This dissertation uses a disease ecology framework to investigate the etiology of hypospadias, a relatively common birth defect affecting the male genitourinary tract. It begins by considering the spatial distribution of hypospadias in North Carolina and whether that spatial distribution can be explained by either compositional or contextual risk factors. It then focuses on a potential contextual risk factor of interest: atrazine, one of the most widely used herbicides in the United States. An endocrine disruptor, atrazine breaks down slowly in soils and water, suggesting that mothers could be exposed to atrazine via contaminated drinking water. This research uses data from the North Carolina Birth Defects Monitoring Program and the National Birth Defects Prevention Study. Three different methods are used to estimate maternal exposure to atrazine via drinking water: total atrazine applied to maternal county of residence; sampling data maintained by the United States Environmental Protection for compliance monitoring; and outputs from surface water and groundwater models from the United States Geological Service. After concluding that the surface and groundwater modeling metric is most appropriate for our dataset, this research concludes by incorporating maternal population and behavioral characteristics into analyses of hypospadias and maternal exposure to atrazine via drinking water. Results indicate statistically significant spatial autocorrelation of hypospadias in eastern central North Carolina, which persists when controlling for compositional risk factors, and which suggests that contextual factors may influence the spatial distribution of hypospadias. Results further suggest possible role played by atrazine in a multi-factorial etiology of hypospadias. When controlling for maternal demographic and behavioral characteristics, hypospadias is found to be marginally significantly associated with daily maternal atrazine consumption during the critical window of genitourinary development (odds ratio = 1.03; p = 0.054). This reinforces the utility of a disease ecology framework in research of diseases of unknown or multifactorial etiology. It also suggests that further research is needed to evaluate the potential teratogenic properties of atrazine.