PLATELETS (THROMBOCYTES) – EFFECTS OF CARBON MONXIDE EXPOSURE

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).