Urinary mutagenicity and bladder cancer risk in northern New England

Author:

Wong Jason Y. Y.12ORCID,Fischer Alexander H.2,Baris Dalsu2,Beane Freeman Laura E.2,Karagas Margaret R.3,Schwenn Molly4,Johnson Alison5,Matthews Peggy P.6,Swank Adam E.6,Hosain G. Monawar7,Koutros Stella2,Silverman Debra T.2,DeMarini David M.6ORCID,Rothman Nathaniel2

Affiliation:

1. Epidemiology and Community Health Branch, National Heart Lung and Blood Institute, National Institutes of Health Bethesda Maryland USA

2. Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics National Cancer Institute, National Institutes of Health Rockville Maryland USA

3. Department of Epidemiology Geisel School of Medicine at Dartmouth Lebanon New Hampshire USA

4. Maine Cancer Registry Augusta Maine USA

5. Vermont Cancer Registry Burlington Vermont USA

6. Office of Research and Development, U.S. Environmental Protection Agency Research Triangle Park North Carolina USA

7. Division of Public Health Services New Hampshire Department of Health and Human Services Concord New Hampshire USA

Abstract

AbstractThe etiology of bladder cancer among never smokers without occupational or environmental exposure to established urothelial carcinogens remains unclear. Urinary mutagenicity is an integrative measure that reflects recent exposure to genotoxic agents. Here, we investigated its potential association with bladder cancer in rural northern New England. We analyzed 156 bladder cancer cases and 247 cancer‐free controls from a large population‐based case–control study conducted in Maine, New Hampshire, and Vermont. Overnight urine samples were deconjugated enzymatically and the extracted organics were assessed for mutagenicity using the plate‐incorporation Ames assay with the Salmonella frameshift strain YG1041 + S9. Logistic regression was used to estimate the odds ratios (OR) and 95% confidence intervals (CI) of bladder cancer in relation to having mutagenic versus nonmutagenic urine, adjusted for age, sex, and state, and stratified by smoking status (never, former, and current). We found evidence for an association between having mutagenic urine and increased bladder cancer risk among never smokers (OR = 3.8, 95% CI: 1.3–11.2) but not among former or current smokers. Risk could not be estimated among current smokers because nearly all cases and controls had mutagenic urine. Urinary mutagenicity among never‐smoking controls could not be explained by recent exposure to established occupational and environmental mutagenic bladder carcinogens evaluated in our study. Our findings suggest that among never smokers, urinary mutagenicity potentially reflects genotoxic exposure profiles relevant to bladder carcinogenesis. Future studies are needed to replicate our findings and identify compounds and their sources that influence bladder cancer risk.

Funder

Division of Cancer Epidemiology and Genetics, National Cancer Institute

Publisher

Wiley

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