By Michael J. Parnham (auth.)
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Additional resources for Advantages and Problems with Non-Opioids in Pain Management: Vancouver, Canada, August 19, 1996
DG-N2-BPDE was the major adduct detected. The adduct levels in fetal tissues increased with benzo[a]pyrene dose, but at a much lower rate that placentae or maternal livers. Preference in binding to DNA of various fetal tissues was more apparent in early gestation compared to late gestation, and at lower doses compared to higher doses. During early gestation and at lower doses, benzo[a]pyrene produced a similar level of DNA binding in fetal lung, liver, maternal liver, and placenta. Individual fetal organ adduct levels correlated significantly with placental adduct levels, indicating placental and/or maternal contribution to adduct formation in fetuses.
Male and female mice were exposed to 0, 175, 350, or 700 mg/kg/day acenaphthene by gavage for 13 weeks (EPA 1989c). No signs of cardiovascular distress were seen during life for any dose group, and no gross or microscopic damage was seen upon necropsy. Similar findings were reported after 13-week administration of 1,000 mg/kg/day anthracene, and 500 mg/kg/day fluoranthene, or 500 mg/kg/day fluorene (EPA 1988e, 1989d, 1989e). Gastrointestinal Effects. Minimal information is available on the gastrointestinal effects of human oral exposure to PAHs.
Intermittent gavage exposure of mice to 67-100 mg/kg benzo[a]pyrene resulted in increased forestomach (100%) and pulmonary tumor incidences relative to controls at 30 weeks of age (Sparnins et al. 1986; Wattenberg and Leong 1970). 0 mg of benzo[a]pyrene once a week for 8 weeks. 3 mg/kg/day) for 30-197 days (Neal and Rigdon 1967, see Table 2-2). The tumor incidence also increased with increasing dose. 48 mg) did not develop tumors. The authors suggest that these findings provide evidence that there are no cumulative carcinogenic effects of benzo[a]pyrene or its metabolites in mice.