Sensory-evoked potentials in rats chronically exposed to trichloroethylene: Predominant auditory dysfunction

Rebert, Charles S.; Day, Virginia L.; Matteucci, Michael J.; Pryor, Gordon T.

doi:10.1016/0892-0362(91)90031-q

Cited by 49 publications

(29 citation statements)

References 26 publications

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“…The data presented here are consistent with previous reports of ototoxicity following inhalation exposure to TCE in the rat (Rebert et al, 1991;Crofton and Zhao, 1993;Jaspers et al, 1993;Crofton et al, 1994). The effective concentrations reported by Rebert et al (1991) for 1-week (3000-3500 ppm, 8 hr/day, 5 days/week), 3-week (2000 ppm, 12 hr/day, 7 days/week), and 12-week exposures (3200 ppm, 12 hr/day, 7 days/week), as well as Jaspers et al (1993) for a 3-week exposure (3000 ppm, 18 hr/day, 5 days/week) and Albee et al (1994) for 13-week exposure (2500 ppm, 6 hr/day, 5 days/week), are fairly consistent with the LOAELs reported here.…”

Section: -Weeksupporting

confidence: 82%

“…(2) The BMC was calculated as the 95% upper limit for the dB15. This threshold was included in the model because previously published data clearly indicated concentrations for which no effects were observed (Rebert et al, 1991;Jaspers et al, 1993;Crofton and Zhao, 1993). Goodness-of-fit statistics were used to determine the significance of the lack-of-fit as follows: The fit was accepted if the test statistic F 1 [F 1 = (sum of squares lack-of-fit)/(Oack-of-fit degrees of freedom) X (pooled mean square pure error))] was less than the quantile in the F distribution corresponding to (1-a) where a = 0.01 (Clement International Corp., Ruston, LA).…”

Section: Reflex Modificationmentioning

confidence: 99%

“…Evidence for the ototoxicity of trichloroethylene has been demonstrated using animal models (Rebert et al, 1991(Rebert et al, , 1993Crofton and Zhao, 1993;Jaspers et al, 1993;Crofton et al, 1994). The use of high concentrations in animal experiments have hampered calculation of noncancer risk estimates for the ototoxicity of long-duration, low-concentration exposures.…”

mentioning

confidence: 99%

“…The use of high concentrations in animal experiments have hampered calculation of noncancer risk estimates for the ototoxicity of long-duration, low-concentration exposures. Animal research has carefully documented exposure concentrations and durations, although all of this research has employed concentrations in the range of 1000 to 4000 ppm (Rebert et al, 1991;Crofton and Zhao, 1993;Jaspers et al, 1993). The question remains as to the relevance of these findings to human environmental exposures, especially to nonoccupational ambient air exposures.…”

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confidence: 99%

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The Ototoxicity of Trichloroethylene: Extrapolation and Relevance of High-Concentration, Short-Duration Animal Exposure Data

Crofton

Zhao

1997

Toxicol Sci

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Inhalation exposure to high concentrations of 1,1,2-trichloroethylene (TCE) has been shown to damage hearing in the mid-frequency range in the rat The present study directly evaluated the adequacy of high-concentration, short-term exposures to TCE for predicting the neurotoxicity produced by longer duration exposures. Adult male Long-Evans rats (n = 10-12 per group) were exposed to TCE via inhalation (whole body) in 1-m 3 stainless steel flow-through chambers for 6 hr/day, 5 days/week. The following exposures were used: 1 day (4000-8000 ppm), 1 week (1000-4000 ppm), 4 weeks (800-3200 ppm), and 13 weeks (800-3200 ppm). Air-only exposed animals served as controls. Auditory thresholds were determined for a 16-kHz tone 3-5 weeks after exposure using reflex modification audiometry. Results replicated previous findings of a hearing loss at 16 kHz for all exposure durations. The dB15 concentrations (concentration that increases thresholds by 15 dB) for 16-kHz thresholds were 6218, 2992, 2592, and 2160 ppm for the 1-day, 1-week, 4-week and 13-week exposures, respectively. These data demonstrate that the ototoxicity of TCE was less than that predicted by a strict concentration x time relationship. These data also demonstrate that simple models of extrapolation (i.e., C X r = k, Habeas Law) overestimate the potency of TCE when extrapolating from short-duration to longer-duration exposures. Furthermore, these data suggest that, relative to ambient or occupational exposures, the ototoxicity of TCE in the rat is a high-concentration effect c 1997 society' of To 1,1,2-Trichloroethylene (TCE) is a volatile organic solvent with widespread human exposure. TCE is used primarily as a metal parts degreaser, with production volume for ' This manuscript has been reviewed by the Health Effects Research Laboratory, U.S. Environmental Protection Agency, and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use.

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Section: -Weeksupporting

confidence: 82%

Section: Reflex Modificationmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The Ototoxicity of Trichloroethylene: Extrapolation and Relevance of High-Concentration, Short-Duration Animal Exposure Data

Crofton

Zhao

1997

Toxicol Sci

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“…The possible ototoxic effect of toluene was fi rst reported in rats by Pryor et al [1], and subsequent studies demonstrated hearing loss in rats after exposure to toluene [2][3][4][5][6][7][8][9][10][11], styrene [8,[12][13][14][15][16][17][18], xylene [8,9,12], ethyl benzene [19,20], trichloroethylene [8,9,[21][22][23][24], chlorobenzene [9], and n-heptane [25]. The ototoxic potency of the different solvents varies signifi cantly [9,14,26], but when rats were exposed to different combinations of organic solvents, the auditory impairment was additive with respect to the potency of the solvents under study [9].…”

Section: Introductionmentioning

confidence: 99%

Hazards to Hearing from Combined Exposure to Toluene and Noise in Rats

Lund

Kristiansen²

2008

International Journal of Occupational Medicine and Environmental Health

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Introduction:The main risk of hearing impairment from workplace exposure to organic solvents may stem from the potentiation of effects caused by concomitant noise exposure. The aim of the present study was to identify the main hazards from combined long-term, low-level exposure to noise and aromatic organic solvents, like toluene, in rats. Material and Methods: The rats were exposed to steady-state, wide-band noise (WBN) and 0 ppm, 100 ppm, 200 ppm and 500 ppm toluene for 90 days. Hearing was assessed using Auditory Brain Stem Responses (ABR) and Distortion Product Oto-Acoustic Emissions (DPOAE) eight weeks after exposure. The impact of noise composition on the interaction between solvent and noise exposure was investigated in rats exposed for 10 days either to 0 ppm, 500 ppm, 1000 ppm or 1500 ppm toluene and either WBN or impulse noise. ABR and DPOAE tests were performed before and two weeks after exposure. Results: Long-term exposure of rats to WBN and toluene at 500 ppm or less did not show any increase in hearing impairment, compared to the rats exposed to noise only. Synergistic interaction was demonstrated in short-term exposure to 1500 ppm toluene and both to WBN and impulse noise, but hearing impairment was much larger when following exposure to impulse noise. Conclusion: In combined exposure to low-levels of noise and toluene, even a long-term exposure did not reveal a potential hazard of hearing impairment. Synergistic interaction in combined short-term exposure to toluene and noise was noted both with respect to WBN and impulse noise, but the impulse noise was much more disruptive than WBN at the same level of noise exposure. The ototoxicity of organic solvents may primarily be a hazard also to human hearing due to the exacerbation of hearing loss by a possible co-exposure to especially harmful noise, such as impulse noise.

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Alteration of brainstem auditory evoked potentials in diethylbenzene and diacetylbenzene‐treated rats

Gagnaire

Becker

Céaurriz

1992

J of Applied Toxicology

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Male Sprague-Dawley rats were treated either with 1,2-diethylbenzene (1,2-DEB) or its putative active metabolite, 1,2-diacetylbenzene (1,2-DAB). Experimental rats and appropriate controls were examined electrophysiologically for brainstem auditory evoked potentials (BAEP). Oral administration of 1,2-DEB (75 or 100 mg kg-1 once a day, 4 days a week, for 8 weeks) and intraperitoneal injection of 1,2-DAB (10 or 15 mg kg-1 once a day, 4 days a week, for 8 weeks) produced time- and dose-dependent increases in the peak latencies of all BAEP components as well as in interpeak (I-V) differences, and a decrease in the amplitudes of all the components. The absolute and interpeak latencies recovered partially during an 8-week (1,2-DEB) or a 10-week (1,2-DAB) recovery period, whereas there were long-lasting decreases in peak amplitudes.

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Sensory-evoked potentials in rats chronically exposed to trichloroethylene: Predominant auditory dysfunction

Cited by 49 publications

References 26 publications

The Ototoxicity of Trichloroethylene: Extrapolation and Relevance of High-Concentration, Short-Duration Animal Exposure Data

The Ototoxicity of Trichloroethylene: Extrapolation and Relevance of High-Concentration, Short-Duration Animal Exposure Data

Hazards to Hearing from Combined Exposure to Toluene and Noise in Rats

Alteration of brainstem auditory evoked potentials in diethylbenzene and diacetylbenzene‐treated rats

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