Our EtG Calculation Methodology
A detailed, scientific explanation of how our calculator estimates EtG detection windows
Our EtG calculator employs established pharmacokinetic principles and peer-reviewed research to provide reliable estimates of Ethyl Glucuronide detection windows. The methodology combines the well-validated Widmark formula for blood alcohol estimation with current understanding of EtG formation and elimination kinetics.
This approach allows us to model the complex relationship between alcohol consumption patterns, individual physiological factors, and the resulting EtG metabolite levels that determine detection windows in standard urine testing protocols.
The foundation of our calculation begins with the Widmark formula, developed by Swedish scientist Erik Widmark in the 1930s and still considered the gold standard for forensic alcohol calculations:
- BAC = Blood Alcohol Concentration (%)
- A = Total alcohol consumed (grams)
- W = Body weight (grams)
- r = Widmark factor (distribution constant)
- Males: r = 0.68
- Females: r = 0.55
These factors account for differences in body water content and alcohol distribution.
Ethyl Glucuronide formation occurs through hepatic glucuronidation, a Phase II metabolic process where ethanol is conjugated with glucuronic acid via UDP-glucuronosyltransferase enzymes. Research indicates that approximately 0.02-0.05% of consumed ethanol is converted to EtG.
Key EtG Formation Characteristics:
- Peak EtG levels occur 2-5 hours after alcohol consumption
- EtG concentration correlates with peak blood alcohol levels
- Formation continues as long as ethanol is present in the system
- Individual variation exists based on genetic polymorphisms in UGT enzymes
Our model estimates peak EtG levels using a conversion factor derived from published studies, typically ranging from 50-100 times the peak BAC value, adjusted for individual factors.
EtG elimination follows first-order kinetics with a well-established half-life of 2-3 hours in most individuals. Unlike ethanol, which is eliminated through hepatic metabolism, EtG is primarily eliminated unchanged through renal excretion.
Elimination Formula:
Where:
- C(t) = EtG concentration at time t
- C₀ = Initial EtG concentration
- k = Elimination rate constant (0.277 hr⁻¹ for 2.5-hour half-life)
- t = Time elapsed (hours)
Our calculator uses a conservative 2.5-hour half-life to account for individual variation and provide reliable estimates across different populations.
Scenario: Social Drinking
- 180 lb (81.6 kg) male
- Widmark factor: 0.68
- 4 standard beers (56g alcohol)
- Last drink: 10:00 PM
BAC = (56g / (81,600g × 0.68)) × 100 = 0.101%
Peak EtG ≈ 0.101% × 75 = 7,575 ng/mL (occurs ~12:30 AM)
t = ln(7,575/500) / 0.277 = 10.0 hours after peak
Estimated clearance: 10:30 AM next day
While our methodology is grounded in established science, several factors can significantly affect accuracy:
Physiological Variables:
- Individual metabolism rates
- Liver function variations
- Kidney function and hydration status
- Genetic polymorphisms in metabolic enzymes
- Age, health status, and medications
Testing Variables:
- Laboratory sensitivity and methods
- Sample collection and storage
- Cutoff levels (100-500 ng/mL range)
- Potential for false positives/negatives
- Quality control procedures
Critical Disclaimer: This calculator provides educational estimates only and should never be used for legal, medical, or safety decisions. Individual results may vary significantly from predictions. Always consult qualified professionals and follow official testing protocols.
1. Widmark, E.M.P. (1932). Die theoretischen Grundlagen und die praktische Verwendbarkeit der gerichtlich-medizinischen Alkoholbestimmung. Urban & Schwarzenberg.
2. Schmitt, G., et al. (1997). Ethyl glucuronide: an unusual ethanol metabolite in humans. Synthesis, analytical data, and determination in serum and urine. Journal of Analytical Toxicology, 21(4), 340-346.
3. Wurst, F.M., et al. (2006). Ethyl glucuronide discloses recent covert alcohol use not detected by standard testing in forensic psychiatric inpatients. Alcoholism: Clinical and Experimental Research, 30(3), 471-476.
4. Helander, A., & Beck, O. (2005). Ethyl sulfate: a metabolite of ethanol in humans and a potential biomarker of acute alcohol intake. Journal of Analytical Toxicology, 29(5), 270-274.