Pack-Years of Tobacco Cigarette Smoking as a Predictor of Spontaneous Pain Reporting and Experimental Pain Reactivity

The pack-years formula is a widely used estimate of lifetime tobacco smoking exposure, and greater pack-years have been associated with greater risk of chronic pain development and poorer pain-related outcomes among smokers with chronic pain. The pathophysiology underlying these associations is poorly understood. Regular tobacco smoking exposure may dysregulate homeostatic pain processes, producing an allostatic state of pain facilitation. Maladaptive pain mechanisms, such as central and peripheral sensitization, are chronic pain risk factors. Yet no published research has examined the relation between lifetime-smoking exposure and dysregulated pain processing. The current study used hierarchical linear regression analyses to test pack-years of tobacco smoking as a predictor of (a) pain reporting (current pain severity, pain frequency in the last 180 days) among a sample of 228 daily smokers without chronic pain, and (b) experimental capsaicin-induced pain reactivity (pain intensity, area of flare, mechanical pain sensitivity, and area of mechanical hyperalgesia) among 101 daily smokers without chronic pain. As hypothesized, results indicated that pack-years smoking was positively and significantly associated with current pain severity, past 180-day pain frequency, experimental pain intensity, mechanical pain sensitivity ratings, and area of mechanical hyperalgesia. Pack-years smoking was not significantly associated with neurogenic flare. These findings implicate central sensitization as a factor that may underlie the association between chronic tobacco smoking and increased risk for persistent pain. Public Health Significance This study showed that pack-years of tobacco smoking was positively and significantly associated with current pain severity, past 180-day pain frequency, experimental pain intensity, and mechanical hyperalgesia. The current study provides preliminary evidence of dysregulated pain processing as a function of smoking exposure among a nonpain sample. Prevention and intervention approaches that target maladaptive pain processes in smokers may reduce the risk for chronic pain development.