Occupational Asthma Reference

Cullinan P, Irritant-induced Asthma from Work Irritant induced asthma from work; What Happens Next?, Am J Respir Crit Care Med, 2009;179:857-858,

Keywords: editorial, irritant induced asthma, rads

Known Authors

Paul Cullinan, Royal Brompton Hospital, London, UK Paul Cullinan

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Abstract

‘‘Inhalation accidents’’ at work are common, particularly in the chemical, plastics, and engineering sectors. In almost all cases, fortunately, the outcome is good, a testament to the remarkable resilience of the human respiratory tract. Factory physicians who registered 383 such accidents in a surveillance program in the United Kingdom, for example, later reported that in just 10% of cases did respiratory symptoms persist for a month or
more and in only 3% was there a persistent asthmatic outcome (1). This experience is probably more representative than that of respiratory specialists to whom, of course, difficult cases are referred. They commonly see patients with persistent respiratory symptomsthat have been attributed to an irritant exposure at work and, in many instances, the prognosis seems poor.

Stuart Brooks and his coauthors were the first to codify this specialist experience with, in 1985, a description of 10 cases of a persistent asthma-like condition that followed a single irritant exposure, of which 8 cases encountered the irritant at work (2); the average duration of symptoms was 3 years. There are at least two critical features of this important paper. First, the initiating exposures were of very high intensity: one patient, for example, was trapped beneath a 55-gallon drum of 35% hydrazine while another was in a bookshop into which an airplane crashed and caught fire. Second, the diagnostic criteria applied by the authors were peculiarly stringent and included measurable bronchial hyperreactivity and a ‘‘documented’’ absence of any preceding respiratory disease. Strict criteria such as these are valuable in assigning causality, but do not eliminate the possibility that high-dose irritant exposures can cause disease in individuals with a preexisting respiratory condition. Moreover,
it is very rarely the case that there are pre-morbid measurements of airway function and thus, in general, it is supposition that an inhalational accident followed by bronchial hyperreactivity is a matter of cause and effect. Brooks and his colleagues coined the term ‘‘reactive airways dysfunction syndrome’’ to describe the experience of their patients. While this was useful as an acronym (RADS), it was not particularly descriptive, and the term has been largely superseded by the near-simile ‘‘irritant-induced asthma.’’ The fate of patients with irritant-induced asthma is often considered to be poor, but this is largely on the basis of anecdote and case experience, since there are very few surveys of prognosis in patient cohorts. Where such information is available, it suggests that many patients find that their symptoms respond poorly to standard asthma medications (3).

Malo and coauthors describe the experience of 29 men and 6 women in Quebec who since 1988 have been compensated for irritant-induced asthma acquired after an inhalation accident at work (4). The diagnosis required an onset of symptoms within 24 hours of the accident, a history absent of any previous asthma or other chronic obstructive lung diseases, and either bronchial hyperresponsiveness (n=30) or ‘‘significant’’ airway obstruction (FEV1 <1.5 L, n=5). After a minimum interval of 4 years and an average of
around 13 years, almost all 35 patients continued to have symptoms consistent with asthma, a third were using inhaled corticosteroids, and a third were still smoking. There was little evidence of any improvement—or deterioration—in spirometry, the mean percent predicted FEV1 and FVC values being approximately 70% at diagnosis and follow up. Twenty-three
patients had repeat measurements of their metacholine responsiveness,
17 (74%) with persistently abnormal results. The remainder underwent spirometry before and after a bronchodilator. From the whole cohort, there was no physiologic evidence of continuing airway hyperreactivity in nine cases (25%); and in a further three, methacholine responsiveness had improved by at least two doubling doses. In this small study there was no
evidence that either the severity or chemical nature of the initial event had any bearing on the outcome. Those with evidence of functional improvement tended to be younger (although few were very young) and to have a higher PC20 at presentation.

What can we learn from these findings? The experience reported is very unlikely to be characteristic of workplace inhalational accidents in general and, in any case, the participation rate (52% of those eligible) raises concerns that a particularly poor prognosis is being presented. Nonetheless it would seem, at least among those who seek compensation for irritant-induced asthma and taking account of the response rate, that more than half will continue to report asthmatic symptoms for many years after what was probably quite a severe inhalational accident, and that more than one third will have persistent airway hyperreactivity. These are useful data. The levels of anxiety and depression in this cohort were quite high, again a feature that will be familiar to experienced physicians and one that raises the question of whether, how, and when psychological treatment might be helpful in improving symptomatic recovery. What is less clear is why some patients fare less well than others. If failure to recover is a consequence of inadequate remodeling after toxic airways damage, then one might expect it to be related to the severity of the initiating injury, or perhaps to its chemical nature. Neither appeared important in this cohort,
although its small size will have limited its power to address these issues and retrospective measurements of severity (hospital attendance in this case) are difficult in individual cases. Nonetheless these findings, except in the instance of a very severe exposure, are in accord with the experience of most physicians. On the other hand, youth may be an advantage as is probably the case in other forms of occupational asthma (5). We do not know, and it will be difficult ever to know, whether workers’ compensation schemes affect, favorably or otherwise, prognosis, even when they are as generous as that in Quebec.

Finding answers to these questions is going to need much larger cohorts of well-characterized patients followed, preferably prospectively, for 5 years or more, which will be a challenge

Plain text: ''Inhalation accidents'' at work are common, particularly in the chemical, plastics, and engineering sectors. In almost all cases, fortunately, the outcome is good, a testament to the remarkable resilience of the human respiratory tract. Factory physicians who registered 383 such accidents in a surveillance program in the United Kingdom, for example, later reported that in just 10% of cases did respiratory symptoms persist for a month or more and in only 3% was there a persistent asthmatic outcome (1). This experience is probably more representative than that of respiratory specialists to whom, of course, difficult cases are referred. They commonly see patients with persistent respiratory symptomsthat have been attributed to an irritant exposure at work and, in many instances, the prognosis seems poor. Stuart Brooks and his coauthors were the first to codify this specialist experience with, in 1985, a description of 10 cases of a persistent asthma-like condition that followed a single irritant exposure, of which 8 cases encountered the irritant at work (2); the average duration of symptoms was 3 years. There are at least two critical features of this important paper. First, the initiating exposures were of very high intensity: one patient, for example, was trapped beneath a 55-gallon drum of 35% hydrazine while another was in a bookshop into which an airplane crashed and caught fire. Second, the diagnostic criteria applied by the authors were peculiarly stringent and included measurable bronchial hyperreactivity and a ''documented'' absence of any preceding respiratory disease. Strict criteria such as these are valuable in assigning causality, but do not eliminate the possibility that high-dose irritant exposures can cause disease in individuals with a preexisting respiratory condition. Moreover, it is very rarely the case that there are pre-morbid measurements of airway function and thus, in general, it is supposition that an inhalational accident followed by bronchial hyperreactivity is a matter of cause and effect. Brooks and his colleagues coined the term ''reactive airways dysfunction syndrome'' to describe the experience of their patients. While this was useful as an acronym (RADS), it was not particularly descriptive, and the term has been largely superseded by the near-simile ''irritant-induced asthma.'' The fate of patients with irritant-induced asthma is often considered to be poor, but this is largely on the basis of anecdote and case experience, since there are very few surveys of prognosis in patient cohorts. Where such information is available, it suggests that many patients find that their symptoms respond poorly to standard asthma medications (3). Malo and coauthors describe the experience of 29 men and 6 women in Quebec who since 1988 have been compensated for irritant-induced asthma acquired after an inhalation accident at work (4). The diagnosis required an onset of symptoms within 24 hours of the accident, a history absent of any previous asthma or other chronic obstructive lung diseases, and either bronchial hyperresponsiveness (n=30) or ''significant'' airway obstruction (FEV1 <1.5 L, n=5). After a minimum interval of 4 years and an average of around 13 years, almost all 35 patients continued to have symptoms consistent with asthma, a third were using inhaled corticosteroids, and a third were still smoking. There was little evidence of any improvement-or deterioration-in spirometry, the mean percent predicted FEV1 and FVC values being approximately 70% at diagnosis and follow up. Twenty-three patients had repeat measurements of their metacholine responsiveness, 17 (74%) with persistently abnormal results. The remainder underwent spirometry before and after a bronchodilator. From the whole cohort, there was no physiologic evidence of continuing airway hyperreactivity in nine cases (25%); and in a further three, methacholine responsiveness had improved by at least two doubling doses. In this small study there was no evidence that either the severity or chemical nature of the initial event had any bearing on the outcome. Those with evidence of functional improvement tended to be younger (although few were very young) and to have a higher PC20 at presentation. What can we learn from these findings? The experience reported is very unlikely to be characteristic of workplace inhalational accidents in general and, in any case, the participation rate (52% of those eligible) raises concerns that a particularly poor prognosis is being presented. Nonetheless it would seem, at least among those who seek compensation for irritant-induced asthma and taking account of the response rate, that more than half will continue to report asthmatic symptoms for many years after what was probably quite a severe inhalational accident, and that more than one third will have persistent airway hyperreactivity. These are useful data. The levels of anxiety and depression in this cohort were quite high, again a feature that will be familiar to experienced physicians and one that raises the question of whether, how, and when psychological treatment might be helpful in improving symptomatic recovery. What is less clear is why some patients fare less well than others. If failure to recover is a consequence of inadequate remodeling after toxic airways damage, then one might expect it to be related to the severity of the initiating injury, or perhaps to its chemical nature. Neither appeared important in this cohort, although its small size will have limited its power to address these issues and retrospective measurements of severity (hospital attendance in this case) are difficult in individual cases. Nonetheless these findings, except in the instance of a very severe exposure, are in accord with the experience of most physicians. On the other hand, youth may be an advantage as is probably the case in other forms of occupational asthma (5). We do not know, and it will be difficult ever to know, whether workers' compensation schemes affect, favorably or otherwise, prognosis, even when they are as generous as that in Quebec. Finding answers to these questions is going to need much larger cohorts of well-characterized patients followed, preferably prospectively, for 5 years or more, which will be a challenge

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