Maternal Passive Smoking Exposure Research Articles

Effectiveness of Integrated Maternal Nutrition Intervention Package on Birth Weight in Rwanda.

Inadequate maternal nutrition before and during pregnancy is a principal risk factor for poor fetal development, resulting in low birth weight (LBW) and subsequently, poor child growth. Most studies focus on the impact of nutritional interventions after birth while only a few interventions consider integrated nutrition service packages. Therefore, there is limited evidence on whether integrated maternal nutrition interventions have a positive effect on birthweight. Thus, a post-program quasi-experimental study was carried out to determine the effectiveness of the integrated maternal nutrition intervention package on low birth weight in Rwanda. A total of 551 mother–baby pairs from the intervention and 545 controls were included in the analysis. Data regarding socio-demographic, maternal anthropometric parameters, and dietary diversity were collected using a structured questionnaire. Birth weight was assessed right after delivery, within 24 h. Logistic regression, linear regression, and path analysis were fitted to determine the effectiveness of the intervention on birth weight. The study found that the intervention reduced LBW by 66.99% (p < 0.001) and increased average birth weight by 219 g (p < 0.001). Logistic regression identified reduced risk of LBW among the intervention group (AOR = 0.23; 95%CI = 0.12–0.43; p < 0.001). It was also observed that the direct effect of the intervention on birth weight was 0.17 (β = 0.17; p < 0.001) and the main indirect mediator was maternal MUAC (β = 0.05; p < 0.001). Moreover, maternal passive smoking exposure and MUAC < 23 cm were found as risk factors for LBW. This study has demonstrated that an integrated maternal nutritional intervention package can significantly reduce LBW in low-income settings and should, therefore, be considered to improve birth weight.

Early-life exposure to indoor air pollution or tobacco smoke and lower respiratory tract illness and wheezing in African infants: a longitudinal birth cohort study

SummaryBackgroundIndoor air pollution (IAP) and environmental tobacco smoke (ETS) are associated with lower respiratory tract illness (LRTI) or wheezing in children. However, the effect of the timing of these exposures, specifically antenatal versus postnatal, and of alternate fuel sources such as the increasingly used volatile organic compounds have not been well studied. We longitudinally investigated the effect of antenatal or postnatal IAP and ETS on LRTI or wheezing prevalence and severity in African infants.MethodsMother and infant pairs enrolled over a 3-year period in a birth cohort study in two centres in Paarl, South Africa, were followed for the first year of life for LRTI or wheezing illness. We measured exposure to IAP (particulate matter, nitrogen dioxide, sulphur dioxide, carbon monoxide, and volatile organic compounds benzene and toluene) using devices placed in homes, antenatally and postnatally. We measured ETS longitudinally by maternal self-report and by urine cotinine measures. Study staff trained in recognition of LRTI or wheeze documented all episodes, which were categorised according to WHO case definition criteria. We used multivariate logistic and Poisson regressions to explore associations.FindingsBetween March 1, 2012, and March 31, 2015, we enrolled 1137 mothers with 1143 livebirths. Of 1065 infants who attended at least one study visit, 524 episodes of LRTI occurred after discharge with a wheezing prevalence of 0·23 (95% CI 0·21–0·26) episodes per child year. Exposures associated with LRTI were antenatal maternal smoking (incidence rate ratio 1·62, 95% CI 1·14–2·30; p=0·004) or particulate matter (1·43, 1·06–1·95; p=0·008). Subanalyses of LRTI requiring hospitalisation (n=137) and supplemental oxygen (n=69) found antenatal toluene significantly increased the risk of LRTI-associated hospitalisation (odds ratio 5·13, 95% CI 1·43–18·36; p=0·012) and need for supplemental oxygen (13·21, 1·96–89·16; p=0·008). Wheezing illness was associated with both antenatal (incidence rate ratio 2·09, 95% CI 1·54–2·84; p<0·0001) and postnatal (1·27, 95% CI 1·03–1·56; p=0·024) maternal smoking. Antenatally, wheezing was associated with maternal passive smoke exposure (1·70, 1·25–2·31; p=0·001) and, postnatally, with any household member smoking (1·55, 1·17 −2·06; p=0·002).InterpretationAntenatal exposures were the predominant risk factors associated with LRTI or wheezing illness. Toluene was a novel exposure associated with severe LRTI. Urgent and effective interventions focusing on antenatal environmental factors are required, including smoking cessation programmes targeting women of childbearing age pre-conception and pregnant women.FundingBill & Melinda Gates Foundation, Discovery Foundation, South African Thoracic Society AstraZeneca Respiratory Fellowship, Medical Research Council South Africa, National Research Foundation South Africa, and CIDRI Clinical Fellowship.

Passive smoking in the etiology of non-syndromic orofacial clefts: a systematic review and meta-analysis.

BackgroundStudies have found a consistent positive association between maternal smoking and non-syndromic orofacial clefts (NSOFC). However, no comprehensive assessment of the association between NSOFC and passive smoking has been undertaken. This systematic review and meta-analysis explores the relationship between maternal passive smoking and NSOFC, and compares the associations between passive and active smoking.Methods and FindingsSearch strategy, inclusion / exclusion criteria, and data extraction from studies reporting maternal passive smoking and NSOFC was implemented without language restrictions. Risks of bias in the identified studies were assessed and this information was used in sensitivity analyses to explain heterogeneity. Meta-analysis and meta-regression of the extracted data were performed. Egger's test was used to test for small study effects. Fourteen eligible articles were identified. Maternal passive smoking exposure was associated with a twofold increase in risk of NSOFC (odds ratio: 2.11, 95% confidence interval: 1.54–2.89); this was apparent for both cleft lip with and without palate (OR: 2.05, 95% CI: 1.27–3.3) and cleft palate (OR: 2.11, 95% CI: 1.23–3.62). There was substantial heterogeneity between studies. In the studies that provided data enabling crude and adjusted odd ratios to be compared, adjustment for potential confounders attenuated the magnitude of association to about a 1.5-fold increase in risk.ConclusionOverall, maternal passive smoking exposure results in a 1.5 fold increase in risk of NSOFC, similar to the magnitude of risk reported for active smoking, but there is marked heterogeneity between studies. This heterogeneity is not explained by differences in the distribution of cleft types, adjustment for covariates, broad geographic region, or study bias/quality. This thorough meta-analysis provides further evidence to minimize exposure to environmental tobacco smoke in policy making fora and in health promotion initiatives.

Cigarette smoke‐induced transgenerational alterations in genome stability in cord blood of human F1 offspring

The relevance of preconceptional and prenatal toxicant exposures for genomic stability in offspring is difficult to analyze in human populations, because gestational exposures usually cannot be separated from preconceptional exposures. To analyze the roles of exposures during gestation and conception on genomic stability in the offspring, stability was assessed via the Comet assay and highly sensitive, semiautomated confocal laser scans of γH2AX foci in cord, maternal, and paternal blood as well as spermatozoa from 39 families in Crete, Greece, and the United Kingdom. With use of multivariate linear regression analysis with backward selection, preconceptional paternal smoking (% tail DNA: P>0.032; γH2AX foci: P>0.018) and gestational maternal (% tail DNA: P>0.033) smoking were found to statistically significantly predict DNA damage in the cord blood of F1 offspring. Maternal passive smoke exposure was not identified as a predictor of DNA damage in cord blood, indicating that the effect of paternal smoking may be transmitted via the spermatozoal genome. Taken together, these studies reveal a role for cigarette smoke in the induction of DNA alterations in human F1 offspring via exposures of the fetus in utero or the paternal germline. Moreover, the identification of transgenerational DNA alterations in the unexposed F1 offspring of smoking-exposed fathers supports the claim that cigarette smoke is a human germ cell mutagen.

Relationship between birth weight and domestic maternal passive smoking exposure

This study aimed to assess the relationship between birth weight and maternal exposure to passive smoking during pregnancy, and to investigate some other determinants of birth weight. A retrospective cohort study in Baghdad, Iraq was conducted during February to August 2004 on a random sample of 300 non-smoker housewife mothers, interviewed 24 hours after delivery: 150 were not exposed to passive smoking at home and 150 were exposed. The mean birth weight of exposed newborns was significantly lower than non-exposed newborns. In exposed newborns, a significant inverse relationship was noticed between birth weight and the number of cigarettes smoked by household members (r = -0.27). Multiple regression analysis showed that after controlling for all the variables studied, birth weight had a significant inverse correlation with the maternal exposure to passive smoking and a positive correlation with adequate antenatal care.

Transforming Growth Factor Beta-3 and Environmental Factors and Cleft Lip with/without Cleft Palate

To identify the interactions among two loci (C641A and G15572-) of transforming growth factor beta 3 (TGFbeta3), and exposures in pregnancy with cleft lip with/without cleft palate (CL/P), a hospital-based case-control study was conducted. Associations among offspring polymorphisms of TGFbeta3 C641A and G15572-, paternal smoking, paternal high-risk drinking, maternal passive smoking, and maternal multivitamin supplement with CL/P were analyzed by logistic regression analysis, and the results showed that maternal passive smoking exposures and maternal multivitamin use were associated with the risk of CL/P but offspring polymorphisms of TGFbeta3 C641A and G15572-, paternal smoking, and paternal high-risk drinking were not. Interactions among these variables were analyzed using the multifactor dimensionality reduction method, and the results showed that the two-factor model, including maternal passive smoking and TGFbeta3 C641A, among all models evaluated had the best ability to predict CL/P risk with a maximum cross-validation consistency (9/10) and a maximum average testing accuracy (0.5892; p = 0.0010). These findings suggested that maternal passive smoking exposure is a risk factor for CL/P, whereas maternal multivitamin supplement is a protective factor. The polymorphism of TGFbeta3 C641A participates in interaction effect for CL/P with environmental exposures, although the polymorphism was not associated with CL/P in single-locus analysis, and synergistic effect of TGFbeta3 C641A and maternal passive smoking could provide a new tool for identifying high-risk individuals of CL/P and also an additional evidence that CL/P is determined by both genetic and environmental factors.

Analysis of interactions between genetic variants of BMP4 and environmental factors with nonsyndromic cleft lip with or without cleft palate susceptibility

A hospital-based case-control study was conducted to identify interactions between the 538(T-->C) polymorphic site of bone morphogenetic protein 4 gene (BMP4T538C) and exposures in pregnancy with nonsyndromic cleft lip, with or without cleft palate (nsCL/P). Associations between offspring polymorphism of BMP4T538C, paternal smoking, paternal high-risk drinking, maternal passive smoking, and maternal multivitamin supplement with nsCL/P were analyzed by logistic regression analysis. BMP4T538C polymorphism, maternal passive smoking exposures and maternal multivitamin use were associated with the risk of nsCL/P but paternal smoking and paternal high-risk drinking were not. Gene-environment interactions were analyzed using the multifactor dimensionality reduction (MDR) method. The two-factor model including maternal passive smoking and BMP4T538C, was the best for predicting nsCL/P risk with a maximum cross-validation consistency (10/10) and a maximum average testing accuracy(0.605; P<0.0001). The findings suggested that: BMP4T538C could be used as a genetic susceptibility marker for nsCL/P; maternal passive smoking exposure is a risk factor for nsCL/P; maternal multivitamin supplements are a protective factor; the synergistic effect of BMP4T538C and maternal passive smoking could provide a new tool for identifying individuals at high risk of nsCL/P, and provides additional evidence that nsCL/P is determined by genetic and environmental factors.

Maternal Passive Smoking Exposure and Offspring Birthweight: A Gene-Environment Study

Maternal Passive Smoking Exposure and Offspring Birthweight: A Gene-Environment Study

Passive smoking and pregnancy outcome in central Poland.

1. The present investigation was undertaken to evaluate the effect of environmental tobacco smoke (ETS) on the risk of preterm delivery (PD) and small-for-gestational age (SGA) infants in a female non-smoking population of central Poland. 2. The study group were 1751 women classified as non-smokers in the comprehensive project on 'Socio-economic and environmental risk factors of preterm delivery and small-for-gestationaI-age babies in central Poland' conducted on a randomly selected population of 2080 women who gave birth to a child between June 1, 1996 and May 31, 1997. The PD group comprised 95 non-smoking women who delivered before 37 weeks of pregnancy and the SGA group included 111 non-smoking mothers of babies with birthweight below the 10th percentile of the standard curves for central Poland. Passive exposure to tobacco smoke was determined based on a structured interview. 3. In the stepwise multiple logistic regression model maternal passive smoke exposure lasting 7 h or more was found to be a significant risk factor for preterm delivery. No significant effect of passive smoking on the risk of SGA was observed. 4. The information about the adverse effects of ETS exposure on pregnancy duration and outcome should be incorporated in the health promotion programmes for women.

Parental cigarette smoking and the risk of spontaneous abortion.

Although cigarette smoking is often considered a risk factor for spontaneous abortion, the epidemiologic literature is actually inconsistent. Therefore, the authors examined maternal and paternal smoking and maternal passive smoke exposure using data from a large case-control study of spontaneous abortion (626 cases and 1,300 controls) conducted in Santa Clara County, California, in 1986 and 1987. No excess risk of spontaneous abortion was seen in the 1% of women who smoked an average of more than 20 cigarettes per day in the first trimester. Moderate smokers (11-20 cigarettes per day) had a slightly elevated crude odds ratio of 1.3 (95% confidence interval 0.9-1.9), which was close to unity after adjustment for covariates. Paternal smoking showed a slight crude elevation for moderate and heavy smoking, but no association after adjustment. In contrast, maternal exposure to environmental tobacco smoke for 1 hour or more per day was associated with spontaneous abortion, even after adjustment (odds ratio = 1.5, 95% confidence interval 1.2-1.9). For both maternal direct and environmental exposure, the association appeared to be stronger in second-trimester abortions. Several studies have found stronger associations of smoking with late versus early abortions, perhaps reflecting smoking-associated placental insufficiency and fetal hypoxia.