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Mary Ward is a senior investigator in OEEB.

Mary H. Ward, Ph.D.

Senior Investigator

NCI Shady Grove | Room 6E138



Dr. Ward received an M.S. in ecology from the University of Tennessee, Knoxville, and a Ph.D. in epidemiology from The Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland. She completed post-doctoral work in the Occupational and Environmental Epidemiology Branch within the Division of Cancer Epidemiology and Genetics, was appointed as a tenure-track investigator in 1999, and received tenure in 2008. Dr. Ward received a DCEG Intramural Research Award in 1999 and an NIH Merit Award in 2000 for her work using geographical information systems for exposure assessment of environmental contaminants. She received the DCEG Mentoring Award in 2011 and the NCI Women Scientist Advisors' Mentoring and Leadership Award in 2016. Dr. Ward is a Fellow of the American College of Epidemiology and an elected member of the American Epidemiological Society.

Research Interests

Dr. Ward’s research focuses on environmental and occupational causes of cancer, with special emphasis on drinking water contaminants, pesticides, and other chemicals in relation to the etiology of childhood leukemia, gastrointestinal cancers, and thyroid cancer. She is examining nitrate in drinking water and the diet with respect to cancers of the bladder, colon, stomach, esophagus, ovary, and thyroid. Dr. Ward is responsible for developmental work using geographic information systems for exposure assessment of environmental contaminants.

Nitrates, Pesticides and Cancer and Environmental Exposure Assessment

Dr. Ward uses innovative methods such as geographic information systems (GIS) to display and analyze environmental exposure data. Using GIS and remote sensing data, she is participating in interdisciplinary collaborations to develop new methods of exposure assessment for epidemiologic studies of cancer risk in relation to drinking water contaminants, agricultural pesticides, and other environmental contaminants.

Nitrates, Nitrite, and N-nitroso Compounds

The endogenous formation of carcinogenic N-nitroso compounds (NOC) can occur following ingestion of nitrate from drinking water. Certain foods are also sources of nitrate and nitrite. Nitrate can also inhibit iodide uptake by the thyroid. Only a limited number of analytic epidemiologic studies have evaluated these exposures with respect to diet and drinking water. Dr. Ward conducted case-control studies that found an increased risk of colon and kidney cancer associated with prior exposure to elevated nitrate in drinking water among those who also had lower intakes of vitamin C and higher intakes of red meat, inhibitors and precursors in the endogenous formation of NOC. Increasing intake of dietary nitrite, a major source of which is processed meats, was associated with increased risk of colorectal adenomas, colon, rectum, pancreas, thyroid, and ovarian cancers in case-control and/or cohort studies. Drinking water nitrate increased the risk of thyroid, bladder, kidney, and ovarian cancers in a cohort of older women in Iowa.

To follow up upon these findings, Dr. Ward led interdisciplinary collaborations to develop GIS-based random forest models to estimate nitrate levels in the drinking water wells of participants of the Agricultural Health Study, a cohort of pesticide applicators and their spouses with high exposure to nitrate through their private wells. 

Pesticides and Other Chemicals

A feasibility study using remote sensing data and a GIS to estimate indirect exposure to pesticides demonstrated that using available data, accurate historical crop maps could be produced and that these could be linked to pesticide use data to estimate probabilities of indirect exposure to agricultural pesticides. This was the first study to estimate the prevalence of potential indirect exposure to agricultural pesticides in the general population. A validation study in Iowa found that increasing acreage of corn and soybean fields within 750 m of homes was associated with significantly elevated concentrations of agricultural herbicides compared with homes with no crops within 750 m even after accounting for the presence of an occupational exposed worker. Dr. Ward and colleagues are applying this exposure assessment approach to estimate residential exposures to agricultural pesticides in studies of childhood cancers in California and Denmark.

In a case-control study of childhood leukemia in California, Dr. Ward and colleagues analyzed carpet dust samples for pesticides and other chemicals. Analyses of persistent organochlorine pesticides, polychlorinated biphenyls (PCB), and polybrominated diphenyl ethers (PBDE) in carpet dust samples revealed an increased risk of acute lymphocytic leukemia among children living in homes with higher levels of PCB and specific PBDE congeners. In a nested-case control study of in the Norwegian Janus Serum Bank cohort, early life exposures to specific organochlorine chemicals were associated with increased risk of thyroid cancer. 

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