The relationship between sunlight or ultraviolet irradiation and subsequent development of skin cancer is well known in both human and veterinary medicine. As with the etiology of human SCC, sunlight has been implicated as a cause of SCC in domestic animals and livestock. This implication is strengthened by the clear dose response relationship that has been shown in both epidemiological and experimental studies. ^28-31 Specifically, light skin pigmentation and chronic sun exposure are associated with development of facial, aural, and nasal planum SCC in white or partially white cats ( Figure 3-1 ) and may play a similar role in some cutaneous SCC lesions in dogs. Ultraviolet-B (UV-B) light, which is in the range of 280 to 320 nm, is the part of the ultraviolet spectrum that is most likely to be responsible for nonmelanotic skin lesions in people and animals. ²⁸ Cumulative long-term exposure to UV-B may induce skin tumors directly by causing genetic mutations (such as p53) or indirectly by impairing the immune response to tumor antigens. ^28,32,33 Companion animals are at greatest risk of UV exposure during the midday hours. Protection from this exposure is warranted, especially in lightly pigmented breeds.

Chronic inflammation can lead to genetic mutations that ultimately result in neoplastic transformation. In four dogs with chronic pigmentary keratitis, neoplastic lesions of the cornea (three SCC and one squamous papilloma) were reported. ³⁴ Although the underlying etiology of the keratitis could not be confirmed, the neoplastic transformation was thought to be related to chronic inflammation. Earlier reports have linked feline intraocular sarcomas to prior ocular trauma and secondary uveitis and lens rupture. ³⁵ Despite the varied histologies, in both examples the underlying etiology was thought to be related to inflammatory changes (see Chapter 20, Section C , for more detail). Another small animal malignancy thought to be associated with inflammation is vaccine-associated feline sarcoma (VAFS). ³⁶ This tumor type is discussed in Chapter 23, Section E , Vaccine site fibrosarcomas have also been reported in dogs and ferrets. ^37,38

A potential link between childhood cancer and chronic low-dose exposure to magnetic fields was first proposed more than 25 years ago. ³⁹ Since that time, multiple studies have attempted to identify links between magnetic fields and a variety of human cancers ranging from hematopoietic malignancies to breast cancer. The extremely low–frequency (<60 Hz) magnetic fields in question are ubiquitous in today’s society and are generated by household appliances, industrial machinery, and electrical power lines. Because pets share our environment and thus have a similar amount of exposure to magnetic fields, it has been suggested that companion animals are at similar risk of cancer development because of this etiology. A 1995 study found the risk for canine lymphoma was highest in dogs from households with the highest measured exposure to magnetic fields. ⁴⁰ This risk was related to both the duration and the intensity of exposure. Dogs that spent more than 25% of the day outdoors were found to be at highest risk. A year later, a report was published by the National Research Council (NRC) at the request of Congress and reviewed over 500 studies on the subject of cancer risk and exposure to electromagnetic fields. ⁴¹ The report concluded that, although a weak association has been shown between development of childhood leukemia and exposure to electromagnetic fields, no clear evidence exists to suggest that exposure to electromagnetic fields is a true threat to human health. To the author’s knowledge, there have been no further reports on the possible link between magnetic fields and cancer in companion animals published since the 1995 report. Still, the magnetic field debate continues in the human oncology literature. The NRC report suggested that other factors including air quality and proximity to high-traffic density are more likely environmental causes of cancer than low-frequency magnetic fields.

The first report of canine cancer developing after therapeutic irradiation dates back almost a quarter century, when orthovoltage radiation was considered state of the art. ⁴² At the time, the term malignant transformation was used to describe the development of epithelial malignancies at the site of prior irradiation for acanthomatous epulides in four dogs. With both the benefit of hindsight and a review of more recent cases, the author of the original report has since suggested that the term malignant transformation is misleading, in that the occurrence of second tumors was unlikely due to a true transformation of epulides into carcinomas. ⁴³ Rather, radiation carcinogenesis is the likely cause of second tumors in radiation fields. In human oncology, most tumors that occur in heavily irradiated treatment fields are of mesenchymal, rather than epithelial, origin. ^44,45 Several reports of sarcomas occurring at sites of prior radiation may be found in the veterinary literature. ^42,46-48 One example is a retrospective review of 57 dogs undergoing definitive megavoltage radiation therapy with ⁶⁰ cobalt photons for acanthomatous epulis. ⁴³ In the report, McEntee et al. ⁴³ described the development of a second tumor (one sarcoma and one osteosarcoma) in two of the 57 irradiated dogs, occurring 5.2 and 8.7 years after the initial treatment, respectively. The overall incidence of second tumors was only 3.5% in the manuscript by McEntee et al. ⁴³ compared with figures of up to 18% in previous reports. ^42,49 The fact that no epithelial tumors were reported in this latest paper may indicate that megavoltage radiation therapy used today more efficiently targets an existing subpopulation of malignant epithelial cells than did orthovoltage. The risk of second tumors at sites of radiation therapy is primarily of clinical concern when treating young dogs that are expected to enjoy long-term survival. Second tumors have also been reported in at least six people who have undergone stereotactic radiosurgery. ⁵⁰ As this radiation technique becomes more commonplace in veterinary medicine, the possibility of second tumors may need to be considered in companion animals as well.

Sarcoma development at the site of metallic implants has been reported in people, dogs, and laboratory animal models. ^51,52 However, it is often difficult to know if sarcoma development is related to fracture fixation devices or to other factors, including wound-healing complications and osteomyelitis. The largest veterinary study to examine the relationship between metallic implants and tumor development in dogs was published in 1993 by Li et al. ⁵² The authors reported on 222 dogs that developed tumors of any kind after fracture fixation, compared with 1635 dogs that underwent fracture fixation but did not subsequently develop tumors. The investigators concluded that use of metallic implants was not a risk factor for bone tumor development. Other types of implants and foreign materials related to surgery are sporadically implicated in carcinogenesis in human and veterinary case reports. Published examples include a dog that developed a myxoma at the site of a subcutaneous pacemaker implantation and another that developed a jejunal osteosarcoma associated with a surgical sponge presumably not retrieved during an abdominal surgery 6 years prior. ^53,54 More recently, it has been suggested that microchips implanted subcutaneously in companion animals for identification purposes may lead to tumor development at the microchip site. ^55,56 This link is yet to be proven but is currently under investigation.