Conscious Hartley guinea-pigs were sensitized with trimellitic anhydride (TMA) or trimeric hexamethylene diisocyanate biuret (Des-N) by repeated intradermal injections or by inhalation exposure. Immediate- and delayed-onset pulmonary reactions were recorded during/after challenges with the hapten or protein conjugate of the hapten, respectively. The positive control was sensitized and challenged with ovalbumin (OA) by inhalation. Homocytotropic antibodies of the IgG1 type were determined to correlate antibody titres and pulmonary responses. Immediate-onset pulmonary reactions were apparent in guinea-pigs sensitized by inhalation of TMA and OA. Animals sensitized intradermally with TMA demonstrated more vigorous immediate-onset reactions than animals sensitized by inhalation. The measurement of breathing parameters demonstrated that the ability to detect immediate-onset airway hyperreactivity was best when the breathing rate and tidal and minute volumes were measured. None of the measurements for delayed-onset reactions presented conclusive results, since sensitized as well as naive guinea-pigs demonstrated a delayed increase of breathing frequency. Antigen-specific IgG1 antibodies were several orders of magnitude higher in intradermally sensitized animals compared with animals sensitized by inhalation. Although Des-N-sensitized guinea-pigs experienced high IgG1-antibody titres, no response of pulmonary hypersensitivity could be elicited after hapten or conjugate challenge. In summary, it would appear that pulmonary hypersensitivity depends on factors other than IgG1 antibody titres. For the screening of chemicals, the dermal induction and inhalation challenge protocol was revealed to be more sensitive than the inhalation induction and inhalation challenge protocol.

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Abstract. In acute and subehronie inhalation studies rats were exposed to trichloroethylene. During the 4-h exposures the concentration was about 50 ppm to 3t60 ppm and more, and in the 14-week study (8 h/day) within the range of the MAC (50 ppm). The behavior of triehloroethylene and its metabolites (chloral hydrate, trichloroethanol and trichloroacetic acid) in the expired air, blood and urine was investigated. For this purpose, analytical methods were developed.With the exception of elevated liver weights, the exposure to a trichloroethylene concentration of 55 ppm over a period of 14 weeks did not cause any p~hologieal changes. The liver enlargement as a consequence of an enzyme induction is discussed. Trichloroethylene was not detectable in the blood, and the concentrations of trichloroethanol and chloral hydrate were not altered significantly. The urinary triehloroethanol excretion increased until the 10 th week and then decreased slowly. In contrast, the trichloroacetic acid remained fairly constant. Corresponding results of the ratio TCE: TCA were found.

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