SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
The skin manifestations associated with boric acid intoxication are particularly striking. We present a case report of a 44-year-old black woman who, following a suicide attempt, demonstrated the classic features of acute boric acid poisoning. She developed generalized erythema creating a "boiled lobster" appearance with massive areas of desquamation. A discussion of the history of the use of boric acid by the medical profession follows the patient presentation.
OBJECTIVES: Both boric acid (H3BO3) and phosphoric acid (H3PO4) are components of dental cements, commonly incorporated into glass (as ingredients in the melt) and occasionally added to the powder or liquid components. This study investigated the effect of boric acid addition to an experimental glass-ionomer powder and the effect of phosphoric acid addition to a glass-ionomer liquid on the 24-h compressive strength. METHODS: Boric acid powder was added in various concentrations to an experimental glass-ionomer powder and, separately, phosphoric acid was added to an experimental glass-ionomer liquid. Powders and liquids were dosed into capsules at various powder:liquid ratios and cements thus formed were assessed for 24-h compressive strength. RESULTS: Incorporation of boric acid in glass-ionomer powder resulted in a pronounced decrease (p < 0.05 at 1% boric acid) in compressive strength. Addition of phosphoric acid produced initially stronger cements (up to 13% increase at 1% phosphoric acid) before also declining. SIGNIFICANCE: The incorporation of less than 2% w/w phosphoric acid in glass-ionomer liquids may improve cement strengths without compromising clinical usefulness. The incorporation of boric acid in glass-ionomer cements is contraindicated.
Equilibrium geometries, energies, and vibrational frequencies of cage-shaped boric acid clusters including the onion-like structure have been calculated at the HF/6-31G and B3LYP/6-31G(d) levels of theory. A family of cage-shaped boric acid clusters becomes evident according to our calculations. Each member of the family is formed by strong O-H...O hydrogen bonds. Higher cage-shaped boric acid clusters are more stable. The calculated stabilization energies for the cage-shaped boric acid clusters appear to steadily increase with the number of boric acid molecules (n) and are nearly linear in n. Similarities between cage-shaped boric acid clusters and fullerenes are also discussed.
Borate products varied in efficacy against larval cat fleas, Ctenocephalides felis felis Bouché, with some effective at rates of 23 micrograms/cm2 when larvae were exposed to the compounds in sand. Powdered boric acid, granular boric acid, and disodium octaborate tetrahydrate (Polybor) at rates of 200 micrograms/cm2 produced < or = 90% mortality of larvae exposed in carpet for 96 h. LC50 values of larvae exposed in treated carpets for 96 h were 23 micrograms/cm2 for powdered boric acid, 40 micrograms/cm2 for granular boric acid, and 47 micrograms/cm2 for polybor.
There is little published experience with the extracorporeal treatment of boric acid overdose, although the pharmacokinetic properties of boric acid suggest a potential role for hemodialysis. We report a rare case of potentially toxic boric acid overdose that was treated successfully with hemodialysis. Based on our experience in this patient and a review of previously reported cases, hemodialysis is effective in decreasing serum boric acid levels and should be considered in the treatment of patients with acute boric acid intoxication.
The improper use of boric acid containing antiseptics is still one of the most common causes of toxic accidents in newborns and infants. Health hazards may also arise from inadvertent absorption of insecticides and household products containing borates as well as from occupational accidents related to production and use of boranes. A variety of boronated agents with hypolipidemic, antiinflammatory or anticancer properties have been developed in recent years. Unfortunately, most of these compounds were found to be highly toxic when tested at the required therapeutic dosages in animals. In this paper, recent information on human toxicology of boron is reviewed, with special emphasis on epidemiological and clinical aspects of boric acid poisoning.
The field of legal medicine has seen a recent increase of poisoning by boric acid and, in cases of emergency, a simple method of making a qualitative analysis of the boric acid content is a necessity. Thus, we have examined curcuma paper (turmeric paper) to see if it can provide a qualitative analysis of the boric acid content in biological materials, so as to identify cases of poisoning. It was found that curcuma paper can provide a preliminary analysis of the quantitative content of boric acid, and that about 0.1 mg/ml of boric acid can be determined. The steps for this testing method follow. First, either blood or urine is acidified with a 6 N concentration of hydrochloric acid, i.e., in the case of urine, 0.5 ml of urine is added to 0.1 ml hydrochloric acid, and for blood, 0.5 ml of blood is added to 0.2 ml hydrochloric acid. If the sample is not sufficiently acidic, more hydrochloric acid is added. Next, a drop of the sample is placed on the curcuma paper and, after drying at room temperature, a red stain results if boric acid is present. (Rosocyanin is formed by the reaction of boric acid and protonated curcumin). Then, a 1 N concentration of sodium hydroxide is dropped onto the stained place, and if rosocyanin is present, the stain will turn blue. Informatively, to make curcuma paper, filter paper (No. 2) is soaked in a saturated curcumin/ethanol solution and then air dried.(ABSTRACT TRUNCATED AT 250 WORDS)
Boric acid (BA) is a naturally occurring agent used in manufacturing processes and numerous consumer products. Because of the potential for both industrial and consumer exposure to boron-containing compounds, and the lack of developmental toxicity data, the National Toxicology Program evaluated the potential for boric acid to cause developmental toxicity in pregnant Swiss (CD-1) mice, Sprague-Dawley rats (n = 26-28/group), and New Zealand rabbits (n = 18-23/group). BA was provided in the feed to mice and rats at 0, 0.1, 0.2, or 0.4% throughout gestation to attain steady-state exposure as early as possible during development. Average doses (mg/kg/day) were 248, 452, or 1003 for mice, and 78, 163, or 330 in rats. A separate group of rats received 0.8% BA in the feed, or 539 mg/kg/day only on gestation days (gd) 6 to 15. Rabbits were given BA (0, 62.5, 125, or 250 mg/kg) by gavage administration on gd 6 to 19. Maternal body weight, food and/or water consumption and signs of toxicity were monitored at regular intervals. At termination, gd 17 (mice), 20 (rats), or 30 (rabbits), the uterus was examined to determine the number of resorptions, dead, or live fetuses. Fetuses were weighed and live fetuses were examined for external, visceral, and skeletal defects. Mouse dams exhibited mild renal lesions (> or = 248 mg/kg/day BA), increased water intake and relative kidney weight (1003 mg/kg/day BA), and decreased weight gain during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
In connection with the discussion on a uniform regulation within the European Communities for baby-care products containing boric acid, it was of interest to which degree boric acid can be absorbed through normal or damaged skin from a common baby ointment. Studies performed by an in vitro permeation method using excised human skin and by a liberation method in the absence of a membrane are described. Boron was not detectable in the acceptor compartment when intact skin was tested, while using damaged skin, prepared by removing the horny layer, a maximum permeation of 2.46 micrograms/cm2 boron, corresponding to 14.1 micrograms/cm2 boric acid, was measured. Accordingly the stratum corneum functions as an effective barrier for the cutaneous permeation of boric acid under the given conditions. Thus there is no cause for concern that the ointment under consideration could evoke unwanted systemic effects when applied to healthy skin. The results showing permeation of boric acid through damaged skin are of special interest, since it has to be taken into account, that skin care preparations for babies may be applied on irritated skin, e.g. in cases of napkin dermatitis. On the basis of the permeation results for damaged skin the possible daily boron uptake of babies, treated with the test product, is estimated and compared to the daily alimental intake of boron. With respect to quantities of boric acid delivered per unit of surface in the skin model and in the liberation system, the permeation through damaged skin amounts to 86% of the release. The results indicate, that the degree of permeation through damaged skin depends on the degree of liberation from the vehicle. The liberation model presented here could be suitable for the assessment to which extent boric acid may be absorbed from an ointment through damaged skin in worst case.
Two strains of boric acid tolerant Vibrio cholerae have been studied in order to identify the characteristics which distinguish them from the 'wild-type' virulent strains. Strain Ib5 requires either amino acid cysteine or methionine while strain Ib5S requires deoxyribonucleic acid (DNA) for growth. Although the strains did not grow on desoxycholate citrate agar (DCA) they grew well on chocolate agar. Morphologically filamentous, bacillary and comma-shaped forms were seen, depending on the media and incubation period. The strains failed to cause accumulation of fluid in gut ligation and permeability factor tests. With the single radial immunodiffusion test, strain Ib5S gave positive reaction in 83% of the tests when DNA was added to the growth medium. On the other hand only 25% of the tests were positive when no DNA was added to the growth medium, even though the antigen was concentrated ten-fold. Strain Ib5 only gave 50% positive tests when the antigen was concentrated ten-fold. It is therefore suggested that Ib5S strain is a cholerangenoid producer in the presence of DNA, and may be useful as an effective vaccine against cholera.
Catecholamines, dopamine and the renal kallikrein-kinin system may participate in the pathogenesis of hypertension. In the past these systems have been studied independently in isolation. Attempts to study the systems together have been hampered by incompatibility of the current urine preservatives for the two assays involved. In order to measure acid-stable catecholamines and acid-labile kallikrein enzyme together, we have established boric acid solution as a preservative by comparing the stability of urinary catecholamines stored in it with the commonly employed preservative, hydrochloric acid (HCl) as well as the stability of urinary kallikrein in untreated urine with and without boric acid at ambient temperatures for 24 and 48 h, and at -20 degrees C for 2 weeks and 1, 2 and 3 months. The stability of other common urine parameters including cortisol, electrolytes, creatinine and protein, was also investigated after storage with boric acid at ambient temperature for 24 h. Our results showed that there was a good agreement between the measurements of urinary catecholamines stored in both HCl and boric acid and that the latter did not interfere with measurements of urinary kallikrein or other common urine parameters.
The influence of boric acid, a boron carrier, on Ehrlich ascites carcinoma (EAC) cell-bearing mice was investigated in view of its importance in the boron neutron capture therapy and the influence of boron on proliferation and progression of cancer cells mediated by proteoglycans and collagen. The present study included the evaluation of boric acid for the effects on total count and viability of EAC cells in addition to their non-protein sulfhydryls (NP-SH) and malondialdehyde (MDA) contents as parameters for conjugative detoxication potency and possible oxidative damage. The EAC cell-bearing animals were also observed for the effect on survival, body weight changes, and histopathological evaluation of the tumors grown at the site of inoculation. The treatment with boric acid significantly increased the total number of peritoneal EAC cells and their viability. A significant increase in the body weight was observed that dose-dependently reached plateau levels by 20 days of treatment. Conversely, a reduction in the duration of survival of these animals was evident with the same protocol. Boric acid treatment resulted in a decrease in NP-SH contents with a concomitant increase in MDA levels in EAC cells as revealed by the results of the biochemical analysis. These data are supported by our results on histopathological investigations, which apparently showed fast growth, in addition to several mitotic figures and mixed inflammatory reaction, after treatment with boric acid. It seems likely that a particular combination of properties of boric acid, rather than a single characteristic alone, will provide useful information on the use of this boron carrier in neutron capture therapy.
The author carried out a study on the effectiveness of the boric acid as a stomach poison for German cockroach control from July to September 1971. The test was performed by the feeding method under conditions of 20 degrees C and 80 per cent relative humidity. The baits were composed of one control group and five different combination groups with boric acid and sugar as follows. 1)10 g sugar only(control group), 2)1 g powedered boric acid to 9 g sugar(1:9 poison baits), 3)2 g powdered boric acid to 8 g sugar(2:8 poison baits), 4)4 g powdered boric acid to 6 g sugar(4:6 poison baits), 5)5 g powdered boric acid to 5g sugar(5:5 poison baits), 6)10 g powdered boric acid only (10:0 poison baits). The insects were composed of 360 female adult German cockroaches collected by traps at the kitchens of restaurants and house holds in Seoul City. The results were as follows: 1.The total mortality by poison baits in 72 hours after treatment were: 1)44.3 % by 1:9 poison baits, 2)79.4 % by 2: poison baits, 3)96.7 % by 4:6 poison baits(the most effective poison baits), 4)88.3 % by 5:5 poison baits, 5)91.1 % by 10:0 poison baits. 2.The peak mortality by the treatment hours were: 1)Up to 21 hours: 23.3 % by 5:5 poison baits, 20.0 % by 10:10 poison baits, 2)From 24 to 48 hours: 71.1 % by 4:6 poison baits, 55.6 % by 10:0 poison baits, 3)From 48 to 72 hours: 21.9 % by 2:8 poison baits, 19.6 % by 1:9 poison baits. The most effective treatment hours was from 24 to 48 hours.
A retrospective chart review was conducted at two regional poison centers to determine the clinical outcome of boric acid ingestions and to assess the relationship between serum boric acid levels and clinical presentation. A total of 784 cases were studied; all but 2 were acute ingestions. No patients developed severe manifestations of toxicity, and 88.3% were entirely asymptomatic. The most common symptoms were vomiting, abdominal pain, and diarrhea. Lethargy, headache, lightheadedness, and atypical rash were seen less frequently. Boric acid levels were obtained in 51 patients and ranged from 0 to 340 micrograms/mL. Blood levels were 70 micrograms/mL or more in 7 patients; 4 remained asymptomatic, whereas the other 3 had nausea or vomiting. Dialysis was performed in 4 of these 7 patients, only 1 of whom had symptoms (vomiting). On the basis of data from 9 patients, the mean half-life of boric acid was determined to be 13.4 hours (range, 4.0 to 27.8). Hemodialysis in 3 patients significantly shortened the half-life compared with pre- and postdialysis half-lives. Our results suggest that acute boric acid ingestions produce minimal or no toxicity and that aggressive treatment is not necessary in most patients.
BACKGROUND: Boron is a ubiquitous element widely distributed in nature in the form of borates at low concentrations in soils and rocks. Boron is released from these minerals by the natural weathering processes in the form of boric acid, which is water soluble and biologically available. High levels of boric acid are naturally found in sea water. Boric acid and borax are used in the greatest quantities and represent the major boron chemical exposures to humans and the environment. The principal use of boric acid and borax is in the manufacture of various types of glass products that do not result in exposure to the consumer. Boric acid and borax are also found in an array of consumer goods including fireproofing for fabrics and wood, insecticides, and in many cosmetics and personal care products as well. Boron may be an essential element for higher animals including humans. HUMAN EXPOSURE: Boric acid and borax are considered to be completely absorbed by the oral route of exposure. Absorption through intact skin is considered negligible, although absorption can occur through denuded or irritated skin. Boron levels in the body do not persist upon cessation of exposure. People may be exposed to boron through three primary sources: 1) consumption of private, municipal, or commercial (bottled) sources of drinking water; 2) dietary consumption of crops and other foodstuffs (including dietary supplements for body building); and 3) inhalation of boron compounds during their mining, manufacturing, and other industrial processing. While boron has been detected in 81.8% of the municipal water systems, it is a minor source of boron in most parts of the U.S. The mean boron concentration is reported as 0.2 mg B/L. However, residents of California and other western states with boron-rich geologic deposits may be regularly exposed to higher levels in drinking water. Individuals who drink bottled mineral water may also increase their exposure to boron. An EPA health advisory, recommends boron concentrations in drinking water not exceed 0.6 mg B/L [0.06 mM B] over a lifetime of exposure. Dietary exposure to boron for an adult typically ranges from ranges from 0.25 to 3.1 mg B/d with an average of 1.5 mg B/d. The high end of the exposure range, 3.1 mg B/d, was selected by the Expert Committee as best estimate of exposure. It should be noted that a diet high in fruits, vegetables, grains, legumes, and other food stuffs with high boron contents may lead to daily exposures as high as 10 mg B/d from diet alone. Some body building supplements contain boron at levels ranging from 1.5 to 10 mg B, with a median of 4 mg B. Use of the supplements containing the median concentration of boron could equal the daily intake an individual receives from diet and drinking water combined. Adults in the U.S. at the high end of the food exposure range may typically ingest up to 3.5 mg B/d, or a daily dose of 0.005 mmol B/kg b.wt., through exposure from diet (3.1 mg B/d) and drinking water (0.4 mg B/d). Individuals who also use body-building supplements may have a total daily boron intake of 7.5 mg B resulting in a daily dose of 0.01 mmol B/kg b.wt./d. Occupational exposure to boron is mainly through inhalation of borate containing dust during mining and manufacturing processes. Current occupational exposures to boron are reported to result in a daily dose of < 0.0001 to 0.2 mmol B/kg b.wt./d. Current U.S. OSHA permissible exposure limit (PEL) for sodium tetraborates is 10 mg/m3, and the California Occupational Safety and Health Administration PEL is 5 mg/m3. An exposure of 5 mg B/m3 translates to approximately 0.01 mmol B/kg b.wt./d that, coincidentally, is the same as exposure levels associated with combined municipal drinking water, diet, and body building supplement consumption. Infants may receive exposures to boric acid when it is used as a household insecticide for cockroach control. Exposure from boric acid-containing cosmetic and personal care products applie
40 g boric acid was by error given instead of glucose solution to a 62-year-old man during an oral glucose test. During an 18-hour dialysis 8.32 g boric acid was eliminated, 8.6 g by forced diuresis and at least 9 g by gastric lavage. A large amount of the poison was also found in the vomitus. The most important signs of posioning were slight metabolic acidosis, total anuria for 14 hours and normochromic anaemia. There was no residual kidney damage or other effects of the poisoning.
The acute oral mean lethal dose of boric acid in 1-day-old chickens was found to be 2.95 +/- 0.35 g/kg of body weight, which classifies this product as only slightly toxic to chickens. One-day-old broiler chicks were housed in floor pens in which litter had been treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.9 m2 of floor space. Boron residue levels in brain, kidney, liver, and white muscle were not statistically elevated following a 15-day exposure period. Boron residue levels in the same types of tissue were not significantly elevated in chicks fed 500 ppm or 1250 ppm boric acid in feed ad libitum for 3 weeks; however, residues were significantly higher in chicks fed 2500 ppm or 5000 ppm boric acid. These data indicate that broilers grown on boric acid-treated litter do not consume enough boric acid to cause elevated boron levels in tissues.
A mixture containing 3 g of boric acid and 300 mg of cinchocaine chloride prescribed due to painful dental protrusion was accidentally ingested by a 12-month-old girl. She developed violent vomiting and coughing. Irritability, tremor, seizures and a delirious reaction. She was treated with diazepam, intubated, sedated and ventilated. Her diuresis was stimulated with furosemide and fluid. Within the first 24 h she was treated with haemodialysis twice on femoral catheters. Her renal function was unaffected. In two days she fully recovered. The maximum measured levels of boric acid and cinchocaine chloride approximately 6 h after ingestion were 26 micrograms/ml and 71 ng/ml respectively. The plasma half-life of boric acid was 7.0 h and decreased to 3.6 and 4.4 h during the two haemodialyses. The total body clearance of boric acid increased correspondingly from 21 ml/min to 41 and 34 ml/min. The in vitro clearance of boric acid of the dialyser was later determined to be 18 ml/min. It is concluded that haemodialysis is valuable in the treatment of boric acid intoxication because it increases the elimination of the drug even in patients without any sign of renal toxicity.