Dataset Information

The accuracy and promise of personal breathalysers for research: Steps toward a cost-effective reliable measure of alcohol intoxication?

ABSTRACT:

Objective

Technology is continuing to shape the way we collect health data, including data on alcohol use. A number of technologies are being developed to objectively measure intoxication 'in the wild' without relying on self-report; the most immediate solution may be the use of personal breathalysers. In this study, we aimed to determine whether a cost-effective personal breathalyser would perform in a similar manner to a device used for roadside breath testing.

Method

We intercepted young adults (n = 337; 45% men) outside three concerts, administered 5-min interviews, and asked for breath samples on two devices (a personal breathalyser and a police-grade breathalyser).

Results

Participants reported having consumed an average of 7.3 standard drinks before the interview and had a mean Blood Alcohol Content of 0.077 g/dl on the police-grade device and 0.085 g/dl on the personal device. Difference scores suggested the personal breathalyser was more likely to over report Blood Alcohol Content (bias = 0.008 g/dl).

Conclusion

Although the personal device was more likely to over report Blood Alcohol Content compared with the police-grade device, the results suggest that personal devices could be used as a measure of Blood Alcohol Content when collecting data outside of the lab.

SUBMITTER: Riordan BC

PROVIDER: S-EPMC6001255 | biostudies-literature | 2017 Jan-Dec

REPOSITORIES: biostudies-literature

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Publications

The accuracy and promise of personal breathalysers for research: Steps toward a cost-effective reliable measure of alcohol intoxication?

Riordan Benjamin C BC Scarf Damian D Moradi Saleh S Flett Jayde A M JAM Carey Kate B KB Conner Tamlin S TS

Digital health 20170101

<h4>Objective</h4>Technology is continuing to shape the way we collect health data, including data on alcohol use. A number of technologies are being developed to objectively measure intoxication 'in the wild' without relying on self-report; the most immediate solution may be the use of personal breathalysers. In this study, we aimed to determine whether a cost-effective personal breathalyser would perform in a similar manner to a device used for roadside breath testing.<h4>Method</h4>We interce ...[more]

PMID: 29942621

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Project description:BackgroundAlcohol intoxication can increase inflammation and worsen injury, yet the mechanisms involved are not clear. We investigated whether acute alcohol intoxication increases microvascular permeability and investigated potential signaling mechanisms in endothelial cells that may be involved.MethodsConscious rats received a 2.5 g/kg alcohol bolus via gastric catheters to produce acute intoxication. Microvascular leakage of intravenously administered fluorescein isothiocyanate (FITC)-conjugated albumin (FITC-albumin) from the mesenteric microcirculation was assessed by intravital microscopy. Endothelial-specific mechanisms were studied using cultured endothelial cell monolayers. Transendothelial electrical resistance (TER) served as an index of barrier function, before and after treatment with alcohol or its metabolite acetaldehyde. Pharmacologic agents were used to test the roles of alcohol metabolism, oxidative stress, p38 mitogen-activated protein kinase (MAPK), myosin light-chain kinase (MLCK), rho kinase (ROCK), and exchange protein activated by cAMP (Epac). VE-cadherin localization was investigated to assess junctional integrity. Rac1 and RhoA activation was assessed by ELISA assays.ResultsAlcohol significantly increased FITC-albumin extravasation from the mesenteric microcirculation. Alcohol also significantly decreased TER and disrupted VE-cadherin organization at junctions. Acetaldehyde significantly decreased TER, but inhibition of alcohol dehydrogenase or application of a superoxide dismutase mimetic failed to prevent alcohol-induced decreases in TER. Inhibition of p38 MAPK, but not MLCK or ROCK, significantly attenuated the alcohol-induced barrier dysfunction. Alcohol rapidly decreased GTP-bound Rac1 but not RhoA during the drop in TER. Activation of Epac increased TER, but did not prevent alcohol from decreasing TER. However, activation of Epac after initiation of alcohol-induced barrier dysfunction quickly resolved TER to baseline levels.ConclusionsOur results suggest that alcohol intoxication increases microvascular permeability to plasma proteins. The data also suggest the endothelial-specific mechanism involves the p38 MAPK, Rac1, and reorganization of VE-cadherin at junctions. Last, activation of Epac can quickly resolve alcohol-induced endothelial barrier dysfunction.

Project description:In adults, alcohol intoxication is associated with prolongation of the QT interval corrected for heart rate (QTc). The QTc is influenced by age and sex. Although alcohol intoxication is increasingly common in adolescents, there are no data on the prevalence of QTc prolongation in adolescents with alcohol intoxication. This study aimed to determine the prevalence of QTc prolongation in adolescents with alcohol intoxication and identify at-risk adolescents. In this observational study including adolescents aged 10-18 years, heart rate and QT interval were automatically assessed from an electrocardiogram (ECG) at alcohol intoxication using a validated algorithm. The QTc was calculated using both the Bazett formula (QTcB) and Fridericia formula (QTcF). If present, an ECG recorded within 1 year of the date of admission to the emergency department was obtained as a reference ECG. A total of 317 adolescents were included; 13.3% had a QTcB and 7.9% a QTcF longer than the sex- and age-specific 95th-percentile. None of the adolescents had a QTcB or QTcF > 500 ms, but 11.8% of the adolescents with a reference ECG had a QTcB prolongation of > 60 ms, while no adolescents had a QTcF prolongation of > 60 ms. QTc prolongation was mainly attributable to an increase in heart rate rather than QT prolongation, which underlies the differences between QTcB and QTcF. Male sex and hypokalaemia increased the likelihood of QTc prolongation.Conclusion: QTc prolongation was seen in approximately 10% of the adolescents presenting with alcohol intoxication, and although no ventricular arrhythmias were observed in this cohort, QTc prolongation increases the potential for malignant QT-related arrhythmias. Clinicians must be aware of the possibility of QTc prolongation during alcohol intoxication and make an effort to obtain an ECG at presentation, measure the QT interval, and give an adequate assessment of the findings. We advocate admitting adolescents with alcohol intoxication and QTc prolongation. During hospital admission, we recommend limiting exposure to QTc-prolonging medication, increasing potassium levels to a high-normal range (4.5-5.0 mmol/L) and obtaining a reference ECG at discharge.

Dataset Information

The accuracy and promise of personal breathalysers for research: Steps toward a cost-effective reliable measure of alcohol intoxication?

Objective

Method

Results

Conclusion

Publications

The accuracy and promise of personal breathalysers for research: Steps toward a cost-effective reliable measure of alcohol intoxication?

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