"Cocaine-Related" Deaths

This article by Linda Wong and myself appeared in the Journal of Drug Issues in 1991. It shows how the media of the day misled the public about the basic facts concerning cocaine use.


A 1989 newspaper story describing twenty-nine cocaine-related deaths in British Columbia is used to illustrate the kinds of unwarranted inferences that are propagated by the news media during the current War on Drugs. The newspaper story conveys the impression that most of the deaths involved well-integrated, moderate drug users, that all twenty-nine deaths were caused by cocaine, and that these deaths provided evidence of an epidemic of dangerous cocaine use sweeping the province. However, the coroner's files on which the story was based, and related research, provide strong evidence that all three frightening inferences are wrong. A more careful analysis of these deaths as a consequence of chronic deterioration in a fringe population can contribute to the development of realistic drug policy.

The Vancouver Province newspaper of 14 May 1989 announced a feature story with the front page headlines "KILLER COKE" and "Drug death 'epidemic' in B.C." The story described twenty-nine cocaine-related deaths that had occurred in 1987 and 1988 in British Columbia (Middleton 1989). We believe that this story is typical of hundreds of dramatic media portrayals that draw invalid inferences from events involving drugs. Further, we believe that such inferences serve to perpetuate the current War on Drugs long after its futility has been amply documented. This article critically examines three key inferences made in this newspaper story and offers a new analysis of the twenty-nine deaths.

The first inference promulgated by the newspaper story is that most of the twenty-nine decedents were well-integrated people who were only moderate cocaine users. For example, the first of a set of capsule case studies begins as follows:

Tom...was 35 when he shot himself up with cocaine and died. He was living with a woman who loved him dearly. He had a comfortable apartment on the west side. He had everything to live for. And he died for a spoonful of white powder. "His story is typical," said Vancouver coroner..."Sad, but true" (Middleton 1989:4).

We systematically polled readers of the story and confirmed that it led them to believe that most of the decedents were well-integrated, physically healthy people who were only moderate users of drugs. This polling seemed necessary since the story does not state these claims explicitly and because it briefly mentions indications that some of the decedents may have been addicted.

Second, the story identifies cocaine as the cause of death in all twenty-nine cases. It unequivocally states: "Cocaine killed at least 11 people in B.C. in 1987 and at least 18 in 1988" (Middleton 1989:4).

Finally, the story uses the first two inferences to support a third inference, that "a cocaine epidemic is sweeping B.C." The article states:

The drug path of death cuts across social and economic lines from bikers to businessman, laborers to lawyers.

"It's an epidemic," Vancouver coroner...told The Sunday Province in an exclusive interview (Middleton 1989:4).

Contrary to the newspaper story, the coroners' files on the twenty-nine deaths suggest that few, if any, of the decedents could be considered well-integrated people with "everything to live for." Most were long-time heroin and cocaine addicts living on the fringe of society. Also contrary to the story, there are substantial reasons to doubt that cocaine was the primary cause of all of these people's deaths. Most of their deaths may be better understood as the outcome of a general deterioration resulting from a prolonged unhealthy, socially deviant lifestyle in which cocaine use was but one element. Finally, the inference that these deaths reveal the existence of an epidemic of dangerous cocaine use among the general population in British Columbia is contradicted by current data on the extent of cocaine use in the province. Each of these issues is examined below.

The Decedents

We searched the coroner's files that the newspaper reporter had used for information on the twenty-nine decedents. Some of the decedents' characteristics could be determined with confidence, such as age, history of intravenous drug use, occupation, and criminal record. Where inferences were required, we attempted to make them from the viewpoint of disinterested observers and submitted our findings to the scrutiny of the author of the original newspaper article and to an official in the coroner's office for critique.

Few of the twenty-nine decedents appeared to have been recreational users or to have led normal lives. In fact, twenty-six were known to have been heavy or addictive users of illicit drugs and/or alcohol (see Table 1). The most frequently mentioned drugs were heroin, methadone, cocaine, alcohol, cannabis, prescription drugs and tobacco. Twenty-three of the decedents were known to have been intravenous users. At least sixteen decedents were heavy users of more than one drug. Ten were known to be alcoholic. On autopsy, thirteen showed lung damage that is typical of chronic intravenous drug users ("junkie lung" ). We concluded from the coroner's reports that at most three could have been only recreational users of illicit drugs.

Apart from drug use, the files suggested that at least twenty-one of the twenty-nine decedents had socially deviant lifestyles (See Table 1). Thirteen of the decedents had criminal records, some of them lengthy. Nine were currently unemployed or were earning their living as professional prostitutes, drug dealers, or thieves. At least twelve were suffering from severe personal problems, such as chronic depression, family and marital problems, suspension from their profession, gambling addiction, and the aftermath of a traumatic childhood. We found only one file that indicated that the decedent led a relatively ordinary life and seven others containing too little background information to justify any conclusion about lifestyle.

In addition to their histories of drug addiction and their deviant lifestyles, twenty-six of the decedents showed signs of chronic physical pathology (See Table 1). Their illnesses will be discussed in more detail below.

Causes of "Cocaine-related" Deaths

There is no doubt that cocaine can kill. However, we do not believe that there is sufficient evidence to attribute all or most of these twenty-nine deaths to it. It seems more probable to us that the larger number of these deaths were the culmination of a long period of deterioration resulting from a socially deviant lifestyle and chronic illness and that cocaine use was only one of several contributing factors. This section first discusses problems involved in attributing deaths to cocaine in general and them examines the twenty-nine cases that are at issue more specifically.


Cocaine overdose is well known in medicine and is readily recognized by dramatic signs and symptoms. Victims generally become excited and confused shortly after a large dose of cocaine, and are subsequently described as undergoing seizures, convulsions, depression, coma and, in severe cases, death from respiratory depression, or occasionally heart failure. Overdose death usually occurs within two hours following a dose of cocaine, often much sooner. This syndrome has been well documented in human beings and experimental animals since the nineteenth century (Finkle and McCloskey 1978; Smart and Anglin 1987). Such deaths will be designated "classical overdose" in this report to distinguish them from other ways in which cocaine may cause death.

Other Ways That Cocaine May Cause Death

Some medical researchers believe that relatively small amounts of cocaine can cause sudden death due to cardiac arrhythmia, particularly in people with pre-existing heart conditions, and that chronic cocaine use leads to an accumulation of heart damage that may eventually produce a fatal heart attack (Gerber and Flaherty 1987; Mittleman and Wetli 1987; Sternberg et al. 1989; Wetli and Fishbain 1985). However, there is no conclusive evidence in the medical literature that deaths of these types actually occur, nor is there a clear description of signs that would confirm the occurrence of these kinds of fatality.

Instead, medical research on this topic appears to be at the stage of attempting to prove the hypothesis that cocaine can cause heart attacks and identifying mechanisms whereby this might occur. In a thorough review of the medical risks associated with cocaine, Bates (1988:441) stated "it is not possible to unequivocally state that cocaine abuse causes myocardial infarction." Sternberg and colleagues (1989:522) point out that "There is accumulating evidence of an association between cocaine use and myocardial infarction, although a direct causal relation remains unproved." These authors also point out that the interpretation of pathologic research on this topic "is complicated by the significant incidence of polysubstance abuse in cocaine users...and by the frequent presence of adulterants in illicit cocaine preparations" (Sternberg et al. 1989:524). Similar reservations about the hypothesis that cocaine causes heart attacks have been made in the medical literature by Haines and Sexter (1987) and Devenyi and McDonough (1988).

There are also substantial uncertainties in medical reports attributing brain hemorrhage deaths to cocaine (Golbe and Merkin 1986; Kaye and Fainstat 1987; Lowenstein et al. 1987; Mody et al. 1988; Tuchman et al. 1987; Wojack and Flamm 1987). In many of these studies there is documentation of neurological defects pre-existing the trauma that was associated with cocaine use and indications that the users were cocaine addicts and/or habitual users of other strong drugs. There is a clear possibility that many, or all, of these deaths would have occurred without cocaine use or could have been caused by adulterants in the street "cocaine" which the decedents consumed.

Blood Levels of Cocaine

In the absence of signs of classical overdose death4 or of pathological evidence to confirm a cocaine-induced fatal trauma, coroners tend to rely heavily on blood levels of cocaine in ruling on the cause of death. However, blood levels are an uncertain indicator, and they generally must be supplemented by other kinds of information.

The generally recognized lethal range for cocaine is 1 to 20 milligrams/liter of blood (Winek 1985). In British Columbia, one milligram of cocaine plus benzoylecgonine (a breakdown product of cocaine) has been accepted as the minimum lethal level for intravenously administered cocaine. However, these values are questionable. Some recent studies have suggested that cocaine can cause death in people with blood levels significantly lower than these values, although numerous other studies suggest that people with less than 1 milligram/liter of cocaine in their bloodstreams rarely report any physical problems (Barnett et al. 1982; Feehan and Mancusi-Ungaro 1976; Jatlow 1988; Javaid et al. 1978; Kosten and Kleber 1988; Paly et al. 1982; Van Dyke et al. 1978).

In fact, there is convincing evidence that plasma levels greater than 1 milligram/liter are normally not lethal and only rarely cause physical symptoms. Fischman and Schuster (1980) experimentally injected varying doses up to 200 milligrams of cocaine per hour intravenously into volunteers who had a history of illicit intravenous cocaine use. Levels of cocaine in blood plasma up to 1.2 milligrams/liter were recorded in some subjects. Out of fifty subjects, some of whom received multiple injections, only one had an adverse reaction. The subject reported an "intense anxiety attack associated with muscle contraction" that lasted about forty-five minutes. Barnett, Hawks and Resnick (1981) injected 200 milligram doses of cocaine into two volunteer subjects and recorded blood levels above 1 milligram/liter for about an hour after the injection. Initial levels were 3.9 and 2.5 milligrams/liter for a three-hour period with a continuous infusion. Ambre, Ruo, Nelson, and Belknap (1988) maintained an experimental subject's blood level of cocaine over 1 milligram/liter for a three-hour period with a continuous infusion. By the end of the three-hour period, the subject's blood levels of cocaine had reached 3 milligrams/liter. No ill effects were reported in either of these studies. Finkle and McCloskey (1978) report NIDA data showing that experienced users had as much as 4 to 7 milligrams/liter of cocaine in their blood following large street doses, that is, four to seven times the minimum lethal level. Unfortunately, we have found no other studies on typical cocaine plasma levels in regular users of cocaine.

Part of the problem of establishing a precise lethal level of cocaine in blood arises because cocaine breaks down quickly in blood, even after death. For this reason it is difficult to determine the cocaine levels that were in the blood at the time death occurred (Basalt 1983; Bates 1988). Toxicologists sometimes use cocaine's inactive breakdown product, benzoylecgonine, to estimate the cocaine level in blood at the time of death. Liu, Budd and Griesemer (1982) showed that the concentration of cocaine and benzoylecgonine in a stored blood sample remained constant, as cocaine was gradually converted to benzoylecgonine. They concluded that the "best procedures are those that detect both cocaine and benzoylecgonine since the total concentration remains constant" (Liu et al. 1982:219).

However, this procedure introduces a major source of error because benzoylecgonine remains in the living body for a longer period than cocaine does. Weiss and Gawin (1988) report elimination half-lives of twenty to ninety minutes for cocaine and six to eight hours for benzoylecgonine. Therefore, it is possible that benzoylecgonine found after death is not representative of the blood levels of cocaine at the time of death, but is an accumulated residual of many previous doses. These high residual levels would not contribute to the death of the user, since benzoylecgonine is inactive. Under these conditions, the combined levels of cocaine and benzoylecgonine could be a substantial overestimate of the amount of cocaine in the blood stream at the time of death. Thus, whereas blood levels of cocaine and benzoylecgonine can provide conventional standards and suggestions of what may have caused a person's death, they do not provide sufficient certainty for critical analysis. This problem is well recognized by the B.C. Coroner's Office and in the technical literature. Comstock (1977:29) states that "toxicological data alone are not sufficient to establish the cause of death." Similar generalizations have been suggested by Helpern (1977) and Noguchi (1977).

Pathologists and coroners we have interviewed agree that the actual decision about which drug is identified as the cause of death on the coroner's report is based on complex factors which are determined by observations at the scene of death, medical histories, and testimony of witness and friends. Pathologists do rely on certain predetermined rules in making their decisions, but there is no hard evidence of the validity of these rules (Alexander et al. 1988).

Coroners' decisions are influenced by social considerations (including the feelings of the relatives and the effect of their reports on insurance companies), public concerns and political pressures (Leon 1978). A U.S. study comparing "drug abuse deaths" in nine cities stated that "each citys medical examiner or coroner may have a somewhat different conception as to what constitutes a drug-involved death" (Gottschalk 1979:18) and that "there are probably consistent differences from city to city, both in ability to recognize cases as being drug involved and in readiness to classify borderline cases as being drug involved" (Gottschalk et al. 1979:13). Ingold (1986:84) pointed out that the criteria for attributing a death to drug abuse differ throughout Europe and that it is "debatable whether these figures are comparable or whether they are indicative of the extent and pattern of drug related deaths in each country."

Classification of the B.C Deaths

There is no evidence in the coroner's files confirming that any of the twenty-nine deaths were classical overdoses. There were no witnesses for twenty-five of the twenty-nine deaths who could have reported the signs of overdose. Most of these deaths were discovered many hours or days after the event. In the four deaths in which witnesses were present, no seizures or convulsions were described and there were no reports of decedents taking doses of cocaine within two hours prior to their death, although the possibility of a dose shortly before death cannot be ruled out from the reports. Only one of the four descriptions, in our judgement, could be taken as possibly compatible with classical overdose.

Nine of the twenty-nine deaths attributed to cocaine in the newspaper story were not attributed to cocaine by the coroners. Two of these nine were judged to have died of morphine overdose, two from chronic intravenous drug abuse, and five from a mixed drug overdose in which cocaine was but one drug involved. In none of these nine was as much as 1 milligram of cocaine per liter of blood reported, although four had combined blood levels of cocaine and benzoylecgonine that exceeded 1 milligram/liter (see Table 2).

The remaining twenty deaths were attributed to cocaine by the coroners. However, we feel there is a significant doubt that all or most of these deaths were caused by cocaine. Of the twenty decedents that were officially judged to have died of cocaine, seven had other powerful drugs in their blood besides cocaine. Methadone and diazepam were detected in two, methadone alone in one, antabuse in one, morphine and alcohol in two, and alcohol in one. The other drugs found in the bodies could have been a factor in a mixed drug overdose, in spite of the coroner's judgement to the contrary. Both opiates and alcohol can cause central nervous system depression which can have fatal consequences when combined with cocaine's effect on the central nervous system, especially if the cocaine effect terminates sooner than the powerful depressant effect of opiates or alcohol (Finkle and McCloskey 1978; Cave 1989).

In three of this group of seven decedents, no cocaine was detected in the blood, but benzoylecgonine levels over 1 milligram/liter were detected (See Table 2). No data were recorded on either chemical in the blood of the other four decedents, although cocaine and/or benzoylecgonine were found in other tissues or in urine. To our knowledge there are no established lethal levels of cocaine or benzoylecgonine for bodily tissues other than for blood or for urine. Benzoylecgonine can be detected in urine many days after cocaine ingestion (Jatlow 1987; Weiss and Gawin 1988).

In the thirteen cocaine deaths in which only cocaine was detected, the blood levels of cocaine ranged from .31 to 6.4 milligrams/liter, with a mean value of 2.2 milligrams/liter (See Table 2). In eleven of the thirteen cases the combined cocaine and benzoylecgonine level exceeded 1 milligram/liter.

In view of the fact that people with blood levels of cocaine comparable to these have often reported no ill effects, it seems reasonable to examine other possible causes of death. Nine of the thirteen decedents that died with only cocaine in their bodies had lung pathologies of a sort that is thought to be due to the adulterants in street drugs (Hailer 1988); ten of the thirteen decedents had coronary artery and or heart pathologies, the most common being arteriosclerotic coronary artery disease. Moreover, six of the thirteen decedents had liver pathologies common to chronic intravenous drug users, including hepatitis and being laden with macrophages, infiltrates and lymphocytes. In a study of deaths attributed to drug abuse in Europe, Ingold (1986:87-88) reported: "it is likely that such acute intoxication is not the sole or principle cause of death in the cases examined, since the impaired general condition and lesions (for example, those affecting the liver and lungs) play such an important role that they alone may be the cause of death." Ingold also pointed out the high probability of suicide by drug overdose in deteriorated and exhausted people.

It seems unreasonable to us to attribute deaths of physically deteriorated, socially deviant polydrug users to the drug they happen to be taking when they expire. Rather, the causes of these deaths must include the conditions that drew the people to their deviant lifestyles and the accumulating damage that such lifestyles produce. Also, if people are addicted to an illegal drug their deaths must be partly attributed to drug laws which make it necessary for them to acquire impure drugs and unhygienic paraphernalia at inflated prices in a criminal milieu.

The Cocaine "Epidemic"

Although cocaine appears to be one of the dangerous components in the already dangerous lifestyles of socially marginal people, we found nothing in these twenty-nine sets of documents that suggests the existence of an epidemic of dangerous cocaine use among the general population of British Columbia. It seems more parsimonious to conclude that these deaths reveal the existence of a socially deviant population in which chronic drug addiction is common, along with crime, prostitution, unemployment and general ill-health. Media tend to superficially attribute deaths in this population to whatever drug is currently in the greatest use. A few years ago, B.C. media were attributing deaths in this population to methadone as uncritically as they now attribute them to cocaine (Alexander et al. 1988).

Existing evidence argues against the existence of an epidemic of dangerous cocaine use among the general population of British Columbia. A recent survey of 1,668 people randomly sampled from voter's lists throughout British Columbia found that 11.2% of the population reported having experimented with cocaine at one time or another. However, over 60% of this 11.2% had not used cocaine at all in the year of the interview and less than 1% of the sample had used it more than 100 times in their life (Coordinated Law Enforcement Unit 1987:28-44). Thus, if there is any epidemic in the general population, it is an epidemic of experimentation or infrequent use. Erickson and Alexander (1989) have elsewhere reviewed the evidence that most people who use cocaine experimentally or moderately do not become addicts.

Moderate use of cocaine does not appear to be extraordinarily dangerous. Less than 20% of the B.C. sample that had used cocaine more than once reported any negative side effects (Coordinated Law Enforcement Unit 1987:56). Studies of moderate cocaine users in Canada (Erickson et al. 1987), the Netherlands (Cohen in press) and Australia (Mugford and Cohen 1989) report few, if any, medical problems after years of use.

In spite of the speculative attention given to hazards associated with cocaine in the recent medical literature, a careful reading of this literature reveals that no substantial evidence has yet been found that moderate use of cocaine is more hazardous to healthy people than other invigorating activities (Alexander 1990). For example, cocaine is routinely applied intranasally in doses of 200 milligrams or more in nasal surgery (Gorden 1987; Haddad 1983; Moore et al.1986). These dosages are comparable to those taken by Canadian recreational users (Erickson et al.1987) and the peek blood levels of cocaine following the medical doses are comparable to those found following administration of doses that produce a "high" in experienced users (Javaid et al. 1978). A survey of plastic surgeons revealed five deaths and thirty-four severe, but non-fatal, reactions in 108,032 medical applications (Feehan and Mancusi-Ungaro 1976). Thus, cocaine proved fatal in five one-thousandths of 1% of applications to people who were undergoing surgery. Many socially accepted practices, such as automobile driving, mountain climbing and sexual intercourse, may be no more dangerous than this.


The newspaper story that provoked this investigation appears typical of many that justify the current War on Drugs. The story asserts or implies that cocaine kills otherwise well-integrated people and that an epidemic of dangerous cocaine use is sweeping the province. A closer examination of the data convinced us that most of the deaths involved long-time intravenous users or alcoholics, whose lives were deviant in many ways, and whose deaths may more productively be attributed to accumulated ill-health, to the conditions that instigated their deviance, or to the current drug laws. We were unable to establish that any of the twenty-nine deaths involved healthy, well-integrated people who were merely recreational users of cocaine.

The decedents do not appear to come from the population of homeless or destitute people, but rather from a group that maintains a veneer of normalcy. For the most part they are young, white adults living in rented homes or apartments with some money, some friends, and sometimes a job. Many questions about this fringe population remain. How large is it? How are new members drawn into it? How do people get out of it, other than by dying? What services do the people who belong to it need? Attention to these difficult questions promises more benefit for public health in the long run than continuing to pursue the simplistic doctrines of the War on Drugs.

There is a long history in North America of scare stories about drugs being publicly accepted for many years before they are finally shown to be invalid (Alexander 1990). Yet, we believe there should be a sense of urgency in the task of disabusing the media and the public of belief in the kind of information presented in the current media. Achieving rational drug policy in Canada requires carefully analyzing cocaine-related deaths and other drug-related tragedies, rather than using these events to frighten the public and to justify dubious policy. Table 1

              Personal Histories of the 29 Decedents


    of heavy or    of IV
     addictive      drug
     drug use       use   Occupation

1    37      +           +    unemployed
2    32      +           +    paper maker
3    38      +           +    land manager
4    26      +           +    student
5    30      +           +    unemployed
6    33      +           +    merchant
7    35      +           +    logger
8    31      +           u    welder
9    42      +           +    just released from prison
10   39      +           +    thief
11   39  possibly -      u    cocaine dealer
12   34      +           +    prostitute
13   22      +           +    secretary
14   33      +           u    u
15   33      +           +    steel fabricator
16   41      +           +    commercial artist
17   31      +           +    1st aid attendant & drug dealer
18   42      +           u    lawyer under suspension
19   34  possibly -      u    computer work at home
20   38      +           +    carpenter
21   47      +           +    salesman
22   31      +           +    cab driver
23   36      +           +    community college instructor
24   31      +           +    waiter
25   24      +           +    unemployed
26   34      +           +    contractor
27   41      +           +    hotel doorman
28   28      +           u    homemaker
29   18      +           +    unemployed



          Severe                                 Severe
          personal           Criminal            physical
          problems            record           pathologies

1         u                   +                   +
2         +                   -                   +
3         u                   +                   +
4         u                   -                   +
5         u                   -                   +
6         u                   +                   +
7         +                   -                   +
8         u                   -                   +
9         +                   +                   +
10        u                   +                   +
11        u                   +                   u
12        +                   +                   +
13        +                   -                   +
14        u                   -                   +
15        u                   -                   +
16        u                   +                   +
17        u                   +                   +
18        +                   +                   u
19        u                   -                   +
20        +                   -                   u
21        u                   +                   +
22        u                   -                   +
23        +                   -                   +
24        +                   -                   +
25        +                   +                   +
26        u                   -                   +
27        +                   +                   +
28        u                   -                   +
29        +                   -                   +

a + = yes

- = no

u = unable to make a conclusion; insufficient information in coroners' files

Table 2

       Coroner's Reports on Blood Levels of Cocaine in 29
                Cocaine-Related Deaths


                  Subjects   Cocaine detected   Cocaine level
                                 in body          in blood

Cocaine                 1            +           0.0
not                     2            +           none stated
official                3            +           0.0
cause                   4            +           0.15 mg/L
of                      5            +           

Alexander, B.K. 1990 Peaceful Measures: Canada's Way Out of the War on Drugs. Toronto: University of Toronto Press.

Alexander, B.K., T.M. MacInnes and B.L. Beyerstein 1988 Methadone and Addict Mortality. British Columbia Medical Journal 30:160-163.

Ambre, J., T.I. Ruo, J. Nelson and S. Belknap 1988 Urinary Excretion of Cocaine, Benzoylecgonine and Ecgonine Methyl Ester in Humans. Journal of Analytical Toxicology 12:301-306.

Barnett, G., R. Hawks and R. Resnick 1981 Cocaine Pharmacokinetics in Humans. Journal of Ethnopharmacology 3:353-366.

Basalt, R.C. 1983 Stability of Cocaine in Biological Fluids. Journal of Chromatography 268:502-505.

Bates, C.K. 1988 Medical Risks of Cocaine Use. Western Journal of Medicine 148:440-444.

Cave, W. 1989 Personal Communication. August 17.

Cohen, P.D A. In press Cocaine Use in Amsterdam in Nondeviant Subcultures. Amsterdam: University of Amsterdam.

Comstock, E.G. 1977 Treatment for survival prior to death and interpretation of postmortem toxicologic findings. In Guide to the investigation and reporting of drug abuse deaths, L.A. Gottschalk, S.L. McGuire, E.C. Dinovo, H. Birch and J.F. Heiser (ed.). Rockville, Maryland: National Institute on Drug Abuse.

Coordinated Law Enforcement Unit 1987 Cocaine: Demand Reduction Strategies. Final Report. Victoria, B.C.: Ministry of the Attorney General.

Devenvi, P. and M.A. McDonough 1988 Cocaine Abuse and Endocarditis. Annals of Internal Medicine 109:82.

Erickson, P.G., E.M. Adlaf, G.F. Murray and R.G. Smart 1987 The Steel Drug: Cocaine in Perspective. Lexington, Massachusetts: D.C. Heath.

Erickson, P.G. and B.K. Alexander 1989 Cocaine and Addictive Liability. Social Pharmacology 3:249-270.

Feehan, H.F. and A. Mancusi-Ungaro 1976 The Use of Cocaine as a Topical Anesthetic in Nasal Surgery: A Survey Report. Plastic and Reconstructive Surgery 57:62-65.

Finkle, B.S. and K.L. McCloskey 1978 The Forensic Toxicology of Cocaine (1971-1976). Journal of Forensic Sciences 23:173-189.

Fischman, M.W. and C.R. Schuster 1980 Experimental investigations of the actions of cocaine in humans. In Cocaine 1980, F.R. Jeri (ed.). Lima, Peru: Pacific Press.

Garber, M.W. and D. Flaherty 1987 Cocaine and sudden death. American Family Physician 36:227-230.

Golbe, L.I. and M.D. Merkin 1986 Cerebral infarction in a user of free-base cocaine (crack). Neurology 36:1602-1604.

Gorden, B.R. 1987 Topical cocaine nasal anesthesia. Archives of Otolaryngology -- Head and Neck Surgery 113:211.

GottsehaIk, L.A., S.L. MeGuire, J.F. Heiser, E.C. Dinovo and H. Birch 1979 Drug Abuse Deaths in Nine Cities: A Survey Report. NIDA Research Monographs 29. Rockville, Maryland: National Institute on Drug Abuse.

Haddad, L.M. 1983 Cocaine. In Clinical Management of Poisoning and Drug Overdose, L.M. Haddad and J.F. Winchester (eds.). Philadelphia: W.B. Saunders.

Haines, J.D. and S. Sexter 1987 Acute myocardial infarction associated with cocaine abuse. Southern Medical Journal 80:1326-1327.

Haller, P.R. 1988 Infections in Intravenous Drug Abusers. Postgraduate Medicine 83:95-114.

Helpern, M. 1977 Certification of death from narcotism and other psychoactive drugs of abuse. In Guide to the investigation and reporting of drug-abuse deaths, Gottschalk, S.L. McGuire, E.C. Dinovo, H. Birch and J.F. Heiser (eds.). Rockville, Maryland: National Institute on Drug Abuse.

Ingold, F.R. 1986 Study of Deaths Related to Drug Abuse in France and Europe. Bulletin on Narcotics 38:81-89.

Jatlow, P. 1987 Drug of Abuse Profile: Cocaine. Clinical Chemistry 33:66B-72B.

Jatlow, P. 1988 Cocaine: Analysis, Pharmacokinetics, and Metabolic Disposition. Yale Journal of Biology and Medicine 61:105-113.

Javaid, J. I., M.W. Fischman, C.R. Schuster, H. Dekirmenjian and J.M. Davis 1978 Cocaine Plasma Concentration: Relation to Physiological and Subjective Effects in Humans. Science 202:227-228.

Kaye, B.R. and M. Fainstat 1987 Cerebral basculitis associated with cocaine abuse. Journal of the American Medical Association 258:2104-2106.

Kosten, T.R. and H.D. Kleber 1988 Rapid Death During Cocaine Abuse: A Variant of the Neuroleptic Malignant Syndrome? American Journal of Drug and Alcohol Abuse 14:335-346.

Leon, J.S. 1978 Methodology and Law: Problems Associated with coroner's Data on Alcohol and Drug Related Deaths. Legal Medical Quarterly 2:29-32.

Liu, Y, R.D. Budd and E.C. Griesemer 1982 Study of the Stability of Cocaine and Benzoylecgonine, its Major Metabolite, in Blood Samples. Journal of Chromatography 248:318-320.

Lowenstein, D.H., S.M. Massa, M.C. Rowbotham, S.D. Collins, H.E. McKinney and R.P. Simon 1987 Acute neurological and psychiatric complications associated with cocaine abuse. American Journal of Medicine 83:841-846.

Middleton, G. 1989 Rush Toward Death. Province 14 May:4-5.

Mittleman, R.E. and C.V. Wetli 1987 Cocaine and Sudden "Natural" Death. Journal of Forensic Sciences 32:11-19.

Mody, C.K., H.B. Miller, S.K. McIntyre, S.K. Cobb and M.A. Goldberg 1988 Neurological complications of cocaine use. Neurology 38:1189-1193.

Moore, G.F., J.M. Emanuel, T.P. Ogren and A.J. Yonkers 1986 Cocaine: Current Clinical Use and Potential Abuse. Nebraska Medical Journal 71:317-321.

Mugford, S. and P. Cohen 1989 Drug Use, Social Relations, and Commodity Consumption: A Study of Recreational Cocaine Users in Sydney, Canberra and Melbourne. A Report to the Research into Drug Abuse Advisory Committee, National Campaign Against Drug Abuse. Department of Sociology, Australian National University.

Noguchi, T.T. 1977 Postmortem examination. In Guide to the investigation and reporting of drug-abuse deaths, L.A. Gottschalk, S.L. McGuire, E.C. Dinovo, H. Birch and J.F. Heiser (eds.). Rockville, Maryland: National Institute on Drug Abuse.

Paly, D., P. Jatlow, C. Van Dyke, F.R. Jeri and R. Byck 1978 Plasma cocaine concentrations During Cocaine Paste Smoking. Life Sciences 30:731-738.

Smart, R.G. and L. Anglin 1987 Do We Know the Lethal Dose of Cocaine? Journal of Forensic Sciences 32:303-312.

Sternberg, R.G., M.D. Winniford, L.D. Hillis, G.P. Dowling and L.M. Buju 1989 Simultaneous acute thrombosis of two major coronary arteries following intravenous cocaine use. Archives of Pathology and Laboratory Medicine 113:521-524.

Tuchman, A.J., M. Daras, P. Zalzal and J. Mangiardi 1987 Intracranial hemorrhage after cocaine abuse. Journal of the American Medical Association 257:1175.

Van Dyke, C., P. Jatlow, J. Ungerer, P.G. Barash and R. Byck 1978 Oral Cocaine: Plasma Concentrations and Central Effects. Science 200:211-213.

Weiss, R.D. and F.H. Gawin 1988 Protracted elimination of cocaine metabolites in long-term high-dose cocaine abusers. American Journal of Medicine 85:879-880.

Wetli, C.V. and D.A. Fishbain 1985 Cocaine-induced Psychosis and Sudden Death in Recreational Cocaine Users. Journal of Forensic Sciences 30:873-380.

Winek, C.L. 1985 Drug and Chemical Blood-Level Data 1985. Pittsburgh: Fisher Scientific.

Wojack, J.D. and E.S. Flamm 1987 Intracranial hemorrhage and cocaine use. Stroke 18:712-715.


 Newest Article:

"My Final Academic Article on Addiction"

Read Now

“Problem Gambling” is Now a Recognized Addiction: Why it Matters!"

Read Now

"Creating Healing Communities in a Toxic Society: Viktor Frankl and Jordan Peterson"

Read Now
"Treatment for Addiction: Why Aren’t We Doing Better?"
Read Now

Addiction: A Hopeful Prophecy From a Time of Despair

Read Here

 "What Shakespeare Knew About Addiction, But We Have Forgotten"
Read Now

Healing Addiction Through Community: A Much Longer Road Than it Seems?

Read Here

Rat Park vs. The NY Times

Read Here

New Revision of "The Rise and Fall of the Official View of Addiction"

Read Here

Addiction, Environmental Crisis, and Global Capitalism

Read Here

Listen to Bruce Alexander
speak with David Crowe on
"The Infectious Myth" 

Dealing with Addiction