Scholarlink

Background <p>Exposure during pregnancy to secondhand smoke (SHS) is associated with a wide range of adverse fetal development effects and perinatal outcomes. This study aimed to measure SHS exposure in pregnant women using urinary cotinine measurements and to evaluate the association between paternal smoking and maternal urine cotinine and birth outcomes in a birth cohort of Israeli mothers and children.</p> Methods <p>We measured cotinine in urine samples taken at birth from 96 non-smoking mothers participating in the EHF (Environmental Health Fund)-Assaf-Harofeh-Ichilov cohort. Half of the partners were smokers, based on the self-reported data. Logistic regression models were used to predict maternal urinary cotinine levels, and potential confounders were included in the model. We analyzed the association between maternal urinary cotinine levels and birth weight.</p> Results <p>In our study of 96 nonsmoking pregnant women, 94% of women with a smoking partner and nearly 60% of those with a non-smoking partner were exposed to SHS and had urine cotinine levels above the Limits of Quantification (LOQ). Paternal smoking was a significant predictor for maternal urinary cotinine levels above the LOQ (aOR 7.83 95%CI [2.01–30.57], p-value = 0.003). There were no statistically significant differences between the birth outcomes (e.g. gestational age, birth weight, birth length, head circumference, and the delivery method) tested in both groups– self-reported smoking status and exposed vs. non-exposed newborns. Maternal urinary cotinine levels were inversely associated with newborns’ birth weight (beta estimate − 281.39, p-value = 0.048). When stratified by sex, in male newborns, maternal urinary cotinine was inversely associated with newborns’ birth weight (beta estimate 470.22, p-value = 0.014), but not in females.</p> Conclusions <p>Our findings support the fact that partners are one of the primary sources of maternal secondhand smoke and may play an essential role in creating and maintaining smoke-free environments.</p> Trial registration <p>ClinicalTrials.gov, ID: NCT03084445. Registered 06 February 2014, <a href="https://clinicaltrials.gov/study/NCT03084445">https://clinicaltrials.gov/study/NCT03084445</a>.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Paternal smoking and maternal secondhand smoke exposure and the effects on the offspring: results from the EHF (Environmental Health Fund) birth cohort

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月8日

查看全文
  • Maya Berlin,
  • Elkana Kohn,
  • Rimona Keidar,
  • Ayelet Livne,
  • Ronella Marom,
  • Amit Ovental,
  • Dror Mandel,
  • Ronit Lubetzky,
  • Moshe Betser,
  • Miki Moskovich,
  • Ariela Hazan,
  • Ludmila Groisman,
  • Efrat Rorman,
  • Matitiahu Berkovitch,
  • Ilan Matok,
  • Laura J. Rosen

摘要

Background

Exposure during pregnancy to secondhand smoke (SHS) is associated with a wide range of adverse fetal development effects and perinatal outcomes. This study aimed to measure SHS exposure in pregnant women using urinary cotinine measurements and to evaluate the association between paternal smoking and maternal urine cotinine and birth outcomes in a birth cohort of Israeli mothers and children.

Methods

We measured cotinine in urine samples taken at birth from 96 non-smoking mothers participating in the EHF (Environmental Health Fund)-Assaf-Harofeh-Ichilov cohort. Half of the partners were smokers, based on the self-reported data. Logistic regression models were used to predict maternal urinary cotinine levels, and potential confounders were included in the model. We analyzed the association between maternal urinary cotinine levels and birth weight.

Results

In our study of 96 nonsmoking pregnant women, 94% of women with a smoking partner and nearly 60% of those with a non-smoking partner were exposed to SHS and had urine cotinine levels above the Limits of Quantification (LOQ). Paternal smoking was a significant predictor for maternal urinary cotinine levels above the LOQ (aOR 7.83 95%CI [2.01–30.57], p-value = 0.003). There were no statistically significant differences between the birth outcomes (e.g. gestational age, birth weight, birth length, head circumference, and the delivery method) tested in both groups– self-reported smoking status and exposed vs. non-exposed newborns. Maternal urinary cotinine levels were inversely associated with newborns’ birth weight (beta estimate − 281.39, p-value = 0.048). When stratified by sex, in male newborns, maternal urinary cotinine was inversely associated with newborns’ birth weight (beta estimate 470.22, p-value = 0.014), but not in females.

Conclusions

Our findings support the fact that partners are one of the primary sources of maternal secondhand smoke and may play an essential role in creating and maintaining smoke-free environments.

Trial registration

ClinicalTrials.gov, ID: NCT03084445. Registered 06 February 2014, https://clinicaltrials.gov/study/NCT03084445.