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Lead Levels in the Eggs of a Chicken With Lead Toxicosis.

Abstract: A 1.5-year-old Polish hen was presented with a history of watery droppings and poor vent tone. Results of diagnostic tests revealed blood lead at levels considered to be toxic. Chelation therapy was started with calcium ethylenediaminetetraacetate. The hen was laying eggs before, during, and after chelation therapy. Eggs were tested for the presence of lead by combining yolk and albumen together. Before chelation therapy, the level of lead in the egg tested was 14 [micro]g. Two days after the end of chelation therapy, results of a second blood lead test revealed a drop to nontoxic levels. No lead was detected in the combined yolks and albumen of eggs collected 7-11 days after the end of chelation therapy. Four weeks after the end of chelation therapy, no lead was identified in the shells of tested eggs.

Key words: lead toxicosis, chelation, poultry, egg, yolk, albumen, avian, chicken

Clinical Report

A 1.5-year-old female Polish hen was presented for examination with a history of watery droppings and poor vent tone. The hen was housed outdoors in an urban backyard with a flock of 6 other chickens of various breeds. They were offered scratch grains, layer pellets, layer mash, shredded leafy greens, and occasional bird seed. The hen was actively laying eggs about once per week, according to the owner at the time of presentation. The other hens in the flock were not laying eggs at the time.

On physical examination, the hen was found to be bright, alert, and responsive with a body condition score of 5 out of 9. The feathers near the vent had adhered dried fecal material, and a clear viscous fluid was leaking from the vent. The vent tone was slightly flaccid. The remainder of the examination was unremarkable. Initial diagnostic tests consisted of a fecal direct cytologic examination and Gram's stain, a complete blood cell count, serum biochemical profile, and radiographs. Results of the direct fecal exam did not reveal any ova or parasites. The fecal Gram's stain showed 90% gram-positive bacteria and 10% gram-negative bacteria, which was interpreted as a normal finding. Results of the complete blood count and biochemical profile were within reference intervals. (1) Radiographs revealed a full-appearing caudal coelom typical of a laying hen with an active reproductive tract. Mineral densities were present within the ventriculus. Because no abnormalities were detected with these results, further diagnostic tests were recommended, and because the hen was part of a flock with a known history of lead, including one bird that was recently treated for lead toxicosis, a blood sample was submitted to measure lead and zinc levels by flame atomic absorption spectrometry. No treatments were administered pending the results of this heavy metal testing.

Five days after presentation, the lead and zinc levels were available. The zinc level was considered normal (1.7 mg/kg [170 [micro]g/dL]; reference interval, <10 mg/kg [<1000 [micro]g/dL]), but the lead level was high (0.75 mg/kg [75 [micro]g/dL]; reference interval, <0.50 mg/kg [<50 [micro]g/dL]). (2) Chelation therapy with calcium ethylenediaminetetraacetate (CaEDTA) was started (35 mg/kg IM q12h for 5 days; CaEDTA, Diamondback Drugs, Scottsdale, AZ, USA). After 5 days of treatment, a 2-day break was given, and the patient then was treated again with the same dosing of CaEDTA. The patient tolerated treatments well. Two days after the last dose of CaEDTA, the hen's lead level was rechecked and found to be less than 0.02 mg/kg (2 [micro]g/dL), which was considered a nontoxic level. Further chelation therapy was not performed.

This hen had been laying eggs before, during, and after treatment. When the lead test results were known, the owner was immediately informed not to consume or compost any eggs from this bird. Treatment with CaEDTA also required a withdrawal time of 6-8 weeks, as directed by the US Food Animal Residue Avoidance Databank. An egg that was produced a day before the initial start of chelation therapy was submitted to the California Animal Health and Food Safety Laboratory for lead testing by inductively coupled mass spectrometry. The albumen and yolk were mixed together, and a level of 14 [micro]g or 0.28 mg/kg (28 [micro]g/ dL), assuming an egg weight of 50 g, was detected in the sample. Combined egg yolk and albumen from 3 eggs collected from days 7 to 11 after cessation of chelation therapy were submitted to the same laboratory. The yolk and albumen were mixed together and tested as a batch. No lead was detectable within this sample. Two weeks later, 2 eggs were collected again over 2 days and submitted to the same laboratory for the shell to be tested for lead. These results showed no detectable lead. At that time, the hen was acting clinically appropriate, and vent tone was normal, with fluid no longer leaking from the vent. No other members of the flock were laying eggs or had signs of lead toxicosis. The owner was instructed not to use the eggs from this bird, even though lead was not detectable at present because of possible rebound toxicosis by lead possibly leaching out of bone stores in the future.

Discussion

Lead is one of the most common toxins identified in avian patients of various species. (2-4) When ingested, the acidic pH of the proventriculus and ventriculus allow lead to be solubilized. Lead is then absorbed into the blood stream through the small intestines. (2,3) More than 90% of the absorbed lead will bind to red blood cells and circulate throughout the body to be distributed to tissues. (2) Blood and well-vascularized organs will hold onto 4% of the lead burden, whereas soft tissue organs will have 2% of the lead burden. (4) The bones will bear most of the lead burden at 94%. (4)

Lead toxicosis can result in various systemic problems. In the gastrointestinal tract, lead directly causes necrosis of the gastrointestinal epithelium and impairment of gastrointestinal motility. (2,5) Lead can alter the hematologic system by interfering with heme synthesis and increasing red blood cell fragility, which will lead to anemia. (2,5) Liver degeneration and necrosis also can occur. (5) Lead can compete with calcium ions and may substitute for calcium in the bone, and it can mimic or inhibit cellular actions of calcium, which can lead to cell death, impair neuronal differentiation, and contribute to cerebral edema. (2) Lead can also have many effects at the cellular level, such as interfering with cellular metabolism in the mitochondria and inhibiting cytochrome P-450 enzymes. (2)

Diagnosis of lead toxicosis is by measuring levels of lead in the blood. (2-5) Radiographs can also be used as a screening test to look for the presence of metallic dense objects within the body. However, the absence of a metallic object on a radiograph does not rule out lead toxicosis, because elevated concentrations of blood lead can cause toxicosis even after the metal has been absorbed or eliminated from the gut. (5) The hen in this report did not show any metallic densities on radiographs, yet lead toxicosis was diagnosed on the basis of the results of blood lead testing.

Patients diagnosed with lead toxicosis can be treated by different methods. Removing the metallic object from the gastrointestinal tract is often recommended to reduce further exposure and absorption. (4) Removal of metal objects can be done through lavage, endoscopy, laparotomy, cathartics, laxatives, or by administering grit to aid in the grinding of the metal particles in the ventriculus to a small enough size that can be passed naturally. (4,6) Chelation therapy is necessary to bind absorbed lead in the blood and allow it to be excreted. Drugs such as CaEDTA, D-penicillamine, and meso-2,3-dimercaptosuccinic acid can be used. (2-5) A rebound effect can occur after therapy is stopped because of the redistribution of compartmentalized lead; therefore, several courses of therapy may be needed to reduce the total lead burden on the body. (4)

Although much is known about the diagnosis and treatment of lead toxicosis in avian patients, less complete information is available about lead in the eggs of birds. Lead can be deposited into the shell, yolk, and albumen of an egg. (7-16) The shell usually has the highest concentration of lead, but some studies show that the yolk can have higher levels. (10,12) Within the contents of the egg, yolk levels are usually highest, and albumen levels are often low to negligible. (10,12,13,15,16) However, when testing for lead in eggs, the yolk and albumen are often tested together because this is the portion consumed by humans. (10)

The mechanism through which lead gets into the egg has yet to be completely elucidated. In one study, the ovarian tissue of postmortem-examined birds with lead toxicosis were found to have high levels of lead. (12) When ovulation occurs, this lead is then present within the yolk of a developing egg and is the source within the egg content. (12) The source of lead in the eggshell is still not completely clear and may occur by various pathways. Because lead is a divalent cation, it can compete with calcium and can be used in place of it in other parts of the body. (2) When calcium is mobilized from the bones for eggshell formation, lead may be able to use the same pathway for calcium deposition into the shell. (10) Lead in eggshells also possibly originates from intestinal sources and uses the same pathways as calcium to enter the shell. (10) Further studies are needed to better understand this pathway.

The hen of this report was treated for lead toxicosis with CaEDTA. As the blood levels of lead dropped to nontoxic levels, lead within the egg was reduced correspondingly to nondetectable levels. In one study, a strong linear relationship was found between blood and yolk lead levels. As the blood lead levels rose, the yolk lead levels increased as well. (12) To the author's knowledge, no studies have been done in chickens to see whether the reverse relationship is true. The clinical course of the case, however, would suggest that as lead levels decrease in the blood, a linear reduction of lead in the yolk is likely, as well. Further studies are needed with a larger number of birds to see if this is the true.

Several recent reports describe lead being found within the eggs of urban and backyard chickens. In a study in Belgium, lead levels ranged from 74 to 116 [micro]g/kg (7.4-11.6 [micro]g/dL) in the homogenized yolk, albumen, and shells of eggs. This correlated well with levels of lead in the soil, which could indicate that soil is a likely source of lead for chickens. (8) In a study in New York City looking at community gardens, lead levels in 48% of eggs tested ranged from 10 to 167 [micro]g/kg (1-16.7 [micro]g/ dL). (9) In a separate study conducted in California, 21 eggs were collected from an urban flock of 10 chickens. The shell of all 21 eggs had lead detected with levels ranging from 0.075 to 1.8 [micro]g/g (7.5-180 [micro]g/dL) wet weight. Twelve of these eggs had lead detected in the pooled albumen and yolk of the egg. (10) In another case conducted in California, eggs were tested from a flock in which high lead levels were found in the liver of a chicken postmortem. Lead was found in the mixed contents of the albumen and yolk at 72 [micro]g/kg (7.2 [micro]g/dL). (11)

Valid concerns have been raised about a potential health risk for humans consuming eggs or meat from birds that have lead toxicosis. (9-12) The half-life and withdrawal time for lead in chickens is unknown, which makes it difficult to know if and when consumption of their products would be appropriate. (12) In humans, blood lead levels above 10 [micro]g/dL are concerning and, according to the Centers for Disease Control and Prevention, levels above 5 [micro]g/dL in children are the level at which public health actions should be initiated. (10,17,18) Treatment of lead toxicosis in children with chelation therapy usually occurs when lead levels are greater than 45 [micro]g/dL. (18) Children and pregnant women may be particularly susceptible to lead toxicosis because the developing nervous system is thought to be more vulnerable to lead's toxic effects. (10,11,17,19) The US Department of Agriculture recommends that the daily maximum of lead intake for children be no more than 6 [micro]g and for adults be no more than 75 [micro]g. (10,20) The amount of lead present in the egg that was submitted from the hen in this case report was 14 [micro]g, which is above the daily limit recommended for children. An adult would have been required to consume 6 eggs with this level of lead to be above the daily limit.

Another intriguing question is whether successful chelation therapy of a bird can make eggs safe for human consumption. After treatment of this hen, lead levels in the yolk and albumen became nondetectable. Although it is difficult to say without further research, one would presume that if chelation therapy can reduce lead to nondetectable levels, the eggs would then be safe for human consumption. However, until studies are done, it may be best to err on the side of caution and advise against eating eggs produced from hens that have been diagnosed with lead toxicosis, even if hens no longer have detectable lead in their blood or eggs.

The ownership of backyard chickens is on the rise, whether it be for companionship or their meat and egg production. (21) However, as this report and others show, lead can be deposited in the eggs of chickens and could thereby be present in the diet of those consuming the eggs, which is a potential public health concern. This case represents the successful chelation of lead from a backyard hen that resulted in potentially toxic lead levels in eggs that then dropped to undetectable levels. This case demonstrates that lead was eliminated from the egg of a hen with appropriate chelation treatment. Further studies are needed to see whether chelation therapy of an individual hen with lead toxicosis can be successful in making eggs lead free and safe for human consumption.

Stephanie K. Lamb, DVM, Dipl AB VP (Avian)

From the Arizona Exotic Animal Hospital. 744 N Center St., No. 101, Mesa, AZ 85201, USA.

References

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(2.) Wismer T. Advancements in diagnosis and management of toxicologic problems. In: Speer BL, ed. Current Therapy in Avian Medicine and Surgery. St Louis, MO: Elsevier; 2016:589-600.

(3.) Dumonceaux G, Harrison GJ. Toxins. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Application. Lake Worth, FL: Wingers; 1994:1030-1052.

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(8.) Waegeneers N, Hoenig M, Goeyens L, DeTemmerman L. Trace elements in home-produced eggs in Belgium: levels and spatiotemporal distribution. Sci Total Environ. 2009;407(15):4397-4402.

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(13.) Doganoc DZ. Distribution of lead, cadmium, and zinc in tissues of hens and chickens from Slovenia. Bull Environ Contam Toxicol. 1996;57(6):932-937.

(14.) Brams E, Anthony W. Cadmium and lead through an agricultural food chain. Sci Total Environ. 1983; 28:295-306.

(15.) Mazliah J, Barron S, Bental E, Reznik I. The effect of chronic lead intoxication in mature chickens. Avian Dis. 1989;33(3):566-570.

(16.) Vogt H, Nezel K, Matthes S. Effect of various lead and cadmium levels in broiler and laying rations on performance of the birds and on the residues in tissues and eggs. Nutr Metab. 1977;21 (suppl 1):203-204.

(17.) Koller K, Brown T, Spurgeon A, Levy L. Recent developments in low-level lead exposure and intellectual impairment in children. Environ Health Perspect. 2004; 112(9):987-994.

(18.) Lead. Centers for Disease Control and Prevention Web site, https://www.cdc.gov/nceh/lead/default.htm. Accessed September 22, 2017.

(19.) Cecil KM, Brubaker CJ, Adler CM, et al. Decreased brain volume in adults with childhood lead exposure. PLoS Med. 2008;5(5):el 12.

(20.) Childhood lead poisoning and prevention branch. California Department of Public Health Web site. http://www.cdph.ca.gov/programs/CLPPB/Pages/ CLPPPIndex.aspx. Accessed September 22, 2017.

(21.) Nixon JB. Laws and regulations governing backyard poultry in the United States. In: Greenacre CB, Morishita TY, eds. Backyard Poultry Medicine and Surgery: A Guide for Veterinary Practitioners. Ames, IA: Wiley Blackwell; 2015:3-17.
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Title Annotation:Clinical Report
Author:Lamb, Stephanie K.
Publication:Journal of Avian Medicine and Surgery
Date:Sep 1, 2018
Words:3005
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