Subject: Re: How toxic of nitric oxide?
From: email@example.com (Joshua B. Halpern)
Date: Nov 18 1995
Martin Ystenes (firstname.lastname@example.org) wrote:
:> NO appears to be one of the most toxic gases known to man. On top of
This is an _absolutely_ false statement. See the MSDS appended to the
end of this letter. NO _is_ bad stuff, but by no means the worst gas
known to man, or even in the top ten list.
The 50% death point for mice (LD50) is 797 ppm for 1 hour. 320 ppm is
the lowest observed leathel dose. 315 ppm is considered immediately
dangereous to life and health. These are relatively high values for
NOs mode of action is to prevent oxygen transport in the blood. However,
at high concentration NO converts to NO2 upon exposure to air,
within a few seconds. NO2 is also a lethel gas, whose mode of action
is to cause fatal reflex choking. o
(See MSDS below for details)
: >that it produces carcenogens with the help of sunlight and hydrocarbons.
: >are "Identified Flying Objects" that produce cancer. Chronic exposure to
: >carcenogens is worse than a one time exposure; amounts being equal.
One of the roles that NO plays in the air pollution story is as a
precursor to ozone. While at high concentrations
NO is readily converted to NO2 by the three body reaction
NO + NO + O2 --> 2NO2
at the sub ppm concentrations found even in LA at drive time, this is too slow
(because it depends on the square of the NO concentration), rather peroxides
and the peroxy radical oxidize the NO via
NO + XO2 --> NO2 + XO where X = H, CH3O, R, etc.
followed by photodissociation of the NO2 by light < 400 nm
NO2 + hv --> NO + O
O + O2 --> O3
with the NO that is produced cycling around to produce more O3.
NO can also play a role in the oxidation of organic pollutants, as in
OH + RCH3 --> H2O + RCH2
RCH2 + O2 --> RCH2 + RCH2O2
RCH2O2 + NO --> RCH2O + NO2
RCH2O + O2 --> RCHO + HO2
HO2 + NO --> OH + NO2
For more detail, see for example "Chemistry of atmospheres" by Richard Wayne
(where I cribbed most of thi :))
Which is the guilty party here, the oxidizers, or the volitile organic
compounds. Note that both can be limited in combustion engines by
controlling the fuel mixture and the tempertures of burning. Unfortunately,
the higher the temperature, the more NO produced, but the lower the
temperature the more VOC produces (general rule, subject to the usual
caveats). However, that why your car's carborator and ignition are now
run by a computer and the gas stations have those wierd vapor recovery
: I do not object in the carcinogenic ability of NO, although I dispute
: the claim "one of the most toxic gases known to man". Sounds like you
: have just read a pamphlet. But the claim that there was an observable dip
: correlated to gas consumption I put in the same bag as so many other
: claims that has been thorougly debunked.
Neither NO nor NO2 are carcinogens. NO is mutagenic
and NO2 is tetragenic, again to some extent.
(See MSDS below)
One other point. I recall that NO _in the human body_ plays an important role
in neural transmission. Can the biochemists tell me if this recollection
N 848071 MSDS-CCOHS
PRODUCT NAME(S): ***Nitric Oxide***
PRODUCT IDENTIFICATION: CAS NUMBER: 10102-43-9
M.S.D.S. #: C674E
MANUFACTURER(S): LIQUID CARBONIC INC
140 Allstate Parkway
Canada L3R 5Y8
Telephone: 905-477-4141 (OFFICE)
Emergency Telephone: 905-477-5571 (24 HOUR)
Note from Liquid Carbonic: Use, handling or storage of the
product described in this MSDS is at the users sole risk. Liquid
Carbonic Inc shall not be liable for any loss or damages of any
nature whatsoever, however arising, relating to the use, handling
or storage of the product or the statements and information
contained in or omitted from this MSDS.
DATE OF MSDS: 30 Aug 1994
MATERIAL SAFETY DATA SHEET
===== PRODUCT IDENTIFIER: Nitric Oxide
===== SECTION I - Product Information *
===== SHIPPING NAME: Nitric Oxide
UN NUMBER: 1660
CAS NUMBER: 10102-43-9
TDG CLASSIFICATION: 2.3 (5.1) (8)
WHMIS CLASSIFICATION: ACD1A
CHEMICAL NAME: Nitric Oxide
MOLECULAR WEIGHT: 30.01
CHEMICAL FAMILY: Oxide of Nitrogen
FACT NAME & SYNONYMS: Nitrogen Monoxide
CHEMICAL FORMULA: NO
===== SECTION II - Hazardous Ingredients of Material
Nitric Oxide 100%
LC50: LC50 115/1hr - inhl.-rat
LCLo 320 ppm/1 hr.
inhl-mouse (Toxic D1A)
LCLo 315 ppm/15 min. inhl-rabbit
WARNING: CLASS A POISON GAS
SECTION III - Physical Data
APPEARANCE & ODOUR: Colourless gas with pungent odour
PHYSICAL STATE (AT N.P.T.): Gas
SPECIFIC GRAVITY (WATER=1): 1.269
ODOUR THRESHOLD (ppm): 0.27-0.9, but rapid olfactory
BOILING POINT: -151.8 deg C (-241.2 deg F)
FREEZING POINT: -163.6 deg C (-263.6 deg F)
SPECIFIC GRAVITY (AIR=1): 1.036 (@ 21.1 deg C/70 deg F)
GAS DENSITY (g/ml): 0.00125 (@ 21.1 deg C/70 deg F)
VAPOUR PRESSURE: 3450 kPa, 500 psig (@ 21.1 deg C/70 deg F)
pH: Not Applicable %
VOLATILE (BY VOLUME): 100
LIQUID DENSITY (g/ml 1.269 (@ Boiling Point)
EVAPORATION RATE: Not Applicable
SOLUBILITY IN WATER (vol/vol): 0.07
COEFFICIENT OF WATER/OIL DISTRIBUTION: Not Applicable
SECTION IV - Fire and Explosion Hazard of Material
FLAMMABILITY [ ] Yes [X] Non flammable but powerful
oxidizer reacts explosively with reducing agents and organic materials.
SPECIAL PROCEDURES In container is exposed to fire, evacuate
all personnel from danger area. Wearing SCBA and full chemical
suit, cool container with water spray from maximum distance.
Fight source fire with media appropriate to it. Absorb vapours
with water fog. Run-off may be acidic and require
neutralization. Container may rupture if subjected to
localized heating. Container has no safety device.
FLASHPOINT (DEG C) AND METHOD: None
LOWER EXPLOSION LIMIT (% BY VOLUME): None
UPPER EXPLOSION LIMIT (% BY VOLUME): None
AUTO IGNITION TEMPERATURE (DEG C): None
TDG FLAMMABILITY CLASSIFICATION: Non Flammable
HAZARDOUS COMBUSTION PRODUCTS: NO2
SENSITIVITY TO MECHANICAL IMPACT: None
RATE OF BURNING: Not Applicable
SENSITIVITY TO STATIC DISCHARGE: None
SECTION V - Reactivity Data
Chemical Stability [X] Yes [ ] No Stable at normal
temperatures at pressures. Above 300 deg C may decompose
to toxic oxides of nitrogen.
Incompatibility to Other Substances [X] Yes [ ] All
combustible materials, Alkali Metals, Alkaline Earths, Hydrides,
Reducing Agents, Non Metals, Carbides, Metal Oxides,
Sulphides, Chlorides, Chlorocarbons, Halogens, Aluminum,
Chromium, Iron, Magnesium, Manganese, Uranium and Ozone.
Reactivity [X] Yes [ ] Reacts with air to form brown NO2
which is more irritating at low concentrations. Forms nitrous
acid, HNO2, (and nitric acid, HNO3, if oxygen is present) in
presence of moisture and becomes corrosive.
SECTION VI - Toxicological Properties of Material
ROUTE OF ENTRY [X] Skin Contact
[X] Skin Absorption
[X] Eye Contact
[X] Inhalation Acute
[X] Inhalation Chronic
WARNING: CLASS A POISON GAS
Extremely dangerous if inhaled due to blood poisoning.
A fatal dose of Nitric Oxide, a CLASS A POISON, may be
inhaled with no smell or warning symptoms during exposure.
In air, nitric oxide (NO) slowly converts to nitrogen
dioxide (NO2) which is also a CLASS A POISON.
Traces of nitrogen dioxide anaesthetize the nose, moderate
exposures attack the lungs reducing respiration, high
exposures can cause reflex choking to death. Chances of
survival are worsened by serious delayed symptoms including
immunological attack of lung tissue up to 6 weeks after
exposure. A few breaths of nitrogen dioxide at the 1,000
ppm range is almost immediatelyfatal, and at the 200-700 ppm
range, will develop potentially fatal symptoms within 30
EFFECTS OF ACUTE EXPOSURE TO MATERIAL
Skin Contact ------------ NO is a mild irritant but NO2 is a
stronger irritant since it will readily form nitric acid in
the presence of moisture causing chemical burns. See symptoms
by concentration range below and chronic effects below.
Skin Absorption --------------- Nitric oxide (NO) can be
slowly absorbed through the skin causing symptoms as per
inhalation. Nitrogen dioxide (NO2) absorbed into the skin
forms nitric acid with moisture causing chemical burns.
Eye Contact ----------- Due to readily available moisture,
the eyes are severely irritated by nitrogen oxides. 50
ppm of NO2 will cause immediate irritation and, if exposure
is prolonged, will cause severe injury. 90 ppm NO2 has
been shown to cause cornea opacity in rabbits in 8 hours.
See symptoms by concentration range below and chronic effects
THE PRIMARY ROUTE OF EXPOSURE TO CLASS A POISON GAS(ES): A
detailed explanation of the effects of exposure is provided
in four sections; Mode of Action; Hazards; Symptoms by
Concentration Range; and Delayed Symptoms.
Mode of Action -------------- The toxic effects of nitric
oxide (NO) are due to its chemistry. It is only mildly
acidic in presence of water, thus it is absorbed into the
blood in the lungs rather than just converting to acid on
the moist lung tissues as NO2 does (causing irritation or
damage). The NO is a potent enough oxidizer however, to
oxidize the iron atom within hemoglobin (forming
Methemoglobin) making it incapable of transporting oxygen
but making it capable of absorbing NO. If NO is transported
in the blood, then released, it affects the vascular smooth
muscles in the walls of the blood vessels causing them to
relax. This allows blood to engorge certain tissues causing
mucous membranes to become brownish-blue; excessive
salivation; vomiting and contributes to the reduction in
oxygen transport efficiency. The primary acute toxic effect
is poisoning of the blood's oxygen transport capacity
causing symptoms such as muscle tremors, increase in
respiratory rate, increase in heart rate, loss of
coordination, drowsiness, vertigo, blackouts, unconsciousness,
coma and death all due to oxygen deficiency in the brain or
An important consideration is that NO is rapidly converted to
NO2 in the air. Nitrogen Dioxide (NO2) does not react with
hemoglobin but slowly forms a strong acid on contact with
moisture such as found in the mucous membranes or lungs. In
trace amounts, it is an irritant to the eyes, nose, throat and
lungs. In slightly higher amounts, it causes airway reactivity
(muscle contractions constricting airways) and serious
potentially fatal lung damage causing delayed pulmonary edema
(weeping of the body fluids into the lung airspaces) and a
potential time delayed immune system attack on the lungs. (The
lungs do not have nerves, so there is no sensation as the damage
progresses but the airways do and thus, they constrict.) Even at
low levels, NO2 can cause acute broncho constriction or
laryngospasm choking off breathing entirely (i.e. reflex choking)
resulting in asphyxiation with convulsions and death. Also
important, is the fact that 4 ppm of NO2 will anaesthetize the
nose in 10 minutes reducing further any potential warning of
Hazards ------- Nitric Oxide (NO) is a potentially lethal
class A poison which decomposes in air into Nitrogen Dioxide
(NO2), also a potentially lethal class A poison. The first
prevents oxygen transport by the blood while the second
seriously impairs lung function or causes reflex choking to
death. Odour is not a reliable warning and many symptoms are
delayed, so a fatal overexposure may not initially exhibit
dangerous symptoms. There is a high degree of synergy in their
toxicology making prompt treatment crucial.
ALL SUSPECTED CASES OF EXPOSURE MUST BE HOSPITALIZED. Where
possible, and without risk, the time of the exposure, duration
of the exposure, container size and concentration of the gas
source, room dimensions, time and description of all symptoms
and this data sheet should be relayed to the attending physician.
Symptoms by Concentration Range -------------------------------
Listed below are the immediate and delayed symptoms for both
nitric oxide and nitrogen dioxide in decreasing concentrations:
Nitric Oxide (NO)
CLASS "A" POISON GAS - Rescue teams must have air packs
(SCBA). -------------------- 8,000 ppm i.e. 0.8% (estimated):
sudden unconsciousness followed by death in 1 minute by
chemical asphyxiation. Higher concentrations may be fatal in
3,000 ppm i.e. 0.3% (estimated): dizziness or drowsiness in
minutes quickly followed by unconsciousness and death in 5
1,600 ppm i.e. 0.16% (estimated): muscular tremors, loss of
coordination, faster breathing, faster heart rate, drowsiness,
dizziness, excess salivation and vomiting may occur in 5 minutes
with unconsciousness in 10 minutes and death in 15 minutes.
800 ppm (estimated): similar to 1,600 ppm above but taking four
times as long. Vomiting may cease after 30 minutes and mucous
membranes may become brownish-blue. Still has potential to be
fatal when Methemoglobin concentration of blood reaches 70-90%
after a 1 hour exposure.
797 ppm (1068 mg/m3): LC50/1 hr inhl-rat. (Lethal concentration
to 50% of rats in 1 hour.)
632 ppm (or more) of NO: each minute 100 ppm NO2 will be formed
(with remainder still NO) which has appearance of faint brown
visible cloud which irritates the eyes and mucous membranes.
400 ppm (estimated): first symptoms, similar to 1,600 ppm above,
appear within 2 hours when Methemoglobin concentration reaches
30-40%. Vomiting may cease and unconsciousness may occur within
3 hours. Still has the potential to be fatal if Methemoglobin
concentration of blood reaches 70- 90%.
320 ppm: LCLO/1 hour inhl-mouse. (Lethal concentration lowest
315 ppm: LC50/15 min. inhl-rabbit. 100 ppm: is considered to be
IDLH (immediately dangerous to life or health).
25 ppm: for 8 hours may be symptom free until 5-48 hours after
exposure when air hunger, tightness or burning in the chest,
and coughing, choking and sleeplessness may develop.
0.3 - 0.9 ppm: pungent odour.
Nitrogen Dioxide (NO2)
CLASS "A" POISON GAS - Rescue Teams must have air packs (SCBA).
1000 ppm: LC50/10 min. inhl-mouse. 805 ppm i.e. 0.08%
(estimated): 15 seconds exposure lethal by reflex choking
if not rescued. Extremely irritating to the eyes, nose and
663 ppm (estimated): 30 seconds exposure lethal by reflex
choking if not rescued. Extremely irritating to the eyes,
nose and throat.
546 ppm (estimated): 60 seconds exposure lethal by reflex
choking if not rescued. Extremely irritating to the eyes,
nose and throat.
348 ppm (estimated): 5 minutes exposure lethal by reflex
choking if not rescued. Extremely irritating to the eyes,
nose and throat.
256 ppm (estimated): lethal to man 15 minutes by reflex
choking. Airway reactivity and resistance makes
breathing more difficult with time. Less than 5 minutes
exposure causes potentially fatal pulmonary edema (See 90 ppm).
211 ppm (estimated): lethal to man in 30 minutes by reflex
choking. Airway reactivity and resistance makes breathing
difficult. (See 90 ppm).
173 ppm (estimated): lethal to man in 60 minutes by reflex
choking. Breathing becomes shallow and laboured with time.
150 ppm: for 10 minutes or less causes; coughing; eye, nose
and throat irritation; headache; nausea and vomiting. Longer
exposure can cause permanent eye damage and potentially fatal
delayed pulmonary edema. (See 90 ppm).
100 ppm: appearance of faint brown visible cloud.
90 ppm: for 40 minutes has caused moderate irritation to the
eyes and mucous membranes and potentially fatal delayed
pulmonary edema. The delay may be up to 70 hours when symptoms
of cyanosis (turning blue), shortness of breath, restlessness,
headache and frothy yellow or brown sputum appear. If untreated,
fluids or froth can flood the lungs (i.e. drowning) or can be
infected by viruses or bacteria resulting in bronchitis or
pneumonia which may be fatal to a weakened patient.
88 ppm: LC50/4 hour inhl-rat.
70 ppm: for 8 hours has caused permanent corneal opacities
(blindness) in rabbits.
50 ppm: is moderately irritating to the eyes and mucous
membranes within 10 minutes and long exposure can cause
permanent eye damage. IDLH (Immediately dangerous to life
30 ppm: LC50/1 hour inhl-guinea pig.
4-5 ppm: for 15 minutes will cause increased airway reactivity
(constriction of airways), airway resistance (more effort needed
to breathe), and decreased diffusion of gases in the lungs.
4 ppm: for 10 minutes anaesthetizes the nose so it can no
1-5 ppm: sweetish acrid odour.
0.1 ppm: for 2 hours can result in increased airway
reactivity for asthmatics or people with chronic bronchitis.
Some individuals who had symptoms of acute exposure with or
without edema developed an immune reaction (bronchiolitis
fibrosa obliterans) 10 days to 6 weeks after exposure. Symptoms
include severe cough, cyanosis (turning blue), fever, hypoxemia
(low oxygen level in blood), reduced pulmonary function,
decreased pulmonary diffusion and X-rays may show fine scattered
nodes in the lungs. Also, lungs are vulnerable to virus and
bacterial infections for several weeks after exposure resulting
in recurrent bronchitis. If pneumonia sets in, there is a
potential of death.
A release of NO could result in exposure to both NO and NO2
Medical treatment can be assisted if notes as to time and
description of symptoms are written down to allow prompt and
appropriate treatment decisions. In most exposures, NO2 will
predominate since the longer NO is in air, the more it will have
converted to NO2. Also, the reaction rate is a function of the
square of the NO concentration, it is very rapid at
concentrations above 10,000 ppm (1%) so exposures to NO in this
range are unlikely. (For this reason, very little data is
available for NO from 300 to 10,000 ppm and the information
provided has been extrapolated from other blood poisons.)
Ingestion --------- An unlikely route of exposure to a gas but
strong irritation of mouth and throat or, in large amounts, as
EFFECTS OF CHRONIC EXPOSURE TO MATERIAL
Skin Contact ------------ Chronic exposure may cause dermatitis
or brownish staining of skin.
Eye Contact ----------- Repeated or prolonged contact may cause
Chronic Exposure ---------------- Exposure to NO has not been
linked to chronic disease in man.
Repeated or prolonged exposure to low concentrations of NO2 may
cause chronic irritation of respiratory tract with coughing,
wheezing, air hunger, moist rales, cyanosis, headache, vertigo,
loss of strength, shallow breathing, dyspnea, loss of appetite
and corrosion of teeth.
Chronic changes may develop if edema or fibrosis occurred and
include chronic bronchitis, asthmatic attacks, pulmonary function
changes and rarely fibrosis or emphysema. Fibrosis
(Bronchiolitis fibrosa obliterans) is an immune system reaction
with the formation of antibodies against some parts of the lung.
The antibody reaction results in the formation of fibrous clumps
which, with continuous exposure, may develop into emphysema.
Rats exposed to 4 ppm NO2 daily for 6 months did not develop this
but, those exposed from 9.8 to 25 ppm for up to 18 months, did
show some emphysema.
EXPOSURE LIMIT(S): For NO TWA 25 ppm OSHA, ACGIH, NIOSH
EXPOSURE LIMIT(S): For NO2 CL (maximum) 5 ppm
OSHA, 1 ppm/15 min
NIOSH STEL 5 ppm
ACGIH TWA 3 ppm
ACGIH IRRITANCY OF MATERIAL: Irritant (NO2)
SENSITIZATION OF MATERIAL: Yes (NO2)
REPRODUCTIVE EFFECTS: Yes (NO2)
TERATOGENICITY: Yes (NO2)
MUTAGENICITY: Yes (NO); Yes (NO2)
SYNERGISTIC MATERIALS: Sodium Chloride Aerosol, Welding
Fumes, Prior Asthma, Reactive Airway or Respiratory Disease,
SECTION VII - Preventive Measures
Gloves: Clean oil-free neoprene gloves.
Respiratory: SCBA or air supplied respirator.
Eyes: Full faceshield and chemical goggles.
Footwear: Safety shoes for container handling, if
Clothing: Chemical resistant clothing such as neoprene.
Other: Air monitoring devices are highly recommended.
(Potentially fatal overexposure can occur
without symptoms.) Buddy system with buddy (similarly
protected) responsible for shutting off supply quickly.
ENGINEERING CONTROLS Corrosion resistant exhaust for
fumehood is acceptable for laboratory use. The exhaust
system must be free of deposits of organic materials
which could become an explosion hazard. Forced
ventilation neutralizing scrubber is required when
large amounts are used in manufacturing. Use only in
closed system which are corrosion resistant and are
verified as being free of air, moisture and organic
contaminants at all times (even when not in use).
Pressure test and purge system prior to and after
each use with inert gas.
A rapid failsafe system to shut off supply is highly
recommended. A thorough purging of the system before
and after use is highly recommended.
Note: A worker with proper respiratory and eye protection
may be ignorant of an elevated level in the air.
No unprotected personnel should be permitted in work area.
Shut off supply and initiate evacuation at the first sign
of any of the following: Monitor gives alarm; Gas leak
heard; Any smell in the mask(s); and Itchy, creepy or
burning skin areas.
LEAK AND SPILL PROCEDURE Self Contained Breathing Apparatus
(SCBA) is needed for all
Large Leak: - Evacuate danger area. - Suppress fumes
with water fog while wearing SCBA and full chemical suit and
shut off supply, if without risk. Run- off water may require
neutralization. Do not walk on spilled material.
Small Leak: - Evacuate immediate area. - Shut off supply
if without risk using SCBA and adequate protective clothing.
- Wait until gas has dissipated or has been removed by exhaust
or scrubbing system.
Shutdown & Purge: - Once the immediate hazard has been
controlled as above, the system must be fully shut down
and purged out. Then, the whole area must be washed down
to remove any corrosive film. Moisten pH paper is useful to
stick to surfaces to check for this.
WASTE DISPOSAL Neutralizing scrubber preferred. Do not
dispose of residual content of container. Return container,
CORROSIVITY Not Applicable.
STORAGE REQUIREMENTS Replace valve plug and container cap,
if applicable. Protect containers from physical damage.
Store in cool, dry, well-ventilated area. Do not allow
temperature to exceed 52 deg C (125 deg F). Secure in upright
position, with full and empty containers segregated.
SPECIAL SHIPPING INFORMATION Shut valve tightly, replace
valve plug if so equipped, replace cap, if applicable and
mark if any residual product is being returned. Replace
container cap, if supplied. Transport secured upright in
well-ventilated truck. Never transport in passenger
compartment, trunk or enclosed vehicle. Special placarding
is required for shipments of gas.
HANDLING PROCEDURES AND EQUIPMENT Due to the extreme toxicity
of this gas, an Emergency Plan is highly recommended. This
should involve a detailed plan, training in breathing air,
rescue, emergency communication and coordination with the
Fire Department and local hospital.
Use a purge system before and after use. For larger scale
work, a very carefully designed system which takes into
account valve and other component failures must be very
carefully cleaned and dried prior to assembly, then
extensively purged until the entire system has the same
moisture content as the purge gas. Safe handling requires
frequent external inspections for corrosion, leaks, pressure
tests, safety valve tests, and also periodic internal
inspections. Any potential suck-back air or liquids is
dangerous and should be eliminated. Keep oil and grease away.
Use only with regulating equipment cleaned for oxygen service
and rated for container pressure. Use only in well ventilated
areas. Do not move container without its cap in place, if
applicable. Use a suitable hand truck for container movement,
if applicable. Secure container when in use. Do not allow
to fall. Use backflow preventive device to prevent suck-back.
Keep container away from heat, flame and sparks. Close valve
after each use and when empty. Replace valve plug as soon as
cylinder is disconnected from the system. Return empty
SECTION VIII - First Aid Measures
Eyes: - Wash promptly with copious amounts of water
for 15 minutes keeping eyelids apart. - Call a
physician. Repeat eye wash.
Skin: - Wash immediately in emergency shower, then
remove contaminated clothing and shoes. - Call a physician
immediately. Wash affected area with mild soap. Treat high
exposure as for inhalation. - Do not use ointments. - Wash
contaminated clothing before re-use and discard shoes.
Inhalation: - Carry (do not allow to walk) victim to fresh air.
- Have victim breathe fresh air (oxygen is an antidote) in all
cases, as hard as possible. Give oxygen immediately.
-Call an ambulance and advise them of case of blood poisoning
due to Nitric Oxide.
- Give artificial respiration with supplemental oxygen, if
- Without delaying the patient's transport to the hospital,
note the time and description of patient's symptoms and
other readily accessible information in Hazards Section above.
Rapid transmission of this information to the physician is vital.
-Fatal symptoms may be delayed up to 48 hours even though
victim may seem normal immediately after exposure.
Symptoms may disappear after a short period, but this
is not a sign of recovery. All suspected cases of exposure
must be hospitalized immediately.
- The purpose of this procedure is to maximize the oxygen
available throughout the body to react with NO forming NO2
which does not cause blood poisoning. Prompt medical
intervention to fight pulmonary edema, and later
bronchitis obliterans, is necessary to prevent chronic
- Rinse mouth promptly with water. If irritated, treat as
Recommendations to Physicians
- Eye pain due to NO2 may be alleviated with 2-3 drops of 0.5%
pontocaine solution but indicates an emergency referral to an
opthalmologist is required to manage collagenase release and
prevent further damage.
- Patients presenting skin or oral burns due to NO2 should also
have level of methemoglobinemia verified.
- Methemoglobinemia due to NO resolves in hours with oxygen
therapy. Treatment as follows may be indicated at 20%
methemoglobinemia in the blood, or onset of cyanosis, prior
atherosclerosis or underlying hypoxemia. Concurrent vascular
smooth muscle relaxation may be inhibited with 1% methylene
blue via I.V. to a total dose of 0.2 ml/kg while perivenous
infiltration is prevented and oxygen therapy continued.
(Additional doses may be required). Periodic verification of
hemolysis, which may require diuresis and hydration to prevent
renal hemoglobin precipitation and damage,is recommended.
Treatment of hypoxemia should be expected to be complicated by
immediate and delayed pulmonary crisis and oxygen under positive
pressure may be indicated. #See Inhalation Acute below.'
+ Inhalation Acute:
NO2 irritation of the lower respiratory tract results in airway
reactivity and resistance and can progress to bronchiospasm or
laryngospasm. These may indicate artificial respiration (with
oxygen), bronchodilators such as metaraminol or albuterol and
an anticholinergic inhalant such at Atrovent. Prior asthma,
reactive airways, exposure to welding fumes or sodium chloride
mist are synergistic and may indicate aggressive treatment.
Severe cases may present laryngedema requiring aspiration and
may indicate tracheotomy. #See Inhalation Delayed below,
Delayed Symptoms above, and Chronic Exposure above.'
+ Inhalation Delayed:
NO forms nitric acid in the lungs that both corrode and
oxidize tissues. After a delay of up to 72 hours, the patient
will present with hypoxemia, carbon dioxide retention,
restrictive or obstructive pulmonary changes arising from
edema. Symptoms include cyanosis, shortness of breath and
frothy yellow or brown sputum. The onset of edema is a very
severe crisis requiring sequential or concurrent management of
acute respiratory failure, cardiogenic shock, unresolved
methemoglobinema, hypoxemia and opportunistic viral and
bacterial infections. Treatment is symptomatic, but pretreatment
with antibiotics may be indicated. #Experimentally, vitamin E
can prevent some of the consequences of NO2 intoxication.'
Immune response; Bronchiolitis fibrosis obliterans may be
prevented by high dose steroids such as 30-80 mg/day in divided
doses of prednisone or equivalent beginning with onset of
delayed symptoms and continued for 3 weeks. #See Delayed
Symptoms above and Chronic Exposure above.'
+ ALL CASES OF SUSPECTED EXPOSURE REQUIRE HOSPITALIZATION
BECAUSE SYMPTOMS MAY NOT BE IMMEDIATELY APPARENT.
EARLY EVALUATION AND TREATMENT ARE CRUCIAL.
Prepared By: Phone Number Date Safety Department
#905' 477-4141 Prepared: September 1988 Liquid Carbonic Inc.
Revised: September 1991
Reviewed: September 1994
M.S.D.S. #: C674E
DATE: 8/30/94 REV: 2