Neutrophils:
Carbon monoxide exposure is associated with discrete changes in blood
neutrophil counts. This gas enhances random migration of human neutrophils. CO
form the normal biochemical milieu that stabilizes the aviculture against
leukocyte adhesion, extrabvasations and vascular permeability (Nasem; 2005,
Wallace; 2007). A study carried out on the effect of carbon monoxide after acid
aspiration; it was found that there was increase in neutrophil counts, in
addition to these aspiration-associcated lung pathology develops biphasic
pattern (Kennedy et al; 1989). A report also has shown in a study carried out
on mice that a reduced neutrophil
associated with decrease in the percentage of
peripheral blood neutrophil expressing CD116 protein.
Due to this CO activate
anti-inflammatory/preconditioning pathways by oxidant-dependent signals (Bavnes
et al 1997). A current study reported that septic lung (caecal
ligation/puncture) leads to pulmonary entrapment proteins and infiltration of
neutrophils (polymorphonuclear leukocyte (PMN) (Mizuguch et al; 2009). Hoever,
little has been studied on this particular work; a similar work carried out was
based on the acute systemic inflammatory response to welding fume exposure on
welders. It was revealed that there was a significant increse in the white
blood cells and neurtophil counts immediately follwing exposure. There was
reduction in lung function which was
only seen in smoking welder, this suggested a possible interation between
welding fume and tobacco smoke on pulmonary responses (Ozdemir elal; 1995, Wang
et al; 1994). In line to study carried out on the effect of smoking and the
intake of pills on the blood count, the study reported that there was a
significant increase in neutrophil counts (Dodsworth et al; 1981). The rise in
neutrophils in this study showed similarly in two separate studies on acute
effects of smoking in humans that increased neutrophils count in
broncho-alveolar lavage fluid one hour after smoking (Morrison et al; 1998) and
increased neutrophil retention in the lung during smoke exposure (MacNee et al;
1989).
Basophils:
studies
have it that CO has effects on the basophils, it causes immunological
activation of human basophils. Hemi (1-100um) a heme oxygenase substrate
analogue significantly increased the formation of bilirubin from partially
purified human’s basophils thus indicating that these cells express heme
oxygenase inhibitor Hemin (100um) also
decreased immunoglobulins G and anti-(anti-IgE)-induced activation of basophils
was measured by the expression of a membraine granules-association protein,
identified by CD63 and by histamine release. Exposure of basophils to exogenous
CO (10m for 30mins) also decreases the action of basophils casusing an effect,
one of the major effect of carbon monoxide is bronchoconstiction (Nadel and
Cornroe; 1961, Sterling; 1967, Walter and Nancy; 1967) the effect is reversible
by smooth muscle contraction as suggested by the study. Anoterh study suggested
that there was a significant difference in the total basophils concentration as
an acute effect of smoking; the study reported that there was a increase before
smoking and lowered after study smoking histamine release was found to be casue
of this (Sampson and Archer; 1967). Another had it that there was a higher
basophil count on smoker after a brief period of abstinence thus showing
significance p<0.05(Samenek and Aviado; 1965).
Eosinophils:
in
a report from the study of the effect of increased exhalation of carabon
monoxide between 0-1 hour induced a greater decrease in blood eosinboophils,
another recorded report was of the opinion that smoking of two cigarettes
acutely suppressed blood eosinophils. Three similar report of the effect of
smoking on blood eosinophils gave the same results as stated above. Eosinophils
showed statistical lower value of p<0.03 in blood from healthy female
smokers within 2 hours after smoking 12 sticks of cigarette (Winkel and
Statland; 1981). In lung tissues of rats after exposure within 6 hours to smoke
(Jeffery and Reid; 1981) and lung lavage fluid of ovalbumin sensitized mice
after three weeks smoke exposure (Melgert et al; 2004) effect by toxic
substances in cigarette smoke which was statistically not significant (Aoshiba
et al; 2001) and the anti-inflammatory substances in cigarette smoke like
carbon monoxide (Siebos et al; 2003, Chapman et al; 2001). A study carried out
on humans who had potroom asthman (PA) was positively associated with blood
eosinophils. An attenuation of blood eosinophil was also observed in smoking
asthmatics, suggesting an immune – modulating effect of smoking.
Smoking
causes increase blood eosonophils compared to non-smokers, after smoking
cessation, heavy smokers had higher blood eosinophil this it was stated that it
is associcated with allergy or a small negative effect on the lung function
with p<0.05 (Juel et al; 1998). A report has it that smoking increased
exhaled CO between some hours and induced a statistically greater decrease in
blood eosinophil observed and there was also a suppressive inflammatory effect
of smoking and in the cause of allergy the cells were found to be significant
p<0.05 (Hester et al; 2005).
Monocytes:
a
study result showed that smoking influences monocytes counts thus lowers the
count in light smokers (Juel et al; 1998). The effect of cigarette smoking in a
recent study shows that there are an increased number of the cells. Monocytes
are known to have originated from a precursor of macrophages that have
defective micropicidal function may represent additional pathogenicity factor
in the diminished host defense observed in smokers (Nielsen; 1985). Smoking
evokes an inflammatory response in both humans and animal models, which is
characterized by the early influx and activation of inflammatory cells together
with the release of chemokines (van der Vaart et al; 2004). The activation
(Rhaman et al; 1996) or inhibition (Ouyang et al; 2000, Witherden; 2004) of
chemokines has been shown to be have effect on monocytes.