A study published within the journal Scientific Reports finds that cigarette smoking can trigger suicidal erythrocyte death, a condition which will increase the chance of anemia and microcirculation impairment.
Study: Smoking is related to increased eryptosis, suicidal erythrocyte death, in a big population-based cohort. Image Credit: sruilk / Shutterstock
Smoking is a number one reason behind premature morbidity and mortality worldwide. Tobacco smoke comprises many harmful substances, including carbon monoxide, formaldehyde, acetaldehyde, benzopyrenes, and nicotine, which might enter the bloodstream through inhalation and cause cardiovascular complications. Furthermore, carbon monoxide can bind to hemoglobin to form carboxyhemoglobin, which reduces the oxygen-carrying capability of hemoglobin and subsequently induces hypoxic effects.
Previous studies investigating the impact of smoking on the red blood cell system provide mixed results. While some studies show higher red blood cell indices in smokers in comparison with non-smokers, some indicate that smoking can induce eryptosis. Eryptosis is a means of erythrocyte (red blood cell) death, characterised by phosphatidylserine externalization and cell shrinkage.
In this massive population-based cohort study, scientists have investigated the impact 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 mean corpuscular hemoglobin concentration (MCHC).
The present study included 2,023 participants from the German National Cohort Study (NAKO), which incorporates greater than 205,000 adult participants across 18 study centers in numerous German states.
Blood samples collected from the 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.
Amongst 2,023 participants included within the study, 1,000 were non-smokers, 418 were current smokers, and 605 were ex-smokers.
The comparative evaluation between smoking habits and eryptosis revealed that smokers have a moderately higher rate of eryptosis than non-smokers and ex-smokers. Specifically, smokers showed 14% and 19% higher percentages of eryptotic cells in comparison with non-smokers and ex-smokers, respectively. Nevertheless, no significant difference in eryptosis was observed between non-smokers and ex-smokers.
Moreover, the study found a positive association between the variety of cigarettes smoked per day and the speed of eryptosis. This association remained the identical for each female and male smokers. Nevertheless, no association between the smoking burden per yr and the speed of eryptosis was observed in all the study population.
A subgroup evaluation including ex-smokers revealed a negative association between the duration of smoking cessation and the speed of eryptosis. The age of smoking cessation and the time since smoking cessation were identified as significant predictors of eryptosis in ex-smokers.
Regarding hematological parameters, no association of eryptosis was observed with erythrocyte count, hemoglobin, hematocrit, and MCV. Nevertheless, there was a moderately positive association between eryptosis and MCH and MCHC.
No significant differences in erythrocyte count and hematocrit were observed between smokers, non-smokers, and ex-smokers. Nevertheless, smokers showed higher levels of hemoglobin, MCV, MCH, and MCHC than the remaining.
The day by day variety of cigarettes smoked, smoking duration, and annual smoking burden showed a moderately positive association with hematocrit, hemoglobin, MCV, and MCH and a negative association with MCHC in current smokers.
The study finds that current smokers have a moderately higher rate of suicidal erythrocyte death than non-smokers and ex-smokers. Nevertheless, despite higher erythrocyte death, smokers have comparatively higher erythrocyte indices. This means that higher eryptosis in smokers has no apparent negative impact on the general red blood cell system.
Based on the available literature, smoking-induced oxidative stress and inflammation may play a task in triggering eryptosis. Carbon monoxide inhaled during smoking has also been found to stimulate eryptosis directly. Furthermore, the p38MAPK/Fas signaling pathway has been found to extend the eryptosis rate in smokers.
Despite higher erythrocyte death, the study found fewer erythrocyte counts amongst smokers. This may very well be on account of enhanced erythropoiesis (the means of producing recent erythrocytes) in smokers to compensate for the eryptosis-mediated lack of erythrocytes.
As mentioned by the scientists, including numerous participants is the study’s major strength. Nevertheless, self-reported smoking status may be subjected to reporting bias. The scientists are looking forward to studying whether increased eryptosis is related to the next risk of heart problems in smokers.