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Discovering the causes of cancer and the means of prevention

Mary H. Ward, Ph.D.

Senior Investigator

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Mary H. Ward, Ph.D.

Mary H. Ward, Ph.D.

Organization:National Cancer Institute
Division of Cancer Epidemiology & Genetics, Occupational and Environmental Epidemiology Branch
Address:9609 Medical Center Drive
Room 6E138


Dr. Ward received an M.S. in ecology from the University of Tennessee and a Ph.D. in epidemiology from The Johns Hopkins School of Hygiene and Public Health. Her 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, non-Hodgkin lymphoma, 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.  She is also examining the etiologic role of environmental exposures to pesticides and other chemicals in relation to childhood leukemia, non-Hodgkin lymphoma, and thyroid cancer. Dr. Ward is responsible for developmental work using geographic information systems for exposure assessment of environmental contaminants. For this effort, she received a DCEG Intramural Research Award in 1999 and an NIH Merit Award in 2000. She received the DCEG Mentoring Award in 2011 and the NCI Women Scientist Advisors' Mentoring and Leadership Award in 2016.

Research Interests

Nitrates, Pesticides and Cancer and Environmental Exposure Assessment

We are using innovative methods such as geographic information systems (GIS) to display and analyze environmental exposure data. Using GIS and remote sensing data, we are 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.


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 this exposure issue with respect to diet and drinking water. We 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, and ovarian cancers in case-control and/or cohort studies. Drinking water nitrate increased the risk of thyroid cancer in a cohort of older women in Iowa. Additional analytic studies are underway to evaluate further the importance of drinking water and dietary sources of nitrate and nitrite in the etiology of urinary tract and gastrointestinal tumors.

To further evaluate the possible role of drinking water nitrate exposure in the development of cancer, we estimated nitrate levels in private wells for participants of the Agricultural Health Study, a large cohort of pesticide applicators and their spouses in Iowa and North Carolina. Annual monitoring data are being used to characterize the population exposed to nitrate through community water systems. Through an interdisciplinary collaboration with colleagues in hydrology, geography, and biostatistics, we used a GIS to characterize land use, fertilizer application rates, the location of livestock feeding operations, soil type, and other factors around the wells, and we used a random forest model to estimate levels of nitrate in the drinking water wells for the study population.


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. A total of 24% of the study population in an agricultural area of Nebraska were determined to live within 500 meters of crop fields likely to have been treated with 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 58% of residences had crops within 500 m of their home, an intermediate distance for primary drift from aerial and ground applications. Six herbicides used almost exclusively in agriculture were detected in 28% of homes. Increasing acreage of corn and soybean fields within 750 m of homes was associated with significantly elevated odds of detecting agricultural herbicides compared with homes with no crops within 750 m even after accounting for the presence of an occupational exposed worker.  In a cohort of postmenopausal women in Iowa, risk of acute myeloid leukemia was increased among women living on farms. The acreage of crops within 750 m of homes was not associated with risk of leukemia among the women, but chronic lymphocyctic leukemia and small cell lymphoma risk increased with increasing crop acres near the homes.

With collaborators in California, we are evaluating agricultural pesticide use near residences as a risk factor for childhood leukemia in an ongoing case-control study. Carpet dust samples have been analyzed for pesticides and other chemicals, and information about the current and historical location of crops near residences was determined. 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; we observed no significant associations with other persistent organochlorine chemicals such as DDT, DDE, or chlordane.


Using a GIS, residential proximity to specific industries, specific chemical releases as reported by the Environmental Protection Agency's Toxic Release Inventory, and dioxin-emitting facilities are being evaluated in a multi-center study of non-Hodgkin lymphoma.