Urol Oncol. 2026 Jun 19;44(9):211-222. doi: 10.1016/j.urolonc.2026.05.014. Online ahead of print.
ABSTRACT
BACKGROUND: While several environmental carcinogens are well-established in the development of bladder and kidney cancer, the role of microplastic exposure remains poorly understood. Micro- and nanoplastics (MNPs), often released during plastics manufacturing and recycling, are emerging pollutants that may carry carcinogenic additives or act as chemical vectors in air and water. Ohio-a major hub for plastics production-has experienced rising rates of bladder and kidney cancer, prompting an investigation into the spatial relationship between cancer incidence and exposure to plastics-processing waste.
METHODS: We conducted a geospatial epidemiological study using data from the Ohio Cancer Incidence Surveillance System (OCISS) from 2013 to 2021, alongside environmental exposure estimates derived from the Environmental Protection Agency (EPA’s) Toxics Release Inventory (TRI) and Risk-Screening Environmental Indicators (RSEI) model. Chemicals were categorized into adjusted plastics-processing waste (APPW), known bladder and kidney carcinogens, and combined exposures. Incidence and exposure data were analyzed at the ZIP Code Tabulation Area (ZCTA) level using spatial statistics (Moran’s I, bivariate Moran’s I, and Mantel tests), local cluster detection, and spatial regression.
RESULTS: Between 2013 and 2021, both bladder and kidney cancer incidence increased across Ohio, with notable geographic clustering of cases. Spatial analysis demonstrated that regions with higher environmental exposure to chemicals used in plastics-processing, particularly via air, had significantly higher rates of both cancers. Airborne bladder carcinogens showed the strongest spatial association with cancer incidence (bivariate Moran’s I = 0.0510, P = 0.004; Mantel P < 0.001), followed by airborne microplastics (bivariate Moran’s I = 0.0589, P = 0.007). Waterborne microplastics, while not spatially clustered on their own, were significantly associated with higher bladder and kidney cancer rates (kidney: bivariate Moran’s I = 0.0940, P = 0.001). When combining all plastics-related exposures, spatial relationships remained robust, suggesting a cumulative effect. These patterns were most prominent in industrial ZIP codes, particularly in northern and southwestern Ohio.
CONCLUSIONS: Our findings reveal significant spatial associations between plastics-related industrial emissions and both bladder and kidney cancer incidence in Ohio. These patterns suggest an environmental component to urologic cancer risk, with airborne exposures showing the strongest spatial alignment. The results warrant deeper mechanistic studies and targeted epidemiological investigations in high-exposure communities to further assess causality and inform public health interventions.
PMID:42320109 | DOI:10.1016/j.urolonc.2026.05.014
