Children Of Nonsmoking Mothers Research Articles

Programmed Obesity?: Study Links Intrauterine Exposures to Higher BMI in Toddlers

Vol. 117, No. 1 EnvironewsOpen AccessProgrammed Obesity?: Study Links Intrauterine Exposures to Higher BMI in Toddlers M. Nathaniel Mead M. Nathaniel Mead Search for more papers by this author Published:1 January 2009https://doi.org/10.1289/ehp.117-a33bAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InReddit To date, there have been relatively few epidemiologic studies investigating the association between intrauterine exposure to chemicals and body mass index (BMI, which characterizes weight in relation to height). Now a prospective birth cohort study in Flanders, Belgium, reveals an association between prenatal exposure to environmental pollutants and elevated BMI during the first three years of life [EHP 117:122–126; Verhulst et al.]. The study also found associations between exposures and birth weight and length.Since the late 1990s, developmental biologists have amassed laboratory data indicating that exposure to endocrine disruptors such as polychlorinated biphenyls (PCBs), dioxins, and bisphenol A during critical phases of fetal development may increase the risk of obesity later in life. In addition, prenatal exposure to cigarette smoke has been linked with the subsequent development of obesity. These exposures likely alter mechanisms involved in weight homeostasis.Using a longitudinal study design, the researchers obtained a random sample of 138 mother–infant pairs by drawing from 26 maternity wards in Flanders between September 2002 and February 2004. These wards were identified within geographic areas with varying environment and pollution characteristics (rural, urban, and industrial). The researchers collected information on the parents that included health status, smoking behavior, age, family composition, socioeconomic status, height, and weight. Children’s height and weight were also analyzed, and umbilical cord blood was collected to enable measurement of levels of hexachlorobenzene, dioxin-like compounds, PCBs, and the pesticide metabolite DDE. Children were then observed over a 3-year period.The main findings were twofold. First, higher PCB congener levels were associated with higher BMI standard deviation scores (SDS) in the children between 1 and 3 years of age. Both maternal smoking and higher PCB levels were positively associated with birth weight SDS. In addition, they showed a statistically significant combined effect. Second, higher DDE levels were associated with a slight increase in BMI SDS in 3-year-old children of nonsmoking mothers, but this effect was further increased in children of smoking mothers. Thus, simultaneous intrauterine exposure to endocrine disruptors might compound the weight-enhancing effects of maternal smoking during pregnancy.The researchers acknowledge a number of study limitations, including the fact that maternal weight gain during pregnancy—an important risk factor for obesity in children—was not recorded in the study. Additionally, the children were only followed for 3 years. Although it remains to be seen whether BMI trends for this particular study population will persist later in life, a higher BMI during toddlerhood is known to be associated with an increased risk of obesity in adulthood.This is the first epidemiologic study to demonstrate the impact of prenatal pollution exposure on BMI during the preschool years, and more large-scale prospective studies are certainly warranted. One research challenge will be to determine which factors mediate the effects of prenatal exposure to endocrine disruptors in terms of subsequent weight dysregulation in the offspring.Certain exposures in utero can affect birth weight, birth length, and later, body mass index.FiguresReferencesRelatedDetails Vol. 117, No. 1 January 2009Metrics About Article Metrics Publication History Originally published1 January 2009Published in print1 January 2009 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact [email protected]. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Intrauterine exposure to environmental pollutants and body mass index during the first 3 years of life.

ObjectiveWe investigated the association between body mass index (BMI) standard deviation score (SDS) and prenatal exposure to hexachlorobenzene, dichlorodiphenyldichloroethylene (DDE), dioxin-like compounds, and polychlorinated biphenyls (PCBs).MethodsIn this prospective birth cohort study, we assessed a random sample of mother–infant pairs (n = 138) living in Flanders, Belgium, with follow-up until the children were 3 years of age. We measured body mass index as standard deviation scores (BMI SDS) of children 1–3 years of age as well as pollutants measured in cord blood.ResultsDDE correlated with BMI SDS, with effect modification by maternal smoking and the child’s age. At 1 year, children of smoking mothers had higher BMI SDS than did children of nonsmoking mothers. At 3 years, this difference was reduced because of the faster rate of decline in BMI SDS in the former group. This relationship held except for children with high levels of DDE. DDE had a small effect on BMI SDS at 3 years of age in children of nonsmoking mothers (difference in BMI SDS for DDE concentrations between the 90th and 10th percentiles = 0.13). On the other hand, smoking enhanced the relation between DDE and BMI SDS at 3 years (difference in BMI SDS for DDE concentrations between the 90th and 10th percentiles = 0.76). Increasing concentrations of PCBs were associated with higher BMI SDS values at all ages (parameter estimate = 0.003 ± 0.001; p = 0.03).ConclusionIn this study we demonstrated that intrauterine exposure to DDE and PCBs is associated with BMI during early childhood. Future studies are warranted to confirm our findings and to assess possible mechanisms by which these pollutants could alter energy metabolism.

Neurology: Secondhand Behavioral Problems

Children whose mothers regularly smoked during pregnancy are known to be more likely to exhibit disruptive and aggressive behavior than children of nonsmoking mothers. A new study now finds that children born even to nonsmoking mothers who were exposed to chronic secondhand smoke (SHS) while pregnant face serious problems of attention deficit/hyperactivity disorder (ADHD) and conduct disorder, which includes fighting, truancy, substance abuse, and stealing. At the University of Washington, psychologists Lisa Gatzke-Kopp and Theodore Beauchaine recruited 171 children aged 7–15 years who had emotional and behavioral problems. Their mothers consisted of 21 women who smoked regularly during the second and/or third trimester, 16 nonsmokers who were exposed during the second and/or third trimester to SHS at work or home, and 96 women who neither smoked nor were exposed to SHS (some of the mothers had more than one child in the study). More symptoms of ADHD and conduct disorder were measured in children of smoking or SHS-exposed mothers, compared with children of smoke-free mothers. In fact, severe symptom scores were about the same for children whether they were exposed in utero to maternal smoking or to SHS. Childhood emotional disorders such as depression and anxiety were not significantly associated with maternal smoking or SHS exposure during pregnancy. ADHD and conduct disorder are “externalizing” behaviors, as opposed to “internalizing” outcomes such as depression and anxiety. Animal models show that nicotine impairs brain development during the second and third trimesters, the formative periods for brain regions that control externalizing behaviors, such as the mesolimbic dopamine system. The study, published online 23 May 2007 ahead of print in Child Psychiatry and Human Development, is the first to link SHS exposure in pregnancy to serious disruptive behavior during childhood. However, the level of SHS exposure studied was “chronic and extreme and all day long,” points out Gatzke-Kopp, now at Pennsylvania State University; therefore “pregnant women should not panic about minor exposures to secondhand smoke.” Still, the researchers hope their results will raise awareness about the potential health consequences of SHS to pregnant women in public places and work environments that still permit smoking (such as restaurants and bars). Lauren Wakschlag, an associate professor of psychology at the University of Illinois Institute for Juvenile Research, says the new study “highlights where we need to go to disentangle the complex relationship of prenatal secondhand smoke exposure and antisocial behavior.” However, with only 16 SHS-exposed participants and 21 smokers, the central emphasis on SHS versus smoking needs to be interpreted cautiously. “These preliminary findings suggest a possibility that secondhand smoke affects behavior,” says Wakschlag, “but we need more systematic exploration of this.”

Early determinants of overweight at 4.5 years in a population-based longitudinal study

The roots of the obesity epidemic need to be traced back as early in life as possible in order to develop effective means for preventing obesity and its health consequences in the future. The aim of this paper is to examine a broad range of factors that may simultaneously contribute to childhood overweight in a population-based cohort of children followed from birth to 4.5 years, to determine which factors exert the most influence in early life. The analyses were performed using data from the Quebec Longitudinal Study of Child Development 1998-2002 (QLSCD). The study follows a representative sample (n=2103) of children born in 1998 in the Canadian province of Quebec. Measured height and weight were available for 1550 children aged 4.5 years. At 4.5 years, BMI was analyzed using the US CDC sex- and age-specific growth charts. In order to study children at their highest weights at various ages, odds ratios were presented for high birth weight, weight-for-stature at or above the 95th percentile at 5 months, and BMI at or above the 95th percentile at 4.5 years. Monthly weight gain between birth and five months has been analyzed. Children were also evaluated by the Z-score obtained from the standardized weight divided by height. Factors potentially related to children's weight include sex, gestational age and birth rank, breastfeeding, mothers' smoking status during pregnancy, family type at child's birth, and family income before pregnancy and when the children were 5 months and 4.5 years old. Other parental factors such as height and overweight/obesity (based on BMI) and other maternal factors (age, education, immigrant status) were also part of the analysis. Being in the highest quintiles of weight gain between birth and 5 months, as well as maternal smoking during pregnancy, almost double the odds of being overweight at 4.5 years. Parental overweight or obesity also increased the odds of being overweight at this age, as well as being raised in middle-income or in poor families. A greater proportion of children born to nonsmoking mothers with higher weights (more than 4000 g) were overweight at 4.5 years, the percentage being greatest for those in the highest weight-gain categories from birth to 5 months. The pattern was different for children born to smoking mothers. The greatest proportion of 4.5-year-old overweight children was seen for children born in the normal weight-range category (3000-4000 g) who were in the highest quintiles of weight gain from birth to 5 months, and for children with high birth weights (more than 4000 g) who were in the lowest quintiles of birth-to-5-months weight gain. Children who were overweight at 4.5 years and who had been born to smoking mothers started life with a birth weight around that for the population means, but they gained more weight in the first 5 months of life than did the children of nonsmoking mothers. This study indicates that behavioral and social factors exert critical influences on the onset of childhood overweight in preschool years. From a population-health perspective, interventions aimed at preventing childhood obesity would do well to target smoking pregnant women, as well as nonsmoking pregnant women at risk for giving birth to high-birth-weight children, paying particular attention to rapid weight gain in the first months of life.

Maternal smoking during pregnancy in relation to child overweight: follow-up to age 8 years

Data from several studies indicate that children of mothers who smoked during pregnancy may be at a risk of overweight compared with children of non-smoking mothers. The size of this relation, however, is unclear, as is the age at which it becomes detectable. Prospective data for 34 866 children enrolled in the US Collaborative Perinatal Project were analysed to examine maternal pregnancy smoking in relation to weight, height, and body mass index (BMI) in offspring at ages 1, 3, 4, 7, and 8 years. Compared with offspring of non-smokers, children of smokers had (i) weight that was lower at birth but then quickly equalled or exceeded that of non-smokers, (ii) consistently decreased height, and (iii) increased risk of overweight, particularly in girls. For example, at age 7 years, the adjusted odds ratio of BMI>or=85th percentile in boys of mothers who smoked on an average>or=20 cigarettes per day while pregnant was 1.22 (95% confidence interval 1.03-1.46), and in girls it was 1.30 (1.08-1.56). In these data, maternal smoking during pregnancy was associated with a modest increase in risk of overweight in children before the age of 8 years.

Maternal concentration of dichlorodiphenyl dichloroethylene (DDE) and initiation and duration of breast feeding

Dichlorodiphenyl dichloroethylene (DDE) has been shown to reduce the duration of breast feeding in two studies. In addition to duration, we examined whether DDE lowers the initiation of breast feeding. Between 1973 and 1991, the Michigan Department of Community Health conducted three surveys to assess polychlorinated biphenyls (PCBs) and DDE serum concentrations in Michigan anglers. Through telephone interviews with parents, we retrospectively ascertained information on breast feeding. Based on repeated maternal serum measurements between 1973 and 1991, we arrived at the level of exposure at the time of delivery by extrapolating PCB and DDE serum levels. One mother may have contributed more than one child; however, serum concentrations varied between children from the same mother. The maternal DDE and PCB serum concentrations were categorised as follows: 0 to <5 microg/L, 5 to <10 microg/L, >or=10 microg/L. Repeated measurement models and survival analyses were used to determine the relationship between DDE and PCBs and characteristics of breast feeding while controlling for cohort effects, maternal age at delivery, education, and smoking during pregnancy. We focused on 176 pregnancies of 91 mothers who had maternal exposure information and gave birth between 1969 and 1995. Initiation of breast feeding was lowered by 39.5% and duration shortened by 66.4% in children of mothers who smoked during pregnancy. In children of non-smoking mothers, the incidence ratio for breast-feeding initiation was 0.45 [95% CI 0.15, 0.94] and 0.42 [95% CI 0.10, 1.03] when maternal DDE concentrations were 5 to <10 microg/L and >or=10 microg/L respectively, compared with the lowest DDE exposure group. In these offspring (of non-smoking mothers), breast-feeding duration was shorter when DDE concentrations were higher: 13 weeks for >or=10 microg/L DDE, compared with 21.7 weeks for lower DDE. We did not detect any association between PCBs and breast feeding. In the absence of the distorting effects of maternal smoking, DDE exposure may decrease initiation and duration of breast feeding.

Household Smoking and Bronchial Hyperresponsiveness in Children with Asthma

This study investigated whether household environmental tobacco smoke (ETS) exposure is associated with increased bronchial hyperresponsiveness (BHR) in children with asthma. Two hundred forty-nine children, ages 7–11 years, sampled from a larger group with reported asthma or multiple asthma symptoms identified in a community survey in Cape Town, underwent histamine challenge testing and had urinary cotinine measured. Parents were interviewed for information on smoking habits and a variety of covariates. Children with asthma whose mothers smoked had a lower frequency of BHR than asthmatic children of nonsmoking mothers, particularly if the mother smoked ≥15 cigarettes daily. BHR was also less common among children sharing a house with four or more smokers vs. fewer or none. BHR was unrelated to paternal smoking. In contrast, FEV1 was lower among children whose mothers currently smoked. The findings do not support a mechanism whereby ETS exposure aggravates existing childhood asthma by increasing BHR. This association may be masked, however, by the degree to which mothers of asthmatic children adjust their smoking. The results are consistent with an adverse effect of maternal smoking on lung function in asthmatic children.

Biomarkers of environmental tobacco smoke in preschool children and their mothers.

Adverse health effects attributable to environmental tobacco smoke (ETS) include respiratory illness and lung cancer in nonsmokers. There is accumulating evidence that children may be at heightened risk of cancer later in life as a result of exposure to carcinogens during their early development. It is of concern that as many as 9 million American children under the age of 5 years may be exposed to ETS. Our goal was to assess whether levels of cotinine and polycyclic aromatic hydrocarbon-albumin (PAH-albumin) are associated with ETS exposure in children and in women of reproductive age, after accounting for background exposures to PAHs in the diet, workplace, and the home environment. The study cohort was composed of 87 Hispanic and African-American mothers and 87 of their preschool children (2-5 years of age). Plasma cotinine was analyzed by gas chromatography; PAH-albumin adducts in peripheral blood were analyzed by enzyme-linked immunosorbent assay. Exposure data were obtained by interview-administered questionnaires. Both cotinine and PAH-albumin were significantly higher in the children whose mothers smoked than in the children of nonsmoking mothers (P < .001 and P < .05, respectively). Among the children of nonsmoking mothers, cotinine levels were also significantly higher in those who had ETS exposure from others in the household compared with the unexposed children. By regression analysis, after adjustment for ethnicity, there was a significant dose-response relationship between cotinine and the number of cigarettes smoked per day by the mother, both in the children (partial r2 = .23; P = .01) and in the mothers (partial r2 = .22; P = .01). Among the nonsmoking mothers, regression of biomarkers against total passive smoking exposure also showed a significant association with cotinine (r2 = .25; P = .04). PAH-albumin did not show the same dose-related response with the smoking variables. Mothers' cotinine levels were significantly correlated with those of their children (r = .76; P < .001) as were PAH-albumin adducts (r = .27; P = .014). ETS exposure of young children via their mothers' smoking is associated with increases not only in the internal dose of ETS (cotinine), which has been previously reported, but also in the biologically effective dose of the carcinogenic (PAH) components of ETS (PAH-albumin adducts). This observation underscores the carcinogenic and public health hazard of ETS. Given the relatively low level of ETS exposure in this study, these results reinforce the need for effective programs aimed at smoking prevention and cessation among women, particularly women of reproductive age and minorities.

Parental smoking and post-infancy wheezing in children: a prospective cohort study.

The contribution of parental smoking to wheezing in children was studied in a subset of all British births between April 5 and 11, 1970 (N = 9,670). Children of smoking mothers had an 18.0 per cent cumulative incidence of post-infancy wheezing through 10 years of age, compared with 16.2 per cent among children of nonsmoking mothers (risk ratio 1.11, 95% CI: 1.02, 1.21). This difference was confined to wheezing attributed to wheezy bronchitis, of which children of smokers had 7.4 per cent, and those of nonsmokers had 5.2 per cent (risk ratio 1.44, 95% CI: 1.24, 1.68). The incidence of wheezy bronchitis increased as mothers smoked more cigarettes. After multiple logistic regression analysis was used to control for paternal smoking, social status, sex, family allergy, crowding, breast-feeding, gas cooking and heating, and bedroom dampness, the association of maternal smoking with childhood wheezy bronchitis persisted. Some of this effect was explained by maternal respiratory symptoms and maternal depression, but not by neonatal problems, the child's allergic symptoms, or paternal respiratory symptoms. There was a 14 per cent increase in childhood wheezy bronchitis when mothers smoked over four cigarettes per day, and a 49 per cent increase when mothers smoked over 14 cigarettes daily.

High-Density Lipoprotein-Cholesterol Subfractions in Adolescent Twins

Data on the levels of high-density lipoprotein-cholesterol (HDL-C) and subfractions in 102 adolescent twin pairs and their parents are presented. Children with a family history of premature cardiovascular death had lower levels of HDL2-C than did those without such a history. White girls reporting a high level of physical activity had higher levels of HDL-C and HDL2-C than did their more sedentary peers. In general, children of mothers who smoked had lower HDL2-C than did children of nonsmoking mothers. These findings suggest that low levels of HDL2-C in children may identify families in which there is an increased risk of coronary heart disease and that parental smoking may contribute to changes in this risk factor in the children of smokers as well as in the smokers themselves.

Thyroglobulin in cord blood. The influence of the mode of delivery and the smoking habits of the mother.

The cord thyroglobulin (Tg) concentration was estimated in 160 full-term newborns of whom 103 were delivered normally, 26 by elective Cesarean section and 31 by vacuum extraction. There was no correlation between the median cord Tg concentration and gestational age at delivery (37-43 weeks), birth weight or sex of the child or the median cord TSH concentration. The median cord Tg concentration was significantly higher in the children born by Cesarean section than in those delivered by vacuum extraction (P less than 0.001). The same tendency was found when smokers and non-smokers were compared separately. Mechanical force on the thyroid gland during labour and delivery therefore does not seem to increase the cord Tg concentration. The influence of maternal cigarette smoking on the cord Tg concentration was studied also. Forty-five mothers were smokers. The median cord Tg concentration in the children of these women was significantly higher than in the children of non-smoking mothers (130 micrograms/l vs 100 micrograms/l, P less than 0.001), whereas the median cord TSH concentration did not differ between these groups. It therefore seems possible that components of cigarette smoke, e.g. thiocyanate, may have a direct effect on the thyroid gland of the fetus.

Indoor air pollution and pulmonary function growth in preadolescent children.

Results are reported from a study of the association between exposure to sidestream cigarette smoke or gas stove emissions and pulmonary function level and growth rate of 7,834 children seen at 2-5 annual visits between the ages of 6-10 years. Children whose mothers smoked one pack of cigarettes per day had levels of forced expiratory volume in one second (FEV1) at age eight that were 0.81% lower than children of nonsmoking mothers (p less than 0.0001), and FEV1 growth rates approximately 0.17% per year lower (p = 0.05). For a child of age eight with an FEV1 of 1.62 liters, this corresponds to a deficit in rate of change of FEV1 of approximately 3 ml/annum and a deficit of 13 ml at age eight. Children whose mothers smoked one pack per day had levels of forced vital capacity (FVC) at age eight that were 0.33% higher than children of nonsmokers (p = 0.12); however, their growth rates of FVC were 0.17% per year lower (p = 0.04). Because few mothers changed their smoking habits during the course of the study, it was not possible to determine whether the difference in rate of growth was due to current exposure or to an effect of prenatal and early childhood exposure on the course of development. The magnitude of the effect on FEV1 is consistent with deficits in FEV1 of up to 3% in early adult life due to childhood exposure to sidestream cigarette smoke. The importance of this relatively small effect will be evaluated further through follow-up of these children as they are exposed to other risk factors such as personal active smoking. The data provide some evidence for an association between gas stove exposure and pulmonary function level, especially at younger ages, but no evidence for an effect of gas stove exposure on growth rate.

Fetal cardiovascular system as influenced by maternal smoking

Primary prevention of atherosclerosis should be initiated early in life, preferably in childhood. Nevertheless, it tends to be forgotten that a child has existed for nine months before birth, and that the newborn child might already have been exposed to agents capable of causing vessel damage. Studies of the umbilical artery, umbilical vein, and vessels of the placental villi (2, 3, 4, 5, 6) revealed that, in this portion of the fetal cardiovascular system, severe damage to the vessel wall is associated with maternal tobacco smoking during pregnancy. These alterations within the fetal cardiovascular system were never found in the children of non-smoking mothers. If similar changes occur in the other vessels of the newborn child, which it seems reasonable to expect, they might give rise to sequelae later in life. It should therefore strongly be advocated that pregnant women abandon tobacco smoking.