Fetal death

In laboratory tests, appHcation of DMAC to the skin of pregnant rats has caused fetal deaths when the dosages were close to the lethal dose level for the mother. Embryonal malformations have been observed at dose levels 20% of the lethal dose and higher. However, when male and female rats were exposed to mean DMAC concentrations of 31,101, and 291 ppm for 6 h per day over several weeks, no reproductive effects were observed (6). 

Animal data consistently show dibutyltin dichloride to cause dose-dependent developmental toxicity, such as fetal deaths, birth defects, and reductions in fetal weight. 

Arbuckle TE, Sever LE. 1998. Pesticide exposures and fetal death A review of the epidemiologic literature. Crit Rev Toxicol 28 229-270. 

It is known that an association exists between maternal UTI during pregnancy and fetal death, mental retardation, and developmental delay.24 Because of this known association, and because up to 7% of pregnant women have an asymptomatic bacteriuria that may progress to pyelonephritis, screening is necessary. In patients with significant bacteriuria, whether symptomatic or asymptomatic, treatment is recommended to avoid the complications discussed above. In the majority... 

Decreased fetal weight and increased fetal death were reported following single intravenous injection of pregnant rats with 241Am (activity level 90 pCi/kg or 3,330 kBq/kg) on gestation day 9 (Rommerein and Sikov 1986). The investigators indicated a tendency toward increased incidences of fetuses with anomalous ribs. 

Information on the transplacental transfer of americium in humans is not available directly, but the information from experiments with americium and other actinides has been used to derive biokinetic models and perform dosimetric models for the human (NCRP 1998 NRC 1996 Sikov and Kelman 1989). Studies in animals that received parenteral injections of americium have shown that absorbed americium is transferred to the fetus (Hisamatsu and Takizawa 1983 Paquet et al. 1998 Sasser at al. 1986 Schoeters et al. 1990 Weiss et al. 1980) (see Section 3.4.2.1). Limited reports indicate that241 Am may induce fetal death and teratogenic effects in rodents (Moskalev et al. 1969 Rommerein and Sikov 1986). 

Adverse effects of copper deficiency can be documented in terrestrial plants and invertebrates, poultry, small laboratory animals, livestock — especially ruminants — and humans. Data are scarce or missing on copper deficiency effects in aquatic plants and animals and in avian and mammalian wildlife. Copper deficiency in sheep, the most sensitive ruminant mammal, is associated with depressed growth, bone disorders, depigmentation of hair or wool, abnormal wool growth, fetal death and resorption, depressed estrous, heart failure, cardiovascular defects, gastrointestinal disturbances, swayback, pathologic lesions, and degeneration of the motor tracts of the spinal cord (NAS 1977). 

Pregnant females given single intrauterine injection Smaller litters, increased fetal deaths 15... 

Dose-related increase in fetal deaths and malformations... 

Arsenic can traverse placental barriers as little as 1.7 mg As+5/kg body weight at critical stages of hamster embryogenesis, for example, can produce fetal death and malformation. 

Permethrin may behave like estrogen in females but antiandrogen in males when administered to immature female and male rats at 10-800 mg/kg [154]. Treatment of rats with permethrin at 10 mg/kg/day during gestation produced fetal death and feminization of male fetuses [155]. Reductions in sperm count and motility and in serum testosterone were noted in a 6-week repeated dose study in mice at 35 mg/kg/day. Permethrin may cause mitochondrial membrane impairment in Leydig cells, resulting in inhibition of testosterone biosynthesis [156]. 

Inversions. When two breaks occur in the same chromosome, the portion between them is detached and becomes reinserted in the opposite way to its original position, that is, the gene order is reversed. This need not cause a genetic problem, but imbalanced gametes could result in congenital malformation or fetal death. 

Khera, K.S. (1985). Maternal toxicity A possible etiological factor in embryo-fetal deaths and fetal malformations of rodent-rabbit species. 

Abortion in pregnant cattle is frequently reported but exact amounts and mechanism of action is not fully understood. The fetus is particularly susceptible to hypoxia induced by the methemoglobinemia. Fetal death and abortion may occur at any stage of pregnancy because of the decreased fetal oxygen and the limited ability of the fetus to metabolize nitrate (Knight and Walter, 2001). 

In a dominant lethal assay, eight male Charles River CD-I mice received single oral doses of 7.5 or 15 mg/kg of a heptachlor heptachlor epoxide mixture (25% 75%) and were bred with three untreated females each week for 6 weeks (Arnold et al. 1977). No adverse effect on the reproductive capacity of male mice was noted therefore, the NOAEL was 15 mg/kg. A LOAEL was not established. Both heptachlor and heptachlor epoxide were also tested separately in another dominant lethal assay in mice. Heptachlor was tested at 5 and 10 mg/kg and heptachlor epoxide at 8 mg/kg/day. Neither agent produced early fetal deaths or preimplantation losses outside the control limits (Epstein et al. 1972). 

Mechanical prosthetic heart valves The use of enoxaparin injection has not been adequately studied for thromboprophylaxis or long-term use in patients with mechanical prosthetic heart valves. Isolated cases of prosthetic heart valve thrombosis have been reported in patients with mechanical prosthetic heart valves who have received enoxaparin for thromboprophylaxis. Some of these cases were pregnant women in whom thrombosis led to maternal and fetal deaths. Frequent monitoring of peak and trough anti-Factor Xa levels and dose adjustment may be needed. 

Reports, primarily from Brazil, of congenital anomalies and fetal death subsequent to use of misoprostol alone, as an abortifacient, have been received. 

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