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To reduce the exposure of the French West Indies population to the pollutant chlordecone (CLD), the contamination of consumed products must be reduced. One of the strategies to secure safe animal products is related to the depuration of contaminated animals. In order to set up this strategy in situ, characterizing CLD distribution and elimination appears to be essential. The aim of this study is to characterize CLD distribution and elimination in ewes, and establish correlations between CLD concentrations in tissues following a continuous oral contamination period and a depuration period. The experiment consisted in a 90-d period of CLD exposure via daily feeding at 0.01 mg kg−1 body weight, followed by a 127-d period of depuration. A total of 24 ewes were sequentially slaughtered and serum, liver, perirenal fat, subcutaneous fat, shaft muscle, longissimus dorsi muscle and heart samples were collected. CLD concentrations in serum and tissues were analyzed by GC-MS/MS and LC-MS/MS, respectively. Whatever the time of sampling, CLD concentrations in liver were significantly higher than in other collected tissues. However, the results showed that fat tissues stored the higher portion of CLD body burden, followed by muscle, liver, serum and heart. CLD half-lives did not differ significantly between tissues including serum and ranged between 20.2 ± 4.0 and 24.1 ± 4.9 d. Two linear models were developed to estimate CLD concentration in tissues from a blood sample. This study illustrates the theoretical methodology to estimate the time required to decontaminate farm animals from a blood sample.

International audience; The former use of chlordecone (CLD) in the French West Indies has resulted in long-term pollution of soils. In this area, CLD may be transferred into eggs of hens reared outdoors, through soil ingestion. In order to assess this risk, a kinetic study involving the contamination of laying hens (22 weeks of age) with a diet containing 500 mu g CLD kg(-1) during 42 d, followed by a depuration period of 35 d was carried out. Forty-four hens were sequentially slaughtered all over the experimental period and their liver, egg, abdominal fat and serum were collected. Two additional edible tissues, pectoral and leg muscles, were collected in hens slaughtered at the end of the contamination period. The depuration half-life of CLD in liver, egg, abdominal fat and serum was estimated at 5.0 +/- 0.38 (mean +/- SE), 5.5 +/- 0.29, 5.3 +/- 0.37 and 5.1 +/- 0.66 d, respectively. CLD concentration at the end of the contamination period reached 1640 +/- 274,460 +/- 41,331 +/- 23, and 213 +/- 8.5 mu g kg(-1) fresh matter (FM), respectively. The corresponding concentrations in pectoral and leg muscles were 119 +/- 8.4, 127 +/- 11 mu g kg(-1) FM, respectively. The steady state carry over rate of CLD in eggs reached 43 +/- 7.6%. This experiment demonstrates the preferential accumulation of CLD in liver, its significant transfer to eggs and its quite short half-life. It is concluded that raising hens on even mildly contaminated areas would lead to products exceeding the regulatory maximum residue limit of 20 mu g CLD kg(-1).

The aim of this study was to determine the tissue distribution of 17 PCDD/Fs following the chronic ingestion of contaminated milk in rats and to assess the "target tissue/milk" BioConcentration Factors (BCFs) of these molecules. Contaminated milk, collected in a polluted area, has been incorporated into the diet of male rats at a low dose (31 pg I-TEQ/day/rat). For this exposure, the accumulation of PCDD/Fs in target tissues (liver and adipose tissue) was limited, the tissue concentrations stabilising between 90 and 120 days of daily intake to levels close to 3 pg/g of tissue (all tissues and molecules combined). The tissue distribution seemed to be governed by the congeners properties and by the tissue characteristics. An increase in the chlorination degree of dioxins caused a decrease in their incorporation in the adipose tissue, and consequently of the BCF values. Moreover, the distribution of dioxins between hepatocytes and adipocytes differed: unlike the liver, the quantities of dioxins in the adipose tissue were significantly (P