Control of food additives and contaminants.
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Precocious puberty is generally defined as the appearance of secondary sex characteristics before age 8 years in girls (or menarche before age 9 years) and before 9 years in boys. The overall incidence of sexual precocity is estimated to be 1:5,000 to 1:10,000 children. The female-to-male ratio is approximately 10:1. In addition to the psychosocial disturbances associated with precocious puberty, the premature pubertal growth spurt (with less time for prepubertal growth) and the accelerated bone maturation result in reduced adult height. Precocious puberty may be gonadotrophin-dependent [i.e. of central origin with premature activation of the gonadotrophin-releasing hormone (GnRH) pulse generator] or gonadotrophin-independent (i.e. peripheral where the GnRH pulse generator is suppressed). This can be determined by GnRH testing. The pathophysiology is the basis for different diagnostic and therapeutic strategies, i.e. in the first case a stimulated LH/FSH ratio >1 and suppressive treatment with GnRH agonists (e.g. in hypothalamic hamartoma), and in the second decreased gonadotrophins and removal or suppression of the endogenous or exogenous sex steroid source (e.g. congenital adrenal hyperplasia). While several cases of gonadotrophin-independent precocious puberty due to oestrogen exposure via the transdermal, oral, or inhalative route have been reported, no case is known with the development of subsequent secondary central precocious puberty. Food contamination with oestrogens is theoretically possible, but would most probably be sporadic and, thus, would not lead to precocious puberty. As steroid hormones in meat production are banned in the European Union, no data on the impact of environmental oestrogenic substances on human maturation are currently available. In conclusion, the risk for children to develop precocious puberty through exposure to oestrogens (or androgens) in the environment or in food is very low. Nevertheless, studies of the effects of defined environmental oestrogenic substances on the human reproductive system and on pubertal development are warranted.
A possible butyltin contamination source in wine was studied in this paper. Agglomerated cork stoppers, which were produced in Portugal, Spain, and Italy, used in wine bottles were examined. The domestic cork products, cork granules, and mucus used for cork products were also analyzed. The levels of mono- and dibutyltin compounds in corks were found in the range from <0.0024 to 3.3 and from <0.0029 to 6.7 microg of Sn/g, respectively. A low level of tributyltin contamination was also found in 2 of 31 tested samples. The presence of butyltin compounds in agglomerated cork stoppers was confirmed by GC-MS. Experimental results indicated that all overseas agglomerated cork stoppers studied contained mono- and/or dibutyltins. Butyltins were not detected in cork granules, mucus, most of the natural cork stoppers, and domestic agglomerated cork products. The concentrations of mono- and dibutyltins increased with the time in a 30-day experiment, showing that butyltin compounds can leach from agglomerated cork to the wine. When the butyltin concentrations in wine samples were compared with their levels in the corresponding agglomerated cork stoppers, a correlation was found. The potential harm of such food contamination was evaluated by the toxic research of butyltin compounds using Daphnia sp. as the experimental model.
Several measures were adopted by European countries in the aftermath of the Chernobyl accident. In this paper these measures are reviewed and the European Communities initiatives for food marketing and exports are analyzed, together with the reference levels for radioactive concentration in the main food matrices chosen in different European countries in the very few days after the accident. A particular attention has been devoted to the emergency management in Italy, outlining exhaustively the laws enforced at the time of the accident and explaining how the reference levels for food contamination were chosen. Finally, a tentative balance about emergency management in Italy is struck and some questions are raised about the commitments undertaken or to be undertaken by international institutions.
EHEC (enterohaemorrhagic E. coli) bacteria are new, only since 1982 recognized zoonotic pathogens. EHEC differ from E. coli intestinal commensales by the fact that they are lysogenic infected with bacteriophages, which carry the genetic information for the production of shigatoxins (Stx type 1 and/or 2). Due to the obligatory released Stx EHEC are classified also among the Shigatoxin producing E. coli (STEC). EHEC are capable of causing a Hemorrhagic Colitis and some sequelae of diseases such as the haemolytic uraemic syndrome. Due to their virulence factors they can be divided into typical and non-typical EHEC. Typical EHEC possess a pathogenicity island (Locus of Enterocyte Effacement) harboring genes, which apart from the characteristic necrotic activity of Stx enable the pathogens to closely attach to the epithelial cells of the intestinal mucosa and to destruct the microvilli. Additionally a so-called virulence plasmid codes for the production of a haemolysin, a peroxidase-katalase, an enterotoxin as well as a serine protease. EHEC are one of the world-wide most important causes of foodborne infections. Depending upon the country, most of the incidences in 1998 varied between 1 to 3 cases per 100,000 inhabitants. Since EHEC are only notifiable in a few countries, one must count however on substantially higher numbers. In Germany the estimated incidence is about 13 cases per 100,000 inhabitants. Since the first EHEC outbreaks were recognized in humans, studies investigating the prevalence of EHEC within animals were repeatedly performed. From the outset one assumed that cattle are a possible reservoir. Actually EHEC were isolated from fecal samples world-wide (typical and non-typical EHEC) from a large percentage of cattle (> 50%). Besides EHEC were isolated sporadically from fecal samples of other animals and healthy humans. The EHEC bacteria are shed by infected humans and animals, in particular by infected ruminants. They are spread over manure, slurry, sewage etc. Humans can get infected directly by contact with infected persons or animals or indirectly by contaminated food, water etc. The clinical outcome within humans appears as aqueous to bloody diarrhea. Beyond that approximately 5 to 10% of the patients develop the haemolytic uraemic syndrome. In contrast to humans, animals are mostly infected clinically inapparent. The therapy is based upon a symptomatic treatment. At present in man the control of EHEC infections concentrates on a particularly strict hand hygiene after the contact with infected humans and animals (above all ruminants). Since EHEC are heat sensitive, the prophylaxis by sufficient heating of risk food (raw milk, ground beef) is of special importance. In veterinary medicine above all EHEC infections must be controlled in ruminants, which are the primary reservoir. Due to the wide spread of EHEC in the ruminant population it is not realistic to demand an EHEC free cattle stock. Since EHEC are spread only via fecal excretion, at present it is most important to reduce the fecal shedding and to avoid fecal contamination of food of animal origin. In detail prophylactic hygienic measures concerning the farm management, the feeding hygiene, the food hygiene, the meat hygiene as well as the food hygiene are available.
Field and glasshouse investigations were conducted on the responses of two legumes (field pea and fodder vetch) and three non-leguminous crops (maize, wheat and rapeseed) to the heavy metals Cd, Cr, Zn, Pb, Cu and Mn in soil with multiple metal contamination. In general, the results indicate that the two legumes and wheat were more susceptible to soil metals than were rapeseed and maize. The dry matter yields of field pea, wheat, fodder vetch, rapeseed and maize decreased by up to 169, 123, 113, 93 and 68%, respectively, in metal-contaminated soil. Among the crops, maize had the highest concentrations of Mn, Zn and Cd, rapeseed had the highest concentrations of Cr, the concentration of Cu was highest in fodder vetch, and wheat was the highest accumulator of Pb. The bioconcentration factors (BCF) of the metals decreased as the soil metal loading rates increased except for Cr in fodder vetch and Cd in wheat, whose BCF increased as the metal loading rate increased. Significant linear correlations were found between plant and soil metal concentrations. Patterns of metal distribution in plant parts varied with different crops and metals, with more Cd and Cu accumulating in the grain of wheat than of maize, suggesting that growing wheat would represent a higher risk of food contamination than growing maize in Cd- or Cu-contaminated soil. The results suggest that on sites with multiple metal contamination, growing maize and rapeseed would be safer than growing wheat or legumes. However, maize could perhaps be used for phytoremediation of lightly contaminated soils, providing that the crop residues were safely disposed of.
AIM: This pilot study attempts to assess how far the standardized questionnaires are a valid tool to detect the food-related burden of acrylamide. Acrylamide is a toxic substance classified by the International Agency of Research on Cancer, as well as the Deutsche Forschungsgemeinschaft, as a probable human carcinogen. METHODS: A venous blood sample was taken in order to determine the smoking-specific acrylnitrile adduct N-cyanoethylvaline and the acrylamide adduct N-2-carbamoylethylvaline in a female study population expecting delivery soon. A standardized questionnaire was used to determine the consumption of acrylamide-contaminated food. The results of our questionnaire were transferred to a linear evaluation system. Finally, anamnestic data of the questionnaire were correlated to objective parameters such as blood levels of hemoglobin adducts of acrylamide and acrylonitrile. RESULTS: A positive correlation between the acrylamide intake and the levels of hemoglobin adducts in our study population was not proven. CONCLUSIONS: Evaluation of food-related exposure to acrylamide is difficult due to several reasons. Firstly, the validity of anamnestic data strongly depends on the patient's ability to remember precisely all consumed food (quality as well as quantity) over a 3-month period. In addition, the contamination of acrylamide in food varies from one product to another; even the contamination of the same product is variable. Therefore, the missing correlation between the questionnaire and hemoglobin adduct rates is rather due to restricted validity of anamnestic data.
A 20-day experiment was conducted to compare the accumulation, distribution, and toxicological effects of dietary As, as arsenate, in lake whitefish (LWF, Coregonus clupeaformis) and lake trout (LT, Salvelinus namaycush). Results of this experiment were used to design an experiment of longer duration in which one of the fish species was selected and exposed three times per week to lower dietary As doses. In the present study each treatment group was exposed to a combination of one of three doses of As (0, 100, or 1000 microg As/g) and one of two types of diet, no brine shrimp (NS) or with brine shrimp (WS) for a total of eight dosing events. Brine shrimp were added to determine whether their presence enhanced consumption of As-contaminated food. Modified feeding behavior occurred in both fish species fed As contaminated diets, with the exception of the 100 microg As/g NS food. Brine shrimp addition did not affect feed consumption of the As contaminated diets. Significant As accumulation occurred in stomach, pyloric caeca, intestine, liver, kidney, and gallbladder, but not in bile or muscle. As exposure did not have a significant effect on hepatic and renal metallothionein concentrations. Concentrations of lipid peroxides were only significantly elevated in the plasma of LT fed the 1000 microg As/g WS food. Liver somatic indices decreased significantly in both species, whereas hematological parameters were not affected in either species. Histological lesions occurred in gallbladder, liver, kidney, pyloric caeca and intestine from LWF. These lesions were not observed in LT; however, gallbladders were not examined in this species. Weight gain was lower in both species fed As contaminated diets, however, condition factors were not affected.
The dissemination in food factories of the organisms I have referred to earlier, represent significant and interesting issues of public health concern. Yet there seem to be difficulties in incorporating material in education-training-information programmes explaining merely the most simple and basic facts about the risk involved in food being contaminated in food factories. Such educational programmes are essential components in the overall scheme of foodborne disease control, yet they often represent the weakest links in the control chain. There has been a decline in the emphasis on food hygiene in some programmes at the level of institutions of higher education, and a de-emphasis on food hygiene has occurred over the past few decades in schools of veterinary medicine in some parts of the world. This committee has taken active steps to improve this situation by convening a professorial consultation on post-graduate teaching in advanced food microbiology, Copenhagen 1989 (Park, 1990). The public, as well as politicians, focus for the time being on chemical contamination of foods, possible presence of residues, thereby ignoring the fact that statistically it is not the residues that cause deaths which count, but, without a shadow of doubt, the foodborne pathogens. This fact emphasizes the need for intensive training in preventive hygienic measures. Since representatives of the food industry are participating in the Symposium, I would like to balance the problems by saying: we all share a responsibility in securing education in food hygiene in food factories.(ABSTRACT TRUNCATED AT 250 WORDS)
Consumption of food contaminated with Fusarium moniliforme causes leucoencephalomalacia and hepatotoxicity in horses, pulmonary edema in pigs and liver cancer in rats, and has been correlated with esophageal cancer in humans. The causative agents are thought to be a family of compounds called fumonisins, which have recently been shown to be potent inhibitors of sphingosine (sphinganine) N-acyltransferase. Because inhibition at this step blocks the formation of complex sphingolipids while leading to accumulation of sphinganine, we hypothesized that exposure of animals to fumonisin-contaminated feed might be detected by analyses of serum sphingolipids. Within days of giving ponies feed contaminated with 15 to 44 micrograms/g fumonisin B1, there was an increase in the amount of free sphinganine (and sometimes sphingosine) and a reduction in complex sphingolipids. Free sphinganine and sphingosine decreased when ponies consumed less of the contaminated feed, and increased again when they consumed more fumonisin. When toxicosis was evident as indicated by other serum markers, complex sphingolipids as well as free sphingosine and sphinganine were elevated, probably due to loss of sphingolipids from dying cells. These findings establish that consumption of fumonisin-contaminated feed disrupts sphingolipid metabolism. Because the changes in sphinganine and sphingosine were seen before liver enzymes were noticeably elevated, they may be an early marker of exposure to fumonisins.
A total of 22 chiral toxaphene congeners were analyzed in organ tissues and eggs of laying hens after they had been fed with food spiked with technical toxaphene. For the analysis, multidimensional high-resolution gas chromatography using a chiral column coated with randomly silylated heptakis(O-tert-butyldimethylsilyl)-beta-cyclodextrin, electron capture detection, and valveless "live column switching" technique was applied. The analytical results were additionally confirmed with mass spectral data, recorded in electron-capture negative ionization mode with selected-ion monitoring mass spectrometry. During both the feeding period of the laying hens with toxaphene-contaminated food (38 weeks, accumulation phase) and the following subsiding period without toxaphenes (another 14 weeks, decontamination phase), organs (liver, kidney, skin/fat), blood, meat, and eggs of the hens served as model matrices for toxaphene uptake. The enantiomeric ratios (ERs) of congeners 26, 31, 32, 40, 41, 42(a+b), 44, 50, and 62--known as the most important components of technical toxaphene occurring in the environment--could be analytically determined. Significant differences were observed with respect to their initial racemic ratios. On the basis of their chemical structures, the metabolic pathways of some congeners could be explained. Astonishingly, some of the toxaphenes applied as racemates could merely be found as single enantiomers at the end of the feeding program, for example, congener 32 in blood and meat samples or congener 44, especially in organ tissues, which showed ERs of zero or infinity. The findings of this study impressively emphasize that it is essential to isolate and analyze individual toxaphene enantiomers in food and biota tissues to be capable of evaluating their toxicity and metabolization more specifically.
A short period of fasting leads, in the mouse, to usually reversible damage to chondrocytes and in patients with rheumatoid arthritis often to a temporary improvement. Slight hypo-alimentation and a low-caloric diet reduce the spontaneous development of osteo-arthritis in the mouse, whereas a high-caloric diet promotes the disease. In man, mice, and, in particular, fattened animals, obesity is often associated with forms of osteo-arthritis. In such cases, it may be assumed that metabolic damage to cartilage is involved as well as damage due to weight-bearing forces. Elderly people, i.e., persons with a predisposition to osteo-arthritis, often suffer from a generalized vitamin deficiency. Vitamins E, B2, and C have been shown to exert an inhibitory effect on osteo-arthritis in animals, and it has been found that supplementation therapy, particularly with vitamin E and the combination of vitamins B1, B6, and B12, can exert a beneficial effect on the symptomatology of human degenerative joint disease. Mineral deficits in calcium, zinc and selenium (Kashin-Beck disease; endemic osteo-arthritis deformans) can provoke skeletal damage in humans and animals. On the other hand, calcium, iron, and copper have been reported to give rise to storage diseases, in some cases with involvement of articular cartilage. There have been indications that chondrotoxic damage may result from food contaminants. So far very little is known about the influence of phytopharmacodynamic substances (other than derivatives of rutin and rhein) on osteo-arthritis. The large gaps in our knowledge of the chondrotropic properties of the constituents of food and common stimulants underline the need for further investigations.
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The identification of host factors that are predictors of changes in serum polyhalogenated biphenyl contaminants over time has been a difficult challenge in epidemiologic studies of exposed individuals. Of particular concern are age at exposure, reproductive and lactational histories, and changes in body mass index. Using both cross-sectional and longitudinal approaches, this study examined factors related to high initial serum PBB and PCB levels and changes in these levels over time among women of varying ages at exposure (n=1772; age range<1 to 45 years). In 1973, PBB exposure occurred through consumption of farm products contaminated with PBB added to cattle feed. Exposures to PCBs began in 1941 through PCB-contaminated silo sealant deteriorating into animal feed. The Michigan Department of Public Health began enrolling participants in 1977 and has continued to follow them through annual updates. At enrollment, questionnaires were administered to obtain demographic, lifestyle, and anthropometric measurements, medical/reproductive and occupational histories, and contaminated food consumption patterns. Blood samples were collected for PBB and PCB analysis at enrollment for all participants; additional serum tests were done on a subset of the population during follow-up. Median serum levels at enrollment were 2.0 ppb PBB and 5.0 ppb PCB. A decline in serum PBB level over an interval that ranged from 1 to 146 months (median=31) was observed for 44.6% of the women (median=1.0 ppb), while 12.2% showed an increase (median=1.0 ppb). PCB levels declined in 50.3% of the women (median=3.0 ppb) while 12.2% increased (median=2.0 ppb). Relative to women whose contaminant levels were stable, higher initial serum level was a predictor of decline for both PBB and PCB (OR=1.66, 95% CI 1.52-1.82; OR=3.26, 95% CI 2.58-4.12, respectively); a yearly increase in interval between tests was related to declining PCBs (OR=1.65, 95% CI 1.46-1.87). In addition, age< or =10 years at exposure (OR=1.72, 95% CI 1.03-2.86) and residence on a quarantined farm (OR=1.40, 95- CI 1.03-1.90) were predictors of a decrease in PBBs. Factors related to an increase in PBB levels were age< or =10 years at exposure (OR=0.30, 95% CI 0.10-0.96) and initial PBB level (OR=1.24, 95% CI 1.15-1.33); and for PCBs, high initial level (OR=1.34, 95% CI 1.17-1.53) and body mass index (OR=1.07, 95% CI 1.01-1.13). One or more live births during the interval between tests were not related to changing levels of either contaminant; breastfeeding data were not available for examination. Early age at exposure appears to be an important predictor of changes in serum PBB levels over time.
To evaluate the main intake source of arsenic by the villagers from arsenic-affected families in Jalangi and Domkol blocks in Mushidabad district, West Bengal-India, we determined the concentrations of arsenic in tube-well water and in food composites, mainly including vegetables and cereals collected from the surveyed families which were cultivated in that region. The daily dietary intakes of arsenic by the villagers were estimated and the excretions of arsenic through urine and hair were determined. The arsenic concentrations in hair and urine of the studied population living in mild (2.78 microg/L), moderate (30.7 microg/L) and high (118 microg/L) arsenic-affected families were 133, 1,391 and 4,713 microg/kg and 43.1, 244 and 336 microg/L, respectively. The linear regressions show good correlations between arsenic concentrations in water vs hair (r(2)=0.928, p<0.001) and water vs urine (r(2)=0.464, p<0.01). Approximately 29.4%, 58.1% and 62.1% of adult population from mild, moderate and high arsenic-affected families were suffering from arsenical skin manifestations. The mean arsenic concentrations of food composites (vegetables and cereals) in high arsenic-affected families are not significantly different from mild arsenic-affected families. The daily dietary intakes of arsenic from water and food composites of the studied population, living in high, moderate and mild arsenic-affected families were 568, 228 and 137 microg, respectively. The linear regressions show good correlations between arsenic concentrations in hair vs daily dietary intake (r(2)=0.452, p<0.001) and urine vs daily dietary intake (r(2)=0.134, p<0.001). The water for drinking contributed 6.07%, 26.7% and 58.1% of total arsenic in our study from mild, moderate and high arsenic-affected families. The result suggested that the contaminated water from high arsenic-affected families should be the main source for intake of arsenic. On contrary, the contribution of arsenic-contaminated food composites from mild and moderate arsenic-affected families might be the main source for intake of arsenic. The Food and Agriculture Organization/World Health Organization (FAO/WHO) provisional tolerable weekly intake (PTWI) values of arsenic in our study were 3.32, 5.75 and 12.9 microg/kg body weight/day from mild, moderate and high arsenic-affected families, respectively, which is higher than the recommended PTWI value of arsenic (2.1 microg/kg body weight/day).
An outbreak of cholera caused by Vibrio cholerae 01, biotype El Tor, serotype Inaba, phage type 4, occurred in an institution for the aged in Singapore in August and September 1984. 96 inmates were infected (21 symptomatic and 75 asymptomatic) and 5 died. The index case was a 72-year-old male inmate who continued to assist in food preparation in the kitchen from the time of onset of diarrhoea until he was seriously ill and hospitalized 4 days later. Another kitchen helper was found to have asymptomatic V. cholerae 01 infection. The infection rate for males was significantly higher than that for females (P less than 0.025), associated with the use of unsanitary toilets. The main mode of transmission was through food contaminated by the 2 kitchen helpers who probably accounted for most of the infections, while poor personal hygiene of the inmates helped to sustain person-to-person spread. The outbreak was confined within the institution as the result of the prompt and effective implementation of control measures.
Mycotoxins are impractical as tactical weapons, butthey can be used by small poor terrorist organizations to poison food and water sources or can be released in crowded, confined areas. Crude concentrated or dried extracts of readily grown fungal cultures can be used as weapons. The production of fungal weapons does not require elaborate facilities for the growth of fungi, sophisticated equipment for the purification of the toxins, or highly trained personnel. Aflatoxin B1, fumonisin B1, ochratoxin A, and the trichothecenes T-2 toxin and deoxynivalenol could be weaponized for bioterrorism. Knowledge of the symptoms of intoxication and the biochemical mechanisms of action of mycotoxins is necessary for the rapid identification of the toxins, the development of prophylactic antidotes, and the design of effective treatments of affected persons. All of these mycotoxins except deoxynivalenol are carcinogens (Stark, A. A., Annu. Rev. Microbiol. 34:235-262, 1980; Stark, A. A., p. 435-445, in P. S. Steyn and R. Vleggaar, ed., Mycotoxins and phycotoxins, 1986; Stark, A. A., p. 47-60, in C. L. Wilson and S. Droby, ed., Microbial food contamination, 2000; Stark, A. A., and N. Paster, p. 60-64, in M. L. Wahlqvist, A. S. Truswell, R. Smith, and P. L. Nestel, ed., Nutrition in a sustainable environment, 1994). Because immediate and widespread death, illness, or panic is the goal of bioterrorists, the mechanisms by which mycotoxins exert acute toxicity are the focus of this article.
The aim of this study was to determine what weaning foods and food preparation practices expose children to a high risk of diarrhoeal disease through exposure to a contaminated diet. Bacterial contamination of 897 food and 896 drinking water samples was assessed in a water and sanitation intervention project. The geometric mean of faecal coliforms per g or ml was 7.5 x 10(3) in left-over rice. 1.4 x 10(2) in other types of boiled rice, 2.5 x 10(2) in milk, 4.8 in household drinking water, and 3.5 in bread. Multiplication of faecal coliforms occurred when there was a delay of more than 4 h between preparation and consumption of food. All samples were more contaminated in the rainy than in the dry season. Strategies to reduce contamination should therefore focus on 'wet' foods, early consumption after preparation, and re-heating of left-over foods. Understanding the reasons for the faulty practices is also essential to the formulation of effective measures.