A study conducted at the University of Missouri found your dog's health - and your own - may be at risk if your dog eats canned food.
According to a university news release, an increase in Bisphenol A - an endocrine-disrupting industrial chemical found in the linings of some metal food cans - was found after a short-term feeding study with canned dog food.
Because of shared environments, the dog's unhealthy BPA exposure from canned foods could have human health hazards.
Elevated BPA concentrations positively correlated with increased plasma bicarbonate concentrations and associated with fecal microbiome alterations. Short-term feeding of canned dog food increased circulating BPA concentrations in dogs comparable to amounts detected in humans, and greater BPA concentrations were associated with serum chemistry and microbiome changes.
Selective BPA uptake by the tumor was found in all animals, the tumor/blood ratios ranged between 2.02 and 3.76, while the tumor/normal thyroid ratio was 6.78. Individual samples had tumor/blood ratios between 8.36 and 0.33. These ratios were related to the two histological patterns observed: homogeneous and heterogeneous tumors. We confirm the selective uptake of BPA by spontaneous UTC in dogs and plan to apply BNCT in the future.
There is a 2- to 3-fold increase in risk of developing hyperthyroidism among cats eating a diet composed mostly of canned cat food and a 3-fold increase in risk among those using cat litter. In contrast, the use of commercial flea products did not retain a strong association.
in a long-gestation species with a similar regulatory scheme of thyroid function as humans that BPA in utero exposure can be associated with hypothyroidism in the newborns.
BPA or Bisphenol A is a hot topic these days with health conscious consumers and petsumers. Pet owners, concerned about the risks associated with BPA are contacting their pet food companies asking if canned pet foods contain the chemical. However, many Pet Food answers to the BPA questions seem to be as varied as pet food itself. Which pet food companies are using BPA lined cans and which are not…you judge by their responses and the available information.
A total of 26 samples (15 samples of cat food and 11 samples of dog food) were prepared for analysis by high-performance liquid chromatography. BPA in the samples was extracted with acetonitrile and fat in the sample extract was removed with hexane. Solid-phase extraction was used for sample clean-up prior to final analysis. The concentration of BPA ranged from 13 to 136 ng/g in canned cat food and from 11 to 206 ng/g in dog food. Also, to confirm that the BPA had originated from the can coating, distilled water was added to each washed empty can and the cans were autoclaved at 121 degrees C for 30 min. The concentration of BPA leached from empty cans was between 7 and 31 ng/ml.
. Products intended for chewing and mouthing uses include toys and training devices that are often made of plastics. The goal of the current study was to determine if a subset of phthalates and bisphenol A (BPA), endocrine disrupting chemicals commonly found in plastics, leach out of dog toys and training devices (bumpers) into synthetic canine saliva. In vitro assays were used to screen leachates for endocrine activity. Bumper leachates were dominated by di-2-ethylhexyl phthalate (DEHP) and BPA, with concentrations reaching low μg mL(-1) following short immersions in synthetic saliva. Simulated chewing of bumpers during immersion in synthetic saliva increased concentrations of phthalates and BPA as compared to new bumpers, while outdoor storage had variable effects on concentrations (increased DEHP; decreased BPA). Toys leached substantially lower concentrations of phthalates and BPA, with the exception of one toy which leached considerable amounts of diethyl phthalate. In vitro assays indicated anti-androgenic activity of bumper leachates, and estrogenic activity of both bumper and toy leachates. These results confirm that toys and training devices are potential sources of exposure to endocrine disrupting chemicals in pet dogs.
two common plasticizers, bisphenol A (BPA) and phthalates, induce adverse health effects in vertebrates; however few studies have addressed their toxicity to non-mammalian species. The aim of this review is to compare the effects of plasticizers in animals, with a focus on aquatic species. In summary, we identified three main chains of events that occur in animals exposed to BPA and phthalates. Firstly, plasticizers affect development by altering both the thyroid hormone and growth hormone axes. Secondly, these chemicals interfere with reproduction by decreasing cholesterol transport through the mitochondrial membrane, leading to reduced steroidogenesis. Lastly, exposure to plasticizers leads to the activation of peroxisome proliferator-activated receptors, the increase of fatty acid oxidation, and the reduction in the ability to cope with the augmented oxidative stress leading to reproductive organ malformations, reproductive defects, and decreased fertility.
we measured the concentration of BPA in convenience samplings of foodstuffs purchased in Dallas, Texas. Sampling entailed collection of 204 samples of fresh, frozen, and canned foods in two rounds in 2010. BPA was positive in 73% of the canned food samples, while it was found in only 7% of non-canned foods at low concentrations. canned food concentrations greatly exceeded non-canned concentrations was consistent with other studies, and underscores the importance of canned foods in the overall exposure of adults of BPA.
This study quantified BPA concentrations in 78 canned and two frozen food products from the U.S. market using an adaptation of a previously reported liquid chromatography-tandem mass spectrometry method. The tested products represented 16 different food types that are from the can food classifications that constitute approximately 65% of U.S. canned food sales and canned food consumption. BPA was detected in 71 of the 78 canned food samples but was not detected in either of the two frozen food samples. Detectable BPA concentrations across all foods ranged from 2.6 to 730 ng/g. Large variations in BPA concentrations were found between different products of the same food type and between different lots of the same product. Given the large concentration ranges, the only distinguishable trend was that fruits and tuna showed the lowest BPA concentrations. Experiments with fortified frozen vegetables and brine solutions, as well as higher BPA concentrations in canned food solids over liquid portions, clearly indicated that BPA partitions into the solid portion of foods.
BPA, BPF, and BPS, were analyzed in foodstuffs (N = 267) collected from Albany, NY, USA, using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Foodstuffs were divided into nine categories of beverages, dairy products, fats and oils, fish and seafood, cereals, meat and meat products, fruits, vegetables, and "others". Bisphenols were found in the majority (75%) of the food samples. The highest overall mean concentration of ΣBPs was found in the "others" category, which included condiments (preserved, ready-to-serve foods). A sample of mustard (dressing) and ginger, placed in the category of vegetables, contained the highest concentrations of 1130 ng/g for bisphenol F (BPF) and 237 ng/g for bisphenol P (BPP). Concentrations of BPs in beverages (mean = 0.341 ng/g) and fruits (0.698 ng/g) were low. The predominant bisphenol analogues found in foodstuffs were BPA and BPF, which accounted for 42 and 17% of the total BP concentrations, respectively. Canned foods contained higher concentrations of individual and total bisphenols in comparison to foods sold in glass, paper, or plastic containers. On the basis of measured concentrations and daily ingestion rates of foods, the daily dietary intakes of bisphenols (calculated from the mean concentration) were estimated to be 243, 142, 117, 63.6, and 58.6 ng/kg body weight (bw)/day for toddlers, infants, children, teenagers, and adults, respectively.
Most studies of the health effects of BPA have focused on endocrine disruption leading to reproductive toxicity, but it displays additional side effects, including liver damage, disrupted pancreatic β-cell function, thyroid hormone disruption, and obesity-promoting effects. In this article, we reviewed specifically on the effects of BPA in energy balance.
recent studies have revealed that early life perturbations can affect the health of subsequent generations. Hypothesized mechanisms of multi- and transgenerational inheritance of abnormal developmental phenotypes include epigenetic misregulation in germ cells. In this review, we will focus on the available data demonstrating the ability of endocrine disrupting chemicals (EDCs), including bisphenol A (BPA), phthalates, and parabens, to alter epigenetic marks in rodents and humans. These epigenetic marks include DNA methylation, histone post-translational modifications, and non-coding RNAs. We also review the current evidence for multi- and transgenerational inheritance of abnormal developmental changes in the offspring following EDC exposure. Based on published results, we conclude that EDC exposure can alter the mouse and human epigenome, with variable tissue susceptibilities. Although increasing data suggest that exposure to EDCs is linked to transgenerational inheritance of reproductive, metabolic, or neurological phenotypes, more studies are needed
in utero and early postnatal exposure to this compound may produce a broad range of adverse effects, including impaired brain development, sexual differentiation, behavior, and immune function, which could extend to future generations. Molecular mechanisms that underlie the long-lasting effects of BPA continue to be elucidated, and likely involve disruption of epigenetic programming of gene expression during development. Several studies have provided evidence that maternal exposure to BPA results in postnatal changes in DNA methylation status and altered expression of specific genes in offspring.
BPA may be one of the influencing factors for thyroid volume and thyroid nodules and its effects are independent of iodine nutrition status in children.
BPA, not able to directly cause genetic damage at environmental dose, may exert an indirect genotoxic activity.
The last six decades have witnessed a massive introduction of hormonally active synthetic chemicals into the environment leading some to postulate that the diverse outcomes documented in human and wildlife populations might be the result of extemporaneous exposure to xenoestrogens during development. The estrogen-mimic bisphenol-A (BPA) is used as a model agent for endocrine disruption. BPA is used in the manufacture of polycarbonate plastics and epoxy resins from which food and beverage containers and dental materials are made. Perinatal exposure to environmentally relevant BPA doses results in morphological and functional alterations of the male and female genital tract and mammary glands that may predispose the tissue to earlier onset of disease, reduced fertility and mammary and prostate cancer.
Research on BPA exposure has accelerated in the past decade with findings suggesting that perinatal exposure to BPA can negatively impact both male and female reproduction, create alterations in behavior, and act as a carcinogen. BPA can have both short term and long term effects with the latter typically occurring through epigenetic mechanisms such as DNA methylation.
BPA exposure was estimated to be associated with 12,404 cases of childhood obesity and 33,863 cases of newly incident coronary heart disease, with estimated social costs of $2.98 billion in 2008. Removing BPA from food uses might prevent 6,236 cases of childhood obesity and 22,350 cases of newly incident coronary heart disease per year, with potential annual economic benefits of $1.74 billion (sensitivity analysis: $889 million-$13.8 billion per year). Although more data are needed, these potentially large health and economic benefits could outweigh the costs of using a safer substitute for BPA.
there seems to be a discrepancy between exposure assessments based on biomonitoring data and those based on food/drink concentrations. Several recent studies indicated also the importance of non-food sources. Although the main use of BPA is polymerization to polycarbonate and epoxy resins, it can also be used as an additive, from which it may be easily released. Several studies have already provided scientific evidence for the contribution of sources for dermal BPA absorption, such as thermal paper where BPA is used as an additive.
Critical care medicine has largely benefited from plastic-containing medical devices. However, bisphenol-A (BPA) and phthalates present in the plastics can leach from such devices. We hypothesized that intensive care unit (ICU) patients are exposed to BPA and phthalates through (plastic) medical devices. Serum (n = 118) and urine (n= 102) samples of adult ICU patients (n = 35) were analyzed for total BPA and phthalate metabolites (PMs). Our results showed that adult ICU patients are continuously exposed to phthalates, such as di(2-ethylhexyl)phthalate (DEHP), as well as to BPA, albeit to a lesser extent. This exposure resulted in detectable high serum and urinary levels in almost every patient and at every studied time point. Moreover, these levels were significantly higher than in controls or compared to referenced literature. The chronology of exposure was demonstrated: pre-operative urinary and serum levels of the DEHP metabolites were often below the detection limit. Plastic-containing medical devices were the main source of DEHP exposure: post-operative patients on hemofiltration, extracorporeal membrane oxygenation or both showed serum levels 100-or 1000-fold higher than the levels in the general population reported in the literature.
Our concern with human exposure to BPA derives from 1) identification of molecular mechanisms mediating effects in human and animal tissues at very low doses, 2) in vivo effects in experimental animals caused by low doses within the range of human exposure, and 3) widespread human exposure to levels of BPA that cause adverse effects in animals.