Background Exposure to secondhand smoke (SHS) is a serious public health threat and represents a preventable cause of morbidity among children. Sleep bruxism is characterised by teeth grinding or clenching movements during sleep and may begin in adulthood as well as in childhood.
Objectives To investigate the association between SHS exposure and sleep bruxism in children.
Methods Sleep bruxism was investigated in 498 children (mean age: 9.2±1.9). Family members were interviewed and asked whether they smoked in the presence of their children. Children were classified according to their exposure to SHS into heavily, moderately, lightly and occasionally exposed. Children with sleep bruxism and exposed to SHS were randomly divided into two groups: children in group 1 were not exposed to SHS for 6 months, whereas children in group 2 were.
Results Thirty-one per cent of the children under investigation suffered from bruxism. Among them, 116 children (76%) were exposed to SHS. Exposed children showed a higher risk of sleep bruxism (p<0.05). After 6 months, sleep bruxism was found in 38% and in 90% of children, in the first and in the second group, respectively, this difference was statistically significant (p<0.05). In group 1, changes were statistically significant in those who were heavily and moderately exposed (p<0.05) but not in those lightly and occasionally exposed (p>0.05). In group 2, changes were not statistically significant (p>0.05).
Conclusion The findings showed that high and moderate exposure to SHS is associated with sleep bruxism in children.
- secondhand smoke
- smoking-caused diseases
- primary healthcare
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Exposure to secondhand smoke (SHS) represents a serious public health threat, remaining a preventable cause of morbidity among children. Adverse health effects have been found in children exposed to SHS, including increased risk of pneumonia, bronchitis, respiratory illness, wheezing, middle ear effusions, otitis media and cardiovascular damage.1–3 Furthermore, in adulthood, SHS increases the risk of lung cancer,2 breast cancer,4 renal cell carcinoma5 and heart diseases.6
Sleep bruxism is characterised by teeth grinding or clenching movements during sleep.7 ,8 Its aetiology has been defined as multifactorial since it is mainly regulated centrally and is influenced by local variables.9 Sleep bruxism may begin in adulthood as well as in childhood and either be confined to a certain time of life or continue throughout the individual's life.7 The following factors have been associated with bruxism: disorders in the dopaminergic system, stress, sleep disturbances, smoking and alcohol consumption as well as age, gender and genetic factors.10 In children, an association between sleep bruxism and oral habits such as pacifier sucking, nail or lip biting has also been highlighted.11
Although the underlying mechanism between smoking and sleep bruxism is not known, there are several possibilities. Nicotine is known to induce acetylcholine and glutamate synaptic transmission and enhance dopamine release. In smokers, nicotine accumulates in the body during the time spent awake, decreasing gradually during sleep. Via an action on acetylcholine receptors, nicotine can enhance glutamatergic synaptic transmission and increase dopamine release. It follows that higher levels of smoking, leading to increased levels of nicotine and dopamine release, could thus be related to increased oromotor activity.12 In addition to this, smoking has been found to have behavioural and cognitive effects, it being associated both with difficulty initiating and maintaining sleep, increasing arousals and motor activity during sleep.13–15
In literature, it is reported that the prevalence and severity of bruxism is greater in smokers than in non-smokers and several studies have shown an association between active smoking and sleep bruxism.10 ,16–20 In spite of this, no previous study has investigated the influence of SHS exposure on bruxism and whether there is an association between these two factors.
The goal of this study was to investigate the association between SHS exposure and sleep bruxism in children.
The parents of 1147 children were asked to participate in a school project related to the risks of SHS exposure; all children were from two elementary schools in Naples, Italy. The project lasted 5 months and included one weekly 2 h lesson about the risk of SHS, each lesson was presented by a psychologist and a doctor and was attended by children together with their parents, out of the regular school timetable. The project was conducted to educate children about the risk of SHS and help parents to either reduce or give up smoking in the presence of their children. The parents of 379 children refused to participate in the project and the main reasons given were either that they were not smokers or that they had no time to attend extra lessons. Therefore, the project involved 768 children, aged between 8 and 11 years (mean age 9.8±1.3), 337 were males and 431 were females. The sample was randomly divided into 25 classes of about 30 families each.
The present parallel, randomised controlled trial was conducted prior to the beginning of the above-mentioned project and included 498 white children of 768, 222 were males and 276 were females with a mean age of 9.2±1.9. Seven children were excluded from the study because they had cleft lip and palate, 18 because they had some forms of disability, 47 because they had respiratory disorders and 171 because they were undergoing orthodontic and/or orthopaedic treatment. The parents of 27 children refused to participate in this study. All parents provided written informed consent with guarantees of confidentiality. The study was approved by the Ethics Committee of the Second University of Naples.
Data were collected in the school setting by self-reported questionnaire and personal interview. During the interview, the interviewer reviewed the answers on the self-reported questionnaire for completeness and internal consistency. The parents of the children under investigation were interviewed and asked if any member of the family was a smoker and smoked in the presence of the child. Children were asked whether they had any smoking habit, and none of them reported having ever smoked before. Exposure to SHS was elicited by response to some questions, such as: “ How many people in the family are smokers?” “How many cigarettes a day do they smoke in the presence of the children?” Furthermore, parents were also asked whether their children had any oral habit that could be related to bruxism such as nail biting, lip biting, finger or pacifier sucking.
Children were classified according to the amount of exposure to SHS into ‘heavily exposed’, if their family member/s smoked >10 cigarettes a day in their presence; ‘moderately exposed’, if their family member/s smoked between 6 and 10 cigarettes a day in their presence; ‘lightly exposed’, if their family member/s smoked between 1 and 5 cigarettes a day in their presence, and ‘occasionally exposed’, if their family member/s smoked in their presence not on daily basis.16 ,21 We considered the total amount of cigarettes smoked in the presence of the child regardless whether smoked by one single parent or by several family members.
The primary outcome of the study was to detect sleep bruxism in children according to criteria proposed by the American Sleep Disorders Association,22 that is, tooth grinding reported by parents, in combination with at least one of the following signs: jaw muscle fatigue, tenderness or pain upon awakening, observation of tooth wear. Wear of anterior teeth on incisal border was considered; when wear of the occlusal posterior teeth was present, individuals were considered bruxers only if open bite was also present.
Dental examinations were carried out by a licensed dentist, in the school setting, by using a mirror and an ordinary examination light in order to observe any tooth wear. The dentist was kept blind to the interview data regarding children exposure to SHS.
The children with sleep bruxism and exposed to SHS were randomly divided into two groups. The smoking members of the families in group 1 were asked not to smoke in the presence of the child for a period of 6 months, while those in group 2 were asked not to change their smoking habits. Parents were told prior to study enrolment that they would not be required to quit smoking as part of study participation, rather they would be asked to reduce children SHS exposure. Parents in both groups were told not to change their children's sleeping habits.
A stratified randomisation procedure was used to allocate patients into the two groups. The strata formed were based on the degree of severity of SHS exposure (occasional, low, moderate and heavy exposure). With randomisation within each stratum, we ensured that the distributions of children exposed to SHS were balanced within the two groups. Computer-generated random numbers were used to assign patients to the two treatment arms within each stratum. The allocation sequence was concealed from the researcher enrolling and assessing participants in sequentially numbered, opaque and sealed envelopes.
After 6 months, data were collected again according to the same criteria mentioned above in order to find out the amount of children in the two groups still bruxing during the night. Furthermore, parents were asked if over 6 months their children had given up any oral habit they had at the beginning of the study. These children were excluded from the study in order to eliminate any confounding variable that might be associated to a reduced bruxing activity.
We estimated a sample size of 51 patients for each group, based on the following assumptions: (1) one primary comparison (sleep bruxism rate with SHS exposure vs sleep bruxism rate without SHS exposure), (2) a two-sided χ2 test of statistical significance, (3) a probability of type I error associated with the two-sided test of 0.05 and (4) a probability of type II error associated with the test of 0.2 (ie, the power of the test is 80%).
The Pearson χ2 test was used to evaluate the difference in prevalences. The RR was evaluated by logistic regression. All analyses were conducted by using Statgraphics Centurion XV.II (Warrenton, Virginia, USA). A p value of <0.05 was considered statistically significant.
Sleep bruxism was found in 153 of 498 children (31%). As many as 116 children (76%), out of those with sleep bruxism, were exposed to SHS. Sixty-seven were heavily exposed, 21 were moderately exposed, 15 were lightly exposed and 13 were occasionally exposed. Children exposed to SHS showed a higher risk of sleep bruxism (p<0.05, RR 3.11, 95% CI 2.24 to 4.32) (table 1). Parents reported that no child had any pacifier-sucking habit, 12 children had finger-sucking habit and 41 had either lip- or nail-biting habit. The 116 bruxing children exposed to SHS were randomly divided into two groups of 58 children each.
After 6 months, parents reported that three children were no longer sucking their finger and six children had given up biting their nails or their lip. These children were excluded from the two groups. Therefore, the first group included 55 children and the second group included 52 children.
In the first group, after 6 months without exposure to SHS, the number of children with bruxism decreased and sleep bruxism was detected in 21 children of 55 (38%). Among these, six children had been heavily exposed, four had been moderately exposed, five had been lightly exposed and six had been occasionally exposed. These changes were statistically significant for those who had been heavily and moderately exposed but not for those who had been lightly and occasionally exposed (p<0.05, RR 4.50, 95% CI 2.17 to 9.35; p<0.05, RR 2.22, 95% CI 1.01 to 4.91; p>0.05, RR 1.23, 95% CI 0.72 to 2.10; p>0.05, RR 0.97, 95% CI 0.61 to 1.55, respectively). The greatest risk difference was found in the heavily exposed group (risk difference (RD) RD 45, 95% CI 41.63 to 47.87) (table 2).
In the second group, after 6 months, sleep bruxism was detected in 46 children of 52 (90%). There were no statistically significant changes in the amount of children with sleep bruxism in those heavily, moderately, lightly and occasionally exposed (table 3).
After 6 months, sleep bruxism was detected in 38% of children in group 1 and in 90% of children in group 2, and this difference was statistically significant (p<0.05, RR 2.19, 95% CI 1.55 to 3.09).
An occurrence of 31% of bruxism in children from 8 to 11 years emerged in our study. Similar occurrence (38%) was found in the paper by Cheifetz and colleagues23 whose children's mean age was 8.1. Other papers presented a different occurrence but included younger age groups; therefore, the comparison is difficult.7 ,11
The results of our study showed that exposure to SHS was associated with sleep bruxism in children. Although our findings agree with previous studies performed on active smokers,10 ,16–20 most of these studies just show the association between smoking and sleep bruxism without analysing different categories of smokers (heavy, moderate, light and occasional).10 ,17–20 Only Rintakoski and colleagues classified smokers as heavy smokers (at least 10 cigarettes daily), light smokers (<10 cigarettes daily), former smokers and never-smokers. They investigated the possible effect of cumulative tobacco use on bruxism in a sample of young adults and found that both weekly and rarely reported bruxism was significantly associated with smoking, and heavy smokers were more than twice as likely to be weekly bruxers compared with never-smokers.16 A follow-up study of 30–50-year-old employees of the Finnish Broadcasting Company highlighted that bruxism was significantly more prevalent among smokers, regardless of age, marital status and gender.17 Epidemiological reports also showed some degree of association between tobacco use and bruxism.10 ,18 A study performed on 18 smokers and 165 non-smokers found that smokers were about three times more likely to experience symptoms of bruxism.19 Lavigne and colleagues20 reported that sleep bruxism prevalence was significantly higher in smokers rather than in non-smokers and that there were five times as many grinding episodes in smokers than in non-smokers.
After 6 months without being exposed to SHS, our data showed a statistically significant decrease of the number of children with sleep bruxism and only 38% still bruxed during the night. Children being heavily exposed showed the highest risk of sleep bruxism. Moderately exposed children also showed a statistically significant risk of sleep bruxism, whereas lightly and occasionally exposed children did not show any statistically significant risk of sleep bruxism. Heavily exposed children were more than twice as likely to be sleep bruxers compared with moderately exposed children and more than three times as likely to be sleep bruxers compared with lightly exposed children. When parents smoke in the presence of their child, smoke permeates the environment and is inhaled by the child. Therefore, nicotine is likely to increase dopamine release and oromotor activity in active as well as in passive smokers.
Based on the results, it is important for parents to be educated about the risks of SHS and its association with sleep bruxism. For this reason, as part of the school project, once the present study was completed, parents in both groups were given psychological support to either reduce or give up smoking in the presence of their children. Furthermore, parents and children in both groups were educated about the risks of SHS. Although parents were told that they were not expected to give up smoking, a limitation of the present study was the determination of fidelity to the recommendation of decreasing children's SHS exposure. Further studies including indoor air quality measurement would be helpful to confirm our results.
SHS exposure is a significant problem: worldwide, 40% of children are exposed to SHS.24 The highest proportions exposed are estimated in Europe and in the western Pacific.24 SHS was estimated to have caused 603 000 premature deaths in 2004.24 The largest number of estimated deaths attributable to SHS exposure was caused by ischaemic heart disease in adults and lower respiratory infections in children.24
The reduction of exposure to SHS in children may be beneficial in terms of reducing sleep bruxism, respiratory illness and cardiovascular damage associated with SHS1–3 and in reducing the initiation of smoking by children due to reduced opportunities to observe smoking modelled by parents.
What this paper adds
Although many studies highlight the association between active smoking and sleep bruxism in adults, no study has ever investigated the association between secondhand smoke and sleep bruxism in children.
This is the first paper to consider the effects of secondhand smoke chemicals on patterns of bruxism in children. Our results show that being both heavily and moderately exposed to secondhand smoke increases the risk of sleep bruxism. This provides additional support for the importance of reducing children's secondhand smoke exposure.
See Editorial, P 383
Competing interests None.
Ethics approval Ethics approval was provided by Second University of Naples.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement The proposed research includes data from 498 children and their families recruited from a school project related to the risks of secondhand smoke exposure. Two elementary schools in Naples, Italy, were considered. Most data were published. However, because of the relatively restricted area from which we recruited the children and because of their age, although further data will be stripped of identifiers prior to release for sharing, we believe that there remains the possibility of deductive disclosure of subjects. We think that it is important to protect minors' privacy; therefore, we will make the data and associated documentation available upon request only under a data-sharing agreement that provides for (1) a commitment to using the data only for research purposes and not to identify any individual participant; (2) a commitment to securing the data using appropriate computer technology and (3) a commitment to destroying or returning the data after analyses are completed.
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