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PubMed1986

Evaluation of the relationship between chemical and biological monitoring of low-level lead poisoning.

Blood lead levels, together with delta-aminolevulinic acid dehydratase activity determinations have been measured on rats dosed with up to 1000 ppm lead acetate in their drinking water for periods up to 5 weeks. Despite evidence of a compensation mechanism developing in the enzyme determinations, enzyme activity ratios, if properly chosen, still correlate reasonably well (r = 0.87) with blood lead levels. Activity ratios using data on the shoulders of pH-activity profiles (e.g. activity ratios of 6.4 and 7.2), however, give much less satisfactory correlations. These data provide a more stringent test of the chemical monitor-biological monitor correlation than has previously been possible.

Animals↗
PubMed1982

Tissue distribution of lead in rat pups nourished by lead-poisoned mothers.

Lead accumulation was studied in rats treated with Pb through the dam's milk from birth to weaning. Dams of experimental litters received lead acetate in drinking water, while dams of control litters received a sodium solution. Fluid consumption by dams and pup weight were monitored daily. No differences were seen in the dams' fluid consumption or in mortality or growth rate of pups. Rats were sacrificed after 5, 10, 16, or 21 d of Pb treatment, or 3 and 3.5 mo after weaning. Samples of heart, brain, liver, kidney, intestine, and bone were solubilized in concentration nitric acid and analyzed for Pb by atomic absorption spectrophotometry. Nitric acid digests of blood samples from pups 10 and 21 d old and from animals allowed a Pb-free period of 3-3.5 mo after treatment were also analyzed for Pb concentration. Levels of Pb in all tissues analyzed progressively increased during the first 10 d of treatment. After the Pb-free period only bone Pb concentration remained elevated. The results indicate that treatment of lactating dams is an efficient method of producing chronic Pb exposure of rat pups. The results also provide a means of comparing studies of Pb toxicity in which different treatment paradigms are used.

Animal Population Groups↗
PubMed1978

Surma and lead poisoning.

Blood lead concentrations were measured in 62 Asian children, of whom 37 had definitely had surma applied to their eyes and 25 were thought not to have done. The mean concentration in those who had not used surma was 0.98 +/- SD 0.42 mumol/1 (20.3 +/- 8.7 microgram/100 ml) compared with 1.65 +/- 0.68 mumol/4 (34.2 +/- 14.1 microgram/100 ml) in those who had. Analysis of 29 different samples of surma showed 23 of them to be composed largely of lead sulphide. We conclude that the use of surma is associated with high blood lead concentrations. In our cases most of it had been obtained abroad, and hence government restrictions might be ineffective in limiting its use: a better method of prevention might be to inform the leaders of Asian communities of the risks.

Asia↗
PubMed1992

Lead poisoning in cattle--transfer of lead to milk.

The transfer of lead to milk in cattle in relation to blood lead levels and the uptake of lead in edible tissues was studied for an accidental exposure over 1 or 2 days to lead in excessive amounts from the licking of burnt storage batteries. The degree of exposure was monitored by determination of blood lead levels. Milk and blood samples were taken from eight cows, without acute symptoms of lead poisoning, during a period of 18 weeks. Two weeks after the accidental exposure, lead levels (mean +/- SD) in milk were 0.08 +/- 0.04 mg kg-1 and in blood 0.36 +/- 0.04 mg kg-1 in six of the cows. The relationship between lead concentration in blood and those in milk was found to be exponential and could be expressed by the equation: log y = 3.19x - 2.36 (r = 0.85, p less than 0.001), where y and x are the lead concentrations in milk and blood, respectively. The lead level in milk was relatively constant up to a blood lead level of 0.2-0.3 mg kg-1, and increased sharply at higher blood levels. The biological half-life of lead in blood was shown to be approximately 9 weeks. In eight acutely sick cows, which were emergency slaughtered, the range of lead levels in edible muscle tissue was 0.23-0.50 mg kg-1 wet weight. Very high concentrations were found in the kidneys, with a range of 70-330 mg kg-1, and in the livers, with a range of 10-55 mg kg-1. Four of the cows were pregnant, in the first or second month of gestation, during the episode of exposure. The lead exposure was not found to disturb the gestation or development of the fetuses.

Animals↗
PubMed1988

Inorganic lead poisoning in an adult.

Lead poisoning is uncommon in the adult population, but must be considered in the differential diagnosis of patients with abdominal pain of obscure etiology. In this paper we present a 38-yr-old male with abdominal pain, a history of alcohol abuse, and exposure to the virus responsible for acquired immunodeficiency syndrome. The cause of pain was elusive until his occupation as a housepainter was appreciated. The diagnosis of lead poisoning then was considered and confirmed by an elevated blood lead level and symptomatic response to therapy. With the increase in renovation of old buildings, it is likely that the incidence of lead poisoning will become more common.

Adult↗
PubMed1983

Lead poisoning from hair spray ingestion.

A 37-year-old alcoholic woman was poisoned by lead from drinking hair spray mixed with water. Laboratory and pathologic findings showed changes due to lead poisoning. Further analysis by Scanning Electron Microscopy (SEM) and Energy Dispersive X-Ray Analysis (EDXA) confirmed the presence of lead in both the tissues and the hair spray. The significance of these findings is discussed.

Adult↗
PubMedDate not supplied

Child and caretaker attributes associated with lead poisoning in young children.

Lead poisoning is one of the major health hazards facing young children. A perplexing aspect is that elevated blood lead levels persist in many children even after education of caretakers in techniques to achieve lead reduction. This study examined attributes of mothers and children that might be associated with recovery after diagnosis. The results showed that mothers who had fewer "masculine" sex-role behaviors, who thought lead poisoning to be less serious, or who thought their children to be more difficult had children who made less improvement after diagnosis. Less improvement was also seen in the children of older mothers or mothers who had more children living with them. Children who were later-born, older, or male made less improvement after diagnosis than first-born, younger, or female children. Nurses should be alert to attributes that may foretell less redovery from lead poisoning and the need for more intensive intervention in these circumstances.

Adolescent↗
PubMed1984

[Biological stigmata of lead poisoning from water and their peculiarities. Application to the choice of diagnostic tests].

We have studied the diagnostic efficiency of some biological tests in 59 consecutive patients whom we suspected to be poisoned by lead from drinking water. This diagnosis was confirmed in 30 patients in whom EDTA-promoted urinary excretion of lead was greater than 800 micrograms/24 hr. The measurement of delta-ALA (delta-aminolevulinic acid) dehydrase was the most sensitive test (89.7 p. 100). Sensitivities of protoporphyrin blood level (64.7 p. 100), of serum lead level (46.2 p. 100), of the presence of erythrocytes with basophilic stippling in blood (44.4 p. 100) were lower. The determinations of urinary coproporphyrin and of delta-ALA levels in blood and urine had no practical diagnostic value. We conclude that the best screening test for the diagnosis of lead poisoning by drinking water is the measurement of delta-ALA dehydrase activity. An increase of the EDTA-promoted urinary excretion of lead is required for a final confirmation of the diagnosis.

Adult↗
PubMed1981

[Excretion of lead in the gastric and duodenal juice of persons with occupational lead poisoning and normal subjects].

Lead was measured in the gastric and duodenal juice of three patients with lead poisoning (blood concentrations of lead: 4.30; 5.16; 5.50 mumol/l). The lead excretion into the gastric juice was 94.6; 29.9 and 18.3 nmol Pb X h-1 for the poisoned persons and 57.9 +/- 38.1 nmol Pb X h-1 for healthy persons (n = 20). Pentagastrin (6 microgram/kg, i.m.) stimulated lead excretion in both groups (normal + 109%, lead poisoned persons: + 180%; + 187%; + 311%). The lead excretion was correlated with an increase of HCl-secretion and volume in healthy persons. The lead excretion into the duodenal juice after secretion (1 unit/kg) amounted to 14.2 +/- 8.8 nmol Ph X h-1 in healthy persons, whereas after secretion plus caerulein 18.8 +/- 7.2 nmol Pb X h-1 were found. In the duodenal juice of the lead poisoned persons 27.5 and 474.9 nmol Ph X h-1 respec. were found after secretion and 58.9 and 491.8 nmol Pb X h-1 respec. after secretion plus caerulein. Lead excretion was correlated with enzyme secretion (trypsin and chymotrypsin).

Ceruletide↗
PubMed2006

Should all patients with unexplained anaemia be screened for chronic lead poisoning?

The global prevalence of lead poisoning is declining. However, the prevalence of lead poisoning in patients with either microcytic or normocytic anaemia is unknown. Blood samples from anaemic patients residing in south-east London without an obvious cause for anaemia had their blood lead concentration (BLC) analysed. A batch of 988 samples was analysed for BLC using atomic absorption spectroscopy. Median haemoglobin was 10.3 g/dL (range: 4.2-10.9) in females, 10.6 g/dL (range: 5.2-11.4) in males and 10.7 g/dL (range: 6.7-10.9) in children. Median BLC was 2.63 microg/dL (0.21-24.0 microg/dL; 95th centile 7.54 microg/dL). Fifteen samples (1.5%) had a BLC > 10.0 microg/dL, five samples (1%) > 15.0 microg/dL and one sample (0.1%) > 20.0 micrg/L. In the 106 children, median BLC was 2.34 microg/dL (0.5-14.5 microg/dL; 95th centile 6.12 microg/ dL). Only one child (14.5 microg/L) had a BLC > 10.0 pg/dL. There was a poor correlation between haemoglobin and BLC (r2 = 0.08). Routine screening for lead poisoning cannot be justified in all patients with unexplained anaemia, unless there is a history or clinical features to suggest lead toxicity. Additionally, we have shown that in this former high-risk area for lead exposure, there is a low point prevalence of significant lead poisoning, even in an anaemic population.

Adolescent↗
PubMed1996

Moderate lead poisoning: trends in blood lead levels in unchelated children.

The appropriate clinical management of children who are moderately poisoned with lead (Pb) is under active investigation. To determine the pattern of change in blood Pb (BPb) levels in the absence of chelation therapy, we followed moderately Pb-poisoned children (initial blood Pb levels 1.21-2.66 mumol/l or 25-55 micrograms/dl) for 6 months with repeated BPb level measurements. Chelation therapy was not administered because all the children had negative lead mobilization tests indicating limited response to the chelating agent, calcium disodium edetate (CaNa2EDTA). Eligible children received the following interventions: notification of the health department to remediate lead hazards; reinforced educational efforts about the toxicity sources and treatment of Pb during 10 clinic and 3 home visits; and iron therapy for children with ferritin levels less than 16 micrograms/l. To quantify the lead paint hazards in the home, we combined a visual rating of the surfaces (intact to peeling) with an X-ray fluorescence (XRF) measurement of the lead content of the painted surface. The sum of these assessments is termed the home environmental score (HES). Data were analyzed from 79 children. BPb levels declined by 27%, on average, over 6 months. HES was correlated with BPb at enrollment, but neither the initial nor later HES measurements predicted BPb at other time points. The HES was highest at enrollment and declined by 50% and 75% at the second and third home visits, respectively. However, only a minority of the children (20%) achieved an HES of 0, indicating no lead paint hazards at home. Despite some ongoing Pb exposure, a parallel fall in BPb levels was observed in subgroups of children with either initially low or high HES (above or below the median HES of 37). Iron status did not account for the change in BPb levels. These data provide evidence that our measure, the HES, is quantifiably related to BPb levels in children, that this correlation is significant only prior to intervention; and that BPb levels decline in children who are moderately poisoned with Pb after they are enrolled in a comprehensive intervention program, even in the absence of chelation therapy and in the presence of ongoing lead paint exposure and Fe deficiency.

Chelation Therapy↗
PubMed1986

Slow, natural reduction in blood lead level after chelation therapy for lead poisoning in childhood.

Lead poisoning is treated with chelating agents. We report the natural decline of blood lead (Pb-B) concentration after treatment(s) (1967 to 1972) in 74 patients whose maximal Pb-B level ranged from 100 to 471 micrograms/dL (4.83 to 22.73 mumol/L). These longitudinal data (range, nine to 17 years) disclose a predictable decrease in Pb-B levels after treatment that is independent of the maximal Pb-B level before therapy. The correlation between age in months and the logarithm of the Pb-B level was significant, and the equation defined by the regression line allows one to predict Pb-B levels at specific ages after chelation therapy. It is important to recognize the slow, natural decline of Pb-B levels after chelation therapy once the level is stable and below 70 micrograms/dL (3.38 mumol/L). Multiple repeated courses of calcium disodium edetate are unlikely to influence the natural decline of the Pb-B level in asymptomatic children.

Chelating Agents↗
PubMed1978

2,3-Dimercaptosuccinic acid: a new agent for the treatment of lead poisoning.

Using minimally lead-poisoned rats, we have measured urinary and fecal lead excretion in response to 2,3-dimercaptosuccinic acid (DMS) administered i.p. or p.o. and compared it to that induced by dimercaptopropanol (BAL) (i.p.), EDTA (i.p.), D-penicillamine (p.o. and i.p.) and the combination of BAL and EDTA (i.p.). At doses of 30 mg/kg, parenterally administered DMS was as effective as i.p. BAL and these two drugs were more effective than the other treatment groups. However, p.o. DMS was only 20% less effective and was as effective as i.p. EDTA and the combination of EDTA + BAL i.p. and significantly more effective than D-penicillamine p.o. or i.p. Unlike BAL, most lead excretion in response to DMS was via the urine, undoubtedly reflecting the greater water solubility of DMS. When mice were fed a diet containing both lead and DMS, the drug prevented the accumulation of porphyrins in erythrocytes. Studies with 210Pb indicate that this prophylactic effect is not due to an inhibition of lead absorption but rather to enhanced excretion of lead. The residual tissue distribution of 210 Pb administered simultaneously with DMS was not different form that of 210Pb alone. Since DMS is orally effective and its LD50 is 30 times greater than that of BAL, we expect this compound to be clinically useful in the treatment of lead poisoning.

Animals↗
PubMed1998

[Occupational lead poisoning in Poland].

During the years 1970-1996, 8,414 cases (8,176 among men and 238 among women) of lead poisoning, recognised as occupational disease, were registered with the peak in 1972-1976 (500-800 cases per year). An in-depth analysis of 7,893 (men) reported in the period between 1970 and 1992 revealed that repeated poisonings in the same person were observed quite frequently. Among 4,556 men poisoned by lead during the period under study, in every third men the disease was diagnosed at least twice. Almost half of men with occupational lead poisoning received the occupational disease certification after the exposure lasting less than five years. The majority of persons poisoned by lead (64.3%) were employed in plants located in the Katowice voivodship. More than half of men with occupational lead poisoning (54.1%) was exposed to maximum concentrations of lead, exceeding MAC values by two hundred times. A diminishing number of occupational lead poisoning observed during the 1990s does not reflect a real-level of occupational exposure. The majority of cases reported apply to large plants or industrial complexes where the prevention of poisonings is rather well organised. But dispersed small production and service enterprises, where acute cases of poisoning may lead to irreversible organic changes create a great problem. One of the prerequisites for effective prevention of occupational lead poisoning is to identify and to make a complete inventory of workplaces where lead occurs, as well as to identify workposts hazardous to worker's health, and to monitor lead concentrations in the air.

Adult↗
PubMed1993

Preventing lead poisoning in New York City: priorities for lead abatement in housing.

The major challenge for lead poisoning prevention programs is to increase the availability of lead-safe housing as quickly as possible. The approach proposed by the City of New York maximizes the impact of the limited resources available to address this problem. The approach, however, is based on an assumption that in the short-term, modest lead hazard reduction measures such as restoring surfaces to an intact condition is adequate for most units and that more extensive abatement should be reserved for the relatively fewer units in which there is a high risk of exposure of lead-poisoned children reside. Ideally, this plan would be implemented with voluntary efforts to abate lead hazards when other renovation or remodeling occurs or when dwellings are vacant and more extensive abatement work can be performed at lower cost and without the attendant difficulty of abating occupied units. Approaches ranking hazards and implementing varying levels of hazard reduction must be fully evaluated and modified as new information becomes available. The specific criteria used to rank hazards should be evaluated to determine what measures best differentiate risk. Given the magnitude of the problem and the numerous obstacle--lack of funding, limited trained workers, and limited technical knowledge--it will probably take years, if not decades, to abate lead hazards in all the dwellings in which they exist. We must not be deterred, however, from beginning this effort in the communities and dwellings that need intervention the most: deteriorated, older housing units in which young children reside. In major urban centers such as New York City the greatest lead hazards will generally be found in areas where poverty is greatest. Thus, every effort must be made to ensure that adequate resources are available to improve housing in the communities in greatest need.

Child↗
PubMed1981

Reassessment of the microcytic anemia of lead poisoning.

Hematologic abnormalities in childhood lead poisoning may be due, in part, to the presence of other disorders, such as iron deficiency or thalassemia minor. In order to reassess increased lead burden as a cause of microcytic anemia, we studied 58 children with class III or IV lead poisoning, normal iron stores, and no inherited hemoglobinopathy. Anemia occurred in 12% and microcytosis in 21% of these children. The combination of anemia and microcytosis was found in only one of 58 patients (2%). When only children with class IV lead poisoning were studied, the occurrence of microcytosis increased to 46%. However, the combination of microcytosis and anemia was found in only one of these 13 more severely affected patients. Microcytic anemia was similarly uncommon in children with either blood lead concentration greater than or equal to 50 microgram/100 ml. These data indicate that microcytosis and anemia occur much less commonly than previously reported in childhood lead poisoning uncomplicated by other hematologic disorders.

Anemia↗
PubMed1990

Acute lead poisoning in nursing home and psychiatric patients from the ingestion of lead-based ceramic glazes.

To our knowledge, acute inorganic lead poisoning from single ingestions of lead compounds has been only rarely reported. During a 14-month period, we were contacted regarding eight instances of acute ingestions of liquid lead-based ceramic glazes by mentally impaired residents of nursing homes or psychiatric facilities participating in ceramic arts programs. While some ingestions did not cause toxic effects, some patients developed acute lead poisoning characterized by abdominal pain, anemia, and basophilic stippling of red blood cells. In the blood of several patients, lead concentrations were far above normal (4 to 9.5 mumol/L). Urinary lead excretions were tremendously elevated during chelation therapy, with one patient excreting 535.9 mumol/L of lead during a 6-day period, the largest lead excretion ever reported in a patient suffering from acute lead poisoning, to our knowledge. All patients recovered following supportive care and appropriate use of chelating agents. Lead-based glazes are commonly found in nursing homes and psychiatric facilities. We suspect that acute or chronic lead poisoning from the ingestion(s) of lead-based ceramic glazes may be an unrecognized but not uncommon problem among such residents. We urge physicians to take ingestions of lead-based glazes seriously and to consider the diagnosis of lead poisoning in nursing home and psychiatric patients who have participated in ceramic crafts programs.

Acute Disease↗