IARC monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans

insignificant); one individual was allergic to mice and one to guinea pigs and IgE antibodies to allergens from these species were not tested; two had skin reactions only (one very mild) and two had mild nasal symptoms only. We would also emphasise that this retrospective group was chosen from individuals who in a previous survey had reported allergic symptoms and our comments about increased antibody levels referred only to this group and should not be taken to indicate that the statement is necessarily true of a larger, controlled population. Even with this proviso our results do not support the statements made by Newman Talor et al in their abstract that "these findings suggest that the immunological mechanisms responsible for asthmatic reactions to laboratory animals are different from those involved in rhinitis and urticaria." ' We fail to see the point of the last paragraph of their letter. There was no intention to conceal anything. The prospective group is, as stated, a clearly defined population of individuals during their first year of employment. We agree that it is crucial to know if those with specific IgE are at particular risk of developing asthma, and this is one of the reasons for the continuing study referred to in our paper. Slovak and Newman Taylor seem to be reading more into our results than is justified from the defined nature of the study. We also agree that the development of specific IgE could become a valuable monitor and that skin prick test conversion may be a significant marker. We are seeking scientific evidence for these assertions. We should further point out that although our observations were "made on a volunteer sample" there was a 100% response; all individuals who began employment during the study period agreed to take part.