Inhalation Injuries Resident Rounds January 30, 2003 Roberto Newtoni Drummondi.

Inhalation Injuries

• Resident Rounds

• January 30, 2003

• Roberto Newtoni Drummondi

Overview

• Exposure to population vs individual• types of inhalational exposure• approach• four cases to illustrate:• simple asphyxia• smoke inhalation• chemical asphyxia• irritant gas exposure

Sallier Papyrus 1650 BC

1650 BC

•

I do not see a sculptor on a missionor a goldsmith on the task of being dispatched (?)but I see the coppersmith at his toilat the mouth of his furnacehis fingers like crocodile skinhis stench worse than fish eggs

• The mat-weaver (lives) inside the weaving-househe 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 Reuchen).This pamphlet describes inhalational hazards of coal smoke, mercury fume, and acid aerosols among goldsmiths

Modern Era

• the use of poison gas in World War Ichlorine, 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 disaster200,000 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, formaldehyde

Laboratory workers.................Solvent vapors, inorganic acid vapors/mists Military personnel...................Zinc chloride smoke

Power plant and oil refinery workers.......... Sulfur dioxide

• Printers, painters...............Solvent vapors Pulp mill workers..............Chlorine, chlorine dioxide, hydrogen sulfide

Railroad personnel, miners, truck drivers...............Diesel exhaust

Refrigeration workers (commercial).........

Ammonia 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

oxides, ozone Woodworkers...................Wood dust

Common Inhaled Toxins Inhalant Source/use Predominant class

•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

soluble 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

Methylbromide.............Fumigant Chemical 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 space

• 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 fashionformation 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)

Exposure level

• 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

Water solubility

• Determines where inhaled gases deposit. • mucus is a watery solution, • gases that are highly water soluble (ammonia, sulfur dioxide, and

hydrogen chloride), • 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

Particle size

•

smaller than 100 microns can enter the airwaysmaller 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

•

Upper airway

• Warns of exposure through protective mechanismMucous, cough, sneeze, glottic closure,Modifies temperature and humidity

• From simple, transient irritation to airway compromisechronic rhinitis , sinusitis, nasal perforationReactive Upper Airways dysfunction syndrome RUDSVocal 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

inflammation develops.

• “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 airways

• usually cytokine mediated, without obvious lung injury

Systemic effects

•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

PHYSIOLOGIC DERANGEMENTS

• 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

History

• 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,.

Physical examination

• 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.

Laboratory examination

• 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 spirometryfull 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

Treatment

• 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 from hemoglobin

• smoke inhalation may require greater fluid resuscitation(no predictable guidelines)

• 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 controversialIn patients with smoke inhalation, steroids have no benefit

• Several experimental treatments ascorbic acid infusions for treatment of inhalation injuries

• 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

Disposition

• 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 mental status.

•

Follow-up care

• 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

CASE

•Coal miner in bellevue underground mine4 miles to the coal facewent down into new seamcanary stopped singing found by partner at the end of shiftvery dead

“I TOT I TAW A PUDDY TAT... I DID, I DID TEE A PUDDDDDD______***”

Physical Asphyxiants

• any gas that displaces sufficient oxygen from the breathable air.

produces tissue anoxia

• asymptomatic if the FiO2 is normal

workplace relatedNitrogen, carbon dioxide, ethane, methane all colourless odourless gasesless 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 minutes..

Dyspnea is not an early finding because hypoxemia vs hypercarbiamost 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

•Nitrogen gas

clear, colorless gasindustrial 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 methaneMethane 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 refrigerant. Methane is lighter than air

• Explosion may occur before death by asphyxiation. suicides with natural gas,.

•

Case

• Firefighter whose respirator malfunctionedFound down in basement of styrofoam factoryunconsious

• singed nasal hairs soot in back of throat

Smoke Inhalation

• 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 particlesdamage the mucosa acid generation and free radical formation,

Early visualization of the airway is critical with early intubation if damage is present.

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 variableThe nature of the fuel determines the composition complex chemistry of heat decomposition and pyrolysisthe toxins of concern are formed de novo

• carbon monoxide and cyanide with smoke inhalation

• the onset of clinical symptomatology is highly variable can be delayedsinged 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 harmful

long-term morbidity, including the development of bronchiolitis obliterans and asthma

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

CHEMICAL ASPHYXIANTS

• tissue hypoxia from interference with oxygen delivery or utilization.

• Carbon monoxide combines with hemoglobin to form carboxyhemoglobinand 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 fire-related death

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 cytochrome

altered mental status, including coma and seizures; extremely abnormal vital signs, including hypotension and cardiac arrest; and metabolic acidosis.

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 controversialLevels .> 25%. 40%

Disposition: Patients with no or mild symptoms (after exposure of less than 5 minutes) who become asymptomatic after a few hours of oxygen therapy and have a CO level below 10%, normal findings on physical examination and on neurologic-cognitive examination, and normal ABG parameters, may be discharged but instructed to return if any signs of neurologic dysfunction arise. Patients with CO poisoning necessitating treatment need follow-up neuropsychiatric examination.

Simultaneous Carbon Monoxide and Cyanide Poisoning (Fire Victim

• a major factor in the mortality associated with exposure to fire smoke. Standard therapy with the nitrite in the cyanide antidote kit produces methemoglobinemia,

• 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, nitroprusside

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 secondsdepletes ATP

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 responsean 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 form cyanomethemoglobin

• inhaled Amyl nitrite followed by (IV) sodium nitrite more effecticvethiosulfate 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 aggressive resuscitation.

Case

•Two men killed in manhole accidentPutting in wires for television companyWaiting over man hole hit by wave of gasHidden 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 daysHe fell forward, paralyzed, directly into the channel of the nine-foot deep manhole. Head injuries from the fall alone would have killed himFriend went into hole to get him died also

Hydrogen SulfideProduction 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 respiration

•

•The treatment of hydrogen urgency as for hydrogen cyanide, and general supportive measures are similar.

• The formation of methemoglobin reverses the effects of hydrogen sulfide • 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 neuropsychiatric symptoms

• 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 airway• 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

Case

• 128 people many of whom were childrenbrought in from pool in Tuebingen found to have irritated eyes, coughsome complaining of inability to smelltwo required intubation for hypoxiadefective bottle found in pump room

IRRITANT GASES

• 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 failure

• Anosmia may also result from chlorine gas exposure

• Pulmonary function studies may show an obstructive pattern bronchiolitis obliterans

• decline in pulmonary function over several years

• Repeated low level exposures may have cumulative effects

Chlorine

•It is greenish-yellow in color and has a pungent odor low odor threshold and good warning properties. Industrial use

• 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 misadventures.

Other Irritant Gases

• PhosgeneTen times as toxic as chlorine not water soluble so has its effect deep in the parenchym

AmmoniaFrom fertiizer a base or alkaliLiquefactive necrosis full thickness tissue destructionBronchiectasis chronic restrictive and obstructive pulmonary changes

Nitrogen DioxideReddish brown gasoccupational 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.

• Ozone • is a bluish gas pungent odor

of photochemical smog Ozone is highly toxic to the respiratory tract. water purification,

Sulfur dioxide

• 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 MetalsInhalation of certain metal fumes or vapors causes acute pneumonitis

Metal Fume Fever, Polymer Fume Fever, and Organic Dust Toxic Syndromehallmark 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 systemic effects

• 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

sulfide poisoning

• Say your prayers when the canary stops singing!!!