Ware G. Kuschner, MD
Paul D. Blanc, MD, MSPH
Potentially hazardous substances may be encountered as airborne toxicants across occupational, vocational, indoor environmental, and ambient exposure scenarios. These substances can exist in one or more of several physicochemical states, including gases, fumes, mists, aerosols, vapors, and smoke. Table 33–1 lists common definitions of these terms. The physicochemical distinctions among categories of airborne toxicants are of limited clinical application, but may be relevant for industrial hygiene monitoring and in interpreting workplace exposure limits. Airborne toxicants cause respiratory tract injury and/or systemic injury beyond local effects on the airways or lungs. Either group of toxic responses can be mediated through a wide variety of mechanisms.
Table 33–1. Definition of terms.
Victims of airborne toxicant exposure may be evaluated and treated across a professional mix of health care providers, including occupational physician or nurse specialists, primary outpatient or inpatient providers, or various subspecialists such as pulmonologists or allergists. Victims of high-intensity exposures are more likely to be managed initially by first responders (eg, paramedics, firefighters, or integrated hazmat teams) and subsequently by emergency department physicians and nurses. Other disciplines (eg, toxicology, otolaryngology, speech therapy, psychiatry, and neurology) may also become involved in the assessment and care of airborne toxicant associated illness depending on the nature of the exposure, the acuity of the presentation, the constellation of signs and symptoms involved, and forensic or medico-legal considerations.
ROUTE OF EXPOSURE & TARGET ORGAN TOXICITY
The respiratory tract may be the toxicant’s route of exposure, the toxicant’s target organ for injury, or both. All of the toxicants discussed in this chapter enter the body principally, if not exclusively, through inhalation (although there are uncommon scenarios where lung injury can occur through ingestion of certain substances not covered here, such as the herbicide paraquat). In addition to being the primary route of exposure, the respiratory tract is also the target organ for many of these airborne toxicants. For example, irritant toxicants such as ammonia cause the abrupt onset of a constellation of respiratory symptoms, including cough, chest tightness, wheeze, and breathlessness. In contrast, carbon monoxide is a nonirritating chemical asphyxiant that exerts its most prominent toxic effects on the central nervous and cardiovascular systems and may be acutely lethal even though causing virtually no respiratory symptoms.
DOSE-RESPONSE & TIME COURSE OF EFFECT
High-intensity exposure to toxic gases and other airborne toxicants may result in clinical findings within seconds, minutes, or hours. These scenarios represent an intensity that is at the far end of the dose-response curve, where most, if not all, exposed individuals will manifest at least some adverse effects.
Some short-term, high-intensity exposures can also cause longer-term sequelae. Examples include anoxic brain injury (eg, caused by carbon monoxide), irritant-induced asthma or reactive airways dysfunction syndrome (“RADS”) (eg, caused by chlorine gas), and bronchiolitis obliterans (eg, caused by nitrogen dioxide).
Chronic health effects caused by repeated subclinical exposures to airborne toxicants are being recognized increasingly as a significant adverse health outcome. Severe bronchiolitis obliterans has been described in microwave popcorn plant workers (called “Popcorn Workers Lung” in that group) as well as in others exposed to the chemical diacetyl, a chemical artificial butter flavorant. An earlier outbreak of severe lung disease marked by organizing pneumonia was reported among workers in Europe and North Africa indolently exposed to a textile coating agent (Ardystil). As another example, repeated intentional (ie, recreational) exposure to volatile solvents, nitrites, and other inhalants can cause a spectrum of chronic health effects that includes liver disease, cognitive disorders, and bone marrow toxicity.
SIMPLE ASPHYXIANTS: METHANE, CARBON DIOXIDE, NITROGEN, NITROUS OXIDE, ETHANE, PROPANE, ACETYLENE, NOBLE GASES
ESSENTIALS OF DIAGNOSIS
Acute effects
• Headache.
• Nausea.
• Confusion.
• Loss of consciousness.
• Coma.
• Anoxic brain injury.
• Cardiac arrest.
Chronic effects
• Residual anoxic injury.
General Considerations
Physical asphyxiant gases displace oxygen and are toxicants insofar as they reduce the fractional inspiratory concentration of oxygen (Table 33–2). These otherwise “inert” gases contrast with toxic asphyxiants (see below) that exert their adverse effects by interfering with the delivery of oxygen to tissues or by disrupting the utilization of delivered oxygen at the cellular level.
Table 33–2. Common asphyxiant gases.
Occupational & Environmental Exposure
Simple asphyxiants are health hazards most commonly when encountered in confined spaces (eg, inside storage tanks or mines). Asphyxiant gases that are heavier than air also may be hazardous in low-lying semi-enclosed areas with little air movement allowing dispersion. Morbidity and death may occur if the exposure is overwhelming and rapid, insidious and occult, or if the victim is unable to flee a confined space. Although any inert gas could act as a simple asphyxiant, the substances of practical importance account for a fairly short list.
Methane gas is most commonly encountered in coal mining, where, because it is lighter than air, it may accumulate in poorly ventilated upper pockets. Methane is also released in other fossil fuel extraction settings and in the presence of organic material breakdown (including landfills). In addition to the danger from asphyxia, methane is also hazardous as an explosive gas, a characteristic shared by several other asphyxiants (eg, propane and acetylene).
Carbon dioxide is a clear and odorless gas used in food preservation. It also may be encountered in: beer and wine fermentation; settings where it is used as a refrigerant, including frozen carbon dioxide (dry ice), especially if a large amount is allowed to sublimate within an enclosed space; and mines, including off-gassing from abandoned mine sites. Carbon dioxide is also used in the leather and textile industries, water treatment, carbonated beverage manufacturing, and in purging pipes and tanks. Natural release of carbon dioxide from a volcanic lake at Lake Nyos, Cameroon, Africa, in 1986, resulted in the deaths of 1700 people and 3500 livestock in surrounding villages. The carbon dioxide is 1.5 times as dense as air, resulting in a dense layer of the gas to accumulate in population centers at the bottom of the hillsides surrounding the lake. This natural environmental calamity was an exception to the general rule that simple asphyxiants are only hazardous in small, confined spaces.
Nitrogen may be encountered in hazardous concentrations in a variety of work settings, including underwater work, mining, metallurgic operations, and pressurization of oil wells. In hyperbaric settings such as tunnels or in deep-sea diving occupations, nitrogen may cause narcosis, leading to behavioral changes and impaired judgment (as well as the complications of decompression; see Chapter 14).
Propane, argon, and other asphyxiant agents may be associated with exposure in high concentrations while filling tanks or when there is a leak from a tank or fuel-delivery system. Whether the substance is heavier or lighter than air, as noted previously, may drive exposure risk in the microenvironment.
Metabolism & Mechanism of Action
By definition, the simple asphyxiants act nonspecifically by displacing oxygen from inspired air. The reduction in the fractional inspired concentration of oxygen results in hypoxia and ultimately frank anoxia. The central nervous and cardiovascular systems are the organ systems most severely affected by hypoxia.
Although carbon dioxide is considered a simple asphyxiant, at high concentrations it also acts as a potent central nervous system depressant (analogous to many solvent vapors that are not considered here as simple asphyxiants; see Chapter 32). It also is a direct acute stimulant to respiration at intermediate concentrations. Tachypnea and dyspnea may be noted with carbon dioxide concentrations greater than 2–3%. Exposure to carbon dioxide in concentrations greater than 10% may be lethal within minutes.
Clinical Findings
A. Symptoms and Signs
Responses to decreased concentrations of inspired oxygen are variable. Important predictors of clinical response include the concentration of the simple asphyxiant (ie, the magnitude of the reduction in fractional inspired concentration of oxygen), the level of physical activity (ie, metabolic activity) and the underlying health status (including the oxygen carrying capacity) of the exposed individual. The normal ambient air oxygen concentration is 21% at sea level (and not <19.5% as noted above). Moderate oxygen deprivation (oxygen concentrations of 10–16%) may cause tachycardia, tachypnea, and exercise intolerance. As the concentration of oxygen decreases to 6–10%, the victim may experience nausea, prostration, and coma. At oxygen concentrations of less than 6%, rapid loss of consciousness and death are typical.
B. Laboratory Findings
There are no specific findings other than the reduction of blood oxygen and associated metabolic derangements (eg, lactic acidosis).
Differential Diagnosis
A brief occupational history may quickly identify a simple asphyxiant as the likely cause of anoxic injury, especially in the context of a confined-space injury. On clinical grounds alone, it may be difficult to differentiate simple physical as opposed to toxic asphyxia (as will be discussed below). Specific laboratory findings may suggest exposure to a chemical (toxic) asphyxiant. Other causes of collapse, such as a primary cardiac or central nervous system event, may need to be excluded depending on the clinical context. Syndromes related to reduced oxygen tension due to hypobaric conditions have a different clinical presentation that is not relevant to displacement of oxygen by simple asphyxiants.
Prevention
Confined-space work should have engineering controls to ensure an adequate air supply. It is important to confirm that the air supply intake does not itself entrain other toxins (eg, carbon monoxide from a compressor). Confined-space injury often occurs in the setting of inadequate safety training, equipment, and procedures (eg, a buddy system).
Treatment
Immediate removal from the exposure can be lifesaving; however, rescuers themselves often are in equal danger without an adequate air supply. Postexposure treatment is supportive and nonspecific, but should include the administration of supplemental oxygen.
Prognosis
Although anoxic brain injury can occur, many survivors of simple asphyxiant gas inhalation make a complete and rapid recovery.
TOXIC ASPHYXIANTS
CARBON MONOXIDE
ESSENTIALS OF DIAGNOSIS
Acute and subacute effects
• Headache.
• Nausea.
• Confusion.
• Cardiac ischemia.
• Coma.
• Anoxic brain injury.
Chronic Effects
• Residual anoxic injury.
General Considerations
Carbon monoxide intoxication is the leading cause of death by gas inhalation. Most fatalities are a result of environmental rather than occupational exposures. In addition to unintentional exposures, carbon monoxide inhalation remains a common method of intentional self-poisoning.
Occupational & Environmental Exposure
Carbon monoxide is a by-product of the incomplete combustion of carbon-based fuels. Significant exposure can occur wherever there is any kind of incomplete combustion of such fuels and inadequate ventilation. The incomplete combustion of biomass fuel, gasoline, kerosene, and propane all result in the generation of carbon monoxide. The internal combustion engine is an important occupational and environmental source of carbon monoxide. Nonelectric forklifts and other vehicles and gas-powered compressors and generators, especially when used indoors, also represent important exposure sources. Carbon monoxide exposures are relevant among firefighters, petroleum refinery workers, indoor garage attendants, mine workers, forklift operators, and furnace operators. Home heating unit malfunction or misuse, structural fires, automobile exhaust, gas-powered recreation equipment, and cigarette smoke are the most common sources of significant nonoccupational environmental carbon monoxide exposure. Exposure also can occur after exposure to methylene chloride (see Chapter 32) because metabolism of this solvent releases carbon monoxide. Massive hemolysis, which can be caused by selected toxins (see arsine gas below) also can be associated with the generation of carboxyhemoglobin (COHb) through metabolism.
Metabolism & Mechanism of Action
Carbon monoxide acts by avidly binding to hemoglobin to form COHb. This has two important effects. First, carbon monoxide competes with oxygen for binding sites on hemoglobin, thereby reducing the oxygen-carrying capacity of the blood. Second, the COHb unit interferes with heme-heme interactions such that the oxygen-hemoglobin dissociation curve is shifted to the left, resulting in decreased release of oxygen from hemoglobin carrier sites to the tissues where the oxygen is required. Carbon monoxide also may bind to
other heme-containing moieties besides hemoglobin and also may affect the mitochondrial cytochrome oxidase system, thus compromising cellular respiration.
Clinical Findings
A. Symptoms and Signs
Acute carbon monoxide toxicity may be nonspecific or, with higher intensity exposures, the neurological or cardiovascular effects may be obvious. The brain and heart are the organs most vulnerable to hypoxia, as noted previously. At high exposures, rapid loss of consciousness, coma, and death occur as with other asphyxiants. In subacute carbon monoxide exposure, symptoms are less marked and can be quite nonspecific, including headache, malaise, nausea, and vomiting. Cardiac ischemia may result from carbon monoxide exposure, particularly in individuals with underlying coronary artery disease. Chronic lower-level exposure to carbon monoxide has been associated with an increase in the incidence of dysrhythmias and, epidemiologically, with the development of atherosclerosis.
B. Laboratory Findings
Elevated COHb is confirmed through co-oximeter blood gas (venous or arterial) analysis. Some newer pulse oximetry devices also estimate COHB. Routine pulse oximetry inaccurately detects this form of hemoglobin as oxygenated, underestimating impairment. A routine blood gas analysis (not done by co-oximetry) reports a calculated rather than measured oxygen saturation that will be falsely preserved in the setting of carbon monoxide intoxication. COHb is increased in active cigarette smoking but should not exceed 10% on this account and usually is less than that (typically 4–7% in a two-pack-per-day cigarette smoker). COHb levels above 30% are associated with moderate to severe symptoms including headache, nausea, vomiting, impaired manual dexterity, and impaired judgment. Levels of 50% can result in seizure, coma, and death. There is a great deal of symptomatic heterogeneity, however, in relation to the absolute COHb level associated with specific findings. In pregnancy, a higher fetal level may be reached than that reflected by the maternal COHb level. Electrocardiographic and biochemical monitoring (eg, serial troponin assays) can be useful because myocardial infarction can occur in carbon monoxide intoxication, even in the absence of typical chest pain symptoms.
Differential Diagnosis
With severe exposure, the differential diagnosis is that of any anoxic injury. For fire victims, it is often difficult to rule out concomitant cyanide intoxication. The differential diagnosis of subacute carbon monoxide intoxication leading to nonspecific symptoms is quite wide and it is likely that many cases go undiagnosed. A high index of suspicion is needed, particularly in winter months when space-heater malfunction is common. Group exposures can be misdiagnosed as food poisoning, for example.
Prevention
Carbon monoxide is odorless and has no warning properties. Internal combustion engines should not be used in indoor environments or near the intake of air supplies. Heating units should be well maintained to ensure proper venting and to avoid partial combustion. Household carbon monoxide alarms are now employed widely. Properly used, these may serve to reduce home heating mishaps. Misuse of gas-powered generators in the face of natural disasters is another source of outbreaks that warrant vigilance in the context of public health protection.
Treatment
Immediate removal from exposure together with supplemental oxygen (100% by non-rebreathing face mask or, in the comatose patient, by endotracheal tube) are the mainstays of initial treatment for carbon monoxide intoxication. On 100% oxygen, the half-life of COHb is reduced to approximately 60–90 minutes from 5–6 hours on room air alone. The role of hyperbaric treatment remains controversial in low-level poisoning. It can play a role in high-level intoxication, presuming that technical access to a hyperbaric chamber is logistically feasible, especially if the chamber allows health care personnel to be in contact with the patient (ie, a multiplace device). In one controlled study, such treatment was found to reduce the risk of selected long-term cognitive deficits following acute carbon monoxide poisoning.
Prognosis
Anoxic brain injury can occur after severe carbon monoxide exposure (ie, intoxication to the point of loss of consciousness). Injury can be nonfocal and subtle, including neurobehavioral abnormalities. Parkinsonian deficits have been documented as a sequela of severe carbon monoxide poisoning.
HYDROGEN CYANIDE
ESSENTIALS OF DIAGNOSIS
Acute and subacute effects
• Dyspnea.
• Headache.
• Gastrointestinal distress.
• Dizziness.
• Loss of consciousness.
• Anoxic brain injury.
Chronic Effects
• Residual anoxic injury.
General Considerations
Hydrogen cyanide is a colorless gas under standard atmospheric conditions. It can be encountered in a wide array of industrial applications. In addition to gas inhalation, exposures occur through ingestion and skin absorption of cyanide salts in solution (eg, potassium cyanide) or ingestion of such liquids. The classic “bitter almond” odor of cyanide cannot be appreciated by a significant proportion of the population, apparently on a genetic basis. Because of its potency and rapidity of action, cyanide has long been important to forensic as well as occupational toxicology.
Occupational & Environmental Exposure
The major current industrial use of cyanide is in metal plating operations and in the extraction of silver and gold salts from ores. This can be an environmental contamination problem as well as occupational exposure scenario. Hydrogen cyanide is also used as an insecticide and rodenticide and in the manufacturing of adiponitrile (for nylon). As with carbon monoxide, cyanide release is a potential hazard in structural fires, primarily as a thermolysis by-product of both natural and synthetic polymers. Toxicity also can occur after exposure to acrylonitrile (see Chapter 32) because metabolism of this solvent releases hydrogen cyanide. Cyanogenic glycosides are an environmental dietary exposure source in much of the developing world, principally from cassava.
Metabolism & Mechanism of Action
Cyanide is quickly absorbed through inhalation and skin exposures. Cyanide exerts its toxicity by binding to ferrous (F++) iron in cytochrome oxidase in the mitochondrial respiratory chain, blocking oxygen utilization. As aerobic metabolism is compromised, anaerobic metabolism ensues resulting in lactic acidosis.
Clinical Findings
A. Symptoms and Signs
Low-level exposure leads to dyspnea, dizziness, headache, confusion, and gastrointestinal distress. Higher exposures cause rapid loss of consciousness, cardiovascular collapse, seizures, and death.
B. Laboratory Findings
Tests of blood cyanide levels are used in forensic examinations but generally are not available in a timely enough fashion to guide acute medical management. Thiocyanate levels, reflecting cyanide metabolism, do not accurately reflect the intensity of cyanide intoxication and should not be used as a proxy.
Differential Diagnosis
The differential diagnosis includes other asphyxiants, especially hydrogen sulfide and, in fire victims, carbon monoxide. Cyanide exposure should be suspected when collapse is very sudden after inhalation, skin contact with contaminated liquids, or ingestion. Profound lactic acidosis raises the suspicion of cyanide intoxication in the appropriate clinical setting.
Prevention
Cyanide gas is released from cyanide salt solutions if the pH falls, such as will occur, for example, from inadvertent mixing of solutions with an acid. As noted, absorption following skin contact with salt solutions also leads to the same toxicity as inhaling cyanide gas.
Treatment
The most widely promoted treatment for cyanide intoxication in the United States had long been the induction of methemoglobin with nitrites (purportedly to compete for cyanide binding, sparing the cytochrome oxidase) and the administration of thiosulfate to promote detoxification of cyanide to thiocyanate. More recently an alternative treatment using hydroxycobalamin has become available. Hydroxycobalamin binds to cyanide, forming Vitamin B12. Because of its challenges, the medical management of cyanide toxicity typically involves consultation with a Poison Control Center.
Prognosis
As with other asphyxiants, anoxic brain injury can occur in survivors of severe acute exposure.
HYDROGEN SULFIDE
ESSENTIALS OF DIAGNOSIS
Acute effects
• Mucous membrane and respiratory tract irritation.
• Loss of consciousness.
• Anoxic brain injury.
Chronic effects
• Residual anoxic injury.
General Considerations
Hydrogen sulfide is a naturally occurring toxicant generated from the breakdown of organic materials. For this reason, it is also sometimes called “sewer gas.” It is associated with a pungent odor of rotten eggs and is detectable by smell in concentrations as low as 0.02 ppm, although this warning property may be lost through olfactory fatigue.
Occupational & Environmental Exposure
Geothermal and fossil-fuel energy extraction are the two major occupational sources of industrial hydrogen sulfide exposure, but other occupational risk groups include farmers (manure processing), sewage workers, fish processors, and roofers or surfacers who work with heated tar and asphalt. Hydrogen sulfide is a particular hazard in confined spaces such as fishing-ship holds, manure pits, and sewers. It is heavier than air and therefore accumulates in low-lying areas.
Metabolism & Mechanism of Action
Like cyanide, hydrogen sulfide exerts its toxicity by blocking oxygen utilization through the cytochrome oxidase pathway. Hydrogen sulfide also has irritant properties and can cause mucous membrane and respiratory tract irritation.
Clinical Findings
A. Symptoms and Signs
High exposure leads to rapid loss of consciousness and death. Intermediate exposures may lead to pulmonary edema and acute lung injury. At lower levels, irritant effects may predominate, including airway irritation and burning eyes. Other findings may include headache, dizziness, nausea, and vomiting.
B. Laboratory Findings
Blood sulfide level measurements generally are not available in clinical laboratories. Industrial hygiene area sampling (eg, with quick-reading sampling tubes) may indicate that exposure has occurred.
Differential Diagnosis
The differential diagnosis includes other asphyxiants, the most important of which is cyanide. Signs or symptoms of mucous membrane or respiratory tract irritation would support the diagnosis because the other toxic asphyxiants are not potent irritants.
Prevention
Confined-space precautions are particularly relevant to the prevention of hydrogen sulfide injury. The odor warning properties of hydrogen sulfide are not reliable as a protective factor.
Treatment
As with cyanide, the specific management of an acutely ill hydrogen sulfide-exposed individual should utilize Poison Control Center consultation.
Prognosis
Anoxic brain injury may result from severe intoxication. In addition, the sequelae of acute irritant inhalant injury represent a potential adverse outcome (see “Irritant Inhalants” below).
IRRITANT AIRBORNE TOXICANTS
ESSENTIALS OF DIAGNOSIS
Acute Effects
• Mucous membrane irritation.
• Cough.
• Stridor.
• Dyspnea.
• Noncardiogenic pulmonary edema.
Chronic Effects
• Irritant-induced asthma (reactive airways dysfunction syndrome).
• Bronchiolitis obliterans.
• Bronchiectasis.
• Chronic respiratory insufficiency.
General Considerations
Irritant airborne toxicants are a heterogeneous group of substances linked by common target-organ effects. The majority of these compounds (but importantly, not all) are moderately to highly water solubleand cause the abrupt onset of irritation of all mucous membranes with which they come in contact, including the eyes, nose, mouth, and throat. Exposure to water-soluble irritants such as chlorine, ammonia, sulfur dioxide, and the acid aerosols leads to tearing, rhinorrhea, and burning of the mouth and throat. Higher-dose exposures that may occur in confined-space mishaps (which can include bathroom cleaning hypochlorite misadventures) or in large ambient releases can lead to lower respiratory tract injury as well. Water-insoluble irritants do not produce marked mucous membrane symptomatology but nonetheless do cause lower respiratory tract injury, including noncardiogenic pulmonary edema and bronchiolitis obliterans (an obstructive airways disease characterized by scarring of the small airways). The most important of these water-insoluble toxicants are nitrogen dioxide, phosgene, and ozone.
Occupational & Environmental Exposure
A. Water-Soluble Airborne Toxicants
Chlorine gas (which is of intermediate solubility) exposures occur through industrial leaks, especially in textile and pulp bleaching (where a related irritant, chlorine dioxide, is also common) and in the production of plastics and resins. Other releases occur primarily in transportation accidents, water-purification mishaps, swimming pool disinfectant accidents, and household cleaning product misadventures (when chlorine is released from hypochlorite up-mixing with an acid; chloramine is a related irritant released from ammonia and hypochlorite combinations). Chlorine gas was used as a chemical weapon in World War I.
Acid aerosol exposure is widespread in a variety of industrial processes. Important compounds include hydrochloric, sulfuric, chromic, and hydrofluoric acids. The anhydrous acid analogues (eg, hydrogen chloride) quickly form acid aerosols in normal atmospheric conditions where humidity is present.
Ammonia exposures result from refrigeration gas leaks, in the manufacture of plastics, and in petroleum refining. High-level exposures also occur when anhydrous ammonia is handled in fertilizer applications.
Other important but less widely encountered water-soluble irritant gases include diborane (microelectronics manufacture), bromine (chemical synthesis, including flame retardants and in water treatment, including in home spas), and methyl isocyanate (pesticide manufacture; a related irritant methyl isothiocyanate is a breakdown product of the pesticide fumigant metam sodium) Formaldehyde, a gas in pure form that also vaporizes easily from solutions (formalin) or off-gasses residual monomer from polymers (ureaformaldehyde resins), is an irritant that may be encountered in plastics, textiles, and paper industries, as well as in smoke and photochemical smog. Acrolein, structurally related to formaldehyde but a more portent irritant, is one of the most important combustion by-product irritants in fire smoke.
B. Water-Insoluble Airborne Toxicants
Nitrogen dioxide inhalation occurs through exposure to gas-shielded electric arc welding, combustion engine exhaust, the manufacture and use of explosives, in the manufacture of fertilizers and dyes, in reactions of nitric acid with various materials, and in silage decomposition (the cause of “silo filler’s disease”).
Phosgene, like chlorine, was important historically as a chemical weapon in World War I. It is still encountered when certain volatile chlorinated hydrocarbons are exposed to heat or ultraviolet light, as in arc welding on or near solvent contaminated (eg, degreased) metals. Phosgene is also used in the production of certain pesticides and in other chemical processes.
Ozone has becoming increasingly important as an alternative to chlorine in pulp paper bleaching and water disinfection. Ozone exposure in the paper industry in Sweden has been shown to be a risk factor for asthma.
Metabolism & Mechanism of Action
The irritants cause tissue injury through heterogeneous mechanisms that may include free-radical or oxidant pathways. In general, these are not substances that specific require metabolic activation (eg, mixed function oxidase modification) in order to exert their toxic effect.
Clinical Findings
A. Symptoms and Signs
Low to moderate exposure to water-soluble airborne toxicants causes mucous membrane irritation marked by lacrimation, rhinorrhea, and burning of the mouth and face. These toxicants have good warning properties, prompting the victim to flee if possible. Higher exposure is associated with hoarseness, cough, and respiratory irritation and also can lead to laryngospasm and tracheal and lower respiratory tract injury. Lower respiratory tract injury may range from mild pulmonary edema to severe injury that manifests clinically as acute respiratory distress syndrome (ARDS). Lower respiratory tract injury becomes evident in the hours immediately following exposure.
The water-insoluble airborne toxicants typically spare the mucous membranes and upper respiratory tract. These toxicants have poor warning properties, permitting significant exposure to occur before symptoms are manifest. In contrast with the immediate onset of symptoms following exposure to water-soluble toxicants, symptoms may be delayed for hours following inhalation of water-insoluble toxicants.
B. Laboratory Findings
After significant symptomatic exposure, laboratory evaluation should include pulmonary function testing, chest radiograph, and assessment of oxygenation.
Differential Diagnosis
The exposure history usually is sufficient to identify irritant inhalation as the cause of respiratory compromise. However, nitrogen dioxide or phosgene exposure sometimes may present as occult causes of ARDS, for which pneumonia and sepsis typically would be the leading alternative etiology. Lower respiratory tract injury without antecedent mucous membrane irritant symptoms is inconsistent with exposure to a water-soluble irritant such as ammonia or chlorine.
Prevention
Precautions in the storage and transport of irritant gases are critical to prevention. Household cleaning product misadventures can be prevented by avoiding hypochlorite mixing with other products, especially acid- or ammonia-containing cleaners. Nitrogen dioxide injury in agriculture can be prevented by proper silo ventilation. Precautions against nitrogen dioxide overexposure also are important during continuous-feed (high-volume) gas-shielded welding operations (eg, tungsten inert gas [TIG] welding), especially in confined or poorly ventilated spaces.
Treatment
The treatment of irritant injury is supportive and nonspecific and includes supplemental oxygen and bronchodilator therapy. Although corticosteroids are used frequently in the treatment of irritant injury in clinical practice, this has not been studied in a controlled clinical trial manner. There is no proven role for prophylactic antibiotic use following such exposures.
Prognosis
In severe exposures leading to ARDS, mortality can be high, but injury of lesser severity resolves without sequelae in most cases. However, irritant-induced asthma (including reactive airways dysfunction syndrome) or, more rarely, bronchiolitis obliterans or bronchiectasis may result from acute irritant inhalation.
SMOKE & OTHER COMBUSTION BY-PRODUCTS
ESSENTIALS OF DIAGNOSIS
Acute effects
• Mucous membrane irritation and cough.
• Stridor and dyspnea.
• Noncardiogenic pulmonary edema.
• Loss of consciousness.
General Considerations
Smoke is a complex mixture of gases and particulates (Table 33–3). The components of smoke depend on the material consumed, the temperature of combustion, and the amount of oxygen present. The principal relevant components of smoke include carbon monoxide, hydrogen cyanide, irritant gases and aerosols as discussed above (particularly hydrogen chloride, formaldehyde, nitric oxide, and acrolein), and carbonaceous particulates (ie, soot). Similarly, the by-products of internal combustion engines are similarly complex and include many of the same key constituents that can vary by engine type and other environmental factors, in particular the oxygen enrichment of the process. Diesel engine exhaust is particularly noteworthy for the fine particulate that it can produce and the relationship this may have to diesel-associated adverse health effects. Incense is made of wood and other plant matter and is impregnated with fragrances and is a source of aromatic chemical aerosols mixed with particulates. Secondhand cigarette smoke is another important source of combustion by-products.
Table 33–3. Common components of smoke from structural fires.
Occupational & Environmental Exposure
Firefighters (urban and wildland) are the largest occupational risk group for smoke inhalation. Home cooking and heating with biomass materials are ubiquitous sources of environmental smoke exposure in the developing world. Residential wood fireplaces are also used widely in industrialized nations for heating and ambiance. Diesel exhaust sources include mobile sources (eg, motor vehicles), stationary area sources (eg, oil- and gas-production facilities, stationary engines, and shipyards), and stationary point sources (eg, chemical-manufacturing facilities and electric utilities). Incense is used worldwide for ceremonial purposes. It represents a source of intentional smoke exposure and is used commonly in confined indoor spaces.
Metabolism & Mechanism of Action
Smoke can exert its toxicity through asphyxia (see “Carbon Monoxide” and “Cyanide” above) or irritant effects. In addition, combustion-related oxidants can cause methemoglobinemia (see Chapter 18). Direct thermal injury typically is not a major sequela of smoke inhalation, in contrast with steam inhalation or flame inhalation in street performers (so called “fire-eaters lung”), where this can be an important cause of respiratory tract injury. The combustion products of biomass fuels such as wood, charcoal, and animal dung contribute to the development of chronic obstructive pulmonary disease, while preexisting asthma and COPD may be exacerbated in indoor environments where biomass fuel smoke is encountered in high concentrations. The precise mechanisms of action, however, are not well delineated.
Clinical Findings
A. Symptoms and Signs
Clinical findings in smoke inhalation injury can include features of both asphyxiant and irritant injury. Carbonaceous sputum and evidence of smoke tainted nares (as well as singed hair) represent findings specific to smoke inhalation.
B. Laboratory Findings
Blood co-oximetry should establish the COHb level and document oxygenation status. After significant symptomatic exposure, laboratory evaluation also should include pulmonary function testing and chest radiography. Profound lactic acidosis may suggest concomitant cyanide exposure.
Differential Diagnosis
The differential diagnostic questions following smoke exposure often center on identifying the potential toxicants of greatest concern, especially following chemical fires. Very acrid smoke suggests the presence of hydrochloric acid or other acid aerosols. These are frequently released when polyvinyl chloride and other halogenated polymers are burned. Other synthetic or natural polymers ranging from polyurethanes to wool can be sources of hydrogen cyanide release through combustion.
Prevention
Appropriate use of a self-contained breathing apparatus is the principal preventive measure used for firefighters combating structural fires, including during clean-up. The use of a breathing apparatus appears to be effective in preventing the development of pulmonary symptoms and in reducing both the deterioration in forced expiratory volume in 1 second and the increase in airway responsiveness caused by smoke inhalation. Limiting exercise in the afternoon on days with poor ambient air quality is one way to limit exposure to ambient-air pollution from combustion releases (eg, wildland fires).
Treatment
The treatment of smoke inhalation includes supplemental oxygen, empirical bronchodilator therapy, and supportive care. As with other irritant exposures, corticosteroids sometimes are used but have not been studied in a controlled manner. Tracheal intubation and mechanical ventilation may be necessary.
Prognosis
Temporary deterioration in pulmonary function and increases in nonspecific airway reactivity have been well documented in persons exposed to smoke, including firefighters and bystanders. In many states, firefighters can receive workers’ compensation on a presumptive basis for lung cancer because of chronic fire smoke exposure. This compensation is based on social policy but does not reflect a well established epidemiologic association. Community environmental exposures following conflagrations can lead to widespread concern over possible chronic effects. Acute respiratory symptoms, including aggravation of preexisting asthma and chronic obstructive pulmonary disease, can be anticipated. Long-term sequelae in the absence of clear-cut acute effects, however, would not be anticipated. High intensity exposure to toxic combustion products can result in chronic respiratory health effects in previously healthy individuals including most commonly irritant-induced asthma. Other respiratory complications could be potentially relevant to those who survive hospitalization requiring intensive care for inhalation injury.
OTHER AIRBORNE RESPIRATORY TOXICANTS
ARSINE
ESSENTIALS OF DIAGNOSIS
Acute Effects
• Malaise and weakness.
• Gastrointestinal distress and dyspnea.
• Hemolysis.
• Hemoglobinuria and hematuria.
Chronic Effects
• Renal damage.
General Considerations
Hemolytic anemia is the most consistent clinical finding. Other findings may include multi-organ-system dysfunction. Arsine gas is colorless, nonirritating, and in high concentrations has a mild garlic odor.
Occupational & Environmental Exposure
Arsine gas can be produced de novo in metal refining and other metal-working processes when arsenic reacts with an acid in the appropriate environment. Preformed arsine gas, often stored under pressure in large quantities, is used widely as a dopant in the microelectronics industry. In addition to a potential occupational hazard, this also presents an environmental risk to surrounding communities. Certain fungi can generate arsine in sewage.
Metabolism & Mechanism of Action
Arsine is toxic to red blood cells, leading to hemolysis. Damage to other tissues may result from secondary damage from hemolysis (eg, kidney deposition of hemoglobin) or from direct toxic effects. Heme metabolism, as noted previously, can be a source of CO leading to elevated COHb levels.
Clinical Findings
A. Symptoms and Signs
The signs and symptoms of arsine toxicity reflect both hemolysis with its sequelae and other systemic toxic manifestations. A triad of abdominal pain, hematuria, and jaundice is characteristic. Clinical findings also may include malaise, headache, renal failure, cerebral edema, intracerebral hemorrhage, dyspnea, cardiovascular collapse, and death.
B. Laboratory Findings
The laboratory findings are those of intravascular hemolysis. Hemolysis may continue up to 4 days after removal from exposure. The blood arsenic level may be elevated, although this is unlikely to be available rapidly enough to aid in early diagnosis. The free hemoglobin level may help to guide management; exchange transfusion has been advocated for free hemoglobin levels greater than 1.2–1.5 g/dL.
Differential Diagnosis
The principal differential diagnosis includes hemolysis as a consequence of other causes. Although chemical oxidant exposures also can cause hemolysis, this would occur in the context of significant methemoglobinemia, which is not present in arsine poisoning. Stibine (antimony hydride) exposure also can cause massive hemolysis, although it is rarely encountered industrially or environmentally.
Prevention
Meticulous control measures and backup procedures should be in place whenever arsine gas is used. This should include hazardous materials (HAZMAT) incident planning relevant to community protection.
Treatment
There is no specific antidote for arsine poisoning. Treatment consists of measures to support vascular, renal, hematologic, and respiratory function. Treatment of massive arsine-caused hemolysis has required exchange transfusion. Alkalinization may reduce hemoglobin precipitation in the kidneys. Interim dialysis may be required if renal failure develops.
Prognosis
Severe arsine exposure is life-threatening. If adequate acute supportive care and transfusion are available, fatalities should be avoidable.
PHOSPHINE
ESSENTIALS OF DIAGNOSIS
Acute Effects
• Respiratory distress.
• Headache and dizziness.
• Gastrointestinal distress.
• Coma.
General Considerations
Phosphine is a systemic toxicant of high potency. It is colorless and has a strong odor that is described either as “fishy” or “garlicky.”
Occupational & Environmental Exposure
Like arsine, phosphine gas is used in the microelectronics industry. Phosphine is also generated from the hydrolysis of aluminum phosphide and zinc phosphide (which occurs spontaneously from contact with air moisture or when ingested), both of which are employed as rodenticides and insecticides, especially in agricultural settings but also in home pest eradication. Phosphine gas exposure has also been reported in the setting of illegal methamphetamine synthesis. Airborne phosphine exposure among veterinary personnel can occur when treating pet animals that have ingested phosphine-containing rodenticide.
Metabolism & Mechanism of Action
When phosphine is inhaled, it can react with moisture to form phosphoric acid, which is an irritant. The systemic toxic mechanisms of phosphine are incompletely understood. A number of end organs are affected, including the central nervous, cardiac, respiratory, hepatic, and renal systems.
Clinical Findings
A. Symptoms and Signs
Multi-organ-system dysfunction can be anticipated following phosphine exposure, with pulmonary, cardiovascular, and central nervous system morbidity most prominent. With lower-level exposure, pulmonary toxicity may be the primary manifestation, marked by dyspnea, cough, chest pain, and delayed-onset pulmonary edema in the hours following exposure.
B. Laboratory Findings
There are no specific laboratory findings in phosphine poisoning. Phosphorus levels are not followed in routine practice in the management of phosphine intoxication.
Differential Diagnosis
Without a history of exposure, it may be difficult to identify phosphine as the cause of the acute multisystem injury this toxicant can induce. Exposure to silos or railroad cars that may have been fumigated should raise the index of suspicion for phosphine exposure.
Prevention
Adequate postuse ventilation and other appropriate reentry restrictions should prevent overexposure in agricultural settings. In industry, strict engineering controls must be enforced. Veterinary and medical personnel should take precautions when handling poisoned animals or humans if phosphine-containing pesticide ingestion exposure is within the differential diagnosis.
Treatment
There is no specific treatment for phosphine toxicity other than general supportive care. The potential for delayed onset of pulmonary edema should be recognized. Hemodialysis is recommended only if renal failure develops. The effectiveness of exchange transfusions is questionable. The value of steroids for phosphine-exposed patients who develop acute pulmonary edema has not been established.
Prognosis
Potential sequelae related to acute lung injury are a possible problem. There are no data on other chronic effects of phosphine poisoning.
METHYL BROMIDE
ESSENTIALS OF DIAGNOSIS
Acute Effects
• Dyspnea and respiratory distress.
• Seizures.
• Coma.
Chronic Effects
• Genotoxicity.
General Considerations
Methyl bromide is a fumigant that has been used widely in agriculture. Its use has become increasingly restricted, however, because of its ozone depleting properties (not is well established human toxicity). In the past, it has been used frequently in structural pest control in the urban environment as well. Methyl bromide, which is heavier than air, is a gas at room temperature but does condense at colder temperatures (<3.3°C [38°F]).
Occupational & Environmental Exposure
Pesticide applicators are the principal occupational risk group. Inadvertent environmental exposure occurs following misapplication or inappropriate reentry to areas treated with methyl bromide. Methyl bromide dissipates rapidly to the atmosphere, so it is most dangerous at or near the fumigation site or at a distance if inadvertently carried through enclosed connections such as piping.
Metabolism & Mechanism of Action
Methyl bromide has multiple toxic actions, including alkylation and enzyme inhibition. It has two principal target-organ effects in humans: acute lung injury and central nervous system toxicity.
Clinical Findings
A. Symptoms and Signs
Dyspnea and pulmonary edema may coincide with neurologic compromise marked by visual disturbance, tremor, altered mental status, and seizure. In severe cases, status epilepticus ensues.
B. Laboratory Findings
Serum bromide may be elevated, but the actual level correlates poorly with symptoms. In some assays, the serum chloride may be falsely elevated because of bromine.
Differential Diagnosis
The exposure history is critical. The combination of neurotoxicity and pulmonary injury represents an unusual constellation of symptoms that should suggest methyl bromide inhalation.
Prevention
Methyl bromide has few warning properties. For this reason, chloropicrin, which is a mucous membrane irritant even at low concentrations, frequently is added to the fumigant. The phasing out of methyl bromide use will be the definitive prevention measure. Unfortunately, methyl iodide, an even more toxic chemical fumigant that is not an ozone depleting agent, has been promoted as one potential substitute.
Treatment
Treatment is nonspecific. Control of status epilepticus is usually the primary focus of care. Dimercaprol and acetylcysteine have been suggested as antidotes based on the postulated mechanism of methyl bromide toxicity. However, no adequate studies have tested the efficacy of these therapies. Accordingly, they cannot be recommended for routine use.
Prognosis
Neurologic compromise that resolves very slowly or that may be persistent has been well documented following methyl bromide intoxication.
MILITARY & CROWD-CONTROL AGENTS & SELECTED AIRBORNE TOXICANTS WITH TERRORISM USE POTENTIAL
ESSENTIALS OF DIAGNOSIS
Acute effects of irritant agents used in crowd-control
• Lacrimation.
• Mucous membrane irritation.
• Dyspnea.
Acute effects of selected incapacitants
• Opioids, benzodiazepines, general anesthetics.
• Stupor.
• Sedation.
• Respiratory depression.
• Anticholinergics.
• Altered consciousness.
• Seizures.
• Dry mouth.
• Constipation.
General Considerations
Tear gases are actually well-dispersed aerosols. Another military agent, the “smoke bomb,” releases zinc chloride aerosol. In October 2002, the Russian military used an incapacitating agent or mixture of incapacitating agents prior to a siege of a theater in Moscow where Chechen terrorists held 800 hostages. Carfentanil, a derivative of the opioid fentanyl, and halothane, a general anesthetic gas, are believed to have been the incapacitants used in that operation. 3-Quinuclidinyl benzylate (BZ) is an anticholinergic agent that has been weaponized and has a spectrum of effects including paranoid hallucinations and other responses typical for anticholinergic toxicity (see Chapter 37).
Occupational & Environmental Exposure
Occupationally, both military and police personnel can be exposed through accidental releases, in training exercises, and in the field. In the latter context, “environmental” exposure may be widespread.
Clinical Findings
A. Symptoms and Signs
The tear gases, principally chloroacetophenone (CN, Mace) and ortho-chlorobenzylidenemalononitrile (CS), are designed to be lacrimators and mucous membrane irritants. Rarely, with severe exposure, lower respiratory injury also can occur. Capsaicin “pepper” spray is a lacrimator used for personal protection and self-defense and as a riot control agent. Pepper spray causes severe irritation to the eyes, including temporary blindness. It also has respiratory tract irritant effects and may produce cough and dyspnea. Depending on the exposure, temporary blindness may last from 15 to 30 minutes, a burning sensation of the skin may last up to one hour, and intense coughing with dyspnea may persist for 3–15 minutes. Zinc chloride, the principal component of smoke bombs, is a severe respiratory irritant. Nonirritant incapacitants cause a spectrum of effects, of which the most important is alterations in mental status.
B. Laboratory Findings
There are no specific laboratory findings.
Differential Diagnosis
The lacrimators (eg, CS and CN) would be anticipated to have similar effects. Involvement of other organs or systemic toxicity suggests other chemical exposures. Capsaicin can trigger severe laryngospasm and, especially in persons with asthma, life threatening bronchoconstriction. Other chemical warfare agents, especially the modern “nerve gases,” cause an entirely different presentation, with systemic illness marked by severe cholinesterase inhibition. The effects of cholinesterase inhibitors are addressed elsewhere in the agricultural chemical context (see Chapter 34). Severe respiratory distress following smoke in a military exercise or other “planned” release should suggest zinc chloride toxicity. This from of zinc inhalation exposure should not be confused with zinc oxide-caused fume fever (see Chapter 31). Another warfare agent, sulfur mustard, although commonly referred to as “mustard gas,” is a vesicant aerosol that leads to skin blistering and bone marrow depression in addition to respiratory injury. Opioid incapacitants may induce respiratory failure, whereas anticholinergic incapacitants may cause systemic symptoms that include altered mental status, hypertension, dry mouth, constipation, and seizures.
Prevention
Confined-space exposures to any of these agents can be associated with adverse outcomes and should be avoided. “Confined space” refers to a space which by design has limited openings for entry and exit, unfavorable natural ventilation which could contain or produce dangerous air contaminants, and which is not intended for continuous employee occupancy. Confined spaces include but are not limited to storage tanks, compartments of ships, process vessels, pits, silos, vats, degreasers, reaction vessels, boilers, ventilation and exhaust ducts, sewers, tunnels, underground utility vaults, and pipelines. Sustained high intensity exposures may occur in confined spaces resulting in significant harm.
Treatment
There are no specific treatments for irritant gases or other lacrimators. After removal from exposure, treatment is supportive. Physostigmine may be used as an antidote for the anticholinergic incapacitants. Flumazenil and naloxone are antidotes for benzodiazepines and opioids, respectively. In any serious illness suspected to be associated with the agents above consultation with a Poison Control Center is warranted for treatment guidance and as a public health notification step.
Prognosis
There are no commonly observed chronic residual health effects of the lacrimators, although case reports of irritant-induced asthma have been documented. Smoke bomb inhalation may lead to the sequelae of acute lung injury. Many of the chemical warfare agents are extremely and rapidly lethal.
INHALANT ABUSE (“RECREATIONAL” INHALANTS)
ESSENTIALS OF DIAGNOSIS
Acute effects
• Alcohol intoxication-like effects.
• Excitation.
• Euphoria.
• Drowsiness.
• Light-headedness.
• Agitation.
• Slurred speech.
• Unconsciousness.
Chronic effects
• Weight loss.
• Inattentiveness.
• Depression.
• Impaired cognition.
• Motor abnormalities.
• Liver toxicity.
General Consideration
Common household products that contain volatile solvents, propellants, gases, nitrites, and aerosols are widely abused to induce psychoactive effects. Products include glues, nail polish remover, lighter fluids, spray paints, deodorants, hair sprays, canned whipped cream, and cleaning fluids. The specific inhalants include amyl nitrite (“poppers”), butyl nitrite (found in video head cleaners), butane (found in lighter fluid), methylene chloride (found in paint thinners), nitrous oxide (“laughing gas”), n-hexane (found in glue), and toluene (found in correction fluid and glue). Inhalants may be sniffed from containers, sprayed into the mouth as aerosols, introduced into a bag as a vapor or aerosol and then inhaled, or inhaled from a soaked rag.
Occupational & Environmental Exposure
Recreational inhalant use refers to intentional inhalational exposure to chemicals in order to produce desired psychoactive and physical effects that may, in turn, have important acute and chronic adverse health consequences. Abuse of common consumer products may be viewed as a form of environmental toxicant exposure, particularly among young adults, adolescents, and children. It also may be viewed as a substance-abuse disorder. It is estimated that over 12 million Americans have abused inhalants at least once in their lives. According to the National Institute on Drug Abuse, 20% of eighth-grade students have engaged in recreational inhalant use. Hair stylists, wood refinishers, and anesthesiologists are occupations that may be at increased risk of experiencing unintentional exposure to some of the same inhalants that have abuse potential.
Metabolism & Mechanism of Action
Inhaled chemicals are absorbed rapidly from the respiratory tract into the bloodstream and delivered quickly to the brain and other organ systems. Alcohol intoxication–like effects may be produced within seconds to minutes. Intoxication may only last a few minutes, which may result in repeated intentional exposures.
Clinical Findings
A. Symptoms and Signs
Recreational inhalants produce a spectrum of acute effects, including euphoria, dizziness, slurred speech, hallucinations, headache, delusions, and loss of consciousness. A single session of inhalant abuse may cause a lethal cardiac dysrhythmia, a sequela termed sudden sniffing death. This can be related to the primary substance inhaled or to carrier propellants, especially if they are halogenated hydrocarbons that can sensitize the myocardium to catecholamine-related dysrhythmia. Long-term health effects from compulsive use include neurotoxicities such as cognitive abnormalities and movement disorders, as well as injury to the heart, liver, bone marrow, and kidneys.
B. Laboratory Findings
There are few specific laboratory findings. Macrocytic anemia has been described in chronic nitrous oxide abuse. Nitrates and oxidants induce methemoglobinemia. Forensic analysis may detect solvents in cases of acute mortality and very high-level exposure. Although various solvent metabolites can be detected in urine and are the basis of biological monitoring in industrial exposure settings, they are generally not relevant to clinical management (but can play a role forensically). Pathologic findings in chronic solvent exposure include brain atrophy (ie, toluene), nerve demyelination (ie, n-hexane), and cirrhosis (ie, hepatotoxic chlorinated solvents).
Differential Diagnosis
An exposure history typically is sufficient to make a diagnosis of acute recreational inhalant use. A spectrum of recreational drugs with psychoactive effects may produce euphoria and other neurologic effects similar to those produced by abused inhalants. The clinical presentation of sudden sniffing death is indistinguishable from sudden cardiac death as a result of congenital or acquired heart disease unless a post-mortem examination is performed (that includes forensic testing). Chronic recreational inhalant use (especially solvents) may produce clinical and pathologic-neurologic syndromes difficult to distinguishable from multiple sclerosis and cirrhosis caused by alcohol.
Prevention & Treatment
The general strategies used to prevent and treat substance abuse are relevant to the public health problem of recreational inhalant abuse.
Prognosis
Intensity, duration, and frequency of exposure and, presumably, host factors are important determinants of prognosis. Chronic neurologic, cardiac, and liver disease may result from long-term abuse.
REFERENCES
Hampson NB: Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. Am J Respir Crit Care Med 2012;186:1095 [PMID: 23087025].
Jacquin L: Short-term spirometric changes in wildland firefighters. Am J Ind Med 2011;54:819 [PMID: 22006591].
Lawson-Smith P: Cyanide intoxication as part of smoke inhalation—a review on diagnosis and treatment from the emergency perspective. Scand J Trauma Resusc Emerg Med 2011;19:14 [PMID: 21371322].
National Institute on Drug Abuse Research Inhalants. Available at: http://www.drugabuse.gov/drugs-abuse/inhalants.
Toon MH: Management of acute smoke inhalation injury. Crit Care Resusc 2010;12:53 [PMID: 20196715].
US Center for Disease Control and Prevention. Confined spaces. Available at: http://www.cdc.gov/niosh/topics/confinedspace/.
US Center for Disease Control and Prevention. Current Intelligence Bulletin 32: Arsine (Arsenic Hydride) Poisoning in the Workplace. Available at: http://www.cdc.gov/niosh/docs/1970/79142_32.html.
US Center for Disease Control and Prevention. Phosphine: Lung Damaging Agent. Available at: http://www.cdc.gov/niosh/ershdb/EmergencyResponseCard_29750035.html.
US Environmental Protection Agency. Methyl Bromide Questions & Answers. Available at: http://www.epa.gov/ozone/mbr/qa.html.
SELF-ASSESSMENT QUESTIONS
Select the one correct answer to each question.
Question 1: High-intensity exposure to toxic gases and other airborne toxicants
a. may result in clinical findings within seconds, minutes, or hours
b. affects only a small number of exposed individuals
c. will manifest only minor adverse effects
d. does not cause longer-term sequelae
Question 2: Simple asphyxiants
a. are health hazards only when encountered in confined spaces
b. are of less concern when they are heavier than air
c. are of no concern when encountered in semienclosed areas
d. include methane gas, argon, carbon dioxide, and nitrogen
Question 3: Methane gas is
a. heavier than air
b. not explosive
c. released in the presence of organic material breakdown
d. not encountered in coal mining
Question 4: Carbon dioxide is
a. lighter than air
b. not a direct acute stimulant to respiration at intermediate concentrations
c. not lethal at any concentration
d. a potent central nervous system depressant at high concentrations
Question 5: Carbon monoxide
a. competes with oxygen for binding sites on hemoglobin
b. increases the oxygen-carrying capacity of the blood
c. is not toxic to fetal hemoglobin
d. is not treated if brain injury has occurred
Question 6: Hydrogen cyanide is
a. encountered in metal plating operations
b. slowly absorbed through inhalation and skin exposures
c. recognized by all workers as a “bitter almond” odor
d. released from cyanide salt solutions if the pH increases to the alkaline range
Question 7: Hydrogen sulfide
a. exerts its toxicity by blocking oxygen utilization through the cytochrome oxidase pathway
b. has good warning properties through smell
c. does not cause mucous membrane and respiratory tract irritation
d. is not associated with burning eyes, headache, dizziness, nausea, and vomiting
Question 8: Smoke inhalation
a. only exerts toxicity through irritant effects
b. results in direct thermal injury
c. does not cause methemoglobinemia
d. produces clinical findings of both asphyxiant and irritant injury
Question 9: Arsine gas
a. is used as a dopant in the microelectronics industry
b. exposure may present as a characteristic triad of abdominal pain, hematuria, and cough
c. may cause headache, renal failure, and purple staining of urine and feces
d. exposure with massive hemolysis does not benefit from exchange transfusion
Question 10: Phosphine gas
a. is not used in agriculture
b. is generated from the hydrolysis of aluminum phosphide and sodium chloride
c. is not associated with chest pain
d. toxicity is marked by delayed-onset pulmonary edema