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Technology &
Development Center
Wildland Firefighter Health and Safety
Recommendations of the April 1999 Conference

Wildland Firefighting and the Immune Response

Steve Wood, Ph.D, R.D.
Senior Clinical Project Leader
Ross Products Division/Abbott Laboratories


Wildland firefighters perform their jobs in a number of conditions (such as smoke, stress, and extreme temperatures) that may suppress their immune systems and ultimately affect their performance and increase the risk of disease or infection. The focus of this review is to examine the influences of external and internal stresses on immune function and present a military example (containing many of the stresses found in wildland firefighting) of a field nutrition study where immune suppression was minimized.

The Immune System

The immune system is an intricate system of organs, tissues, cells, and molecules that maintain balance between the environment and man. Stress such as physical exertion, sleep deprivation, malnutrition, extreme temperatures, psychological pressures, and endocrine changes all influence the body’s defense system and alter its equilibrium.

The environment in which we live contains a great variety of infectious microbes (viruses, bacteria, fungi, parasites, and protozoa). If these multiply unchecked within a host, they can cause sickness, disease, and ultimately death. Our bodies combat these microorganisms through immune responses. For example, the first line of defense is the skin. Few infectious agents can penetrate intact skin; however they may gain access across epithelia, or gastrointestinal or urogenital tracts. Once an organism has gained access into the body, the immune system must recognize the pathogen or foreign material and mount an attack (immune response).

Immune responses are coordinated primarily by white blood cells (leukocytes). Leukocytes include monocytes, lymphocytes, basophils, eosinophils, and neutrophils. Each cell type typically performs several functions (Figure 1). The initial response to an invading organism is both nonspecific (innate) and specific (adaptive or acquired) recognition. Once the white blood cells identify the foreign material, the immune system mounts an attack to bind and destroy it (for instance, through phagocytosis). The immune response is like an orchestra. When cells and organs (the instruments) are working together, it functions very effectively; if cells are not functioning properly, there is dysregulation (disharmony). The risks of disease and illness are greater.

Diagram showing leukocytes in the immune system.
Figure 1—Leukocytes and the immune system.

Immune cells communicate by lymphokines (cytokines) that are small proteins secreted by leukocytes to act as molecular signals. As cellular communication molecules, they are analogous to hormones or neurotransmitters. In most cases, cytokines bind to specific receptors on cellular surfaces. These cytokines are not antigen specific, but perform a function to transduce or amplify a signal that ultimately translates into a cellular response. Cytokines may also have a systemic effect. For example, with an infection, leukocytes are stimulated and produce cytokines that can elevate the normal temperature (along with pyrogens from the invading organisms), causing fever. The effectiveness of the immune system can be evaluated by the quantification of the specific cytokines (the level at which they are secreted by leukocytes) and by the number of cells secreting specific cytokines.

Energy and sleep deprivation, mental stress, and intense physical exertion affect both innate and specific immunity [such as cellmediated humoral (antibody production) and lymphocyte proliferation (multiplication of cells) following in vitro mitogen stimulation)]. The specificity and effectiveness of the immune system is the result of interaction and function of specific lymphocyte subsets. Immune effector cells, B-lymphocytes, natural killer cells (large granular lymphocytes), and T-lymphocytes interact to mount a defense against invading pathogens or abnormal cells. B-lymphocytes are involved with antibody production, while T-lymphocytes are most commonly associated with cell-mediated immunity. T-lymphocytes, in addition to their role as “killer cells,” have important roles in regulating B-lymphocyte functions and in “directing” cellular trafficking in the development of highly specific antibody responses. In a clinical setting, numerous laboratory tests can be performed to evaluate immune function.

Examples of laboratory immune functions assessment:

White Cell Numbers

Automated cell count (complete blood count)

Flow cytometry (differential cell population analysis by immunophenotype analysis)

Cell Function

Lymphocyte proliferation following mitogenic stimulation

Gene Regulation


Cytokine Production

T- and B-lymphocyte cooperation

Immunoglobulin production

In Vivo Immunity

Cutaneous reaction

Resistance to viral infections

Incidence of infectious disease

Immune cells are identified by their morphology (size and structure), function, and specific proteins on their surface. Immune cells can be analyzed by flow cytometry. There are also a number of ways to evaluate the functions or numbers of immune cells.

In vitro tests may not, in all cases, be indicative of clinically relevant immune deficiencies because they provide a limited view of immune status. Furthermore, in vitro studies need to be performed on fresh blood samples. A single test will usually not be indicative of overall immune system status. When evaluating immune status or competency, it is important to evaluate a variety of cellular functions or components. It is also important to attempt to quantify overall immune system effectiveness by using clinical measures such as delayed type-skin hypersensitivity (DTH), rate of infection, or response to pathogen or vaccine. DTH tests can be easily administered by placing small amounts of proteins that cause a reaction (antigens) into the epidermis and superficial dermal tissue. Circulating T-lymphocytes that have had prior contact with the antigen induce a specific immune response that causes lymphocytes to undergo mitosis (proliferation) and release a number of soluble mediators (cytokines). The intensity of the response reaches its peak within 24 to 72 hours (thus the term delayed). The diameter of the bump (induration) can be measured in millimeters. The larger the induration, the better the immune response. Lack of a response is called anergy. Anergy indicates functional impairment of the immune system (with the assumption that the individual has had prior exposure to the antigen). Experience with DTH over the last several years has shown good correlations between lack of DTH reactivity (anergy) and risk of infection and mortality in a hospital setting (Table 1).

Table 1—Infection and death rates based on Delayed Type-Skin Hypersensivity (DTH) skin testing of 4,289 hospitalized patients (Christou et al. 1995).

  Infection Rates Death Rates of Infected

Reactive‡ 172/2509 (7%) 33/172 (19%)
Relative Anergy* 109/666 (16%) 35/109 (32%)
Anergy† 289/1114 (25%) 147/289 (51%)

‡Intradermal injection into the forearm of Candida, mumps skin test antigen, purified protein derivative, trichophyton and varidase. Reactive was defined as a diameter of induration equal to or greater than 5 mm.
*Response to one of five antigens.
†No response to any of the antigens.

Patients who are DTH reactive have a much lower rate of infection. Those patients who are anergic and become infected have a poor prognosis. A reduction in cell-mediated immune responses can limit the development of an effective immune response against intracellular pathogens, including viruses, bacteria, fungi, and protozoa. DTH has also been used to evaluate the immune function of malnourished, trauma, or immune-suppressed patients.

Stresses of Firefighting and Influence on Immune Function

The immune response can be influenced by a number of factors, including the intensity and duration of physical and/or psychological stress, concentrations of hormones and cytokines, body temperatures, hydration status, hormones, and ambient temperature. Wildland firefighters are exposed to many “stresses” that can impact their health and influence their immune systems. In addition to the psychological challenges, wildland firefighters are exposed to a number of physical challenges (such as environmental toxins, injuries, smoke inhalation, abrasions, laceration, and burns) that suppress the immune system. Although there have been many studies evaluating the effectiveness of firefighting equipment for the wildland firefighter, little research has focused on the firefighter’s health [other than respiratory health (Harrison et al. 1995)]. Therefore, we will examine other scenarios to evaluate some of the factors that may influence the immune system of the wildland firefighter.

Stress and Infection

The first question is: What happens to the immune system as a result of stress? Secondly, do these changes translate into increased susceptibility? Peterson et al. (1991) reviewed stress and the pathogenesis of infectious disease. The authors reviewed many studies in which stressors (swimming or running, electric shock, isolation or crowding, and exposure to cold temperatures) were imposed on animals and mortality was studied. Table 2 is a sampling of results showing the effects of physical stress on the susceptibility of animals and humans to viral infections.

Table 2—Animal models of stress and viral infection (modified from table of Peterson et al. 1991).


Poliomyelitis Mouse Forced exercise Increased Mortality, paralysis
Coxsackievirus B Mouse Forced Exercise Increased Mortality
Herpes simplex Mouse Restraint Increased Mortality
Influenza A Mouse Forced exercise Increased Mortality
Infectious Mononucleosis Human Pressure to achieve academically Increased Clinical illness
Upper respiratory tract infection Human Life events Increased Frequency and severity
Upper respiratory tract infection Human (Marines) Delayed promotion Increased Frequency
Epstein-Barr virus
Human (Medical school students) Academic Stress Increased level of antibody, indicating high infection rate

Research indicates that moderate exercise enhances immunity while more strenuous exercise and prolonged training appear to suppress it (Simon 1987; Nieman 1991; Nieman et al. 1993). There have been studies of relatively short-term physical stress, yet few studies have examined the chronic stress that may be experienced by wildland firefighters. This offers a unique opportunity for investigation.

Cowles reported in 1918 that pneumonias were associated with intensive exercise. It has more recently been shown that unusually high rates of upper respiratory tract infections (URTI) can be attributed to either a single bout of exhausting exercise or overtraining (Douglas and Hanson 1978; Peters and Bateman 1983; Nieman et al. 1989). Table 3 shows several animal studies that linked increased mortality by bacteria with forced exercise and crowding.

The idea that high-intensity training might reduce immune function was first postulated in 1932, based on the observation that muscular fatigue predisposed individuals to infections, especially respiratory pathogens (Baetjer 1932). Several epidemiological studies have documented an increased incidence of URTI following strenuous exercise (Neiman et al. 1989; Peters 1983; Peters et al. 1993). Conversely, persons performing moderate exercise have lower risk of infection than sedentary controls (Heath et al. 1992; Neiman et al. 1993). These results are also supported by studies in which mice undergoing moderate exercise training had reduced susceptibility to bacterial and protozoan infections compared to sedentary controls (Cannon and Kluger 1984; Chao et al. 1992).It appears that the effect of moderate exercise can convey enhanced immunological responses. More chronic and severe stress, as in military training such as the U.S. Army Special Forces Assessment and Selection School (SFAS), decreases immune function and increases susceptibility to environmental pathogens.

Table 3—Increased mortality by bacteria in animals with forced exercise and crowding.


Bacillus anthrcis Rat Forced exercise Increased Mortality
Staphylococcus aures Rabbit Forced exercise Increased Mortality
Salmonella typimurium Mouse Crowding Increased Mortality
Mycobacterium tuberculosis Mouse, rat Forced exercise Increased Mortality

Ambient temperatures can also influence immune function and susceptibility to infection. For example, Shimizu et al. (1978) found that pigs maintained at 30 °C (86 °F) remained disease-free after a challenge with coronavirus. However, the pigs experienced diarrhea from the virus challenge when the ambient temperature was lowered to 4 oC (39 °F). Similarly, temperature changes (stress) can also influence susceptibility to bacteria. For example, Previte and Berry (1962) demonstrated that mice exposed to temperatures of 5 °C (41 °F) had markedly increased susceptibility to bacteria or lipopolysaccharide.

One area that has not received much attention is the gender-specific influence of stress upon infectious morbidity or mortality. Tobach and Bloch (1956) injected female and male mice with Mycobacterium tuberculosis and then imposed the stress of crowding on the animals. They found that crowding female mice offered protection to the infection while the stress of crowding male mice increased the death rate.

Lack of sleep has been shown to adversely affect immune function. For example, it has been shown that sleep deprivation in the rat causes drastically increased food consumption (hyperphagia), yet the rats experience body weight loss (malnutrition-like symptoms) and succumb to lethal opportunistic systemic infection. Furthermore, sleep-deprived rats develop skin lesions that are not inflamed, indicating immune dysregulation (Kushida et al. 1989). Other researchers noted that cutaneous changes were often the first signs of primary alteration in the susceptibility of the host to pathogens. The immune system was the first system to fail after sleep deprivation (Everson 1995).

Complaints by wildland firefighters of upper respiratory tract problems are the main reasons for visits to the medical clinics. URTI can result from decreased immune function from fatigue, sleep deprivation, smoke exposure, inadequate nutrition, or a combination of stresses.

Readiness and Impact on Time Lost

The influence stress has on immunological defenses that result in lost hours or prevent readiness for wildland firefighters has not been reported. However, military studies can be used to establish the impact of immune changes observed during military environments and infection rates or nonbattle injuries. Historical studies examined findings from research conducted during military conflicts. For example, in several of the major military conflicts involving the United States, disease and nonbattle injuries (DNBI) have accounted for significant loss of manpower (Palinkas and Coben 1988). During World War II the ratio of Navy and Marine Corps hospital admission for DNBI and combat-related wounds and injuries was 88:1. In Marine Corps personnel serving in Vietnam, for every 100 men wounded in action, 128 men were hospitalized for DNBI (Palinkas and Coben 1988). Exposure to pathogens from environmental factors and crowded living quarters contribute to disease susceptibility of military units even during routine peacetime operations. Seay (1995) found that after a 10-day port visit to Rhodes, Greece, by the crew of the USS Forrestal, 777 cases of gastroenteritis were reported. This accounted for 15% of the work force and a cost of 462 man-days of lost work. Major Wallace J. Seay stated, “...lost duty days, and the burden of providing medical confinement may be more criticalthan fatal illnesses. Fatalities may be replaced but sick soldiers continue to occupy positions, decrement performance, and consume large quantities of medical supplies (Seay 1995, pp. 3-4).” While many factors may contribute to susceptibility to infection and disease during military operations, the effect of both physical and psychological stress undoubtedly have a significant impact on host defense mechanisms. Therefore, it would be important to evaluate the stress that is experienced by wildland firefighters, its impact on immune function, and its influence on firefighters’ readiness to perform.

Physical and Nonphysical Stresses

There is evidence to suggest that with chronic physical exertion, immune dysregulation occurs [low immunoglobulin and complement levels, increased neutrophil concentration yet decreased phagocytosis, decreased NK cell activity, decreased lymphocytic proliferative response and T lymphocyte numbers (Nieman 1997)]. Furthermore, infections and intense exercise have similar immunological responses [leukocytosis, lymphopenia—primarily T lymphocytes, degranulation of neutrophils, and decreased lymphocytes’ responsiveness to mitogens (Heath et al. 1992)].

Stress, such as exertion and extreme environmental temperature, can play a role in immune dysregulation. The resulting changes are similar to nonphysical stresses (such as isolation). Comparisons of the effects of cold, exertion, and isolation on immune function were studied in a cold-water, swimming mouse model and in an isolation model. Ben-Nathan and Feuerstein (1990) exposed mice to cold water (5 min/day) for 8 to 10 days and also stressed a group of mice by isolation. Animals were then exposed to a West Nile Virus (WNV-brain specific virus) at the initiation and after 5 days of cold stress (Figure 2a). It was found that physical (cold water and swim stress) or nonphysical (crowding stress) had a significant impact on reducing the weight of important immune organs (thymus and spleen) as well as increasing mortality rates (Figure 2a, Figure 2b).

Graph showing the effect of cold stress on the mortality of mice inoculated with West Nile Virus.
Figure 2a—The effect of cold stress on the mortality
of mice inoculated with West Nile Virus: Cold-Virus
(not infected), Virus (Control), Cold+Virus d1 (cold stressed
and infected on day 1 with 50 PFU), Cold+Virus d5
(cold stressed and infected with 50 PFU on day 5 of stress).
*p < 0.05 that the difference was due to chance.
**p < 0.001 that the difference was due to chance.

Graph showing the effect of isolation or crowding stress.
Figure 2b—The effect of isolation or crowding stress on the
mortality of mice inoculated with WNV. 18 M/Cage
(18 mice/cage), 12 M/Cage (12 mice/cage), 6 M/
cage (6 mice/cage-normal housing), 1 M/Cage (1 mouse/cage),
*p < 0.01 compared to normal housing.
(modified from Ben-Nathan and Feuerstein 1990).

In human studies, nonphysical and physical stress can produce immunological changes. Spousal caregivers of patients having Alzheimer’s or dementia disease have been shown to have lower immune responses (response to vaccine and cytokine response). Caregivers were vaccinated with a trivalent influenza vaccine. Their antibody responses were compared to a control group (noncaregivers). Although caregivers and noncaregivers had similar baseline antibody titers, the caregivers responded less often and with less magnitude than the control group. Furthermore, the cytokine response was lower in the stressed caregiver group as well (Figure 3).

Graph showing percentage of caregivers and controls with a four-fold increase in antibody.
Figure 3a—Percentage of caregivers and controls with a
four-fold increase in antibody 30 days after vaccination. The
ELISA assay has greater sensitivity, while the hemagglutinin
inhibition (HAI) assay has greater specificity.

Figure 3b—IL-1 ßresponses of monocytes to lipopolysaccharide
stimulation (mean ±SEM) of caregivers and controls
before and 30 days after influenza vaccination
(from Kiecolt-Glaser et al. 1996).

The caregivers’ stress adversely affected the immune response (as measured by antibody and cytokine responses), placing them at increased risk of infection.


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