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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.
GINA conducts continuous review of scientific publications on asthma and is a leader in disseminating information about the care of patients with asthma. [2] GINA publishes resources such as evidence-based guidelines for asthma management, and runs special events such as World Asthma Day. GINA's guidelines, revised each year, are used by ...
The prevalence of asthma increased 75% from 1980 to 1994. Asthma prevalence is 39% higher in African Americans than in Europeans. [148] 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
"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.
As result of his work, he has provided evidence on asthma and allergy to the Lords Select Committee on Science and Technology in 2006 [12] and has been interviewed by mainstream media. [ 13 ] [ 14 ] [ 15 ] In 2014, he contributed to a European Respiratory Society video about the Burden of COPD - ERS Vision.
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]
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.