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.
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
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:
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.
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
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
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
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
(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.
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
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
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.
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
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.
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