Editing Asthma (section)

==Causes==
Asthma is caused by a combination of complex and incompletely understood environmental and genetic interactions.<ref name=Martinez2007>{{cite journal | vauthors = Martinez FD | title = Genes, environments, development and asthma: a reappraisal | journal = The European Respiratory Journal | volume = 29 | issue = 1 | pages = 179–84 | date = January 2007 | pmid = 17197483 | doi = 10.1183/09031936.00087906 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Miller RL, Ho SM | title = Environmental epigenetics and asthma: current concepts and call for studies | journal = American Journal of Respiratory and Critical Care Medicine | volume = 177 | issue = 6 | pages = 567–73 | date = March 2008 | pmid = 18187692 | pmc = 2267336 | doi = 10.1164/rccm.200710-1511PP }}</ref> These influence both its severity and its responsiveness to treatment.<ref>{{cite journal | vauthors = Choudhry S, Seibold MA, Borrell LN, Tang H, Serebrisky D, Chapela R, Rodriguez-Santana JR, Avila PC, Ziv E, Rodriguez-Cintron W, Risch NJ, Burchard EG | display-authors = 6 | title = Dissecting complex diseases in complex populations: asthma in latino americans | journal = Proceedings of the American Thoracic Society | volume = 4 | issue = 3 | pages = 226–33 | date = July 2007 | pmid = 17607004 | pmc = 2647623 | doi = 10.1513/pats.200701-029AW}}</ref> It is believed that the recent increased rates of asthma are due to changing [[epigenetic]]s ([[heritable]] factors other than those related to the [[DNA sequence]]) and a changing living environment.<ref name="pmid21575714">{{cite journal | vauthors = Dietert RR | title = Maternal and childhood asthma: risk factors, interactions, and ramifications | journal = Reproductive Toxicology | volume = 32 | issue = 2 | pages = 198–204 | date = September 2011 | pmid = 21575714 | doi = 10.1016/j.reprotox.2011.04.007 | bibcode = 2011RepTx..32..198D }}</ref> Asthma that starts before the age of 12 years old is more likely due to genetic influence, while onset after age 12 is more likely due to environmental influence.<ref>{{cite journal | vauthors = Tan DJ, Walters EH, Perret JL, Lodge CJ, Lowe AJ, Matheson MC, Dharmage SC | title = Age-of-asthma onset as a determinant of different asthma phenotypes in adults: a systematic review and meta-analysis of the literature | journal = Expert Review of Respiratory Medicine | volume = 9 | issue = 1 | pages = 109–23 | date = February 2015 | pmid = 25584929 | doi = 10.1586/17476348.2015.1000311 | s2cid = 23213216 }}</ref>

===Environmental===
{{See also|Asthma-related microbes}}

Many environmental factors have been associated with asthma's development and exacerbation, including allergens, air pollution, and other environmental chemicals.<ref name="pmid21623970">{{cite journal |vauthors=Kelly FJ, Fussell JC |date=August 2011 |title=Air pollution and airway disease |journal=Clinical and Experimental Allergy |volume=41 |issue=8 |pages=1059–71 |doi=10.1111/j.1365-2222.2011.03776.x|pmid=21623970 |s2cid=37717160 }}</ref> There are some substances that are known to cause asthma in exposed people and they are called [[asthmagen]]s. Some common asthmagens include ammonia, latex, pesticides, solder and welding fumes, metal or wood dusts, spraying of isocyanate paint in vehicle repair, formaldehyde, glutaraldehyde, anhydrides, glues, dyes, metal working fluids, oil mists, moulds.<ref>{{cite web | url=https://www.health.ny.gov/environmental/workplace/lung_disease_registry/toolkit/asthmagens.htm | title=Occupational Asthmagens – New York State Department of Health}}</ref><ref>{{cite web | url=https://www.hse.gov.uk/foi/internalops/og/og-00016.htm | title=Occupational Asthmagens – HSE}}</ref> [[Smoking and pregnancy|Smoking during pregnancy]] and after delivery is associated with a greater risk of asthma-like symptoms.<ref name="GINA2011_p6">{{harvnb|GINA|2011|p=6}}</ref> Low [[Air quality index|air quality]] from environmental factors such as [[Exhaust gas|traffic pollution]] or high [[ozone]] levels<ref name="GINA2011_p61">{{harvnb|GINA|2011|p=61}}</ref> has been associated with both asthma development and increased asthma severity.<ref name="Gold">{{cite journal|vauthors=Gold DR, Wright R|year=2005|title=Population disparities in asthma|journal=Annual Review of Public Health|volume=26|pages=89–113|doi=10.1146/annurev.publhealth.26.021304.144528|pmid=15760282|s2cid=42988748 |doi-access=}}</ref> Over half of cases in children in the United States occur in areas when air quality is below the [[EPA]] standards.<ref>{{cite journal|title=Urban Air Pollution and Health Inequities: A Workshop Report|journal=Environmental Health Perspectives |volume=109 |issue=s3 |year=2001 |pages=357–374 |issn=0091-6765 |doi=10.2307/3434783|doi-access=free |jstor=3434783 |pmc=1240553 |pmid=11427385 |author1=American Lung Association }}</ref> Low air quality is more common in [[Socioeconomic status|low-income]] and minority communities.<ref>{{cite journal| vauthors = Brooks N, Sethi R |date=February 1997|title=The Distribution of Pollution: Community Characteristics and Exposure to Air Toxics|journal=Journal of Environmental Economics and Management|volume=32|issue=2|pages=233–50|doi=10.1006/jeem.1996.0967|doi-access=free|bibcode=1997JEEM...32..233B }}</ref>

Exposure to indoor [[volatile organic compounds]] may be a trigger for asthma; [[formaldehyde]] exposure, for example, has a positive association.<ref name="pmid20064771">{{cite journal|vauthors=McGwin G, Lienert J, Kennedy JI|date=March 2010|title=Formaldehyde exposure and asthma in children: a systematic review|journal=Environmental Health Perspectives|volume=118|issue=3|pages=313–7|doi=10.1289/ehp.0901143|pmc=2854756|pmid=20064771|bibcode=2010EnvHP.118..313M }}</ref> [[Phthalate]]s in certain types of [[PVC]] are associated with asthma in both children and adults.<ref>{{cite journal|vauthors=Jaakkola JJ, Knight TL|date=July 2008|title=The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis|journal=Environmental Health Perspectives|volume=116|issue=7|pages=845–53|doi=10.1289/ehp.10846|pmc=2453150|pmid=18629304|bibcode=2008EnvHP.116..845J }}</ref><ref name="pmid20059582">{{cite journal|vauthors=Bornehag CG, Nanberg E|date=April 2010|title=Phthalate exposure and asthma in children|journal=International Journal of Andrology|volume=33|issue=2|pages=333–45|doi=10.1111/j.1365-2605.2009.01023.x|pmid=20059582|doi-access=free}}</ref> While exposure to [[pesticide]]s is linked to the development of asthma, a cause and effect relationship has yet to be established.<ref name="MamJune2015">{{cite journal|vauthors=Mamane A, Baldi I, Tessier JF, Raherison C, Bouvier G|date=June 2015|title=Occupational exposure to pesticides and respiratory health|journal=European Respiratory Review|volume=24|issue=136|pages=306–19|doi=10.1183/16000617.00006014|pmid=26028642|pmc=9487813 |doi-access=free}}</ref><ref name="MamSept2015">{{cite journal|vauthors=Mamane A, Raherison C, Tessier JF, Baldi I, Bouvier G|date=September 2015|title=Environmental exposure to pesticides and respiratory health|journal=European Respiratory Review|volume=24|issue=137|pages=462–73|doi=10.1183/16000617.00006114|pmid=26324808|pmc=9487696 |doi-access=free}}</ref> A [[meta-analysis]] concluded gas stoves are a major risk factor for asthma, finding around one in eight cases in the U.S. could be attributed to these.<ref>{{cite journal | vauthors = Gruenwald T, Seals BA, Knibbs LD, Hosgood HD | title = Population Attributable Fraction of Gas Stoves and Childhood Asthma in the United States | journal = International Journal of Environmental Research and Public Health | volume = 20 | issue = 1 | pages = 75 | date = December 2022 | pmid = 36612391 | pmc = 9819315 | doi = 10.3390/ijerph20010075 | doi-access = free }}</ref>

====Pregnancy====
The evidence does not support a causal role between [[paracetamol]] (acetaminophen) or antibiotic use and asthma.<ref>{{cite journal | vauthors = Heintze K, Petersen KU | title = The case of drug causation of childhood asthma: antibiotics and paracetamol | journal = European Journal of Clinical Pharmacology | volume = 69 | issue = 6 | pages = 1197–209 | date = June 2013 | pmid = 23292157 | pmc = 3651816 | doi = 10.1007/s00228-012-1463-7 }}</ref><ref>{{cite journal | vauthors = Henderson AJ, Shaheen SO | title = Acetaminophen and asthma | journal = Paediatric Respiratory Reviews | volume = 14 | issue = 1 | pages = 9–15; quiz 16 | date = March 2013 | pmid = 23347656 | doi = 10.1016/j.prrv.2012.04.004 }}</ref> A 2014 systematic review found that the association between paracetamol use and asthma disappeared when respiratory infections were taken into account.<ref>{{cite journal | vauthors = Cheelo M, Lodge CJ, Dharmage SC, Simpson JA, Matheson M, Heinrich J, Lowe AJ | title = Paracetamol exposure in pregnancy and early childhood and development of childhood asthma: a systematic review and meta-analysis | journal = Archives of Disease in Childhood | volume = 100 | issue = 1 | pages = 81–9 | date = January 2015 | pmid = 25429049 | doi = 10.1136/archdischild-2012-303043 | s2cid = 13520462 | url = https://epub.ub.uni-muenchen.de/37262/ }}</ref> Maternal [[psychological stress]] during pregnancy is a risk factor for the child to develop asthma.<ref>{{cite journal | vauthors = van de Loo KF, van Gelder MM, Roukema J, Roeleveld N, Merkus PJ, Verhaak CM | title = Prenatal maternal psychological stress and childhood asthma and wheezing: a meta-analysis | journal = The European Respiratory Journal | volume = 47 | issue = 1 | pages = 133–46 | date = January 2016 | pmid = 26541526 | doi = 10.1183/13993003.00299-2015 | doi-access = free }}</ref>

====Allergens====
Asthma is associated with exposure to indoor allergens.<ref name="pmid21301330">{{cite journal | vauthors = Ahluwalia SK, Matsui EC | title = The indoor environment and its effects on childhood asthma | journal = Current Opinion in Allergy and Clinical Immunology | volume = 11 | issue = 2 | pages = 137–43 | date = April 2011 | pmid = 21301330 | doi = 10.1097/ACI.0b013e3283445921 | s2cid = 35075329 }}</ref> Common indoor allergens include [[dust mite]]s, [[cockroach]]es, [[animal dander]] (fragments of fur or feathers), and mould.<ref name=Arshad>{{cite journal | vauthors = Arshad SH | s2cid = 30418306 | title = Does exposure to indoor allergens contribute to the development of asthma and allergy? | journal = Current Allergy and Asthma Reports | volume = 10 | issue = 1 | pages = 49–55 | date = January 2010 | pmid = 20425514 | doi = 10.1007/s11882-009-0082-6 }}</ref><ref>{{cite journal | vauthors = Custovic A, Simpson A | title = The role of inhalant allergens in allergic airways disease | journal = Journal of Investigational Allergology & Clinical Immunology | volume = 22 | issue = 6 | pages = 393–401; qiuz follow 401 |year=2012 | pmid = 23101182 }}</ref> Efforts to decrease dust mites have been found to be ineffective on symptoms in sensitized subjects.<ref name=Gotzsche2008/><ref>{{cite journal | vauthors = Calderón MA, Linneberg A, Kleine-Tebbe J, De Blay F, Hernandez Fernandez de Rojas D, Virchow JC, Demoly P | title = Respiratory allergy caused by house dust mites: What do we really know? | journal = The Journal of Allergy and Clinical Immunology | volume = 136 | issue = 1 | pages = 38–48 | date = July 2015 | pmid = 25457152 | doi = 10.1016/j.jaci.2014.10.012 | doi-access = free }}</ref> Weak evidence suggests that efforts to decrease mould by repairing buildings may help improve asthma symptoms in adults.<ref>{{cite journal | vauthors = Sauni R, Verbeek JH, Uitti J, Jauhiainen M, Kreiss K, Sigsgaard T | title = Remediating buildings damaged by dampness and mould for preventing or reducing respiratory tract symptoms, infections and asthma | journal = The Cochrane Database of Systematic Reviews | volume = 2015 | issue = 2 | pages = CD007897 | date = February 2015 | pmid = 25715323 | pmc = 6769180 | doi = 10.1002/14651858.CD007897.pub3 }}</ref> Certain viral respiratory infections, such as [[respiratory syncytial virus]] and [[rhinovirus]],<ref name=M38/> may increase the risk of developing asthma when acquired as young children.<ref name=NHLBI07p11>{{harvnb|NHLBI Guideline|2007|p=11}}</ref> Certain other infections, however, may decrease the risk.<ref name=M38/>

====Hygiene hypothesis====
The [[hygiene hypothesis]] attempts to explain the increased rates of asthma worldwide as a direct and unintended result of reduced exposure, during childhood, to non-pathogenic bacteria and viruses.<ref>{{cite journal | vauthors = Ramsey CD, Celedón JC | title = The hygiene hypothesis and asthma | journal = Current Opinion in Pulmonary Medicine | volume = 11 | issue = 1 | pages = 14–20 | date = January 2005 | pmid = 15591883 | doi = 10.1097/01.mcp.0000145791.13714.ae | s2cid = 44556390 }}</ref><ref>{{cite journal | vauthors = Bufford JD, Gern JE | title = The hygiene hypothesis revisited | journal = Immunology and Allergy Clinics of North America | volume = 25 | issue = 2 | pages = 247–62, v–vi | date = May 2005 | pmid = 15878454 | doi = 10.1016/j.iac.2005.03.005 }}</ref> It has been proposed that the reduced exposure to bacteria and viruses is due, in part, to increased cleanliness and decreased family size in modern societies.<ref name=Brook2013>{{cite journal | vauthors = Brooks C, Pearce N, Douwes J | title = The hygiene hypothesis in allergy and asthma: an update | journal = Current Opinion in Allergy and Clinical Immunology | volume = 13 | issue = 1 | pages = 70–7 | date = February 2013 | pmid = 23103806 | doi = 10.1097/ACI.0b013e32835ad0d2 | s2cid = 23664343 }}</ref> Exposure to bacterial [[endotoxin]] in early childhood may prevent the development of asthma, but exposure at an older age may provoke bronchoconstriction.<ref>{{cite journal | vauthors = Rao D, Phipatanakul W | title = Impact of environmental controls on childhood asthma | journal = Current Allergy and Asthma Reports | volume = 11 | issue = 5 | pages = 414–20 | date = October 2011 | pmid = 21710109 | pmc = 3166452 | doi = 10.1007/s11882-011-0206-7 }}</ref> Evidence supporting the hygiene hypothesis includes lower rates of asthma on farms and in households with pets.<ref name=Brook2013/>

Use of [[antibiotic]]s in early life has been linked to the development of asthma.<ref>{{cite journal | vauthors = Murk W, Risnes KR, Bracken MB | title = Prenatal or early-life exposure to antibiotics and risk of childhood asthma: a systematic review | journal = Pediatrics | volume = 127 | issue = 6 | pages = 1125–38 | date = June 2011 | pmid = 21606151 | doi = 10.1542/peds.2010-2092 | s2cid = 26098640 }}</ref> Also, delivery via [[caesarean section]] is associated with an increased risk (estimated at 20–80%) of asthma&nbsp;– this increased risk is attributed to the lack of healthy bacterial colonization that the newborn would have acquired from passage through the birth canal.<ref>{{harvnb|British Guideline|2009|p=72}}</ref><ref name="pmid21645799">{{cite journal | vauthors = Neu J, Rushing J | title = Cesarean versus vaginal delivery: long-term infant outcomes and the hygiene hypothesis | journal = Clinics in Perinatology | volume = 38 | issue = 2 | pages = 321–31 | date = June 2011 | pmid = 21645799 | pmc = 3110651 | doi = 10.1016/j.clp.2011.03.008 }}</ref> There is a link between asthma and the degree of affluence which may be related to the hygiene hypothesis as less affluent individuals often have more exposure to bacteria and viruses.<ref name="pmid14763924">{{cite journal | vauthors = Von Hertzen LC, Haahtela T | title = Asthma and atopy – the price of affluence? | journal = Allergy | volume = 59 | issue = 2 | pages = 124–37 | date = February 2004 | pmid = 14763924 | doi = 10.1046/j.1398-9995.2003.00433.x | s2cid = 34049674 | doi-access = free }}</ref>

===Genetic===
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
|+ CD14-endotoxin interaction based on CD14 SNP C-159T<ref name=Martinez_CD14 />
|-
! Endotoxin levels !! CC genotype !! TT genotype
|-
! High exposure
| Low risk || High risk
|-
! Low exposure
|High risk || Low risk
|}

Family history is a risk factor for asthma, with many different genes being implicated.<ref name=El2010>{{cite book| vauthors = Elward G, Douglas KS |title=Asthma|year=2010|publisher=Manson Pub.|location=London|isbn=978-1-84076-513-7|pages=27–29|url=https://books.google.com/books?id=gS4BsugTBvoC&pg=PA27|url-status=live|archive-url=https://web.archive.org/web/20160517002458/https://books.google.com/books?id=gS4BsugTBvoC&pg=PA27|archive-date=May 17, 2016}}</ref> If one identical twin is affected, the probability of the other having the disease is approximately 25%.<ref name=El2010/> By the end of 2005, 25 genes had been associated with asthma in six or more separate populations, including [[Glutathione S-transferase Mu 1|GSTM1]], [[Interleukin 10|IL10]], [[CTLA-4]], [[SPINK5]], [[Leukotriene C4 synthase|LTC4S]], [[Interleukin-4 receptor|IL4R]] and [[ADAM33]], among others.<ref name=Hoffjan/> Many of these genes are related to the immune system or modulating inflammation. Even among this list of genes supported by highly replicated studies, results have not been consistent among all populations tested.<ref name=Hoffjan /> In 2006 over 100 [[gene]]s were associated with asthma in one [[genetic association]] study alone;<ref name=Hoffjan>{{cite journal | vauthors = Ober C, Hoffjan S | title = Asthma genetics 2006: the long and winding road to gene discovery | journal = Genes and Immunity | volume = 7 | issue = 2 | pages = 95–100 | date = March 2006 | pmid = 16395390 | doi = 10.1038/sj.gene.6364284 | s2cid = 1887559 | doi-access =  }}</ref> more continue to be found.<ref name="pmid20298365">{{cite journal | vauthors = Halapi E, Bjornsdottir US | title = Overview on the current status of asthma genetics | journal = The Clinical Respiratory Journal | volume = 3 | issue = 1 | pages = 2–7 | date = January 2009 | pmid = 20298365 | doi = 10.1111/j.1752-699X.2008.00119.x | s2cid = 36471997 | doi-access =  }}</ref>

Some genetic variants may only cause asthma when they are combined with specific environmental exposures.<ref name=Martinez2007/> An example is a specific [[single nucleotide polymorphism]] in the [[CD14]] region and exposure to [[endotoxin]] (a bacterial product). Endotoxin exposure can come from several environmental sources including tobacco smoke, dogs, and farms. Risk for asthma, then, is determined by both a person's genetics and the level of endotoxin exposure.<ref name=Martinez_CD14>{{cite journal | vauthors = Martinez FD | title = CD14, endotoxin, and asthma risk: actions and interactions | journal = Proceedings of the American Thoracic Society | volume = 4 | issue = 3 | pages = 221–5 | date = July 2007 | pmid = 17607003 | pmc = 2647622 | doi = 10.1513/pats.200702-035AW }}</ref>

===Medical conditions===
A triad of [[atopic eczema]], [[allergic rhinitis]] and asthma is called atopy.<ref name="Bolognia" /> The strongest risk factor for developing asthma is a history of [[atopy|atopic disease]];<ref name=NHLBI07p11/> with asthma occurring at a much greater rate in those who have either [[eczema]] or [[Rhinitis|hay fever]].<ref name="GINA2011_p4">{{harvnb|GINA|2011|p=4}}</ref> Asthma has been associated with [[eosinophilic granulomatosis with polyangiitis]] (formerly known as Churg–Strauss syndrome), an autoimmune disease and [[vasculitis]].<ref name="ChapelHill">{{cite journal | vauthors = Jennette JC, Falk RJ, Bacon PA, Basu N, Cid MC, Ferrario F, Flores-Suarez LF, Gross WL, Guillevin L, Hagen EC, Hoffman GS, Jayne DR, Kallenberg CG, Lamprecht P, Langford CA, Luqmani RA, Mahr AD, Matteson EL, Merkel PA, Ozen S, Pusey CD, Rasmussen N, Rees AJ, Scott DG, Specks U, Stone JH, Takahashi K, Watts RA | display-authors = 6 | title = 2012 revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides | journal = Arthritis and Rheumatism | volume = 65 | issue = 1 | pages = 1–11 | date = January 2013 | pmid = 23045170 | doi = 10.1002/art.37715 | doi-access = free }}</ref> Individuals with certain types of [[urticaria]] may also experience symptoms of asthma.<ref name="Bolognia">{{cite book | vauthors = Rapini RP, Bolognia JL, Jorizzo JL |title=Dermatology: 2-Volume Set |publisher=Mosby |location=St. Louis |year=2007 |isbn=978-1-4160-2999-1 }}</ref>

There is a correlation between [[obesity]] and the risk of asthma with both having increased in recent years.<ref>{{cite journal | vauthors = Beuther DA | title = Recent insight into obesity and asthma | journal = Current Opinion in Pulmonary Medicine | volume = 16 | issue = 1 | pages = 64–70 | date = January 2010 | pmid = 19844182 | doi = 10.1097/MCP.0b013e3283338fa7 | s2cid = 34157182 }}</ref><ref name=holguin>{{cite journal | vauthors = Holguin F, Fitzpatrick A | title = Obesity, asthma, and oxidative stress | journal = Journal of Applied Physiology | volume = 108 | issue = 3 | pages = 754–9 | date = March 2010 | pmid = 19926826 | doi = 10.1152/japplphysiol.00702.2009 }}</ref> Several factors may be at play including decreased respiratory function due to a buildup of fat and the fact that adipose tissue leads to a pro-inflammatory state.<ref name="Woods 2009">{{cite journal | vauthors = Wood LG, Gibson PG | title = Dietary factors lead to innate immune activation in asthma | journal = Pharmacology & Therapeutics | volume = 123 | issue = 1 | pages = 37–53 | date = July 2009 | pmid = 19375453 | doi = 10.1016/j.pharmthera.2009.03.015 }}</ref>

[[Beta blocker]] medications such as [[propranolol]] can trigger asthma in those who are susceptible.<ref name="pmid17998992">{{cite journal | vauthors = O'Rourke ST | title = Antianginal actions of beta-adrenoceptor antagonists | journal = American Journal of Pharmaceutical Education | volume = 71 | issue = 5 | pages = 95 | date = October 2007 | pmid = 17998992 | pmc = 2064893 | doi = 10.5688/aj710595 }}</ref> [[Cardioselective beta-blockers]], however, appear safe in those with mild or moderate disease.<ref>{{cite journal | vauthors = Salpeter S, Ormiston T, Salpeter E | title = Cardioselective beta-blockers for reversible airway disease | journal = The Cochrane Database of Systematic Reviews | issue = 4 | pages = CD002992 |year = 2002 | volume = 2011 | pmid = 12519582 | doi = 10.1002/14651858.CD002992 | pmc = 8689715 }}</ref><ref>{{cite journal | vauthors = Morales DR, Jackson C, Lipworth BJ, Donnan PT, Guthrie B | title = Adverse respiratory effect of acute β-blocker exposure in asthma: a systematic review and meta-analysis of randomized controlled trials | journal = Chest | volume = 145 | issue = 4 | pages = 779–786 | date = April 2014 | pmid = 24202435 | doi = 10.1378/chest.13-1235 }}</ref> Other medications that can cause problems in asthmatics are [[angiotensin-converting enzyme inhibitors]], [[Acetylsalicylic acid|aspirin]], and [[NSAIDs]].<ref name="pmid15579370">{{cite journal | vauthors = Covar RA, Macomber BA, Szefler SJ | title = Medications as asthma triggers | journal = Immunology and Allergy Clinics of North America | volume = 25 | issue = 1 | pages = 169–90 | date = February 2005 | pmid = 15579370 | doi = 10.1016/j.iac.2004.09.009 }}</ref> Use of acid-suppressing medication ([[proton pump inhibitors]] and [[H2 blockers]]) during pregnancy is associated with an increased risk of asthma in the child.<ref>{{cite journal | vauthors = Lai T, Wu M, Liu J, Luo M, He L, Wang X, Wu B, Ying S, Chen Z, Li W, Shen H | display-authors = 6 | title = Acid-Suppressive Drug Use During Pregnancy and the Risk of Childhood Asthma: A Meta-analysis | journal = Pediatrics | volume = 141 | issue = 2 | pages = e20170889 | date = February 2018 | pmid = 29326337 | doi = 10.1542/peds.2017-0889 | doi-access = free }}</ref>

===Exacerbation===
Some individuals will have stable asthma for weeks or months and then suddenly develop an episode of acute asthma. Different individuals react to various factors in different ways.<ref name=Baxi2010>{{cite journal | vauthors = Baxi SN, Phipatanakul W | title = The role of allergen exposure and avoidance in asthma | journal = Adolescent Medicine | volume = 21 | issue = 1 | pages = 57–71, viii–ix | date = April 2010 | pmid = 20568555 | pmc = 2975603 }}</ref> Most individuals can develop severe exacerbation from a number of triggering agents.<ref name=Baxi2010/>

Home factors that can lead to exacerbation of asthma include [[dust]], animal [[dander]] (especially cat and dog hair), cockroach [[allergen]]s and [[Mold (fungus)|mold]].<ref name=Baxi2010/><ref>{{cite journal | vauthors = Sharpe RA, Bearman N, Thornton CR, Husk K, Osborne NJ | title = Indoor fungal diversity and asthma: a meta-analysis and systematic review of risk factors | journal = The Journal of Allergy and Clinical Immunology | volume = 135 | issue = 1 | pages = 110–22 | date = January 2015 | pmid = 25159468 | doi = 10.1016/j.jaci.2014.07.002 | doi-access = free }}</ref> [[Perfume]]s are a common cause of acute attacks in women and children. Both [[virus|viral]] and bacterial [[infection]]s of the upper respiratory tract can worsen the disease.<ref name=Baxi2010/> Psychological [[stress (biological)|stress]] may worsen symptoms&nbsp;– it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.<ref name=Gold/><ref name="Chen2007">{{cite journal | vauthors = Chen E, Miller GE | title = Stress and inflammation in exacerbations of asthma | journal = Brain, Behavior, and Immunity | volume = 21 | issue = 8 | pages = 993–9 | date = November 2007 | pmid = 17493786 | pmc = 2077080 | doi = 10.1016/j.bbi.2007.03.009 }}</ref>

Asthma exacerbations in school-aged children peak in autumn for 8 weeks, shortly after children return to school. This might reflect a combination of factors, including poor treatment adherence, increased allergen and viral exposure, and altered immune tolerance. There is limited evidence to guide possible approaches to reducing autumn exacerbations, but while costly, seasonal [[omalizumab]] treatment from four to six weeks before school return may reduce autumn asthma exacerbations.<ref name="PikeAkhbari2018">{{cite journal | vauthors = Pike KC, Akhbari M, Kneale D, Harris KM | title = Interventions for autumn exacerbations of asthma in children | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | issue = 3 | pages = CD012393 | date = March 2018 | pmid = 29518252 | pmc = 6494188 | doi = 10.1002/14651858.CD012393.pub2 }}</ref>