Human adipose samples collected in Tokyo, Japan in 1970 and 2000 were analyzed for the presence of polybrominated dibenzo-p-dioxins (PBDDs), dibenzofurans (PBDFs), and diphenyl ethers (PBDEs), and the concentrations in the two groups were compared. As far as we know, the concentrations of the PBDD/Fs in adipose tissue from the general Japanese population are reported for the first time. Three PBDD/F congeners were found in the following adipose tissues: 2,3,7,8-TeBDD, 2,3,7,8-TeBDF, and 2,3,4,7,8-PeBDF. The median concentrations (ranges) of three PBDD/Fs in 1970 and 2000 were 5.1 (3.4-8.3) and 3.4 (1.9-5.3) pg/g lipid wt (l.w.), respectively. For PBDEs, seven PBDE congeners were determined in the following samples: 2,4,4'-tribromodiphenyl ether (BDE-28), 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), 2,2',4,4',5-pentabromodiphenyl ether (BDE-99), 2,2',4,4',6-pentabromodiphenyl ether (BDE-100), 2,2',4,4',5,5'-hexabromodiphenyl ether (BDE-153), 2,2',4,4',5',6-hexabromodiphenyl ether (BDE-154), and 2,2',3,4,4',5',6-heptabromodiphenyl ether (BDE-183). Median concentrations (ranges) of PBDEs showed a significant increase from 29.2 (6.8-78.4) pg/g l.w. in 1970 to 1288 (466-2,753) pg/g l.w. in 2000. BDE-47, the major congener of PBDEs, was 56.2% and 35.6% of the total in 1970 and 2000, respectively, whereas the BDE-153 was < 1% and 29.7% of the total in 1970 and 2000, respectively. This may indicate that the source of PBDEs had changed during this period. Further analysis of archived human samples from 1970 to 2000 is needed to describe the details of the contamination trends of PBDD/Fs and PBDEs in the Japanese population. Furthermore, PBDD/F monitoring, particularly 2,3,7,8-TeBDD and 2,3,7,8-TeBDF, may give more toxicological information based on TeCDD toxic equivalents (TEQs).

Neonicotinoids, a widely used group of pesticides designed to selectively bind to insect nicotinic acetylcholine receptors, were considered relatively safe for mammalian species. However, they have been found to activate vertebrate nicotinic acetylcholine receptors and could be toxic to the mammalian brain. In the present study, we evaluated the developmental neurotoxicity of acetamiprid (ACE), one of the most widely used neonicotinoids, in C57BL/6J mice whose mothers were administered ACE via gavage at doses of either 0 mg/kg (control group), 1.0 mg/kg (low-dose group), or 10.0 mg/kg (high-dose group) from gestational day 6 to lactation day 21. The results of a battery of behavior tests for socio-sexual and anxiety-related behaviors, the numbers of vasopressin-immunoreactive cells in the paraventricular nucleus of the hypothalamus, and testosterone levels were used as endpoints. In addition, behavioral flexibility in mice was assessed in a group-housed environment using the IntelliCage, a fully automated mouse behavioral analysis system. In adult male mice exposed to ACE at both low and high doses, a significant reduction of anxiety level was found in the light-dark transition test. Males in the low-dose group also showed a significant increase in sexual and aggressive behaviors. In contrast, neither the anxiety levels nor the sexual behaviors of females were altered. No reductions in the testosterone level, the number of vasopressin-immunoreactive cells, or behavioral flexibility were detected in either sex. These results suggest the possibility that in utero and lactational ACE exposure interferes with the development of the neural circuits required for executing socio-sexual and anxiety-related behaviors in male mice specifically.

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