Chronic bronchitis causes: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
| Line 5: | Line 5: | ||
==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. | 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=== | ===Common Causes=== | ||
====Smoking==== | ====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.<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> | * 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> | ||
* 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. | * 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. | ||
* 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.<ref>{{cite doi|10.1016/S0140-6736(06)68516-4}}</ref> | * 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==== | ====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]] | * 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 | | pmid = 16690673 | ||
| pmc = 1459603 | | pmc = 1459603 | ||
| Line 27: | Line 30: | ||
}}</ref> | }}</ref> | ||
* Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. | * 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> | * 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> | * 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==== | ====Air Pollution==== | ||
* People who live in large cities have a higher rate of 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> | * 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 COPD, as it is thought to slow the normal growth of the lungs. Long-term research is needed to confirm this link. | * 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 COPD/asthma-aggravating compound, [[sulfur dioxide]], and an inverse relationship between the blue lichen '' | * 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 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> | * 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==== | ====Genetics==== | ||
* A [[gene]]tic 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.<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> | * 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. | * 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.<ref>{{MedlinePlus|000091}}</ref> | * [[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==== | ====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> | |||
* There is mounting evidence that there may be an autoimmune component to 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> | * 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==== | ====Other Risk Factors==== | ||
* A characteristic of asthma, also common in 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. | * 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. | * 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. | ||
| Line 165: | Line 167: | ||
===Causes in Alphabetical Order=== | ===Causes in Alphabetical Order=== | ||
{{Columns-list|3| | |||
*Abnormal activity of tissue inhibitors of [[metalloproteinase]] (TIMP-1) | *Abnormal activity of tissue inhibitors of [[metalloproteinase]] (TIMP-1) | ||
*[[Age]] | *[[Age]] | ||
| Line 205: | Line 208: | ||
*[[Vitamin E]] deficiency | *[[Vitamin E]] deficiency | ||
*[[Zanamivir]] | *[[Zanamivir]] | ||
}} | |||
==External Links== | ==External Links== | ||
Revision as of 15:21, 6 April 2017
|
Chronic bronchitis Microchapters |
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Chronic bronchitis causes On the Web |
|
American Roentgen Ray Society Images of Chronic bronchitis causes |
|
Risk calculators and risk factors for Chronic bronchitis causes |
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
- A characteristic of asthma, also common in 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.[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
| 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}}.
3External Links
http://www.cdc.gov/copd/index.htm
References
- ↑ 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) - ↑ 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.
- ↑ 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.
- ↑ 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) - ↑ 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)