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ON CANCER, |
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TOBACCO ROW 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. AIR QUALITY: 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. CARBON
MONOXIDE: 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. SECONDHAND
SMOKE: 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.
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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). ONE-TWO PUNCH 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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