Hazardous Chemical Information System (HCIS)

Exposure Standard Documentation


SUBSTANCE NAME:Glutaraldehyde
Potentiated Acid Glutaraldehyde
CAS Number:111-30-8
Exposure Standard:TWA: 0.1 ppm (0.41 mg/m3)
STEL: - ppm - mg/m3

Exposure standard adopted in December 1995

Peak limitation notice: Forsome rapidly acting substances and irritants, averaging of airborneconcentration over an eight hour period is inappropriate. These substancesmay induce acute effects after relatively brief exposure to highconcentrations and so the exposure standard for these substances represents amaximum or peak concentration to which workers may be exposed. See Chapter 6:Guidance Note on the Interpretation of Exposure Standards for AtmosphericContaminants in the Occupational Environment, published by WorksafeAustralia.

Sensitizer notice: Some substancescan cause a specific immune response in some people. Such substances arecalled sensitisers and the development of a specific immune response istermed `sensitisation'. Exposure to a sensitiser, once sensitisation hasoccurred, may manifest itself as a skin rash or inflammation or as anasthmatic condition, and in some individuals this reaction can be extremelysevere. See Chapter 12: GuidanceNote on the Interpretation of Exposure Standards for Atmospheric Contaminantsin the Occupational Environment, published by Worksafe Australia.

Documentation notice: Thisdocumentation is substantially based upon the National Industrial ChemicalsNotification and Assessment Scheme (NICNAS), Full Public Report onGlutaraldehyde (Priority Existing Chemical No. 3) Australian GovernmentPublishing Service, Canberra, 1994. The reader is referred to thispublication for more detailed information on glutaraldehyde.


CAS Number:111-30-8
IUPAC name:1,5-pentanedial
Potentiated Acid Glutaraldehyde
Molecular formula:C5H8O2
Structural formula:O=CH(CH2)3CH=O
Molecular weight:100.11


The following physical properties are for 100% glutaraldehyde (unlessotherwise stated):

Appearance:colourless, oily liquid.
Boiling point:188oC
Density (water = 1):0.72
Relative density (air = 1):3.4
Vapour pressure (20oC):2.03 Pa (50% aqueous solution)
Vapour density:4.1 g/L
Solubility:Soluble in all proportions in water and ethanol; soluble in benzene and ether.
pH:mildly acid (50% aqueous solution)
Partition coefficient log POW:-0.01 (50% aqueous solution)
Hydrolysis:Stability decreases with increasing pH.
* pH 5, half life 508 days;
* pH 7, half life 102 days;
* pH 9, half life 46 days.

Aqueous solutions of glutaraldehyde are stable for long periods of timeand have a mildly acid pH. By buffering aqueous solutions to an alkaline pH,such as with sodium bicarbonate, glutaraldehyde can act as an antimicrobial(sporocidal, bactericidal, viricidal, fungicidal).

In the vapour state, glutaraldehyde has a pungent odour, with an odourthreshold of 0.04 ppm.

Glutaraldehyde tends to polymerise in solution. Commercial glutaraldehydemay contain numerous species including oligomers, unsaturated derivatives andcyclic aldehydes (1).


Glutaraldehyde as a pure chemical is not manufactured in Australia. It isimported into the country mostly as 25%, 45% or 50% w/w aqueous solutions, in200-litre drums. The total volume of glutaraldehyde imported into Australiaper year is in excess of 100 tonnes.

Glutaraldehyde is used mainly as an aqueous solution, ranging inconcentration from 50% w/w to less than 1% w/w. It is used primarily as abiocide but it also has wide use in X-ray film processing, leather tanning,and some use as a therapeutic agent. Approximately 55% of glutaraldehyde isused in Australia as a cold-sterilising disinfectant and approximately 20%for X-ray film processing.


Workers may be exposed to aqueous solutions of glutaraldehyde from 50% toless than 1% by skin contact and by inhalation of the vapours liberated fromthe solutions. The risk of adverse health effects from exposure willincrease with the strength of glutaraldehyde solution handled and temperatureas the atmospheric concentration of glutaraldehyde vapour will increase.

Glutaraldehyde aqueous solutions imported into Australia are usually mixedwith other ingredients and diluted further with water in a closed system.

A large number of workers are potentially exposed to glutaraldehyde inAustralia, mostly in the health care industry, where workers such asendoscopy nurses and technical assistants in hospitals may be exposed to 1%and 2% solutions. Radiographers may be exposed to higher concentrationsthrough the use of glutaraldehyde in X-ray film processing developers. TheX-ray developers are usually supplied as a 50% w/w glutaraldehyde concentrateand are diluted to <2% working solutions. The working solutions are generally used in high temperature, automated film processing equipment.

Occupational exposure to glutaraldehyde also occurs through its use intanning, water treatment, animal housing and electron microscopy and throughits use as a general biocide but, in general, the number of workers exposedin these industries is relatively low.


Monitoring can be carried out at a fixed location or by personalmonitoring of the worker. Commonly high performance liquid chromatography(HPLC) and gas chromatography are used to determine atmosphericglutaraldehyde levels.

Examples of HPLC methods include OSHA Method 64 (7), NIOSH Method 2532 (8) and HSE Method No. FM/2 (9). The OSHA method involves sample collectiononto glass fibre filters treated with 5% 2,4-dinitrophenyl-hydrazinehydrochloride (2,4-DNPH) and phosphoric acid, extraction with acetonitrileand UV detection at 360 nm. The reported detection limit is 0.268 µgfor a 15-litre air sample (7). NIOSH Method2532 involves air sampling onto silica gel coated with 2,4- DNPH, extractionwith acetonitrile and UV detection at 365 nm. The reported limit ofdetection is 0.3 µg per sample and the working range is 0.01 to 0.3 ppmfor a 20-litre air sample (8) (Note thismethod is partially validated). The HSE FM/2 method is currently in draftform (9) and is based on OSHA method 64. Ithas a reported detection limit of 0.008 ug/L based on a two-litre air sampleand corresponds to 80 pg of material on the column (9).


6.1 Toxicokinetics

A material balance study (10) was carried out in male and female Fischer344 rats and New Zealand White rabbits by intravenous injection and dermalapplication of aqueous 14C-glutaraldehyde. The results of thisstudy with solutions of glutaraldehyde up to 7.5% showed that prolonged skincontact can lead to absorption via the skin. This is supported by theresults (11) of in vitro testing usinghuman skin tissue, where 3-14% of an applied dose penetrated the stratumcorneum of the chest and abdomen and 3-4% penetrated the epidermis. In amore recent study, <1% of applied glutaraldehyde penetrated the skin of humans, rats, mice, rabbits and guinea pigs (12).

In the same material balance study (10) themetabolites of glutaraldehyde were not identified. However, the reportproposed that the metabolism of glutaraldehyde probably involved initialoxidation to the corresponding carboxylic acids by aldehyde dehydrogenase,and then further oxidation via an acidic intermediate to CO2. Nospecific target site for distribution was identified.

Glutaraldehyde reacts readily with proteins as a cross-linking agent (12).

6.2 Health Effects in Humans

Symptoms reported in workers after exposure to glutaraldehyde haveincluded headache, nausea and light-headedness (13).

In Western Australia, palpitations and tachycardia were reported in sevenhealth care workers after regular exposure to glutaraldehyde (14), but the reports have not been confirmed byscientific and toxicological evidence.

6.2.1. Irritation


Both a Swedish (15) and a South Australian(6) study have revealed health effects inhospital workers exposed to glutaraldehyde occur at levels below the currentoccupational exposure standard of 0.2 ppm.

A study of Swedish hospital workers involved in cold sterilisation workusing 2% glutaraldehyde has been reported (15).The aims of the study were to determine firstly, the levels of exposure toglutaraldehyde during cold sterilisation work in medical services andsecondly, the acute health effects of this exposure. The study involved bothpersonal and environmental monitoring in seven areas where cold sterilisationoccurred. Two areas had automated cold sterilisation, one with goodventilation and the other with poor. The remaining five were areas whereglutaraldehyde was handled manually. All staff working in these five areas(irrespective of whether they handled glutaraldehyde or not) were given aretrospective questionnaire to complete on health effects experienced in theprevious six months.

The exposed group (n=39), that is, those handling glutaraldehyde reporteda significantly increased prevalence of certain airway symptoms from the nose(catarrh and obstruction) and throat (smarting) than in the non-exposed group(n=68) (15). Other symptoms such as headache,nausea, eczema and hand-rashes were reported to be significantly higher inthe exposed group. A dose-response effect was found between the frequency ofexposure to glutaraldehyde and the number of symptoms (15). No case of contact allergy toglutaraldehyde was found (15).

The results from environmental monitoring were not reported but werestated to be below the detection limit of the method. The results frompersonal monitoring are as follows: In manual cold sterilisation work areasglutaraldehyde measurements ranged from <0.01 mg/m3 to 0.14mg/m3, with a single measurement of 0.57 mg/m3; Inautomatic cold sterilisation work areas the measurements ranged from 0.1mg/m3 to 0.3 mg/m3 (well ventilated) and 0.13mg/m3 to 0.18 mg/m3 (poorly ventilated) (15).

In South Australia a survey (6) wasconducted on hospital-employed endoscopy nurses occupationally exposed toglutaraldehyde. Included in the survey were work-site exposure measurements(both personal and environmental) and the completion of a retrospectivequestionnaire of symptoms experienced in the previous year by glutaraldehydeexposed and non-exposed nurses. As well as completion of a retrospectivequestionnaire, a subset of exposed nurses were also questioned about acutesymptoms experienced at the end-of-day on the day exposure measurements wereperformed.

In the year prior to interview, nurses exposed to glutaraldehyde (N=135)were significantly more likely to report skin, eye and throat symptoms, aswell as headache and tiredness compared with the control group (N=132) (6). No significant differences were found fornasal symptoms, pulmonary symptoms, nausea or stress (6).

Of 72 personal exposure measurements, four were above 0.2 ppm, and afurther six measurements were between 0.1 ppm and 0.2 ppm. The mean of theenvironmental exposure levels was 0.017 ppm.

Simple comparisons were made to investigate whether high personalexposures were associated with an increased risk of reporting symptoms in the12-month retrospective questionnaire. The personal exposure measurementswere arbitrarily categorised into high exposure (> 0.032 ppm) and lowexposure (<0.032 ppm). Symptoms were more common in nurses with glutaraldehyde exposures < 0.032 ppm compared with those exposed to> 0.032ppm. The occurrence of skin, eye and throat symptoms appeared to beunrelated to airborne exposure (6).

On the day of exposure monitoring, a subset of glutaraldehyde exposed nurses(N=63) were questioned on any acute symptoms experienced during that day.The prevalence of acute symptoms were compared for high and low (as above)inhalation exposure groups. Skin symptoms were reported in 2/30 of the highexposure group and 5/33 of the low exposure group. Corresponding values forany eye symptoms were 4/30 vs 3/33, any throat symptoms 5/30 vs 3/33, anynasal symptoms 11/30 vs 11/33 and headache 4/30 vs 6/33. No statisticaldifference existed between high and low exposure groups.

From this study it appears that no obvious dose-response relationshipexists between inhalation exposure and symptoms (either end of day acutesymptoms or those pertaining to a 12 month period) (6).

Other cases of respiratory irritation experienced by workers exposed toglutaraldehyde vapours have been reported (16,17,18,19,20,21,21,23).


Skin irritation has been experienced in workers exposed to glutaraldehydesolutions (usually 2% or higher) and vapours, with numerous cases of contactdermatitis reported in the literature (5,15,16,17,24,25). In Australia, dermatitishas been observed in a number of different types of workers, includingendoscopy nurses, hospital cleaners, radiographers and dental assistants (26). In a South Australian study (2) hand dermatitis was reported in dentalassistants, and facial irritation was reported in egg collectors sprayingeggs with a glutaraldehyde sanitising solution.


Eye irritation has occurred in hospital workers exposed to 2%glutaraldehyde or atmospheric concentrations of 0.5 ppm v/v (16,18,19,21,27). In a case (28) where 2% glutaraldehyde was accidentallysplashed in the eye, irritation, pain and an increased sensitivity to lightresulted.

Human evidence indicates that skin and respiratory irritant effects areexacerbated on repeated exposure to glutaraldehyde.

6.2.2 Sensitisation

Allergic skin reactions have been reported (29,30,31,32,33,34,35,36,37,38) in workersexposed to glutaraldehyde. Positive responses in patch testing have confirmedthat glutaraldehyde is a skin sensitiser (39,40). Photosensitisation testing (41,42) on volunteers did not produce a positivephototoxic or photoallergic response.

A number of reports (23,25,43,44,45,46,47,48,49) of occupationalasthma and/or rhinitis have been linked with exposure to glutaraldehyde inthe workplace, with some cases concerning workers with no past history ofallergic response. Difficulties have arisen in determining whether theresponse in each case is due to an irritant effect or to an allergichypersensitivity. The type of allergic mechanism that causes asthma afterexposure to glutaraldehyde is not yet known, and no specific antibody hasbeen identified (43).

6.2.3 Carcinogenicity and reproductive toxicity

Limited epidemiological data is available on the long-term effects ofglutaraldehyde.

In a mortality study (50) of 186 malesemployed during the period 1959 - 78 at a glutaraldehyde production unit inthe United States, the number of cancer deaths and the total number of deathswere compared to those of white males in the United States and to that of29,000 other chemical workers during the period 1959-78. The number ofdeaths was 14 (25.4 expected) and the total number of cancer deaths four (6.1expected). There was no evidence of glutaraldehyde being carcinogenic, butthe study was hampered by the relatively short observation period and thenumber of subjects still young.

A study in hospital staff engaged in chemical disinfection of instrumentsfound that an increased frequency of spontaneous abortions did not correlatewith exposure to glutaraldehyde (51). A laterstudy comparing 164 nurses who had suffered miscarriage with 464 who hadnormal births indicated that glutaraldehyde exposure was similar in bothgroups (52). The same study (52) gave similar results when comparing nurseswho have borne malformed children with those producing normal babies.

6.3 Toxicity in Animals

6.3.1 Acute toxicity

The oral LD50 using 50% w/w glutaraldehyde in male and femaleSprague Dawley rats is 123 and 77 mg/kg, respectively (53). In another acute oral study (10) in male and female rats, the results forLD50s for glutaraldehyde in the range 5-50% show that largeramounts of glutaraldehyde are required to produce mortality at the higherconcentrations. For example at 50% w/w glutaraldehyde the LD50 inmale rats is 733 mg/kg; and at 15% w/w glutaraldehyde the LD50 is183 mg/kg. This is contrary to what is expected.

The dermal LD50 of 50% w/w glutaraldehyde in male rabbits is1430 mg glutaraldehyde/kg (10). For femalerabbits the dermal LD50 of a 45% w/w glutaraldehyde is 1360 mg/kg(10).

The inhalation LC50 in male and female Fisher rats exposed toheated glutaraldehyde vapours is 23.5 ppm and 40.1 ppm, respectively (54).

6.3.2 Irritation

In a series of skin irritation tests (55),New Zealand white rabbits were treated with solutions of glutaraldehydebetween 1% and 50% for four hours. At 45% and 50%, the aqueous solution wascorrosive to the skin of rabbits. Signs of skin irritation were stillpresent with a 2% aqueous solution, but no effects were observed with a 1%solution.

Other animal tests (56,57,58) were carriedout with 1% or 10% solutions, where the duration of skin contact was longer,for example 24 hours, and the effects observed were more severe.

A study (55) measuring the eye irritancy ofglutaraldehyde (5%, 2%, 1% aqueous w/w) was conducted on New Zealand whiterabbits. The tests indicated that the 5% solution was a severe irritant tothe eye of the rabbit, and that dilute solutions such as 1% and 2% weremoderately irritating to the eye. Further acute eye irritation studies (10) in the rabbit showed that the minimaltransient eye irritation threshold was 0.2-0.5%, and that the minor transientcorneal injury threshold was 1% glutaraldehyde.

Acute inhalation (59) studies in testanimals showed that the vapour from glutaraldehyde solutions was a severe eyeirritant at low vapour concentrations, for example 3 ppm v/v.

Groups of four ND4 Swiss Webster mice were exposed (head only) toconcentrations of glutaraldehyde vapour (1.64 - 36.7 ppm) for 30 minutes (60). Results of the study showed that thebreathing rate of mice was significantly reduced at all vapourconcentrations, no level of tolerance being achieved. The RD50 wascalculated to be 13.8 ppm.

6.3.3 Sensitisation

A skin sensitisation study (61) was carriedout in Dunkin Hartley albino guinea pigs using either aqueous or alkalised 2%glutaraldehyde. The aqueous solution was a moderate to strong skinsensitiser in guinea pigs and the alkalised solution was a weak to moderateskin sensitiser. The results (62) of amouse-ear swelling test confirmed that glutaraldehyde is a skin sensitiser.

6.3.4 Repeated dose toxicity

Short term repeated dose inhalation studies on F344/N rats exposed forsix-hours per day to either 0.3, 1.1 and 3.1 ppm glutaraldehyde for nine-days(63) or 0.16, 0.5, 1.6, 5, and 16 ppmglutaraldehyde for two-weeks (64) producedsimilar results. Respiratory irritation occurred at 0.2 ppm and greater thanor equal to 0.5 ppm, and lesions of the upper respiratory tract were detectedat greater than or equal to1 ppm and 5 ppm respectively (63,64). Signs of irritation included labouredbreathing and discharge and encrustation around the eyes and nose.

In a 13-week sub-chronic study (64), F344/Nrats were exposed for six hours/day to 0.0625, 0.125, 0.25, 0.5 and 1 ppm.The NOAEL was determined at 0.125 ppm for nasal lesions. Dose-relatedincreases in nasal cavity lesions were detected at glutaraldehydeconcentrations of 0.250 ppm and above. Breathing difficulty was noted at 1ppm. In a similar 14-week study (65), ratswere exposed to 0.021, 0.049 and 0.194 ppm glutaraldehyde. Signs ofrespiratory irritation occurred at 0.049 ppm. No lesions of the nasal cavitywere detected at any of the dose levels.

In corresponding two-week and 13-week studies (64) in B6C3F1 mice, mortalityoccurred at 1.6 ppm and 0.500 ppm respectively. Lesions of the upperrespiratory tract were detected at 0.5 ppm and above for the two-week studyand for the 13-week study lesions were detected at all dose levels for femalemice and at 0.25 ppm and above for male mice. Signs of nasal irritationoccurred at the lowest dose (0.0625 ppm) in the 13-week study.

A short term dermal study (10) in male C3H/Jmice exposed to aqueous glutaraldehyde (0.5 - 50% w/w) showed that severecumulative toxicity and mortality may occur by repeated skin contact to25-50% glutaraldehyde, but there was no evidence of cumulative toxicity at 5%or less.

In a 13-week subchronic drinking water study (66) female and male Fisher rats received nominalconcentrations of 0, 50, 250 or 1000 ppm w/v glutaraldehyde in their drinkingwater. At 1000 ppm w/w glutaraldehyde was slightly toxic and 250 ppmproduced physiological changes at 250 ppm.

In a two-year drinking water study (67)female and male Fisher rats received nominal concentrations of 0, 50, 250 or1000 ppm w/v glutaraldehyde in their drinking water. An increased incidenceof large granular cell lymphatic leukaemia (LGLL) was found in the liver andspleen of females only at all dose levels, but as the strain of rats used inthe study has a high natural susceptibility to LGLL the findings were notconclusive.

6.3.5 Reproductive toxicity and teratogenicity

In one study (68) groups of 25 pregnantWistar rats received 50, 250 or 750 ppm w/v glutaraldehyde in their drinkingwater. The maternal NOEL for glutaraldehyde was five mg/kg body weight/day,and for the foetus a NOEL of 68 mg/kg body weight/day.

Gavage studies (69) in groups of 15pregnant Himalayan rabbits receiving 5, 15, or 45 mg/kg bodyweight ofglutaraldehyde for 13 days resulted in maternal toxicity and embryolethalityat 45 mg/kg body weight/day, with a NOEL of 15 mg/kg body weight/day.

In the above two studies, there was no evidence of teratogenicity.

6.4 Genotoxicity

6.4.1 In vitro

Recent studies have indicated that glutaraldehyde is mutagenic inbacterial assays (64).

Glutaraldehyde has been shown to induce mutations in mouse lymphoma L5178Ycells (64), human TK6 lymphoblasts (70) and sister chromatid exchanges in Chinesehamster ovary (CHO) cells (64) in vitro.Chromosome aberration studies in CHO are generally negative, with theexception of a weak positive response (without S9 metabolic activation) inone study (64).

6.4.2 In vivo

Glutaraldehyde did not induce micronuclei (71) chromosome aberrations (72) or unscheduled DNA synthesis (13) in in vivo test systems.Glutaraldehyde was negative in the mouse dominant lethal test (12).


Irritation of the nose and throat have been experienced by workers exposedto glutaraldehyde vapours. In studies in Sweden and South Australia onhospital workers, respiratory irritation was experienced at concentrationsbelow 0.2 ppm. Case studies and patch testing have shown that glutaraldehydeis a skin sensitiser. Human evidence indicates that occupational exposure toglutaraldehyde at the current exposure standard of 0.2 ppm may result inirritation of the skin, eyes and respiratory system, particularly afterrepeated exposure.

Short term (nine-day or two-week) repeated-dose inhalation rat studiesresulted in nasal irritation at levels down to approximately 0.2 ppm.Lesions of the nasal cavity and larynx were observed at 0.5 ppm. In twosubchronic (13-14-weeks) rat studies, signs of irritation were observed atlower concentrations, with a NOAEL of 0.125 ppm in one study and signs ofnasal irritation at 0.049 ppm in the other. In corresponding two-week and13-week studies in mice, signs of nasal irritation were noted at the lowestdose (0.0625 ppm) in the 13-week study. The results highlighted the toxicityand irritancy of glutaraldehyde by inhalation at low vapour concentrationsand the harmful effects of repeated or prolonged exposure to the vapours.


ACGIH:0.2 ppm ceiling limit.
Germany:0.1 ppm MAK; Peak 0.2 ppm (5 minutes, 8 Times/shift).
Sweden:0.2 ppm Ceiling limit;
United Kingdom HSE:0.2 ppm STEL (10 minutes).


In view of the results of animal testing and the human experience, whereirritant effects have been observed at or below 0.2 ppm, the ExposureStandards Expert Working Group recommends that the exposure standard forglutaraldehyde be lowered to 0.1 ppm.


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Footnotes: Peak limitation notice:

Peak - means a maximum or peak airborne concentration of a particular substance determined over the shortest analytically practicable period of time which does not exceed 15 minutes.Documentation notice:

Entries carrying a notice for National Occupational Health and Safety Commission documentation indicate that these substances have been reviewed in detail by the Exposure Standards Expert Working Group and that documentation supporting the adopted national values is available in the National Commission's Documentation of the Exposure Standards [NOHSC:10003(1995)].