Concentrations of trace elements in American alligators (Alligator mississippiensis) from Florida, USA.

Concentrations of 28 trace elements (Li, Mg, Al, V, Cr, Mn, Fe, Co, Ni, Cu, Zn, Ga, As, Se, Rb, Sr, Mo, Ag, Cd, In, Sn, Sb, Cs, Tl, Hg, Pb, and Bi) in the livers of juvenile and adult American alligators inhabiting two central Florida lakes, Lake Apopka (LA), and Lake Woodruff National Wildlife Refuge (LW) and one lagoon population located in Merritt Island National Wildlife Refuge (MINWR; NASA), were determined. In juveniles from MINWR, concentrations of nine elements (Li, Fe, Ni, Sr, In, Sb, Hg, Pb and Bi) were significantly higher, whereas six elements (V, Fe, As, Sr, Hg and Bi) were elevated in adults (p<0.05) obtained from MINWR. Significant enrichment of some trace elements in adults, relative to juveniles, was observed at all three sampling areas. Specifically, Fe, Pb and Hg were significantly elevated in adults when compared to juveniles, suggesting age-dependent accumulation of these elements. Further, As, Se and Sn showed the same trend but only in animals collected from MINWR. Mean Fe concentrations in the livers of adults from LA, LW and MINWR were 1770 µg g(-1) DW, 3690 µg g(-1) DW and 5250 µg g(-1) DW, respectively. More than half of the adult specimens from LW and MINWR exhibited elevated hepatic Fe concentrations that exceed the threshold value for toxic effects in donkey, red deer and human. These results prompted us to express our concern on possible exposure and health effects in American alligators by some trace elements derived from NASA activities.

Hypoxia-induced exposure of isaza fish to manganese and arsenic at the bottom of Lake Biwa, Japan: experimental and geochemical verification.

In December 2007, a mass mortality of isaza (Gymnogobius isaza), a goby fish in Lake Biwa, Japan, was observed under severe hypoxia. Considering the level of manganese and arsenic in the dead isaza during the event was much higher than that in live isaza, hypoxia-induced mobilization of manganese and arsenic and subsequent exposure could be the reason for this adverse effect. However, secondary accumulation of manganese and arsenic after the mortality event could not be ruled out. To test this hypothesis, we conducted tissue distribution/speciation analysis and absorption tests on dead specimens. All the results, particularly the limited absorption of arsenic in the absorption tests, indicated that the isaza were exposed to arsenic before the mortality event. Parallel to this, the geochemical behavior of manganese and arsenic in oxygen-rich conditions (June) and oxygen-poor conditions (December) was investigated to verify the mechanism of exposure. Considerable enrichment of manganese and arsenic in a thin surface layer of sediment was a common feature in all seven stations studied. In the water at the bottom of the lake, a clear increase of arsenite in December was observed, and the manganese level was several hundred times higher in both seasons than the average level of the lake. Although further verification is needed, the data provided here support exposure to manganese and arsenic under hypoxia.