Physico-Chemical Characterization and Assessment of Cytotoxic and Genotoxic Effects of Poly-Ethylene-Glycol Coated and Uncoated Gold Nanoparticles on Human Kidney (HK-2) Cells.

Although gold nanoparticles (Au-NPs) have been widely used in medicine for the diagnosis and treatment of patients due to their unique physicochemical properties, chemical stability and biocompatibility, recent reports have also highlighted their potential to induce toxicity to humans. In the present study, we investigated the toxic effects of uncoated and polyethylene glycol (PEG)-coated AuNPs on human kidney (HK-2) cells. Both forms of AuNP were synthesized and characterized using standard protocols. Dynamic Light Scattering (DLS), Zeta Sizer Nano ZS analyzer, Transmission Electron Microscopy (TEM), and Inductively Coupled Plasma-Optical Emission Spectroscopy (ICP-OES) were used to measure their distribution, zeta potential/surface charge, morphological size, and Au concentrations, respectively. Cytotoxicity was measured by Cyto-Tox assay and trypan blue exclusion test. Oxidative stress (OS) was assessed by quantifying the levels of Glutathione (GSH), and Mitochondria Membrane Potential (MMP). Genotoxicity was assessed by single cell gel electrophoresis (Comet assay) and Chromosomal Aberration (CA) assay. Uncoated AuNPs significantly reduced cell viability, increased ROS, decreased GSH, depolarized the MMP, and induced significant DNA damage and chromosomal alterations including chromosome gaps, centric rings, breaks, deletions, and intra and inter-chromosome exchanges, in a concentration-dependent manner. PEG-coated AuNPs displayed lower cytotoxic and genotoxic effects, and did not produce any significant increase in ROS or significant decrease in GSH along with negligible polarization of the MMP. Hence, PEG-coated AuNPs are relatively less toxic than uncoated AuNPs and therefore, may have potential applications in nanomedicine.

Thrombospondin-1 and microRNA-1 expression in response to multiwalled carbon nanotubes in alveolar epithelial cells.

Thrombospondin-1 (TSP-1) is a glycoprotein that plays a role in extracellular matrix (ECM) remodeling. Previously, we have shown that multiwalled carbon nanotubes (MWCNT) regulate ECM components TGFß and its target Col3A1 in alveolar epithelial cells. In this study, we investigated the effect of MWCNT on TSP-1 and microRNA-1 (miR-1) in the regulation of TGFß in ECM remodeling using alveolar epithelial A549 cells. A549 cells were treated with MWCNT (20 or 50 µg/mL) for 6 or 24 h and the expression of TSP-1 and miR-1, and the exogenous miR-1 effect on cell morphology were analyzed. MWCNT induced in a time- and dose-dependent manner the expression of TSP-1. miR-1 was suppressed by MWCNT after 6 or 24 h of treatment regardless of the dose. TSP-1 and miR-1 negatively correlated with each other, r = -0.58. Exogenous administration of miR-1 induced alveolar epithelial cell morphology changes including cell clustering, whereas inhibition of miR-1 induced less cell to cell contact, cell rounding, and cellular projections. IntAct molecular network interactions analysis revealed that TSP-1 interacts with 21 molecular factors including ECM genes, and molecules. These results indicate a relationship between that TSP-1, MWCNT, and TGFß, and suggest TSP-1 may play a role in MWCNT-induced TGFß and ECM remodeling. Moreover, these data also suggest an inverse relationship between TSP-1 and miR-1 and a potential role of miR-1 in MWCNT-induced fibrotic signaling. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1596-1606, 2017.

Effects of lipopolysaccharide, multiwalled carbon nantoubes, and the combination on lung alveolar epithelial cells.

Multiwalled carbon nanotubes (MWCNT) have been shown to induce lung fibrosis in animal models, however the underlying molecular factors/mechanisms are still unclear. In this study, we investigated the effects of lipopolysaccharide (LPS), MWCNT, and the combination of LPS and MWCNT on the expression of matrix metalloproteinase-9 and metalloproteinase-12 (MMP-9, MMP-12), collagen 3A1 (Col3A1), and transforming growth factor beta (TGFß) in alveolar epithelial A549 cells. MMPs are proteinases that degrade extracellular matrix and play a role in lung fibrosis. A549 cells were exposed to LPS (1 ng/mL), MWCNT (20 µg/mL), and the combination and analyzed for paracellular permeability, TGFß, Col3A1, MMP-9, MMP-12, NF-κB activation, and cell migration by real-time PCR and immunofluorescence. LPS, the combination of LPS and MWCNT, and MWCNT only at the highest tested dose induced blue dextran extravasation. LPS and MWCNT increased the expression of TGFß and its downstream target gene Col3A, and MMP-9 and MMP-12 mRNA. MWCNT potently induced cell migration toward wound healing, whereas LPS slightly induced cell migration. Both, LPS and MWCNT, induced NF-κB nuclear translocation. Our results indicate that MWCNT activated alveolar epithelial cells to promote fibrogenesis, and that LPS differentially primes molecular factors involved in lung remodeling. These findings suggest a role of alveolar epithelial cells in fibrogenesis and also may aid in the design and development of tests for screening of fibrogenic agents. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 445-455, 2017.

Biochemical and Histopathological Evaluation of Graphene Oxide in Sprague-Dawley Rats.

Graphene and its derivatives are promising material for important biomedical applications due to their versatility. A detailed comprehensive study of the toxicity of these materials is required in context with the prospective use in biological setting. We investigated toxicity of Graphene Oxide (GO) in rats following exposure with respect to hepatotoxicity and oxidative stress biomarkers. Four groups of five male rats were orally administered GOs, once a day for five days, with doses of 10, 20 and 40mg/Kg GO. A control group consisted of five rats. Blood and liver were collected 24h after the last treatment following standard protocols. GO's exposure increased induction of Reactive Oxygen Species (ROS), activities of liver enzymes (Alanine ALT, Aspartate AST, Alkaline Phosphates ALP), concentration of Lipid Hydro Peroxide (LHP) and morphological alterations of liver tissue in exposed groups compared to control. The highest two doses, 20 and 40mg/kg, showed statistically significant (p<0.05) increases in the induction of ROS, activities of ALT, ALP, LHP concentration, and morphological alterations of liver tissue compared to control. However, AST activity showed no effect. The results of this study demonstrate that GO may be hepatotoxic, and its toxicity might be mediated through oxidative stress.

Comparative Study of Epidemiological and Anthropological Aspects of Diabetes and Hypertension in Cameroon.

The traditional medicine in Africa in general and specifically in Cameroon does not manage diabetes and arterial hypertension very well. Yet, these pathologies are becoming more prevalent among the populations that need adequate knowledge to fight against them. Therefore the present study was designed to determine the knowledge, attitudes and practices of indigenous people regarding diabetes and hypertension control, and to assess the epidemiological aspects of these diseases in order to reinforce their health education and promote a better health care through traditional medicine. To achieve this objective, 1,131 households including 70 traditional healers, 114 diabetics, 167 hypertensive patients, 30 hypertensive patients-diabetics and other Cameroonians were questioned on their ethnomedical knowledge of diabetes and arterial hypertension. Fifty-eight randomly distributed tribes were taking in account. The elucidation of anthropological and epidemiological aspects of diabetes and hypertension improved the beliefs of indigenous people and facilitated the modernization of diabetes and hypertension comprehension that remained focused on the elucidation of diseases' causes and complications, as well as on the behaviors that could help translate biomedical terms into locally meaningful metaphors.

Groundwater vulnerability to pollution mapping of Ranchi district using GIS.

Groundwater pollution due to anthropogenic activities is one of the major environmental problems in urban and industrial areas. The present study demonstrates the integrated approach with GIS and DRASTIC model to derive a groundwater vulnerability to pollution map. The model considers the seven hydrogeological factors [Depth to water table (D), net recharge (R), aquifer media (A), soil media (S), topography or slope (T), impact of vadose zone (I) and hydraulic Conductivity(C)] for generating the groundwater vulnerability to pollution map. The model was applied for assessing the groundwater vulnerability to pollution in Ranchi district, Jharkhand, India. The model was validated by comparing the model output (vulnerability indices) with the observed nitrate concentrations in groundwater in the study area. The reason behind the selection of nitrate is that the major sources of nitrate in groundwater are anthropogenic in nature. Groundwater samples were collected from 30 wells/tube wells distributed in the study area. The samples were analyzed in the laboratory for measuring the nitrate concentrations in groundwater. A sensitivity analysis of the integrated model was performed to evaluate the influence of single parameters on groundwater vulnerability index. New weights were computed for each input parameters to understand the influence of individual hydrogeological factors in vulnerability indices in the study area. Aquifer vulnerability maps generated in this study can be used for environmental planning and groundwater management.

Influence of local meteorology and NO2 conditions on ground-level ozone concentrations in the eastern part of Texas, USA.

The influence of local climatic factors on ground-level ozone concentrations is an area of increasing interest to air quality management in regards to future climate change. This study presents an analysis on the role of temperature, wind speed, wind direction, and NO2 level on ground-level ozone concentrations over the region of Eastern Texas, USA. Ozone concentrations at the ground level depend on the formation and dispersion processes. Formation process mainly depends on the precursor sources, whereas, the dispersion of ozone depends on meteorological factors. Study results showed that the spatial mean of ground-level ozone concentrations was highly dependent on the spatial mean of NO2 concentrations. However, spatial distributions of NO2 and ozone concentrations were not uniformed throughout the study period due to uneven wind speeds and wind directions. Wind speed and wind direction also played a significant role in the dispersion of ozone. Temperature profile in the area rarely had any effects on the ozone concentrations due to low spatial variations.

EFFECT OF COPPER OXIDE NANOPARTICLES TO SHEEPSHEAD MINNOW (CYPRINODON VARIEGATUS) AT DIFFERENT SALINITIES.

Nanotechnologies research has become a significant priority worldwide. Many engineered nano-sized materials have been increasingly used in consumer products. But the adverse effects of these nanoparticles on the environment and organisms have recently drawn much attention. The present study investigated the effects of different concentrations of copper oxide nanoparticles (CuO NPs) on the sheepshead minnow (Cyprinodon variegatus) at different salinity regimes, since it is able to withstand a wide range of salinities. The results indicated that CuO NPs could cause behavioral changes in the fish, such as increased mucus secretion, less general activity and loss of equilibrium. No mortality was observed at the presence of CuO NPs during the experiments. But higher oxidative stress was determined at half strength seawater than seawater exposure medium, which can be associated with the decreasing toxicity of CuO NPs as salinity increases. In addition, Cu contents in the tissues of the fish were significantly higher (p<0.05) in the low salinity. The order of Cu accumulation in the fish's organs was intestine > gills > liver.

Induced mitogenic activity in AML-12 mouse hepatocytes exposed to low-dose ultra-wideband electromagnetic radiation.

Ultra-wideband (UWB) technology has increased with the use of various civilian and military applications. In the present study, we hypothesized that low-dose UWB electromagnetic radiation (UWBR) could elicit a mitogenic effect in AML-12 mouse hepatocytes, in vitro. To test this hypothesis, we exposed AML-12 mouse hepatocytes, to UWBR in a specially constructed gigahertz transverse electromagnetic mode (GTEM) cell. Cells were exposed to UWBR for 2 h at a temperature of 23 degrees C, a pulse width of 10 ns, a repetition rate of 1 kHz, and field strength of 5-20 kV/m. UWB pulses were triggered by an external pulse generator for UWBR exposure but were not triggered for the sham exposure. We performed an MTT Assay to assess cell viability for UWBR-treated and sham-exposed hepatocytes. Data from viability studies indicated a time-related increase in hepatocytes at time intervals from 8-24 h post exposure. UWBR exerted a statistically significant (p < 0.05) dose-dependent response in cell viability in both serum-treated and serum free medium (SFM) -treated hepatocytes. Western blot analysis of hepatocyte lysates demonstrated that cyclin A protein was induced in hepatocytes, suggesting that increased MTT activity after UWBR exposure was due to cell proliferation. This study indicates that UWBR has a mitogenic effect on AML-12 mouse hepatocytes and implicates a possible role for UWBR in hepatocarcinoma.

Freshwater microcosms-based assessment of eco-toxicological effects of a chemical effluent from the Pilcam industry in Cameroon.

We studied the acute toxicity of a raw effluent from a battery manufacturing plant (Pilcam) in Douala, Cameroon, to a freshwater fish (Oreochromis niloticus), and subsequently evaluated its sub-acute effects on water quality and the biota in freshwater microscosms. The acute toxicity test was based on 96 hrs static renewal bioassays that resulted in 96-h LC50 and LC90 values of 16 and 20.7% (v/v), respectively. The sub-acute experiments were conducted by exposing several species of aquatic organisms (plankton, macroinvertebrates and mollusks) to lower effluent concentrations [1.6%, 8.0%, 16% (v/v)] for six weeks, and monitoring their survival rates, as well as the physical and chemical characteristics of water. These concentrations were based on 10%, 50%, and 100% of the 96 h - median lethal concentrations (LC50) of the effluent to the freshwater fish, Oreochromis niloticus. Significant effects on functional parameters, such as, chlorophyll-a and total protein could not be demonstrated. However, the activity of alkaline phosphatase was significantly inhibited at all concentrations tested. Phytoplankton, zooplankton, macro-invertebrate communities and snails were negatively affected by the effluent application at concentrations ? 8% (v/v), with chlorophyta, ciliates, ostracoda, annelida, planaria and snails being the most sensitive groups. The snails were eliminated after 24 h exposure from microcosms treated with effluent at concentration ? 8% (v/v). Effluent exposure also caused significant effects on water quality parameters (DO, pH, hardness, conductivity, color, turbidity, ammonia) in general at concentrations ? 8% (v/v). Temperature and alkalinity were not significantly affected. Overall, data from this research indicate that a dilution of the Pilcam effluent down to 1.6% does not provide protection against chronic toxicity to aquatic organisms. Further studies are needed to determine the no observable adverse effect level (NOAEL), as well as a chronic reference concentration for this effluent.

Arsenic trioxide-induced transcriptional activation of stress genes and expression of related proteins in human liver carcinoma cells (HepG2).

Arsenic is a naturally occurring element, but anthropogenic activities can lead to a substantial contamination of the environment. Exposure to arsenic has been associated with a significant number of adverse health effects in humans including: cardiovascular disease, diabetes, hearing loss, developmental abnormalities, anemia, neurologic and neurobehavioral disorder, leukopenia, eosinophilia, fibrosis of the liver and the kidney and various neoplasms. However, the cellular and molecular events associated with arsenic toxicity are poorly understood. Also, the precise mechanisms by which arsenic acts as a carcinogen in humans remain to be elucidated. In the present study, we used human liver carcinoma (HepG2) cells as a model to study the molecular mechanisms of arsenic-induced toxicity and carcinogenesis. We hypothesized that arsenic-induced expression of stress genes and related proteins may play a role in the cellular and molecular events leading to toxicity and tumorigenesis in liver cells. To test this hypothesis, we performed the MTT-assay for cell viability, the CAT-Tox (L) assay for gene induction, and the Western Blot analysis to assess the expression of cellular proteins including c-fos, HMTIIA, HSP70 and p53. Data obtained from the MTT assay indicated a strong dose-response relationship with respect to arsenic trioxide toxicity. Upon 48 hr of exposure, the chemical dose required to cause 50% reduction in cell viability (LD50) was computed to be 8.55 +/- 0.58 microg/ml. The CAT-Tox (L) assay showed statistically significant inductions (p<0.05) of c-fos, HMTIIA, and HSP70. Western blot analysis also demonstrated a dose-response relationship with regard to expression of specific cellular proteins. The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p<0.05) between treated and control cells. The lack of a significant induction of p53 may be due to the potential mitogenic effect of arsenic at low levels of arsenic exposure.

Effects of tetrachloroethylene on the viability and development of embryos of the Japanese medaka, Oryzias latipes.

We evaluated the acute toxicity of Tetrachloroethylene (C(2)Cl(4)), and investigated its sub-chronic effects on the embryonic development of Japanese medaka (Oryzias latipes). One-day-old eggs/embryos of this fish species were exposed, under static renewal conditions, to serial concentrations (0, 20, 40, 60, and 80 mg/L) of C(2)Cl(4) for 96 h (acute) and 10 days (sub-chronic) time periods. The toxic endpoints evaluated included: egg/embryo viability, hatchability, and morphological/developmental abnormalities. The acute toxicity test resulted in a 96 h-LC(50) of 27.0 (19.5-32.9) mg/L for egg viability. Exposure of eggs to sub-chronic concentrations (0, 1.5, 3, 6, 12, and 25 mg/L) of C(2)Cl(4) significantly reduced hatchability and larval survival, in a concentration dependent manner. At the highest tested concentration (25 mg/L) of the sub-lethal exposure, larval survival was greatly reduced to within three days post-hatch. The lowest tested concentration (1.5 mg/L) produced a significant number of developmental effects to the Japanese medaka, including abnormal development of the circulatory system, yolk-sac edema, pericardial edema, scoliosis, hemorrhaging, blood pooling, and defects in heart morphology. The severity of these abnormalities was concentration-dependent. It can be concluded from these results that tetrachloroethylene is teratogenic to the Japanese medaka.

Cytotoxicity and transcriptional activation of stress genes in human liver carcinoma cells (HepG2) exposed to cadmium chloride.

Epidemiological studies have shown that there exists some correlation between cadmium exposure and human cancers. The evidence that cadmium and cadmium compounds are probable human carcinogens is also supported by experimental studies reporting induction of malignant tumors formation in multiple species of laboratory animals exposed to these compounds. In vitro studies with mammalian cells have also shown that cadmium is clastogenic, but its mutagenic potential is rather weak. In this research, we performed the MTT assay for cell viability to assess the cytotoxicity of cadmium chloride (CdCl2), and the CAT-Tox (L) assay to measure the induction of stress genes in thirteen different recombinant cell lines generated from human liver carcinoma cells (HepG2), by creating stable transfectants of different mammalian promoter-chloramphenicol acetyltransferase (CAT) gene fusions. Cytotoxicity experiments with the parental cell line yielded a LC50 of 6.1 +/- 0.8 microg/mL, upon 48 h of exposure. Four (metallothionein--HMTIIA, 70-kDa heat shock protein--HSP70, xenobitic response element--XRE, and cyclic adenosine monophosphate response element--CRE) out of the 13 constructs evaluated showed statistically significant inductions (p < 0.05). The induction of these genes was concentration-dependent. Marginal inductions were also recorded for the c-fos, and 153-kDa growth arrest DNA damage (GADD153) promoters, indicating a potential for CdCl2 to damage DNA. However, no significant inductions (p > 0.05) of gene expression were recorded for cytochrome P4501A1--CYP1A1, glutathion-S-transferase Ya subunit--GST Ya, nuclear factor kappa (B site) response element--NFkappaBRE, tumor suppressor protein response element--p53RE, 45-kDa growth arrest DNA damage--GADD45, 78-kDa glucose regulated protein--GRP78, and retinoic acid response element--RARE. As expected, these results indicate that metallothioneins and heat shock proteins appear to be excellent candidates for biomarkers for detecting cadmium-induced proteotoxic effects at the molecular and cellular levels. Induction of XRE indicates the potential involvement of CdCl2 in the biotransformation process in the liver, while activation of CRE indicates stimulation of cellular signaling through the protein kinases pathway.

Atrazine potentiation of arsenic trioxide-induced cytotoxicity and gene expression in human liver carcinoma cells (HepG2).

Recent studies in our laboratory indicated that arsenic trioxide has the ability to cause significant cytotoxicity, and induction of a significant number of stress genes in human liver carcinoma cells, HepG2. However, similar investigations with atrazine did not show any significant effects of this chemical on HepG2 cells, even at its maximum solubility of 100 microg/mL in 1% dimethyl sulfoxide (DMSO). Further cytogenetic studies were therefore carried out to investigate the combined effects of arsenic trioxide and atrazine on cell viability and gene expression in immortalized human hepatocytes. Cytotoxicity was evaluated using the MTT-assay for cell viability, while the CAT-Tox (L) assay was performed to measure the induction of stress genes in thirteen different recombinant cell lines generated from human liver carcinoma cells (HepG2), by creating stable transfectants of different mammalian promoter-chloramphenicol acetyltransferase (CAT) gene fusions. Cytotoxicity experiments yielded LC50 values of 11.9 +/- 2.6 microg/mL for arsenic trioxide in de-ionized water, and 3.6 +/- 0.4 microg/mL for arsenic trioxide in 100 microg/mL atrazine; indicating a 3 fold increase in arsenic toxicity associated with the atrazine exposure. Co-exposure of HepG2 cells to atrazine also resulted in a significant increase in the potency of arsenic trioxide to upregulate a number of stress genes including those of the glutathione-S-transferase Ya subunit--GST Ya, metallothioneinIIa--HMTIIA, 70-kDa heat shock protein--HSP70, c-fos, 153-kDa growth arrest and DNA damage (GADD153), 45-kDa growth arrest and DNA damage (GADD45), and 78-kDa glucose regulated protein--GRP78 promoters, as well as the xenobiotic response element--XRE, tumor suppressor protein response element--p53RE, cyclic adenosine monophosphate response element--CRE, and retinoic acid response element--RARE. No significant changes were observed with respect to the influence of atrazine on the modulation of cytochrome P450 1A1-CYP 1A1, and nuclear factor kappa (B site) response element--NFkappaBRE by arsenic trioxide. These results indicate that co-exposure to atrazine strongly potentiates arsenic trioxide-induced cytotoxicity and transcriptional activation of stress genes in transformed human hepatocytes.

Transcriptional activation of stress genes and cytotoxicity in human liver carcinoma cells (HepG2) exposed to 2,4,6-trinitrotoluene, 2,4-dinitrotoluene, and 2,6-dinitrotoluene.

The CAT-Tox (L) assay has recently been developed and validated for detecting and quantifying the specific molecular mechanisms that underlie toxicity of various xenobotic chemicals. We performed this assay to measure the transcriptional responses associated with 2,4,6-trinitrotoluene (TNT) and 2 of its byproducts [2,4 and 2,6-dinitotoluenes (DNTs)] to 13 different recombinant cell lines generated from human liver carcinoma cells (HepG2) by creating stable transfectants of mammalian promoter chloramphenicol acetyltransferase (CAT) gene fusions. Cytoxicity test with the parental HepG2 cells, using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide]-based assay for cell viability, yielded LC50 values of 105 +/- 6 mg/mL for TNT in 1% dimethyl sulfoxide (DMSO), and > 300 mg/mL for DNTs, upon 48 h of exposure. TNT appeared to be more toxic than 2,4-DNT, which also showed a higher toxicity compared to 2,6-DNT. Of the 13 recombinant constructs evaluated, 8 (CYP 1A1, GST Ya, XRE, HMTIIA, c-fos, HSP70, GADD153, and GADD45), 5 (c-fos, HSP70, GADD153, GADD45, and GRP78), and none showed inductions to significant levels (p < 0.05), for TNT, 2,4-DNT, and 2,6-DNT, respectively. For most constructs, the induction of stress genes was concentration-dependent. These results show the potential for TNT and 2,4-DNT to cause protein damage and/or perturbations of protein biosynthesis (HSP70 and GRP78), alterations in DNA sequence or its helical structure (c-fos, GADD153, GADD45), and the potential involvement of TNT in the biotransformation process (CYP 1A1, GST Ya, XRE), and in the toxicokinetics of metal ions (HMTIIA). Within the range of concentrations tested (0-300 mg TNT or DNT/mL in 1% DMSO), no significant inductions (p > 0.05) of NFKBRE, p53RE, CRE, and RARE were found.

Physicochemical and bacteriological assessment of water quality at the Ross Barnett reservoir in central Mississippi.

The Ross Barnett Reservoir serves as a source of water supply for the city of Jackson, Mississippi, U.S.A. and is an important site for recreational activities for many residents of Mississippi counties. A broad spectrum of illness is associated with water-contact activities like bathing and swimming in recreational waters. In the present research, we assessed the bacteriological quality of water in the Ross Barnett Reservoir and compared the levels of bacteria with the recommended criteria for public health protection. From June 12, 1999 to October 2, 1999, we collected water samples weekly from two different sites in the reservoir and tested them for the following bacteriological parameters: heterotrophic plate counts, total coliforms, fecal coliforms, and fecal streptococci. The samples were also tested for basic physical and chemical characteristics of water. The results of the study indicate that the respective mean concentrations of bacteria (colony forming units per 100 mL of water) in water samples collected from the reservoir were 5.6 x 10(6)+/-1.5 x 10(6) (heterotrophic plate counts), 4.5 x 10(4) +/- 5.3 x 10(4) (total coliforms), 5.0 x 10(2) +/- 1.6 x 10(2) (fecal coliforms), and 9.1x10(1)+/-7.3x10(1) (fecal streptococci). The values of all physical and chemical parameters were at acceptable levels. The bacterial densities, however, often exceeded federal/state guidelines by several orders of magnitude, raising considerable public health concerns. Steps should therefore be taken to develop and implement strategies to improve the water quality and to reduce or eliminate the potential health risks associated with water-contact activities in the Ross Barnett Reservoir.

Assessment of lead toxicity to the marine bacterium, Vibrio fischeri, and to a heterogeneous population of microorganisms derived from the Pearl River in Jackson, Mississippi, USA.

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.

Climate change and its potential impacts on the Gulf Coast region of the United States.

The Gulf Coast region of the United States abuts five states, including Alabama, Florida, Louisiana, Mississippi, and Texas. In general, the Gulf of Mexico has a surface area of 1.63 million square kilometers (630,000 square miles) and a watershed area of 4.69 million square kilometers (1.81 million square miles) in the United States. This region is one of the nation's largest ecological systems and is closely linked to a significant portion of the nation's economy. In the Gulf Coast region, energy, fisheries, agriculture, and tourism rank among the most significant sectors of the economy. The Gulf has five of the top ten fishing ports in the United States, and commercial fisheries in the Gulf annually produce nearly 2 billion tons of fish, oysters, shrimps, and crabs. Gulf ports handle one-half of the nation's import-export tonnage. Petroleum produced in the Gulf represents about 80% of the nation's offshore production. The Gulf Coast region largely relies on many natural resources to fuel many important sectors of its economy. But nevertheless, the health and vitality of the Gulf have declined in recent years, caused in part by increasing populations along its coast and the growing demand upon its resources and in part by the accumulation of years of careless depletion, abuse, and neglect of the environment. Equally important are the impacts of natural and human-induced climate change on the economy and on the quality of life for millions of people living in the Gulf Coast region. The results have generated alarming increases in damage to and destruction of the ecosystems and habitats of the Gulf. This paper reviews the nature of global environmental change and addresses the potential health and environmental impacts that may occur in the Gulf Coast region of the United States as a consequence of various environmental alterations resulting from global change.

Important considerations in the development of public health advisories for arsenic and arsenic-containing compounds in drinking water.

Drinking water contamination by arsenic remains a major public health problem. Acute and chronic arsenic exposure via drinking water has been reported in many countries of the world; especially in Argentina, Bangladesh, India, Mexico, Thailand, and Taiwan, where a large proportion of drinking water (ground water) is contaminated with a high concentration of arsenic. Research has also pointed out significantly higher standardized mortality ratios and cumulative mortality rates for cancers of the bladder, kidney, skin, liver, and colon in many areas of arsenic pollution. General health effects that are associated with arsenic exposure include cardiovascular and peripheral vascular disease, developmental anomalies, neurologic and neurobehavioral disorders, diabetes, hearing loss, portal fibrosis of the liver, lung fibrosis, hematologic disorders (anemia, leukopenia, and eosinophilia), and carcinoma. Although, the clinical manifestations of arsenic poisoning appear similar, the toxicity of arsenic compounds depends largely u[on the chemical species and the form of arsenic involved. On the basis of its high degree of toxicity to humans, and the non-threshold dose-response assumption, a zero level exposure is recommended for arsenic, even though this level is practically non-attainable. In this review, we provide and discuss important information on the physical and chemical properties, production and use, fate and transport, toxicokinetics, systemic and carcinogenic health effects, regulatory and health guidelines, analytical methods, and treatment technologies that are applied to arsenic pollution. Such information is critical in assisting the federal, state and local officials who are responsible for protecting public health in dealing with the problem of drinking water contamination by arsenic and arsenic-containing compounds.

The urgent need for environmental sanitation and a safe drinking water supply in Mbandjock, Cameroon.

Studies were conducted to assess the physical, chemical, and bacteriological qualities of drinking water in Mbandjock, Cameroon. Study results indicated that the vast majority of drinking water sources possessed acceptable physical and chemical qualities, according to the World Health Organization standards. However, microbiological analyses revealed that only the waters treated by the Cameroon National Water Company (SNEC) and the Sugar Processing Company (SOSUCAM) were acceptable for human consumption. All spring and well waters presented evidences of fecal contamination from human and/or animal origin. Water from these sources should, therefore, be treated before use for drinking. Since the majority of the population gets its water from wells and springs, there is an urgent need to develop a health education program, within the framework of primary health care, with respect to environmental sanitation and safe drinking water supply in this community.