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1985 H M (focal areas of highly vocuolated cells, elevated serum glutamic oxaloacetic transaminase) Vernot et al. 1985 H Reproductive 37 Rat (Fischer-344) 1 yr 5 d/wk 6 hr/d 5 B (atrophy of the ovaries and inflammation of the endometrium and uterine tube) Vernot et al. 1985 H TABLE 2-1. 25 M Less serious (ppm) Serious (ppm) Reference Chemical Form 1 M (senile testicular atrophy) Vernot et al. 1985 H Cancer a 39 Rat (Fischer-344) 1 yr 5 d/wk 6 hr/d 1 M (CEL: nasal adenomatous polyps in males) 5 M (CEL: thyroid carcinoma in males) Vernot et al.

1979). Although these data are limited, they suggest that fetal development is not adversely affected by hydrazine or 1,2-dimethylhydrazine. These NOAEL values for developmental effects resulting from oral exposure to hydrazines are recorded in Table 2-2 and plotted in Figure 2-2. 7 Genotoxic Effects No studies were located regarding genotoxic effects in humans after oral exposure to hydrazines. Alkylation of liver DNA was reported in rats acutely exposed to 30–90 mg/kg hydrazine for 1–3 days (Becker et al.

Although the levels of hydrazine and 1,1-dimethylhydrazine exposure were not determined, these studies indicate qualitatively that the liver is a target for both hydrazines. 5 weeks, cytoplasmic degeneration of the liver was observed (Haun 1977). Hemosiderosis of the spleen was observed in dogs exposed intermittently to 5 ppm 1,1-dimethylhydrazine for 26 weeks, and the same effect was observed in the Kupffer cells of the liver after exposure to 25 ppm for 13 weeks (Rinehart et al. 1960). Dogs exposed to 5 ppm 1,1-dimethylhydrazine for 6 months showed transitory increases in serum glutamic pyruvic transaminase (SGPT) levels which returned to normal during the postexposure recovery period (Haun et al.

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