Inhalation of Alcohol Vapor: Measurement and Implications
Robert Ross MacLean, Gerald W. Valentine, Peter I. Jatlow, and Mehmet Sofuoglu
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Department of Psychiatry (RRM, GWV, MS), School of Medicine, Yale University, West Haven, Connecticut; VA Connecticut Healthcare System (RRM, GWV, MS), West Haven, Connecticut; and Laboratory Medicine (PIJ), Yale University, West Haven, Connecticut
Reprint requests: Robert Ross MacLean, PhD, Department of Psychiatry, Yale University, VA Connecticut Healthcare System, 950 Campbell Ave, Bldg. 35LL, West Haven, CT06516; Tel.: 203-932-5711; Fax: 203-937-3472; [email protected]
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Decades of alcohol research have established the health risks and pharmacodynamic profile of oral alcohol consumption. Despite isolated periods of public health concern, comparatively less research has evaluated exposure to alcohol vapor. Inhaled alcohol initially bypasses first-pass metabolism and rapidly reaches the arterial circulation and the brain, suggesting that this route of administration may be associated with pharmacological effects that increase the risk of addiction. However, detailed reviews assessing the possible effects of inhaled alcohol in humans are lacking. A comprehensive, systematic literature review was conducted using Google Scholar and PubMed to examine manuscripts studying exposure to inhaled alcohol and measurement of biomarkers (biochemical or functional) associated with alcohol consumption in human participants. Twenty-one publications reported on alcohol inhalation. Fourteen studies examined inhalation of alcohol vapor associated with occupational exposure (e.g., hand sanitizer) in a variety of settings (e.g., naturalistic, laboratory). Six publications measured inhalation of alcohol in a controlled laboratory chamber, and 1 evaluated direct inhalation of an e-cigarette with ethanol-containing “e-liquid.” Some studies have reported that inhalation of alcohol vapor results in measurable biomarkers of acute alcohol exposure, most notably ethyl glucuronide. Despite the lack of significantly elevated blood alcohol concentrations, the behavioral consequences and subjective effects associated with repeated use of devices capable of delivering alcohol vapor are yet to be determined. No studies have focused on vulnerable populations, such as adolescents or individuals with alcohol use disorder, who may be most at risk of problems associated with alcohol inhalation.
Keywords: Ethanol Vapor, Alcohol Inhalation, Alcohol Without Liquid, Vaportini, Vaping
ALCOHOL USE IS a significant health problem that often co-occurs with other addictive disorders and mental health diagnoses (Bradizza et al., 2006; Falk et al., 2006; Grant et al., 2004; RachBeisel et al., 1999). While scores of human and animal studies have exhaustively characterized the behavioral and neurocognitive effects resulting from oral ingestion over a wide range of doses, the evaluation of effects from alternative routes of alcohol absorption has received comparatively little attention. Notably, alcohol inhalation in humans has been documented within contexts associated with incidental exposure (e.g., occupational or environmental) as well as intentional, or inadvertent, exposure while using devices that deliver alcohol vapor.
Concerns about the negative health impact of exposure to inhaled alcohol have been present for decades (e.g., Lester and Greenberg, 1951). The majority of research on incidental exposure to alcohol vapor has largely focused on occupational exposure, namely healthcare professionals that frequently use commercial alcohol-containing products such as hand sanitizer; but emerging research suggests that another source of exposure to inhaled alcohol is from the use of e-cigarettes that contain ethanol (EtOH) in the “e-liquid.” E-cigarettes are battery-operated devices that use an electrical current to heat small metal coils that then generate aerosols from an e-liquid reservoir (i.e., tank or saturated wicking material). E-liquids typically contain a “base mixture” of glycerol and propylene glycol to which various flavoring ingredients and nicotine are added. In addition, EtOH is a variable, but frequent constituent of e-liquids (Cai and Kendall, 2009; Ellicott, 2009; Herrington and Myers, 2015; Tygat, 2007; Valance and Ellicott, 2008; Varlet et al., 2015) and alcohol has been detected in the aerosols produced from them (Herrington et al., 2015; Laugesen, 2008). Furthermore, some Internet-based e-cigarette forums include recipes that recommend alcohol as an ingredient in self-made e-liquids. Consequently, the fact many e-cigarette users are repeatedly inhaling variable levels of alcohol during routine e-cigarette use has potential health implications.
In addition, “alcohol vaporizers” that use heat or physical agitation to generate alcohol vapor or aerosols in an enclosed system that are then inhaled have periodically been publicized as a novel mode of recreational alcohol use (Le Foll and Loheswaran, 2014). For example, one such method known as “alcohol without liquid” used a nebulizer to mix alcohol and oxygen to create a mist (Lovell, 2004). Although the specter of a public health menace from inhaled alcohol use emerged with these early reports, widespread recreational use of inhaled alcohol or of other routes of administration failed to materialize and these alternative forms of alcohol use have largely been relegated to Internet-based curiosities (Stogner et al., 2014). Collectively, the absence of sustained, identifiable public health risks resulting from recreational or coincidental exposure to inhaled alcohol, combined with the absence of evidence for acute safety risks within extant literature on studies simulating occupational exposure, has resulted in an implicit presumption that inhaled alcohol poses negligible risks as compared to the well-established consequences of ingested alcohol. With that said, the scientific assessment of harm from inhaled alcohol is incomplete because it has been based upon comparisons to the effects of ingested alcohol and has relied on methods and assumptions that do not address more subtle behavioral, cognitive, and physical manifestations that may result from the possibly dissimilar pharmacodynamics of inhaled alcohol (Fig. 1).
Further exploration of the behavioral and pharmacological profile of inhaled alcohol use is particularly relevant for drugs of abuse, because the rate of delivery to brain receptor sites is positively correlated with their abuse potential and addiction risk (Allain et al., 2015). In well-controlled human laboratory studies, faster delivery of fixed doses of opioids, benzodiazepines, cocaine, and stimulants produce greater positive subjective drug effects (Marsch et al., 2001; de Wit et al., 1992). Preclinical studies suggest that greater psychomotor sensitization and immediate early gene expression are potential mechanisms by which rate of delivery impacts the behavioral effects for drugs of abuse (Samaha et al., 2005). As with smoked drugs such as nicotine and cocaine, inhaled alcohol bypasses first-pass metabolism and, compared with other routes of administration, should rapidly reach arterial circulation in the brain. Consequently, inhaled alcohol may be associated with enhanced behavioral effects including increased risk of addiction. Indeed, in rodents, chronic exposure to alcohol vapor was found to be the most effective mechanism for inducing alcohol dependence (Gilpin et al., 2008). If similar effects are present in humans, inhaled alcohol may produce a “priming” effect for alcohol consumption when small doses of alcohol are rapidly delivered. To determine the influence of inhaled alcohol, it is helpful to first evaluate whether exposure to alcohol vapor can be detected via established alcohol biomarkers.
The purpose of this focused review is to (i) summarize the translational foundation of alcohol inhalation and evaluate possible effects of exposure in humans, (ii) establish the objective evidence for systemic alcohol absorption after human inhalation, and (iii) discuss the most common contexts of alcohol inhalation and their differential risk profiles.
ANIMAL MODELS OF EXPOSURE TO ALCOHOL VAPOR
Preclinical studies provide the best evidence to date for characterizing possible risks associated with inhalation of alcohol vapor. Compared with oral administration, EtOH vapor provides a faster, more reliable method of inducing alcohol dependence in animal models (e.g., Heilig and Koob, 2007; Koob et al., 2009; Martin et al., 2012; Sommer and Spanagel, 2013; for review, see Vendruscolo and Roberts, 2014). The use of alcohol vapor inhalation for the induction of dependence has several advantages over other methods of forced alcohol administration (e.g., oral gavage, intragastric intubation) such as precise control of the dose, duration, and pattern of exposure that correspond to key features of alcohol dependence including withdrawal severity and tolerance (Gilpin et al., 2008; Goldstein and Pal, 1971; Rimondini et al., 2003). In a seminal study, Rogers and colleagues (1979) compared alcohol exposure via an inhalation chamber, intubation, and liquid diet in rats. Of these, alcohol inhalation was the only method to safely induce tolerance and dependence by producing sustained blood alcohol levels above 100 mg/dl while permitting rats to move normally and match nutritional needs between the control and experimental groups (Rogers et al., 1979). In subsequent operant conditioning paradigms, rats permitted to self-administer EtOH vapor achieved sustained blood alcohol levels between 100 and 150 mg/dl that significantly reduced the severity and presence of withdrawal criteria (Roberts et al., 1996). Withdrawal-associated increases in operant self-administration of EtOH vapor in alcohol-dependent rats has also been shown to persist for 4 to 8 weeks after induction of dependence (Roberts et al., 2000). Another study comparing liquid diet and vapor inhalation in rats concluded both routes of administration consistently produced alcohol withdrawal; however, vapor inhalation, relative to the liquid diet, was associated with a greater peak and average severity of withdrawal symptoms and a higher average blood alcohol level at the time of withdrawal (217.8 mg/dl vs. 94.3 mg/dl, respectively) (Macey et al., 1996). Finally, self-administration of an alternative reinforcer (i.e., saccharin) in rodents exposed to intermittent vapor was not significantly different than no alcohol controls, suggesting that the motivational mechanisms driving self-administration are likely specific to alcohol (Becker and Lopez, 2004; O’Dell et al., 2004).
Animal models using alcohol vapor have also contributed to our understanding of the impact of EtOH on the brain and other vital organs as well as in evaluating the mechanisms and efficacy of possible pharmacological interventions for chronic alcohol use. Alcohol vapor exposure in rodents results in alcohol-induced alterations in neural pathways that have been associated with alcohol use in humans such as dopamine (Budygin et al., 2007; Hirth et al., 2016), GABA (Roberto et al., 2004), glutamate (Rimondini et al., 2002; Roberto et al., 2006), and corticotrophin-releasing factors (Sommer et al., 2008; for review, see Heilig and Koob, 2007). Preclinical research using alcohol vapor to induce repeated cycles of intoxication and withdrawal has elucidated mechanisms critical to the development and evaluation of pharmacological intervention (Czachowski and Delory, 2009; Gewiss et al., 1991; Rimondini et al., 2002; for review, see Meinhardt and Sommer, 2015). For example, the administration of acamprosate blocks exposure-induced, but not basal, EtOH vapor intake and the resultant changes in gene expression mirror those in human models of alcohol dependence (Rimondini et al., 2002). Chronic intermittent EtOH vapor exposure in rats also produces widespread significant tissue injury including hepatic, pulmonary, and cardiovascular changes (Mouton et al., 2016). In sum, the use of alcohol vapor to induce dependence in preclinical models is an effective approach for evaluating motivational, biological, and pharmacological factors associated with chronic alcohol use and intoxication.
INHALED ALCOHOL IN HUMANS: POSSIBLE REINFORCING EFFECT
Although alcohol vapor is arguably the most effective method of inducing a state of dependence in animal models, there is a paucity of research on the behavioral and pharmacological profile of inhaled alcohol in humans. A cursory Internet search typically yields multiple news articles, instructional blogs, and user-uploaded videos of consumer and commercial devices that are designed to deliver alcohol vapor for recreational use. Most appear to be targeted to young adults and often include anecdotal evidence of a rapid “high” that quickly subsides. Additionally, patterns of use closely resemble binge drinking where the device is used frequently for a short period of time to achieve subjective levels of intoxication. Despite the digital presence of alcohol vaping devices and media reports of increasing use, no studies have directly compared behavioral and pharmacological profiles of oral and inhaled routes of alcohol administration in humans. As such, the relative reinforcing strength of vaporized alcohol transmitted to the brain via arterial uptake is largely unknown. By analogy, arterial levels of inhaled nicotine are reported to be as much as 10-fold higher than concurrent venous concentrations in blood (Benowitz, 2008; Hukkanen et al., 2005). Thus, the immediate impact of inhaled alcohol on brain sites of action may be out of proportion to those predicted from blood alcohol content (BAC) measurements.
Although oral and inhaled alcohol use likely entail differences in pharmacodynamics, human neuroimaging studies using oral and/or inhaled alcohol as conditioned reinforcers reveal meaningful similarities in cue reactivity in response to small doses of alcohol. Oral administration of just 1 ml of preferred brand of alcohol to humans during an fMRI scan is associated with increased craving and activation in reward-related regions of the brain, including the nucleus accumbens, amygdala, precuneus, dorsal striatum, and insula (Claus et al., 2011; Filbey et al., 2008; Ray et al., 2014). Furthermore, activation of these regions is positively associated with alcohol use disorder severity (Claus et al., 2011). Alcohol odors have also been used as conditioned reinforcers in human fMRI studies by forcing air into a closed container of alcohol that volatilizes alcohol into a nasal cannula attached to the participant (Lowen and Lukas, 2006; Lukas et al., 2013; Schneider et al., 2001). Exposure to inhaled alcohol, relative to neutral odors, has been associated with brain activation in the nucleus accumbens, amygdala, and ventral tegmental area (Kareken et al., 2004; Schneider et al., 2001). Thus, exposure to even a small amount of alcohol or inhalation of vaporized alcohol has analogous and potentially additive effects on brain regions known to be involved in the development and maintenance of addiction.
ACUTE BIOCHEMICAL AND FUNCTIONAL BIOMARKERS FOR ALCOHOL EXPOSURE
A biomarker is an objectively measured characteristic that is evaluated as a therapeutic indicator of a pharmacologic response to intervention or a diagnostic indicator to assess the risk or presence of a disease (Biomarkers Definitions Work Group, 2001; Gutman and Kessler, 2006). As inhaled alcohol is likely associated with low levels of alcohol exposure and not necessarily associated with chronic alcohol consumption, the current review will focus on the biomarkers of acute alcohol exposure (see Ingall, 2012).
Acute Biochemical Biomarkers
Two direct biochemical markers that have been used to study the bioavailability of inhaled alcohol are breath alcohol and the urinary alcohol metabolites, ethyl glucuronide (β-D-6-glucuronide or EtG) and ethyl sulfate (EtS).
Breath/Blood Alcohol Content
In both forensic and clinical settings, breath alcohol content (BrAC) is accepted as a valid estimation of BAC (Jones, 1993; Martin et al., 1984). The pharmacodynamic profile of ingested alcohol is well established. The principle effects (i.e., subjective, motor, cognitive) of acute alcohol exposure are most evident in the rising BAC curve (Friel et al., 1995; Wilkinson, 1980); moreover, individuals are typically more responsive to changes in BAC than to the absolute level of BAC (Martin et al., 2006). Although the pharmacodynamics of inhaled alcohol have not been established, it is possible that inhalation of alcohol vapor may correspond to low levels of total exposure that share features of the rising curve after acute oral alcohol exposure. Alterations in alcohol-specific motivational and attention processes are also evident at low BAC levels, including increasing craving and attention to alcohol-related stimuli (Schoenmakers et al., 2008). Collectively, these studies highlight the clinical importance of even a low dose of oral alcohol, particularly in the rising BAC curve, and possible shifts in motivation that are evident after exposure to relatively small amount of alcohol.
Ethyl Glucuronide and Ethyl Sulfate
Two additional direct biochemical biomarkers are EtG and EtS (Jatlow and O’Malley, 2010; Wurst et al., 2015). While they are only minor metabolites of EtOH, accounting for less than 0.1% of total EtOH dispersion (Helander et al., 2009), both EtG and EtS can detect alcohol a few hours after exposure (Wurst et al., 2006; Zimmer et al., 2002) and remain detectable for days depending upon the dose (Helander and Beck, 2005; Jatlow et al., 2014; Wurst et al., 2015). Particularly relevant to alcohol inhalation, EtG and EtS are effective at confirming that alcohol has been absorbed even in the absence of a positive BAC.
Acute Functional Biomarkers
The primary action of ingested alcohol is dose-dependent central nervous system depression exemplified by functional changes in multiple cognitive and motor domains (Little, 1991). Much of the existing literature on functional biomarkers has focused on deficits at or above the legal limit for intoxication (i.e., 80 mg/dl); but deficits in reaction time, response inhibition, working memory, and visuo-motor control are observable at BAC under the traditional cutoff for intoxication (for review, see Brick and Erickson, 2009; Chamberlain and Solomon, 2002). A review of over 100 studies on low-dose alcohol exposure suggested that functional impairment of skills related to driving begin with any departure from a BAC of zero (Moskowitz and Fiorentino, 2000). All of the above studies are based on oral ingestion and subsequent peripheral (venous) measurement or estimation of BAC, which may not be the most effective for quantifying alcohol after inhalation. Although the impairments associated with low-level alcohol exposure may not be sufficient to endanger personal safety (e.g., driving under the influence), subjective effects and functional impairments associated with alcohol consumption could trigger alcohol-specific expectancies that may increase reactivity to alcohol cues and motivate drinking behavior.
MATERIALS AND METHODS
Literature searches were performed in PubMed and Google Scholar using the following search terms: “alcohol OR ethanol AND inhalation OR vapor,” without any restrictions on date of manuscript publication. Potential studies were limited to those with human participants that included both exposure to inhaled alcohol and measurement of biomarkers (biochemical or functional) associated with alcohol consumption. Upon completion of literature search, the reference sections of identified articles and reviews (e.g., Stogner et al., 2014) were used to locate additional studies that met inclusion criteria.
A total of 21 publications met criteria to be included in the review. A summary of findings can be found in Table 1. Fourteen studies examined inhalation of alcohol vapor associated with occupational exposure (e.g., hand sanitizer) in a variety of settings (e.g., naturalistic, laboratory). Six publications measured alcohol inhalation of alcohol in a controlled laboratory chamber, and 1 evaluated direct inhalation of an e-cigarette with EtOH-containing e-liquid.
Summary of Literature Review of Inhaled Alcohol
|Article||Type of alcohol||Source of alcohol||Method of exposure||Study design||Biomarkers for alcohol exposure||Main finding|
|Ahmed-Lecheheb and colleagues (2012)||70% EtOH||Hand-sanitizing gel||Sanitizer: 3 ml several times over 4-hour shift||Naturalistic||BrAC; urine and plasma levels of EtOH, acetaldehyde, and acetate||↑ BrAC in 33% of participants|
|Ali and colleagues (2013)||62% EtOH||Hand-sanitizing gel||Sanitizer: 3 groups with varying amounts and drying procedures||Between subjects; 3 conditions: 1.5 ml with hand rubbing, 1.5 ml no rubbing, 3.0 ml no rubbing||BrAC||↑ BrAC (median, dose dependent)|
|Arndt and colleagues (2012)||30% propan-1-ol; 45% 2-propanol||Hand-sanitizing gel||Sanitizer: 5 individuals applying every 15 minutes for 8 hours||Within subjects; 2 conditions: 2 individuals present in room but did not apply sanitizer (inhaled only)||EtG||↑ EtG in 6 of 7 including both participants in inhaled only condition|
|Arndt and colleagues (2014)||96% EtOH||Hand-sanitizing gel||Sanitizer: 3 ml 4 times per hour for 8 hours||Between subjects; dermal and inhalation versus inhalation only||EtG||↑ EtG 6 hours after exposure|
|Below and colleagues (2012)||70% propan-1-ol; 63.14% propan-2-ol; 45% propan-2-ol with 30% propan-1-ol||Hand-sanitizing gel||Sanitizer: 10 surgical hand rubs (4 ml repeated 5 times) over 80 minutes||Between subjects; dermal and inhalation of 3 sanitizers||Plasma propanol levels||↑ In median propanol from dermal and inhalation|
|Brown and colleagues (2007)||70% EtOH or 70% isopropanol||Hand-sanitizing gel||Sanitizer: 1 squirt (1.2 to 1.5 ml) every 2 minutes||Naturalistic||BrAC, serum||↑ BrAC in 30% of participants within 2 minutes of exposure|
|Brugnone and colleagues (1983)||Occupational exposure to isopropanol||Isopropanol concentration in air||Air sample before shift, 30 minutes later, and hourly for next 7 hours||Naturalistic||Isopropanol in alveolar air, BAC, and urine||↑ Alveolar concentration that correlated with environmental air; not detected in blood or urine|
|Campbell and Wilson (1986)||1,000 ppm of EtOH air concentration||Inhaled alcohol||Inhaled alcohol for 3 hours||Case study, time series; blood assessed throughout 3 hours||BAC||No increases in EtOH blood content|
|Dumas-Campagna and colleagues (2014)||125 to 1,000 ppm of EtOH air concentration||Inhaled alcohol||Inhaled alcohol for 4 hours in each condition||Within subjects; exposed to 5 concentrations over 6 days (excluding exercise condition)||BAC||Detectable BAC in all conditions with highest in 1,000 ppm after 4 hours (0.30 mg/dl)|
|Ernstgard and colleagues (2003)||142 ppm of 2-propanol air concentration||Inhaled alcohol||Inhaled alcohol over 2 hours during light physical exercise||Within subjects; propanol and clean air exposures||BAC, urine, BrAC||↑ 2-Propanol in BAC, urine, and blood up to 6 hours after exposure|
|Ernstgard and colleagues (2005)||0,100,200 ppm of methanol||Inhaled alcohol||Inhaled alcohol over 2 hours in each condition with light physical exercise||Within subjects; exposed to 3 concentrations||BAC, urine, BrAC||Dose-dependent increase in methanol in BAC, urine, and BrAC|
|Hautemaniere and colleagues (2013a)||70% EtOH||Hand-sanitizing gel||Sanitizer: used ad libitum over the course of a 4-hour shift||Naturalistic||BrAC, urine, and plasma levels of EtOH, acetaldehyde, and acetate||↑ BrAC within 2 minutes of exposure|
|Jones and colleagues (2006)||62% EtOH||Hand-sanitizing gel||Sanitizer: 0.5 g once per hour for 8 hours||Time series; urine assessed throughout 8 hours and next morning (18 hours)||EtG, EtS||↑ EtG and EtS|
|Kramer and colleagues (2007)||95, 85, and 55% EtOH||Hand-sanitizing gel||Sanitizer: 4 ml applied for 10 seconds repeated 20 times or 20 ml for 3 minutes repeated 10 times||Within subjects; 3 conditions: 55, 85, and 95% EtOH with 2 exposure durations||Blood levels of EtOH and acetaldehyde||Dose-dependent increase in median blood EtOH concentration|
|Miller and colleagues (2006)||62% EtOH||Hand-sanitizing gel||Sanitizer: 5 ml applied 50 times over 4 hours||Within subjects; pre–post, repeated application||Plasma levels of EtOH||No increases in plasma EtOH levels|
|Nadeau and colleagues (2003)||0 to 1,000 ppm of EtOH air concentration||Inhaled EtOH||Inhaled EtOH for 6 hours at each level||Within subjects; exposed to 4 concentrations (in ppm) over 4 days||Plasma levels of EtOH||Increases in plasma EtOH to 0.443 mg/dl at highest concentration (1,000 ppm)|
|Reisfield and colleagues (2011)||62% EtOH||Hand-sanitizing gel||Sanitizer: 1 pump (~1 ml) every 5 minutes for 10 hours||Repeated measures; sanitizer procedure repeated for 3 days||EtG, EtS||↑ EtG in all but 1 participant|
|Rohrig and colleagues (2006)||62% EtOH||Hand-sanitizing gel||Sanitizer: applied 15 minutes for 4 hours||Between groups; sanitizer applied at various frequencies||EtG||↑ EtG in 1 participant in the most frequent application group|
|Rosano and Lin (2008)||61% EtOH||Hand-sanitizing gel||Sanitizer: 1 ml applied 20 times during 8 to 12 hours||Within subjects; comparing EtG after hand sanitizer and oral EtOH challenge||EtG||↑ EtG in next day urine in 90% of sample|
|Skipper and colleagues (2009)||62% EtOH||Hand-sanitizing gel||EthGel applied 2 squirts on hands every 4 minutes for 1 hour||Between groups; 4 conditions: control, skin exposure, vapor exposure or both||BrAC, EtG||↑EtG with gel exposure, especially vapor|
|Valentine and colleagues (2016)||23.5% EtOH||Electronic cigarette “liquid”||E-cigarette: Two 20-minute ad lib smoking sessions||Within subjects; pre–post smoking e-cigarette in high and low EtOH content||BrAC, EtG, EtS||No elevated BrAC, 38% of participants positive for EtG after high EtOH exposure|
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Occupational Exposure via Hand Sanitizers
One possible complicating factor when studying hand sanitizer use is the ability to isolate inhalation of alcohol vapor, and not dermal resorption, of alcohol. To address this, a double-blind, randomized, 3 times crossover study included either dermal application of 74.1% EtOH, 10% 2-propanol, or a combination of both, to the participant’s back (thus reducing opportunity to inhale alcohol vapor) (Kirschner et al., 2009). All 3 conditions resulted in undetectable BAC suggesting that increases in alcohol biomarkers are unlikely to result from transdermal resorption. To determine whether use of hand sanitizer presents an opportunity for inhaled alcohol exposure, 1 study used a specialized apparatus that measures alcohol vapor in the breathing zone (150 cm) above individuals exposed to 3 ml of hand sanitizer (Bessonneau and Thomas, 2012). Results suggest that alcohol levels within the breathing zone peaked around 1.3 to 1.4 mg/dl after 30 seconds of exposure and 1.8 to 2.0 mg/dl after 40 seconds of exposure. Assuming an average breathing frequency, the authors calculated that after 30 seconds and 90 seconds of hand disinfection, the total inhaled dose of EtOH were 74.9 mg and 328.9 mg, respectively (Bessonneau and Thomas, 2012). Therefore, although transdermal alcohol absorption remains a possibility, it is more likely that the positive tests for alcohol biomarkers after hand sanitizer use reviewed below are due to inhalation of alcohol vapor and not dermal resorption of alcohol.
Healthcare workers have been the focus of many studies because infection control plans encourage the repeated use of alcohol-based hand sanitizers. To evaluate whether a naturalistic exposure to alcohol-containing hand sanitizers results in an increase in alcohol biomarkers, Hautemaniere and colleagues (2013a) repeatedly measured alcohol concentrations present in blood, breath, and urine at the beginning of a work shift and 4 hours later. Participants were asked to maintain their typical frequency of hand sanitizer use during the course of the study. Four hours into a shift, EtOH was not detectable in blood or urine; however, mean alcohol in inhaled air was 46.2 mg/m3 and expelled air contained 0.003 mg/dl of alcohol up to 2 minutes after exposure (Hautemaniere et al., 2013a). In a similar study with a larger sample of 86 healthcare workers tested before and after a 4-hour shift, alcohol was not detected in blood and urine, but approximately one-third of healthcare workers demonstrated an elevated mean expired EtOH level of 0.008 mg/dl within 2 minutes of exposure (Ahmed-Lecheheb et al., 2012). Furthermore, another study found a significant positive correlation between the amount of hand sanitizer used and EtOH concentration in inhaled air, suggesting that increased sanitizer use will increase inhaled alcohol exposure (Hautemaniere et al., 2013b).
Another set of experimental studies have evaluated direct biomarkers for alcohol exposure after replicating various recommended hand-sanitizing procedures in the laboratory. With notable exceptions (Miller et al., 2006), multiple studies have reported increases in BAC after exposure to alcohol vapor during hand-sanitizing protocols modeled from clinical settings. For example, Kramer and colleagues (2007) evaluated 3 hand rubs (95, 85, and 55% EtOH) in hygienic (4 ml applied 20 times) and surgical (20 ml applied 10 times) hand disinfection. The highest median blood levels of EtOH 30 minutes postexposure in the hygienic (2.1 mg/dl) and surgical (3.0 mg/dl) conditions were low, but still demonstrate a small dose-dependent increase in blood EtOH levels after exposure to alcohol vapor from hand sanitizer (Kramer et al., 2007). Additional studies using other hand-sanitizing protocols that mimic healthcare settings have reported consistent increases in BAC (Below et al., 2012; Brown et al., 2007) and BrAC (Ali et al., 2013; Brown et al., 2007) with the median BrAC at times exceeding the legal limit (119 mg/ dl after 3.0 ml) (Ali et al., 2013). Taken together, these results suggest that incidental exposure to alcohol vapor from hand sanitizer corresponds to inconsistent or extremely small increases in BrAC and BAC biomarkers.
In contrast, a number of studies have evaluated EtG and EtS levels after exposure to alcohol vapor. For example, in a simulation of a typical clinical shift, individuals used 3 ml of 96% EtOH sanitizer 4 times an hour for 8 hours and then provided repeated urine samples over 24 hours (Arndt et al., 2014). Use of sanitizer was associated with elevated EtG levels up to 2,100 ng/ml and individuals who were exposed only to alcohol vapor demonstrated concentrations between 600 and 800 ng/ml (Arndt et al., 2014). Notably, application of hand sanitizer under an exhaust fan (i.e., no vapor) resulted in undetectable EtG, further supporting the likelihood that positive biomarkers are a result of alcohol inhalation and not dermal resorption. In another study, daily pre- and posturinary analyses revealed that use of 1 ml of 62% EtOH hand sanitizer every 5 minutes for a 10-hour period on 3 consecutive days resulted in positive EtG levels in 90% of participants with a mean EtG of 278 ng/ml (range = 0 to 2,001 ng/ml). Positive urine EtS was present in 72% of the sample with a mean value of 9 ng/ml (range = 0 to 84 ng/ml) (Reisfield et al., 2011). Several other studies report detectable EtG and EtS after exposure to alcohol vapor from hand sanitizer (Arndt et al., 2012; Jones et al., 2006; Rohrig et al., 2006; Rosano and Lin, 2008) with reported average peak concentrations sometimes exceeding clinical thresholds commonly used to indicate alcohol consumption (Skipper et al., 2009). Therefore, in contrast to BAC, urine EtG may at least for a short period time document systemic exposure to alcohol after incidental exposure to EtOH vapor from hand sanitizer.
Other Occupational Exposure to Alcohol Vapor and Laboratory Alcohol Vapor Chambers
Compared with the numerous studies on biochemical biomarkers associated with exposure to alcohol vapors from hand sanitizer, we identified only 6 studies that explored possible functional biomarkers associated with direct exposure to inhaled alcohol. One study measured environmental air concentration of isopropanol in a printing works while measuring corresponding isopropanol concentration in alveolar air, blood, and urine of workers (Brugnone et al., 1983). This occupational exposure resulted in detectable levels in alveolar air (range 4 and 437 mg/m3), but not in blood or urine. While 1 study reported no detectable increases in blood EtOH content after exposure to vaporized EtOH (1,000 parts per million [ppm]) (Campbell and Wilson, 1986), 2 other studies combined alcohol vapor exposure with light exercise and reported increases in blood, urine, and BrAC after exposure to 142 ppm of 2-propanol vapor (Ernstgard et al., 2003) and a dose-dependent increase after exposure to 3 concentrations (0, 100, 200 ppm) of methanol (Ernstgard et al., 2005). Another study reported that exposure to 6 EtOH concentrations (125 to 1,000 ppm) in an inhalation chamber resulted in peak BAC of 0.3 (men) and 0.27 (women) mg/dl after 4 hours in the highest concentration (Dumas-Campagna et al., 2014). Finally, associations between BrAC and performance on neuromotor tasks, including reaction time, body sway, postural tremor, and velocity of hand movements, were evaluated during 6 hours of EtOH inhalation at 4 concentrations: 0, 250, 500, and 1,000 ppm (Nadeau et al., 2003). Results demonstrated negative BrAC in all conditions except for a negligible increase after 3 and 6 hours at the highest concentration and neuromotor effects were largely nonsignificant at all concentrations. This study was limited in that the total sample consisted of only 5 males and neuromotor tests were associated with high variability (Nadeau et al., 2003). Assessment of BAC/BrAC has been established after oral ingestion of alcohol, but arterial or brain levels may prove more relevant. If true, even a modest BAC or detectable EtG in a larger sample could potentially reflect functional impairment.
Alcohol Inhalation via E-Cigarette
A recent study measured motor performance and urine EtG after inhaling from an e-cigarette filled with e-liquids that contained high or low alcohol concentrations (Valentine et al., 2016). The e-liquids used in an e-cigarette contain numerous chemicals which have as-yet-unknown toxicities. Ethyl alcohol (alcohol) is one such constituent, but has received little scientific interest in this context (Hutzler et al., 2014; Varlet et al., 2015). The study evaluated the acute effects of puffing from commercially available e-liquids containing 23% or trace (<0.4%) alcohol in young adult social drinkers who also smoke cigarettes. While no differences in subjective drug effects were observed between alcohol conditions, puffing from an e-liquid with 23% alcohol was associated with diminished performance on the Purdue Pegboard Dexterity Test, a test known to be sensitive to alcohol exposure (Breckenridge and Berger, 1990; Buddenberg and Davis, 2000; Marczinski et al., 2012; Tarter et al., 1971). Further, in 3 of the 8 subjects with undetectable baseline urine EtG levels, just 1 test session of puffing from the e-cigarette with 23% alcohol resulted in positive EtG levels (average 371 ng/ml) verifying systemic exposure (Valentine et al., 2016). Importantly, the results may underestimate the intensity of exposure that could result after repeated, heavy e-cigarette use with alcohol-containing e-liquid.
The current review of the literature highlights that biomarkers of alcohol exposure in humans are measurable after inhalation of alcohol vapor, but at levels that are generally considered subthreshold for legal intoxication based on oral ingestion of alcohol. Thus, it is not surprising that inhalation of alcohol vapor is commonly perceived as innocuous; however, the acute pharmacodynamics of inhaled alcohol are presently unknown. Guided by preclinical and addiction literature, it is possible that inhaled alcohol is especially reinforcing due to immediate and rapid transmission to the brain. As such, the usual methods of quantifying alcohol exposure (i.e., BAC and BrAC) may be largely irrelevant to the behavioral and pharmacological impact of inhaled alcohol. That is, compared with oral consumption of alcohol, a “hit” of alcohol to brain is not likely to produce analogous BAC levels that are associated with well-characterized impairments in cognitive and motor performance. The most sensitive biomarkers for alcohol inhalation seem to be EtG (and/or EtS), and the presence of EtG confirms that some amount of alcohol has been absorbed and metabolized. With that said, the literature reviewed above generally reflect very low levels of exposure (e.g., alcohol vapor from hand sanitizer) that may not reflect the levels or exposure resulting from the recreational inhalation of alcohol.
Recreational use of alcohol vapor is most likely to resemble a binge-like pattern where inhalation occurs repeatedly in short bursts (e.g., e-cigarette inhalation, recreational alcohol vaping). Based on animal literature highlighting that intermittent, relative to continuous, EtOH vapor exposure results in rapid increases in self-administration and greater overall intake (O’Dell et al., 2004; Rimondini et al., 2002), the reinforcing effect of taking “hits” of alcohol vapor may be greater than, or serve to enhance, oral ingestion. Furthermore, akin to oral alcohol use, the volume of alcohol inhaled may be a critical factor in determining the clinical effect of repeated exposure over the course of day. Therefore, positive biomarkers found in the above studies, especially EtG, may significantly underestimate the clinical significance of recreational alcohol vapor exposure. It may also be possible that home-made vaporizers, relative to commercial products, may deliver higher volumes of alcohol vapor, potentially resulting in greater levels of alcohol exposure. Additional research is needed to characterize the consequences of different methods of alcohol inhalation (e.g., deliberate vaping, inadvertent exposure) and, perhaps, the likely pharmacokinetics of brain exposure as reflected by arterial levels. The behavioral consequences of alcohol inhalation also need to be better defined and measured after repeated intentional exposures that simulate recreational binge patterns of use.
Overall, the immediate safety concerns for inhaled alcohol may be relatively minor. However, there may be specific contexts of use that are more likely to result in acute behavioral effects such as while using high-powered electronic cigarette designs in combination with high-alcohol-content e-liquids. The psychomotor impact of repeated intentional inhalation of alcohol vapor has not been comprehensively studied in a controlled laboratory setting. Such studies are needed to determine whether the amount or frequency of inhaled alcohol poses similar risks to complex tasks, such as driving. Safety concerns aside, the clinical significance of inhaled alcohol is likely to dependent on the specific populations or individuals exposed. For example, subtle changes in interoceptive states resulting from inhaled alcohol may serve as conditioned reinforcers for alcohol use, regardless of whether they are consciously perceived or attributed to the inhalation of alcohol. Therefore, it is noteworthy that the existing studies on inhaled alcohol deliberately exclude vulnerable populations such as those with alcohol use disorder.
Prior research in clinical populations has suggested that reactivity to drug cues can be consciously perceived via controlled processing or subject to automatic processing that is unavailable to introspection (Ryan, 2002). Drug expectancy plays a critical role in the generation of craving such that an individual can experience craving after becoming aware of drug-related stimuli or interpreting a state (e.g., physiological arousal) as representing a need for drug use. Exposure to the odor of a preferred alcoholic beverage is an example of a consciously perceived drug cue that can readily generate craving and motivate drinking behavior. Exposure to “preattentive,” or subliminal, drug cues, is also associated with increased craving, motivation for drug seeking behavior, and activation of reward-related limbic brain regions (Childress et al., 2008; Franken et al., 2000; Wetherill et al., 2014; Young et al., 2014). Compared with similarly masked control images, alcohol cues that were presented for 30 ms were associated with deceleration of heart rate in heavy drinkers that is thought to be indicative of an orienting index for the automatic analysis of a stimulus (Ingjaldsson et al., 2003b), and this effect was more pronounced within “high cravers” (Ingjaldsson et al., 2003a). Additionally, exposure to subliminal alcohol-related, but not nonalcoholic, words resulted in activation of alcohol expectancy-consistent aggressive behavior (Friedman et al., 2007; Subra et al., 2010) and cognitive impairment (van Koningsbruggen and Stroebe, 2011). Thus, it may not be important that incidental or inadvertent (e.g., e-cigarettes) exposure to alcohol vapor results in biomarkers above or even near to legal limits; instead, the level of absorption after inhaling alcohol may only need to be sufficient to produce interoceptive or subjective states that have previously been associated with oral alcohol intoxication. Therefore, exposure to even small amounts of alcohol vapor by individuals in recovery from alcohol use disorders may facilitate relapse via reinforcement of alcohol-related expectancies that increase craving and/or attention to alcohol cues.
An alternative scenario is that exposure to alcohol vapor may influence the susceptibility to problematic or habitual oral alcohol use. The etiology of alcohol use disorders is complex and believed to be associated with a host of individual factors such as positive family history of alcohol problems, age of alcohol use onset, and co-occurring mental health and substance use disorders (for review, see Moss et al., 2007; de Wit and Phillips, 2012). In general, subjective positive effects resulting from initial drug use are believed to play a key role in escalation of problematic use and the development of drug use disorders (de Wit and Griffiths, 1991) and measures of drug liking have been posited to be both sensitive and reliable indicators of likelihood of abuse (Carter and Griffiths, 2009; Griffiths et al., 2003; McColl and Sellers, 2006). For example, evidence suggests that positive effects of nicotine are associated with abuse liability and increased smoking behavior while a sensitivity to negative or aversive subjective effects of nicotine may prevent both the initiation of tobacco product use as well as the amount of nicotine intake in established tobacco users (Carter et al., 2009; Hu et al., 2011; Jensen et al.,2015; Sartor et al.,2010). The neuropharmacological and behavioral effects of oral alcohol intoxication in heavy drinkers are believed to be multifaceted and include concurrent dimensions of reinforcement and punishment (Ray et al., 2009). Models that describe the development of alcohol use disorders are equally complicated with some highlighting increased experience of reinforcing effects of alcohol (e.g., Newlin and Thomson, 1990) and others emphasizing a reduced sensitivity to unpleasant effects of alcohol (e.g., Schuckit, 1994). Consistent with anecdotal and proposed behavioral and pharmacological consequences of inhaled alcohol, successive “hits” of alcohol may result in more reinforcing positive effects, and absent or attenuated aversive effects, when compared to oral alcohol consumption. As such, similar to the proposed etiology of nicotine addiction (Fowler and Kenny, 2014; Laviolette and van der Kooy, 2003; Riley, 2011), the potential for inhalation of alcohol vapor to influence susceptibility to the development of habitual alcohol use may be a function of the relative balance between inhaled alcohol’s positive and negative/aversive effects and is likely moderated by established risk factors for problematic drinking (e.g., positive family history).
Exposure to subthreshold doses of inhaled alcohol may also maintain or facilitate development of addiction to other substances, most notably nicotine. The frequent covariation of alcohol use and cigarette smoking is well documented with about 20% of those dependent on tobacco also dependent on alcohol, and with half of those who are alcohol dependent also being dependent on nicotine (Falk et al., 2006; Grant et al., 2004). Use of alcohol and nicotine together may lead to a greater reinforcement than either substance alone. Indeed, co-administration of subthreshold doses of nicotine and alcohol induces dopamine release in the nucleus accumbens, a region implicated in the reinforcing effects of drugs of abuse (Tizabi et al., 2007). In human laboratory studies, acute alcohol administration increases urges to smoke, smoking behavior, and satisfaction from smoking in both heavy and light smokers (Kahler et al., 2014; King et al., 2009; McKee et al., 2006; Sayette et al., 2005). Collectively, numerous studies across varying levels of analysis indicate that the development of nicotine addiction may be facilitated by the use of combustible tobacco products or e-cigarettes that also contain alcohol. Considering the rapid rise in e-cigarette use, particularly among adolescents (Bunnell et al., 2015), more research on the prevalence and patterns of alcohol absorption from e-cigarette use, and on the biological effects of co-administered nicotine and alcohol, is needed to understand the influence of inhaled alcohol vapors from e-cigarette use on the development of nicotine addiction, especially in specific populations with increased vulnerability.
CONCLUSIONS AND FUTURE RESEARCH
This review of the current literature evaluating inhaled alcohol use has revealed a predominate focus on the inhalation of alcohol vapor from hand sanitizer use, a ubiquitous behavior in the healthcare worker population. When using standards established by decades of research on oral ingestion, exposure to alcohol vapor is often assumed to pose a negligible risk. However, many studies have reported that inhalation of alcohol vapor can result in measurable biomarkers of alcohol exposure, most notably EtG and/or EtS documenting systemic alcohol exposure by the inhalation route. Importantly, the acute behavioral consequences and subjective effects of repeated exposure using devices capable of delivering alcohol vapor await further characterization. Finally, inhalation exposure may also be especially important in individuals with an alcohol use disorder, or those at risk of developing alcohol use disorder for whom priming doses of alcohol, as might occur with inadvertent inhalation via e-cigarettes or from other sources, may lead to greater craving and further alcohol use.
Research reported in this publication was supported by the VA New England Mental Illness Research, Education, and Clinical Center (MIRECC) and by the P50DA036151 (Yale TCORS) from the National Institute on Drug Abuse of the National Institutes of Health and the U.S. Food and Drug Administration Center for Tobacco Products. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or of the U.S. Food and Drug Administration. Drs. MacLean, Valentine, Jatlow, and Sofuoglu declare they have no conflicts of interest.
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Inhaling Alcohol: Dangerous Trend, Expert Says
Some college students are experimenting with inhaling alcohol by pouring it over dry ice and “smoking” the vapors, according to an expert who says the practice is dangerous.
Young adults are inhaling alcohol to get high without ingesting calories, the Daily News reports.
Dr. Harris Stratyner, Regional Clinical Vice President of Caron Treatment Centers in New York, told the newspaper, “When you inhale alcohol, it goes directly into the lungs and circumnavigates the liver. The liver is what metabolizes alcohol, but when you inhale it, it goes directly from the lungs to the brain.”
The practice is more likely to lead to deadly alcohol poisoning than drinking liquor, he said. Inhaling alcohol vapors can dry out the nasal passages and mouth, making a person more susceptible to infection, Stratyner added.
“One of the things that prevents alcohol poisoning is that you usually vomit,” he noted. “When you circumvent the stomach and go straight to the lungs, you don’t have that ability.”
Inhaling alcohol has become more popular in the past year and a half, Stratyner said. “This is a stupid, highly dangerous thing to do. The fact that youngsters in particular can purchase the equipment for a relatively cheap price…this has to be made illegal.”
Can You Use Rubbing Alcohol to Extract THC From Weed?
Extracting compounds such as THC and CBD from marijuana enables users to benefit from a high concentration of a specific cannabinoid. For example, proper THC extraction allows you to create cannabis concentrates, which could have a THC level of over 90%! Extraction via alcohol is one of the most common methods.
When it is performed correctly, it is a safe form of extraction, BUT you must choose the right type of alcohol. Do NOT select denatured alcohol because it contains harmful ingredients which make it unfit for human consumption.
What is Rubbing Alcohol?
There are several types of alcohol, and not all of them are suitable for drinking! The alcohol we drink in the form of beer, wine, or spirits, is ethyl alcohol produced by yeast. In winemaking, for example, the yeast consumes the sugar in grape juice and creates alcohol.
Ethanol is the same kind of alcohol found in whiskey and is also used as car fuel. It is different from the stuff you drink because it has been distilled to the point where it is almost entirely alcohol. The denatured alcohol you find at the drug store is also ethanol, but it is poisoned to prevent people from drinking it. Food grade ethanol is a popular solvent for THC and CBD extraction and is still used by several big sellers.
Rubbing alcohol is the term used to describe either ethanol-based liquids or isopropyl alcohol. While denatured alcohol is classified as a methylated spirit, rubbing alcohol is a surgical spirit. It is widely used in medicine as a topical application. It is often a form of denatured alcohol made from a unique solution of 70% ethanol or isopropyl alcohol in concentrated form.
The term ‘rubbing alcohol’ is actually a generic term to describe ethyl or isopropyl-based products with similar qualities. In the UK, rubbing alcohol is often referred to as ‘surgical spirit.’ In North America, methyl salicylate is added to rubbing alcohol, which is commonly known as wintergreen oil. In Canada and the United States, manufacturers are allowed to use their own standards of formulation, as long as the isopropyl or ethanol alcohol content is labeled and ranges from 70% to 99%.
Both ethanol (chemical formula C2H5OH [also written as C2H5OH]) and isopropyl alcohol (chemical formula C3H8O) are used as disinfectants. However, while ethanol has no lasting short-term effects when consumed, isopropyl alcohol gets converted into acetone in the liver; which means it is incredibly toxic.
The term ‘rubbing alcohol’ was first used during the prohibition era in the 1920s. It was used as an ointment in massages and was rubbed into the skin. As it was an age where the consumption of alcoholic beverages was illegal, it was necessary to distinguish the type of alcohol one drank from the kind used in medicine.
Is it Safe to Use Rubbing Alcohol for THC Extraction?
There is some confusion over whether rubbing alcohol is even safe for use as a solvent for THC extraction. While it is true that isopropyl rubbing alcohol and denatured alcohol share similarities, their chemical structures, toxicity, and means of production are different.
Neither version is suitable for human consumption. Indeed, only food grade ethanol or ethyl alcohol can be safely consumed. Isopropyl alcohol is the name of a substance, whereas denatured alcohol is a commercial product which can contain several materials including ethanol and isopropyl alcohol. It also includes denaturants which make it unsafe for consumption.
However, there are different types of rubbing alcohol. In the United States, in accordance with ATF rules, all preparations classified as rubbing alcohol must have toxic additives to limit human consumption and prevent alcohol abuse. These forms of rubbing alcohol must have between 87.5% and 91% of absolute ethyl alcohol. The rest of the solution contains denaturants, water, and perfume oils.
There are also specific isopropyl rubbing alcohols with anywhere between 50% and 99% isopropyl alcohol. Therefore, if you are going to use rubbing alcohol for THC extraction, you will ideally choose one with up to 99% isopropyl alcohol.
Although you CAN use isopropyl based rubbing alcohol to extract THC or other cannabinoids from marijuana, it is safer to use ethanol. If you plan to use isopropyl alcohol for whatever reason, the process is known as Quick Wash Isopropyl (QWISO).
How to Perform QWISO THC Extraction
Isopropyl extraction involves stripping the trichomes from marijuana flowers to create potent hash oil. If you want to use this method of extraction, you’ll need the following equipment:
- A metal screen or filter (you can use a permanent coffee filter)
- A clean glass bowl
- Paper coffee filters
- A glass pot (a coffee pot works well)
- A glass mason jar
- A plastic storage container
- A large sieve; we recommend a large and a small sieve if you are using more than 10 grams of bud
- Cutting utensils
- A fan
- An oven
- 100-200ml of isopropyl alcohol
- At least 10 grams of bud
- A razor blade to gather the extract
Preparing for the Extraction Process
When it comes to THC extraction using isopropyl alcohol, preparation is crucial and begins several hours before you attempt the process. Make sure every container you plan on using is extremely clean and dry. Next, grind up your buds into a small jar and put it, and the alcohol, in a freezer for a few hours (you can even do this overnight) to ensure they are as cold as possible. Isopropyl alcohol’s freezing point is approximately -128.2 degrees Fahrenheit, so there is nothing to worry about!
You need to freeze the bud because its trichomes fall off far more efficiently at very low temperatures. You can attempt the extraction process without freezing, but it will result in a far smaller amount of THC.
Final preparation steps include placing a coffee filter into your jar to create a type of bag. If you plan on extracting THC from a large amount of bud, cover the entire surface area of your large sieve with filters and place the smaller strainer on top.
Extracting THC Using Isopropyl Alcohol
Pour all of the alcohol into the jar containing the weed. Make sure the ground buds are entirely submerged in the alcohol. Close the lid and tighten it securely. Shake the jar vigorously for 30 seconds. Don’t shake the jar for too long because you could extract too much chlorophyll, which will leave a bitter taste.
Next, pour everything through a sieve and filter the contents in a jar. The filtering process could take up to an hour, so be patient! If you have any alcohol left over, pour it into the jar to ensure no leftover trichomes are remaining. Filter this additional solution.
The process works because the cannabinoids in the weed dissolve in the alcohol. The sieve filters the plant material, while the coffee filter refines the liquid by removing tiny parts of the remaining plant. As all of the cannabinoids have been dissolved, they are now in liquid form. The coffee filter enables liquid to pass through but prevents solid particles from doing so.
Once the filtering process has been completed, you are left with a jar containing a fairly clear liquid with a hint of green. Now, your precious THC is contained in the liquid, which means we must remove the alcohol.
Pour the contents of the jar into a container with a flat surface. If you have a fan, you can set it to blow into your liquid at its lowest setting. Please note that the alcohol must be stored in a well-ventilated area because you are evaporating a toxic and flammable substance. It could take up to 24 hours for the evaporation process to be completed.
The evaporation process is only completed when you see no traces of liquid on the flat surface. Get your razor blade and a clean mason jar, and gather the solid substance. A toothpick is a handy item to have as it can remove pieces of material that get stuck to the razor blade.
Don’t be dismayed when you see such a small amount of material. It should contain at least 70% THC (depending on the strain), and a little goes a VERY long way.
Final Thoughts on Using Rubbing Alcohol to Extract THC From Weed
The answer to the title question is ‘yes,’ but with a fair number of caveats. Firstly, you should NEVER use denatured alcohol as it is designed to be poisonous. If you are going to use rubbing alcohol as your solvent of choice, it must be isopropyl-based; ideally up to 99%.
There is a significant amount of confusion when it comes to distinguishing between different types of alcohol. Ethyl, or grain, alcohol is used in the recreational beverages that millions of people enjoy. Manufacturers denature ethyl alcohol by including poisonous substances which render the solution undrinkable.
Isopropyl alcohol, on the other hand, is already unfit for human consumption. Ingesting it can cause intestinal bleeding, vomiting, and occasionally, death. It is less toxic than denatured alcohol but is still poisonous to humans.
Therefore, if you insist on using isopropyl alcohol for THC extraction, extreme caution is advised. You need to ensure that all of the alcohol has been evaporated before using the leftover cannabis concentrate. It is a common solvent in DIY extraction, but we would recommend using food grade ethanol instead.
Once again, you need the ethanol to completely evaporate before using the concentrate. However, if you don’t remove 100% of the ethanol, and consume marijuana, you should not feel too many ill effects since ethanol is safe for human consumption. In fact, it is often used as an additive and food preservative.
Published on: 19 Jun, 2019
How Do You Smoke Alcohol?
Alcohol can be converted into a vapor by either heating up the alcohol over a significant heat source or by pouring it over dry ice and using an air pump.
These vapors that result from this process may then be inhaled through a straw, or through the use of an alcohol vaporizer. An alcohol vaporizer is a machine specifically designed to allow users to inhale alcohol vapors. However, because many states in America have banned the sale or purchase of these machines, many people have turned to make their own devices through do-it-yourself methods.
Is Smoking Alcohol Safer Than Drinking?
Although there is limited research on alcohol inhalation, experts have made it clear that there is no reason to believe that smoking alcohol is any safer than drinking it.
In fact, there are actually several ways than inhaling alcohol may actually pose additional risks to a person’s mental and physical health, leading some medical officials to actually deem it more dangerous than consuming it the traditional way.
The Dangers Of Vaping Alcohol
One major thing that has attracted people to the idea of smoking alcohol is what it can provide that traditional drinking can’t: near-instant intoxication.
Unfortunately, this appeal is also one of the most dangerous aspects of the activity.
By inhaling alcohol vapors, the alcohol bypasses the usual process of absorbing alcohol, instead of being absorbed directly into the bloodstream. This can cause an intense high almost immediately, coming about much more rapidly than if you were to drink it.
Compare the 15 to 20 minutes it may take for your body to process liquid alcohol to the near-instantaneous intoxication you get from smoking its vapors – and you might start to see why this can be harmful. Binge-drinking, and the effects of it, can occur within mere seconds before a person even realizes how much of the alcohol vapor they have inhaled.
In addition, beyond the risks involved with getting drunk faster, there are several other dangers that have been tied to this new method of ‘drinking’. These include:
- Higher risk for overdose or alcohol poisoning: By vaping alcohol, you can inhale several drinks within seconds, and this greatly heightens the risk of serious consequences such as overdose or alcohol poisoning.
- Less control: When you’re inhaling the alcohol vapors, it is much more difficult to gauge just how much of the vapor is going into your lungs. This lack of control that comes with vaping alcohol can pose serious consequences
- Lung damage: Not unlike smoking tobacco or other drugs, experts have stated that the heated vapor can cause damage to the lungs. It may also put you at risk of developing long-term breathing problems.
- Effects on the stomach: Drinking alcohol in heavy amounts can sometimes lead to vomiting, which – if painfully – can be considered a protective measure by the body to help limit how much alcohol your body absorbs. But because the vapor of heated alcohol goes directly to the brain, vomiting is not as common a consequence. This can lead to consequences such as losing consciousness or experiencing slowed breathing.
- Negative effects on the brain: The increase of alcohol absorption that occurs with vaping alcohol poses harm to the brain, with additional risk for those whose brains are still developing, such as kids and teenagers.
- Increased anxiety: Studies on alcohol inhalation with rats have shown that those who are exposed to this method of intoxication may experience an increase in anxious behaviors. The anxiety can also become worse during the withdrawal period in cases where a person has developed a dependency.
Myths of Vaping Alcohol
1. Vaping alcohol is a calorie-free way to get drunk — FALSE
The rumor that vaping alcohol is the zero-calorie way to get yourself drunk is one of the more popular myths that has circulated about smoking the often calorie-laden liquid. However, there are not yet any reports to back up this claim and experts have routinely debunked it as false.
Thus, if you’ve considered vaping alcohol to save on calories, don’t bother. It has not proven to be an effective method for calorie control.
2. You might be less likely to get addicted to alcohol if you smoke it — FALSE
Just as with drinking alcohol, you are still at risk for developing a dependency or addiction by smoking it. The potential for developing an addiction actually rises the faster that drugs like alcohol reach the brain.
Both binge-drinking and ‘binge-vaping’ therefore carry the risk of developing a dependency.
3. You don’t have to worry about alcohol withdrawal syndrome (AWS) if you vape it — FALSE
Those who become dependent on alcohol through vaping are still subject to the symptoms of withdrawal and are at risk of developing alcohol withdrawal syndrome (AWS). Some documented symptoms that can occur with withdrawal from alcohol inhalation include tremors, anxiety, chills, sweating, and seizures.
4. If you are under 21, you can vape alcohol without facing legal consequences because you’re technically not drinking it — FALSE
This is another myth that has been debunked because it is the consumption of alcohol that is illegal for persons under the age of 21. The detail that it has to be drunk is not specified.
More than 25 states have also already created laws targeting alcohol inhalation specifically, including bans on the buying and selling of alcohol vaporizers.
5. Smoking alcohol is at least as risky as drinking it — TRUE
This is not a myth.
Although there is limited research on the short and long-term effects of alcohol inhalation, what experts have already learned tells us that vaping alcohol is at least as risky as drinking it, if not more so.
The Bottom Line
There is no way to consume alcohol that comes without risks, and that includes by means of inhaling it. There is also no reason to believe that it is safer to vape alcohol than to drink it, particularly because one is still at risk of becoming addicted to alcohol through exposure to its vapor.
If you are interested in more information about vaping alcohol or are concerned about a loved one’s drinking habits, contact one of our specialists today.
Rubbing alcohol smoking
Method of administering ethanol directly into the respiratory system
Alcohol inhalation is a method of administering alcohol (also known as ethanol) directly into the respiratory system, with aid of a vaporizing or nebulizing device. It is chiefly applied for recreational use, when it is also referred to as alcohol smoking, but it has medical applications for testing on laboratory rats, and treatment of pulmonary edema and viral pneumonia.
To inhale alcohol, it must be first converted from liquid into gaseous state (vapor) or aerosol (mist). For recreational use, a variety of methods have been invented. Alcohol can be vaporized by pouring it over dry ice in a narrow container and inhaling with a straw. Another method is to pour alcohol in a corked bottle with a pipe, and then use a bicycle pump to make a spray. Alcohol can be vaporized using a simple container and open-flame heater. Medical devices such as asthma nebulizers and inhalers were also reported as means of application.
The practice gained popularity in 2004, with marketing of the device dubbed AWOL (Alcohol without liquid), a play on the military term AWOL (Absent Without Leave). AWOL, created by British businessman Dominic Simler, was first introduced in Asia and Europe, and then in United States in August 2004. AWOL was used by nightclubs, at gatherings and parties, and it garnered attraction as a novelty, as people 'enjoyed passing it around in a group'.
AWOL was gimmicked as an alcohol "vaporizer", implying that it would heat the liquid until it entered a gaseous state, but is in fact a nebulizer, a machine that agitates the liquid into an aerosol. AWOL's official website states that "AWOL and AWOL 1 are powered by Electrical Air Compressors while AWOL 2 and AWOL 3 are powered by electrical oxygen generators", which refer to a couple of mechanisms used by the nebulizer drug delivery device for inhalation. Although the AWOL machine is marketed as having no downsides, such as the lack of calories or hangovers, Amanda Shaffer of Slate describes these claims as "dubious at best". Although inhaled alcohol does reduce the caloric content, the savings are minimal.
After expressed safety and health concerns, sale or use of AWOL machines was banned in a number of American states. The AWOL device was later followed by new products for alcohol inhalation, such as "Vaportini", created in 2009, which uses simple thermal vaporization.
Effects and health concerns
There are occupational health and safety risks of inhaling alcohol vapor and mists. Inhalation devices make it "substantially easier to overdose on alcohol" than drinking, because the alcohol bypasses the stomach and liver and goes directly into the bloodstream, and because the user does not have a reliable way of determining how much alcohol they have taken in. Inhaled alcohol cannot be purged from the body by vomiting, which is the body's main protection against alcohol poisoning. Inhaled alcohol can dry out nasal passages and make them more susceptible to infection. There is also a potential increased risk of addiction.
Inhalation of vapor obtained by nebulization of water and ethanol in oxygen has been used in treatment of pulmonary edema in humans. Alcohol vapor acts as an anti-foaming agent in the lungs, so the sputum becomes more liquid, and can be easily expelled. The method has also been used to reduce the alcohol withdrawal syndrome in patients who had intestinal tract surgeries.
In the United States, many state legislatures have banned alcohol inhalation machines. Support for such legislation comes from groups fighting underage drinking and drunk driving, including alcohol companies such as Diageo and industry groups such as the Distilled Spirits Council of the United States (DISCUS).
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To get drunk, people are getting creative. But a new form of drinking, known as “smoking” alcohol, has doctors concerned.
Whatever happened to taking shots? Any sort of excessive drinking is dangerous, be it via beer bongs or pouring shots into the eye socket. But now some drinkers are taking it even further and “smoking” alcohol. The questionable practice, which has potentially scary consequences, has various permutations.
An individual can pour alcohol over dry ice and inhale it directly or with a straw, or make a DIY vaporizing kit using bike pumps. The alcohol of choice is poured into a bottle, the bottle is corked, and the bicycle pump needle is poked through the top of the cork. Air is pumped into the bottle to vaporize the alcohol, and the user inhales.
In 2004, the U.S. saw a brief emergence of the trend with the availability of the AWOL (Alcohol Without Liquid) device, but the product was quickly banned in the U.S. and lost its following.
(MORE:If Drinking Starts at Puberty, It’s More Likely to Lead to Alcohol Problems)
Nearly a decade later, clinicians are seeing evidence that the practice is gaining some traction — and not just among college kids and adolescent risk takers. It’s popular among people who want to lose weight and don’t want the calories that come from consuming alcohol. “People think it is a great way to get the effects of alcohol without gaining the weight because alcohol has an enormous amount of empty calories. You can’t be ingesting a lot of alcohol if you’re on a diet and want to lose weight,” says Dr. Deni Carise, the deputy chief clinical officer at CRC Health Group, a treatment- and educational-program provider for individuals struggling with behavioral issues, chemical dependency and eating disorders. “I think adolescents are also particularly susceptible to this because it is novel and exciting.”
In Fox’s KCTV-5 coverage of the trend, a North Texas man, Broderic Allen, says he stopped drinking to lose 80 lb. (36 kg) and started smoking alcohol to avoid calories:
(MORE:Brain Scans Can Predict Which Alcoholics Are Most Likely to Relapse)
When alcohol vapor is inhaled, it goes straight from the lungs to the brain and bloodstream, getting the individual drunk very quickly. Because the alcohol bypasses the stomach and liver, it isn’t metabolized, and the alcohol doesn’t lose any of its potency.
Drinkers feel the effects almost instantly, but the risks are also much higher. People who smoke their alcohol are at a much greater risk of getting alcohol poisoning and potentially overdosing. When people drink too much alcohol, they tend to vomit. Getting sick is one of the ways that prevents an alcohol overdose, but when alcohol circumvents the stomach and liver, the body can’t expel it.
It’s also much harder to know just how much alcohol you’re consuming in one sitting if you’re not stringently measuring. If a cup of alcohol is poured into a bottle and then vaporized, the drinker cannot tell if they are inhaling a few sips or the whole cup, since the liquid remains in the bottle.
“It’s also terrible for your lungs and nasal passages,” says Carise. “Your lungs are not meant to inhale something that can turn back into a liquid. When you think of liquid in the lungs, you think of drowning.”
(MORE:Safety Board Recommends Defining Legally Drunk With Lower Blood-Alcohol Level)
The prevalence of the trend is unclear, since there are no current studies tracking the cases, says Carise. But like other drinking fads, YouTube videos of drinkers inhaling and smoking alcohol have increasingly popped up online.
The trend is also picking up in the bar scene, with vaporizing methods like the Vaportini, which is legally sold in all 50 states. The site boasts: “This has the advantage of no calories; no carbs, no impurities and the effects of consuming alcohol are immediately felt, making it easier to responsibly imbibe.”
Fortunately, these beverages are usually consumed in a wide glass, so the effect is not as concentrated, says Carise. Still, she finds the concept disturbing. “It is amazing what our culture will do to get drunk,” she says.
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