ALCOHOL CONCENTRATIONS IN BREATH AND VENOUS BLOOD AND ALCOHOL EFFECTS. U. Loos and U. Heifer

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1 ALCOHOL CONCENTRATIONS IN BREATH AND VENOUS BLOOD AND ALCOHOL EFFECTS U. Loos and U. Heifer Department of Forensic Medicine, University of Bonn D-5300 Bonn 1, Fed. Rep. of Germany Introduction Numerous studies about the correlation between the alcohoi^concentrations in blood (BAC) and in breath (BrAC) have been conducted. Additionally, we ask for the time course of the alcohol effects in relationship to the alcohol concentrations (12).because the former parameters are the primary indicator for the alcoholic impairment. Two aspects are well known. Firstly, during the gastro-intestinal resorption the BrAC rises in advance of the peripheral venous BAC. Secondly, in this phase the alcohol impairment Is overshooting as compared With the elimination period. But how does the temporal correlation of alcohol concentrations in breath and blood and of alcoholic effects appear? Does the BrAC possibly describe the overshooting alcoholic impairment during the invasion phase? Methods We tried to answer these questions in a drinking experiment. After a fasting period of at least four hours 15 sober students (11 male and 4 female) consumed vodka of 40 volume-per-cent in the dosage of 1 g ethanol per kg body weight, within 55 minutes. The alcohol concentrations in the venous blood and in the breath, and the alcoholic ef- The word alcohol in this article refers to ethanol. 1087

2 fects were investigated over a period of four hours, at time intervals of 15 or 30 minutes. The cubital (elbow) vein BAC was determined as the average of three gas chromatographic values. Before and after each blood sampling a breath test was carried out. The BrAC was measured by a device - based on infrared photometry - which was calibrated by a breath-alcohol simulator (1). We received the results from the persons tested as the calculated average of two breath tests in the unit 1 mg ethanol per litre expired air. During the drinking period the breath analysis was only performed after a thorough mouth rinse with water for we wanted to avoid disturbances by remaining mouth alcohol. In order to estimate the influence of different expiration techniques on the BrAC measurement, our collective was divided in two groups: - the first seven test persons expired, after having inhaled some air, in four seconds into the instrument, and, then, stopped their exhalation. The BrAC was analysed in a defined expiratory air. - the other eight test persons breathed out, after inhaling, their total air volume into the measuring chamber which recorded the last 100 ml of the inblown quantity. In the second group the BrAC was ascertained in end-expiratory (=alveolar) air. As the first example for alcoholic intoxication we measured the total amplitude of the ost-rotational fixation nystagmus (PFN) by electronystagmography (8). In general, this eye movement increases pathologically if an alcoholized person optically fixates an object, after some rotations around his axis. As a second example we studied the sensory-motor er- 1088

3 formance (SMP) under alcohol influence with a test device which demanded correct reactions of the hands and the feet on optical and acoustic stimuli in two manners: - in the determination test (D-test) the stimuli were time-controlled: each 0.9 second one of a total of 180 impulses appeared. The correct and the delayed correct reactions (which means that the correct reaction took place only at the next stimulus) were used by us. - in the reaction test (R-test) a new. stimulus was created when the subject pressed the correct key. Within 120 seconds the test person should obtain as many right reactions as possible. We determined the BAC, the BrAC, the PFN, and the SMP only at certain points in time. With the help of interpolating theoretical model curves (10, 11, 12) we got the continuous time course of these parameters. In particular, on this basis we are able to find their peak times. Results Figure 1 illustrates the correlation between the breath and blood test. It contains the data of the resorption and the elimination phase of the whole collective tested. A regression analysis yields a standard error for the BAC's estimate from the breath analysis of mg ethanol/ml blood in the elimination phase (if the regression formula BAC (mg/ml) = 2,161 * BrAC (mg/ml air) is used ; indicates that during the evasion phase the alcohol concentration in the peripheral venous blood is higher than in the pulmonary blood, vice versa as in the invasion period (14)). This appears to be a reasonable precision (13). The error would have been lower if we had allowed only one expiration technique. With the results of the blood and breath tests we can calculate the venous blood/breath alcohol concentration ratio. This temperature dependent quotient states the 1089

4 BAC IN MG/ML BLOOD <* K * o o o O 0 = RESORPTION PHASE X = ELIMINATION PHASE i i i i t BRAC IN MG/L EXPIRED AIR Figure 1. Correlation between the breath and the blood test. BLOOD/BREATH ALCOHOL RATIO ,400 EXPIRATORY T X TIME IN MINUTES AFTER THE BEGINNING OF DRINKING Figure 2. Time course of the blood/breath alcohol ratio for the defined expiratory and end-expiratory air group (mean + standard deviation). 1090

5 ratio of the alcohol amount in 1 ml blood to 1 ml breathing air. Figure 2 shows this quotient for the defined expiratory and end-expiratory air group. During the invasion the ratio is lower than in the evasion phase, since the BrAC rises more quickly than the peripheral BAC. Because the expiratory BrAC is smaller than the end-expiratory, the data points of the former group - in figure 2 - are above those of the latter. In the elimination phase the blood/ breath alcohol ratio amounts to (mean + standard deviation) 2, for the defined expiratory air group (range 2, ,804). - 2, for the end-expiratory air group (range 1, ,308). There is a large change in the quotient by employing a different expiration technique which may be a considerable error source in breath alcohol analysis. Our result for end-expiratory air corresponds satisfactorily with Harger's value of 2,100 at 34 C temperature (5, 6). The figures 3 to 6 illustrate the test-collective's mean time courses of the vein BAC, the BrAC, the PFN, and the D- and R-test. The BrAC is converted into a BAC by multiplying with the mean individual blood/breath alcohol ratio of the elimination phase. The results of the D-test are expressed as a percentage of all possible correct reactions, those of the R-test as the mean reaction time per correct reaction (=test time of 120 seconds divided by the number of correct reactions). The graphs in the figures are derived from our theoretical models. The curves are slightly delayed at about the half way point of the drinking time because the alcohol consumption was interrupted for a test period. In the invasion phase the BrAC exceeds the cubital vein BAC. The PFN and the SMP reach their peak and begin to fall off before the alcohol concentrations become maximal (overshooting effects). 1091

6 ALCOHOL CONCENTRATION IN MG/G BLOOD TIME IN MINUTES Figure 3. Time course of the BrAC (broken line) and the venous BAC (full line). (Figures 3 to 6: The means + standard deviations of the collective's data and the fitted theoretical curves are shown.) TOTAL AMPLITUDE IN ANGULAR DEGREES Figure 4. Time course of the PFN. 1092

7 REACTIONS IN PER CENT Figure 5. Time course of the D-test results. REACTION TIME IN MILLISECONDS TIME IN MINUTES Figure 6. Time course of the reaction time in the R-test. 1093

8 MEAN + SD OF THE PEAK TIMES BAC < P < O.OOl BRAC i P < 0.01 SMP i P < PFN RINKING I I TIME IN MINUTES Figure 7. Peak times of the PFN, SMP, BrAC, and the cubital vein BAC after the drinking period (mean + standard deviation). P = statistical significancies for the differences of the peak times. Figure 7 presents the peak times (mean + standard deviation of the collective) of the alcohol impairment and concentrations. The Wilcoxon matched pairs signed rank test provides the statistical significancies (P) for the differences of the peak times in the collective. The overlapping of the intervals in figure 7 should not be misunderstood. The following temporal order of the maxima is nearly fixed for each test person: (sooner) PFN - SMP - BrAC - cubital vein BAC (later). This means that at first the PFN is maximal, then the SMP has the largest defects. There is no difference between D- and R-Eest. The highest alcohol levels appear after the peak alcohol effects. The specific time differences between the maxima will depend on the drinking manner. Discussion In the introduction we asked if the BrAC - as a better representative for the brain's alcohol concentration than venous blood - can describe the overshooting alcoholic effects in the resorption phase. We see now that it does not. The reason why the BrAC exceeds the cubital vein BAC during the invasion is the following: after oral intake the 1094

9 alcohol is resorbed by the gastro-intestinal tract and transported into the liver. Then the right heart chamber pumps the blood stream through the lungs. Here a part of the alcohol molecules diffuses in the alveolar membrane, evaporates to the alveolar space forming the breath alcohol. Now the left heart chamber conveys the alcohol to the body's periphery, especially to the extremities, which have a low rate of blood flow per kg of tissue. Therefore the cubital vein BAC rises slowly. The discrepancy between BrAC and venous BAC can be comprehended as arterio-venous difference of the alcohol concentration. In the literature this phenomenon and the brain's richer specific blood flow are mentioned as reasons for the overshooting alcohol impairment during the invasion phase (4). But the explanation is not sufficient since it does not apply to the BrAC that is a good representative of the brain alcohol, but which lags behind the alcohol effects. We think that the rise in the rate of the alcoholic concentration, as a second factor, plays a role with respect to the greater alcoholic impairment in the invasion period. The central nervous system seems to react not only on the alcohol "stimulus", but also on its variation speed. The PFN has its peak value earlier than the SMP because the nystagmus represents a reflex system and the test person may try to compensate the deficits in the SMP by stronger efforts as long as possible. In some countries breath alcohol methods are accepted by the courts in traffic cases, in others - like Western Germany - only blood alcohol analysis is admitted. On the one hand the expenditure for the breath check is less, and the BrAC's time course is more "parallel" to that of the impairment. On the other hand the BrAC does not reproduce it and considerably depends on the expiration technigue (e.g. expiratory or end-expiratory air) and other conditions. 1095

10 Therefore the forensic admissibility of the breath alcohol analysis is so far denied in Germany. For screening purposes and scientific investigations the new modern breath alcohol instruments are surely very useful. Conclusions 1. In breath alcohol analysis the kind of the employed exhaled breath is very important for a correct measurement. As previously shown, a defined expiratory and the end-expiratory air lead to variation in the results for the alcohol levels. 2. After oral ingestion the breath alcohol concentration rises more quickly than the cubital vein blood alcohol level. It does not describe the overshooting alcoholic impairment in the invasion phase. Besides the brain's richer specific blood flow, as compared with the upper extremities, the rise in the rate of the alcohol concentration plays a role with respect to the greater impairment during the resorption period. References 1. Adrian W: Ein neues Gerat zur Blutalkoholbestimmung iiber die Messung der Atemalkoholkonzentration. Unfall- und Sicherheitsforschung, StraBenverkehr (ed. by Bundesanstalt fur StraBenwesen, Cologne), No. 10: , Bschorr R: Studien iiber den Ablauf der Alkoholintoxikation unter besonderer Berticksichtigung der pharmakopsycnologischen Beziehungen in der Resorptionsphase bei AlkoholgewOhnten. Dtsch Zschr ges gerichtl Med 40: , Forney RB, Hughes FW, Harger RN, Richards AB: Alcohol distribution in the vascular system. Concentration of orally administered alcohol in blood from various points in the vascular system, and in rebreathed air, 1096

11 during absorption. Quart J Stud Ale 2J5: , Gostomzyk JG, Gyalog G, Reulen H J : Anflutung und Verteilung von Alkohol bei oraler Resorption. Z f Rechtsmed 70: 46-52, Harger RN, Forney RB, Barnes HB: Estimation of the level of blood alcohol from analysis of breath. J Lab Clin Med 36: , Harger RN, Forney RB, Baker R S : Estimation of the level of blood alcohol from analysis of breath. Quart J Stud Ale 12: 1-18, Harger RN: Blood source and alcohol level; errors from using venous blood during active absorption. Proceed.Third Intern. Conf. on Alcohol and Road Traffic British Medical Association, London, Pp Heifer U, Sellier K, Kutzner M: Experimentelle und statistische Untersuchungen iiber den alkoholbedingten postrotatorischen Fixationsnystagmus. Blutalkohol 3^: , Heifer U: Die Beurteilung der Fahruntiichtigkeit nach Sturztrunk. Kraftfahrt und Verkehrsrecht No. 3: 1-7, Kniipling H: Untersuchung iiber die Dynamik von Pharmakonkonzentration und -wirkung, dargestellt an Teilfunktionen des Zentralnervensystems. Habil.-Schrift, Bonn, Loos U: Postrotatorischer Fixationsnystagmus und sensomotorische Leistung unter Alkoholeinwirkung. Experimentelle Untersuchung und modellmsbige Beschreibung. Inaug.-Diss., Bonn, not yet published. Loos U, Heifer U: Uber den zeitlichen Verlauf von Atemund venoser Blutalkoholkonzentration und von Alkohol wirkungen. Blutalkohol , Noordzij PC: Comparison of blood and breath testing under field conditions. Proceed. Sixth Intern.Conf. on Alcohol, Drugs, and Traffic Safety. Addiction Re-

12 search Foundation of Ontario, Toronto, Canada, Pp Sedman AJ, Wilkinson PK, Wagner JG: Concentration of ethanol in two segments of the vascular system. J'Forens Sci 21; ,