Freshness Packet in Beef Jerky Toxic Humans
J Med Toxicol. 2012 Mar; 8(one): 76–79.
Iron Intoxication in a Dog Consistent to the Ingestion of Oxygen Absorber Sachets in Pet Treat Packaging
A. M. Brutlag
Pet Toxicant Helpline and SafetyCall International, PLLC, Minneapolis, MN USA
C. T. C. Flintstone
Pet Poison Helpline and SafetyCall International, PLLC, Minneapolis, MN United states
B. Puschner
Department of Molecular Biosciences and the California Animal Wellness and Food Rubber Laboratory Arrangement, School of Veterinary Medicine, University of California, Davis, CA USA
Abstract
Oxygen absorbers are normally used in packages of dried or dehydrated foods (east.grand., beef jerky, dried fruit) to prolong shelf life and protect nutrient from discoloration and decomposition. They normally contain reduced iron as the active ingredient although this is rarely stated on the external packaging. Although reduced atomic number 26 typically has minimal oral bioavailability, such products are potential sources of iron poisoning in companion animals and children. We nowadays a case of canine ingestion of an oxygen absorber from a bag of dog treats that resulted in iron intoxication necessitating chelation therapy. A vii-calendar month-old female Jack Russell terrier presented for evaluation of vomiting and melena 8–12 h after ingesting ane–2 oxygen absorber sachets from a packet of canis familiaris treats. Serum atomic number 26 concentration and ALT were elevated. The dog was treated with deferoxamine and supportive care. Clinical signs resolved fourteen h post-obit treatment, simply the ALT remained elevated at the 3-calendar month recheck. The ingestion of reduced iron in humans has been reported to crusade balmy elevation of serum iron concentration with minimal clinical furnishings. To our cognition, no cases of atomic number 26 intoxication following the ingestion of oxygen absorbers have been reported. The lack of ingredient information on the packaging prompted assay of contents of oxygen absorber sachets. Results indicate the contents contained l–lxx% full iron. This case demonstrates that iron intoxication can occur post-obit the ingestion of such products. Human and veterinary medical personnel demand to exist enlightened of this upshot and monitor serum iron concentrations as chelation may be necessary.
Keywords: Heavy metal poisoning, Nutrient preservatives, Chelation therapy, Deferoxamine, Reduced fe, Oxygen scavenger
Introduction
Packages of dried foods, nuts, and processed meats often contain oxygen absorber sachets (2–30 g net weight) that are added to prolong the shelf life and protect food from the discoloration and decomposition caused by oxidation or aerobic microorganisms (Fig.i). The nearly mutual active ingredient in food-grade oxygen scavenging systems is reduced fe, used for its power to eat oxygen via conversion to iron oxide [1]. Reduced iron is a term generally used to refer to the end production of atomic number 26 oxide that has been reduced with hydrogen or carbon monoxide. This form of elemental iron is a common iron fortificant of foods.
A collection of oxygen absorber sachets from human-course and pet food packaging purchased in the USA by the authors. Only one of the 5 sachets mentions atomic number 26 on the packaging. (Courtesy of Dr. Ahna G. Brutlag, Pet Poison Helpline, Minneapolis, MN)
With respect to oxygen absorbers, the ingredient information is not typically included on the exterior packaging making it challenging for physicians and veterinarians to determine the proper course of treatment when faced with patient exposures. Fifty-fifty in cases where the outer packaging lists iron every bit an ingredient, the label does not land the specific salt formulation or total amount of elemental iron. Determining this information is difficult even for experienced clinical toxicologists, and therefore creates difficulty computing the hazard of toxic exposure following ingestion. Adding to the defoliation, such sachets may easily exist mistaken for desiccants containing silica gel, a relatively inert and not-toxic ingredient.
Example summary
A 7-calendar month-old female intact Jack Russell terrier weighing 5.eighteen kg presented to a veterinary clinic for evaluation of vomiting of 3 h duration. In the 8–12 h preceding examination, the domestic dog had chewed into an unopened package of rawhide pet treats as well equally the 2 oxygen cushion sachets that were included in the rawhide packaging. One of the oxygen absorber packets was completely emptied, and the other was punctured and spilled. There was no known exposure to other toxins or foreign fabric, and the canis familiaris had no known health problems.
The physical exam revealed lethargy, melena, and a tense abdomen with the residuum being unremarkable. Abdominal radiographs revealed granular, radiopaque material within the distal colon consequent with granular iron. The serum iron concentration was 436 μg/dl (reference 94–220 μg/dl). Complete claret count (CBC) and activated clotting fourth dimension (Human action) results were within reference ranges. The fecal flotation exam was normal except for the presence of black stool with mucous. Results of a express serum biochemical assay were inside reference ranges with the exceptions of mildly elevated ALT (ALT = 175 U/l; reference x–100 U/fifty) and mildly elevated BUN (BUN = 31 mg/dl; reference 7–27 mg/dl).
Treatment for iron intoxication commenced with milk of magnesia (v ml PO in one case), sucralfate (100 mg/kg slurry PO q eight h), and famotidine (i mg/kg IM or Iv q 12 h). 2 hours after access one sixty-ml warm water enema was administered, and the dog defecated dark tarry feces, black granular material believed to be the contents of the oxygen absorber sachets, and white liquid resembling milk of magnesia. Chelation therapy was instituted with a abiding rate infusion of deferoxamine (15 mg/kg/h IV for 21 h) and supportive care including IV fluids (Normosol-R at 3.86 ml/kg/h) and oral metronidazole (x mg/kg PO q 12 h). The dog's urine was a gold color iii h afterwards instituting deferoxamine and a dark amber color six h after.
Three hours following presentation the dog vomited once more; maropitant (1.5 mg/kg, SQ, 104 once) was administered maropitant (i.5 mg/kg, SQ, once) and the vomiting resolved. The canis familiaris'due south lethargy resolved approximately 8 h following the initial exam, and melena was last noted 14 h following the initial test. Twenty hours subsequently the initial presentation ALT was reduced to 136 U/l and all other values were within reference ranges. Twenty-6 hours later on the initial exam, the dog was discharged on oral sucralfate, oral metronidazole, and a banal diet. During a follow-up telephone call the week afterward ingestion, the pet possessor reported that the domestic dog remained asymptomatic following belch. Three months later a recheck exam and labs revealed a normal physical exam, an elevated ALT (217 U/l), mildly elevated BUN (31 mg/dl), and normal CBC and urinalysis. The possessor did not render the dog for recheck of liver enzymes.
Discussion
To the all-time of our cognition, this is the showtime documented case of iron intoxication following ingestion of iron-containing oxygen scavengers. Reported sources of unintentional iron intoxication in humans and animals include prenatal vitamins, multi-vitamins with iron, iron supplements (prescription or OTC), or, less commonly ferric chloride, parenteral iron, iron-based slug allurement and fertilizers, and reduced-atomic number 26 containing products such as instant hand/foot warmers [two–4]. Reduced iron, the active ingredient believed to be in iron-based oxygen scavengers, is reported to have poor solubility in water and weak acids, which likely results in low oral bioavailability. Until recently, the reduced iron contained in products such as oxygen absorbers or instant mitt/foot warmers was not deemed to be of toxicological significance [3, five]. Notwithstanding, the particle size of reduced fe is critically important to determine the bioavailability; the smaller the iron particle, the greater its bioavailability [6].
The mechanisms of iron absorption in mammals are extremely complex and continue to be the subject field of intense investigation. The chemical form of atomic number 26 influences absorption and transport mechanisms, simply many other factors including pH, bounden components, transporter proteins, and reducing enzymes affect iron uptake [7]. Although ferrous (2+) and ferric (3+) salts have similar solubility, ferric (3+) salts have by and large lower bioavailability. The rate at which reduced (elemental) iron dissolves in the stomach and duodenum is largely unknown but is greatly influenced by particle size. Thus, cognition of the chemic form of iron and the particle size of reduced iron is critical in order to gauge the bioavailability and risk of toxicity. Fe oxide, the end product of iron-based oxygen scavengers, has very poor oral bioavailability and is non thought to be problematic following ingestion [4]. Thus, it is likely that oxidized or "spent" oxygen scavengers pose minimal toxicological threat to humans or animals following ingestion. Withal, because the caste of oxidation cannot be adamant by the outward appearance of the packet, medical professionals cannot easily determine the bioavailability and wellness hazard. Complicating the calculation of run a risk in these exposures is the lack of readily bachelor information regarding the scavenger's ingredients or amount of elemental atomic number 26. In this case, such information was not easily accessible.
Following ingestion, the absorption of fe is also regulated past the body's current iron stores. At therapeutic concentrations, atomic number 26 is primarily absorbed in the duodenal enterocytes past divalent metal transporter ane (DMT1) from where it is either transported to the systemic circulation via transferrin or stored as ferritin and discarded as the prison cell is sloughed. However, in cases of oral overdose, iron asserts its toxic effect via the creation of iron-induced reactive oxygen species (ROS) that direct damage the gastrointestinal (GI) epithelium, resulting in the dysfunction and bypass of the intestinal regulatory system which allows for increased passive assimilation of iron downwardly its concentration gradient. One time the reserve of transferrin has been saturated, "complimentary" or unbound reactive atomic number 26 results in the formation of additional ROS.
The generation of ROS as a effect of iron intoxication is due to the fact that, equally a transition metallic, iron is a key participant in both the Fenton and Haber–Weiss reactions, resulting in the creation of hydroxyl radicals. As physiologic defenses for the detoxification of ROS go overwhelmed, ROS outcome in direct cellular impairment such equally lipid membrane devastation (via hydroxyl radical initiated lipid peroxidation), along with damage to mitochondria and macromolecules [4, 8]. The organ systems almost affected include the GI tract, liver, and vasculature. Early signs of fe intoxication include vomiting, diarrhea, abdominal pain, sluggishness, and GI hemorrhage with possible hemodynamic compromise. Progressive cellular harm results in metabolic acidosis, hepatic harm and coagulopathy, capillary leak syndrome, stupor, and expiry [two, 4, 8]. In rare cases, gastric outflow obstruction due to stricture formation occurs 2–8 weeks following ingestion [ii].
The range of toxicity for humans and dogs post-obit oral atomic number 26 exposure is similar. Ingestions of less than 5–20 mg/kg of elemental iron typically consequence in mild clinical signs but are non probable to consequence in meaning toxicosis [4, 9, 10]. Ingestions between 20 and 60 mg/kg of elemental iron can develop mild to moderate clinical signs, necessitating handling or monitoring [2, iv, 11]. Ingestions greater than 60 mg/kg can upshot in serious poisoning or death. In animals and humans, oral doses between 100 and 250 mg/kg are potentially lethal [4, 8, 9, 12].
Ingestions of more than than twenty–40 mg/kg elemental iron or, in cases such as this where the amount of elemental atomic number 26 is not known and clinical signs are visible, obtaining serum atomic number 26 concentrations is warranted [2, four]. In oral overdose, peak concentrations of atomic number 26 occur 2–6 h post-obit ingestion, depending on the conception. As absorption rates vary with product dissolution (surface area) and serum concentrations may change apace, obtaining a serum iron concentration 4–6 h after the ingestion of most intact products is recommended. In the case of liquid or chewable fe formulations, serum concentrations should be nerveless 2–3 h after ingestion. Additionally, monitoring the iron concentration every 6–8 h during chelation therapy can help to guide the elapsing of treatment. In humans and dogs, height serum iron concentrations greater than 500 μg/dl are associated with meaning toxicosis including metabolic acidosis and daze, and chelation with deferoxamine is often necessary. Regardless of the serum iron concentration, if the amount of ingested iron is believed to be greater than 20 mg/kg and the patient is displaying signs consistent with intoxication (beyond mild vomiting), decontamination, abdominal radiographs, deferoxamine, and supportive care including GI protectants and IV fluids are recommended. In this example, the patient presented too late for effective oral decontamination; withal, due to the presence of radiopaque material in the distal colon, decontamination was performed via an enema (versus emesis or whole bowel irrigation). The domestic dog was also treated with oral milk of magnesia in hopes of precipitating iron in the GI tract as insoluble atomic number 26 hydroxide. Famotidine and sucralfate were administered to decrease gastric and abdominal acidity and thereby decrease the solubilization and absorption of iron likewise as aid in the reduction of gastric harm and reduce the take a chance of stricture formation. Metronidazole was administered to aid in the management of astute colitis. Additional supportive therapies such as maropitant (antiemetic) were administered due to the domestic dog'south persistent vomiting, and Iv fluids were utilized at a twice maintenance rate in order to maintain acceptable organ perfusion and correct for ongoing losses.
The oxygen cushion sachets ingested by this domestic dog independent no ingredient information on the packaging, nor was the salt formulation or amount of elemental iron bachelor from customary sources (MSDS, medical databases such equally Micromedex, the manufacturer). Thus, in effort to estimate the amount of atomic number 26, chemic analysis of three randomly chosen brands of oxygen absorbers found in packages of human-grade food products was performed. Unfortunately, analysis of the oxygen absorber ingested by the dog in this example was not possible as the sample was non saved. The samples were digested in a combination of nitric and muriatic acid at 180°C and quantitatively analyzed by inductively coupled argon plasma atomic emission spectrometry (ICP-AES; FISONS, Accuris Model, Thermo Optek Corporation, Franklin, MA). The oxygen absorbers independent 42%, 69% and 71% fe with depression concentrations of chloride (less than 0.five%), sulfate (less than 0.004%), and phosphorus (less than 0.03%). Based on these findings, the oxygen absorbers most probable contained metallic iron pulverisation, which would be consistent with the term reduced iron.
Assuming iron-based oxygen absorbers contain a l% concentration of elemental iron in a bioavailable class, a 5-kg dog would only demand to ingest 0.1–0.3 g of the contents to exceed a toxic dose (xx–60 mg/kg elemental atomic number 26). Likewise, a fifteen-kg kid or domestic dog need only ingest 0.3–0.9 g of contents to exceed the same dose. As the typical sizes of oxygen scavenger sachets range from 2–thirty thousand (internet weight), the ingestion of such an amount is hands believable.
As evidenced by the patient'south clinical signs, serum iron concentrations, radiographic evidence, and exposure history, the dog was diagnosed with fe intoxication secondary to the ingestion of iron-based oxygen absorbers. This case demonstrates that the reduced fe contained in oxygen absorbers, when ingested, can upshot in iron intoxication. Human and veterinary medical personnel need to be aware of this upshot and monitor serum iron concentrations as chelation may be necessary.
Acknowledgments
The authors are grateful to the staff at the California Animal Health and Food Safety Laboratory System, especially Mr. Larry A. Melton and Mr. Ian Holser for their technical assistance.
Disharmonize of involvement
None.
Footnotes
This case written report was presented at the 2011 American Clan of Veterinary Laboratory Diagnosticians/U.s.a. Animate being Health Association (AAVLD/USAHA) annual coming together in Buffalo, NY, September 28 - October 5, 2011.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550222/
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