Risk of bladder cancer and lymphoma in dogs is associated with pollution indices by county of residence.

Human urothelial cell carcinoma (UCC) and non-Hodgkin lymphoma are considered environmental cancers in people, but less is known about environment risk for UCC and lymphoma in dogs. The objective of this study was to determine whether dogs with these cancers, compared to unaffected control dogs, live in counties with higher tap water contaminants or higher levels of air pollution as measured by the Environmental Protection Agency (EPA) and by National Air Toxics Assessment chemical exposure risk estimates. Dogs with available home addresses from two previously published case-control populations were included: 66 dogs with UCC and 70 unaffected controls; and 56 boxer dogs with lymphoma and 84 unaffected boxer controls. Tap water total trihalomethanes, which are water disinfection by-products, were more than threefold higher in UCC case counties of residence compared to controls (p < .0001), and a higher proportion of dogs with UCC lived in counties exceeding EPA ozone limits (41.8%) compared to controls (13.6% p = .0008). More boxers with lymphoma lived in counties exceeding EPA ozone limits (52.1%) compared to controls (29.0%; p = .018), with higher exposure risk estimates for airborne 1,3-butadiene and formaldehyde (p = .004-.005). These data support the hypothesis that tap water contaminants and airborne environmental pollutants contribute to the risk of both urothelial carcinoma and lymphoma in dogs. If these findings reflect causal relationships, then it is possible that tap water filtration units and more effective air pollution controls could decrease the overall incidence of these cancers in dogs.

Environmental chemical exposures in the urine of dogs and people sharing the same households.

INTRODUCTION: Urothelial carcinoma (UCC) develops in both humans and dogs and tracks to regions of high industrial activity. We hypothesize that dogs with UCC may act as sentinels for human urothelial carcinogen exposures. The aim of this pilot study was to determine whether healthy people and dogs in the same households share urinary exposures to potentially mutagenic chemical carcinogens. METHODS: We measured urinary concentrations of acrolein (as its metabolite 3-HPMA), arsenic species, 4-aminobiphenyl, and 4-chlorophenol (a metabolite of the phenoxyherbicide 2,4-D) in healthy dogs and their owners. We assessed possible chemical sources through questionnaires and screened for urothelial DNA damage using the micronucleus assay. RESULTS: Biomarkers of urinary exposure to acrolein, arsenic, and 4-chlorophenol were found in the urine of 42 pet dogs and 42 owners, with 4-aminobiphenyl detected sporadically. Creatinine-adjusted urinary chemical concentrations were significantly higher, by 2.8- to 6.2-fold, in dogs compared to humans. Correlations were found for 3-HPMA (r = 0.32, P = 0.04) and monomethylarsonic acid (r = 0.37, P = 0.02) between people and their dogs. Voided urothelial cell yields were inadequate to quantify DNA damage, and questionnaires did not reveal significant associations with urinary chemical concentrations. CONCLUSIONS: Healthy humans and pet dogs have shared urinary exposures to known mutagenic chemicals, with significantly higher levels in dogs. Higher urinary exposures to acrolein and arsenic in dogs correlate to higher exposures in their owners. Follow-up studies will assess the mutagenic potential of these levels in vitro and measure these biomarkers in owners of dogs with UCC.