The Effect of Secondary Smoking on Platelet Count

Secondary smoking, or environmental tobacco smoke (ETS), is the involuntary action of inhaling the smoke produced by a smoker. This inhaled smoke can be either sidestream smoke, which is the smoke produced by a burning cigarette, or mainstream smoke, which is the smoke exhaled by the smoker. Inhaled secondary smoke includes the same toxic chemicals that are inhaled by smokers, including more than 60 chemical compounds which are known human carcinogens, or cancer-causing agents.

What Platelets Are

• Platelets, also known as thrombocytes, are disc-shaped cells which circulate in the plasma of human blood under normal conditions. Platelets play a major role in hemostasis, which is the process of stopping bleeding after an injury and keeping the blood within the damaged blood vessel by the formation of a plug or blood clot. Under normal conditions, when you cut yourself, this is beneficial and prevents excessive bleeding. When activated after an injury, the platelets rush to the site of the cut and form finger-like projections, which help the platelets stick together to form the plug or a scab. This helps to reduce bleeding through a process called aggregation. If injury occurs under the skin, the aggregation of platelets forms a blood clot and reduces bleeding from the blood vessel.

When Platelet Counts Go Wrong

• Elevated platelet counts lead to blood clots developing in the blood vessels, which can lead to stroke, myocardial infarction (death of heart tissue brought about by obstruction of blood flow; otherwise known as a heart attack) and embolisms. Reduced platelet count can lead to excessive bleeding.

Effect of Smoking on Platelet Count in Smokers

• There is an increase in arterial thrombosis in smokers. This change is brought about primarily by a disturbance in platelet function rather than platelet count, and more specifically by an increase in platelet activation. Also the natural anticoagulant properties (called "endogenous anti-aggregatory power") in the plasma of smokers is significantly decreased.

Effect of Passive Smoking on Platelet Count

• There is no significant change in platelet count after passive smoking, but rather an increase in the activation of platelets in the blood, as has been demonstrated in smokers. Passive smokers show evidence of increased thrombus formation (a thrombus is a blood clot formed within a blood vessel that remains attached where it was formed, causing an obstruction), which is brought about by increased activation of platelets leading to excessive aggregation. In fact, it has been shown that platelet activation and aggregation increase within 20 minutes of exposure to passive smoke. The effects are very similar to the effects seen in smokers. When long-term exposure to passive smoke is suddenly stopped, there can be a corresponding rapid decrease in platelet aggregation, which is a key factor in the development of coronary syndromes (a group of symptoms related to the heart). Subtypes include myocardial infarction, coronary thrombosis and unstable angina. Increased platelet activation and aggregation play an active role in the development of atherosclerosis and arterial thrombosis.

Conclusions

• Passive smoking has been cited as the leading cause of preventable death and can lead to a 25 to 30 percent increase in coronary heart disease in otherwise healthy subjects. Secondary smoke is especially harmful to children and can lead to an increased risk of respiratory disease and middle ear infection.

  Passive smoking has not been proven to have any significant impact on actual platelet count, but rather on the behavior of platelets in the body. Passive smoking has been shown to cause similar effects on the platelet behavior of passive smokers to those of smokers---namely increased platelet activation and corresponding platelet aggregation, potentially leading to increased risk of thrombosis and other related complications, including coronary syndromes.