💾 Archived View for spam.works › mirrors › textfiles › drugs › crackinf.drg captured on 2023-11-14 at 09:26:36.
⬅️ Previous capture (2023-06-14)
-=-=-=-=-=-=-
I want first to express my personal opinion that freebasing is a very bad thing to do for your body and mind. I have seen a few people hooked on it, and it is not a nice thing to see. I strongly disrecommend doing it. It is easy to overdose and die of cardiac arrest. Some people doing freebase will exhibit the same kind of behavior as those rats whose pleasure centers are electrically stimulated: they will do it until either the supply runs out, or until they die. The recipes are readily available. In fact, a few years ago, police officers would go to great lengths explaining how crack was made when given interviews (at least in Montreal)! There was also an article in Time a few years ago explaining the procedures. I have never tried any of those procedures or smoked freebase, and will never do it. The information I post comes from a used booklet I bought a long time ago ("Cocaine Handbook", by Davis). Crack is actually a impure form of freebase. Procedures for both substances are based on the fact that while cocaine hydrochloride is very soluble in water, base cocaine is almost insoluble. freebase: mix about 1 g of coke in 10 ml of water in a small vial. Slowly add drops of ammonia to the solution. A white milky precipitate will form. Stop adding ammonia when additional drops no longer result in precipitation. Add 5 ml of ethyl ether, close vial, and shake. The precipitate (freebase) will dissolve in the ether. Siphon off the ether with a pipette (ether and water don't mix), and slowly drip it on a plate. As the ether evaporates, white crystals will form. This is the evil freebase. Crush the crystals and put under a heat lamp for at least 24 hrs to let the solvent evaporate. ETHYL ETHER IS EXTREMELY FLAMMABLE. IN THE PRESENCE OF AIR IT CAN FORM PEROXIDES WHICH WILL SPONTANEOUSLY EXPLODE! ALSO, ETHER CAN "CRAWL" FROM AN OPEN BOTTLE AND TRIGGER AN EXPLOSION MANY FEET AWAY. This is how Richard Pryor almost died. A lot of untrained people killed themselves doing that procedure, and this is why crack is now more popular. crack: mix 2 parts ok coke HCL for 1 part baking soda in 20 ml of water. Heat solution gently until white precipitates form, and stop heating when precipitation stops. Filter and keep precipitate. wash precipitate once with water (this procedure usually omitted in street product). Dry 24 hours under heat lamp. Voila. The product is much less pure (there is lots of baking soda left) but the procedure is safer. ============================================================================= Date: Fri, 13 Nov 92 09:21:26 -0500 From: (anonymous) Subject: Crack / Rock Cocaine Let me first say that this is also freebase. Its not as pure as the other recipe and has a *much smaller return* than using ammonia (no one really does the ether part, just ammonia and heat it). [previous crack "recipe" deleted -cak] After gentle heating, it will float to the top, any excess soda will precipitate to the bottom. Given that, you'd never filter it, and the 24 hour heat lamp thing is unrealistic, too. Note that what you're trying to do is start and sustain a chemical reaction (bonding the hcl with the base-soda) so as long as the reaction is happening you don't have to continue heating. ============================================================================= In article <1993Mar4.215558.9171@midway.uchicago.edu> bagg@midway.uchicago.edu writes: >I suspect that freebase cocaine is probably not too bad for your lungs. After writing this, I bopped onto Medline and yanked the following abstracts for the sake of thoroughness: 1. Khalsa ME; Tashkin DP; Perrochet B. Smoked cocaine: patterns of use and pulmonary consequences. Journal of Psychoactive Drugs, 1992 Jul-Sep, 24(3):265-72. (UI: 93058148) Abstract: This article offers a perspective on the use of volatilized alkaloidal cocaine in its freebase and crack forms and on the pulmonary consequences of such use. The inhalational route of administration of freebase and crack cocaine exposes the lung to their combustion products, raising concern about possible adverse pulmonary effects. A brief historical review of cocaine and its methods of use precedes the presentation of data concerning current modes and patterns of use and some pulmonary complications of crack and freebase use. Results from a systematic study of a large sample of cocaine users document a high frequency of occurrence of acute respiratory symptoms in temporal association with cocaine smoking. No relationship was detected between the prevalence of acute pulmonary symptoms and identifiable aspects of techniques of cocaine administration. These results suggest that the respiratory consequences of alkaloidal cocaine are most likely attributable to the inhaled cocaine itself, rather than to variable characteristics of usage. 2. Oh PI; Balter MS. Cocaine induced eosinophilic lung disease. Thorax, 1992 Jun, 47(6):478-9. (UI: 92358464) Abstract: A patient developed fever, bronchoconstriction, hypoxaemia, pulmonary infiltrates, and serum and bronchoalveolar lavage fluid eosinophilia on two occasions after inhaling crack cocaine. Transbronchial biopsy specimens showed normal lung parenchyma but a dense eosinophilic infiltrate within the bronchial wall. Both episodes resolved promptly after treatment with corticosteroids. Eosinophilic lung disease may be a steroid responsive complication of crack cocaine abuse. 3. Perper JA; Van Thiel DH. Respiratory complications of cocaine abuse. Recent Developments in Alcoholism, 1992, 10:363-77. (UI: 92270885) Pub type: Journal Article; Review; Review, Tutorial. Abstract: Upper respiratory and pulmonary complications of cocaine addiction have been increasingly reported in recent years, with most of the patients being intravenous addicts, users of freebase, or smokers of "crack." The toxicity of cocaine is complex and is exerted via multiple central and peripheral pathways. Recurrent snorting of cocaine may result in ischemia, necrosis, and infections of the nasal mucosa, sinuses, and adjacent structures. Pulmonary complications of cocaine toxicity include pulmonary edema, pulmonary hemorrhages, pulmonary barotrauma, foreign body granulomas, cocaine related pulmonary infection, obliterative bronchiolitis, asthma, and persistent gas-exchange abnormalities. Respiratory manifestations are nonspecific and include shortness of breath, cough, wheezing, hemoptysis, and chest pains. Severe respiratory difficulties have been reported in neonates of abusing mothers. In the absence of a cocaine-abuse history, it may be difficult to recognize the etiological role of cocaine, especially in the absence of needle tracks pointing to previous intravenous drug abuse and/or negative toxicology. 4. Ferre C; Sirvent JM; Vidaller A. [Hemoptysis and pulmonary infiltrates following crack poisoning (letter)]. Medicina Clinica, 1992 Mar 7, 98(9):358. Language: Spanish. (UI: 92261122) Pub type: Letter. 5. Tashkin DP; Khalsa ME; Gorelick D; Chang P; Simmons MS; Coulson AH; Gong H Jr. Pulmonary status of habitual cocaine smokers. American Review of Respiratory Disease, 1992 Jan, 145(1):92-100. (UI: 92117426) Abstract: We determined the prevalence of respiratory symptoms and lung dysfunction in a large sample of habitual smokers of freebase cocaine ("crack") alone and in combination with tobacco and/or marijuana. In addition, we compared these findings with those in an age- and race-matched sample of nonusers of crack who did or did not smoke tobacco and/or marijuana. A detailed respiratory and drug use questionnaire and a battery of lung function tests were administered to (1) a convenience sample of 202 habitual smokers of cocaine (cases) who denied intravenous drug abuse and (2) a reference sample of 99 nonusers of cocaine (control subjects). The cocaine smokers (85% black) included the following: 68 never-smokers of marijuana, of whom 43 currently smoked tobacco and 25 did not, and 134 ever-smokers of marijuana (42 current and 92 former), of whom 92 currently smoked tobacco and 42 did not. The control subjects (96% black) included the following: 69 never-smokers of marijuana, of whom 26 currently smoked tobacco and 43 did not, and 30 ever-smokers of marijuana (18 current and 12 former), of whom 21 currently smoked tobacco and 9 did not. Cases smoked an average of 6.5 g cocaine per week for a mean of 53 months. The median time of the most recent use of crack prior to study was 19 days (range less than 1 to 180 days). After controlling for the use of other smoked substances, frequent crack use was associated with: (1) a high prevalence of at least occasional occurrences of acute cardiorespiratory symptoms within 1 to 12 h after smoking cocaine (cough productive of black sputum [43.7%], hemoptysis [5.7%], chest pain [38.5%], usually worse with deep breathing, and cardiac palpitations [52.6%]) and (2) a mild but significant impairment in the diffusing capacity of the lung.(ABSTRACT TRUNCATED AT 250 WORDS) 6. O'Donnell AE; Mappin FG; Sebo TJ; Tazelaar H. Interstitial pneumonitis associated with "crack" cocaine abuse. Chest, 1991 Oct, 100(4):1155-7. (UI: 92006753) Abstract: A 33-year-old woman developed acute bilateral pulmonary infiltrates after the intense use of rock cocaine (crack). She subsequently had progressive deterioration of pulmonary function to the point of being ventilator-dependent. Open lung biopsy showed a chronic interstitial pneumonia with extensive accumulation of free silica within histiocytes associated with mild pulmonary fibrosis. This pattern of interstitial pneumonia has not been previously reported in crack users. 7. Susskind H; Weber DA; Volkow ND; Hitzemann R. Increased lung permeability following long-term use of free-base cocaine (crack). Chest, 1991 Oct, 100(4):903-9. (UI: 92006781) Abstract: The clearance of inhaled 99mTc DTPA aerosol from the lungs is used as an index of lung epithelial permeability. Using the radioaerosol method, we investigated the effects of long-term "crack" (free-base cocaine) inhalation on lung permeability in 23 subjects. Eighteen control subjects (12 nonsmokers and 6 cigarette smokers) with no history of drug use were also studied. Subjects inhaled approximately 150 muCi (approximately 5.6 MBq) of 99mTc DTPA aerosol and quantitative gamma camera images of the lungs were acquired at 1-min increments for 25 minutes. Regions of interest (ROIs) were selected to include the following: (1) both lungs; (2) each individual lung; and (3) the upper, middle, and lower thirds of each lung. 99mTc DTPA lung clearance was determined from the slopes of the respective time-activity plots for the different RIOs. Radioaerosol clearance half-times (T1/2) for the seven nonsmoking crack users (61.5 +/- 18.3 minutes) were longer than for the seven cigarette-smoking crack users (27.9 +/- 16.9 minutes) and nine cigarette-smoking crack plus marijuana users (33.5 +/- 21.6 minutes). T1/2 for the nonsmoking crack users was significantly shorter (p less than 0.001) than for the nonsmoking control group (123.8 +/- 28.7 minutes). T1/2 for the cigarette-smoking drug users was similar to that of the cigarette-smoking control group (33.1 +/- 17.8 minutes), suggesting a similar mechanism of damage from the smoke of crack and tobacco. From these groups, one nonsmoker and 11 cigarette smokers displayed biexponential 99mTc DTPA clearances, indicative of greater lung injury than found in the usual cases of monoexponential clearance. The upper lungs of all crack users groups cleared faster than the lower lungs. The faster and biexponential clearance properties of inhaled 99mTc DTPA aerosol were the principal functional abnormalities found in all the drug users. In contrast, 19 of 23 crack users had normal spirometry and gas exchange. These results indicate that 99mTc DTPA may provide a sensitive and useful assay to evaluate the physiologic effects of cocaine inhalation in the lung. 8. McCarroll KA; Roszler MH. Lung disorders due to drug abuse. Journal of Thoracic Imaging, 1991 Jan, 6(1):30-5. (UI: 91116637) Pub type: Journal Article; Review; Review, Academic. Abstract: Drug-related diseases of the lungs have been noted with increasing frequency in urban patients. These entities are also being seen in smaller urban and suburban settings, however. The spectrum of pathology is also changing coincident with the marked increase in crack cocaine use. The incidence of abnormal chest radiographs in cocaine users admitted with pulmonary complaints has ranged from 12% to 55%. Findings have included focal air space disease, atelectasis, pneumothorax, pneumomediastinum, and pulmonary edema. Pulmonary complications related to injections of illicit drugs have included pulmonary infection, pulmonary edema, particulate embolism, and talcosis. The "pocket shot" places the patient at risk for a unique set of complications. Radiologists should be aware of this wide spectrum of pulmonary disease that may be related to this increasingly frequent social problem. 9. Smart RG. Crack cocaine use: a review of prevalence and adverse effects. American Journal of Drug and Alcohol Abuse, 1991, 17(1):13-26. (UI: 91247446) Pub type: Journal Article; Review; Review, Tutorial. Abstract: Crack is a potent form of cocaine which results in rapid and striking stimulant effects when smoked. This paper reviews epidemiological research on the extent of use as well as reports of adverse effects. Crack is used by a small minority of adult and student populations but by a large proportion of cocaine users and heavy drug-using groups. Use does not appear to be increasing in general populations, but there are no trend studies for high-risk groups. Crack users tend to be young, heavy polydrug users, many of whom have serious drug abuse problems. The adverse reactions to crack are similar to those of cocaine and include effects on offspring, neurological and psychiatric problems, as well as pulmonary and cardiac abnormalities. However, two adverse reactions unique to crack have been reported. One relates to lung infiltrates and bronchospasm. The other involves neurological symptoms among children living in crack smoke-filled rooms. There is a need for improved treatment and preventive programs for crack use. 10. Forrester JM; Steele AW; Waldron JA; Parsons PE. Crack lung: an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. American Review of Respiratory Disease, 1990 Aug, 142(2):462-7. (UI: 90343162) Abstract: In this report, we review the hospital course of four patients who presented with an acute pulmonary syndrome after inhaling freebase cocaine and compare them with previously described case reports. Two patients had prolonged inflammatory pulmonary injury associated with fever, hypoxemia, hemoptysis, respiratory failure, and diffuse alveolar infiltrates. Lung tissue specimens from both patients revealed diffuse alveolar damage, alveolar hemorrhage, and interstitial and intraalveolar inflammatory cell infiltration notable for the prominence of eosinophils. Immunofluorescent staining performed on one of the biopsy specimens showed a striking deposition of IgE in both lymphocytes and alveolar macrophages. Both patients were treated with systemic corticosteroids and rapidly improved. In contrast, two patients presented acutely with diffuse pulmonary alveolar infiltrates associated with dyspnea and hypoxemia, but without fever, and within 36 h of discontinuing cocaine their pulmonary infiltrates and symptoms had spontaneously resolved. Our report further supports the finding that an acute pulmonary syndrome can occur after inhalation of freebase cocaine. Furthermore, the lung injury may respond to systemic corticosteroid therapy when it is associated with a prominent inflammatory cell infiltration. 11. Hannan DJ; Adler AG. Crack abuse. Do you known enough about it? Postgraduate Medicine, 1990 Jul, 88(1):141-3, 146-7. (UI: 90310821) Pub type: Journal Article; Review; Review, Tutorial. Abstract: Crack use has increased dramatically because the drug is cheap, highly addictive, and easy to use. As a result, an increased frequency of cocaine-related medical problems has been noted. The effects of crack abuse on fetal outcome and neurobehavioral development are becoming more apparent. In addition, the role of crack use in furthering transmission of sexually transmitted diseases has been documented, and the implications for AIDS transmission have been speculated on. Crack use enhances social disorganization, particularly in poor urban areas, where increased child abuse, neglect, and prostitution are common. Ever present are the financial incentives to increase the number of crack users. Cocaine was once considered a drug for the elite, rich, and famous. Crack clearly has changed that notion. 12. Tashkin DP. Pulmonary complications of smoked substance abuse. Western Journal of Medicine, 1990 May, 152(5):525-30. (UI: 90273700) Pub type: Journal Article; Review; Review, Tutorial. Abstract: After tobacco, marijuana is the most widely smoked substance in our society. Studies conducted within the past 15 years in animals, isolated tissues, and humans indicate that marijuana smoke can injure the lungs. Habitual smoking of marijuana has been shown to be associated with chronic respiratory tract symptoms, an increased frequency of acute bronchitic episodes, extensive tracheobronchial epithelial disease, and abnormalities in the structure and function of alveolar macrophages, key cells in the lungs' immune defense system. In addition, the available evidence strongly suggests that regularly smoking marijuana may predispose to the development of cancer of the respiratory tract. "Crack" smoking has become increasingly prevalent in our society, especially among habitual smokers of marijuana. New evidence is emerging implicating smoked cocaine as a cause of acute respiratory tract symptoms, lung dysfunction, and, in some cases, serious, life-threatening acute lung injury. A strong physician message to users of marijuana, cocaine, or both concerning the harmful effects of these smoked substances on the lungs and other organs may persuade some of them, especially those with drug-related respiratory complications, to quit smoking. 13. Brody SL; Slovis CM; Wrenn KD. Cocaine-related medical problems: consecutive series of 233 patients [see comments]. American Journal of Medicine, 1990 Apr, 88(4):325-31. (UI: 90224989) Abstract: PURPOSE: Little information describing common cocaine-related medical problems is available. This study examined the nature, frequency, treatment, incidence of complications, and emergency department deaths of patients seeking medical care for acute and chronic cocaine-associated medical problems. PATIENTS AND METHODS: A consecutive series of 233 hospital visits by 216 cocaine-using patients over a 6-month period during 1986 and 1987 was studied. Medical records were retrospectively reviewed to determine patient characteristics, nature of complications, treatment, and outcome. RESULTS: Patients most commonly used cocaine intravenously (49%), but freebase or crack use was also common (23.3%). Concomitant abuse of other intoxicants, especially alcohol, was frequently seen (48.5%). The vast majority of complaints were cardiopulmonary (56.2%), neurologic (39.1%), and psychiatric (35.8%); multiple symptoms were often present (57.5%). The most common complaint was chest pain though rarely was it believed to represent ischemia. Altered mental status was common (27.4%) and ranged from psychosis to coma. Short-term pharmacologic intervention was necessary in only 24% of patients, and only 9.9% of patients were admitted. Acute mortality was less than 1%. CONCLUSION: Most medical complications of cocaine are short-lived and appear to be related to cocaine's hyperadrenergic effects. Patients usually do not require short-term therapy or hospital admission. Acute morbidity and mortality rates from cocaine use in patients presenting to the hospital are very low, suggesting that a major focus in the treatment of cocaine-related emergencies should be referral for drug abuse detoxification and treatment. 14. Wallach SJ. Medical complications of the use of cocaine. Hawaii Medical Journal, 1989 Nov, 48(11):461-2. (UI: 90077816) Abstract: There are many serious medical problems that are associated with the use of cocaine and "crack" cocaine. 15. Eurman DW; Potash HI; Eyler WR; Paganussi PJ; Beute GH. Chest pain and dyspnea related to "crack" cocaine smoking: value of chest radiography. Radiology, 1989 Aug, 172(2):459-62. (UI: 89316319) Abstract: The chest radiographs of 71 patients who had chest pain or shortness of breath following the smoking of highly potent "crack" cocaine were retrospectively evaluated. Nine patients had abnormal findings on radiographs as follows: atelectasis or localized parenchymal opacification in four, pneumomediastinum in two, pneumothorax in one, hemopneumothorax in one, and pulmonary edema in one. Radiographic detection of these abnormalities was important in the clinical management of these patients. This spectrum of findings is presented with a discussion of the pathophysiologic mechanisms responsible. 16. Cherukuri R; Minkoff H; Feldman J; Parekh A; Glass L. A cohort study of alkaloidal cocaine ("crack") in pregnancy. Obstetrics and Gynecology, 1988 Aug, 72(2):147-51. (UI: 88276400) Abstract: The recent dramatic increase in the use of alkaloidal cocaine ("crack") has led to concern about possible deleterious fetal effects associated with its use during pregnancy. Crack, which is not destroyed by heating, can be smoked, and delivers a large quantity of cocaine to the vascular bed of the lung, producing an effect similar to that from intravenous injection. To describe the association of crack use with pregnancy outcome, we conducted a retrospective matched cohort study of 55 women who admitted to the use of crack during pregnancy and 55 non-drug-using women who delivered during the same period. The groups were matched for age, parity, socioeconomic status, alcohol use, and presence or absence of prenatal care. A significantly larger number of women using crack delivered at 37 weeks or earlier (50.9 versus 16.4%; P = .001). Crack-exposed infants were 3.6 times more likely to have intrauterine growth retardation (P less than .006) and 2.8 times more likely to have a head circumference less than the tenth percentile for gestational age (P less than .007). Premature rupture of the membranes was 1.8 times more common in the crack group (P less than .03). Sixty percent of crack-using mothers received no prenatal care. Abnormal neurobehavioral symptoms were present in a minority of infants and were usually mild. 17. Snyder CA; Wood RW; Graefe JF; Bowers A; Magar K. "Crack smoke" is a respirable aerosol of cocaine base [published erratum appears in Pharmacol Biochem Behav 1988 Apr;29(4):835]. Pharmacology, Biochemistry and Behavior, 1988 Jan, 29(1):93-5. (UI: 88177036) Abstract: The smoking of cocaine base [corrected] ("crack") has emerged as a significant substance abuse problem. A detailed characterization of cocaine smoke is a prerequisite for studies of its pharmacokinetics, abuse potential and toxicity. Model pipes were used to generate cocaine smoke analogous to that inhaled by human "crack" abusers. Using procedures to minimize pyrolysis, cocaine base smoke was determined to be 93.5% cocaine particles with the remainder being cocaine vapor. The average particle size generated from all model pipes was 2.3 mu which is small enough to ensure deposition into the alveolar region of the human lung. Although this particle size is eminently respirable [corrected] by primates, a much smaller fraction will reach the alveolar region of rodents. Special generating procedures would therefore be required to expose rodents to meaningful doses of airborne cocaine that mimic the rapid absorption achieved by "crack" smokers.