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__NOTOC__
__NOTOC__
{{Asthma}}
{{Asthma}}
'''Editor(s)-in-Chief:''' [[C. Michael Gibson, M.S., M.D.]] [mailto:mgibson@perfuse.org] Phone:617-632-7753; [[Philip Marcus, M.D., M.P.H.]] [mailto:pmarcus192@aol.com]; {{AOEIC}} {{VK}}
{{CMG}}; [[Philip Marcus, M.D., M.P.H.]] [mailto:pmarcus192@aol.com]; {{AE}} {{VK}}


==Overview==
==Overview==
Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not yet fully understand.<ref name=Martinez_geneenvir>{{cite journal |author=Martinez FD |title=Genes, environments, development and asthma: a reappraisal |journal=Eur Respir J |volume=29 |issue=1 |pages=179–84 |year=2007 |pmid=17197483 |doi=10.1183/09031936.00087906}}</ref> These factors can also influence how severe a person’s asthma is and how well they respond to medication.<ref>{{cite journal |author=Choudhry S, Seibold MA, Borrell LN "et al." |title=Dissecting complex diseases in complex populations: asthma in latino americans |journal=Proc Am Thorac Soc |volume=4 |issue=3 |pages=226–33 |year=2007 |pmid=17607004 |doi=10.1513/pats.200701-029AW}}</ref> As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all studies posing such claims have been verified by further studies. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may affect asthma only when combined.
Asthma is caused by a complex interaction of environmental and [[genetic]] factors that researchers do not yet fully understand.<ref name="Martinez_geneenvir">{{cite journal |author=Martinez FD |title=Genes, environments, development and asthma: a reappraisal |journal=Eur Respir J |volume=29 |issue=1 |pages=179–84 |year=2007 |pmid=17197483 |doi=10.1183/09031936.00087906}}</ref> These factors can also influence how severe a person’s asthma is and how well they respond to medication.<ref>{{cite journal |author=Choudhry S, Seibold MA, Borrell LN "et al." |title=Dissecting complex diseases in complex populations: asthma in latino americans |journal=Proc Am Thorac Soc |volume=4 |issue=3 |pages=226–33 |year=2007 |pmid=17607004 |doi=10.1513/pats.200701-029AW}}</ref> As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all studies posing such claims have been verified by further studies. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may affect asthma only when combined.<ref name="pmid27180590">{{cite journal| author=Liu WY, Yu Q, Yue HM, Zhang JB, Li L, Wang XY et al.| title=[The distribution characteristics of etiology of chronic cough in Lanzhou]. | journal=Zhonghua Jie He He Hu Xi Za Zhi | year= 2016 | volume= 39 | issue= 5 | pages= 362-7 | pmid=27180590 | doi=10.3760/cma.j.issn.1001-0939.2016.05.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27180590  }} </ref>


==Differential Diagnosis of Underlying Etiology==
==Causes==
(By organ system)
===Causes by Organ System===
{|style="width:70%; height:100px" border="1"
{| style="width:70%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
| style="width:25%" bgcolor="LightSteelBlue" ; border="1" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
| style="width:75%" bgcolor="Beige" ; border="1" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Dermatologic'''
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
| '''Drug Side Effect'''
|bgcolor="Beige"| [[Aspirin]] hypersensitivity, [[beta-adrenergic receptor blocker]]s
| bgcolor="Beige" | [[Artemether and lumefantrin]], [[Aspirin]] hypersensitivity, [[beta-adrenergic receptor blocker]]s, [[Bicalutamide]], [[Cefpodoxime]], [[Chlorpromazine]], [[Choline Magnesium Trisalicylate]], [[Cidofovir]], [[diclofenac (patch)]], [[Flurbiprofen]], [[Leflunomide]], [[Meropenem]], [[Oxaprozin]], [[Oxcarbazepine]], [[Polidocanol]], [[Pramipexole]], [[Pentamidine Isethionate]], [[Tiagabine]], [[Zanamivir]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-  
|-  
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Endocrine'''
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-  
|-  
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Environmental'''
| '''Environmental'''
|bgcolor="Beige"| Environmental allergens such as house dust mites, animal allergens (cat and dog), cockroach allergens, and fungi. [[Passive smoking|Environmental tobacco smoke]], especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.<ref name=Gold /> Poor [[air Quality Index|air quality]], from traffic pollution or high [[ozone]] levels<ref name=childrens_health_study>{{cite web | url = http://www.arb.ca.gov/research/chs/chs.htm | title = California Children's Health Study}}</ref>. Exposure to cold or dry air are also known to cause [[bronchospasm]].
| bgcolor="Beige" | Environmental allergens such as house dust mites, animal allergens (cat and dog), cockroach allergens, and fungi. [[Passive smoking|Environmental tobacco smoke]], especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.<ref name="Gold" /> Poor [[air Quality Index|air quality]], from traffic pollution or high [[ozone]] levels<ref name="childrens_health_study">{{cite web | url = http://www.arb.ca.gov/research/chs/chs.htm | title = California Children's Health Study}}</ref>. Exposure to cold or dry air are also known to cause [[bronchospasm]].
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
| '''Gastroenterologic'''
|bgcolor="Beige"| Gastroesophageal reflux disease<ref name="pmid10903216">{{cite journal| author=Harding SM, Guzzo MR, Richter JE| title=The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms. | journal=Am J Respir Crit Care Med | year= 2000 | volume= 162 | issue= 1 | pages= 34-9 | pmid=10903216 | doi= | pmc= | url= }} </ref>
| bgcolor="Beige" | Gastroesophageal reflux disease<ref name="pmid10903216">{{cite journal| author=Harding SM, Guzzo MR, Richter JE| title=The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms. | journal=Am J Respir Crit Care Med | year= 2000 | volume= 162 | issue= 1 | pages= 34-9 | pmid=10903216 | doi= | pmc= | url= }} </ref>
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Genetic'''
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Hematologic'''
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Iatrogenic'''
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Infectious Disease'''
| '''Infectious Disease'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Neurologic'''
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| [[Obesity]]<ref name="pmid10573048">{{cite journal| author=Camargo CA, Weiss ST, Zhang S, Willett WC, Speizer FE| title=Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. | journal=Arch Intern Med | year= 1999 | volume= 159 | issue= 21 | pages= 2582-8 | pmid=10573048 | doi= | pmc= | url= }} </ref>
| bgcolor="Beige" | [[Obesity]]<ref name="pmid10573048">{{cite journal| author=Camargo CA, Weiss ST, Zhang S, Willett WC, Speizer FE| title=Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. | journal=Arch Intern Med | year= 1999 | volume= 159 | issue= 21 | pages= 2582-8 | pmid=10573048 | doi= | pmc= | url= }} </ref>
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| [[Caesarean section]]s have been associated with asthma when compared with vaginal birth<ref name="pmid18352976">{{cite journal| author=Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell CR| title=A meta-analysis of the association between Caesarean section and childhood asthma. | journal=Clin Exp Allergy | year= 2008 | volume= 38 | issue= 4 | pages= 629-33 | pmid=18352976 | doi=10.1111/j.1365-2222.2007.02780.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18352976  }} </ref>. Increased maternal age, [[Premature birth]], Maternal smoking and prenatal exposure to tobacco smoke
| bgcolor="Beige" | [[Caesarean section]]s have been associated with asthma when compared with vaginal birth<ref name="pmid18352976">{{cite journal| author=Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell CR| title=A meta-analysis of the association between Caesarean section and childhood asthma. | journal=Clin Exp Allergy | year= 2008 | volume= 38 | issue= 4 | pages= 629-33 | pmid=18352976 | doi=10.1111/j.1365-2222.2007.02780.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18352976  }} </ref>. Increased maternal age, [[premature birth]], maternal smoking and prenatal exposure to tobacco smoke
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Oncologic'''
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Opthalmologic'''
| '''Opthalmologic'''
|bgcolor="Beige"| Use of [[beta-adrenergic receptor blocker]]s in [[glaucoma]]
| bgcolor="Beige" | Use of [[beta-adrenergic receptor blocker]]s in [[glaucoma]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
| '''Overdose / Toxicity'''
|bgcolor="Beige"| Household sprays, Paint fumes
| bgcolor="Beige" | Household sprays, Paint fumes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Psychiatric'''
| '''Psychiatric'''
|bgcolor="Beige"| Emotional stress<ref name="Chen2007">{{cite journal |author=Chen E, Miller GE |title=Stress and inflammation in exacerbations of asthma. |journal=Brain Behav Immun. |volume=21 |issue=8 |pages=993-9 |year=2007 |pmid=17493786 |doi=}}</ref>
| bgcolor="Beige" | Emotional stress<ref name="Chen2007">{{cite journal |author=Chen E, Miller GE |title=Stress and inflammation in exacerbations of asthma. |journal=Brain Behav Immun. |volume=21 |issue=8 |pages=993-9 |year=2007 |pmid=17493786 |doi=}}</ref>
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Pulmonary'''
| '''Pulmonary'''
|bgcolor="Beige"| Chronic [[sinusitis]] or [[rhinitis]]
| bgcolor="Beige" | Chronic [[sinusitis]] or [[rhinitis]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
| '''Renal / Electrolyte'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Aspirin]] hypersensitivity
| bgcolor="Beige" | [[Aspirin]] hypersensitivity
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Sexual'''
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Trauma'''
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Urologic'''
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="Beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="LightSteelBlue"
| '''Miscellaneous'''
| '''Miscellaneous'''
|bgcolor="Beige"| Occupational exposure such as farming, painting, janitorial work, and plastics manufacturing; Exposure to cold or dry air are also known to cause [[bronchospasm]]. Family history or genetic predisposition to asthma<ref name="pmid16395390">{{cite journal| author=Ober C, Hoffjan S| title=Asthma genetics 2006: the long and winding road to gene discovery. | journal=Genes Immun | year= 2006 | volume= 7 | issue= 2 | pages= 95-100 | pmid=16395390 | doi=10.1038/sj.gene.6364284 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16395390  }} </ref>.
| bgcolor="Beige" | Occupational exposure such as farming, painting, janitorial work, and plastics manufacturing; Exposure to cold or dry air are also known to cause [[bronchospasm]]. Family history or genetic predisposition to asthma<ref name="pmid16395390">{{cite journal| author=Ober C, Hoffjan S| title=Asthma genetics 2006: the long and winding road to gene discovery. | journal=Genes Immun | year= 2006 | volume= 7 | issue= 2 | pages= 95-100 | pmid=16395390 | doi=10.1038/sj.gene.6364284 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16395390  }} </ref>.
|-
|-
|}
|}


==Environmental==
===Environmental Factors===
Many environmental [[risk factor]]s have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a [[meta-analysis]] of several studies to support their direct association.
* Many environmental [[risk factor]]s have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a [[meta-analysis]] of several studies to support their direct association.
* [[Passive smoking|Environmental tobacco smoke]], especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.<ref name="Gold" />
* Poor [[air Quality Index|air quality]], from traffic pollution or high [[ozone]] levels, has been repeatedly associated with increased asthma [[morbidity]] and has a suggested association with asthma development that needs further research.<ref name="Gold">{{cite journal |author=Gold DR,Wright R |title=Population disparities in asthma |journal=Annu Rev Public Health |volume=26 |pages=89–113 |year=2005 |pmid=15760282 |doi=10.1146/annurev.publhealth.26.021304.144528}}</ref><ref name="childrens_health_study">{{cite web | url = http://www.arb.ca.gov/research/chs/chs.htm | title = California Children's Health Study}}</ref>
* [[Caesarean section]]s have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).<ref name="Thavagnanam" />
* Psychological [[stress (biological)|stress]], has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.<ref name="Gold" /><ref name="Chen2007">{{cite journal |author=Chen E, Miller GE |title=Stress and inflammation in exacerbations of asthma. |journal=Brain Behav Immun. |volume=21 |issue=8 |pages=993-9 |year=2007 |pmid=17493786 |doi=}}</ref>
* Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.<ref name="Gold" /><ref name="Thorax2006-Terttu">{{cite journal |author=Harju TH, Leinonen M, Nokso-Koivisto J, ''et al'' |title=Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma |journal=Thorax |volume=61 |issue=7 |pages=579–84 |year=2006 |pmid=16517571 |doi=10.1136/thx.2005.056291}}</ref><ref name="Cochrane2005-Richeldi">{{cite journal |author=Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG |title=Macrolides for chronic asthma |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD002997 |year=2005 |pmid=16235309 |doi=10.1002/14651858.CD002997.pub3}}</ref>
* [[Antibiotic]]use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify [[gut flora]], and thus the immune system (as described by the [[hygiene hypothesis]]).<ref name="Marra" />
* The [[hygiene hypothesis]] is an [[hypothesis]] about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, C-sections, and cleaning products.<ref name="Marra">{{cite journal |author=Marra F, Lynd L, Coombes M "et al." |title=Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis |journal=Chest |volume=129 |issue=3 |pages=610–8 |year=2006 |pmid=16537858 |doi=10.1378/chest.129.3.610}}</ref><ref name="Thavagnanam">{{cite journal |author=Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell, CR |title=A meta-analysis of the association between Caesarean section and childhood asthma |journal=Clin. And Exper. Allergy |volume=online ahead of print |year=2007 |doi=10.1111/j.1365-2222.2007.02780.x  | pages = 629}}</ref><ref name="europe_study">{{cite web | author=Jeremy Laurance | url=http://www.belfasttelegraph.co.uk/health/article3056797.ece | title = Asthma blamed on cleaning sprays and air fresheners}}</ref> All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.


[[Passive smoking|Environmental tobacco smoke]], especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.<ref name=Gold /> Poor [[air Quality Index|air quality]], from traffic pollution or high [[ozone]] levels, has been repeatedly associated with increased asthma [[morbidity]] and has a suggested association with asthma development that needs further research.<ref name=Gold>{{cite journal |author=Gold DR,Wright R |title=Population disparities in asthma |journal=Annu Rev Public Health |volume=26 |pages=89–113 |year=2005 |pmid=15760282 |doi=10.1146/annurev.publhealth.26.021304.144528}}</ref><ref name=childrens_health_study>{{cite web | url = http://www.arb.ca.gov/research/chs/chs.htm | title = California Children's Health Study}}</ref>
===Genetic Predisposition===
 
Over 100 [[gene]]s have been associated with asthma in at least one [[genetic association|genetic association study]].<ref name="Hoffjan">{{cite journal |author=Ober C,Hoffjan S |title=Asthma genetics 2006: the long and winding road to gene discovery |journal=Genes Immun |volume=7 |issue=2 |pages=95–100 |year=2006 |pmid=16395390 |doi=10.1038/sj.gene.6364284}}</ref> However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:<ref name="Hoffjan" />
[[Caesarean section]]s have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).<ref name=Thavagnanam />
 
Psychological [[stress (biological)|stress]], has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.<ref name=Gold /><ref name="Chen2007">{{cite journal |author=Chen E, Miller GE |title=Stress and inflammation in exacerbations of asthma. |journal=Brain Behav Immun. |volume=21 |issue=8 |pages=993-9 |year=2007 |pmid=17493786 |doi=}}</ref>
 
Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.<ref name=Gold /><ref name="Thorax2006-Terttu">{{cite journal |author=Harju TH, Leinonen M, Nokso-Koivisto J, ''et al'' |title=Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma |journal=Thorax |volume=61 |issue=7 |pages=579–84 |year=2006 |pmid=16517571 |doi=10.1136/thx.2005.056291}}</ref><ref name="Cochrane2005-Richeldi">{{cite journal |author=Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG |title=Macrolides for chronic asthma |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD002997 |year=2005 |pmid=16235309 |doi=10.1002/14651858.CD002997.pub3}}</ref> [[Antibiotic]] use early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify [[gut flora]], and thus the immune system (as described by the hygiene hypothesis).<ref name=Marra />
The [[hygiene hypothesis]] is an [[hypothesis]] about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, c-sections, and cleaning products.<ref name=Marra>{{cite journal |author=Marra F, Lynd L, Coombes M "et al." |title=Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis |journal=Chest |volume=129 |issue=3 |pages=610–8 |year=2006 |pmid=16537858 |doi=10.1378/chest.129.3.610}}</ref><ref name=Thavagnanam>{{cite journal |author=Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell, CR |title=A meta-analysis of the association between Caesarean section and childhood asthma |journal=Clin. And Exper. Allergy |volume=online ahead of print |year=2007 |doi=10.1111/j.1365-2222.2007.02780.x  | pages = 629}}</ref><ref name=europe_study>{{cite web | author=Jeremy Laurance | url=http://www.belfasttelegraph.co.uk/health/article3056797.ece | title = Asthma blamed on cleaning sprays and air fresheners}}</ref>  All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.
 
==Genetic Predisposition==
Over 100 [[gene]]s have been associated with asthma in at least one [[genetic association|genetic association study]].<ref name=Hoffjan>{{cite journal |author=Ober C,Hoffjan S |title=Asthma genetics 2006: the long and winding road to gene discovery |journal=Genes Immun |volume=7 |issue=2 |pages=95–100 |year=2006 |pmid=16395390 |doi=10.1038/sj.gene.6364284}}</ref> However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:<ref name=Hoffjan />


{{Multicol}}
{{Multicol}}
<small>
* Glutathione S-transferase Mu 1 (GSTM1)
* Glutathione S-transferase Mu 1 (GSTM1)
*[[Interleukin 10|IL10]]
*[[Interleukin 10|IL10]]
Line 140: Line 137:
*[[SPINK5]]
*[[SPINK5]]
*[[Leukotriene C4 synthase|LTC4S]]
*[[Leukotriene C4 synthase|LTC4S]]
  {{Multicol-break}}
{{ColBreak}}
<small>
* lymphotoxin alpha (LTA)
* lymphotoxin alpha (LTA)
* GRPA
* GRPA
Line 147: Line 143:
* CC16
* CC16
* GSTP1
* GSTP1
  {{Multicol-break}}
{{ColBreak}}
<small>
*[[STAT6]]
*[[STAT6]]
*[[NOS1]]
*[[NOS1]]
Line 154: Line 149:
*[[Thromboxane receptor|TBXA2R]]
*[[Thromboxane receptor|TBXA2R]]
*[[TGFB1]]
*[[TGFB1]]
  {{Multicol-break}}
{{ColBreak}}
<small>
*[[Interleukin 4|IL4]]
*[[Interleukin 4|IL4]]
*[[Interleukin 13|IL13]]
*[[Interleukin 13|IL13]]
Line 161: Line 155:
*[[Beta-2 adrenergic receptor|ADRB2]] (β-2 adrenergic receptor)
*[[Beta-2 adrenergic receptor|ADRB2]] (β-2 adrenergic receptor)
*[[HLA-DRB1]]
*[[HLA-DRB1]]
  {{Multicol-break}}
{{ColBreak}}
<small>
*[[HLA-DQB1]]
*[[HLA-DQB1]]
*[[Tumor necrosis factors|TNF]]
*[[Tumor necrosis factors|TNF]]
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* Interleukin-4 receptor (IL4R)
* Interleukin-4 receptor (IL4R)
*[[ADAM33]]
*[[ADAM33]]
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Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.<ref name=Hoffjan /> This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences ([[single nucleotide polymorphism]]s in [[Chromosome 17 (human)|17q21]]) was associated with asthma that develops in childhood.<ref name="pmid18923164">{{cite journal |author=Bouzigon E, Corda E, Aschard H, ''et al'' |title=Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma |journal=The New England journal of medicine |volume= |issue= |pages= |year=2008 |month=October |pmid=18923164 |doi=10.1056/NEJMoa0806604 |url=}}</ref>
Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.<ref name="Hoffjan" /> This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences ([[single nucleotide polymorphism]]s in [[Chromosome 17 (human)|17q21]]) was associated with asthma that develops in childhood.<ref name="pmid18923164">{{cite journal |author=Bouzigon E, Corda E, Aschard H, ''et al'' |title=Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma |journal=The New England journal of medicine |volume= |issue= |pages= |year=2008 |month=October |pmid=18923164 |doi=10.1056/NEJMoa0806604 |url=}}</ref>


==Gene-environment Interactions==
===Gene and Environment Interactions===
Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.<ref name=Martinez_geneenvir />
* Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.<ref name="Martinez_geneenvir" />
 
* The genetic trait, CD14 [[single nucleotide polymorphism]] (SNP) C-159T  and exposure to [[endotoxin]] (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s [[genotype]] at CD14 C-159T and level of endotoxin exposure.<ref name="Martinez_CD14">{{cite journal |author=Martinez FD |title=CD14, endotoxin, and asthma risk: actions and interactions |journal=Proc Am Thorac Soc |volume=4 |issue=3 |pages=221–5 |year=2007 |pmid=17607003 |doi=10.1513/pats.200702-035AW}}</ref>
The genetic trait, CD14 [[single nucleotide polymorphism]] (SNP) C-159T  and exposure to [[endotoxin]] (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s [[genotype]] at CD14 C-159T and level of endotoxin exposure.<ref name=Martinez_CD14>{{cite journal |author=Martinez FD |title=CD14, endotoxin, and asthma risk: actions and interactions |journal=Proc Am Thorac Soc |volume=4 |issue=3 |pages=221–5 |year=2007 |pmid=17607003 |doi=10.1513/pats.200702-035AW}}</ref>


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[[Category:Disease]]
[[Category:Pulmonology]]
[[Category:Pulmonology]]
[[Category:Immunology]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]
[[Category:Mature chapter]]
[[Category:Up-To-Date]]
[[Category:Up-To-Date pulmonology]]
{{WH}}
{{WS}}

Latest revision as of 20:30, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Philip Marcus, M.D., M.P.H. [2]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [3]

Overview

Asthma is caused by a complex interaction of environmental and genetic factors that researchers do not yet fully understand.[1] These factors can also influence how severe a person’s asthma is and how well they respond to medication.[2] As with other complex diseases, many environmental and genetic factors have been suggested as causes of asthma, but not all studies posing such claims have been verified by further studies. In addition, as researchers detangle the complex causes of asthma, it is becoming more evident that certain environmental and genetic factors may affect asthma only when combined.[3]

Causes

Causes by Organ System

Cardiovascular No underlying causes
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect Artemether and lumefantrin, Aspirin hypersensitivity, beta-adrenergic receptor blockers, Bicalutamide, Cefpodoxime, Chlorpromazine, Choline Magnesium Trisalicylate, Cidofovir, diclofenac (patch), Flurbiprofen, Leflunomide, Meropenem, Oxaprozin, Oxcarbazepine, Polidocanol, Pramipexole, Pentamidine Isethionate, Tiagabine, Zanamivir
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental Environmental allergens such as house dust mites, animal allergens (cat and dog), cockroach allergens, and fungi. Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[4] Poor air quality, from traffic pollution or high ozone levels[5]. Exposure to cold or dry air are also known to cause bronchospasm.
Gastroenterologic Gastroesophageal reflux disease[6]
Genetic No underlying causes
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal / Ortho No underlying causes
Neurologic No underlying causes
Nutritional / Metabolic Obesity[7]
Obstetric/Gynecologic Caesarean sections have been associated with asthma when compared with vaginal birth[8]. Increased maternal age, premature birth, maternal smoking and prenatal exposure to tobacco smoke
Oncologic No underlying causes
Opthalmologic Use of beta-adrenergic receptor blockers in glaucoma
Overdose / Toxicity Household sprays, Paint fumes
Psychiatric Emotional stress[9]
Pulmonary Chronic sinusitis or rhinitis
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Aspirin hypersensitivity
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Occupational exposure such as farming, painting, janitorial work, and plastics manufacturing; Exposure to cold or dry air are also known to cause bronchospasm. Family history or genetic predisposition to asthma[10].

Environmental Factors

  • Many environmental risk factors have been associated with asthma development and morbidity in children, but a few stand out as well-replicated or that have a meta-analysis of several studies to support their direct association.
  • Environmental tobacco smoke, especially maternal cigarette smoking, is associated with high risk of asthma prevalence and asthma morbidity, wheeze, and respiratory infections.[4]
  • Poor air quality, from traffic pollution or high ozone levels, has been repeatedly associated with increased asthma morbidity and has a suggested association with asthma development that needs further research.[4][5]
  • Caesarean sections have been associated with asthma when compared with vaginal birth; a meta-analysis found a 20% increase in asthma prevalence in children delivered by Cesarean section compared to those who were not. It was proposed that this is due to modified bacterial exposure during Cesarean section compared with vaginal birth, which modifies the immune system (as described by the hygiene hypothesis).[11]
  • Psychological stress, has long been suspected of being an asthma trigger, but only in recent decades has convincing scientific evidence substantiated this hypothesis. Rather than stress directly causing the asthma symptoms, it is thought that stress modulates the immune system to increase the magnitude of the airway inflammatory response to allergens and irritants.[4][9]
  • Viral respiratory infections at an early age, along with siblings and day care exposure, may be protective against asthma, although there have been controversial results, and this protection may depend on genetic context.[4][12][13]
  • Antibioticuse early in life has been linked to development of asthma in several examples; it is thought that antibiotics make one susceptible to development of asthma because they modify gut flora, and thus the immune system (as described by the hygiene hypothesis).[14]
  • The hygiene hypothesis is an hypothesis about the cause of asthma and other allergic disease, and is supported by epidemiologic data for asthma. For example, asthma prevalence has been increasing in developed countries along with increased use of antibiotics, C-sections, and cleaning products.[14][11][15] All of these things may negatively affect exposure to beneficial bacteria and other immune system modulators that are important during development, and thus may cause increased risk for asthma and allergy.

Genetic Predisposition

Over 100 genes have been associated with asthma in at least one genetic association study.[16] However, such studies must be repeated to ensure the findings are not due to chance. Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[16]

  • lymphotoxin alpha (LTA)
  • GRPA
  • NOD1
  • CC16
  • GSTP1

Template:Multicol-end

Many of these genes are related to the immune system or to modulating inflammation. However, even among this list of highly replicated genes associated with asthma, the results have not been consistent among all of the populations that have been tested.[16] This indicates that these genes are not associated with asthma under every condition, and that researchers need to do further investigation to figure out the complex interactions that cause asthma. One theory is that asthma is a collection of several diseases, and that genes might have a role in only subsets of asthma. For example, one group of genetic differences (single nucleotide polymorphisms in 17q21) was associated with asthma that develops in childhood.[17]

Gene and Environment Interactions

  • Research suggests that some genetic variants may only cause asthma when they are combined with specific environmental exposures, and otherwise may not be risk factors for asthma.[1]
  • The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. Endotoxin exposure varies from person to person and can come from several environmental sources, including environmental tobacco smoke, dogs, and farms. Researchers have found that risk for asthma changes based on a person’s genotype at CD14 C-159T and level of endotoxin exposure.[18]
CD14-endotoxin interaction based on CD14 SNP C-159T[18]
Endotoxin levels CC genotype TT genotype
High exposure Low risk High risk
Low exposure High risk Low risk

References

  1. ↑ 1.0 1.1 Martinez FD (2007). "Genes, environments, development and asthma: a reappraisal". Eur Respir J. 29 (1): 179–84. doi:10.1183/09031936.00087906. PMID 17197483.
  2. ↑ Choudhry S, Seibold MA, Borrell LN; et al. (2007). "Dissecting complex diseases in complex populations: asthma in latino americans". Proc Am Thorac Soc. 4 (3): 226–33. doi:10.1513/pats.200701-029AW. PMID 17607004.
  3. ↑ Liu WY, Yu Q, Yue HM, Zhang JB, Li L, Wang XY; et al. (2016). "[The distribution characteristics of etiology of chronic cough in Lanzhou]". Zhonghua Jie He He Hu Xi Za Zhi. 39 (5): 362–7. doi:10.3760/cma.j.issn.1001-0939.2016.05.006. PMID 27180590.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 Gold DR,Wright R (2005). "Population disparities in asthma". Annu Rev Public Health. 26: 89–113. doi:10.1146/annurev.publhealth.26.021304.144528. PMID 15760282.
  5. ↑ 5.0 5.1 "California Children's Health Study".
  6. ↑ Harding SM, Guzzo MR, Richter JE (2000). "The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms". Am J Respir Crit Care Med. 162 (1): 34–9. PMID 10903216.
  7. ↑ Camargo CA, Weiss ST, Zhang S, Willett WC, Speizer FE (1999). "Prospective study of body mass index, weight change, and risk of adult-onset asthma in women". Arch Intern Med. 159 (21): 2582–8. PMID 10573048.
  8. ↑ Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell CR (2008). "A meta-analysis of the association between Caesarean section and childhood asthma". Clin Exp Allergy. 38 (4): 629–33. doi:10.1111/j.1365-2222.2007.02780.x. PMID 18352976.
  9. ↑ 9.0 9.1 Chen E, Miller GE (2007). "Stress and inflammation in exacerbations of asthma". Brain Behav Immun. 21 (8): 993–9. PMID 17493786.
  10. ↑ Ober C, Hoffjan S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun. 7 (2): 95–100. doi:10.1038/sj.gene.6364284. PMID 16395390.
  11. ↑ 11.0 11.1 Thavagnanam S, Fleming J, Bromley A, Shields MD, Cardwell, CR (2007). "A meta-analysis of the association between Caesarean section and childhood asthma". Clin. And Exper. Allergy. online ahead of print: 629. doi:10.1111/j.1365-2222.2007.02780.x.
  12. ↑ Harju TH, Leinonen M, Nokso-Koivisto J; et al. (2006). "Pathogenic bacteria and viruses in induced sputum or pharyngeal secretions of adults with stable asthma". Thorax. 61 (7): 579–84. doi:10.1136/thx.2005.056291. PMID 16517571.
  13. ↑ Richeldi L, Ferrara G, Fabbri LM, Lasserson TJ, Gibson PG (2005). "Macrolides for chronic asthma". Cochrane Database Syst Rev (4): CD002997. doi:10.1002/14651858.CD002997.pub3. PMID 16235309.
  14. ↑ 14.0 14.1 Marra F, Lynd L, Coombes M; et al. (2006). "Does antibiotic exposure during infancy lead to development of asthma?: a systematic review and metaanalysis". Chest. 129 (3): 610–8. doi:10.1378/chest.129.3.610. PMID 16537858.
  15. ↑ Jeremy Laurance. "Asthma blamed on cleaning sprays and air fresheners".
  16. ↑ 16.0 16.1 16.2 Ober C,Hoffjan S (2006). "Asthma genetics 2006: the long and winding road to gene discovery". Genes Immun. 7 (2): 95–100. doi:10.1038/sj.gene.6364284. PMID 16395390.
  17. ↑ Bouzigon E, Corda E, Aschard H; et al. (2008). "Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma". The New England journal of medicine. doi:10.1056/NEJMoa0806604. PMID 18923164. Unknown parameter |month= ignored (help)
  18. ↑ 18.0 18.1 Martinez FD (2007). "CD14, endotoxin, and asthma risk: actions and interactions". Proc Am Thorac Soc. 4 (3): 221–5. doi:10.1513/pats.200702-035AW. PMID 17607003.

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