Abstract

CD-1 mice were continuously exposed to ozone (O3) from 6 days before the formation of breeding pairs to Day 17 of pregnancy. The concentrations used were 0, 0.2, 0.4, and 0.6 ppm; the lowest-observed-effect levels for eye irritation and respiratory function are in the range of 0.08–0.2 ppm for both humans and animals (47). Ozone failed to produce significant effects on either reproductive performance, postnatal somatic and neurobehavioral development (as assessed by a Fox test battery) or adult motor activity (including within-session habituation). In social interaction tests performed in the pre-juvenile period (23–25 days) and the juvenile period (43–45 days), social response endpoints were not modified in O3 mice, but exploration and self-grooming showed concentration dependent effects (decrease and increase, respectively). Performance at 84–98 days in an eight-arm radial maze with water reinforcement was initially impaired in O3 mice, but the results were not entirely consistent; e.g., the data failed to show a concentration dependence of the effects. Overall, the data confirm previous results of an experiment with more limited exposure [pregnancy Days 7–17 (6)] by showing that prenatal O3 exposure, even when extended to include a period before the start of pregnancy and the preimplantation phase, does not produce major or widespread somatic and neurobehavioral effects. Some of the results, however, point to subtle or borderline behavioral deficits which deserve to be considered both in further animal experiments and in the assessment of risk to developing humans. In fact, the latter are often exposed to O3 concentrations which exceed the lowest-observed-effect levels indicated above as well as those of the prolonged exposure guideline in WHO recommendations [0.05–0.06 ppm (47)].

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