Granular parakeratosis secondary to benzalkonium chloride exposure from common household laundry rinse aids.

AIM: Granular parakeratosis (GP) is a benign dermatosis characterised by a rash at intertriginous sites. The pathogenesis is uncertain although it is proposed to be an irritant contact reaction with cases related to benzalkonium chloride (BAC) reported. Our experience is that patients often have delayed diagnosis. This study aims to review the clinical presentation and histopathological features of GP. METHODS: This study is a retrospective case series of adult and paediatric patients seen at dermatology clinics in Auckland, New Zealand. Information was collected on patient demographics, presentation, investigations and management. RESULTS: Thirteen cases (seven adults; six children) are included. The typical presentation of GP was erythematous or brown, scaly papules and plaques with desquamation in a predominantly flexural distribution. All patients reported recent exposure to BAC in laundry rinse solution. Nine biopsies were taken from four patients. Psoriasiform and eczematous findings were common on histopathology. The mainstay of treatment was cessation of BAC exposure. CONCLUSION: GP has a distinct clinical pattern although histopathological findings are varied. Clinicians should have a high index of suspicion for GP in patients presenting with erythematous flexural eruptions and seek a history of BAC exposure, especially in the context of the COVID-19 pandemic and increased antiseptic use.

Liquid chromatography-tandem mass spectrometry detection of benzalkonium chloride (BZK) in a forensic autopsy case with survival for 18 days post BZK ingestion.

We report a forensic autopsy case of an elderly man who ingested unknown amount of germicidal disinfectant containing 50% benzalkonium chloride (BZK). He survived for 18 days after BZK ingestion and then died because of pneumonia. A liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was used to detect three BZK compounds (C12-BZK, C14-BZK and C16-BZK) in the blood. Extraction of BZK was carried out according to a modified QuEChERS method. Chromatographic separation was achieved on an ODS column and detection was performed in selected reaction monitoring mode. The accuracy and the precision were acceptable for quantitative analysis in the concentration range of 10-200 ng/mL for the three BZK compounds. BZK was detected in heart and femoral vein blood samples even 18 days after BZK ingestion. Taking into consideration clinical information during 18 days hospitalization and the autopsy findings, the cause of death was attributed to BZK poisoning. Several toxico-kinetic factors regarding absorption and excretion of BZK in the body were also discussed to elucidate the detection of BZK such a long time after ingestion.

Benzalkonium chloride exposure in cats: a retrospective analysis of 245 cases reported to the Veterinary Poisons Information Service (VPIS).

Benzalkonium chloride is commonly found in household products. This retrospective study examined 245 cases of feline exposure to benzalkonium chloride-containing products reported to the Veterinary Poisons Information Service (VPIS). A single route of exposure was reported in 188 cats (ingestion 126, skin 58, buccal 4); 57 cats had multiple routes. The common products involved were household antibacterial cleaners (43.6 per cent), household disinfectants (22.3 per cent) and patio cleaners (17.5 per cent). The most common signs were hypersalivation/drooling (53.9 per cent), tongue ulceration (40.4 per cent), hyperthermia (40.4 per cent) and oral ulceration (22.9 per cent). The mean time recorded for onset of the first clinical sign was 6.4 hours (range five minutes to 48 hours, median 4.5 hours, n=60), however, the VPIS was not contacted until 14.0 ± 13.2 hours after exposure (n=120). This figure also reflects the time of presentation. The most common treatments given were antibiotics (82.0 per cent), fluids (50.2 per cent), analgesia (45.3 per cent), gastroprotectants (31.0 per cent), dermal decontamination (24.1 per cent) and steroids (22.7 per cent). 13 cats (5.3 per cent) received syringe or nasogastric feeding. Of 245 cats, 12 (4.9 per cent) remained asymptomatic, 230 (93.9 per cent) recovered and three died (1.2 per cent). The time to recovery ranged from 1 to 360 hours (n=67) with a mean of 100.4 ± 82.0 hours (4.2 ± 3.4 days, median 72 hours).

Benzalkonium chloride intoxication caused by intravenous self-injection.

BACKGROUND: Benzalkonium chloride (BZK) is widely used as a germicide in hospitals and other places. Although several cases of accidental oral intake of BZK have been reported, there have been few reported cases of BZK toxicity due to intravenous injection. CASE REPORT: A male nurse in his 40 s injected 15 mL of 10% BZK (Osvan S) directly into his left antebrachial vein while at home, as a suicide attempt. The patient was admitted to our hospital 1 hour later. Acute respiratory distress syndrome (ARDS) was diagnosed by blood gas analysis, chest X-ray, and CT scan. Due to extracorporeal blood purification therapy, including hemoperfusion and plasma exchange, serum BZK became undetectable. However, the ARDS was not improved. Extracorporeal blood purification therapy consisting of continuous hemodiafiltration (CHDF) was continued to treat the ARDS. After performing CHDF for the next 36 hours, improvement of both the PaO2/FiO2 ratio and chest X-ray findings was noted. Tracheal extubation was performed on day 9 and no further complications occurred after this period, he was discharged on day 21. CONCLUSION: Extracorporeal blood purification therapy is probably effective for treatment of BZK intoxication by intravenous injection.

A rare and preventable cause of respiratory insufficiency: ingestion of benzalkonium chloride.

Caustic agents stored in ordinary containers can be ingested by children. These materials should be stored in soft distinctive bottles and in safe places. The probability of ingestion of a caustic agent is low in the newborn period, and caustic burns have been reported infrequently. In this case study, a newborn baby with severe respiratory insufficiency after ingestion of benzalkonium chloride is reported.

A collaborative evaluation of the cytotoxicity of two surfactants by using the human corneal epithelial cell line and the WST-1 test.

This study was undertaken to investigate the use of the in vitro test WST-1, an assay of cell proliferation and viability, for a preliminary safety evaluation of topical ophthalmic preparations. The cytotoxicity of two surfactants, benzalkonium chloride (BAC) and polyoxyethylene-20-stearyl ether (Brij78, PSE) was independently investigated in four laboratories in the EU by using an immortalized human corneal epithelial (HCE) cell line. The HCE cells were exposed to BAC and PSE for 5 min, 15 min, and 1 hour, and the results of the HCE-WST-1 tests were collected and compared. After one-hour exposure, the EC(50) values in BAC-treated cells in the presence of serum ranged between 0.0650 +/- 0.0284 (mean +/- SD) mM, and those in the absence of serum 0.0296 +/- 0.0081 mM. The corresponding values for PSE were 0.0581 +/-.0300 mM and 0.0228 +/-.0063 mM. There were variations in the results between different laboratories, with coefficients of variation ranging from 31 to 121%, mean 58%. The use of one-hour exposure time is to be preferred, and the elimination of serum in the culture medium is recommended to avoid both underestimation of toxic effects and variability of the test results.

Comparison of an immortalized human corneal epithelial cell line and rabbit corneal epithelial cell culture in cytotoxicity testing.

The cytotoxicity of benzalkonium chloride (BAC) and disodium edetate (EDTA) was evaluated in vitro in rabbit corneal epithelial primary cells and in the immortalized human corneal epithelial cell line SV40. Cell injury was assessed by lactate dehydrogenase (LDH) leakage and by reduction of the tetrazolium salt WST-1 to formazan by mitochondrial metabolic activity. Cell cultures were exposed to test compounds both in serum-free and in serum-containing medium. Although WST-1 and LDH tests measured different physiological endpoints, they yielded comparable results. However, the LDH test seemed less reliable due to great variation. The use of serum was found to result in lower toxicity of the compounds in both tests. The rabbit primary cell culture and the human corneal cell line were quite similar in their responses to BAC and EDTA. The human cell line is a promising in vitro alternative in oculotoxicity testing.

A case of fatal benzalkonium chloride poisoning.

Five elderly persons with senile dementia accidentally ingested Hoesmin, a 10% aqueous solution of benzalkonium chloride (BAC). The condition of one patient, an 84-year-old woman whose lips and oral cavity became erythematous, gradually deteriorated. Although gastric lavage was performed, the patient died 3 h after ingestion of Hoesmin. Autopsy revealed corrosive changes of the mucosal surfaces of the tongue, pharynx, larynx, esophagus and stomach which may have come in contact with BAC. In addition, BAC was detected in the serum. We conclude that the patient died of BAC poisoning. Fatal BAC poisoning is rare and autopsy findings in only a few cases of BAC poisoning have been reported. Our findings emphasize the risk of oral ingestion of BAC.

A combined respiratory and cutaneous hypersensitivity syndrome induced by work exposure to quaternary amines.

The quaternary amine, benzalkonium chloride, has been associated with cutaneous and mucosal delayed hypersensitivity reactions and with paradoxical bronchoconstriction after use of aerosolized asthma medications. Until now, quaternary amines have not been reported to cause occupational asthma. We describe a case of occupational asthma caused by prolonged exposure to a cleaning solution containing benzalkonium chloride in the workplace. Single-blind, placebo-controlled, open-room challenges were performed to determine the specific agent responsible for the patient's symptoms. Pulmonary function and epicutaneous challenge tests were also performed. The patient had positive responses to challenges with a liquid toilet bowl cleaner containing benzalkonium chloride but was unreactive to other agents tested. Removal from the workplace resulted in complete resolution of symptoms. The exact mechanisms responsible for occupational asthma induced by quaternary amines remain unknown; however, this case emphasizes the importance of recognizing reactive chemicals as possible causes.

Ocular toxicity of beta-blockers and benzalkonium chloride in pigmented rabbits: electrophysiological and morphological studies.

Subconjunctival injection of 0.2 ml of the following solutions was carried out once a day for two weeks in the albino and pigmented rabbit: commercial 0.5% timolol or 1% befunolol ophthalmic solutions, both containing benzalkonium chloride, and also these drug solutions containing no preservative, ophthalmic base solutions containing benzalkonium chloride, physiological saline solution or phosphate buffer solution. One week after daily injections of the commercial drug solutions or base solutions with benzalkonium chloride, the electroretinogram (ERG) showed a marked reduction in the a- and b-wave amplitudes in the pigmented rabbit, but the ERG changes were slight in the albino rabbit. After two weeks of injections, histological studies of the pigmented rabbit eyes revealed retinal detachment, visual cell loss and atrophy of the retinal pigment epithelium and choroid; the changes in the albino rabbit eyes were minimal. Injections of the beta-blockers containing no benzalkonium resulted in no significant changes in the ERG or in the tissue structures of all rabbits. Injections of only physiological saline or phosphate buffer had no deleterious effects. Therefore, the ocular toxicity of the beta-blockers was thought to be minor and the toxic effects seen in this study were thought to be due to benzalkonium chloride, which possibly accumulates in the ocular pigments.

Quaternary ammonium compound toxicity in chickens.

Two commercial White Leghorn flocks of 41,000 and 57,000 25-week-old hens experienced death losses of 676 and 1,089 birds in a week. Six birds from each flock were presented for necropsy to the Animal Disease Diagnostic Laboratory at Purdue University with a clinical history of excessive deaths, unsatisfactory production, and dehydration. Gross lesions were present on the tongue and on oral and pharyngeal mucosa as uniformly pale or white areas with interspersed multifocal sites of ulceration. Other changes were cyanotic, shriveled combs and wattles and ruptured ovarian follicles with concurrent egg yolk peritonitis. Microscopic examination revealed large areas of coagulative necrosis with multifocal epithelial ulceration of the oral and pharyngeal mucosae. There was an intense inflammatory, heterophilic response at the periphery of affected areas. Alterations in the abdominal viscera were limited to egg yolk peritonitis. The high death rate and oral lesions were attributed to accidental use of excessive levels of a quaternary ammonium disinfectant in the drinking water.