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Clandestine Drug Lab Cleanup a HAZWOPER Supplement

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Clandestine Drug Lab Cleanup a HAZWOPER Supplement UC Davis Extension continuing education Since 1891 Clandestine Drug Lab Cleanup A HAZWOPER Supplement April 25, 2006 Instructors: Mark Cameron, CIH Elise Rothschild Mark Trask Western Region Universities Consortium (WRUC) - NIEHS Grant UC Davis Extension Occupational & Environmental Management 1333 Research Park Drive Davis, CA 95616 (530) 757-8607 CLANDESTINE DRUG LAB CLEANUP - A HAZWOPER SUPPLEMENT Learn the new regulations (AB 1078) related to the cleanup of drug lab contaminated properties. Identify the likely chemicals used at drug labs and discuss the possible risks to personnel associated with these chemicals. Explore the analytical methods used for detecting residue and determine applicable cleanup levels. You will also discuss the appropriate cleanup methods used at contaminated properties. This course is designed for HAZWOPER (40 hour) trained personnel who develop cleanup plans, perform actual cleanup and are planning to do inspections of drug lab contaminated facilities. It is also applicable for regulatory personnel who oversee cleanup of drug lab contaminated facilities. MARK CAMERON, SENIOR INDUSTRIAL HYGIENIST ELISE ROTHSCHILD, SUPERVISING ENVIRONMENTAL SPECIALIST MARK TRASK, ENVIRONMENTAL SPECIALIST UC DAVIS EXTENSION Janis Heple, program director Nathan Sands, program representative Whitney Hughes, program assistant Occupational and Environmental Management 1333 Research Park Drive, Room 251 Davis, CA 95616 (530) 757-8607 Western Region Universities Consortium (WRUC) is supported by grant number ES006173 from the National Institute of Environmental Health and Science (NIEHS), NIH. Its contents are solely the responsibility of the authors, and do not necessarily represent the official views of the NIEHS, NIH. Introduction Chemistry Sampling & Cleanup Regulations Sacramento County Methamphetamine: “What’s the big deal?” Amphetamine/Methamphetamine Methylated version of amphetamine Name d-N-methylamphetamine d-deoxyephedrine 1-phenyl-2- methylaminopropane CAS: N,a-dimethyl benzenethanamine Meth 2-15x more potent than amphetamine Street Names for Methamphetamine Crystal Tina Meth Crissy Crystal Meth Glass Speed Ice Tweak/Tweek Uppers Product Yaba Crank Shabu shabu Methamphetamine History Amphetamine synthesized 1887 by German chemist, L. Edeleano Recent research has shown that methamphetamine was first produced by Dr. Nagayoshi Nagiai of Tokyo Imperial University in 1888 by reducing ephedrine with HI and Red Phosphorus Methamphetamine synthesized from methylamine and phenyl-2- propoanone 1919 by Japanese researcher, A. Ogata 1927 (USA): Dextro-levo-amphetamine synthesized as substitute for ma huang (chinese name for the herb ephedra) 1930: Amphetamine discovered to increase blood pressure. Marketed in 1932 as “benzedrine” in an over-the-counter inhaler to treat nasal congestion 1935: Amphetamine’s stimulant effect first recognized and used to treat narcolepsy (compulsion to sleep) 1937: Amphetamine first approved by AMA for sale in tablet form. Sold by prescription for treatment of narcolepsy, ADHD and 37 other conditions. Meth History Cont. 1938: First published report of amphetamine addition and psychosis 1940: “Methedrine” commercial trade name for methamphetamine Both amphetamine and methamphetamine used as performance enhancer by Japanese, German and Americans in WWII. Led to addiction problems in Japanese after the war. 1950-53: amphetamine distributed to US troops in Korean war 1951: U.S. Congress passes a law requiring prescriptions for all oral and injectable amphetamines used commonly to treat obesity, narcolepsy and depression. 1954: Height of Japanese addiction: 2 million users in 88.5 million population 1959: first report of IV injection of contents of benzedrine inhaler. OTC Benzedrine Inhalers within drawn from market. OTC Methedrine inhalers offered. Meth History, cont. 1962: early reports of illicit domestic production by biker gangs 1965: OTC Methedrine inhalers withdrawn from market. 31 million prescriptions written: mostly to women. Amphetamine and methamphetamine become Schedule II drugs in 1971 Motorcycle gangs synthesized drug using phenyl-2-propanone until late 1980’s. P2P became restricted substance, so chemistry shifted to making P2P from phenyl acetic acid or other ways 1987, DEA busts first HI/Red Phosphorus lab in the country in California. This method has a higher yield and more potent methamphetamine. Mexican nationals take over the market from biker gangs with this method. Current methods (Iodine/Red P or Lithium/Ammonia) using pseudoephedrine became popular as other chemicals became illegal 1990 1994 1997 CA 227 419 946 DEA 520 306 1238 (nationwide) Source: http://www.usdoj.gov/dea/concern/map_lab_seizures.html accessed October 18, 2005 Source: http://www.usdoj.gov/dea/concern/map_lab_seizures.html accessed October 18, 2005 Modes of Administration • Harms associated with each: • Slamming (Injection) • Snorting • Swallowing (crystal-laced drinks; homemade pills: wrapped in tissue paper and ‘popped’ with water) • Smoking • ‘Booty bumping’ (rectal administration) Physiological Effects Increases heart rate (tachycardia) and blood pressure Increases shallow breathing (tachypnea) Raises internal body temperature (hyperthermia) Causes sweating, often profusely Decreases appetite Enlarges pupils Causes dry mouth and bad breath (halitosis) Causes pounding headaches Increases motor activity (can’t keep still) “Tweaking” • Tweaking lasts 8-12 hours, depending on dose and purity; may last several days from repeated dosing • Major symptoms may include: Teeth grinding Dilated pupils and staring/trance state Bad breath Source: Severe paranoia and hallucinations http://www.usdoj.gov/dea/concern/meth_effects.html Rapid body movement; jerking ‘Meth bugs’ (parethesias, caused by an imbalance in sensory neurons) and may lead to picking one’s skin Increased motor activity/performing repetitive acts “Crashing” Withdrawal effect: Extreme exhaustion Sleep disorder Suicidal ideation Increased generalized anxiety and/or other anxiety disorders (agoraphobia) Can lead to continued use (“crash avoidance”) Using ‘downs’(sleeping pills) and/or opiates to alleviate withdrawal Consequences Additional problems with meth: • Impaired cognitive functioning and short-term memory loss, notably abstract thinking and judgment • A person’s ability to perceive risks and consequences while tweaking is diminished (person may engage in high risk sexual behavior, linked to HIV infection and syphilis) • Mixing drugs when crashing: pain killers; sleeping pills (may cause Substance Induced Amnesia if the person doesn’t fall asleep) Consequences of Long-term Use Addiction Sexual compulsivity Anorexia; distorted body image, or phobia about weight gain Lethality results from kidney failure, dehydration, seizures (can occur after single use); cardiovascular events such as heart attack or stroke “Meth mouth”: Lack of saliva production causes bacteria to grow, causing tooth decay “Meth-induced osteoporosis”: structural deterioration of bone tissue, which leads to bone fragility and loss of teeth Meth Mouth When meth is ingested, it causes the user's blood vessels to shrink, limiting the steady blood supply that the mouth needs in order to stay healthy. With repeated shrinking, these vessels die and the oral tissues decay. Similarly, meth use leads to "dry mouth" (xerostomia), and without enough saliva to neutralize the mouth's harsh acids, those acids eat away at the tooth and gums, causing weak spots that are susceptible to cavities. The cavities are then exacerbated by behavior common in users on a meth high: a strong desire for sugary foods and drinks, compulsive tooth grinding, and the general neglect of regular brushing and flossing. In case you have doubt about the hazards of meth use… Source: http://www.usdoj.gov/dea/con cern/meth_effects.html Accessed October 18, 2005 Crystal Releases Neurotransmitters Meth crosses the blood brain barrier and causes release of neurotransmitters: Dopamine: provides feelings of reward and pleasure Serotonin: provides sense of emotional stability Norepinephrine: stimulates arousal, drive Dopamine Normally, dopamine is released, excites receptor cell, is released and pumped back into adjacent nerve ending. Drug effects on dopamine Meth and heroin block the return pump, allowing dopamine to sit on receptor cell and continue firing. Heroin lasts an hour Meth lasts up to 12 hrs Damage to Dopamine Transport System Although speed cause initial flood of dopamine, in the long term, dopamine transport system is damaged. This results in dopamine deficits Damage, although probably not permanent, is long-lasting and persistent Damage to Dopamine Transport System Sensitization Persistence of psychotic symptoms Resumption of psychoses with each use Psychosis can be triggered by other substances Cognitive impairment Cognitive Impairment Memory Verbal Learning Judgment Reasoning Planning, impulsivity Meth Mimics Adrenaline Adrenaline prepares the body for emergencies -- to either fight or run. This is known as the “fight or flight” response. The body experiences crystal meth as an emergency, prompting appropriate physiological responses. “Fight or Flight” Response The body prepares for an emergency, possible injury: Pupils dilate to admit more light. Cutaneous blood vessels constrict. Bronchial muscles relax increased respiration. Heart rate and body temp increase. Ureters, intestines and urinary muscles constrict.
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