Analysis of breast milk to assess exposure to chlorinated contaminants in Kazakstan: high levels of 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) in agricultural villages of southern Kazakstan.

Abstract

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 World Health Organization protocol from 92 donors that were representative of 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 now been confirmed by three analytical laboratories.ImagesFigure 1Figure 2Figure 3Figure 4

Induction of the transferrin receptor gene by benzo[a]pyrene in breast cancer MCF‐7 cells: Potential as a biomarker of PAH exposure

“…However, our results cannot rule out the possibility that B[a]P-induced TfR expression may be due, at least in part, to induction of reactive oxygen species, a known byproduct of PAH metabolism [Penning et al, 1996;Glaze et al, 2001]. Although it could be argued that the concentrations of B[a]P used in these and other [Gwinn et al, 2005] studies may not occur in the human breast, the possibility exists that acute exposure to individual PAHs or complex mixtures [Hooper et al, 1998;Weiss et al, 2003] with various binding affinities for the AhR [Piskorska-Pliszczynska et al, 1986] combined with genetic polymorphisms in activation and detoxifying enzymes [Landi et al, 1999] may facilitate accumulation of PAHs in breast tissue at levels sufficient to alter TfR expression.…”

Mouse breast cancer model-dependent changes in metabolic syndrome-associated phenotypes caused by maternal dioxin exposure and dietary fat

“…At PND 0, body mass was determined by dividing the total litter mass by the number of pups within the litter. Individual body masses were evaluated at PND 4,7,10,14,21,35,49,63,90,120,150,180,210,240,270, 300, and 330. At PND 35,90, and 180, all mice were placed under isoflourane anesthesia for ϳ5 min while undergoing dual-energy X-ray absorptiometry (DEXA; GE Lunar PIXImus, Madison, WI) to evaluate percent body fat.…”

“…Longitudinal models are depicted per diet with 95% confidence intervals, and diet-based mean is plotted for LFD (E) and HFD (F). For body weight measurement at PND 0, 4,7,10,14,18,21,28,35,49,63,90,120,150,180,210,240,270 Germany), and luciferase activity in each well was measured over 10 s after a 2-s delay following automatic injection of 50 l Promegastabilized luciferase reagent (15,39,50). Luciferase activity in each well was expressed relative to the maximal inducing concentration of the respective positive control (E 2, DHT, or TCDD).…”

“…In A-C, longitudinal models are depicted per diet with 95% confidence intervals, and diet-based mean is plotted for LFD (E) and HFD (F). For body weight measurements at PND 0, 4,7,10,14,18,21,28,35,49 Age at maximum growth rate, PND 18.9 (0.45)* 17.6 (0.41)*…”

“…Individuals that have metabolic syndrome or that are obese usually have higher consumption of fatty foods from animal origin, which is associated with a greater body burden of lipophilic endocrine disruptors such as 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD) (16,18,21,34). Elimination of TCDD is slowed substantially as body fat increases (10,32).…”