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Do all occupational respiratory sensitisers follow the united airways disease model?
  1. M J Seed,
  2. M Carder,
  3. M Gittins,
  4. R M Agius
  1. Occupational and Environmental Health Research Group, University of Manchester, Manchester, UK
  1. Dr M J Seed, Occupational and Environmental Health Research Group, Faculty of Medical and Human Sciences, University of Manchester, Oxford Road, Manchester M13 9PL, UK; martin.seed{at}

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Castano et al1 applied specific inhalational challenge testing to examine the important relationship between occupational rhinitis (OR) and occupational asthma (OA) in 43 subjects. Using this approach they found that OR occurred in 76.4% of confirmed cases of OA, and this provides strong evidence that the united airways disease model does apply to occupational causation overall. However, as they readily acknowledge, an attempt to stratify this relationship according to whether the causative agent is of high molecular weight (HMW) or low molecular weight (LMW) is limited by the small size of the study population. An epidemiological approach offers a means of complementing the observations from this type of clinical study in order to better characterise how the frequency of rhinitis varies with type of exposure.

National reporting schemes for occupational diseases such as The Health and Occupation Reporting (THOR) network2 in the UK provide data on the causative agents for a large number of cases of OR and OA reported by networks of respiratory and occupational physicians. In a preliminary study we have determined the number of cases of rhinitis (with or without asthma) as a proportion of the total number of cases of rhinitis and/or asthma for the 15 respiratory sensitisers most frequently reported to THOR during the decade 1997–2006.3

The data suggest significant differences in the rhinitis:asthma ratio between the various causative agents. Few, if any, of the cases of OR reported to THOR would have been confirmed by acoustic rhinometry, and their diagnosis is probably based on a history of nasal symptoms, sometimes accompanied by rhinoscopy, which can have poor specificity. This, together with potential reporting biases, limits conclusions that can be drawn from these provisional THOR data. They do, however, raise the possibility that respiratory sensitisers differ in the extent to which they cause rhinitis compared with asthma. This is particularly evident when the rhinitis:asthma ratio is compared for the two most frequently reported respiratory sensitisers—laboratory animals and isocyanates—with a much higher proportion of rhinitis associated with the former.

A number of toxicokinetic factors, such as particle size or solubility, could determine the relative distribution of a sensitiser in the upper and lower airways. Toxicodynamic factors might relate to molecular weight, with the suggestion from the data that higher molecular weight agents might be preferentially associated with rhinitis. The THOR data are consistent with the hypothesis that OR (when in conjunction with OA) is more likely to be caused by sensitisers that cause disease through IgE-mediated mechanisms. On the other hand, LMW agents such as diisocyanates, which may cause OA by non-IgE mechanisms, do not associate strongly with OR. Morphine, which had the highest rhinitis:asthma ratio in our study, may act through direct mast cell degranulation.4 Further clinical and epidemiological research could help to substantiate such mechanistic hypotheses. Castano and colleagues have shown that the united airways disease can apply to occupational causation, but this might not be consistent across the diverse range of respiratory sensitisers.


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  • Competing interests: None.