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==Overview==
==Overview==
Chronic bronchitis as a main category of [[COPD]] is caused by multiple environmental and genetic factors. Smoking is the leading cause of chronic bronchitis.


==Causes==
== Causes ==
[[Chronic bronchitis]] is a long-term [[condition]]. People have a [[cough]] that produces excessive [[mucus]]. To be diagnosed with [[chronic bronchitis]], you must have a [[cough]] with [[mucus]] most days of the month for at least 3 months.
 
[[Chronic bronchitis]] is one type of [[chronic obstructive pulmonary disease]], or [[COPD]] for short. ([[Emphysema]] is another type of [[COPD]].)
===Common Causes===
The following things can make [[bronchitis]] worse:                                                                             
 
*Air pollution                                                                                                         
====Smoking====
*[[Allergies]]                                                                                                            
* The primary risk factor for [[COPD]] is chronic tobacco smoking. In the [[United States]], 80 to 90% of cases of [[Chronic obstructive pulmonary disease|COPD]] are due to [[smoking]].<ref name="medcauses">[http://www.medicinenet.com/chronic_obstructive_pulmonary_disease_copd/page3.htm MedicineNet.com - COPD causes]</ref><ref>{{cite journal |author=Young RP, Hopkins RJ, Christmas T, Black PN, Metcalf P, Gamble GD |title=COPD prevalence is increased in lung cancer, independent of age, sex and smoking history |journal=Eur. Respir. J. |volume=34 |issue=2 |pages=380–6 |year=2009 |month=August |pmid=19196816 |doi=10.1183/09031936.00144208 }}</ref>
*Certain occupations (such as coal mining, textile manufacturing, or grain handling)                                          
* Exposure to cigarette smoke is measured in [[pack-years]],<ref>{{cite web |url=http://www.cancer.gov/Templates/db_alpha.aspx?CdrID=306510 |title=Definition of pack year - NCI Dictionary of Cancer Terms |format= |work= |accessdate=}}</ref> the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking.
*[[Infections]]
* The likelihood of developing [[Chronic obstructive pulmonary disease|COPD]] increases with age and cumulative smoke exposure. Majority of life-long smokers will develop [[COPD]], provided that smoking-related extrapulmonary diseases ([[cardiovascular]], [[Diabetes mellitus|diabetes]], [[cancer]]) do not claim their lives beforehand.<ref>{{cite doi|10.1016/S0140-6736(06)68516-4}}</ref>
 
====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.<ref>{{cite journal
| pmid = 16690673
| pmc = 1459603
| title = Definition, epidemiology, and risk factors
| year = 2006
| journal = BMJ
| volume = 332
| issue = 7550
| pages = 1142–4
| doi = 10.1136/bmj.332.7550.1142
| month = May
| author = Devereux, Graham
}}</ref>
* 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.<ref>{{cite journal |author=Hnizdo E, Vallyathan V |title=Chronic obstructive pulmonary disease due to occupational exposure to silica dust: a review of epidemiological and pathological evidence |journal=Occup Environ Med |volume=60 |issue=4 |pages=237–43 |year=2003 |month=April |pmid=12660371 |pmc=1740506 |doi=10.1136/oem.60.4.237}}</ref>
* The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of [[cigarette smoking]].<ref name="Harrisons">{{cite book |author=Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. |title=Harrison's Principles of Internal Medicine |edition=17th |publisher=McGraw-Hill Professional |year=2008 |isbn=0-07-146633-9}}</ref>
 
====Air Pollution====
* People who live in large cities have a higher rate of [[Chronic obstructive pulmonary disease|COPD]] compared to people who live in rural areas.<ref>{{cite journal |author=Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM |title=Global burden of COPD: systematic review and meta-analysis |journal=Eur. Respir. J. |volume=28 |issue=3 |pages=523–32 |year=2006 |month=September |pmid=16611654 |doi=10.1183/09031936.06.00124605 }}</ref>
* Urban [[air pollution]] may be a contributing factor for [[Chronic obstructive pulmonary disease|COPD]], as it is thought to slow the normal growth of the lungs. Long-term research is needed to confirm this link.
* Studies have demonstrated a direct relationship between the waste gas and [[Chronic obstructive pulmonary disease|COPD]]/[[asthma]]-aggravating compound, [[sulfur dioxide]], and an inverse relationship between the blue lichen ''Xanthoria'' (usually found abundantly in the countryside, but never in towns or cities) and the exacerbation of [[Chronic obstructive pulmonary disease|COPD]].
* In many developing countries, indoor air pollution from cooking fire smoke (often using [[biomass fuel]]s such as wood and animal dung) is a common cause of [[Chronic obstructive pulmonary disease|COPD]], especially in women.<ref>{{cite journal |author=Kennedy SM, Chambers R, Du W, Dimich-Ward H |title=Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?|journal=Proceedings of the American Thoracic Society|volume=4 |issue=8 |pages=692–4 |year=2007 |month=December |pmid=18073405 |url=http://pats.atsjournals.org/cgi/content/full/4/8/692 |doi=10.1513/pats.200707-094SD}}</ref>
 
====Genetics====
* A [[gene]]tic component appears to be required for susceptibility in developing [[Chronic obstructive pulmonary disease|COPD]], even in heavy smokers. [[Chronic obstructive pulmonary disease|COPD]] is more common among relatives of COPD patients who smoke than unrelated smokers.<ref>{{cite journal |author=Silverman EK, Chapman HA, Drazen JM, ''et al.'' |title=Genetic epidemiology of severe, early-onset chronic obstructive pulmonary disease. Risk to relatives for airflow obstruction and chronic bronchitis |journal=Am. J. Respir. Crit. Care Med. |volume=157 |issue=6 Pt 1 |pages=1770–8 |year=1998 |month=June |pmid=9620904 |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=9620904}}</ref>
* 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 [[Chronic obstructive pulmonary disease|COPD]] cases. 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.<ref>{{MedlinePlus|000091}}</ref>
 
====Autoimmune Disease====
* There is mounting evidence that there may be an autoimmune component to [[Chronic obstructive pulmonary disease|COPD]], triggered by lifelong smoking.<ref>{{cite journal |author=Agustí A, MacNee W, Donaldson K, Cosio M. |title=Hypothesis: Does COPD have an autoimmune component? |journal=Thorax |volume=58 |issue=10 |pages=832–4 |year=2003 |pmid=14514931 |doi=10.1136/thorax.58.10.832 |pmc=1746486}}</ref>
* Many individuals with COPD who have stopped smoking have active inflammation in the lungs.<ref name="Rutgers00">{{cite journal |author=Rutgers SR, Postma DS, ten Hacken NH, ''et al.'' |title=Ongoing airway inflammation in patients with COPD who do not currently smoke |journal=Thorax |volume=55 |issue=1 |pages=12–8 |year=2000 |month=January |pmid=10607796 |pmc=1745599 |doi= 10.1136/thorax.55.1.12|url=}}</ref> The disease may continue to progress for many years after smoking cesssation due to this ongoing inflammation.<ref name="Rutgers00" /> This sustained inflammation is thought to be mediated by [[autoantibodies]] and autoreactive T cells.<ref name="Rutgers00" /><ref>{{cite journal |author=Feghali-Bostwick CA, Gadgil AS, Otterbein LE, ''et al.'' |title=Autoantibodies in Patients with Chronic Obstructive Pulmonary Disease |journal=Am. J. Respir. Crit. Care Med. |volume=177 |issue=2 |pages=156–63 |year=2008 |month=January |pmid=17975205 |doi=10.1164/rccm.200701-014OC |pmc=2204079 }}</ref><ref>{{cite journal |author=Lee SH, Goswami S, Grudo A, ''et al.'' |title=Antielastin autoimmunity in tobacco smoking-induced emphysema |journal=Nat. Med. |volume=13 |issue=5 |pages=567–9 |year=2007 |month=May |pmid=17450149 |doi=10.1038/nm1583 }}</ref>
 
====Other Risk Factors====
* A characteristic of asthma, also common in [[Chronic obstructive pulmonary disease|COPD]] patients is the tendency for airways to suddenly constrict in response to inhaled irritants ([[bronchial hyperresponsiveness]]). In COPD, the presence of [[bronchial hyperresponsiveness]] predicts poorer prognosis of the disease.<ref name="Harrisons" /> 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===
 
{|style="width:75%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"|[[Silicosis]], Isocyanates, [[Cigarette smoking]], [[Cadmium]], [[Sulfur dioxide]]
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| [[Goserelin]], [[Pramipexole]], [[Zanamivir]]
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"|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
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"|[[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)
 
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"|[[Pulmonary tuberculosis]], History of childhood [[respiratory infections]]
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"|[[Vitamin C]] deficiency, Deficiency of [[antioxidant]] [[vitamins]], [[Vitamin E]] deficiency
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"|[[Bronchitis]], [[Bronchiectasis]], [[Bronchiolitis obliterans]], Early childhood recurrent [[Pneumonia]], [[Silicosis]], Increased airway responsiveness, [[Bronchopulmonary dysplasia]], [[Asthma]] (controversial), [[Pulmonary tuberculosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Atopy]]
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"|[[Gender]] (controversial), more common in male
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| [[Nicotine addiction]], Low socioeconomic status, First-degree relatives with severe premature [[COPD]], [[Age]]
|-
|}
 
===Causes in Alphabetical Order===
{{Columns-list|3|
*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==
[http://www.example.org http://www.cdc.gov/copd/index.htm]


==References==
==References==
{{Reflist|2}}
{{reflist|2}}
 
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}
 
[[Category:Pulmonology]]
[[Category:Emergency medicine]]
[[Category:Disease]]
[[Category:Up-To-Date]]
[[Category:Infectious disease]]

Latest revision as of 20:56, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Overview

Chronic bronchitis as a main category of COPD is caused by multiple environmental and genetic factors. Smoking is the leading cause of chronic bronchitis.

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.[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. Majority of life-long smokers will develop COPD, provided that smoking-related extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.[4]

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.[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

  • 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. Long-term research is needed to confirm this link.
  • Studies have demonstrated a direct relationship between the waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and an inverse relationship between the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) and the exacerbation of COPD.
  • 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

  • A genetic component appears to be required for susceptibility in developing COPD, even in heavy smokers. 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 COPD cases. 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

  • 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 progress for many years after smoking cesssation 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

Causes by Organ System

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

The unnamed parameter 2= is no longer supported. Please see the documentation for {{columns-list}}.
3

External Links

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

References

  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)
  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.
  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)
  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)
  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)
  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.
  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)
  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)
  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)


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