Objective: To study cytogenetic damage in order to estimate the effect of pre-pregnancy smoking on
pregnant women and their foetuses.
Study design: Lymphocyte cultures were obtained from peripheral blood of 20 women who quit smoking
during pregnancy, and umbilical cord blood of their newborns at delivery. Cytogenetic analyses were
performed for sister chromatid exchanges (SCEs), proliferation rate index (PRI) and mitotic index (MI)
using the Fluorescence Plus Giemsa staining technique. Twenty non-smoking women and their
newborns were evaluated as controls. CPT-11, a known antineoplastic, was used as a positive genotoxic
agent in order to correlate non-smoking women with smoking women and reveal any underlying
chromosome instability. Statistical evaluation of SCE frequencies, PRI and MI was based on independent
samples t-test in order to estimate the effect of pre-pregnancy smoking on mothers and their newborns.
Results: SCEs were induced in the cord blood lymphocytes of newborns whose mothers smoked before
pregnancy when they were exposed to the mutagenic agent CPT-11 (p < 0.01). A similar increase in SCEs
was observed in both non-smoking and smoking mothers exposed to CPT-11. Newborns in both groups
had significantly lower SCE levels than their mothers (p < 0.01).
Conclusion: Pre-pregnancy smoking results in cytogenetic damage for both mothers and newborns, and
is an important risk factor for cancer and/or other genetic-related diseases. Smoking cessation needs to
occur well before conception in order to avoid the strong cytogenetic association between pre-pregnancy
smoking by mothers and their newborns.
Objective: To study cytogenetic damage in order to estimate the effect of pre-pregnancy smoking on
pregnant women and their foetuses.
Study design: Lymphocyte cultures were obtained from peripheral blood of 20 women who quit smoking
during pregnancy, and umbilical cord blood of their newborns at delivery. Cytogenetic analyses were
performed for sister chromatid exchanges (SCEs), proliferation rate index (PRI) and mitotic index (MI)
using the Fluorescence Plus Giemsa staining technique. Twenty non-smoking women and their
newborns were evaluated as controls. CPT-11, a known antineoplastic, was used as a positive genotoxic
agent in order to correlate non-smoking women with smoking women and reveal any underlying
chromosome instability. Statistical evaluation of SCE frequencies, PRI and MI was based on independent
samples t-test in order to estimate the effect of pre-pregnancy smoking on mothers and their newborns.
Results: SCEs were induced in the cord blood lymphocytes of newborns whose mothers smoked before
pregnancy when they were exposed to the mutagenic agent CPT-11 (p < 0.01). A similar increase in SCEs
was observed in both non-smoking and smoking mothers exposed to CPT-11. Newborns in both groups
had significantly lower SCE levels than their mothers (p < 0.01).
Conclusion: Pre-pregnancy smoking results in cytogenetic damage for both mothers and newborns, and
is an important risk factor for cancer and/or other genetic-related diseases. Smoking cessation needs to
occur well before conception in order to avoid the strong cytogenetic association between pre-pregnancy
smoking by mothers and their newborns.
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