著者

Mitsuru Yoshida Marino Isamu Kazuhiro Chiku

出版者

Food Safety Commission, Cabinet Office, Government of Japan

雑誌

Food Safety (ISSN:21878404)

巻号頁・発行日

vol.5, no.2, pp.54-60, 2017 (Released:2017-06-30)

参考文献数

16

被引用文献数

5

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Acrylamide has neurotoxicity, carcinogenicity, and genotoxicity in experimental animals and cellular systems. Fried potato is one of the major intake sources of acrylamide in food, and fried onion was reported to contain up to 100 ng/g level of acrylamide. To determine acrylamide concentration in potato and onion stir-fried prior to boiling for simmered dishes such as curry, stew, and Niku-jaga, a typical Japanese meat/potato/onion cuisine, we collected samples stir-fried at homes of volunteers who intended voluntarily to cook these simmered dishes. Acrylamide level was analyzed by GC-MS after the xanthydrol derivatization. Among 53 stir-fried potato samples, median and average values of acrylamide were found to be 2.0 ng/g and 11 ng/g, respectively. Acrylamide levels of 27 samples (51%) were less than limit of detection (LOD) (4 ng/g), and those of 13 samples (25%) were less than limit of quantification (LOQ) (10 ng/g). In cases with less than LOD and less than LOQ of acrylamide levels, one-half of LOD and average of LOD and LOQ were adopted, respectively, to calculate the median and average. This median was markedly lower than those of fried potato (180 ng/g) and potato snacks including potato chips (550 ng/g) reported in monitoring in 2013 fiscal year in Japan. Among 58 stir-fried onion samples, acrylamide level of only one sample (2%) was less than LOD (3 ng/g), and those of 15 samples (26%) were less than LOQ (8 ng/g). The median and average values in the stir-fried onion were 14 ng/g and 36 ng/g, respectively. These values are comparable to those for stir-fried onion reported by Ministry of Agriculture, Forestry and Fisheries, Japan (median 19 ng/g, average 25 ng/g). But the maximum value of stir-fried onion 420 ng/g in the present study is much higher than the reported maximum value (70 ng/g).

著者

Ann Abraham Kathleen R. El Said Leanne J. Flewelling

出版者

Food Safety Commission, Cabinet Office, Government of Japan

雑誌

Food Safety (ISSN:21878404)

巻号頁・発行日

vol.6, no.1, pp.33-43, 2018 (Released:2018-03-30)

参考文献数

46

被引用文献数

6

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Monitoring and management programs for marine toxins in seafood depend on efficient detection tools for their success in protecting public health. Here we review current methods of detection for neurotoxic shellfish poisoning (NSP) toxins, and current knowledge in brevetoxin metabolism in shellfish. In addition, we discuss a novel approach to developing monitoring tools for NSP toxins in molluscan shellfish. NSP is a seafood-borne disease caused by the consumption of brevetoxin-contaminated shellfish. Brevetoxins are a suite of cyclic polyether compounds found in blooms of the marine dinoflagellate Karenia brevis (K. brevis) and are potent neurotoxins. Preventive controls for NSP in the U.S. currently rely upon environmental monitoring of K. brevis blooms and assessment of their shellfish toxicity by mouse bioassay. The mouse bioassay for NSP approved by National Shellfish Sanitation Program was developed in the 1960s when very little information on the structural and toxicological properties of brevetoxins in algae and shellfish was available. Alternative methods to mouse bioassay based on current scientific knowledge in the area are needed for monitoring NSP toxins. It is now established that brevetoxins are metabolized extensively in shellfish. Algal brevetoxins undergo oxidation and reduction, as well as conjugation with fatty acids and amino acids in shellfish. Recently, three metabolites have been identified as biomarkers of brevetoxin exposure and toxicity in Eastern oyster (Crassostrea virginica) and hard clam (Mercenaria sp.). The role of these biomarkers in monitoring NSP toxins in K. brevis exposed molluscan shellfish is reviewed. Comparisons of biomarker levels by liquid chromatography-mass spectrometry (LC-MS) with composite toxin as measured by enzyme linked immunosorbent assay (ELISA), and shellfish toxicity by mouse bioassay, support the application of these biomarkers as a dynamic and powerful approach for monitoring brevetoxins in shellfish and prevention of NSP.

著者

Zachary Marsh Minesh P. Shah Mary E. Wikswo Leslie Barclay Hannah Kisselburgh Anita Kambhampati Jennifer L. Cannon Umesh D. Parashar Jan Vinjé Aron J. Hall

出版者

Food Safety Commission, Cabinet Office, Government of Japan

雑誌

Food Safety (ISSN:21878404)

巻号頁・発行日

pp.2017028, (Released:2018-05-25)

参考文献数

32

被引用文献数

32

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Noroviruses are the leading cause of acute gastroenteritis and foodborne disease in the United States (U.S.). About 1 in 5 reported norovirus outbreaks are spread through foodborne transmission, presenting opportunities for prevention. We describe the epidemiology of U.S. foodborne norovirus outbreaks reported to national surveillance systems, including differences between genotypes. Foodborne outbreaks that occurred during August 2009–July 2015 with norovirus reported as a single confirmed etiology to the National Outbreak Reporting System (NORS) were matched with outbreaks reported to CaliciNet, a U.S. laboratory norovirus outbreak surveillance network. We analyzed these matched outbreaks stratified by genotype for epidemiologic characteristics, including setting, size and duration, health outcomes of case-patients, implicated food, and outbreak contributing factors. Four hundred ninety-three confirmed foodborne norovirus outbreaks were reported in both NORS and CaliciNet. The most common norovirus genotypes reported were GII.4 (52%), GII.6 (9%), and GI.3 (8%). Compared to non-GII.4 outbreaks, GII.4 outbreaks had higher hospitalization rates (12.8 vs. 4.8 per 1,000 cases, P < 0.01). While contaminated foods were identified and reported in only 35% of outbreaks, molluscan shellfish (4% overall) were more often implicated in non-GII.4 outbreaks than in GII.4 outbreaks (7% vs. 1%, P = 0.04). Of the 240 outbreaks reporting at least one contributing factor, food workers were implicated as the source of contamination in 182 (76%), with no difference between GII.4 and non-GII.4 (73% vs 79%, P = 0.3). Foodborne norovirus outbreaks are frequently reported in the U.S., most of which are caused by GII.4 noroviruses. Viruses of this genotype are associated with higher rates of hospitalization; non-GII.4 noroviruses are more frequently associated with contaminated molluscan shellfish. These surveillance data highlight the diversity of noroviruses causing foodborne disease and can help guide appropriate food safety interventions, including worker hygiene, improved food handling and preparation, and further development of norovirus vaccines.

著者

Justin J. Greenlee Robert A. Kunkle Jodi D. Smith M. Heather West Greenlee

出版者

内閣府食品安全委員会

雑誌

Food Safety (ISSN:21878404)

巻号頁・発行日

vol.4, no.4, pp.110-114, 2016 (Released:2016-12-22)

参考文献数

33

被引用文献数

8

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A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. We conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Scrapie inoculum was a pooled 10% (w/v) homogenate derived from the brains of clinically ill sheep from the 4th passage of a serial passage study of the U.S scrapie agent (No. 13–7) through susceptible sheep (homozygous ARQ at prion protein residues 136, 154, and 171, respectively). Pigs were inoculated intracranially (n=19) with a single 0.75 mL dose or orally (n=24) with 15 mL repeated on 4 consecutive days. Necropsies were done on a subset of animals at approximately six months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease (primarily lameness). Brain samples were examined by immunohistochemistry (IHC), western blot (WB), enzyme immunoassay (EIA), and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At six-months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more methods: IHC (n=4), WB (n=3), or EIA (n=4). Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie.

著者

Yasuhisa Ano Akikazu Sakudo Ryuta Uraki Juri Kono Masayoshi Yukawa Takashi Onodera

出版者

内閣府食品安全委員会

雑誌

Food Safety (ISSN:21878404)

巻号頁・発行日

vol.1, no.1, pp.2013005-2013005, 2013 (Released:2013-11-20)

参考文献数

51

被引用文献数

3

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Infectious prion diseases include Kuru and its variant, Creutzfeldt-Jakob disease, in humans, scrapie in sheep, and bovine spongiform encephalopathy in cattle. In these diseases, the pathogenic prion protein (PrPSc) enters the host through the gastrointestinal tract and migrates to the central nervous system, where PrPSc induces characteristic pathological changes. The mechanisms underlying this intercellular transfer are not fully understood. After oral administration, PrPSc withstands the digestive process and may be incorporated by microfold cells (M cells) or villous columnar epithelial cells in the intestine. Based on Western Blot with specific markers, liquid chromatography, and morphological analysis, the cellular prion protein (PrPC) and PrPSc in the cells are associated with exosomes, membranous vesicles that are secreted upon fusion of multivesicular endosomes with the plasma membranes. Exosomes may play a role in PrP transportation through intestinal epithelium. Cells may exploit the nature of endosome-derived exosomes to communicate with each other in normal and pathological situations, providing for a novel route of cell-to-cell communication and therefore of pathogen transmission in the intestinal epithelium. In addition, since most bovine spongiform encephalopathy cases were exposed to the agent in the first six months of life, developmental alteration of the intestinal defense and immune system may also be involved in the susceptibility to infection.