Lead poisoning and other human-related factors cause significant mortality in white-tailed eagles.

The white-tailed eagle (Haliaeetus albicilla) suffered a severe population decline due to environmental pollutants in the Baltic Sea area ca. 50 years ago but has since been recovering. The main threats for the white-tailed eagle in Finland are now often related to human activities. We examined the human impact on the white-tailed eagle by determining mortality factors of 123 carcasses collected during 2000-2014. Routine necropsy with chemical analyses for lead and mercury were done on all carcasses. We found human-related factors accounting for 60% of the causes of death. The most important of these was lead poisoning (31% of all cases) followed by human-related accidents (e.g. electric power lines and traffic) (24%). The temporal and regional patterns of occurrence of lead poisonings suggested spent lead ammunition as the source. Lead shot was found in the gizzards of some lead-poisoned birds. Scavenging behaviour exposes the white-tailed eagle to lead from spent ammunition.

Vermeer: los colores tóxicos del plomo y del mercurio / Vermeer: the toxic colours of lead and mercury

¿Qué sucede con Vermeer?, se preguntan los historiadores y amantes del arte. El enigmático pintor permaneció en la oscuridad después de su muerte hasta el siglo XIX, en donde capturaría la imaginación y el gusto estético de los tiempos modernos. Aunque han llegado a nosotros sólo treinta y seis de sus obras, su originalidad y refinamiento le colocan entre los más grandes artistas holandeses del siglo XVII. La vida de Vermeer sólo puede recompuesta a través de actas notariales y su dramático final es conocido por boca de su viuda. Nosotros pretendemos aportar un nuevo punto de vista de las razones de su muerte a causa de una intoxicación por plomo y mercurio, y las repercusiones que esta causa tuvo en su pintura (AU)

What is it about Johannes Vermeer? contemporary art lovers and historians ask. The enigmatic painter lapsed into obscurity after his death only to surface again in the 19th century and capture the imagination and esthetic taste of modern times. Even though he produced no more than 40 paintings, their originality and refinement place him among the greatest 17th-century Dutch artists. Vermeer's life story can only be patched together from public records, and the dramatic end of Vermeer`s life was told by his widow after his death.We contribute our point of view of the reason of his death because of a poisoning for lead and mercury and the repercussions that it had in his painting (AU)

Mercury poisoning in a free-living northern river otter (Lontra canadensis).

A moribund 5-year-old female northern river otter (Lontra canadensis) was found on the bank of a river known to be extensively contaminated with mercury. It exhibited severe ataxia and scleral injection, made no attempt to flee, and died shortly thereafter of drowning. Tissue mercury levels were among the highest ever reported for a free-living terrestrial mammal: kidney, 353 microg/g; liver, 221 microg/g; muscle, 121 microg/g; brain (three replicates from cerebellum), 142, 151, 151 microg/g (all dry weights); and fur, 183 ug/g (fresh weight). Histopathologic findings including severe, diffuse, chronic glomerulosclerosis and moderate interstitial fibrosis were the presumptive cause of clinical signs and death. This is one of a few reports to document the death of a free-living mammal from presumed mercury poisoning.

DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury.

Acute effects of mercuric chloride (HgCl2) were evaluated on mice. Mice received a single dose of HgCl2 (4.6 mg/kg, subcutaneously) for three consecutive days. Thirty minutes after the last injection with HgCl2, mice received one single injection of 2,3-dimercapto-1-propanesulfonic acid (DMPS) or N-acetylcysteine (NAC) or diphenyl diselenide (PhSe)2. DMPS, NAC and (PhSe)2 were utilized as therapy against mercury exposure. At 24 h after the last HgCl2 injection, blood, liver and kidney samples were collected. delta-Aminolevulinate dehydratase (delta-ALA-D) and Na+, K- (+) ATPase activities, thiobarbituric acid-reactive substances (TBARS), non-protein thiols (NPSH) and ascorbic acid concentrations were evaluated. Plasma aspartate (AST) and alanine (ALT) aminotransferase activities, as well as urea and creatinine levels were determined. The group of mice exposed to Hg + (PhSe)2 presented 100% of lethality. Exposure with HgCl2 caused a decrease on the body weight gain and treatments did not modify this parameter. delta-ALA-D, AST and ALT activities, TBARS, ascorbic acid levels and NPSH (hepatic and erythrocytic) levels were not changed after HgCl2 exposure. HgCl2 caused an increase in renal NPSH content and therapies did not modify these levels. Mice treated with (PhSe)2, Hg + NAC and Hg + DMPS presented a reduction in plasma NPSH levels. Creatinine and urea levels were increased in mice exposed to Hg + NAC, while Hg + DMPS group presented an increase only in urea level. Na+, K- (+) ATPase activity was inhibited in mice exposed to Hg + DMPS and Hg + NAC. In conclusion, therapies with (PhSe)2, DMPS and NAC following mercury exposure must be better studied because the formation of more toxic complexes with mercury, which can mainly damage renal tissue.

[Choice of safety criteria during accidents occurring at the dangerous industrial objects during work using cadmium and metallic mercury]. / O vybore kriteriev bezopasnosti pri vozniknovenii avarii na opasnykh proizvodstvennykh ob"ektakh v protsesse raboty s kadmiem i metallicheskoi rtut'iu.

Based on the systematization of the experimental and epidemiological data on the toxicity of the compounds of mercury and cadmium and on the concept of a reasonable risk, the author has developed qualitative indices (criteria) required to analyze the safety of work associated with metallic mercury and cadmium at the dangerous industrial objects while declaring their safety. The fulfillment of these criteria ensures the high level of safety of mercury- and cadmium-associated work; it is in accord with the current trends in approaches to evaluating the safety of devices using toxically dangerous substances. The criteria considers the risk of human death due to the simultaneous intake of mercury vapors and cadmium oxide aerosols during accidents, as well as the level of chronic intake of these substances in different groups of persons on secondary dust formation (evaporation) after an accident.

Occupational exposure to mercury in dentistry and dentist mortality.

In response to public concern, Health Canada recently conducted a review of amalgam safety and released a position statement entitled The Safety of Dental Amalgam. Essentially, the department has concluded that the levels of mercury absorbed by the body due to the release of mercury vapor from amalgam restorations, while detectable, do not approach those recognized to cause illness. It has therefore confirmed that amalgam restorations can be used safely in most patients, with some notable caveats. Despite Health Canada's position statement in support of amalgam, patient doubts about amalgam safety remain, including the tenuous hypothesized link between amalgam restorations and specific diseases. This article reviews the available studies of dentist mortality to identify possible links between mercury exposure and negative health effects. A lack of evidence to suggest a detrimental health outcome in dentists who are occupationally exposed to higher levels of mercury than their patients, and are known to have higher levels of mercury in their blood, provides an important reassurance concerning the safety of amalgam. The reviewed data indicates that the 10 leading causes of death in the United States and Canada are the same for both dentist and non dentist population groups, and that the percentage of deaths by the same cause are remarkably similar. By 1975, the year of the most recent U.S. study, the average age at death for white male dentists was about three years higher than for all adult white males. Although suicide standard mortality rates are known to be higher for dentists, suicide deaths have also been shown to be a factor in many other occupations, particularly those where there is easy access to drugs. Although updated actuarial data for dentist mortality are needed, the available data indicate no reduction in the life expectancy of practising dentists, nor any specific or disproportionate rates of disease associated with high mercury exposure. In fact, the available mortality studies are generally optimistic about the health of dentists, which should reassure patients about the safety of dental amalgam.

Influence of dietary protein levels on the acute toxicity of methylmercury in mice.

The influence of dietary protein levels on the acute toxicity of methylmercury (MeHg) was investigated using C57BL/6N male mice fed either a 24.8% protein diet (normal protein diet, NPD) or a 7.5% protein diet (low protein diet, LPD). When MeHg was administered to each group of mice, all mice died at a medium or high dose (80 or 120 mumol/kg, respectively) within 16 or 7 days, respectively, but not at a low dose (40 mumol/kg) in both dietary groups. Although no difference was observed in the survival rate at a medium dose, NPD-fed mice died earlier despite lower brain Hg than LPD-fed mice at a high dose. Accordingly, death, in our observations, could not be due to neural damage by MeHg. When a high dose of MeHg was administered to mice, plasma aspartate aminotransferase and alanine aminotransferase activities increased in NPD-fed mice but not in LPD-fed mice in spite of similar hepatic Hg levels. Therefore, the higher susceptibility of the liver could be reason for the shorter survival period in NPD-fed mice. Since plasma creatinine increased within 24 h after MeHg administration at a medium or high dose, renal dysfunction could be a major factor in death. The present results suggest that susceptibility to acute MeHg toxicity was higher in NPD-fed mice than in LPD-fed mice, possibly due to the difference in hepatic susceptibility.

Intoxicación crónica por mercurio: reacción de las mucosas orales / Chronic mercury poisoning: oral mucosal reaction

Los efectos crónicos y acumulativos de pequeñas dosis constantes de mercurio, pueden hacer episodios de agudización del cuadro clínico de intoxicación, ofreciendo riesgos de importancia en la morbimortalidad de una comunidad. Los desapercibidos clínicamente, tatuajes de las mucosas orales, son estudiados desde el punto de vista anatomopatológico.

The cronic and acumulatives effects of small dosis of mercury can produce moments of agudization of its toxicity and risks of importance en relation with human morbi-mortality. The so called amalgan tatoes of the oral mucosa are studied from the amatomopathological point of view.

A cohort study of workers compensated for mercury intoxication following employment in the fur hat industry.

This article presents the preliminary results of a follow-up study (1950-1992) of 1,146 subjects (person-years = 30,954; 23,055 for women) receiving compensation for mercury poisoning. In a province of Tuscany in central Italy, severe exposure to mercury occurred during fur hat production. A deficit in all causes of mortality was observed in both sexes, whereas mortality due to cancer was slightly higher than expected. Mortality from stomach cancer was significantly elevated for men and women. A significant excess of lung cancer was observed in women only. Whereas the excess of stomach cancer probably reflects elevated rates in the study area rather than exposure to mercury, the excess of lung cancer mortality does appear to be related to mercury exposure. Smoking habits or other exposures at work do not seem to explain the excess of lung cancer.

Respiratory failure and death following acute inhalation of mercury vapor. A clinical and histologic perspective.

A family of four was exposed to toxic levels of mercury vapor while attempting to extract silver from mercury amalgam. All four suffered respiratory failure and subsequent death despite chelation therapy with dimercaprol. Histologic findings at autopsy were similar in all four cases demonstrating a progression of acute lung injury that appeared related to postexposure day survival. There were no clinical signs of extrapulmonary manifestations despite toxic serum mercury levels. Although serum mercury levels decreased in response to the mercury chelating agent dimercaprol, serum levels remained in the toxic range and no clinical response was observed. Acute inhalational exposure to high concentrations of mercury vapor causes pneumonitis that can lead to respiratory failure and death. This continues to be a health hazard in both the workplace and the home environment.

Mortality and survival for Minamata disease.

Analysis of mortality of 439 deaths that occurred among 1483 patients with Minamata disease (MD) in Kumamoto Prefecture, Japan was performed from the end of 1981. Causes of death and survival rates were studied by means of the standardized mortality ratio (SMR) and life-table technique. Of the 439 deaths (29.6%) in MD cases, the first death occurred in 1954. There was a first peak incidence in 1956 when MD was initially reported, however, the majority of deaths occurred after 1972 when a second and much larger peak was evident. In 1970 an important milestone occurred when the Public Nuisance Relief Law (an anti-pollution law) was enacted. Among its provisions, this law required and enabled verification of MD among people suspected of having been exposed. In contrast to the early cases, later cases of MD were older and their mean age-at-death was not different from that of the general population. The mortality rate for all causes of death was significantly higher in both sexes compared to the general population. Significantly lower survival rates were noted for older patients. The cause-specific mortality rates also showed significantly increased SMRs for liver diseases and nephritis-nephrosis-nephrotic syndrome in male patients, and for nephritis-nephrosis-nephrotic syndrome and other diseases in females. On the other hand, the SMR for senility without mention of psychosis was significantly lower than expected in both sexes.

Causes of death in Minamata disease: analysis of death certificates.

The causes of death in Minamata disease were analyzed and compared with those of control subjects. Of the 1422 Minamata disease patients in the Kumamoto Prefecture, 378 had died by the end of 1980. Of these 378, the first death occurred in 1954 with a peak incidence in 1956 when Minamata disease was officially reported for the first time. The number of deaths increased rapidly after 1972 with a second peak in 1976. The male:female ratio was 1.8:1 and the mean age-at-death was 67.2 years (SD = +/- 18.65). The mean age-at-death was younger in the cases of the initial outbreak than in those recently. There were, on the average, 2.8 causes of death per person. Of these cases, 157 (41.5%) had Minamata disease indicated on the death certificate, though 64 (16.9%) had Minamata disease coded as the underlying cause. Minamata disease and the noninflammatory diseases of the central nervous system (CNS) were the main underlying causes of death between 1954 and 1969, while, in the multiple cause data, pneumonia and non-ischemic heart disease were the most prevalent. Cerebrovascular diseases (18.0%) were the main underlying causes of death followed by malignant neoplasms (14.7%), cardiovascular diseases (14.1%) and Minamata disease (14.1%) in 1970 or later, while cardiovascular diseases (18.6%), Minamata disease (14.5%), cerebrovascular diseases (10.4%) and malignant neoplasms (7.1%) were the major multiple causes of death. As compared with the control, the proportions of deaths due to noninflammatory diseases of CNS and pneumonia were higher in the initial outbreak. Although the difference in the causes of death was less apparent recently, malignant neoplasms and hypertensive diseases tended to be lower. These results suggest that there is a need for a long-term follow-up of Minamata disease patients. The data also show the potential value of multiple causes of death coding in analyses of mortality.