Influence of passive smoking on learning in elementary school

Jorge, Juliana Gomes; Botelho, Clóvis; Silva, Ageo Mário Cândido; Moi, Gisele Pedroso

doi:10.1016/j.jped.2015.08.010

Cited by 6 publications

(3 citation statements)

References 21 publications

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“…1 Previous studies have reported that prenatal smoking exposure, premature birth, and asphyxia are linked to an increased risk of ADHD. 17,20 Likewise, our findings suggest that prenatal smoking exposure and premature birth increase ADHD comorbidity in children with SLD. EEG abnormality is present in 6.1 to 53.1% of children with ADHD.…”

Section: Discussionsupporting

confidence: 57%

“…14 Previous studies have suggested that premature birth, expressive language delay, and prenatal smoking exposure increase the risk of SLD. 1,[15][16][17][18] Children with a developmental history of expressive language delay are more likely to suffer from poor academic performance and various learning disorders. 19 These manifestations are more significant when dyslexia and dysgraphia are present.…”

Section: Discussionmentioning

confidence: 99%

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Clinical Significance of Electroencephalography in Children with Specific Learning Disorders

et al. 2019

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A specific learning disorder (SLD) is a neurodevelopmental disorder in which academic skills, such as reading, writing, and mathematics ability, are below the expected range. This study was conducted to determine the relationship between spike-wave index and SLD in children. We recruited 110 child psychiatry outpatients (38 girls, 72 boys) with SLDs for this study between January 2015 and March 2018. The mean ± standard deviation patient age was 9.17 ± 1.87 years. Electroencephalography (EEG) findings were abnormal in 20.9% of children. We found that children with expressive language delay and who were born prematurely had a significantly higher risk of spike-wave index. Attention deficit/hyperactivity disorder was present in 55.5% of children with SLD. This comorbidity was significantly higher in children with a history of prenatal smoking exposure or premature birth. The EEG findings were particularly important in cases of SLD in children who were born prematurely and had expressive language delay. The spike-wave index is a potential marker of SLD and can be easily and noninvasively detected by EEG.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Clinical Significance of Electroencephalography in Children with Specific Learning Disorders

et al. 2019

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“…Although we adjusted for some potentially confounding factors which are known to be associated with infant development such as maternal socioeconomic status,21 maternal education,22 low birth weight,23 maternal exposure to passive smoking24 and maternal obesity,25 we were unable to adjust for those on which we had no data, such as maternal nutrition,26 depressive illness,27 stress and anxiety28 and alcohol consumption29 which could also potentially influence infant development but which were not measured in the SNAP trial. There remains therefore, the potential for residual confounding.…”

Section: Discussionmentioning

confidence: 99%

Is the apparently protective effect of maternal nicotine replacement therapy (NRT) used in pregnancy on infant development explained by smoking cessation?: secondary analyses of a randomised controlled trial

et al. 2019

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ObjectiveTo investigate relationships between maternal smoking status in pregnancy and infant development. The largest randomised controlled trial of nicotine replacement therapy (NRT) for smoking cessation in pregnancy, the smoking, nicotine and pregnancy (SNAP) trial, found that at 1 month after randomisation, smoking cessation rates were doubled in the NRT group compared with the placebo group. At delivery, there was no significant difference in cessation rates between groups. Surprisingly, infants born to women randomised to NRT were more likely to have unimpaired development at 2 years. We hypothesised that this apparently protective effect was due to smoking cessation caused by NRT and so, investigate this relationship using the same cohort.DesignSecondary analysis of a randomised controlled trial.SettingSeven antenatal hospitals in the Midlands and North-West England.ParticipantsEight hundred and eighty-four pregnant smokers randomised to receive either NRT patches or visually-identical placebo in the SNAP trial. Participants’ smoking behaviour were recorded at randomisation, 1 month after their target quit date and at delivery.MethodsUsing logistic regression models, we investigated associations between participants’ smoking measures and infant development (assessed using the Ages and Stages questionnaire) at 2 years.Main outcome measures2 year infant development.ResultsDevelopmental impairment was reported for 12.7% of study 2 year olds. Maternal heaviness of smoking at randomisation (OR: 1.26, 95% CI: 0.82 to 1.96, p=0.091), validated smoking abstinence recorded at 1 month after a quit date (OR: 1.02, 95% CI: 0.60 to 1.74, p=0.914) and validated smoking abstinence recorded at both 1 month after a quit date and at the end of pregnancy (OR: 1.52, 95% CI: 0.81 to 2.85, p=0.795) were not independently associated with infant developmental impairment at 2 years.ConclusionWe found no evidence that NRT treatment improved infants' developmental outcomes through smoking cessation.Trial registration numberCTA03057/0002/001-0001; Post-results

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Inhibition of the receptor for advanced glycation end-products (RAGE) protects from secondhand smoke (SHS)-induced intrauterine growth restriction IUGR in mice

et al. 2017

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Intrauterine growth restriction (IUGR) is a disease affecting 10% of all pregnancies. IUGR is associated with maternal, fetal, or placental abnormalities. Studies investigating the effects of secondhand smoke (SHS) exposure and IUGR are limited. The receptor for advanced glycation end-products (RAGE) is a pro-inflammatory transmembrane receptor increased by SHS in the placenta. We tested the hypothesis that inhibition of RAGE during SHS exposure protects from smoke-induced IUGR. C57BL/6 mice were exposed to SHS or SHS + semi-synthetic glycosaminoglycan ethers (SAGEs) known to inhibit RAGE signaling. Trophoblast cells were treated with cigarette smoke extract (CSE) with or without SAGEs in order to address the effects of RAGE inhibition during trophoblast invasion in vitro. SHS-treated mice demonstrated a significant reduction in fetal weight (7.35-fold, P ≤ 0.0001) and placental weight (1.13-fold, P ≤ 0.0001) compared with controls. Mice co-treated with SHS and SAGEs were protected from SHS-induced fetal weights decreases. SHS treatment of C57BL/6 mice activated placental extracellular signal-regulated kinase (ERK) (3.0-fold, P ≤ 0.05), JNK (2.4-fold, P ≤ 0.05) and p38 (2.1-fold, P ≤ 0.05) and the expression of inflammatory mediators including TNF-α (1.34-fold, P ≤ 0.05) and IL-1β (1.03-fold, P ≤ 0.05). SHS-mediated activation of these molecules was reduced to basal levels when SAGE was co-administered. Invasion of trophoblast cells decreased 92% (P < 0.002) when treated with CSE and CSE-mediated invasion was completely reversed by SAGEs. We conclude that RAGE inhibition protects against fetal weight loss during SHS-induced IUGR. These studies provide insight into tobacco-mediated IUGR development and clarify avenues that may be helpful in the alleviation of placental complications.

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Influence of passive smoking on learning in elementary school

Abstract: The study demonstrated an association between passive exposure to tobacco smoke and learning difficulties at school.

Cited by 6 publications

References 21 publications

Clinical Significance of Electroencephalography in Children with Specific Learning Disorders

Clinical Significance of Electroencephalography in Children with Specific Learning Disorders

Is the apparently protective effect of maternal nicotine replacement therapy (NRT) used in pregnancy on infant development explained by smoking cessation?: secondary analyses of a randomised controlled trial

Inhibition of the receptor for advanced glycation end-products (RAGE) protects from secondhand smoke (SHS)-induced intrauterine growth restriction IUGR in mice

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