Evaluation of the Association between Maternal Smoking, Childhood Obesity, and Metabolic Disorders: A National Toxicology Program Workshop Review

and Division of National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA.
Environmental Health Perspectives (Impact Factor: 7.98). 12/2012; 121(2). DOI: 10.1289/ehp.1205404
Source: PubMed


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.

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    • "Given the increasing concern regarding the potential involvement of pollutants in metabolic disease etiology, the U.S. National Institute of Environmental Health Sciences/National Toxicology Program (NIEHS/NTP) (NTP 2011) organized a workshop in 2011 that resulted in the generation of a publicly accessible database containing > 200 human studies linking environmental pollutants to diabetes and obesity (NTP 2012). The role of pollutants in diabetes and obesity was compelling in the series of papers published following this volume 121 | number 11-12 | November-December 2013 • Environmental Health Perspectives workshop (Behl et al. 2013; Maull et al. 2012; Taylor et al. 2013; Thayer et al. 2012) as well as in other reviews (Alonso-Magdalena et al. 2011; Hatch et al. 2010; Hectors et al. 2011; Neel and Sargis 2011; Tang-Péronard et al. 2011). With regard to IR in particular, several studies have investigated the potential association between pollutants and markers of insulin sensitivity (e.g., Barregard et al. 2013; Chang et al. 2010, 2011; Chen et al. 2008; Dirinck et al. 2011; Faerch et al. 2012; Kern et al. 2004; Lee et al. 2007, 2011; Nelson et al. 2010; Raafat et al. 2012; Wang et al. 2012). "
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    ABSTRACT: The metabolic disruptor hypothesis postulates that environmental pollutants may be risk factors for metabolic diseases. Because insulin resistance is involved in most metabolic diseases and current health care prevention programs predominantly target insulin resistance or risk factors thereof, a critical analysis of the role of pollutants in insulin resistance might be important for future management of metabolic diseases. We aim at critically reviewing the available information linking pollutant exposure to insulin resistance and intend to open the discussion on future perspectives for metabolic disruptor identification and prioritization strategies. PubMed and Web of Science were searched for experimental studies reporting on linkages between environmental pollutants and insulin resistance. A total of 23 studies were identified as the prime literature. Recent studies specifically designed to investigate the effect of pollutants on insulin sensitivity show a potential causation of insulin resistance. Based on these studies, a table of viable test systems and endpoints can be composed which allows to gain insight into what is missing and what is needed to create a standardized insulin resistance toxicity testing strategy. It is clear that current research predominantly relies on top-down identification of insulin resistance-inducing metabolic disruptors and that one of the major future research needs is the development of dedicated in vitro or ex vivo screens to allow animal sparing and time- and cost-effective bottom-up screening.
    Environmental Health Perspectives 09/2013; 121(11-12). DOI:10.1289/ehp.1307082 · 7.98 Impact Factor
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    ABSTRACT: In the same way as medicines are delivered to produce effects in the endocrine system, environmental chemicals can be similarly delivered to produce unwanted endocrine effects, resulting in a staggering increase in several diseases. These effects on endocrine and other physiological systems can have significant population-level impacts and thus require public health approaches to disease control.
    Trends in Endocrinology and Metabolism 05/2013; 24(7). DOI:10.1016/j.tem.2012.12.005 · 9.39 Impact Factor
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    ABSTRACT: Aims/hypothesis: The primary aim of the study was to investigate the risk of developing gestational diabetes in women who were exposed to tobacco smoke in utero. Secondary aims were to assess the risk of obesity and non-gestational diabetes. Methods: Data were retrieved from the Medical Birth Register of Sweden for women who were born in 1982 (when smoking data were first registered) or later and who had given birth to at least one child; 80,189 pregnancies were included. The associations between in utero smoking exposure (three categories: non-smokers, 1-9 cigarettes/day [moderately exposed] and >9 cigarettes/day [heavily exposed]) and subsequent gestational diabetes (n = 291), non-gestational diabetes (n = 280) and obesity (n = 7,300) were assessed. Results: The adjusted ORs (aORs) of gestational diabetes were increased among women who were moderately (1.62, 95% CI 1.24, 2.13) and heavily (1.52, 95% CI 1.12, 2.06) exposed. The corresponding aORs of obesity were 1.36 (95% CI 1.28, 1.44) and 1.58 (95% CI 1.48, 1.68), respectively. A reduced OR for non-gestational diabetes was seen in the offspring of heavy smokers (aOR 0.66, 95% CI 0.45, 0.96). Conclusions/interpretation: Women exposed to smoking during fetal life were at higher risk of developing gestational diabetes and obesity.
    Diabetologia 05/2013; 56(8). DOI:10.1007/s00125-013-2936-7 · 6.67 Impact Factor
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