Biomarkers of mercury exposure in two eastern Ukraine cities.

This study evaluates biomarkers of mercury exposure among residents of Horlivka, a city in eastern Ukraine located in an area with geologic and industrial sources of environmental mercury, and residents of Artemivsk, a nearby comparison city outside the mercury-enriched area. Samples of urine, blood, hair, and nails were collected from study participants, and a questionnaire was administered to obtain data on age, gender, occupational history, smoking, alcohol consumption, fish consumption, tattoos, dental amalgams, home heating system, education, source of drinking water, and family employment in mines. Median biomarker mercury concentrations in Artemivsk were 0.26 µg/g-Cr (urine), 0.92 µg/L (blood), 0.42 µg/g (hair), 0.11 µg/g (toenails), and 0.09 µg/g (fingernails); median concentrations in Horlivka were 0.15 µg/g-Cr (urine), 1.01 µg/L (blood), 0.14 µg/g (hair), 0.31 µg/g (toenails), and 0.31 µg/g (fingernails). Biomarkers of mercury exposure for study participants from Horlivka and Artemivsk are low in comparison with occupationally exposed workers at a mercury recycling facility in Horlivka and in comparison with exposures known to be associated with clinical effects. Blood and urinary mercury did not suggest a higher mercury exposure among Horlivka residents as compared with Artemivsk; however, three individuals living in the immediate vicinity of the mercury mines had elevated blood and urinary mercury, relative to overall results for either city. For a limited number of residents from Horlivka (N = 7) and Artemivsk (N = 4), environmental samples (vacuum cleaner dust, dust wipes, soil) were collected from their residences. Mercury concentrations in vacuum cleaner dust and soil were good predictors of blood and urinary mercury.

The effects of enhanced zinc on spatial memory and plaque formation in transgenic mice.

There is considerable evidence suggesting that metals play a central role in the pathogenesis of Alzheimer's disease. Reports suggest that elevated dietary metals may both precipitate and potentiate an Alzheimer's disease phenotype. Despite this, there remain few studies that have examined the behavioral consequences of elevated dietary metals in wild type and Alzheimer's disease animals. To further investigate this in the current study, two separate transgenic models of AD (Tg2576 and TgCRND8), together with wild type littermates were administered 10 ppm (0.153 mM) Zn. Tg2576 animals were maintained on a zinc-enriched diet both pre- and postnatally until 11 months of age, while TgCRND8 animals were treated for five months following weaning. Behavioral testing, consisting of "Atlantis" and "moving" platform versions of the Morris water maze, were conducted at the end of the study, and tissues were collected for immunohistochemical analysis of amyloid-beta burden. Our data demonstrate that the provision of a zinc-enriched diet potentiated Alzheimer-like spatial memory impairments in the transgenic animals and was associated with reduced hippocampal amyloid-beta plaque deposits. Zinc-related behavioral deficits were also demonstrated in wild type mice, which were sometimes as great as those present in the transgenic animals. However, zinc-related cognitive impairments in transgenic mice were greater than the summation of zinc effects in the wild type mice and the transgene effects.

Anthropogenic sources of arsenic and copper to sediments in a suburban lake, Northern Virginia.

Mass balances of total arsenic and copper for a suburban lake in densely populated northern Virginia were calculated using date collected during 1998. Mass-balance terms were precipitation; stream inflow, including road runoff; stream outflow; and contributions from leaching of pressure-treated lumber. More mass of arsenic and copper was input to the lake than was output the 1998 lake-retention rates were 70% for arsenic and 20% for copper. The arsenic mass balance compared well with a calculated annual mass accumulation in the top 1 cm of the lake sediments; however, the calculated contribution of copper to the lake was insufficient to account for the amount of copper in this zone. Leaching experiments were conducted on lumber treated with chromated copper arsenate (CCA) to quantify approximate amounts of arsenic and copper contributed by this source. Sources to lake sediments included leaching of CCA-treated lumber (arsenic, 50%; copper, 4%), streamwater (arsenic, 50%; copper, 90%), and atmospheric deposition (arsenic, 1%; copper, 3%). Results of this study suggest that CCA-treated lumber and road runoff could be significant nonpoint sources of arsenic and copper, respectively, in suburban catchments.