Occupational Health - Public Health Poster Session
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Introduction
The literature data from the last 20 years certify the impact of lead and cadmium on the calcium metabolism. The Pb/Ca interaction is done at the level of the intestinal absorption, distribution and excretion mechanisms. It is accepted that a lead exposure lead to a hipocalcemia with hipercalciuria and it is also known the hipercalciuria by the proximal tube injury in the cadmium intoxication. The competition between lead and calcium at different levels (intestinal absorption, transport, bones deposit and mobilisation, renal excretion) it's well known 1,2,3,4,5/. In the same time it is also known the cadmium impact with the calcium metabolism, especially at the kidney 6,9,10/. In moderate lead exposure, Koo has demonstrated decreases in serum calcium. There are few papers concerning the concomitant action of lead and cadmium on the calcium metabolism. Epidemiological studies, carried out in population exposed to cadmium, demonstrated an increase of calcium excretion and hipocalcemia, consecutively to a proximal tube injury, and decreased of the D vitamine and paratiroidian hormone. On the other hand, Myahara 8/ demonstrated an increase of the prostaglandine PGE2 concentration due to lead the lead exposure, which increased calcium mobilization from bones and consecutively hipercalcemia.
Materials and Methods
179 males (17-52 years), workers from a non-ferrous plant were examined. The average time of exposure was 7,5 -± 6,2 years (1-30 years). The lead concentration at the workplaces was between 0.2 and 5 mg/m3 air. Cadmium exposure was inconstant and the cadmium concentrations were between 0.05 and 0.3 mg/m3 air. Were determined: The blood lead concentration, total serum calcium and ionic calcium. The results were compared with a control group (50 unexposed workers).
Results
The concentration of blood lead, total serum calcium and ionic calcium are showed in the table 1.
Table 1: Blood lead, total calcium level and ionic calcium level.
The blood lead concentrations were significantly high. At the exposed group (fig.1) total serum calcium is not significantly different than at control. The percentage of cases with hipocalcemia is not significantly different (fig. 2) in both groups. There are a high percent of cases with hipercalcemia (23%). The ionic calcium is slightly decreased in the exposed group, but the percent of cases with low values is significantly higher (fig.3).
Fig. 1: Blood lead level and exposed and control group.
Fig. 2: Prevalence of hipocalcemia cases (total serum calcium) at exposed and control group.
Fig. 3: Prevalence of hipocalcemia cases (ionic calcium) at exposed and control group.
Discussion and Conclusion
- 1. Lead and cadmium exposure found in the non-ferrous metallurgy, resulted in calcium metabolism disorder and finally in the modification of the blood calcium level.
- 2. It was observed high percents of cases with hipocalcemia but with hipercalcemia also. Here appear probably disorders of intestinal calcium absorption and also disorders in transport, distribution, deposit and excretion of calcium by the direct action of lead on the cells membranes, but also on the parathhormone, osteocalcine, calcitonine, 1,25 D dihydroxyvitamine.
- 3. Cadmium cause a reduced renal tubular reabsorption function with increase of urinary excretion of calcium.
- 4. The major target organs of cadmium and lead are different from one person to another, depending on some individual particularities which are not well known yet.
References
- 1. AUNGST B I, FUNG H L. The effects of dietary calcium on lead absobtion, distribution and elimination kinetics in rats. J. Toxicol. and Environ. Health, 16, 147-159, 1985
- 2. BARNEVELD A., C. VAN DEN HAMER- Influence of Ca and Mg on the uptake and deposition of Pb and Cd in mice.Toxicol. and Appl. Pharmacol., 79, 1-10, 1985.
- 3. BELLINGER D., LEVITON A., WATERNAUX C., NEEDLEMAN H., RABINOWITZ M.-Low-level lead exposure, social class and infant developement. Neurotoxicol. and Teratol., vol. 10, pp. 497-503, 1989.
- 4. BRONNER F. BONE AND CALCIUM HOMEOSTASIS. -Neurotoxicology. 13(4)-775-82, 1992 Winter.
- 5. FULLMER C.S. -Dietary calcium levels and treatment interval determine the effects of lead ingestion on plasma 1,25-dihydroxyvitamin D concentration in chicks. Journal of Nutrition. 125(5)-1328-33, May 1995.
- 6. HINKLE P. M., KINSELLA P. A., OSTERHOVA T. - Cadmium uptake and toxicity in voltage-sensitive calcium chanells. J. Biol. Chem., 262, 34, 16333-16338, 1987.
- 7. KOO W. W., SUCCOP P. A., BORHSCHEIN H. L., KRUG WISPE S. K.- Serum Vitamin D metabolites nad bone mineralisation in young children with low to moderate lead exposure. Pediatrics, 87(5), 680-687, May 1991.
- 8. MIYAHARA T.. KOMIYAMA H.. MIYANISHI A.. TAKATA M.. NAGAI M.. KOZUKA H.. HAYASHI T.. YAMAMOTO M.. ITO Y.. ODAKE H. et al. - Stimulative effects of lead on bone resorption in organ culture. Toxicology. 97(1-3)-191-7, Mar 31,1995.
- 9. SORENSEN E.M.B., ACOSTA B., HEALON B.C.: - Effect of cadmium and calcium on the fluidity of plasma membranes. Toxicol. letters, 25,119-126, 1985.
- 10. STAESSEN J., AMERY A. - Effects of exposure to cadmium on calcium metabolism. Brit. J. Ind. Med., 48, 710-714, 1991.
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