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Showing papers by "Frederica P. Perera published in 1988"


Journal ArticleDOI
TL;DR: IntroductIOn 255 Methods and human appllcnion, biological rationa/.
Abstract: IntroductIOn 255 Methods and human appllcnion, 256 Biological rationa/., for adduct measurcmcnh 257 Car..:inogcn expo,ure and DNA/protein adduct" 'dIN:-response' 258 Observed rciationship hCl"een adduct, and induction o[ gene mutation 260 Quantitative relationshiP between DNA adducts and can:inogeniCltv 261 Relallonship hct"'cell adduct> and specics or tissue susceptibility, 262 Possihle factors determining carCinogenic effect nf adducts , , 263 Condusion 264

125 citations


Journal ArticleDOI
TL;DR: The assumptions and data set upon which the HERPs were based were analyzed, concluding that such a simplified approach to set public health policy is inappropriate given the underlying uncertainties.
Abstract: In 1987, investigators concluded that the risks of man-made industrial carcinogens and pesticides (outside of the workplace) are trivial compared with the risks of naturally occurring carcinogens found mostly in the diet. They used a ranking system based on human exposure and rodent potency (HERP) data to arrive at this conclusion. As a result, they recommend that regulatory agencies, such as the Environmental Protection Agency and the Food and Drug Administration, base their priorities in this area on their HERP system. We analyzed the assumptions and data set upon which the HERPs were based, concluding that such a simplified approach to set public health policy is inappropriate given the underlying uncertainties. However, we note that when comparisons are consistently based on estimates of average daily exposure to common carcinogens, the HERP scores of many man-made pollutants are comparable to those of naturally occurring carcinogens in the diet.158 references.

27 citations


Journal ArticleDOI
11 Mar 1988-Science

11 citations


Book ChapterDOI
01 Jan 1988
TL;DR: The actual amount of carcinogen that has interracted with target cellular molecules such as DNA, RNA, or protein is found to be the biologically effective dose of the carcinogenic substance.
Abstract: Traditionally, the field of chemical carcinogenesis has relied upon estimates of adminis tered dose and/or human exposure in constructing dose-response curves and assessing cancer risk. Of far greater relevance to risk is the actual amount of carcinogen that has interracted with target cellular molecules such as DNA, RNA, or protein—the biologically effective dose of the carcinogenic substance.

8 citations