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Asthma as a result of (or worsened by) workplace exposures is a commonly reported occupational disease. [122] Many cases, however, are not reported or recognized as such. [123] [124] It is estimated that 5–25% of asthma cases in adults are work-related.
Airway remodelling is a multifaceted process involving multiple airway tissues. These include goblet cell hyperplasia, leading to increased mucus production, and airway smooth muscle hypertrophy (or smooth muscle cell hyperplasia), leading to the release of pro-inflammatory and pro-fibrotic messengers contributing to subepithelial fibrosis.
Thus, basing asthma treatment plans on a single sputum eosinophil measurement may be misleading. It is not known to what extent asthma phenotypes can change in the long term. [3] GINA presently recognises 5 asthma phenotypes: allergic asthma, non-allergic asthma, adult-onset asthma, asthma with persistent airflow limitation, and asthma with ...
An estimated 22 million American adults had asthma in the US that year, according to the Centers for Disease Control and Prevention. Nearly 30,800 US adults with asthma were included in the study.
While the acronyms are similar, reactive airway disease (RAD) and reactive airways dysfunction syndrome (RADS) are not the same. [1]Reactive airways dysfunction syndrome was first identified by Stuart M. Brooks and colleagues in 1985 as an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke.
In some subjects, the constriction does not return to normal, and recurs after three to four hours, which may last up to a day or more. The first is named the early asthmatic response, and the latter the late asthmatic response. Bronchoconstriction can occur as a result of anaphylaxis, even when the allergen is not inhaled.
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