Blood alcohol content (BAC), also called blood alcohol concentration or blood alcohol level, is a measurement of
alcohol intoxication used for legal or medical purposes;[1] it is expressed as mass of alcohol per volume of blood. For example, a BAC of 0.10 (0.10% or one tenth of one percent) means that there is 0.10
g of alcohol for every 100
mL of blood.[2] A BAC of 0 is
sober. In different countries the maximum permitted BAC when driving ranges from the
limit of detection to 0.08%.[3][4] BAC levels over 0.08% are considered impaired; above 0.40% is potentially fatal.[1]
At BAC 0.01–0.05%, people may experience mild relaxation and reduced
social inhibition, along with impaired judgment and coordination. At BAC 0.06–0.20%, effects can include emotional swings, impaired vision, hearing, speech, and
motor skills. The
NIAAA defines the term "
binge drinking" as a pattern of drinking that brings a person's blood alcohol concentration (BAC) to 0.08 grams percent or above.[5]
Beginning at a BAC greater than 0.2%, people may experience
urinary incontinence,
vomiting, and symptoms of
alcohol intoxication. At a BAC greater than 0.3%, people may experience total loss of consciousness and show signs of severe alcohol intoxication. A BAC of 0.4% or higher is potentially fatal and can result in a
coma or
respiratory failure.[6][7] The magnitude of sensory impairment may vary in people of differing weights.[8]
Estimation
Direct measurement
Blood samples for BAC analysis are typically obtained by taking a venous blood sample from the arm. A variety of methods exist for determining blood-alcohol concentration in a blood sample.[9] Forensic laboratories typically use
headspace-gas chromatography combined with mass spectrometry or flame ionization detection,[10] as this method is accurate and efficient.[9] Hospitals typically use
enzyme multiplied immunoassay, which measures the co-enzyme
NADH. This method is more subject to error but may be performed rapidly in parallel with other blood sample measurements.[11]
The amount of
alcohol on the breath can be measured, without requiring drawing blood, by blowing into a
breathalyzer, resulting in a breath alcohol content (BrAC). The BrAC specifically correlates with the concentration of alcohol in arterial blood, satisfying the equation BACarterial = BrAC × 2251 ± 46. Its correlation with the standard BAC found by drawing venous blood is less strong.[12] Jurisdictions vary in the statutory conversion factor from BrAC to BAC, from 2000 to 2400. Many factors may affect the accuracy of a breathalyzer test,[13] but they are the most common method for measuring alcohol concentrations in most jurisdictions.[14]
By intake
Blood alcohol content can be estimated by a model developed by Swedish professor Erik Widmark in the 1920s.[15] The model corresponds to a
pharmacokinetic single-compartment model with instantaneous absorption and
zero-order kinetics for elimination. The model is most accurate when used to estimate BAC a few hours after drinking a single dose of alcohol in a fasted state, and can be within 20%
CV of the true value.[16][17] It is less accurate for BAC levels below 0.2 g/L (alcohol is not eliminated as quickly as predicted) and consumption with food (overestimating the peak BAC and time to return to zero).[18][19] The equation varies depending on the units and approximations used, but in its simplest form is given by:
where:
EBAC is the estimated blood alcohol concentration (in g/L)
A is the mass of alcohol consumed (g).
T is the amount time during which alcohol was present in the blood (usually time since consumption began), in hours.
β is the rate at which alcohol is
eliminated, averaging around 0.15 g/L/hr
Vd is the
volume of distribution (L); typically body weight (kg) multiplied by 0.71 L/kg for men and 0.58 L/kg for women
Examples:
A 80 kg man drinks 2 US
standard drinks (3 oz) of 40% ABV vodka, containing 14 grams of ethanol each (28 g total). After two hours:
A 70 kg woman drinks 63 g of 40% ABV vodka, containing 21 grams of ethanol. After two hours:
The volume of distribution Vd contributes about 15% of the uncertainty to Widmark's equation[20] and has been the subject of much research. It corresponds to the volume of the blood in the body.[15] In his research, Widmark used units of mass (g/kg) for EBAC, thus he calculated the apparent mass of distribution Md or mass of blood in kilograms. He fitted an equation of the body weight W in kg, finding an average rho-factor of 0.68 for men and 0.55 for women. This ρm has units of dose per body weight (g/kg) divided by concentration (g/kg) and is therefore dimensionless. However, modern calculations use weight/volume concentrations (g/L) for EBAC, so Widmark's rho-factors must be adjusted for the density of blood, 1.055 g/mL. This has units of dose per body weight (g/kg) divided by concentration (g/L blood) - calculation gives values of 0.64 L/kg for men and 0.52 L/kg for women, lower than the original.[19] Newer studies have updated these values to population-average ρv of 0.71 L/kg for men and 0.58 L/kg for women. But individual Vd values may vary significantly - the 95% range for ρv is 0.58-0.83 L/kg for males and 0.43-0.73 L/kg for females.[21] A more accurate method for calculating Vd is to use
total body water (TBW) - experiments have confirmed that alcohol distributes almost exactly in proportion to TBW. TBW may be calculated using
body composition analysis or estimated using anthropometric formulas based on age, height, and weight. Vd is then given by , where is the water content of blood, approximately 0.825 w/v for men and 0.838 w/v for women.[22]
The elimination rate from the blood, β, is perhaps the more important parameter, contributing 60% of the uncertainty to Widmark's equation.[20] Similarly to ρ, its value depends on the units used for blood.[19]β varies 58% by occasion and 42% between subjects; it is thus difficult to determine β precisely, and more practical to use a mean and a range of values. The mean values for 164 men and 156 women were 0.148 g/L/h and 0.156 g/L/h respectively. Although statistically significant, the difference between sexes is small compared to the overall uncertainty, so Jones recommends using the value 0.15 for the mean and the range 0.10 - 0.25 g/L/h for forensic purposes, for all subjects.[23] Explanations for the gender difference are quite varied and include liver size, secondary effects of the volume of distribution, and sex-specific hormones.[24] Elaborating on the secondary effects, zero-order kinetics are not an adequate model for ethanol elimination; the elimination rate is better described by
Michaelis–Menten kinetics. M-M kinetics are approximately zero-order above a BAC of 0.15-0.20 g/L, but below this value alcohol is eliminated more slowly and the elimination rate more closely follows first-order kinetics. This change in behavior was not noticed by Widmark because he could not analyze low BAC levels.[19] A 2023 study using a more complex two-compartment model with M-M elimination kinetics, with data from 60 men and 12 women, found statistically small effects of gender on maximal elimination rate and excluded them from the final model. Eating food in proximity to drinking increases elimination rate significantly.[25]
In terms of
fluid ounces of alcohol consumed and weight in pounds, Widmark's formula can be simply approximated as[15]
for a man or
for a woman, where EBAC and β factors are given as g/dL (% BAC), such as a β factor of 0.0015% BAC per hour.[15]
The examples above define a standard drink as 0.6
fluid ounces (14 g or 17.7 mL) of ethanol, whereas other definitions exist, for example 10 grams of ethanol.
Approximate blood alcohol percentage (by volume)[26] Based on one drink having 0.5 US fl oz (15 mL) alcohol by volume
Drinks
Sex
Body weight
40 kg 90 lb
45 kg 100 lb
55 kg 120 lb
64 kg 140 lb
73 kg 160 lb
82 kg 180 lb
91 kg 200 lb
100 kg 220 lb
109 kg 240 lb
1
Male
–
0.04
0.03
0.03
0.02
0.02
0.02
0.02
0.02
Female
0.05
0.05
0.04
0.03
0.03
0.03
0.02
0.02
0.02
2
Male
–
0.08
0.06
0.05
0.05
0.04
0.04
0.03
0.03
Female
0.10
0.09
0.08
0.07
0.06
0.05
0.05
0.04
0.04
3
Male
–
0.11
0.09
0.08
0.07
0.06
0.06
0.05
0.05
Female
0.15
0.14
0.11
0.10
0.09
0.08
0.07
0.06
0.06
4
Male
–
0.15
0.12
0.11
0.09
0.08
0.08
0.07
0.06
Female
0.20
0.18
0.15
0.13
0.11
0.10
0.09
0.08
0.08
5
Male
–
0.19
0.16
0.13
0.12
0.11
0.09
0.09
0.08
Female
0.25
0.23
0.19
0.16
0.14
0.13
0.11
0.10
0.09
6
Male
–
0.23
0.19
0.16
0.14
0.13
0.11
0.10
0.09
Female
0.30
0.27
0.23
0.19
0.17
0.15
0.14
0.12
0.11
7
Male
–
0.26
0.22
0.19
0.16
0.15
0.13
0.12
0.11
Female
0.35
0.32
0.27
0.23
0.20
0.18
0.16
0.14
0.13
8
Male
–
0.30
0.25
0.21
0.19
0.17
0.15
0.14
0.13
Female
0.40
0.36
0.30
0.26
0.23
0.20
0.18
0.17
0.15
9
Male
–
0.34
0.28
0.24
0.21
0.19
0.17
0.15
0.14
Female
0.45
0.41
0.34
0.29
0.26
0.23
0.20
0.19
0.17
10
Male
–
0.38
0.31
0.27
0.23
0.21
0.19
0.17
0.16
Female
0.51
0.45
0.38
0.32
0.28
0.25
0.23
0.21
0.19
Subtract approximately 0.01 every 40 minutes after drinking.
By training
If individuals are asked to estimate their BAC, then given accurate feedback via a breathalyzer, and this procedure is repeated a number of times during a drinking session, studies show that these individuals can learn to discriminate their BAC, to within a mean error of 9 mg/100 mL (0.009% BAC).[27] The ability is robust to different types of alcohol, different drink quantities, and drinks with unknown levels of alcohol. Trained individuals can even drink alcoholic drinks so as to adjust or maintain their BAC at a desired level.[28] Training the ability does not appear to require any information or procedure besides breathalyzer feedback, although most studies have provided information such as intoxication symptoms at different BAC levels. Subjects continue to retain the ability one month after training.[29]
Post-mortem
After fatal accidents, it is common to check the blood alcohol levels of involved persons. However, soon after death, the body begins to
putrefy, a biological process which produces ethanol. This can make it difficult to conclusively determine the blood alcohol content in autopsies, particularly in bodies recovered from water.[30][31][32][33] For instance, following the 1975
Moorgate tube crash, the driver's kidneys had a blood alcohol concentration of 80 mg/100 mL, but it could not be established how much of this could be attributed to natural decomposition.[34] Newer research has shown that vitreous (eye) fluid provides an accurate estimate of blood alcohol concentration that is less subject to the effects of decomposition or contamination.[35]
Units of measurement
BAC is generally defined as a fraction of weight of alcohol per volume of blood, with a
coherent unit of grams per liter. Countries differ in how this number is normally expressed. Common formats are listed in the table below. For example, the US and many international publications present BAC as a percentage, such as 0.05%. This would be interpreted as 0.05 grams per deciliter of blood. This same concentration could be expressed as 0.5‰ or 50 mg% in other countries.[36]
United Kingdom[40] Ireland, Canada, New Zealand[19]
It is also possible to use other units, but these have become uncommon. For example, in the 1930s Widmark measured alcohol and blood by mass, and thus reported his concentrations in units of g/kg or mg/g, weight alcohol per weight blood. 1 mL of blood has a mass of approximately 1.055 grams, thus a mass-volume BAC of 1 g/L corresponds to a mass-mass BAC of 0.948 mg/g. Sweden, Denmark, Norway, Finland, Germany, and Switzerland use mass-mass concentrations in their laws,[19] but this distinction is often skipped over in public materials.[41]
For purposes of law enforcement, blood alcohol content is used to define intoxication and provides a rough measure of impairment. Although the degree of impairment may vary among individuals with the same blood alcohol content, it can be measured objectively and is therefore legally useful and difficult to contest in court. Most countries forbid operation of motor vehicles and heavy machinery above prescribed levels of blood alcohol content. Operation of boats and aircraft is also regulated. Some jurisdictions also regulate bicycling under the influence. The alcohol level at which a person is considered legally impaired to drive varies by country.
Test assumptions
Extrapolation
Retrograde
extrapolation is the mathematical process by which someone's blood alcohol concentration at the time of driving is estimated by projecting backwards from a later chemical test. This involves estimating the absorption and elimination of alcohol in the interim between driving and testing. The rate of elimination in the average person is commonly estimated at 0.015 to 0.020 grams per deciliter per hour (g/dL/h),[43] although again this can vary from person to person and in a given person from one moment to another. Metabolism can be affected by numerous factors, including such things as body temperature, the type of alcoholic beverage consumed, and the amount and type of food consumed.
In an increasing number of states, laws have been enacted to facilitate this speculative task: the blood alcohol content at the time of driving is legally presumed to be the same as when later tested. There are usually time limits put on this presumption, commonly two or three hours, and the defendant is permitted to offer evidence to rebut this presumption.
Forward extrapolation can also be attempted. If the amount of alcohol consumed is known, along with such variables as the weight and sex of the subject and period and rate of consumption, the blood alcohol level can be estimated by extrapolating forward. Although subject to the same infirmities as retrograde extrapolation—guessing based upon averages and unknown variables—this can be relevant in estimating BAC when driving and/or corroborating or contradicting the results of a later chemical test.
Metabolism
Alcohol is absorbed throughout the gastrointestinal tract, but more slowly in the stomach than in the small or large intestine. For this reason, alcohol consumed with food is absorbed more slowly, because it spends a longer time in the stomach.[44] Furthermore,
alcohol dehydrogenase is present in the stomach lining. After absorption, the alcohol passes to the liver through the
hepatic portal vein, where it undergoes a first pass of metabolism before entering the general bloodstream.[45]
Alcohol is removed from the bloodstream by a combination of
metabolism, excretion, and evaporation. Alcohol is metabolized mainly by the group of six
enzymes collectively called alcohol dehydrogenase. These convert the ethanol into
acetaldehyde (an intermediate more toxic than ethanol). The enzyme
acetaldehyde dehydrogenase then converts the acetaldehyde into non-toxic acetic acid.
Many physiologically active materials are removed from the bloodstream (whether by
metabolism or excretion) at a rate proportional to the current concentration, so that they exhibit
exponential decay with a characteristic
half-life (see
pharmacokinetics). This is not true for alcohol, however. Typical doses of alcohol actually saturate the enzymes' capacity, so that alcohol is removed from the bloodstream at an approximately constant rate. This rate varies considerably between individuals. Another sex-based difference is in the elimination of alcohol. For females, the concentration of alcohol in breast milk produced during lactation is closely correlated to the individual's blood alcohol content.[46] People under 25, women,[47] or people with liver disease may process alcohol more slowly. Falsely high BAC readings may be seen in patients with kidney or liver disease or failure.[citation needed]
Such persons also have impaired acetaldehyde dehydrogenase, which causes acetaldehyde levels to peak higher, producing more severe
hangovers and other effects such as flushing and tachycardia. Conversely, members of certain ethnicities that traditionally did not use alcoholic beverages have lower levels of alcohol dehydrogenases and thus "sober up" very slowly but reach lower aldehyde concentrations and have milder hangovers. The rate of detoxification of alcohol can also be slowed by certain drugs which interfere with the action of alcohol dehydrogenases, notably
aspirin,
furfural (which may be found in
fusel alcohol), fumes of
certain solvents, many
heavy metals, and some
pyrazole compounds. Also suspected of having this effect are
cimetidine,
ranitidine, and
acetaminophen (paracetamol).
Currently, the only known substance that can increase the rate of alcohol metabolism is
fructose. The effect can vary significantly from person to person, but a 100 g dose of fructose has been shown to increase alcohol metabolism by an average of 80%. Fructose also increases false positives of high BAC readings in anyone with proteinuria and hematuria, due to kidney-liver metabolism.[48]
The peak of blood alcohol level (or concentration of alcohol) is reduced after a large meal.[44]
There have been reported cases of blood alcohol content higher than 1%:
In 1982, a 24-year-old woman was admitted to the UCLA emergency room with a serum alcohol content of 1.51%, corresponding to a blood alcohol content of 1.33%. She was alert and oriented to person and place and survived.[49] Serum alcohol concentration is not equal to nor calculated in the same way as blood alcohol content.[50]
In 1984, a 30-year-old man survived a blood alcohol concentration of 1.5% after vigorous medical intervention that included
dialysis and
intravenous therapy with
fructose.[51]
In 1995, a man from
Wrocław, Poland, caused a car accident near his hometown. He had a blood alcohol content of 1.48%; he was tested five times, with each test returning the same reading. He died a few days later of injuries from the accident.[52]
In 2004, an unidentified Taiwanese woman died of alcohol intoxication after immersion for twelve hours in a bathtub filled with 40% ethanol. Her blood alcohol content was 1.35%. It was believed that she had immersed herself as a response to the
SARS epidemic.[53]
In South Africa, a man driving a
Mercedes-Benz Vito light van containing 15 sheep allegedly stolen from nearby farms was arrested on December 22, 2010, near
Queenstown in
Eastern Cape. His blood had an alcohol content of 1.6%. Also in the vehicle were five boys and a woman, who were also arrested.[54][dubious –
discuss]
On 26 October 2012, a man from
Gmina Olszewo-Borki, Poland, who died in a car accident, recorded a blood alcohol content of 2.23%; however, the blood sample was collected from a wound and thus possibly contaminated.[52]
On 26 July 2013 a 30-year-old man from
Alfredówka, Poland, was found by Municipal Police Patrol from
Nowa Dęba lying in the ditch along the road in Tarnowska Wola. At the hospital, it was recorded that the man had a blood alcohol content of 1.374%. The man survived.[55][56]
Notes
^In Germany, Finland, Netherlands and Sweden, the local language term promille is used; this is occasionally provided as a courtesy in English texts.[39]
^Gullberg, Rod G. (October 2007). "Estimating the uncertainty associated with Widmark's equation as commonly applied in forensic toxicology". Forensic Science International. 172 (1): 33–39.
doi:
10.1016/j.forsciint.2006.11.010.
PMID17210238.
^
abMaskell, Peter D.; Cooper, Gail A. A. (September 2020). "The Contribution of Body Mass and Volume of Distribution to the Estimated Uncertainty Associated with the Widmark Equation". Journal of Forensic Sciences. 65 (5): 1676–1684.
doi:
10.1111/1556-4029.14447.
PMID32421216.
S2CID218677989.
^Maskell, Peter D.; Jones, A. Wayne; Heymsfield, Steven B.; Shapses, Sue; Johnston, Atholl (November 2020). "Total body water is the preferred method to use in forensic blood-alcohol calculations rather than ethanol's volume of distribution". Forensic Science International. 316: 110532.
doi:
10.1016/j.forsciint.2020.110532.
PMID33099270.
S2CID224966411.
^Jones, Alan Wayne (July 2010). "Evidence-based survey of the elimination rates of ethanol from blood with applications in forensic casework". Forensic Science International. 200 (1–3): 1–20.
doi:
10.1016/j.forsciint.2010.02.021.
PMID20304569.
^Dettling, A.; Skopp, G.; Graw, M.; Haffner, H.-Th. (May 2008). "The influence of sex hormones on the elimination kinetics of ethanol". Forensic Science International. 177 (2–3): 85–89.
doi:
10.1016/j.forsciint.2007.11.002.
PMID18079079.
^Huber, H; Karlin, R; Nathan, P E (January 1976). "Blood alcohol level discrimination by nonalcoholics. The role of internal and external cues". Journal of Studies on Alcohol. 37 (1): 27–39.
doi:
10.15288/jsa.1976.37.27.
PMID2811.
^Rowan, D. C. (March 1978). "The Role of Blood Alcohol Level Estimation in Training Alcoholics to become Controlled Drinkers". British Journal of Addiction to Alcohol & Other Drugs. 73 (3): 316–318.
doi:
10.1111/j.1360-0443.1978.tb00159.x.
PMID280356.
^Kelly, Alexandra R.; Fillmore, Mark T. (24 August 2023). "Use of mindfulness training to improve BAC self-estimation during a drinking episode". Psychology of Addictive Behaviors.
doi:
10.1037/adb0000955.
PMC 10907993.
PMID37616096.
S2CID261098937.
^
ab"Absorption Rate Factors". BHS.UMN.edu. Archived from
the original on 18 January 2013. Retrieved 6 March 2018. When food is ingested, the pyloric valve at the bottom of the stomach will close in order to hold food in the stomach for digestion and thus keep the alcohol from reaching the small intestine. The larger the meal and closer in time to drinking, the lower the peak of alcohol concentration; some studies indicate up to a 20% reduction in peak blood alcohol level. Stress causes the stomach to empty directly into the small intestine, where alcohol is absorbed even faster. Liquor mixed with soda or other bubbly drinks speeds up the passage of alcohol from the stomach to the small intestine, which increases the speed of absorption.
Patel, AR; Paton, AM; Rowan, T; Lawson, DH; Linton, AL (August 1969). "Clinical studies on the effect of laevulose on the rate of metabolism of ethyl alcohol". Scottish Medical Journal. 14 (8): 268–71.
doi:
10.1177/003693306901400803.
PMID5812044.
S2CID3067691.
Lowenstein, LM; Simone, R; Boulter, P; Nathan, P (14 September 1970). "Effect of fructose on alcohol concentrations in the blood in man". JAMA. 213 (11): 1899–901.
doi:
10.1001/jama.1970.03170370083021.
PMID4318655.
Soterakis, J; Iber, FL (March 1975). "Increased rate of alcohol removal from blood with oral fructose and sucrose". The American Journal of Clinical Nutrition. 28 (3): 254–7.
doi:
10.1093/ajcn/28.3.254.
PMID1119423.
Rawat, AK (February 1977). "Effects of fructose and other substances on ethanol and acetaldehyde metabolism in man". Research Communications in Chemical Pathology and Pharmacology. 16 (2): 281–90.
PMID847286.
Iber, FL (September 1977). "The effect of fructose on alcohol metabolism". Archives of Internal Medicine. 137 (9): 1121.
doi:
10.1001/archinte.137.9.1121.
PMID901079.
Bode, JC; Bode, C; Thiele, D (1 February 1979). "Alcohol metabolism in man: effect of intravenous fructose infusion on blood ethanol elimination rate following stimulation by phenobarbital treatment or chronic alcohol consumption". Klinische Wochenschrift. 57 (3): 125–30.
doi:
10.1007/bf01476052.
PMID439778.
S2CID8813046.
Sprandel, U; Tröger, HD; Liebhardt, EW; Zöllner, N (1980). "Acceleration of ethanol elimination with fructose in man". Nutrition & Metabolism. 24 (5): 324–30.
doi:
10.1159/000176278.
PMID7443107.
Meyer, BH; Müller, FO; Hundt, HK (6 November 1982). "The effect of fructose on blood alcohol levels in man". South African Medical Journal (Suid-Afrikaanse Tydskrif vir Geneeskunde). 62 (20): 719–21.
PMID6753183.
Crownover, BP; La Dine, J; Bradford, B; Glassman, E; Forman, D; Schneider, H; Thurman, RG (March 1986). "Activation of ethanol metabolism in humans by fructose: importance of experimental design". The Journal of Pharmacology and Experimental Therapeutics. 236 (3): 574–9.
PMID3950864.
Mascord, D; Smith, J; Starmer, GA; Whitfield, JB (1991). "The effect of fructose on alcohol metabolism and on the [lactate]/[pyruvate] ratio in man". Alcohol and Alcoholism. 26 (1): 53–9.
PMID1854373.
Onyesom, I; Anosike, EO (June 2004). "Oral fructose-induced changes in blood ethanol oxidokinetic data among healthy Nigerians". The Southeast Asian Journal of Tropical Medicine and Public Health. 35 (2): 476–80.
PMID15691159.
^O'Neill, Shane; Tipton, KF; Prichard, JS; Quinlan, A (1984). "Survival After High Blood Alcohol Levels: Association with First-Order Elimination Kinetics". Archives of Internal Medicine. 144 (3): 641–2.
doi:
10.1001/archinte.1984.00350150255052.
PMID6703836.
Carnegie Library of Pittsburgh. Science and Technology Department. The Handy Science Answer Book. Pittsburgh: The Carnegie Library, 1997.
ISBN978-0-7876-1013-5.
Perham, Nick; Moore, Simon C.; Shepherd, Jonathan; Cusens, Bryany (2007). "Identifying drunkenness in the night-time economy". Addiction. 102 (3): 377–80.
doi:
10.1111/j.1360-0443.2006.01699.x.
PMID17298644.
Taylor, L., and S. Oberman. Drunk Driving Defense, 6th edition. New York: Aspen Law and Business, 2006.
ISBN978-0-7355-5429-0.