3.4 Respiratory diseases

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3.0 Background

3.1 Tobacco—a leading preventable cause of death and disease

3.2 Cardiovascular diseases

3.3 Lung cancer

3.4 Respiratory diseases

3.5 Other cancers caused by or associated with smoking

3.6 Reproductive health and smoking

3.7 Pregnancy and smoking

3.8 Infant health and smoking

3.9 Increased susceptibility to infection in smokers

3.10 Eye diseases

3.11 Dental diseases

3.12 Gastrointestinal diseases

3.13 Bone density and risk of fractures

3.14 Effects of smoking on the skin

3.15 Smoking and complications in medical treatment

3.16 Smoking and diabetes

3.17 Poorer levels of general health

3.18 Smoking, motor vehicle crashes and other injuries

3.19 Burns and fires caused by tobacco use

3.20 Tobacco poisoning

3.21 Health effects for younger smokers

3.22 Genetic influences on tobacco-caused disease

3.23 Smoking, dementia and cognitive decline

3.24 Lung disease, smoking and occupational exposures

3.25 Air pollution, cigarette smoking and ill health

3.26 Health effects of smoking brands that claim to deliver lower levels of tar, nicotine and carbon monoxide

3.27 Health effects of smoking tobacco in other forms

3.28 Health 'benefits' of smoking?

3.29 Morbidity (ill health) attributable to tobacco-caused disease

3.30 Deaths attributable to tobacco by disease category

3.31 Morbidity and mortality due to tobacco-caused disease and socioeconomic disadvantage

3.32 Health effects of smoking other substances

3.33 Health effects of chewing tobacco, and of other smokeless tobacco products

3.34 Public perceptions of tobacco as a drug, and knowledge and beliefs about the health consequences of smoking

3.35 Health benefits of cessation

3.36 The global tobacco pandemic

Acknowledgments

References

Smoking interferes with the body's methods of filtering inhaled air. Chemicals within the smoke, especially hydrogen cyanide, acrolein, ammonia, nitrogen dioxide and formaldehyde, have a direct damaging effect on the cilia, part of the natural lung clearance mechanism in humans.22 Cilia are tiny hair-like structures that line the bronchial tubes, collecting and sweeping away impurities that have been inhaled. Interference with this system can result in an accumulation of mucus and toxins in the lungs, and reduce the lungs' ability to respond to infection. These factors increase the likelihood of developing lung disease.

3.4.1 Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) arises from progressive, permanent damage to the airways and airway sacs of the lungs. It is a major underlying cause of death in Australia, accounting for almost 4% of all deaths in 2004.28

COPD comprises three separate but often interconnected disease processes. These are:29

• Chronic over-secretion of mucus, resulting in chronic cough and phlegm production. This may be associated with low-grade infection in the airways (chronic bronchitis).
• Airway thickening and narrowing resulting in difficulty breathing.
• Damage to the small airways within the lung, eventually causing destruction of elastic fibres and the airway sacs (alveoli) where oxygen is transferred to red blood cells and carbon dioxide is removed from the bloodstream. This disease process, known as emphysema, restricts the lungs' capacity to contract and expand, and decreases the amount of lung tissue through which gas exchange can occur.

All three processes of COPD lead to progressive loss of lung function,29 and it is considered probable that most smokers have COPD to at least some extent.30 Although they may not necessarily develop disabling respiratory impairment, with increased duration of smoking almost all smokers can be expected to fulfil diagnostic criteria for the disease, are at increased risk of suffering from respiratory illness, and could potentially benefit from treatment.30 The chronic nature of these diseases means that those who develop them may continue to live for many years, with various degrees of discomfort and disability. Even individuals with mild COPD have reduced quality of life.31 At their worst, sufferers may be dependent on life support systems.

While smoking is the primary cause of COPD, it may also occur in non-smokers with a long history of asthma, or in individuals with a rare, genetically-determined deficiency in the protein a1-anti-trypsin. Smokers with this genetic risk factor experience a much more rapid decline in lung function.31 Up to 2% of cases of COPD occur in patients with a1-anti-trypsin deficiency.31 Exposure to air pollution and certain occupational pollutants (such as dusts and other particles, and toxic gases) are also implicated as risk factors, and the combination of smoking with adverse occupational exposures may lead to an even higher risk of developing COPD. About 20% of cases of COPD are likely to be related to occupational exposures.31

Death rates for COPD have been in decline for males over the past thirty years, while rates for women increased up until the early 1990s and have since stabilised. This is likely to reflect changing patterns in cigarette smoking28 rather than any improvement to health due to changes in the toxicity of cigarettes smoked, for which the evidence is currently equivocal.5

In Australia in 2004–05, it is estimated that of all deaths in people aged over 35 caused by COPD, 77% of cases in males and 71% of cases in females were attributable to smoking.20

3.4.2 Other chronic respiratory diseases

Chronic respiratory diseases include symptoms such as phlegm production, cough and wheezing, and reduced lung capacity.5 These symptoms arise from the direct deleterious effect of smoking on the lungs, as described above. Continued smoking leads to the development of chronic obstructive pulmonary disease (see above).

There is some evidence that cigarettes with lower tar levels may have reduced the incidence of cough and mucus hypersecretion.5

3.4.3 Acute respiratory illnesses

Acute respiratory illnesses include bronchitis, bronchiolitis, pharyngitis, influenza and pneumonia, and are bacterial or viral in origin. Smoking reduces the lungs' ability to resist infection by directly damaging lung defences in the airways (cilia movement and mucus clearance) and by impairing the lungs' immune response to infection.5

Smoking causes acute respiratory illnesses, including pneumonia, in individuals who do not already have underlying smoking-related chronic obstructive lung disease.5 In Australia in 2004–05, it is estimated that about 15% of all deaths due to lower respiratory tract infection in men aged over 35, and 12% in women of the same age, were caused by smoking.20

3.4.4 Respiratory effects in utero and infancy

Maternal smoking during pregnancy causes reduced lung function in infants, and may also cause an increase in the number of lower respiratory tract infections during infancy. The effects of maternal smoking in utero may also be related to an increased risk of having impaired lung function in childhood and adulthood.5 In Australia in 2004–05, about 13% of all deaths due to lower respiratory tract infections in babies under the age of one were attributable to exposure to tobacco smoke.7

3.4.5 Respiratory effects in childhood and adolescence

Exposure to secondhand smoke during infancy and childhood, and active smoking during childhood and adolescence, cause impaired lung growth and an increased risk of developing more serious respiratory diseases.5 Active smoking in children and teenagers causes respiratory symptoms including coughing, phlegm production, dyspnea (breathing difficulty) and asthma-related symptoms such as wheezing. Active smoking causes the early onset of decline in lung function during late adolescence and early adulthood.5

3.4.6 Respiratory effects in adulthood

Smoking in adulthood is a cause of all major respiratory symptoms, including coughing, phlegm production, dyspnea and wheezing. Smokers who are also asthmatic are more likely to experience difficulty in controlling their asthma than non-smokers. All adults experience a loss of lung function as they age, but this process occurs earlier and at a greater rate among smokers than non-smokers.5

Snoring is more common in smokers and former smokers than in never smokers. Frequency of snoring increases with the amount of tobacco smoked, and is independent of obesity, another well-established risk factor for snoring. Snoring is likely to occur in response to the effects of tobacco smoke on the airways, including upper airway inflammation, cough and sputum production.32

Being a smoker is also associated with having an impaired sense of smell (hyposmia).33, 34 Smoke directly damages the olfactory sensory neurons, located in the nasal airways, which detect different odours.33 Smokers are about twice as likely to have olfactory impairment compared to non-smokers. Following quitting, sense of smell is restored to levels of a never smoker.34