TOBACCO AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

1. TOBACCO AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Mini Lecture 2 Module: Effects of Tobacco on the Respiratory System

2. Objectives of the Mini Lecture GOAL OF MINI LECTURE: Provide students with knowledge about the harmful effects of tobacco on chronic obstructive pulmonary disease (COPD), and the importance of smoking cessation counseling for COPD patients. LEARNING OBJECTIVES Students will be able to: • Describe the burden of smoking among COPD patients. • Describe the association between smoking and COPD and the impact of smoking on COPD. • Understand the importance of cessation counseling for COPD patients.

3. Contents Core Slides Optional Slides COPD Prevalence in India Pathophysiology of COPD Immunological Aspect of COPD Smoking, Chronic Bronchitis, and COPD Mortality • Global Burden of COPD • Smoking: A Risk Factor for COPD • Smoking and Respiratory Infection: Mechanisms • Secondhand Smoke and COPD • Indoor Air Pollution and COPD • Smoking Cessation: COPD Patients • Cessation Messages: COPD Patients

4. CORE SLIDES Tobacco and Chronic Obstructive Pulmonary Disease (COPD) Mini Lecture 2 Module: Effects of Tobacco on the Respiratory System

5. Global Burden of COPD • COPD is an inflammatory lung disease that is characterised by almost irreversible airflow limitation.1 • In 2002, COPD was the 5th leading cause of death in the world, and it is predicted to cause 7.8% of global deaths in 2030.2 1. Calverley and Walker 2003; 2. Mathers and Loncar 2006

6. Smoking: A Risk Factor for COPD • Smoking leads to airway inflammation, and hence induces hyper-production of mucus.1 • Chronic mucus production can lead to COPD, with contributions from other factors: genetic, life-style, infections, etc.1 • Chronic bronchitis is a strong predictor of COPD leading to higher COPD hospitalisation and death rates.1 1. Pelkonen 2008

7. Smoking and RespiratoryInfection: Mechanisms Structural changes: • Peribronchiolar inflammation and fibrosis • Mucosal permeability increase and changes in pathogen adherence • Impairment of the mucociliary clearance • Disruption of the respiratory epithelium1 Immunologic mechanisms: • Decreased immune response & circulating immunoglobulins • Impaired cellular immunity1 1. Arcavi and Benowitz 2004

8. Secondhand Smoke and COPD • Exposure to SHS at home or at work, particularly high levels of exposure, increases the chances of COPD by as much as 50%.1 • In China, about 11.6% of deaths among never smokers are attributable to COPD.1 1. Yin et al 2007

9. Indoor Air Pollution and COPD • Indoor air pollution is cumulative: combustion of solid fuels+ indoor smoking • Increases risk of COPD, particularly in women and children • To reduce indoor air pollution: • Substitute solid fuels with LPG or electricity • Locate kitchen outside living/sleeping areas • Adequately ventilate kitchens • Minimize exposure (e.g., smokeless chullahs) • Stop/minimize indoor smoking Jindal 2004

10. Smoking Cessation: COPD Patients • Smoking accelerates progression of COPD.1 • Smoking cessation programs can help COPD patients quit for the long term. • Even in severe COPD cases, cessation slows the loss of lung function and improves survival.2 1. Sundblad et al. 2008; 2. Godtfredsen et al. 2008

11. Cessation Messages:COPD Patients • Smoking cessation is of critical importance for patients with COPD. • Doctors should ask all COPD patients about smoking and second hand smoke exposure. • Doctors should advise all COPD patients to quit smoking and avoid second hand smoke.

12. OPTIONAL SLIDES Tobacco and Chronic Obstructive Pulmonary Disease (COPD) Mini Lecture 2 Module: Effects of Tobacco on the Respiratory System

13. COPD Prevalence in India • Prevalence of COPD from India (from different population-based studies): highly variable • Male subjects: 2.12% to 9.4% (North India), 1.4% to 4.08% (South India) • Female subjects: 1.33% to 4.9% (North India), 2.55% to 2.7% (South India) • Median prevalence rates (>30 years): Male – 5%, Female – 2.7% • More common in males • Median male to female ratio: 1.6:1 Jindal et al. 2004

14. Pathophysiology of COPD • Basic mechanism: innate and adaptive inflammatory immune response.1 • Airway limitation in COPD patients can occur through: • Infiltration of inflammatory cells and occlusion of airway by inflammatory exudates. • Thickening of airway walls due to repair and remodeling process—hyperactivity of epithelial cells. • Decrease of elastic recoil pressure at respiratory bronchioles.2 1. Calverley and Walker 2003; 2. Hogg and Timens 2009

15. Immunological Aspect of COPD • “Danger hypothesis” by Matzinger: immune system is triggered not by the infective material, but by the cellular stress or tissue damage.1 • Three-step mechanisms leading to COPD: • Step 1: Activation of macrophages and neutrophils as initial response to cigarette smoke (a healthy smoker) • Step 2: T-cell activation and proliferation (Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 1 or stage 2, with progression to GOLD 3 or 4 with severe failure) • Step 3: Adaptive immune response (GOLD 3 or 4)1 1. Cosio et al. 2009

16. Smoking, Chronic Bronchitis,and COPD Mortality • Smoking is a risk factor for chronic bronchitis, COPD, deteriorating lung function, and mortality as end point.1 • 40% of smoker will develop chronic bronchitis, 25% of smoker will develop COPD.1 • Deterioration of lung function and obstruction of airways among patient with chronic bronchitis will lead to COPD.1 • Patients with rapid decline of FEV1 have 40% higher probability of hospitalization and COPD-related death.1 1. Pelkonen 2008

17. The most important health message a doctor can give to patients is to quit smoking.