UKPID MONOGRAPH
ZIRCONIUM
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service
(Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
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
Service.
ZIRCONIUM
Toxbase summary
Type of product
Zirconium is used in a number of metal alloys, explosive primers and
flash bulbs. Zirconium compounds have been used in deodorant and
dermatitis treatments.
Toxicity
Most zirconium compounds have low systemic toxicity due to their poor
solubility. However, some soluble compounds, such as zirconium
tetrachloride, are irritants and may cause corrosive injury. In
addition, skin and lung granulomas have been reported following
repeated zirconium exposure.
Features
Dermal and inhalational exposure are reported most commonly.
Dermal
- Most zirconium compounds are considered inert to the skin.
- Zirconium tetrachloride is irritant and may cause corrosive
injury.
- Development of granulomas has been reported following
application of zirconium-containing deodorants and
dermatitis treatments to broken skin.
Ocular
- Eye irritation, lacrimation, blurred vision and
conjunctivitis may occur.
- Some soluble compounds may cause corrosive damage.
Inhalation
- Most zirconium dusts and vapours will cause only mucosal
irritation.
- Some corrosive compounds may cause hoarseness, dyspnoea and,
in severe cases, stridor due to laryngeal oedema.
- Pulmonary oedema has been reported after exposure to
zirconium tetrachloride (Cordasco and Stone, 1973) and may
be delayed for up to 36 hours.
- Pulmonary granulomas have been reported in workers
chronically exposed to zirconium dusts (Bartter et al, 1991;
Liippo et al, 1993).
Ingestion
- There are no reports of zirconium intoxication, although
ingestion of a soluble salt may cause corrosive injury.
Management
Dermal
1. Irrigate with copious lukewarm water.
2. Zirconium-induced granulomas are managed most effectively by
discontinuing exposure. Topical or systemic steroids may hasten
resolution in severe cases.
Ocular
1. Irrigate immediately with lukewarm water or preferably saline for
at least 10 minutes.
2. Application of local anaesthetic may be required for pain relief
and to overcome blepharospasm to allow thorough decontamination.
3. Ensure no particles remain lodged in the conjunctival recesses.
4. Corneal damage may be detected by the instillation of
fluorescein.
5. If symptoms do not resolve rapidly or if there are abnormal
examination findings, refer for an ophthalmological opinion.
Inhalation
1. Remove from exposure and administer supplemental oxygen by
face-mask if there is evidence of respiratory distress.
2. Intubation and assisted ventilation may be necessary.
3. Rarely tracheostomy may be required for life-threatening
laryngeal oedema.
4. Corticosteroids in high dosage (prednisolone 60-80 mg/day) may be
considered for laryngeal and pulmonary oedema but there is no
confirmed evidence that they improve prognosis.
5. Chronic exposure may precipitate a pulmonary granulomatous
reaction. Initial assessment involves chest X-ray and lung
function tests. Specialist referral may be indicated.
Ingestion
1. Ingestion of most common zirconium compounds will require
symptomatic and supportive care as dictated by the patient's
condition.
2. If corrosive injury is suspected management is as for acid
ingestion (see Corrosives).
References
Anderson KD, Rouse TM, Randolph JG.
A controlled trial of corticosteroids in children with corrosive
injury of the esophagus.
N Engl J Med 1990; 323: 637-40.
Baler GR.
Granulomas from topical zirconium in poison ivy dermatitis.
Arch Dermatol 1965; 91: 145-8.
Bartter T, Irwin RS, Abraham JL, Dascal A, Nash G, Himmelstein JS,
Jederlinic PJ.
Zirconium compound-induced pulmonary fibrosis.
Arch Intern Med 1991; 151: 1197-201.
Cordasco EM, Stone FD.
Pulmonary edema of environmental origin.
Chest 1973; 64: 182-5.
Hadjimichael OC, Brubaker RE.
Evaluation of an occupational respiratory exposure to a
zirconium-containing dust.
J Occup Med 1981; 23: 543-7.
Jeng L-BB, Chen H-Y, Chen S-C, Hwang T-L, Jan Y-Y, Wang C-S, Chen M-F.
Upper gastrointestinal tract ablation for patients with extensive
injury after ingestion of strong acid.
Arch Surg 1994; 129: 1086-90.
Liippo KK, Anttila SL, Taikina-Aho O, Ruokonen E-L, Toivonen ST, Tuomi
T.
Hypersensitivity pneumonitis and exposure to zirconium silicate in a
young ceramic tile worker.
Am Rev Respir Dis 1993; 148: 1089-92.
Marcus RL, Turner S, Cherry NM.
A study of lung function and chest radiographs in men exposed to
zirconium compounds.
Occup Med 1996; 46: 109-13.
Romeo L, Cazzadori A, Bontempini L, Martini S.
Interstitial lung granulomas as a possible consequence of exposure to
zirconium dust.
Med Lav 1994; 85: 219-22.
Rubin L, Slepyan AH, Weber LF, Neuhauser I.
Granulomas of the axillas caused by deodorants.
JAMA 1956; 162: 953-5.
Shelley WB, Hurley HJ.
The allergic origin of zirconium deodorant granulomas.
Br J Dermatol 1958; 70: 75-101.
Skelton HG, Smith KJ, Johnson FB, Cooper CR, Tyler WF, Lupton GP.
Zirconium granuloma resulting from an aluminium zirconium complex: a
previously unrecognized agent in the development of hypersensitivity
granulomas.
J Am Acad Dermatol 1993; 28: 874-6.
Zargar SA, Kochhar R, Nagi B, Mehta S, Mehta SK.
Ingestion of corrosive acids. Spectrum of injury to upper
gastrointestinal tract and natural history.
Gastroenterology 1989; 97: 702-7.
Substance name
Zirconium
Origin of substance
Found in rare earth minerals, zircon, malacon, baddeleyite,
zirkelite, eudialyte and in monazite sand. Invariably associated
with hafnium. (MERCK, 1996)
Synonyms
Zircat (HAZARDTEXT, 1997)
Chemical group
A group IV B (d block) transition metal.
Reference numbers
CAS 7440-67-7 (DOSE, 1994)
RTECS ZH7070000 (RTECS, 1997)
UN 2858, 2009 (dry);
2008 (powder, dry);
1358 (powder, wetted) (DOSE, 1994)
HAZCHEM NIF
Physicochemical properties
Chemical structure
Zr (DOSE, 1994)
Molecular weight
91.22 (DOSE, 1994)
Physical state at room temperature
Solid (MERCK, 1996)
Colour
A grey-white metal or a blue-black powder.
(MERCK, 1996)
Odour
NIF
Viscosity
NA
pH
NIF
Solubility
Insoluble in hot or cold water.
Slightly soluble in acids.
Soluble in hydrogen fluoride and aqua regia.
(HSDB, 1997)
Autoignition temperature
NIF
Chemical interactions
Zirconium reacts with hydrofluoric acid, aqua regia and hot
phosphoric acid.
Zirconium is slightly attacked by hot concentrated sulphuric acid
or hydrochloric acid and avidly attacked by fused potassium
hydroxide or nitrate.
Treatment of zirconium powder with hydrogen fluoride solution (1
per cent) desensitizes it to electrostatic ignition.
Zirconium dust may explode when mixed with alkali hydroxides,
alkali metal chromates, dichromates, molybdates, sulphates,
tungstates, borax, carbon tetrachloride, cupric oxide, lead, lead
oxide, phosphorus, potassium chlorate, potassium nitrate and
nitryl fluoride.
(MEDITEXT, 1997; SAX'S, 1996; MERCK, 1996)
Major products of combustion
Zirconium oxide (SAX'S, 1996)
Explosive limits
0.16 g/L in air (SAX'S, 1996)
Flammability
Highly flammable. Dust may ignite spontaneously.
(SAX'S, 1996)
Boiling point
3577°C (DOSE, 1994)
Density
6.5 at 20°C (DOSE, 1994)
Vapour pressure
NIF
Relative vapour density
NIF
Flash point
NIF
Reactivity
When exposed to heat and flame, zirconium dust is a very
dangerous fire hazard. A 10 to 70 per cent zirconium lead alloy
will ignite if hit by a hammer.
(MEDITEXT, 1997; SAX'S, 1996)
Uses
Pure zirconium (hafnium free) is used in structural materials in
nuclear reactors.
In constructing rayon spinnerets in lamp filaments and flash
bulbs.
In explosive primers.
As weighting agents, in welding rod manufacture and sandblasting
applications.
In moulds and furnaces in the aluminium, brass, steel and glass
industries.
As a reflective surface on satellites.
In deodorants. (MERCK, 1996; DOSE, 1994; PATTY, 1994)
Hazard/risk classification
Index no.
Zirconium powder (pyrophoric) 040-001-00-3
Risk phases
R15-17 - Contact with water liberates extremely flammable gases.
Spontaneously flammable in air.
Safety phases
S7/8 - 43 - Keep container tightly closed and dry. In case of
fire, use (indicate in the space the precise type of fire
fighting equipment). If water increases the risk add - Never use
water.
EEC no. 231 - 176 - 9 (CHIP2, 1994)
INTRODUCTION
Zirconium is a transition metal usually existing in valence state +4,
although it can form compounds in the +3 and +2 states (PATTY/Beliles,
1994). It is believed to have low systemic toxicity due to the low
solubility of many of its compounds (including the silicate, carbonate
and oxide). Some soluble zirconium salts, such as zirconium
tetrachloride, are irritants and may cause corrosive injury.
Furthermore, zirconium may contain uranium and thorium presenting a
potential radiation hazard to those exposed (Castello et al, 1992).
EPIDEMIOLOGY
Exposure to zirconium and its compounds is mainly as dust and fumes in
the metallurgical industry. Although several studies have found no
adverse health effects following occupational zirconium exposure
(Hadjimichael and Brubaker, 1981; Marcus et al, 1996) a number of case
reports have linked zirconium to respiratory disease (Bartter et al,
1991; Liippo et al, 1993; Romeo et al, 1994).
The use of zirconium compounds in deodorants (Rubin et al, 1956;
Anon.,1958; Obermayer, 1969) and dermatitis treatments (Baler, 1965)
has led to the development of "allergic" granulomas; Shelley and
Hurley (1958) reported 70 cases between 1956 and 1958.
Exposure of bare feet to zirconium-rich clay in Ethiopia has been
associated with non-filarial elephantiasis (Frommel et al, 1993).
MECHANISMS OF TOXICITY
In vitro studies demonstrate zirconium induces lymphocyte
proliferation and may augment the T-cell mediated immune response to
other agents via interaction with macrophages (Price and Skilleter,
1986). However, evidence that the development of lung granulomas in
exposed individuals is a T- cell mediated delayed hypersensitivity
response is inconclusive, unlike the case of beryllium
hypersensitivity (Parkes, 1994).
Some zirconium compounds, for example zirconium tetrachloride, have a
direct irritant or corrosive effect on the skin, eyes and mucous
membranes.
TOXICOKINETICS
Absorption
Zirconium compounds are absorbed poorly following ingestion
(PATTY/Beliles, 1994).
The uptake of insoluble zirconium compounds following inhalation is
low (PATTY/Beliles, 1994). Coal miners exposed to unstated zirconium
concentrations had up to 14 ppm zirconium in heavily pigmented
sections of lung and 22 ppm in pulmonary lymph nodes. Blood zirconium
concentrations were up to 100 µg/L and urine concentrations up to 12
µg/L (PATTY/Beliles, 1994).
Zirconium-induced skin granulomas are associated typically with areas
of damaged skin indicating that absorption through intact skin is
poor.
Distribution
Zirconium was found to be widely distributed in specimens from four
autopsies of non-poisoned patients with particularly high
concentrations in liver and body fat (Schroeder and Balassa, 1966).
Excretion
There are very little data available but most absorbed zirconium
appears to be eliminated in bile with only small amounts appearing in
urine (HSDB, 1997).
CLINICAL FEATURES: ACUTE EXPOSURE
Dermal exposure
Most commonly used zirconium compounds are insoluble and considered
inert to the skin, although some salts, such as zirconium
tetrachloride, are skin irritants. The severity of injury will depend
on concentration or extent of exposure.
Development of axillary granulomas has been reported rarely following
a single application of a zirconium-containing deodorant. However,
prior sensitization, possibly from inhalation of zirconium compounds,
is believed to have occured (Shelley and Hurley, 1958).
Ocular exposure
Ocular exposure to zirconium compounds may cause eye irritation,
lacrimation, blurred vision and conjunctivitis. More severe damage may
be expected following exposure to a corrosive salt such as zirconium
tetrachloride. There are no clinical case data.
Inhalation
Most zirconium compounds cause only irritation when inhaled as dusts
or vapours although pulmonary oedema has been reported following
exposure to zirconium tetrachloride which is corrosive (Cordasco and
Stone, 1973).
Early features following corrosive inhalation include cough and
retrosternal discomfort. Hoarseness, dyspnoea and, in severe cases,
stridor due to laryngeal oedema may follow. Where pulmonary oedema
ensues its onset may be delayed for up to 36 hours.
Ingestion
There are no reports of zirconium poisoning by ingestion. Most
zirconium compounds are absorbed poorly from the gastrointestinal
tract although some salts such as zirconium tetrachloride may cause
corrosive injury.
Gastrointestinal toxicity
Common early features of corrosive ingestion include immediate pain in
the mouth, pharynx and abdomen, intense thirst, vomiting, haematemesis
and diarrhoea. Gastric and oesophageal perforation and chemical
peritonitis may also occur.
Late features include antral or pyloric stenosis, jejunal stricture
formation, achlorhydria, protein-losing gastroenteropathy and gastric
carcinoma.
Pulmonary toxicity
Features associated with corrosive ingestion include hoarseness,
stridor, respiratory distress and, in severe cases, laryngeal or
epiglottal oedema. Chemical pneumonitis and adult respiratory distress
syndrome (ARDS) are recognized.
Nephrotoxicity
Renal failure secondary to acute tubular necrosis may complicate
ingestion of a corrosive zirconium salt.
Cardiovascular toxicity
Circulatory collapse is likely in patients with extensive
gastrointestinal burns.
Haemotoxicity
Disseminated intravascular coagulation and haemolysis may complicate
concentrated corrosive ingestions.
Injection
Two individuals developed vertigo following intravenous administration
of 50 mg zirconium malate (Hathaway et al, 1991).
CLINICAL FEATURES: CHRONIC EXPOSURE
Dermal
The use of soluble zirconium salts, notably sodium zirconium lactate,
in deodorants (Rubin et al, 1956; Anon.,1958; Shelley and Hurley,
1958) has been associated with the development of axillary granulomas.
These appear as red-brown or flesh coloured, mildly or non-pruritic
papules which may form linear streaks, often associated with shaving
and restricted to areas of deodorant application. Histologically they
resemble sarcoid granulomas with epithelioid and multinucleate giant
cells. Onset of the lesions is usually delayed for days to weeks after
exposure with complete recovery within six to twelve months if
exposure ceases.
A more recent report linked the use of an aluminium zirconium complex
to granuloma formation (Skelton et al, 1993). A 27 year-old woman
developed a right axillary mass after some two years use of an
antiperspirant containing aluminium zirconium tetrachlorohydrex
glycerine. A year after its development the mass became acutely
inflamed and was excised. Histological examination showed typical
features of zirconium-induced granulomas and chemical analysis
confirmed the presence of zirconium. The use of the antiperspirant was
discontinued and no recurrence was reported after one year (Skelton et
al, 1993).
Similar lesions were reported in a 15 year old girl following
treatment of poison ivy dermatitis with four per cent zirconium oxide
cream. No granulomas appeared on intact skin areas indicating dermal
damage is necessary for zirconium penetration. Oral prednisone (dose
not stated), topical fluocinolone and intralesional injection of
triamcinolone (6 mg/mL) each cleared the lesions leaving only areas of
pigmentation. However, there was a complete recurrence on cessation of
treatment and untreated granulomas showed no evidence of improvement
over 20 months (Baler, 1965). The author noted that although cutaneous
reactions to zirconium seemed less common following exposure to
insoluble (e.g. zirconium oxide) than soluble (e.g. zirconium lactate)
salts, once initiated reactions to insoluble salts were more likely to
persist due to prolonged retention in dermal tissue.
The development of lymph node sclerosis, leading to non-filarial
elephantiasis has been associated with increased soil concentrations
of zirconium and beryllium in Southwest Ethiopia (Frommel et al,
1993). The exposure of bare feet to zirconium rich soil is thought to
be exacerbated by the corrosive nature of the clay particles.
Inhalation
Epidemiological studies of industrial exposure to zirconium compounds
have found no evidence of impaired pulmonary function although
individual cases of zirconium-induced lung disease have been reported.
No zirconium-attributed abnormalities were reported in 22 workers
exposed to fumes in a zirconium reduction plant for one to five years
(Reed, 1956).
A group of 32 male metal handfinishers exposed to zirconium dust for
one to 17 years were examined for any adverse pulmonary function
compared to a control group matched for age, sex, payroll status and
smoking history. No significant difference in self-reported symptoms,
chest X-rays or expiratory lung function tests were found
(Hadjimichael and Brubaker, 1981).
The pulmonary function of 178 men exposed to zirconium dust (mainly
less than 10 mg/m3; maximum measured concentration 30.0 mg/m3) was
monitored between 1975 and 1988 (Marcus et al, 1996). No abnormal
chest X-ray findings (in 1975, 1978 and 1982) or impaired pulmonary
function were found to have resulted from zirconium exposure.
Conversely, Bartter et al (1991) described a 62 year-old man with
apparent zirconium-induced pulmonary fibrosis. He was employed for 39
years at a lens grinding company where he was responsible for mixing a
powder containing 90 per cent zirconium dioxide. He was a smoker and
wore no respiratory protection during the course of his work. Over 25
years he became increasingly dyspnoeic, and was originally diagnosed
with emphysema. Examination revealed clubbing of the fingers and toes
with diffuse crackles and wheeze in both lungs. A series of X-rays
taken between 1969 and 1988 showed progressive interstitial fibrosis
with honeycombing in the lower zones bilaterally. Pulmonary function
tests showed a restrictive picture with total lung capacity 56 per
cent predicted, carbon monoxide diffusing capacity 37 per cent
predicted and modest hypoxia (pO2 9.3 kPa; pCO2 normal). An open
lung biopsy showed end-stage fibrosis and honeycombing but no
granulomas. Polarizing light microscopy revealed a moderate number of
birefringent particles. Further scanning electron microscope analysis
revealed 69 x 106 particles/cm3, 60 x 106 of which contained
zirconium oxide, zirconium silicate or zirconium aluminium silicate
(normal < 1 x 106/cm3). Zirconium-specific proliferation studies
on peripheral lymphocytes and pulmonary lymphocytes obtained via
bronchoalveolar lavage were negative. The patient died of pneumonia
with sepsis two years after initial examination (Bartter et al, 1991).
Zirconium-induced hypersensitivity pneumonitis was considered the
underlying cause of death in a 25 year old female ceramic tile worker
(Liippo et al, 1993) who had a history of atopy. The patient had
worked for 1.5 years as a glazier where she was exposed to
0.8-5.8 mg/m3 dust containing 10-30 per cent zirconium silicate. She
previously had worked for two years as a sorter where dust
concentrations were 0.5 - 2.6 mg/m3 and one month with special
shaped ceramics where dust concentrations were as high as 8.6 mg/m3.
At presentation she gave a two month history of dry cough and
exertional breathlessness. Examination revealed crackles in both lungs
with bilateral interstitial fibrosis and small discrete nodules on
chest X-ray. Respiratory function was markedly decreased with FEV1 32
per cent predicted, FVC 34 per cent predicted and carbon monoxide
diffusing capacity 36 per cent predicted. Oral prednisolone 1 mg/kg
for nine months gave no improvement. An open lung biopsy was performed
but was complicated by pneumothorax which precipitated acute right
heart failure and fatal splenic rupture one week later. At autopsy the
lungs showed features compatible with hypersensitivity pneumonitis
with widespread interstitial lymphocytic inflammation, mild fibrosis
and multiple noncaseating epithelioid granulomas with some
multinucleate cells. Scanning electron microscopy revealed 1.3 x 109
zirconium silicate particles per gram dry weight of lung (Liippo et
al, 1993).
Zirconium-induced lung disease has been implicated also in a 29 year
old male worker with suspected pneumoconiosis following eight years
exposure to 1.1 mg/m3 inhalable dust containing zirconium silicate.
Pulmonary function tests were normal though chest X-ray showed diffuse
interstitial reticular opacities. A transbronchial biopsy revealed
small interstitial granulomas which histologically contained
epithelioid and giant cells with no central necrosis (Romeo et al,
1994).
A recent review has concluded that while prolonged zirconium dust
inhalation undoubtedly may cause a benign pneumoconiosis, there is
insufficient evidence to confirm zirconium as a cause of a delayed
(type IV) granulomatous hypersensitivity reaction as seen among
beryllium workers (Parkes, 1994).
Ingestion
There are no reports of chronic ingestion of zirconium or its
compounds.
MANAGEMENT
Dermal exposure
Ensure adequate self protection before attempting treatment. If
possible the patient should remove any contaminated clothing
him/herself. Affected areas of skin should be washed with copious
quantities of water. Pay special attention to skin folds, fingernails
and ears. Burns should be treated conventionally as for thermal burns
(e.g. silver sulphadiazine dressing). Surgery may be required for deep
burns.
Dermal granulomas usually clear spontaneously six to twelve months
after removal from exposure (PATTY/Beliles, 1994; Obermayer, 1969),
although they may remain for longer periods in individuals exposed to
insoluble zirconium compounds (Baler, 1965). Topical and/or systemic
steroids may hasten granuloma resolution.
Ocular exposure
Irrigate immediately with lukewarm water or preferably saline for at
least 10-15 minutes. A local anaesthetic may be indicated for pain
relief and to overcome blepharospasm. Specialist ophthalmic advice
should be sought if any abnormality is detected or suspected on
examination and in those whose symptoms do not resolve rapidly.
Inhalation
Immediate management involves removal from exposure, establishment of
a clear airway and administration of supplemental oxygen if necessary.
Rarely mechanical ventilation may be required or tracheostomy if there
is life-threatening laryngeal oedema. The administration of
prednisolone 60-80 mg daily may be considered if laryngeal or
pulmonary oedema are present but there is no confirmed evidence that
their use alters prognosis. Discussion with a NPIS physician is
recommended.
Ingestion
Decontamination
Ingestion of most common zirconium compounds will require only
symptomatic and supportive care as dictated by the patient's
condition. However, if ingestion is of a corrosive salt a more
aggressive approach may be required.
Gastric aspiration/lavage following corrosive ingestion is
contraindicated. There may be some benefit of attempting oral dilution
with milk or water, if performed immediately, though this is
controversial.
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
injuries.
Supportive measures
Airway support and analgesia should be provided as required. Treat
shock with intravenous colloid/crystalloid and/or blood. Monitor
biochemical and haematological profiles and acid/base status.
Administer antibiotics for established infection only.
Symptoms and signs are unreliable predictors of the extent of injury
following corrosive ingestion (Zargar et al, 1989) and therefore in
symptomatic patients panendoscopy should be carried out, ideally
within 12-24 hours to gauge the severity of injury.
Grade 0: Normal examination
1: Oedema, hyperaemia of mucosa
2a: Superficial, localized ulcerations, friability, blisters
2b: Grade 2a findings and circumferential ulcerations
3: Multiple, deep ulceration, areas of necrosis (Zargar et al,
1989).
Following corrosive acid ingestion endoscopic findings within the
first 36 hours have been successfully used to guide management. In a
series of 41 patients (Zargar et al, 1989) those with grade 0 to 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 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.
In view of the high morbidity associated with corrosive-induced upper
gastrointestinal perforation and the high incidence of later
complications requiring surgery, an aggressive surgical approach is
recommended (Jeng et al, 1994). Surgery should therefore be
considered:
1. If symptoms or signs of gastrointestinal tract perforation are
evident at initial presentation.
2. When endoscopy reveals evidence of grade 3 burns with full-
thickness necrosis (black, ulcerated mucosa) of the stomach or
oesophagus.
Corticosteroids
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 hours 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, 1990). 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).
MEDICAL SURVEILLANCE
Ensure adequate ventilation and air concentrations below the
occupational exposure standard.
Appropriate respiratory and dermal protective equipment should be
available. In particular, the exposure of broken skin to zirconium
compounds must be avoided.
People with respiratory disease should be identified prior to
employment if inhalational exposure is likely.
Normal zirconium concentrations in biological fluids
NIF
OCCUPATIONAL DATA
Occupational exposure standard
Short-term exposure limit (15 minute reference period) 3.8 mg/m3.
Long term exposure limit 1.3 mg/m3 (8 hour TWA reference period)
(Health and Safety Executive, 1997).
OTHER TOXICOLOGICAL DATA
Carcinogenicity
There is no evidence regarding the carcinogenicity of zirconium in
humans (REPROTEXT, 1997). However, there is an increased risk of
gastric cancer following severe mucosal damage after corrosive
ingestion.
Reprotoxicity
There is no conclusive evidence that zirconium is reprotoxic in man
(REPROTEXT, 1997).
Genotoxicity
Salmonella typhimurium TA98, TA100, TA102, TA1537, TA2637 negative.
When tested in combination with 9-aminoacridine, the mutation rate was
higher than that for 9-aminoacridine alone (zirconium tetrachloride)
(DOSE, 1994).
Fish toxicity
LC50 (96hr) fish (unspecified) bioassay >20 mg/L (DOSE, 1994).
EC Directive on Drinking Water Quality 80/778/EEC
NIF
WHO guidelines for drinking water quality
NIF
AUTHORS
WN Harrison PhD CChem MRSC
SM Bradberry BSc MB MRCP
JA Vale MD FRCP FRCPE FRCPG FFOM
National Poisons Information Service (Birmingham Centre),
West Midlands Poisons Unit,
City Hospital NHS Trust,
Dudley Road,
Birmingham
B18 7QH
UK
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
28/1/98
REFERENCES
Anonymous.
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A controlled trial of corticosteroids in children with corrosive
injury of the esophagus.
N Engl J Med 1990; 323: 637-40.
Baler GR.
Granulomas from topical zirconium in poison ivy dermatitis.
Arch Dermatol 1965; 91: 145-48.
Bartter T, Irwin RS, Abraham JL, Dascal A, Nash G, Himmelstein JS,
Jederlinic PJ.
Zirconium compound-induced pulmonary fibrosis.
Arch Intern Med 1991; 151: 1197-1201.
Castello G, Vigo F, Gallelli G, Beccaria AM.
Determination of radioactive impurities in zirconium minerals used in
the ceramic industry and risk analysis for exposed workers.
Int J Environ Stud 1992; 42: 271-9.
CHIP2/Chemicals (Hazard Information and Packaging for Supply)
Regulations 1994.
Health and Safety Commission.
Sudbury: Heath and Safety Executive, 1994.
Cordasco EM, Stone FD.
Pulmonary edema of environmental origin.
Chest 1973; 64: 182-5.
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See Also:
Toxicological Abbreviations
Zirconium (ICSC)