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Case Report

Delayed local chemical burns following dermal exposure to bromoacetic acid: a case report

ORCID Icon, , , , &
Article: 2325791 | Received 22 Dec 2023, Accepted 27 Feb 2024, Published online: 11 Mar 2024

Abstract

Bromoacetic acid is an alkylating agent that can cause chemical burns after dermal exposure. We describe a case of chemical burns resulting from dermal exposure to bromoacetic acid, a toxic chemical commonly used in pharmaceutical and industrial settings. A 54-year-old female chemist presented to the emergency department with skin lesions on her right hand. She reported they appeared a day after exposure to bromoacetic acid through a hole in her protective glove. On exam, she had multiple partial thickness burns to the first, second, third, and fourth digits. Her wounds were managed with bedside debridement by the burn service followed by daily wound care. A four-week follow-up visit in clinic revealed well-healing wounds. Dermal exposure to bromoacetic acid cause delayed chemical burns managed with debridement and local wound care.

Introduction

Bromoacetic acid (BAA) is an organobromide and appears as a colorless solid (). Both its acid and esters are found in various industrial processes, including chemical synthesis and by-products of drinking water disinfection [Citation1]. Various reports on animal exposure to BAA demonstrates cytotoxic, genotoxic, mutagenic, carcinogenic, and teratogenic effects [Citation2–4]. We present, in accordance with the CARE Guidelines (https://www.care-statement.org), a case of dermal exposure to BAA and its associated clinical findings and course.

Figure 1. Chemical structure of bromoacetic acid [Citation1].

Figure 1. Chemical structure of bromoacetic acid [Citation1].

Case

A 54-year-old female chemist presented to the emergency department with complaints of painless skin lesions on her right hand. The patient reported transferring BAA at work three days prior to presentation. She was wearing nitrile gloves but noticed that there was a hole in her right glove after handling the material. She had no pain at the time and washed her hands immediately. The next day, she noticed discoloration over the dorsal aspect of her third and fourth digits. She initially presented to an urgent care clinic where she received antibacterial ointment and a tetanus vaccination. The next day, she presented to the emergency department as she had two additional areas of discoloration at the distal tips of her first and second digits. The lesions were not painful. Upon examination, we observed partial thickness burns with discolored bullae over the dorsal aspect of the third and fourth digits, and tip of the second digit (). There was also a small 3 to 4 mm vesicle on the palmar surface of the first digit (). The burn surgery service was consulted and performed a bedside debridement and dressed the wounds with collagenase ointment and xeroform gauze (). In a four-week follow up visit in an outpatient burn clinic, the patient’s skin ulcers had improved with appropriate daily wound care (). Serum complete metabolic panel was normal at the time of presentation to the ED.

Figure 2. Photographs demonstrating multiple partial thickness burns to the (a) first digit, (b) second and third digits, and (c) third and fourth digits 2 days after exposure.

Figure 2. Photographs demonstrating multiple partial thickness burns to the (a) first digit, (b) second and third digits, and (c) third and fourth digits 2 days after exposure.

Figure 3. Photograph demonstrating wounds post bedside debridement to the (a) second and third digits and (b) third and fourth digits on day of emergency department presentation.

Figure 3. Photograph demonstrating wounds post bedside debridement to the (a) second and third digits and (b) third and fourth digits on day of emergency department presentation.

Figure 4. Photograph demonstrating wounds to the (a) second digit and (b) third and fourth digits four weeks after initial exposure.

Figure 4. Photograph demonstrating wounds to the (a) second digit and (b) third and fourth digits four weeks after initial exposure.

Discussion

Dermal exposure to BAA leads to delayed presentations of chemical burns and skin ulcers. BAA shares structural and functional similarities with alkylating agents (e.g. nitrogen mustards, alkyl sulfonates, nitrosureas, and triazines) through binding of its alkyl group to cellular macromolecules including DNA [Citation5]. Covalent bonds to DNA leads to DNA cross-links, strand breaks, and the formation of DNA adducts [Citation5]. These DNA alterations results in mutations, cell cycle arrest, and apoptosis. Most alkylating agents in the medical field are used as chemotherapy agents and have effects on many organ systems. Dermal side effects from chemotherapy treatment include mucositis, alopecia, skin sensitivity, rashes, and dry skin. These side effects occur after intravenous treatment opposed to direct skin exposure. In order to limit occupational exposure to chemotherapy agents, medical staff who handle these agents are strongly recommended to don personal protective equipment which includes at the minimum one to two pairs of gloves (most common are latex and nitrile gloves) and a gown made from material with low permeability [Citation6]. There are no reported cases of human dermal exposure to BAA in the current literature. Topical exposure to chemical weapons containing sulfur mustard, a potent alkylating agent, produced similar dermal injuries in World War I, the disaster at Bari, Italy in World War II, and in the Iran-Iraq Wars in the 1980s [Citation7, Citation8]. Dermal exposure to these agents caused painful blister formation that often required debridement and daily wound care [Citation9, Citation10].

There are multiple in vitro studies on both human cells and animal models that demonstrate BAA toxicity. BAA disrupts uric acid metabolism causing renal oxidative damage in chickens exposed to oral BAA in drinking water [Citation2]. In an in vitro model using mouse oocytes, BAA disrupts cytoskeletal dynamics, damages epigenic modifications, and induces accumulation of DNA damage [Citation3]. In another in vitro study on non-transformed human cells, BAA exposure causes DNA breaks as well as upregulation and downregulation of pathways involving DNA repair, apoptosis, cell cycle regulation, stress response, and xenobiotic metabolism [Citation4].

Conclusion

In summary, this report describes a case of dermal toxicity following occupational topical exposure to BAA.

Disclosure statement

All authors have nothing to disclose.

Data availability statement

Data sharing is not applicable to this article as no new data were created or analyzed in this study.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.

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