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Published on: February 24, 2011
Effect of passive smoking on blood lymphocyte apoptosis in children
Moustafa A El-Hodhod1, Ahmed M Hamdy, Manal B Ahmed
1Department of Pediatrics, Faculty of Medicine, Ain Shams University, Cairo, Egypt. moshodhod@yahoo.com
Insights
Passive smoking in children increases lymphocyte apoptosis and alters lipid profiles, potentially increasing infection risk. This study links secondhand smoke exposure to these adverse health effects.
Area of Science:
- Environmental Health
- Immunology
- Pediatrics
Background:
- Passive smoking is a known risk factor for respiratory infections and abnormal lipid profiles.
- The relationship between passive smoking, lymphocyte survival, and lipid profile alterations requires investigation.
Purpose of the Study:
- To investigate the impact of passive smoking on lymphocyte apoptosis and lipid profiles in children.
- To explore potential links between altered lipid profiles and increased lymphocytic apoptosis in children exposed to secondhand smoke.
Main Methods:
- Assessed urinary cotinine and creatinine levels, lipid profiles, and peripheral blood lymphocyte (PBL) apoptosis via flow cytometry.
- Compared 26 children with indoor passive smoking exposure to 14 matched controls.
Main Results:
- Passive smoking children exhibited higher triglycerides, cholesterol, LDL, and lower HDL levels.
- Urinary cotinine levels correlated positively with triglycerides and LDL, and negatively with HDL.
- Early apoptosis of PBL was significantly higher in children exposed to passive smoking.
Conclusions:
- Passive smoking in children may enhance lymphocytic apoptosis.
- Altered lipid profiles might contribute to the increased health risks associated with passive smoking.
- Lymphocytic derangement due to passive smoking could impact the frequency of infections.
Background:
Passive smoking is a well-known risk factor for both recurrent respiratory infections and disturbed lipid profile. Whether passive smoking problems are related to altered lymphocyte survival and its relation to altered lipid profile are the points of concern in this work.
Materials And Methods:
Urinary cotinine and creatinine levels as well as lipid profile and flow cytometric assessment of apoptosis of peripheral blood lymphocytes (PBL) were assessed in 26 children with history of indoor exposure to cigarette smokers in comparison with 14 matched children with no such history.
Results:
Lipid profile showed significantly higher mean levels of triglycerides, cholesterol and low-density lipoprotein (LDL) and significantly lower mean levels of high-density lipoprotein (HDL) in passive smoking children compared to nonpassive-smoking ones. Furthermore, cotinine parameters were positively correlated with triglycerides and LDL and negatively correlated with HDL. Early apoptosis of PBL was significantly higher in exposed vs nonexposed ones.
Conclusions:
Passive smoking in children could be a risk factor for enhanced lymphocytic apoptosis. It is possible that altered lipid profile may play a role in the increased risk. The impact of this lymphocytic derangement on increased frequency of infections is noticeable.
