ACUTE L.,2V'3UZ-' TO CL;ArL7L."Z S:-,'O7KI' AS UUSE: Go- IN-607-T-ri,
William 11.
Previous invcs:igatilon of acute c---.po,.;ura to cinarattc smolw as a
cause oAz artarial hypo-.@_-a havc been for the cost pnrt negative. Mo s t
of these studies vcra parZormcd before the availability of pO.) electrodes
and thus are studies of oxyhe;noglobin sazuracion and were done on
relatively small numbers of essentially normal people.
This study was conducted on 16 subjects with COM and 16 without
to determaine the possible fraquency oz arrazial hypoxia following
exposure to ci.'-aratce snok-a and its machanism.. Baseline studies of
alvco"ar-arterial -as w-chan-e ware done before and im:zzediataly after
smoking 6 cm of a cigarette containing approximately 27 mg tar and
1.9 ming nicotine. Tho studios were repezz-ad at the 5-7 and 15-17 minute
-intervals after smokinbo. EiZht of the 32 sustained a significant decrease
in PaO2 a"e-- this decrease av,-ra;--.,, 10.4 mm F- at the 0-2
minute leval after smao'King, S.2 mr, at 5-7 -minutes and 5.2 ran bet-,.eon
15 and 17,minutes. -Lhasa results are, sign"-;ctntly different from the
,group of 24 who did decrease in ?a0j. Of these
remainin- not have
8 individuals, 2 had COM, I interstitial pulmonary fibr@sis, 2 were
recova@-in- from pneic@monia, 1 Inad rheumatoid arthritis and I a chronic
derm.atitis. Since ?aCO2 did not chan-e in .:-.ase eight -individuals,
the decrease in ?aO2 must be due to altered V/@ relationships.
The results o.-- the A-a gas exchange studies divide the 8 individuals
with hypox--a into a group of 6 with prado-.Jnaatly bronchoconstrictor
effects and 2 subjects with vasoconstriction. in comparing the 6 with
a broncblocoastrictor effect to the 24 subjects whose PaO2 did not change
after smoking, the 6 had an increase in 547. in the A-a gradient, more
than a 100% increase in alveolar shurt fraczion of the lun- and a 90%
increase in venous admixture. The 2 individuals with a vasoconstrictor
effect did not have chlangas in any of the above, but did have an
increase Of -the alveolar dead space fractions and an increase in
physiological dead space.
Work is presently underway to determine if the development of a
decreased PaO2 is a difference in individual response to cigarette smoke.
or a phenomenon related to the amount of smoke inhaled.
The decrease in PaO2 found in the 8 subjects, when combined with the
development of carboxyhemoglobin in cigarette smoke will significantly
0
decrease oxygen delivery at the cellular level in such individuals.
NJ
BATCo document for Province of British Columbia 19 April 1999