[RADIOACTIVE CONTAMINATION BY FALLOUT IN FOODS. II. CONTAMINATION BY SR 90 IN FOODS SAMPLED IN THE MUNICIPALITY OF BERGAMO DURING THE YEAR 1963].
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Contamination of food products with pepsin resistant allergens is generally believed to be a serious threat to patients with severe food allergy. A sandwich type enzyme-linked immunosorbent assay (ELISA) was developed to measure pepsin resistant hazelnut protein in food products. Capturing and detecting rabbit antibodies were raised against pepsin-digested hazelnut and untreated hazelnut protein, respectively. The assay showed a detection limit of 0.7 ng/mL hazelnut protein or <1 microg hazelnut in 1 g food matrix and a maximum of 0.034% cross-reactivity (peanut). Chocolate samples spiked with 0.5-100 microg hazelnut/g chocolate showed a mean recovery of 97.3%. In 9/12 food products labeled "may contain nuts", hazelnut was detected between 1.2 and 417 microg hazelnut/g food. It can be concluded that the application of antibodies directed to pepsin-digested food extracts in ELISA can facilitate specific detection of stable proteins that have the highest potential of inducing severe food anaphylaxis.
"Dioxins" are used to specify polychlorinated dibenzo-p-dioxins (PCDD), dibenzo-furanes (F) and dioxin-like polychlorinated biphenyls (PCB's). Many of the congeners proved to be highly toxic; 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) is the most toxic congener, and probably the most toxic compound ever synthesized by man (the natural occurance of this substance is very low). The total concentration/-toxicity of a mixture of congeners (WHO-PCDD/F-TEQ, or including the PCB's WHO-PCDD/F-PCB-PCB-TEQ) is calculated by addition of the individual concentrations multiplied by respective toxicity equivalence factors TEF; the most toxic congener TCDD is defined as 1. The tolerable weekly intake TWI set by the European Commission is 14pg WHO-PCDD/F-TEQ/kg bw. The "body burden" of adults in industrial countries is about 2-6 ng WHO-PCDD/F-TEQ/kg bw., or about double this value if PCB's are also considered. There is a very broad range of toxic effects of "dioxins". Many of the congeners can induce toxic responses at very low "body burdens". The most sensitive effects are immunosuppression, developmental and reproductive toxicity, as well as neurological behavioral effects. These effects occur at "body burdens" whih are close to background exposure of the human. Cancerogenic effects are induced at higher exposure (Seveso, industrial exposure). TCDD was considered a "complete carcinogen" by the IARC (Group 1). There is a broad range of carcinogenic effects, and there is no "hallmark" effect. Most toxic effects induced by TCDD are mediated by binding to the Ah-receptor (Ah-R) which binds together with a second protein, ARNT, to the respone elements of a number of target genes, and thus modulates gene expression. "Dioxins" are strong promotors, but weak initiators. The multitude of interactions of the Ah-R and ARNT ("receptor cross-talk") results in numerous molecular and cellular effects. The TCDD-Ah-R complex can also bind to the response element of the estrogen receptor, and thus can block the effects of es-trogens. This explains the fact that TCDD can be an estrogen antagonist reducing or preventing mamma carcinoma. Other Ah-R ligands occur in vegetables (e.g. indoles, flavones) and will possibly be developed in the future as functional substances. PCB's have similar properties to TCDD if they can exist in a planar configuration (dioxin-like PCB's). The non-dioxin-like PCB's always occur together with "dioxins"; their toxixty cannot be adequately determined although they occur in high concenrations. The consumption of food contaminated with "dioxins" need not directly lead to a toxic effect. Due to the continous cumulation of "dioxins" repeated ingestion of contaminated food could result in an increase of the "body burden" and thus chronic toxicity. This shows that the exposure of the human to dioxins should be minimized wherever possible.
In conjunction with the programme of monitoring the food contamination by one of the most widely distributed contaminants--phthalic acid esters--the present investigation was focused on the elucidation of metabolic transformations of phthalates in the organism of the rat and humans and on assessment of the phthalate content of beef and pork liver. As a model substance di-(2-ethylhexyl)phthalate was selected. The paper contains new information on the mechanism of metabolic oxidative phthalate degradation in the rat, identifies the structure of intermediary products and suggests a reaction breakdown pattern. The balance of phthalate excretion from experimental animals in faeces and urine was examined, their metabolized ratio was defined and the phthalate load of the decisive parts of the organism was evaluated, i.e. in the liver, kidneys, spleen, brain and muscular tissue. Subsequent monitoring of phthalates in urine of human volunteers exposed only to the natural phthalate intake from contaminated food revealed the presence of some oxidative metabolites in body fluids. It provided also evidence of the possible endogenous formation of 2-ethyl-3-carboxypropylphthalic acid the presence of which may signalize metabolic oxidation by a pathway terminated by possible hepatocellular carcinogenicity of phthalates. The probability of introduction of oxidative phthalate metabolites from meat of domestic animals seems minimal.
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High hydrostatic pressure processing (HPP) has been shown to be an effective non-thermal means of inactivating microorganisms from various food products. Little information is available regarding the effects of HPP on metazoan parasites. Outbreaks of food-borne disease have been associated with importation of food contaminated with fecal material. Ascaris suum is used as a surrogate model metazoan parasite for the human roundworm, Ascaris lumbricoides, to study the effects of treatments on the inactivation of eggs in sludge. The present study was conducted to determine the effects of HPP on A. suum eggs. Unembryonated A. suum eggs were subjected to 138-552 megapascals (MPa) for 10-60s in a commercial HPP unit. Embryonation was induced after HPP treatments by incubating eggs in 0.01N sulfuric acid at room temperature. After 21 days, 100 eggs were examined per treatment using a light microscope and the percent of embryonated eggs was determined. Embryonation was induced in 38-76% eggs that were subjected to 138 and 270MPa. No embryonation was observed in eggs exposed to pressures of 241MPa or more for 60s or in eggs exposed to 276MPa for 10-30s. These results indicate that HPP treatment could be used to protect contaminated food items by inactivating A. suum eggs and may also have potential in reducing food-borne illness resulting from fecal contamination.
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In order to improve the knowledge of host/pathogenic agent interaction and to obtain a more careful estimation of risk related to ingestion of food contaminated by Vibrio spp., the effects of bile extracts have been studied. The growth of one V. fluvialis, two V. alginolyticus, and three V. parahaemolyticus strains, isolated from mollusks and crustaceans, has been determined to evaluate their adaptability to intestinal environment. Moreover, the expression of virulence factors responsible for the colonization, as bacterial "swarming mobility", biofilm production, adherence on epithelial cells and hydrophobicity, has been evaluated. Using a bile concentration of 1.5%, all examined strains showed a constant inhibitory effect, quite moderate in the first growth phases. Bile increased the "swarming mobility" and biofilm production; also the adherence was favored, but only after adaptation and during the early logarithmic phase. The decreased hydrophobicity could explain the reduction of adherence during the stationary phase. Studying the phenotypic expression of virulence factors in "minor vibrios" in the presence of bile, it was possible to extend the knowledge about their pathogenetic mechanisms owing to the ingestion of contaminated food. That permits a more careful estimation of risk related to the contamination, considering the high frequency of isolation of these species in some seafood.
Cases of stramonium poisoning due to deliberate abuse by young adults have been widely reported. There are also a few reports of accidental poisoning in children from contaminated food. The taste and shape of Datura stramonium makes it unattractive to both man and animals and, therefore, ingestion by children in ignorance of its toxicity is rare. Three such cases are described in this paper. In Saudi Arabia stramonium abuse is unheard of and poisoning of children as a result of food contamination is very unlikely. Cases of ingestion in ignorance are, however, likely to occur frequently since D. stramonium grows in many parts of the country. The doses taken under the circumstances, though toxic, were small. The patients, therefore, suffered mainly the peripheral signs of the anti-cholinergic action of atropine, the principal D. stramonium alkaloid. Central nervous system manifestations and toxic psychosis were minimal in contrast to intentional misuse or accidental poisoning. Due to the special susceptibility of children to atropine toxicity and the relatively small lethal dose (less than or equal to 10 mg), treatment with the specific antidote, physostigmine salicylate, is emphasized for all but the mildest cases, in addition to any symptomatic treatment that might be needed.
In order to elucidate the effects upon the human immune system of aflatoxin B1 produced by the food-contaminating mould Aspergillus flavus, phagocytosis, microbicidal activity, superoxide production and intrinsic antiviral activity were studied in monocytes exposed to aflatoxin B1 for different times at concentrations ranging from 0.1 to 1 pg/ml. Phagocytosis and microbicidal activity were significantly impaired (p < 0.05) by aflatoxin B1 at doses as low as 0.1 pg/ml. However, pretreatment of monocytes with aflatoxin B1 did not modify intrinsic antiviral activity or superoxide production. These results confirmed data obtained from animals fed with mycotoxin-contaminated foods. The potential danger to human health of exposure to mycotoxins demonstrates the necessity for careful microbiological control of food.
Disease associated with exposure to mycotoxins is known as the "Great Masquerader" of the 21st century because of its complex natural history involving different tissues and resembling different diseases at each stage in its evolution. It can present with a variety of nonspecific clinical signs and symptoms such as rash, conjunctivitis, epistaxis, apnea, cough, wheezing, nausea, and vomiting. Some cases of vomiting illness, bone marrow failure, acute pulmonary hemorrhage, and recurrent apnea and/or "pneumonia" are associated with exposure to mycotoxins. Familiarity with the symptoms of exposure to the major classes of mycotoxins enables the clinician to ask pertinent questions about possible fungal exposures and to remove the infant or child from the source of exposure, which could be contaminated food(s), clothing and furniture, or the indoor air of the home. Failure to prevent recurrent exposure often results in recurrent illness. A variety of other conditions, including hepatocellular and esophageal cancer and neural tube defects, are associated with consumption of foods contaminated with mycotoxins. Awareness of the short- and long-term consequences of exposures to these natural toxins helps pediatricians to serve as better advocates for children and families.
The selection of synthetic antibody fragments from large phage libraries has become a common method for the generation of specific antibodies. The technique is particularly valuable when antibodies against small, non-immunogenic molecules (haptens) or highly toxic substances have to be produced. In addition, haptens are usually coupled to protein carriers, bearing the risk that the free hapten is not detectable. Here, a single variable chain antibody (scFv) against the highly toxic mycotoxin fumonisin B1 has been produced. The hapten was coupled via a linker to biotin. Using this conjugate and a naive scFv library, it was possible to circumvent both the necessity of immunization and the risk of a disguised hapten. The scFv obtained after three panning rounds was found to bind specifically to both free fumonisin B1 and fumonisin-biotin conjugate. Also fumonisin B2 was bound by the scFv. Modeling of both scFv and fumonisin B1 molecule revealed a good fitting of structures. The antibody obtained can potentially be used for developing a rapid and affordable immunoassay for detection of food contamination and can be applied in immunoaffinity chromatography, usually carried out prior to HPLC analysis of mycotoxin-contaminated food and feed.
Addition of penicillin, Terramycin, or kanamycin to the drinking water of adult mice rapidly induced in them an enlargement of the cecum. In all animals, this occurred within 12 hr after the beginning of drug administration-the effect being most pronounced with penicillin. The cecums remained enlarged and generally continued to increase in size as long as the antibacterial drugs were administered. The increase in wet weight of the cecums was due primarily to an accumulation of water in the lumens during the first 24-48 hr of drug administration. At that time, there were no detectable histological changes in any case, but the bacteriological picture differed from drug to drug. The cecums were free of bacteria in animals receiving penicillin, fusiform-shaped bacteria and bacteroides were present in those receiving Terramycin, and lactobacilli and bacteroides in those receiving kanamycin. After the initial 48 hr, an abundant and complex secondary microflora developed in all treated animals, its composition being characteristic for each type of antibacterial drug. When penicillin was administered for 2 wk, the cecal weights and microbial populations did not return to normal levels for over 14 days after discontinuance of the drug. This recovery period could be shortened to 10 days by giving the mice food contaminated with cecal homogenates prepared from normal animals. A period of 7 or 8 days was required for the cecal weights and microflora to reach normal levels when the administration of penicillin lasted only 24 hr; this period could not be shortened by giving the animals contaminated food. The effects of drugs on the size and bacterial contents of the cecum have been discussed in the light of earlier findings concerning the characteristics of the huge cecums uniformly found in germfree mice. Taken together, these observations support the hypothesis that certain elements of the intestinal microflora-not yet completely identified-play an essential role in maintaining the integrity of the water-transport mechanism in the intestinal epithelium.
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Soils from beaches in northwestern Alaska have been found to contain Clostridium botulinum type E, providing evidence of one environmental source of food contamination.