SM Bradberry BSc MB MRCP

    National Poisons Information Service
    (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    B18 7QH

    This monograph has been produced by staff of a National Poisons
    Information Service Centre in the United Kingdom.  The work was
    commissioned and funded by the UK Departments of Health, and was
    designed as a source of detailed information for use by poisons
    information centres.

    Peer review group: Directors of the UK National Poisons Information


    Toxbase summary

    Type of product

    Used in smoke bombs, soldering fluxes, disinfectants, fire-proofing
    agents, the textile industry and cements.


    Zinc chloride is corrosive by ingestion and highly irritant by



         -    Topical zinc chloride causes ulceration and burns and
              chronic exposure has been associated with anorexia, fatigue
              and weight loss.


         -    Zinc chloride is highly corrosive and ingestion of only 10
              mL of a 35 per cent solution has caused oropharyngeal and
              gastric burns, epigastric tenderness, pharyngeal oedema,
              haematemesis and melaena (Chew et al, 1986).
         -    Respiratory insufficiency and CNS depression may occur in
              severe cases. Recovery may be complicated by
              gastrointestinal stricture formation and/or pancreatic
         -    Hyperglycaemia, hypokalaemia, increased alkaline
              phosphatase, amylase and liver transaminase activities have
              been reported.


         -    Zinc chloride inhalation from smoke screen generators or
              smoke bombs may cause transient cough, sore throat,
              hoarseness, a metallic taste and chest pain.
         -    Exposure to high zinc chloride concentrations produces a
              chemical pneumonitis with marked dyspnoea, a productive
              cough, fever, chest pain and cyanosis. Pneumothorax and the
              adult respiratory distress syndrome (ARDS) have been
              reported. Fatalities have occurred (Hjortsœ et al, 1988).



    1.   Symptomatic and supportive measures as indicated by the severity
         of the burn.


    1.   Irrigate with copious lukewarm water or 0.9 per cent saline for
         at least ten minutes.
    2.   A topical anaesthetic may be required for pain relief and to
         overcome blepharospasm.
    3.   Ensure removal of any particles in conjunctival recesses.
    4.   Fluorescein staining allows identification of corneal burns.
    5.   Seek ophthalmological advice if symptoms persist or any
         significant abnormality is detected on examination.


    1.   Most patients will vomit spontaneously. Gastric lavage is
         contraindicated following zinc chloride ingestion as this salt is
    2.   Symptomatic and supportive measures with adequate fluid
         resuscitation are paramount.
    3.   Endoscopic examination may be required (ideally within the first
         24 hours).
    4.   Save blood and urine for zinc concentration estimations.
    5.   Monitor the blood count and biochemical profile including serum
         amylase activity.
    6.   The value of chelation therapy following zinc ingestion has not
         been confirmed. Discuss with NPIS if patient is symptomatic.


    1.   Remove from exposure after ensuring adequate self-protection.
    2.   Administer supplemental oxygen by face mask.
    3.   Symptomatic patients and those with abnormal respiratory physical
         signs should have a chest X-ray.
    4.   The possibility of delayed-onset chemical pneumonitis, pulmonary
         oedema and development of ARDS must be considered.
    5.   There is no established role for the routine use of inhaled or
         systemic corticosteriods in patients with pulmonary
    6.   The use of antibiotics should be reserved for established
         infection only.
    7.   The value of chelation therapy following zinc chloride inhalation
         has not been confirmed. Discussion of individual cases with an
         NPIS physician is recommended.


    Allen MB, Crisp A, Snook N, Page RL.
    'Smoke-bomb' pneumonitis.
    Respir Med 1992; 86: 165-6.

    Chew LS, Lim HS, Wong CY, Htoo MM, Ong BH.
    Gastric stricture following zinc chloride ingestion.
    Singapore Med J 1986; 27: 163-6.

    Chobanian SJ.
    Accidental ingestion of liquid zinc chloride: local and systemic
    Ann Emerg Med 1981; 10: 91-3.

    Hjortsœ E, Qvist J, Bud MI, Thomsen JL, Andersen JB, Wiberg-Jœgensen
    F, Jensen NK, Jones R, Reid LM, Zapol WM.
    ARDS after accidental inhalation of zinc chloride smoke.
    Intensive Care Med 1988; 14: 17-24.

    McKinney PE, Brent J, Kulig K.
    Acute zinc chloride ingestion in a child: local and systemic effects.
    Ann Emerg Med 1994; 23:1383-7.

    Potter JL.
    Acute zinc chloride ingestion in a young child.
    Ann Emerg Med 1981; 10: 267-9.

    Substance name

         Zinc chloride

    Origin of substance

         Formed during ignition of zinc oxide/hexachloroethane incendiary
         devices.                                (DOSE, 1994)


         Butter of zinc
         Zinc dichloride
         Zinc muriate                            (DOSE, 1994)

    Chemical group

         A compound of zinc, a group II B (d block) transition element.

    Reference numbers

         CAS            7646-85-7                (DOSE, 1994)
         RTECS          ZH1400000                (RTECS, 1997)
         UN             2331 (anhydrous) 1840 (solution)   (DOSE, 1994)
         HAZCHEM CODE   2X (solution)            (DOSE, 1994)

    Physicochemical properties

    Chemical structure
         ZnCl2                                   (DOSE, 1994)

    Molecular weight
         136.28                                  (DOSE, 1994)

    Physical state at room temperature
         Solid                                   (MERCK, 1996)

         White                                   (MERCK, 1996)

         Fume has an acrid odour.                (HSDB, 1997)


         The aqueous solution is acid to litmus; pH about 4.
                                                 (MERCK, 1996)

         Water: 432 g/L at 25°C, 614 g/L at 100°C.
         Soluble in methanol, ethanol, diethyl ether and dimethyl ether.
                                            (MERCK, 1996; SAX'S, 1996)

    Autoignition temperature

    Chemical interactions
         Zinc chloride forms an explosive reaction with copper (II)
         Soluble zinc salts are precipitated as zinc hydroxide by ammonium
         A mixture of potassium and zinc chloride produces a strong
         explosion on impact.               (SAX'S, 1996; HSDB, 1997)

    Major products of combustion
         Fumes of chloride and zinc oxide        (SAX'S, 1996)

    Explosive limits

         Not flammable                           (HSDB, 1997)

    Boiling point
         732°C                                   (DOSE, 1994)

         2.907 at 25°C                           (DOSE, 1994)

    Vapour pressure
         133.322 Pa at 428°C                     (DOSE, 1994)

    Relative vapour density

    Flash point

         When heated to decomposition it emits toxic fumes of chloride and
         zinc oxide.                             (SAX'S, 1996)


         In smoke bombs used for crowd dispersal, fire-fighting exercises
         and military screens.
         In dentifrices.
         Treatment of skin complaints.
         Flux in plating, soldering and welding.
         In wood preservatives and fire-proofing agents.
         Astringent.                             (DOSE, 1994)

    Hazard/risk classification

    Index no. 030-003-00-2
    Risk phrases
         C; R34. Causes burns.
    Safety phrases
         S(1/2) 7/8-28-45. Keep locked up and out of the reach of
         children. Keep container tightly closed and dry. After contact
         with skin, wash immediately with plenty of (to be specified by
         the manufacturer). In case of accident or if you feel unwell,
         seek medical advice immediately (show label where possible).
    EEC No:   231-592-0                          (CHIP2, 1994)


    Zinc is an essential trace element required for the function of over
    200 metallo-enzymes, including alkaline phosphatase and carbonic
    anhydrase (Sandstead, 1994). Zinc also plays a critical role in the
    regulation of DNA and RNA synthesis (via interaction with DNA binding
    proteins), in hormone-receptor interactions and in the
    "second-messenger" system of cellular signal transduction (Walsh et
    al, 1994).

    Zinc chloride is an acidic salt encountered most frequently in solder
    fluxes or as a constituent of 'smoke-bomb' emissions when zinc oxide
    and hexachloroethane are burned together.


    Inhalational exposure to low zinc chloride concentrations typically
    occur during military or civilian fire-drill exercises (Schenker et
    al, 1981; Allen, 1992). In an early report the accidental ignition of
    several smoke generators at a storage site led to severe zinc chloride
    poisoning affecting 70 persons, ten of whom died (Evans, 1945).

    There are several reported cases of accidental or deliberate self-harm
    involving zinc chloride ingestion, usually as soldering flux
    (Chobanian, 1981; Hedtke et al, 1989; McKinney et al, 1994). No deaths
    have occurred but debilitating sequelae include gastrointestinal
    stricture formation (secondary to corrosive damage) and chronic
    pancreatic insufficiency (McKinney et al, 1994).


    Excess zinc has been shown to reduce serum free thiol groups and
    disrupt hepatic enzyme activities (IPCS, 1996).

    Zinc chloride is directly corrosive to the mucous membranes of the
    respiratory and gastrointestinal tracts. Anaemia resulting from excess
    zinc uptake is usually due to zinc-induced copper deficiency via
    impaired gastrointestinal copper absorption. This probably involves
    zinc-induced increased metallothionein synthesis with increased
    copper-metallothionein retention in intestinal mucosal cells (Fischer
    et al, 1981).



    Zinc chloride exposure occurs primarily via inhalation and ingestion.
    Available zinc toxicokinetic data involve exposure to non-corrosive
    zinc salts. Gastrointestinal zinc absorption is a function of a
    cysteine-rich intestinal protein (CRIP) which sequesters zinc within
    enterocytes prior to active transport into plasma (Hempe and Cousins,
    1992; Walsh et al, 1994). Metallothionein contributes to zinc
    homeostasis at higher exposures, primarily via retaining excess zinc
    within mucosal cells which are subsequently shed into the intestinal
    lumen (Hempe and Cousins, 1992). Zinc absorption is affected by diet;
    it is inhibited by calcium, phosphorus and phytates and facilitated by
    dietary protein (Hunt et al, 1991). In one study less than 15 per cent
    of dietary zinc was absorbed from a high phytate diet compared to 40
    per cent from a diet with a high animal protein content (Sandstrom,

    In ten healthy volunteers Nčve et al (1991) observed a peak serum zinc
    concentration some 2-3 hours after ingestion of 45 mg zinc (as zinc

    Workers occupationally exposed to zinc fumes may have increased urine
    zinc concentrations (Hamdi, 1969) as evidence of systemic zinc uptake
    via the lungs. However, some inhaled zinc is undoubtedly swallowed
    (and absorbed via the gastrointestinal tract) following clearance via
    the mucociliary mechanism. Systemic zinc uptake following zinc
    chloride inhalation may also occur due to damage to the mucosal
    barrier. In two soldiers who died following zinc chloride inhalation,
    plasma zinc concentrations gradually increased during their illness
    although at autopsy zinc concentrations in major organs and tissues
    were normal save for a slightly increased lung zinc concentration in
    one case (Hjortsœ et al, 1988).

    Zinc is absorbed through broken skin when zinc oxide paste is used to
    treat wounds and burns (Hallmans, 1977).


    Most intravascular zinc is contained within erythrocytes. Plasma zinc
    is bound predominantly to albumin, the remainder bound to other
    proteins, particularly alpha2-macroglobulin, for distribution to
    tissues. Excess zinc is stored as a metallothionein complex, mainly in
    the liver (Abdel-Mageed and Oehme, 1990; IPCS, 1996).

    Some ninety per cent of total body zinc is in muscle and bone (Wastney
    et al, 1986).

    Appreciable amounts of zinc are found also in the kidney, lung, spleen
    and brain (IPCS, 1996).

    Zinc crosses the placenta slowly and is found in breast milk (Agency
    for Toxic Substances and Disease Registry, 1997).


    Most ingested zinc is eliminated in faeces via bile, pancreatic fluid
    and intestinal mucosal cells, with up to ten per cent appearing in
    urine (Abdel-Mageed and Oehme, 1990). Zinc is also eliminated in sweat
    and saliva. The kidneys do not play an important role in regulating
    total body zinc (IPCS, 1996).

    The whole-body zinc half-life is some 5-16 months (IPCS, 1996).


    Dermal exposure

    Topical zinc chloride exposure causes ulceration (Beliles, 1994) and
    burns (Evans, 1945; Chew et al, 1986). Contact dermatitis also has
    been described but without reference to original case data (Poisindex,

    Ocular exposure

    Zinc chloride is highly irritant to the eyes causing pain and erythema
    (Evans, 1945) which may be complicated by corneal oedema, burns and
    ulceration, iritis, glaucoma and cataract formation. Discrete grey
    spots on the lens ("glaukomflecken") as typically seen in acute
    glaucoma also have been described (Grant and Schuman, 1993).

    A plumber who was accidently splashed in the eye with a 30 per cent
    zinc chloride solution experienced an immediate reduction in visual
    acuity with conjunctival haemorrhage and inflammation, corneal
    opacification, a bullous keratopathy and "glaukomflecken" (Houle and
    Grant, 1973).


    Pulmonary toxicity

    Exposure to zinc chloride fumes occurs primarily from smoke screen
    generators or smoke bombs when equal quantities of zinc oxide and
    hexachloroethane are burnt together. Following detonation of a smoke
    bomb participants in an airport disaster drill experienced cough, sore
    throat, hoarseness and chest pain in association with gastrointestinal
    upset (Schenker et al, 1981). Most symptoms resolved within 48 hours
    and none experienced permanent injury.

    In contrast, exposure to high zinc chloride concentrations produces a
    chemical pneumonitis with productive cough, dyspnoea, fever, chest
    pain, cyanosis and diffuse pulmonary infiltrates (Allen et al, 1992).
    In one study these features occurred following exposure to a zinc
    chloride concentration of approximately 4075 mg/m3 (1955 mg
    zinc/m3) (Johnson and Stonehill, 1961). The development of
    emphysematous bullae (which may be complicated by pneumothorax) has
    been reported (Matarese and Matthews, 1986). Severe cases may develop
    non-cardiogenic pulmonary oedema (the adult respiratory distress
    syndrome) (Hjortsœ et al, 1988) sometimes after several days of
    apparent clinical stability (Homma et al, 1992).

    Hjortsœ et al (1988) described two soldiers who died following
    exposure to fumes (for one and two minutes respectively) from smoke
    ammunition bombs (primarily zinc chloride). The first (exposed for two
    minutes) experienced immediate cough and dyspnoea but initial chest
    examination was unremarkable. Inhaled steroids (beclomethasone 100 µg
    qds) were prescribed. The following day he was pyrexial (38.4°C) with
    bilateral lower zone pulmonary infiltrates. Oral prednisolone 40 mg
    daily plus oral antibiotics were instituted. Sputum cultures were
    negative but the patient gradually deteriorated and some 15 days post
    exposure required mechanical ventilation for worsening hypoxia.
    Pulmonary angiography on the 17th day showed diffuse vascular
    obstruction. On day 19 the patient was commenced on intravenous and
    nebulized N-acetylcysteine plus intravenous L-3,4-dehydroproline 35
    mg/kg/day in an attempt to inhibit pulmonary fibrosis. Despite these
    measures hypoxaemia and hypercapnia progressed and the patient died 32
    days after exposure. A similar clinical course was observed in the
    second patient who died on the 25th day.

    Adverse effects occurred in 34 of 70 persons exposed in a tunnel to a
    mixture of zinc chloride (estimated concentration 33,000 mg
    zinc/m3), carbon and carbon dioxide following accidental ignition of
    several smoke bomb generators (Evans, 1945). Immediate symptoms
    included dyspnoea, hoarseness, chest pain and a productive cough. Two
    individuals died before reaching hospital; both showed severe
    respiratory distress and one had aspirated their stomach contents.
    Among the 15 patients admitted to hospital, all had evidence of upper
    respiratory tract (and eye) mucosal irritation, with haemoptysis,
    stridor, cyanosis and persisting chest pain in the majority, often
    accompanied by neurological, cardiovascular and gastrointestinal

    features (see below). Initially there were minimal pulmonary
    auscultatory findings but a chemical pneumonitis with fever and
    consolidation ensued in several patients during the next few days. Six
    of 15 patients died. Autopsy showed respiratory tract mucous membrane
    necrosis with pulmonary haemorrhage and oedema. Autopsy findings in
    other cases have included diffuse pulmonary microvascular obliteration
    with widespread pulmonary artery occlusion (Hjortsœ et al, 1988; Homma
    et al, 1992) and interstitial fibrosis (Milliken et al, 1963; Hjortsœ
    et al, 1988; Homma et al, 1992).

    Gastrointestinal toxicity

    A metallic taste, nausea, vomiting and epigastric pain have been
    reported following zinc chloride inhalation (Evans, 1945; Schenker et
    al, 1981). Gastrointestinal inflammation has been noted at autopsy of
    patients who died following severe zinc chloride poisoning (Evans,

    Cardiovascular toxicity

    Hypotension and tachycardia have accompanied the pulmonary features of
    significant zinc chloride inhalation (Evans, 1945).


    Agitation and restlessness have been described as early features
    accompanying pulmonary symptoms in those exposed to zinc chloride
    smoke (Evans, 1945).


    Gastrointestinal toxicity

    Zinc chloride ingestion causes corrosive damage. Initial symptoms
    include burning of the mouth and pharynx with vomiting. An erosive
    pharyngitis, oesophagitis and gastritis may ensue which may be
    complicated by gastrointestinal haemorrhage and acute pancreatitis
    (Chobanian, 1981; Potter, 1981).

    In one case (Chobanian, 1981) oesophagitis, pharyngitis and acute
    pancreatitis occurred in a patient who ingested some 85 mL "Ruby Red"
    solder flux containing an unstated concentration of zinc chloride. An
    initial serum zinc concentration (some four hours post ingestion) was
    1.46 mg/L (normal 0.5-0.9 mg/L). The patient recovered over five days.

    A 26 year-old woman who ingested 10 mL of a correction fluid
    containing zinc chloride (35 per cent) and methanol (0.5 per cent)
    presented four hours post ingestion with oropharyngeal and gastric
    burns, epigastric tenderness, dysphagia and diarrhoea. Examination
    revealed gross oral mucosal and pharyngeal oedema with surgical
    emphysema of the neck and upper chest wall (presumably due to
    pharyngeal perforation). Serum zinc on the third hospital day was
    normal (0.9 mg/L). The patient subsequently experienced haematemesis

    and melaena necessitating multiple blood transfusions. Recovery was
    delayed further by formation of a gastric stricture requiring subtotal
    gastrectomy (Chew et al, 1986).

    Hedtke et al (1989) reported a 13 month-old child who ingested 9300 mg
    of a moss killer containing 68 per cent zinc chloride. He presented
    with vomiting, gastric mucosal erosions, hyperglycaemia and increased
    alkaline phosphatase and amylase activities. The peak serum zinc
    concentration was 14.2 mg/L (normal range 0.68 - 1.36 mg/L) one hour
    post ingestion.

    A 16 month-old child who ingested approximately one tablespoon of
    soldering flux liquid (containing zinc chloride 22.5 per cent and
    ammonium chloride 5.5 per cent, pH 2) immediately vomited then
    developed dysphagia with inability to swallow his own saliva (McKinney
    et al, 1994). Severe gastrointestinal corrosive effects ensued
    (oropharyngeal, oesophageal and gastric burns). Severe gastric
    scarring and outlet obstruction necessitated a gastric antrectomy. The
    peak plasma zinc concentration was 12 mg/L (normal range 0.6-1.0 mg/L)
    14 hours post ingestion (McKinney et al, 1994). Five months later
    pancreatic exocrine insufficiency was diagnosed with an on-going
    requirement for pancreatic enzyme supplements (McKinney et al, 1995).

    Pulmonary toxicity

    An asthmatic patient who ingested correction fluid developed an acute
    episode of bronchospasm and severe oropharyngeal and laryngeal
    inflammation leading to stridor and dysphonia (Chew et al, 1986). She
    eventually recovered.

    A child who immediately started coughing after ingesting a tablespoon
    of soldering flux (see above) was noted 20 minutes later to have
    widespread coarse breath sounds and wheeze in addition to features of
    severe gastrointestinal toxicity. A chest X-ray some five hours later
    revealed a right pleural effusion with basal atelectasis. The
    pulmonary features resolved with supportive care although the child
    had ongoing gastrointestinal problems (McKinney et al, 1994).


    Microscopic haematuria without associated renal failure (Chobanian,
    1981; Chew et al, 1986) and mild albuminuria (Chew et al, 1986) have
    occurred following zinc chloride ingestion.


    Within 20 minutes of ingesting one tablespoon of solder flux
    (containing zinc chloride 22.5 per cent and ammonium chloride 5.5 per
    cent, pH 2) a 16 month-old became comatose and later developed
    agitation and lethargy which persisted for several days (McKinney et
    al, 1994).

    Somnolence and lethargy occurred in a 13 month-old (Hedtke et al,
    1989) and a two year-old (Potter, 1981) following zinc chloride

    Cardiovascular toxicity

    Premature atrial beats were reported in a 13 month-old child following
    the supposed ingestion of 9.3 g moss killer containing 68 per cent
    zinc chloride (Hedtke et al, 1989).

    Hypotension secondary to intravascular volume depletion is likely in
    those with severe corrosive damage following zinc chloride ingestion.

    The 16 month-old child described above who ingested solder flux
    containing zinc chloride presented with clinical signs consistent with
    hypovolaemic shock (pulse 120 beats per minute, blood pressure 88/62
    mmHg) but following intravenous fluid resuscitation and an upper
    gastrointestinal endoscopy, became hypertensive (figure not given)
    requiring hydralazine and labetalol therapy. The cause of hypertension
    in this case was not known but occurred prior to commencement of
    chelation therapy.


    Severe gastrointestinal corrosive effects following zinc chloride
    ingestion have been associated with transiently increased liver enzyme
    activities (McKinney et al, 1994).


    Gastrointestinal ulceration and burns following zinc chloride
    ingestion may precipitate an acute fall in the haemoglobin
    concentration. Intravascular haemolysis may occur in severely poisoned
    patients (McKinney et al, 1994).


    Dermal exposure

    In an early report chronic topical zinc chloride exposure in the
    pillow manufacturing industry was claimed to result in anorexia,
    weight loss, fatigue and leg pains, microcytic anaemia and
    thrombocytopenia (du Bray, 1937). The causative role of zinc chloride
    could not be confirmed but the patient's symptoms and abnormal
    investigation findings resolved when exposure ceased.


    Occupational asthma associated with raised serum IgE concentrations
    occurred in two men after several months working with soldering fluxes
    containing zinc chloride and ammonium chloride (Weir et al, 1989)
    although in one patient there was no reduction in FEV1 after exposure
    to zinc chloride alone.


    Dermal exposure

    Decontaminate with soap and water ensuring adequate self-protection.
    Ideally, patients should remove their own contaminated clothing. Treat
    burns conventionally. Consider the possibility of systemic zinc
    uptake, particularly where the skin is broken.

    Ocular exposure

    Irrigate with copious amounts of lukewarm water for at least ten
    minutes. A topical anaesthetic may be required for pain relief and to
    overcome blepharospasm. Ensure removal of any particles lodged in the
    conjunctival recesses. The instillation of fluorescein allows
    detection of corneal damage. Specialist ophthalmological advice should
    be sought if any significant abnormality is detected on examination
    and in those whose symptoms do not resolve rapidly.


    Remove the subject from exposure after ensuring adequate
    self-protection. Symptomatic and supportive measures are the mainstay
    of management. Symptomatic patients and those with abnormal
    respiratory signs should have a chest X-ray, receive supplemental
    oxygen and bronchodilators if necessary and be observed until symptoms

    The possibility of developing a chemical pneumonitis, delayed-onset
    pulmonary oedema and/or ARDS must be considered. In these
    circumstances high flow oxygen is mandatory but the value of inhaled
    or systemic corticosteriods has not been confirmed. Steroid therapy
    did not favourably influence the course of a soldier who died from
    ARDS 32 days after a two minute exposure to zinc chloride smoke
    (Hjortsœ et al, 1988). He received inhaled beclomethasone 100 µg qds
    within hours of exposure substituted on the second hospital day with a
    two week course of oral prednisolone 40 mg daily.

    In chemical pneumonitis and ARDS it generally is recommended that
    antibiotics should be reserved for established infection only. The
    patient described by Hjortsœ et al (1988) (see above) also received
    oral penicillin the day following zinc chloride exposure but sputum
    cultures were negative and the antibiotics were discontinued after
    seven days.

    Intravenous L-3,4-dehydroproline (35 mg/kg/day) was administered to a
    patient with zinc chloride smoke-induced ARDS in an attempt to inhibit
    pulmonary fibrosis but without modification of the progressively
    deteriorating course. The patient died 32 days after exposure.


    Effective management primarily involves rapid appropriate symptomatic
    and supportive care. The role of chelating agents is discussed below.

    Decontamination and dilution

    Vomiting is likely to occur spontaneously following significant zinc
    chloride ingestion. Gastric lavage is contraindicated due to the
    corrosive nature of the salt. There may be some benefit in attempting
    oral dilution, if performed immediately, though this is controversial.

    Burkhart et al (1990) advocated whole-bowel irrigation as an effective
    gut decontamination method following zinc sulphate ingestion but there
    are no controlled data to support this view.

    Fluids should not be offered if the patient is not fully conscious, is
    unable to swallow or protect his/her own airway, has respiratory
    difficulty or severe abdominal pain. Possible complications of fluid
    administration include vomiting, aspiration, perforation of the
    gastrointestinal tract and worsening of oesophageal or gastric

    Supportive measures

    Airway support and analgesia should be provided as required. Treat
    hypovolaemic shock with intravenous colloid/crystalloid or blood.
    Monitor biochemical and haematological profiles and acid/base status.
    Antibiotics should be reserved for established infection only.

    If corrosive oesophageal or gastric damage is suspected panendoscopy
    should be carried out, ideally within 12-24 hours, to gauge the
    severity of injury (Knapp et al, 1994). A severity score based on acid
    ingestions may be useful:

    Grade 0:  Normal examination
          1:  Oedema, hyperaemia of mucosa
          2a: Superficial, localized ulcerations, friability, blisters
          2b: Grade 2a findings and circumferential ulceration
          3:  Multiple, deep ulceration, areas of necrosis (Zargar et al,

    Zargar et al (1989) illustrated the important prognostic value of this
    grading system in the management of acid ingestions. In their series
    of 41 patients endoscoped within the first 36 hours of acid ingestion,
    those with grade 0 and 1 burns were discharged within one or two days,
    those with grade 2a burns required only supportive care for a little
    longer, whereas those with grade 2b and 3 burns required nutritional
    support via jejunostomy feeding (total parenteral nutrition is an
    alternative). All patients with grade 0, 1 and 2a injury recovered
    without sequelae. Acute complications and death were confined to those
    with grade 3 burns although several patients with grade 2b burns
    developed oesophageal or gastric strictures.

    An early surgical opinion should be sought if there is any suspicion
    of pending gastrointestinal perforation or where endoscopy reveals
    evidence of grade 3 burns.


    There is no evidence to suggest any role for corticosteroid therapy in
    the management of zinc chloride ingestion. In a controlled trial of
    steroid use among 60 children with oesophageal burns following
    corrosive ingestion (alkalis in the majority) the use of steroids
    (intravenous prednisolone 2 mg/kg within 24 h and daily until oral
    intake was resumed then prednisolone 2.5 mg/kg orally daily for at
    least three weeks) did not influence outcome (Anderson et al, 1996).
    Smaller case series have also concluded that systemic corticosteroids
    confer no benefit following acid ingestion and may exacerbate or mask
    symptoms of pending perforation (Hawkins et al, 1980).


    Animal studies

    Domingo et al (1988) investigated the antidotal potential of DTPA
    (trisodium calcium diethylene triamine-pentaacetate), CDTA
    (cyclohexane diamine tetraacetate), d-penicillamine, sodium
    calciumedetate, DMSA (dimercapto-succinic acid) and the sodium salt of
    DMPS (dimercaptopropanesulphonate) on reducing mortality in rodents
    poisoned with intraperitoneal zinc acetate 66-330 mg/kg. This dose
    range was selected to span the previously calculated intraperitoneal
    LD50 (108 mg/kg) and LD99 (216 mg/kg) for this zinc salt.

    Chelation therapy (or 0.9 per cent saline as control) was administered
    intraperitoneally to ten mice ten minutes after dosing with zinc.
    Antidote doses and outcome (measured as survival at 14 days) are
    summarized in Table 1.

    The very high antidote doses employed in this study necessitate
    caution in interpreting the results with regard to potential clinical
    value. Nevertheless at a zinc acetate dose in excess of the LD99
    there was 100 per cent survival following treatment with DTPA,
    d-penicillamine and DMPS. DMSA was not an impressive antidote under
    these conditions.

    The same research group (Llobet et al, 1988) undertook a similar
    study. Intraperitoneal zinc acetate 0.49 mmol/kg (a dose approximately
    equivalent to its LD50) and 1.15 mmol/kg (approximately the LD99)
    was administered immediately before antidote administration to ten
    mice. Outcome was measured as survival ratio. Sodium calciumedetate
    (2152 mg/kg), DTPA (2262 mg/kg) and d-penicillamine (857 mg/kg),
    completely protected against mortality at the LD99 for zinc acetate.
    Under exactly the same conditions (each chelating agent at a dose of
    5.75 mmol/kg) the survival ratios for CDTA, DMPS and DMSA were 80, 50
    and 70 per cent respectively.

    Table 1. Survival (%) following parenteral chelation therapy in mice
    after a single zinc acetate injection (after Domingo et al, 1988)


    Chelating agent     Antidote dose     Zinc acetate dose
                           (mg/kg)             (mg/kg)
                                           66    153     241

    Control             -                  40     20       0
    Na2CaCDTA           1360              100     90      90
    Na2CaEDTA           1644              100     90      90
    Na2CaDTPA           1569              100    100     100
    d-Penicillamine      857              100    100     100
    DMSA                 619               80     30      10
    DMPS                 273              100    100     100

    Several antidotes have been investigated for their potential to
    enhance zinc elimination. Domingo et al (1988) measured 24 hour faecal
    and urinary zinc excretion in mice administered 88 mg/kg
    intraperitoneal zinc acetate followed ten minutes later by an
    intraperitoneal dose of chelating agent (or saline in the control
    group). The same chelating agents and doses were used as in Table 1,
    again with ten mice in each treatment group. In the control group
    urine zinc elimination was less than half faecal excretion. CDTA
    enhanced urine zinc excretion some six fold and DTPA, DMSA and DMPS
    each some four fold. d-Penicillamine enhanced 48 hour urine zinc
    elimination by some 80 per cent. Sodium calciumedetate did not enhance
    urine zinc excretion but was the only antidote to increase 24 hour
    faecal zinc elimination (by some 20 per cent).

    The effect of increasing the time delay between zinc dosing and DTPA
    or CDTA administration was investigated by Llobet et al (1989).
    Intraperitoneal zinc acetate 0.4 mmol/kg (LD50 0.49 mmol/kg) was
    followed 0-24 hours later by a single intraperitoneal dose of
    chelating agent to give a chelating agent: zinc acetate molar ratio of
    approximately 10:1.

    Urine and faecal zinc elimination were monitored for 48 hours with
    five mice in each treatment group. Urine and faecal zinc elimination
    were increased significantly (p < 0.05) by both chelating agents when
    administered up to two hours after poisoning but only DTPA
    significantly enhanced the 48 hour urine and faecal zinc excretion
    when the antidotes were given 12 hours after zinc dosing.

    When there was a 24 hour delay between zinc acetate injection and
    antidote administration, DTPA significantly (p < 0.05) enhanced urine
    but not faecal 48 hour zinc elimination (CDTA was not effective).

    In summary, animal studies suggest DTPA is the most effective zinc
    antidote as judged by improved survival (100 per cent following a zinc
    acetate dose in excess of the LD99) and increased zinc elimination.
    CDTA produced 90 per cent survival and increased urine zinc excretion
    some six fold. d-Penicillamine also gave excellent results in
    mortality studies, with 100 per cent survival following administration
    of zinc acetate at a dose exceeding the LD99. However,
    d-penicillamine did not enhance zinc elimination significantly. Sodium
    calciumedetate improved survival (90-100 per cent) and in one study
    (Domingo et al, 1988) was the only chelating agent to increase faecal
    zinc elimination. DMPS 273 mg/kg completely protected mice against the
    lethal effects of zinc acetate at a dose in excess of the LD99 and
    the same antidote dose enhanced urine zinc excretion some four fold
    following administration of 88 mg/kg zinc acetate. By contrast DMSA
    619 mg/kg resulted in only 10 per cent survival following 241 mg/kg
    zinc acetate.

    Clinical studies

    Although increased renal zinc excretion has been noted during
    chelation therapy instituted to enhance elimination of other toxic
    heavy metals, there is no convincing evidence of benefit in human zinc
    poisoning. In health, most zinc is eliminated via the gastrointestinal
    tract with only a small contribution made by renal excretion. No data
    have been found regarding the effect of chelation therapy on biliary
    zinc excretion in man.


    McKinney et al (1994) reported improved mental status in a patient
    with severe zinc chloride poisoning (by ingestion) following
    administration of intramuscular dimercaprol 12 mg/kg/day for 24 hours
    and intravenous sodium calciumedetate 1 g/m2 for five days. This
    treatment was instituted 74 hours post ingestion. Chelation therapy
    was not associated with increased urine zinc elimination.

    Intramuscular dimercaprol 4 mg/kg qds was instituted less than four
    hours after the ingestion of 3 g each of zinc sulphate and copper
    sulphate by an 86 year-old woman. This patient also received oral
    d-penicillamine (see below) but both antidotes were discontinued after
    48 hours due to deteriorating renal function. The patient made a full
    recovery over 20 days.

    A 16 year-old who ingested 12 g elemental zinc was treated some nine
    days later with intramuscular dimercaprol 2.3-9.2 mg/kg daily.
    Chelation was associated with clinical improvement and a reduction in
    the blood zinc concentration but urine zinc concentrations were not
    measured (Murphy, 1970).

    Sodium calciumedetate

    A 24 year-old man who developed erosive pharyngitis and oesophagitis,
    hyperamylasaemia, microscopic haematuria and a serum zinc
    concentration of 1.46 mg/L (normal range 0.5-0.9 mg/L) after ingesting
    liquid zinc chloride, made an uneventful recovery following supportive
    care and intravenous sodium calciumedetate 45 mg/kg in divided doses
    over 36 hours. No zinc excretion data were given (Chobanian, 1981).

    Potter (1981) utilized intravenous sodium calciumedetate 150 mg in the
    management of a 28 month-old child who had ingested a zinc chloride
    solution; no urine zinc excretion data were given.

    The patient reported by McKinney et al (1994) who was severely
    poisoned after ingesting one tablespoon of a zinc chloride-containing
    soldering flux was treated with intravenous sodium calciumedetate 1
    g/m2 for five days. The urine zinc excretion in the eight hours
    preceding chelation was 950 µg. Urine zinc excretion was not increased
    by sodium calciumedetate with only 1000 µg/24 h removed on the fourth
    day of treatment (no interim data were given).


    In response to a rising serum zinc concentration, a soldier who
    developed adult respiratory distress syndrome following two minutes
    inhalation of zinc chloride smoke was administered intravenous (140
    mg/kg/day for three days) and nebulized (100 mg qds for 13 days)
    N-acetylcysteine between days 19 and 32 in an attempt to enhance zinc
    elimination. The urine zinc excretion increased from some 125 µmol/24h
    on day 20 to 260 µmol/24h on day 22 (coinciding with intravenous
    N-acetylcysteine administration) then rose to nearly 300 µmol/day (the
    maximum observed zinc excretion) on day 24. Unfortunately no
    pre-chelation zinc excretion measurements were made. There was no
    clinical improvement with therapy and the patient died in respiratory
    and renal failure on day 32.


    An 86 year-old woman who developed chemical pneumonitis, gastritis,
    cardiac and renal failure following the ingestion (and partial
    aspiration) of 3 g each of zinc and copper sulphate, received 250 mg
    oral d-penicillamine qds (in addition to intramuscular dimercaprol 4
    mg/kg qds) commenced less than four hours after zinc ingestion
    (Hantson et al, 1996). Unfortunately there were no pre-chelation urine
    zinc excretion data and treatment was discontinued after 48 hours due
    to deteriorating renal function. The maximum 24 hour urine zinc
    excretion, achieved on the first day of chelation therapy was some
    6000 µg.

    Another patient with zinc chloride poisoning by inhalation survived
    following treatment with oral penicillamine 125 mg twice daily (Allen
    et al, 1992). No blood or urine zinc concentrations were measured.

    Antidotes: Conclusions and recommendations

    1.   There are no controlled clinical data of chelation therapy in
         zinc poisoning and animal studies must be interpreted with
         caution in view of the extremely high antidote doses employed.
         Nevertheless, animal studies suggest that of the antidotes
         readily available for clinical use, sodium calciumedetate is the
         preferred agent with d-penicillamine or DMPS potential
    2.   Although case reports claim clinical benefit following parenteral
         administration of dimercaprol, sodium calciumedetate and d-
         penicillamine, urine and/or faecal zinc excretion data to support
         these claims are lacking.
    3.   Chelation therapy cannot be advocated routinely in the management
         of zinc poisoning; symptomatic cases should be discussed with the


    Patients with haemochromatosis are at greater risk of zinc toxicity
    due to iron-induced increased metallothionein concentrations since
    metallothionein has a greater affinity for zinc than iron.


    Serum zinc concentrations are increased in acute zinc poisoning. The
    24 hour urine zinc excretion is useful when monitoring chronic
    exposure although there is no well established relationship between
    the extent of exposure and urine zinc concentration. Hair zinc
    concentrations are not useful (Agency for Toxic Substances and Disease
    Registry, 1997).

    Normal zinc concentrations in biological fluids

    Plasma and serum: 1.1-1.3 mg/L (IPCS, 1996).
    Whole blood: 6.8-10.8 mg/L (IPCS, 1996).
    24 hour urine excretion: less than 500 µg (IPCS, 1996).


    Occupational exposure standard
    Zinc chloride, fume: Long-term exposure limit (8 hour TWA reference
    period) 1 mg/m3.



    There is no evidence to suggest zinc chloride is carcinogenic in
    humans (Leonard and Gerber, 1989) and the Environmental Protection
    Agency has concluded zinc is not classifiable with regard to its human
    carcinogenicity (Agency for Toxic Substances and Disease Registry,

    Marrs et al (1988) demonstrated a high incidence of pulmonary
    carcinoma in experimental zinc oxide/hexachloroethane smoke poisoning.
    However, a recent  in vitro and  in vivo study failed to show a
    significant genotoxic effect and the authors concluded the smoke was
    "not .... a major health hazard" (Anderson et al, 1996).

    Severe gastric burns following corrosive ingestion are associated with
    an increased risk of gastric carcinoma.


    There is no conclusive evidence regarding the reprotoxicity of zinc
    chloride in humans (Reprotext, 1996). There were no adverse effects
    following the administration of oral zinc sulphide (providing 20 mg
    elemental zinc daily) to 494 women during the last two trimesters of
    pregnancy (Mahomed et al, 1989).

    A relationship between high amniotic fluid or maternal serum zinc
    concentrations and foetal neural tube defects has been proposed, but
    evidence for this is inconsistent (Reprotext, 1996; Reprotox 1996).

    Pre-eclampsia, abnormal deliveries, anencephaly, and an increased
    incidence of stillbirths have been associated with  low maternal
    serum zinc concentrations. Zinc deficiency also has been associated
    with delayed sexual maturity (Reprotext, 1996; Reprotox, 1996).

    Low seminal fluid zinc concentrations have been implicated in male
    infertility but the use of zinc supplements to treat this condition
    remains controversial (Reprotext, 1996; Reprotox, 1996).


     Escherichia coli WP2 (lambda) microscreen assay-positive.

     Salmonella typhimurium TA98, TA100, TA102, TA1537, TA2637-negative.

     In vitro human lymphocytes, chromosomal aberrations-positive.

     In vitro human lymphocytes, low concentrations stimulated DNA
    synthesis, high concentrations inhibited DNA synthesis.

     In vivo mouse bone marrow cells, chromosomal aberrations were
    induced in calcium deficient mice but not in normal calcium
    supplemented mice (DOSE, 1994).

    Fish toxicity

    Lethal to fathead minnow at less than 80 mg/L as zinc (exposure
    unspecified) (DOSE, 1994).

    EC Directive on Drinking Water Quality 80/778/EEC

    Zinc: Guide level 100 µg/L at supply works, 5000 µg/L after 12 hour
    contact with consumers' pipework. Chlorides: Guide level 25 mg/L
    (DOSE, 1994).

    WHO Guidelines for Drinking Water Quality



    SM Bradberry BSc MB MRCP

    National Poisons Information Service (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    B18 7QH

    This monograph was produced by the staff of the Birmingham Centre of
    the National Poisons Information Service in the United Kingdom. The
    work was commissioned and funded by the UK Departments of Health, and
    was designed as a source of detailed information for use by poisons
    information centres.

    Date of last revision


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