Halogenated Aromatic Hydrocarbons Research Articles

In vitro induction of CYP1A1‐associated activities in human and rodent cell lines by commercial and tissue‐extracted halogenated aromatic hydrocarbons

AbstractDespite reports of species‐specific differences, the rat cell line H4IIE continues to be used to assess the toxicity of many halogenated aromatic hydrocarbon (HAH) contaminants for diverse populations using an approach that relates aryl hydrocarbon (Ah) receptor‐mediated responses by HAHs to that of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD). To assess the relevance of H4IIE for human populations, we examined levels of aryl hydrocarbon hydroxylase (AHH) and ethyoxyresorufin O‐deethylase (EROD) activities in H4IIE rat liver, HepG2 human liver, and MCF‐7 human breast cells treated with TCDD and three coplanar polychlorinated biphenyl (PCB) congeners (77, 126, 169), alone or in combination, and to fractions extracted from the muscle tissue of Lake Ontario rainbow trout (Oncorhynchus mykiss). H4IIE was generally more sensitive to all HAH treatments. Both AHH and EROD activities were induced in all cells treated with TCDD and PCB‐126, alone or combined with each other. In contrast, neither activity was induced in human cells treated with PCB‐77 or PCB‐169. For inducing concentrations of PCBs, the induction response in all cell lines treated with 5 nM TCDD‐PCB mixtures was generally nonadditive; only the response in H4IIE treated with 10−3 nM TCDD–PCB mixtures was generally additive. With tissue extracts, induction was restricted to H4IIE cells treated with TCDD/PCB‐or organochloride pesticide‐containing fractions. Our initial results suggest that differences in the properties of each HAH or in levels of Ah receptor in each cell line are not likely to underlie the significant differences in the murine/human induction responses.

Regulation of Prostaglandin Endoperoxide H Synthase-2 Expression by 2,3,7,8-Tetrachlorodibenzo-p-dioxin

We have examined the molecular mechanisms for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-stimulated prostaglandin synthesis in Mardin Darvey canine kidney cells (MDCK). TCDD stimulates prostaglandin synthesis in these cells, at least in part, by elevating prostaglandin endoperoxide H2synthase-2 (PGHS-2) levels. TCDD-stimulated transcription of the PGHS-2 gene was maximal (6-fold) within 2 h and resulted in a 100-fold increase in PGHS-2 mRNA and a 25-fold increase in PGHS-2 protein levels by 4 h. Transient transfection experiments using luciferase-reporter plasmids demonstrated that control element(s) responsible for TCDD activation of the murine PGHS-2 promoter in MDCK cells are located in the first 965 nucleotides upstream from the PGHS-2 transcriptional initiation site. A canonical xenobiotic response element, similar to those that control transcription of other well-known TCDD-sensitive genes, is present at position −157, but does not appear to be sufficient for halogenated aromatic hydrocarbon (HAH) activation of the PGHS-2 promoter. TCDD failed to stimulate transcription from the PGHS-2 promoter when reporter plasmids were transfected into Hepa 1c1c7 cells, a line which contains the functional aryl hydrocarbon receptor. It seems likely that inappropriate expression of PGHS-2 may contribute to the toxic effects of TCDD and other HAHs. In particular, PGHS-2 expression may affect those toxic reactions that involve inappropriate cellular growth, such as dermal hyperplasia and tumor formation. It is also likely that elevated synthesis of prostaglandins, which are potent regulators of immune function, could play a role in the immunotoxicity associated with HAH exposure.

Identification of dioxin-specific binding proteins in marine bivalves

Epidemiological investigations of germ cell tumors of Maine soft shell clams ( Mya arenaria) and hard shell clams ( Mercenaria spp.) from Florida demonstrate the prevalence of histogenically similar gonadal cancers as high as 40 and 60%, respectively. Human mortality rates due to ovarian cancer from the same areas are significantly greater than the national average. Since further investigation revealed that there was a heavy use of herbicides at these sites, we proposed to investigate their possible role in the etiology of the clam tumors. One avenue of investigation was to determine whether clams had a mechanism similar to the vertebrate Ah receptor which could be activated by halogenated aromatic hydrocarbons (HAH). We used the TCDD photoaffinity analog [ 125-I]-2-azido-3-iodo-7,8-dibromodibenzo- p-dioxin to detect two cytosolic proteins (28 and 39 kDa) in Mercenaria mercenaria and one (35 kDa) in Mya arenaria which specifically bound this ligand. Expression of both proteins in Mercenaria is tissue specific with the highest levels observed in cytosols from gill and gonad. Females exhibit higher levels of the 39 kDa protein in gonadal tissue than do the males. Studies to determine the relationship of these proteins to vertebrate Ah receptors, as well as their possible role in gonadal tumor development, are in progress.

In vitro modulation of 17-β-estradiol-induced vitellogenin synthesis: Effects of cytochrome P4501A1 inducing compounds on rainbow trout ( Oncorhynchus mykiss) liver cells

Cytochrome P4501A1 (CYP1A1) induction, particularly in liver, is a useful marker of exposure of fish to polycyclic- and halogenated-aromatic hydrocarbons. However, the relationship between toxicity and CYP1A1 induction in fish is uncertain. Some compounds that induce CYP1A1 are antiestrogenic in mammalian bioassay, and this effect is linked to aryl hydrocarbon (Ah) receptor and/or increased catabolism of 17-β-estradiol. Liver of fish synthesizes estrogen-inducible egg yolk precursor protein vitellogenin (Vg) which is critical for oocyte maturation and ovarian development. To determine if CYP1A1-associated endocrine modulation could occur in fish liver, primary cultures of rainbow trout liver cells were co-administered 17-β-estradiol and CYP1A1 inducing compounds or mixtures. Protein synthesis and enzyme activity of cells were optimal when cultured in a modified HEPES buffered Medium 199 at 15 °C. Vg and albumin (Alb), estimated by ELISA measurement of concentration in the media 48 h after treatment, formed the basis for the test. Equivalent viability (mitochondrial dehydrogenase activity) and secretory functional capacity (Alb synthesis) were estimated and correlated with other results. In descending order, 2,3,4,7,8-pentachlorodibenzofuran (10 −12 to 10 −8 M) > 2,3,7,8- tetrachlorodibenzo-p- dioxin ( TCDD) ≊ 2,3,7,8- tetrachlorodibenzofuran (10 −11 to 10 −8 M) > β- naphthoflavone (10 −7 to 10 −6 M) inhibited Vg synthesis in 17-β-estradiol treated liver cells. Potency of inhibition directly related to strength as an inducer of CYP1A1 protein. At 10 −8 M, PCB congeners 77, 126, 156 did not inhibit Vg synthesis and induced no to moderate levels of CYP1A1 protein or EROD activity. At 10 −8 M, congener 114, a weak EROD inducer, potentiated Vg synthesis relative to cells treated with 17-β-estradiol alone. The results of this study increase our understanding of the consequences of hepatic CYP1A1 induction, forewarn of reproductive impairment of sexually maturing fishes exposed to CYP1A1 inducing compounds and argue for further, more detailed in vivo investigation.

Immunosuppressive potential of several polycyclic aromatic hydrocarbons (PAHs) found at a Superfund site: new model used to evaluate additive interactions between benzo[ a]pyrene and TCDD

Exposure to environmental pollution is rarely limited to a single compound or even a single class of compounds. The Superfund site located in Massena, NY, is contaminated by both halogenated aromatic hydrocarbons (HAHs) and polycyclic aromatic hydrocarbons (PAHs). Since representatives of both HAHs and PAHs are capable of binding to the aromatic hydrocarbon receptor ( AhR), two well-documented AhR-mediated effects, immunosuppression and induction of hepatic aryl hydrocarbon hydroxylase (AHH) activity, were used to evaluate the individual and interactive toxicity of these compounds. Fifteen PAHs were first screened for their ability to suppress the antibody response in C57BL/6 ( Ah +/+) mice immunized 12 h after a single oral dose of 0.1, 1, 10, or 100 mg/kg. Acenaphthene, anthracene, benzo[ g, h, i]perylene, fluoranthene, fluorene, naphthalene, phenanthrene, and pyrene had little or no effect. Seven PAHs caused > 50% suppression at 100 mg/kg. Listed in order of decreasing potency they were benzo[ k]fluoranthene, benzo[ b]fluoranthene, indeno[1,2,3, c, d]pyrene, benzo[ a]pyrene, chrysene, dibenzo[ a, h]anthracene, and benz[ a]anthracene. Chrysene and benzo[ a]pyrene (B[ a]P), were further evaluated to determine the dependence of these effects on the Ah phenotype by comparing responses of C57BL/6 and congenic B6.D2 ( Ah −/−) mouse strains. Chrysene immunosuppression was maximal at 0.1 mg/kg and was Ah phenotype-independent whereas chrysene AHH induction was Ah phenotype-dependent, but a 100-fold less sensitive indicator of exposure. In contrast, B[ a]P immunosuppression and AHH induction were coincident in B6 mice and Ah phenotype-dependent. In the final phase, a new approach was used to evaluate toxic interactions. This approach considers the mechanism of action of each compound and accounts for the fact that the extent of increase in toxic response caused by an incremental change of dose is determined by its position on the dose-response curve rather than on the absolute amount of dose administered. Thus, the immunotoxic effects of combined exposure to B[ a]P and the AhR ligand, 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD), a representative HAH, were evaluated by combining the ED 20 of B[ a]P with the difference between the ED 20 and ED 40 of TCDD, and vice versa, to produce 40% suppression. The results of the combination were consistent with additivity regardless of the composite arrangement or phenotype although some antagonism could not be excluded with certainty.

Halogenated aromatic hydrocarbon-induced suppression of the plaque-forming cell response in B6C3F1 splenocytes cultured with allogenic mouse serum: Ah receptor structure activity relationships

The immunsuppressive effects of halogenated aromatic hydrocarbons (HAHs) were investigated in B6C3F1 female mice and in mouse splenocytes cultured with allogenic mouse serum using the Mishell-Dutton model for in vitro immunization to trinitrophenyl-lipopolysaccharide (TNP-LPS). Exposure to 2,3,7,8-tetrachlorodibenzo- P-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 1,2,3,7,8-PeCDF, 1,3,6,8-tetrachlorodibenzofuran (TCDF), 3,3′,4,4′,5-pentachlorobiphenyl (pentaCB), or 3,3′,4,4′,5,5′-hexaCB resulted in a dose-dependent suppression of the splenic plaque-forming cell (PFC) response both in vivo and in vitro. The effective dose required to decrease 50% (ED 50) of the response to 2,3,7,8-TCDD, 2,3,4,7,8-PeCDF, 1,2,3,7,8-PeCDF, 1,3,6,8-TCDF, 3,3′,4,4′,5-pentaCB, or 3,3′,4,4′,5,5′-hexaCB in vivo was 14.1, 5.5, 1695, 34800, 21, and 19 nmol/kg, respectively, and in vitro was 7.0, 10.6, 149, 2325, 9.1 and 9.1 nM, respectively. There was an excellent rank order and linear correlation between the in vivo versus in vitro activities for these HAHs ( r < 0.99) and the relative immunosuppressive potencies of these compounds paralleled their binding affinities for the aryl hydrocarbon (Ah) receptor. These results show that splenocytes cultured with allogenic mouse serum is an Ah-responsive in vitro assay which can be used for quantitating the immunosup-pressive effects of HAHS.

Production of a novel recombinant cell line for use as a bioassay system for detection of 2,3,7,8-tetrachlorodibenzo-P-dioxin-like chemicals

Exposure to specific halogenated aromatic hydrocarbons (HAHs), such as 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), can produce a wide variety of species- and tissue specific toxic and biological effects The presence of HAHs in environmental samples as complex mixtures has made it difficult to predict the biological and toxic potency of these chemicals We have used aspects of the molecular mechanism of action of these chemicals to develop a species-specific bioassay system for detection of bioactive HAHs in complex mixtures Here we describe construction and utilization of a recombinant expression vector that responds to these HAHs with the induction of an easily measurable gene product, heat-stable human placental alkaline phosphatase (PAP) This vector contains the PAP gene under TCDD-inducible control of four dioxin-responsive DNA enhancer elements HAH inducible expression of PAP from the recombinant vector occurs in a dose- and Ah-receptor- (AhR-) dependent manner Stable transfection of this vector into mouse hepatoma cells has produced a novel cell line in which AhR-dependent induction of gene expression can easily be measured This transfected cell line can readily be used for detection and relative quantitation of AhR agonists in complex mixtures of environmental and biological samples and for identification and characterization of novel AhR agonists

Suppression of prolactin and cytotoxic T-lymphocyte activity in PCB-treated mice

Halogenated aromatic hydrocarbons (HAH) are ubiquitous environmental contaminants. Studies in rats have shown that HAH treatment can lead to dysregulation of circulating hormone levels, including prolactin. Reduction of prolactin levels in both rats and mice is inhibitory to immune function. Previous studies have reported suppression of alloantigen-specific cytotoxic T-lymphocyte (CTL) activity in mice treated with 3,3′,4,4′,5,5′-hexachlorobiphenyl (HxCB). Here we report that treatment of mice with HxCB (10 mg/kg body weight) leads to a significant reduction of serum prolactin levels (by 89% to 3.7 ng/ml) on day 10 post alloantigen injection (P815 mastocytoma), the day of peak alloantigen-specific CTL activity. Prolactin levels were not altered on day 3 post alloantigen injection. Treatment with bromocryptine (5 mg/kg/day) reduced serum prolactin levels slightly on day 3 and significantly (94% to 2.1 ng/ml) on day 10 post alloantigen injection. Splenic CTL activity was not altered by treatment with bromocryptine. The data presented here suggest that reduction of prolactine levels alone, to the extent observed in HxCB-treated mice, is not causative for CTL suppression.

Development of bioassays and approaches for the risk assessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds.

Polychlorinated biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and related halogenated aromatic hydrocarbons (HAHs) are industrial compounds or by-products that have been identified as contaminants in almost every component of the global ecosystem. 2,3,7,8- Tetrachlorodibenzo-p-dioxin (TCDD) is the most toxic HAH, and studies in rodents have shown that this compound is a carcinogen. Analysis of environmental samples for HAHs has shown that these extracts contain complex mixtures of isomers and congeners, and this greatly complicates risk assessment due to the paucity of data available for most of the individual compounds. Extensive research has demonstrated a common receptor-mediated mechanism of action for TCDD and related toxic HAHs, and this has led to the development of a mechanism-based risk assessment approach for HAHs. Toxic equivalency factors (TEFs; relative potency compared to TCDD) have been developed for selected HAH congeners, and the TEF values can be used to determine "toxic equivalents" (TEQs) for HAH mixtures. In addition, several bioassays that use receptor-mediated end points have been developed and can be used directly to determine the TEQs for HAH mixtures. The applications of the TEF/TEQ approach for the risk assessment of HAHs are considerable, particularly with the conversion of complex analytical data into TEQs. However, there appear to be several limitations to this approach, particularly with PCBs because their potential nonadditive (antagonistic), interactive effects with "2,3,7,8-TCDD-like" compounds may invalidate the use of the risk assessment procedure for some environmental matrices.

A rapid and sensitive cell culture bioassay for measuring ethoxyresorufin-o-deethylase (EROD) activity in cultured hepatocytes exposed to halogenated aromatic hydrocarbons extracted from wild bird eggs

An improved method for determining the effect of polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs) and other halogenated aromatic hydrocarbons (HAHs) on ethoxyresorufin-O-deethylase (EROD) activity in primary cultures of chicken embryo hepatocytes is described. Cells were cultured in 48-well plates, and EROD activity was determined with a computer-operated fluorescence multi-well plate reader. Assays were carried out directly within multi-well plates, and dose-response curves were obtained approximately 100 times faster than other methods. The method can be used to measure EROD-inducing potencies of complex mixtures of HAHs extracted from wild bird eggs. It may have potential use as a cost-effective screening tool for determining the toxic potencies of complex mixtures of HAHs in environmental samples.

Development, validation and limitations of toxic equivalency factors

Halogenated aromatic hydrocarbons (HAHs) such as the polychlorinated dibenzo- p-dioxins (PCDDs), dibenzofurans (PCDFs) and biphenyls (PCBs) are complex mixtures of industrial compounds or by-products which have been identified as contaminants in almost every component of the global ecosystem. High resolution analytical techniques can unequivocally identify and quantitate most of the individual HAH congeners present in different matrices. 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 HAHs have been determined relative to TCDD ( i.e. toxic equivalency factors, TEFs). The derived toxic equivalents (TEs or TEQs) can be used for hazard and risk assessment of halogenated aromatic mixtures. This approach can be used for estimating the TEQs from high resolution analytical data obtained for PCBs, PCDDs and PCDFs; however, it is clear that this approach can only be used for those congeners which exhibit TCDD-like activity.

Ethoxyresorufin-O-deethylase (EROD) and porphyriainduction in chicken embryo hepatocyte cultures — A new bioassay of PCB, PCDD, and related chemical contamination in wildlife

Ethoxyresorufin-O-deethylase (EROD) and porphyria induction potencies of extracts from polychlorinated biphenyl (PCB) and 2,3,7,8-tetrachloro dibenzo-p-dioxin (TCDD) contaminated eggs of Herring Gulls, Larus argentatus from the Great Lakes of North America, and Great Blue Herons, Ardea herodias from British Columbia were measured in primary cultures of chicken embryo hepatocytes. The results show that EROD and porphyria induction in these cells have potential for determining the toxic potencies of complex mixtures of halogenated aromatic hydrocarbons (HAHs) extracted from wildlife tissue.

Tetrachlorodibenzo- [formula omitted]-dioxin (TCDD) and 3,3′,4,4′,5,5′,-hexachlorobiphenyl (HxCB) enhance anti-CD3-induced T cell activation

The effect of two immunosuppressive halogenated aromatic hydrocarbons (HAH), TCDD and HxCB, on T cell activation in vivo were evaluated using the monoclonal antibody (145-2C11) to the CD3 portion of the murine T cell receptor complex. Briefly, mice were injected in both rear footpads with either 25 μg anti-CD3 or hamster IgG. After 24 hr, popliteal and inguinal lymph node cells were pooled, and T cell activation was measured by 3H-TdR incorporation and flow cytometric analyses (DNA cell cycle; CD3 and IL-2 receptor (IL-2R) expression). The immunosuppressive drug, cyclosporin A (CsA, 50 mg/kg, ip), was used as a positive control. CsA inhibited anti-CD3-induced 3H-TdR incorporation, IL-2-driven 3H-TdR incorporation, and IL-2 receptor (IL-2R) expression. In contrast, TCDD (2 or 20 μg/kg, po) dose-dependently increased anti-CD3-induced 3H-TdR incorporation and the percentage of both CD4 + and CD8 + cells cycling in S/G 2M. In addition, IL-2-driven 3H-TdR incorporation increased without an increase in IL-2R expression. Similar increases in anti-CD3-induced T cell activation were observed following HxCB treatment (30 mg/kg, po).

Halogenated aryl hydrocarbon-induced suppression of the in vitro plaque-forming cell response to sheep red blood cells is not dependent on the Ah receptor

The immunosuppressive effects of the halogenated aromatic hydrocarbons (HAHs), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 1,2,3,7,9-PeCDF and 1,3,6,8-TCDF were investigated utilising the Mishell-Dutton model for in vitro immunization. The selected polychlorinated dibenzofuran congeners and 2,3,7,8-TCDD caused a concentration-dependent suppression of the splenic plaque-forming cell response to sheep red blood cells using cell cultures derived from C57BL/6 (Ah responsive) mice. Previous studies showed that there was up to a 14900-fold difference in the in vivo immunotoxicity of these compounds, however in the in vitro studies, their immunosuppressive potencies were comparable. In addition, these congeners also exhibited similar potencies using spleen cell cultures from DBA/2 (Ah-nonresponsive) mice. Previous research demonstrated that α-naphthoflavone was relatively inactive in the in vitro splenic assay system and that co-treatment of cells from C57BL/6 mice with α-naphthoflavone (10 μM) plus 2,3,7,8-TCDD (20 mM) resulted in a significant inhibition of the immunotoxicity of 2,3,7,8-TCDD. In these studies, comparable interactive effects were also observed in cells treated with α-naphthoflavone plus 1,3,6,8-TCDF, a weak in vivo Ah receptor agonist. Collectively, the results from this study suggest that there may be mechanism(s) of action for HAH-induced suppression of the in vitro murine humoral response to sheep red blood cells which are independent of the Ah receptor protein.

Immunomodulation in C57BI/6 mice following consumption of halogenated aromatic hydrocarbon‐contaminated coho salmon(Oncorhynchus kisutch)from lake Ontario

This report describes studies designed to assess the immunomodulatory effects associated with the consumption of coho salmon containing halogenated aromatic hydrocarbons (HAHs) and other compounds naturally bioaccumulated from Lake Ontario. Diets containing 33% coho salmon from Lake Ontario or the Pacific Ocean were fed to juvenile C57Bl/6 mice for 2-4 mo. Following 60 d, the mice that consumed Lake Ontario salmon had reduced IgM, IgG, and IgA plaque-forming cell responses to sheep erythrocytes. No changes were observed in total numbers of spleen lymphocytes, total T-lymphocytes or T-lymphocyte subsets as determined by flow cytometry. Cellular immunity, assessed by the cytotoxic T-lymphocyte response to allogeneic tumor target cells, was not altered following dietary exposure to Lake Ontario coho salmon for 4 mo. The observed humoral immunomodulation correlated with elevated PCB levels in the Lake Ontario salmon diets. The levels of pollutants such as mercury, tin compounds and other metals, PCDDs, and PCDFs were not examined.

Dietary exposure of rainbow trout ( Salmo gairdneri) to Great Lakes coho salmon ( Oncorhynchus kisutch Walbaum). Bioaccumulation of halogenated aromatic hydrocarbons and host resistance studies

Great Lakes coho salmon ( Oncorhynchus kisutch walbaum) contain a gradient of halogenated aromatic hydrocarbons (HAHs) naturally bioaccumulated from their environment which have immunomodulatory potential. Juvenile rainbow trout ( Salmo gairdneri) were fed diets of coho salmon from Lakes Michigan and Ontario, the Pacific Ocean and control trout chow, for a 20 weak period. The body burdens of organochlorines bioaccumulated in rainbow trout were similar to levels in the dietary coho salmon. The effect on natural resistance was assessed by challenge with a titrated dose of Vibrio anguillarum (VA-58). The ability to mount a protective immune response was determined by immunization with a VA-58 bacterin followed by challenge with virulent VA-58. These parameters of host resistance of rainbow trout were not compromised following dietary exposure to Great Lakes coho salmon.

ChemInform Abstract: HEALTH EFFECTS OF HALOGENATED AROMATIC HYDROCARBONS

Chemischer InformationsdienstVolume 10, Issue 43 Reviews ChemInform Abstract: HEALTH EFFECTS OF HALOGENATED AROMATIC HYDROCARBONS - -, - -Search for more papers by this author - -, - -Search for more papers by this author First published: October 23, 1979 https://doi.org/10.1002/chin.197943359Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume10, Issue43October 23, 1979 RelatedInformation

REPRODUCTIVE EFFECTS OF HALOGENATED AROMATIC HYDROCARBONS ON NONHUMAN PRIMATES

Annals of the New York Academy of SciencesVolume 320, Issue 1 p. 419-425 REPRODUCTIVE EFFECTS OF HALOGENATED AROMATIC HYDROCARBONS ON NONHUMAN PRIMATES* J. R. Allen, J. R. Allen Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this authorD. A. Barsotti, D. A. Barsotti Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this authorL. K. Lambrecht, L. K. Lambrecht Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this authorJ. P. VAN Miller, J. P. VAN Miller Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this author J. R. Allen, J. R. Allen Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this authorD. A. Barsotti, D. A. Barsotti Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this authorL. K. Lambrecht, L. K. Lambrecht Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this authorJ. P. VAN Miller, J. P. VAN Miller Department of Pathology and Regional Primate Research Center University of Wisconsin Madison, Wisconsin 53706Search for more papers by this author First published: May 1979 https://doi.org/10.1111/j.1749-6632.1979.tb56623.xCitations: 112 * This investigation was supported in part by United States Public Health Service grants ES00958, ES00472, ES01339, ES01839 and RR00167 from the National Institutes of Health, and the University of Wisconsin Sea Grant Program. A portion of this research was conducted at the University of Wisconsin-Madison Biotron, a controlled environmental facility funded by the National Science Foundation and the University of Wisconsin-Madison. Primate Center Publication No. 18-004. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume320, Issue1Health Effects of Halogenated Aromatic HydrocarbonsMay 1979Pages 419-425 RelatedInformation

ASSESSMENT OF IMMUNOLOGIC ALTERATIONS CAUSED BY HALOGENATED AROMATIC HYDROCARBONS

Annals of the New York Academy of SciencesVolume 320, Issue 1 p. 572-578 ASSESSMENT OF IMMUNOLOGIC ALTERATIONS CAUSED BY HALOGENATED AROMATIC HYDROCARBONS Michael I. Luster, Environmental Biology and Chemistry Branch National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709Search for more papers by this authorRobert E. Faith, Environmental Biology and Chemistry Branch National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709 Biological Research Center, Oral Roberts University, Tulsa, Oklahoma 74171.Search for more papers by this author Michael I. Luster, Environmental Biology and Chemistry Branch National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709Search for more papers by this authorRobert E. Faith, Environmental Biology and Chemistry Branch National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709 Biological Research Center, Oral Roberts University, Tulsa, Oklahoma 74171.Search for more papers by this author First published: May 1979 https://doi.org/10.1111/j.1749-6632.1979.tb56635.xCitations: 4 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Citing Literature Volume320, Issue1Health Effects of Halogenated Aromatic HydrocarbonsMay 1979Pages 572-578 RelatedInformation

ChemInform Abstract: A CHAIN PHOTOREACTION OF SODIUM BOROHYDRIDE WITH HALOGENATED AROMATIC HYDROCARBONS, EVIDENCE FOR INITIATION BY ARYL RADICALS

Chemischer InformationsdienstVolume 4, Issue 40 Preparative Organic Chemistry ChemInform Abstract: A CHAIN PHOTOREACTION OF SODIUM BOROHYDRIDE WITH HALOGENATED AROMATIC HYDROCARBONS, EVIDENCE FOR INITIATION BY ARYL RADICALS J. A. BARLTROP, J. A. BARLTROPSearch for more papers by this authorD. BRADBURY, D. BRADBURYSearch for more papers by this author J. A. BARLTROP, J. A. BARLTROPSearch for more papers by this authorD. BRADBURY, D. BRADBURYSearch for more papers by this author First published: October 2, 1973 https://doi.org/10.1002/chin.197340157Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume4, Issue40October 2, 1973 RelatedInformation