Most people know that smoking causes coronary heart disease and cancer. However, did you know that smoking is a contributing factor to back pain and neuropathic pain? It is true. Being a smoker can significantly contribute to symptoms, and even increase pain associated with degenerative disc disease (DDD) and nerve-related pain. Smoking cessation may have a dual benefit of increased health and decreased neuropathic pain.
Smoking introduces and releases toxic substances that damage the interior lining of blood vessels. Small blood vessels, such as those that feed the heart and intervertebral discs will be affected first. In addition smoking will introduce carbon monoxide into the blood stream. This will decrease the oxygen carrying capacity of the blood, thereby causing tissue starvation, degeneration, and death. This is the mechanism by which the discs in the spine begin to degenerate. This degeneration leads to weakening of the disc wall, which in turn leads to disc pain and herniations. In addition, Nicotine receptors have been implicated in pain perception.
People who smoke cigarettes during adult life can expect to live 7 to 10 years less than nonsmokers. Cigarette smoking not only affects the quantity of life, but also the quality of life, especially in later years. The consequences of smoking result in a huge cost in health care in the United States. The Centers for Disease Control and Prevention estimates that tobacco-related diseases result in more than 400,000 deaths among adults in the United States each year. Direct medical costs attributable to smoking total about $50 billion a year.
· Smokers experience a decrease in bone mineral (osteoporosis), resulting in fragile bones that are susceptible to fracture. Elderly smokers have a 41 percent increase in the rate of hip fracture.
· Smoking often delays healing of fractures and wounds.
· People who smoke may also experience more low back pain than nonsmokers.
· Smoking is associated with an increase in the incidence of rheumatoid arthritis.
· Nicotine, the most powerful substance in tobacco, ultimately causes a decrease in blood flow to all tissues in the human body. This is most pronounced in the hands and feet. Decreased blood flow in the hands and feet due to smoking can lead to death of tissue, requiring amputation of a hand or foot. Smokers also have a higher incidence of hand contraction and nerve problems.
· Patients who smoke have a higher complication rate from surgery than nonsmokers. Outcomes following surgical bone procedures in smokers are not as satisfactory as for nonsmokers.
Every tissue in the human body is affected by smoking, including the musculoskeletal system--bones, muscles, tendons, ligaments and nerves. Cigarette smoking represents a risk factor, which can be avoided by the individual and the effects are potentially reversible. The potential for savings in health care expenditure is enormous.
“The American
Academy of Orthopedic Surgeons (AAOS) is concerned that the American public is
not fully aware of the harmful musculoskeletal effects of smoking. The AAOS
strongly recommends avoidance of smoking due to the severe and negative impact
on the musculoskeletal system--the bones, muscles, tendons, ligaments and
nerves in the body.”
- December
2000
There's no question smoking is dangerous to your health. Tobacco smoke contains more than 4,000 substances that can damage your heart and blood vessels and cause cancer. Smoking also contributes to chronic pain by increasing fatigue and muscle weakness. Carbon monoxide in tobacco smoke replaces oxygen in your red blood cells. Less oxygen means less energy and fewer nutrients for your body tissues. Carbon monoxide has a much higher affinity for hemoglobin than does oxygen (210 times more), and high percentages of carboxyhemoglobin in the blood impairs the normal transport of oxygen by the blood. Cigarette smoke contains over four thousand chemicals with some being proven carcinogens. Among the many harmful ingredients are nicotine, tar, carbon monoxide and arsenic. Smoking alters anti-oxidant levels in the blood and has the ability to cause genetic damage. It causes chronic obstructive pulmonary disease, peripheral arterial disease and contributes to hypertension, osteoporosis, musculoskeletal injury, diabetes and many cancers. Smoking also stimulates the antidiuretic hormone with its associated problems. Whenever you smoke your muscles and nerves are exposed to these potentially harmful influences, and you risk infection, poor wound healing, injury, disability, deformity and possible amputation. However smoking cessation will result in immediate health benefits. While most people equate smoking deaths to cancer and lung disease, in fact many more people will die from circulatory conditions from smoking than die from cancer or other lung diseases. Also, in general, they will die at much younger ages from these problems. We would have many more lung cancers than we do if smokers could live long enough to get them. When many people with fatal heart attacks or strokes are autopsied, there are often precancerous lesions found that indicate that if these people had a few more years to live they would have eventually succumbed to these smoking induced diseases. As for heart and other circulatory diseases, the two chemicals in cigarettes that stand out as the biggest problems are nicotine and carbon monoxide. Nicotine, besides being addictive, has very powerful effects on arteries throughout the body. Nicotine is a stimulant, speeding up the heart by about 20 beats per minute with every cigarette, it raises blood pressure, is a vasoconstrictor - which means it makes arteries all over the body become smaller making it harder for the heart to pump through the constricted arteries - and it causes the body to release its stores of fat and cholesterol into the blood. The heart has to work harder to overcome all of these effects. To work harder the heart, like every other muscle in the body, needs extra amounts of oxygen for the additional workload. The oxygen has to be transported through the blood. But carbon monoxide from tobacco smoke literally poisons the oxygen carrying capacity of the blood. So this results in the heart having to work harder to get more blood to itself to work harder, because it's working harder. This is a circle. A vicious and deadly circle when it comes down to it.
But this clogging/clotting effect is not limited to just major organs like the heart or brain. These chemicals affect arteries throughout the entire body. These affects may not be as deadly as cutting off circulation to the heart or brain, but in a real way they can show the true potential of the grip of the nicotine addiction. Peripheral circulation, arteries going to the extremities are also highly susceptible to the vasoconstrictor effects of nicotine as well as the increase of clots and clogging risks posed by smoking. Smoking is a primary cause of much of the peripheral vascular disease seen as well as a powerful aggravating factor for people who have other preexisting conditions causing circulation problems to the extremities. One condition though stands out as being truly unique and in many ways, demonstrates the real addictive nature of nicotine better than any other cause. The condition is known as Berger's Disease (thromboangiitis obliterans.) Buerger's Disease is a condition where there is a complete cutoff of circulation to the finger or toes, resulting in gangrene. Smokers of all ages have been shown to have a higher risk of suffering tendinitis, bursitis, sprains or fractures. Efficient muscle function is also threatened due to the harmful effects of smoking on lung growth and function which results in less available oxygen for muscles during activity. Smokers are three times more likely to suffer from short breath than non-smokers
(American Academy of Orthopedic Surgeons, 2000).
A
recent Swedish study found that people who smoke have higher rates of low back,
neck, and generalized muscle and bone pain than do nonsmokers. Researchers think
smoking may block circulation in tiny blood vessels in the spine, causing
permanent damage to spinal disks. Smokers often have other problems that can
contribute to pain; these include poor physical fitness, osteoporosis (a
bone-thinning disease that can lead to fractures), and persistent coughing.
Finally, say experts, some smokers may have "pain-prone"
personalities. Unfortunately, quitting doesn't seem to help. Former smokers
have rates of pain close to those of current smokers. The best strategy? Don't
light up in the first place.1
Andersson HI,
Ejlertsson G, Leden I. Widespread Musculoskeletal Chronic Pain Associated With
Smoking. Scand J Rehab Med 1998:30:185-191.
It's
a well known fact that cigarette smoking increases the risk of lung cancer and
heart disease. More evidence now exists which adds rheumatoid arthritis
to the list of diseases linked to smoking. Rheumatoid arthritis (RA) is an
autoimmune disease which causes chronic inflammation of the joints, the tissue
surrounding the joints, and possibly other organs in the body. RA affects more
than two million people in the United States and is three times more common in
women than men. New research was presented at the American College of
Rheumatology Annual Scientific Meeting (October 29-November 2, 2000 in
Philadelphia, Pennsylvania). Based on an analysis of the records of more
than 30,000 women (age 55-69) enrolled in the Iowa Women's Health Study since
1986 statistically significant correlations were found between:
· the incidence of elderly onset rheumatoid arthritis and the number of cigarettes smoked per day
· the incidence of elderly onset rheumatoid arthritis and how long the individual was a smoker
It
was found that the risk of developing rheumatoid arthritis was nearly double
for current smokers compared to non-smokers. The risk of developing
rheumatoid arthritis appeared lower for former smokers compared to current
smokers but higher than for people who never smoked. Women who had
stopped smoking at least 10 years prior to the start of the study did not have
an increased risk. Researchers are not certain why smoking increases the risk
of RA for women. An interaction between smoking and the woman's immune
system and/ or estrogen level has been suggested. It is thought that
smoking may lower the level of estrogen. It has also been observed that smoking
raises the level of rheumatoid factor in the body. Future studies will focus on
determining the exact connection between smoking and rheumatoid arthritis.
Smoking May Increase Risk Of
Developing Rheumatoid Arthritis, ACR 10/29/00
A
new study strengthens the link between smoking and lower back pain, and also
sheds light on the causes of degenerative lumbar spine problems.
The
study, which prospectively examined 1,337 physicians who graduated from Johns
Hopkins University between 1948 and 1964, followed some participants for more
than 50 years. Researchers discovered that smoking history, hypertension and
coronary artery disease, all of which are risk factors for atherosclerosis, or
occlusion of the arteries, were significantly associated with the development
of lower back pain.
These
same risk factors, along with abnormally high blood cholesterol levels, were
also significantly associated with the development of lumbar spondylosis. The
findings provide support for the hypothesis that atherosclerosis causes lower
back pain and degenerative disorders of the intervertebral discs. The study
results, which were reported at the 2001 annual meeting of the American
Association of Orthopedic Surgeons in San Francisco, lend support to the theory that the mechanism of injury in
low back pain is damage to the vascular structures of the discs and joints. Numerous
researchers have proposed a link between smoking and back pain, but the exact
nature of that link had remained largely untested in terms of long-term
prospective studies. "Because we had the subjects' medical records and
answers from self-reported questionnaires over such a long period of time, a
53-year period of time for the oldest patients, we were able to determine if
the risk factors, such as smoking or high cholesterol, preceded the development
of the disease years later," said Nicholas U. Ahn, Chief Resident in the
Department of Orthopedic Surgery at the Johns Hopkins Hospital in Baltimore and
co-author of the study. "To prove a causative association from a long-term
prospective study is very powerful because one can show that the cause occurred
before the effect as opposed to the other way around," Dr. Ahn explained.
The study concluded that development of lower back pain was significantly
associated with smoking history and hypertension, and development of lumbar
spondylosis was significantly associated with smoking history, and hypertension
and high cholesterol. No significant association was reported between diabetes
and lower back pain or lumbar spondylosis.
A
survey of nearly 13,000 individuals found that smokers complain more often of
discomforting or disabling musculoskeletal pain than never-smokers.
The
association was found "even in ex-smokers," suggesting that smoking
may cause long-term damage to muscle tissues or changes in the neurological
pain response, according to researchers led by Dr. K. T. Palmer of Southampton
General Hospital in Southampton, UK. Writing in the January issue of Annals of
Rheumatic Diseases, the UK team notes that previous studies have suggested
links between smoking and pain, especially chronic back pain. However, most of
these studies did not factor out lifestyle factors, such as on-the-job manual
labor, as a possible contributing cause. . .
Annals of Rheumatic
Diseases; 2002;62:33-36. Eriksen WB et al:
A
large number of studies show that smoking has profound pathophysiological
effects on the human body. However, there is little knowledge of the role
smoking may play in the pathogenesis of musculoskeletal (MS) pain. This study
investigated the relationship between smoking and the intensity of MS pain,
with the hypothesis that persons with MS pain experience more intense pain if
they smoke. This study was based on data from the Norwegian Health Survey
conducted in 1985 which found that smoking was associated with MS pain from any
region of the body. From a gross sample of 13,438 persons, 10,576 were
interviewed and a sample of 4,490 adult respondents who reported MS pain were
selected for inclusion in the study. All subjects were asked about somatic and
mental complaints during the survey period of 14 days. For the present study,
persons with MS pain were defined as having at least slight pain in at least
one of the three regions of the body. A person's intensity of pain was defined
as the pain intensity in the most painful region of the body. A smoker was
defined as a person who smoked daily at the time of the interview. This study
revealed that young and middle-aged smokers (with or without a self-reported MS
disease) experienced considerable pain, and intense pain more frequently than
nonsmokers or elderly smokers. In young and middle-aged persons, neck/upper
limb pain, back pain, and hip/lower limb pain were significantly more intense
among smokers. Intense pain was statistically significantly related to smoking,
increased age, being married/cohabitating, being a pensioner, having a MS
disease, and having a high level of mental distress. Smoking was associated
with intense pain for subjects who reported having a MS disease, and for those
who did not. In subjects who were working, even after adjusting for workplace
factors, intense pain was significantly related to smoking, increased age,
having a MS disease, mental distress, and hectic job. There are several
possible explanations for the association between smoking and the intensity of
pain in the present study. First, smoking could have an aggravating effect on
MS pain, perhaps through blood flow reduction and local hypoxia, or through a
long term effect on the nervous system. Second, a high intensity of pain could
stimulate occasional smokers to become daily smokers, or make it more difficult
for smokers to quit smoking. Several studies indicate that smoking is used as a
coping strategy to regulate emotional states, and nicotine has been shown to
increase the tolerance for cold pressure in ex-smokers and nicotine-deprived
smokers. Third, the smoking/pain connection may be due to psychological or
social factors not measured in this study, but with impact both on smoking and
the genesis of MS pain. It is not obvious why age should be an effect modifier
on the relationship between smoking and pain intensity. However, age frequently
interacts with other biological variables. The authors conclude that there was
an independent association between smoking and high intensity of pain in
persons with MS pain.
Scand J Rheumatol,
26(1):49-54, 1997.
NEW
YORK (Reuters Health) - On top of its other ill effects, smoking may also be a literal
pain in the neck--and back, knees and other joints, researchers report.
A
survey of nearly 13,000 Britons found that smokers complain more often of
discomforting or disabling musculoskeletal pain than never-smokers. The
association was found "even in ex-smokers," suggesting that smoking
may cause long-term damage to muscle tissues or changes in the neurological
pain response, according to researchers led by Dr. K. T. Palmer of Southampton
General Hospital in Southampton, UK. Writing in the January issue of Annals of
Rheumatic Diseases, the UK team notes that previous studies have suggested
links between smoking and pain, especially chronic back pain. However, most of
these studies did not factor out lifestyle factors, such as on-the-job manual
labor, as a possible contributing cause. In their study, Palmer's team had
12,907 adults fill out detailed questionnaires that covered topics such as
smoking history, work activities and levels of sporadic or chronic
musculoskeletal pain. They found that, compared with those who had never
smoked, current smokers had about a 50% higher incidence of reporting
"pain in the past year preventing activity," meaning pain so severe
it precluded the individual from going to work or performing housework or hobby
activities. Pain at all sites--lower back, shoulders, elbows, hands, neck and
knees--was higher in smokers than never-smokers. What's more, this association
held even among respondents who had white-collar or other jobs that did not
require heavy lifting or moving.
Why
might smoking raise pain levels? Studies have suggested numerous explanations.
First, nicotine is a powerful stimulant that "could affect the manner in
which the brain processes sensory stimuli and the central perception of
pain," the researchers say--effectively cranking up the smoker's pain
response. Secondly, "tobacco smoking might cause general damage to
musculoskeletal tissues" by reducing blood supply to these tissues,
raising clotting risks, or reducing the flow of nutrients to muscles and joints.
On the other hand, those who choose to take up smoking might be psychologically
predisposed to simply feel and report pain at lower thresholds than
non-smokers, the researchers say. They point to previous studies that suggest
that smokers react more quickly to painful stimuli than nonsmokers. Whatever
the reason, the fact that even ex-smokers reported discomfort more frequently
than never-smokers leads researchers to conclude that the pain-related effects
of smoking can last for years, due to "tissue damage or a prolonged
resetting of the threshold for pain."
Annals of Rheumatic
Diseases; 2002;62:33-36.
Questionnaires
were completed by 12 907 (58%) subjects, including 6513 who had smoked at some
time, among whom 3184 were current smokers. Smoking habits were related to age,
social class, report of headaches, tiredness or stress, and manual activities
at work. After adjustment for potential confounders, current and ex-smokers had
higher risks than lifetime non-smokers for pain at all of the sites considered.
This was especially so for pain reported as preventing normal activities (with
PRs up to 1.6 in current v never smokers). Similar associations were found in
both sexes, and when analysis was restricted to non-manual workers. Conclusions: There is an association
between smoking and report of regional pain, which is apparent even in
ex-smokers. This could arise from a pharmacological effect of tobacco smoke
(for example, on neurological processing of sensory information or nutrition of
peripheral tissues); another possibility is that people with a low threshold
for reporting pain and disability are more likely to take up and continue
smoking.
K T Palmer, H Syddall, C
Cooper and D Coggon
In
order to explore the relationship between smoking habits and regional pain in
the general British population, researchers KT Palmer and colleagues from the
MRC Environmental Epidemiology Unit at the University of Southampton, UK
administered a questionnaire to men and women around the country. They asked
questions about pain in the low back, neck, and upper and lower limbs during
the past 12 months; smoking habits; physical activities at work; headaches; and
tiredness or stress. 12,907 men and woman aged 16-64 completed the
questionnaire. This included 6,513 people who had smoked at some time, among
whom 3,184 were current smokers. Smoking habits were related to age, social
class, report of headaches, tiredness or stress, and manual activities at work.
Current and ex-smokers had higher risks than lifetime non-smokers for pain at
all of the sites considered. This was especially true for pain reported as
preventing normal activities. They found similar results in both sexes, and
when analysis was restricted to non-manual workers. The researchers conclude
that there is an association between smoking and the report of regional pain,
which is apparent even in non-smokers. They suggest that the association could
arise from a pharmacological effect of tobacco smoke (for example, on the
brain's ability to process sensory information or nutrition of peripheral
tissues), or that people with a low threshold for reporting pain and disability
are more likely to take up and continue smoking.
STUDY DESIGN: A structured review of the epidemiologic literature was performed. Thirty-eight studies published in peer-reviewed journals were reviewed. The methodologic strengths and weaknesses of the studies were described and assessed qualitatively. Four studies were excluded because of difficulties in design or interpretation. OBJECTIVES: To provide a systematic analysis of the literature to assess the evidence as to whether smoking is associated with the prevalence and incidence of nonspecific back pain and related outcomes. SUMMARY OF BACKGROUND DATA: Evidence has been gathering regarding the association of smoking with nonspecific back pain and other back disorders, but a comprehensive summary and evaluation of the data have not been published. RESULTS: Positive associations between current smoking and nonspecific back pain were found in 18 of 26 studies in men and 18 of 20 studies in women. For sciatica and herniated discs, there were four of eight and one of five positive studies in men and women, respectively. The majority of these studies were cross-sectional (18 in men and 16 in women), with only a handful of prospective studies. Positive associations between past smoking and nonspecific back pain were reported in five of nine studies in men and five of six studies in women. In addition, increases in the prevalence and/or incidence of nonspecific back pain were found in the majority of studies in which level of consumption was analyzed and reported. An attempt was made to assess whether these results could be artifactual arising from selection bias, confounding bias, publication bias, or errors in measurement. As well, the biologic mechanisms were summarized that have been suggested by various investigators. CONCLUSIONS: The available data are consistent with the notion that smoking is associated with the incidence and prevalence of nonspecific back pain, but there are too few studies to make any conclusions for the other end points (e.g., sciatica, herniated discs). It cannot be ruled out that the association is a statistical artifact arising from either selection or confounding factors, because the evidence for nonspecific low back pain derives mostly from cross-sectional studies. In addition, it cannot be stated unequivocally that smoking preceded back pain. Long-term follow-up studies are needed to eliminate the possibility that chronic back pain preceded smoking, to better estimate dose-response correlations, and to perform biologic measurements to elucidate possible mechanisms.
Goldberg MS, Scott
SC, Mayo NE. Spine. 2000 Apr 15;25(8):995-1014
STUDY DESIGN: A retrospective cohort study of adolescent idiopathic scoliosis. A comparison group of persons without scoliosis was also selected randomly from the general population. OBJECTIVES: To estimate the association between level of cigarette smoking and the prevalence and severity of back pain. METHODS: A postal questionnaire was used to elicit information on smoking histories, a variety of indices of low back pain, and potential confounding factors. The association between smoking and back pain was estimated separately for men and women in the cohort and in the comparison group using ordinal regression models. RESULTS: The questionnaire was completed by 1287 women and 184 men who had adolescent idiopathic scoliosis and by 1130 women and 621 men in the comparison population who did not have scoliosis. Statistically significant associations between back pain and current cigarette smoking were found in the two groups of women and men with scoliosis, but not among men selected from the general population. In the three former groups, proportional odds ratios comparing current smokers to persons who never smoked ranged from 1.4 to 1.9. Among current smokers, the prevalence of back pain increased with cigarette consumption, and the proportional odds ratios ranged from 1.2 to 1.8 per 10 pack-years (no. of cigarettes smoked per day x no. of years/20). In these three groups, intensity, frequency, and duration of episodes of back pain also were found to increase with smoking consumption. CONCLUSION: The finding that smokers have more frequent episodes of back pain may imply that smoking exacerbates back pain, and the observation that stronger associations between back pain and smoking were found in the scoliosis cohort suggests that smoking may have a greater impact on persons with damaged spines.
Scott SC, Goldberg
MS, Mayo NE, Stock SR, Poitras B. Spine. 1999 Jun 1;24(11):1090-8.
STUDY DESIGN: A cross-sectional postal survey of 29,424 people aged 12-41 years obtained from a population-generated panel of twin individuals. OBJECTIVES: To study whether smoking causes low back pain. SUMMARY OF BACKGROUND DATA: Despite insufficient evidence in the epidemiologic literature, it has become increasingly accepted that smoking causes low back pain and that discontinuation of smoking is a suitable means of secondary prevention. METHODS: Dose-response was examined for smoking (daily use, number of years smoked, and total cigarette use during the years of smoking) in correlation with low back pain (occurring 1-7 days, 8-30 days, and > 30 days in the past year). A possible modifying effect was studied for age, gender, and body mass index. A negative gradient was sought in relation to the time since smoking was discontinued. The prevalence of low back pain was studied in monozygotic twin pairs, only one of whom smoked. RESULTS: There was a significant positive association between smoking and low back pain that increased with the duration of low back pain: occurring 1-7 days (odds ratio, 1.4), 8-30 days (odds ratio, 2.1), and more than 30 days (odds ratio, 3) in the past year. However, these differences in reports of low back pain disappeared in monozygotic twin pairs discordant on present smoke status. There was no biologic gradient for any of the low back pain definitions or measures of smoking-dose, and the prevalence of low back pain did not decrease with the number of years since smoking was stopped. Smaller people (youngsters, women, people with low body mass index) were not more vulnerable to development of low back pain with smoking. CONCLUSIONS: There is a definite link between smoking and low back pain that increases with the duration and frequency of the low back pain problem, but this link is unlikely to be causal. Leboeuf-Yde C, Kyvik KO, Bruun NH. Spine. 1998 Oct 15;23(20):2207-13; discussion 2214.
Recently smoking has been increasingly implicated as a possible risk factor for low-back pain. One explanation for this finding is confounding by occupation. To investigate this possibility, the relationship between smoking and self-reported back pain was studied within 13 occupations. A relationship between smoking and back pain was observed only in occupations that require physical exertion. The relationship between smoking and other musculoskeletal pain also was explored. Pain in the extremities turned out to be related more clearly to smoking than to pain in the neck or the back. This suggests confounding or a general influence of smoking on pain. It is concluded that prevention of back pain could be a beneficial side-effect of anti-smoking campaigns. However, the prime target for prevention of low-back pain would have to be other factors.
Boshuizen HC, Verbeek JH, Broersen JP, Weel AN. Spine. 1993 Jan;18(1):35-40.
Data on smoking and pain symptoms from a random sample (n = 1806) of a general population were used to evaluate the association between chronic pain at various locations and smoking. In both genders current smoking was associated with reports of increased pain in low back, neck and with multiple locations. In a multiple logistic regression analysis current smoking was associated with an increase in widespread chronic musculoskeletal pain (OR 1.60, CI 1.04-2.46, in relation to non-smokers) and chronic low back pain (OR 1.58, CI 1.13-2.20, in relation to non-smokers). A dose-response relationship was found between the daily cigarette consumption and the prevalence of chronic low back pain. Smoking is associated not only with low back pain but also with chronic widespread musculoskeletal pain.
Andersson H,
Ejlertsson G, Leden I. Scand J Rehabil Med. 1998 Sep;30(3):185-91.
OBJECTIVES: To investigate (a) whether there is a causal link between smoking and low back pain (LBP), (b) whether smoking is uniquely associated with symptoms in the lumbar spine and (c) the role of respiratory problems in the possible link between smoking and LBP. STUDY DESIGN: Data were collected through questionnaires in a cross-sectional study of a representative sample of the general Danish population, consisting of 1370 men and women aged 30-50 yr, with a response rate of 69%. BACKGROUND: In some epidemiological studies (mostly those of cross-sectional design) smoking has been associated with LBP; this association, however, is not consistently present in all reports. Several theories exist that attempt to explain a possible association between the two; only rarely have these theories been systematically tested. However, cross-sectional data can also be used to obtain answers to questions relating to causes and mechanisms. METHOD: A list of expectations was produced that related to three hypotheses previously forwarded in the epidemiological literature. The fit of the data in the present study was then considered in the light of these expectations. RESULTS: There is evidence in favor of a causal link between smoking and some definitions of LBP. Smoking was not uniquely associated with the lumbar spine. Respiratory symptoms seemed to be positively associated with LBP but only when linked with smoking. CONCLUSIONS: The clinical significance of these findings is limited, but it needs to be considered in future research. Abstinence from smoking may, however, be a useful means of primary prevention of certain types of LBP.
Leboeuf-Yde C, Yashin
A, Lauritzen T. J Manipulative Physiol Ther. 1996 Feb;19(2):99-108.
OBJECTIVE: To examine the association between musculoskeletal pain and smoking. DESIGN: Cross sectional, national interview survey. SETTING: All individuals in a representative sample of households in Norway in 1985. SUBJECTS: A total of 6681 persons aged 16 to 66 years old. people in institutions were not included. OUTCOME MEASURES: Gender specific and age specific prevalence rates for pain in the cervical region/upper limbs, back, and lower limbs. RESULTS: Current smoking was independently associated with musculoskeletal pain (odds ratio (OR) 1.69; 95% confidence interval (95% CI) 1.45, 1.97) after adjustment for gender, age, comorbidity, mental distress, lifestyle factors, and occupation related factors. The association was of similar strength regarding cervical/upper limb pain (OR 1.87; CI 1.56, 2.25) and back pain (OR 1.84; CI 1.50, 2.25) but weaker in respect of lower limb pain (OR 1.37; CI 1.10, 1.71). Musculoskeletal pain was often present in more than one site. CONCLUSION: Smoking was significantly associated with musculoskeletal pain after adjustment for other relevant factors.
Brage S, Bjerkedal T.
J Epidemiol Community Health. 1996 Apr;50(2):166-9.
The present study was based on data from the Norwegian Health Survey 1985, a nationwide interview survey with members of a representative sample of households. Our sample comprised all adult respondents who had reported musculoskeletal pain (n = 4490). Smokers experienced more intense pain than nonsmokers. The association between smoking and considerable/intense pain was, however, only seen in persons younger than 67 years. In this age group, smoking was related to intense pain in a logistic regression analysis (OR = 1.58; 95% CI: 1.24-2.00; p < 0.001), adjusting for age, gender, socioeconomic status, civil status, having children under 16, physical exercise, the presence of a musculoskeletal disease, and mental distress. The association remained significant after adjusting for workplace factors, social network factors, alcohol consumption, and intake of cod liver oil as dietary supplement.
Eriksen WB, Brage S,
Bruusgaard D. Scand J Rheumatol. 1997;26(1):49-54.
OBJECTIVES: To explore the relation between smoking habits and regional pain in the general population. METHODS: A questionnaire was mailed to 21 201 adults, aged 16-64 years, selected at random from the registers of 34 British general practices, and to 993 members of the armed services, randomly selected from pay records. Questions were asked about pain in the low back, neck, and upper and lower limbs during the past 12 months; smoking habits; physical activities at work; headaches; and tiredness or stress. Associations were examined by logistic regression and expressed as prevalence ratios (PRs). RESULTS: Questionnaires were completed by 12 907 (58%) subjects, including 6513 who had smoked at some time, among whom 3184 were current smokers. Smoking habits were related to age, social class, report of headaches, tiredness or stress, and manual activities at work. After adjustment for potential confounders, current and ex-smokers had higher risks than lifetime non-smokers for pain at all of the sites considered. This was especially so for pain reported as preventing normal activities (with PRs up to 1.6 in current v never smokers). Similar associations were found in both sexes, and when analysis was restricted to non-manual workers. CONCLUSIONS: There is an association between smoking and report of regional pain, which is apparent even in ex-smokers. This could arise from a pharmacological effect of tobacco smoke (for example, on neurological processing of sensory information or nutrition of peripheral tissues); another possibility is that people with a low threshold for reporting pain and disability are more likely to take up and continue smoking.
Palmer KT, Syddall H,
Cooper C, Coggon D. Ann Rheum Dis. 2003 Jan;62(1):33-6.
Data from a community-based four-year prospective study were used to test the hypothesis that heavy physical work is a stronger predictor of low back pain in smokers than in non-smokers. Of 708 working responders without low back pain during the entire year prior to 1990, 562 (79%) completed a questionnaire four years later in 1994. A job involving heavy lifting and much standing in 1990 was a strong predictor of low back pain in smokers four years later [odds ratio (OR) = 5.53, 95% confidence interval (CI) = 1.93-15.84, p < 0.01) after having adjusted for other job characteristics, demographic factors, emotional symptoms, physical exercise and musculoskeletal pain elsewhere. In non-smokers, having a job with heavy lifting and much standing was not associated with low back pain. One explanation may be that smoking leads to reduced perfusion and malnutrition of tissues in or around the spine and causes these tissues to respond inefficiently to mechanical stress.
Eriksen W, Natvig B,
Bruusgaard D. Occup Med (Lond). 1999 Apr;49(3):155-60.
BACKGROUND: Passive smoking has been reported to induce intervertebral disc degeneration in rats, and the objective of the present study was to histologically investigate changes in smoking-induced intervertebral disc degeneration after cessation of smoking. METHODS: Four-week-old rats were subjected to passive smoking for 8 weeks in a smoking box [20 cigarettes a day: one cigarette an hour (inhaled over 3 minutes and followed by ventilation with room air for 5 minutes)] to induce intervertebral disc degeneration. Smoke-free periods of different lengths were then established, and intervertebral discs were histologically analyzed. RESULTS: Immediately after 8 weeks of passive smoking, intervertebral discs exhibited cracks, tears, and misalignment of the annulus fibrosus, and increased fibrous tissue was seen in the nucleus pulposus. In addition, the level of interleukin-1beta in intervertebral discs was higher in the smoking group than in the non-smoking group. After cessation, progression of degeneration ceased, and the matrix of the nucleus pulposus and annulus fibrosus exhibited increased fibrous connective tissue and proteoglycan. However, there were no changes in annulus fibrosus misalignment. Interleukin-1beta levels also remained significantly elevated after 8 weeks of cessation. CONCLUSIONS: While the annulus fibrosus degeneration caused by smoking was partially irreversible after cessation of smoking, the amount of mucin (proteoglycan) in the nucleus pulposus and annulus fibrosus tended to increase after cessation, thus suggesting the possibility that smoking-induced intervertebral disc degeneration can be repaired to some degree by cessation of smoking.
J Orthop Sci. 2006
Mar;11(2):191-7.
Department of Orthopedic
Surgery, Nihon University School of Medicine, 30-1 Oyaguchi-kamimachi,
Itabashi-ku, Tokyo 173-8610, Japan.
PMID: 16568393 [PubMed - indexed for MEDLINE]
We have investigated the intervertebral discs of rat-smoking models to demonstrate that smoking is a cause of degenerative intervertebral disc disease. A smoking box was developed for this study. We exposed 8-week-old rats to indirect tobacco smoke inhalation. Each rat was forced to inhale the smoke from one cigarette per hour. The mean blood nicotine level of rodents exposed to cigarette smoke corresponds to about twice that of ordinary human smokers. Histological and immunological studies were then performed to assess the effects of smoking for varying periods of time. After 8 weeks, the chondrocytes in the disordered annulus fibrosus layer tended to grow larger and attain a rounder form than normal chondrocytes. The interleukin-1beta level in the 8-week smoking group was significantly higher than that of the control group. Tobacco smoke inhalation increased local production and release of inflammatory cytokines and resultant decomposition of chondrocyte activity.
J Orthop Sci.
2004;9(2):135-41.
Department of Orthopedic
Surgery, Nihon University Hospital, 30-1 Oyaguchi-Kamimachi, Itabashi-ku, Tokyo
173-8610, Japan.
PMID: 15045541
[PubMed - indexed for MEDLINE]
STUDY DESIGN: This study attempts to determine the molecular changes in intervertebral disc degeneration of rats induced by passive cigarette smoking. OBJECTIVES: To quantitate and compare the gene expression levels in intervertebral discs from passively cigarette smoking rats and nonsmoking rats. SUMMARY OF BACKGROUND DATA: The molecular mechanism of intervertebral disc degeneration has been investigated mainly in vitro but little in vivo, and gene expression analysis has been performed in a few studies. The cigarette smoking is a risk factor of low back pain. We developed a smoking box to create a rat model of intervertebral disc degeneration induced by passive cigarette smoking. METHODS: Total RNA was extracted from intervertebral discs of rats that were raised in a cigarette-smoking box for 2 to 7 weeks. After synthesis of cDNA, the quantitative analysis of gene expression was performed by the real-time PCR. The remaining spines were subjected to the histologic examination. RESULTS: Histologic changes of the nucleus pulposus and the annulus fibrosus were detected after 2 weeks of smoking and were frequently found after 7 weeks. Collagen genes were down regulated remarkably after 7 weeks of smoking. No significant increase was observed in the expressions of matrix metalloproteinase-3, but the expression of tissue inhibitor of metalloproteinases-1 started to increase at 4 weeks of smoking. Aggrecan also started to be up-regulated at 4 weeks. CONCLUSIONS: Changes in gene expression by passive cigarette smoking precede the histologic changes in the intervertebral discs. Reactions to suppress the destruction of tissue matrix and to regenerate the intervertebral discs are occurring at the same time as the degenerative histologic changes.
Spine. 2006 Mar
1;31(5):510-4.
Department of Orthopedic
Surgery, Nihon University School of Medicine, Tokyo, Japan.
PMID: 16508543
[PubMed - indexed for MEDLINE]
STUDY DESIGN: Experimental investigation to determine the effect of nicotine on intervertebral spinal disc nucleus pulposus (NP) cells cultured in vitro. OBJECTIVES.: To evaluate the effects of nicotine on cell proliferation, extracellular matrix production, and viability of NP cells in three-dimensional alginate constructs cultured in vitro. SUMMARY OF BACKGROUND DATA: Numerous studies confirm that smoking is a strong risk factor for back pain. The most widely accepted explanations for the association between smoking and disc degeneration is malnutrition of spinal disc cells by carboxy-hemoglobin-induced anoxia or vascular disease. Nicotine, a constituent of tobacco smoke, present in most body fluids of smokers is known to have detrimental effects on a variety of tissues. It may also be directly responsible for intervertebral disc (IVD) degeneration by causing cell damage in both the nucleus pulposus and anulus fibrosus. The effect of nicotine on IVD cells has not previously been investigated. METHODS: Bovine chondrocytic intervertebral disc cells were isolated by sequential digestion of nucleus pulposus and seeded in 2% alginate. The constructs were cultured for 21 days either in growth medium containing freebase nicotine (Sigma) at concentrations found in the serum of smokers (25 nmol/L-300 nmol/L) or in standard nicotine free-medium as controls. Samples were collected at time points 3, 7, 14, and 21 days and a quantitative assay was performed for DNA, glycosaminoglycans (GAG), and hydroxyproline. Samples were also processed for qualitative histologic analysis including immunolocalization of collagen types I and II. RESULTS: There was both a dose- and time-dependent response to nicotine, with constructs cultured in low-nicotine concentration media demonstrating an early increase in DNA, GAG, and collagen content, while constructs cultured in high nicotine concentration media demonstrated a late decrease in these parameters. At 25 nmol/L dose of nicotine, there was a significant increase (P < 0.05) in the above parameters at day 7 compared with the controls. At higher doses, there was a significant dose-dependent decrease (P < 0.05) in these parameters compared to controls; however, this was only significant at day 14 for the 300 nmol/L group and at day 21 for the 100 nmol/L, 200 nmol/L, and 300 nmol/L groups. Adverse morphologic changes were observed on histology, which included reduced cell proliferation, disrupted cell architecture, disintegration of cells, and extracellular matrix. Immunohistochemistry revealed the presence of type I collagen in the extracellular matrix rather than the normal type II collagen seen in the controls. CONCLUSIONS: Nicotine has an overall detrimental effect on NP disc cells cultured in vitro. There was significant inhibition of cell proliferation and extracellular matrix synthesis. Nicotine in tobacco smoke may have a role in pathogenesis of disc degeneration.
Spine. 2004 Mar
1;29(5):568-75.
Institute of Orthopedics
& Royal National Orthopedic Hospital, Stanmore, UK.
M.Akmal@orthopaedics.com
PMID: 15129075 [PubMed - indexed for MEDLINE]
Clinically, we have observed that a large proportion of patients presenting with low back pain as the chief complaint are smokers. It was therefore postulated that smoking might affect the intervertebral disc. We investigated the histological and functional effects of nicotine on intervertebral discs in rabbits. Rabbits were implanted subcutaneously with minipumps for the delivery of 200 microg/ml nicotine for 4 or 8 weeks. The selected dose produced blood nicotine levels equivalent to those found in heavy smokers (30 cigarettes/day). Nicotine injection caused necrosis and fibrous tissue and vitreous formation in the nucleus pulposus of the intervertebral disc, as well as hypertrophy of the fibrous ring, with partial cracks and detachment. Measurement of collagen and proteoglycan production in intervertebral discs showed reduced synthesis of these proteins in nicotine-treated rabbits compared with the control findings. Our results indicated that the harmful effects of nicotine on the integrity of the intervertebral disc might be mediated by the direct effect of nicotine, or indirectly, by causing vasoconstriction of the vascular network surrounding the intervertebral discs.
J Orthop Sci.
2001;6(2):177-82.
Department of
Orthopedic Surgery, Nihon University School of Medicine, 30-1
Oyaguchi-kamimachi, Itabashi-ku, Tokyo 173-8610, Japan.
PMID: 11484105
[PubMed - indexed for MEDLINE]
STUDY DESIGN: The effects of nicotine on intervertebral discs in rabbits were studied experimentally. OBJECTIVES: To investigate the effects of nicotine on the vascular buds in rabbits for elucidating the mechanism of nicotine-induced vertebral disc degeneration. BACKGROUND DATA: Several groups have suggested that cigarette smoking is associated with low back pain, but the exact mechanism is not yet fully understood. METHODS: The pump was filled with a diluted nicotine solution, then implanted under the skin of rabbits for 8 weeks. This model was designed to maintain blood nicotine concentration at approximately 110 ng/mL. Rabbits receiving physiologic saline were used as control animals. RESULTS: Nicotine treatment resulted in necrosis and hyalinization of the nucleus pulposus in all rabbits. The anulus fibrosus showed a disturbance of the pattern of overlapping laminae with and without clefts and separation. These resulted in changes indicative of stenosis of vascular buds and perivascular calcification. Nicotine treatment resulted in hypertrophy of vascular walls, necrotic changes in endothelial cells, and narrowing of the vascular lumen. Nicotine treatment resulted in delineation of vascular buds in the vicinity of the vertebral endplate and a reduction of their numbers. However, the control animals showed a dense vascular network. The number of vascular buds decreased in nicotine treatment. CONCLUSION: The authors believe that both reduction in the density of vascular buds and narrowing of the vascular lumen result in decreased oxygen tension, leading to decreased synthesis of proteoglycan and collagen, thus facilitating degeneration of the disc.
Spine. 2002 Jul
1;27(13):1396-401.
Department of Orthopedic
Surgery, Nihon University School of Medicine, Tokyo, Japan.
masaki3@ms.tokyo.jcom.ne.jp
PMID: 12131735
[PubMed - indexed for MEDLINE]
BACKGROUND CONTEXT: Cigarette smoking has been implicated in low back pain and intervertebral disc degeneration; however, there is no conclusive evidence that cigarette smoking is an important contributing factor to intervertebral disc degeneration. PURPOSE: The objective of this study is to determine whether heavy cigarette smoking is a contributing factor to the development and severity of degenerative disc disease of the cervical spine. STUDY DESIGN: This is a comparative roentgenographic study of degenerative changes of the cervical spine in age- and sex-matched smokers and nonsmokers. PATIENT SAMPLE: Two hundred asymptomatic subjects, 100 women and 100 men, were equally divided into 50 nonsmokers and 50 heavy smokers. OUTCOME MEASURES: A numerical grading system previously developed was used to grade the presence and severity of degenerative changes at each cervical level, and cervical lordosis was measured. This was performed on a lateral cervical spine roentgenogram. METHODS: A single lateral roentgenogram of the cervical spine was taken in each individual, and in the smokers a short questionnaire was administered to determine the amount and duration of smoking. The roentgenograms were read by the three authors. Average values of all three observers were used for statistical analysis. RESULTS: There were no statistically significant differences between smokers and nonsmokers. CONCLUSIONS: Based on the evidence of the plain roentgenograms used in this study, we found no evidence to suggest that cigarette smoking is a causative factor in asymptomatic people in the development of degenerative disc disease in the cervical spine. Whether cigarette smoking has a significant effect in people with neck symptoms cannot be determined by this study.
Spine J. 2006 Sep-Oct;6(5):557-60.
Epub 2006 Jul 11.
2920 Superior Avenue,
Sheboygan, WI 53081, USA.
PMID: 16934727
[PubMed - in process]
STUDY DESIGN: A prospective cohort study. OBJECTIVE: To study the relationship of smoking and overweight with severe back disorders leading to hospitalization. SUMMARY OF BACKGROUND DATA: Many epidemiological studies have shown an association between smoking or overweight and back pain, but the results are still equivocal. Longitudinal studies are few. METHODS: A cohort of metal industry employees (n = 902) was studied for lifestyle, work history, and health in 1973 by questionnaire and interview. The weight of the subjects was measured and body mass index (kg/m2) was calculated. Based on intensity and duration, smoking was categorized as: never smoked (reference), stopped smoking, smoked <or=9 or >9 pack-years. Information on hospital admissions from 1973 to 2000 from the Finnish Hospital Discharge Register was linked to the data. Seventy-five individuals had been admitted to hospital because of back disorders. Intervertebral disc disorders and other common back disorders were analyzed separately. Cox proportional hazards regression was used to estimate the time between the assessment of potential risk factors and the first hospitalization for a back disorder. RESULTS: The rate ratio of heavy smokers (>9 pack-years) for hospitalization because of intervertebral disc disorders was 3.4 (95% confidence interval 1.3-9.0) as compared with never-smokers, allowing for other risk factors. Accordingly, the rate ratio of body mass index >27.5 kg/m2 was 2.7 (1.1-6.45) as compared with people with normal weight. The results retained when patients with chronic back disease at baseline were excluded from the analyses. Other back-related diagnoses of hospitalization were not consistently associated with smoking or overweight. CONCLUSION: Heavy smoking and overweight predicted hospitalization for intervertebral disc disorders.
Spine. 2003 Aug
15;28(16):1860-8.
Finnish Institute of
Occupational Health, Helsinki, Finland. Leena.Kaila-Kangas@ttl.fi
PMID: 12923477
[PubMed - indexed for MEDLINE]
Cigarette smokers have an increased risk of low back pain which may be caused by disc degeneration and spinal instability, for example. 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. Along with degeneration, the primary avascular disc turns vascular. There is some evidence that disc degeneration of cigarette smokers is of more severe degree than that of non-smokers. Cigarette-smoking increases serum proteolytic activity by releasing proteolytic enzymes from neutrophils in alveolar capillaries, and by inhibiting the activity of alpha-1-antiprotease, the most potent protease inhibitor. We hypothesize 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 resulting in spinal instability. These processes may explain the increased risk of low back pain of cigarette smokers. Copyright 2001 Harcourt Publishers Ltd.
Med Hypotheses. 2001
Apr;56(4):537-9.
Department of
Neurology, University of Helsinki, Helsinki, Finland. r.fogel@saunalahti.fi
PMID: 11339862 [PubMed - indexed for MEDLINE]
Nicotinic receptors have been implicated in pain perception. It is unclear to what extent these 2 cases generalize to the Spinal Cord Injury population. Smoking cessation may have a dual benefit of increased health and decreased neuropathic pain.
J. Scott Richards,
PhD, Stephen C Kogos, Jr, PhD, T. J Ness, MD, PhD, and Christina V Oleson, MD
Department of Physical Medicine and Rehabilitation, University of Alabama at Birmingham, Birmingham, Alabama. J Spinal Cord Med. 2005; 28(4): 330-332.
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