Tobacco and Chronic

Obstructive Pulmonary
Diseases (COPD)
Mini Lecture 2
Module: Tobacco effects on
respiratory system

Objectives of the Module

GOAL OF MINI LECTURE: Provide students with knowledge
on the harmful effects of tobacco on chronic obstructive
pulmonary diseases (COPD), and skill to address smoking
and to provide smoking cessation counseling for COPD
patients
LEARNING OBJECTIVES
Learners will be able to:
Understand the burden of smoking among COPD patients
Understand the association between smoking and COPD,
and impact of smoking on COPD
Conduct counseling to encourage COPD patients to quit
smoking

CORE SLIDES

Tobacco and COPD

Mini Lecture 2
Module: Tobacco effects on
respiratory system

Global burden of COPD

COPD is an inflammatory lung disease which
characterised by almost irreversible airflow limitation
low ratio of FEV1/FEC and lower vital capacity (<0.7)
(Calverley and Walker, 2003)

Meta-analysis from 37 studies during 1990-2004 revealed

the pooled estimate of COPD was 7.6%, chronic
bronchitis alone 6.4%, and emphysema alone 1.8%.
(Halbert et al., 2006)

In 2002, COPD was the 5th leading cause of death in the

world, and it is predicted to cause 7.8% of global death in
2030.
(Mathers and Loncar, 2006)

Smoking: a risk factor for COPD

Smoking leads to airway inflammation, and hence
induces hyper-production of mucus chronic bronchitis
and later accelerated decline in FEV1.
Chronic mucus production can lead to COPD, with
contribution from other factors: genetic, life-style,
infections, etc.
Chronic bronchitis is a strong predictor of COPD.
Progressive decline of FEV1 leads to higher COPD
hospitalisation and death rates.
(Pelkonen, 2008)

Smoking and Respiratory

Infection the mechanisms
Structural changes
peribronchiolar inflammation and fibrosis
mucosal permeability and changes in pathogen adherence
impairment of the mucociliary clearance
disruption of the respiratory epithelium
Immunologic mechanisms
decreased immune response & circulating immunoglobulins
CD4 lymphopenia, CD8+ lympocyte counts
depressed phagocyte activity, and decreased release of
proinflammatory cytokines.
(Arcavi and Benowitz, 2004)

Passive smoking and COPD

Exposure to SHS at home or at work, particularly high
level of exposure, increases the chance to experience
COPD by 50%.
In China, about 11.6% of deaths among never smoker
are attributable to COPD.
An excess of 1.9 millions deaths due to COPD is
expected if over half of their non-smoker population
(about 60% of total adult) is exposed to high level of SHS
exposure (>5 years with 40 hours exposure per week).
(Yin et al., 2007)

Smoking cessation for COPD

patients (i)
Smoking cessation is the only most effective and costeffective way to reduce COPD mortality.
Smoking cessation prevents or delays the development
of airflow limitation, and reduces its progression.
Doctor should offer intensive smoking cessation
intervention for people at risk of COPD and those with
COPD already.
(Global Initiative for Chronic Obstructive Lung Disease, 2009)

Smoking cessation for COPD

patients (ii)
Intensive smoking cessation program can help COPD
patients quitting, remain in abstinence in long-term, and
have less sick-leave from work due to their COPD.
(Sundbald et al., 2008)

Even among the most severe COPD cases, cessation

slows the progressivity of lung function decline and
improve survival. However, at long term, the decline in
FEV1 will follow the function of ageing.
(Godtfredsen et al., 2008)

Hospitalization related to COPD exacerbation increased

during the 90s significantly among those 65+.
(Calverley and Walker, 2003)

OPTIONAL SLIDES

Tobacco and COPD

Mini Lecture 2
Module: Tobacco effects on
respiratory system

COPD Prevalence in Indonesia

No good registry data on COPD hospitalization and
mortality are available in Indonesia.
The projected prevalence of COPD in Indonesia was
5.6% ( a total of 4.8 millions moderate to severe COPD
cases) in those 30 years old and older in 2003.
70% were smoking-related COPD cases.

(Regional COPD Working Group, 2003)

Pathology of COPD
Basic mechanism: innate and adaptive inflammatory
immune response
Airway limitation in COPD patients can occurred through:
Infiltration of inflammatory cells and occlusion of airway
by inflammatory exudates
Thickening of airways wall due to repair and
remodeling process hyperactivity of epithelial cells
Decreased of elastic recoil pressure at respiratory
bronchioles
(Hogg and Timens, 2009)

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.
Three steps 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 (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)
(Cosio et al., 2009)

Smoking, chronic bronchitis and

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