A blood alcohol concentration is a measurement from a particular biological specimen at a particular time. It is not a direct measurement of the concentration of ethanol in the brain, even though the brain is the principal target organ for many of alcohol’s behavioral and neurological effects. That distinction matters whenever a toxicology opinion moves from an analytical result to a conclusion about impairment.
A small magnetic-resonance spectroscopy study by Thierauf-Emberger and colleagues directly compared ethanol concentrations in several brain regions with serum ethanol concentrations. The investigators reported that brain ethanol concentrations, normalized to tissue water, were lower than the paired serum values and were comparatively homogeneous across the measured regions. The highest reported brain value was 0.68 g/L, while the maximum serum concentration reached 1.19 g/L. The brain concentration-time curve also appeared flatter than the serum curve. The study was small, but it illustrates an important forensic principle: the specimen tested in the laboratory is a proxy for exposure at a target organ, not the target organ itself.
That principle becomes more important when timing is uncertain. Ethanol concentration changes during absorption, distribution, and elimination. A serum or blood result obtained after an event therefore does not automatically reveal the concentration at the time of driving, an injury, or another disputed act. Any backward estimation requires assumptions about drinking history, absorption status, specimen timing, and elimination kinetics. A pharmacokinetic model can formalize those assumptions, but it cannot make uncertain inputs certain.
A separate study by Lim and colleagues demonstrates both the power and the limits of model-based reconstruction. Using a previously developed alcohol pharmacokinetic model, defendant-specific information, and Bayesian estimation, the researchers produced a predicted alcohol concentration over time with a 95% prediction interval. The method did not reduce the result to a single supposedly exact number; it expressed the reconstruction as a range of plausible values. That is the scientifically responsible way to communicate uncertainty.
Forensic interpretation should therefore separate three questions. First, what did the analytical method actually measure? Second, what can pharmacokinetics reasonably infer about the concentration at another time? Third, what behavioral or neurological conclusion is justified by the available evidence? A numerical BAC may answer the first question well while leaving the second and third questions contested.
This is also why categorical statements such as “a BAC of X proves impairment” deserve scrutiny. Alcohol-related impairment is real and well documented, but the magnitude and manifestation of impairment depend on more than one number. The scientific record should be evaluated alongside timing, observed behavior, testing conditions, individual variability, and the uncertainty of any extrapolation.
The most defensible toxicology opinion is one that identifies the specimen, the analytical method, the sampling time, the pharmacokinetic assumptions, and the limits of inference. Precision in the laboratory should not be confused with certainty about what happened earlier in time or inside the brain.
No. Blood or serum is a surrogate specimen. Research using magnetic-resonance spectroscopy has shown that measured brain ethanol concentrations can differ from paired serum concentrations.
Sometimes, but the reliability depends on the quality of the drinking history, timing, absorption assumptions, and the pharmacokinetic model. A range with stated uncertainty is more scientifically defensible than an unsupported exact value.
Thierauf-Emberger A, et al. International Journal of Legal Medicine. 2020. doi:10.1007/s00414-020-02325-w.
Lim H-S, Soung JH, Bae K-S. Translational and Clinical Pharmacology. 2017. doi:10.12793/tcp.2017.25.1.5.