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1/2. harm reduction--a treatment approach for resistant smokers with tobacco-related symptoms.

    Smokers with chronic obstructive pulmonary disease (COPD) appear to represent a hard-core group, and this presents a dilemma for chest physicians. A reduction in cigarette smoking benefits health, and nicotine replacement therapy (NRT) can aid smoking reduction. Hence we studied the efficacy of nicotine gum in helping hard-core smokers with severe COPD to quit. Seventeen smokers with severe COPD (FEV(1) 38-47% of predicted normal) who smoked >30 cigarettes/day but were unable to quit were encouraged to reduce their smoking as much as possible by using 4-mg nicotine gum. Five gradually reduced their daily tobacco consumption and, 18 months after starting NRT, were smoking an average of 6 cigarettes/day while still using nicotine gum. Compared to baseline, their respiratory symptoms had improved, and both FEV(1) and FVC had increased. There was no improvement in pulmonary function in the group of smokers who did not reduce their cigarette consumption. No adverse events relating to nicotine occurred among the patients who used NRT to reduce their smoking. We propose that this reduction approach should be considered for patients with respiratory disease who are unable or unwilling to stop smoking.
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keywords = tobacco
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2/2. A 26-year-old welder with severe non-reversible obstructive lung disease.

    A 26-year-old white male, lifelong non-smoker presented with a history of increased shortness of breath, for approximately 1 year. He had a history of welding aluminum parts. He had evidence of partially reversible reactive airways disease with a non obstructive component as well. VATS biopsy revealed evidence of airway and parenchymal inflammation consistent with aluminum pneumoconiosis. Approximately 5-10% of COPD is attributable to non-smoking causes including occupational exposures. There are studies to suggest that the persistence of aluminum particulate may cause ongoing inflammation despite removal from exposure. It is possible that the persistence of particulate matter from tobacco smoke remaining in the lung may contribute to the persistent inflammatory response found in former smokers. Further study is required to examine the importance of this potential inflammatory mechanism both in occupationally exposed and in cigarette smokers. Reduction of certain particulate components of cigarette smoke may have implications for prevention of disease or at least disease progression in some COPD patients.
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keywords = tobacco
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