Glenn C. Millner

University of Arkansas at Little Rock, Little Rock, Arkansas, United States

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Publications (5)8.81 Total impact

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    ABSTRACT: IntroductionComplaints of poor water quality and skin rashes among workers at a US cardboard manufacturing facility were investigated to determine potential causes.Methods Employees were interviewed regarding work duties and health symptoms. Areas of dermatitis in affected employees were visually examined. Collected water samples were tested for potential chemical and microbial contaminants.ResultsA total of 27 employees were identified with complaints of recent skin rashes affecting primarily the upper and lower extremities. Dermatitis complaints were associated with water contact and work in areas with poor water quality. Water testing showed high levels of Pseudomonas aeruginosa. Other tested substances were not at levels of concern.Conclusions Overgrowth of P. aeruginosa occurred in the water system shortly after the facility switched to a closed-loop water recycling system and was the most likely cause of the observed dermatitis. To our knowledge, this is the first reported outbreak of Pseudomonas folliculitis in an industrial setting. Am. J. Ind. Med. 49:895–899, 2006. © 2006 Wiley-Liss, Inc.
    No preview · Article · Nov 2006 · American Journal of Industrial Medicine
  • David J. Hewitt · Glenn C. Millner · Alan C. Nye · Margaret Webb · R. Gail Huss
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    ABSTRACT: Elevated surface soil arsenic levels over 100 mg/kg were identified in residential areas near a Superfund site in Fort Valley, GA, at which arsenical pesticides previously had been manufactured. Arsenic levels in drinking water and air were not significantly elevated. A baseline risk assessment suggested an increased potential for adverse health effects due to incidental ingestion of soil. To address community concerns and guide remediation goals, arsenic exposure in residents living and working near the facility was assessed through measurement of total urinary arsenic in random and 24-hour samples during the summer of 1993. Of225 urine samples obtained from 115 individuals, over 90% had undetectable levels of arsenic (less than 10 pg/1). None exceeded 34 μg/1 (laboratory normal value is less than 100 μg/1). The mean urinary arsenic concentration for participants was approximately 6 μg/1 assuming a concentration of one-half the detection limit for samples in which arsenic was not detected. Urinary arsenic concentration was not associated with gender, age, race, home location, or property arsenic soil concentration. These results suggest there was not an increased level of arsenic exposure in the community. The regulatory implications of the study results are discussed.
    No preview · Article · Sep 1995 · Human and Ecological Risk Assessment
  • Glenn C. Millner · Robert C. James · Alan C. Nye
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    ABSTRACT: Soil cleanup guidelines were developed for diesel fuel No. 2 that are protective of human health. Guidelines were conservatively based on a residential land use scenario. This scenario estimates human health risks associated with long‐term exposure to site soil via the inhalation, dermal, and ingestion routes of exposure. Lifetime dermal cancer studies were selected as the basis for deriving a safe level of diesel fuel in soil. Soil cleanup guidelines for diesel fuel No. 2 ranged from 1166 to 11,287 mg/kg for adult or child residents and represent contaminant levels that pose acceptable health risks for both present and proposed future uses of a site.
    No preview · Article · Jan 1992 · Soil and Sediment Contamination (formerly Journal of Soil Contamination)
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    ABSTRACT: Previous studies have suggested a significant role for reproductive tract glutathione in protecting against chemical-induced germ-cell mutations. Therefore, a number of compounds were tested for their ability to perturb glutathione levels in the testes and epididymides as well as liver following single acute dosages to rats. Phorone (250 mg/kg), isophorone (500 mg/kg), and diethyl maleate (500 mg/kg) significantly reduced glutathione in the liver and in both reproductive organs examined. Methyl iodide (100 mg/kg), trimethyl phosphate (600 mg/kg), naphthalene (500 mg/kg), acetaminophen (1500 mg/kg), and pentachlorophenol (25 mg/kg) affected hepatic and epididymal glutathione, but had little or no effect on testicular levels. The ability of isophorone to enhance the covalent binding of tritiated ethyl methanesulfonate (3H-EMS) to spermatocytes was assessed. Perturbation of reproductive tract glutathione by isophorone treatment significantly enhanced the extent of 3H-EMS-induced binding to sperm heads. The temporal pattern of ethylations in sperm heads was consistent with the stage of sperm development known to be susceptible to ethylations by EMS. Therefore, chemical-induced lowering of glutathione in the male reproductive tract may be a mechanism for potentiation of chemical-induced germ-cell mutations.
    No preview · Article · Feb 1990 · Journal of Toxicology and Environmental Health
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    ABSTRACT: It has recently been demonstrated that morphine produces a loss of hepatocellular glutathione in mice by virtue of its action within the central nervous system. The ability of opioid receptor antagonists to abolish morphine's effect on hepatic glutathione suggests that this action is opioid-receptor mediated. The involvement of opioid receptors in this phenomenon is confirmed in the present study in mice by the ability of naltrexone, 100 micrograms administered intracerebroventricularly (i.c.v.), to completely block the decrease in hepatic glutathione induced by an i.c.v. injection of 100 micrograms of morphine. Intracerebroventricular administration of the selective mu (mu) opioid receptor agonist, (D-Ala2,N-MePhe4,Gly-ol5)enkephalin (DAGO; 25-50 micrograms), or the selective delta (delta) opioid agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE; 3-50 micrograms), like morphine, produced significant decreases in hepatic glutathione 3 h after administration. The selective kappa (kappa) opioid receptor agonists, ethylketocyclazocine (1-30 micrograms) and trans-(+/-)3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl] benzeneacetamide-methane sulfonate (U50 488; 10-300 micrograms), as well as the selective sigma (sigma) opioid agonists, phencyclidine (PCP; 50-300 micrograms) and N-allylnormetazocine (SKF 10,047; 1-30 micrograms), had no effect on the concentrations of glutathione in the liver. It appears from these data that stimulation of mu- or delta-, but not kappa- or sigma-opioid receptors within the central nervous system results in a loss of hepatocellular glutathione.
    Full-text · Article · Nov 1988 · Toxicology