Acta Med Scand 207: 493498, 1980

Noise as a Contributory Factor in the Development of Elevated Arterial Pressure

A Strrcly o f t l i t Mrchiriiistiis h! u*hicli Noise tnrry Rrrise Blood P w s s i i w i n M a n

Lennart Andren, Lennart Hansson, Martin Bjorkman and Anders Jonsson

Fvonl the Hj1pertension Section, Department qf' Medicine. 0 ~ 1 1 ~ 1 Hospitctl. ond the Drptrrtments qf' Eniironmentcrl Hygiene irnd Occrrpciriontrl Medicine,

University qf Cijteborg, Cijteborg, Snqeden

ABSTRACT. Arterial pressure and other hemo- dynamic variables (stroke volume (SV), cardiac output and total peripheral resistance) were studied in 18 healthy males before and during exposure to recorded industrial noise. All measurements took place under strictly standardized conditions in a noise laboratory. The frequency distribution and level of noise used for stimulation were continuously moni- tored and kept constant within close limits through- out the experiments. SV was measured with imped- ance cardiography. Indirect blood pressure (BP) in the brachial artery was measured with an automatic device and the derived parameters, cardiac output and total peripheral resistance, were calculated from these measurements. Compared with resting condi- tions at 40 dBA, stimulation with industrial noise at 95 dBA caused significant increases in diastolic BP, mean arterial pressure and total peripheral resist- ance. Minor but statistically significant reductions of SV and cardiac output were seen. Heart rate and systolic BP did not change. These alterations of the hemodynamic variables persisted throughout 20 min of noise stimulation and were maintained for 5 min following cessation of noise stimulation. All variables had returned to their initial levels 10 min after discontinuation of noise stimulation. This study suggests that exposure to industrial noise at levels prevailing during several industrial processes may cause acute elevations of arterial BP and peripheral vascular resistance. In animal studies, repeated elevations of BP due to exposure to noise have been shown to cause a permanent elevation of BP. There- fore, we suggest that noise may be one of several external stimuli contributing to the development of arterial hypertension in man.

K L , ~ il~wd..d.~: hypertension, noise. hemodynamics.

Acta Med Scand 207: 493, 1980.

The etiology of hypertension in man is not ful ly known. Few would oppose the opinion that heredi- tary factors play an important role. Great interest has also been devoted to external variables, e.g. ingestion of salt (41, either as primary causes of hypertension or as modulating influences.

Among several conceivable external factor5 which may affect the development of hypertension. we became interested in noise after having ob- served that industrial workers with a severe noise- induced impairment of hearing, indicating pro- longed and severe exposure to industrial noise, had significantly higher blood pressures (BPI than sub- jects of the same age and sex but with normal hear- ing, and that the rate of hypertension was higher in the group exposed to noise ( 8 ) . Previous animal studies, mainly in rats, have shown acute rises of BP during stimulation with noise (12. 19). Repeated exposure of animals to alerting stimuli has also been shown to produce a permanent elevation of BP (3, 16).

This report describes the acute hernodynamic ef- fects of exposure to industrial noise under carefully standardized conditions. The purpose has been to establish whether exposure to noise at levels which frequently occur in occupational life may cause a rise of BP also in man and, if so. by which hemodynamic mechanism.

METHODS Eighteen normotensive male volunteers took part in the investigation. All had normal auditory acuity (subjectively

Abbre\~iutions: BP = blood pressure. SV = stroke volume. HR=heart rate.

494 L . AtidrPti ct (11.

t

dB re1 20 pPa

l o t

A

90 --

80 - -

70 - -

60 - -

50 - -

40

L 0 E 5 /

c ~ " : " ~ " ~ " : " ; " : " ; " : ' ~ " ' ; + 16 32 63 125 250 500 1000 2000 4000 8000 16000

10

a, Is,

L 0 s

: 5--

Systolic

A

--

NS NS A

NS NS A

75 85 95

Diastolic

- I

n=8 n=8 n=18 75 85 95

Hz

Fig. 1 . Frequency analysis and sound levels of the in- dustrial noise induced in the noise laboratory.

Fig. 2. Changes in systolic and diastolic BP during stimulation with 75.85 and 95 dBA for periods of 10 min compared with initial levels following 20 min of rest at 40 dBA.

Noise trnd elelwted blood presslire 495

10

5 a, 0 c m 1 0 s

0

-5

Heart Rate

U NS

n=a 75

NS NS

n=8 n=ia a5 95

Stroke Volume

IT NS

Pc0.05

n=a n=a 75 85

Noise Level (dBA)

and tested with audiometry). Their average age was 26 years (range 23-31). None of them had taken medication of any kind on the day of investigation. Their average recumbent BP after 20 min rest was 120/70 mmHg.

The hemodynamic variables were studied with non-in- vasive methods. Systolic and diastolic BPs were meas- ured indirectly in the brachial artery using an automatic BP recorder (Bosch Bosomat). The accuracy of this equipment had been assessed by simultaneous compari- sons with BP measurements with a mercury sphyg- mometer. The correlation coefficient between simul- taneous measurements was r=0.93, p<O.Ool.

Stroke volume (SV) was measured with impedance car- diography (IFM Minnesota 304A) in the recumbent posi- tion. Two conductive Mylar strip electrodes (Electrode Tape No. M6001, 3M Co) were placed around the neck and separated as widely as possible. A third electrode was placed around the thorax at the level of the xiphoid pro- cess and a fourth around the upper abdomen not less than 3 cm from the third electrode. The output signals of the cardiograph were recorded on a Siemens-Elema Recorder (34 T). SV was calculated according to the AZ-formula (5 ) :

Fig. 3. Changes in HR and SV induced by noise stimulation at 75, 85 and 95 dBA for periods of 10 min compared with initial val- ues following 20 min of rest at 40 dBA. -

PCO.001

n.18 95

where A is the cross section area of the thorax at the level of the third electrode, L the distance between the second and the third electrode (average of ventral and dorsal measurements), AZ the maximal amplitude of the wave- formed impedance change during systole, and Z,, the basic impedance between the second and the third electrode.

This method correlates very well with other ways of determining SV and cardiac output. In our laboratory we compared this method with the dye-dilution method using a densitometer (Cardiognost, Atlas) and indocyanine green (Cardio-Green) in 13 paired experiments. The mean value of cardiac output determined by the impedance car- diography method did not differ significantly from that obtained by the dye-dilution method (8.39 I/min vs. 7.49 I/min, t = 1.86, n.s.). A statistically significant correlation was found between measurements obtained by the two methods (r=0.78, p<0.002) .

All experiments were performed in a specially equipped noise laboratory. The subjects rested comfortably in the

496 L . AiidrPn et NI.

T Pc 0.01

NS -

NS n=a n=a n=ta 75 a5 95

Noise Level (dBA Fig. 4 . Changes in cardiac output induced by noise stimu- lation at 75,85 and 95 dBA for periods of 10 rnin compared with initial values following 20 rnin of rest at 40 dBA.

recumbent position on a couch in the center of an expos- ure room with eight loudspeakers built into the walls. Tape recorders, amplifiers and equipment for acoustical measurements were placed in an adjacent control room. Recorded industrial noise was replayed through the loudspeakers. The noise level in the exposure room was measured continuously throughout the studies at the ear level approximately 10 cm from the subject's head. The A-weighted noise level and the frequency spectrum of the noise were analyzed (Fig. 1). This made it possible to maintain a constant noise level ( + I dBA) over the entire frequency spectrum throughout the experiments. The equipment for acoustical measurements was manufac- tured by Bruel & Kjaer (microphone type 4145, preamplifier type 2619, real time analyzer type 3347, sound level recorder type 2305, sound level analyzer type 4426). Measurements were made after 20min of recum- bent rest at 40 dBA and again after exposure to noise at 95 dBA for 20 min. In eight subjects recordings were made also after stimulation for 10 rnin at 75 and 85 dBA. Finally, recordings were made at 5 , 10 and IS rnin after cessation of noise stimulation.

Standard methods were used for calculation of the mean, S.D. and r-value. The hypothesis of no difference in means was tested by the f-test for paired data. Only two-tailed tests were used and differences were con- sidered significant forp-values <0.05.

RESULTS

Following 20 min of recumbent rest at 40 dBA the average systolic BP was 120k2.9 mmHg, diastolic

BP 70k2.0 mmHg, mean arterial pressure 8727.0 mmHg, heart rate (HR) 61k2.5 beatslmin. SV 113k5.6 ml, cardiac output 7.0k0.5 Ilmin, total peripheral resistance 13.7_+ 1.3 PR units. During stimulation with noise at 95 dBA, a statistically significant increase in diastolic BP but no change in systolic BP occurred (Fig. 2 ) .

No significant changes in HR occurred during stimulation with noise at either 75 , 85 or 95 dBA. whereas significant reductions of SV were seen at the two highest levels of stimulation (Fig. 3) . The reduction of SV also caused a significant reduction of cardiac output at the highest level of stimulation (Fig. 4). Statistically significant increments of mean arterial pressure and total peripheral resistance occurred during stimulation with noise at the 95 dBA level (Fig. 5 ) .

The observed hemodynamic changes remained virtually unaltered 5 rnin after cessation of the noise stimulus. All hemodynamic variables had, how- ever, returned to their initial levels 10 min after discontinuation of noise stimulation.

DISCUSSION

Short-lasting stimulation with industrial noise at 95 dBA under carefully standardized conditions in a noise laboratory caused a statistically significant increase in diastolic BP in 18 healthy volunteers but no change in systolic BP. This agrees with findings by others during stimulation with aircraft and traffic noise (13, 14). The increase in diastolic BP could be ascribed to a significant rise of total peripheral re- sistance. A noise-induced increase in diastolic BP concomitant with vasoconstriction in peripheral vascular beds has previously been reported ( I 1 ) . This pattern of hemodynamic responses resembles in part those seen during the "defense reaction" ( I ) . The lack of cardiac participation in the rise of BP (no increase in HR or SV) is reflected by the un- changed systolic BP. This is most likely caused by reflex inhibitory effects on the heart through the baroreceptor mechanism. Thus, the suppression of the baroreceptor reflex seen during more fulminant forms of the "defense reaction" (7) does not seem to take place during stimulation with noise at the sound levels employed in the present study.

Previous studies in animals have shown marked acute elevation of BP in some species during stimu- lation with noise (12, 16, 19). Noise alone and com-

, A 1 111 M I 4 s< llllll207

Resistance Mean Arterial Pressure

- I NS n=a n=a n=ia 75 a5 95

L Pe0.05 NS I

n=a n=a 75 a5

Noise Level (dBA)

bined with other stress stimuli can also induce per- manent hypertension in animals (17).

Evaluating the present results against this background, it is conceivable that stimulation with noise, e.g. in the form of industrial noise, is one of several external stimuli by which persistently ele- vated BP may be elicited in man. In other words, if normotensive individuals are exposed to noise levels severe enough to cause an acute rise of BP, it i s conceivable that repeated exposure to such stimuli could cause persistent hypertension. Our findings that industrial workers with a noise-in- duced impairment of hearing had higher BPs and a higher incidence of hypertension than individuals with normal hearing (8) support indirectly this view. This suggestion is corroborated by the fact that a severe noise-induced impairment of auditory acuity frequently requires almost daily exposure to noise for periods longer than 10 years (10). The view that prolonged exposure to noise may cause hyperten- sion is further supported by the recent observation that the prevalence of hypertension and other car-

-

- 0.c

n=1a 95

- I

Fig. 5 . Changes in total peripheral resist- ance and mean arterial BP induced by noise stimulation at 75, 85 and 95 dBA for periods of 10 min compared with initial levels following 20 min of rest at 40 dBA.

diovascular disorders was approximately SO % higher in areas exposed to aircraft noise (9). It has also been shown that the prevalence of borderline and established hypertension is significantly higher among weavers in textile mills exposed for several years to daily noise levels of more than 90 dBA (mean 96) than among workers not exposed to noise (15). On the other hand, no relation between expos- ure to noise and hypertension has been found in some other studies (2, 18).

We found no linear relationship between noise level and BP response. The reason for this could be that the more abrupt change in noise from 40 to 75 dBA induced a greater shift in noise level than did the change from 75 to 85 dBA. Another possible explanation could be that the initial hemodynamic changes at 75 dBA might be secondary to a com- bination of the exposure to noise and “expectancy stress”.

Obviously, it is not possible to draw definite con- clusions concerning the importance of audiogenic stimulation in the pathogenesis of essential hyper-

498 L . Andrbii et trl.

tension. Genetic factors are likely to be of great importance in determining the susceptibility to noise stimulation. This can be illustrated by studies in rats, where one strain developed hypertension whereas another, exposed to the same kind of noise, did not (16). It is also conceivable that indi- viduals with a genetic predisposition to devel- op hypertension may "hyper-react" to stressful stimuli in analogy with observations by Hallback (6). who noted a more pronounced rise of BP in young " prehypertensive" spontaneously hyperten- sive rats, e.g. during exposure to noise. than in normotensive rats.

Thus, noise could be one of several external fac- tors contributing to the development of hyperten- sion in man, particularly in genetically suspectible individuals. The relative importance of noise in this respect is difficult to evaluate. Nevertheless, it is interesting that increased sensitivity to salt has been noted in animals with audiogenic hypertension (16), a finding that further illustrates the complexity of this matter.

In conclusion, short-lasting exposure of healthy volunteers to industrial noise caused an acute rise of diastolic BP due to an increase in vascular resist- ance. It is conceivable that repetition of such stimuli may cause a persistent elevation of BP and that noise therefore could be one of several external factors contributing to the development of hyper- tension.

ACKNOWLEDGEMENTS

Supported in part by grants from The Swedish Work Envi- ronment Fund and Astra/Hassle, Ltd.

REFERENCES I . Abraham, V. C., Hilton. S. M. & Zbrozyna, A. W.:

The role of active muscle vasodilatation in the alerting stage of the defense reaction. J Physiol 171: 189, 1964.

2. Drettner, 8.. Hedstrand, H., Klockhoff, I. & Sved- berg, A.: Cardiovascular risk factors and hearing loss. Acta Otolaryngol79: 366, 1975.

3. Folkow, B. & Rubinstein, E. H.: Cardiovascular ef- fects of acute and chronic stimulations of the hypothalamic defense area in the rat. Acta Physiol Scand 68: 48. 1966.

4. Freis, E. D.: Salt, volume and the prevention of hypertension. Circulation 53: 589. 1976.

5. Granerus, G. & Elg, R.: Hjartminutvolymbestamning med impedanskardiografi. Berlkning av slagvolymen frin den icke deriverade signalen (AZ). LakaresaII- skapets Riksstamma. p. 157, 1975.

6. Hallback, M.: Interaction between central neurogenic mechanisms and changes in cardiovascular design in primary hypertension. Acta Physiol Scond (Suppl) 424. 1975.

7. Hilton, S. .M.: Inhibition of baroreceptor reflexes on hypothalamic stimulation. J Physiol 165: 56. 1963.

8. Jonsson, A. & Hansson. L.: Prolonged exposure to ;1 stressful stimulus (noise) as a cause of raised blood pressure in man. Lancet 1: 86. 1977.

9. Knipschild, P.: Medical effects of aircraft noise: Community cardiovascular survey. Int Arch Occup Environ Health 40: 185. 1977.

10. Kylin, B.: Temporary threshold shift and auditory trauma following exposure to steady-state noise. Acta Otolaryngol (Suppl) 152: I , 1960.

11. Lehmann, G. & Tamm. J.: Uber Veranderungen der Kreislaufdynamik des ruhenden Menschen unter Einwirkung von Gerauschen. Int Z Angew Physiol 16:217, 1956.

12. Medoff, H. S. & Bongiovanni. A. M.: Blood pressure in rats subjected to audiogenic stimulation. Am J Physiol 143: 300, 1945.

13. Mosskov, J. I. & Ettema. J. H.: Extra-auditory ef- fects in short-term exposure to aircraft and traffic noise. Int Arch Occup Environ Health 40: 165. 1977.

14. - Extra-auditory effects in long-term exposure to aircraft and traffic noise. I n t Arch Occup Environ Health 40: 177, 1977.

IS. Parvizpoor, D.: Noise exposure and prevalence of high blood pressure among weavers in Iran. J Occup Med 18: 730, 1976.

16. Rothlin, E., Cerletti, A. & Emmenegger, H.: Ex- perimental psycho-neurogenic hypertension and its treatment with hydrogenated ergot alkaloids (Hyder- gine). Acta Med Scand (Suppl) 312: 27, 1956.

17. Smookler, H., Goebel, K., Siegel, M . & Clarke. E.: Hypertensive effects of prolonged auditory. visual and motion stimulation. Fed Proc 32: 2105. 1973.

18. Takala, J., Varke, S. . Vaheri. E. & Severs, K.: Noise and blood pressure. Lancet 2: 974. 1977.

19. Yeakel, E. H., Shenkin, H. A.. Rothballer, A. B. & McCann. S. McD.: Blood pressures of rats subjected to auditory stimulation. Am J Physiol 155: 118, 1948.