3.2 Respiratory diseases (excluding lung cancer)

Last updated: March 2015 
Suggested citation: Peters, M, Greenhalgh, EM & Winstanley, MH. 3.2 Respiratory diseases. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2015. Available from http://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-2-respiratory-diseases

The airways and lungs, being the route of tobacco smoke exposure, are exposed to higher concentrations of the toxic constituents of smoke than any other system in the body. The adverse effects of smoking range from impairment of the protective mechanisms in the lungs that reduce the risk of infection to actual lung destruction.1,2

3.2.1 Impairment of pulmonary immune and protective responses

The lungs are continually exposed to gases, particles and micro-organisms in the air. 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 chronic disease.1

Every time we breathe, we inhale particles. Some are harmless dust and others are potentially injurious particles, viruses, or bacteria. Large and very small particles are mostly trapped in the nose and upper airway and cleared without reaching the lung at all. Intermediate sized particles, between 0.001 and 10 microns, penetrate deep into the lungs.1 From here they are cleared by the mucociliary system: particles become trapped in the mucus blanket on the surface of the cells lining the airways, and are swept out of the lung by the synchronised movement of cilia, which are tiny hair-like structures on the surface of airway cells.3

About 60% of the particles from cigarette smoke are deposited in the lung. Exposure to cigarette smoke reduces the clearance rate of particles from the lung.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.3–6 This impairment of the mucociliary system increases the risk of infection.1 Smokers also 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

Lying under the mucociliary system, 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, increasing its permeability, which leads to inflammation.1,9,10

Smoking compromises the immune system, provoking an inflammatory response and increasing the potential for infection.1,9,11 The ability of the lung's immune system to sense and eliminate viruses and bacteria is impaired.10,12 All smokers have inflammation in their lungs, which may persist for many years after smoking cessation.1,13

3.2.2 The effect of smoking on acute respiratory illnesses

Adults who smoke are more likely to develop acute respiratory illnesses, including bronchitis, bronchiolitis, influenza, legionnaires disease, and pneumonia.12,14 The risk of pneumococcal infection, the most common cause of severe pneumonia, is two- to four-fold in smokers compared to non-smokers, with the risk increasing as daily cigarette consumption increases.14,15 Smokers are more likely to be infected with influenza in an epidemic. Seasonal influenza is more common and severe in non-vaccinated smokers.12,14

Smoking also causes active tuberculosis disease and death from tuberculosis.11 Tuberculosis in not common in Australia, but there are groups vulnerable to TB infection including Aboriginal Australians, migrants from countries where TB is common and people with HIV.17 Smoking cessation and avoiding secondhand smoke reduces the risk of tuberculosis disease.18

In Australia in 2004–5, 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.19

3.2.3 Smoking and respiratory symptoms

Active smoking causes respiratory symptoms in adults, teenagers and children, including coughing, phlegm, wheezing and dyspnea (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.12

3.2.4 Smoking and lung function

Active smokers in childhood and adolescence have both reduced lung function and impaired lung growth.20 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.12 Among smokers, there appears to be a sliding scale of susceptibility to loss of lung function.21,22 A few smokers may lose lung function almost as slowly as non-smokers, but for a significant minority of smokers, their rapid loss of lung function becomes disabling or fatal.1,9,21 Most smokers will fall between these groups.22 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.13

3.2.5 Major diseases caused by smoking

3.2.5.1 Chronic bronchitis

Bronchitis is defined by symptoms of cough together with frequent and increased production of sputum or phlegm. Chronic bronchitis is diagnosed when these symptoms are present for three months in each of two successive years.1 It occurs in about half of all heavy smokers.13 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 a greater frequency of respiratory infections.1,23 In persons who also have chronic obstructive pulmonary disease (COPD), symptoms of chronic bronchitis increase the risk of death from respiratory infections.24

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.1,12 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.1,13

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.13 In people with severe COPD, chronic cough associated with chronic bronchitis is more likely to persist after smoking cessation.23

3.2.5.2 Chronic Obstructive Pulmonary Disease (COPD)

Chronic obstructive pulmonary disease (COPD) is characterised by airflow limitation that is usually progressive and not fully reversible.1 In 2011, COPD was the fifth leading cause of death in Australia, representing 4.4% of all deaths in people aged 55 and over.25 These statistics may underestimate the contribution of highly prevalent, slowly progressive, chronic diseases such as COPD to mortality, as the reported number of deaths is based on the underlying cause of death only. In Australia, only 40% of all deaths with COPD as any cause had COPD recorded as the underlying cause of death for the period 2007–2011.25

Death rates from COPD have declined over time.25 COPD is more prevalent among the elderly, when it has important interactions with many other acute and chronic illnesses.17,26 The evidence also suggests that women may be more susceptible to developing severe COPD at younger ages.11 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.17 Even individuals with mild COPD have reduced quality of life, which worsens as the disease becomes more severe.27

The greatest cause of COPD by far is smoking.25 In 2004–5, it is estimated that of all deaths in Australians aged over 35 caused by COPD, 77% of cases in males and 71% of cases in females were attributable to smoking.19 In 2007-08, among Australians aged 55 years and over who had self-reported COPD, 20% were current smokers, 52% were former smokers, and 28% had never smoked.28 Limited data suggests that, of the current smokers who survive to their mid-70s, around half may develop mild to severe COPD.29

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 are inflammation, oxidative stress, and an imbalance of proteases (enzymes that affect proteins) and antiproteases in the lung. Oxidative stress is the result of highly reactive 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.1,13

Different disease processes result in the airflow limitation that characterises COPD. The main diseases are obstructive bronchiolitis and emphysema.1,13 Chronic bronchitis often co-occurs with COPD (as described above). Smokers have different susceptibilities to each disease process and this will influence their symptoms.

Obstructive bronchiolitis

Inflammation in the small airways is seen to some extent in all smokers.12,30 Obstruction of the small airways 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 lumen (airway space).1 In addition, excess mucus accumulates in the small airway lumen.9 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.9 Smoking cessation slows lung function decline.12 In some smokers, airway inflammation persists, possibly for life, after stopping smoking.13

Emphysema

Emphysema is irreversible loss 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 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.4,26

Smoking causes oxidative stress, which tips the protease–anti-protease balance towards proteases.1 Proteases are enzymes that degrade structural proteins, such as elastin and collagen, in the lungs airways and alveoli.12 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.1,9 In advanced emphysema, the inelastic lungs enlarge leading to a large barrel-shaped chest.

Course of COPD after smoking cessation

Smoking cessation is the only action known to protect from rapid declines in lung function.31 In populations with COPD, there is a small 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.13 Reduction in the number of cigarettes smoked does not change the loss of lung function.32 Former smokers have a reduced risk of hospitalisation related to COPD and death from COPD compared with those who continue to smoke.13,33

3.2.6 Other respiratory illnesses related to smoking

3.2.6.1 Asthma

In Australia, one in ten people suffer from asthma.34 Smoking rates in people with asthma are at least as high as those without asthma.28 Active smoking is associated with an increased risk for asthma in adolescents and adults. Smoking exacerbates asthma in adults and research suggests that it may also do so in children and adolescents.11 Smoking increases asthma symptoms and impairs the response to asthma treatment.28,35 People with asthma who smoke are more likely to have accelerated loss of lung function.11,36,37 The risk of severe asthma events, such as hospitalisation, use of emergency services and death, are increased in smokers.11,37,38 Smoking cessation improves asthma control.39,40

3.2.6.2 Interstitial Lung Diseases (ILD)

Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal fibrotic interstitial lung disease. It has the worst prognosis of all idiopathic interstitial diseases of the lung, with a median survival time of three to four years.41 Although its cause is unknown, evidence suggests that both genetic and environmental factors are involved in its development. The latest Surgeon General’s report concluded that cigarette smoking is associated with an increased risk of IPF.16

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.42,43 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.42

3.2.6.3 Histiocytosis X (Langerhan's Cell Histiocytosis)

Histiocytosis X is rarer than RB-ILD. It 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.42 Smoking cessation is strongly encouraged, because case reports show improvement after quitting, and even restoration of normal or near-normal lung structure.42,40

3.2.7 Other respiratory conditions related to smoking

3.2.7.1 Sense of smell

Being a smoker is associated with having an impaired sense of smell (hyposmia).45,46 Smoke directly damages the olfactory sensory neurons, located in the nasal airways, which detect different odours.45 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.46,47 (Also see section 3.22.5 )

3.2.7.2 Snoring

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.48 (Also see section 3.22.4 )

Recent news and research

For recent news items and research on this topic, click here (Last updated June 2018)  

References

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, 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, 2010. Available from: http://www.surgeongeneral.gov/library/tobaccosmoke/report/index.html

2. Churg A, Cosio M and Wright JL. Mechanisms of cigarette smoke-induced COPD: insights from animal models. American Journal of Physiology and Lung Cell Molecular Physiology 2008;294(4):L612-31. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18223159

3. Leopold P, O'Mahony M, Lian X, Tilley A, Harvey B and Crystal R. Smoking is associated with shortened airway cilia. PLoS One 2009;4(12):e8157. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790614/?tool=pubmed

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: http://www.cdc.gov/tobacco/data_statistics/sgr/pre_1994/index.htm

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: http://www.ncbi.nlm.nih.gov/pubmed/18223159

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 Physiolgy and Lung Cell Molecular Physiology 2005;288(5):L894-902. Available from: http://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: http://www.ncbi.nlm.nih.gov/pubmed/10414423

8. Ramos EM, De Toledo AC, Xavier RF, Fosco LC, Vieira RP, Ramos D, et al. Reversibility of impaired nasal mucociliary clearance in smokers following a smoking cessation programme. Respirology 2011;16(5):849-55. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21545372

9. Hogg JC. Pathophysiology of airflow limitation in chronic obstructive pulmonary disease. The Lancet 2004;364(9435):709-21. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15325838

10. 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: http://www.ncbi.nlm.nih.gov/pubmed/19330016

11. 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: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/

12. 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: http://www.cdc.gov/tobacco/data_statistics/sgr/index.htm

13. International Agency for Research on Cancer, IARC Handbooks of cancer prevention, Tobacco Control, Vol. 11: reversal of risk after quitting smoking. Lyon, France: IARC; 2007.

14. Arcavi L and Benowitz NL. Cigarette smoking and infection. Archives of Internal Medicine, 2004; 164(20):2206−16. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15534156

15. Nuorti JP, Butler JC, Farley MM, Harrison LH, McGeer A, et al. Cigarette smoking and invasive pneumococcal disease. Active Bacterial Core Surveillance Team. New England Journal of Medicine, 2000; 342(10):681−9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15534156

16. U.S. Department of Health and Human Services. The Health Consequences of Smoking: 50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: U.S. 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, Printed with corrections, January 2014. Available from: http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf 

17. Australian Institute of Health and Welfare. Australia's health 2010. Canberra: AIHW, 2010. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2010/contents/table-of-contents

18. Slama K, Chiang CY, Enarson DA, Hassmiller K, Fanning A, et al. Tobacco and tuberculosis: a qualitative systematic review and meta-analysis. Internatioanl Journal Tuberculosis of Lung Disease, 2007; 11(10):1049−61. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17945060

19. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004–05. Canberra: Department of Health and Ageing, 2008. Available from: http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Content/mono64/$File/mono64.pdf

20. 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/

21. Fletcher C and Peto R. The natural history of chronic airflow obstruction. British Medical Journal, 1977; 1(6077):1645−8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/871704

22. Rennard S and Vestbo J. COPD: the dangerous underestimate of 15%. The Lancet, 2006; 367:1216−19. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16631861

23. Braman SS. Chronic cough due to chronic bronchitis: ACCP evidence-based clinical practice guidelines. Chest, 2006; 129(1 suppl.):104S−115S. Available from: https://www.ncbi.nlm.nih.gov/pubmed/16428699

24. 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: http://www.ncbi.nlm.nih.gov/pubmed/7489800

25. Australian Institute of Health and Welfare, Poulos LM, Cooper SJ, Ampon R, Reddel HK, et al. Mortality from asthma and COPD in Australia. Cat. no. ACM 30 Canberra 2014. Available from: http://www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=60129548230 .

26. Australian Institute of Health and Welfare. Chronic diseases and associated risk factors in Australia, 2001. cat. no. PHE 33.Canberra: AIHW, 2002. Available from: http://www.aihw.gov.au/publication-detail/?id=6442467343

27. Devereux G. The ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. British Medical Journal, 2006; 332:1142−4. Available from: http://www.bmj.com/cgi/reprint/332/7550/1142.pdf

28. 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: Australian Institute for Health and Welfare, 2011. Available from: http://www.aihw.gov.au/publication-detail/?id=10737420159&tab=2

29. Lundback B, Lindberg A, Lindstrom M, Ronmark E, Jonsson AC, et al. Not 15 but 50% of smokers develop COPD?--Report from the Obstructive Lung Disease in Northern Sweden Studies. Respiratory Medicine, 2003; 97(2):115−22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12587960

30. 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: http://www.ncbi.nlm.nih.gov/pubmed/8016769

31. Barnes PJ. Chronic obstructive pulmonary disease. New England Journal of Medicine, 2000; 343(4):269−80. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10911010

32. 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: http://www.ncbi.nlm.nih.gov/pubmed/12403880

33. Godtfredsen N, Lam T, Hansel T, Leon M, Gray N, et al. COPD-related morbidity and mortality after smoking cessation: status of the evidence. The European Respiratory Journal, 2008; 32(4):844–53. Available from: http://erj.ersjournals.com/cgi/content/full/32/4/844

34. Australian Institute of Health and Welfare. Asthma, 2015. Available from: http://www.aihw.gov.au/asthma

35. 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: http://www.ncbi.nlm.nih.gov/pubmed/11867826

36. 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: http://www.ncbi.nlm.nih.gov/pubmed/15486340

37. Thomson NC and Spears M. The role of cigarette smoking on persistent airflow obstruction in asthma. Annals of Respiratory Medicine, 2010; ii(1). Available from: https://www.researchgate.net/publication/228471299_The_Role_of_Cigarette_Smoking_on_Persistent_Airflow_Obstruction_in_Asthma

38. 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: http://www.ncbi.nlm.nih.gov/pubmed/7606941

39. 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: http://www.ncbi.nlm.nih.gov/pubmed/16645173

40. 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: http://www.ncbi.nlm.nih.gov/pubmed/15804686

41. Behr J. The diagnosis and treatment of idiopathic pulmonary fibrosis. Deutsches Ärzteblatt International, 2013; 110(51-52):875. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928534/

42. 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: http://www.ncbi.nlm.nih.gov/pubmed/16738193

43. 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: http://www.ncbi.nlm.nih.gov/pubmed/17356078

44. 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: http://www.ncbi.nlm.nih.gov/pubmed/17551600

45. Vent J, Robinson A, Gentry-Nielsen M, Conley D, Hallworth R, et al. Pathology of the olfactory epithelium: smoking and ethanol exposure. Laryngoscope, 2004; 114:1383−8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15280712

46. Murphy C, Schubert C, Cruickshanks K, Klein B, Klein R, et al. Prevalence of olfactory impairment in older adults. The Journal of the American Medical Association, 2002; 288(18):2307−12. Available from: http://jama.ama-assn.org/cgi/reprint/288/18/2307

47. Frye RE, Schwartz BS, and Doty RL. Dose-related effects of cigarette smoking on olfactory function. The Journal of the American Medical Association, 1990; 263(9):1233−6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2304239

48. Franklin K, Gíslason T, Omenaas E, Jõgi R, Jensen E, et al. The influence of active and passive smoking on habitual snoring. American Journal of Respiratory and Critical Care Medicine, 2004; 170:799−803. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15242843

      Previous Chapter Next Chapter