International Journal of Pediatric Otorhinolaryngology 78 (2014) 4649

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International Journal of Pediatric Otorhinolaryngology

journal homepage: www.elsevier.com/locate/ijporl

Dose passive smoking induce sensorineural hearing loss in children?

Hossam Sanyelbhaa Talaat a,*, Mohamed Akram Metwaly b,1, Ahmed Hafez Khafagy c,2, Hatem Ragaa Abdelraouf d,3
a

Audiology Unit, ENT Department, Menouya University, Egypt ENT Department, Menouya University, Shebien Elkoom, Egypt c ENT Department, Ain Shams University Hospital, Cairo, Egypt d ENT Department, National Research Center, Cairo, Egypt
b

A R T I C L E I N F O

A B S T R A C T

Article history: Received 10 August 2013 Received in revised form 19 October 2013 Accepted 21 October 2013 Available online 30 October 2013 Keywords: Second-hand smoke Environmental tobacco smoke Minimal sensorineural hearing loss Audiometry

Objectives: Smoking plays major role in development of vascular and respiratory serious diseases. It has been reported that negative smoker children are prone for conductive hearing impairment due to repeated attacks of Eustachian tube dysfunction and middle ear effusion. This study aims to identify negative smoking as potential risk factor for development of sensorineural hearing loss. Study: This study was done between January 2010 and November 2012. 411 children aged 5-11 years (8.2 1.5) participated in this study; they were children attending the Ear, Nose, and Throat clinic of a tertiary care hospital and their siblings. The inclusion criteria were: (i) normal speech and language, (ii) absence of any disease or condition that may cause sensorineural hearing loss, and (iii) normal middle ear function on the day of hearing assessment. They were divided into three groups according to the exposure to second-hand smoke at home; group of no exposure whereas no smoker in the family (131 children), group of mild exposure whereas the father was the only smoking parent and smoking was prohibited at home (155 children), and group of heavy exposure, whereas the mother was smoking, or the father was freely smoking at home and in the presence of his children (125 children). Audiological evaluation in the form of pure tone and speech audiometry and immitancemetry was done for the study group. Results: Audiological evaluation revealed that the prevalence of hearing loss was 3.8%, 4.5% and 12% in the no exposure, mild exposure, and heavy exposure groups, respectively. Signicant difference was only detected between the high exposure group and the other two groups. All children had minimal sensorineural hearing loss, i.e. threshold of frequencies showing hearing loss was 20 or 25 dB HL. The risk ratios (95% condence interval) for hearing loss in the study subgroups were 1.18 (0.38, 3.64) for mild exposure group (p > 0.05), 3.14 (1.18, 8.3) for heavy exposure group (p < 0.05). Conclusions: Passive smoking in childhood correlates with sensorineural hearing loss, and it is an important risk factor for development of minimal hearing loss. Strict prevention of children exposure to second-hand smoke should be encouraged by every mean. 2013 Elsevier Ireland Ltd. All rights reserved.

1. Introduction and rationale Cigarette smoking has become a common tendency worldwide; in 2003, tobacco was consumed by approximately 1.3 billion of the worlds population. It is predicted that 1.51.9 billion people will be smokers in 2025 [1]. Smoking plays major role in development of serious vascular and respiratory diseases. Many studies conrmed the relation between hearing loss and smoking [2].

* Corresponding author at: ENT Department, Hadiclinic Hospital, Elgabriya, P.O. box 44630, Hawally 32061, Kuwait. Tel.: +20 965 66753572. 1 Tel.: +20 965 97668805. 2 Tel.: +20 965 97215597. 3 Tel.: +20 965 97692411. 0165-5876/$ see front matter 2013 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijporl.2013.10.016

Moreover, it was reported that smoking accelerates age related [3] and noise induced hearing loss [4]. The hazards of smoking are not limited to the smokers; it extends to the surrounding people especially for children and infants. Passive smoking (also called second-hand smoke exposure or environmental tobacco smoke exposure) became a profound public health problem, with more than half of children in the United States exposed [5]. Passive smoking has been associated with lung cancer, ischemic heart disease, sudden infant death syndrome, asthma in children and adults, severe headache, and hearing loss [6]. There is mounting evidence that passive smoking is a risk factor of hearing loss; in a cohort of infants, exposure to cigarette smoke was associated with a 4.9 times increase in the prevalence of hearing decits [7]. The children of smoking parents are more prone to develop recurrent [8] or persistent [9] otitis media with

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effusion. It was noticed that hearing loss was more prevalent when the mother was the smoking parent, because the mother is more likely to spend time with the child and, if she smokes, the child is more likely to be exposed to the tobacco smoke [10]. Sensorineural hearing loss in smokers and passive smokers was reported in many studies in adults and teenagers [11,12]. This study aims to test the prevalence of sensorineural hearing loss in children experiencing passive smoking. 2. Materials and methods 2.1. Subjects This study was conducted in a tertiary referral center, between January 2010 and November 2012 in Hadiclinic Hospital, Kuwait. The study group included 411 children (188 males, 223 females), with age range 5-11 years (8.2 1.5). They were children of 290 families attending the ENT clinic; only 89 of these families (131 children) had non smoking parents. Informed consent was obtained from the parents of the children participating in the study, and the study was approved by the Ethics Committee at Hadiclinic Hospital. 2.2. Methods

determine the presence or absence of hearing loss the hearing threshold of all the frequencies 250 through 8000 Hz were considered, if all the frequencies showed threshold 15 dB HL then normal hearing was reported. If any frequency had hearing threshold greater than 15 then we would move to the next step, calculating the degree of the hearing loss. The pure tone average only for frequencies 500, 1000 and 2000 was calculated, if it was 25 dB HL this was considered minimal hearing loss. Other degrees of hearing loss such as mild, moderate or severe would have been considered if the average was 26 dB HL or more [14]. Low frequency hearing loss was considered if the affected frequencies were 2 kHz. High frequency hearing loss was considered if the affected frequencies were 3 kHz [11]. 3. Results 3.1. Demographic distribution Table 1 shows the demographic distribution of the study group. One way ANOVA and Chi square test were done, they showed no statistical signicant difference as regards age or gender distribution (p > 0.05). 3.2. Audiological assessment

The entire study group was subjected to detailed history of any condition causing hearing loss, e.g. ototoxic drug intake, family history of hearing loss, head trauma, etc.; otoscopy; immittancemetry; tympanometry and acoustic reex testing. Pure tone (air and bone conduction) and speech audiometry, speech reception threshold (SRT) and word discrimination scores (WDS) were done using Madsen, Orbiter 922 ver.2 audiometer. Hearing testing was undertaken inside a sound treated booth, with the test environment meeting the specications detailed in Maximum Permissible Ambient Noise Levels for Audiometric Test Rooms (ANSI S3.11999) [13]. Smoking history was ascertained by self-report obtained from the parents. The inclusion criteria for this study were: (i) normal speech and language development, (ii) absence of any disease or condition that may cause sensorineural hearing loss, and (iii) normal otoscopic examination and middle ear function on the day of hearing assessment. All the parents of the families participating in the current study replied to a questionnaire concerned with the smoking habits in the family (if any). The questionnaire questions were concerned with identifying the following: (1) awareness of the parents to the hazards of smoking and passive smoking especially on children. (2) Ascertaining parental tobacco consumption, smoking by household members other than parents, e.g. by visitors to the house or child care providers. (3) Does the parents permit smoking in the home in the presence or absence of the children? According to the data obtained by the smoking questionnaire the children in the study group were divided into three groups according to the exposure to second-hand smoke at home: (1) Group of no exposure whereas no smoker in the family (131 children, 89 families), (2) Group of mild exposure whereas the father was the only smoking parent and smoking was prohibited at home, and in the presence of the children (155 children, 120 families), and (3) Group of heavy exposure whereas the mother was smoking, or the father was freely smoking at home or in the presence of his children (125 children, 81 families). Hearing loss was identied when pure-tone threshold in any of the tested frequencies was greater than 15 dB hearing level (HL) in the worse ear. The degree of hearing loss was determined according to the pure tone average of 500, 1000 and 2000 Hz. Subjects with hearing loss and pure tone average 25 were considered minimal hearing loss. In other words in order to

According to the inclusion criteria of the present study, the entire study had normal middle ear functions. This was conrmed by the normal otoscopic testing, type (A) tympanogram and intact acoustic reexes in the entire study group. No air bone gap was detected in any subjects in this study. Table 2 shows the mean and SD of the air conduction pure tone thresholds, SRT and WDS of both the right and left ears in the study group (822 ears). One way ANOVA test revealed no statistical signicant difference as regard hearing threshold in all of the frequencies (p > 0.05). Table 3 shows demographic and audiological features of hearing loss in the different study groups. All of them had minimal hearing loss. Statistical analysis showed insignicant differences in age and gender distribution between children with hearing loss and those with normal hearing, only signicant difference was reported in the prevalence of hearing loss in the high exposure group compared with the other 2 groups. 3.3. Risk ratios The risk ratios (95% condence interval) for hearing loss in the study subgroups were 1.18 (0.38, 3.64) for mild exposure group (p > 0.05), 3.14 (1.18, 8.3) for heavy exposure group (p < 0.05). 4. Discussion Many studies reported a correlation between passive smoking and hearing loss in infants, children, adolescents and adults [7,10,12]. Several possible mechanisms may account for the relationship between smoking and sensorineural hearing loss;

Table 1 Demographic distribution of the study group. No exposure No. Age (years), mean SD Females (131/411) 31.9% 8.2 1.5 (74/131) 56.5% Mild exposure (155/411) 37.7% 8.2 1.4 (83/155) 53.5% Heavy exposure (125/411) 30.4% 8.1 1.5 (66/125) 52.8%

No., number and percent of children in each subgroup.

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Table 2 Mean and SD of the air conduction pure tone threshold, SRT and WDS of both the right and left ears of the study group. Freq. (Hz) No exposure Mild exposure Heavy exposure 250 8.3 5.5 8.5 5.8 8.2 5.7 500 7.9 5.1 8.5 5.2 8 5.9 1000 7.6 5.2 7.3 5.2 7.6 5.5 2000 7.6 4.8 7.4 4.8 7.5 5.2 3000 8.3 4.8 8.1 5.1 8.1 4.6 4000 7.3 4.6 7.6 4.8 8.4 5.2 6000 7.2 4.9 8.1 5.1 8.3 5.1 8000 7.3 5.1 8.2 5.1 8.4 5.4 SRT 8 3.1 8.2 3.6 8.2 3.3 WDS 96.3 3.3 95 3.9 95.3 3.9

nicotine has direct ototoxic effect on the hair cells and induces vasospasm and arteriosclerosis in the cochlear blood vessels [15]. It has also been suggested that the carbon monoxide in tobacco smoke causes a rise in the carboxyhaemoglobin levels in smokers, which reduces the oxygen perfusion for the organ of Corti [16]. Genetic variability in the cochlear antioxidant system (GSTM1 deletion) renders smokers at increased risk for noise induced hearing loss than for never smokers [17]. Neonatal nicotine exposure impairs temporal processing and gap detection in rates implying an impairment of the normal development of auditory temporal processing by inducing changes in the efferent cholinergic systems [18]. Maternal smoking has also been found to be harmful to fetal brain development and may lead to auditory cognitive dysfunction [19]. Cotinine, the major proximate metabolite of nicotine, has been widely used as a biomarker of exposure to tobacco, in both active and passive smokers [20]. Cotinine serum level may not be available for many cohorts; this enhanced the application of questionnaires to quantify the second-hand smoke exposure at work, at home and in social settings. These questionnaires proved to be rapid, cheap, and have strong correlation with the serum cotinine level. So it can be used to distinguish relative levels of exposure to second-hand smoke exposure [21]. In this study quantifying the second-hand smoke exposure was done through self-ascertained questionnaire. According to the questionnaire the families and their children participating in the study group were divided into 3 subgroups. 201 families participating in the study had at least one smoking parent (69.3%). Only 120 families (59.7%) of these smoking families were vigilant for the dangers of the passive smoking and trying to keep their children away from second-hand smoke exposure; this shows the need for awareness media campaigns which can positively affect smokers knowledge of the dangers of passive smoking to protect others from second-hand smoke [22]. In the current study, the hearing threshold at all frequencies, SRT and WDS showed no signicant difference between the study groups (Table 2). Table 3 showed that the prevalence of hearing loss was nearly the same in children of no exposure group (3.8%) and mild exposure group (4.5%), but the heavy exposure had signicant higher prevalence of hearing loss (12%). The risk ratio

for developing hearing loss in smokers and their households ranged between 1.33 and 4.9 in different studies [7,2]. In the present study the risk ratio was 3.14. Passive smoking was signicantly associated with all congurations of sensorineural hearing loss; there was increased risk of low-, mid- and highfrequencies denoting global injury of the cochlea [12,18]. There was increased risk for development of either unilateral or bilateral hearing loss [12]. In the present study 80% of the hearing loss in the heavy exposure group was low frequency hearing loss, and it was unilateral hearing loss in 46.7%. The children with unilateral sensorineural hearing loss may represent early stage of hearing loss, which by time may progress to be bilateral. Though Kumar et al. [3] reported that the sensorineural hearing loss degree in passive smoker children was mild, all children with hearing loss in the current study had minimal hearing loss. Again this may represent early stage of hearing loss which may progress to more severe degrees with continuing exposure to second-hand smoke. Minimal hearing loss affects about 5% of children. Hearing aid tting is not a choice in patients with minimal hearing loss, though they may be at risk academically due to their poorer speech perception in the noisy classrooms [14]. The current study indicates that passive smoking is an important attributing factor for development of minimal hearing loss. 5. Conclusions Passive smoking in childhood correlates with minimal sensorineural hearing loss, and it may be a risk factor for development of minimal hearing loss. Strict prevention of children exposure to second-hand smoke should be encouraged by every mean. References
[1] O. Shafey, S. Dolwick, G.E. Guindon, The Tobacco Control Country Proles, American Cancer Society, Atlanta, 2003. [2] K. Nomura, M. Nakao, T. Morimoto, The effect of smoking on the hearing loss: the quality assessment and meta-analysis, Prev. Med. 40 (2005) 138214. [3] A. Kumar, R. Gulati, S. Singhal, A. Hasan, A. Khan, The effect of smoking on the hearing status a hospital based study, J. Clin. Diagn. Res. 7 (2) (2013) 210214. [4] S. Ferritite, V. Santana, Joint effects of smoking, noise exposure, and age on hearing loss, Occup. Med. 55 (2005) 4853. [5] K. Yolton, K. Dietrich, P. Auinger, B.P. Lanphear, R. Hornung, Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents, Environ. Health Perspect. 113 (1) (2005) 98103. [6] C. Iribarren, G. Friedman, A. Klatsky, M. Eisner, Exposure to environmental tobacco smoke: association with personal characteristics and self reported health conditions, J. Epidemiol. Community Health (55) (2001) 721728. [7] R. Lyons, Passive smoking and hearing loss in infants, Ir. Med. J. 85 (1992) 111112. ka nyi, A. Czinner, J. Spangler, T. Rogers, G. Katona, Relationship of environ[8] Z. Csa mental tobacco smoke to otitis media (OM) in children, Int. J. Pediatr. Otorhinolaryngol. 76 (7) (2012) 989993. lu, M. Yener, I. Ozdemir, M. Ku lekc [9] E. Gultekin, N. Develiog i, Prevalence and risk factors for persistent otitis media with effusion in primary school children in Istanbul, Turkey, Auris Nasus Larynx 37 (2) (2010) 145149. [10] K. Bennett, M. Haggard, Accumulation of factors inuencing childrens middle ear disease: risk factor modeling on a large population cohort, J. Epidemiol. Community Health 52 (1998) 786793. [11] K. Cruichanks, R. Klien, B. Klien, T. Wiley, Cigarette smoking and hearing loss, the epidemiology of hearing loss study, J. Am. Med. Assoc. 21 (279) (1998) 17151719. [12] A. Lalwani, Y. Liu, M. Weitzman, Secondhand smoke and sensorineural hearing loss in adolescents, Arch. Otolaryngol. Head Neck Surg. 137 (7) (2011) 655662.

Table 3 Demographic and audiological features of hearing loss in the different study groups. No. exposure No. Age Females Bilateral Low frequency High frequency (5/131) 3.8% 8.2 1.5 (3/5) 60% (2/5) 40% (3/5) 60% (2/5) 40% Mild exposure (7/155) 4.5% 8.1 1.5 (4/7) 57.1% (3/7) 42.9% (4/7) 57.1% (3/7) 42.9% Heavy exposure (15/125) 12% 8.3 1.5 (7/15) 46.7% (7/15) 53.3% (12/15) 80% (3/15) 20%

No., number and percent of children with hearing loss in every subgroup; Bilateral, number and percent of children with bilateral hearing loss in every subgroup.

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[18] W. Suna, A. Hansena, L. Zhanga, J. Lua, D. Stolzberga, K. Krausa, Neonatal nicotine exposure impairs development of auditory temporal processing, Hear. Res. 245 (12) (2008) 5864. [19] A.P. Key, M. Ferguson, D.L. Molfese, K. Peach, C. Lehman, V.J. Molfese, Smoking during pregnancy affects speech-processing ability in newborn infants, Environ. Health Perspect. 115 (2007) 623629. [20] N. Benowitz, Cotinine as a biomarker of environmental tobacco smoke exposure, Epidemiol. Rev. 18 (2) (1996) 188204. [21] D. Nondahl, K. Cruickshanks, C.R. Schubert, A questionnaire for assessing environmental tobacco smoke exposure, Environ. Res. 97 (1) (2005) 7682. [22] K. King, R. Vidourek, S. Creighton, S. Vogel, Smokers willingness to protect children from secondhand smoke, Am. J. Health Behav. 27 (5) (2003) 554563.