Portuguese Version

Year:  2003  Vol. 69   Ed. 5 - (14º)

Artigo Original

Pages: 681 to 689

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Distortion product otoacoustic emissions in workers exposed to lead & noise

Author(s): Kátia de F. Alvarenga1,
Lilian C. B. Jacob2,
Carlos Henrique F. Martins3,
Orozimbo A. Costa4,
Carmem Z. V. Coube5,
Jair Mendes Marques6

Keywords: lead, otoacoustic emissions, noise, hearing loss

Abstract:
Currently, legislations concerning worker's health only require periodic monitoring of individuals who are noise-exposed at work, and exposure to chemicals are not taken into consideration. However, the scientific literature indicates a very clear concern regarding the effects of lead on the auditory system, demonstrating that there are negative effects to the auditory system following occupational exposure to this metal. Aim: The aim of this study was to evaluate the amplitude of distortion product otoacoustic emissions (DPOAEs) among individuals with a history of exposure to lead and noise. Study design: Transversal Cohort. Material and method: We evaluated 69 individuals divided in 3 groups: Group I (GI): composed by 29 workers occupationally exposed to both lead and noise; Group II (GII): composed by 11 noise-exposed workers with no other exposure to ototraumatic, and Group III (GIII): composed by 11 individuals with normal hearing and no history of exposure to noise or lead. Results: The results showed no effect of lead exposure on the otoacoustic emission results, since the smaller EOEPD amplitudes were observed in the noise-exposed group, despite the fact that the lead and noise exposed workers had a long history of lead exposure, and a wide variability in blood lead levels.

INTRODUCTION

Currently, the occupational national legislation in Brazil requires hearing to be monitored only when there is occupational exposure to noise, disregarding exposure to chemicals. However, the scientific literature is very specific in presenting its concerns about the effects of such toxic agents in hearing systems.

Specifically considering lead, Jacob et al.1 conducted a critical analysis of the literature showing evidence of the harmful effects of occupational exposure to this metal in the hearing system. However, there are still some obscure issues, especially concerning the difficulties to define a cause-effect relation, owing to the variables common to industry workers, such as simultaneous and/or previous exposure to noise. This and other flaws in the methodology employed by many clinical trials have been questioned by the studies of Repko and Corum2 and Cary et al.3.

The studies conducted in laboratory with guinea pigs treated with daily doses of lead allow the precise control of variables such as duration of exposure and lead levels in the body, without concomitant exposure to other toxic agents to the hearing system. Thus, such experiments are extremely important to define the real effect of lead, but they do not reflect the reality of the workers who normally present previous or current history of exposure to other harmful hearing agents, such as noise.

There are studies that confirmed with histopathological analyses the absence of cochlear lesion in guinea pigs exposed to lead, reaching a consensus about the impairment of neural structures (Gozdzik-Zolnierkiewicz and Moszynski4; Yamamura et al.5,6; Lilienthal et al.7; Lasky et al.8); conversely, there are clinical studies developed in lead-exposed workers that showed contradictory results. The significant correlation between level of blood lead and hearing loss was described by Repko and Corum2, Otto et al. 9, Guedes et al.10; Farahat et al.11; Forst et al.12 , but it was not confirmed by Baloh et al.13. In a publication about hearing prevention programs 4, it was reported the absence of interaction between lead and noise in the onset of hearing affections, however, Counter and Buchanan15 stated that environmental noise exposure is a determinant factor in the occurrence of hearing loss found in subjects occupationally exposed to lead.

Such contradictory results, especially concerning alterations of pure tone detection, seem to be explained by the action of lead in the hearing system, that is, the hearing loss caused by this metal is probably not perceived at the cochlea level, but rather results from the impairment of nervous impulse conduction. This observation was described by Rice16 in the studies with guinea pigs, in which they observed high thresholds with disordered patterns of responses, quite differently from those found in cochlear pathologies caused by agents that damage the outer hair cells of Corti's organ.

The results of current studies are directed to the neurotoxic effects of lead in the hearing system, demonstrated by audiological procedures that allow a more precise and segmented assessment of this system.

Within such context, we can point out the study of otoacoustic emissions, which allows the functional assessment of outer hair cells. In the area of occupational audiology, the effect of noise over the cochlea has been widely discussed and confirmed by investigations with otoacoustic emissions. Conversely, studies with lead and distortion product otoacoustic emissions (DPOAE) in an experimental study 7 or clinical study (Buchanan et al.17) suggested little or no clinical or sub-clinical evidence that high lead blood levels have a toxic effect over the cochlea.

Based on this premise and the involvement in studies in this area, in 1998, the University of Sao Paulo - Campus Bauru - together with Universidade Tuiuti do Paraná, created a research study whose main objective was to investigate the effects of lead in the hearing system using complementary and electrophysiological tests.

The present study aimed at analyzing the effects of lead intoxication in the cochlea using otoacoustic emissions in subjects with history of lead and noise exposure.

MATERIAL AND METHOD

The data collection was conducted at Centro de Pesquisas Audiológicas do Hospital de Reabilitação de Anomalias Craniofaciais, University of Sao Paulo.

Characterization of the sample
The study gathered 66 subjects subdivided into 3 groups:

a) Group I (GI): comprising 21 workers exposed to lead and simultaneous exposure to noise in a battery plant;
b) Group II (GII): comprising 21 workers exposed to occupational noise without simultaneous or previous exposure to other hearing harmful agents; and
c) Group III (GIII): comprising 24 subjects with normal hearing, without history of occupation noise exposure or other risk factors that lead to hearing loss.

Considering the total exposure time, based on data collected in the clinical history, we concluded that GI presented mean exposure of 9.2 years and GII of 10 years, being that the current noise exposure was similar for groups I and II, ranging from 86 to 108 dBSPL. The mean age of GI was 34.03 years; GII, 40 years, and GIII, 36.05 years.

Workers in Group I presented mean value of serum lead (Pbs) of 36.31mg/dl, being that the minimum value was 8.6 mg/dl and the maximum value was 80 mg/d, with mean lead exposure time of 7 years, ranging from 11 months to 21 years.

All subjects were submitted to ENT and audiological assessment comprising initial interview, pure tone audiometry, speech audiometry and acoustic immittance measures (tympanometry and acoustic reflex) to characterize the hearing status of subjects participating in the study. We excluded subjects who had middle ear affections.

Pure tone audiometry had air thresholds tested in frequencies 0.5 to KHz and bone conduction in 0.5 to 4 KHz. The device used was audiometer brand Siemens SD 50. We considered 25 dBHL as the acceptable threshold for normal range hearing in the area of occupation health 18. As the result, considering the assessed ears, 48% of the assessed ears in GI presented hearing loss. In GII, we observed a high percentage of affection, totaling 55% of the assessed ears. The present study was approved by the Research Ethics Committee of Hospital de Reabilitação de Anomalias Craniofaciais, University of Sao Paulo.

Distortion product otoacoustic emissions (DPOAE)
The assessment of amplitude of otoacoustic emissions was conducted by using distortion product study (DPOAE gram). Primary frequencies selected for the assessment were geometric means of f1 and f2, of about 1, 2, 3, 4 and 6 kHz (Chart 1), the proportion f2/f1= 1.22 and the mean sound stimuli (L1 = L2) of 70 dB SPL. The test was conducted in steps of 3 points/octave. We used the device Distortion Product Analyzer ILO92DP and Transient OAE Analysis (Otodynamics Ltda.).

Statistical analysis
We conducted the descriptive and comparative analysis of amplitude of DPOAE between the 3 groups using the t Student test, Variance and Tukey test, considering the total number of ears assessed in each group.

Chart 1. Primary frequencies f1 and f2 and mathematical relation 2f1 - f2.



Table 1. Descriptive statistics considering amplitude of distortion product otoacoustic emissions, total of assessed ears in groups I, II and III.



Table 2. Comparison of amplitude of distortion production otoacoustic emissions between groups I, II and III.

* Statistically significant at p < 0.05 (5%).



Table 3. Descriptive statistics considering amplitude of distortion production otoacoustic emissions (dBSPL) in ears without hearing loss in groups I, II and III.



Table 4. Comparison of amplitude of distortion production otoacoustic emissions between groups I and II, considering ears without hearing loss and ears in group III.

* Statistically significant difference at p < 0.05 (5%).

RESULTS

Table 1 and Graph 1 present the statistical description considering amplitude of DPOAE in the total ears of each assessed group. In Table 2, we can find the comparative statistical analysis of amplitude of DPOAE between groups I, II and III.

A similar analysis was conducted considering the ears without hearing loss detected in pure tone audiometry in groups I and II. Table 3 and Graph 2 present descriptive statistics considering amplitude of DPOAE in the ears without hearing loss in groups I and II. In Table 4 we can see the comparative statistical analysis of amplitude of DPOAE obtained in the ears without hearing loss in groups I, II and III.

Graph 1. Mean amplitude of distortion product otoacoustic emissions in the assessed frequencies for groups I, II and III.



Graph 2. Mean amplitude of distortion product otoacoustic emissions in the assessed frequencies considering the ears without hearing loss in groups I and II and ears in group III.

DISCUSSION

In the specific literature, the concern with the effects of lead in the hearing system is evident, being that many studies have been developed in experimental form or in human beings. Initially, the studies conducted with lead exposed workers attributed the affections to pure tone observed in audiometry to the toxic effect of the metal to the cochlea 2, 9, 10, 11, 12. However, other studies, especially in guinea pigs, did not confirm these findings 1, 3, 5, 6, 7, 8.

Despite the technological advance of the area of audiology, through which devices that allow the assessment of specific structures of the hearing system were made available, the effects of lead over them are still very widely discussed, especially the definition of the structures that are damaged by exposure to the metal.

In the present study, considering the total number of assessed ears, we found a mean amplitude in DPOAE in group I of 2.51 dBSPL, 3.77 dBSPL, -1.62 dBSPL, 1.75 dBSPL and 1.50 dBSPL, in frequencies of 1, 2, 3, 4 and 6 KHz, respectively (Table 1 and Graph 1). For group II, the values were 4.63 dBSPL, 1.71 dBSPL, 0.16 dBSPL, -1.34 dBSPL and -3.74 dBSPL, respectively (Table 1 and Graph 1). Therefore, it was possible to confirm that amplitude of DPOAE was lower in frequencies of 2, 4, and 6 kHz than in the group exposed only to noise (GII), when compared to the subjects exposed simultaneously to noise and lead (GI), with a significant difference in frequency of 6kHz (Table 2). This finding was in agreement with the audiometry since the group exposed only to noise presented higher occurrence of hearing loss (55% of the total ears in GII compared to 48% in the GI group) and consequently there was lower amplitude in DPOAE. Probably, the differences in noise exposure previous to the conduction of the study would justify this findings, being that it is a common variable when studying hearing in industry workers, which is very difficult to control 1, 2, 3.

The importance of considering noise in the analysis of hearing loss found in lead exposed workers has already been described 4.

Considering GIII, the mean amplitude of DPOAE was 6.23 dBSPL, 7.24 dBSPL, 5.74 dBSPL, 8.68 dBSPL and 13.48 dBSPL for frequencies de 1, 2, 3, 4 and 6 KHz, respectively (Table 1 and Graph 1). It is possible to observed that the mean amplitudes of DPOAE in groups I and II were lower than in GIII, which did not have history of noise and/or lead occupational exposure, with statistically significant difference in all tested frequencies except for the frequency of 1kHz in both groups and 2kHz in GI (Table 2).

The findings described above demonstrate that the mechanisms of cochlear amplification of outer hair cells of Corti's organ is affected in both groups with history of exposure to noise and/or lead. However, the toxic effect of lead in the cochlea was not evidenced, since the lower values of DPOAE amplitude were observed in the group exposed only to noise, even considering the subjects had long period of lead exposure (ranging from 11 months to 21 years, mean period of 7 years) as well as the wide variation of serum lead levels, from 8.6 mg/dl to 80 mg/d, mean value of 36.31 mg/dl. Similar results were described in previous studies 8, 15, reinforcing the hypothesis that reduced amplitude of DPOAE in lead exposure population would probably be related to simultaneous exposure to noise.

Taking into account only the ears of GI and GII that presented normal pure tone audiometry, the mean amplitudes of DPOAE in groups I and II, respectively were 5.26 dBSPL and 6.51 dBSPL, in frequency of 1 KHz; 6.67 dBSPL and 4.13 dBSPL in frequency of 2 KHz; 1.85 dBSPL and 3.13 dBSPL in frequency of 3 KHz; 3.91 dBSPL and 2.76 dBSPL in frequency of 4 KHz, and 5.36 dBSPL and -2.26 dBSPL in frequency of 6 KHz (Table 3 and Graph 2).

In Table 4 we can find the comparative analysis of amplitude of DPOAE in groups I and II without hearing loss with group III, which demonstrated statistically significant difference for the frequency of 6kHz when we compared groups I and III, and 4 and 6 kHz when we compared groups GII and normal subjects in GIII. As to GI and GII, the statistically significant difference was maintained when we analyzed the frequency of 6kHz as previously observed. These data show that the study of otoacoustic emissions is a test capable of evidencing functional alterations of outer hair cells by noise exposure, even before hearing acuity is affected, with thresholds of £25 dB17.

CONCLUSION

The results obtained in the present study led us to the conclusion that:

 amplitude of distortion product otoacoustic emissions was lower in the group of subjects exposed to noise and noise and lead simultaneously when compared to subjects without exposure to these agents;
 the investigation of otoacoustic emissions can be affected in subjects exposed to noise and noise and lead simultaneously even with hearing thresholds at 25 dB, proposed as the normal range for industry workers; and,
 the toxic effect of lead to the cochlea was not evidenced, since lower otoacoustic emissions amplitudes were observed in the group exposed only to noise, even considering that the subjects presented a long period of lead exposure, as well as high variation of serum lead levels.

REFERENCES

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16. Rice DC. Effects of lifetime lead exposure in monkeys on detection of pure tones. Fundam Appl Toxicol 1997; 36:112-8.
17. Buchanan LH, Counter SA, Ortega F, Laurell, G. Distortion product oto-acoustic emissions in Andean children and adults with chronic lead intoxication. Acta Otolaryngol 1999; 119:652-8.
18. Nudelmann, AA, Costa EA, Seligman J, Ibañez RN. Atualização sobre os documentos do Comitê Nacional de Ruído e Conservação Auditiva. In Nudelmann, AA, Costa EA, Seligman J, Ibañez RN. PAIR - Perda Auditiva Induzida Por Ruído. Rio de Janeiro: Ed Revinter, Vol II; 2001. 241p.

ANNEX - Amplitude of DPOAE in the three groups.

Key: 1 - absence of hearing loss; 2 - presence of hearing loss; DPOAE - distortion production otoacoustic emissions.

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1 Ph.D., Professor, Department of Speech and Hearing Pathology, School of Dental Sciences, Bauru. Hearing pathologist, researcher of Centro de
Pesquisas Audiológicas do Hospital de Reabilitação de Anomalias Craniofaciais de Bauru, University of Sao Paulo, campus of Bauru.
Department of Speech and Hearing Pathology
School of Dental Sciences, University of Sao Paulo
Al Dr Octávio Pinheiro Brisolla, 9-75 - CEP 17012-901
Bauru-SP - e-mail: katialv@fob.usp.br
2 Ph.D., Professor, Program of Post-graduation, Master in Human Communication Disorders, Universidade Tuiuti do Paraná, Curitiba/PR.
3 Otorhinolaryngologist, Centro de Pesquisas Audiológicas do Hospital de Reabilitação de Anomalias Craniofaciais de Bauru, University of Sao Paulo, campus Bauru.
4 Otorhinolaryngologist, Coordinator of Centro de Pesquisas Audiológicas do Hospital de Reabilitação de Anomalias Craniofaciais de Bauru. Full Professor, Department of Speech and Hearing Pathology, School of Dental Sciences, Bauru; University of Sao Paulo, campus Bauru.

5Ph.D., Professor, Department of Speech and Hearing Pathology, School of Dental Sciences, Bauru. Hearing pathologist, researcher of Centro de Pesquisas Audiológicas do Hospital de Reabilitação de Anomalias Craniofaciais de Bauru, University of Sao Paulo, campus Bauru.
6Ph.D., Professor, Program of Post-Graduation, Master in Human Communication Disorders, Universidade Tuiuti do Paraná, Curitiba/PR.
Article submitted on May 05, 2003. Article accepted on August 24, 2003.

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