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11 Articles in Volume 6, Issue #4
Assessing Secondary Gain In Chronic Pain Patients
Chronic Overuse Sports Injuries
Introducing Low Level Laser Therapy to Pain Management
Managing Diabetic Peripheral Neuropathic Pain (DPNP)
Moral Virtue and the Pain Physician
Non-pharmacologic Therapy for Chronic Opioid-dependent Sickle Cell Pain
Osteoarthritis of the Knee
Smoking and Low Back Pain
Temporal Tendinitis Migraine Mimic
The Underutilization of Intrathecal Treatment
Tumblin’ Dice–Why Does Random Matter?

Smoking and Low Back Pain

A review of research findings regarding the relationship of smoking and low back pain.

The purpose of this article is to provide an update on the evidence, or the lack of, that exists between low back pain and cigarette smoking. This relationship has been researched and studied extensively within the past 25 years. Several and extensive reviews on this subject, many of which are described in this article, proved inconclusive. Despite these studies, there seems to be an overwhelming agreement that all researchers, as well and many clinicians, feel that there is an association between cigarette smoking and back pain. Proving this link, however, is not as simple as making that assumption.

Review of Pertinent Articles

In order to assess the association between cigarette smoking and the development of nonspecific back pain and related outcomes, Goldberg et al. reviewed 38 epidemiological studies published between 1976 and 1997 in peer-reviewed journals. This review included twelve population-based cross-sectional studies, four occupational cross-sectional studies, five prospective- general population and work place studies, three population studies, seven occupational studies combining cross-sectional and prospective follow-up studies, three case control studies, two retrospective cohort studies in the general population, one workplace study, and one retrospective cohort and cross-sectional general population study. They found positive associations between current smoking and nonspecific back pain in 18 of 28 studies in men, and 18 of 20 studies in women. For sciatica and herniated discs, there were four of eight studies for men and one of five studies for women where positive associations were found.

However, a majority of these studies were cross-sectional (18 in men and 16 in women) with only a few prospective studies (five of nine studies on men and five of six studies on women) making causal inferences problematic. The authors concluded that the research studies that were reviewed through 1997 supported the notion that smoking is associated with the incidence and prevalence of nonspecific back pain, but the evidence was too scarce to reach any conclusion regarding smoking and back pain with specific diagnoses such as sciatica and herniated discs. Furthermore, the possibility that this perceived association is an artifact arising from either selection bias or confounding factors cannot be ruled out due to the cross-sectional nature of the research.

A separate systematic and independent review by Leboeuf-Yde2 included forty-one original research reports that included 47 studies, published between 1974 and 1996. This review was undertaken to assess whether smoking causes low back pain and whether cessation of smoking reduces the incidence and/or prevalence of low back pain. The findings were disappointing in that there was no consistency of statistically significant positive associations found between smoking and low back pain.

The author pointed out that, when present, the association was usually weak and was found only in studies using very large samples. When restricting the analysis to studies with large sample size, no consistent findings were found in relation to dose-response, temporality, or reversibility. Evidence of possible causality was present only in the study with the largest sample size (N> 30,000). The author concluded that smoking should be considered a weak risk factor and not a cause of low back pain.

“...there is the hint of a link between cigarette smoking and back pain. While the link may be causal, it is safer to state that abstinence from smoking may be a useful means of primary prevention of certain types of low back pain.”15

In a separate study, Leboeuf-Yde and Yashin3 identified research that challenged their initial findings with additional “test factors” using multivariate analysis. Twenty-four publications, reporting on 126 epidemiological studies, were located and systematically reviewed by the two authors independently and jointly. The authors concluded that, of the thirteen studies that had found a preliminary positive association, the association remained in only eight of them after multivariate analysis was performed. The authors suggested that, due to their unique presence in the studies where the initial positive association was lost, marital status and occupation should be further investigated.

One study did investigate the possible confounding effect of occupation on the relationship between smoking and low back pain.4 Thirteen occupations were studied in regard to this relationship. The results indicated that smoking and low back pain were significantly correlated only in occupations that require physical exertion. Interestingly, pain in the extremities was more clearly related to smoking than low back pain. The study concluded that smoking may have a general influence on pain but a clear association between smoking and low back pain was not evident. Furthermore, the study indicated that other extraneous factors such as occupation could confound the relationship between smoking and low back pain.

In order to study causal link between smoking and back pain, one has to identify and rule out the effects of extraneous variables that could influence this relationship. This is extremely difficult to do since multiple factors could influence the experience of pain and smoking behavior. One way to get around this is to utilize, as subjects, monozygotic (identical) twins. They are genetically identical and usually have identical upbringing. One such study involved the Danish Twin Register that contains 20,888 twin pairs.5 Results indicated an association between smoking and low back pain that was found to be stronger for low back pain of longer duration. However, there was no dose-response correlation and smokers of smaller stature were not more susceptible to back pain. Furthermore, the study found no evidence linking smoking cessation with lower prevalence of this pain. The authors concluded that smoking is associated with the report of nonspecific low back pain and, in particular, recurrent low back pain or low back pain of long duration but that the relationship is unlikely to be causal.

A major criticism of the literature on smoking and spinal pain has been the cross-sectional design used in a majority of these studies. A recent prospective study has been completed in Canada in which 502 high school students were followed for one and one half years and assessed at six month intervals.6 The primary outcome for low back pain was defined as “low back pain occurrence at a frequency of at least once a week within the past six months.” Secondary outcomes included medication use for pain and disability. The results indicated that low back pain is prevalent among adolescents, with a cumulative annual incidence of 17%. Risk factors associated with the development of this pain in adolescents were a high growth spurt, poor quadriceps and hamstrings, working during school year, and smoking. The authors concluded that smokers were more likely to develop low back pain, at least among the adolescents studied.

Potential Mechanism of Action

It is not surprising that given the inconsistent findings on the relationship between smoking and low back pain, there has not been a well-accepted mechanism of action, to date. While recent literature has revealed cigarettes contain multiple chemical ingredients, much of the research on mechanism has focused on the role of nicotine. For instance, coronary endothelium has been identified as the major site of abnormal vasomotor response in long-term smokers.7 Smoking is associated with impaired endothelium-dependent dilatation in human arteries and veins. In particular, acute local exposure to nicotine in vivo is associated with an impaired response to endothelium-derived nitric oxide in human veins.8 The endothelium is involved in the control of vascular tone and homeostasis.9 Cigarette smoking causes vasoconstriction, an increase in coronary vascular resistance, and a decrease in coronary blood flow despite an increase in myocardial oxygen demand. Cigarette smoking also induces diffuse or segmental coronary artery spasm.10

The relationship between smoking and the adrenergic nervous system has been of interest to many researchers. The acute rise in blood pressure and heart rate that accompanies smoking is associated with a rise in plasma catecholamines believed to be the result of the stimulation of the adrenergic system. Taking this a step further, Grassi, et al11 were able to show that peripheral (adrenal gland stimulation, reduction in norepinephrine uptake, reduction in catecholamines clearance, etc); rather than central mechanisms; explain the adrenergic involvement in the acute homodynamic effect of smoking. The central sympathetic drive was inhibited rather than excited due to baro-receptor stimulation. Other research has confirmed the finding that nicotine stimulates catecholamines release via the activation of nicotine acetylcholine receptors localized on peripheral post-ganglionic sympathetic nerve endings and the adrenal medulla.12 The effect of cigarette smoke on passive smokers has been shown to have the same acetylcholine-induced coronary artery dilation, in other words, coronary endothelial dysfunction.13

While the toxic effects of smoking on health have been well researched and the understanding about the mechanism behind smoking and addiction has significantly increased in the last decade,14 the mechanisms behind smoking and low back pain have remained largely unknown. The obstacle is that it is difficult to conduct a prospective study utilizing an experimental design whereby cause and effect can be established.

From the above summary and the studies cited there is the hint of a link between cigarette smoking and back pain. While the link may be causal, it is safer to state that abstinence from smoking may be a useful means of primary prevention of certain types of low back pain.15

More recent studies16 emphasized the negative impact of nicotine on revascularization of damaged tissue, including that of the back. Their study revealed that the percentage of males smoking increased as the smoking level increased. Also, the level of smoking increased as the level of education decreased, and the percentage of patients completing rehabilitation programs decreased. In an another study led by Vogt MT, et al,17 this multi-center, cross-sectional analysis concluded that, among the approximately 25,000 patients studied, smokers and nonsmokers had symptoms of similar duration but the smokers reported more severe symptoms and which lasted longer. Also the smokers had lower physical and mental health status scores, based on the SF-36, than did the nonsmokers.

In 2001, a study out of Finland by Fogelholm RR and Alho AV18 had a very interesting study that shed light on the ‘molecular’ effects of cigarette smoking. The study concluded that cigarette smokers have an increased risk of low back pain that may be caused by disc degeneration and spinal instability. Ischemia, apoptosis, faulty synthesis of disc macromolecules, and an imbalance between disc matrix proteinases and their inhibitors may be involved in the pathogenesis of disc degeneration. There was some evidence that disc degeneration of smokers is more severe than that of non-smokers. The authors hypothesized that the high serum proteolytic activity of cigarette-smokers gets access to a previously degenerated neovascularized disc and speeds up the degenerative process. The increased proteolytic activity may also weaken the spinal ligaments and indirectly result in spinal instability.

Possible Links

Traditional wisdom would dictate that controlled experimental design and the “double blind control” types of research are necessary for establishing a mechanism of action. When such studies are difficult, if not impossible to conduct, the authors would suggest that clinical experience, in addition to the published data, could be a rich source for developing hypotheses about the mechanism of action.

Since there has not been, to the authors’ knowledge, a unified theory about the mechanism(s) of action behind smoking and low back pain, a hypothesis is presented as follows and is consistent with the present evidence. Clinical practitioners, in particular, are reminded that these are only postulated theories and are not, by any means, interpretation of causality:

  • Nicotine increases flow of catecholamines.
  • Catecholamines cause muscle spasm which is translated, in part, to pain.
  • Catecholamines also cause vasoconstriction.
  • Vasoconstriction (on a continuous basis) may lead to decreased blood supply in the back structures which results in “angina-like” pain.
  • Nicotine decreases the healing process of the back, especially an injured one or one with predisposing factors (e.g. Scoliosis).
  • Nicotine increases de-conditioning and worsening of health that leads to decreased activity and exercise, and resulting muscle disuse.
  • Nicotine, as a centrally-acting neurotransmitter, may interfere with the medications used to treat low back pain (e.g., CNS depressants like opioids, narcotics, muscle relaxants, benzodiazapines).
  • Nicotine possibly heightens the perception of pain as evidenced by reported higher pain scores.
  • Degenerative joint disease is more common in smokers than non-smokers, possibly due to higher proteolytic activities.
  • Smoking may induce chronic cough. This, in turn, can increase the intra-epidural pressure and cause worsening of disc herniations and ligament sub-laxity and instability, thereby contributing to back and radicular pain.


It is important to note that the evidence, if any, associating cigarette smoking with cases of mechanical back pain may differ from that of back pain with radicular leg pain. Ironically, these differences, as we reviewed the data published thus far, seem to be overlooked and back pain (radicular or non) is somewhat used interchangeably, except in a few articles. Although a great deal has been accomplished in researching the link between smoking and low back pain, much research still needs to be done in this field. The authors suggest a prospective study that would be expected to yield the strongest results and eliminate any bias. n


The intention of this article is only to highlight the scientific and clinical findings that were researched and observed clinically and should not be misconstrued as a negative depiction of smoking or smokers.

Last updated on: December 28, 2011
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