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Showing papers by "Frederica P. Perera published in 1987"



Journal ArticleDOI
TL;DR: The results support the need for batteries of markers to detect and to quantify the carcinogenic dose to humans resulting from both specific and "background" environmental exposures.
Abstract: In order to validate markers of internal dose and biologically effective dose of carcinogens, a battery of measurements was made on blood samples from 22 smokers and 24 nonsmokers. The markers included immunoreactivity in an enzyme-linked immunosorbent assay (ELISA) quantified in white blood cells with the use of a polyclonal anti-benzo[a]pyrene diol epoxide-I-DNA antibody, 4-aminobiphenyl hemoglobin (4-ABP-Hb) adducts measured by negative chemical ionization mass spectrometry, sister chromatid exchange (SCE) in cultured lymphocytes, and cotinine in plasma measured by radioimmunoassay. Several blood samples were drawn from each subject. In blood samples 1 and 3 having detectable levels of DNA adducts, mean femtomole-per-microgram levels were consistently higher among smokers compared to nonsmokers. The borderline significance of this difference may be attributable to the small numbers of subjects. Consistently higher adduct levels were seen in females compared to males. In sample 3, adduct levels were significantly correlated with measurements of active smoking in smokers and with passive smoking in nonsmokers. By contrast to the ELISA data, which may reflect cumulative exposure from multiple background sources, the 4-ABP-Hb assay was able to distinguish clearly between smokers and nonsmokers. SCEs were significantly elevated in the smokers compared to nonsmokers. Also observed were significant correlations between 4-ABP-Hb and both cotinine and SCEs, as well as a positive correlation between the 4-ABP-Hb and DNA adduct levels (sample 3) that was highly significant. The correlation between DNA and 4-ABP-Hb adducts was significant in smokers but not nonsmokers (sample 3). These results support the need for batteries of markers to detect and to quantify the carcinogenic dose to humans resulting from both specific and "background" environmental exposures.

123 citations


Journal ArticleDOI
TL;DR: The growing body of data regarding carcinogen-DNA and protein adducts as illustrative markers of biologically effective dose of carcinogens illustrates considerable human inter-individual variation in binding and the presence of significant "background" levels ofadducts, which support the absence of human population thresholds for exposure to carcinogens.
Abstract: Substantial data have been generated during the last 5 years in experimental systems and human populations which shed light on the potential usefulness of biological markers in human cancer risk as...

55 citations


Journal ArticleDOI
TL;DR: A review of risk assessment at the Environmental Protection Agency points out the serious lack of toxicological testing data for commercial chemicals and pesticides as well as a disturbing trend toward undue reliance on quantitative risk assessment and cost-benefit analysis.
Abstract: A review of risk assessment at the Environmental Protection Agency (EPA) points out the serious lack of toxicological testing data for commercial chemicals and pesticides as well as a disturbing trend toward undue reliance on quantitative risk assessment (QRA) and cost-benefit analysis (CBA). The apparent precision of quantitative estimates of risk masks the many underlying value judgments and uncertainties. In an attempt to address the uncertainties in QRA, EPA has recently published Guidelines on Risk Assessment for Carcinogens. The Guidelines are generally sound; however, they do not address human variability in response and possible synergistic interactions which can lead in some cases to an underestimate of risk. Moreover, they offer a simplistic carcinogen classification scheme which has already been misused to justify less stringent regulation of waterborne carcinogens. Since 1982, EPA's ever greater use of QRA coupled to CBA has led to relaxed standards or decisions not to regulate certain sources of environmental pollutants such as benzene and radionuclides. Risk managers should not be seduced by the precision of the numbers into using QRA and CBA as the primary tool in setting public health policy. When estimated risk is inserted into a cost-benefit analysis under “benefits” or cancers avoided, its own uncertainties are compounded by those regarding the true economic impacts of the regulation.

6 citations