Chronic obstructive pulmonary disease causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Priyamvada Singh, MBBS [3]
Overview
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive airway disease (COAD), is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders. It is most often due to tobacco smoking,[1] but can be due to other airborne irritants such as coal dust, asbestos or solvents, congenital conditions such as alpha-1-antitrypsin deficiency and as well as preserved meats containing nitrites. In the United States, tobacco use is a key factor in the development and progression of COPD, but asthma, exposure to air pollutants in the home and workplace, genetic factors, and respiratory infections also play a role. In the developing world, indoor air quality is thought to play a larger role in the development and progression of COPD than it does in the United States.
Causes
Common Causes
Smoking
The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking.[2][3] Exposure to cigarette smoke is measured in pack-years,[4] the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.[5]
Occupational Exposures
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers.[6] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[7] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.[8]
Air Pollution
Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas.[9] Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.[10]
Genetics
Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.[11] The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.[12]
Autoimmune Disease
There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking.[13] Many individuals with COPD who have stopped smoking have active inflammation in the lungs.[14] The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.[14] This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.[14][15][16]
Other Risk Factors
A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.[8] It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD.
Causes by Organ System
| Cardiovascular | Congestive heart failure |
| Chemical / poisoning | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | No underlying causes |
| Ear Nose Throat | No underlying causes |
| Endocrine | No underlying causes |
| Environmental | No underlying causes |
| Gastroenterologic | No underlying causes |
| Genetic | Alpha1-Antitrypsin Deficiency |
| Hematologic | No underlying causes |
| Iatrogenic | No underlying causes |
| Infectious Disease | No underlying causes |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional / Metabolic | No underlying causes |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | No underlying causes |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | No underlying causes |
| Psychiatric | No underlying causes |
| Pulmonary | Bronchitis, Emphysema, Pulmonary embolism, Chronic Asthma, Bronchiectasis , Bronchiolitis obliterans, Lung tumor, Pneumonia, Silicosis, Lymphangioleiomyomatosis |
| Renal / Electrolyte | No underlying causes |
| Rheum / Immune / Allergy | No underlying causes |
| Sexual | No underlying causes |
| Trauma | No underlying causes |
| Urologic | No underlying causes |
| Miscellaneous | Nicotine addiction |
External Links
http://www.cdc.gov/copd/index.htm
References
- ↑ Devereux G. ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. BMJ 2006;332:1142-1144. PMID 16690673
- ↑ MedicineNet.com - COPD causes
- ↑ Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD (2009). "COPD prevalence is increased in lung cancer, independent of age, sex and smoking history". Eur. Respir. J. 34 (2): 380–6. doi:10.1183/09031936.00144208. PMID 19196816. Unknown parameter
|month=ignored (help) - ↑ "Definition of pack year - NCI Dictionary of Cancer Terms".
- ↑ Template:Cite doi
- ↑ Devereux, Graham (2006). "Definition, epidemiology, and risk factors". BMJ. 332 (7550): 1142–4. doi:10.1136/bmj.332.7550.1142. PMC 1459603. PMID 16690673. Unknown parameter
|month=ignored (help) - ↑ Hnizdo E, Vallyathan V (2003). "Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence". Occup Environ Med. 60 (4): 237–43. doi:10.1136/oem.60.4.237. PMC 1740506. PMID 12660371. Unknown parameter
|month=ignored (help) - ↑ 8.0 8.1 Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's Principles of Internal Medicine (17th ed.). McGraw-Hill Professional. ISBN 0-07-146633-9.
- ↑ Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (2006). "Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): 523–32. doi:10.1183/09031936.06.00124605. PMID 16611654. Unknown parameter
|month=ignored (help) - ↑ Kennedy SM, Chambers R, Du W, Dimich-Ward H (2007). "Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?". Proceedings of the American Thoracic Society. 4 (8): 692–4. doi:10.1513/pats.200707-094SD. PMID 18073405. Unknown parameter
|month=ignored (help) - ↑ Silverman EK, Chapman HA, Drazen JM; et al. (1998). "Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis". Am. J. Respir. Crit. Care Med. 157 (6 Pt 1): 1770–8. PMID 9620904. Unknown parameter
|month=ignored (help) - ↑ MedlinePlus Encyclopedia 000091
- ↑ Agustí A, MacNee W, Donaldson K, Cosio M. (2003). "Hypothesis: Does COPD have an autoimmune component?". Thorax. 58 (10): 832–4. doi:10.1136/thorax.58.10.832. PMC 1746486. PMID 14514931.
- ↑ 14.0 14.1 14.2 Rutgers SR, Postma DS, ten Hacken NH; et al. (2000). "Ongoing airway inflammation in patients with COPD who do not currently smoke". Thorax. 55 (1): 12–8. doi:10.1136/thorax.55.1.12. PMC 1745599. PMID 10607796. Unknown parameter
|month=ignored (help) - ↑ Feghali-Bostwick CA, Gadgil AS, Otterbein LE; et al. (2008). "Autoantibodies in Patients with Chronic Obstructive Pulmonary Disease". Am. J. Respir. Crit. Care Med. 177 (2): 156–63. doi:10.1164/rccm.200701-014OC. PMC 2204079. PMID 17975205. Unknown parameter
|month=ignored (help) - ↑ Lee SH, Goswami S, Grudo A; et al. (2007). "Antielastin autoimmunity in tobacco smoking-induced emphysema". Nat. Med. 13 (5): 567–9. doi:10.1038/nm1583. PMID 17450149. Unknown parameter
|month=ignored (help)