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4
HAZARDS ASSOCIATED WITH FIRES
moment.
Fires generate three main sources of hazard--heat,
smoke, and depletion of oxygen--all of which can interact
in exerting their effects. The relative contribution of
each to the overall hazard depends on the physical charac-
teristics of the fire, namely, heat release rate, fuel
source, and oxygen supply. These characteristics combine
with others, such as structural configuration and distance
from the heat source, to constitute the hazard at any
In a real fire, many of these characteristics
are changing continuously. This chapter reviews briefly
some of the information that is available on the potential
hazards associated with the components of fires.
HEAT
The most obvious hazard associated with fires is heat.
Although most fire deaths are due to smoke inhalation,
many are caused by burns from the heat of the flame
itself .6 3 6 4 2 0 3 A skin temperature of about 45°C is
associated with pain. 2 ~ 4
Burn injury caused by the inhalation of air heated to
150 °C or higher is ordinarily confined to the oropharynx
and upper airway (above the vocal cords) . 4 4 ~ 5 4 Even
very hot air is rapidly cooled before it reaches the
lower respiratory tract, because of the tremendous heat-
exchanging efficiency of the oropharynx and mesopharynx.
The inhalation of hot steam, however, can cause a burn as
deep as the major bronchioles. 4 4
62
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63
OXYGEN DEPLETION
A decrease in arterial PO2* stimulates the peripheral
chemoreceptors in the aortic and carotid bodies and causes
hyperventilation.90
damage if the oxygen (02)
more than about 3 min.90
The brain suffers irreversible
supply is interrupted for
The extent to which O2 depletion and the resulting
hypoxia are important in fires depends on various physical
characteristics of the fire and its environment, e.g.,
the size of the fire and the available air supply. O2
depletion is not generally thought to be a major problem.
However, when flashover occurs (see Chapter 2), O2 can
be depleted over a large area, even if the fire is con-
tained in one room. A 3-MOO fire in an average-sized house
will consume all the O2 in the house within about 30 s.
SMOKE
Smoke is defined here to include all the airborne
products of the pyrolysis and combustion of materials.
Smoke consists of particles (soot), gases (e.g., carbon
monoxide), volatilized organic molecules of varied com-
plexity, aerosols, and free radicals. The extent to
which these components contribute to the overall hazard
associated with smoke is discussed briefly below. Recent
reviews contain more detailed and comprehensive treatments
of the subject. 3
WATER
Water is a frequent product of combustion, although
the amount varies greatly. Unlike steam, water is not an
important factor in smoke-inhalation injury, except that
. .
* p" denotes partial pressure (also called tension) of
any gas in a mixture. It is the pressure that that gas
would exert if it alone were present. The partial
pressure of any gas is the product of the total pressure
of the gas mixture and the fractional concentration of
that gas.
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64
water droplets can serve as a vehicle for the transport
of absorbed acids, such as hydrochloric
acid.39 54 93 97 168
PARTICLES ( SOOT AND AEROSOLS )
Soot and aerosols are the visible components of smoke.
A wide range of particle sizes, from 0.1 Am to above 10
Am (mass median diameter), can be found in fire smokes.
Those larger than 10 Am in diameter are too large to
reach the alveoli, so their role in causing parenchymal
lung injury is debatable. 3 3 3 4 Particles can contribute
to hazard by reducing visibility and otherwise impeding
escape. The extent to which the decrease in visibility
caused by particles and soot is a hazard in real fires
is, like incapacitation, strongly suspected from anecdotal
evidence, but its exact role is largely undetermined.
However, it is clear a priori that any impediment to
escape will increase the hazard associated with a fire.
If the particles are also highly irritating to the eyes
and cause lacrimation, vision will be impaired, even if
the density of the particles is not great. But the
presence of particles can also speed fire detection and
thus aid early escape by serving as a visible warning or
by triggering smoke detectors.
Some investigators believe that such hydrophilic
pyrolysates as hydrogen chloride (HC1) can adhere to
smoke particles and thus be transported into the tracheo-
respiratory tree, where they can directly damage membranes
and cause edema.58 However, estimates from laboratory
modeling suggest that less than 2% of the predicted amount
of HC1 produced is adsorbed on soot.~27 How much of
this reaches the lower airways is uncertain.
GASES
Carbon Dioxide
Carbon dioxide (CO2) is a major combustion product.
Its concentration in air can reach 15% in some fires. 2 0 4
The most important physiologic effect of CO2 is to
stimulate the respiratory center. The normal pulmonary
ventilation rate is 5-7 L/min, at a PCO2 of 35-45 mm Hg.
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An increase of 2 mm Hg in blood PCO2 doubles the
ventilation rate,90 which increases the rate of exposure
of the lungs to smoke. CO2 also contributes to an
abnormal acid-base balance when inhaled at the concentra-
tions and for the durations common in fires.
In addition to its effects on the respiratory center,
CO2 at sufficient concentrations can cause headache,
somnolence, mental confusion, hyporeflexia, lassitude,
revere necrologic disturbances, such
and eventually more _
as tremors, flaccid paralysis, unconsciousness, and
eventually, death.~° 6
Carbon Monoxide
Carbon monoxide (CO) is an odorless and colorless gas.
It is the major product of combustion that has been
clearly established as contributing to death in fires.~9~
CO is toxic because of its high affinity for hemoglobin.
It forms carboxyhemoglobin (COHb) by binding to hemo-
globin, for which its affinity is 250 times greater than
the affinity of O2 for hemoglobin and thus reduces the
O2-carrying capacity of the blood and causes hypoxia.
The formation of COHb also increases the affinity of O2
for the remaining hemoglobin. That shifts the oxyhemo-
globin dissociation curve to the left; as a result, tissue
O2 tensions must fall to lower than normal for the O2
to be released from hemoglobin. This effect causes
greater hypoxia than would be expected only from the
COHb-related decrease in the O2-carrying capacity of
the blood. The concentration of COHb achieved in
blood depends on both the concentration of CO in inhaled
air and the duration of exposure. 6 ~ CO also binds to
myoglobin in muscles.
COHb concentrations as low as 5% in the blood have
been associated with angina and dysrhythmias in persons
with ischemic heart disease. 23 These effects might
explain some fire fatalities, such as sudden death in
susceptible persons at what would normally be considered
sublethal concentrations of CO.
A person can manifest
psychomotor and judgment ~nett~ciencies at a COHb concen-
tration of about 10~. At about 10-20%, exertional dyspnea
is present. Headaches are common at 20-30%, and nausea,
dizziness, and muscular weakness can occur at 30-40%. At
40-50%, there is syncope, and at 50-60%, convulsions.
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66
Concentrations of 60-70% lead to coma and, with long
exposure, death. COHb at 80% is rapidly fatal. 2 2 7
The central nervous system and myocardium are most
sensitive to the O2 deprivation caused by CO poisoning.
Because they cause hypoxia, sublethal exposures to CO
can impair performance and thus impede escape from a fire.
In some animal studies (mostly with rats), performance
changes in conditioned behaviors were observed at CO
concentrations of 200-400 ppm, corresponding to COHb of
13-15%.~ 24 In other studies, higher CO concentrations
(600-800 ppm) were required to disrupt behavior during
60-min exposures. 2 ~ The effect of these exposures
tended to be increased pausing in whatever behavior was
taking place, not necessarily with any increase in
errors; at higher CO concentrations, all behavior would
cease. Using the more stressful task of avoidance of
unsignaled shock, Sette and Annau200 reported that
behavioral disruption in rats occurred at 60% COHb (CO at
1,000 ppm) during a 30-min exposure. More recently,
monkeys trained in a lever-pressing task that required
crossing a cage to obtain positive reinforcement after a
correct response suffered performance decrements with CO
at 900 ppm in about 20 min. After 30 min. COHb
ranged from 25 to 30~; performance disruption was complete
in some monkeys (total collapse), and the others completed
only about 50% of the trials.
These data suggest that a wide range of CO concentra-
tions can disrupt behavior in rodents and that the monkey
responds similarly, at least at high concentrations. With
human subjects in a simulated task of driving an auto-
mobile, the task became impossible at 45% COHb, and the
subjects were near collapse.~°
Laties and Merigan~ 2 4
concluded that, although there was a lack of well-
controlled human studies with clear-cut effects, the COHb
threshold for detectable, if not necessarily reliable,
changes in human performance was around 10~.
A partial explanation for the wide disparity in the
behaviorally disruptive CO threshold is that organisms
respond to hypoxia challenge by increasing cerebral blood
flow202 and that this compensatory mechanism can sustain
function only up to a point, after which a precipitous
decline might occur.
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67
Because CO-induced hypoxia decreases the total amount
of O2 delivered to the brain, all regions of the brain
might be expected to be equally affected.
But neuropatho-
logic examination of human fatalities and the results or
animal studies suggest that some brain regions are more
vulnerable than others to CO-induced hypoxia insult.
Vogel223 described a case in which a man survived a
fire and lived on a respirator for 5 months before dying
of pneumonia. Neuropathologic examination of his brain
showed marked destruction of several cortical layers and
damage to the hippocampus, basal ganglia, and cerebellum.
In a more extensive examination of human brain injury
after various hypoxia insults, Ginsberg 7 concluded
that lesions of the white matter were prominent. Monkeys
exposed to severe CO intoxication exhibited essentially
the same neuropathologic pattern. Ginsberg 7 also
described a delayed onset of symptoms sometimes seen in
human cases of severe CO intoxication. Such patients
recovered from the acute intoxication rapidly and were
discharged from the hospital, only to undergo progressive
deterioration that began 2-6 weeks later. This deteriora-
tion was characterized by disorientation, confusion,
excitement, restlessness, defective motor control, and
even frank psychosis. In some cases, a vegetative
neurologic state eventually led to death.
_
. . . . . ~
Hydrogen Cyanide
Cyanide inactivates heavy-metal enzymes by forming
stable complexes with them. Of these enzymes, cytochrome
oxidase is the most sensitive to cyanide. Formation of
the complexes compromises oxidative metabolism and
phosphorylation and blocks electron transfer to molecular
O2. The peripheral tissue O2 tensions increase, and
the unloading gradient for oxyhemoglobin decreases. 2 0 5
Although hydrogen cyanide (HCN) can be formed in many
fires, its contribution to toxic hazard is uncertain. It
can be produced at appreciable concentrations only if the
fuel contains both carbon and nitrogen. Inhalation of
HCN can be rapidly fatal. Toxic symptoms occur at blood
cyanide concentrations greater than 0.2 mg/L, and 10 mg/L
is lethal.205 Symptoms of cyanide poisoning include
salivation, nausea without vomiting, anxiety, confusion,
vertigo, giddiness, lower jaw stiffness, convulsion,
paralysis, coma, cardiac arrhythmia, and transient
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68
respiratory stimulation followed by respiratory
failure.2 US
Moss et al.~55 compared the effects of CO and HCN--
alone and together--in rats. Whereas rats exposed to CO
were calm and remained quiet until they collapsed from
anoxia, HCN-exposed rats displayed a brief period of
violent escape behavior followed by unconsciousness and
death. Rats exposed to CO and HCN together exhibited the
typical response pattern seen after exposure to HCN alone.
The authors reported that CO at 5,000 ppm was lethal in
30 min. as was HCN at 50 ppm. The combination of CO at
only 2,000 ppm and HCN at 16 ppm was sufficient to kill
animals in 30 min.
Purser et alms 7 studied the effects of HCN in
monkeys sitting in chairs, with gas administered by
mask. Incapacitation was defined as a semiconscious
state with loss of motor tone. With HCN at about 150
ppm, incapacitation was seen after 8 min. At 100 ppm,
the lowest concentration tested, the monkeys became
incapacitated in 19 min.
Ginsberg 7 reviewed the neuropathologic consequences
of cyanide intoxication. The lesions produced in the
brain closely resemble those seen after CO exposure. In
acute, high-dose cyanide intoxication, the victim goes
into respiratory arrest. Although the mechanism of
cyanide toxicity is completely different from that of CO
toxicity, the resulting neuropathology resembles that
caused by other hypoxia-inducing agents.
IRRITANTS
Many respiratory irritants are generated in fires,
including ammonia, oxides of nitrogen, hydrogen chloride,
sulfur dioxide, isocyanates, and acrolein.~ 2 0 2 ~ 7 The
site of injury after exposure to these substances is
determined largely by their solubility. Highly water-
soluble gases, if they are also highly reactive with
surface components (e.g., ammonia) are readily absorbed
and cause injury to proximal mucosal surfaces and the
upper respiratory tract. Deposition of insoluble gases
(e.g., some oxides of nitrogen) in the lower respiratory
tract causes injury that might be delayed by 24-48 h.
Other factors that affect the site--and extent--of injury
include chemical form, dose, and duration of exposure.
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Survivors of acute injury have a highly variable
prognosis. Some recover fully within weeks with no
permanent sequelae, whereas others have a spontaneous,
usually mild, recurrence of pneumonitis several weeks
after the exposure. 27 Although most survivors gradually
recover, others are left with productive cough and
residual obstructive deficits with or without bronchial
hyperreactivity. Restriction impairment sometimes
remains. A serious but rare complication is bronchiolitis
obliterans, in which spontaneous deterioration begins
about 4-6 weeks after injury and pulmonary function shows
a restrictive or mixed obstructive-restrictive process.
Respiratory failure and death can ensue; there are
usually permanent residue among those who recover.89
Hyrdrogen Chloride
Airborne HCl exists in the anhydrous state and as an
aerosol. Because anhydrous HC1 is very hydroscopic,
exposure to it is potentially more dangerous to biologic
systems than exposure to HC1 aerosols. Anhydrous HC1
injures not only by corrosion, as does the acid, but also
by desiccation. However, its very affinity for water
makes exposure to anhydrous HC1 extremely unlikely.
The main nonlethal effects of HCl are irritation of
the mucous membranes that results in breathing difficulty
and lacrimation that obstructs vision, both of which can
cause panic. Air concentrations of HCl below lOO ppm are
considered tolerable, whereas concentrations near l,OOO
ppm are rapidly fatal in rats.92
Hydrogen Fluoride
The physiologic effects of hydrogen fluoride (HF) are
the same as those of HC1. 2 ~ 3 However, HF is more potent
than HC1. Acute inhalation of HF at lOO ppm can cause
death in only a few minutes. Like HCl, HF can cause
delayed death from cardiotoxicity and from such pulmonary
sequelae as infection. 2 ~ 3
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70
Sulfur Dioxide
On contact with moisture, sulfur dioxide (SO2) forms
sulfurous acid. Death resulting from SO2 exposure is
usually caused by respiratory arrest and asphyxia, which
culminates in massive tracheobronchial mucosal necrosis
and gross pulmonary edema, with no evidence of an inflam-
matory reaction. 4 6 Delayed irreversible reactions
include chronic airflow obstruction and bronchitis.
Associated symptoms (dyspnea at rest and on exertion) and
disability can be severe. Other common symptoms include
cough, wheeze, rates, hypoxemia, marked abnormality in
pulmonary function, bronchiolitis obliterans, peri-
bronchiolar fibrosis, and a general decrease in small-
airway diameters. There is one report of severe left
main stem bronchial stenosis. 4 6 Reduced resistance or
increased susceptibility to infection can ensue days or
months after what is at first considered to be a mild
exposure to SO2.~8 Delayed deaths from pulmonary
infection (occurring 17 days to 16 months after exposure)
have also been reported.
Nitrogen Dioxide
The thermal oxidation products of nitrogen are usually
found only in association with extreme combustion tempera-
tures (about 2500°F or 1370°C) .6 ~ The immediate effect
of an intense exposure to nitrogen dioxide (NO2) is
rapid death from respiratory spasm or pulmonary edema.
Exposures to high, sublethal concentrations can cause
severe delayed pulmonary edema and chemical pneumonitis.
There is some evidence, mainly from animal experiments,
that a single brief exposure can cause persistent lung
damage, such as emphysema and interstitial fibrosis.
Severe discomfort with lacrimation, coughing, and
respiratory distress is induced by somewhat less intense
exposures than those requiring hospitalization, and a
milder pulmonary edema with reversible respiratory
impairment is possible.~45 Single exposures to NO2
at concentrations that cause slight, but tolerable,
discomfort in humans have been shown in animal experi-
ments to cause a reversible increase in susceptibility to
respiratory infection and aggravated reactions to aller-
gens. Even lower concentrations, at or below the
threshold of sensory perception and below the current
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71
federal occupational standard (5 ppm), can cause
reversible impairment of respiratory functions. 6 6
Hydrogen Sulfide
Hydrogen sulfide (H2S) is characterized by the smell
of rotten eggs. It is an irritant gas that induces
inflammation of the moist membranes of the eye and
respiratory tract. The consequences of exposure have
been grouped into three phases: acute, subacute, and
chronic. At high acute doses (over 1,000 ppm), H2S
causes immediate collapse with respiratory failure.
Artificial respiration is required to restore the victims,
who might have necrologic symptoms later. At lower doses
(300-500 ppm), subacute exposures cause severe eye and
respiratory tract irritation. After a few hours, pul-
monary edema might set in. Exposure at 50-100 ppm is
characterized by nonspecific necrologic symptoms, such as
fatigue." 6 ~ ~ 6 s Recent animal studies have shown that
subacute exposures are followed by reduction in protein
synthesis, probably caused by inhibition of cytochrome
oxidase.~9 7 The resulting cellular hypoxia is suggested
to be the critical toxic effect of H2S intoxication.
The slow dissociation of the cytochrome-H2S complex
could explain the persistence of the biochemical effects
and the cumulative effects of repeated exposure.
ALIPHATIC AND AROMATIC HYDROCARBONS
~-
Most hydrocarbons have an anesthetic or narcotic
effect when inhaled. The aromatic hydrocarbons, in
addition to their narcotic effect, have varied irritant
properties. 3 6 Some can be absorbed through the skin.
Some, notably benzene, are carcinogens.~°8 Although
their presence is not uncommon in fires, their concen-
trations are usually very low and insignificant in
proportion to those of other pyrolysates.~ 36
FREE RADICALS
Considerable attention has recently been focused on
the presence of stable free radicals formed during
combustion. 4 ~ ~ 3 7 Free radicals have been identified
at concentrations up to 1,200 ppm in fire environments
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where CO did not exceed 500 ppm.t 3 7 Unidentified, but
stable, free radicals were found in laboratory tests to
cause rapid unconsciousness, owing to the peroxidation of
the pulmonary surfactant, which caused an increase in
surface tension, atelectasis, and concomitant hypoxia.) 3 7
This mechanism also potentiated CO asphyxia and might be
related directly to alveolar injury of type I pneumocytes
and to the inhibition of alveolar macrophages and ensuing
pulmonary sepsis (Lowry et al., unpublished data).
INTERACTIONS AMONG COMPONENTS
This brief review of the toxic hazards associated with
fires suggests that fatalities due to smoke inhalation
are in reality caused by complex mixtures of gases,
particles, and other less well-characterized products of
combustion. Results of the few well-conducted fire-
fatality studies available 8 3 5 indicate that most fire
fatalities are associated with CO poisoning and, to a
much smaller extent, with HCN intoxication. Although
these two chemicals have been identified with some
certainty, examination of the blood of victims has
revealed that in many cases neither chemical was present
at a concentration sufficient to cause death. Other
chemicals, such as free radicals, have recently been
identified as potentially lethal, but difficulties in
detecting them in human victims leave their contribution
to fire fatalities uncertain. The most serious potential
hazard, of course, is the combination of a mixture of
combustion products with high temperatures that can
increase their toxicity.
There is evidence that exposure to a combination of
two or more toxic agents can have effects not completely
explained by knowledge of the effects of exposure to the
individual agents alone. Similarly, although data are
insufficient for drawing firm conclusions, the combination
of numerous respiratory irritants can be expected to
induce toxic pulmonary effects not anticipated on the
basis of the effects induced by exposure to any single
toxicant at lower concentrations. Understanding of these
interactions will increase what is now our very limited
ability to extrapolate from some fire model systems to
actual human experience of fire exposures.
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HEALTH EFFECTS OF SMOKE INHALATION
~ . .
ON HUMANS EXPOSED TO FIRES
The health effects of smoke inhalation on humans can
be grouped into three phases: immediate or in-fire
effects, early postexposure effects, and long-term
sequelae.
IMMEDIATE EFFECTS
Immediate effects are defined as those which occur at
the fire scene. They include the effects of exposure to
heat, CO, increased concentration of CO2, O2 depletion,
and irritants. Causes of death at the fire scene include
heat, burns, and necrologic and cardiorespiratory
collapse 43 79 132 153 154 180 230-232
EARLY POSTEXPOSURE EFFECTS
Early postexposure effects are defined as those which
are seen after rescue or entry into the emergency care
system and in the resuscitation and shock phase--a period
of up to several days. Myocardial infarction can be
precipitated by the physical and psychologic stresses of
the fire. Common sequelae are edema of the upper airways
and edema and bronchospasm throughout the respiratory
tract. In this period, sepsis might complicate recovery
and contribute to a fatal outcome.
A moderate smoke-inhalation injury can produce chemical
tracheobronchitis concentrated in the large and medium
airways ~ 0 7 7 ~ 6 ~ 5 3 ~ ~ 3 BrOnChOrrhea is common after
smoke inhalation and is often accompanied by large amounts
of sooty sputum. Sloughing of the bronchial mucosa can
also occur. Depending on whether sepsis occurs, the
condition usually improves by the tenth day.
LONG-TERM SEQUELAE
The difficulties of identifying acute effects of
single high-dose exposures to fire are compounded when
one tries to define the chronic effects of such exposures.
Few followup studies to characterize the nature and
extent of chronic sequelae have been performed;
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interpretation of those which have been done is limited
by problems related to selected populations (selected
with respect to types of exposures and extent of illness
at presentation for medical care), variability of
follownp intervals and measured outcomes, and loss of
subjects to followup. Much of our knowledge about
potential and known long-term sequelae of exposures to
fire has been derived from animal and human data on
exposures to constituents of fire smoke in nonfire
settings, such as intentional exposure to CO in auto-
motive exhaust. It must be kept in mind that interactive
effects of the numerous constituents of smoke probably
increase the risk of injury.
Lonq-Term Sequelae after Single Exposures
Fire victims have been shown to have chronic obstruc-
tive pulmonary disease after single exposures.5 3 ~ ~ 9
Followup studies among smoke-inhalation victims have
demonstrated various types and degrees of persistent
pulmonary dysfunction. Whitener et al. performed serial
pulmonary function measurements in 28 patients after
acute burn injury and smoke inhalation. 2 2 6 Among the
six with smoke inhalation only (without burns), signifi-
cant pulmonary obstruction was observed within hours of
exposure, and further recovery of function was seen at
final followup, 5 months after injury; that all six were
smokers might preclude the generalization of these
persistent effects to all smoke victims. Among patients
with both smoke inhalation and surface burns, the pul-
monary function abnormalities were more severe than in
those with either alone, and decrements of function were
still resolving at the 5-month followup. Recent animal
studies of pulmonary effects of wood smoke and thermal
decomposition products of plasticized poly(vinyl chloride)
have shown that smoke from Douglas fir diminished ventila-
tory response to 10% CO2. 2 2 9 Wood smoke was one-tenth
as potent as smoke from poly(vinyl chloride), and animals
recovered from the effects of wood smoke much more
rapidly. 2 2 ~
Other delayed sequelae of inhalation are attributed
not only to thermal injury (e.g., tracheal stenosis), but
to toxic exposures of the tracheobronchial tree (tracheo-
bronchitis, bronchiolitis obliterans, bronchial stenosis,
and bronchiectasis).~ 3 0 ~ 7 6
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Long-Term Sequelae after Repeated Exposures
Although long-term pulmonary impairment is the most
commonly recognized and studied sequela of acute exposure,
risk factors for chronic respiratory dysfunction, the
prevalence of dysfunction among fire victims, and the
degree of permanent impairment are still poorly charac-
terized. Firefighters have been a useful cohort for
investigations of respiratory morbidity. Caution needs
to be applied, however, in generalizing results from
studies in this group, which faces recurrent exposures
and different exposures in postfire overhauls, to the
population of victims of single exposures.
Although a number of studies among firefighters have
identified acute pulmonary complications of smoke
inhalation, the reported chronic sequelae are variable.
Tashkin and co-workers' initial evaluation of 21 fire-
fighters exposed to the combustion products of poly(vinyl
chloride) found transient hypoxemia in 19; at 1 month,
respiratory symptoms and pulmonary function abnormalities
did not exceed those in matched controls. Musk et
al.,~59 however, found significant decrements in forced
expiratory volume at 1 s (FEV1) among a group of 39
Boston firefighters after intense smoke inhalation.~59
Loke et al. 3 4 found an excess of changes consistent
with small-airway disease among 54 firefighters and
persistent significant obstructive airway disease in one
after a single severe exposure. Unger et al. 2 2 ~ studied
a group of 30 firefighters after a severe smoke exposure
and found decrements in both FEV1 and forced vital
capacity (FVC) with a preserved ratio of FEV1 to FVC,
which is consistent with a restrictive ventilatory defect.
This defect persisted at 6-week and 18-month followups. 2 2
Because baseline spirometric data were not available, it
was not possible to establish whether the decrement in
function resulted from repeated exposures or from a
single intense exposure; for various reasons, the author
favored the former as the cause.
Chronic pulmonary function changes attributed to
s
repeated smoke exposure have been found in three studies
of firefighters.) 7 S ~ 7 ~ 2 °8 The largest was a study of
pulmonary function among Boston firefighters: 1,430
firefighters studied in 1970 and again in 1972 were found
to have greater than twice the degree of pulmonary func-
tion loss that would have been anticipated in the
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intervening 2 years; the decline was significantly
correlated with the frequency of fire exposures. 7 ~
However, 3- and 6-year followup studies of this cohort
showed no further abnormal loss of pulmonary
function.~5 7 USA The authors attributed the apparent
resolution of accelerated functional impairment to
absence of the most affected subjects from followup and
to job transfer (away from continued exposures) within
the fire service. A recent 1-year followup study of a
cohort of London firemen showed a greater than expected
decline in FEV1 and FVC, particularly among cigarette-
smokers. 6 7
Firefighters have also been found to have both acute
and chronic respiratory and necrologic dysfunction after
serious exposures to toluene diisocyanate,22 ~ 28 com-
bustion products of pesticides,~99 and poly(vinyl
chloride) wire insulation. 2 2 4
Cancer
Because the products of fire contain a number of known
and suspected human carcinogens, concern has been raised
about the potential carcinogenic risk associated with
exposures to fire. Unlike the pulmonary sequelae of fire
exposure, excess cancer risk would be expected to show a
dose-response relationship: the greatest risk would be
among those with repeated exposures--firefighters. After
his review of the literature failed to reveal any studies
that showed a pattern of excess cancer risk among fire-
fighters,~ 4 ~ Mastromatteo investigated the mortality
experience of a cohort of city firefighters and found no
evidence of excess cancer risk.) 4 2 The absence of excess
cancer risk was also demonstrated some 20 years later,
when Musk et al. studied the mortality experience of
Boston firefighters employed from 1915 to 1975.~ 5 6
The possibility that firefighters have excess cancer
risks has been suggested by a number of other epidemio-
logic studies, with no consistent pattern of excess
identified. These studies reported increases in brain
cancer and lymphatic and hematopoietic cancers, 44 in
lung cancer,70 ~79 and in gastrointestinal cancer.7 6
More recent studies, by Feuer and Rosenman7 6 and N. J.
Heyer and L. Rosenstock (personal communication), have
identified an excess of lymphatic and hematopoietic
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cancers in a group of city firefighters with long
exposure histories.
In sum, the data available are inconsistent and
contradictory and show no convincing pattern of excess
risk of cancer at specific sites. Some studies have
shown an absence of excess cancer risk, 4 2 ~ 5 9 and
others have shown excesses of lung, gastrointestinal,
hematopoietic, and brain cancers.~° 144 179
SUMMARY
The most studied and best recognized chronic sequelae
of exposure to fire smoke are in the respiratory system.
Smoke inhalation, with and without burn injury, has been
demonstrated to cause persistent and sometimes irrevers-
ible impairment in pulmonary function. The impairment is
predominantly obstructive, but isolated restrictive and
mixed deficits have also been observed. Tracheal and
bronchial stenosis, polyposis, bronchiolitis, and
bronchiectasis have been identified. The prevalence and
extent of these sequelae, however, are not well known.
Although there is ample evidence that toxic gases are
primarily responsible for these sequelae, differences in
the effects of various combustion products are not well
established.
Other chronic sequelae are rare; they include the
delayed necrologic effects of exposure to CO and other
asphyxiants. Excess cancer risk has been suggested in
studies of firefighters who sustained chronic exposures,
but, although plausible, remains unmeasurable among
single-episode victims.
Representative terms from entire chapter:
pulmonary function
