This study addresses the risk factors for adult-onset asthma, including cigarette smoking, atopy, and obesity. Asthma denotes a pulmonary disease characterized by increased airways responsiveness to stimuli, such as allergens and irritants that cause blockages. Noteworthy, asthma can attack anybody and at any stage of life. The major symptoms of asthma include recurring episodes of dyspnea, wheezing, and cough, mostly during night time. In adults, the occurrence of asthma is referred to as adult-onset asthma. If an adult is newly diagnosed with asthma, the symptoms are persistent rather than intermittent, like in children. Cigarette smoking exposes victims to harmful chemical compounds that constrict airway muscles, cause inflammation and swelling, as well as increased mucus secretions. Atopy refers to the genetic tendency of developing allergic reactions, such as allergic rhinitis, eczema, and asthma. When an individual’s immune response is activated, the body produces antihistamines that cause inflammation and swelling of pulmonary airways. Obesity or being overweight is another cause of asthma. While adipokines act to cause inflammation of the airways, mechanical obstructions limit the amount of air, such that individuals breathe slowly than usual. However, more women than men are likely to suffer from obesity-related asthma due to concurrent development of excess body fat, type II diabetes, as well as shared inherited and immunological factors.
Health Research on the Risk Factors for Adult-onset Asthma
Recurrent episodes of dyspnea, wheezing, and cough suggest a potential asthmatic attack. Asthma denotes an increased airways’ responsiveness to various stimuli, such as irritants and allergens that cause obstructions. In the case study, ‘Whistling in the Dark’ (Solomon, Fanta, Levy, & Loscalzo, 2012), a 38-year-old patient complained to her physician that these conditions worsen at night. Her medical history designates that several identifiable triggers might have triggered the disease. Some of these exposures include respiratory tract infections, congestive heart failure, and prolonged cigarette smoking. According to Solomon et al. (2012), the risk factors for adult-onset asthma include atopy, cigarette smoking, and obesity (p.1725).
Based on the case study, the following research question and hypothesis can be developed for further analysis:
Research Question: How do cigarette smoking, atopy, and obesity contribute to the development of adult-onset asthma?
Hypothesis: Cigarette smoking, atopy, and obesity trigger asthmatic attack through increased sensitization, inflammation, bronchial hyper-responsiveness, and reversible airways obstruction
3.0.Effects of Cigarette Smoking
An asthmatic attack can occur at any time in an individual's life. Adults can develop asthma in their 50s, 60s, or even later, thus acquiring adult-onset asthma. Unlike kids who demonstrate intermittent symptoms, newly diagnosed adults have persistent symptoms. Cigarette smoking exposes individuals to chemical irritants that offset breathing due to constricted airway muscles, inflammation, swelling, and increased mucus secretions. According to Jaakkola, Hernberg, Lajunen, Sripaijboonkij, Malmberg, & Jaakkola (2019), smoking is a primary determinant of mortality and morbidity around the world. It is also known to cause chronic illnesses, including chronic obstructive pulmonary disease (COPD) (Jaakkola et al., 2019), and coronary heart ailments. Approximately 4,000 irritants and carcinogenic compounds are found in tobacco smoke (Jaakkola et al., 2019). Unfortunately, cigarette smoking has become rampant in low- and middle-income nations, particularly among women.
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Adult-onset asthma is a heterogeneous disorder that can progress from mild to severe. According to Moazed & Calfee (2015), several cross-sectional studies have provided various features of patients who have adult-onset asthma. Nonetheless, there is insufficient data to show which patients are at risk of developing mild or severe asthmatic attacks. Some other previous studies have demonstrated that most adult-onset asthma patients were smokers (Moazed & Calfee, 2015). There is a definite relationship between cigarette smoke and asthma development in adults. Noteworthy, cigarette smoke contributes to the pathogenesis of asthma, augmented Th2 pathway activation, allergic sensitization, and airway hyperactivity (Moazed & Calfee, 2015).
Moazed & Calfee (2015) testify to a study by Coogan and colleagues that addressed the relationship between adult-onset asthma and active/passive smoking. Coogan et al. recruited African American women as participants in a “Black Women’s Health Study” from 1995 to 2011 (Moazed & Calfee, 2015). Approximately 46,182 women respondents without baseline asthma were engaged for an average of 14.7 years (Moazed & Calfee, 2015). The findings exhibited that active and passive smoking had a direct relationship with adult-onset asthma. However, the utilization of a multivariable model adjusted for potential confounders, such as body mass index (BMI), parental history of asthma, female hormone usage, education level, age, and access to healthcare (Moazed & Calfee, 2015). Both the ex- and active smokers showed a dose-response relationship between adult-onset asthma and smoking. The higher the number of pack-years smoked, the higher the incidence of adult-onset asthma. When the subjects were stratified for age and BMI, the relationship between smoking and adult-onset asthma was higher in individuals older than 50 years and with a BMI lower than 30 kg/m2 (Moazed & Calfee, 2015). It was, nonetheless, interesting that these populations are typically thought to have a lower risk for adult-onset asthma.
Both smokers and non-smokers have an increased risk of asthma (Jaakkola et al., 2019). Most asthmatic adults in developed countries, such as the U.S. and U.K., are cigarette smokers. In such cases, the interaction of asthma with active cigarette smoking causes decreased lung function and impaired response to short-term corticosteroids. Although limited data is found on airway pathology, it has been established that smoking causes inflammations associated with asthma. Most of the evidence, however, shows that complications result from the combination of suppressed and heightened inflammatory responses in asthmatic smokers compared to nonsmoking asthma patients (Jaakkola et al., 2019). Corticosteroid resistance in smoking asthmatic patients is attributed to the alterations of airway inflammatory cell phenotypes, such as reduced eosinophils or increased neutrophils (Jaakkola et al., 2019). Some other possible mechanisms include modifications in the glucocorticoid receptor -α to -β ratio (Jaakkola et al., 2019), augmented activation of pro-inflammatory transcription factors (Jaakkola et al., 2019), or abridged histone deacetylase activity.
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Jaakkola et al. (2019) cite a study by Jayes and colleagues that active cigarette smoking is highly associated with the development of asthma in adults. In eight different studies that were published from 1985 to 2013, Jayes et al. established that the summary-effect estimate was 1.61. The risk for asthmatic smokers was 1.33 (95% CI 1.00 to 1.77) (Jaakkola et al., 2019), while that of ex-smokers was 1.49 (1.12 to 1.97) (Jaakkola et al., 2019). The risk among the current smokers rose to 14 cigarettes daily, and the trend was replicated in cumulative smoking. Jaakkola et al. (2019) resolved that asthma was common among working-age adults. Consequently, it would be vital to address smoking and the adverse effects it causes lung function in asthmatic adults.
4.0.Effects of Atopy
Atopy describes the genetic tendency of developing allergic conditions, including asthma, eczema, and allergic rhinitis. Most often, atopy is associated with activated immune responses to allergens, particularly food and inhaled allergens. In adult-onset asthma, the condition is typically non-atopic, more severe, and causes a fast reduction in lung function (Thomsen, 2015). Clinical scientists have routinely described asthma as an atopic condition following a theoretical paradigm in allergen exposure, atopic sensitization, airways inflammation, reversible airway obstruction, and bronchial hyper-responsiveness (Thomsen, 2015).
The genetic predisposition to adult-onset asthma is less studied than the atopic onset of asthma in childhood. In adults, a familial history of asthma is deficient because atopy is less familiar than in the general population. Thomsen (2015) cites a study conducted in the Chinese Han population, which shows a significant relationship between adult-onset asthma and genetic variants in chromosome 17q21. The study also noted that a similar connection was established in childhood asthma. Although the study was limited by self-reported age at asthma onset, it provides vital information on the similarity of childhood and adulthood-onset asthma, such as exposure to infection or pollution.
Rhinitis is a well-known risk factor for asthma in adults. Deriving from the case study, the California-based patient had seasonal allergic rhinitis attributed to atopy. Thomsen (2015) states that chronic nasal polyposis and rhinosinusitis play a crucial role in the development of asthma in adulthood. A previous study also pinpointed the relationship between chronic rhinosinusitis and asthma (Thomsen, 2015). Notably, the link between the two factors was established devoid of nasal allergies, which are also related asthma. The investigators tried to outline the relationship between aspirin intolerance and nasal polyps with adult-onset asthma. Unfortunately, the mechanisms underlying the connection between nasal polyps and asthma provided poor outcomes. BACHERT and colleagues, however, established that IgE against Staphylococcus aureus enterotoxin caused severe upper airways inflammation and comorbid asthma (Thomsen, 2015). Consequently, bacteria play a vital role in lower and upper airway infections.
5.0.Effects of Obesity
The risk of adult-onset asthma is higher in overweight or obese people. Most often, women are associated with overweight-related asthma due to metabolic syndrome. Women mostly suffer due to the development of additional body fat, type II diabetes, and shared inherited and immunological factors. Also, obesity contributes to asthmatic attacks and reduces the effectiveness of inhaled corticosteroids. According to Thomsen (2015), the incidence of adult-onset asthma increases by 50% in obese and overweight individuals. Two recent observational studies assessing waist circumference demonstrated that abdominal obesity was independently associated with increased incidence and prevalence of asthma (Thomsen, 2015). Although the contribution of obesity to asthma is complicated, several mechanisms have been established with this relationship.
Obesity-related asthma results from increased adipokines, including leptin in the visceral adipose tissue. Adipokines may have a direct impact on the airways by promoting inflammation, which may induce asthma (Thomsen, 2015). Secondly, mechanical factors have a crucial role in asthmatic attacks. Obese or overweight individuals breathe at a slower rate than healthy individuals. As a result, there is limited residual capacity, increased expiratory flow restrictions, and airway closure and hyperresponsiveness. The primary effect of obesity is reduced lung function, even in the absence of pulmonary diseases (Thomsen, 2015). It can thus exaggerate the existence of simple airway infection. Thirdly, obesity may inflate the risk of other pulmonary infections, such as gastroesophageal reflux infection and sleep-disordered breathing. Due to the high rate of obesity, asthma associated with the condition may be an epidemic in the future.
The findings comprehensively respond to the research question in that cigarette smoke, atopy, and obesity are risk factors to asthmatic attacks. Likewise, the hypothesis was addressed through multifactorial characteristics, such as airways inflammation, hyperactivity, and subsequent obstruction that induces asthma. Tobacco smoke has over 4,000 chemical compounds that cause irritation and are also carcinogenic. It is these chemicals that trigger various mechanisms related to the pathogenesis of asthma, such as allergic sensitization, airway hyperactivity, and increased Th2 pathway activation. The strong impact of previous smoking and nonlinear relationship with pack-years address behavioral change and response to triggering the symptoms. The genetic contributions to adult asthmatic attacks include family history of the disease and allergic rhinitis. A Chinese-based study with the Han population demonstrated that adult-onset asthma is significantly related to the genetic variants in chromosome 17q21. With rhinitis, chronic nasal polyposis and rhinosinusitis contribute to adult-onset asthma. Obesity contributes to asthmatic attacks through increased adipokines in the visceral adipose tissue. Women are more susceptible than men due to concurrent development of excess body fat, type II diabetes, and shared inherited and immunological factors. Nevertheless, the question of whether female participants are more affected due to unique biological susceptibility and its relationship with different factors requires further research.
- Jaakkola, J. J., Hernberg, S., Lajunen, T. K., Sripaijboonkij, P., Malmberg, L. P., & Jaakkola, M. S. (2019). Smoking and lung function among adults with newly onset asthma. BMJ open respiratory research, 6(1). DOI: https://doi.org/10.1136/bmjresp-2018-000377
- Moazed, F., & Calfee, C. S. (2015). Clearing the air. Smoking and incident asthma in adults. DOI: https://doi.org/10.1164/rccm.201411-2098ED
- Solomon, D. A., Fanta, C. H., Levy, B. D., & Loscalzo, J. (2012). Whistling in the Dark. New England Journal of Medicine, 366(18), 1725-1730. DOI: https://doi.org/10.1056/NEJMcps1106363
- Thomsen, S. F. (2015). Epidemiology and natural history of atopic diseases. European clinical respiratory journal, 2(1), 24642. DOI: https://doi.org/10.3402/ecrj.v2.24642
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