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PubMed1991

Development of testicular lesions in F344 rats after treatment with boric acid.

Boric acid is an inorganic acid that impairs fertility in male rodents. A reproductive assessment by continuous breeding study found that male rats treated with boric acid had decreased fertility and sperm motility. In order to determine the cell type that is first affected by boric acid, we have examined the development of the boric acid-induced testicular lesion by light and electron microscopy. Adult F344 male rats were fed 9000 ppm boric acid in NIH-07 rat chow for up to 4 weeks. The first testicular lesion noted was an inhibition of spermiation, which appeared by Day 7. Widespread exfoliation of apparently viable germ cells, and pachytene cell death in stages VII and XIV, appeared as exposure continued. After 28 days of dosing, extreme epithelial disorganization and germ cell loss were evident. To determine if there was a hormonal component to the boric acid-induced testicular lesion, serum levels of basal, hCG-, and LHRH-stimulated testosterone levels were measured. After 4 days of dosing, basal testosterone levels were lower than controls and remained low during dosing. However, serum testosterone levels were similar in both boric acid-treated and control animals after either hCG or LHRH challenge. To determine if boron was preferentially accumulated by the testis, boron levels in testis, epididymis, liver, kidney, and blood were measured. Boron levels had effectively reached steady-state levels by Day 4 and were not differentially concentrated in the tissues examined. Thus, these studies characterize the testicular lesion produced by boric acid exposure and identify a decrease in basal serum testosterone levels in the absence of selective accumulation of boron in the testis.

Androgen-Binding Protein↗

PubMed1977

[Electron microscopic study of the seminiferous tubules of white rats exposed to boric acid].

Boric acid in a dose of 1 g/kg was given orally to albino rats for a period of 2 weeks, daily. Changes in the nucleus and the cytoplasm of both the spermatozoids and spermatides were revealed at the early stages of their formation. The appearance of numerous multinuclear cells with an even and odd number of nuclei (from 2 to 10 and over) was noted. The formation of multinuclear cells can be apparently attributed to the action of boric acid on the prolonged processes of meiotic division of the spermatogenic epithelium cells (spermatocytes, spermatides).

Animals↗

PubMed1992

Clinical management of boric acid ingestion: pharmacokinetic assessment of efficacy of hemodialysis for treatment of acute boric acid poisoning.

Seven hours after suicidal ingestion of about 21 g of boric acid, a 26-year-old female admitted to our hospital in a state of slightly impaired consciousness, with frequent vomiting, shivering, fever and skin flush. Immediately, gastric lavage, followed by administration of activated charcoal and laxative (MgSO4), was performed. In order to ensure her urination, fluid infusion therapy was conducted with the aid of diuretics (furosemide). Since the serum concentrations of boric acid was very high, hemodialysis was carried out twice during the first 39 h. She responded well to the above mentioned treatment and was discharged 12 d post-admission without any sequelae. The concentrations of boric acid in serum and urine were measured in appropriate intervals with our modified Miyamoto's method, and the pharmacokinetics of boric acid were analyzed. The concentration of boric acid in serum and urine at the beginning of treatment was 465 micrograms/ml and 3.40 mg/ml, respectively. The half-life of boric acid in serum was 13.46 h, whereas it was shortened to 3.76 h during hemodialysis. The total body clearance was 0.99 l/h, while it increased to 3.53 l/h by hemodialysis. The additional removal of boric acid by hemodialysis was estimated to be about 5 g. It was concluded that the hemodialysis was very useful in the treatment of boric acid poisoning, because it accelerated the elimination of boric acid about four times faster than with conventional treatment.

Acute Disease↗

PubMed1986

Boric acid toxicity.

Although boric acid was widely used therapeutically in the past and resulted in significant toxicity, the past few years have seen a decline in its usage. Ninety-nine per cent boric acid powder is now being used as a household pesticide. Physicians therefore should be aware of the potential for boric acid toxicity.

Absorption↗

PubMed1986

Ingestion of boric acid by infants.

Boric acid solution was inadvertantly used to dilute concentrated formula and was fed to 24-day-old and 14-month-old siblings. Total amounts ingested were 2.6 g and 1.95 g, respectively. Symptoms of toxicity included irritability, diarrhea, and perineal erythema (in the younger child only). Peak boric acid levels were 147 micrograms/ml in the 24-day-old and 56 micrograms/ml in the 14-month-old. Peritoneal dialysis was utilized in the younger child, while the older child required only symptomatic care. Serum boric acid half-lives were approximately ten hours (24-day-old) and eight hours. Neither child developed severe toxicity; both were asymptomatic at one-month follow-up.

Boric Acids↗

PubMed1991

[Study on the histochemical staining of boric acid].

The detection of boric acid in the tissue is of significance in investigating its toxicity. Because of this, we have devised a histochemical staining method to detect the presence of boric acid. The outline of this method follows. Frozen 12-14 microns sections, cut by a cryostat, are fixed in anhydrous ethanol and stained for 20 minutes in a protonated curcumin solution. Washing in acetic acid follows, and a red stain results if boric acid is present. This method causes a reaction, in which rosocyanin is formed by the reaction of boric acid and the protonated curcumin, and this principle is now used when an analysis of boric acid is needed. As to procedure, a 1 N concentration of sodium hydroxide is dropped onto a part of the stain to be tested, and the presence of rosocyanin is confirmed if the stain turns blue. Consequently, this staining confirms the presence of boric acid.

Animals↗

PubMed1990

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↗

PubMed1986

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↗

PubMed1990

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↗

PubMedDate not supplied

Human toxicology of boron with special reference to boric acid poisoning.

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.

Adult↗

PubMed1989

[Determination of boric acid in biological materials by curcuma paper].

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 Acids↗

PubMed1987

[Liberation and in vitro skin permeation of boric acid from an ointment].

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.

Boric Acids↗

PubMed1988

Clinical manifestations of toxicity in a series of 784 boric acid ingestions.

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.

Adolescent↗

PubMed1975

[Haemodialysis in the treatment of acute boric acid poisoning (author's transl)].

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.

Acidosis↗

PubMedDate not supplied

Acute toxicity of boric acid and boron tissue residues after chronic exposure in broiler chickens.

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.

Animal Feed↗

PubMed1988

Combined boric acid and cinchocaine chloride poisoning in a 12-month-old infant: evaluation of haemodialysis.

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.

Boric Acids↗

PubMed1989

[Spectrophotometric determination of boric acid by the curcumin method].

We have contrived an improved curcumin method for a spectrophotometric determination of the boric acid content, suitable for use on biologic materials to determine cases of poisoning. The use of this method enables detection of boric acid from a level of 10 micrograms/ml up to 5 mg/ml. The steps of this measurement method follow. Initially, boric acid was extracted by using a modification of Agazzi's method, i.e., to 1 ml of the sample solution, 0.2 ml of a 50% solution of sulfuric acid is added, along with 4 ml of 10 v/v% 2-ethyl-1,3-hexanediol/chloroform (an EHD solution). This mixture was then shaken for 5 min and then centrifuged for 10 min at 3,000 rpm. The extract of this chloroform phase was dehydrated with anhydrous sodium sulfate and used for the coloring reaction sample. The colorimetry procedure for determining the boric acid content follows. Fifty microliters of the extract solution was placed into a dry tube, to which 0.5 ml of a 0.3% curcumin/acetic acid solution and 50 microliters concentrated sulfuric acid were added, and the contents mixed thoroughly. The reaction mixture was then allowed to stand for 30 min at room temperature. (Rosocyanin is formed by the reaction of boric acid and protonated curcumin). Next, ethanol (3-138 ml) was added to the reaction mixture to decompose the excess protonated curcumin. Then, the absorbancy of the resulting solution was measured at 550 nm against a blank test solution. Ethanol was added to enable the measurement of the absorbancy (ethanol amounts tested were 3, 6, 12, 24, and 138 ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Boric Acids↗

PubMed1992

Developmental toxicity of boric acid in mice and rats.

Boric acid (BORA), an ingredient of many cosmetics, pharmaceuticals, and pesticides, was tested for developmental toxicity in timed-pregnant Swiss mice and Sprague-Dawley rats (n = 26-28/group). BORA (0, 0.1, 0.2, or 0.4% in feed) was provided throughout gestation to attain steady-state exposure as early as possible during prenatal development. Average doses (mg/kg/day) were 248, 452, or 1003 in mice, and 78, 163, or 330 in rats. To limit prenatal mortality, BORA (0.8% or 539 mg/kg/day) was provided to an additional group of rats on Gestational Days (GD) 6 to 15 only. On GD 17 (mice) or 20 (rats), fetuses were weighed and examined for malformations (external, visceral, skeletal). Mouse dams exhibited mild renal lesions (greater than or equal to 0.1%), increased water intake and relative kidney weight (0.4%), and decreased weight gain (0.4%) during treatment. There was a reduction of fetal body weight (greater than or equal to 0.2%) and an increased incidence of resorptions and malformed fetuses per litter (0.4%). Morphological changes included an increased incidence of short rib XIII (a malformation) and a decreased incidence of rudimentary or full rib(s) at lumbar I (an anatomical variation). Maternal rats exhibited increased liver and kidney weights at greater than or equal to 0.2%, altered water and/or food intake at greater than 0.2%, and decreased weight gain at greater than 0.4%. Average fetal body weight/litter was reduced at all doses. Prenatal mortality was increased only at 0.8%. The incidence of fetal malformations was significantly increased at greater than or equal to 0.2%. The most frequently observed malformations were enlarged lateral ventricles of the brain and agenesis or shortening of rib XIII. In rats, the no-observable-adverse-effect level (NOAEL) for maternal toxicity was 78 mg/kg (0.1%), while in mice the low dose of 248 mg/kg (0.1%) approached the maternal NOAEL with mild renal lesions in only 2 of 10 females. Embryo/fetal toxicity occurred in all groups of rats at greater than or equal to 78 mg/kg (greater than or equal to 0.1%) while the NOAEL for developmental toxicity in mice was 248 mg/kg (0.1%). Thus developmental toxicity occurred below maternally toxic levels in rats as well as in the presence of maternal toxicity in mice and rats.

Abnormalities, Drug-Induced↗