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Usefulness of forced diuresis for acute boric acid poisoning in an adult.

BACKGROUND: Boric acid is generally not recognized as a poisonous substance. However, boric acid has potentially fatal actions such as hypotension, metabolic acidosis and oliguria. Death may result from circulation collapse and shock. OBJECTIVE: We present a clinical case history of the successful use of forced diuresis with furosemide and intravenous fluid for boric acid poisoning. SUBJECT: A 26-year-old female who attempted suicide by consuming a large quantity of boric acid. She was brought to the hospital in a state of clouded consciousness, fever and erythema 14 h after ingestion. METHOD: 3.25 L of intravenous fluid and 100 mg of furosemide were administered over a period of 4 h in the intensive care unit and the serum and urinary concentrations of boric acid measured. RESULTS: The elimination rate of boric acid obtained with diuresis was similar to that obtained with haemodialysis on a previous occasion when the same patient attempted suicide with boric acid. The patient showed only temporary emesis and diarrhoea along with erythema, and was moved to the general ward 4 h after admission. Although in the general ward the patient's fever persisted and nausea, vomiting and headache often recurred, possibly because of an insufficient dose of furosemide, the patient's condition steadily improved over the 64 h after admission. CONCLUSION: Forced diuresis without haemodialysis is recommended early after admission for boric acid poisoning.

Adult↗

Gastro-intestinal absorption and in vitro release of boric acid from water-emulsifying ointments.

Boric acid taken orally by six male volunteers in a cross-over study was absorbed to equal extents from a water solution and a 3% waterless, water-emulsifying ointment, though with a slight initial delay in the latter case. Virtually complete gastro-intestinal absorption and renal excretion were indicated by the 96-hr urinary recovery, amounting to 89.1-98.3% (mean 93.9%) and 89.2-97.5% (mean 92.4%) of the dose ingested as solution and ointment, respectively, normal daily boron excretion having been taken into account. The in vitro release of boric acid, measured for 24 hr by dialysis in water at 37 degrees C, reached 95% from a purely water-based jelly but only about 5% from the water-emulsifying ointment. The low boric acid release from the ointment was not significantly influenced when the ointment was dialysed against buffer solutions of pH 2.5 and 9.6 instead of water, or when the maximum possible amount of water (26.9% w/w) was incorporated into the ointment before dialysis. The 24-hr boric acid release from a number of other oil-based ointments, either hydrophobic or water-emulsifying and containing 1-3% boric acid and 0-28.5% water, was also low (0.9-18.3% of the boric acid content). This indicates that the formulation of the ointment is an important factor in determining the extent of release of boric acid when the ointment is applied externally, but that it does not alter the absorption of boric acid should the ointment be ingested.

Administration, Oral↗

Toxicity of boric acid to Blattella germanica (Dictyoptera: Blattellidae) and analysis of residues in several organs.

Pestiferous cockroach species are associated closely with humans and are important from medical and public health points of view. Conventional insecticides have been used widely to control cockroaches which have developed resistance to these compounds. Thus, interest has again centered on lesser-used compounds such as boric acid. Boric acid has been used as an insecticide for many years, especially against cockroach. Its mode of action on insects has not been satisfactorily established. In Algeria, Blattella germanica (Dictyoptera: Blattellidae) is a serious pest in the urban environment and their infestation were controlled for many years by organophosphate, carbamate or pyrethroid insecticides. In order to obtain more information on the mode of action of boric acid, we first evaluated the oral toxicity of boric acid on B. germanica adults. Then, the compound was determined in several organs by an colorimetric method. This insecticide was incorporated into the diet and orally administered at different concentrations ranging from 1 to 40% (w/w) to newly emerged adults. Mortality was recorded at different times during treatment (24, 48, 72 and 144 h). Treatment resulted in a dose-dependent mortality since the LD50 (%) recorded are 85 at 24 h, 67 at 48 h, 39 at 72 h and 8 at 144 h, respectively. Then the quantity of boric acid accumulated in several organs (hemolymph, gut, ovaries, testicles and fat body) was determined as function the duration of treatment (1 to 5 days) for two doses (LD50 and LD90). Results revealed that bioaccumulation of residues in these organs increased as function the duration of treatment. In addition, relatively important amounts of residues, are detected in fat body.

Adipose Tissue↗

Boric acid bait kills adult mosquitoes (Diptera: Culicidae).

The toxicity of boric acid solutions to adult Anopheles quadrimaculatus Say, Culex nigripalpus Theobald, and Aedes albopictus Skuse was evaluated in the laboratory. Median lethal concentrations (LC50 in %) at 24-h exposure for male and female An. quadrimaculatus were 0.317 and 0.885, respectively; for Cx. nigripalpus, 0.273 and 0.560, respectively; and for Ae. albopictus, 0.174 and 0.527, respectively. The LC50 values at 48-h exposure for male and female An. quadrimaculatus were 0.101 and 0.395, respectively; for Cx. nigripalpus, 0.098 and 0.255, respectively; and for Ae. albopictus, 0.078 and 0.244, respectively. In laboratory tests, access for 48 h to sucrose (10%) water containing 1% boric acid (boric acid bait) resulted in 98% mortality in blood fed, gravid, and parous Ae. albopictus. When offered a choice between boric acid bait and sucrose water, 52% of male and 33% of female Ae. albopictus ingested sufficient boric acid bait in 24 h to cause death; after 48 h, respective percent mortalities were 88 and 58%. In outdoor tests, in a walk-in screened cage (156 m3) containing 1,250 female Ae. albopictus, mosquito biting rates on the exposed forearm of a human subject in 3-min exposure were reduced > or = 78% for the boric acid bait treatment, compared with a sucrose water control.

Aedes↗

Developmental toxicity NOAEL and postnatal recovery in rats fed boric acid during gestation.

Boric acid (BA), an essential plant micronutrient, occurs naturally in fruits, vegetables, and other foods. It is widely used in the manufacture of glass, ceramics, and other products. In a prior study, gestational exposure to BA was associated with developmental toxicity in the rat, including fetal growth retardation and altered skeletal morphology. In order to establish the developmental toxicity no-observed-adverse-effect level (NOAEL) in the rat, BA (0, 0.025, 0.05, 0.075, 0.1, or 0.2% in feed) was administered to timed-mated rats (60/group) from gestational day (gd) 0 to gd 20. Approximately half the dams were terminated on gd 20, and the remaining dams delivered their litters. Pup growth and viability were monitored until postnatal day (pnd) 21. Dams sacrificed on gd 20 (pnd 21) ingested average doses of 0(0), 19(19), 36(37), 55(56), 76(74), or 143(145) mg BA/kg/day. Maternal clinical signs, body weight, and food and water intake were measured at regular intervals during gestation and lactation. At termination, maternal liver and right kidney were weighed, and live fetuses (gd 20) and pups (pnd 21) were weighed, sexed, and examined for morphological anomalies (external, visceral, skeletal). Maternal effects were limited to increased relative kidney weight at 0.2% BA. Viability of the offspring was unaffected. On gd 20, fetal body weight was 94 and 88% of controls at 0.1 and 0.2% BA, but recovery was complete at birth (approximately gd 22). The incidence of short rib XIII was increased on gd 20 at > or = 0.1% BA, but only at 0.2% on pnd 21. The incidence of wavy rib was increased on gd 20 at > or = 0.1% BA, but the reversibility of this effect was confirmed on pnd 21. A slight decrease in extra lumbar ribs was observed at 0.2% BA on gd 20, and extra lumbar ribs were not found in any pups on pnd 21. Thus, the developmental toxicity NOAEL in the rat was 0.075% BA (55 mg/kg/day) on gd 20 and 0.1% BA (74 mg/kg/day) on pnd 21.

Administration, Oral↗

The developmental toxicity of boric acid in rabbits.

Boric acid (BA), an ingredient of many pharmaceutical, cosmetic, and pesticide products, was previously shown to induce reproductive and developmental toxicity in laboratory rodents. In this study, BA (0, 62.5, 125, or 250 mg/kg/day, po) was administered on Gestational Days (GD) 6-19 to New Zealand White rabbits (18-23 pregnant/group). Maternal body weight, food consumption, and clinical condition were monitored at regular intervals throughout gestation. At termination (GD 30), the numbers of uterine implantations, resorptions, dead fetuses, and live fetuses were determined. Fetuses were weighed, and live fetuses examined for external, visceral, and skeletal defects. Maternal food intake decreased during treatment at 250 mg/kg/day and increased at >/=125 mg/kg/day after treatment. Maternal body weight (GD 9-30), weight gain during treatment, gravid uterine weight, and number of ovarian corpora lutea decreased at 250 mg/kg/day. In contrast, maternal corrected gestational weight gain increased at >/=125 mg/kg/day. Maternal liver weight was not affected. Relative (but not absolute) maternal kidney weight increased at 250 mg/kg/day, and microscopic evaluation revealed no treatment-related renal pathology. At 250 mg/kg/day, prenatal mortality was increased (90% resorptions/litter vs 6% for controls), the proportion of pregnant females with no live fetuses was increased (73% vs 0%), and live litter size was reduced (2.3 fetuses/litter vs 8.8). As a result, there were only 14 live fetuses (6 live litters) available for evaluation in the high-dose group, compared to 153-175 live fetuses (18-23 live litters) in the other groups. The percentage malformed fetuses/litter was increased at 250 mg/kg/day, primarily due to cardiovascular defects in 72% of high-dose fetuses vs 3% of controls. The most prevalent cardiovascular malformation (interventricular septal defect) was observed in 57% of high-dose fetuses compared to 0.6% among controls. At 250 mg/kg/day, average fetal body weight/litter was 92% of the average control weight (not statistically significant). In summary, no definitive maternal or developmental toxicity was observed at 62.5 or 125 mg/kg/day BA. Mild maternal effects and severe developmental toxicity were observed at 250 mg/kg/day.

Abnormalities, Drug-Induced↗

Toxicology of selected pesticides, drugs, and chemicals. Boric acid.

With the advent of boric acid insecticides, accidental ingestion of the compound can be encountered in animals. Toxic levels of boric acid most commonly cause vomiting, depression, and, occasionally, diarrhea. Boric acid is, however, cytotoxic to all cells. If a sufficiently high level is ingested, seizures, renal tubular nephrosis, and, rarely, hepatotoxicity may be noted. Gastrointestinal evaluation and supportive care are usually of primary therapeutic importance, although in severe cases, exchange transfusion and/or peritoneal dialysis may be required to decrease blood boron concentrations.

Animals↗

Acute ingestions of boric acid.

Four patients with elevated serum boric acid levels after single, acute ingestions of 10 to 297 grams were reported to the Rocky Mountain Poison and Drug Center (RMPDC) between January 1983 and August 1985. Systemic effects were absent. In 1983-4, 364 cases of boric acid exposure were reported to the RMPDC with only one fatality from a probable chronic ingestion. Vomiting, nausea, diarrhea, and abdominal cramps were rather common. Systemic effects were notably absent in acute ingestions. Five of three hundred sixty-four patients had measured serum levels and were the only ones hospitalized. These observations suggest that significant poisoning is unlikely to result from a single, acute ingestion of boric acid. Serum boric acid levels appear to correlate poorly with clinical toxicity following acute ingestion.

Acute Disease↗

Effects of ultrasound on the reaction step of boric acid production process from colemanite.

Colemanite is one of the most important boron minerals used for production of boric acid. Boric acid (H(3)BO(3)) is produced by the reaction of colemanite (2CaO.3B(2)O(3).5H(2)O) with sulfuric acid in a heterogeneous solid-liquid reaction leading to crystallization of gypsum as a byproduct. The influence of ultrasound on the dissolution of colemanite in H(2)SO(4) solution and on the precipitation of the gypsum during the reaction was investigated. Experiments have been carried out in a batch stirred vessel at 85 degrees C in the absence and presence of ultrasound. The stirring rates were chosen as 600 rpm (for 500-600 microm) and 800 rpm (for 1000-1180 microm) to provide a homogeneous suspension during the reaction. The boric acid and calcium ion concentrations in the solution were determined as a function of time. The results showed that ultrasound enhances the dissolution of colemanite and precipitation rate of the gypsum in the solution after 1h. It has been shown that the use of ultrasound decreases the size of gypsum crystals.

Journal Article↗

Toxic effects of boric acid on the German cockroach.

Boric acid is a slow-acting, inorganic insecticide whose mode of action has not been satisfactorily elucidated. Reported here is evidence which shows that ingested boric acid destroys the cellular lining of the foregut of German cockroaches, Blattella germanica (L.). This effect appears to be sufficient to bring about the death of the insects, perhaps ultimately by starvation. This finding is important because resistance to conventional insecticides may re-establish boric acid as a prominent cockroach control chemical.

Animals↗

BORIC ACID POISONING: REPORT OF 11 CASES.

Boric acid poisoning in 11 infants, occurring in the newborn nursery as a result of the accidental and inadvertent use of 2.5% boric acid in the preparation of the formulae, is reported. Five of the infants died. All except two exhibited the classical symptomatology of acute boric acid poisoning, namely, diarrhea, vomiting, erythema, exfoliation, desquamation of the skin, and marked central nervous system irritation. Early manifestations of poisoning were nonspecific, and one patient died before skin manifestations were noted. Peritoneal dialysis, instituted in nine cases, was found to be the most effective method of treatment. It is recommended that boric acid, which is of doubtful therapeutic value, should be completely removed from hospitals, dispensaries and pharmacopoeias.

Acidosis↗

N-alkyl-4-boronopyridinium halides versus boric acid as catalysts for the esterification of alpha-hydroxycarboxylic acids.

[reaction: see text] Boric acid is a highly effective catalyst for the dehydrative esterification reaction between equimolar mixtures of alpha-hydroxycarboxylic acids and alcohols. In contrast, N-methyl-4-boronopyridinium iodide (2a) is a more effective catalyst than boric acid for the similar esterification in excess alcohol. A heterogeneous catalyst, such as N-polystyrene-bound 4-boronopyridinium chloride, is also an effective catalyst and can be recovered by filtration.

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of Boric Acid (CAS No. 10043-35-3) in B6C3F1 Mice (Feed Studies).

Boric acid is a component of cosmetics and pharmaceuticals and is also used in numerous industrial processes. Earlier long-term studies did not demonstrate a carcinogenic effect in Sprague-Dawley rats. Because of potential widespread human exposure, corroborative evidence was sought in a second species. Toxicology and carcinogenesis studies were conducted by feeding technical-grade boric acid (99.7% pure) to groups of male and female B6C3F1 mice for 14 days, 13 weeks, and 2 years. In the 14-day studies (five mice per group), mortality occurred in mice fed 25,000 ppm, 50,000 ppm, or 100,000 ppm boric acid; hyperplasia and/or dysplasia of the forestomach was also seen in these dose groups. No compound-related gross pathologic or histopathologic effects were seen in male or female mice exposed at concentrations up to 12,500 ppm in feed. In the 13-week studies, groups of 10 male and 10 female mice were fed boric acid at concentrations up to 20,000 ppm; 8 male mice and 1 female mouse receiving 20,000 ppm and 1 male receiving 10,000 ppm boric acid died before the end of the studies. Male and female mice receiving 20,000 ppm boric acid weighed 23% and 18% less, respectively, than did the controls at the end of the studies. Testicular atrophy in 8/10 male mice, hyperkeratosis and acanthosis of the stomach in 8/10 male and female mice, and extramedullary hematopoiesis of the spleen in all male and female mice receiving 20,000 ppm boric acid indicated that the testis, stomach, and spleen were potential target organs in the 2-year studies. Based on these results, 2-year toxicology and carcinogenesis studies were conducted by feeding diets containing boric acid at concentrations of 0, 2,500, or 5,000 ppm to groups of 50 male and 50 female mice. Survival of high dose male mice after week 63 and of low dose mice after week 84 was lower than that of the controls (final survival: control, 41; low dose, 30; high dose, 22), which may have reduced the sensitivity of the carcinogenicity study; the numbers of female mice (33; 33; 37) that survived to the end of the studies were considered adequate for toxicologic evaluation. Body weight gain was reduced in each sex after week 30; mean final body weights were 7% and 13% below control values for exposed male mice and 7% and 20% below those of controls for exposed female mice. No chemically related clinical signs were reported. At the top dose, boric acid caused an increased incidence of testicular atrophy (control, 3/49; low dose, 6/50; high dose, 27/47) and interstitial cell hyperplasia (0/49; 0/50; 7/47) inmale mice. The testicular atrophy was characterized by variable loss of spermatogonia, primary and secondary spermatocytes, spermatids, and spermatozoa from the seminiferous tubules. The seminiferous tubules contained primarily Sertoli cells and variable numbers of spermatogonia. In some mice, there were accumulations of interstitial cells, indicating hyperplasia. In low dose male mice, there were increased incidences of hepatocellular carcinomas (5/50; 12/50; 8/49) and hepatocellular adenomas or carcinomas (combined) (14/50; 19/50; 15/49) and an increased incidence of subcutaneous tissue fibromas, sarcomas, fibrosarcomas, or neurofibrosarcomas (combined) (2/50; 10/50; 2/50). No increased incidence of subcutaneous tissue neoplasms was seen in male mice receiving 5,000 ppm. Because the incidence of subcutaneous tissue tumors is variable in historical controls, because there was no corresponding increase in the high dose male mice, and because the incidence of hepatocellular tumors was not significant by the incidental tumor test and was within the historical control range, neither of these tumors was considered to be related to the administration of boric acid. Boric acid was not mutagenic in the Salmonella/microsome assay with Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537. Boric acid was negative in the mouse lymphoma L5178Y/TK+/- assay and did not induce sister-chromatid exchanges or chromosomal aberrations in Chinese hamster ovary cells. All assays were preformed with anhamster ovary cells. All assays were preformed with and without metabolic activation. The data, documents, and pathology materials from the 2-year studies of boric acid were audited at the NTP Archives. The audit findings show that the conduct of the studies is documented adequately and support the data and results given in this Technical Report. Under the conditions of these 2--year feed studies, there was no evidence of carcinogenicity of boric acid at doses of 2,500 or 5,000 ppm for male or female B6C3F1 mice. Testicular atrophy and interstitial cell hyperplasia were observed in high dose male mice. The decrease in survival of dosed male mice may have reduced the sensitivity of this study. Synonyms: orthoboric acid; boracic acid

Journal Article↗

[Clinical studies on zinc oxide ointment replacing boric acid and zinc oxide ointment (JP8)].

A boric acid and zinc oxide ointment (J.P. VIII) is an unique preparation in Japan, which consist of boric acid (5%), zinc oxide (10%), vegetable oil (usually soybean oil or sesame oil) and yellow wax. The ointment is widely used in the area of Hokkaido, because not only of the customary prescription but also of the characteristic clinical efficiency. However, boric acid has been recognized to be harmful in these days. Therefore, a zinc oxide ointment consisting 10% zinc oxide, soybean oil and white beeswax was tentatively made and evaluated. The zinc oxide ointment presented the same consistency as the boric acid and zinc oxide ointment, measured with penetrometer. The clinical efficiency was also confirmed on six patients with chronic eczema and seven patients with psoriasis vulgaris. The effect on wound healing of the donor site of skin graft was as good as the previous preparation.

Boric Acids↗

Bacteriostatic and bactericidal actions of boric acid against bacteria and fungi commonly found in urine.

Boric acid has been used for over 20 years to preserve urine while in transit for bacteriological examination. It has been suggested that it may be toxic for some urinary pathogens. To investigate this several strains of bacteria and fungi commonly found in urine were exposed to different concentrations of boric acid in nutrient broth. Viable counts were made at the outset and at intervals for up to 24 hours at room temperature to detect bacteriostatic or bactericidal effects. At concentrations between 10 and 20 g/l boric acid was bacteriostatic or fungistatic for very nearly all the common urinary pathogens. At 10 g/l boric acid was weakly bactericidal for some strains of Acinetobacter calcoaceticus and Pseudomonas aeruginosa, though higher concentrations were bacteriostatic only. Group B streptococci varied in their response to boric acid, but for most of them 10 or 20 g/l was satisfactorily bacteriostatic. It is concluded that boric acid is rarely toxic, and when it is, the effect is usually sufficiently delayed to be of only theoretical importance.

Acinetobacter↗

Application of boric acid baits to plant foliage for adult mosquito control.

Boric acid (1%) in 5% sugar water bait solution was applied as a spray to the foliage, stems, and other surfaces of plants for control of adult Aedes albopictus, Culex nigripalpus, and Ochlerotatus taeniorhynchus. Initial studies outdoors in small (1.42-m3) screened cages showed that exposure of male and female mosquitoes to 1% boric acid bait for 48 h resulted in 80 to 100% mortality in Ae. albopictus and > or = 98% mortality in Cx. nigripalpus and Oc. taeniorhynchus. At 48 h posttreatment, in large (1,178-m3) outdoor screened cages, 1% boric acid bait applied as a spray to plant surfaces significantly reduced the landing rates of Ae. albopictus and Cx. nigripalpus on a human subject as well as the numbers of these two species captured in mechanical traps, compared with responses for adults exposed to 5% sugar water solution only (control). Boric acid bait treatments in large screened cages did not significantly reduce landing rates or trap captures of Oc. taeniorhynchus. The application of boric acid baits to plant surfaces may be an effective adulticidal method for selected species of pest and disease vector mosquitoes.

Aedes↗

Crystallisation of amorphous mannitol is retarded using boric acid.

An approach to inhibit the crystallisation of amorphous mannitol was investigated. Boric acid was selected as a model additive for a fundamental study of its ability to retard crystallisation and to facilitate characterisation of the properties of the amorphous solid. At concentrations above 5% (w/w) of boric acid, the DSC scans indicated that a totally amorphous solid could be prepared by cooling the melted pre-mixture under ambient conditions. An increase in the glass transition temperature (T(g)) was observed with a corresponding increase in boric acid content, and their relationship was well fitted by the Gordon-Taylor equation. This result suggested that mannitol and boric acid mixed homogeneously. The crystallisation profiles of the resultant amorphous compositions were best described by the Avrami-Eroféev equation (n=1/3), which indicated that random nucleation and three-dimensional crystal growth was the best-fitting mechanism of this crystallisation. The activation energy of crystallisation decreased with increasing boric acid content, indicating that the temperature dependency for crystallisation decreased with increasing boric acid content. Furthermore, the rate of crystallisation at 30 degrees C for mannitol alone was 7000 times higher than that of mannitol containing 7.5% (w/w) of boric acid.

Boric Acids↗

Individual and combined genotoxic response of boric acid and aflatoxin B1 in Escherichia coli PQ37.

The genotoxic potentials of boric acid in Escherichia coli PQ37 was assessed along in the presence of aflatoxin B1 using SOS chromotest. Boric acid induced beta-galactosidase synthesis on the tester bacteria both on the presence and absence of S9 activation mixture. Therefore, the inorganic acid may not require metabolic activation to be genotoxic for this bacteria. When present together with aflatoxin B1 in the assay medium, boric acid increased the degree of beta-galactosidase synthesis induced by the maximal inducing concentration of aflatoxin B1 before the toxin's activation. However, the degree of enzyme synthesis induced was significantly decreased when boric acid was present after aflatoxin activation. This suggests that boric acid may not interfere with nor block the expoxidation of aflatoxin B1. It may however interact with the expoxide thereby inhibiting its activity. Boric acid may be a genotoxin and could possibly act as a syngenotoxic and/or a cogenotoxic agent.

Aflatoxin B1↗