Search tips
Search criteria 


Logo of noisehealthHomeCurrent issueInstructionsSubmit article
Noise Health. 2015 Jul-Aug; 17(77): 233–236.
PMCID: PMC4900486

Simultaneous effects of noise exposure and smoking on OAEs


Noise is one of the most pervasive hazardous factors in the workplace. Noise-induced hearing loss (NIHL) is the most common disorder related to noise exposure. Smoking is probably associated with hearing loss. The simultaneous effect of noise and smoking on hearing is a recent concern. In this study, we assessed the simultaneous effect of noise and smoking on standard pure tone audiometry (PTA) and distortion product otoacoustic emissions (DP-OAEs). This was an historical cohort study on 224 workers exposed to noise who were divided into two groups: Smokers and nonsmokers. DP-OAE response amplitudes were assessed. Data were analyzed by SPSS software (version 19) using Student's t-test and Mann-Whitney U test. One hundred and five subjects were smokers (case group) and 119 individuals were nonsmokers (control group). All the subjects were exposed to 91.08 ± 2.29 dBA [time-weighted average (TWA) for an 8 h work shift]. Mean DP-OAE response amplitude at frequencies higher than 1,000 Hz was significantly higher in the smokers than the nonsmokers. This study showed that smoking can aggravate the effect of noise on hearing in DP-OAEs.

Keywords: Audiometry, distortion product otoacoustic emissions (DP-OAEs), noise-induced hearing loss (NIHL), noise, smoking


Noise is a common physical exposure in the workplace and noise-induced hearing loss (NIHL), the most frequent outcome of this exposure, is the second acquired cause of hearing loss after presbycusis.[1,2,3] According to the report of the US Department of Labor in 2002, about 10 million workers suffer from NIHL in the US.[4] The European agency for safety and health at work have estimated that about 28% of workers are exposed to noise level approximately between 85 dBA and 90 dBA in the Europian Union.[5] Despite the implementation of hearing conservation program (HCP) in many workplaces, NIHL is still a common occupational disorder. It could not be treated but can be prevented.[1]

HCP is required for workplaces when noise exposure exceeds 85 dBA according to the Occupational Safety and Health Administration (OSHA) guidelines. The main aspect of this program is the screening of hearing thresholds by pure tone audiometry (PTA).[6]

NIHL typically affects high frequencies bilaterally and by continuation of exposure to noise, it may extend to lower frequencies, that is, speech frequencies that may impair the worker's normal hearing.[2,3,7] Detection of early changes in the hearing threshold before development of clinical hearing loss can help prevent hazardous effects of noise on hearing.[8] Hearing thresholds in workers exposed to hazardous noise are performed by PTA, but recently other diagnostic tests such as extended high-frequency audiometry (HFA) and otoacoustic emissions (OAEs) were introduced.[9,10] OAEs are routinely performed for diagnosis of functional hearing loss. Some studies have proved a higher sensitivity of OAEs for the detection of NIHL than standard PTA.[11,12]

Recent literature shows that smoking may cause sensorineural hearing loss as well.[13,14,15,16] It is also proposed that hearing loss is directly associated with pack/years of smoking[17] although some studies have not shown the association between smoking and hearing loss.[18,19,20,21] Nakanishi et al. found 4,000 Hz as the frequency mostly affected by smoking.[16] Paschoal et al. found that 1,000 Hz and 4,000 Hz in OAEs are frequencies with the most sensitivity to smoking.[13]

A recent issue comprises the simultaneous effects of noise and smoking on hearing. Some studies have shown that smoking and noise may have additive or multiplicative effects on the hearing threshold in standard PTA.[17,22] We could not find a study on the simultaneous effects of noise and smoking on OAEs.

In this study, we aimed to assess the simultaneous effects of noise and smoking on standard PTA and distortion product OAEs (DP-OAEs) among workers exposed to noise.


In a cross-sectional study, we assessed the simultaneous effects of noise and smoking on DP-OAE response amplitude in workers exposed to industrial noise higher than 85 dBA. Subjects were randomly selected from workers in the tile and ceramic industry who were exposed to noise higher than 85dBA. The subjects were asked to avoid loud noise for 16 h before testing.

Exclusion criteria included: Conductive hearing loss, diabetes mellitus, history of exposure to ototoxic substances or ototoxic drugs, history of head trauma, congenital hearing loss, and unilateral hearing loss. Ex-smokers were also excluded from the study. Subjects were divided into two groups: 105 smokers and 119 nonsmokers.

Data about smoking were obtained from each participant's self-report at the time of health evaluation. Smokers were assessed by pack/years of smoking (i.e., the number of cigarettes smoked per day divided by 20 multiplied by years of smoking). In this study, smokers were those who smoked at least 1 pack/year. None of the workers wore hearing protection devices regularly.

The noise in each unit of the factory (i.e., spray drying, forming, drying, glazing, firing, packing, and loading) was measured and the mean exposure of the subjects according to their workstation was calculated. An 8-h equivalent continuous noise level in A-weighted network (LAeq8h) was measured by a calibrated sound level meter (Casella CEL-383, Bedford, England). Measuring time was around 3-5 min in each square, the sound level meter was read at a time interval of 60 s over the measurement duration, and arithmetic mean was calculated.

Then, otoscopic examination was performed for all subjects by an occupational medicine resident (6 subjects were excluded due to abnormal otoscopic examination). Then DP-OAEs were recorded for all subjects (device: Madsen's Capella 1089, Denmark) in the fast screen mode by the DPgram method. The f2/f1 (pure tone frequencies) ratio was kept at 1.2:1. At first, noise floor was measured for all frequencies. Frequency from 1,000 Hz to 8,000 Hz was tested. Primary tone intensity levels for f1 (L1) was 65 dB-SPL and for f2 (L2) was 55 dB SPL. Testing was conducted for 3 min in each ear across the frequency range. All testing was conducted in a quiet test room, according to the guidelines of ISO8253-1.[23] All tests were performed by an audiologist blinded to the study. Abnormal result of DP-OAE was considered as lower than 10 dB sound pressure level (SPL) response amplitude above noise floor in each frequency.[24]

The study was approved by the Ethics Committee of Shahid Sadoughi University of Medical Sciences (number ≠ 2428). Informed consent was obtained from all participants. Data were analyzed by SPSS software (IBM Corp. Released 2010. IBM SPSS Statistics for Windows, Version 19.0. Armonk, NY: IBM Corp.) using Student's t-test and Mann-Whitney U test. Kolmogorov-Smirnov test was used to evaluate the normality of data.


A total of 224 tile and ceramic workers exposed to hazardous noise (higher than 85 dB) were evaluated. One hundred and five subjects were smokers (case group) and 119 individuals were nonsmokers (control group). The mean age and work experience of the subjects were 34.45 ± 5.36 years (range: 21-50 years) and 10.23 ± 5.06 years (range: 2-24 years), respectively. All subjects were exposed to 91.08 ± 2.29 dBA [time-weighted average (TWA) for an 8 h work shift]. There was no statistically significant difference between the two groups regarding age, work experience, and exposure to noise [Table 1].

Table 1
Comparison of demographic data between the case group and the control group

Kolmogorov-Smirnov test showed that DP-OAE response amplitudes at all frequencies did not obey normal distribution (P < 0.001 for all frequencies in each ear). DP-OAE response amplitudes were compared between smokers and nonsmokers and the difference was significant at all frequencies [Table 2].

Table 2
Comparison of mean response amplitudes obtained by DP-OAEs between the two groups (Mann-Whitney U test)

Table 3 shows the frequency of abnormal amplitudes of OAEs in different frequencies in each ear while comparing the noise floor.

Table 3
Frequency of abnormal response amplitude of OAEs in each ear in different frequencies considering smoking status


NIHL is an irreversible occupational disorder that can be prevented by HCP. Periodic evaluations of hearing among workers with exposure to noise constitute one of the main activities in HCP, which helps in early case finding. Recently, OAEs have been proposed as a test for the early diagnosis of NIHL. Some studies have shown OAEs to be more sensitive to noise than PTA.[10,25]

Smoking as a risk factor for hearing loss is a concern but data are controversial about its effect on hearing and its impact on NIHL when a worker is simultaneously exposed to noise and smoking. Similar to noise, smoking affects 4,000 Hz most frequently than other frequencies.[16,22,26] In a study, it has been shown that smoking affects 1,000 Hz and 4,000 Hz in transient evoked OAEs (TE-OAEs).[13]

In this study, we evaluated the simultaneous effects of noise and smoking on DP-OAE response amplitude in workers exposed to hazardous noise. The workers were selected from the tile and ceramic industry and their demographic data and noise exposure were similar.

In the current study, we found that both smokers and nonsmokers suffered from hearing loss. DP-OAE response amplitude was significantly lower among smokers. Abnormal response amplitude was observed most frequently at 6,000 Hz followed by 4,000 Hz in both ears, probably due to the noise spectrum in the tile and ceramic industry. Smokers more frequently showed abnormal DP-OAE response amplitude based on noise floor measurements. We could not find other studies on the effect of smoking and noise on OAEs.

This study had some advantages. In this study, the simultaneous exposure to noise and cigarette on hearing was evaluated by DP-OAEs in addition to conventional audiometry. We compared DP-OAE response amplitude among two similar groups regarding the exposure to noise, age, and work experience. This study had some limitations as well. We could not assess how the workers used hearing protection devices in detail. We excluded the females due to their small number, so the results could not be extrapolated to female workers.


This study showed that smoking can aggravate the effect of noise on response amplitudes of DP-OAEs.


Source of Support: Nil

Conflicts of Interest: None declared.


1. Schindler DN, Jackler RK, Robinson ST. Hearing loss. In: Ladou J, editor. Occupational and Environmental Medicine. 4th ed. New York: McGraw-Hill; 2007. pp. 104–20.
2. Robinowitz PM, Rees TS. Occupational hearing loss. In: Rosenstock L, editor. Clinical Occupational and Environmental Medicine. 2nd ed. Philadelphia: Saunders; 2005. pp. 426–35.
3. Hong O. Hearing loss among operating engineers in American construction industry. Int Arch Occup Environ Health. 2005;78:565–74. [PubMed]
4. U.S. Department of Labor. Occupational Safety and Health Administration (USDOL OSHA) Noise and Hearing Conservation. 2002. [Last accessed on 2014 May 12]. Available from: http://www.osha- .
5. Luxembourg: European Agency for Safety and Health at Work (EASHW); 2000. European Agency for Safety and Health at Work (EASHW). Monitoring: The State of Occupational Safety and Health in the European Union — Pilot Study.
6. US Department of Labor (USDL). Occupational Safety and Health Administration (OSHA). Occupational Noise Exposure, Hearing Conservation Amendment: Final Rule. Fed Regist. 1983;48:9738–85.
7. Meyer JD, McCunney RJ. Occupational exposure to noise. In: Rom WN, editor. Environmental and Occupational Medicine. Philadelphia: Lippincott Williams & Wilkins; 2007. pp. 1296–310.
8. Daniell WE, Swan SS, McDaniel MM, Stebbins JG, Seixas NS, Morgan MS. Noise exposure and hearing conservation practices in an industry with high incidence of workers’ compensation claims for hearing loss. Am J Ind Med. 2002;42:309–17. [PubMed]
9. Mehrparvar AH, Mirmohammadi SJ, Ghoreyshi A, Mollasadeghi A, Loukzadeh Z. High-frequency audiometry: A means for early diagnosis of noise-induced hearing loss. Noise Health. 2011;13:402–6. [PubMed]
10. Baradarnfar MH, Karamifar K, Mehrparvar AH, Mollasadeghi A, Gharavi M, Karimi G, et al. Amplitude changes in otoacoustic emissions after exposure to industrial noise. Noise Health. 2012;14:28–31. [PubMed]
11. Desai A, Reed D, Cheyne A, Richards S, Prasher D. Absence of otoacoustic emissions in subjects with normal audiometric thresholds implies exposure to noise. Noise Health. 1999;1:58–65. [PubMed]
12. Sliwinska-Kowalska M, Kotylo P, Hendler B. Comparing changes in transient-evoked otoacoustic emission and pure-tone audiometry following short exposure to industrial noise. Noise Health. 1999;1:50–7. [PubMed]
13. Paschoal CP, Azevedo MF. Cigarette smoking as a risk factor for auditory problems. Braz J Otorhinolaryngol. 2009;75:893–902. [PubMed]
14. Ohgami N, Kondo T, Kato M. Effects of light smoking on extra-high-frequency auditory thresholds in young adults. Toxicol Ind Health. 2010;27:143–7. [PubMed]
15. Oliveira DC, Lima MA. Low and high frequency tonal threshold audiometry: Comparing hearing thresholds between smokers and non-smokers. Braz J Otorhinolaryngol. 2009;75:738–44. [PubMed]
16. Nakanishi N, Okamoto M, Nakamura K, Suzuki K, Tatara K. Cigarette smoking and risk for hearing impairment: A longitudinal study in Japanese male office workers. J Occup Environ Med. 2000;42:1045–9. [PubMed]
17. Foda NM, Fouad HM, Mostafa PM. Combined effect of smoking and occupational noise exposure on hearing. Bull Alex Fac Med. 2008;44:785–93.
18. Lindgren T, Wieslander G, Dammstrom BG, Norback D. Hearing status among commercial pilots in a Swedish airline company. Int J Audiol. 2008;47:515–9. [PubMed]
19. Karlsmose B, Lauritzen T, Engberg M, Parving A. A five-year longitudinal study of hearing in a Danish rural population aged 31-50 years. Br J Audiol. 2000;34:47–55. [PubMed]
20. Starck J, Toppila E, Pyykkö I. Smoking as a risk factor in sensory neural hearing loss among workers exposed to occupational noise. Acta Otolaryngol. 1999;119:302–5. [PubMed]
21. Brant LJ, Gordon-Salant S, Pearson JD, Klein LL, Morrell CH, Metter EJ, et al. Risk factors related to age-associated hearing loss in the speech frequencies. J Am Acad Audiol. 1996;7:152–60. [PubMed]
22. Mizoue T, Miyamoto T, Shimizu T. Combined effect of smoking and occupational exposure to noise on hearing loss in steel factory workers. Occup Environ Med. 2003;60:56–9. [PMC free article] [PubMed]
23. Kemp DT. Otoacoustic emissions, their origin in cochlear function, and use. Br Med Bull. 2002;63:223–41. [PubMed]
24. Gettke JT, Robinette MS. Otoacustic emission. In: Roeser RJ, Valente M, Hosford-Dunn H, editors. Audiology: Diagnosis, Treatment and Practice Management. 2nd ed. New York: Thieme Medical Publishers; 2007. pp. 478–94.
25. Attias J, Horovitz G, El-Hatib N, Nageris B. Detection and clinical diagnosis of noise-induced hearing loss by otoacoustic emissions. Noise Health. 2001;3:19–31. [PubMed]
26. Uchida Y, Nakashimat T, Ando F, Niino N, Shimokata H. Is there a relevant effect of noise and smoking on hearing? A population-based aging study. Int J Audiol. 2005;44:86–91. [PubMed]

Articles from Noise & Health are provided here courtesy of Wolters Kluwer -- Medknow Publications