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PubMed2003

Determination of high molecular mass polycyclic aromatic hydrocarbons in a typical Italian smoked cheese by HPLC-FL.

High-performance liquid chromatography with fluorescence detection was used for the analysis of polycyclic aromatic hydrocarbons (PAHs), in "Diavoletto" smoked cheese. Such cheese is typically produced in the Sorrento peninsula, and it is smoked commonly with different materials of vegetable origin. The importance of the smoking generation material is proven by the attention that the EU is paying in indicating the list of wood that may be used to produce smoking flavor agents. The PAHs considered are classified as "probable human carcinogens" by the U.S. Environmental Protection Agency for sufficient data from animal bioassays. The smoked samples contained high molecular mass PAHs with different levels ranging from 0.12 to 6.21 microg/kg. The determination was carried out also on liquid smoking flavor agents, smoke-flavored cheese, and nonsmoked cheese to measure the level of contamination before the treatment.

Carcinogens↗
PubMed2002

Thresholds of carcinogenicity of flavors.

Fifteen compounds approved by the FEMA (Flavor and Extract Manufacturers Association) expert panel as GRAS (Generally Recognized As Safe) and structurally related compounds have been reported to be carcinogenic in rodent studies. The dose response of the 15 compounds in these studies was scrutinized by attempting to plot the percentage of animals with tumors against the dose of the compound on a logarithmic scale in molecules of compound per kg per day (the Rozman scale). Four compounds had either no or an inverse dose response: benzaldehyde, furfural, 3,4-dihydroxycoumarin, and gamma-buterolactone. Three had a response at one dose only: anethole, estragole (2 studies), and isophorone. Obviously, a dose-response curve could not be generated for these 7 compounds. Four compounds had an increasing response at two doses (benzyl acetate, cinnamyl anthranilate, ethyl acrylate, and estragole); three compounds had increasing responses at three doses (citral, 2,4-hexadienal, and pyridine); one compound had increasing responses at four doses (methyl eugenol). The three compounds with three doses fit a linear plot with a correlation coefficient of at least 0.9; the four doses in male rats of methyl eugenol fit a linear plot with a correlation coefficient of 0.999983. The intercept at zero percentage tumors of these linear fits was at least several orders of magnitude greater than the estimated daily dose of these flavoring agents to individuals in the United States. This is interpreted to indicate that these flavoring agents have a clear threshold for carcinogenicity in animals that is well above the levels currently approved for use in foods; consequently, these animal studies should not be a cause for concern for carcinogenicity of these compounds in humans. Rather, the animal studies should be viewed as providing evidence for the safety of these compounds at current levels of human exposure.

Animals↗
PubMed2004

Activated charcoal administration in a pediatric emergency department.

OBJECTIVES: Activated charcoal is the commonest form of gastrointestinal decontamination offered to potentially poisoned children within United States emergency departments. Our aim was to describe this practice with regard to timing, route of administration, use of flavoring agents, and occurrence of adverse events other than vomiting. METHODS: Descriptive data were prospectively collected from consecutive administrations of single-dose activated charcoal, within an urban, academic pediatric emergency department, over a period of 2.5 years. RESULTS: Two hundred seventy-five subjects were enrolled. The median time elapsed between ingestion and emergency department arrival was 1.2 hours. Although 55% of children were administered charcoal within 1 hour of emergency department presentation, only 7.8% received charcoal within 1 hour of poisoning exposure. Forty-four percent of children younger than 6 years, 50% of 6-year to 12-year olds, and 89% of 12-year to 18-year olds drank the charcoal voluntarily (P < 0.01). Medical staff chose not to offer charcoal orally to 42 asymptomatic children among the 176 subjects under the age of 6 years. Of the 114 young children offered oral charcoal, 36 (32%) refused or were intolerant. Nurses added flavoring agents to the charcoal in 59% of oral administrations, but this act did not enhance observed palatability. Among children younger than 6 years, the median time from first sip to complete ingestion of charcoal slurry was 15 minutes. One pulmonary aspiration event and a case of constipation were noted. CONCLUSIONS: Despite published guidelines, children treated in an emergency department rarely received charcoal within 1 hour of ingestion. Gastric tube administration of charcoal varies by age and is partly subjective in its application. We found no evidence that excipient flavoring of charcoal improved success of administration. Pulmonary aspiration of charcoal, although uncommon, should be considered when assessing the risk of therapy. We offer a report of symptomatic constipation from single-dose charcoal.

Administration, Oral↗
PubMed1994

Nursing attitudes towards charcoal administration--impact on patient care.

In 1990, the American Association of Poison Control Centers identified that for the first time activated charcoal (AC) use had surpassed that of syrup of ipecac. As nurses are given the primary responsibility for AC administration, it was important to determine how AC was being administered, as well as nursing attitudes towards AC that have an impact on patient care. Surveys were mailed to the Emergency Departments (EDs) of 60 hospitals served by the Pittsburgh Poison Center (PPC); 6 nurses/ED, 2 from each shift, were asked to respond. Forty-four EDs responded (73.3%) providing 237 surveys. Eighty-two percent of nurses stated they disliked administering AC for the following reasons: Patients did not like AC (64.4%); AC soiled clothing (54.7%); and AC took too long to give (35.5%). Prior to administration, 70.9% of the nurses responded that they shook the AC a minimum of 20 times; 9.3% commented that AC still failed to resuspend. Specific administration techniques included attempts to mask the appearance the the AC (67.1%) and attempts to increase AC's palatability by adding a flavoring agent (37.6%) or by using AC with sorbitol instead of aqueous AC (25.7%). Of note was that the flavoring agents used were those known to decrease AC's ability to adsorb toxins. As the majority of problems with AC involved its poor resuspendibility and palatability, an AC fact sheet was developed and mailed to EDs to provide suggestions on AC resuspension and means of enhancing patient acceptance without compromising AC's adsorptive capacity. By surveying nursing attitudes toward AC and the administration techniques being utilized, the PPC was able to identify specific problems and address nursing concerns in a way that positively impacts patient care.

Attitude of Health Personnel↗
PubMed1999

NTP Toxicology and Carcinogenesis Studies of Isobutyraldehyde (CAS No. 78-84-2) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

Isobutyraldehyde, a branched alkyl aldehyde, is used as a chemical intermediate and flavoring agent. It was nominated by the National Cancer Institute for toxicity and carcinogenicity studies by the NTP. Reasons for nomination and selection of isobutyraldehyde for study included its high potential for human exposure as suggested by its high production volume, its use as a chemical intermediate and food flavoring agent, suspicion of carcinogenicity due to an increased incidence of cancer at an aldehyde manufacturing plant where workers were exposed to a variety of aldehydes, its structural relationship to formaldehyde (a nasal carcinogen in rats), and the lack of toxicity and carcinogenicity studies on isobutyraldehyde in animals. Although human exposure occurs orally, dermally, or via inhalation, the inhalation route of exposure was selected for these animal studies because of the instability of isobutyraldehyde in water and feed. Male and female F344/N rats and B6C3F1 mice were exposed to isobutyraldehyde (approximately 99% pure) by inhalation for 13 weeks or 2 years. Genetic toxicology studies were conducted in vitro in Salmonella typhimurium, L5178Y mouse lymphoma cells, and cultured Chinese hamster ovary cells; in vivo tests were conducted in Drosophila melanogaster germ cells and bone marrow cells of rats and mice. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female F344/N rats were exposed to 0, 500, 1,000, 2,000, 4,000, or 8,000 ppm isobutyraldehyde by inhalation, 6 hours per day, 5 days a week, for 13 weeks. All rats exposed to 8,000 ppm died before the end of the study. Three male rats and six female rats in the 4,000 ppm groups and one female in the 500 ppm group died before the end of the study. The final mean body weight of male rats in the 4,000 ppm group and the body weight gains of 4,000 ppm males and females were significantly less than those of the chamber controls. Clinical findings in rats exposed to 4,000 or 8,000 ppm included abnormal respiratory sounds, decreased activity, nasal discharge, prostration, and slowed respiration. A minimal mature neutrophilia, evidenced by increased segmented neutrophil numbers, occurred in exposed groups of male and female rats. Exposure to isobutyraldehyde resulted in minimal increases in alanine aminotransferase activity in all groups of male and female rats. Spermatozoal motility in 500 and 1,000 ppm males was significantly reduced and females exposed to 4,000 ppm differed significantly from the chamber control females in the relative time spent in the estrous stages. No gross lesions were observed at necropsy that could be associated with isobutyraldehyde exposure. In the 8,000 ppm groups, severe necrosis of the epithelium, and occasionally of the entire mucosa, of the nasal turbinates accompanied by an acute inflammatory reaction was observed. Increased incidences of squamous metaplasia and mild acute inflammation occurred in male and female rats exposed to 4,000 ppm. Minimal to mild degeneration of the olfactory epithelium was observed in all male rats in the 2,000 and 4,000 ppm groups. Male rats exposed to 4,000 or 8,000 ppm and females exposed to 4,000 ppm had mild osteodystrophy of the turbinate bone. The incidences of necrosis/degeneration of the larynx and trachea were increased in male rats in the 8,000 ppm group. The incidences of mild to moderate lymphoid depletion of the spleen and thymus and lymphoid necrosis of the thymus were significantly increased in male and female rats exposed to 8,000 ppm. 13-WEEK STUDY IN MICE: Ten male and 10 female B6C3F1 mice were exposed to 0, 500, 1,000, 2,000, 4,000, or 8,000 ppm isobutyraldehyde by inhalation, 6 hours per day, 5 days per week, for 13 weeks. One male in the chamber control group, one male in the 1,000 ppm group, nine males and all females in the 4,000 ppm groups, and all males and females in the 8,000 ppm groups died before the end of the study. The final mean body weight and body weight gain of female mice in the 1,000 ppm group were significantly less than those of the chamber controls. Clinical findal findings included decreased activity, tremors, prostration, and slower and labored respiration. The absolute and relative kidney weights of males in the 1,000 and 2,000 ppm groups were significantly increased. There were no gross lesions observed at necropsy that could be associated with isobutyraldehyde exposure. Histopathologically, the nasal cavity and lymphopoietic tissues were considered target organs, with changes similar, but not identical, to those observed in rats. Increased incidences of nonneoplastic lesions of the nasal cavity were observed in male and female mice exposed to 1,000 ppm or greater. These lesions included necrosis, inflammation, hyperplasia, and squamous metaplasia of the epithelium; serous and suppurative exudate within the nasal passages; olfactory epithelial degeneration; and osteodystrophy of the turbinate bone. Mild to moderate lymphoid depletion and/or lymphoid necrosis were observed in the thymus of male and female mice exposed to 8,000 ppm. 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female F344/N rats were exposed to 0, 500, 1,000, or 2,000 ppm isobutyraldehyde by inhalation, 6 hours per day, 5 days per week, for 105 weeks Survival, Body Weights, and Clinical Findings No differences in survival rates between exposed and chamber control rats were found. The mean body weights of male and female rats were generally similar to those of the chamber controls throughout the study. Pathology Findings No increase in neoplasm incidences that could be attributed to exposure to isobutyraldehyde was observed in male or female rats. Nonneoplastic lesions related to isobutyraldehyde exposure were limited to the nose and consisted of squamous metaplasia of the respiratory epithelium, degeneration of the olfactory epithelium, and suppurative inflammation. Incidences of minimal to mild squamous metaplasia in 1,000 and 2,000 ppm males and females and in 500 ppm females were significantly greater than those in the chamber controls. Another lesion associated with isobutyraldehyde exposure was minimal to mild degeneration of the olfactory epithelium in 2,000 ppm males and females. The incidences of suppurative inflammation (rhinitis) in male and female rats exposed to 2,000 ppm were increased compared to the chamber controls. 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female B6C3F1 mice were exposed to 0, 500, 1,000, or 2,000 ppm isobutyraldehyde by inhalation, 6 hours per day, 5 days per week, for 105 weeks. Survival, Body Weights, and Clinical Findings There was an exposure-related decrease in survival of male mice, and the survival of males exposed to 2,000 ppm was marginally lower than that of the chamber controls. The mean body weights of female mice exposed to 1,000 or 2,000 ppm were lower than those of the chamber controls during the second year of the study. Pathology Findings No neoplasms that could be attributed to iso butyraldehyde exposure were observed in mice. Non neoplastic lesions related to isobutyraldehyde exposure were limited to the nose. The incidences of olfactory epithelial degeneration in 1,000 and 2,000 ppm males and females were significantly greater than in the chamber controls. GENETIC TOXICOLOGY: Isobutyraldehyde is mutagenic in vitro and in vivo, with the strongest responses observed in mammalian cell assays that measured chromosomal damage. Results of an initial mutagenicity test in S. typhimurium were negative; a second test, con ducted with different strains and varying concentrations of induced S9 activation enzymes, gave equivocal results. Strongly positive responses were obtained in the mouse lymphoma assay for mutation induction in L5178Y cells without S9 and in cytogenetic tests for induction of sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells. Sister chromatid exchanges were significantly increased with and without S9, but induction of chromosomal aberrations was noted unequivocally only in the absence of S9. No induction of sex-linked recessive lethal mutations was observed in germ cells of male D. melanogaster administered isobutyraldehyde by feeding or by injection. In vivo, isobutyraldehyde was demonstrated to induce chromosomal aberrations in bone marrow cells of male mice, but no increases in micronuclei were observed in bone marrow cells of mice or rats after administration of isobutyraldehyde. All these in vivo cytogenetic studies used doses that reached lethality CONCLUSIONS: Under the conditions of these 2-year inhalation studies, there was no evidence of carcinogenic activity of isobutyraldehyde in male or female F344/N rats or male or female B6C3F1 mice exposed to 500, 1,000, or 2,000 ppm isobutyraldehyde. In male and female rats, exposure to isobutyraldehyde induced squamous metaplasia and suppurative inflammation of the nasal respiratory epithelium and degeneration of the nasal olfactory epithelium. In male and female mice, exposure to isobutyraldehyde caused degeneration of the nasal olfactory epithelium. Synonyms: Dimethylacetaldehyde; 2-formylpropane; isobutanal; isobutylcarboxaldehyde; isobutyral; isobutyric aldehyde; isobutyrylaldehyde; isopropylformaldehyde; 2-methylpropanal; 2-methyl-1-propanal; a-methylpropionaldehyde; 2-methylpropionaldehyde; valine aldehyde

Journal Article↗
PubMed1994

Adverse reactions to food additives in children with atopic symptoms.

In a multicenter study conducted at four Danish hospital pediatric departments, the parents of 472 consecutive children were informed of this project to determine the incidence of intolerance of food additives among children referred to an allergy clinic with symptoms of asthma, atopic dermatitis, rhinitis, or urticaria. After a 2-week period on an additive-free diet, the children were challenged with the eliminated additives. The food additives investigated were coloring agents, preservatives, citric acid, and flavoring agents. Carbonated "lemonade" containing the dissolved additives was used for the open challenge. Two doses were used: a low dose and a 10-fold higher dose. Gelatin capsules were used for a double-blind challenge. The children were 4-15 years old, and they were attending an outpatient pediatric clinic for the first time. Of the 379 patients who entered the study, 44 were excluded and 335 were subjected to open challenge. A total of 23 children developed positive reactions after the open challenge. Sixteen of these patients accepted the double-blind challenge, and six showed a positive reaction to preservatives (atopic dermatitis, asthma, rhinitis), coloring agents (atopic dermatitis, asthma, urticaria, gastrointestinal symptoms), and citric acid (atopic dermatitis, gastrointestinal symptoms). The incidence of intolerance of food additives was 2% (6/335), as based on the double-blind challenge, and 7% (23/335), as based on the open challenge with lemonade. Children with atopic skin symptoms had a statistically increased risk of a positive reaction. This may have consequences for the future clinical investigation of children with atopic cutaneous symptoms.

Adolescent↗
PubMed1991

[The mutagenic effects of sodium nitrite and monosodium glutamate used as food additives demonstrated by the Salmonella microsome test system].

In this study, the mutagenicity of sodium nitrite (an antimicrobial agent) and monosodium glutamate (a flavoring agent), which are widely used as food additives, have been evaluated. They were tested for mutagenicity in the Salmonella/microsome test system by employing plate-incorporation test in the absence and presence of rat-liver fraction, S 9. No mutagenic activity was seen for monosodium glutamate in the Salmonella/microsome test system by using the tester strains Salmonella typhimurium TA98, TA100, TA1535 and TA1538. Sodium nitrite was found mutagenic on S. typhimurium TA1535, whereas it was found weakly mutagenic on S. typhimurium TA100, in the presence and absence of rat-liver fraction, S 9.

Animals↗
PubMed2000

Recent studies on the biofunctions and biotransformations of curcumin.

Curcumin is a major component of Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. Curcumin has shown anti-carcinogenic activity in animals as indicated by its ability to block colon tumor initiation by azoxymethane and skin tumor promotion induced by phorbol ester TPA. Curcumin possesses anti-inflammatory activity and is a potent inhibitor of reactive oxygen-generating enzymes such as lipoxygenase/cyclooxygenase, xanthine dehydrogenase/oxidase and inducible nitric oxide synthase. Curcumin is also a potent inhibitor of protein kinase C, EGF-receptor tyrosine kinase and IkappaB kinase. Subsequently, curcumin inhibits the activation of NFkappaB and the expressions of c-jun, c-fos, c-myc and iNOS. It is proposed that curcumin may suppress tumor promotion through blocking signal transduction pathways in the target cells. Curcumin was first biotransformed to dihydrocurcumin and tetrahydrocurcumin and that these compounds subsequently were converted to monoglucuronide conjugates. These results suggest that curcumin-glucuronide, dihydro-curcumin-glucuronide, tetrahydrocurcumin-glucuronide and tetrahydrocurcumin are major metabolites of curcumin in mice.

Animals↗
PubMedDate not supplied

The influence of salivary variables on fluoride retention in dental plaque exposed to a mineral-enriching solution.

This study was carried out to examine interindividual differences in salivary variables related to plaque accumulation and to estimate their influence on the fluoride retention in plaque in vivo by a mineral-enriching solution. Two saliva samples were taken from 10 subjects, once after brushing and once after 24 h without brushing. Calcium, phosphate and monofluorophosphatase (MFPase) activity in the saliva samples were determined. The salivary flow rate and the debris index were also recorded. After plaque had formed over 3 days within in situ plaque-generating devices, subjects were instructed to rinse with a mineral-enriching mouthrinse three times a day on 4 consecutive days. Plaque exposed to distilled water plus flavoring agents served as a control. Fluoride-free dentifrice was used during the experimental period. Twenty-four hours after the last rinsing, the samples were removed from the mouth, and fluoride and mineral distributions in plaque analyzed using a method previously reported by the authors. Salivary flow, MFPase activity and calcium concentration in saliva were significantly higher after 24 h of plaque accumulation. Rinsing with the mineral-enriching solution produced retention of fluoride and phosphate in the outer and middle layers of plaque. Salivary calcium concentration had a direct effect on fluoride uptake in plaque, but no obvious relationship was found between other salivary variables and the plaque fluoride retention. The salivary calcium effect may be due to enhanced bacterial cell wall binding of fluoride via calcium bridging.

Adult↗
PubMedDate not supplied

Enamel demineralization by snack foods.

The amount of enamel destroyed by salivary fermentation of snack foods and confections was not dependent on their sugar content; starch, flavoring agents, and other components also played a part. Most enamel destruction was produced by fruit-flavored candies in which the inherent acid or high sugar concentration or both inhibited bacterial fermentation.

Acids↗
PubMed2004

Flavor analysis in a pharmaceutical oral solution formulation using an electronic-nose.

Flavors are commonly used in pharmaceutical oral solutions and oral suspensions to mask drug bitterness and to make the formulation more palatable. Flavor analysis during product development is typically performed by human organoleptic analysis, which is often expensive and less objective. A novel approach using a metal oxide sensor-based instrument (electronic-nose) for headspace analysis was explored to replace human sensory perception for consistent qualitative and quantitative analysis of flavors in a pharmaceutical formulation. The use of the electronic-nose technique to qualitatively distinguish among six common flavoring agents (raspberry, red berry, strawberry, pineapple, orange, and cherry) in placebo formulations was demonstrated. The instrument was also employed to identify unknown flavors in drug formulation placebos. Raspberry flavor samples from different lots made by the same manufacturer, as well as freshly prepared and aged samples, were also distinguished by electronic-nose. Therefore, the instrument can potentially be used for identity testing of different flavor raw materials and the flavored solution formulations. The electronic-nose was also employed successfully for quantitative analysis of flavors in an oral solution formulation. The quantitative method might be used to assay the flavor concentration during release testing of the oral solution formulation or to monitor flavor shelf-life in the marketed container. It can also be implemented for packaging selection for the formulation in order to ensure the flavor shelf-life. Chemometric methodologies including principal component analysis (PCA), discriminant factorial analysis (DFA), and partial least squares (PLS), were used for data processing and identification.

Administration, Oral↗
PubMed1988

Oral mucosal reactions to cinnamon-flavored chewing gum.

Oral lesions induced by contact with cinnamon flavoring agents are relatively uncommon, and are probably unrecognized as such by many clinicians. Ten patients with these lesions seen during the past 6 years are described in this report. Most patients had a "burning sensation" as their primary symptom. Clinically, lesions appeared as erythematous patches with varying degrees of superimposed keratosis or ulceration, or both. The lesions were usually confined to the buccal mucosa and lateral border of the tongue. The offending agent was almost always cinnamon-flavored chewing gum, and symptoms typically resolved within 1 to 2 days of discontinuing the product containing cinnamon.

Adult↗
PubMed2004

Effect of vanillin on toxicant-induced mutation and mitotic recombination in proliferating somatic cells of Drosophila melanogaster.

Vanillin (VA; C8H8O3) is a flavoring agent that in previous studies has both increased and decreased the genotoxicity of chemical agents, depending on the nature of both the agent and the genetic event measured. The ability of VA to modulate the mutagenicity and recombinogenicity of three different monoalkylating agents, N-ethyl-N-nitrosourea (ENU), N-methyl-N-nitrosourea (MNU), and ethyl methanesulfonate (EMS), and the intercalating agent bleomycin (BLEO) was examined using the somatic mutation and recombination test (SMART) in Drosophila melanogaster. While neither the mutagenicity nor the recombinagenicity of ENU or MNU was modified by posttreatment with VA, EMS-induced genetic toxicity was enhanced by as much as 30%. This overall enhancement included a synergistic increase in mitotic recombination and a lesser decrease in mutation. Posttreatment with VA also produced an increase in the genotoxicity of BLEO, which was characterized by increases of 120% and 180% for 0.5% and 1% VA, respectively. This enhancement was restricted to an increase in recombinational events, since no alteration in BLEO-induced mutation was observed. The data suggest that the major VA-modulatory action on genotoxicity in D. melanogaster is related to its synergistic effects on somatic recombination, which has a greater consequence on overall genotoxicity than its antimutagenic effects. Since the SMART assay is specifically sensitive to mitotic crossing-over, our data suggest that VA promotes toxicant-induced homologous recombination, at least in the proliferative cells of Drosophila.

Alkylating Agents↗
PubMed2004

Analysis of thresholds for carcinogenicity.

Re-evaluations of large prominent studies, e.g. the ED01 study and N-nitrosodiethylamine, unequivocally have demonstrated that thresholds exist for carcinogenicity when the dose-response curves for animal studies done at high doses are calculated according to fundamental principles of chemistry. This requires dose to be on a logarithmic scale and percent tumors on a linear scale. Fifteen compounds approved by the Flavor and Extract Manufacturers Association (FEMA) expert panel as Generally Recognized As Safe (GRAS) have been reported to be carcinogenic in rodent studies. The thresholds for tumors of these flavors were at least several orders of magnitude greater than the estimated daily dose of these flavoring agents to individuals in the United States. Similarly, comparisons of thresholds of carcinogenicity of chemicals and drugs to which humans are exposed with their exposure levels suggest that experimental animals are more sensitive to carcinogenicity than humans. The animal studies should be viewed as providing evidence for the safety of these flavors and other compounds at current levels of human exposure.

Animals↗
PubMed2006

Clinical features of cinnamon-induced contact stomatitis.

Cinnamon flavoring agents are known to act on the mucosa as irritants or sensitizers. The objective of this study was to report on clinical and histologic features important in the diagnosis of cinnamon-induced contact stomatitis. We examined 37 past cases of contact stomatitis and identified clinical signs and symptoms and possible causes. The most common cause in the 37 cases was toothpaste; other causes were chewing gum and foods. Although various clinical findings were observed, some characteristics were evident. The most commonly affected site was the gingiva, which showed diffuse or generalized erythema and epithelial sloughing. It is important to identify the causative agents of such a disorder by understanding characteristic signs and symptoms and conducting an appropriate inquiry.

Adult↗
PubMed2001

The science and complexity of bitter taste.

Food choices and eating habits are largely influenced by how foods taste. Without being the dominant taste sensation, bitter taste contributes to the complexity and enjoyment of beverages and foods. Compounds that are perceived as bitter do not share a similar chemical structure. In addition to peptides and salts, bitter compounds in foods may include plant-derived phenols and polyphenols, flavonoids, catechins, and caffeine. Recent studies have shown that humans possess a multitude of bitter taste receptors and that the transduction of bitter taste may differ between one compound and another. Studies of mixture interactions suggest further that bitter compounds suppress or enhance sweet and sour tastes and interact with volatile flavor molecules. Caffeine, a natural ingredient of tea, coffee, and chocolate, has a unique flavor profile. Used as a flavoring agent, it enhances the sensory appeal of beverages. Research developments on the genetics and perception of bitter taste add to our understanding of the role of bitterness in relation to food preference.

Aging↗
PubMedDate not supplied

Exhaled nitric oxide measurement in workers in a microwave popcorn production plant.

Airways obstruction in microwave-popcorn workers has been attributed to inhalation of flavoring agents. Two former workers at a microwave-popcorn plant were found by lung biopsy to have bronchiolitis obliterans. The study's aim was to determine whether exhaled nitric oxide (FENO) levels were associated with exposure levels, respiratory symptoms, or airways obstruction. A questionnaire, spirometry, and FENO measurements were completed by 135 workers. The FENO levels of workers with high flavoring exposures (n = 107) were compared with those of workers with low exposures (n = 28) and healthy external controls (n = 31). FENO levels were significantly lower in the high-exposure group (p < 0.05). There is no indication that FENO is useful as a marker of lung injury in a flavoring-exposed worker population with a substantial lung disease burden, but the finding of low FENO in the high-exposure group should not be dismissed.

Adolescent↗