Effects of polychlorinated biphenyls, hexachlorocyclohexanes, and mercury on human neutrophil apoptosis, actin cytoskelton, and oxidative state.

Apoptosis, or programmed cell death, has been proposed as a biomarker for environmental contaminant effects. In this work, we test the hypothesis that in vitro assays of apoptosis are sensitive indicators of immunological effects of polychlorinated biphenyls, hexachlorocyclohexanes, and mercury on human neutrophils. Apoptosis, necrosis, and viability as well as the related indicators F-actin levels, and active thiol state were measured in purified human neutrophils after treatment with contaminants. Effective concentrations observed were 0.3µM (60µg/L) mercury, 750µg/L Aroclor 1254, and 50µM (14,500µg/L) hexachlorocylcohexanes. Concentrations of contaminants that induced apoptosis also decreased cellular F-actin levels. Active thiols were altered by mercury, but not organochlorines. Comparison of these data with levels of contaminants reported to be threats to human health indicate neutrophil apoptosis is a sensitive indicator of mercury toxicity.

Aquatic toxicity of four alkylphenols (3-tert-butylphenol, 2-isopropylphenol, 3-isopropylphenol, and 4-isopropylphenol) and their binary mixtures to microbes, invertebrates, and fish.

The acute and chronic toxicity of four simple alkylphenols with butyl and propyl substitutions was evaluated with aquatic microbes, invertebrates, and fish. These alkylphenols-3-tert-butylphenol, 2-isopropylphenol, 3-isopropylphenol, and 4-isopropylphenol-have been detected in various environmental media, but their impact on aquatic fauna has seldom been evaluated. Relative susceptibility to each phenolic varied by test species. The marine bacterium Vibrio fischeri was the most susceptible to the alkylphenols, up to 3 orders of magnitude more sensitive than species of higher trophic levels. For 4-isopropylphenol, the 5-min Microtox EC(50) value was 0.01 mg/L, whereas the EC(50) for Ceriodaphnia after a 48-h exposure was 10.1 mg/L. Notable differences in sensitivity to the alkylphenols was also observed with the Microtox assay: 4-isopropylphenol was > 200 times more toxic to V. fischeri than was 2-isopropylphenol (EC(50) = 2.72 mg/L). For V. fischeri, the mixture toxicity of the alkylphenols was additive in nature and was predicted by a concentration addition model. The energy of the lowest unoccupied molecular orbital (ELUMO) explained the observed toxicity of the individual alkylphenols to V. fischeri (r(2) = 0.92, p < 0.05). These results suggest that the mode of action of polar narcotic alkylphenols to V. fischeri is different than that of other test organisms, possibly because of the differences in the cell structure of the prokaryotic V. fischeri.

The toxicity of fluoranthene to Hyalella azteca in sediment and water-only exposures under varying light spectra.

In the US Environmental Protection Agency methods for sediment toxicity testing, the light regimen is specified as a 16:8 light dark cycle with 500-1000 lx. The potential for photoinduced toxic effects from this requirement is evaluated. Hyalella azteca were exposed to fluoranthene in both water only and sediment to examine the impact of light spectra on the toxicity of fluoranthene. The light sources included gold fluorescent light (lambda > 500 nm), cool white fluorescent light, and UV-enhanced fluorescent light. Toxicity was determined as mortality after 10 days of exposure. The extent of mortality was determined both as LC(50) and LR(50) (median lethal body residue). In water-only exposures, the toxicity of fluoranthene was greatest under the UV-enhanced spectra, followed by fluorescent light, and least toxic under the gold light. Both the LC(50) and LR(50) values exhibited the same pattern. The toxicity under gold light gave an LR(50) of 0.81 mmol kg(-1) (0.82-0.79, 95% CI) similar to values expected for the acute toxicity of nonpolar narcotic (anesthetic) compounds. The LR(50) values under the other two light sources were substantially lower, 4 and 58 times lower for the fluorescent and UV-enhanced exposures, respectively. In sediment, toxicity was not significantly affected by the light source. Toxicity occurred only when the body residue concentration approached that of the LR(50) under gold light from the water-only exposures. Thus, H. azteca were significantly protected from the light by burrowing into the sediment.

In vitro toxicity and interactions of environmental contaminants (Arochlor 1254 and mercury) and immunomodulatory agents (lipopolysaccharide and cortisol) on thymocytes from lake trout (Salvelinus namaycush).

The immunotoxicity of chemical combinations commonly encountered by the lake trout (Salvelinus namaycush) immune system was the focus of this study. It was hypothesised that combinations of an environmental contaminant (mercuric chloride or Aroclor 1254) and an immunomodulatory agent (bacterial endotoxin or cortisol) might interact to produce a greater toxicity than that of the environmental contaminant alone at concentrations typically encountered in piscine blood and other tissues. Thus lake trout thymocytes were isolated and treated with mercuric chloride or Aroclor 1254 in the presence and absence of cortisol or lipopolysaccharide. Incubations were performed for 6 or 20 h at 4 degrees C or 10 degrees C. Lipopolysaccharide did not affect the toxicity of either contaminant. In contrast, cortisol enhanced the toxicity of both environmental contaminants. Hence, stressors that lead to increased cortisol production, but not lipopolysaccharide directly, may increase the toxicity of mercury and Aroclor 1254 to lake trout thymocytes.