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Different levels of polybrominated diphenyl ethers (PBDEs) and chlorinated compounds in breast milk from two UK regions.

Research output: Contribution to journalJournal articlepeer-review

<mark>Journal publication date</mark>07/2004
<mark>Journal</mark>Environmental Health Perspectives
Issue number10
Number of pages7
Pages (from-to)1085-1091
Publication StatusPublished
<mark>Original language</mark>English


Polybrominated diphenyl ether (PBDE) congeners are constituents of flame retardants, and there is growing concern regarding their persistence, bioaccumulation, and toxicity. We collected breast milk samples between late 2001 and early 2003 from 54 U.K.-resident mothers. Of these, 27 originated from southeast England (London) , and the other 27 originated from northwest England (Lancaster) . Analysis of milk-fat extracts by gas chromatography-mass spectrometry was performed to determine the levels of 15 PBDE congeners, 15 polychlorinated biphenyl (PCB) congeners, and other selected chlorinated compounds. PCB and organochlorine (OC) levels in southeast samples were consistently higher, and significant differences (p < 0.05) were observed. PBDE levels ranged from 0.3 to 69 ng/g lipid (geometric mean, 6.6 ng/g) , and PBDE-47 was the most abundant congener. PCB levels ranged from 26 to 530 ng/g lipid (geometric mean, 150 ng/g) and were composed mainly of PCB-153 (26%) , PCB-138 (20%) , and PCB-180 (13%) . OC levels for 1,1,1-trichloro-2,2-bis(p-chlorophenyl) ethane (p,p´-DDT) and its metabolites (DDX) ranged from 24 to 2,300 ng/g lipid (geometric mean, 160 ng/g) ; hexachlorobenzene ranged from nondetectable levels to 180 ng/g lipid (geometric mean, 17 ng/g) ; and hexachlorocyclohexane levels ranged from 1.2 to 1,500 ng/g lipid (geometric mean, 16 ng/g) . Using nuclear magnetic resonance-based metabonomics, samples (n = 7) containing the highest contaminant levels were compared with samples (n = 7) containing the lowest levels. Excellent separation along the first principal component implied that the chemical constituents of the two groups were significantly different. Although reasons for such differences remain obscure, lifestyle factors associated with a more heterogeneous London cohort could be responsible. Identifying primary routes of contaminant exposures and their biologic effects is of great importance.