Body burdens of brominated flame retardants and other persistent organo-halogenated compounds and their descriptors in US girls

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Abstract

Background

Levels of brominated flame retardants are increasing in US populations, yet little data are available on body burdens of these and other persistent hormonally active agents (HAAs) in school-aged children. Exposures to such chemicals may affect a number of health outcomes related to development and reproductive function.

Objective

Determine the distribution of biomarkers of polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and organo-chlorinated pesticides (OCPs), such as DDT/DDE, in children, and their variation by key descriptor variables.

Methods

Ethnically diverse cohorts of girls 6–8 y old at baseline are being followed for growth and pubertal development in a multi-site, longitudinal study. Nearly 600 serum samples from the California and Ohio sites were analyzed for lipids, 35 PCB congeners, 11 PBDE congeners, and 9 OCPs. The biomarker distributions were examined and geometric means compared for selected analytes across categories of age, race, site, body mass index (BMI), parental education, maternal age at delivery, and breast feeding in adjusted models.

Results

Six PBDE congeners were detected among greater than 70% of samples, with BDE-47 having the highest concentration (median 42.2, range 4.9–855 ng/g lipid). Girls in California had adjusted geometric mean (GM) PBDE levels significantly higher than girls in Ohio. Furthermore, Blacks had significantly higher adjusted GMs of all six PBDE congeners than Whites, and Hispanics had intermediate values. GMs tended to be lower among more obese girls, while other variables were not strongly associated. In contrast, GMs of the six PCB congeners most frequently detected were significantly lower among Blacks and Hispanics than Whites. PCBs and the three pesticides most frequently detected were also consistently lower among girls with high BMI, who were not breast-fed, whose mothers were younger, or whose care-givers (usually parents) were less educated. Girls in California had higher GMs than in Ohio for the pesticides and most PCB congeners, but the opposite for CB-99 and -118.

Conclusions

Several of these potential HAAs were detected in nearly all of these young girls, some at relatively high levels, with variation by geographic location and other demographic factors that may reflect exposure pathways. The higher PBDE levels in California likely reflect differences in fire regulation and safety codes, with potential policy implications.

Introduction

During the last few decades, concern has grown about the health effects of exposure to environmental contaminants that have hormonally active properties. While some of the chemicals of original concern were banned in many Westernized countries (such as DDT/DDE and PCBs), they are persistent in the environment. More recently, levels of a class of brominated flame retardants, the polybrominated diphenyl ethers (PBDEs), have been found to be increasing in the environment and subsequently in human biospecimens, and are present at higher concentrations in human serum and milk in the US than in Europe (Hites, 2004; Norstrom et al., 2002; Sjodin et al., 2004a). In contrast, levels of PCBs have been declining since the 1970s (Sjodin et al., 2004a). The PBDE studies have tended to include only adults (Bradman et al., 2007a, Bradman et al., 2007b; Hites, 2004; Petreas et al., 2002; Sjodin, 2004a; Schecter et al., 2005; Thomsen et al., 2002) and although there is much data on PCBs and DDT/DDE in adults and newborns, levels of these compounds are not routinely monitored in children under age 12 y. The Centers for Disease Control and Prevention (CDC, 2005) reports concentrations of these potential hormonally active agents (HAAs) in older children (12–19 y) in the National Health and Nutrition Examination Survey (NHANES); more recent data on PBDEs were published separately (Sjodin et al., 2008) and in the very recent new report (CDC, 2009).

Exposure to these persistent compounds in children is primarily through the diet (including breast feeding), as well as dust or inhalation for PBDEs (Lorber, 2008). As the reproductive system does not fully mature until later puberty during adolescence, chemicals that affect the endocrine system might potentially alter such development. The observed trend towards pubertal development occurring at younger ages (Hermann-Giddens et al., 1997; Euling et al., 2008) has raised the possibility that exogenous exposures may be contributing factors. Due to these concerns and the association of early menarche with increased risk of breast cancer, a study of determinants of puberty in girls is being conducted within the NIEHS/NCI-sponsored Breast Cancer and the Environment Research Centers (BCERC), which include transdisciplinary research collaborations integrated across biologic, epidemiologic, and community outreach projects. Of primary interest are exposures to potential HAAs in young girls before breast development (Hiatt et al., 2009). Working with community representatives, laboratory staff at the National Center for Environmental Health of the Centers for Disease Control and Prevention (CDC), and the relevant literature, we identified numerous compounds for evaluation in a small pilot sample of girls who provided urine and serum specimens (Pinney et al., 2008; Windham et al., 2008; Wolff et al., 2007a). Factors considered in determining which chemical families were subsequently measured in the entire cohort included high detection frequency and adequate variability. This current analysis focuses on persistent organo-halogenated compounds measured in serum, which was collected at two sites. To provide data lacking on children of this age (6–9 y), our goal was to characterize the distribution of these compounds and to compare them by geographic and other common demographic variables.

Section snippets

Study population

In the BCERC epidemiologic studies, girls ages 6–8 y at enrollment are being followed to measure onset and progression of pubertal maturation, including breast and pubic hair development. This longitudinal study began in 2005 at three sites: (1) Mount Sinai School of Medicine, which recruited girls through clinics, schools, and neighborhood centers in East Harlem in New York City; (2) Cincinnati Children’s Hospital/University of Cincinnati, Ohio (abbreviated as OH site), which recruited through

Results

Age at blood draw ranged from 6 to 10 y (the only 10-year-old had recently turned 10), with the majority aged 7–8 y old (Table 1). The sample was racially diverse with 52% white overall, and of fairly high socioeconomic status (SES) based on education level of the care-giver. About one-third of the girls had a BMI indicating risk for obesity and the majority had been breast-fed (Table 1). There were some differences between the two sites with girls from CA being older at blood draw, having older

Discussion

Our results show that many of these potential hormonally active agents, most of which have been little studied previously in children of this age, were detectable in a large proportion of young girls, some at relatively high levels. Concentrations of many, most consistently the PBDEs, varied by geographic location with higher levels found in the California site. There were variations by race, with Blacks having the highest mean PBDE levels, but about 50% lower mean PCB levels and slightly lower

Acknowledgments

We wish to acknowledge the contributions of numerous BCERC collaborators, including Drs. Mary Wolff, Susan Teitelbaum and Antonia Calafat, as well as the field staff at each site; Janice Barlow, M. Kathryn Brown and other members of the Community Outreach and Translation Core; and Dr. Gwen Collman. We thank Isaac J. Ergas, Lixia Zhang, Ling Shen, and Lusine Yaghjyan for initial data management and analyses.

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    Funding Sources: This work was funded by the National Institute of Environmental Health Sciences (NIEHS) and the National Cancer Institute (NCI), NIH, DHHS to the Breast Cancer & the Environment Research Centers at the University of California San Francisco Helen Diller Family Comprehensive Cancer Center (U01 ES012801) and the University of Cincinnati/Cincinnati Children’s Hospital Medical Center (U01 ES12770), with support from the University of Cincinnati Center for Environmental Genetics (P30-ES006096), the CA Department of Public Health (CDPH), and the NIH/NCRR-sponsored UCSF Center for Translational Science Institute (UL1 RR024131). The contents of this report are solely the responsibility of the authors and do not necessarily represent the official views of the NIEHS, the NCI, the CDC, or the CDPH. Before initiation of the study, human subjects approval was obtained from the IRBs of the institutions carrying out subject recruitment and data collection, e.g. Kaiser Permanente, Northern California (no.: CN-04LKush-04-H, last re-approved on 14 October 2008) and the University of Cincinnati (CCHMC IRB no. 03-18-05, last re-approved on 1 November 2008).

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