Maternal Tobacco Smoke Exposure Research Articles

Maternal environmental tobacco smoke exposure and adverse birth outcomes in Egypt: a cross sectional study

Maternal environmental tobacco smoke exposure and adverse birth outcomes in Egypt: a cross sectional study

Tobacco smoke exposure in early childhood and later risk of inflammatory bowel disease: A Scandinavian birth cohort study.

To examine the association between early-life smoking exposure and later risk of inflammatory bowel disease (IBD). We followed 115,663 participants from the Norwegian Mother, Father and Child (MoBa) and All Babies in Southeast Sweden (ABIS) cohorts from birth (1997-2009) through 2021. IBD was identified through national patient registers. Validated questionnaire data defined maternal smoking during pregnancy, maternal environmental tobacco smoke (ETS) exposure during pregnancy, and child ETS exposure by age 12 and 36 months. Cox regression was used to estimate adjusted hazard ratios (aHRs) for sex, maternal age, education level, parental IBD and origin. Cohort-specific estimates were pooled using a random-effects model. During 1,987,430 person-years of follow-up, 444 participants developed IBD (ABIS, n=112; MoBa, n=332). Any vs. no maternal smoking during pregnancy yielded a pooled aHR of 1.30 (95%CI=0.97-1.74) for offspring IBD. Higher level of maternal smoking during pregnancy (compared to no smoking, average ≥6 cigarettes/day: pooled aHR=1.60 [95%CI 1.08-2.38]) was associated with offspring IBD, whereas a lower smoking level was not (average 1-5 cigarettes/day: pooled aHR=1.09 [95%CI=0.73-1.64]). Child ETS exposure in the first year of life was associated with later IBD (any vs. no ETS, pooled aHR=1.32 [95%CI=1.03-1.69]). Estimates observed for child ETS exposure by 36 months were similar but not statistically significant. In this prospective Scandinavian cohort study, children exposed to higher levels of maternal smoking during pregnancy or ETS during the first year of life were at increased risk of later IBD.

Investigating associations between maternal stress, smoking and adverse birth outcomes: evidence from the All Our Families cohort

BackgroundIndependently, active maternal and environmental tobacco smoke exposure and maternal stress have been linked to an increased risk of preterm birth and low birth weight. An understudied relationship is the potential for interactive effects between these risk factors.MethodsData was obtained from the All Our Families cohort, a study of 3,388 pregnant women < 25 weeks gestation recruited from those receiving prenatal care in Calgary, Canada between May 2008 and December 2010. We investigated the joint effects of active maternal smoking, total smoke exposure (active maternal smoking plus environmental tobacco smoke) and prenatal stress (Perceived Stress Scale, Spielberger State-Trait Anxiety Inventory), measured at two time points (< 25 weeks and 34–36 weeks gestation), on preterm birth and low birth weight.ResultsA marginally significant association was observed with the interaction active maternal smoking and Spielberger State-Trait Anxiety Inventory scores in relation to low birth weight, after imputation (aOR = 1.02, 95%CI: 1.00-1.03, p = 0.06). No significant joint effects of maternal stress and either active maternal smoking or total smoke exposure with preterm birth were observed. Active maternal smoking, total smoke exposure, Perceived Stress Scores, and Spielberger State-Trait Anxiety Inventory scores were independently associated with preterm birth and/or low birth weight.ConclusionsFindings indicate the role of independent effects of smoking and stress in terms of preterm birth and low birthweight. However, the etiology of preterm birth and low birth weight is complex and multifactorial. Further investigations of potential interactive effects may be useful in helping to identify women experiencing vulnerability and inform the development of targeted interventions.

The effects of maternal environmental tobacco smoke exposure on periodontal health and mother-infant bonding in relation to salivary cotinine level

Background: Environmental tobacco smoking is produced by active smokers burning the tip of a cigarette and breathed by nonsmokers and measured by cotinine level. It has the potential to raise the risk of periodontal disease. One of the most frequent chronic diseases in adults is periodontal disease. The lower maternal-fetal attachment has been found to predict smoking status in previous studies, but no research has examined whether maternal-fetal attachment predicts environmental tobacco smoking. This study assessed the effects of maternal environmental tobacco smoke exposure on periodontal health and mother-infant bonding concerning salivary cotinine levels. Materials and methods: This is a comparative cross-sectional study comparing environmental tobacco smoke on exposed and non-exposed mothers aged between 20-35 years with their infants aged up to one year who attended primary health care centers in rural areas of AL-Karkh sector/Baghdad. Along with the essential socio-demographic data, a secondhand smoke exposure scale and postpartum bonding questionnaire were employed. Collection of unstimulated saliva from mothers was done according to Navazesh and Kumer in 2008. After that, the clinical Assessment of gingival bleeding and periodontal pockets was performed by using Community Periodontal Index according to the world health organization in 1997. Results: Out of 150 subjects,67(44.66%) were exposed to environmental tobacco whereas the non-exposed mothers were composed of 83 (55.33%). The highest mean number of CPI0(healthy gingiva) and CPI1(gingival bleeding) were among the non-exposed mothers while the highest mean number of CPI2(dental calculus), CPI3 (shallow pocket 4-5mm) and CPI4(deep pocket 6mm or more) were among the exposed mothers. The mean value of cotinine level among the non-exposed mothers was lower than exposed mothers with significant results. A higher salivary cotinine level was linked to a lower maternal-fetal bonding score. Conclusions: Mother’s exposure to environmental tobacco smoke significantly negatively impacts periodontal disease. Furthermore, mothers who have a stronger sense of attachment and affiliation to their fetus have lower salivary cotinine concentrations than mothers who have a less sense of fetal attachment.

Utilisation of supplementary prenatal screening and diagnostics in Germany: cross-sectional study using data from the KUNO Kids Health Study

BackgroundAppropriate health system utilisation during pregnancy is fundamental for maintaining maternal and child’s health. To study the use and determinants of supplementary prenatal screening and diagnostics in Germany this study provides comprehensive data.MethodsWe obtained data from a recently established prospective German birth cohort study, the KUNO Kids Health Study. Analyses are based on Andersen’s Behavioural Model of health system use, which distinguishes between predisposing (e.g. country of birth), enabling (e.g. health insurance) and need factors (e.g. at-risk pregnancy). We examined bi- and multivariate association with the use of supplementary prenatal screening and diagnostics using logistic regression.ResultsThe study has a sample size of 1886 participating mothers. One fifth of the mothers investigated did not use any supplementary prenatal screening or diagnostics. Notably, the chance of using supplementary prenatal screening and diagnostics more than doubled if the pregnant woman had a private health insurance (OR 2.336; 95% CI 1.527–3.573). Higher maternal age (OR 1.038; 95% CI 1.006–1.071) and environmental tobacco smoke exposure (OR 1.465 95% CI 1.071–2.004) increased the use of supplementary prenatal screening and diagnostics. However, regarding need factors only having an at-risk-pregnancy (OR 1.688; 95% CI 1.271–2.241) showed an independent association.ConclusionThe important role of the type of health insurance and the relatively small influence of need factors was surprising. Especially with respect to equity in accessing health care, this needs further attention.

Maternal tobacco smoke exposure is associated with increased DNA methylation at human metastable epialleles in infant cord blood.

Metastable epialleles (MEs) are genomic regions that are stochastically methylated prior to germ layer specification and exhibit high interindividual but low intra-individual variability across tissues. ME methylation is vulnerable to environmental stressors, including diet. Tobacco smoke (TS) exposure during pregnancy is associated with adverse impacts on fetal health and maternal micronutrient levels as well as altered methylation. Our objective was to determine if maternal smoke exposure impacts methylation at MEs. Consistent with prior studies, we observed reductions in one-carbon pathway micronutrients with gestational TS exposure, including maternal folate (P = 0.02) and vitamins B6 (P = 0.05) and B12 (P = 0.007). We examined putative MEs BOLA3, PAX8, and ZFYVE28 in cord blood specimens from 85 Newborn Epigenetics STudy participants. Gestational TS exposure was associated with elevated DNA methylation at PAX8 (+5.22% average methylation; 95% CI: 0.33% to 10.10%; P = 0.037). In human conceptal kidney tissues, higher PAX8 transcription was associated with lower methylation (Rs = 0.55; P = 0.07), suggesting that the methylation levels established at MEs, and their environmentally induced perturbation, may have meaningful, tissue-specific functional consequences. This may be particularly important because PAX8 is implicated in several cancers, including pediatric kidney cancer. Our data are the first to indicate vulnerability of human ME methylation establishment to TS exposure, with a general trend of increasing levels of methylation at these loci. Further investigation is needed to determine how TS exposure-mediated changes in DNA methylation at MEs, and consequent expression levels, might affect smoking-related disease risk.

Decreased head circumference at birth associated with maternal tobacco smoke exposure during pregnancy on the Japanese prospective birth cohort study

Maternal tobacco smoke exposure during pregnancy impairs fetal body size, including head circumference (HC) at birth; however, the mechanism still remains unclear. This analysis using a large prospective cohort study evaluated the impact of maternal tobacco exposure on their offspring’s HC and the relationship with placental weight ratio (PWR) and placental abnormalities. Parents-children pairs (n = 84,856) were included from the 104,065 records of the Japan Environmental and Children’s Study. Maternal perinatal clinical and social information by self-administered questionnaires, offspring’s body size, and placental information were collected. Data were analyzed with binominal logistic regression analysis and path analysis. Logistic regression showed significantly elevated adjusted odds ratio (aOR) (1.653, 95% CI 1.387–1.969) for the impact of maternal smoking during pregnancy on their offspring’s smaller HC at birth. Maternal exposure to environmental tobacco smoke in the non-smoking group did not increase aOR for the smaller HC. Path analysis showed that maternal smoking during pregnancy decreased the offspring’s HC directly, but not indirectly via PWR or placental abnormalities. The quitting smoking during pregnancy group did not increase aOR for the smaller HC than the non-smoking group, suggesting that quitting smoking may reduce their offspring’s neurological impairment even after pregnancy.

Maternal tobacco smoke exposure and determination of the optimal urinary cotinine cut-off values: a cross-sectional birth study

Maternal tobacco smoke exposure and determination of the optimal urinary cotinine cut-off values: a cross-sectional birth study

Association between prenatal metals exposure and childhood lung function

BACKGROUND AND AIM: Previous cross-sectional research has shown metals are associated with decreases in lung function in children. The influence of prenatal metals exposure on childhood lung function remains understudied. This study aimed to determine if prenatal metals exposure predicts childhood lung function, and assess effect modification by child sex. METHODS: We assessed 217 mother-child dyads enrolled in the Programming Research in Obesity, Growth, Environment, and Social Stressors birth cohort in Mexico City. Maternal blood samples were measured for lead, arsenic, and manganese in pregnant women during their 2nd trimester using plasma-mass spectrometry. Between 8-11 years of age, lung function was tested by pre- and post- bronchodilator spirometry. Outcomes included z-scores for forced expiratory volume in one second (FEV1), forced vital capacity (FVC), FEV1/FVC and forced expiratory flow at 25-75% of the pulmonary volume (FEF25-75) in separate models. We conducted multiple linear regression to evaluate the association between prenatal metals and post-bronchodilator childhood lung function adjusting for maternal age, education, and environmental tobacco smoke exposure and mutually adjusting for other metals. Models were then stratified by child sex to assess effect modification. RESULTS:Prenatal blood lead (1.13+0.60) was marginally associated with lower FEV1 (β -0.20, 95% CI: -0.43, -0.03), and lower FVC (β: -0.20, 95% CI: -0.42, 0.03). We did not find significant main effects of arsenic or manganese on lung function outcomes. When stratified by sex, lead was associated with lower FEF25-75% (β: -0.27, 95% CI: -0.53, -0.02) among boys but not in girls (β: 0.07, 95% CI: -0.32, 0.46). CONCLUSIONS:Prenatal lead was marginally associated with decreased lung function in childhood and appeared to be modified by child sex. These findings underscore the need to consider prenatal metal effects on childhood lung function. KEYWORDS: children's environmental health, heavy metals, pediatric lung function

Urinary cotinine assessment of maternal smoking and environmental tobacco smoke exposure status and its associations with perinatal outcomes: a cross-sectional birth study

Tobacco consumption and environmental tobacco smoke (ETS) exposure remains an important public health concern. Pregnant women require particular attention as active and passive smoking during pregnancy are associated with multiple adverse perinatal outcomes. This study aimed to biochemically validate self-reported smoking and ETS exposure status among pregnant women, to more precisely ascertain its association with adverse perinatal outcomes. Data refers to 595 pregnant women who sought prenatal care in a public hospital in Porto, Portugal. A standard questionnaire on smoking and ETS-related variables was completed. Urinary cotinine (UC) concentrations were assessed by solid-phase competitive ELISA, in maternal urine samples collected on the day of delivery. The results showed that the optimal UC cut-off value to distinguish smokers from non-smokers and within non-smokers those who were exposed to ETS from those non-exposed in the third trimester of pregnancy was 74.1 ng/mL (sensitivity and specificity of 96.7% and 98.0%, respectively) and 1.6 ng/mL (sensitivity of 66.2% and specificity of 75.7%, respectively). The agreement between maternal self-reported and UC-based smoking status was very good (κ=0.919, p<0.001), but much lower for ETS exposure (κ=0.386, p<0.001). Maternal active smoking in the third trimester of pregnancy was associated with a significant decrease in birth weight, length and head circumference of 157.66 g (95% CI: −245.81, −69.52; p<0.001), 0.78 cm (95% CI: −1.22, −0.34; p=0.001) and 0.39 cm (95% CI: −0.70, −0.07; p=0.016), respectively. Maternal ETS exposure in the third trimester of pregnancy was associated with a non-significant increase in birth weight of 38.37 g (95% CI: −28.91, 105.64; p=0.263). Furthermore, maternal smoking cessation was associated with the increase of approximately 172 g in birth weight (95% CI: 50.00, 293.19). As such, there is an urgent need for increased public health awareness campaigns to encourage smoking cessation during pregnancy, in order to improve perinatal outcomes.

Prenatal Exposure to Gutkha, a Globally Relevant Smokeless Tobacco Product, Induces Hepatic Changes in Adult Mice.

Maternal exposures during pregnancy affect the onset and progression of adult diseases in the offspring. A prior mouse study indicated that maternal tobacco smoke exposure affects hepatic fibrosis in adult offspring. Gutkha, a broadly used smokeless tobacco (ST) product, is widely used by pregnant woman in many countries. The objective of this murine study was to evaluate whether oral maternal exposure to gutkha during pregnancy alters non-alcoholic fatty liver disease (NAFLD) in adult offspring: risk factors for the progression of NAFLD to cirrhosis in adults remain elusive. Buccal cavity ‘painting’ of pregnant mice with gutkha began on gestational days (GD) 2–4 and continued until parturition. Beginning at 12 weeks of age, a subset of offspring were transitioned to a high-fat diet (HFD). Results demonstrated that prenatal exposure to gutkha followed by an HFD in adulthood significantly increased the histologic evidence of fatty liver disease only in adult male offspring. Changes in hepatic fibrosis-related cytokines (interleukin (IL)-1b and IL-6) and in hepatic collagen mRNA expression were observed when comparing adult male offspring exposed to gutkha in utero to those not exposed. These findings indicate that maternal use of gutkha during pregnancy affects NAFLD in adult offspring in a sex-dependent manner.

Maternal waterpipe tobacco smoke exposure during lactation induces hormonal and biochemical changes in rat dams and offspring.

Waterpipe smoking is common among pregnant and breastfeeding women. Herein, the effects of waterpipe tobacco smoke (WTS) exposure during lactation on milk composition, hormonal levels and biochemical profile in dams and pups were investigated. Lactating Wistar rats were randomly assigned to receive either WTS (2hours per day) or fresh air (control group). Milk was collected on day 21 and analysed for protein, lactose and total fat. Blood, from dams and pups, was analysed for insulin, glucose, lipid profile, leptin, prolactin and corticosterone. WTS exposure during lactation increased the blood level of HDL and corticosterone in dams (P<.05). However, the level of milk lactose and blood glucose was reduced in dams after the exposure to WTS during lactation (P<.05). WTS during lactation significantly increased levels of triglycerides, LDL and leptin (P<.05), and a trend of increase in blood level of nicotine and prolactin in pups. Levels of other parameters were not affected by WTS exposure in dams and pups. In conclusion, WTS exposure during lactation altered the milk composition and altered lipid profile, glucose homeostasis and hormonal levels in dams and pups. It is necessary to adopt strategies to enhance tobacco cessation during breastfeeding.

Chronic Maternal Tobacco Smoke Exposure and/or Alpha-Lipoic Acid Treatment Causes Long-Term Deterioration of Testis and Sexual Behavior in Adult Male Rats

BackgroundTobacco use during pregnancy is known to have several negative effects on the offspring's reproductive health in the long term. The use of alpha-lipoic acid (ALA) as a dietary supplement during pregnancy has increased greatly in recent years and has been known to have positive effects on various pregnancy outcomes including miscarriage, diabetic embryopathy, preterm delivery, and congenital malformations. AimTo evaluate the effects of tobacco smoke exposure (TSE) on sexual behavior, reproductive parameters, and testicles in adult male rats and to reveal the possible role of ALA administration on these parameters. MethodsPregnant rats (n = 7 per group) were treated with tobacco smoke (TS), ALA (20 mg/kg), and TS + ALA for a total of 11 weeks. The following parameters were compared with 8 control rats: puberty parameters, sexual behavior; levels of serum gonadotropins and testosterone, total antioxidant status, and total oxidant status; the expression of the apoptotic protease-activating factor-1 and caspase 9 mRNA levels in the testis; and assessment of immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick end labeling assay of testis. Main Outcome MeasureSexual behavior, changes in puberty parameters, and hormonal and genetic alterations were the outcomes analyzed in this study. ResultsMaternal TSE caused a significant decrease in the number of intromissions compared to the control group. Similarly, ALA decreased erectile function in sexual behavior by decreasing the number of intromissions and intromission ratio in the ALA group compared to the control group. In addition, TSE and ALA treatment caused an impairment of some consummatory sexual behaviors. Also, in parallel with this inhibitory effect, the age of pubertal onset was significantly delayed in the TS + ALA group compared to other groups. Also, histopathological changes in testicular tissue, oxidative stress markers, apoptotic index, and mRNA levels of apoptosis-related genes increased in all treatment groups. Clinical ImplicationsThe use of ALA and/or tobacco products during pregnancy may adversely affect the reproductive health of male newborns in the long term. Strengths & LimitationsTo the best of our knowledge, this study is the first to show the effects of maternal ALA treatment and/or TSE on the sexual behavior and reproductive parameters in male rats; however, the study is based on an animal model, and the present findings partially reflect the characteristics of human sexual behavior. ConclusionMaternal TSE and/or ALA treatment may impair sexual behavior in adulthood in male rats because of testicular damage caused by oxidative stress during gonadal development.Yardimci A, Akkoc RF, Tektemur A, et al. Chronic Maternal Tobacco Smoke Exposure and/or Alpha-Lipoic Acid Treatment Causes Long-Term Deterioration of Testis and Sexual Behavior in Adult Male Rats. J Sex Med 2020;17:1835–1847.

Maternal Tobacco Smoke Exposure Causes Sex-Divergent Changes in Placental Lipid Metabolism in the Rat.

Maternal tobacco smoke exposure (MTS) affects fetal acquisition of long-chain polyunsaturated fatty acids (LCPUFA) and increases the risk of obesity and cardio-metabolic disease in the offspring. Alterations in fetal LCPUFA acquisition in maternal smoking are mediated by the placenta. The handling of LCPUFA by the placenta involves protein-mediated transfer and storage. Molecular mediators of placental LCPUFA handling include PPARγ and the fatty acid transport proteins. We previously demonstrated, in a rat model, that MTS results in programming of adult-onset obesity and metabolic disease in male, but not female, offspring. In this study, we test the hypothesis that in utero MTS exposure alters placental structure, placental LCPUFA handling, and fetal fatty acid levels, in a sex-divergent manner. We exposed pregnant rats to tobacco smoke from embryonic day 11 to term gestation. We measured placental and fetal fatty acid profiles, the systolic/diastolic ratio (SD ratio), placental histology, and expression of molecular mediators in the placenta. Our primary finding is that MTS alters fatty acid profiles in male, but not female fetuses and placenta, including increasing the ratio of omega-6 to omega-3 fatty acids. MTS also increased SD ratio in male, but not female placenta. In contrast, the expression of PPARγ and FATPs was upregulated in female, but not male placenta. We conclude that MTS causes sex-divergent changes in placental handling of LCPUFA in the rat. We speculate that our results demonstrate an adaptive response to MTS by the female placenta.

Effect of waterpipe tobacco smoke exposure during lactation on learning and memory of offspring rats: Role of oxidative stress

AimsThe prevalence of waterpipe tobacco smoking is increasing among breastfeeding women. Herein, the effect of maternal waterpipe tobacco smoke (WTS) exposure during lactation on learning and memory of adult offspring rats was examined. Main methodsLactating rats received either fresh air or mainstream WTS (1 h twice daily) from day 4 to day 21. Learning and memory was examined by the radial arm water maze and the levels of brain derived neurotrophic factor (BDNF) and oxidative stress biomarkers superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and thiobarbituric acid reactive substances (TBARS) were assessed in the hippocampus of adult male offspring rats. Key findingsMaternal exposure to WTS during lactation impaired the long-term memory and reduced levels of BDNF (P < 0.05) in hippocampus in adult male offspring rats. The activity of SOD, GPx and catalase were reduced (P < 0.05) while level of TBARS was increased (P < 0.05). SignificanceMaternal WTS exposure during lactation impaired the long-term memory of adult male offspring that was associated with low levels of BDNF and altered oxidative stress balance. Therefore, careful measures should be taken to enhance waterpipe smoking cessation during breastfeeding.

Associations between Maternal Tobacco Smoke Exposure and the Cord Blood [Formula: see text] DNA Methylome.

Background:Maternal tobacco smoke exposure has been associated with altered DNA methylation. However, previous studies largely used methylation arrays, which cover a small fraction of CpGs, and focused on whole cord blood.Objectives:The current study examined the impact of in utero exposure to maternal tobacco smoke on the cord blood DNA methylome.Methods:The methylomes of 20 Hispanic white newborns ( exposed to any maternal tobacco smoke in pregnancy; unexposed) from the Maternal and Child Health Study (MACHS) were profiled by whole-genome bisulfite sequencing (median coverage: ). Statistical analyses were conducted using the Regression Analysis of Differential Methylation (RADMeth) program because it performs well on low-coverage data (minimizes false positives and negatives).Results:We found that 10,381 CpGs were differentially methylated by tobacco smoke exposure [neighbor-adjusted p-values that are additionally corrected for multiple testing based on the Benjamini-Hochberg method for controlling the false discovery rate (FDR) ]. From these CpGs, RADMeth identified 557 differentially methylated regions (DMRs) that were overrepresented () in important regulatory regions, including enhancers. Of nine DMRs that could be queried in a reduced representation bisulfite sequencing (RRBS) study of adult cells ( smokers; nonsmokers), four replicated (). Additionally, a CpG in the promoter of SLC7A8 (percent methylation difference: comparing exposed to unexposed) replicated () in an EPIC (Illumina) array study of cord blood cells ( exposed to sustained maternal tobacco smoke; unexposed) and in a study of adult cells across two platforms (EPIC: smokers; nonsmokers; 450K: smokers; nonsmokers).Conclusions:Maternal tobacco smoke exposure in pregnancy is associated with cord blood DNA methylation in key regulatory regions, including enhancers. While we used a method that performs well on low-coverage data, we cannot exclude the possibility that some results may be false positives. However, we identified a differentially methylated CpG in amino acid transporter SLC7A8 that is highly reproducible, which may be sensitive to cigarette smoke in both cord blood and adult cells. https://doi.org/10.1289/EHP3398

Do traditional fermented foods protect against infantile atopic dermatitis.

Environmental and dietary factors during pregnancy may affect development of infantile atopic dermatitis (AD). This study analyzed whether maternal consumption of selected Turkish fermented foods (FF) and other factors during pregnancy affect the development of AD during the first 2years of life. Eighty-four children with physician-diagnosed AD (aged between 2 and 24months) and mothers, and 56 similarly aged, healthy children and mothers were studied. Physician-administered questionnaires retrospectively surveyed maternal consumption of FF during pregnancy. The intake frequency of 8 selected Turkish FF was classified as either (1) daily or (2) less than daily. Other possible demographic and environmental risk factors were also analyzed. Daily maternal consumption of yogurt, fermented olive, and cheese in the control group was significantly higher than the AD group (P<0.001, P=0.017, and P=0.011, respectively). Exposure to environmental tobacco smoking (ETS) was more common in the AD group than the control group (P=0.025). In multivariate logistic regression analysis, maternal ETS exposure during pregnancy was associated with increased risk of infantile AD, and daily consumption of yogurt was associated with a reduced risk (odds ratio [OR]: 2.60, 95% confidence interval [CI]: 1.11-6.1, and OR: 0.22, CI: 0.09-0.54, respectively). The diversity of consumed FF during pregnancy was found to have a protective effect against infantile AD (OR: 0.27, CI: 0.14-0.53). Daily maternal intake of yogurt and diversity of consumed Turkish FF during pregnancy may reduce the risk of AD. Maternal tobacco smoke exposure is associated with increased risk of infantile AD.

Environmental tobacco smoke exposure during pregnancy has limited effect on infant birthweight and umbilical vein endothelial nitric oxide synthase

Women who smoke, deliver significantly smaller infants. These infants have reduced levels of the vasodilator endothelial nitric oxide synthase (eNOS) levels in the umbilical vessels, which may reduce fetal growth. Serum cotinine, the degradation product of nicotine, can be used to determine the level of tobacco exposure. Newborns of environmental smokers are suggested to be smaller and shorter in weight, length, and head circumference. eNOS levels have not yet been studied in these infants. We investigated the existence of a relation between maternal environmental tobacco smoke exposure, eNOS activity, concentration, and birthweight. We included 263 healthy singleton pregnancies categorized into three groups according to measured cotinine levels: 175 nonsmokers, 38 smokers, and 50 environmental smokers. Cotinine was quantified by mass spectrometry with a detection limit of .2ng/mL; eNOS activity and concentration were measured in endothelial cells (ECs) of the umbilical vein. Infants born to environmental smokers had similar weights to infants born to nonsmokers (47g heavier, P=.48). Cotinine concentrations were .06/.09/.12ng/mL (quartiles) in infants born to nonsmokers, .27/.37/.81ng/mL in infants born to women exposed to environmental tobacco smoke, and 43.0/63.8/108.1ng/mL in infants born to smokers. The eNOS concentration was 1.65±.92ng/106 ECs (mean±SD) in nonsmokers and 1.71±1.00ng/106 ECs in environmental smokers. The eNOS activity was 52.0±20.6pmol l-citrulline/min/106 ECs in nonsmokers and 48.7±19.8pmol l-citrulline/min/106 ECs in environmental smokers. Infants born to environmental smokers, as judged by umbilical serum cotinine levels close to .2ng/mL, are not associated with lower birthweight or reduced eNOS activity, or concentration in the fetal vascular bed.

The investigation of effect of alpha lipoic acid against damage on neonatal rat lung to maternal tobacco smoke exposure.

This study was carried out to determine the changes in the lungs of the rat pups exposed to tobacco smoke during pregnancy period and to investigate the protective effects of alpha lipoic acid, which is administered during pregnancy, on these changes. Spraque-Dawley female rats were divided into four groups: control, tobacco smoke (TS), tobacco smoke + alpha lipoic acid (TS + ALA) and alpha lipoic acid (ALA). The rats in control group were untreated. Rats were exposed to TS twice a day for one hour starting from eight weeks before mating and during pregnancy. 20 mg / kg of ALA was administered to rats. On 7th and 21st days 7 of the pups from each group were decapitated. Histological, morphometric, biochemical and quantitative real-time RT-PCR analyzes were performed. Histopathological and biochemical changes were observed in TS group. While a significant decrease was observed both in SP-A and VEGF immunoreactivities and mRNA levels, caspase-3 immunoreactivity and TUNEL positive cells were increased in TS group. It is suggested that prenatal TS exposure leads to morphological and histopathological changes on lung development by causing oxidative damage in lungs of neonatal rats and the maternal use of ALA can provide a limited protective effect on the neonatal lung development against this oxidative stress originating from TS. Although pregnant women are increasingly aware on health risks of smoking, environmental tobacco smoke exposure is still a widespread problem. For this reason, it is thought that this damage can be partially reduced by some antioxidant supplements in pregnancy.

Effect of Prenatal Exposure to Waterpipe Tobacco Smoke on Learning and Memory of Adult Offspring Rats.

Waterpipe tobacco smoking has increased in prevalence worldwide, including among pregnant women. In this study, we investigated the effect of prenatal maternal waterpipe tobacco smoke (WTS) exposure during different stages of pregnancy on learning and memory of adult offspring rats. Pregnant rats received either fresh air or mainstream WTS (2 hours daily) during early, mid, late, or whole gestational period. Male offspring rats were followed through 20 weeks. Outcomes included (1) spatial learning and memory using the radial arm water maze (RAWM), (2) levels of brain derived neurotrophic factor (BDNF) in the hippocampus, and (3) oxidative stress biomarkers (superoxide dismutase, catalase, glutathione peroxidase and thiobarbituric acid reactive substances). Relative to offspring whose mothers were exposed to fresh air, prenatal exposure to WTS at any stage of pregnancy resulted in short- and long-term memory impairment in adult offspring rats (p < .05). This impairment was associated with reduced levels of BDNF in hippocampus (p < .05). However, prenatal WTS did not affect the level of oxidative stress biomarkers in hippocampus. Prenatal WTS during late gestation increased the activity of catalase as compared to control. Prenatal maternal WTS exposure can impair the memory of adult male offspring. These results support development of interventions that target pregnant women who smoke waterpipe during pregnancy. We examined for the first time the effect of prenatal waterpipe tobacco smoke exposure on learning and memory of offspring. The results showed that in utero exposure to waterpipe tobacco smoke was associated with impaired memory and decreased brain derived neurotrophic factor in hippocampus of adult male offspring rats.