Smoking can cause polycythemia, a condition characterized by an elevated red blood cell count. This condition is known as secondary polycythemia (erythrocytosis) and is a direct physiological response to inhaled tobacco smoke. The body attempts to compensate for a reduced oxygen-carrying capacity by increasing the production of red blood cells. The resulting high red blood cell count significantly impacts overall cardiovascular health.
Understanding High Red Blood Cell Count
Polycythemia describes a state where the body has an abnormally high number of circulating red blood cells, measured by elevated hemoglobin or hematocrit levels. Hemoglobin is the oxygen-carrying protein in red cells, and hematocrit is the percentage of blood volume made up by red cells. When these values rise above the normal range, the blood becomes thicker, a state known as increased viscosity.
This thickening forces the heart to work harder to pump blood throughout the circulation. Increased blood viscosity slows blood flow, which raises the risk of dangerous complications. The slower, thicker blood is more prone to forming clots (thrombosis), which can block vessels in the brain or heart, increasing the risk of stroke or heart attack.
The Mechanism: How Smoking Triggers Overproduction
The primary driver of smoking-related polycythemia is the inhalation of carbon monoxide (CO), a toxic gas released during tobacco combustion. Carbon monoxide binds to hemoglobin in red blood cells much more readily than oxygen. When CO binds to hemoglobin, it forms a stable compound called carboxyhemoglobin (COHb), effectively taking up the sites that would normally transport oxygen.
The presence of carboxyhemoglobin reduces the blood’s overall oxygen-carrying capacity, creating a state known as functional anemia or tissue hypoxia. This lack of oxygen signals the kidneys.
In response to the perceived hypoxia, specialized cells in the kidneys increase the secretion of a hormone called erythropoietin (EPO). EPO travels to the bone marrow, where it acts as a stimulant. The EPO signal instructs the bone marrow to accelerate the production of new red blood cells.
This increased production is the body’s compensatory mechanism to restore oxygen delivery. However, because carbon monoxide exposure continues, newly produced red blood cells also become saturated with CO, leading to a vicious cycle of overproduction and thickened blood. This results in a chronically elevated red blood cell count that raises the risk of clotting.
Differentiating Smoking-Related and Primary Polycythemia
The form of polycythemia caused by smoking is classified as secondary polycythemia, distinguishing it from other types based on its origin. Secondary polycythemia is a reactive condition where the bone marrow responds normally to an external stimulus, such as chronic oxygen deprivation. In this type, the production of red blood cells is stimulated by high levels of erythropoietin.
This is fundamentally different from primary polycythemia, most commonly known as Polycythemia Vera (PV), which is a rare type of blood cancer. Polycythemia Vera is caused by an internal problem, typically an acquired genetic mutation (often JAK2) in the bone marrow. This mutation causes the bone marrow cells to produce excessive red blood cells autonomously, regardless of the body’s actual oxygen needs.
A key clinical difference used for diagnosis is the level of erythropoietin (EPO) in the blood. In secondary polycythemia, EPO levels are typically normal or high because the hormone is driving the cell production in response to hypoxia. Conversely, in Polycythemia Vera, EPO levels are often low because the autonomous, overactive bone marrow production suppresses the regulatory hormone. Differentiating these two conditions is important for treatment because secondary polycythemia focuses on removing the external trigger, while Polycythemia Vera requires managing the underlying bone marrow disorder.
Reversing the Condition Through Cessation
For smoking-induced secondary polycythemia, the primary treatment is complete smoking cessation. When the chronic exposure to carbon monoxide is removed, the hypoxic stimulus to the kidneys rapidly disappears. Carbon monoxide levels in the blood begin to drop within hours after quitting.
As the body’s oxygen-carrying capacity improves, the kidneys stop overproducing erythropoietin. The normalization of EPO levels allows the bone marrow to slow its excessive red blood cell production. Since the lifespan of a red blood cell is approximately 120 days, the elevated red cell mass typically begins to decrease within a few weeks and can normalize within three to six months as the older, CO-affected cells are naturally cleared from the bloodstream.
In some cases, especially when the blood viscosity is dangerously high, a procedure called phlebotomy might be used temporarily. Phlebotomy involves drawing a specific amount of blood to immediately reduce the red blood cell count and lower the risk of clotting complications like stroke or heart attack. However, this is often a short-term measure until smoking cessation can resolve the root cause and restore normal blood parameters.