A study published in the journal Scientific report discovered that cigarette smoking can trigger suicidal erythrocyte death, a condition that can increase the risk of anemia and microcirculation impairment.
Study: Smoking is associated with increased eryptosis, suicidal erythrocyte death in a large population-based cohort. Image credit: sruilk/Shutterstock
Smoking is a major cause of premature morbidity and mortality worldwide. Tobacco smoke contains many harmful substances, including carbon monoxide, formaldehyde, acetaldehyde, benzopyrene, and nicotine, which can enter the bloodstream through inhalation and cause cardiovascular complications. Furthermore, carbon monoxide can form carboxyhemoglobin with hemoglobin, which reduces the oxygen-carrying capacity of hemoglobin and subsequently induces a hypoxic effect.
Previous studies investigating the effects of smoking on the red blood cell system have provided mixed results. Although some studies show higher red blood cell indices in smokers than nonsmokers, some indicate that smoking may induce eryptosis. Eryptosis is a process of erythrocyte (red blood cell) death, characterized by phosphatidylserine externalization and cell shrinkage.
In this large population-based cohort study, scientists investigated the effects of smoking on eryptosis and vital hematological parameters, including red blood cell count, hematocrit, hemoglobin, mean corpuscular cell volume (MCV), mean corpuscular hemoglobin (MCH). , and the mean. Corpuscular hemoglobin concentration (MCHC).
The current study included 2,023 participants from the German National Cohort Study (NAKO), which includes 205,000 adult participants at 18 study centers in different German states.
Blood samples collected from participants were analyzed for eryptosis and hematological parameters. Eryptosis was determined using flow cytometry and red blood cell indices were determined using a hematological analyzer.
Of the 2,023 participants included in the study, 1,000 were non-smokers, 418 were current smokers and 605 were ex-smokers.
Comparative analysis between smoking habits and eryptosis showed that smokers had moderately higher rates of eryptosis than nonsmokers and ex-smokers. Specifically, smokers showed 14% and 19% more eryptotic cells than nonsmokers and ex-smokers, respectively. However, no significant difference in eryptosis was observed between non-smokers and ex-smokers.
Furthermore, the study found a positive correlation between the number of cigarettes smoked per day and the rate of eryptosis. This association was similar for both male and female smokers. However, no association was observed between smoking burden per year and the rate of eryptosis in the entire study population.
A subgroup analysis including ex-smokers revealed a negative association between duration of smoking cessation and the rate of eryptosis. Age at smoking cessation and timing of smoking cessation were identified as significant predictors of eryptosis in ex-smokers.
Regarding hematological parameters, no correlation of eryptosis with erythrocyte count, hemoglobin, hematocrit and MCV was observed. However, there was a moderately positive correlation between eryptosis and MCH and MCHC.
No significant differences in erythrocyte count and hematocrit were observed between smokers, non-smokers and ex-smokers. However, smokers had higher hemoglobin, MCV, MCH, and MCHC levels than the rest.
Daily number of cigarettes smoked, smoking duration, and annual smoking burden showed a moderate positive association with hematocrit, hemoglobin, MCV, and MCH and a negative association with MCHC in current smokers.
Significance of the study
Studies have shown that current smokers have a moderately higher rate of suicidal erythrocyte death than nonsmokers and ex-smokers. However, despite higher erythrocyte mortality, smokers have relatively higher erythrocyte indices. This indicates that elevated eryptosis in smokers has no apparent negative effect on the overall red blood cell system.
According to the available literature, smoking-induced oxidative stress and inflammation may play a role in triggering eryptosis. Carbon monoxide inhaled during smoking has also been found to directly stimulate eryptosis. Furthermore, the p38MAPK/Fas signaling pathway has been shown to increase eryptosis rates in smokers.
Despite higher erythrocyte mortality, studies have found lower erythrocyte counts in smokers. This may be due to increased erythropoiesis (the process of making new erythrocytes) in smokers to compensate for the eryptosis-mediated loss of erythrocytes.
Mentioned by scientists, the main strength of research with a large number of participants. However, self-reported smoking status may be subject to reporting bias. Scientists look forward to studying whether increased eryptosis is associated with a higher risk of cardiovascular disease in smokers.