What Is the Normal Alcohol Level in the Body

Alcohol

George F. Koob , ... Michel Le Moal , in Drugs, Addiction, and the Brain, 2014

Blood alcohol levels are measured in gram%. The degree of intoxication throughout the United States is measured by a blood alcohol level, and the legal limit is 0.08   gram%. For example, 0.08grams alcohol/100ml = 0.08gram% = 17mM. Generally, for a male who weighs 150   lbs, 4   ounces of spirits (100 proof = 50% alcohol), four glasses of wine, or four beers will result in a blood alcohol level of approximately 0.10   gram%. For a female who weighs 150   lbs, these same amounts of alcohol will result in a blood alcohol level of 0.12   gram%. The difference in blood alcohol levels in males and females has been attributed to differences in the distribution of body fat, with more fat per kilogram (thus less water) for females, and lower gastric levels of the alcohol-metabolizing enzyme alcohol dehydrogenase in females.

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Alcohol a double-edged sword

Amitava Dasgupta , in Alcohol, Drugs, Genes and the Clinical Laboratory, 2017

Physiological effects of various blood alcohol levels

Blood alcohol depends on many factors including number of drinks, gender (females show higher blood alcohol than males for consuming same amounts of alcohol when body weights are comparable), and body weight. Moreover, peak blood alcohol level is lower if alcohol is consumed with food and if alcohol is sipped instead of consumed rapidly. The presence of food not only reduces blood alcohol level but also stimulates its elimination through the liver. Alcohol is first metabolized to acetaldehyde by the enzyme alcohol dehydrogenase and then by aldehyde dehydrogenase into acetate. Acetate finally breaks down into carbon dioxide and water. For higher alcohol consumption, liver CYP2E1 plays a role in alcohol metabolism.

Substantial research has established that the effect of alcohol on the human depends on the blood alcohol concentration. At a very low blood alcohol level people usually feel relaxation and mild euphoria and some loss of inhibition or shyness. However, at blood alcohol levels that exceed the legal limit for driving in United States, significant impairment of motor skills may occur. At a blood alcohol level of 0.3% and higher, complete loss of consciousness may occur and a blood alcohol level of 0.5% and higher may even cause death (Table 1.2). Drinking excessive alcohol in one occasion may cause alcohol poisoning which if not treated promptly may be fatal. Celik et al. reported that postmortem blood alcohol levels ranged from 136 to 608   mg/dL in 39 individuals who died due to alcohol overdose. Most of those deceased were male [5]. The mechanism of death from alcohol poisoning is usually attributed to paralysis of respiratory and circulatory centers in the brain causing asphyxiation.

Table 1.2. Physiological effects of various blood alcohol levels

Blood alcohol level	Physiological effect
0.01–0.04% (10–40   mg/dL)	Mild euphoria, relaxation, and increased social interactions.
0.05–0.07% (50–70   mg/dL)	Euphoria with loss of inhibition making a person more friendly and talkative. Some impairments of motor skills may take place in some individuals, and as a result, in some countries, e.g., Germany, the legal limit of driving is 0.05%.
0.08% (80   mg/dL)	Legal limit of driving in United States. Some impairment of driving skills may be present in some individuals.
0.08–0.12% (80–120   mg/dL)	Moderate impairment to significant impairment of driving skills depending on drinking habits. Emotional swings and depression may be observed in some individuals.
0.12–0.15% (120–150   mg/dL)	Motor function, speech, and judgement are all severely affected at this height of blood alcohol. Staggering, and slurred speech, may be observed. Severe impairment of driving skills.
0.15–0.2% (150–200   mg/dL)	This is the blood alcohol level where a person appears drunk and may have severe visual impairment.
0.2–0.3% (200–300   mg/dL)	Vomiting, incontinence, symptoms of alcohol intoxication.
0.3–0.4% (300–400   mg/dL)	Signs of severe alcohol intoxication and a person may not be able to move without the help of another person. Stupor, blackout, and total loss of consciousness may also happen.
0.4–0.5% (400–500   mg/dL)	Potentially fatal and a person may be comatose.
Above 0.5% (500   mg/dL)	Highly dangerous/fatal blood alcohol level.

Impairment of motor skills may occur at blood alcohol levels lower than 0.08%. Phillips and Brewer commented that accident severity increases when the driver is merely "buzzed" compared to sober drivers because buzzed drivers are significantly more likely to speed, and the greater the blood alcohol, the greater the speed as well as the severity of the accident. Moreover, a buzzed driver may not put the seatbelt on properly. Usually alcohol-related traffic accidents are more likely to take place on weekends, in the months of June–August, and from 8   pm to 4   am [6].

Falleti et al. demonstrated that cognitive impairment associated with 0.05% blood alcohol is similar to staying awake for 24   h [7]. Moreover, many industrialized countries such as Austria, France, Germany, and Italy have set legal limit of driving at 0.05%. Although the legal limit of driving in Canada is 0.08%, in some Canadian provinces, 0.05% blood alcohol is considered as the "warning range" limit at which officers may suspend a driver's license for 1–7 days. The National Transportation Safety Board in 2014 recommended lowering the legal limit of driving in the United States to 0.05%, but it is not adopted as the law. Scientific research has shown that even at 0.05% blood alcohol virtually all drivers are impaired regarding at least some driving practices [8]. For avoiding driving while intoxicated in United States, consumption of alcohol with food is highly recommended. For men, up to 2 standard drinks consumed with food in a 2   h period (1 drink per hour) and for women up to 1 drink with food consumed in a 2   h period should produce blood alcohol levels below 0.08%.

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Alcohol Withdrawal Seizures

PROSPER N'GOUEMO , MICHAEL A. ROGAWSKI , in Models of Seizures and Epilepsy, 2006

Blood Sampling and Measurement of Blood Alcohol Concentrations

Blood alcohol concentrations are typically measured during intoxication, at the onset of withdrawal symptoms, and during the fully developed withdrawal syndrome. Blood samples are usually collected from the tail vein in mice or by intracardiac sampling in deeply anesthetized rats using large-bore (21-gauge) needles to prevent hemolysis. Blood samples are stored in tubes containing heparin or the anticoagulant potassium oxalate and sodium fluoride (Becton Dickinson Vacutainer Systems, Rutherford, NJ). Blood ethyl alcohol concentrations are measured using gas chromatography (Brown and Long, 1988) or determined in the plasma using the alcohol dehydrogenase method, which requires a spectrophotometer to measure the absorbance at 340 nm (Pointe Scientific, Canton, MI).

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Toxicology/Alcohol

A. Stowell , in Encyclopedia of Forensic Sciences (Second Edition), 2013

Abstract

Although blood alcohol concentrations are most commonly used to assess the degree of alcohol intoxication, blood is not always available for analysis, and it may be in poor condition, especially in postmortem investigations. Therefore, analysis of alcohol in other body fluids is common in forensic laboratories. The alcohol concentration in a body tissue or fluid is generally proportional to the water content of that tissue or fluid. For example, if the water content of a body tissue is 10% higher than that of blood, the tissue's alcohol content should be 10% higher than that of blood. This is the basis for estimating blood alcohol concentrations from alcohol concentrations in other body fluids and tissues. Knowledge of the alcohol content of oral fluid, sweat, and tears can be used to make reliable estimates of coexisting blood alcohol concentrations. However, such estimates are more complicated when dealing with body fluids existing in isolated compartments where there is slow or very little exchange of alcohol between blood and the isolated fluid, for example, bile, eye fluid, and urine. Nevertheless, in postmortem investigations, knowledge of the alcohol content of any one of these and other fluids can often be used to estimate the minimum blood alcohol concentration existing some time before death.

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The Effects of Alcohol on the Human Nervous System

Kathleen T. Brady , in The Effects of Drug Abuse on the Human Nervous System, 2014

2.2 Acute Intoxication

As blood alcohol levels increase in humans, the impact of alcohol on cognitive abilities, psychomotor performance, and vital physiologic functions increases (Naranjo and Bremner, 1993, Table 2).

Table 2. Clinical Manifestations of Blood Alcohol Concentration

Blood Alcohol Level mg%	Clinical Manifestations
20–99	Loss of muscular coordination Changes in mood, personality, and behavior
100–99	Neurologic impairment with prolonged reaction time, ataxia, incoordination, and mental impairment
200–299	Very obvious intoxication, except in those with marked tolerance nausea, vomiting, marl-zed ataxia
300–399	Hypothermia, severe dysarthria, amnesia, Stage 1 anesthesia
400–799	Onset of alcoholic coma, with precise level depending on degree of tolerance Progressive obtundation, decreases in respiration, blood pressure and body temperature Urinary incontinence or retention, reflexes markedly decreased or absent
600–800	Often fatal because of loss of airway protective reflexes from airway obstruction by flaccid tongue, from pulmonary aspiration of gastric contents, or from respiratory arrest from profound central nervous system obstruction

Source: Reproduced with permission (Mayo-Smith, 2009)

With chronic use, tolerance to the effects of alcohol develops, so the functional impact of a specific amount of alcohol is dependent on a number of factors including degree of tolerance, rate of intake, body weight, percentage of fat and gender.

Alcohol intoxication initially impacts the frontal lobe region of the brain, causing disinhibition, impaired judgment, and cognitive and problem-solving difficulties. At blood alcohol concentrations between 20   mg% and 99   mg%, along with increasing mood and behavioral changes, the effects of alcohol on the cerebellum can cause motor-coordination problems. With blood alcohol levels of 100–199   mg%, there is neurologic impairment with prolonged reaction time, ataxia, and incoordination. Blood alcohol levels of 200–399   mg% are associated with nausea, vomiting, marked ataxia and hypothermia. Between 400   mg% and 799   mg% blood alcohol level, the onset of alcohol coma can occur. Serum levels of alcohol between 600   mg% and 800   mg% are often fatal. Progressive obtundation develops with decreases in blood pressure, respiration, and body temperature. Death may be caused by the loss of protective airway reflexes, aspiration of gastric contents or respiratory/cardiac arrest through depressant effects of alcohol on the medulla oblongata and the pons (Table 2, and Mayo-Smith, 2009).

Severely intoxicated individuals may require admission to the hospital for management in specialized units with close monitoring and respiratory support. In individuals with coma, alternative causes must always be investigated, such as head injury, other drug use, hypoglycemia, or meningitis.

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Biochemical Mechanisms of Fatty Liver and Bioactive Foods

R. Sharma , in Bioactive Food as Dietary Interventions for Liver and Gastrointestinal Disease, 2013

3 Diagnosis of Fatty Liver Disease

3.1 Elevated Liver Enzymes

Serum ADH, serum transaminases aspartate transaminase [AST] and ALT are major indicators of alcohol-induced injury. Author established hepatocyte and Kupffer cell enzymes participating in liver injury and drug metabolism at different points in cell as shown in Figure 41.2. In fatty liver, diffused liver injury was shown associated with elevated liver tissue metabolite contents, serum metabolites and nuclear magnetic resonance (NMR) relaxation data with visible changes in liver magnetic resonance imaging (MRI) scan (see Figure 41.4; Table 41.1).

Figure 41.4. Focal hepatic steatosis is shown by different imaging modalities including US (a), CT (b), in phase MRI (c), out phase MRI (d), T ₂wt MRI (e), T ₂FS MRI (f), T ₁Grad MRI (g), and out of phase susceptibility MRI (h).

Source: http://radiopaedia.org/articles/focal_fat_infiltration.

Table 41.1. Comparative NMR Biochemical Correlation Analysis of Liver with Diffused Injury by Different Methods Using NMR Relaxation Times, In Vitro NMR Spectroscopy, In Vivo MR Spectroscopy, Tissue Metabolites, and Serum Enzyme Levels

Method	Normal liver	Diffused liver injury
In vitro pulsed NMR T 1 ms T 2 ms	448   ±   20   ms 88   ±   7   ms	939   ±   11   ms 144   ±   9   ms
In vitro NMR spectroscopy   Phosphocreatine/creatine   Phosphorylcholine   Taurine	0.48   mM 7.2   mM 5.75   mM	1.06   mM 61.3   mM 23   mM
In vivo NMR spectroscopy   Glutamine   Aspartate	36.1   mM 6.27   mM	35.2   mM 2.7   mM
Biochemical tissue metabolites   Phospholipids   Triglycerides	113.8   ±   3.9   mg% 89.7   ±   4.8   mg%	168.9   ±   5.6   mg% 139.9   ±   3.6   mg%
Biochemical serum levels a   Serum glutamate pyruvate transaminase   Alkaline phosphatase   Bilirubin	18.5   ±   1.9 IU 39.5   ±   7.8 IU 1.5   ±   0.2   mg%	140.9   ±   15.4 IU 239.9   ±   23.4 IU 4.2   ±   0.6   mg%

a

IU is defined as μ moles substrate used per minute per mg enzyme protein.

Source: Sharma, R., 1995. PhD (MRI) dissertation thesis submitted at Indian Institute of Technology, New Delhi.

3.2 Imaging of Fatty Infiltration

Liver imaging is emerging as theradiagnostic tool to image liver tissue changes with localization of cellular or molecular lesions or infiltration. MRI is choice of microimaging of soft tissues. Due to soft tissue of liver and active metabolism in hepatocytes, sequential changes in liver acini offer a window to assess metabolic changes and fatty infiltration as shown in Figure 41.2.

3.3 Focal Hepatic Steatosis

Focal hepatic steatosis (focal fat infiltration of the liver) is common and seen in a number of clinical settings, essentially the same as those that contribute to diffuse hepatic steatosis:

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Diabetes mellitus

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Obesity

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Alcohol abuse

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Exogenous steroids

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Drugs (amiodarone, methotrexate, chemotherapy)

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IV hyperalimentation

In general treatment of the underlying condition will reverse the findings.

3.4 Location

A characteristic location for focal fatty change is the medial segment of the left lobe of the liver (segment IV) either anterior to the porta hepatis or adjacent to the falciform ligament. This distribution is the same as that seen in focal fatty sparing and is thought to relate to variations in vascular supply. This also would account for focal fatty change/sparing sometimes seen related to vascular lesions.

3.5 Radiographic Features

3.5.1 Ultrasound

Ultrasound features only become apparent when the amount of fat reaches 15–20%. Features include the following:

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Increased hepatic echogenicity

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Hyperattenuation of the beam

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Mild or absent positive mass effect

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Geographic borders

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No distortion of vessels

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Inability to visualize the portal vein walls (as the parenchyma is as bright as the wall)

3.5.2 Computed tomography

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Decreased attenuation (noncontrast computed tomography (CT))

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normal liver 50 57 HU

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decreases by 1.6 HU per mg of fat in each gram of liver

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Decreased attenuation (postcontrast CT)

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liver and spleen should normally be similar on delayed (70   s) scans

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earlier scans are unreliable as the spleen enhances earlier than the liver (systemic supply rather than portal)

3.5.3 Magnetic resonance imaging

MRI is the imaging modality of choice in any case where the diagnosis is felt to be less than certain:

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Increased T1 signal

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Signal dropout in out of phase imaging

•

Ability to quantify fat fraction

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Alcohol: Absorption, Metabolism, and Physiological Effects

R. Rajendram , ... V. Preedy , in Encyclopedia of Human Nutrition (Third Edition), 2013

Effects of Food on Blood Ethanol Concentration

The peak BEC is reduced when alcohol is consumed with or after food. Food delays gastric emptying into the duodenum. This attenuates the sharp early rise in BEC seen when alcohol is taken on an empty stomach. Food also increases elimination of ethanol from the blood. The area under the BEC/time curve (AUC) is reduced (Figure 4). The contributions of various nutrients to these effects have been studied, but small, often conflicting, differences have been found. It appears that the caloric value of the meal is more important than the precise balance of nutrients.

Figure 4. Blood ethanol concentration curve after oral dosing of ethanol. A subject ingested 0.8   g   kg⁻¹ ethanol over 30 minutes either after an overnight fast or after breakfast. The peak blood ethanol concentration and the area under the curve are reduced if ethanol is consumed with food.

In animal studies ethanol is often administered with other nutrients in liquid diets. The AUC is less when alcohol is given in a liquid diet than with the same dose of ethanol in water. The different blood ethanol profile in these models may affect the expression of pathology.

However, food increases splanchnic blood flow, which maintains the ethanol diffusion gradient in the small intestine. Food-induced impairment of gastric emptying may be partially offset by faster absorption of ethanol in the duodenum.

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Alcohol: Acute and Chronic Use and Postmortem Findings

A.W. Jones , in Encyclopedia of Forensic and Legal Medicine (Second Edition), 2016

Reporting Blood–Alcohol Concentrations

The statutory BAC limits for driving a motor vehicle differ fourfold between countries, and this seems to depend on historical traditions, lifestyle, and various political forces and public opinion about driving after drinking alcohol (Table 2). In most European nations, the statutory BAC limit is 50   mg/100   ml, whereas Norway, Sweden, and Poland have adopted a limit of 20   mg/100   g blood (21   mg/100   ml). The current (2014) legal BAC limit for driving in the UK and throughout the USA, as well as all Canadian provinces, is 80   mg/100   ml, although lowering this to 50   mg/100   ml has been suggested to reduce alcohol-related crashes (Fell and Voas, 2014).

Table 2. Statutory concentration limits of alcohol in blood and breath for operating a motor vehicle in various countries and the blood/breath ratio of alcohol used for legal purposes

Country where limits apply	Blood alcohol concentration	Breath alcohol concentration	Blood/breath ratio of alcohol
Most European nations	0.50   g/l	0.25   mg/l	2000:1
The Netherlands	0.50   mg/ml	220   µg/l	2300:1
Ireland	50   mg/100   ml	22   µg/100   ml	2300:1
Norway, Poland, Sweden a	0.20   mg/g	0.10   mg/l	2100:1
Finland	0.50   mg/g	0.22   mg/l	2260:1
USA	0.08   g/100   ml	0.08   g/210   l	2100:1
UK b	80   mg/100   ml	35   µg/100   ml	2300:1
Canada	80   mg/100   ml	80   mg/100   ml c	2100:1

Source: Reproduced from Jones, A.W. 2011a. Driving under the influence of alcohol. In: Moffat, A.C., Osselton, M.D., Widdop, B., Watts, J. (Eds.), Clarke's Analysis of Drugs and Poisons. London: The Pharmaceutical Press, pp. 87–114.

a

BAC of 0.20   mg/g is equivalent to 0.21   mg/ml.

b

The threshold concentration for alcohol in urine is 107   mg/100   ml.

c

The result of a breath alcohol test is converted into presumed blood alcohol.

The units used to report BAC for clinical and forensic purposes are expressed as either mass per unit volume (e.g., g/l, mg/ml, or g/100   ml) or mass per unit mass (e.g., g/kg or mg/g). In most nations mass/volume units are used, although for historical reasons in Germany and the Nordic countries BAC for legal purposes is defined as mass/mass. Because the specific gravity of whole blood is 1.055 on average, 100   mg/100   ml blood is close to 95   mg/100   g blood (Dettmeyer et al., 2014).

In hospital clinical laboratories, alcohol is determined in specimens of plasma or serum, not in whole blood. This needs to be considered if and when results from clinical laboratories are used in criminal cases, such as drunk driving. Because the water content of serum and plasma (~92% w/w) is higher than in an equal volume of blood (~80% w/w), the concentrations of ethanol will also be higher. Direct measurements have shown that the average distribution ratio for ethanol between serum (plasma) and whole blood is 1.15:1, with a range from 1.10:1 to 1.20:1 (Charlebois et al., 1996). Moreover, clinical laboratories report ethanol concentrations in mmol/l, where 21.7   mmol/l = 100   mg/100   ml or 0.1% w/v.

The concentrations of ethanol determined in serum or plasma can be converted to the concentration in blood using known values of the serum/blood concentration ratios. The following conversion factors are recommended depending on whether results are intended for research, clinical, or legal purposes.

$\mathrm{For}\mathrm{research}\mathrm{and}\mathrm{clinical}\text{purposes}:\mathrm{Blood}\mathrm{alcohol}\mathrm{concentration}=\mathrm{plasma}(\mathrm{serum})\mathrm{concentration}/1.15$

$\mathrm{For}\mathrm{legal}\text{purposes}:\mathrm{Blood}\mathrm{alcohol}\mathrm{concentration}=\mathrm{plasma}(\text{serum})\mathrm{concentration}/1.20$

Table 3 compares blood ethanol concentrations when expressed in different units as adopted for forensic purposes in various countries; the equivalent concentrations in mmol/l are also shown for comparison.

Table 3. Relationships between ethanol concentrations expressed in different units for forensic purposes and in clinical chemistry laboratories

UK and Ireland mg/100   ml	USA and Australia g/100   ml (g%)	Most European nations, g/l	Nordic countries and Germany, mg/g or g/kg a	Clinical laboratories, mmol/l b
50	0.05	0.50	0.47	10.9
80	0.08	0.80	0.76	17.4
100	0.10	1.00	0.95	21.7
150	0.15	1.50	1.42	32.6
200	0.20	2.00	1.89	43.4

a

The specific gravity of whole blood is taken as 1.055, where density is 1.055   g/ml.

b

Molecular weight of alcohol taken to be 46.07.

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Ethanol- and Drug-Facilitated Crime

Christian Staub , Aline Staub Spörri , in Toxicological Aspects of Drug-Facilitated Crimes, 2014

2.7 Determination of Urine Alcohol Concentration (UAC)

The methods used for blood alcohol analysis can also be used to determine the amount of ethanol in urine samples. The quantitative relationship between the urine alcohol concentration (UAC) and the BAC has been extensively studied by Jones. ^14,15 In addition to the higher water content in urine (≈99%) compared to whole blood (≈80%), the concentration–time curves are shifted in time. In an interesting study from the same group, ¹⁶ the UAC/BAC ratio was determined after volunteer subjects drank a standard dose of ethanol (0.85   g/kg body weight) in the form of neat whiskey over 25   min on an empty stomach. The subjects emptied their bladders of any residual urine before starting to drink, and further voids were collected every 60 minutes for up to 8 hours. Temporal variations in the UAC/BAC ratio were measured, and the mean ratio was less than unity for the 60 minute void, whereas at 120 minutes (the post-resorption phase) and all later times, the UAC/BAC ratio was 1.25 or more (a ratio equal to 3.6 after 8 hours). After 360 minute post-drinking, as the BAC decreased below 0.5   g/kg, the mean UAC/BAC increased significantly and continued to increase as the BAC approached zero. Therefore, when the time between the alleged crime and the blood sampling is more than 8 hours or when the BAC is close to 0   g/kg, it is recommended to collect one urine sample and to determine the urine alcohol (ethanol).

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Alcohol: Breath Analysis

A.W. Jones , in Encyclopedia of Forensic and Legal Medicine (Second Edition), 2016

Statutory Limits of Breath-Alcohol Concentration

In most countries punishable BAC limits for driving existed long before the use of evidential breath-alcohol instruments was considered feasible. An exception was the USA because of constitutional issues about unreasonable search and seizure and self-incrimination it was more problematic to obtain blood samples for analysis in criminal cases. When the first drink-driving laws were enforced the suspects were expected to provide samples of breath or urine for analysis of alcohol concentration.

When in the 1980s European nations began to use evidential breath-alcohol instruments, it was considered more scientifically sound to establish a threshold BrAC instead of converting the result into a BAC. Unfortunately, different countries opted to use different BBRs to arrive at statutory BrAC limits ranging from 2000:1 to 2400:1   as indicated by the information in Table 1.

The UK Road Transport Act of 1981 stipulated 35   µg/100   ml as the punishable BrAC limit and this was derived from the pre-existing BAC limit of 80   mg/100   ml. This assumed a BBR of 2300:1 (80/35×1000=2286:1, which rounds up to 2300:1). The Republic of Ireland, the Netherlands, and Belgium also adopted a 2300:1 BBR when setting their respective BrAC limits. Other European nations such as France and Spain approved a BBR of 2000:1.

The situation in Germany and the Nordic countries is more complicated because the statutory BAC limit is reported in mass/mass concentration units (e.g., 0.50   mg/g or 0.50   g/kg), which is the same as 0.527   mg/ml (density of blood=1.055   g/ma). Dividing 0.527   mg/ma by 2100 (BAC/BrAC ratio) gives a threshold BrAC of 0.25   mg/l ((0.50/2100)×1000=0.25   mg/l). The statutory BAC and BrAC limits that operate in Germany and the Nordic countries are also shown in Table 1.

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What Is the Normal Alcohol Level in the Body

Source: https://www.sciencedirect.com/topics/immunology-and-microbiology/alcohol-blood-level

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