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Boron Compounds and Their Toxicity

-Boric acid (BO3H3),
-Sodium tetraborate, anhydrous or Anhydrous Borax (Na2B4O7), these two materials are mainly used in the manufacture of boron frits.
- Sodium tetraborate, decahydrate or Borax or Decahydrate Borax (Na2B4O7.10H2O),
-Ulexite (NaCaB5O9.8H2O),
-Colemanite (2CaO.3B2O3.5H2O),
-Gerstley Borate (North America), see our comprehensive report on this site :
-Boron frits,
-Lead-boro silicate.
General information :
The natural forms include boric acid and the borates.
Boric Acid, Borates, Boron Oxide :
Since these products have similar metabolism and toxicity, we will discuss them together
I- Boric Acid :
Boric acid (H3BO3, CAS # 10043-35-3) has a pH of 4 in a saturated aqueous solution. It has antibacterial and antifongic properties, hence it is used as a colourless disinfectant for the skin and the mucous membranes, ocular, oto-rhino-laryngologeal and vaginal.
European standards have set authorized concentrations of boric acid at 0.5% for oral hygiene products and at 5% for talcs and cosmetics.
It is used in the nuclear industry, for its capacity to absorb neutrons, for control and emergency regulation of reactions.
II-Borates :
Borates, among which sodium borate or borax, are also used in :
-the glass industry, ceramics, enamels,
-the manufacture of cosmetics, paints, dyes,
-the treatment of leather and wood,
-weedkillers, insecticides
-retardings of combustion
III-Boron Oxide :
Boron oxide, B2O3 CAS# 1303-86-2, formed by the thermal fusion of boric acid, is used in the glass industry.
Toxicological properties :
I- Absorption :
A-Digestive absorption :
Digestive absorption is fast and almost complete; the blood peak is located at the second hour.
B-Cutaneous absorption :
These products are little absorbed by a healthy or slightly scarified skin. Skin absorption by a seriously injured or burned skin can be significant and be the source of intoxication in the case of a local treatment containing boron.
C-Differences of preparation :
There is a significant difference of absorption between the hydrated forms (< 1%) and the gel forms (20%).
II-Distribution :
The distribution in the body is ubiquitous; the concentration in body fluids is identical to that of the plasma.
There are however two exceptions: the bone, where it concentrates (two to three times the plasmatic levels), and the fat tissue where one finds only 20% of the plasmatic levels. There is no active transfer between the blood compartment and tissues.
III-Bio-transformation :
In the body, borates are metabolized to boric acid which remains unchanged.
IV-Excretion :
Whatever the route of entry, excretion is mainly urinary (80 to 85% of the absorbed amount) in the form of boric acid, and less in the form of borates. Small amounts are found in the feces and perspiration.
Although not properly evaluated, its half-life of elimination is less than 20 hours. In the case of massive ingestion, elimination is biphasic, 50% in 12 hours and 50% in 1 to 3 weeks.
V-Acute Intoxication :
A-Oral Lethal Dose (LD) :
In man, the oral LD may be estimated in the following manner :
1-Newborn= 1 to 3 g.
2-Child= 5g.
3-Adult= 15 to 20 g.
B-Latency Period :
whatever the route of intoxication, a delay of a few hours precedes symptomatology.
C-Clinical Findings :
1-Digestive disorders : nausea, vomiting, abdominal pains.
2-Neurological disorders : headaches, tremors, agitation, convulsions, hallucinations.
3-Severe intoxication : coma, collapse, metabolic acidosis, cyanosis, fever and respiratory depression.
4-Renal impairment : tubular necrosis may occur (oliguria and proteinuria, possibly anuria).
5-Cutaneous disorders (after a few days) : extensive desquamative dermatitis beginning with erythema involving the palms of the hands, the soles of the feet and the buttocks, with the possibility of a secondary generalization (formation of bubbles, massive exfoliation), similar to Ritter's syndrome (exfoliative dermatitis of the newborn). Alopecia may be observed.
Death occurs due to infections, shock, neurological complications, the autopsy showing renal tubular necrosis, cerebral oedema, hepatitis and gastro-enteritis.
D-Laboratory Findings :
The intoxication is confirmed by measuring boron in blood, which is detectable below 1µg/L. by many techniques:
1-In adults:
a-toxic effects are observable from 15 to 20 mg/L. of blood boron,
b-signs of severity are seen as low as 40 mg/L,
c-the presence of more than 40 mg/L. suggests a serious intoxication,
d-the evolution may be fatal for concentrations equal to 500 mg/L.
2-In newborns :
a-toxic effects have been observed for blood boron levels as low as 4 mg/L.
E-Mortality :
In studies dating from the 50s, mortality is estimated at more than 50%; it relates primarily to accidental intoxications in children.
As from the 80s, in an American series, intoxications are generally asymptomatic (88.3%), and never fatal. This difference may be explained by a better way of dealing with these intoxications.
F-Treatment :
Above all, treatment is aimed at purifying (skin and mucous membranes wash, gastric wash, hemodialysis, peritoneal dialysis ), and symptomatic.
G-Skin Irritation :
1-Borax: is a severe eye irritant.
2-Boron and borates: are not or only slight skin irritants.
3-Boron oxide: causes slight irritation of the skin and mucous membranes (skin irritation, ocular irritation, nosebleed, dryness of the mouth, the throat and the nose, pharyngeal pain, sputum, cough), disappearing at the end of exposure without pulmonary impairment, nor long-term effect.
VI-Chronic Intoxication :
In man, the repeated inappropriate use of boric acid has caused, particularly in children, chronic intoxications characterized primarily by cutaneo-mucous, hair and nails disorders.
-red coloured tongue,
-cracks of the lips,
- loss of hair,
-digestive disorders,
-neurological disorders
These effects are close to those observed at the time of acute intoxication and are related to boron accumulation in the body. These disorders are usually reversible at the cessation of its use; they are enhanced by the presence of a pre-existing kidney insufficiency.
Workers exposed to dust of borates or boron oxide present signs of rhinitis, conjunctivitis or cough. In the long run, no pulmonary impairment has been found.
In the case of chronic intoxication, blood boron levels are frequently higher than 30 mg/L.
Effects on reproduction :
A-Experimentally :
Animal experimentation has revealed disorders of reproduction related to boric acid and borax exposure. These were testicular and fertility effects.
The mechanism of this toxicity is not completely elucidated. In the female rat, an increase in the number of spontaneous abortions and a fall in the number of litters were observed.
A study relating to development shows that boric acid causes birth defects in three (3) species studied (rat, rabbit, mouse).
B-In Man :
A previous study carried out in Russia with exposure levels varying from 20 to 83 mg/m3 at 50% of the studied workstations i.e. 2 to 8 times the currently allowed exposure limit, showed a reduction of sexual activity and a deterioration of the quality of the sperm
In the USA, these results were not confirmed in a study of 542 workers whose average exposure was 19.7 mg/m3.
As far as birth defects in man are concerned, there does not seem to be any case reported in the literature.
Carcinogenesis and Mutagenesis :
A-Experimentally :
1-Boric acid has not caused genetic mutations nor chromosomal abnormalities in a series of in vitro experiments on bacteria or eucaryotic cells.
2-In the rat and in the mouse, no carcirogenic effect due to boric acid has been found during a 2 year experiment.
B-In man :
Epidemiologic studies have also been negative.
Exposure Limits :
I-Gerstley Borate :
VEMP (Quebec) : 5 mg/m3
II-Boron oxide :
A-IDLH (Immediate danger to life and health) 2,000 mg/m3
B-VEMP : 10mg/m3
III-Sodium tetraborate, anhydrous or Anhydrous Borax (Na2B4O7) :
VEMP : 1 mg/m3
IV-Sodium tetraborate, decahydrate or Borax or Decahydrate Borax :
VEMP : 5 mg/m3
Prevention :
Laws on Occupational Health and Safety aim at the elimination of hazards at the source.
When engineering methods and modifications of working methods are not able to sufficiently reduce the exposure to these substances, the wearing of personal protective gears may become necessary. These protective gears must be in conformity with regulation.
References :
1-CSST-Quebec, Repertoire Toxicologique, 2002
2-Toxicologie Industrielle et Intoxications Professionnelles, Lauwerys R., last edition.
3-Potterycrafts-MSDS, United Kingdom, avril 2002.
4-Sax's Dangerous Properties of Industrial Materials, Lewis C., last edition.
5-Bore et ses composés, Encyclopédie Médico-Chirurgicale, Toxicologie-Pathologie Professionnelle, M. Falcy, mai 2002.
6-Clay and Glazes for the Potter, Rhodes Daniel, 1973.

Related Information


Typecodes Article by Edouard Bastarache
Edouard Bastarache is a well known doctor that has written many articles on the subject of toxicity of ceramic materials and books on technical aspects of ceramics. He writes in both English and French.
Materials Borax Decahydrate
Materials Anhydrous Borax
Materials Borax Pentahydrate
Minerals Borate Minerals

By Edouard Bastarache

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