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
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
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.