Effects of postirradiation temperature on the yields of radiation-induced single- and double-strand breakage in SV40 DNA

This report describes a case of lead poisoning occurring in an electrician as the result of an unusual personal habit, namely, the chewing of lead-containing coatings of electric wires. A coating chewing test showed that a few minutes after beginning chewing, saliva lead concentration increased from 10 micrograms/l to several milligrams per liter. This case is an example of poisoning caused by an occupationally related source (coatings containing lead) as a consequence of a singular and unconventional worker's habit.     

Lead poisoning from an unexpected source in a 4-month-old infant

Childhood lead poisoning is characteristically a disease that occurs between the second and third years of life, generally resulting from the child's ingestion of lead-based paint or dust. However, lead poisoning may also appear in the first year of life. The case of a 4-month-old infant is reported in which the preparation of infant formula in a lead-soldered samovar (urn) resulted in venous blood lead levels as high as 46 microg/dl. The samovar had been brought into the United States by the parents while on a visit to Iran. The infant was placed on chelation therapy with parenteral CaNa2EDTA followed by oral meso-2,3-dimercaptosuccinic acid (DMSA) and d-penicillamine. This resulted in a rapid and substantial reduction in the blood lead level. Lead poisoning in infancy may have unusual etiologies such as in utero transmission of lead by lead-poisoned women. Because sources of lead poisoning in infancy may be unusual, a detailed environmental investigation may be necessary to identify the exact source. Children exposed to lead in the first 2 years of life have a special vulnerability to the neurotoxicity of lead, with the risk of enduring developmental handicaps. Continued public health initiatives to remove lead from the environment, in conjunction with routine lead screening of young children, will be key in meeting the goal of the Centers for Disease Control and Prevention to eliminate childhood lead poisoning by the year 2011.     

Lead poisoning in a dog

A case of lead poisoning caused by ingestion of a lead roof-washer is described in a one-year-old, spayed Fox Terrier bitch, presented with nervous signs, and basophilic stippling of red blood cells. Blood concentrations of lead were in the low toxic range. Radiography of the abdomen revealed radio-dense objects in the stomach, which on gastrotomy included a lead roof-washer. Prior to removal of the foreign bodies, the dog showed remarkable improvement on non-specific symptomatic treatment alone, and recovered well after surgery, only to die unexpectedly several hours later. Concentrations of lead in the liver and kidneys were extremely high, and histology revealed typical intracellular inclusions and organ degeneration. In the light of these findings, it is suggested that all cases of suspected or confirmed lead poisoning be given specific chelation therapy.     

Methylmercury poisoning, Clinical follow-up and sensory nerve conduction studies

Methylmercury poisoning occurred in four cases after passage of methylmercury through the food chain. The neurological damage in all four cases was severe. The damage was greater at younger ages with maximum involvement in the case of transplacental poisoning. Significant recovery occurred in two cases, but on six-year follow-up two cases remained severely impaired. Clinical and electrophysiological evidence suggests that damage to peripheral sensory nerves may not be the cause of the late sensory symptomatology.     

Jaw and leg claudication in a patient with temporal arteritis, chronic sialoadenitis and previous hepatitis C virus infection

OBJECTIVES: Poisoning by organophosphate insecticides causes cholinergic toxicity. Organophosphate induced delayed polyneuropathy (OPIDP) is a sensory-motor distal axonopathy which usually occurs after ingestion of large doses of certain organophosphate insecticides and has so far only been reported in patients with preceding cholinergic toxicity. Surprisingly, it was recently reported by other authors that an exclusively sensory neuropathy developed in eight patients after repeated unquantified exposures to chlorpyrifos, which did not cause clear-cut cholinergic toxicity. The objective was to assess whether an exclusively sensory neuropathy develops in patients severely poisoned by various OPs. METHODS: Toxicological studies and electrophysiological measurements were performed in peripheral motor and sensory nerves in 11 patients after acute organophosphate poisoning among which two subjects were poisoned with chlorpyrifos. RESULTS: Three patients developed OPIDP, including one poisoned by chlorpyrifos. Exclusively sensory neuropathy was never seen after either single or repeated acute organophosphate poisoning. A mild sensory component was associated with a severe motor component in two of the three cases of OPIDP, the other was an exclusively motor polyneuropathy. CONCLUSION: A sensory-motor polyneuropathy caused by organophosphate insecticides might occur after a severe poisoning and the sensory component, if present, is milder than the motor one. Bearing in mind the toxicological characteristics of these organophosphate insecticides, other causes should be sought for sensory peripheral neuropathies in patients who did not display severe cholinergic toxicity a few weeks before the onset of symptoms and signs.     

Pulmonary tuberculosis: diagnostic delay in Ghanaian adults

Pica (pica = magpie) is an eating disorder that is manifested by a craving for oral ingestion of a given substance that is unusual in kind (nonfood items) or quantity (food items). Pica has been described as a world wide phenomenon, but there are more frequent occurrences of selected substances among selected groups--especially young children and black pregnant and nonpregnant women in the southern part of the USA. In Central Europe and Germany this syndrome has not been described in the moderne literature. For this reason, we report a case of pica for starch associated with severe iron deficiency anemia in Germany. Iron deficiency anemia and--less often-potassium and zinc deficiency are the main complications of an excessive starch or clay ingestion, followed by gastrointestinal obstructions due to gastroliths or impaction. Additionally, naphtalene poisoning (in pica for toilet air-freshener blocks), phosphorus poisoning (in matches pica), mercury poisoning (in paper pica), and lead poisoning (in dried paint pica) have been described.     

Are pediatricians ready for the new guidelines on lead poisoning?

In 1991 the Centers for Disease Control established new guidelines for the definition of and screening for lead poisoning. OBJECTIVE. To assess: (1) pediatricians' knowledge of lead poisoning including the most recent literature on the subject, and (2) their screening practices. DESIGN, SETTING, SUBJECTS. A 22-item questionnaire was developed and validated. The survey was mailed to 1183 physicians in Virginia who were self-designated as pediatricians in the state medical registry. RESULTS. Sixty-nine percent (391/556) of those responding They were evenly distributed throughout the state. Of the respondents, 62% were male, 86% were white, and 72% trained at a university program. The median year for training completion was 1978. Demographic differences were not demonstrated (chi 2) between primary care pediatricians and subspecialists. Responses demonstrated an overall deficiency in physicians' knowledge of lead poisoning with specific deficiencies in knowledge of the literature, with mean +/- SD correct responses of 15.7 +/- 3.4. Primary care pediatricians scored significantly better than subspecialists: 16.2 +/- 3.0 vs 14.7 +/- 4.1 (P < .001, t-test). Twelve percent of the total group and 13.5% of primary care physicians were screening all their patients. CONCLUSIONS. Although primary care pediatricians (self-designated) are more knowledgeable about lead poisoning than their subspecialist colleagues, there are still deficiencies, and screening practices must be modified in both groups. To successfully implement the new Centers for Disease Control and Prevention guidelines, physician education must be a priority.     

Diagnostic and therapeutic management of ethylene glycol poisoning. Importance of crystalluria. Apropos of a case

During the course of a case of ethylene glycol poisoning with ensuing oliguric renal failure despite early dialysis, we show the importance of early diagnosis of this intoxication in underlined. Characteristics of ethylene glycol poisoning are: metabolic acidosis with anion gap (without lactic acidosis or keto-acidosis) and high plasma osmolarity. Awaiting the result of blood and urinary toxic values, crystalluria, by typical needle monohydrate calcium oxalate crystals finding, evokes the diagnosis and permits to start a specific treatment. This treatment is based on: principles of intensive care, ethanol administration (or 4-methyl-pyrazole now available), also thiamine and pyridoxine administration and finally, dialysis therapy. We can hope, with early and intensive management of this poisoning, to prevent the renal failure, principal complication of ethylene glycol ingestion, which can lead to chronic renal failure. Therefore, crystalluria, an easy and specific diagnosis technic, is of great interest.     

Lysosomal enzyme activity in the serum of rats with experimental lead poisoning

Examination of the effect of experimental lead poisoning on permeability of lysosomal membranes in albino rats demonstrated activation of lysosomal enzymes (alpha-manosidase and beta-acetylglucosaminidase) in the blood serum as soon as the third day after daily administration of lead acetate (20 mg/kg). Apparently damage of the lysosomal membrane played an important role in the pathogenesis of lead poisoning.     

Current problems of lead poisoning]

In collaboration with private associations and public services, we screened a targeted population for serum lead levels and observed lead poisoning (serum Pb > 100 micrograms/l) in 6 out 44 children living in precarious conditions in Poitiers, France. This observation underscores some of the major problems encountered in the battle against lead poisoning in western countries. First, the social, economical or legal situation of the population at risk often results in exclusion from the normal health care network. If after a coordinated effort based on mutual trust, children exposed to lead poisoning can be identified, the second problem is to identify the source of intoxication. Scaling paint in the current housing may be incriminated, but how can the true source be identified when the populations concerned change residence often and may be unwilling to disclose their previous residence due to fear of reprisals for themselves or the new occupants? And if the source is identified, the cost of rehabilitation or the illegal situation of the family may raise further problems requiring adapted solutions. The prevention of lead poisoning calls for a targeted screening program, combined efforts of public authorities and health care workers, and close cooperation with private associations. All intoxicated children should be removed from the source of exposure and their families protected from the risk of sanctions. Only an active and practical public health policy can provide the solution to this continuing public health problem.     

Neuromaturation and behavior development: The case of childhood lead poisoning.

Presents a rationale for the study of the role of neuromaturation in cognitive and behavioral development. Early childhood lead poisoning is discussed in terms of physiological mechanisms and known cognitive sequelae. 18 children, 4–6 yrs old, with past histories of lead poisoning, were compared to matched controls on a 6-factor cognitive and neuromotor battery that included the WPPSI and the PPVT. A developmental hypothesis that specific cognitive sequelae of lead poisoning would depend on and vary with the age of the child at the time of lead ingestion was tested. Previous findings in the literature on asymptomatic childhood lead poisoning, which cited either language-linguistic or visuospatial skill decrements in nonoverlapping populations, were elucidated. When the performances of Ss who had suffered early (before 24 mo), middle (24–36 mo), and late (after 36 mo) exposure were compared on language-linguistic and spatial factors in this sample, significant differences were suggested. Ss who experienced increased lead consumption showed reductions in 3 motor and visual-motor skills. This finding illustrates the differential effects of interruptions in maturational processes on cognitive behavior as a function of age. Although the interaction of maturational and environmental events is acknowledged, the results imply that more attention to the structure-function relationship is needed in the study of behavior development and in the development of measures of cognitive functioning. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Severe lead poisoning caused by an ingested fishing weight

Authors describe the case-history of a 17 year old male who accidentally ingested a fishing weight that was retained in the stomach and caused a serious lead poisoning. It is worth mentioning that beside the wellknown symptoms and signs of lead intoxication also the liver was seriously affected. The histologically verified toxic lesion of the liver presumably can be attributed to the large quantities of lead absorbed within a short period. This also explains the appearance of symptoms and signs indicating to encephalopathy beside the young age of the patient. The foreign body could not be removed by means of gastroscopy, therefore a gastrotomy was carried out followed by chelating treatment with i.v. CaNa2EDTA that resulted in complete clinical and laboratory recovery. The case history draws the attention to the importance of the quick removal of the retained lead containing objects out of the gastrointestinal tract.     

The peak latency of orbital presaccadic spike potential with horizontal eye movements

A case of Macrozamia riedlei seed poisoning is described in a young Dachshund. Vomiting and depression commenced within 6 h of ingestion; other signs that developed included severe hepatopathy, jaundice, abdominal pain that was unresponsive to analgesics, severe gastro-intestinal haemorrhage and thrombocytopenia as well as crystalluria and marrow dyserythropoiesis. The dog was euthanased 6 days after ingestion of the seeds.     

Childhood lead poisoning: the promise and abandonment of primary prevention

In 1991, the Public Health Service published the Strategic Plan for the Elimination of Childhood Lead Poisoning. This document marked a fundamental shift in federal policy from finding and treating lead-poisoned children to authentic primary prevention. It spelled out a 15-year strategy to achieve this goal and provided a cost-benefit analysis showing that the monetized benefits far exceeded the costs of abatement. A strong national effort to eliminate the disease developed. Now, 7 years after publication of the plan, primary prevention of lead exposure has been abandoned. This article examines the role of some prevailing attitudes and institutions in derailing the effort. Some institutions--the lead industry, real estate interests, and insurance interests--behaved as anticipated. Others, including private pediatricians, the American Academy of Pediatrics, some federal agencies, and a public interest group ostensibly dedicated to eliminating lead poisoning, also played an unexpected part in derailing the plan.     

The effect of pharmacologic prophylaxis with Panpal on acetylcholinesterase activity in the diaphragm and various parts of the brain in rats during treated and untreated Soman poisoning

BACKGROUND: The pharmacological prophylaxis protecting the organism against organophosphorus compounds could increase the effect of antidotal treatment of poisoning with organophosphates. METHODS AND RESULTS: The influence of the pharmacological prophylaxis with Panpal (pyridostigmine in combination with benaetyzine and trihexyphenidyle) on acetylcholinesterase activity in diaphragm and various parts of brain at 1 and 3 h following non-treated and treated (the oxime HI-6 in combination with atropine) soman poisoning was tested on male rats. While Panpal did not significantly influence the acetylcholinesterase activity in brain following non-treated as well as treated soman poisoning. Panpal increased so many-induced acetylcholinesterase inhibition following non-treated poisoning and decreased the reactivating effect of the oxime HI-6 following treated soman poisoning in diaphragm. CONCLUSIONS: Our data confirm the importance of the combination of reversible acetylcholinesterase inhibitor pyridostigmine with anticholinergic drugs in the pharmacological prophylaxis of soman poisoning because of the elimination of consequences of pyridostigmine-induced increasing in acetylcholinesterase inhibition in the peripheral compartment.     

Cost-effectiveness analysis of lead poisoning screening strategies following the 1997 guidelines of the Centers for Disease Control and Prevention

OBJECTIVE: To compare blood lead (BPb) poisoning screening strategies in light of the 1997 recommendations by the Centers for Disease Control and Prevention, Atlanta, Ga. DESIGN: Cost-effectiveness analysis from the perspective of the health care system to compare the following 4 screening strategies: (1) universal screening of venous BPb levels; (2) universal screening of capillary BPb levels; (3) targeted screening of venous BPb levels for those at risk; and (4) targeted screening of capillary BPb levels for those at risk. Costs of follow-up testing and treatment were included in the model. RESULTS: Only universal venous screening detected all BPb levels of at least 0.48 micromol/L (10 microg/dL). Universal capillary screening detected between 93.2% and 95.5% of cases, depending on the prevalence of elevated BPb levels. Targeted screening was the least sensitive strategy for detecting cases. Venous testing identified between 77.3% and 77.9% of cases, and capillary testing detected between 72.7% and 72.8% of cases. In high-prevalence populations, universal venous screening minimized the cost per case ($490). In low- and medium-prevalence populations, targeted screening using venous testing minimized the cost per case ($729 and $556, respectively). In all populations, regardless of screening strategy, venous testing resulted in a lower cost per case than capillary testing. Sensitivity analyses of all parameters in this model demonstrated that this conclusion is robust. CONCLUSIONS: Universal screening detects all cases of lead poisoning and is the most cost-effective strategy in high-prevalence populations. In populations with lower prevalence, the cost per case detected using targeted screening is less than that of universal screening. The benefit of detecting a greater number of cases using universal screening must be weighed against the extra cost of screening. Regardless of whether a strategy of universal or targeted screening is used, the cost per case using venous testing is less than that of capillary testing.     

Combined therapeutic potential of meso-2,3-dimercaptosuccinic acid and calcium disodium edetate on the mobilization and distribution of lead in experimental lead intoxication in rats

Asymptomatic lead poisoning remains a serious public health problem in developed and developing countries. Chelation therapy particularly with calcium disodium ethelenediamine tetracetic acid (CaNa2EDTA) is often used therapeutically to reduce the body burden of lead. This chelating drug has serious side effects and drawbacks primarily related to redistribution of lead, nephrotoxicity, and essential metal depletion. The present study was planned to determine the effectiveness of CaNa2EDTA and meso-2,3-dimercaptosuccinic acid (DMSA) used in combination. Both drugs, when administered individually, resulted in significant urinary excretion of lead and lowered the tissue lead burden. Combined treatment with CaNa2EDTA and DMSA elicits an additive response in promoting urinary lead elimination, depleting body lead burden, and restoring altered lead-sensitive biochemical variables. Further, no redistribution of lead to brain or any other soft organ following combined DMSA-CaNa2EDTA treatment was observed indicating a definite advantage of combined therapy over the conventional treatment with CaNa2EDTA or DMSA alone. However, an elevation of serum transaminase activity, creatinine level, and depletion of blood zinc level may limit the usefulness of this combined treatment.     

Hyperkalemia and acidosis in lead nephropathy

Defective potassium excretion with clinical acidosis, associated with fixed moderate sodium wasting, has been found to be a common abnormality in lead nephropathy. Lead poisoning has been shown by others to be associated with depression of the renin-aldosterone system and of sodium and potassium activated adenosinetriphosphatase (ATPase). Since these hormonal defects may contribute to the hyperkalemia and are reversible, lead poisoning should be treated aggressively. Management also requires proper regulation of dietary sodium, correction of acidosis, limitation of dietary potassium, and minimal use of antihypertensive agents, as well as the administration of allopurinal for urate control.     

A patient with parkinsonism presenting hyperintensity in the globus pallidus on T1-weighted MR images: the correlation with manganese poisoning

We report a 55-year-old woman who developed symptoms resembling parkinsonism. Her psychiatric symptoms in the early stage, cervical dystonia and tremor increasing on movement were consistent with manganese poisoning. Manganese levels were elevated to 1.5 micrograms/l in the serum (normal; 0.3-1.1 micrograms/l) and to 1.4 micrograms/l in the urine (normal; less than 1.2 micrograms/l). Intravenous infusion of calcium disodium editate (CaEDTA; chelating agent) was followed by the marked excretion of manganese (27.3 micrograms/l) in the urine. These findings support manganese poisoning. Manganese poisoning is a disease which results from chronic exposure to manganese, but the source of manganese exposure remained obscure in this patient. T1-weighted MRI of the brain showed symmetric high signal intensity in the globus pallidus without any abnormality on T2-weighted images. There is a report that manganese induced brain lesions in Macaca fascicularis as revealed by MRI and the fascicularis developed signs of unsteady gait and hypoactivity. The patient responded to treatment with CaEDTA and the second MRI demonstrated regression of abnormal signal intensity. This may be due to enhanced manganese excretion. To our knowledge, this is the first case of probable manganese-induced human parkinsonism whom changes in MRI were noted after treatment with CaEDTA.