Concentration of carbon monoxide (CO) in postmortem human tissues: effect of environmental CO exposure.

We studied how carbon monoxide (CO) is distributed within the human body through quantitation of CO concentrations in postmortem tissue samples from fatalities including possible CO exposure. Stored, frozen tissues were diced, sonicated in water, and 0.01-8.0 mg wet weight (ww) tissues were incubated with sulfosalicylic acid in CO-purged, septum-sealed vials. CO released into the headspace was quantitated by reduction gas chromatography. Mean tissue CO concentrations (pmol/mg ww) from subjects diagnosed to have no known CO exposure (control, N=14), died from fire (N=13), and CO asphyxiation (N=7), respectively, were: adipose (2;13;9), brain (3;13;65), muscle (15;97;297), heart (30;99;371), kidney (22;432;709, lung (54;690;2638), spleen (73;1366;3548), and blood (162;2238;5070). Carboxyhemoglobin concentrations were 1.4%, 25.2%, and 69.1% of total hemoglobin, respectively. We conclude that measurements of CO concentration in a variety of tissues can be used as markers for the degree of exogenous CO exposure and the identification of possible causes of death.

Lung tissue concentrations of nicotine in sudden infant death syndrome (SIDS).

OBJECTIVE: To compare lung concentrations of nicotine and cotinine in cases of sudden infant death syndrome (SIDS) and controls. DESIGN/METHODS: We measured lung tissue concentrations of nicotine and cotinine in SIDS (n = 44) and non-SIDS cases (n = 29) stratified according to household smoking status. RESULTS: When all the SIDS and non-SIDS cases were compared regardless of smoking status, there was a significantly higher nicotine concentration in the SIDS cases than in the non-SIDS cases, (P =.0001). Upon stratifying for smoking status, there was a nonsignificant trend toward more nicotine in SIDS versus non-SIDS lungs that had come from a reported smoking environment. In the nonsmoking group, there were significantly higher nicotine concentrations in SIDS than non-SIDS cases (P =.001). CONCLUSIONS: Children who died from SIDS tended to have higher concentrations of nicotine in their lungs than control children, regardless of whether smoking was reported. These results are based on an objective, biochemical test rather than history, and they further support the relationship between environmental tobacco smoke and the risk of SIDS.