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PubMed2003

Preventing lead poisoning in children: can the US experience inform other countries? The case of Poland.

Exposure to excess lead during childhood is preventable, but nowhere has that goal been achieved. In the US, recommendations for prevention of childhood lead poisoning are issued by the Centres for Disease Control and Prevention, based on periodically updated population-based data on the prevalence of lead poisoning by age and blood lead level. A well developed public health infrastructure is to provide case management to the lead exposed children. In Poland, the social and economic transitions of the last decade changed the potential for childhood lead exposure, and there has been a profound restructuring of the health care system. Blood lead testing in children is performed outside the primary care. Data on blood lead levels are not collected and analysed centrally. The range of follow-up services may differ among the regions, depending on the local expertise. An updated approach to prevention of childhood lead poisoning, making better use of the existing expertise and involving primary care providers, needs consideration. Complex public health programs like this of lead poisoning prevention cannot be transplanted whole to other countries. However, experiences gained by the US might provide valuable suggestions for others, even though the US policy has flaws and is not fully implemented. Discussing proposal for Poland in light of the current US practice highlights the necessity of reliable estimates of the exposed population for rational policy. It also helps to define research questions relevant to public health practice in Poland, and confirms that prevention of lead poisoning in children requires the coordinated work of different professionals.

Child↗
PubMed2006

Epidemiologic investigation of lead poisoning in trumpeter and tundra swans in Washington State, USA, 2000-2002.

An observational study was conducted to determine the proportionate mortality of wild trumpeter (Cygnus buccinator) and tundra (Cygnus columbianus columbianus) swans that died during the winters of 2000-02 in northwestern Washington State, USA. Among 400 swans necropsied, 81% were lead poisoned (302/365 trumpeter swans; 20/35 tundra swans). Mortality started in mid-November and peaked from late December through mid-February; swan mortality that was not associated with lead poisoning was uniformly lower throughout the winter months. Lead poisoning was 24 times more likely to be the cause of death in swans found in Whatcom County compared to swans found in other locations in northwestern Washington State (95% CI: 12.7, 47.0). Mortality attributable to lead poisoning was twice as likely in adults as in juveniles (95% CI: 1.0, 4.2). Aspergillosis was documented in 62 trumpeter and two tundra swans, including 37 swans in which mortality was caused by lead poisoning. Males were twice as likely as females to have aspergillosis (95% CI: 1.1, 3.8). Traumatic injuries were documented in 37 trumpeter and seven tundra swans, including seven trumpeter swans with concurrent lead poisoning. Dead swans found outside Whatcom County were four times more likely to have traumatic injuries compared to those found in Whatcom County (95% CI: 1.6, 10.0). Overall, lead-poisoned swans were significantly less likely to have concurrent aspergillosis or traumatic injuries. There was no apparent association between grit ingestion (total mass or mass categorized by size) and lead poisoning or number of lead shot. Not surprisingly, lead-poisoned swans were more likely to have one or more lead shot compared to swans that died from other causes (OR 294; 95% CI: 92, 1,005); lead-poisoned swans were also more likely to have one or more nontoxic shot compared to swans that were not poisoned (OR 63; 95% CI: 19, 318). The source(s) of shot are unknown but likely are in or near Whatcom County, Washington.

Animals↗
PubMed2001

Primary prevention of childhood lead poisoning through community outreach.

BACKGROUND: The prevalence of childhood lead poisoning has substantially decreased in Milwaukee, Wisconsin over the past decade. Nevertheless, by the mid 1990s, 30% of children were still found to have elevated blood levels. OBJECTIVE: To extend the reach of the Milwaukee Health Department (MHD) to previously underserved families in 1 inner city neighborhood with extremely old housing, the Sixteenth Street Community Health Center (SSCHC) implemented, in 1995, the Community Lead Outreach Project (CLOP). Going door-to-door, CLOP attempted to identify children 6 months to 6 years old with elevated blood lead levels (BLL), referring those > or = 20 micrograms/dL to MHD and enrolling those with BLLs 10-19 micrograms/dL in a program of prevention education and environmental clean-up with the specific aim of preventing BLLs increasing to 20 micrograms/dL and above. METHODS: A team of community outreach workers led by a nurse-coordinator visited, over a 4-year period, families in their homes in 13 census tracts surrounding the SSCHC. During the home visits, capillary blood samples for BLLs were drawn, environmental assessments and scoring were conducted, lead poisoning prevention education provided and repair and cleaning of household lead hazards demonstrated. For control and comparison, BLL data for the entire city by ZIP Code and provider were obtained from the Milwaukee Health Department. Odds ratios for changes in the proportions of children screened > or = 10 micrograms/dL were calculated and compared for the years 1996 through 1999. The odds ratios of changes for various populations were compared for significant differences using tests of homogeneity. To control for age confounding, proportions of elevated BBLs for all groups and for all years were age-standardized, using the direct method. RESULTS: Over the entire study, 20.9% of the children screened had BLLs > or = 10 micrograms/dL and 3.0% were > or = 20 micrograms/dL. For 395 children with BLLs 10-19 micrograms/dL enrolled in the CLOP follow-up program, the mean BLL was 12.9 micrograms/dL. Mean levels at the first, second and third follow-up visits were 10.8, 10.3 and 9.8 micrograms/dL respectively, showing an overall decline of 3.1 micrograms/dL or 24%. At the first follow-up visit, 97% of the children tested were < 20 micrograms/dL while 76% were < 10 micrograms/dL. By the second follow-up visit, 100% were < 20 micrograms/dL. Initial environmental scores averaged 24.7, declining to 19.0 at first, 17.8 at second and 14.8 at third follow-up visits. For the entire CLOP population, the proportion of children testing > 10 micrograms/dL declined each year from 46.3% in 1996 to 22.5% in 1999. The geographic area in which CLOP operated recorded the highest screening penetration rate in the city: 61%. The odds ratio for CLOP clients to have elevated blood lead levels at the end of the study period, in contrast with the beginning, was 0.34 compared to 0.55 for the entire city and 0.75 for private physicians serving the same general population. Comparison of odds ratios showed the CLOP target population enjoyed a decrease in rate of elevated BLL 1.6 times that of the city-wide average, p-value = 0.016 and more than double that of the patients of area private providers. CONCLUSIONS: We conclude that the Sixteenth Street Community Health Center Childhood Lead Outreach Project has successfully accessed populations of children with high rates of lead poisoning who had escaped more traditional screening venues and effectively intervened to reduce their BLLs to < 10 micrograms/dL. Moreover, CLOP produced impressive and unanticipated primary prevention benefits in the community at large. The demonstrated ability of community outreach workers to access high-risk populations and reduce exposure to lead hazards suggests the potential of this strategy for extension to other geographic areas, to the patients of private physicians and to address other prevalent, urban health problems like asthma, injuries and violence.

Child↗
PubMed2006

Adverse effects of childhood lead poisoning: the clinical neuropsychological perspective.

Elevated blood lead levels in children can result in brain injury and, as a consequence, have negative effects on cognitive functioning and behavior. Risk assessment studies have focused on psychological measures, especially IQ, and also school achievement and behavioral adjustment as endpoints. Such studies, like epidemiological work in other areas, by necessity examine effects in large groups rather than in individuals. Since the peer-reviewed literature primarily describes those adverse effects noted in epidemiological studies, little or no attention has been directed to what is observed in the individual. The present review describes the presentation of individual lead-poisoned children from the perspective of the clinical neuropsychologist. The sequelae of lead poisoning typically observed in evaluation of individuals provide information in addition to that gained from risk assessment studies and has implications for the mechanisms and treatment of this disease. In addition, attention to certain aspects of individual case presentation does provide information relevant to issues of public health.

Child↗
PubMed1984

Free erythrocyte protoporphyrin (FEP) and zinc protoporphyrin (ZnP) as biological parameters for lead poisoning.

Lamola et al. (1974) reported that free erythrocyte protoporphyrin (FEP) is not present as free type protoporphyrin ( FPP ) but rather is chelated with zinc in lead poisoning and iron deficiency anemia. In our fluorometric study of FEP and zinc protoporphyrin ( ZnP ) in erythrocytes of lead-poisoned rabbits and lead workers, the co-existence of ZnP and FPP was observed in the severe stage of acute lead poisoning in rabbits. The ratio of ZnP to FEP in erythrocytes decreased with the progress of lead intoxication, and the amount of FPP was greater than that of ZnP in the severe stage of intoxication. This FPP accumulated in the erythrocytes was easily converted to ZnP by incubation of the hemolysate with zinc. On the other hand, increased protoporphyrin (PP) in bone marrow was present as FPP in lead intoxication. From these results, ZnP in peripheral erythrocytes is considered to be a secondary product, not a primary one. Therefore, the determination of total FEP ( FPP + ZnP ) by the acid solvent extraction method might be more reasonable than using ZnP -determination as the biological parameter of lead poisoning. We propose that erythrocyte porphyrin in lead intoxication should be expressed as FEP, not as ZnP , for the parameter. The present study also suggests that the form of erythrocyte FPP in erythropoietic protoporphyria (EPP) patients is a little different from that in lead-poisoning patients, because of its high chelation reactivity with zinc.

Anemia, Hypochromic↗
PubMedDate not supplied

An overview of the laboratory diagnosis of lead poisoning.

Four tests for the evaluation of lead poisoning are reviewed from both the clinical and methodological aspects. Whole blood or erythrocyte lead measurements appear to provide the best means of assessing the bodily burden of lead with electrothermal and Delves cup flame atomic absorption spectorphotometric techniques providing accurate and precise results. Urine lead is less reliable as a screening test for lead poisoning but is excellent for monitoring the course of ethylenediamine tetraacetic acid (EDTA) therapy. Atomic absorption methods for urine are made difficult by the variable matrix of urine but satisfactory electrothermal and flame procedures have been described. Erythrocyte delta-aminolevulinic acid dehydratase activity is a very sensitive index of lead exposure,--perhaps too sensitive. Analytical procedures for measuring this enzyme are subject to errors and many complicating factors such as lack of stability of the specimen limit the usefulness of the test. Urine delta-aminolevulinic acid is of questionable value as a screening procedure and also is subject to analytical problems.

Clinical Enzyme Tests↗
PubMed1986

Lead poisoning from retained missiles. An experimental study.

The problem of lead poisoning from bullets has been investigated by surgically implanting discs of lead, each enriched in a different natural isotope, into the tissue of two mongrel dogs and monitoring by mass spectrometry the release of the lead into each animal's blood over the course of 3 years. Lead placed in the knee underwent vigorous attack by the synovial fluid, far in excess of what would be expected from corrosion theory, and reached a maximum concentration in blood 4-6 months after operation. Thereafter, lead concentration exponentially declined as the remaining fragments became encapsulated. The disc placed in muscle was sparingly soluble immediately following implantation. It is concluded that the greatest danger of lead poisoning from an injury involving many fragments having collectively a large surface area will occur within a month, and that the cases of lead poisoning resulting from bullets in joints that occur 5 or more years after injury are caused by continual wear of metal on a joint surface, storage of lead so released in the skeleton, and its subsequent resorption during a change in osteocyte activity.

Animals↗
PubMed1999

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.

Adolescent↗
PubMed1975

Acute lead poisoning: Five cases resulting from self-injection of lead and opium.

Five cases of acute lead poisoning resulted from the self-injection of lead and opium pills which were crushed, heated and suspended in water. Two of the five patients died of illnesses in which hepatic failure and reversible acute tubular necrosis were prominent features. One of these two had a severe neuropathy, with flaccid quadriplegia and respiratory paralysis. The other three patients had relatively minor symptoms but unequivocal biochemical evidence of lead toxicity. Autopsy changes included hepatic degeneration with inclusion bodies, regenerating renal tubular epithelium and wasting of skeletal muscle. Hepatic lead content was extremely high in one case. Chelation therapy in the other fatal case resulted in a fall in blood lead to within normal limits and a clinical improvement, which was terminated by massive haemorrhage from a ruptured innominate artery.

Acute Disease↗
PubMed1983

[Heme synthesis and iron turnover in rabbits with experimental lead poisoning].

The nature of anemia formation in lead poisoning is still unknown, especially of its mechanism. Rimington proposed a hypothesis that lead interferes with a specific enzyme (ferrochelatase) system, which is responsible for incorporating iron into the protoporphyrin IX molecules to form heme. In the present study, heme synthesis in mitochondria (Mt) of liver and bone marrow, and 59Fe behavior in vivo were investigated in rabbits to verify his hypothesis. The experimental five groups were as follows: 1) lead (Pb) poisoning by administration of 10-20 mg Pb/kg at a time, subcutaneously injected 10 times in all during 30 days, 2) phenylhydrazine (PH) poisoning, 10 mg PH/kg, 3 times subcutaneously during 3 days, 3) bleeding of about 105 ml of blood in total by venesection through 7 times treatments, 4) low feeding, synthetic feeding pellets of 30 g/d/cap. or 70 g/d/cap. 5) control, by administration of 5% glucose instead of lead injection with 120 g/d/cap. of the feeding pellets, with drinking water 300 ml/d/cap. for 30 days. 59Fe-plasma was prepared by the following procedure: 5 ml of plasma from each rabbit having been incubated with 5 microCi of 59Fe citrate at 37 degrees C for 30 minutes, 59Fe-plasma was purified partially by Borova's method. The prepared 59Fe-plasma was injected intravenously into the rabbits in each group. Urinary coproporphrin (CP-U), erythrocyte protoporphyrin (FFP), Hb, Ht, MCHC, reticulocyte (Rt), and protoheme formed by Mt, were determined to examine the relationship between lead and porphyrinheme metabolism. 59Fe behavior was estimated by detecting the plasma iron disappearance rate (half life time of 59Fe in plasma), 59Fe intake into erythrocytes, and the retention of 59Fe in tissues. Increase of FEP in lead poisoning was not caused by hemolysis, because FEP did not increase in PH group (Table 1). CP-U slightly increased in PH group, but not in the bleeding group (Table 2). This increase of CP-U must be due to acceleration of hematopoiesis in PH poisoning, because PH and bleeding groups showed an increase of Rt, counting 222.2 and 85.3%, respectively, at the termination of the treatment, while the Pb group did not show any obvious reticulocytosis (Table 3). PH, bleeding, and Pb(10 mg/kg) groups showed shorter half life time of 59Fe in plasma, while the 30 g/d-feeding group showed longer time (Table 8). During 100 minutes after 59Fe injection, incorporation of 59Fe into erythrocytes was higher in PH and bleeding groups than those in other treatment groups and the control (Table 9).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Lessons from a primary-prevention program for lead poisoning among inner-city children.

This study evaluated the impact on childhood lead poisoning of a primary-prevention educational-intervention program for pregnant women in St. Louis, Missouri. The women were predominantly poor and of African-American, Hispanic, Asian, and Caucasian backgrounds. The interventions, tailored for each woman on the basis of responses to a survey and environmental measurements, included case management with hands-on instruction on cleaning techniques, property maintenance, hygiene, and nutrition to reduce exposure of newborns to lead. It was hypothesized that the probability of lead poisoning (blood lead levels greater than 10 microg/dL) would be reduced among mothers who received the interventions compared with those who received only printed educational material. Contrary to expectations, none of the interventions reduced the likelihood of lead poisoning among participating children. In the process of the study, however, a number of valuable lessons related to recruitment and commitment of participants emerged that can inform future efforts of this nature.

Environmental Exposure↗
PubMedDate not supplied

Lead poisoning in upland-foraging birds of prey in Canada.

We examined the degree of lead exposure, based on tissue-lead concentrations, in 184 raptors of 16 species found dead across Canada. The most prevalent species available for examination were Red-tailed hawks, Great horned owls, and Golden eagles (n = 131). The majority of individuals examined had very low lead accumulation, however 3-4% of total mortality in these 3 most commonly encountered species was attributed to lead poisoning. In addition, 1 of 9 Bald Eagles found dead far from aquatic environments was lead poisoned; and a single Turkey Vulture had a highly elevated bone-lead concentration (58 microg/g dry weight). Evidence from our study, along with other published research, indicates that upland-foraging birds of prey and scavengers that typically include game birds and mammals in their diets, are at risk for lead poisoning from the ingestion of lead projectiles from ammunition used in upland hunting. The use of non-lead ammunition for hunting upland game would effectively remove the only serious source of high lead exposure and lead poisoning for upland-foraging raptors.

Animals↗
PubMed1989

[Lead poisoning in two families from a car battery workshop].

Lead poisoning resulting from exposure to lead in a domestic car battery workshop is reported in 10 children in 2 families. 2 girls, aged 2 10/12 and 1 8/12 years, respectively, from 1 of the families were hospitalized for investigation of nausea, vomiting, progressive muscular weakness and peripheral neuropathy. Serum lead levels were 52 and 49 mcg/dl, respectively. Subsequent screening of all members of this family, as well as those of the other family who lived in the same house, revealed abnormally elevated levels of serum lead in all the members of both families. The 2 girls were treated with chelating agents and improved clinically and their serum lead levels decreased to 29 and 34 mcg/dl, respectively. The domestic workshop was closed and the 2 families moved to another neighborhood. These cases illustrate the need to screen all family members and contacts of patients with lead poisoning, as well as the hazards of the uncontrolled use of lead in domestic workshops.

Chelating Agents↗
PubMed1991

Residential deleading: effects on the blood lead levels of lead-poisoned children.

Acute elevations of venous blood lead levels (PbB) are periodically reported in children with chronic lead poisoning, during deleading of their houses. To evaluate this phenomenon 114 preschool children who entered the Massachusetts Childhood Lead Poisoning Prevention Program case management system during 1984 and 1985 were retrospectively studied. PbB increased from a mean (+/- SE) of 1.76 +/- 0.03 mumol/L (36.4 +/- 0.6 micrograms/dL) prior to deleading to 2.03 +/- 0.07 mumol/L (42.1 +/- 1.5 micrograms/dL) during deleading (P less than .001). Among 41 subjects for whom deleading was done by dry scraping and sanding, the mean mid-deleading PbB was higher than the pre-deleading PbB by 0.44 +/- 0.12 mumol/L (9.1 +/- 2.4 micrograms/dL). However, when deleading was done by covering or replacement of painted surfaces in the residences of 12 subjects, mid-deleading PbB decreased 0.11 +/- 0.12 mumol/L (2.25 +/- 2.4 micrograms/dL) (P less than .005). In a subset of 59 subjects who had no chelation therapy and were available for follow-up 250 +/- 14 days after completion of deleading, PbB had decreased from 1.72 +/- 0.04 mumol/L (35.7 +/- 0.9 micrograms/dL) to 1.24 +/- 0.04 mumol/L (25.5 +/- 0.9 micrograms/dL) (P less than .001). The long-term effect of deleading is a significant reduction in PbB. However, deleading resulted in a significant, albeit transient, increase in PbB.

Age Factors↗
PubMed1976

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

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

Acetylglucosaminidase↗
PubMedDate not supplied

Management of childhood lead poisoning: clinical impact and cost-effectiveness.

OBJECTIVES: No consensus exists regarding the preferred treatment of childhood lead poisoning. The authors used decision analysis to compare the clinical impacts and cost-effectiveness of four management strategies for childhood lead poisoning, and to investigate how effective chelation therapy must be in reducing neuropsychologic sequelae to warrant its use. METHODS: The model was based on a 2-year-old child with moderate lead poisoning [blood lead level 1.21 to 1.88 mumol/L (25 to 39 micrograms/dL)]. The following strategies were compared: 1) no treatment; 2) EDTA provocation testing, followed by chelation if testing is positive (PROV); 3) penicillamine chelation with crossover to EDTA provocation testing if toxicity occurs (PCA); 4) EDTA provocation testing with crossover to penicillamine chelation if testing is negative (EDTA). RESULTS: The EDTA and PCA strategies prevented 22.5% of the cases of reading disability and resulted in an increase of 1.02 quality-adjusted life years compared with no treatment. When the costs of outpatient EDTA testing and chelation are considered, the EDTA strategy is more cost-effective than the PCA strategy; when inpatient costs are considered, the PCA strategy becomes more cost-effective. When costs of remedial education are considered, all strategies are cost-saving compared with no treatment if chelation reduces the risk of lead-induced reading disability by more than 20%. CONCLUSIONS: Treatment strategies for childhood lead poisoning vary in clinical impact, cost, and cost-effectiveness. Chelation of the 1.4% of United States preschoolers whose blood lead levels are 2.21 mumol/L (25 micrograms/dL) or higher could prevent more than 45,000 cases of reading disability, and save more than $900 million per year in overall costs when the costs of remedial education are considered.

Chelation Therapy↗
PubMedDate not supplied

Primary prevention of childhood lead poisoning: a goal for the 1990s.

Childhood lead poisoning remains a common problem in America today. The U.S. Department of Health and Human Resources has recently released a strategic plan on eliminating childhood lead poisoning, and health care professionals should become familiar with the basic elements of the plan.

Child, Preschool↗