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1 clinical investigations Risk Factors in a General Population for Snoring* Importance of Cigarette Smoking and Obesity John W. Bloom, M.D., F.C.C.P.;t Walter T. Kaltenborn, M.S.; and Stuart F. Quan, M.D., F.C.C.P. In order to study risk factors associated with snoring in a general adult population, 2,187 subjects in the Tucson Epidemiologic Study of Obstructive Airways Disease were surveyed to determine the prevalence of snoring. Major independent risk factors for snoring were male gender, age between 40 and 64 years, obesity, and current cigarette smoking. Furthermore, greater intensity of cigarette smoking also was associated with higher snoring prevalence rates. Snoring prevalence remained elevated in subjects who recently quit smoking, but declined in ex-smokers to the level of never smokers within four years of smoking cessation. The presence of cough or sputum production was associated with an increase in snoring prevalence especially in ex-smokers. Snoring prevalence was slightly increased in subjects who regularly used alcohol or medications as aids to sleep. We conclude that cigarette smoking, obesity, male gender, age over 40, and use of alcohol or sleep medications are important risk factors for snoring. We propose that the effect of smoking may be related to the production of upper airway inflammation and edema by cigarette smoke, and that smoking cessation may eventually reduce snoring risk. TTistorically, snoring during sleep has been considered to be only an annoyance to the snorer s bed partner. However, recent studies demonstrate an increased prevalence of hypertension, stroke, and ischemic heart disease in those who snore. 1 " 5 In addition, heavy snorers are more likely to hypoventilate during sleep, 6 and there may be a relationship between long-term heavy snoring and the development symptomatic obstructive sleep apnea. 78 Snoring is the audible result of vibration of the palate and other soft tissues in the oropharynx, and represents partial obstruction of the upper airway. 9 Cigarette smoking frequently results in a chronic productive cough 10 and smokers often have evidence of upper airway inflammation." Alcohol attenuates the activity of the pharyngeal dilator musculature, 1213 and it has been suggested that sedative-hypnotic medications have a similar effect. 14 Obese men have a higher prevalence rate of obstructive sleep apnea 8 and may have a higher resistance to airflow in the upper airway. 15 *From the Department of Internal Medicine, Division of Respiratory Sciences, Sleep Disorders Center, University of Arizona College of Medicine, Tucson. Presented in part at the Annual Meeting, American Thoracic Societv, New Orleans, May 13, Supported by SCOR Grant No HL trecipient of Pulmonarv Academic Award from National Heart, Lung, and Blood Institute (HL00838). Manuscript received July 6; revision accepted September 14. Reprint requests: Dr. Bloom, Respiratory Sciences, Arizona Health Sciences Center, Tucson of These observations suggest that cigarette smoking, obesity, respiratory symptoms, and use of alcohol and sedative-hypnotic medications are factors which may compromise the patency of the upper airway during sleep and should be associated with a higher prevalence of snoring. In order to test this hypothesis, we surveyed subjects in the Tucson Epidemiologic Study of Airways Obstructive Disease to determine the relationship of these factors to the prevalence of snoring in a random sample of a general population. METHODS Data were obtained from the seventh (October 1981-February 1983), eighth (April 1983-April 1984), and ninth (May 1984-October 1985) surveys of subjects participating in the Tucson Epidemiologic Study of Airways Obstructive Diseases, a prospective longitudinal study of the natural history of obstructive lung disease that was begun in The study sample represents a random, stratified sample of the white, non-hispanic population of Tucson, Arizona. A detailed description of the methodology of population selection has been published previously. 18 In each survey, health information is obtained for the study population using a self-administered questionnaire. In the ninth survey, additional questions were included pertaining to the presence and frequency of snoring and the use of alcohol or medications as aids to sleep. The question concerning snoring was: How often do you snore loudly? 1. Every night 2. Most nights 3. Some nights 4. Rarely 5. Don't know 678 Risk Factors for Snoring (Bloom, Kaltenborn, Quan)

2 Thirty-seven percent of subjects did not know whether they snored. This group of "don't knows" included significantly more women ("don't know" = 68.4 percent female vs "know" = 49.7 percent female, p <. 001) and older subjects (over 64 years of age, "don't know" = 39.6 percent vs "know" = 20.3 percent, p <.001). Fewer of the "don't know" group (45 percent) than the "know" group (78 percent) were presently married (p <.001). Thus, the marital status of these "don't know" subjects indicates that they were more likely to sleep alone. Because we could not determine accurately the snoring status of these subjects, we excluded this "don't know" group from the analysis. The prevalence of snoring "every" or "most nights" was 16.8 percent in the overall adult population. This prevalence rate was similar to that for heavy snoring in previous epidemiologic studies of snoring. Therefore, for this analysis we considered heavy snorers to be those who snored on every or most nights. 2,3 Smoking status was determined from data obtained in the ninth survey. Current smokers were asked how many cigarettes per day they smoked. In ex-smokers, duration and intensity of smoking and years since quitting were obtained from data in the eighth and ninth surveys. Information regarding respiratory symptoms was determined from questions in the ninth survey pertaining to the occurrence of cough, sputum production, wheezing, and rhinitic symptoms. The prevalence of cough or sputum production was defined as a "yes" response to the presence of cough, phlegm, sputum, or mucus production regardless of frequency, time of day, or weather conditions. Subjects were asked if their chests ever sounded wheezy or whistling. The presence of wheezing was defined as a "yes" response irrespective of symptom frequency or the presence of concurrent respiratory infection. The prevalence of rhinitis was defined as a "yes" response to the question asking whether subjects had hay fever or other allergy which resulted in a runny nose or nasal stuffiness, An index of obesity was calculated as body weight divided by height squared" using data from the ninth survey. We considered subjects as obese if they were in the upper 25th percentile of the obesity index for each gender. Data regarding the use of alcohol or medications as aids to sleep were drawn from the ninth survey questionnaire. However, total alcohol consumption was determined from the seventh survey because this specific question was not included in the ninth survey. For some analyses, subjects were stratified according to age and gender. Inasmuch as we were interested in studying an adult population, we included only subjects who were older than 17 years. Three age groups (less than 40 years of age, years of age, and greater than 64 years of age) were chosen to represent young, middle-aged, and elderly subgroups, Statistical comparisons of prevalence rates between groups were made using chi square analysis with Yates' correction for continuity where indicated. Analysis of trends in proportions among groups was done using trend chi square analysis. Multiple logistic regression was used to evaluate the simultaneous effect of several potentially confounding variables on the risk of snoring. ** GENDER AGE M W + M LT 40 W M W G T 64 FIGURE 1. Snoring prevalence according to gender and age. M = men. W = women. LT 40 = age less than 40 years; = age 40 to 64 years; GT 64 = age greater than 64 years. * = snoring prevalence significantly greater in men compared to women, p <.001. ** = snorning prevalence significantly greater in men compared to women, p<,01. + = snoring prevalence signficantly increased compared to age group less than 40 years of same gender. ing except in the under 40-year-old age group. In this subgroup, the proportion of men in the study population was less than in the group of nonparticipants (47.0 percent vs 57.1 percent, p < ). There were 1,359 subjects who knew whether or not they snored. Of these 1,359 subjects, there were 636 subjects (326 men, 310 women) under 40 years of age, 447 subjects (236 men, 211 women) years of age, and 276 subjects (121 men, 155 women) 65 + years old. Snoring prevalence for age and gender groups is shown in Figure 1. In the less than 40 and age groups, snoring prevalence was significantly greater in men than women. In both men and women, snoring prevalence was lowest in the subjects and increased youngest significantly (under 40 yrs) in middle age (40-64 yrs). Although there appeared to be a decline in snoring prevalence in elderly (65 + yrs) men, this was not statistically significant. The effect of obesity on snoring is shown in Figure 2 by age and gender. Regardless of gender, snoring prevalence was greater in obese subjects in each of the age groups. T h e effect of obesity was most pronounced in young women ( < 4 0 years of age). T h e snoring prevalence of obese subjects in this group was over RESULTS three-fold greater than nonobese subjects. Data were available for 2,187 (82.9 percent) of the As shown in Figure 3, cigarette smoking was associ- 2,639 subjects over 17 years of age. Data were not ated with a higher rate of snoring. For both men and available in 452 subjects because they could not be women, snoring prevalence was greater in present located (57.3 percent), refused (29.8 smokers than in subjects who had never smoked. For percent), or were too ill to complete the questionnaires ex-smokers, the snoring prevalence appeared inter- (12.9 percent). T h e mean age of these individuals mediate between present and never smokers, although (47.1 ± years, m e a n ± S D ) was not significantly this did not reach statistical significance. T h e effect of different from the study population (49.1 ± 19.7 years). smoking was greater in nonobese subjects. In non- There was no difference distribution obese women, the prevalence of snoring in present between the study population and those not participat- smokers (18.1 percent) was almost four times higher to participate in the gender CHEST / 93 / 4 / APRIL,

3 MEN WOMEN 40 N FRY 3 L Y J N N LT 4 0 N G T 64 N LT 4 0 than the rate in never smokers (p <.001). In nonobese men, the prevalence of snoring in present smokers (29.3 percent) was almost 2.5-times the rate in never smokers (p <.001). In obese present smokers of either sex, the prevalence of heavy snoring was over 40 percent. The risk of snoring increased with cigarette smoking intensity. The rate was 43.9 percent in smokers of more than 30 cigarettes/day compared to 24.3 percent in smokers of 30 or fewer cigarettes/day (p <.01). This effect of smoking intensity was observed in both men and women. In addition, the risk of snoring increased with pack-years of cigarette smoking (cigarettes per day divided by 20 X years smoked). The prevalence of snoring in present smokers with 30 or more pack-years of smoking (38.3 percent) was higher than the rate (19.7 percent) in present smokers with less than 30 pack-years of smoking (p <.01). There was a relationship between several respiratory symptoms and the prevalence of heavy snoring. The most prominent association was with cough or sputum production. The snoring prevalence was increased two-fold in subjects with cough or sputum production (26.4 percent vs 13.7 percent, p <.001). The relamen SMOKING STATUS PS ES WOMEN NS PS ES NS FIGURE 3. The effect of cigarette smoking on snoring prevalence. PS = present smokers; ES = ex-smokers; NS = never-smokers. Snoring prevalence was significantly different in smoking groups for both men and women (p <.001), except that ex-smokers were not significantly different from never-smokers, 680 N N G T 64 FIGURE 2. The effect of obesity on snoring prevalence. = obese subjects. N = nonobese subjects. LT 40 = age less than 40 years; = age 40 to 64 years; GT 64 = age greater than 64 years; * = snoring prevalence in obese subjects greater than nonobese subjects, p <, 0 5 ; p =.10 in men age years. tionships of age, gender, obesity, and smoking to snoring were not affected by the presence of cough or sputum production except in ex-smokers. The snoring rate in ex-smokers with cough or sputum production (31.7 percent) approached the rate in present smokers (35.1 percent). In ex-smokers without cough or sputum production, the snoring prevalence (17.5 percent) was similar to the rate in never smokers (16.5 percent). Wheezing complaints were also associated with an increased snoring prevalence (25.2 percent vs 13.2 percent, p <.01). There was no relationship between rhinitis and snoring in this population. There was a slight increase in the prevalence of snoring related to the use of alcohol or medications as aids to sleep. The prevalence of snoring in subjects who used alcohol or medications regularly as aids to sleep was 23.6 percent compared to 15.9 percent in non-users (p <. 05). However, we found no relationship between overall alcohol use and snoring. Because smokers were more likely to use alcohol or medications as sleep aids (present smokers 15.7 percent, never smokers 8.6 percent), w e determined the relationship of smoking to snoring separately in users and non-users of alcohol and medicinal sleep aids. In users of alcohol or medicinal sleep aids, the prevalence of snoring was 35.4 percent in present smokers compared to 10.2 percent in never smokers (p <.01). In nonusers of alcohol or medicinal sleep aids, the snoring rate in present smokers was 26.1 percent compared to 11.8 percent in never smokers (p <.001). In both groups, the snoring prevalence in ex-smokers appeared intermediate between present and never-smokers. A multiple logistic regression analysis of the data was performed to consider the simultaneous effect of potential risk factors related to snoring. Current cigarette smoking, obesity, gender, and age were significantly related to heavy snoring (p <.005), as were cough or sputum production, wheezing, and use of alcohol or medicinal sleep aids (p <.05). However, exsmoking was not significant in the model. Inasmuch as there was considerable heterogeneity among the exrisk Factors for Snoring (Bloom, Kaltenborn, Quan)

4 RELATIVE NEVER SMOKING NONESE 1.0 FEMALE LT40 PRESENT SMOKING NONESE 2.9 FEMALE LT40 NEVER SMOKING NONESE 3.7 MALE LT40 PRESENT SMOKING NONESE 10.1 MALE LT40 PRESENT SMOKING NONESE MALE PRESENT SMOKING ESE MALE SNORING PREVALENCE 40 DISCUSSION We have investigated the risk factors for snoring in a random, stratified sample of the population of Tucson, Arizona. Snoring status was determined from questionnaire responses. Self-reported snoring has been shown to correlate well with sleep laboratory findings, especially for habitual snorers. W e defined snoring as loud snoring every or most nights because this type of heavy habitual snoring has been associated with a higher prevalence of hypertension, ischemic heart disease, and stroke. In addition, a large percentage of heavy snorers may have mild obstructive sleep apnea. We elected to exclude subjects from our analyses who did not know whether or not they snored FIGURE 4. The relative risk of snoring for several combinations of age, gender, obesity, and smoking. LT 40 = age less than 40 years; = age 40 to 64 years; GT 64 = age greater than 64 years. 50 (%) smokers with regard to prior smoking intensity and duration since quitting, another multiple logistic regression analysis limited to ex-smokers was performed to determine whether these factors explained the absence of an ex-smoking effect in the overall multiple logistic regression. This analysis suggested that duration since quitting contributed to the risk of snoring in ex-smokers ( p =. 0 7 ). Subsequent examination of the data showed that there was no ex-smoking effect observed if the time since quitting exceeded four years. The effect of prior smoking intensity (packyears) was not significant. The relative risk of snoring associated with several of the factors identified in this study is shown in Figure 4. The lowest rate of snoring (2.8 percent) was found in young, nonobese, never-smoking women. Present smoking in this group increased the relative risk 2.9fold. Young, nonobese, never-smoking men had a 3.7fold increase in relative risk of snoring compared to the same category of women. T h e addition of present smoking in young, nonobese men markedly increased the relative risk to T h e addition of middle-age and obesity increases the prevalence of snoring to greater than 40 percent in the middle-aged obese male smoker with a relative risk of snoring 14.8 times that of the young nonobese female nonsmoker. 21 RISK It would seem likely that these subjects are not heavy snorers. Therefore, it is possible that actual snoring prevalence rates are lower than those w e observed. However, because the overall prevalence for heavy snoring found in this study is similar to that of Lugaresi et al and Norton and Dunn, we think it unlikely that the actual snoring prevalence rates differ markedly from the data w e report. 2 3 We found that cigarette smoking, male gender, age greater than 40 years, obesity, respiratory symptoms (cough or sputum production, and wheeze), and the use of alcohol or medications as aids to sleep were associated with an increased prevalence of snoring. Our data agree with previous reports that have noted the association of gender and age with snoring preval e n c e. Although our finding that snoring is more common in men and older individuals has been universal, the mechanism is unclear. However, recent evidence suggests upper airway caliber may be relatively smaller in men. White et al have demonstrated that pharyngeal resistance is higher in men than women. In addition, pharyngeal resistance increased with age in men but not in women. Therefore, the greater prevalence of snoring in men and its increase in middle age may be a result of an anatomically less patent pharyngeal airway. However, these findings do not explain our observations of a decline in snoring prevalence in men after age 64 and an increase in snoring prevalence in middle-aged women. 24 2,3 13 Previous studies also have noted a strong association between obesity and an increase in snoring preval e n c e. It is tempting to speculate that this finding is related to a reduction in pharyngeal airway diameter produced by deposits of adipose tissue in obese individuals. In support of this hypothesis, White et al have observed that pharyngeal resistance in men correlates with increasing weight-to-height ratio, although this finding was confounded by a simultaneous effect of aging. Nevertheless, computerized tomographic scans in individuals with sleep apnea have failed to demonstrate localized deposits of fat adjacent CHEST / 93 / 4 / APRIL,

5 to the pharynx in spite of the observation that subjects with sleep apnea had a smaller pharyngeal airway than control subjects Norton and Dunn reported an association between 3 cigarette smoking and snoring in a survey of patients from a family practice clinic. We confirm this strong association in a general population sample, and extend these findings to present evidence that the increased prevalence of snoring in cigarette smokers is actually the result of smoking. First, we found a dose-effect of smoking on snoring. In present smokers, those smoking more than 30 cigarettes/day had a greater prevalence of snoring than those who smoked less. Secondly, the snoring prevalence in ex-smokers appeared to be intermediate between never-and present smokers. This effect was the result of an increased prevalence rate in recent ex-smokers. Ex-smoking was not a risk factor for snoring if the time since quitting exceeded four years. We found that the effect of smoking on snoring prevalence was not the result of a relationship between smoking and another risk factor for snoring. The smoking relationship was independent of age, gender, obesity, the use of alcohol and medications as aids to sleep, and respiratory symptoms. It has been demonstrated that nonobese snorers with or without sleep apnea have a smaller pharyngeal cross-sectional area than non-snorers. Thus, it is 24 possible that pharyngeal narrowing may predispose to snoring by increasing upper airway resistance and producing turbulent airflow. We hypothesize that the irritant effect of smoking causes edema and inflammation of the pharynx resulting in narrowing. This pharyngeal narrowing may predipose smokers to heavy snoring. If our hypothesis is correct, we would expect to see a continuing effect of smoking in exsmokers which declines with increasing time after smoking cessation. Therefore, our observations that ex-smokers have a snoring prevalence rate intermediate between present and never-smokers and that only recent ex-smoking is a risk factor for snoring support this hypothesis. Moreover, these findings make it unlikely that the increase in snoring prevalence in smokers is a result of an acute effect produced by cigarette smoke. We observed an increased prevalence of snoring associated with the respiratory symptoms of cough or sputum production, and wheezing. However, we did not find a relationship in this population between symptoms of nasal stuffiness or rhinitis and snoring although nasal obstruction has been reported occasionally to produce sleep apnea. Interestingly, exsmokers with cough or sputum production had rates of 2527 snoring that approached those in present smokers, and asymptomatic ex-smokers were similar to neversmokers. Thus, symptoms in ex-smokers may be a marker of continuing airway inflammation resulting in pharyngeal narrowing. Although we did not find a relationship between overall alcohol intake and snoring, the use of alcohol or medications as aids to sleep was associated with an increased prevalence of snoring. Alcohol previously has been shown to increase upper airway resistance and snoring This may be the result of a decrease in pharyngeal muscle tone. Alcohol selectively decreases neural input and electromyographic activity of pharyngeal dilator muscles, 1213 and a similar mechanism has been suggested for the effect of sedative-hypnotic drugs. 14 Therefore, after ingestion of alcohol or a sedative-hypnotic medication, the normal inspiratory increase in the pharyngeal dilator muscle tone during sleep may be reduced, predisposing to upper airway narrowing or collapse and snoring or obstructive sleep apnea. Heavy snoring may be more than just a social liability. It has been associated with an increased prevalence of hypertension, stroke, and ischemic heart disease. 15 Furthermore, heavy snorers may have or may develop symptomatic obstructive sleep apnea. 7 8,21 These data argue in favor of some treatment for heavy snoring. Avoidance of sleep in the supine position has been suggested as a method of eliminating snoring, but a definite benefit has not been demonstrated. 30 Our data and those of others 2,3 would suggest that obese snorers might improve by losing weight, but compliance with weight loss programs is poor. 31 Furthermore, our data suggest that avoidance of alcohol or medications as sleep aids may decrease snoring. Inasmuch as we observed a lower prevalence of snoring in ex-smokers compared to present smokers, smoking cessation may be an effective treatment for smokers who snore. In summary, we have identified that smoking, obesity, male gender, and middle age are risk factors for snoring. We believe this is the first report documenting risk factors for snoring in a randomly selected sample of a general population. The strong association between cigarette smoking, respiratory symptoms, and snoring is especially intriguing and requires further study. ACKNOWLEDGMENTS: The authors thank Mrs. Ellen Dunn and Mrs. Sandra Testa for secretarial assistance and Mr. Philip Thomas for computer programming assistance. REFERENCES 1 Partinen M, Palomaki H. Snoring and cerebral infarction. Lancet 1985; 2: Lugaresi E, Cirignotta F, Coccagna G, Piana C Some epidemiological data on snoring and cardiocirculatory disturbances. Sleep 1980; 3: Norton PG, Dunn EV. Snoring as a risk factor for disease: an epidemiological survey. Br Med J 1985; 291: Koskenvuo M, Partinen M, Sarna S, Kaprio J, Langinvainio H, Heikkila K. Snoring as a risk factor for hypertension and angina 682 Risk Factors for Snoring (Bloom, Kaltenborn, Quan)

6 pectoris. Lancet 1985; 1: Koskenvuo M, Kaprio J, Telakivi T, Partinen M, Heikkila K, Sarna S. Snoring as a risk factor for ischaemic heart disease and stroke in men. Br Med J 1987; 294: Lugaresi E, Coccagno G, Farneti M, Mantovani M, Cirignotta F. Snoring. Electroencephalogr and Clin Neurophysiol 1975; 39: Zwillich C. The clinical significance of snoring. Arch Intern Med 1979; 139:24 8 Guilleminault C, van den Hoed J, Mitler MM. Clinical overview of the sleep apnea syndromes. In: Guilleminault C, Dement WC, eds. Sleep apnea syndromes. New York:Alan R. Liss, 1978; Lugaresi E, Coccagna G, Cirignotta F. Snoring and its clinical implications. In: Guilleminault C, Dement WC, eds. Sleep apnea syndromes. New York:Alan R. Liss, 1978: Burrows B, Lebowitz MD. Characteristics of chronic bronchitis in a warm, dry region. Am Rev Respir Dis 1975; 112: Bowen-Davies A. Pharyngitis-acute and chronic. In: Ballantyne J, Groves J, eds. Diseases of the ear, nose and throat. London: Butterworths, 1971:75 12 Bonora M, Shields GI, Knuth SL, Bartlett D, St. John WM. Selective depression by ethanol of upper airway respiratory motor activity in cats. Am Rev Respir Dis 1984; 130: Krol RC, Knuth SL, Bartlett D. Selective reduction of genioglossal muscle activity by alcohol in normal human subjects. Am Rev Respir Dis 1984; 129: Remmers JE. Obstructive sleep apnea. Am Rev Respir Dis 1984; 130: White DP, Lombard RM, CadieuxRJ, Zwillich CW. Pharyngeal resistance in normal humans: influence of gender, age and obesity. J Appl Physiol 1985; 58: Lebowitz MD, Knudson RJ, Burrows B. Tucson epidemiologic study of obstructive lung disease. I: Methodology and prevalence of disease. Am J Epidemiol 1975; 102: Revicki DA, Israel RG. Relationship between body mass indicies and measures of body adiposity. Am J Public Health 1986; 76: Zar JH. Biostatistical analysis. Englewood Cliffs, New Jersey :Prentice Hall, 1974:127-29, , Armitage E Statistical methods in medical research, 8th ed. New York:Blackwell Scientific Publications, 1983: Kelsey JL, Thompson WD, Evans AS. Methods in observational epidemiology. New York:Oxford University Press, 1986: Berry RB, Block AJ. Positive nasal airway pressure eliminates snoring as well as obstructive sleep apnea. Chest 1984; 85: Suratt PM, Dee P, Atkinson RL, Armstrong P, Wilhoit SC. Fluoroscopic and computed tomographic features of the pharyngeal airway in obstructive sleep apnea. Am Rev Respir Dis 1983; 127: Haponik EF, Smith PL, Bohlman ME, Allen RP, Goldman SM, Bleecker ER. Computerized tomography in obstructive sleep apnea. Am Rev Respir Dis 1983; 127: Bradley TD, Brown IG, Grossman RF, Zamel N, Martinez D, Phillipson EA, et al. Pharyngeal size in snorers, nonsnorers, and patients with obstructive sleep apnea. N Engl J Med 1986; 315: Zwillich CW, Pickett C, Hanson FN, Weil JV. Disturbed sleep and prolonged apnea during nasal obstruction in normal men. Am Rev Respir Dis 1981; 124: Taasan V, Wynne JW, Cassisi N, Block AJ. The effect of nasal packing on sleep-disordered breathing and nocturnal oxygen desaturation. Laryngoscope 1981; 91: McNicholas WT, Tarlo S, Cole P, Zamel N, Rutherford R, Griffin D, et al. Obstructive apneas during sleep in patients with seasonal allergic rhinitis. Am Rev Respir Dis 1982; 126: Issa FG, Sullivan CE. Alcohol, snoring and sleep apnea. J Neurol, Neurosurg, and Psychiatry 1982; 45: Robinson RW, White DP, Zwillich CW. Moderate alcohol ingestion increases upper airway resistance in normal subjects. Am Rev Respir Dis 1985; 132: Koskenvuo M, Partinen M, Kaprio J. Snoring and disease. Ann Clin Res 1985; 17: Orr WC. Sleep-related breathing disorders; an update. Chest 1983; 4: CHEST / 93 / 4 / APRIL,

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