1,1,1-Trichloroethane Marine Risk Assessment with Special Reference to the Osparcom Region: North Sea

This risk assessment on 1,1,1-trichloroethane was carried out specifically for the marine environment, accordingly to the methodology laid down in the EU risk assessment Regulation (1488/94) and the Guidance Document of the EU New and Existing Substances Regulation (TGD, 1996). 1,1,1-trichloroethane is being phased out of most uses because of its ozone depletion potential (ODP) under the Montreal Protocol. Production for emissive uses has already been phased out end 1995 in Europe and 1996 in the United States, Japan and other industrial countries. The risk assessment study consists of the collection and evaluation of data on effects and environmental concentrations from analytical monitoring programmes in large rivers and estuaries in the North Sea area. The risk is indicated by the ratio of the Predicted Environmental Concentration (PEC) and the Predicted No-Effect Concentration (PNEC) for the marine aquatic environment. In total 14 studies for fish, 7 studies for invertebrates and 9 studies for algae have been evaluated. Both acute and chronic studies have been taken into account and the appropriate assessment factors have been used to calculate a PNEC value of 21 microg/l based on long term exposure. The PEC was derived from monitoring data. The PEC was set at 0.206 microg/l (worst case) and 0.024 microg/l (typical case) for coastal waters and estuaries and 0.6 microg/l (worst case) and <0.1 microg/l (typical case) for river waters. The calculated PEC/PNEC ratios, which do not take into account any dilution factor within the sea, correspond to a safety margin of 35 to 1000 between the aquatic effect and the exposure concentration. 1,1,1-trichloroethane is not a 'toxic, persistent and liable to bioaccumulate' substance according to the criteria as mentioned by the Oslo and Paris Conventions for the Prevention of Marine Pollution (OSPAR-DYNAMEC). It can be concluded that the present use of 1,1,1-trichloroethane does not present a risk to the marine aquatic environment.     

Trace elements and organochlorines in surf scoters from San Francisco Bay, 1985

Surf scoters (Melanitta perspicillata) were collected from 6 locations in San Francisco Bay during January and March 1985. Overall, mean concentrations of cadmium and zinc were higher in livers of scoters from the southern region of the Bay, whereas mean iron and lead were higher in those from the northern Bay region. Mean concentrations of arsenic, copper, lead, zinc, aluminum (January only) and iron (January) also differed among individual locations. Mean concentrations of copper and zinc increased, arsenic decreased, and cadmium remained the same between January and March. Selenium and mercury concentrations in scoter livers were not significantly correlated (P>0.05), but cadmium concentrations in livers and kidneys were positively correlated (P<0.0001), and body weight was negatively related to mercury concentration in the liver (P<0.05). Body weight differed among locations but not between January and March. Body weight was correlated with lipid content (P<0.0001). DDE and PCBs were each detected in 34 of 36 scoter carcasses. DDE increased significantly between January and March at Richmond Harbor, but BCBs did not differ between January and March at the 3 locations that could be tested.     

Induction of oxidative stress by non-lethal dose of mercury in rat liver: possible relationships between apoptosis and necrosis

Sprague Dawley strain of male rats weighing 200 +/- 10.0 g, were exposed intramuscularly to non-lethal dose of mercury for short acute duration of 24 and 48 hr. Mercury treatment increased thio-barbituric acid reactive substance (TBARS) and conjugated diene (CD) content with increase in duration when compared with control. This reflects possible increase in lipid peroxidation, revealing that sufficient intoxication was generated by non-lethal dose of mercury. Furthermore, mercury treatment decreased tissue glutathione (GSH) content to 2.07 and 1.49 microg GSH mg protein(-1) with concomitant decrease in glutathione-S-transferase (GST) activity by 26.06 and 36.40% after 24 and 48 hr of exposure respectively. The elevations of aspartate transaminase (AST) and alanine transaminase (ALT) levels measured exhibited increase of 287.5 and 214.5% after 48 hr of exposure respectively which were found to be highly significant compared with control. Western blot analysis indicated upregulation of caspase-9 and upsurge in effect or caspase-3 activity leading to apoptosis. The concluded findings of the present investigation suggests possible role of early mercury exposure in inducing oxidative stress mediated apoptosis in mammalian model systems as an indicator component of environmental toxicology.