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Prenatal and Postnatal Exposure to Persistent Organic Pollutants and Infant Growth: A Pooled Analysis of Seven European Birth Cohorts.

Iszatt N, Stigum H, Verner MA, White RA, Govarts E, Murinova LP, Schoeters G, Trnovec T, Legler J, Pelé F, Botton J, Chevrier C, Wittsiepe J, Ranft U, Vandentorren S, Kasper-Sonnenberg M, Klümper C, Weisglas-Kuperus N, Polder A, Eggesbø M, OBEL - Environ. Health Perspect. (2015)

Bottom Line: Growth was change in weight-for-age z-score between birth and 24 months.Due to heterogeneity across cohorts, this estimate cannot be considered precise, but does indicate that an association with infant growth is present on average.Prenatal p,p'-DDE was associated with increased infant growth, and postnatal PCB-153 with decreased growth at European exposure levels.

View Article: PubMed Central - PubMed

Affiliation: Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway.

ABSTRACT

Background: Infant exposure to persistent organic pollutants (POPs) may contribute to obesity. However, many studies so far have been small, focused on transplacental exposure, used an inappropriate measure to assess postnatal exposure through breastfeeding if any, or did not discern between prenatal and postnatal effects.

Objectives: We investigated prenatal and postnatal exposure to POPs and infant growth (a predictor of obesity).

Methods: We pooled data from seven European birth cohorts with biomarker concentrations of polychlorinated biphenyl 153 (PCB-153) (n = 2,487), and p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) (n = 1,864), estimating prenatal and postnatal POPs exposure using a validated pharmacokinetic model. Growth was change in weight-for-age z-score between birth and 24 months. Per compound, multilevel models were fitted with either POPs total exposure from conception to 24 months or prenatal or postnatal exposure.

Results: We found a significant increase in growth associated with p,p'-DDE, seemingly due to prenatal exposure (per interquartile increase in exposure, adjusted β = 0.12; 95% CI: 0.03, 0.22). Due to heterogeneity across cohorts, this estimate cannot be considered precise, but does indicate that an association with infant growth is present on average. In contrast, a significant decrease in growth was associated with postnatal PCB-153 exposure (β = -0.10; 95% CI: -0.19, -0.01).

Conclusion: To our knowledge, this is the largest study to date of POPs exposure and infant growth, and it contains state-of-the-art exposure modeling. Prenatal p,p'-DDE was associated with increased infant growth, and postnatal PCB-153 with decreased growth at European exposure levels.

No MeSH data available.


Related in: MedlinePlus

Associations between change in weight-for-age z-score and total exposure from conception to 2 years, prenatal exposure (unadjusted and adjusted for postnatal exposure) and postnatal exposure (unadjusted and adjusted for prenatal exposure) to (A) PCB-153 and (B) p,p’-DDE. Results are per IQR increase (ng/g lipid). PCB-153 IQRs: total exposure 152 ng/g, prenatal exposure 120 ng/g, postnatal exposure 183 ng/g. p,p’-DDE IQRs: total exposure 515 ng/g, prenatal exposure 388 ng/g, postnatal exposure 571 ng/g. Models were adjusted for birth weight, parity, gestational age, maternal smoking during pregnancy, maternal age at birth, maternal height and weight, Roma ethnicity, and breastfeeding, and were fitted with random slope (p,p’-DDE) and slope (PCB-153) by cohort. Prenatal unadjusted: prenatal exposure adjusted for covariates except postnatal. Prenatal adjusted: prenatal exposure adjusted for covariates including postnatal. Postnatal unadjusted: postnatal exposure adjusted for covariates except prenatal. Postnatal adjusted: postnatal exposure adjusted for covariates including prenatal.
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f1: Associations between change in weight-for-age z-score and total exposure from conception to 2 years, prenatal exposure (unadjusted and adjusted for postnatal exposure) and postnatal exposure (unadjusted and adjusted for prenatal exposure) to (A) PCB-153 and (B) p,p’-DDE. Results are per IQR increase (ng/g lipid). PCB-153 IQRs: total exposure 152 ng/g, prenatal exposure 120 ng/g, postnatal exposure 183 ng/g. p,p’-DDE IQRs: total exposure 515 ng/g, prenatal exposure 388 ng/g, postnatal exposure 571 ng/g. Models were adjusted for birth weight, parity, gestational age, maternal smoking during pregnancy, maternal age at birth, maternal height and weight, Roma ethnicity, and breastfeeding, and were fitted with random slope (p,p’-DDE) and slope (PCB-153) by cohort. Prenatal unadjusted: prenatal exposure adjusted for covariates except postnatal. Prenatal adjusted: prenatal exposure adjusted for covariates including postnatal. Postnatal unadjusted: postnatal exposure adjusted for covariates except prenatal. Postnatal adjusted: postnatal exposure adjusted for covariates including prenatal.

Mentions: Figure 1 shows the secondary analyses assessing which of prenatal and postnatal exposure is the more important contributor toward associations with total exposure. After adjustment for prenatal exposure, postnatal PCB-153 was associated with a significant decrease in change in weight-for-age z-score (β = –0.10; 95% CI: –0.19, –0.01 for an IQR increase of 183 ng/g lipid) (Figure 1A). Prenatal p,p´-DDE was associated with a significant increase in change in weight-for-age z-score (β = 0.12; 95% CI: 0.03, 0.22 for an increase of 388 ng/g lipid) after adjustment for postnatal exposure (Figure 1B).


Prenatal and Postnatal Exposure to Persistent Organic Pollutants and Infant Growth: A Pooled Analysis of Seven European Birth Cohorts.

Iszatt N, Stigum H, Verner MA, White RA, Govarts E, Murinova LP, Schoeters G, Trnovec T, Legler J, Pelé F, Botton J, Chevrier C, Wittsiepe J, Ranft U, Vandentorren S, Kasper-Sonnenberg M, Klümper C, Weisglas-Kuperus N, Polder A, Eggesbø M, OBEL - Environ. Health Perspect. (2015)

Associations between change in weight-for-age z-score and total exposure from conception to 2 years, prenatal exposure (unadjusted and adjusted for postnatal exposure) and postnatal exposure (unadjusted and adjusted for prenatal exposure) to (A) PCB-153 and (B) p,p’-DDE. Results are per IQR increase (ng/g lipid). PCB-153 IQRs: total exposure 152 ng/g, prenatal exposure 120 ng/g, postnatal exposure 183 ng/g. p,p’-DDE IQRs: total exposure 515 ng/g, prenatal exposure 388 ng/g, postnatal exposure 571 ng/g. Models were adjusted for birth weight, parity, gestational age, maternal smoking during pregnancy, maternal age at birth, maternal height and weight, Roma ethnicity, and breastfeeding, and were fitted with random slope (p,p’-DDE) and slope (PCB-153) by cohort. Prenatal unadjusted: prenatal exposure adjusted for covariates except postnatal. Prenatal adjusted: prenatal exposure adjusted for covariates including postnatal. Postnatal unadjusted: postnatal exposure adjusted for covariates except prenatal. Postnatal adjusted: postnatal exposure adjusted for covariates including prenatal.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4492262&req=5

f1: Associations between change in weight-for-age z-score and total exposure from conception to 2 years, prenatal exposure (unadjusted and adjusted for postnatal exposure) and postnatal exposure (unadjusted and adjusted for prenatal exposure) to (A) PCB-153 and (B) p,p’-DDE. Results are per IQR increase (ng/g lipid). PCB-153 IQRs: total exposure 152 ng/g, prenatal exposure 120 ng/g, postnatal exposure 183 ng/g. p,p’-DDE IQRs: total exposure 515 ng/g, prenatal exposure 388 ng/g, postnatal exposure 571 ng/g. Models were adjusted for birth weight, parity, gestational age, maternal smoking during pregnancy, maternal age at birth, maternal height and weight, Roma ethnicity, and breastfeeding, and were fitted with random slope (p,p’-DDE) and slope (PCB-153) by cohort. Prenatal unadjusted: prenatal exposure adjusted for covariates except postnatal. Prenatal adjusted: prenatal exposure adjusted for covariates including postnatal. Postnatal unadjusted: postnatal exposure adjusted for covariates except prenatal. Postnatal adjusted: postnatal exposure adjusted for covariates including prenatal.
Mentions: Figure 1 shows the secondary analyses assessing which of prenatal and postnatal exposure is the more important contributor toward associations with total exposure. After adjustment for prenatal exposure, postnatal PCB-153 was associated with a significant decrease in change in weight-for-age z-score (β = –0.10; 95% CI: –0.19, –0.01 for an IQR increase of 183 ng/g lipid) (Figure 1A). Prenatal p,p´-DDE was associated with a significant increase in change in weight-for-age z-score (β = 0.12; 95% CI: 0.03, 0.22 for an increase of 388 ng/g lipid) after adjustment for postnatal exposure (Figure 1B).

Bottom Line: Growth was change in weight-for-age z-score between birth and 24 months.Due to heterogeneity across cohorts, this estimate cannot be considered precise, but does indicate that an association with infant growth is present on average.Prenatal p,p'-DDE was associated with increased infant growth, and postnatal PCB-153 with decreased growth at European exposure levels.

View Article: PubMed Central - PubMed

Affiliation: Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway.

ABSTRACT

Background: Infant exposure to persistent organic pollutants (POPs) may contribute to obesity. However, many studies so far have been small, focused on transplacental exposure, used an inappropriate measure to assess postnatal exposure through breastfeeding if any, or did not discern between prenatal and postnatal effects.

Objectives: We investigated prenatal and postnatal exposure to POPs and infant growth (a predictor of obesity).

Methods: We pooled data from seven European birth cohorts with biomarker concentrations of polychlorinated biphenyl 153 (PCB-153) (n = 2,487), and p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) (n = 1,864), estimating prenatal and postnatal POPs exposure using a validated pharmacokinetic model. Growth was change in weight-for-age z-score between birth and 24 months. Per compound, multilevel models were fitted with either POPs total exposure from conception to 24 months or prenatal or postnatal exposure.

Results: We found a significant increase in growth associated with p,p'-DDE, seemingly due to prenatal exposure (per interquartile increase in exposure, adjusted β = 0.12; 95% CI: 0.03, 0.22). Due to heterogeneity across cohorts, this estimate cannot be considered precise, but does indicate that an association with infant growth is present on average. In contrast, a significant decrease in growth was associated with postnatal PCB-153 exposure (β = -0.10; 95% CI: -0.19, -0.01).

Conclusion: To our knowledge, this is the largest study to date of POPs exposure and infant growth, and it contains state-of-the-art exposure modeling. Prenatal p,p'-DDE was associated with increased infant growth, and postnatal PCB-153 with decreased growth at European exposure levels.

No MeSH data available.


Related in: MedlinePlus