Internal Lead Dose

Because of its wide distribution in the body, biologic measures of lead dose in a nmnber of tissues—including blood, plasma, umbiUcal cord blood, hair, fingernails and toenails, breast ntilk, urine, semen, soft tissue, and bone— are available (see review by Hu et al. 2007). The excretion of lead in urine can be enhanced by CaNa2EDTA or DMSA, and chelatable lead has been used to estimate lead dose (Schiitz et al. 1987 Tell et al. 1992 Lee et al. 1995, 2000 Schwartz et al. 2001). Because CaNa2EDTA can partially chelate bone lead 

Potential Health Risks to DOD Firing-Range Personnel 

FIGURE 3-2 Schematic of a hypothetical worker s dose over time. Used with permission of Brian Schwartz, Johns Hopkins Bloomberg School of Public Health. 

Given the importanee of enmulative lead dose to health (discussed in Chapters 4 and 5) and the laek of wide availabihty of XRF systems for measuring bone lead, this argues that more frequent longitudinal monitoring of BLLs, with attention to the CBLI over time, would have much greater utihty than heretofore required under the OSHA lead standard. 

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Health Effects Associated with Exposure to Lead and Internal Lead Doses in Humans... 

As discussed in the introduction to Section 2.2, the bulk of the human data on the health effects of lead are expressed in terms of internal exposure, or PbB levels, rather than external exposure levels (i.e., mg/m3 or mg/kg/day). For the general population, exposure to lead occurs primarily via the oral route with some contribution from the inhalation route, whereas occupational exposure is primarily by inhalation with some oral. Therefore, it is difficult to distinguish specific routes and levels of exposure. For this reason, the human health effects data for lead will be presented in terms of PbB levels in this section. Health effects associated with human exposures to lead and internal lead doses are shown in Table 2-1. 

Low-level environmental exposure to Cd may thus promote skeletal demineralization, which may lead to increased bone fragility and raised risk of fractures. Therefore it has been proposed that a CdU value of 2 pg Cd/g creatinine should be regarded as the maximum tolerable internal Cd dose for individuals from the general population. Hence, one may assume that in the early 1990 s about 10% of the general population in Belgium exceeded this threshold value and that it amoimted to 20% in the rural area with historical pollution by Cd from non-ferrous smelters. In this area, a clear-cut impact of a preventive action to decrease the Cd transfer from the environment to the inhabitants was observed, because the Cd concentration... 

Lead is classified as a probable cancer-inducing subtance for human beings . Research work on animals has shown that even ingestion of low doses may induce kidney cancer. However, it is worth mentioning that international institutions such as EPA and WHO have still to quantify the cancerogenic potential (or Slope Factor, SF), i.e. the slope of the plot probability of a tumor vs. lead dose. 

Bonithon-Kopp et al. (1986b) investigated another potential marker for lead exposure. Maternal and infant hair lead levels, determined from hair samples taken at birth, were found to be correlated inversely with results on neurobehavioral tests (McCarthy Scales of Children s Abilities) when the children were tested at 6 years of age. Other studies have also reported associations between hair lead levels and behavioral or cognitive test scores, but measures of lead in hair may not accurately reflect internal body burden of lead, and such data should not be used to evaluate internal dose-response relationships (EPA 1986a). 

Dose (blood lead)-effect data are available in the study by Fowler et al. (1980). Rats exposed to lead acetate in the drinking water through the dams during gestation and lactation and then directly until 9 months of age had the following external exposures (ppm lead), internal exposures ( pg lead/dL in blood), and renal effects 0 ppm (controls), 5 pg/dL, no lesions 0.5 ppm, 4.5 pg/dL, no lesions 5 ppm,... 

Effects at even lower external and internal exposure levels were reported by Hayashi (1983). Lead acetate at 0.7 mg lead/kg/day in the drinking water of rats for the first 18 or 21 days of pregnancy resulted in decreased ALAD activity in the fetal and maternal erythrocytes and increased ALAD activity in fetal but not maternal liver. Fetal, but not maternal, hematocrits and hemoglobin levels were decreased in the group treated for 21 days. Fetal PbB levels were 27 pg/dL and 19 pg/dL in the 18-day and the 21-day treated groups, respectively. Maternal PbB levels were approximately 4 pg/dL in treated and control groups. The study is limited by the use of one dose level, which precluded assessment of dose response. 

Studies in rodents, dogs, and non-human primates have demonstrated all of the major types of health effects of lead that have been observed in humans, including cardiovascular, hematological, neurodevelopmental, and renal effects (EPA 1986a). These studies also provide support for the concept of blood lead concentration as a metric of internal dose for use in dose-response assessments in humans. 

Bolla-Wilson K, Bleecker ML, Agnew J. 1988. Lead toxicity and cognitive functioning A dose response relationship. 16th Annual International Neuropsychological Society Meeting, January 27-30, 1988. J Clin Exp Neuropsychol 10 88. 

Chisolm JJ Jr. 1981. Dose-effect relationships for lead in young children Evidence in children for interactions among lead, zinc, and iron. In Lynam DR, Piantanida LG, Cole JF, eds. Environmental Lead Proceedings on the Second International Symposium on Environmental Lead Research, December, 1978, Cincinnati, Ohio. New York, NY Academic Press, 1-7. 

Hammond PB, Bomschein RL, Succop P. 1985. Dose-effect and dose-response relationships of blood lead to erythrocytic protoporphyrin in young children. In Bomschein RL, Rabinowitz MB, eds. The Second International Conference on Prospective Studies of Lead, Cincinnati, OH April, 1984. Environ Res 38 187-196. 

Needleman HL, Bellinger DC. 1989. Type II fallacies in the study of childhood exposure to lead at low dose A critical and quantitative review. In Smith M, Grant LD, Sors A, eds. Lead exposure and child development An international assessment. Lancaster, UK Kluwer Academic Publishers. 

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