The incidence of cancer in dogs has increased substantially, largely due to greater canine longevity (1). Cancer, a multifactorial disease, is now the primary cause of death in dogs and cats, underscoring the importance of veterinary oncology and cancer epidemiology (2). The most frequent malignant oral neoplasms in dogs are melanomas, squamous cell carcinomas, and fibrosarcomas (3–5).

Malignant oral melanomas, which originate from melanocytic cells, are the most common oral tumors in dogs, particularly in elderly dogs of pigmented breeds such as Chow Chows, Cocker Spaniels, and Poodles. Squamous cell carcinomas arise from keratinocytes, while fibrosarcomas, of mesenchymal origin, are also prevalent and display variable invasiveness (6, 25). Although internal factors such as genetic mutations and immune dysfunction contribute to tumorigenesis, external influences, including environmental exposures, are also critical.

Approximately 6% of malignant neoplasms in dogs occur in the oral cavity, making it the fifth most common site of tumor development (4, 7, 8). A survey of 1,813 canine tumors diagnosed between 1993 and 2002 at the Animal Pathology Service of the University of São Paulo showed that oral squamous cell carcinoma accounted for 5% of epithelial tumors (9). Oral cavity tumors and tumor-like lesions are often detected during routine examinations. These lesions may cause pain, discomfort, or anorexia, but can also be incidental findings, frequently associated with periodontal disease. Owners often present dogs for evaluation due to sialorrhea, halitosis, or mastication difficulties (10). In early stages, these neoplasms may be misdiagnosed as inflammatory processes like gingivitis or stomatitis, highlighting the importance of comprehensive clinical examination.

Definitive diagnosis of solid oral tumors requires histopathological confirmation via incisional or excisional biopsy. Persistent irritation and chronic inflammation from conditions like chronic gingivitis may promote malignant transformation. Additional proposed risk factors include passive exposure to tobacco smoke, use of flea-control collars, and dietary or environmental influences (11). Specifically, the rationale for examining exposures to indoor pollutants like incense and water source composition stems from their documented carcinogenic potential in humans and other species, where they are linked to mucosal irritation and oxidative stress (12, 13). This study aims to identify key epidemiological and etiological factors, including these specific environmental and lifestyle variables, associated with solid oral tumors in dogs.

This study examined the epidemiological and etiological factors associated with the development of solid oral tumors in dogs. Age emerged as a major risk factor, with affected dogs being significantly older than healthy counterparts. This aligns with previous research showing that cancer is largely a disease of aging, influenced by the accumulation of genetic mutations, diminished DNA repair capacity, and persistent inflammatory processes over time (14–16).

Body size was also associated with a higher risk of oral tumors. This finding supports earlier evidence that larger breeds have greater cancer susceptibility, potentially due to accelerated cell turnover and prolonged exposure to growth factor signaling, both of which contribute to oncogenic transformation (17). Reproductive status was significantly associated with oral tumor development, with intact dogs demonstrating a higher risk than neutered dogs. A plausible explanation is that intact dogs may experience different lifestyle patterns, including reduced veterinary care and fewer preventive interventions, which could contribute to later-stage diagnoses. Furthermore, hormonal influences on oral mucosal tissue may differ from those documented in mammary or prostate tumors, underscoring the need for further investigation into the role of sex hormones in oral oncogenesis.

Environmental exposures were also significant predictors, with barbecue smoke showing a positive association with oral tumor development. This finding is consistent with the well-documented carcinogenic potential of polycyclic aromatic hydrocarbons (PAHs) released during the combustion of organic material (18). PAHs have been strongly associated with multiple cancers in humans and animals, and their presence in airborne barbecue smoke may contribute to oral mucosal irritation and chronic inflammation, creating a pro-tumorigenic environment. Prolonged exposure to these compounds may also promote the accumulation of DNA damage in oral epithelial cells.

An unexpected and paradoxical finding was the apparent protective effect of incense exposure against oral tumors. This result appears counterintuitive, as incense burning releases volatile organic compounds and particulate matter, several of which are recognized carcinogens (12). However, this association should be framed cautiously. Incense exposure may function as a proxy for other unmeasured lifestyle variables—such as specific hygiene practices, household stress levels, or dietary patterns—that influence cancer susceptibility. This likely represents residual confounding rather than a biological protective effect. Further studies with more detailed exposure assessments are required to clarify this relationship.

Similarly, the consumption of mineral water was associated with a reduced risk. This may indicate a protective role of specific minerals or the absence of harmful contaminants found in tap water, such as heavy metals and chlorine byproducts (13). Nevertheless, this finding may also reflect confounding by socioeconomic factors, as owners providing bottled water may engage in other health-conscious practices, such as offering higher-quality diets and ensuring more consistent veterinary care.

Dietary habits were significant determinants; dogs fed a mixed diet demonstrated a higher likelihood of tumors, whereas those consuming fruits and vegetables exhibited a lower risk. The risk from mixed diets may stem from processed human foods containing preservatives or additives with carcinogenic potential (19, 20). Conversely, the protective effect of fruits and vegetables supports evidence that bioactive compounds like polyphenols mitigate oxidative stress (21, 22).

Finally, the association between periodontal disease and professional dental cleaning and increased tumor risk may represent reverse causality or surveillance bias. Dogs receiving frequent dental procedures often have chronic inflammation, a well-established precursor to neoplasia (23, 24). Therefore, this association likely reflects enhanced veterinary surveillance in dogs predisposed to oral pathology rather than a direct tumor-promoting effect of dental procedures.

Overall, these findings emphasize the multifactorial nature of canine oral tumors. Due to the observational design, causality cannot be confirmed, and limitations such as recall bias and residual confounding must be acknowledged. Future research should prioritize prospective cohort studies to validate these associations.

These findings underscore the importance of preventive strategies in veterinary oncology. Minimizing exposure to established carcinogens, optimizing dietary practices, and promoting oral health may be critical in reducing cancer risk. Additionally, the unexpected protective associations observed for certain exposures highlight the need for a more nuanced and cautious understanding of environmental contributions to cancer biology. Because of the observational nature of this study, these results should be viewed as significant associations rather than confirmed causal links. Integrating epidemiological evidence with molecular research will be essential for future studies to advance the understanding of canine oral tumor etiology and to guide the development of more effective prevention and treatment strategies.