Original ArticlesChildhood growth and exposure to dichlorodiphenyl dichloroethene and polychlorinated biphenyls☆,☆☆,★
Section snippets
Study population
After obtaining permits from the Data Protection Agency of the State of Hamburg, Germany, from the Ministry of Cultural Affairs of Hesse, Germany, and from the local school committees, we asked the parents of 1091 second grade school children in 18 townships to participate in our study. Informed consent, according to the requirements of the Ethical Committee of the Board of Physicians and the Data Protection Agency of the State of Hamburg, was obtained from all participating parents. Parents
Results
The proportion of participation was 61.5% (671/1091). We obtained blood samples from 350 children, and complete organo chlorine analyses could be conducted in 343 samples. Overall information (ie, from the Child's Health Card, the questionnaires, and on DDE and PCB determination) could be analyzed statistically in 343 children. The number of patients with complete data that could be analyzed for the various cross-sectional height models ranged from 212 at both 4 and 10 years of age to 313 at
Discussion
We analyzed the relationship between growth and DDE concentration at 8 years of age. At the onset of the study, we did have the previous hypothesis that growth in exposed children is reduced. However, we did not specify which exposure we would focus on, DDE or PCB. Because of budget limitations, the investigation had to select a subgroup of the total sample for blood analyses. Although we restricted phlebotomy to children who had lower ETS exposure in their homes to reduce the potentially
Acknowledgements
We thank the reviewers for their thoughts and contributions, with special emphasis regarding those comments that led to the addition of BMI to the statistical models.
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2019, Encyclopedia of Environmental HealthAssociations of maternal o,p′-DDT and p,p′-DDE levels with birth outcomes in a Bolivian cohort
2016, Environmental ResearchCitation Excerpt :Specifically, p,p′-DDE has been found to cause adipocyte dysfunction and obesity through interaction with the release of leptin, resistin, and adiponectin (Howell and Mangum, 2011). Numerous authors have observed a positive association between prenatal p,p′-DDE exposure and weight or weight gain during the first years of life (Iszatt et al., 2015; Karmaus et al., 2002; Mendez et al., 2011; Valvi et al., 2014; Verhulst et al., 2009; Warner et al., 2014), although the available literature is not entirely consistent (Cupul-Uicab et al., 2010; Garced et al., 2012). Interestingly, Robledo et al. (2014) reported that preconception maternal and parental p,p′-DDE concentrations were positively associated with the newborn ponderal index, although statistical significance was only reached for paternal levels.
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2012, Environmental ResearchCitation Excerpt :In comparison with other studies, our sample was small and this could have been a possible source of error due to lack of statistical power. Our DDE concentration levels were lower than those reported in other studies (Verhulst et al., 2009; Jusko et al., 2006; Ribas-Fitó et al., 2006; Gladen et al., 2004; Karmaus et al., 2002). No information of DDE levels on maternal milk was available for this study, limiting our ability to draw conclusions about potential exposures from this source.
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Supported by the Ministry of Environment, Energy, Youth, Family and Health, Hesse, Germany.
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The work of Scott Asakevich was covered by a grant from the Agency for Toxic Substances and Disease Registry, No. H75/ATH582536-06.
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Reprint requests: Wilfried Karmaus, MD, MPH, Associate Professor, Department of Epidemiology, Michigan State University, 4660 S Hagadorn Rd, Suite 600, East Lansing, MI 48823.