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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 45C 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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65 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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69 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 2500F or 1370C) .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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72 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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73 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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74 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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75 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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76 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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77 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.