Lead Chelation Study; Detoxamin Lead Poisoning in Children Study
Abstract: The effect of lead poisoning in children on high percentages of the pediatric population is cause for concern and it is one of the most common and preventable pediatric health problems today. Currently, the primary form of lead chelation medical intervention for lead poisoning in children consists of an expensive and painful CaNa2 EDTA intramuscular injection. The availability of an easily administered effective lead chelation treatment is an important component in controlling lead poisoning in children worldwide. This lead chelation and lead poisoning in children study utilizes a new form of lead chelation with the administration of CaNa2 EDTA, Detoxamin® suppositories. Detoxamin EDTA suppositories (2000mg) were administered once per evening to 20 children for 10 consecutive days, no treatment after the following 10 consecutive days and re-administration of the initial suppository dose for another 10 consecutive days. Lead toxicity in blood showed continual excretion from the pre-lead chelation treatment concentration of 66.64μg/dL to 83.67μg/dL post treatment at the end of the 30 trial period. Lead toxicity in urine levels rose from a baseline of 4.23μg/g creatinine to 325.55μg/g creatinine after only one lead chelation treatment via detoxamin EDTA suppository administration. The lead in urine levels then dropped to 61.45μg/g creatinine within the first 10 days of Detoxamin lead chelation treatment, and decreased to 9.94μg/g creatinine after the next 10 consecutive days of no treatment and rose to 22.71μg/g creatinine after the last 10 days of suppository administration. These data indicate significant and consistent excretion of lead toxicity in both blood and lead in urine with the use of Detoxamin EDTA suppositories for lead chelation in children. Detoxamin EDTA suppositories offer a simple, convenient, non-invasive and cost- effective means of effective lead chelation for lead poisoning in children.
Introduction: Lead poisoning in children is one of the most common pediatric health problems in the world today, and it is entirely preventable and reversible. Enough is now known about the sources and pathways of lead toxicity exposure, about ways of preventing lead poisoning in children, and about ways of reducing the lead content of the body to eradicate this disease permanently. The persistence of lead poisoning in children, in light of all that is known, presents a singular and direct challenge to public health authorities, clinicians, regulatory agencies, and society. Lead is ubiquitous in the human environment as a result of industrialization. It has no known physiological value. Children are particularly susceptible to lead's toxic effects. Lead poisoning in children, for the most part, is silent: most poisoned children have no symptoms. The vast majority of lead poisoning cases, therefore, go undiagnosed and untreated. Lead poisoning is widespread. It is not solely a problem of inner city or minority children. No socioeconomic group, geographic area, or racial or ethnic population is spared. Previous lead toxicity statements issued by the Centers for Disease Control (CDC) have acknowledged the adverse effects of lead at lower and lower lead levels.
In the most recent previous CDC lead statement, published in 1985, the threshold for action was set at a blood lead level of 25 μg/dL, although it was acknowledged that adverse effects for lead poisoning in children occur below that level. In the past several years, however, the scientific evidence for lead poisoning in children showing that some adverse effects occur below levels at least as low as 10 μg/dL in children has become so overwhelming and compelling that it must be a major force in determining how we approach lead poisoning in children. It is not possible to select a single number to define lead poisoning in children. Epidemiological studies have identified harmful effects of lead in children at blood lead levels at least as low as 10 μg/dL. Some studies have suggested harmful effects of lead toxicity at even lower levels, but the body of information accumulated so far is not adequate for effects below about 10 μg/dL to be evaluated definitively. As yet, no threshold has been identified for the harmful effects of lead toxicity. Because 10 μg/dL is the lower level of range at which effects are now identified, primary prevention activities are typically directed at lead chelation by reducing children's blood lead levels below 10 μg/dL or 14 μg/dL. While the overall goal of lead chelation should be to reduce children's blood lead levels below 10 μg/dL, there are entrenched reasons for not attempting to do interventions directed at individual children to lower blood lead levels of 10-14 μg/dL. First, practical lead chelation medical interventions for children with blood lead levels in this range have previously been unavailable. Second, the sheer numbers of children in this range would preclude effective case management in established intravenous lead chelation therapy. Clearly, a simply and effective therapy such as suppository is needed for more accessible lead chelation.
The single, all-purpose definition of childhood lead poisoning has been replaced with a
multi-tiered approach, described in the following table:
Lead is a poison that affects virtually every system in the body. The risks of lead exposure are not based on theoretical calculations. They are well known from studies of children themselves and are not extrapolated from data on laboratory animals or high-dose occupational exposure. Since 1970, our understanding of childhood lead poisoning has changed substantially. As investigators have used more sensitive measures and better study designs, the generally recognized level for lead toxicity has progressively shifted downward. Before the mid-1960s, a level above 60 μg/dL was considered toxic(Chisholm and Harrison, 1956). By 1978, the defined level of toxicity had declined 50% to 30 μg/dL.
Lower blood lead levels cause adverse effects on the central nervous system, kidney and hematopoietic system. Blood lead levels as low as 10 μg/dL, which do not cause distinctive symptoms, are associated with decreased intelligence and impaired neurobehavioral development (Davis and Svendsgaard, 1987; Mushak et al, 1989).
The concern about adverse effects on central nervous system functioning at blood lead levels as low as 10 μg/dL is based on a large number of rigorous epidemiological and experimental studies. Several well-designed and carefully conducted cross-sectional and retrospective cohort studies in many different countries have been conducted (Lansdown et al., 1986; Fulton et al., 1987; Fergusson et al., 1988; Silva et al., 1988; Bergomi et al., 1989; Hansen et al., 1989; Hatzakis et al., 1989; Winneke et al., 1990; Lyngbye et al., 1990; Needleman et al., 1990; Yule et al., 1981; Hawk et al., 1986; Schroeder et al., 1985).
Some inconsistencies can be found in the results of these studies, but the weight of the evidence clearly supports the hypothesis that decrements in children's cognition are evident at blood lead levels well below 25 μg/dL. No threshold for the lead-IQ relationship is discernible from these data. Recent evaluation of 24 major cross-sectional studies provides strong support for the hypothesis that children's IQ scores are inversely related to lead burden (Needleman and Gatsonis, 1990).