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Polybrominated diphenyl ethers (PBDEs) are brominated flame retardants that act as endocrine disruptors, affecting thyroid hormone homeostasis. As a follow-up to a recent study showing high PBDE levels in household cats and linking PBDE levels with cat hyperthyroidism, we measured PBDEs, polychlorinated biphenyls (PCBs), and organochlorinated pesticides (OCPs) in serum samples from 26 California household cats (16 hyperthyroid, 10 controls) using liquid-liquid extraction and high-resolution gas chromatography/high-resolution mass spectrometry. In the present pilot study, we found that PBDE levels in California house cats were extremely high (ΣPBDEs median = 2,904 ng/g lipid; range, 631-22,537 ng/g lipid). This is approximately 50 times higher than levels in California residents (ΣPBDEs geomean = 62 ± 8.9 ng/g lipid, National Health and Nutrition Examination Survey), who have among the highest human levels in the world. Polybrominated diphenyl ethers congener patterns (BDE-99 major congener, BDE-209 significant) differed markedly from patterns found in California residents (BDE-47 major) or wildlife but resembled patterns found in house dust. Polychlorinated biphenyls and OCPs in cats were highly correlated, consistent with a shared dietary source or pathway of exposure, but did not correlate with PBDEs. This suggests a different source or pathway of exposure for PBDEs, which was most likely house dust. The authors found no evidence that linked levels of PBDEs, PCBs, or OCPs with hyperthyroidism. This may be because of the small sample size, competing or confounding risk factors, or complicated causal mechanisms. Environ. Toxicol. Chem. 2012;31:301-306. © 2011 SETAC [ABSTRACT FROM AUTHOR]

High (maximum of 4.1 ppm lipid weight) levels of BDE-209 and other higher brominated diphenyl ethers (BDEs) found in California, USA, peregrine falcon (Falco peregrinus) eggs (n = 95) provided an opportunity to examine homolog profiles of nona-, octa-, and hepta-BDEs as possible evidence for biological debromination of BDE-209. We found two congeners in eggs, an unidentified hepta-BDE (BDE-heptaUNK) and BDE-202 (octa-BDE) that are not present in commercial mixtures. In addition, BDE- 208 (nona-BDE) was present at much higher (10-fold) proportions in eggs than in commercial mixtures. To examine whether these unusual homolog patterns arose from assimilation of environmentally degraded BDE commercial mixtures, we compared nona-hepta- BDE homolog profiles of peregrine falcon eggs with those of weathered BDEs present in various abiotic matrices (sludge, sediment, and dusts). We found the profiles differed significantly: BDE-207 was the major nona-BDE in eggs, whereas BDE-206 was the major nona-BDE in abiotic matrices. Thus, the evidence for the biological debromination of BDE-209 in peregrine falcons is twofold: Eggs have two congeners (BDE-202 and -heptaUNK) that are not reported for any commercial mixtures nor in the abiotic matrices examined thus far, and eggs have higher-brominated BDE homolog patterns that are different from those found in commercial mixtures or environmental matrices. [ABSTRACT FROM AUTHOR]

Presents a study which compared the Toxicity Characteristic Leaching Procedure, the Waste Extraction Test and the Synthetic Precipitation Leaching Procedure with actual municipal solid waste leachates. Experimental section; Results and discussion.

Evaluates the limits of quantitation (LOQ) for a quadrupole ion storage tandem-in-time mass spectrometry (QISTMS) method through replicate analysis of chlorine-substituted polychlorodibenzofurans. Limits of quantitation appropriate for animal foods; Methodology of the study conducted; Analysis on high-fat food pool.

Evaluates the effectiveness of breast milk monitoring programs as an early warning system for polyhagenated polychlorinated persistent organic pollutants. Graph showing persistent organochloride pollutant levels in breast milk; Tetracholodibenzo-p-dioxin levels in breast milk and serum.

To assess levels of chlorinated contaminants in breast milk, we measured organochlorine pesticides, polychlorinated biphenyls, polychlorinated dibenzo-p-dioxins (PCDDs), and polychlorinated dibenzofurans (PCDFs) in breast milk samples collected in 1994 according to the WorldHealth Organization protocol from 92 donors that were representativeof regional populations in southern Kazakstan. High levels (10-120 pg/g fat) of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic of the PCDD/PCDF congeners, were found in breast milk samples from an agricultural region. TCDD was the major contributor (75%) to the international toxicity equivalents of these samples. The same distinctive PCDD/PCDF congener pattern was found in 15 breast milk samples and 4 serum samples collected in 1996 in a follow-up study, and has nowbeen confirmed by three analytical laboratories. [ABSTRACT FROM AUTHOR]

Concentrations of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) were measured in 169 avian eggs. We analyzed randomly collected eggs of two species of piscivorous birds: Caspian tern (Sterna caspia) (n =78) and Forster’s tern (Sterna forsteri) (n =76). We also analyzed fail-to-hatch eggs from two species protected under the Federal Endangered Species Act of 1973, that breed in the San Francisco Bay region: the piscivorous California Least tern (Sterna antillarum brownii) (n =11) and the omnivorous California Clapper rail (Rallus longirostris obsoletus) (n =4). San Francisco Bay eggs were collected annually for four years (2000–2003), and additional 20 eggs were collected and analyzed from Gray’s Harbor, Washington in 2001. Geometric mean PBDE concentrations did not significantly differ in the three tern species, but concentrations in eggs from the fail to hatch California Clapper rail eggs were significantly lower than those found in the randomly collected tern eggs. Median concentrations of ∑PBDEs in Caspian tern eggs for 2000–2003 were 2410, 4730, 3720 and 2880ng/g lipid weight (lw), respectively, in Forster’s terns 1820, 4380, 5460 and 3600ng/g lw, respectively, and in California Least terns for 2001 and 2002 were 5060 and 5170ng/glw, respectively. In contrast, median ∑PBDEs concentration in California Clapper rail eggs for 2001 was 379ng/glw. Five PBDEs were the major congeners found and decreased in the order BDE-47, -99, -100, -153, and -154. BDE-32, -28, -71, -66, -85, -183 were less prevalent, minor congeners, as was BDE-209, which was measured in a subset of samples. PBDE concentrations in bird eggs from San Francisco Bay were site related. There was no significant difference in PBDE concentrations in Caspian tern eggs from San Francisco Bay and Gray’s Harbor, WA. Average PBDE concentrations in eggs did not significantly increase over the period 2000–2003. [Copyright &y& Elsevier]

Breast milk samples from 40 first-time mothers from the Pacific Northwest of the US and Canada were analyzed for polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs). Total PBDEs (∑PBDEs), calculated by summing values for the 12 PBDEs congeners analyzed, ranged from 6 to 321ppb (lipid weight) (mean=96ppb; median=50ppb). In ∼40% of the women (15/40), ∑PBDEs>100ppblw in their milk, and four samples had levels >250ppblw. PBDE 47 was the dominant congener in most samples, whereas PBDE 153 was predominant in a few (3/40). ∑PCBs were calculated by summing values for the 82 PCB congeners analyzed, and ranged from 49 to 415ppb (lipid weight) (mean=147ppb; median=126ppb). ∼30% of the mothers (13/40) have ∑PBDEs>∑PCBs in their milk samples, and ∼65% (25/40) have BDE 47>PCB 153 in breast milk samples, with BDE 47 averaging 3-fold greater levels than PCB 153. Clearly, the lower brominated PBDEs are surpassing PCBs as a major environmental concern in North America, and are likely affecting significant portions of the populations in these regions. PBDEs have become a major persistent organic pollutant. However, there are no positive correlations between levels of ∑PBDEs and ∑PCBs, or between levels of PBDE 47 and PCB 153, suggesting there may be some differences in exposure pathways for PBDEs and PCBs in humans. [Copyright &y& Elsevier]

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.

High levels (microg/g lw) of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) were measured in peregrine falcon eggs from California (n = 90 eggs from 52 birds, 38 nest sites, collected 1986-2007, SigmaPBDEs median = 4.53, range = 0.08-53.1). Over the past 22 years, PBDE levels more than tripled each decade in the eggs, whereas PCB levels had no significant changes. PBDE levels were highest in eggs from major California cities ("Big Cities"), whereas PCBs showed no difference across the regions. For PBDEs, Big City eggs had markedly different patterns from Coastal eggs: BDE-209 and the higher brominated PBDEs (hexa-nona) were dominant congeners in Big City eggs, while BDE-47 and -99 were dominant in Coastal eggs. In many of the birds that gave multiple eggs over time ("time series"), PBDE patterns changed over time: the high proportions of BDE-209 and higher brominated PBDEs (short half-lives) in young birds contrasted with increasingly higher proportions of BDE-153 (long half-life) and other lower brominated PBDEs as the birds aged. These data are consistent with metabolic debromination of BDE-209 (t(1/2) = 1-2 weeks) to the lower brominated PBDEs, with accumulation over time of BDE-153 (t(1/2) = 3-4 years). In contrast, PCB patterns showed no differences by locations, and did not change over time. Diet (prey birds) may explain the urban PBDE pattern, as the patterns in urban pigeons and peregrines were similar, with high proportions of BDE-209 and the higher-brominated PBDEs. Also, our prey data (feathers from peregrine nests) showed urban peregrines having a higher proportion (>2 fold) of granivorous/opportunistic birds (e.g., "introduced feral" pigeons, mourning doves, starlings) in their diet than coastal peregrines. In summary, these data indicate that BDE-209 exits consumer products as an environmental contaminant to be taken up by wildlife (particularly in urban locations), and undergoes metabolic debromination to the banned lower-brominated PBDEs. High levels of the higher-brominated PBDE congeners, especially in urban locations, permitted accurate measures of relative proportions of homologues in each of the hexa-nona congener classes. Using the major hexa-nona homologues in each of these classes, we propose a pathway for the stepwise, metabolic debromination of BDE-209.

Epidemiologic methods only seldom identify causes of childhood cancer associated with relative risks below a factor of 1 1/2-2. Children are at risk of exposure to over 15,000 high-production-volume chemicals 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 factors are potentially important. Infants and children are exposed to higher levels of some environmental toxicants and may also be more sensitive. During intrauterine development and childhood, cells divide frequently, and the mutant frequency rises rapidly. Endocrine-related cancers or susceptibility to cancer 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 childhood cancers is indicated by associations of enzyme polymorphisms with risk.