Occupational asthma: allergen exposure and lung function decline

Loss of lung function over time has been reported in patients with asthma in longitudinal prospective and retrospective studies. An accelerated decline in lung function occurs in some patients. Risk factors include young age, longer duration of disease, black ethnicity, more prominent eosinophilic airway inflammation, asthma exacerbations, smoking and continuous exposure to causative agents. However, accelerated decline is not invariable. Many asthmatics retain normal or close to normal lung function throughout life, showing reversibility from acute worsening. Conversely, some patients develop "irreversible" asthma, as seen in population-based studies and in specialist-treated patients whose obstruction persisted despite bronchodilators and oral corticosteroids. In occupational asthma, continued exposure to the causative agent is recognized as being associated with a greater decline in lung function in asthmatic workers during the periods of exposure than after removal of allergens.  Also reduction of occupational exposure seems not to reduce the decrease in lung function over time, in fact, it has been shown that, after 12 years of observation, lung function decay slopes of persistently exposed workers (even reduced by preventive measures in the work place) appear steeper and significantly greater with respect to those of asthmatics that avoided the exposure to causative allergens. This difference became evident after 4  years of allergen reduction. Allergen exposure seems to be among the most important factors determining the entity of the decline in lung function in allergic asthmatics. Its importance seems greater that smoking habit (almost between ex- and non-smokers) and the entity of FEV1 variability at diagnosis. In conclusion, recent literature data show that allergen avoidance is crucial in the long term preservation of lung function in patients with occupational asthma. Not only the persistence of allergen exposure accelerates the decline of lung function, but determines an inflammatory state that is barely controlled by drugs.