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Dive into the research topics where C.Stuart Baxter is active.

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Featured researches published by C.Stuart Baxter.


Journal of Occupational and Environmental Medicine | 2010

Ultrafine particle exposure during fire suppression--is it an important contributory factor for coronary heart disease in firefighters?

C.Stuart Baxter; Clara Sue Ross; Thomas Z. Fabian; Jacob L. Borgerson; Jamila Shawon; James M. Dalton; James E. Lockey

Objective: Coronary heart disease (CHD) is the primary cause of death among US firefighters during fire suppression. In other populations, exposure to respirable particles, including ultrafine particles, has been widely implicated as a risk factor for CHD. This study is the first to report detailed characterization of respirable particles released by combustion of an automobile and model residential structures under firefighter exposure conditions. Methods: Characterization was performed when feasible during knockdown and routinely during overhaul. Results: Ultrafines accounted for >70% of particles in all fire suppression stages, occurring in concentrations exceeding background by factors between 2 (automobile) and 400 (bedroom), consistent among all structures. Conclusions: Exposure to ultrafine particles during fire suppression should be considered a potential contributing factor for CHD in firefighters. Of major significance is their predominance during overhaul, where firefighters frequently remove respiratory protection.


Journal of Occupational and Environmental Hygiene | 2014

Exposure of Firefighters to Particulates and Polycyclic Aromatic Hydrocarbons

C.Stuart Baxter; Joseph D. Hoffman; Michael J. Knipp; Tiina Reponen; Erin N. Haynes

Firefighting continues to be among the most hazardous yet least studied occupations in terms of exposures and their relationship to occupational disease. Exposures are complex, involving mixtures of particles and chemicals such as polycyclic aromatic hydrocarbons (PAHs). Adverse health effects associated with these agents include elevated incidences of coronary heart disease and several cancers. PAHs have been detected at fire scenes, and in the firehouse rest area and kitchen, routinely adjoining the truck bay, and where firefighters spend a major part of each shift. An academic-community partnership was developed with the Cincinnati Fire Department with the goal of understanding active firefighters’ airborne and dermal PAH exposure. PAHs were measured in air and particulates, and number and mass concentrations, respectively, of submicron (0.02–1 μm) and PM2.5 (2.5 μm diameter and less) particles during overhaul events in two firehouses and a University of Cincinnati administrative facility as a comparison location. During overhaul firefighters evaluate partially combusted materials for re-ignition after fire extinguishment and commonly remove Self-Contained Breathing Apparatus (SCBA). Face and neck wipes were also collected at a domestic fire scene. Overhaul air samples had higher mean concentrations of PM2.5 and submicron particles than those collected in the firehouse, principally in the truck bay and kitchen. Among the 17 PAHs analyzed, only naphthalene and acenaphthylene were generally detectable. Naphthalene was present in 7 out of 8 overhaul activities, in 2 out of 3 firehouse (kitchen and truck bay) samples, and in none collected from the control site. In firefighter face and neck wipes a greater number of PAHs were found, several of which have carcinogenic activity, such as benzofluoranthene, an agent also found in overhaul air samples. Although the concentration for naphthalene, and all other individual PAHs, was very low, the potential simultaneous exposure to multiple chemicals even in small quantities in combination with high ultrafine particle exposure deserves further study. It is recommended that personal respiratory and skin protection be worn throughout the overhaul process.


Journal of Occupational and Environmental Hygiene | 2014

Plasticizer Contamination of Firefighter Personal Protective Clothing – A Potential Factor in Increased Health Risks in Firefighters

Barbara Alexander; C.Stuart Baxter

Chemical exposures may be responsible for firefighters’ elevated incidences of cancer and cardiovascular disease. This study characterized semivolatile chemical contamination on firefighter personal protective clothing to assess exposure of firefighters to these chemicals. Samples from used firefighter protective clothing, including gloves, hood, and one coat wristlet, were extracted with methylene chloride and analyzed by EPA method 8270 for semivolatile contaminants, including 20 polycyclic aromatic hydrocarbons (PAHs) and 6 phthalate diesters. Twenty-two of the chemicals of interest were found on at least one clothing swatch. Only di-(2-ethylhexyl) phthalate (DEHP), a plasticizer, added to polyvinyl chloride (PVC) to increase flexibility, was found on every swatch. DEHP concentrations were the highest of any chemical measured, and were 52 to 875 times higher than any PAH concentration measured. DEHP was also detected on most items of unused firefighter personal protective clothing, although at much lower levels. These findings suggest that firefighters are exposed to high levels of DEHP, a probable human carcinogen, and at levels much higher than PAHs, the semivolatile toxic combustion products most extensively studied historically. Firefighter exposure to DEHP and other phthalate diesters therefore merits further study.


Cardiovascular Toxicology | 2004

Gene expression profiles of mouse aorta and cultured vascular smooth muscle cells differ widely, yet show common responses to dioxin exposure

Alvaro Puga; Maureen A. Sartor; Ming-ya Huang; J. Kevin Kerzee; Yu-Dan Wei; Craig R. Tomlinson; C.Stuart Baxter; Mario Medvedovic

Exposure to environmental toxicants may play a role in the onset and progression of cardiovascular disease. Many environmental agents, such as dioxin, are risk factors for atherosclerosis because they may exacerbate an underlying disease by altering gene expression patterns. Expression profiling of vascular tissues allows the simutaneous analysis of thousands of genes and may provide predictive information particularly useful in early disease stages. Often, however, in vivo experiments are unfeasible for material or ethical reasons, and data from cultured cells must be used instead, even though it may not be known whether cultured cells and live tissues share common global responses to the same toxicant. In a search for gene responsive to dioxin exposure, we used oligonucleotide microarrays with DNA sequences from 13,433 genes to compare global gene expression profiles of C57BL/6 mice aortas with cultured vascular smooth muscle cells (vSMCs) of the same mice. Aorta segments and vSMCs differed in the expression of more than 4500 genes, many showing expression differences greater than 1000-fold. Integration of microarray data into Gene Ontology Project annotations showed that many of the genes differentially expressed belonged to the same biological process or metabolic pathway. Notwithstanding these results, a subset of 35 genes responded in the same fashion to dioxin exposure in both systems. Genes in this subset encoded phase I and phase II detoxification enzymes, signal transduction kinases and phosphatases, and proteins involved in DNA repair and the cell cycle. We conclude that vSMCS may be useful aorta surrogates to study early gene expression responses to dioxin exposure, provided that analyses focus on this subset of genes.


Journal of Occupational and Environmental Medicine | 2012

Hypomethylation of dual specificity phosphatase 22 promoter correlates with duration of service in firefighters and is inducible by low-dose benzo[a]pyrene

Bin Ouyang; C.Stuart Baxter; Hung-Ming Lam; Samrat Yeramaneni; Linda Levin; Erin N. Haynes; Shuk-Mei Ho

Objective: Firefighters (FFs) are chronically exposed to smoke and products of incomplete combustion, which frequently contain polycyclic aromatic hydrocarbons (PAHs). This study examined the possibility of an association between PAH-induced epigenetic alterations and occupational firefighting exposure. Methods: Promoter methylation was analyzed in four genes in blood DNA from 18 FFs and 20 non-FFs (controls). Jurkat and human normal prostate epithelial cells were treated with benzo[a]pyrene to ascertain the epigenetic effects of this type of agent. Results: Firefighters had a higher prevalence of dual specificity phosphatase 22-promoter hypomethylation in blood DNA (P = 0.03) and the extent of hypomethylation correlated with duration of firefighting service (P = 0.04) but not with age. Benzo[a]pyrene reduced promoter methylation and increased gene expression of the same gene in Jurkat and normal prostate epithelial cells. Conclusions: Cumulative occupational exposure to combustion-derived PAHs during firefighting can cause epigenetic changes in promoters of specific genes.


Biochemical and Biophysical Research Communications | 1986

Phorbol diester synergistically stimulates agonist-induced lipoxygenase product formation in murine macrophages☆

Howard E. Wey; C.Stuart Baxter

Murine peritoneal macrophages were preincubated with 12-O-tetradecanoylphorbol-13-acetate (100 ng/ml) and then exposed to various concentrations of calcium ionophore A23187. This combined treatment resulted in an elevated release of arachidonic acid metabolites that was synergistic in nature. Resolution of the [3H]products released into the medium revealed that the effect on the cyclooxygenase products 6-keto PGF1 and PGE2 were additive to less than additive (A23187 concentration dependent), the production of lipoxygenase products was synergistically enhanced, and the largest effect was on 12-HETE production.


Mutation Research\/dna Repair Reports | 1984

DNA damage and repair in embryonic mouse limbs exposed to teratogenic doses of methylnitrosourea

Rita Loch-Caruso; C.Stuart Baxter

The alkaline elution assay was used to monitor DNA single-strand breaks in embryonic tissue following exposure to the DNA-damaging teratogen N-methyl-N-nitrosourea (MNU, CAS No. 694-93-5). An animal model was developed in which nearly every fetus exposed to the highest dose of MNU had malformations of the hindlimbs while the fetuses exposed to the lowest dose of MNU had none. Hindlimbs pooled within litters were analyzed for DNA single-strand breaks by alkaline elution conducted at rapid (0.35 ml/min) and slow (0.35 ml/min) speeds. Breaks in the DNA of hindlimbs exposed to teratogenic doses of MNU were readily detected by alkaline elution only if slower speeds were used in the assay. Using the more sensitive procedure, DNA breakage was monitored over a 24-h period. DNA breakage peaked in the MNU-exposed hindlimbs in a dose-dependent manner 4 h after injection. While the elution profiles of hindlimbs exposed to the lower doses of MNU returned to control levels 8 h after injection, single-strand breaks persisted in the hindlimbs exposed to the highest dose of MNU for at least 20 h. These latter data suggest that the highly teratogenic dose of MNU induced DNA damage that was more slowly repaired than that produced at lower doses, possibly by saturation of DNA repair systems. Although some necrosis did occur in hindlimbs exposed at teratogenic dose levels, it was not severe and it did not appear to influence the alkaline elution results. These experiments show that alkaline elution is a sensitive assay for the detection of DNA damage in embryonic tissues.


Toxicology and Applied Pharmacology | 1981

Murine lymphocyte comitogenesis by phorbol esters, and its inhibition by retinoic acid and inhibitors of polyamine biosynthesis☆☆☆

Larry A. Fish; C.Stuart Baxter; Jerry A. Bash

Abstract 12- O -Tetradecanoyl-phorbol-13-acetate (TPA) and other phorbol-derived tumor-promoting agents were shown not to be mitogenic per se, but to enhance mitogenesis in concanavalin A (Con A)- and phytohemagglutinin (PHA)-stimulated splenic lymphocytes for the first time in the mouse, the species in which the phenomenon of tumor promotion was first established. The comitogenesis observed was dose-dependent, and a good correlation was established between degree of proliferative enhancement and previously reported potency as skin tumor promoter in the same animal species among the phorbol esters examined. Phorbol, the unesterified parent polyhydric alcohol which lacks skin tumor promoting capability, was inactive. Comitogenesis could be inhibited, without concurrent effect on mitogenesis, by retinoic acid and α,α-difluoromethylornithine, an inhibitor of the synthesis of the polyamine putrescine. In the latter respect the murine cells differed from their bovine counterparts. In contrast methyglyoxal bis(guanylhydrazone), an inhibitor of the spermidine and spermine synthesis, inhibited both mitogenesis and comitogenesis over the same dose range. Since retinoids have also been shown to inhibit induction of polyamine synthesis by TPA, our findings are consistent with the theory that polyamines play a key role in both epidermal tumor promotion and lymphocyte comitogenesis in the same species. Our results further suggest, however, that in the same animal model, the mouse, the two ostensibly dissimilar events share a similar, but not identical, biochemical basis.


Immunobiology | 1984

Carrageenan-Induced Suppression of T-Lymphocyte Proliferation in the Rat: Abrogation of Suppressor Factor Production by the Prostaglandin Synthesis Inhibitors, Indomethacin and ETYA

Felicia R. Cochran; C.Stuart Baxter

Carrageenan, an algal polygalactan reputed to be selectively toxic for macrophages, is widely employed as a tool to dissect pathways of cell-mediated immunity. In the present study, corn oil-elicited rat peritoneal macrophages after 72 h culture with 10 micrograms/ml Seakem 9 Carrageenan secreted a soluble suppressor factor capable of abrogating T-cell activation by phytohemagglutinin-P (PHA). Addition of the prostaglandin synthesis inhibitors Indomethacin or 5,8,11,14-eicosatetraynoic acid (ETYA) prevented inhibitor synthesis by Carrageenan-conditioned macrophages. Seakem 9 and lambda Carrageenans added directly into spleen cell cultures failed to diminish lymphocyte proliferation, but rather stimulated spleen cell division. Macrophages cultured with low concentrations of Carrageenan appeared to be activated on the basis of enhanced tumoristatic capacity against Schmidt-Ruppin sarcoma cells. Thus, macrophages activated by low concentrations of Carrageenan in vitro appear to secrete a product of arachidonic acid metabolism which is a potent inhibitor of PHA-induced spleen cell mitogenesis.


Toxicology | 1981

Reduced prevalence and growth rate of urethane induced lung adenomas in ageing adult strain a mice

Michael Dourson; C.Stuart Baxter

Following administration of 1.0 mg of urethane/g body wt the average diameter and prevalence of lung adenomas in adult strain. A mice were found to be progressively smaller in animals of progressively greater age at initiation of treatment. Reduction of tumor diameters below detectibility in animals in the older treatment groups could not account for the concurrent reduction in prevalence. Explanations for the observed data in ageing animals based on considerations of reduced immunocompetence or on decreased urethane metabolism or distribution were also considered insufficient. Possible mechanisms for the observed data are discussed.

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Larry A. Fish

University of Cincinnati

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Howard E. Wey

University of Cincinnati

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Jerry A. Bash

University of Cincinnati

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Alvaro Puga

University of Cincinnati Academic Health Center

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Barbara Alexander

Cincinnati Children's Hospital Medical Center

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Erin N. Haynes

University of Cincinnati

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