Work-related asthma encompasses both new-onset asthma and aggravation of pre-existing asthma from work exposures/conditions. New-onset asthma can be caused by exposure to an irritant or a substance that causes sensitization. Approximately 350 substances have been identified by which exposure at work can lead to sensitization and asthma. When the term occupational asthma is used, it generally does not include work-aggravated asthma. Some authors limit the use of occupational asthma to new-onset asthma from sensitization to a substance at work, while others also include new-onset asthma from exposure to an irritant at work under this category. New-onset asthma from an acute single exposure is called reactive airways dysfunction Syndrome (RADS) (note this is not the same as reactive airways disease). New-onset asthma from repeated chronic exposure to an irritant at work as a cause of asthma has also been described, but it is not as well accepted as an entity as RADS. Aggravation of pre-existing asthma by work can occur from any exposure as well as stress, physical activity, and temperature/humidity. Unlike the work-related lung diseases such as the pneumoconioses, which cause irreversible fibrosis, work-related asthma is potentially completely reversible if diagnosed soon after onset of symptoms and the patient’s exposure to the etiologic agent ceases. Beginning in the early 1900s, asthma from exposure at work to plant material and metals first began to be reported in the medical literature. In the 1970s, Dr. Jack Pepys from England markedly advanced the identification of etiological agents by developing a practical way to perform specific inhalation challenge testing. The field has continued to advance with the recognition of an increased number of etiological agents, an understanding of the pathophysiology, an understanding of the prognosis and factors associated with a better prognosis, and the initiation of work on the interaction with genetic variability. At least in more developed countries, such as in European countries and the United States, which have implemented controls or banned the use of the mineral dusts (i.e., asbestos, silica) that have caused the most common pneumoconioses, work-related asthma has become a more important cause of new-onset work-related lung disease than the more traditional pneumoconioses.
Can reactive airways dysfunction syndrome (RADS) transform into occupational asthma due to "sensitisation" to isocyanates?
