Kim Hooper

Children show highest levels of polybrominated diphenyl ethers in a California family of four: a case study.

Polybrominated diphenyl ethers (PBDEs), a major class of flame retardants, are ubiquitous environmental contaminants with particularly high concentrations in humans from the United States. This study is a first attempt to report and compare PBDE concentrations in blood drawn from a family. Serum samples from family members collected at two sampling occasions 90 days apart were analyzed for PBDE congeners. Concentrations of the lower-brominated PBDEs were similar at the two sampling times for each family member, with children’s levels 2- to 5-fold higher than those of their parents. Concentrations of, for example, 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) varied from 32 ng/g lipid weight (lw) in the father to 60, 137, and 245 ng/g lw in the mother, child, and toddler, respectively. Decabromodiphenyl ether (BDE-209) concentrations differed significantly between the two samplings. September concentrations in the father, mother, child, and toddler were 23, 14, 143, and 233 ng/g lw, respectively. December concentrations (duplicate results from the laboratory) were 2 and 3, 4 and 4, 9 and 12, and 19 and 26 ng/g lw, respectively. Parents’ ∑PBDE concentrations approached U.S. median concentrations, with children’s concentrations near the maximum (top 5%) found in U.S. adults. The youngest child had the highest concentrations of all PBDE congeners, suggesting that younger children are more exposed to PBDEs than are adults. Our estimates indicate that house dust contributes to children’s higher PBDE levels. BDE-209 levels for all family members were 10-fold lower at the second sampling. The short half-life of BDE-209 (15 days) indicates that BDE-209 levels can decrease rapidly in response to decreased exposures. This case study suggests that children are at higher risk for PBDE exposures and, accordingly, face higher risks of PBDE-related health effects than adults.

Depuration of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) in breast milk from California first-time mothers (primiparae).

Background Little is known about the rates of loss (depuration) of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) from mothers during lactation. Depuration rates affect infant exposure to chemicals during breast-feeding, and fetal and lactational transfers during subsequent pregnancies. Objective Our objective in this study was to estimate depuration rates of PBDEs and PCBs using serial samples of breast milk. Method Nine first-time mothers (primiparae) each collected samples at 4, 6, 8, 12, 16, 20, and 24 weeks after birth. Nine additional primiparae each collected two samples at varying time intervals (18 to > 85 weeks after birth). Analytical precision was assessed to evaluate the accuracy of measured monthly percentage declines in PBDEs and PCBs. Results The four major PBDE congeners decreased 2 or 3% ± 1% per month over the 6-month period. These decreases were consistent over a 50-fold range (21–1,330 ng/g lipid weight) of initial PBDE concentrations in breast milk. The change in PCB-153 ranged from + 0.3% to –0.6% per month, with heterogeneous slopes and greater intraindividual variability. PBDE and PCB concentrations declined 1% per month over longer periods (up to 136 weeks). Conclusions Our data indicate that PBDEs and PCBs are not substantially (4–18%) reduced in primiparae after 6 months of breast-feeding. Consequently, the fetal and lactational exposures for a second child may not be markedly lower than those for the first. Participants were volunteers from a larger study population (n = 82), and were typical in their PBDE/PCB levels and in many demographic and lifestyle factors. These similarities suggest that our results may have broader applicability.

Polybrominated Diphenyl Ether (PBDE) Levels in Peregrine Falcon (Falco peregrinus) Eggs from California Correlate with Diet and Human Population Density

Peregrine falcons are now considered a conservation success story due in part to the phasing out of harmful contaminants that adversely affected reproduction. Recent studies have shown that peregrine eggs collected from California cities, however, have high levels of the higher-brominated polybrominated diphenyl ethers (SigmaPBDE(183-209)), a class of industrial flame retardants, in comparison to published data for other wildlife. Sources of these high PBDE levels and unusual PBDE profiles are unknown. Here we analyzed the stable carbon (delta(13)C), hydrogen (deltaD), and nitrogen (delta(15)N) isotope composition of peregrine eggs collected from urban and nonurban habitats. We found that delta(13)C values were significantly higher in urban versus nonurban eggs, suggesting that urban peregrines indirectly receive anthropogenic subsidies via their consumption of prey reliant on corn-based anthropogenic foods. delta(15)N and deltaD values were significantly lower in urban versus nonurban eggs, reflecting differences in dietary diversity and food/water sources available to peregrines in each habitat. These patterns suggest a link between an anthropogenic diet and high levels of SigmaPBDE(183-209) in California peregrines, and identify anthropogenic food as a potentially important PBDE exposure pathway for urban wildlife. If diet is an important PBDE exposure pathway for peregrines, continued high body burdens of SigmaPBDE(183-209) may be a potential risk to ongoing peregrine conservation efforts in California.

High Postnatal Exposures to Polybrominated Diphenyl Ethers (PBDEs) and Polychlorinated Biphenyls (PCBs) via Breast Milk in California: Does BDE-209 Transfer to Breast Milk?

Breast milk samples collected during 2003-2005 from 82 first-time mothers in 24 communities located throughout California contained levels of polybrominated diphenyl ethers (∑(tri-hexa (8))PBDEs; median = 53.3 ng/g lw, range = 9.60-1291) and polychlorinated biphenyls (∑(12)PCBs; median = 73.4 ng/g lw, range = 22.2-433) that are among the highest in the world. PBDE levels varied 100-fold. BDE-47 was the dominant PBDE congener, with levels exceeding the U.S.EPA Reference Dose (RfD) for neurodevelopmental toxicity (100 ng/kg/day) in most (60%) breast milk samples. In some samples, BDE-209 (2/82) and/or BDE-153 (5/82) were the dominant congeners, suggesting that BDE-209 can transfer to breast milk and/or break down in the mother and transfer to the nursing infant as the lower-brominated PBDEs associated with adverse effects. PBDE levels in California breast milk are approaching those of PCBs, and the trend PBDEs > PCBs may continue as PBDEs migrate from products to the indoor and outdoor environments.

Human somatic mutation assays as biomarkers of carcinogenesis.

This paper describes four assays that detect somatic gene mutations in humans: the hypoxanthine-guanine phosphoribosyl transferase assay, the glycophorin A assay, the HLA-A assay, and the sickle cell hemoglobin assay. Somatic gene mutation can be considered a biomarker of carcinogenesis, and assays for somatic mutation may assist epidemiologists in studies that attempt to identify factors associated with increased risks of cancer. Practical aspects of the use of these assays are discussed.

Unrecognized or potential risk factors for childhood cancer

Abstract Epidemiologic methods only seldom identify causes of childhood cancer associated with relative risks below, a factor of(1/2−2. Children are at risks of exposure to over 15,000 high-production-volume chemical and are certainly exposed to many, carcinogens. The individual impacts of most of these agents are too small to be detected, but collectively these unrecognized facors are potentially important. Infants and children are exposed to higher levels of some environmental toxicants and may also be more sensitive. During intrauterine developtnent a childhood cells divide frequently, and the mutant frequency rises rapidly. Endocrine-related cancer or susceptibility to canser may result from developmental exposures rather than from exposures , existing at or near the time of diagnosis. That environmental exposures may be important causes of childrood cancers is indicated, by associations of enzyme polymorphisms with risk.