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In 2000-2001 asthma prevalence was monitored at 6.5%; by 2010-2011 a 4.3% increase was shown, with asthma prevalence totaling 10.8% of Canada's population. [29] Furthermore, asthma prevalence varies among the provinces of Canada; the highest prevalence is Ontario at 12.1%, and the lowest is Nunavut at 3.8%. [29]
Asthma phenotyping and endotyping has emerged as a novel approach to asthma classification inspired by precision medicine which separates the clinical presentations of asthma, or asthma phenotypes, from their underlying causes, or asthma endotypes. The best-supported endotypic distinction is the type 2-high/type 2-low distinction.
Childhood asthma is a chronic respiratory condition characterized by inflammation and narrowing of the airways, leading to recurrent episodes of wheezing, shortness of breath, chest tightness and coughing. Around 4.9 million children in the US suffer from asthma [1]. It is difficult to diagnose asthma in children younger than 6 years of age.
The prevalence of asthma increased 75% from 1980 to 1994. Asthma prevalence is 39% higher in African Americans than in Europeans. [135] 5.7 million (about 9.4%). In six- and seven-year-olds asthma increased from 18.4% to 20.9% over five years, during the same time the rate decreased from 31% to 24.7% in 13- to 14-year-olds. Atopic eczema
Sensitizer-induced occupational asthma is an immunologic form of asthma which occurs due to inhalation of specific substances (i.e., high-molecular-weight proteins from plants and animal origins, or low-molecular-weight agents that include chemicals, metals and wood dusts) and occurs after a latency period of several weeks to years. [1]
"The influence of sensitisation to pollens and moulds on seasonal variations in asthma attacks" European Respiratory Journal. 42: 935-945. Ghosh RE, Cullinan P, Fishwick D, Hoyle J, Warburton CJ, Strachan DP, Butland BK, Jarvis D (2013). "Asthma and occupation in the 1958 birth cohort" Thorax. 68: 365-371.
It is unclear whether ACO is a separate disease entity or a clinical subtype of asthma and COPD. The pathogenesis of ACO is poorly understood, but it is thought to involve both type 2 inflammation (usually seen in asthma) as well as type 1 inflammation (seen in COPD). The incidence and prevalence of ACO are not well known.
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