Photograph of a 120Vold carbon monoxide detector device Carbon Monoxide Gas Guide
CO Exposure, Carbon Monoxide CO Poisoning Symptoms, Carbon Monoxide Exposure Limits, Cause of Death, Chronic Exposure Effects, CO Gas Testing Procedures

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Carbon monoxide (CO) gas hazards home page: carbon monoxide alarms, effects, tests, exposure limits, medical effects. This article describes the toxicity and exposure limits for exposure to carbon monoxide gas (CO).

In companion articles we also describe procedures for inspecting buildings for evidence of carbon monoxide hazards, including visual clues that may suggest a safety problem even if CO testing is not detecting carbon monoxide at the time of the inspection. We describe carbon monoxide testing methods, the medical effects of carbon monoxide exposure, and we cite authorities who set the limits on carbon monoxide exposure in different environments.

We give references and explanation regarding Toxicity of Carbon Monoxide, based on literature search and including research on OSHA, NIOSH, and at the old Compuserve's Safety Forum. This is background information, obtained from expert sources. This text may assist readers in understanding these topics.

We also provide a MASTER INDEX to this topic, or you can try the page top or bottom SEARCH BOX as a quick way to find information you need.

Guide to Inspecting buildings for Visible Evidence of Conditions Likely to Produce Dangerous Carbon Monoxide Gas

Discussed here: Guide to Inspecting buildings for Visible Evidence of Conditions Likely to Produce Dangerous Carbon Monoxide Gas,

IF YOU SUSPECT CARBON MONOXIDE POISONING GO INTO FRESH AIR IMMEDIATELY and get others out of the building, then call your fire department or emergency services for help. Links on this page also direct the reader to carbon dioxide gas information in a separate document.

Seek prompt advice from your doctor or health/safety experts if you have any reason to be concerned about exposure to toxic gases. Carbon monoxide poisoning can be fatal but exposure at lower limits can produce flu-like symptoms and headaches that are often mistaken for ordinary illness.

The fact that you cannot see nor smell dangerous carbon monoxide gas does not mean that there is nothing to look for when assessing the safety of heating equipment. Not only are there easily spotted installation errors (the first list below), there may be more subtle but easily visible errors if you know what to look for (the second list below).

Safety Suggestions: Install Carbon Monoxide Detectors in addition to Smoke Detectors

Carbon monoxide detectors are inexpensive and readily available, both as a battery-operated unit and as a unit that plugs into an electrical outlet in the home. No home should be without this safety protection, and homes with gas-fired equipment (natural gas or LP propane), space heaters, or other sources of risk should be extra cautious. Smoke detectors do not protect against carbon monoxide poisoning, and the opposite is also true. Carbon monoxide detectors do not warn of smoke or fire.

Examples of visible building conditions risking carbon monoxide hazards

This is by no means the complete list of errors that can cause dangerous carbon monoxide exposure in buildings, but here are some common foul ups outside of the workplace that can cause dangerous levels of indoor carbon monoxide:

Other clues which can suggest a risk of carbon monoxide hazards in buildings

Procedures for Testing for Carbon Monoxide Gas Leaks, Exposure, Hazards

In addition to the installation of CO monitoring alarms in buildings, a variety of electronic and gas sampling equipment is available to make spot checks for hazardous gases. I have and have used a variety of these devices under a wide range of conditions.

While a "positive" indication of a gas is an important indicator of a hazard, a "negative" or "not found" result is nothing to rely on.

The fact that dangerous levels of CO are not present in a building at a particular instant is absolutely no guarantee that dangerous levels of CO (for example) may not occur even moments later. For example, opening a window, turning on a fan or clothes dryer, closing a door, and similar innocent acts can significantly change air flow, combustion air, and other building conditions.

Therefore spot tests for dangerous gases should not be relied upon to guarantee building safety. This is why the list of visual inspection items and proper heating equipment maintenance are so important.

MEDICAL EFFECTS of CO - Medical effects of Carbon Monoxide (CO) Poisoning

Watch out: the immediate and most severe effect of carbon monoxide exposure and poisoning can be death, typically loss of consciousness followed by death. In a recent example of carbon monoxide fatality, the manager of a Legal Seafoods restaurant in Huntington Long Island (New York) died and twenty-seven others were sickened as a result of carbon monoxide poisoning traced to a faulty water heating equipment vent.

News media noted that while CO detectors are required in homes just about everywhere, laws requiring carbon monoxide detectors in the workplace are not (as of February 2014) in place in New York where this death occurred. The LA Times news report illustrates the pernicious odorless nature of carbon monoxide gas: when restaurant workers reported that the assistant-manager was unconscious, apparently from a head injury due to a fall, rescue workers, themselves sickened when working in the building, found the restaurant manager also unconscious, but he was later pronounced from carbon monoxide poisoning. - Los Angeles Times (2014)

Here we discuss the effects of CO exposure or chronic CO exposure at less severe levels when death, the ultimate penalty, has not been incurred.

Many sources I (DF) reviewed indicated that if carbon monoxide exposure was sub-acute, that is if the person did not lose consciousness and was removed from the CO exposure before losing consciousness, then any medical effects were temporary. Indeed detection of CO exposure at a hospital is problematic since CO leaves the bloodstream quickly once a person is exposed to normal air.

However there is evidence that lasting physical damage may occur from carbon monoxide exposure, though the popular press has not (2006) discussed the exposure level and duration necessary for these effects.

Heart muscle damage occurs from Carbon Monoxide (CO) exposure, screening recommended

31 January 2006 - The New York Times Science Section reports on a new study, released in JAMA's January 25 2006 Magazine Issue, and which indicated that people exposed to carbon monoxide suffer damage to their heart muscles and are at much greater risk for heart attacks in later years.

The Times article asserted that CO Poisoning results in 40,000 emergency visits a year in the United States - the most common accidental poisoning event in the U.S. with an annual average accidental death rate of about 1000 people and average suicidal death rate of about 2400 people. [U.S. CDC] Five percent of such patients die in the hospital. Research was not cited regarding sub acute exposures and exposures which do not result in a visit to a hospital. -- New York Times Science Section, January 31, 2006 p. F6, "After Crisis, Carbon Monoxide Still Takes a Toll."

The carbon monoxide exposure and heart muscle damage study was led by Christopher R. Henry, Minneapolis Heart Institute Foundation, in the current [Jan 2006] Journal of the American Medical Association The study examined the medical history of 230 people exposed to carbon monoxide and treated at hospital between 1994 and 2002, following their health to 2005.

After 7 1/2 years, in this otherwise low risk (of heart failure) population, 25% of the originally-surviving patients had died - a rate about three times the average heart failure death rate statistic. For people who had suffered heart muscle damage the mortality rate was 38% with half of the mortalities being (apparently) traced to cardiovascular problems.

The study concludes that people who are exposed to carbon monoxide should be screened for heart muscle damage. Heart muscle damage from CO poisoning (in the study) was characterized by elevated levels of cardiac troponin I (a type of protein) or creatine kinase-MB (a type of enzyme), and/or changes in diagnostic electrocardiogram (ECG). -- DJ Friedman paraphrasing the NY Times article and JAMA's news release regarding this study.

More references for this study:
see: Heart Injury Due to Carbon Monoxide Poisoning Increases Long-Term Risk of Death, JAMA January 25 2006. AMA news release 2006. This study was supported by an unrestricted educational grant from the Minneapolis Heart Institute Foundation. Study copies may be available from the JAMA/Archives Media Relations Department at 312/464-JAMA (5262) -

Carbon Monoxide Poisoning Information From U.S. Army Field Manual 8-285:

Pathology of CO poisoning: Asphyxiation is caused by the inactivation of blood hemoglobin through a combination with CO. The resultant anoxia may produce nervous system changes. Postmortem examinations reveal little beyond the characteristic cherry red color of the blood and hemorrhages in the brain

Symptoms of CO poisoning: Carbon monoxide is very insidious in its action and poisoning may occur without appreciable initial signs. The symptoms progress from throbbing headaches, vertigo, yawning, and poor visual acuity, to the development of cherry red mucous membranes, weakness and coma, subnormal temperature, feeble pulse, and death.

Diagnosis of CO poisoning: The diagnosis is made from the circumstances of exposure and the appearance of
cherry red skin and mucous membranes color.

Protection against CO poisoning: In general, exposure to CO should be avoided whenever possible.

Adequate ventilation should be provided for all enclosed spaces where CO may be produced. The safety of air in the space for people to breathe may be tested by standard CO indicator or detector devices. Individuals required to enter closed areas where high concentrations of CO are (known or suspected to be) present must be provided with respiratory protective devices. For the approved devices, refer to TB MED 502.

Note: For a helpful discussion of just what constitutes "adequate venitlation", see Offermann, Francis (Bud) J., P.E., C.I.H., ASHRAE & Mark Nicas, Ph.D., MPH, C.I.H., USE WITH ADEQUATE VENTILATION ? [PDF], ASHRAE Journal, May 2018.

Treatment for Carbon Monoxide Poisoning: Remove the victim to pure air. If respirations are weak or absent, begin assisted ventilation at once. Oxygen, if available, should be given by a face mask, preferably under pressure (up to 3 atmospheres). The patient should be kept warm and at rest (sedated, if necessary).

After resuscitation, initial supportive measures (such as the need for parenteral fluids and pressor drugs) can best be decided by the medical officer. Ordinarily, methylene blue solution, morphine, and atropine should NOT be used (TB MED 269).

Prognosis for people exposed to carbon monoxide poisoning: The longer the period of the coma,
the less the chance for recovery. Most mildly exposed individuals recover with early treatment. Tachycardia and dyspnea may continue for months. There may be CNS disturbances ranging from simple neuritis to mental deterioration.

CO EXPOSURE LIMITS - Carbon monoxide exposure limits PEL and TLV set by OSHA and NIOSH

This section has been moved to CO EXPOSURE LIMITS.

To convert between % and ppm concentration of carbon monoxide air see CONVERT PPM to % CONCENTRATION

Carbon Monoxide Hazards - Carboxyhemoglobin levels and related health effects on people

Quoting from CPSC Indoor Air Pollution Book Online Copy

Carbon monoxide is an asphyxiant. An accumulation of this odorless, colorless gas may result in a varied constellation of symptoms deriving from the compound's affinity for and combination with hemoglobin, forming carboxyhemoglobin (COHb) and disrupting oxygen transport. The elderly, the fetus, and persons with cardiovascular and pulmonary diseases are particularly sensitive to elevated CO levels.

Methylene chloride, found in some common household products, such as paint strippers, can be metabolized to form carbon monoxide which combines with hemoglobin to form COHb. The following chart shows the relationship between CO concentrations and COHb levels in blood.

Tissues with the highest oxygen needs -- myocardium, brain, and exercising muscle -- are the first affected. Symptoms may mimic influenza and include fatigue, headache, dizziness, nausea and vomiting, cognitive impairment, and tachycardia. Retinal hemorrhage on funduscopic examination is an important diagnostic sign19, but COHb must be present before this finding can be made, and the diagnosis is not exclusive.

Studies involving controlled exposure have also shown that CO exposure shortens time to the onset of angina in exercising individuals with ischemic heart disease and decreases exercise tolerance in those with chronic obstructive pulmonary disease (COPD)20.

Note: Since CO poisoning can mimic influenza, the health care provider should be suspicious when an entire family exhibits such symptoms at the start of the heating season and symptoms persist with medical treatment and time.

Graph of the relationship between CO and COHb levels in blood

Relationship between carbon monoxide (CO) concentrations and carboxyhemoglobin (COHb) levels in blood

Predicted COHb levels resulting from 1- and 8-hour exposures to carbon monoxide at rest (10 l/min) and with light exercise (20 l/min) are based on the Coburn-Foster-Kane equation using the following assumed parameters for nonsmoking adults: altitude = 0 ft; initial COHb level = 0.5%; Haldane constant = 218; blood volume = 5.5 l; hemoglobin level = 15 g/100ml; lung diffusivity = 30 ml/torr/min; endogenous rate = 0.007 ml/min.

Source: Raub, J.A. and Grant, L.D. 1989. "Critical health issues associated with review of the scientific criteria for carbon monoxide." Presented at the 82nd Annual Meeting of the Air Waste Management Association. June 25-30. Anaheim, CA. Paper No. 89.54.1, Used with permission.

Table of Carboxyhemoglobin levels and related health effects on people

% COHb in blood

Effects Associated with this COHb Level




Loss of consciousness; death if exposure continuesa


Confusion; collapse on exercisea


Headache; fatigue; impaired judgmenta


Statistically significant decreased maximal oxygen consumption during strenuous exercise in healthy young menb


Statistically significant diminution of visual perception, manual dexterity, ability to learn, or performance in complex sensorimotor tasks (such as driving)b


Statistically significant decreased maximal oxygen consumption and exercise time during strenuous exercise in young healthy menb

Below 5

No statistically significant vigilance decrements after exposure to COb


Statistically significant decreased exercise capacity (i.e., shortened duration of exercise before onset of pain) in patients with angina pectoris and increased duration of angina attacksb


Statistically significant decreased (about 3-7%) work time to exhaustion in exercising healthy menb

- SOURCE: a U.S. EPA (1979); b U.S. EPA (1985)

Nitrogen dioxide (NO) and sulfur dioxide (SO2) act mainly as irritants, affecting the mucosa of the eyes, nose, throat, and respiratory tract. Acute S02-related bronchial constriction may also occur in people with asthma or as a hypersensitivity reaction. Extremely high-dose exposure (as in a building fire) to N02 may result in pulmonary edema and diffuse lung injury. Continued exposure to high N02 levels can contribute to the development of acute or chronic bronchitis.

The relatively low water solubility of N02 results in minimal mucous membrane irritation of the upper airway. The principal site of toxicity is the lower respiratory tract. Recent studies indicate that low-level N02 exposure may cause increased bronchial reactivity in some asthmatics, decreased lung function in patients with chronic obstructive pulmonary disease, and an increased risk of respiratory infections, especially in young children.

The high water solubility of S02 causes it to be extremely irritating to the eyes and upper respiratory tract. Concentrations above six parts per million produce mucous membrane irritation. Epidemiologic studies indicate that chronic exposure to S02 is associated with increased respiratory symptoms and decrements in pulmonary function21. Clinical studies have found that some asthmatics respond with bronchoconstriction to even brief exposure to S02 levels as low as 0.4 parts per million22


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