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Evaluation of the Role of Carbon Monoxide and Nicotine in the Pathogenesis of Arteriosclerosis and Cardiovascular Disease

Date: 19790000/EP
Length: 11 pages
81211273-81211283
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Author
Schievelbein, H.
Type
PSCI, SCIENTIFIC PUBLICATION
BIBL, BIBLIOGRAPHY
CHAR, CHART/GRAPH/MAPS
FOOT, FOOTNOTE
Area
LIBRARY/SUBJECT BOXES
Site
G39
Request
R1-080
Named Organization
Ahf, American Health Foundation
Comm on Medical + Biological Effects O
Federal Health Office
Subcomm on Carbon Monoxide of 770000
Named Person
Anderson
Armitage
Aronow
Astrup
Ayres
Davies
Dawber
Dinman
Doll
Doyle
Fisher
Forbes
Gijka
Goldsmith
Grosgogeat
Grundke
Helovaara
Hernberg
Hill
Issac
Jones
Kannel
Kjeldsen
Kuller
Langone
Rand
Robinson
Schievelbein, H.
Scott
Sinclair
Surgeon General
Topper
Turner
Vanvunakis
Date Loaded
20 Dec 2001
Master ID
81211048/1331
Related Documents:
Litigation
Feda/Produced
Author (Organization)
Academic Press
German Heart Center
Preventive Medicine
Characteristic
DRFT, DRAFT
UCSF Legacy ID
upm54c00

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F o4'^ - H. SCHIEVELBEIN COHb levels were slightly higher in sudden death due to arteriosclerotic heart disease than in sudden death due to other causes. Cigarette smokers who died suddenly due to arteriosclerotic heart disease had higher postmortem COHb levels than nonsmokers. AIl elevated COHb levels could be related to either cigarette smoking-or environmental exposure. But there was no relationship be- tween cardiac parthologic 5ndings and postmortem COHb_ levels among patients dy_ing-su_ddenly of arterioscierotic disease. Helovaara and co-workers (29) found a weak correlation between COHb levels, smoking history, and CVD. If the smoking history was eliminated, the correlation between COHb levels and CVD remained. The authors themselves stated that their results were far from conclu- sive and further studies should be conducted. - No conclusive data can be obtained from reports on risk of CVD of Gre fighters (11, 12) as measured by ECG responses. heart rate, and cholesterol levels- assum- ing that this profession is exposed to extreme ambient CO levels. No correlation regarding arterial disease was found by Jones and Sinclair (33) in blast furnace workers despite the finding that COHb levels were increased in this group com- pared with a nonexposed control group. Hernberg and co-workers (30) found a clear dose-response relationship between angina pectoris and CO exposure from -either occupation, smoking, or both but no ECG findings suggesting CVD in foundry workers. - - As has been done for nicotine, the same question regarding the-upfake of CO in smokers should be discussed. In Table 3, the measurments by different authors of the COHb level in cigarette smokers are comparable and justified by the experi- ments described below. Modern technical equipment and the improved analytical techniques are now available (2Si and the very high COHb levels measured in older investigations, estigations, i.e., 15% COHb_, should not be considered relevant. With the ~~- ------ TABLE3 - CARBO%YHENOGLO9IN LES'EtS L\ SkIOKERS AFD NOFSY05ER5 Mean or range of percentaee COHb Description Nonsmokers Smokers United Kingdom - pregnant women 1.1 3.6 Meat porters 1.6 - 5.1 - Office workers (Hawkins. 1976) I-3 6' London office workers 1.12 5.5 (Cale, 1975) _ 0.1-2.7 _.'_-13.0 - 29,000 USA blood donors 1.39 5.57 (Stewart er al., 1974) 0.4-6.9 0.8-1 L9 3,311 California longshoremen 1.3 5.9 (Goldsmith and Landaw, 19681 Munich pupulation 2.36 7.38 - Rural Bacarians 1.03 6.06 (Schcidemandel and Daum, 1973) Munich population ?.98 4 87 (Schie,elbein, 1978) 1.5-4.9 2.8-9.6 b ;e x io tiead~,~re.

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