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Reproductive toxicity stillbirths

The reproductive toxicity of high-level lead exposure is well known and supported by an extensive literature (Rom, 1976). Much of this literature focuses on an increased incidence of spontaneous abortions and stillbirths associated with lead exposures in the workplace (Oliver, 1911 Lane, 1949). Based on a renewed awareness of these earlier findings, women have been largely excluded from occupational lead exposure. Therefore, exposures have declined and the attention of researchers and regulatory agencies has shifted to more subtle manifestations of lead-related reproductive toxicity in the general population. [Pg.307]

As already described earlier, NHP also experience significant loss at term and shortly thereafter [45], Hence in a pre-/postnatal toxicity study overall reproductive failure (prenatal loss, stillbirth, neonatal and infant death) can amount to 40% or even 50% losses in single experimental groups. For developmental toxicity studies naive animals are frequently requested. Female animals with proven fertility and breeding experience might improve this... [Pg.391]

SAFETY PROFILE A poison by intravenous and subcutaneous routes. Moderately toxic by ingestion and intraperitoneal routes. Human teratogenic effects by an unspecified route developmental abnormalities of the central nervous system effects on embryo or fetus fetal death, extra embryonic structures. Human reproductive effects by an unspecified route stillbirth. An experimental teratogen. Experimental reproductive effects. Human mutation data reported. When heated to decomposition it emits acrid smoke and irritating fumes. [Pg.1173]

This chapter presents the toxicological evidence for lead as a potent reproductive and intrauterine developmental toxicant. Sections of the chapter deal with male and female gametotoxicity, embryotoxicity, fetotoxicity, and various gross indices of fetal injury such as spontaneous abortion, stillbirth, and neonatal survival. Prenatal developmental effects as they affect the whole organism are presented here, while prenatal effects on various systems and organs are discussed in system- and organ-specific chapters. For example, developmental neurotoxicity of lead as it occurs in utero is discussed in Chapter 12. [Pg.537]

By the first decade of the twentieth century, recognition of reproductive and prenatal harm and subsequent responses greatly reduced the adverse effects of lead in utero during worker pregnancies through constraints on women of childbearing age in the lead workplace. In particular, the prevalence and incidence of such gross Pb toxicity outcomes as spontaneous abortions, stillbirths, and depressed early natal survival declined markedly. [Pg.537]


See other pages where Reproductive toxicity stillbirths is mentioned: [Pg.555]    [Pg.1571]    [Pg.47]    [Pg.856]    [Pg.978]    [Pg.407]    [Pg.123]    [Pg.401]    [Pg.44]    [Pg.246]    [Pg.263]    [Pg.1208]    [Pg.35]    [Pg.195]    [Pg.144]    [Pg.341]    [Pg.474]    [Pg.113]    [Pg.371]    [Pg.308]    [Pg.50]    [Pg.39]   
See also in sourсe #XX -- [ Pg.537 , Pg.540 , Pg.541 ]




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Reproductive toxicants—

Stillbirth

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