OBJECTIVES: This study was performed to investigate the effect of drink containing sodium benzoate on the change of urinary hippuric acid (UHA) and methyl hippuric acid (UMHA) excretion among workers coexposed to low toluene and xylene. METHODS: Study subjects were 55 male shipbuilders who were divided into 3 groups; nonexposed group (n=10, who were not exposed to organic solvent and had drunk sodium benzoate), exposed A group (n=24, who were coexposed to toluene and xylene, and had drunk sodium benzoate), and exposed B group (n=21, who were coexposed to toluene and xylene, and had not drunk sodium benzoate). The study methodology consisted of questionnaire survey, urinary analysis for metabolites of toluene and xylene before and after drinking with or without sodium benzoate, and personal air sampling of toluene and xylene. RESULTS: Before drinking, there was no significant difference in UHA or UMHA between the exposed A and B groups. After 1.5 hour of drinking, UHA of the exposed A group was significantly higher than that of the exposed B group. After 3 hours, however, UHA of the exposed A group was decreased to the level of the exposed B group, regardless of the ambient toluene level. UMHA exhibited no significant difference between the exposed A and B groups regardless of time and ambient toluene level. The regression model showed that drinking of sodium benzoate was positively correlated with UHA after 1.5 hours of drinking, but not after 3 hours. In addition, sodium benzoate didn't affect UMHA. CONCLUSIONS: This study showed that sodium benzoate initially increased UHA temporally but that its effect disappeared after 3 hours. In the medical examination of toluene exposure workers, the ingestion of drink containing sodium benzoate should be forbidden during the 3 hours prior to urinary sampling.
Drinking ; Eating ; Humans ; Male ; Questionnaires ; Sodium Benzoate* ; Sodium* ; Toluene* ; Xylenes*

Objective and METHOD: In order to identify the aggravating agents for intrinsic asthma, we performed ASA- and food additive-challenge tests on 182 subjects diagnosed as having intrinsic asthma. The following tests were performed: Lysine-aspirin bronchoprovocation test to confirm aspirin-sensitivity, sodium bi-sulfite (40-200mg) oral provocation test for sulfite sensitivity, tartrazine oral provocation test (50mg) for tartrazine sensitivity, and sodium benzoate (400mg) oral provocation test for sodium benzoate sensitivity. Positive reaction was defined as decrease in FEV, by more than 20% from the baseline value after the provocation. RESULT: Seventy-five (41.2%) of 182 subjects showed positive responses to more than one agent among the aspirin and three food additives challenged. The prevalence of aspirin-sensitivity was the highest (22.5%), followed by sulfite-sensitivity (8.8%), and then concurrent sensitivity to both aspirin and sulfite (6.0% ), to both aspirin and tartrazine (1.6% ), to aspirin, sulfite and tartrazine (1.1%) and to aspirin, sulfite and sodium benzoate (0.5%). Rhino-sinusitis was noted in 62.5% of aspirin-sensitive asthmatic subjects, 60% of sulfite-sensitive ones, and 80% of tartrazine-sensitive ones. Urticaria was noted in 21.4% of aspirin-sensitive asthmatic subjects, 16.6% of sulfite-sensitive ones and 6.3% of tartrazine-sensitive ones. Thirty-seven to 83% of positive responders had no adverse reaction history. CONCLUSION: These findings suggest that ASA and food additive challenge tests should be considered as a screening test to evaluate any aggravating factors in subjects with intrinsic asthma, even though they may not have experienced any adverse reactions.
Aspirin* ; Asthma* ; Food Additives* ; Mass Screening ; Prevalence ; Sodium ; Sodium Benzoate ; Tartrazine ; Urticaria

The role of food additives in chronic urticaria (CU) is still under investigation. In this study, we aimed to explore the association between food additives and CU by using the basophil activation test (BAT). The BAT using 15 common food additives was performed for 15 patients with CU who had a history of recurrent urticarial aggravation following intake of various foods without a definite food-specific IgE. Of the 15 patients studied, two (13.3%) showed positive BAT results for one of the tested food additives. One patient responded to monosodium glutamate, showing 18.7% of CD203c-positive basophils. Another patient showed a positive BAT result to sodium benzoate. Both patients had clinical correlations with the agents, which were partly determined by elimination diets. The present study suggested that at least a small proportion of patients with CU had symptoms associated with food additives. The results may suggest the potential utility of the BAT to identity the role of food additives in CU.
Basophils* ; Diet ; Food Additives* ; Humans ; Hypersensitivity ; Immunoglobulin E ; Sodium Benzoate ; Sodium Glutamate ; Urticaria*

Antihistamines are commonly used for the treatment of urticaria. Some antihistamines contain dyes and preservatives which have themselves been shown to produce or exacerbate urticaria. Tartrazine is used predominantly as an additive in food and drugs. To stimulate awareness of this problem, the author reports a case of recurrent urticaria induced by tartrazine in an antihistamine in a 25-year-old male patient. His skin lesions recurred after treatment with oral antihistamine containing tartrazine. The provocation tests with 0.1mg of tartrazine and the antihistamine containing tartrazine induced urticaria within two hours. The provocation tests with aspirin and sodium benzoate were negative.
Adult ; Aspirin ; Coloring Agents ; Histamine Antagonists ; Humans ; Male ; Skin ; Sodium Benzoate ; Tartrazine* ; Urticaria*

Objective To establish an infrared spectroscopic method for the rapid qualitative and quantitative analysis of caffeine and sodium benzoate in Annaka samples. Methods Qualitative and quantitative modeling samples were prepared by mixing high-purity caffeine and sodium benzoate. The characteristic absorption peaks of caffeine and sodium benzoate in Annaka samples were determined by analyzing the infrared spectra of the mixed samples. The quantitative model of infrared spectra was established by partial least squares （PLS）. Results By analyzing the infrared spectra of 17 mixed samples of caffeine and sodium benzoate （the purity of caffeine ranges from 10% to 80%）, the characteristic absorption peaks for caffeine were determined to be 1 698, 1 650, 1 237, 972, 743, and 609 cm^-1. The characteristic absorption peaks for sodium benzoate were 1 596, 1 548, 1 406, 845, 708 and 679 cm^-1. When the detection of all characteristic absorption peaks was the positive identification criteria, the positive detection rate of caffeine and sodium benzoate in 48 seized Annaka samples was 100%. The linear range of PLS quantitative model for caffeine was 10%-80%, the coefficient of determination （ R²） was 99.9%, the root mean square error of cross validation （RMSECV） was 0.68%, and the root mean square error of prediction （RMSEP） was 0.91%; the linear range of PLS quantitative model for sodium benzoate was 20%-90%, the R² was 99.9%, the RMSECV was 0.91% and the RMSEP was 1.11%. The results of paired sample t test showed that the differences between the results of high performance liquid chromatography method and infrared spectroscopy method had no statistical significance. The established infrared quantitative method was used to analyze 48 seized Annaka samples, the purity of caffeine was 27.6%-63.1%, and that of sodium benzoate was 36.9%-72.3%. Conclusion The rapid qualitative and quantitative analysis of caffeine and sodium benzoate in Annaka samples by infrared spectroscopy method could improve identification efficiency and reduce determination cost.
Caffeine ; Chromatography, High Pressure Liquid ; Least-Squares Analysis ; Sodium Benzoate ; Spectroscopy, Near-Infrared

Aspirin(ASA) and NSAIDs can induce bronchoconstriction in 10~20% of adult asthmatics patients. Inhalation of lysine-ASA(L-ASA) has been described as an alternative method for diagnosis of ASA-sensitive asthma. To further understand the characterlstics of ASA-sensitive asthmas. we studied 38 asthmatic patients with ASA -sensitivity (36 intrinsic and 2 extrinsic asthma) proven by L-ASA bronchoprovocation test (BPT). Most were female (male to female ratio was 27:73). Twenty (53%) of them had no previous history of adverse reactions when exposed to ASA. Twenty nine (79%) had rhino-sinusitis symptoms. Early asthmatic response was observed in 16 (42%) patients, late only response in 16(42%), and dual response in 6(16%) patients. The threshold of L-ASA to provoke a positive response ranged from 11.2 to 180 mg/ml and most (68.3%) had a positive response after the inhalation of 180 mg/ml. Concurrent sensitivity to sulfite was noted in 14 (36%) patients, followed by sensitivity to tartrazine in one (3%) patient. None showed a positive response to sodium benzoate. After the avoidance from ASA/ NSAIDs with administration of anti-asthmatic medications, symptom and medication scores reduced in 26(87%) patients among 30 followed patients. They were classified into the improved group: four (13%) patients belonged to the not-improved group. There were no significant differences in clinical characteristics between the improved and not- improved group (p>0.05). In conclusion, L-ASA BPT could be considered as a useful method to diagnose ASA -sensitive asthma and be used to screen the causative agent for asthmatic patients with intrinsic type, especially in female patients with rhino-sinusitis and/or nasal polyp, even though they do not have arty history of adverse reactions. Cessation of exposure and proper treatment may allow to reduce symptom and medication scores.
Adult ; Anti-Inflammatory Agents, Non-Steroidal ; Asthma* ; Bronchoconstriction ; Diagnosis ; Female ; Humans ; Inhalation ; Nasal Polyps ; Sodium Benzoate ; Tartrazine

PURPOSE: This study was undertaken to determine whether lipid peroxidation induced by hydroxyl radicals play a critical role in cisplatin(cis-diamminedichloroplatinum II)-induced acute renal failure. METHODS: Animals received cisplatin at a single i.p. dose of 5 mg/kg, and changes in renal function were measured at 48 hr after cisplatin injection. RESULTS: Cisplatin caused an increase in serum creatinine level, which was accompanied by reduction in GFR. The fractional excretion of Na(+), glucose, and inorganic phosphate was increased in animals treated with cisplatin alone. Cisplatin treatment in vivo inhibited PAH uptake by renal cortical slices and Na(+)-K(+)-ATPase activity in microsomal fraction. Lipid peroxidation was increased in cisplatin-treated kidneys. When animals received the antioxidant N,N'-diphenyl-p-phenylenediamine(DPPD), the iron chelator deferoxamine, and hydroxyl radical scavengers dimethylthiourea and sodium benzoate before cisplatin injection, alterations in renal function and lipid peroxidation induced by cisplatin were significantly prevented. Exposure of renal cortical slices to cisplatin in vitro caused an increase in LDH release and lipid peroxidation, which were completely prevented by DPPD and deferoxamine. By contrast, hydroxyl radical scavengers(dimethylthiourea and thiourea) did not prevent cisplatin-induced LDH release despite they inhibited cisplatin-induced lipid peroxidation. CONCLUSION: These results suggest that the lipid peroxidation resulting from generation of hydroxyl radicals may play a role in cisplatin-induced acute renal failure. In addition, the protective effects of hydroxyl radical scavengers in vivo studies are different from the results obtained from in vitro studies using renal cortical slices.
Acute Kidney Injury* ; Animals ; Cisplatin ; Creatinine ; Deferoxamine ; Glucose ; Hydroxyl Radical ; Iron ; Kidney ; Lipid Peroxidation* ; Rabbits* ; Reactive Oxygen Species ; Sodium Benzoate

Citrullinemia is an inborn error of urea cycle metabolism caused by deficiency of arginosuccinate synthetase. It is characterized by hyperammonemia and high citrulline level in serum, CSF and urine. The clinical symptoms include vomiting, lethargy, seizure, coma and ultimately death if hyperammonemia is not controlled. We report a case of 9- day old male with citrullinemia who was initially treated with sodium benzoate during acute stage followed by gradual weaning to discontinuation. Hyperammonemia was well controlled by low protein milk diet and arginine.
Arginine* ; Citrulline ; Citrullinemia* ; Coma ; Diet* ; Humans ; Hyperammonemia ; Lethargy ; Ligases ; Male ; Metabolism ; Milk ; Seizures ; Sodium Benzoate ; Urea ; Vomiting ; Weaning

Atomic force microscope (AFM) was used to study biotoxicity of food preservative sodium benzoate (SB) at the single cellular level. Lymphocyte morphology and membrane ultrastructure treated with SB at different concentrations and time were analyzed visually. As compared to the normal lymphocyte, the cell morphology and membrane was significantly changed and its ultrastructure was also complicated. After treated with SB, the Rp-v, Rq, Ra and Z values were changed. The statistical analysis of lymphocytes after treated with SB was studied, and discussed its mechanism.
Animals ; Cell Membrane ; ultrastructure ; Lymphocytes ; drug effects ; pathology ; Mice ; Mice, Inbred BALB C ; Microscopy, Atomic Force ; Sodium Benzoate ; toxicity

Urea cycle disorder (UCD) is a group of inherited metabolic diseases with high disability or fatality rate, which need long-term drug treatment and diet management. Except those with Citrin deficiency or liver transplantation, all pediatric patients require lifelong low protein diet with safe levels of protein intake and adequate energy and lipids supply for their corresponding age; supplementing essential amino acids and protein-free milk are also needed if necessary. The drugs for long-term use include nitrogen scavengers (sodium benzoate, sodium phenylbutyrate, glycerol phenylbutyrate), urea cycle activation/substrate supplementation agents (N-carbamylglutamate, arginine, citrulline), etc. Liver transplantation is recommended for pediatric patients not responding to standard diet and drug treatment, and those with severe progressive liver disease and/or recurrent metabolic decompensations. Gene therapy, stem cell therapy, enzyme therapy and other novel technologies may offer options for treatment in UCD patients. The regular biochemical assessments like blood ammonia, liver function and plasma amino acid profile are needed, and physical growth, intellectual development, nutritional intake should be also evaluated for adjusting treatment in time.
Humans ; Child ; Citrullinemia/drug therapy* ; Urea Cycle Disorders, Inborn/therapy* ; Arginine ; Sodium Benzoate/therapeutic use* ; Liver Transplantation