Polybrominated diphenyl ethers (PBDEs) are used as flame retardants in plastics (concentration, 5--30%) and in textile coatings. Commercial products consist predominantly of penta-, octa-, and decabromodiphenyl ether mixtures, and global PBDE production is about 40,000 tons per year. PBDEs are bioaccumulated and biomagnified in the environment, and comparatively high levels are often found in aquatic biotopes from different parts of the world. During the mid-1970--1980s there was a substantial increase in the PBDE levels with time in both sediments and aquatic biota, whereas the latest Swedish data (pike and guillemot egg) may indicate that levels are at steady state or are decreasing. However, exponentially increasing PBDE levels have been observed in mother's milk during 1972--1997. Based on levels in food from 1999, the dietary intake of PBDE in Sweden has been estimated to be 0.05 microg per day. Characteristic end points of animal toxicity are hepatotoxicity, embryotoxicity, and thyroid effects as well as maternal toxicity during gestation. Recently, behavioral effects have been observed in mice on administration of PBDEs during a critical period after birth. Based on the critical effects reported in available studies, we consider the lowest-observed-adverse-effect level (LOAEL) value of the PBDE group to be 1 mg/kg/day (primarily based on effects of pentaBDEs). In conclusion, with the scientific knowledge of today and based on Nordic intake data, the possible consumer health risk from PBDEs appears limited, as a factor of over 10(6) separates the estimated present mean dietary intake from the suggested LOAEL value. However, the presence of many and important data gaps, including those in carcinogenicity, reproduction, and developmental toxicity, as well as additional routes of exposure, make this conclusion only preliminary. Moreover, the time trend of PBDEs in human breast milk is alarming for the future.

Polybrominated diphenyl ethers (PBDEs) are used as flame retardants in plastics (concentration, 5--30%) and in textile coatings. Commercial products consist predominantly of penta-, octa-, and decabromodiphenyl ether mixtures, and global PBDE production is about 40,000 tons per year. PBDEs are bioaccumulated and biomagnified in the environment, and comparatively high levels are often found in aquatic biotopes from different parts of the world. During the mid-1970--1980s there was a substantial increase in the PBDE levels with time in both sediments and aquatic biota, whereas the latest Swedish data (pike and guillemot egg) may indicate that levels are at steady state or are decreasing. However, exponentially increasing PBDE levels have been observed in mother's milk during 1972--1997. Based on levels in food from 1999, the dietary intake of PBDE in Sweden has been estimated to be 0.05 microg per day. Characteristic end points of animal toxicity are hepatotoxicity, embryotoxicity, and thyroid effects as well as maternal toxicity during gestation. Recently, behavioral effects have been observed in mice on administration of PBDEs during a critical period after birth. Based on the critical effects reported in available studies, we consider the lowest-observed-adverse-effect level (LOAEL) value of the PBDE group to be 1 mg/kg/day (primarily based on effects of pentaBDEs). In conclusion, with the scientific knowledge of today and based on Nordic intake data, the possible consumer health risk from PBDEs appears limited, as a factor of over 10(6) separates the estimated present mean dietary intake from the suggested LOAEL value. However, the presence of many and important data gaps, including those in carcinogenicity, reproduction, and developmental toxicity, as well as additional routes of exposure, make this conclusion only preliminary. Moreover, the time trend of PBDEs in human breast milk is alarming for the future.

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In this study, the modulation of aflatoxin B 1 (AFB 1 ) uptake in rats by administration of the probiotic Lactobacillus rhamnosus GG was demonstrated. Fecal AFB 1 excretion in GG-treated rats was increased via bacterial AFB 1 binding. Furthermore, AFB 1 -associated growth faltering and liver injury were alleviated with GG treatment.Aflatoxins are toxic and carcinogenic fungal metabolites that frequently contaminate staple crops (1). Interventions in aflatoxin exposure focus either on improving crop quality and storage (20) or on altering aflatoxin bioavailability on the individual level, using various adsorbents (5, 18). However, no safe means are presently available to completely protect humans from aflatoxin exposure. Our previous work with lactic acid bacteria revealed that the probiotic strain Lactobacillus rhamnosus strain GG (ATCC 53013) efficiently binds several mycotoxins, including aflatoxin B 1 (AFB 1 ) and aflatoxin M 1 (AFM 1 ), its hydroxylated metabolite, in vitro (6,7,9,10,19). Even though heat-killed bacteria have the highest binding capacities, most studies use viable bacteria, which are more relevant in probiotic products intended for human consumption. Acid, intestinal enzymes, and intestinal mucus were shown not to interfere with AFB 1 binding of this probiotic (6,7,11,12). GG was subsequently demonstrated to bind AFB 1 and to reduce its uptake into intestinal tissue in the ligated duodenal loops of 1-week-old chicks (8). However, this ex vivo method has its limitations in simulating intestinal conditions, and we therefore conducted an in vivo single-dose experiment in rats, investigating the effects of GG on AFB 1 absorption and toxic effects. Five-week-old Han-Wistar rats were kept individually in metabolic cages on standard powdered feed and water ad libitum. After acclimatization, the rats (n ϭ 12/group) received either vehicle (phosphate-buffered saline [PBS]) or probiotic suspension (5 ϫ 10 10 CFU GG/0.5 ml PBS, prepared by directly suspending lyophilized bacteria in PBS) by oral gavage daily for 3 days before and 3 days after a single oral dose of AFB 1 (1.5 mg or 4.8 mol/kg of body weight in dimethyl sulfoxide [Sigma-Aldrich, St. Louis, Mo.]). Four additional rats served as untreated controls. Body weight was recorded at the beginning of the study (prior to GG treatment), on the day of AFB 1 dosing, and at the end of the study. Urine and fecal samples were collected daily, weighed, and stored at Ϫ20°C. At the end of the study, blood samples were taken by cardiac puncture and centrifuged, and the plasma was stored at Ϫ20°C. The experiments were approved by the University of Kuopio animal ethics committee.Extraction of fecal samples was modified from a method developed in our laboratory (17). The samples were mixed with 2.5 volumes of 0.2 M sodium acetate in 10% NaCl, and aliquots (2 ml) were spiked with aflatoxin G 2 (AFG 2 ) (18.6 pmol/sample) as an internal standard and centrifuged (3,000 ϫ g; 15 min; 4°C). The pellets were suspended in 4 ml 80% methanol (in 10% NaCl [vol/vol]) and h...

Polychlorinated dibenzo-p-dioxins (PCDDs) are highly toxic environmental contaminants, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent dioxin. Here, we studied the effects of TCDD on bone. Two rat strains, Han/Wistar (H/W) and Long-Evans (L-E), were used because they exhibit a 1000-fold sensitivity difference in acute lethality of TCDD, which difference is related to the aryl hydrocarbon receptor (AHR). TCDD inhibited the tibial growth dose dependently, the effect being manifested at lower doses in the more sensitive L-E strain. In H/W rats the effect of TCDD was seen only at the high dose of 170 microg/kg (p < 0.05), whereas in the sensitive L-E rats a significant reduction of bone growth was already seen at 1.7 microg/kg (p < 0.01). This reduction was caused by the smaller tibial size because the diaphyseal bone mineral density (BMD) did not change. The three-point bending breaking force of the tibia was significantly reduced in H/W rats at 170 microg/kg (p < 0.05), but tibial stiffness was lower already at the dose of 17 microg/kg (p < 0.05). In the sensitive L-E strain, both breaking force and stiffness were reduced at the dose of 17 microg/kg (p < 0.001). These results indicate that TCDD dose-dependently interferes with bone growth, modeling, and mechanical strength. The altered transactivation domain of AHR is associated with a lower sensitivity of bone to TCDD in H/W rats, suggesting that AHR plays a role in modulating the effects of dioxins on bone.