Occurrence of acute lead toxicosis in western Canadian cattle herds: A decade of diagnostic case records (2014 to 2024)

Abstract

Background

Acute lead toxicosis is a leading toxic etiology in western Canadian cattle herds. Automotive batteries are commonly accepted as the main source of lead for grazing cattle.

Objective

The objective was to characterize cases of acute lead poisoning in cattle in western Canada (British Columbia, Alberta, Saskatchewan, and Manitoba) based on submissions to a veterinary diagnostic laboratory from 2014 to 2024.

Procedure

This study was a diagnostic records review.

Results

From January 1, 2014 to December 31, 2024, 352 cattle were poisoned from 233 herds. Cases occurred annually (median: 33 cases, 13 herds). Most submissions occurred in June (n = 110); however, cases were documented monthly (median: 18 cases, 21 herds). Cases and herds affected were most frequent in Saskatchewan (51 and 49%, respectively), followed by Alberta > Manitoba > British Columbia. Diagnosis was made most often on a postmortem basis, particularly with fresh liver (n = 213; range: 1.7 to 1663 mg/kg wet weight). There were 128 cases diagnosed antemortem using whole blood (range: 0.33 to 6.5 mg/L). Most herds affected were beef breeds (98%). Poisoning was most frequently diagnosed in calves (n = 174).

Conclusion and clinical relevance

Acute lead poisoning continues to be a regular occurrence in western Canada. Pre-weaned calves during the months of May through July were at the greatest risk of lead poisoning in this study population.

INTRODUCTION

For the past several decades in Canada, acute lead toxicosis has been a regular occurrence in cattle, particularly beef cattle (1–8). Lead is highly toxic to numerous organ systems; however, acute lead poisoning in cattle manifests as neurotoxicosis. Clinical signs can be localized to the forebrain and include blindness, bruxism, head-pressing, circling, focal tremors, and tonic-clonic seizures (9,10). The earliest signs of acute lead toxicosis are often depression and anorexia; however, it is not uncommon for cattle to be observed with neurologic signs or found dead without premonitory signs. The mechanism of neurotoxicosis is damage to cerebral blood vessels leading to cerebral edema and subsequent neuronal necrosis [e.g., polioencephalomalacia (PEM)] (9). Reported lethal doses of lead in calves and mature cattle are 200 to 400 mg/kg BW and 600 to 800 mg/kg BW, respectively (9,11,12).

Outbreaks of lead poisoning can be devastating to cattle producers. Case histories submitted to the diagnostic laboratory often describe multiple cattle sick or dead. Often, infectious causes of neurologic disease are considered. In addition, the source of lead to cattle is commonly unknown to the producer. Management of lead-poisoned cattle is also challenging for veterinarians, as there are limited effective treatment options available. In theory, based on studies of experimental lead poisoning in cattle (13–15), chelation therapy (e.g., succimer, calcium edetate) could be attempted. However, chelators may be impractical to administer and difficult to acquire, and many symptomatic cattle die despite treatment. This is further complicated by the highly variable half-life of the body burden of lead, with elimination half-life values ranging from 3 to 2507 d in various reports (6,13–15). Further, herd-wide testing is necessary to prevent lead-exposed cattle entering the food chain.

The objective of this study was to retrospectively characterize cases of acute lead poisoning in cattle in British Columbia, Alberta, Saskatchewan, and Manitoba, based on submissions to a veterinary diagnostic laboratory from 2014 to 2024. This study serves as a follow-up to a previous publication that documented acute lead poisoning in cattle in western Canada from 1998 to 2013 (7).

MATERIALS AND METHODS

Records of lead poisoning in cattle from January 1, 2014 to December 31, 2024, were retrieved from the veterinary toxicology laboratory archives of Prairie Diagnostic Services (Western College of Veterinary Medicine, Saskatoon, Saskatchewan). Submissions received by the laboratory were either submitted specifically for lead testing or as part of a larger investigation of other diseases. A case of lead poisoning was defined as single tissue submission from a single animal, whereas a herd was defined as > 1 sample from individual animals submitted by a veterinarian on behalf of the same owner or operation.

Lead poisoning was diagnosed by a veterinary toxicologist based on published tissue concentrations (16). The diagnostic thresholds for lead poisoning in whole blood, liver, and kidney were > 0.35 ppm, > 5.0 ppm (wet-weight basis), and > 5.0 ppm (wet-weight basis), respectively. Information on year of case submission, month of case submission, province of animal origin, animal age, commodity (i.e., dairy or beef), breed of cattle, tissue specimen submitted, and tissue lead concentrations was retrieved, if available, from each diagnostic case record. Any available clinical pathology data [i.e., complete blood (cell) count (CBC) and blood chemistry panel] were tabulated. Signs described in case histories were used to identify common presentations, and these were categorized on a multi-pleanimal basis or an individual-animal basis. Suspected sources of lead described in case histories were noted. Case data were reviewed manually and entered into a commercial spreadsheet for analysis (Microsoft Excel, Microsoft 365, Version 16; Microsoft Corporation, Redmond, Washington, USA). In addition to recording numeric age (if available), cattle were categorized into the following groups based on age: calf (≤ 12 mo), yearling (> 12 mo to ≤ 24 mo), and adult (> 24 mo).

Concentration of lead in whole blood (heparin or EDTA) was determined using anodic stripping voltammetry (LeadCare I or LeadCare II; Magellan Diagnostics, North Billerica, Massachusetts, USA) or inductively coupled plasma mass spectroscopy [iCAP Q inductively coupled plasma mass spectrometry (ICP-MS); ThermoFisher, Franklin, Massachusetts, USA]. Lead concentrations in liver, kidney, brain, rumen contents, and lung were determined using ICP-MS, following addition of nitric acid and microwave digestion, according to laboratory protocol. The limit of detection for the anodic stripping voltammetry method was 0.033 ppm. The limit of detection for lead analysis with ICP-MS was 2.6 ppt. Concentrations of lead in tissues were reported as parts per million (mg/kg for tissues or mg/L for blood) on a wet-weight basis (as received).

RESULTS

Acute lead poisoning was diagnosed in 352 cattle and 233 herds over the 10-year period of study. Occurrence of acute lead poisoning in cattle by province of submission, month of submission, and year of submission are described in Table 1. Cases occurred on an annual basis. The highest number of cases documented in a year was 49 in 2018, corresponding to the highest number of herds affected (n = 36). The lowest number of case submissions occurred in 2014 and 2023 (13 cases each), corresponding to the lowest number of herds affected (9 and 12, respectively). Most cases of acute lead poisoning occurred in Saskatchewan (SK; 51% of cases and 49% of herds), followed by Alberta (AB), Manitoba (MB), and British Columbia (BC). Lead poisoning was reported in each month of the year. However, submissions were most frequent in June (n = 110), which corresponded to the highest number of herds affected by month (n = 70). Submissions were also frequent in May and July, which also corresponded to the higher numbers of herds affected in those months. Cases in these 3 months accounted for 63% of total cases and 61% of total herds affected.

TABLE 1.

Geographic and temporal characteristics of acute lead poisoning in cattle in western Canada from 2014 to 2024. Lead poisoning was confirmed in 352 cattle in 233 herds by antemortem and postmortem tissue analysis at a Saskatchewan veterinary diagnostic laboratory^a.

Characteristic	No. submissions (%)	No. herds (%)
Province of submission
BC	23 (6.5)	8 (3.4)
AB	120 (34)	83 (36)
SK	178 (51)	114 (49)
MB	31 (8.8)	28 (12)
Mean ± SD	88 ± 74	58 ± 49
Median	76	56
Year of submission
2014	13 (3.7)	9 (3.9)
2015	33 (9.4)	25 (11)
2016	24 (6.8)	14 (6.0)
2017	47 (13)	29 (12)
2018	49 (14)	34 (15)
2019	32 (9.1)	27 (12)
2020	45 (12)	27 (12)
2021	47 (13)	20 (8.6)
2022	18 (5.1)	15 (6.4)
2023	13 (3.7)	12 (5.2)
2024	34 (9.4)	22 (9.0)
Mean ± SD	32 ± 14	19 ± 19
Median	33	13
Month of submission
January	3 (0.9)	3 (1.3)
February	11 (3.1)	3 (1.3)
March	9 (2.5)	6 (2.6)
April	20 (5.7)	15 (6.4)
May	53 (15)	36 (16)
June	110 (31)	70 (30)
July	61 (17)	36 (16)
August	22 (6.2)	18 (7.7)
September	12 (3.4)	9 (3.9)
October	18 (5.1)	13 (5.6)
November	18 (5.1)	12 (5.2)
December	16 (4.5)	13 (5.6)
Mean ± SD	29 ± 31	21 ± 8
Median	18	21

AB — Alberta; BC — British Columbia; MB — Manitoba; SD — Standard deviation; SK — Saskatchewan.

^aPrairie Diagnostic Services (Western College of Veterinary Medicine, Saskatoon, Saskatchewan).

There were 6 herds that experienced multiple years of lead poisoning incidents; 4 were from SK and 2 were from AB. Three of these herds experienced poisoning within 1 y of the first documented case (i.e., 2015 and 2016, 2017 and 2018, 2020 and 2021). The other 3 herds had poisoning cases 3 years after the first documented cases (i.e., 2015 and 2018, 2018 and 2021, 2021 and 2024). In all these herds, the histories provided to the laboratory did not include descriptions of repeat pasture use.

Most cases were diagnosed post-mortem. Tissues used to make the diagnoses included liver, kidney, brain, rumen contents, and lung tissue (Table 2). Of these tissues, there were 3 instances in which multiple tissues from the same animal were submitted for lead quantification. In the case of a 2-month-old Charolais calf from SK in 2015, liver and rumen contents contained 12.5 ppm and 3873 ppm lead, respectively. From another SK herd in 2015, the liver and kidney from a 3-year-old Charolais cow contained 19.6 ppm and 39.9 ppm lead, respectively. Last, in an Angus cow of unknown numeric age from SK, the liver contained 10.4 ppm lead whereas the rumen contents contained 14 320 ppm lead. There were 6 cases in which acute lead poisoning was diagnosed based on liver concentrations less than the accepted diagnostic threshold of 5 ppm (16). Concentrations of hepatic lead ranged from 4.0 to 4.4 ppm and were interpreted as toxic, based on the veterinarian-provided history compatible with acute lead toxicosis. In 2 of these cases, batteries were found on pasture.

TABLE 2.

Lead concentrations (ppm wet weight; mean ± SD) in bovine tissues submitted for toxicology testing at a Saskatchewan veterinary diagnostic laboratory^a from 2014 to 2024. Concentrations in non-blood tissues were determined by ICP-MS. Whole-blood lead concentration was determined by anodic stripping voltammetry or by ICP-MS.

Sample	[Pb]	Min.	Max.	No.b
Liver	43 ± 122	4.0	1663	211
Whole blood	1.2 ± 0.82	0.33	6.5	128
Kidney	82 ± 52	27	173	7
Brain	9.2 ± 14	0.33	30	4
Rumen contents	6573 ± 6811	1527	14 320	3
Lung	1.7	N/A	N/A	1

ICP-MS — Inductively coupled plasma mass spectrometry; N/A — Not applicable.

^aPrairie Diagnostic Services (Western College of Veterinary Medicine, Saskatoon, Saskatchewan).

^bThree cattle had multiple tissues submitted (liver/rumen contents, liver/kidney, liver/rumen contents).

Antemortem diagnosis with whole blood was documented in 127 cases (heparin: n = 89, EDTA: n = 19 where blood tube additive was specified). There were 2 cases in which acute lead poisoning was diagnosed based on whole-blood concentrations less than the accepted diagnostic threshold of 0.35 ppm (16). In both cases, acute lead poisoning was suspected in the history provided to the laboratory and blood lead concentrations were 0.33 and 0.34 ppm, respectively.

A limited number of cases had blood clinical pathology data; these data are presented in Tables S1 and S2 (available online from: Supplementary Materials). Thirteen cattle had CBC testing completed. Commonalities in CBC results included hemoconcentration, as evidenced by elevated erythrocyte count (n = 10; range: 7.64 to 10.6 × 10¹²/L), elevated hemoglobin concentration (n = 8; range: 134 to 155 g/L), and elevated hematocrit (n = 10; range: 0.332 to 0.418 L/L). Erythrocyte distribution width was also elevated in 10 cattle (range: 19.9 to 25.6%). Serum chemistry testing was available for 17 cattle. Commonalities in serum chemistry results included elevated creatinine kinase (n = 15; range: 395 to 8911 U/L), hyperbilirubinemia (n = 10; range: 7.4 to 23.9 mmol/L), elevated creatinine (n = 10; range: 96 to 175 mmol/L), elevated aspartate aminotransferase (n = 10; range: 132 to 507 U/L), hyperglycemia (n = 9; range: 4.5 to 9.9 mmol/L), hyperalbuminemia (n = 9; range: 39 to 45 g/L), hypercalcemia (n = 7; range: 2.63 to 3.01 mmol/L), elevated glutamate dehydrogenase (n = 6; range: 38 to 138), high anion gap (n = 6; range: 31 to 46 mmol/L), and hypomagnesemia (n = 6; range: 0.67 to 0.8 mmol/L).

Numeric age of cattle was specified in 232 cases. Case history also allowed for subsequent categorization of 54 cases. Age was not available or described for 66 cases. Most cases were documented in calves (n = 174; 49% of total cases and 75% of cases in which numeric age or category was described). The age distribution of calves diagnosed with acute lead poisoning is provided in Figure 1. Calves in most cases were ≤ 4 mo old (n = 120; 34% of cases). The youngest calves diagnosed with acute lead poisoning were 3 wk old (2 calves from the same herd). There were 27 cases of poisoning in yearlings and 85 in adult cattle. The oldest animal poisoned was 11 y old.

FIGURE 1.

Age distribution of calves diagnosed with acute lead poisoning in western Canada from 2014 to 2024.

Commodity of cattle was described for 159 herds and not described for 73 herds. Most herds were beef cattle (n = 156; 98%). The 4 dairy herds affected had Holstein-Friesian cattle. Owner-reported beef breeds affected, including crosses, were Angus (n = 99 herds), Charolais (n = 19), Simmental (n = 18), Hereford (n = 4), shorthorn (n = 4), Gelbvieh (n = 2), longhorn (n = 2), Limousin (n = 1), Maine-Anjou (n = 1), and Speckle Park (n = 1). There were 5 herds described as “mixed-breed beef.”

Signs of lead poisoning were described in the veterinarian-submitted histories in 200 cases (Table S3, available online from: Supplementary Materials). Of these cases, 118 described signs in > 1 animal, whereas 82 cases described signs in 1 animal only. The 5 most common signs described in individual cattle were blindness (n = 49), acute death (n = 24), tremors or seizures (n = 21), salivation/frothing (n = 16), and abnormal mentation (n = 14). The 5 most common signs described in multiple individuals were acute death (n = 72), blindness (n = 53), being found dead (n = 32), tremors or seizures (n = 26), and abnormal mentation (n = 18). A complete table of signs in individuals and multiple animals is presented in Table S2 (available online from: Supplementary Materials).

The suspected sources of lead were described in a limited number of case histories. These included automotive/machinery batteries (n = 36), debris piles (n = 1), old vehicles/metal waste (n = 1), old machinery/metal scraps (n = 1), old shingles (n = 1), an old yard site (n = 1), and a burning barrel (n = 1). In addition, 7 veterinarian-submitted histories described finding metallic content in the reticulorumen. Metallic particles in rumen contents of 2 deceased cattle diagnosed with lead poisoning are shown in Figure 2.

FIGURE 2.

Photographs showing lead particles in the reticulorumen of poisoned cattle. A — Rumen contents from a deceased beef cow during an on-farm postmortem examination (Saskatchewan, June 2024). B — Reticulum contents from a deceased beef cow (British Columbia, June 2024).

DISCUSSION

The present study expanded on previous studies of acute lead toxicosis in Canadian cattle by documenting herds affected rather than only reporting on case submissions. Throughout the 10-year period of study, lead poisoning occurred in herds annually and in all months of the year, especially in Saskatchewan and Alberta. The higher proportion of cases in these provinces is most likely related to the high cattle population (17) rather than to more sources of lead accessible to cattle. There were a small number of cases in which poisoning was diagnosed below the accepted thresholds for lead toxicosis. This was possible because detailed histories were submitted to the diagnostic laboratory, which underscores the importance of providing a complete history and physical examination findings to the laboratory to contextualize diagnostic results.

In Canada, lead poisoning has been the most diagnosed form of poisoning of cattle for at least 60 y. Results of the present study were consistent with those from previous Canadian studies of lead poisoning in cattle (1,3,4,7) in multiple areas (age of cattle, time of year, and commodity of cattle). A study from Ontario reported 175 cases from 1954 to 1969 (1). In a study of case records from 1968 to 1982 submitted to the diagnostic laboratory primarily from Saskatchewan, 294 cases of lead poisoning were documented in cattle (4). In Alberta, 738 cases of lead poisoning were recorded between 1964 and 1985 (5). From 1998 to 2013, 525 cases were documented in western Canada (7). Although the number of diagnosed cases appears to be decreasing over time, diagnosed cases cannot be considered a true representation of the breadth of the problem; most producers or bovine practitioners submit samples from a limited number of poisoned animals to establish a diagnosis. Although cases may be decreasing numerically over time, the problem persists.

Determining the extent of lead exposure in a herd with confirmed cases is achieved by testing the entire herd. Other reports of lead poisoning in cattle have indicated that significant portions of the herd are asymptomatic-yet-exposed. A study of lead poisoning in 3 Canadian beef cattle herds reported that 4 to 40% of cattle without any signs of acute or subacute lead poisoning could have elevated or toxic concentrations of lead in their blood (6). Similarly, in a study describing lead poisoning in 12 Saskatchewan cattle herds, the asymptomatic-yet-exposed prevalence in lead-exposed herds ranged from 0 to 15.6% (8), also supporting the rationale to test all potentially exposed cattle in a herd. Consequently, the authors of that study recommend pooled blood testing for clinically normal animals, to save on costs associated with outbreaks. A study of 9 farms with accidental lead exposure (14) indicated that only 1 of every 7 cattle with elevated blood lead concentrations exhibited clinical signs of poisoning. Further, a recent report from Australia indicated that the number of asymptomatic-yet-exposed cattle ranged from 7 to 40% (18). This phenomenon of underestimation of exposed cattle in herds with lead poisoning has been known for decades (2). Although herd-wide testing is the best practice for identification of exposed cattle, the costs of testing can be substantial. Best et al (2022) reported that costs of testing cattle herds with cases of lead poisoning ranged from CAD ~$220 to $42 000 (median: $3300) (8).

Most cases documented herein occurred in calves, especially those ≤ 4 mo of age. This finding was consistent with other surveys of bovine lead poisoning in Canada (3,7). A survey of cases from 1968 to 1975 documented that 72% of cattle with lead poisoning were < 12 mo of age and ~50% were calves ≤ 6 mo old (3). A survey of diagnostic records from 1998 to 2013 in western Canada reported that 54% of cases occurred in calves ≤ 6 mo old (7). Calves are considered more vulnerable to lead poisoning due to their curious nature, the ability to fit into smaller areas that may contain lead sources, a greater degree of lead absorption from the gastrointestinal tract (especially with milk-based diets) (19), a proclivity of pre-ruminants to ingest soil (20), and an immature blood-brain barrier (6). In a study of demographics of cattle poisoned by lead, calves ≥ 2 mo but ≤ 6 mo of age had significantly higher odds of poisoning (21). Given this age predisposition in cattle, lead poisoning should be considered as a top differential diagnosis in any case of calves presenting with neurologic signs on pasture.

Seasonality of lead poisoning cases documented in the present study was consistent with other studies from Canada (3,5–7) and elsewhere (10,12,20,22). In beef cattle production, this period coincides with calving in commercial beef herds and the start of the grazing season. Recent pasture change was noted in many of the histories submitted to the diagnostic laboratory. Although cases occurred throughout the year during the period of study, the highest-risk period for lead poisoning in cattle appeared to be May through July. Beef cattle had the majority of documented lead poisoning cases in the present study. This finding was perhaps unsurprising, as most cattle in western Canada are beef breeds, particularly Angus (21).

In modern beef cattle production, extensive management with pasture grazing is a key component of the production cycle for many operations. In contrast to beef cattle, dairy cattle are intensively managed but are often not on pasture for prolonged intervals as beef care are, leading to fewer opportunities for lead exposure. The predominant concern with dairy cattle becoming poisoned is contamination of milk. Lead from poisoned cattle can be excreted in milk at various concentrations (23–26); however, if testing bulk tank milk, false negative results are possible due to sample dilution. Despite the predominance of lead poisoning in beef cattle, very few reports describe lead testing of meat from poisoned and exposed beef cattle. One study of lead-exposed cattle reported no correlation between blood lead concentration and lead concentration in skeletal muscle (27). Moreover, the lead concentration in skeletal muscle was as high as ~30 mg/kg (dry matter basis). Further research is required to understand the transfer of lead to edible tissue in beef cattle and the degree of risk this poses to beef consumers.

An inherent difficulty of dealing with lead poisoning in cattle is the highly variable half-life of its elimination from blood, which impairs the ability of veterinarians and veterinary diagnosticians to provide accurate recommendations on when cattle products can enter the food chain (either meat or milk). Reported half-lives for lead in blood of poisoned cattle include 68 to 266 d (13), 3 to 577 d (14), 48 to 2507 d (15), and 34 to 107 d (interquartile range) (6). However, disappearance from blood is the main indicator of when cattle are considered “safe” for the food supply. The major disadvantage of relying on blood lead elimination for safety is that lead disappearance from blood does not mean an animal is “lead free.” Following absorption from the gastrointestinal tract, lead partitions to viscera such as the liver and kidney (in which concentrations can be high) and eventually to cancellous bone (6). In an outbreak of lead poisoning in an Australian yearling cattle herd, the authors noted that a small proportion of exposed cattle had elevated blood lead concentrations 19 mo after the outbreak (18). Subsequent necropsy of those cattle revealed lead particles in the reticulorumen, serving as a continuous source of lead. The major conclusion of that report was that asymptomatic animals with elevated blood lead concentrations quadrupled their time at the feedlot (18).

As there are limited treatment options for lead poisoning in cattle, prevention of exposure to lead sources is essential. Often, this matter is complicated if the presence of lead is unknown to the current landowner or the producer is using leased/rented land. In the present study, sources of lead were inconsistently reported in histories provided to the diagnostic laboratory. In the limited studies that did report suspected sources, automotive batteries were most cited. Multiple deaths on pasture prompt the producer/veterinarian to inspect the pasture for a potential source of lead (i.e., a reactive approach). It is a challenge to proactively prevent lead poisoning, as searching pasture before turn-out can be time consuming and fruitless. In addition, some producers graze the same pasture for years without problem. Historically, sources of lead for cattle included engine oil from leaded gasoline, automotive/machinery batteries, and lead-based paint (3,9,10,14,20,28). There have also been reports of cattle becoming poisoned through consumption of lead ammunition on pasture (29–31). Pastures contaminated by industrial byproducts and waste have also resulted in poisoning (28,32–34).

In the present study, the most common signs of lead poisoning in the veterinarian-provided histories were blindness and acute death. Lead causes blindness in cattle through forebrain damage, thereby inducing a “cortical blindness.” In the author’s opinion and experience, the finding of blindness in calves during the summer months is acute lead poisoning until proven otherwise. The cluster of signs of blindness, “stargazing,” opisthotonus, and tremors/seizures are often referred to as PEM. Although originally (and still) a histologic diagnosis of the brain (i.e., cerebrocortical necrosis or liquefactive necrosis of the grey matter), the term has become a widely used clinical diagnosis in production animal medicine.

Acute lead poisoning is a differential diagnosis for PEM; others include salt poisoning [i.e., sodium-ion water deprivation toxicosis (35)], sulfur poisoning, and thiamine deficiency. Thiamine deficiency is more of a phenomenon of feedlot cattle, related to rapid dietary transition that results in prevalence of thiaminolytic bacteria in the rumen (36). Thiamine deficiency can likely be ruled out if cattle are on pasture at the time of a PEM outbreak. History information, including water source and availability, water quality, and type of feed being consumed on pasture (e.g., Brassica spp.), is essential for directing diagnostic testing to differentiate the toxic causes of PEM. Postmortem testing for salt poisoning and lead poisoning is available at most veterinary diagnostic laboratories; submission of fresh brain is used for sodium quantification and submission of fresh liver (or other tissue) for lead quantification. To the author’s knowledge, there is currently no confirmatory tissue test available for sulfur toxicosis; therefore, diagnosis is supported by a finding of high total dietary sulfur intake, including water (37).

Due to the retrospective nature of this study, there were numerous limitations worthy of mention. Diagnostic histories were heavily relied upon for description of clinical signs; therefore, clinical signs were skewed toward cases in which more in-depth histories were provided to the laboratory. Similarly, there were numerous cases in which complete case information was not provided, including age, breed, and other pertinent details. The diagnostic laboratory rarely received follow-up testing results from affected herds; therefore, information on lead depuration could not be provided. In certain provinces, such as Alberta, diagnosis of lead poisoning in a herd triggers a regulatory process involving quarantine and follow-up blood lead testing in exposed cattle that is managed by the Alberta Ministry of Agriculture. In contrast, in Saskatchewan, there is currently no regulatory requirement for follow-up testing in herds with diagnosed cases of lead poisoning.

Given the clear temporal pattern of bovine lead poisoning in Canada, a paradigm shift is required to prevent cases. Based on the data provided herein, this is especially important for pre-weaned calves, though cattle of any age can become poisoned. Beef breeds are at greatest risk due to extensive management on pasture, where the sources of lead are located. Harmonization of regulatory oversight and investigation strategies across western Canada could be considered to better understand trans-provincial movement of exposed cattle and provide a standard framework for bovine veterinarians. In herds with documented cases of lead poisoning, testing of the entire herd should become regular practice to prevent asymptomatic-yet-exposed cattle from entering the food chain. Pooled sampling can be considered to minimize costs.