Carbon disulfide potentiates the effects of impulse noise on the organ of Corti

•Carbon disulfide exposure has raised concerns for hearing in low-frequency regions.•Despite similar energy, impulse and continuous noises do not have the same traumatic impact on cochlea.•Carbon disulfide potentiates the effects of impulse noise.•Exposure to moderate carbon disulfide concentrations...

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Published inNeurotoxicology (Park Forest South) Vol. 59; pp. 79 - 87
Main Authors Carreres Pons, Maria, Chalansonnet, Monique, Venet, Thomas, Thomas, Aurélie, Nunge, Hervé, Merlen, Lise, Cosnier, Frédéric, Llorens, Jordi, Campo, Pierre
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.03.2017
Elsevier BV
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Abstract •Carbon disulfide exposure has raised concerns for hearing in low-frequency regions.•Despite similar energy, impulse and continuous noises do not have the same traumatic impact on cochlea.•Carbon disulfide potentiates the effects of impulse noise.•Exposure to moderate carbon disulfide concentrations reduced the auditory damage caused by continuous noise. Occupational noise can damage workers’ hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents are known to provoke chemical-induced hearing loss, but little is known about the effects on hearing of carbon disulfide (CS2) when combined with noise. Co-exposure to CS2 and noise may have a harmful effect on hearing, but the mechanisms involved are not well understood. For instance, CS2 is not thought to have a cochleotoxic effect, but rather it is thought to cause retrocochlear hearing impairment. In other words, CS2 could have a distal neuropathic effect on the auditory pathway. However, a possible pharmacological effect of CS2 on the central nervous system (CNS) has never been mentioned in the literature. The aim of this study was to assess, in rats, the effects of a noise (continuous vs. impulse), associated with a low concentration of CS2 [(short-term threshold limit value) x 10 as a safety factor] on the peripheral auditory receptor. The noise, whatever its nature, was an octave band noise centered at 8kHz, and the 250-ppm CS2 exposure lasted 15min per hour, 6h per day, for 5 consecutive days. The impact of the different experimental conditions on hearing loss was assessed using distortion product oto-acoustic emissions and histological analyses. Although the LEX,8h (8-h time-weighted average exposure) for the impulse noise was lower (84dB SPL) than that for the continuous noise (89dB SPL), it appeared more damaging to the organ of Corti, in particular to the outer hair cells. CS2 exposure alone did not have any effect on the organ of Corti, but co-exposure to continuous noise with CS2 was less damaging than exposure to continuous noise alone. In contrast, the cochleo-traumatic effects of impulse noise were significantly enhanced by co-exposure to CS2. Therefore, CS2 can clearly modulate the middle-ear reflex function. In fact, CS2 may have two distinct effects: firstly, it has a pharmacological effect on the CNS, modifying the trigger of the acoustic reflex; and secondly, it can make the organ of Corti more susceptible to impulse noise. The pharmacological effects on the CNS and the effects of CS2 on the organ of Corti are discussed to try to explain the overall effect of the solvent on hearing. Once again, the results reported in this article show that the temporal structure (continuous vs. impulse) of noise should be taken into consideration as a key parameter when establishing hearing conservation regulations.
AbstractList Occupational noise can damage workers' hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents are known to provoke chemical-induced hearing loss, but little is known about the effects on hearing of carbon disulfide (CS2) when combined with noise. Co-exposure to CS2 and noise may have a harmful effect on hearing, but the mechanisms involved are not well understood. For instance, CS2 is not thought to have a cochleotoxic effect, but rather it is thought to cause retrocochlear hearing impairment. In other words, CS2 could have a distal neuropathic effect on the auditory pathway. However, a possible pharmacological effect of CS2 on the central nervous system (CNS) has never been mentioned in the literature. The aim of this study was to assess, in rats, the effects of a noise (continuous vs. impulse), associated with a low concentration of CS2 [(short-term threshold limit value) x 10 as a safety factor] on the peripheral auditory receptor. The noise, whatever its nature, was an octave band noise centered at 8kHz, and the 250-ppm CS2 exposure lasted 15min per hour, 6h per day, for 5 consecutive days. The impact of the different experimental conditions on hearing loss was assessed using distortion product oto-acoustic emissions and histological analyses. Although the LEX,8h (8-h time-weighted average exposure) for the impulse noise was lower (84dB SPL) than that for the continuous noise (89dB SPL), it appeared more damaging to the organ of Corti, in particular to the outer hair cells. CS2 exposure alone did not have any effect on the organ of Corti, but co-exposure to continuous noise with CS2 was less damaging than exposure to continuous noise alone. In contrast, the cochleo-traumatic effects of impulse noise were significantly enhanced by co-exposure to CS2. Therefore, CS2 can clearly modulate the middle-ear reflex function. In fact, CS2 may have two distinct effects: firstly, it has a pharmacological effect on the CNS, modifying the trigger of the acoustic reflex; and secondly, it can make the organ of Corti more susceptible to impulse noise. The pharmacological effects on the CNS and the effects of CS2 on the organ of Corti are discussed to try to explain the overall effect of the solvent on hearing. Once again, the results reported in this article show that the temporal structure (continuous vs. impulse) of noise should be taken into consideration as a key parameter when establishing hearing conservation regulations.
•Carbon disulfide exposure has raised concerns for hearing in low-frequency regions.•Despite similar energy, impulse and continuous noises do not have the same traumatic impact on cochlea.•Carbon disulfide potentiates the effects of impulse noise.•Exposure to moderate carbon disulfide concentrations reduced the auditory damage caused by continuous noise. Occupational noise can damage workers’ hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents are known to provoke chemical-induced hearing loss, but little is known about the effects on hearing of carbon disulfide (CS2) when combined with noise. Co-exposure to CS2 and noise may have a harmful effect on hearing, but the mechanisms involved are not well understood. For instance, CS2 is not thought to have a cochleotoxic effect, but rather it is thought to cause retrocochlear hearing impairment. In other words, CS2 could have a distal neuropathic effect on the auditory pathway. However, a possible pharmacological effect of CS2 on the central nervous system (CNS) has never been mentioned in the literature. The aim of this study was to assess, in rats, the effects of a noise (continuous vs. impulse), associated with a low concentration of CS2 [(short-term threshold limit value) x 10 as a safety factor] on the peripheral auditory receptor. The noise, whatever its nature, was an octave band noise centered at 8kHz, and the 250-ppm CS2 exposure lasted 15min per hour, 6h per day, for 5 consecutive days. The impact of the different experimental conditions on hearing loss was assessed using distortion product oto-acoustic emissions and histological analyses. Although the LEX,8h (8-h time-weighted average exposure) for the impulse noise was lower (84dB SPL) than that for the continuous noise (89dB SPL), it appeared more damaging to the organ of Corti, in particular to the outer hair cells. CS2 exposure alone did not have any effect on the organ of Corti, but co-exposure to continuous noise with CS2 was less damaging than exposure to continuous noise alone. In contrast, the cochleo-traumatic effects of impulse noise were significantly enhanced by co-exposure to CS2. Therefore, CS2 can clearly modulate the middle-ear reflex function. In fact, CS2 may have two distinct effects: firstly, it has a pharmacological effect on the CNS, modifying the trigger of the acoustic reflex; and secondly, it can make the organ of Corti more susceptible to impulse noise. The pharmacological effects on the CNS and the effects of CS2 on the organ of Corti are discussed to try to explain the overall effect of the solvent on hearing. Once again, the results reported in this article show that the temporal structure (continuous vs. impulse) of noise should be taken into consideration as a key parameter when establishing hearing conservation regulations.
Occupational noise can damage workers' hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents are known to provoke chemical-induced hearing loss, but little is known about the effects on hearing of carbon disulfide (CS ) when combined with noise. Co-exposure to CS and noise may have a harmful effect on hearing, but the mechanisms involved are not well understood. For instance, CS is not thought to have a cochleotoxic effect, but rather it is thought to cause retrocochlear hearing impairment. In other words, CS could have a distal neuropathic effect on the auditory pathway. However, a possible pharmacological effect of CS on the central nervous system (CNS) has never been mentioned in the literature. The aim of this study was to assess, in rats, the effects of a noise (continuous vs. impulse), associated with a low concentration of CS [(short-term threshold limit value) x 10 as a safety factor] on the peripheral auditory receptor. The noise, whatever its nature, was an octave band noise centered at 8kHz, and the 250-ppm CS exposure lasted 15min per hour, 6h per day, for 5 consecutive days. The impact of the different experimental conditions on hearing loss was assessed using distortion product oto-acoustic emissions and histological analyses. Although the LEX,8h (8-h time-weighted average exposure) for the impulse noise was lower (84dB SPL) than that for the continuous noise (89dB SPL), it appeared more damaging to the organ of Corti, in particular to the outer hair cells. CS exposure alone did not have any effect on the organ of Corti, but co-exposure to continuous noise with CS was less damaging than exposure to continuous noise alone. In contrast, the cochleo-traumatic effects of impulse noise were significantly enhanced by co-exposure to CS . Therefore, CS can clearly modulate the middle-ear reflex function. In fact, CS may have two distinct effects: firstly, it has a pharmacological effect on the CNS, modifying the trigger of the acoustic reflex; and secondly, it can make the organ of Corti more susceptible to impulse noise. The pharmacological effects on the CNS and the effects of CS on the organ of Corti are discussed to try to explain the overall effect of the solvent on hearing. Once again, the results reported in this article show that the temporal structure (continuous vs. impulse) of noise should be taken into consideration as a key parameter when establishing hearing conservation regulations.
Occupational noise can damage workers' hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents are known to provoke chemical-induced hearing loss, but little is known about the effects on hearing of carbon disulfide (CS2) when combined with noise. Co-exposure to CS2 and noise may have a harmful effect on hearing, but the mechanisms involved are not well understood. For instance, CS2 is not thought to have a cochleotoxic effect, but rather it is thought to cause retrocochlear hearing impairment. In other words, CS2 could have a distal neuropathic effect on the auditory pathway. However, a possible pharmacological effect of CS2 on the central nervous system (CNS) has never been mentioned in the literature. The aim of this study was to assess, in rats, the effects of a noise (continuous vs. impulse), associated with a low concentration of CS2 [(short-term threshold limit value) x 10 as a safety factor] on the peripheral auditory receptor. The noise, whatever its nature, was an octave band noise centered at 8 kHz, and the 250-ppm CS2 exposure lasted 15 min per hour, 6 h per day, for 5 consecutive days. The impact of the different experimental conditions on hearing loss was assessed using distortion product oto-acoustic emissions and histological analyses. Although the LEX,8 h (8-h time-weighted average exposure) for the impulse noise was lower (84 dB SPL) than that for the continuous noise (89 dB SPL), it appeared more damaging to the organ of Corti, in particular to the outer hair cells. CS2 exposure alone did not have any effect on the organ of Corti, but co-exposure to continuous noise with CS2 was less damaging than exposure to continuous noise alone. In contrast, the cochleo-traumatic effects of impulse noise were significantly enhanced by co-exposure to CS2. Therefore, CS2 can clearly modulate the middle-ear reflex function. In fact, CS2 may have two distinct effects: firstly, it has a pharmacological effect on the CNS, modifying the trigger of the acoustic reflex; and secondly, it can make the organ of Corti more susceptible to impulse noise. The pharmacological effects on the CNS and the effects of CS2 on the organ of Corti are discussed to try to explain the overall effect of the solvent on hearing. Once again, the results reported in this article show that the temporal structure (continuous vs. impulse) of noise should be taken into consideration as a key parameter when establishing hearing conservation regulations.
Author Merlen, Lise
Chalansonnet, Monique
Cosnier, Frédéric
Campo, Pierre
Carreres Pons, Maria
Nunge, Hervé
Venet, Thomas
Thomas, Aurélie
Llorens, Jordi
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Keywords LEX,8 h
Combined exposure
IHC
Rats
CNS
IS
OHC
STEL
SD
Carbon disulfide
FFT
SDH
Risk assessment
Impulse noise
DPOAEs
SEM
dB (A)
dB SPL
MER
NIHL
TWA
Middle-ear reflex
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SSID ssj0015769
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Snippet •Carbon disulfide exposure has raised concerns for hearing in low-frequency regions.•Despite similar energy, impulse and continuous noises do not have the same...
Occupational noise can damage workers' hearing, and the phenomenon is even more dangerous when noise is associated with an ototoxic solvent. Aromatic solvents...
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pubmed
elsevier
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StartPage 79
SubjectTerms Acoustic emission
Acoustic emission testing
Acoustic noise
Acoustic Stimulation
Analysis of Variance
Animals
Auditory Threshold - drug effects
Carbon disulfide
Carbon Disulfide - pharmacology
Central nervous system
Combined exposure
Continuous noise
Damage
Disease Models, Animal
Ear
Exposure
Female
Hair cells
Hearing loss
Hearing Loss - etiology
Human exposure
Impulse noise
Microscopy, Electron, Scanning
Middle-ear reflex
Noise
Noise - adverse effects
Noise levels
Occupational health
Organ of Corti
Organ of Corti - drug effects
Organ of Corti - pathology
Organ of Corti - ultrastructure
Otoacoustic Emissions, Spontaneous - drug effects
Otoacoustic Emissions, Spontaneous - physiology
Ototoxicity
Outer hair cells
Pharmacology
Psychoacoustics
Rats
Rats, Long-Evans
Risk assessment
Safety factors
Solvents - adverse effects
Time Factors
Workers
Title Carbon disulfide potentiates the effects of impulse noise on the organ of Corti
URI https://dx.doi.org/10.1016/j.neuro.2017.02.003
https://www.ncbi.nlm.nih.gov/pubmed/28189717
https://www.proquest.com/docview/1943255017
https://search.proquest.com/docview/1867985037
Volume 59
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