Pulmonary Effects of Maternal Smoking on the Fetus and Child: Effects on Lung Development, Respiratory Morbidities, and Life Long Lung Health.
Ontology highlight
ABSTRACT:
SUBMITTER: McEvoy CT
PROVIDER: S-EPMC5303131 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:To explore associations of maternal prenatal smoking and child psychological problems and determine the role of causal intrauterine mechanisms.Maternal smoking and child psychological problems were explored in 2 birth cohorts in Pelotas, Brazil (n = 509, random subsample), and the Avon Longitudinal Study of Parents and Children (ALSPAC) in Britain (n = 6735). Four approaches for exploring causal mechanisms were applied: (1) cross-population comparisons between a high-income and a middle-income country; (2) multiple adjustment for socioeconomic and parental psychological factors; (3) maternal-paternal comparisons as a test of putative intrauterine effects; and (4) searching for specific effects on different behavioral subscales.Socioeconomic patterning of maternal prenatal smoking was stronger in the ALSPAC compared with the Pelotas cohort. Despite this difference in a key confounder, consistency in observed associations was found between these cohorts. In both cohorts, unadjusted maternal smoking was associated with greater offspring hyperactivity, conduct/externalizing problems, and peer problems but not with emotional/internalizing problems. After adjusting for confounders and paternal prenatal smoking, only the association with conduct/externalizing problems persisted in both cohorts (conduct problems in the ALSPAC cohort, odds ratio [OR]: 1.24 [95% confidence interval (CI): 1.07-1.46], P = .005; externalizing problems in the Pelotas cohort, OR: 1.82 [95% CI: 1.19-2.78], P = .005; ORs reflect ordinal odds ratios of maternal smokers having offspring with higher scores). Maternal smoking associations were stronger than paternal smoking associations, although statistical evidence that these associations differed was weak in 1 cohort.Evidence from 4 approaches suggests a possible intrauterine effect of maternal smoking on offspring conduct/externalizing problems.
| S-EPMC3605780 | biostudies-literature
Project description:Background and objectiveNon-invasive techniques for measuring lung mechanics in infants are needed for a better understanding of lung growth and function, and to study the effects of prenatal factors on subsequent lung growth in healthy infants. The forced oscillation technique requires minimal cooperation from the individual but has rarely been used in infants. The study aims to assess the use of the forced oscillation technique to measure the influence of antenatal exposures on respiratory mechanics in unsedated infants enrolled in a birth cohort study in Cape Town, South Africa.MethodsHealthy term infants were studied at 6-10 weeks of age using the forced oscillation technique. Respiratory impedance was measured in the frequency range 8-48 Hz via a face mask during natural sleep. Respiratory system resistance, compliance and inertance were calculated from the impedance spectra.ResultsOf 177 infants tested, successful measurements were obtained in 164 (93%). Median (25-75%) values for resistance, compliance and inertance were 50.2 (39.5-60.6) cmH2 O.s.L(-1), 0.78 (0.61-0.99) mL.cmH2 O(-1) and 0.062 (0.050-0.086) cmH2 O.s(2) .L(-1), respectively. As a group, male infants had 16% higher resistance (P = 0.006) and 18% lower compliance (P = 0.02) than females. Infants whose mothers smoked during pregnancy had a 19% lower compliance than infants not exposed to tobacco smoke during pregnancy (P = 0.005). Neither maternal HIV infection nor ethnicity had a significant effect on respiratory mechanics.ConclusionsThe forced oscillation technique is sensitive enough to demonstrate the effects of tobacco smoke exposure and sex in respiratory mechanics in healthy infants. This technique will facilitate assessing perinatal influences of lung function in infancy.
| S-EPMC4670479 | biostudies-literature
Project description:IntroductionOur aim was to understand the strength of association between parental smoking and child environmental tobacco smoke (ETS) exposure in order to inform the development of future tobacco control policies. ETS was measured using child cotinine levels below the active smoking threshold.MethodsParticipants were drawn from the Avon Longitudinal Study of Parents and Children and included 3,128 participants at age 7 years and 1,868 participants at age 15 years. The primary outcome was cotinine levels of nonsmoking children, to investigate the relationship between maternal smoking and child cotinine levels. The secondary outcome was cotinine levels of all individuals to investigate the relationship between child smoking and child cotinine levels. Maternal and child smoking behavior was assessed by self-report questionnaire. We adjusted for several sociodemographic variables.ResultsWe found an association between maternal smoking and child cotinine at age 7 years (mean cotinine = 1.16ng/ml serum, ratio of geometric means = 3.94, 95% CI = 2.86-5.42) and at age 15 years (mean cotinine = 0.94ng/ml serum, ratio of geometric means = 5.26, 95% CI = 3.06-9.03), after adjustment for potential confounders.ConclusionsThe magnitude of this association for children whose mothers were heavy smokers was comparable with the quantity of half the levels of cotinine observed among children who were irregular (i.e., nonweekly) active smokers, and it was greater than five times higher than that seen in nonsmoking children whose mothers didn't smoke. This provides further evidence for the importance of public health interventions to reduce smoking exposure in the home.
| S-EPMC3819976 | biostudies-literature
Project description:Early child neurodevelopment has major impacts on future human capital and health. However, not much is known about the impacts of prenatal risk factors on child neurodevelopment. This study evaluates the effects of maternal smoking during pregnancy on child neurodevelopment between 3 and 24 months of age and interactions with socioeconomic status (SES). Data from a unique sample of children from South America are employed. Smoking has large adverse effects on neurodevelopment, with larger effects in the low SES sample. The study results highlight the importance of early interventions beginning before and during pregnancy for enhancing child development and future human capital attainment.
| S-EPMC3262676 | biostudies-literature
Project description:Use of e-cigarettes, especially among the young, is increasing at near-exponential rates. This is coupled with a perception that e-cigarettes are safe and with unlimited advertising geared toward vulnerable populations, the groups most likely to smoke or vape during pregnancy. There is now wide appreciation of the dangers of maternal smoking during pregnancy and the lifelong consequences this has on offspring lung function, including the increased risk of childhood wheezing and subsequent asthma. Recent evidence strongly supports that much of the effect of smoking during pregnancy on offspring lung function is mediated by nicotine, making it highly likely that e-cigarette use during pregnancy will have the same harmful effects on offspring lung function and health as do conventional cigarettes. In fact, the evidence for nicotine being the mediator of harm of conventional cigarettes may be most compelling for its effects on lung development. This raises concerns about both the combined use of e-cigarettes plus conventional cigarettes by smokers during pregnancy as well as the use of e-cigarettes by e-cigarette-only users who think them safe or by those sufficiently addicted to nicotine to not be able to quit e-cigarette usage during pregnancy. Thus, it is important for health professionals to be aware of the risks of e-cigarette usage during pregnancy, particularly as it pertains to offspring respiratory health.
| S-EPMC4824926 | biostudies-literature
Project description:IntroductionMaternal smoking is a well-known risk factor for youth smoking, yet whether this relationship is causal remains unresolved. This study utilizes propensity score methods for causal inference to robustly account for shared risk factors between maternal and offspring smoking.MethodsAn 8-year longitudinal cohort of 900 adolescents in the Chicago area were followed starting from approximately age 15.6. The effects of maternal lifetime smoking (MLS) and prenatal tobacco exposure (PTE) (among participants reporting MLS) on offspring's past 30-day smoking, daily smoking status and smoking frequency were examined using logistic regression and Poisson regression after nearest-neighbor propensity matching. Age dependency of this relationship was then examined across the age range of 15-25 using time-varying effect modeling.ResultsPropensity matching yielded 438 and 132 pairs for MLS and PTE study samples, respectively. MLS demonstrated significant associations with past 30-day smoking (RR 1.09; 95% CI 1.04-1.14), daily smoking (RR 1.08; 95% CI 1.05-1.12), and smoking frequency of offspring (RR 1.32; 95% CI 1.15-1.52), with stable effects across age. Among participants reporting MLS, having PTE showed significant additional effects on daily smoking (RR 1.09; 95% CI 1.02-1.17) and age-dependency that showed significance during young adulthood but not adolescence.ConclusionThe relationship between maternal and offspring smoking was not fully accounted for by shared risk factors, suggesting possible causation with PTE having a delayed effect across age. Targeted prevention efforts should be made on maternal smoking-exposed adolescents to mitigate their risks of developing heavy smoking habits in adulthood.
| S-EPMC8194413 | biostudies-literature
Project description:Maternal smoking during pregnancy has been consistently related to low birthweight. However, older mothers, who are already at risk of giving birth to low birthweight infants, might be even more susceptible to the effects of maternal smoking. Therefore, this study aimed to examine the modified association between maternal smoking and low birthweight by maternal age.Data were obtained from a questionnaire survey of all mothers of children born between 2004 and 2010 in Okinawa, Japan who underwent medical check-ups at age 3 months. Variables assessed were maternal smoking during pregnancy, maternal age, gestational age, parity, birth year, and complications during pregnancy. Stratified analyses were performed using a logistic regression model.In total, 92641 participants provided complete information on all variables. Over the 7 years studied, the proportion of mothers smoking during pregnancy decreased from 10.6% to 5.0%, while the prevalence of low birthweight did not change remarkably (around 10%). Maternal smoking was significantly associated with low birthweight in all age groups. The strength of the association increased with maternal age, both in crude and adjusted models.Consistent with previous studies conducted in Western countries, this study demonstrates that maternal age has a modifying effect on the association between maternal smoking and birthweight. This finding suggests that specific education and health care programs for older smoking mothers are important to improve their foetal growth.
| S-EPMC4721610 | biostudies-other
Project description:BackgroundMaternal smoking is a risk factor for pediatric lung disease, including asthma. Animal models suggest that maternal smoking causes defective alveolarization in the offspring. Retinoic acid signaling modulates both lung development and postnatal immune function. Thus, abnormalities in this pathway could mediate maternal smoking effects. We tested whether maternal smoking disrupts retinoic acid pathway expression and functioning in a murine model.MethodsFemale C57Bl/6 mice with/without mainstream cigarette smoke exposure (3 research cigarettes a day, 5 days a week) were mated to nonsmoking males. Cigarette smoke exposure continued throughout the pregnancy and after parturition. Lung tissue from the offspring was examined by mean linear intercept analysis and by quantitative PCR. Cell culture experiments using the type II cell-like cell line, A549, tested whether lipid-soluble cigarette smoke components affected binding and activation of retinoic acid response elements in vitro.ResultsCompared to tobacco-naïve mice, juvenile mice with tobacco toxin exposure had significantly (P < 0.05) increased mean linear intercepts, consistent with an alveolarization defect. Tobacco toxin exposure significantly (P < 0.05) decreased mRNA and protein expression of retinoic acid signaling pathway elements, including retinoic acid receptor alpha and retinoic acid receptor beta, with the greatest number of changes observed between postnatal days 3-5. Lipid-soluble cigarette smoke components significantly (P < 0.05) decreased retinoic acid-induced binding and activation of the retinoic acid receptor response element in A549 cells.ConclusionsA murine model of maternal cigarette smoking causes abnormal alveolarization in association with altered retinoic acid pathway element expression in the offspring. An in vitro cell culture model shows that lipid-soluble components of cigarette smoke decrease retinoic acid response element activation. It is feasible that disruption of retinoic acid signaling contributes to the pediatric lung dysfunction caused by maternal smoking.
| S-EPMC3479035 | biostudies-literature
Project description:Cystic fibrosis (CF) is characterized by recurrent respiratory infections and progressive lung disease. Although environmental factors account for 50% of the variation in CF lung function, few specific exposures have been identified. Studies using small study samples focusing on environmental allergies in CF have had inconsistent results. Our objective was to examine the role of environmental allergies in upper and lower respiratory tract morbidities in CF.A total of 1,321 subjects with CF were recruited through the U.S. CF Twin-Sibling Study. Questionnaires were used to determine the presence/absence of environmental allergies. Questionnaires, chart review, and U.S. CF Foundation Patient Registry data were used to track outcomes.Within the study sample 14% reported environmental allergies. Environmental allergies were associated with a higher risk of sinus disease (adjusted OR: 2.68; P < 0.001) and nasal polyps (adjusted OR: 1.74; P?=?0.003). Environmental allergies were also associated with a more rapid decline in lung function (additional -1.1%/year; P?=?0.001). However, allergies were associated with a later median age of acquisition of Pseudomonas aeruginosa (6.6 years vs. 4.4 years; log rank P?=?0.027). The reported use of common allergy medications, anti-histamines and leukotriene inhibitors, did not alter the frequency of respiratory morbidities.Environmental allergies are associated with an increased risk of sinus disease and nasal polyps and a more rapid decline in CF lung function, but may have a protective effect against the acquisition of P. aeruginosa. Prospective studies are needed to confirm these associations which have implications for more aggressive management of allergies.
| S-EPMC3572264 | biostudies-literature
Project description:Background and objectiveThe lung microbiome was previously thought to be a sterile environment where only gaseous exchange takes place, but recent studies have shown the presence of microbiota in the lung. This review investigates the current literature on the effects of an environmental driven dysbiosis on the healthy oral and respiratory microbiome and its relationship to lung cancer risk in never-smokers.MethodsAn online electronic search was performed on PubMed of all English-language literature using combinations of the following keywords: "lung cancer", "dysbiosis", "non-smokers", "oral microbiome", and "respiratory microbiome". All population-based studies reporting results on oral and/or respiratory microbiome in adults were considered for our narrative review.Key content and findingsMetagenomic analyses have been performed on isolated samples from healthy participants and compared to samples from those with lung cancer. Research shows that a decrease in alpha diversity of microbes in the oral microbiome is associated with increased risk of lung cancer, along with differences in beta diversity in the sputum of lung cancer cases and healthy controls. Further, several studies have observed that significant changes in the abundance of genera such as increased abundance of Lactobacillales, Bacilli, and Firmicutes associated with an increased lung cancer risk among participants with exposure to certain household solid fuels.ConclusionsThese findings suggest potential carcinogenic processes such as increased inflammation associated with changes in flora. Additionally, studies showed that increase in certain taxa such as Bacteroides and Spirochetes might have a protective effect on lung cancer risk. The review also provides insight into how understanding the microbial changes can be beneficial for lung cancer treatment and disease-free survival. Larger studies in different populations need to be performed to strengthen the current associations between microbial diversity and lung cancer risk.
| S-EPMC10482636 | biostudies-literature