3.2.1 Damage to the lungs caused by smoking
The primary function of the human respiratory tract is gas exchange. Air is inhaled through the upper respiratory tract (nasal cavity, pharynx and larynx) into the lungs, which together with the trachea and bronchi make up the lower respiratory tract. Gas exchange occurs between the alveoli and pulmonary capillaries, where oxygen passes into the blood and carbon dioxide from the blood into the lungs for exhalation. This gas exchange occurs through a very thin membrane, over an extremely large surface area within the lungs. Gas exchange occurs due to disequilibrium of the concentrations of gases in the blood and air. Other gases in disequilibrium may also be exchanged, including those present in tobacco smoke.1
Particles and gases are inhaled in each breath. These include harmless dust, chemicals that may be harmful, allergens such as pollen, and pathogens (viruses, bacteria, fungal spores and tiny parasites). Gases pass directly into the lungs. Large and very small particles are mostly trapped in the nose and upper airway and cleared without reaching the lungs. Intermediate sized particles, between approximately 0.005 and 2.5 micrometres in diameter, may penetrate deep into the lungs.1 The lungs are protected by an anti-microbial respiratory defence system and mucociliary clearance system that physically moves particles out of the lungs.
The respiratory system, being the route of tobacco smoke exposure, is exposed to higher concentrations of the toxic constituents of smoke than any other system in the body. Smoke is inhaled through the mouth and nose, travels into the lungs via the upper and lower respiratory tracts. In each part of the respiratory system, smoke causes damage and leads to diseases such as cancer and chronic obstructive pulmonary disease (COPD).1 2 This Section describes the major non-cancerous respiratory diseases caused by or associated with smoking.
22.214.171.124 Impairment of pulmonary immune and protective responses
About 60% of the particles from mainstream cigarette smoke are deposited in the lungs. These particles cause structural and immunological damage to the lungs. Particles from smoke also enter the blood stream through the lungs and circulate all over the body. To avoid the ill effects from these potential insults, the respiratory system employs a set of protective mechanisms. Cigarette smoke can impair or overwhelm the lungs’ defences, leading to acute or chronic disease.1
The particles from cigarette smoke and other sources are trapped by the mucus blanket on the surface of the cells lining the airways. They are cleared by mechanisms such as mucociliary clearance, coughing and alveolar clearance. During mucociliary clearance, particles in the mucous are swept out of the airways by the synchronised movement of cilia, which are tiny hair-like structures on the surface of airway cells.3
Exposure to cigarette smoke reduces the clearance rate of particles from the lungs.1 This is in part due to shortening, loss or disco-ordination of cilia, but may also be due to changes in the thickness of mucus that reduces the effective propulsion of the mucus by the cilia.3 4 5 6 Acrolein and formaldehyde in cigarette smoke are suspected to be causes of this damage to respiratory cilia.1
Impairment of the mucociliary system also increases the risk of infection.1 Smokers become increasingly reliant on coughing to clear mucus, rather than the normal clearance process which is more effective and less irritating.7 Long-term smokers retain a substantial amount of particles in their lungs.1 Smoking cessation improves mucocilary clearance in the nose after two weeks, and in the lungs after three months.4 8
Innate immunity in the respiratory system
Innate immune respiratory responses consist of fast-acting peptides, proteins and leukocytes aimed at blocking and killing infectious pathogens that enter the airways. The innate immune system also directs the adaptive immune system, leading to antibody and cytotoxic cellular responses that protect against infectious agents such as the influenza virus.9
The ability of the lung’s immune system to sense and eliminate viruses and bacteria is impaired by smoking.10 11 Smoking compromises the innate immune system, provoking an inflammatory response and increasing the potential for infection.1 12 13 Inflammation is one type of innate immune response against pathogens. It should be a fast and temporary response, resolving after the threat is removed, as chronic inflammation is damaging. Due to regular damage from tobacco, smokers usually have damaging chronic inflammation in their lungs.1 14 The 2020 report of the US Surgeon General on smoking cessation determine that the evidence was suggestive but insufficient to infer that this airways inflammation persists for months to years after smoking cessation.15
Some specific chemicals from tobacco smoke are predicted to damage the lung immune responses based on experimental evidence. In mouse experiments, acrolein from cigarette smoke disrupted the ability of surfactant proteins to inhibit bacterial growth and activate the protective functions of alveolar macrophages (leukocytes that ingest and destroy bacteria).16 Cadmium from cigarette smoke can alter the regulation of innate immunity and inflammation. Increased tissue levels of cadmium are associated with COPD, which is usually caused by smoking.17
126.96.36.199 Damage to lung function
Lying under the mucociliary system in the lungs, the outer layer of lung cells lining the airway form a physical barrier between lung tissue and airspace. Chronic exposure to cigarette smoke damages this protective barrier, causing inflammation and increasing its permeability.1 12 11
Cigarette smoke triggers an inflammatory response that leads to destruction of lung parenchyma (the functional tissue, taking part in gas exchange). This is promoted through the cellular release of proteinases that damage the extracellular matrix of the lung, programmed cell death due to oxidative stress, and loss of matrix–cell attachment and ineffective repair of elastin and other extracellular matrix components act to enlarge the airspace.1, 13
Active smokers in childhood and adolescence have both reduced lung function and impaired lung growth.18 Smoking causes the early onset of decline in lung function during late adolescence and early adulthood. 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.10 Among smokers, there appears to be a sliding scale of susceptibility to loss of lung function.19 20 A few smokers may lose lung function almost as slowly as non-smokers. . A significant minority of smokers, their rapid loss of lung function becomes disabling or fatal.1 12 19 Most smokers will fall between these groups.20 A diagnosis of chronic obstructive lung disease (COPD) can be made after a significant and non-reversible loss of lung function. In the population of smokers without COPD, the age-related rate of lung function decline slows down to that seen in people who have never smoked within five years of smoking cessation. However, they do not regain the lung function they have already lost.14 Cessation of smoking is the only established intervention that reduces the loss of lung function over time, for people with COPD.15
3.2.2 Smoking and respiratory symptoms
Active smoking causes respiratory symptoms in adults, teenagers and children, including coughing, phlegm, wheezing and dyspnoea (difficulty breathing and shortness of breath). These symptoms are associated with a number of acute and chronic respiratory illnesses. They may also indicate underlying lung injury and disease. The population prevalence of these symptoms decreases with smoking cessation.10
3.2.3 The effect of smoking on acute respiratory infections
Adults who smoke are more likely than non-smokers to develop acute respiratory infections such as pneumonia. For more details see Section 3.9.
3.2.4 Major chronic respiratory conditions caused by smoking
188.8.131.52 Chronic Obstructive Pulmonary Disease (COPD)
Chronic obstructive pulmonary disease (COPD) is characterised by persistent respiratory symptoms and airflow limitation that is usually progressive.21 The chronic airflow limitation is caused by a mix of small airways disease (obstructive bronchitis) and destruction of the gas-exchanging surfaces of the lung due to chronic inflammation (referred to as emphysema). The relative contributions of both pathologies vary from person to person. The changes do not always occur together, and they evolve at different rates over time. Chronic respiratory symptoms may precede the airways obstruction that characterises COPD.21
Using self-reported data from the 2017–18 ABS National Health Survey, the prevalence of COPD in Australians aged 45 and over was estimated to be 4.8%.22 In 2018, 7,113 people were recorded as having died from COPD in Australia, making it the fifth leading cause of death.23
Death rates from COPD have declined over time.23 COPD is more prevalent among middle-aged and older people, at which stage it has important interactions with many other acute and chronic illnesses.23 24 The evidence also suggests that women may be more susceptible to developing severe COPD at younger ages.13 Beyond the effect on mortality, the chronic nature of COPD means those who develop COPD may live for many years, with various degrees of discomfort and disability.24 Even individuals with mild COPD have reduced quality of life, which worsens as the disease becomes more severe.25
Smoking as a cause of COPD
According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD), the causes of COPD include tobacco smoking, exposure to secondhand smoke, genetic factors, lung developmental factors, exposure to some chemicals and pollutants, and other chronic diseases that increase the risk of COPD.21
Smoking is the main cause of COPD. It’s estimated that 15-20% of long-term, regular smokers will develop COPD, and that smoking causes the majority of cases of COPD.14 A meta-analysis of 133 studies found that current smokers had a 3.5-fold increased risk of COPD compared to non-smokers.26 The 2004 report of the US Surgeon General has found sufficient evidence demonstrating that active smoking causes morbidity and mortality from COPD.10 The 2014 US Surgeon General’s report concluded that smoking is the dominant cause of COPD in the United States. Smoking causes all elements of the COPD phenotype, including emphysema and damage to the airways of the lungs.13
Smoking is the main cause of COPD in Australia. In 2015, 68.3% of the burden of COPD disease was attributable to tobacco use in men and 76.5% in women in Australia.27
People with COPD who continue to smoke may have worse symptoms and more exacerbations. Current smokers with COPD may have significantly poorer health-related quality of life than ex-smokers.28 29 However, some studies have found similar rates of exacerbations between current and former smokers with COPD.30 31 Smoking may also increase the risk of acute respiratory infections in people with pre-existing COPD.10
Pathophysiology of COPD
COPD arises from progressive, permanent damage to the airways and airway sacs (alveoli) of the lungs. The main processes thought to be important in the development of COPD that is caused by smoking are inflammation, oxidative stress, and an imbalance of proteases (enzymes that break up specific proteins) and antiproteases in the lung.1 10 Oxidative stress results from highly reactive free radicals and oxidant chemicals in tobacco smoke creating an imbalance between oxidants and antioxidants in the lung. Oxidative stress can directly damage lung cells, promote inflammation, and contribute to the protease-antiprotease imbalance.
While all smokers have inflammation of the lungs, not all develop COPD. People who develop COPD are thought to have an enhanced or abnormal inflammatory response to noxious particles or gases (typically from cigarette smoke).1 14 There are some known genetic causes of COPD. People with alpha-1 antitrypsin deficiency, a common inherited condition,1, 13 21 or those with rare inherited condition called cutis laxa, are at greater risk of COPD.13
Different disease processes result in the airflow limitation that characterises COPD. The main diseases are obstructive bronchiolitis and emphysema.1 14 Chronic bronchitis often co-occurs with COPD (as described below). Smokers have different susceptibilities to each disease process, and this will influence their symptoms.
Inflammation in the small airways is seen to some extent in all smokers, with some experiencing chronic bronchitis (described below).10 32 Obstruction of the small airways (obstructive bronchitis) occurs when abnormally heightened inflammation and remodelling occur in the small bronchi and bronchioles in the lungs. The term ‘remodelling’ describes a cycle of injury and repair in the presence of inflammation, that results in the thickening of the airway wall and narrowing of the airway spaces. The underlying cause may be related to overproduction and hypersecretion of mucus by goblet cells.12 21 33 This process obstructs air flow through the small airways to the lung’s air sacs (alveoli) where gas exchange occurs. For as long as smoking continues, the condition progresses. The main symptom is breathlessness, because the gradually altered lung structure cannot allow increases in the flow of air that is needed to exercise comfortably.12 Smoking cessation slows lung function decline and sustained cessation is necessary to return the decline in lung function to that of a non-smoker.10
Emphysema is the irreversible destruction of the walls of the alveoli—the small air sacs where gas exchange occurs. As this framework is lost, the alveoli walls cannot regenerate, and the air spaces enlarge. The resulting loss of the surface area where gas exchange occurs reduces the capacity of the lungs to transfer oxygen to red blood cells and remove carbon dioxide from the bloodstream—its essential functions.4 34 The lung becomes less elastic, restricting its capacity to contract and expand. The loss of elastic recoil reduces the force driving the air out the lungs, so it takes longer to breathe out.1 12 In advanced emphysema, the inelastic lungs enlarge leading to a large barrel-shaped chest.
Smoking leads to a shift in the protease–antiprotease balance towards proteases.1 Proteases are enzymes that degrade specific proteins. Emphysema involves an excess activity of proteases that degrade extracellular matrix proteins such as elastin and collagen in the airways and alveoli.10 Acting against this protein degradation are anti-proteases, such as alpha-1 antitrypsin. It’s believed that people with an inherited lower antiprotease activity are more susceptible to COPD. However, the protease-antiprotease balance does not completely explain the damage that underpins COPD, indicating that other mechanisms also underly this disease process.35
Course of COPD after smoking cessation
Smoking cessation is the only established intervention that reduces the loss of lung function among people with COPD.15 36 Smoking cessation also reduces the risk of developing COPD in cigarette smokers.15 In people with COPD, there is a small average improvement in lung function in the year after smoking cessation. Thereafter, age-related decline in lung function that is less than half of that seen in continuing smokers.14 Reduction in the number of cigarettes smoked does not change the loss of lung function.37 Former smokers have a reduced risk of hospitalisation related to COPD and death from COPD compared with those who continue to smoke.14 38
184.108.40.206 Chronic bronchitis
Chronic bronchitis is defined by symptoms of cough together with frequent and increased production of sputum or phlegm. It is diagnosed when these symptoms are present for three months in each of two successive years.1 Chronic bronchitis is associated with inflammation in the large and small bronchial airways, which results in the enlargement of mucus-producing glands and remodelling (thickening) of the airway walls. People with chronic bronchitis have more frequent respiratory infections.1 39 In persons who also have chronic obstructive pulmonary disease (COPD), symptoms of chronic bronchitis increase the risk of death from respiratory infections.40
Chronic bronchitis often co-occurs with COPD, but it does not influence airflow limitation unless the inflammation extends into the small airways.1 Having symptoms of chronic bronchitis is associated with an accelerated decline in lung function as seen in COPD.1 10 It was previously thought that chronic bronchitis was a necessary first step in the development of COPD. However, since then research has shown that airflow limitation can develop without symptoms of chronic bronchitis.1 Also, in people with normal lung function, the presence of chronic bronchitis does not increase their likelihood of developing COPD.1 14
Smoking is a long-recognised cause of chronic bronchitis.41 1 26 A meta-analysis of 101 studies from 2011 found that current smokers have a 3.4-fold higher risk of chronic bronchitis compared to non-smokers.26 Symptoms of chronic bronchitis decrease by one to two months after smoking cessation, and the population prevalence of cough and phlegm returns to the level of never smokers within five years.14 In people with severe COPD, chronic cough associated with chronic bronchitis is more likely to persist after smoking cessation.39
3.2.5 Other respiratory conditions related to smoking
Asthma is a common chronic respiratory disease affecting approximated one in nine people in Australia.42 People with asthma have airways obstruction (narrowing) that leads to wheezing, shortness of breath, coughing, chest tightness and/or fatigue. Severe asthma can be life-threatening, causing 389 deaths in Australia in 2018.43 Triggers for asthma symptoms include tobacco smoke, allergens, respiratory infection and exposure to some chemicals.
Asthma usually starts in childhood and often becomes less frequent over time. However, it may continue for some people, reoccur, or begin later in life. These time periods can mean that it is difficult to be certain if exposure to tobacco smoke has preceded the disease onset, complicating studies of causality.
The 2014 US Surgeon General’s report reviewed 12 studies of asthma risk among adolescent smokers. Many of these studies showed an increased risk of asthma among adolescent smokers, but there were a limited number of high-quality studies. The report concluded that the available evidence suggested but is insufficient to conclude that active smoking is a cause of asthma in adolescents. Similarly, this report also concluded that the evidence suggested, but was insufficient to conclude that smoking increases the incidence of asthma in adults.
Smoking exacerbates asthma in adults and leads to poor asthma control.10 13 44 Three randomised controls determined that inhaled corticosteroids were of less benefit to smokers with asthma compared to non-smokers.13 45 46 47 In one of these studies, smokers had 6-fold higher rate of exacerbations whilst taking corticosteroids to control their asthma, compared to non-smokers.47 People with asthma who smoke are more likely to have accelerated loss of lung function.13 48 49 In the Copenhagen City Heart Study, adult smokers with asthma had a greater decline in lung function over time than non-smokers.50 The risk of severe asthma events, such as hospitalisation, use of emergency services and death, are increased in smokers.13 49 51
The 2014 US Surgeon General’s report concluded that the evidence suggested, but was insufficient to demonstrate causation that smoking caused exacerbations in asthma among children and adolescents.13
Smoking cessation may improve asthma control.52 53 15 However, the 2020 report of the US Surgeon General concluded that whilst the evidence suggested that smoking cessation reduced asthma symptoms, improved treatment outcomes and asthma specific quality-of-life scores, and improved lung function in smokers, it was currently insufficient to infer causality.15
See Section 3.8 for more information about the effects of parental, grandparental and perinatal smoking on asthma in children.
220.127.116.11 Interstitial lung disease (IDL)
Interstitial lung diseases are a group of disorders that are mostly characterised by progressive scarring of interstitial alveolar tissue. The pathophysiology is often fibrosis (scar tissue formation) and inflammation. Some of these disorders are caused or triggered by exposure to toxic materials, or associated with auto-immune diseases, connective tissue diseases or the use of certain drugs.54 The 2014 Lung Disease in Australia report stated that interstitial lung diseases lead to 4,050 hospitalisations and 1,161 deaths in 2011 – 2012.55
Idiopathic pulmonary fibrosis is a progressive, fatal fibrotic interstitial lung disease. It is one of the most common and most severe interstitial lung diseases. It has the worst prognosis of all idiopathic interstitial diseases of the lung, with a median survival time of three to four years.56 Although its causes are unknowns, evidence suggests that both genetic and environmental factors are involved in its development.57 The incidence and prevalence of idiopathic pulmonary fibrosis in Australia are currently difficult to estimate.55
The 2014 report of the US Surgeon General reviewed 12 studies on the risk of idiopathic pulmonary fibrosis in smokers.13 All but one found an increased risk of this disease in smokers. The two largest studies reported odds ratios of 1.59 and 1.57 for idiopathic pulmonary fibrosis in ever smokers compared to never smokers. However, there are some problems with the quality of the epidemiological studies, such as inconsistent adjustment for potential confounders. The 2014 report concluded that the evidence suggested but was insufficient to conclude that smoking is a cause of idiopathic pulmonary fibrosis.13
Respiratory bronchiolitis-interstitial lung disease (RB-ILD) is seen in very heavy smokers, typically those smoking more than 30 cigarettes per day. Unlike typical COPD, it can be seen in young smokers.58 59 RB-ILD is a greatly exaggerated form of bronchiolitis that spreads to create inflammation in the nearby alveoli. RB-ILD impairs lung function and has an abnormal appearance on chest X-rays. Smoking cessation is recommended.58
18.104.22.168 Pulmonary histiocytosis X (Pulmonary Langerhan’s Cell Histiocytosis)
Histiocytosis X is a rare cancer that causes damage to variable regions of the body. Pulmonary histiocytosis X involves the development of inflammatory nodules in the lung along with cystic degeneration of the lungs themselves. It has a distinct appearance on X-rays. Patients are commonly young adults and the vast majority have a history of smoking.58 Smoking cessation is strongly encouraged, because case reports show improvement after quitting, and even restoration of normal or near-normal lung structure.58 60 61 Smoking may therefore be a cause of this disease, but current research is insufficient to make this conclusion.
22.214.171.124 Sense of smell
See Section 3.22.6.
See Section 3.22.4.
Relevant news and research
For recent news items and research on this topic, click here. ( Last updated May 2023)
1. US Department of Health and Human Services. How tobacco smoke causes disease: the biology and behavioral basis for smoking-attributable disease. A report of the US Surgeon General, Atlanta, Georgia: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Available from: https://www.ncbi.nlm.nih.gov/books/NBK53017/.
2. Churg A, Cosio M, and Wright JL. Mechanisms of cigarette smoke-induced COPD: insights from animal models. American Journal of Physiology. Lung Cellular and Molecular Physiology, 2008; 294(4):L612-31. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18223159
3. Leopold PL, O'Mahony MJ, Lian XJ, Tilley AE, Harvey BG, et al. Smoking is associated with shortened airway cilia. PLoS ONE, 2009; 4(12):e8157. Available from: https://www.ncbi.nlm.nih.gov/pubmed/20016779
4. US Department of Health and Human Services. The health consequences of smoking: Chronic Obstructive Lung Disease. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1984. Available from: https://profiles.nlm.nih.gov/spotlight/nn/catalog/nlm:nlmuid-101584932X476-doc.
5. Stanley PJ, Wilson R, Greenstone MA, MacWilliam L, and Cole PJ. Effect of cigarette smoking on nasal mucociliary clearance and ciliary beat frequency. Thorax, 1986; 41(7):519-23. Available from: https://www.ncbi.nlm.nih.gov/pubmed/3787531
6. Kreindler JL, Jackson AD, Kemp PA, Bridges RJ, and Danahay H. Inhibition of chloride secretion in human bronchial epithelial cells by cigarette smoke extract. American Journal of Physiology. Lung Cellular and Molecular Physiology, 2005; 288(5):L894-902. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15626749
7. Houtmeyers E, Gosselink R, Gayan-Ramirez G, and Decramer M. Regulation of mucociliary clearance in health and disease. European Respiratory Journal, 1999; 13(5):1177-88. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10414423
8. Ramos EM, De Toledo AC, Xavier RF, Fosco LC, Vieira RP, et al. Reversibility of impaired nasal mucociliary clearance in smokers following a smoking cessation programme. Respirology, 2011; 16(5):849-55. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21545372
9. Riches DWH and Martin TR. Overview of innate lung immunity and inflammation. Methods in Molecular Biology, 2018; 1809:17-30. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29987779
10. US Department of Health and Human Services. The health consequences of smoking: a report of the Surgeon General. Atlanta, Georgia: US Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available from: https://www.cdc.gov/tobacco/data_statistics/sgr/2004/index.htm.
11. Stampfli MR and Anderson GP. How cigarette smoke skews immune responses to promote infection, lung disease and cancer. Nature Reviews. Immunology, 2009; 9(5):377-84. Available from: https://www.ncbi.nlm.nih.gov/pubmed/19330016
12. Hogg JC. Pathophysiology of airflow limitation in chronic obstructive pulmonary disease. Lancet, 2004; 364(9435):709-21. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15325838
13. US Department of Health and Human Services. The health consequences of smoking - 50 years of progress. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Available from: https://www.ncbi.nlm.nih.gov/books/NBK179276/
14. International Agency for Research on Cancer. Reversal of risk after quitting smoking. IARC handbooks of cancer prevention, tobacco control, 11 Vol. 11.Lyon, France: IARC, 2007. Available from: https://publications.iarc.fr/Book-And-Report-Series/Iarc-Handbooks-Of-Cancer-Prevention/Tobacco-Control-Reversal-Of-Risk-After-Quitting-Smoking-2007.
15. US Department of Health and Human Services. Smoking cessation. A report of the Surgeon General. Atlanta, GA U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Centre for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health 2020. Available from: https://www.cdc.gov/tobacco/data_statistics/sgr/2020-smoking-cessation/.
16. Takamiya R, Takahashi M, Maeno T, Saito A, Kato M, et al. Acrolein in cigarette smoke attenuates the innate immune responses mediated by surfactant protein D. Biochimica et Biophysica Acta - General Subjects, 2020; 1864(11):129699. Available from: https://www.ncbi.nlm.nih.gov/pubmed/32738274
17. Knoell DL and Wyatt TA. The adverse impact of cadmium on immune function and lung host defense. Seminars in Cell and Developmental Biology, 2020. Available from: https://www.ncbi.nlm.nih.gov/pubmed/33158728
18. US Department of Health and Human Services. Preventing tobacco use among young people: A report of the Surgeon General. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2012. Available from: http://www.cdc.gov/tobacco/data_statistics/sgr/2012/.
19. Fletcher C and Peto R. The natural history of chronic airflow obstruction. British Medical Journal, 1977; 1(6077):1645-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/871704
20. Rennard SI and Vestbo J. COPD: the dangerous underestimate of 15%. Lancet, 2006; 367(9518):1216-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16631861
21. Global Initiative for Chronic Obstructive Pulmonary Disease. Global strategy for the diagnosis, management, and prevention of chronic obstrictove pulmonary disease. 2018 report. 2018. Available from: https://goldcopd.org/wp-content/uploads/2017/11/GOLD-2018-v6.0-FINAL-revised-20-Nov_WMS.pdf.
22. Australian Bureau of Statistics. National Health Survey: First Results, 2017–18. Cat no. 4364.0.55.001 Canberra, Australia: ABS, 2018. Available from: https://www.abs.gov.au/statistics/health/health-conditions-and-risks/national-health-survey-first-results/latest-release.
23. Australian Institute for Health and Welfare. Chronic obstructive pulmonary disease (COPD). Canberra, Australia: AIHW, 2020. Available from: https://www.aihw.gov.au/reports/chronic-respiratory-conditions/copd/contents/copd.
24. Australian Institute of Health and Welfare, Australia's health 2010. Australia's health series no. 12. AIHW cat. no. AUS 122. Canberra: AIHW; 2010. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2010/contents/table-of-contents.
25. Devereux G. ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. British Medical Journal, 2006; 332(7550):1142-4. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16690673
26. Forey BA, Thornton AJ, and Lee PN. Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema. BMC Pulmonary Medicine, 2011; 11:36. Available from: https://www.ncbi.nlm.nih.gov/pubmed/21672193
27. Australian Institute of Health and Welfare. Burden of tobacco use in Australia: Australian Burden of Disease Study 2015. Canberra 2019. Available from: https://www.aihw.gov.au/getmedia/953dcb20-b369-4c6b-b20f-526bdead14cb/aihw-bod-20.pdf.aspx?inline=true.
28. Cheruvu VK, Odhiambo LA, Mowls DS, Zullo MD, and Gudina AT. Health-related quality of life in current smokers with COPD: factors associated with current smoking and new insights into sex differences. International Journal of Chronic Obstructive Pulmonary Disease, 2016; 11:2211-9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27695308
29. Riesco JA, Alcazar B, Trigueros JA, Campuzano A, Perez J, et al. Active smoking and COPD phenotype: distribution and impact on prognostic factors. International Journal of Chronic Obstructive Pulmonary Disease, 2017; 12:1989-99. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28740378
30. Baris SA, Onyilmaz T, Basyigit I, Boyaci H, and Yildiz F. Frequency of exacerbations and hospitalizations in COPD patients who continue to smoke. Acta Medica Okayama, 2017; 71(1):11-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28238005
31. Tal S, Adir Y, Stein N, Shalom H, Lache O, et al. COPD exacerbator phenotype is inversely associated with current smoking but not with haptoglobin phenotype. Israel Medical Association Journal, 2019; 21(1):19-23. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30685900
32. Hogg JC, Wright JL, Wiggs BR, Coxson HO, Opazo Saez A, et al. Lung structure and function in cigarette smokers. Thorax, 1994; 49(5):473-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/8016769
33. Kim V and Criner GJ. Chronic bronchitis and chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 2013; 187(3):228-37. Available from: https://www.ncbi.nlm.nih.gov/pubmed/23204254
34. Australian Institute for Health and Welfare. Chronic diseases and associated risk factors in Australia, 2001. cat. no. PHE 33, Canberra, Australia: AIHW, 2002. Available from: https://www.aihw.gov.au/reports/chronic-disease/associated-risk-factors-australia-2001/contents/table-of-contents.
35. Lomas DA. Does protease-antiprotease imbalance explain chronic obstructive pulmonary disease? Annals of the American Thoracic Society, 2016; 13 Suppl 2:S130-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27115947
36. Barnes PJ. Chronic obstructive pulmonary disease. New England Journal of Medicine, 2000; 343(4):269-80. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10911010
37. Godtfredsen NS, Vestbo J, Osler M, and Prescott E. Risk of hospital admission for COPD following smoking cessation and reduction: a Danish population study. Thorax, 2002; 57(11):967-72. Available from: https://www.ncbi.nlm.nih.gov/pubmed/12403880
38. Godtfredsen NS, Lam TH, Hansel TT, Leon ME, Gray N, et al. COPD-related morbidity and mortality after smoking cessation: status of the evidence. European Respiratory Journal, 2008; 32(4):844-53. Available from: https://www.ncbi.nlm.nih.gov/pubmed/18827152
39. Braman SS. Chronic cough due to chronic bronchitis: ACCP evidence-based clinical practice guidelines. Chest, 2006; 129(1 Suppl):104S-15S. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16428699
40. Prescott E, Lange P, and Vestbo J. Chronic mucus hypersecretion in COPD and death from pulmonary infection. European Respiratory Journal, 1995; 8(8):1333-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/7489800
41. US Department of Health and Education and Welfare, Smoking and Health: A report of the Advisory Committee to the Surgeon General of Public Health Service. Publication no (PHS) 1103 Washington: US Department of Health, Education and Welfare, Public Health Service, Center for Disease Control; 1964. Available from: https://profiles.nlm.nih.gov/spotlight/nn/catalog/nlm:nlmuid-101584932X202-doc.
42. Australian Institute for Health and Welfare. Asthma. Canberra, Australia: AIHW, 2020. Available from: https://www.aihw.gov.au/reports/chronic-respiratory-conditions/asthma/contents/asthma.
43. Australian Institute for Health and Welfare. General Record of Incidence of Mortality (GRIM) books. Canberra, Australia: AIHW, 2020. Available from: https://www.aihw.gov.au/reports/life-expectancy-deaths/grim-books/contents/grim-excel-workbooks.
44. Australian Centre for Asthma Monitoring. Asthma in Australia 2011: with a focus chapter on chronic obstructive pulmonary disease. AIHW asthma series no. 4, cat. no. ACM 22, Canberra, Australia: AIHW, Available from: https://www.aihw.gov.au/reports/chronic-respiratory-conditions/asthma-in-australia-2011-with-chapter-on-copd/contents/table-of-contents.
45. Chalmers GW, Macleod KJ, Little SA, Thomson LJ, McSharry CP, et al. Influence of cigarette smoking on inhaled corticosteroid treatment in mild asthma. Thorax, 2002; 57(3):226-30. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11867826
46. Lazarus SC, Chinchilli VM, Rollings NJ, Boushey HA, Cherniack R, et al. Smoking affects response to inhaled corticosteroids or leukotriene receptor antagonists in asthma. American Journal of Respiratory and Critical Care Medicine, 2007; 175(8):783-90. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17204725
47. Tomlinson JE, McMahon AD, Chaudhuri R, Thompson JM, Wood SF, et al. Efficacy of low and high dose inhaled corticosteroid in smokers versus non-smokers with mild asthma. Thorax, 2005; 60(4):282-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15790982
48. James AL, Palmer LJ, Kicic E, Maxwell PS, Lagan SE, et al. Decline in lung function in the Busselton Health Study: the effects of asthma and cigarette smoking. American Journal of Respiratory and Critical Care Medicine, 2005; 171(2):109-14. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15486340
49. Thomson NC and Spears M. The role of cigarette smoking on persistent airflow obstruction in asthma. Annals of Respiratory Medicine, 2011; 2(1):47. Available from: https://www.researchgate.net/publication/228471299_The_Role_of_Cigarette_Smoking_on_Persistent_Airflow_Obstruction_in_Asthma
50. Lange P, Parner J, Vestbo J, Schnohr P, and Jensen G. A 15-year follow-up study of ventilatory function in adults with asthma. New England Journal of Medicine, 1998; 339(17):1194-200. Available from: https://www.ncbi.nlm.nih.gov/pubmed/9780339
51. Ulrik CS and Frederiksen J. Mortality and markers of risk of asthma death among 1,075 outpatients with asthma. Chest, 1995; 108(1):10-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/7606941
52. Chaudhuri R, Livingston E, McMahon AD, Lafferty J, Fraser I, et al. Effects of smoking cessation on lung function and airway inflammation in smokers with asthma. American Journal of Respiratory and Critical Care Medicine, 2006; 174(2):127-33. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16645173
53. Tonnesen P, Pisinger C, Hvidberg S, Wennike P, Bremann L, et al. Effects of smoking cessation and reduction in asthmatics. Nicotine and Tobacco Research, 2005; 7(1):139-48. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15804686
54. Zibrak JD and Price D. Interstitial lung disease: raising the index of suspicion in primary care. NPJ Primary Care Respiratory Medicine, 2014; 24:14054. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25208940
55. Prasad J, Holland AE, Glaspole I, and Westall G. Idiopathic pulmonary fibrosis: an Australian perspective. Internal Medicine Journal, 2016; 46(6):663-8. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27257148
56. Behr J. The diagnosis and treatment of idiopathic pulmonary fibrosis. Deutsches Ärzteblatt International, 2013; 110(51-52):875-81. Available from: https://www.ncbi.nlm.nih.gov/pubmed/24529303
57. Walters GI. Occupational exposures and idiopathic pulmonary fibrosis. Current Opinion in Allergy and Clinical Immunology, 2020; 20(2):103-11. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31895128
58. Caminati A and Harari S. Smoking-related interstitial pneumonias and pulmonary Langerhans cell histiocytosis. Proceedings of the American Thoracic Society, 2006; 3(4):299-306. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16738193
59. Portnoy J, Veraldi KL, Schwarz MI, Cool CD, Curran-Everett D, et al. Respiratory bronchiolitis-interstitial lung disease: long-term outcome. Chest, 2007; 131(3):664-71. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17356078
60. Negrin-Dastis S, Butenda D, Dorzee J, Fastrez J, and d'Odemont JP. Complete disappearance of lung abnormalities on high-resolution computed tomography: a case of histiocytosis X. Canadian Respiratory Journal, 2007; 14(4):235-7. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17551600
61. Kinoshita Y, Watanabe K, Sakamoto A, and Hidaka K. Pulmonary Langerhans cell histiocytosis-associated pulmonary hypertension showing a drastic improvement following smoking cessation. Internal Medicine, 2016; 55(5):491-5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26935369