Effet du tabagisme sur l’implantation embryonnaire et la placentation précoce et facteurs influençant la toxicité tabagique sur la reproduction (Partie II)

Background An inverse association between maternal smoking and preeclampsia has been frequently observed in epidemiologic studies for several decades. In the May 2015 issue of this journal, Lisonkova and Joseph described a simulation study suggesting that bias from left truncation might explain the inverse association. The simulations were based on strong assumptions regarding the underlying mechanisms through which bias might occur. Methods To examine the sensitivity of the previous authors’ conclusions to these assumptions, we constructed a new Monte Carlo simulation using published estimates to frame our data generating parameters. We estimated the association between smoking and preeclampsia across a range of scenarios that incorporated abnormal placentation and early pregnancy loss. Results Our results confirmed that the previous authors’ findings are highly dependent on assumptions regarding the strength of association between abnormal placentation and preeclampsia. Thus, the bias they described may be less pronounced than was suggested. Conclusions Under empirically-derived constraints of these critical assumptions, left truncation does not appear to fully explain the inverse association between smoking and preeclampsia. Further, when considering processes in which left truncation may result from the exposure, it is important to precisely describe the target population and parameter of interest before assessing potential bias. We comment on the specification of a meaningful target population when assessing maternal smoking and preeclampsia as a public health issue. We describe considerations for defining a target population in studies of perinatal exposures when those exposures cause competing events (e.g., early pregnancy loss) for primary outcomes of interest.

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“…8 Regarding assumption 3, smoking during pregnancy has been associated with increased risk of impaired placental development. 9,10 …”

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confidence: 99%

Left Truncation Bias to Explain the Protective Effect of Smoking on Preeclampsia

et al. 2017

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“…Egg quality, influenced by its follicular microenvironment, is susceptible to a range of physiological, biochemical, and environmental The forest of subgroup analyses of the effect of ETS on infertility. (35,36). Cigarette smoke components contribute to follicular lipid peroxidation and DNA damage, as evidenced in animal studies showing its effects on oocyte depletion, apoptosis, and oxidative stress, leading to fewer ovulating follicles (37).…”

Section: Discussionmentioning

confidence: 99%

Unraveling the link: environmental tobacco smoke exposure and its impact on infertility among American women (18–50 years)

Peng,

Luo,

Cao

et al. 2024

Front. Public Health

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PurposeThe detrimental effects of environmental tobacco smoke (ETS) on women’s reproductive health have been widely recognized. However, the detailed association between exposure to environmental tobacco smoke and the incidence of infertility remains under-explored. This investigation focuses on exploring this potential connection.MethodsFor this analysis, we extracted data from the US National Health and Nutrition Examination Survey (NHANES) database, covering the years 2013 to 2018, focusing on individuals with recorded serum cotinine levels and infertility information. ETS exposure and fertility status were analyzed as independent and dependent variables, respectively. We applied weighted multivariate logistic regression method to evaluate the impact of ETS on infertility, including subgroup analyses for more detailed insights.ResultsThe study encompassed 3,343 participants. Logistic regression analysis revealed a notable positive correlation between ETS exposure and infertility, with an odds ratio (OR) of 1.64 (95% Confidence Interval [CI]: 1.14–2.36). We observed a non-linear relationship between ETS exposure and infertility risk. Notably, infertility risk increased by 64% in serum cotinine levels above 0.136 compared to that in serum cotinine levels below 0.011. Further, subgroup analysis and interaction tests showed consistent results across different segments, underscoring the robustness of the ETS-infertility link.ConclusionOur findings suggest that environmental tobacco smoke exposure may be a contributing factor to infertility. These results reinforce the recommendation for women in their reproductive years to avoid ETS exposure, especially when planning for pregnancy.

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“…Scientific literature strengthens this hypothesis, underlining the β 2 GPI presence only as a phospholipid antigen in trophoblasts cell membrane and placental endothelial cells, especially at the implantation site, as well as in the liver [6]. The pathological conditions taken into account are characterized by an aberrant implantation process, caused by anomalies in the immunological (RPL and ahT) and oxidative stress (RPL and smoking) physiological balances, leading to placental endothelial dysfunction, dysregulation in neo-angiogenesis pathways and accelerated apoptotic processes in trophoblast cell line [24, 32–35]. The presence of anti-β 2 GPI Abs in the AF could represent a direct marker of placental dysfunction and of abnormal implantation, since an accelerated apoptotic process could expose the β 2 GPI antigen from trophoblast cells disrupted membrane.…”

Section: Discussionmentioning

confidence: 99%

Amniotic fluid antiphospholipid antibodies: potential role in antiphospholipid syndrome-independent aberrant implantation process

Bruno

Nuccetelli

Ticconi

et al. 2019

Reprod Biol Endocrinol

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Background The direct role of antiphospholipid antibodies (aPL) at maternal-fetal interface has not been fully investigated, especially whether they are involved in physiological and pathological implantation conditions, in an antiphospholipid syndrome (APS)-independent manner. In fact, trophoblast cells and placental endothelial cells at the implantation site express potential aPL targeted-phospholipid antigens (PL Ags); thus, the local production and presence of their specific antibodies, not related to APS (characterized by aPL presence in the peripheral blood), could be a potential marker of aberrant invasion, implantation and fetal-maternal immune tolerance processes. Methods Anti-Beta2glycoprotein I (anti-β2GPI) and anticardiolipin (aCL Ab) antibodies (the most clinically relevant aPL) were detected by immunoenzymatic assay (ELISA), in the amniotic fluid (AF) of 167 women with physiological and complicated common pregnancy conditions, sharing an aberrant implantation process, such as recurrent pregnancy loss (RPL), autoimmune hypothyroidism (ahT) and smoking. All women included in the study were negative to peripheral blood aPL. Results aCL and anti-β2GPI antibodies were detectable in all the AF samples. RPL, ahT and smoking patients had higher level of anti-β2GPI Abs (IgM) compared to women with physiological pregnancies (p < 0.0001). Since IgM cannot cross the placenta, their local production in response to maternal-fetal interface stimuli, could be hypothesized. Conclusions The presence of aPL in the AF (not related to APS) could reveal a potential clinical significance at maternal-fetal interface in selected pregnancy complications, in which an aberrant implantation process, and in turn an impaired fetal-maternal immune tolerance cross-talk, could occur.

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Effet du tabagisme sur l’implantation embryonnaire et la placentation précoce et facteurs influençant la toxicité tabagique sur la reproduction (Partie II)

Cited by 15 publications

References 104 publications

Left Truncation Bias to Explain the Protective Effect of Smoking on Preeclampsia

Left Truncation Bias to Explain the Protective Effect of Smoking on Preeclampsia

Unraveling the link: environmental tobacco smoke exposure and its impact on infertility among American women (18–50 years)

Amniotic fluid antiphospholipid antibodies: potential role in antiphospholipid syndrome-independent aberrant implantation process

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