Invisible Wounds of Motherhood: How Smoking During Pregnancy Fuels Postpartum Depression
Poster #: 167
Session/Time: B
Author:
Reem Sharaf-Alddin, MD, MS
Mentor:
Qi(Harry) Zhang B.A., PhD
Research Type: Review Article
Abstract
INTRODUCTION:
Postpartum Depression (PPD) is the most common mental health complication of childbirth. PPD has both short-term and long-term consequences for the mother and child alike. PPD is a function of several factors, including biological, social, behavioral, and environmental factors, which together predispose individuals to PPD. A major modifiable risk factor for PPD is prenatal exposure to nicotine (PEN), which can occur through Active Tobacco Smoking (ATS), Secondhand Smoking (SHS), or Electronic Nicotine Products (ENPs) use. This systematic review and meta-analysis aim to summarize and evaluate all current evidence regarding the relationship between all types of prenatal exposure to nicotine and PPD.
MAIN BODY:
We searched the following databases, PubMed, Medline, Cochrane, EMBASE, and CINHAL, for all studies published between Jan 1, 2000, and Sep 19, 2024, with the outcome PPD. The quality of the included studies was assessed using the Newcastle-Ottawa Scale for observational studies. Pooled prevalence was calculated using the Freeman-Tukey Double Arcsine Transformation method. The Pooled Odds Ratio (pooled-OR) was compared for women with prenatal exposure to nicotine compared to women with no prenatal exposure to nicotine using a random effects model. The sensitivity analysis was conducted using the leave-one-out technique. Out of the 29 studies in the systematic review, 26 met the inclusion criteria for meta-analysis. The pooled prevalence of PPD was 0.15 (95% CI [0.12 - 0.17]; I2=99.80%, p<0.001). The pooled-OR was 1.74 (95%CI [1.44 - 2.12]; Z=5.59, p<0.001) for overall prenatal exposure to nicotine, 1.96, (95%CI 1.59 - 2.41; Z=6.46, p<0.001) for prenatal ATS, 1.22 (95%CI 0.69 - 2.18, Z=0.69, p=0.49) for prenatal SHS, and 1.14 (95%CI 0.82 - 1.58, Z=0.78, p=0.43) for prenatal ENPs use. Funnel plots and the Egger test showed no evidence of publication bias. Sensitivity analysis confirmed the robustness of the findings.
CONCLUSION:
This meta-analysis reveals that the accumulated evidence shows a significant association between prenatal ATS and PPD; however, no clear conclusion could be drawn about prenatal SHS or ENPs use due to the limited number of studies. There is a need for future studies that prospectively assess the impact of SHS and ENP on PPD.
Postpartum Depression (PPD) is the most common mental health complication of childbirth. PPD has both short-term and long-term consequences for the mother and child alike. PPD is a function of several factors, including biological, social, behavioral, and environmental factors, which together predispose individuals to PPD. A major modifiable risk factor for PPD is prenatal exposure to nicotine (PEN), which can occur through Active Tobacco Smoking (ATS), Secondhand Smoking (SHS), or Electronic Nicotine Products (ENPs) use. This systematic review and meta-analysis aim to summarize and evaluate all current evidence regarding the relationship between all types of prenatal exposure to nicotine and PPD.
MAIN BODY:
We searched the following databases, PubMed, Medline, Cochrane, EMBASE, and CINHAL, for all studies published between Jan 1, 2000, and Sep 19, 2024, with the outcome PPD. The quality of the included studies was assessed using the Newcastle-Ottawa Scale for observational studies. Pooled prevalence was calculated using the Freeman-Tukey Double Arcsine Transformation method. The Pooled Odds Ratio (pooled-OR) was compared for women with prenatal exposure to nicotine compared to women with no prenatal exposure to nicotine using a random effects model. The sensitivity analysis was conducted using the leave-one-out technique. Out of the 29 studies in the systematic review, 26 met the inclusion criteria for meta-analysis. The pooled prevalence of PPD was 0.15 (95% CI [0.12 - 0.17]; I2=99.80%, p<0.001). The pooled-OR was 1.74 (95%CI [1.44 - 2.12]; Z=5.59, p<0.001) for overall prenatal exposure to nicotine, 1.96, (95%CI 1.59 - 2.41; Z=6.46, p<0.001) for prenatal ATS, 1.22 (95%CI 0.69 - 2.18, Z=0.69, p=0.49) for prenatal SHS, and 1.14 (95%CI 0.82 - 1.58, Z=0.78, p=0.43) for prenatal ENPs use. Funnel plots and the Egger test showed no evidence of publication bias. Sensitivity analysis confirmed the robustness of the findings.
CONCLUSION:
This meta-analysis reveals that the accumulated evidence shows a significant association between prenatal ATS and PPD; however, no clear conclusion could be drawn about prenatal SHS or ENPs use due to the limited number of studies. There is a need for future studies that prospectively assess the impact of SHS and ENP on PPD.