Michele Morin Doody, M.S.
|Organization:||National Cancer InstituteDivision of Cancer Epidemiology & Genetics, Radiation Epidemiology Branch|
|Address:||Executive Plaza SouthRoom 7051|
Captain Doody received a B.S. in Biology from Stonehill College in 1977 and an M.S. in Epidemiology from the University of Massachusetts School of Public Health in 1980. She joined the Environmental Epidemiology Branch in the Division of Cancer Cause and Prevention in 1980 as a Commissioned Officer in the U.S. Public Health Service, and transferred to the Radiation Epidemiology Branch shortly after its inception in 1984. Captain Doody received several U.S. Public Health Service awards for epidemiological studies that provided new information on the role of low-level radiation in carcinogenesis, including quantifying risk for breast cancer following diagnostic x-rays, and for research administration of a landmark program to assess cancer risk following protracted low-dose occupational radiation exposure. She also earned an NIH award for leading a team of researchers in developing the first comprehensive historical dose reconstruction for a large cohort of medical radiation workers spanning multiple decades. Captain Doody was medically retired from the Commissioned Corps in 2007 and immediately resumed work as a Civil Servant.
Although cancer risks following radiation exposure have been widely studied, to date quantitative estimates of risk have been derived largely from studies of the Japanese atomic bomb survivors who received a single acute exposure. To quantify the risk of radiogenic cancers following protracted low-to-moderate dose radiation exposures that occur in occupational and environmental settings, and to clarify mechanisms of radiation carcinogenesis, a nationwide cohort of 146,000 radiologic technologists has been evaluated from the American Registry of Radiologic Technologists. The U.S. Radiologic Technologists (USRT) cohort is predominantly female (73%), affording a unique opportunity to quantify breast cancer risk associated with low-dose-rate (protracted) exposures, which animal studies have shown to be less carcinogenic than high-dose-rate (acute) exposures because of the opportunity for DNA repair. Results to date have shown that breast cancer risk is significantly increased among technologists who first worked before 1940, when radiation exposures were likely high, compared to those who began working in 1970 or later (Doody et al, 2006). The USRT dosimetry team recently completed an historical dose reconstruction which provides annual estimates through 2006 of personal dose equivalent (badge dose) and radiation absorbed doses to twelve organs and tissues for 110,000 cohort members who completed at least one baseline survey. We will estimate cancer dose-response risks and assess potential effect modifiers. For information on USRT biodosimetry studies and genetic studies of breast and thyroid cancer, see the biography of Dr. Alice Sigurdson.
Radiation exposure to the chest, especially at young ages, is associated with increased breast cancer risk. Few epidemiologic studies can address potentially susceptible stages of breast development. A cohort of 5,573 women with scoliosis who underwent routine diagnostic x-rays of the spine during childhood and adolescence were evaluated to quantify the breast cancer radiation dose-response relationship, assess whether known breast cancer risk factors modify the dose-response, and to explore possible age intervals of increased radiation sensitivity. Scoliosis patients were found to have a statistically significant 70% excess risk of dying from breast cancer compared to women in the general population and risk increased significantly with increasing radiation dose to the breast (Doody et al, 2000). An analysis of radiation-related breast cancer incidence among 3,010 women who completed a survey in 1992 revealed a borderline-significant breast cancer radiation dose-response (ERR/Gy=2.86; p=0.058, 1-tailed p=0.029) based on 78 cases, after adjustment for established breast cancer risk factors (Ronckers et al, 2008). Ninety-five percent of daily breast dose increments (when exposure occurred) were under 2.4 cGy, with a mean dose of 1.1 cGy per day. Assuming that repair of radiation-related DNA damage requires at most a few hours, these data argue against the existence of a low-dose threshold on the order of 1-3 cGy for radiation exposure contributing to breast carcinogenesis. Reproductive factors did not affect the dose-response, but the dose-response slope was significantly greater for women who reported a family history of breast cancer in first or second degree relatives than for women without a family history of breast cancer. Although some variation in dose-response was seen by breast development stage at exposure, the differences were not statistically significant. A further follow-up of this cohort is in the planning stages.