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Embryos/fetuses

NCRP. 1998. Radionuclide exposure of the embryo/fetus. Bethesda, MD National Council on Radiation Protection and Measurements. NCRP REPORT No. 128. [Pg.252]

Sensitivity of the immune system to Pb appears to differ across life stages, and studies in rodents suggest that the gestational and neonatal periods are the most sensitive. Compared to adults, the increased dose sensitivity of the embryo-fetus would appear to fall in the range of 3-12X depending upon the immune endpoint considered. Recent studies have suggested that exposure of embryos to Pb producing neonatal BLLs below 10 pg/dL can also produce later-life immunotoxicity (Table 12.2). Furthermore,... [Pg.218]

Studies in animals suggest that, unlike some other phthalate esters, the potential for adverse reproductive or developmental effects following exposure to di-n-octylphthalate by the route most relevant to human exposure (oral) is very low (Foster et al. 1980 Gray and Butterworth 1980 Hardin et al. 1987 Heindel et al. 1989 Mann et al. 1985 Morrissey et al. 1989 NIOSH 1983 NTP 1985 Oishi 1990 Oishi and Hiraga 1980). Therefore, it does not appear that individuals of child-bearing age or embryos/fetuses are likely to be unusually susceptible to the effects of di-n-octylphthalate. No other information is available on populations with above-average susceptibility to di-n-octylphthalate. [Pg.69]

Generally, it appears that effects of xenobiotics on organs or endpoints may be similar in children and adults, e.g., liver necrosis observed in adults will also be observed in children. As regards toxicodynamics, age-dependent differences are primarily related to the specific and unique effects that substances may have on the development of the embryo, fetus, and child in that the physiological development of the nervous, immune, and endocrine/reproductive systems continues until adolescence (12 to 18 years). Furthermore, receptors and other molecular targets for various xenobiotics are continuously developing during the embryonic, fetal, and infant periods. This may cause age-dependent differences in the outcome of receptor-xenobiotic interactions and even result in opposite effects of xenobiotics in infants and adults. The available data are insufficient to evaluate... [Pg.245]

The placenta plays an important role in the development of the embryo/fetus, and therefore macroscopic evaluation of the placenta... [Pg.49]

Indications of maternal toxicity include mortality or morbidity, clinical signs, reduced body weight gain, reduced food consumption, and differences in organ weights and organ/tissue lesions. Slight maternal toxicity does not necessarily result in developmental effects on the embryos, fetuses, or pups. Severe maternal toxicity, however, will always impact on the litter. [Pg.78]

Quality Assurance and Measurement in Diagnostic Radiology Radiation Exposure and Potentially Related Injury Radiation Received in the Decontamination of Nuclear Facilities Guidance on Radiation Received in Space Activities Effects of Radiation on the Embryo-Fetus... [Pg.165]

Chemicals that cross the placental barrier can act directly on the embryo/fetus, and it is likely that the majority of chemicals that cause developmental toxicity act in this way. Teratogenic chemicals are most likely to act directly on the fetus. Some chemicals cause maternal toxicity at high doses but interfere with embryonic or fetal development at lower doses, and these chemicals are of concern in reproductive toxicology. Many of the most widely recognized embiyotoxic or teratogenic chemicals are selectively active in this manner, and the dose that causes developmental toxicity can be much lower than the dose that is toxic to the mother (Khera, 1984). [Pg.91]

Embryotaxicity (Fetotoxicity) Injury to the embryo (fetus), which may result in death or abnormal development or growth alteration. [Pg.170]

Although embryos, fetuses, and nursing infants may be exposed to relatively high amounts of PBBs and PBDEs during sensitive periods of development, it is not known if the susceptibility of children to the health effects of these chemicals differs from that of adults. Younger children may be particularly... [Pg.237]

Alterations to the development of the embryo, fetus, or neonatal animal, either morphological or functional, and caused by chemicals is termed "developmental toxicology." The result may involve interference with normal growth, homeostasis, development, differentiation, and/or behavior. [Pg.237]

Radionuclide Exposure of the Embryo/Fetus (1998) Recommended Screening Limits for Contaminated Surface Soil and Review of Factors Relevant to Site-Specific Studies (1999) Biological Effects and Exposure Limits for Hot Particles (1999) Scientific Basis for Evaluating the Risks to Populations from Space Applications of Plutonium (2001)... [Pg.413]

As noted above, the lowest effective doses in adults and young are often similar. However, the type and severity of effects from an exposure may be very different. This becomes an important consideration, especially in evaluating prenatal animal studies. Because the developing embryo/fetus is exposed in the maternal animal, it has been argued that if maternal toxicity is observed, any developmental toxicity could be due to the compromised maternal system. However, several issues should be considered. The difference between the lowest maternally toxic dose and the developmentally toxic dose may at times be related to the relative thoroughness with which endpoints are evaluated in dams and offspring, as well as to the sensitivity of the end-points. Moreover, the severity of the effects must be considered the developmental effects may be permanent, while the maternal effects may be reversible. From a risk assessment perspective, developmental toxicity in the presence of maternal toxicity cannot be simply considered secondary to maternal toxicity and discounted (USEP A, 1991). [Pg.235]

The incidence of prenatal loss in the marmoset was 17%, and losses were detected between GD 36 and GD 102 [40]. Prenatal loss consistently affected all embryos/fetuses per female. Heger and colleagues reported a 20% to 35% postimplantation loss in the marmoset [50]. [Pg.391]

Embryo/fetus Occupational exposure during entire pregnancy 0.5... [Pg.195]

The inclusion of different patient populations reveals regional differences, especially for women with child bearing potential. There is a high level of concern for unintentional exposure of an embryo/fetus. [Pg.773]

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]

The maternal capacities that provide a homeostatic environment and metabolic deactivation of potential toxicants, along with the repair and regenerative capabilities of the embryo/fetus, are believed to impart a threshold phenomenon to developmental toxicity. The supposition of a threshold implies that a maternal dose exists at which a toxicant will elicit no adverse effect on the conceptus. This is in contrast to the threshold principle of carcinogenesis, which assumes that exposure to any amount of carcinogen, even a single molecule, can potentially lead to cancer. [Pg.841]

When conducting an evaluation of an agent for potential reproductive and developmental toxicity, the Navy should assess several types of data human exposure data, general toxicity data in humans and experimental animals, and reproductive and developmental toxicity data in humans and experimental animals. Complete assessments should consider potential adverse effects on the male and female reproductive systems and on the embryo, fetus, and child. [Pg.31]

Human exposure data are evaluated to identify populations that might be exposed, to identify potential pathways of exposure, and to estimate the range of exposure so that quantitative estimates of exposure can be made that are associated with each pattern of use. Exposure conditions that are unique for reproductive and developmental toxicity should be considered because the embryo, fetus, neonate, juvenile, young adult, and older adult differ in susceptibility. Human exposure data are important for accurate evaluation of the risk potential of an agent, but data of sufficient quality and quantity are often unavailable. [Pg.31]

Seizures, even mild seizures, may cause harm to the embryo/fetus... [Pg.4]


See other pages where Embryos/fetuses is mentioned: [Pg.332]    [Pg.369]    [Pg.43]    [Pg.319]    [Pg.417]    [Pg.56]    [Pg.39]    [Pg.92]    [Pg.431]    [Pg.431]    [Pg.431]    [Pg.415]    [Pg.262]    [Pg.88]    [Pg.138]    [Pg.239]    [Pg.157]    [Pg.169]    [Pg.372]    [Pg.360]    [Pg.36]    [Pg.38]   
See also in sourсe #XX -- [ Pg.909 , Pg.911 ]




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