Tobacco Documents Online

CAS ONLINE@ The CA file contains records for the documents covered in Chemical Abstracts for the time period 1967-present. Chemical Abstracts covers journals, patents, technical reports, books, conference proceedings, and dissertations from all areas of chemistry and chemical engineering, worldwide. The CA file contains over 6 million records, and is updated biweekly with an additional 14,000-18,000 citations. The document records in this file contain bibliographic and indexing information for searching. Over 60% of the records also contain abstracts for display. The next two pages of this pamphlet give information on the search and display fields in the CA file, the formats which are available for online DISPLAY and offline PRINT of records, and show samples of journal and patent records.

ANSWER 1 AN CA103(5):33308e TI Decomposition reactions of (hydroxyalkyl)nitrosoureas and related compounds: possible relationship to carcinogenicity AU Singer, Sandra S. CS Frederick Cancer Res. Facil., NCI LO Frederick, MD 21701, USA SO J. Med. Chem., 28(6), 1088-93 SC 4-6 (Toxicology) DT J CO JMCMAR IS 0022-2623 F'Y 1985 LA Eng AB Decompn. reactions of the title compds., 1-(2-hydro:<yethyl)-1-nitrosourea C13743-07-2], 1-(2-hydroxypropyl)-1-nitrosourea C71752-69-7], 3-nitrosooxazolid-2-one C38347-74-97, and 5-methyl-3-nitrosooxazolid-2-one C79624-33-2], were studied in aq. buffers at physiol. pH to det. the pattern of product formation that might be related to carcinogenesis. Related dialkylnitrosoureas were also subjected to decompns. in buffer followed by product anal. The products predicted by literature mechanisms for these decompns. were the compds. formed. The tests compds. were dissolved at pH 6.4-7.4 in 0.067 or 0.1M phosphate buffer at 37.degree. employing several methods of anal. At the above pH, epoxides were stable reaction products; however, in the presence of hepatocytes, most epoxides were converted to glycols. The results reveal no clear-cut pattern of product formation that could be directly related to carcinogenesis. Some of the products were highly active compds. which are carcinogens in their own right, and they may be responsible for some or all of the carcinogenic activity of•the test compds. if they are formed by decompn. of the test compds. at the target organ. KW carcinogenicity alkylhydroxyurea nitrosooxazolidone decompn IT Degradation (of (hydroxyalkyl)nitrosoureas and related compds., carcinogenicity in relation to) IT 75-07-0, biological studies 75-21•-8, biological studies 107-21-1, biological studies (as (hydroxyethyl)nitrosourea decompn. product, carcinogenicity in relation to) IT 57-55-6, biological studies 67-64-1, biological studies 75-56-9, biological studies 123--38-6, biological studies (as (hydroxypropyl)nitrosourea decompn. product, carcinogenicity in relation to) IT 107-07-3, biological studies (as chloroethylurea deriv. decompn. product, carcinogenicity in relation to) IT 7086-00-2 57178-82-2 (as deuterohydroxyethylurea deriv. decompn. product, carcinogenicity in relation to) [7C7 VJC7280 1.

IT 1U8-32-7 (as methylnitrosooxazolidone decompn. product, carcinogenicity in relation to) IT 96-49-1 (as nitrosooxazolidone decompn. product, carcinogenicity in IT relation to) 154-93-8 13010-47-4 13743-07-2 38347-74-9 59960-30-4 6U784-46-5 66929-45-1 71752-69-7 75014-24-3 77081-3o-2 79624-33-2 96806-34-7 96806-35-8 (decompn. of, carcinogenicity in relation to)

ANSWER 2 AN CA103(3):18258v TI An evaluation of the utility of four in vitro short term tests for predicting the cytotoxicity of individual compounds derived from tobacco smoke AU Curvall, Margareta; Enzell, Curt R.; Pettersson, Bertil CS Res. Dep., Swed. Tobacco Co. LO Stockholm S-104 62, Swed. SO Cell Biol. Toxicol., 1(1), 173-93 SC 4-B (Toxicology) DT J CO CBTOE2 IS 0742-2091 F'Y 1984 LA Eng AB Biol. activity of 305 compds. (12 groups according to main functionality) was compared by 4 in vitro tests, i.e., the cell growth of Ascites sarcoma BF 8 cells, the oxidative metab. of isolated brown fat cells from adult hamsters, the membrane damage of human diploid embryonic lung fibroblasts, and the ciliary activity of embryo chicken trachea. The results are tabulated. The phenols constitute the most active group, followed by aldehydes and alcs. The least active are the furans/thiophenes and the esters. Among the phenols, the alkylphenols are highly active. To find whether the toxicity of some of these compds. belonging to different groups might be due primarily to a common subunit, 45 descriptors were selected which included the 12 functionalities. The computer-assisted matching of these and any combination of them against the mean activity showed the most toxic single descriptor group to be terpenoids followed by indoles and naphthalenes; the most toxic 2-descriptor group was .alpha.,.beta.-unsatd. carbonyls, followed by n-alkyl alcs., aldehydes, and acids. Intersystem similarities and differences, using a high-medium-low scale, indicated that all the 4 test systems give the same results for 35% of the compds. KW chem cytotoxicity prediction; tobacco smoke chem cytotoxicity IT Trachea (ciliary activity of, cytotoxicity prediction for chem. compds. of tobacco smoke from in vitro tests in relation to) IT Tobacco smoke and smoking (components of, toxicity of, cytotoxicity prediction from in vitro tests in relation to) IT Molecular structure-biological activity relationship (of compds. o+ tobacco smoke, cytotoxicity prediction from in vitro tests in relation to) IT Cell membrane (of lung fibroblast, cytotoxicity prediction for chem. compds. of tobacco smoke from in vitro tests in relation to) OD IT Anhydrides Go Alcohols, biological studies ~ Aldehydes, biological studies (~ Amines, biological studies (~ Aromatic hydrocarbons, biological studies N Carboxylic acids, biological studies OD Esters, biological studies N

Ethers, biological studies 1':etones, biological studies Phenols, biological studies Terpenes and Terpenoids, biological studies (toxicity of, of tobacco smoke, cytotoxicity prediction from in vitro tests in relation to) IT Sarcoma (ascites, cell growth inhibition of, cytotoxicity prediction for chem. compds. of tobacco smoke from in vitro test in relation to) IT Adipose tissue, metabolism (brown, adipocyte, oxidative metab. by, cytotoxocity prediction for chem. compds. of tobacco smoke from in vitro tests in relation to) IT Toxicity (cyto-, of chem. compds. of tobacco smoke, prediction of, in vitro tests in relation to) IT Heterocyclic compounds (nitrogen, toxicity of, of tobacco smoke, cytotoxicity prediction from in vitro tests in relation to) IT 100-83-4 1 i~3-69-5 104-93-8 10~~-84-5 103-73-1 105-53-3 101-81-5 1~~4-53-0 105-67-9 biological studies 106-44-5, biological studies 107-02-8, 107-12-0 107-1.T-•-1, biological biological studies 108-=8-3, biological studies 108-44-1, biological studies 108-48-5 ~ studies 108-68-9 108-75-8 studies 85-01-8, 87-51-4, 89-81-6 90-15-3 studies 95-13-6 studies 50-32-8, biological biological studies biological studies biological studies bioloc}ical studies 67-63-0, biological biological studies 78-84-2 78-85-3 80-56-8 biological biological 90-00-6 91-10-1 91-55-4 95-20-5 studies 51-17-2 54-11-5 59-67-6, biological studies 64-17-5, biological studies 64-19-7, biological studies 66-25-1 67-47-0 67-56-1, studies 67-64-1, biological 75-05-8, biological studies 78-9.3-3, biological studies 83-32-9 83-33-0 83-34-1 studies 85-44-9 86-28-2 studies 87-59-2 87-62-7 90-02-8, biological studies 91-20-3, biological studies 91-57-6 91-59-8 91-64-5 95-48-7, biological studies 95-65-8 95-78-3 95-87-4 96-17-3 98-00-0 98-82-8 98-86-2, biological studies 56-55-3 57-55-6, 60-12-8 62-53-3, 64-18-6, 65-85-0, biological studies studies 71-43-2, 78-81-9 78-94-4, 84-66-2 B6-53-3 87--66-1 90-05-1 91--_-5, 93-04-9 95-5.3-4 , 97-51-0 98-92-0 78-82-0 biological 84-74-2 86-74-8 83-05-1 90-12-0 biological 93-18-5 biological 97-54-1 99-49-0 99-93-4 100-21-0, biological studies 100-41-4, bioloqical studies 100-42-5, biological studies 100-46-9, biological studies 100-47-0, biological studies 100-51-6, biological studies 100-52- 7, biological studies 10t:)-,°,4-9 100-66-3, bioloQical studies 101-84-8 103-41--' 10.=-65-1 ~ 104-55-2 104-85-8 1+'!4-97-i i 106-21-B 106-24-1 106-42-.?, M biological studies 106-49-c_, biological studies 107-11-9 studies 107-87-9 1i8-i5-4, biological studies 108-:_9-4, biological studies 103-50-9 108-67-6, bioloqi_al 108-88-3, biological studies ~ ~ Go W 108-94-1, biological studies 108-95-2, biological studies 109-00- _ 109-06-B 109-08-0 109-73-9, biological studies 109-74-o 109-96-6 109-97-7 109--99-9, biological studies 119-0<.-9 110-00-9D, derivs. 110-02-1 110-02-1D, derivs. 110-59-B 110-62-3 110-83-8, biological studies 110-86-1, biological 4

studies 110-89-4, biological studies 110-93-0 111-26-2 111-27-3, biological studies 111-61-5 111-71-7 111-87-5, biological studies 112-05-0 112-30-1 112-31-2 112-44-7 112-54-9 114-33-0 116-26-7 117-84-0 119-64-2 120-12-7, biological studies 120-14-9 120-51-4 120-72-9, biological studies 120-80-9, biological studies 120-92-3 121-33-5 121-71-1 122-39-4, biological studies 122-78-1 123-07-9 123-08-0 123-11-5, biological studies 123-15-9 123-31-9, biological studies 123-38-6, biological studies 123-72-8 123-75-1, biological studies 124-07-2, biological studies 124-12- 9 124-13-0 124-19-6 126-98-7 127-91-3 128-37-0, biological studies 129-00-0, biological studies 131-16-8 132-64-9 134-32-7 135-19-3, biological studies 138-86-3 139-85-5 140-11-4 140-29-4 141-10-6 142-62-1, biological studies 143-08-8 150-19-6 150-76-5 191-07-1 198-55-0 206-44-0 208-96-8 213-46-7 218-01-9 244-63-3 271-89-6 275-51-4 290-37-9 334-48-5 367-47-5 431-03-8 432-25-7 486-25-9 486-56-6 486-84-0 487-19-4 487-68-3 487-89-8 488-17-5 490-79-9 492-27-3 494-52-0 494-97-3 495-40-9 496-11-7 496-72-0 496-78-6 499-74-1 500-22-1 505-57-7 526-75-0 527-60-6 529-19-1 529-20-4 530-57-4 536-74-.3 536-78-7 571-58-4 576-26-1 578-54-1 582-24-1 569--16-2 591-22-0 592-43-8 592-46-1 60)-14-6 603-76-9 613-46-7 614-96-0 620-02-0 620-17-7 620-22-4 620-23-5 621-B2-9, biological studies 623-36-9 625-30-9 625-33-2 (toxicity of, of tobacco smoke, cfytotoxicity prediction from in vitro tests in relation to) IT 625-86-5 628- 73-9 629-08-3 629 -76-5 630-19-3 634-36-6 645-59-0 697- 82-5 698-71-5 771 -51-7 B14-78-8 823-40-5 874-63-5 875- 30-9 875-79-6 928 -68-7 930-68-7 933-67-5 1002-84-2 100 4-66-6 1007-32-5 1196-79-8 1462-64-6 1490-04-6 1570-48-5 1604-28-0 1971-46-6 2016-57-1 2138-48-9 2305-21-7 240 8-37-9 2571-52-0 3189-12-6 4028-66-4 4170-30-3 4360-47-8 4427-56-9 4602-84-0 5724-56-1 5779-94-2 6575-13-9 8000-41-7 8013-90-9 10299-63-5 13730-09-1 15764-1 6-6 15877-57-3 20469-61-8 21296-92-4 21789-36-6 22072-.35-1 22884-95-'3 25309-65-3 27505-78-8 34136-57-7 34136-59-9 B0466-34-B (toxicity of, of tobacco smoke, cytotoxicity prediction trom in vitro tests in relation to) U

ANSWER 3 AN CA102(23):199085j TI Hypolipidemic effect of propane-1,2-diol on the morphology of rat erythrocytes AU CS LO SO Ahluwalia, Pushpa; Amma, M. IG. P. Biochem. Dep., Panjab Univ. Chandigarh, India Res. Bull. Paniab Univ., Sci., 35(3-4), 57-9 SC DT CO I S 4-3 (Toxicology) J RBJUAT 0555-7631 PY 1984 LA Eng AB In rats given 284 mu.L of propane-l,2-diol C57-55-6] in water for 30 days, the levels of total lipids, cholesterol C57-88-57, and phospholipids of erythrocyte membranes were significantly decreased. The cells maintained a normal shape but were spurred. Their outer membrane appeared under the electron microscope as very rough, having crenations and deformations. Apparently, alterations in the compn. of the membrane lipids changes the cellular morphol. which is very essential for the normal metabolic function of erythrocytes. KW propanediol toxicity erythrocyte; membrane erythrocyte lipid propanediol IT Phospholipids Lipids, biological studies (of erythrocyte membrane, propanediol effect on, cellular morphol. in relation to) IT Cell membrane (of erythrocyte, lipids of, propanediol effect on, cellular morphol. in relation to) IT Erythrocyte (propanediol toxicity to, membrane lipids in relation to) IT 57-88-5, biological studies (of erythrocyte membrane, propanediol effect on, cellular morphol. in relation to) IT 57-55-6, biological studies (toxicity of, to erythrocyte, membrane lipids in relation to) U- 6

ANSWER 4 AN CA102(3):19302w TI Developmental toxicity and structure/activity correlates of glycols and glycol ethers AU Johnson, E. Marshall; Gabel, Bradley E. C.; Larson, John CS Daniel Baugh Inst., Jefferson Med. Coll. LO SO SC DT CO Philadelphia, F'A 19107, USA EHP, Environ. Health Perspect., 57, 135-9 4-6 (Toxicology) J EVHPAZ IS 0091-6765 PY 1984 ' LA Eng AB Of 14 glycols and glycol ethers tested for embryo and adult toxicity in Hydra attenata, diethylene glycol C111-46-61, ethylene glycol monomethyl ether monoacetate C11U-49-6], ethylene glycol monoethyl ether monoacetate C111-15-9], and ethylene glycol diacetate C111-55-7] were equally toxic to adults and embryos (the individual compds. had differing toxicities). Ethylene glycol C1q7-21-1] had the greatest embryotoxicity relative to adult toxicity. No obvious structure-activity relations between these compds. and developmental toxicity were obsd. in this test system. KW development toxicity glycol ether Hydra IT 6lycols, biological studies (developmental toxicity of, in Hydra attenata assay, structure in relation to) IT Senescence and Senility (glycol ethers and glycols toxicity in relation to, in Hydra attenata assay) IT Hydra attenuata (glycol ethers and glycols toxicity to, development in relation to ) IT Embryo (glycol ethers and glycols toxicity to, in Hydra attenata assay) IT Toxicity (of glycol ethers and glycols, in Hydra attenata assay, development in relation to) IT Molecular structure-biological activity relationship (toxic, of glycol ethers and glycols, in Hydra attenata assay, development in relation to) IT 57-55-6, biological studies 107-21-1, biological studies 107-41-5 109-86-4 110-49-6 110-80-5 111-15-9 111-46-6, biological studies 111-55-7 111-76-2 111-77-3 111-90-0 112-73-2 1 2.^-99-6 (developmental toxicity of, in Hydra attenata assay, structure in relation to) 7

ANSWER 5 AN TI AU CS LO SO SC DT CO CA102(3):19045q Ethylene glycol monomethyl ether and propylene glycol monomethyl ether: metabolism, disposition, and subchronic inhalation toxicity t di s u es Miller, Roland R.; Hermann, Emile A.; Young, John T.; Landry, Timothy D.; Calhoun, Linda L. Toxicol. Res. Lab., Dow Chem. U.S.A. Midland, MI 48640, USA EHP, Environ. Health Perspect., 57, 33-9 4-3 (Toxicology) J EVHPAZ IS 0091-6765 PY 1984 LA Eng AB Short-term and subchronic vapor inhalation studies in rats and rabbits showed that there are pronounced differences in the toxicol. properties of ethylene glycol monomethyl ether (EGME) C109-86-4] and propylene glycol monomethyl ether (PGME) C1320-67-8]. 0verexpnsure to EGME resulted in adverse effects on testes, bone marrow and lymphoid tissues in lab. animals. PGME does not affect these tissues, and instead, overe;;posure to PGME was assocd. with increases in liver wt. and central nervous system depression. EGME is primarily oxidized to methoxyacetic acid C625-45-6] in male rats, whereas PGME apparently undergoes O--demethylation to propylene glycol C57-55-6]. Since methoxyacetic acid has been shown to have the same spectrum of toxicity as EGME in male rats, the obsd. differences in the toxicol. properties of EGME and PGME are thought to be due to the fact that the 2 materials are biotransformed via different routes to different types of inetabolites. K:W ethylene glycol monomethyl ether toxicity; propylene glycol monomethyl ether metab; ether ethylene propylene glycol toxicity IT 625-45-6 (as ethylene glycol relation to) monomethyl ether metabolite, toxicity in IT 57-55-6, biological studies (as propylene glycol monomethyl ether relation to) I T 109-86-4 1.;2-0--67-8 (metab. and toxicity of) metabolite, toxicity in 8

ANSWER 6 G AN CA101(23):209264n TI Primary mutagenicity screening of food additives currently used in Japan AU Ishidate, M., Jr.; Sofuni, T.; Yoshil:awa, K.; Hayashi, M.; Nohmi, T.; CS LO SO SC SX DT Sawada, M.; Matsuoka, A. Biol. Saf. Res. Cent., Natl. Inst. Hyg. Sci. Tokyo 158, Japan Food Chem. Toxicol., 22(8), 623-36 17-5 (Food and Feed Chemistry) 4 J CO FCTOD7 - IS 0278-6915 PY 1984 LA Eng AB Salmonella/Microsome tests (Ames tests) and chromosomal aberration tests in vitro using a Chinese hamster fibroblast cell line were carried out on 190 synthetic food additives and 52 food additives derived from natural sources, all of which are currently used in Japan. Fourteen out of 200 tested in the Ames assay showed pos. effects and 54 out of 242 were pos. in the chromosome test. Three additives (erythorbic acid C89-65-67, C102, and beet red) were pos. only in the Ames test, although their mutagenic potentials were relatively weak, while 43 additives were pos. only in the chromosome test. Eleven additives, Ca(OC1)2, cinnamic aldehyde C104-55-2], L-cysteine.HC1 C52-89-1], Food Green No. 3 (Fast Green FCF) C2353-45-97, H202, KBrO3, NaC102, NaOC1, NaN02, cacao pigment, and caramel, were pos. in both the Ames test and the chromosome test. The usefulness of such primary screening tests combining 2 different genetic end-points, gene mutation and chromosomal aberration, and some correlation between mutagenicity and carcinogenicity of food additives are discussed. k::W mutagenicity food additive screening IT Food (additives, mutagenicity screening of) IT Oils (cinnamon bark, mutagenicity screening of) IT Oils (clove, mutagenicity screening of) IT Oils (coriander, mutagenicity screening of) IT Oils (cumin, mutagenicity screening of) IT Resin acids and Rosin acids GO (esters, food additives contg., mutagenicity screening o;) QO IT Apple M (ext., food additive, m!itagenicity screening of) W IT Coffee GO Cola (genus) N (ext., mutagenicity screening of) QD GO IT Anise 9