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Reproductive toxicology developmental effects

CERHR (2003) National Toxicology Program—Centre for the Evaluation of risks to human reproduction. Monograph on the Potential Human Reproductive and Developmental Effects of Di-Isodecyl Phthalate (DIDP). NIH Pub No. 03-4485. US Department of Health and Human Services, April 2003. http //ntp.niehs.nih.gov/ntp/ohat/phthalates/didp/DIDP Mono-graph Pinal.pdf... [Pg.332]

Toxicology. Dibutyl phthalate (DBP) is of low-order acute toxicity reproductive and developmental effects have been reported in animal studies. [Pg.217]

DART is a bibliographic database that covers the literature on teratology and other aspects of reproductive and developmental toxicology. DART is an essential resource to the Navy for gathering information on the potential reproductive and developmental effects of agents because it greatly simplifies the process for searching for literature in this area. [Pg.115]

National Toxicology Program Center for the Evaluation of Risks to Human Reproduction Monographs on the Potential Human Reproductive and Developmental Effects of di-isodecyl phthalate, di-n-octyl phthalate, di-n-hexyl phthalate, hutyl henzyl phthalate, di-isononyl phthalate and di-n-hutyl phthalate. Available at http //cerhr.niehs.nih.gov/ Accessed August 8, 2003. [Pg.554]

Lead induces reproductive and developmental effects in laboratory rats after gestational or lactational exposure. Many of the effects occur in a concentration-dependent manner and have been observed at maternal BLLs that do not result in overt maternal toxicity (under 40 pg/dL). Animal studies have further demonstrated that effects of lead exposure during early development include impairment of retinal development and alterations in the developing hematopoietic and hepatic systems. Toxicology studies in male animals have reported de-... [Pg.103]

National Toxicology Program (NTP). NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Styrene. NIH Publication 06-4475. Eeb. 2006 2006. [Pg.253]

As it was stated earlier, many studies have suggested that PAEs and their metabolites produce reproductive and developmental toxicities in laboratory animals. Although the most of these animals were exposed to PAEs at relatively high level to exam toxicological effects, some studies showed that relatively low doses of PAEs caused toxic effects [88, 117, 118]. Thus, there is a question of whether humans are exposed to PAEs at a severe enough level to generate human health effects. [Pg.319]

Hood RD, MiUer DB (2006) MaternaUy-mediated effects on development. In Hood RD (ed) Developmental and reproductive toxicology, a practical approach, 2nd edn. CRC, Boca Raton, pp 93-124... [Pg.324]

Results of acute, short-term and long-term toxicity studies, reproduction studies, developmental studies, genotoxicity studies, and studies of the toxicity of metabolites and impurities, and other adverse effects. Data on human toxicology, the no observable effect level, acceptable daily intake, and proposed and safety directions... [Pg.377]

Previous reproductive toxicology studies in laboratory animals examining the effects of prenatal exposure to fumonisin demonstrated a potential risk to the developing fetus. Studies using an aqueous extract of contaminated maize-culture material of F. verticillioides reported that fumonisin was developmentally toxic in hamsters (Floss et al., 1994 Penner et al., 1998). In addition, purified fumonisin Bi was shown experimentally to cause fetal toxicity in rats and mice (Collins et al., 1998 Reddy et al., 1996). In another study, pregnant CD1 mice treated with a semipurified extract... [Pg.155]

The survival of all species depends on the integrity of its reproductive system. Reproductive toxicology may be defined as the study of the effects of physical and chemical agents on the reproductive and neuroendocrine systems of adult males and females, as well as those of the embryo, fetus, neonate, and prepubertal animal. This chapter focuses primarily on the potential sites of toxic insult in the reproductive systems of adult mammals, the biochemical mechanisms of such toxicants, and the manifestations that may result. The latter part of the above definition is a subspecialty of developmental toxicology (Chapter 34) and is discussed only in brief. [Pg.805]

Pharmacokinetic studies in reproductive and developmental toxicology are most useful if they are conducted in animals during the stages in which reproductive and developmental insults occur. The correlation of pharmacokinetic parameters and reproductive and developmental toxicity data might enhance our understanding of both the effects observed and of their predictive value (Kimmel and Young 1983 Hansen et al. 1999). [Pg.67]

When assessing manifestations of toxicity, evaluators might base their conclusions about relevance on the mechanism that produces a toxicological effect however, a basic default assumption is that any manifestation of reproductive or developmental toxicity is relevant to humans unless the mechanism by which it occurs is impossible in humans. For example, if a toxic effect occurs in animals through an inhibition of folic acid synthesis, that effect would not be considered relevant for humans because humans do not synthesize folic acid. It is unusual, however, to have such detailed knowledge about mechanisms of toxicity from experimental animal studies. [Pg.88]


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