The phasing out of leaded gasoline for transportation vehicles between 1973 and 1995 and the removal of lead from paint by federal mandate by 1978 have resulted in substantial lowering of mean blood lead levels in all segments of the U.S. population. However, because lead is a persistent metal, it is still present in the environment – in water, brass plumbing fixtures, soil, dust, and imported products manufactured with lead. Diagnosis of lead toxicity has traditionally been based on significantly elevated blood lead levels. However, data now implicates low-level exposures and blood lead levels previously considered normal as causative factors in cognitive dysfunction, neurobehavioral disorders, neurological damage, hypertension, and renal impairment. Chelation is the conventional recommendation in the case of blood levels associated with acute toxicity and encephalopathic damage. Issues surrounding the assessment of body lead burden and the consequences of low-level environmental exposure are critical in the treatment of chronic disease related to lead toxicity. (Altern Med Rev 2006;11(1):2-22)

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Lead Toxicity, A Review of the Literature. Part I: Exposure, Evaluation, and Treatment

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Toxicological profile for nickel

Normal levels of trace elements in human blood plasma or serum

The physiology, pharmacology, and biochemistry of the eccrine sweat gland

Although considerable progress has been made in recent years in reducing human exposures to lead, the potential for high intake of this contaminant still exists in millions of homes and in many occupational settings. Moreover, there is growing evidence that levels of lead intake considered inconsequential just a few years ago can result in subtle, adverse health effects, particularly in children. Consequently, there have been increased efforts by health protection agencies to develop credible, versatile methods for relating levels of lead in environmental media to levels in blood and tissues of exposed humans of all ages. In a parallel effort motivated largely by the Chernobyl nuclear accident, the International Commission on Radiological Protection (ICRP) is assembling a set of age-specific biokinetic models for calculating radiation doses from environmentally important radionuclides, including radioisotopes of lead. This paper describes a new age-specific biokinetic model for lead originally developed for the ICRP but expanded to include additional features that are useful for consideration of lead as a chemical toxin. The model is developed within a generic, physiologically motivated framework designed to address a class of calciumlike elements. This framework provides a useful setting in which to synthesize experimental, occupational, and environmental data on lead and exploit common physiological properties of lead and the alkaline earth elements. The modular design is intended to allow researchers to modify specific parameter values or model components to address special problems in lead toxicology or to incorporate new information. Transport of lead between compartments is assumed to follow linear, first-order kinetics provided the concentration in red blood cells remains below a nonlinear threshold level, but a nonlinear relation between plasma lead and red blood cell lead is modeled for concentrations above that level. The model is shown to be consistent with data on human subjects exposed to lead under a variety of experimental and natural conditions.

An age-specific kinetic model of lead metabolism in humans.

Ni, Cu, Zn, and Pb were measured by atomic absorption spectrometry in sweat samples obtained by the arm-bag technique from 48 healthy adult subjects (33 ♂, 15 ♀ ) during sauna bathing (15 min at 93 °C, dry heat). The men sweated more profusely than the women (volume, in milliliters, of sweat collected: mean, SD, and range: 23 ± 12 (3-55) and 7 ± 3 (2-13), respectively. The concentrations, in µg/liter, (mean, SD, and range) of trace metals in sweat of men and women, respectively, were: nickel , 52 ± 36 (7-180) and 131 ± 65 (39-270); copper , 550 ± 350 (30-1440) and 1480 ± 610 (590-2280); zinc , 500 ± 480 (130-1460) and 1250 ± 770 (530-2620); and lead , 51 ± 42 (8-184) and 118 ± 72 (49-283). In sweat samples from 11 women on oral contraceptives, concentrations of Ni, Cu, Zn, and Pb did not differ significantly from the values in the 15 control women. Sweating is a demonstrably significant route for excretion of trace metals, and sweating may play a role in trace-metal homeostasis. Essential trace metals could conceivably be depleted during prolonged exposure to heat; conversely, sauna bathing might provide a therapeutic method to increase elimination of toxic trace metals.

Atomic Absorption Spectrometry of Nickel, Copper, Zinc, and Lead in Sweat Collected from Healthy Subjects during Sauna Bathing

Nickel was measured, by atomic absorption spectrometry, in serum and urine specimens from: ( a ) healthy hospital employees (age 19-62) who had resided >1 year in Sudbury, Ontario, and ( b ) healthy hospital employees (age 18-62) who had resided >1 year in Hartford, Connecticut. Subjects in groups a and b were matched according to age and sex. None of the subjects had occupational exposure to nickel. Nickel was analyzed in duplicate on a "blind" basis with specimens from groups a and b interspersed within each run. In population a , serum nickel concentrations averaged 4.6 ± 1.4 µg/liter (n = 25), urine nickel excretion 7.9 ± 3.7 µg/day (n = 19). In population b , serum nickel concentrations averaged 2.6 ± 1.0 µg/liter (n = 26), urine nickel excretion 2.5 ± 1.4 µg/ day (n = 20). These population means were all significantly different ( P <0.001, t test). Serum and urinary nickel concentrations were not significantly influenced by age or sex, nor were they correlated with length of residence in either location. Nickel concentrations in municipal tap water averaged 200 ± 43 µg/liter in Sudbury (seven sites), and 1.1 ± 0.3 µg/liter in Hartford (five sites). Measurements of nickel in serum and urine are valid biological indices of environmental exposure to nickel.

Measurements of Nickel in Serum and Urine as Indices of Environmental Exposure to Nickel

Nickel concentrations were measured by atomic absorption spectrometry in sera. The mean concentration of nickel in sera of 47 healthy adults was 2.6 SD ± 0.8) µg/liter. Abnormally high mean concentrations (µg/liter) of serum nickel were found in patients with: ( a ) acute myocardial infarction (13-36 h after onset), mean = 5.2 ± 2.8, N = 33, P 25% body surface, 37-72 h after injury), mean = 7.2, N = 3, range = 4.1-10.9. Diminished mean concentrations of serum nickel were found in patients with: ( a ) hepatic cirrhosis, mean = 1.6 ± 0.8, N = 18, P <0.005; and ( b ) chronic uremia, mean = 1.7 ± 0.7, N = 12, P = <0.005. Normal mean concentrations of serum nickel were found in patients with: ( a ) acute myocardial ischemia without infarction (13-36 h after onset), mean = 3.3 ± 1.6, N = 22; ( b ) acute trauma with fractured bones (13-36 h after injury), mean = 2.7 ± 0.9, N = 19; ( c ) acute delirium tremens (13-36 h after admission), mean = 2.3 ± 0.9, N = 25; and ( d ) muscular dystrophy, mean = 2.3 ± 1.4, N = 10. In sera collected from 12 mothers immediately after normal delivery, the mean concentration of nickel was 3.0 ± 1.2 µg/liter, the same values as for sera from the umbilical cords of their 12 full-term infants.

Abnormal Concentrations of Nickel in Serum in Cases of Myocardial Infarction, Stroke, Burns, Hepatic Cirrhosis, and Uremia

Indices of Environmental Exposure to Nickel"2

Diminishedmean concentrationsofserum nickel were found in patients with:(a)hepaticcirrhosis, mean = 1.6± 0.8,N = 18,P <0.005;and (b) chronicuremia,mean = 1.7± 0.7,N = 12,P = <0.005.Normal mean concen trations of serum nickel were found inpatientswith:(a)acutemyocardial ischemiawithoutinfarction (13-36h after onset), mean = 3.3± 1.6,N = 22;(b) acutetrauma withfracturedbones (13-36h afterinjury), mean = 2.7 ± 0.9, N = 19;(c) acutedelirium tremens (13-36h after admission), mean = 2.3± 0.9,N 25;and (d) musculardystrophy,mean = 2.3± 1.4,N = 10. Insera collected from 12 mothers immediatelyafternormal delivery, the mean concentrationofnickelwas 3.0± 1.2pg/liter, the same values as for sera from theumbilicalcordsoftheir12full-term infants.

Maria W. Nechay

Papers

Atomic Absorption Spectrometry of Nickel, Copper, Zinc, and Lead in Sweat Collected from Healthy Subjects during Sauna Bathing

Measurements of Nickel in Serum and Urine as Indices of Environmental Exposure to Nickel

Abnormal Concentrations of Nickel in Serum in Cases of Myocardial Infarction, Stroke, Burns, Hepatic Cirrhosis, and Uremia

Indices of Environmental Exposure to Nickel"2

Abnormal Concentrations of Nickelin Serumin Cases of Myocardial Infarction, Stroke,Burns, HepaticCirrhosis, andUremia"2