Talk:Carbon monoxide poisoning

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1 Strength of Ligands
2 Another possible treatment for CO poisoning
3 Resolving the disputed tag
4 Reduction of O2 delivery isn't often relevant?
5 CO and heart disase
6 Carbon Monoxide toxicity
7 Out of place
8 Palladium compounds
9 Carbon Monoxide Poisoning - Long Term Effects
10 Hb tetramer effect
11 Real-world concentrations
12 Air quality data

[edit] Strength of Ligands

Though CO and Cyanide are both strong ligands why do they proceed in two parallel routes in their mechanism for poisoning the human body? --Curieous 09:58, 14 October 2007

[edit] Another possible treatment for CO poisoning

I found this on the "iron" article:

Humans also use iron in the hemoglobin of red blood cells, in order to transport oxygen from the lungs to the tissues and to export carbon dioxide back to the lungs. And iron is an essential component of myoglobin to store oxygen in muscle cells.

The human body needs iron for oxygen transport. That oxygen is required for the production and survival of all cells in our bodies.

This seems like taking an iron tablet would help. -Usernamefortonyd

Maybe to combat the effects of chronic low-level exposure. Taking iron isn't going to help if most haemoglobin has been rendered useless by acute CO exposure, the body isn't going to make new haemoglobin fast enough. Also remember WP:NOR M0ffx 11:09, 12 October 2007 (UTC)

Then you have to deal with the effects of iron overload as well; iron is pretty toxic (like most minerals) when outside it's normal dosage; case in point, haemochromotosis. For the treatment to be effective, the iron would need to be a form easily and quickly absorbed into the bloodstream, and capable for readily forming a stable, non-toxic complex with CO. The iron in an iron tablet is not in such a form. —Preceding unsigned comment added by 58.161.19.90 (talk)

[edit] Resolving the disputed tag

I've left a message with User:Physchim62 asking him for information on the disputed tag. --Arcadian 16:58, 9 December 2005 (UTC)

The following paragraph was queried on the Reference Desk:

"With chronic low-level exposure, similar neurologic injury may occur. Carbon monoxide acts as a potent neurotoxin, creating irreversible lesions in the brain's white matter (i.e., the myelin sheath). Such lesions, which are similar to those found in multiple sclerosis, can result in severe cognitive impairment."

As with most of the article, its source is unclear; I have however managed to track down the paper, which appears to be Penney, D. G.; Verma, K.; Hull, J. A. (1989). "Cardiovascular, metabolic and neurologic effects of acute carbon monoxide poisoning in the rat". Toxicol. Lett. 45(2/3):207–13. As the title suggests, this study concerned an acute exposure in an animal model, not chronic exposure in humans.

The use of the term neurotoxin is more than ambiguous: such neurological damage may not be solely related to primary anoxia, but other animal studies suggest that secondary hypertension, secondary acidosis and elevated blood glucose levels are also involved (Penney, D. G. (1990). "Acute carbon monoxide poisoning: animal models: a review". Toxicology 62(2):123–60.)

"The effect of prolongued exposure to low levels of carbon monoxide [in humans] is still a very controversial subject. It seems however that a long term toxic effect on the cardiovascular system cannot be excluded." Institut national de recherche et de sécurité (1996). "Oxyde de carbone". Fiche toxicologique n°. 47, 6pp. (PDF, in French) And how can you discuss possible chronic effects without noting that heavy cigarette smokers have HbCO levels of 10% or over (compared to 1–2% for non-smokers in the countryside: Source Sax's Dangerous Properties of Industrial Materials)

Unfortunately, such imprecisions seem common throughout the article, which should be completely rewritten from trustable sources: I certainly don't object to carbonmonoxidekills.com being an external link, but if it is really the only source then we should just start again from scratch.

Physchim62 (talk) 10:24, 10 December 2005 (UTC)

[edit] Reduction of O2 delivery isn't often relevant?

The reduction in oxygen delivery (DO2) caused by carboxyhaemoglobin is seldom relevant, but often quoted as the mechanism of the observed tissue hypoxaemia. For example, if total Hb is 15 g/dL and CarboxyHb is 33%, then this still leaves 10 g/dL of normal OXYHAEMOGLOBIN. So at worst, CO poisoning has caused a mild functional anaemia. This can hardly be responsible for tissue hypoxia to any degree. Whilst it is true that the P50 of this oxyhaemoglobin is left shifted, this has a minor effect in the context of tissue acidosis which mostly overcomes it. The principal mechanism of tissue hypoxia is poisoning of cytochrome oxidase, with failure of electron transport and reduction of molecular O2. The value of measuring Carboxyhaemoglobin is that it merely serves as a useful marker of exposure to CO.

Symptoms?

I personaly think a section describing the symptoms of carbon monoxide poisoning would enhance this article.

Yes. Also, some information on prognosis. How fast do the symptoms of minor poisoning fade with time (or do they), what treatments are used, and how effective are they?--Srleffler 23:07, 12 February 2006 (UTC)

I can answer this from experience, as I used to work with the stuff and suffered minor poisoning on a couple of occasions. First symptoms are lethargy and/or a headache. Treatment is to remove the source of intoxication (I used to take myself off home for the afternoon), recovery is complete within hours. I'll see if I can come up with more citable sources for the article. Physchim62 (talk) 00:21, 13 February 2006 (UTC)

Recommeded reading: Henry CR et al: Myocardial injury and long-term mortality following moderate to severe carbon monoxide poisoning. JAMA 2006; 295: 398-402.

[edit] CO and heart disase

Missing from this article seems to be a discussion of the link between CO and heart disease. --Badger151 19:56, 16 April 2006 (UTC)

Is this painless?

[edit] Carbon Monoxide toxicity

Should the term carbon monoxide toxicity redirect to this site?

Does Carbon Monoxide poisoning have any relation to cancer? Such as Bladder Cancer or Lung Cancer?

[edit] Out of place

Smething seems out of place here

Because carbon monoxide binds to haemoglobin several hundred times more strongly than oxygen, its effects are cumulative and long-lasting, causing oxygen starvation throughout the body. Prolonged exposure to fresh air (or pure oxygen) is required for the CO-tainted hemoglobin (carboxyhaemoglobin) to clear. Carbon monoxide detectors for homes are now readily available and are increasingly being required by municipal building codes.

The last sentence seems very out of place and I think it should be moved to a different section (I tihnk it is already mentioned somewhere else anyway).Father Time89 05:10, 7 November 2006 (UTC)

[edit] Palladium compounds

"The carbon monoxide can be easily detected by the filtering paper impregnated by the solution of the palladium chloride. Carbon monooxide reduces the palladium monoxide to the black metallic palladium. This reaction is very sensitive."

Well, which one is it? The oxide or the chloride? —The preceding unsigned comment was added by MikaelRo (talk • contribs) 19:09, 6 December 2006 (UTC). --MikaelRo 19:11, 6 December 2006 (UTC)

[edit] Carbon Monoxide Poisoning - Long Term Effects

The long-term effects of Carbon Monoxide poisoning seems to have been left out of the general Carbon Monoxide catagory. One might survive CM poisoning but what then? The University of Kentucky did a study on this and found that men my experience impotence and women may experience premature sexual aging. Cardiovascular disease and Parkinson's disease have also been cited. When a person is CM poisoned it's the equivalent if being at the bottom of a lake with no air except that this time it is being caused by a poison. Linda Dohse 00:51, 19 January 2007 (UTC)

[edit] Hb tetramer effect

In the "Toxic mechanism" section under "Hemoglobin" the article says:

Because hemoglobin is a tetramer with four oxygen binding sites, binding of CO at one of these sites also increases the oxygen affinity of the remaining 3 sites, which interferes with normal release of oxygen. This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.

How does that cause–effect relationship work? Seems like a CO molecule would knock one iron of the four out-of-play, having no effect on the other three. The statement gives a cite of PMID 12679050, but I don't see any discussion of Hb tetramers or of enhanced Hb affinity for O2 during CO exposure in that article. DMacks 17:41, 11 April 2007 (UTC)

The binding CO to a haem iron atom causes the haemoglobin chain to distort. Because a haemoglobin molecule is a tetramer, the distortion of one protein chain will cause distortions in the other chains, which prevents the release of oxygen. —Preceding unsigned comment added by 58.161.19.90 (talk)

[edit] Real-world concentrations

Please add some real-world concentration numbers, typical CO ppm ranges:

atmosphere: baseline, suburban, urban, in traffic, upper atmosphere
candle flame, kerosene lantern flame, natural gas burner flames
internal combustion exhaust: before and after catalytic converter, diesel

-69.87.199.142 00:20, 24 August 2007 (UTC)

"Several natural sources of CO of both biological origins have also been identified but their contributions to urban atmospheric concentrations are thought to be small. Background levels of CO (resulting from natural and technological sources) found in relatively unpolluted air range from 0.025 to 1.0 ppm. Urban carbon monoxide is produced primarily by motor vehicles.

Because motor vehicle traffic is the major source of CO, daily concentration peaks coincide with morning and evening rush hours. The worst carbon monoxide problems are found where large numbers of slow moving cars congregate. These problems are further aggravated when they occur in a "street canyon" situation. When there are large amounts of slow moving traffic in a street canyon situation, with the wind blowing perpendicular to the street, carbon monoxide can be trapped in the canyon and build up to unhealthful levels.

CO problems are usually worse in winter because: 1) cold weather makes motor vehicles run dirtier and requires more combustion for space heating; and 2) on winter nights a strong inversion layer develops in the atmosphere, that traps pollution near the ground, preventing it from mixing with cleaner air above."[1]

"No standards for CO have been agreed upon for indoor air. The U.S. National Ambient Air Quality Standards for outdoor air are 9 ppm (40,000 micrograms per meter cubed) for 8 hours, and 35 ppm for 1 hour." "Average levels in homes without gas stoves vary from 0.5 to 5 parts per million (ppm). Levels near properly adjusted gas stoves are often 5 to 15 ppm and those near poorly adjusted stoves may be 30 ppm or higher."[2]

"undiluted cigarette smoke contains about 30,000 ppm of CO, undiluted warm car exhaust about 7,000 ppm, and the chimney of a home wood fire about 5,000 ppm. Clean countryside air contains about 0.02 ppm of CO. The smoke from one pack of cigarettes, if distributed uniformly throughout an average sized house, could result in a CO concentration of up to 14 ppm.

An average healthy person at sea level is just barely affected by prolonged exposure to concentrations of 9 ppm, but the presence of other pollutants aggravates the situation, and respiratory and cardiac problems pose an increased risk. Chronic exposure to high concentrations of CO (30 to 100 ppm), such as in a poorly vented garage, can lead to long-term deterioration of the cardiovascular system." (1983)[3] -69.87.199.142 01:09, 24 August 2007 (UTC)

[edit] Air quality data

It would be great if there were one integrated website people could go to for current or historic carbon monoxide measurement data for any particular locations. This is the best I've been able to find so far: