Hydrogen Cyanide
Poisoning from Inhalation of Smoke Produced in Fires
Much warning has been given
on the dangers of carbon monoxide poisoning resulting from fires. But there is
another danger to firefighters and victims in structural fires which is less recognized,
and that is acute cyanide poisoning. The dangerous hydrogen cyanide fumes can
be given off even after the fire is out but the material is still smoldering.
Very mild cases might be shrugged off as a headache, but concentrations of a
couple of hundred parts per million in air can kill within a few minutes.
Antidotes are available which are effective if administrated quickly, but the
wrong diagnosis can also result in death. It is important to recognize the
difference between hydrogen cyanide and carbon monoxide poisoning.
The
Providence Journal
carried an article [see
http://www.firerescue1.com/print.asp?act=print&vid=102408 ] about a
50-year-old firefighter who had collapsed while fighting two house fires in Providence R.I. on 24 March 2006. Fortunately, the correct diagnosis of cyanide poisoning
was made at the local hospital, and the firefighter was given the correct
antidote. Other firefighters at the house fires also had elevated cyanide
levels in their blood stream. But there have been many other instances where
people have died as the result of inhalation of hydrogen cyanide produced
during fires. Even with administration of an antidote, survivors can still
suffer long-term damage to the nervous system.
The First Responder
published a similar article in October 2003, titled “Fires: What’s in That
Smoke”.
Where Does the Hydrogen
Cyanide Come From?
No, we are not talking about
a release from a cylinder of hydrogen cyanide or someone adding acid or water
to cyanide salts stored somewhere. We are talking about ordinary materials of
everyday life (e.g. insulation, furniture coverings, carpets, even some
clothing, etc.) which can release cyanide if they catch fire.
The culprit is nitrogen
which makes up the combustible material. Even the nitrogen gas which makes up
the major part of the air can contribute under the right circumstances to form
a minute amount of cyanide during burning of combustibles. High temperatures
and low oxygen concentrations favor the formation of cyanide gas. Smoke from
the combustion of grass clippings, green wood, tobacco, cotton, paper, wool,
silk, weeds, and animal carcasses will likely contain some hydrogen cyanide
gas. But the real offender is from the combustion of man-made plastics and
resins containing nitrogen, especially if the fire is hot and occurs in an
enclosed space. Common man-made materials which generate cyanide gas during
combustion include nylon, polyurethane, melamine, and acrylonitrile. These
materials are present everywhere in building furnishings and our vehicles, foam
insulation, furniture, carpets, draperies, appliances, many plastics, and
articles of clothing.
How Much Hydrogen Cyanide
Gas Can Kill?
The Occupational Safety and
Health Administration (OSHA) website [see http://www.osha.gov] lists the
threshold odor concentration for detection of hydrogen cyanide as 0.58 parts
per million (ppm) by the most sensitive individuals, but firefighters and other
exposed to smoke from burning materials will not be able to smell the gas.
Also possibly 40% of the human population are unable to smell hydrogen cyanide
because of genetic and other factors.
Hydrogen cyanide causes
rapid death by metabolic asphyxiation. The Lethal Concentration in air (LC50,
concentration estimated to kill 50% of people) require to kill humans (cited in
the same OSHA website) depends upon the duration of exposure, as shown in table
1:
Table 1. LC50 in Air
Estimated for Humans [source: Hathaway et al. 1991. Proctor and Hughes’
Chemical Hazards of the Workplace. 3
rd ed Van Nostrand Reinold, N.Y., N.Y.]
LC50, ppm, estimated
|
Exposure Duration
|
3404 ppm
|
1 minute
|
270 ppm
|
6 to 8 minutes
|
181 ppm
|
10 minutes
|
135 ppm
|
30 minutes
|
The numbers are a little
misleading when applied to unprotected emergency responders because other
chemicals in smoke such as carbon monoxide can have synergistic effects with
hydrogen cyanide. Also, emergency responders will be breathing more heavily.
The American Conference of
Governmental Industrial Hygienists reported (cited in same OSHA website) that
workers exposed to hydrogen cyanide concentrations ranging from 4 to 12 ppm for
7 years reported increased headaches, weakness, changes in taste and smell,
throat irritation, vomiting, effort dyspnea, lacrimation (tearing), abdominal colic,
precordial pain, and nervous instability. Also workers exposed to low
concentrations of hydrogen cyanide developed enlarged thyroid glands.
The OSHA permissible
exposure limit (PEL) for hydrogen cyanide is 10 ppm as an 8‑hour
time-weighted average (TWA) concentration. The National Institute for
Occupational Safety and Health (NIOSH) lists a lower limit of 4.7 ppm for
worker short term exposure limit; the American Conference of Industrial
Hygienists (ACGIH) has assigned 4.7 ppm as a worker ceiling limit. This is
more conservative than OSHA. [the PEAC tool goes with the more conservative
NIOSH/ACGIH listing of 4.7 ppm]. The word “SKIN” by the NIOSH and OSHA listing
means that hydrogen cyanide can be absorbed also by the skin and eyes in
addition to inhalation. The NIOSH “Immediately Dangerous to Life and Health
(IDLH)” listing for a 30-minute exposure is listed as 50 ppm for HCN.
Recently, the IDLH level was lowered to 25 mg/m
3 as cyanide
including inhaling salts. [reference http://www.cdc.gov/niosh/idlh/cyanides.html].
The lethal oral dose of cyanide salt for an adult (70 kg) is 50 to 100 mg as
cyanide.
As mentioned before,
hydrogen cyanide causes rapid death by metabolic asphyxiation. More precisely,
cyanide prevents tissue utilization of oxygen by inhibiting the tissue enzyme
cytochrome oxidase. Symptoms of acute exposure to cyanide include general
weakness, headache, confusion, anxiety, and occasionally nausea and vomiting.
Respiratory rate and depth may be initially increased but later become slow and
gasping. Coma and convulsions may follow. Respiration may cease or become
inadequate. If exposure is severe, collapse may be almost instantaneous
followed by convulsions and unconsciousness and death.
Symptoms of Exposure to
Smoke Inhalation-associated Cyanide Poisoning
Firefighters and victims
inhaling hydrogen cyanide associated with smoke as in the burning of plastic
materials often experience cognitive dysfunction and drowsiness that can impair
the ability to escape or to perform rescue operations. Exposure to low
concentrations (or initial exposure to higher concentrations) may result in
stupor, confusion, flushing, anxiety, perspiration, headache, drowsiness,
tachypnea (rapid breathing), dyspnea (labored, uncomfortable breathing), and
tachycardia (rapid heart rate, over 100 beats per minute in adult). Exposure
to higher concentrations of hydrogen cyanide result in prostration, tremors,
cardiac arrhythmia (irregular heartbeat), coma, respiratory depression,
respiratory arrest, and cardiovascular collapse.
If the concentrations are
high (>1,000 ppm), symptoms may occur 15 seconds after inhalation.
Convulsions may occur in 15 to 30 seconds, and respiratory arrest in 2 or 3
minutes. Cardiac arrest follows within 6 to 8 minutes of exposure. If
concentrations are lower, symptoms may not occur until after several minutes.
Eventually respiratory and cardiac arrest occurs.
Other harmful chemicals may
be in that smoke including carbon monoxide. Breathing the hot gas and smoke
may cause thermal injury in the upper airway (mucosal damage, ethyhema
[abnormal redness due to inflammation], ulceration, and oedema [tissue swelling
due to fluid buildup]). There may be blistering and soot deposits in the nose
and mouth. There may be adsorption of other toxins. Upper airway oedema
usually becomes apparent within 24 hours of injury and usually resolves itself
within 3 to 5 days. Some toxins in the smoke irritate the bronchial mucosa
causing airway inflammation, resulting in coughing, breathlessness, wheezing,
and excess bronchial secretions. Pulmonary oedema (fluid buildup in lungs) may
occur in severe cases.
Carbon monoxide binds to
heamogloblin in the blood reducing the blood oxygen carrying capacity. The
concentration of carboxyheamoglobin in the blood increases. The victim may
suffer from both carbon monoxide and hydrogen cyanide poisoning.
Distinguishing Between
Hydrogen Cyanide and Carbon Monoxide Poisoning
Carbon monoxide poisoning is
associated with malfunctioning furnaces, automobile exhaust, hot water heaters,
kerosene heaters, and stoves, as well as fires. Carbon monoxide occurs when
the combustion of fuel is incomplete. Hydrogen cyanide is associated with the
burning of plastics, especially if the fire is hot and in a confined space.
The burning of plastic materials in a confined space can also result in carbon
monoxide.
Carbon monoxide
concentrations of at least 1,500 ppm are associated with significant
mortality. Ambient carbon monoxide concentrations can reach 1000 to 15,000 ppm
during actual firefighting. Carbon monoxide poisoning is estimated to cause
roughly 50% of all fire-related fatalities.
Many of the symptoms of
exposure are the same for hydrogen cyanide and carbon monoxide: headache,
nausea, vomiting, drowsiness, and poor coordination. In the case of mild
carbon monoxide poisoning, the person recovers when moved to fresh air. Severe
carbon monoxide poisoning will result in confusion, chest pain, shortness of
breath, unconsciousness, and coma.
Differences between symptoms
of hydrogen cyanide and carbon monoxide poisoning are subtle and difficult to
characterize. Hydrogen cyanide inhalation will result in difficulty breathing,
the person gasping for air even when he/she is brought out to fresh air whereas
in the case of carbon monoxide poisoning he/she may simply feel sleepy but
breath normally. A bright, red color of venous blood is a symptom of acute
cyanide poisoning because of inability of tissue cells to utilize oxygen.
Blood depleted in oxygen content will appear bluish or purple. Bright red skin
and the absence of cyanosis (bluish or purple skin) have been described in
patients with cyanide poisoning. Caution is indicated because cherry red skin
may also be seen in some severe carbon monoxide poisoning cases [reference:
Myers et al, “Cutaneous Blisters and Carbon Monoxide Poisoning,
Ann. Emerg.
Med. 14(6), 1985, pages 603-6]. Also, a firefighter may experience both
hydrogen cyanide and carbon monoxide poisoning.
The eye pupils may be normal
or slightly dilated in cyanide poisoning. There may be diaphoresis (excessive
sweating).
Sometimes carbon monoxide
poisoning is misdiagnosed as influenza But influenza is accompanied with a
fever, and carbon monoxide poisoning is not accompanied with a high temperature
as the flu does. Caution here is still required for diagnosis in the case of
firefighters because the firefighting effort can still elevate the body
temperature somewhat.
Blood tests can conclusively
distinguish between carbon monoxide and hydrogen cyanide poisoning, but tests
take time. The blood tests include:
- Measurement of blood
oxygen concentration (hospitals and some responders have a device that
attaches to the end of a finger) gives useful information but may be
misleading. Pulse oximetry alone cannot distinguish between COHb and
oxyhemoglobin and is not a reliable measurement of oxyhemoglobin
saturation.
- Measurement of blood
cyanide concentrations. Nonsmokers: < 0.02 μg/ml; smokers
typically 0.04 to 0.05 μg/ml; toxic > 0.2 μg/ml; tachycardia
and flushing 0.5 to 1 μg/ml; coma 1 to 2.5 μg/ml; death >3
μg/ml.
- Measurement of
carboxyhaemoglobin (COHb) concentration. Normal COHb levels for
non-smokers breathing clean air are 0.3% to 0.7% (e.g. 0.3% to 0.7% of
hemoglobin is bound with carbon monoxide forming COGb). Smokers may be
as high as 8%. COHb levels above 25% are considered toxic (symptoms:
throbbing headache, slight confusion). COHb readings above 50% could
result in unconsciousness. CoHb readings above 60% could result in
death. Caution is indicated because patients receiving 100% oxygen
treatment might have a normal COHb reading even though the carbon monoxide
is not completely flushed out. Again, pulse oximetry is not a reliable
estimate of oxyhemoglobin saturation.
- Measurement of carbon
monoxide in the blood. If the person is breathing, some carbon monoxide
may be detected in the gases exhaled.
- Measurement of plasma
lactate concentration. A high plasma lactate (>10 mmol/L) in the
absence of severe burns or hypotension is an indicator of cyanide
toxicity.
- An increased mixed venous
PO2 and a decreased difference in arteriovenous oxygen content
suggests concurrent carbon monoxide and hydrogen cyanide poisoning.
Funduscopic examination of
eyes may reveal erythematous (reddish) retinal veins in the case of cyanide
poisoning.
A portable carboxyhemoglobin
oximeter (the RAD-57) is manufactured by Masimo Corporation in Irvine, California (www.masimo.com). It is also a pulse oximeter.
Technical details on Carbon
monoxide poisoning and treatment can be obtained at the government website at
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~MCvzk8:1. See also
Postgraduate Medicine on line, vol 105(1), Jan. 1999, Carbon Monoxide
Poisoning, at http://www.postgradmed.com.
Technical details on
Hydrogen cyanide poisoning and treatment can be obtained at the government
website at http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~k0AwBW:1.
See also Postgraduate Medicine on line, vol 105(2), Feb. 1999, Smoke Inhalation
Injury, at http://www.postgradmed.com.
Treatment
Remove the incapacitated
person from the fire scene. If the person is wearing an air pack or other respiratory
protection it should not be removed until after he/she is brought to clean
air. Implement appropriate emergency treatment, including treatment of trauma.
Give high flow humidified
oxygen to smoke inhalation victims. Consider early intubation if there is
respiratory distress or coma. Consider early intubation if there are facial or
neck burns, erythema (reddening of skin), blistering, or oedema (fluid buildup)
in the orophaeynx (airway).
Richard Alcortaf, MD, FACEP,
and EMS director for Maryland Institute for Emergency Medical Systems, writes
[see http://www.fireresque1.com/hazards/articles/102410/]:
“Prehospital
management of acute cyanide poisoning in the smoke inhalation victim involves
moving the victim from the source of exposure (while maintaining appropriate
provider respiratory protection, SCBA), restoring or maintaining airway
patency, administering 100% oxygen via non-rebreather mask or bag-valve mask
technique, aggressive advanced airway management, including early intubation,
providing cardiopulmonary support and stabilizing vital signs, including the
use of trauma and burn management (Parkland formula). When clinically
indicated, anticonvulsants (benzodiazpines) should be given for seizures,
epinephrine and antiarrhythmics to stabilize cardiovascular function, and
sodium bicarbonate to correct metabolic acidosis if known.”
These instructions are
also similar to those recommended at the government TOXNET website for
Emergency Medical Treatment for Carbon Monoxide {see http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./etemp/~MCvzk8:1:emt
].
Teofilo L. Lee-Chiong
Jr., MD, writes in the Feb. 1999 issue of Postgraduate Medicine [see
http://www.postgradmed.com/issues/1999/02_99/chiong.htm]:
“Most fatalities
resulting from burn injuries can be attributed to smoke inhalation. Patients
who were trapped in an enclosed space or lost consciousness during a fire are
at increased risk for significant smoke inhalation. Prompt evaluation is
important and can include chest films, pulmonary function testing, arterial
blood gas analysis, and bronchoscopy. Positive findings require aggressive
treatment with adequate oxygenation, ventilation, pulmonary toilet, and fluid
resuscitation. “
The treatments for
carbon monoxide poisoning and hydrogen cyanide poisoning are different after
these initial steps described above. Treatment for cyanide requires
administration of an antidote. Treatment for carbon monoxide requires
administration of oxygen until the carbon monoxide is flushed out of the
system. The danger is that the standard treatment for cyanide (administration
of amyl nitrite, thiosulfate, sodium nitrate) used in the United States has certain risks, among them being that it can worsen or be even fatal to a
victim suffering from carbon monoxide poisoning. A safer antidote
(hydroxocobalamin) has been used in France and other European countries. The
decision is compounded because antidote administration must be started before
all laboratory tests are available.
Treatment for carbon
monoxide requires administration of oxygen. An increase in oxygen tension in
the blood promotes the disassociation of carbon monoxide and hemoglobin. The
carbon monoxide is excreted by the lungs. The half-life of carbon monoxide in
the blood is 3 to 4 hours in room air, 30 to 40 minutes with 100% oxygen
therapy, and 22 minutes with 2.5 atm hyperbaric oxygen therapy. There may also
be complications in administrating hyperbaric oxygen, and some physicians feel
there is no distinct advantage over 100% oxygen. More details are at
Postgraduate Medicine on line, vol 105(2), Feb. 1999, Smoke Inhalation Injury,
at http://www.postgradmed.com.
Supportive oxygen treatment
may benefit cyanide poisoning victims as well. Theoretically, oxygen will not
rid or flush out cyanide from the body, and oxygen therapy should not help. In
practice, oxygen treatment has helped in a number of cases with cyanide
poisoning, especially with smoke inhalation situations where there is also some
carbon monoxide poisoning.
Antidotes for
Hydrogen Cyanide Poisoning
- Taylor Kit; Lilly Kit; Pasadena Kit: Amyl
nitrate, thiosulfate, and sodium nitrite. The amyl nitrite is first
administrated via a mechanical ventilation device or by a gauze sponge for
inhalation. This is followed by intravenous administration of sodium
nitrite and thiosulfate. The nitrites supplied in the kit reduces the
blood’s oxygen-carrying capacity by binding with hemoglobin to form
methemoglobin, which in turn binds and neutralizes cyanide. The problem
is that the nitrite treatment also reduces the bloods capacity to carry
oxygen which could be fatal to a victim with carbon monoxide poisoning.
Another risk is that the antidote may cause severe hypotension (low blood
pressure) leading to shock. Vomiting may occur. Amyl nitrite is also a
controlled substance in the United States.
- Hydroxocobalamin (available in Europe as
Cyanokittm, Hydro Cobrex, Merck-Santé s.a.s). The Cyanokittm
kit contains two vials of 2.5 grams of hydroxocobalamin lyophilizate for
reconstitution with 100 mL saline per vial and two sterile transfer kits
which are injected intravenously. The usual dose in Europe is 70 mg of
hydroxocobalamin per kg of body weight. The hydroxocobalamin neutralizes
cyanide by fixing it to form cyanocobalamin (vitamin B12) which is
excreted in the urine. It does not have the problem of reducing the
blood’s capacity to carry oxygen as in the case of nitrite
administration. Hydroxocobalamin is red in color and will turn the mucous
membranes, skin, and urine red, which could interfere with clinical
laboratory tests which depend on color.
- Dicobalt-EDTA (Kelocyanor) and
4-dimethylaminophenyl: Available in Europe and used prior to development
of hydroxocobalamin treatment but has safety concerns similar to use of
the Taylor kit.
Should the Taylor Kit
be used for treatment of smoke inhalation victims if this is the only antidote
available? Richard Alcortaf, MD, cited above, writes:
- Consider antidotal therapy if [cyanide
poisoning] diagnosis is strongly suspected.
- Begin antidotal therapy without waiting for
laboratory conformation.
- Avoid the sodium nitrate portion of the Taylor cyanide antidote kit in patients with smoke inhalation unless the carboxyhemoglobin
(COHb) concentration is very low (<10%).
Dr. Alcortaf further
writes that injection of sodium nitrite portion of the Taylor kit involves
online medical control. Anticonvulsants may be needed for general seizures.
Vasopressors (e.g. epinephrine) are indicated for hypotension not responsive to
a fluid challenge.
The use for hydroxocobalamin
is expected to get fast track approval by the U.S. Food and Drug Administration
for use in the United States for treatment of smoke inhalation victims, with
possible approval by January 2007. The drug is already used to treat other
medical conditions, but the doses required to treat cyanide are large. It is
even available as a vitamin supplement (vitamin B12a). Dosages and adverse
side effects are being studied with reference to cyanide poisoning. A
treatment reported by Evanston Northwestern Healthcare [see
http://www.enh.org/healthandwellness/bioterrorism/hf065250.aspx?lid=1093] under
study in the United States uses a combination of hydroxocobalamin (4 grams) and
sodium thiosulfate (8 grams) injected intravenously as a solution; a 5 gram dose
of hydroxocobalamin appears to bind all cyanide ions in patients with initial
cyanide levels up to 40 μmol/L (= 1 μg/ml). Co-administration of
folic acid may be required. Possible adverse side effects with patients using
certain other medications need to be better defined. The study notes reddening
of the skin, stools, and urine as side effects along with possible pulmonary
edema, diarrhea, and anaphylactoid reactions (adverse immunologic response) in
some patients.
A French study examined the
results of prehospital use of hydroxocobalamin by the Paris Fire Brigade during
the period Jan. 1998 to Dec. 2002 [reported in
http://www.jems.com/data/pdf/smoke-poisoning.pdf]. Over this period,
hydroxocobalamin (usually a 5 gram dose) was administrated to 81 smoke
inhalation patients in structural or closed space fires; of these patients, 70
recovered cardiac and/or respiratory function at the fire scene and 11 patients
died. Of the 81 patients, 29 were in cardiac arrest before hydroxocobalamin
administration, and of the 29 patients, 18 spontaneously recovered following hydroxocobalamin
(plus adrenalin and supportive care) administration in an average time of 19.3
minutes. Twelve (12) of 15 patients where were hemodynamically unstable
(systolic blood pressure < 90 mm Hg) recovered systolic blood pressure in an
average of 29 minutes after hydroxocobalamin infusion.
Additional reading: see
http://emedicine.com/emerg/topic118.htm
Respiratory
Protection Required
Firefighters and other
emergency response personnel must wear airpacks / SCBA when entering a building
or any confined area where a fire is taking place. The danger of hydrogen
cyanide and/or carbon monoxide poisoning is very real even after the fire is
out but the structure and contents are still smoldering. Theoretically, 10
pounds of furnishings based on acrylonitrile-type polymer could under
air-starved conditions form as much 5 pounds of hydrogen cyanide. In a room
measuring say 20 by 30 feet and 9 feet high, the concentration of hydrogen
cyanide might reach in the ballpark of 14,000 ppm (more or less depending upon
what the temperature is in the room). Considering that a concentration of
3,400 ppm can kill in one minute and a concentration of 180 ppm can kill in 10
minutes, air packs are required when entering structures or other confined
spaces. Concentrations of carbon monoxide might also be high, in excess of
1,000 ppm.
Occupational Safety and
Health Administration regulations (see 29 CFR 1910.1000) require the use of a
full-facepiece, pressure demand self-contained breathing apparatus (SCBA)
meeting the requirement of the National Fire Protection Association Standard
1981 (see rules for Open-Circuit Self-Contained Breathing Apparatus for Fire
Fighters available at http://www.nfpa.org) when entering structures in
firefighting efforts.
Even if firefighters do
not enter the structure and remains outside, there have been instances of
hydrogen cyanide poisoning when SCBA is not used.
An air-purifying
respirator using a cartridge will not provide adequate protection against
either carbon monoxide or hydrogen cyanide. Some may provide limited
protection against hydrogen cyanide, but none are certified for firefighting
use.
Dr. Richard Alcorta,
referenced earlier, estimated that smoke inhalation causes between 5,000 and
10,000 deaths annually in the United States, plus more than 23,000 injuries
including 5,000 firefighters. Hydrogen cyanide poisoning or the combination of
hydrogen cyanide and carbon monoxide poisoning is believed to play a
significant role in these deaths.