Pediatric Care for Lead Exposure
Child Lead Exposure
Childhood lead poisoning is recognized as the most important preventable pediatric environmental health problem in the United States. The adverse health effects of lead exposure in early childhood are well documented.
Lead poisoning is defined as exposure to environmental lead that results in whole blood lead concentrations ≥ 10 µg/dl. (micrograms/deciliter) (US Centers for Disease Control and Prevention, 1992).
Exposure to environmental lead begins in the prenatal period when physiologic stress mobilizes lead from its storage in maternal bone into the blood, where it easily crosses the placenta and is deposited in fetal tissue.
Dependent on the level of lead present in the environment, the exposure can continue as infants and children develop. Absorption of lead is dependent on age and nutritional status; young children and those who have diets high in fats are most susceptible.
Lead is most
commonly ingested through exposure to lead-contaminated paint and the resulting
dust, soil, and paint chips. Once ingested, lead is distributed in the blood
and eventually is deposited in bone and teeth.
Diagnostic Criteria
Whole blood lead levels (BLL) greater than 10 µg/dl. put children at risk for developing a variety of health problems. At high level exposures (BLL> 20 µg/dL), damage to the nervous, hematopoietic, endocrine, and renal systems can occur.
At lower-level exposures, these health problems include altered cognitive and neurobehavioral processes. Researchers have suggested that some of these effects may be seen in children with BLL as low as 5 ug/dL. (Lamphear, Deitrich, Aligner, & Cox, 2000; Landrigan, 2000; Needleman & Landrigan, 2004).
Direct results of primary and secondary efforts at prevention of lead toxicity have significantly reduced BLL among young US children within the last 30 years.
The major sources of environmental lead exposure have been greatly decreased through the elimination of lead in gasoline, the banning of lead-based paint for residential use, and the elimination of lead solder from food and beverage cans.
Despite the success of these efforts, lead poisoning
continues to occur in about 5% of children 5 years of age and younger, and much
higher levels of lead poisoning have consistently been documented among
low-income, urban, and African-American children living in older housing in the
Midwest and Northeast (Pirkle et al., 1994).
Historical Overview Of Lead Poisoning
Childhood lead poisoning was first described in the late 1800s by Gibson and colleagues (Gibson, Love, Hendel, Bancroft, & Turner, 1892), who encountered a case of peripheral paralysis in a young child and described the similarities of the case to that of chronic lead poisoning in adults.
Gibson speculated that the source of the lead poisoning was paint, and he described the long-lasting effects of the exposure. Unfortunately, most of Gibson's observations were ignored, as the prevailing view of the time was that once a child survived lead poisoning, there were no lasting effects.
It was not until the early 1970s that cross-sectional and longitudinal studies of low-level lead exposure were conducted.
Early Studies On Lead Exposure
These early studies of lead exposure involved comparisons of a lead-exposed group and a comparison group on intelligence test measures.
As knowledge accumulated and research strategies became more sophisticated, researchers began to assess the influence of covariates, such as parental intelligence, socioeconomic status, and parental education level ( Gatsonis & Needleman, 1992).
Though
conflicting results were common, lead exposure and neurobehavioral deficits
remained significantly associated.
Nursing Researches On Lead Poisoning
Although few nurse researchers have investigated the effects of low-level lead exposure on the neurobehavioral development of children, low-level lead exposure certainly falls within the realm of the phenomena of concern to the discipline.
Lead exposure is unquestionably of clinical significance; until all lead is removed from the environment, clinicians will be faced both with screening children for lead exposure and treating the effects of this preventable public health problem.
The deleterious effects of lead exposure have been known for a hundred years; how-ever, progress in prevention has been slow. Some of the reasons for this are related to society's indifference to problems of poor and vulnerable populations.
Until recently, lead exposure was thought to be a problem only. for poor inner-city minority populations, and parenting practices were thought to contribute to the problem.
Also, many considered the elimination of lead in gasoline and paint sufficient to eradicate the problem of lead poisoning.
The Centers for Disease Control (CDC), in 1992, issued comprehensive guidelines for preventing and treating the problem of childhood lead exposure.
These guidelines were issued after the CDC accumulated large
amounts of scientific evidence from animal and human studies that supported the
hypothesis that the deleterious effects of lead exposure occurred at levels
previously thought to be harmless.
Diagnostic Levels Of lead Poisoning And Clinical Symptoms
The earliest studies of lead poisoning were conducted on children who had BLL≥60 µg/dl. and were symptomatic. During the 1970s, researchers focused on asymptomatic children who had BLL in the 40-50 µg/dL.
Conclusions about the effects of lead exposure were difficult to make from these studies because of their methodological shortcomings. In 1979, researchers conducted a major investigation of large cohorts of asymptomatic children and used shed deciduous teeth rather than BLL to measure lead exposure (Needleman et al., 1979).
These researchers controlled for major confounding variables and concluded that BLL was associated with lower IQ, decreased attention span, and poor speech and language skills in the children studied.
Long-term follow-up of these children led the researchers to conclude that the effects of low-level lead exposure (equivalent to BLL 25 µg/dl) persisted throughout young adulthood; failure to complete high school, reading disabilities, and delinquency were behaviors exhibited by children who had elevated BLL at age 7 (Needleman, Riess, Tobin, Biesecker, & Greenhouse, 1996).
Scientists criticized the work done by Needleman and his colleagues (1979) because the study lacked baseline data about early cognitive abilities of the subjects.
For instance, it was proposed that the affected children may have had neurological deficits at birth that would lead them to certain behaviors (increased mouthing) that predisposed them to be lead exposed.
To address this issue, subsequent studies were designed to follow large numbers of subjects from birth through early school age and major outcomes (eg, IQ level, motor development, cognitive development) were measured, while large numbers of covariates were controlled.
Numerous investigators using comparable designs reported similar findings; Thus a solid consensus among investigators began to emerge that lead was toxic at extremely low concentrations.
Research with lead-exposed primates strengthened the
consensus, and the toxic level of lead was redefined by the CDC as a BLL ≤ 10
µg/dL.
L ow-Level Lead Exposure
Researchers continue to study the effects of low-level lead exposure on the development of children. While these efforts are worthwhile, future efforts could focus on:
(a) identifying mediators of lead exposure effects
(b) investigating the effects of lowering blood lead levels (chelation) on the neurobehavioral outcomes of children
(c) investigating the synergistic effects of other environmental exposures on neurocognitive development
(d) investigating the effects of providing educational materials about reducing environmental lead exposure to families of low-level exposed children.
Any efforts that address the primary
prevention of the problem would help to protect thousands of children against
the long-lasting effects of lead exposure.
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