The effects of wood dusts on the redox status and cell death in mouse macrophages (RAW 264.7) and human leukocytes in vitro.

Wood dusts are classified as carcinogenic to humans and also produce other toxic, allergic, and acute effects in woodworkers. However, little is known about causative agents in wood dusts and their mechanisms of action. The effects of different tree species and particle size for biological activity were studied. The differences in the production of reactive oxygen species (ROS) and cell death (necrotic and apoptotic) between mouse macrophage (RAW 264.7) cells and human polymorphonuclear leukocytes (PMNL) for pine, birch, and beech dust exposures were investigated in vitro. The pine and birch dust exposure (1-100 microg/ml) produced concentration-dependent ROS production in both the cells, which was one order of magnitude higher with pine dust. The ROS production was faster in human PNML than murine RAW cells. The higher concentrations (500 and/or 1000 microg/ml) decreased ROS formation. With pine and birch dust exposure, this was probably due to the necrotic cell death. The pine dust concentrations of 500 and 1000 microg/ml were cytotoxic to human PMNL. The beech dust exposure activated the ROS production and decreased the cell viability only at the highest concentrations, being least potent of the three dusts. A sign of the apoptotic cell death in the murine RAW cells was observed at the pine dust concentration of 100 microg/ml. The exposure to the birch and beech dusts with a smaller particle size (<5 microm) produced greater ROS production than exposure to the corresponding dust with a wide range of particle sizes. However, changing the particle size did not affect the cell viability. The results indicate that the type of wood dust (tree species and possibly particle size) has a significant impact on the function and viability of phagocytic cells.

Chlorinated drinking water is mutagenic and causes 3-methylcholanthrene type induction of hepatic monooxygenase.

Acid/neutral fractions of 4 chlorinated drinking water samples were tested for mutagenicity in the Ames' test and injected intraperitoneally to 10- and 20-day-old Wistar rats at doses of 200 and 100 liters of water/kg body weight. Cytochrome P-450 mediated enzyme activities of ethylmorphine-N-demethylase (EMND), 7-ethoxycoumarin-O-deethylase (ECOD), 7-ethoxyresorufin-O-deethylase (EROD) and 7-pentoxyresorufin-O-dealkylase (PEROD) were determined in the 9000 g supernatant fraction of liver homogenate. EROD was introduced by the concentrates. The induction was related to the mutagenic activity. About 4-fold increase in activity was observed with the most mutagenic sample. PEROD was also slightly enhanced. EMND and ECOD activities were not affected by the lower dose, but the higher dose caused inhibition of 30-40%. Although the extracts were not toxic to bacteria, they were unexpectedly toxic to rats. It is concluded that the samples contained 3-methylcholanthrene (3-MC) type inducer(s).

High levels of mutagenic activity in chlorinated drinking water in Finland.

The organic extract from the drinking water of Kuopio, Eastern Finland, turned out to be highly mutagenic in the Ames test. The direct mutagenic activities of the acid/neutral fractions of 48 drinking water samples were on an average 1700 net revertants/l in strain TA100. The highest activities were more than 6000 net revertants/l, and one drinking water sample exceeded 10 000 net revertants/l. The drinking water of Kuopio is produced from lake water which has a relatively high content of humic substances. Water processing involved two chlorination phases. The organic constituents of the water samples were isolated either by continuous liquid-liquid extraction or by absorption on XAD 8 resin.