The Role of Anxiety Sensitivity in the Relation between Pain Intensity with Substance Use and Anxiety and Depressive Symptoms among Smokers with Chronic Pain

Abstract

Background:

The additive effect of experiencing chronic pain in the context of nicotine addiction places smokers with chronic pain at elevated risk for experiencing physical and mental health problems. Isolating factors that explain linkages between pain and health-related outcomes among smokers with chronic pain is an important next step. Therefore, the current study examined the explanatory role of anxiety sensitivity in relations between pain intensity and current opioid misuse, severity of opioid dependence, tobacco-related problems, and anxiety/depressive symptoms.

Method:

Participants were 187 (M_age = 39.02, SD = 9.94, 74.9% female) daily smokers with chronic pain who completed a battery of self-report measures on pain experience, anxiety sensitivity, tobacco and opioid use, and anxiety/depression symptoms. Indirect effect analyses were conducted to examine anxiety sensitivity as a mediator of the relations between pain intensity and health-related outcomes.

Results:

A significant indirect effect emerged for pain intensity, through anxiety sensitivity, on opioid misuse (ab = 0.83, SE = 0.24, 95% CI [0.39, 1.34], CSE = 0.17), severity of opioid dependence (ab = 0.17, SE = 0.05, 95% CI [0.08, 0.26], CSE = 0.16), tobacco use problems (ab = 0.16, SE = 0.06, 95% CI [0.07, 0.28], CSE = 0.11), and anxiety/depressive symptoms (ab = 0.20, SE = 0.06, 95% CI [0.10, 0.31], CSE = 0.19).

Conclusion:

The current investigation highlights the potential importance of anxiety sensitivity in terms of the experience of pain with severity of substance use and anxiety/depressive symptoms among smokers with chronic pain.

Substantial empirical evidence suggests smoking and chronic pain co-occur at high rates [i.e., 28.3%; ¹]. Moreover, estimates suggest that the prevalence of smoking among persons with chronic pain is steadily increasing whereas prevalence of smoking in the general population is declining [1]. Some work suggests that smokers with greater dependence on tobacco are more likely to experience chronic pain [2]. Importantly, the comorbidity between smoking and chronic pain is not attributable to sociodemographic factors [e.g., race/ethnicity, age; ³]. Research has also found that pain intensity, regardless of chronic pain status, is related to smoking rate [4–8].

Ditre and colleagues [9] have forwarded an influential integrative model of smoking-pain comorbidity. This and other similar theoretical models [10, 11] suggest that smoking and pain interplay in the manner of a positive feedback loop, resulting in greater pain and the maintenance of tobacco dependence [9]. Indeed, pain has been shown to be a motivator of smoking urge and behavior [12–14] and sensitivity to pain has been shown to predict smoking relapse [15]. Smokers with chronic pain also identify distraction from both physical pain and pain-related distress as a primary smoking motive [16, 17]. Not surprisingly, smokers with co-occurring pain report having greater difficulty quitting and being less confident in their ability to sustain abstinence [18, 19]. The close interconnectedness of smoking and chronic pain highlights the public health significance of the concurrent manifestation of these problems. Indeed, individuals suffering from chronic pain who smoke cigarettes are at heightened risk for a broad array of negative outcomes [e.g., non-tobacco substance misuse, mental health problems; ^20–23].

One central objective of continuing research should be to isolate factors that explain linkages between pain experience and multiple health problems among smokers with chronic pain. Opioid dependence and misuse, severity of tobacco problems (e.g., problems quitting), and anxiety/depressive symptoms may be of particular importance given these problems represent the most common substance use and mental health problems in the general population [24, 25].

A theoretically relevant construct to better understand the smoking-pain connection is anxiety sensitivity. Anxiety sensitivity refers to the extent to which individuals believe anxiety and anxiety-related sensations have harmful consequences [26]. Extant work has implicated anxiety sensitivity with both smoking and chronic pain [27]. For example, anxiety sensitivity has been linked to greater likelihood of smoking, greater cigarettes smoked per day, smoking relapse, and greater tobacco dependence [27]. As it relates to chronic pain, elevated anxiety sensitivity has been shown to contribute to an increased propensity to avoid activities that are believed to exacerbate pain [27]. The pattern of avoiding activities because of anticipatory pain is likely a learned behavior that develops from increased attention to and hypervigilance of physical and interoceptive experiences. Increased sensitivity to these experiences leads to an inaccurate attribution for these experiences as harmful, which reinforces the initial pattern of avoidance. As such, stressful events like more intense pain may contribute to the development of anxiety sensitivity by engaging a learning process that involves increased self-focused attention to bodily sensations and to physical and cognitive symptoms of anxiety and pain, as well as increased thought about the adverse consequences of those symptoms. Such cognitive processes may lead to the development of anxiety sensitivity.

Notably, extant research has not yet examined anxiety sensitivity as a mechanistic construct linking the experience of pain as it relates to severity of substance use and anxiety/depressive symptoms among smokers with chronic pain. Given that severity of substance use and mental health problems are consistently related to poorer treatment response and course of illness [28–30], there is clinical utility in evaluating such a model. For example, to the extent that anxiety sensitivity helps explain relations between the experience of pain with substance use and anxiety/depressive symptoms, there may be clinical utility in focusing efforts on informing the development of targeted interventions to offset the relative risk of more severe addictive and psychological problems. Conceptually, greater pain intensity among smokers with chronic pain may be related to greater anxiety sensitivity. Heightened reactivity to pain-based perturbation may be associated with greater tendency to use substances (including opioids and tobacco) to downregulate aversive symptoms. Such coping-oriented use would theoretically be linked to heightened risk for more severe substance use trajectories [e.g., greater dependence and risk of problems, such as inability to quit or cut down use; ³⁸]. Further, this same account could extend to negative emotional states, such as anxiety/depressive symptoms. That is, anxiety sensitivity may amplify the perceived threat meaning of pain symptoms and ability to regulate such symptoms [27]. With a lessened ability to control pain-related symptoms and cognition, risk for more severe anxiety/depressive symptoms may be elevated. Overall, this theoretical model posits a mediational role for anxiety sensitivity in the context of smoking and chronic pain for both substance use and anxiety/depressive symptoms.

The degree to which pain intensity, anxiety sensitivity, and severity of substance use and anxiety/depressive symptoms generalize to smokers with chronic pain remains uninvestigated. Indeed, we are not aware of any empirical studies that have explored the extent to which anxiety sensitivity is an explanatory mechanism in the context of pain experience for opioid misuse/dependence, tobacco use problems, and anxiety/depressive symptoms among smokers with chronic pain. Consequently, there is a need to explore whether pain intensity is related to these outcomes via anxiety sensitivity among smokers with chronic pain. Thus, the present study empirically evaluated anxiety sensitivity as an explanatory factor in the relation between pain intensity and opioid misuse/dependence, tobacco use problems, and anxiety/depressive symptoms among smokers with chronic pain (see Figure 1). It was hypothesized that greater levels of past-month pain intensity would be associated with greater opioid misuse and dependence, severity of tobacco use problems, and anxiety/depressive symptoms via greater anxiety sensitivity. We expected these relations to be apparent over and above variance accounted for by clinically significant covariates including age [32, 33] and sex [34–36].

Figure 1.

Note. a path = Effect of X on M; b path = Effect of M on Y; c paths = Total effect of X on Y; c’ path = Direct effect of X on Y controlling for M. A single path was conducted (Y), with the independent variable (X).

METHOD

Measures

Demographics Questionnaire.

The demographics questionnaire collected sociodemographic information, including sex, race, age, employment, and income.

Graded Chronic Pain Scale.

The Graded Chronic Pain Scale (GCPS) is an 8-item measure of self-reported pain severity and pain disability currently and over the past 3 months [37]. Pain severity items are rated on 10-point scale from 0 (no pain) to 10 (pain as bad as could be) while pain disability items are rated on a 10-point scale from 0 (no interference) to 10 (unable to carry on activities). Higher scores reflect greater pain severity and disability. Although, research suggests that pain-related disability is an important predictor of substance use, when accounting for pain intensity, pain intensity is the only variable of the two that has been shown to differentiate substance misusers from non-misusers [38]. Thus, only the GCPS pain intensity (α = .86) scale was used as an independent variable.

Anxiety Sensitivity Index-3.

The Anxiety Sensitivity Index-3 (ASI-3) is an 18-item self-report measure of sensitivity to and fear of anxiety-related symptoms and sensations [39]. Respondents indicate their level of concern about the possible negative consequences of anxiety-related symptoms and sensations on a 5-point scale from 0 (very little) to 4 (very much). Example items include “When I feel pain in my chest, I worry that I’m going to have a heart attack” or “When my stomach is upset, I worry that I might be seriously ill.” The ASI-3 total score was used as the mediator variable (α = .97).

Current Opioid Misuse Measure.

The Current Opioid Misuse Measure (COMM) is a 17-item questionnaire developed to detect opioid misuse among chronic pain patients on opioid therapy [40]. The items are rated on a 5-point scale from 0 (never) to 4 (very often) and are summed to yield a total score. Test-retest reliability has been established and construct validity was demonstrated via positive correlations with urine toxicology results [40, 41]. The COMM total score has been used as a criterion variable (α = .97).

Severity of Dependence Scale.

The Severity of Dependence Scale (SDS) is a 5-item measure of the level of dependence to substances (e.g., heroin, cocaine, amphetamine) and has also been validated for opioid use [42]. In the current study, responses were specifically anchored to problems associated specifically with opioid use, as has been done in prior research [43, 44]. Responses are rated on a 4-point scale from 0 (never) to 3 (always) and are summed to generate a total score [43]. The SDS total score was used as a criterion variable (α = .86).

Patient Health Questionnaire-4.

The Patient Health Questionnaire-4 (PHQ-4) is a 4-item self-report measure designed to assess symptoms of anxiety and depressive symptoms [45] and is rated on a 5-point Likert scale from 0 (not at all) to 4 (nearly every day). The PHQ-4 is comprised of the PHQ-2 for depressive symptoms (e.g., “Over the last 2 weeks, how often have you have you been bothered by feeling down, depressed or hopeless”) and the GAD-2 (e.g., “Over the last 2 weeks, how often have you have you been bothered by feeling nervous, anxious or on edge”) for anxiety [45, 46]. The PHQ-4 produces a composite anxiety/depressive symptoms score [47] and in the current study, the PHQ-4 total score was used as a criterion variable (α =.92).

The Alcohol, Smoking, and Substance Involvement Screening Test.

The Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST) is a 8-iem assessment for lifetime and current (i.e., past three month) use of common substances [e.g. tobacco, alcohol, cannabis, cocaine, stimulants, inhalants, sedatives, hallucinogens, and opioids; ⁵³]. Five items assess for related problems with each substance. Example items include, “During the past three months, how often have you had a strong desire or urge to use tobacco” and “Have you ever tried and failed to control, cut down or stop using tobacco.” For each substance, a risk score is derived by summing the responses to six questions (range = 0–39; WHO ASSIST Working Group, 2002). In the current study, the total score of the ASSIST tobacco problems subscale was calculated and used as a criterion variable (α = .56).

Procedure

Participants were recruited nationally through Qualtrics, an online open survey management system. Past research suggests that such survey management methodology yields valid and reliable data [49–52]. Adults with a Qualtrics Panels account that endorsed moderate to severe chronic pain and current use of opioid pain medication were sent a survey advertisement. Respondents were screened for eligibility and directed to the online anonymous survey. Qualtrics implements safeguards to prevent multiple attempts to complete the survey by the same respondent, including recording IP addresses and the ‘Prevent Ballot Box Stuffing’ option which places a cookie on the participant’s browser when they submit a response. Participants provided informed consent prior to completing the survey, which included information regarding the length of the survey (~30 minutes) and were informed that no identifying information would be collected. Participants entered data directly into the survey, and data were retained on the Qualtrics.com secure server. Additionally, to ensure reliability of the data, responses completed in less than half of the median response time were not included in the final dataset. Qualtrics provided a final dataset of only the complete participants, and therefore, it is not possible to comment on the number of participants removed due to these quality checks.

Participants could opt to receive their payment in varying forms (e.g., cash-based incentives [i.e., gift cards], rewards miles, rewards points, etc.). Although the forms were different, the level of compensation remained consistent across respondents. The study protocol was approved by the Institutional Review Board at a large Southwestern University.

Analytic Strategy

First, sample descriptive statistics and zero-order correlations among study variables were examined. Second, indirect effect analyses were conducted in SPSS version 25 using the PROCESS macro [53]. Specifically, anxiety sensitivity was examined as a mediator between pain intensity with substance use (ASSIST, SDS, and COMM) and anxiety/depressive symptoms (PHQ-4). Direct, total, and indirect effects are reported. The confidence intervals (CIs) for indirect effects were subjected to 10,000 bootstrap re-samplings and 95-percent CIs were estimated [54–56]. Statistical significance of the effects is supported if the CIs around their product do not include zero [56]. Completely standardized point estimates (CSE) were used as a measure of effect size for the current study. CSE is interpreted as small (.014), medium (.36), and large (.51) [57]. To test specificity of the models, reverse models (switching the independent and mediator variables) were run and effect sizes were compared between the original model and the reverse model [56]. All models controlled for age [32, 33] and sex [34–36].

RESULTS

Participants

Participants were 187 daily smokers (M_age = 39.02, SD = 9.94, 74.9% female) with moderate to severe chronic pain [often defined as pain lasting longer than standard healing time or greater than 3 months; ⁶³] who currently use prescribed opioids for pain management. Eligible participants were between the ages of 18–64 years, reported current moderate to severe chronic pain that persisted at least 3 months, endorsed current use of opioid pain medication, and reported current daily smoking [defined as self-reported “daily or almost daily” use of tobacco products for the past three months; ⁵³]. Participants were excluded if they were younger than 18 years, a non-English speaker (to ensure comprehension of the study questions), and were unable to provide informed, voluntary, written consent to participate. The current study is based on secondary analyses of data with previous publications [see ^{59, 60}].

Most participants were non-Hispanic/Latino White (82.9%), with 9.6% identifying as African American, 8.0% Hispanic/Latino, 4.3% Native American, 1.1% Asian, 2.1% multi-racial, and the remaining participants reported ‘other’ for their race/ethnicity. In terms of income, 35.8% reported earning less than $25,000, with 26.2% earning between $25,000 and $49,999, 19.3% earning between $50,000 and $74,999, and the remainder earning more than $75,000. About half (38.5%) were employed full time, 8.6% employed part time, 29.0% were either homemakers, students, retired, or unemployed, and 24.1% were not working due to disability. Participants reported an average pain level of 7.89/10 and indicated pain prevented participation in normal daily activities a mean of 8.2 (SD = 2.38) days out of the past 90 days.

Bivariate Correlations

See Table 1 for all bivariate correlations. The ASI-3 total score was significantly positively associated with all criterion variables, and pain intensity was significantly positively associated with substance use and anxiety/depressive symptoms.

Table 1.

Bivariate Correlations and Descriptive Statistics

	1.	2.	3.	4.	5.	6.	7.	Mean (SD)/% (n)
1. Age	-							39.02 (9.94)
2. Sex (female)	−.032	-						74.9% (140)
3. ASI-3 Total	−.230**	.102	-					33.48 (23.45)
4. Pain Intensity	.138	.004	.253**	-				7.89 (1.38)
5. COMM Total	−.283**	.199**	.698**	.316**	-			21.27 (19.53)
6. SDS Total	−.290**	.220**	.635**	.215**	.756**	-		5.14 (4.21)
7. PHQ-4 Total	−.174*	.112	.699**	.233**	.622**	.517**	-	4.58 (4.27)
8. ASSIST Tobacco	−.143	.055	.360**	.002	.372**	.325**	.326**	20.72 (6.55)

^*p<0.05,

^**p<0.01. ASI-3 Total – Anxiety Sensitivity Index – 3 Total Score [39]; Pain Intensity – GCPS Pain Intensity subscale [37]; COMM Total – Current Opioid Misuse Measure Total Score [40]; SDS Total – Severity of Opioid Dependence Scale Total Score [42]; PHQ-4 Total – Patient Health Questionnaire 4 Total [Anxiety/Depressive symptoms; ⁴⁷]; ASSIST Tobacco – Tobacco problems score [48].

Indirect Effect Analyses

Current Opioid Misuse.

In terms of COMM total scores, the total effect model was significant (F [3, 172] = 19.00, b = 1.76, SE = 0.32, p < .001, R² = .25). Further, there was a significant indirect effect of pain intensity, through ASI-3 total score, on the COMM total score (ab = 0.83, SE = 0.24, Bootstrapped 95% CI [0.39, 1.34], CSE = 0.17). There remained a significant direct effect of pain intensity on the COMM total score after controlling for ASI-3 (b = 0.93, SE = 0.26, p = .004).

Severity of Opioid Dependence.

For SDS total scores, the total effect model was significant (F[3, 172] = 14.06, b = 0.28, SE = 0.07, p = .001, R² = .20). Further, there was a significant indirect effect of pain intensity, through ASI-3 total score, on the SDS total score (ab = 0.17, SE = 0.05, Bootstrapped 95% CI [0.08, 0.26], CSE = 0.16). After controlling for the effect of ASI-3 total score, there was not a significant direct effect of pain intensity on the SDS total score (b = 0.11, SE = 0.06, p = .06.

Tobacco Problems.

Regarding ASSIST tobacco problems from pain intensity (including ASI-3 and covariates), the total effect model was not significant (F[3, 172] = 1.44, b = 0.09, SE = 0.12, p = .23, R² = 0.02). There was, however, a significant indirect effect of pain intensity, through ASI-3 total score, on ASSIST tobacco problems score (ab = 0.16, SE = 0.06, Bootstrapped 95% CI [0.07, 0.28], CSE = 0.11). After controlling for the effect of ASI-3 total score, there was not a significant direct effect of pain intensity on ASSIST tobacco problems score (b = −0.07, SE = 0.12, p = .52).

Anxiety/Depressive Symptoms.

For PHQ-4 total scores, the total effect model was significant (F[3, 172] = 7.95, b = 0.30, SE = 0.07, p = .001, R² = .12). Further, there was a significant indirect effect of pain intensity, through ASI-3 total score, on PHQ-4 total score (ab = 0.20, SE = 0.06, Bootstrapped 95% CI [0.10, 0.31], CSE = 0.19). After controlling for the effect of ASI-3 total score there was not a significant direct effect of pain intensity on PHQ-4 total score (b = 0.10, SE = 0.06, p = .10).

Specificity Analyses

Specificity analyses revealed a significant indirect effect of ASI3 total score, through pain intensity, on the COMM total score (ab = 0.05, SE = 0.02, Bootstrapped 95% CI [0.02, 0.09], CSE = 0.06) and SDS total score (ab = 0.01, SE = 0.003, Bootstrapped 95% CI [0.004, 0.01], CSE = 0.03). However, there were no significant indirect effects observed for ASSIST tobacco problems (ab = −0.004, SE = 0.001, Bootstrapped 95% CI [−0.02, 0.01], CSE = −0.01) or PHQ-4 total scores (ab = 0.01, SE = 0.004, Bootstrapped 95% CI [−0.001, 0.01], CSE = 0.03).

Discussion

Although there is a well-established comorbidity between smoking and chronic pain [11], few studies have explored constructs that explain linkages between the experience of pain and tobacco, opioid, and anxiety/depressive symptoms among this population. Therefore, the present study examined whether anxiety sensitivity explained, in part, the relation between pain intensity and opioid misuse/dependence, tobacco problems, and anxiety/depressive symptom severity among smokers with chronic pain.

In terms of opioid misuse and dependence, results were generally in line with prediction. Specifically, anxiety sensitivity significantly explained the relation between pain intensity and opioid misuse and dependence. Effect sizes can be characterized as moderate across the studied models. These results are consistent with the theoretical perspective that anxiety sensitivity may represent a transdiagnostic mechanism underlying the relation between the pain intensity and opioid misuse/dependence. Although indirect effects of the reverse models for opioid misuse and dependence were significant, thus supporting the notion of bi-directional relations, the magnitude of these effects were smaller in the tests of specificity than in the hypothesized models. For tobacco use problems, a similar pattern emerged, though there was no significant effect for the reverse model. Collectively, these results suggest that complex interrelations are apt to be at play in associations between pain intensity and opioid/tobacco use problems among smokers with chronic pain. Indeed, both pain experience (intensity) and anxiety sensitivity in the current data are involved in relations to opioid misuse and dependence as well as tobacco use problems. However, there may also be bi-directional relations between pain intensity and anxiety sensitivity for opioid misuse and dependence among smokers with chronic pain. Although the present tests were theoretically driven, there is a need to extend and corroborate these findings using prospective and laboratory-based research designs to isolate temporal ordering.

For anxiety/depressive symptoms, results were consistent with expectations. Specifically, anxiety sensitivity was found to explain relations between pain intensity and anxiety/depressive symptoms among smokers with chronic pain. The observed effect size can be characterized as medium in magnitude. These results indicate that anxiety sensitivity may, at least partially, explain relations between pain intensity and anxiety/depressive symptoms among the studied high-risk smoking sample. Specifically, among smokers with chronic pain taking prescribed opioid medication, more intense pain symptoms could be related to more fearful and aversive responding to such pain states, and such sensitivity could, in turn, be related to more severe anxiety/depressive symptomatology. This finding and conceptualization is in line with extant theories on pain-related beliefs (e.g., catastrophizing [61]), among chronic pain samples [62, 63]. Indeed, anxiety sensitivity may magnify the threat meaning of the pain experience and engender lower self-efficacy for coping with pain [27]. In the context of lessened ability to regulate or mitigate pain-related cognitions, there would likely be a greater risk for experiencing anxiety/depressive symptoms. Further, although the cross-sectional nature of our research design does not permit explication of temporal ordering, the alternative anxiety/depressive symptoms model was rejected. As such, significant indirect effects provide initial empirical evidence for anxiety sensitivity as an underlying factor between the experience of more intense pain and increased anxiety/depressive symptoms among smokers with chronic pain.

These and future results could have direct clinical implications for addressing substance use and anxiety/depressive symptoms among smokers with chronic pain. Indeed, to the extent to which anxiety sensitivity serves as a mechanism in the experience of pain with substance use and anxiety/depressive symptom trajectories, there may be merit to assessing and intervening on this construct in an effort to offset the relative risk for exacerbating comorbid substance use and anxiety/depressive symptoms. Given long-standing recognition that greater comorbidity is related to worse clinical outcomes for smoking [30, 64–66] and chronic pain [67, 68], improvements (i.e., reductions) in anxiety sensitivity may also lessen the severity of concurrent anxiety/depressive symptoms and addictive disorders in this vulnerable group of smokers. Indeed, anxiety sensitivity is as a malleable treatment target [69] and several evidenced-based psychosocial treatments have been found to reduce anxiety sensitivity in controlled trials [70–72]. Among smokers, reducing anxiety sensitivity has been shown to both improve smoking cessation outcomes [73, 74] and reduce the severity of mental health problems [75]. Drawing from such work, there may be clinical utility in adapting anxiety sensitivity reduction programs for smokers with chronic pain.

Several study limitations should be highlighted. First, the cross-sectional study design cannot address causal relations. As such, additional research is needed to replicate these findings using alternative designs. For example, by employing a laboratory-based paradigm that involved experimental manipulation of pain experience among smokers with chronic pain, it may be possible to illuminate the mediational effects of anxiety sensitivity on acute tobacco craving or acute severity of emotional distress. Second, given that the sample was mostly comprised of female participants, generalizability to male smokers with chronic pain remains unclear. Further, most of the sample was non-Latinx White. Future research would benefit from including smokers with chronic pain from more diverse racial/ethnic backgrounds. Third, although online data collection has been found to yield valid and reliable data [76], there are inherent potential biases to this method of sampling. It is possible, for instance, that certain persons (e.g., those without internet access) may be less likely to participate. Future research should employ complementary methods of data collection (e.g., recruitment from smoking or chronic pain clinics). Additionally, given that methods of data collection were based on self-report, bias in the assessment instruments could be operative. For this reason, future work should replicate and extend the present findings with multimethod protocols that can cross-index drug use behavior (e.g., via toxicology screens) and anxiety/depressive symptoms (e.g., via structured clinical interview). Fourth, internal consistency for the ASSIST was low (α = .56). Thus, future studies should employ alternative measurement approaches that may yield higher reliability to further validate the proposed models. Fifth, by design, we focused the present investigation on anxiety sensitivity as explanatory construct. However, it is possible that other constructs may also serve explanatory roles. For example, distress tolerance [77], pain-related anxiety [78], and pain-specific catastrophic thinking [27] are all theoretically relevant factors that could be explored in future research. In such pursuits, it may be advisable to utilize a multi-mediation model wherein the general and specific variance explained by such individual difference factors could be contextualized. Finally, although we assessed chronic pain status and severity of pain, we did not assess the source or location of pain (e.g., low back pain, migraine). Therefore, there is a need for future research to examine the relative generalizability of the current model to specific chronic pain conditions.

Overall, the current investigation highlights the potential importance of anxiety sensitivity in terms of the experience of pain with severity of substance use and anxiety/depressive symptoms among smokers with chronic pain. These data build systematically from previous research on anxiety sensitivity among non-smokers with chronic pain that largely focused on the main effects of this construct in terms of the severity of pain symptoms [79]. Future research is needed to explore the present model using longitudinal research methodology to refine theoretical models of smoking-chronic pain comorbidity and their clinical correlates.

Informed consent:

Informed consent was obtained from all individual participants included in the study