Mode of action

Methylene chloride is a CNS depressant and can cause profound CNS depression at high concentrations. The CNS depressant effects are thought to be due to methylene chloride itself rather than an effect of its conversion to carbon monoxide. Fatalities have occurred after methylene chloride inhalation where, although carboxyhaemoglobin concentrations were high, they were not sufficient to cause death. In some of these cases, very high blood concentrations of methylene chloride have been found, suggesting that methylene chloride itself may be responsible for deaths or that high concentrations of toxic metabolites formed from the non-saturable glutathione conjugation pathway are involved. These include formaldehyde and formic acid, which may induce tissue hypoxia and metabolic acidosis (Manno et al., 1992).

It is thought that the neurotoxic effects of methylene chloride depend on a direct, non-specific narcotic action on the CNS as well as an equally non-specific carbon monoxide-induced hypoxic effect (Winneke, 1981). The carbon monoxide produced by the metabolism of methylene chloride binds reversibly to the oxygen carrying sites of the haemoglobin molecule. Carbon monoxide has an affinity for haemoglobin 200 to 300

times greater than oxygen itself, and carboxyhaemoglobin is formed which is then unavailable for oxygen transportation. The metabolic formation of carboxyhaemoglobin after methylene chloride exposure may result in greater cardiovascular stress than that induced by a comparable concentration of carboxyhaemoglobin after exposure to carbon monoxide itself (Stewart and Hake, 1976). This may be particularly problematic for those with pre-existing cardiac disease.

An increased amount of markers of cell damage (protein, hexose, sialic acid, lactate dehydrogenase, acid and alkaline phosphatase) were found in cell-free lavage effluents from lungs of rats exposed to methylene chloride by inhalation, compared to controls (Sahu et al., 1980).

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