PubMed · 278929
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I L Shannon, E N Starcke. 1978. Higher performance denture cleansers.. https://pubmed.ncbi.nlm.nih.gov/278929/
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A method of quantitating uronic acids and uronic acids from pectin in particular is described. The method uses carbazole in 80% sulfuric acid with borate ions added. The assay is carried out at 60 degrees C. This assay has some cross reactivity with aldose sugars and must be timed precisely. A further method that is specific for galacturonic acid is also described. This method uses concentrated sulfuric acid and carbazole only. Of the biological substances tested, only formaldehyde and glyceraldehyde showed a reactivity of more than 10% that of galacturonic acid on a weight to weight basis.
An outbreak of an illness suggestive of boric acid poisoning occurred among 51 persons who had eaten lunch at the cafeteria of the United States Agency for International Development in Islamabad, Pakistan, on February 11, 1990. Affected patients had headache and severe myalgias 2 to 4 hours after eating lunch. Fever, nausea and vomiting, red eyes, and photophobia were also reported. Among 25 patients (49%), a sunburn-like inflammation of the skin of the face developed, which subsequently desquamated. One patient required hospitalization for 1 day because of dehydration. Among all patients, the only symptoms remaining 72 hours after the meal were mild headache, fatigue, and peeling skin. Those persons who became ill were more likely to have eaten one particular food item (minestrone soup) for lunch than were those who did not become ill. A similar illness has been described following ingestion of boric acid. However, the results of an analysis of serum samples collected 3 days after the lunch from 24 patients did not show boron above normal background levels. Because of boron's short half-life, however, these data do not rule out the possibility that patients may have had higher boron levels at the onset of the illness.
A 45-year-old white man ingested approximately two cups of boric acid crystals dissolved in water in a suicide attempt. Nausea, vomiting, greenish diarrhea, and dehydration occurred shortly thereafter. Two days later, he presented to the hospital with hypotension, metabolic acidosis, oliguric renal failure, a generalized erythematous rash, and several superficial skin abrasions. His condition failed to improve despite intravenous fluids and vasopressors. He later developed atrial fibrillation with a rapid ventricular response and could not be converted to a sinus rhythm. This rhythm deteriorated to electromechanical dissociation, and the patient died 17 hours after admission. The urine and whole blood boric acid concentrations approximately 52 hours after ingestion were 160 and 42 mg/dL, respectively. These results are equivalent to urine and blood boron concentrations of 28 and 7 mg/dL, respectively. A postmortem urine boron concentration was 29.4 mg/dL. The autopsy report listed boron toxicity as the cause of death. This is the only adult reported to die from acute boric acid ingestion in recent years and may be atypical since the patient was untreated for 3 days and presented with dehydration and renal function impairment. This case suggests that lack of adequate urine flow and dehydration increases the risk of boron toxicity.