DNA adducts, protein adducts, and sister chromatid exchange in cigarette smokers and nonsmokers.

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.

A dose-response model incorporating nonlinear kinetics.

This paper introduces a dose-response model for toxic quantal response data based on hit theory applied to the dose unit as transformed by a nonlinear kinetic equation. When spontaneous background response is included in the model, the resulting dose-response model has four parameters. The maximum likelihood estimators and their large-sample properties are given.

Assessing the power and quality of epidemiologic studies of asbestos-exposed populations.

This paper briefly discusses criteria for evaluating epidemiologic studies for risk assessment purposes, using asbestos as an example. Asbestos is one of the few carcinogens for which substantial data exist on exposures to humans. However, there are major difficulties in using these data for conducting risk assessments.

Risk assessment for fetal toxicity.

This paper reviews the problem of performing risk assessments using data on fetal toxic effects. It briefly discusses the usual dose-response models and their inappropriateness for application to such data. The paper then considers tests for determining whether the fetal toxic effect is increased over that of the control group.