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

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Chronic obstructive pulmonary disease (COPD), is most often due to tobacco smoking; 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

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### Common Causes

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#### Smoking

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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.[1][2] Exposure to cigarette smoke is measured in pack-years,[3] 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, extra-pulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.[4]

#### Occupational Exposures

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Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, iso-cyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in non-smokers.[5] 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.[6] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.[7]

#### Air Pollution

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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.[8] 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.[9]

#### Genetics

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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.[10] 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.[11]

#### Autoimmune Disease

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Main article: Autoimmunity

There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking.[12] Many individuals with COPD who have stopped smoking have active inflammation in the lungs.[13] The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.[13] This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.[13][14][15]

#### Other Risk Factors

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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.[7] 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

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Cardiovascular | No underlying causes

|

Chemical / poisoning | Silicosis, Isocyanates, Cigarette smoking, Cadmium, Sulfur dioxide
Dermatologic | No underlying causes
Drug Side Effect | Goserelin, Pramipexole, Zanamivir
Ear Nose Throat | No underlying causes
Endocrine | No underlying causes
Environmental | Use of biomass fuels for cooking, Second hand smoking, Occupational pollution exposure to dusts and chemicals, Fumes from welding, Environmental air pollution such as coal, grain
Gastroenterologic | No underlying causes
Genetic | Tumor necrosis factor-alpha (TNF-a) gene polymorphisms, Several SNPs of the leptin receptor (LEPR) gene,

Several gene polymorphisms of Transforming growth factor beta 1, Metalloproteinase dysregulation, Increased Matrix metalloproteinases ( MMP)-9 (gelatinase B), Increased Matrix metalloproteinases (MMP)-8 (Collagenase 2), Increased Matrix metalloproteinases (MMP)-2 (gelatinase A), Heredity, Genetic influences, Excess elastase, Decreased glutathione S-transferase P1 activity, Decreased glutathione levels, Decreased function of microsomal epoxide hydrolase, Decreased function of microsomal epoxide hydrolase, Alpha-1-antitrypsin deficiency, Abnormal activity of tissue inhibitors of metalloproteinase (TIMP-1)

Hematologic | No underlying causes
Iatrogenic | No underlying causes
Infectious Disease | Pulmonary tuberculosis, History of childhood respiratory infections
Musculoskeletal / Ortho | No underlying causes
Neurologic | No underlying causes
Nutritional / Metabolic | Vitamin C deficiency, Deficiency of antioxidant vitamins, Vitamin E deficiency
Obstetric/Gynecologic | No underlying causes
Oncologic | No underlying causes
Opthalmologic | No underlying causes
Overdose / Toxicity | No underlying causes
Psychiatric | No underlying causes
Pulmonary | Bronchitis, Bronchiectasis, Bronchiolitis obliterans, Early childhood recurrent Pneumonia, Silicosis, Increased airway responsiveness, Bronchopulmonary dysplasia, Asthma (controversial), Pulmonary tuberculosis
Renal / Electrolyte | No underlying causes
Rheum / Immune / Allergy | Atopy
Sexual | Gender (controversial), more common in male
Trauma | No underlying causes
Urologic | No underlying causes
Miscellaneous | Nicotine addiction, Low socioeconomic status, First-degree relatives with severe premature COPD, Age

### Causes in Alphabetical Order

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* Abnormal activity of tissue inhibitors of metalloproteinase (TIMP-1)
* Age
* Alpha-1-antitrypsin deficiency
* Asthma (controversial)
* Atopy
* Bronchopulmonary dysplasia
* Cadmium
* Cigarette smoking
* Decreased function of microsomal epoxide hydrolase
* Decreased function of microsomal epoxide hydrolase
* Decreased glutathione levels
* Decreased glutathione S-transferase P1 activity
* Deficiency of antioxidant vitamins
* Environmental air pollution such as coal, grain
* Excess elastase
* First-degree relatives severe premature COPD
* Fumes from welding
* Gender (controversial)
* Genetic influences
* Heredity
* History of childhood respiratory infections
* Increased airway responsiveness
* Increased Matrix metalloproteinases (MMP)-2 (gelatinase A)
* Increased Matrix metalloproteinases (MMP)-8 (Collagenase 2)]]
* Increased Matrix metalloproteinases ( MMP)-9 (gelatinase B)]]
* Isocyanates
* Low socioeconomic status
* Metalloproteinase dysregulation
* Occupation pollution exposure to dusts and chemicals
* Pulmonary tuberculosis
* Second hand smoking
* Several gene polymorphisms of Transforming growth factor beta 1
* Several SNPs (Several gene polymorphisms) of the leptin receptor (LEPR) gene
* Silicosis
* Sulfur dioxide
* Tumor necrosis factor-alpha (TNF-a) gene polymorphisms
* Use of biomass fuels for cooking
* Vitamin C deficiency
* Vitamin E deficiency
* Zanamivir

## External Links

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http://www.cdc.gov/copd/index.htm

## References

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1. ↑ MedicineNet.com - COPD causes
2. ↑ 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)CS1 maint: Multiple names: authors list (link)
3. ↑ "Definition of pack year - NCI Dictionary of Cancer Terms".
4. ↑ Template:Cite doi
5. ↑ 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)
6. ↑ 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)
7. ↑ 7.0 7.1 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.CS1 maint: Multiple names: authors list (link)
8. ↑ 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)CS1 maint: Multiple names: authors list (link)
9. ↑ 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)CS1 maint: Multiple names: authors list (link)
10. ↑ 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)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
11. ↑ MedlinePlus Encyclopedia 000091
12. ↑ 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.CS1 maint: Multiple names: authors list (link)
13. ↑ 13.0 13.1 13.2 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)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
14. ↑ 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)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
15. ↑ 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)CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)

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