NIOSH Publication No. 2007-133:
Preventing Fire Fighter Fatalities Due to Heart Attacks and Other Sudden Cardiovascular Events
The National Institute for Occupational Safety and Health (NIOSH) requests assistance in preventing on-duty cardiovascular deaths among U.S. fire fighters. To reduce these deaths, NIOSH recommends that fire departments and fire fighters follow established medical screening guidelines, adopt risk reduction measures during fire fighting operations, and develop and participate in comprehensive wellness/fitness programs. To bring the information and recommendations in this Alert to the attention of the fire service community, NIOSH requests help from the following individuals and organizations: fire commissioners, fire chiefs, State and local fire district administrators, State fire marshals, safety and health officials, health care providers (physicians, nurses, etc.), human resource specialists, unions, labor organizations, insurance companies and editors of trade journals and other publications.
Sudden cardiac death represents the most common cause of a fire fighter fatality. In 2005, the National Fire Protection Association (NFPA) reported 44% (440/1006) of on-duty fire fighter fatalities during the ten-year period 1995–2004 were due to sudden cardiac death [Fahy 2005]. For 308 (70%) of these 440 deaths, NFPA was able to obtain some medical information (e.g., death certificate and/or post mortem examination) about the decedent. One hundred thirty-four (44%) of the 308 had prior known coronary artery disease (CAD) as determined by a heart attack, bypass surgery, or angioplasty/stent procedures. However, NFPA was unable to describe the medical screening or fitness for duty evaluations conducted before these deaths. Therefore, additional information would be helpful to determine whether prevention efforts should be directed toward exploring reasons why fire departments and fire department physicians do not follow NFPA 1582, Standard on Comprehensive Occupational Medical Programs for Fire Departments, or toward revising the cardiovascular component of NFPA 1582.
Heart attacks and CAD are two conditions under the umbrella term, cardiovascular disease (CVD). Not all sudden cardiovascular events result in sudden death. In 2005, an estimated 765 fire fighters suffered an on-duty cardiovascular event that did not result in sudden death [Karter 2006].
In 1998, Congress funded the NIOSH Fire Fighter Fatality Investigation and Prevention Program to conduct investigations of on-duty fire fighter fatalities and formulate recommendations for preventing future deaths and injuries. From 1998 to 2004, NIOSH investigated 131 (43%) of the 304 sudden cardiac death fatalities. The NIOSH investigations included a review of the deceased fire fighter’s personal medical records.
To share lessons from the NIOSH investigations, this document
Coronary artery disease among fire fighters is due to a combination of personal and workplace factors. The personal factors are well known: age, gender, family history, diabetes mellitus, hypertension, smoking, high blood cholesterol, obesity, and lack of exercise [AHA 2007]. Not as widely known, however, is that fire fighters have exposures to workplace factors that are associated with adverse cardiovascular outcomes. Fire departments have a responsibility to implement effective prevention programs for workplace risk factors for cardiovascular disease.
Cardiac and Cardiovascular Effects Associated with Fire Smoke
Fire smoke is complex mixture of heated gases, vapors, and particulate matter. The composition of the smoke is determined not only by the fuel source, but also by fire conditions (e.g. oxygen availability, temperature, etc.) [Kulig 1991; Levin 2005]. While hundreds of decomposition products are found, two of the more common and well known gases with cardiovascular effects are carbon monoxide and hydrogen cyanide.
Carbon monoxide, a by-product of incomplete combustion, is present in virtually all fire environments. A number of studies have quantified a fire fighter’s exposure during various phases of fire suppression [Gold 1978; Brandt-Rauf 1988; Jankovic 1991]. High concentrations of carbon monoxide have been documented not only during knockdown, but also during overhaul when fire fighters frequently remove their self contained breathing apparatus (SCBA) [Bolstad-Johnson 2000]. If inhaled, carbon monoxide disrupts the blood’s transport of, and intracellular use of, oxygen [Ernst 1998]. The resulting hypoxia can cause myocardial injury [Satran 2005].
Hydrogen cyanide is formed during the incomplete combustion of substances containing carbon and nitrogen (e.g., paper, cotton, wool, silk, plastics, etc). Hydrogen cyanide frequently has been detected in structure fires and levels have been shown to exceed established exposure limits [Jankovic 1991; Brandt-Rauf 1988; Gold 1978]. Like carbon monoxide, hydrogen cyanide disrupts the intracellular use of oxygen, resulting in intracellular hypoxia with cardiac manifestations [Purser 1984].
Fire fighters have significant exposure to fire smoke particulate matter during fire suppression [Treitman 1980; Brandt-Rauf 1988]. Studies in the general population suggest particulate matter, as a component of air pollution, has cardiovascular effects [Brook 2004]. For example, long-term repeated exposure to elevated concentrations of particulate matter has been associated with cardiovascular mortality and the initiation/progression of atherosclerosis [Dockery 1993; Pope 2002, 2004]. In addition, short-term exposure to fine particulates has been associated with triggering heart attacks, particularly among people with pre-existing heart disease [Peters 2001; Pope 2006]. These findings have implications for the fire service given fire fighters’ exposure to fire smoke particulate matter [Treitman 1980].
Cardiac and Cardiovascular Effects Associated with the Work Environment
Increased Heart Rates and Heavy Physical Exertion
A significant portion of the fire fighters’ work-day is spent at rest or doing light work around the fire station. However, the station’s alarm may sound at any time, and fire fighters are expected to rapidly deploy to the incident scene. Fire fighters react to these emergency calls with an increase in their heart rates, probably due to a surge in sympathetic nervous system activity (e.g. the flight or fight response) [Barnard 1975; Kuorinka 1981]. The increase in heart rate frequently persists through the course of fire suppression activities; a finding not surprising given the heavy physical demands of structural fire fighting [Lemon 1977; Hurley 1980; Manning 1983; Guidotti 1992; Smith 1995]. The pattern of sedentary periods interrupted by catecholamine surges and heavy physical exertion has been suspected to put fire fighters at increased risk for acute heart attacks. Epidemiologic studies in the general population report that heavy physical exertion sometimes immediately precedes and triggers the onset of acute heart attacks and sudden cardiac death [Willich 1993; Mittleman 1993; Siscovick 1984; Tofler 1992; Albert 2000].
Heat stress and heat illnesses are well recognized hazards of fire fighting. Fire suppression can increase body temperature resulting in sweating and fluid loss, which can cause serum electrolyte changes, lower stroke volume (the volume of blood pushed during each contraction of the heart), or lower cardiac output [Rossi 2003; Smith 2001; Costrini 1979]. Heat stroke has been reported to increase the risk of myocardial ischemia, arrhythmias, and conduction abnormalities [Akhtar 1993].
Fire fighters’ noise exposures are obvious: sirens, air horns, diesel engines, and the roar of a large structure fire itself. During emergency operations, sound levels exceeding 120 decibels have been measured [Tubbs 1995]. Studies of community and occupational groups have found an association between noise exposure and hypertension, and possibly an association with ischemic heart disease [Van Kempen 2002; Davies 2005; Willich 2006; McNamee 2006]. It is important to note that fire fighters’ noise exposure (short duration, high intensity) differs from that studied in community and in other occupational groups [lower intensity for a longer duration (e.g. full-shift)]. However, given the extent of the noise-induced hearing loss found in fire fighters, it is plausible that noise exposure increases the risk of hypertension and possibly ischemic heart disease among fire fighters [Tubbs 1995].
Shift Work and Overtime
Several studies suggest a modest association between rotating shifts (e.g., a week of days, a week of evenings, a week of nights, with weekends off) and heart disease [Steenland 2000]. Because most career fire departments work 24-hour shifts and volunteers fire fighters do not work shifts at all, these findings may have limited application to the fire service. A 24-hour shift, however, is long, stressful, and fatiguing. The literature also suggests long hours can increase blood pressure and lead to increased heart disease, independently of other stressful conditions at work [Steenland 2000].
Environmental Tobacco Smoke
In 2006, the Surgeon General confirmed a causal relationship between exposure to secondhand smoke and increased risks of coronary heart disease morbidity and mortality [USDHHS 2006]. An estimated 46,000 cardiac deaths occur each year due to secondhand smoke in the United States [Cal/EPA 2005]. Since not all fire stations are smoke free, involuntary exposure to tobacco smoke continues to present cardiovascular risks for fire fighters.
Fire Fighting and Heart Disease
Over 25 published studies examine the relationship between heart disease and fire fighting. Results of these studies are conflicting (e.g., some studies support the association while others do not). In 1995, Guidotti published a review of the fire fighter mortality literature. He concluded, “Sudden death, myocardial infarction, or fatal arrhythmia occurring on or soon after near-maximal stress of the job are likely to be [work] related…” [Guidotti 1995]. It is important to recognize, however, the limitations of the scientific method used in these studies. The major concern is a problem known as the healthy worker effect (HWE) [Choi 1992]. This problem arises because working populations are usually selected for employment in such a way that they have better health (corresponding to a lower death rate) than the general population to whom the workers are compared. For example, before placement, fire fighter candidates are screened for many cardiovascular conditions and risk factors (e.g., diabetes and hypertension). This leads to a strong healthy hired effect, one component of the HWE [Arrighi 1994]. In 2000, Choi re-assessed 23 standardized mortality ratio studies addressing the relationship between fire fighting and heart disease after attempting to control for the HWE. He concluded that, “(1) there is strong evidence of an increased risk of death overall from heart disease among firefighters; …. (3) there is insufficient evidence, even after considering the HWE, for a relationship between firefighting and any heart disease subtype, such as acute myocardial infarction” [Choi 2000].