Tobacco use continues to be a leading preventable cause of death and disability in the USA. Early patterns of use in adolescence and early adulthood often develop into chronic forms of nicotine addiction for approximately one in three users (Colby, Tiffany, Shiffman, & Niaura, 2000). Despite a reduction in smoking prevalence over the past 25 years, approximately 45–48 million (approximately 22–25%) adults in the USA currently smoke (Centers for Disease Control and Prevention [CDC], 1996). Though nearly 70% of these smokers are motivated to quit (CDC, 2002), approximately 90–95% of smokers who try to quit smoking on their own (Cohen et al., 1989), and 60–80% of smokers who attend treatment programs, relapse (CDC, 2002).

Cigarette smoking is more prevalent among individuals with panic psychopathology, as well as other certain types of anxiety disorders, than it is among individuals without panic psychopathology or other types of psychological disorders. This work has predominately focused on individuals seeking treatment for anxiety disorders (McCabe et al., 2004), but has more recently expanded to include representative samples of the general population (Goodwin, Zvolensky, & Keyes, 2008). Current rates of daily smoking among those diagnosed with panic disorder have been as high as 56% and have not meaningfully varied when lifetime histories of smoking are examined (Zvolensky, Feldner, Leen-Feldner, & McLeish, 2005). Rates of current daily smoking among those with panic disorder are typically greater than those found among individuals without psychiatric problems and other anxiety disorders, with the exception of posttraumatic stress disorder. For example, McCabe et al. (2004) reported that 40% of treatment-seeking individuals with panic disorder were current smokers compared with 19% of those with social anxiety disorder and 22% of persons with obsessive–compulsive disorder, who also were seeking treatment for their anxiety problems at the same clinic.

Studies have found that smoking, compared to nonsmoking, among young adults or adolescents is related to an increased risk for panic attacks, panic disorder, and agoraphobia (Breslau & Klein, 1999; Breslau, Novak, & Kessler, 2004; Isensee, Wittchen, Stein, Hofler, & Lieb 2003). For example, Johnson et al. (2000) found adolescents who smoked 20 or more cigarettes per day were at significantly greater risk for panic disorder and agoraphobia as young adults. Studies also have suggested that smoking among those with nonclinical panic attacks (Zvolensky, Forsyth, Fuse, Feldner, & Leen-Feldner 2002) and panic disorder with and without agoraphobia (Zvolensky et al., 2004; Zvolensky, Schmidt, & McCreary, 2003) compared to nonsmokers with these same problems is related to more severe panic symptoms and life impairment. These smoking-panic effects are moderated by individual differences in affect-relevant vulnerability variables (McLeish, Zvolensky, Bonn-Miller, & Bernstein, 2006). For example, Zvolensky, Kotov, Antipova, and Schmidt (2003) found that high levels of anxiety sensitivity moderated the relation between smoking rate and agoraphobic avoidance, such that higher levels of anxiety sensitivity and smoking rates were associated with the greatest levels of panic symptoms.

There also is evidence that panic psychopathology may play a formative role in the maintenance of smoking. This work is derived from integrative conceptual models that suggest that smokers with panic psychopathology may have a particularly difficult time quitting smoking by virtue of their emotional reactivity to aversive interoceptive cues that routinely occur during smoking abstinence, as well their tendency to smoke as a way of avoiding or regulating negative affect (Zvolensky & Bernstein, 2005; Zvolensky, Schmidt, & Stewart, 2003). In fact, some work suggests that daily smokers with a history of panic attacks report significantly more intense anxiety-related withdrawal symptoms (e.g., anxiety, restlessness) compared to smokers without such a history, but not other tobacco withdrawal symptoms (Zvolensky, Lejuez, Kahler, & Brown, 2003). Other studies are consistent with these findings (Zvolensky, Feldner, Eifert, & Brown, 2001).

Alcohol use disorders are among the most prevalent mental disorders in the USA. Indeed, the National Institute on Alcohol Abuse and Alcoholism’s (NIAAA) 2001–2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC; Grant et al., 2003) indicated that the 12-month prevalence of DSM-IV alcohol abuse and dependence is approximately 8% in the general population (Grant et al., 2006). Such problems are associated with impairment across numerous life spheres. For instance, chronic heavy drinking is an etiological factor for certain cancers, liver cirrhosis, immune system disorders, and brain damage (Grant et al., 2003). Alcohol use problems co-occur with panic psychopathology at rates that exceed those found among individuals without psychopathology and many other psychological disorders (Kushner, Sher, & Beitman, 1990). Studies have suggested that individuals seeking treatment for alcohol use problems and dependence often meet diagnostic criteria for panic attacks, panic disorder, and agoraphobia. Tómasson and Vaglum (1996), for example, reported that over 30% of individuals seeking treatment for alcohol use problems met diagnostic criteria for panic disorder with or without agoraphobia. Other investigations have examined rates of alcohol use problems among individuals seeking treatment for panic psychopathology. In a classic study in this area, Otto, Pollack, Sachs, O’Neil, and Rosenbaum (1982) found that approximately 25% of persons seeking treatment for panic disorder had a history of alcohol dependence. Importantly, these co-occurrence rates among treatment-seeking populations are consistent with those observed in epidemiological studies. For example, Regier, Narrow, and Rae (1990) reported that in the Epidemiological Catchment Area survey, panic disorder was associated with an elevated risk for alcohol dependence, even relative to other anxiety disorders.

Bidirectional associations may exist between alcohol problems and panic psychopathology. Here, perhaps one of the most influential perspectives has been that panic psychopathology may promote maladaptive alcohol use via its use as a coping strategy for dampening aversive internal states and panic attacks (Kushner et al., 1990). There is empirical evidence consistent with this perspective. For example, research suggests that panic attacks and panic disorder predict the future onset of alcohol abuse (Zimmerman et al., 2003). Other work suggests that acute alcohol administration does, in fact, dampen anxiety reactions in controlled, laboratory studies, especially among panic-vulnerable individuals (Kushner et al., 1996; MacDonald, Baker, Stewart, & Skinner, 2000). Thus, it is plausible that individuals with panic psychopathology or even pre-morbid risk factors for such problems may learn to use alcohol to cope with distressing anxiety or related negative mood symptoms. The significance of such data for understanding relapse problems among individuals with co-occuring alcohol-panic psychopathology has not been extensively studied. Moreover, there is little understanding thus far of the factors that may mediate or moderate panic-to-alcohol problem associations.

Problematic alcohol use also may contribute to the maintenance of panic psychopathology. For instance, problems resulting from heavy alcohol use, such as withdrawal or physical dysregulation related to intoxication, may induce acute anxiety states and perpetuate panic psychopathology (Kushner, Sher, & Erikson, 1999). Emerging data are consistent with this perspective. Rassovsky et al. (2004), for example, conducted a study comparing recently detoxified alcohol-dependent individuals to nonalcoholic social drinkers during a biological challenge. Results indicated that individuals in the alcohol-dependent group displayed a greater anxiety response to the challenge than the control group, suggesting that withdrawal symptoms may indeed play a role in the induction of panic (Rassovsky et al., 2004). Such findings highlight the potential clinical significance of problematic alcohol use in exacerbating preexisting panic states.

Marijuana has been the most widely used illicit substance in the USA for 30 consecutive years (Johnston, O’Malley, & Bachman 2003), with approximately 25 million people in the USA (8.6% of the population) having used marijuana in the past year (Johnston, O’Malley, Bachman, & Schulenberg, 2004). An estimated 10% of persons who have ever used marijuana will become daily users (Johnston, O’Malley, & Bachman 1995). Lifetime marijuana dependence is estimated at 4% of the general population, a rate that is the highest of any illicit drug (Anthony, Warner, & Kessler, 1994). These rates of marijuana use, abuse, and dependence in the USA represent a significant public health concern, as there are a number of negative consequences associated with certain patterns of use of the substance (e.g., increased risk of severe medical disease; Bloom, Kaltenborn, Paoletti, Camilli, & Lebowitz, 1987).

Interest in marijuana use and panic attacks was initially stimulated by clinical observations that using marijuana may elicit acute episodes of elevated anxiety (Hollister, 1998). For example, many clinical reports have documented that marijuana use in certain contexts (e.g., novel situations) can trigger an acute fear response (Thomas, 1996). In one study, Hathaway (2003) found that among adult weekly users of marijuana (n  =  140), approximately 40% reported having had at least one panic attack related to such use. Studies addressing marijuana–panic psychopathology associations using representative sampling tactics are now emerging. For example, Zvolensky et al. (2006) found, among a representative sample of adults, that a lifetime history of marijuana dependence was significantly related to an increased risk of meeting lifetime diagnostic criteria for panic attacks. More recently, Zvolensky, Cougle, Johnson, Bonn-Miller, and Bernstein (2010) examined the prevalence rates between marijuana and panic psychopathology among a representative sample of adults in the USA. Results indicated that lifetime history of comorbid marijuana use and panic attacks or panic disorder were approximately 36.8% and 8.5%, respectively; these rates were significantly higher than the 22.0% and 4.4% evident for those with no history of marijuana use and evident when adjusting for a large number of sociodemographic factors and lifetime alcohol as well as drug abuse/dependence (Zvolensky et al., 2010).

Zvolensky et al. (2006) examined a representative sample from the general adult population (n  =  4,745; 52% female). After controlling for polysubstance use, alcohol abuse, and demographic variables, lifetime history of marijuana dependence, but not use or abuse, was significantly related to an increased risk of panic attacks. Additionally, among participants reporting a lifetime history of both panic attacks and marijuana use, the age of onset of panic attacks (M  =  19.0 years) was significantly earlier than for individuals with a lifetime panic attack history but no marijuana use (M  =  27.6 years). This work is indirectly supported by other investigations showing that daily or weekly users of marijuana report greater levels of panic-relevant anxious arousal (i.e., symptoms of somatic tension and arousal such as feeling dizzy) compared to nonusers (Bonn-Miller, Zvolensky, Leen-Feldner, Feldner, & Yartz 2005). In another investigation, adolescent marijuana use and dependence were significantly prospectively associated with increased odds for the development of panic attacks and panic disorder in adulthood (Zvolensky et al., 2008). However, the marijuana use and dependence effects in relation to the onset of panic psychopathology (both panic attacks and panic disorder) were not evident after controlling for daily cigarette smoking (Zvolensky et al., 2008). Most recently, Zvolensky et al. (2010) examined the relations between marijuana use and panic attacks and panic disorder using a large representative survey of adults (n  =  5,672; 53% female; M _age  =  45.05, SD  =  17.9). After adjusting for sociodemographic variables (age, marital status, income, education, race, and sex) and the presence of a lifetime substance use disorder, lifetime marijuana use was significantly associated with increased odds of a lifetime panic attack history. Lifetime marijuana use also was significantly associated with an increased risk of current (past year) panic attacks; however, this relation was not significant when controlling for nicotine dependence. Lifetime marijuana use was significantly associated with an increased odd of a lifetime diagnosis of panic disorder as well as a current (past year) diagnosis of panic disorder. These results appear to suggest that although there are often consistent statistically significant relations between these problems, there may be distinct and bidirectional pathways between marijuana use and panic psychopathology.

Notably, there are currently no studies examining the role of panic psychopathology in relapse among individuals attempting to stop using marijuana. Based upon panic-tobacco relapse work (Zvolensky & Bernstein, 2005), one would expect that panic-related factors may play a functional role in problems discontinuing marijuana use as well as shaping the nature of the “quit experience.”

Empirical work suggests that substance use is common among persons with panic psychopathology, and clinically relevant bidirectional associations are evident between panic psychopathology and various forms of tobacco, alcohol, and marijuana use and misuse. Therefore, assessment strategies aimed at understanding and addressing the co-occurrence of anxiety and substance use are theoretically and clinically important.

There can be many purposes for the assessment of substance use disorders in the context of anxiety psychopathology (e.g., treatment planning, determination of readiness to enter occupation, early intervention). In most instances, the procedures employed to execute assessment activities are highly influenced by the underlying conceptual framework (Kazdin, 1982). For example, the level of analysis for assessment of substance use in the context of anxiety psychopathology is largely influenced by the conceptualization of the problem behavior in question. In most cases, assessment activities for anxiety psychopathology-substance use disorder co-occurrence focus on symptom presentation (e.g., number of days missed per week due to substance use), psychopathology phenotype (e.g., alcohol abuse versus dependence), or the operative system components (cognitive, behavioral, physiocal, and context). The level of analysis employed will directly affect the extent to which specific aspects of problematic behavior are assessed.

Assessment at the symptom level focuses on individual behavior (e.g., number of drinks per drinking episode); it is a unidimensional approach. Assessment at the phenotypic level focuses on the symptoms that covary, and therefore, is multidimensional (e.g., facets of distinct elements of drinking behavior); this approach encompasses more elements of the individuals’ substance use behavior (e.g., frequency, amount, consequences). Assessment at the system level tends to be more inclusive, assuming various systems involved affect one another in a direct fashion; for example, substance use behavior affects anxiety and related mood states and vice versa (Drasgow & Kanfer, 1985). Although more inclusive theoretically, the challenge to using the system level approach historically has been in the titration of the accuracy operative conceptual model in terms of the pragmatic aspects of the assessment processes (e.g., isolating the appropriate level to assess problem behavior relative to existing scientific information about it).