DOSE PARADIGMS FOR INHALED VAPORS OF PRIMARY CARCINOGENS AND THEIR IMPACT ON RISK ASSESSMENT

Notice - This site contains archived material(s)

Archive disclaimer
Archive disclaimer
Archived files are provided for reference purposes only. These files are no longer maintained by the Agency and may be outdated. For current EPA information, go to www.epa.gov. It is EPA's policy to support reasonable accommodation to persons with disabilities, pursuant to the Rehabilitation Act of 1973, 29 U.S.C. 791. If you need assistance with accessing archived files, contact EPA's Reasonable Accommodations or submit a request using the Contact Us form.


Abstract

In the assessment of risk, several factors affect predictions: election of reactive agent, selection of tumor incidence data, modeling of dose, scaling across species, adjustment for differences in duration and frequency of exposure, and selection of the most suitable risk extrapolation model. f the end points, exposure regimen, and the model for risk extrapolation are constant, then the review of dose paradigms will illustrate the effect of dose modeling on risk, since by definition the reactive agent is the primary carcinogen. he response incidence in lifetime inhalation bioassays of two primary carcinogens, ethylene oxide and formaldehyde, was used with different dose paradigms to estimate risk from maximum lifetime occupational exposures. he dose paradigms that will be considered include: oncentration, concentration time product, retained dose, integrated blood concentration, and tissue exposure. he basis for across-species scaling and the assumptions underlying each dose paradigm were discussed.

Citation

Beliles, R. AND J. Parker. DOSE PARADIGMS FOR INHALED VAPORS OF PRIMARY CARCINOGENS AND THEIR IMPACT ON RISK ASSESSMENT. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-89/494 (NTIS PB91149815).

Additional Information

Journal of the Health Physics Society 57(1):333-340, 1989