Index Home About Blog
Subject: Re: How toxic of nitric oxide?
From: (Joshua B. Halpern)
Date: Nov 18 1995
Newsgroups: sci.chem

Martin Ystenes ( 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
dangerous gases.

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.  
: >These
: >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
is correct?

Josh Halpern

N   848071  MSDS-CCOHS
PRODUCT NAME(S):   ***Nitric Oxide***
                            M.S.D.S. #:  C674E
                            140 Allstate Parkway
                             Markham Ontario
                             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)
 CHEMICAL NAME:         Nitric Oxide
 CHEMICAL FAMILY:       Oxide of Nitrogen
 FACT NAME & SYNONYMS:  Nitrogen Monoxide
 Uses:                  Various 
===== SECTION II - Hazardous Ingredients of Material 
Hazardous Ingredients
Nitric Oxide        100%
     LD50:  None 
     LC50:  LC50 115/1hr - inhl.-rat 
             LCLo 320 ppm/1 hr.
             inhl-mouse (Toxic D1A)
             LCLo 315 ppm/15 min. inhl-rabbit 
 SECTION III - Physical Data 
APPEARANCE & ODOUR: Colourless gas with pungent odour 
ODOUR THRESHOLD (ppm):      0.27-0.9, but rapid olfactory 
fatigue occurs 
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 
 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.
RATE OF BURNING:                       Not Applicable 
 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
               [X] Ingestion
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 
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 
Inhalation ----------
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 
vital tissues.
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.  
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
less time. 
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 
and health). 
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 
longer smell. 
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 
per inhalation. 
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 NO2  CL (maximum) 5 ppm 
OSHA,                                           1 ppm/15 min 
NIOSH                              STEL         5 ppm 
ACGIH                              TWA          3 ppm 
CARCINOGENICITY:             None 
TERATOGENICITY:              Yes (NO2) 
MUTAGENICITY:                Yes (NO); Yes (NO2) 
SYNERGISTIC MATERIALS:       Sodium Chloride Aerosol, Welding 
Fumes, Prior Asthma, Reactive Airway or Respiratory Disease,
Heart 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
 Emergency Procedures:
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, 
if applicable.
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 
breathing stops. 
- 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 
after affects.
- 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.'
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 

Index Home About Blog