Editor's
Note:Th/s/stheeighty-ninth
ina •eries
ofreoieto
andtutorial
papers
onvarious
aspects
ofacoustics.
Noise-induced hearing loss as influenced by other agents and by
some physical characteristics of the individual
LarryE. Humes
Division
ofHearing
andSpeech
$cience•
Vanderbilt
University
School
ofMedicine,
Nashville,
Tennessee
'
37232and TheBill WiikersonHearingand SpeechCenter,Nashville,Tennessee
37212
(Received10June1983;accepted
for publication22 June1984)
The interaction
of noisewith a varietyof otheragentsandwith somephysicalcharacteristics
of
the individualto producenoise-induced
hearinglossis reviewedcritically. The reviewis
restricted,
for themostpart,to publications
since1970.Otheragentsinteractingwithsteady-state
noisethat arereviewedhereinclude:{1)ototoxicdrugs{kanamycin,
neomyein,ethacrynieacid,
furosemide,
andsalieylates),
{2)impulsenoise,and(3)whole-bodyvibration.Physical
characteristics
of theindividual
thatarereviewed
are:(1)age,(2)presence
ofprevious
hearingloss
frompriornoiseexposure,
(3)eyecolor,and{4)race.Suggestions
forfutureresearch
in thisgeneral
areaarealsomade.Someof thesesuggestions
areasfollows:(1)to extendstudiesof theinteraction
of steady-state
noisewith impulsenoise,salieylates,
andwhole-bodyvibrationto encompass
a
broaderrangeof exposure
conditions,
includingexposure
conditions
typicallyencountered
bythe
worker,{2)to developan animalmodelof presbyeusis
to exploretheinteractionsof noise-induced
hearinglossandpresbyeusis,
and{3)to explorethepotentialinteractions
resultingfrom
concurrent
exposure
to multipleagents,suchasimpulsenoiseandototoxiedrugs,in younger,
moresusceptible
animals.
PACS numbers:43.10.Ln,43.50.Qp,43.66.Sr
INTRODUCTION
The hazardouseffectsof noiseon hearinghavebeenof
interestfor over a century. Over the past few decadeswe
have gainedconsiderableinsightinto the mechanismsand
featuresof noise-induced
hearingloss.For a varietyof reasons,much of our presentknowledgeabout noise-induced
heatingloss,whethertemporaryor permanentin nature,has
beenconcernedwith continuousexposures
to steady-state
sound{typicallya noiseof sometypeor a puretone).Sincea
considerable amount of information
on noise-induced hear-
ing lossresultingfrom continuous
exposures
to steady-state
soundhadbeenobtainedby thelate 1960s,onethrustof such
researchfromapproximately1970to thepresenthasbeento
examineinteractions
of variousagentswith suchnoisein the
productionof hearingloss.Prior to 1970,for example,there
wasapparentlyonlyonepubh'shed
study(DarrouzctandSobrinho,1963}ontheinteractionof noisewithototoxicdrugs.
By 1983,on the otherhand,at leastnine publicationshave
appearedon the interactionof noisewith oneototoxicdrug
alone--kanamycin.A similarcasecanbemadefor the interactionof noisewith personalcharacteristics
of the individual. Prior to 1970, for example,there was apparentlyonly
one study ILutovats, 1969} that demonstratedany effect of
age on the amount of noise-induced
hearinglossobserved
followingexposureto loud sound.Sincethen, however,at
least11 suchstudiesappearedin the literature.
The purposeof thepresentarticleisto providea review
of the literature in these two areas of research. A sufficient
number of studies have been conducted since 1970 in these
two areasto warranta synthesis
of thisliterature.It ishoped
that this synthesis
will identifyareasthat requireadditional
research. The remainder of this review is divided into three
1318
major sections:See. I discussesinteractionsof noise with
other agents,Sec. II discussesinteractionsof noise with
physicalcharacteristics
of the individual,andSec.III proridesa generalsummary.
I. INTERACTIONS
WITH OTHER AGENTS
For thepurpose
of thisreviewanagentissaidto "interact"withnoiseif thedamage
(assessed
withanatomical,
physiological,
orbehavioral
methods)
resulting
fromexposure
to
bothagentsis greaterthanthat produced
by eitheragent
acting
byitself.Thisisalsoreferred
tofrequently
as"poten~
fiation"of thedamagedueto noiseby theotheragent."Additivity" is a specialcaseof interactionin whichthe total
damage
resulting
fromanexposure
to bothagents
isapproximatelyequalto thesumof theeffects
dueto eitheragent
alone.Finally,a "synergistic"
effectisanotherspecialtype
of interaction
in whichthedamage
produced
by theircom-
binedpresentation
exceeds
thatpredicted
byadditivity.
In
mostcases
ofsynergy
reviewed
here,additivity
predicted
no
damageor hearingloss(neitheragentactingalonewasharmful),yetsomelossor damagewasobserved
whenpresented
together.
A. Noise and drugs
Research
on the interactionof noiseanddrugsin the
productionof hearinglossis moreextensive
than for any
othercombination
studied.
Amongthevariousdrugsstudied,kanamycin
hasreceived
themostattention.
TableI proridesa summary
of thestudies
examining
theinteraction
of
noiseandkanamycin
overthepast13years.Fromthestudies summarized in Table I several conclusionscan be drawn.
As notedin thefar rightcolumnof TableI all but threeof the
J. Acoust.Soc.Am.76 (5),Novernber
1984 0001-4966/84/111318-12500.80
¸ 1984Acouslical
SocietyofAmerica
1318
TABLEI. Stsmmnry
of•'Mdies
e•*mining
theinto'action
ofn•
S•y
S•
Day•elai.(1971}
•
pig
43' L• •cu•mrnoi•
•
•
pig
180 p• no•, 113dB,
(1973)
N
N•
•
• 70 dB, •S w•
•g d•e
Mc•
•me
1•,•, or1• m•g,
H• •un•
mild
syner•stic
e•t
•5 w•
noisefollowedby kanamycin
yieldedgreaterHC lossthan
eitheralone;not true for
kanamy½infollowedby noise
1 •k
Kroclunalska
(1974}
guinea
pig 250 industrial
noise
(MFd); 30mg/kg,
I or2
~92 dB;1,2,3,4,6,
CMdand
weeks
WNAPd
no interaction;noiseand
kanamyeinsameasnoisealone
and 12 weeks
Dnyal
andBareit
(1975) guinea
pig
38 BBNd,90dB,5weeks 100mF/kg,
5weeks HCcounts
noiseandkanamycinyield
greater
lossthaneither
alone
Marqum
etal.(1975} guinea
pig 7
OB
Nd(CF= 8kHz}, 200
mg/kl•,
I week CMand
HC
100dB, 8 h/day,
counts
1 week
noiseandkanamycinor noise
preceding
kunamycin
yielded
moredamagethan eitheralone
or reverse sequence
HawkinsetaL(1975
)guinea
pig
?
OBN{CF=0.5,1,2,
or 100m•/kg,
lweek
CMandHC
8 kl-Iz),BBN, 90,
counts
8 h/day, I week
chinehilln 16 BBN(I.4-5.6
kHz),
100(lB, 1 h
level )100 dB and NIHL
coincideswith regionof loss
due to kanamycin
10o, 106 dB,
RyanandBone
(1978)
interactiononly when noise
150ms/ks
•
behavioral findingssameasQuante(1973}
audiossam
(seeabove)
and HC count
Bone
and
Ryan
(1978) chinchilla 6 BBN
(1.4-5.6
kHz),
100dB, 1 h
150
m•/kg
b
behavioral noiseextendedrangeof lossto
audiossam
and HC
count
Winkeletai. (1978}
bumnn
91
(4-6years}
Rychkova
and]•[nllnkln 8Uin•tpig
?
(1979)
incubator
noise,
10ms/kS,
rctrospec-
noevidence
ofkanam
ycin
and
60-70dBA,7
> 5days
tirestudy
of
incubatornoisebeingworsethan
PTd (2.5kHz),
4 ms/kg,8days
100riB,lh
Browneta/.(1980}
guinea
pig
50•
lowerfrequencies
in 1/2 of
subjects;
noeffectin other
subjects
audiosrams
incubator alone
HC
no interaction
nuclear
volume
BBN,115or45dB,
200,300,
or400
CMandHC
10h/day,7 days
m•/kg, ? days
count
at all kanamycindoses,noise
andkanamycinyieldedgreater
damagethaneitheragentalone
ßN for Ssoups
typically(5.
bDosage
wascontinued
untilh•aringlossat 6 kHz reached
30-40dB.
CTenSsoups
of N----5.
dLF---lowfrequency;
MF---midfrequency;
BBN= broadband
noise;
OBN-- octave
band
noise;
CF---center
frequency;
HC= haircell;CM= cochlear
microphonic;
WNAP----whole-nerve
actionpotential;
PT -- puretone.
studies
listedhaveindicated
a significant
interaction
ofnoise
withkanamycin.
Thethreestudies
thathavenotobserved
a
regimens
andnoiseexposures
thattrulymimic"reallife"
strong
interaction
(DayaletaL, 1971;Kl'ochm•lslta,
1974;
Winkeletal.,1978)haveused
thelowest
dosages
ofkanamycinandthelowest
noiseleveh(,92 dBSPL).Hawkinsetal.
{1975),
however,
haveindicated
thatinteraction
ofnoise
and
kanamycin
in theguineapig'isnotobserved
unless
noise
rationapproximating
two-thirds
oftheanimal's
lifeexpec-
levelsare • 100 dB SPL. Moreover,they indicatethat the
conditions
forindustrial
employees
(e.g.,noiseexposure
dutancy)haveyetto beexamined.
Most often the interactionobservedhasbeenlessthan
thatexpected
fromanadditive
relationship
between
thetwo
agents.
Another
result
thatargues
against
simple
additivity
is thesequential
interaction
observed
by several
inveStiga-
reportthatnoiseexposure
foldamage
produced
bythenoise
mustoccur
inthesame
region tors.Thatis,severalstudies
lowed
by
kanamycin
intoxication
results
in
an
interactive
of thecochlea
asthatdamaged
bythekanamycin.
Thusone
bykanamycin
doesnot(Darrouwouldnotexpect
toobserve
aninteraction
between
kanamy- effectwhilenoisepreceded
zet
and
Sobrinho,
1963;
Quante,
1973;
Marques
etal., 1975;
cin and low-levelnoiseor noisecontainingprimarilylow-
Simple
addifivity
isinsensitive
tothe
frequency
energy
such
astheincubator
noise
used
byDayal RyanandBone,1978).
etal. (1971)andWinkeletal. (1978).It isinteresting,
however,that thosestudies
usingdrugdosages
typicalfor humanscoupled
withnoiseexposures
moreclosely
approximating
conditions
encountered
byhumanworkers
observed
little,if any,interaction
inanimals.
Ontheotherhand,drug
1319
J.Acoust.
Sec.Am.,Vol.76,No.5,November
1984
orderin whichtheagentsareappliedandmustthereforenot
applyto thenoise/kanamycin
interaction.
Another feature of the studesoutlined in Table I that is
readilyobserved
is that thevastmajorityof datahavebeen
obtainedfroma singlespecies,
theguineapig.It is unclear,
LarryE.Humes:
Noise-induced
hearing
loss
1319
therefore,howmuchthedatacanbegeneralized
to theother
species,includingman.
Severalother ototoxic agentshave been examinedin
recentyearsfor possibleinteractionswith noise.The agents
includeneomycin,ethacrynieacid,furosemide,and salicylates. The studies and their outcomes are summarized in Ta-
bleII. The limiteddataavailableon neomycinindicatesthat
neomycindoesinteractwith noiseto producegreaterhearing lossthan eitheragentalone.The data, however,come
fromonespecies
andareavailablefor onlyonedrugdosage.
The equallysparsedataavailablefrom studiesof loopdiuretics (ethacrynicacid and furosemide)suggestno interaction
sureandsalicylate
intoxication
produce
onlytemporary
loss
of hearing.Hence,oneagentcanbe appliedand following
recoverythe secondagentor a combinationof agentscanbe
applied.The studyby Woodfordet al. (1978)on the other
hand, utilized a between-subjects
designin which small
groups(n= 5) of animalsweresubjected
to eitheragent
aloneor bothagentsin combination.
The significant
vari-
abilityobserved
in theanimalsexposed
to noisealonemakes
anyconclusions
drawnfromthemeandatafor eachgroup
somewhattenuous.If between-subject
designsare usedto
explorethe noise/salicylate
interaction,then it wouldseem
that the large individual differencesin responseto noise
with noise.
alonewoulddictatethe useof 15-20 animalsper group.
At least four recent studies have examined the interacChen and Aberdeen{1980)usedfive groups,eachcontion of noisewith sodiumsalicylate.Only one study(Woodt•|nirlgapproximately25 animals,to studytheinteractionof
ford et al., 1978) failed to observeinteractionof the two
noisewith salicylate.Theseinvestigators
observedsequenagents.Interaction hasbeenobservedin mice, chinchillas, tial effectsin the resultinginteraction.The greatestinteracand humans. In two of the three studies that demonstrated
tion wasobservedfor noiseexposure6 h after injectionof
interaction
(Eddyeta•.,1976;McFadden
andPiattsmier, sodiumsalicylate.Injections24 h prior to exposureand at
1983)a within-subjectsdesignwas usedin which the same
both 1 and 24 h followingexposureresultedin lessinteracsubjects
wereexposed
to eachagentseparately
andthenboth
tion. The uniqueness
of the behavioralmeasureof hearing
in combination.This is possiblein that boththe noiseexpodamage(primingforandiogenic
seizure)
andthesoundexpoTABLE II. Summaryof studiesexaminingtheinteractionof noiseexposure
with ototoxicdrugsotherthankanamycin.
Drug
Study
Species
Neomycin
Jauhiainen
etat
guineapig
N
Noiseexposure
Drugdosage
32 OBN{CF= 8.0kHz), 200mg/kg,7 days CM andHC
(1972)
115dB, 70 h
( 10 h/day?}
Brownet al. (1978)
guineapig
32 BBN, 115dB,
count
200 mg/kg, 7 days CM andHC
10 h/day, 7 days
Ethacrynic
VemonetaL 0977)
guineapig
Method
15 BBN, 120or78dB,
acid
Outcome
combination
yieldedgreater
damagethan eitheralone
confirmedabovefindings
count
40mg/kg, 1 day
24 h
CMandHC
count
damagedue to EA and noise
not greaterthan noisealong
EA producedno permanent
effects
IOsieiandBobbin
guineapig
4O P'r{4.okHz),
(1982)
Furosemide
•0 mg/kg
CM and WNAP
loss same for noise alone as
for noise and EA
100mg/kg,1 day
CM and HC
count
furosemide
andnoiseyielded
no greaterdamagethan noise
200mg/cma,
behavioral
•S
14 injectionsin
audiogram
and salicylates
greaterthan
from eitheragentalone
AER thresholds
and HC count
TTS from combination no
primingfor
audiogenic
combinedexposureto
salicylateand noise
-- 1I0 and 135 dB,
Vemonetal.(1977} guineapig
15 BBN, 120or78dB,
24h
alone
Salicylates
Eddyet aL (1976)
chinchilla
7 BBN,85dBA,48h
72 h
Woodford
et aL
chinchilla
39 OBN (CF ----2.8 kHz),
400 mg/kg
95dB, 1 hor
(1978}
OBN (CF = 4.0 kltz),
at 1.0 kHz due to noise -
greaterthan from the single
agentproducinggreaterloss
80riB, 96hot
50 impulses,158da peak, l/win
Chen and Aberdeen
BALB/cmice 134 127-dB"beil
500mg/kg
sound," 10 s
(1980)
seizures
produced
greaterpriming
effect than noise
alone;
greatestinteraction for
saUcylateadministered6 h
before noise
McFadden and
Plattsmier(1983)
1320
humans
4
PT (2.5 kHz},
10 m/n, levd
determined
4 g/day,
-3 daysto
0.5 g/day
individually
(2 h beforetest)
J. Acoust.
Soc.Am.,Vol.76, No.5, November
1984
behavioral
combination resulted in
greaterTTS at 3550 Hz than
eitheralone;
additive effects
LarryE.Humes:
Noise-induced
hearing
loss
1320
'sure
stimulus
(a127-dB
"bell
sound"),
however,
necessitates
at thesamefacility,aresummarized
in TableIlL
furtherexamination
of sequential
effects/n
the/nteraction
of
no/sew/thsalicylate.
It isinteresting
thatalthough
sequential effectswereapparentin theinteractionof noiseandkanamycin,the directionof the sequence
observed
therewas
opposite
to thatobserved
forsalicylate.
Specifically,
whereas
interaction
wasapparentwhennoiseexposure
wasfollowed
by kanamycin
intoxication,
interaction
appears
to begreatestforsalicylates
whenthedrugprecedes
thenoheexposure.
The studieson the interactionof noisewith salicylate
needto beexpanded
to systematically
encompass
a broader
rangeof combinations
of noiseexposure
anddrugdosage.
In
ß•idition, moreresearch
w/th humansubjects
couldbeconductedbecause
of the reversible
natureof the hear/rigloss.
Of thefourstudies
appearing
in TableII thathaveexamined
theno/se/sal/cylate
interaction,onlythat of McFaddenand
Plattsm/er(1983)usedhumansubjects.
Finally,the magnitudeof interaction
resulting
fromchronicexposures
to noise
and chronic ingestionof salicylateshouldbe examined.
Many workersin industry,especiallyarthritissufferers,
ingesta considerable
amountof sal/cylateon a daily basis
whilebeingexposed
to intensenoiseovera periodof several
years.
-
B. Nols• and Impuls• nois•
Fourof the
eightstudiesoutlinedin TableIII havefailedto observe
an
interactionbetweensteady-state
andimpulsendise•/alker,
1972;Yamamuraet aL, 1974;ArlingerandMellberg,1980;
HamerniketaL, 1981a).In addition,theresultsof oneof the
remainingfourstudies
(OkadaetaL, 1972a)cannotbemeaningfullyinterpretedin that the TTS for an/repulse-alone
conditionwas not measured.One can not conclude,there-
fore,thattheTTS for thecombined
exposure
isgreaterthan
that from eitheragentalone.For the mostpart, the studie/
reportingnointeractionemployed
anhnpulselevelthatwas
muchlowerthanin the remaininginvestigations.
The resultsfromthethreestudiesthat supportan interaction of steady-state
and hnpulsenoisecan be generally
summarizedby statingthat interactionoccurswhenthe two
typesof noiseexposure
overlapin time(i.e.,apparentlythere
areno sequential
effects)
andtheimpulselevelequalsor exceeds147 dB. The valueof 147 dB appearsto be a critical
valueforthechinchillawhenpermanent
effects,
asmeasured
either by behavioralthresholdsor cytocochleogra.
m.%are
usedto determinethe presence
of an interaction.When temporarythresholdshiftis usedasthe measureof interaction,
then 137 dB appearsto be more appropriate.Finally, the
studybyBlakesleeet al. (1977}suggests
that interactionis
reducedas the degreeof spectraloverlapbetweenthe two
The interactionof steady-state
noiseandimpulsenoise noises is reduced.
The useof a between-subject
designand mean data
hasbeenthetopicofatleasteightinvestigations
overthepast
decade.
Eightof thesestudies,
fourof whichwereconducted fromsmallgroups
(n -- 5)in thestudies
demonstrating
interTABLE IlL Interactionof cxposurmto steady-state
noise.andimpulsenoise.
Study
Species
Oltsd•_
et aL (1972a)
human
N
7
S•.•y-state noise
BBN, 98 dBA, I h '
Impulsenoise
Method
Outcome
104dB, ?{B),
behavioral
TTS ß
TTS for combinedexposure
greaterthan steady-statenoise
20/rain, lh
aion• TTS not measured,however,
for impulsealone
Walker (1972}
Hametalk et at
human
11
et
96-132 dB, 75 ms(B},
20 rain
3.2/s, 20 rain
behavioralTTS
TTS for combined
exposure
not
greaterthanfor singlemost
hazardousagent
chinchilla
29 OBN(CF=3.1kHz},15•dB,
40ps{A), AERandiogram
damagegreaterfor combination
0974)
Y•mnmura
BBN, 78-96 dBA,
human
8
95 dB, I h
l/rain, 50 min, or
175dB,
and HC count
than for eitheralone;
synergisticeffectobservedin PTS
BBN, 90 dB, 40 rain
105or 120dB,
25 or 100ms{B),
behavioralTTS
At low impulselevelno interactions;
at 120-dBimpulselevd, combined
exposureproducedmoreTTS
(1974}
0.5/s, 40 rain
thansteady-state
alonebutless
thanor equalto impulsealone
HuntetaL(1976)
ehinehillg30 OBN{CF= 3.1kHz),
95 dB, I h
137-158
dB,
AERaudiogram Potentiationfor TTS andsynergistic
40ps(A}, i/rain,
and HC count
effectfor PTSwhenimpulselevel
> 147 dB
Blakeslee
et al. (1977} chinchilla 15
OBN (CF = 0.707kHz},
100dB, 1 h
158dB, 40ps{A},
1/m/n, 50 min
AER or
audiogramand
synergisticeffectreducedwith
spectralmismatch
HC count
Adingerand
Mellberg{1980)
human
10 OBN (CF ----2 kHz),
95 dBA, 20 rain
119.5dBA, I ms{B),
10/s, 20 min
behavioral
•
TI'S from combinedexposure
not greaterthan steady-state
noise alone
Hamerniket al.
{1981a)
1321
chinchill• 23
BBN, 75-85 dB,
8 h/day,
5 days/week,4 or 8
103dB, 7(B),
l/s, 8 h/day,
5 days/week,
weeks
4 or 8 weeks
J. Acoust.SOC.Am.,Vol.76, No.5, November1984
behavioral
audiogram
no interactions observed
LarryE. Humes:Noise-induced
hearingloss
1321
ßaction,however,
detractssomewhat
fromthestrengthof the
findings.Often, for example,the differencein hearing
threshold
between
thegroupsreceiving
combined
exposures
andthe groupsexposedto eachagentaloneis lessthan the
standarddeviationobservedin measurement
of pre-exposurethresholds.
Further,all thestudies
reportinganinteraction havebeenconductedwith onespecies,
the chinchilla.
The generalityof thesefindingswouldbe enhancedconsiderablyby work with other species.Finally, implicationsof
thisresearchfor the humanworkerexposedto bothsteadystateand impulsenoiseare unclear.The chinchilla,for example,is considerably
more susceptible
to noise-induced
hearinglossthan man (Trahiotis,1976;Saundersand Rosowski,1979).Perhapsinteractionfor manwouldnot occur
until theimpulselevelfar exceeded
a value6f 147dB. Indeed,the onestudythat usedexposureconditionssimilarto
thoseencounteredin industrydid not observeany interac-
tion, despitethe useof the moresusceptible
chinchilla(Hamerniketa!., 198la). Previousresearchhasestablished
that
an interactioncanoccurbetweensteady-state
noiseandimpulsenoiseundercertainexposureconditions
and with the
chinchillaser•dngas the subject.Future work shoulduse
largergroupsof animals,a restricted
setof exposure
conditionsthoughtto be representative
of the workplace,and a
wider varietyof species.
Despitethe divergentexperimentalconditionsand
methods
employed
in thesefourinvestigations,
theyall reportthathearinglossisgreaterfornoiseexposure
administeredduringwhole-body
vibrationthanadministered
alone.
In only onestudydid exposure
of the subjectto vibration
aloneproduce
anylossofhearing
(OkadaetaL, 1972b).
This
hearing
loss,however,
wasveryslight(5dB)andtemporary.
Hence,interaction
isevident
whenthehearing
lossresulting
fromnoiseandvibrationisgreaterthannoisealone.Of the
two studi• usinghumansassubjects
the leastconvincing
demonstration of interaction between noise and vibration is
provided
byOkadaetal. {1972b).
At 1000Hz, forexample,
thetemporary
hearinglossfollowingnoiseexposure
alone
wasapproximately
4 dB whilethatresultingfromcombined
exposureto noiseand vibrationwasonly 7 dB. Comparable
values at 4000 Hz were 19 and 23 dB for noise alone and the
combinationof noise and vibration, respectively.Differencesof 3-4 dB are certainlysmalland approximatetestretestdifferencesexpeetedfrom replicationsof the noisealone condition.
The two demonstrations
of interactionin thechinchilla,
morcover,
areweakened
by theuseof a between-subject
de-
signanda smallnumberof subjects
pergroupwhilereportingonlymeanvalues.The considerable
variabilityobserved
in the hearinglossfrom the impulsenoisealoneand the
impulseandvibrationconditions
reduces
the significance
of
the small interaction effect evident in the mean data. There is
C. Noi•e and vibration
At leastfour investigators
haveexaminedthe issueof
the interactionof noisewith whole-bodyvibration.As indicatedin Table IV, thesefour studiescan be further subdivid-
alsoconsiderable
overlapin thecytocochleograms
of theimpulse-onlygroup(Blakeslee
et aL, 1978)and the impulseplus-vibration
group(Hamerniket aL, 198lb). At least60%
of theanimalsof theimpulse-only
groupmanifested
hair-cell
damagecomparable
to thatobserved
in thegroupexposed
to
ed into two pairsof investigations.
Onepair of studiesutilizeda smallnumberof humansubjects,
a within-subjects both noise and vibration.
design,
exposure
to a broadband
noiseat approximately
100
Hence,althoughall four studiesexhibitevidenceof indBfor20rain,andmeasured
theresulting
TTS (Okadaeta!.,
teractionbetweennoiseand whole-bodyvibration,the evi1972b;Yokoyamaetal., 1974).Theotherpairofstudiesused denceis not overwhelming
in thisregard.Furtherwork apsmallgroupsof chinchillas
assubjects,
a between-subjects pearsnecessary.
Suchcombinations
of noiseexposureand
design,combined
exposures
of impulsenoisewith vibration, whole-bodyvibrationare apparenfiyvery commonin the
and measuredtemporaryand permanentchangesin beha- workplace(Wasserman
etaL, 1978).A parametric
studyexvioralheating(Hamerniket aL, 1980,1981b).
ploringa rangeof noiseexposures
andvibrations,
including
TABLE IV. Studiesexaminingthe interactionof noiseand whole-bodyvibration.
Study
Species
Okadaetal.(1972b)
human
N
5
Noiseexposure
VibrationporametersMethod
Outcome
BBN, 101dB, 20 rain
10 and 20 Hz, 1000
cm/s• or 5, 10,
TTSat
behavioralTTS
I and 4 kHz due to
combinationgreater than that
due to either alone;additive
and 20 Hz, 500
cm/$ 2 or
2, 5, and 10Hz,
100 cm/s 2, 20
relationship
rain or • 60 rain
Yokoyamaet al. (1974) human
71
BBN, 100dB
("82 dB SL"},
5 at 6 ram, or
TTS at 4 kHz due to combination
16.7 Hz at
greaterthan that due to either
20 min
3 nun, 20 rain
alone;vibrationaloneproduced
no TTS
Hamernik
etaL(1980) chinchilla15 155-dB
impulse
30Hz, 1g,50rain
AERaudiograminteractionandsynergistic
effects
113-dBimpulse,
30Hz, 1 g,
behavioralor
l/s, 10 days
10 days
l/rain, 50 rain
Hamemiketal.(1981b)chinchilla 13
1322
J.Acoust.
Soc.Am.,VoL76,No.5, November
1984
evident
interaction evident in TTS and
AER audiogram PTS measurements
and HC counts
LarryE.Humes:
Noise-induced
hearing
loss
1322
apparent
opposition
to thisconclusion
is theevidence
supportingtheexistence
of a "criticalperiod"of susceptibility
to noise-induced
heatinglossin themouseandthehamster
II. INTERACTIONS WITH PHYSICAL
(Saunders
andHirsch,1976;Staneket al., 1977;Beckand
CHARACTERISTICS
Seifter,1978).The so-calledcriticalperiodof susceptibility
A. Age
manifests
itself,in a plotof noise-induced
hearinglossasa
The influence
of thesubject's
ageon subsequent
noise- functionof age,asa sharppeakin thefunctionat approxiinduceddamageto the auditorysystemis a topicthat has mately18daysof agefor themouseanda roundedpeakfirst
receivedmuchattentionduringthepastdecade.Studiesof appearing
at approximately
30 daysof agefor thehamster.
in noise-induced
damageat ageslessthan 18
thiskindcanbedividedintotwotypesaccording
to theend The decrease
of theagecontinuum
with whichtheyhavedealt.TableV
and30daysforthemouse
andhamster,
respectively,
canbe
however,by developmental
changes
in the perisummarizes
l 1studies
dealing
withtheyoungendoftheage explained,
Relkinet al. (1979),for
continuum.
Eachstudyin TableV suggests
that younger pheralpartof theauditorysystem.
animalsaremoresusceptible
to hearingdamagethanadult instance,noted that the admittanceof the hamster'smiddle
with age up to approximately35 days,after
animals.A widevarietyof measures
of damageof the audi- ear increases
some
simulations
ofactualworkconditions,
wouldappear
to
bepartio_•larly
valuable.
which it remainsfairly constant.Thus a soundexposure
tory systemhavebeenused,althoughonly onestudymade
useof behavioral
measures.
Moreover,fivedifferentspecies
monitored in the ear canal of the hamster will not reveal the
have been studied.
decrease in the effective stimulation of the inner ear of ani-
Ol•ecan$nmmal'ize
thedatabestby statingthat,once mals youngerthan 35 days.Thus the reductionin noisetheperipheral
auditory
system
isfullydeveloped,
theyounger inducedhearinglossbelowan ageof 30 daysin thehamster
theanimal,thegreaterthedamage
fromnoiseexposure.
In
maysimplyreflectthegreaterattenuation
of thenoisebythe
TABLE V. Summary
of studies
examining
theinteraction
of noisewithsubject
age--youth.
Study
Species
N
Noiseexposure
Ages
Falk etaL {1974)
guineapig
30
BBN, • ] 20 dB,
2days,$days,$months HC counts
Method
30h
Outcome
bothyoungergroups
demonstrated
greaterHC loss
than adults
Coleman11976)
guineapig
45
PT (4 kHz),
3, 10,49 weeks
HC counts
greaterHC lossin youngest
groupcomparedto eitherof
othergroups
8 weeks,adult
CM, HC
CM indicategreaterIo•sin
youngergroupsfor 115-rib
levelbut not others;no
differencein HC lossfollowing
exposureat any level
! 19dB, 2 h
- Price(1976)
cat
I11
PT (5 kH_z),
•105, 115, 135
dB', $0min
Saunders and Hirsch
C$7BL/6J mouse
OBN (CF = ! 1.3
kHz), 110dB,
(1976)
count
14, 18, 28,
38, 58 days
CM
"criticalperiod"for age-related
susceptibility
changes;IS-day~
old nn;malsmostsusceptible
2, 120days
behavioral
threshold at
gkHz
younggroupdemonstrated
• 20 dB greaterPTS at 8 kHz
11, 15, 19,23,
27, 31, 40, 48,
55, 62, 75 days
CM
criticalperioddemonstrated
again;broadpeakfrom28to 55-day-oldalaimnl.•
15,28,40,54,
85 days
CMand
criticalperiodobserved
with
evokedresponse40<lay-oldanimalsexhibiting
greatestloss
16,22,28,40,
WNAP
greaterlossof WNAP, both
temporaryand permanent.in
16-to 22-day-oldanimals;PTS
oRlyill animals <40.-daysold
HC count
results consistent with above
WNAP
loss(WNAPthreshold)
increased
2min
DantoandC•;•,,o
0977}
guineapig
StaneketaL (1977)
hamster
6
NBN (CF- 4 kHz),
1 I$ dB, I h
143 OBN (CF = 7.07
kHz), 125dB,
2 1/2 min
BeckandSeifter{1978) hamster
25 PT (3 kHz),
110dB, 10 rain
LenoiretaL{1979}
72 BBN, 120dB,
rat
30 rain
60, 100days
LenoirandPujol(1980) rat
72 BBN, 120dB,
3Orain
Henry(1982)
44 OBN(CF= 1.7kHz), 60,90, 120,360days
mouse
16,22, 28, 40,
6O, 100days
124 dB, 5 min
YanzandAbbas{1982} mouse
160 BBN(4-20kUz•
as agedecreasedbelow 120days
18,28days
WNAP
lossgreatestin youngeranlrnal•
115 or 120
only at higher exposurelevel
10rain
(120dB}andonlyfor thresholds
measured30 dayspostexposure
'Actual exposurelevelsweredeterminedindividuallyusingthe input level yieldingthe maximumCM on the CM input-out function(MAX + 0,
MAX 4- 10,and MAX 4- 30 dB).
1323
d. Acoust.Sec.Am.,VoL76, No.5, November1984
LarryE. Humes:Noise-induced
hearingloss
1323
middleearsofanimalsyounger
than35days.We•ter (1982)
tary dataon permanent
noise-induced
hearingloss.
The studiesby Macrae 11971)and Welleschikand
matureuntil approximately18 daysof age.Thusthissame Raber(1978}indicatethatthelossof hearingassociated
with
explanation
appliesto thecriticalperiodobserved
in thedata
the agingprocess(presbycusis}
interactswith that due to
frommice.The criticalperiod,therefore,is notinterpreted noiseexposure.
More specifically,
bothstudiessupportthe
asan exceptionto thegeneralization
described
earlier.
concept
ofadditivitybetween
presbycusis
andnoise.Thatis,
In light of the verystrongsupportfor the existence
of
thehearinglossdueto noisealoneandthat dueto agealone
age-dependentchangein susceptibilityto noise-induced addto describe
thelossfrombothfactorstogether.Thisfindhearingdamageonemightaskwhethera similareffectmaniing is consistent
with the previouswork of Mo!lica (1969).
indicates,moreover, that the middle ear of the mouseis not
festsitseftin someof the interactionsof other agentswith
noise.Apparentlythisquestionhasnot beenposedpreviously. It is nonetheless
an importantconsideration.Many neonatesin intensivecare units,for example,are exposedto a
fair amount of noise. This is demonstratedin Table VI,
Novotny's survey(1975b)of a smallernumber of industrial
workers(n ----80},however,failedto observeadditivity.The '
hearinglossobservedin two differentagegroupsexposedto
presumably
identicalnoisefor either5 or 10 yearswasthe
sameforbothagegroupsdespite
thepresence
ofpresbycusis
which summarizes several studies of noise levels in neonatal
in the older group.Novotny(1975b}hasalsoobservedno
intensivecareunits.The neonateis subjectedto thesenoise differencein temporary noise-induced
hearing loss for
levels24 h/day typicallyfor 3-4 weekswhilesimultaneously youngand elderlyadults.
beingadministeredantibioticssuchas kanamycin.MoreData on the interaction
of presbycusis
andnoiseexpoover,the datafrom Besset al. 11979)indicatethat the neosureareof considerable
practicalimportance.
For example,
natesare alsofrequentlysubjectedto impulsivesoundsapadditivityof presbycusis
andhearinglossdueto noiseexposure is assumed in the determination of the amount of comproximating130-140 dB SPL. The noise/drugand noise/
impulseinteractionhas been reviewedabove.The issue pensable
hearinglossto whichan employee
isentitled.If a
raisedhereis whetherthe magnitudeof theseinteractionsis
threshold
of40 dBHTL ismeasured
in thehighfrequencies
increased
furtherfor youngeranimals.In thisregard,it is of
fora 60-year-old
industrial
employee
and25 dBof hearing
interestto notethatBernard(1981)hasreportedthatyoung lossisexpected
duetoagealone,then15dBofhearing
loss
kittensare moresusceptible
to kanamyeinototoxieitythan
(40-25dB)wouldbeascribedto exposure
to industrialnoise.
adult animals.McDowell {1982},on the otherhand,failedto
Asidefromtheissueof thedetermination
of compensable
observea comparableeffectof ageon gentamyeinototoxihearingloss,the interactionof presbycusis
and noise-incityin theguineapig.The youngest
ageexploredin thelatter
ducedhearinglosspermeates
virtuallyall large-scale
retrostudy, however,was only 4 weeks. Perhapsthe use of
spective
studies
of noise-induced
hearinglossin man.Hearyoungeranimalsin the study of McDowell would have reinglevelsin suchstudies
are"agecorrected"
by subtracting
yealedageeffectssimilarto thosereportedby Bernard.
presbyeusis
valuesfrom the measured
hearinglevels.Thus Turningnowto theotherendof theagecontinuum,the
additivityis assumed.
issueof the interactionof agewith noise-induced
hearing
losshasreceivedsurprisingly
little attention.
TableVII sum-
If an appropriate
animalmodelof presbycusis
canbe
found,then the issueof additivitycanbe addressed
more
marizes the recent work in this area. Of the four studies
directly.One possibleapproachwould be as follows.A
shownhere,all havebeenconducted
with humansubjects, noise-induced
hearinglosswouldbe createdin younganiandthreeof thefourrepresent
analysisof industrialor milimals(adults),
andthenthe animals,aswell asa groupof
TABLE ¾I. Summaryof studiesmeasuring
noiselevelsin neonatalintensive
careunits.
Study
Equipment
or location
Noiselevel(dBSPL)
Selenyand Streczyn(1969)
incubators
68-82 dB Lin at 125Hz
ICU
55-60 dB Lin
Leagueet al. (1972)
infantoxygentent
80 dBC
incubators
ICU
72-74 dBC
62 dBC
Hoffmanet al. (1972)
Pressurebox
80-86 dB Lin
Falk andWoods(1973)
incubator
ICU
80 dB Lin (66dBA)
73 dB Lin [60dBA)
Blennow
etal. (1974)
incubator
80dBLin (61dBA)
Vidyasagaret al. (1976)
ICU
60-70 dBA
Shenai(1977)
Bess
etaI. (1979)
incubatorin nursery
58-68 dBA
incubator in transit
70-103 dBA
incubators
73dBC(55dBA)
incubators with life
support
equipment
80dBC(60dBA)
strikingsideof
incubator
1324
J. Acoust.
Soc.Am.,Vol.76,No.5, November
1984
! 30-140dBpeSPL
LarryE.Humos:
Noise-induced
hearing
loss
1324
TABLE VII. Summaryof studiesex•minlngthe interactionof noisewith subjecta•e--elderly.
$fudy
Sl•ci•s
N
Noiseexposure
Ages
Method
O•tcome
Macrae(1971)
human
~200
militaryveterans
30-75 years
longitudinalstudy additiverelationshipbetween
of HL at ! and
NIHL andpresbycusis
4 kHzin
militaryveterans
no longerexposed
to noise
Novotny(197Yo)
human
80
industrialemployees
30-59 years
cross-sectional
study;compared
HI..s of work•m
for equalexposuredurations
(5 or 10years),bothagegroups
showedidenticalHLs; not
enteringat
additive
young age
(20-25 years)to
thoseentering
later (50-55 yea•}
Welleschik
andRaber
(1978)
human
25 544
industrialemployees; 20-60 years
levelsrangingfrom
> 97 dB{A}to < 85
cross-sectional
study;compared
additivityapparentexceptat
3 and4 kHz for age > 55 yearsand
NIHLa
duration < 15 years
dBA and duration
workersgrouped
by age{<25,
from0 to > 25 yearn
of
26-35, 36-45,
46-55, and
> 55 years)and
yearsof
exposure{0,
1-$. 6-15,
16-25, and
> 26 years)
Novotny(1975a)
human
160
BBN, 85 dB,
3min.
30-64 years
'ITS in
fourgroupsof
TTS samein all agegroups
listeners
having
=highfrequency
SN hearing
loss
ginningthe noiseexposurewith a 30 dB SPL threshold
wouldalsoshiftto a thresholdof 40 dB SPL resultingin a 10dB thresholdshift.This typeof tradeoffbetweenpre-exposure thresholdand thresholdshift has been observedby
Mills (1973}and Man eta/. (1975).Often, however,this perfect tradeoff is not observedas noted severalyears ago
be needed.
(C}1origeta!., 1961; Ward, 1973) and more recentlyby
Howell {1978)and BoReand Variot (1979).This imperfect
B. Previous noise-induced hearing loss
tradeoffbetweenpre-exposure
thresholdshiftandpre-expoAt leastsixseparate
investigations
haveaddressed
the surethreshold
canbeexplained
to a largedegreebylessthan
issueof whethernoiseexposure
interactswith preexisting perfectagreement
between
theregionofpreexistinghearing
noise-induced
hearinglossto produce
greaterlossof hearing lossand the regionaffectedby the new exposure{Humes,
thanthatobserved
in normalhearers(essentially
the "noise 1980;Humesand Koval, 1981}.
Thesecondconclusion,
drawnprimarilyfromthestudy
exposurealone"condition).Table VIII summarizes
these
ofPye {1974},is that whenthe regionofpre-existingdamage
investigations.
The resultsof the studiessuggest
the followfailsto overlapwith the regionaffectedby the experimental
'ins two generalconclusions.
First, whenthe regionof preexistingnoise-induced
hearinglosscoincides
withtheregion noiseexposure,thetotal regionof damageisthe simplesum
of thetwo.Thusif noiseexposure
A produces
a 20-dBlossof
affectedby the noiseexposure,
thethresholdshiftis lessin
hearing
at
4000
Hz
and
exposure
B
produces
a
20-dBlossat
the impairedear, but the resultingshiftedthresholdsare
500
Hz,
when
presented
together
the
composite
hearingloss
identical.Shiftedthreshold
issimplythesoundpressure
levwill be 20 dB at 500 Hz and 20 dB at 4000 Hz. Thus a lowel of the toneat thresholdfollowingnoiseexposure.Thus if
frequency
noiseexposure
doesnotinteractwith a high-frean individualbeginstheexposure
with a thresholdof 10dB
quency
exposure
and
vice
versa.This, of course,assumes
SPLandshiftsto a threshold
of 40dBSPLfollowing.
noise
exposure
resultsin a shiftconfined
to
exposure,
a 30-dBthreshold
shifthasresulted
fromthenoise thatthelow-frequency
regionof thehearingorgan.
exposure
(shifted
threshold
= 40dBSPL).An individualbe- thelow-frequency
nonexposed
controlanimals,wouldbe followedlongitudinally. A secondapproachwould be to exposeseparate
groupsdifferingin ageand,therefore,pre-exposure
hearing
loss(otherwiseno presbycusis),
to the samenoise,and to
observethedifferences
in resultanthearinglossand underlyingdamage.A controlgroupfor eachagestudiedwouldalso
1325
J. Acoust.Sec. Am., Vo1.,76.No. 5. November1984
Larry E. Humes;Noise-inducedhearingloss
1325
TABLB VIII. S. mm*ryof studies
examining
interaction
of noisewith previous
noisedamage.
Study
Species
Mills(1973)
chinchilla
N
4
Noiseexposure
Method
Outcome
OBN(4kHz),
behavioral
threshold
at 5.7kl-Iz
shifted thresholds identical for
normaland hearing-impaired
80 dB, $ days
anmals
Pye{1974)
guineapig
24
PT 120dB,2 k.H•
nodirefence
in patterns
of
HC cotmrs
damagebetweenthosehaving
normalcochle•andthosehaving
priorthma•eat otherfrequency
I'C•OH
20 !d-L• • 0r •
rain; 3-4 week•
betweenexposures
ManetaL {1975)
hunch
17
military
longitudinalstudy;subjects
had mild unilateralhighfrequencysensorineural
hearinglossdueto noiseat
impairedear changesvery little
while normal ear shifts to
mild high-frequency
•en•orineural
hearingloss
•-3 years•ater
Howell{1978)
h.mnr•
449
industrial noise at
behavioral threshold at 6 kHz
> 100, 90-99, or
<90 dBA over
threshold shifts about 5 dB
greater(15vs 10dB}for tho•e
workershavingbetterhearing
thresholdsat thebeginning
(HL < 20 versusHL • 39 dB)
7-yearperiod
Voidrich(1979)
guineapig
10
histological
examination
of organ
145 dB, 5 min,
30min
of Corti; half exposedto both
noisesand half receivedonly
the moreintense;controlgroup
run at 90 dB only
PT {2.67kHz},
TTS at 4 kHz from 2-10 rain
•I'S less(•7 vs •20 riB) in
96dB, 30rain
post exposure
three listeners wiht mild-moderate
noise at 90 dB for
6
extentof lesionalongbasilar
membranegreaterfor combined
exposures
(7.25mm) than for
moreintenseonly (2.73nun};
1/30BN (1 kHz),
followedby same
Bette
and
V•iot{1979}bumnn
wheneachgroupis standaxdized
for ageand noiselevel>90 dBA,
nosignificant
damage
in controls
high-frequency
sensorineural
HL
The studyby Voidrich(1979)in TableVIII isan interestingone.Voidrichdemonstrated
a sequential
interaction
between
pre-existing
injuryandsubsequent
noiseexposure.
The novelfeatureof thi.•studyis that the exposureproduc-
eyecoloronsubsequent
noise-induced
hearing
loss,
onlythe
studiesof Hoodet aL (1976),CarlinandMcCroskey(1980),
and Garberet al. (1982)can be considered
as supportfor
suchan interaction.The studiesof Hood et al. (1976)and
ingthe"preexisting
injury"wasfollowed
immediately
by Garberet al. (1982),however,measuredthe temporary
followinga l-rain expotheexperimental
noiseexposure.
Theregionof injurywas thresholdshiftat 10spostexposure
sure
to
an
intense
1000-Hz
pure
tone.
The generalization
of
extended
considerably
whena moderate
levelnoiseexposure
the
data
to
the
sound
exposures
typical
of
the
workplace
is
waspreceded
imm•ately bya moreintense
exposure
tothe
apparently
poor,asevidenced
bythestudies
ofCarter(1980),
samenoisethanwheneithernoisewaspresented
alone.A
Carteret al. (1981),Thomaset al. (1979),andCunningham
smallnumberof animalsweretested,however,and the proof Hoodetal. (1976),moreceduresandresultswerenot describedin detail.The findings andNorris(1982).The findings
over,
do
not
offer
strong
support
for the relationship
of Voidrich(1979},therefore,needto be replicatted.
betweeneyecolorandnoise-induced
hearingloss.Of thefive
C. Degree of melanlzatlon
exposure
levelsusedby theseinvestigators,
for instance,
eye
Melaninis a substance
presentin theinnerearthat is colorinteractedwith TTS at only the highestlevel(127 dB
theseinvestigators
suggest
thatblue-eyed
subthoughtby someto beimportantfor normalphysiological SPL).Second,
greaterlossofhearingfollowing
function(Fisch,1959).Melaninin theirisof theeyeandin jectsnotonlydemonstrated
but alsomanifesttheskinisresponsible,
in largepart,forthepigmentation
of noiseexposurethanbrown-eyedsubjects,
as
thesetwoorgans.Considering
eyecolorfirst,severalinvesti- ed delayedrecovery.Recovery,however,wasexpressed
Consider,
gatorshavesuggested,
onthebasisof noiseexposure
experi- percentrecoveryat 30 and 50 s postexposure.
however,thefollowinghypothetical
case.Suppose
thatbluemenCs,
thatthoseindividualshavinglessmelanincontentin
manifesta 20-dBthresholdshiftat 10spostextheiris(blueorgreyeyes)
exhibitgreaternoise-induced
hear- eyedsubjects
subjects
exhibita 10-dBshiftin
ing lossthan thosewith greatermelanincontent(brown posurewhilebrown-eyed
eyes).Thisnotionwasapparentlyfirstadvanced
byTota and threshold.Now assumefurther that both groups exhibit
identicalrecoveryratesof 5 dB every20 s. At 30 and 50 s
Becel{1967).
postexposure
bothgroupswill recoverby 5 and l0 dB, reSeveralinvestigations
of thisissue,summarized
in TaExpressed
aspercentage
recovery,
however,the
ble XX, havebeenconducted
overthe pastdecade.Of the spectively.
shift(brown-eyed
subeightinvestigations
examining
theinfluence
of thesubject's grouphavingonlya 10-dBthreshold
1326
J. Acoust.So(:.Am.,Vol.76, No.•. November1984
LarryE. Humes:Noise-induced
hear'ngloss
1326.
TABLE
IX.Interaction
ofnoise
with
thedegree
ofsubject's
meJanization
asmanifested
ineye
color
andrace.
ManifestationStudy
Eyecolor
Karlovich
(1975}
N
40
Noiseexposure
Method
Outcome
PT (I kHz},110dB, TTSo.3,
TFS•
nodependence
oneyecolor
3 rain
at 1.414 kHz
PT {I kHz),
•So.•6 at I kHz
usingcontinuous
usingpulsedtone
Hoodetal. 0976}
38
87-127 dB in
effectof eyecolorobserved
onlyat 127-dB
exposure
level
tone
lmin
Carter{1980)
257
industrial,
3 years retrospective
significant
difference
onlyat 4 kHz in lea ear
analysis
of NIPTS
at sevenfrequencies
in each ear and for
two categories
of
eyecolor
Carteret oL
{1981}
1! 8
military,
•8 years
retrospective
significant
'difference
onlyat 3 kHzinleftear
analysis
of NIPTS
at sevenfrequencies
in each ear and for
two extremesof eye
color continuum
Carlinand
McCroskey( 1980}
100
employees
of
oil refinery
retrospective
analysis
of HL
at 1, 2, 3, 4, and
no difference in His between brown- and
blue-eyedsubjects,
but grey-eyedsubjects
demonstrated
greaterloss
6 kHz
Thomaset aL
(1979}
675
Naval aviators
ratio of blue-eyedto brown-eyedmen was
longitudinal
only shghtyhigherin impairedsub•cts
studyover20-year
period;audiograms
divided into normal
{< 25 dB HL, 0.5-6
kHz} andimpaired
(>50dBHLat
somefrequency)
Garberetal.
30
(1982)
Cunninghamand
Norris{1982}
PT(I kHz,
107and
117dB. I rain}
130
onlys'•nificantdifferencewasbetweenalbinos
and brown-eyedsubjects
continuoustone
for albinos,
blue-eyed
subjects,and
brown-eyedsubjects
TTS.,6for l-kHz
industrial,
78-92 dBA,
retrospective
analysisof His
9-14years
(• I
forthreegroups
of
no effectof eyecolorwhencontrolledfor
ageand yearsof exposure
eyecolor
Karsalet al.
(1972}
Roysteret al.
{1978}
836
10000
longshoremen
retrospective
for I to :>40years analysisof
HIS
blackAmericansshow15-20dB lesshigh-frequenoy
lossat all durationsof employment
varietyof
industrial
whitemales(WM} appearclearlyseparated
fromother
threegroups(WF, BM, BF) andhave-- 10dB poorer
retrospective
analysis
of His
exposures
-'10-1• ye• •)
high-frequency
thresholds
jects)will haverecoverypercentages
of 50% and 100%at 30
and50 s postexposure,
respectively.
Comparable
valuesfor
the subjectshavinggreaterinitial losswould be 25% and
50% at 30 and 50 s postexposure,
respectively.
Thus the
delayedrecoveryobserved
by Hood etal. (1976)may simply
reflecttheuseofpercentage
recoveryto describe
thedataand
may not existwhenexpressed
in termsof dB/s. Consistent
with this explanation,differencesin percentagerecovery
greaterhearinglossthan eitherblue-eyedor brown-eyed
subjects.There was no difference,however,for blue-eyed
and brown-eyedsubjects.
The grey-eyedsubjects,
however,
were much smallerin number(n ----12 vs n ----33--40),approximately5-8 yearsolder,and exposedto noise3-5 years
longerthan the other two groups.Perhapsthesefactorsare
responsible
for theirhigherhearinglevels.
were observedonly at the soundlevel (127 dB) manifesting
noiseexposure.This is especiallytrue for noiseexposures
morerepresentative
of industrialor military settings.
differences
in thresholdshiftat 10s postexposure.
In the studyby Carlin and McCroskey(1980)a retrospective
analysis
of thehearinglevelsof 100employees
of an
oil refinery indicatedthat grey-eyedsubjectsexhibited
1327
J. Acoust.Soc. Am., Vol. 76, No. 5, November1984
Insummary,
eyecolor
does
notappear
tointeract
with
As mentionedpreviously,melanizationalsomanifests
itseffinskinpigmentation
(darkerpigmentation
correspondingto greatermelanization).
Karsaietal. (1972)andRoyster
Larry E. Humes:Noise-inducedhearingloss
1327
et aL (1978}bothobserved
greaterlossof hearingin white
workersthan in black workersin retrospective
studiesof
hearinglevelsin'industrialpopulations.
Thusit wouldappearthat thoseemployees
havinggreatermelanization
evidencelesshearinglossfromindustrialnoiseexposure
than
thosehavinglessmelaninin their systems.More recently,
however,Royster and Royster{1982}indicatedthat black
individualsmay not necessarilyhave lessindustry-related
noise-induced
hearingloss.When hearingthresholdsfrom
an industrialnoise-ex•
populationare comparedto
thosefrom a nonindustrialnoise-exposed
populationthat
hassimilarhistoriesof ear disease,
recreationalnoiseexposure,etc.,theyshowthatapproximately
thesameamountof
industry-related
noise-induced
hearinglosswasobserved
for
bothwhiteandblackworkers.Theracedifference
in hearing
thresholdsfor the nonindustrial
noise-exposed
individuals,
however,hasnot beenexplainedfully.
The assumptionunderlyingthe hypothesisthat interactionsof eyecolorand'racewith noise-induced
hearingloss
are due to difference in melanin content of the inner ear
posures
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assumes
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further assumption
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physiologically.
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The recentliteratureon the interactionsof otheragents
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exist betweenexposuresto steady-statenoiseand several
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of an interaction
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The presenceof an interactionbetweennoiseand wholebodyvibrationislesswellestablished.
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ACKNOWLEDGMENTS
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Thiswork wassupportedin part by a contractawarded
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