Methylene chloride poisoning in a cabinet worker.

Abstract

More than a million workers are at risk for methylene chloride exposure. Aerosol sprays and paint stripping may also cause significant nonoccupational exposures. After methylene chloride inhalation, significant amounts of carbon monoxide are formed in vivo as a metabolic by-product. Poisoning predominantly affects the central nervous system and results from both carboxyhemoglobin formation and direct solvent-related narcosis. In this report, we describe a case of methylene chloride intoxication probably complicated by exogenous carbon monoxide exposure. The worker's presentation of intermittent headaches was consistent with both methylene chloride intoxication and carbon monoxide poisoning. The exposures and symptoms were corroborated by elevated carboxyhemoglobin saturations and a workplace inspection that documented significant exposures to both methylene chloride and carbon monoxide. When both carbon monoxide and methylene chloride are inhaled, additional carboxyhemoglobin formation is expected. Preventive efforts should include education, air monitoring, and periodic carboxyhemoglobin determinations. Methylene chloride should never be used in enclosed or poorly ventilated areas because of the well-documented dangers of loss of consciousness and death. Images Figure 1

Bilateral hearing loss after dichloromethane poisoning: A case report

“…The formation rate of COHb is quite variable according to concentration and duration of exposure, so the peak value of COHb can be reached even several hours after an incident [Fagin et al, 1980]. Once exposure is terminated, DCM stored in the body continues to be converted to CO [Mahmud and Kales, 1999]. The CO produced by DCM metabolism has a half-life of 13 hr, compared to 5.3 hr of inhaled CO [Goulle et al, 1999].…”

Evaluation of three physiologically based pharmacokinetic (PBPK) modeling tools for emergency risk assessment after acute dichloromethane exposure

“…Via this pathway, DCM is metabolised to carbon monoxide (CO), leading to increased HbCO levels, causing a decrease in oxygen transport capacity and tissue oxygenation. HbCO can peak hours after exposure ceases, as fat and other tissues continue to release accumulated DCM (Rioux and Myers, 1989;Mahmud and Kales, 1999). The second pathway involves GSH-conjugation via glutathione (GSH) and results in carbon dioxide, with formaldehyde and formic acid as metabolic intermediates.…”

Antagonistic Effect of Dichloromethane on Oreochromis mossambicus and Immune Stimulation Activity of Aloe Vera

“…However, data on DCM's acute toxicities have rarely been analyzed (Bos et al, 2006) because DCM is sparingly soluble in water and is the least toxic of all the chloromethanes (Watanabe et al, 2007;Kim and Carlson, 1986). Several studies have reported the effects of DCM exposure on mental consciousness (Mahmud and Kales, 1999) and on the inhibition of acetylcholine neurotransmitters in industrial settings (Pacheco et al, 2016). The solvent's harmful effects can be direct or indirect, as with the release of carbon monoxide, which is a by-product of this solvent (Wirkner et al, 1997).…”