Dogs: High levels of plasticizers,
grease-proof chemicals,and
fire retardants
35 chemicals detected – 40% at higher levels
in dogs than people

Cats: notably high levels of fire
retardants, high levels of plasticizers,
and grease-proofing chemicals
46 chemicals detected – 96% at higher levels
in cats than people

Chemical exposures and pets’ health

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.

Who is protecting pets?

The Toxics Substances Control Act (TSCA) is the cornerstone in our system of health protections for industrial chemical exposures. Passed in 1976, it is the only major public health and environmental law in the U.S. that has never been updated. It allows nearly all industrial chemicals on the market and in consumer products with no mandate for safety testing, and with no requirement that companies prove their products are safe for children and others who are vulnerable before they are sold. The result of this weak law is a body burden of industrial chemicals found in every member of every household in this country, pets and people alike. Congress and public health agencies attempt to hold together the threadbare safety net provided by TSCA with a series of other programs and laws targeted at particular kinds of exposures, including laws and regulations that provide some oversight on the safety of drugs, pesticides in food, cosmetics, and food additives. But even with this hodgepodge of programs, we’ve seen recent glaring evidence of safety gaps, with potential health risks from exposures that include everything from antifreeze in toothpaste (FDA 2007b) and lead and asbestos in children’s toys (CDC 2007, 2008), to cancer-inducing chemicals in cosmetics and personal care products (EWG 2007; Brody 2007; Darbre 2006; Irigaray 2007) and unregulated contaminants in overseas-produced food and drugs (Armstrong 2008). As weak as the system of protections is for people, it’s even weaker for pets. Public health agencies have little authority and few resources to ensure that products produced for pets are safe (FDA CVM 2007a).

A massive pet food recall in 2007 brought attention to the most urgent issues in pet food safety such as regulations, ingredients and additives in commercial foods and accountability of pet food manufacturers to government agencies and to the general public (AVMA 2007). Illnesses and deaths of pets caused by melamine-contaminated food have contributed to a loss of public confidence in pet food safety, raising many questions about the role of the government in this important area (FDA 2008).

Basic common sense suggests that commercially distributed pet food should be held to the same health and safety standards as human food. Indeed, the FDA Center for Veterinary Medicine (CVM) describes its mission as a “consumer protection organization [that fosters] public and animal health by approving safe and effective products for animals” (FDA CVM 2000a). In this position, CVM is “responsible for the evaluation, approval and/or surveillance of animal drugs, food additives, feed ingredients, and animal devices” (FDA CVM 2000b). These public statements indicate that, similar to the FDA’s Center for Food Safety and Applied Nutrition (CFSAN) which oversees 80% of food intended for human consumption in the United States (FDA 2002), the CVM is in a position to provide leadership, oversight, and targeted regulations in order to assure the safety of pet food. However, the current reality falls far short of this worthy goal. When it comes to the presence of dubious food additives, chemical pollutants or untested ingredients in pet food, pets and pet owners are still largely on their own. For human food, the FDA CFSAN regulates food additives, colorants, and chemical contaminants in food such as pesticide residues. Together with CFSAN, other government agencies oversee the safety of human food supply, including the Food Safety and Inspection Service of the U.S. Department of Agriculture, Environmental Protection Agency, and state and local governments. Even with this system, food additives and preservatives that may pose health risks are sometimes approved for use in human food (FDA 1993, 2007c). Recent studies, for instance, demonstrate links between attention deficit/hyperactivity disorders and common food additives (McCann 2007; McCann 2008). The adequacy of health protections for food additives has been called into question many times (Barrett 2007). But food manufactured for pets falls outside of even this flawed system. Significantly less stringent oversight is applied to pet food compared to food standards for people. Unlike their role in human food safety, FDA and USDA are doing and are required to do close to nothing for pet food safety under the current laws and regulations. Some standards and mandates for government oversight of pet foods do exist (FDA CVM 2007a; Syverson 2007a, b). In practice, these regulations have massive gaps. To draw a comparison, for human food additives companies need to submit an application to obtain pre-clearance approval from FDA. Provisions for the similar pre-clearance mechanism for pet food additives are defined in Title 21 Code of Federal Regulations (CFR) subchapter on animal drugs, feeds, and related products. Such a petition should contain a description of the chemical identity, manufacturing process and controls, human food safety data, target animal safety data, product labeling, and in some cases an environmental assessment. For some additives, tolerance limitations need to be established in order to ensure their safety. Yet despite having the power to do so, the CVM does not scrutinize manufacturer’s practices with regard to pet food additives. As described on the CVM website (FDA CVM 2007a):

CVM has used regulatory discretion and not required food additive petitions for substances that do not raise any safety concerns. In this case, we ask the company to submit the information needed to list the ingredient in the Official Publication of the Association of American Feed Control Officials (AAFCO). This ingredient definition process is done to conserve agency resources, as food additive approval is time-consuming. CVM reviews the data to ensure the ingredient has utility and can be manufactured consistently to meet product specifications. Although ingredients used under regulatory discretion are still unapproved food additives, we agree we will not take regulatory action as long as the labeling is consistent with the accepted intended use, the labeling or advertising does not make drug claims, and new data are not received that raise questions concerning safety or suitability.

As a result, companies are not required to notify FDA before they use a chemical additive in pet food, as they are for human food. Instead, pet foods can legally contain unapproved food additives whose safety has not been adequately examined by scientific experts. This state of affairs puts the health of pets into a version of a hit-or-miss game. Several case studies of toxic chemicals in commercial pet foods illustrate the problems inherent in this lack of regulation. Antioxidant preservative ethoxyquin is a controversial additive that is currently allowed at levels up to 150 parts per million (ppm, equivalent to microgram of additive per gram of food) in animal feeds and canned pet food, as described in 21 CFR section 573.380 (FDA 1996a). Presence of ethoxyquin in dog food has been linked to numerous adverse effects in dogs, such as liver, kidney, thyroid and reproductive dysfunction, teratogenic and carcinogenic effects, allergic reactions, and skin and hair abnormalities (Dzanis 1991). Although FDA acknowledges that 150 ppm levels of ethoxyquin may be hazardous for lactating female dogs and puppies, no action has been taken by the agency beyond a request to the pet food industry that ethoxyquin in complete dog foods be voluntarily lowered to 75 parts per million (FDA 1997; FDA CVM 2007b). At the moment, pet owners cannot know what levels of this additive may be found in a can of pet food; they can only hope that the levels are less than what could harm their dogs. It is relatively easy for a manufacturer to include a chemical ingredient in pet food. Any food additive that has been cleared by the FDA under the extensive “Generally Recognized As Safe” (GRAS) category is permitted. So far so good. However, if a company wishes to add a new, untested chemical substance into pet food, it merely needs to notify the voluntary AAFCO organization. Under current standards, that is sufficient – no FDA notification is required. In contrast to the wide range of permitted animal food additives and all the potentially present unapproved food additives, EWG analysis found only one chemical prohibited by FDA from use in pet food. Water-retaining additive propylene glycol has been used as an ingredient in soft-moist pet foods (FDA 1996b). Propylene glycol causes inactivation and clumping of hemoglobin in the red blood cells of cats, thereby causing anemia and other adverse effects in cats consuming the substance at levels that used to be commonly present in soft-moist food (Christopher 1989). Current regulations expressly prohibit the presence of propylene glycol in cat foods. Nevertheless, this is just one ingredient among many whose safety or even quantity in pet food is not adequately studied and publicly available. As the government, general public and the media are well aware, even with all the standards in place for human food safety, the agencies and companies make huge mistakes and leave gaps that put human health at risk. So, we can readily imagine how unreliable the safety of food supply is for dogs and cats where there is almost no oversight from the government at all. Indeed, this is exactly what happened in the melamine crisis of 2007. Congressional hearings that followed the crisis revealed blatant gaps in pet food safety in the United States. Not only has there been no adequate monitoring system for the chemical composition of pet foods, but there was also a huge delay in companies’ response to the crisis. Nearly three weeks passed between the first report of cat illness (received by the Menu Foods on February 22, 2007) and the date when Menu Food notified FDA of the problem and initiated the recall (March 15, 2007). This long delay resulted in a lot of preventable illnesses and even deaths of many pets (Burns 2007a). Following a great public outcry and congressional investigation, legislation was passed in September 2007 to protect the health of both animals and humans (Food and Drug Administration Amendments Act 2007; Nolen 2007). The new legislation amends the Federal Food, Drug, and Cosmetic Act to require companies to immediately notify FDA of any food contamination problems. It also requires the Secretary to establish: (1) processing and ingredient standards for pet food; (2) update standards for pet food labeling; and (3) set in place an early warning system to alert the public about unsafe pet food. Although bought at a high cost of needless animal suffering, this Act has the potential to increase the safety of pet food – if the FDA issues appropriately strict rules and regulations and ensures ongoing oversight and surveillance of pet food manufacturing practices. In the meanwhile, more gaps than standards are evident as the lack of government supervision over pet food and other pet products continues to put companion animals at risk over and over again. In the absence of government oversight, the safety of products intended for pets is almost completely within the purview of the manufacturers themselves. The pet food industry, as represented by the manufacturers’ association known as the Pet Food Institute (PFI), is largely self-regulating. However, as the melamine crisis clearly demonstrated, this model of voluntary compliance and internal setting of manufacturing criteria has not functioned successfully. The only organization that reviews standards on pet food is the Association of American Feed Control Officials (AAFCO). AAFCO has no regulatory authority, although it publishes a code, known as Model Pet and Specialty Pet Food Regulation. As stated on the CVM website, AAFCO responsibility for the pet food products is necessary “because FDA has limited enforcement resources that are focused on human food safety issues” (FDA CVM 2007a). Yet, would it not be better for pets and their owners, more secure, and more scientifically defensible if the FDA itself issued binding pet food regulations instead of relying on a voluntary organization to provide guidelines and suggestions to the industry? For example, for years cat owners have worried about the presence of ash in cat food because of its potential links to kidney problems and chronic renal failure (Hughes 2002). Within the ash, there is calcium, magnesium, calcium, potassium and other trace minerals; greater quantities of ash are produced when low quality meat parts are included in pet food. On its website, FDA states that ash per se is not related to the incidence of feline lower urinary tract disease (FDA CVM 2007c). However, a pet owner cannot help but wonder how high can be the levels of ash that a pet food manufacturer can legally include in a product? Who is setting these levels and has their safety being adequately demonstrated? Another issue of significant concern is the safety of pet products, such as pet toys, pet beds, and pet clothing, and numerous other products developed and marketed for pets. There are no government standards in this area, leaving the industry group itself, the American Pet Product Manufacturers Association, to adopt whatever manufacturing practices it wishes. As a result, pet toys can contain endocrine-disrupting and asthma-inducing phthalates and pet beds and clothing may have toxic flame retardants in them. Nobody is looking and nobody bears legal responsibility – hardly a situation that inspires confidence in pet owners. Again, a comparison between products for human use and products for pets points out how the lack of safety standards endangers the health of pets. The Consumer Product Safety Commission (CPSC) oversees the safety of human products. This agency is entrusted by the Congress “to protect the public against unreasonable risks of injuries and deaths associated with consumer products” (CPSC 2007). Specifically, the Consumer Product Safety Act sec. 31 (2) (A) states that the CPSC, with the assistance of a Chronic Hazard Advisory Panel, has the authority to review whether a substance in a product may be a carcinogen, mutagen, or a teratogen. When such a determination is made, the Panel needs to report an estimate of the probable harm to human health that will result from exposure to the substance. This process allows CPSC to issue rules and regulations under the Federal Hazardous Substances Act that will ensure safety of consumer products from chemical contaminants. In contrast to CPSC control over products for human consumption, it has no power over products for pets. In a letter to EWG, CPSC stated: “The Commission does not have the authority to require labeling that warns of dangers to animals.” Instead, only a “personal” injury or illness of a human consumer can constitute grounds for CPSC action. Thus, as EWG found out, reports of hundreds of deaths of pet birds due to Teflon cookware falls outside the interests of this regulatory agency (EWG 2003b). All these examples point in a single direction: food and products for pets receive hardly any government oversight, standards, or regulations. This situation puts the health of pets into danger. Pets are sentinels for the urgent need for a system of health protections that requires companies to prove their products are safe before they are sold. Modernizing public health laws now more than 30 years old is a critical step to protecting the health of all members of American households, whether they walk on two legs or four.

Study Methodology

Introduction. For 20 dogs and 37 cats, a trip to the vet in December and January included a special procedure – the donation of a small amount of blood or urine needed for an exploratory study of industrial pollutants in pets. In the most comprehensive tests ever conducted on companion animals, we analyzed samples for a broad battery of industrial chemicals and pollutants – 70 chemicals in total, from 5 chemical classes. To our knowledge this work includes the first reported biomonitoring tests for 23 of the targeted chemicals in pets. Information below describes the components of this new study, detailing the sample collection procedures, sample preparation and analysis methods, and the quality assurance and quality control provisions included in the study design. Blood and urine sample acquisition and storage. Samples were collected from dogs and cats visiting the Hanover Animal Hospital in Mechanicsville, Virginia. Each pet owner was informed of the nature of the study, and signed a consent form in order to participate. A dog typically can safely provide 3 to 4 mL of blood and 1 mL of urine, while due to smaller size, a cat typically can safely provide only 1 to 2 mL of blood and 1 mL of urine. Number of pets sampled, sample medium, and sample storage container varied depending on the class of chemicals targeted for analysis:

• 5 dogs and 10 cats provided blood samples stored and processed in plastic vacutainers and vials for perfluorochemicals analysis;
• 5 dogs and 5 cats provided urine samples for phthalates and BPA analysis;
• 10 dogs and 17 cats provided blood samples stored and processed in glass vacutainers and vials for PBDEs analysis;
• 5 dogs and 10 cats provided blood samples stored in EDTA-treated plastic vacutainers for metals analysis.

Blood samples collected for perfluorochemical and PBDE analyses were allowed to clot for 30 minutes, then centrifuged. The serum was extracted and stored for analysis. Blood samples collected for metals analysis were used whole. Serum, whole blood, and urine samples were frozen and shipped at the end of the collection period to Axys Analytical Services in British Columbia, Canada. There, individual samples were combined to create a single dog and a single cat serum sample for perfluorochemicals analysis, a single dog and a single cat urine sample for phthalates and BPA analysis, and a single dog and a single cat serum sample for PBDEs analysis. Whole blood samples were shipped to Brooks Rand in Seattle, Washington, where they were composited to create a single dog sample and a single cat sample for metals analysis. Samples were stored at -20 degrees C until analyzed.

Analysis of Perfluorochemicals (PFCs). Analysis for perfluorochemicals was conducted on approximately 0.5 mL of serum. The sample was first spiked with three 13C-labeled perfluorochemical surrogate standards prior to extraction using formic acid on a solid phase extraction cartridge. The extract was spiked with labeled recovery standards and analyzed by liquid chromatography tandem mass spectrometry (LC/MS/MS) using a Micromass Quattro Ultima MS/MS coupled with a Waters 2690 high performance liquid chromatographic (HPLC) system. Target compounds are quantified using the internal standard method, comparing the area of the quantification ion to that of the 13C-labeled standard and correcting for response factors. Final sample concentrations were determined by isotope dilution/internal standard quantification against matrix-matched calibration standards carried through the analysis procedure alongside the samples. Measurements are reported in nanograms per milliliter (wet weight) of blood serum. Analysis of Phthalate Metabolites and Bisphenol A (BPA). Phthalate metabolites and BPA were co-extracted from 1 mL urine samples. Urine samples were first buffered with ammonium acetate, and spiked with 13C-labeled phthalate monoesters, d6-bisphenol A, 13C4-4-methylumbelliferone, and 4-methylumbelliferyl glucuronide. Urine samples were also spiked with beta-glucuronidase enzyme (for deconjugation of glucuronidated forms of the target analytes). The treated samples were incubated to hydrolyze the glucuronides (the completeness of hydrolysis was monitored by the recovery of 4-methylumbelliferone). Samples were extracted and cleaned up using solid phase extraction (SPE) procedures. Extracts were spiked with labeled recovery standards for both phthalate metabolites and BPA, split into 2 portions, and each portion was analyzed separately by LC/MS/MS using a Micromass Quattro Ultima MS/MS coupled with a Waters 2695 HPLC system. The method determined the total of the free and the glucuronidated phthalate metabolites and bisphenol A. Analyte concentrations were determined using isotope dilution quantification. Values are reported in units of micrograms per gram creatinine, a urine protein, to account for variation in the dilution of the urine samples due to different levels of fluid intake by the participating animals. Analysis of Polybrominated Diphenyl Ethers (PBDEs). Analyses for PBDEs were achieved using a 6 gram serum sample. Samples were spiked with a suite of 13C-labeled surrogate standards, extracted and cleaned up using solid phase extraction (SPE) procedures, followed by acid silica clean up. Extracts were spiked with labeled recovery standards and analyzed by gas chromatography with high-resolution mass spectrometric detection (GC/HRMS) in accordance with EPA method 1614. GC/HRMS analyses were performed using a Micromass Ultima high-resolution mass spectrometer equipped with a Hewlett-Packard 6890 gas chromatograph. Quantification of target analytes was achieved by isotope dilution quantification using the 13C-labeled surrogate standards. Values are reported in units of nanograms per gram of lipid in the blood serum, as PBDEs accumulate in the lipid fraction of blood. Analysis of Metals. Analysis for metals was conducted by Brooks Rand LLC (Seattle, WA). To measure methylmercury, 0.1 gram whole blood samples were subjected to alkaline digestion, followed by ethylation, then purging and trapping of the resulting ethylated mercury derivatives. The mercury compounds were thermally desorbed and transferred to a gas chromatography column, which separated the species by mass. Ethylated mercury compounds were heated to form elemental mercury, which was measured using cold vapor atomic fluorescence spectroscopy (CVAFS). Values are reported in units of micrograms per liter (wet weight) of whole blood. To measure total mercury, 1 gram whole blood samples were subjected to acid digestion and oxidation. Mercury ions in the sample were reduced to elemental mercury, then purged and trapped. The concentrated mercury was measured using CVAFS. Values are reported in units of micrograms per liter (wet weight) of whole blood. To measure lead, 200 microliter whole blood samples were first diluted by a factor of 50 in a 1% nitric acid solution and filtered. Analysis was conducted using inductively couple plasma – mass spectrometry (ICP-MS). Values are reported in units of micrograms per deciliter (wet weight) of whole blood. Procedures for quality assurance and quality control (QA/QC). All organic analyses were conducted in accordance with AXYS’ accredited QA/QC program including regular analysis of QC samples and participation in international inter-laboratory comparison programs. Each analysis batch included a procedural blank to demonstrate cleanliness and a spiked laboratory control sample to monitor precision and recovery. The sample results were reviewed and evaluated in relation to the QA/QC samples worked up at the same time. The sample surrogate standard recoveries and detection limits, procedural blank data and the laboratory control sample data were evaluated against method criteria to ensure acceptable data quality. All metal analyses were conducted in accordance with Brooks Rand’s accredited QA/QC program. Samples were analyzed in conjunction with NIST 966 standard-spiked blanks, and 4 method blanks.

References

Armstrong D. 2008. For FDA, Congress Readies a Bitter Pill. CQ Weekly (April 7): 867-77. AVMA (American Veterinary Medical Association). 2007. Pet Food Recall Frequently Asked Questions. Available:http://www.avma.org/aa/petfoodrecall/faq.asp [accessed April 10 2008]. Barrett JR. 2007. Diet & nutrition: hyperactive ingredients? Environ Health Perspect 115(12): A578. Bertone ER, Snyder LA, Moore AS. 2002. Environmental tobacco smoke and risk of malignant lymphoma in pet cats. Am J Epidemiol 156(3): 268-73. Bertone ER, Snyder LA, Moore AS. 2003. Environmental and lifestyle risk factors for oral squamous cell carcinoma in domestic cats. J Vet Intern Med 17(4): 557-62. Betts K. 2007. PBDEs, cats, and children. Environ Sci Technol 41(18): 6319-20. Blandford TB, Seamon PJ, Hughes R, Pattison M, Wilderspin MP. 1975. A case of polytetrafluoroethylene poisoning in cockatiels accompanied by polymer fume fever in the owner. Vet Rec 96(8): 175-8. Bornehag CG, Sundell J, Weschler CJ, Sigsgaard T, Lundgren B, Hasselgren M, et al. 2004. The association between asthma and allergic symptoms in children and phthalates in house dust: a nested case-control study. Environ Health Perspect 112(14): 1393-7. Booth J. 2007. Eli Lilly launches first Prozac for dogs. Times Online April 25, 2007. Available: http://www.timesonline.co.uk/tol/news/uk/science/article1705299.ece [accessed April 15 2008]. Brody JG, Rudel RA, Michels KB, Moysich KB, Bernstein L, Attfield KR, et al. 2007. Environmental pollutants, diet, physical activity, body size, and breast cancer: where do we stand in research to identify opportunities for prevention? Cancer 109(12 Suppl): 2627-34. Bukowski JA, Wartenberg D. 1997. An alternative approach for investigating the carcinogenicity of indoor air pollution: pets as sentinels of environmental cancer risk. Environ Health Perspect 105(12): 1312-9. Burns K. 2007a. Chief executive officers testify about recall of pet food. J Am Vet Med Assoc 230(11): 1600-04. Burns K. 2007b. Recall shines spotlight on pet foods. J Am Vet Med Assoc 230(9): 1285-8. Casteel SW. 2001. Metal toxicosis in horses. Vet Clin North Am Equine Pract 17(3): 517-27. CDC (Centers for Disease Control and Prevention). 2007. Toy Jewelry and Childhood Lead Exposure. Available: http://www.cdc.gov/nceh/lead/faq/jewelry.htm [accessed April 10 2008]. CDC (Centers for Disease Control and Prevention). 2008. Lead Recalls: Toys. Available: http://www.cdc.gov/nceh/lead/Recalls/toys.htm [accessed April 10 2008]. Christopher MM, Perman V, Eaton JW. 1989. Contribution of propylene glycol-induced Heinz body formation to anemia in cats. J Am Vet Med Assoc 194(8): 1045-56. Colt JS, Lubin J, Camann D, Davis S, Cerhan J, Severson RK, et al. 2004. Comparison of pesticide levels in carpet dust and self-reported pest treatment practices in four US sites. J Expo Anal Environ Epidemiol 14(1): 74-83. CPSC (U.S. Consumer Product Safety Commission). 2007. Who We Are – What We Do for You. Available: http://www.cpsc.gov/cpscpub/pubs/103.html [accessed April 4 2008]. Darbre PD. 2006. Environmental oestrogens, cosmetics and breast cancer. Best Pract Res Clin Endocrinol Metab 20(1): 121-43. Dorn CR, Taylor DO, Frye FL, Hibbard HH. 1968. Survey of animal neoplasms in Alameda and Contra Costa Counties, California. I. Methodology and description of cases. J Natl Cancer Inst 40(2): 295-305. Dorn CR, Taylor DO, Schneider R, Hibbard HH, Klauber MR. 1968. Survey of animal neoplasms in Alameda and Contra Costa Counties, California. II. Cancer morbidity in dogs and cats from Alameda County. J Natl Cancer Inst 40(2): 307-18. Dye JA, Venier M, Zhu L, Ward CR, Hites RA, Birnbaum LS. 2007. Elevated PBDE levels in pet cats: sentinels for humans? Environ Sci Technol 41(18): 6350-6. Dzanis DA. 1991. Safety of ethoxyquin in dog foods. J Nutr 121(11 Suppl): S163-4. Edinboro CH, Scott-Moncrieff JC, Janovitz E, Thacker HL, Glickman LT. 2004. Epidemiologic study of relationships between consumption of commercial canned food and risk of hyperthyroidism in cats. J Am Vet Med Assoc 224(6): 879-86. Edlich RF, Winters KL, Long WB, 3rd. 2005. Treated wood preservatives linked to aquatic damage, human illness, and death–a societal problem. J Long Term Eff Med Implants 15(2): 209-23. EWG (Environmental Working Group). 2007. EWG Research Shows 22 Percent of All Cosmetics May Be Contaminated With Cancer-Causing Impurity. Available: http://www.ewg.org/node/21286 [accessed April 11 2008]. EWG (Environmental Working Group). 2003a. Canaries in the kitchen: teflon toxicosis. Washington, DC. Available: http://www.ewg.org/reports/toxicteflon [accessed April 8 2008]. EWG (Environmental Working Group). 2003b. EWG Petition to the CPSC. Available: http://www.ewg.org/reports/toxicteflon [accessed April 4 2008]. EWG (Environmental Working Group). 2003c. PFCs: A chemical family that contaminates the planet. Available: http://www.ewg.org/reports/pfcworld [accessed April 8 2008]. FDA (U.S. Food and Drug Administration). 1993. A Fresh Look at Food Preservatives. Available:http://www.cfsan.fda.gov/~dms/fdpreser.html [accessed April 10 2008]. FDA (U.S. Food and Drug Administration). 1996a. 21 CFR section 573.380 Ethoxyquin in animal feeds. [accessed April 4, 2008 at http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=573.380]. FDA (U.S. Food and Drug Administration). 1996b. 21 CFR section 582.1666 Propylene glycol. [accessed April 4, 2008 at http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=582.1666]. FDA (U.S. Food and Drug Administration). 1997. FDA requests that ethoxyquin levels be reduced in dog foods. Available:http://www.fda.gov/cvm/september97.htm#2728 [accessed March 26 2008]. FDA (U.S. Food and Drug Administration). 2002. Keeping the Nation’s Food Supply Safe: FDA’s Big Job Done Well. Available:http://www.fda.gov/opacom/factsheets/justthefacts/2cfsan.html [accessed April 2 2008]. FDA (U.S. Food and Drug Administration). 2007a. FDA’s ongoing pet food investigation. Available:http://www.fda.gov/consumer/updates/petfoodrecallup.html [accessed March 28 2008]. FDA (U.S. Food and Drug Administration). 2007b. FDA Advises Consumers to Avoid Toothpaste From China Containing Harmful Chemical. Available: http://www.fda.gov/bbs/topics/NEWS/2007/NEW01646.html [accessed April 10 2008]. FDA (U.S. Food and Drug Administration). 2007c. How Safe are Color Additives? Available:http://www.fda.gov/consumer/updates/coloradditives121007.html [accessed April 10 2008]. FDA (U.S. Food and Drug Administration). 2008. Pet Food Recall (Melamine)/Tainted Animal Feed. Available:http://www.fda.gov/oc/opacom/hottopics/petfood.html [accessed March 26 2008]. FDA CVM (U.S. Food and Drug Administration Center for Veterinary Medicine). 2000a. Mission Statement. Available:http://www.fda.gov/cvm/mission.htm [accessed April 2 2008]. FDA CVM (U.S. Food and Drug Administration Center for Veterinary Medicine). 2000b. Vision Statement. Available:http://www.fda.gov/cvm/visionstatement.htm [accessed April 2 2008]. FDA CVM (U.S. Food and Drug Administration Center for Veterinary Medicine). 2007a. FDA’s Regulation of Pet Food. Available:http://www.fda.gov/cvm/petfoodflier.html [accessed March 17 2008]. FDA CVM (U.S. Food and Drug Administration Center for Veterinary Medicine). 2007b. Interpreting Pet Food Labels. Available:http://www.fda.gov/cvm/petlabel.htm [accessed March 25 2008]. FDA CVM (U.S. Food and Drug Administration Center for Veterinary Medicine). 2007c. Interpreting Pet Food Labels – Special Use Foods. Available:http://www.fda.gov/cvm/labelint.htm [accessed April 11 2008]. Filby AL, Neuparth T, Thorpe KL, Owen R, Galloway TS, Tyler CR. 2007. Health impacts of estrogens in the environment, considering complex mixture effects. Environ Health Perspect 115(12): 1704-10. Food and Drug Administration Amendments Act. 2007. Elements of the Human and Pet Food Safety Act of 2007 were enacted in the Food and Drug Administration Amendments Act of 2007, Public Law 110–85—Sept. 27, 2007. Glickman LT, Domanski LM, Maguire TG, Dubielzig RR, Churg A. 1983. Mesothelioma in pet dogs associated with exposure of their owners to asbestos. Environ Res 32(2): 305-13. Glickman LT, Raghavan M, Knapp DW, Bonney PL, Dawson MH. 2004. Herbicide exposure and the risk of transitional cell carcinoma of the urinary bladder in Scottish Terriers. J Am Vet Med Assoc 224(8): 1290-7. Glickman LT, Schofer FS, McKee LJ, Reif JS, Goldschmidt MH. 1989. Epidemiologic study of insecticide exposures, obesity, and risk of bladder cancer in household dogs. J Toxicol Environ Health 28(4): 407-14. Gunn-Moore D. 2005. Feline endocrinopathies. Vet Clin North Am Small Anim Pract 35(1): 171-210. Harbison ML, Godleski JJ. 1983. Malignant mesothelioma in urban dogs. Vet Pathol 20(5): 531-40. Hayes HM, Jr., Hoover R, Tarone RE. 1981. Bladder cancer in pet dogs: a sentinel for environmental cancer? Am J Epidemiol 114(2): 229-33. Hayes HM, Tarone RE, Cantor KP. 1995. On the association between canine malignant lymphoma and opportunity for exposure to 2,4-dichlorophenoxyacetic acid. Environ Res 70(2): 119-25. Hayes HM, Tarone RE, Cantor KP, Jessen CR, McCurnin DM, Richardson RC. 1991. Case-control study of canine malignant lymphoma: positive association with dog owner’s use of 2,4-dichlorophenoxyacetic acid herbicides. J Natl Cancer Inst 83(17): 1226-31. Hayes HM, Tarone RE, Casey HW. 1995. A cohort study of the effects of Vietnam service on testicular pathology of U.S. military working dogs. Mil Med 160(5): 248-55. Hayes HM, Tarone RE, Casey HW, Huxsoll DL. 1990. Excess of seminomas observed in Vietnam service U.S. military working dogs. J Natl Cancer Inst 82(12): 1042-6. Hayes T, Haston K, Tsui M, Hoang A, Haeffele C, Vonk A. 2002. Herbicides: feminization of male frogs in the wild. Nature 419(6910): 895-6. Hayes TB, Case P, Chui S, Chung D, Haeffele C, Haston K, et al. 2006. Pesticide mixtures, endocrine disruption, and amphibian declines: are we underestimating the impact? Environ Health Perspect 114 Suppl 1: 40-50. Horwitz DF. 2001. Behavior Problems in Senior Dogs. Atlantic Coast Veterinary Conference 2001. Available: http://www.vin.com/vindbpub/searchpb/proceedings/pr05000/pr00315.htm [accessed April 15 2008]. Hughes KL, Slater MR, Geller S, Burkholder WJ, Fitzgerald C. 2002. Diet and lifestyle variables as risk factors for chronic renal failure in pet cats. Prev Vet Med 55(1): 1-15. Irigaray P, Newby JA, Clapp R, Hardell L, Howard V, Montagnier L, et al. 2007. Lifestyle-related factors and environmental agents causing cancer: an overview. Biomed Pharmacother 61(10): 640-58. Kang JH, Kondo F. 2003. Determination of bisphenol A in canned pet foods. Res Vet Sci 73: 177-182. Kass PH, Peterson ME, Levy J, James K, Becker DV, Cowgill LD. 1999. Evaluation of environmental, nutritional, and host factors in cats with hyperthyroidism. J Vet Intern Med 13(4): 323-9. Kelsey JL, Moore AS, Glickman LT. 1998. Epidemiologic studies of risk factors for cancer in pet dogs. Epidemiol Rev 20(2): 204-17. Knight TE, Kumar MS. 2003. Lead toxicosis in cats-a review. J Feline Med Surg 5(5): 249-55. Khan BI, Solo-Gabriele HM, Townsend TG, Cai Y. 2006. Release of arsenic to the environment from CCA-treated wood. 1. Leaching and speciation during service. Environ Sci Technol 40(3): 988-93. Knight TE, Kumar MS. 2003. Lead toxicosis in cats-a review. J Feline Med Surg 5(5): 249-55. Koya G. 1964. [Experimental Study on Etiology of Minamata Disease, Especially on Intoxication of Methylmercuric Sulfide Compounds in Cats]. Kumamoto Igakkai Zasshi 38: 100-39. Kucera E. 1988. Dogs as indicators of urban lead distribution. Environmental Monitoring and Assessment 10(1): 51-57. Landrigan PJ. 2001. Children’s environmental health. Lessons from the past and prospects for the future. Pediatr Clin North Am. 2001 48(5): 1319-30. Linnett PJ. 2008. Permethrin toxicosis in cats. Aust Vet J 86(1-2): 32-5. Marino PE, Landrigan PJ, Graef J, Nussbaum A, Bayan G, Boch K, et al. 1990. A case report of lead paint poisoning during renovation of a Victorian farmhouse. Am J Public Health 80(10): 1183-5. Martin KM, Rossing MA, Ryland LM, DiGiacomo RF, Freitag WA. 2000. Evaluation of dietary and environmental risk factors for hyperthyroidism in cats. J Am Vet Med Assoc 217(6): 853-6. McCann D, Barrett A, Cooper A, Crumpler D, Dalen L, Grimshaw K, et al. 2007. Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. Lancet 370(9598): 1560-7. McCann KJ, Ottensmeier CH, Callard A, Radcliffe CM, Harvey DJ, Dwek RA, et al. 2008. Remarkable selective glycosylation of the immunoglobulin variable region in follicular lymphoma. Mol Immunol 45(6): 1567-72. McDuffie HH, Pahwa P, McLaughlin JR, Spinelli JJ, Fincham S, Dosman JA, et al. 2001. Non-Hodgkin’s lymphoma and specific pesticide exposures in men: cross-Canada study of pesticides and health. Cancer Epidemiol Biomarkers Prev 10(11): 1155-63. Miller S, Bauk TJ. 1992. Lead toxicosis in a group of cats. J Vet Diagn Invest 4(3): 362-3. Morgan MK, Sheldon LS, Thomas KW, Egeghy PP, Croghan CW, Jones PA, et al. 2008. Adult and children’s exposure to 2,4-D from multiple sources and pathways. J Expo Sci Environ Epidemiol. in press Morgan RV. 1994. Lead poisoning in small companion animals: an update (1987-1992). Vet Hum Toxicol 36(1): 18-22. Muraki K. 1965. [Experimental studies on the cause of Minamata disease in the cat. (2). Hg content of organs chronically intoxicated with fish and Hg-ethyl phosphates]. Nippon Yakurigaku Zasshi 61(4): 269-78. National Research Council (NRC). 1991. Animals as Sentinels of Environmental Health Hazards. Washington, DC: National Academies Press. Newman SJ, Smith SA. 2006. Marine mammal neoplasia: a review. Vet Pathol 43(6): 865-80. Nolen RS. 2007. Congress strengthens pet food safety regulations. J Am Vet Med Assoc 231(9): 1320-1. Olczak J, Jones BR, Pfeiffer DU, Squires RA, Morris RS, Markwell PJ. 2005. Multivariate analysis of risk factors for feline hyperthyroidism in New Zealand. New Zealand Veterinary Journal 53 (10): 53-8. Overall KL, Dunham AE. 2002. Clinical features and outcome in dogs and cats with obsessive-compulsive disorder: 126 cases (1989-2000). J Am Vet Med Assoc 221 (10): 1445-52. Paoloni MC, Khanna C. 2007. Comparative oncology today. Vet Clin North Am Small Anim Pract 37(6): 1023-32. Paoloni M, Khanna C. 2008. Translation of new cancer treatments from pet dogs to humans. Nat Rev Cancer 8(2): 147-56. Peterson ME, Ward CR. 2007. Etiopathologic findings of hyperthyroidism in cats. Vet Clin North Am Small Anim Pract 37(4): 633-45, v. Potera C. 2007. Chemical exposures: cats as sentinel species. Environ Health Perspect 115(12): A580. Prescott CW. 1983. Clinical findings in dogs and cats with lead poisoning. Aust Vet J 60(9): 270-1. Purdue University Department of Veterinary Pathobiology. 2000. Breed Health Surveys. Available http://www.vet.purdue.edu/epi/[accessed April 15 2008] Reif JS. 2006. The epidemiology of cancer in pet animals. In: Small Animal Clinical Oncology (Withrow SJ, Vail DM, eds). Amsterdam: Elsevier, 68-76. Reif JS, Bruns C, Lower KS. 1998. Cancer of the nasal cavity and paranasal sinuses and exposure to environmental tobacco smoke in pet dogs. Am J Epidemiol 147(5): 488-92. Reif JS, Dunn K, Ogilvie GK, Harris CK. 1992. Passive smoking and canine lung cancer risk. Am J Epidemiol 135(3): 234-9. Reynolds PM, Reif JS, Ramsdell HS, Tessari JD. 1994. Canine exposure to herbicide-treated lawns and urinary excretion of 2,4-dichlorophenoxyacetic acid. Cancer Epidemiol Biomarkers Prev 3(3): 233-7. Roza MR, Viegas CA. 2007. The dog as a passive smoker: effects of exposure to environmental cigarette smoke on domestic dogs. Nicotine Tob Res 9(11): 1171-6. Schilling RJ, Steele GK, Harris AE, Donahue JF, Ing RT. 1988. Canine serum levels of polychlorinated biphenyls (PCBs): a pilot study to evaluate the use of animal sentinels in environmental health. Arch Environ Health 43(3): 218-21. Seidel WC, Scherer KV, Jr., Cline D, Jr., Olson AH, Bonesteel JK, Church DF, et al. 1991. Chemical, physical, and toxicological characterization of fumes produced by heating tetrafluoroethene homopolymer and its copolymers with hexafluoropropene and perfluoro(propyl vinyl ether). Chem Res Toxicol 4(2): 229-36. Shusterman DJ. 1993. Polymer fume fever and other fluorocarbon pyrolysis-related syndromes. Occup Med 8(3): 519-31. Stapleton HM, Dodder NG, Offenberg JH, Schantz MM, Wise SA. 2005. Polybrominated diphenyl ethers in house dust and clothes dryer lint. Environ Sci Technol 39(4): 925-31. Syverson D. 2007a. Association of American Feed Control Officials Pet Food Committee: How Pet Food is Regulated. Available: http://www.aafco.org/OtherInformation/tabid/73/Default.aspx [accessed April 2, 2008]. Syverson D. 2007b. Association of American Feed Control Officials Pet Food Committee: Questions and Answers Concerning Pet Food Regulation. Available: http://www.aafco.org/OtherInformation/tabid/73/Default.aspx [accessed April 2, 2008]. Texas A&M Veterinary Medical Center. 2008. What is the incidence of cancer in our pets? Available: http://www.cvm.tamu.edu/oncology/faq/FAQ.html [accessed March 29 2008]. Thomas CW, Rising JL, Moore JK. 1975. Blood lead concentrations in three groups of dogs from a suburban Illinois community. J Am Vet Med Assoc 167(11): 995-9. Thomas CW, Rising JL, Moore JK. 1976. Blood lead concentrations of children and dogs from 83 Illinois families. J Am Vet Med Assoc 169(11): 1237-40. Tsuchiya K. 1992. The discovery of the causal agent of Minamata disease. Am J Ind Med 21(2): 275-80. van der Schalie WH, Gardner HS, Jr., Bantle JA, De Rosa CT, Finch RA, Reif JS, et al. 1999. Animals as sentinels of human health hazards of environmental chemicals. Environ Health Perspect 107(4): 309-15. von Lindern IH, Spalinger SM, Bero BN, Petrosyan V, von Braun MC. 2003. The influence of soil remediation on lead in house dust. Sci Total Environ 303(1-2): 59-78. Waters DJ, Wildasin K. 2006. Cancer clues from pet dogs. Sci Am 295(November 12): 94-101. Wells RE. 1983. Fatal toxicosis in pet birds caused by an overheated cooking pan lined with polytetrafluoroethylene. J Am Vet Med Assoc 182(11): 1248-50. Wormuth M, Scheringer M, Vollenweider M, Hungerbuhler K. 2006. What are the sources of exposure to eight frequently used phthalic acid esters in Europeans? Risk Anal 26(3): 803-24. Ylitalo GM, Stein JE, Hom T, Johnson LL, Tilbury KL, Hall AJ, et al. 2005. The role of organochlorines in cancer-associated mortality in California sea lions (Zalophus californianus). Mar Pollut Bull 50(1): 30-9.

All test results

The Environmental Working Group has conducted a study of industrial chemicals in samples of blood and urine from 20 dogs and 40 cats collected at a Virginia veterinary clinic. For each of 70 chemicals, two composite samples were analyzed, one for dogs and one for cats. The table below gives the detailed findings from the study. The results shown, which reflect an average level in the animals tested, are compared to arithmetic average levels found in national studies of chemicals in people, conducted by the Centers for Disease Control and Prevention (CDC 2008), and the Environmental Working Group (EWG 2008) when data from CDC were not available.