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Chemical exposures and pets’ health

Polluted Pets: Chemical exposures and pets’ health

April 17, 2008

Pets, who share their living environment with humans, are exposed to scores of human-produced chemicals by inhaling indoor air with contaminated dust, strolling in industrial urban neighborhoods, drinking tap water full of disinfection byproducts, eating factory-made pet food laden with numerous chemicals, and contacting a variety of house and garden products, from herbicides to flame retardants. As a result of these multiple exposures, pet cats have 23 times higher levels of brominated flame retardants (polybrominated diphenyl ethers, or PBDEs) in their serum compared to humans, while dogs are contaminated with perfluorinated chemicals (PFCs) at levels 2.4 times higher than typical amounts found in people. The EWG investigation detected 48 of 70 (68%) different chemicals that were tested in cats and dogs. Companion animals have long been viewed as sentinels of chemical hazards to human health (Bukowski 1997; Potera 2007; van der Schalie 1999). However, this EWG study demonstrates for the first time the extent to which pets themselves are at risk from human industrial activities and pervasive presence of hazardous chemicals in the environment.

Pet cats and dogs have been noted to suffer harmful health effects from chemical pollution in the environment, often earlier than humans. In Minamata Bay in Japan during the 1950s, neurobehavioral symptoms were first observed in cats that consumed mercury-contaminated fish (Koya 1964; Muraki 1965; Tsuchiya 1992). The disturbed behavior of suffering animals has been dubbed by the locals as “dancing cat fever.” Compared to humans, cats and dogs live shorter lives. They also have correspondingly shorter latency periods for the development of life-threatening diseases such as cancer (Kelsey 1998). At the same time, behavioral patterns of pets (living close to the ground, ingesting dust, chewing on domestic objects, licking and self-grooming) are similar to the behavior of human toddlers (Betts 2007). Thus, the presence of toxic chemicals in cats and dogs sounds a cautionary warning for the present and future health of children. As emphasized in a report by the National Academy of Science, "Animals as Sentinels of Environmental Health Hazards," systematic evaluation of chemical exposure-related diseases of companion animals could lead to identification of unsuspected chemical hazards to vulnerable human populations that might otherwise go unnoticed (National Research Council 1991).

EWG reviewed veterinary research literature published over the past three decades, and identified numerous studies documenting illnesses linked to chemical exposures in companion animals. The list spans diverse diseases and exposures starting from lead toxicosis in cats and dogs to asbestos-related canine mesothelioma and oral carcinoma in cats related to use of flea and tick products. Ten examples of key research observations in the scientific literature are:

  • Mesothelioma in dogs and exposure to asbestos. Dog owners employed in a profession with asbestos exposure carry traces of asbestos fibers home on their working gear and apparel. The presence of asbestos fibers in home insulation serves as another significant source of asbestos exposure to both people and dogs. In a Purdue University study, the asbestos exposures of dog owners were associated with an eight-fold increase in risk of mesothelioma in their pets. The authors wrote: “Because of the short latent period for tumor development in dogs, their mesothelioma would often precede human disease by many years” (Glickman 1983). In the same study study, lung tissue from three dogs with mesothelioma and from one dog with squamous cell carcinoma of the lung had higher levels of chrysolite asbestos fibers than lung tissue from control dogs. In a second study, asbestos bodies were found in three of five dogs with mesotheliomas but rarely were found in control dogs (Harbison 1983).

  • Bladder cancers in dogs and local industrial activity. In a study of 8,760 pet dogs at 13 veterinary teaching hospitals, a significant positive correlation was seen between the morbidity ratios for canine bladder cancer and the overall level of industrial activity in the host county of the hospital, suggesting environmental exposure to carcinogens (Hayes 1981). Strikingly, human mortality from bladder cancer in the same counties showed a similar correlation with industrial activity (Hayes 1981). While this study did not identify specific chemical exposures that lead to bladder cancer in dogs, pet dogs living in chemically polluted area were found to have high levels serum levels of toxic chemicals such as polychlorinated biphenyls (PCBs) (Schilling 1988). Association with urban pollution has also been observed for tonsillar carcinoma in dogs in several studies (Reif 2006).

  • Bladder cancers in dogs and the use of insecticides and herbicides. In a case-control study of bladder cancer in household dogs, cancer risk was significantly increased by the use of topical insecticides. For 1-2 topical applications per year, bladder cancer risk was increased by 1.6 times, while more than 2 applications per year the risk was 3.5 times greater (Glickman 1989). As the authors noted in their publication, in addition to active insecticides, flea and tick dip products contain up to 96% organic solvent carriers such as benzene, toluene, and xylene, all known carcinogens, which could act as additional risk factors for bladder cancer (Glickman 1989; Kelsey 1998). A more recent study demonstrated that the risk of bladder carcinoma was significantly increased among dogs exposed to lawns or gardens treated with both herbicides or insecticides (7.2 times greater risk) or with herbicides alone (3.6 times greater risk), and was also increased for dogs exposed to lawns or gardens treated with insecticides alone (1.6 times greater risk), compared with dogs exposed to untreated lawns (Glickman 2004).

  • Canine malignant lymphoma and yard herbicide application. As demonstrated by a study of over 1400 dogs performed by National Cancer Institute (NCI) researchers, exposure to a common herbicide, 2,4-dichlorophenoxyacetic acid (2,4-D) which is associated with non-Hodgkin’s lymphoma in humans (McDuffie 2001), increases the risk of malignant lymphoma in dogs (Hayes, Tarone and Cantor 1995; Hayes 1991). High concentrations of 2,4-D were found in urine of dogs exposed to 2,4-D treated lawns, providing evidence that dogs living in and around residences with recent 2,4-D treatments absorb measurable amounts of the herbicide through normal activities and behaviors (Reynolds 1994). Although the NCI study was attacked by the pesticide industry and the Professional Lawn Care Association of America, the conclusion remains strong: lawn application of insecticides puts the health of household animals at risk (Hayes, Tarone and Cantor 1995; Reif 2006); as discussed above, herbicides and insecticides are also a risk factor for bladder cancer in dogs (Glickman 2004). 2,4-D herbicide remains a potential health hazard for pets and for children, who share similar exposures to environmental sources that can be contaminated with this insecticide such as soil, outdoor air, indoor air, and carpet dust (Morgan 2008)

  • High rates of various testicular cancers in military dogs. A two-fold excess lifetime risk for seminomas was found among military working dogs who had served in the Vietnam war (Hayes 1990). Furthermore, pathology study of tissues from 1,048 military dogs that died in Vietnam noted significant excesses of testicular hemorrhage, epididymitis/orchitis, sperm granuloma, testicular degeneration, and seminoma (Hayes, Tarone and Casey 1995). Military working dogs served in close proximity with their human handlers, sharing common exposures to war-related activity, infectious agents, chemical pesticides, phenoxy herbicides, and extensive use of therapeutic drugs (Hayes 1990). These studies noted another similarity: both the dogs and their handlers shared a higher risk for testicular cancers (van der Schalie 1999).

  • Oral squamous cell carcinoma in cats and the use of flea control products. In a study by epidemiology researchers at University of Massachusetts, Amherst, flea control product use and canned food intake were significantly associated with risk of oral squamous cell carcinoma in cats (Bertone 2003). Further, the same group of researchers noted that household tobacco smoke increased the risk of both oral carcinoma and malignant lymphoma (Bertone 2002, 2003). In addition to concern for cancer risk, acute toxicosis in cats from flee control products has also been reported (Linnett 2008); and anti-flea products used regularly on cat’s bed or bedding have been linked to a high risk for hyperthyroidism (Olczak 2005).

  • High levels of brominated flame retardants (polybrominated biphenyls or PBDEs) in cats. In a 2007 paper published in the journal Environmental Science and Technology, total PBDE serum concentrations of 4.3-12.7 ng/mL have been reported in cats (Dye 2007). For comparison, the EWG study detected the sum of PBDEs in cat serum at 5.2 ng/ml concentration. As demonstrated by these two studies, PBDE levels in cats are 20- to 100-fold greater than median levels in US adults (0.1-0.2 ng/mL). A significant portion of PBDEs in pet cats may come from dietary sources; at the same time, cats likely ingest 7-fold more dust than adult humans (Dye 2007), and household dust is laden with flame retardant chemicals (Stapleton 2005). One of the hypotheses posed by the researchers in this study was that high PBDE levels in cats could be linked to hyperthyroidism, a feline disease that has increased dramatically since 1980s (Peterson 2007). Although high sample variability precluded detection of association between PBDE levels and hyperthyroidism in this study, other studies have noted the connection of this disease with consumption of canned cat food (Edinboro 2004; Kass 1999; Martin 2000).

  • Lead toxicosis in dogs and cats. Prior to the 1970s' federal regulation of lead, lead toxicosis was considered the most common accidental poisoning in small animals (Knight 2003). Lead poisoning is clinically and epidemiologically similar in dogs and human infants (Morgan 1994; National Research Council 1991; Prescott 1983). Historically, small children and pet animals pick up the same sources of lead exposure such as peeling old lead paint or proximity to traffic (Kucera 1988). In a 1976 study of 83 dog-owning families in Illinois, high blood levels in dogs were significantly linked to high blood levels in a child within the same household (Thomas 1975, 1976). Neurologically disturbed behavior of the pets could be noted as the first sign of trouble, such as “shaking and twisting” of pet dogs (Marino 1990) or anorexia in pet cats (Miller 1992). Often, these symptoms appear following remodeling of old houses and subsequent exposure to lead fumes and dust (Knight 2003).

  • Teflon toxicosis or “polymer fume fever” in birds. As noted in the National Academies of Sciences report (National Research Council 1991), polymer fume fever in birds has been known since the 1970s. Upon heating, olytetrafluoroethylene or PTFE, a common coating on non-stick cookware, undergoes pyrolysis (heat-induced breakdown) and forms solid particle fumes (Seidel 1991). These fumes coat the inside surface of lungs, causing shortness of breath, shivering, dizziness, and death by asphyxiation in pet birds (Blandford 1975; Wells 1983), as well as severe flu-like symptoms in bird owners (National Research Council 1991; Shusterman 1993).

  • Chemical contamination of pet food. A massive recall was initiated in March 2007 after many pets became sick or died after eating certain brands of pet foods (FDA 2007). Poisonings of pets were traced to the presence of melamine and cyanuric acid in imported wheat gluten that was used for pet food production (Burns 2007a, b). These events highlighted the vulnerability of pets and their owners who, due to insufficient government oversight over chemicals present in pet food, are left to trust that the pet food industry will regulate itself. Following hearings in the House and Senate on the need for additional food safety regulations, Human and Pet Food Safety Act was passed in September 2007 (Nolen 2007). This act set in place an early warning system to alert the public about unsafe pet food; however, much yet remains to be done to protect both animal and human food supply before dangerous incidents occur.

These 10 examples help to situate within the existing research literature EWG demonstration of high levels of industrial chemicals in pets and dogs. Clearly, companion animals are at risk from the environmental pollution. In light of this fact, it is striking that we are still lacking national-level statistics on diseases that companion animals. Overall, data for incidence rates of cancer and other diseases in dogs and cats are limited to a few sources, most of which are badly outdated (Kelsey 1998; Reif 2006). For example, the most commonly cited cancer statistics come from the California Animal Neoplasm Registry which is based on the data more than 40 years old that was published in 1968 (Dorn, Taylor, Frye 1968; Dorn, Taylor, Schneider 1968). A lot has changed in the intervening period. For example, greater awareness of health impact of environmental tobacco smoke has changed hazard perceptions and attitudes towards smoking, especially indoor smoking. This is great news for pets’ health as well, since environmental tobacco smoke is associated with lung and nasal cancers in dogs (Reif 1998; Reif 1992; Roza 2007) and malignant lymphoma in cats (Bertone 2002). Other environmental changes have not been so beneficial. For example, as noted by the Environmental Protection Agency researchers, a rise in feline hyperthyroidism has coincided with the widespread introduction of brominated flame-retardants into household materials (Dye 2007), while the hazards of over-heated non-stick cookware to pet birds have been documented with countless reports of bird owners (EWG 2003a, c). We need to look at the issue of pet animal health in the context of overall health of animals, wild and domesticated. As evidenced by research observations and news stories about feminized fish in sewage effluent locations (Filby 2007), hermaphroditic frogs in areas of high pesticide use (Hayes 2002; Hayes 2006) and high rates of cancers in California sea lions and in St. Lawrence estuary beluga whales due to chemical contamination with PCBs and DDT (Newman 2006; Ylitalo 2005), the health of animals everywhere is imperiled. It is thus up to us, humans, to come up with policies that will protect the health of animals – and our own.