[DECONTAMINATION OF MILK FROM RADIOELEMENTS].
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The programs of the Food and Drug Administration (FDA), which operates under a broad mandate of regulatory authority provided by the Congress in the form of the Food, Drug, and Cosmetic Act, demonstrate the way in which science and law interact to protect public health through the regulatory process. In particular, sections 402, 406, and 409 of the Act provide the means for regulating both new and old food products approved for use by the petition process as well as foods which present a potential hazard because of environmental accidents which result in residues of undesirable or dangerous chemical substances. The episodes of foods contaminated with polychlorinated biphenyls (PCBs) or polybrominated biphenyls (PBBs), and the manner in which action levels or guidelines were developed to regulate the allowable levels of these chemicals in foods, describe the pragmatic way in which FDA protects public health by restricting the allowable levels of chemical substances in foods.
More than 50% of the electricity in the United States is produced by coal-burning power plants. The byproduct of coal-burning plants is coal fly ash, which contains increased concentrations of trace metals and is disposed of in collection basins. Southern toads (Bufo terrestris) frequently use these basins for reproduction. Male toads were collected in spring 2001 and 2002 from an ash basin and a reference site and divided into four groups: toads collected at the control site and maintained on (1) control substrate and food or (2) ash and contaminated food and toads collected at the ash site and maintained in (3) control or (4) ash conditions. Blood was collected periodically during 5 months to determine testosterone and corticosterone concentrations. Reference to ash toads exhibited a significant, transient increase in corticosterone at 4 weeks, but neither corticosterone nor testosterone continued to increase beyond this time. In contrast, toads caught and maintained on ash did not exhibit increased corticosterone. Testosterone in these toads appeared to be unrelated to ash exposure. This unexpected lack of a corticosterone response and no effect on testosterone suggests that toads chronically exposed to trace metals can acclimate to a polluted environment, but they may still experience subtle long-term consequences.
Penicillic acid (PA) is a carcinogenic food contaminant produced by several food-borne fungi. PA was resolved as a sharp peak by reversed-phase high-performance liquid chromatography on a small-particle (10 micrometer) column in 3-4 min by an elution system composed of acetonitrile (AN), water and glacial acetic acid (AC) with detection by ultraviolet (UV) absorbance at 254 nm. Peak height and peak area were related linearly to the amount of PA injected over a range of 5-500 ng. Reproducibility of retention time, peak height and peak area was demonstrated. The lower detection limit was 5 ng in two elution systems [AN-H2O-AC(45:55:2), flow-rate (F) 1 ml/min; AN-H2O-AC(40:60:2), F = 1.2 ml/min] and 10 ng in a third system [AN-H2O-AC(25:75:2), F = 1.6 ml/min]. Based on the sensitivity and separation of PA from (40:60:2), F = 12 ml/min; urine, AN-H2O-AC (25:75:2), F = 1.6 ml/min. Good recovery (89-98%) over a range of 1-50 microgram/ml of PA was obtained from PA-spiked plasma samples treated first with 25% HPO3 followed by extraction with chloroform. A single peak detected either by UV absorbance or by radioactivity was obtained when plasma samples spiked with [14C]PA were extracted. Good recovery (92-105%) of PA also was obtained from spiked urine and bile samples.
A methodology has been developed to assess potential hazards from low-level exposures to radioactive pollutants. Estimates of dose rates to reference organs from internal and external exposure pathways (inhalation of contaminated air, ingestion of contaminated food or water, immersion in contaminated air, and exposure to contaminated ground surfaces) are computed with contemporary dosimetric models. These dose rates are used in a life-table analysis to estimate the radiation-induced cancer deaths and resultant years of life lost in an exposed cohort of 100,000 persons, all simultaneously liveborn and subject to the same risks of dying from competing causes (including natural background radiation). Estimates of the potential health risk are tabulated for approx. 150 radionuclides for each of the exposure pathways; results are summarized in terms of the probability of premature radiation-induced death for a member of the cohort due to incremental radiation exposure, and the average number of years of life lost per incremental fatality. The estimates of radiation-induced mortality generated by these methods provide a useful means of quantifying radiation risk; however, these estimates may be subject to large uncertainties, and can be best interpreted as a measure of the relative degree of hazard associated with exposures to various radionuclides through several exposure pathways.
Ochratoxin A (OA) is produced mainly by Penicillium verrucosum, Aspergillus ochraceus and A. carbonarius and it was found as a contaminant in the large number of agricultural commodities, feedstuffs and animal organs such as kidney and liver of pig. Toxicological studies indicated that OA is a teratogenic, mutagenic and carcinogenic mycotoxin with the strong toxic effects on liver and kidney. In some endemic areas in the world, OA was suspected to be related to swine nephropathy and has been detected in blood samples from inhabitants in these areas as well. More and more attention was paid to the relationship between the consumption of food contaminated with OA and human health. In this paper, OA--producing fungi, the contamination of it to the agricultural commodities, its toxicity and risk assessment are reviewed.
OBJECTIVE: To evaluate the role of foods in sporadic listeriosis. DESIGN: Microbiologic survey of foods collected from refrigerators of patients with listeriosis identified through active laboratory-based surveillance. Patient and food Listeria monocytogenes isolates were subtyped to identify foods contaminated with the same strain of L monocytogenes that caused illness in the patient; samples of these foods were obtained from the retail source. SETTING: Multistate population-based study conducted between 1988 and 1990. RESULTS: Listeria monocytogenes grew from at least one food specimen in the refrigerators of 79 (64%) of 123 listeriosis patients; 11% of more than 2000 food specimens collected in the study contained L monocytogenes. Twenty-six (33%) of 79 refrigerators with foods that grew L monocytogenes contained at least one food isolate of the same strain as that in the corresponding patient, a frequency much higher than would be expected by chance (P less than .001). Multivariate analysis showed that of the food specimens that grew L monocytogenes, foods that were ready-to-eat, foods that grew L monocytogenes by a direct-plating method (a measure of the level of contamination), and foods that contained serotype 4b isolates were independently associated with an increased likelihood of containing the patient-matching strain. CONCLUSION: We identified specific food and L monocytogenes isolate characteristics--ready-to-eat foods, foods containing higher concentrations of L monocytogenes, and foods containing serotype 4b--which were associated with disease-causing strains. These results can provide guidance to industry and regulatory agencies in developing strategies to prevent listeriosis.
Aflatoxins are known to be hepatotoxic, carcinogenic, and teratogenic. A positive correlation has been established between the consumption of aflatoxin-contaminated foods and the increased incidence of liver cancer worldwide. A survey of Egyptian corn and corn-based products and by-products shows that the majority of the samples had higher limits of aflatoxin. We have conducted experiments to determine the fate and distribution of aflatoxin during wet-milling process fractions and investigate the aflatoxin destruction during starch conversion to glucose syrup. The present results showed that about half of the aflatoxin content (48.1%) in the infected corn grain was found to be lost in steep liquor, depending upon the aflatoxin type, arranged in the order G1 > G2 > B1 > B2. After wet-milling aflatoxins were distributed into starch, gluten, fiber, and germ. Gluten, fiber, and germ were the most highly contaminated fractions. The loss of aflatoxin during process of starches reached 54.4% in steep water and water process. Although the gluten fraction represents only 9.6% of corn, the higher percentage (25.3%) of aflatoxin was found in this fraction, the fiber and germ account for nearly 29% of the milled corn and contain 11.6% of the aflatoxin. On the other hand, 8.7% of the total aflatoxins in start corn was found in starch fraction which accounts 61% of the milled corn. Aflatoxins G1 and G2 were found lost in higher concentrations compared to the aflatoxin B1 and B2. A higher percentage of AfG1 (86.35%) and AfG2 (78.36%) and a lower percentage of AfB1 (16.3%) and AfB2 (14.7%) were found in starch fraction. The conversion percent of contaminated starch was 89.5% compared with control starch. It can be concluded that aflatoxins were destroyed during starch conversion. Consequently, glucose syrup produced from contaminated starch was found aflatoxin-free.
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This report presents the conclusions of a Joint FAO/WHO Expert Committee convened to evaluate the safety of various food additives and contaminants, with a view to recommending acceptable daily intakes for humans, and to prepare specifications for the identity and purity of food additives. The first part of the report contains a general discussion of principles governing the toxicological evaluation of food additives and contaminants, including flavouring agents, and the establishment and revision of specifications, with comments concerning limits for arsenic, lead and heavy metals. The toxicological significance of proliferative lesions of the adrenal medulla in rats fed polyols and other poorly digestible carbohydrates is also discussed. A summary follows of the Committee's evaluations of toxicological data on various specific food additives (dodecyl, octyl and propyl gallate, glycerol ester of wood rosin, ethyl esters, isoamyl alcohol and related esters, allyl esters, alitame, konjac flour, benzyl acetate, benzyl alcohol, benzaldehyde, benzoic acid, the benzoate salts, and sucrose acetate isobutyrate) and the contaminants aflatoxins. Annexed to the report are a table summarizing the Committee's recommendations for acceptable daily intakes of these substances, changes in the status of specifications and further toxicological studies required, and toxicological data on the ethyl and isoamyl esters considered.
In this review many examples are given of the complexities involved in using some biomarkers in relation to assessing the effects of dietary exposure, when there is frequently a need to determine changes following long-term low level exposure to dietary components. These range from understanding why the biomarker might be valuable and how best it can be measured, to the pitfalls which can occur in the interpretation of data. Analytical technique is considered in relation to folate and selenium, and flavonoid and carotenoid species are used to illustrate how the metabolism of a compound may alter the validity or adequacy of a marker. Vitamin A is discussed in relation to the difficulties which can arise when there are several biomarkers that may be available to assess exposure to one nutrient. Vitamin B12 is discussed in relation to the dietary choices made by individuals. Possible interactions and the role of measuring total antioxidant capacity is considered in some detail. In contrast to most nutrients, there is a marked lack of biomarkers of either exposure or effect for most non-nutrients. The role of biological effect monitoring is considered for dietary contaminants, fumonisins and polyhalogenated aromatic hydrocarbons. Aflatoxins are discussed to exemplify food contaminants for which the biomarker approach has been extensively studied. Finally some compounds which are deliberately added to foods and some which appear as processing contaminants are each considered briefly in relation to the requirement for a biomarker of exposure to be developed.
Probable pathways of food contamination with environmental chemical mutagens and factors responsible for the formation of mutagens in food during cooking are reviewed, and natural and synthetic food components with mutagenic properties are described. The data discussed provide evidence for the expediency of further analyzing mutagenicity of various food components and developing chemical analytical methods for their detection and identification. Antimutagenic compounds present in food are characterized. The adequacy of methods for estimating the activity of these compounds and perspectives for their use as antimutagenic chemopreventive agents are discussed. Emphasis is placed on the necessity of being extremely cautious in employing food antimutagens because of the probable inversion of their effects. Several examples are provided to demonstrate the possibility of reducing mutagenicity of prepared food by modifying food processing technology.