Abstract  #311 chemicals were tested under code, for mutagenicity, in Salmonella typhimurium; 35 of the chemicals were tested more than once in the same or different laboratories. The tests were conducted using a preincubation protocol in the absence of exogenous metabolic activation, and in the presence of liver S-9 from Aroclor-induced male Sprague-Dawley rats and Syrian hamsters. Some of the volatile chemicals were also tested in desiccators. A total of 120 chemicals were mutagenic or weakly mutagenic, 3 were judged questionable, and 172 were non-mutagenic. The remaining 16 chemicals produced different responses in the two or three laboratories in which they were tested. The results and data from these tests are presented.

Abstract  The emissions of polycyclic aromatic hydrocarbons (PAHs) were quantified for two joss paper furnaces burning two kinds of joss papers (recycled paper made and virgin bamboo made). A cyclone and a wet scrubber were installed in series on one of the two furnaces. Particulate and gaseous PAHs were collected with a sampling system meeting the criteria of U.S. EPA Modified Method 5. Twenty-one species of PAH were analyzed by GC/MS. Individual PAH emission factors vary from less than 1 mg kg(-1) fuel to several tens of mg kg(-1) fuel. The total (sum of 21 compounds) and the carcinogenic PAH (benz[a]anthracene, chrysene, benzo[b] fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, indeno[1,2,3,-cd]pyrene, dibenz[a,h] anthracene) emission factors were not statistically different for the two furnaces and averaged 71.0 and 3.2 mg kg(-1), respectively. The PAH profiles showed a predominance of naphthalene (58.1%), phenanthrene (11.7%) and fluorene (7.5%). Of the two joss papers examined, bamboo-made joss paper showed less emission in both particulate and gaseous PAHs. For particulate and gaseous PAHs, the removal efficiencies of total PAHs by the air pollution control devices were 42.5% and 11.7%, respectively. PAH emission factors in high airflow conditions were generally lower than those in low airflow condition. (c) 2005 Elsevier Ltd. All rights reserved.

Abstract  Emissions of polycyclic aromatic hydrocarbons (PAHs, 2-7 ring) and regulated air pollutants (CO, HC, NOx, PM) from 2-stroke carburetor (2-Stk/Cb), 4-stroke carburetor (4-Stk/Cb) and 4-stroke fuel injection (4-Stk/Fl) motorcycles were investigated by testing these vehicles on a chassis dynamometer. Exhaust samplings were carried out on diluted exhausts in a dilution tunnel connected to a constant volume sampling system. Measurements were performed On a standard driving cycle. The results reveal that low molecular weight PAHs (especially naphthalene) dominated in the exhaust gas. The averages of soluble organic fractions were 86.4%. 46.3% and 48.9% for the 2-Stk-/Cb. 4-Stk/Cb and 4-Stk/Fl motorcycles, respectively. PAH emissions are greater from cold-start driving than those from hot-start driving cycle for all these three kinds of motorcycles. Total PAH emission factors were 8320. 5990 and 3390 mug km(-1) for the in-used 2-Stk/Cb, 4-Stk/Cb and 4-Stk/Fl motorcycles, respectively. PAH emission factors were the largest for the 2-Stk/Cb motorcycles. Besides, the 2-Stk/Cb motorcycle had the largest total BaP equivalent emission factor of 10.8 mug km(-1) indicating that the emission exhaust from the 2-Stk/Cb motorcycle was most carcinogenic. HC. PM and PAH emissions were the lowest for the 4-Stk/Fl motorcycles. The correlation coefficient between CO and total PAH emissions for all the test motorcycles was 0.51, indicating that CO and PAH emissions are not highly correlated. (C) 2004 Elsevier Ltd. All rights reserved.

Abstract  Much of the biological activity of cigarette smoke resides in the neutral fraction of the particulate phase. Since the volatile constituents of this material, the semivolatiles, are accessible to selective filtration, some of the biological activity of cigarette smoke might be reduced. In view of this, the genotoxic and cytotoxic effects and the chemical composition of the semivolatile neutral material of a cigarette smoke condensate was investigated. Cigarette smoke condensate obtained from domestic American blend type cigarettes, was separated into a volatile, a nonvolatile and a semivolatile fraction. The semivolatile constituents were fractionated by liquid-liquid extraction into 4 subfractions: acids, phenols, bases and neutrals. The neutral material was separated further by silica gel chromatography into 7 subfractions of varying polarity. The major components of these were identified by gas chromatography-mass spectrometry. These fractions were studied using 4 in vitro short-term tests, of which 2, the Ames test and induction of sister-chromatid exchanges, provided information on their genotoxicity and the other 2 provided information on their cytotoxicity by measuring inhibition of cell growth and inhibition of oxidative metabolism. Sister-chromatid exchanges were induced by the neutral fraction and the 7 subfractions, the activities of which increased with increasing polarity. Neither the total neutral material, nor the subfractions showed any mutagenic activity in the Ames test. The cytotoxic effect of the fractions of medium polarity, was greater than that of the total neutral material, while the most and the least polar fractions were less toxic.

Abstract  The mutagenicities of organic chemical contaminants in city water and related compounds were examined by the Salmonella/microsome test {Ames test}. Out of 21 chemicals tested, 1,2-dichloroethane was mutagenic in S. typhimurium TA100 in the presence of S9 mix. The other 20 compounds including the 3 isomers of trichlorobenzene 1,1-dichloroethane, chlorobenzene, were not mutagenicin the present test system.

Abstract  Since statistical analysis proved the intercorrelation of tissue-gas partition coefficients of chemicals with similar chemical structures, bioavailability is controlled by one parameter dependent on the physicochemical properties of the chemicals and two constants distinguishing the tissues. Oil-gas partition coefficients are suggested to describe the biosolubility of volatile halogenated aliphatic chemicals. Tissue-gas partition coefficients derived from oil-gas partition coefficients were substituted in a pharmacokinetic model in order to study the effect of biosolubility on uptake, distribution, and elimination of inhaled chemicals. The simulation was focused on occupational exposures (8 h/day, 5 days/wk). Desaturation curves for all tissues show three exponential decays. The analysis of the simulation data indicates three patterns in behavior of inhaled vapors and gases in the body. Tissue uptake of poorly soluble chemicals (oil-gas partition coefficient less than 10) is flow limited at the beginning of exposure, but the partial pressures of such chemicals in the body equilibrate very rapidly with ambient air. Increased pulmonary uptake compensates for metabolic clearance. The rapid response of tissue concentrations to changes in exposure concentrations indicates that the toxic effect can easily be induced by short-term increase of exposure concentration, and that emergence from the reversible effect is rapid when exposure ceases. Tissue uptake of chemicals with oil-gas partition coefficients between 10 and 10(4) is flow limited during the entire 8-h exposure. Tissue concentrations increase slowly. Pulmonary uptake, being restricted by alveolar ventilation, compensates at steady state only for the amount of chemical removed by metabolic clearance. Therefore, tissue concentrations at steady state are lower than biosolubility. Accumulation during occupational exposure is obvious. Dumping of inhaled chemicals in adipose tissue protects the target organ from the occasional short-term increases in the exposure concentration. Tissue uptake of highly soluble chemicals (oil-gas partition coefficients greater than 10(4)) is limited by alveolar ventilation and exposure concentration. The rising and declining of tissue concentrations is very slow, half-times being in the magnitude of months and years. Metabolism reduces the half-time significantly. A lagging acute toxic effect can develop as the chemical accumulates in the body; the effect is most likely to persist long after the termination of the exposure.

Abstract  Repeated exposure to coal liquefaction products produces a broad range of systemic effects. Among these, growth suppression, anaemia, leucocytosis and other haematological disorders are most prominent. Bone marrow, liver and kidney are the target organs affected by treatment. The effects are more severe with heavy distillates and male rats are more sensitive than females. Other changes included increased serum transaminases, alkaline phosphatase and cholesterol. Depending on the route of administration, the skin or lung may also be affected. Inhalation exposure produces the most severe changes, and oral exposure the least. Distillates containing N-PAHs and sulphur-containing PAHs are also more biologically active. Teratological effects were only observed if animals were exposed to the heavy distillate. Similarly, heavy distillates have mutagenic or carcinogenic properties. Teratological effects, as well as mutagenicity and carcinogenicity, of the coal liquefaction distillates seem to be linked to their PAH content, especially the N-PAHs. From the data presented in this review, it should become evident that the potential effects of coal liquefaction products on human health could be severe, especially with long-term exposure. Limited information exists on the occupational effects to coal liquefaction materials because most of the work to date has been with pilot plants. Careful and good judgement is required in order to extrapolate data from pilot plants to commercial-scale production. Experience in health effects of workers in the petroleum industry and coke-oven operations can serve as a guide for the implementation of industrial hygiene programmes for coal liquefaction operations. These programmes include engineering controls, health education, personal monitoring and hygienic practices, medical surveillance and long-term epidemiology studies, and they should be implemented to make coal liquefaction a healthy and environmentally sustainable industry.

Abstract  Tabershaw Occupational Medicine Associates, PA (TOMA) performed medical examinations and evaluations of the workers at Koppers' Bridgeville, Pennsylvania plant in May and June 1981. Of the 246 eligible workers, 139 (56.5%) were examined. While this is not a large proportion of workers, there is fairly good representation across all age groups. The medical examinations, tests, and evaluations were geared specifically for the potential occupational exposures at the plant. Special tests were therefore used to detect abnormalities in physiology and health that might be caused by work exposures. There were no diseases or abnormalities found that can be definitely related to effects of work exposures. There was one case of lung cancer detected in a 64-year-old cigarette smoker. It is not possible to say definitely if there is any relationship between work exposures and the development of lung cancer in this man, but the long history of cigarette smoking would implicate this as a causative factor. There were nine cases of possible minimal pneumoconiosis by chest x-ray. In addition, four of these individuals also had pleural thickening. Three others had pleural thickening without other complications. We do not have any information to indicate there were work exposures at this plant that would cause these abnormalities detected in the x-ray. There were no other abnormalities detected in the workers in greater proportion than in the general population of the same age groups. Specifically, there were fewer than expected skin lesions and no skin cancers found. There was no evidence of thyroid or immunological abnormalities. There also was no excess number of abnormalities in the hematological system. In the 1978 study, 13 cases of eosinophilia were observed, a higher than expected prevalence. Only seven of these 13 were retested in 1981. The results were all normal except for one case and his results were only slightly elevated. Five other workers also had elevated eosinophils, but the levels were not severe and there was no evidence of associated disease. There were several workers who bad abnormalities, generally minor, not related to work. Each worker was counseled about the findings and advised to see his/her personal physician as appropriate.

Abstract  1. Naphthalene (1g./kg.) was fed daily by stomach tube to rabbits. 2. In more than half of the rabbits opacities in the lens and degeneration of the retina were visible in vivo. 3. Dissection of eye tissues revealed some or all of the following changes: a browning of the lens and eye humours, blue fluorescence of the eye humours and crystals in the retina and vitreous body. 4. The ascorbic acid concentration of the eye humours was decreased. 5. Some metabolites of naphthalene [1,2-dihydro-1,2-dihydroxynaphthalene, 2-hydroxy-1-naphthyl sulphate and (1,2-dihydro-2-hydroxy-1-naphthyl glucosid)uronic acid] are converted enzymically by the tissues of the eye into 1,2-dihydroxynaphthalene. 6. Changes in the eye are consistent with 1,2-dihydroxynaphthalene's being the primary toxic agent. The properties and reactions of this substance are described. 7. 1,2-Dihydroxynaphthalene is readily autoxidizable in neutral solution to form the yellow 1,2-naphthaquinone and hydrogen peroxide. This oxidation is reversed by ascorbate. 8. Ascorbate is oxidized catalytically by 1,2-naphthaquinone. This may account for the disappearance of ascorbate from the aqueous and vitreous humours of the eye after naphthalene feeding. It may also account for the appearance of crystals of calcium oxalate in the eye. 9. The brown colour of the lens of the naphthalene-fed rabbit is due to presence of naphthaquinone-protein compounds.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM REVIEW NEUROTOXICITY CARCINOGENESIS TERATOGENESIS MUTAGENESIS

Abstract  National Center for Toxicological Research; Electric Power Research Institute. #Current methods to estimate the quantitative cancer risk of complex mixtures of polycyclic aromatic hydrocarbons (PAH) such as coal tar assume that overall potency can be derived from knowledge of the concentration of a few carcinogenic components such as benzo[a] pyrene (B[a]P). Genotoxic damage, such as DNA adducts, is thought to be an essential aspect of PAH-induced tumorigenesis and could be a biomarker for exposure useful for estimating risk. However, the role of B[a]P and the relationship of adduct formation in tumorigenosis have not been tested rigorously in models appropriate for human health risk assessment. Therefore, we directly compared tumor induction and adduct formation by B[a]P and coal tars in several experimental protocols, including one broadly accepted and used by regulators. We found that B[a]P content did not account for tumor incidences after exposure to coal tars. DNA adducts were found in both tumors and tumor-free tissue and tumor outcomes were not predicted by either quantitation of total DNA adducts or by the DNA adduct formed by B[a]P. These data suggest that risk assessments based on B[a]P content may not predict accurately risk to human health posed by environmental PAH.

Abstract  Naphthalene, a murine Clara cell cytotoxicant, is metabolized by cytochrome P450 monooxygenases to unstable, chiral epoxide metabolites which can conjugate with glutathione in the presence of glutathione transferases. Analysis of the three diasteriomeric glutathione adducts produced from conjugation of naphthalene oxides was used in these studies to characterize the stereochemistry of naphthalene epoxidation in preparations of nasal mucosa, lung and liver of the mouse, rat, hamster and monkey. The highest rates of naphthalene metabolism were observed in mouse lung and liver microsomal incubations. Rat, hamster and monkey lung microsomal preparations metabolized naphthalene at 12, 37, and 1%, respectively, of the rate observed in mouse lung. The ratio of chiral epoxides produced in microsomal incubations was dependent upon the concentration of naphthalene. At high substrate concentrations (0.25-1.0 mM), the ratio of 1R,2S- to 1S,2R-naphthalene oxide, as assessed by the glutathione adducts generated (adduct 2/adducts 1 + 3), in murine lung microsomal incubations was 10:1 and at low concentrations (0.062 mM and below) varied from 13.8:1 to 30:1. In contrast, the ratio of 1R,2S- to 1S,2R-naphthalene oxide produced in murine liver microsomes varied from 1:1 at high substrate concentrations to 5:1 at low substrate concentrations. The ratio of naphthalene oxides was unaffected by the concentration of glutathione in the incubation. In contrast to the preferential formation of 1R,2S-naphthalene oxide observed in mouse lung microsomal preparations, lung microsomes derived from the rat, hamster and monkey yielded 1R,2S- to 1S,2R-epoxide ratios of 0.48, 0.61 and 0.12, respectively, at 0.5 mM naphthalene.

Abstract  Male, weanling Blue-Spruce rats were treated with naphthalene (p.o.) in defined dose increments up to 750 mg/kg body weight over 9 weeks. At necropsy, treated rats showed a 20% decrease in body weight compared to controls. Naphthalene treatment resulted in enhanced peroxidation (p less than 0.001) only in the liver. This increased peroxidation was associated with reductions (p less than 0.05) in the activity of the selenoenzyme glutathione peroxidase in hepatic cytosolic fractions and an associated increase (p less than 0.05) in the selenium-independent glutathione peroxidase. No increase in peroxidation was observed in the lung, eye or heart of these rats and the activities of the selenoenzyme and the selenium-independent glutathione peroxidases were also unaffected by naphthalene in these organs. Naphthalene also did not affect superoxide dismutase activity in any of the organs examined. Thus, in addition to the known effects of naphthalene on tissue glutathione, naphthalene-induced reductions in the selenoenzyme glutathione peroxidase can also contribute to peroxidation in the liver and must be considered as a contributing factor in naphthalene toxicity in vivo.

Abstract  Hemolysis following accidental ingestion of naphthalene in black females deficient in glucose-6-phosphate dehydrogenase (G-6-PD) has not been previously reported. A 20-month-old black female is presented and the literature reviewed. Although G-6-PD deficiency is X-linked, health care providers must be aware that hemolysis may occur in females who are deficient in G-6-PD after exposure to naphthalene.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN

Abstract  BIOSIS COPYRIGHT: BIOL ABS. Some data on a newly developed filter/sorbent indoor air SVOC sampling device for thermal desorption analysis are described. Thermal desorption of SVOCs spiked on Tenax had response factors identical to on-column injection except for highly polar compounds like fatty acids. SVOCs spiked on quartz fiber filters had for non-oxygen compounds). Low nanogram on-tube amounts of lower desorption efficiency. In addition, it was indicated that the "memory" effect was an important source of background contaminations that might impair analysis of low nanogram on-tube amounts of some SVOCs. Polar SVOCs in the gas phase appear to adsorb to the quartz fiber filters. This functions as a precleaning of the sample and thus minimizes the problem with coeluting peaks. The relative standard deviations of air concentrations of 10 SVOCs in an office estimated from nine duplicate samples appeared to be sufficiently low to distinguish a day to day variation.

Abstract  Analytical Institute of the University of Vienna. A method for the quantitative determination of polycyclic aromatic hydrocarbons (PAHs) in tobacco smoke condensate has been developed and was applied to the analysis of the Kentucky Reference cigarette 1R4F. The procedure uses extraction of the filters with methanol, dilution with water, automated solid-phase extraction (SPE) on a C18 column for cleanup purposes and elution with cyclohexane prior to gas chromatography-mass spectrometry for quantification. Concentration values for 17 PAHs are given and compared to results of former publications.

Abstract  This paper presents the results of an extensive literature survey and data analysis conducted to determine uncontrolled and controlled pollutant emission factors (mass pollutant emitted per mass waste incinerated) for medical waste incinerators (MWI). Pollutant emission factors were calculated separately by type of medical waste (red bag, general hospital, and pathological waste), and add-on air pollution control (APC) equipment (wet scrubber systems, or dry scrubber/baghouse combinations). Pollutants for which emission factors were determined are particulate matter, carbon monoxide, hydrogen chloride, sulfur dioxide, nitrogen oxides, various metals, dioxins/furans, and selected volatile organic compounds (VOCs). In addition, the combustion gas produced per mass of waste incinerated was determined in order to compute expected pollutant concentrations in the exhaust gases based on the pollutant emission factors. Data from 40 MWIs burning various forms of medical waste and equipped with or without add-on air pollution control equipment were used to develop pollutant emission factors. Technical reports of emission tests were reviewed in detail, and calculations were made to convert reported outlet stack gas concentrations (before and after APC equipment) to pollutant emission rates. Reported waste feed rates were combined with the pollutant emission rates to produce emission factors. The emission factors were then grouped and averaged within appropriate groups to give best-estimate emission factors for various pollutants. Also, air pollution control equipment efficiencies were determined for each pollutant. Wide variations were observed for many of the pollutant emission factors, both controlled and uncontrolled. These variations are most likely a result of different operating conditions of APC equipment (e.g., caustic feed rates, water feed rates, and inlet temperatures), variable waste compositions, and differing incinerator operations among the reported MWI facilities. Based on the data examined, it appears that control of dioxins/furans by wet scrubber systems is, on the average, twice as good as that by dry scrubber/baghouse combinations. However, control of metals by dry scrubber/ baghouse combinations appears to be far superior to that of wet scrubber systems.

Abstract  BIOSIS COPYRIGHT: BIOL ABS. Select polycyclic aromatic hydrocarbons (PAHs), their derivatives, and nicotine were measured in eight homes in Columbus, Ohio, during the winter of 1986/1987 by Chuang et al. (1988, Technical Report EPA/600/4-28/028, U.S. EPA). These homes had different indoor PAH sources, namely, environmental tobacco smoke, gas cooking/beating, and electrical cooking stoves. We use a combination of correlation analysis, factor analysis and multiple regression to identify and apportion the different sources of PAHs. We find that, of all the sources, environmental tobacco smoke appears to have the greatest impact on the total indoor PAH concentrations. In smokers' homes, more than 87% of the total PAH is due to this source. Background sources are the largest contributor to PAHs in nonsmokers' homes. We also study the source apportionment of total extractable organic material (EOM) measured in the homes. In smokers' homes, EOM can be attributed mainly to environmental tobacco smoke (49%

Abstract  The determination of S-(1,2-dicarboxyethyl)glutathione and reduced glutathione (GSH) in the rabbit lens and liver was developed using an isotachophoretic analyser. The recovery of S-(1, 2-dicarboxyethyl)GSH from the rabbit liver after ion-exchange treatment was 96.8 +/- 11.3% (n=3). The contents of S-(1,2-dicarboxyethyl)GSH in the rabbit lens and liver were 219.9 +/- 29.1 (n=5) and 44.0 +/- 13.5 (n = 8) nmol/g, respectively. The contents of S-(1, 2-dicarboxyethyl)GSH in the lens and GSH in the lens and liver of naphthalene-treated rabbits was also determined by this method 24 hours after naphthalene administration, at which time the axial opacity "spichen" was observed at the equatorial region of the lens. The content of S-(1,2-dicarboxyethyl)GSH in the lens decreased in proportion to the content of GSH. During the further development of true lens opacity after naphthalene administration, the S-(l, 2-dicarboxyethyl)GSH content further compared with that in the spichen stage, but the S-(1, 2-dicarboxyethyl)GSH content of the lens that did not develop true opacity after naphthalene administration returned to the normal level. The change of S-(1, 2-dicarboxyethyl)GSH content of the lens in the spichen and true opacity stages coincided with that of GSH content. On the other hand, the content of GSH of the liver decreased markedly until 24 hours after naphthalene administration, then returned to normal, irrespective of whether true opacity did or did not subsequently develop.

Abstract  Exposure of rat hepatocytes to hydrazine, carbon tetrachloride or 1,4-naphthoquinone results in cytotoxicity determined as uptake of Trypan blue and leakage of lactate dehydrogenase (LDH). After exposure of hepatocytes to hydrazine and 1,4-naphthoquinone, ATP was also measured and was found to be depleted. Addition of the beta-amino acid taurine to the hepatocyte incubation buffer partially protects the cells against the cytotoxicity of these three different cytotoxic compounds, as indicated by Trypan blue uptake and LDH leakage. Taurine also reduces the depletion of ATP caused by 1,4-naphthoquinone but not hydrazine. It is suggested that taurine may have a cytoprotective effect in vitro and may be a useful tool for the investigation of mechanisms of cytotoxicity.