Smokers' polycythemia is a secondary erythrocytosis, an increase in red blood cell mass linked to tobacco-related factors, such as carbon-monoxide (CO) exposure or chronic hypoxia. [4] CO binds to hemoglobin to form carboxyhemoglobin (COHb), which reduces effective oxygen delivery; the body compensates by increasing erythropoietin-driven red blood cell production, thereby raising hemoglobin and hematocrit levels. This mechanism helps explain marked increases in hematocrit after tobacco use, including reported hookah-related CO toxicity with resultant polycythemia, and provides a clue to differentiate smokers' polycythemia from bone marrow disease like polycythemia vera (PV). [1][2]

Clinically, smokers' polycythemia usually presents in the setting of tobacco use history (such as cigarettes, cigars, or alternative products like hookah) or with co-existing pulmonary disease (for example, COPD) that results in sustained hypoxia. Key practical clues are:

• A history of smoking, elevated carboxyhemoglobin (COHb)
• Evidence of hypoxia
• Improvement in hematocrit after smoking cessation or correction of hypoxia

Given that smoking-related cases may improve with smoking cessation or pulmonary optimization, initial management focuses on confirming tobacco exposure and addressing reversible drivers; persistent erythrocytosis after proper cessation and oxygen correction warrants hematology evaluation for primary causes such as polycythemia vera. [3][4]

At the core of smokers' polycythemia are two related mechanisms: carbon-monoxide (CO) exposure and hypoxia. CO from tobacco smoke binds to hemoglobin with high affinity to form carboxyhemoglobin (COHb), which reduces the blood’s oxygen-carrying capacity [1]. The kidney may sense reduced tissue oxygen delivery and increase erythropoietin (EPO) production, thereby driving an increase in red blood cell mass. Heavy or non-combustible tobacco exposures (for example, intense hookah use) can produce markedly elevated COHb and clinically apparent erythrocytosis. [2][6]

Chronic lung disease, most commonly COPD, in smokers, adds a sustained hypoxemic stimulus that similarly increases EPO and red blood cell production [3]. Notably, several studies show that smoking cessation or correction of hypoxemia (for example, with proper COPD management) may help decrease hemoglobin and hematocrit, supporting the role of these reversible drivers. [1][3][4][5]

Smokers’ polycythemia is context-driven and sometimes reversible: it arises when tobacco smoke (or alternative exposures such as hookah) raises carboxyhemoglobin (COHb) and produces hypoxia, triggering a compensatory rise in red blood cell mass that might fall after smoking cessation or correction of hypoxia. [1][2][3][4][6]

In contrast, when erythrocytosis persists despite removing reversible drivers, or when the clinical picture lacks clear smoking or hypoxia evidence, that warrants concerns for a primary cause and prompt hematology evaluation. In practice, a history of smoking combined with documented carbon-monoxide exposure or hypoxia, along with improvement after smoking cessation,supports smoking as the secondary cause of erythrocytosis. [1][2][5][6] Use a practical, stepwise bedside approach to separate the two:

• Confirm active tobacco exposure and measure CO burden and oxygenation
• Treat or optimize any contributing lung disease (e.g., COPD)
• Reassess blood counts after a structured cessation or oxygenation period

If hematocrit and hemoglobin levels decrease following tobacco quitting and/or correction of oxygen, this supports the possibility of smokers' polycythemia. [1][4] If they do not, or if there are atypical features (e.g., unexplained thrombosis, progressive splenomegaly, or persistently high blood counts), refer to hematology for evaluation of primary erythrocytosis. Also be alert for complications more often described with secondary polycythemia (for example, eye blood vessel damage from low oxygen reported to improve with smoking cessation). [5]

Smokers' polycythemia can be more than a lab abnormality; watch for hyperviscosity symptoms (headache, visual disturbance, dizziness, fatigue).

Two pragmatic consequences to keep front of mind:

1. Ocular ischemic symptoms have been reported in a case report polycythemia contexts and may improve after smoking cessation, so new visual symptoms warrant urgent assessment, and
2. Smokers with polycythemia commonly carry concurrent cardiometabolic risk (hypertension, dyslipidemia, or abnormal cholesterol, insulin resistance) that increases overall vascular risk and should be actively managed.

These findings support a management approach that addresses hematologic findings alongside cardiovascular risk reduction and timely smoking-cessation support. [5]

1. What is “smokers' polycythemia”?

A secondary rise in red blood cells caused by tobacco-related CO exposure and hypoxia. It often improves after quitting smoking. [1][2][4]

2. How do you tell it apart from polycythemia vera (PV)?

Look for active smoking, elevated COHb or hypoxia, and a decrease in Hgb and Hct after smoking cessation or oxygen correction. Persistently high blood counts despite these steps or atypical features may warrant hematology evaluation for PV (JAK2 testing, EPO level). [2][3]

1. Smith, J. R., & Landaw, S. A. (1978). Smokers' polycythemia. New England Journal of Medicine, 298(1), 6-10.
2. Anaqrah, H., & McCabe, D. J. (2022). Severe chronic carboxyhemoglobinemia and polycythemia due to smoking hookah. The American Journal of Emergency Medicine, 55, 226.e1.
3. Zhang, J., DeMeo, D. L., Silverman, E. K., Make, B. J., Wade, R. C., Wells, J. M., Cho, M. H., & Hobbs, B. D. (2021). Secondary polycythemia in chronic obstructive pulmonary disease: Prevalence and risk factors. BMC Pulmonary Medicine, 21, 235.
4. Ilkkilic, K., Karadogan, D., Telatar, T. G., Cure, O., & Klisic, A. (2025). Effect of smoking and smoking cessation on hematological parameters in polycythemic patients. Open Medicine, 20(1), 20251181.
5. Sung, S. Y., Chang, Y. C., Wu, H. J., & Lai, H. C. (2022). Polycythemia‑related proliferative ischemic retinopathy managed with smoking cessation: A case report. International Journal of Environmental Research and Public Health, 19(13), 8072.
6. Tadmor, T., Mishchenko, E., Polliack, A., & Attias, D. (2011). Hookah (narghile) smoking: a new emerging cause of secondary polycythemia. American journal of hematology, 86(8), 719-720.