• Resident Rounds
• January 30, 2003
• Roberto Newtoni Drummondi
• Exposure to population vs individual
• types of inhalational exposure
• four cases to illustrate:
• simple asphyxia
• smoke inhalation
• chemical asphyxia
• irritant gas exposure
Sallier Papyrus 1650 BC
I do not see a sculptor on a mission
or a goldsmith on the task of being dispatched (?)
but I see the coppersmith at his toil
at the mouth of his furnace
his fingers like crocodile skin
his stench worse than fish eggs
• The mat-weaver (lives) inside the weaving-house
he is worse off than a woman,
with his knees up to his stomach,
unable to breathe in any air
1473 AD - Ellenbog
• The first treatise devoted solely to occupational health,
"On the poisonous evil vapors" (Von den gifftigen besen Tempffen und
This pamphlet describes inhalational hazards of coal smoke,
mercury fume, and acid aerosols among goldsmiths
• the use of poison gas in World War I
chlorine, phosgene, and mustard gases
respiratory rather than systemic toxins.
• World War I also spurred heightened governmental
interest in and funding for industrial hygiene
Exposures that affect huge communities
• Bhopal chemical disaster
200,000 people were exposed to a cloud of methyl isocyanate
6000 deaths were caused by acute respiratory failure
• 2001 World Trade Center terrorist attack in New York City,
inhalation injury was the most frequent reason medical attention
• Wartime use of chemical agents, such as mustard gas,
resulted in severe inhalation injuries to combatants
Individual Exposure harder to detect
• Hard to diagnose can be covert and indolent
May know only that a toxic release occurred without details
must take thorough occupational history
diagnosis of inhalation injury is largely clinical,
• Despite the array of possible toxic inhalants,
identification of a specific inhalant is often unnecessary because
therapy is based primarily on the clinical manifestations
Table 1. Selected occupational irritants
Agricultural workers....... Ammonia, nitrogen dioxide, hydrogen sulfide
Custodians ................ . Ammonia, bleach (hypochlorite), chloramines
Firefighters.............. Smoke, hazardous materials releases
Food service workers........ Cooking vapors, cigarette smoke
Health professionals ........ Glutaraldehyde,
Laboratory workers.................Solvent vapors, inorganic acid vapors/mists
Military personnel...................Zinc chloride smoke
Power plant and oil refinery workers..........
• Printers, painters...............Solvent vapors
Pulp mill workers..............Chlorine, chlorine dioxide, hydrogen sulfide
Railroad personnel, miners, truck drivers...............Diesel exhaust
Refrigeration workers (commercial).........
Roofers, pavers...................Asphalt vapors, PAHsa
Swimming pool service workers......................Chlorine (hypochlorite), hydrogen chloride
Waste water treatment workers.....................Chlorine, hydrogen sulfide
Welders...........metalic oxide fumes, nitrogen
Common Inhaled Toxins Inhalant Source/use
Acrolein.....................Combustion Irritant, highly soluble
Ammonia Fertilizer.................combustion Irritant, highly soluble
Carbon dioxide....................Fermentation, complete combustion, fire extinguisher Simple; systemic effects
Carbon monoxide...................... Incomplete combustion, methylene chloride Chemical
Chloramine.........Mixed cleaning products
(hypochlorite bleach and ammonia) Irritant, highly
Chlorine....................Swimming pool disinfectant, cleaning products Irritant, intermediate solubility
Chlorobenzylidenemalononitrile/choroacetophenone ................Tear gas Irritant
Ethane.................Natural gas, refrigerant Simple
Hydrogen chloride.................Tanning and electroplating industry Irritant, highly soluble
Hydrogen cyanide................Combustion of plastics, acidification of cyanide salts (e.g., jewelry) Chemical
• Hydrogen fluoride Hydrofluoric acid...............Irritant, highly soluble; systemic effects
Hydrogen sulfide ................Decaying organic matter, oil industry, mines, asphalt Chemical; irritant, highly
Methane.............................Natural gas, swamp gas Simple
Nitrogen......................... Mines, scuba divers (nitrogen narcosis, decompression sickness)
Nitrous oxide .....................Inhalant of abuse, whipping cream, racing fuel booster Simple
Noble gases....................(e.g. helium) Industry, laboratories
Oxides of nitrogen....................Silos, anesthetics, combustion Irritant, intermediate solubility
Oxygen..................Medical use, hyperbaric conditions Irritant, free radical; systemic effects
Ozone...................... Electrostatic energy Irritant, free radical
Phosgene.......................Combustion of chlorinated hydrocarbons Irritant, poorly soluble
Phosphine ...................Hydration of aluminum or zinc phosphide (fumigants) Chemical
Smoke .......................(varying composition) Combustion Variable, but may include all classes
Sulfur dioxide ........................Photochemical smog (fossil fuels) Irritant
Occupational and Environmental Lung Disease
Fatal Work-Related Inhalation of Harmful Substances in the United States Francesca Valent MD
MARCH 2002 CHEST
• USA 1992 to 1998, a total of 523 workers died The overall mortality rate was
• 0.56 deaths per 1,000,000 worker-years
• women had lower mortality rates than men
• Worse if >65
• Carbon monoxide was more frequently involved in fatal inhalations
• irritants, particularly chlorine gas the most common sources of emergency
department visits not requiring hospitalization.
Exposure to carbon monoxide was a major problem across industries
• result not of fires but of malfunctioning machines
exposure to other substances was more industry specific
• CDC identified mining, agriculture, forestry, fishing, and construction as the
industries with the highest rates fatal inhalations.
• auto and miscellaneous repair services to be an industry with increased
inhalation mortality rate.
• one fourth of the victims were doing repair or maintenance.
PHYSICAL AND CHEMICAL QUALITIES
• Gases formless state of matter can expand to occupy an available
• Fumes condensing vapour in cooler air
• Dusts suspensions solid particles in air
• Smoke incomplete combustion of carbon containing material
• Mists airborne finely divided fluid droplets
• Aerosols very fine liquid droplets suspended in air prolonged time
Mechanisms of toxicity
• common target airway epithelium.
– disruption of the integrity protective barrier.
– edema, inflammation, smooth muscle contraction, and stimulation of afferent neurons
• not always respiratory disorders
(eg, lead poisoning from fume inhalation),
• conversely:ingested toxins effects on the lung paraquat and hydrocarbon
• irritants damage cells in a nonimmunologic fashion
formation of an acid, alkali, or reactive oxygen species.
• tissue depletion of glutathione, a free radical scavenger
• direct thermal injury to cells and tissue (steam especially)
• The intensity of the exposure
• Controlled industrial vs uncontrolled explosion
• Environment confined space vs outdoors
• The Occupational Health and Safety Administration (OSHA)
– permissible exposure limits for many chemical substances
• Determines where inhaled gases deposit.
• mucus is a watery solution,
• gases that are highly water soluble (ammonia, sulfur dioxide, and hydrogen
• acute irritant injury to mucus membranes, ( eyes nose upper airway)
• spare the lower respiratory tract
• Unpleasant symptoms protective
• Gases of intermediate solubility( chlorine) widespread irritant effectst.
• less water-soluble( nitrogen dioxide and phosgene) travel distally
• result in delayed onset chemical pneumonitis
smaller than 100 microns can enter the airway
smaller than 10 microns can reach the lower respiratory tract,
smaller than 5 microns can deposit in the lung parenchyma
• Host factors
Patients with pre existing disease COPD etc
Site of injury
• Warns of exposure through protective mechanism
Mucous, cough, sneeze, glottic closure,
Modifies temperature and humidity
• From simple, transient irritation to airway compromise
chronic rhinitis , sinusitis, nasal perforation
Reactive Upper Airways dysfunction syndrome RUDS
Vocal Cord Dysfunction chronic pharyngitis
Conducting airway injury
• Damage to the epithelial cells and tight junctions
increases mucosal permeability
leads to inflammation and cellular damage.
• Results in bronchoconstriction,.
• irritant effects include tracheitis and bronchitis.
• exacerbates underlying reactive airway disease
• More intense exposures airway constriction,
even in individuals without a history of reactive airways disease.
• Airway obstruction may worsen over the first 24 hours after exposure as
• “reactive airways disease syndrome”
• Classically, RADS develops after a single, high dose exposure, but it may also
occur after repeated lower level exposure
Injury to lower respiratory tract
• lower water solubility and particles less than 5 microns
• Diffuse bronchiolar inflammation can occur
• Atelectasis may result from disruption of the pulmonary surfactant
• Pneumonitis is the most common acute manifestation
dyspnea, cough, and hypoxemia
• pulmonary edema or ARDS.
• Chronic effects bronchiolitis obliterans, bronchiolitis obliterans organizing
pneumonia (BOOP), and pulmonary fibrosis.
• Fixed airway obstruction granulation and interstitial fibrosis extending into small
• usually cytokine mediated, without obvious lung injury
Inhalation of mercury vapor : a toxic pneumonitis with pulmonary edema fever,
tremors, and chest pain.
• Metal fume fever: flu-like symptoms from metal oxides fumes, including zinc ,
copper, and magnesium oxides.
• Organic toxic dust syndrome: agricultural workers after exposure to moldy
grains flu-like syndrome cough, fever, myalgias and dyspnea
• Exposure to high doses of hydrofluoric acid hypocalcemia and hypomagnesemia
• Loss of airway patency secondary to mucosal edema
• Bronchospasm secondary to inhaled irritants
• Intrapulmonary shunting from small airway occlusion caused by mucosal edema
and sloughed endobronchial debris
• Diminished compliance secondary to alveolar flooding and collapse
• Pneumonia and tracheobronchitis associated with loss of ciliary clearance
• Respiratory failure progressing to multiple-organ dysfunction
Approach to the patient with inhalation injury
• what the individual was doing at the time of the exposure
• the substances involved and the intensity and duration of exposure.
• If eye or upper airway mucus membrane irritation occurred, and when such
• irritation began provides information about the water solubility of a substance.
• The occurrence of symptoms in coworkers
• If material safety data sheets or container warnings
• Other respiratory symptoms include cough, sputum production, wheezing, chest
pain, and shortness of breath. taste sensations, central nervous system
symptoms such as lightheadedness or dizziness,
fever or malaise.
• The past medical history underlying lung disease such as asthma or COPD,
whether the patient is a smoker,.
• signs that indicate the severity of injury.
• Heart rate, respiratory rate, temperature, blood pressure and oxygen saturation
may initially be normal, even in the setting of a significant inhalation injury.
• The skin, hair and nares, and oropharynx should be examined for signs of burns
or chemical injury.
• It is important to remember that significant injury can occur without visible
abnormalities in these structures.
• The presence of stridor.
of wheezes or crackles.
cyanosis, confusion, tachycardia, pulsus paradoxus, and fever.
• pulse oximetry and an arterial blood gas
• If smoke inhalation is suspected, a carboxyhemoglobin level should be obtained.
CBC lytes specific toxin mercury eg
• elevated plasma lactate levels may indicate cyanide toxicity
• If cyanide toxicity is suspected, a cyanide level should be drawn, but treatment
should not be delayed if clinical suspicion is high.
• A chest radiograph may be normal early in the course of the event
Bilateral patchy infiltrates suggest the development of pneumonitis, whereas air
trapping suggests airway obstruction
• laryngoscopy, or less commonly, bronchoscopy may be helpful looking for
deposits of soot or edema
• indicates a higher risk for respiratory failure and a potential need for intubation.
• peak flow measurements and spirometry
full pulmonary function testing can help determine whether restrictive or
obstructive pulmonary disease is present
• findings at the time of initial evaluation frequently do not correlate with the
ultimate clinical course
• In general, treatment of inhalation injury is supportive.
• An exception is for exposures, such as hydrofluoric acid, that may benefit from
treatment with a specific antidote.
• oxygen to ensure adequate oxygenation and to help displace carbon monoxide
• smoke inhalation may require greater fluid resuscitation(no predictable
• Pulmonary toilet
• Intubation or tracheotomy may be necessary if there is significant upper airway
compromise or respiratory failure
• The role of steroids in the treatment of inhalation injury is controversial
In patients with smoke inhalation, steroids have no benefit
• Several experimental treatments ascorbic acid infusions for treatment of
• In an animal model, hyperbaric oxygen and free radical scavenging medications
reduced the severity of smoke-induced pulmonary edema
• intubation for standard indications, positive pressure ventilation, pulmonary
toilet, and antibiotics for established infection.
• no value to prophylactic intubation, steroids, or antibiotics
• support such patients while they go through a predictable 7- to 21-day period of
endobronchial slough, secondary failure of gas exchange and compliance,
infection, and healing.
• Survivors are left with a variable degree of permanent lung dysfunction
• Death following burns and other forms of trauma is frequently the result of
multiple organ system failure
• knowledge of the agent involved, and the intensity and duration of exposure
• Inhalation of certain agents, such as phosgene, can produce few initial
symptoms, yet progress to significant pulmonary edema, ARDS, and respiratory
failure within 12 to 24 hours of exposure.
• Indicators of poor prognosis include progressive respiratory difficulty, presence
of rales on physical examination, burns to the face, hypoxemia, and altered
• often self-limited events,
• For mild exposures, a follow-up appointment should be made several days after
the initial exposure, with clear instructions to the patient to seek medical care
immediately if symptoms are worsening.
• serial spirometry
• methacholine challenge test
• psychological and social support to avoid post-traumatic stress disorder
• Social issues, related to returning to work and work restrictions, as well as
workers compensation programs, may be present.
• consultation with an industrial hygienist or a regional occupational and
environmental health center
Coal miner in bellevue underground mine
4 miles to the coal face
went down into new seam
canary stopped singing found by partner at the end of shift
“I TOT I TAW A PUDDY TAT... I DID, I
DID TEE A PUDDDDDD______***”
• any gas that displaces sufficient oxygen from the breathable air.
produces tissue anoxia
• asymptomatic if the FiO2 is normal
Nitrogen, carbon dioxide, ethane, methane all colourless odourless gases
less commonly encountered are the inert gases argon, neon, and helium
A consistent history, an appropriate spectrum of complaints, and rapid
resolution on removal from exposure
• oxygenation, and supportive care.
• the differential diagnosis is extensive
• scene investigation
• (interestingly deaths related to intentions inhalation of automotive exhaust
result from simple asphyxiation and not CO)
headache, hyperventilation, nausea, confusion, loss of consciousness, apnea,
and death. At high concentrations of gas, unconsciousness may occur within
Dyspnea is not an early finding because hypoxemia vs hypercarbia
most patients present with resolving symptoms.
• failure to improve may suggest complications of ischemia
(e.g., seizures, coma, cardiac arrest) and is associated with a poor prognosis
clear, colorless gas
industrial processes, underground mines;
when accompanied by carbon dioxide in coal mines, black damp
• Carbon dioxide
• clear, odorless gas
used in its gaseous, liquid, or solid form.
textile, leather, wine, and chemical industries,
in food preservation, in welding, as a fire extinguisher,
• Methane and ethane
low-molecular-weight hydrocarbons that are colorless and odorless.
Mercaptan is usually added to methane
Methane is the principal component of natural gas (85%)
formed from decaying organic matter such as from swamps
Ethane is a small component of natural gas (9%) and is also used as a
Methane is lighter than air
• Explosion may occur before death by asphyxiation.
suicides with natural gas,.
• Firefighter whose respirator malfunctioned
Found down in basement of styrofoam factory
• singed nasal hairs soot in back of throat
• 4000 persons die or are injured by residential fires in the United States
Smoke inhalation injury is typically irritant in nature.
Irritant toxins produced by the fire are adsorbed onto carbonaceous particles
damage the mucosa
acid generation and free radical formation,
Early visualization of the airway is critical with early intubation if damage is
Inhalation injury commonly accompanies burning and is a major determinant of
length of intensive care unit stay
air has such a low heat capacity that it rarely produces lower airway damage.
• Smoke is always undefined and nonuniform very variable
The nature of the fuel determines the composition
complex chemistry of heat decomposition and pyrolysis
the toxins of concern are formed de novo
• carbon monoxide and cyanide with smoke inhalation
• the onset of clinical symptomatology is highly variable can be delayed
singed nasal hairs and soot in the sputum suggest substantial exposure but are
not sufficiently sensitive or specific to be practical.
• filtered smoke (e.g., in a different room) or to relatively smokeless combustion
(e.g., engine exhaust) inhale predominantly CO, cyanide, and metabolic poisons
and do not suffer irritant exposure.
• ongoing bacterial pneumonitis. Staphylococcus and pseudomonas
• bronchoalveolar lavage to assist with pulmonary toilet
No lavage of carbonaceous material
• Corticosteroids, whether inhaled or systemic, are not indicated and potentially
long-term morbidity, including the development of bronchiolitis obliterans and
Patients with concerning clinical findings (e.g., hoarseness, respiratory distress)
and those with identifiers of substantial exposure (e.g., closed-space exposure,
carbonaceous sputum) should be admitted to a critical care unit or transferred
to a burn center
• tissue hypoxia from interference with oxygen delivery or utilization.
• Carbon monoxide combines with hemoglobin to form carboxyhemoglobin
and interferes with oxygen delivery,
• hydrogen cyanide and hydrogen sulfide
• oxidative enzymes and impair oxygen utilization.
THIRTEEN FACTS ABOUT CARBON MONOXIDE
• most common cause of acute poisoning death and the most common cause of
CO poisoning can be obscure and subacute with flu h/a symptoms
incomplete combustion of virtually all carbon-containing products.
interacts with deoxyhemoglobin to form carboxyhemoglobin (COHb),
which cannot carry oxygen. (approximately 240 times greater than for oxygen)
be overcome by high tissue levels of oxygen.
4 to 6 hours on room air, 90 minutes with 100% oxygen at 1 atm,
30 minutes on 100% oxygen at 3 atm of pressure.
The affinity of fetal hemoglobin for CO is even greater, hcg on all women
• affects myoglobin, and interferes with oxidative phophorylation through
altered mental status, including coma and seizures;
extremely abnormal vital signs, including hypotension and cardiac arrest; and
cigarettes contains 3% to 6% carbon monoxide,
or an average exposure of 400 ppm during inhalation.
By comparison, the work-place standard allowed by OSHA is 50 ppm.
cherry-red color is a postmortem finding
The ABG measurement cannot be used as a diagnostic test
• HBO therapy in patients with CO poisoning are controversial
Levels .> 25%. 40%
Simultaneous Carbon Monoxide and Cyanide Poisoning
• a major factor in the mortality associated with exposure to fire smoke
. Standard therapy with the nitrite in the cyanide antidote kit produces
• worsens carcon monoxide poisoning
Sodium thiosulfate, administered alone is safe
• A standard dose of 12.5 g
therapy in an HBO chamber may receive nitrite therapy while pressurized
FIFTEEN FACTS About Hydrogen Cyanide
• Hydrogen cyanide is a colorless liquid or gas
• widespread industrial use,. Combustion of various plastics.... found in fruit pits,
Hydrogen cyanide is nonirritating...... odor of bitter apricot
rapidly absorbed distributed to the oxygen-utilizing body tissues.
Inhibition of oxidative metabolism by binding to complex IV of the electron
transport chain within mitochondria occurs within seconds
high venous oxygen content aterialization of venous blood Fundal veins and
arteries may appear equally red.
• An increased anion gap metabolic acidosis should be present, and the serum
lactate level should be elevated. A lactate level greater than 10 mmol/L in a fire
victim is highly predictive of cyanide poisoning.
stimulates chemoreceptors in the aorta and carotid artery, causing hyperpnea.
acyanotic patient with respiratory and cns symptoms
Contact with cyanide salts may also cause direct respiratory, mucous
membrane, and skin irritation, as well as skin burns from the caustic solution.
mild acute poisoning is uncommon
high index of suspicion with rapid response
an appropriate history of exposure or ingestion.
• Specific therapy the production of methemoglobin, inducing methemoglobinemia
which competes with the cytochrome oxidase system for binding of cyanide.
Cyanide has a high affinity for MetHb and readily leaves cytochrome oxidase to
inhaled Amyl nitrite followed by (IV) sodium nitrite more effecticve
thiosulfate component, should be administered immediately
The last part of the antidote kit is the sulfur-containing compound sodium
thiosulfate. The adult dose is 12.5 gms. Cyanide and cyanomethemoglobin are
detoxified by sulfur transferase sulfur donor
• The best results are attained when the kit is used in combination with
Two men killed in manhole accident
Putting in wires for television company
Waiting over man hole hit by wave of gas
Hidden in the trees, around the bend of the river, was a lake of raw sewage
created from the overflowing line. In all, there was about 2,750 feet of 18- and
15-inch pipe filled with septic sewage behind the plugs. It had been standing in
the pipes for at least 40 days
He fell forward, paralyzed, directly into the channel of the nine-foot deep
manhole. Head injuries from the fall alone would have killed him
Friend went into hole to get him died also
Production and Uses
• Rapid tests for hydrogen sulfide are not available,
• Although not routinely available, blood sulfide levels can be measured.
• presence of blackened copper coins in the.pockets
• Hydrogen sulfide is a colorless gas heavier than air,accumulates at the bottom
of a confined space with a characteristic rotten-egg odor
• low olfactory threshold, at 0.02 ppm,
• (olfactory fatigue can occur at concentrations of 100 to 150 ppm,)
• Hydrogen sulfide is used industrially
– oil refineries decompostion of organic material mining
• potent cytotoxic asphyxiant, impairing cytochrome oxidase and cellular
The treatment of hydrogen urgency as for hydrogen cyanide, and
general supportive measures are similar.
• The formation of methemoglobin reverses the effects of hydrogen
• rapid cardiovascular collapse and death
a mechanism identical to that for cyanide poisoning.
Hydrogen sufide spontaneously dissociates from the mitochondria
allowing patients to survive after exposure
• inhalation of amyl nitrite followed by infusion of 10 mL of a 3% solution
of sodium nitrite over 2 to 4 minutes.
• sodium thiosulfate not generally recommended. (hydrogen sulfide is
not detoxified by rhodanese)
• A potential role for the use of HBO not uniformly acceptedfor delayed
• All patients with symptomatic cyanide or hydrogen sulfide admitted
• Workers can experience a knockdown with one inhalation
• often fall away from gas exposure into fresh air
• three most common causes of death are
• a fall into water, into machinery, into a space with compromised
• antidotes are usually not useful because once the patient is
removed from source recover quickly
• permanent damage is caused by hypoxic injury
• awaken suddenly spontaneously with overwhelming air hunger
• 128 people many of whom were children
brought in from pool in Tuebingen
found to have irritated eyes, cough
some complaining of inability to smell
two required intubation for hypoxia
defective bottle found in pump room
• Irritant gases cause pulmonary damage by direct injury
• The severity of injury depends upon the duration of exposure,
concentration of the irritant, and physical and chemical properties.
• More water-soluble irritants, such as ammonia, formaldehyde and chlorine,
cause upper airway injury and burning and watery eyes or cough
Severe exposure may result in pulmonary edema, hypoxemia, and respiratory
• Anosmia may also result from chlorine gas exposure
• Pulmonary function studies may show an obstructive pattern
• decline in pulmonary function over several years
• Repeated low level exposures may have cumulative effects
It is greenish-yellow in color and has a pungent odor
low odor threshold and good warning properties.
• Transported in pressurize containers as liquid
• Prolonged exposure: chlorine is denser than air remains at ground level.
• industrial leaks, environmental releases occurring primarily in transport, water
purification, swimming pool-related events, and household-cleaning product
Other Irritant Gases
Ten times as toxic as chlorine not water soluble so has its effect deep in the
From fertiizer a base or alkali
Liquefactive necrosis full thickness tissue destruction
Bronchiectasis chronic restrictive and obstructive pulmonary changes
Reddish brown gas
occupational exposure manufacture of nitric and sulfuric acids,
explosives, fertilizers, cellulose compounds, and dyes. metal etching and
photoengraving and the cleaning of copper and brass.
Nitric oxide is produced in welding.
• is a bluish gas pungent odor
of photochemical smog
Ozone is highly toxic to the respiratory tract.
• Sulfur dioxide (SO2) gas is a byproduct of the combustion of sulfur-containing
fossil fuels. major component of air pollution smog.
• Hydrofluoric acid
• (hydrogen fluoride), irritant effects, clinically significant hypocalcemia A specific
antidote, calcium gluconate, is available for topical use, and is also available in
an inhaled form.
Crowd control agents ("tear gasses”)
to incapacitate persons via immediate mucous membrane irritation
chloroacetophenone ("mace"), and orthochlorobenzamalonitrile
lower respiratory injury with high-intensity exposure
Inhalations With Systemic Effects
• Cadmium, Mercury, and Other Toxic Metals
Inhalation of certain metal fumes or vapors causes acute pneumonitis
Metal Fume Fever, Polymer Fume Fever, and Organic Dust Toxic Syndrome
hallmark is chills, fever, malaise, and myalgia with onset 4 to 8 hours after Metal
fume fever is associated with zinc oxide inhalation from welding galvanized
metal or brass working
Take Home Points
• Inhalation injury most common form of industrial accident
• Identify agent with occupational history
• Inhalation injury caused by four mechanisms, simple
asphyxiation, chemical asphyxiation, irritant exposure and
• Carbon Monoxide is the most common inhalational agent
• Think cyanide poisoning in smoke inhalation
• There is a three stage antidote kit for cyanide and hydrogen
• Say your prayers when the canary stops