Talk:Abnormal Development - Smoking - Revision history

Z8600021 at 05:58, 23 October 2018

2018-10-23T05:58:27Z

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	==2018==		==2018==

			===Toxic Effect of Cigarette Smoke on Brainstem Nicotinic Receptor Expression: Primary Cause of Sudden Unexplained Perinatal Death===

			Toxics. 2018 Oct 18;6(4). pii: E63. doi: 10.3390/toxics6040063.

			Lavezzi AM1.

			Abstract

			Among the neurotoxicants contained in tobacco smoke, if absorbed during pregnancy, nicotine significantly affects α7-nicotinic acetylcholine receptors, which play essential roles in the development of the brainstem regions receiving cholinergic projections in perinatal life. Immunohistochemical procedures for analysing formalin-fixed and paraffin-embedded brainstem samples from 68 fetuses and early newborns, with smoking and non-smoking mothers, who died of known and unknown causes, were carried out in order to determine if nicotine had activated the α7-nicotinic acetylcholine receptors. High α7-nicotinic acetylcholine receptor expression levels were only observed in the victims with smoking mothers. Frequently, these findings were associated with the hypoplasia of the brainstem structures controlling vital functions. The results of this study indicate that the exposition to nicotine in pregnancy exerts a strong direct effect on α7-nicotinic acetylcholine receptor activity especially in perinatal life and may be one of the primary risk factors leading to the sudden unexplained death of fetuses and newborns.
			KEYWORDS:
			Kölliker-Fuse nucleus; brainstem; immunohistochemistry; nicotine; nicotinic acetylcholine receptors; sudden fetal death; sudden neonatal death
			PMID: 30340403 DOI: 10.3390/toxics6040063


	===Nicotine exposure of male mice produces behavioral impairment in multiple generations of descendants===		===Nicotine exposure of male mice produces behavioral impairment in multiple generations of descendants===

Z8600021 at 05:53, 23 October 2018

2018-10-23T05:53:59Z

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	==2018==		==2018==

			===Nicotine exposure of male mice produces behavioral impairment in multiple generations of descendants===

			PLoS Biol. 2018 Oct 16;16(10):e2006497. doi: 10.1371/journal.pbio.2006497. eCollection 2018 Oct.

			McCarthy DM1, Morgan TJ Jr1, Lowe SE1, Williamson MJ1, Spencer TJ2, Biederman J2, Bhide PG1.

			Abstract

			Use of tobacco products is injurious to health in men and women. However, tobacco use by pregnant women receives greater scrutiny because it can also compromise the health of future generations. More men smoke cigarettes than women. Yet the impact of nicotine use by men upon their descendants has not been as widely scrutinized. We exposed male C57BL/6 mice to nicotine (200 μg/mL in drinking water) for 12 wk and bred the mice with drug-naïve females to produce the F1 generation. Male and female F1 mice were bred with drug-naïve partners to produce the F2 generation. We analyzed spontaneous locomotor activity, working memory, attention, and reversal learning in male and female F1 and F2 mice. Both male and female F1 mice derived from the nicotine-exposed males showed significant increases in spontaneous locomotor activity and significant deficits in reversal learning. The male F1 mice also showed significant deficits in attention, brain monoamine content, and dopamine receptor mRNA expression. Examination of the F2 generation showed that male F2 mice derived from paternally nicotine-exposed female F1 mice had significant deficits in reversal learning. Analysis of epigenetic changes in the spermatozoa of the nicotine-exposed male founders (F0) showed significant changes in global DNA methylation and DNA methylation at promoter regions of the dopamine D2 receptor gene. Our findings show that nicotine exposure of male mice produces behavioral changes in multiple generations of descendants. Nicotine-induced changes in spermatozoal DNA methylation are a plausible mechanism for the transgenerational transmission of the phenotypes. These findings underscore the need to enlarge the current focus of research and public policy targeting nicotine exposure of pregnant mothers by a more equitable focus on nicotine exposure of the mother and the father.
			PMID: 30325916 DOI: 10.1371/journal.pbio.2006497

	===Developmental effects of maternal smoking during pregnancy on the human frontal cortex transcriptome===		===Developmental effects of maternal smoking during pregnancy on the human frontal cortex transcriptome===

Z8600021 at 01:28, 24 September 2018

2018-09-24T01:28:13Z

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	==2018==		==2018==

			===Developmental effects of maternal smoking during pregnancy on the human frontal cortex transcriptome===

			{{#pmid:30131587}}

			Semick SA1, Collado-Torres L1,2, Markunas CA3, Shin JH1, Deep-Soboslay A1, Tao R1, Huestis MA4, Bierut LJ5, Maher BS6, Johnson EO7, Hyde TM1,8,9, Weinberger DR1,8,9,10,11, Hancock DB3, Kleinman JE12,13, Jaffe AE14,15,16,17,18.
			Author information
			Abstract
			Cigarette smoking during pregnancy is a major public health concern. While there are well-described consequences in early child development, there is very little known about the effects of maternal smoking on human cortical biology during prenatal life. We therefore performed a genome-wide differential gene expression analysis using RNA sequencing (RNA-seq) on prenatal (N = 33; 16 smoking-exposed) as well as adult (N = 207; 57 active smokers) human postmortem prefrontal cortices. Smoking exposure during the prenatal period was directly associated with differential expression of 14 genes; in contrast, during adulthood, despite a much larger sample size, only two genes showed significant differential expression (FDR < 10%). Moreover, 1,315 genes showed significantly different exposure effects between maternal smoking during pregnancy and direct exposure in adulthood (FDR < 10%)-these differences were largely driven by prenatal differences that were enriched for pathways previously implicated in addiction and synaptic function. Furthermore, prenatal and age-dependent differentially expressed genes were enriched for genes implicated in non-syndromic autism spectrum disorder (ASD) and were differentially expressed as a set between patients with ASD and controls in postmortem cortical regions. These results underscore the enhanced sensitivity to the biological effect of smoking exposure in the developing brain and offer insight into how maternal smoking during pregnancy affects gene expression in the prenatal human cortex. They also begin to address the relationship between in utero exposure to smoking and the heightened risks for the subsequent development of neuropsychiatric disorders.
			PMID: 30131587 DOI: 10.1038/s41380-018-0223-1

	===Impact on birth weight of maternal smoking throughout pregnancy mediated by DNA methylation===		===Impact on birth weight of maternal smoking throughout pregnancy mediated by DNA methylation===

Z8600021 at 02:43, 28 April 2018

2018-04-28T02:43:25Z

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			==2018==

			===Impact on birth weight of maternal smoking throughout pregnancy mediated by DNA methylation===
			BMC Genomics. 2018 Apr 25;19(1):290. doi: 10.1186/s12864-018-4652-7.

			Witt SH1, Frank J2, Gilles M3, Lang M2, Treutlein J2, Streit F2, Wolf IAC3, Peus V3, Scharnholz B3, Send TS3, Heilmann-Heimbach S4,5, Sivalingam S4,5, Dukal H2, Strohmaier J2, Sütterlin M6, Arloth J7, Laucht M8,9, Nöthen MM4,5, Deuschle M3, Rietschel M2.

			Abstract
			BACKGROUND:
			Cigarette smoking has severe adverse health consequences in adults and in the offspring of mothers who smoke during pregnancy. One of the most widely reported effects of smoking during pregnancy is reduced birth weight which is in turn associated with chronic disease in adulthood. Epigenome-wide association studies have revealed that smokers show a characteristic "smoking methylation pattern", and recent authors have proposed that DNA methylation mediates the impact of maternal smoking on birth weight. The aims of the present study were to replicate previous reports that methylation mediates the effect of maternal smoking on birth weight, and for the first time to investigate whether the observed mediation effects are sex-specific in order to account for known sex-specific differences in methylation levels.
			METHODS:
			Methylation levels in the cord blood of 313 newborns were determined using the Illumina HumanMethylation450K Beadchip. A total of 5,527 CpG sites selected on the basis of evidence from the literature were tested. To determine whether the observed association between maternal smoking and birth weight was attributable to methylation, mediation analyses were performed for significant CpG sites. Separate analyses were then performed in males and females.
			RESULTS:
			Following quality control, 282 newborns eventually remained in the analysis. A total of 25 mothers had smoked consistently throughout the pregnancy. The birthweigt of newborns whose mothers had smoked throughout pregnancy was reduced by >200g. After correction for multiple testing, 30 CpGs showed differential methylation in the maternal smoking subgroup including top "smoking methylation pattern" genes AHRR, MYO1G, GFI1, CYP1A1, and CNTNAP2. The effect of maternal smoking on birth weight was partly mediated by the methylation of cg25325512 (PIM1); cg25949550 (CNTNAP2); and cg08699196 (ITGB7). Sex-specific analyses revealed a mediating effect for cg25949550 (CNTNAP2) in male newborns.
			CONCLUSION:
			The present data replicate previous findings that methylation can mediate the effect of maternal smoking on birth weight. The analysis of sex-dependent mediation effects suggests that the sex of the newborn may have an influence. Larger studies are warranted to investigate the role of both the identified differentially methylated loci and the sex of the newborn in mediating the association between maternal smoking during pregnancy and birth weight.
			KEYWORDS:
			Birth weight; DNA methylation; Mediation analysis; Smoking
			PMID: 29695247 DOI: 10.1186/s12864-018-4652-7

Z8600021 at 16:12, 1 March 2015

2015-03-01T16:12:03Z

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			==2015==

			===The effects of electronic cigarette emissions on systemic cotinine levels, weight and postnatal lung growth in neonatal mice===
			PLoS One. 2015 Feb 23;10(2):e0118344. doi: 10.1371/journal.pone.0118344. eCollection 2015.

			McGrath-Morrow SA1, Hayashi M2, Aherrera A2, Lopez A3, Malinina A4, Collaco JM1, Neptune E4, Klein JD5, Winickoff JP6, Breysse P7, Lazarus P8, Chen G8.

			Abstract

			BACKGROUND/OBJECTIVE:
			Electronic cigarette (E-cigarettes) emissions present a potentially new hazard to neonates through inhalation, dermal and oral contact. Exposure to nicotine containing E-cigarettes may cause significant systemic absorption in neonates due to the potential for multi-route exposure. Systemic absorption of nicotine and constituents of E-cigarette emissions may adversely impact weight and lung development in the neonate. To address these questions we exposed neonatal mice to E-cigarette emissions and measured systemic cotinine levels and alveolar lung growth.
			METHODS/MAIN RESULTS:
			Neonatal mice were exposed to E-cigarettes for the first 10 days of life. E-cigarette cartridges contained either 1.8% nicotine in propylene glycol (PG) or PG vehicle alone. Daily weights, plasma and urine cotinine levels and lung growth using the alveolar mean linear intercept (MLI) method were measured at 10 days of life and compared to room air controls. Mice exposed to 1.8% nicotine/PG had a 13.3% decrease in total body weight compared to room air controls. Plasma cotinine levels were found to be elevated in neonatal mice exposed to 1.8% nicotine/PG E-cigarettes (mean 62.34± 3.3 ng/ml). After adjusting for sex and weight, the nicotine exposed mice were found to have modestly impaired lung growth by MLI compared to room air control mice (p<.054 trial 1; p<.006 trial 2). These studies indicate that exposure to E-cigarette emissions during the neonatal period can adversely impact weight gain. In addition exposure to nicotine containing E-cigarettes can cause detectable levels of systemic cotinine, diminished alveolar cell proliferation and a modest impairment in postnatal lung growth.

			PMID 25706869

			http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0118344

	==2014==		==2014==

Z8600021 at 05:01, 7 August 2014

2014-08-07T05:01:33Z

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	==2014==		==2014==
			===Fetal Exposure to Parental Smoking and the Risk of Type 2 Diabetes in Adult Women===
			Diabetes Care. 2014 Aug 4. pii: DC_131679.

			Jaddoe VW1, de Jonge LL2, van Dam RM3, Willett WC4, Harris H5, Stampfer MJ4, Hu FB4, Michels KB6.

			Abstract

			OBJECTIVE:
			We evaluated the associations of both maternal and paternal smoking during pregnancy with the risk of type 2 diabetes in daughters and explored whether any association was explained by weight at birth or BMI throughout life.
			RESEARCH DESIGN AND METHODS:
			We used data from 34,453 participants of the Nurses' Health Study II. We used Cox proportional hazards models to examine the associations of maternal and paternal smoking during pregnancy with incidence of type 2 diabetes in daughters between 1989 and 2009.
			RESULTS:
			Maternal smoking during first trimester only was associated with the risk of type 2 diabetes in the offspring, independent of confounders, birth weight, and later-life BMI (fully adjusted hazard ratio 1.34 [95% CI 1.01, 1.76]). In the age-adjusted models, both continued maternal smoking during pregnancy and paternal smoking tended to be associated with an increased risk of type 2 diabetes in daughters. Perinatal and adult life variables did not explain these associations, but additional adjustment for current BMI fully attenuated the effect estimates.
			CONCLUSIONS:
			The associations of maternal and paternal smoking during pregnancy with the risk of type 2 diabetes in daughters were largely explained by BMI throughout the life course. Further studies are needed to explore the role of first-trimester-only maternal smoking on insulin resistance in the offspring. Also, similar effect estimates for maternal and paternal smoking suggest that the associations reflect shared family-based or lifestyle-related factors.
			© 2014 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

			PMID 25092685


	===Helping pregnant smokers to quit===		===Helping pregnant smokers to quit===

Z8600021 at 07:25, 14 March 2014

2014-03-14T07:25:46Z

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 ==2013==
 ===Influence of Smoking and Alcohol during Pregnancy on Outcome of VLBW Infants===
 Z Geburtshilfe Neonatol. 2013 Dec;217(6):215-219. Epub 2013 Dec 20.

Z8600021 at 07:03, 14 March 2014

2014-03-14T07:03:47Z

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	~~Original page http~~:/~~/embryology~~.~~med~~.~~unsw~~.~~edu~~.~~au/Defect/~~smoking.~~htm~~		==2014==

			===Helping pregnant smokers to quit===
			Brose LS.
			BMJ. 2014 Mar 11;348:g1808. doi: 10.1136/bmj.g1808.

			Although most smokers manage to quit during pregnancy, a proportion does not. In England, 26% of women smoke in the year before their pregnancy and 12% smoke through to delivery.1 The rate is similar in other high income countries, whereas in low and middle income countries, smoking rates are more variable and seem to be increasing among young women.2 In addition to the countless negative consequences for the smoker’s own mental and physical health, smoking in pregnancy is linked to a wide range of poor health outcomes for the child.3 Thus there is an urgent need to help pregnant smokers who find it difficult to quit.

			PMID 24620362

	==2013==		==2013==
	===Influence of Smoking and Alcohol during Pregnancy on Outcome of VLBW Infants===		===Influence of Smoking and Alcohol during Pregnancy on Outcome of VLBW Infants===

Z8600021 at 01:49, 27 Ocak 2014

2014-01-27T01:49:17Z

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	Original page http://embryology.med.unsw.edu.au/Defect/smoking.htm		Original page http://embryology.med.unsw.edu.au/Defect/smoking.htm
			==2013==
			===Influence of Smoking and Alcohol during Pregnancy on Outcome of VLBW Infants===
			Z Geburtshilfe Neonatol. 2013 Dec;217(6):215-219. Epub 2013 Dec 20.

			Spiegler J1, Jensen R2, Segerer H3, Ehlers S4, Kühn T5, Jenke A6, Gebauer C7, Möller J8, Orlikowsky T9, Heitmann F10, Boeckenholt K11, Herting E1, Göpel W1.
			Author information

			Abstract

			Nicotine and alcohol consumption have been associated with premature delivery and adverse neonatal outcome. We wanted to analyze the influence of self-reported nicotine and alcohol consumption on outcome of VLBW infants.In an ongoing multicenter study 2 475 parents of former very low birth weight (VLBW) infants born between January 2009 and December 2011 answered questionnaires about maternal smoking habits and alcohol consumption during pregnancy. 2 463 (99.5%) completed questions on alcohol consumption and 2 462 (99.5%) on smoking habits. These infants were stratified to reported maternal smoking and alcohol consumption during pregnancy. We compared the reasons for premature delivery, neonatal outcome and parental reports on bronchitis during the first year of life, as well as growth and development at age 2 years to pregnancy exposure.In nicotine exposed infants intrauterine growth restriction (31 vs. 21%, p<0.01), a birth weight below the 10th percentile (26 vs. 17%, p<0.01) and placenta abruption (9.2 vs. 5.8%, p<0.05) was seen more often. Premature rupture of membranes (24 vs. 30%, p<0.05) or HELLP syndrome (6 vs. 11%, p<0.01) was less frequent. A birth weight below the 3rd percentile was seen more frequently in mothers with reported alcohol consumption (13 vs. 6%, p<0.05). We noted an increased rate of BPD and ROP if mothers reported smoking during pregnancy (p<0.05). Growth parameters and scores on Bayley Sscales of infant development at age 2 years did not differ.Smoking during pregnancy results in a high rate of growth restricted VLBW infants. Prenatal exposition to nicotine seems to increase postnatal complications such as BPD und ROP.
			© Georg Thieme Verlag KG Stuttgart · New York.
			PMID 24363249
	==2011==		==2011==

Z8600021: /* 2011 */

2012-10-15T03:42:39Z

2011

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 Original page http://embryology.med.unsw.edu.au/Defect/smoking.htm
 ==2011==
 ===Effects of chronic carbon monoxide exposure on fetal growth and development in mice===