scholarly journals Tobacco smoke exposure in early life and adolescence in relation to lung function

2018 ◽  
Vol 51 (6) ◽  
pp. 1702111 ◽  
Author(s):  
Jesse D. Thacher ◽  
Erica S. Schultz ◽  
Jenny Hallberg ◽  
Ulrika Hellberg ◽  
Inger Kull ◽  
...  

Maternal smoking during pregnancy is associated with impaired lung function among young children, but less is known about long-term effects and the impact of adolescents' own smoking. We investigated the influence of maternal smoking during pregnancy, secondhand smoke exposure and adolescent smoking on lung function at age 16 years.The BAMSE (Barn/Child, Allergy, Milieu, Stockholm, Epidemiology) birth cohort collected information on participants' tobacco smoke exposure through repeated questionnaires, and measured saliva cotinine concentrations at age 16 years. Participants performed spirometry and impulse oscillometry (IOS) at age 16 years (n=2295).Exposure to maternal smoking during pregnancy was associated with reduced forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratio of −1.1% (95% CI −2.0 to −0.2%). IOS demonstrated greater resistance at 5–20 Hz (R5–20) in participants exposed to maternal smoking during pregnancy. Adolescents who smoked had reduced FEV1/FVC ratios of −0.9% (95% CI −1.8 to −0.1%) and increased resistance of 6.5 Pa·L–1·s (95% CI 0.7 to 12.2 Pa·L–1·s) in R5–20. Comparable associations for FEV1/FVC ratio were observed for cotinine concentrations, using ≥12 ng·mL−1 as a cut-off for adolescent smoking.Maternal smoking during pregnancy was associated with lower FEV1/FVC ratios and increased airway resistance. In addition, adolescent smoking appears to be associated with reduced FEV1/FVC ratios and increased peripheral airway resistance.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tadashi Shiohama ◽  
Aya Hisada ◽  
Midori Yamamoto ◽  
Kenichi Sakurai ◽  
Rieko Takatani ◽  
...  

AbstractMaternal 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.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Regina Grazuleviciene ◽  
Sandra Andrusaityte ◽  
Inga Uzdanaviciute ◽  
Jolanta Kudzyte ◽  
Rimantas Kevalas ◽  
...  

Aim. To investigate the association between maternal smoking during pregnancy, second-hand tobacco smoke (STS) exposure, education level, and preschool children’s wheezing and overweight.Methods. This cohort study used data of the KANC cohort—1,489 4–6-year-old children from Kaunas city, Lithuania. Multivariate logistic regression was employed to study the influence of prenatal and postnatal STS exposure on the prevalence of wheezing and overweight, controlling for potential confounders.Results. Children exposed to maternal smoking during pregnancy had a slightly increased prevalence of wheezing and overweight. Postnatal exposure to STS was associated with a statistically significantly increased risk of wheezing and overweight in children born to mothers with lower education levels (OR 2.12; 95% CI 1.04–4.35 and 3.57; 95% CI 1.76–7.21, accordingly).Conclusions. The present study findings suggest that both maternal smoking during pregnancy and STS increase the risk of childhood wheezing and overweight, whereas lower maternal education might have a synergetic effect. Targeted interventions must to take this into account and address household smoking.


2007 ◽  
Vol 26 (6) ◽  
pp. 535-544 ◽  
Author(s):  
E. Köhler ◽  
S. Avenarius ◽  
A. Rabsilber ◽  
C. Gerloff ◽  
G. Jorch

Meconium samples collected from 115 neonates were analysed for nicotine, cotinine and trans -3-hydroxycotinine (OH-cotinine) by means of high-performance liquid chromatography (HPLC) to identify prenatal smoke exposure. The self-reported maternal smoking status during pregnancy was determined by means of a questionnaire and verified by measurements in urine prior to childbirth. The total sum of nicotine and its metabolites (Sumtot) of the first passed meconium samples was 1560 ± 1024 pmol/g in newborns of smoking mothers. Smoking of less than five cigarettes was clearly detected. Sumtot remained constant in all meconium samples passed by a neonate in succession. However, the proportion of nicotine decreased with the time of passage after birth and the OH-cotinine proportion increased, whereas cotinine hardly changed. Nicotine or its metabolites were not detectable in meconium (detection limit < 20 pmol/g), when the mothers were only exposed to environmental tobacco smoke (ETS) using the HPLC method. The hypothesis that the content of nicotine metabolites in meconium reflects long-term smoke exposure could not be confirmed in newborns whose mothers had quit smoking during the latter half of pregnancy. Determining Sumtot enables the intensity of continuous smoking during pregnancy to be estimated in all meconium samples passed by a newborn. Human & Experimental Toxicology (2007) 26: 535—544


2003 ◽  
Author(s):  
Αναστασία Σταθοπούλου

Prenatal exposure to cigarette smoke causes chronic fetal hypoxia, dysregulation of endocrineequilibrium, and disruption of fetal neurodevelopment associated with brain malfunction, all of whichpotentially could induce vulnerability to schizophrenia. A total of 212 schizophrenia patients aged 14-30 years, and 212 matched controls were studied. Prenatal tobacco smoke exposure of theschizophrenia patients was compared to that of the normal controls by applying logistic regressionanalysis and controlling for several confounding factors The outcomes of interest were comparison ofthe frequency of maternal and paternal smoking between patients and controls as well as the severity ofpositive and negative symptoms between the offspring of smoking and nonsmoking parents.Furthermore, we investigated the relative frequency of subtypes of schizophrenia among offspring ofsmoking and non-smoking parent. Among the mothers of schizophrenia patients and controls, 92(43.4%) and 46 (21.7%) smoked, respectively. Maternal smoking during pregnancy had a significantunique contribution on increasing the risk for development of schizophrenia (p=0.001), and a greaterseverity of negative symptoms (p=0.023). Simultaneously, logistic regression analysis showed thatmaternal smoking during pregnancy had significantly unique contribution to increased risk for thedevelopment of schizophrenia with possible ratio = 2.32, 95% CI = 1.41-3.81, p = 0.001 and frequencyof non-paranoid subtypes as potential ratio = 2.94,95% CI = 1.50-5.76, p = 0.002. Paternal smokingdid not have a significant effect on the risk of schizophrenia, or severity of negative symptoms. Thefindings suggest that maternal smoking during pregnancy puts offspring at an increased risk for laterschizophrenia, with increased severity of negative symptoms. Given the wide practice of smokingduring pregnancy, fetal exposure to tobacco smoke could be a major preventable neurodevelopmentalfactor that increases vulnerability to schizophrenia.


2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e22011-e22011
Author(s):  
Nurdan Tacyildiz ◽  
Adil Güzel ◽  
Filiz Bakar Ateş ◽  
Derya Özyörük ◽  
Emel Cabi Unal ◽  
...  

e22011 Background: The incidence of childhood cancers increased by 1 % per year over the last three decades. Life style changes and increased variety of environmental exposures are accused of this trend. One of these environmental factors is cigarette smoking and parental smoking is the main source of tobacco smoke exposure of children. There are strong reasons for considering parental smoking behaviour as a risk factor for childhood cancers. Many tobacco related compounds are detected in fetal tissues, breast milk and tissues of children of smoking parents. However, it is hard to make causal relationship between parental smoking and childhood cancers. One of the reasons is the difficulty to detect tobacco smoke exposure. Questionnaires, commonly used method to detect tobacco smoke exposure, are prone to biases. Cotinine is the main metabolite of nicotine which is the abundant organic compound in tobacco and a good biomarker to detect tobacco smoke exposure. Methods: 104 newly diagnosed, 0-18 years aged pediatric cancer patients from two pediatric oncology centers ( Ankara University Children’s Hospital and Ankara City Hospital) and 99 healthy children aged 0-18 applied to the Ankara University Children’s Hospital participated our study. Parental smoking behaviours (preconceptional, during pregnancy and current smoking) and environmental tobacco smoke exposures (ETS) of children were compared between two groups. ETS exposures of cancer patients and healthy children were evaluated by hair cotinine ELISA analysis and questionnaire. For hair cotinine analysis, 30 mg of hair samples were taken from occipital part of scalp by a stainless scissors. Samples were processed according to manufacturer's instructions. Parents of two groups were surveyed about their smoking behaviours and ETS exposures of their children. Results: We found no differences between two groups by means of maternal preconceptional smoking, smoking during pregnancy and current smoking behaviours. Paternal preconceptional smoking and smoking during pregnancy rates were significantly low in cancer patients (p < 0,05) according to questionnaire. Environmental tobacco smoke exposures were found statistically low in cancer patients according to questionnaire (p < 0,05). However, quantitative exposure assessment by hair cotinine analysis revealed that cancer patients are exposed to tobacco smoke more than healthy children (p < 0,001). Conclusions: Our findings support that smoking could be a risk factor for childhood cancers. This study also revealed that questionnaires could cause biases. We thought, social desirability bias of father of cancer patients could be a reason of their low smoking rates according to questionnaire. We suggest that cotinine analysis along with validated questionnaires can be used to prevent biases in studies of tobacco smoke in the etiology of childhood cancers.


CHEST Journal ◽  
2019 ◽  
Vol 155 (1) ◽  
pp. 94-102 ◽  
Author(s):  
Xin Dai ◽  
Shyamali C. Dharmage ◽  
Gayan Bowatte ◽  
Nilakshi T. Waidyatillake ◽  
Jennifer L. Perret ◽  
...  

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