The risk of acute cutaneous intoxication appears to be negligible given its low transcutaneous absorption index.
Boric acid can be absorbed in toxic quantities through the gastrointestinal tract, by inhalation or through skin lesions.
As a result of the use of large quantities of boric acid on wounds or sores, cases of poisoning and death have occurred, especially in children. The mechanism of the toxic action is unknown and numerous organs and systems are affected, in particular the skin, kidney and digestive tract. The toxic effects also affect the CNS and the lung with lesions, mainly hemorrhagic, of obscure origin. The main symptoms of boric acid poisoning are vomiting, diarrhea, visceral pain, peeling skin rash, CNS stimulation followed by depression, restlessness, headache. Metabolic acidosis and severe water and salt imbalances are also frequent. Furthermore, boric acid in these situations can cause seizures, changes in body temperature and kidney damage which can be evidenced with oliguria. Death from circulatory collapse and untreated shock can occur within 3-5 days. Cyanosis, delirium, seizures and coma (HSDB) can also occur. Cases of severe intoxication have resulted in gastrointestinal disturbances (73%), on the central nervous system (67%) and skin lesions (76%).
Symptoms of chronic poisoning include anorexia, confusion, debilitation, dermatitis, menstrual disorders, anemia, seizures, and alopecia.
No treatment is needed if the dose taken is less than 50 mg / kg. For ingestion of higher doses, gastric lavage is performed with activated charcoal suspension and saline purgative. If the absorbed quantity exceeds 100 mg / kg, even if the patient is still asymptomatic, forced diuresis must be instituted immediately, in order to accelerate elimination and protect the kidney from toxic effects; at the first signs of renal insufficiency and water overdose, forced diuresis should be replaced with peritoneal dialysis or hemodialysis. The remaining therapy is symptomatic and resuscitation.