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Despite the observation that select nicotine receptor agonists have analgesic effects, smokers report higher pain scores and more functional impairments than lifelong nonsmokers, attributable to exaggerated stress responses, receptor desensitization, and altered pharmacokinetics compounded by accelerated structural damage resulting from impaired bone healing, osteoporosis, and advancement of disk disease. We hypothesized that smoking diminishes the analgesic response to spinal cord stimulation (SCS) in patients with chronic spine–related pain conditions.A retrospective cohort study was performed at Cleveland Clinic by collecting and assessing data of 213 patients who had been implanted with SCS for spine-pain indications. History of tobacco smoking was subcategorized into 3 categories: past (former smoker), present (current smoker), or those who had never previously smoked (lifelong nonsmokers), and a multivariable linear regression was run to measure the correlation, if any, between smoking status and numerical rating scale pain score. In addition, opioid consumption at baseline and 12-month follow-up, expressed in milligram oral morphine equivalents, was collected and compared.Adjusted for differences, at 1-year follow-up, current smokers (n = 62) reported numerical rating scale pain score of 7.0, which is 1.93 (P < 0.001) and 1.32 (P = 0.001) points higher than those of lifelong nonsmokers (n = 77) and former smokers (n = 74), respectively. Opioid intake was 2.4 times higher (P = 0.004) in smokers than in lifelong nonsmokers.Among our SCS-implanted sample, a positive correlation was observed between tobacco use and degree of pain reduction as early as 12 months postimplant; this was evident by the reported higher pain scores and opioid use in current smokers in comparison with former smokers and lifelong nonsmokers.