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Drug Testing

TASC Collection Center
Redwood Toxicology Laboratory

Located at 19 N. 6th Street on the first floor of the SAM Building, the TASC Urine Collection Center is open from Monday through Thursday from 7:30 AM until 6:00 PM. Using the federally accepted standards for chain of custody in collecting urine samples, TASC contracts with Redwood Toxicology, which conducts all specimen testing. While a standard 6-panel test screens for marijuana, amphetamine/methamphetamine, cocaine, benzodiazepines, opiates, and oxycodone, Redwood can test for a multitude of substances, including synthetic cannabis (K2), Ecstasy, Ethyl Glucoronide (EtG), anabolic steroids, and common antidepressants.

All donors are observed by gender appropriate staff when submitting a urine specimen. Results will be released only to the entities as specified on the Consent to Release Confidentiality form that is presented to each donor. If referred by an agency affiliated with the Court of Common Pleas (i.e. APO, BCCYS, BCPS, etc.), donor cost for testing is $5, payable by cash at the time of collection. Test results are available to the referral source via Redwood’s ToxAccess online system within 48-72 hours.

Confirmation testing via GC/MS (gas chromatography/mass spectrometry) or LC/MS/MS (liquid chromatography-tandem mass spectrometry) is available upon request at a cost of $35. If the confirmation test is negative, the $35 fee is reimbursed.

Diluted Specimens
To be a valid, all urine samples must contain an acceptable concentration of creatinine. Creatinine is a metabolic by-product of muscle metabolism, and normally appears in urine in relatively constant quantities over a 24 hour period with “normal” liquid intake. Abnormal liquid consumption within 2-5 hours of submitting a sample, sometimes referred to as “water loading,” will cause the urine creatinine level to decrease. The following creatinine levels,  as determined by the Federal Department of Health and Human Services, Substance Abuse Mental Health Services Administration (SAMHSA), are indicative of “water loading” or specimen substitution:

<20 mg/dL : Diluted specimen caused by short-term water loading or flushing

<2.0 mg/dL : Abnormally diluted specimen not consistent with human urine

Poppy Seeds
Poppy seeds contain trace amounts of codeine and morphine which can result in a positive drug screen for opiates. It is recommended that donors refrain from consuming any products that contain poppy seeds, such as bagels, cakes, etc.

EtG Testing
Ethyl Glucoronide (EtG) is a direct metabolite of alcohol. The presence of EtG in urine may be used to detect recent ethanol ingestion, even after ethanol is no longer measurable. Sometimes called the “Monday morning test,” the presence of EtG in urine is an indicator that ethanol was ingested and can be detected in urine for up to 80 hours after ingestion.

Synthetic Cannabinoids (K2)
The Redwood Toxicology laboratory test for synthetic marijuana (i.e. K2) is a specialized test that screens for over 70 compounds commonly detected in street level K2.  Working in conjunction with law enforcement, Redwood Toxicology provides the most up to date testing for K2 that has been confiscated on the streets, broken down into its component parts, and included as part of Redwood’s detection process.

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Drugs of Abuse Information Guide

Amphetamine & Methamphetamine

Classification

Amphetamine and methamphetamine are Schedule II drugs included in a group of chemicals called sympathomimetic amines, which contain a phenethylamine chemical nucleus. Sympathomimetic amines mimic the effects of the endogenous neurotransmitters such as epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine. Also included in this group are various over-the-counter drugs such as phenylpropanolamine, pseudoephedrine, ephedrine as well as the Schedule I drug methylenedioxymethamphetamine (MDMA or Ecstasy). The amphetamines are powerful central nervous system stimulants and can be taken orally, intravenously, snorted or smoked. Methamphetamine is one of the most commonly abused drugs in the Western United States. It is readily synthesized, with ephedrine being used as the primary precursor.
Metabolism
Amphetamines are rapidly absorbed from the gastrointestinal tract and are either deactivated by the liver or excreted unchanged into the urine. Methamphetamine is excreted primarily unchanged (44%) and some of the drug (6%) is metabolized and excreted as amphetamine. Amphetamine is also excreted largely unchanged (30%) with 20-25% being metabolized to deaminated (hippuric and benzoic acids) and hydroxylated metabolites. The elimination rate of amphetamines varies with the pH of the urine, as at low pH the excretion of unchanged drug increases, while at high pH the excretion of unchanged drug decreases. Within a few hours after any type of administration, amphetamines appear in the urine and can typically be detected for up to 72-96 hours.
Abuse
Amphetamines, particularly methamphetamine, are among the most popular drugs of abuse. Common street names include speed, crank, crystal, meth, and ice. Ice and crystal meth are crystals of methamphetamine HCL. Snot and glue are oils formed from methamphetamine free base and baking soda. Methamphetamine is frequently smoked in a glass pipe as it is easily volatilized into a gas that is inhaled. Although the ice form is primarily found in Hawaii, it has gained the most notoriety mainly due to the fact that it is 98-100% pure methamphetamine HCL and its effects are rapid, intense, and of longer duration than other forms of methamphetamine.

The signs and symptoms associated with the abuse of methamphetamine depend upon the amount used and the duration of use. With infrequent or low dose use, a person may experience euphoria, lowered anxiety, talkativeness, decreased appetite, increased sexual arousal, increased alertness, and decreased fatigue. Physiologically there can be increased heart rate and blood pressure. With increased dose or prolonged abuse (either binge or chronic), an individual may experience a set of secondary effects that can include increased anxiety, irritability, aggressiveness, paranoia and hypersexuality. Physiological effects can include dilated pupils, dry mouth, hippus, increased body temperature and tachycardia. In overdose situations, a person may experience hallucinations, coma or death. Crash symptoms typically follow binge abuse of methamphetamine. This phase is marked by extreme fatigue, depression, mental exhaustion and prolonged periods of sleep.


Benzodiazepines Drug Information

Classification
The benzodiazepines are a class of drugs primarily classified as anti-anxiety, sedatives, or hypnotics. All contain a benzene ring fused to a 7-membered diazepine ring, hence the term benzodiazepine. Various modifications and substitutions of the ring structure yield compounds of similar activities. The clinical effects of these drugs result from actions on the central nervous system and these effects include sedation, hypnosis, muscle relaxation, and anticonvulsant activity.
Metabolism
The benzodiazepines are well absorbed after oral administration and are rapidly distributed throughout the body. They are extensively metabolized by the liver, and in general, slowly excreted in the urine as pharmacologically inactive conjugated metabolites. Some metabolites may possess some pharmacological activity of their own, thus displaying the “next day” effects of some benzodiazepines. Oxazepam is a common urinary metabolite of several benzodiazepines such as diazepam and temazepam. Duration of detectability in urine is varied. Ingestion of therapeutic dosages may be detectable for 1-3 days while extended usage over a period of months or years can extend excretion times up to 4-6 weeks after cessation of use (depends on dosage & benzodiazepine)
Abuse
The benzodiazepines are considered one of the most widely prescribed drugs in the United States, thus leading to its widespread abuse. Diazepam (Valium®) and alprazolam (Xanax®) are two of the most widely abused of the benzodiazepines. Many abusers will attempt to accentuate the effects of benzodiazepines by the concomitant use of alcohol or other CNS depressant drugs.As a result, benzodiazepines are involved in approximately one third of all drug self induced poisonings. Other commonly abused benzodiazepines are chlordiazepoxide, flurazepam, clonazepam, and lorazepam. Prolonged high doses of benzodiazepines can cause dependency and a withdrawal syndrome may occur following abrupt cessation of use.
Chemical Name Trade Name
Alprazolam Xanax®
Chlordiazepoxide Librium®
Clonazepam Klonopin®
Clorazepate Tranxene
Diazepam Valium®
Flunitrazepam Rohypnol®
Flurazepam Dalmane®
Lorazepam Ativan®
Midazolam Versed®
Oxazepam Serax®
Prazepam Centrax®
Temazepam Restoril®
Triazolam Halcion®


Cocaine Drug Information

Classification
Cocaine (benzoylmethylecgonine) is a central nervous system stimulant derived from the leaves of the coca plant. Cocaine has two major pharmacological actions; one is a local anesthetic, and the other is an indirect acting sympathomimetic having many of the properties of an amphetamine. The drug is either in the salt/powder form (cocaine HCL) which can be administered by snorting or intravenous injection or in the free base “crack” form which is smoked.
Metabolism
After smoking, cocaine is rapidly absorbed with peak plasma concentrations occurring at about 5 minutes, versus 30-40 minutes following intranasal ingestion. Cocaine is extensively metabolized by the liver and blood enzymes with approximately one percent of the dose excreted in the urine unchanged. The major metabolite found in the urine is benzoylecgonine (25-40% of the dose), followed by ecgonine methyl ester (18-22%). Depending upon the dosage ingested, frequency of use, and metabolic variation, benzoylecgonine can remain detectable in the urine for as long as 48-96 hours post ingestion.
Abuse
Cocaine produces a short-lived, intense high which is extremely addictive. The signs and symptoms associated with the abuse of cocaine depend upon the amount used and the duration of use. With infrequent or low dose use a person may experience euphoria, lowered anxiety, talkativeness, decreased appetite, increased sexual arousal, increased alertness, and decreased fatigue. Physiologically there can be increased heart rate and blood pressure.
With increased dose or prolonged abuse (either binge or chronic) an individual may experience a set of secondary effects that can include increased anxiety, irritability, aggressiveness, paranoia and hypersexuality. Physiological effects can include dilated pupils, dry mouth, hippus, increased body temperature and tachycardia. In overdose situations, a person my experience hallucinations, coma or death. Crash symptoms typically follow binge abuse of cocaine. This phase is marked by extreme fatigue, depression, mental exhaustion and prolonged periods of sleep.
Laboratory drug testing: Methods of Analysis
Enzyme immunoassay (EIA) is a widely used screening method designed to specifically detect benzoylecgonine and to a lesser extent, cocaine and ecgonine methyl ester (secondary cocaine metabolite). Commonly used confirmation methods include gas chromatography/mass spectrometry (GC/MS) and liquid chromatography/tandem mass spectrometry (LC/MS/MS). These methods offer excellent sensitivity and specificity and are the methods of choice for the confirmation of the immunoassay positive screens.


Synthetic Cannabinoids Drug Information

Classification
Synthetic Cannabinoids are chemicals that act as cannabinoid receptor agonists. Chemically they are not similar to cannabinoids but the term “Synthetic Cannabinoids” or “Cannabinomimetics” is widely used to refer to them as they’re cannabinoid-like in their activity.
The synthetic cannabinoid receptor agonists fall into seven major structural groups:
• Naphthoylindoles (e.g. JWH-018, JWH-073, JWH-081, AM-2201)
• Naphthylmethylindoles* (JWH-185, JWH-199)
• Naphthoylpyrroles* (JWH-369, JWH-370)
• Naphthylmethylindenes* (JWH-176)
• Phenylacetylindoles (JWH-250, RCS-4)
• Cyclohexylphenols (e.g. CP 47,497 and homologues of CP 47,497)
• Classical cannabinoids (e.g. HU-210)
*Compounds in these groups have not been detected in herbal blends so far.
Metabolism
Little is known about the detailed pharmacology and toxicology of the synthetic cannabinoids and few formal human studies have been published.
Synthetic Cannabinoids metabolize extensively in humans via oxidation and glucuronide conjugation. Following a single low dose, the hydroxylated synthetic cannabinoids and the carboxylated synthetic cannabinoids metabolites can be detected up to 72 hours in urine. Very little parent drug excreted in human urine has been reported. In case of chronic use the detection window could be longer.
Presence of parent drug in saliva confirms ingestion; average detection window up to 24-48 hours.
It is possible that, apart from high potency, some other synthetic cannabinoids could have particularly long half-lives, potentially leading to a prolonged psychoactive effect. In addition, there is considerable inter-and intra-batch variability in smoking mixtures, both in terms of substances present and their quantity. Thus, there is a higher potential for overdose than with cannabis.
Abuse
Initially, JWH-018 and JWH-073 were the two most common synthetic cannabinoid chemicals found in a variety of herbal smoking blends. Others like AM-1248, AKB-48, UR-144, and XLR-11 have started appearing in newer synthetic cannabinoid products and preparations. Reportedly offering a high 4 times stronger than marijuana, these compounds are commonly associated with herbal smoke and incense products sold under names such as K2, K3 Legal, Spice, Syn, Haze, Cloud Nine, Serenity and many others.
Synthetic cannabinoid chemicals are often laced in the herbal smoking products that are readily available via the Internet and in many “head-shops” around the country.
Users looking for a “high” often turn to these herbal smoking or incense products because they do not show up on a standard urine drug test. Users smoke the product by wrapping joints, smoking it in pipes, or inhaling fumes via vaporizers. Users also report that herbal blends or pure chemical concoctions can be ingested with an infusion or solvent process; purportedly allowing them to manage the potency and dose of the active ingredient(s).
Users indicate the high comes on slow at first, then with surprising potency. There have been many reports about the adverse effects including agitation, rapid heart rate, confusion, dizziness and nausea.
According to the American Association of Poison Control Centers, the number of human exposure calls relating to synthetic cannabinoids increased 139% between 2010 and 2011.
Long-term effects from these research chemicals are unknown.
In July 2012, the DEA banned synthetic cannabinoids based on their structural classification, explicitly naming 15 chemicals, citing numerous calls to poison control centers around the nation. Plans to Emergency Schedule three more drugs were announced in April 2013. However, newer generation compounds continually emerge—making it more vital than ever to target synthetic marijuana.


Marijuana Drug Information

Classification
Marijuana is a preparation derived from the leaves and flowering tops of cannabis plants (Cannabis sativa) that is capable of producing psychoactive effects when ingested. One of the primary classes of compounds found in marijuana is called cannabinoids. There are up to 60 cannabinoids in marijuana with delta-9-tetrahydrocannabinol (THC) being the primary psychoactive constituent.
Metabolism
When marijuana is smoked, THC is rapidly absorbed through the lungs and enters the bloodstream in minutes. Following oral ingestion, THC does not reach the bloodstream for approximately 1.5-3 hours. Once in the blood, THC is bound to blood proteins and carried throughout the body where it is either absorbed into body tissues (including the brain, heart, and fat) or transformed by the liver into the water soluble metabolites 11-hydroxy-THC and carboxy-THC. These water soluble metabolites, are readily excreted into the urine, with the inactive metabolite carboxy-THC being the predominant metabolite detected. Initially, THC is quickly absorbed into the body tissues and then is slowly released back into the blood stream where it is carried to the liver and metabolized. Because THC tends to be stored in fatty tissues, it accumulates faster than it can be eliminated in chronic repetitive smokers. This leads to extended retention of THC which is then eliminated from the body at a relatively constant rate with an average elimination half-life being estimated at 18-30 hours. Urinary concentrations of THC are very difficult to interpret due to variables such as dosage of THC ingested, frequency of use, timing of urine collection relative to last exposure to marijuana, rate of release of stored cannabinoids in adipose tissue, and an individual’s hydration state. Therefore, the detection of THC metabolites in the urine is only an indication of past marijuana use and is not related to the degree of intoxication or impairment.
Abuse
The psychological effects of THC include an increased sense of well being or euphoria, relaxation, slowed psycho-motor response, an altered sense of time, short term memory impairment and impairment of multi-tasking performance.
THC Retention Time
• Infrequent (less than twice/week) Smoking: When screening assays of 50 ng/mL or greater are used, urine samples will generally be positive for 1-3 days.
• Regular (several times per week) Smoking: May result in urine specimens testing positive for 7-21 days.
• Chronic (daily) Smoking: An individual who smokes marijuana daily for prolonged periods of time can test positive for 30 days or longer.
• Oral Ingestion: Metabolic profiles in urine samples cannot generally differentiate between marijuana ingested orally versus marijuana ingested by smoking. However, oral ingestion requires approximately three times more THC than smoking to produce similar effects or “highs”; therefore, visual detection of the marijuana in the ingested item would seem reasonable, thus ruling out unknown consumption. Retention time of orally ingested marijuana ranges from 1-5 days.
• Passive Inhalation: In general, routine passive exposure to marijuana smoke will not result in a positive result for cannabinoids in excess of a 50 ng/mL screening cut-off.


Opiates Drug Information

Classification
The term “opioid” refers to all drugs, natural or synthetic, with morphine-like properties. Both morphine and codeine are naturally occurring alkaloids derived from the seed pod of the opium poppy. Semi-synthetic opiates include heroin, a diacetyl derivative of morphine; hydromorphone, hydrocodone, and oxycodone derived by a simple modification of the morphine molecule. Synthetic opiates such as methadone and meperidine, mimic opiate effects but are not prepared from the poppy. The drugs may be administered by snorting, subcutaneous or intravenous injection, or smoking. Opioid compounds have analgesic and antitussive properties.
Metabolism
Morphine is rapidly absorbed. Plasma peak levels following an oral dose occur after 15-60 minutes, and following IV injection occur after 15 minutes. Extensively metabolized by the liver, only 2-12% is excreted as unchanged drug, while 60-80% is excreted as morphine-3-glucuronide. The half-life of morphine is 1.7-4.5 hours. Heroin is rapidly metabolized (plasma half-life is 3 minutes), first to 6-monoacetylmorphine (6-MAM) and further to morphine. The urinary excretion profile is similar to morphine, in that 7% is excreted as unchanged morphine and 50-60% as glucuronides. Trace amounts of 6-MAM, a specific metabolite of heroin, are also excreted for approximately 6-8 hours following heroin use. Following an oral dose, codeine is also rapidly absorbed and metabolized, principally to codeine-6-glucuronide, with 10-15% metabolized to morphine and norcodeine. Opiates may be detected in urine for 2-4 days following ingestion.
The interpretation of results for urines positive for opiates merit special consideration. Since codeine is metabolized to morphine, both substances may appear in the urine following codeine ingestion. However, the codeine concentration is generally greater than that of morphine. Street heroin also contains acetylcodeine, which metabolizes to codeine, therefore, both codeine and morphine may be present in the urine of some heroin users, although morphine generally predominates. In cases of low morphine and codeine concentrations in urine, it is not possible to determine whether codeine, morphine, or heroin were ingested. The presence of morphine alone would generally indicate either clinical morphine use or illicit morphine or heroin use. A specific metabolite of heroin, 6-monoacetylmorphine, is also at times detected and would definitely confirm illicit drug (heroin) use. Poppy seeds, which have not been effectively washed, contain trace amounts of codeine and morphine. When consumed in sufficient amounts, poppy seeds may produce urines which test positive for opiates.
Abuse
Opioid compounds have effects on the CNS and usually on the bowel. They produce analgesia, respiratory depression, euphoria, mood changes, confusion, and constipation. Tolerance and dependence develop with repeated use, with overdose being characterized by coma, respiratory depression, and pinpoint pupils. Discontinuing the drug in a dependent individual will precipitate a withdrawal syndrome. Heroin and morphine are the most commonly abused opioid compounds; however codeine, propoxyphene, oxycodone, hydrocodone, etc. are also extensively abused, as they are more readily available. Most heroin and morphine abusers inject or “mainline” the drugs intravenously, as this produces the most immediate and intense effects. The heroin or morphine “rush” is the most desired sensation which is characterized by an intense orgasmic sensation centered in the abdomen.


Oxycodone Drug Information

Classification
Oxycontin® is the trade name of one of numerous Schedule II prescription drugs that contain the opioid oxycodone as the active ingredient. Opioids refer to a class of drugs, natural and synthetic, with morphine-like actions. Oxycodone is reported to have equivalent potency to that of morphine. Other prescription drugs that contain oxycodone include Percodan® and Percocet®. Schedule II drugs are those which are approved for medical use and have a high potential for abuse and may lead to severe physical and psychological dependence. Oxycontin® was first introduced by Purdue Pharma in 1996 as a controlled sustained release formulation for pain relief. It was estimated that almost 6 million prescriptions for Oxycontin® were filled in the year 2000 and sales reached 1 billion dollars. It is legitimately prescribed for moderate to severe chronic or long-lasting pain. Oxycontin® is available in tablet forms containing 10, 20, 40, and 80 mg. A 160 mg oxycodone tablet was available which was discontinued in May 2001. By comparison, Percocet® typically contains 5 mg of oxycodone. Thus, one 160 mg tablet of Oxycontin® contained the equivalent amount of oxycodone as 32 Percocet® (5 mg) tablets.
One of the primary benefits of Oxycontin® is that because it is controlled release, it only needs to be taken orally every 12 hours. In contrast, short acting oxycodone tablets like Percocet® require the dosage be taken every 4-6 hours to maintain pain relief. Thus, the controlled release formulation allows for continuous pain relief for a substantial period of time when compared to traditional Percodan® or Percocet® tablets.
Metabolism
A large portion of oxycodone is N-dealkylated to noroxycodone during first-pass metabolism. Oxymorphone, is formed by the O-demethylation of oxycodone. The metabolism of oxycodone to oxymorphone is catalyzed by CYP2D6. Free and conjugated noroxycodone, free and conjugated oxycodone, and oxymorphone are excreted in human urine following a single oral dose of oxycodone. Approximately 8% to 14% of the dose is excreted as free oxycodone over 24 hours after administration. Following a single, oral dose of oxycodone, the mean ± SD elimination half-life is 3.51 ± 1.43 hours.
Abuse
The attraction of Oxycontin® as a preferred drug of abuse over other oxycodone containing products has several reasons. The large amounts of oxycodone per tablet versus Percodan® or Percocet® are one of the primary reasons, while a second factor is that Percodan® and Percocet® additionally contain 325 mg of aspirin or up to 650 mg of acetaminophen, respectively while Oxycontin® has neither. Thus, the oxycodone high will not be associated with any toxic side effects that may result from either excessive aspirin or acetaminophen. Oxycontin® tablets are to be taken whole to allow for the controlled release of oxycodone. Abusers will destroy the controlled release capabilities of Oxycontin® by either chewing the tablets prior to swallowing, crushing the tablets and snorting the powder or they may be crushed, dissolved in water and injected. This allows for a rapid and large absorption of oxycodone into the blood stream producing a powerful euphoric high. This rapid, bolus absorption is also thought to be responsible for an apparent increase in oxycodone related overdoses in the east. Several Oxycontin® street slang’s include “OC”, “OXY”, “Oxy-Coffins”, Hillbilly Heroin, Poor-Mans Heroin and Killers. Diversion of the prescription has also been a problem associated with Oxycontin®. It has been reported that while a single 160 mg tablet may retail for up to $14, it can fetch up to $1 per mg on the street. Thus, a 160 mg tablet, known as a “blue bomber”, may sell for up to $160 with its illicit sale. Interestingly, Oxycontin® is sometimes referred to as poorman’s heroin. We recently encountered a case in California in which a parolee who was being prescribed Oxycontin® was suspected of diverting his prescription to purchase heroin. Specific analysis of his urine determined no detectable level of oxycodone but the primary heroin metabolite, morphine, was present in his urine in excess of 2,000 ng/mL. Thus, offering scientific support to the diversion suspicion.


Phencyclidine Drug Information

Classification
Phencyclidine (l-phencyclohexylpiperidine, PCP) is prepared from l-piperidinocyclohexane-carbonitrile in a Grignard reaction, as first performed in 1956 for use as an intravenous anesthetic. Pharmacologically PCP is classified as a dissociative anesthetic. PCP is currently a popular drug of abuse and was once used as a veterinary tranquilizer. A structural analog, ketamine, is currently used as a veterinary tranquilizer. PCP is self-administered either by smoking (drug-laced tobacco, marijuana, or parsley), by nasal insufflation and intravenous injection, or by oral ingestion.
Metabolism
PCP is a lipophilic drug with a large volume of distribution. It undergoes extensive hepatic oxidative metabolism with about 10-15% of a dose excreted unchanged in urine, and about 65% excreted as hydroxylated metabolites and other polar metabolites. Renal excretion of PCP (pKa 8.5) is enhanced when urine is acidic, and it is reduced when urine is alkaline. Frequent or chronic PCP users may excrete PCP for 2-10+ days following last use. Urine concentrations may range from <0.1 mcg/mL to 340 mcg/mL.
Abuse
Phencyclidine’s pharmacological actions are complex, since it interacts with several neurotransmitter systems (i.e., GABAergic, dopaminergic, cholinergic, and adrenergic). As a result, PCP has stimulant, depressant, hallucinogenic, and analgesic properties. Adverse effects are unpredictable and include agitation, delusions of grandeur, anxiety, hostility, stupor, paranoia, and coma. Death has been known to result following the ingestion of 120 mg of PCP (toxic dose 10-20 mg).

 

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