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. Author manuscript; available in PMC: 2014 Jul 31.
Published in final edited form as: Arch Otolaryngol Head Neck Surg. 2011 Jul;137(7):655–662. doi: 10.1001/archoto.2011.109

Second Hand Smoke is Associated with Sensorineural Hearing Loss in Adolescents

Anil K Lalwani 1,2,3, Ying-Hua Liu 2,5, Michael Weitzman 2,4,5
PMCID: PMC4117391  NIHMSID: NIHMS582150  PMID: 21768409

Abstract

Background

Second hand smoke (SHS) exposure, either in utero or during childhood, has been linked to low birth weight, sudden infant death syndrome, upper and lower respiratory infections, increased asthma severity, dental caries, behavioral problems, ADHD, emotional problems, and otitis media (OM).To our knowledge, no previous study has examined the possible association between SHS and sensorineural hearing loss (SNHL) in adolescent.

Objectives

The study objectives were to (1) exam risk factors for sensorial hearing loss in different age, gender, race, and income/poverty groups among adolescents (age 12 to 19) in the U.S. using data from most recent waves of NHANES (2005–2006); and, (2) evaluate the independent association between SHS and sensorial hearing loss among adolescents.

Design

Cross-sectional analysis of nationally representative data.

Setting

National Health and Nutrition Examination Survey 2005–2006.

Participants

1533 non-institutionalized adolescents age 12–19 who underwent audiometric testing, had serum cotinine levels available, and were not actively smoking.

Measurements

The serum cotinine levels, presence of household smokers, and self-report of smoking were used to determine SHS exposure and active smoking. Low frequency hearing loss was defined as the average pure tone level greater than 15 dB for 500, 1000, and 2000 Hz; high frequency hearing loss was defined as the average pure tone level greater than 15 dB for 3, 4, 6, and 8 kHz.

Results

SHS exposure was associated with elevated pure tone hearing levels at 2, 3 and 4 kHz. and 1.8 fold increased risk of unilateral low frequency SNHL in multivariate analyses (95% C.I.: 1.08-3.46). The incidence of SNHL was directly related to level of SHS exposure as reflected in serum cotinine levels. In addition, nearly 82% of adolescents with low frequency SNHL did not report hearing difficulty.

Conclusions

SHS is associated with increased incidence of LFSNHL that is directly related to level of exposure. The affected individuals are unaware of the hearing loss. Therefore, early identification and prevention of hearing loss related to SHS may produce significant public health benefits.

Keywords: Second hand smoke (SHS), low frequency sensorineural hearing loss, high frequency sensorineural hearing loss, serum cotinine levels

INTRODUCTION

Second hand smoke (SHS) is a profound public health problem with more than half of children exposed1. While exposure rates may vary across regions, by socioeconomic status, ethnicity, or sex, its detrimental effects have been demonstrated across all demographics groups. Specifically, prenatal tobacco, or childhood SHS exposure have been linked to low birth weight2, Sudden Infant Death Syndrome3,4,5, upper and lower respiratory infections6,7, increased asthma severity8, behavioral problems9,10, cognitive problems11, and otitis media (OM)12. A variety of mechanisms have been proposed to explain the detrimental effects of SHS, including disruption of normal in utero development 13 , alteration of the immune system 14 , postnatal deterioration of body function, and altered hemodynamics15.

In the auditory system, SHS is a known risk factor for OM12. Recurrent acute OM is more common in the nearly 60% of children exposed to SHS in the United States. While the exact mechanism remains unclear, the increased risk of OM may be through suppression or modulation of the immune system, enhancement of bacterial adherence factors, the consequence of exposure to toxins within SHS, and impairment of the respiratory mucociliary apparatus leading to Eustachian tube dysfunction16.

SHS may also have the potential to impact auditory development leading to sensorineural hearing loss (SNHL) because of its negative impact on in utero development of the fetus and low birth weight. To our knowledge, no previous study has examined the possible association between SHS and SNHL among adolescents. The present study exams risk factors for SNHL in different age, gender, race, and income/poverty groups among adolescents (age 12 to 19) and investigates the independent association between SHS and SNHL among adolescents.

METHODS

Participants

Data from 2,288 subjects, 12 to 19 years of age, from the National Health and Nutrition Examination Survey (NHANES 2005 to 2006) were examined 17 . The survey was conducted by the National Center for Health Statistics (NCHS) of the Centers for Disease Control and Prevention (CDC) and was reviewed and approved by the NCHS institutional review board. NHANES 2005–2006 is a cross-sectional health survey that used a complex, multistage design to achieve a nationally representative sample of the non-institutionalized civilian population in the United States17.

Participants were evaluated with a home interview to determine family medical history, current medical conditions, medication use, self-report of the presence of any smokers in the household, and socioeconomic and demographic information. Additionally, each person was randomly assigned to undergo a morning, afternoon, or evening examination at a mobile examination center consisting of physical examinations and laboratory testing using blood and urine samples.

Audiometric Measures

The NHANES 2005–2006 protocol for audiometry included otoscopic examination. The ears were examined with a Welch-Allyn Model 25020 otoscope with rechargeable handle and disposable specula. The Micro Audiometrics Earscan Acoustic Impedance Tympanometer (Murphy, NC) was used to perform tympanometry to evaluate the functional health of the middle ear system. Tympanometry was performed from −312 dekaPascals (daPa) to +200 daPa. The quality of the tympanogram was noted along with the peak response. Audiometry was conducted in a special sound booth (manufactured by Acoustic Systems, model Delta 143, Ceder Park, TX) built into the mobile examination center by trained examiners using a standardized protocol. An audiometer (Interacoustic Model AD226, Assens, Denmark) with standard TDH-39P headphones (Telephonics Corporation, Farmingdale, New York), and insert earphones (EARTone 3A, Etymotic Research, Elk Grove Village, Illinois) was used for testing hearing. The audiometer was calibrated with the same specifications at the start and end of testing at each field location using Quest Model BA-201-25 acoustic simulator (Oconomowoc, WI). Additional information regarding the methods, calibration equipment and calibration protocol is available at http://www.cdc.gov/nchs/data/nhanes/nhanes_05_06/AU.pdf. Air-conduction thresholds were measured for each ear at 0.5, 1, 2, 3, 4, 6, and 8 kHz, with testing repeated at 1 kHz across an intensity range of −10 to 120 dB. The correlation of the threshold for the 1-kHz first test with the retest was 0.9 (P<.001) for the left and right ears of each child. The 1-kHz first test was the value used for this analysis18.

The response to the following question was also used to determine the self recognition of hearing impairment: “Which statement best describes {your/SP’s} hearing (without a hearing aid)? Would you say {your/his/her} hearing is excellent, good, that {you have/s/he has} a little trouble, moderate trouble, a lot of trouble, or {are you/is s/he} deaf?

Definition: Hearing loss

Hearing loss can be categorized by where or what part of the auditory system is damaged. There are three basic types of hearing loss: sensorineural hearing loss, conductive hearing loss (CHL), and mixed hearing loss (MHL). SNHL was inferred when the otoscopic exam was normal and there was adequate or good quality tympanogram with a peak of >0.3 mol. Thus, individuals with abnormal otoscopy, poor quality tympanogram, or peak response less than 0.3 mol were excluded from further analyses as these individuals may have CHL or MHL. Among 2,288 adolescents age 12 to 19, only 32 were excluded based on these criteria.

Low and high frequency hearing threshold was defined as the average of pure tone hearing levels at 0.5, 1, and 2 kHz, and 3, 4, 6 and 8 kHz, respectively. Low and high frequency hearing loss was defined as low and high frequency hearing threshold above 15 dB. 19,20 Unilateral low or high frequency hearing loss was defined as pure-tone average of greater than 15 dB HL in the worse ear. The hearing loss was deemed to be bilateral when the better ear pure-tone average was greater than 15 dB HL.

Definition: Active Smoking and SHS Exposure

Cotinine, a metabolite of nicotine, was used as a biomarker for both active smoking and exposure to SHS. In 424 individuals, cotinine levels were not available and, thus, they were excluded from further analyses. In addition to cotinine, NHANES includes adolescent self-report of smoking status. Consistent with previously published studies, active smokers were defined as those with cotinine levels ≥15 ng/mL or those who reported smoking in the past 5 days. Those with serum cotinine levels that were detectable but <15 ng/mL and who did not report smoking in the past 5 days were defined as exposed to SHS21. A cotinine level of <0.05 ng/mL was below the detection limit. Those with undetectable serum cotinine levels, and without self-reported smoking were defined as unexposed. In the analysis assessing the impact of exposure level on hearing loss, the observed cotinine levels were grouped in quartiles: quartile 1- ≤0.0876 ng/mL; qualtile 2- > 0.0876 ng/mL and ≤0.217 ng/mL; quartile 3- >.217 ng/mL and ≤0.858 ng/mL; quartile 4- >0.858 ng/mL). To study the effect of SHS only, active smokers (either self-report of smoking in last five days or cotinine levels ≥15 ng/mL; n=299) were excluded from the study.

Sociodemographic Variables and Hearing-Related Covariates

The adolescent subjects were divided into two age groups: 12 to 15 years and 16 to 19 years. Race-ethnicity was classified as non-Hispanic black, non-Hispanic white, or Mexican American. The “all other” race-ethnicity category (eg, other Hispanics, Asians, and Native Americans) was too small to be analyzed separately, but was included in all totals (n=40). These 4 race-ethnicity groups are mutually exclusive. The poverty-income ratio (PIR) was defined as the total family income divided by the poverty threshold, as determined by the US Bureau of the Census, for the year of the interview. Income was classified as poverty (PIR below 1) and not poverty (PIR greater than 1).

Prematurity, diabetes, greater than 3 episodes of otitis media, allergy and eczema are recognized risk factor for hearing loss 22,23,24,25. In NHANES 2005–2006, the Early Childhood section of the Sample Person Questionnaire provides personal interview data for children (age below 15), including the age of the biological mother when the child survey participant was born, smoking habits of the mother while she was pregnant with the participant, birth weight, and whether the participant received care in an neonatal intensive care unit, premature nursery, or any other type of special care facility. Moreover, NHANES 2005–2006 survey included questions about otitis media, asthma, allergy, and eczema.

Statistical Analyses

After excluding for inadequate smoking history, active smoking status, and findings suggestive of CHL/MHL, the sample size available for the study was 1,533 adolescents age between 12 and 19. X2-test was used for bivariate analyses to test for associations between independent variables investigated and the unilateral/bilateral, low/high frequency hearing loss. The Cochran-Armitage trend test was used to test for trends. Two additional analyses were performed: one on second hand smoking exposed quartile levels and the other on second hand smoking exposure and its association with different speech-frequency levels (using t-tests for 0.5, 1, 2, 3, 4, 6, and 8 KHZ). All analyses were conducted with SAS26; the SUDAAN statistical software27 was used to account for the complex sample design of the NHANES and to apply sampling weights to produce national estimates by adjusting for the oversampling of young children, older adults, Mexican Americans, and blacks.

RESULTS

Table 1 shows the prevalence of a given levels of auditory thresholds (≤15 dB, >15 and ≤25 dB, >25 and ≤40 dB, and >40 dB) for individuals with and without SHS exposure. For example, among adolescents aged 12 to 19, using 15 dB as the threshold for hearing loss, the overall rate of unilateral low frequency hearing loss, bilateral hearing low frequency loss, unilateral high frequency loss, and bilateral high frequency loss was 9.55%, 2.19%, 15.38%, and 3.68% respectively. The prevalence of hearing loss is greater among individuals exposed to SHS for unilateral low and high frequency hearing and bilateral low and high frequency hearing compare to non-exposed. SHS is associated with increased incidence of elevated auditory thresholds at unilateral low frequency hearing loss and bilateral high frequency hearing loss (trend p=0.03 and 0.04, respectively).

Table 1.

Incidents of Hearing loss with and without SHS among adolescents in NHANES 2005–2006

N ≤15dB >15 dB, ≤25 dB > 25 dB, ≤40dB >40dB p
0.03
Unilateral Low frequency 1,533 90.45% 7.33% 1.17% 1.06%
Non Exposed 754 92.47% 6.15% 0.86% 0.52%
Exposed 799 88.18% 8.65% 1.51% 1.65%
0.18
Bilateral low frequency 1,533 97.81% 2.07% 0.04% 0.07%
Non Exposed 754 98.35% 1.65%
Exposed 799 97.20% 2.54% 0.09% 0.17%
0.29
Unilateral high frequency 1,533 84.62% 11.18% 2.53% 1.67%
Non Exposed 754 86.14% 10.10% 2.69% 1.07%
Exposed 799 82.91% 12.39% 2.36% 2.33%
0.04
Bilateral high frequency 1,533 96.32% 3.18% 0.33% 0.17%
Non Exposed 754 97.46% 2.31% 0.16% 0.07%
Exposed 799 95.03% 4.17% 0.51% 0.29%

The vast majority of adolescents with unilateral low or high frequency hearing loss are unaware of their hearing impairment. Only 18% with low frequency and 11% with high frequency hearing loss reported “a little trouble, moderate trouble, a lot of trouble” with hearing (Table 2).

Table 2.

Pure Tone Hearing Level at Each Frequency with and without SHS among adolescents in NHANES 2005–2006

Average (right and left ear) Worse ear (among right and left ear)
Frequency
(kHz)
Exposed Unexposed p Exposed Unexposed p
MEAN STD MEAN STD MEAN STD MEAN STD
0.5 9.87 0.51 8.86 0.51 0.133 12.72 0.65 11.55 0.57 0.150
1 5.23 0.58 4.43 0.36 0.225 8.37 0.78 7.16 0.37 0.137
2 5.99 0.35 3.50 0.41 <0.001 9.11 0.53 6.16 0.41 <0.001
3 5.56 0.48 4.11 0.35 0.026 8.65 0.65 6.87 0.44 0.041
4 6.20 0.54 4.28 0.50 0.015 9.71 0.69 7.41 0.51 0.010
6 12.10 0.73 11.59 0.55 0.532 16.48 0.89 15.91 0.64 0.554
8 8.46 0.82 7.64 0.60 0.276 12.37 0.92 11.75 0.74 0.543

The effect of SHS on hearing level at 0.5, 1, 2, 4, 5, 6 and 8 kHz was evaluated using both the average threshold for the right and left ear, as well as, hearing level of the worst ear (Table 3). Across all frequencies, the mean pure tone hearing level was elevated in adolescents exposed to SHS when compared to individuals without SHS. Specifically, second hand smoking is significantly associated with elevated thresholds at 2, 3, and 4 kHz under both conditions.

Table 3.

Risk factor for SNHL among adolescents in NHANES 2005–2006

Low Frequency(>15)1 High Frequency(>15)2
N % of
unilateral
SNHL
p
value
% of
bilateral
SNHL
p
value
% of
unilateral
SNHL
p value % of
bilateral
SNHL
p
value
1533* 9.54% 2.19% 15.38% 3.68%
SHS3 0.04 0.36 0.3428 0.10
  Non Exposed 754 7.53% 1.65% 13.86% 2.54%
  Exposed 779 11.82% 2.80% 17.09% 4.97%
SHS exposure level4 0.02 0.16 0.37 0.16
  Non-Exposed 754 7.53% 1.65% 13.86% 2.54%
  Exposed level Quarter 1 190 7.71% 0.42% 15.64% 3.79%
  Exposed level Quarter 2 188 10.54% 1.56% 13.95% 7.60%
  Exposed level Quarter 3 201 12.08% 4.14% 19.85% 1.49%
  Exposed level Quarter 4 200 17.05% 5.14% 18.80% 6.90%
Prenatal Smoking5 0.11 0.24 0.34 0.48
  Yes 129 16.78% 4.10% 18.48% 5.73%
  No 703 6.40% 1.63% 13.47% 3.13%
Birth Weight5 0.53 0.41 0.58 0.72
  Low BW (<=5.5pds) 76 16.48% 5.87% 17.89% 3.94%
  Normal (>5.5 pds) 709 7.77% 1.88% 13.98% 3.06%
Very Low BW5 0.52 0.45 0.46
  Very Low BW (<=3.3pd) 12 42.32% 42.32% 0.41 60.36% 15.41%
  Low BW (<=5.5pds) 64 12.95% 0.89% 12.08% 2.37%
  Normal (>5.5 pds) 709 7.77% 1.88% 13.98% 3.06%
Received NICU5 0.01 0.4 0.82
  Yes 111 16.30% 18.07% 3.04%
  No 722 7.35% 13.74% 3.50%
Sex 0.69 2.73% 0.42 0.14 0.21
  Male 737 8.56% 1.64% 14.66% 3.66%
  Female 796 10.56% 15.49% 3.70%
Age group 0.60 0.99 0.33 0.99
12~15 847 8.47% 2.18% 14.35% 3.52%
16~19 686 11.08% 2.20% 16.83% 3.63%
Race 0.33 NA 0.52 0.02
Mexican 539 7.75% 1.56% 13.92% 2.87%
Other Hispanic 40 3.37% 0.00% 12.78% 4.59%
White 359 10.36% 2.14% 15.99% 3.46%
Black 523 10.10% 3.80% 17.24% 6.06%
Poverty 0.61 0.65 0.81 0.94
Poor 432 9.74% 1.92% 14.77% 3.52%
Not poor 1,043 8.54% 2.28% 15.67% 3.63%
OM6 0.23 0.48 0.64 0.49
Yes 408 12.95% 2.63% 16.54% 4.25%
No 1,114 7.29% 1.90% 14.68% 3.22%
Allergy 0.78 0.63 0.76 0.21
Yes 395 9.88% 2.74% 14.66% 2.73%
No 1,136 9.21% 1.98% 15.49% 4.08%
Eczema 0.85 <.01 0.98 0.86
Yes 132 10.28% 2.40% 15.49% 3.37%
No 1,397 9.49% 0.29% 15.39% 3.72%
1

Low frequency: average (0.5, 1, and 2 kHz)

2

High Frequency: average (3, 4, 6, and 8 kHz)

3

SHS: with serum cotinine levels that were detectable but <15 ng/mL and who did not report smoking in the past 5 days

4

SHS exposure levels: 1- ≤0.0876 ng/mL; 2- >0.0876 ng/mL and ≤0.217 ng/mL; 3- >.217 ng/mL and ≤0.858 ng/mL; 4- >0.858 ng/mL

5

Prenatal smoking, Low Birth weight, very Low birth weight, Receive NICU are only available for adolescents below age 15

6

OM: greater than 3 episodes of otitis media

Bivariate analyses were used to investigate the relationship of hearing loss with a variety of variables shown in Table 4. SHS exposure was associated with significantly higher incidence of unilateral low frequency hearing loss (11.82% vs. 7.53%, p=0.04); while the incidence of unilateral high frequency hearing loss was greater in the SHS exposed group (17.09% vs. 13.86%), it was not statistically significant (p=0.34). Greater SHS, as reflected by the higher cotinine level, was associated with higher incidence of hearing loss (see below in dosage analysis). Eczema and Black race were significantly associated with bilateral low frequency hearing loss and bilateral high frequency hearing loss, respectively. Adolescents who received care in the NICU were found to have significantly higher incidence of low frequency hearing loss. Despite a higher incidence, low birth weight was not significantly associated with hearing loss likely reflecting a small sample size of low birth weight babies in the population. Similarly, while the data suggest an association between prenatal smoking, and ear infections and low frequency unilateral hearing loss, these associations were not significant at 0.05 level.

Table 4.

Independent Associations with Unilateral SNHL1 for Adolescents 12 to 19 (NHANES, 2005–2006)

OR 95% CI
SHS2
  Non Exposed
  Exposed 1.83 1.08–3.46
SHS level3
  Non-Exposed
  Exposed level Quarter 1 1.14 0.60–2.20
  Exposed level Quarter 2 1.72 0.71–4.18
  Exposed level Quarter 3 1.94 0.72–5.32
  Exposed level Quarter 4 2.64 1.34–5.19
Sex
  Male 1.31 0.76–2.25
  Female
Age group
  12~15
16~19 1.63 1.10–2.41
Race
Mexican American 0.92 0.53– 1.60
Other Hispanic 0.33 0.04–2.90
Non-Hispanic White
Non-Hispanic Black 1.09 0.54–2.19
Poverty
Poor 0.88 0.52–1.50
Not poor
OM4
Yes 1.87 0.86–4.07
No
Allergy
Yes 0.96 0.55–1.67
No
Eczema
Yes 0.96 0.47–1.99
No
1

Unilateral Hearing loss: worse ear (0.5+1+2)KHZ/3>15 dB.

2

SHS: SHS: with serum cotinine levels that were detectable but <15 ng/mL and who did not report smoking in the past 5 days

3

SHS exposed level: I (<=0.540), II (>0.54, <=1.35); (>1.35, <15 ng/ML) SHS level was tested in seperated multivariate model adjusted by age, gender, race, poverty, allergy, eczema, and OM.

4

OM: greater than 3 episodes of otitis media

Multivariable logistic regression analyses was used to determine if SHS was independently associated with low frequency hearing loss controlling for age group, gender, race, poverty, ≥3 episodes of otitis media, allergy and eczema (Table 5). Only SHS exposure and older age were significantly associated with unilateral hearing loss. Adolescents with exposure to SHS were 1.83 times more likely to have low frequency hearing loss (95% CI, 1.08–3.46) compared to non-exposed individuals. Older adolescents (age 16–19) were 1.31 times more likely to have low frequency hearing loss than younger adolescents (age 12 to 15 years) (95% CI, 1.10–2.41).

Table 5.

Self-reportinga of Hearing Difficulty Among Adolescents With and Without Sensorineural Hearing Loss (NHANES 2005–2006)b

Self-Report of Hearing Loss

Low Frequencyc High Frequencyd

Pure-Tone
Frequency
Hearing
Participants
No.
Excellent
or Good
%
A Little
Moderate
or Lot of
Trouble, %
Participants
No.
Excellent
or Good
%
A Little
Moderate
or Lot of
Trouble, %
Normal 1833 95.41 4.59 1701 95.23 4.77
Hearing loss 185 81.57 18.43 309 88.57 11.43
a

Which statement best describes {your/Sample Person’s} hearing (without a hearing aid)? Would you say {your/his/her} hearing is excellent, good, that {you have/she or he has} a little trouble, moderate trouble, a lot of trouble, or {are you/is she or he} deaf?

b

See Analytic and Reporting Guidelines: The National Health and Nutrition Examination Survey (NHANES).16

c

Low-frequency hearing loss: average of hearing thresholds at 0.5, 1, and 2 kHz greater than 15 dB HL.

d

High-frequency hearing loss: average of hearing thresholds at 3, 4, 6, and 8 kHz greater than 15 dB HL.

To assess a dose-response relationship between exposed levels and unilateral low frequency hearing loss, the exposed group was classified into four levels of exposure based upon the serum cotinine quartiles. Higher serum cotinine levels were associated with greater incidence of unilateral low frequency hearing loss: the incidence of hearing loss was 7.43% for non exposed group, and 7.60%, 10.30%, 11.89%, and 16.82% for exposure level 1, 2, 3 and 4, respectively (p<0.01, Table 4). In multivariable logistic regression analyses, controlling for other covariates, a dose-response relationship was found for group level 4 (odds ratio 2.64, 95% CI: 1.34–5.79; Table 5).

DISCUSSION

SHS exposure has been linked to diverse pathology in humans, affecting the unborn to the elderly. In this study, based on a large, nationally representative sample with an objective biochemical marker of tobacco exposure, an exposure to SHS is found to be associated with hearing loss in US adolescents. Furthermore, this risk to auditory function is directly related to serum cotinine level, a biomarker of tobacco exposure. Specifically, SHS was associated with elevated pure tone threshold at 0.5, 1, 2, 3, 4, 6, and 8 kHz suggesting that the injury to the inner ear is global. The elevated threshold for pure tones was significantly higher at 2, 3 and 4 kHz in individuals with SHS exposure when compared to those without exposure. These mid to high frequencies are critical for hearing in humans and are responsible for the clarity of hearing allowing us to discriminate between similar sounding words. Accelerated hearing loss associated with smoking has been previously reported in adults28. Finding of elevated threshold in adolescents suggests that the inner ear injury responsible for hearing loss associated with smoking in adults may begin at a very early age.

Furthermore, the incidence of unilateral and bilateral low frequency, and unilateral and bilateral high frequency hearing loss, is greater in adolescents exposed to SHS; it is significantly higher for unilateral low frequency hearing loss. There is also a direct dos-response relationship between incidence of hearing loss and exposure level: higher serum cotinine levels are associated with higher incidence of hearing loss. In the multivariate analysis, controlling for sex, age, race, poverty, multiple OM, allergy and eczema, exposure to tobacco smoke is associated with a 1.83-fold increased risk of unilateral low frequency hearing loss among adolescents. The rate of hearing loss increased with exposure level: the increased risk was 1.14, 1.72, 1.94 and 2.64 fold higher for cotinine quartile levels 1 to 4, respectively. Findings of the bivariate and multivariate analysis are consistent with the hypothesis that the deterioration in auditory function observed is a direct consequence of SHS exposure.

Children with untreated hearing loss above 35 dB in the better ear have significant negative impact on speech, language, and cognitive development; these children also go on to have difficulties with academic and vocational achievement 29,30,31 . While controversial, mild hearing loss (>15 dB and <35 dB) has been shown to be similarly detrimental to children’s development. As a result of their hearing loss, they may miss up to 10% of speech and respond inappropriately. Mild hearing loss in the sensitive speech and language acquisition period has been associated with delays similar to children with more severe hearing loss32. Children with mild hearing loss have been shown to have academic problems (Bess et al. 1998) 33. Similarly, their social interactions may be affected. Children with hearing loss are often labeled troublemakers due to their inappropriate responses based on misunderstood verbal instructions34. The effects of mild SNHL during adolescence remain to be elucidated.

A variety of mechanisms may be implicated in how SHS affects auditory function including its effect on the microvasculature35, endocrine function36, and oxidative stress37. Tobacco smoke is known to have detrimental effect on the microvasculature. As an active energy producing and consuming organ, the inner ear is exquisitely dependent on adequate blood supply and thus may be susceptible to tobacco mediated alterations in blood flow. Smoking’s effect on the cardiovascular system and diabetes may both also affect hearing; both are independently associated with hearing loss. Hypoxemia due to SHS may be deleterious to the inner ear. Direct injury to the inner ear by nicotine or other toxin in SHS could also be implicated.

As more than 50% of adolescents are exposed to SHS1, the association of the mild SNHL with SHS has significant implications for public health in the United States. While there is active screening for hearing loss in newborns and young children, adolescents are not routinely evaluated for hearing loss. Based on the findings in this report, at risk adolescents should also undergo hearing screening. Self-reporting of hearing loss alone is inadequate for identifying affected individuals as more than 80% were unaware of hearing difficulty in our sample population. Thus, adolescents who are exposed to SHS should be more closely monitored for hearing loss. In homes where there is active smoking, parents and caretakers should be made aware of risk to hearing in their children. Health care providers should refer these young adults for routine complete audiologic evaluation to identify early hearing loss.

There are several limitations to these data and their analysis. While large and comprehensive, the NHANES data set is cross-sectional and causal inferences cannot be made. Further, prenatal SHS exposure history is available for some but not all of the participants, and is based on retrospective report, thus limiting the validity of this measure The data also does not provide the source of the SHS exposure, thus limiting the development of effective public health interventions to prevent SHS mediated hearing loss.

SUMMARY

This study demonstrates, for the first time, a relationship between tobacco exposure and hearing loss among adolescents in the United States. Data comes from a large, nationally representative sample with objective biochemical rather than exclusive self-report measures of smoking status. The findings indicate that exposure to tobacco smoke is associated with a 1.8-fold increase in the risk of hearing loss among adolescents. These findings may have profound implications in light of the high exposure rates among adolescents in the United States. Future studies need to investigate the adverse consequences of this early hearing loss on social development, academic performance, behavioral and cognitive function and public health costs.

ACKNOWLEDGMENT

This work was supported, in part, by grants from the Zausmer Foundation (Principal Investigators: Drs. Lalwani, Liu, and Weitzman) and NIH/NCMHD 5P60 MD000538-06 (Principal Investigator: Michael Weitzman, MD).

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