Reply

Dr Barber and colleagues propose that the changes in peak expiratory flow (PEF) which we found in workers with allergic alveolitis were more likely to be due to reversible airflow obstruction than to parallel reductions in lung volumes due to restriction which we proposed. They cite frequently found biopsy evidence of bronchiolitis, the mosaic attenuation on high-resolution computed tomography (HRCT) and the obstructive spirometry found in some case series. They cite a body of evidence demonstrating asthma in some patients with extrinsic allergic alveolitis (EAA).

We agree with much of this. Bronchiolitis is often found on lung biopsies, sufficient for many to prefer the term bronchiolar-alveolitis, and this may manifest as air trapping in acini seen as mosaic attenuation on HRCT. This was the most common CT abnormality of EAA seen in our series [1]. We also agree that asthma may co-exist with allergic alveolitis, with the same cause. We believe that this was probably the case in one of our workers who had immediate reactions at work with additional evidence of alveolitis; we do, however, have problems in attributing all the changes in PEF to reversible airflow obstruction (i.e. asthma). Mead describes the bronchioles as the ‘silent area’ of the lung as changes there were barely represented by spirometry or PEF, so any airflow obstruction that might result from the bronchiolitis would be an unlikely cause for reduced PEF [2]. The PEF changes that we presented changed over hours, also unlikely if this was due to airflow obstruction in the small airways with the occlusive changes often seen histologically.

If airflow obstruction is the cause of the PEF changes, there should be other evidence of airflow obstruction. Stănescu found that the best measures independent of spirometry are a raised total lung capacity (TLC) and residual volume (RV), and a raised RV/TLC ratio [3], a value >40% is usually taken to represent air trapping. We have contemporary lung volume measurements in 14/16 of the workers with allergic alveolitis in our paper [4], shown in Table 1 (the worker with co-existing asthma was one of the two with missing values). These results provide no evidence of airflow obstruction in the allergic alveolitis group. We therefore stand by our original conclusions that the majority of the changes in PEF shown in the allergic alveolitis group were due to reductions in lung volume rather than co-existing asthma. It is, however, interesting that the magnitude of the changes in PEF seen were similar in both groups, but that the immediate and flat hourly reactions were a feature of the asthmatic rather than the alveolitic group. Serial measurements of PEF remain a valid method of identifying the source of allergic alveolitis as well as their more usual use for identifying the cause of asthma.

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