Impact of exposure to wood dust on genotoxicity and cytotoxicity in exfoliated buccal and nasal cells

Wood dust was classified by the IARC as a human carcinogen, which causes sinonasal tumours. However, the exposure in different industries varies strongly and the risks of workers depend on the specific situation, which can be assessed by the use of biomonitoring methods. The aim of this study was to investigate the workers who are exposed to low dust levels (below the permitted concentrations) with cytogenetic and biochemical methods. Micronuclei (MNi), which are indicative for genomic damage, nuclear buds which reflect gene amplification, binucleated cells which are caused by mitotic disturbances and acute cytotoxicity parameters (pyknosis, karyorrhexis, condensed chromatin, karyolysis) were monitored in buccal and nasal cells of workers of a veneer factory (n = 51) who are exposed to volatile wood-derived compounds, in carpenters of a furniture factory which use no synthetic chemicals (n=38) and in a control group (n = 65). Additionally, markers were measured in blood plasma which reflect inflammations (C-reactive protein, CRP) and the redox status, namely malondialdehyde (MDA) and oxidised low density proteins (oxLDL). No induction of micronucleated cells was observed in both epithelia in the two exposure groups while all other nuclear anomalies except pyknosis were increased; also one health-related biochemical marker (MDA) was significantly elevated in the workers. Taken together, the results this study shows that exposure to low levels of wood dust does not cause formation of MNi indicating that the cancer risks of the workers are not increased as a consequence of genetic damage while positive results were obtained in earlier studies with workers who are exposed to high dust levels. However, these findings indicate that wood dust causes cytotoxic effects which may lead to inflammations.

Authors: Wultsch G, Nersesyan A, Kundi M, Wagner KH, Ferk F, Jakse R, Knasmueller S. ;Full Source: Mutagenesis. 2015 May 9. pii: gev034. [Epub ahead of print] ;