Risk Finnishforestryworkers · Br J Ind Med: first published as 10.1136/oem.46.7.439 on 1 July 1989. Downloaded from . 440 recumbentposition,andthemeanvalueoftheleft and right arm

British Journal ofIndustrial Medicine 1989;46:439446

Risk factors in the genesis of sensorineural hearingloss in Finnish forestry workersI PYYKKO,' K KOSKIMIES,2 J STARCK,2 J PEKKARINEN,2 M FARKKILA,3R INABA2

From the Department ofOtolaryngology,' University Hospital ofHelsinki, SF00290 Helsinki; Institute ofOccupational Health,2 Helsinki; and Department ofNeurology,3 University ofHelsinki, Helsinki, Finland

ABSTRACT A detailed analysis of risk factors for the development of sensorineural hearing loss(SNHL) was carried out in 199 forest workers. The hearing threshold of both ears at 4000 Hz wasmeasured, and the effect of age, exposure to noise, blood pressure, presence of vibration inducedwhite finger (VWF), tobacco smoking, plasma LDL-cholesterol concentration, and consumption ofdrugs were evaluated by multiple linear regression analysis. Aging was the major risk factor, followedby exposure to occupational noise and the presence ofVWF. Plasma LDL-cholesterol concentrationand the use of antihypertensive drugs also correlated significantly with SNHL. These main factorswere able to explain about 28% of the SNHL variance. Additional factors in the analysis, includingsmoking, systolic and diastolic blood pressure, and consumption of salicylates did not significantlycontribute to the genesis of SNHL.

Despite the careful application of the equal energyprinciple in the analysis of populations exposed tonoise, variability in the development of sensorineuralhearing loss (SNHL) is a dominant feature. Whereasthe hearing of some people is resistant to the harmfuleffect of noise, some are exceptionally vulnerable. Ithas been suggested that this individual resistanceagainst occupational noise depends on heredity, diet,pigmentation, drugs, blood pressure, non-occu-pational exposure to noise, etc."A Recently we haveshown a link between vibration induced white finger(VWF) and SNHL56 suggesting that factors disturbingthe peripheral circulation may influence cochlearfunction and hearing. The relative role of differentfactors in the genesis of SNHL is, however, poorlyunderstood.

In the present study we have examined a populationof workers exposed to noise and vibration. Thepurpose of the study was to evaluate the relativeimportance of selected risk factors in the aetiology ofSNHL.

Subjects and methods

The investigation was carried out in 1986 in connec-tion with a compulsory health survey in the county ofSuomussalmi in north eastern Finland. The popula-tion in this area was stable and we have followed up

Accepted 4 July 1988

these workers since 1972 in a longitudinal survey.7 Allthe professional forest workers of the major employ-ing company (National Board of Forestry) took partin the study. During a physical examination the earswere inspected, and workers with bilateral middle eardisease were excluded from the study. The studycomprised altogether 199 professional forest workers.Their mean age was 43-1 years (range 25-60) and meanexposure to chain saw noise was 15-370 hours (range0-32 200).

Hearing was tested in an acoustically treated butnon-isolated room after absence of occupationalexposure to noise for 15 to 48 hours using a pure toneaudiometer (Maico Ma-19). A more detailed discrip-tion of the threshold evaluation is given elsewhere.89For the characterisation of individual SNHL meanhearing threshold at 4000 Hz was used. In cases ofunilateral ear disease the hearing ofthe healthy ear wasused.A history ofwork habits (daily chain saw operating

hours, alternative working tasks) were obtainedannually during a longitudinal survey to get anestimation of exposure. The use of earmuffs, a historyof vibration syndrome, and smoking habits were alsorecorded. Subjects were divided into six categoriesdepending on the extent of their smoking.9 If morethan ten years had passed since giving up smoking thesubject was classified as a non-smoker.A cbmplete medical examination was performed.7

Blood pressure was measured in both arms in the439

on March 22, 2020 by guest. P

rotected by copyright.http://oem

.bmj.com

/B

r J Ind Med: first published as 10.1136/oem

.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

440

recumbent position, and the mean value ofthe left andright arm for systolic and diastolic blood pressuremeasurements was taken after the subject had beensupine for 20 to 30 minutes.For each subject, serum high density lipoprotein-

cholesterol (HDL-cholesterol) and total cholesterollevels were measured. Low density lipoprotein-choles-terol (LDL-cholesterol) content was calculated forrisk analysis.A history of head injuries, noisy activities during

free time, annual consumption of salicylates and otherantiphlogistic drugs, as well as the use of antihyper-tensive drugs, was recorded. Other possible sources ofSNHL were noted. It was found that noisy free timeactivities or head injuries did not significantlycontribute to SNHL and they are therefore notcommented on in the present report.

RISK EVALUATION BASED ON ROBINSON'S MODELMeasured hearing loss was compared with estimatedmean hearing loss evaluated using Robinson's modelwhich gives the age corrected hearing level that isrelated to A-weighted equivalent noise level in thefollowing way.'"

HTL = 275 (1 + tanhEAi Lf+UP)+U + Cf(N-20)2 (1)

HTL = actual hearing level exceeded by p percent of the population

EAi = LAqi + 10 lOg(Ti)EAi = A-weighted noise immission level

LAcqi = A-weighted equivalent dB level (8 h/d,5 d/w)

Ti = exposure time in years

Ni = age in years

Cf and Lf = coefficients depending on audiometricfrequency

Up = constant depending on the selected per-centage p.

This model was applied to the data in two differentways for comparison with actual HTL valuesmeasured among forest workers in Suomussalmi.Firstly, HTL was calculated using age, exposure time,and exposure level as independent factors for eachindividual. Exposure time (in years) was related to thetotal sawing time (in hours) assuming a working timeof 1000 hours yearly. The exposure level depended onthe period of earmuff use and calculated for eachworker separately using logarithmic conversion.Secondly, the effect of age alone was examined byfixing the exposure level to the median value of thewhole population and increasing age one year at a timefrom 20 to 60. The median exposure time was 16-0years.

Pyykko, Koskimies, Starck, Pekkarinen, Farkkila, Inaba

For risk evaluation, the audiometric frequency was4000 Hz and the constants Cf = 0-012 and Lf = 112-5dB. The values were calculated for median (p = 50%)andUp = 0. Thus equation (1) becomes:

HTL 27)51+tan0A +0012(N-20)2 (2)

ex -x

where tan h (x) = ex e,

StatisticsIn risk evaluation a multiple linear regression analysiswas used. To determine the significance of regressionthe determination coefficients for each factor weretested with Student's t test. For individual factors thesubjects were divided into two groups depending onthe risk level of each factor. The difference in hearingbetween the groups was evaluated with age correctedSNHL. When p was less than 0 05 the result wasconsidered statistically significant.

Results

LINEAR REGRESSION ANALYSISThe measured hearing loss for the group was 27-3 dBat 4000 Hz. In the linear regression analysis aging wasthe most important single risk factor for SNHL andexplained 25% of the variance in SNHL at 4000 Hz.Exposure to noise explained 9% of the variance inSNHL at 4000 Hz. A statistically significant correla-tion was also found with the presence ofVWF, serumLDL-cholesterol concentration, and use of antihyper-tensive drugs, and SNHL at 4000 Hz (table). Acombination of these risk factors explained about 28%of the variance observed in the SNHL at 4000 Hz. Allthese significant risk factors also correlated with age.Thus exposure (r = 0 612, p < 0.001), LDL-choles-terol(r = 0O34,p < 0 01),VWF(r = 0-251,p < 0 05),

Individual partial correlation coefficients, their cut-offlevel inrisk analysis, and their effect on hearing (n = 199)

Partial Effect oncorr hearing

Factor coeff Cut offlevel (dB)

Age 0-514 - 7.6*Exposure 0 318 - 17.8*VWF 0-202 Present or not 1.5LDL-cholesterol 0-156 50 mmol/l 0 5Salicylate 0-064 50 tablets a year 0 9Smoking 0100 Smoker or not 0 4Antihypertensive

drugs 0-165 User or not 1.0Diastolic blood

pressure 0046 90 mm Hg 0 1

*Estimated according to Robinson's model.'"



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

Riskfactors in the genesis ofsensorineural hearing loss in Finnishforestry workersForest workers, n 199 (1986)

0 .

* -00

_.*S 0.0 0~~~AK0

@00

8.00* 0

0.0a08-10

10 20 30 40 50 60 70 80

Hearing level, measured at 4000 Hz (dB)

Fig 1 Relation between estimated hearing loss according to Robinson's model' and measured hearing loss inforest workers.

and use of antihypertensive drugs (r = 00.05) were age dependent. The sensorineurloss did not correlate significantly with thetion of salicylates, diastolic and systolic bsure, and smoking.The table gives the partial correlation e

1.0 20 3C 4-0 5.0LDL-CHOL (rnol/l)

60

Fig 2 Distribution ofsubjects according to plasmcholesterol concentration.

'-215, p <ral hearingconsump-

for determination as well as the cut off level of eachrisk factor and their effects on hearing.

)lood pres- EXPOSURE AND AGEThe mean A-weighted equivalent noise level measured

coefficients outside the earmuffs was 96-103 dB(A) and therespective figures inside the earmuffs were 83-91dB(A). The mean duration of exposure for noise was16-0 years with a standard deviation of 6-4 years; theaverage percentage use of earmuffs was 79% duringthe exposure period. When the wearing time ofearmuffs was taken into account, the median exposurelevel to noise inside the earmuffs was 94 7 dB.9 Asignificant correlation was found between exposure tonoise and SNHL at 4000 Hz (r = 0-317, p < 0 001).Aging, according to Robinson's model applied to thepresent data, explained 7-3 dB of hearing loss onaverage. When the effect of age was removed by usingthe age correction provided by Robinson,'" the meanSNHL at 4000 Hz measured for the group was about19-7 dB. This is about the same (17-8 dB) as predicted

7T0 8'0 from a theoretical model calculated with fixedexposure time and level.9 The results indicate that the

:a LDL- combination of hand/arm vibration with noise doesnot contribute excessively to SNHL. Moreover, the

441

0

S0

*o0S

0 000

* 0

0

0

S

00

00 3

00

0

0

00

00

00

-10

00

0

30-

>, 24-

4,ac

1! 18-to

4,

12-

&6-

0-



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/


100-

450-in00z

10-

0 r

40-

32-

& 24-.O.

c 16-

8-

0 20 40 60 80 100 200Tablets/year

Fig 3 Distribution ofsubjects according to annual salicylateconsumption: one tablet contains 0O5 g ofsalicylate.

measured data showed wide case to case variationwhen values were compared with calculated valuesderived from Robinson's model (fig 1). Measuredvalues ranged from 0 to 70 dB, whereas Robinson'smodel ranged from 5 to 50 dB.

120-

100-

80-

V60-

40-

20

~~~0-

1-2 3 4 5 6Smoking class

Fig 4 Distribution ofsubjects according to smoking habits.

o-7

I I

60 80 100 120Diastolic blood pressure (mm Hg)

Fig 5 Distribution ofsubjects according to diastolic bloodpressure.

PERIPHERAL VASCULAR DISTURBANCESThe vascular component of the vibration syndrome,known as VWF, correlated significantly with SNHL at4000 Hz (r = 0-201, p < 0-01). When the subjects withVWF were removed, the average gain in age correctedhearing loss at 4000 Hz was 1 5 dB.

SERUM LIPID CONCENTRATIONWe found a significant correlation between serumLDL-cholesterol level and SNHL (r = 0155, p <0 05). Removal of subjects with raised LDL-choles-terol improved the average age corrected SNHL at4000 Hz with 0-5 dB (fig 2).

SALICYLATESThe effect ofsalicylate consumption on SNHL was notsignificant (r = 0 100, p = NS). When heavy users ofsalicylates (50 tablets or more a year) were removedfrom the group, the age corrected hearing wasimproved by 0 9 dB (fig 3).

SMOKINGSmoking was not significantly correlated with SNHLat 4000 Hz (r = 0 100, p = NS). When smokers wereremoved the average age corrected hearing level at4000 Hz improved by 0 4 dB (fig 4).

BLOOD PRESSURENeither the systolic (r = 0-029, p = NS) nor thediastolic blood pressure (r = 0-046, p = NS)correlated with SNHL. The increase in diastolic bloodpressure explained only 0 1 dB of the reduction of theage corrected hearing level (fig 5).

AA')

I

0- r-



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

Riskfactors in the genesis ofsensorineural hearing loss in Finnish forestry workersFrequency (Hz)

2000

443

4000 8000

Salicylate (n=82)

,Smoking (n=48)

LDL-CHOL (n=74)

Fig 6 Sensorineural hearing loss in 199forest workers at different frequencies. Hearing level is shown after exclusion ofdifferent riskfactors. Number ofsubjects remaining in analysis is shown in parentheses. VWF = Vibration induced whitefinger; neuropathy = subjects with history of vibration neuropathy; LDL-CHOL = raised cholesterol level; drugs = users ofantihypertensive drug; smoking = smokers; DBP = raised diastolic bloodpressure. Vertical bars indicate SD.

ANTIHYPERTENSIVE TREATMENTWe found a positive correlation between treatment ofantihypertensive drugs and SNHL (r = 0165, p <

0 05). Possibly, therefore, the lack of an associationbetween raised blood pressure and SNHL was maskedby treatment. When the subjects with antihypertensivetreatment were removed, the mean age correctedhearing level was improved in the remaining subjectsby 1 0dB.

Figure 6 gives the mean age corrected audiogram forthe group at frequencies of500-4000 Hz after stepwiseelimination of subjects owing to different risk factors.Removal of the different risk factors described aboveimproved the average age corrected hearing level at4000 Hz by 2-9 dB. At 200 Hz the improvement was

16 dB.

Discussion

In Finland noise induced SNHL is the leadingoccupational hazard in the 1980s and accounts forabout 2000 new cases annually-that is, 0-1% of theworking population. In the present study we com-

pared our noise exposure data with population dataon normal hearing reported by Robinson andSutton." " According to Robinson it is not generallyrealistic to compare the hearing of a noise exposedpopulation with an age matched "otologically nor-

mal" baseline, since the noise exposed population will

include those with adventitious hearing loss as well as

those with noise related loss.'3The age related hearing loss accounted in the

present study for an average of 7 3 dB. When, based onthis data, the noise induced hearing loss was cal-culated, the measured noise induced hearing loss (19 2dB) was close to that predicted from Robinson'smodel (17-8 dB). In risk assessment based on Robin-son's model we used a median percentile criterion thatgives the risk of hearing impairment expressed as

percentage of population exceeding the specified hear-ing threshold. The amount of age correction differs inthe available models for SNHL-for example, the ISOstandard proposal would give on average 3-5 dBgreater age correction for a population with a mean

age of 43 than Robinson's model does.'4 The variancecaused by risk factors cannot be eliminated by more

severe age correction.

EFFECT OF AGING ON NOISE INDUCED HEARING

LOSSIn the present study age, according to linear regressionanalysis, accounted for 25% ofthe variance at 4000 Hzbut there is no indication that age should be construedas a cause of sensorineural hearing impairment. Moreprobably, as individuals get older they will have beenexposed to, or suffered from, factors responsible forsuch impairment.'5The hearing loss caused by aging is gradual and

05-

500 1000

m102

-.'

I

20



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

444

forms a part of the progressive functional deteriora-tion associated with the degeneration of sensoryorgans.'6 17

Several factors have been suspected as contributoryfactors to presbycusis, including hypertension, diet,drugs, and exposure to social noise.' 18-22 In the presentstudy the age of the workers had a high correlationwith factors provoking SNHL. Thus exposure to noisecould explain 25% of the variance of age relatedSNHL. LDL-cholesterol was significantly correlatedwith age, as was antihypertensive treatment and VWF.The older subjects suffered more often from pain thandid the younger and consequently used more salicy-lates. Thus presbycusis is contaminated by severalfactors each of which impedes hearing, but throughsomewhat different mechanisms. The histopatho-logical findings presented by Schuknecht'7 may all becaused by these different, age related environmentalconfounding factors. Based on the present study wetend to disregard age as the primary reason for hearingimpairment in modern society.

INTERACTION OF NOISE AND VIBRATIONThe forest workers in the present study were exposedto noise of LAeq97-102 dB and weighted vibration of2-18 m/s2 in their work.5 We were unable to confirm thatcombined exposure to noise and hand/arm vibrationgenerates more SNHL than exposure to noise alone.So far, relatively few studies have considered the

combined effects of noise and vibration. One study ontractor drivers showed more SNHL than could bepredicted on the basis of the drivers' exposure tonoise.23 This was assumed to be the consequence ofexposure to vibration. A hazardous interaction be-tween noise and vibration has also been proposed byTaniewski and Banaszkiewics2' who found a connec-tion between VWF and SNHL, but there was noconclusive evidence for an interaction between hand/arm vibration and aggravated SNHL. Moreover, inthe present study we found that Robinson's model forSNHL estimated rather accurately the measuredSNHL, when the effect of age and exposure to noise,including the protection efficiency of earmuffs, wereconsidered in the calculation.

EFFECT OF VWF AND SNHLIn previous studies we5 6 8 9 and others25 26 have found acorrelation between VWF and SNHL. The reason forthe potentiating effect of VWF and SNHL is notknown, but we have speculated that vibration maycause "vasospasm" in the cochlea through auto-nomous vascular reflexes.8

Possibly, during exposure to noise and vibration,the sympathetic nervous system participates in thecontrol of the circulation of the inner ear-for exam-ple, by disturbing the local compensatory changes in


capillary flow during high local energy demands, asoccurs during exposure to noise. Vascular changes inthe circulation of the inner ear provoked by theactivation of sympathetic reflexes could aggravateSNHL in this manner. The mechanism that causesexcessive SNHL in people with VWF may beanalogous to the development of disturbed fingercirculation-that is, a continuous bombardment ofcentral autonomic vasoconstrictor reflexes on themalfunctioning local vascular flow.27 Nevertheless, therole of the autonomic nervous system in controllingthe cochlear circulation is still vague.28 29

EFFECT OF SMOKINGCigarette smoking is widely accepted as one of the riskfactors related to vascular disease, particularly tocoronary heart disease, but its role in hearing loss iscontroversial. Studies by Weston,30 Zelman,3' andChung et al' showed a positive correlation betweentobacco smoking and loss of hearing. In risk evalua-tion Chung et al showed that compared with non-smokers, heavy smoking increased SNHL at 4000 Hzby 6 dB.4 The mechanism is uncertain but it has beensuggested that higher carboxyhaemoglobin levels32may reduce the available oxygen for the organ ofCorti.4 The direct ototoxic effect of nicotine has alsobeen suggested.33

In line with some other investigators3435 we were notable to show that smoking is a significant individualrisk factor for SNHL. According to the linear regres-sion analysis smoking cannot be more than a minorconfounder36 and decreased hearing by only 0 4 dB.

EFFECT OF CARDIOVASCULAR FACTORS ON SNHLRosen et at'8 and Rosen and Olin37 suggest thatcardiovascular risk factors are closely related toSNHL. In these and some other studies SNHL seemsto be related to serum levels of fatty acids andcholestrerol."33'3 In the present study we confirmedthat the serum LDL-cholesterol concentrationcorrelated significantly with SNHL. A combinationof information of triglyceride level or cholesterolratio may provide additional data on the genesis ofSNHL.3940

Reports on the effects of hypertension are stillcontroversial. Although a correlation with raisedarterial blood pressure and SNHL has been shown4' 42the reciprocal connection is unknown. It has beenproposed that exposure to noise may cause an increasein blood pressure that may lead to aggravated hearingloss. Furthermore, not all studies have shown arelation between raised arterial blood pressure andSNHL.434 In animal studies there is, however, anindication that arterial hypertension aggravates agerelated hearing loss.43-45 In the present study we couldnot confirm that raised diastolic blood pressure sig-



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

Riskfactors in the genesis ofsensorineural hearing loss in Finnishforestry workers

nificantly contributes to SNHL, but this presumablywas due to treatment, since treatment with antihyper-tensive drugs correlated significantly with SNHL.

EFFECT OF SALICYLATES ON HEARINGThere is still uncertainty of the effect of salicylates onhearing. What seems to be well established is thatsalicylates produce loss of hearing and that this loss isreversible. After high doses of salicylates few morpho-logical changes occur in the inner ear.' Hawkins wasone of the first to show that salicylates reduce cochlearblood flow by causing capillary narrowing,47 whichappears to be produced by swollen endothelial cellsand possibly pericyte contraction.' In man the criticalototoxic salicylaemic level is remarkably high49 andcorresponds to the ingestion of 5-10 g of salicylicacid.5' The acute symptoms of hearing deficit arecharacterised by sudden onset followed by recoverywithin 1-10 days.' Such doses of salicylates were notreported by any of the forest workers in our study.

Salicylates seem to potentiate the hearing lossinduced by acute exposure to noise.5" Eddy et alshowed in acute experiments on chinchillas that thetemporary threshold shift produced by combinednoise and salicylate was significantly greater (55 dB)than that produced by noise (35 dB) or salicylate (30dB) alone.52 It is not known whether continual andprolonged salicylate intake in combination withenvironmental noise would promote SNHL in man. Inthe present study the moderate use of salicylates didnot appear to aggravate SNHL in the working popula-tion. Nevertheless, in the age corrected hearing level,the exclusion of salicylate consumers from the rest ofthe forest workers caused a gain in the average hearinglevel of 0 9 dB. Such an increase, though not statis-tically significant, suggests that even moderate use ofsalicylates in conjunction with environmental noisemay in some subjects be hazardous to cochlearfunction.

Requests for reprints to: Dr Ilmari Pyykko,Department of Otolaryngology, University Hospitalof Helsinki, Haartmanink 4, SF-00290 Helsinki,Finland.

References

I Hinchcliffe R. Epidemiology of sensori-neural hearing loss.Audiology 1973;12:446-52.

2 Hawkins JE. Comparative otopathology: aging, noise andototoxic drugs. Adv Otorhinolaryngol 1973;20:125-41.

3 Burns W, Robinson DW. Hearing and noise in industry. London:HMSO, 1973.

4 Chung DY, Willson GN, Gannon RP, Mason K. Individualsusceptibility to noise. In: Hamernik RP, Henderson D, Salvi R,eds. New perspectives on noise-induced hearing loss. New York:Raven Press, 1982:511-9.

5 Pyykk6 I, Starck J, Farkkili M, Hoikkala M, Korhonen 0,Nurminen M. Hand-arm vibration in the aetiology of hearingloss in lumberjacks. Br JInd Med 1981;38:281-9.

6 Pyykk6 I, Starck J. Vibration syndrome in the etiology ofoccupational hearing loss. Acta Otolaryngol suppl 1982;386, 296-300.

7 Pyykko I, Korhonen 0, FirkkilfaM, Starck J, Aatola S, Jintti V.Vibration syndrome among Finnish forest workers. A follow-up study from 1972 to 1983. ScandJ Work Environ Health 1986;12:307-12.

8 Pyykk6 I, Starck J, Pekkarinen J. Further evidence of a relationbetween noise-induced permanent threshold shift andvibration-induced digital vasospasms. Am J Otolaryngol1986;4:391-8.

9 Pyykk6 I, Pekkarinen J, Starck J. Sensory neural hearing lossduring combined noise and vibration exposure: an analysis ofrisk factors. Int Arch Occup Environ Health 1987;59:439-54.

10 Robinson DW. Estimating the risk of hearing loss due tocontinuous noise. In: Robinson DW, ed. Occupational hearingloss. London: Academic Press, 1971:43-62.

11 Robinson DW, Sutton GJ. A comparative analysis ofdata on therelation ofpure-tone audiometric thresholds to age. Teddington:National Physical Laboratory, 1978. (NPL report Ac 84.)

12 Robinson DW, Sutton GJ. Age effects in hearing-a comparativeanalysis of published threshold data. Audiology 1979;18:320-34.

13 Robinson DW. Threshold of hearing as a function of age and sexfor the typical unscreened population. BrJAudiol 1988;22:5-20.

14 International Organisation for Standardisation. Acoustics-deter-mination of occupational noise exposure and estimation of noiseinduced hearing impairment. Geneva: IOS, 1985. (IOS/DIS1999.2.)

15 BrowingGG,Davis AC. Clinical characterization ofthe hearinginthe adult British population. Adv Otorhinolaryngol 1986;31:217-23.

16 Friedman I. Pathology of the cochlea. In: Booth JB, ed. Scott-Brown's otolaryngology. London: Butterworths, 1987:110-4.

17 Schuknecht HF. Pathology of the ear. Cambridge, MA: HarvardUniversity Press, 1974.

18 Rosen S, Plester D, El-Mofty A, Rosen HV. Relation of hearingloss to cardiovascular disease. Transactions of the AmericanAcademy of Ophthalmology and Otolaryngology 1964;68:433-44.

19 Driscoll DP, Royester L. Comparisons between the medianhearing threshold levels for an unscreened black non-industrialnoise exposed population (NINEP) and four presbycusis databases. Am Ind Hyg Assoc J 1984;45:577-93.

20 Stephens SGD. What is acquired hearing loss in elderly people. In:Glendening F, ed. Acquired hearing loss in elderly people. Stoke-on-Trent: Beth Johnsson Foundation, 1982:9-26.

21 Lim D, Stephens SDG. Clinical investigation of hearing loss in theelderly. J Irwin. Causes of hearing loss in adults. Adultaudiology. In: Stephens D, ed. Scott-Brown's otolaryngology.London: Butterworths, 1987.

22 Humes LE. Noise-induced hearing loss as influenced by otheragents and by some physical characteristics of the individual.J Acous Soc Am 1984;76:1318-29.

23 Pinter I. Hearing loss of forest workers and of tractor operators(interaction of noise with vibration). In: Proceedings of theinternational congress on noise as a public health problem,Arlington, Virginia, 1973. Washington: USA EnvironmentalProtection Agency, Office of Noise Abatement and Control,1973:315-27.

24 Taniewski M, Banaszkiewicz T. Hearing in persons exposed tovibration. Biul Inst Med Morsk Gdansku 1973;24:35-46.(English abstract.)

25 Iki M, Kurumatani N, Hirata K, Moriyama T, Itoh J, Arai T. Anassociation between vibration-induced white finger and hearingloss in forestry workers. Scand J Work Environ Health 1986;12:365-70.

445



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

446

26 Miyakita T, Miura H, Futatsuka M. Noise-induced hearing loss inrelation to vibration-induced white finger in chain-saw workers.ScandJ Work Environ Health 1987;13:32-6.

27 Pyykko I, Hyvarinen J. The physiological basis of the traumaticvasospastic disease: a sympathetic vasoconstrictor reflex trig-gered by high frequency vibration. Work Environmental Health1973;10:36-47.

28 Lawrence M. Control mechanisms of inner ear microcirculation.Am J Otolaryngol 1980;1:324-33.

29 Hultcrantz E. The effect of noise on cochlear blood flow in theconscious rabbit. Acta Physiol Scand 1979;106:27-37.

30 Weston TET. Presbycusis: a clinical study. J Laryngol 1964;78:273-85.

31 Zelman S. Correlation of smoking history with hearing loss.JAMA 1973;223:920.

32 Stewart RO. The effect of carbon monoxide on humans. J OccupMed 1976;18:304-9.

33 Wright MI. Pathology of deafness. Manchester: ManchesterUniversity Press, 1971.

34 Drettner B, Hedstrand H, Klockhoff I, Svedberg A. Cardio-vascular risk factors and hearing loss. Acta Otolaryngol1975;79:366-71.

35 Friedman GD, Siegelanb AB, Seltzer CC. Cigarette smoking andexposure to occupational hazards. Am J Epidemiol 1969;98:175-83.

36 Starck J, Pyykko I. Effect of smoking on sensorineural hearingloss. In: Claussen CF, ed. Vertigo, nausea, tinnitus andhypoacusis in metabolic disease. (Exerpta Medica InternationalCongress series, 377-50.) Amsterdam: Elsevier (in press).

37 Rosen S, Olin P. Hearing loss and coronary heart disease. ArchOtolaryngol 1965;82:236-43.

38 Spencer JT. Hyperlipoproteinemia and inner ear disease.Otolaryngol Clin North Am 1975;8:483-92.

39 Castelli WP, Abbot RD, McNamara P. Summary of estimates ofcholesterol used to predict coronary heart disease. Circulation1983;67:730-4.

40 Pyykko I, Starck J, Pekkarinen J, Farkkila M. Serum cholesterol

Pyykkoi, Koskimies, Starck, Pekkarinen, Fdrkkila, Inabaand triglyceride in the etiology ofsensori-neural hearing loss. In:Claussen CF, ed. Vertigo, nausea, tinnitus and hypoacusis inmetabolic disease. (Exerpta Medica International Congressseries 335-8.) Amsterdam: Elsevier (in press).

41 Johnsson A, Hansson L. Prolonged exposure to a stressfulstimulus (noise) as a cause of raised blood pressure in man.

Lancet 1977;i:86-7.42 Andr6n L, Hansson L, Bjorkman M, Jonsson A. Noise as a

contributory factor in the development of elevated arterialpressure. Acta Med Scand 1980;207:493-8.

43 Borg E. Noise-induced hearing loss in normotensive and sponta-neously hypertensive rats. Hearing Res 1982;8:1 17-30.

44 McCormic JG, Harris DT, Hartley CB, Lassiter RBH. Sponta-neous genetic hypertension in the rat and its relationship toreduce cochlear potentials: implications for preservation ofhuman hearing. Proc Natil Acad Sci USA 1982;79:2668-72.

45 Tachibana M, Yamamichi I, Nakae S, Hirasugi Y, Machino M,Mizukoshi 0. The site of involvement of hypertension withinthe cochlea. Acta Otolaryngol 1984;97:257-65.

46 Meyers EN, Bernstein JM. Salicylate ototoxicity. Arch Otolaryn-gol 1965;82:483-93.

47 Hawkins JE. Vascular patterns of the membranous labyrinth. In:Graybiel A, ed. Third symposium on the role of the vestibularorgans in space exploration. Washington: NASA, 1967:241-58.

48 Smith I, Lawrence M, Hawkins JE. Effects ofnoise and quinine onthe vessels of the stria vascularis: an image analysis. Am JOtolaryngol 1985;5:260-5.

49 Graham JDP, Parker WA. The toxic manifestation of sodiumsalicylate therapy. Q J Med 1948;17:153-63.

50 Grifo S. Aspirin ototoxicity in the guinea pig. ORL J 1975;37:24-34.

51 Mitchell C, Brummett R, Himes D, Vernon J. Electro-physiological study of the effect of sodium salicylate upon thecochlea. Arch Otolaryngol 1973;98:297-301.

52 Eddy LB, Morgan RJ, Carney HC. Hearing loss due to combinedeffects ofnoiseand sodium salicylate. ISA Transactions 1976;15:103-8.

Correspondence and editorialsThe British Journal of Industrial Medicine wel- the understanding that they may be subject tocomes correspondence relating to any of the editorial revision and shortening.material appearing in the journal. Results from The journal now also publishes editorialspreliminary or small scale studies may also be which are normally specially commissioned. Thepublished in the correspondence column if this Editor welcomes suggestions regarding suitableseems appropriate. Letters should be not more topics; those wishing to submit an editorial, how-than 500 words in length and contain a minimum ever, should do so only after discussion with theof references. Tables and figures should be kept to Editor.an absolute minimum. Letters are accepted on



.bmj.com

/B


.46.7.439 on 1 July 1989. Dow

nloaded from

http://oem.bmj.com/

Documents

Risk Finnishforestryworkers · Br J Ind Med: first published as 10.1136/oem.46.7.439 on 1 July 1989. Downloaded from . 440 recumbentposition,andthemeanvalueoftheleft and right arm