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Secondhand Smoke & Carbon Monoxide



In the spirit of public service I am sharing information that the 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 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 time3s higher, about 5% (but level up to 12% have been reported).  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.  The principle one caused by incomplete combustion is carbon monoxide.  It is this that 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 corinary disease.   to  This is  particularly significant as I shall develop carbon monoxides link to atheroscrlerosis and the conclusion that more people die early from tobacco because of coronary problems than they do from cancer.]

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 studys 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) was used to measure the progress of the formation of plaque deposits over a 3-year period in 10,914 participants in the common carotid artery.  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 were not exposed to secondhand smoke (122).  Moreover, the effect of secondhand 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 secondhand 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.



Published by the Cardiovascular Institue of the South
article by Bart G. Denys, M.D., Medical Director

JAMA, Oct 6, 2004, Vol. 292, No,. 13, p. 1542


Study Finds Carbon Monoxide Can Trigger Brain-Damaging Attack by Immune System

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 the overactivation 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 (www.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 was 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 came 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 lest 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.

POTENTIAL THERAPIES? 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 do to disturb ii," said Thorn. Obvious candidates are immunosuppressants.  If 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 Thom.

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment.