Cocaine Essay, Research Paper
This chapter introduces the pharmacology of crack cocaine to help readers evaluate the claims that have been made regarding its danger to individual users and society. Because, materially and pharmacologically, crack is cocaine, most of what is known about cocaine applies to crack as well. The fact that crack is smoked rather than sniffed, swallowed, or injected is significant. Our review of the evidence indicates, however, that its importance has been exaggerated. Clearly, using either cocaine powder or crack entails risks, but both can also be used in less or more risky ways. In fact, among the things we will show is that the amount of harm resulting from the use of powder cocaine and crack has less to do with their pharmacological properties than with the social circumstances of their use.
FROM COCA LEAVES TO CRACK
For centuries, people have consumed cocaine to enhance work performance, forestall drowsiness, lift mood, and produce feelings of elation and euphoria. In the South American Andes, for over a thousand years people have ingested cocaine by chewing coca leaves or brewing them into a tea. This form of consumption seems not to be associated with significant biological harm or social dysfunction (Aldrich and Barker, 1976; Antonil, 1978; Forno et al., 1981; Weil, 1986) and has not, by and large, been subjected to repressive government control (Henman, l990; Morales, 1989).
There was little use of coca in the United States or Europe until the mid-nineteenth century, when the plant’s principal active ingredient was extracted and made available as a water-soluble powder cocaine hydrochloride Western physicians soon discovered that cocaine was an effective local anesthetic; they also used it, although less effectively, as an antidepressant, asthma remedy, and a treatment for opiate addiction About the same time, cocaine was added to numerous patent medicines and tonics that people purchased without prescription to combat a variety of common ailments, including chronic fatigue.
During the late nineteenth century, Americans also consumed cocaine recreationally, often in beverage form. Vin-Mariani wine and Coca-Cola for example, were popular cocaine-based drinks and the latter was even marketed as a “temperance beverage” to people wishing to avoid alcohol (Pendergrast, 1993). There is less information available about the recreational use of cocaine powder during the nineteenth century, but it seems to have been most common among members of the “criminal underworld” (Grinspoon and Bakalar, 1985; Inciardi, 1992; Musto, 1987) a fact that helped fuel public support for increased government controls. Also precipitating anticocaine legislation around the turn of the twentieth century were growing concern about cocaine’s potentially harmful physical effects (Alexander, 1990; Courtwright, 1982; Grinspoon and Bakalar, 1985) and fear, especially in the South, that the drug caused blacks to behave violently (Morgan, 1981; Musto, 1987; Pendergrast, 1993). However, because this was an era of increasing government control over most available intoxicants including alcohol the laws regulating cocaine may have had little to do with this drug’s particular characteristics and effects.
As early as 1887, states began passing anticocaine laws (Ashley, 1976); and in 1906, with enactment of the first Pure Food and Drug Act, the federal government began requiring that products with cocaine (and some other drugs) be labeled as to content. Then, in 1914, Congress passed the Harrison Act, which originally only imposed tax and registration requirements on the legitimate providers of certain drugs, including cocaine. However, courts soon interpreted this law as giving federal drug enforcement officials the power to decide what constituted “legitimate” use of these drugs; and, through this power, they quickly transformed the Harrison Act into a law prohibiting all recreational use of cocaine.
One immediate consequence of cocaine prohibition was the elimination of cocaine tonics and beverages. Another was the emergence of an organized black market in cocaine hydrochloride, which was smuggled into the country from South America. Almost certainly, the purity of the product available to users declined, the price rose far above the $2 an ounce that had been common during the previous century (Courtwright, 199l), and use became even more concentrated in deviant subcultures (Ashley, 1976; Grinspoon and Bakalar, 1985; Inciardi, 1992).
After 1930, when a number of synthetic stimulants (particularly amphetamine) became available, cocaine use may have decreased further, although it continued to be used by some artists and entertainers, who generally sniffed it, and by intravenous heroin users, who employed it either as an occasional alternative to heroin or mixed with heroin to form a “speed-ball” (Grinspoon and Bakalar, 1985). During the 1960s, as part of the more general increase in the use of illegal drugs among more “mainstream” Americans, the use of cocaine probably increased as well, although in 1972, still less than 3% of the population (aged twelve and over) said they had tried it (Johnson and Muffler, 1992).
During the remainder of the 1970s and into the early 1980s, cocaine use increased steadily, especially among young adults aged eighteen to twenty-five (NIDA, 1991a). Probably contributing to cocaine’s appeal was the government’s success, first, in curtailing diverted medicinal amphetamine (Brecher, 1972; Inciardi, 1987; Morgan and Kagan, 1978) and, second, in interdicting enough marijuana substantially to decrease its availability and increase its price (Cowan, 1986; Hamid, 1992; Lazare, 1990). As the demand for cocaine increased, supplies increased as well, and by 1982, approximately 28% of eighteen-to twenty-five-year-olds had at least tried it (NIDA, 1991a). However, because of cocaine’s relatively high price up to $100 for a gram of powder in the early 1980s use was most prevalent among the middle and upper classes (Grinspoon and Bakalar, 1985). The typical mode of ingestion was to sniff cocaine hydrochloride powder into the nose, which permits absorption through the nasal mucosa.
Today, essentially all cocaine enters the U.S. in the form of hydrochloride powder. This powder is extracted in a process that begins by mixing pulverized coca leaves with a solvent (such as ether or gasoline) and partially drying it. Then, to make the product water-soluble, this “coca paste” is treated with hydrochloric acid and dried to a white powder. In this form, cocaine can be sniffed, swallowed, or dissolved in water for injection, but it cannot be smoked because igniting it degrades the cocaine before it will volatilize. However, through a series of fairly simple chemical procedures, cocaine can be turned into “freebase” a product that resembles the smokeable coca paste. To produce freebase, cocaine hydrochloride is mixed in water with a liquid base (such as ammonia, baking soda, or sodium hydroxide) to remove the hydrochloric acid. The resulting alkaloidal cocaine is then dissolved in a solvent (such as ether) and gently heated, causing most of the liquid to evaporate. The product created, when placed in a glass pipe and ignited, produces vapors of relatively pure cocaine.
Inhaling cocaine vapor into the lungs delivers the drug more rapidly to the bloodstream and therefore to the brain than does sniffing the powder; as a consequence, it produces quicker, more intense effects. Most cocaine users do not want this more dramatic experience especially because it means, as well, a more rapid diminishing of the drug’s effects. Also reducing freebase’s attractiveness is the somewhat complicated conversion process which occasionally can be dangerous because some of the solvent used in the preparation may remain in the product being ignited. Nonetheless, freebasing did increase in popularity in the early 1980s (Hamid, 1992; Inciardi, 1987; Siegel, 1984), mainly attracting people who were already fairly heavy users of powder cocaine (Siegel, 1984; Waldorf et al., 1991; Washton et al., 1986).
Around 1985, another form of smokeable cocaine called “rock” or “crack” became available. Its production resembles that of freebase, but without the final purification process: cocaine hydrochloride is dissolved in water, sodium bicarbonate (baking soda) is added, and the mixture is heated and then dried into hard, smokeable pellets. These pellets contain not only alkaloidal cocaine, but sodium bicarbonate and whatever other fillers and adulterants had been added earlier to the powder; thus, crack is not as highly purified as freebase, and street samples tend to range from 10 to 40% cocaine by weight (Inciardi, 1987). Still, igniting crack produces a vapor that is largely pure cocaine (Snyder et al., 1988), making the experience of smoking crack quite similar to that of smoking freebase. However, unlike freebase, which users generally produced themselves from the powder, crack was usually cooked (or “cracked up”) by drug dealers who then sold it in ready-to-smoke form (Hamid, 1990).
Crack quickly gained in popularity, although it never became as popular as cocaine powder. For example, in 1991, nearly twenty-four million Americans (aged twelve and over) said they had tried cocaine, compared to less than four million for crack (NIDA, 1991b). Although the price of cocaine had been decreasing and its quality increasing during the early 1980s, it was still, in 1985, too expensive to be used very much by the poor. What crack did was to lower dramatically the cost of the “cocaine high.” Simply because smoking delivers a drug more efficiently to the brain than does snorting, an amount of cocaine too small to produce an effect in powder form becomes an effective dose when converted to crack. In 1986, a single dose of crack could be purchased for as little as $5 or $10; and, over the next few years as the price of cocaine powder fell even further, the price of a pellet of crack fell as low as $2 in some parts of the country (Cohn, 1986). Thus, by the late 1980s, what had once been called “the champagne of drugs” had become available to the poor and its use spread especially quickly in impoverished urban areas where enterprising youth turned powder cocaine into crack and sold it on the streets (Fagan and Chin, 1989; Hamid, 1990; Williams, 1992).
As Chapter 2 showed, once crack had been introduced to the inner-city poor, the “crack epidemic” became a major media event with literally thousands of articles appearing in newspapers and magazines in 1986 alone. At the time, no scientific studies of the drug had been conducted, but journalists found and quoted a handful of “experts” mostly law enforcement officials and drug treatment providers who had decided that crack was “the most dangerous drug known to man.” They claimed that crack was highly potent and highly toxic, causing record numbers of heart attacks, seizures, and strokes. They blamed crack for recent increases in crime, family violence, and child abandonment. They claimed that crack was “instantly addicting,” making moderate and controlled use impossible. And when used by pregnant women, crack was said to produce babies so severely damaged that they would never fully recover.
Before long, articles supporting these claims appeared in the drug abuse and medical literatures. Although clothed in scientific garb, most of these “studies” were simply “case reports” of crack and cocaine users enrolled in drug abuse treatment programs a self-selected and nonrepresentative sample (Gold et al., 1986; Honer et al., 1987; Isaacs et al., 1987; Miller et al., 1989; Mody et al., 1988; Spitz and Rosecan, 1987; Washton et al., 1986; Weiss and Mirin, 1987). Even today, few of the “facts” that are “well known” about cocaine and crack come from careful scientific studies. Nonetheless, they have made their way into government documents, drug education materials, and anti-drug public service announcements particularly those of the Partnership for a Drug-Free America. In addition, although a number of journalists have been critical of the media’s handling of the crack story (Gladwell, 1986; Martz, 1990; Morley, 1989; Weisman, 1986), exaggerated tales of cocaine- and crack-caused horror still appear regularly in the popular press.
The faulty assumption on which such drug horror stories are based is that a drug’s pharmacology holds the key to understanding the patterns of its use and the behavior of its users. One of our goals in this chapter is to demonstrate that this “pharmacocentrism” is misleading. In doing so, we are not suggesting that a drug’s pharmacology is unimportant. After all, for a drug to be used recreationally, people have to like how it makes them feel, and how a drug makes people feel is a product of its “pharmacological fit” with the human organism. However, a description of this “fit” cannot explain why only some people use a particular drug, why only some of them become regular users, or why fewer still use it in a volume and frequency that disrupts their lives. In short, to explain how a drug works in the brain reveals no more about why and how people use it than explaining how a specific food is processed by the body reveals why and how people eat it. Like food consumption, drug consumption must be understood, primarily, as a social-psychological phenomenon. In fact, one of the things we hope to show in the following overview of crack cocaine’s pharmacology is how little it reveals about the drug’s popularity or the social consequences of its use.
COCAINE’S INTERACTION WITH THE HUMAN ORGANISM
Like all stimulant drugs, those prescribed by physicians as well as those taken recreationally, cocaine produces a psychoactive effect by interacting with the central nervous system, stimulating it to perform its ordinary functions more intensely. This system operates through the release of various neurochemical transmitters (from the nerve cells in which they are produced) and their binding to receptor sites on neighboring cells. The constant release and binding of these neurotransmitters forms a pathway of “messages” that travel throughout the body, sustaining life and making possible the organism’s response to environmental stimuli.
Cocaine also has an impact in the autonomic (or involuntary) division of the central nervous system, which helps regulate a variety of bodily functions that are generally free of volitional impact, including respiration, circulation, digestion, and body temperature. Ordinarily, these functions are maintained at relatively stable levels throughout the day. But they are slowed down during periods of rest through diminished production, release, and binding of neurotransmitters and can be speeded up, as needed, through increased neurotransmitter activity. Cocaine operates in this system by increasing the concentration and binding activity of the body’s own neurotransmitters particularly dopamine. Thus, what people experience as cocaine’s stimulant effect is an intensification of the body’s normal stimulatory mechanisms.
Cocaine is both a quick-acting and a short-acting drug. When cocaine enters the bloodstream directly, via injection, it reaches the brain quickly, and users feel its effects within minutes. Inhalation also delivers cocaine quickly to the brain because air passages in the lungs are positioned close to capillary accesses to the bloodstream. When cocaine is sniffed, the onset of effect is slower because the drug must pass through the nasal mucosa before entering the bloodstream. Swallowing cocaine delays delivery to the brain even more because most of the drug is passed through the gastrointestinal tract before it crosses through cell membranes into the bloodstream.
Controlling for dose, sniffing and swallowing also produce less intense effects. This is not only because these routes of administration cause active cocaine molecules to reach the brain more gradually, and therefore in lower concentrations, but also because the additional passage of time allows more of the cocaine molecules to be transformed into inactive byproducts (or metabolites) before they reach the brain. Both injection and inhalation deliver a greater number of active cocaine molecules per dose to the brain than snorting.
Whatever the route of administration, within thirty to sixty minutes, the processes of biotransformation and excretion cut in half cocaine’s concentration in the blood which is one reason its effects are of relatively short duration. However, even before this decline, cocaine’s effects are diminished through other “protective mechanisms.” The most important is the rapid distribution of the drug from the bloodstream to the rest of the body, including to sites with no cocaine receptors. Thus, the same activity that delivers cocaine rapidly to active sites in the brain and heart also removes it from these sites, thereby reducing the drug’s effects. At the same time, cocaine’s effects are also diminished through homeostatic mechanisms that reduce neurotransmitter activity at receptor sites the same mechanisms that operate when factors other than drugs cause an increase in neurotransmitter activity. It is this diminishing of effects prior even to the decline in the drug’s concentration in the blood that cocaine users experience as “acute tolerance.” That is, to maintain a stable effect over time, users must follow each dose of the drug with a larger subsequent dose. However, acute tolerance also can be viewed as a preexisting protective mechanism because it diminishes cocaine’s potentially harmful effects on the cardiovascular and central nervous systems.
Cocaine’s Psychostimulant Effects
The intensity of cocaine’s impact on the central nervous system depends largely on dose. At low doses, cocaine’s effects are fairly similar to those of caffeine: it combats drowsiness and fatigue, increases energy and alertness, and enhances mental acuity. With increasing doses, most users begin to experience negative effects such as nervousness, jitteriness, sleeplessness, and agitation and at very high doses, feelings of suspicion, hypervigilance, and paranoia are common (Cohen, 1989; Erickson et al., 1987; Spotts and Shontz, 1980; Waldorf et al., 1991).
Extremely high does of cocaine like extremely high doses of many stimulant drugs can produce a toxic psychosis, with symptoms similar to the delirium of high fever. However, toxic psychoses appear to be rare among cocaine users, probably because of the body’s protective mechanisms referred to previously. In addition, because cocaine is relatively short acting, when psychosis does occur, it tends to be short-lived (Weil, 1986). Permanent psychosis is found occasionally among cocaine users (Washton, 1989; Weiss and Mirin, 1987), but there is no evidence of a causal link, and, for most people, even heavy and prolonged use appears to have no permanent impact on mental health, personality, mood, cognition, memory, or perception.
Among people predisposed to behave violently, cocaine may increase the likelihood of their involvement in violent episodes, but there is no evidence that cocaine causes generally nonviolent people to behave violently. Some researchers have identified crack as more violence producing than cocaine powder (Peterson, 199l; Washton, 1989), and journalists have been prone to attribute increases in violent crime to the pharmacological properties of crack. However, a growing number of social scientists refute these claims.
Crack use by women has also been blamed for rising rates of child abuse (Peterson, 199l). However, to the extent that crack users seem to “lose their mothering instinct” and begin abusing or neglecting their children, it is probably due less to the pharmacology of the drug than to the lifestyle that accompanies heavy involvement in the street drug scene regardless of the drug (Rosenbaum et al., 1990). In fact, research on a variety of drugs shows that the same drug is associated with very different behaviors in different cultures, which indicates that there is no direct link between any specific drug and any specific behavior (see, e.g., MacAndrew and Edgerton, 1969; Zinberg, 1984). In this culture, crack like alcohol is associated with violence primarily because it is often used by people already at high risk for behaving violently and because it is often used in social settings in which violence is already common (Williams, 1992). No drug directly causes violence simply through its pharmacological action.
Cocaine’s Physiological Effects
Because it constricts blood vessels and speeds up the heart, cocaine has the potential to produce cardiovascular disease. However, at low doses, the increases in blood pressure and heart rate caused by cocaine are fairly similar to those associated with over-the-counter appetite suppressants and are less dramatic than those experienced by most people during aerobic exercise, urban driving, or sex. With larger doses, cocaine’s cardiovascular effects become more pronounced, and users face an increased risk of harm to the heart through coronary artery constriction or arrhythmia. High-dose users also face an increased risk of adverse stimulant effects in the central nervous system, including seizures, convulsions, and strokes (Cregler and Mark, 1986).
Because intravenous injection allows the rapid delivery of a large dose of cocaine, injectors are more likely to experience adverse physiological effects. Rapid consumption of multiple doses increases the risk associated with other routes of administration, but the body’s capacity quickly to diminish cocaine’s effects protects even most high-dose smokers, sniffers, and swallowers from serious harm. Oral ingestion clearly has the greatest safety margin, although an extremely large dose swallowed can be dangerous, as indicated by the death of “body packers” people who swallow balloons or condoms filled with cocaine to smuggle it across borders (Amon et al., 1986; Suarez et al., 1977).
Although most people can consume a fairly high dose of cocaine with out serious harm, even a low dose can be dangerous for people with preexisting central nervous system or cardiac abnormalities (Isner et al., 1986; Mittleman and Wetli, 1987). People with enzyme deficiencies that interfere with cocaine’s biotransformation may also be at higher risk (Devenyi, 1989). There is recent evidence that consuming alcohol with cocaine may be risky, especially for persons with heightened sensitivity to cocaine’s effects (Karch, 1992).