Effects of Toxic Gas Exposure in buildings

Effects of exposure to various gases that may occur in buildings, including Ammonia, Arsine, Arsenic, Bromine, Carbon Dioxide, Carbon Monoxide, Hydride, Hydrogen Sulfide, Nitrogen Oxide Gas, Propylene, Propane, LP gas Sewer Gas, Sulphur dioxide, & others
Questions & Answers about the toxicity of various gases found in buildings
References

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What are the effects on humans of exposure to various toxic gases? This document gives basic information about exposure to and potential health hazards from a number of common toxic gases that may be found indoors or in or around buildings. We describe symptoms of exposure to these gases, industry recommendations for gas exposure limits, how gases may be measured, and how to track down and cure the sources of gas leaks in buildings.

Potential Health Hazards of Exposure to Certain Gases

In addition to reviewing the gas exposure limits in this document, see Toxic Gas Exposure Standards - Summary for Indoor gases and also Indoor Gas Sampling Plan for Residential buildings which lists many other toxic indoor gases which are among almost 300 toxic gases we can test for, depending on the building complaint, building conditions, and individual health concerns. Portions of this material are quoted from comments by Jack Peterson at a public CompuServe safety forum in 1989. At Volatile Organic Compounds VOCs we discuss several chemicals and gases found indoors and offer advice for reducing indoor exposure.

For details about exposure to various toxic and irritating gases see GAS EXPOSURE LIMITS & STANDARDS. Also see ODORS & SMELLS DIAGNOSIS & CURE for procedures to diagnose and cure all kinds of odors in and around buildings.

Gas exposure hazard evaluation consists of comparing measurements of exposure (or dose) with exposures (doses) known to be safe or known to be hazardous. For the most part, because of biological variation, "no effect" levels are much easier to estimate than are "first effect" or other levels indicative of injury.

Watch out: When considering the possible toxicity or health hazards of exposure to gases in buildings, readers should note that

Individual sensitivity and potential health effects on individuals may vary widely and
There may be multiple (un-cited) recommended or allowable exposure limits coming from various sources.
We have seen wide variation in allowable exposure limits, for example, for Carbon Monoxide permissible exposure limits -(CO PELs).

Of the several industrial hygiene standards-setting groups in this country, the most important and/or most quoted are the National Institute for Occupational Safety and Health (NIOSH), the Occupational Safety and Health Administration (OSHA), and the American Conference of Governmental Industrial Hygienists (ACGIH).

Only those standards promulgated by OSHA (called Permissible Exposure Limits or PELs) have the force of law; the others are advisory except that OSHA has claimed the power to force compliance with NIOSH "Recommended Standards" if it chooses to do so. The main advantage of ACGIH Threshold Limit Values (TLVs) is that they are reviewed and updated annually; neither NIOSH nor OSHA updates its standards with any regular frequency.

Health Hazards of some Gases, Jack E. Peterson, P.E., CIH, Ph.D., May, 1987

Ammonia Gas Exposure Hazards

Ammonia is very soluble in water and, in water, hydrolyzes to ammonium hydroxide, a strong base. These properties insure that ammonia gas is an upper respiratory tract and eye irritant. It dissolves in the water of mucous membranes (or tears), hydrolyzes and irritates rapidly mainly because of the high pH that results.

Because of this biological property of prompt irritation, most people cannot tolerate a concentration of ammonia in air sufficiently high to be harmful. Its warning properties assure a negligible hazard from ammonia inhalation if escape is possible. As with formaldehyde and other good upper respiratory tract irritants, people can become "hardened" to the irritation of ammonia and after several exposures can tolerate much higher concentrations than can an unexposed individual.

Under some circumstances, a hardened person can accept an exposure that will result in inflammation of the throat, bronchi, and possibly eyes. An exposure to 300 to 500 ppm for 30 to 60 minutes would cause such an effect and might be hazardous to health.

The current TLV for ammonia is 25 ppm with a short-term exposure limit of 35 ppm. Both were designed to be low enough to cause no irritation in unhardened people. The OSHA PEL for ammonia is 50 ppm, as is the NIOSH Recommended Standard.

Ammonia Gas Properties, Exposure Pathology, Symptoms, Treatment, Prognosis

The following information about exposure to ammonia gas hazards is based on information from U.S. Army Field Manual 8-285 Chapter 10, Noxious Chemicals:

Physical Properties of ammonia:

Ammonia is a colorless gas, soluble in water, with a pungent odor. Liquid ammonia is a vesicant.

Occurrence if Ammonia gas in Military Operations or in Civilian Environments:

Ammonia gas has not been used in warfare but may be encountered in industrial accidents, bombings involving refrigeration plants, and holds of ships as a product of decomposing material.

Pathology of Human Exposure to Ammonia or Ammonia Gas

Exposure to high concentrations of ammonia produces prompt and violent irritation of the eyes and respiratory tract. There may be spasm a nd edema of the glottis or necrosis of the laryngeal mucous membranes. Pulmonary edema may develop and may be complicated by bronchopneumonia.

Symptoms of Exposure to Ammonia or Ammonia Gas

High concentrations produce violent, burning pain in the eyes and nose, lacrimation, sneezing, pain in the chest, cough, spasm of the glottis, and pulmonary edema. Often there is a temporary reflex cessation of respiration with spasm of the glottis. Edema of the glottis at a later period may seriously interfere with breathing. Concentrations of 0.1 percent are intolerable to humans.

Treatment for Exposure to Ammonia Gas

Treatment for ammonia gas exposure consists of prompt removal to pure air and administration of assisted ventilation. Later measures are directed toward the treatment of pulmonary edema, bronchitis, and pneumonia.

Prognosis for Humans Exposed to Ammonia Gas

The mortality for people exposed to ammonia gas is high following severe exposure. With low concentrations, recovery is usually rapid although bronchitis may persist.

Arsine Gas Exposure Hazards - Arsenic Hydride

Arsine is arsenic hydride, the combination of arsenic metal and hydrogen gas. Arsine is a water-soluble gas. It is given off whenever freshly-generated hydrogen contacts metallic arsenic especially in an acid environment. As a lead-acid storage battery approaches full charge (in formation or boosting or simply charging), some hydrogen evolves. When arsenic is present in the grids of that battery, some arsine is formed and escapes through the vent caps. If the battery is seriously overcharged, much hydrogen (and arsine if a lead-arsenic alloy is used in the plates) may be given off; an ignition source can then cause the gases to explode.

The main acute effects of arsine on people are lung irritation and hemolysis (destruction of red blood cells). Both effects are usually delayed and do not appear until several hours after the exposure that typically occurs during the acid washing of a tank that has contained an arsenical slag.

Of the two, hemolysis is usually the more serious and is first indicated by pink or red urine that becomes darker with successive voidings. Debris from damaged red cells "clogs up" the kidneys, leading to extremely severe pain and, eventually, to a stoppage of urine flow. Because red cells have been destroyed, severe anemia results so that oxygenation of tissue is impaired. In addition, there may be severe lung irritation (impeding proper oxygenation of blood); death may result from asphyxiation a few days after the exposure.

These effects of arsine are completely avoided if 8-hr exposures are kept at or below 200 ug/cu. m, (0.05 ppm), the TLV and PEL. Whether or not arsine has any chronic effects (such as the causation of cancer) is not known because there has been no study of people or animals chronically exposed to this material.

There are, therefore, no data available indicating that arsine is a carcinogen. Of the three "standards setting" groups, NIOSH is the only one that recommends extremely strict control (2.0 ug/cu. m as determined by 15-min samples) of arsine exposures.

All of the information upon which NIOSH based its Recommended Standard was (and is) available to anyone, including ACGIH and OSHA, of course. If half of the arsine inhaled is excreted in the urine (as seems to be the case for particulate arsenic compounds), then, inhalation of 200 ug/cu. m should result in a urinary concentration on the order of 666 ug/L. Under these circumstances, then, urinary arsenic concentrations might well be useful as indices of arsine exposure/absorption. However, there is very little data in the literature concerning urine concentrations resulting from measured arsine exposures.

Also see ARSENIC IN WATER for more information about arsenic poisoning symptoms and effects.

Bromine Gas Exposure Hazards

Bromine is the only halogen that is a liquid at room temperature. Its color is a dark rust red as a liquid and as a gas. As opposed to the "upper respiratory tract" irritants and "lower respiratory tract" irritants, bromine is a "whole respiratory tract" irritant.

That is, its main effects are exerted on the deep lung and may be delayed for some time after the exposure, but it does have far better warning properties than do the lower respiratory tract irritants such as nitrogen dioxide, phosgene, and ozone. Bromine causes eye irritation and lacrimation (tearing) in concentrations below 1 ppm but above the TLV (and PEL) of 0.1 ppm.

Concentrations irritating to the eyes should not be tolerated for more than 15 minutes. Prolonged overexposure to bromine can cause dizziness, headache, and cough followed by abdominal pain and, later, lung edema and pneumonia if the exposure is severe enough. None of these signs/symptoms is at all likely, however, if irritation (eye or respiratory tract) is used as a warning to leave the area of exposure.

Carbon Dioxide Gas Exposure Hazards

Our CO2 articles include:

CARBON DIOXIDE - CO₂
  CO₂ POISONING SYMPTOMS
  CO₂ HEALTH EFFECTS
  CO₂ EXPOSURE LIMITS
  TYPICAL CO₂ LEVELS
OXYGEN - O₂
GAS DETECTION INSTRUMENTS

The highest TLV (and PEL) assigned to any material is assigned to carbon dioxide, namely 5000 ppm (NIOSH has recommended a Standard of 1.0% or 10 000 ppm for a 10-hr work shift with a ceiling of 3.0% or 30 000 ppm for any 10-min period). Furthermore, these concentrations are far more an expression of good practice than a line between "safe" and "dangerous."

Actually, the concentration of carbon dioxide must be over about 2% (20 000 ppm) before most people are aware of its presence unless the odor of an associated material (auto exhaust or fermenting yeast, for instance) is present at lower concentrations. Above 2%, carbon dioxide may cause a feeling of heaviness in the chest and/or more frequent and deeper respirations. If exposure continues at that level for several hours, minimal "acidosis" (an acid condition of the blood) may occur but more frequently is absent.

As the carbon dioxide concentration climbs above a few percent, the concentration of oxygen in the air inhaled begins to be affected. At 6% carbon dioxide, for instance, the concentration of oxygen in air has decreased from 20.96 to 19.9%. OSHA has indicated that the lowest oxygen concentration for shift-long exposure is 19.5%, corresponding to a carbon dioxide concentration well above 60 000 ppm (6%). Carbon dioxide concentration, not oxygen concentration, is limiting in such circumstances.

Details about Carbon Dioxide Poisoning:See Carbon Dioxide Gas Toxicity hazard levels, poisoning symptoms, & testing. Our CO2 articles include:

CARBON DIOXIDE - CO₂
  CO₂ POISONING SYMPTOMS
  CO₂ HEALTH EFFECTS
  CO₂ EXPOSURE LIMITS
  TYPICAL CO₂ LEVELS

Carbon Monoxide Gas Exposure Hazards

Our CO articles include:

CARBON MONOXIDE - CO
  CO ALARM CAUSES
  CO EXPOSURE LIMITS
  CARBON MONOXIDE INSPECTION
  CO DETECTOR OPTIONS
  MEDICAL EFFECTS of CO
  POISONING SYMPTOMS - CO

Carbon monoxide is a colorless, odorless, tasteless gas that, physiologically, is a chemical asphyxiant. When inhaled, it combines with hemoglobin more readily than does oxygen, displacing oxygen from hemoglobin and thereby interfering with oxygen transport by the blood.

A person suffering from carbon monoxide (CO) intoxication may first experience euphoria (similar to the effect of a martini or two), then headache, followed by nausea and possibly vomiting as the concentration of carboxyhemoglobin in the blood increases.

To prevent these effects, OSHA has established a PEL of 50 ppm for an 8-hr exposure, identical to the TLV. NIOSH, on the other hand, has decided to be more conservative and recommends a standard of 35 ppm. All of these concentrations refer to exposures with durations of 8 hr/day, 40 hr/week for a working lifetime and all are attempts to establish a "no effect" level.

Details about Carbon Monoxide Poisoning:See Carbon Monoxide Gas Toxicity hazard levels, poisoning symptoms, & testing

Nitrogen Oxides Gas Exposure Hazards

The only oxides of nitrogen of concern in most industrial and commercial enterprises are nitric oxide (NO) and nitrogen dioxide (NO2). The main source of both gases is combustion and only under special conditions are appreciable concentrations of nitric oxide formed. Nitric oxide oxidizes in air to nitrogen dioxide which is the more toxic of the two gases.

Nitric oxide, when inhaled, combines with hemoglobin to form nitrosohemoglobin, a carboxyhemoglobin-like material that rather rapidly is oxidized to methemoglobin. That is, its main effect is to inhibit transportation of oxygen

by the blood. Its TLV and PEL are both 25 ppm. Nitrogen dioxide is a deep lung irritant. That is, this gas is not very soluble in water and thus is capable of penetrating deeply into the lung where it undergoes hydrolysis to other materials (acids) that are the actual irritants. Because hydrolysis is a necessary condition for irritation and because hydrolysis takes an appreciable amount of time (several hours in many cases), nitrogen dioxide is known as a delayed-action lung irritant.

Nitric oxide is colorless and may have little or no odor. Nitrogen dioxide (and/or its dimer, nitrogen tetraoxide) is rust red and has a "typical" odor quite notable at 5 ppm and causes eye and nose irritation at 10 to 20 ppm. Currently (1987), the TLV is 3.0 ppm with an STEL of 5.0 ppm; the PEL is 5.0 ppm. NIOSH has recommended 1.0 ppm for a Standard.

Oxides of Nitrogen Gas Properties, Exposure Pathology, Symptoms, Treatment, Prognosis

The following information about exposure to ammonia gas hazards is based on information from U.S. Army Field Manual 8-285 Chapter 10, Noxious Chemicals:

Physical Properties of Nitrogen Oxide Gas

The term “oxides of nitrogen” applies to a mixture consisting of nitric oxide, nitrogen dioxide, and nitrogen tetroxide. Nitric oxide is colorless. The other oxides are red-brown gases.

Occurrence of Nitrogen Oxide Gas in Military Operations or Civilian Exposure

(1) The danger of nitrous fume poisoning is or cordite) are burned or detonated in poorly ventilation areas. This may occur in gun pits, armored vehicles, ship magazines, and turrets. This may also occur in mining and tunneling operations.

(2) In addition, nitrous fumes are emitted from fuming nitric acids (white and red) and are generated by the combustion of certain plastics.

Watch out: improper use of ozone generators to try to kill mold or odors may oxidize certain common plastics found in buildings, leading to the hazards discussed here. [OPINION-DF]. See OZONE HAZARDS and OZONE for MOLD OR ODORS.

Pathology of Human Exposure to Nitrogen Oxide Gases

Inhalation of nitric oxide causes the formation of methemoglobin and does not appear to lead to any tissue lesions. Inhalation of nitrogen dioxide results in the formation of nitrite that leads to a fall in blood pressure and to the production of methemoglobin. Inhalation of high concentrations of nitrogen dioxide (above 0.5 mg per liter) causes rapid death without the formation of pulmonary edema.

Somewhat lower concentrations of nitrogen oxide gas exposure result in death with the production of yellow, frothy fluid in the nasal passages, mouth, and trachea and marked pulmonary edema. The findings in other tissues are negligible.

Symptoms of Exposure to Nitrogen Oxide Gases

The symptoms following inhalation of nitrous fumes are due chiefly to nitrogen dioxide. The symptoms presented depend upon the concentration of the gas. Exposures to higher concentrations cause severe local irritation with choking and burning in the chest, violent coughing, yellow staining of the mucous membranes, expectoration of yellow-colored sputum, headache, and vomiting.

Often, these early symptoms may be mild or entirely absent. After 2 to 24 hours, symptoms start with coughing, nausea, vomiting, frothy sputum, dyspnea, cyanosis, convulsions, and signs of lung edema. This train of symptoms may result in death.

At nitrogen gas exposures to very high concentrations for short periods of time, the onset of symptoms is very sudden and marked. Convulsions, unconsciousness, and respiratory arrest occur within a short time and death may follow rapidly.

Diagnosis of Nitrogen Oxide Gas Exposure

The diagnosis is made from the history, symptoms described, and sometimes the pungent odor of the gas or the yellow discoloration of the exposed mucous membranes.

Treatment for Exposure to Nitrogen Oxide Gas

Treatment of casualties with symptoms of pulmonary irritation is the same as for CG poisoning (chap 5).

Prognosis for People Exposed to Nitrogen Oxide Gases

The few cases with symptoms referable to the CNS either die quickly or, on removal to fresh air, recover spontaneously. Fatal cases usually die within 48 hours. Bronchopneumonia and varying degrees of pulmonary fibrosis and emphysema often follow recovery from the acute stage.

NOX Reference: Toxicity of Oxides of Nitrogen

Nitrogen Oxides: Air Quality Criteria for Oxides of Nitrogen, Vol III of III, US EPA, EPA600/8-91/049cF, August 1993, web search 08/28/2010, original source: http://nepis.epa.gov [Large PDF 25MB]
Key chapters in this document evaluate the latest scientific data on (a) health effects of NOx measured ill laboratory animals and exposed human populatIOns and (b) effects of NOx on agricultural crops, forests, and ecosystems, as well as (c) NOx effects on visibility and nonbiological materials. Other chapters describe the nature, sources, distribution, measurement, and concentratiOns of NOx m the environment These chapters were prepared and peer revived by experts from various state and Federal government offices, academia, and private industry for use by EPA to support decision makIng regarding potentIal risks to public health and the enVIronment Although the document IS not intended to be an exhaustIve literature reVIew, It IS intended to cover all the pertinent literature through early 1993

Ozone Gas Exposure Hazards

Ozone is a kind (called an "allotrope") of oxygen . It is formed in the ionosphere by the action of ultraviolet radiation from sunlight on oxygen. Lightning strokes are another natural source of ozone and the characteristic odor of that material can often be noted during and after a thunderstorm.

When pollutants are emitted into the air either by man or nature, almost all are eventually removed by one or more of several processes including reaction under the influence of ultraviolet radiation. One series of such reactions results in the formation of ozone as a "secondary" (formed by reaction in the air) air pollutant, often in rather high concentrations (several tenths of a part per million).

As ozone can be formed by nature's sparks (lightning), it can also be formed by man's. Whenever an electrical spark or corona occurs in air, some ozone is formed. This accounts for the characteristic odor noted near an operating electric motor such as an electric shaver.

Because ozone is found in so many places, its toxicity (ability to injure a living organism by other than mechanical means) has been investigated extensively since the early 1900s. Experimentation has shown that the odor of ozone can be detected and identified by most people at a concentration of from 0.02 to 0.05 ppm (parts ozone per million parts air + ozone). As the concentration increases to a few tenths of a part per million, the first effect noted is likely to be a feeling of dryness in the back of the throat. If a concentration on the order of 0.2 or 0.3 ppm is inhaled more or less continuously for several hours to a few days some lung irritation may result.

Higher concentrations of ozone can produce several kinds of toxic effects if exposures are sufficiently prolonged. Eye irritation (despite newspaper and TV accounts seemingly indicating otherwise) occurs only at concentrations high enough to result in other, more severe, toxic effects.

Ozone is a very reactive substance. It will readily react with just about any material capable of being oxidized, and with many that are not. The material with which it reacts may be a gas or vapor, a particle floating in the air (a mold spore, for example), or a solid (or liquid) surface. For this reason, when ozone is present in most enclosed spaces its concentration declines quite rapidly with time. Of course, if ozone is being generated more rapidly than it is destroyed by reaction, its concentration can build up. This is the main reason why devices that produce relatively large amounts of ozone are safe only in relatively large enclosures and why the ozone generation rate should be reduced in small enclosures.

Ozone is well known for its ability to eliminate certain odors. How this is accomplished is controversial. At concentrations just above the odor threshold, some odors do seem to vanish. The main reason for this may be ozone's ability to desensitize the olfactory apparatus so that the odors can no longer be perceived. Some evidence indicates that this may be the case at least occasionally. Other evidence indicates that ozone may react with the odor-causing substances, eliminating them from the air (this is probably the only mechanism that operates when concentrations are below the odor threshold).

Finally, some people have insisted that even if ozone does not paralyze the olfactory sense, its odor is such that it "masks" other odors. Perhaps all three mechanisms operate, each in its own area of effectiveness. As with all other materials, ozone has a dose-effect relationship with a threshold. That is, once the threshold dose has been exceeded, toxic effects are proportional to dose.

For inhaled gases, dose is proportional to both time and concentration. If the duration of exposures cannot be controlled (as is usually the case), then the concentration must be kept low enough so that no injury will occur even from prolonged and repeated exposures.

For ozone, that "threshold" concentration is 0.1 ppm. So long as concentrations are kept at or below that level, injury is not expected even in the most sensitive workers so long as their exposure durations coincide reasonably well with or are less than the 8 hr/day, 40 hr/wk regimen. This "threshold" level is accepted by the American Conference of Government al Industrial Hygienists (and is called the Threshold Limit Value by that organization) and by the Occupational Safety and Health Administration, OSHA.

The TLV or OSHA's Permissible Exposure Level (PEL) is not a fine line between safe and non-safe. Instead, it represents the best judgment of a group of experts of the highest concentration that can be inhaled repeatedly by a population of workers with no resulting injury. Higher concentrations may or may not have any particular effect on a specific individual.

Ozone is a highly toxic gas but even highly toxic substances can be encountered safely. The main concern with this material is that concentrations to which people are exposed do not average more than 0.1 ppm over an 8-hr day, and do not exceed that value by more than a factor of 2 or 3 during the exposure.

More depth: see Ozone Warnings - Use of Ozone as a "mold" remedy is ineffective and may be dangerous. Our complete list of articles about ozone can be found at these links:

OZONE as a "CURE" for TOXIC INDOOR MOLD
WHAT IS OZONE- O₃
OZONE AIR PURIFIER WARNINGS
OXYGEN - O₂
OZONE HAZARDS
OZONE EXPOSURE STANDARDS
OZONE TESTS
OZONE MSDS
OZONE TOXICITY
OZONE ODORS, MOLD, REFS

Propane Gas or LP Gas Exposure Hazards

The greatest LP gas or propane gas exposure risk other than fire or explosion, would be not the exposure to LP gas or propane gas itself but the prolonged absence of sufficient oxygen if someone is enclosed in a space with high concentration of propane. No long term exposure health risks associated with LP gas or propane have been reported at low concentrations.

At air concentrations below 1000 ppm propane is virtually non-toxic. Brief exposures to 10,000 ppm cause no symptoms; 100,000 ppm can produce slight dizziness after a few minutes of exposure, but is not noticeably irritating to the nose and throat.

Propane is a simple asphyxiant. High concentrations of propane can displace oxygen and cause asphyxiation. Oxygen content in the atmosphere must not be allowed to fall below 18%.

Effects of oxygen deficiency are: 12-16% breathing and pulse rate increased, muscular co-ordination slightly disturbed; 10-14% emotional upset, abnormal fatigue, disturbed respiration; 6-10%: nausea and vomiting, collapse or loss of consciousness; below 6%: convulsive movements, possible respiratory collapse and death.

The gas does not affect the skin. Contact with liquified gas escaping from its high pressure cylinder may cause frostbite. Symptoms of mild frostbite include numbness, prickling and itching in the affected area. Symptoms of more severe frostbite include a burning sensation and stiffness of the affected area. The skin may become waxy white or yellow. Blistering, tissue death and gangrene may also develop in severe cases.

Close range contact with liquefied propane gas may cause injury characteristic of a thermal burn with swelling, fluid accumulation and extreme redness. Tissue death and gangrene may also develop.

The gas does not cause eye irritation. Contact with liquified gas escaping from its high pressure cylinder may cause freezing of the eye. Permanent eye damage or blindness could result. - Canadian Centre for Occupational Health and Safety

In some areas propane gas and similar fuels may be referred to by the name of their distributor, such as "Cadac" gas referring to the blue fuel gas cylinders and related products sold in South Africa.

Propylene Gas Exposure Hazards

Propylene is a simple asphyxiant (that is, it acts by dilution of oxygen) and a rather poor anesthetic. Extremely high concentrations are required to produce any effect at all.

No TLV or PEL has ever been established for this material and NIOSH has not recommended a Standard. Its lower explosive limit is 2% in air (the upper is 11.1%) and a reasonable value for a maximum permissible concentration (suggested by Gerarde in Patty's Industrial Hygiene and Toxicology, vol 2, p. 1204, Interscience, New York, 1963) is 1/5 of the LEL or 4000 ppm.

Sulfur Dioxide Gas Exposure Hazards & Effects

For sulfur dioxide, the TLV had been 5.0 ppm for many years, but in 1978 ACGIH announced its intention to reduce that TLV to 2.0 ppm; that was done in 1980. The reason for this was recent information indicating that chronic (long term, repeated) exposure to sulfur dioxide concentrations near 5.0 ppm was found to have some minimal effects on working populations.

Sulfur dioxide is an upper respiratory tract irritant and acute (single or short-term) exposures cause nothing but irritation of the nose and throat. Long term exposures to sulfur dioxide concentrations in excess of 2.0 ppm can be expected in some cases to cause minor lung changes.

Potential Symptoms of sulfur dioxide gas exposure: Eye, nose, throat irritation; rhinorrhea, nosebleeds; choking, coughing, shortness of breath, chest pain, pulmonary edema, cyanosis; reflex bronchoconstriction; eye, skin burns; frostbite (on contact with liquid); asthma; chronic bronchitis. [12]

Affected organs: eyes, skin, respiratory system.

Health Effects of sulfur dioxide gas exposure: Irritation-Eye, Nose, Throat, Skin---Marked (HE14) Mutagen (HE2); Respiratory effects--- Bronchoconstriction, pulmonary edema, reactive airways dysfunction syndrome (HE9 and HE11); Suspect reproductive effects (HE5)

Affected Organs: Eyes, skin, respiratory system

OSHA Note:

Sulfur dioxide is listed by the FDA as generally recognized as safe when used in accordance with good manufacturing practice as a preservative of fruits or vegetables (21 CFR 182.3862). [12]

Sulfur Oxides Toxicity and Exposure Limits References:

Sulphur dioxide Sulfur dioxide SO2 exposure limits (PELS typically are at 5 ppm or less by some standards) are at Sulfur Dioxide Gas in our article titled: GAS EXPOSURE LIMITS & STANDARDS

Watch out: NIOSH Immediately Dangerous To Life or Health Concentration (IDLH): 100 ppm

Sulfur dioxide & other Oxides: Air Quality Criteria for Particulate Matter and Sulfur Oxides, Vol. III, US EPA, Environmental Criteria and Assessment Office, Research Triangle Park NC 27711, Dec. 1982, EPA-600/8/2-029c. Web search 08/26/2010, original source: http://nepis.epa.gov [large PDF]

OSHA citations for sulphur dioxide hazards & effects:[12]

NIOSH Pocket Guide to Chemical Hazards: Sulfur dioxide.
International Chemical Safety Cards (WHO/IPCS/ILO): Sulphur dioxide.
Koksal, N., Hasanoglu, H.C., Gokirmak, M., Yildirim, Z. and Gultek, A.: Apricot sulfurization: an occupation that induces an asthma-like syndrome in agricultural environments. Am. J. Ind. Med. 43(4): 447-453, 2003.
Piirilä, P.L., Nordman, H., Korhonen, O.S. and Winblad, I.: A thirteen-year follow-up of respiratory effects of acute exposure to sulfur dioxide. Scand. J. Work Environ. Health 22(3): 191-196, 1996.
Pohanish, R.P. (editor): Sulfur Dioxide. In, Sittig's Handbook of Toxic and Hazardous Chemicals and Carcinogens, Fourth Ed., Vol. 2. Norwich, NY: Noyes Publications, William Andrew Publishing, 2002, pp. 2116-2119.

Frequently Asked Questions (FAQs) about toxicity of various gases and gas exposure limits

Question: Sulphur dioxide SO₂ exposure limits?

[This question originally appeared in reader comments at CARBON DIOXIDE - CO2] - Ed.]

This article is interesting. I think I understand the concept but I have an application that use an analyzer.
To calibrate this instrument, I need to use an 8% SO2 compress gas cylinder (cylinder capacity 5m3). This is located in a sealed 10x10x10 room, so my room is 1000m3 and unventilated.
Worst case scenario, the cylinder empties in this room. Is this an accute risk knowing that 3000 ppm is the LC50 (1/2hour) limit and the bottle contains 80000ppm? I have a bit of difficulties to put some math around this. Could you please explain?

I think 8% concentration x 5m3 cylinder = 0.4m3 of SO2 release in the room.
The gas will occupy 0.4m3/1000m3 = 0.04% of the room volume which is 400ppm.
400ppm < LC50 3000ppm = Low Risk?

- Syl

Reply:

Syl, your question was a bit unclear and makes me worry that you are messing with gases without proper education or preparation. You are asking about Sulphur dioxide (SO₂) in an article about Carbon dioxide (CO₂) - in any event, if you are asking about recommended exposure limits for Sulphur dioxide SO2,

OSHA PELs for SO₂ and other recommended exposure limits are given at Sulfur Dioxide Gas in our article titled: GAS EXPOSURE LIMITS & STANDARDS. Depending on the standard, SO₂ PELs range among 0.25 ppm, 2 ppm, or 5 ppm. - all significantly less than your 400 ppm.