Maternal Prenatal Hair Cortisol Is Associated with Child Wheeze among Mothers and Infants with Tobacco Smoke Exposure and Who Face High Socioeconomic Adversity.
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SUBMITTER: Scherman A
PROVIDER: S-EPMC7967280 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPrenatal exposure to tobacco is associated with adverse health outcomes for the mother and child, and has been associated with an increased risk of tobacco smoking and nicotine dependence in offspring. The objective of this study was to examine the risk of prenatal smoking, among daughters, associated with maternal prenatal smoking.MethodsWe used a population-based cohort study design, with linked vital records data of mothers and daughters delivering 1984-96 and 1996-2013, respectively, in Washington State. The exposure of interest was mothers' prenatal smoking (any vs. no smoking at any time during pregnancy), while the outcome was daughters' prenatal smoking (similarly assessed). We used multivariable log-binomial regression to obtain estimates of the relative risk (RR) and 95% confidence interval (CI).ResultsDaughters exposed to maternal prenatal smoking were more likely to smoke during their pregnancy, compared to unexposed daughters (RR 1.78, 95% CI 1.72, 1.84, adjusted for the year the daughter delivered, her marital status and educational attainment, and the mothers' race/ethnicity).ConclusionsIn this relatively young population, we found that daughters exposed to maternal prenatal smoking have an increased risk of smoking later on during their own pregnancy, emphasizing the importance of exposures during the prenatal period. The mechanisms leading to prenatal smoking are multifactorial and likely include behavioural, genetic, epigenetic and environmental factors. An understanding of this risk factor for prenatal smoking may guide health care providers to better target smoking cessation interventions to at-risk populations.
| S-EPMC5195902 | biostudies-literature
Project description:IntroductionTobacco use remains the single most modifiable cause of adverse pregnancy outcomes. It is crucial to be able to accurately quantify the burden of tobacco exposure on both the mother and fetus to have better measures of efficacy with interventions being studied.MethodsThis is a descriptive and exploratory study conducted within a randomized controlled trial. Pregnant smoking and non-smoking women were followed from ≤22 weeks' gestation through delivery with monthly maternal smoking questionnaires, urine cotinine levels, and collection of maternal and infant hair and nail samples, at delivery. Nicotine was extracted and measured (ng/mg) using high-performance liquid chromatography with electrochemical detection.ResultsForty-six mother-infant dyads (34 pregnant smokers and 12 pregnant non-smokers) had successful completion of maternal and infant hair and nails samples. The median hair nicotine levels of the smoking mothers and their infants was significantly higher than those of the non-smokers (1.015 vs 0.037 ng/ mg, p<0.05 for the mothers; 0.445 vs 0.080 ng/mg, p<0.01 for the infants). Similarly, the median nail nicotine levels for smoking mothers and their infants were significantly higher than the non-smokers (2.130 vs 0.056 ng/mg, p<0.01 for the mothers; 0.594 vs 0.132 ng/mg, p<0.05 for the infants). We found a moderate but significant correlation between maternal hair and nail nicotine (r=0.64, p<0.001), infant hair and nail nicotine (r=0.64; p<0.001), maternal and infant hair nicotine (r=0.61, p<0.001), and maternal and infant nail nicotine levels (r=0.58, p<0.001).ConclusionsOur study shows that both infant hair and nail nicotine levels are valid biomarkers of intrauterine tobacco smoke exposure, and can be used to identify prenatal smoke exposure, correlating well with the level of maternal nicotine exposure.
| S-EPMC8693083 | biostudies-literature
Project description:BackgroundAlthough studies show that maternal smoking during pregnancy increases the risks of respiratory outcomes in childhood, evidence concerning the effects of household environmental tobacco smoke (ETS) exposure remains inconsistent.MethodsWe conducted a population-based study comprised of 5,019 seventh and eighth-grade children in 14 Taiwanese communities. Questionnaire responses by parents were used to ascertain children's exposure and disease status. Logistic regression models were fitted to estimate the effects of ETS exposures on the prevalence of asthma, wheeze, and bronchitic symptoms.ResultsThe lifetime prevalence of wheeze was 11.6% and physician-diagnosed asthma was 7.5% in our population. After adjustment for potential confounders, in utero exposure showed the strongest effect on all respiratory outcomes. Current household ETS exposure was significantly associated with increased prevalence of active asthma, ever wheeze, wheeze with nighttime awakening, and bronchitis. Maternal smoking was associated with the increased prevalence of a wide range of wheeze subcategories, serious asthma, and chronic cough, but paternal smoking had no significant effects. Although maternal smoking alone and paternal smoking alone were not independently associated with respiratory outcomes, joint exposure appeared to increase the effects. Furthermore, joint exposure to parental smoking showed a significant effect on early-onset asthma (OR, 2.01; 95% CI, 1.00-4.02), but did not show a significant effect on late-onset asthma (OR, 1.17; 95% CI, 0.36-3.87).ConclusionWe concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.
| S-EPMC2828425 | biostudies-literature
Project description:To investigate whether paternal tobacco smoke (PTS) was associated with prenatal epigenetic programming of CG site methylation, 20 cord blood DNA samples from newborns with and without PTS were subjected to microarray assay of 1,505 CG loci in 807 genes by Illumina GoldenGate® technology bead system to obtain high-throughput DNA Methylation profiles. Samples included 14 newborns without PTS exposure, and 6 newborns with PTS exposure.
2019-04-13 | GSE129751 | GEO
Project description:PURPOSE:To investigate whether prenatal exposure to indoor fine particulate matter (PM?.?) and environmental tobacco smoke (ETS) affects susceptibility to respiratory tract infections (RTIs) in infancy, to compare their effects between prenatal and postnatal exposure, and to determine whether genetic factors modify these environmental effects. METHODS:The study population consisted of 307 birth cohort infants. A diagnosis of RTIs was based on parental report of a physician's diagnosis. Indoor PM?.? and ETS levels were measured during pregnancy and infancy. TaqMan was used for genotyping of nuclear factor erythroid 2-related factor (Nrf2) (rs6726395), glutathione-S-transferase-pi (GSTP) 1 (rs1695), and glutathione-S-transferase-mu (GSTM) 1. Microarrays were used for genome-wide methylation analysis. RESULTS:Prenatal exposure to indoor PM?.? increased the susceptibility of lower RTIs (LRTIs) in infancy (adjusted odds ratio [aOR]=2.11). In terms of combined exposure to both indoor PM?.? and ETS, prenatal exposure to both pollutants increased susceptibility to LRTIs (aOR=6.56); however, this association was not found for postnatal exposure. The Nrf2 GG (aOR=23.69), GSTM1 null (aOR=8.18), and GSTP1 AG or GG (aOR=7.37) genotypes increased the combined LRTIs-promoting effects of prenatal exposure to the 2 indoor pollutants. Such effects of prenatal indoor PM?.? and ETS exposure were not found for upper RTIs. CONCLUSIONS:Prenatal exposure to both indoor PM?.? and ETS may increase susceptibility to LRTIs. This effect can be modified by polymorphisms in reactive oxygen species-related genes.
| S-EPMC4605930 | biostudies-literature
Project description:BackgroundSmoking while pregnant is associated with a myriad of negative health outcomes in the child. Some of the detrimental effects may be due to epigenetic modifications, although few studies have investigated this hypothesis in detail.ObjectivesTo characterize site-specific epigenetic modifications conferred by prenatal smoking exposure within asthmatic children.MethodsUsing Illumina HumanMethylation27 microarrays, we estimated the degree of methylation at 27,578 distinct DNA sequences located primarily in gene promoters using whole blood DNA samples from the Childhood Asthma Management Program (CAMP) subset of Asthma BRIDGE childhood asthmatics (n?=?527) ages 5-12 with prenatal smoking exposure data available. Using beta-regression, we screened loci for differential methylation related to prenatal smoke exposure, adjusting for gender, age and clinical site, and accounting for multiple comparisons by FDR.ResultsOf 27,578 loci evaluated, 22,131 (80%) passed quality control assessment and were analyzed. Sixty-five children (12%) had a history of prenatal smoke exposure. At an FDR of 0.05, we identified 19 CpG loci significantly associated with prenatal smoke, of which two replicated in two independent populations. Exposure was associated with a 2% increase in mean CpG methylation in FRMD4A (p?=?0.01) and Cllorf52 (p?=?0.001) compared to no exposure. Four additional genes, XPNPEP1, PPEF2, SMPD3 and CRYGN, were nominally associated in at least one replication group.ConclusionsThese data suggest that prenatal exposure to tobacco smoke is associated with reproducible epigenetic changes that persist well into childhood. However, the biological significance of these altered loci remains unknown.
| S-EPMC4070909 | biostudies-literature
Project description:BackgroundPreviously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure.MethodsPrenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap.ResultsA significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years.ConclusionsCombined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.
| S-EPMC3081952 | biostudies-literature
Project description:Rationale: Little is known about effects of paternal tobacco smoke (PTS) on the offspring's asthma and its prenatal epigenetic programming. Objective: To investigate whether PTS exposure was associated with the offspring's asthma and correlated to epigenetic CG methylation of potential tobacco-related immune genes: LMO2, GSTM1 or/and IL-10 genes. Measurements and Main Results: In a birth cohort of 1,629 newborns, we measured exposure rates of PTS (23%) and maternal tobacco smoke (MTS, 0.2%), cord blood DNA methylation, infant respiratory tract infection, childhood DNA methylation, and childhood allergic diseases. Infants with prenatal PTS exposure had a significantly higher risk of asthma by the age of 6 than those without (p = 0.026). The PTS exposure doses at 0, <20, and ≧20 cigarettes per day were significantly associated with the trend of childhood asthma and the increase of LMO2-E148 (p = 0.006), and IL10_P325 (p = 0.008) CG methylation. The combination of higher CG methylation levels of LMO2_E148, IL10_P325, and GSTM1_P266 corresponded to the highest risk of asthma by 43.48%, compared to other combinations (16.67-23.08%) in the 3-way multi-factor dimensionality reduction (MDR) analysis. The LMO2_P794 and GSTM1_P266 CG methylation levels at age 0 were significantly correlated to those at age of 6. Conclusions: Prenatal PTS exposure increases CG methylation contents of immune genes, such as LMO2 and IL-10, which significantly retained from newborn stage to 6 years of age and correlated to development of childhood asthma. Modulation of the LMO2 and IL-10 CG methylation and/or their gene expression may provide a regimen for early prevention of PTS-associated childhood asthma. Descriptor number: 1.10 Asthma Mediators. Scientific Knowledge on the Subject: It has been better known that maternal tobacco smoke (MTS) has an impact on the offspring's asthma via epigenetic modification. Little is known about effects of paternal tobacco smoke (PTS) on the offspring's asthma and its prenatal epigenetic programming. What This Study Adds to the Field: Prenatal tobacco smoke (PTS) can program epigenetic modifications in certain genes, such as LMO2 and IL-10, and that these modifications are correlated to childhood asthma development. The higher the PTS exposure dose the higher the CG methylation levels are found. The combination of higher CG methylation levels of LMO2_E148, IL10_P325 and GSTM1_P266 corresponded to the highest risk of asthma. Measuring the DNA methylation levels of certain genes might help to predict high-risk populations for childhood asthma and provide a potential target to prevent the development of childhood asthma.
| S-EPMC6554446 | biostudies-literature
Project description:RationalePrenatal exposure to tobacco smoke increases the risk for diseases later in the child's life that may be mediated through alterations in DNA methylation.ObjectivesTo demonstrate that differences in DNA methylation patterns occur in children exposed to tobacco smoke and that variation in detoxification genes may alter these associations.MethodsMethylation of DNA repetitive elements, LINE1 and AluYb8, was measured using bisulfite conversion and pyrosequencing in buccal cells of 348 children participating in the Children's Health Study. Gene-specific CpG methylation differences associated with smoke exposure were screened in 272 participants in the Children's Health Study children using an Illumina GoldenGate panel. CpG loci that demonstrated a statistically significant difference in methylation were validated by pyrosequencing. Estimates were standardized across loci using a Z score to enable cross-comparison of results.Measurements and main resultsDNA methylation patterns were associated with in utero exposure to maternal smoking. Exposed children had significantly lower methylation of AluYb8 (beta, -0.31; P = 0.03). Differences in smoking-related effects on LINE1 methylation were observed in children with the common GSTM1 null genotype. Differential methylation of CpG loci in eight genes was identified through the screen. Two genes, AXL and PTPRO, were validated by pyrosequencing and showed significant increases in methylation of 0.37 (P = 0.005) and 0.34 (P = 0.02) in exposed children. The associations with maternal smoking varied by a common GSTP1 haplotype.ConclusionsLife-long effects of in utero exposures may be mediated through alterations in DNA methylation. Variants in detoxification genes may modulate the effects of in utero exposure through epigenetic mechanisms.
| S-EPMC2742762 | biostudies-literature
Project description:BackgroundMaternal psychopathology is associated with altered HPA axis functioning in offspring. Most studies have focused on mildly affected populations, but less is known about the effect of severe maternal psychopathology. In our explorative study we investigated in a heterogenic sample of mothers with severe and long-lasting psychiatric disorders, if a diagnosis of depression and severity of general maternal psychiatric symptomatology were associated with infant salivary cortisol reactivity to the Face-to-Face Still-Face (FFSF) paradigm at 6 months of age.MethodsA clinical sample of 36 mother-infant dyads was explored. All mothers fulfilled criteria for a severe psychiatric disorder and had psychiatric complaints for the last two consecutive years. Maternal diagnosis was established during pregnancy using a diagnostic interview and general maternal psychiatric symptom severity was established by self-report at the time of the FFSF procedure. The FFSF paradigm was used to assess infants' response to social stress at the age of 6 months. Infant saliva samples were collected at three time points: 5 min before and 15 and 30 min after the social stressor. Cortisol reactivity was operationalized as incremental Area Under the Curve (AUCi). Potential confounders were identified and adjusted for.ResultsIn regression analyses, a negative relationship was found between infant cortisol reactivity (AUCi) during the FFSF paradigm at 6 months and general maternal symptom severity at time of the FFSF paradigm (unadjusted n = 36, ß = -0.331, B = -9.758, SE 4.8, p = .048; adjusted n = 36, ß = -0.335, B = -9.868, SE 4.5, p = .039) and for diagnosis of perinatal depression at trend level (unadjusted n = 36, ß = -0.293, B = -8.640, SE 4.8, p = .083; adjusted n = 36, ß = -0.317, B = -9.347, SE 4.6, p = .052). Analyses were adjusted for gestational age.ConclusionsPreliminary results on cortisol reactivity in 6-month-old infants of mothers with severe and long-lasting psychiatric disorders show a significant reduction in the group of mothers who experienced a high level of psychiatric symptoms in the post-partum period, compared to mothers with lower levels of psychiatric symptomatology. The same trend was found for mothers with and without a diagnosis of perinatal depression. Since these infants are considered to be at increased risk for later psychopathology, our study suggests that future longitudinal studies should investigate whether reduced cortisol reactivity in babies could be a marker for any adverse outcomes, besides other possible risk factors (e.g. (epi)genetic phenomena).
| S-EPMC9216463 | biostudies-literature