Interview with David Tinkelman, MD
June/July 2009, Vol 2, No 4 - COPD
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In this interview, Dr Tinkelman discusses the clinical approach to the diagnosis and treatment of chronic obstructive pulmonary disease and the effects of this airways disease on employees and employers. He stresses that smoking, much more than occupational exposure, causes this chronic and irreversible lung disease. Progressive loss of lung function reduces productivity in workers whose jobs require physical exertion. A significant number of employees with this disease become disabled. Therefore, companies would do well to support employees in their efforts to quit smoking to lower the impact of this debilitating disease in their workplace. The case study typifies the etiology and progression of this disease. [AHDB. 2009;2(4):195-197.]

F. Randy Vogenberg, RPh, PhD: Could you begin by addressing the differential diagnosis of chronic obstructive pulmonary disease (COPD) in relation to asthma?

David Tinkelman, MD: Both asthma and COPD are inflammatory airway diseases, which is an important fact because these conditions may be similar in their clinical presentation. They both involve inflammation, but the inflammation is mediated by different pathways and has entirely different triggers.1 In COPD, the inflammation leads to destruction and to irreversible airway changes. In asthma, the inflammatory process causes the airways to become hyperresponsive, which enables them to go into spasm, and the airways become thickened due to the inflammation; but these changes are reversible. The essential difference between COPD and asthma is that asthma is a fully reversible lung disease, and COPD is an irreversible or only partially reversible lung disease.

The causes of COPD and asthma are also different.1 COPD is predominantly, although not exclusively, caused by smoking. In contrast, a large percentage of asthma cases are caused by allergy. In some people, asthma is caused by an infectious disease process. Unlike COPD, asthma is not a destructive airway disease.

Vogenberg: What are the guidelines for COPD diagnosis?

Tinkelman: For COPD, the world truly changed in 2001, with publication of the guidelines from the Global Initiative for Obstructive Lung Disease (GOLD initiative).2 Before that, the term “COPD” was not used very much and was referred to as “emphysema” or “chronic bronchitis.” However, each of these terms describes something different: emphysema describes a pathologic change, with destruction of the terminal airways resulting in air trapping; chronic bronchitis describes a clinical presentation, with hypersecretion of mucus and months of coughing, predominantly in the morning. The original GOLD initiative guidelines adopted the term COPD, which encompasses both emphysema and chronic bronchitis, and heightened awareness to the condition.

The American Thoracic Society (ATS) also issued its own guidelines in 2004.3 Whereas the GOLD initiative criteria for COPD focused onmeasured lung function, by forced expiratory volume in 1 second (FEV1)and forced vital capacity, the ATS criteria incorporated clinical symptoms in addition to lung function measurements. When the GOLD initiative guidelines were updated in 2007, clinical symptoms were added to the definition.4 Almost 60% of primary care physicians never do a lung function test on patients with respiratory symptoms.5 A COPD definition exclusive of symptoms may not lead to a correct diagnosis of this condition.

Vogenberg: How is COPD diagnosed and confirmed?

Tinkelman: Patients with COPD typically present with coughing and increasing shortness of breath over time. Some features in the history are critical to the diagnosis. A critical feature is that the symptoms progressively get worse. COPD is not a condition that gets better and worse, better and worse—that is the typical history for asthma. Another key feature is a history of exposure to toxins. Predominantly, that exposure is to cigarette smoke. Sometimes it is a work-related exposure in a specific industry. Rarely, it is a genetic cause—alpha1 antitrypsin deficiency—found in younger people.

Patients, however, generally do not tell the physician the truth about their smoking.6 They do not tell how much they smoke, and they may not admit that they are still smoking.6 To make a COPD diagnosis, the clinician has to find out whether a patient has an airway obstruction that is either partially or completely irreversible. The only way to make a definitive diagnosis is with spirometry.

Vogenberg: In the working-age population, those under 65 years, what would be a typical profile of a COPD patient?

Tinkelman: The typical patient has a loss in lung function, manifested by an increase in shortness of breath.7 The patient may say, “I used to be able to walk up the steps,” or “I used to be able to play golf.” That indicates that this patient’s lung capacity has progressively worsened. Many people deny this or attribute it to getting older. In fact, they have lost significant lung function and are unable to do things that they should be able to do at their age.

Loss of lung function—manifested as the change in their ability to function in their daily activities—is what usually brings people with COPD to the doctor. They become frightened: they can ignore the wheezing and the coughing, but when they cannot do what they used to, that is when they present at the office.

The second cardinal symptom is coughing. “I get up in themorning and I cough,” is a common complaint. Many people cough when they get up, but those with COPD regularly get up in the morning with a productive cough. They have lung destruction, chronic bronchitis, and mucus production, and they cough to clear their lungs.

The third sign is wheezing. As soon as a patient says “wheezing” to a primary care physician, that physician often thinks that the patient may have asthma, because wheezing is a hallmark of asthma.5,8 But many patients with COPD wheeze as well.

Vogenberg: What are the comorbidities of COPD common in the working-age population?

Tinkelman: Other body systems besides the lungs are affected by cigarette smoking. Osteoporosis in postmenopausal women is a major problem, because of the risk for fractures. Smoking aggravates that risk, because tobacco changes the calcium metabolism pathway.

The incidence of depression is much higher with COPD than with many other chronic diseases. This may be a direct effect of cigarette smoke on the central nervous system, but more likely, patients with COPD are depressed because they have lived a lifetime of hearing people say, “You should not smoke,” “You’re doing this to yourself,” “What are you going to do when you get older?” Now they have crossed that chasm and they are depressed. The inevitable has occurred, and they did nothing about it for the past 40 years.

The cardiovascular effects of COPD are linked to congestive heart failure rather than to the calcium buildup characteristic of atherosclerosis.

Vogenberg: Are there manifestations of COPD related to productivity that employers may be seeing and not realizing?

Tinkelman: Loss of lung function means that people lose the ability to take effective deep breaths. For working people with a sedentary job, productivity may not be affected all that much, except that, if they are still smoking, they have to go outside or move away from the building to smoke. For people in a job that requires some degree of activity, they will become short of breath earlier than they would if their lungs were functioning in a normal way. With any type of exertion in which they have to take deep breaths, they will have more problems.

There are 2 types of lost productivity. Direct loss of productivity occurs when people are sick and do not show up for work. Patients with COPD are more prone to lung infections, especially in the fall and winter, and their functioning is more impaired when they have an attack. Indirect loss of productivity occurs in presenteeism, when people are at work but their productivity is reduced. Workers with COPD may have to stop more often and take more breaks. The indirect loss is hard to measure, but it is there.

In the railroad industry, for example, loss of productivity is a huge problem. Smoking is prevalent among railroad workers, as well as among truckers and blue collar workers who have jobs that require physical activity. Smoking for a long period of time is associated with a higher incidence of comorbid conditions, leading to direct and indirect effects on productivity.

Vogenberg: What is the economic impact of COPD in the workplace, as it affects the patient and the employer?

Tinkelman: Disability from COPD is not always considered a workplace issue, but it is a major problem for which billions of dollars are spent.9,10 As staggering as these figures are, the more sobering realization is that the true figures are almost double the reported numbers. Because of misdiagnosis and underdiagnosis, the true burden of COPD is not known. For example, a 55-yearold woman who has COPD but was diagnosed with asthma for the first 5 years is counted in the economic burden associated with asthma, not with COPD. Our research showed that among patients with COPD under age 65, there is a significant amount of long-term disability.10,11 These are people who should be working.

Vogenberg: What can be done to mitigate or better manage the loss of worker productivity from COPD?

Tinkelman: The first thing is to get people to stop smoking. It is important to identify whether the patient is currently smoking. The patient in the case study above exemplifies the difficulty of this task. She admits to smoking on and off, but what she admits to, and what she is truly doing, may not be the same.6 Pharmacotherapy for COPD is not the only answer; there has not been a major change in therapy for COPD in years. Formulations of atropine, tiotropium, and beta agonists are useful, but these are not new drug classes. Inhaled steroids work mainly for those who have a mixed cause of COPD (up to 40% of patients).12 Many patients are diagnosed too late, and steroids do not reverse airway destruction. The number of deaths from COPD is larger than from asthma. It is the only prevalent chronic illness in which the mortality rate is increasing.

Vogenberg: What is being done to heighten awareness of COPD in the United States?

Tinkelman: Some companies have done a great job heightening awareness to this condition. They use the term COPD, and they run ads on TV. The National Institutes of Health has conducted an entire campaign to raise awareness to COPD that is directed not just to consumers but also to physicians. At many different levels, the message is getting out. The Occupational Safety and Health Administration has also been involved in raising awareness to this disease for many years.

Only about 10% to 20% of patients with COPD are nonsmokers.13 The number of people who get COPD from environmental exposure is relatively low. Different industries present different kinds of exposures to COPD risk, such as vapors, gases, toxic dusts, and certain strong odors. Smoking makes the effects of exposure to such materials much worse. Many industries recognized this several years ago and now use robotics in certain areas, such as spray painting.14

Vogenberg: When you talk with medical directors at large companies, what do you tell them they could be doing differently to prevent COPD?

Tinkelman: I try to dispel their fear of making a COPD diagnosis, because they think it is going to be costly. I try to start them thinking about prevention and helping people with COPD. I suggest that they change the culture of their workplace to be nonsmoking. They also need to provide resources for their smokers, to help them get into smoking-cessation programs. Many employees do not take advantage of these programs, because they are afraid of being fired. Companies need to remove that threat. If employees are afraid to tell their employer that they want to quit smoking, they will not tell. Companies have to support them. Large companies have nurses and other medical staff who can offer smoking-cessation information and programs. Wellness programs can benefit everyone.


1. Tinkelman DG, Price DB, Nordyke RJ, et al. Symptom-based questionnaire for differentiating COPD and asthma. Respiration. 2006;73: 296-305.
2. Global strategy for the diagnosis, management, and prevention of chronic pulmonary disease: National Heart, Lung, and Blood Institute and World Health Organization Global Initiative for Chronic Obstructive Lung Disease (GOLD): executive summary. Respir Care. 2001; 46:798-825.
3. American Thoracic Society/European Respiratory Society Task Force. Standards for the Diagnosis and Management of Patients with COPD. Version 1.2. September 8, 2005. Accessed June 11, 2009.
4. Rabe KF, Hurd S, Anzueto A, et al; for Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. Am J Respir Crit Care Med. 2007;176:532-555.
5. Tinkelman DG, Price DB, Nordyke RJ, Halbert RJ. Misdiagnosis of COPD and asthma in primary care patients 40 years of age and over. J Asthma. 2006;43:75-80.
6. Price DB, Tinkelman DG, Halbert RJ, et al. Symptom-based questionnaire for identifying COPD in smokers. Respiration. 2006;73:285-295.
7. Price DB, Tinkelman DG, Nordyke RJ, et al. Scoring system and clinical application of COPD diagnostic questionnaires. Chest. 2006;129: 1531-1539.
8. Tinkelman DB, Price D,Nordyke RJ,Halbert RJ. COPD screening efforts in primary care: what is the yield? Prim Care Respir J. 2007;16:41-48.
9. Foster TS,Miller JD,Marton JP, et al. Assessment of the economic burden of COPD in the U.S.: a review and synthesis of the literature. COPD. 2006;3:211-218.
10. Tinkelman D, Nordyke RJ, Isonaka S, et al. The impact of chronic obstructive pulmonary disease on long-term disability costs. J Manag Care Pharm. 2005;11:25-32.
11. Tinkelman D, George D, Halbert RJ. Chronic obstructive pulmonary disease in patients under age 65: utilization and costs from a managed care sample. J Occup Environ Med. 2005;47:1125-1130.
12. Burge PS, Calverley PM, Jones PW, et al. Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ. 2000;320:1297-1303.
13. Global Initiative for Chronic Obstructive Lung Disease. Guidelines: global strategy for diagnosis, management, and prevention of COPD. November 2008. Accessed June 10, 2009.
14. Blanc PD, Iribarren C, Trupin L, et al. Occupational exposures and the risk of COPD: dusty trades revisited. Thorax. 2009;64:6-12.

Dr Tinkelman is Vice President of Health Initiatives, National Jewish Health, and Professor of Pediatrics at National Jewish Health, and the University of Colorado Health Sciences Center, Denver, CO; Dr Vogenberg is Principal, Institute for Integrated Healthcare, and Chief Strategic Officer, Employer-Based Pharmaceutical Strategies, Sharon, MA.

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Last modified: November 10, 2011
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