The Problem of Breath Alcohol Concentration and Exhaled Volume

In forensic breath alcohol testing, there persists a naive belief that as a subject blows into a breath alcohol analyzer, breath alcohol concentration (BrAC) will quickly rise and reach a plateau, at which point the subject’s breath alcohol concentration will no longer increase [1]. This old paradigm of alcohol diffusion into the breath is frequently touted by forensic scientists in the courtroom and promulgated in training materials related to breath alcohol testing [1–4].

Figure 1. The old model of BrAC

In reality, alveolar concentration is never reached, and the BrAC continues to rise throughout exhalation [5,6]. Jones has pointed out that a mechanistic understanding of alcohol exchange in the lungs using only Henry’s law is insufficient to explain alcohol exchange in breath [7]. In 2010, Hlastala called the simplistic model of alcohol exchange in the lungs the “old paradigm” [5]. Other mechanisms such as diffusion, perfusion, ventilation, and differential solubilities must be accounted for when describing alcohol exchange in the lungs and airways.

While Henry’s law accurately describes the exchange of alcohol in a breath alcohol simulator when used to calibrate a breath analyzer, it does not capture the complexities of the alcohol exchange in the lungs [8,9]. In particular, Henry’s law does not consider the complex dynamic interaction of alcohol diffusion in the lungs and mucous membranes of the airways leading to the lungs in vivo [10–14].