Evaluating risk factors across the lifespan (using the life course perspective) is important when considering the role of environment on BCa risk. Spatial cluster detection methods offer unique opportunities to identify shared exposures of individuals with BCa on the local level and formulate hypotheses about the potential role of environmental exposures. This study tests for evidence of spatial clustering of BCa incidence based on neighborhoods defined as 1940 US Census enumeration districts (ED). Data were extracted from the Utah Population Database (UPDB). UPDB holds birth, death, historic US Census, and driver license records that allow tracking of an individual’s location across the lifespan. UPDB is linked to the Utah Cancer Registry, an original member of the Surveillance, Epidemiology, and End Results program. Incident BCa cases from 1966 to 2017 were identified in the UCR or by death records and linked to UPDB. We geocoded all 1940 US Census ED centroids in Utah using US Census maps and ArcGIS software. The cohort comprises all individuals age 0–40 years at the time of the 1940 Census (Ncohort=343,521). We excluded individuals with an absence of follow-up information (Nexcluded=82,726). Our final cohort size was 260,795 individuals who contributed 13,816,670 person-years. SatScan software was used to identify spatial clustering of EDs with high rates of BCa. BCa was diagnosed in 2,654 individuals during follow-up (rate=19.2 cases per 100,000 person-years). Approximately 78.4% of cases were male. Average follow-up time was 53 years (range 1-78 years). We identified a circular cluster of 1.54 kilometers in diameter containing 23 ED centroids in an urban area, with a rate of 32.7 cases per 100,000 person-years (relative risk = 1.73, p=0.0023). We found evidence of spatial clustering of BCa incidence in an urban area of Salt Lake City, Utah for individuals in early life (0-40 years) at the time of the 1940 US Census. Individuals residing in this shared space were significantly more likely to develop BCa later in life, with a 73% increase in the incidence rate. Shared space in this context is presumed to be a proxy for environmental exposures. Environmental exposures including arsenic in drinking water and exposure to carcinogenic chemicals are associated with bladder cancer incidence. While this study was hypothesis generating and did not test for contaminants directly, future studies would benefit from the inclusion of contamination data. Additionally, we were limited by the use of residential history at a single time point and lack of data on personal behaviors (e.g., smoking). Strengths of this study include large cohort size, long follow-up time, and ability to expand to an early census. A life course perspective on cancer incidence provides for innovative methods to explore the environmental contexts of disease.

Citation Format: Claire L. Leiser, Marissa Taddie, Rebecca Richards-Steed, James A. VanDerslice, Brock O’Neil, Heidi A. Hanson. Neighborhood clustering of bladder cancer incidence in Utah: Analyzing census data linked to cancer records [abstract]. In: Proceedings of the AACR Special Conference on Environmental Carcinogenesis: Potential Pathway to Cancer Prevention; 2019 Jun 22-24; Charlotte, NC. Philadelphia (PA): AACR; Can Prev Res 2020;13(7 Suppl): Abstract nr A11.