Physics, Physiological, and Meteorological Effects of Heat Exposure

Increasing heat and humidity affect the body’s ability to maintain its homeostatic balance, but similar heat indexes (temperatures and humidity) will affect individuals differently based on personal, geographical, sheltering, and other aspects of the mini-climates in which they live. The temperature of the air, its humidity and motion, and the amount of radiant heat energy to which an individual is exposed are the most important factors in human heat stress. Of these, air temperature can have the greatest impact.²⁷ Although there may be intense temperature fluctuations on the outer surfaces and extremities of the human body, thermal homeostatic mechanisms attempt to maintain a relatively stable core temperature. There are four aspects to this homeostatic process: 1) metabolic heat gain; 2) heat loss from perspiration/evaporation; 3) conductive and invective heat loss or gain; and 4) the effects of radiant energy.⁹ When air temperature is low, heat generated metabolically is more easily lost from the body to the air. As air temperature increases, convective heat loss is no longer possible, and heat can be gained from the air. High humidity limits the cooling effects of perspiration evaporation.⁹

The interpretation of any heat index value will be affected by differences in an individual’s age, medications, clothing, and body habitus. In addition, these numbers will fluctuate significantly when compared with other values obtained if one could measure the various microclimates to which individuals are exposed.⁹ For example, those older than age 52 tend to produce significantly less perspiration than those who are younger.²⁸ Differences in hydration patterns can complicate the application of general heat indices to individuals or groups. Elderly populations with little shelter from the sun’s direct rays, or those shuttered tightly within steaming, unventilated brick buildings in inner-cities will experience drastically different reactions to the heat than middle-class, middle-aged suburban dwellers with air-conditioned homes.

Increasing temperatures, humidity, and direct exposure to the sun can increase the heat stress that individuals experience during EHEs. Heat index tables often assume that temperatures are taken in a shaded area, with little wind. In addition, most heat index tables note that direct sunlight can increase heat index figures by up to approximately 8°C and that exposure to dry winds can further increase health risks by promoting rapid dehydration (Figure 41.3).²⁹ Ultimately, any meteorological conditions that increase heat indexes will increase heat stress and health risk. All else being equal, the shock effect of the increased heat is greater the earlier in the summer the EHE occurs.^30,31 In a similar fashion, health risks increase with the duration of the EHE, the amount of time spent above minimum temperature thresholds, and the rapidity of the rise in the heat index.^17,32–36 Residents become increasingly acclimated to the heat as the season progresses. It is not absolute temperature, but rather the extent of upward deviation from usual local summer temperatures that seems to be the key variable affecting mortality.³⁵ As Table 41.1 demonstrates, there is striking similarity across the continents (with the exception of Antarctica) in the array of the highest-ever recorded temperatures.

Figure 41.3.

Likelihood of Heat Disorders with Prolonged Exposure or Strenuous Activity.

Source: NOAA, http://www.srh.noaa.gov/ssd/html/heatwv.htm. Reviewed/modified by Tom Javorcic, 2013.

Diagnosis and Treatment of Heat Stress Illnesses

There are several clinical syndromes that comprise heat stress illnesses or conditions: 1) heat cramps; 2) heat edema; 3) heat syncope; 4) heat exhaustion; and 5) heat stroke. They represent variations and overlap in a continuum of heat illness, from minor complaints to overwhelming heat stress that can lead to death.³⁶

Heat cramps present as pain and spasm in heavily exercised muscles. Their presentation can vary, from the parade marcher who complains of abdominal pain, to the athlete with cramping in the calves. The mechanism is thought to result from an imbalance in water and sodium intake, leading to hyponatremia, either measurably or locally at the cellular level. Clinically the body temperature is normal, with little evidence of frank dehydration. Measurement of electrolytes may reveal hypokalemia, hyponatremia, respiratory alkalosis, hypomagnesemia, and hypophosphatemia. On the scale of severity, this is usually a benign condition, treatable with rest, removal from the heat source, and oral or parenteral fluid and electrolyte replacement. Pitfalls that may occur include the attribution of abdominal cramping to heat cramps, when in fact the patient has an alternate diagnosis, such as infectious peritonitis or internal bleeding from a ruptured viscus or hemorrhagic ovarian cyst. Additionally, rhabdomyolysis can occur in the setting of severe exertion or repetitive muscular contraction, leading to myoglobinuric renal failure and life-threatening hyperkalemia with its attendant effects on cardiac conduction. Thus, evaluation in the setting of significant muscle pain should include laboratory studies that can detect these conditions.

Heat edema is a mild condition resulting in swelling of the hands or feet, related to prolonged peripheral vasodilation followed by orthostatic pooling of blood in the extremities. It is usually responsive to elevation of the affected limbs. It must be differentiated from renal failure, deep vein thrombosis, and congestive heart failure in susceptible populations.

Heat syncope is characterized by sudden loss of consciousness and is also related to peripheral venous blood pooling with subsequent orthostatic hypotension. It occurs with prolonged standing, or rising quickly from a sitting position. Such persons should not be “held up” or supported, but rather gradually lowered to the ground. First aid treatment consists of laying the patient on the ground and lifting the legs up slightly to restore blood flow to the head. Maintaining the patient in an upright position may prolong the period of poor cerebral perfusion. Rehydration should ensue, and an electrocardiogram should be obtained to ensure no heart blocks or other cardiac conduction abnormalities are occurring.

Heat exhaustion occurs in the setting of excess diaphoresis in a hot, humid environment, leading to volume depletion. Core body temperature will be elevated above normal, but typically remains less than 40.5°C, which usually defines the level for heat stroke. Symptoms are profuse sweating, malaise, fatigue, headache, dizziness, nausea, and vomiting. If left untreated, the condition will likely progress to classic heat stroke. Tachycardia and hypotension may be present, but major neurological dysfunction does not occur. Treatment consists of cooling, oral rehydration, or intravenous rehydration in someone who is hypotensive or fails to respond to oral fluid replacement within a few hours.

Heat stroke is the most life-threatening condition related to heat stress. It is defined as an elevated core body temperature usually equal to or greater than 40.5°C in association with significant acute mental status or behavioral changes. Mental status changes can consist of confusion, bizarre behavior, hallucinations, delirium, unresponsiveness, seizures, posturing, or coma. Loss of sweating as a mechanism for body cooling is a late finding. The observation that sweating ceases is found in only 50% of cases, and those patients with exertion-related hyperthermia are more likely to be sweating. Heat stroke is a medical emergency and occurs when heat production exceeds physiological cooling capacity such that heat dissipation no longer occurs. Hyperthermia is characteristically differentiated from fever, in that fever occurs due to an upward adjustment of the temperature set point in the hypothalamus. In hyperthermia, the hypothalamus set point is normal, but the body is unable to eliminate acquired or self-generated heat, leading to excessive body temperature.

With the onset of heat stroke, widespread cellular and organ damage ensues, characterized initially by tachycardia, increased cardiac index, and central venous dilation. Critical deterioration continues, progressing to hypotension, acute renal and hepatic failure, gut ischemia, rhabdomyolysis and cardiovascular collapse. Manifestations include coagulopathy in association with hepatic, renal, and cardiac failure. Hemostatic disturbances are marked by drops in platelet counts and fibrinogen and consumption of clotting factors. Although usually attributed to direct cellular injury by heat, a contribution from inflammation has been proposed in the last decade. Specifically, a role of the systemic inflammatory response syndrome (SIRS) in the development of multi-organ system dysfunction is theorized.³⁷ Thermal injury to the vascular endothelium³⁸ activates platelet aggregation, which is irreversible, even following cooling. Excess deposition of fibrin ensues in arterioles and capillaries, which may lead to vascular thrombosis causing occlusion of blood supply in various organ beds. Coagulation often persists until platelets and coagulation proteins are consumed at a faster rate than they are produced, even after normalization of fibrinolysis following cooling. As coagulation proceeds, platelets and coagulation proteins are consumed, resulting in blood loss from multiple tissue sites, such as gums and venipuncture wounds. High circulating levels of cytokines correlate with morbidity and mortality in heat stroke. Few controlled studies have been performed examining the efficacy of anti-cytokine, anti-endotoxin or anti-coagulation drugs on patient outcome with heat stroke.³⁷

Classic heat stroke is described during EHEs, particularly in the elderly. Exertional heat stroke may also occur in young, fit populations such as athletes and military recruits undergoing training. Several high-profile deaths in professional athletes have been reported by the media, demonstrating the importance of prevention when weather conditions increase the risk of such heat stress. In that setting, marked rhabdomyolysis and myoglobinuric renal failure are often observed along with acute hepatic failure and disseminated intravascular coagulation. Mortality ranges from 10–70% in series of heat stroke patients, with higher mortality rates found when treatment is delayed more than 2 hours.³⁹ Predictors of multi-organ dysfunction include respiratory failure, metabolic acidosis, elevated creatinine phosphokinase, and liver function test elevations greater than twice normal.⁴⁰

Treatment requires rapid cooling to avoid further cellular and organ damage by extreme hyperpyrexia. In the field or on arrival to the ED, ice or cold liquids should be placed in contact with the patient (especially in the axillae and groin), and additional cooling measures instituted as available, while airway, breathing, and circulation are assessed and managed. Airway management may include endotracheal intubation. If severe hyperpyrexia is suspected, use a rapid sequence paralytic agent that does not induce hyperkalemia, i.e., avoid using succinylcholine. Due to altered mental status, an immediate glucose determination is needed to allow rapid diagnosis and treatment of hypoglycemia. Breathing assessment should include oxygen saturation monitoring. Circulatory support includes cardiac monitoring and fluid resuscitation when indicated to support blood pressure, perfusion, and urine output. Caution is necessary when managing the geriatric population that may have antecedent cardiac, pulmonary, and/or renal disease. In addition to ice packing, when fans are available, cooling can be accomplished by spraying the undressed patient with tepid (not cold) water while blowing air from large fans across the body surface to maximize evaporative heat loss. More invasive methods such as ice water lavage of the stomach through a nasogastric tube or the peritoneum through a peritoneal lavage catheter, and even cardiopulmonary bypass have had reported anecdotal success. These aggressive treatments have limited evidence of benefit, however, and may actually be harmful and are therefore not recommended by some experts.^41,42 A newer modality of using intravenous catheters containing cooling coils offers an additional treatment option.⁴³ Frequent monitoring of the core body temperature is essential to avoid overshooting and creation of further problems due to hypothermia. It is not necessary to reduce body temperature to normal, but only to the level thought not to produce cellular injury; a goal of 38.9°C is reasonable. Risks and benefits of each of these techniques have been reviewed.⁴⁴

Recreational drug use may also contribute to heat-related mortality. The number of fatal cocaine overdoses appears to correlate with higher ambient temperatures. In a New York City study, the mean daily number of cocaine overdose deaths increased by 33% on days with a maximum temperature of 31.1°C or higher, in comparison to days when the mean temperature was below this point.⁴⁵ This appears to be related to the fact that both cocaine and heat stress cause significant thermoregulatory instability. Other risk factors for developing heat stroke found in the New York City EHEs were neighborhood poverty, lack of access to working air conditioning, chronic medical and psychiatric conditions, and obesity.⁴

Emergency Medical Services, the ED, and Extreme Heat Events

In nations with well-developed emergency services, prehospital emergency medical services (EMS) and the ED play significant roles during EHEs. The EMS system is the triage and transportation system that initiates patient contact when dispatched, often initiates treatment in the field, and transports patients to EDs. During EHEs, just as the number of patients increases, so too do the requests for ambulances. The average number of ambulance calls increased by 10% on those days considered oppressively hot over the 4-year period from 1999 to 2002 in a study in Toronto, Canada.⁴⁶ Data from two EHEs in Adelaide, Australia, in 2008 and 2009 demonstrated a 10% increase in ambulance calls in the first event, and 16% in the second.⁴⁷ In the Sydney, NSW, Australia study of the 8-day EHE in 2011, a 10% increase in ambulance calls was noted in the age group <75 years old, while it increased 17% in the age group >75 years old.⁴⁸ Augmentation of EMS capabilities may be a reasonable intervention during an EHE.

EDs are the major hospital point of entry for most victims suffering heat-related illnesses and therefore have a large role in preventing escalating morbidity and mortality. EDs should be prepared to manage surges of EHE patients with adequate cooling equipment. Thus, ED managers must ensure sufficient supplies of water spray bottles, cooling packs, fans, cooling catheters, and ice during EHEs. Informational handouts can be printed as part of discharge instructions in advance of such emergencies as well as during the events. This should become part of the general community educational program, much as is done for other types of safety issues. Increased visits to the EDs in affected areas should be expected.

Using a wide variety of measures to predict EHEs is a complex process that can involve a national weather service, local health departments and emergency management agencies, first response EMS agencies, hospitals, medical examiners/coroners’ offices, and many other local agencies and community organizations. No matter how effective the ED may be as a heat mortality sentinel, it cannot provide sufficient warning to reduce the impact of these emergencies. Systems designed to predict EHEs in a timely manner should augment rather than substitute for the longer-range prediction times that air mass monitoring systems allow. The EHE has already started by the time patients begin presenting to EDs. Earlier real-time identification of presenting symptoms of patients to the EMS system may identify the onset of an EHE sooner. A study of atmospheric circulation phenomena identified a five-wave pattern of anomalous planetary waves that tended to precede the onset of heat waves by 15 to 20 days. This was not necessarily linked to tropical heating, suggesting that EHEs are predictable beyond the typical weather forecast range of 7 to 10 days.⁴⁹ EHEs tend to quickly generate many patients so that, in systems where it is permitted, many EDs implement diversion status. As three Institute of Medicine (IOM) reports delineate, the U.S. emergency medical care system “is woefully inadequate and unprepared for a pandemic, bioterrorist attack, natural disaster or other national crisis.”⁵⁰ IOM found the U.S. emergency care system to be underfunded, too fragmented to communicate and cooperate effectively across levels and geographical areas, and possessing little surge capacity to manage a disaster. The IOM also found that emergency care staff members are often inadequately trained to respond to large-scale disasters or to care for pediatric patients. While this analysis focused on the United States, findings are likely similar in other countries.

During Chicago’s July 1995 EHE, there were 1,072 more hospital admissions than average for comparative weeks, with 838 (35%) more patients aged 65 years and older being admitted than expected. There was also strong anecdotal evidence of increased ED visits. An analysis of excess hospital admissions during the heat wave defines who was admitted and why. The primary reasons for a hospital visit were dehydration, heat stroke, or heat exhaustion. The susceptible population at risk for admission had comorbid cardiovascular illnesses, endocrine disorders, liver and kidney diseases, or nervous system disorders. Within this population, the elderly were disproportionately represented, in large part due to their altered thirst perception and related conditions.⁵¹ On the second day of the EHE, only a few Chicago EDs were on diversion and directing ambulances to other hospitals. By the fourth day, however, eighteen city EDs were diverting patients to other facilities.⁷ A study of the 1993 heat wave in Philadelphia found a 26% increase in total mortality and a 98% increase in cardiovascular mortality associated with the EHE. In adjacent counties, the risk for dying of cardiovascular disease rose significantly for people older than 65 years, for both sexes and all races.⁵²

During the European heat wave of 2003, heat-related deaths in a Parisian hospital occurred mostly in elderly patients (mean age 84), and 69% were women. Patients who died differed from those who survived.⁵³ The former were characterized by greater levels of dependency and by a more abnormal initial clinical presentation (such as elevated temperature, lower blood pressure, and altered mental states). They were also more likely to have existing ischemic cardiomyopathies and to be taking psychotropic medications.⁵³ In London during the same period, 2,091 deaths occurred (17% more than for the same period in earlier years); 23% of the deaths were among those 75 years of age or older.⁵⁴ Investigators report similar findings in Australia, where high environmental temperatures are common, although it is rare that these exceptional conditions produce elevated levels of heat-related morbidity and mortality. In four major teaching hospitals in Adelaide, most patients presenting with heat-related conditions (85%) were aged 60 years or older, with 20% from institutional care, and 30% with poor mobility. Peak presentation followed high daily temperatures for 4 consecutive days. Severity was related to existing cognitive impairment, diuretic use, presenting temperature, heart rate, blood pressure, serum sodium, and serum creatinine. The mortality rate was 12%, and 17% required a more dependent level of residential care on discharge.⁵⁵ There were comparable findings in a 1999 study in Wisconsin where heat-related illnesses led to twenty-one deaths. Death rates were highest among the elderly; particularly those aged 65–84 years (2.2/100,000). Heat was attributed as the underlying cause of death for twelve of the twenty-one victims. Cardiovascular conditions resulted in another eight deaths and were a contributing cause for an additional seven.⁵⁶

Hospital/ED Surge Capacity and Extreme Heat Events

For years, emergency managers have considered “surge capacity” in their catastrophic planning (see Chapter 3). Although an EHE would likely stress existing healthcare facility resources, it is unlikely that most EHEs would last long enough and generate enough patients to necessitate the use of external surge facilities. A review of surge capacity, however, is helpful to the extent that the strategies similar to those used for external expansion can be used to support and extend services within existing fixed facilities.

U.S. hurricanes in 2004 and 2005 provide an example of the devastating health and medical effects of weather disasters. Hurricanes Katrina and Rita and subsequent flooding caused the same types of damage to many local healthcare facilities as they did to other types of buildings. Many hospitals and federal and state medical support agencies were forced to establish operations in temporary locations such as shuttered retail stores and veterinary hospitals.⁵⁷ Freestanding or support/augmentation facilities were also constructed at airports, sports complexes, and adjacent to existing institutions. These surge hospitals addressed the increase in demand for medical care and contained triage, treatment, and sometimes surgical capacities.⁵⁷

Using the United States as an example, federal disaster support to hospitals is only a small part of the national emergency management system. This system is a complex network of public, private, and nonprofit organizations (ranging from the American Red Cross to professional organizations such as the American Hospital Association, local hospital councils, and community groups in the vicinity of hospitals) as well as individual benefactors. It also includes federal, state, and local government agencies, special districts and quasigovernmental bodies, nonprofit service and charitable organizations, ad hoc volunteer groups and individuals, and private sector firms that provide governmental services by contract.⁵⁸ Collaboration with this huge array of emergency preparedness agencies and entities in a coordinated and effective manner requires hospital preparedness staff whose perspectives are broader than just the individual hospital’s concerns. Planners must also be knowledgeable about the complex and rapidly growing scientific evidence base related to disasters.

Surge planning in U.S. hospitals includes consideration of The Joint Commission requirements for: 1) establishing hospital incident command systems as the chain of command for disasters; 2) all-hazard emergency management plans; 3) mutual aid agreements and processes with other hospitals, systems, and local, state, and federal agencies; 4) coordination with local emergency management agencies; and 5) the requirement to maintain comprehensive documentation on decision making, victim destinations, patient tracking, and reimbursement.⁵⁹ Existing rules and waivers under the federal Medicare program can also significantly influence a hospital’s ability to manage surge requirements. Other recommendations that address surge planning appear in the publication Medical Surge Capacity and Capability: A Management System for Integrating Medical and Health Resources during Large-Scale Emergencies.⁶⁰ Those that have the most relevance to EHEs include:

The U.S. National Foundation for Trauma Care has made several key recommendations for improving the capacity of trauma centers to provide care to victims of a terrorist event.⁶¹ Those relevant to EHE surge planning include:

Auf der Heide published response strategies for hospitals during disasters. Those that are directly applicable to EHEs are:

The Joint Commission found that legal and reimbursement issues are among the most critical, non-patient, care-related challenges that hospitals face when developing surge capacity.⁵⁷ During surge conditions, state and federal waivers can protect emergency medical workers. During Hurricane Katrina, for example, the governor of Louisiana waived state licensure restrictions for those practitioners licensed out of state. The Department of Health and Human Services (HHS) afforded liability protection to healthcare workers who volunteered, and waived the Emergency Medical Treatment and Active Labor Act. A number of U.S. laws and agreements (e.g., the Emergency System for Advanced Registration of Volunteer Health Professionals) as well as a proposed hospital-based credentialing system have made it potentially easier to accommodate volunteers who respond to a disaster.

Other U.S. federal and state programs that can provide healthcare staff resources during surge conditions include the National Disaster Medical System, the U.S. Public Health Service Commissioned Corps, and the Medical Reserve Corps. The Emergency Management Assistance Compact, administered by NEMA, can also provide volunteers (Table 41.3). Individuals recruited by this program (31,000 for Hurricanes Katrina and Rita alone) played important roles in the responses to the four hurricanes in 2004 and to Katrina and Rita the following year.^57,63

Mortality and Morbidity from Heat Exposure

There is a relatively consistent correlation between mortality and increases in heat measured by temperatures, heat index (a measure of temperature and humidity), or by air-mass conditions. ^{12,14,64–66} Using sophisticated air-mass models, researchers demonstrated a clear relationship between heat-related mortality and EHEs in forty-four major U.S. metropolitan areas.¹⁴ In a study of twenty-eight metropolitan areas within the United States, heat-related deaths during EHEs significantly exceeded the expected totals for time of year and were in substantial agreement with the previous findings.¹⁹ Overall, however, heat-related mortality trends declined between 1964 and 1998, as temperatures and heat stress conditions have risen. This suggests that a relative “desensitization” of the U.S. metropolitan population to weather-related heat stress has occurred. Such desensitization can be attributed to a variety of factors, including improved medical care, increased air conditioning use, better public awareness programs, and both human physiological and urban medical/emergency response systems adaptations. The irony is clear: traditionally hotter metropolitan areas have lower heat-related mortality.

EHEs also increase morbidity. The majority of studies emphasize the most serious incidents that result in ED visits and hospital admissions.⁶⁷ Semenza studied 1,072 hospital admissions during the 1995 Chicago EHE and found the majority of excess admissions were due to dehydration, heat stroke, and heat exhaustion among people with existing conditions. ⁵¹ Rydman also studied intense heat-related morbidity from the same event through an analysis of ED visits and found that heat-related morbidity was an antecedent of mortality.⁶⁸ Knowlton et al.⁶⁹ collected data from the 2006 California heat wave showing a substantial rise in morbidity, with dramatic increases across a wide range of morbidities statewide. ED visits far exceeded excess hospitalizations. Heat-related illnesses, electrolyte imbalances, acute renal failure, nephritis and nephrotic syndrome, diabetes and cardiovascular diseases were the main reasons for the increase in ED visits. Heat-related ED visits increased 6-fold statewide, and more than a 10-fold increase was seen in heat-related hospitalizations. Kilbourne searched for the most effective responses to heat-related illnesses and determined that universal access to air conditioning may be the most effective intervention, even with the relatively high costs of providing this service to the poor.³⁵ More recent studies found that basic behavioral changes and adaptations (e.g., use of air conditioning, adequate hydration, heat emergency plans, warning systems, and illness management plans) could significantly mitigate heat-related morbidity and mortality.⁷⁰

The most precise definition of mortality related to heat waves is that given by a medical examiner or a coroner in the formal determination of death. After serious EHEs in Philadelphia in 1993, and in Chicago in 1995, the National Association of Medical Examiners recommended the following definition of heat-related death: “a death in which exposure to high ambient temperature either caused the death or significantly contributed to it.”⁷¹ The committee also recommended that the diagnosis of heat-related death be based on a history of exposure to high ambient temperature and the reasonable exclusion of other causes of hyperthermia. The diagnosis may be established from the circumstances surrounding the death, investigative reports concerning environmental temperature, or measured antemortem body temperatures at the time of collapse being at least 40.6°C. Under those conditions, the cause of death should be certified as heatstroke or hyperthermia. In cases in which the antemortem body temperature cannot be established, but the environmental temperature at the time of collapse was high, appropriate heat-related diagnosis should be listed as the cause of death or as a significant contributing factor.⁷¹

Heat stroke survivors have been shown to have significant elevations in their 30-year mortality rates when compared with individuals that never experienced heat stroke. Many heat stroke victims in Europe succumbed to multi-organ failure during the weeks, months, and years following the heat event, despite acute hospital treatment.^72,73

Demographic and Individual Factors in Heat Exposure

Individuals at highest risk of becoming ill or dying during EHEs are the very young, the elderly (socially isolated, without access to air conditioning, bedridden, and with ischemic heart disease or other chronic conditions), the poor, minorities, and those taking certain medications such as neuroleptics or antiparkinson agents.^{9,28,55,66,68,74–79} Behaviors that can result in heat stroke from dehydration and impaired judgment include strenuous exercise or work in hot or humid weather (even by the young and physically fit), alcohol consumption, and the use of some nonprescription drugs (e.g., antihistamines and sleeping pills).^9,80 Cocaine overdose, which is associated with hypertension, tachycardia, coronary vasospasm, arrhythmias, and increased core temperature, was linked with a significant increase in mortality in Marzuk’s 1998 study of New York City.^45,78

Use of cooling centers by individuals was not shown to be significantly protective, probably because so few visited them.⁷⁴ Walking down flights of stairs, with the mobility limitations often accompanying older age, and crossing potentially unsafe streets to attend cooling centers are unlikely options for many of the at-risk elderly.⁷⁴ European mortality patterns in the August 2003 heat wave mirrored those seen in the United States, with 70% of those dying from heat-related causes being 75 years or older.⁸¹ Accurate demographic estimates and projections of those sickened or dying from heat-related causes are complicated because susceptible groups often remain in the city, creating a bias in predicted excess deaths.⁸² Most often, there are more females affected by adverse heat-related conditions than males. This probably reflects the higher proportion of women in the elderly population, their possible higher susceptibility, and their higher rates of living alone (Figure 41.4).⁸²

Figure 41.4.

The Demographic and Individual Risk Factors of Heat-Related Mortality.

During Chicago’s 1995 heat wave, hospital admissions were up 11% for the week of the heat event, with a 35% increase for patients 65 years of age and older. The majority of the excess admissions (59%) represented patients requiring treatments for dehydration, heat stroke, and heat exhaustion. With the exception of acute renal failure, no other primary discharge diagnoses were significantly elevated. In contrast, analysis of comorbid conditions revealed 23% excess admissions for underlying cardiovascular diseases, 30% for diabetes, 52% for renal diseases, and 20% excess admissions related to nervous system disorders. Patient admissions for emphysema and epilepsy were also significantly elevated during the heat event.⁵¹ Other risk factors for developing heat stroke found in the New York City EHEs were neighborhood poverty, lack of access to working air conditioning, chronic medical and psychiatric conditions, and obesity.⁴

Geographical Factors in Heat Exposure

Average summer temperatures appear to have no effect on heat deaths. Kilbourne observed that it is not the absolute temperature value, but rather the extent of upward deviation from the usual summer temperature that seems to influence mortality.³⁵ For example, in the United States, southwestern cities such as Phoenix, Arizona, have fewer heat-related deaths but have higher average temperatures than midwestern cities such as St. Louis, Missouri, or Chicago, Illinois, which have experienced high mortality from heat waves. Neither excess mortality nor prominent heat-related health effects were noted in Phoenix in July 1980 despite temperatures that averaged 2.4°C above baseline and a highest monthly temperature of 46°C. As expected, based on reports in the international literature, cities that normally have a cool climate (those located in the north) reported the highest excess mortality.⁸³ Reasons for these differences have not been studied extensively. Possible explanations include differences in population age/acclimatization, architectural style/building materials, and air conditioning use. In 2002, researchers at the University of Delaware reported a list of temperature levels that raise mortality and morbidity in select, large American cities whose populations have been subjected to various degrees of heat stress. These are listed in the emergency response plan of the City of New York (Table 41.3).⁸⁵

There is evidence of a geographical and physiological basis for the lower death rates in urban areas that have higher average temperatures. Kilbourne observed that heat seems to cause fewer health problems in characteristically warm areas than in those that are more variable in climate; the temperature level required to increase mortality is actually higher in hotter climates.^14,35,85 DiMaio reported that when individuals live in a temperate zone, many of their nascent sweat glands become permanently inactive during childhood.⁸⁶ If, however, the individual lives in the tropics, the glands remain functional throughout life. Other adaptations include reduction in sodium loss from sweat to 3–5 g/day, after 4–6 weeks of acclimatization. A person who sweats profusely may lose as much as 15–30 g/day of sodium chloride until becoming acclimated.

Chestnut demonstrated geographical patterns in heat-related mortality.⁸⁷ The highest hot weather–related mortality rates are in northern metropolitan areas of the United States, even though average summer temperatures are higher in southern metropolitan areas. This suggests that biological/behavioral adaptations occur in areas that are consistently hot, but not where minimum daily temperature variability is great. The availability of air conditioning, standards of living, and housing quality contribute to differences in mortality, but these explain a much smaller share of the fatalities than does variability in minimum daily temperatures.⁸⁷ Kalkstein found that consecutive days of hot, oppressive weather caused a continued rise in mortality.⁸⁸ Chestnut also reported that areas with higher average temperatures and more frequent hot weather episodes do not necessarily experience more hot weather–related mortality during summer months.⁸⁷ Several southern metropolitan areas with very hot, humid summer weather experience much lower or no statistically significant hot weather–related mortality. It remains unclear whether these data apply to the degree of mortality or morbidity from increases in the temperature, duration, and frequency of hot weather episodes in the tropics.¹

Death rates related to EHEs do not occur on the days with the highest average temperatures. In a study of heat-related mortality from the September 1970 heat wave in New York and other eastern seaboard cities, the highest mortality levels occurred on the third day, when the temperatures were less than those on the first 2 days (Figure 41.5).^9,89,90 In Chicago’s 1995 EHE, a slightly different pattern manifested, with the number of deaths peaking 2 days after the maximum heat-index recording.⁹¹ This is consistent with previous studies demonstrating that during EHEs, the maximum number of heat deaths tends to lag behind the days with the highest temperatures.^92,93 It has also been suggested that EHE-related mortality may reflect the tendency of heat stress to precipitate death in persons who are already ill from a wide variety of chronic diseases and would die in the near future.⁹ Evidence of this potential effect has been sought but not found. For example, no significant decrease in the number of deaths was reported following the EHE in New York in 1972.^9,89,90

Figure 41.5.

Heat-Related Deaths, Chicago, July 1995.

Source: National Synthesis Team, U.S. Global Change Research Program, published in 2000.

Urban Heat Island and Bioclimates

The long-established concept of the “urban heat island” is pervasive in the American and European literature on EHEs, and applies, to a lesser extent, to urban areas in developing countries.^94,95 This phenomenon describes urban and suburban temperatures that are 1°C–6°C hotter than in nearby rural areas. Elevated temperatures can affect communities by increasing peak energy demand, air conditioning costs, air pollution levels, and heat-related illness and mortality.⁹⁶ A typical urban heat island profile is shown in Figure 41.6. Important aspects of the urban heat island literature include themes regarding poverty, social isolation, social class, race/minority status, crime, poor housing, inadequate healthcare, and mobility limitations. Ultimately, most of these factors are related to poverty and unemployment. Studies of heat islands do not generally indicate bioclimatic aspects (effects of weather and climate on life forms, including humans) and are therefore of limited use for urban planners.⁹⁷

Figure 41.6.

Urban Heat Island Profile.

Source: Environmental Protection Agency, http://www.epa.gov/heatisland/about. Reviewed/modified by Tom Javorcic, 2013.

Urban areas tend to be warmer because of their “masses of stone, brick, concrete, asphalt, and cement.”²⁷ These darker surfaces, which absorb more solar heat during the day, radiate that energy into the environment at night.⁸⁴ All of these factors, including diminished wind and cooling air currents create the heat storing and absorbing urban heat island. The Atlanta Metropolitan Area Heat Profile appears in Figure 41.7 with red, and dark and light orange and yellow denoting hotter and colder areas. Heat wave response planning is of interest in intensely developed urban areas that are large enough, dense enough, and often old enough to have potentially damaging urban heat islands. U.S. studies analyzing data from the last 100 years confirm this finding and recognize associations among: 1) large masses of cityscape (e.g., cement, asphalt, and high percentages of multiple unit dwellings); 2) a relative lack of trees and other vegetation; and 3) poor wind and air circulation patterns. These areas have experienced relatively high EHE-related morbidity and mortality.^9,34,84,87 Klinenberg termed urban heat islands “Urban Loneliness Islands,” referring to the physical and social isolation of many elderly heat victims.⁹⁸

Figure 41.7.

Atlanta Metropolitan Area Heat Profile.

Source: Environmental Protection Agency, http://www.epa.gov/heatisland/about/measurement.html. Reviewed/modified by Tom Javorcic, 2013.

After the deadly Chicago heat wave of 1995, the National Oceanic and Atmospheric Administration (NOAA) observed, “There is sufficient circumstantial evidence to conclude that the urban heat island was at least partially responsible for…conditions in Chicago’s south side.…[T]he elderly and infirm…in urban areas are in the greatest danger during heat waves.”⁷ During EHEs, health risks are magnified by increasing exposure time and maximum temperature.²

Urban populations in non-industrialized countries are likely to be particularly vulnerable to such effects when compounded by climate change.⁹⁹ Worsening economic conditions exacerbate this impact. A statement by Lord May, President of the British Royal Society, makes clear that climate change and its related and unexpected costs could ruin efforts to elevate Africa out of poverty.⁴ Vulnerable populations can, however, be spared many of the effects of EHEs through relatively uncomplicated human interventions, including the use of advanced early warning systems and providing access to potable water, shelter, emergency medical care, and air conditioning.¹⁷

Concentrations of asphalt, concrete, stone, and brick are relatively new, and make up relatively smaller parts of urban areas in developing nations. Poor immigrants to the city, and even the emerging middle class, usually live in a different environment. These areas are characterized by quasi-traditional, owner-constructed, single- or extended-family housing, frequently densely packed, and usually with dirt rather than asphalt or cement roads. These typically large barrios, favelas, kampungs, or townships are not really heat islands, due to their lack of a genuine urban infrastructure. Yet these communities are where almost all deaths and illnesses from EHE events occur.

Heat in the Indoor Environment

Kovats and Jendritzky found that there are three main factors associated with indoor heat exposure.¹⁰⁰

Givoni categorized the variables that influence the inner bioclimate:^97,101,102

Givoni also described aspects of external design that influence urban climate.

There is a need for further health research on the relationship between housing types and heat effects. In addition, there is little information about how people behave in their homes. When do they use their air conditioners? What is the effect of electrical costs? When do they open their windows for cooling or when do they close them to keep out pollution or noise?

Air Conditioning

Air conditioning is a “special case” in Europe, which relies much less on air conditioning than the United States, even in many healthcare institutions. The European research on air conditioning is not definitive, but supports the use of unit-wide, central air conditioning as opposed to single room air conditioning. The latter has been found to be minimally, if at all protective, unless the housing unit has enough window air conditioners to approximate the coverage of central air conditioning.¹⁰³ Although Europeans recognize the protective nature of air conditioning in EHEs, they stress that air conditioning requires sealed buildings that create stagnant, polluted air issues, and that air conditioning itself uses energy that contributes to global warming. When power grids fail, people are often left in relatively airtight buildings.⁹⁷ In Europe, air conditioning is advised only in cases in which ill health is present.¹⁰⁰

The Extreme Heat Event Planning Process

Despite the many examples of deadly EHEs, a 2004 review of plans from 18 U.S. cities at risk for heat-related mortality found that many had inadequate plans or no plans at all.¹⁰⁴ Another study of 120 of the largest U.S. cities found that only 29 had developed single-purpose response plans and these were of varying quality and scope. In a 2010 review, 31 cities were found to have adopted plans.^105,106,107 Although there is no mechanism for coordinated U.S. EHE response planning, there has been significant activity at the federal level. These efforts include the development and mass circulation of a comprehensive, interagency extreme heat event guide (2006), the federally sponsored Heat Wave Workshop in 1996, the National Weather Service’s (NWS) growing use of sophisticated air mass prediction systems, CDC’s coverage of EHEs in its Morbidity and Mortality Weekly Reports, and study results published on multiple Web pages by EPA, CDC, and NOAA.

Urban EHE response planning has developed into a unique policy area with its own literature that is scattered among larger disciplines. It is supported by a growing public awareness and constantly reinforced by heat wave alerts. During recent decades, a modestly growing number of urban governments in Europe, Canada, and the United States, have reacted to EHEs by developing EHE response plans. These include alert/watch/warning systems based on an analysis of deadly air masses that provide more “early warning time” than previous systems. In addition to such strategies, existing urban EHE response plans have included the following: 1) public utility bill forgiveness or modified bill payment; 2) free air conditioner distributions; 3) public cooling centers; 4) public information hotlines; 5) public education and information systems; 6) registries for the elderly and other at-risk populations; and 7) aggressive outreach programs. Such policies could be adopted in developing countries, although international donors may need to supply the necessary resources. The most plausible cooling sites are usually government offices and elite hotels, places often reluctant to admit poor people. Khogali and Rosenfeld divide response strategies into primary, secondary, and tertiary levels. Their recommendations are specific and proactive with the goal to reduce heat-related disease in the workplace and at sports venues.¹⁰⁷

Primary prevention addresses adequate and effective building design to maximize comfortable cooling and ventilation, and to reduce radiant and convective heat using mechanical aids.

Secondary prevention includes a wide variety of workplace and sports-related preventative measures that are placed in two groups. The first is referred to as selection and acclimation. These interventions can include pre-event deployment and placement of medical examination resources/equipment in occupational settings and pre-event medical examinations of those participating in sports activities. The second measure is appropriate administrative personnel behavior. This emphasizes modification of the work–rest cycle or the exercise–rest cycle and provision of cool rest areas with fluids.

Tertiary prevention strategies aim at diagnosing heat illness syndromes as early as possible. Khogali and Rosenfeld stress workplace and organized athletic participation.

Certain characteristics are associated with individual municipalities that have developed an EHE response plan. A logistic regression analysis of the twenty-nine U.S. cities with such documents showed that cities with larger populations, higher percentages of multiple unit dwellings, fewer residents age 25 or older with bachelor’s degrees, higher violent crime rates, and a member of a heat wave advocacy coalition working or living within the jurisdiction were more likely to have developed a plan. Violent crime was a significant predictor. If such correlations are not spurious, they offer further evidence of widespread perceptions that heat waves are law-and-order problems to the extent that dangerous neighborhoods will tend to minimize people traveling to cooling centers, opening windows to let in cooler night air (when that is available), or have the social cohesion of safer neighborhoods. Cities with a political rather than a professional administration are more likely to have a plan, suggesting “political” solutions as more plausible than purely “technocratic” ones.

Well-designed EHE plans can be cost-effective. Semenza, for example, concluded that those at greatest risk of dying during Chicago’s 1995 heat wave were people with medical illnesses, socially isolated, and without air conditioning. Such groups could benefit from simple interventions.⁶⁶

In both Chicago and Milwaukee during the 1995 events, NWS issued warnings of the developing heat wave several days in advance and these were quickly broadcast by the local media. Given this advance warning, many of the heat-related deaths associated with this event were preventable.¹⁰⁸ Despite these timely warnings and effective media coverage, this information either failed to reach or was not used effectively by the people who succumbed to heat-related deaths. This included the victims themselves as well as members of the healthcare community who did not always understand the scope of the impending calamity.⁷ Much more than effective media announcements are needed to avoid serious heat wave mortality and morbidity.^{66,68,109–112} The development of pre-event plans that integrate public and private assets is necessary to coordinate and effectively deploy lifesaving resources.

It is difficult to use scientific evidence to judge the post facto efficiency of EHE response plans because no two heat waves are the same, and because of the large number of interrelated variables. Researchers analyzed the 1995 EHEs in St. Louis and Chicago and compared them to the 1999 EHEs in those same cities. Although noting differences, they saw more effective and faster responses in 1999 that appeared to save lives that would have been lost in 1995. These cities learned from prior experiences and improved their EHE response plans.

The only intervention that was not widely reflected in the content of existing plans was equipment grant subsidies (e.g., for air conditioners) for poor residents. Not surprisingly, bill forgiveness, bill postponement, and related programs involve real losses for utility companies. Such programs reflect a confluence of creativity, resources, cooperation, and public spirit. In developing countries, air conditioners would rank low among priorities for the poor as compared with receiving advanced notice of the impending increase in temperature, better education, potable water, adequate shelter, and healthcare. In addition, a large number of air conditioners would likely cause local circuits to fail or create a demand that electricity-generating facilities could not fulfill.