One of the most insidious pollutants in our environment is the heavy metal element Cadmium. An important new study is the first research report on the effects of Cadmium on human fetal sex organ tissues. The authors of the abstract below make the following introductory points in their paper:
- Exposure to Cadmium is usually the result of environmental contamination by waste from human activities such as the residues found in mining waste, those released by the combustion of fossil fuels and industry, and the run-off from agricultural land.
(Note: the term "apoptosis" refers to programmed cell death, a process that ends with the death and dissolution of a living cell. It's a common consequence of exposure to chemicals toxic to living systems.)
The Abstract:
Title: Cadmium Increases Human Fetal Germ Cell Apoptosis.
Gaëlle Angenard, Vincent Muczynski, Hervé Cof?gny, Catherine Pairault, Clotilde Duquenne, René Frydman, René Habert, Virginie Rouiller-Fabre, and Gabriel Livera.
Journal: Environmental Health Perspectives.
doi: 10.1289/ehp.0900975
Online 14 October 2009.
BACKGROUND: Cadmium (Cd) is a common environmental pollutant and a major constituent of tobacco smoke. Adverse effects of this heavy metal on reproductive function have been identified in adults however no studies have examined its effects on human reproductive organs during development.
OBJECTIVES: Using our previously developed organ culture system, we investigated the effects of Cadmium chloride on human gonads at the beginning of fetal life, a critical stage in the development of reproductive function.
METHODS: Human fetal gonads were recovered during the first trimester (7-11 weeks post conception), and cultured with or without Cd. Different concentrations of Cd were used and results compared to those obtained with mouse fetal gonads at similar stages.
RESULTS: Cadmium, at concentrations as low as 1 µM, significantly decreased the germ cell density in human fetal ovaries. This correlated with an increase in germ cell apoptosis while there was no effect on proliferation. Similarly, in the human fetal testis, Cd (1 µM) reduced germ cell number without affecting testosterone secretion. In mouse fetal gonads, Cd increased only female germ cell apoptosis.
CONCLUSIONS: This is the first experimental demonstration that Cd, at low concentrations, alters the survival of male and female germ cells in humans. Considering data demonstrating extensive human exposure, we think that current environmental levels of Cd could be deleterious to early gametogenesis.
Research Installations: Laboratory of Differentiation and Radiobiology of the Gonads, Fontenay aux Roses, France. Université Paris Diderot-Paris 7, F-92265, Fontenay aux Roses, France. INSERM, Unité 967, F-92265, Fontenay aux Roses, France. Service de Gynécologie-Obstétrique, Université Paris Sud, UMR 782, Hôpital A. Béclère, Clamart, France. INSERM, Unité 782, F-92141 Clamart, France.
