Dataset Information

Evaluation of the association between maternal smoking, childhood obesity, and metabolic disorders: a national toxicology program workshop review.

ABSTRACT:

Background

An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life.

Objective

Here we assess the association between these health outcomes and exposure to maternal smoking during pregnancy as part of a broader effort to develop a research agenda to better understand the role of environmental chemicals as potential risk factors for obesity and metabolic disorders.

Methods

PubMed was searched up to 8 March 2012 for epidemiological and experimental animal studies related to maternal smoking or nicotine exposure during pregnancy and childhood obesity or metabolic disorders at any age. A total of 101 studies-83 in humans and 18 in animals-were identified as the primary literature.

Discussion

Current epidemiological data support a positive association between maternal smoking and increased risk of obesity or overweight in offspring. The data strongly suggest a causal relation, although the possibility that the association is attributable to unmeasured residual confounding cannot be completely ruled out. This conclusion is supported by findings from laboratory animals exposed to nicotine during development. The existing literature on human exposures does not support an association between maternal smoking during pregnancy and type 1 diabetes in offspring. Too few human studies have assessed outcomes related to type 2 diabetes or metabolic syndrome to reach conclusions based on patterns of findings. There may be a number of mechanistic pathways important for the development of aberrant metabolic outcomes following perinatal exposure to cigarette smoke, which remain largely unexplored.

Conclusions

From a toxicological perspective, the linkages between maternal smoking during pregnancy and childhood overweight/obesity provide proof-of-concept of how early-life exposure to an environmental toxicant can be a risk factor for childhood obesity.

SUBMITTER: Behl M

PROVIDER: S-EPMC3569686 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature

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Publications

Evaluation of the association between maternal smoking, childhood obesity, and metabolic disorders: a national toxicology program workshop review.

Behl Mamta M Rao Deepa D Aagaard Kjersti K Davidson Terry L TL Levin Edward D ED Slotkin Theodore A TA Srinivasan Supriya S Wallinga David D White Morris F MF Walker Vickie R VR Thayer Kristina A KA Holloway Alison C AC

Environmental health perspectives 20121211 2

<h4>Background</h4>An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life.<h4>Objective</h4>Here we assess the association between these health outcomes and exposure to maternal smoking during pregnancy as part of a broader effort to develop a research agenda to better understand the role of environmental chemicals as potential risk factors for obesity and metaboli ...[more]

PMID: 23232494

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Project description:There has been increasing interest in the concept that exposures to environmental chemicals may be contributing factors to the epidemics of diabetes and obesity. On 11-13 January 2011, the National Institute of Environmental Health Sciences (NIEHS) Division of the National Toxicology Program (NTP) organized a workshop to evaluate the current state of the science on these topics of increasing public health concern.The main objective of the workshop was to develop recommendations for a research agenda after completing a critical analysis of the literature for humans and experimental animals exposed to certain environmental chemicals. The environmental exposures considered at the workshop were arsenic, persistent organic pollutants, maternal smoking/nicotine, organotins, phthalates, bisphenol A, and pesticides. High-throughput screening data from Toxicology in the 21st Century (Tox21) were also considered as a way to evaluate potential cellular pathways and generate -hypotheses for testing which and how certain chemicals might perturb biological processes related to diabetes and obesity.Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the "developmental obesogen" hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life. Research on environmental chemical exposures and type 1 diabetes was very limited. This lack of research was considered a critical data gap. In this workshop review, we outline the major themes that emerged from the workshop and discuss activities that NIEHS/NTP is undertaking to address research recommendations. This review also serves as an introduction to an upcoming series of articles that review the literature regarding specific exposures and outcomes in more detail.

Project description:BackgroundTobacco use and obesity are major public health problems and part of the leading causes of preventable disease and death worldwide. The prevalence of overweight children has escalated over the years; making the weight gain in children a critical issue for health professionals and academics alike. This study examines the association between maternal tobacco use and body weight abnormalities among South African children.Data and methodsThe study uses data from the National Income Dynamics Study (NIDS), conducted from 2008 to 2017. The survey is available in five waves which have been merged into a panel dataset of 211,718 children aged between 0 to 5 years old, drawn from a nationally representative sample of households followed across time. Thus, the subgroup of children aged between 6 and 15 years old was excluded from the analysis. The empirical investigation employs a logistic regression model to estimate the marginal effect of maternal smoking on childhood overweight prevalence measured by three anthropometric based proxies, namely risk of child overweight, child overweight and child obesity. This framework assumes unobserved child characteristics to be uncorrelated with independent variables (random effect assumption); hence allowing to control for time-invariant sociodemographic factors which are likely to affect child nutritional health.ResultsIn addition to sociodemographic and health characteristics of mothers, empirical findings suggest that maternal smoking exhibits a significant odds and/ or probability of weight abnormalities in children. Notably, children of smoking mothers are likely to be obese, overweight, or at risk of becoming overweight with a possible coexistence of mother-child overweight. Similarly, weight irregularities in children are likely to increase with mother's age. Conversely, married mothers although associated with increased odds of children having high BMI, display a reduced probability of children being abnormally weighted. Finally, child support grant has the potential to improve children nutritional health as children whose mothers are recipient of such grant have a negative probability of having high BMI.ConclusionOverall, maternal smoking contributes to child overweight and/or obesity in south Africa; suggesting that maternal healthy lifestyle could be an alternative strategic tool to fight against overweight in children. However, mothers' inability to remain and/or follow a healthy life style is plausible as age increases, with spillover effect on child care. Thus, policymakers should prioritize programs to reduce smoking, especially amongst pregnant women and caregivers, to minimise the risk of overweight in children. Promoting the consumption of healthy foods accompanied by physical activity may reduce mothers' stress levels and their incentive to self-medicate using tobacco substances. In addition, comprehensive action programs including child support grant and recommendations for treatment plans that address the problems of children who are already suffering from overweight, remain essential.

Project description:Childhood obesity is associated with chronic low-grade inflammation considered as a precursor to metabolic disease; however, the underlying mechanisms for this remain unclear. Studies in adults have implicated gut derived gram-negative bacterial fragments known as lipopolysaccharide or endotoxin, activating the inflammatory response, whilst the importance in childhood obesity is unclear. The aim of this research is to understand the relationship between circulating endotoxin in childhood obesity, and its' association with inflammatory and cardiovascular (CV) injury biomarkers.Fasted blood was obtained from children with varying degrees of obesity (age: 13.9 ± 2.3Yr; BMI: 35.1 ± 5.2 Kg/m(2); n = 60). Multiplex CVD biomarker immunoassays were used to determine systemic levels of inflammatory and vascular injury biomarkers, such as tumour necrosis factor-α (TNF-α), interleukin (IL-) 1β, 6, 8 and 10, plasminogen activator inhibitor-1 (PAI-1), soluble intercellular adhesion molecule type-1 (sICAM-1), matrix metalloproteinase-9 (MMP-9), myeloperoxidase (MPO) and vascular endothelial growth factor (VEGF) as well as endotoxin levels.Endotoxin levels demonstrated a significant and positive correlation with the markers for inflammation, vascular injury and atherogenesis (TNF-α: r(2) = 0.077, p < 0.05; PAI-1: r(2) = 0.215, p < 0.01; sICAM-1: r(2) = 0.159, p < 0.01; MMP-9: r(2) = 0.159, p < 0.01; MPO: r(2) = 0.07, p < 0.05; VEGF: r(2) = 0.161, p < 0.01). Males demonstrated significantly higher circulating endotoxin than females (Males: 9.63 ± 5.34 EU/ml; p = 0.004; Females: 5.56 ± 4.06 EU/ml; n = 60) in these BMI and age-matched cohorts.The present study demonstrates for the first time a significant association between circulating endotoxin and biomarkers of metabolic risk in children as young as 11 years. Thus, endotoxin-mediated sub-clinical inflammation during childhood obesity may be a key contributor to T2DM and CVD development later in life.

Dataset Information

Evaluation of the association between maternal smoking, childhood obesity, and metabolic disorders: a national toxicology program workshop review.

Background

Objective

Methods

Discussion

Conclusions

Publications

Evaluation of the association between maternal smoking, childhood obesity, and metabolic disorders: a national toxicology program workshop review.

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