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Cigarette smoking causes the largest human exposure to carbon monoxide.  The COHb [C = carbon, O = oxygen, CO = carbon monoxide, Hb = hemoglobin] content in an average nonsmoker is about 0.5%, while in a smoker it is ten time3s higher, about 5% (but level up to 12% have been reported).  Toxics A to Z, Jim Harte et al, U. of Cal. Press, 1991, p. 25.


Lowered level of hemoglobin is minor compared to its effect upon the arteries.  The formation of plack is primarily a healing response brought on by reactive chemicals.  What clogs the arties is not just cholesterol, but also includes cells from the artery wall.  The principle reactive chemical from smoking is carbon monoxide.  Carbon monoxide is the principle culprit that accounts for why a person who averages a pack or more a day is over two-and-one half times more likely in any given year to die of a coronary disease.  Given the prevalence early from tobacco because of coronary problems than they do from cancer. 

It was in April of 1979 in Scientific American that an article presented the evidence in an organized way on the link to carbon monoxide with coronary disease.  That evidence still stands.--JK



Study Finds Carbon Monoxide can Trigger Brain-Damage Attack by Immune System

JAMA, October 6, 2004—Vol. 292, No. 13


Tracy Hampton, PhD


CARBON MONOXIDE'S REPUTATION as a stealth toxin goes be­yond its odorless, colorless properties. The gas can also surrepti­tiously cause delayed permanent brain damage, an effect that scientists have been unable to explain.  But now they are no longer in the dark. A new study reveals that the dam­age arises from over activation of im­mune cells that attack proteins that help insulate nerves.

The findings were published in the September 1 online issue of the Pro­ceedings of the National Academy of Science (vvvvw.pnas.org).


Annually in the United Stales, about 40,000 individuals are treated for car­bon monoxide poisoning, the leading agent of injury and death by poison­ing worldwide.  The gas' initial effect on the body is a result of its high affinity for hemo­globin.  This causes hypoxic stress, and affected patients are generally treated with oxygen. 

Stephen Thorn, MD, PhD, of the University of Pennsylvania in Phila­delphia, has been studying carbon monoxide’s second effect—permanent brain damage, which can become evi­dent between 4 days and 3 weeks fol­lowing exposure. Thorn and col­leagues have found that this effect occurs because carbon monoxide exposure modifies myelin basic protein, found in the insulating cells around neurons.  "It turns out that the altered myelin basic protein is now recognized by the body as an invader or a foreign sub­stance," said Thorn. "The big surprise in our findings vas that once the immune system is turned on, the lymphocytes also recognize normal myelin basic pro­tein as abnormal.  As these immune cells continue to lash out against normal myelin basic protein, permanent brain damage can result.  Thorn and the research learn carne to their conclusions when they found that rats engineered to be incapable of mounting an immune response against myelin basic protein did not develop brain damage following carbon monoxide exposure. These rats also performed normally in a maze test that mea­sures cognitive and motor function.  Control rats did not fare as well. Their brain cells exhibited measur­able biochemical damage and the ani­mals performed poorly in the maze test.  "We think that that's also a clinical correlate—that is to say, patients who suffer serious carbon monoxide poi­soning and don't get early treatment, they have perhaps as much as a 50% chance of suffering what is called de­layed neurological sequelae." said Thorn. "So it's a clinically very important problem," one that can result in im­paired learning and concentration prob­lems, he said.



The study's findings suggest potential therapies. "One of the next steps is to go back to the animal model and say, now that we have this pathway figured out, what can we what can we do to disturb it," said Thorn. Obvious candidates an immunosuppressants. It they prove effective in ani­mal studies, then "we rather quickly could be going to clinical trials to see if we can do something for patients," said Thorn. D


1542    JAMA

This ties in well with the fact that an active immune system will stimulate healing response, which in turn results in the build up of plaque—see above article.--JK 


Vascular Biology

Relationship Between Homocysteine and Superoxide Dismutase in Homocystinuria

Possible Relevance to Cardiovascular Risk

David E. L. Wilcken; Xing Li Wang; Tetsuo Adachi; Hirokazu Hara; Natalia Duarte; Kathryn Green; Bridget Wilcken

From the Department of Cardiovascular Medicine (D.E.L.W., X.L.W., N.D.), Prince of Wales Hospital, and University of New South Wales Centre for Thrombosis and Vascular Research, Sydney, Australia; the Laboratory of Clinical Pharmaceutics (T.A., H.H.), Gifu Pharmaceutical University, Gifu, Japan; and the NSW Biochemical Genetics Service (K.G., B.W.), the Royal Alexandra Hospital for Children, Sydney, Australia.

Correspondence to Professor David Wilcken, Cardiovascular Genetics Laboratory, Edmund Blacket Building, Prince of Wales Hospital, Randwick, NSW 2031, Australia. E-mail d.wilcken@unsw.edu.au

AbstractA modest homocysteine elevation is associated with an increased cardiovascular risk. Marked circulating homocysteine elevations occur in homocystinuria due to cystathionine -synthase (CS) deficiency, a disorder associated with a greatly enhanced cardiovascular risk. Lowering homocysteine levels reduces this risk significantly. Because homocysteine-induced oxidative damage may contribute to vascular changes and extracellular superoxide dismutase (EC-SOD) is an important antioxidant in vascular tissue, we assessed EC-SOD and homocysteine in patients with homocystinuria. We measured circulating EC-SOD, total homocysteine (free plus bound), and methionine levels during the treatment of 21 patients with homocystinuria, 18 due to CS deficiency, aged 8 to 59 years, and 3 with remethylating defects. We measured total homocysteine by immunoassay, EC-SOD by ELISA, and methionine by amino acid analysis and assessed interindividual and intraindividual relationships. There was a significant, positive relationship between EC-SOD and total homocysteine. For the interindividual assessment, levels were highly correlated, r=0.746, N=21, P<0.0001. This relationship was maintained after taking into account intraindividual patient variation (r=0.607, N=62, P<0.0001). In 2 newly diagnosed CS-deficient patients, treatment that lowered the markedly elevated pretreatment homocysteine level (from 337 to 72 and from 298 to 50 mol/L) reduced the associated elevated EC-SOD in each by 50%. EC-SOD and methionine levels were unrelated (r=0.148, n=39, P=0.368). The positive relationship between circulating EC-SOD and homocysteine could represent a protective antioxidant response to homocysteine-induced oxidative damage and contribute to reducing cardiovascular risk in homocystinuric patients.  EC-SOD levels may be relevant to the pathogenesis of vascular disease in other patient groups.

Key Words: homocysteine superoxide dismutase oxidative stress vascular disease cystathionine -synthase deficiency

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