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

Behl M, Rao D, Aagaard K, Davidson TL, Levin ED, Slotkin TA, Srinivasan S, Wallinga D, White MF, Walker VR, Thayer KA, Holloway AC - Environ. Health Perspect. (2012)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Kelly Government Solutions, Research Triangle Park, North Carolina, USA.

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.

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Human studies on exposure to smoking during pregnancy related to T1D. Studies are grouped by the nature of the smoke exposure (maternal, paternal, or secondhand smoke during childhood). Studies are then sorted by specific outcome measure (e.g., GAD Ab+), and presented alphabetically within a given outcome measure. Abbreviations: ABIS, All Babies in Southeast Sweden cohort; adjHR, adjusted hazard ratio; autoAb, auto antibodies; BBC, British Birth Cohort; BCS70, 1970 British Birth Cohort study; BPASU, British Paediatric Association Surveillance Unit; CC, case–control; cross-sect, cross-sectional; DAISY, Diabetes Autoimmunity Study in the Young; ESPED, German pediatric surveillance unit; GADA, glutamic acid decarboxylase antibodies; IA-2A, insulinoma antigen 2A; NCDS, National Child Development Study; pros, prospective; retro, retrospective; SHS, secondhand smoke. aRelative risk estimates [crudeRR] calculated based on data presented in the paper using an open source epidemiology statistics programs, OpenEpi (http://www.openepi.com/menu/openEpiMenu.htm).
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f2: Human studies on exposure to smoking during pregnancy related to T1D. Studies are grouped by the nature of the smoke exposure (maternal, paternal, or secondhand smoke during childhood). Studies are then sorted by specific outcome measure (e.g., GAD Ab+), and presented alphabetically within a given outcome measure. Abbreviations: ABIS, All Babies in Southeast Sweden cohort; adjHR, adjusted hazard ratio; autoAb, auto antibodies; BBC, British Birth Cohort; BCS70, 1970 British Birth Cohort study; BPASU, British Paediatric Association Surveillance Unit; CC, case–control; cross-sect, cross-sectional; DAISY, Diabetes Autoimmunity Study in the Young; ESPED, German pediatric surveillance unit; GADA, glutamic acid decarboxylase antibodies; IA-2A, insulinoma antigen 2A; NCDS, National Child Development Study; pros, prospective; retro, retrospective; SHS, secondhand smoke. aRelative risk estimates [crudeRR] calculated based on data presented in the paper using an open source epidemiology statistics programs, OpenEpi (http://www.openepi.com/menu/openEpiMenu.htm).

Mentions: T1D. The existing human studies do not provide support for an association between maternal or paternal smoking during pregnancy and childhood T1D (Figure 2). Only 2 of the 13 studies assessing end points related to T1D following exposure during pregnancy reported findings consistent with an association (Sipetic et al. 2005; Wahlberg et al. 2011). In the study by Sipetic et al. (2005), the frequency of maternal smoking during pregnancy was higher in T1D cases compared with controls (37.2% vs. 24.8%, p = 0.023 or unadjusted OR = 1.79; 95% CI: 1.08, 2.97). Although the univariate finding was statistically significant, the authors did not include maternal smoking in the multivariate analysis conducted to identify risk factors for T1D. In the study by Wahlberg et al. (2011), a positive association was observed for one indicator of β-cell autoimmunity in T1D, tyrosine phosphatase (IA-2A) + antibody status (unadjusted OR = 1.6; 95% CI: 1.2, 2.2), and not for glutamic acid decarboxylase (GAD) + antibody status (data not shown). None of the five prospective studies reported a positive association between maternal or paternal smoking during pregnancy and T1D (Hummel et al. 2001; Johansson et al. 2008; Rosenbauer et al. 2007; Stene et al. 2004; Toschke et al. 2007a; Wadsworth et al. 1997), including two studies of children who were considered at high risk for developing the disease (Hummel et al. 2001; Stene et al. 2004). Several studies reported that T1D was less likely among children whose mothers smoked during pregnancy than among the children of nonsmoking mothers (Dahlquist and Kallen 1992; Marshall et al. 2004; Svensson et al. 2005) for T1D. Hummel et al. (2001) reported a nonsignificant negative association between islet-cell antibodies (a marker of β-cell autoimmunity) and maternal smoking during pregnancy among children considered at high risk because one or both parents had T1D. However, the number of cases in this study was small (47 of 1,043 children). One hypothesis that may explain evidence of a protective effect of exposure to smoking relates to the hygiene theory of autoimmune disease; this suggests that the risk of autoimmune disease may be increased if the environment is “cleaner,” which might be manifest in the households of nonsmokers (Johansson et al. 2008; Marshall et al. 2004). Alternatively, smoking may affect immune function, resulting in a reduced risk of developing autoimmune disorder (Prescott 2008).


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

Behl M, Rao D, Aagaard K, Davidson TL, Levin ED, Slotkin TA, Srinivasan S, Wallinga D, White MF, Walker VR, Thayer KA, Holloway AC - Environ. Health Perspect. (2012)

Human studies on exposure to smoking during pregnancy related to T1D. Studies are grouped by the nature of the smoke exposure (maternal, paternal, or secondhand smoke during childhood). Studies are then sorted by specific outcome measure (e.g., GAD Ab+), and presented alphabetically within a given outcome measure. Abbreviations: ABIS, All Babies in Southeast Sweden cohort; adjHR, adjusted hazard ratio; autoAb, auto antibodies; BBC, British Birth Cohort; BCS70, 1970 British Birth Cohort study; BPASU, British Paediatric Association Surveillance Unit; CC, case–control; cross-sect, cross-sectional; DAISY, Diabetes Autoimmunity Study in the Young; ESPED, German pediatric surveillance unit; GADA, glutamic acid decarboxylase antibodies; IA-2A, insulinoma antigen 2A; NCDS, National Child Development Study; pros, prospective; retro, retrospective; SHS, secondhand smoke. aRelative risk estimates [crudeRR] calculated based on data presented in the paper using an open source epidemiology statistics programs, OpenEpi (http://www.openepi.com/menu/openEpiMenu.htm).
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569686&req=5

f2: Human studies on exposure to smoking during pregnancy related to T1D. Studies are grouped by the nature of the smoke exposure (maternal, paternal, or secondhand smoke during childhood). Studies are then sorted by specific outcome measure (e.g., GAD Ab+), and presented alphabetically within a given outcome measure. Abbreviations: ABIS, All Babies in Southeast Sweden cohort; adjHR, adjusted hazard ratio; autoAb, auto antibodies; BBC, British Birth Cohort; BCS70, 1970 British Birth Cohort study; BPASU, British Paediatric Association Surveillance Unit; CC, case–control; cross-sect, cross-sectional; DAISY, Diabetes Autoimmunity Study in the Young; ESPED, German pediatric surveillance unit; GADA, glutamic acid decarboxylase antibodies; IA-2A, insulinoma antigen 2A; NCDS, National Child Development Study; pros, prospective; retro, retrospective; SHS, secondhand smoke. aRelative risk estimates [crudeRR] calculated based on data presented in the paper using an open source epidemiology statistics programs, OpenEpi (http://www.openepi.com/menu/openEpiMenu.htm).
Mentions: T1D. The existing human studies do not provide support for an association between maternal or paternal smoking during pregnancy and childhood T1D (Figure 2). Only 2 of the 13 studies assessing end points related to T1D following exposure during pregnancy reported findings consistent with an association (Sipetic et al. 2005; Wahlberg et al. 2011). In the study by Sipetic et al. (2005), the frequency of maternal smoking during pregnancy was higher in T1D cases compared with controls (37.2% vs. 24.8%, p = 0.023 or unadjusted OR = 1.79; 95% CI: 1.08, 2.97). Although the univariate finding was statistically significant, the authors did not include maternal smoking in the multivariate analysis conducted to identify risk factors for T1D. In the study by Wahlberg et al. (2011), a positive association was observed for one indicator of β-cell autoimmunity in T1D, tyrosine phosphatase (IA-2A) + antibody status (unadjusted OR = 1.6; 95% CI: 1.2, 2.2), and not for glutamic acid decarboxylase (GAD) + antibody status (data not shown). None of the five prospective studies reported a positive association between maternal or paternal smoking during pregnancy and T1D (Hummel et al. 2001; Johansson et al. 2008; Rosenbauer et al. 2007; Stene et al. 2004; Toschke et al. 2007a; Wadsworth et al. 1997), including two studies of children who were considered at high risk for developing the disease (Hummel et al. 2001; Stene et al. 2004). Several studies reported that T1D was less likely among children whose mothers smoked during pregnancy than among the children of nonsmoking mothers (Dahlquist and Kallen 1992; Marshall et al. 2004; Svensson et al. 2005) for T1D. Hummel et al. (2001) reported a nonsignificant negative association between islet-cell antibodies (a marker of β-cell autoimmunity) and maternal smoking during pregnancy among children considered at high risk because one or both parents had T1D. However, the number of cases in this study was small (47 of 1,043 children). One hypothesis that may explain evidence of a protective effect of exposure to smoking relates to the hygiene theory of autoimmune disease; this suggests that the risk of autoimmune disease may be increased if the environment is “cleaner,” which might be manifest in the households of nonsmokers (Johansson et al. 2008; Marshall et al. 2004). Alternatively, smoking may affect immune function, resulting in a reduced risk of developing autoimmune disorder (Prescott 2008).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Kelly Government Solutions, Research Triangle Park, North Carolina, USA.

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.

Show MeSH
Related in: MedlinePlus