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Journal of Feline Medicine and Surgery logoLink to Journal of Feline Medicine and Surgery
. 2016 Jun 25;5(5):249–255. doi: 10.1016/S1098-612X(03)00047-0

Lead toxicosis in cats—a review

TE Knight 1,*, MSA Kumar 1
PMCID: PMC10822269  PMID: 12948499

Abstract

Although the incidence of lead toxicosis in small animals continues to decrease, it remains a significant malady. We have reviewed the literature of the past 45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis, pathology and treatment of feline lead toxicosis are reviewed.

In 84% of these cases the source of lead was old paint usually from home renovation. The most common signs in cats are anorexia, vomiting, and seizures. The younger individuals seem more likely to show CNS signs. Since signs are often vague, lead toxicosis may be significantly under diagnosed in cats. The gold standard of diagnostic tests is blood lead concentration, although it does not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs. Diagnostic tests including erythropoietic protoporphyrin (EPP), urine aminolevulinic acid, and others are discussed. Gross findings on necropsy are few and include a yellow-brown discoloration of the liver often with a nutmeg-like appearance. Histological examination may reveal pathognomonic inclusion bodies in liver and renal tissues. Characteristic histological changes in the CNS include neuronal necrosis and demyelination.

Treatment of lead toxicosis in cats, as in any species, involves removing the exposure, decontaminating the individual and the environment, supportive care and chelation therapy. The most recently available chelator is succimer (meso 2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a wide margin of safety.

A high index of suspicion of lead toxicosis is warranted in cats since they often present with vague and non-specific signs. With any consistent history owners need to be asked about home renovation. Early diagnosis and treatment affords a good prognosis.

Introduction

At one time lead toxicosis was considered the most common accidental poisoning in small animals (Zook et al 1969, 1972, Clark 1973, Hamir 1986, Bratton and Kowalczyk 1989). Federal regulations enacted in the 1970s led to decrease in the amount of lead allowed inresidential paints, leaded gasoline, and other household products, and a significant decrease in incidence of lead toxicosis in humans and domestic species has been seen over the past two decades (Morgan et al 1991a, Graeme and Pollac 1998). Lead now ranks behind more common accidental poisons in small animals such as rodenticides, antifreeze, insecticides, and human pain relievers such as ibuprofen and acetaminophen in cats (Bratton and Kowalczyk 1989, Berny et al 1992). Reports of lead poisoning represented approximately 0.5% of the calls received at the National Animal Poison Control Center (NAPCC) from 1985 to 1989 (Berny et al 1992). Nevertheless, lead remains an important source of toxicity in small animals.

Lead toxicosis in cats is infrequently reported. Review of the literature from the past 45 years has revealed 70 cases (Valler and Virat 1956, Scott 1963, Priester and Hayes 1974, Zook and Carpenter 1977, Turner and Fairburn 1979, McLeavey 1980, Jacobs 1981, Watson 1981, Prescott 1983, Hoffheimer 1988, Maddison and Allan 1990, Morgan et al 1991a, Hawke and Maddison 1992, Miller and Bauk 1992, Maddison et al 1993, Van Alstine et al 1993, Knight et al 2001). Incomplete data precluded analysis of an additional report of 64 cats (Anonymous 1979). This compares with over 800 cases of lead poisoning reported in dogs in the same time period (Scott 1963, Zook et al 1969, 1972, Schrimsher 1971, Priester and Hayes 1974, Kowalczyk 1976, Knecht et al 1979, Hamir 1981, O'Brien 1981, Hamir and Handson 1982, Prescott 1983, Koh 1985, Hamir et al 1986, Morgan et al 1991a, Khanna et al 1992, Ramsey et al 1996). This disparity has traditionally been ascribed to the more fastidious dietary habits in felines (Aronson 1972, Van Alstine et al 1993). Constant grooming, however, makes cats more susceptible to ingestion of paint dust or soil contamination on the coat and footpads. Other factors which may help explain this disparity include physiological differences in susceptibility between species, although, to our knowledge, no data concerning cats are available; under diagnosis due to the often vague, non-specific presenting signs in cats (Priester and Hayes 1974, Miller and Bauk 1992, Maddison et al 1993); and historically more households have owned dogs as pets (AVMA, 1997). In the following paragraphs we review sources, signs, diagnosis, pathology, and treatment of lead toxicosis in cats.

Sources

Numerous sources of lead exposure for small animals include old paint and other building materials such as linoleum, caulking compounds, plumbers solder, carpet padding, and roofingmaterials (Bratton and Kowalczyk 1989). Automotive related sources include storage batteries, wheel weights, used motor oil, and emissions from gasoline engines. Sporting goods such as golf balls, ammunition, and fishing weights are also potential sources (Zook et al 1972, McLeavey 1980, Bratton and Kowalczyk 1989, Morgan et al 1991a,b, Van Alstine et al 1993). Miscellaneous sources are contaminated water or soil (Scott 1963), newspaper and magazine print (Hankinet al 1974), pottery glazes (Schrimsher 1971, Turner and Fairburn 1979), lead dust from shooting galleries (Khanna et al 1992), and leaded glass artwork and curtain weights (Fenner 1989, Morgan et al 1991b). In our review of studies specifically involving cats the source of leadexposure was determined in 74% of cases (32/43) with old paint being responsible 84% of the time (27/32) (Scott 1963, Turner and Fairburn 1979, Jacobs 1981, Watson 1981, Prescott 1983, Hoffheimer 1988, Maddison and Allan 1990, Morgan et al 1991a, Miller and Bauk 1992, Van Alstine et al 1993). Old paint is the most commonly identified source not only in lead poisoned cats, but dogs and humans as well (Maddison et al 1993). Renovation of older houses involving the sanding and scraping of lead-based paint is the primary means of exposure (Maddison et al 1993). Federal regulations have limited the lead content of residential paint to <0.06% since 1977 (Morgan et al 1991a, Ramsey et al 1996). However, 74% of the occupied houses in the United States built before 1980 still contain hazardous quantities of lead paint (Graeme and Pollac 1998). Other sources of exposure were contaminated soil from a nearby lead mine in at least three cats (Scott 1963) and contamination of the integument of a cat with lead silicate used in pottery glazing (Turner and Fairburn 1979).

Signs

Lead toxicosis in domestic species characteristically involves the gastrointestinal and neurological systems. Ingested lead is distributed first to soft tissues including blood, liver, kidneys, and the central nervous system with clinical signs reflecting dysfunction of these organs. With more chronic exposure bone becomes the primary reservoir (Bratton and Kowalczyk 1989, Hong and Han 1994). The most common clinical signs in cats are anorexia, which may be the only presenting sign (McLeavey 1980, Miller and Bauk 1992, Maddison et al 1993), vomiting, and seizures(Table 1). Constitutional signs of lethargy and weight loss are common. Among the more unusual signs reported are ataxia of cerebellar (Hoffheimer 1988) or vestibular (Knight et al 2001) origin, vertical nystagmus indicating central vestibular dysfunction (Knight et al 2001), polyuria/polydipsia (Valler and Virat 1956, Morgan et al 1991a) presumably from renaltubular damage, and megaesophagus with dysphagia which resolved 8–10 weeks following treatment (Maddison and Allan 1990) (Table 1). The age of the cat may affect which organ system is involved. For example, in a report of 10 cats (mean age 3.5 years) from Boston the most frequent signs were anorexia, vomiting, and seizures (Morgan et al 1991a), while a study of 13 cats from Australia (mean age 8.8 years) reported vomiting and anorexia but no neurological signs. This was ascribed to the older age of the cats in that report (Maddison et al 1993). In our review the average age of cats with lead toxicosis, in reports where the age was given, was 6.1 years (median age4.5 years, n=35). Cats presenting with CNS signs (seizures, ataxia, and hysteria) with or without gastrointestinal signs had an average age of 4.1 years, and cats presenting with gastrointestinal signs (vomiting, colic, constipation, diarrhea, and regurgitation) without CNS signs had an average age of 8.3 years. The trend of this small number of cases indicates that younger cats may develop CNS signs more readily. The explanation may be that younger individuals of any domestic species have increased permeability of the blood–brain barrier (O'Brien 1981, Reid and Oehme 1989, Maddison et al 1993), greater gastrointestinal absorption of ingested lead (Bratton and Kowalczyk 1989, Reid and Oehme 1989), and less efficient detoxification and excretory pathways (Prescott 1983, Bratton and Kowalczyk 1989, Maddison et al 1993), all resulting in higher lead concentrations in the CNS.

Table 1.

Signs of lead toxicosis in cats

Signs No. of cats References
Anorexia 48 Valler and Virat (1956), Turner and Fairburn (1979), McLeavey (1980), Jacobs (1981), Watson (1981), Prescott (1983), Hoffheimer (1988), Maddison and Allan (1990), Morgan et al (1991a), Miller and Bauk (1992), Hawke and Maddison (1992), Van Alstine et al (1993), Maddison et al (1993), and Knight et al (2001)
Vomiting 30 Valler and Virat (1956), Turner and Fairburn (1979), Watson (1981), Jacobs (1981), Prescott (1983), Hoffheimer (1988), Morgan et al (1991a), Maddison et al (1993), and Van Alstine et al (1993)
Seizures 23 Valler and Virat (1956), McLeavey (1980), Prescott (1983), Hoffheimer (1988), Morgan et al (1991a), Van Alstine et al (1993), and Knight et al (2001)
Lethargy 17 Morgan et al (1991a), Van Alstine et al (1993), Hawke and Maddison (1992), Jacobs (1981), and Maddison et al (1993)
Weight loss 17 Morgan et al (1991a), Van Alstine et al (1993), Hawke and Maddison (1992), Jacobs (1981), Maddison et al (1993), and Knight et al (2001)
Ptyalism 10 Van Alstine et al (1993), and Hoffheimer (1988)
Depression 7 Maddison and Allan (1990), Turner and Fairburn (1979), and Maddison et al (1993)
Hyperexcitability 7 Valler and Virat (1956), Maddison and Allan (1990), McLeavey (1980),Maddison et al (1993), and Knight et al (2001)
Hysteria 5 Morgan et al (1991a) and Valler and Virat (1956)
Colic 4 Morgan et al (1991a), Maddison and Allan (1990), Hawke and Maddison (1992), and Maddison et al (1993)
Constipation 4 Valler and Virat (1956), Prescott (1983), and Turner and Fairburn (1979)
Ataxia 3 Hoffheimer (1988) and Knight et al (2001)
PU/PD 3 Morgan et al (1991a) and Valler and Virat (1956)
Dysphagia 2 Valler and Virat (1956) and Maddison and Allan (1990)
Diarrhea 2 Morgan et al (1991a) and Maddison et al (1993)
Vertical nystagmus 2 Knight et al (2001)
Head tremor 2 Knight et al (2001)
Regurgitation 1 Hawke and Maddison (1992)
Hypermetria 1 Hoffheimer (1988)
Failure to groom 1 Hawke and Maddison (1992)
Third eyelid prolapse 1 Maddison et al (1993)
Megaesophagus 1 Maddison and Allan (1990)
Blindness 1 Hawke and Maddison (1992)
Circling NS McLeavey (1980)
Mydriasis NS McLeavey (1980)
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NS=not stated.

Diagnosis

Blood lead concentrations are considered the best diagnostic test for lead toxicosis. Toxic blood levels in cats are >30–35 μg/dl (Fenner 1989, Van Alstine et al 1993, Puls 1994) or >60 μg/dl (Reid and Oehme 1989). However, it is important to be aware that blood lead concentrations fluctuate and due to sequestration in other organs do not necessarily correlate with total body burden of lead or with metabolic effects including clinical signs (Bratton and Kowalczyk 1989, Hong and Han 1993, Maddison et al 1993). Some animals with clinical lead toxicosis will not have a diagnostic elevation of blood lead while some animals may have elevated blood concentrations with few if any clinical signs (Maddison et al 1993). Making the diagnosis of lead toxicosis in cats requires consistent physical examination findings with confirmatory concentrations of blood lead. Lead concentration in the blood should not be the sole basis for diagnosis.

Less reliable diagnostic laboratory tests include urine lead or urine δ-aminolevulinic acid (ALA) concentrations and blood zinc protoporphyrin (ZPP) levels. Although urine lead concentrations diagnostic for lead toxicosis have not been established for cats, some authors suggest concentrations >50 μg/dl should be considered toxic with background concentrations in cats being <20 μg/dl (Scott 1963, Van Alstine et al 1993). Enzymes of the heme synthetic pathway are especially sensitive to lead and their substrate concentrations may aid in the diagnosis of lead toxicosis. Erythropoietic protoporphyrin (EPP) accumulates in red blood cells (RBCs) residing in the bone marrow due to inhibition of ferrochelatase by lead. The majority of EPP in the cat will bind zinc and exist as ZPP. Blood levels of ZPP >50–54 μg/100 ml (Hawke and Maddison 1992, Hong and Han 1993) indicate lead toxicosis. Since elevated ZPP will be found only in those RBCs which have left the bone marrow subsequent to exposure, ZPP levels are not a good indicator of acute lead exposure. Likewise, the ZPP remains in the RBCs even after chelation therapy has been completed, and is thus not a good indicator for following the success of treatment. Additionally, elevated ZPP is not specific to lead toxicosis. Iron deficiency, for example, gives similar results (Hawke and Maddison 1992). Inhibition of δ-aminolevulinic dehydrase results in accumulation of the substrate δ-ALA in blood and urine. Urinary ALA increases acutely with exposure to lead but is not specific for lead toxicosis and may be elevated in chronic liver disease and some porphyrias. A value greater than 87 μmol/l is suggestive of lead toxicosis, although wide variation in urinary ALA concentration in healthy cats requires correlation with clinical signs and blood lead levels (Hawke and Maddison 1992, Maddison et al 1993).

‘Lead lines’ on radiographs are caused by lead sequestration in the metaphyses of long bones in growing animals and can potentially be helpful diagnostically (Bratton and Kowalczyk 1989). The term ‘lead lines’ also refers to a dark blue linear discoloration of the gingiva near the teeth caused by hydrogen sulfide of decaying food particles reacting with blood borne lead to form a lead sulfide precipitate (Jones et al 1997). To our knowledge, radiographic or gingival ‘lead lines’ have not been reported in cats. Perhaps the most valuable use of radiography to diagnose lead poisoning in cats is to reveal radiodense specks of lead in the gastrointestinal tract, although bone chips may appear similar.

Hemogram evaluation for lead toxicosis in cats is usually normal and not helpful. The abnormalities most commonly found are nucleated RBCs (McLeavey 1980, Prescott 1983, Bratton and Kowalczyk 1989), followed by anemia (Valler and Virat 1956, Scott 1963, Priester and Hayes 1974, Zook and Carpenter 1977) and then basophilic stippling (Priester and Hayes 1974, Bratton and Kowalczyk 1989). Although nucleated RBCs(normoblastemia) in the absence of anemia are regarded as classic hemograms in lead poisoned animals, this finding is unusual in cats.

Lead causes toxic effects primarily in thehepatocytes and renal tubular epithelial cells by forming complexes with sulfhydryl groups in crucial sulhydryl-dependent proteins resulting in enzyme inhibition and ultimately cell death (Graeme and Pollac 1998). This results in elevated liver enzymes on serum chemistry analysis and glycosuria, proteinuria, and granular cast formation on urinalysis (Hoffheimer 1988, Bratton and Kowalczyk 1989, Morgan et al 1991a). A postmortem diagnosis can be made by analyzing lead concentration in tissues. The liver and kidneys are primary soft tissue organs of distribution with lead toxicosis. Higher doses and more acute exposure increase the proportion of lead found in the liver, kidneys, and brain (eg 36, 20, and 1%, respectively) relative to amounts found in bone (eg 42%). With chronic exposure bone may contain higher levels (eg 82%), with smaller amounts in the liver, kidney, and brain (eg 7, 8, and 2%, respectively) (Hong and Han 1994). Analysis of lead concentration in the liver is used most frequently. Levels >3.6–10 μg/g by wet weight of liver tissue is diagnostic of lead toxicosis (Bratton and Kowalczyk 1989, Puls 1994, Jones et al 1997).

Pathology

Reports of pathology findings in cats with lead toxicosis are rare. Experimental lead poisoning in a study of 30 cats revealed on gross necropsy examination yellow-brown discoloration of the liver in 11 cats often with a nutmeg-like appearance. Enlarged mesenteric lymph nodes were also seen in five cats although no specific histological changes were found (Hong and Han 1994). Pathognomonic, intranuclear, acid fast inclusion bodies or intranuclear or cytoplasmic inclusion bodies seen on H&E and orcein stained specimens may be seen in hepatocytes and in epithelial cells of the proximal renal tubules (Jubb et al 1993, Hong and Han 1994, Jones et al 1997). Lesions of the CNS are not found on gross necropsy (Van Alstine et al 1993, Hong and Han 1994), but histological findings include neuronal necrosis, demyelination, and astrocyte proliferation in the gray matter of the cerebrum. The cerebellum may have degeneration of Purkinje cells (Hong and Han 1994). Brain stem histology may reveal multifocal hemorrhages, vacuolated and dilatedperiaxonal spaces, eosinophilic shrunken nerve cell bodies with astrocytosis and microgliosis (Van Alstine et al 1993), and demyelination with neuronal necrosis (Hong and Han 1994).

Neurological signs correlate with necropsy findings in the CNS. Seizures, the most commonly reported neurological sign, as well as hyperexciteability, hysteria, and depression are consistent with abnormalities in the cerebral cortex. Hypermetria, ataxia, and head tremor may reflect cerebellar dysfunction while brainstem lesions could result in ataxia, nystagmus, dysphagia, and ptyalism. Anorexia, vomiting, and ptyalism may result from CNS or gastrointestinal dysfunction.

Treatment

Treatment of lead toxicosis in the cat, as in other species, involves prevention of further exposure, decontamination of the environment and the individual (ie bathing, cathartics, and/or enemas), supportive therapy, and chelation teatment. Magnesium sulfate (epsom salt) or sodium sulfate cathartics are preferred since lead will precipitate in the gastrointestinal tract as lead sulfate which is not absorbed (Bratton and Kowalczyk 1989). The recommended dose in cats is 2–5 g given orally while enema solutions of these agents should be avoided in cats due to possible electrolyte imbalances (Plumb 1999). The first chelating agent available was calcium disodium ethylenediaminetetraacetic acid (CaNa2 EDTA, calcium edetate, CaEDTA; Calcium Disodium Versenate, 3M Pharma., St. Paul, MN). This agent has the advantage of a proven track record in many species and can be administered by any route. For cats CaEDTA may be given subcutaneously at 27.5 mg/kg in 15 ml of D5W qid for 5 days, and repeated in 2 or 3 weeks if blood lead concentration remains >0.2 ppm. CaEDTA may also be given slowly IV at a dose of 5 mg/kg in divided daily doses (Reid and Oehme 1989). CaEDTA acts primarily on lead sequestered in bone which may be from 42 to 82% of total body lead burden depending on length of exposure and concentration of ingested lead. With lower doses and longer exposures proportionately more lead is sequestered in bone (Jubb et al 1993, Hong and Han 1994). The lead chelator complex is then excreted in the urine. Significant side effects of CaEDTA include pain at injection sites (especially when given IM), potential nephrotoxicity, and depletion of essential minerals like calcium, zinc, and iron. Also, when given alone it may paradoxically worsen lead encephalopathy within the first 2 days of therapy (Graziano et al 1978, 1985, Fikes and Dorman 1994, Ramsey et al 1996). This is apparently caused by lead being redistributedfrom soft tissue to the brain. Some authors recommend that British anti-lewisite (dimercaprol, BAL; BAL in Oil, Becton Dickinson) be given as an intramuscular (IM) injection before instituting CaEDTA therapy. BAL, a dithiol agent, works primarily by chelating lead from soft tissue with excretion of the complex in urine and bile. BAL therapy prior to calcium edetate helps prevent exacerbation of encephalopathy (Fikes and Dorman 1994, Ramsey et al 1996, Graeme and Pollac 1998) and the two agents act synergistically. CaEDTA is given parenterally or, if necessary, may be given orally in dogs (Hamir et al 1986) while BAL is given by IM injection. Because the therapeutic index is low for both agents they are best given in a hospital setting (Graziano et al 1978, 1985). BAL in veterinary medicine is primarily used in arsenic toxicosis. In our review we found no reports of use in cats, and we have no experience treating lead toxicosis in cats with BAL. The dosage for arsenic toxicosis in cats (and presumably for lead toxicosis) is 2.5–5 mg/kg IM q 4 h for 48 h, then q 12 h until recovery. The drug causes pain with IM injection and should be used cautiously in patients with renal compromise and always with IV fluid support (Reid and Oehme 1989). D-penicillamine (Cuprimine, Merck, West Point, PA) is a monothiol, oral chelating agent which is often given (125 mg q 12 h. p.o. for 5 days) as an outpatient drug to follow-up CaEDTA therapy in cats particularly if the blood lead concentration remains >0.2 ppm at3–4 weeks after CaEDTA therapy (Reid andOehme 1989). Vomiting is a common side effect but may be cirvumvented by giving with food or giving smaller, more frequent dosing (same total dose). Cuprimine may also increase the amount of lead absorbed from the gastrointestinal tract. Enemas or purgatives should therefore be given prior to use, especially if radiodense specks are seen in the gastrointestinal tract on radiographs. CaEDTA, Cuprimine and BAL are all potentially nephrotoxic (Fikes and Dorman 1994, Graeme and Pollac 1998).

Succimer (meso 2,3-dimercaptosuccinic acid, DMSA; Chemet, Sanofi-Synthelabo, New York, NY), an analog of BAL, is the most recent chelating agent to become available. Succimer has been used for decades in other countries but was first approved for human use in the United States in the mid-1990s. Oral dosing is an advantage, and it may be given rectally as a solution in vomiting patients. Excretion is via bile and urine (Graziano et al 1978, Ramsey et al 1996). Succimer has been used successfully in dogs (Ramsey et al 1996) and cats (Knight et al 2001), but does not have FDA approval for use in veterinary patients. In the only report of use in cats, two 5-year-old female littermate cats with lead toxicosis presented with anorexia, head tremors, central vestibular signs, and developed seizures soon after admission. They were successfully treated with oral succimer and suffered no side effects from the drug. Within 48 h of beginning treatment the signs began to resolve and blood lead concentrations were normal after 1 week of therapy. The cats were clinically normal 3 weeks after discharge (Knight et al 2001). Succimer appears to be a safe drug with no potential for nephrotoxicity. Toxicity studies with beagles given three times the recommended dose (105 mg/kg/day) for 15 times the recommended duration (22 weeks) showed no adverse effects and no clinical, biochemical, or pathological abnormalities (Graziano et al 1978). Standard dosage for dogs and cats is 10 mg/kg, p.o., q 8 h for 10 days (Graziano et al 1978, Knight et al 2001). Maximal response to succimer, in terms of amount of lead excreted, can be expected in the first day of treatment (Graziano et al 1978, 1985, Knight et al 2001). A rebound in blood lead levels after completion of the first course of therapy may necessitate a subsequent course (Graziano et al 1985, Ramsey et al, 1996).

Conclusions

Lead toxicosis remains a significant malady in feline patients and warrants a high index of suspicion since cats often present with vague, non-specific signs. With any consistent history, owners should be asked specifically about home renovations. Making the diagnosis is usually straightforward by finding elevated blood lead concentrations with consistent clinical signs. Supportive therapy, eliminating the source of lead and early treatment with chelating agents afford a good prognosis. Succimer has worked well in dogs and appears to work well in cats. More experience with this drug in cats will be helpful in determining safety profile, alternate routes of administration (eg efficacy when given per rectum in cats), and potential for rebound of lead concentrations after treatment.

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