Environmental Medicine

0025-7125/90 $0.00

+

.20

Heat, Cold, Noise, and Vibration Steven M. Horvath, MD, PhD, * and John F. Bedi, PhDt

Environmental stressors tax the ability of both normal and diseased individuals to maintain the homeokinetic state. The human organism responds to the environmental stressors of heat, cold, noise, and vibration with the general stress syndrome. Prolonged or high-intensity exposures may cause changes at the organ level. Humans are subtropical animals who have the capacity to develop physiological adaptations and mechanisms that maximize their potential to survive. In the context of this review, it is apparent that this capacity has limitations; for example, adaptative mechanisms for heat exposure are quite effective, whereas the ability to acclimate to cold environments is limited. 17 The heat balance equation provides the basic information for evaluating the maintenance of a relatively constant internal environment:

o =

(M - W) ± R ± C ± D - E ± S

where M = heat production, R = radiation, C = convection, D = conduction, S = heat storage, and E = evaporation. These factors and the equations related to predictions of the various factors are presented in detail in Nadel and Horvath. 31 Although the core temperature is usually closely regulated near 37°C, individual temperatures on the surface and in various organs can differ considerably from this homeostatic level. Furthermore, there are daily (circadian) rhythms, ambient environmental conditions, menstrual cycle variations and menopause, food ingestion, drug usage, and physical activity that alter this quasisteady state to various degrees. For example, Maron and associates 28 reported rectal temperatures exceeding 41°C in competitive marathon runners. Heat stroke, circulatory collapse, and coma have followed ingestion of amphetamines associated with vigorous exercise. AcciFrom the Environmental Stress Laboratory, Neuroscience Research Institute, University of California, Santa Barbara, California *Professor of Physiology and Biomedical Engineering t Associate Research Physiologist

Medical Clinics of North America-Vo!' 74, No. 2, March 1990

515

516

Sn:n::-.I .\1.

HORVATII AND JOHN

F.

BED!

dental hypothermic core temperatures as low as 17°C have been reported, with some survivors having minimal central nervous system damage or peripheral injuries. Howevcr, in general, core temperatures of approximately 3.5°C are considcred to be diagnostic of hypothermia. Certain reflex eflects associated with local cold exposure in individuals with cardiorespiratory disease have an impact on the quality of life in these individuals.

COLD ENVIRONMENTS Exposure of humans to cold induces two important physiologic protective mechanisms: increased heat production and marked peripheral resistance. The former is primarily a consequence of increased muscular activity (shivering and pilomotor), whereas the second results in a reduction of core-peripheral temperature gradients, tending to maintain core temperature by preventing heat loss from the surface. If the core temperature falls progressively, heat production diminishes, shivering ceases, and the individual becomes hypothermic. Development of the hypothermic state is usually not recognized by the individual and consequently can become more severe before treatment is undertaken. Hypothermia has been classified as mild (core temperature 34 to 35°C), in which the individual is awake, uncomfortable, and shivering; moderate (core temperature 30 to 34°C), in which the individual is obtunded and shivering; and severe (core temperature below 30°C), in which the individual is obtunded, unconscious, and not shivering and the breathing and heart rates are markedly depressed. Hypothermia can occur in individuals of all ages,6, 7. 18, 27. 3H but the most concern has been expressed for the pediatric and geriatric populations, with somewhat lesser interest in those adults with "hiker's hypothermia." Accidental hypothermia, a pathophysiological state in which core temperature is below ,35°C, is frequent in elderly individuals. Its occurrence exhibits a wide national difference, being apparently more common in the United Kingdom 6 . lb and nonexistent in Scandinavia. It has occurred frequently in the US, notably in Alaska. Hypothermic incidents have occurred in diabetics. Treatment varies with the magnitude of core temperature depression. Rewarming is by either external or internal means. External warming procedures are passive or active, whereas all internal ones are active. Active rewanning is the method of choice for patients with core temperatures below 30°C. There are considerable differences of opinion as to the most effective method, which ranges from passive insulation of the individual to rapid rewarming by immersion in a hot tub (40°C water). Fluid volume shifts occur and require correction. The most serious complication is the susceptibility of the myocardium to fibrillation and the difficulty of defibrillation when cardiac temperatures are below 28°C. Hypoxia can be an additional consideration. There are a number of factors to consider in the development of hypothermia in the aged. Thermal preference is impaired, perception of temperature changes is reduced, metabolic heat production is lower, and there may bc a lack of adequate nutrition and heating systems. G, 7. 18 In a

517

HEAT, COLD, NOISE, A'JD VIBRATIOl\

study comparing the responses of nude patients ages ,52 to 76 years and 20 to 25 years to a cool (lO°C) environment, Horvath and associates 19 found that all younger subjects complained of discomfort in the cold, whereas the older ones did not. The younger subjects had immediate metabolic responses and the older minimal and delayed responses. Core temperatures were maintained in the young but fell in the older group. Submersion hypothermia and near-drowning have received considerable attention, especially as it occurs in small children in whom the rate of eooling is proportionally faster (larger surface area and smaller fatty insulaticm). The apparently successful treatment outcome in some of these patients with core temperatures as low as 24°C and submersion times of up to 40 minutes reflects primarily on the coordinated and intensive efforts of the recovery personnel. The numbers of nonsurviving or brain-damaged individuals remain large. Hiker's hypothermia generally occurs when the wind chill factor is high, the individual is wet and sweating, evaporation heat loss is high, and physical activity is moderate or intense. The wet clothing and large heat losses then lead to hypothermia. Ifi If alone, the hiker is in an uncompromising situation. If observed (and usually emergency personnel and methods are u~available), simple procedures can be followed with a successful outcome. Conductive heat losses and evaporative heat losses need to be reduced. Because some 20 per cent of heat losses come from the head, covering the head, mouth, and nose with a cap and scarf is helpful. Exercise, if the person is capable and supported, can be helpful but is not recommended for the severely hypothermic. Cutaneous diseases occur in individuals exposed to low ambient conditions. Chilblains (baggy swelling of skin) are found in individuals persistently exposed to cold damp climates. Frostbite (superficial or deep freezing of skin) may occur. Immersion foot is a nonfreezing injury consequent to long-term exposure to a wet, cold environment. Certain individuals suffering from various diseases apparently are markedly influenced by exposure to cold air whether they are resting or engaged in modest physical activity. In some patients with coronary heart disease, cold exposure can induce attacks of angina pectoris or lower the threshold for external angina, possibly by increasing peripheral resistance while myocardial oxygen demand increases. 17 Patients with asthma have considerable exaggeration of their airway obstruction, sometimes at rest but generally during exercise, in a cold environment. Hay fever subjects are less influenced by such exposure but may be affected. Aged individuals are less tolerant of cold water immersion, and shipwreck studies clearly indicate the smaller survival rate of older subjects. Some individuals have an extraordinary sensitivity to cold exposure, as manifested by an allergic response: headaches, flushing, fall in blood pressure, syncope and urticaria. Deaths in swimmers in cold water have been attributed to this response.

HEAT Environmental heat leads to positive and definitive reactions in humans. The increased body heat content leads to alterations in the circula-

518

STEVE'i ~1. HORVATII AND JOH'i

F.

BEDI

tory, respiratory, endocrine, and temperature regulatory systems. Sweating or lack of sweating imposes further loads. The thermoregulatory system can maintain the core temperature within narrow limits, and consequently, the amount of heat gained must equal the amount of heat lost. Calculations of this exchange can be made from the heat balance equation. A schematic outline of the events and actions that lead to heat stress is presented in Figure 1. Various inadequate responses to heat stress have been noted in the medical literature, which have been categorized by the World Health Organization and brought up to date by Dinman and Horvath. 8 The most serious consequence is heat stroke. Other significant forms are heat exhaustion, heat cramps, heat fatigue, and heat rash. Anhidrotic heat exhaustion has been more commonly observed in military operations. Heat is a potent stressor of the human body, not only in the natural environment but also in the artificial one presented by certain industrial situations. Successful resistance to this stress depends on the development and utilization of adequate physiological mechanisms. In industry, different work schedules and modifying work loads and conditions with radiation screens and garment protectors are required to reduce the work load. 35 A number of attempts to describe the environment and so determine the conditions under which individuals could work without undue heat stress have been offered. At present, although there is no general agreement, several organizations have promulgated a scheme of threshold limit values. The Wet Bulb-Globe Temperature Index (WBGT) is the simplest and most suitable technique to measure environmental factors. I, It is calculated as follows: Outdoors with solar loads: WBGT

= 0.7 WB + 0.2 GT + 0.1 DB

Indoors or outdoors with no solar load; WBGT = 0.7 WB

+

0.3 GT

where WB = natural wet bulb temperature, DB = dry bulb temperature, and GT = globe thermometer temperature. Although this measure provides some valuable information, the missing factor for evaluating human heat load is the heat production during rest and activity and the time devoted to each. Heat exposure cannot be determined reliably unless all of the information is available (see NIOSH Recommendations for Occupational Safety and Health Standards 1988). It should be noted that heat-related deaths are common during a sudden natural heat wave. Most of these occur on the second through the fourth days of the heat wave. The young and the aged are the most susceptible to heat morbidity and mortality.1O Although the data for the 1988 heat wave are not yet available, it is clear that numerous deaths did occur (the actual number may be much larger because of the extensive nature of this heat wave).

~

\J1 ......

+

Circulatory Shock (Rapid, Weak Pulse: Low Blood Pressure Core Temperature May be Normal) HEAT EXHAUSTION

t

I I

__ -

t

~

I

Figure 1. Mechanisms involved in heat injury.

Rapid Rise in Core Temperature HEAT STROKE

t

~-

(Often an Inadequate Stimulus)

Thirst

" . _ Dehydration ~

Increased Metabolism

"""

~"

f Diminished Sweating

Fatigue and Impairment of Performance I

t

I

~

--

.....

Gastric -- Burning Nausea

H2 0 Intake

-

-

_ _ _ Unevaporated Sweat Useless for Cooling

Heat Loss by EVAPORATION

_ SWEATING / ~ ~ - - - Salt Intake / ~ . ____ Faiigue of Drain on Drain on _ Sweat 11ands BOdY,Water ~BOdY Salt

__ -

Rise in Body Temperature

-~

__ PRICKLY HEAT

"-..

Second-Line Defenses

Failure of Central Control Mechanisms (Sweating Ceases)

Inadequate Venous Prolonged Exposure Return to Heart Increased Blood Volume "(Acclimatization) ....... #' Inadequate Skin Inadequate Blood Circulation Flow to Vital Areas --_

First-Line Defense

/

Receptors for Warmth Are Activated

~ Skin Temperature Rises; Nervous

AUGMENTED SKIN CIRCULATION / " (Vasodilation) I

~

~

Increased Heat Flow From Body Core With Rise in Skin Temperature

Greater Heat Loss (or less gain) by RADIATION TCONVECTlON

HEAT STRESS Mean Heat Losses by RADIATION AND CONVECTION are less than produciion of METABOLISM

HEAT CRAMPS

520

STEVEN

:'vI.

IIoRvATH AKO JOHN

F.

BED!

In the 1980 heat wave, some 1700 deaths (as defined by a core temperature of 41 DC or higher or 40 DC with anhidrosis) were attributed to the high ambient conditions. Because the mortality records do not specifically require statements about "heat related," the actual number of deaths may have been much greater. Estimates of morbidity are not available, but the toll probably was large. Not all cases of heat injuries result in death. An incomplete analysis of heat-related illness involving worker's compensation claims indicate that claims were high in industry: 9, 6, 5, and 3 per cent of employees in agriculture, construction, mining, and manufacturing, respectively.21 The claims were primarily for heat stroke and heat exhaustion. Probably heat cramps did not result in claims because they were treated locally. The principal factors inducing death, especially in the aged, are limitations in circulatory capacity (cardiovascular disease plus age-related decrements), dehydration, drug therapies, poor physical fitness, alcohol, cessation of sweating, and reduced salt intake. Fluid loss in excess of 2 per cent of body weight is a predisposing factor for heat injuries. Treatment is designed to reduce core temperatures, replace fluid volume, and establish a proper electrolyte balance. Preventive measures involve simple steps such as encouraging fluid intake, adequate salt intake (not salt tablets), activity during cooler portions of the day, keeping out of the sun, and seeking and using cool areas. 17 The last-named measure may be counterproductive for some workers, as it eliminates the basic physiological mechanism for improved tolerance. Acclimatization to a hot environment is essential for an enhanced tolerance to it and can be attained only by working in the heat. Unfortunately, full acclimatization does not develop quickly: exposures of as much as 10 days are required, although tolerance does improve with each succeeding day. All individuals, regardless of age, can become acclimatized, although older persons require a longer exposure to develop full acclimatization. This mechanism is not retained, being lessened with each successive day of cool environmental exposure. . NOISE The young adult is capable of hearing sounds ranging in frequency from 20 to 20,000 Hz. Hearing at any frequency is dependent on the energy of the noise at that frequency, generally measured in decibels (dB). Sound meter measurements of noise give a frequency-weighted energy reading. In excess of 85 db, noise is considered loud. Hearing loss occurs with age at all frequencies. Exposure to abrupt loud noise causes temporary threshold shifts (TIS) , and long-duration exposure can result in permanent threshold changes. Changes in blood pressure and heart rate on exposure are consistent with a general stress reaction and show adaptation within the exposure period. Linden,26 studying 63 men and women exposed to 90 dB of white noise, concluded that initial blood pressure and heart rate reactivity and adaptation are unaffected by noise distraction. Bartsch and coworkers,3 in a study of 38 subjects exposed to noise in excess of 90 dB, found an increase in reaction time, a decrease in systolic blood pressure, and a rise

HEAT, COLD, l\orSE, AI\D VIBRATION

521

in diastolic pressure during exposure to seven noise types (long and short impulse and interruptions including a no-noise condition). Those investigators concluded that there were no eflects on blood pressure with various noise structures, although they observed different patterns ofTTS with the different structures. Body sway in 60 subjects exposed to gunshot noise, with various degrees of TTS, was significantly greater than in 115 controls.23 Sway increased in subjects with greater TfS at 4 and 6 kHz. This result may indicate disturbance of the vestibular system by impulse noise. An evaluation of noise and vigilance interaction was performed by Koelega and Brinkman,24 who looked at the effect of variable and intermittent noise on 21 sensory visual performance tasks. Those investigators concluded that nothing was known about the effects of variable noise on sustained attention because of the many types of noise and measures of performance used. It was also concluded that disparate task definitions contributed to the inconsistent results on vigilance. Studies in the workplace have evaluated relative risk factors of age, sex, race, occupation, diabetes, blood pressure conditions, smoking history, and maternal history for hearing loss. Risk factor analysis on sensorineural hearing, assessed in 127 forest workers aged 30 to 55 years, suggested that age, vibration-induced white finger, and elevated diastolic blood pressure accounted for 26 per cent of the variance in hearing loss. Smoking, systolic pressure, and use of ear muffs did not contribute significantly to the regression of sensorineural hearing loss. 34 However, Barone and colleagues 2 found a significant relative risk for smokers compared with nonsmokers, with significant risk for pack years and packs per day, for hearing loss in 2348 white men. Hodgson and associates!5 studied 28 diabetic participants and controls working in high- and low-noise industrial plants, conducting analyses of variance at each of seven hearing threshold frequencies. They found no evidence of higher hearing threshold shifts in diabetics at the same noise levels. Wu and coworkers 37 found in 151 steel mill workers with the highest hearing thresholds at 4000 Hz that blood pressure was unrelated to the degree of hearing loss. Van Dijk36 found no correlation between blood pressure and total noise exposure after corrections for age, weight, and other confounding variables in 539 male workers from seven industries. Results of auditory threshold tests performed on 28 white and matched black medical service fire fighters exposed to ambulance siren noise suggested that whites were more susceptible to noise-induced hearing loss in the mid- and high-frequency regions. 22 There is evidence that exposure during pregnancy to noise in excess of 85 dB may result in hearing loss in the offspring. 2.5 Although exposure to loud noise causes a sympathetic reaction consistent with the general stress reaction, there is little evide'1ce to suggest alteration of any functional system, either locally or systemically, other than hearing. Only the increase in body sway during exposure to impulse noise and the greater hearing loss with vibration-induced white finger would suggest changes in blood flow. 23

522

STEVEN

M.

HORVATl! AND JOHN

F.

BEDI

VIBRATION Individuals are exposed to whole-body vibrations and local vibrations at the tool-body interface in tool users. Whole-body vibrations, noise, and motion (traveling or large machine operation) can result in motion sickness, and there is epidemiologic evidence of connections with low back pain and early degeneration of the lumbar spinal region. 9 . 20 Local vibration experienced by grinders, chainsaw operators, pneumatic drill operators, and others can result in a disorder-vibration-induced white finger-that has the same etiology as Raynaud's disease and may be referred to as vibration syndrome, Raynaud's phenomenon, or secondary Raynaud's disease. It was originally believed that the symptom complex was attributable to an overreactive sympathetic system. The initial symptoms of vibration-induced phenomena include intermittent tingling in the fingers followed by intermittent numbness and by blanching of one or more fingertips with or without tingling and numbness. These conditions can occur without interfering with normal activities. However, one or more fingers may turn white triggered by cold exposure, with stiff and clumsy hands, which may interfere with normal activity. In extreme cases, gangrene supervenes. The latency period-the time between the first exposure to vibration and the blanching of the digits-may be several years and is related to the amplitude of the vibration. The shorter the latency, the more rapid the progression of the disorder. The prevalence of the disorder in workers can be related to total operating time (there was no difference in prevalence between controls and chainsaw operators with less then 2000 hours of operation 12) and to vibration acceleration (prevalence below 2 meters per second was zero) and frequency (10 Hz was a suggested lower limit). Low-intensity vibration rarely causes white finger. The symptoms would suggest changes in neurologic fUllction and vascular properties in the affected area. Measures of fingertip temperature, 5 blood flow and recovery response to cold provocation,5 and blood pressure 24 in the fingers substantiate this view that changes in the blood vessels are important. Hypertrophy of the media and decreased lumen, resulting in a reduced blood flow, account for some of the changes. A decrease in finger sensitivity to touch, decreases in nerve conduction velocity,14 and loss of muscular strength l l imply local neuropathy. There is radiographic evidence of bone anomalies (cysts, vacuoles, enostoses) in the hand, wrist, and elbow joint,4 although there is some question about whether vibration exposure is involvedY There is also evidence of increased blood viscosity. 33 The magnitude of the sympathetic vasoconstrictor response to cold, estimated as the blood-pressure response to exposure in the affected fingers minus the same variable with nerve blockade, was twice as large as the local response to 6°C of body cooling during blockade, implying that the sympathetic vasoconstrictor response to cold plays a significant role in white finger episodes. 32 The prognosis for the patient suffering from vibration-induced white finger is uncertain, although there is some information suggesting a positive prognosis. The percentage of workers in certain industries who have the

IIEAT, COLD, NOISE, A0ID VIBHATION

523

condition has decreased. For example, 40 per cent of the lumberjacks in one district who used chainsaws had white finger in 1972. This was reduced to 7 per cent in 1980. There appears to be a decrease in the condition in chainsaw operators. Most workers with white finger who continued the exposure but with saws designed to dampen the vibration at the handles had a lessening of the disease compared with controls who continued to use the original saws. The improvement in this industry thus could be secondary to improvement in chainsaw design. In 46 grinders, subjective symptomatology, digital blood pressure, and digital temperature showed improvement that increased with the number of years removed from vibration exposure. The percentage of subjects showing improvement was approximately 50 for digital pressure and symptomatology after 2 years. However, digital temperature improvement was only 15 per cent after 2 years. Numbness in the hands and arms takes longer to reverse than does white finger. 12 If exposure is to continue, vibration isolation and tool maintenance must be adhered to. It also has been suggested that vitamin E or a calcium antagonist may be beneficial as a prophylactic agent, because these agents reduce the response of arterial smooth-muscle preparations to norepinephrine. Interruption of continuous vibration also reduces the response of these preparations, suggesting that interval work times may help prevent the vibration syndrome. 1

SUMMARY Exposure to a cold environment induces a number of physiological alterations, the most serious being hypothermia. This state can occur in all individuals, but the very young and the elderly are more susceptible. Environmental and industrially generated high ambient temperature can place further stress on aged individuals and workers, resulting in a complex symptom picture. Morbidity and death may result from such exposures. Causative factors have been identified. Noise exposure induces hearing losses above those secondary to the aging process. Psychophysiological effects during noise exposure are considered to result from the sympathetic activity secondary to a general stress reaction. Vibration from the use of power tools results in Raynaud's phenomenon. However, modification of power tools has reduced the symptoms associated with vibration exposure. Termination of exposure to vibration appears eventually to reduce symptoms related to white-finger spasms. Interaction between these stressors has not been clarified because of the complex effects of each. The need for additional information about the response to these stressors is evident.

REFERENCES 1. Azuma T, Ohhashi T: Pathophysiology of vibration induced white finger: Etiological considerations and proposals for prevention: In Brammer AJ, Taylor VV (eds): Vibration Effects on the Hand and Arm in Industry. New York, John Wiley and Son, 1984, p 31

524

STEVEN

.\1.

HORVATII AND JOHN

F. BED!

2. 13arone JA, Peters JM, Garahrant )) H, et al: Smoking as a risk factor in noise induced hearing loss. J Qccup Med 29:741, 1987 :3. Bartsch R, Bruckner C, DierofI HG: Influence of different kinds of noise on the ear and some physiological and psychological parameters. Int Arch Qc-cup Environ Health 58:217, 1986 4. Bovenzi M, Fiorito A, Volpe C: Bone and joint disorders in the upper extremities of chipping and grinding operators. Int Arch Qccup Environ Health 59:189, 1987 5. Bovenzi M, Giansante KC, Fiorito A, et al: Relation of haemostatic function, neurovascular impairment, and vibration exposure in workers with different stages of vibration induced white finger. Br J Ind Med 42:25:3, 198,5 6. Collins KF, Exton-Smith AN: Urban hypothermia: Thermoregulation, thermal perception and thermal comfort. In Adams JM (ed): Hypothermia: Ashore and Afloat. Proceedings of the 1979 Conference on Disasters Caused by Cold. Aberdeen, Scotland, Aberdeen University Press, 1981, p 1.581 I. Cooper KDE, Fergllson AV: Thermoregulation and hypothermia in the elderly. In Pozos RS, Wittmers LE Jr (eds): The Nature and Treatment of Hypothermia. Minneapolis, University of l\linnesota Press, 198:3, p :3:3 8. Dinman BD, Horvath 5,\1: Heat disorders ill industry: A reevaluation of diagnostic criteria. J Occup Med 26:489, 1984 9. Dllpuis H, Zerletti G: Whole-body vibration and disorders of the spine. Int Arch Qccup Environ Health ,59::32:3, 1987 10. Ellis FP: Mortality from heat illness and heat aggravated illness in the United States. Environ Res 5:1, 1972 11. Farkkila M, Aatola 5, Starck J, et al: Hand-grip force in lumberjacks: Two-year followup. Int Arcb Qccup Euviron Health 58:20:3, 1986 12. Futatsuka NI, Ueno T, Sakurai T: Follow up study of vibration induced white finger in chain saw operators. Eur J Appl Physiol 56:267, 1987 1:3. lIarkonen H, Hiihimaki H, Tola S, et al: Symptoms of vibration syndrome and radiographic findings in the wrists oflumberjacks. Br J Ind Med 41:1:3:3, 1984 14. Ho ST, Yu HS: A study of neurophysiological measurements and various function tests on workers occupationally exposed to vibration. Int Arch Occup Environ Health ,58:259, 1985 1.5. Hodgson MJ, Talbot E, Helmkamp JC, et al: Diabetes, noise exposure, and hearing loss. J Occup \Ied 29:576, 1987 16. lIorvath SM: Exercise in a cold environment. Exerc Sport Sci Hev 9:26,5, 1981 17. Horvath Sl\1: Hot and cold environments. In Cralley LV, Cralley LJ (eds): Patty's Industrial Hygiene and Toxicology, vol :3B. New York, John Wiley and Sons, 1985, p 481 18. Horvath SM, Rochelle RD: Hypothermia in the ageing. Environ Health Perspect 20:127, 1977 19. Horvath SM, Hadclifle CE, Hutt BR, et al: Metabolic response of old people to a cold environment. J Appl Physiol 8:145, 19,58 20. Hulshof C, van Zanten BV: Whole-body vibration and low-back pain: A review of epidemiologic studies. Int Arch Occup Environ Health 59:20,5, 1987 21. Jensen RC: \Vorkers compensation claims relating to heat and aggravated cold exposure. Professional Safety, September 19, 198:3 22. Jerger J, Jerger 5, Pepe P, et al: Hace difference in susceptibility to noise-induced hearing loss. Am J Otol 7:1425, 1986 2:3. Juntunen J. Ylikoski J, Qjala M, et al: Postural body sway and exposure to high energy impulse noise. Lancet 2:261, 1987 24. Koelega H5, Brinkman JA: Noise and vigilance: An evaluative review. Hum Factors 28:465, 1986 2.5. Lalande NM, Hetu R, Lambert J: Is occupational noise exposure during pregnancy a risk factor of damage to the auditory system of the fetus? Am J rnd Med 10:427, 1986 26. Linden W: Effect of noise distraction during mental arithmetic on phasic cardiovascular activity. Psychophysiology 24::328, 1987 27. Lybarger JA, Kilbourne EM: Hyperthermia and hypothermia in the elderly. In Davis BB, Woods WG (eds): Homeostatic Function and Aging. New York, Raven Press, 1985, p 149 28. Maron MB, Wagner JA, Horvath SM: Thermoregulatory responses during competitive marathon running. J Appl Physiol 42:909, 1977

I1K"T, COLD, NorSE, A'JD VIBRATIO:'-l

525

29. \'Iatikainen E, Leinonen H, Jukntunen J, et al: The efleet of exposure to high and low frequency hand-ann vibration on finger systolic pressure. Eur J Appl Physiol .56:440, 1987 30. Miyashita K, Shiomi S, !toh N, et al: Epidemiological study of vibration syndrome ill response to total hand tool operating time. Br J Ind Med 40:92, 1983 31. I'\adel ER, Horvath SM: Optimal evaluation of cold tolerance in men. In Horvath SM, Kondo S, Matsue H, et al (eds): Comaparative Studies on Human Adaptability of Japanese, Caucasians, and Japanese-Americans. Tokyo, University of Tokyo Press, 1975, p 89 32. Olsen N, Fjeldborg P, Brochner-Mortensen .\: Sympathetic and local vasoconstrictor response to cold in vibration induced white finger. Eur J Appl Physiol 56:272, 1987 33. Okada A, Ariizumi M, Fujinaga H: Diagnosis of vibration syndrome by blood viscosity. In Brammer AI. Taylnr W (eds): Vibration Efl"cts on the Hand and Arm in Industry. New York, John Wiley and Sons, 1984, p 67 34. Pyyko I, Pekkarinen J, Starck J: Sensory-neural hearing loss during comhined noise and vibration exposure: An analysis of risk factors. Int Arch OCCIlP Em'iron Health 59:439, 1987 :35. Rosenstock H, Cullen MR (eds): Clinical Occupational Medicine. Philadelphia, WB Saunders, 1986 36. van Dijk FJ: :-..ion-auditory effects of noise in industry: Introduction and study objectives. Int Arch Oecup Environ Health 58:321, 1986 37. \Vu TN, Chou FS, Chang PY: A study of noise induced hearing Inss and blood pressure in steel mill workers. Int Arch Occup Environ Health 59:529, 1987 38. Young RSK, l\larks KH: Hvpothermia and the pediatric patient. In Pozos HS, Witlmers LE Jr (eds): The I'\ature and Treatment of Hypothermia. Minneapolis, University of Minnesota Press, 1983, p 20 Address reprint requests to Steven \,1. Horvath, MD Environmental Stress Laboratory I\'euroscience Hesearch Institute II niversitv of California Santa Ba;bara, CA 93106