Grant Number:	5R01CA074413-04 Interpret this number
Primary Investigator:	Herrick, Robert
Organization:	Harvard University (Sch Of Public Hlth)
Project Title:	Identification and Control of Cancer Risk
Fiscal Year:	2000

DESCRIPTION: (Adapted from Applicant's Abstract). The major goal of this study is to test the hypothesis that the excess cancer risk among asphalt workers is a result of their occupational exposure, and to assess the role of asphalt exposure as a cancer risk. In addition to investigating the degree to which the observed marker for cancer risk is attributable to occupational asphalt exposure, the relative importance of inhalation and dermal routes of exposure will be assessed to provide the basis for an intervention strategy to reduce that risk. There have been approximately 20 epidemiologic studies done on cancer risk among roofers and highway maintenance workers, and excess risk of cancer for several sites (lung, stomach, non-melanoma skin, and leukemias) have been reported with roofers consistently demonstrating greater risks than highway maintenance workers. Occupational exposure to PAHs has been proposed to explain the excess risk in these two groups, but no detailed exposure assessments have been done to support this association. The plan is to conduct a prospective study, including comprehensive assessment of exposure, to examine the association between exposure to PAH and a biological marker of carcinogen damage in the form of PAH-DNA adducts. The proposed research will: 1) recruit a population of at least 100 workers employed in roofing and highway paving with a range of asphalt exposures; 2) conduct a comprehensive evaluation of their occupational PAH exposure using their work task as the central organizing principle of the exposure assessment; 3) develop a task-based model for estimating the PAH exposures during the one-year prospective study; 4) measure the change in PAH-DNA adduct levels in mononuclear cells of these workers over the working year; 5) evaluate by linear regression the contribution of dermal and respiratory PAH exposure, smoking, diet and other factors to the level of PAH-DNA adducts; 6) develop an intervention strategy to reduce the risk of cancer resulting from occupational PAH exposures, using the information on the relative significance of inhalation and dermal exposure and the task-specific measures of exposure.





None