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PubMed1991

A case of lead poisoning recovered by transposition of the work post.

A case of lead poisoning in a secondary lead refinery was reported. A 58 year old man working at the post of lead refining complained of severe lassitude and diarrhea. By increased urine coproporphyrin excretion, he was suspected of a case of lead poisoning. Clinical data from the health examinations revealed that he had been affected by lead. The patient was transposed to another work post where lead was not handled and rapidly recovered from the poisoning.

Follow-Up Studies↗
PubMed1994

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.

Centers for Disease Control and Prevention, U.S.↗
PubMed1983

Childhood lead poisoning. A controlled trial of the effect of dust-control measures on blood lead levels.

Lead-contaminated house dust is one factor in childhood lead poisoning; however, most lead-reduction programs do not emphasize the control of house dust. We studied whether lead-reduction plus dust-control measures would lower blood lead levels in children with Class II or III poisoning (blood lead levels, 30 to 49 micrograms per deciliter) more effectively than lead reduction alone. An experimental group of 14 children and a control group of 35 children whose homes had already been treated were studied. In experimental homes, sites with elevated lead levels (greater than 100 micrograms per 930 cm2) were wet-mopped twice monthly and families were encouraged to clean and to wash the child's hands frequently. After one year blood lead levels fell an average of 6.9 micrograms per deciliter in the experimental group, as compared with 0.7 micrograms per deciliter in controls (P less than 0.001). Children in the experimental group with the highest blood lead levels had the most marked reduction. Four children in the control group (and none in the experimental group) required chelation therapy for blood levels greater than 50 micrograms per deciliter. These results show that a focused dust-control program can reduce blood lead levels more than standard lead removal in the home.

Child↗
PubMed2005

Unraveling the mystery of why there was no childhood lead poisoning.

Despite widespread use of leaded paints, classic life-threatening lead poisoning in small children began to be diagnosed as such only in the 1914-30 period. The diagnosis became suddenly more common in the 1950s and 1960s, but only in some areas of the United States. Experts focused on interior leaded paints as the source of the poison. Archival study of cases from Cincinnati and material from Denver, along with reevaluation of the medical literature, suggests that the problem should be reframed in terms of localized accident, not an epidemic. Very likely clinicians' reports accurately reflected social and material reality. Housing patterns hitherto not fully explored or understood explain why diagnoses were or were not reported. Moreover, evidence suggests the hypothesis that exterior (not interior) paint applied to middle-class houses (not mansions) may account for most cases not traced to repainted furniture and windowsills.

Child↗
PubMed2004

Correlation between clinical indicators of lead poisoning and oxidative stress parameters in controls and lead-exposed workers.

The present study was undertaken to investigate the involvement of oxidative damage in lead-induced toxicity in humans and to enlighten whether oxidative stress indicators are correlated with the known indices of lead toxicity. For these purposes, selected oxidative stress parameters along with some clinical indices of lead poisoning were determined in blood of battery plant workers and control subjects. Workers had significantly increased erythrocyte malondialdehyde (MDA) levels, catalase and glucose-6-phosphate dehydrogenase (G6PD) activities, and decreased blood glutathione:glutathione disulfide ratio compared to the controls. Increased blood lead concentrations and zinc protoporphyrin (ZPP) levels, and decreased delta-aminolevulinic acid dehydratase (ALAD) activity were used as clinical indices of lead toxicity. Statistically significant correlation between oxidative stress parameters and clinical indices implies that disrupted prooxidant/antioxidant balance might contribute to lead-induced toxicity in erythrocytes. A significant correlation was found between ALAD activity and blood lead levels in human subjects. Similarly significant correlation between ALAD activity and erythrocyte MDA concentrations was shown. Present data indicates that ALAD can serve as a valuable biomarker of oxidative stress in lead-exposed hematological system as well as being a biochemical indicator of lead exposure.

Adult↗
PubMed2001

[Occupational lead poisoning due to deficient protective measures at the work place].

UNLABELLED: Occupational lead poisoning due to deficient protective measures at the work place. HISTORY AND ADMISSION FINDINGS: A 27-year-old man who was working in the mixing plant of a company manufacturing synthetic materials, was admitted with colicky upper abdominal pain, loss of appetite and postprandial nausea for 3 weeks. On examination he had pain without guarding over the abdomen. INVESTIGATIONS: He had a normochronic anaemia (haemoglobin 12.5. g/dl). Ultrasound of the abdomen revealed splenomegaly. Gastroscopy excluded an ulcer. Deep duodenal biopsy showed Giardia intestinalis histologically. DIAGNOSIS, TREATMENT AND COURSE: As part of the differential diagnosis of abdominal colic and anaemia, lead poisoning was found, with the lead level markedly elevated to 1776 microgram/l. Penicillamine treatment rapidly reduced the blood lead level, but it had not yet become normal after 4 months. Exposure to lead at his work place was discovered. Subsequent tests there by the federal agency for occupational protection revealed massive deficiencies in protective measures. CONCLUSION: In present conditions abdominal colic must be viewed as a cardinal symptom of lead poisoning. Blood levels must be obtained as part of the differential diagnosis of abdominal pain of uncertain aetiology. If the diagnosis has been established and an occupational risk is possible, the appropriate occupational organizations and, if necessary, federal agency must be informed in order to exclude occupational exposure to lead. In Germany there still exist marked deficiencies in the protection of workers occupationally exposed to lead. Notification is essential to protect others similarly at risk.

Adult↗
PubMed2002

[Lead poisoning--an overview].

MATERIAL AND METHODS: We present a review of the history, pathophysiology, diagnosis and treatment of lead poisoning based on relevant literature. RESULTS AND INTERPRETATION: The human body does not metabolize lead, and lead accumulation may cause organ failure. Lead poisoning may cause serious health defects, including anaemia, central nervous system problems and various organ defects. Sources of lead may be found in the home as well as in the workplace or elsewhere in our environment, but lead poisoning is an infrequent condition. Prevention is important, but manifest lead poisoning can be treated effectively.

Acute Disease↗
PubMed2005

[Occupational lead poisoning 1892-1936].

The first Norwegian factory inspection act was passed in 1892. Until 1931, little attention was paid to occupational lead poisoning. In 1915 the physician Olai Lorange (1876-1965) was appointed chief of the factory inspectorate. In 1916 he initiated a registration of lead poisoning in Norway. In 1920 he also called on Norwegian doctors to report diseases considered to be of occupational origin. The results were scanty. Attention was paid to occupational lead poisoning in a draft legislation put forward in 1923. However, the motion was not put to vote during the depression after the First World War and was not passed until 1936. Historically, lead exposure has in periods been forgotten as a cause of disease, only to reappear. In Norway, occupational lead poisoning attracted attention in 1931-33, when 46 cases were reported from a shipyard. The inspectorate laid down regulations and the government granted compensations and pensions to 40 of the workers. Based on worker protection acts and regulations, yearbooks from the factory inspectorate, and medical literature, the article describes attitudes towards occupational lead poisoning in the early years after the first Norwegian factory inspection act was implemented.

History, 19th Century↗
PubMed2004

Lead poisoning associated with ayurvedic medications--five states, 2000-2003.

Although approximately 95% of lead poisoning among U.S. adults results from occupational exposure, lead poisoning also can occur from use of traditional or folk remedies. Ayurveda is a traditional form of medicine practiced in India and other South Asian countries. Ayurvedic medications can contain herbs, minerals, metals, or animal products and are made in standardized and nonstandardized formulations. During 2000-2003, a total of 12 cases of lead poisoning among adults in five states associated with ayurvedic medications or remedies were reported to CDC. This report summarizes these 12 cases. Culturally appropriate educational efforts are needed to inform persons in populations using traditional or folk medications of the potential health risks posed by these remedies.

Adult↗
PubMed2004

Cognitive deficits and magnetic resonance spectroscopy in adult monozygotic twins with lead poisoning.

Seventy-one-year-old identical twin brothers with chronic lead poisoning were identified from an occupational medicine clinic roster. Both were retired painters, but one brother (J.G.) primarily removed paint and had a history of higher chronic lead exposure. Patella and tibia bone lead concentrations measured by K-X-ray fluorescence in each brother were 5-10 times those of the general population and about 2.5 times higher in J.G. than in his brother (E.G.). Magnetic resonance spectroscopy (MRS) studies examined N-acetylaspartate:creatine ratios, a marker of neuronal density. Ratios were lower in J.G. than in his brother. Scores on neurocognitive tests that assess working memory/executive function were below expectation in both twins. Short-term memory function was dramatically worse in J.G. than in his brother. These results demonstrate some of the more subtle long-term neurologic effects of chronic lead poisoning in adults. In particular, they suggest the presence of frontal lobe dysfunction in both twins, but more dramatic hippocampal dysfunction in the brother with higher lead exposure. The MRS findings are consistent with the hypothesis that chronic lead exposure caused neuronal loss, which may contribute to the impairment in cognitive function. Although a causal relation cannot be inferred, the brothers were genetically identical, with similar life experiences. Although these results are promising, further study is necessary to determine whether MRS findings correlate both with markers of lead exposure and tests of cognitive function. Nevertheless, the results point to the potential utility of MRS in determining mechanisms of neurotoxicity not only for lead but also for other neurotoxicants as well.

Aged↗
PubMed1996

Severe lead poisoning from an imported clothing accessory: "watch" out for lead.

CASE REPORT: A case of severe lead poisoning following ingestion of an imported clothing accessory is reported. The child presented with abdominal pain, vomiting, and anemia but did not develop encephalopathy. RESULTS: Prompt removal of the object in conjunction with whole bowel irrigation and chelation therapy led to a favorable outcome.

Child, Preschool↗
PubMed1989

Height and weight following lead poisoning in childhood.

The effect of lead on growth was examined in 104 lead-poisoned subjects (Pb-B [blood lead concentration], 4.82 to 22.73 mumol/L) and 27 sib-controls (Pb-B, 0.48 to 1.88 mumol/L). Blood lead concentration, height, and weight are reported for 1974 (the year of their first posttreatment recall for evaluation) and for 1985 (the year of their sixth recall). In 1974, when their mean age was 8 years and their mean Pb-B was 1.68 mumol/L, about 70% of the patients and sib-controls were in the 50th to 95th percentiles for height and weight. In 1985, when their mean age was 18 years and all Pb-Bs were less than 1.20 mumol/L, height and weight percentiles were similar to those of 1974. Lead did not seem to affect the genetic predisposition for height attainment, at high or low blood lead levels.

Adolescent↗
PubMed1987

Deleading dilemma: pitfall in the management of childhood lead poisoning.

Deleading is a dangerous process which, if improperly done, can result in acute lead intoxication. The following case report illustrates what happened to an already-lead-poisoned child's lead level when he was not excluded from his apartment during deleading. Supportive evidence is provided from 12 additional cases recently seen by the same pediatric practice. The issues behind the failure of these families to vacate their apartments during deleading are discussed, and the need for lead-poisoning prevention programs to address these issues, particularly that of providing alternative shelter during deleading, is stressed. Society should adequately fund such programs so that they become a reality.

Chelating Agents↗
PubMed1998

[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.

Air Pollutants↗
PubMedDate not supplied

[The infraclinical diagnosis of lead poisoning (author's transl)].

Laboratory study of 16 workers handling lead made it possible to define a state of infraclinical lead poisoning. Estimation of alpha-dehydrase and of free erythrocytic protoporphyrins is the most sensitive test for diagnostic purposes. The estimation of erythrocytic pyrimidine 5' Nucleotidase would seem to be of value in the diagnosis of mild lead poisoning. The urinary lead tolerance test confirms the diagnosis and indicates the degree of intoxication. Its repetition make it possible to treat the intoxication.

Erythrocytes↗
PubMed1982

[Changes of hemoglobinemia during chelating therapy in lead poisoning].

The modifications of the Hb level of 32 subjects in which a lead poisoning occurred were studied during chelation therapy. 27 subjects showed a subclinical lead poisoning picture; 5 subjects suffered for a mild anemia. At the end of therapy, the mean Hb value of the whole group increased from 14.5 g/100 ml to 15.8 g/100 ml; the 5 subjects with anemia showed a remission and their mean Hb level increased from 12.3 to 15.1 g/100 ml. A group of 12 subjects with Hb values at the lower normal limits and 10 subjects with "apparently normal" values of Hb showed a significant increase in the Hb level following the treatment. The results obtained confirm the inhibitory activity exerted by lead on the heme synthesis also during preclinic lead poisoning and suggesting the opportunity of a constant evaluation of the Hb levels in order to decide the doses and the lengths of the chelation therapy and to lead the decision about the readmission to the working activity.

Adult↗