Paint chip poisoning of Laysan albatross at Midway Atoll

Epizootic mortality occurred in Laysan albatross (Diomedea immutabilis) fledgings at Midway Atoll in 1983. Heavy metal toxicity from ingestion of weathered paint chips was one of the causes. Sick albatrosses were unable to retract their wings, causing a "droop-wing" appearance. Five normal and 12 droop-winged fledglings were captured, killed, and examined. Paint chips found in the proventriculus of the affected fledglings contained up to 144,000 ppm lead. Blood, liver, and kidney concentrations of lead in affected birds were higher than in normal fledglings, and acid-fast intranuclear inclusion bodies were present in the kidneys. Degenerative lesions were present in the myelin of some brachial nerves. Weathered paint samples collected from 12 buildings contained up to 247,250 ppm lead and 101 ppm mercury. Lead poisoning was diagnosed in 10 of the droop-winged albatrosses and was one of the causes of morbidity. Mercury toxicosis and plastic impaction were other possible causes.     

Intranuclear inclusions in urinary cytology

Twenty-one urinary cytology specimens from 16 patients showed red intranuclear inclusion bodies. The literature pertinent to these inclusions mainly suggests that lead poisoning is a cause for such inclusions. Histories were reviewed for possible causes, particularly lead poisoning, associated medications, associated illness or relationship to neoplasia. The only consistent associations found were that all the patients were women over the age of 50 and that all inclusions were found in voided urine specimens. Four slides containing inclusions were stained by acid-fast methods, with negative results. The origin of these inclusions remains unknown.     

Lead poisoning from lead-soldered electric kettles.

Lead poisoning occurred in two infants, causing lead encephalopathy in one but no symptoms in the other. Both infants had been fed a formula prepared with water boiled in a lead-soldered electric kettle. The diagnosis was suggested by dense metaphyseal bands in radiographs, illustrating the importance of careful examination of "routine" radiographs, particularly in asymptomatic infants.     

Lead poisoning in whooper and tundra swans

Six weak whooper swans (Cygnus cygnus) and two weak tundra swans (Cygnus columbianus) were found at Swamp Miyajima (Hokkaido, Japan) in May 1998. Anorexia, depression, green watery feces, pale conjunctiva, and anemia were observed. Radiographs showed from six to 38 suspected lead pellets in the gizzard. Blood lead concentrations were 2.5-6.7 microg/g (mean+/-SD=4.6+/-1.14 microg/g) on day 1. After blood collection, the birds were treated with calcium disodium ethylenediaminetetraacetate (CaEDTA) given intravenously and force fed. Despite treatment, seven birds died the next day. Green, bile-stained livers and pale or green kidneys were observed on necropsy. Microscopically, bile pigment was widespread in the liver and acid-fast intranuclear inclusion bodies were observed in renal tubular epithelium. Lead concentrations in livers and kidneys were 14.0-30.4 microg/g and 30.2-122 microg/g wet weight, respectively. Only one bird survived and this whooper swan continued to be treated with CaEDTA and activated charcoal. No lead shot was observed in the proventriculus and gizzard by radiography on day 64 and the blood lead concentration decreased from 2.9 microg/g to 0.09 microg/g during that same period. After 4 mo of rehabilitation, the whooper swan was returned to the wild. Lead intoxication continues to be a problem at Swamp Miyajima.     

Lead poisoning in woodpeckers in Sweden

Lead poisoning was demonstrated in two gray-headed woodpeckers (Picus canus) and one white-backed woodpecker (Dendrocopus leucotos) in Sweden; they had liver lead levels between 9.4 and 26.2 mg(-1) wet weight. At necropsy one gray-headed woodpecker showed signs of emaciation and the other one had severe traumatic injuries, caused by a cat. The white-backed woodpecker died in the transportation box during a translocation program. The source of the lead could not be determined, but it was suspected that it may have originated from lead pellets shot into trees and picked out by the woodpeckers during food search.     

Retrospective analysis of an outbreak of B virus infection in a colony of DeBrazza's monkeys (Cercopithecus neglectus)

In 1981, an outbreak of herpetic disease developed in a colony of DeBrazza's monkeys (Cercopithecus neglectus). In seven of eight infected animals, clinical signs of infection included vesicular and ulcerative lesions on the lips, tongue, and/or palate. Histologic examination of lesions revealed intranuclear inclusion bodies, and electron microscopy revealed nucleocapsids and virions with typical herpesvirus morphology. Although a virus was isolated that appeared similar to monkey B virus, techniques available at the time did not allow precise identification of the virus. Analysis of serum from one surviving monkey collected 12 years after the outbreak revealed a pattern of reactivity characteristic of B virus-positive serum on the basis of results of ELISA and western immunoblot analysis. Polymerase chain reaction analysis of archived paraffin-embedded tissue specimens and molecular analysis of the one viral isolate obtained from a DeBrazza's monkey indicated that the virus responsible for the outbreak was a new genotype of B virus. Testing of sera from lion-tailed macaques (Macaca silenus) housed in an adjacent cage at the same zoo indicated that these animals harbored this virus and, thus, were the likely source of the virus that infected the DeBrazza's monkeys. This study documents usefulness of archiving samples from disease outbreaks for later analysis. In addition, this incident underscores the importance of considering herpes B virus infection when outbreaks of disease having characteristics of herpetic infections develop in nonhuman primates kept at institutions that also house macaques.     

The unique kidney of the spider monkey (Ateles geoffroyi).

Among nonhuman primates, the renal anatomy of the spider monkey (Ateles geoffroyi) is unique, as it is multipyramidal and multipapillary. Renal function parameters (glomerular filtration rate, renal plasma flow, and concentrating ability) are compared to man and other primates. The kidneys of the spider monkey are similar both anatomically and functionally to man.     

Aluminum Chloride Causes the Dysfunction of Testes Through Inhibiting the ATPase Enzyme Activities and Gonadotropin Receptor Expression in Rats

Lead, one of the most harmful heavy metals, can cause various hazardous effects on living organisms. This study was undertaken to evaluate the antagonistic and protective effects of two economically important laver species, Pyropia yezoensis and P. haitanensis, against subchronic lead poisoning in rats by a 30-day feeding test. Sixty-four healthy Wistar rats were randomly divided into eight groups with eight rats (4♂ + 4♀) per group, among which, one group was served as the control, the others were respectively treated with lead acetate (5 mg/kg b w), and a combination of lead acetate and P. yezoensis or P. haitanensis at different dosages. Weight gain of rats was observed and recorded. Changes in antioxidant indexes, and liver and renal function markers were determined to evaluate the antagonistic effect. Lead content in rats was determined to investigate lead excretion effect of laver. The results showed that exposure to lead caused lead accumulation in kidney and liver, thus leading to significant oxidative damage and impaired liver and renal function compared to the control group. The co-treatment of laver slightly increased body weight compared to the lead-treated group. The co-administration of laver restored liver and renal function of rats by preventing the increment in the activities of alanine transaminase (ALT), alkaline phosphatase (ALP), and aspartate transaminase (AST), and the levels of blood urea nitrogen (BUN) and creatinine (Cr). The increasing of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities, and lowering of the enhanced malondialdehyde (MDA) contents of rats were observed in the laver co-treated groups, which indicated that laver enhanced the antioxidative capacity of rats. The laver also enhanced lead content in feces and reduced it in liver and kidney. The results indicated that P. yezoensis and P. haitanensis could maintain or promote the normal physiological and biochemical function of lead-induced subchronic poisoning of rats, probably owing to their enhancements of antioxidant capacity and lead excretion.     

Adverse health effects in Canada geese (Branta canadensis) associated with waste from zinc and lead mines in the Tri-State Mining District (Kansas, Oklahoma, and Missouri, USA)

Lead and zinc poisoning have been recorded in a variety of bird species, including migrating waterfowl such as Canada Geese (Branta canadensis), at sites contaminated with mine waste from lead and zinc mines in the Tri-State Mining District, Kansas, Oklahoma, and Missouri, USA. The adverse health impacts from mine waste on these birds may, however, be more extensive than is apparent from incidental reports of clinical disease. To characterize health impacts from mine waste on Canada Geese that do not have observable signs of poisoning, four to eight apparently healthy birds per site were collected from four contaminated sites and an uncontaminated reference site, and examined for physical and physiologic evidence of metals poisoning. Tissue concentrations of silver, aluminum, arsenic, barium, cadmium, cobalt, chromium, copper, iron, magnesium, manganese, molybdenum, nickel, lead, selenium, thallium, vanadium, and zinc were determined by inductively coupled plasma mass spectroscopy. Adverse health effects due to lead were characterized by assessing blood δ-aminolevulinic acid dehydratase (ALAD) enzyme activity. Adverse effects associated with zinc poisoning were determined from histologic examination of pancreas tissues. Elevated tissue lead concentrations and inhibited blood ALAD enzyme activities were consistently found in birds at all contaminated sites. Histopathologic signs of zinc poisoning, including fibrosis and vacuolization, were associated with elevated pancreatic zinc concentrations at one of the study sites. Adverse health effects associated with other analyzed elements, or tissue concentrations indicating potentially toxic exposure levels to these elements, were not observed.     

Spatial and temporal variation in lead levels related to body condition in the Mississippi Valley population of Canada geese

Concern over lead poisoning led to progressive prohibition of toxic shot to harvest waterfowl in the 1980's. Nevertheless, waterfowl remain susceptible to ingestion of lead shot because illegal use continues and spent shot persists in soil and wetland substrates. While mortality due to lead toxicosis has subsided, sublethal effects may still affect survival and reproduction. We measured liver lead levels and body condition in 732 Canada geese (Branta canadensis interior) during July 1984 to April 1989 in southern Illinois (USA), east-central Wisconsin (USA), and northern Ontario (Canada). Although we sampled only individuals that were visibly healthy, 55 of 732 (7.5%) geese had elevated liver lead levels (> 2 ppm). Lead levels of 46 (6.3%) geese indicated subclinical poisoning (2-6 ppm) and 9 (1.2%) geese had lead levels indicative of clinical poisoning (> 6 ppm). A greater proportion of juveniles (14.3%) had elevated lead levels than did adults (6.0%), but there was no difference between genders. Lead levels were highest in autumn and winter in southern Illinois, but were low during nesting and summer, despite legal use of lead shot in northern Ontario during our study. Lead poisoning (> or = 5% of the population) was still evident during all seasons in juveniles, and during autumn and winter in adults, 5 to 10 yr after toxic shot was banned from areas where we collected geese during migration and winter. Elevated lead levels did not affect total body mass, lipid reserves, or mineral levels of geese we collected. Protein levels also were unaffected below 10 ppm, but there was evidence of decline at higher concentrations. Thus, it seems unlikely that lead exposure currently affects survival or reproduction of Mississippi Valley Population (MVP) geese via body condition, although other sublethal effects cannot be discounted.     

Lead poisoning.

Lead poisoning is the most common disease of environmental origin in the United States today. Adult lead poisoning results primarily from exposure by inhalation in the workplace. Pediatric lead poisoning results principally from the ingestion of lead from environmental media, including paint chips, dust, soil, drinking water, ceramics, and medications. Lead is toxic to many organ systems, among them developing erythrocytes, the kidneys, and the nervous system. Lead-induced toxicity to the central nervous system causes delayed development, diminished intelligence, and altered behavior. In young children, this effect has been demonstrated convincingly to occur at blood lead levels between 10 and 20 micrograms per dl. The Centers for Disease Control and Prevention has recommended that a blood lead level of 10 micrograms per dl or higher be considered evidence of increased lead absorption, and the National Academy of Sciences has concurred in that recommendation. Unresolved issues in need of further study include the frequency of screening young children for lead, the question of whether women should be offered screening for lead before conceiving a pregnancy, the role of x-ray fluorescence analysis in assessing lead in bone, and the appropriate legislative response of the United States government to lead-based paint abatement.     

Lead poisoning and heavy metal exposure of golden eagles ( Aquila chrysaetos ) from the European Alps

Lead poisoning and organ levels of the non-essential heavy metals lead, cadmium and mercury of seven free-ranging golden eagles (Aquila chrysaetos) from the European Alps, and of one 23-year-old captive golden eagle are reported. All birds were found dead or moribund during the years 2000 and 2001 in Austria, Germany and Switzerland. One golden eagle from Switzerland with extraordinarily high lead residues in its liver and kidney was clearly identified as lethally lead poisoned. Another bird from the same region was found still alive and died in a wildlife rehabilitation center, showing lead residues in its organs known for acute lead poisoning with detrimental physiological effects, such as nervous disorders and the inhibition of the hemoglobine synthesis. Concentrations of cadmium, mercury and lead residues in the organs of the other five free-ranging birds, and in the long-lived captive golden eagle, were low and represent the natural background levels in birds of prey of the terrestrial food web. This is the first published report of lead poisoning in golden eagles from Switzerland. Sources for lead poisoning in golden eagles in the Alpine region are discussed.     

Epidemiologic investigation of lead poisoning in trumpeter and tundra swans in Washington State, USA, 2000-2002

An observational study was conducted to determine the proportionate mortality of wild trumpeter (Cygnus buccinator) and tundra (Cygnus columbianus columbianus) swans that died during the winters of 2000-02 in northwestern Washington State, USA. Among 400 swans necropsied, 81% were lead poisoned (302/365 trumpeter swans; 20/35 tundra swans). Mortality started in mid-November and peaked from late December through mid-February; swan mortality that was not associated with lead poisoning was uniformly lower throughout the winter months. Lead poisoning was 24 times more likely to be the cause of death in swans found in Whatcom County compared to swans found in other locations in northwestern Washington State (95% CI: 12.7, 47.0). Mortality attributable to lead poisoning was twice as likely in adults as in juveniles (95% CI: 1.0, 4.2). Aspergillosis was documented in 62 trumpeter and two tundra swans, including 37 swans in which mortality was caused by lead poisoning. Males were twice as likely as females to have aspergillosis (95% CI: 1.1, 3.8). Traumatic injuries were documented in 37 trumpeter and seven tundra swans, including seven trumpeter swans with concurrent lead poisoning. Dead swans found outside Whatcom County were four times more likely to have traumatic injuries compared to those found in Whatcom County (95% CI: 1.6, 10.0). Overall, lead-poisoned swans were significantly less likely to have concurrent aspergillosis or traumatic injuries. There was no apparent association between grit ingestion (total mass or mass categorized by size) and lead poisoning or number of lead shot. Not surprisingly, lead-poisoned swans were more likely to have one or more lead shot compared to swans that died from other causes (OR 294; 95% CI: 92, 1,005); lead-poisoned swans were also more likely to have one or more nontoxic shot compared to swans that were not poisoned (OR 63; 95% CI: 19, 318). The source(s) of shot are unknown but likely are in or near Whatcom County, Washington.     

Gasoline sniffing and lead encephalopathy.

Gasoline sniffing is endemic in northern Manitoba and perhaps throughout much of northern Canada. Its most serious complication is lead encephalopathy, which can be fatal. Most of the toxic effects are thought to be due to tetraethyl lead and its metabolites. The specific treatment is chelation therapy, for which a protocol has been developed at the Health Sciences Centre, Winnipeg. Lead encephalopathy, however, is a manifestation of social, cultural and psychologic malaise.     

Influences of thiamin on lead intoxication,lead deposition in tissues and lead hematological responses of Tilapia zillii

1. Lead levels in the blood, kidney, liver, brain and muscle of fish receiving only lead were elevated markedly over the values of both controls and thiamin-treated fish.2. No statistical difference was observed between the lead levels in bone samples of both fish receiving only lead and thiamin-treated fish.3. In contrast to the fish receiving only lead the fish treated with thiamin appeared to be healthy and had no lead poisoning signs.4. Over the period of study, hemoglobin content and red blood cell counts of fish receiving only lead showed significant decreases from the values of both controls and fish treated with thiamin.5. Hematocrit values and white blood cell counts were uninfluenced by either lead exposure or thiamin treatment at all intervals.6. The data suggest that thiamin can serve as a promising natural chelator to prevent fish mortality, not only in short term, but also in prolonged exposure.     

Global approach to reducing lead exposure and poisoning

Lead poisoning is an important environmental disease that can have life-long adverse health effects. Most susceptible are children, and most commonly exposed are those who are poor and live in developing countries. Studies of children's blood-lead levels (BLLs) are showing cognitive impairment at increasingly lower BLLs. Lead is dangerous at all levels in children. The sources of lead exposure vary among and within countries depending on past and current uses. Sources of lead may be from historic contamination, recycling old lead products, or from manufacturing new products. In all countries that have banned leaded gasoline, average population BLLs have declined rapidly. In many developing countries where leaded gasoline is no longer used, many children and workers are exposed to fugitive emissions and mining wastes. Unexpected lead threats, such as improper disposal of electronics and children's toys contaminated with lead, continue to emerge. The only medical treatment available is chelation, which can save lives of persons with very high BLLs. However, chelating drugs are not always available in developing countries and have limited value in reducing the sequelae of chronic low dose lead exposure. Therefore, the best approach is to prevent exposure to lead. Because a key strategy for preventing lead poisoning is to identify and control or eliminate lead sources, this article highlights several major sources of lead poisoning worldwide. In addition, we recommend three primary prevention strategies for lead poisoning: identify sources, eliminate or control sources, and monitor environmental exposures and hazards.     

Lead Poisoning in Rural Scotland

Nine people from four families living in rural parts of Scotland have been found to suffer from clinical or biochemical effects of lead poisoning. Five had symptoms and four had unequivocal evidence of excessive lead exposure. The source of lead has been traced to the domestic water supply which in all cases was grossly contaminated with lead acquired from lead plumbing systems, including lead storage tanks. Clinical improvement followed the replacement of lead piping in two families studied. Lead poisoning is a possible cause of chronic ill health in areas of plumbosolvent water.     

Influences of thiamin on lead intoxication, lead deposition in tissues and lead hematological responses of Tilapia zillii.

1. Lead levels in the blood, kidney, liver, brain and muscle of fish receiving only lead were elevated markedly over the values of both controls and thiamin-treated fish. 2. No statistical difference was observed between the lead levels in bone samples of both fish receiving only lead and thiamin-treated fish. 3. In contrast to the fish receiving only lead the fish treated with thiamin appeared to be healthy and had no lead poisoning signs. 4. Over the period of study, hemoglobin content and red blood cell counts of fish receiving only lead showed significant decreases from the values of both controls and fish treated with thiamin. 5. Hematocrit values and white blood cell counts were uninfluenced by either lead exposure or thiamin treatment at all intervals. 6. The data suggest that thiamin can serve as a promising natural chelator to prevent fish mortality, not only in short term, but also in prolonged exposure.     

Ameloblastic odontoma in a cynomolgus monkey (Macaca fascicularis)

An ameloblastic odontoma occurred in an adult cynomolgus monkey (Macaca fascicularis). The neoplasm involved the upper left maxilla as a disfiguring, fleshy growth. The tissue and cellular changes were consistent with an ameloblastic odontoma which is rare in man, nonhuman primates (NHP), and other vertebrate animals. The monkey was one of 50 adult, single-caged housed cynomolgus monkeys. No additional clinical signs of disease were present. Hematology and serum chemistries were within normal limits. There have been three reports in the literature of ameloblastic odontomas in NHP; however, this is the first reported case of an ameloblastic odontoma in a cynomolgus monkey.