Loading AI tools
Hallucinogenic drug From Wikipedia, the free encyclopedia
Lysergic acid diethylamide, commonly known as LSD (from German Lysergsäure-diethylamid), is a potent psychedelic drug that intensifies thoughts, emotions, and sensory perception.[12] Often referred to as acid or lucy, LSD can cause mystical, spiritual, or religious experiences.[13][14] At higher doses, it primarily induces visual and auditory hallucinations.[15][16] While LSD does not cause physical addiction, it can lead to adverse psychological reactions, such as anxiety, paranoia, and delusions.[7] Additionally, it may trigger "flashbacks," also known as hallucinogen persisting perception disorder, where individuals experience persistent visual distortions after use.[17][18]
Clinical data | |
---|---|
Pronunciation | /daɪ eθəl ˈæmaɪd/, /æmɪd/, or /eɪmaɪd/[1][2][3] |
Trade names | Delysid |
Other names | LSD, LSD-25, LAD, acid, lucy, among others |
AHFS/Drugs.com | Reference |
Pregnancy category |
|
Dependence liability | Low[4] |
Addiction liability | None[5] |
Routes of administration | By mouth, under the tongue |
Drug class | Serotonergic psychedelic (hallucinogen) |
ATC code |
|
Legal status | |
Legal status |
|
Pharmacokinetic data | |
Bioavailability | 71%[6] |
Protein binding | Unknown[7] |
Metabolism | Liver (CYP450)[6] |
Metabolites | 2-Oxo-3-hydroxy-LSD[6] |
Onset of action | 30–40 minutes[8] |
Elimination half-life | 3.6 hours[6][9] |
Duration of action | 8–20 hours[10] |
Excretion | Kidneys[6][9] |
Identifiers | |
| |
CAS Number | |
PubChem CID | |
IUPHAR/BPS | |
DrugBank | |
ChemSpider | |
UNII | |
KEGG | |
ChEBI | |
ChEMBL | |
PDB ligand | |
CompTox Dashboard (EPA) | |
ECHA InfoCard | 100.000.031 |
Chemical and physical data | |
Formula | C20H25N3O |
Molar mass | 323.440 g·mol−1 |
3D model (JSmol) | |
Melting point | 80 to 85 °C (176 to 185 °F) |
Solubility in water | 67.02[11] mg/mL (20 °C) |
| |
| |
(verify) |
The effects of LSD begin within 30 minutes of ingestion and can last up to 20 hours, with most trips averaging 8–12 hours.[19][20] It is synthesized from lysergic acid and commonly administered via tabs of blotter paper.[21] LSD is mainly used recreationally or for spiritual purposes.[19][22] As a serotonin receptor agonist, LSD's precise effects are not fully understood, but it is known to alter the brain’s default mode network, leading to its powerful psychedelic effects.[12][23][24]
The drug was first synthesized by Swiss chemist Albert Hofmann in 1938 and became widely studied in the 1950s and 1960s.[19][17] It was used experimentally in psychiatry for treating alcoholism and schizophrenia.[25] However, its association with the counterculture movement of the 1960s led to its classification as a Schedule I drug in the U.S. in 1968.[26] It was also listed as a Schedule 1 controlled substance by the United Nations in 1971 and remains without approved medical uses.[19]
Despite its legal restrictions, LSD remains influential in scientific and cultural contexts. Its therapeutic potential has been explored, particularly in treating mental health disorders.[12][27] As of 2017, about 10% of people in the U.S. had used LSD at some point, with 0.7% having used it in the past year.[28] Usage rates have risen, with a 56.4% increase in adult use in the U.S. from 2015 to 2018.[29]
LSD is commonly used as a recreational drug.[30]
LSD can catalyze intense spiritual experiences and is thus considered an entheogen. Some users have reported out of body experiences. In 1966, Timothy Leary established the League for Spiritual Discovery with LSD as its sacrament.[31][32] Stanislav Grof has written that religious and mystical experiences observed during LSD sessions appear to be phenomenologically indistinguishable from similar descriptions in the sacred scriptures of the great religions of the world and the texts of ancient civilizations.[33]
LSD currently has no approved uses in medicine.[34][35] A meta analysis concluded that a single dose was shown to be effective at reducing alcohol consumption in people suffering from alcoholism.[36] LSD has also been studied in depression, anxiety,[37][38] and drug dependence, with positive preliminary results.[39][40]
LSD is exceptionally potent, with as little as 20 μg capable of producing a noticeable effect.[19]
LSD can induce physical effects such as pupil dilation, decreased appetite, increased sweating, and wakefulness. The physical reactions to LSD vary greatly and some may be a result of its psychological effects. Commonly observed symptoms include increased body temperature, blood sugar, and heart rate, as well as goose bumps, jaw clenching, dry mouth, and hyperreflexia. In cases of adverse reactions, users may experience numbness, weakness, nausea, and tremors.[19]
The primary immediate psychological effects of LSD are visual hallucinations and illusions, often referred to as "trips". These effects typically begin within 20–30 minutes of oral ingestion, peak three to four hours after ingestion, and can last up to 20 hours, particularly with higher doses. An "afterglow" effect, characterized by an improved mood or perceived mental state, may persist for days or weeks following ingestion.[43] Positive experiences, or "good trips", are described as intensely pleasurable and can include feelings of joy, euphoria, an increased appreciation for life, decreased anxiety, a sense of spiritual enlightenment, and a feeling of interconnectedness with the universe.[44][45]
Negative experiences, commonly known as "bad trips", can induce feelings of fear, agitation, anxiety, panic, and paranoia.[7][46] While the occurrence of a bad trip is unpredictable, factors such as mood, surroundings, sleep, hydration, and social setting, collectively referred to as "set and setting", can influence the risk and are considered important in minimizing the likelihood of a negative experience.[47][48]
LSD induces an animated sensory experience affecting senses, emotions, memories, time, and awareness, lasting from 6 to 20 hours, with the duration dependent on dosage and individual tolerance. Effects typically commence within 30 to 90 minutes post-ingestion, ranging from subtle perceptual changes to profound cognitive shifts. Alterations in auditory and visual perception are common.[49][50]
Users may experience enhanced visual phenomena, such as vibrant colors, objects appearing to morph, ripple or move, and geometric patterns on various surfaces. Changes in the perception of food's texture and taste are also noted, sometimes leading to aversion towards certain foods.[49][51]
There are reports of inanimate objects appearing animated, with static objects seeming to move in additional spatial dimensions.[52] The auditory effects of LSD may include echo-like distortions of sounds. Basic visual effects often resemble phosphenes and can be influenced by concentration, thoughts, emotions, or music.[53] Auditory effects may include echo-like distortions and an intensified experience of music. Higher doses can lead to more intense sensory perception alterations, including synesthesia, perception of additional dimensions, and temporary dissociation.
LSD, a classical psychedelic, is deemed physiologically safe at standard dosages (50–200 μg) and its primary risks lie in psychological effects rather than physiological harm.[23][56] A 2010 study by David Nutt ranked LSD as significantly less harmful than alcohol, placing it near the bottom of a list assessing the harm of 20 drugs.[57]
LSD can induce panic attacks or extreme anxiety, colloquially termed a "bad trip". Despite lower rates of depression and substance abuse found in psychedelic drug users compared to controls, LSD presents heightened risks for individuals with severe mental illnesses like schizophrenia.[58][59] These hallucinogens can catalyze psychiatric disorders in predisposed individuals, although they do not tend to induce illness in emotionally healthy people.[23]
While research from the 1960s indicated increased suggestibility under the influence of LSD among both mentally ill and healthy individuals, recent documents suggest that the CIA and Department of Defense have discontinued research into LSD as a means of mind control.[60][61][62][non-primary source needed]
Flashbacks are psychological episodes where individuals re-experience some of LSD's subjective effects after the drug has worn off, persisting for days or months post-hallucinogen use.[63][64] These experiences are associated with hallucinogen persisting perception disorder (HPPD), where flashbacks occur intermittently or chronically, causing distress or functional impairment.[18]
The etiology of flashbacks is varied. Some cases are attributed to somatic symptom disorder, where individuals fixate on normal somatic experiences previously unnoticed prior to drug consumption.[65] Other instances are linked to associative reactions to contextual cues, similar to responses observed in individuals with past trauma or emotional experiences.[66] The risk factors for flashbacks remain unclear, but pre-existing psychopathologies may be significant contributors.[67]
Estimating the prevalence of HPPD is challenging. It is considered rare, with occurrences ranging from 1 in 20 users experiencing the transient and less severe type 1 HPPD, to 1 in 50,000 for the more concerning type 2 HPPD.[18] Contrary to internet rumors, LSD is not stored long-term in the spinal cord or other body parts. Pharmacological evidence indicates LSD has a half-life of 175 minutes and is metabolized into water-soluble compounds like 2-oxo-3-hydroxy-LSD, eliminated through urine without evidence of long-term storage.[7] Clinical evidence also suggests that chronic use of SSRIs can potentiate LSD-induced flashbacks, even months after stopping LSD use.[68]: 145
Several psychedelics, including LSD, are metabolized by CYP2D6. Concurrent use of SSRIs, potent inhibitors of CYP2D6, with LSD may heighten the risk of serotonin syndrome.[68]: 145 Chronic usage of SSRIs, TCAs, and MAOIs is believed to diminish the subjective effects of psychedelics, likely due to SSRI-induced 5-HT2A receptor downregulation and MAOI-induced 5-HT2A receptor desensitization.[7][68]: 145 Interactions between psychedelics and antipsychotics or anticonvulsants are not well-documented; however, co-use with mood stabilizers like lithium may induce seizures and dissociative effects, particularly in individuals with bipolar disorder.[68]: 146 [69][70] Lithium notably intensifies LSD reactions, potentially leading to acute comatose states when combined.[7]
The lethal oral dose of LSD in humans is estimated at 100 mg, based on LD50 and lethal blood concentrations observed in rodent studies.[56]
LSD shows significant tachyphylaxis, with tolerance developing 24 hours after administration. The progression of tolerance at intervals shorter than 24 hours remains largely unknown.[71] Tolerance typically resets to baseline after 3–4 days of abstinence.[72][73] Significant cross-tolerance occurs between LSD, mescaline and psilocybin.[74][75] A slight cross-tolerance to DMT is observed in humans highly tolerant to LSD.[76] Tolerance to LSD also builds up with consistent use,[77] and is believed to result from serotonin 5-HT2A receptor downregulation.[72] Researchers believe that tolerance returns to baseline after two weeks of not using psychedelics.[78]
LSD is widely considered to be non-addictive, despite its potential for abuse.[5][23][79][80] Attempts to train laboratory animals to self-administer LSD have been largely unsuccessful.[23] Although tolerance to LSD builds up rapidly, a withdrawal syndrome does not appear, suggesting that a potential syndrome does not necessarily relate to the possibility of acquiring rapid tolerance to a substance.[81] A report examining substance use disorder for DSM-IV noted that almost no hallucinogens produced dependence, unlike psychoactive drugs of other classes such as stimulants and depressants.[82][83]
The mutagenic potential of LSD is unclear. Overall, the evidence seems to point to limited or no effect at commonly used doses.[84] Studies showed no evidence of teratogenic or mutagenic effects.[7]
There have been no documented fatal human overdoses from LSD,[7][85] although there has been no "comprehensive review since the 1950s" and "almost no legal clinical research since the 1970s".[7] Eight individuals who had accidentally consumed an exceedingly high amount of LSD, mistaking it for cocaine, and had gastric levels of 1000–7000 μg LSD tartrate per 100 mL and blood plasma levels up to 26 μg/ml, had suffered from comatose states, vomiting, respiratory problems, hyperthermia, and light gastrointestinal bleeding; however, all of them survived without residual effects upon hospital intervention.[7][86]
Individuals experiencing a bad trip after LSD intoxication may present with severe anxiety and tachycardia, often accompanied by phases of psychotic agitation and varying degrees of delusions.[56] Cases of death on a bad trip have been reported due to prone maximal restraint (commonly known as a hogtie) and positional asphyxia when the individuals were restrained by law enforcement personnel.[56]
Massive doses are largely managed by symptomatic treatments, and agitation can be addressed with benzodiazepines.[87][88] Reassurance in a calm, safe environment is beneficial.[89] Antipsychotic agents such as neuroleptics and haloperidol are not recommended as they may have adverse psychotomimetic effects.[87] Gastrointestinal decontamination with activated charcoal is of little use due to the rapid absorption of LSD, unless done within 30–60 minutes of ingesting exceedingly huge amounts.[87] Administration of anticoagulants, vasodilators, and sympatholytics may be useful for treating ergotism.[87]
Many novel psychoactive substances of 25-NB (NBOMe) series, such as 25I-NBOMe and 25B-NBOMe, are regularly sold as LSD in blotter papers.[90][91] NBOMe compounds are often associated with life-threatening toxicity and death.[90][92] Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD,[93] and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently".[85] Researchers state that the alleged physiological toxicity of LSD is likely due to psychoactive substances other than LSD.[56]
NBOMe compounds are reported to have a bitter taste,[85] are not active orally,[a] and are usually taken sublingually.[95] When NBOMes are administered sublingually, numbness of the tongue and mouth followed by a metallic chemical taste was observed, and researchers describe this physical side effect as one of the main discriminants between NBOMe compounds and LSD.[96][97][98] Despite its high potency, recreational doses of LSD have only produced low incidents of acute toxicity, but NBOMe compounds have extremely different safety profiles.[85][92] Testing with Ehrlich's reagent gives a positive result for LSD and a negative result for NBOMe compounds.[99][100]
Most serotonergic psychedelics are not significantly dopaminergic, and LSD is therefore atypical in this regard. The agonism of the D2 receptor by LSD may contribute to its psychoactive effects in humans.[101]
LSD binds to most serotonin receptor subtypes except for the 5-HT3 and 5-HT4 receptors. However, most of these receptors are affected at too low affinity to be sufficiently activated by the brain concentration of approximately 10–20 nM.[23] In humans, recreational doses of LSD can affect 5-HT1A (Ki = 1.1 nM), 5-HT2A (Ki = 2.9 nM), 5-HT2B (Ki = 4.9 nM), 5-HT2C (Ki = 23 nM), 5-HT5A (Ki = 9 nM [in cloned rat tissues]), and 5-HT6 receptors (Ki = 2.3 nM).[102] Although not present in humans, 5-HT5B receptors found in rodents also have a high affinity for LSD.[103] The psychedelic effects of LSD are attributed to cross-activation of 5-HT2A receptor heteromers.[104] Many but not all 5-HT2A agonists are psychedelics and 5-HT2A antagonists block the psychedelic activity of LSD. LSD exhibits functional selectivity at the 5-HT2A and 5-HT2C receptors in that it activates the signal transduction enzyme phospholipase A2 instead of activating the enzyme phospholipase C as the endogenous ligand serotonin does.[105]
Exactly how LSD produces its effects is unknown, but it is thought that it works by increasing glutamate release in the cerebral cortex[23] and therefore excitation in this area, specifically in layer V.[106] LSD, like many other drugs of recreational use, has been shown to activate DARPP-32-related pathways.[107] The drug enhances dopamine D2 receptor protomer recognition and signaling of D2–5-HT2A receptor complexes,[108] which may contribute to its psychotropic effects.[108] LSD has been shown to have low affinity for H1 receptors, displaying antihistamine effects.[109][110]
LSD is a biased agonist that induces a conformation in serotonin receptors that preferentially recruits β-arrestin over activating G proteins.[111] LSD also has an exceptionally long residence time when bound to serotonin receptors lasting hours, consistent with the long-lasting effects of LSD despite its relatively rapid clearance.[111] A crystal structure of 5-HT2B bound to LSD reveals an extracellular loop that forms a lid over the diethylamide end of the binding cavity which explains the slow rate of LSD unbinding from serotonin receptors.[112] The related lysergamide lysergic acid amide (LSA) that lacks the diethylamide moiety is far less hallucinogenic in comparison.[112]
LSD, like other psychedelics, has been found to increase the expression of genes related to synaptic plasticity.[113] This is in part due to binding to brain-derived neurotrophic factor (BDNF) receptor TrkB.[114]
The acute effects of LSD normally last between 6 and 10 hours depending on dosage, tolerance, and age.[116][117] Aghajanian and Bing (1964) found LSD had an elimination half-life of only 175 minutes (about 3 hours).[102] However, using more accurate techniques, Papac and Foltz (1990) reported that 1 μg/kg oral LSD given to a single male volunteer had an apparent plasma half-life of 5.1 hours, with a peak plasma concentration of 5 ng/mL at 3 hours post-dose.[118]
The pharmacokinetics of LSD were not properly determined until 2015, which is not surprising for a drug with the kind of low-μg potency that LSD possesses.[6][9] In a sample of 16 healthy subjects, a single mid-range 200 μg oral dose of LSD was found to produce mean maximal concentrations of 4.5 ng/mL at a median of 1.5 hours (range 0.5–4 hours) post-administration.[6][9] Concentrations of LSD decreased following first-order kinetics with a half-life of 3.6±0.9 hours and a terminal half-life of 8.9±5.9 hours.[6][9]
The effects of the dose of LSD given lasted for up to 12 hours and were closely correlated with the concentrations of LSD present in circulation over time, with no acute tolerance observed.[6][9] Only 1% of the drug was eliminated in urine unchanged, whereas 13% was eliminated as the major metabolite 2-oxo-3-hydroxy-LSD (O-H-LSD) within 24 hours.[6][9] O-H-LSD is formed by cytochrome P450 enzymes, although the specific enzymes involved are unknown, and it does not appear to be known whether O-H-LSD is pharmacologically active or not.[6][9] The oral bioavailability of LSD was crudely estimated as approximately 71% using previous data on intravenous administration of LSD.[6][9] The sample was equally divided between male and female subjects and there were no significant sex differences observed in the pharmacokinetics of LSD.[6][9]
Neuroimaging studies using resting state fMRI recently suggested that LSD changes the cortical functional architecture.[119] These modifications spatially overlap with the distribution of serotoninergic receptors. In particular, increased connectivity and activity were observed in regions with high expression of 5-HT2A receptor, while a decrease in activity and connectivity was observed in cortical areas that are dense with 5-HT1A receptor.[120] Experimental data suggest that subcortical structures, particularly the thalamus, play a synergistic role with the cerebral cortex in mediating the psychedelic experience. LSD, through its binding to cortical 5-HT2A receptor, may enhance excitatory neurotransmission along frontostriatal projections and, consequently, reduce thalamic filtering of sensory stimuli towards the cortex.[121] This phenomenon appears to selectively involve ventral, intralaminar, and pulvinar nuclei.[121]
LSD is a chiral compound with two stereocenters at the carbon atoms C-5 and C-8, so that theoretically four different optical isomers of LSD could exist. LSD, also called (+)-d-LSD,[122] has the absolute configuration (5R,8R). 5S stereoisomers of lysergamides do not exist in nature and are not formed during the synthesis from d-lysergic acid. Retrosynthetically, the C-5 stereocenter could be analysed as having the same configuration of the alpha carbon of the naturally occurring amino acid L-tryptophan, the precursor to all biosynthetic ergoline compounds.
However, LSD and iso-LSD, the two C-8 isomers, rapidly interconvert in the presence of bases, as the alpha proton is acidic and can be deprotonated and reprotonated. Non-psychoactive iso-LSD which has formed during the synthesis can be separated by chromatography and can be isomerized to LSD.
Pure salts of LSD are triboluminescent, emitting small flashes of white light when shaken in the dark.[116] LSD is strongly fluorescent and will glow bluish-white under UV light.
LSD is an ergoline derivative. It is commonly synthesized by reacting diethylamine with an activated form of lysergic acid. Activating reagents include phosphoryl chloride[123] and peptide coupling reagents.[110] Lysergic acid is made by alkaline hydrolysis of lysergamides like ergotamine, a substance usually derived from the ergot fungus on agar plate; or, theoretically possible, but impractical and uncommon, from ergine (lysergic acid amide, LSA) extracted from morning glory seeds.[124] Lysergic acid can also be produced synthetically, although these processes are not used in clandestine manufacture due to their low yields and high complexity.[125][126]
The precursor for LSD, lysergic acid, has been produced by GMO baker's yeast.[127]
A single dose of LSD is typically between 40 and 500 micrograms—an amount roughly equal to one-tenth the mass of a grain of sand. Threshold effects can be felt with as little as 25 micrograms of LSD.[128][129] The practice of using sub-threshold doses is called microdosing.[130] Dosages of LSD are measured in micrograms (μg), or millionths of a gram.
In the mid-1960s, the most important black market LSD manufacturer (Owsley Stanley) distributed LSD at a standard concentration of 270 μg,[131] while street samples of the 1970s contained 30 to 300 μg. By the 1980s, the amount had reduced to between 100 and 125 μg, dropping more in the 1990s to the 20–80 μg range,[132] and even more in the 2000s (decade).[131][133]
"LSD," writes the chemist Alexander Shulgin, "is an unusually fragile molecule ... As a salt, in water, cold, and free from air and light exposure, it is stable indefinitely."[116]
LSD has two labile protons at the tertiary stereogenic C5 and C8 positions, rendering these centers prone to epimerisation. The C8 proton is more labile due to the electron-withdrawing carboxamide attachment, but the removal of the chiral proton at the C5 position (which was once also an alpha proton of the parent molecule tryptophan) is assisted by the inductively withdrawing nitrogen and pi electron delocalisation with the indole ring.[citation needed]
LSD also has enamine-type reactivity because of the electron-donating effects of the indole ring. Because of this, chlorine destroys LSD molecules on contact; even though chlorinated tap water contains only a slight amount of chlorine, the small quantity of compound typical to an LSD solution will likely be eliminated when dissolved in tap water.[116] The double bond between the 8-position and the aromatic ring, being conjugated with the indole ring, is susceptible to nucleophilic attacks by water or alcohol, especially in the presence of UV or other kinds of light. LSD often converts to "lumi-LSD," which is inactive in human beings.[116]
A controlled study was undertaken to determine the stability of LSD in pooled urine samples.[134] The concentrations of LSD in urine samples were followed over time at various temperatures, in different types of storage containers, at various exposures to different wavelengths of light, and at varying pH values. These studies demonstrated no significant loss in LSD concentration at 25 °C for up to four weeks. After four weeks of incubation, a 30% loss in LSD concentration at 37 °C and up to a 40% at 45 °C were observed. Urine fortified with LSD and stored in amber glass or nontransparent polyethylene containers showed no change in concentration under any light conditions. The stability of LSD in transparent containers under light was dependent on the distance between the light source and the samples, the wavelength of light, exposure time, and the intensity of light. After prolonged exposure to heat in alkaline pH conditions, 10 to 15% of the parent LSD epimerized to iso-LSD. Under acidic conditions, less than 5% of the LSD was converted to iso-LSD. It was also demonstrated that trace amounts of metal ions in the buffer or urine could catalyze the decomposition of LSD and that this process can be avoided by the addition of EDTA.
LSD can be detected in concentrations larger than approximately 10% in a sample using Ehrlich's reagent and Hofmann's reagent. However, detecting LSD in human tissues is more challenging due to its active dosage being significantly lower (in micrograms) compared to most other drugs (in milligrams).[136]
LSD may be quantified in urine for drug testing programs, in plasma or serum to confirm poisoning in hospitalized victims, or in whole blood for forensic investigations. The parent drug and its major metabolite are unstable in biofluids when exposed to light, heat, or alkaline conditions, necessitating protection from light, low-temperature storage, and quick analysis to minimize losses.[137] Maximum plasma concentrations are typically observed 1.4 to 1.5 hours after oral administration of 100 μg and 200 μg, respectively, with a plasma half-life of approximately 2.6 hours (ranging from 2.2 to 3.4 hours among test subjects).[138]
Due to its potency in microgram quantities, LSD is often not included in standard pre-employment urine or hair analyses.[136][139] However, advanced liquid chromatography–mass spectrometry methods can detect LSD in biological samples even after a single use.[139]
... affected by a remarkable restlessness, combined with a slight dizziness. At home I lay down and sank into a not unpleasant intoxicated-like condition, characterized by an extremely stimulated imagination. In a dreamlike state, with eyes closed (I found the daylight to be unpleasantly glaring), I perceived an uninterrupted stream of fantastic pictures, extraordinary shapes with intense, kaleidoscopic play of colors. After some two hours this condition faded away.
Swiss chemist Albert Hofmann first synthesized LSD in 1938 from lysergic acid, a chemical derived from the hydrolysis of ergotamine, an alkaloid found in ergot, a fungus that infects grain.[19][17] LSD was the 25th of various lysergamides Hofmann synthesized from lysergic acid while trying to develop a new analeptic, hence the alternate name LSD-25. Hofmann discovered its effects in humans in 1943, after unintentionally ingesting an unknown amount, possibly absorbing it through his skin.[141]