To investigate whether occupational exposure to lead is genotoxic, we evaluated data from 103 lead-exposed workers and 78 matched controls. These data correspond to three different sampling periods, and we measured genetic damage as increases in the frequency of binucleated cells with micronuclei (BNMN) in peripheral blood lymphocytes. The levels of exposure were determined according to the lead levels in blood. Clearly significant increases in BNMN were observed in the exposed groups when compared to the control group. In addition, for the overall population (n = 181), we observed a clear relationship between lead levels in blood and BNMN (r = 0.497; p < 0.001). When we examined four exposure levels--very low exposure (< 1.20 microM/L), low exposure (1.20-1.91 microM/L), high exposure (1.92-2.88 microM/L), and very high exposure (> 2.88 microM/L)--we found significant differences in the genetic damage induction. We conclude that exposure to levels of lead higher than 1.20 microM/L may pose an increase in genetic risk. In addition, our data show that blood lead level is a good indicator of genetic damage induction.

Antikinetochore antibodies and fluorescence in situ hybridization with an alphoid centromeric probe were applied to the cytokinesis-block micronucleus (MN) assay to study the suitability of these methodologies to detect clastogenic/aneugenic activity in isolated human lymphocytes. The chemicals selected for this study were the herbicide alachlor, the clastogen mitomycin-C (MMC), and the aneugen vinblastine sulphate (VBL). Furthermore, MN frequencies obtained from slides stained with May-Grünwald-Giemsa (MGG) and with the DNA fluorochrome 4',6'-diamidino-2-phenylindole (DAPI) were compared to check if the DNA-specific DAPI facilitated a more accurate recording of MN than the unspecific MGG. The results showed that the detection of kinetochores (KC) or centromeres (CM) within MN are equally reliable and sensitive techniques to study the mode of action of clastogenic and aneugenic agents. The comparison of CM and KC detection in control cultures suggested that up to 17% of spontaneous chromosome-containing MN may be due to KC disruption, whereas the majority are caused by dysfunction in other components of the mitotic apparatus. Alachlor (7.5-20 micrograms/ml) and MMC (0.6 microM) acted as pure clastogens without aneugenic activity, inducing exclusively KC- and CM-negative MN. VBL produced primarily KC- and CM-positive MN, in accordance with its known mechanism of action. A comparison between CM and KC data in the VBL treatment suggested that some 7% of KC-containing MN may not be detected by the probe. The frequencies of MN were generally higher in slides stained with DAPI than in those stained with MGG, especially in controls and clastogen-treated cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine whether occupational exposure to a complex mixture of pesticides results in a significant increase in the level of cytogenetic damage, a follow-up study was planned on 39 greenhouse workers from Almería (southeastern Spain). Taking into account that pesticide exposure can be season-related, two blood samples were taken from each individual at different times: one in a period of high exposure (sample A, spring-summer) and the other in a period of lower exposure (sample B, autumn-winter). Using the cytokinesis block micronucleus technique the frequency of binucleated cells with micronuclei (BNMN) and the cytokinesis blocked proliferation index (CBPI) were determined in peripheral blood lymphocytes. The results obtained indicate that there were no statistically significant differences in BNMN frequencies between the two sampling periods nor between exposed and controls. ANCOVA analysis of repeated measures revealed that the age of the individuals showed a direct relation with BNMN in the first study period. With regard to CBPI, a significant and season-related effect was found.

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Two chromium(VI) compounds (potassium chromate and potassium dichromate) and one chromium(III) compound, chromium chloride, were evaluated for genotoxic effects in the wing spot test of Drosophila melanogaster following standard procedures. This assay detects both somatic recombination and mutational events. The genotoxic effects were determined from the appearance of wing spots in flies transheterozygous for the third chromosome recessive markersmultiple wing hairs (mwh) and flare‐3 (flr3), as well as in flies heterozygous formwh and the multiply inverted TM3 balancer chromosome. Genetic changes induced in somatic cells of the wing's imaginal discs lead to the formation of mutant clones on the wingblade. Single spots are due to different genotoxic mechanisms: point mutation, deletion, chromosome breakage, and mitotic recombination; while twin spots are produced only by mitotic recombination. From our results it appears that both chromium(VI) compounds clearly increase the incidence of mutant clones by inducing high increases in the frequency of all types of clones recorded. On the contrary, chromium(III) did not increase the frequency of mutant clones. A high proportion of the total spot induction was due to mitotic recombination, confirming previously reported data on the strong recombinogenic activity of chromium(VI) compounds. Environ. Mol. Mutagen. 34:47–51, 1999 © 1999 Wiley‐Liss, Inc.