Environmental heat

Ambient or environmental heat affecting the worker and the worker’s ability to transfer body heat to the environment is determined by four environmental factors: (i) air or dry-bulb temperature (T_db), (ii) air moisture content or wet-bulb temperature (T_wb), (iii) air velocity, and (iv) radiant heat (solar and infrared). Microwave radiation may also be a source of environmental heat in some work situations (see Chapter 15). Various measures of ambient heat load, reflecting the factors influencing heat transfer, are available for use in the industrial setting.¹¹ The most commonly used instruments for quantifying the thermal environment are described in Table 6.2.

Metabolic heat

Heat production in the body is the by-product of normal basal metabolism and occurs mostly in the liver, brain, heart, and skeletal muscles. During exercise or work, skeletal muscle activity greatly increases metabolic heat production. A measurement of metabolic heat production or, at least, an estimate of metabolic heat is essential in determining a worker’s total heat stress and in calculating workplace heat exposure limits. Direct or indirect measurement of each worker’s level of work and quantity of heat produced in the occupational setting is not practical. Therefore, tables of the workload or energy cost of various tasks have been developed and are used to estimate metabolic heat (Table 6.3).

Heat stress indexes

The guidelines currently used for worker exposure to heat stress are based on indexes developed through subjective and objective testing of workers or from combinations of external heat measurements. Earlier examples include the effective temperature index, resultant temperature, equivalent temperature, the Oxford index, the Botsball, the heat stress index, and the wet globe temperature index. It is important to note that some of these are indicators of subjective thermal comfort and not of heat stress.¹² Today, the most commonly used index is the Wet-Bulb Globe Temperature (WBGT) index, which was originally developed in an effort to reduce the incidence of heat illness during Marine Corps basic training at Parris Island.¹³

The WBGT index is recommended by OSHA, NIOSH, and American Conference of Governmental Industrial Hygienists (ACGIH) and required by the US Armed Forces.^14,15

The WBGT index is calculated from measurements of the natural wet-bulb (T_wb), the black globe (T_g), and the dry-bulb (T_db) temperatures.

For outdoor environments with a solar heat source, the WBGT formula is

For indoor use or for outdoor settings without a solar load, the formula is

The necessary measurements require relatively simple instrumentation and can be easily obtained in an industrial environment. Automated heat stress monitors that measure all three temperatures and calculate the WBGT index temperature are also available. An example of a manual WBGT monitor is shown in Figure 6.1. The WBGT index was developed for men exercising outdoors in military fatigues. Therefore, if different types of clothing are worn, correction factors are required. This index is not applicable in settings where sweat-impermeable clothing is required and may not be as effective as other indices in preventing heat casualties in extreme heat stress conditions.

Heat strain indicators

Under identical heat stress conditions, the heat strain experienced by different individuals may vary widely, which may require estimation of the physiologic responses to environmental heat stress. Historically, the cumbersome nature of monitoring equipment and its lack of durability have limited our ability to make real-time measurements of a workers’ core temperature or heart rate. As technology improves and durable and convenient monitors and sensors become available, the physiologic measures of heat strain may take on increasing importance, especially for workers in heavy protective clothing.

Heart rate is easily measured and may be a reliable indicator of overall heat strain, rising with both increasing workload and increasing core temperature. Utilizing this physiologic response to heat, a method of measuring oral temperature, postwork heart rate, and recovery heart rate to monitor for heat strain has been developed. Heat stress exposure should be discontinued if (i) sustained heart rate is in excess of 180 bpm minus the individual’s age in years or (ii) recovery heart rate at 1 minute after peak work effort is greater than 120 bpm.¹⁴ The availability of inexpensive electronic pulse monitors and timers has made this method easier, and it can be a valuable indicator of heat strain in certain settings.

Body core temperature appears to be a more reliable indicator of heat stress than heart rate. The World Health Organization recommends that body core temperature should not, under circumstances of prolonged daily work and heat, be permitted to exceed 38°C (100.4°F) rectally or 37.5°C (99.5°F) orally.² Though this heat strain index may seem ideal, monitoring internal or core body temperature with rectal or esophageal probes is not acceptable to many workers. Oral temperatures, while easy to obtain, may be inaccurate measures of core temperatures because of mouth breathing or drinking hot or cold liquids immediately before using a thermometer. An ingestible capsule containing a temperature sensor and a device producing a telemetry signal is available to monitor real-time internal temperatures as the capsule passes through the gastrointestinal tract. Validation studies suggest that given appropriate time to exit the stomach, this method is an acceptable surrogate for rectal or esophageal temperature.^16,17 Tympanic membrane temperature monitors may also provide an acceptable measurement of core temperature, but use of these monitors is uncommon because of ear discomfort and the need for a good seal in the ear canal. Mathematical models to predict core temperature and/or heat strain risk from noninvasive inputs have been developed; further validation and packaging in an end-user-friendly interface are necessary before they can be utilized in the occupational setting.¹⁸

Estimation of fluid loss or hydration status by regular weight measurements prior to work and throughout the day has also been proposed as an indicator of heat strain. Based upon weight measurements (assuming that the worker was fully hydrated before beginning work), the heat-exposed worker can be encouraged to drink liquids to maintain hydration and constant body weight throughout the day. Urine specific gravity measurements before, during, and after work have also been used to assess hydration status in workers. Weight loss of greater than 1.5% of body weight over the course of a normal shift may indicate that an individual is at greater risk of heat illness.¹⁴

Heat exchange

Heat exchange between the body and the environment is influenced by air temperature and humidity, skin temperature, air velocity, evaporation of sweat, radiant temperature, and the clothing worn.²⁵ The heat balance equation describes the major modes of heat exchange or loss by the body (Table 6.5).

Calculated heat loss by radiation and convection is typically estimated from the skin-air thermal gradient. Consequently as T_db approaches skin temperature, heat loss via R + C is diminished, and there is an increased reliance on evaporative heat loss. If T_db exceeds skin temperature, heat will be gained rather than lost. Conductive heat exchange, where there is direct transfer of heat to air or objects in contact with the body, is rarely an important source of heat gain or loss in clothed workers in most occupational settings. However, conductive heat exchange may be an important mode of heat transfer for some workers, such as divers working in hot or cold water.

In addition to elevated ambient temperature, an increase in the water vapor content of the air and clothing will limit heat dissipation to the environment. Relative humidity is the most common way of expressing water vapor content of the air, but comparisons between different levels of humidity are appropriate only when the air temperature is the same. The evaporation of sweat is dependent on the vapor pressure gradient between the skin and the air, which is temperature dependent. As an example, the vapor pressure of air at 30°C, 40%RH, is approximately equal to that at 40°C, 20%RH. Clothing insulates the body from heat loss via radiation, and convection will also serve as a barrier to the evaporation of sweat. Protective clothing, especially sweat-impermeable clothing, which effectively eliminates any body cooling from sweat evaporation, places workers at significantly greater risk for heat strain and heat-related illnesses.

Numerous acute and chronic medical conditions, medications, and individual characteristics may diminish the body’s ability to tolerate heat stress and dissipate internal heat (Table 6.6).²⁶ Dehydration from any cause, whether due to increased sweating or associated with underlying illness, fever, vomiting, or diarrhea, increases the risk of hyperthermia. Many medications, especially antihypertensive or cardiac medications that affect the cardiovascular or renal systems or medications with anticholinergic effects on sweat glands, may alter a worker’s physiologic responses to heat and therefore increase the risk of heat illness. Previous heat-related illness, especially heatstroke, has historically been considered an indicator of both heat intolerance and a possible underlying defect in the individual’s thermoregulatory system. One investigation of 10 individuals with previous exertional heatstroke found that nine of them readily acclimatized to heat while one displayed evidence of persistent heat intolerance for almost 1 year following heatstroke. The investigators concluded that a small percentage of individuals with previous heatstroke may be heat intolerant.²⁷

Heat-related skin conditions

Heat rash, or miliaria, is caused by sweat duct obstruction and resultant sweat retention within the sweat gland. Obstruction of the sweat duct leads to duct rupture and an inflammatory reaction surrounding the duct. Because the rupture of the sweat ducts may occur within different layers of the skin, three forms of miliaria—crystalline, rubra, and profunda—are described.²⁸

Miliaria crystallina is a mild, asymptomatic skin condition consisting of small, clear vesicles resulting from sweat duct rupture within the surface layers of skin. Small erythematous macules resulting from sweat duct rupture within the middle layers of the skin and associated with burning and itching is known as miliaria rubra or “prickly heat.” Miliaria rubra commonly affects the skin of the trunk and intertriginous areas of the body. Extensive cases of miliaria rubra involving large numbers of sweat glands can impede body heat dissipation and contribute to more severe heat-related illness.²⁹ Miliaria profunda results from sweat duct rupture deep within the skin. The lesions, which usually appear only after prolonged periods of miliaria rubra, are small, white to flesh-colored papules and occur most commonly on the trunk. Sunburned skin and occlusive clothing that precludes the free evaporation of sweat increase the risk of all forms of miliaria. Treatment involves reducing sweating in the affected individual and keeping the skin cool and dry. In workers whose jobs require sweat-impermeable protective clothing, the treatment of miliaria may include a temporary transfer to a job not requiring protective clothing or into an air-conditioned workspace. Miliaria rubra usually resolves within a week. Complete resolution of miliaria profunda may take several weeks in a cool environment.

Heat edema

Heat edema is often not considered a true heat-related disorder. It is a rather a common condition in which the extremities swell during the first 7–10 days of exposure to higher temperatures. Typically it is found in unacclimatized individuals, often women or military trainees, who stand or sit for long periods during hot weather and is not associated with cardiac or renal impairment. The etiology of heat edema is uncertain, but it may involve local vasomotor changes or be associated with changes in aldosterone activity.²⁴ It is sometimes prominent in pregnancy, when heat can aggravate the underlying condition of pregnancy-associated edema. Heat edema usually resolves spontaneously within a few days as the individual acclimatizes. Diuretic therapy does not provide significant relief and is not indicated. Symptomatic treatment—elevation of the legs, compression stockings, and gradual exposure to heat—is generally all that is required.

Heat cramps

Heat cramps are painful muscle spasms that occur during or following intense physical exercise in hot environments. The affected individual is usually acclimatized to heat and gives a history of heavy exertion in the heat, profuse sweating, drinking large quantities of water, and minimal salt or electrolyte replacement. Inadequate electrolyte replacement is probably associated with the underlying mechanism responsible for the muscle spasm.^24,30

The muscles involved in the spasm are usually the same muscles used during the preceding exercise, such as the abdominal muscles or the large muscles of the thigh. Heat cramps may be heralded by fasciculations, and while multiple muscle spasms may occur simultaneously, usually only a small section of the muscle is involved. Individual heat-induced muscle spasms last less than a minute; but if untreated, attacks of intermittent heat cramps may last for 4–8 hours.

Heat cramps respond to rest in a cool place and ingestion of 0.1% saline solution (one teaspoon of salt in a quart of water) or fluids containing electrolytes. Salt tablets should not be given. If nausea and vomiting preclude administration of oral solutions, intravenous electrolyte solutions may be necessary. Heat cramps can be prevented by ensuring that workers, especially acclimatized workers, maintain adequate dietary salt intake in addition to adequate fluid replacement.

Heat syncope

Heat syncope occurs in individuals who stand for prolonged periods, who make sudden postural changes, or who exercise strenuously in the heat. The underlying mechanism of heat syncope is similar to that of orthostatic syncope. Venous return to the heart is reduced by pooling of blood in dependent extremities or in dilated peripheral vessels, and cardiac output is inadequate to maintain cerebral circulation and consciousness. Heat syncope is not associated with elevated body temperature, and the syncope victim may remember a typical prodrome of nausea, sweating, and dimming of vision before loss of consciousness. Following syncope and falling to a recumbent position, consciousness returns rapidly. Heat syncope is generally a benign “faint.” The primary health concern is the potential for falling and injury, especially for workers on roofs and scaffolding.

Following an episode of heat syncope, the worker should be allowed to recover in a cool area. To ensure that he or she has not been injured by the fall, a medical examination should be performed. The employer should make sure that the worker is properly hydrated and acclimatized before returning to a job that requires heavy exertion or standing in a hot environment.

Heat exhaustion

Heat exhaustion is a mild to moderate illness characterized by an inability to sustain cardiac output during strenuous work or exercise in the heat that is necessary to meet the combined demands of blood flow for metabolic and thermoregulatory requirements.¹⁵ The signs and symptoms include weakness, ataxia, fatigue, headache, nausea, hypotension, tachycardia, and transient alterations in mental status. Since the symptoms of heat exhaustion are similar to those of early heatstroke, all heat exhaustion victims must be evaluated to eliminate the diagnosis of heatstroke (see Heat Stroke below). Heat exhaustion occurs more commonly in workers who are unacclimatized to heat and who are without adequate water and salt replacement. Treatment of heat exhaustion must be individualized based upon the severity of the presenting symptoms and the underlying cause. Mild heat exhaustion may be treated by having the worker rest in a cool area and providing oral fluid and salt replacement. Severe cases of heat exhaustion—especially severe water-depletion type requiring intravenous fluids—need to be referred to an emergency room for careful replacement of body water. Timing of return to work after heat exhaustion has not been fully studied, but it seems prudent to allow at least 24–72 hours for full rehydration and correction of electrolyte abnormalities before the individual returns to work.

Hyponatremia occurs when electrolyte replacement is insufficient and/or fluid replacement is overly aggressive and can lead to potentially serious and sometimes fatal outcomes. Exercise- or work-related hyponatremia is due to overdrinking, both in absolute (related to total volume consumed) and relative (related to sodium loss via sweating) terms.³¹ In the occupational setting, as hyponatremia rarely occurs, specific prevention measures beyond encouraging appropriate fluid replacement and consumption of salt-containing foods are not necessary.

Heat injury and heatstroke

Heat injury is a moderate to severe illness characterized by tissue (muscle and gut) and organ (liver, renal) injury resulting from work or exercise during heat exposure.²⁶ Individuals with exertional heat injury do not demonstrate sufficient neurological abnormalities to meet the usual definition of heatstroke. Organ and tissue damage may not manifest early in the presentation of heat injury, making it difficult to distinguish it from heat exhaustion, and a thorough clinical evaluation, including assessment of possible organ damage, is necessary.¹⁵

Heatstroke is a life-threatening medical condition. Symptoms include altered mental status and rectal temperatures are often but not always >40°C (104°F).²⁶ However, core temperature >40°C should not be used as a universal diagnostic criteria, as well-conditioned individuals can have core temperatures above this threshold yet remain asymptomatic of heat illness.^32,33 During physical work in the heat, skin blood flow is high, reducing perfusion of the intestines and other viscera, which can result in ischemia, endotoxemia, systemic inflammatory response, and multiorgan damage.

Heatstroke requires immediate, aggressive cooling of the affected individual. Classic heatstroke occurs during summer heat waves predominantly in infants or elderly individuals. The condition is most common in poor and/or elderly individuals who take medications for underlying medical conditions and live in poorly ventilated housing without air conditioning. After days of hot, humid environmental conditions, their ability to maintain body heat balance fails, and heatstroke occurs. A second form of heatstroke, exertional heatstroke, occurs in workers, athletes, or military recruits who perform vigorous exercise in hot, humid conditions and is the focus of this section. Mental status changes are the predominant initial presenting symptom. Heatstroke victims may present with any form of mental status change ranging from irrational behavior, poor judgment, and confusion to delirium, seizures, and coma. Sweating, characteristically absent in classic heatstroke, may be present in exertional heatstroke. The rectal temperature is often >40°C (104°F) and may be much higher; the pulse is elevated; the blood pressure is normal or low; and hyperventilation is common. Nausea, vomiting, and diarrhea may be present.

Initial laboratory findings often include proteinuria, with red blood cells and granular casts also present in the urine, an elevated white blood cell count, and a decreased platelet count. Serum electrolyte levels will vary with level of hydration, acid–base status, and underlying tissue damage. Serum enzymes—lactic dehydrogenase, creatinine phosphokinase, aspartate aminotransferase, and alanine aminotransferase are characteristically elevated. With hyperventilation, respiratory alkalosis may be present; but in exertional heatstroke, lactic acidosis may be the presenting acid–base abnormality. Abnormalities of blood clotting consistent with disseminated intravascular coagulation—including decreased fibrinogen, prolonged prothrombin time and partial thromboplastin time, and elevated levels of fibrin split products—may be present on initial evaluation.

The treatment for all heatstroke victims is immediate initiation of cooling and appropriate resuscitation. The method of cooling used in military settings is immersion of the victim in ice water or wrapping the victim in wet sheets. Even though this type of cooling will cause cutaneous vasoconstriction and shivering, thereby decreasing conductive heat loss and increasing metabolic heat formation, it is still probably the most effective method of cooling outside of a healthcare facility. Rapid cooling to a core temperature <38.3°C (101°F) has been associated with no mortality and an attenuation of organ damage.^34,35 Other rapid cooling methods used for heatstroke include packing the individual in ice or applying ice packs and/or spraying with cold water. Once cooling has been initiated, the victim should be transferred immediately to a hospital for continuous monitoring of core temperature and definitive care. Endotracheal intubation and invasive cardiovascular monitoring are often needed during resuscitation and follow-up care.

The severity of sequelae and mortality in heatstroke is determined by the degree and duration of the elevated temperature. After initial resuscitation of an individual with heatstroke, failure or disruption of the function of multiple organ systems is common and should be expected. Frequent sequelae to heatstroke include liver function abnormalities, disseminated intravascular coagulation, rhabdomyolysis, and acute renal failure.²⁴ Other reported complications of heatstroke include pancreatitis, pulmonary edema, myocardial infarction, and central and peripheral nervous system damage.

Return to Work Considerations

Return to work/play guidelines are often “common sense” recommendations based on a return to normal laboratory parameters and an asymptomatic state.³⁶ Recent data indicates that these criteria may not be appropriate, as tissue damage and/or impaired organ function may persist after the individual appears to have recovered. Biological markers of exertion heat illness (EHI) severity are lacking; however, recent evidence from a rat model of heatstroke suggests that there are novel patterns of core temperature responses to mild, moderate, and severe pathophysiology that may assist in the differential diagnosis. Additionally, associations between hemodynamic changes during heat exposure, high circulating cardiac troponin I levels, and histopathological changes in cardiac muscle during recovery were identified.³⁷ Whether similar or other biomarkers of EHI severity and/or recovery exist in humans remains to be determined.

The return-to-play recommendations from the American College of Sports Medicine are to refrain from exercise for 1 week after release from medical care, with follow-up examination, testing, and imaging as appropriate prior to resuming exercise. Work intensity, duration, and heat stress should be gradually increased until tolerance to vigorous exercise in the heat has been demonstrated. Development of clinical aids and/or biomarkers of EHI injury severity and recovery are necessary, as well as determination of the long-term health consequences, if any, of exertional heatstroke.