|Year : 2014 | Volume
| Issue : 2 | Page : 34-39
Smoking and chronic pain
Joel D' Silva, Sumana Devadiga, Prasanna Kumar Dengody, Mahabaleshwar Chalathadka, Mimansa Bhoj, Vaibhav Jain
Department of Oral and Maxillofacial Surgery, Kurunji Venkataramana Gowda Dental College and Hospital, Karnataka, India
|Date of Web Publication||4-Feb-2015|
Joel D' Silva
Department of Oral and Maxillofacial Surgery, KVG Dental College and Hospital, Sullia, Dakshina Kannada, Karnataka
Source of Support: None, Conflict of Interest: None
Smoking has become a trend among individuals nowadays and, thus a major health problem. Since a long time, smoking has been associated with problems like vascular stenosis, lung cancer, heart attack, and chronic obstructive pulmonary disease. Experiments have shown that nicotine released by cigarette smoking has analgesic property. However, along with this, studies have also shown it to be a factor that causes musculoskeletal problems. Therefore, it becomes a matter of scientific concern. This review article will discuss about how smoking induces both acute and chronic pain. Also, it will enlighten us about the pharmacology and pathophysiology behind smoking-induced pain. Quitting smoking reverses or prevents most of its harmful effects. Therefore, smoking cessation plays an important role. We will also discuss about the various steps taken to help smokers quit the habit.
Keywords: Musculoskeletal, nicotine, pain, tobacco
|How to cite this article:|
D' Silva J, Devadiga S, Dengody PK, Chalathadka M, Bhoj M, Jain V. Smoking and chronic pain. J Health Res Rev 2014;1:34-9
|How to cite this URL:|
D' Silva J, Devadiga S, Dengody PK, Chalathadka M, Bhoj M, Jain V. Smoking and chronic pain. J Health Res Rev [serial online] 2014 [cited 2020 Sep 25];1:34-9. Available from: http://www.jhrr.org/text.asp?2014/1/2/34/150794
| Introduction|| |
Smoking is a major public health problem. Cigarette smoking delivers nicotine in humans and has been found to cause profound changes in the physiological architecture. Mortality due to the habit of smoking is high, and death happens as a result of cancers, breathing problems, strokes, etc. It even causes disabilities, pain, and makes the smokers prone to many diseases. Pain is one thing which significantly interferes with the quality of life, as it affects the physical as well as mental status of an individual.  One of the major health problems is the musculoskeletal complaints. Its prevalence rate seems to be increasing and it poses an economic burden to the society.  This review article focuses on pain perception, both acute and chronic pain, in smoking. and also explains the mechanism to understand the association between smoking and pain.
Chronic pain is one of the major challenging health concerns faced in day-to-day life. Before looking into the effects of acute and chronic exposure to nicotine in cigarette smoke in acute and chronic painful conditions, one should know the relevant pharmacology of nicotine and other ligands at nicotine acetylcholine receptor (nAChR). This is important to know the mechanics as well as for identifying the potential targets for the management of smoking-associated pain, as well as important in the development of drugs. 
| Pharmacology Of nAhR|| |
Nicotinic receptors are of two types: Nm and Nn. Nm is located in the neuromuscular junction, which causes the contraction of skeletal muscles by way of end-plate potentials (EPPs). Nn causes depolarization in autonomic ganglia, resulting in post-ganglionic impulse. Nicotinic receptors cause the release of catecholamine from the adrenal medulla and also site-specific excitation or inhibition in brain. Both Nm and Nn are Na+ and k+ channel linked, but Nn is also linked with Ca++ channel.
Nicotine affects through nAChR, which is a pentameric complex of transmembrane protein that has a central pore permeable to sodium, calcium, and potassium ions.  The structure of nAChR is different in adult and fetus muscle. For adults, it is (α1) 2β1δε and for fetus, it is (α1) 2β1δγ.  Neuronal nAChRs have different combinations of α(α2-α10) and for nonα, it is β2-β4.  Ach binds at the interface between α subunit and the neighboring subunit, and thus, binding with nAChRs depends on their subunit composition.
These nAChRs are widely distributed in the central and peripheral nervous systems. Homomeric receptor α7 and heteromeric α4β2 are mainly present in the central nervous system.  This α4β2 receptor has two binding sites for agonist and competitive antagonist and α7 nAChRs have five binding sites. , In the dorsal horn of the spinal cord, thalamus, and other brain regions, α4β2 receptors are present that are associated with nociceptive transmission and modulation. , Similarly, in the dorsal root ganglia, leukocyte, vestibular and cochlear mechanosensory hair cells, and other tissues, α9α10 nAChR is present. 
Direct excitatory neuronal effects are produced by activation of post-synaptic nAChRs via cationic channels. Activation of presynaptic nAChR causes release of neurotransmitters like dopamine, glutamate, serotonin, histamine, and norepinephrine. Thus, the effect of nicotine and other nAChR ligands is produced by the released neurotransmitter. , Multiple ligands and modulators such as neurosteroid, local anesthetic, phencyclidine, and MK801 are responsible for neuronal nAChRs.  In relevant doses, inhibitors for α4β2 and α3β4 are volatile anesthetic and ketamine. The pharmacological action is complex as the nAChR subunits have varying selectivity. Along with this, kinetic of nAChR channel opening also varies. With a high concentration and short exposure of Ach, there is fast opening of nAChRs, while prolonged and chronic exposure leads to closed and desensitized state.  Change in receptor number or function can also occur during prolonged exposure. Animal experiments have shown twofold increase in nAChR due to prolonged exposure of low-level nicotine which is similar to what is seen in chronic smokers. , When compared in smokers and non-smokers, positron emission tomography showed greater densities of high-affinity AChRs in the brain. These aspects of nAChR pharmacology are important for understanding the mechanics as well as for designing definitive management measures and drug therapy. 
| An overview of the literatures|| |
Tobacco smoking causes dependence and the reason behind this is the chemical agent in the cigarette, known as nicotine. During smoking, numerous chemical agents are produced, but the addictive agent is nicotine alone. During smoking, nicotine is quickly absorbed into the blood stream and within a time gap of 30 s, it reaches the brain. It stimulates the brain to release various chemicals, namely epinephrine, which gives a pleasurable euphoric effect.  This effect is short-lived and fades away, but crave for the pleasure that has been felt remains and this explains the addiction to cigarette smoking. It should be kept in mind that many of the studies regarding chronic pain and smoking found that smoking rates are higher in certain population than others, and moreover, researchers are categorizing the patients as smokers and non-smokers in pain-related complaints. 
Brage and Bjerkedal were among the first researchers who did a study on smoking and its relation to pain in Norway. They conducted a study on 6681 smokers and reported the subjects to be suffering from musculoskeletal pain, especially in the neck, back, and upper limbs.  Population-based studies showed that current smokers as well as former heavy smokers reported a much higher pain intensity than non-smokers.  Many studies have been conducted in the US on this; a survey has found that one in five Americans smoke and around 20.6% of the American adult population consists of current smokers and various pain studies have quoted the smoking rates to be high in the group. 
It is a proven fact that smoking of tobacco causes the production of rheumatoid factors or anti-cyclic citrullinated peptide autoantibodies (anti-CCP Abs), which is a risk factor for the development of rheumatoid arthritis.  But looking into the literature reports and the studies conducted worldwide, the results obtained are debatable and the cause for the uncertainty is lack of clear-cut causal mechanism to prove the relation.  Numerous hypotheses have been put forward to discover the relation of smoking and chronic pain, but it is a challenging to prove and disprove these hypotheses because the data which exist are cross sectional and, also, there are many factors which precipitate the pain. So, it is challenging to point out the causal relation until and unless it is particularly strong. 
Tobacco is used in various forms other than smoking, such as chewable and snuff forms, and no relation with pain was found in individuals using these forms of tobacco, but a relation was found in individuals who were past smokers. But the study failed to state the time period for which the users had given up the habit.  Considering confounding factors such as socioeconomic status, psychological factors, as well as the lifestyle and nature of the occupation, they do play a role in tobacco smoking. Among smokers, those with an occupation that involved standing for long and lifting heavy loads were predicted to have back pain within 4 years, whereas it was not predictable among non-smokers; it came out to be true for other confounding factors as well. It was also well proven that individuals with low educational status were more likely to present with the complaint of low back pain. ,,,
A population-based cohort study conducted by Kvalheim et al. showed 20% increased risk for chronic musculoskeletal disorders. This was especially evident in those individuals who were more than 50 years of age. The study had sufficient sample size to be statistically sound. The authors suggested that as smoking is a modifiable risk factor in musculoskeletal pain, it has to be considered in the health intervention programs, although they pointed out that the effect of age-dependant smoking on musculoskeletal pain is not obvious. Many epidemiological studies have shown a positive relation between smoking and chronic musculoskeletal pain, but only a few studies have been conducted taking age as a factor and showing the interaction.  However, a meta-analysis conducted among young individuals showed a stronger association between smoking and chronic low back pain. This study stated that adolescents are more vulnerable to the effects of smoking than adults. The explanation given is that chronic musculoskeletal pain is less tolerated by young individuals and tobacco smoke containing nicotine, which has antinociceptive property, acts as a pain modulator, thereby relieving the individual from stress. In these individuals, smoking is continued due to its stress relieving effect, and they rarely give up the habit. ,
In addition to the relation of smoking and pain, studies conducted have proved that smokers have comparatively more number of painful sites in addition to the increased pain intensity.  There is a positive relation between smoking and depression  and it has been observed that smokers use more number of cigarettes when they are depressed. Smoking also makes the individual who is depressed more prone to pain than a normal smoker.  A study has been conducted taking into account the multivariate association of smoking with depression as well as pain. This study showed a positive relation of smoking and pain, but this association weakened when controlling for depression. A study conducted among adolescent smokers found that daily smoking affected multiple aspects of somatic and psychological health. Psychological health is a known factor influencing the musculoskeletal disorders, so this study reported that smoking, through its indirect effect on the psychological health status, results in chronic musculoskeletal painful condition. ,,, This throws light into the interlinking factor, depression.  Testimonials of smokers reveal that smoking elevates their mood and it has been considered as a self-medication by them for depression.  The study data draws us to the conclusion that in outpatient clinics, patients presenting with chronic pain were high in number and so also the smoking rates. Patients who smoked presented with the most severe painful condition. Taking depression as a major factor helps up to draw a better conclusion in the relation of pain and smoking. 
An overview of the literatures in relation to cigarette smoking and pain showed that there was no statistical difference in the number of cigarettes smoked per day and pain, and therefore, this study signifies that for prevention of musculoskeletal pain, one should stop smoking and reducing the number of cigarettes per day will not have any effect.  Cigarette smoking is habitual because of the cognitive effect of nicotine in the tobacco smoke. It has been documented in literatures that longer the duration of quitting smoking, lesser will be the severity of pain, but more studies have to be conducted to prove this statement.  A result of a cohort study conducted showed that students of age approximately14 years who smoked had a high risk of low back pain. A longitudinal study conducted among the blue collar workers in Finland concluded that smoking is a predictive factor for musculoskeletal pain and also cessation of smoking leads to relief from musculoskeletal pain symptoms. 
Smoking does not only aggravate chronic back pain, but also pain in shoulders, hands, neck, elbows, and knees. A study focused on the orofacial pain in relation to smoking, and it reported that there is an increased incidence of temporomandibular joint (TMJ) pain in smokers than in other individuals. The physiology behind this is that nicotine gets accumulated in the body during the day hours and decreases once the individual rests; so, the action of nicotine in the ACh receptors can enhance glutamatergic synaptic transmission which will result in increased dopamine release, and this is followed by increased nicotine concentration in turn followed by increased dopamine release, and this relates to the increased oromotor activity.  Looking into the clinical aspect, it was found that after third molar surgery, individuals who smoked more than 10 cigarettes a day required higher dosage of pain killers, when compared with non-smokers. 
Although controversial, smoking is said to be a major factor in the risk of getting macrovascular diseases such as diabetes mellitus and is also associated with macroproteinuric neuropathy in insulin-dependent diabetes mellitus individuals.  It has also been reported in literature that tobacco use is associated with an increased incidence of tooth ache as well as other oral soft tissue pain and the impact of pain reduces after the cessation of the tobacco habits.  Scot et al. did a comparative study on smoking and low back pain in adolescent idiopathic scoliosis (AIS) group and a control group; they found a closer association with the AIS group. Eriksen et al. conducted a study and the result showed that the odds ratio was higher in heavy physical workers who were smokers than in non-smokers. These studies draw us to a conclusion that smoking acts as a modifying factor in people having damaged spine, as well as in people with heavy workloads, which causes increased damage and thereby aggravates the pain. 
An association of smoking and chronic pain and its relation to the poor socioeconomic status as well as psychosocial status has been described. It is seen that people of low socioeconomic status as well as people affected with heir psychosocial status like low education, divorced individual, unemployment, and so on are not able to cope up with their pain symptoms that, in turn, contributes to chronic pain. 
A reasonable question comes to our mind whether a former smoker will have the same effect as a current smoker or will he have the benefit of a non-smoker. Epidemiological studies conducted have shown differences between a former smoker and a non-smoker in relation to pain, and former smokers were found to have pain of comparatively more severity than non-smokers.  But many other studies reported that the former smokers had the same pain intensity and differences between them were negligible.  This knowledge is an important factor for the management of pain in the smoking population and necessary measures should be taken to make the individual quit the habit as it may have positive impact on outcomes. Specific outcome results cannot be drawn because little attention has been given for habit cessation in the management of chronic pain in the smoking population on an outpatient basis. Point conclusions cannot be drawn because of ineffective measures and reported low cessation rates during the management.  More experimental studies are needed to draw valuable data and clear the path for designing management measures.
With regard to gender factor, literatures report that ladies who are chronic users of tobacco experience more pain than men, but this statement lacks a definitive backbone.  But post gynecological surgery in females, it was found that more opioid was needed for the pain management in smokers when compared to never smokers.  A positive relation was derived in a study conducted among twins and it was concluded in the study that there was no gross difference in back pain in monozygotic twins in which one was a smoker and the other was not.  In another study between monozygotic twins where one smoked and the other did not, it was found that the bone density of the individual who smoked was less compared to the other, again supporting the pathology behind smoking.  In a study regarding rheumatoid arthritis and its relation to smoke, it was found out that the response rate of the therapy and severity of pain were more in people who were more exposed to smoking.  Similarly, it was observed in a study that there is high pain severity as well as more depressive symptoms in the smokers as compared to non-smokers, and this makes it a challenging task for the management of pain in these individuals. 
A multi-disciplinary pain rehabilitation program was conducted for 3 weeks by Hooten et al. It was an observational study and the results are of great concern in the management of pain in chronic smokers. Smokers had severe pain and functional impairment as compared to the never smokers group. The treatment program also included various efforts in order to taper the opioid dosage in individuals who showed opioid dependency. Results obtained at the end of study were surprising. Nearly all the participants of the study discontinued opioid use. The treatment outcomes were similar or improved in smokers. The study shows that successful cognitive behavioral therapy and rehabilitation for pain is not dependant on the smoking status. 
| Possible pathology behind the relation|| |
Nicotine has analgesic property, but it is found that chronic smokers are associated with chronic pain.  This fact seems surprising and the possible reasons [Figure 1] for this relation are described below
- In a normal individual, the psychological stress is anticipated by the sympathetic system and the hypothalamic-pituitary-adrenal (HPA) axis, but in smokers, this HPA system is suppressed 
- Smoking causes degenerative changes in the body like osteoporosis lumbar disc diseases and also impairs bone healing. These factors make the smokers prone to injury as well as compromised healing, and this leads to chronic pain. The tissues get hypoxic due to the impaired oxygen perfusion caused by increased sympathetic outflow as well as increased carboxyhemoglobin levels 
- Psychological factors have also shown a positive relation. Smokers are found to have high rates of psychological disturbances like depression and anxiety than non-smokers and these mood variations are associated with more chronic pain. The exact relation of smoking, depression, and chronic pain is complex and not yet understood completely. But it has been said in literatures that pain and depression are thought to have a common neurophysiological pathway, hence depressed smokers can experience more pain due to this interaction 
- Smoking leads to reduced perfusion to the spine tissue, thereby causing tissue anoxia and malnutrition of the spinal tissues, making it more prone to any mechanical injury during stress. So, any stress in physical form will induce more injury to the tissues as compared to normal tissues. Reason behind this is that the catecholamine released and other toxic chemical products produced during smoking, such as cadmium, nicotine, cyanide, and carbon monoxide, reduce the blood flow ,
- Increase in the viscosity of the blood due to the induced erythropoiesis by increased carboxyhemoglobin and long-term inhibition of prostaglandin E2 production by nicotine 
- Among the patients taking opioid analgesics for chronic pain, smokers were found to take high doses than non-smokers and yet, pain was not relieved. The reason behind this is that the polycyclic aromatic hydrocarbons in the tobacco smoke induce P450 enzymes involved in morphine metabolism, thereby reducing the bio-availability of the drug 
- Although nicotine has antinociceptive action, once deprived, it will result in easy perception of pain and reduced tolerance to pain
- Nicotine can increase the concentration of calcium ions which will result in muscle contractions, thus causing fatigue and pain 
- Smoking causes reduction in the bone density and also reduction of blood supply to the vertebrae, which makes them prone to injury as well as pain. The mechanism behind this is carboxyhemoglobin formation, vasoconstriction, arthrosclerosis, and hematological impairment. 
| Smoking cessation approaches|| |
Quitting smoking is quite difficult because of unpleasant withdrawal syndrome that consists of frustration, depression, anxiety, reduced heart rate, increased weight, depressed mood, and difficulty in concentration. Because of all these withdrawal symptoms, individuals who try to quit start up again very soon. 
Clinical practice guidelines for treating tobacco use and dependence were released by the US public health services in 2000. The guidelines briefed about the techniques for quitting cigarette smoking. It was found that for people who are willing to quit the habit, counseling and medications are helpful and this approach has produced efficient results.  There are specific FDA approved medications for smoking cessation [Table 1].
|Table 1: FDA-approved medication for smoking cessation (smoke cessation)|
Click here to view
It has been reported that currently of the adult cigarette smokers in the US, 68.8% individuals want to quit the habit completely. Most of the smokers can quit the habit without using evidence-based treatment. Despite this fact, many of the following treatment modalities have been found to be successful in individuals who wanted to quit the habit. 
This can be in the form of a brief intervention when a doctor gives advice for a few minutes regarding quitting the habit.
It can be held as group, individual, or telephone counseling. A relatively newer form of telephone counseling called proactive telephone calls is found to be effective. Problem-solving approach is also found to be effective in many smokers. Under this approach, individuals are asked about when they mostly want to smoke, and then work is planned out at that time. This would help to distract them and reduce their urge for smoking. Support, caring attitude, and encouragement by family members and friends (extra-treatment social support) and by healthcare providers (intra-treatment social support) also help in quitting the habit successfully. 
Five medicines are approved by the US Food and Drug Administration (FDA) for quitting the habit. These include four nicotine replacement therapy agents and one non-nicotine agent. Replacement therapy includes gum, inhaler, patch, and nasal spray. This therapy not only relieves withdrawal symptoms and reduces the urge to smoke, but also decreases the smoker's exposure to carbon monoxide, tar, and other carcinogens. Non-nicotinic agent includes bupropion. 
OTC indicates over the counter. Zyban, Nicorette, and Nicoderm are products of GlaxoSmithKline; Nicotrol is a product of Pharmacia, Inc.
Since smoking is highly addictive in nature, patient should be counseled again and again regardless of the number of unsuccessful attempts. Repeated attempts should be made not only by the individual but also by the family members and the society. 
| Conclusion|| |
As we all know, smoking is an environmental risk factor and has many deleterious effect on human body. A study conducted in England about smoking concluded that smoking is disadvantageous to an individual in multiple dimensions, i.e. physical, mental, as well as social health.  This concludes that smoking acts like a confounding factor or a supporting factor which would soon lead to the pathological conditions. More studies have to be conducted for discovering the definitive explanation for the relation. Also, more studies have to be conducted to throw light on the gender difference and effects, as well as statistically sound studies are required to discover the frequency and duration of the habit and the relation.
Smoking is a health hazard. This is a well-known fact and the noxious effects are multiple. So, for management of pain in smokers, necessary steps have to be taken in order to help them quit the habit. Cognitive behavioral therapy or anti-depressant therapy in the management of pain of depressed patients who are smokers has shown good results in a rehabilitation center. This approach has proved effective. Also, some classes of anti-depressants have analgesic property too, aiding in effective pain relief to the individuals.  Smoking cessation too should be considered as the prime goal in the management of these patients and they will experience the dramatic benefits of stopping the habit in a long-term basis. ,
| References|| |
Nirogi R, Goura V, Abraham R, Jayarajan P. α4β2* Neuronal nicotinic receptor ligands (agonist, partial agonist and positive allosteric modulators) as therapeutic prospects for pain. Eur J Pharmacol 2013;712;22-9.
Kvalheim S, Sandven I, Hagen K, Zwart JA. Smoking as a risk factor for chronic musculoskeletal complaints is influenced by age. The HUNT study. Pain 2013;154:1073-9.
Taly A, Corringer PJ, Guedin D, Lestage P, Changeux JP. Nicotinic receptors: Allosteric transitions and therapeutic targets in the nervous system. Nat Rev Drug Discov 2009;8:733-50.
Aceto MD, Awaya H, Martin BR, May EL. Antinociceptive action of nicotine and its methiodide derivatives in mice and rats. Br J Pharmacol 1983;79:869-76.
Gotti C, Clementi F. Neuronal nicotinic receptors: From structure to pathology. Prog Neurobiol 2004;74:363-96.
Le Novère N, Corringer PJ, Changeux JP. The diversity of subunit composition in nAChRs: Evolutionary origins, physiologic and pharmacologic consequences. J Neurobiol 2002;53:447-56.
Cucchiaro G, Chaijale N, Commons KG. The dorsal raphe nucleus as a site of action of the antinociceptive andbehavioral effects of the alpha4 nicotinic receptor agonist epibatidine. J Pharmacol Exp Ther 2005;313:389-94.
Rashid MH, Furue H, Yoshimura M, Ueda H. Tonic inhibitory role of alpha4beta2 subtype of nicotinic acetylcholine receptors on nociceptive transmission in the spinal cord in mice. Pain 2006;125:125-35.
Pereira EF, Hilmas C, Santos MD, Alkondon M, Maelicke A, Albuquerque Ex. Unconventional ligands and modulators of nicotinic receptors. J Neurobiol 2002;53:479-500.
Benwell ME, Balfour DJ, Anderson JM. Evidence that tobacco smoking increases the density of (-)-[3H] nicotine binding sites in human brain. J Neurochem 1988;50:1243-7.
Sallette J, Pons S, Devillers-Thiery A, Soudant M, Prado de Carvalho L, Changeux JP, et al
. Nicotine upregulates its own receptors through enhanced intracellular maturation. Neuron 2005;46:595-607.
Mukhin AG, Kimes AS, Chefer SI, Matochik JA, Contoreggi CS, Horti AG, et al
. Greater nicotinic acetylcholine receptor density in smokers than in nonsmokers: A PET study with 2-18F-FA-85380. J Nucl Med 2008;49:1628-35.
The Patient Education Institute. 1995-2010. Available from: http://www.X-Plain.com. [Last accessed on 2014 Nov 17].
Pirouzi S, Ghanbari A, Moslemi Haghighi F, Ghafarinejad F, Pouya F, Motiallah T. The prevalence of musculoskeletal pain in male cigarette smoking students at Shiraz University of Medical Sciences, Iran. Addict Health 2011;3:125-9.
Goesling J, Brummett CM, Hassett AL. Cigarette smoking and pain: Depressive symptoms mediate smoking-related pain symptoms. Pain 2012;153:1749-54.
Westhoff G, Rau R, Zink A. Rheumatoid arthritis patients who smoke have a higher need for DMARDs and feel worse, but they do not have more joint damage than non-smokers of the same serological group. Rheumatology (Oxford) 2008;47:849-54.
Eriksen W, Natvig B, Bruusgaard D. Smoking, heavy physical work and low back pain: A four-year prospective study. Occup Med (Lond) 1999;49:155-60.
Jakobsson U. Tobacco use in relation to chronic pain: Results from a Swedish population survey. Pain Med 2008;9:1091-7.
Otani T, Iwasaki M, Ohta A, Kuroiwa M, Yosiaki S, Suzuki S, et al
. Low back pain and smoking in a community sample in Japan. J Occup Health 2002;44:207-13.
Inoue M, Harada N. Habitual smoking and musculoskeletal symptoms in japanese blue-collar workers. J Occup Health 2002;44:315-20.
Unrod M, Kassel JD, Robinson M. Effects of smoking distraction and gender on pain perception. Behav Med 2004;30:133-9.
Palmer KT, Syddall H, Cooper C, Coggon D. Smoking and musculoskeletal disorders: Findings from a British national survey. Ann Rheum Dis 2003;62:33-6.
John U, Hanke M, Meyer C, Völzke H, Baumeister SE, Alte D. Tobacco smoking in relation to pain in a national general population survey. Prev Med 2006;43:477-81.
Shi Y, Hooten WM, Roberts RO, Warner DO. Modifiable risk factors for incidence of pain in older adults. Pain 2010;151:366-71.
Benjamin S, Morris S, McBeth J, Macfarlane GJ, Silman AJ. The association between chronic widespread pain and mental disorder: A population-based study. Arthritis Rheum 2000;43:561-7.
Edwards RR, Klick B, Buenaver L, Max MB, Haythornthwaite JA, Keller RB, et al
. Symptoms of distress as prospective predictors of pain-related sciatica treatment outcomes. Pain 2007;130:47-55.
Mantel N. Chi-square tests with one degree of freedom. Extensions of the Mantel-Haenszel procedure. J Am Stat Assoc 1963;58:690-700.
Pincus T, Burton AK, Vogel S, Field AP. A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine (Phila Pa 1976) 2002;27:E109-20.
Ahlberg J. Smoking and orofacial pain-do we need to add bruxism, psychology, or sleep? Pain 2009;147:13-4.
Benbow SJ, Williams G, MacFarlane IA. Smoking habits and painful diabetic neuropathy. J Diabetes Complications 1997;11:334-7.
Mitchell MD, Mannino DM, Steinke DT, Kryscio RJ, Bush HM, Crofford LJ. Association of smoking and chronic pain syndromes in Kentucky women. J Pain. 2011 Aug;12(8):892-9.
Hooten WM, Townsend CO, Bruce BK, Schmidt JE, Kerkvliet JL, Patten CA, et al
. Effects of smoking status on immediate treatment outcomes of multidisciplinary pain rehabilitation. Pain Med 2009;10:347-55.
Freedman MK, Saulino MF, Overton EA, Holding MY, Kornbluth ID. Interventions in chronic pain management. 5. approaches to medication and lifestyle in chronic pain syndromes. Arch Phys Med Rehabil 2008;89(Suppl 1):S56-60.
Shi Y, Weingarten TN, Mantilla CB, Hooten MW, Warner DO. Smoking and pain, Pathophysiology and clinical implications. Anesthesiology 2010;113:977-92.
Smoking cessation strategies for the 21 st
Century. W.B. 2014.
Jorenby DE. Smoking cessation strategies for 21 st
century. Circulation 2001;104:e51-2.
Edwards R, McElduff P, Harrison RA, Watson K, Butler G, Elton P. Pleasure or pain? A profile of smokers in Northern England. Public Health 2006;120:760-8.
Weingarten TN, Shi Y, Mantilla CB, Hooten WM, Warner DO. Smoking and chronic pain: A real-but-puzzling relationship. Anesth Analg 2009;108:308-15.
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