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PubMed1995

Polyfluorinated dibenzodioxins and dibenzofurans--synthesis, analysis, formation and toxicology.

The 75 congeners of the polyfluorinated dibenzodioxins (PFDDs) and about half of the 135 polyfluorinated dibenzofurans (PFDFs) have been synthesized by pyrolysis of fluorophenols and fluorobenzenes. The individual congeners were characterized by GC/MS. 2,3,7,8-TFDD was also characterized by 1H-, 13C- and 19F-NMR spectroscopy. The retention behaviour of PFDDs and PFDFs during gaschromatographic separation is entirely different from that of PCDDs/PCDFs or PBDDs/PBDFs. The PFDDs/PFDFs elute earlier than the PCDDs/PCDFs and the order of the elution is not governed by the degree of substitution, O8FDD eluting e.g. much earlier than the M1FDDs. A preliminary toxicological evaluation of 2,3,7,8-TFDD was carried out. The elimination of 2,3,7,8-TFDD from mice after a single i.p. injection is biphasic with a very rapid elimination half-life of 5 minutes and a slower phase of 165 minutes. This means a dramatically reduced half-life compared to 2,3,7,8-TCDD with 8.5 d. In liver the TFDD level reaches a maximum 30 minutes after injection and also declined in a biphasic manner. In rat hepatocytes a primary culture induction of CYP4501A1-catalyzed EROD activity could be demonstrated, indicating that 2,3,7,8-TFDD activates the dioxin receptor. In rat hepatocyte cultures similar EC50 values were found for 2,3,7,8-TCDD and 2,3,7,8-TFDD. So far no de novo synthesis of PFDD/PFDF could be detected under conditions were PCDDs/PCDFs are formed. Also, formation of PFDDs/PFDFs could not be detected during thermal treatment of fluorotrichloromethane or Teflon.

Animals↗

PubMed1988

Polydimethylsiloxanes associated with indoor and outdoor airborne particles.

Electrical contacts are subject to damage by interaction with silicone oils. These oils, which can cause catastrophic failure of electrical contacts, can arise as vapors or aerosols from components of the environment in which the contacts operate. To assess the potential environmental burden of silicones which could be transferred from source to sink (electrical contact), an aerosol sampling methodology was developed which collects silicone-bearing aerosols. These aerosols, collected with impactors and Teflon filters, are then analyzed by a pyrolysis/mass spectrometric method. As little as 0.1 ng of a given viscosity silicone fluid may be detected using this analytical approach. The fingerprint pyrolysis fragments in this study are cyclic dimethylsiloxanes such as hexamethylcyclotrisiloxane (molecular weight = 222), the detection of which is characteristic of polymeric silicone-bearing contaminants in the atmosphere surrounding the silicone-vulnerable electrical contacts.

Air Pollutants↗

PubMed1988

"Crack smoke" is a respirable aerosol of cocaine base.

The smoking of cocaine base [corrected] ("crack") has emerged as a significant substance abuse problem. A detailed characterization of cocaine smoke is a prerequisite for studies of its pharmacokinetics, abuse potential and toxicity. Model pipes were used to generate cocaine smoke analogous to that inhaled by human "crack" abusers. Using procedures to minimize pyrolysis, cocaine base smoke was determined to be 93.5% cocaine particles with the remainder being cocaine vapor. The average particle size generated from all model pipes was 2.3 mu which is small enough to ensure deposition into the alveolar region of the human lung. Although this particle size is eminently respirable [corrected] by primates, a much smaller fraction will reach the alveolar region of rodents. Special generating procedures would therefore be required to expose rodents to meaningful doses of airborne cocaine that mimic the rapid absorption achieved by "crack" smokers.

Aerosols↗

PubMed1996

Methylecgonidine coats the crack particle.

Crack is a form of cocaine base self-administered by smoking. When heated, it volatilizes and may partially pyrolyze to methylecgonidine (MEG). Upon cooling, a condensation aerosol forms. Heating cocaine base in model crack pipes produced particles of about 1 micron in diameter, regardless of the amount heated; however, MEG concentration increased from < or = 2% at 10 mg per heating to as much as 5% at 30 mg per heating. Methylecgonidine was < or = 1% of the recovered material when cocaine was vaporized off a heated wire coil, but the particles were larger (2-5 microns), and the distribution disperse. The vapor pressure of MEG was higher [log P(mm Hg) = 9.994 - 3530/T] than cocaine base, consistent with MEG coating the droplet during condensation, and with evaporation during aging or dilution. Disappearance of MEG from a chamber filled with crack smoke was a two-component process, one proceeding at the rate of cocaine particle removal, and the other at the desorption rate from other surfaces. Particle diameter influences the deposition site in the respiratory tract; thus, the likely different patterns of deposition in the respiratory tract of humans and animals of crack aerosols produced by different techniques warrant consideration, as they may influence our understanding of immediate and delayed sequelae of the inhalation of cocaine and its pyrolysis product, MEG.

Administration, Inhalation↗

PubMed1992

An isotopic biogeochemical study of the Green River oil shale.

Thirty-five different samples from three different sulfur cycles were examined in this stratigraphically oriented study of the Shell 22x-l well (U.S.G.S. C177 core) in the Piceance Basin, Colorado. Carbon isotopic compositions of constituents of Green River bitumens indicate mixing of three main components: products of primary photoautotrophs and their immediate consumers (delta approximately -30% vs PDB), products of methanotrophic bacteria (delta approximately -85%), and products of unknown bacteria (delta approximately -40%). For individual compounds synthesized by primary producers, delta-values ranged from -28 to -32%. 13C contents of individual primary products (beta-carotane, steranes, acyclic isoprenoids, tricyclic triterpenoids) were not closely correlated, suggesting diverse origins for these materials. 13C contents of numerous hopanoids were inversely related to sulfur abundance, indicating that they derived both from methanotrophs and from other bacteria, with abundances of methanotrophs depressed when sulfur was plentiful in the paleoenvironment. gamma-Cerane coeluted with 3 beta(CH3),17 alpha(H),21 beta(H)-hopane, but delta-values could be determined after deconvolution. gamma-Cerane (delta approximately -25%) probably derives from a eukaryotic heterotroph grazing on primary materials, the latter compound (delta approximately -90%) must derive from methanotrophic organisms. 13C contents of n-alkanes in bitumen differed markedly from those of paraffins generated pyrolytically. Isotopic and quantitative relationships suggest that alkanes released by pyrolysis derived from a resistant biopolymer of eukaryotic origin and that this was a dominant constituent of total organic carbon.

Alkanes↗

PubMed1994

Partial resolution of sources of n-alkanes in the saline portion of the Parachute Creek Member, Green River Formation (Piceance Creek Basin, Colorado).

Systematic variations in the 13C contents of individual extractable n-alkanes (C16-C29) can be modelled quantitatively and interpreted as indicating contributions from at least five distinct sources. These appear to be cyanobacterial (C16-C18, delta 13C = -37% vs PDB), phytoplanktonic (C16-C23, delta = -32%), chemoautotrophic bacterial (C20-C29, delta = -38%), phytoplanktonic or heterotrophic bacterial (C20-C29, delta = -30%), and vascular plants (C23-C29, delta = -29%). Hydrous pyrolysis of related kerogens yields large quantities of additional n-alkanes with different and much more uniform delta values. The latter materials are apparently derived from the thermolysis of aliphatic biopolymers whose presence in the Green River Oil Shale has been recognized visually.

Alkanes↗

PubMed1990

Metabolism of dietary genotoxins by the human colonic microflora; the fecapentaenes and heterocyclic amines.

The microflora of the human colon is a complex ecosystem of anaerobic bacteria which have the capability of enzymatically transforming a variety of dietary (or biliary) compounds to genotoxic metabolites. In the past, most investigators studying the interplay between diet and colonic flora and its role in the etiology of cancers focused on the reductive and glycosidic potential of the bacterial enzymes--many of which reverse the oxidative and conjugative reactions performed by the liver. Recent work in our laboratory has focused on the metabolism of two relatively new classes of genotoxins, the fecapentaenes and the heterocyclic amines (pyrolysis carcinogens). The fecapentaenes (conjugated ether lipids) are produced in the colon by Bacteroides spp. from polyunsaturated ether phospholipids (plasmalogens) whose natural origin and function are unknown. The fecapentaenes are potent direct-acting genotoxins that are detected in the feces of most individuals on normal western diets. The heterocyclic amines, which originate from fried or broiled proteinaceous foods, normally require activation by the liver before being potent mutagens or carcinogens. However, the "IQ" subclass (e.g. IQ and MeIQ) can be activated in the colon by Eubacterium and Clostridium species to a 7-hydroxy form which is directly mutagenic in Salmonella. Although there is no direct evidence that the fecapentaenes or the 7-hydroxy "IQ" compounds influence risk for colon cancer, the potency and prevalence of these bacterial metabolites is cause for concern.

Amines↗

PubMed1994

Potential genotoxic, mutagenic and antimutagenic effects of coffee: a review.

Coffee and caffeine are mutagenic to bacteria and fungi, and in high concentrations they are also mutagenic to mammalian cells in culture. However, the mutagenic effects of coffee disappear when bacteria or mammalian cells are cultured in the presence of liver extracts which contain detoxifying enzymes. In vivo, coffee and caffeine are devoid of mutagenic effects. Coffee and caffeine are able to interact with many other mutagens and their effects are synergistic with X-rays, ultraviolet light and some chemical agents. Caffeine seems to potentiate rather than to induce chromosomal aberrations and also to transform sublethal damage of mutagenic agents into lethal damage. Conversely, coffee and caffeine are also able to inhibit the mutagenic effects of numerous chemicals. These antimutagenic effects depend on the time of administration of coffee as compared to the acting time of the mutagenic agent. In that case, caffeine seems to be able to restore the normal cycle of mitosis and phosphorylation in irradiated cells. Finally, the potential genotoxic and mutagenic effects of the most important constituents of coffee are reviewed. Mutagenicity of caffeine is mainly attributed to chemically reactive components such as aliphatic dicarbonyls. The latter compounds, formed during the roasting process, are mutagenic to bacteria but less to mammalian cells. Hydrogen peroxide is not very active but seems to considerably enhance mutagenic properties of methylglyoxal. Phenolic compounds are not mutagenic but rather anticarcinogenic. Benzopyrene and mutagens formed during pyrolysis are not mutagenic whereas roasting of coffee beans at high temperature generates mutagenic heterocyclic amines. In conclusion, the mutagenic potential of coffee and caffeine has been demonstrated in lower organisms, but usually at doses several orders of magnitude greater than the estimated lethal dose for caffeine in humans. Therefore, the chances of coffee and caffeine consumption in moderate to normal amounts to induce mutagenic effects in humans are almost nonexistent.

Animals↗

PubMed1982

Genetic effects of fresh cigarette smoke in Saccharomyces cerevisiae.

Ability of fresh cigarette smoke from University of Kentucky reference cigarette 2R1 to induce gene conversion, reverse mutation and mitotic crossing-over in strain D7 of Saccharomyces cerevisiae was examined. A closed cell suspension-recycle system using 2 peristaltic pumps interconnected to a single-port reverse-phase smoking machine was developed to provide complete exposure of cells to smoke within 0.2--10 sec of its generation. The exposed cells showed a dose-dependent increase in the frequency of all the 3 genetic endpoints examined. Cell age was an important factor with younger cells being more sensitive than older. Filtration studies showed that the gas phase possessed as much as 25% of the total whole-smoke activity. Activated charcoal reduced the activity of smoke in direct proportion to its amount in the filter. Acetate filter did not appreciably alter the activity. A comparison of whole smoke from various cigarettes showed that: (1) the nicotine content of a cigarette does not affect the genetic activity of smoke; (2) burley and flue-cured tobaccos have differential activity in gene conversion and reverse mutation systems; and (3) the genetic effects of whole smoke are not peculiar to tobacco pyrolysis because similar effects are produced by smokes from lettuce and other non-tobacco cigarettes. It is concluded that the yeast D7 system can be used effectively for the quantitative evaluation of genetic effects of smoke from different cigarettes, and both whole cigarette smoke and its gas phase possess mutagenic as well as recombinogenic activity that can be modified by the use of filters.

Crossing Over, Genetic↗

PubMedDate not supplied

Mutagenicity of smoked, dried bonito products.

Mutagens have been found in smoked, dried bonito products, popular items in Japanese foods. The mutagens were isolated by means of blue cotton, an absorbent cotton preparation with covalently bound trisulfo-copper-phthalocyanine residues, and by means of XAD-2 resin. The mutagenicity was positive in Salmonella typhimurium strain TA98 with metabolic activation. The mutagens are produced during the process of smoking-and-drying bonito (a process called baikan). The activity was much higher than that expected from the content of benzo[a]pyrene. In contrast to benzo[a]pyrene, the mutagens were not inhibited by ellagic acid. The mutagenicity was not abolished by treatment with nitrite. Thin-layer and high-performance liquid chromatographic analysis gave two mutagenic fractions, both of which were distinguishable from benzo[a]pyrene and from the pyrolysis products Trp-P-1, Trp-P-2, Glu-P-1, Glu-P-2, A alpha C and MeA alpha C. The major mutagenic component was not chromatographically distinguishable from IQ and MeIQx, and the minor one was very similar to MeIQ. The smoked, dried bonito products contained free fatty acids, which were inhibitory to the mutagenicity of the bonito products.

Animals↗

PubMed1991

Indoor sources of mutagenic aerosol particulate matter: smoking, cooking and incense burning.

The emission of aerosol particles and their mutagenic activity as well as the emission of some gaseous pollutants has been studied experimentally in order to compare the emission from some indoor pyrolysis processes. Cigarette (tobacco and herbal) smoking, incense and mosquito-coil burning and frying of experimental lean minced pork emitted particulate matter. Their extracts were mutagenic in the Ames Salmonella test with TA98 and activation as well as, with a higher response, in a microsuspension test with the same strain and activation condition. The response of the particles from the smoking and burning processes varied from 3000 to 50,000 revertants per gram of smoked or burnt material in the conventional Salmonella test and from 50,000 to 350,000 revertants per gram in the microsuspension assay. The frying of lean minced pork gave an airborne emission of about 53 and 560 revertants per gram of fried pork, respectively, in the 2 assays. The frying of some common food items following cookbook recipes also emitted mutagenic aerosol particles but the emitted activity was less than that in the pork experiment. Carbon monoxide, isoprene and benzene were present in the emissions from the smoking and burning processes but were not detectable in the frying fumes. The results suggest that incense and mosquito-coil burning can cause indoor air pollution akin to that from cigarette smoking. Indoor air pollution from cooking requires further study.

Aerosols↗

PubMed1992

Mutagenic activity of a series of synthetic and naturally occurring heterocyclic amines in Salmonella.

26 synthetic and naturally occurring heterocyclic amines were tested in the Salmonella/microsome assay (Ames test) using tester strains TA98 and TA100 in the presence of an Aroclor-induced rat-liver S9 fraction. 9 of the compounds were protein-pyrolysis products which had previously been shown to be mutagenic. Mutagenic potencies similar to previously reported values were demonstrated for these compounds with the exception that Trp-P-1 was only mutagenic in strain TA98 in our study, although it had previously been reported to be weakly mutagenic in strain TA100. 17 structurally diverse heterocyclic amines were synthesized and tested for mutagenicity. The structural diversity of these synthetic heterocyclic amines will enhance the sensitivity of future quantitative structure-activity relationship (QSAR) studies by demonstrating the structural characteristics essential for mutagenicity. The results of this study provide a large data base for the mutagenicity of this important class of compounds.

Amines↗

PubMed1983

Comparative induction of somatic eye-color mutations and sex-linked recessive lethals in Drosophila melanogaster by tryptophan pyrolysates.

The mutagenicities of the products of pyrolysis of tryptophan, Trp-P-1 and Trp-P-2, on Drosophila melanogaster were examined by measuring the effects of these compounds in inducing recessive lethals and somatic eye-color mutations. Since negative results have already been obtained by the standard procedure in males, Trp-P-1 and Trp-P-2 (0.75 to 6 mg/ml) in sucrose solution were given to females for assay of recessive lethal mutations in X-chromosomes. These compounds caused a marginal increase above the control level in the mutation frequency. For the assay of effects on somatic eye-color mutations, Trp-P-1 (200 and 400 ppm) and Trp-P-2 (400 and 800 ppm) were fed to male larvae of a tester strain carrying a genetically unstable marker set of z and w+ on the X-chromosome. These compounds caused dose-dependent increases above the control level in somatic eye-color mutations in adults. It is concluded that, under the conditions used, the somatic eye-color mutation system was more sensitive than the recessive lethal system to the mutagenic effects of tryptophan pyrolysates.

Animals↗

PubMed1991

Enhanced liver metabolism of mutagens and carcinogens in fish living in polluted seawater.

Specimens of the seawater fish annular seabream (Diplodus annularis) were caught from a polluted harbor area and from a clean reference area. Seawater concentrates and fish-muscle extracts were not mutagenic in the Salmonella reversion test. Liver preparations of fish from the 2 sources were comparatively assayed for microsomal mixed-function oxidases and cytosolic biochemical parameters, as well as for the ability of S12 fractions to activate promutagens or to detoxify direct-acting mutagens. A shift of the cytochrome P-450 peak from 450.3 to 448.5 was accompanied by a 4.5-fold increase in arylhydrocarbon hydroxylase activity in fish living in the polluted environment. At the same time, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were doubled in the cytosol of the same animals, while reduced glutathione (GSH) peroxidase and GSH S-transferase were slightly yet significantly depressed. No significant difference was recorded for other biochemical parameters, including GSH, oxidized glutathione (GSSG) reductase, NADH- and NADPH-dependent diaphorases, and DT diaphorase. In parallel, fish exposed to polluted seawater exhibited a significant and marked enhancement of the metabolic activation of the pyrolysis product Trp-P-2 and of benzo[a]pyrene-trans-7,8-diol, and at the same time were less efficient in detoxifying the antitumor compound ICR 191. Liver S12 fractions from both sources efficiently decreased the direct mutagenicity of sodium dichromate, and failed to activate benzo[a]pyrene and aflatoxin B1 to mutagenic metabolites. These results provide evidence that both biochemical parameters and the overall capacity of fish liver to activate or detoxify certain mutagens can be assumed to be sensitive indicators of exposure to mixed organic pollutants in the marine environment.

Animals↗

PubMed1989

Catecholamine melanins. Structural changes induced by copper ions.

Melanins synthesized from adrenaline and dopamine in the presence or absence of copper ions were characterized by pyrolysis-gas chromatography-mass spectrometry and by IR and ESR methods. It was shown that Cu2+ are able to induce changes in the melanin structure. Melanins obtained from adrenaline-Cu2+ and dopamine-Cu2+ complexes are composed mainly from monomeric units of the indole type. Melanins synthesized from these catecholamines without Cu2+ contain additionally large amounts of unindolized monomeric units. The structure differences in both types of melanins are reflected in their sorptive abilities and spectroscopic characteristics.

Chloroquine↗

PubMedDate not supplied

Hypersensitivity of xeroderma pigmentosum cells to dietary carcinogens.

Xeroderma pigmentosum patients, in addition to ultraviolet-induced skin cancers, have an increased prevalence of neoplasms occurring in sites shielded from ultraviolet radiation. We postulated that these internal neoplasms might be related to ingestion of dietary carcinogens. As model dietary carcinogens, we studied the tryptophan pyrolysis products, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2). These dietary compounds bind to DNA and are highly mutagenic and carcinogenic. Cytotoxicity of these compounds was examined in cultured lymphoblastoid cell lines from xeroderma pigmentosum patients in complementation groups A, B, C, D and E and the variant form and from normal donors. All xeroderma pigmentosum lymphoblastoid cell lines showed a greater reduction in viable cell concentration than the 2 normal lymphoblastoid cell lines following addition of Trp-P-1 or Trp-P-2 (5 micrograms/ml) to the culture medium. Possible differences in cellular activation of these compounds were overcome by treating the cells with rat-liver microsome-activated Trp-P-2. There was a greater reduction in viable cell concentration in the xeroderma pigmentosum group A and D cells than in the normal lymphoblastoid cell lines after treatment with activated Trp-P-2. These data suggest that the xeroderma pigmentosum DNA-repair system is defective in repairing Trp-P-1 and Trp-P-2 induced DNA damage in addition to being defective in repairing ultraviolet-induced DNA damage. Thus xeroderma pigmentosum patients may be at increased risk of toxicity from some dietary carcinogens.

Aryl Hydrocarbon Hydroxylases↗

PubMed1994

Management and control of a large outbreak of diarrhoea due to Clostridium difficile.

In the six-month period 1 November 1991 to 1 May 1992 175 patients developed diarrhoea due to Clostridium difficile in three hospitals in Manchester, UK. Most patients (90%) were over 60 years old and had been admitted to acute geriatric or medical wards with other illnesses. Infection is thought to have contributed to 17 deaths. Twenty-two patients relapsed clinically after antibiotic treatment. The outbreak began in one ward and affected 15 patients and two nurses. During the following months cases occurred on 34 wards. The pattern of spread suggested that a ward index case was followed by several secondary cases. Pyrolysis mass spectrometry showed that 79% of isolates of C. difficile belong to a single cluster and this putative outbreak strain also extensively colonizes the hospital environment. It was also responsible for a smaller outbreak in 1991 and many 'sporadic' cases in our hospitals before then. An outbreak control team was convened at an early stage and expert opinion co-opted. Infection control measures included: intensive education of staff; increased vigilance; strict enteric precautions; cohort nursing in a designated ward; rigorous cleaning procedures including emptying and 'deep' cleaning of wards where several cases had occurred; restriction of staff and patient movement; and restriction of antibiotic use. Subsequent to these measures there has been a substantial and sustained decrease in the number of new cases.

Aged↗

PubMed1991

Relative acute toxicities of hydrogen fluoride, hydrogen chloride, and hydrogen bromide in nose- and pseudo-mouth-breathing rats.

Hydrogen fluoride (HF), hydrogen bromide (HBr), and hydrogen chloride (HCl) gases can be generated during the pyrolysis of a variety of materials and they may be encountered in numerous industrial settings. Although injury to the respiratory tract has been characterized following the inhalation of halide gases via the nasal route, essentially no experimental information is currently available about their injurious effects when they are inhaled during mouth breathing. In this study, we simulated mouth breathing by using a pseudo-mouth-breathing (MB) rat model in order to: (1) characterize the profiles and magnitudes of respiratory tract injury that result from the acute inhalation of relatively high mass concentrations of the above halides when the upper airway is bypassed, and (2) assess the relative toxicities of HF, HBr, and HCl when inhaled by way of either the nasal or the oral pathways. Tracheal tubes connected to mouthpieces were inserted into temporarily anesthetized rats, i.e., mouth breathers. Awake rats were placed into whole body flow plethysmographs for pulmonary ventilation studies while they were exposed either to air or to 1300 ppm of HF, HBr, or HCl for 30 min. Similarly pretreated rats were also exposed but without the mouthpiece, i.e., nose breathers (NB). The animals were euthanized 24 hr after exposure for histopathologic analyses of their upper and lower respiratory tracts and for lung gravimetric measurements. Tissue injury following NB exposure to the halides was confined to the nasal region, e.g., epithelial and submucosal necrosis, accumulations of inflammatory cells, exudates, and the extravasation of erythrocytes. MB exposure caused higher mortality rates and major tissue disruption in the trachea, including epithelial, submucosal, glandular, and cartilage necrosis, and accumulations of inflammatory cells and exudates. More peripheral lung damage was manifested by lung gravimetric increases and histopathologic changes primarily in the larger conducting airways. The results of this study demonstrate that the injurious response profiles to HF, HBr, and HCl markedly differ as a function of the route by which they are inhaled. Furthermore, examinations of the magnitudes of injury caused by exposure to the halides during nose or mouth breathing in conjunction with animal ventilatory data obtained during exposure to the halides suggest that HF, HBr, and HCl are quantitatively similar in their toxic effects in the respiratory tract.

Acids↗