A negative urinary ethyl sulfate result does not, by itself, establish that ethanol in postmortem blood was produced after death. In a 79-case study, Al-Asmari and colleagues reported urine containing ethyl glucuronide despite negative ethyl sulfate results. Discordance requires interpretation of both markers, reporting thresholds and specimen history.
What was studied?
The investigators developed a hydrophilic interaction liquid chromatography–electrospray ionization ion-trap tandem mass spectrometry method for ethyl glucuronide (EtG) and ethyl sulfate (EtS), then applied it to autopsy urine from 79 medicolegal cases submitted in Glasgow.
Cases were grouped by blood ethanol: 31 in the high group, described as above 200 mg/100 mL; 21 in the 80–200 mg/100 mL group; and 27 in the 10–80 mg/100 mL group. These selected ethanol-positive cases were not a random sample of all deaths or a controlled drinking study.
Blood came from femoral, subclavian or jugular veins and contained 1–2% potassium fluoride. Autopsy intervals ranged from 24 hours to several days, and specimens were refrigerated until analysis. A uniform blood site and case-specific urine preservation history were not supplied. Ethanol was measured by headspace GC–FID; urinary metabolites were measured separately by LC–MS/MS.
Individual cases show why both markers matter
In Table V, case 27 had urinary EtG of 3.9 mg/L with EtS reported as not detected. In the low-ethanol group, Table VII lists case 61 with blood ethanol 11 mg/100 mL, urinary EtG 10.6 mg/L and no detected EtS. Urine ethanol was also reported as not detected in that case.
The authors regarded EtG-positive discordant cases as evidence of antemortem exposure. Their findings do not establish that EtS is useless or that EtG is infallible. They show that a rule requiring both markers to be positive could classify some EtG-positive cases as lacking evidence of exposure.
Negative markers supported a hypothesis, not a measured microbial fraction
The authors attributed ethanol in eight cases with neither marker detected to postmortem synthesis. Six were in the low-blood-ethanol group, with reported blood concentrations of 11–47 mg/100 mL; the other two had blood ethanol of 133 and 180 mg/100 mL.
That attribution was an interpretation of the case findings, not a direct measurement of the quantity produced by microbes. The study did not establish each person’s predeath ethanol concentration through an independent reference specimen. Negative findings alone therefore cannot supply a validated subtraction from the blood ethanol result.
A positive metabolite finding likewise does not establish that every part of the measured blood ethanol originated from drinking. Evidence of exposure and possible postmortem formation can coexist; the study did not validate a method for separating their amounts in an individual.
Reporting cutoffs and stability qualify the comparison
The study used reporting cutoffs of 1 mg/L for EtG and 0.1 mg/L for EtS. A negative classification must be read against those thresholds rather than equated automatically with molecular absence. The paper also contains inconsistencies in its printed analytical limits and some aggregate counts, so individual table entries are preferable to an unreconciled headline detection percentage.
Fortified-urine experiments supported stability under the specific conditions tested. They did not establish identical behavior in every infected or putrefied authentic specimen. The design did not isolate the cause of each discordant result, and detection of either metabolite is not a measure of impairment.
A practical interpretive boundary
Review both biomarkers, their actual numerical results and thresholds, ethanol in other matrices, decomposition and storage records. Do not convert a positive urine marker into a blood ethanol concentration: the authors found poor associations between the metabolite concentrations and blood or urine ethanol.
For direct evidence of change after collection, see serial ethanol testing of a preserved specimen. That is a different evidentiary question from whether a metabolite supports prior exposure.
Primary source
Al-Asmari AI, Anderson RA, Appelblad P. Direct Determination of Ethyl Glucuronide and Ethyl Sulfate in Postmortem Urine Specimens Using Hydrophilic Interaction Liquid Chromatography–Electrospray Ionization-Tandem Mass Spectrometry. Journal of Analytical Toxicology. 2010;34(5):261–272. doi:10.1093/jat/34.5.261.
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