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four columns correspond to models tted over 12 hour time periods while the fth column corresponds to models tted over the whole dataset. It is rather interesting to note the huge variations in the value of the discrepancy for all models except the Weibull one. This is another indication that only the Weibull and none of the other models yields a satisfying t even over the different time periods.

The guinea pig intratracheal test has been used to establish the relative potency of different detergent enzymes and establish safe occupational exposure levels As the name implies, guinea pigs are sensitized by intratracheal exposure and induction of cytophilic antibodies are assessed Dose responses obtained for new enzymes are compared to a reference enzyme for which safe exposure levels have been established The relative potency of the new enzyme to this reference is used to establish a safe exposure level for the new enzyme Exposure to certain low (<3000) molecular weight compounds (haptens) has also been associated with the development of occupational asthma Highly reactive compounds such as the diisocyanates or acid anhydrides have the capacity to react with protein and induce an immune response Toluene diisocyanate (TDI) and trimellitic anhydride are the compounds that have been most extensively studied in this regard.

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Target of Inhibition ISG transcription IFNs binding to receptors JAK and/or p48 expression IRF 3 STAT and/or p48

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There is a great deal of interest in developing a test to screen chemicals for this type of effect in order to avoid induction of immune responses that could lead to occupational asthma Although speci c IgE antibodies have been detected in some individuals with TDI asthma, it has not been uniformly present and some of these individuals exhibit the late phase but not the immediate response Hence, unlike proteins, there is less certainty about the mechanisms underlying respiratory allergic responses to low molecular weight compounds Structure activity approaches similar to those described for contact sensitizers have been developed, but this approach has limitations because the database of known respiratory sensitizers is small compared to contact sensitizers and the underlying mechanisms are less well de ned.

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interferon-a (IFN-a)13 In addition, such cultures were impaired in IFN-a production if treated with dsRNA that normally should lead to IFN production13 Basler et al14 reported that Ebola virus protein VP35 blocked dsRNA- and virus-mediated induction of the IFN-stimulated response element reporter gene and also inhibited dsRNA- and virus-mediated induction of the IFN-b promoter Moreover, Ebola virus VP35 protein inhibits activation of the interferon regulatory factor-3 (IRF-3), a key component in the initiation of the host cell interferon response, through inhibition of IRF-3 phosphorylation15 IRF-3 subsequently cannot dimerize and translocate to the nucleus Dengue virus nonstructural proteins NS2A, NS4B, and NS4A have been shown to downregulate IFN-b-stimulated gene19 Table 171 shows the mechanism of action and inhibition for some viruses that target the signaling and transcriptional responses of IFNs Viruses have evolved mechanisms that target products of the IFN pathway and render them ineffective.

At the other extreme guinea pigs have been exposed by inhalation for a number of days, rested, and then challenged at a later date by inhalation with subsequent monitoring of respiratory responses Although this approach has produced a good model of TDI asthma, it is too cumbersome and expensive for routine testing Because the capacity to interact with protein is a pre-requisite to allergenicity, it has been suggested that testing for protein reactivity in vitro could provide an initial screening test for chemicals Also, because it appears that respiratory sensitizers are a subset of chemicals that produce positive results in a contact sensitivity test, it has been suggested that the LLNA test be used as the rst tier in screening chemicals for this effect The problem then becomes separating chemicals that are strictly contact sensitizers from those that have the capacity to cause respiratory sensitization.

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Efforts have been made to determine whether differences in responses to dermal application of these chemicals could provide a means for making this distinction One proposal is to assess total serum IgE following dermal exposure, assuming that respiratory sensitizers would produce a bigger IgE signal Another approach has been to assess cytokine pro les in the draining lymph node following dermal exposure Different subsets of T helper (Th) cells, have been associated with type I immediate (Th2) and type IV delayed (Th1) responses These different populations of T cells are distinguished by different cytokine pro le and efforts are underway to use these differing pro les to distinguish respiratory from contact sensitizers However, there is as yet no well-validated, well-accepted test to assess low molecular weight chemicals for the capacity to induce respiratory allergy This remains a subject of intense research..

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