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TOBACCO SMOKE, an overview--jk

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In the spirit of public service I am sharing information that ought to be known by all because tobacco causes the early death each year of 500,000 American, and 8 times that number world-wide. 



How concerned can we be about air quality when we so many have chosen for the sake of personal transportation the single greatest source of pollution and when 26% of the adult population turn their lungs into a filter system. 



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 times higher, about 5% (but level up to 12% have been reported). 

While lung cancer gets the main attention, all cancers are increased, and even more significant in terms of total mortality is cigarette’s smokes effect upon the heart.  Smoking a pack a day increases the risk of death from coronary disease by 2.09 times, compared to a nonsmoker.

Toxics A to Z, Jim Harte et al, U. of Cal. Press, 1991, p. 25.



A ten-year carefully controlled investigation whose results were reported this past year found that women who are constantly exposed to secondhand smoke, at work or at home, are almost twice as likely as others to have a heart attack.  And even women who are only occasionally exposed experience a 58% increase in risk, according to the study lead author, epidemiologist Ichiro Kawachi of the Harvard School of Public Health.  [Harvard is noted for the quality of their studies].  Discover, p. 58, January 1994.


This consequence was verified as to the development of atherosclerosis in a study where an imagining technique (B-mode real-time ultrasound) of the common carotid artery was used to measure the progress of the formation of plaque deposits over a 3-year period in 10,914 participants.  The study found that there was a 50% increase in the progression of atherosclerosis is attributed to current smoking versus those who never smoked and also were not exposed to secondhand smoke (122).  Moreover, the effect of second-hand smoke was quantified to be 34% as great as the impact of active smoking on the progression of atherosclerosis (123).  Thus the increased progression of atherosclerosis associated with ETS exposure should be considered in light of the estimated 30,000 to 60,000 annual deaths in the United states attributable to ETS [exposure to second-hand smoke] 123.  Uncovered in the study was the fact that pack-years of smoking but not current vs. past smoking was associated with progression of atherosclerosis progression suggested that some adverse effect of smoking might be cumulative and irreversible (119).  The Atherosclerosis Risk in Communities Study, Howard et al, Journal of American Medical Association, January 14, 1998, Vol. 279, No. 2.


The greatest health impact of tobacco upon users is from vascular disease (atherosclerosis).  A person who smokes a pack a day is twice as likely to die from this effect through mitochondria infraction that a non-smoke.  This increased mortality eclipses the increased risk of death from cancer. 

In 1979 Scientific American came out with an article which shown that arteriosclerosis primary cause is insult to the artery walls. The insult it was shown results in an immune response. Smoking a pack a day doubles the risk of death by a coronary failure.  Carbon monoxide and to a lesser extent the other reactive chemical is tobacco smoke are the reason for this risk. This articles ties into those conclusions. 


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 darn-age 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



The mechanism by which carbon monoxide causes arteriosclerosis is through the white blood cells which respond to it presence by emitting a polypeptide which causes the cells of the artery walls to build up plaque—a sort of protective coating.  Over twenty or more years of repetitive exposure to high levels of carbon monoxide, the arteriosclerosis develops--jk.




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