Search tips
Search criteria

Results 1-25 (1222734)

Clipboard (0)

Related Articles

1.  The Diagnosis of Industrial Lead Poisoning 
A series of 100 lead workers from different industries, 91 at work and nine admitted to hospital with lead poisoning, was studied in order to define more clearly the clinical and biochemical criteria of lead poisoning in three stages—(A) a presymptomatic state of lead exposure (37 men), (B) a state of mild symptoms or mild anaemia (45 men), and (C) frank lead poisoning with severe symptoms and signs (18 men).
The tests used were haemoglobin, reticulocyte count, and blood lead, and urinary lead, coproporphyrin, δ-aminolaevulinic acid (ALA), and porphobilinogen (PBG) estimations. Of these, the urinary lead was similar for all three groups and the blood lead estimation was of less value for determining the clinical group of the men than the haemoglobin and urinary coproporphyrin or ALA estimations, which correlated well with the clinical assessment and with each other but showed no correlation with the urinary and blood lead levels. PBG levels became raised only with the onset of symptoms of lead poisoning.
A haemoglobin of 13 g./100 ml. (90%) or less is a cautionary sign. Urinary coproporphyrin above 80 μg./100 mg. creatinine (800 μg./litre), ALA above 2·0 mg./100 mg. creatinine (2·0 mg.%), and PBG above 0·15 mg./100 mg. creatinine (0·15 mg.%) were almost always associated with symptoms or signs and were therefore considered to be the upper safety limits. Although the blood lead level does not differentiate between lead toxicity and lead exposure, values above 60 μg. lead/100 g. blood should alert the physician to carry out other tests.
In addition to the above tests, blood pressure, blood urea, and serum uric acid estimations were performed on all the men in order to elucidate the possible role of lead in the production of renal damage. Blood pressure and serum uric acid levels were similar for all three groups but the blood urea level was raised in group C. The reason for this finding was not established.
It was found that scrap metal burning, battery manufacturing, and ship-breaking constituted the gravest lead hazards encountered in this survey whereas wire manufacture constituted the least. Workers in the most modern factory, a car-body pressing plant, gave average values just below the danger levels for the urinary coproporphyrin and ALA estimations despite apparently efficient protective measures. This finding underlines the importance of the medical supervision of lead workers.
PMCID: PMC1008661  PMID: 5642647
2.  The Value of Mobilization of Lead by Calcium Ethylene-diamine-tetra-acetate in the Diagnosis of Lead Poisoning 
Traditional laboratory tests for lead poisoning tend to fail in cases where a considerable interval has elapsed since exposure. We have used calcium ethylene-diamine-tetra-acetate (CaNa2EDTA) for the quantitative mobilization of lead for diagnostic purposes.
In a control group of 50 individuals who had never worked with lead it was found that the average urinary excretion of lead in 24 hours amounted to 0·031 to 0·043 mg. The maximum value did not exceed 0·100 mg. After intravenous injection of CaNa2EDTA the amount of excreted lead rose considerably, but did not exceed 0·350 mg./24 hr.
In a group of 47 individuals who had formerly worked with lead or who were still engaged in this work but did not show any symptoms of poisoning, the urinary lead levels before injection were higher than in the control group. After injection of CaNa2EDTA the lead excretion in 24 hours increased considerably. After injection of CaNa2EDTA, patients suffering from chronic lead poisoning showed a considerable increase of urinary lead excretion, which attained the order of milligrams in 24 hours.
The fractionated examination of the urine of 10 unexposed individuals, undertaken at intervals of three hours, showed after injection of CaNa2EDTA no higher lead concentration than 0·500 mg./litre, the highest concentrations being observed six hours after injection. In the urine of individuals exposed to lead or suffering from lead poisoning a higher urinary lead concentration was found than in the control group, and the maximum was in these cases found at various time intervals.
It is concluded that the mobilization of lead may be of considerable value in the diagnosis of atypical cases of chronic lead poisoning, but the results can be evaluated only in association with the general clinical picture.
PMCID: PMC1039180  PMID: 13651558
3.  Description of 3,180 Courses of Chelation with Dimercaptosuccinic Acid in Children ≤5 y with Severe Lead Poisoning in Zamfara, Northern Nigeria: A Retrospective Analysis of Programme Data 
PLoS Medicine  2014;11(10):e1001739.
Jane Greig and colleagues from the medical humanitarian organization Médecins Sans Frontières describe the use of the oral chelating agent dimercaptosuccinic acid (DMSA) in several thousand young children with severe lead poisoning as a result of an environmental disaster in Zamfara, northern Nigeria.
Please see later in the article for the Editors' Summary
In 2010, Médecins Sans Frontières (MSF) discovered extensive lead poisoning impacting several thousand children in rural northern Nigeria. An estimated 400 fatalities had occurred over 3 mo. The US Centers for Disease Control and Prevention (CDC) confirmed widespread contamination from lead-rich ore being processed for gold, and environmental management was begun. MSF commenced a medical management programme that included treatment with the oral chelating agent 2,3-dimercaptosuccinic acid (DMSA, succimer). Here we describe and evaluate the changes in venous blood lead level (VBLL) associated with DMSA treatment in the largest cohort of children ≤5 y of age with severe paediatric lead intoxication reported to date to our knowledge.
Methods and Findings
In a retrospective analysis of programme data, we describe change in VBLL after DMSA treatment courses in a cohort of 1,156 children ≤5 y of age who underwent between one and 15 courses of chelation treatment. Courses of DMSA of 19 or 28 d duration administered to children with VBLL ≥ 45 µg/dl were included. Impact of DMSA was calculated as end-course VBLL as a percentage of pre-course VBLL (ECP). Mixed model regression with nested random effects was used to evaluate the relative associations of covariates with ECP. Of 3,180 treatment courses administered, 36% and 6% of courses commenced with VBLL ≥ 80 µg/dl and ≥ 120 µg/dl, respectively. Overall mean ECP was 74.5% (95% CI 69.7%–79.7%); among 159 inpatient courses, ECP was 47.7% (95% CI 39.7%–57.3%). ECP after 19-d courses (n = 2,262) was lower in older children, first-ever courses, courses with a longer interval since a previous course, courses with more directly observed doses, and courses with higher pre-course VBLLs. Low haemoglobin was associated with higher ECP. Twenty children aged ≤5 y who commenced chelation died during the period studied, with lead poisoning a primary factor in six deaths. Monitoring of alanine transaminase (ALT), creatinine, and full blood count revealed moderate ALT elevation in <2.5% of courses. No clinically severe adverse drug effects were observed, and no laboratory findings required discontinuation of treatment. Limitations include that this was a retrospective analysis of clinical data, and unmeasured variables related to environmental exposures could not be accounted for.
Oral DMSA was a pharmacodynamically effective chelating agent for the treatment of severe childhood lead poisoning in a resource-limited setting. Re-exposure to lead, despite efforts to remediate the environment, and non-adherence may have influenced the impact of outpatient treatment.
Please see later in the article for the Editors' Summary
Editors' Summary
Lead, a toxic metal that occurs naturally in the earth's crust, is now present throughout the environment because of human activities. For many years, lead was added to paint and gasoline and used in solder for water pipes. In addition, the mining, smelting, and refining of some metallic ores releases lead into the environment. Inhalation of contaminated air, consumption of contaminated food and water, and contact with dust that contains lead raises venous blood lead levels (VBLLs) and causes many health problems, particularly in children. Children who ingest large amounts of lead can develop anemia, muscle weakness, kidney damage, and life-threatening encephalopathy (brain swelling). Although fatal lead poisoning is now rare in resource-rich countries, it nevertheless remains a major global health problem. Over a three-month period in early 2010, for example, about 400 young children died in Zamfara State, Nigeria, from unexplained, intractable fits. By May 2010, it was clear that recently expanded gold mining had caused widespread environmental lead contamination in the region, and an environmental management program was begun to reduce lead levels in the surface soils.
Why Was This Study Done?
In response to the lead poisoning outbreak, the not-for-profit organization Médecins Sans Frontières (MSF) began a medical management program to reduce VBLLs that included treatment with the oral chelation agent dimercaptosuccinic acid (DMSA). Chelation agents bind metal ions and facilitate their removal from the body, thereby reducing the likelihood of lead moving from the blood to the brain. Lead encephalopathy has been commonly treated by injecting another chelator called CaNa2EDTA, but the discovery of more than 1,000 cases of childhood lead poisoning in rural villages in Nigeria meant that MSF needed a chelation approach that could be applied rapidly in a remote resource-limited setting. Additionally, although CaNa2EDTA has been in common use for severe lead poisoning for longer than DMSA, and is commonly recommended in guidelines, the evidence base does not support one treatment as superior. Here, in a retrospective analysis of MSF program data, the researchers evaluate the changes in VBLLs before and after courses of oral DMSA treatment in children aged five years and below living in Zamfara to gain new insights into this understudied treatment for severe childhood lead poisoning.
What Did the Researchers Do and Find?
The researchers measured VBLLs before and after treatment with DMSA in 1,156 children (inpatient and outpatient) with high amounts of lead in their blood who underwent one or more courses of chelation treatment lasting 19 or 28 days by calculating each child's end-course VBLL as a percentage of the child's pre-course VBLL (ECP). Considering all the treatment courses given between June 2010 and June 2011, the mean (average) ECP was 74.5%. That is, on average, VBLLs measured at the end of treatment courses were reduced by a quarter compared to VBLLs at the start of treatment courses. Among 159 inpatient courses of DMSA, the ECP was 47.7% (a halving of pre-course VBLLs). The ECP after 19-day courses was lower in older children, after first-ever courses, after courses with a longer interval since a previous course, after courses that included more directly observed doses (DMSA given in the presence of a health-care worker), and in children with higher pre-course VBLLs. Nine of the children included in this analysis died during the study period; lead poisoning was probably involved in three of these deaths. Importantly, no clinically severe adverse effects related to DMSA were seen during the study period, and no laboratory findings were recorded that required treatment discontinuation.
What Do These Findings Mean?
Because many changes were made to the treatment given to the affected children in Zamfara during the study period and because no information is presented here on clinical outcomes, these findings cannot be used to reach any definitive conclusions about the effectiveness or safety of oral DMSA as a treatment for lead poisoning in young children. However, these findings show that chelation was associated with a large reduction in the death rate among probable or suspected cases of childhood lead poisoning in Zamfara and provide new information about oral chelation that may help agencies such as MSF provide urgent treatment for lead poisoning in resource-limited settings where intravenous chelation is not feasible. Moreover, the finding of a lower ECP after inpatient treatment courses compared to after outpatient courses suggests that re-exposure to lead and non-adherence to treatment may have influenced the impact of outpatient treatments. Thus, it is essential that medical management of lead poisoning in resource-limited settings be accompanied by environmental remediation and that efforts are made to support adherence to treatment in the community by implementing directly observed treatment wherever possible.
Additional Information
Please access these websites via the online version of this summary at
A related PLOS ONE Research Article by Greig et al. provides information about the association between VBLLs and neurological features in children affected by the acute lead poisoning outbreak in Zamfara
MSF provides information about the lead poisoning crisis in Zamfara State
Human Rights Watch, an international organization that works to uphold human dignity and advance the cause of human rights for all, also provides information about lead poisoning in Zamfara State, including photographs and a video
Tox Town, an interactive site about environmental health concerns from the US National Library of Medicine, provides information on exposure to lead (in English and Spanish)
The US Environmental Protection Agency provides information on lead and lead poisoning (in English and Spanish)
The US Centers for Disease Control and Prevention provides information about lead in the environment and about its lead poisoning prevention program
MedlinePlus provides a list of links to further information about lead poisoning (in English and Spanish)
PMCID: PMC4188566  PMID: 25291378
4.  Urinary non-precipitable lead in lead workers. 
Sixty-six workers engaged in lead-glazing pottery with a presumed moderate exposure to lead were studied. The group comprised 20 men with long-term exposure to lead and positive laboratory signs of increased lead absorption (Group A); 22 with long-term exposure and negative laboratory signs (Group B); 11 with short-term exposure and positive laboratory signs (Group C); and 13 with short-term exposure and negative laboratory signs (Group D). In addition, 14 workers employed in casting the kelmet alloys with presumed heavy exposure to lead (Group E) and seven healthy individuals (Group F) were included. Urine samples from all the subjects were analysed to determine, first, the total lead using the ashing technique, and then the precipitable lead using the coprecipitation technique of Cholak, Hubbard, and Burkey (1948), but modified slightly by us. Thus, the non-precipitable lead fraction in urine was the difference between the two measurements and this was also expressed as a percentage of the total lead. The mean total lead and the mean proportion of non-precipitable lead were 0.62 mumol/l and 48.7%, 0.35 mumol/l and 44.9%, 0.40 mumol/l and 48.9%, 0.17 mumol/l and 24.6%, 1.43 mumol/l and 44.3%, 0.14 mumol/l and 18.8% for Groups A, B, C, D, E, and F respectively, showing that a large part of urinary lead was eliminated as precipitable lead in Groups D and F who had normal lead excretion, while about half was eliminated as non-precipitable lead in the other four groups who had excessive lead excretion. No essential difference in the proportion of non-precipitable lead among Groups A, B and C excluded the possibility that the proportion might be directly related to the period of exposure to lead and to the laboratory findings of excessive lead absorption. The mean proportion of non-precipitable lead for the physiological (up to 0.240 mumol/l), intermediate (0.241 to 0.721 mumol/l), and excessive (above 0.722 mumol/l) total lead levels was 26.7, 41.3, and 52.3% respectively, in the lead workers comprising Groups A, B, C, and E each showing increased lead excretion when grouped together. these data suggested that, when urinary lead is within the normal range, it is excreted largely as precipitable lead even in individuals exposed to lead, and that the principal conditions determining the excretion of non-precipitable lead would be the current or recent degree of lead absorption. The excretory mechanisms and the biological significance of the non-precipitable lead are also discussed.
PMCID: PMC1008133  PMID: 963004
5.  Studies in Lead Poisoning: Oral Therapy with Penicillamine: Relationship between Lead in Blood and other Laboratory Tests 
Fifteen workers with lead poisoning of varying degrees were treated with penicillamine given by mouth. The effect on symptoms and pathological laboratory values was satisfactory, side effects were generally mild and the drug is considered to be a good alternative to Ca-EDTA, which must be given intravenously. Previous studies on the reliability of different laboratory tests in evaluating the degree of lead poisoning and the effect of the therapy were extended with special respect to the lead levels in blood.
The correlations between lead in blood and lead in urine, coproporphyrins in urine and lead excreted during treatment were of the same order as those found between delta-aminolaevulic acid (ALA) in urin and the same parameters. As could be expected, the correlation between the initial values of lead in blood and ALA in urine was very strong (p<0·001). It also persisted during treatment.
It is concluded that penicillamine is efficient and useful in the treatment of lead poisoning. Determinations of lead in blood and ALA in urine are equivalent as expressions of lead poisoning, provided that the lead level in blood is not temporarily raised because of an acute exposure.
PMCID: PMC1008466  PMID: 5926893
6.  Treatment of Lead Poisoning: A Comparison between the Effects of Sodium Calciumedetate and Penicillamine Administered Orally and Intravenously1 
In 16 workers with lead poisoning of varying degrees, a comparison was made between the therapeutic efficacy of sodium calciumedetate (Ca-EDTA) and penicillamine (PCA), administered intravenously and orally. The question of comparable dosages of ligands, forming metal complexes in different ways, is discussed. With the dosages given, intravenous Ca-EDTA promoted the greatest output of lead in the urine, followed by intravenous and oral PCA. These three agents also had a very satisfactory effect on the output δ-aminolaevulinic acid (ALA) in urine. Oral Ca-EDTA was found to be greatly inferior in both these respects.
In order to study the absorption of the agents and the renal excretion of the formed lead complexes, the urine was collected quantitatively and fractionated in consecutive 4-hour periods, after which the lead excretion during each period was determined. It was found that the oral absorption of PCA was rapid and quantitatively great, whereas the oral absorption of Ca-EDTA was very slow and quantitatively small. The possible resorption of ligand-lead complexes is discussed and indications were found of resorption of the Ca-EDTA-lead complex but not of the PCA-lead complex. The renal excretion of the different ligand-lead complexes was very effective and reached its maximal level within four hours. However, in some subjects excretion of the Ca-EDTA-lead complex showed some delay. An investigation, in four subjects, of a blocking effect of probenecid on the renal excretion of PCA and/or PCA-lead complexes gave no conclusive results. It is concluded that oral PCA is satisfactory in most cases of lead poisoning. However, in more severe cases intravenous treatment is preferable. Which agent should be chosen, Ca-EDTA or PCA, appears to be unimportant as both are quite satisfactory from the point of view of treatment, but it seems that Ca-EDTA may cause more serious side-effects. Oral Ca-EDTA is quite unsatisfactory and there is good evidence to indicate that the agent causes a resorption of Ca-EDTA-lead complexes from the gastro-intestinal tract.
PMCID: PMC1008620  PMID: 4965262
7.  Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels. 
Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).
PMCID: PMC1008609  PMID: 508643
8.  Interrelationships between lead in blood, lead in urine, and ALA in urine during lead work 
Selander, S., and Cramér, K. (1970).Brit. J. industr. Med.,27, 28-39. Interrelationships between lead in blood, lead in urine and ALA in urine during lead work. One hundred and seventy-seven workers from a storage battery factory were examined for lead in blood and lead and δ-aminolevulinic acid (ALA) in urine. The workers were selected at random from those who had been employed for more than one month;most had been employed for several years at the same job. Thirty-six workers were from departments with no lead exposure. In three departments with high exposure a rotating system with three weeks' exposure and three weeks' non-exposed work was applied. As the aim of the study was to establish the relationships between the three parameters during constant exposure, the values from these men were treated separately.
The relationship between lead in blood and urinary ALA was best described by a curvilineat function: ALA = 100·0157 Pbb-1·0985, while the regression lines for ALA on lead in urine, and lead in urine on lead in blood were straight.
Workers from the departments with the rotating system showed lower values for urinary lead and ALA, compared with non-rotating workers with the same level of lead in blood. All these workers were examined during their second or third week of lead work, i.e., with an accumulating lead body burden. This system may be beneficial, especially in departments where prophylactic measures are difficult to install, or for notoriously careless workers.
Those who showed comparatively high ALA and urinary lead values in relation to their blood lead level were found to be workers with repeated incidents of metabolic lead influence, in whom the ALA values had seldom been normal.
The mean values from different factory departments were of the same order as would be expected from previous studies in storage battery plants.
The results are discussed in relation to present concepts of lead absorption and poisoning.
PMCID: PMC1009038  PMID: 5418917
9.  Clinical lead poisoning in England: an analysis of routine sources of data 
OBJECTIVE: To examine the occurrence of clinical lead poisoning in England based on routine sources of data. METHODS: Three routine data sources were examined, over different periods according to availability of data: (a) mortality for England, 1981-96; (b) hospital episode statistics data for England, for the 3 years 1 April 1992-31 March 1995; (c) statutory returns to the Health and Safety Executive under the reporting of injuries, diseases, and dangerous occurrences regulations (RIDDOR), also for the period 1 April 1992-31 March 1995. Also, analyses of blood lead concentrations carried out by the Medical Toxicology Unit, Guy's and St Thomas' Hospital Trust in London during the period 1 January 1991-31 December 1997 were examined. The analyses were performed both for industrial screening purposes and in response to clinicians' requests where lead poisoning was suspected. This is one of several laboratories carrying out such analyses in the United Kingdom. RESULTS: One death, of a 2 year old girl, was coded to lead poisoning in England during 1981-96. Analysis of hospital episode statistics data identified 83 hospital cases (124 admissions) over 3 years with any mention of lead poisoning, excluding two with admissions dating from 1965 and 1969. For these 83 cases the median hospital stay per admission was 3 days (range 0-115 days). Five were coded as having received intravenous treatment. Further clinical details of these cases beyond what is routinely recorded on the hospital episode statistics database were not available, except for blood lead concentrations in cases also identified on the Medical Toxicology Unit database. Eighteen cases (22%) were below 5 years of age of whom 10 (56%) came from the most deprived quintile of electoral wards. There was evidence to suggest spatial clustering of cases (p = 0.02). Six occupational cases were reported under RIDDOR in England during the period of study, two of whom were identified on the hospital episode statistics database. One further occupational case was identified on hospital episode statistics. Blood lead analyses for 4424 people carried out by the Medical Toxicology Unit (estimated at about 5% of such analyses in England over 7 years) found that among 547 children aged 0-4, 45 (8.2%) had a blood lead concentration in excess of 25 micrograms/dl, the action level in the United Kingdom for investigation, or removal of environmental sources of lead. At all ages, there were 419 (9.5%) such people, including 106 adults with no mention of industrial exposure. CONCLUSIONS: Both mortality and hospital admission ascribed to lead poisoning in England are rare, but cases continue to occur and some, at least, seem to be associated with considerable morbidity. Lead poisoning was confirmed as a probable cause of clinical signs and symptoms in only a small proportion of those in whom a blood lead concentration was requested. Where indicated, appropriate remedial action for the safe removal of environmental sources of lead should be taken.
PMCID: PMC1757691  PMID: 10658538
10.  Lead Poisoning in an Adult: Lead Mobilization by Pregnancy? 
Journal of General Internal Medicine  2007;22(8):1212-1215.
We report a case of acute lead poisoning in an adult female who had last been exposed to lead 7 years ago. She presented with abdominal pain, knee pain, and neurological symptoms, hypertension, chronic kidney disease, and anemia with basophilic stippling and lead gum lines. Compared to during her recent pregnancy, her lead level had almost tripled in 5 months to 81 mcg/dL. Chelation therapy was initiated and improved the patient’s symptoms and lead level significantly. In the absence of any new lead exposure or other reasons for increased bone turnover, this acute lead increase was likely due to skeletal mobilization caused by increased resorption from mineralized tissue during and after her pregnancy. This case report illustrates the seriousness of long-term health effects associated with lead poisoning at a multi-organ level, even years after the initial exposure. Thus, patient care should not be limited to the acute treatment of increased lead levels, but also include prevention of increased mobilization and bone turnover and appropriate patient education. In this context, we review various aspects of lead toxicity, especially during pregnancy and lactation.
PMCID: PMC2305731  PMID: 17562116
lead; toxicity; pregnancy; mobilization; gum line
11.  STUDIES IN LEAD POISONING: Comparison between different Laboratory Tests 
The urinary output of δ-aminolaevulic acid (ALA), coproporphyrins, and lead in 15 leadintoxicated workers was determined and correlated with the degree of intoxication. Raised levels of ALA in the urine show the best agreement with clinical evidence of intoxication.
In addition these values were correlated with the amount of lead excreted after treatment with a total dosage of 9 g. penicillamine. Weak correlations were found between therapeutically excreted lead and initial values for lead and coproporphyrin in urine. In contrast the initial values for ALA correlate very closely (P < 0·001). It is concluded that determinations of the output of ALA are to be preferred in the evalution of lead intoxication and that they point directly to the amount of metabolically active lead in the organism.
PMCID: PMC1069384  PMID: 5836572
12.  Moderate lead poisoning: trends in blood lead levels in unchelated children. 
Environmental Health Perspectives  1996;104(9):968-972.
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.
PMCID: PMC1469468  PMID: 8899376
13.  Primary prevention of lead poisoning in children: a cross-sectional study to evaluate state specific lead-based paint risk reduction laws in preventing lead poisoning in children 
Environmental Health  2014;13:93.
Children younger than 72 months are most at risk of environmental exposure to lead from ingestion through normal mouthing behavior. Young children are more vulnerable to lead poisoning than adults because lead is absorbed more readily in a child’s gastrointestinal tract. Our focus in this study was to determine the extent to which state mandated lead laws have helped decrease the number of new cases of elevated blood-lead levels (EBLL) in homes where an index case had been identified.
A cross-sectional study was conducted to compare 682 residential addresses, identified between 2000 and 2009, in two states with and one state without laws to prevent childhood lead poisoning among children younger than 72 months, to determine whether the laws were effective in preventing subsequent cases of lead poisoning detected in residential addresses after the identification of an index case. In this study, childhood lead poisoning was defined as the blood lead level (BLL) that would have triggered an environmental investigation in the residence. The two states with lead laws, Massachusetts (MA) and Ohio (OH), had trigger levels of ≥25 μg/dL and ≥15 μg/dL respectively. In Mississippi (MS), the state without legislation, the trigger level was ≥15 μg/dL.
The two states with lead laws, MA and OH, were 79% less likely than the one without legislation, MS, to have residential addresses with subsequent lead poisoning cases among children younger than 72 months, adjusted OR = 0.21, 95% CI (0.08-0.54).
For the three states studied, the evidence suggests that lead laws such as those studied herein effectively reduced primary exposure to lead among young children living in residential addresses that may have had lead contaminants.
PMCID: PMC4240897  PMID: 25380793
Children; Prevention; Law; Lead Poisoning
14.  Lead poisoning in a group of demolition workers. 
The incidence of lead poisoning in industry has fallen dramatically since the beginning of the twentieth century. This reduction has been partly attributable to increased awareness, improved ventilation and hygiene facilities, and technical changes which have allowed other substances to replace lead, but improved medical surveillance of workers exposed to lead in certain defined industries has also been important. Not all industries where lead exposure can occur are at present covered by specific regulations dealing with lead, however. We report the diagnosis and treatment of eleven oxyacetylene metal burners involved in the demolition of a railway station, who rapidly developed frank lead poisoning. The most suitable measurements to employ in evaluating such a population are considered. The selection, based on blood lead and haemoglobin measurements, of those who should receive further treatment is discussed. Symptoms were found to be more nearly related to indices of effect or toxicity of lead than to indices of exposure or absorption. The effects of chelation therapy upon symptoms, blood lead, haemoglobin and urinary porphyrins are recorded. The need for careful follow-up is illustrated.
PMCID: PMC1008280  PMID: 412513
15.  Human Arsenic Poisoning Issues in Central-East Indian Locations: Biomarkers and Biochemical Monitoring 
The study reports the use of three biomarkers i.e. total arsenic in hair and nails, total arsenic in blood, and total arsenic in urine to identify or quantify arsenic exposure and concomitant health effects. The main source of arsenic was inorganic exposure through drinking water. The arsenic levels and the health effects were analyzed closely in a family having maximum symptoms of arsenic. Based on the result of this study it is reported that there exist a correlation between the clinically observable symptoms, the blood and urine arsenic level, and the arsenic intake through drinking water. An intensive study on the urinary arsenic levels was carried out in which the urine levels of arsenic and the urine sufficiency tests were performed. A composite picture of body burden of arsenic has been obtained by carrying out a complete biochemical analysis of a maximum affected family. This confirms pronounced chronic exposure of the arsenic to these people. A combined correlation study on the arsenic levels measured in whole blood, urine, hair, nails and age present a remarkable outcome. Accordingly, the arsenic levels in blood are negatively correlated with the urine arsenic levels, which indicate either the inadequacy of the renal system in cleaning the blood arsenic or a continuous recirculation of the accumulated arsenic. This is an important conclusion about arsenical metabolism in humans. The study also raises the issues of the prospects of complete elimination of the accumulated arsenic and the reversibility of the health effects. Based on the work in Kourikasa village we report that there are very remote chances of complete purging of arsenic and thus reversibility of the health effects owing to various factors. The paper also discusses the various issues concerning the chronic arsenic poisoning management in the affected locations.
PMCID: PMC3719954  PMID: 17431310
Arsenic; biomonitoring; biochemical arsenic monitoring; central-east India
16.  A neurological and biochemical study of early lead poisoning 
ABSTRACT Changes in nerve conduction velocity were found in 94 workers exposed to lead in a battery factory compared with 94 age-matched controls. There was no clinical evidence of nerve damage in the lead workers. The mean blood lead concentration in the 94 lead workers was 2·9 μmol/l (60 μg/100 ml) and their length of exposure to lead ranged from 6 months to 33 years.
All mean maximum motor nerve conduction velocities (MMCV) measured were highly statistically significantly lower in the lead-exposed group when compared with their age-matched controls. Thus mean ulnar MMCV was 53·4 m/s in lead workers and 55·6 m/s in control subjects (p < 0·0005); mean median MMCV was 55·9 m/s in lead workers and 57·3 m/s in control subjects (p < 0·01); mean radial MMCV was 63·9 m/s in lead workers and 71·1 m/s in control subjects (p < 0·0005); mean peroneal MMCV was 46·1 m/s in lead workers and 47·6 m/s in control subjects (p < 0·005).
The amplitude of the muscle action potential produced by proximal stimulation of a nerve was expressed as a percentage of the amplitude of the muscle action potential produced by distal stimulation and the percentage amplitude thus obtained used as an indicator of the conduction velocity of slower fibres (SFCV). Peroneal nerve percentage amplitude of lead workers was statistically significantly lower (p < 0·005) than in the control group (means 86·6% and 90·3% respectively). There were, however, no significant differences in the percentage amplitude in the ulnar and median nerves. It is suggested that percentage amplitude is an inappropriate indicator of SFCV in ulnar and median nerves.
There was no statistically significant correlation to indicate that progressive slowing of nerve conduction (MMCV and SFCV) was associated with increasing exposure to lead (as indicated by blood and urine lead concentrations) or with the commonly measured biochemical changes associated with disturbed haemopoiesis in lead exposure (δ-aminolaevulinic acid dehydrase; free erythrocytc protoporphyrin; haemoglobin and urinary δ-aminolaevulinic acid). MMCV of the ulnar nerve was the only conduction velocity statistically significantly correlated with length of exposure to lead. Increased length of exposure to lead was associated with a decrease in the ulnar MMCV.
Only 13 of the subjects had been exposed to lead for two years or less and in none of them had the blood lead ever risen above 3·9 μmol/l (80 μg/100 ml) in three-monthly tests (mean blood lead concentration at time of testing: 2·8 μmol/l). In these subjects the MMCV of ulnar, radial, and peroneal nerves and the peroneal percentage amplitude were statistically significantly reduced. The results from this group suggest that the onset of nerve conduction changes occurs within two years and at concentrations of lead in blood of less than 3·9 μmol/l (80 μg/100 ml).
PMCID: PMC1008680  PMID: 7426463
17.  Current approaches of the management of mercury poisoning: need of the hour 
Mercury poisoning cases have been reported in many parts of the world, resulting in many deaths every year. Mercury compounds are classified in different chemical types such as elemental, inorganic and organic forms. Long term exposure to mercury compounds from different sources e.g. water, food, soil and air lead to toxic effects on cardiovascular, pulmonary, urinary, gastrointestinal, neurological systems and skin. Mercury level can be measured in plasma, urine, feces and hair samples. Urinary concentration is a good indicator of poisoning of elemental and inorganic mercury, but organic mercury (e.g. methyl mercury) can be detected easily in feces. Gold nanoparticles (AuNPs) are a rapid, cheap and sensitive method for detection of thymine bound mercuric ions. Silver nanoparticles are used as a sensitive detector of low concentration Hg2+ ions in homogeneous aqueous solutions. Besides supportive therapy, British anti lewisite, dimercaprol (BAL), 2,3-dimercaptosuccinic acid (DMSA. succimer) and dimercaptopropanesulfoxid acid (DMPS) are currently used as chelating agents in mercury poisoning. Natural biologic scavengers such as algae, azolla and other aquatic plants possess the ability to uptake mercury traces from the environment.
PMCID: PMC4055906  PMID: 24888360
Mercury compounds; Chelating agents; Poisoning; Gold nanoparticles; Natural biologic scavengers
18.  Electroencephalographic studies on petrol intoxication: comparison between nonleaded and leaded white petrol 
Saito, K. (1973).British Journal of Industrial Medicine,30, 352-358. Electroencephalographic studies on petrol intoxication: comparison between nonleaded and leaded white petrol. The effect of nonleaded and leaded petrol on the brains of rats was studied electroencephalographically. Bipolar electrodes were implanted on the brain surface between the frontal and occipital lobes of the left hemisphere. The rats were divided into two groups and were given by intraperitoneal injection 1 ml of either nonleaded white petrol (WP) or leaded petrol (LP) containing 1 000 ppm of tetraethyl lead per 100 g body weight. The electrocorticogram was observed for 10 days and the lead content of the brain, liver, and kidney was estimated.
The rats injected with leaded petrol showed excessive tension and excitement by the sixth or seventh day, and their body weight had diminished significantly by 10 days. One to three days after both LP and WP injection, the δ, θ, and α waves decreased significantly but the electrocorticogram from six or seven days after LP injection showed marked α and θ waves. The lead content in organs of the LP group was far greater than in those of the WP group and a correlation between the electrocorticogram and lead content was recognized.
PMCID: PMC1069475  PMID: 4753718
19.  Environmental Lead Exposure in Polish Children: Blood Lead Levels, Major Sources and Principles of the Lead Poisoning Prevention 
In Poland, children are exposed to lead from the combustion of leaded gasoline and industrial processes. Since the early 1990s, emission levels have declined, and a ban on leaded petrol is anticipated in 2005. Major industrial sources are located in Silesia Province and the copper mining centre (Legnica region). Concerns about, lead exposure in children date back to the 1980s; mean blood lead levels (BILL)reported in children living near lead smelters in Silesia exceeded 20ug/dl. in the 1990s, mean BLLs were decreasing, both in urban children and those living near lead industry. Lower than the CDC action level of 101ug/dl, they were however higher than mean values in children from the other countries, where leaded gasoline had already been banned. Childhood lead poisoning prevention requires a comprehensive approach, involving different sectors. Medical prevention focuses on the early detection of exposed child by the blood lead testing and individual case management. An increasing body of evidence, indicating adverse effects even below the current “safe” level of 101ug/dl, argues for intensification of the primary prevention, which requires legal, economic and technical measures. Public health efforts should contribute to the reduction and elimination of sources of exposure in child’s environment and public education campaigns.
PMCID: PMC2267063  PMID: 18365064
20.  Counseling to prevent childhood lead poisoning. 
Excessive lead exposure continues to be a pervasive and serious threat to the health and well-being of the nation's children. The current guidelines issued by the Centers for Disease Control and Prevention (CDC) recommend education (during well-child visits) regarding the major preventable sources of lead and how to prevent excessive exposure. To determine if parents receive counseling to prevent excessive lead exposure in their children, a survey of parental knowledge on prevention of lead exposure was administered to parents of children recently identified as having elevated blood lead levels. Surveys were administered by lead program outreach workers prior to an educational visit in urban neighborhoods of Boston, Massachusetts. Parents of 139 children (88% ethnic minorities; mean age: 31 months) with recently identified elevated blood lead levels (mean: 1 mumol/L) participated. Fifty-one percent first learned of their child's elevated lead level at the time they were contacted by an outreach worker. Seventy-one percent did not recall having been counseled regarding lead poisoning or its prevention prior to this contact. Before the outreach visit, 17% had been counseled but after the elevated lead was detected. Only 12% of the parents had received preventive counseling prior to detection of the elevated lead level. We conclude that despite CDC recommendations, adequate counseling for preventing lead poisoning does not occur for a substantial number of children who have elevated lead levels.
PMCID: PMC2608075  PMID: 8803429
21.  Biological Fractionation of Lead Isotopes in Sprague-Dawley Rats Lead Poisoned via the Respiratory Tract 
PLoS ONE  2012;7(12):e52462.
It was considered that lead isotope ratios did not change during physical, chemical, or biological processes. Thus, lead isotope ratios have been used as fingerprints to identify possible lead sources. However, recent evidence has shown that the lead isotope ratios among different biological samples in human are not always identical from its lead origins in vitro. An animal experiment was conducted to explore the biological fractionation of lead isotopes in biological systems.
24 male Sprague-Dawley (SD) rats were divided into groups that received acute lead exposure (0, 0.02, 0.2, or 2 mg/kg body weight of lead acetate) via the respiratory route every day for 5 days. Biological samples (i.e., blood, urine, and feces) were collected for comparison with the lead acetate (test substance) and the low-lead animal feed (diet) administered to the rats. The lead isotope ratios were determined by inductively coupled plasma mass spectrometry (ICP-MS).
There are significant differences (p<0.05) in lead isotope ratios between blood, urine, and feces. Moreover, a nonlinear relationship between the blood lead concentration and the blood lead isotope ratios was observed. There is also a threshold effect to the fractionation function. Only the blood isotope ratio of 204Pb/206Pb matches the test substance well. As for feces, when 204Pb/206Pb ratio is considered, there is no significant difference between feces-test substance pairs in medium and high dose group.
The biological fractionation of lead isotopes in SD rats was observed. Moreover, there might be a threshold for the biological fractionation of lead isotopes which is depending on whole blood lead level. It is considered to be more reliable that we compared the isotope ratios of potential lead hazards with both blood and feces lead fingerprints especially for 204Pb/206Pb ratio under high-dose exposure.
PMCID: PMC3530463  PMID: 23300678
22.  A Case of Lead Poisoning due to a Mixture of Talisman Ash 
Lead is a metal that has no biological function useful for the human body. In Korea, non-occupational exposure to lead has mostly occurred through taking oriental medicine. However, in this paper we report a case of lead poisoning caused by ingesting talisman material.
Case presentation
A 16-year-old male patient complained of severe abdominal pain after taking cinnabar, a talisman material. He was diagnosed with lead poisoning accompanied by acute hepatitis. We confirmed that the cinnabar the patient took contained about 10% elemental lead. After symptom management, the patients’ symptoms, liver function test results, and blood lead concentration level improved.
Lead poisoning can be accompanied by hepatitis, although rarely. As we have confirmed that cinnabar as a talisman material is harmful to the human body, measures to prevent its misuse are needed.
PMCID: PMC3923338  PMID: 24472628
Lead poisoning; Talisman; Cinnabar; Acute hepatitis
23.  Severe Neurotoxicity Following Ingestion of Tetraethyl Lead 
Journal of Medical Toxicology  2010;6(1):31-34.
Organic lead compounds are potent neurotoxins which can result in death even from small exposures. Traditionally, these compounds are found in fuel stabilizers, anti-knock agents, and leaded gasoline. Cases of acute organic lead intoxication have not been reported for several decades. We report a case of a 13-year-old Iraqi male who unintentionally ingested a fuel stabilizer containing 80–90% tetraethyl lead, managed at our combat support hospital. The patient developed severe neurologic symptoms including agitation, hallucinations, weakness, and tremor. These symptoms were refractory to escalating doses of benzodiazepines and ultimately required endotracheal intubation and a propofol infusion. Adjunctive therapies included chelation, baclofen, and nutrition provided through a gastrostomy tube. The patient slowly recovered and was discharged in a wheelchair 20 days after ingestion, still requiring tube feeding. Follow-up at 62 days post-ingestion revealed near-resolution of symptoms with residual slurred speech and slight limp. This case highlights the profound neurotoxic manifestations of acute organic lead compounds.
PMCID: PMC3550442  PMID: 20306169
Organic lead; Tetraethyl lead; Poisoning; Chelation
24.  Nephropathy in Chronic Lead Poisoning 
This paper presents a study of renal function in 102 patients with lead poisoning admitted to the Occupational Diseases Clinic in Bucharest during the past 10 years; nearly half the patients had no history of lead colic. Every possible cause of renal damage, other than lead, was excluded by a careful differential diagnosis.
Renal function was investigated by repeated determinations of blood urea, creatinine and uric acid, urea clearance, and endogenous creatinine clearance tests.
Significant decreases of the clearance values (less than 50 ml./min. urea clearance and less than 80 ml./min. creatinine clearance), persistent high blood urea (more than 50 mg./100 ml.), and high blood creatinine (more than 1·2 mg./100 ml.) were found in a significant number of cases. These signs of impaired renal function were more frequent in the group of patients with chronic lead poisoning who had had several episodes of colic and an occupational exposure of more than 10 years. A high blood pressure was also found more frequently in this group of patients.
Undercompensated and decompensated renal failure was found in 17 patients, most of whom had been exposed to lead for more than 10 years and had a history of several attacks of colic. Arterial hypertension accompanied the chronic renal failure in 13 patients, the renal impairment generally preceding the rise in blood pressure by several years.
The duration of occupational lead exposure, the high absorption in the past, and the long period of observation of these patients, most of whom were repeatedly hospitalized, may explain the relatively high incidence (17 cases) of nephropathy with chronic renal failure in the present group.
Impairment of urea clearance seems to be the earliest sign, at a time when the creatinine clearance is still normal. As the duration of exposure lengthens and the patient is subjected to active episodes of poisoning the creatinine clearance also deteriorates. Persistent urea retention and high creatininaemia may follow in time, accompanied rather frequently by arterial hypertension. A study of some of the cases followed for several years demonstrated this progressive evolution of lead nephropathy.
A functional and transitory impairment of renal function is very probably caused by an impairment of intrarenal circulation, resulting from marked vasoconstriction of the renal vessels, forming part of the generalized vasoconstriction of lead poisoning. Prolonged exposure and frequently recurring episodes of acute poisoning may lead to progressive impairment of renal function and to the development of organic lesions.
Special attention should be paid to renal function tests in all cases with prolonged exposure to lead in order to prevent the development of severe lead nephropathy.
PMCID: PMC1008772  PMID: 5663423
25.  Evaluation, diagnosis, and treatment of lead poisoning in a patient with occupational lead exposure: a case presentation 
Amongst toxic heavy metals, lead ranks as one of the most serious environmental poisons all over the world. Exposure to lead in the home and the workplace results in health hazards to many adults and children causing economic damage, which is due to the lack of awareness of the ill effects of lead. We report the case of a 22 year old man working in an unorganized lead acid battery manufacturing unit, complaining about a longer history of general body ache, lethargy, fatigue, shoulder joint pain, shaking of hands and wrist drop. Patient had blue line at gingivodental junction. Central nervous system (CNS) examination showed having grade 0 power of extensors of right wrist & fingers. Reflexes: Supinator- absent, Triceps- weak and other deep tendon reflexes- normal. Investigations carried out during the admission showed hemoglobin levels of 8.3 g/dl and blood lead level of 128.3 μg/dl. The patient was subjected to chelation therapy, which was accompanied by aggressive environmental intervention and was advised not to return to the same environmental exposure situation. After repeated course of chelation therapy he has shown the signs of improvement and is on follow up presently.
PMCID: PMC2000868  PMID: 17718907

Results 1-25 (1222734)