Document N2d3km1edNNxLa1Q3724QJD3w
im m
1 GGB 3/15/94
BENEFITS OF UPDATING INTER-INDUSTRY STUDY OF VINYL CHLORIDE WORKERS
Product Stewardship - Demonstrates to workers, community residents, customers, and other audiences our collective commitment to characterize cancer risks associated with employment in VCM/PVC processes.
Scientific Knowledge - Refines the estimate of the number of cases of human angiosarcoma of the liver (ASL) associated with operating VCM/PVC plants in the pre-1972 era in North America. - Provides basis for refining human cancer risk assessments which are used by government agencies for permitting facilities, etc. - Contributes ASL cases to the international registry. - Helps to resolve unanswered questions about alleged links to cancers of the brain, lung, and hematopoeitic system as well as address non cancer causes of death such as emphysema.
Litigation Defense - VCM/PVC manufacturers continue to face toxic tort litigation alleging that numerous other types (non-ASL) of cancer are related to VCM/PVC employment. This type of research is useful in defending such litigation.
GGB 3/15/94
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BENEFITS OF UPDATING INTER-INDUSTRY STUDY OF VINYL CHLORIDE WORKERS
(cont.) Chlorine Issue
- VCM/PVC continue to be a part of the general debate on health and environmental impacts of chlorinated organics. This type of research serves a valuable role in helping to debate the issues on the basis of good science.
GGB 3/15/94
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m i m o s a <nfa
CHEMICAL MANUFACTURERS ASSOCIATION Vinyl Chloride Panel
Vinyl Chloride Research Coordinators Tentative Agenda
DATE: TIME: PLACE:
May 19, 1994
10:00 a.m. - 3:00 p.m., EDT
CMA Offices 2501 M Street, NW Washington, D.C.
1.0 Approval of February 14, 1994 Record of Meeting
2.0 Discussion of Scope of Work of the Epidemiology Study
3.0 Discussion of Potential Contractors for the Epidemiology Study
4.0 Discussion of Cost Sharing Formula for the Epidemiology Study
5.0
Presentation by Richard Reitz on Predicting Cancer Risk from Vinyl Chloride Exposure with a Physiologically-Based Pharmacokinetic Model - TENTATIVE
6.0 Discussion of Course of Action with EPA on Vinyl Chloride Risk Assessment
7.0 Discussion of ATSDR Research Data Needs for Vinyl Chloride
8.0 Discussion of Course of Action with ATSDR on Its Priority Data Needs
9.0 Financial Statement
10.0 Schedule Date for Next Meeting or Conference Call
Subject to Approval
Hasmukh C. Shah, Ph.D. Manager, Vinyl Chloride Panel
ANTITRUST CHECKLIST FOR CMA MEETINGS
o
This antitrust checklist is for use by CMA staff and member representatives in die conduct of CMA-sponsored meetings, =ftoaibitcd discussion topics apply equally to social gatherings incidental to CMA-sponsored meetings. The Checklist is ndgexhaustive and does not address antitrust issues relating to activities ocher than CMA meetings. Participants in CMA meeting&aiso should be thoroughly familiar with: (1) "Antitrust Guide for OdA Committee Members" and, (2) "General Principles Applica ble to die Structure and Operations of Committees." Both of these documents may be found in the CMA Directory. ^
DO
Ensure said performance In areas of:
OVERSIGHTYSUPERVISION.
Have a CMA. staff representative at each CMA-sponsored meet ing (unless an exception has been authorized by the appro priate CMA vice-president);
ccnsu/r with an anomey ofthe CMA Office ofGenera/ Counsel on aS amicus questions relating to CMA-sponsored meetfogs;
limit meeting discussions to agenda topics (unless additional topics have been approved by the appropriate CMA staff rep resentative), and
provide each member company representative and Q*1A staff representative attending a CMA-sponsored meeting with a copy of this checklist, and have a copy available lot reference at aD CMA-sponsored meetings.
RECORDKEEPING:
Have an agenda and minutes which accurately reflect the mai lers which occur:
provide agendas and minutes to the CMA Office of General Counsel for review and approval in advance of distribution; and.
futh' describe the purposes and authorities of all task groups, work groups, ad hoc or other standing committee subgroups in the minutes of the appropriate parent committee.
VIGILANCE:
Protest against any discussion or meeting activities which ap pear to violate this checklist: disassociate yourself from any auch discussion or activities and leave any meeting in which they continue.
Revised 3'0O (single page version) Reformated 1 '89 MDB
DON'T
Do not, in factor appearance, discuss or exchange infor mation on:
PRICES, XNCUJDKNGi
Individual company prices, price changes, price differentials, markups, discounts, allowances, credit terms, etc.:
todividual company data on costs, production, capacity*, inventories, sales, etc* and.
industry pricing policies, price levels, price changes, differen tials, me.
PRODUCTION, INCLUDING}
Plans ofindividual companies concerning the design, produc tion, distribution or marketing of particular products, includ ing proposed territories or customers: and.
changes in indussy production, capacity or inventories.
TRANSPORTATION RATES:
Rates or rate policies for individual shipments, including bas ing point systems, zone prices, freight equalization, etc.
MARKET PROCEDURES, INCLUDING?
Company bids on contracts for particular products: company procedures for responding to bid invitations: and.
matters relating to actual or potential individual suppliers or customers that might have the effect of excluding them from any market or influencing the business conduct of firms to ward them.
CONSENT DECREE SUBSTANCE:
Any matter relating to trisodiuffl phosphate (a restriction re quired by a 1962 consent decree to which CMA is a party).
VRD 0B02&27469
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CHEMICAL MANUFACTURERS ASSOCIATION
A
April 15, 1994
Dear Vinyl Chloride Research Coordinators:
The next VCRC meeting is scheduled for May 19, 1994. The agenda for the meeting is enclosed. Also enclosed are: 1) a draft scope of work for an update of the mortality among vinyl chloride workers; 2) an historical perspective on inter-industry vinyl chloride study; and, 3) the benefits of updating the inter-industry study of vinyl chloride workers. Please review these documents in conjunction with Dr. Richard Reitz's abstract on physiologically-based pharmacokinetics model for vinyl chloride and the ATSDR Federal Register notice on vinyl chloride research data needs that were sent to you with my March 30 letter.
I am looking forward to seeing you on May 19.
Sincerely,
Enclosures
Hasmukh C. Shah, Ph.D. Manager, Vinyl Chloride Panel
2501 M Street, NW, Washington, DC 20037 Telephone 202-887-1100 Fax 202-887-1237
Responsible Care * 11 APuofcCommftment
HISTORICAL PERSPECTIVE ON INTER-INDUSTRY VINYL CHLORIDE STUDY
1960- 1963
Report published documenting anesthetic effects in animals and humans and liver injuiy in animals from chronic exposure.
1967
Acroosteolysis reported in humans exposed to high levels of VCM.
1971
Carcinogenicity of VCM discovered in animals, including angiosarcoma of the liver.
1973
CMA sponsors Tabershaw-Cooper Associates to conduct an epidemiologic study of 8,384 vinyl chloride workers from 34 plants.
1974
First reports of angiosarcoma of the liver cases in VCM workers.
1974
Tabershaw-Cooper report preliminary results confirming high risk of angiosarcoma of the liver and suggesting excess cancers of respiratory system, brain and lymphoma.
GGB 3/15/94
HISTORICAL PERSPECTIVE ON INTERINDUSTRY VINYL CHLORIDE STUDY
(cont.)
1974
OSHA holds hearings and revises PEL down to 1 ppm.
1981
Cooper expands original epidemiology study to include 10,173 workers from 37 plants-- reports show angiosarcoma and brain cancer to be in excess through 1972.
1986
EHA updates inter-industiy study with follow-up through 1982reports angiosarcoma, brain cancer and emphysema to be in excess--no excess respiratory cancer or lymphoma/ leukemia.
1991
EHA study is published.
1993
CMA letter to the editor and EHA response are published clarifying the brain cancer and emphysema findings.
1994
GGB 3/15/94
CMA Vinyl Chloride Research Coordinators meet to discuss updating study.
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DIALOG File 159: CANCERLIT(R)_1963-1994/Apr (c) format only 1994 Enzyme No.: EC 2.4.2.8 .(Hypoxanthlne Phosphor 1bosyltransfer
ase) Gene Symbol: hprt
Di slog Info.Svcs.
01080252
94142774
MEDL/94142774
Evaluation of the yeast DEL assay with 10 compounds
by the International Program on Chemical Safety
evaluation of short-term'tests for carcinogens. Carls N; Schlestl'Rtf
selected for the
01080254
94142776
MEDL/94142776
Detection of 1,2,4-benzenetrlol induced aneuploldy and
microtubule disruption by fluorescence in situ hybridization
and immunocytochemistry.
Zhang L; Venkatesh P; Creek ML; Smith MT
Department of Molecular and School of Public Health, Boston,
Mutat Res; 320(4):293-303 1994 Journal Code: NNA
Languages: ENGLISH
Cellular Toxicology, MA 02115.
ISSN 0165-1110
Harvard
Department of Biomedical and Environmental Health Sciences, School of Public Health, University of California, Berkeley 94720.
Mutat Res; 320(4):315-27 1994 ISSN 0165-1110 Journal Code: NNA
Document Type: JOURNAL ARTICLE
Journal Announcement: 9404
Subfile:
L; M
The Saccharomyces cerevlslae DEL
variety of nonmutagenlc carcinogens
assay detects (Schtestl et al.
wide (1989)
Contract/Grant No.: P42-ES04705, ES, NIEHS; P30-ES01896, ES.
NIEHS
Languages: ENGLISH
Document Type: JOURNAL ARTICLE
Journal Announcement: 9404
Subfile;
L; M
Fluorescence
In situ hybridization (FISH) Is becoming
Increasingly used to detect chromosomal changes In cancer
cytogenetics. Here, we report Its use In human HL60 cells to
Carcinogenesis, IQ, 1445-1455). This study shows the effect on
DEL recombination of 8 carcinogenic compounds (o-to 1u1dine,
hexamethy1phosphoram1de,
saf role,
aery1 on11 r11e. benzene,
d1ethy1hexy1phtha1 ate, phenobarb1tal and d1ethy1st11bestrol)
and 2 noncarclnogenlc compounds (caprolactam and benzoin).
These chemicals have been selected by the Program on Chemical
Safety for the evaluation of short-term tests for carcinogens,
because sufficient carcinogenicity data for these compounds
exist, and because they are difficult to detect with the
detect aneuploldy Induced by the benzene metabolite.
Salmonella assay. 5 of 8 carcinogens reproduclbly gave a
1.2,4-benzenetrlol (BT). Human centromerlc probes specific for chromosomes 9 and 7 were used. Untreated HL60 cells were 0.72
strong positive response and the noncarcinogen benzoin was negative. Thus, 60% of the chemicals tested In this study have
+/- 0.29% hyperdiploid for chromosome 9. Treatment,w1th 5 mlcroM BT Increased this level 3-fold to 2.20 +/- 0.87% and 50 mlcroM Increased It 4-fold to 2.96 +/- 0.74%. Similar results were obtained with the chromosome 7 probe. The Induction of aneuploldy by BT Is therefore not chromosome-spec 1f1c nor is
been correctly Identified with the DEL assay compared to only 20% with the Salmonella assay.
Tags: Support, U.S. Gov't, Non-P.H.S. Major Descriptors: *Carc1nogens--Tox1c1ty--TO: *Mutagen1c1ty Tests--Methods--MT; *Saccharomyces cerev1s1ae--Drug Effects
It artlfactual. Immunocytochemfcal staining with anti-tubulin
antibodies
also
showed
that
BT disrupted microtubule
- -DE Minor
Descriptors:
Aery 1 on 1tr11e--Toxic1ty--TO; Benzene
organization at these concentrations. Thus, mitotic spindle disruption probably plays an Important role In BT-Induced
--Toxicity --TO: --Tox1c1ty --TO;
Chromosome Deletion; Diethylhexyl Phthalate
lethy1sti1bestrol--Tox1c1ty--TO;
Hempa
aneuploidy. Trisomy and not tetrasomy accounted for the majority of the hyperdlploldy Induced by BT In the two C-group chromosomes 7 and 9. Since trisomy of C-group chromosomes Is commonly observed In leukemia, BT-induced aneuploldy may be
--Toxicity --TO;
Phenobarb1ta1 --Tox1c1ty--TO;
Saccharomyces
cerev1s1ae --Genet 1cs--GE;
Safrole--Toxic1ty--TO; Toluldlnes
--Toxicity --TO
CAS Reg istry No.: 0
.(Carcinogens); 0
.(Tolu1dines);
Involved in benzene-induced leukemia.
107-13-1 .(Aery1onltr11e); 117-81-7 .(Diethylhexyl Phthalate)
Tags: Human; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
Major Descriptors: *Aneuplo1dy: ^Chromosomes, Human, Pair 7; Chromosomes, Human, Pair 9; *Hydroqu1nones--ToxIc1ty--TO; *M1crotubules--Drug Effects--DE
; 50-06-6 680-31-9 95-53-4
.(Phenobarbltal); .(Hempa); 71-43-2 (2-toluldlne)
56-53-1
.(Diethylstllbestrol );
.(Benzene); 94-59-7 .(Safrole);
Minor
Descriptors:
Chromosome
Aberrations; Colchicine
--Toxlclty--T0; Immunohistochemlstry; In Situ Hybridization,
01079808 94140140 MEDL/94140140 [Genetic effects of lead*, nitrate on seeds of chronically
Fluorescence;
Leukemia,
Myelocytic,
Acute--Genet1cs--G;
irradiated populations of Arabidopsis thalfana]
Leukemia, . Myelocytic, Acute--Pathology--PA; Tumor Cells,
Genet 1cheskle posledstvllu delstvlla nltrata svlntsa na
Cultured
CAS
Registry
No.:
O
.(Hydroqu1 nones);
533-73-3
semena khronicheskl thalIana.
obluchaemykh populiatsll Arabidopsis
.(hydroxyhydroqu1 none); 64-86-8 .(Colchicine)
Dlneva SB; Abramov VI; Shevchenko VA
Genetlka; 29(11):1914-20 1993 ISSN 0016-6758 Journal Code: FNN
001459
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DIALOG File 159: CANCERLIT(R)_1963-1994/Apr (c) format only 1994
Tags: Humar^
Major
Descriptors:
`Breast
Neoplasms--Chem1stry--CH;
`Proto-Oncogene Prote1ns--Analys1s--AN; `Receptors, Epidermal
Growth Factor-Urogastrone--Analys1s--AN
Minor Descriptors: Breast Neoplasms--Et1o1ogy--ET; Breast
Neoplasms--Metabol1sm--ME: Prognosis; Proto-Oncogene Proteins
--MetabolIsm--ME;
Proto-Oncogene Prote1 ns--Physlology--PH;
Receptors, Epidermal Growth Factor-Urogastrone--Metabol1sm--ME
; Receptors. Epidermal Growth Factor-Urogastrone-`Phys1ology
- - PH
CAS Registry No.: Inase); 0 .(proto-oncogene protein erbB-2)
;O
. (Proto-Oncogene Proteins); 0 .(Receptors, Epidermal
Growth Factor-Urogastrone)
Enzyme No.: EC 2.7.1.- .(Epidermal Growth Factor Receptor
Protein-Tyrosine K
Gene Symbol: EGFR; neu
01077006
94126838
MEDL/94126838
Carcinogenicity of TCDD In laboratory animals: Implications
for risk assessment. (177 Refs)
Lucler G; Clark G; Hlermath C; Tritscher A; Sewall C; Huff J
Laboratory
of
Biochemical
Risk Analysis. N.I.E.H.S.,
Research Triangle Park, NC 27709.
Toxicol Ind Health; 9(4):631-68 1993 ISSN 0748-2337
Journal Code: VWS
Languages: ENGLISH
Document Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
Journal Announcement: 9404
Subfile:
L; M
Tags: Animal; Female; Human; Male
Major Descriptors: *Tetrachlorod1benzod1ox1n--Tox1clty--T0
Minor Descriptors: Biological Assay; Carclnogenlclty Tests;
Hamsters; Mice; Rats; Risk Factors
CAS Registry No.: 1746-01-6 .(Tetrachlorodlbenzodloxln)
01077005
94126837
MEDL/94126837
Effects of acute and subchronic exposure of topically
applied fullerene extracts on the mouse skin.
Nelson MA; Domann FE; Bowden GT; Hooser SB; Fernando 0;
Carter DE
Pathology Department, University of Arizona, Tucson 85724.
Toxicol Ind Health; 9(4):623-30 1993 ISSN 0748-2337
Journal Code: VWS
Contract/Grant No.: ES05533-02. ES. NIEHS; CA-40584, CA. NCI
Languages: ENGLISH
Document Type: JOURNAL ARTICLE
Journal Announcement> 9404
Subfile:
L; M
The recent discovery that fullerenes (C60) can be produced
in macroscopic quantities has sparked much Interest in the
chemistry of this unusual molecule. Concerns have also arisen
about the potential carcinogenic effects of this molecule. We
have addressed the potential acute and subchronic toxic
effec'
of fullerenes applied in benzene on the mouse skin.
The
e toxic effects measured In this study Included
001464
lalog Info.Svcs.
epidermal
DNA synthesis and the Induction of ornithine
decarboxylase activity in the epidermis. At the topical dose
of fullerenes used In.(these studies (l.e., 200 micrograms), we found no effect''"'in 'either DNA synthesis or ornithine
decarboxylase activity over a 72 hour time course after
treatment. The subchronic effects of the fullerenes as a mouse skin tumor promoter was assessed by repeatedly applying the
chemical to the skin after Initiation with the polycyclic
aromatic
hydrocarbon,
7,12-dimethyl benzanthracene (DMBA).
Repeated administration of the fullerenes for up to 24 weeks
post-in11lat1 on did not result In either benign or malignant
skin tumor formation, whereas promotion with the phorbol
ester, 12-0-tetradecanoyl-phorbol- 13-acetate (TPA) resulted in the formation of benign skin tumors. Our data Indicate that fullerenes applied in benzene at a likely industrial exposure
level do not cause acute toxic effects on the mouse skin
epidermis.
Tags: Animal; Female; Support. U.S. Gov't, P.H.S.
Major
Descriptors:
`Carbon--Tox1c1ty--TO;
`Skin --Drug
Effect5--DE
Minor
Descriptors:
Administration,
Cutaneous;
Carbon
--Administration and Dosage--AD; Carbon--Pharmacok1net1cs--PK
; Carcinogenicity Tests; DNA--Biosynthes1s--BI;
DNA--Drug
Effects--DE; Enzyme Induct ion--Drug Effects--DE; Hyperplasia
--Chemically
Induced--CI;
Mice;
Ornithine Decarboxylase
--B1osynthesis--BI; Ornithine Decarboxylase--Drug Effects--DE
; Skin Neoplasms--Chem1cal1y Induced--CI; Time Factors;
9,10-D1methyl - 1,2-benzanthracene CAS Registry No.: 115383-22-7
.(fullerene C70); 57-97-6
.(9,10-Dimethy 1-1,2-benzanthracene);
7440-44-0
.(Carbon);
9007-49-2 .(DNA); 99685-96-8 .(fullerene C60)
Enzyme No.: EC 4.1.1,17 .(Ornithine Decarboxylase)
01076864
94126081
MEDL/94126081
Review of the genotoxicity of nitrogen oxides.
Vlctorln K
Institute of Environmental Medicine, Karolinska Institutet,
Stockholm, Sweden.
Mutat Res; 317(1):43-55 1994 ISSN 0165-1110
Journal Code: NNA
Languages: ENGLISH
Document Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
Journal Announcement: 9404
Subfile:
L; M
Nitrogen oxides (NOx) are formed in combustion processes and
are major pollutants in urban air. Relatively few studies on
the genotoxlclty of N02 and NO have been performed. These
studies Indicate that N02 Is genotoxlc in vitro, but the
effect of NO seems to be very slight. One In vivo study showed chromosome aberrations and 'mutations In lung cells after
Inhalation of N02 (and NO), but tests for chromosome
aberrations in lymphocytes and spermatocytes or micronuclei in
bone marrow were negative after Inhalation of N02. Based on
present studies, there Is no clear evidence of a carcinogenic
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DIALOG File 40: Envlrol1ne(R)_1970-1993/Jan (c) 1994 ClSr Inc. Information Service.)
SPECIAL FEATURES: 5 graph(s); 14 reference(s); 1 table(s)
MAJOR DESCRIPTORS:
CRUSTACEANS; BIOLOGICAL INDICATORS. WATER
; AGE COMPARISONS; DIAZINON; SURFACTANTS; COPPER; CADMIUM;
ZINC; SEDIMENT;
REVIEW CLASSIFICATION: 02
00255504
ENVIROLINE NUMBER: 94-00829
Effects of Contaminants from Chromated Copper Arsenate-Treated
Lumber on Benthos
Weis. J. S.. (Rutgers University, Newark, NJ); Weis, P.,
(University of Medicine and Dentistry of New Jersey,
Newark)
JOURNAL: Arch Environ Contam Toxicol v26, nl, p103(7)
PUBLICATION DATE: Jan 94
DOCUMENT TYPE: research article
LANGUAGE: English
ABSTRACT: Toxic chemicals are known to leach from chromated copper arsenate (CCA) -treated bulkheads and adsorb onto fine-grained sediment. Sediment samples were collected In the vicinity of two CCA-treated bulkheads In Florida, and the effects of Cu. chromium, and arsenic at varying distances were Investigated on benthic community structure and sediment toxicity. Except for Cu, concentrations of the contaminants were highest Immediately adjacent to each bulkhead, and they decreased with distance. Copper and As concentrations were elevated In Neanthes succlnea found nearest the CCA-treated wood. In worms living at 1, 3, and 10 m from the bulkheads, Cu and As concentrations decreased with distance. Mortality of amphipods was highest In sediment collected nearest the bulkheads. Species diversity was reduced significantly nearest the bulkheads 'compared to controls. While the contamination was very localized, the high numbers of CCA-treated bulkheads in coastal waters makes the contamination problem significant. (Full text available from Congressional Information Service.)
SPECIAL FEATURES: 8 graph(s); 1 map(s); 23 reference(s); 1
table(s)
MAJOR DESCRIPTORS:
SEDIMENT; COPPER; ARSENIC; CHROMIUM;
BENTHIC COMMUNITIES; BIOACCUMULATION, ANIMAL;
REVIEW CLASSIFICATION: 02
00255494
ENVIROLINE NUMBER: 94-00819
Congener-Specific Analysis of Polychlorinated Biphenyls
White-Tailed Sea Eagles Hallaeetus albicllla Collected
Poland
Falandysz, J.. University of Gdansk, Poland; Yamashlta, N.;
Tanabe, S-; Tatsukawa, R.; Rucinska, L.; Mlzera, T.;
Jakuczun, B.
JOURNAL: Arch Environ Contam Toxicol v26, nl, p13(l0)
PUBLICATION DATE: Jan 94
DOCUMENT TYPE: research article
LANGUAGE: English
In In
ABSTRACT: PCB congeners were determined In white-tailed sea
000701
eagles collected In Poland over the period 1982-90. All samples were analyzed-by gas chromatography/mass spectrometry. In breast muscles, the most persistent PCBs were found to be the congeners 153, 13^^ .180 118, 187, 99, and an unidentified congener. The extremely high PCB congener concentrat1ons in the sea eagles collected from the Baltic coast appeared to be related to relatively high contamination levels in animals of the lower food chain In the area. Apart from PCBs, the sea eagles were also probably highly contaminated with other persistent organochlorlnes, including highly toxic dioxins and furans, as well as dleldrln. The dioxin toxic equivalents of the coplanar PCBs are presented. The high PCB concentrations found In females were correlated with the high contamination of eggs, and may be associated with eggshell thinning and the low reproduction success of these birds. (Full text available from Congressional Information Service.)
SPECIAL FEATURES: 14 graph(s); 30 reference(s); 3 table(s)
MAJOR DESCRIPTORS:
POLAND; POLYCHLORINATED BIPHENYLS;
BIOACCUMULATION, BIRD; EAGLES;
REVIEW CLASSIFICATION: 02
00255477
ENVIROLINE NUMBER: 94-00802
Toxic Effects of Pollutants on the Mineralization of Acetate
in Methanogenic River Sediment
van Vlaardlngen, Peter L. A.; van Beelen, Patrick, National
Institute of Public Health and Environ Protection,
Bllthoven, Netherlands
JOURNAL: Bull Environ Contam Toxicol v52, nl, p46(8)
PUBLICATION DATE: Jan 94
DOCUMENT TYPE: research article
LANGUAGE: English
ABSTRACT: The sediments of the Rhine River, the Netherlands, are highly polluted with organic compounds and heavy metals. The organic matter Is converted to acetate by acetogenic bacteria. The mineralization of acetate under methanogenic conditions Is then performed by a few specialized methanogenic bacteria. Results are presented from a study on the effect of six toxicants on the anaerobic mineralization of acetate. The toxicants Include: benzene, chloroform, 1,2-d1ch1oroethane, pentachlorophenol, mercury, and zinc. Sediment microcosms were prepared using sediment samples from the Rhine River. Highest Inhibition of acetate mineralization was found for chloroform, 1.2-dlchloroethane, and pentachlorophenol. Benzene was the least toxic of the organic compounds for acetate mineralization. Even at their highest concentrations, Hg and Zn had no observable effects on the anaerobic acetate mineralization. (Full text available from Congressional Information Service.)
SPECIAL FEATURES: 3 graph(s); 22 reference(s); 3 table(s)
MAJOR DESCRIPTORS:
SEDIMENT; RHINE RIVER; BENZENE;
PENTACHLOROPHENOL; CHLOROFORM; MERCURY; ZINC; BACTERIA;
WATER POLLUTION EFFECTS;
(cont. next page)
DIALOG
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DIALOG File 40: Enviroline(R) 1970-1993/Jan (c) 1994 CIS. Inc.
SPECIAL FEATURES: 1 diagram(s7; 6 reference(s): S table(s)
MAJOR DESCRIPTORS:
FERTILIZERS. ORGANIC; SEWAGE APPLICATION.
LAND; HEAVY METALS; CADMIUM; COPPER; LEAD; BIOACCUMULATION,
PLANT;
REVIEW CLASSIFICATION: 02
00255264
ENVIROLINE NUMBER: 94-00525
Increased Risk of Proteinuria Among a Cohort of Lead-Exposed
Pregnant Women
Factor-L1tvak, Pam, Columbia School of Public Health, New
York, NY; Stein, Zena; Grazlano, Joseph
JOURNAL: Environ Health Perspec vIOI, n5, p418(4)
PUBLICATION DATE: Oct 93
DOCUMENT TYPE: research article
LANGUAGE: English
ABSTRACT: Exposure to environmental lead and pregnancy outcomes were studied In two Yugoslavian towns to determine risks of proteinuria. Blood lead levels were 17.1 and 5.1 (gr)rog/dl In a smelter town and nonexposed town, respectively. The adjusted odds ratio for proteinuria was 4.5, and for trace proteinuria was 2.3. These results support other studies that found an association between chronic exposure to lead and renal dysfunction manifested as proteinuria. (Full text available from Congressional Information Service.)
SPECIAL FEATURES: 2 graph(s); 41 reference(s); 4 table(s)
MAJOR DESCRIPTORS:
TOXICOLOGY; PREGNANCY; BLOOD LEAD LEVEL;
KIDNEY DISEASE; SYNERGISTIC EFFECTS;
REVIEW CLASSIFICATION: 02
00255240
ENVIROLINE NUMBER: 94-00499
Identification of 6-Hydroxy-trans,trans-2,4-hexadienoic Acid,
a Novel Ring-Opened Urinary Metabolite of Benzene
Kline, Stanley A., University of Medicine and Dentistry,
Plscataway, NJ; Robertson, J. Forbes; Grotz, V. Lee;
Goldstein, Bernard D.; Witz, Glsela
JOURNAL: Environ Health Perspec vIOI, n4, p310(3)
PUBLICATION DATE: Sep 93
DOCUMENT TYPE: research article
LANGUAGE: English
ABSTRACT: Research has shown that benzene toxicity arises from the formation of metabolites in the liver. One of these metabolites is the open-ringed intermediate trans,trans-muconlc acid (MA). One such compound has been Identified In the laboratory as the dialdehyde trans,trans-muconaldehyde (MU), which as been shown to be hematotoxlc when injected Into mice. Two of the endproducts of MUC are MA and 6-hydroxy-trans,trans-hexadlenolc acid (HH). Using CO-1 mice treated with MUC, the identification of HHA as a urinary metabolite of benzene Is confirmed, showing the Intermediacy of MUC In benzene metabolism. (Full text available from Congressional information Service.)
SPECIAL FEATURES: 3 dlagram(s); 14 reference(s); 2 table(s)
MAJOR DESCRIPTORS:
BENZENE; BIOLOGICAL INDICATORS; METABOLIC
000703
ACTIVATION; CHEMICAL ANALYSIS; BIOACCUMULATION, ANIMAL; REVIEW CLASSIFICATION: 02
00255071
ENVIROLINEWNUMBER: 94-00295
A Survey of Some Waste-to-Energy (W-E) Issues: Ash Residues and Mercury
Shaub, Walter A.
JOURNAL: Solid Waste Assoc of North Am 30th Annu Int Expo,
Orlando, FL p395(36)
PUBLICATION DATE: Aug 3-6. 92
DOCUMENT TYPE: conf paper
LANGUAGE: English
ABSTRACT: Waste-to-Energy (W-E) facilities are gaining in popularity among communities seeking to reduce landfill utilization while saving energy. A number of issues that must be considered when evaluating designs for W-E facilities are examined, Including the need to effectively manage ash and other residues, and the need to manage mercury compounds. The proposed techniques were developed for the express purpose of protecting the environment from undue Impacts. To prevent the buildup of contaminants In ashes and residues, It will probably be necessary to screen wastes being Introduced Into the combustors to weed out potentially dangerous Items, such as fluorescent lights and lead batteries. (Full text available from Congressional Information Service.)
MAJOR DESCRIPTORS:
SOLID WASTE ENERGY; ENV CONSTRAINTS,
SOLID WASTE ENERGY; INCINERATORS; TOXIC SUBSTANCES; MERCURY
; AIR POLLUTION CONTROL; EMISSION CONTROL PROGRAMS; ASH;
REVIEW CLASSIFICATION: 17
00254863
ENVIROLINE NUMBER: 94-00081
Monitoring Heavy Metals in the Gulf of Thailand Using Mussel
Watch Approach
Sukasem, Phaka; Tabucanon, Monthlp S., Environ Research and
Training Center, Bangkok, Thailand
JOURNAL: Scl Total Environ V139-140, p297(9) PUBLICATION DATE: Nov 1, 93
DOCUMENT TYPE: conf paper
LANGUAGE: English
ABSTRACT: Due to rapid Industrial development along the major
rivers In Thailand that drain Into the Gulf of Thailand,
marine water concentrations of zinc, manganese, copper,
chromium, nickel, and cadmium have Increased. Green mussels
Perna vlrldls were collected from ten locations along the gulf
coast and analyzed for concentrations of the toxic metals. All
mussel samples were analyzed by spectrophotometry. Differences
In metal concentrations In mussels from different areas were
relatively large for Zn, Mn, Cr, and Cd, but less for Cu and
N1. Highest metal concentrations were found in the regions
adjacent to river discharges. When compared to similar data
compiled In 1986. metal concentrations had remained relatively
unchanged, with the exception of Mn and N1. which had
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SPECIAL FEATURES: 6 graph(s); 1 map(s): 11 reference(s); 3
table(s)
MAJOR DESCRIPTORS:
THAILAND; MUSSELS; HEAVY METALS;
BIOACCUMULATION, ANIMAL; BIOLOGICAL INDICATORS, MARINE; REVIEW CLASSIFICATION: 02
00254860
ENVIROLINE NUMBER: 94-00078
Utilization of Vegetation Sample Bank as an Indicator of
Environmental State In the Areas of Industrial Pollution
Kovnatsky, Evgeny F.; Surnln, Valery A., Institute of
Experimental Meteorology, Obninsk, Russia
JOURNAL: Scl Total Environ V139-140, p271(7)
PUBLICATION DATE: Nov 1, 93 DOCUMENT TYPE: conf' paper
LANGUAGE: English
ABSTRACT: In the villages of Ust-Kamenogorsk and Glubokoje in Russia, poplar leaves were studied for their use as biological Indicators of industrial pollution. Circular zones were established around the Industrial town centers. Mult1-element analysis was used to separate the elements according to purely technogenic origin and those derived from soil dust. It was found that calcium, potassium, strontium, lead, Iron, and manganese were natural pollutants caused by transport and sedimentation of soil dust, which enters leaf surfaces through the root system. Zinc, Pb, copper, and arsenic were found to be technogenic elements, since their concentration decreased with distance from the Industrial center. Besides these toxic elements. It Is suggested that mercury, antimony, cobalt, and chromium be Included for chemical analysis In the leaves. Overall results indicated that poplar leaves are a good biological Indicator of Industrial pollution.
SPECIAL FEATURES: 2 reference(s); 3 table(s)
MAJOR DESCRIPTORS:
BIOLOGICAL INDICATORS, AIR;
BIOACCUMULATION. PLANT; METAL CONTAMINATION; .ELEMENTAL
ANALYSIS;
REVIEW CLASSIFICATION: 02
schemes are provided. Such toxicants should be considered priority compounds for use reduction, should be excluded from use as substitutes for other toxic chemicals, and should be phased out. Compensation for workers displaced by plant closings should be considered. Coordination of efforts among environmentalists, business, and government Is required. ( Full text available from Congressional Information Service.)
SPECIAL FEATURES: 11 reference(s); 2 table(s)
MAJOR DESCRIPTORS:
REPRODUCTION, HUMAN; CHEMICAL
CONTAMINATION; CHEMICAL REDUCTION; LEGISLATION,
LOCAL; POLICY-PLANNING, STATE AND LOCAL;
REVIEW CLASSIFICATION: 02
STATE
AND
00254805
ENVIROLINE NUMBER: 94-00023
Protecting. Reproductive Health and the
Reduction
Gelser, Kenneth, Unlv of Massachusetts
JOURNAL: Environ Health Perspec vIOI,
PUBLICATION DATE: JuT 93
DOCUMENT TYPE: conf paper
LANGUAGE:
Environment: Toxics Use
Lowel1 supplement 2, p221(5)
Engl 1sh
ABSTRACT: Several states have passed laws that mandate reductions In the use of toxic chemicals as a method of managing hazardous materials. Since some of the regulated compounds are reproductive and developmental toxicants, reductions In use should Improve pregnancy outcome. These Include lead, mercury, solvents, pesticides, ethylene oxide, PCBs, - * ethylene glycol ethers, for which use reduction
000704
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01075247
9412Q233
MEDL/94120233
[H2 antagonists as Inhibitors of cytochrome P-450 In rat
liver: In vitro and In vivo effects]
Antagonlstas H2, como Inhlbldores del cltocromo P-4SO en
hlgado de ratas: efecto In vitro e In vivo.
Carrasco M; Gaule C; Vega P; del Vlllar E
Servlclo de Medlclna Interna, Hospital Regional de Coplapo.
Rev Med Chi 1 : 120(5):539-44 1992 ISSN 0034-9887
Journal Code: SHD
Languages: SPANISH
Document Type: JOURNAL ARTICLE
English Abstract
Journal Announcement: 9403
Subfile:
L; M
The Allium anaphase-telophase- test was evaluated to find out If It could be recommended in the screening of wastewater for genotoxlclty. Five mUl?gen1c or carcinogenic chemicals usually
found In wastewater
anaphase-telophase
test.
were
tested
In
Sodium dichromate
the
Allium
(25 mlcroM),
benzene
(100 mlcroM), d1 chioromethane (175 mlcroM) and
1, 1, 1-trIchloromethane (175 mlcroM) Increased the frequency of
chromosome aberrations In the root cells, whereas formaldehyde (1 mM) was found to be non-mutagenlc In this test system.
Journal Announcement: 9403
Subfile:
L
Cytochrome
P-50
Is a well known participant In the
metabolism of xenoblotles as well as an activator or
Inactivator of hepatotoxlc substances and carcinogenic agents.
Other studies where chemicals were tested In the Allium test were reviewed. For 15 chemicals the results were compared with results from the Ames test, the Microscreen assay, and
carcinogenicity tests In rodents. The sensitivity of the Alll/jm test was calculated to be 82%. In conclusion the Allium
H2 antagonists, clmetldlne, famotidine and ranitidine were
used to Inhibit cytochrome P-450 in rat liver. After 200 mg
clmetldlne, 85% Inhibition of cytochrome P-450 In vitro and
50%
In vivo were demonstrated through demethyl at Ion of
test Is recommended for the screening of wastewater because It has a high sensitivity. Is cheap, rapid, easy to handle, and because It can be used on wastewater without pretreatment of the sample.
amlnopyrlne. Inhibition was further confirmed by differential
Major Descriptors: *A11 1um--Drug Effects--DE; *Industrial
absorption spectra (Type II). The percentage Inhibition
obtained with famotidine or ranitidine were lower than those
obtained
with clmetldlne. Inhibition of the microsomal
oxidative
system by clmetldlne could lead to decreased
production of superoxide radicals and protection against
damage induced by toxic agents activated In the liver.
Tags: Animal; Comparative Study; Male
Major
Descriptors:
*Cytochrome P-450 --Antagonists and
Inh1b1tors--AI;
*H1stamine H2 Receptor Blockaders
--Pharmacology--PD; *M1crosomes, LIver--Drug Effects--DE
Minor
Descriptors:
Administration,
Oral:
Amlnopyrlne
--MetabolIsm-nME;
B1otransformat1on--Drug
Effects--DE;
Waste--Adverse Effects--AE; *Mutagen1 clty Tests--Methods--MT;
Mutagens--Toxlclty--T0; *Water Pollutants. Chemical--Toxicity
--TO
Minor DescrIptors: All 1 urn--Genet 1cs--GE: Benzene--Toxiclty
--TO;
Chromates--Toxic1ty--T0;
Chromosome
Aberrations;
Formaldehyde--ToxId ty--T0; Genes, PI ant--Drug Effects--DE;
Methylene Chi or 1de--Tox1c1ty--TO; Tr1chloroethanes--Tox1c1ty
--TO
CAS Registry No.: 0 .(Chromates); 0 .(Industrial Waste); 0
.(Mutagens); 0
.(TrIchloroethanes); 0 .(Water Pollutants,
Chemical);
10588-01-9
.(sodium bichromate);
50-00-0
.(Formaldehyde); 71-43-2 .(Benzene); 71-55-6 .(1,1,1-trIchlor
Clmetldlne--Pharmacology--PD; Enzyme Induct Ion--Drug Effects --DE; Famot1d1ne--Pharmacology--PD; Hemeprotelns--Metabol Ism
oethane); 75-09-2 .(Methylene Chloride)
--ME;
Methylat1on--Drug Effects--DE;
Mlcrosomes,
Liver
--Enzymology--EN; Mixed Function Oxidases --Antagonists and
01074863 94118541 MEDL/94118541
Inhlbltors--AI; Oxldatlon-ReductIon; RanitIdlne--Pharmacology
--PD; Rats; Rats, Wlstar; Suparox1des--Metabol1sm--ME
CAS Registry No.: 0
.(Hemeprotelns); 0 .(Histamine H2
Receptor Blockaders); 11062-77-4 .(Superoxides); 51481-61-9
.(Clmetldlne);
58-15-1
.(Amlnopyrlne);
66357-35-5
.(Ranitidine):
76824-35-6
.(Famotidine);
9035-51-2
.(Cytochrome P-450)
Enzyme No.: EC 1.13.12. .(Mixed Function Oxidases)
A randomized phase II study of low-dose cytosine arablnoslde (LD-AraC) plus granulocyte-macrophage colony-stimulating factor (rhGM-CSF) In myelodysplastlc syndromes (MDS) with a high risk of developing leukemia. EORTC Leukemia Cooperative Group.
Gerhartz HH; Marcus R; Delmer A; Zwierzlna H; Suclu S;
Oardenne M; Solbu G; de Witte T; Jacobs A; Vlsanl G; et al Medical Dept. Ill, Kllnlkum Grosshadern, Munich, Germany.
Leukemia; LEU
8(l):16-23
1994
ISSN 0887-6924
Journal Code:
01075018
94119131
MEDL/94119131
Evaluation of the Allium anaphase-telophase test In relation
to genotoxlclty screening of Industrial wastewater.
Rank J; Nielsen MH
Department of Environment, Technology and Social Studies,
Roskllde University, Denmark.
Mutat Res; 312(1):17-24 1994 ISSN 0165-1110
Journal Code: NNA
Languages: ENGLISH
Document Type: JOURNAL ARTICLE
Contract/Grant
No.:
5U10-C111488-18;
5U10-C111488-19;
5U10-C111488-20; +
Languages: ENGLISH
Document Type: CLINICAL TRIAL; CLINICAL TRIAL. PHASE II;
JOURNAL ARTICLE; MULTICENTER' STUDY; RANDOMIZED CONTROLLED
TRIAL
Journal Announcement: 9403
Subfile:
X; L; M
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showed a similar requirement for MgATP and were equally
contaminated with creosote, polycyclic aromatic hydrocarbons
enhanced by protein kinase C activator
(PAHs),
polychlorinated
dibenzo-p-dloxlns
(PCDDs),
and
12-0-tetradecanoylphorbol 13-acetate (TPA) but not by kinase A activator 8-bromoadenoslne 3',5'-cycl1c monophosphate free
polychlorinated dlbenzofurans (PCDFs). This paper compares the results of the current LISEPA point estimate (deterministic)
base. The protein kinase C Inhibitor staurosporlne blocked the
approach for predicting:, the health risks associated with
TPA-stlmulated component of secretion but had no effect on the
exposure to PCDDs/PCDFs In soil with the results of a
NE release In the absence of TPA. Calmldazollum, an Inhibitor
probabilistic approach which uses a Monte Carlo analysis. At
of calmodulin, inhibited the secretion evoked by both metals
many of these wood treatment sites the hazard posed by the
to similar extent. Agents Interacting with microtubules (colchicine and vinblastine) or microfilaments (cytochalasln 8 and phalloldln) had no effect on secretion induced by either
PAHs, and especially pentachlorophenol, can be much greater than that due to PCDD and PCDFs; however, because at this site the health risk associated with PAHs was deemed negligible by
metal cation. These observations indicate that both Pb2+ and Ca2+ act at a common site and activate the exocytotic release
ATSDR, only PCDDs/PCDFs were evaluated. Octachlorodlbenzo-p-dl oxln (OCDO) and octachlorodibenzofuran (OCDF) congeners were
of NE by an analogous mechanism.
evaluated Independently from the other congeners due. to their
Tags: Animal; Comparative Study: Support, U.S. Gov't, P.H.S.
prevalence in the environment and the availability of
Major
Descriptors:
"Adrenal
Medulla--Phys1ology--PH;
congener-spedf1c data. The results of the reevaluation of the
Calclum--Pharmacology--PD; *Lead--Tox1c1ty--T0; "Noreplnephrl
rodent bioassay data for 2,3,7,8-TCDD were considered in the
ne--MetabolIsm--ME
probability distribution for the cancer potency factor. The
Minor Descriptors: Adenosine Triphosphate--Pharmacology--PD;
authors' analyses indicate that when assessing exposure to
Adrenal Medul1a--Drug Effects--DE; A1kalolds--Pharmacology--PD
soil via inhalation, ingestion, and dermal contact, the
; Calc1um--Metabollsm--ME; Calmodulin --Antagonists and
current regulatory approach used to estimate the reasonable
Inhlbltors--AI; Cattle: Cell Membrane Permeability; Cells, Cultured; Cyclic AMP-Dependent Protein K1nases--Metabo11sm--ME
maximally exposed Individual (RMEI) (USEPA, Risk Assessment Guidance for Superfund, Vol. 1, Part A, 1989) can predict
; Dose-Response Relationship, Drug; Egtazlc Ac1d--Pharmaco!ogy
risks which are 10- to 100-fold greater than the 95th
--PD;
Enzyme
Activation;
Imidazoles--Pharmacology--PD;
percentile risk predicted by a Monte Carlo analysis.
Kinetics; Lactate Dehydrogenase--Analys1s--AN; Protein Kinase
Tags: Animal; Case Report: Comparative Study; Female; Human
C--Antagon1sts
and
Inhlbltors--AI;
Protein
Kinase
C
Major Descriptors: "Environmental Pol 1ut1on--Stat 1st1 cal and
--Metabol1sm--ME;
Spectrophotometry.
Atomic
Absorption;
Numerical Data--SN; "Industry; "Soil Pol 1utants--Analys1s--AN;
Tetradecanoylphorbol Acetate--Pharmacology--PD; 8-Bromo Cyclic
"Wood
Adenos1ne Monophosphate--Pharmacology--PD
CAS Registry No.: 0
.(Alkaloids); . 0
.(Calmodulin); 0
Minor Descriptors: Abnormalities, Drug-Induced--Ep1dem1ology
--EP;
Algorithms;
Benzofurans--Analys1s--AN;
Benzofurans
.(Imidazoles); 16561-29-8
.(Tetradecanoylphorbol Acetate);
--Pharmacok1 net 1cs--PK; Benzofurans--Tox1c1ty--TO; Dose-Respo
23583-48-4 .(p-Bromo Cyclic Adenosine Monophosphate); 51-41-2
nse
Relationship, Drug; Environmental Pollution --Adverse
.(Norepinephrine);
56-65-5
.(Adenosine Triphosphate);
Effects--AE; Mice; Monte Carlo Method; Pregnancy; Probability;
57265-65-3
.(R 24571); 62996-74-1 .(staurosporlne); 67-42-5
Risk;
Soil
PolIutants--Tox1city--T0;
Structure-Activity
.(Egtazlc Acid); 7439-92-1 .(Lead); 7440-70-2 .(Calcium)
Relationship;
Tetrachlorodlbenzodlox1n
--Analogs
and
Enzyme 2.7.1.-
No.: EC 1.1.1.27
.(Protein
Kinase
.(Lactate Dehydrogenase); EC
C);
EC 2.7.10.-
.(Cyclic
Deri vat Ives--AA; Tetrachlorodlbenzodloxln--Analys1s--AN; Tet rachlorodlbenzod1 ox1n--Pharmacok1 net 1cs--PK; Tetrachlorod1ben
AMP-Dependent Protein Kinases)
zod1ox1n--Tox1c1ty--T0;
United
States;
United
States
Environmental Protection Agency
CAS
Registry
No.: 0
.(chlorinated dlbenzofurans); 0
01072196
94105459
MEDL/94105459
.(polychlorodlbenzo-4-dloxln); 0
.(Benzofurans); 0 .(Soil
Comparing the results of a Monte Carlo analysis with EPA's
Pol 1utants); 1746-01-6 .(Tetrachlorodlbenzodloxln)
reasonable maximum exposed individual (RMEI): a case study of
a former wood treatment site.
Copeland TL; Paustenbach DJ; Harris MA; Otanl J
01072032
94104627
MEDL/94104627
ChemRIsk, 92714.
a Division of McLaren/Hart, Irvine, California
Base
incorporation
and
extension at a site-specific
ethenocytoslne by Escherichia coll DNA polymerase I Klenow
Regul Toxicol Pharmacol; 18(2):275-312 1993 ISSN 0273-2300
fragment.
Journal Code: RBH
Slmha D; Yadav D; Rzepka RW; Palejwala VA; Humayun MZ
Languages: ENGLISH
Department of Microbiology and Molecular Genetics, UMD-New
Document Type: JOURNAL ARTICLE
Jersey Medical School, Newark 07103-2714.
Journal Announcement: 9403
Mutat Res; 304(2):265-9 1994 ISSN 0165-1110
Subfile:
L; M
Journal Code: NNA
In the United States, there are about 250 former sites that
Contract/Grant No.: CA47234, CA, NCI
treated wood with preservatives that are now In need of some degree of remediation. The soil at many of these sites Is
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Journal Announcement: 9403
Subfile:
L; M
Ethenocytoslne (epsilon C) is a highly mutagenic exocycllc
DNA lesion Induced by carcinogens vinyl chloride and urethane.
We have examined base Incorporation and extension at a
site-specific
epsilon
C residue by a quantitative gel
electrophoretic assay using an exonuclease-deficlent version
of Escherichia coll DNA polymerase I (Klenow fragment) as the
model enzyme. The data show that the KM for 1ncorporat1 on of
adenine or thymine opposite epsilon C by Is about 5 orders of
magnitude higher than that for the Incorporation of guanine
opposite normal cytosine. The KM for base extension past
epsilon C:A and epsilon C:T pairs is 1-2 orders of magnitude
higher than that observed for a C:G pair. Although adenine
mlslnsertlon Is favored over that of thymine, base extension
occurs more readily when the base incorporated opposite
epsilon C Is thymine.
Tags: Support, ll.S. Gov't, P.H.S.
Major Descriptors: *Cytosine--Analogs and Derlvat1ves--AA;
*DNA--MetabolIsm--ME; *DNA Damage; *DNA Polymerase I--Genetics
--GE; *Mutagenes1s, Site-Directed; *Mutagens--Metabol1sm--ME
Minor
Descriptors:
Alkylating Agents--Metabol1sm--ME;
Alkylating Agents--Toxlc1ty--T0;
Base Composition; Base
Sequence; Cytos1ne--Chem1stry--CH; Cytos1ne--Metabol1sm--ME;
Cytos1ne--Tox1c1ty--T0; DNA--Chem1stry--CH; DNA Polymerase I
--Metabol1sm--ME; Escherichia col 1--Enzymology--EN; Escherlch
la col1--Genet1cs--GE; Molecular Sequence Data; Mutagens
--Toxicfty--T0;
01IgodeoxyrIbonucleotIdes--MetabolIsm--ME;
Templates
CAS Registry No.: 0 .(Alkylating Agents): 0 .(Mutagens); 0
.(01IgodeoxyribonucleotIdes); 0
.(3,N(4)-ethenocytoslne);
71-30-7 .(Cytosine); 9007-49-2 .(DNA)
Enzyme No.: EC 2.7.7.- .(DNA Polymerase I)
01071935
94104039
MEDL/94104039
Tobacco-specific
N-nltrosamlnes
and
Areca-derlved
N-nltrosamlnes: chemistry, biochemistry, carcinogenicity, and
relevance to humans.
Hoffmann D; Brunnemann KD; Prokopczyk B; Djordjevic MV
American Health Foundation, Valhalla, New York 10595.
J Toxicol Environ Health; 4l(l):1-52 1994 ISSN 0098-4108
Journal Code: KAA
Contract/Grant No.: CA-29580, CA, NCI; CA-17613. CA, NCI
Languages: ENGLISH
Document Type: JOURNAL ARTICLE; REVIEW; REVIEW. ACADEMIC
journal Announcement: 9403
Subfile:
X; L; M
Nicotine and the minor tobacco alkaloids give rise to
tobacco-specific
N-nltrosamlnes
(TSNA)
during
tobacco
processing anp during smoking. Chemical-analytleal studies led
to the Identification of seven TSNA In smokeless tobacco (< or
= 25 mlcrograms/g) and In mainstream smoke of cigarettes (1.3
micrograms TSNA/cigarette). Indoor air polluted by tobacco
smoke
~y contain up to 24 pg/L of TSNA. In mice, rats, and
001560
DIs log Info.Svcs.
hamsters,
three
TSNA,
N'-nitrosonornicot1ne
(NNN),
4-(methylnltrosamlno)-1 -(3-pyrIdy1)-1-butanone
(NNK),
and
4-(methylnltrosamlno)-1 -(3-pyrIdyl)-1-butanol
(NNAL),
are
powerful carcinogens; , two TSNA are moderately active as
carcinogens; and twc^TSMA appear not to be carcinogenic. The
TSNA
are
procarcfnogeris, agents that require metabolic
activation. The active forms of the carcinogenic TSNA react
with cellular components, Including DNA, and with hemoglobin
(Hb).
The Hb adducts In chewers and smokers serve as
biomarkers
for
the uptake and metabolic activation of
carcinogenic TSNA and the urinary excretion of NNAL as free
alcohol and as glucuronlde for the uptake of TSNA. The review
presents evidence that strongly supports the concept that TSNA
contribute to the increased risk for cancer of the upper
digestive tract In tobacco chewers and for the Increased risk
of lung cancer, especially pulmonary adenocarcinoma. In
smokers. The high Incidence of cancer of the upper digestive
tract especially among men on the Indian subcontinent has been
causally associated with chewing of betel quid mixed with
tobacco. In addition to the TSNA, the betel quid chewers are
exposed to four N-nltrosamlnes that are formed during chewing
from the Areca alkaloids, two of these N-nltrosamlnes are
carcinogens. The article also reviews approaches toward the
reduction of the carcinogenic potency of smokeless tobacco,
betel quid-tobacco mixtures, and cigarette smoke. Although the
safest way to reduce the risk for tobacco-related cancers Is
to refrain from chewing and smoking, modif1 cat ions of
smokeless tobacco and of cigarettes are indicated to lead to
less toxic products. Another more recent approach for reducing
the carcinogenic effect of tobacco products is the application
of chemopreventlve agents, primarily of micronutrients. Future
aspects In tobacco carcinogenesis, especially as It relates to
TSNA, are expected in the field of molecular biochemistry and
In biomarker studies, with the goal of identifying those
tobacco and betel quid chewers and tobacco smokers who are at
especially high risk for cancer. (250 Refs)
Tags: Animal; Human; Support, U.S. Gov't, P.H.S.
Major
Descriptors:
*Areca--Chem1stry--CH;
*Carcinogens
--Toxlclty--T0; *Neoplasms--Chemically Induced--Cl; *N1trosaml
nes--Toxicity--TO; Tobacco--Chemlstry--CH
Minor Descriptors: Carc1nogens--Analysis--AN; Carcinogens
--Chem1stry--CH; Hamsters; Mice; Neoplasms --Prevention and
Control--PC;
Nitrosamlnes--Analys1s--AN;
Nitrosamlnes
--Chem1stry--CH;
Rats;
Tobacco Smoke Pollution --Adverse
Effects--AE;
Tobacco Smoke Pollut1on--Analysis--AN; Tobacco,
Smokeless--Adverse Effects--AE; Tobacco, Smokeless--Chemlstry
- -CH
CAS Registry No.: 0 .(Care 1 nogens); 0 .(Nltrosamines); O
.(Tobacco, Smoke1 ess)
01069997
94094449
MEDL/94094449
The intensity of vanad1um(V)-1nduced cytotoxicity and
morphological transformation In BALB/3T3 cells Is dependent on
glutathione-mediated bioreduction to vanadlum(IV).
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DIALOG File 159: CANCERLXT(R)_19B3-1994/Mar (c) format only 1994
Sabblonl E; Pozzl G; Devos S; Plntar A; Casella L; Flschbach M
Commission of the European Communities, Environment
Institute, Joint Research Centre-Ispra Site, Varese, Italy.
Carcinogenesis; 14(12):2565-8 1993 ISSN 0143-3334
Journal Code: C9T
`Languages: ENGLISH
Document Type: JOURNAL ARTICLE
Journal Announcement: 9403
Subfile:
X; L; M
Cytotoxicity
and morphologlea 1 transformat1 on has been
studied In BALB/3T3 Cl A31-1-1 mouse embryo cells for ammonium vanadate [vanadium(V)] and vanadyl sulphate [vanadlum(IV)]
alone or In combination with d1ethy1ma1eate (DEM), a cellular
glutathione (GSH)-deplet1ng agent. Cells exposed for 24 h to 10(~5) M vanadlum(V) alone or In combination with 3 x 10(-6) M
DEM
showed
the characteristic hyperflne EPR signal of
vanad1um(IV), which was more obvious In the case of exposure
to vanadlum(V) alone. This suggests that the amount of
vanadlum(V) reduced to vanadlum(IV) decreased In GSH-depleted
cells. While vanadlum(IV) at concentrations of 3 x 10(-6) M
and 10(-5) M was not transforming In the cells, vanadlum(V)
showed neoplastic transforming activity (P < 0.025 and P <
0.001 for the two doses, respectively) in comparison to
controls
(vanadium unexposed cells).
Cytotoxicity and
morphological transformation in cells exposed to vanadlum(V)
In combination with 3 x 10(-6) M DEM were significantly more
Intensive (P < 0.005 and P < 0.01 for the two doses of
vanadate tested) compared to the corresponding values observed
in cells exposed to vanadlum(V) alone. This suggests that the
final transforming activity response .Is dependent on the
intracellular GSH-medlated mechanism of reduction of
vanadlum(V)
(to vanadlum(IV):
(1) the extent to which
vanadlum(V) should be bioreduced to less toxic vanadlum(IV)
via intracellular GSH Is a key point In determining the
Intensity
of the observed neoplastic action; (11) the
carcinogenic potential of vanadlum(V) should be strictly
dependent on Its IntracelTular persistence which could lead to
changes In normal metabolic patterns of vanadlum(V) In the
oxidized form due to lack of GSH-medlated reduction.
Tags: Animal
Major Descriptors: *Cell Transformation, Neoplast1c--Drug
Effects--DE; *G1utath1one--Metabol1sm--ME; *Vanad1um Compounds
--Tox1 clty--TO
Minor Descriptors: Biotransformat ion; Cell Survival--Drug
Effects--DE; Electron Spin Resonance Spectroscopy; Maleates
--Pharmacology--PD;
Mice;
Mice,
Inbred
BALB
C;
OxldatIon-Reduct Ion: Vanadium Compounds--MetabolIsm--ME; 3T3
Cells
CAS Registry No.: 0 .(Maleates); 0 .(Vanadium Compounds);
141-05-9
.(diethyl maleate); 27774-13-6 .(vanadyl sulfate);
70-18-8 .(Glutathione)
001561
Dialog info.Svcs.
01069982
94094434
ME0L/94094434
Benzene and phenol metabolism by mouse and rat liver
mlcrosomes.
Schlosser PM; Bond JA,; Medlnsky MA
Chemical Industry Institute of Toxicology, Research Triangle
Park, NC 27709.
Carcinogenesis; 14(12):2477-86 1993 ISSN 0143-3334
Journal Code: C9T
Languages: ENGLISH
Document Type: JOURNAL ARTICLE Journal Announcement: 9403
Subfile:
X; L; M
Benzene, an Important Industrial solvent and constituent of unleaded gasoline, causes leukemia and aplastic anemia in
humans. Mice are more sensitive than rats to benzene toxicity,
though neither species has been shown to respond consistently
with benzene-Induced leukemia. Benzene biotransformation in
liver to phenol, hydroqu1 none, catechol and/or mucona1dehyde
Is thought to be necessary for Its hematotoxlc1ty and/or
genotox1c1ty. Our goal Is to develop a mathematical simulation
model capable of describing the pathways and kinetics of
benzene metabolism by rat and mouse liver mlcrosomes and to
assess the role of species metabolic differences In species
sensitivity.
Mlcrosomes
were
Incubated
with 4 mlcroM
(U-14CJ-benzene or 4 mlcroM [U-14Cjphenol. Metabolite
production was quantified by extraction Into ethyl acetate,
HPLC separation and liquid scintillation spectroscopy. After
45 min, mouse liver mlcrosomes converted 20% of the benzene to
phenol, 31% to hydroquinone and 2% to catechol. Rat liver
mlcrosomes
converted
23% of benzene to phenol, 8% to
hydroquinone and 0.5% to catechol. Production of hydroquinone
and catechol continued for 90 min for mouse liver mlcrosomes.
while production by rat liver mlcrosomes had virtually ceased
by 90 min. Muconic acid production by mouse liver mlcrosomes
was < 0.2% and < 0.04% from benzene and phenol respectively
after 90 min. A quantitative simulation model was constructed
to describe the In vitro metabolism of benzene, 1ncorporat1ng
the reaction sequences: benzene-->phenol-->catechol-->tr1hydro
xybenzene and pheno1 -->hydroqu1 none-->tr1hydroxybenzene. In
the model, all of the reaction steps are assumed to be
catalyzed by the same enzyme(s), cytochrome(s) P450, and
benzene, phenol, hydroquinone and catechol in solution are all
assumed to compete, through reversible binding, for the same
reaction site(s) on cytochrome(s) P450. The simulation model
accurately described both the benzene and phenol kinetic data,
supporting this proposed mechanism. In particular, this model
suggests that the observed inhibition of benzene on phenol
metabolism, and of phenol on benzene metabolism, occurs
through competition for a common reaction site, which can also
bind catechol and hydroquinone.
Tags: Animal; In Vitro; Male; Support, Non-U.S. Gov't
Major Descriptors: *Benzene--MetabolIsm--ME; ^Mlcrosomes,
L1ver--Metabol1sm--ME; *Phenols--Metabol1sm--ME
Minor
Descriptors:
Biotransformation;
Mice;
Models,
Biological; Rats; Rats, Inbred F344
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CAS
Registry No.: O
.(Phenols); 108-95-2
.(phenol);
71-43-2 .(Benzene)
01069781
94093257
MEDL/94093257
[Handling of red silica gravel on sports, play and resort
surfaces with special reference to new toxicologic results]
Umgang mlt Kieselrot auf Sport-, Spiel- und Frelzeltflachen
unter Berucks1cht1gung neuer toxikolog1scher UntersuchUngserge
bnlsse.
Heudorf U
Gesundhe1tsamt der Stadt Frankfurt am Main.
Gesundheitswesen; 55(10):521-6 1993 ISSN 0941-3790
Journal Code: BFD
Languages: GERMAN
Document Type: JOURNAL ARTICLE
English Abstract
Journal Announcement: 9403
Subfile:
L
In 1991
"Kieselrot", a material with extremely high
PCDD/PCDF-contaminatlon up to about 200.000 ng TEQ/kg was
detected on many leisure centres and sports fields In Germany.
The contaminated grounds were closed, and covered up. The
following examinations to prepare the planned decontamination
are described here. The need for decontamination of those
"K1ese1rot"-areas Is discussed with special reference to its
relevance on behalf of environmental toxicology and preventive
medicine. Risk estimates, based on mathematical models had
shown a considerable health and cancer risk for the users of
such play- and sports grounds. However, recent studies
conducted with sportsmen, groundsmen, and residents after many
years of contact with "Kleselrof-covered grounds did not
reveal any additional PCDD/PCDF blood fat burden. But raised
TEO-levels and a typical congeneric pattern pointing to a
"K1eselrot"-load could be seen in some of the examined
children. Following these results It was concluded that
children play grounds contaminated with "Kieselrot" should
remain closed and should be decontaminated, whereas sports
fields could be used again. Another possibility could be the
adaption of the decontamination concepts and methods to the
proven low bloavallabi11ty of PCDD/PCDF from "Kieselrot".
Tags: Female; Human; Male
Major Descriptors: *Benzofurans--Analysis--AN; *Env1ronmenta
1 PolIutants--Analys1s--AN; *Polymers--Ana1ys1s--AN; *So11
PolIutants--Analys1s--AN; *Tetrachlorod1benzod1ox1n --Analogs
and Derlvatlves'-AA
Minor Descriptors: Adolescence; Adult; Aged; Aged, 80 and
over; Benzofurans--Tox1c1ty--T0; Body Burden; Child; Child,
Preschool; Infant; Leisure Activities; Maximum Permissible
Exposure Level; Middle Age; Play and Playthings; Polymers
--Tox1city--T0; Sports; Tetrach1orodibenzodiox1n--Analys1s--AN
; Tetrachlorodibenzodiox in--Toxicity--TO
CAS
Registry
No.: O
.(polychlorodibenzo-4-dloxin); 0
.(polychlorodlbenzofuran); 0 .(Benzofurans); 0 .(Environments
1
Pollutant^);
O
.(Polymers); 0
.(Soil Pollutants);
1746-01-6 .(Tetrachlorodibenzodioxln)
001562
Dialog Info.Svcs.
01069668 94092366
MEDL/94092366
Methods development toward the measurement of polyaromatic
hydrocarbon-DNA adducts by mass spectrometry.
Glese RW; Vouros P .x` Department of Medicinal. Chemistry, Northeastern University,
Boston. Ma 02115.
Res Rep Health Eff Inst; (61): 1-25; discussion 27-36 1993
ISSN 1041-5505
Journal Code: AH8
Languages: ENGLISH
Document Type: JOURNAL ARTICLE
Journal Announcement: 9403
Subfile:
L; M
The measurement of DNA adducts in human samples Is at an
early stage. The accuracy of some of the current measurements
Is not defined, the structures are unknown for a significant
number of the adducts that have been detected, and there is
little Information about how many adducts remain to be
discovered. This Is due largely to the trace amounts of human
DNA adducts In any sample. A consequence of this Is that the
true potential of DNA adducts as Indicators of exposure and
risk
in human toxicology Is far from realized. Mass
spectrometry, a powerful technique for organic analysis, is
the key to exploiting fully the usefulness of human DNA
adducts as biomarkers of human exposure and risk. Mass
spectrometry can make accurate measurements, discover unknown
compounds, and determine the structures of these unknown
compounds. However, the trace (very small) amounts of human
NA adducts have limited mass spectrometry's usefulness In
analyzing such samples. This project focused on Increasing the
sensitivity of mass spectrometry for measuring human DNA
adducts. Advances In sensitivity have been achieved for two-
modes of mass spectrometry applied to standards related to DNA
adducts: gas chromatography with electron-capture negative ion
mass
spectrometry,
and
fast-atom-bombardment
mass
spectrometry. These advances Involve both sample preparation
and Instrument conditions.
Tags: Animal; Human; Support, U.S. Gov't, Non-P.H.S.
Major Descriptors: *DNA--Analysis--AN; DNA--Chem1stry--CH;
*DNA
Damage;
*Polycycl1c
Hydrocarbons--Analysis--AN;
Polycyclic Hydrocarbons--Chem1stry--CH; *Spectrum Analysis,
Mass
Minor Descriptors: Benzene--Chem1stry--CH: Benzo(a)pyrene
--Analogs and Der1vat1ves--AA; Benzo(a)pyrene--Chem1stry--CH;
Carcinogens, Environmental--Chem1stry--CH; Chromatography, Gas
--Methods--MT;
Chromatography,
High
Pressure
Liquid;
DeoxyadenosInes--Chem1stry--CH; Deoxyguanos1ne --Analogs and
Derivat1ves--AA
Deoxyguanos1ne--Chemistry--CH; E1ectrophores
1s--Methods--MT
F1uorenes--Chem1stry--CH;
Hydraz1nes
--Chemistry--CH
HydrogenatIon; 0x1dat1on-Reduct1 on; Pyrenes
--Chem1stry--CH
Spectrometry, Mass, Fast Atom Bombardment;
Spectrum Analysis, Mass--Methods--MT; Superoxldes--Chemlstry
--CH; 2-Acetylamlnofluorene--Chemistry--CH
CAS
Registry No.: 0
.(benzo(a)pyrene-DNA adduct); 0
.(Carcinogens,
Environmental);
0
.(DeoxyadenosInes); 0
. (Fluorenes); 0 .(Hydrazines); 0 .(Polycyclic Hydrocarbons);
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DIALOG File 55: BIOSIS PREVIEWS(R)_198S-1994/MAR ISS 12 (c) 1994 Concept Codes:
*00512 . General Biology-Conservation Resource Management *22506 . Toxicology-Environmental and Industr1a 1 Tox1co1ogy *37015 . Public Health: Environmental Health-Air, Water and
Soil Pollution 10059 . Btochemlcal Methods-Mlnerals
10932578
BIOSIS Number: 97132578
Modeling the concentrations of gas-phase toxic organic air
pollutants: Direct emissions and atmospheric formation
Harley R A: Cass G R
Environ. Eng. Scl. Dep., Calif. Inst. Technology, Pasadena,
CA 91125, USA
Environmental Science & Technology 28 (l). 1994. 88-98.
Full Journal Title: Environmental Science & Technology
ISSN: 0013-936X
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 006 Ref.
082471
An Eulerlan photochemical air quality model Is described for
the prediction of the atmospheric transport and chemical
reactions of gas-phase toxic organic air pollutants. Model
performance was examined In the Los Angeles, CA (USA), area
over the period August 27-28, 1967. The organic compounds were drawn from a list of 189 species selected for control as
hazardous air pollutants In the Clean Air Act amendments of
1990.
The
species
considered Include benzene, various
alkylbenzenes,
phenol,
cresols, 1,3-butadiene, acrolein,
formaldehyde,
acetaldehyde,
and perchloroethylene among
others. It Is found that photochemical generation contributes
significantly to formaldehyde, acetaldehyde, acetone, and
acrolein concentrations for the 2-day period studied. Phenol
concentrations are dominated by direct emissions, despite the
existence of a pathway for atmospheric formation from benzene
oxidation. The finding that photochemical production can be a
major contributor to the total concentratIons of some toxic
organic species Implies that control programs for those
species must consider more than just direct emissions.
Descriptors/Keywords: RESEARCH ARTICLE; AIR QUALITY MODEL;
PHENOL; 1,3-BUTADIENE; ACROLEIN; FORMALDEHYDE; ACETALDEHYDE;
PERCHLOROETHYLENE; ACETONE
Concept Codes:
*07504 . Ecology; Environmental Blology-BloclImatology and
B1ometeoro1ogy
*22506 . Toxicology-Environmental and Industrial Toxicology
*37015 . Public Health: Environmental Health-Air, Water and
Sol 1 Pollutlon
10050 . Biochemical Methods-General
10932564
BIOSIS Number: 97132564
Toxicity, Bloavallabl1 tty and metal spedat ion
Jonnalagaddd S B: Rao P V V P
Dep. Chemistry, University Zimbabwe, Box MP 167, Mt.
Pleasant, Harare, RHO
Comparative Biochemistry and Physiology C Comparative
015462
BIOSIS
Pharmacology and Toxicology 106 (3). 1993. 585-595.
Full Journal Title: Comparative Biochemistry and Physiology
C Comparative Pharmacology and Toxicology
ISSN: 0742-8413
,-
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 006 Ref.
082440
1. Environmental toxicology emphasizes the difference from
traditional toxicology in which pure compounds of interest are
added to purified diets, or Injected Into the test animals.
When the objective Is to study the fate an& effects of trace
elements in the environment, knowledge of the speclatfon of
the elements and their physico-chemical forms Is Important. 2.
Cadmium salts such as the sulfides, carbonates or oxides, are
practically
Insoluble
In water. However, these can be
converted to water-soluble salts in nature under the Influence
of oxygen and acids. Chronic exposure to Cd Is associated with
renal toxicity In humans once a critical body burden Is
reached. 3. The solubility of As(III) oxide In water Is fairly
low, but high In either acid or alkali. In water, arsenic Is
usually in the form of the arsenate or arsenlte. As(III) Is
systemically more poisonous than the As(V), and As(V) Is
reduced to the As(III) form before exerting any toxic effects.
Organic arsenlcals also exert their toxic effects In vivo In
animals by first metabolizing to the trlvalent arsenoxlde
form.
Some
methyl arsenic compounds, such as dl- and
trImethylars1nes, occur
naturally
as a consequence of
biological activity. The toxic effect of arsenlte can be
potentiated by dlthlols, while As has a protective effect
against the toxicity of a variety of forms of Se in several
species. 4. Selenium occurs In several oxidation states and
many selenium analogues of organic sulfur compounds exist In
nature. Selenium in selenate form occurs in alkaline soils,
where It is soluble and easily available to plants. Selenite
binds tightly to Iron and aluminum oxides and thus is quite
Insoluble In soils. Hydrogen selenlde Is a very toxic gas at
room temperature. The methylated forms of Se are much less
toxic for the organism than selenite. However, the methylated
Se derivatives have strong synergistic toxicity with other
minerals such as arsenic. 5. Aquatic organisms absorb and
retain Hg In the tissues, as methyl mercury. although most of
the environmental Hg to which they are exposed is Inorganic.
The methyl mercury
In fish arises from the bacterial
methylatlon of inorganic Hg. Methylmercury In the human diet
Is almost completely absorbed into the bloodstream. The
nervous system Is the principal target tissue affected by
methylmercury in adult human beings, while kidney Is the
critical organ following the Ingestion of Hg(II) salts.
Descriptors/Keywords: LITERATURE REVIEW; HUMAN; PLANT; FISH;
CADMIUM; ARSENIC; SELENIUM; METHYLMERCURY; ENVIRONMENTAL
EXPOSURE; RENAL; NERVOUS SYSTEM TOXICITY
Concept Codes:
*13010 . Metabolism-Minerals
*15506 . Urinary System and External Secretions-Pathology
*20506 . Nervous System-Pathology
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DIALOG File 55: BIOSZS PREVIEWS(R)_1985-1994/MAR ISS 12 (c) 86190 . Prlmates-Unspecifled 86375 . Murldae
Super Taxa: Animals; Chordates; Vertebrates; Nonhuman Vertebrates; Mammals; Nonhuman Mammals; Primates; Nonhuman Primates; Rodents
1994
10926075
BIOSIS Number: 97126075
Structure-activity studies of human tumour necrosis factors
Van Ostade X; Tavernier J; Flers W
Inst. Med. Vet. Scl., Div. Human Immunol., PO Box 14 Rundle
Mall Post Office, Adelaide 5000, South Australia, AUL Protein Engineering 7 (1). 1994. 5-22.
Full Journal Title: Protein Engineering
ISSN: 0269-2139
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 006 Ref. 075947
The mechanism by which tumour necrosis factors (TNF and lymphotoxin, also called TNF-alpha and TNF-beta respectively)
exert their cytotoxic activity on many malignant cells,
remains largely unknown. Furthermore, the broad array of
differentiation (gene Induction) and mitogenic activities towards many primary cells Is still a subject of Intensive
Investigation. TNF Is an Important mediator Inflammation,
Immune responses and Infection-related phenomena and these
activities contribute to the severe toxicity seen when TNF is
used as an anticancer agent. The first step In the mechanism
of action Is the specific binding of the ligand to its
receptors and dissection of the molecular mechanism Involved In this Interaction is the subject of this review. The reasons
for the interest in this aspect are obvious: first, the
development of strong antagonistic TNF analogues can be useful
In dampening the potentially lethal or debilitating effects of
an overproduction of the cytokine (as In septic shock or
rheumatoid arthritis). . Secondly, since two distinct TNF
receptors exist, construction of TNF muteins that distinguish
between both types may lead to derivatives of this plelotroplc agent with a more restricted biological activity pattern. Ideally, one would like to develop a TNF mutant that has
retained Its cytotoxic action on tumour cells without Inducing the deleterious systemic toxicity. Such an optimized TNF molecule could become a potent anticancer agent.
Descriptors/Keywords: LITERATURE REVIEW; MOUSE; TUMOR NECROSIS
FACTOR; HORMONE-DRUG; ANTINEOPLASTIC-DRUG; PHARMACODYNAMICS;
TUMOR NECROSIS FACTORS; LYMPHOTOXIN; INFLAMMATION; ACTION
MECHANISM; MOLECULAR SEQUENCE OATA; AMINO ACID SEQUENCE; PROTEIN ENGINEERING
Concept Codes: *10010 . Comparative Biochemistry, General *10064 . Biochemical Studles-Protelns, Peptides and Amino
Acids *10506 . Biophysics-Molecular Properties and Macromolecules
*12508 . Pathology, General and Miscellaneous-Inflammation and Inflammatory Disease
*12512 . Pathology, General and Miscellaneous-Therapy (1971-
015469
BIOSIS
)
*15008 . Blood, Blood-Forming Organs and Body
F1u1ds-Lymphat1c Tissue and Reticuloendothelial
System
,
* 17002 . Endocr1ne Systern-Genera1
*22005
Pharmacology-Clinical Pharmacology (1972- )
*22016 . Pharmacology-Endocrine System
*24008 . Neoplasms and Neoplastic Agents-Therapeutlc Agents;
Therapy
10068 . Biochemical Studies-Carbohydrates
Blosystemat1c Codes: 86215 . Homlnldae
86375 . Murldae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans;
Nonhuman Vertebrates; Nonhuman Mammals; Rodents
10925475
BIOSIS Number: 97125475
Benzene and phenol metabolism by mouse and rat liver
mlcrosomes
Schlosser P M; Bond J A; Medlnsky M A
Chemical Industry Inst. Toxicol., 6 Davis Dr., PD Box 12137,
Research Triangle Park, NC 27709, USA
Carcinogenesis (Oxford) 14 (12). 1993. 2477-2486.
Full Journal Title: Carcinogenesis (Oxford)
ISSN: 0143-3334
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 006 Ref.
075344
Benzene, an important.industrial solvent and constituent of
unleaded gasoline, causes leukemia and aplastic anemia In
humans. Mice are more sensitive than rats to benzene toxicity,
though neither species has been shown to respond consistently
with benzene-Induced leukemia. Benzene b.lotransformatlon in
liver to phenol, hydroqulnone, catechol and/or muconaldehyde
Is thought to be necessary for its hematoxlclty and/or
genotoxlclty. Our goal is to develop a mathematical' simulation
model capable of describing the pathways and kinetics of
benzene metabolism by rat and mouse liver mlcrosomes and to
assess the role of species metabolic differences In species
sensitivity.
Mlcrosomes
were
Incubated
with
4-mu-M
(U-14C)-benzene or 4-mu-M (U-14C)phenol. Metabolite production
was
quantified
by extraction into ethyl acetate, HPLC
separation and liquid scintillation spectroscopy. After 45
min, mouse liver mlcrosomes converted 20% of the benzene to
phenol, 31% to hydroqulnone and 2% to catechol. Rat liver
mlcrosomes
converted
23% of benzene to phenol, 8% to
hydroqulnone and 0.5% to catechol. Production of hydroqulnone
and catechol continued for 90 min for mouse liver mlcrosomes,
while production by rat liver mlcrosomes had virtually ceased
by 90 min. Muconlc acid production by mouse liver mlcrosomes
was It 0.2% and It 0.04% from benzene and phenol respectively
after 90 min. A quantitative simulation model was constructed
to describe the In vitro metabolism of benzene. Incorporating
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the reaction sequences: benzene fwdarw phenol fwdarw catechol
fwdarw trlhydroxybenzene and phenol fwdarw hydroqulnone fwdarw
trlhydroxybenzene. In the model, all of the reaction steps are
assumed to be catalyzed by the same enzyme(s), cytochrome(s)
P450, and benzene, phenol, hydroqulnone and catechol In
solution are all assumed to compete, through reversible
binding, for the same reaction slte(s) on cytochrome(s) P450.
The simulation model accurately described both the benzene and
phenol kinetic data, supporting this proposed mechanism. In
particular, this model suggests that the observed Inhibition
of benzene on phenol metabolism, and of phenol on benzene
metabolism, occurs through competition for a common reaction
site, which can also bind catechol and hydroqulnone.
Descriptors/Keywords: RESEARCH ARTICLE; HUMAN; CARCINOGENS;
LEUKEMIA
Concept Codes:
*02506 . Cytology and Cytochemistry-Animal
*13002 . Metabolism-General Metabolism; Metabolic Pathways
*14004 . Digestive System-Physiology and Biochemistry
15006 . Blood, Blood-Forming Organs and Body Flulds-Blood,
Lymphatic and Reticuloendothelial Pathologies
*15008 . Blood, Blood-Forming Organs and Body
Flulds-Lymphatlc Tissue and Reticuloendothelial
System
22501
Toxicology-General; Methods and Experimental
*24006 . Neoplasms and Neoplastic Agents-Blochemlstry
*24007 . Neoplasms and Neoplastic Agents-Carclnogens and
Care1 nogenes1s
*24010 . Neoplasms and Neoplastic Agents-Blood and
Retlculoendothellal Neoplasms
10060 . Biochemical Studles-General
32600 . In Vitro Studies, Cellular and Subcellular
Blosystematic Codes:
86215 . Horn1n1dae
86375 . Mur 1dae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans;
Nonhuman Vertebrates;*Nonhuman Mammals; Rodents
10925453
BIOSIS Number: 97125453
The Intensity of vanadium-(V)-Induced cytotoxicity and
morphological transformation In BALB-3T3 cells is dependent on
glutathione-mediated bloreduction to vanadlum-(IV)
Sabblonl E; Pozzl G; Devos S; Plntar A; Casella L; Flschbach
M
Commission European Communities, Environment Inst., Joint
Res. Centre Ispra Site, 21020 Ispra, ITL
Carcinogenesis (Oxford) 14 (12). 1993. 2565-2568.
Full Journal Title: Carcinogenesis (Oxford)
ISSN: 0143-3334
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 006 Ref.
075348
Cytotoxicity and morphological transformation has been
studied In BALB/3T3 Cl A31-1-1 mouse embryo cells for ammonium
vanadate (vanad1um(V)) and vanadyl sulphate (vanadium (IV))
015470
alone or In combination with dlethylmaleate (DEM), a cellular
glutathione (GSH)-depletlng agent. Cells exposed for 24 h to
10-5 M vanadlum(V) alone or In combination with 3 times 10-6 M
DEM showed the characteristic hyperflne EPR signal of vanadium
(IV), which was mor'e: obvious In the case of exposure to
vanadlum(V)
alone.
This
suggests
that the amount of
vanadlum(V) reduced to vanadlum(IV) decreased In GSH-depleted
cells. While vanadlum(IV) at concentrations of 3 times 10-6M
and 10-5M was not transforming In the cells, vanadium(V)
showed neoplastic transforming activity (P It 0.025 and P It
0.001 for the two doses, respectively) In comparison to
controls
(vanadium unexposed cells).
Cytotoxicity and
morphological transformat1 on In cells exposed to vanadium (V)
In combination with 3 times 10-6 M DEM were significantly more
Intensive (P It 0.005 and P It 0.01 for the two doses of
vanadate tested) compared to the correspond 1ng values observed
In cells exposed to vanadlum(V) alone. This suggests that the
final transforming activity response Is dependent on the
Intracellular GSH-medlated mechanism of reduction of
vanadlum(V)
to vanadlum(IV): (1) the extent to which
vanadium(V) should be bioreduced to less toxic vanadlum(IV)
via Intracellular GSH Is a key point In determining the
intensity of the observed neoplastic action; (11) the
carcinogenic potential of vanadium(V) should be strictly
dependent on Its Intracellular persistence which could lead to
changes In normal metabolic patterns of vanadlum(V) in the
oxidized form due to lack of GSH-medlated reduction.
Descriptors/Keywords: RESEARCH ARTICLE; MOUSE FIBROBLASTS;
AMMONIUM VANADATE; VANADYL SULFATE; CARCINOGENS;
DIETHYLMALEATE; METABOLIC-DRUG
Concept Codes:
*02506 . Cytology and Cytochemistry-Animal
*13010 . Metabolism-Minerals
*13012 . Metabolism-Proteins, Peptides and Amino Acids
*22003 . Pharmacology-Drug Metabolism; Metabolic Stimulators
*22501 . Toxicology-General; Methods and Experimental
*24005 . Neoplasms and Neoplastic Agents-Neoplast1c Cell
L1 nes
*24006 . Neoplasms and Neoplastic Agents-Bloehemistry
24007 . Neoplasms and Neoplastic Agents-Carclnogens and
Carcinogenesis
10060 . Biochemical Studles-General
10064 . Biochemical Studles-Protelns, Peptides and Amino
Acids
10069 . Biochemical Studles-Minerals
18004 . Bones, Joints, Fasciae, Connective and Adipose
Tissue-Physiology and Biochemistry
32500 . Tissue Culture, Apparatus, Methods and Media
Blosystematic Codes:
86375 . Mur 1dae
Super Taxa:
Animals; Chordates: Vertebrates; Nonhuman Vertebrates;
Mammals; Nonhuman Mammals; Rodents
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DIALOG File 55: BIOSIS PREVIEWS(R)_1985-1994/MAR ISS 12 (c) Super Taxa:
Animals; Chordates; Vertebrates; Nonhuman Vertebrates; Mammals; Nonhuman Mammals; Carnivores; Primates; Humans
1994
10917672
BIOSIS Number: 97117672
Sinus histiocytosis of pelvic lymph nodes after hip
replacement: A histiocytic proliferation Induced by
cobalt-chromium and titanium
Albores-Saavedra J; Vultch F; Delgado R; Wiley E; Hagler H
Dlv. Anat. Pathol., Dap. Pathol., UT-Southwestern Med.
Cent., 5323 Harry Hines Blvd., Dallas, TX 75235-9072, USA
American Journal of Surgical Pathology 18 (1). 1994. 83-90.
Full Journal Title: American Journal of Surgical Pathology
ISSN: 0147-5185
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 006 Ref.
067550
Descriptors/Keywords: RESEARCH ARTICLE; HUMAN; TOXICITY;
IMMUNOHISTOCHEMIS-TRY
Concept Codes:
*02508 . Cytology and Cytochemistry-Human
*10511
B1ophys1cs-B1oeng1neer1ng
*15006
Blood, Blood-Forming Organs and Body Flulds-Blood,
Lymphatic and Reticuloendothelial Pathologies
*15008
Blood, Blood-Forming Organs and Body
Flulds-Lymphatlc Tissue and Reticuloendothelial
System
*18006
Bones, Joints. Fasciae, Connective and Adipose
Tissue-Pathology
01056
Microscopy Technlques-Hlstology and Histochemistry
10069
B1ochemleal Stud1es-M1nera1s
11316
Chor^date Body Reglons-Pelvis (1970- )
Blosystematlc Codes:
86215 . Homlnldae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans
10915693
BIOSIS Number: 97115693
Twenty-efght-day repeated dose toxicity tests of
O-nltrotoluene in VMstar rats
Kaneko T; Shimo T; Yasuhara X; HI rose A; Ogawa Y; Suzuki 5;
NakaJ1 Y; Kurokawa Y
Dlv. Toxicol., Biol. Safety Res. Cent., Natl. Inst. Health'
Scl., JAP
Journal of Toxicological Sciences 18 (4). 1993. 422.
Full Journal Title: 20th Annual Meeting of the Japanese
Society of Toxicological Sciences, Chiba, Japan, July 29-30,.
1993. Journal of Toxicological Sciences
ISSN: 0388-1350
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS Print Numberi Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 044586
Descriptors/Keywords: MEETING PAPER; LIVER; SPLEEN; HEMOLYTIC
ANEMIA: NITROBENZENE TOXICITY
015475
ISIS
Concept Codes:
*14006 . Digestive System-Pathology
*15006
Blood, Blood-Forming Organs and Body Flulds-Blood,
Lymphatic and Reticuloendothelial Pathologies
*15008
Blood, Bloocf-Formlng Organs and Body
Flulds-Lymphatlc Tissue and Reticuloendothelial
System
*22501
Toxicology-General; Methods and Experimental
00520
General Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
10060
Biochemical Studies-General
Blosystematlc Codes:
86375 . Muridae
Super Taxa:
Animals; Chordates; Vertebrates; Nonhuman Vertebrates;
Mammals; Nonhuman Mammals; Rodents
i
10914606
BIOSIS Number: 97114606
Density, diversity and incidence of deformities of benthic
invertebrates near a vinyl chloride discharge point source In
the Niagara River watershed
Dlckman M 0; Ryglel G
Biol. Scl. Dep., Brock Univ., St. Catharines, ON L2S 3A1, CAN
0 (0). 1993. 663-680. Full Journal Title: Gorsuch, J. W., et al. (Ed.). ASTM (American Society for Testing and Materials) Special Technical Publication, 1216. Environmental toxicology and risk assessment, 2nd volume; Symposium on Environmental Toxicology
and Risk Assessment: Aquatic, Plant, and Terrestrial, Pittsburgh, Pennsylvania, USA, April 26-30, 1992. x11+730p. American Society for Testing and Materials (ASTM):
Philadelphia. Pennsylvania, USA. ISBN 0-8031-1485-0.
ISSN: 0066-0558 Language: ENGLISH Document Type: BOOK; CONFERENCE PROCEEDINGS Print Number: Biological Abstracts/RRM Vol. Ref. 043499
046
Iss.
003
Descriptors/Keywords: BOOK CHAPTER; MEETING PAPER; CHIRONOMID: ENVIRONMENTAL TOXICITY; TERATOGENICITY
Concept Codes:
*07508
Ecology; Environmental Biology-Animal
*07514
Eco1ogy; Env1ronmental B1ology-L1mnology
*22506 *25503
Toxicology-Environmental and Industrial Toxicology Developmental B1ology-Embryology-Pathoiogleal
*25552
Developmental B1ology-Embryology-Descr1pt1ve
Teratology and Teratogenesls
*64078
Invertebrata, Comparative and Experimental Morphology. Physiology and
00520
Pathology-Insecta-Pathology General Biology-Symposia, Transactions and Proceedings of Conferences, Congresses, Review
Annuals
(cont. next page)
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DIALOG File 55: 8X0SXS PREVIEWS(R)_1985-1994/MAR XSS 12 (c) 1994 10060 . Biochemical Studles-General
Blosystematlc Codes: 75314 . Dlptera
Super Taxa: Animals: Invertebrates: Arthropods; Insects
10914597
BI0SI5 Number: 97114597
Metal accumulation In blood and milk of dairy cows grazed or
fed by fodder grown on a sewage water disposal site
Varadarajan K; Pallwal K; Rajamanlckam C
Sch. Biol. Scl., Madurai Kamaraj Unlv., Madurai 625 021. IND
0 (0). 1993. 510-520.
Full Journal Title: Gorsuch, d. W., et al. (Ed.). ASTM
(American Society for Testing and Materials) Special Technical
Publication. 1216. Environmental toxicology and risk
assessment, 2nd volume; Symposium-on Environmental Toxicology
and Risk Assessment: Aquatic, Plant, and Terrestrial,
Pittsburgh, Pennsylvania, USA, April 26-30, 1992. x11+730p.
American Society for Testing and Materials (ASTM):
Philadelphia, Pennsylvania, USA. ISBN 0-8031-1485-0.
ISSN: 0066-0558
Language: ENGLISH
Document Type: BOOK; CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 043490
Descriptors/Keywords: BOOK CHAPTER; MEETING PAPER: LEAD; IRON.;
ZINC; ENVIRONMENTAL TOXICITY
Concept Codes:
*13010 . Metabolism-Minerals
*15002 . Blood, Blood-Forming Organs an.d Body Flulds-BJood
and Lymph Studies
* 16506
Reproductive System-Pathology
*22506
Toxicology-EnvIronmental and Industrial Toxicology
*25502
Developmental B1ology-Embryology-Genera1 and
Descriptive
*26504
Animal Production-Feeds and Feeding
*37014
Public Health: Environmental Health-Sewage Disposal
and Sanitary Measures
*38004
Veterinary Science-Pathology
00520
General Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
10069
Biochemical Studies-Mlnerals
13518
Food Technology-Dairy Products
Blosystematlc Codes:
85715 . Bovldae
Super Taxa:
Animals; Chordates; Vertebrates; Nonhuman Vertebrates;
Mammals; Nonhuman Mammals; Artlodactyls
10914575
BIOSIS Number: 97114575
A short-tenb test for dioxin teratogenicity using chicken
embryos
Henshel D S; Hehn B M; Vo M T; Steeves J D
India***' Unlv. Sch. Public Environ. Affairs, Bloomington. IN
015476
BIOSIS
47405, USA
O (0). 1993. 159-174.
Full Journal Title: Gorsuch, J. W., et al. (Ed.). ASTM
(American Society for Testing and Materials) Special Technical
Publication, 1216. Environmental toxicology and risk
assessment. 2nd volume; Symposium on Environmental Toxicology
and Risk Assessment: Aquatic, Plant, and Terrestrial,
Pittsburgh, Pennsylvania, USA, April 26-30, 1992. x11+730p.
American Society for Testing and Materials (ASTM):
Philadelphia, Pennsylvania, USA. ISBN 0-8031-1485-0.
ISSN: 0066-0558
Language: ENGLISH
Document Type: BOOK; CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 043468
Descrlptors/Keywords: BOOK CHAPTER; MEETING RAPER;
ENVIRONMENTAL TOXICITY TESTING METHOD
Concept Codes:
*22501 . Toxicology-General; Methods and Experimental
*22506 . Toxicology-Environmental and Industrial Toxicology
*25503 . Developmental B1ology-Embryology-Pathoioglcal
*25552 . Developmental Biology-Embryology-DescriptIve
Teratology and Teratogenes1s
*37015 . Public Health: Environmental Health-Air, Water and
Sol 1 Pollution
00520 . General Biology-Symposia, Transactions and
Proceedings of Conferences. Congresses, Review
Annuals
10060
Biochemical Studies-General
Blosystematlc Codes:
85536 . Galllformes
Super Taxa:
Animals; Chordates; Vertebrates; Nonhuman Vertebrates;
B1 rds
10911371
BIOSIS Number: 97111371
Enhanced fatty-acid synthase (FAS) activity In hypertrophic
alveolar type II cells from silica-treated rats: Studies on
function and messenger RNA levels
Rami J; Stenzel W; Puel-M'RInl C; Besombes J P; Rooney S A
INSERM CJF 9107, 31054 Toulouse, FRA
Molecular Biology of the Cell 4 (SUPPL.). 1993. 335A.
Full Journal Title: Thirty-third Annual Meeting of the
American Society for Cell Biology, New Orleans, Louisiana,
USA, December 11-15, 1993. Molecular Biology of the Cell
ISSN: 1059-1524
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 040264
Descriptors/Keywords: MEETING ABSTRACT; MEETING POSTER;
TOXICITY; CHOLINE PHOSPHATE CYTIDYLYLTRANSFERASE
Concept Codes:
*02506 . Cytology and Cytochemistry-Animal
(cont. next page)
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DIALOG File 55: BXOSIS PREVIEWS(R)_1935-1994/MAR ISS 12 (c) 1994
10908624
BIOSIS Number: 97108624
Volatilizing toxic metals from soil
Clifford D A; Chen S-S; Reznik C; Hampton M
Dep. Civil and Environ. Eng., Unlv. Houston, Houton, TX
77204-4791, USA
Waste Management 13 (5-7). 1993. 520.
Full Journal Title: Symposium on Emerging Technologies:
Metals, Oxidation, and Separation, Belmont, Texas, USA, February 25-26, 1993. Waste Management
ISSN: 0956-053X
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 iss. 003
Ref. 037517
Descriptors/Keywords: MEETING ABSTRACT; LEAD; LEAD SULFIDE;
LEAD SULFATE; LEAD NITRATE; LEAD CARBONATE; LEAD OXIDE; CADMIUM; MERCURY; ZINC; ARSENIC; SELENIUM
Concept Codes: *22506 . Toxicology-Environmental and Industrial Toxicology
*37014 . Public Health: Environmental Health-Sewage Disposal
and Sanitary Measures
*37015 . Public Health: Environmental Health-Air, Water and
Sol 1 Pollution
*52005 . Soil Science-Physics and Chemistry (1970- )
00520 . General Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
10059 . Biochemical Methods-Mlnerals
10908606
BIOSIS Number: 97108606
Volatilizing toxic metals from soil
Clifford D A; Chen S-S; Reznik C
Dep. Civil and Environ. Eng., Unlv. Houston, Houston, TX
77204-4791, USA
Waste Management 13 (5-7). 1993. 467-479.
Full Journal Title: Symposium on Emerging Technologies:
Metals, Oxidation, and Separation, Belmont, Texas, USA,
February 25-26, 1993. Waste Management
ISSN: 0956-053X
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 037499
Descriptors/Keywords: MEETING PAPER; LEAD SULFATE; LEAD
CARBONATE; LEAD NITRATE; LEAD; CADMIUM; MERCURY; ZINC;
ARSENIC; SELENIUM; BATTERY WASTE SITE
Concept Codes:
*22506 . Toxicology-Environmental and Industrial Toxicology
*37014 . Public Health: Environmental Health-Sewage Disposal
and Sanitary Measures
,*37015 . Public Health: Envlronmenta1 Health-Air, Water and
Soil Pollution
*52805 . SoM Science-Physics and Chemistry (1970- )
00520 . General Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
015478
BIOSIS 10059
Biochemical Methods-Mlnerals
10905778
BIOSIS Number: 97105778
Generation of reactive oxygen from the copper-mediated
oxidation of the benzene metabolite, 1,4-hydroqulnone: Role In
DNA damage
LI Y; Kuppusamy P; Zweier J L; Trush M A
Johns Hopkins Med. Inst., Baltimore, MD, USA
Free Radical Biology & Medicine 15 (5). 1993. 540.
Full Journal Title: 1st Annual Meeting of the Oxygen
Society on Oxygen, Charleston, .South Carolina, USA, November
12-17, 1993. Free Radical Biology & Medicine
ISSN: 0891-5849
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 034671
Descriptors/Keywords: MEETING ABSTRACT; TOXICITY
Concept Codes:
*13002 . Metabolism-General Metabolism; Metabolic Pathways
*13010 . Metabolism-Minerals
*22501 . Toxicology-General; Methods and Experimental
00520 . General Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
* Annuals
10012 . Biochemistry-Gases (1970- )
10060 . Biochemical Studles-General
10062 . Biochemical Studles-Nuclelc Acids, Purines and
Pyrimidines
10069 . Biochemical Studles-Mlnerals
Blosystemat1c Codes:
33000 . Animalla-Unspeolfled Super Taxa:
Animals
10904133
BIOSIS Number: 97104133
Leukemia induced by chemicals
Snyder R
Joint Graduate Program Toxicol., Environmental Occupational
Health Sci. Inst., Rutgers State Unlv. New Jersey/UMDNJ-Robert
Wood Johnson Med. Sch., 681 FrelInghuysen Road, Plscataway, NJ
08855-1179, USA
Annals of Hematology 67 (SUPPL.). 1993. A119.
Full Journal Title: Annual Meeting of the German and the
Austrian Society of Hematology and Oncology, Essen. Germany,
October 10-13, 1993. Annals of Hematology
ISSN: 0939-5555
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 033026
Descriptors/Keywords: MEETING ABSTRACT; HUMAN; BENZENE;
ENVIRONMENTAL TOXICITY; APLASTIC ANEMIA; ANALYTICAL METHOD
(cont. next page)
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DIALOG File 55: BIOSIS PREVIEWS(R)_1985-1994/KAR XSS 12 (c) 1994
Concept Codes:
*15001 . Blood, Blood-Forming Organs and Body
Flulds-General; Methods
* 15006
Blood, Blood-Forming Organs and Body Flulds-Blood,
Lymphatic and Reticuloendothelial Pathologies
*15008
Blood, Blood-Forming Organs and Body Flulds-Lymphatlc Tissue and Reticuloendothelial
System
*22506
Toxicology-EnvIronmental and Industrial Toxicology
*24007
Neoplasms and Neoplastic Agents-Carclnogens and
Card nogenes 1 s
*24010
Neoplasms and Neoplastic Agents-Blood and
Retlculoendothellal Neoplasms
*37015
Public Health: Environmental Health-Air. Water and
Sol 1 Pollutlon
00520
General Biology-Symposia. Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
10050 . Biochemical Methods-General
10060 . Biochemical Studles-General
Blosystematlc Codes:
86215 . HornInidae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans
10901738
BrOSrS Number: 97101738
Blood lead levels and neuropsychologic function in elderly
women
Muldoon S B; Cauley J A; Kuller L; Scott J
Univ. Pittsburgh, Pittsburgh, PA 15261,. USA
American Journal of Epidemiology 138 (8). 1993. 644-645.
Full Journal^, Title: Twenty-sixth Annual Meeting of the
Society for Epidemiologic Research, Keystone, Colorado, USA,
June 16-18, 1993. American Journal of Epidemiology
ISSN: 0002-9262
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref. 030631
Descriptors/Keywords: MEETING ABSTRACT; HUMAN; TOXICITY;
EPIDEMIOLOGY; DIAGNOSIS; PATHOLOGY; COGNITIVE FUNCTION;
PSYCHOMOTOR SPEED; SENSORIMOTOR FUNCTION
Concept Codes:
*15006 . Blood, Blood-Forming Organs and Body Flulds-Blood,
Lymphatic and Reticuloendothelial Pathologies
*20506 . Nervous System-Pathology 21002 . Psychiatry-Psychopathology; Psychodynamics and
Therapy
*22501 . Toxicology-General; Methods and Experimental
*24500 . Gerontology
*37054 . Public Health: Epidemiology-Organic Diseases and
Neoplasms 00520 . Gerleral Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
10060 . Biochemical Studles-General
015479
BXOSIS 10069 . Biochemical Studles-Mlnerals 12512 . Pathology, General and Miscellaneous-Therapy (1971-
)
Blosystematlc Codes: . 86215 . Homlnldae '
Super Taxa: Animals; Chordates; Vertebrates; Mammals; Primates; Humans
10901732
BIOSIS Number: 97101732
Blood lead levels among radiator repair workers in Colorado
Dalton C B; McCammon J B; Hoffman R E
Colorado Dep. Health. Denver, CO 80222, USA
American (Journal of Epidemiology 138 (8). 1993. 643. Full Journal Title: Twenty-sixth Annual Meeting of the
Society for Epidemiologic Research, Keystone, Colorado, USA,
June 16-18, 1993. American Journal of Epidemiology
ISSN: 0002-9262
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 003
Ref.' 030625
Descriptors/Keywords: MEETING ABSTRACT; HUMAN; EPIDEMIOLOGY:
OCCUPATIONAL HEALTH; TOXICITY
Concept Codes:
*15006 . Blood, Blood-Forming Organs and Body Flulds-Blood,
Lymphatic and Retlculoendothellal Pathologies
*22501 *37013
Toxicology-General; Methods and Experimental Public Health: Environmental Health-Occupational
Health
*37054
Public Health: Epidemiology-Organic Diseases and
Neoplasms
00520
General Biology-Symposia, Transactions and Proceedings of Conferences, Congresses, Review
Annuals
10060
Biochemical Studles-General
10069
Biochemical Studles-M1nera1s
Blosystematlc Codes:
86215 . Homlnldae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans
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DIALOG File 55: BIOSIS PREVIEWS(R)_1985-1994/Mar Iss 16 (c) 1994
115697
The Province of Ontario has had a surveillance program for
workers in dusty industries for almost 70 years. This paper
reports
the detection rates of silicosis among 68,701
silica-exposed Individuals who were first exposed to dust In
1950 or later, and who were still employed In 1979 or later.
The detection rate varied strongly with latency, being less
than two new cases per 10,000 examinations during the first
two decades from first exposure, reaching two new cases per
1,000 examinations at 27 years from first exposure, and
averaging between
two
and
four new cases per 1,000
examinations thereafter. The silicosis incidence rate among
miners was only about half that among foundry workers.
Cigarette smoking was also found to be a risk factor for the
diagnosis of silicosis. These data were used to model the
detection rate of new cases of silicosis as a function of the
time Interval between examinations, and results are presented
for examination cycles between 2 and 10 years.
Descriptors/Keywords: RESEARCH ARTICLE; HUMAN; OCCUPATIONAL
TOXICITY; DIAGNOSIS; CANADA
Concept Codes:
*12504 . Pathology, General and Miscellaneous-Diagnostic
*16006 . Respiratory System-Pathology
*22506 . Toxicology-Environmental and Industr/lal Toxicology
*37013 . Public Health: Environmental Health-Occupational
Health
10069 . Biochemical Studies-Minerals
Blosystematlc Codes:
86215 . Hominidae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals: Primates; Humans
10982025
BIOSIS Number: 97182025
Chewing electric wire coatings: An unusual source of lead
poisoning
Franco G; Cottica D; M'inoia C
Cattedra di Med. dellavoro del 1'Universita di Modina, via
Campl 287, 1-41100 Modena, ITL
American Journal of Industrial Medicine 25 (2). 1994.
291-296.
Full Journal Title: American Journal of Industrial Medicine
ISSN: 0271-3586
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 008 Ref.
115695
This report describes a case of lead poisoning occurring in
an. electrician as the result of an unusual personal habit,
namely, the chewing of lead-containing coatings of electric
wires. A coating chewing test showed that a few minutes after
beginning chewing, saliva lead concentration Increased from 10
mu-g/1 to several milligrams per liter. This case Is an
example of (poisoning caused by an occupationally related
source (coatings containing lead) as a consequence of a
singular and unconventional worker's habit.
Descriptors/Keywords: CASE STUDY; HUMAN; EMPLOYEE BEHAVIOR;
HYGJ'
OCCUPATIONAL TOXICOLOGY
014804
BIOSIS Concept Codes: *21002 . Psychiatry-Psychopathology; Psychodynamics and
Therapy *22506 . Toxicology,^Environmental and Industrial Toxicology *37013 . Public Health: Environmental Health-Occupational
Health 07004 . Behavioral Biology-Human Behavior 10060 . Biochemical Studles-General Blosystematlc Codes: 86215 . Hominidae Super Taxa: Animals; Chordates; Vertebrates; Mammals; Primates; Humans
10982024
BIOSIS Number: 97182024
Muconic acid in urine: A reliable indicator of occupational
exposure to benzene
Lauwerys R R: Buchet J-P; Andrlen F
Industrial Toxicology Occupational Med. Unit, Fac. Med.,
Catholic Univ. Louvain, 30.54. cios Chapelle-aux-Champs, 1200
Brussels, BEL
American Journal of Industrial Medicine 25 (2). 1994.
297-300.
Full Journal Title: American Journal of Industrial Medicine
ISSN: 0271-3586
Language: ENGLISH
Print Number: Biological Abstracts Vol. 097 Iss. 008 Ref.
115694
In male subjects not occupationally exposed to benzene, the
concentration of muconic acid (MA) in urine Is usually below
0.5 mg/g creatinine. At ambient levels of benzene exposure
(below 0.01 ppm), the mean MA level was greater in 21 smokers
than In 14 nonsmokers. In 38 male subjects employed In garages
and coke ovens, a statistically significant correlation was
found between the airborne concentration of benzene measured
with passive monitors and MA in postshift urine. The.mean
postshift MA concentrations corresponding to a benzene 8-hour
time-weighted average exposure (TWA) of 0.5 and 1 ppm were 0.8
and 1.4 mg/g creatinine, respectively.
Descriptors/Keywords: RESEARCH ARTICLE; HUMAN; OCCUPATIONAL
TOXICOLOGY
Concept Codes:
*15506 . Urinary System and External Secretlons-Pathology
*22506 . Toxicology-Environmental and Industrial Toxicology
*37013 . Public Health: Environmental Health-Occupational
Hea1th
10060 . Biochemical Studles-General
Blosystematlc Codes:
86215 . Hominidae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans
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DIALOG File 55: BIOSIS PREVIEWS(R)_198S-1994/Mar Iss 16 (c) 1994
Investigative Dermatology and the Western Student Medical
Research Committee, Carmel, California, USA, February 9-12,
1994. Clinical Research
ISSN: 0009-9279
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 004
Ref. 055034
Descriptors/Keywords: MEETING ABSTRACT; RAT; LUTEINIZING
HORMONE; GONADOTROPIN; GONADOLIBERIN; LHRH; TRANSCRIPTIONAL
MESSENGER RNA LEVEL; MALE REPRODUCTIVE TOXTCITY
Concept Codes:
*03506 . Genetics and Cytogenetics-Animal
*03510 . Genetics and Cytogenetics-Sex Differences
10300 . Replication, TranscrIpt1 on. Translation
*13014 . Metabolism-Nucleic Acids, Purines and Pyrimidines
16506 . Reproductive System-Pathology
*17006 . Endocrine System-Gonads and Placenta
*17014 . Endocrine System-Pituitary
*17020 . Endocrine System-Neuroendocrinology (1972- )
20504 . Nervous System-Physiology and Biochemistry
*22501 . Toxicology-General; Methods and Experimental
00520 . General Biology-Symposia, Transactions and
Proceedings of Conferences, Congresses, Review
Annuals
10062
Biochemical Studles-Nuclelc Acids, Purines and
Pyrimidines
10064
Biochemical Studles-Protelns, Peptides and Amino
Acids
10068
Biochemical Studies-Carbohydrates
10069
Biochemical Studies-Minerals
Blosystemat1c;Codes:
86375 . Muridae
Super Taxa:
Animals; Chordates; Vertebrates; Nonhuman Vertebrates;
Mammals; Nonhuman Mammals; Rodents
10957542
BIOSIS Number: 97157542
Monitoring occupational exposure to some industrial
chemicals by the determination of hemoglobin adducts
Van Sittert N J; Van VI let E W N
Shell Internationale Petroleum Maatschappl B.V., Health
Safety and Environment Dlv., P.0. Box 162, 2501 AN The Hague,
NET
Naunyn-Schmledeberg's Archives of Pharmacology 348 (SUPPL.).
1993. R174.
Full Journal Title: Deutsche Gesellschaft fuer
Pharmakologle und Toxlkologle (German Society for Pharmacology
and Toxicology) Fifth Winter Meeting, Hannover, Germany,
December 1-3, 1993. Naunyn-Schmledeberg's Archives of
Pharmacology
ISSN: 0028-1298
Language: ENGLISH
Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 004
Ref. Of
3
rt i/n ir
ISIS
Descriptors/Keywords:- MEETING ABSTRACT; HUMAN; ETHYLENE OXIDE;
PROPYLENE OXIDE; ETHYLENE; 1.3-BUTADIENE; TOXICITY
Concept Codes:
,1
*10006 . Clinical Biochemistry: General Methods and
Applications
*10054 . Biochemical Methods-Prote1 ns, Peptides and Amino
Acids
*22506 . Tox1 cology-Envlronmenta1 and Industrial Toxicology
*37013 . Public Health: Environmental Health-Occupational
Health
00520 . General B1ology-Symposla, Transactions and
Proceedings of Conferences, Congresses, Review
Annua 1s
10060
B lochemlca1 Studies-Genera 1
10064
Biochemical Studles-Protelns. Peptides and Amino
Ac Ids
10065
Biochemical Studfes-Porphyr1ns and Bile Pigments
B1osystemat1c Codes:
86215 . Homlnldae
Super Taxa:
Animals; Chordates; Vertebrates; Mammals; Primates; Humans
10957540
BIOSIS Number: 97157540
Biomonitoring and subcllnlcal effect In tetraethyl lead
exposed persons in Hubei, China
Zhang W; Golka K
Inst. Occupational Med., Tonglj Med. Unlv., Wuhan/Hubei,
430030, CHN Naunyn-Schmledeberg's Archives of Pharmacology 348 (SUPPL.).
1993. R174.
Full Journal Title: Deutsche Gesellschaft fuer
Pharmakologle und Toxlkologle (German Society for Pharmacology
and Toxicology) Fifth Winter Meeting. Hannover, Germany,
December 1-3, 1993. Naunyn-Schmledeberg's Archives of
Pharmaco1ogy
ISSN: 0028-1298
Language: ENGLISH Document Type: CONFERENCE PROCEEDINGS
Print Number: Biological Abstracts/RRM Vol. 046 Iss. 004
Ref. 054141
Oescriptors/Keywords: MEETING ABSTRACT; TOXICOLOGY; GASOLINE
ADDITIVE; OCCUPATIONAL HEALTH; URINE
Concept Codes:
*15504
Urinary System and External Secretlons-Physlology
*22506
and Biochemistry Toxicology-Environmental and Industrial Toxicology
*37013
Public Health: Environmental Health-Occupational
Health
00520
General Biology-Symposia, Transactions and Proceedings of Conferences, Congresses, Review
Annuals
10069
Biochemical Studles-Minerals
Blosystemat1c Codes:
86215 . Homlnldae
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dysfunctional
despite
continued
oxygen
ventilation.
Spontaneous breathing and cardiovascular performance following
STX-induced apnea could all be promptly restored (typically in
less than a minute) by combined oxygen/antitoxin therapy.
Notable also was a state of uncompensated acidemia (as
revealed by changes in arterial pH and C02 tension) which
persisted throughout the course of therapeutic Intervention.
Notwithstanding, the ventilatory frequency continued to be
low,
the
central respiratory activity pattern remained
aberrant, and the ECoG amplitudes were still depressed. In
consideration of these findings, and of the large molecular
weight of alpha-STX antitoxin (> 150,000 Da) which limits its
entry into the CNS, we are of the opinion that the therapeutic
effects of antitoxin are probably confined primarily to the
periphery.
Tags: Animal
Descriptors:
*Ant 1 toxins--Immunology--IM;
*Antitoxins
--Therapeutic
Use--TU;
`Cardiac Output. Low --Chemically
Induced--CI;
*Cardlac Output, low--Therapy--TH; `Respiratory
Insuff1c1ency--Chemleal 1y Induced--CI; `Respiratory Insuffici
ency--Therapy--TH;
*Sax1toxin--Immunology--IM;
`Saxltoxin
--Toxlclty--T0; Adrenal Glands--Drug Effects--DE; Antibodies
--Therapeut1c Use--TU; Cardiac Output, Low--Phys1opathology
--PP; Cardiovascular System--Drug Effects--DE: Electrocardiogr
aphy; Electrophysiology; Guinea Pigs: Oxygen Inhalation
Therapy;
PerIssodactyla;
Respiratory
Insufficiency
--Phys1opatho1ogy--PP
CAS Registry No.: 0
.(Antibodies); 0
.(Antitoxins);
35523-89-8 .(Saxltoxln)
08805516
9f120516
Pharmacokinetic interaction between benzene metabolites,
phenol and hydroquInone, in B6C3F1 mice.
Legathe A; Hoener BA; Tozer TN
Department of Pharmacy, School of Pharmacy, University of
California at San Francfsco 94143-0446.
Toxicol Appl Pharmacol (UNITED STATES)
Jan 1994, 124 (1)
p131-8, ISSN 0041-008X
Journal Code: VWO
Contract/Grant No.: ES 04705, ES, NIEHS
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
There Is strong evidence that metabolites are responsible
for
adverse
effects of benzene. Benzene myelotoxicity,
reproduced by coadministering phenol (PH) and hydroqutnone
(HO) but not when these benzene metabolites were administered
alone, has been postulated to be induced by PH stimulating the
myeloperoxidase-mediated oxidation of HO to the toxic
1.4-benzoquinone In bone marrow. A pharmacokinetic Interaction
between PH and HO is also hypothesized to contribute to the
observation.! Both
metabolites
are
sulfoconjugated and
glucuronoconjugated. Sulfoconjugation of phenolic substrates
has been shown to approach saturation at high concentrations
in rats. Thus, more PH may be converted to HO and HO
conjur * on may be diminished. These effects would Increase
101714
the amounts of PH and HO present and result (by further
oxidation) in the formation of more 1,4-benzoqu1 none. To test
this hypothesis, we investigated the pharmacokinetics in blood
and the recovery of 'hydroqu1 none and phenol in urine when the
metabolites were administered 1ntraperitoneal1y alone or in
combination at 75 mg/kg each to B6C3F1 mice. The combination
resulted in a 2.6-fold Increase in the area under the blood
concentration-time curve (AUC) of HQ compared to the sum of
AUC values observed after administration of each compound
alone. The half-life of HQ was also increased from 9 +/- 2 to
15 +/- 3 min. The AUC of PH was increased by a factor of 1.4.
The clearance of phenol decreased from 89 +/- 13 ml/min per
kilogram when injected alone to 62 +/- 7 ml/min per kilogram
after coadministration. A decreased clearance of formation of
each conjugate demonstrated that both conjugation pathways
were diminished. This interaction may contribute to the
observed production of myelotoxicity when these metabolites
are coatim1n1stered.
Tags: Animal; Male; Support, Non-U.S. Gov't; Support. U.S.
Gov't, P.H.S.
Descriptors:
`Benzene--Toxic1ty--TO;
`Hydroquinones
--Pharmacokinetics--PK; `Phenols--Pharmacokinetics--PK; Benzen
e - - Metabol 1 sro- -ME ; Drug I r> teract 1 ons; G1 ucuronates--Ur 1 ne- - UR ;
Hydroqu!nones--Blood--BL;
Hydroqu!nones--Pharmacology--PD;
Hydroquinones--Ur 1ne--UR; Mice; Mice, Inbred Strains; Models,
Biological;
Phenols--B1ood--BL;
Phenol s--Pharmaco1ogy--PD:
Phenols--Ur1ne--UR; Sulfates--Ur1ne--UR
CAS Registry No.: 0 .(G1ucuronates); 0 .(Hydroquinones); 0
.(Phenols); 0
.(Sulfates); 108-95-2
.(phenol); 123-31-9
.(hydroquinone); 71-43-2 .(Benzene)
08805515
94120515
Role of quinone reductase in In vivo ethanol metabolism and
toxicity.
Chung JH; Cha YN; Rubin RJ
Division of Toxicological Sciences, School of Hygiene and
Public Health, Johns Hopkins University, Baltimore, Maryland
21205.
Toxicol Appl Pharmacol (UNITED STATES)
Jan 1994, 124 (1)
p123-30, ISSN 0041-008X
Journal Code: VWO
Contract/Grant No.: RO1-AA06O49, AA, NIAAA
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
Quinone reductase
(QR). In the presence of suitable
substrate, results in the regeneration of NAD+ from NADH. To
test the hypothesis that QR can play a role in ethanol
metabolism and toxicity, we studied the effect of a quinone as
well as of Induced levels.of QR on ethanol administered in
vivo to male rats and mice. Butylated hydroxyanlsole (BHA) Is
known both to induce QR and to be metabolized to tert-butyl
quinone (TBQ). Dietary BHA (0.75% for 10 days), followed by
oral ethanol (4 g/kg, by gavage), increased the rate of
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Tags: Animal
Descriptors: *Acet1c Aclds--Tox1city--TO; *Furans--Toxicity
--TO;
`Water
Supply; Acetic Ac 1ds--Pharmacok1 net 1cs--PK;
Carcinogenicity
Tests; Furans--Pharmacok1 net 1cs--PK; Mice;
Mutagenicity Tests; Research; Sa1 monel 1 a--Drug Effects--DE;
Sa1mone1 la--GenetIcs--GE; Sterilization
CAS Registry No.: 0 .(Acetic Acids); 0 .(Furans)
08791828 94106828
Presence and Importance of organochlorlne solvents and other
compounds In Germany's groundwater and drinking water.
Dieter HH; Kerndorff H
Institute for Water-. Soil- and Air Hygiene of the Federal
Health Office of Germany (BGA), Berlin.
Ann 1st Super Sanlta (ITALY)
1993, 29 (2) p263-77, ISSN
0021-2571
Journal Code: 5BP
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
Organochlorlne compounds are widely used in Germany although
the Inland production of chlorinated solvents has greatly
decreased since 1985. Data on groundwater contamination are
incomplete, but there are some regional data sets from the
States (Lander). Approximately 25% of the groundwater samples
contain more than 1 mlcrogram/1 of a single solvent, the most
prominent
ones
being
tri-
and
tetrachloroethene,
1,1,1 -tr1 chioroethane
and
dichloromethane,
but
also
chloroform. The most Important causes for contaminations of
the groundwater are unprotected storage and leaking sewage
systems.
Abandoned waste sites are. besides chlorinated
compounds, aiso a source of many other contaminants. A ranking
procedure
according
to
their
exposure
potential
(concentration.
Incidence,
toxicology) is proposed. The
compound of greatest concern Is vinyl chloride, which Is
formed
from
tri-
and tetrachloroethene under reducing
conditions In the subsoil. The most important contaminant In
drinking
water
is
tetrachloroethene
followed
by
1,1,1-tr1 chioroethane and tr1 chioroethane. Chlorobenzene may
also be present on occasion, while only about 20% of the
finished drinking waters contain more chloroform after
treatment than before. Only about 10% of all analyses of
drinking water derived from groundwater shows the presence of
organochlorlne
solvents
and
most of these show total
concentrations less than 2 m1crograms/1. The degradation
product, vinyl chloride, was found up to now only In different
groundwaters. To stabilize and to Improve the situation, which
still
Is much more favorable for drinking than for
groundwater, precautions are going to be taken which should
assure that these and other problematic substances which
endanger water are used only in closed systems and rigid
safety measures be Imposed on their disposal and transport.
Descriptors:
`Hydrocarbons,
Chlorinated--Analys1s--AN:
*So1vents--Ana1ysis--AN; `Water Pollutants, Chemical--Analysis
--AN; `Water Pollution, Chemical; `Water Supply--Ana 1ys1s--AN
; Gerr
/; Hydrocarbons, Chlorinated--Metabol1sm--ME; Solvents
101728
-Metabol1sm--ME; Water Pol 1utants, Chemical --Metabol1sm--ME
CAS
Registry
No.: 0
.(Hydrocarbons, Chlorinated); 0
(Solvents); 0 .(Watqr Pollutants, Chemical)
08791780 94106780
Effects of alcohol
carbon tetrachloride, and choline
deficiency on iron metabolism in the rat.
Batey RG; Johnston R
Department of Medicine, Westmead Hospital , New South Wales,
Austra11a.
Alcohol Clin Exp Res (UNITEO STATES)
Oct 1993, 17 (5)
p931-4. ISSN 0145-6008
Journal Code: 35X
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
The effects of alcohol on hepatic iron uptake and Intestinal
Iron transport were studied In rats fed a nutritionally
replete liquid diet containing varying quantities of ethanol.
Results were compared with those from animals exposed to
carbon tetrachloride (CCJ4) to produce hepatocellular necrosis
or a choline-deficient diet to produce steatosis and
cirrhosis. A high ethanol intake for 4 or 10 weeks produced
hepatic steatosis. CC14 produced hepatocellular necrosis.
Choline
deficiency
was
associated
with steatosis +/-
cirrhosis.
Intestinal
Iron transport was unaffected by
ethanol, CC14, or choline deficiency. Hepatic Iron uptake was
significantly
depressed In rats consuming 11.7 g/kg/day
ethanol (p < 0.01) for 4 weeks. Choiine-defIclent animals
studied at 14 weeks also had significantly decreased hepatic
Iron uptake (p < 0.01); results were similar In the cirrhotic
and noncirrhotic animals. Conversely, CC14 exposure produced a
significant 5-foJd Increase in hepatic Iron uptake (p <
0.001). Results suggest that ethanol consumption, fatty liver,
and cirrhosis are not responsible for any Increase In iron
absorpt1 on or of hepatic Iron uptake In the rat model. Acute
hepatocelfular Injury is followed by increased hepatic Iron
uptake.
Tags: Animal; Female; Support, Non-U.S. Gov't
Descriptors:
Alcohol,
Ethy1 --Tox1c1ty--TO;
`Carbon
Tetrachlor 1de--Tox1c1ty--TO; `Choline DefIdency--Blood--BL;
`Hepatitis, Toxic--Blood--BL; `Intestinal .Absorption --Drug
Effects--DE; * Iron--B1ood--BL;
*L1ver--Drug
Effects--DE;
`Liver
Diseases, A1cohol1c--B1ood--BL; Choline Deficiency
--Pathology--PA; Fatty Liver, A1cohol1c--B1ood--BL; Fatty
Liver, A1cohol1c--Patho1ogy--PA; Hepatitis. Tox1c--Pathology
--PA; Intestinal Absorpt1 on--Phys1ology--PH; L1ver--Metabol1sm
--ME; L1ver--Patho1ogy--PA; Liver Cirrhosis, A1cohol1c--B1ood
--BL;
Liver Cirrhosis,
A1cohol1c--Pathology--PA; Liver
Diseases, A1cohol1c--Pathology--PA; Rats; Rats, Wistar; Weight
Gain--Drug Effects--DE; Weight Ga1n--Phys1ology--PH
CAS Registry No.: 56-23-5 .(Carbon Tetrachloride); 64-17-5
.(Alcohol, Ethyl); 7439-89-6 .(Iron)
Dinner
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08791583 94106583
~
Intracellular mechanism of Pb(2+)-Induced norepinephrine
release from bovine chromaffin cells.
Tomslg JL; Suszklw JB
Department of Physiology and Biophysics, UUnni viveersrs1ity of
Cincinnati College of Medicine, Ohio 45267-0576.
Am J Physiol (UNITED STATES)
Dec 1993,
265
(6 Pt 1)
pC1630-6, ISSN 0002-9513
Journal Code: 3U8
Contract/Grant No.: ES-04090, ES, NIEHS
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
The Intracellular mechanism of Pb(2+)- 1nduced release of
norepinephrine (NE) was investigated In comparison with Ca2+
In bovine chromaffin cells permeab111 zed with staphylococcal
alpha-toxin. Pb2+ activated NE release at considerably lower
concentrations
(concentration of free metal giving half
maximal meta1-dependent release (K0.5) 4.6 nM] than Ca2+ (K0.5
2.4 mlcroM). The release of NE was associated with the release
of dopamine-beta-hydroxylase but not lactate dehydrogenase.
The maximal secretory responses produced by Pb2+ and Ca2+ were
similar and nonadditive. Pb(2+)- and Ca(2+)-dependent releases
showed a similar requirement for MgATP and were equally
enhanced
by
protein
kinase
C activator
12-0-tetradecanoylphorbol 13-acetate (TPA) but not by kinase A
activator 8-bromoadenos1ne 3',5'-cyclic monophosphate free
base. The protein kinase C Inhibitor staurosporlne blocked the
TPA-stlmulated component of secretion but had no effect on the
NE release in the absence of TPA. Calmldazollum, an Inhibitor
of calmodulin. Inhibited the secretion evoked by both metals
to similar extent. Agents interacting with microtubules
(colchicine and vinblastine) or mlcrof1 laments (cytochalasln B
and phalloldln) had no effect on secretion Induced by either
metal cation. These observations Indicate that both Pb2+ and
Ca2+ act at a common site and activate the exocytotlc release
of NE by an analogous mechanism.
Tags: Animal; Comparative Study; Support, U.S. Gov't, P.H.S.
Descriptors:
*Adrenal
Medulla--Phys1ology--PH; -Calcium
--Pharmacology--PD;
* Lead--Tox1c1ty--TO;
`Norep 1nephr1ne
--Metabol1sm--ME; Adenosine Tr1phosphate--Pharmacology--PD;
Adrenal Medulla--Drug Effects--DE; A1ka1 olds--Pharmacology--PD
; Calc1um--Metabol1sm--ME;
Calmodulin --Antagonists
and
Inhlbltors--AI; Cattle; Cell Membrane Permeability; Cells,
Cultured; Cyclic AMP-Dependent Protein K1nases--Metabol1sm--ME
; Dose-Response Relationship, Drug; Egtazlc Ac Id--Pharmaco1ogy
--PD;
Enzyme
Activation;
Imldazoles--Pharmacology--PD;
Kinetics; Lactate Dehydrogenase--Ana1ysis--AN; Protein Kinase
C--Antagon1sts
and Inhlbltors--AI;
Protein
Kinase
C
--Metabol1sm--ME;
Spectrophotometry,
Atomic
Absorption;
Tetradecanoylphorbol Acetate--Pharmacology--PD; B-Bromo Cyclic
Adenos1ne Monophosphate--Pharmaco1ogy--PD
CAS Registry No.: 0
.(Alkaloids); 0
.(Calmodulin); 0
. (Imidazoles)*; 16561-29-8
. (Tetradecanoylphorbol Acetate);
23583-48-4 .(8-Bromo Cyclic Adenosine Monophosphate); 51-41-2
.(Norepinephrine);
56-65-5
.(Adenosine Triphosphate);
57265-6K-3
.(R 24571); 62996-74-1 .(staurosporine); 67-42-5
101729
.(Egtazlc Acid); 7439-92-1 .(Lead); 7440-70-2 .(Calcium)
Enzyme No.: EC -1.1.1.27
.(Lactate Dehydrogenase); EC
2.7.1.-
.(Protein Kinase
C);
EC 2.7.10.-
.(Cyclic
AMP-Dependent Prote1n/K1nases)
08791132
94106132
[Correction of disorders in the monooxygenase system
function
with
dlethylnlcotinamlde
(cord1 amine)
In
tetrachloromethane- Induced and viral hepatitis]
Korrekts11a dletllnlkotlnamldom (kordlamlnom) narushenlla
funktsll monooks1genazno1 slstemy prl tetrakh1ormetanovom 1
vlrusnom gepatltakh.
Zavodnlk LB; Luklenko PI; Bushma MI; Shoka AIu; Tsyrkunov VM
Vopr Med Khlm (RUSSIA)
Sep-Oct 1993, 39 (5) p45-7, ISSN
0042-8809
Journal Code: XIQ
Languages: RUSSIAN
Summary Languages: ENGLISH
Document type: JOURNAL ARTICLE
English Abstract
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
Content of cytochromes P-450 and b5 and the rate of
oxidative dealkylation In liver mlcrosomes as well as the
antipyrlne pharmacok1 net 1cs were normalized in rats with acute
CCl4-lnduced hepatitis
after
treatment with cordiamine
(diethyl nicotinamide) at a dose of 40 mg, subcutaneously, 2
times dally within 4 days. Cordiamine (30 drops 3 times dally
within S days)
contributed
to normalization of the
hydroxylating reaction in liver tissue of patients with viral
hepatitis A, estimated by the "antipyrlne" test. The drug
exhibited stabilizing effect on hydrophobic interactions In
microsomal
membranes;
diethyl
nicotinamide possessed
antiradical and vitamin properties.
Tags: Animal; Female; Human; Male
Descriptors:
`Carbon
Tetrachloride; `Cytochrome
b5
--Antagonists
and
Inhlb1 tors--AI;
`Cytochrome
P-450
--Antagonists and Inhlbitors--AI; `Hepatitis A--Drug Therapy
--DT;
`Hepatitis,
Toxic--Drug
Therapy--DT; `Nikethamide
--Therapeutic Use--TU; Adolescence; Adult; Mlcrosomes, Liver
--Enzymology--EN; Rats
CAS Registry No.: 56-23-5 .(Carbon Tetrachloride); 59-26-7
.(Nikethamide); 9035-39-6
.(Cytochrome
b5);
9035-51-2
.(Cytochrome P-450)
08790738
94105738
[Hematologic changes In patients chronically exposed to
benzene]
Alteracoes hemato 1ogicas em pacientes expostos cronlcamente
ao benzeno.
Ruiz MA; Vassallo J; de Souza CA
Setor de Hematol ogia, Fa,culdade de Cienclas Medicas de
Santos (FCMS), SP, Brasil.
Rev Saude Publlca (BRAZIL)
Apr 1993, 27 (2) p145-51,
ISSN 0034-8910
Journal Code: T5X
Languages: PORTUGUESE
Summary Languages: ENGLISH
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Document type: JOURNAL ARTICLE
English Abstract
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
A study was carried out Into the hematological abnormalities
of peripheral blood bone marrow in patients chronically
exposed to benzene. The metabolic biotransformat ion and the
mechanisms Involved In toxicity are described. Hematological
data are described and discussed. Macrocytosls and lymphopenia
are the earliest hematological signs of benzene toxicity. Bone
marrow abnormalitles are demonstrated by the complementary
methods of cytology and histology. Global hypocel1u1ar1ty was
mainly
due
to
the
granulocytic series. Mastocytosis,
eosinophil la
and magakarlocy11c
abnormalities are also
presented.
Inflammatory
abnormalitles
and
signs
of
dismyelopolese could also be observed. The importance of
peripheral blood abnormalities and the need for a critical
approach to this Important public health problem are
emphasized.
Tags: Human; Support. Non-U.S. Gov't
Descriptors: *Benzene--Po1sonlng--PO; ^Hematologic Diseases
--Chemical 1y Induced--Cl; *0ccupatlonal Diseases--Chemically
Induced--CI;
*0ccupat1onal
Exposure--Adverse Effects--AE ;
Benzene--Metabo11sm--ME; Bone Marrow--Drug Effects--DE; Bone
Marrow--Patho1ogy--PA;
Hematologic
Diseases--B1ood--BL;
Occupational Dlseases--Blood--BL; Risk Factors
CAS Registry No.: 71-43-2 .(Benzene)
08790460
94105460
Scientific principles for evaluating the potential for
adverse effects from chlorinated organic chemicals In the
environment. ;
Wines RF; Nestmann ER; Miller PA; Orr JC; Munro IC
CanTox Inc., Mississauga, Ontario, Canada.
Regul Toxicol Pharmacol (UNITED STATES)
ct 1993, 18 (2)
p313-56, ISSN 0273-2300. Journal Code: RBH
Languages: ENGLISH
Document type: JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
The term chlorinated chemicals Is used to describe diverse
groups of chemicals of varying chemical structure, including
those used In water disinfection, as well as numerous
aliphatic, aromatic, and polycyclic chlorinated substances.
This report elaborates a number of scientific principles that
govern the evaluation of the potential for chlorinated organic
chemicals to cause adverse effects on the environment and to
human health. The purpose of the report Is to demonstrate the
Importance of applying these scientific principles In the
evaluation of potential adverse effects of chlorinated organic
chemicals. The four major principles upon which such a
scientific analysis must be based are: (1) the fate and
biological activity of a compound are determined by the
chemical properties of the compound; (2) compounds do not show
adverse effects below certain threshold concentrations, and
the mannltude of response Is related to dose; (3) inherent
metabc
processes allow organisms to accommodate low doses
of chlorinated organic chemicals; (4) observations associated
with the presence of a certain compound must be biologically
plausible effects, b^sed on the specificity of the compound's
activity In experimental systems. With respect to the first of
these principles, there Is abundant scientific evidence that
the physical and chemical properties of chlorinated organic
chemicals
govern
their
bioaccumulatfve
potential,
toxicological properties, and thus their potential behavior
and effects in the environment. Chemicals that have low
solubility in water are highly lipophilic and have Tow vapor
pressure, tend to accumulate in biological systems, and
degrade
slowly
in the environment. Chlorinated organic
chemicals that possess these characteristics Include those
having a carbon ring structure and multiple chlorine
substitution. Other chlorinated organic chemicals with lesser
degrees
of chlorine substitution,
such
as
2.4-dlchlorophenoxyacetic
acid
(2,4-D) ,
tr1 chiorophenol,
chloroform, and dlchloroethane, do not share the physical and
chemical properties of the high molecular weight, cyclic, polychlorinated compounds and, as such, do not have the same
potential
to bioaccumulate.
These
differences
among
chlorinated organic chemicals with respect to their physical
and chemical properties and behavior in the environment
preclude
the
generalization that all organic chemicals
containing chlorine behave similarly In the environment and
act as persistent, bloaccumulative chemicals. The reactivity
of chlorinated organic chemicals and hence their potential to
produce biological effects depends on their specific molecular
features.
The substitution of chlorine into an organic
molecule
may
Increase or may
reduce its biological
activity.(ABSTRACT TRUNCATED AT 400 WORDS) (204 Refs.)
Tags: Animal; Human; Support, Non-U.S. Gov't
Descriptors:
Envlronmenta1
Po11utants--Toxic1ty--TO;
Hydrocarbons,
Chi or 1nated--Tox1city--TO;
Environmental
Pol 1utants--Analysis--AN; Hydrocarbons, Chi orinated--Chemistry
--CH
CAS
Registry
No.:
0
.(Environmental Pollutants): O
.(Hydrocarbons, Chlorinated)
08790459
94105459
Comparing the results of a Monte Carlo analysis with EPA's
reasonable maximum exposed Individual (RMEI): a case study of
a former wood treatment site.
Copeland TL; Paustenbach DJ; Harris MA; Otani J
ChemRisk, a Division of McLaren/Hart, Irvine, California
92714.
Regul Toxicol Pharmacol (UNITED STATES)
Oct 1993, 18 (2)
P275-312, ISSN 0273-2300 Journal Code: RBH
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
In the United States, there are about 250 former sites that
treated wood with preservatives that are now in need of some
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serum,
brain,
liver, kidney and uterus were Increased
significantly by HCH and malathlon exposure. Irrespective of
the protein content In the diet. The incorporation of
[1.2-14C]acetate into the hepatic lipids was stimulated by
both HCH and malathlon, suggesting a higher rate of lipid
synthesis In the liver of normal and protein-deficient diet
fed dams. The low protein content In the diet intensified the
pest 1cide-1nduced changes and more severe alterations were
noticed in HCH exposed dams than In malathlon exposed dams.
Tags: Animal; Female
Descriptors: *Benzene Hexachloride--Tox1c1ty--TO; *L1plds
--Metabolism--ME;
*Malath1 on--Tox1c1ty--TO;
*Pregnancy
Complicat1ons--Metabol1sm--ME; *Pregnancy, Anima1 --Metabol1sm
--ME; *Prote1n-Energy Mainutrltion--Metabol1sm--ME; Cholestero
1 --Metabol1sm--ME: G1ucosephosphate Dehydrogenase--Metabol1sm
--ME; Hydroxymethy1glutary1 CoA Reductases--Metabo11sm--ME;
K1dney--0rug Effects--DE; Kidney--Metabol1sm--ME; Llpolysls
--Drug Effects--DE; Lipoprotein LIpase--Metabo11sm--ME; Liver
--Drug
Effects--DE;
L1ver--Metabol1sm--ME;
Malate
Dehydrogenase--Metabol1sm--ME; PhospholIplds--Metabol1sm--ME;
Pregnancy;
Rats;
Rats,
Sprague-Dawley;
Triglycerides
--Metabol1sm--ME
CAS Registry No.: 0
.(Lipids); O
.(Phospholipids); 0
.(Triglycerides);
121-75-5
.(Malathlon);
57-88-5
.(Cholesterol); 50-89-9 .(Benzene Hexachloride)
Enzyme No.:
EC 1.1.1.37
.(Malate Dehydrogenase); EC
1.1.1.49
.(Glucosephosphate Dehydrogenase); EC 1.1.1.88
.(Hydroxymethy1g1utary1
CoA Reductases);
EC
3.1.1.34
.(Lipoprotein Lipase)
08787258
94402258
Identification
of 6-hydroxy-trans,trans-2,4-hexadienoic
acid, a novel ring-opened urinary metabolite of benzene.
Kline SA; Robertson JF; Grotz VL; Goldstein BD; Witz G
Department
of Environmental
and
Community Medicine,
University of Medicine and Dentistry-New Jersey, Robert Wood
Johnson Medical School, Plscataway.
Environ Health Perspect (UNITED STATES)
Sep 1993, 101 (4)
P310-2, ISSN 0091-6765 Journal Code: EIO
Contract/Grant No.; ES02558, ES, NIEHS; ES05022, ES. NIEHS
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEOICUS
We studied the In vivo metabolism of benzene in mice to
ring-opened compounds excreted In urine. Male CD-I mice were
treated Intraperltoneally
with benzene (110-440 mg/kg),
[14C]benzene (220 mg/kg) or trans, trans-muconaldehyde (MUC; 4
mg/kg), a microsomal, hematotoxlc metabolite of benzene.
Urine, collected over 24 hr, was extracted and analyzed by
HPLC
with
a diode-array detector and by scintillation
counting. Inaddition to trans.trans-muconic acid, previously
the only known ring-opened urinary benzene metabolite, a new
metabol1te, 6-hydroxy-trans,trans-2.4-hexadienolc acid, was
detected In urine of mice treated with either benzene or MUC.
We Idr fled the new metabolite based on coelution of
101735
metabolites and UV
spectral comparison with authentic
standards in unmethylated and methylated urine extracts.
Results presented here are consistent with the Intermediacy of
MUC In the in vivo metabolism of benzene to ring-opened
metabolites.
Tags: Animal; Male; Support. U.S. Gov't. P.H.S.
Descriptors: ^Benzene--Metabolism--ME; *Sorb1c Ac 1d--Analogs
and Derivat1ves--AA; 8enzene--Toxic1ty--T0;. Mice; Mfcrosomes,
L1ver--Metabol1sm--ME;
Sorbic Ac Id--Chem1stry--CH;
Sorbic
Acid--Metabol1sm--ME
CAS
Registry
No.: 110-44-1
.(Sorbic Acid); 505-70-4
.(muconlc
acid);
71-43-2
.(Benzene);
88973-47-1
.(6-hydroxy-2,4-hexadlenolc acid)
087B6126
94101126
A community-based epidemiologic study of health sequelae of
exposure to hydrofluoric acid.
Dayal HH; Brodwlck M; Morris R; Baranowskl T; Trleff N;
Harrison JA; Llsse JR; Ansarl GA
University of Texas Medical Branch, Galveston 77550.
Ann Epidemiol (UNITED STATES)
May 1992, 2 (3) p213-30,
ISSN 1047-2797
Journal Code: BX8
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
An accident at an oil refinery in Texas City, Texas,
released around 40.000 lb of hydrogen fluoride, exposing the
community to the highly toxic and corrosive substance. A
population-based epidemiologic study was conducted to evaluate
the Impact of the accident on the health of the community.
Exposure assessment was done using a multipronged approach
through a door-to-door survey of 10,811 individuals. A symptom
survey resulting in 1994 completed Interviews was conducted
with a stratified random sample selected from the exposure
study database. The sampling was balanced with respect to age,
gender, and predisposition across the three ordinal exposure
categories. The results show a strong dose relationship (P <
10(-4)) between the exposure and symptoms reported following
the accident and 2 years later, most notably breathing and eye
symptoms. However. substantial improvement In health was
reported over the 2-year period regardless of the level of
exposure. Problems of recall bias and behavioral sensitization
are considered and It Is recognized that the study may have
overestimated the effect. It Is also recognized that the study
may not have completely unraveled the relative Importance of
exposure and host response In health outcome, since the two
were probably conflated in the exposure measure. Nevertheless,
the independence of predlsposltIon and reported level of
exposure, the magnitude of effect and its consistency, the
unmistakable dose response, the large sample size, and the
mutual corroboration of various findings make It difficult to
dismiss the interpretation that the hydrofluoric acid exposure
indeed caused health problems in the community that continued
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vanad1uro(IV), which was more obvious In the case of exposure
to vanadlum(V) alone. This suggests that the amount of
vanadium(V) reduced to vanadlum(IV) decreased In GSH-depleted
cells. While vanadlum(IV) at concentrations of 3 x 10(-6) M
and 10(-5) M was not transforming in the cells, vanadlum(V)
showed neoplastic transforming activity (P < 0.025 and P <
0.001 for the two doses, respectively) In comparison to
controls
(vanadium
unexposed
cells).
Cytotoxicity and
morphological transformat1 on In cells exposed to vanadlum(V)
in combination with 3 x 10(-6) M DEM were significantly more
Intensive (P < 0.005 and P < 0.01 for the two doses of
vanadate tested) compared to the corresponding values observed
in cells exposed to vanadlum(V) alone. This suggests that the
final transforming activity response Is dependent on the
Intracellular GSH-medlated mechanism of
reduction of
vanadlum(V)
to vanadium(IV):
(1) the extent to which
vanadlum(V) should be bioreduced to less toxic vanadlum(IV)
via Intracellular GSH Is a key point In determining the
intensity of
the observed neoplastic action; (li) the
carcinogenic potential of vanadlum(V) should be strictly
dependent on Its Intracellular persistence which could lead to
changes In normal metabolic patterns of vanadlum(V) In the
oxidized form due to lack of GSH-medlated reduction.
Tags: Animal
Descriptors: `Cell Transformat Ion, Neop1ast1c--Drug Effects
--DE;
*G1utathlone--Metabol1sm--ME;
`Vanadium Compounds
--Toxlclty--T0; Biotransformation; Cell Survival--Drug Effects
--DE;
Electron
Spin
Resonance
Spectroscopy;
Maleates
--Pharmac'ology--PD;
Mice;
Mice.
Inbred
BALB
C;
Oxidation-Reduction; Vanadium Compounds--Metabollsm--ME; 3T3
Cel 1 s
CAS Registry No.: 0 .(Maleates); O .(Vanadium Compounds);
141-05-9
.(diethyl maleate); 27774-13-6 .(vanadyl sulfate);
70-18-8 .(Glutathione)
08779434 94094434 Benzene and phenol
metabolism by mouse and rat liver
mlcrosomes.
Schlosser PM; Bond JA; Med Insky MA
Chemical Industry Institute of Toxicology, Research Triangle
Park, NC 27709.
Carcinogenesis (ENGLAND)
Dec 1993, 14 (12) p2477-86,
ISSN 0143-3334
Journal Code: C9T
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
Subfile:
INDEX MEDICUS
Benzene. an Important Industrial solvent and constituent of
unleaded gasoline, causes leukemia and aplastic anemia In
humans. Mice are more sensitive than rats to benzene toxicity,
though neither species has been shown to respond consistently
with benzene-Induced leukemia. Benzene biotransformation in
liver to phenol, hydroqulnone, catechol and/or muconaldehyde
Is thought to be necessary for Its hematotoxlclty and/or
genotoxlclty. Our goal Is to develop a mathematical simulation
model
pable of describing the pathways and kinetics of
101740
benzene metabolism by rat and mouse liver mlcrosomes and to
assess the role of species metabolic differences in species
sensitivity.
Mlcrosomes
were
Incubated
with 4 microM
{U-14C ]-benzene
or-./ a' microM
[U-l4C]phenol . Metabolite
production was quantified by extraction Into ethyl acetate,
HPLC separation and liquid scintillation spectroscopy. After
45 min, mouse liver mlcrosomes converted 20% of the benzene to
phenol, 31% to hydroqulnone and 2% to catechol. Rat liver
mlcrosomes
converted
23% of benzene to phenol, 8% to
hydroqulnone and 0.5% to catechol. Production of hydroquinone
and catechol continued for 90 min for mouse liver mlcrosomes.
while production by rat liver mlcrosomes had virtually ceased
by 90 min. Muconic acid production by mouse liver mlcrosomes
was < 0.2% and < 0.04% from benzene and phenol respectively
after 90 min. A quantitative simulation model was constructed
to describe the in vitro metabolism of benzene, 1ncorporat1ng
the reaction sequences: benzene-->phenol-->catechol-->tr1hydro
xybenzene and phenol-->hydroquinone-->tr1hydroxybenzene. In
the model, all of the reaction steps are assumed to be
catalyzed by the same enzyme(s), cytochrome(s) P450, and
benzene, phenol, hydroqulnone and catechol In solution are all
assumed to compete, through reversible binding, for the same
reaction slte(s) on cytochrome(s) P450. The simulation model
accurately described both the benzene and phenol kinetic data,
supporting this proposed mechanism. In particular, this model
suggests that the observed Inhibition of benzene on phenol
metabolism, and of phenol on benzene metabolism, occurs
through competition for a common reaction site, which can also
bind catechol and hydroqulnone.
Tags: Animal; In Vitro; Male; Support, Non-U.S. Gov't
Descriptors: `Benzene--MetabolIsm--ME; `Mlcrosomes, Liver
--Metabol1sm--ME; `Phenols--Metabol1sm--ME; B1otransformation;
Mice; Models, Biological; Rats; Rats, Inbred F344
CAS
Registry No.: 0
.(Phenols); 108-95-2
.(phenol);
71-43-2 .(Benzene)
08779365 94094365 Liver accumulation of 2,3,7,8-tetrachloro-[3H]d1benzofuran
In mice: modulation by treatments with polychlorinated biphenyls.
Darnerud PO; Tornwall U; Bergman A; Brandt I Department of Toxicology, Uppsala University, Sweden.
Chem Biol Interact (IRELAND)
Dec
ISSN 0009-2797
Uournal Code: CYV
Languages: ENGLISH
Document type: JOURNAL ARTICLE
JOURNAL ANNOUNCEMENT: 9404
1993,
89 (2-3) p89-102,
Subfile:
INDEX MEDICUS
The
distribution of 2,3,7,8-tetrachloro-[3H]d1benzof uran
([3H]TCDF; 40 micrograms/kg.) resembled that earlier reported
for 2.3,7,8-tetrachlorodibenzo-p-dioxin,
with
a
strong
accumulation in the liver and a selective uptake In the nasal
olfactory mucosa of adult and fetal mice. Pretreatments with a series of selected congeners of polychlorinated biphenyls
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