The Role of Physical Therapists in Smoking Cessation: Opportunities for Improving Treatment Outcomes

Tobacco use constitutes one of the greatest threats to public health worldwide. As a preventable cause of mortality and chronic disease, tobacco use in the United States results in an estimated 443,000 deaths each year through both direct exposure and secondhand smoke.1 An additional 8,600,000 people across the nation have chronic illness due to smoking.1 As physical therapists, we must realize that tobacco use affects all areas of our practice, including cardiovascular, musculoskeletal, neurological, and integumentary health throughout the life span. In order to provide optimal care for the clients we serve, it is essential for physical therapists to screen for tobacco use and incorporate cessation strategies as part of our interventions.2 There is a substantial unmet demand and opportunity for our profession to promote tobacco cessation.2 Despite evidence that links successful cessation to counseling by health care providers, fewer than 40% of insured adults report receiving such advice.3 In addition, receiving advice from 2 or more health care practitioners more than doubles the odds of successful cessation,4 further supporting the need for physical therapists and physical therapist assistants to contribute our skills and expertise as part of the interdisciplinary health care team. Successful cessation efforts have been demonstrated by other health care professionals, including physicians, dentists, dental hygienists, nurses, and pharmacists, and are an important component of preventive medicine and population health.5 According to the US Medical Expenditure Panel Survey, in 2007, physical therapists conducted a total of 88 million ambulatory visits for approximately 9 million adults aged 18 years and over.6 The number of visits (an average of 9.6 per patient, per episode)6 and nature of our interactions, which include extended, personalized, one-on-one care, present a unique opportunity for physical therapists and physical therapist assistants to provide support for tobacco cessation2 as a means of enhancing treatment outcomes and health-related quality of life. In addition, due to the nature of our clientele, physical therapists are in a prime position to address serious health care disparities. People with disabilities have limited access to health care and follow-up visits and have an average smoking prevalence of 30.5% compared with a rate of 21.7% for those without disabilities.7 Furthermore, the health effects of tobacco use may be magnified in people with disabilities due to the clustering of other risk factors, such as obesity and the tendency toward a sedentary lifestyle.7 According to the Guide to Physical Therapist Practice, the physical therapist's scope of services includes assessment and intervention designed to “promote not only optimal physical function but optimal wellness…and optimal quality of life.”8(p13) Furthermore, as we advance toward the attainment of Vision 20209 and direct access enables physical therapists to become practitioners of choice for people seeking better health, the profession needs to become more proactive and skilled in recognizing and promoting behavioral changes that have widespread effects at all levels of the International Classification of Functioning, Disability and Health (ICF model), from pathophysiology to impaired individual capacity and performance.10 Tobacco cessation counseling is consistent with the role of our profession in promoting wellness, improving immediate health, and preventing secondary complications of chronic disease.2,11 Therefore, the aims of this article are: (1) to identify the impairments commonly managed by physical therapists that are negatively affected by tobacco use and (2) to provide a rationale and guidelines to enable physical therapists and physical therapist assistants to successfully engage in smoking cessation interventions. The adverse effects of tobacco use on cardiopulmonary function are well established and recognized.12 Less evident, but equally important, is its impact on all aspects of physical therapist practice, including integumentary, musculoskeletal, and neuromuscular health. Adverse effects of smoking occur throughout the life span, from prenatal exposure, through childhood, adolescence, and all phases of adulthood. As tobacco use has the potential to affect multiple physiologic systems, it is likely that cessation efforts will improve outcomes for many of the conditions and impairments treated by physical therapists. Many pathophysiologic changes caused by tobacco use can be traced to the pro-inflammatory effects of cigarette smoke. This inflammation is a product of oxidative tissue injury and is evidenced by increased levels of inflammatory cytokines in smokers, such as interleukin-6 (IL-6), tumor necrosis factor–alpha (TNF-alpha), and C-reactive protein.13 At the cellular level, smoking contributes to mutations in proteins that can later manifest as tumors.14 Smoking also can lead to adverse changes in the mitochondria and impaired function along the respiratory chain, causing increased cellular stress and decreasing the ability to produce new, healthy tissue.14 In addition, hemoglobin's affinity for carbon monoxide in cigarette smoke is 200 times higher than its affinity for oxygen.15 Due to this effect, increased levels of carbon monoxide within the bloodstream decrease oxygen saturation16 and interfere with the electron transport chain within the mitochondria, leading to a decrease in cytochrome C oxidase.17 This effect can be especially pronounced in tissues with a high metabolic rate, such as skeletal muscle, and the central nervous system.17 Smoking also interferes with oxygen transport by reducing the proliferation of red blood cells.15 In addition, as part of this cycle, smoking decreases concentrations of antioxidant vitamins and nutrients such as folate and riboflavin,18 vitamins E and C,19 and melatonin.20 Melatonin is not only an important antioxidant but also functions as an anticarcinogenic.20 Smokers also experience impaired lipid metabolism. The oxidation of low-density lipoproteins leads to a cytotoxic environment and may promote platelet adhesion, DNA damage, and apoptosis.21 Metabolic disturbances in smokers also include impaired glycolysis.21 These factors are particularly harmful given the tendency for smokers to engage in other unhealthy behaviors such as the consumption of a high-fat diet, which often is rich in simple carbohydrates and deficient in antioxidant nutrients,21 and can result in a clustering of dangerous risk factors for chronic illness. Smoking also leads to tissue damage through accelerated vascular aging. In addition to its impact on the cardiac system, accelerated vascular aging has been implicated in increased risk of cardiovascular accident and vascular dementia.14 This effect is due to the presence of heavy metals and toxins in cigarette smoke14 and the effects of nicotine.22 Nicotine increases systemic blood pressure by stimulating sympathetic nerve endings, leading to vasoconstriction and increased vascular resistance,22 which contribute to tissue hypoxia throughout the body. Peripheral vascular disease and reduced blood flow also increase the risk of other health problems, including metabolic syndrome,23 a precursor to diabetes. Cessation is an important step in limiting systemic inflammation and oxidative tissue injury, thereby enhancing current healing and future health. Tobacco use impedes tissue healing through several mechanisms. Smoking not only causes transient deficiencies in tissue oxygenation, but once oxygen delivery has been restored, reperfusion injury also may occur.17 At the integumentary level, smoking has been shown to reduce cutaneous blood flow by as much as 40% due to the effect of nicotine on cholinergic fibers, which supply the vascular bed.24 Nicotine suppresses immune response and decreases the proliferation, viability, and function of lymphocytes,24 increasing the likelihood of infection. In neutrophils, nicotine stimulates the release of proteases, which may accelerate tissue destruction and further inhibit repair.25 During the proliferative phase, tobacco use reduces the ability of fibroblasts to migrate and interferes with wound contraction.24 It also decreases plasma levels of vitamin C needed for collagen formation.24 Furthermore, nicotine not only lowers the formation of collagens but also decreases synthesis of procollagens I and II and hydroxyproline,15 all of which are required for production of ground substance. Overall, for those who use tobacco, collagen production is slowed, scar tissue is weaker, and healed tissues break down more easily,15,24 increasing risk of recurrent injury. Smoking has been shown to contribute to musculoskeletal problems in many different ways. It results in reduced quadriceps muscle strength26 and increased muscle fatiguability.27 In a study comparing the strength of back extensors among male athletes, smokers had a higher rate of perceived exertion as well as fatigue,28 and these effects were observed in people as young as 18 years of age.28 It has been speculated that these problems may be due to oxidative damage to muscle proteins26 and mitochondrial impairment.27 As people age, smoking may lead to increased weakness and reduced balance. One study examining physical functioning in women aged 65 years and older showed that smokers had less strength, poorer balance, and lower physical performance scores for agility, coordination, and gait compared with their nonsmoking counterparts.29 In another population of older women, smokers had impaired performance on timed rise and walk tests and grip strength.30 It is speculated that atherosclerotic damage in the lower extremities may perpetuate these functional limitations by reducing tolerance to physical activity.29 Through its effects on metabolism and circulation, tobacco use also leads to bone demineralization. Smoking can increase fracture risk by depleting estrogen, which can contribute to osteoporosis.14 Tobacco use has been shown to interfere with the absorption of calcium and vitamin D.31 Elevated cortisol levels32 associated with smoking contribute to bone reabsorption.32 Additionally, smoking inhibits the differentiation of osteoclasts, leading to the reduced formation of new bone.14 These factors work collectively to decrease bone density and increase the risks of fracture33 and fracture nonunion.34 Among clients typically seen in physical therapy settings, tobacco cessation limits damage to muscles and bones, preventing future decline and optimizing current recovery of function. Toxic effects of tobacco use also have been established within the neuromuscular system. Nicotine readily crosses the blood-brain barrier15 and has a detrimental effect on cerebral circulation. Smokers were shown to have a 1.8 times greater risk of silent cerebral infarct compared with nonsmokers.35 Risk increased with higher doses of tobacco.35 The lifetime accumulation of heavy metals such as lead due to smoking has been associated with lower levels of language processing, hand-eye coordination, executive functioning, verbal and visual memory, learning, and global function and with higher rates of white matter lesions and cerebral atrophy in older adults.35 Among the heavy metals contained in cigarette smoke, vinyl chloride has been implicated as a causative agent for brain tumors.35 Heavy smoking in midlife is associated with a higher risk of dementia and Alzheimer disease36 and a 150% higher risk of amyotrophic lateral sclerosis than among nonsmokers.37 In animal studies, prenatal exposure to carbon monoxide led to decreased deposition of myelin in peripheral nerves,38 possibly increasing the likelihood of neuropathy. It has been suggested that nicotine, free radicals, and other toxins in cigarette smoke may cause degeneration or interfere with axonal conduction, particularly in fibers that have already been damaged or demyelinated.38 Chronic exposure to carbon monoxide from smoking increases levels of hemeoxygenase within the bloodstream, a factor that may contribute to the development of neuropathic pain.39 Smoking may enhance excitatory transmission in the dorsal horn of the spinal cord by stimulating nicotinic acetylcholine receptors, thereby increasing the intensity of neuropathic pain.40 In terms of other neuropathologic impairments, people who smoked 20 to 40 cigarettes per day had twice the risk of developing multiple sclerosis compared with nonsmokers.41 Among those who already had multiple sclerosis, smokers were more likely to have the more severe form of primary progressive disease and more severe symptoms and functional disability.41 Due to links between smoking and cognitive function, neuropathic pain, and impairment, tobacco cessation should be a key element in physical therapy interventions to address prevention and restoration in neuromuscular pathologies. Smoking has been linked to an increased likelihood of autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythmatosis.13 The relative risk of RA in current smokers is 3.8 times higher than in nonsmokers,13 and among those with the disease, smokers are less likely to respond to anti-TNF alpha pharmacotherapy,13 such as infliximab. The link between smoking and RA is thought to be related to the production of proinflammatory cytokines within the synovium.42 The association between tobacco use, RA, and systemic lupus erythmatosis should be reflected in our clinical practice patterns when planning for care of people with these conditions. 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