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|Year : 2013
: 15 | Issue : 62 | Page
|Effect of cigarette smoking on noise-induced hearing loss in workers exposed to occupational noise in China
Liyuan Tao1, Robert Davis2, Nicholas Heyer3, Qiuling Yang4, Wei Qiu2, Liangliang Zhu4, Nan Li5, Hua Zhang5, Lin Zeng5, Yiming Zhao1
1 Research Center of Clinical Epidemiology; Research Center of Occupational Medicine, Peking University 3rd Hospital, Beijing 100191, China
2 Auditory Research Laboratory, State University of New York at Plattsburgh, 107 Beaumont Hall, Plattsburgh, New York 12901, USA
3 Battelle Centers for Public Health Research and Evaluation, Seattle, WA, USA
4 Dongfeng Institution of Occupational Disease Prevention, Shi Yan 442001, China
5 Research Center of Clinical Epidemiology, Peking University 3rd Hospital, Beijing 100191, China
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|Date of Web Publication||14-Feb-2013|
Excessive exposure to high noise level environments has the potential to cause noise-induced hearing loss (NIHL), and cigarette smoking has also been shown to have a potential adverse effect on hearing. The aim of this study was to determine whether smoking interacts with noise in the development of hearing loss, and if so, the extent of the contribution from smoking on NIHL. A cross-sectional study was designed to assess the effect of smoking on NIHL in 517 male workers (non-smokers: N = 199; smokers: N = 318) exposed to a high-level industrial noise environment in China. Shift-long temporal waveforms of the noise that workers were exposed to for evaluation of noise exposures, and audiometric threshold measures were obtained on all selected subjects. The subjects used hearing protection devices only within the last 1-2 years. The results suggest that smoking has an adverse effect on NIHL in workers exposed to high level industrial noise, i.e., the median high frequency hearing thresholds were significantly greater in smokers than non-smokers exposed to noise for more than 10 years. This effect was observed at 4.0 and 6.0 kHz. Smoking did not have an adverse effect on NIHL in workers exposed to noise less than 10 years. Multivariate regression analysis revealed that the odds ratio (OR) for high frequency hearing loss (i.e., hearing threshold greater than 40 dB at 4.0 kHz) were 1.94 for smokers in comparison to non-smokers. The results suggest that: (1) smokers have a higher risk of developing high frequency hearing loss than non-smokers with a similar occupational noise exposure, and (2) the interaction between cigarette smoking and high-level noise exposure may be additive. There is a need to develop and analyze a larger database of workers with well-documented exposures and smoking histories for better understanding of the effect of smoking on NIHL incurred from high-level industrial noise exposures. A better understanding of the role of smoking may lead to its incorporation into hearing risk assessment for noise exposure.
Keywords: Cigarette smoking, hearing loss, occupational noise exposure study
|How to cite this article:|
Tao L, Davis R, Heyer N, Yang Q, Qiu W, Zhu L, Li N, Zhang H, Zeng L, Zhao Y. Effect of cigarette smoking on noise-induced hearing loss in workers exposed to occupational noise in China. Noise Health 2013;15:67-72
|How to cite this URL:|
Tao L, Davis R, Heyer N, Yang Q, Qiu W, Zhu L, Li N, Zhang H, Zeng L, Zhao Y. Effect of cigarette smoking on noise-induced hearing loss in workers exposed to occupational noise in China. Noise Health [serial online] 2013 [cited 2020 Aug 6];15:67-72. Available from: http://www.noiseandhealth.org/text.asp?2013/15/62/67/107159
| Introduction|| |
Noise is one of the most pervasive and important physical hazards in industrial working environments.  Excessive noise can cause many adverse effects, including elevated blood pressure, reduced performance, sleeping difficulties, annoyance and stress, tinnitus and noise-induced hearing loss (NIHL). The most serious health effect is NIHL resulting from irreversible damage to the inner ear. , NIHL results in a large social and economic burden on the society. It is estimated that there are approximately 278 million people with hearing disabilities in the world,  and 22 million U.S. workers are exposed to hazardous noise levels at work.  Hearing loss (adult onset) is the 15 th greatest cause of the burden of disease as defined by a disability-adjusted life year in both sexes and all ages.  NIHL is permanent and irreversible, but it is completely preventable.  Cigarette smoking is one of the most common habits in the world, especially in China. According to the World Health Office, China has 320 million smokers which represent about one third of the world's total smokers.  The underlying pathogenic mechanisms are the established vascular changes which include cochlear hypoxia, capillary vasoconstriction, and increased blood viscosity related to smoking. ,,
Cigarette smoking as a risk factor for NIHL has been analyzed in several studies. Studies have associated cigarette smoking with poorer hearing thresholds. ,, A few studies have established a positive association between smoking and NIHL, ,, and the presence of a synergistic effect between smoking and noise exposure. , One study concluded the combined effect is additive.  In contrast, very little to no effect of smoking on hearing loss has also been reported in several studies. ,,,, In light of the above conflicting results, additional research is needed to better understand of the effect of smoking as a risk factor for NIHL. The objective of this study, therefore, is to determine whether smoking is an independent risk factor for NIHL, and the extent, if any, of the interaction between smoking and noise exposure.
| Methods|| |
Study design and subject selection
A cross-sectional approach was adopted in this study. Subjects included male workers (N0 = 517) employed in an auto manufacturer in Shiyan, China. Female workers were not included in this study because of their low-noise exposure and incidence of smoking. Of the 517 workers, 199 were non-smokers and 318 were smokers. All candidate subjects were required to complete a physical examination and health- related information questionnaire, which was followed by a face-to-face interview for quality control (to clarify and affirm responses).
The average age and noise exposure duration (NED) were 37.87 years (±6.38) and 17.28 years (±7.60), respectively. Exposure to excessively high noise levels (LAeq,8h ) ≥80 dB(A)] was the only occupational hazard in this factory. The workforce, processes and machinery were stable for a number of years. Workers were employed in high level noise environments consisting of unsteady continuous and impact noise. There was no use of hearing protective devices (HPD) by workers prior to the recent use of HPDs mandated in the last 1-2 years of employment.
The subjects for this study were selected based on the following inclusion criteria: (1) The noise exposure level (LAeq,8h ) ≥80 dB(A), (2) NED ≥ 1 year, and (3) male workers who had a stable occupational noise exposure history. Exclusion criteria included the following: (1) asymmetrical hearing loss (>10 dB at any one frequency between the ears) or conductive hearing loss, (2) uncontrolled systemic illness, (3) frequent recreational noise exposure, (4) history of head injury or otologic surgery, (5) history of ototoxic drug use, (6) chronic middle ear pathology, and (7) family history of hearing loss. Subjects were introduced to the purpose of and procedures to be followed in this study by an occupational physician. The research protocol was approved by the Ethics Committee, and all subjects participated voluntarily in this study.
Smoking status survey
Health-related lifestyle information, including drinking and smoking data, was obtained at the time of the physical examination, using a face-to-face interview. Queries on smoking habit included smoking status (non-smokers and smokers), the start date, and daily doses for smokers.
Audiometry and hearing loss classification
Each subject that passed the screening protocol was given a general physical and an otologic examination. Pure tone audiometry was performed according to ISO 8253 standards in an isolated acoustic room with a calibrated pure-tone audiometer (MADSEN ITERA) by an audiologist. Hearing thresholds were measured at frequencies of 0.5, 1, 2, 3, 4 and 6 KHz in each ear and at least 16 h after the subjects' last occupational noise exposure. The following indicators were adopted to categorize hearing status: (1) high-frequency hearing thresholds (HFHT: Average hearing threshold at 3, 4 and 6 KHz in both ears), (2) low frequency hearing thresholds (LFHT: Average hearing threshold at 0.5, 1 and 2 KHz in both ears), (3) high -frequency hearing loss (HFHL: Hearing threshold greater than 40 dB at 4 kHz in the worse ear), and (4) low frequency hearing loss (LFHL: Hearing threshold greater than 25 dB at 1 kHz in the worse ear.
Noise exposure measurement
Each subject's NED was determined from their occupational history. Noise exposure levels were measured using personal noise dosimeters (Aihua, Model AWA5610B, Hangzhou, China) to determine the equivalent continuous A-weighted sound pressure level over 8 h (LAeq,8h ). The high stability of the subjects' job status and associated noise exposure afforded us the advantage of obtaining relatively accurate NED and LAeq,8h .
Calibrations were performed before and after each usage with a Model AWA6221A Sound Level Calibrator (Aihua Instruments, Hangzhou, China). Dosimeters were worn by each worker over an 8.5 h period in 1 day. The microphone was covered with a windscreen and placed near the workers' collars. The logging period was 2 s which allowed for the collection of 14,400 two seconds A-weighted equivalent continuous sound levels (LAeq,2s ) over the noise assessment period. The results revealed a noise exposure level ranging between 80.10 and 118.40 dB(A) among the subjects. The mean noise exposure level was 91.02 (±6.12) dB(A).
The cumulative noise exposure (CNE), a composite noise exposure index was used to quantify the noise exposure for each subject. The CNE is defined as:
Where is the equivalent continuous A-weighted noise exposure level normalized to 8 h working day, in decibels, occurring over the time interval Ti in years; n is the total number of different noise levels (i.e., different working tasks/environments) the subject was exposed to during their employment history and Tref = 1 y. Since all subjects in this study were employed in one working environment, n was set equal to 1 and Ti simplified as T. Thus, for the subjects in this study n = i = 1 and equation 2 can be written as follows: 
LAeq,8h is the equivalent continuous A-weighted noise exposure level normalized to an 8-h working day, and T is occupational history in years.
Data were analyzed using predictive analytics software statistics (Release 18.0.0). The quantitative parameters followed the normal distribution, expressed as and tested by independent t-tests. The audiometric data were expressed as median values and analyzed by the non-parametric Mann-Whitney Test between the high and low NED, and smoking status groups. Pearson's Chi-square test and Fisher's exact test were applied to examine differences between the groups for categorical parameters. Association of hearing loss with smoking status was examined by multivariable binary logistic regression. The variables of age, CNE and smoking status (age and CNE as continuous variables, smoking status as categorical variable) were included in a logistic regression model using Backward Stepwise (Likelihood Ratio). All reported P values were two tailed, and P < 0.05 was established as the level of significance.
| Results|| |
The descriptive statistics of workers in the non-smoking and smoking groups are illustrated in [Table 1]. No significant difference was detected in the frequency of HPD use between the smoking and non-smoking groups ( x2 = 0.202, P = 0.904). Since the subjects used HPD (e.g., earplugs) only within the last 1-2 years, with the use of HPD virtually non-existent before that time, the effects of using HPDs were equivalent in the smoker and non-smoker groups.
|Table 1: Descriptive statistics of workers in non-smoking and smoking groups|
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The average age and the NED in non-smokers were significantly less than in smokers ( P < 0.05). Since the NED was a major risk factor for hearing loss, the data were divided into two groups, e.g., low NED (≤10 years) and high NED (>10 years). As shown in [Table 2], the average age, NED, LAeq,8h and CNE in non-smokers were very similar to that in smokers in both the low and high NED groups. In the high NED group, the median HFHT in smokers was significantly poorer (7.1 dB) than in non-smokers ( P = 0.001).
|Table 2: Descriptive statistics of non-smokers and smokers in two separate noise exposure duration groups|
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The average hearing thresholds in the workers who smoked and did not smoke for both the low (≤10 years) and high (>10 years) NED groups are shown in [Figure 1]. In the high NED group, significantly poorer (8-10 dB) thresholds at 4 and 6 kHz were observed in smokers than in non-smokers ( P = 0.01). There were no significant effects of smoking in the low NED group. Thresholds were generally poorer in smokers by approximately 2-3 dB at most test frequencies in each NED group, although this difference was not significant at test frequencies except at 4 and 6 kHz in the high NED group. The results in [Table 3] also illustrate the significant effect (i.e., poorer hearing thresholds) of smoking on the HFHL (i.e., hearing threshold at 4 kHz greater than 40 dB in the worse ear) in the high NED group. Approximately, 50% of smokers ( N = 133 out of 272) demonstrated hearing thresholds at 4.0 kHz greater than 40 dB in the worse ear in the high NED group. In comparison, only 34% of non-smokers illustrated this same effect. In contrast, smoking did not have a significant effect for the LFHL (i.e., hearing threshold at 1 kHz greater than 25 dB in the worse ear) or HFHL indicators in the low NED group.
A multivariable binary logistic regression analysis was employed to assess the relationships among HFHL, age, CNE, and smoking status [Table 4]. The dependent variable was HFHL, and the independent variables were age, CNE, smoking status and the interaction of CNE with smoking status (age and CNE as continuous variables). The results showed that age, CNE and smoking status were significant (P < 0.05). The workers who smoked were 1.94 times more likely to have a HFHL than non-smokers (95% confidence interval, 1.31-2.88). The same analysis performed with age adjusted hearing levels also revealed similar results (e.g., the OR of smoking for hearing loss was 2.23 (95% CI = 1.46-3.39).
|Figure 1: Comparison of the binaural hearing thresholds' median between smokers and non - smokers in low (a) and high (b) noise exposure duration groups *Significant differences (P < 0.05)|
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|Table 3: Comparison of hearing loss between non-smokers and smokers in low and high noise exposure duration groups|
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|Table 4: Adjusted odds ratio and 95% confidence intervals for high frequency hearing loss for age, cumulative noise exposure, and smoking status|
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| Discussion|| |
The results indicated that smoking can have an adverse effect (i.e., additive) on the hearing status of workers exposed to high levels of industrial noise found in this study (noise exposure level ranged between 80.10 and 118.40 dB(A) and mean noise exposure level was 91.02 (±6.12) dB(A). Thus, smoking should be considered an important variable in determining the hazards to hearing posed by a high-level industrial noise environment for hearing conservation purposes. This conclusion is based on the results which showed that: (1) the average hearing thresholds at 4 and 6 kHz in smokers were significantly higher (8-10 dB) than in non-smokers
(P < 0.05), and (2) there was a significantly higher incidence of HFHL in smokers (48.9%) than non-smokers (33.8%) in the high NED group. This outcome is consistent with several studies on the relationship between cigarette smoking and NIHL, ,,,,,,,, which indicated that smoking can increase the probability of hearing impairment. The multivariable binary logistic regression analysis adopted in our study indicated that the OR for HFHL (hearing threshold at 4 kHz greater than 40 dB in the worse ear) compared with non-smokers was 1.94 for smokers (95% CI = 1.31-2.88). This result is similar to that revealed in several studies (OR = 1.48-2.20). ,, but below that reported in others (OR = 4.20-21.0). ,, One important variable contributing to this difference may be due to the different hearing loss criterion adopted among studies. That is, our study used the hearing threshold at 4 kHz greater than 40 dB in the worse ear as the hearing loss criterion, whereas, other studies employed the hearing threshold at 4 kHz of more than 25 dB in the better ear as the criterion.
In light of the above results, it should be noted that recent studies, , which have attempted to evaluate the ISO-1999 database commonly used to compensate for age-related hearing loss [i.e., to determine noise-induced permanent threshold shift (NIPTS)], revealed the following results: (1) there was a greater amount of NIPTS in men (65-74 years) than that observed in the 1999-2006 National Health and Nutrition Examination Survey (NHNES), i.e., prevalence of hearing impairment was lower in the 1999-2006 NHNES in comparison to the 1959-1962 database,  and (2) using the 1999-2002 NHNES (N = 3527), occupational noise exposure was significantly associated with several non-occupational noise factors (e.g., smoking, educational level, leisure time and firearm noise).  The implication of the findings above suggest that: (1) the use of the 1999-2006 NHNES database (instead of ISO-1999) would result in greater NIHL in unscreened older male adults, and (2) an overestimation of NIHL may occur using the ISO-1999 age-correction database if non-occupational noise factors (e.g., smoking, educational level, leisure time and firearm noise) are not considered.
The results from our study indicate an additive effect between smoking and occupational noise exposure. This conclusion is based on the following: (1) the interaction of CNE and smoking status was removed from our logistic model, and (2) the OR of smoking in noise exposed subjects (1.31-2.88) was similar to that reported in others studies (1.7-3.2) without occupational noise exposure. ,,,, While a few studies formed a different conclusion, ,, (i.e., synergistic effect between smoking and occupational noise exposure), the present study is the only large-scale study to assess the association between cigarette smoking and NIHL using personal noise dosimeters to measure the workers' noise exposure. Previous studies used work place environmental noise or a job exposure matrix to estimate the subjects' real noise exposure. ,,,,,,,, Only one other study employed personal noise dosimetry in a comparatively small group of 18 employees. 
One limitation of this study was the inability to establish a dose-response relationship between the amount of cigarette smoking and NIHL. Although surveys were confidential and answers recorded anonymously, there was a lack of subject-reporting of the amount of smoking on a daily basis. However, a few studies have reported a dose-response relation between the number of cigarettes and hearing impairment among noise-exposed workers. , Additional research should focus attention on the evidence for synergistic effects from smoking, noise and age on hearing loss.
The large variability in NIHL has been attributed to the variation in acoustic transfer characteristics of the external auditory meatus,  contribution of the stapedius reflex to protection from noise exposures, , and/or genetic factors. , Recently, gene expression differences induced by a noise exposure were demonstrated in mice.  Other intrinsic factors such as gender, race, hypertension, diabetes, and external factors, ,, which include ototoxicity, leisure noise exposure, smoking, solvents  and use of HPD, have been reported. These potential factors, combined with the parameters of the noise exposure itself (e.g., Leq , duration, interrupted, intermittent, and time varying) contribute, in varying ways, to the probability of developing NIHL and the magnitude of NIHL among individuals exposed to equal acoustic energy exposures.
The results from this present study support a simple additive effect from smoking and noise on hearing which may be consistent with a potentiation of NIHL caused by simultaneous carbon monoxide exposure , from smoking and to exposure to hazardous noise over time.  Evidence for synergistic effects from smoking, noise and age on hearing loss  and a multiplicative effect from smoking and age on hearing loss  have been reported. The underlying pathogenic mechanisms are the established vascular changes (i.e., cochlear hypoxia, capillary vasoconstriction, and increased blood viscosity) related to smoking and also to long-term intense noise exposure. ,,,, Compounding the effects noted above may be the age-related degenerative changes of neural fibers and vascular structures of the cochlea which affect the high frequencies.  Additionally, cigarette burning, which releases organic solvents (i.e., toluene, styrene, xylene and also lead, mercury and carbon monoxide), have been described as independent factors and in synergism for the combined effects of noise and organic solvents. 
The results from the present study (i.e., additive effect between smoking and noise exposure on hearing loss), suggest that hearing conservation programs should educate workers about the increased risk of developing NIHL from smoking and exposure to high occupational noise levels exceeding 85 dB(A). These workers should be encouraged to quit smoking and be closely monitored for changes in hearing status, e.g., audiometric evaluation should be increased to more than once per year. Consideration for removing workers who smoke from high (>85 dB(A)) to lower noise level environments may be made to help reduce the risk for developing NIHL and related occupational compensation claims.
| Conclusion|| |
The results from the present study suggest that smokers have a higher risk of developing HFHL than non-smokers with a similar occupational noise exposure, i.e., cigarette smoking and occupational noise exposure may act in an additive manner in the production of hearing loss. However, the inherent large variability in NIHL among subjects, in combination with the relatively small sample sizes in several studies, emphasize the need to develop and analyze a larger database of workers with well-documented exposures and smoking behavior (i.e., dose) to better understand the interaction effect of smoking on NIHL from high level industrial noise exposures. This will enable us to define the variables (e.g., duration, amount, age) associated with smoking that is needed to increase the risk and/or magnitude of NIHL. A better understanding of the role of smoking in NIHL may lead to its incorporation into a new generation of more predictive hearing risk assessment for noise exposure provided that smoking behavior, noise exposure, and hearing loss data can continue to be acquired from suitably designed epidemiological studies.
| Acknowledgments|| |
We expressed our appreciation to all the employees and the Dongfeng Institution of Occupational Disease Prevention for their valuable cooperation for this study. This work was supported by Grant No. 1-R01-OH-002317 from the National Institute for Occupational Safety and Health.
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Research Center of Occupational Medicine, Research Center of Clinical Epidemiology, Peking University Third Hospital, Beijing 100191
Source of Support: Grant No. 1.R01.OH.002317, National Institute for Occupational Safety and Health,, Conflict of Interest: None
[Table 1], [Table 2], [Table 3], [Table 4]
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