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PubMed2001

Food contamination monitoring in Croatia.

The Croatian National Institute of Public Health Implements the statistical food safety monitoring programme for foods marketed in Croatia in accordance with effective laws and regulations. Laboratories for food safety control, certified by the Ministry of Health, report their findings in quarterly notifications, using the standard forms and issue statements of compliance or non-compliance with current regulations, specifying the cause in case of the latter. This paper brings the results for the period 1993-99 as an illustration of the monitoring programme.

Croatia↗
PubMed2000

Chronic ingestion of a potential food contaminant induces gastrointestinal inflammation in rats: role of nitric oxide and mast cells.

Chronic ingestion of xenobiotics could be pathogenic in the gastrointestinal tract. Recently, we showed that acute low administration of a food contaminant (diquat) induced intestinal secretion involving mast cells and nitric oxide. This work aimed to determine in rats: (1) the influence of a low level (0.1 mg/kg/day per os) chronic ingestion of diquat on gastrointestinal immune cells, and (2) the participation of nitric oxide synthases (NOS) in these effects. Diquat increased both gastric and jejunal myeloperoxidase activities, tissue histamine in vitro release after stimulation by 48/80, and mast cell numbers. Diquat did not alter gastric NOS but increased intestinal inducible NOS (iNOS) activity. L-NAME prevented diquat-induced gastric and intestinal mastocytosis and gastric but not intestinal inflammation. L-NAME reduced gastric constitutive NOS (cNOS) activity and reestablished control iNOS activity. Chronic low level ingestion of diquat induces a low-grade gastric and intestinal inflammation with mastocytosis and enhancement of intestinal iNOS activity.

Animals↗
PubMed2002

Pathways involved in mild gastrointestinal inflammation induced by a low level exposure to a food contaminant.

Chronic gut inflammation is associated with radical oxygen species (ROS) genesis. ROS may activate certain transcription factors such as nuclear factor kappa beta (NF-kappaB), which regulates cyclooxygenase-2 (COX-2). Diquat, a food contaminant, is responsible for oxidative stress. This work aimed to establish the involvement of ROS and prostanoids on diquat-induced gastrointestinal inflammation and mast cell hyperplasia. Diquat increased gastrointestinal MPO activity and mast cell number. Its effect on gastric MPO activity was reversed by PD 138,387 (a COX-2 selective inhibitor) and PDTC (an inhibitor of NF-kappaB activation) but not by DMSO (a hydroxyl radical scavenger) and allopurinol (a xanthine oxidase inhibitor). In contrast, increased jejunal MPO activity was blocked by both DMSO, PD 138,387, and PDTC, while allopurinol enhanced it. PD 138,387 and PDTC reduced gastrointestinal mast cell number while DMSO and allopurinol did not Diquat-induced inflammation involves a gastrointestinal NF-kappaB activation and COX-2 dependent proinflammatory prostanoid synthesis. Furthermore, the hydroxyl radical is involved in intestinal but not gastric inflammation.

Animals↗
PubMed2002

Probabilistic intake assessment and body burden estimation of dioxin-like substances in background conditions and during a short food contamination episode.

The objective was to perform a dioxin body burden estimate based on a probabilistic intake assessment of PCDDs, PCDFs and dioxin-like PCBs because of the so-called 1999 'Belgian dioxin incident'. Monte Carlo simulation techniques were used to combine detailed 7-day food intake data on the individual level from a sample of 14-18-year-old adolescents with 'background' and 'incident-related' food contamination data. In background conditions, 3% of the adolescents had an intake <1 pg TEQ kg(-1) bw day(-1), while 85% had <4 pg TEQ kg(-1) bw day(-1). Milk and other dairy products were the basic source of dioxin-like contaminants, while fish constituted the main source at the higher percentiles of intake. During the dioxin incident, the estimated median dioxin intake showed a moderate increase. At the 99th percentile, the highest intake level, and the 95% upper bound uncertainty level, peak body burden-23.73 ng TEQ kg(-1) bw-remained below body burdens that in the experimental animal or in man are accompanied by a population-based observable increase in the incidence of adverse effects. The 1999 Belgian dioxin incident most likely did not affect public health in Belgium in a measurable way, although exceptions remain possible on the individual level.

Adolescent↗
PubMed1986

Enumeration by DNA colony hybridization of virulent Yersinia enterocolitica colonies in artificially contaminated food.

A genetic probe was used to identify and enumerate virulent Yersinia enterocolitica colonies in 11 artificially contaminated foods. Efficiency of enumeration, determined by autoradiography after DNA colony hybridization, ranged from 66 to 100% (average, 86%) and was influenced by the number of indigenous bacteria. The use of nitrocellulose filters and agar medium had little effect on efficiency of enumeration.

Aerobiosis↗
PubMed1994

National food contamination monitoring programmes-levels of mercury, lead and cadmium in Chinese foods.

Six hundred and thirty-four food samples of six kinds were collected from Beijing, Shanghai, Jiangsu, Sichuan, Jilin and Guangdong areas, China and Hg, Pb, Cd contents were determined. The results showed that their levels in the Chinese foods were low; their levels in meat, egg, milk and fish were generally below the national hygienic standard. The average daily dietary intake of Hg, Pb, Cd were 7.25 micrograms, 103.77 micrograms and 30.72 micrograms respectively and they were all less than the ADI established by WHO.

Adult↗
PubMed2004

The role of aflatoxin-contaminated food materials and HCV in developing hepatocellular carcinoma in Al-Sharkia Governorate, Egypt.

Aflatoxins, particularly aflatoxin B1 (AFB1) have been recognized as one of the most potent chemical carcinogen. In Egypt, HCV is prevalent. The progressive nature of HCV-related liver diseases was found to be influenced by other factors. In this paper, the role of aflatoxin contamination in the onset of liver cancer in HCV-infected patients was studied. The quantitative identification of the possible aflatoxins contamination in six urban and eleven rural areas using high performance liquid chromatography technique, revealed that corn, wheat, pea nut, lupine "termis", white rice, cowpea "lobiya", fava bean and brown rice showed the prevalence of AFB1 to be 64.7%, 53%, 53%, 47%, 47%, 41%, 29.4% & 29.4% respectively. A positive correlation was found between aflatoxin and positive HCV-PCR together with liver disease progression to G3S3, the indicative of hepatocellular carcinoma. Such correlation was not fully understood, but the oncogene amplification caused by HCV-infection may be aggravated by the consumption of aflatoxin contaminated raw food materials or their products.

Aflatoxins↗