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Author

Gary P. Carlson

Other affiliations: RMIT University
Bio: Gary P. Carlson is an academic researcher from Purdue University. The author has contributed to research in topics: Styrene oxide & Styrene. The author has an hindex of 27, co-authored 127 publications receiving 3195 citations. Previous affiliations of Gary P. Carlson include RMIT University.


Papers
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01 Jan 2002
TL;DR: Members Ahti Anttila, Finnish Cancer Registry, Institute for Statistical and Epidemiological Cancer Research, Liisankatu 21 B, 00170 Helsinki, Finland Ramesh V. Bhat, National Institute of Nutrition, Indian Council of Medical Research, Jamai-Osmania PO, Hyderabad-500 007 AP, India.
Abstract: Members Ahti Anttila, Finnish Cancer Registry, Institute for Statistical and Epidemiological Cancer Research, Liisankatu 21 B, 00170 Helsinki, Finland Ramesh V. Bhat, National Institute of Nutrition, Indian Council of Medical Research, Jamai-Osmania PO, Hyderabad-500 007 AP, India James A. Bond, Chemico-Biological Interactions, Toxcon, 5505 Frenchmans Creek, Durham, NC 27713, USA Susan J. Borghoff, CIIT Centers for Health Research, 6 Davis Drive, Box 12137, Research Triangle Park, NC 27709-2127, USA F. Xavier Bosch, Epidemiology Unit and Cancer Registry, Catalan Institute of Oncology, Av. Gran via s/n, Km. 2.7, 08907 L’Hospitalet del Llobregat, Spain Gary P. Carlson, School of Health Sciences, 1338 Civil Engineering Building, Purdue University, West Lafayette, IN 47907-1338, USA Marcel Castegnaro, Les Collanges, 07240 Saint-Jean-Chambre, France George Cruzan, ToxWorks, 1153 Roadstown Road, Bridgeton, NJ 08302-6640, USA Wentzel C.A. Gelderblom, Programme on Mycotoxins and Experimental Carcinogenesis, Medical Research Council (MRC), PO Box 19070, Tygerberg, South Africa 7505 Ulla Hass, Institute of Food Safety and Toxicology, Morkhoj Bygade 19, 2860 Soborg, Denmark Sara H. Henry, 5100 Paint Branch Parkway, College Park, MD 20740-3835, USA Ronald A. Herbert, Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, PO Box 12233, Mail Drop B3-08, Research Triangle Park, NC 27709-2233, USA Marc Jackson, Integrated Laboratory Systems, Inc., PO Box 13501, Research Triangle Park, NC 27709, USA IARC WORKING GROUP ON THE EVALUATION OF CARCINOGENIC RISKS TO HUMANS: SOME TRADITIONAL HERBAL MEDICINES, SOME MYCOTOXINS, NAPHTHALENE AND STYRENE

836 citations

Journal ArticleDOI
TL;DR: This study highlights the importance of knowing the carrier and removal status of canine coronavirus, as a source of infection for other animals, not necessarily belonging to the same breeds.
Abstract: (2002). A COMPREHENSIVE EVALUATION OF THE POTENTIAL HEALTH RISKS ASSOCIATED WITH OCCUPATIONAL AND ENVIRONMENTAL EXPOSURE TO STYRENE. Journal of Toxicology and Environmental Health, Part B: Vol. 5, No. 1-2, pp. 1-263.

119 citations

Journal ArticleDOI
TL;DR: It is concluded that styrene respiratory tract toxicity in mice and rats, including mouse lung tumors, are mediated by CYP2F-generated metabolites, and the PBPK model predicts that humans do not generate sufficient levels of these metabolites in the terminal bronchioles to reach a toxic level.

80 citations

Journal ArticleDOI
TL;DR: Results demonstrated the greater role of epoxide hydrolase in styrene oxide detoxification and increased its hepatotoxicity, while buthionine sulfoxamine, a glutathione depletor, did not.
Abstract: The purpose of this study was to investigate the toxicity of styrene and styrene oxide in the lung in comparison to the toxicity in the liver. Pneumotoxicity caused by styrene or styrene oxide was measured by elevations in the release of gamma-glutamyltranspeptidase (GGT) and lactate dehydrogenase (LDH) into bronchoalveolar lavage fluid (BALF), while hepatotoxicity was measured by increases in serum sorbitol dehydrogenase (SDH) in non-Swiss Albino (Hsd:NSA) mice. Intraperitoneal administration of styrene at doses of 500-1000 mg/kg caused consistent dose-dependent increases in both sets of biomarkers with the hepatic effect appearing earlier than the pulmonary effect. Pyridine, phenobarbital, and beta-naphthoflavone, inducers of CYP2E1, CYP2B, and CYP1A, respectively, increased the toxicity of styrene. Pyridine and phenobarbital treatments increased mortality due to styrene. Styrene oxide exists in two enantiomeric forms: (R)- and (S)-styrene oxide, and the differential toxicities of the two enantiomers and racemic styrene oxide were compared. In all studies, (R)-styrene oxide caused greater toxicity than the (S) enantiomer, especially in the liver. Trichloropropene oxide, an epoxide hydrolase inhibitor, was used to inhibit styrene oxide detoxification and increased its hepatotoxicity, while buthionine sulfoxamine, a glutathione depletor, did not. These results demonstrated the greater role of epoxide hydrolase in styrene oxide detoxification.

77 citations

Journal ArticleDOI
TL;DR: Commercial preparations of fire retardant brominated diphenyl ethers and bis (p-bromophenyl) ether are inducers of xenobiotic metabolism with activity dependent upon degree of bromination.

69 citations


Cited by
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Journal ArticleDOI
TL;DR: A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.
Abstract: Cancer constitutes an enormous burden on society in more and less economically developed countries alike. The occurrence of cancer is increasing because of the growth and aging of the population, as well as an increasing prevalence of established risk factors such as smoking, overweight, physical inactivity, and changing reproductive patterns associated with urbanization and economic development. Based on GLOBOCAN estimates, about 14.1 million new cancer cases and 8.2 million deaths occurred in 2012 worldwide. Over the years, the burden has shifted to less developed countries, which currently account for about 57% of cases and 65% of cancer deaths worldwide. Lung cancer is the leading cause of cancer death among males in both more and less developed countries, and has surpassed breast cancer as the leading cause of cancer death among females in more developed countries; breast cancer remains the leading cause of cancer death among females in less developed countries. Other leading causes of cancer death in more developed countries include colorectal cancer among males and females and prostate cancer among males. In less developed countries, liver and stomach cancer among males and cervical cancer among females are also leading causes of cancer death. Although incidence rates for all cancers combined are nearly twice as high in more developed than in less developed countries in both males and females, mortality rates are only 8% to 15% higher in more developed countries. This disparity reflects regional differences in the mix of cancers, which is affected by risk factors and detection practices, and/or the availability of treatment. Risk factors associated with the leading causes of cancer death include tobacco use (lung, colorectal, stomach, and liver cancer), overweight/obesity and physical inactivity (breast and colorectal cancer), and infection (liver, stomach, and cervical cancer). A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.

23,203 citations

Journal Article
TL;DR: A case study explores the background of the digitization project, the practices implemented, and the critiques of the project, which aims to provide access to a plethora of information to EPA employees, scientists, and researchers.
Abstract: The Environmental Protection Agency (EPA) provides access to information on a variety of topics related to the environment and strives to inform citizens of health risks. The EPA also has an extensive library network that consists of 26 libraries throughout the United States, which provide access to a plethora of information to EPA employees, scientists, and researchers. The EPA implemented a reorganization project to digitize their materials so they would be more accessible to a wider range of users, but this plan was drastically accelerated when the EPA was threatened with a budget cut. It chose to close and reduce the hours and services of some of their libraries. As a result, the agency was accused of denying users the “right to know” by making information unavailable, not providing an adequate strategic plan, and discarding vital materials. This case study explores the background of the digitization project, the practices implemented, and the critiques of the project.

2,588 citations

Journal ArticleDOI
TL;DR: In this paper, the current state of knowledge is reviewed and areas for further research recommended to improve future monitoring and risk assessment efforts, and the authors suggest that the occurrence of high concentrations of certain PBDE isomers may be sufficient to elicit adverse effects in some wildlife.

2,536 citations

Journal ArticleDOI
TL;DR: The most toxic halogenated aromatic is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and based on in vivo and in vitro studies the relative toxicities have been determined relative to TCDD (i.e., toxic equivalents).
Abstract: Halogenated aromatic compounds, typified by the polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), biphenyls (PCBs), and diphenylethers (PCDEs), are industrial compounds or byproducts which have been widely identified in the environment and in chemical-waste dumpsites. Halogenated aromatics are invariably present in diverse analytes as highly complex mixtures of isomers and congeners and this complicates the hazard and risk assessment of these compounds. Several studies have confirmed the common receptor-mediated mechanism of action of toxic halogenated aromatics and this has resulted in the development of structure-activity relationships for this class of chemicals. The most toxic halogenated aromatic is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and based on in vivo and in vitro studies the relative toxicities of individual halogenated aromatics have been determined relative to TCDD (i.e., toxic equivalents). The derived toxic equivalents can be used for hazard and risk assessment of halogenated aromatic mixtures; moreover, for more complex mixtures containing congeners for which no standards are available (e.g., bromo/chloro mixtures), several in vitro or in vivo assays can be utilized for hazard or risk assessment.

1,756 citations

01 Jan 1990
TL;DR: The most toxic halogenated aromatic is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as discussed by the authors.
Abstract: Halogenated aromatic compounds, typified by the polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), biphenyls (PCBs), and diphenylethers (PCDEs), are industrial compounds or byproducts which have been widely identified in the environment and in chemical-waste dumpsites. Halogenated aromatics are invariably present in diverse analytes as highly complex mixtures of isomers and congeners and this complicates the hazard and risk assessment of these compounds. Several studies have confirmed the common receptor-mediated mechanism of action of toxic halogenated aromatics and this has resulted in the development of structure-activity relationships for this class of chemicals. The most toxic halogenated aromatic is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and based on in vivo and in vitro studies the relative toxicities of individual halogenated aromatics have been determined relative to TCDD (i.e., toxic equivalents). The derived toxic equivalents can be used for hazard and risk assessment of halogenated aromatic mixtures; moreover, for more complex mixtures containing congeners for which no standards are available (e.g., bromo/chloro mixtures), several in vitro or in vivo assays can be utilized for hazard or risk assessment.

1,730 citations