Maternal Tobacco Exposure Research Articles

Home environment and indoor air pollution exposure in an African birth cohort study

BackgroundHousehold indoor air pollution (IAP) is a global health problem and a risk factor for childhood respiratory disease; the leading cause of mortality in African children. This study aimed to describe the home environment and measure IAP in the Drakenstein Child Health Study (DCHS), an African birth cohort. MethodsAn antenatal home visit to assess the home environment and measure IAP (particulate matter, sulphur dioxide, nitrogen dioxide, carbon monoxide and volatile organic compounds (VOCs)) was done on pregnant women enrolled to the DCHS, in a low-socioeconomic, peri-urban South African community. Urine cotinine measured maternal tobacco smoking and exposure. Dwellings were categorised according to 6 household dimensions. Univariate and multivariate analysis explored associations between home environment, seasons and IAP levels measured. Results633 home visits were completed, with IAP measured in 90% of homes. Almost a third of participants were of the lowest socio-economic status and the majority of homes (65%) lacked 2 or more of the dwelling category dimensions. Most households had electricity (92%), however, fossil fuels were still used for cooking (19%) and heating (15%) in homes. Antenatal maternal smoking prevalence was 31%; 44% had passive smoke exposure. Of IAP measured, benzene (VOC) was significantly above ambient standards with median 5.6μg/m3 (IQR 2.6–17.1). There were significant associations between the use of fossil fuels for cooking and increased benzene [OR 3.4 (95% CI 2.1–5.4)], carbon monoxide [OR 2.9 (95% CI 1.7–5.0)] and nitrogen dioxide [OR 18.6 (95% CI 3.9–88.9)] levels. A significant seasonal association was found with higher IAP levels in winter. ConclusionIn this low-socioeconomic African community, multiple environmental factors and pollutants, with the potential to affect child health, were identified. Measurement of IAP in a resource-limited setting is feasible. Recognising and quantifying these risk factors is important in effecting public health policy changes.

Maternal passive smoking during pregnancy and age of menarche in daughters: a study of elementary and middle school students in Shanghai.

The objective of this study was to estimate the prevalence and determinants of passive smoking in pregnancy and to examine its association with an earlier age of menarche in offspring. This retrospective study enrolled 751 students 8 to 20 years old in Shanghai selected by stratified cluster sampling. Data were obtained through structured self-administered questionnaires and physical examinations. It was found that daughters with maternal tobacco exposure experienced relatively earlier menarche and had shorter cycle lengths, although both findings were not statistically significant. The unadjusted odds ratio for prenatal tobacco smoke exposure on the relatively earlier onset of menarche was 1.84 (95% confidence interval = 1.05-3.22) compared with no exposure, and the associations remained statistically significant after adjusting for birth weight, birth length, maternal age of menarche, and present height and weight. In conclusion, our study provides limited evidence supporting the hypothesis that maternal passive smoking during pregnancy leads to an earlier age of menarche of daughters.

Risk factors for juvenile dermatomyositis: exposure to tobacco and air pollutants during pregnancy.

To evaluate the influence of exposure to inhaled environmental factors during pregnancy on the diagnosis of juvenile dermatomyositis (DM). We performed a case–control study comprising 20 juvenile DM patients and 56 healthy controls matched by age and sex who were residents in the metropolitan region of a large city. A questionnaire assessed demographic data and environmental inhalation exposure during pregnancy (occupational exposure to demolition, chalk, construction and/or quarry dust, paints, varnish, gasoline vapor, and/or battery fluids; stationary sources of inhaled pollution near the mother's home; and maternal tobacco exposure). Daily concentrations of inhaled particulate matter, SO2, NO2, O3, and carbon monoxide (CO) were evaluated throughout the gestational period. Maternal occupational exposure to school chalk dust/gasoline vapor in the juvenile DM group was significantly higher compared with controls (50% versus 4.6%; P = 0.001). Smoking mothers and secondhand smoke exposure at home during pregnancy were significantly higher in the juvenile DM group versus controls (smoking mothers: 20% versus 1.7%; P = 0.01, and secondhand smoke: 35% versus 19%; P = 0.07). In univariate logistic regression models, maternal smoking, occupational exposure to inhaled agents, and the highest tertile of tropospheric CO (3.2–5.4 parts per million) in the third trimester were significantly associated with juvenile DM (P ≤ 0.05). In the multivariate analysis, smoking mother (odds ratio [OR] 13.26 [95% confidence interval (95% CI) 1.21–144.29], P = 0.03), occupational exposure (OR 35.39 [95% CI 1.97–632.80], P = 0.01), and CO (third tertile) exposure in the third trimester of gestation (OR 12.21 [95% CI 1.28–115.96], P = 0.03) remained risk factors for juvenile DM. Inhaled pollutants and tobacco smoking during fetal development may contribute to juvenile DM.

Lead, mercury, and cadmium exposure and attention deficit hyperactivity disorder in children

BackgroundThere is limited research examining the relationship between lead (Pb) exposure and medically diagnosed attention deficit hyperactivity disorder (ADHD) in children. The role of mercury (Hg) and cadmium (Cd) exposures in ADHD development is even less clear. ObjectivesTo examine the relationship between Pb, Hg, and Cd and ADHD in children living inside and outside a Lead Investigation Area (LIA) of a former lead refinery in Omaha, NE. MethodsWe carried out a case-control study with 71 currently medically diagnosed ADHD cases and 58 controls from a psychiatric clinic and a pediatric clinic inside and outside of the LIA. The participants were matched on age group (5–8, 9–12 years), sex, race (African American or Caucasians and others), and location (inside or outside LIA). We measured whole blood Pb, total Hg, and Cd using inductively coupled plasma mass spectrometry. ResultsInside the LIA, the 27 cases had blood Pb geometric mean (GM) 1.89µg/dL and the 41 controls had 1.51µg/dL. Outside the LIA, the 44 cases had blood Pb GM 1.02µg/dL while the 17 controls had 0.97µg/dL. After adjustment for matching variables and maternal smoking, socioeconomic status, and environmental tobacco exposure, each natural log unit blood Pb had an odds ratio of 2.52 with 95% confidence interval of 1.07–5.92. Stratification by the LIA indicated similar point estimate but wider CIs. No associations were observed for Hg or Cd. ConclusionsPostnatal Pb exposure may be associated with higher risk of clinical ADHD, but not the postnatal exposure to Hg or Cd.

Perinatal programming of obesity: an introduction to the topic

Perinatal programming of obesity: an introduction to the topic

Second trimester amniotic fluid adiponectin level is affected by maternal tobacco exposure, insulin, and PAPP-A level

Adiponectin is an adipocyte-derived plasma protein with insulin-sensitizing and antiatherosclerotic properties. The objectives of the present study were to determine the amniotic fluid (AF) concentration of adiponectin during the second trimester of pregnancy and to demonstrate its association with maternal and fetal variables and AF concentrations of insulin, leptin, and pregnancy-associated-plasma-protein A (PAPP-A). We performed a cross-sectional study of 222 pregnant women who underwent amniocentesis at 15-18 weeks for genetic reasons. No malformation or chromosomal disorder was found in the newborn after birth. AF adiponectin, leptin, PAPP-A, and insulin concentrations were measured using commercially available assays. All maternal, fetal, and biochemical variables were studied using univariate and multivariate linear regression analysis to determine their association with the AF concentration of adiponectin. Adiponectin concentration was negatively correlated with maternal smoking status (β=-5.208; p<0.001) and positively correlated with levels of insulin (β=0.621; p=0.002) and PAPP-A (β=40.150; p<0.001). Non-significant correlations were found between adiponectin concentration and maternal age, maternal body mass index, gestational age at amniocentesis, fetal gender, and AF level of leptin. These findings suggest that the fetus and its membrane adipocytokines, in relationship with maternal and other fetal variables, play a dynamic role in the regulation of energy and oxidative stress homeostasis due to its insulin-sensitizing and antiatherosclerotic effects. The association of these molecules with maternal tobacco consumption during pregnancy could have perinatal implications.

Obesity and Endocrine Dysfunction Programmed by Maternal Smoking in Pregnancy and Lactation

Obesity is a global epidemic, and maternal smoking has been shown to be associated with the development of childhood obesity. Overall, approximately 40% of children worldwide are exposed to tobacco smoke at home. It is well known that environmental changes within a critical window of development, such as gestation or lactation, can initiate permanent alterations in metabolism that lead to diseases in adulthood, a phenomenon called programming. It is known that programming is based on epigenetic alterations (changes in DNA methylation, histone acetylation, or small interfering RNA expression) that change the expression pattern of several genes. However, little is known concerning the mechanisms by which smoke exposure in neonatal life programs the adipose tissue and endocrine function. Here, we review several epidemiological and experimental studies that confirm the association between maternal nicotine or tobacco exposure during gestation or lactation and the development of obesity and endocrine dysfunction. For example, a positive correlation was demonstrated in rodents between increased serum leptin in the neonatal period and exposure of the mothers to nicotine during lactation, and the further development of leptin and insulin resistance, and thyroid and adrenal dysfunction, in adulthood in the same offspring. Thus, a smoke-free environment during the lactation period is essential to improving health outcomes in adulthood and reducing the risk for future diseases. An understanding of the pathophysiological mechanisms underlying the effects of smoking on programming can provide new insights into therapeutic strategies for obesity.

Maternal smokeless tobacco use in Alaska Native women and singleton infant birth size

To examine the effects of maternal prenatal smokeless tobacco use on infant birth size. A retrospective medical record review of 502 randomly selected deliveries. Singleton deliveries to Alaska Native women residing in a defined geographical region in western Alaska, 1997-2005. A regional medical center's electronic records were used to identify singleton deliveries. Data on maternal tobacco exposure and pregnancy outcomes were abstracted from medical records. Logistic models were used to estimate adjusted mean birthweight, length and head circumference for deliveries to women who used no tobacco (n=121), used smokeless tobacco (n=237) or smoked cigarettes (n=59). Differences in mean birthweight, length and head circumference, 95% confidence intervals and p-values were calculated using non-users as the reference group. Infant birthweight, crown-heel length and head circumference. After adjustment for gestational age and other potential confounders, the mean birthweight of infants of smokeless tobacco users was reduced by 78 g compared with that of infants of non-users (p=0.18) and by 331 g in infants of smokers (p<0.01). No association was found between maternal smokeless tobacco use and infant length or infant head circumference. We found a modest but non-significant reduction in the birthweight of infants of smokeless tobacco users compared with infants of tobacco non-users. Because smokeless tobacco contains many toxic compounds that could affect other pregnancy outcomes, results of this study should not be construed to mean that smokeless tobacco use is safe during pregnancy.

Comparison of Biomarkers and Parent Report of Tobacco Exposure to Predict Wheeze

To identify the optimal measure of active and passive prenatal tobacco exposure to predict wheeze in early life. We conducted a birth cohort study of 398 mother-infant dyads enrolled during the second trimester of pregnancy and followed through age 2 years. We measured tobacco exposure with maternal report, serum cotinine level, and meconium cotinine level. We assessed wheeze with parent report every 6 months. We used a repeated measures logistic regression model. Of 367 children with respiratory data, 26% percent had parent reported active or passive prenatal maternal tobacco exposure, but cotinine was detected in 61% of mothers during pregnancy. Compared with children of mothers in the fifth percentile of tobacco exposure, children of mothers in the 95th percentile had increased odds of wheeze when exposure was measured with maternal serum cotinine level (adjusted OR, 2.6; 95% CI, 1.3-5.2; P < .006) versus meconium cotinine level (adjusted OR, 2.0; 95% CI, 1.0-4.0; P = .04) and total parent-reported exposure (adjusted OR, 1.7; 95% CI, 1.1-2.7; P = .01). Serum cotinine, a biomarker of tobacco exposure, was more strongly associated with wheeze than parent-reported exposure. Studies that rely on parent report of prenatal tobacco exposure may underestimate risk of wheeze.

Hair Biomarkers as Measures of Maternal Tobacco Smoke Exposure and Predictors of Fetal Growth

Most biomarker studies of the effects of maternal smoking on fetal growth have been based on a single blood or urinary cotinine value, which is inadequate in capturing maternal tobacco exposure over the entire pregnancy. We used hair biomarkers to compare the associations of maternal self-reported smoking, hair nicotine, and hair cotinine with birth weight for gestational age (BW for GA) among active and passive smokers during pregnancy. We collected maternal hair in the immediate postpartum period and measured nicotine and cotinine concentrations averaged over the pregnancy in 444 term controls drawn from 5,337 participants in a multicenter nested case-control study of preterm birth. BW for GA Z-score and small for gestational age (SGA) were based on Canadian population-based standards. The addition of hair nicotine to multiple linear regression models containing self-reported active smoking, hair cotinine, or both explained significantly more variance in the BW for GA Z-score (p = .01, .03 and .04, respectively). Similarly, women with hair nicotine, but not cotinine, at or above the median value had a significant increase in the risk of SGA birth (odds ratio: 3.07, 95% CI: 1.25-7.52). No significant association was observed between maternal passive smoking and BW for GA based on hair biomarkers. Hair nicotine is a better predictor of reductions in BW for GA than either hair cotinine or self-report. Our negative results for passive smoking suggest that previously reported small but significant effects may be explained by misclassification of active smokers as passive smokers based on self-report.

Tobacco and pregnancy

This paper will review the epidemiology of the impact of cigarette smoking and other forms of tobacco exposure on human development. Sources of exposure described include cigarettes and other forms of smoked tobacco, secondhand (environmental) tobacco smoke, several forms of smokeless tobacco, and nicotine from nicotine replacement therapy. Exposure is immense and worldwide, most of it due to smoking, but in some parts of the world and in some populations, smoking is exceeded by smokeless tobacco use. Nicotine and carbon monoxide exposure are of large concern, but cigarette smoke contains over 4000 chemical constituents and additives including known carcinogens, toxic heavy metals, and many chemicals untested for developmental toxicity. The impact of tobacco on human development will be reviewed. Fertility, conception, survival of the conceptus, most phases and aspects of development studied to date, as well as postnatal survival and health are adversely impacted by maternal tobacco use or exposure. Effects in surviving offspring are probably life-long, and are still being elucidated. It is hoped that this review will serve to keep a focus on the critical and continuing problem of tobacco use impacting human development.

Genetic variability of HVRII mtDNA in cord blood and respiratory morbidity in children

Genetic polymorphisms were examined using direct sequencing of the hypervariable region II (HVRII) in the D-loop of mtDNA in the cord blood of 355 children living in two areas of the Czech Republic – the industrial district of Teplice and the agricultural district of Prachatice. The incidence of the most frequent nucleotide variants of HVRII, C150T (10.1%), T152C (19.7%), T195C (19.7%) and 309.nC (41.4% for 309.2C and 13.8% for 309.3C), and the respiratory morbidity at the ages of 0–2 years and 2–6 years were investigated, considering many other factors such as locality, gender, ethnicity, heating by coal in household, maternal age, asthma bronchiale, allergic rhinitis, pollinosis, conjunctivitis and maternal tobacco exposure during and after pregnancy. We found that the T195C transversion in HVRII is connected with an increased risk of early childhood (0–2 years) bronchitis (RR 1.38, p = 0.034, 95% CI 1.04–1.85) and with increased risk of otitis media in children aged 2–6 years (RR 1.62, p = 0.032, 95% CI 1.04–2.53). Another polymorphism, 309.nC, is associated with an increased risk of bronchitis in children aged 2–6 years (RR 1.46, p = 0.030, 95% CI 1.04–2.06). The results indicate that genetic polymorphisms in mtDNA may be an important factor not only for various types of cancers and neurodegenerative diseases, but also for respiratory morbidity in children.

Tobacco and pregnancy: Overview of exposures and effects

This opening article will review the epidemiology of the effects of cigarette smoking and other forms of tobacco exposure on human development. Sources of exposure described include cigarettes and other forms of smoked tobacco, secondhand (environmental) tobacco smoke, several forms of smokeless tobacco, and nicotine from nicotine replacement therapy. Exposure is immense and worldwide, most of it due to smoking, but in some parts of the world and in some populations, smoking is exceeded by smokeless tobacco use. Nicotine and carbon monoxide exposure are of large concern, but cigarette smoke contains over 4000 chemical constituents and additives including known carcinogens, toxic heavy metals, and many chemicals untested for developmental toxicity. The impact of tobacco on human development will be reviewed. Fertility, conception, survival of the conceptus, most phases and aspects of development studied to date, as well as postnatal survival and health are adversely impacted by maternal tobacco use or exposure. Effects in surviving offspring are probably life-long, and are still being elucidated. It is hoped that this review and those to follow in this issue will serve to keep a focus on the critical and continuing problem of tobacco use impacting human development.

Maternal active or passive smoking causes oxidative stress in cord blood

The aim of this study was to assess the influence of active and passive maternal smoking on cord blood total oxidant/antioxidant status at term. The levels of cord blood catalase (CAT), paraoxonase 1 (PON1), ceruloplasmin, total thiol and lipid hydroperoxide (LOOH), total antioxidant capacity (TAC), total oxidant status (TOS) and the oxidative stress index (OSI) were measured in samples of fetal cord blood serum from 29 nonsmokers who were not exposed to active or passive smoke, 30 passive smokers and 21 active smokers. The gestation period of all pregnancies was between 37 and 40 weeks, the pregnancies were uncomplicated and the infants were delivered vaginally. The weights of infants borne to the active smokers were significantly (P < 0.01) lower than those borne to the controls. Significantly lower concentrations of CAT, PON1 and TAC were found in the cord blood of the smokers than in that of the nonsmokers (P < 0.018). The cord blood levels of LOOH and TOS and OSI were significantly higher in the active and passive smokers than in the controls (P < 0.01). A significant positive correlation was found between maternal tobacco exposure and cord blood OSI (P < 0.001). Active or passive maternal smoking is associated with important alterations in the balance of oxidants and antioxidants in fetal cord blood and causes potent oxidative stress.

Perinatal Outcomes among Infants 24-32 Weeks Gestation Delivered between 1/1998 and 12/2003 ± Antenatal Maternal Tobacco Exposure

Perinatal Outcomes among Infants 24-32 Weeks Gestation Delivered between 1/1998 and 12/2003 ± Antenatal Maternal Tobacco Exposure

Assessing nicotine metabolism in pregnancy—a novel approach using hair analysis

Nicotine and its metabolite cotinine are important biochemical markers to determine active or passive exposure to cigarette smoke. The amount of nicotine and cotinine in hair provides a cumulative index of tobacco exposure. This study uses segmental hair analysis to assess changes in nicotine metabolism in a cohort of pregnant women who smoked steadily during the whole gestational period according to their self-report. Maternal hair was collected at the time of delivery and sectioned into segments representing the three trimesters of pregnancy. The concentrations of nicotine and cotinine in each section of hair were measured by radioimmunoassay. Hair concentration of nicotine decreased during pregnancy without any reported reduction in smoking, while the cotinine concentration remained constant. The nicotine–cotinine ratio in these consistent smokers was: 1st trimester 20.6, 2nd trimester 19.9, and 3rd trimester 13.3. These findings are consistent with results from other studies showing increased nicotine metabolism during pregnancy. Our data suggest that the results of segmental hair analysis should be carefully examined in pregnancy. Both nicotine and cotinine levels should be evaluated in order to confirm any significant change in maternal tobacco exposure during pregnancy.

Measures of maternal tobacco exposure and infant birth weight at term.

This study was undertaken to determine the relation between self-reported number of cigarettes smoked per day and urine cotinine concentration during pregnancy and to examine the relations between these two measures of tobacco exposure and birth weight. Data were obtained from the Smoking Cessation in Pregnancy project, conducted between 1987 and 1991. Cigarette smoking information and urine cotinine concentration were collected for 3,395 self-reported smokers who were receiving prenatal care at public clinics in three US states (Colorado, Maryland, and Missouri) and who delivered term infants. General linear models were used to quantify urine cotinine variability explained by the number of cigarettes smoked per day and to generate mean adjusted birth weights for women with different levels of tobacco exposure. Self-reported number of cigarettes smoked per day explained only 13.9% of the variability in urine cotinine concentration. Birth weight declined as tobacco exposure increased; however, the relation was not linear. The sharpest declines in birth weight occurred at low levels of exposure. Furthermore, urine cotinine concentration did not explain more variability in birth weight than did number of cigarettes smoked. These findings should be considered by researchers studying the effects of smoking reduction on birth outcomes.

Effects of maternal and early tobacco exposure on the development of asthma and airway hyperreactivity.

In 1999 a comprehensive review was published in Thorax that evaluated the role of exposure to tobacco smoke products (TSPs) in respiratory disease. The present review addresses papers published within the past 12 months on the effects of TSPs on childhood asthma and atopic disease, along with a few reports on possible mechanisms by which TSPs exert their adverse effects. Most of the observational studies published during the past year support the conclusion that both in-utero and, to some degree, passive (environmental) tobacco smoke (ETS) exposure adversely affect pulmonary function, and predispose to asthma symptoms and possibly bronchial hyperresponsiveness in childhood, but play little or no role in atopy development. However, in TSP-induced pulmonary disease, a mechanism of upregulation of pulmonary neuroendocrine cells has been hypothesized. An interventional study clearly demonstrated a need for a total (instead of partial) ban on indoor smoking in the homes of children with asthma in order to achieve significant reductions in levels of urinary cotinine. Because there is a large body of evidence for adverse effects of in-utero TSP as well as ETS exposure on respiratory health in children, we are in dire need of studies to elucidate when TSP exposure causes most damage, the mechanisms that underlie this damage, and how we can prevent unnecessary harm to the respiratory system in the vulnerable child.

Effects of maternal and early tobacco exposure on the development of asthma and airway hyperreactivity

Effects of maternal and early tobacco exposure on the development of asthma and airway hyperreactivity

Maternal Tobacco Exposure and Cotinine Levels in Fetal Fluids in the First Half of Pregnancy

Maternal Tobacco Exposure and Cotinine Levels in Fetal Fluids in the First Half of Pregnancy