Irritant-Induced Asthma
Irritant-Induced Asthma
Purpose of review To describe the recent insights into the definition, causes, natural outcome, and key elements of irritant-induced asthma (IIA) management.
Recent findings IIA is a subtype of occupational asthma without immunologic sensitization and includes the typical reactive airway dysfunction syndrome (RADS) and a more gradual form called not-so-sudden IIA, when onset of asthma follows repeated low-dose exposure to irritants. The World Trade Center tragedy brought new insight in the understanding of IIA, suggesting that it can exhibit a prolonged interval between exposure and recognition of clinical symptoms and disease. Dimethyl sulfate has been recently reported to cause RADS and repeated diesel exhaust exposure to cause not-so-sudden IIA in patients who worked in a bus garage. Cleaning workers who are exposed to a large variety of irritants and sensitizers are especially at risk of occupational asthma and IIA.
Summary IIA includes RADS and not-so-sudden IIA. Outcome of IIA is as poor as occupational asthma with sensitization. Treatment of IIA does not differ from standard asthma treatment, but high-dose vitamin D could be assessed further for possible therapeutic benefit.
In 2008, the ACCP (American College of Chest Physician) published their updated state-of-the-art consensus statement on the 'Diagnosis and Management of Work-Related Asthma'. Work-related asthma can be divided in two major entities shown in Fig. 1. The term occupational asthma encompasses all workers who develop new respiratory symptoms and obstructive airways physiology consistent with the diagnosis of asthma, and the cause can be directly attributed to an exposure in the workplace. The key element is that occupational asthma is asthma caused by exposure(s) to an organic protein, chemical, or other compound that is unique to the workplace. Occupational asthma is further split into two subtypes – sensitizer-induced occupational asthma (>90% of the cases) and irritant-induced asthma (IIA) that includes reactive airway dysfunction syndrome (RADS). Work-exacerbated, or work-aggravated, asthma (WEA) refers to previously diagnosed asthma that is worsened, but not caused, by agents found in the workplace. The distinction between these two entities is not superfluous as it impacts treatment strategies and medicolegal decisions.
(Enlarge Image)
Figure 1.
Classification scheme for the major types of asthma in the workplace. This scheme is based on the American College of Chest Physicians 2008 guidelines and is adapted with permission. Reproduced from [2].
Abstract and Introduction
Abstract
Purpose of review To describe the recent insights into the definition, causes, natural outcome, and key elements of irritant-induced asthma (IIA) management.
Recent findings IIA is a subtype of occupational asthma without immunologic sensitization and includes the typical reactive airway dysfunction syndrome (RADS) and a more gradual form called not-so-sudden IIA, when onset of asthma follows repeated low-dose exposure to irritants. The World Trade Center tragedy brought new insight in the understanding of IIA, suggesting that it can exhibit a prolonged interval between exposure and recognition of clinical symptoms and disease. Dimethyl sulfate has been recently reported to cause RADS and repeated diesel exhaust exposure to cause not-so-sudden IIA in patients who worked in a bus garage. Cleaning workers who are exposed to a large variety of irritants and sensitizers are especially at risk of occupational asthma and IIA.
Summary IIA includes RADS and not-so-sudden IIA. Outcome of IIA is as poor as occupational asthma with sensitization. Treatment of IIA does not differ from standard asthma treatment, but high-dose vitamin D could be assessed further for possible therapeutic benefit.
Introduction
In 2008, the ACCP (American College of Chest Physician) published their updated state-of-the-art consensus statement on the 'Diagnosis and Management of Work-Related Asthma'. Work-related asthma can be divided in two major entities shown in Fig. 1. The term occupational asthma encompasses all workers who develop new respiratory symptoms and obstructive airways physiology consistent with the diagnosis of asthma, and the cause can be directly attributed to an exposure in the workplace. The key element is that occupational asthma is asthma caused by exposure(s) to an organic protein, chemical, or other compound that is unique to the workplace. Occupational asthma is further split into two subtypes – sensitizer-induced occupational asthma (>90% of the cases) and irritant-induced asthma (IIA) that includes reactive airway dysfunction syndrome (RADS). Work-exacerbated, or work-aggravated, asthma (WEA) refers to previously diagnosed asthma that is worsened, but not caused, by agents found in the workplace. The distinction between these two entities is not superfluous as it impacts treatment strategies and medicolegal decisions.
(Enlarge Image)
Figure 1.
Classification scheme for the major types of asthma in the workplace. This scheme is based on the American College of Chest Physicians 2008 guidelines and is adapted with permission. Reproduced from [2].
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