Lactic acidosis due to carbon monoxide poisoning

Carbon monoxide poisoning will result in lactic acidosis by decreasing the oxygen-carrying capacity of blood.

There are several ways in which one can decrease the delivery of oxygen to one’s tissues. One of the more popular ways is to have one’s haemoglobin  disabled by the stubborn carbon monoxide molecule.

There are a few ways to get enough carbon monoxide into oneself. The conventional route of delivery is by smoke inhalation; there are some easily googled statistics regarding the annual mortality burden of smoke inhalation injuries.

There are some other exciting and exotic ways to develop carbon monoxide poisoning. A simple compound known variably as dichloroethane or methylene chloride (C2Cl2) yields carbon monoxide as a result of its hepatic metabolism; this results in gradual intoxication with carbon monoxide which may not become obvious until several hours after the exposure. For the suicidal person, this stuff is thankfully difficult to get a hold of, though it enjoys wide use as a solvent and as a plastic bonding glue for the model-building  enthusiasts. Among its pleasant properties is the ability to penetrate easily though human skin and dissolve the underlying fatty tissue, which as far as I am aware has never been investigated as a rapid weight loss treatment.

Tissue hypoxia due to carbon monoxide

Apart from decreasing the oxygen-carrying capacity of the blood by merely decreasing the availability of haemoglobin, carbon monoxide also penetrates into cells and binds to myoglobin (forming carboxymyoglobin) and thus diminishing intracellular oxygen stores. The oxyhemoglobin dissociation curve shifts to the left. Goldfranks manual of toxicologic emergencies also reports that carbon monoxide binds to various components of the mitochondrial cytochrome oxidase, directly interfering with mitochondrial function.

Sounds great, where do I get some?

One’s routine metabolic function generates small amount s of CO; among other pathways the breakdown of heme leads to the generation of small amount of CO, and therefore a healthy person’s gas will contain a small amount of carb. More frequently, it is encountered as a product of combustion – when some sort of carbon-based fuel is combusted in the absence of sufficient  oxygen (of course if you had enough oxygen to combust with, you would produce carbon dioxide instead, which is a more stable molecule). Carbon monoxide is flammable, and in the presence of oxygen it will burn with a blue flame, generating carbon dioxide.

Indeed Wikipedia helpfully informs us that “coal gas” used for indoor heating and ovens contained a considerable amount of carbon monoxide, which would explain how one could successfully off oneself by sticking one’s head into an oven in the 1960s. In these enlightened times, one may find carbon monoxide in large quantities as a participant in plastic manufacturing.

The beautiful beef steak you recently bought from the supermarket is only attractively pink because of carbon monoxide treatment (this cosmetic technique  is Generally Recognised As Safe).

How much carbon monoxide do I need to develop symptoms?

One measures a carboxyhemoglobin concentration in the victims of CO poisoning, and it is expressed as a percentage of total hemoglobin.  If you are a one-pack-a-day smoker, your carboxyhemoglobin is about 6%, but could be as high as 10%.

At around 15%, one becomes dizzy and ataxic; a nasty headache  develops.  At 25% consciousness may be lost. Survival is unlikely at concentrations of 50% or more.

After the carbon monoxide exposure stops, carboxyhaemoglobin is slow to clear; the halflife is said to be six hours. In the presence of a large concentration of oxygen the halflife can be as brief as 30 minutes, because oxygen competes for the same hemoglobin molecules.

What is the evidence that carbon monoxide ever causes lactic acidosis?

A study from 1975 narrates the biochemical exploits of a  group of four firefighters, who became exposed to carbon monoxide while trapped in a burning restaurant. The carboxyhemoglobin values ranged from 13% to 37%; the lactate ranged from 5.1 to 9.3 mmol/L. The authors have concluded that the most likely cause of the lactic acidosis was the impaired systemic oxygen delivery.


Buehler JH, Berns AS, Webster JR, Addington WW, Cugell DW: Lactic acidosis from carboxyhemoglobinemia after smoke inhalation. Ann Intern Med 82:803–805, 1975.


Rioux JP, Myers RA (1988). "Methylene chloride poisoning: a paradigmatic review". J Emerg Med 6 (3): 227–238


Kubic VL, Anders MW, Engel RR, Barlow CH, Caughey WS. Metabolism of dihalomethanes to carbon monoxide. I. In vivo studies. Drug Metab Dispos. 1974 Jan-Feb;2(1):53–57.


Zikria, B. A., et al. "Smoke and carbon monoxide poisoning in fire victims." The Journal of Trauma and Acute Care Surgery 12.8 (1972): 641-645.