Asthma
During an asthma attack, the airways become swollen and full of mucus.
Pronunciation	UK: /ˈæsmə, ˈæsθmə/ US: /ˈæzmə/
Specialty	Pulmonology
Symptoms	Recurring episodes of wheezing, coughing, chest tightness, shortness of breath
Complications	Gastroesophageal reflux disease (GERD), sinusitis, obstructive sleep apnea
Usual onset	Childhood
Duration	Long term
Causes	Genetic and environmental factors[1]
Risk factors	Air pollution, allergens[2]
Diagnostic method	Based on symptoms, response to therapy, spirometry[3]
Treatment	Avoiding triggers,[4]: 42–44  inhaled corticosteroids,[4]: 53–61  salbutamol[4]: 24–28
Frequency	Approximately 262 million (2019)[5]
Deaths	Approximately 461,000 (2019)[5]

Asthma is a common long-term inflammatory disease of the airways. It is characterized by variable and recurring symptoms and reduced lung function. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. A sudden worsening of asthma symptoms sometimes called an 'asthma attack' or an 'asthma exacerbation' can occur when allergens, pollen, dust, or other particles, are inhaled into the lungs, causing the bronchioles to constrict and produce mucus, which then restricts oxygen flow to the alveoli. These may occur a few times a day or a few times per week.^[2] Depending on the person, asthma symptoms may become worse at night or with exercise.^[2]

Asthma is thought to be caused by a combination of genetic and environmental factors.^[1] Environmental factors include exposure to air pollution and allergens.^[2] Other potential triggers include medications such as aspirin and beta blockers.^[2] Diagnosis is usually based on the pattern of symptoms, response to therapy over time, and spirometry lung function testing.^[3] Asthma is classified according to the amount of medication required to control symptoms or mechanisms underlying the condition.

There is no known cure for asthma, but it can be controlled.^[2] Symptoms can be prevented by avoiding triggers, such as allergens and respiratory irritants, and suppressed with the use of inhaled corticosteroids.^{[6]: 169–172 [7]: 57, 72–73} Long-acting beta agonists (LABA) or antileukotriene agents may be used in addition to inhaled corticosteroids if asthma symptoms remain uncontrolled.^{[7]: 77–78, 90 [8]} Treatment of rapidly worsening symptoms is usually with an inhaled short-acting beta₂ agonist such as salbutamol and corticosteroids taken by mouth.^[6]: 214 In very severe cases, intravenous corticosteroids, magnesium sulfate, and hospitalization may be required.^{[6]: 373–375}

In 2019, asthma affected approximately 262 million people and caused approximately 461,000 deaths.^[5] Most of the deaths occurred in the developing world.^[2] Asthma often begins in childhood,^[2] and the rates have increased significantly since the 1960s.^[9] Asthma was recognized as early as Ancient Egypt.^[10] The word asthma is from the Greek ἆσθμα (âsthma), which means 'panting'.^[11]

Wheezing

The sound of wheezing as heard with a stethoscope

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Asthma is characterized by recurrent episodes symptoms of wheezing, shortness of breath, chest tightness, and coughing.^[12] Symptoms are usually worse at night and in the early morning or in response to exercise or cold air.^[13]: 8 Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may react frequently and readily and experience persistent symptoms.^{[7]: 22–24}

A number of other health conditions occur more frequently in people with asthma, including gastroesophageal reflux disease (GERD), rhinosinusitis, and obstructive sleep apnea.^[14] Psychological disorders are also more common,^[15] with anxiety disorders occurring in between 16 and 52% and mood disorders in 14–41%.^[16] It is not known whether asthma causes psychological problems or psychological problems lead to asthma.^[17] Current asthma, but not former asthma, is associated with increased all-cause mortality, heart disease mortality, and chronic lower respiratory tract disease mortality.^[18] Asthma, particularly severe asthma, is strongly associated with development of chronic obstructive pulmonary disease (COPD) as found in Asthma-COPD Overlap.^[19][20][21] Those with asthma, especially if it is poorly controlled, are at increased risk for radiocontrast reactions.^[22]

Due to the diversity in onset, symptoms, outcomes, and response to treatment, asthma is often considered a syndrome — a collection of signs and symptoms — rather than one single condition.^[23][24] Historically asthma was classified as caused by external factors such as allergens (extrinsic) or by internal factors, unrelated to allergies (intrinsic).^[24] Currently asthma is most commonly classified according to severity, control of symptoms, phenotypes and endotypes.^[24][25]

Although asthma is a chronic obstructive condition, it is not considered as a part of chronic obstructive pulmonary disease, as this term refers specifically to combinations of disease that are irreversible such as bronchiectasis and emphysema.^[26] Unlike these diseases, the airway obstruction in asthma is usually reversible; however, if left untreated, the chronic inflammation from asthma can lead the lungs to become irreversibly obstructed due to airway remodelling.^[27] In contrast to emphysema, asthma affects the bronchi, not the alveoli.^[28] The combination of asthma with a component of irreversible airway obstruction has been termed the asthma-chronic obstructive disease (COPD) overlap syndrome (ACOS). Compared to other people with "pure" asthma or COPD, people with ACOS exhibit increased morbidity, mortality, and possibly more comorbidities.^[29]

An asthma exacerbation, commonly referred to as an asthma attack, are episodes of increased symptoms (shortness of breath, wheezing, coughing, chest tightness), and decreased lung function.^[7]: 160

Signs occurring during an asthma attack include the use of accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck), there may be a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest.^[30] A blue colour of the skin and nails may occur from lack of oxygen.^[31]

The level of peak expiratory flow rate (PEFR) is determined as follows:

• A mild exacerbation is ≥200 L/min, or ≥50% of the predicted best.^[32]
• Moderate is defined as between 80 and 200 L/min, or 25% and 50% of the predicted best.
• Severe is defined as ≤ 80 L/min, or ≤25% of the predicted best.^[32]

Acute severe asthma, previously known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators and corticosteroids.^[33] Half of cases are due to infections with others caused by allergen, air pollution, or insufficient or inappropriate medication use.^[33]

Brittle asthma is a kind of asthma distinguishable by recurrent, severe attacks. However brittle asthma is best regarded as a historical disease descriptor rather than a distinct diagnostic category. While it remains useful for understanding older literature it is no longer routinely used in contemporary clinical practice.^[34]

A phenotype is the way in which a condition presents itself, such as when the disease first starts to affect a person and what symptoms an individual displays. An endotype is the mechanisms that underlie the condition.^[35] Asthma is most commonly divided into two endotypes, T2-high and T2-low (non-T2). Within the two main endotypes there are subpopulations (phenotypes), some of which overlap or can be categorized under both of the two endotypes.^[23]

The two endotypes are distinguished based on the type of inflammation present, with the type-2 high endotype involving the type 2 immune system response and type-2 low involving type 1 immune system response. Type-2 high is characterized by increased eosinophils, increased Fractional exhaled nitric oxide (FeNO), or allergens. Type-2 low asthma is the absence of these inflammatory markers and the mechanisms are not well researched. The phenotypes included under the type-2 high endotype include early-onset allergic asthma, late-onset eosinophilic asthma, and Aspirin-exacerbated respiratory disease. Type-2 low asthma phenotypes include asthma associated with obesity, neutrophilic asthma, asthma associated with cigarette smoke, and paucigranulocytic asthma.^[35] Occupational asthma can be further split into separate phenotypes, irritant-induced asthma — caused by exposure to airway irritants such as cleaning products and dust — and sensitizer-induced occupational asthma — developed hypersensitivity. Irritant-induced asthma is a type-2 low phenotype while sensitizer-induced occupational asthma is a type-2 high phenotype.^[23][35] Asthma-COPD overlap (ACO) currently lacks a consistent definition making it hard to categorize it into either endotype.^[23]

Exercise can trigger bronchoconstriction both in people with and without asthma.^[36] It occurs in most people with asthma and up to 20% of people without asthma.^[36] Exercise-induced bronchoconstriction is common in professional athletes. The highest rates are among cyclists (up to 45%), swimmers, and cross-country skiers.^[37] Asthma symptoms may occur under a wide range of weather conditions but are more frequently triggered by changes in weather.^[7]: 24 Inhaled beta₂ agonists do not appear to improve athletic performance among those without asthma;^[38] however, oral doses may improve endurance and strength.^[39][40]

Alcohol may worsen asthmatic symptoms in up to a third of people.^[41] This may be even more common in some ethnic groups, such as the Japanese and those with aspirin-exacerbated respiratory disease.^[41] Other studies have found improvement in asthmatic symptoms from alcohol.^[41]

Infectious asthma is an easily identified clinical presentation.^[42] When queried, asthma patients may report that their first asthma symptoms began after an acute lower respiratory tract illness. This type of history has been labelled the "infectious asthma" (IA) syndrome,^[43] or as "asthma associated with infection" (AAWI)^[44] to distinguish infection-associated asthma initiation from the well known association of respiratory infections with asthma exacerbations. Reported clinical prevalences of IA for adults range from around 40% in a primary care practice^[43] to 70% in a specialty practice treating mainly severe asthma patients.^[45]

Asthma is caused by a mixture of genetic and external factors. The disease manifests when those with a genetic susceptibility to asthma are exposed to specific environmental factors.^[46] Environmental factors can also trigger asthma symptoms.^[47]

Factors during pregnancy that have been linked to the development of asthma include weight gain or obesity in the mother, stressful pregnancy, smoking while pregnant, the use of certain medications while pregnant and caesarean section. Early childhood exposure to secondhand smoke, high levels of stress in parents, respiratory infections, and indoor mold or fungi have also been associated with asthma development.^[48]

Respiratory tract infections, especially during early childhood or if they are severe and recurring can lead to decreased lung function and subsequent asthma.^[47][49] Conversely, there has been research suggesting that certain infections during childhood may lessen the risk of developing asthma. This theory is known as the “hygiene hypothesis”.^[47]

Prenatal or childhood exposure to cigarette smoke increases the likelihood of a child developing asthma. Children whose maternal grandmother smoked during pregnancy are also more likely to develop asthma, regardless of if their mothers developed asthma or smoked. Nicotine is believed to be the cause of these effects and nicotine is linked to changes in DNA.^[49]

Chronic exposure to air pollution increases the risk of developing asthma. Outdoor air pollution includes nitrogen dioxide and traffic pollution while indoor air pollution includes biomass, pesticides, building materials such as asbestos and formaldehyde, mold, dust mites, cockroaches, and endotoxins.^[49][47]

Asthma is more commonly seen in urban environments than in rural environments. This is believed to be due to the higher presence of certain risk factors for asthma such as traffic pollution, secondhand smoke, social inequality, and industrialization in urban settings as well as protective factors such as less air pollution, exposure to allergens and bacteria and higher levels of physical activity associated with rural environments.^[48]

In those who are affected by allergies, exposure to allergens can trigger asthma symptoms. ^[49] However, some research has suggested that early exposure to allergens in childhood may help desensitize individuals from allergies. Other studies have shown that early exposure may increase risk of allergies and the development of allergies is multifactorial. Allergens also play a role in the development of adult-onset asthma.^[48]

Adult-onset asthma is caused by relations between genetics, lifestyle factors such as obesity and smoking, and environmental factors such as an urban or rural environment, occupational exposures, and air pollution.^[48] Unlike childhood asthma, which is more prevalent in males, in adults asthma is more prevalent in females.^[47] Over 400 occupational exposure have been linked to asthma. Exposure to asthmagens, allergens and substances that are known to cause asthma; the amount and length of time that an individual was exposed to the substance; genetics; allergies; and smoking can affect the development of occupational asthma.^[49]

Asthma is highly polygenic, with hundreds of common and rare genetic variants of small effect contributing to disease susceptibility, age of onset, and inflammatory phenotypes.^[50][51][52] Twin studies and family studies support a substantial heritable component, with estimates that roughly half or more of asthma susceptibility is explained by genetics^[52] that is further modulated by environmental and epigenetic factors.^[53] Large genome-wide association studies (GWAS) and sequencing efforts indicate that risk reflects the cumulative effects of numerous common genetic variants together with a more limited contribution from rare variants, rather than a small number of loci of large effect.^[50][51][54]

Meta-analyses now report over 200 genome-wide significant susceptibility loci, many mapping to immune and epithelial genes and explaining a measurable, though still incomplete, fraction of heritability. Pathway analyses consistently highlight type 2 inflammation, epithelial barrier function, and both innate and adaptive immune signalling, including loci near or within IL33, IL1RL1/IL18R1, TSLP, MHC class II, and GATA3.^[50][51] The chromosome region 17q12–21 remains the most robustly replicated asthma locus, with effects strongest for childhood-onset disease.^[55] Multiple genes in this region, including ORMDL3 and GSDMB, appear to act primarily through regulatory mechanisms, with gene-environment interactions and age-dependent effects on airway epithelial responses, particularly to early-life viral infections.^[56][57][51]

Genetic correlation analyses demonstrate substantial overlap between asthma and other atopic disorders such as eczema and allergic rhinitis, as well as with lung function traits. Multi-trait studies identify shared risk genes across asthma, hay fever, and eczema, supporting partially common pathways involving type 2 immunity and epithelial barrier dysfunction.^[51][54][58] Consistent with this architecture, polygenic risk scores (PRS) derived from multi-ancestry GWAS can stratify individuals by asthma risk, with higher predictive performance for childhood-onset than adult-onset disease. Individuals in the highest PRS percentiles show several-fold increased odds of childhood asthma, and PRS analyses have helped delineate heterogeneity across asthma–COPD overlap and related comorbid traits, although clinical implementation remains investigational.^{[56][59][60][61]}

Many asthma-associated variants act within regulatory elements, with effects that are highly cell-type specific and modulated by environmental exposures such as allergens, air pollution, and respiratory infections. Integrative genomic and epigenomic studies show enrichment of risk alleles in enhancers active in airway epithelial and immune cells, and indicate that DNA methylation and other epigenetic modifications mediate part of the gene-environment interaction underlying asthma susceptibility and phenotypic heterogeneity.^[51][56]

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.^[62] Most individuals can develop severe exacerbation from a number of triggering agents.^[62]

Home factors that can lead to exacerbation of asthma include dust, animal dander (especially cat and dog hair), cockroach allergens and mold.^[62][63] Perfumes are a common cause of acute attacks in women and children. Both viral and bacterial infections of the upper respiratory tract can worsen the disease.^[62] Psychological stress may worsen symptoms – it is thought that stress alters the immune system and thus increases the airway inflammatory response to allergens and irritants.^[64][65]

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.^[66]

Asthma is the result of chronic inflammation of the conducting zone of the airways (most especially the bronchi and bronchioles), which subsequently results in increased contractability of the surrounding smooth muscles.^{[7]: 22, 24–25} This among other factors leads to bouts of narrowing of the airway and the classic symptoms of wheezing. The narrowing is typically reversible with or without treatment. Occasionally, the airways themselves change.^{[7]: 22–25} Typical changes in the airways include an increase in eosinophils and thickening of the lamina reticularis.^[11] Chronically, the airways' smooth muscle may increase in size along with an increase in the number of mucous glands.^[11] Other cell types involved include T lymphocytes, macrophages, and neutrophils. There may also be involvement of other components of the immune system, including cytokines, chemokines, histamine, and leukotrienes among others.^[11]

Asthma is defined by the Global Initiative for Asthma as:^[7]: 22

... a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms, such as wheeze, shortness of breath, chest tightness and cough, that vary over time and in intensity, together with variable expiratory airflow. Airflow limitation may later become persistent.

There is currently no precise test for the diagnosis, which is typically based on the pattern of symptoms and response to therapy over time.^[3][11] Asthma may be suspected if there is a history of recurrent wheezing, coughing, or difficulty breathing, and these symptoms occur or worsen due to exercise, viral infections, allergens, or air pollution.^[67] Spirometry is then used to confirm the diagnosis.^[67] In children under the age of six, the diagnosis is more difficult as they are too young for spirometry.^{[7]: 181–184}

Spirometry, which measures the lung function in terms of the amount and speed of air as it is exhaled and inhaled, is recommended to aid in diagnosis and management.^{[68][6]: 64–68 [4]: 18–22} It is the single best test for asthma. If the FEV₁ measured by this technique improves more than 12% and increases by at least 200 millilitres following administration of a bronchodilator such as salbutamol, this is supportive of the diagnosis. It however may be normal in those with a history of mild asthma, not currently acting up.^[11] As caffeine is a bronchodilator in people with asthma, the use of caffeine before a lung function test may interfere with the results.^[69] Single-breath diffusing capacity can help differentiate asthma from COPD.^[11] It is reasonable to perform spirometry every one or two years to follow how well a person's asthma is controlled.^[70]

The methacholine challenge involves the inhalation of increasing concentrations of a substance that causes airway narrowing in those predisposed. If negative, it means that a person does not have asthma; if positive, however, it is not specific for the disease.^[11]

Other supportive evidence includes:^[71]

• A ≥20% difference in peak expiratory flow rate on at least three days in a week for at least two weeks,
• A ≥20% improvement of peak flow following treatment with either salbutamol, inhaled corticosteroids or prednisone, or
• A ≥20% decrease in peak flow following exposure to a trigger.

Testing peak expiratory flow is more variable than spirometry, however, and thus not recommended for routine diagnosis. It may be useful for daily self-monitoring in those with moderate to severe disease and for checking the effectiveness of new medications. It may also be helpful in guiding treatment in those with acute exacerbations.^[72]

Many other conditions can cause symptoms similar to those of asthma. In children, symptoms may be due to other upper airway diseases such as allergic rhinitis and sinusitis, as well as other causes of airway obstruction including foreign body aspiration, tracheal stenosis, laryngotracheomalacia, vascular rings, enlarged lymph nodes or neck masses.^[73] Bronchiolitis and other viral infections may also produce wheezing.^[74] According to European Respiratory Society, it may not be suitable to label wheezing preschool children with the term asthma because there is lack of clinical data on inflammation in airways.^[75] In adults, COPD, congestive heart failure, airway masses, as well as drug-induced coughing due to ACE inhibitors may cause similar symptoms. In both populations vocal cord dysfunction may present similarly.^[73]

Chronic obstructive pulmonary disease can coexist with asthma and can occur as a complication of chronic asthma. After the age of 65, most people with obstructive airway disease will have asthma and COPD. In this setting, COPD can be differentiated by increased airway neutrophils, abnormally increased wall thickness, and increased smooth muscle in the bronchi. However, this level of investigation is not performed due to COPD and asthma sharing similar principles of management: corticosteroids, long-acting beta-agonists, and smoking cessation.^[76] It closely resembles asthma in symptoms, is correlated with more exposure to cigarette smoke, an older age, less symptom reversibility after bronchodilator administration, and decreased likelihood of family history of atopy.^[77][78]

Currently, the only methods of preventing asthma that have been endorsed by clinical guidelines are avoiding the use of broad-spectrum antibiotics in the first year of a child life, eliminating exposure to tobacco smoke both in utero and following birth, appropriate assessment and treatment of vitamin D deficiency during pregnancy, and vaginal birthing when possible.^[7]: 213 Other proposed preventative measures such as dietary changes, breastfeeding, supplements, and early exposure to pets or other common allergens do not currently have enough evidence to support their effectiveness.^{[7]: 209–211}

The goal of asthma management is to reduce symptoms minimize the risk of complication such as exacerbations, reduced lung functioning, and medication side effects.^[7]: 50 This is done by evaluating asthma control and the risk of exacerbation, providing education and guidance on how to manage the disease, finding triggers and ways to minimize them, and medication.^[79][80] Asthma control should be reviewed during doctors appointments so that treatment can be adjusted accordingly.^{[13]: 63 [7]: 52–53}

After a diagnosis of asthma is made the person receiving the diagnosis and their family should receive education about the disease and a plan for management.^[80][79] Education includes information about avoiding triggers, self monitoring of symptoms or peak expiratory flow, an asthma action plan, asthma control and treatment options.^{[13]: 28–30 [7]: 114} Asthma action plans include management options to prevent and treat exacerbations as well as how to modify treatment based on symptoms or seek additional medical care.^{[79][7] : 115} School based education programs on how to manage asthma decrease hospitalizations for asthma in school-aged children.^[7]: 116

Non-medical strategies to manage asthma consist of avoiding exposure to triggers and management of factors that contribute to asthma severity or symptoms.^[12] Exposure to cigarette smoke, from smoking or second-hand smoke, negatively affects asthma control and it is therefore recommended for those with asthma to refrain from smoking and limit exposure to second-hand smoke.^{[79][7]: 59–60} For those with occupational asthma, it is recommended that sensitizers and allergens at work be avoided.^{[7]: 60–61} Due to the variety of potential allergens and the difficulty of eliminating exposure to allergens, current guidelines do not recommend that those with asthma avoid indoor or outdoor allergens.^{[79][7]: 61–64} Certain medications such as Aspirin, beta-blockers, and nonsteroidal anti-inflammatory drugs (NSAIDs) can worsen asthma symptoms in some individuals. It is still considered safe for those with asthma to take these medications, unless they have caused adverse reactions in the past.^[7]: 61

Guidelines encourage those with asthma to maintain a balanced and healthy diet due to benefits on overall wellbeing. Regular physical activity is encouraged for those with asthma due to its positive effects on overall health, however, it does not result in any direct improvement in asthma symptoms and no specific form of exercise is more beneficial. For some, exercise may trigger asthma symptoms and therefore it is recommended that inhalers be used beforehand. Pulmonary rehabilitation may be used to increase tolerance to exercise. Obesity can cause asthma symptoms to be harder to control or cause more severe symptoms, weight loss in obese individuals is therefore recommended.^{[7]: 60, 63}

There is not enough evidence that dietary changes, including restrictive diets or supplements are helpful in managing asthma.^[81] Alternative treatments such as acupuncture, air ionizers, manual therapies (osteopathic, chiropractic, physiotherapeutic and respiratory therapeutic manoeuvres), and breathing exercises are not recommended by clinical guidelines due to a lack of evidence that they are effective.^[82] Breathing exercises do not decrease asthma exacerbations or improve lung functioning, however they can be used alongside medications to help control symptoms.^{[7]: 63–64}

Medications for asthma are generally divided into three categories, controllers — taken daily to control symptoms, reduce exacerbations and decrease inflammation — relievers — taken as needed for severe symptoms or exacerbations — and additional medications added on to manage more severe asthma.^{[80][7]: 69} Medications are prescribed at the lowest dose possible while still treating symptoms and preventing exacerbations.^[79]

Devices for inhaled medications include pressurized metered dose inhaler (pMDI), dry-powder inhalers (DPI), mist inhalers and nebulizers. The choice of delivery method depends on the type of medication used, local availability, age, and ability to use the inhaler properly.^{[7]: 109–111} DPIs are difficult for children to use and are therefore discouraged in those under six years of age. Spacers are used alongside pMDIs to increase the amount of medication inhaled.^[79][80]

The choice of medication used for asthma management depends on symptom control, risk factors, availability, adherence, ability to use the medication, cost and environmental impact.^[7]: 72 It typically takes one or two weeks for symptoms to improve after starting inhaled corticosteroids (ICS) and the response to medication is monitored whenever it is adjusted.^{[79][7]: 73} If asthma symptoms and exacerbations remain well controlled after two or three months, the dosage of medication can be gradually reduced to achieve symptom control at the lowest possible dose of medication.^[7]: 73 If asthma symptoms and exacerbations persist despite two to three months of treatment with ICS factors such as inhaler technique, adherence, exposure to triggers, comorbidities, and alternative diagnoses are assessed before medication dosage is increased.^{[79][7]: 73}

The first line treatment of asthma for children are ICS, for teenagers and adults guidelines recommend a combined ICS and long-acting beta₂ agonist (LABA) inhaler.^[80] After a diagnosis of asthma is confirmed, ICS are started as soon as possible. Guidelines also recommend that everyone diagnosed with asthma have access to a reliever inhaler in case of symptom flare ups.^{[7]: 72 [79]} In children younger than five, higher doses of ICS are used to treat persistent symptoms while older individuals may be treated with an additional medication. Medical guidelines recommend referring people who have persistent symptoms despite adequate treatment to an asthma specialist (usually a respirologist or allergist).^[80]

Historically, asthma was treated with short-acting β2 agonists (SABA) as needed and ICS were only used if symptoms persisted. Due to research suggesting that management with SABA over ICS was insufficient to prevent exacerbations, guidelines now prefer ICS over SABA.^{[12][13]: 20}

For those over the age of twelve, if asthma isn’t well controlled with an ICS/formoterol inhaler then guidelines recommend that medications be taken daily instead of on an as needed basis and gradually increased until symptoms are controlled.^{[13]: 18–19} If higher doses of ICS/formoterol aren’t enough to control symptoms then there are several different medications that may be added in to help manage asthma. These include the leukotriene receptor antagonists (LTRA) montelukast, a mist inhaler containing the LAMA tiotropium, and azithromycin.^{[13]: 19 [7]: 92 [80]} In those with sensitization to aeroallergens, allergen-specific immunotherapy can increase tolerance to allergens by slowly introducing the allergen to an effected person. This is done through two different methods; subcutaneous immunotherapy — injections — and sublingual immunotherapy — under the tongue.^{[80][7]: 104–105} Biologics can be used to reduce inflammation that may play a role in asthma symptoms.^[80] Finally, oral corticosteroids or bronchial thermoplasty may be used as last resorts for severe asthma.^{[7]: 93, 106–107}

In children under the age of five who have comorbid atopic disorders and intermittent asthma symptoms or severe flare-ups a 8-12 week trial of low dose ICS as maintenance treatment and a SABA for flare-ups is recommended by NICE guidelines. If symptoms clear up during the trial then medication can be stopped and symptoms are monitored in the following months to watch for returning symptoms or exacerbation, in which case ICS and SABA can be started again. Persistent symptoms are treated with increasing doses of ICS and an LTRA.^{[13]: 24–25}

Low doses of ICS for maintenance and SABA as needed are used to manage asthma in children ages six to eleven, with ICS used whenever SABA are needed to treat flare-ups. If symptoms persist then the dose of ICS may be gradually increased, a LTRA can be added on top of inhalers or a low-dose ICS-LABA or ICS-formoterol can be used instead of ICS.^{[13]: 22–23 [7]: 97–98}

Treatment of asthma exacerbations involves several doses of bronchodilators, oral corticosteroids, and oxygen supplementation. Salbutamol (albuterol) is commonly used for treating exacerbations with several doses being administered every couple of hours until symptoms lessen. When exacerbations are severe or don’t subside with inhaled medications, oral corticosteroids are used and continued for a week after the exacerbation. Oxygen therapy is also used to maintain a healthy oxygen saturation.^{[7]: 169–170} Ipratropium, a short-acting anticholinergic, can also be used alongside other treatments to manage exacerbations in those experiencing moderate or severe symptoms. Both intravenous magnesium sulfate and helium–oxygen therapy are not recommended by clinical guidelines for the management of exacerbations, however they may be used in those whose symptoms do not react to other first-line treatment options.^{[7]: 175–176, 207}

Staying with a treatment approach for preventing asthma exacerbations can be challenging, especially if the person is required to take medicine or treatments daily.^[83] Reasons for low adherence range from a conscious decision to not follow the suggested medical treatment regime for various reasons including avoiding potential side effects, misinformation, or other beliefs about the medication.^[83] Problems accessing the treatment and problems administering the treatment effectively can also result in lower adherence. Various approaches have been undertaken to try and improve adherence to treatments to help people prevent serious asthma exacerbations, including digital interventions.^[83]

The prognosis for asthma is generally good, especially for children with mild disease.^[84] Mortality has decreased over the last few decades due to better recognition and improvement in care.^[85] In 2010 the death rate was 170 per million for males and 90 per million for females.^[86] Rates vary between countries by 100-fold.^[86]

Globally, it causes moderate or severe disability in 19.4 million people as of 2004 (16 million of which are in low and middle-income countries).^[87] Of asthma diagnosed during childhood, half of the cases will no longer carry the diagnosis after a decade.^[88] Airway remodelling is observed, but it is unknown whether these represent harmful or beneficial changes.^[89] More recent data find that severe asthma can result in airway remodelling and the "asthma with chronic obstructive pulmonary disease syndrome (ACOS)" that has a poor prognosis.^[90] Early treatment with corticosteroids seems to prevent or ameliorate a decline in lung function.^[91] Asthma in children also has negative effects on the quality of life of their parents.^[92]

• 
  Asthma deaths per million persons in 2012

    0–10

    11–13

    14–17

    18–23

    24–32

    33–43

    44–50

    51–66

    67–95

    96–251
• 
  Disability-adjusted life year for asthma per 100,000 inhabitants in 2004^[93]

    no data

    0-100

    100–150

    150–200

    200–250

    250–300

    300–350

    350–400

    400–450

    450–500

    500–550

    550–600

    >600

In 2019, approximately 262 million people worldwide were affected by asthma, and approximately 461,000 people died from the disease.^[5] Rates vary between countries, with prevalences between 1 and 29%.^[7]: 24 It is more common in developed than developing countries.^[7]: 24 One thus sees lower rates in Asia, Eastern Europe, and Africa.^[11] Within developed countries, it is more common in those who are economically disadvantaged, while in contrast, in developing countries, it is more common in the affluent.^[7]: 24 The reasons for these differences are unclear.^[7]: 24 Low- and middle-income countries make up more than 80% of the mortality.^[94]

While asthma is twice as common in boys as girls,^[7]: 24 severe asthma occurs at equal rates.^[95] In contrast adult women have a higher rate of asthma than men^[7]: 24 and it is more common in the young than the old.^[11] In 2010, children with asthma experienced over 900,000 emergency department visits, making it the most common reason for admission to the hospital following an emergency department visit in the US in 2011.^[96][97]

Global rates of asthma have increased significantly between the 1960s and 2008^[9][98] with it being recognized as a major public health problem since the 1970s.^[11] Rates of asthma have plateaued in the developed world since the mid-1990s, with recent increases primarily in the developing world.^[99] Asthma affects approximately 7% of the population of the United States^[100] and 5% of people in the United Kingdom.^[101] Canada, Australia, and New Zealand have rates of about 14–15%.^[102]

The average death rate from 2011 to 2015 from asthma in the UK was about 50% higher than the average for the European Union and had increased by about 5% in that time.^[103] Children are more likely see a physician due to asthma symptoms after school starts in September.^[104]

Population-based epidemiological studies describe temporal associations between acute respiratory illnesses, asthma, and development of severe asthma with irreversible airflow limitation (known as the asthma-chronic obstructive pulmonary disease "overlap" syndrome, or ACOS).^{[105][106][19]} Additional prospective population-based data indicate that ACOS seems to represent a form of severe asthma, characterized by more frequent hospitalizations, and to be the result of early-onset asthma that has progressed to fixed airflow obstruction.^[20]

As of 2005, more "westernized," urbanized countries had much higher rates of asthma than "less developed" countries. However, exposure to urbanization alone has not been able to explain these disparities.^[107]

In the United States, the burden of asthma falls disproportionately on racial and ethnic minorities and economically underprivileged populations.^[108] As of 2016, the prevalence of asthma was highest in non-Hispanic black and Puerto Rican children. The prevalence of asthma was also over 1.5 times higher in Americans 100% below the poverty level than those 450% of the poverty level or higher.^[109] As of 2021, the mortality rate for black Americans with asthma was two times higher than for white Americans.^[108]

Neighborhoods in the United States with predominantly racial and ethnic minority populations are affected to a greater extent than predominantly white neighborhoods by air pollutants, which are a significant factor in the occurrence of asthma. Additionally, residents of areas that were more likely to be redlined have asthma emergency department visit rates 2.4 times higher than residents of areas that were less likely to be redlined.^[108]

From 2000 to 2010, the average cost per asthma-related hospital stay in the United States for children remained relatively stable at about $3,600, whereas the average cost per asthma-related hospital stay for adults increased from $5,200 to $6,600.^[110] In 2010, Medicaid was the most frequent primary payer among children and adults aged 18–44 years in the United States; private insurance was the second most frequent payer.^[110] Among both children and adults in the lowest-income communities in the United States, there was a higher rate of hospital stays for asthma in 2010 than in the highest-income communities.^[110]

The Egyptian Ebers Papyrus (c.1550 BC ), detailing a treatment for asthma

The Chinese Gold-dust Book of Cold Damage, dated the "1st year of the Zhengyuan reign period of the Yuan dynasty" (1341)

Asthma was recognized in ancient Egypt and was treated by drinking an incense mixture known as kyphi.^[10] It was officially named as a specific respiratory problem by Hippocrates c. 450 BC, with the Greek word for "panting" forming the basis of our modern name.^[11] In 200 BC, it was believed to be at least partly related to the emotions.^[16] In the 12th century, the Jewish physician and philosopher Maimonides wrote Maqāla fī al-Rabw ("Treatise on Asthma") in Arabic.^[111] In the work, he described the symptoms of asthma, proposed dietary and therapeutic treatments, and emphasized the importance of clean air and climate in managing the condition.^[112][111] Traditional Chinese medicine also offered medication for asthma, as indicated by a surviving 14th-century manuscript curated by the Wellcome Foundation.^[113]

A well-documented case in the 19th century was that of young Theodore Roosevelt (1858–1919). At that time there was no effective treatment. Roosevelt's youth was in large part shaped by his poor health, partly related to his asthma. He experienced recurring nighttime asthma attacks that felt as if he was being smothered to death, terrifying the boy and his parents.^[114]

In 1873, one of the first papers in modern medicine on the subject tried to explain the pathophysiology of the disease while another in 1872, concluded that asthma can be cured by rubbing the chest with chloroform liniment.^[115][116] Medical treatment in 1880 included the use of intravenous doses of a drug called pilocarpine.^[117] In 1886, F. H. Bosworth theorized a connection between asthma and hay fever.^[118]

At the beginning of the 20th century, treatment was focused on avoidance of allergens and the use of selective beta₂-adrenergic agonists as treatment strategies.^[119][120]

Epinephrine (adrenaline) was first referred to as a treatment of asthma in 1905.^[121] The asthma was relived with this treatment by what was described as "vasomotor ataxia of the relaxing variety". The successful results of using epinephrine provided encouraging medical data on the hypothesis that asthma was due to vasodilation and the subsequent inflammation of the swelling of the bronchial mucosa.^[122]

In the 1930s, U.S. physician Alvin Barach created, by means of spirometry, the quantification of expiratory flow rates to nebulized epinephrine for those with asthma, which was the first published medical report on the effectiveness of bronchodilation.^[123][124]

During the 1930s to 1950s, asthma was known as one of the "holy seven" psychosomatic illnesses. Its cause was considered to be psychological, with treatment often based on psychoanalysis and other talking cures.^[125] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, they considered the treatment of depression to be especially important for individuals with asthma.^[125]

In the 1940s, the first pure β-agonist to be synthesized was isoprenaline. Both isoprenaline and adrenaline are catecholamines. However, isoprenaline was an effective bronchodilator that was more selective than epinephrine.^[126] The efficacy of anecdotal applications of oral corticosteroids (OCS) for the asthma was published in 1952.^[127] In 1958, the association between a treatment strategy of OCS and a reduction in eosinophils in the sputum was published.^[128]

The use of a pressurized metered dose inhaler was developed in the mid-1950s for the administration of adrenaline as well as isoproterenol, and was later used as a beta₂-adrenergic agonist. Inhaled corticosteroids and selective short-acting beta agonists came into wide use in the 1960s.^[129][130] In 1967, adrenergic receptors were classified into the two subtypes of the β₁ and the β₂ adrenergic receptors.^[131] The β₂ adrenergic receptors were found to be dominant in the lungs as well as present in the alveolar airspace.^[132][133] The discovery of the β₂ adrenergic receptors allowed for the discovery and development of beta2 agonists. Specifically, it allowed for the development of selective β2-agonists starting in the 1960s.^[134]

Between 1970 and 1985, the following countries saw a general rise in reported asthma mortality in people aged 5 to 34: Singapore, Australia, Japan, England/Wales, West Germany, Israel, United States, Netherlands, Canada, and France. Additionally, New Zealand experienced a major epidemic of asthma in this period, which may have been due to inadequate maintenance therapy and long-term management of the disease amongst those affected, as well as delays in receiving care in emergencies.^[135]

• WHO fact sheet on asthma