scholarly journals Smoking during pregnancy, birth outcomes, and discordance between biomarker and self-reported smoking status.

2022 ◽  
Vol 226 (1) ◽  
pp. S527
Author(s):  
Jaclyn M. Hall ◽  
Dominick J. Lemas ◽  
Ramzi Salloum ◽  
HeeDeok Cho ◽  
Mildred Maldonado-Molina ◽  
...  
Author(s):  
Magdalena Chełchowska ◽  
Jadwiga Ambroszkiewicz ◽  
Joanna Gajewska ◽  
Joanna Mazur ◽  
Leszek Lewandowski ◽  
...  

Smoking tobacco can impair proper vascular endothelial functioning. This is exhibited through reduced nitric oxide synthesis as well as activity due to accompanying oxidative stress. We examined the relationship between nitric oxide and markers of oxidative stress/antioxidant defense in serum of smoking and non-smoking pregnant women. Subjects included 99 healthy pregnant women, who were tested for nitric oxide (NO), endothelial (eNOS) and inducible (iNOS) nitric oxide synthase, total oxidant capacity (TOC), and total antioxidant capacity (TAC). NO, eNOS, and TAC serum concentrations were significantly lower (p < 0.005), but iNOS (p < 0.05) and TOC (p < 0.001) were higher in smokers than in non-smokers. Multivariate regression analysis showed associations between NO concentration and eNOS, TAC, and smoking status in the whole group of patients. In the model estimated separately for smokers, the highest impact of eNOS (β = 0.375; p = 0.021) and cotinine (β = −0.323; p = 0.037) was indicated for NO concentration. In the model of non-smokers, eNOS (β = 0.291, p = 0.030) and TAC (β = 0.350; p = 0.015) were important for NO level. Smoking during pregnancy could exacerbate oxidative stress, impair the action of nitric oxide synthases, and adversely affect the balance of oxygen and nitrogen metabolism. Relationships between NO concentrations and TAC in the studied women’s blood can confirm the antioxidant nature of nitric oxide.


2007 ◽  
Vol 26 (6) ◽  
pp. 535-544 ◽  
Author(s):  
E. Köhler ◽  
S. Avenarius ◽  
A. Rabsilber ◽  
C. Gerloff ◽  
G. Jorch

Meconium samples collected from 115 neonates were analysed for nicotine, cotinine and trans -3-hydroxycotinine (OH-cotinine) by means of high-performance liquid chromatography (HPLC) to identify prenatal smoke exposure. The self-reported maternal smoking status during pregnancy was determined by means of a questionnaire and verified by measurements in urine prior to childbirth. The total sum of nicotine and its metabolites (Sumtot) of the first passed meconium samples was 1560 ± 1024 pmol/g in newborns of smoking mothers. Smoking of less than five cigarettes was clearly detected. Sumtot remained constant in all meconium samples passed by a neonate in succession. However, the proportion of nicotine decreased with the time of passage after birth and the OH-cotinine proportion increased, whereas cotinine hardly changed. Nicotine or its metabolites were not detectable in meconium (detection limit < 20 pmol/g), when the mothers were only exposed to environmental tobacco smoke (ETS) using the HPLC method. The hypothesis that the content of nicotine metabolites in meconium reflects long-term smoke exposure could not be confirmed in newborns whose mothers had quit smoking during the latter half of pregnancy. Determining Sumtot enables the intensity of continuous smoking during pregnancy to be estimated in all meconium samples passed by a newborn. Human & Experimental Toxicology (2007) 26: 535—544


2014 ◽  
Vol 22 (3) ◽  
pp. 153-158 ◽  
Author(s):  
Cristian I. Meghea ◽  
Ioana A. Rus ◽  
Răzvan M. Cherecheş ◽  
Nicolae Costin ◽  
Gabriela Caracostea ◽  
...  

2019 ◽  
Author(s):  
Todd M. Everson ◽  
Marta Vives-Usano ◽  
Emie Seyve ◽  
Andres Cardenas ◽  
Marina Lacasaña ◽  
...  

AbstractMaternal smoking during pregnancy (MSDP) contributes to poor birth outcomes, in part through disrupted placental functions, which may be reflected in the placental epigenome. We meta-analyzed the associations between MSDP and placental DNA methylation (DNAm) and between DNAm and birth outcomes within the Pregnancy And Childhood Epigenetics (PACE) consortium (7 studies, N=1700, 344 with any MSDP). We identified 1224 CpGs that were associated with MSDP, of which 341 associated with birth outcomes and 141 associated with gene expression. Only 6 of these CpGs were consistent with the findings from a prior meta-analysis of cord blood DNAm, demonstrating substantial tissue-specific responses to MSDP. The placental MSDP associated CpGs were enriched for growth-factor signaling, hormone activity, inflammation, and vascularization, which play important roles in placental function. We demonstrate links between placental DNAm, MSDP and poor birth outcomes, which may better inform the mechanisms through which MSDP impacts placental function and fetal growth.


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