Work-Related Asthma

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.

Updated review of reported cases of reactive airways dysfunction syndrome

Background A previous systematic review of the diagnosis of reactive airways dysfunction syndrome (RADS), undertaken from 1985 to 2004, found a lack of standardization of case reporting, thus misattribution of symptoms can occur. Aims We aimed to update the systematic review, update the list of reported causes and see whether a more structured approach to reporting has been adopted. Methods We undertook a systematic literature review, using the databases EMBASE and Ovid MEDLINE, with search terms ‘reactive airways dysfunction syndrome’ or ‘asthma AND acute irritant’, and reported according to PRISMA guidelines. We included papers and abstracts published from January 2005 to September 2019, and articles were grouped by the presence or absence of diagnostic features: ‘definite’ RADS (met Brooks’ criteria) or ‘possible’ RADS (Brooks’ criteria not met or insufficient data). We collected demographic and diagnostic data for cases, where given. Results Eleven papers and six conference abstracts met the inclusion criteria, 13 of which were case series or reports, and comprised 752 cases in total; seven articles met Brooks’ criteria for RADS diagnosis. A variety of agents were implicated, with chlorine or chlorine-releasing molecules most frequently reported. Conclusions A lack of standardized reporting of RADS remains. The majority of published articles and conference abstracts either do not meet, or contain insufficient data to judge against, Brooks’ criteria, particularly in relation to onset of symptoms and bronchial hyper-reactivity or variability of airflow obstruction. Some novel agents are described, in keeping with recognized structural taxonomies.

Environmental Causes of Asthma

Environmental factors which cause asthma are those that induce airway inflammation with eosinophils (more common) or neutrophils along with airway hyperresponsiveness (AHR). The most common of these (indeed the most common cause of asthma) are IgE-mediated inhalant allergen exposures. Allergen-induced AHR and inflammation are both associated with the allergen-induced late asthmatic response (LAR). Although allergens were previously recognized only as causes of symptoms and bronchoconstriction in asthmatics, we now appreciate them as causes of the fundamental pathophysiologic features of asthma. Low-molecular-weight chemical sensitizers, causes of occupational asthma, also cause asthma in a manner analogous to allergen. Acute irritant-induced asthma (reactive airways dysfunction syndrome) following a very heavy irritant exposure and chronic irritant-induced asthma following repeated high exposures can also induce persistent or permanent changes (inflammation and AHR) consistent with asthma. Textile dust exposure produces a different form of airway disease (byssinosis) which is less frequently observed currently. Environmental exposure to tobacco smoke facilitates the development of asthma in children. Personal smoking and environmental air pollution have an inconsistent and likely generally small effect in causing asthma.