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 an 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.