The synthetic industrial chemical hexachlorobenzene (HCB) is a white crystalline solid compound. The substance is a bioaccumulative, persistent, and toxic pollutant. Historically HCB was commonly used as a pesticide and fungicide. Although HCB production and use has ceased in many countries, the compound is still generated inadvertently, as a byproduct and/or impurity in the manufacture of various chlorinated compounds, and released into the environment. Hexachlorobenzene is ubiquitous in air, water, soil, and biological matrices, as well as in major environmental compartments. Exposure to this substance is a public health concern because of its association with a wide range of adverse health effects. The International Agency for Research on Cancer and the United States Environmental Protection Agency classify HCB as a probable human carcinogen. Although globally the consumption of HCB-contaminated food is the principal source of environmental exposure, exposure can also occur through the inhalation of HCB-contaminated air, by dermal contact, or through in utero exposure and breast milk. In addition to cancer, the human health effects associated with HCB exposure involve systemic impairment (thyroid, liver, bone, skin), as well as damage to the kidneys and blood cells and the immune, endocrine, developmental, and nervous systems. In this review, we discuss the sources of HCB and the potential for human exposure, as well as systemic, carcinogenic, and teratogenic health effects.

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Microorganisms are known to be excellent test organisms because of the relative ease for handling and suitability for analysis related to their small size, large number and convenient growing conditions. In this research, we tested the toxic effects of lead against a marine bacterium (Vibrio fischeri), and a heterogeneous population of bacteria derived from the Pearl River in Jackson, Mississippi. Using the level of bioluminescence in the Microtox Assay (V. fischeri), and the kinetics of dissolved oxygen uptake and growth (mixed bacterial population) as measures of toxicity, lead concentrations effecting a 50% reduction in these parameters (EC50) were determined as the toxic end-points. The activity quotients were also computed to determine the degrees of toxicity. Optical density (measure of growth) and oxygen uptake were measured over an extended period of time (20 h). EC50 values of 0.34 +/- 0.03, 3.10 +/- 0.01, and 3.80 +/- 0.02 mg/L were recorded for bioluminescence, growth, and oxygen uptake, respectively. As expected, the results indicated that the sensitivity to lead toxicity of V. fischeri was about one order of magnitude (10 times) greater than that of the mixed population of Pearl River microorganisms. Reductions in bioluminescence, growth, and oxygen uptake were directly correlated to lead concentrations, with toxic levels ranging from slightly toxic in lower concentrations to extremely toxic in higher concentrations. Upon 20 h of exposure, the times required to produce 50% reduction in dissolved oxygen uptake were (TD50S) 8.01 +/- 0.44, 9.60 +/- 0.46, 11.29 +/- 0.46, 13.03 +/- 0.57, 17.32 +/- 0.95, and 20.00 +/- 0.00 h in 0, 1, 2, 3, 4, 5, and 6 mg/L of lead, respectively, indicating a time-response relationship with respect to lead toxicity.

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