Habitual drinking, either in social settings or at home, is common among Japanese middle-aged men.1 A 1980 national survey in Japan indicated that 47% of men aged 30 years and over were current daily drinkers, but only 4% of women were.2 The habit of frequent drinking in Japanese middle-aged men has drawn attention because evidence suggests that alcohol is an important risk factor for cardiovascular disease.3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
Investigators consistently report that heavy drinking increases the risk of coronary heart disease3 4 5 and total mortality.4 5 6 7 However, evidence of an association between heavy drinking and stroke is sparse and less consistent. Several retrospective case-control studies showed an increased risk of stroke in relation to alcohol intoxication and heavy drinking.8 9 10 A follow-up study of Japanese male physicians6 showed a 70% increase in stroke deaths in heavy drinkers. However, a large prospective case-control study from the Kaiser Permanente Program showed no association for either stroke death or incidence.3 4
Data on the effect of moderate alcohol intake on cardiovascular disease has been available mostly from studies of whites and Japanese Americans. Moderate alcohol intake has been found to reduce the risk of coronary heart disease11 12 and to increase the risk of hemorrhagic stroke.13 14 Several prospective studies also have reported a lower risk of total stroke and nonhemorrhagic stroke associated with moderate alcohol consumption.14 15 16 17 18 Previous reports of Japanese cohorts19 20 21 22 23 were based on limited stratification of two or three drinking categories and did not explore carefully an effect of moderate alcohol intake on cardiovascular disease incidence.
Understanding the relation of alcohol intake to stroke and other cardiovascular diseases is important for the formulation of public health recommendations; Japan has both a high rate of heavy drinking in men and a very high stroke mortality rate.24 We used the data from a 10.5-year follow-up study of men in three rural Japanese populations with a wide range of alcohol intake to examine the relation of alcohol to the incidence of cardiovascular disease. The relation of alcohol intake to stroke type, determined primarily by computed tomography (CT), was examined because of suggestions that the alcohol-stroke relation may vary by stroke type.13 14 17 23
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Subjects and Methods |
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The population surveyed included 2985 men aged 40 to 69 years who were examined between 1975 and 1979 in two northeast rural Japanese communities, Ikawa and Honjo, and between 1981 and 1985 in a central rural community, Kyowa. The overall participation rate was 65%. Persons with a history of stroke (n=75) or coronary heart disease (n=20) were excluded, and the data of 2890 men were used for the analyses (n=842 in Ikawa, 518 in Honjo, and 1530 in Kyowa). We did not examine the relation of alcohol intake to cardiovascular disease in women because only 6% of the 3908 female participants aged 40 to 69 years were current drinkers.
Subjects were followed up to determine cardiovascular disease end points occurring by the end of 1987 in Honjo and by the end of 1992 in other communities. Only 61 (2%) persons moved out of the communities during the follow-up, and 322 (11%) persons died. They were censored at the date of moving out or the date of death. The average follow-up for the participants was 10.5 years. Cardiovascular disease end points were ascertained through six sources25 : (1) national insurance claims, (2) reports by local physicians, (3) ambulance records, (4) death certificates, (5) reports by public health nurses and health volunteers, and (6) cardiovascular risk surveys. From death certificates, case subjects with underlying cause of death (International Classification of Diseases, 9th Revision: stroke, codes 430-438; coronary heart disease, codes 410-414, 428 and 429) were selected.
To validate the diagnosis, all living patients were visited or invited to complete risk-factor surveys. Study physicians obtained a medical history and a standard electrocardiogram (ECG) for coronary heart disease patients and a history and neurological examination from stroke patients. For deaths, histories were obtained from the families, and medical records were reviewed.
Stroke was defined as a focal neurological disorder with rapid onset that persists 24 hours or more. Thus, transient ischemic attack was not included. Determination of type of stroke (ie, intracerebral hemorrhage, subarachnoid hemorrhage, and nonhemorrhagic stroke) was done primarily by CT in a standardized way.26 Stroke cases that were diagnosed clinically but showed no lesion on CT were regarded as unclassified stroke. CT films were available for 72% of the stroke cases. Stroke cases without CT films were classified according to the clinical criteria27 based on Millikan's criteria.28
The criteria for coronary heart disease were modified from those of a World Health Organization expert committee.29 Painless types of coronary heart disease were not investigated because of difficulty with complete ascertainment. "Definite" myocardial infarction was indicated by typical chest pain (lasting for 30 minutes or longer) with the appearance of abnormal and persistent Q or QS waves, by changes in cardiac enzyme activity, or both. "Suspect" myocardial infarction was indicated by typical chest pain without positive ECG and enzyme activity findings. Angina pectoris was defined as repeated episodes of chest pain during effort, especially when walking, usually disappearing rapidly after the cessation of effort or by use of sublinguinal nitroglycerin. Definite or suspect myocardial infarction and angina pectoris were combined and presented as coronary heart disease. Unclassified sudden death was defined as death within 24 hours from the abrupt onset of symptoms that was unassociated with a previous diagnosis of coronary heart disease, stroke, or other identified causes of death. Using these standardized criteria, final diagnoses were made by a panel of three or four study physician-epidemiologists who were blinded to the data of the baseline examination.
Cardiovascular disease risk factors were measured at the baseline
examinations when the men were first examined. An interviewer assessed
usual weekly intake of alcohol in units of go (a Japanese
traditional unit of volume corresponding to 28 g), which were converted
to grams of ethanol per day. One go is 180 mL of sake, and
it corresponds to one bottle (663 mL) of beer, two single shots (75 mL)
of whisky, or two glasses (180 mL) of wine. Men who reported consuming
0.3 go or more per week were regarded as drinkers. Subjects
were classified as never-drinkers, ex-drinkers, or current drinkers who
averaged 1 to 20 g/d, 21 to 41 g/d, 42 to 69 g/d, or 70 g/d of
ethanol. Ex-drinkers were defined as abstainers for the past 3 months
and over. Distribution of ethanol intake in the surveyed populations
(Table 1
) was somewhat higher than that in the 1990
national representative sample.30 Drinking status
after 5 years in average from the baseline was examined for 65% of the
participants. The proportions of men who remained in the same category
of drinking status were 90% for never-drinkers, 63% for ex-drinkers,
39% for drinkers of 1 to 20 g/d ethanol, 36% for drinkers of 21 to 41
g/d ethanol, 58% for 42 to 69 g/d ethanol, and 60% for 70 g/d
ethanol. If drinkers of 1 to 20 g/d and of 21 to 41 g/d ethanol were
combined, the respective proportion was 58%.
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We measured several potential confounders: serum total cholesterol
level, blood pressure, body mass index, cigarette smoking, history of
diabetes mellitus, hypertensive ophthalmoscopic changes, and ECG
evidence of left ventricular hypertrophy. Serum total cholesterol level
was measured by the Liebermann-Burchard direct method using the
Autoanalyzer II (Technicon).31 The laboratory had been
standardized by the Lipid Standardization Program, Centers for Disease
Control and Prevention, Atlanta, Ga, and successfully met the criteria
of precision and accuracy of cholesterol measurements.32
Blood pressures were measured by trained observers using standard
mercury sphygmomanometers on the right arm of seated participants who
had rested for 5 minutes.33 Hypertension was defined as
systolic blood pressure of 160 mm Hg, diastolic blood pressure of
95 mm Hg, and/or current treatment with antihypertensive medication,
while normotension was defined as systolic blood pressure of <140
mm Hg and diastolic blood pressure of <90 mm Hg and no
antihypertensive medication. Subjects with blood pressures between
these categories were classified as having borderline hypertension.
Height in stocking feet and weight in light clothing were measured.
Body mass index was calculated as weight (kilograms) divided by the
square of height (meters squared). An interview was conducted to
ascertain the number of cigarettes smoked per day and use of
medications for diabetes mellitus. Diabetes mellitus was defined as a
fasting glucose level of 7.8 mmol/L or more, a nonfasting glucose level
of 11.1 mmol/L or more, and/or use of medication for diabetes.
A color photograph of the right ocular fundus was taken and coded according to Scheie's classification.34 Hypertensive or arteriosclerotic changes of grades 2 or higher were regarded as a significant hypertensive change in the retinal arterioles. Reliable photographs for the grading were obtained for 90% of the participants. A resting ECG was obtained with the subject in the supine position and coded according to the Minnesota Codes, second version.29 We regarded Minnesota Codes 3-1 plus (4-1 to 4-3 or 5-1 to 5-3) as left ventricular hypertrophy.
Incidence rates per 1000 person-years were calculated according to the six categories of drinking status. Rates were adjusted for age by the direct method of standardization to the age distribution of the total cohort of 2890 men.
For statistical analyses, differences in age-adjusted mean values and
the prevalence of potential confounding factors among six
categories of drinking status were tested by ANCOVA and
2 test, respectively. When the overall difference
was significant (P<.05), comparison of confounding factors
between never-drinkers and the other drinking categories was made using
a t test or 2 test. The relative risks
and 95% confidence intervals (CI) relative to never-drinkers were
calculated adjusting for age and other potential confounding factors
using the Cox proportional hazards model. Potential confounding factors
were the hypertension category (normotension, borderline hypertension,
and hypertension), serum total cholesterol level (millimoles per
liter), body mass index (kilograms divided by meters squared),
cigarette smoking (number per day), a history of diabetes mellitus (yes
versus no), hypertensive ophthalmoscopic changes (yes versus no), and
left ventricular hypertrophy (yes versus no). Because the relationship
between alcohol intake and cardiovascular disease was similar among the
three populations sampled, we presented the results for the
combined cohort.
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Results |
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Mean±SD values of selected cardiovascular risk characteristics were 140±21 mm Hg for systolic and 83±12 mm Hg for diastolic blood pressures and 4.58±0.92 mmol/L for serum total cholesterol. During the 10.5-year follow-up, there were 178 strokes, 34 coronary heart disease events, and 19 unidentified sudden deaths. The total number of cardiovascular disease events was 225 because six case subjects suffered from both stroke and coronary heart disease. Among strokes, there were 40 intracerebral hemorrhages, 18 subarachnoid hemorrhages, 104 nonhemorrhagic strokes, and 16 unclassified strokes.
The age-adjusted incidence rate of stroke (per 1000 person-years) was 5.9 in the total population, which varied among the three populations (10.3 in Honjo, 5.9 in Ikawa, and 4.0 in Kyowa; difference, P<.001). The population difference in stroke incidence corresponded with a difference in the proportion of hypertensive subjects (43%, 38%, and 28%, respectively; P<.001).
Compared with that in never-drinkers, the age-adjusted incidence rate
of all stroke was approximately 1.5 times higher in ex-drinkers and
drinkers of 42 to 69 g/d ethanol and 2.5 times higher in drinkers of
70 g/d (Table 1
). The rate of stroke in the lighter drinkers did not
differ so much from the rate in never-drinkers. For intracerebral
hemorrhage, the three categories of drinkers of 1 to 69 g/d showed
about two to three times higher risk, and drinkers of 70 g/d showed
seven times higher risk than never-drinkers. Although there was a small
number of cases, an excess risk of subarachnoid hemorrhage was shown in
drinkers of 70 g/d. For nonhemorrhagic stroke, the rate was two times
higher in drinkers of 70 g/d and 30% lower in drinkers of 1 to 20
g/d than never-drinkers. Unclassified stroke, although a small number
of cases, showed a similar pattern as nonhemorrhagic stroke. The rate
of coronary heart disease was lower in current drinkers than
never-drinkers, but a dose-response relation among current drinkers was
not evident. The rate of sudden death was over 10 times higher in
drinkers of 70 g/d than in never-drinkers.
To examine confounders for alcohol-disease associations, mean age and
age-adjusted values of selected risk factors at baseline were compared
among drinking-status categories (Table 2). Compared
with that in never-drinkers, mean age was 3 years older in ex-drinkers
and 3 to 4 years younger in drinkers of 42 g/d ethanol. Current
drinkers showed higher systolic and diastolic blood pressure levels
than never-drinkers, and there was a dose-response relationship between
alcohol intake and blood pressure levels. The percentage of men on
antihypertensive medication was 19% in ex-drinkers, 16% to 23% in
current drinkers, and 10% in never-drinkers. The prevalence of
hypertension was high in drinkers of 70 g/d, intermediate in drinkers
of <70 g/d, and ex-drinkers, and it was lowest in never-drinkers.
Current drinkers had mean serum total cholesterol concentrations about
0.25 mmol/L (10 mg/dL) lower than those of never-drinkers. The
prevalence of diabetes mellitus, although low across the
drinking-status categories, was two or three times higher in current
and ex-drinkers than in never-drinkers. Mean number of cigarettes was
higher in drinkers of 42 g/d than in never-drinkers. The prevalence
of hypertensive ophthalmoscopic changes was two or three times higher
in drinkers of 21 g/d ethanol than in never-drinkers. Drinking status
was not related to body mass index or left ventricular hypertrophy.
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Table 3 presents the relative risk of cardiovascular
disease relative to never-drinkers. The age-adjusted relative risk of
all stroke was 2.7 for drinkers of 70 g/d ethanol, and the relative
risks for other categories of alcohol intake were not statistically
significant. Adjusting for age, hypertensive status, serum total
cholesterol level, and cigarette smoking, the relative risk for heavy
drinkers was reduced to 1.9 but remained statistically significant. The
age-adjusted relative risk of hemorrhagic stroke for heavy drinkers was
6.2, which was reduced to 3.4 with adjustment for covariates. The
reduction of the adjusted relative risks was due mostly to the effect
of hypertension. When only age and hypertension category were
controlled for, the adjusted relative risk for heavy drinkers was 2.0
(95% CI, 1.2 to 3.2) for all stroke and 3.6 (95% CI, 1.3 to 9.8) for
hemorrhagic stroke.
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The age-adjusted relative risk of nonhemorrhagic stroke in heavy drinkers was 2.1, and the multivariate-adjusted relative risk was 1.7, which did not reach statistical significance (P=.12). The relative risk in ex-drinkers and drinkers of <42 g/d was <1.0, although it was not statistically significant. Thus, a J-shaped relation was suggested between alcohol intake and nonhemorrhagic stroke. Current drinkers had a relative risk of <1.0 for coronary heart disease, although it was not statistically significant. The age-adjusted risk of sudden death was 10 in heavy drinkers and remained largely unchanged after we controlled for the covariates. The relative risk of total cardiovascular disease was similar to that of all stroke.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In our cohort of Japanese men, heavy drinking of
70 g/d
ethanol was associated with an elevated risk of all stroke incidence,
in particular hemorrhagic stroke. Our results support previous findings
of case-control studies in white men.8 9 10 The excess risk
of stroke was much reduced when the hypertension category was taken
into account, suggesting that hypertension was a strong mediator of a
causal association between alcohol intake and stroke.35 A
causal link between alcohol and hypertension is acceptable on the basis
of many experimental, clinical, and epidemiological
studies.36 In the present study, blood pressure
levels and hypertension-related variables were strongly
associated with alcohol intake. Ex-drinkers were more likely to be
hypertensive than were light drinkers, as reflected by their higher
usage of antihypertensive medication. We assume that treatment of
hypertension triggered cessation of alcohol drinking, probably due to
advice from physicians and other health professionals. The present study also showed a 10-times higher risk of unclassified sudden death in heavy drinkers compared with never-drinkers. The excess risk did not change so much with adjustment for the covariates, which suggests that the excess risk was probably due to drinking per se or other unknown drinking-related factors. We assume that a considerable proportion of unclassified sudden deaths was due to heart disease. Underlying causes of death for the 19 cases of unclassified sudden death were coronary heart disease (n=6), heart failure or other heart disease (n=8), other acute cerebrovascular disease (n=3), and other causes (n=2). One of the plausible mechanisms for the excess risk of sudden death is cardiac arrhythmia occurring in the early stage of cardiomyopathy due to chronic heavy drinking.37 38 Another possible mechanism is ventricular arrhythmia due to subarachnoid hemorrhage, for which heavy drinkers had a higher risk.39
The results of the present study suggest an elevated risk of hemorrhagic stroke and a reduced risk of nonhemorrhagic stroke in men with light or moderate alcohol consumption. These alcohol-stroke relations are consistent with models of a linear relation with hemorrhagic stroke and a J-shaped relation with nonhemorrhagic stroke, reported by Camargo35 based on a systematic literature review. A linear relationship between alcohol intake and hemorrhagic stroke was reported from two prospective studies: one for men, the Honolulu Heart Study,13 and the other for women, the Nurses' Health Study.14 Both studies indicated that the linear relation was due mostly to the relation of alcohol to subarachnoid hemorrhage. For intracerebral hemorrhage, the slope of the positive association was smaller and not statistically significant.13 Mechanisms for the alcohol–hemorrhagic stroke relation are not fully understood except for an effect mediated by high blood pressure. It is possible that alcohol induces changes in hemostatic factors that increase the risk of hemorrhage in intracerebral arterioles. An experimental study of healthy volunteers demonstrated that ingestion of a moderate amount of alcohol prolonged bleeding time and reduced platelet aggregability.40 Alcohol also enhances fibrinolytic activity through increased secretion of plasminogen activator from endothelial cells.41
A J- or
U-shaped association of alcohol intake with
all stroke or nonhemorrhagic stroke has been found predominantly in
white populations. A recent report of 32 years of follow-up in the
Framingham Heart Study17 showed that, among men, moderate
drinkers (<24 g/d ethanol) had a significantly lower incidence rate of
stroke than heavy (24 g/d) or nondrinkers. A study of women showed a
similar U-shaped relation, although it was
not statistically significant.17 Prospective studies of
men in Yugoslavia15 and in Albany16 both
showed a significant U-shaped relation
between alcohol consumption and all stroke deaths. The Nurses' Health
Study,14 a prospective study of 87 526 American female
nurses showed a U-shaped relation between
alcohol intake and all stroke incidence, which was composed of a
positive association with subarachnoid hemorrhage and an inverse
association with nonhemorrhagic stroke. However, the Honolulu Heart
Study,13 a prospective study of 7878 American Japanese
men, showed a linear positive relation between alcohol intake and all
stroke incidence because of a linear positive association with
hemorrhagic stroke and a flat association with nonhemorrhagic stroke. A
recent report of the Hisayama study,23 a prospective study
of 1621 Japanese men and women, reported a nonsignificant linear
positive relation of alcohol intake and hemorrhagic stroke and a
nonsignificant J-shaped relation of alcohol
intake and nonhemorrhagic stroke. In the Hisayama study, the
categorization of alcohol intake was nondrinkers, drinkers of 1 to 34
g/d ethanol, and drinkers of 34 g/d, and they did not differentiate
between never-drinkers and ex-drinkers. The present study examined
the effect of a wide range of alcohol drinking and found a
J-shaped relation in Japanese men.
Potential mechanisms by which light or moderate alcohol intake could reduce the incidence of nonhemorrhagic stroke were addressed previously42 ; the mechanisms are similar for the case of coronary heart disease. Moderate alcohol consumption increases prostacyclin in vascular walls, a potential vasodilator and inhibitor of platelet aggregation, which prevents thrombus formation in cerebral and carotid arteries.43 Enhanced fibrinolysis via increased secretion of plasminogen activator from endothelial cells41 may be another potential mechanism. Elevated high-density lipoprotein cholesterol levels may protect against atheroma formation in cerebral and carotid arteries.44 Change in hemostatic variables such as reduced plasma fibrinogen45 may be another contributing factor. The increased risk of nonhemorrhagic stroke in heavy drinkers is explained by hypertension-induced atherosclerosis or arteriosclerosis,46 reduced cerebrovascular blood flow by spasm of cerebral arteries and arterioles,47 or by alteration of cerebral metabolism.48
There have been a number of prospective studies indicating that moderate alcohol consumption reduces the risk of coronary heart disease.12 The results of the present study do not conflict with previous reports, but the inverse relation was weak and not statistically significant, being based on a small number of cases. The low incidence of coronary heart disease was not surprising because serum total cholesterol level was much lower in the surveyed populations than in white populations.49 In our 6-year prospective investigation of 11 987 urban male employees aged 40 to 59 years, in whom the mean serum cholesterol level was higher at 5.04 mmol/L (195 mg/dL) and there were 83 subsequent coronary heart disease events, we observed a significant inverse association with alcohol intake.50 Mechanisms of the reduced risk of coronary heart disease may be similar to those of nonhemorrhagic stroke.41 43 44
Although a strength of the present study was the availability of CT examinations for stroke typing, a potential drawback was that 28% of stroke case subjects did not have CT examination data, necessitating the use of clinical criteria. We found no difference in the proportion of men with missing CT data between hemorrhagic and nonhemorrhagic stroke cases: 29% for hemorrhagic and 32% for nonhemorrhagic stroke. The validity of stroke diagnosis by the clinical criteria was tested by autopsy findings in our previous study51 : 90% of the cases diagnosed as hemorrhagic stroke and 75% of the cases diagnosed as nonhemorrhagic stroke were correctly diagnosed according to autopsy findings. Among the stroke cases with CT in the present study, all 25 cases diagnosed as hemorrhagic stroke by the clinical criteria were found to be hemorrhagic stroke by CT. On the other hand, 11 of the 88 cases (13%) diagnosed as nonhemorrhagic stroke by the clinical criteria were found to be hemorrhagic stroke by CT. All of the misdiagnosed cases showed a small hematoma without perforation to a ventricular system. The results suggest that clinical discrimination between hemorrhagic and nonhemorrhagic stroke was done well.
The relation between alcohol intake and total cardiovascular
disease was similar to the relation for all stroke; stroke cases
comprised 79% of the cardiovascular disease in the surveyed
populations. Age-adjusted incidence rates were significantly higher in
drinkers of 42 g/d ethanol than in never-drinkers, whereas no excess
risk was found in drinkers of <41 g/d. Therefore, according to results
of this study in Japanese men, three drinks per day or fewer is
recommended for current drinkers to prevent cardiovascular disease,
which is similar to the recommendations for western
populations.3 4 12 18 35
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Acknowledgments |
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The authors thank Professor Aaron R. Folsom, University of Minnesota, for valuable advice on the manuscript.
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Footnotes |
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Reprint requests to Hiroyasu Iso, MD, Institute of Community Medicine, University of Tsukuba 1-1-1, Tsukuba-shi, Ibaraki-ken, 305 Japan.
Received January 10, 1995; revision received February 14, 1995; accepted February 14, 1995.
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