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==Environmental== | ==Environmental== | ||
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 /> | |||
[[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> | * 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 /> | |||
[[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]] | |||
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> | * 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> | |||
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 /> | * 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. | ||
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> | |||
==Genetic Predisposition== | ==Genetic Predisposition== | ||
Revision as of 15:53, 3 October 2011
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Asthma Microchapters |
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Asthma causes On the Web |
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American Roentgen Ray Society Images of Asthma causes |
Editor(s)-in-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-632-7753; 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.
Differential Diagnosis of Underlying Etiology
(By organ system)
| Cardiovascular | No underlying causes |
| Chemical / poisoning | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | Aspirin hypersensitivity, beta-adrenergic receptor blockers |
| 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.[3] Poor air quality, from traffic pollution or high ozone levels[4]. Exposure to cold or dry air are also known to cause bronchospasm. |
| Gastroenterologic | Gastroesophageal reflux disease[5] |
| 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[6] |
| Obstetric/Gynecologic | Caesarean sections have been associated with asthma when compared with vaginal birth[7]. 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[8] |
| 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[9]. |
Environmental
- 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.[3]
- 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.[3][4]
- 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).[10]
- 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.[3][8]
- 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.[3][11][12]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).[13]
- 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.[13][10][14]
- 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.[15] 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:[15]
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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.[15] 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.[16] Gene-environment InteractionsResearch 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.[17]
References
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