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Chronic Nasal Congestion at Night Is a Risk Factor for Snoring in a Population-Based Cohort Study
Terry Young, PhD;
Laurel Finn, MS;
Mari Palta, PhD
Arch Intern Med. 2001;161:1514-1519.
ABSTRACT
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Background Nasal congestion at night is thought to have a role in snoring and sleep
apnea, but this hypothesis has not previously been tested in a population-based
study.
Methods Baseline and 5-year follow-up data on self-reported nocturnal nasal
congestion and snoring frequency were collected from a population-based sample
of 4916 men and women (age range, 30-60 years at baseline) enrolled in the
ongoing Wisconsin Sleep Cohort Study. In-laboratory polysomnography was performed
on a subset (n = 1032) of the study population to determine the frequency
of apnea and hypopnea episodes during sleep. Logistic regression was used
to estimate odds ratios for snoring with chronic nasal congestion at night.
Results Nocturnal nasal congestion frequency was independently associated with
snoring frequency in cross-sectional analyses. The odds ratios (adjusted for
sex, age, body habitus, and smoking) for habitual snoring with severe (always
or almost always) nasal congestion vs none was 3.0 (95% confidence interval,
2.2-4.0). This association was not explained by habitual snorers with frank
sleep apnea (ie,  5 apnea and hypopnea episodes per hour of sleep). Prospective
analyses showed that persons with chronic severe nasal congestion had a high
risk of habitual snoring according to the data from the 5-year follow-up survey:
the odds ratio for habitual snoring and reporting congestion always or almost
always at both baseline and follow-up was 4.9 (95% confidence interval, 2.8-8.8).
Conclusions Nocturnal nasal congestion is a strong independent risk factor for habitual
snoring, including snoring without frank sleep apnea. Intervention studies
are needed to determine if snoring can be reduced with treatment of nasal
congestion.
INTRODUCTION
SEVERAL population-based studies have linked self-reported snoring to
adverse health outcomes, including hypertension and ischemic heart disease,1 daytime sleepiness,2-4
and accidents.5 Most recently, the role of
snoring in the development of cardiovascular conditions was investigated prospectively
in the Nurses Health Study, a study of 72 231 nurses who have been followed
up repeatedly since 1976.6 The significant
associations of snoring with incident hypertension and cardiovascular disease
found in this study add strong support to a causal role of snoring in adverse
health outcomes.
Snoring is the audible result of upper airway dynamics that underlie
sleep disordered breathing (SDB), including increased sleep-induced compliance
and narrowing of the upper airway, turbulent airflow, and fluctuating pressure
differentials between the atmosphere and the intrathoracic space.7 The severity of SDB can range from inspiratory breaths
with increased resistance requiring greater respiratory effort to the frequently
repeated episodes of partial or complete airway closures characteristic of
sleep apnea syndrome.8 Thus, a person reporting
snoring may lie anywhere on the SDB severity continuum. However, most self-reported
snorers have few detectable breathing pauses and are at the milder end of
the SDB spectrum. This level of SDB is often referred to as simple snoring.8
The public health importance of snoring as a potential source of morbidity
is enormous because its prevalence is so high. Prevalence estimates for habitual
snoring vary according to population characteristics, such as age and body
habitus, but several studies of fairly similar populations in the United States,
Australia, Great Britain, and Poland have indicated that roughly 40% and 20%
of middle-aged men and women, respectively, report habitual snoring.2, 9-11 With
mounting evidence that snoring is a source of morbidity, there is a clear
need to reduce this prevalence. However, the number of people who snore and
the lack of effective therapy make this a daunting task.
Currently, concerned snorers are advised to seek polysomnographic evaluation
for sleep apnea. Snorers found to have frequent apnea and hypopnea events
would be candidates for nasal continuous positive air pressure, an effective
treatment for sleep apnea, which splints open the upper airway to prevent
breathing pauses. This therapy, however, is not appropriate for the large
remainder of individuals with simple snoring, for whom there is little in
the way of effective treatment. Consequently, the most rational strategy to
reduce the prevalence of simple snoring must be risk factor reduction.
Several population-based investigations indicate that common risk factors
for sleep apnea of obesity, middle age, male sex, and smoking are also independent
correlates of self-reported snoring. Identification of risk factors that could
be modified by intervention may hold the best promise of reducing the prevalence
of snoring. Unfortunately, most of the hypothesized risk factors for snoring
cannot be eliminated, such as sex and aging, or are difficult to modify, such
as smoking and obesity.
One potential modifiable risk factor is chronic nasal congestion during
sleep. A biological basis for nasal congestion as a cause of SDB lies in the
importance of nasal breathing to an adequate pressure differential between
the atmosphere and the intrathoracic space.12-13
Nasal congestion leads to breathing with increased resistance and lower flow
velocity, which in turn may cause an increased pressure differential and a
tendency for airway collapse.14
Most previous research has focused on nasal congestion as a predictor
of SDB, rather than of snoring in general. Some, but not all, of these studies
have shown that nasal congestion is related to the frequency and duration
of breathing pauses in patients with sleep apnea.15-17
Also, breathing pauses have been provoked in persons without SDB by experiments
in which nasal congestion is simulated by packing or taping the nose.18-19 Limited analyses secondary to other
study aims from 2 population-based studies have indicated that nasal congestion
is linked to snoring. Stradling and Crosby,20
in a study of 1001 men, found that habitual snorers were significantly more
likely to report nasal congestion. In a previous investigation of the association
of nasal resistance and SDB, we also found evidence for the congestion-snoring
link.21 To date, a study specifically designed
to test the hypothesis that nasal congestion is related to snoring has not
been conducted, to our knowledge.
We used data from the Wisconsin Sleep Cohort Study, an ongoing population-based
prospective study of the natural history of SDB, to investigate the association
of nocturnal nasal congestion with snoring. Data from baseline (n = 4916)
and 5-year follow-up surveys (n = 3446) on a sample of middle-aged men and
women and in-laboratory overnight studies on a subsample (n = 1032) of the
study population provided a unique opportunity to investigate the role of
nocturnal nasal congestion in the occurrence of self-reported habitual snoring.
Also, objective data from polysomnograpy permitted us to assess the role of
nasal congestion across the SDB spectrum, from simple snoring to sleep apnea.
PARTICIPANTS AND METHODS
The study protocol and informed consent procedure were approved by the
Committee for the Protection of Human Subjects, University of Wisconsin School
of Medicine.
SAMPLE
A population-based random sample of men and women aged 30 to 60 years
(n = 6569) was drawn from a sampling frame of employee payroll records of
4 state of Wisconsin agencies. This sample served as the source of participants
for 2 mailed questionnaires, conducted 5 years apart, and for a subsample
that was studied by in-laboratory polysomnography (n = 804). Seventy-five
percent of the target sample completed the first questionnaire (n = 4916),
and of these, 3446 completed the second questionnaire as well. The participants
did not differ from the target sample on characteristics available from the
payroll records, including sex, age, salary, and job classification.
From the sample of baseline survey participants, a weighted probability
sample was selected for extensive overnight studies to be conducted every
4 years. Recruitment is ongoing. To date, 1400 men and women from this sample
have completed an overnight study at least once. The response rate for the
overnight studies has averaged 50% for the first study, 75% for the 4-year
follow-up, and 85% for the 8-year follow-up. We were able to assess potential
bias by comparing participants with the recruitment sample on numerous items
taken from the first questionnaire. The items included lifestyle, sleep problems,
medical history, and demographics. A healthy volunteer bias was seen; the
participants, on average, had attained a higher educational level and salary,
had less hypertension, and reported slightly more insomnia. When necessary,
care is taken in analyses to account for a potential bias due to these factors.
The characteristics of the baseline sample are given in Table 1.
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Table 1. Sample Characteristics at Baseline (N = 4916)
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DATA COLLECTION
Snoring Status
Snoring status was derived from participants' reported snoring frequency
reported on the questionnaire and from the number of apnea and hypopnea episodes
per hour of sleep determined by polysomnography. The question was phrased
as follows: "According to what others have told you, please estimate how often
you snore." Response categories included "never," "rarely," "sometimes, a
few nights per month," "irregular but at least once a week," "several nights
(3-5 nights per week)," "every night or almost every night," and "do not know."
Sleep-disordered breathing was measured by 18-channel polysomnography.
The polysomnography consisted of a standard montage of surface leads to record
analog data on cardiopulmonary function during sleep. Sleep state was monitored
by electroencephalography, electro-oculography, and submental electromyography.
Airflow was detected at the nares by end-tidal carbon dioxide detection (capnograph)
and at the mouth by thermistry (Thermister; Pro-Tec, Henderson, Tenn). Respiratory
effort was measured by chest and abdominal excursions using calibrated inductance
plethysmography (Respitrace; Ambulatory Monitoring, Ardsley, NY). Arterial
oxygenation was recorded by finger pulse oximetry (Ohmeda 3740; Ohmeda, Englewood,
Colo).
The polysomnography records were manually scored using conventional
criteria.22 Each 30-second epoch of the recordings
was scored for sleep stage, presence of an apnea (absence of airflow for 10
seconds or more with either no respiratory effort or opposing chest and abdomen
excursions indicating attempt to breathe against a closed airway), and presence
of a hypopnea (reduction in respiratory effort with a 4% dip in oxygen
saturation). A polysomnographic study of acceptable quality was defined by
adequate sleep and breathing signals throughout the night, at least 4 hours
of objectively measured sleep, and at least 1 period of rapid eye movement
sleep.
The total number of scored apneas and hypopneas, divided by the number
of hours of sleep (apnea-hypopnea index [AHI]) was determined for each participant
as the summary measure of SDB.
Nighttime Nasal Congestion
Nighttime nasal congestion was assessed by questions on its frequency
and cause on the mailed questionnaire and in an interview conducted during
the overnight study. One question asked how often nocturnal nasal congestion,
obstruction, or discharge is experienced. Response categories included "never,"
"rarely," "sometimes," "often" and "always or almost always." A different
set of questions was asked to determine the cause of regular nocturnal nasal
stuffiness, if present. For this, participants were asked (yes or no) if they
experienced nightttime nasal stuffiness regularly. If yes, the causes of the
stuffiness were requested. The causes were grouped into allergy, structural,
or other.
Covariates
Smoking and asthma were assessed by questionnaire and by interview.
Persons who reported that they currently smoked at least 1 pack of cigarettes
per week were coded as current smokers. Asthma was considered present if the
participant reported physician-diagnosed asthma. Standard anthropomorphic
techniques were used to measure weight, height, skin folds, and circumferences
of waist, hips, and neck.
ANALYSIS
Definitions
Habitual snoring was defined as a response to the snoring frequency
question of "several nights per week to every night." Simple snoring was defined
as habitual snoring without frequent apnea or hypopnea events (ie, <5 polysomnographically
determined apnea and hypopnea episodes per hour of sleep, or AHI <5).
Nighttime nasal congestion was used as a categorical variable with all
the response categories ("never," "rarely," "sometimes," "often," and "always
or almost always"). For the longitudinal analysis, severe nasal congestion
was defined as nasal congestion at night always or almost always. Chronic
nasal congestion was severe congestion reported at both baseline and 5-year
follow-up; intermittent congestion was severe congestion at only 1 time point.
A binary variable was used for current smoking (yes, at least 1 pack
per week; no, all others) and for physician-diagnosed asthma (yes, no). Body
habitus was indicated by a continuous variable for body mass index (BMI).
Statistical Procedures
Data were analyzed with SAS procedures for descriptive statistics, contingency
tables, and logistic regression.23 Multiple
logistic regression was used to assess the strength of association of nasal
congestion and snoring. This technique allows multiple regression of conditions
with a binary outcome (eg, habitual snoring present vs habitual snoring not
present). The odds ratio (OR) estimated by this technique expresses how likely
it is that individuals who have the risk factor being investigated (eg, nasal
congestion), relative to those who do not have the risk factor (eg, the reference
category of no nasal congestion), have the outcome of interest (eg, habitual
snoring). Age, sex, BMI, and smoking were added to the regression models as
potential confounding factors or effect modifiers. Statistical significance
for differences between proportions was assessed by  2 tests
and that for logistic regression coefficients by the Wald 2
test. Two-tailed P values of less than .05 indicated
statistical significance.
RESULTS
ANALYSES OF CROSS-SECTIONAL DATA
Adjusted ORs for nasal congestion and habitual snoring estimated by
logistic regression are given in Table 2. The cross-sectional analysis shows a dose-response relationship
between the frequency of nocturnal nasal congestion and habitual snoring,
independent of sex, age, smoking, BMI, and asthma. Persons with severe nasal
congestion (occurring every night or almost every night) compared with those
with no congestion had 3 times the odds of being a habitual snorer (OR, 3.00;
95% confidence interval [CI], 2.2-4.0). Concordant with previous studies of
self-reported snoring, smoking, obesity, age, and male sex were also significantly
related to habitual snoring. Interestingly, asthma was also associated with
snoring. Persons reporting physician-diagnosed asthma, compared with those
without asthma, had 40% greater odds of being a habitual snorer.
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Table 2. Logistic Regression Model of Habitual Snoring (N = 4557)*
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Table 3 shows the results
of more detailed analyses to determine if nasal congestion is associated with
simple snoring. From the total of 1032 participants on whom polysomnography
was performed, those with an AHI of 5 or greater were excluded. The logistic
regression model using this subsample (n = 804) compares simple snorers (ie,
habitual snorers with an AHI <5) with those with no SDB (nonhabitual snorers
and nonsnorers and an AHI <5). The results show a strong association between
nasal congestion and simple snoring (OR, 3.33; 95% CI, 1.79-6.21), with a
dose-response relationship suggested by the increasing OR as the frequency
of nasal congestion increases. Thus, the association between congestion and
self-reported habitual snoring is not explained by those snorers with sleep
apnea.
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Table 3. Logistic Regression Model of Simple Snoring (N = 804)*
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To determine if the risk of habitual snoring with nasal congestion varied
by cause, we used the variable for regular nasal stuffiness at night, with
3 categories: "yes due to allergies," "yes due to other causes" (eg, deviated
septum), and "no regular congestion." There was no difference in the ORs for
congestion due to allergy or congestion due to other causes. Similarly, we
tested an interaction of the nocturnal nasal congestion variable and a variable
for the presence of allergies, but found no evidence for a difference in associations
by allergy status.
ANALYSES OF LONGITUDINAL DATA
The data on nasal congestion and snoring at baseline and follow-up were
first examined to determine the degree to which responses changed over the
5-year interval. The report of habitual snoring appeared to be quite stable
over time. Of those reporting habitual snoring at baseline, fewer than 2%
reported snoring never or rarely at follow-up, while 80% reported habitual
snoring at follow-up. However, there was more change over this period in the
frequency categories for nasal congestion.
Only 39% of those reporting congestion "always or almost always" at
baseline remained in this category at follow-up; 50% reported less frequent
congestion (sometimes, often). Overall, the longitudinal data indicate that
while self-reported snoring status is quite stable, nasal congestion frequency
among those reporting any congestion at baseline changed appreciably.
The changes in congestion frequency over time are not unexpected, as
they are likely to reflect seasonal exposure to allergens or changes in other
exposures. However, the changes may also reflect a lack of validity of the
congestion question as an indicator of a chronic condition. To address this,
we created a variable for chronic nasal congestion. We thought that individuals
who reported severe congestion (always/almost always) at both time points
were most likely to have a chronic congestion condition, while those with
no congestion at both time points were a more specific comparison group of
persons who were free of nocturnal congestion. Table 4 shows the results of the logistic regression model estimating
the association of chronic severe vs no severe congestion and intermittent
severe congestion vs no severe congestion with habitual snoring based on the
longitudinal data. Controlling for age, sex, smoking, BMI, and asthma, the
ORs suggest that individuals with chronic severe nocturnal nasal congestion
have a 3.6-fold greater odds of being a habitual snorer at baseline and that
the odds increase over time, with a 4.9-fold greater odds of being a habitual
snorer at follow-up.
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Table 4. Logistic Regression Model of Chronic Severe Nocturnal Nasal
Congestion and Habitual Snoring at Baseline and 5-Year Follow-up*
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COMMENT
The results of this investigation identify nocturnal nasal congestion
as a risk factor for simple snoring, as well as for habitual snoring (which
includes snorers with sleep apnea). Nocturnal nasal congestion occurring always
or almost always was associated with a 3-fold increase in the likelihood of
habitual snoring for persons with or without sleep apnea, independent of sex,
age, BMI, smoking, and asthma. The ORs for habitual and simple snoring increased
with increasing category of nasal congestion frequency. We did not find that
congestion due to allergies, compared with other causes, was a stronger predictor
of snoring. Most importantly, chronic severe nocturnal nasal congestion (ie,
nocturnal nasal congestion occurring always or almost always at both baseline
and 5-year follow-up) was most strongly related to snoring, and the strength
of the association increased from an OR of 3.60 (95% CI, 2.1-6.3) (to an OR
ratio of 4.9 (95% CI, 2,8-8.8) over time.
We found no evidence that this association was driven by a strong relationship
between nasal congestion and more severe SDB, eg, snorers with 5 or more apnea
and hypopnea episodes per hour of sleep. The equivalent OR for snorers with
and without frank SDB is compatible with a natural history scheme whereby
simple snoring is an early manifestation of SDB: exposure to factors that
cause SDB leads first to episodic upper airway resistance overtly manifested
as snoring. With worsening airway dynamics over time, simple snoring may,
in a significant proportion of people, progress to more severe SDB.24
If snoring is an early marker for progressive SDB, risk factor intervention
that reduces or prevents the onset and progression of simple snoring could
prevent the development of clinically significant SDB. However, in considering
the natural history path of SDB from early stage to severe sleep apnea, it
is important to note that not all significant episodic upper airway resistance
results in snoring. "Silent" breathing events defined by increasing airway
resistance and terminating in brief arousals from sleep, termed respiratory effort related arousals, may lead to upper airway resistance
syndrome (UARS), characterized by the frequent occurrence of these events,
in combination with resultant daytime sleepiness.3, 25
As part of the SDB spectrum, it is likely that respiratory effort–related
arousals and UARS are associated with the same risk factors as is snoring.
Unfortunately, very little is known about the epidemiology of UARS, and without
having the necessary measure of esophageal pressure to identify UARS events
in our participants, we are not able to address this hypothesis.
To our knowledge, this is the only study in which risk factors for simple
snoring have been identified. Similarly, the role of chronic nasal nocturnal
congestion over several years has not been examined as a risk factor for snoring.
Thus, we are not able to compare these associations with existing reports.
However findings from the few studies of other risk factors, eg, BMI, smoking,
age, sex, and general snoring, are consistent with our results, providing
some confidence in the validity of our methodology.2, 6, 10-11,26
It is possible that our findings are attributable to study limitations,
including sample bias or incomplete control for confounding factors. However,
it is difficult to explain how limitations in our study could account for
the strong, persistent associations of congestion and snoring that we found.
Sample bias would require the overrepresentation of habitual snorers with
nasal congestion. However, the longitudinal analyses yielded even stronger
findings than those from cross-sectional analyses. Participation bias can
cause spurious findings in cross-sectional analyses, but this is less of a
concern in longitudinal analyses. For this type of bias to occur, participation
would have to be differentially greater in habitual snorers with nasal congestion
who were also destined to have nasal congestion 4 years into the future. Finding
an even stronger relationship with the longitudinal data further reduces this
concern with participation bias.
We were able to account for several potential confounding factors, but
it is possible that an unknown factor related to both snoring and nasal congestion
is responsible for part or all of the associations reported herein. However,
such a factor would have to be extremely influential to account for the relatively
high ORs found, particularly in the longitudinal analyses.
Misclassification of nocturnal nasal congestion and of snoring is possible,
as both of these measures relied on self-report. Although there have been
a few very small validation studies that show self-reported snoring to be
of variable accuracy,27 there have been no
studies on reported nasal congestion, to our knowledge. Our classification
of the cause of congestion is subject to variation in participants' knowledge
as well as to the severity of the congestion. We had data on allergy medication
use, but the interpretation of findings using this variable is limited: medication
may reduce congestion, but it is also likely to be used by the persons with
the most severe congestion. Misclassification of nasal congestion or snoring,
if random, would result in reducing the magnitude of true ORs. However, if
misclassification was differential to one of the exposure or outcome variables
with respect to the other, then bias could result. Such a situation would
arise if there were a tendency of individuals who snore to exaggerate any
other nocturnal condition, including nocturnal nasal congestion. Unfortunately,
we were not able to address this possible bias.
The particular strengths of this study are the large, population-based
sample, longitudinal data on congestion and snoring over a 5-year interval,
and the ability to identify simple snorers using data from in-laboratory polysomnography.
Prevalences of common conditions such as smoking, seasonal allergic rhinitis,
hypertension, and asthma indicate that our sample is representative of the
general middle-aged population. However, our sample lacks racial heterogeneity,
and thus the findings may not apply to races other than white.
Recent population-based studies indicate that simple snoring, in addition
to snoring accompanied by episodes of apnea and hypopnea, is linked to significant
morbidity. If associations with morbidity are causal, the highly prevalent
condition of habitual snoring could account for a significant proportion of
adverse health outcomes, including pathologic sleepiness, accidents, and cardiovascular
disease. Furthermore, habitual snoring can impair the sleep of bed partners
and cause interpersonal stress. We found that regular nocturnal nasal congestion,
particularly that which is chronic over several years, is a strong risk factor
for snoring with and without frank SDB. This relationship may be particularly
important because nasal congestion can be controlled pharmacologically. If
this association is causal, the substantial magnitude of the OR, in conjunction
with the high prevalence of nasal congestion, suggests that intervention may
reduce the prevalence of snoring significantly. At present, there are no firm
data from a randomized controlled clinical trial testing the efficacy of pharmacological
intervention to reduce snoring. The findings of the present investigation
underscore the importance of continuing to investigate this modifiable risk
factor for snoring.
AUTHOR INFORMATION
Accepted for publication November 8, 2000.
This study was supported in part by grants R01HL62252 and RR03186 from
the National Institutes of Health, Bethesda, Md, and a grant from Integrated
Therapeutics Group Inc, Kenilworth, NJ.
We are grateful for the technical expertise and contributions of Linda
Evans, Katherine Pluff, Katherine Kennison, Leah Steinberg, Anthony Jacques,
Steven Weber, PhD, James Skatrud, MD, Jerome Dempsey, PhD, and Safwan Badr,
MD.
Corresponding author and reprints: Terry Young, PhD, 502 N Walnut
St, Madison, WI 53705.
From the Departments of Preventive Medicine (Dr Young and Ms Finn)
and Biostatistics and Informatics (Dr Palta), University of Wisconsin at Madison.
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The role of the nose in the pathogenesis of obstructive sleep apnoea and snoring
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Snoring Is Not Relieved by Nasal Surgery Despite Improvement in Nasal Resistance
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Patient- and Bed Partner-Reported Symptoms, Smoking, and Nasal Resistance in Sleep-Disordered Breathing
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The Influence of Active and Passive Smoking on Habitual Snoring
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Am. J. Respir. Crit. Care Med. 2004;170:799-803.
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Risk Factors and Natural History of Habitual Snoring
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Intranasal corticosteroid therapy for obstructive sleep apnoea in patients with co-existing rhinitis
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Thorax 2004;59:50-55.
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The Nose and Sleep-Disordered Breathing: What We Know and What We Do Not Know
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Chronic Nasal Congestion at Night is a Risk Factor for Snoring in a Population-Based Cohort Study
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Epidemiology of Obstructive Sleep Apnea: A Population Health Perspective
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