Prenatal Cigarette Smoke Research Articles

Prenatal cigarette smoke exposure sensitizes acetaminophen-induced liver injury by modulating miR-34a-5p in male offspring mice.

Introduction: Cigarette smoke (CS) exacerbates the severity of diseases not only in lungs, but also in systemic organs having no direct contact with smoke. In addition, smoking during pregnancy can have severe health consequences for both the mother and the fetus. Therefore, our aim was to evaluate effects of prenatal exposure to CS on acetaminophen (APAP)-induced acute liver injury (ALI) in offspring. Methods: Female C57BL/6 mice on day 6 of gestation were exposed to mainstream CS (MSCS) at 0, 150, 300, or 600μg/L for 2h a day, 5days a week for 2weeks using a nose-only exposure system. At four weeks old, male offspring mice were injected intraperitoneally with a single dose of APAP at 300mg/kg body weight to induce ALI. Results: Maternal MSCS exposure significantly amplified pathological effects associated with ALI as evidenced by elevated serum alanine aminotransferase levels, increased hepatocellular apoptosis, higher oxidative stress, and increased inflammation. Interestingly, maternal MSCS exposure reduced microRNA (miR)-34a-5p expression in livers of offspring. Moreover, treatment with a miR-34a-5p mimic significantly mitigated the severity of APAP-induced hepatotoxicity. Overexpression of miR-34a-5p completely abrogated adverse effects of maternal MSCS exposure in offspring with ALI. Mechanistically, miR-34a-5p significantly decreased expression levels of hepatocyte nuclear factor 4 alpha, leading to down-regulated expression of cytochrome P450 (CYP)1A2 and CYP3A11. Discussion: Prenatal exposure to MSCS can alter the expression of miRNAs, even in the absence of additional MSCS exposure, potentially increasing susceptibility to APAP exposure in male offspring mice.

Early-life exposure to cigarette smoke primes lung function and DNA methylation changes at Cyp1a1 upon exposure later in life.

Prenatal and early-life exposure to cigarette smoke (CS) has repeatedly been shown to induce stable, long-term changes in DNA methylation (DNAm) in offspring. It has been hypothesized that these changes might be functionally related to the known outcomes of prenatal and early-life CS exposure, which include impaired lung development, altered lung function, and increased risk of asthma and wheeze. However, to date, few studies have examined DNAm changes induced by prenatal CS in tissues of the lung, and even fewer have attempted to examine the specific influences of prenatal versus early postnatal exposures. Here, we have established a mouse model of CS exposure which isolates the effects of prenatal and early postnatal CS exposures in early life. We have used this model to measure the effects of prenatal and/or postnatal CS exposures on lung function and immune cell infiltration as well as DNAm and expression of Cyp1a1, a candidate gene previously observed to demonstrate DNAm differences on CS exposure in humans. Our study revealed that exposure to CS prenatally and in the early postnatal period causes long-lasting differences in offspring lung function, gene expression, and lung Cyp1a1 DNAm, which wane over time but are reestablished on reexposure to CS in adulthood. This study creates a testable mouse model that can be used to investigate the effects of prenatal and early postnatal CS exposures and will contribute to the design of intervention strategies to mediate these detrimental effects.NEW & NOTEWORTHY Here, we isolated effects of prenatal from early postnatal cigarette smoke and showed that exposure to cigarette smoke early in life causes changes in offspring DNA methylation at Cyp1a1 that last through early adulthood but not into late adulthood. We also showed that smoking in adulthood reestablished these DNA methylation patterns at Cyp1a1, suggesting that a mechanism other than DNA methylation results in long-term memory associated with early-life cigarette smoke exposures at this gene.

A prospective birth cohort study of maternal prenatal cigarette smoking assessed by self-report and biomarkers on childhood risk of overweight or obesity.

Most studies on the association of in utero exposure to cigarette smoking and childhood overweight or obesity (OWO) were based on maternal self-reported smoking status, and few were based on objective biomarkers. The concordance of self-report smoking, and maternal and cord blood biomarkers of cigarette smoking as well as their effects on children's long-term risk of overweight and obesity are unclear. In this study, we analyzed data from 2351 mother-child pairs in the Boston Birth Cohort, a sample of US predominantly Black, indigenous, and people of color (BIPOC) that enrolled children at birth and followed prospectively up to age 18 years. In utero smoking exposure was measured by maternal self-report and by maternal and cord plasma biomarkers of smoking: cotinine and hydroxycotinine. We assessed the individual and joint associations of each smoking exposure measure and maternal OWO with childhood OWO using multinomial logistic regressions. We used nested logistic regressions to investigate the childhood OWO prediction performance when adding maternal and cord plasma biomarkers as input covariates on top of self-reported data. Our results demonstrated that in utero cigarette smoking exposure defined by self-report and by maternal or cord metabolites was consistently associated with increased risk of long-term child OWO. Children with cord hydroxycotinine in the fourth quartile (vs. first quartile) had 1.66 (95% confidence interval [CI] 1.03-2.66) times the odds for overweight and 1.57 (95% CI 1.05-2.36) times the odds for obesity. The combined effect of maternal OWO and smoking on offspring risk of obesity is 3.66 (95% CI 2.37-5.67) if using self-reported smoking. Adding maternal and cord plasma biomarker information to self-reported data improved the prediction accuracy of long-term child OWO risk. This longitudinal birth cohort study of US BIPOC underscored the role of maternal smoking as an obesogen for offspring OWO risk. Our findings call for public health intervention strategies to focus on maternal smoking - as a highly modifiable target, including smoking cessation and countermeasures (such as optimal nutrition) that may alleviate the increasing obesity burden in the United States and globally.

Effect of maternal cigarette smoking and alcohol consumption during pregnancy on birth weight and cardiometabolic risk factors in infants, children and adolescents: a systematic review protocol

IntroductionTobacco smoking and alcohol consumption during pregnancy are particularly prevalent in low socioeconomic status populations, with an adverse association with birth outcomes and cardiometabolic risk factors. However, the direct and...

Prenatal and Postnatal Cigarette Smoke Exposure Is Associated With Increased Risk of Exacerbated Allergic Airway Immune Responses: A Preclinical Mouse Model

Increased exposure to household air pollution and ambient air pollution has become one of the world’s major environmental health threats. In developing and developed countries, environmental cigarette smoke (CS) exposure is one of the main sources of household air pollution (HAP). Moreover, results from different epidemiological and experimental studies indicate that there is a strong association between HAP, specifically CS exposure, and the development of allergic diseases that often persists into later life. Here, we investigated the impact of prenatal and postnatal CS exposure on offspring susceptibility to the development of allergic airway responses by using a preclinical mouse model. Pregnant BALB/c mice were exposed to either CS or air during pregnancy and lactation and in order to induce allergic asthma the offspring were sensitized and challenged with house dust mite (HDM). Decreased lung function parameters, like dynamic compliance and pleural pressure, were observed in PBS-treated offspring born to CS-exposed mothers compared to offspring from air-exposed mothers. Maternal CS exposure significantly increased the HDM-induced airway eosinophilia and neutrophilia in the offspring. Prenatal and postnatal CS exposure increased the frequency of Th2 cells in the lungs of HDM-treated offspring compared to offspring born to air-exposed mothers. Offspring born to CS-exposed mothers showed increased levels of IL-4, IL-5 and IL-13 in bronchoalveolar lavage fluid compared to offspring from air-exposed mothers. Ex-vivo restimulation of lung cells isolated from HDM-treated offspring born to CS-exposed mothers also resulted in increased IL-4 production. Finally, serum immunoglobulins levels of HDM-specific IgE and HDM-specific IgG1 were significantly increased upon a HDM challenge in offspring born to CS-exposed mothers compared to offspring from air-exposed mothers. In summary, our results reveal a biological plausibility for the epidemiological studies indicating that prenatal and postnatal CS exposure increases the susceptibility of offspring to allergic immune responses.

Cigarette smoking cessation and mental health treatment receipt in a U.S national sample of pregnant women with mental illness.

To (1) compare the probability of cigarette smoking cessation for pregnant women with and without past-year mental illness by the trimester of pregnancy; and (2) examine the association between the receipt of past-year mental health treatment and prenatal cigarette smoking cessation among pregnant lifetime-smokers with mental illness. We conducted secondary analysis of data from the National Survey on Drug Use and Health (NSDUH) 2008-2014. The NSDUH included 2019 pregnant lifetime smokers aged 18-44years, 528 of whom had a mental illness. We used multiple logistic regression to model the probability of prenatal cigarette smoking cessation. Pregnant lifetime-smokers with mental illness had a lower rate of cigarette smoking cessation than women without mental illness (47.9% vs. 61.7%, p=0.001). Compared to pregnant women without mental illness, pregnant women with mental illness had a significantly lower odds of smoking cessation in the first trimester (Adjusted Odds Ratio [AOR]: 0.34, 95% Confidence Interval [CI]: 0.18-0.66), but not in the second (AOR: 0.87, 95% CI: 0.46-1.63) and third trimesters (AOR: 0.94, 95% CI: 0.51-1.72). The likelihood of quitting smoking did not differ significantly for pregnant lifetime-smokers with mental illness who received and did not receive mental health treatment (AOR: 1.69, 95% CI: 0.87-3.28). Pregnant lifetime-smokers with mental illness are less likely to quit smoking than those without mental illness; overall, pregnant women tended to quit smoking as they progressed in their pregnancy. The receipt of mental health treatment was not associated with quitting smoking. Mental health care providers need to screen for cigarette use among pregnant women and strengthen smoking cessation efforts. Pregnancy presents a unique opportunity for mental health care providers to screen for cigarette use in women with mental illness and support their smoking cessation efforts.

Adverse Birth Outcomes Associated With Prepregnancy and Prenatal Electronic Cigarette Use.

To evaluate the risk of adverse birth outcomes among adults who use electronic cigarettes (e-cigarettes) before and during pregnancy. Data from the 2016-2018 PRAMS (Pregnancy Risk Assessment Monitoring System) were used to assess the association between e-cigarette use during the 3 months before and last 3 months of pregnancy among 79,176 individuals with a recent live birth and the following birth outcomes: preterm birth, small for gestational age, and low birth weight (LBW). Adjusted prevalence ratios were generated using average marginal predictions from multivariable logistic regression models. Models were stratified by prenatal combustible cigarette smoking and frequency of e-cigarette use (daily or less than daily use). In the 3 months before pregnancy, 2.7% (95% CI 2.6-2.9%) of respondents used e-cigarettes; 1.1% (95% CI 1.0-1.2%) used e-cigarettes during the last 3 months of pregnancy. Electronic cigarette use before pregnancy was not associated with adverse birth outcomes. Electronic cigarette use during pregnancy was associated with increased prevalence of LBW compared with nonuse (8.1% vs 6.1%; adjusted prevalence ratio 1.33; 95% CI 1.06-1.66). Among respondents who did not also smoke combustible cigarettes during pregnancy (n=72,256), e-cigarette use was associated with higher prevalence of LBW (10.6%; adjusted prevalence ratio 1.88; 95% CI 1.38-2.57) and preterm birth (12.4%; adjusted prevalence ratio 1.69; 95% CI 1.20-2.39). When further stratified by frequency of e-cigarette use, associations were seen only for daily users. E-cigarette use during pregnancy, particularly when used daily by individuals who do not also smoke combustible cigarettes, is associated with adverse birth outcomes.

Effect of prenatal cigarette smoke exposure on sevoflurane-induced respiratory suppression in neonatal rats and the protective role of hydrogen sulfide

Prenatal cigarette smoke (CS) exposure causes numerous respiratory health problems in infants. This study aimed to investigate the effect of prenatal CS exposure on sevoflurane-induced respiratory suppression in neonatal rats and the protective role of H2S. We found that at baseline, minute ventilation (V’E), respiratory frequency (fR), and tidal volume (VT) were similar among tested groups, whereas sigh frequency (fS) was lower in CS group than in the Control group. During 3 % sevoflurane anesthesia, V’E was decreased, fR was slowed, VT was increased, and fS was reduced in all groups; however, the decline in fR and increase in VT was greater in CS group than in the Control group. During the recovery, fS remained lower in CS group. The above changes of respiratory response caused by prenatal CS exposure were alleviated by NaHS pretreatment (a donor of H2S, 56 μmol/kg/d, intraperitoneal injection). These results indicated that prenatal CS exposure alters the breathing into a much slower and deeper manner in neonatal rats during sevoflurane anesthesia, and H2S mitigates this respiratory change.

Low birthweight of children is positively associated with mother\u2019s prenatal tobacco smoke exposure in Shanghai: a cross-sectional study

IntroductionLow birthweight (LBW) is a significant public health issue, and maternal smoking is the most prevalent preventable cause of LBW. But there is limited evidence on association of LBW among children and cigarette smoke exposure in mothers in China. In this cross-sectional study, we try to explore if the LBW in children is positively associated with mothers’ prenatal cigarette smoke exposure.MethodsWe selected 8, 586 mothers and their singleton children in 2018 in Songjiang district, Shanghai. Birthweight of children and gestational weeks of mother was identified by birth records in the hospital, we classified mothers’ prenatal cigarette smoke status into the first-hand smoke (FHS) exposure and the second-hand smoke (SHS) exposure. We use SAS 9.1.3 software to calculate the prevalence of children’s LBW and the prevalence of mothers’ prenatal cigarette smoke exposure including FHS and SHS. Chi-square test and logistic regression were used to analyze the difference.ResultsIn 8, 586 women, The prenatal FHS and SHS exposure prevalence was 0.9 and 20.8%, respectively. The mean birthweight of children was 3315.5 g with a standard deviation of 497.2 g, the mean birthweight was 167.7 g and 66.1 g lower in children born to mothers with prenatally FHS and SHS exposure compared with those children whose mother were not exposed, respectively. The children’s LBW prevalence was 4.7% in this study. By comparing with children whose mother were not exposed, the LBW prevalence was higher among children whose mother were prenatally exposed to FHS [OR (Odds Ratios) = 2.91, 95% confidence interval (CI) (1.49, 5.68)], and SHS [OR = 2.35, 95% CI (1.90, 2.89)].ConclusionsChildren’s LBW is positively associated with mothers’ prenatal tobacco smoke exposure both for FHS and SHS. So implementing tobacco control measures is crucial to lower smoking prevalence among women, and decrease smoking prevalence of their family members as well as work fellows.

Decreasing smoking during pregnancy: Potential economic benefit of reducing sudden unexpected infant death

Sudden Unexpected Infant Death (SUID) remains the leading cause of death among U.S. infants age 1–12 months. Extensive epidemiological evidence documents maternal prenatal cigarette smoking as a major risk factor for SUID, but leaves unclear whether quitting reduces risk. This Commentary draws attention to a report by Anderson et al. (Pediatrics. 2019, 143[4]) that represents a breakthrough on this question and uses their data on SUID risk reduction to delineate potential economic benefits. Using a five-year (2007–11) U.S. CDC Birth Cohort Linked Birth/Infant Death dataset, Anderson et al. demonstrated that compared to those who continued smoking, women who quit or reduced smoking by third trimester decreased the adjusted odds of SUID risk by 23% (95% CI, 13%–33%) and 12% (95% CI, 2%–21%), respectively. We applied these reductions to the U.S. Department of Health and Human Services' recommended value of a statistical life in 2020 ($10.1 million). Compared to continued smoking during pregnancy, the economic benefits per woman of quitting or reducing smoking are $4700 (95% CI $2700–$6800) and $2500 (95% CI, $400–$4300), respectively. While the U.S. obtained aggregate annual economic benefits of $0.58 (95% CI, 0.35–0.82) billion from pregnant women who quit or reduced smoking, it missed an additional $1.16 (95%CI 0.71–1.60) billion from the women who continued smoking. Delineating the health and economic impacts of decreasing smoking during pregnancy using large epidemiological studies like Anderson et al. is critically important for conducting meaningful economic analyses of the benefits-costs of developing more effective interventions for decreasing smoking during pregnancy.

Dual use of cigarettes and electronic nicotine delivery systems during pregnancy and the risk of small for gestational age neonates

PurposeThe purpose of this study was to estimate the effect of cigarette smoking and electronic nicotine delivery systems (ENDS) use during pregnancy on small for gestational age (SGA). MethodsWe used data from the 2016-2017 Arkansas Pregnancy Risk Assessment Monitoring System, estimated the risk ratio (RR) for SGA for maternal prenatal cigarette smoking–only use, cigarette smoking, and ENDS use (i.e., dual use), with no prenatal tobacco use as referent, accounting for the complex survey design. We also explored these effects for women who stopped smoking cigarettes during pregnancy among cigarette smokers and dual users. ResultsEstimated adjusted RR for SGA for cigarette-only users was 1.7 (95% confidence interval [CI]: 1.1, 2.7), and 1.8 (95% CI: 1.0, 3.4) for dual users. These RR estimates increased after correcting for tobacco use misclassification. Women who were dual users (cigarette smokers and ENDS users) and continued using ENDS but stopped smoking cigarettes had an increased risk for SGA compared with nontobacco users, 3.2 (95% CI: 1.5, 6.6). ConclusionsOur results in a population representative sample are consistent with the hypothesis that exposure to both maternal cigarette smoking and ENDS use increased the risk of SGA. Dual users still had an elevated risk of SGA after smoking cessation.

Prenatal cigarette smoking as a mediator between racism and depressive symptoms: The Biosocial Impact on Black Births Study.

This study examined whether cigarette smoking mediated the association of racial discrimination with depressive symptoms among pregnant Black women. Cross-sectional. Two hundred Black women at 8-29weeks gestation. Women completed questionnaires including the Experiences of Discrimination and the Center for Epidemiologic Studies-Depression (CES-D) scales, as well as questions about sociodemographic characteristics and cigarette smoking. The mean age of the sample was 26.9±5.7years and the mean gestational age at data collection was 15.6±5.7weeks. Approximately 17% of women reported prenatal cigarette smoking; 27% had prenatal CES-D scores ≥23, which have been correlated with depression diagnoses; and 59% reported ever (lifetime) experiencing discrimination in at least one situation (e.g., at work). Path analysis results indicated that the standardized indirect effect of experiences of racial discrimination on CES-D scores through prenatal smoking was statistically significant (standardized indirect effect=0.03; 95% CI: 0.001, 0.094; p=.042). Cigarette smoking during pregnancy partially mediated the association between lifetime experiences of racial discrimination and prenatal depressive symptoms among pregnant Black women. Smoking cessation programs should focus on identifying and treating depressive symptoms among pregnant Black women.

Prenatal cigarette smoke exposure slightly alters neurobehavioral development in neonatal rats: Implications for developmental origins of health and disease (DoHAD).

Numerous studies indicate that smoking during pregnancy exerts harmful effects on fetal brain development. The aim of this study was to determine the influence of maternal smoking during pregnancy on the early physical and neurobehavioral development of newborn rats. Wistar rats were subjected to whole-body smoke exposure for 2 × 40 min daily from the day of mating until day of delivery. For this treatment, a manual closed-chamber smoking system and 4 research cigarettes per occasion were used. After delivery the offspring were tested daily for somatic growth, maturation of facial characteristics and neurobehavioral development until three weeks of age. Motor coordination tests were performed at 3 and 4 weeks of age. We found that prenatal cigarette smoke exposure did not alter weight gain or motor coordination. Critical physical reflexes indicative of neurobehavioral development (eyelid reflex, ear unfolding) appeared significantly later in pups prenatally exposed to smoke as compared to the control group. Prenatal smoke exposure also resulted in a delayed appearance of reflexes indicating neural maturity, including hind limb grasping and forelimb placing reflexes. In conclusion, clinically relevant prenatal exposure to cigarette smoke results in slightly altered neurobehavioral development in rat pups. These findings suggest that chronic exposure of pregnant mothers to cigarette smoke (including passive smoking) results in persisting alterations in the developing brain, which may have long-lasting consequences supporting the concept of developmental origins of health and disease (DoHAD).

Infant neurobehavioural consequences of prenatal cigarette exposure: A systematic review and meta-analysis.

AimPrenatal exposure to cigarettes leads to alterations in brain development during pregnancy. This has an impact on postnatal psychological and behavioural processes, affecting an infant's neurobehavioural profile with little known about which aspects are affected. The evidence was synthesised to assess the effects of prenatal cigarette smoke exposure on neurobehavioural outcomes within the first year of life.MethodsSix databases were searched (Web of Science Core Collections, MEDLINE, PsycINFO, CINAHL, EBSCOhost eBook Collection and OpenGrey) in November 2018. Eligible studies (n = 17) had to include a measure of prenatal cigarette exposure and a neurobehavioural assessment ≤1 year of age.ResultsIn the first year of life, specific areas of neurobehavioural functioning are related to prenatal cigarette exposure with eight out of 10 areas of neurobehaviour having significant medium (negative affect, attention, excitability, irritability and orientation) or small (muscle tone, regulation and difficult temperament) pooled effect sizes. Only lethargy and stress did not show any significant pooled effects.ConclusionPrenatal cigarette exposure affects a significant range of behaviours during the first year of life.

Predisposing Factors to Risk of Low Birth Weight in Premature Baby in Bengkulu Indonesia

Introduction: Birth weight is the most important factor which determines the survival of newborns. Low birth weight (LBW) is one of the challenges in maternal and child health and most are caused by preterm labor. Exposure to prenatal or postnatal cigarette smoke has a detrimental effect on fetal and infant health including premature birth. This study was conducted in Bengkulu Province which aims to determine the magnitude of maternal predisposing factors influence on the LBW in preterm birth. Method: This was research with a cross-sectional design which used a questionnaire on 95 premature babies born in January to October 2018 in the Bengkulu Province, Indonesia. Predisposing factors studied including smokers in family members, mother’s age, mother’s education level, mother’s occupation, gestational age and gender of the baby. Data were analyzed using multivariate logistic regression. Result: On average, premature babies were born at 32.9 weeks of gestation, 81.1% of babies born with LBW, most of the samples have family member who smokes (85.3%), most mothers participated aged 2635 years (46.3%), most mother’s education level was moderate (45.3%), and most mother’s occupation was house wived (70.5%). In the multivariate variable analysis, the predisposing risk of experiencing very low birth weight (VLBW) including smoker in a family member (OR=8.79, 95% CI 1.54-50.35), gestational age (OR=0.63, 95% CI 0.49-0.82), and mother’s age of 26-35 years (OR=1.47, 95% CI 1.59-134.73). Conclusion: Smoker in a family member, Mother’s age, gestation age, and Mother’s private employee has a significant risk of LBW in premature babies in Bengkulu Province.

Screening, Brief Intervention, and Referral to Treatment for Prenatal Alcohol Use and Cigarette Smoking: A Survey of Academic and Community Health Care Providers.

Objectives:Prenatal alcohol and cigarette smoking are associated with numerous adverse pregnancy outcomes. Screening, Brief Intervention, and Referral to Treatment (SBIRT) represents a standardized approach; however, implementation in routine pregnancy care remains a challenge. The purpose of the study was to determine current practices, barriers to implementation, and education needs of healthcare providers utilizing SBIRT to address prenatal alcohol and cigarette smoking.Methods:We conducted a survey of 118 providers including family physicians, midwives, and obstetricians practicing at 2 Toronto hospitals: community-based teaching site and fully affiliated academic health sciences center.Results:The response rate was 79%. Almost all providers reported screening every pregnant woman for alcohol and smoking status. Brief intervention was offered by fewer providers. Education and supportive counseling were reported by a higher percentage of providers for prenatal cigarette smoking in comparison to alcohol use. Furthermore, up to 60% referred pregnant women to treatment programs for alcohol and cigarette smoking. A significantly higher number of community-based providers reported referring pregnant women to addiction treatment programs. Barriers to interventions included a perceived lack of appropriate resources, training, and clinical pathways.Conclusion:Healthcare providers report universal screening for prenatal alcohol and cigarette smoking; however, brief intervention and referral to treatment are more limited practices. There is a need for education of all providers regarding effective brief counseling strategies and referral to appropriate treatment resources. Development of clinical care pathways may also increase adoption of all components of SBIRT for prenatal alcohol use and cigarette smoking.

Reproductive Indices and Oxidative Stress Biomarkers of Male Wistar Rats Prenatally Exposed to Cigarette Smoke.

The negative influence of cigarette smoking on developing fetus is well documented but reports of prenatal cigarette smoking on male reproductive hormones are controversial. However, shortened anogenital distance (AGD) has been established to be an indicator of potential male infertility. We therefore investigated the effects of prenatal exposure to passive cigarette smoke on AGD, reproductive hormones and oxidative stress biomarkers of Wistar rats. Female rats were randomly divided into two groups (n=5) and cohabited with male. Group 1 was exposed to smoke from an idling cigarette from day 1 of gestation till parturition, while Group 2 served as control (no-exposure). Morphometric variables of the litters were recorded on postnatal day 1 (PND1) and at 6th week postnatal life. The male offspring were then sacrificed by cervical dislocation. Testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were analysed using ELISA. Serum levels of Catalase, sodium dismutase (SOD), malondialdehyde (MDA), lipid profile and liver function biomarkers were examined spectrophotometrically. On PND1, crown rump length and total body length of rats prenatally exposed to cigarette smoke were significantly shorter. Significantly shorter AGD and crown rump length were also observed at 6th week. Testosterone, LH and FSH were not significantly affected. Cigarette smoke exposure significantly decreased Catalase and SOD while MDA increased. Liver function biomarkers, HDL and LDL were not affected but serum levels of total cholesterol and triglyceride significantly increased. The observed decline in AGD and precipitation of oxidative stress by intrauterine cigarette smoke exposure may predispose to male infertility at adulthood.

Effects of prenatal cigarette smoke exposure on BDNF, PACAP, microglia and gliosis expression in the young male mouse brainstem

Cigarette smoke exposure during pregnancy into infancy affects brain growth and development in both short and long term (into adulthood). Using a mouse model of pre- into post- natal cigarette smoke exposure (SE), we aimed to determine the effects on brain derived neurotrophic factor (BDNF) and its receptor TrkB, neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) and its receptor PAC1, and astrocyte (GFAP) and microglia (Iba-1) immunohistochemical expression, in seven nuclei of the medulla and the facial (FAC) nucleus of the pons. Male pups of dams exposed to two cigarettes (nicotine <1.2 mg, CO <15 mg) twice daily for six weeks prior to mating, during gestation and lactation (n = 5; SE), were compared to pups exposed to air under the same condition (n = 5; SHAM) at postnatal day 20. Expression changes were only evident for BDNF, TrkB and PAC1 and included decreased BDNF in the hypoglossal (XII) nucleus and nucleus of the solitary tract (NTS), increased TrkB in XII but decreased TrkB in the FAC, and increased PAC1 in 4 nuclei of the medulla including the NTS. These results suggest that the effect of SE on the brainstem are region and marker selective, affecting regions of respiratory control (XII and NTS), and restricted to the BDNF system and PAC1, with no effect on activation states of astrocytes or microglia.

Effect of Prenatal Waterpipe Tobacco Smoke Exposure on Cardiac Biomarkers in Adult Offspring Rats.

The prevalence of waterpipe tobacco smoke (WTS) consumption is increased among pregnant woman. Prenatal cigarette smoke exposure increased the risk of developing cardiovascular diseases in offspring. The current study examined the effect of prenatal WTS exposure on inflammatory profile, oxidative stress, and cardiac biomarkers in adult offspring rats. Female rats received WTS (2 hours per day) or fresh air 1 day prior to mating and throughout the pregnancy period. The body and heart masses were measured in male offspring rats. The level of oxidative stress biomarkers, nitrate, inflammatory mediators (interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α]), and gene expression of protein kinase C epsilon, angiotensin 2 receptor one, and transforming growth factor beta1 were measured in cardiac tissue homogenates of 13-week-old male offspring rats. Prenatal WTS exposure reduced body weight and increased heart to body weight ratio (P < .05). Prenatal WTS exposure did not affect oxidative stress biomarkers (superoxide dismutase, glutathione peroxidase, and thiobarbituric acid reactive substances) but significantly increased catalase activity and nitrate level (P < .05) in cardiac tissue of adult male offspring rats. In addition, prenatal exposure to WTS did not affect cardiac level of TNF-α and IL-6 as well as the gene expression of different cardiac modulators in adult male offspring rats (P > .05). Prenatal WTS exposure has detrimental consequences on adult offspring rats by increasing the ratio of heart to body mass, increasing the catalase activity and nitrate level in cardiac tissue of adult male offspring rats.

E-cigarette minimum legal sale age laws and traditional cigarette use among rural pregnant teenagers

Teenagers under 18 could legally purchase e-cigarettes until states passed minimum legal sale age laws. These laws may have curtailed teenagers' use of e-cigarettes for smoking cessation. We investigate the effect of e-cigarette minimum legal sale age laws on prenatal cigarette smoking and birth outcomes for underage rural teenagers using data on all births from 2010 to 2016 from 32 states. We find that the laws increased prenatal smoking by 0.6 percentage points (pp) overall. These effects were concentrated in prepregnancy smokers, with no effect on prepregnancy non-smokers. These results suggest that the laws reduced cigarette smoking cessation during pregnancy rather than causing new cigarette smoking initiation. Our results may indicate an unmet need for assistance with smoking cessation among pregnant teenagers.