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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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Related in: MedlinePlus

Human studies on exposure to smoking during pregnancy and findings related to T2D or metabolic syndrome. The primary grouping is whether the outcome was related to T2D, glucose, or insulin or metabolic syndrome. Studies are then sorted by specific outcome measure (e.g., HOMA-IR) and presented alphabetically within a given outcome measure. Abbreviations: A1C, glycosylated haemoglobin A1c; adjMR, adjusted mean ratio; BBC, British Birth Cohort; cig, cigarettes; cross-sect, cross-sectional; GINIplus, German Infant Nutritional Intervention study; HOMA-IR, Homeostatic model assessment for insulin resistance; LISAplus, Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood study; MoBa, Norwegian Mother and Child Cohort Study; NCDS, National Child Development Study; NS, not significant; pros, prospective; trim, trimester.
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f3: Human studies on exposure to smoking during pregnancy and findings related to T2D or metabolic syndrome. The primary grouping is whether the outcome was related to T2D, glucose, or insulin or metabolic syndrome. Studies are then sorted by specific outcome measure (e.g., HOMA-IR) and presented alphabetically within a given outcome measure. Abbreviations: A1C, glycosylated haemoglobin A1c; adjMR, adjusted mean ratio; BBC, British Birth Cohort; cig, cigarettes; cross-sect, cross-sectional; GINIplus, German Infant Nutritional Intervention study; HOMA-IR, Homeostatic model assessment for insulin resistance; LISAplus, Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood study; MoBa, Norwegian Mother and Child Cohort Study; NCDS, National Child Development Study; NS, not significant; pros, prospective; trim, trimester.

Mentions: T2D and metabolic syndrome. Fewer studies have looked at associations between maternal smoking during pregnancy and T2D, blood glucose, blood insulin, or metabolic disease (Horta et al. 2011; Huang et al. 2007; Montgomery and Ekbom 2002; Thiering et al. 2011; Thomas et al. 2007) (Figure 3). It is not possible to reach conclusions with confidence based on the existing literature because of the variation in health outcomes assessed among the studies [i.e., HbA1C (hemoglobin A1C); fasting glucose, nonfasting glucose, HOMA-IR (homeostatic model assessment–insulin resistance), blood insulin; T2D; and metabolic syndrome. In addition, although most of the studies do not report positive associations with these outcomes, the age at assessment in many of the studies was relatively young, and additional follow-up may be required. It is worth noting that no association with HbA1C ≥ 6% was found in the oldest and largest cohort assessed [7,518 men and women from the 1958 British birth cohort enrolled in the Perinatal Mortality Survey (PMS) evaluated at 45 years of age] (Thomas et al. 2007). This finding does not confirm an earlier report for the same cohort of an association between heavy smoking during pregnancy and T2D in offspring at 33 years of age (adjOR = 4.02; 95% CI: 1.14, 14.14) (Montgomery and Ekbom 2002). A related analysis of the cohort by Power et al. (2010) also reported no association with HbA1C in adults at 45 years of age (fully adjusted mean difference = 0.13; 95% CI: –0.33, 0.58). Power et al. (2010) reported a positive association between maternal smoking during pregnancy and metabolic syndrome based on an unadjusted model [unadjusted OR = 1.21; 95% CI: 1.05, 1.39), but there was a significant negative association between maternal smoking and metabolic syndrome after adjustment for adult life covariates such as social class, education, physical activity and inactivity (television/computer use), smoking, and consumption of fruit/vegetables, cakes/sweets, and alcohol (adjOR = 0.55; 95% CI: 0.47, 0.64).


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 and findings related to T2D or metabolic syndrome. The primary grouping is whether the outcome was related to T2D, glucose, or insulin or metabolic syndrome. Studies are then sorted by specific outcome measure (e.g., HOMA-IR) and presented alphabetically within a given outcome measure. Abbreviations: A1C, glycosylated haemoglobin A1c; adjMR, adjusted mean ratio; BBC, British Birth Cohort; cig, cigarettes; cross-sect, cross-sectional; GINIplus, German Infant Nutritional Intervention study; HOMA-IR, Homeostatic model assessment for insulin resistance; LISAplus, Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood study; MoBa, Norwegian Mother and Child Cohort Study; NCDS, National Child Development Study; NS, not significant; pros, prospective; trim, trimester.
© Copyright Policy - public-domain
Related In: Results  -  Collection

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

f3: Human studies on exposure to smoking during pregnancy and findings related to T2D or metabolic syndrome. The primary grouping is whether the outcome was related to T2D, glucose, or insulin or metabolic syndrome. Studies are then sorted by specific outcome measure (e.g., HOMA-IR) and presented alphabetically within a given outcome measure. Abbreviations: A1C, glycosylated haemoglobin A1c; adjMR, adjusted mean ratio; BBC, British Birth Cohort; cig, cigarettes; cross-sect, cross-sectional; GINIplus, German Infant Nutritional Intervention study; HOMA-IR, Homeostatic model assessment for insulin resistance; LISAplus, Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood study; MoBa, Norwegian Mother and Child Cohort Study; NCDS, National Child Development Study; NS, not significant; pros, prospective; trim, trimester.
Mentions: T2D and metabolic syndrome. Fewer studies have looked at associations between maternal smoking during pregnancy and T2D, blood glucose, blood insulin, or metabolic disease (Horta et al. 2011; Huang et al. 2007; Montgomery and Ekbom 2002; Thiering et al. 2011; Thomas et al. 2007) (Figure 3). It is not possible to reach conclusions with confidence based on the existing literature because of the variation in health outcomes assessed among the studies [i.e., HbA1C (hemoglobin A1C); fasting glucose, nonfasting glucose, HOMA-IR (homeostatic model assessment–insulin resistance), blood insulin; T2D; and metabolic syndrome. In addition, although most of the studies do not report positive associations with these outcomes, the age at assessment in many of the studies was relatively young, and additional follow-up may be required. It is worth noting that no association with HbA1C ≥ 6% was found in the oldest and largest cohort assessed [7,518 men and women from the 1958 British birth cohort enrolled in the Perinatal Mortality Survey (PMS) evaluated at 45 years of age] (Thomas et al. 2007). This finding does not confirm an earlier report for the same cohort of an association between heavy smoking during pregnancy and T2D in offspring at 33 years of age (adjOR = 4.02; 95% CI: 1.14, 14.14) (Montgomery and Ekbom 2002). A related analysis of the cohort by Power et al. (2010) also reported no association with HbA1C in adults at 45 years of age (fully adjusted mean difference = 0.13; 95% CI: –0.33, 0.58). Power et al. (2010) reported a positive association between maternal smoking during pregnancy and metabolic syndrome based on an unadjusted model [unadjusted OR = 1.21; 95% CI: 1.05, 1.39), but there was a significant negative association between maternal smoking and metabolic syndrome after adjustment for adult life covariates such as social class, education, physical activity and inactivity (television/computer use), smoking, and consumption of fruit/vegetables, cakes/sweets, and alcohol (adjOR = 0.55; 95% CI: 0.47, 0.64).

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