[Paralysis of the arms due to lead poisoning occurring a year after exposure to lead; fraudulent prolongation of the poisoning or excessive activity of lead due to therapy].
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OBJECTIVE: To evaluate the effectiveness of parental education on reducing lead exposure of children by examining the changes in blood lead levels of children whose parents receiving or not receiving educational intervention. METHODS: Two hundred children with confirmed blood lead levels beyond 100 microg/L were selected. They were randomized into two groups, 107 children in study group and 93 in control. At the beginning of the study, parents of both study and control groups were called for interview to complete KABP questionnaire and lead study questionnaire. The study group was provided with interventional measures while control group was not contacted until the end of study. Intervention of parental education was undertaken by means of a TV program, a set of slides and a brochure, and focused on the questions regarding harmful effects of lead poisoning, the sources of environmental lead and prevention of this preventable disease. Tests for blood lead level were repeated for both study and control groups 3 months after the determination of the initial blood lead level. RESULTS: All the relevant knowledge of health effect, lead sources and prevention of childhood lead poisoning of participating parents of study group were improved significantly (chi(2) = 14.06, 13.07, 10.08, 28.26, P < 0.01) after educational intervention while parents control group also were significantly improved in the sub-catalogs of concept and prevention (chi(2) = 7.69, 8.64, P < 0.01), but not the health effect and sources of childhood lead poisoning. Children and parents' behavior in study group was improved accordingly and significantly. Less children ate popcorn (chi(2) = 4.08, P < 0.05), less children drank tap-water in the morning (chi(2) = 23.04, P < 0.01), more kids washed their hands before eating (chi(2) = 5.82, P < 0.05), less kids played on road side (chi(2) = 9.60, P < 0.01), and more parents changed their coat or took shower or washed hands before going home after work (chi(2) = 4.00, P < 0.05). But in the control group only the number of kids playing on road side was decreased significantly (chi(2) = 9.60, P < 0.01). A general decline in blood lead levels was detected in both groups with statistical significance at P < 0.01. However, the decrease in blood lead levels was more remarkable in the study group. There was average reduction of 55 microg/L (35%) in blood lead levels for study group (t = 4.979, P < 0.01) and an almost 33 microg/L (20%) for control (t = 3.398, P < 0.01). The reduction in blood lead level was 22 microg/L greater in study group (t = 3.531, P < 0.01). The study also showed that the effectiveness of the educational interventions depended upon various aspects. Fourteen variables were included in the stepwise multiple regression equation of blood lead level changes. Such as parents' occupational exposure to lead, the improvement of knowledge about prevention of childhood lead poisoning, the chang of habit of snacks intake, parents' education levels, the change of attitude of parents for the childhood lead poisoning, etc. CONCLUSION: Educating parents is proved to be an effective approach for children with mild and moderate lead poisoning.
Lead poisoning of unknown source was diagnosed histologically in 2 rhesus monkeys (Macaca mulatta) by finding acid-fast intranuclear inclusion bodies in the epithelial cells of renal cortical tubules. The presence of lead in the inclusions was determined by scanning electron microscopy/energy dispersive x-ray analysis using sections from paraffin embedded tissues. This observation indicates the usefulness of this technique for the detection and cellular localization of lead in tissues, even from archival material.
Lead (Pb) is everywhere in our environment and all children are exposed to lead to some degree. The Center for Disease Control (CDC) has recently declared that a blood lead level of 25 micrograms/dL and an erythrocyte protophoryrin of 35 micrograms/dL or above indicate an excessive absorption of lead in children and constitutes grounds for intervention. A study reported that about 780,000 (4%) of American children age 6 months to 5 years had blood lead levels of 30 micrograms/dL or higher. If the current level of 25 micrograms/dL had been used as a criterion in this study, the number of children involved would be much higher. It has been clearly stated by the American Academy of Pediatrics that ideally, all pre-school children should be screened for lead absorption by means of the erythrocyte protophoryrin test. The following is a review of lead poisoning in children and the serious consequences which may follow if it is not recognized early.
While lead poisoning among children is on the decline, it is still a serious health problem that affects an estimated 930,000 children between the ages of one and five. Baltimore health care providers have--with great success--turned to the tools of disease management to cut blood lead levels in children while simultaneously cutting overall costs.
Little attention was paid to lead poisoning in Norway before 1930. In 1931-33, however, Dr Harald Engelsen, a naval surgeon, reported to the National Insurance Administration more than 40 cases among shipyard workers. The first worker in which he diagnosed lead poisoning had consulted other doctors, but only got a symptomatic diagnosis. Dr Engelsen was then consulted by several others with similar symptoms. At the outset his diagnosis was doubted and a considerable disagreement ensued with colleagues and yard representatives; he was compared with Dr Stockmann in Henrik Ibsen's play An Enemy of the People. The controversy escalated. A commission appointed by the government to examine the matter concluded that there had been cases of lead poisoning in the shipyard, that mandatory requirements had not been strictly complied with, and that monitoring of working conditions had been fragmentary. Most of the workers were granted compensation and pensions. For a publication on lead poisoning, Dr Engelsen was awarded the University of Oslo's gold medal, and for his work for improving seamen's health and welfare he was awarded the St. Olav Order. In 1938 he was appointed head of medical services in the Royal Norwegian Navy.
In October 1991, the Centers for Disease Control issued new recommendations lowering the acceptable blood lead level. This change was based on data indicating that irreversible adverse neurodevelopmental effects occur in children with chronic low-level exposure to lead. The primary source of lead poisoning is still lead-based paint, particularly in older urban housing. Other sources of lead poisoning are also common. Almost all U.S. children are considered at risk of lead poisoning and should be screened for lead poisoning. Parents should be provided with information about potential sources of lead during routine well-child visits. Multidisciplinary efforts should be made to reduce all lead exposure. Oral chelation therapy on an outpatient basis is now available to treat less severe cases of lead poisoning.
This article identifies four culturally shaped sources of lead exposure in human societies: modern and historic technological sources: food habits; culturally defined health beliefs; and beauty practices. Examples of these potential sources of lead poisoning are presented from current cultures. They include the use of lead-glazed cooking pottery in Mexican-American households; folk medical use of lead in Hispanic, Arabic, South Asian, Chinese, and Hmong communities; as well as the use of lead as a cosmetic in the Near East, Southeast Asia, and South Asia. Four interacting cultural conditions that create barriers to the reduction of lead exposure and lead poisoning are identified and discussed. These are knowledge deficiencies, communication resistance, cultural reinterpretations, and incongruity of explanatory models.
In summary, LXRF estimates of Pb in tibial cortical bone have yielded highly relevant clinical data relating to the efficacy of chelation therapy with CaNa2EDTA in lead poisoned children; diagnostic approach(es) to childhood lead poisoning; and evaluations of exposure in children, teenagers, and adults in lead-exposed and non-lead-exposed suburban communities. It is anticipated that KXRF and LXRF estimates of Pb in bone will yield new information concerning the epidemiology of hypertension, osteoporosis, and the contribution of maternal Pb to the developing fetus. It would be premature to delineate the age-developmental time boundaries over which these two systems [KXRF, LXRF] can be viewed as operated optimally. Consequently, it is appropriate to view the two approaches as providing complementary information. All such information might, in fact, be required to obtain a complete exposure profile and a comprehensive framework for assessment of health risks.
Evaluation of occupational lead poisoning and resultant permanent work disability calls for a procedure which is not easy to conduct. This is because vague, non-manifest lead poisonings and transient pre-poisoning states have lately prevailed over clearly manifested, obvious lead poisonings as were found earlier due to unfavourable working conditions. A reason for this further lies in non-specific clinical symptoms of lead poisoning as well as in lack of a strict set of rules--especially when it comes to assessing biological indicators of abnormal lead absorption in the body--for experts in the disability assessment boards to go by. In view of that the conduct of those taking part in the evaluation procedure (general practitioner of patient's own choice and team of experts in pension and disability assessment boards) is analysed. Many assessments have been found deficient. An amendment to the rules for expert evaluation is proposed.
Lead poisoning, the leading environmental illness in this country, is a challenge to our health care and social systems. Because they provide routine health care in a variety of settings, including care to children from poor inner city families, who are most at risk for plumbism, nurse practitioners should be knowledgeable about this illness and prepared to care for children who have it. This article describes the role of a pediatric nurse practitioner in a specialty program who cares for children with lead poisoning and informs the general practitioner about prevention, education, treatment, coordination of care, and long-term follow-up for these children and their families.
Information pertaining to 294 cases of bovine lead poisoning that occurred during the 15-year period from 1968 to 1982 was collected from the toxicology laboratory records at the Western College of Veterinary Medicine. Lead poisoning was seen more often in younger cattle, with 51.9% of the cases reported in animals 6-months of age or less. A statistically significant seasonal incidence was seen (p less than 0.0001) with 60.9% of the cases occurring from May to August. Lead poisoning was more common in dairy breeds than beef breeds. The relative rates in the daily and beef breeds per 1,000 cattle were 0.022 and 0.0065 respectively. No specific breed susceptibility was associated with any of the major dairy or beef breeds. Statistically significant sex-related differences for lead poisoning were not seen (p = 0.11). The most suitable biological samples utilized to confirm lead poisoning were blood, kidney and liver. These samples produced the most reliable results, with rumen and fecal samples exhibiting a high degree of variability.
Lead poisoning and other causes of mortality of 115 trumpeter (Cygnus buccinator) and 21 tundra (C. columbianus) swans from northwestern Washington (USA) from 1986 to 1992 are reported. Necropsies were performed on all 136 swans, liver lead analysis conducted on 110, and differentiation between lead and steel shot pellets recovered from gizzards in 97 swans. Shot pellets were detected in 44 (32%) of 136 gizzards. Lead shot was recovered from 32 (33%) of 97 gizzards and steel shot from 16 (16%). Mean intensity of lead shot in gizzards was nearly five times greater than steel shot. Thirty-nine (35%) of 110 livers had lead concentrations diagnostic of lead poisoning (> 6 ppm, wet weight). Mean (+/- SE) weight for 61 non-lead poisoned trumpeter swans was 9.8 (+/- 0.30) kg, significantly heavier (P < 0.05) than 30 lead poisoned trumpeters (mean = 6.8 +/- 0.23 kg). There was no significant difference (P > 0.05) in weights between lead poisoned (n = 9) and non-lead poisoned (n = 12) tundra swans. Lead poisoning was the primary cause of death, accounting for 29% of the mortalities. Other causes of mortality identified were aspergillosis (17%), illegally shot (11%), and other traumatic factors (12%). The cause of death for 43 swans was not determined. Lead poisoning from the ingestion of lead shot continues to be a principal cause of mortality in swans overwintering in northwestern Washington.
Lead poisoning remains a common environmental threat for children today. The majority of cases of lead poisoning are caused by oral intake of lead dust or lead-containing paint flakes and thus occur during the second and third years of life. An unusual case of severe lead poisoning in a breast-feeding infant girl is here presented; the source proved to be a nipple shield made of a lead-containing metal. Despite the severity of the intoxication, by the end of treatment and for a year afterwards the infant has been well and her psychokinetic development has been normal.
Childhood lead poisoning is characteristically a disease that occurs between the second and third years of life, generally resulting from the child's ingestion of lead-based paint or dust. However, lead poisoning may also appear in the first year of life. The case of a 4-month-old infant is reported in which the preparation of infant formula in a lead-soldered samovar (urn) resulted in venous blood lead levels as high as 46 microg/dl. The samovar had been brought into the United States by the parents while on a visit to Iran. The infant was placed on chelation therapy with parenteral CaNa2EDTA followed by oral meso-2,3-dimercaptosuccinic acid (DMSA) and d-penicillamine. This resulted in a rapid and substantial reduction in the blood lead level. Lead poisoning in infancy may have unusual etiologies such as in utero transmission of lead by lead-poisoned women. Because sources of lead poisoning in infancy may be unusual, a detailed environmental investigation may be necessary to identify the exact source. Children exposed to lead in the first 2 years of life have a special vulnerability to the neurotoxicity of lead, with the risk of enduring developmental handicaps. Continued public health initiatives to remove lead from the environment, in conjunction with routine lead screening of young children, will be key in meeting the goal of the Centers for Disease Control and Prevention to eliminate childhood lead poisoning by the year 2011.
Lead poisoning in children imposes both immediate and long-term financial burdens on taxpayers. The District Board of Health of Mahoning County, Ohio, quantified some of the direct costs to taxpayers of providing medical care and public health services to the 279 children diagnosed with lead poisoning in the county in 2002, using methods described by Katrina Korfmacher at the University of Rochester. The Board of Health also attempted to quantify the longer-term costs of special education and juvenile justice services attributable to lead exposure. The realization that lead poisoning costs local government on the order of 0.5 million dollars each year has mobilized community leaders in education and juvenile justice to demand more aggressive action against rental property owners who fail to remediate lead hazards.
With long-term exposure to lead, lead accumulates in bone, where it is stored for years. These quiescent lead stores are mobilised when increased bone turnover occurs, and latent lead toxicity may then become symptomatic. Although Graves' disease is a common cause of increased bone turnover, to date hyperthyroidism has been implicated in lead poisoning only twice. We describe herein two cases of hyperthyroidism, one caused by toxic multinodular thyroid enlargement, the second by Graves' disease, leading to lead poisoning. Treatment of hyperthyroidism with radioactive iodine cured both hyperthyroidism and lead poisoning and no chelating agent therapy was necessary. Lead poisoning is an important environmental health problem, and physicians must be aware of the endocrine disorders such as hyperthyroidism and hyperparathyroidism that increase bone turnover, favouring lead mobilisation. Atypical symptoms should draw the physician's attention to the possibility of lead poisoning, particularly in workers with occupational exposure to lead and in areas where lead poisoning is endemic.
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