Epidemiological evidence indicates that exposures at work are responsible for 15% of the incidence of asthma among adults (1). Yet, the numbers of cases of asthma that are actually diagnosed – let alone compensated – as being of occupational origin are consistently much lower than this figure would suggest. This discrepancy may indicate that the epidemiologically derived estimates are too high and/or that many cases of occupational asthma are missed by clinicians and occupational physicians. However, the discrepancy may also indicate that occupational exposures do contribute to asthma in many subjects, but that this manifests itself as typical occupational asthma in only few patients. In other words, only a small minority of work-related asthma is caused by sensitization to high molecular weight agents (proteins from animal, vegetal or microbial origin) or low molecular weight chemicals (synthetic chemicals such as isocyanates; metallic agents; some natural compounds). In contrast, a large proportion of work-related asthma would then be due to other, non-sensitizing agents. In this presentation, evidence will be provided that exposure to irritants (in the workplace or elsewhere) may contribute to the development (and not only the clinical manifestations) of asthma. 

It is now well established that persistent asthma may be induced by a single accidental exposure to a non-sensitizing irritant. This condition has been labeled “Reactive Airways Dysfunction Syndrome” (RADS) (2). It is often assumed that RADS only occurs after exposure to very high levels of an irritant causing a clinically severe inhalation injury. However, there are indications from cohort studies that the initial insult does not need to be very severe to lead to persistent bronchial hyperreactivity in some subjects. The most convincing evidence comes from the follow-up studies of the firemen and emergency personnel involved in the WTC collapse of 11 September 2011 (3;4).  

The possibility that repeated exposure to non-sensitizing irritants can also lead to occupational asthma is less universally accepted, especially by compensation agencies. One possible reason for this reluctance to recognize “irritant-induced asthma” is that such occupational asthma cannot be “proven” by specific inhalation challenges. However, there is ample anecdotal evidence that such irritant-induced asthma does exist (5). Moreover, emerging epidemiological studies also show that the risk of asthma (or at least persistent respiratory symptoms), including severe asthma, is increased among people exposed to irritants (6-9). This has been especially well studied among cleaners (10;11). Although, one cannot exclude that cleaners may become asthmatic as a result of allergic sensitization to specific ingredients of cleaning agents, it appears more likely that it is their exposure to irritants (chlorine-derived agents, sprayed compounds) that increases the risk of asthma. A limited number of experimental studies are supportive of this notion (12).

The issue of the role of exposure to irritants is not limited to that of occupational asthma; it is also relevant with regard to asthma in general. Thus, exposure to irritants within the home environment (13) or in other indoor environments (such as chlorinated swimming pools) (14), as well as in the outdoor environment (15) may also contribute to the occurrence of asthma among children.

In conclusion, further clinical-epidemiological as well experimental research must be conducted to understand the relation between irritants and asthma. However, even in the absence of more evidence, occupational exposures to inhaled irritants should be kept to a minimum. Occupational asthma should be recognized not only in workers with asthma caused by sensitization, but also in workers with substantial exposure to irritants.

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     (2)   Brooks SM, Weiss MA, Bernstein IL. Reactive airways dysfunction syndrome (RADS). Persistent asthma syndrome after high level irritant exposures. Chest 1985;88:376-84.

     (3)   Banauch GI, Alleyne D, Sanchez R, Olender K, Cohen HW, Weiden M, et al. Persistent hyperreactivity and reactive airways dysfunction in World Trade Center firefighters. Am J Respir Crit Care Med 2003;168:54-62.

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    (10)   Zock JP, Plana E, Jarvis D, Anto JM, Kromhout H, Kennedy SM, et al. The use of household cleaning sprays and adult asthma: an international longitudinal study. Am J Respir Crit Care Med 2007;176:735-41.

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    (12)   Hox V, Vanoirbeek JA, Callebaut I, Bobic S, De Vooght, V, Ceuppens J, et al. Airway exposure to hypochlorite prior to ovalbumin induces airway hyperreactivity without evidence for allergic sensitization. Toxicol Lett 2011;204:101-7.

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    (14)   Weisel CP, Richardson SD, Nemery B, Aggazzotti G, Baraldi E, Blatchley ER, III, et al. Childhood asthma and environmental exposures at swimming pools: state of the science and research recommendations. Environ Health Perspect 2009;117:500-7.

     (15)      Gehring U, Wijga AH, Brauer M, Fischer P, De Jongste JC, Kerkhof M, et al. Traffic-related air pollution and the development of asthma and allergies during the first 8 years of life. Am J Respir Crit Care Med 2010;181:596-603.