P Apostoli

Biological monitoring of tungsten (and cobalt) in workers of a hard metal alloy industry.

ObjectivesTo evaluate a combined biomonitoring approach based on both cobalt and tungsten determination in workers of the hard metal alloy sector.MethodsWe enrolled 55 workers from a factory producing cutting tools for carpentry. Combined workroom air and biological monitoring of both cobalt and tungsten relied on inductively coupled plasma mass spectrometry determinations. Metals were determined on plasma, blood and urine samples. Urine samples from 34 unexposed subjects were also analyzed.ResultsTungsten was determined in every collected sample. Workers showed significantly higher urinary tungsten levels than controls (pre-shift values of 4.12 vs. 0.06xa0μg/l on average; Pxa0<xa00.0005). Both airborne and biological levels of tungsten prevailed among workers involved in wet-grinding activities. The element was excreted at higher urinary levels than cobalt and showed lower circulating (blood, plasma) concentrations. Exposure–dose relationships were apparent for tungsten biomarkers.ConclusionsObtained results may contribute to the development of biomarkers of exposure to tungsten. The association of such biomarkers to traditional determinations of cobalt in blood and/or urine may substantially improve the exposure assessment of workers employed in cemented carbide industries.

Interactions by Carcinogenic Metal Compounds with DNA Repair Processes

Some metal compounds, including arsenic, beryllium, cadmium, chromium and nickel have long been recognized as human and animal carcinogens, while for other as antimony, cobalt, lead and vanadium their carcinogenic action are probable or possible. Except chromium (VI), carcinogenic metals are only weak mutagens in mammalian cells and often inactive in bacterial assays. Since the mutagenicity in bacterial assays indicates reactivity with DNA, metals are thought to exert genotoxicity mainly by indirect mechanisms. The four main, partly overlapping, DNA repair pathways operating in mammalian cells are base excision, mismatch, nucleotide excision and recombinational repair; each of repair pathways is involved in the removal of the specific DNA lesions. In addition, many carcinogenic metal compounds at low concentrations have been identified as inhibitors of the repair of DNA damage caused by other xenobiotics or endogenous factor. Furthermore, DNA is not only damaged by environmental mutagens including UV-light and polycyclic aromatic hydrocarbons, but also by reactive oxygen species generated from the same metallic elements. Failure to repair DNA damage can result in the accumulation of damaged DNA, mutation and carcinogenesis.

Effects of Metallic Elements on Reproduction and Development

Abstract Many factors can influence the reproductive or developmental outcomes of human exposure to metallic elements, including metallic element speciation, dose, timing, route and duration of exposure, dose-response relationship, bioavailability, and the distribution and accumulation of metallic elements in various organs. Experimental and epidemiological studies have reported the adverse effects of many metallic elements on male and female reproductive function, for example infertility or subfertility, malformations, abortion, and developmental alterations. Different mechanisms of action have been suggested: increased reactive oxygen species or decreased activity of the cellular antioxidant defense system; direct damage on the testes or ovaries; interaction with the embryonic structure; disruption of reproductive hormones; and, finally, immune suppression and neurotransmitter alterations. The targets and effects can be different and specific to each metallic element (e.g. neurotoxicity of Pb and methylmercury in the developing brain or the action of Cd on the testicle) or similar for large groups of metallic elements (reduced sperm motility caused by As, Cr, Hg, Ni, and Pb). Knowledge of these mechanisms may be useful to occupational physicians by providing a better understanding of the dose-response relationship, as well as the choice of current indicators of dose and their effects. Use of the diagnostic approach in occupational medicine is necessary to achieve adequate evidence for a causal relationship between exposure and clinical findings.