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Medical Genetics Centre, South-West Netherlands, Department of Radiation Genetics and Chemical Mutagenesis, Leiden University Medical Centre, 2300 RA Leiden, The Netherlands

This is with reference to the comments of Dr. R. J. Albertini on our study (Czene et al., 2002). The points raised by Dr. Albertini are relevant. We have clearly stated that in our report about the preliminary nature of this study, as well as that the possible exposures other than PO to the workers cannot be ruled out.

As regards to SCEs, this end point is only a reflection of an exposure to genotoxic agents and needs not directly lead to any genetic consequence. However, the increased frequencies of SCEs in workers in our study cannot be attributable to higher incorporation of BrdUrd in these cultures compared with the controls, because all these cultures were carried out under identical conditions and at the same time. It is very unlikely that control cultures had incorporated less BrdUrd, and the immunostaining did not show any visible difference between the controls and exposed.

Of course, it is ideal to look for stable chromosome aberrations, such as translocations, but this is not practical in such a study, as low PO exposures can induce only few chromatid types of aberrations, and only a small fraction can be transformed into chromosome types of aberrations.

We appreciate the concern by Dr. Albertini and agree that one should not rely only on the data on SCEs, especially in exercises aiming at cancer risk assessments after exposures to genotoxic agents.

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