To determine whether prenatal smoking affects systemic cytokine distribution.
Planned secondary analysis of a prospective, longitudinal multicenter trial.
Regional prenatal clinics.
Smoking and nonsmoking pregnant women (81) with singleton gestation.
Cytokine biomarkers (IL-1α, IL-1β, IL-2, IL-6, IL-8, IL-10, TNFa) and C-reactive protein (CRP) were measured using a multiplex bead lyte assay on a Luminexx IS-100. At each time point, smoking status was collected via self-report (survey) and validated by preset urine cotinine limits. Cytokine data were log transformed. Statistical analysis included descriptive statistics, analysis of variance, t-tests, and Spearman's rank correlation coefficient using Statistical Analysis Software (SAS) version 9.3.
Eighty-one women underwent evaluation in the first trimester, 76 in the second, and 69 in the third. Thirty-nine of the participants (48%) were smokers and self-report smoking status was strongly correlated with urine cotinine (ρ = .68). Less than 10% of women who stated they were nonsmokers were classified as smokers based on urine cotinine limits. First trimester serum CRP was significantly higher in women who smoked (p = .04). Furthermore, proinflammatory cytokines in the second and trimester (IL-6 and IL-1α) were also significantly different between women who smoke and do not smoke during pregnancy (p = .04; p = .02, respectively). No significant differences were observed in other serum cytokine concentrations, including anti-inflammatory IL-10.
Conclusion/Implications for Nursing Practice
Maternal tobacco use and systemic immune responsiveness are individually associated with preterm birth (PTB), and the interaction of tobacco use on systemic cytokines requires further study. Currently, there is limited evidence on the impact of prenatal smoking status on serum cytokines and stress. Prenatal tobacco may affect the critical balance between pro- and anti-inflammatory cytokines/molecules. Both elevated CRP and proinflammatory mediators can trigger oxidative stress, potentially impacting endothelial/endocervical structure. Furthermore, upregulation of proinflammatory cytokines in the second and third trimesters may stimulate an unnecessary inflammatory response and increase the risk for PTB. Nurses and other healthcare professionals need to consistently screen for prenatal tobacco use and offer evidenced-based smoking cessation interventions to reduce PTB risk. Further research is needed to investigate the role of maternal tobacco use on local and systemic immune response during pregnancy.