A
study carried out on dogs suggested that there may be a transient
increase invivo platelet
activity with each exposure to cigarette
smoke. Exacerbation of
acute platelet thrombus
formation in stenosed coronary arteries
with smoke from a non tobacco
burning cigarette (Gering and folts;
1990). Similarly, a study carried
out on
30 smokers revealed that they were exposed for 30 minutes in a closed room
to air polluted by automobile
fumes showed not significant (P>0.05).
A study carried out on platelet
aggregates, blood viscosity,
carboxyhaemoglobin levels and P50 were
estimated and the result showed that
there was a release in
platelet aggregation and blood
viscosity this was not directly
correlated with either the decrease
in CO levels or with the reduced
P50 STD levels and it can be reasonably concluded
that the observed alterations were due
to gasoline exhaust fumes
exposure (air pollution by
gasoline exhaust fumes: 1889).
A
research study found it that diesel exhaust increased clot formation
and blood paatelet activity in healthy
volume this can lead to heart attack and
stroke and it was suggested that even an individual
is exposed to high levels of diesel exhaust for a short time, the blood is more likely to clot. There was also an increased arterial thrombus and this is brought about by a disturbance in platelet function rather than
platelet count and more
specifically by an increase in plagtelet
activation (Campbell and Neil,
2008) . a study carried out by researchers found that clot formation
occurred after workers at diesel industries where exposed to exhaust fumes and there was a
significant increase in platelet – neutrophil aggregation.
However, clot formation occurs usually on neutrophils and moncytes
(Andrew L; 2007) leading to stroke
or heart attack.
2.10 erythrocyte sedimentation rate:
In
a study carried out in relation of educational level to inflammation-sensitive biomarker level it was observed that there
was a statistically significance in the
ESR vlue of smokers
invomved in the process (STEINVIL ET AL,
2008) CIGARETTE smoke indices endothelial damage thus producing free
radicals such as nitric acid
and hydrogen peroxide thereby
leading to an increase in ESR values
(Tappia et al, 1995, Bennudez et al, 2002; DeMatt
ET AL, 1996). Nicotine found in
cigarettes as well as carbon monoxide stimulates
cathecolamines resulting in lipolysis
and increased concentration
of plasma free fatty acids
(EFA’S ) thus causing a
significant increase (P>0.05)
in ESR (Rustogi et al, 198, Simons
et al, 1984, Muscat and Harris,
1991).