Restraint has been used as a procedure to study the effects of stress on gestation outcome in rodents. The effects of restraint could potentially be used as a model for the impact of general stress produced by high doses of toxicants and other interventions. In mice, restraint in the peri-implantation period leads to implantation failure, and restraint at appropriate times in organogenesis produces cleft palate, supernumerary ribs, and resorption. In rats, there is some evidence for an association with restraint for implantation failure, but not for the morphological anomalies. Restraint in late gestation alters adult sexual behavior of male rat offspring, but consequences for their fertility are not known. Intrauterine growth retardation is not commonly associated with gestational restraint. In the few studies where they have been directly compared, different restraint procedures produced graded, qualitatively different, or no effects. Adrenocortical hormones have been implicated as mediating the effect of restraint on cleft palate, but not on supernumerary ribs, implantation failure, or sexual differentiation. Given the variety of restraint procedures and the varying species-dependent consequences, it is not possible to infer a generalizable pattern of developmental effects due to gestational stress from the restraint literature. As an alternative approach, contemporary methods in gene expression and developmental biology could profitably be applied to understanding different patterns of stress-mediated effects of toxicant exposures on intrauterine development. Birth Defects Res B 71:26-36, 2004. r 2004 Wiley-Liss, Inc.

Fetal developmental delays, endocrine disruption, and mammary tumors resulted from simazine treatment. Systemic and maternal/fetal effects determined the critical NOELs used in risk assessment. Margins of exposures for most scenarios were below acceptable levels, especially for children who may be bystanders where simazine is applied and children who exhibit pica. This risk characterization raises a concern for long-term effects in humans.

An outbreak of human illnesses associated with West Nile Virus (WNV) occurred in New York City in 1999. Since then, it has gradually spread westwards, reaching northern California for the first time in 2005. WNV is transmitted by several mosquito species and birds serve as the main reservoir. Several control measures have been used, targeting both the aquatic larvae and the adult mosquitoes. In the latter case, roosting birds in trees are sprayed with pyrethroid insecticides because these are highly toxic to mosquitoes, but have low avian toxicity. A request was made to use a resmethrin-containing insecticide during the month of October 2005 in California. Because resmethrin was not registered for use on growing crops, concerns were raised about potential crop contamination. Therefore, an expedited dietary risk assessment was conducted on resmethrin. Developmental toxicity in the rat (NOELs of 25 or 40 mg/kg/day) was used as the acute endpoint and dietary exposure was assessed using the DEEM-FCIDTM computer program. Only crops growing above ground during October were considered. Margins of Safety (MOS) were found to be above 100, the level generally considered to be sufficient to protect public health when using an animal NOEL.

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