4 | DISCUSSION
4.1 | Social demography
To our knowledge, this is one of the largest epidemiologic research
studies carried out in Sichuan Province to examine the HS prevalence
among children aged 2–14 years. We found a 30.38% prevalence of HS in
this age group. This HS prevalence is higher than the 10.5–27.39%
previously reported in other Chinese studies2,8,9. A
possible reason for this inconsistency might be heterogeneity between
studies in participant age and area of residence. We speculate that
another principal reason might be that our questionnaire was completed
voluntarily. Guardians of children who snore habitually and have related
symptoms may have been more likely to participate and complete the
questionnaire.
Herein, there was an increased prevalence of HS in younger children. The
prevalence rate in children under age 7 years was 51.84%, and 26.6% in
children 7 years and older. Two studies using large samples of children,
by Li et al.2 and Anuntaseree et
al.10, also showed interesting age differences in HS
prevalence: a significant initial increase from ages 5–6 to 7 years and
then a gradual decline. HS prevalence tended to decrease with age
because of an increase in pharyngeal cross-sectional area with growth.
This is consistent with the fact that lymphoid tissues in the larynx
(i.e., adenoids, tonsils) gradually degenerate after age 7
years10,12.
Co-sleeping is also common among children under 7 years, which may have
resulted in higher rates of reported snoring by their parents compared
with the parents of older children.
We found a higher prevalence of HS in boys than in girls; however, this
difference was not significant in our sample of 1524 children. In
adults, HS is more common in men, for which the influence of sex
hormones on respiratory control and/or body fat distribution has been
suggested to play a crucial role. Clearly, these factors would be much
less prominent in prepubertal children13. Papaioannou
and colleagues have also reported that growing adenotonsillar tissue
narrows the upper airway during early life, and adenotonsillar
hypertrophy has been reported as a major determinant of OSA in children
but not in adolescents14. Lumeng and Chervin have
suggested that studies showing sex differences often include children
over age 13 years, so there may be a potential mediating effect of
puberty-related hormonal changes on the higher SDB prevalence in
boys15.
Obesity has long been thought to be an important cause of snoring, but
in our study, we did not find any significant difference between BMI
among the three snoring groups or between the HS group and other groups.
Two potential reasons for this result may be: (1) Obesity-related
anatomic risk factors, other than BMI, including enlargement of
parapharyngeal fat pads, lateral pharyngeal walls, the tongue, and total
upper airway soft tissue16; (2) Some studies have
shown that waist circumference (abdominal and hip fat), not BMI, are the
most important causes of snoring in children17,18.
Ours was an epidemiological survey study for which BMI was calculated
based on parents’ answers (height and weight values), and we were unable
to measure abdominal and hip fat. Therefore, it is possible that BMI is
not particularly reasonable for assessing risk for HS.
We found that the HS group had a higher proportion of children whose
mother had a college-level or more education. In China, it is often the
case that mothers are more focused on their children’s growth and living
habits compared with fathers. We speculate that mothers with a higher
education had more access to information about HS-related diagnoses and
symptoms and may have been more concerned about the impact of HS on
their children’s cognition and behavior.
In our survey, 77 mothers had pregnancy complications, including
diabetes, hypertension, and hypothyroidism. An interesting finding was
that the prevalence of HS was significantly lower in children born to
mothers with three or more diseases during pregnancy. The mechanism of
this cannot be explained at present.
Breastfeeding duration was significantly shorter within the HS group
compared with the other groups. A meta-analysis by Sun et
al.19 indicated that breastfeeding was associated with
reduced risk of HS in children. There are two potential explanations
underlying an impact of breastfeeding on HS risk. First, breastfeeding
has a beneficial effect on mandibular development. Oral cavity features,
such as high palates, retruded chin, and narrow dental arches are
additional risk factors for snoring in children which may be partly
prevented by breastfeeding. Second, breast milk may provide
immunoglobulins that may help prevent viral respiratory infections and
thus reduce the chronic upper airway inflammation and adenotonsillar
hypertrophy which facilitate snoring20.
Family history of HS was another strong risk factor for childhood HS. Li
et al. found that having one habitually snoring parent increased the
child’s HS risk by nearly 3.4-fold13. Genetic factors
contribute to craniofacial structure, body composition, and
neuromuscular control of the upper airway and interact to produce a
phenotype21,22. A potential association has been
suggested between the presence of a child’s tonsillar hypertrophy and
the presence of pharyngeal lymphoid tissue hypertrophy in their siblings
and parents21,23.
Numerous disorders have been associated with HS, including upper
respiratory tract infection (asthma, AR, sinusitis, tonsillitis, and
pneumonia/bronchitis) 12,24. These may narrow the
upper airway, causing inflammation that increases flow resistance and
hence snoring propensity. Inflammatory mediators including histamine,
CysLTs, IL 1β, and IL-4, found in high levels in AR, also worsen sleep
quality in those with OSA. Montelukast sodium and mometasone furoate
have obvious anti-inflammatory effects, which has indirectly confirmed
upper respiratory tract infection as an important cause of HS. Previous
studies have reported a positive association between snoring and asthma.
Herein, we could not detect a significant association between asthma and
HS prevalence, likely due to the small number of positive cases.
In relation to the domestic environment, passive smoking was identified
as a major risk factor for HS, consistent with other studies This was
because we assert that maternal smoking during pregnancy, maternal
exposure to secondhand smoke during pregnancy, and child exposure to
secondhand smoke all result in child smoke exposure. Parent-reported
smoking, particularly maternal smoking, has been associated with
increased child snoring, and nighttime respiratory symptoms are
exacerbated by such exposure12,25. Multivariate
analyses by Subramanyam et al. show that children aged 3–18 years with
severe OSA and tobacco smoke exposure have a 1.48 increased odds of
developing OAHI than do those unexposed to tobacco
smoke26. Studies by Urschitz et
al.12 and Zhu27,28 have shown a
positive association between household smoking and incidence of
sleep-related hypoxia and HS, respectively. Cigarette smoke exposes the
nasal and respiratory mucosa to large amounts of endotoxin, resulting in
a potent inflammatory reaction29. It is likely that
cessation of secondhand smoke exposure may also reduce oropharyngeal
mucosal inflammation. Cigarette smoke causes ciliary dysfunction and
proliferation of goblet cells with increased mucus production, in
addition to mucosal inflammation30. Thus, inflammatory
reactions and mucus production lead to respiratory tract narrowing and
HS.
In conclusion, our epidemiological investigation shows that the
prevalence of HS is higher in preschool children. Family history of
snoring, having parents with less education, passive smoking, upper
respiratory tract inflammation, and shorter breastfeeding durations are
important HS risk factors.