This study is the first to identify the correlates of DSM-IV lifetime cocaine dependence among a community sample of long-term crack users, the majority of whom had used the drug for a decade or longer. Although the results suggest it is possible to smoke crack for many years without becoming addicted to it, they clearly show that cocaine dependency is the most common outcome. The findings also suggest that race/ethnicity and comorbid psychiatric disorders are important indicators of who avoids and who succumbs to addiction. Interestingly, the groups did not differ in the mean age of crack initiation or the frequency of recent crack use, suggesting that duration and amount of use, while unquestionably being critically important factors in the development of cocaine addiction, are not its sole determinants.
Even though the results show that proportionately fewer African-Americans than whites had experienced cocaine dependence, the role of race/ethnicity in its development is far from clear. One possible explanation is that the influence of race/ethnicity on cocaine addiction is mediated through other psychiatric disorders. For example, there is a strong relationship between ASPD and substance abuse. Robins has noted that this is due, in part, to the overlapping symptoms of the disorders and shared risk factors. Further, she has argued that ASPD can actually cause substance use disorders (Robins, 1998
). Thus, there is reason to consider ASPD a consequential factor in the development of addiction to illicit drugs like crack.
Earlier research offers additional insight into this complex issue. For example, an AIDS-oriented study of 425 people admitted to treatment facilities in St. Louis in the early 1990s found significantly lower rates of lifetime comorbid drug and non-drug disorders, including ASPD, among African-Americans than among whites (Compton et al., 2000
). In a study on the typology of cocaine abusers, researchers assessed 399 users drawn from treatment and community samples in Connecticut, and found proportionately fewer African-Americans and women suffered the more severe form of cocaine dependence disorder. They also found that ASPD and alcoholism were more common among persons who experienced the more severe form of cocaine dependence (Ball et al., 1995
). Although these studies demonstrate the nexus of race/ethnicity, ASPD, and drug addiction, the question persists as to why white crack users appear to be disproportionately affected by ASPD and cocaine dependence. The answer may lie in the social milieu of the crack scene.
The roots of crack use in the United States are embedded in its inner-cities (Inciardi, 1992
), in neighborhoods that were and still are very largely populated by minorities, often by African-Americans, as is the case in the Dayton area. As crack cocaine became integrated into the social ecology of these neighborhoods, residents were, as a matter of course, exposed to the drug and its users. Residents did not have to engage in extraordinary efforts to obtain crack. In contrast, many white users had to venture into minority neighborhoods to secure the drug. For example, they made drive-though crack purchases, exposing themselves to myriad risks (Inciardi, 1992
; Carlson and Siegal, 1991
). Personality traits like impulsivity and recklessness support such behavior and also help define ASPD. In turn, these may help explain the higher rates of the disorder among white crack users. Further, if ASPD makes an individual more susceptible to drug dependence, this would help explain the higher rate of cocaine dependence among the white users in our sample, since proportionately more of them had ASPD.
Even though there were no significant differences between the dependent and non-dependent groups in terms of current marital status, education, or employment, the study sample, with an average age of 46 years, had very low levels of marriage, educational achievement, and employment. Regardless of whether these behaviors are a cause or an effect of crack use, they are reflective of disengagement from traditional social institutions, and further help explain the marginalization of crack users (Fischer and Coghlan, 2007
). It is worth noting that some researchers have linked problematic drug use to the disconnect between a group’s socioeconomic expectations and its ability to achieve them (Agar and Reisinger, 2001
), an ongoing problem in places like Dayton where the industrial base, and the employment opportunities tied to it, have continued to decline. For a variety of reasons, this problem, sometimes called ‘open marginality’, can differentially impact racial and ethnic groups’ drug use practices (Broz and Ouellet, 2008
), and may have been operating at some level among the crack users in this study.
Attention deficit/hyperactivity disorder was considered in the analysis because there are reports in the literature suggesting people with the problemsometimes use cocaine to address it (Gawin and Ellinwood, 1988
; Khantzian, 1997
; Levin et al., 1998
; Wilens, 2004
). The 22.2% prevalence rate among the cocaine-addicted group is about 5 times greater than the rate in the non-addicted group and nearly 3 times greater than that found in the general population (Kessler et al., 2005
). This finding suggests that it is not unreasonable to consider AD/HD, a disorder, like ASPD, rooted in childhood, a risk factor for cocaine dependence.
The results on alcohol dependence are similar to those of Ball and his colleagues (1995)
who found higher rates of alcohol problems among cocaine abusers with the more severe form of cocaine dependency disorder. In addition, our findings on race/ethnicity and alcoholism are in line with the National Epidemiologic Survey on Alcohol and Related Conditions data showing African-Americans significantly less likely than whites to develop alcohol dependence (Hasin et al., 2007
The partial correlation analysis results show associations between cocaine dependence and other substance use disorders as well as non-drug psychiatric disorders. These findings are consistent with a substantial literature documenting a strong relationship between drug use disorders and other comorbid psychiatric disorders (Kessler et al., 1996
; Stinson et al., 2005
; Hasin et al., 2005
; Compton et al., 2007
). Given the sample’s mean age of crack use initiation (28.1 years), there is some reason to believe that the onset of symptoms of the comorbid disorders assessed preceded crack involvement. Thus, these disorders, or their symptoms, may be markers or risk factors for addiction to crack.
At least several limitations affect the generalizibility of this study’s results. First, it is not known how representative our sample is of long-term crack smokers, although in terms of age, gender, and race/ethnicity, it appears to be reasonably reflective of the current generation of users in the United States (Substance Abuse and Mental Health Services Administration, 2005
). Second, the study relies on self-reports of drug use. Although not without problems, there is good evidence to suggest such self-report data can be valid and reliable (Adair et al., 1995
; Darke, 1998
). Third, our research is limited in scope. Clearly, factors other than those addressed in this study play a crucial role in the development of addiction. For example, research has identified genetic risks for substance use disorders (Langbehn et al., 2003