Dietary intake patterns and relationships to polybrominated diphenyl ether (PBDE) and phthalate body burden

Polybrominated diphenyl ethers (PBDEs) and phthalates are chemicals of concern because of high levels measured in people and the environment as well as the demonstrated toxicity in animal studies and limited epidemiological studies. Exposure to these chemicals has been associated with a range of toxicological outcomes, including developmental effects, behavioral changes, endocrine disruption, effects on sexual health, and cancer. Previous research has shown that both of these classes of chemicals contaminate food in the United States and worldwide. However, how large a role diet plays in exposure to these chemicals is currently unknown. To address this question, an exploratory analysis of data collected as part of the 2003-04 National Health and Nutrition Examination Survey (NHANES) was conducted. Associations between dietary intake (assessed by 24-hour dietary recalls) for a range of food types (meat, poultry, fish, and dairy) and levels PBDEs and phthalate metabolites were analyzed using multiple linear regression modeling. Levels of individual PBDE congeners 28, 47, 99, 100 as well as total PBDEs were found to be significantly associated with the consumption of poultry. Metabolites of di-(2-ethylhexyl) phthalate (DEHP) were found to be associated with the consumption of poultry, as well as with an increased consumption of fat of animal origin. These results, combined with results from previous studies, suggest that diet is an important route of intake for both PBDEs and phthalates. Further research needs to be conducted to determine the sources of food contamination with these toxic chemicals as well as to describe the levels of contamination of US food in a large, representative sample.^

THE RECOVERY OF ENTEROPATHOGENS FROM CONTAMINATED COOKED FOODS AT HOLDING TEMPERATURES

Hot foods served in foodservice establishments, institutions and homes, have always been regarded as safe, since cooking temperatures are more likely to kill the bacterial agents that may cause foodborne diseases. However, foods that are otherwise served hot have been epidemiologically incriminated for causing foodborne diseases. This situation arises due to the possible post-cooking food contamination. Post-cooking contamination of hot-held food is most threatening for it gives the contaminating agents the possibility of proliferation. On one hand, post-cooking contamination is least understood and on the other, hot-holding of food gives the consumer a false sense of freedom from foodborne diseases. In this study, the dynamics of food contamination before or after cooking and during hot-holding are discussed and a food contamination dynamics model is presented.^ The literature on foodborne cholera, cholera-like diarrhea, shigellosis and E. coli gastroenteritis together with the literature on the occurrence and growth of the causative enteropathogens; 01 V. cholerae, non-01 V. cholerae, S. sonnei, S. flexneri and E. coli were reviewed. The literature on the infective doses of these organisms were also cited.^ In the study, four cooked food types held hot at 40-60(DEGREES)C were deliberately contaminated with 01 V. cholerae, non-01 V. cholerae, S. sonnei, S. flexneri and E. coli, one at a time at each of the hot-holding temperatures. Tested food samples for the recovery of these enteropathogens were withdrawn at various time intervals of hot holding.^ The results showed bacterial recovery to decline with increasing temperature and with increasing hot-holding time within each holding temperature. All the bacterial types except V. cholerae were recovered even after holding the food at 60(DEGREES)C for one hour. V. cholerae was not recovered after hot-holding the food at 50-60(DEGREES)C at certain holding periods. After 48 hrs incubation, V. cholerae was recovered on TCBS agar plates that read negative after the initial 24 hrs of incubation. Effective hot-holding temperatures were determined for each of the food types contaminated by each of the bacterial types.^ Statistical analysis of the collected data showed temperature, bacterial type and their interaction to be significant in enteropathogen recovery. Food type and its interactions with temperature and bacterial type were found not significant. ^

Experimental models for p53, hepatitis B and aflatoxin hepatocarcinogenesis

The major risk factors for liver cancer in Southeast Asia: HBV infection, aflatoxin exposure and p53 expression/mutation, were examined in experimental models. Four groups were examined for development of hepatocellular carcinoma (HCC) with and without neonatal exposure to aflatoxin (AFB$\sb1)$: (Group I.) Transgenic HBsAg mice with one p53 allele. (Group II) Transgenic HBsAg mice with two p53 alleles. (Group III) Non-transgenic litter mates with one p53 allele. (Group IV) Non-transgenic litter mates with two p53 alleles. HCC developed in Group I animals exposed to aflatoxin at an earlier time and were of a higher grade than those seen later in other groups. These results provide an explanation for as to why p53 is a target for deletion and/or mutation in human HCC especially when found in high risk areas where HBV infection and Aflatoxin B1 food contamination is high, and nicely illustrates a synergistic interaction among these three factors. None of the tumors analyzed had loss or mutation in the p53 gene.^ To determine the significance of the specific p53ser249 mutation found in HBV/aflatoxin associated human hepatomas in an in-vivo experimental model using transgenic mice, a two-nucleotide change in the mouse p53 gene at amino acid position 246, which is equivalent to that of 249 in human p53, was introduced. Transgenic mice with mutant p53 controlled by the albumin promoter were generated and shown to express the p53ser246 mutant RNA and protein specifically in liver. Three groups were examined for development of HCC with and without neonatal exposure to aflatoxin: (Group V) Transgenic p53ser246 mice with two p53 alleles. (Group VI) Transgenic p53ser246 mice with one p53 allele. (Group VII) Double transgenic for p53ser246 and HBsAg with two p53 alleles. One hundred percent of male mice with the three risk factors injected with aflatoxin developed high grade liver tumors, compared to 66.6% from group VI and only 14.2% of group V suggesting synergistic interaction between HBsAg and this particular ser246 p53 mutation.^ In order to examine the growth properties of hepatocytes and correlation with p53 loss and/or mutation, cell proliferation and ploidy analysis of liver from normal heterozyous, homozygous null mice and from transgenic mutant p53ser246, mice were studied. Loss of wild-type p53 increased G1/G0 ratios of cells as well as proliferation and decreased cell ploidy. The mutant p53ser246 did not show a significant effect on cell ploidy or proliferation. However a striking 5-10X increase in G1/G0 ratio suggests that this specific mutation specifically induces G0 to G1 transition, which in turn further predisposes hepatocytes to the damaging effect of Aflatoxin. (Abstract shortened by UMI.) ^