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Tobacco smoke exposure and the risk of childhood acute lymphoblastic leukemia and acute myeloid leukemia
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Abstract
Objective:
Tobacco smoke contains carcinogens known to damage somatic and germ cells. In this study, we investigated the effect of tobacco smoking on the risk of childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML).
Methods:
Information about tobacco smoking exposures of the mother before, during, and after pregnancy was collected via PubMed, Embase, and Web of Science databases through November 5, 2018. We performed to evaluate the association between smoking exposure and the risk of childhood ALL and AML. Study selection, data abstraction, and quality assessment were performed by 2 independent reviewers. Random effects models were used to obtain summary odds ratios (ORs) and 95% confidence intervals (CIs).
Results:
Nineteen case–control studies of childhood leukemia (age < 15 years) conducted in 9 countries from 1974 to 2018. Maternal smoking exposures did not a significant association with childhood ALL (OR = 1.004, 95% CI 0.953–1.058, P = .881) and AML (OR = 0.92, 95% CI 0.815–1.038, P = .177) during exposure time windows. However, there was an association with paternal smoking and ALL (OR = 1.15, 95% CI 1.038–1.275, P = .007). Paternal smoking in AML showed there was no association with smoking exposures and childhood AML (OR = 1.133, 95% CI 0.943–1.362, P = .181). Next, maternal daily cigarettes consumption showed no associations with ALL (OR = 1.08, 95% CI 1.000–1.168, P = .051) during pregnancy. No association with maternal daily smoking and AML (OR = 0.909, 95% CI 0.682–1.211, P = .514). Paternal daily cigarettes consumption was associated with increased risks of childhood ALL (OR = 1.200, 95% CI 1.112–1.302, P = .000). The higher consumption of paternal smoking (more than 10 per day) was significantly related to childhood ALL. Paternal daily smoking consumption also was related to AML (OR = 1.242, 95% CI 1.031–1.496, P = .022).
Conclusion:
Maternal smoking before, during, or after pregnancy was not associated with childhood ALL or AML. However, paternal smoking was related to a significantly elevated risk of childhood ALL during pregnancy, but not for AML. Maternal daily smoking consumption was not associated with ALL or AML during pregnancy. The higher consumption of paternal smoking were, the higher the risk of childhood ALL or AML.
Ovid Technologies (Wolters Kluwer Health)
Title: Tobacco smoke exposure and the risk of childhood acute lymphoblastic leukemia and acute myeloid leukemia
Description:
Abstract
Objective:
Tobacco smoke contains carcinogens known to damage somatic and germ cells.
In this study, we investigated the effect of tobacco smoking on the risk of childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML).
Methods:
Information about tobacco smoking exposures of the mother before, during, and after pregnancy was collected via PubMed, Embase, and Web of Science databases through November 5, 2018.
We performed to evaluate the association between smoking exposure and the risk of childhood ALL and AML.
Study selection, data abstraction, and quality assessment were performed by 2 independent reviewers.
Random effects models were used to obtain summary odds ratios (ORs) and 95% confidence intervals (CIs).
Results:
Nineteen case–control studies of childhood leukemia (age < 15 years) conducted in 9 countries from 1974 to 2018.
Maternal smoking exposures did not a significant association with childhood ALL (OR = 1.
004, 95% CI 0.
953–1.
058, P = .
881) and AML (OR = 0.
92, 95% CI 0.
815–1.
038, P = .
177) during exposure time windows.
However, there was an association with paternal smoking and ALL (OR = 1.
15, 95% CI 1.
038–1.
275, P = .
007).
Paternal smoking in AML showed there was no association with smoking exposures and childhood AML (OR = 1.
133, 95% CI 0.
943–1.
362, P = .
181).
Next, maternal daily cigarettes consumption showed no associations with ALL (OR = 1.
08, 95% CI 1.
000–1.
168, P = .
051) during pregnancy.
No association with maternal daily smoking and AML (OR = 0.
909, 95% CI 0.
682–1.
211, P = .
514).
Paternal daily cigarettes consumption was associated with increased risks of childhood ALL (OR = 1.
200, 95% CI 1.
112–1.
302, P = .
000).
The higher consumption of paternal smoking (more than 10 per day) was significantly related to childhood ALL.
Paternal daily smoking consumption also was related to AML (OR = 1.
242, 95% CI 1.
031–1.
496, P = .
022).
Conclusion:
Maternal smoking before, during, or after pregnancy was not associated with childhood ALL or AML.
However, paternal smoking was related to a significantly elevated risk of childhood ALL during pregnancy, but not for AML.
Maternal daily smoking consumption was not associated with ALL or AML during pregnancy.
The higher consumption of paternal smoking were, the higher the risk of childhood ALL or AML.
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