Zinc chloride

Direct observations: clinical cases, poisoning incidents and other

Administrative data

Endpoint:

direct observations: clinical cases, poisoning incidents and other

Type of information:

migrated information: read-across based on grouping of substances (category approach)

Adequacy of study:

key study

Study period:

Not reported

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

other: Study well documented, meets generally accepted scientific principles, acceptable for assessment.

Cross-reference

Cross-reference 1

Reason / purpose for cross-reference:

reference to same study

Cross-reference 2

Reason / purpose for cross-reference:

reference to other study

Data source

Reference

Reference Type:

publication

Title:

Unnamed

Year:

1994

Materials and methods

Study type:

poisoning incident

Endpoint addressed:

acute toxicity: oral

Principles of method if other than guideline:

Case report of accidental ingestion of liquid zinc chloride/ammonium chloride in a 16-month-old boy.

GLP compliance:

no

Test material

Test material information

Constituent 1

Reference substance name:

Diammonium tetrachlorozincate(2-)

EC Number:

238-687-6

EC Name:

Diammonium tetrachlorozincate(2-)

Cas Number:

14639-97-5

IUPAC Name:

diammonium tetrachlorozincate(2-)

Details on test material:

- Name of test material (as cited in study report): Denver Soldering Flux®
- Physical state: Liquid
- Composition of test material, percentage of components: Zinc chloride 22.5 %, Ammonium chloride 5.5 %, pH 2

Method

Type of population:

general

Subjects:

- Number of subjects exposed: One
- Sex: Male
- Age: 16-month
- Demographic information: Colorado
- Known diseases: None

Ethical approval:

not applicable

Route of exposure:

oral

Reason of exposure:

accidental

Exposure assessment:

estimated

Details on exposure:

Ingested an estimated one tablespoon of liquid from a small glass. The product was used for stained glass work.

Examinations:

- Vital signs (blood pressure, pulse, respirations, and oral temperature), physical examination, clinical biochemistry (potassium, chloride, glucose, SGOT, SGPT, and alkaline phosphatase), hematology (WBC count, hemoglobin, and hematocrit), chest radiograph, urine analysis, endoscopy, plasma and urine Zinc levels were estimated after admission of the patient approximately 20 min after ingestion

Medical treatment:

After initial evaluation, the oropharynx was irrigated with saline and suction. Initial treatment consisted of IV fluids, 100 mL bolus of D5LR followed by D51/4NS with 20 mEq/L potassium phosphate at a rate of 50 mL/h and 250,000 U penicillin IV every 6 h.
On the second hospital day, the patient became more lethargic and hypertensive, requiring hydralazine and labetalol for blood pressure control. The empirically chosen chelation regimen consisted of BAL 3 mg/kg IM every 6 h and calcium disodium EDTA 1,000 mg/m2 IV in four daily divided doses. BAL was stopped after 24 h, and EDTA was stopped after five days.

Results and discussion

Clinical signs:

Immediately after ingestion, child coughed and soon vomited. Enroute, the child became lethargic and was responsive to painful stimuli. Physical examination showed 1-cm2 partial thickness burn to the lower lip mucosa, coarse breath sounds and wheezes in all lung fields, and lethargy with response to verbal stimuli.

Results of examinations:

- Vital signs (20 min after ingestion): blood pressure, 88/62 mm Hg; pulse, 120; respirations, 32; and oral temperature, 37.5 °C.
- Laboratory examination (1 h after ingestion): Potassium 2.9 mEq/L; CO2 content 19.3 mEq/L; chloride 108 mEq/L; glucose 183 mg/dL; SGOT 98 U/L; SGPT 123 U/L; and alkaline phosphatase 527 U/L. Electrolytes (8 h after ingestion) were normal except for chloride 111 mEq/L and biocarbonate 14 mEq/L. Creatinine, BUN, urinalysis, calcium, and glucose were normal for age.
- Hematology: WBC count 20,000/mm2; hemoglobin 14 g/dL; and hematocrit 43.5 %. Hemoglobin (8 h after ingestion) dropped to 12.7 g/dL with few fragmented RBCs noted on the peripheral smear.
- Chest radiograph (6 h after ingestion): Peribronchial prominence with right pleural effusion and left basilar and retrocardiac atelectasis.
- Endoscopy (18 h after ingestion): Sloughed mucosa in the mouth and posterior pharynx. The right aryepiglottic fold was erythematous and edematous with ulceration and the vocal cords were edematous. Inflammation, ulceration, mucosal slough, and mucopurulent exudate were seen from the vocal cords to the carina. Esophagus showed edema and first-degree burns of the entire esophagus, with whitish exudate and circumferential second-degree burns at the gastroesophageal junction. The stomach was diffusely erythematous, with several areas of third degree burns at the antrum.
- Plasma Zinc (normal plasma Zinc range, 60-100 µg/dL) fell from 1,199 µg/dL (at 14 h after ingestion) to 160 µg/dL (at 74 h after ingestion) before any chelation therapy. Initial 8-h urine collection for Zinc immediately before chelation contained 950 µg/ 8 h of collection. During the fourth day of the five-day course of chelation, urinary Zinc excretion was 1,000 µg/24 h (normal urinary Zinc excretion, 140-800 µg/24 h).

Effectivity of medical treatment:

After initial treatment, mild stridor, retractions, and tachypnea were seen and resolved over five days, requiring only supplemental humidified oxygen.
After chelation therapy, improvement of mental status and resolution of hypertension occurred within the first 24 h of chelation. Hepatobiliary and pancreatic dysfunction (peak measured amylase was 178 IU/mL) resolved by the third hospital day. A progressive decline in hemoglobin to 8.4 g/dL occurred, presumed secondary to gastrointestinal losses, and required transfusion of 110 mL of packed RBCs. Repeat endoscopy performed nine days after admission showed the airway to be normal, with the exception of slight erythema along the arytenoids. The upper esophagus was normal, but there were persistent ulcerations in the stomach, most marked at the antrum. The duodenum was normal. The child tolerated oral feedings poorly because of vomitings. An upper gastrointestinal barium study demonstrated significant antral scarring. The patient was discharged home on a full liquid diet supplemented by home total parenteral nutrition. After several weeks, persistent gastric outlet obstruction necessitated a gastric antrectomy with primary reanastomosis. Ten months after ingestion, there are no residual effects.

Outcome of incidence:

The patient recovered within 10 months.

Any other information on results incl. tables

None

Applicant's summary and conclusion

Conclusions:

Zinc chloride/ammonium chloride soldering flux ingestion can results in significant local corrosive effects as well as systemic toxicity including central nervous system depression, hypertension, metabolic acidosis, hepatocelluar destruction and hyperamylasemia.

Executive summary:

The case report of accidental ingestion of liquid zinc chloride/ammonium chloride in a 16-month-old boy was presented.

 

Accidental ingestion of an estimated one tablespoon of liquid from a small glass caused sever local burns, metabolic acidosis, hepatic damage, hyperamylasemia, lethargy, and hypertension. Peak measured plasma Zinc was 1,199 µg/dL. Because of persistent signs of systemic toxicity, he was chelated with dimercaprol (BAL) and EDTA. Although clinical improvement was noted coincident with the initiation of chelation, there was no apparent increase in urinary Zinc excretion. Scarring in the gastric antrum necessitated an antrectomy.

 

The child recovered without other apparent complications.