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Introduction to Asthma

Asthma is a chronic inflammatory disease that leads to the constriction of the airways, as well as, airway hyperresponsiveness (Keller, 2002). Approximately 300 million people are affected worldwide and this number is expected to rise over the upcoming years (Lambecht & Hammad, 2015). As well, approximately 250,000 people die annually (Pawankar, 2014). Asthma most commonly affects infants (Reed, 2006). A study found that babies in their first year of life had a 3% likelihood of developing asthma (Reed, 2006). This incidence rate drops to 0.9% for 1-4 year olds (Reed, 2006). Due to this, most of research is focused on the development of asthma in children as opposed to adults or seniors (Reed, 2006). Asthma can be divided into allergic asthma and non-allergic asthma. Allergic asthma is mostly commonly found in children, but are also found in 50% of adults (Lambrecht & Hammad, 2015). In children, the disease begins with allergic sensitization, which involves the interaction between the IgE antibody present in the body, and the inhaled or ingested allergin (such as dust mites, pollen) (Lambrecht & Hammad, 2015). This interaction leads to a cascade of allergic reactions, and is accompanied by atopic eczema in the early stages of life (Lambrecht & Hammad, 2015). In later life, these children develop allergic rhinitis, when leads to the progression of the asthma. (Lambrecht & Hammad, 2015). Non-allergic asthma occurs in individuals later in life and does not involve the interaction of IgE antibodies with the allergen (allergic sensitization) (Lambrecht & Hammad, 2015). Non-allergic asthma is most commonly found in women (Lambrecht & Hammad, 2015). This form of asthma is more difficult, takes a longer time to treat and leads to chronic rhinosinusitis, nasal polyps as well as obesity (Lambrecht & Hammad, 2015)

Epidemiology

The prevalence of asthma varies worldwide (Keller, 2002). However, it has been found that developed countries, such as Canada, Unites States, and Australia, have the highest prevalence rates of asthma (Keller, 2002). The world is exhibiting an increase in rates of this illness in all variables: age, gender and racial groups (Keller, 2002). As a result, more people are dying over time, which is leading to higher economic costs for countries (Keller, 2002). In the United States, there was a 75% increase in prevalence of asthma observed between 1980 and 1994, in which, greater increases were found in children and young adults (Keller, 2002). The prevalence of asthma in the United States is much higher than most other countries in the world, but drastically varies between among ethnic groups (Gold & Wright, 2005). However, it has been speculated that this increase may be due to the public awareness and improvements in detecting the disease in earlier stages (Keller, 2002).

Risk Factors

There are several factors that make one more prone to this disease:

  • Heredity:A toddler has an 80 - 90% chance of contracting this illness if both parents are asthmatic, however, if one parent has the disease, then the toddler would be 30 - 40% at risk of contracting the illness (Duffy, 1997). There are several studies that looked at monozygotic and dizygotic twins and found that monozygotic twins have a 19% chance of presenting with the same disease, whereas dizygotic twins only have a 4.8% chance of presenting with the same disease (Edfors-Lubs, 1971). An individual with a family history of this disease is four times as likely of getting the disease (Ronmark et al., 1971).
  • Fetal environment:Studies have found a relationship between the fetal environment and the development of the atopic disease later in life (Keller, 2002). It is more likely for the child to contract the disease if the mother has the disease as opposed to the father (Keller, 2002). The risk for a child to develop asthma in later life has been correlated with a mother’s exposure to allergins in the first 22 weeks of gestation (Warner et al., 2000). Bronchial hyperresponsiveness has been shown to be more commonly found in infants with lower birthweight as opposed to infants with a higher birthweight (Keller, 2002). Moreover, It has been found that mothers who smoke and are younger than 20 years, were more likely to have a child who suffers from asthma (Keller, 2002). Moreover, maternal prenatal stress has also shown to be a possible risk factor for developing asthma (Sears, 2014). Research has also looked at the relationship between different modes of delivery and the likelihood of developing asthma. It was found that mothers who had undergone a caesarean section, were 10% to 20% more likely at risk to get an asthmatic child (Sears, 2014).
  • Environmental Factors:There are several environmental and genetic determinants for Asthma, that interact together to form a genetic-environmental interface (Keller, 2002). Firstly, environmental exposures to allergens early in life can raise the risk of allergy in later life and increase the incidence for developing asthma (Keller, 2002). Infants who develop this disease later in life usually have an unbalanced immune system (Keller, 2002). In order to reduce an individual’s risk of developing asthma, they must ensure that they are living in a clean environment, with a hygienic lifestyle. The overuse and misuse of medications such as antibiotics has also shown to increase the likelihood of developing this disease in children, by disrupting the normal development of the immune system (Keller, 2002). Moreover, research has also shown that diets low in Omega 3, vitamin C and high in fat have been linked the development of asthma (Weiss, 1997). An indoor and sedentary lifestyle, which is typically seen in urban environments, can increase the likelihood as well (Keller, 2002). Studies have shown that physical activity has the potential in protecting against wheezing illnesses (Skloot, 1995).

Works Cited

Skloot G, Permutt S,Togins A. (1995). Airway hyperresponsiveness in asthma: a problem of limited smooth muscle relaxation with inspiration. J Clin Invest, 96, 2393–2403.

Duffy DL. (1997). Genetic epidemiology of asthma. Epidemiol Rev, 19, 129–143.

Warner JA, Jones CA, Jones AC, et al. (2000). Prenatal origins of allergic disease. J Allergy Clin Immuno. 2(2), 493–498.

Weiss ST. Diet as a risk factor for asthma. In: Chadwick D, Cardew G, eds. The Rising Trends in Asthma. New York: Wiley; 1997:244–253

Lambrecht, B., Hammad, H. (2015). The Immunology of Asthma. Nature Immunology, 16(1), 45-56.

Pawankar. (2014). Allergic diseases and asthma: a global public health concern and a call to action. World Allergy Organ J., 7(1), 12.

Keller, M., Lowenstein, S. (2002). Epidemiology of Asthma. eminars in Respiratory and Critical Care Medicine, 23(4). 317-329.

Edfors-Lubs M. (1971). Allergy in 7000 twin pairs. Acta Allergol, 26:249–285

Ronmark E, Lundback B, Jonsson EA, et al. (1997). Incidence of asthma in adults—report from the Obstructive Lung Disease in Northern Sweden study. Allergy, 52:1071–1081.

Sears, M. (2014). Trends in the Prevalence of Asthma. Chest, 145(2), 219-225. Gold DR & Wright R. (2005). Population disparities in asthma. Annu Rev Public Health 26: 89–113. Reed, C. (2006). The natural history of asthma. Journal of Allergy and Clinical Immunology, 118( 3), 549-550.

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