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- genetics
- mold
- air pollution
- pets
- dust mites

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-Stay away from allergen triggers
-Avoid smoke of any kind
-Immunotherphy Allergy Shots

-Combination Inhaler
-Inhaled corticosteroids

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- chest pain
- cough
- wheezing
- shortness of breath
- mucus production
- inflammation

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-Asthma is more common in people under 40
-Approximately 1 in 13 Americans have asthma
-There is no cure for asthma but it can be managed with treatment and prevention of asthma attacks
-Asthma is more common in boys than in girls
-On average, 10 Americans die from asthma each day
-Asthma is one of the countries more costly/common diseases
-More than 300 million people have asthma all over the world

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-Asthma is a major non-communicable disease

-Asthma is a disease that make your airways contract/become smaller and produce mucus, making it difficult to breathe

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This video discusses what an asthma attack looks like in a persons body and all the contributing factors

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How does asthma work? - Christopher E. Gaw

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https://www.webmd.com/asthma/what-is-asthma
https://www.aafa.org/asthma-facts/
https://www.cdc.gov/asthma/triggers.html
https://www.webmd.com/asthma/guide/asthma-prevention
https://www.who.int/news-room/fact-sheets/detail/asthma#:~:text=Key%20facts,of%20breath%20and%20chest%20tightness.

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This article talks about how asthma attack/reaction can differ with age

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Division of Pediatric Pulmonology, Department of Pediatrics, University of Massachusetts Medical School, Worcester, MA, United States

Department of Population and Quantitative Health Sciences, University of Massachusetts Medical School, Worcester, MA, United States

Department of Respiratory Medicine, Alfred Hospital, Melbourne, VIC, Australia

Public Health and Preventive Medicine, Monash University, Melbourne, VIC, Australia

Asthma varies considerably across the life course. Childhood asthma is known for its overall high prevalence with a male predominance prior to puberty, common remission, and rare mortality. Adult asthma is known for its female predominance, uncommon remission, and unusual mortality. Both childhood and adult asthma have variable presentations, which are described herein. Childhood asthma severity is associated with duration of asthma symptoms, medication use, lung function, low socioeconomic status, racial/ethnic minorities, and a neutrophilic phenotype. Adult asthma severity is associated with increased IgE, elevated FeNO, eosinophilia, obesity, smoking, and low socioeconomic status. Adult onset disease is associated with more respiratory symptoms and asthma medication use despite higher prebronchodilator FEV1/FVC. There is less quiescent disease in adult onset asthma and it appears to be less stable than childhood-onset disease with more relapses and less remissions.

Childhood Onset Asthma

Introduction to Childhood Asthma

Asthma is considered a chronic disease of childhood however there are periods of time during which disease can go into remission or resolve altogether. Important risk factors for the development of childhood asthma have been identified. The phenotypes of childhood asthma and varied presentations are best defined through the periods of the pediatric life course and are described herein.

Childhood Asthma Risk Factors

The perinatal period has been implicated in the development of childhood asthma. Several cohort studies have unveiled risk factors for the development of asthma in offspring, with factors that span from genetic and environmental risk factors to features such as child's sex and presence of atopy.

Genetic Risk Factors

The genetics of asthma are an emerging and complicated topic. Multiple genes are thought to contribute to asthma and rapidly changing technology continues to build our current understanding of the genetic risk factors for asthma development. This is a complex topic that we will only briefly describe herein. Genome-wide Association Studies (GWAS) have dramatically improved our understanding of asthma susceptibility genes. Briefly, the following genes have been determined to have significant association with asthma susceptibility: the 17q21 locus with the ORMDL3 and GSDML genes, the IL33 gene on chromosome 9p24, the HLA- DR/DQ gene on chromosome 6p21, the IL1RL1/IL18R1gene on chromosome 2q12, the WDR36/ TSLP gene on chromosome 5q22 and the IL13gene on chromosome 5q31 ( 7). Interestingly, GWAS have shown evidence that loci may be specific to racial/ethnic populations, such PHYNN1 observed in African-Americans with asthma ( 8). However, as with other common diseases, for individuals, only a small degree of heritability of asthma can be explained by the genes observed in GWAS. Therefore, emerging and multi-genetic approaches are needed to further study the genetic susceptibility to asthma ( 7).

Environmental Risk Factors

Environmental perinatal risk factors are also important to consider for childhood asthma. Maternal tobacco smoking during pregnancy has been shown to increase the risk of childhood asthma ( 9). Maternal diet in pregnancy has also been implicated as an asthma risk factor with reports of maternal diets higher in vitamin E, zinc, and polyunsaturated fatty acids as protective against the development of childhood asthma ( 10- 12). In contrast, high sugar intake in the maternal diet during pregnancy has been associated with increased risk of asthma in offspring ( 13). Other maternal dietary factors have been studied but with less conclusive results including the intake of vitamin D, vitamin C, and a Mediterranean diet. Other perinatal risk factors for childhood asthma that have been reported are neonatal jaundice, maternal preeclampsia, and cesarean section delivery, all which have been associated with higher risk of childhood asthma development ( 14- 16).

Ultimately gene-environment interactions (the genetic-environmental axis) are critical for the development of asthma in a child ( 8).

Natal Risk Factors

Sex

Boys are more likely to develop childhood asthma, as compared with girls, at least until the point of puberty. This has been explained by smaller airway size in boys compared with girls under age 10 years, which predisposes to worsened airway reactivity, as compared with girls of the same age, height and weight ( 21).

Family History

Both maternal and paternal histories of asthma are associated with increased risk of asthma in offspring. Interestingly, maternal asthma history is more strongly associated with asthma development in the child ( 22).

Medical History

Presence of atopy (having IgE antibodies to specific allergens) is strongly associated with childhood asthma ( 23). Specifically the "atopic march" is a pattern that is described clinically in individuals with atopic disease. This "atopic march" begins as atopic dermatitis (or eczema) in infancy, develops on to allergic rhinitis (or hayfever) and then asthma later in childhood ( 24). Specific indoor allergen sensitization in early life have been of interest with regard to asthma development. Sensitization to house dust mite, alternaria mold, and cockroach allergens have been associated with increased risk of asthma ( 25, 26), whereas early life exposure to cat and dog allergens have been associated with both increased and decreased risk of asthma in different studies ( 27, 28).

Medication Exposure

Exposures to antibiotics ( 29) and antipyretics ( 30) in infancy have been described to be associated with increased risk of developing childhood asthma however the data has been conflicting and the study results have been concerning for uncontrolled confounding bias. Therefore, further studies are warranted before conclusions can be made about these associations.

Presentation of Asthma: Early Childhood (0-6 Years)

Often, clinicians including pediatric asthma specialists (pulmonologists and allergists) define asthma in this age group as symptoms of airway inflammation that reverse with bronchodilator therapy. However, given the diagnostic challenge in this age group, the Asthma Predictive Index (API) was developed to guide the diagnosis of childhood asthma in children under age 3 years ( 34). The API has limited sensitivity but reasonable specificity. The API major criteria were defined as physician-diagnosed eczema or parental asthma. The minor criteria were defined as physician-diagnosed allergic rhinitis, wheezing apart from colds, and serum eosinophilia >4%. Positive loose index were defined as parental report of wheezing on surveys at age 2 or 3 years and either 1 major or 2 minor criteria. Positive stringent index was defined as frequent wheezing on surveys at age 2 or 3 years and either 1 major or 2 minor criteria. Children with a positive loose index were found to be four times more likely to have active asthma on surveys at age 6, 8, 11, and 13 years (sensitivity 42%, specificity 85%). Children with a positive stringent index were seven times more likely to have asthma on a school-age survey (sensitivity 16%, specificity 97%). The API is most useful for its negative predictive value and thus, when negative, is an essential tool for determining who is not likely to go on to having later asthma. While not a perfect tool, a slightly modified API, with criteria of a higher score of frequent wheezing and replacing "physician-diagnosed allergic rhinitis" with skin prick testing, is endorsed by the US National Asthma Education and Prevention Program Expert Panel Report 3 for use in diagnosing asthma in this young age group ( 35).

Often in this age group, particularly over 0-3 years, symptoms are virally triggered rather than allergically triggered. Infants will often have very few symptoms until they experience an upper respiratory infection, which can trigger a significant and severe inflammatory cascade.

Presentation of Asthma: Late Childhood (7-11 Years)

By this age, children can more reliably perform spirometry, and reversible airway obstruction on spirometry can be a helpful diagnostic tool. However, it is important to note that in children with asthma, spirometry values can be normal despite significant disease and morbidity ( 37). Therefore, in children, spirometry is often used as a monitoring tool for asthma symptoms after the diagnosis has been established through other assessments ( 38).

Symptoms in this age group transition more from discrete episodes of wheezing in response to viral infections to allergic triggered exacerbations. In this age group, exercise-induced symptoms manifest more clearly which may be due to a true change in the clinical presentation of asthma in this age group or also due to sports and exercise becoming a more discreet activity for children of this age wherein caretakers are able to appreciate the symptoms of dyspnea or cough with exertion. In children who avoid or develop a loss of interest in exercise or physical activities, it is important to consider that asthma may be underlying.

Some children in this age group will have few day-to-day symptoms, but have severe asthma attacks in response to specific triggers such as cold weather, cigarette smoke, or seasonal allergies. Virally triggered asthma exacerbations occur in this age group but less often than in the 0-6 year age range and may contribute to the lower rates of healthcare utilization in this age group as compared with younger years of 0-4 years ( 2).

Presentation of Asthma: Adolescence (12-18 Years)

Puberty has an interesting impact on childhood asthma, specifically relating to sex. Prior to puberty, asthma risk is higher among male children. At the time of puberty, the risk of asthma is approximately equal between males and females, and after puberty, girls have a higher risk of asthma ( 39). Some of these differences could be explained by the differences in airway development between the sexes. The fetal lung is less developed in boys from 16 to 26 weeks, measured by mouth movements that reflect fetal breathing, a critical determinant of lung development. In the last 4 weeks of gestation, airway resistance is higher in males ( 21). Boys up to 10 years old appear to have smaller airways in relation to lung size as compared with girls of the same age, height, and weight ( 21). After puberty, smaller airway caliber is then observed in the female sex ( 39). The known sex differences in asthma may also be due to other factors such as hormonal effects, genetic susceptibility, immunologic response, and differences in consultation practices and health-seeking behaviors by sex ( 4, 40).

Asthma symptoms in this age group are most predominantly shortness of breath with exertion, wheezing in response to triggers, chest pain, chest tightness, and cough. In this age group, asthma symptoms can significantly impact sleep, school, sports, and social engagements. Children are more aware of symptoms in this age range and often feel more embarrassment or stigma around using an inhaler and in particular a spacer, often leading to under treatment of asthma symptoms ( 40).

Wheezing and Asthma Phenotypes in Childhood

Childhood wheezing phenotypes have been explored given that nearly 50% of children experience wheezing before age 1, yet only 20% of those children progress to have continued wheezing later in childhood ( 44). While there are several longitudinal birth cohorts that have described wheezing phenotypes, we will describe the classifications according to the earliest of these studies: the Tucson Children's Respiratory Study and the most recent systematic comparison of the clinical and epidemiologic classifications ( 45).

Wheezing Phenotypes (44, 45):

Never/Infrequent Wheeze

This Describes Children who do not Experience any Wheezing.

The Transient Wheeze

This describes children who have their first wheeze before the age of 3 years with resolved wheezing by age 6 years. Transient wheeze is not strongly related to atopy and genetic risk; there are only mild impairments in lung function in this phenotype, and medication use is very uncommon ( 45).

The Persistent Wheeze

This describes children who experience first wheezing before age 3 year, however go on to have continued wheezing at age 6 years. Persistent wheeze was strongly related to the asthma risk locus on chromosome 17, however this phenotype appears to be unrelated to environmental determinants. Interestingly, bronchodilator administration dramatically improved any compromises in lung function for children with this phenotype ( 45).

Intermediate Onset Wheeze

This describes children who experience rare (or no) wheezing before 18 months of age, but persistent wheeze thereafter. Intermediate-onset wheeze has associations with atopy, but only to pollen sensitization ( 45).

The Late Onset Wheeze

These children develop wheezing between age 3 and 6 years. Late-onset wheeze is strongly associated with fractional exhaled nitric oxide levels and sensitization to inhaled allergens at 6 years and at 4 years. There appears to be severe and irreversible reduction in lung function in this phenotype and asthma medication use is common ( 45).

Childhood Asthma Clinical Phenotypes

Asthma Diagnosis (45)

Physician's diagnosis of asthma at least once per lifetime or recurrent diagnoses of spastic, obstructive, or asthmatic bronchitis as reported by the parents at age 6 years.

Frequent Wheeze (45)

Wheeze on a monthly basis for at least 1 year between age 1 and 6 years.

Unremitting Wheeze (45)

Having symptoms between wheezing episodes or having wheeze without a cold at least once between age 1 and 6 years.

Recurrent Unremitting Wheeze (45)

Having s ymptoms between wheezing episodes or wheeze without a cold for 2 or more years between age 1 and 6 years.

Multi-Trigger Wheeze (45)

Having at least 2 common asthma triggers leading to wheeze between ages 3-6 years.

Episodic Wheeze (45)

Wheezing episodes associated only with viral upper respiratory infection between age 1 and 6 years.

Severe, Difficult to Control Asthma, Steroid-Resistant Asthma

Eosinophilic Predominant

Neutrophilic Predominant

While initially most childhood asthma was thought to be eosinophilic in nature, a neutrophilic predominance has emerged as an important phenotype. In this phenotype, children generally have low IgE levels, low serum and sputum eosinophil counts with very little allergic symptoms. Neutrophil-predominant asthma is the most severe asthma phenotype with poor corticosteroid response ( 54) and may explain some of the children who have not respond well to standard asthma therapy.

Other Childhood Asthma Clinical Presentations:

In clinical practice, there are different clinical presentations of symptoms that point to an underlying diagnosis of childhood asthma, and clinical improvement can occur in response to starting a child on preventive asthma therapy, such as a daily-inhaled corticosteroid and use of bronchodilator therapy for acute episodes.

Recurrent Croup

Croup, inflammation of the upper airway, which presents as barky cough and stridor, is a common isolated entity in infancy and early childhood. However, the presence of recurrent croup may indicate the presentation of underlying asthma in childhood. Recurrent croup has been shown to be a risk factor for childhood asthma and airway hyperreactivity ( 56) as well as strongly associated with bronchial asthma in children ( 57).

Middle Lobe Syndrome

Recurrent Pneumonia

In a child with recurrent multi-lobar pneumonia, with a normal immune function evaluation, asthma should be considered as an underlying cause of the recurrent chest infections. Many children referred to specialty care with recurrent chest infections will be found to have undiagnosed or undertreated asthma. Often the history reveals that most have recurrent episodes of cough, wheeze and breathlessness, with trigger factors of upper respiratory tract infections, exercise, cold air, emotional upset, or exposure to pets and other aero-allergens suggestive of asthma ( 62). In several studies, asthma was the main underlying cause for recurrent pneumonia in children ( 63).

Association Between Childhood Asthma and COPD

Children with asthma have an increased risk of developing chronic obstructive pulmonary disease (COPD) in adulthood. Specifically, it has been shown that children who smoke tobacco and also have asthma are at increased risk for developing low lung function and COPD as adults, when compared to smokers who did not have asthma in childhood ( 64).

Remission and Mortality in Childhood Asthma

Asthma remission occurs most commonly between the ages of 14-21 years ( 65). However, large longitudinal studies have also shown that, among children who wheezed before age 3 years, more than 50% had stopped wheezing either by 6 years of age ( 44) or by 12 years of age, ( 36, 66) depending on the study. Remission rates of childhood asthma have been reported between 16 and 60% by early adulthood, according to prior longitudinal studies ( 41, 65, 67). The wide variation in reported remission rates is likely due to diverse study designs, varying follow-up periods, and different study populations. In longitudinal studies, children with the following characteristics had higher remission rates: episodic asthma (rather than persistent asthma), milder initial asthma severity, less allergic sensitization, less allergic rhinitis, less atopic dermatitis, and male sex ( 36, 65).

While the morbidity of childhood asthma is significant, fortunately, mortality from childhood asthma is rare with an estimated 28 deaths per million children with asthma ( 2). As with childhood asthma morbidity, there are grave racial disparities in childhood asthma mortality, and black, and Hispanic children suffer disproportionately from the highest mortality rates ( 2).

Adult-Onset Asthma

Introduction to Adult-Onset Asthma

Asthma is increasingly recognized as an umbrella term for a heterogenous group of conditions that has been likened to the term "arthritis" in Rheumatology-not a specific diagnosis but a term that describes a diverse group of conditions clinically and biologically ( 68). Some have suggested discarding the term asthma altogether ( 69).

Table 1. Comparison of childhood and adult asthma.

Phenotypes

Phenotypes of asthma can be broadly categorized into clinical, biological, and molecular although there is considerable overlap between these and, ultimately, it is the combination of the three that is likely to form the asthma phenotypes of the future.

Clinical

These phenotypes have been further refined with the addition of biologic markers to five groups; early-onset allergic, late-onset eosinophilic, exercise-induced, obesity-related and neutrophilic ( 68). These will be discussed in more detail below.

The extension of the development of more detailed clinical phenotypes is whether these phenotypes represent distinct clinical entities with different treatment strategies. There is considerable work being done currently in this space.

There are, however, a number of clinical phenotypes amongst adults with asthma that are distinct, including those with occupational asthma, aspirin-associated asthma, and asthma associated with other conditions such as allergic bronchopulmonary aspergillosis and chronic obstructive airways disease (COPD) ( 86- 88). Some of these subtypes have more developed clinical characteristics associated with them, biological mechanisms, management, and natural history.

Biologic

As phenotyping of asthma has progressed there has been progressive attempts to describe the endotype, or biologic pathway, behind different clinical phenotypes.

The most developed of these is the distinction between the presence or absence of Type 2 inflammation (T2) in asthma ( 89). It has long been recognized that for many, but not all, patients with asthma there is upregulation of Type 2 inflammation. This is characterized by an stimulus at the level of the airway epithelium that results in production of IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) that stimulate release of IL-4, IL-5, and IL-13 and, in turn eosinophils and antibodies that lead to the pathogenic airway changes characteristic of asthma ( 90). This upregulation of the Type 2 inflammatory response in asthma has important clinical implications because this inflammation tends to be responsive to corticosteroids.

Unlike in children, amongst adults there is a significant proportion of non-T2 high disease. This group of patients is less well-understood than their T2-high disease counterparts and accounts for a significant proportion of mild-moderate adult-onset asthma ( 91). Although these patients are poorly characterized there are significant implications for treatment as they tend to be less steroid responsive than those with T2-high disease and it is unclear what the best treatment strategy for these patients is ( 92).

Molecular

Molecular phenotyping has potential implications for treatment with those with T2-high asthma based on genetic profile having a response to inhaled corticosteroids and those with T2-low disease having no response ( 90, 95).

Adult Phenotypes of Asthma

Late Onset Eosinophilic

Characterized by both clinical and biologic features of later onset, predominately female, and elevated sputum and serum eosinophils. Late-onset eosinophilic asthma is defined clinically by adult-onset, severe disease and is associated with sinusitis and less allergic sensitization compared to early onset disease. Biologically patients have increased IL-5 and IL-13 in the airways and elevated eosinophils in the sputum and serum ( 96- 98). No cut off for sputum and serum eosinophils have been universally agreed upon however it is generally accepted that a sputum eosinophil count of >2% or a serum eosinophil count of >300 cells/uL (or in some cases >150 cells/uL) indicates eosinophilic asthma ( 99- 101). Despite a high prevalence of positive skin prick tests this form of asthma appears to be less allergic but is often associated with sinusitis, nasal polyps, and aspirin exacerbated respiratory disease ( 96). A family history of asthma is seen less frequently than those with early onset asthma ( 96). This type of asthma can be relatively steroid resistant but biologic therapies targeting T2 pathways have been shown to be highly effective in this group of patients ( 102- 105).

Obesity-Related Asthma

Obesity-related asthma is not well-understood. It is unclear whether it is a comorbidity common in asthma that confers greater likelihood of breathing pattern disorder, gastroesophageal reflux and deconditioning or whether it is the driver for a proinflammatory state that results in asthma ( 106- 109). Higher body mass index (BMI) is associated with increased levels of TNFa, IL-6, and leptins and less eosinophils, FeNO and corticosteroid responsiveness ( 108, 109). Clinically there appears to be a group of older non-allergic, obese females who have significant symptoms but minimal healthcare utilization ( 76, 77). The interaction between BMI and eosinophils is more complex, with those who have early onset T2-high asthma having a correlation between duration of asthma and BMI, lower activity levels, and corticosteroid exposure that does not appear to exist in those with T2-low disease ( 110). Bariatric surgery has been shown to improve outcomes in asthma patients with late onset, non-allergic asthma but not in those with allergic disease ( 111).

Neutrophilic Asthma

Neutrophilic asthma is poorly defined and there is no consensus about the characterization of this entity. Adding to the confusion is the fact that corticosteroid treatment commonly suppresses eosinophils and causes neutrophilia making the assessment of corticosteroid-dependant patients difficult ( 112- 114). The clinical phenotype remains controversial and inconsistent but has been suggested to be that of adult-onset, severely obstructed with only partial reversibility and a high healthcare utilization ( 77, 78). Smoking may also play a role. Furthermore, neutrophilic asthma can occur in those with elevated eosinophils conferring a particularly severe clinical phenotype ( 115). These patients tend to be less corticosteroid responsive and other treatment strategies have been tried including use of macrolide antibiotics ( 116). Although IL-17 has been suggested as a potential therapeutic target in neutrophilic asthma a biologic targeted at this interleukin did not result in improvement in asthma control and so far this area remains disappointing ( 117, 118). The initial disappointment with targeted therapies such as the anti-IL-17 and anti-TNFa agents has been tempered by positive preliminary results with a newer biologic agent targeting TSLP that has showed promise in Phase 2 studies in a non-eosinophilic group ( 119, 120).

Aspirin-Associated Asthma

Aspirin-associated asthma, a subset of aspirin exacerbated respiratory disease (AERD) has been described for many years ( 85). It tends to occur in adulthood at an average age of 34 years and is more common amongst females ( 86). This is a subset of late-onset eosinophilic asthma and is associated with sinusitis, nasal polyps and sensitivity to cyclooxygenase-1 inhibitors including aspirin ( 86). Biologically it is characterized by upregulation of the cysteinyl leukotriene pathway and elevated eosinophils ( 96). Molecularly genes related to the leukotriene pathway have been implicated and periostin, a biomarker of IL-13 activity, has been found in nasal polyps present in patients with AERD ( 97, 121). These patients are often relatively corticosteroid resistant, requiring high doses for control, but can be responsive to leukotriene antagonists ( 122, 123). More recently biologic therapies that target T2 pathways including IL-4, IL-13, and IL-5 have been shown to be effective in patients with asthma and nasal polyps ( 124- 126).

Allergic Bronchopulmonary Aspergillosis

Allergic bronchopulmonary aspergillosis (ABPA) was first described in the 1950s and is caused by allergic sensitization to fungal colonization of the lower airways with Aspergillus fumigatus ( 127, 128). It occurs in 1-2% of asthma patients, although has been detected in up to 13% of the population in asthma clinics, predominately adults, and causes asthma exacerbations, deterioration of pulmonary function, mucous plugging, central bronchiectasis, and transient pulmonary infiltrates with characteristic biologic features including elevated total and Aspergillus-specific IgE as well as peripheral eosinophilia ( 88, 128, 129). The diagnosis is based on presence of asthma, proximal bronchiectasis, sensitization to Aspergillus, and an elevated total IgE ( 129). It is important to diagnose ABPA because of the progressive nature of the bronchiectasis in the absence of treatment ( 129). The mainstay of treatment for ABPA is systemic corticosteroids and, in some cases, antifungal agents ( 88).

Link Between Early Transient Wheeze and COPD

Asthma-smoking associations have been described in both early and late onset asthma ( 133). Smoking remains a key risk factor for airflow obstruction in normal and asthmatic individuals, however the risk appears to be greatest in those with late onset disease ( 74).

Natural History

The natural history of asthma in adults is different to that of asthma in children with less remission of adult-onset asthma than that occurring in childhood.

Adult onset asthma has many different forms and the risk factors appear to be different to that of childhood-onset disease. Compared to childhood asthma, major associations with adult-onset disease are female sex, current smoking, and low socio-economic status but not atopy or a family history of asthma ( 74). Other risk factors include; clinical-historical symptoms of wheeze, rhinitis, chronic cough; physiological-lower lung function, bronchial hyperresponsiveness, lower height; comorbidities-higher BMI, nocturnal gastroesophageal reflux disease, habitual snoring, IgE reactivity to Timothy grass; and lifestyle-low physical activity amongst men ( 75, 107, 140- 144). The evidence for smoking as a risk factor is mixed with two large cohort studies from Australia and Sweden showing that this is a risk factor for adult-onset asthma and other studies showing that it doesn't appear to be ( 74, 75, 141, 144).

Despite the differences in risk factors for adult-onset asthma compared to childhood onset disease the prevalence of asthma amongst adults was shown to be increasing in the second half of the twentieth century similar to that of childhood asthma ( 73, 148).

Young Adults

Middle Age

Older Adults

Remissions

Lung Function

Mortality

Contrasts

Table 2. Asthma presentations across the lifecourse.

Severe asthma in children is distinct from severe asthma in adults and approaches to severe asthma in adults should not be extrapolated to children. In children the factors associated with severity have been found to be asthma duration, medication use and lung function rather than Type 2 inflammatory markers such as increased IgE and elevated FENO that are markers of severity in adult-onset disease ( 93).

Author Contributions

MT and ED made substantial contributions to: The conception or design of the work; or the acquisition, analysis, or interpretation of data for the work; Drafting the work or revising it critically for important intellectual content; Provide approval for publication of the content; Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Funding

The manuscript described was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through Grant KL2TR001454. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Asthma in Children and Adults-What Are the Differences and What Can They Tell us About Asthma?

# data[].attributes.attachment_link.description
Asthma varies considerably across the life course. Childhood asthma is known for its overall high prevalence with a male predominance prior to puberty, common remission, and rare mortality. Adult asthma is known for its female predominance, uncommon remission, and unusual mortality. Both childhood and adult asthma have variable presentations, which are described herein.

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This is podcast for kids that discusses basic facts about asthma