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.