SCOEL/SUM/134
August 2010
For second consultation
Recommendation of the Scientific Committee
on Occupational Exposure Limits
for Hydrogen peroxide
1
8 hour TWA
0.2 ppm
STEL (15 min)
0.5 ppm
Notation
-
Substance identification
Hydrogen peroxide
Synonyms
dihydrogen dioxide, hydrogen dioxide
EINECS No.
231-765-0
CAS No.
7722-84-1
Molecular formula
H2O2
Structural formula
H-O-O-H
Molecular weight
34.02 gmol-1
Conversion factors
At 25°C 1ppm H2O2 = 1.3914 mg/m3; 1 mg/m3 = 0.763 ppm
EU-Classification
O; R8 (contact with combustible material may cause fire)
C: R34 (causes burns)
In aqueous solution
R5 (Heating may cause an explosion)
O; R8 (contact with combustible material may cause fire)
C; R35 (causes severe burns)
Xn; R20/22 (harmful by inhalation and if swallowed)
Specific concentration limits
100 - 70%
O; R5-8
C; R20/22-35
50 - 70%
O; R8
C; R20/22-34
35 - 50%
Xn; R22-37/38-41 (irritating to respiratory system and skin, risk of serious
damage to eyes)
1
8 - 35%
Xn; R22-41 (harmful if swallowed, risk of serious damage to eyes)
5 - 8%
Xi; R36 (irritating to eyes)
(see co-existing CLP/GHS classification in Annex).
This document is mainly based on the EU-RAR (2003) document, completed with data coming
from recent studies described in the peer-reviewed literature.
2
Physico-chemical properties
Hydrogen peroxide is a colourless liquid that is normally handled as an aqueous solution. Several
types of stabilizers may be added to the H2O2 solution to prevent potentially violent
decomposition. Such additives include phosphoric acid, sodium phosphate, stannate and silicate,
ammonium sulphate, acetanilide, 8-hydroxyquinoline, pyridine, tartaric, benzoic and carboxylic
acids. Nitrate salts can be added as passivators to improve the chemical resistance of stainless
steel and aluminium against H2O2 (EU-RAR, 2003).
The melting point of hydrogen peroxide is 0.43-0.40°C and it decomposes at 150-152°C. At 25°C
it has a density of 1.4425 g/cm3 and a vapour pressure of 3hPa. It is miscible with water at all
proportions and has a pKa of 11.62 at 25°C.
Hydrogen peroxide can act as both an oxidising and as a reducing agent.
3
Occurrence/Use
The main method by which hydrogen peroxide is produced industrially is by anthraquinone autooxidation. Anthraquinone derivate is hydrogenated to anthrahydroquinone using a palladium or
nickel catalyst. Hydrogen peroxide is formed when anthrahydroquinone is oxidised back to
anthraquionone by bubbling air or oxygen through the solution. Crude H2O2 is extracted with
water from the organic solution which is returned to the first hydrogenation step to give a cyclic
process. The extracted crude aqueous solution contains about 20-40% H2O2 and is normally
purified in two or three stages by extraction with organic solvent. The aqueous solution is
distilled to give 50-70% H2O2 solutions. Older production methods are based on the electrolysis
of aqueous ammonium sulphate or sulphuric acid solution in water. An organic process based on
2-propanol is used in the former Soviet Union.
The EU risk assessment estimated that 750,000 tonnes per year of hydrogen peroxide were
produced in Europe in 1995 out of which 670,000 tonnes were used within the EU. During the
1990s the production increased sharply as hydrogen peroxide replaced chlorine in various
bleaching processes.
The main use (48%) of hydrogen peroxide in the EU is for bleaching pulp. Other uses include
chemicals manufacture and use as an intermediate in the synthesis of chemicals such as sodium
perborate, sodium percarbonate, hydroquinone, hydrazine, organic peroxides and many others. It
is used in the bleaching of textiles and other products, wastewater and waste gas treatment,
disinfection, beverage packing, surface treatment, etching and cleaning. Small quantities are used
in consumer products such as cosmetics, toothpastes and deodorants.
2
4
Methods of exposure monitoring and analysis
OSHA has published two partially validated methods for the measurement of airborne
concentrations of hydrogen peroxide. No fully validated methods are available. OSHA method
VI-6 is based on sample collection using a midget fritted glass bubbler TiOSO4 and analysis by
colorimetry. The limit of detection is 2 µg H2O2 and the method is suitable for concentrations of
0.06 to 3.0 mg/m3 H2O2. OSHA Method ID-126-SG uses the same sampling procedure but
analysis is by differential pulse polarography at a dropping mercury electrode. The detection limit
is 0.14 mg/m3 for a 100 L air sample and the working analytical range is 5 to 100 µg H2O2 on
sample (OSHA 1990).
INRS proposes a method based on air sampling with filters impregnated with titanium oxysulfate
followed by spectrophotometric measurement of the coloured Ti-H2O2 complex (INRS, 2004)
No biological monitoring methods are available.
5
Health Effects
5.1
Toxicokinetics
Human studies
The toxicokinetics of hydrogen peroxide are reviewed in the EU-RAR (2003). Hydrogen
peroxide is present as a normal metabolite in aerobic cells and plays a role in the cellular defence
mechanism. It passes readily across cell membranes giving rise to high levels of absorption
through the mucous membranes, skin and the lungs leading to extensive penetration of adjacent
tissues and blood vessels.
At low physiological concentrations, hydrogen peroxide is mainly decomposed by glutathione
peroxidase but at higher concentrations it is mainly decomposed by catalase. Red blood cells
have very high catalase activities and efficiently remove hydrogen peroxide from the blood.
It appears that H2O2, in human airways, is mainly consumed by the lactoperoxidase system, an
enzyme oxidizing the thiocyanate anion to an antibiotic product that prevents the growth of
bacteria, fungi, and viruses in airways (El Chemaly et al, 2003).
At high levels of exposure, the degradation of hydrogen peroxide to oxygen can lead to the
formation of oxygen micro bubbles and mechanical injury of tissues and/or blood vessels may
result. Normally, however, the lung is an effective filter for micro bubbles, preventing serious
injury to blood vessels.
There are no data on the systemic fate of hydrogen peroxide following occupational exposure.
The EU-RAR concluded that it is unlikely that occupational exposure would affect the
endogenous steady state of hydrogen peroxide, although there are currently no methods available
to allow investigation of the fate of hydrogen peroxide absorbed from the respiratory system or
through the skin.
3
The EU-RAR also noted that hydrogen peroxide may undergo iron-catalysed reactions that may
result in the formation of hydroxyl radicals that are toxic to cells. Certain genetic traits may
render some humans more susceptible to peroxide toxicity (eg acatalasaemia, glucose-6phosphate dehydrogenase deficiency of red blood cells). This traits render cells less able to
reduce oxidised glutathione and thus less able to detoxify hydrogen peroxide through glutathione
peroxidase.
5.2
Acute toxicity
Human data
There are no good human data for inhalation exposure. In an undated guidance document on their
website (www.osha.gov), the US Occupational Health and Safety Administration cite
information from secondary sources that indicated that inhalation of high concentrations of the
vapour or mist may cause extreme irritation of the nose and throat. Even short periods of
exposure, may cause stinging and watering of the eye and exposure to 7 ppm (9.2 mg/m3) has
been reported to cause lung irritation in humans. Higher levels of exposure may cause headache,
dizziness, vomiting, diarrhoea, tremors, numbness, convulsions, pulmonary oedema,
unconsciousness, and shock.
A number of cases of human poisoning following ingestion of aqueous hydrogen peroxide
solutions have been reported but few include information about dose. The EU-RAR identified
two cases where it was possible to make some estimation of the dose received. A 16 month-old
baby died following ingestion of about 600 mg/kg body weight as a 3% solution and an 84-year
man experienced severe brain damage following ingestion of about 150 mg/kg body weight as a
35% solution. In another case, irrigation of an infected wound with a 3% solution of hydrogen
peroxide caused transient shock and coma, probably as a result of systemic embolisation of
oxygen micro bubbles. The received dose was believed to be about 15 mg/kg body weight.
Animal data
A number of acute inhalation studies were reviewed by the EU-RAR. The main effects of
exposure to low concentrations are irritation of the respiratory tract and eyes. Exposure to higher
concentrations is associated with congestion of the lungs and trachea, emphysema and damage to
the cornea. Corneal damage may continue to develop even after cessation of exposure. Very high
levels of exposure give rise to rapid mortality resulting from oxygen embolism. The lowest
reported lethal dose is 160 mg/m3 for H2O2 vapour in mice (4 hours exposure) and 9,400 mg/m3
for H2O2 aerosol in rats (15 minutes exposure). No 4 hour LC50 is available for hydrogen
peroxide aerosol. The 4 hour LC50 for the vapour has been reported as 2,000 mg/m3. Rats
exposed to vapour concentrations between 338 and 427 mg/m3 for 4 to 8 hours showed few
symptoms.
The EU-RAR reviewed several poorly described toxicity studies where dermal application of
hydrogen peroxide gave rise to systemic toxicity and death. Apparent LD50 values following
dermal application of a 90% solution of H2O2 range from 700 to 5,000 mg/kg body weight. There
is interspecies variability in response to dermal exposure with rabbits being sensitive and rats
being relatively insensitive.
4
The EU-RAR also reviewed the oral toxicity of H2O2. Reported oral LD50 values in rats range
from about 800 mg/kg body weight (70% solution) to >5,000 mg/kg (10% solution), although an
LD50 of about 1,500 mg/kg (9.6% solution) was reported in another study. Animals showed
lethargy, immobility, irregular respiration and effects on the tongue, oesophagus, stomach,
duodenum and peritoneal cavity. Degenerative ulceration and regenerative hyperplasia of the
pyloric antrum of the stomach was found at all dose levels.
5.3
Irritation
Human data
The EU-RAR cites several reports linking hydrogen peroxide to irritation of the respiratory tract
and eyes. Seven dairy workers exposed to a mean concentration of about 12 mg/m3 experienced
eye and throat irritation (Kaelin et al, 1988) and slight nasal irritation was reported in workers
filling drums and tanks with H2O2, exposed to a maximum mean concentration of 3.5 mg/m3 over
a one hour period (CEFIC, 1996).
In a briefly reported study by Kondrashov (1977, cited by EU-RAR, 2003), 32 volunteers were
exposed to hydrogen peroxide vapour at variable concentrations and for variable durations
through nose breathing using a face mask. Respiratory irritation depended primarily on the
concentration, and only slightly on the duration of exposure. The exposures, lasting from 5 min to
4 h, revealed an apparent LOAEL of 10 mg/m3 and NOAEL of 5 mg/m3 for respiratory irritation
(the method is not described). The authors cite Russian industrial experience that workers had
respiratory irritation symptoms at 10 mg/m3, in agreement with the experimental results.
In 2005 and 2006 Mastrangelo and coworkers (Mastrangelo et al., 2009) performed two crosssectional studies on workers in a beverage processing plant to investigate the association between
low hydrogen peroxide exposure and symptoms of irritation (2005 study) and to investigate the
effect of wearing respiratory protection (2006 study). The study comprised 69 workers exposed
to hydrogen peroxide in sterile chambers and/or at the bottling lines and 65 unexposed controls
working in automatic mineral water bottling lines. The exposure was estimated by combining air
measurements (performed once a year, 6 measurements per location) and work task information
from employment records. The duration of exposure in the sterile chambers was in average
around 30 min per visit. The average exposure levels (geometric means and upper 95%
confidence limits, n=6) in the sterile chambers (personal sampling) were 0.82 (1.5) mg/m3 in
2005 and 0.47 (2.3) mg/m3 in 2006, whereas the corresponding levels in the bottling lines
(stationary sampling) were 0.13 (0.58) and 0.07 (0.25) mg/m3, respectively.
The symptoms experienced during the last week were graded for severity using a 10-point visual
analog scale, where 1 corresponds to none and 10 to unbearably severe symptoms. In the 2005
study symptoms of irritation (teary, sore and red eyes, throat irritation, nasal secretion,
obstruction and itching, sneezes and cough) were significantly more severe (p<0.001) among
exposed workers compared to controls and the average ratings on the 10-point scale being
between 3.8 and 1.5 units higher among the exposed. There was also a significant (p= 0.0001)
exposure-effect relationship between the number of entries in a sterile chamber in the past 12
month and the severity of sore eyes, teary eyes, redness of eyes, nasal secretion and throat
irritation. There were no significant differences in symptom ratings between the control group
and a group of workers engaged only at the bottling lines, thus never entering the sterile
5
chambers. The study 2006 suggests that respiratory protection (full-face mask) provided an
effective protection from irritative symptoms (Mastrangelo et al., 2009).
Overall, the Mastrangelo (2009) study indicates that an average exposure at 0.82 mg H2O2/m3
(30-min TWA) causes irritative symptoms in eyes, nose and throat, whereas exposure at
0.13 mg/m3 (full shift TWA) does not.
The main effects of eye contact with hydrogen peroxide have been reported to be burning,
redness and blurry vision (Dickson and Caravati, 1994). In the past, solutions of 1 to 3% H2O2
were applied to the eye as an antibacterial treatment. Solutions of 5 to 10% H2O2 cause
cloudiness in the cornea, severe pain and intraocular inflammation.
The main effects of skin contact with hydrogen peroxide have been reported to be paresthesia,
whiteness and blistering (Dickson and Caravati, 1994). In a volunteer experiment described by
Kondrashov (1977), the thresholds for skin irritation following exposure to H2O2 vapour were 20
mg/m3 for 4 hour exposure, 80 mg/m3 for 1 hour, 110 mg/m3 for 30 minutes, 140 mg/m3 for 15
minutes and 180 mg/m3 for 5 minutes. The measured skin deposition of H2O2 vapour associated
with irritation was 110 to 170 mg/m2 compared with a no effect level of 5 to 8 mg/m2.
Animal data
Respiratory irritation has been demonstrated in animal experiments (EU-RAR). The
concentration associated with a 50% reduction in the respiratory rate has been reported as 665
mg/m3.
A number of studies have also demonstrated that hydrogen peroxide is irritating to the skin and
eyes and high concentrations of hydrogen peroxide are corrosive causing epidermal necrosis
(EU-RAR). The threshold for detection of eye irritation is about 0.1%. The thresholds for mild
irritation, severe irritation and corrosion of the skin are 10, 35 and 50%.
5.4
Sensitization
The EU-RAR concluded that the potential of hydrogen peroxide to cause skin sensitisation is
extremely low. There are no reports of respiratory sensitisation. As an irritant, hydrogen peroxide
would be expected to exacerbate pre-existing asthma and high levels of exposure might give rise
to Reactive Airways Dysfunction Syndrome (RADS).
5.5
Repeated dose toxicity
Human data
The EU-RAR reviewed several studies that provide limited information about the levels of
occupational exposure to hydrogen peroxide that may be associated with adverse effects (Table
1). The data suggest that less than 3 years of exposure to peak concentration of 11 mg/m3 (around
9 ppm) and 8h-TWA concentrations of 2-3 mg/m3 combined with intermittent skin contact is
associated with irritation of the eyes and airways, headaches, temporary loss of olfaction, effects
on skin and bleaching of hair (Riihimäki et al, 2002).
6
In an earlier study from the same beverage processing plant as described previously (see 5.3
Irritation – Human data), Mastrangelo et al. (2005) report a longitudinal study on lung function.
Changes over time in forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC) and
FEV1/FVC, all expressed as per cent of predicted, were evaluated by multiple regression analysis
using sparse lung function measurements collected 1993-2002 from 43 exposed and 31
unexposed workers. Sparse stationary air measurements conducted between 1997 and 2001
indicated average air levels between 0.15 and 0.48 (range 0.1-1.0) mg/m3. Whereas FEV1 was
significantly lower in smokers compared to nonsmokers, this measure was uncorrelated to
hydrogen peroxide exposure. In contrast, the ratio FEV1/FVC decreased with increasing exposure
to hydrogen peroxide. The authors interpret the decrease in FEV1/FVC as a consequence of a
positive correlation between FVC and exposure. Considering the development of lung function
over time (and disregarding the sparse exposure measurements), both FEV1 and FVC decreased
by about 15% in the exposed group whereas FEV1/FVC was unaffected.
Overall, although the number of examined workers was small, the air measurements were sparse
and the increase in FVC with exposure is unexplained, the Mastrangelo (2005) study indicates
that average exposure levels of 0.15-0.48 mg/m3 do not significantly impair lung function,.
The EU-RAR suggested that peak levels of exposure may be of particular importance in
determining effects.
Animal data
The EU-RAR reviewed a number of inhalation studies that were considered to be of limited
quality (Table 2). It was concluded that the lowest concentration associated with local adverse
effects on skin, the respiratory tract and the lungs is about 10 mg/m3 in rats (Oberst et al, 1954).
The toxicity of hydrogen peroxide following repeated oral administration is better established but
none of the key studies cited by the EU-RAR are in the peer reviewed literature. The EU-RAR
established that exposure of rats to between 50 and 500 mg/kg body weight/day is associated
with a reduction in body weight gain and effects on a range of other parameters including
decreased red blood cell count, haemocrit, plasma protein concentration and plasma catalase. In a
drinking water study, the NOEL was established at about 26 mg/kg/day in males and 37
mg/kg/day in females. The LOEAL was 76 mg/kg/day in males and 103 mg/kg/day for females
based on reduced food and water consumption and the finding of duodenal mucosal hyperplasia
in one animal. At higher levels of exposure (239 mg/kg/day and above), reversible hyperplasia
was found in all animals. At 547 mg/kg/day (males) and 785 mg/kg/day (females), total plasma
protein and globulin concentrations were reduced.
7
Table 1: Studies of the effects of workplace exposure to hydrogen peroxide (TWA = time-weighted average)
Type of
study
Case report
Study population
Exposure
Effects
Study
Operator of milk
packaging machine
Long term exposure to 12 mg/m3 with short
term exposures to up to 41 mg/m3, daily
exposure over 6 mo preceded by exposure 2
d/wk for 3 years
Kaelin et al
(1988)
Pulmonary
function
testing
All employees of H2O2
production facility over
2-3 years
Typical exposure levels nondetectable to 0.79
mg/m3 (0.6 ppm)
Health
surveillance
110 production workers
at 4 sites, 80 with more
than 10 years exposure
Health
surveillance
Small group of works
exposed to H2O2 during
the packaging of fruit
juices
Shift mean levels well below 1.4 mg/m3 (1.1
ppm), short term concentrations up to 5
mg/m3, some accidental exposures up to 10
mg/m3
Employees had less than 3 years exposure to
peak concentrations of 11 mg/m3, and 8-h
TWA concentrations of 2-3 mg/m3 combined
with intermittent skin contact
Pulmonary
function
testing
43 exposed and
31 controls in beverage
processing plant
Geometric mean 0.15-0.48 mg/m3, range 0.11.0 mg/m3 (0.1- 0.4 ppm)
(stationary measurements 1997-2001)
Crosssectional
study
65 exposed and
69 controls in beverage
processing plant
Sterile chambers: geometric mean 0.82
mg/m3 (0.6 ppm), upper 95% CI limit 2.3 (1.8
ppm) (personal sampling, 30-min TWA).
Bottling lines: geometric mean 0.13 mg/m3
(0.1 ppm), upper 95% CI limit 0.6 (0.5 ppm)
(stationary sampling, 5.5-h TWA)
Eye and throat irritation and gradual bleaching of the hair,
Progressive dyspnoea, bilateral diffuse nodular infiltrates of the
lung. Dyspnoea resolved within 1.5 months of exposure ceasing.
The individual had smoked 2 packs of cigarettes per day for 25
years.
Repeated lung function testing on all employees of a hydrogen
peroxide production facility for a period of 3-5 y showed no
evidence of adverse effects attributable to occupational exposure.
At the same plant there had been reports of hair bleaching, nose
bleeds, and eye or respiratory irritation in the past. Since the
operating procedures were improved there were few reported
incidents.
No effects on lung function, occasional skin irritation and
whitening following accidental H2O2 exposure at two plants, past
reports of hair bleaching at one plant, one case of acute throat
irritation.
Irritation of the eyes and airways, headaches, temporary loss of
olfaction, effects on skin and bleaching of hair. Skin contact was
associated with burning and pricking of fingers, drying of hands
and face, decrease in skin elasticity and dry, rough bleached hair.
A subsequent reduction in concentrations was associated with a
reduction in symptoms.
FVC increased, FEV1 unchanged and FEV1/FVC decreased with
increasing exposure.
FVC and FEV1 decreased and FEV1/FVC unchanged over time in
exposed group.
FEV1 significantly lower in smokers than in non-smokers.
Self-reported irritation was more severe (p<0.001) among
exposed workers. Severity of symptoms correlated with number
of entrances in sterile chambers. No significant differences in
symptom ratings between controls and workers engaged only at
the bottling lines.
8
CEFIC 1996,
cited by EURAR 2003
Degussa-Huls,
1999, described
by EU-RAR
2003
Riihimäki et al
(2002)
Mastrangelo et
al (2005)
Mastrangelo et
al (2009)
Table 2: Repeated dose animal inhalation experiments reviewed by the EU-RAR
Species
Rat
Mouse
Dog
Rat
Exposure regime
Exposure of 23 rats to 93
mg/m3 H2O2 vapour for 6
weeks, 6 hours/day, 5
days/week
Exposure of groups of 10 mice
to 79 mg/m3 or 107 mg/m3
H2O2 vapour for 6 weeks, 6
hours/day, 5 days/week
Exposure of 2 dogs to 10 mg/m3
H2O2 vapour for 6 months, 6
hours/day, 5 days/week
NOEL
Exposure of groups of 5 rats at
0, 2.9, 14.6 or 33 mg/m3 of
H2O2 vapour for 6 hours/day, 5
days/week for 28 days
2.9 mg/m3
(2.2 ppm)
LOEL
93 mg/m3
79 mg/m3
10 mg/m3
14.6
mg/m3
Effects
After 2 weeks: nasal discharge, oedema of the feet, skin
irritation in the groin region
Study
Comstock et al
(1954)*, Oberst
et al (1954)*
After 5 weeks: hair loss
Remarks
Restricted study
design,
incomplete
reporting
Sneezing, lachrymation, external skin irritation, bleaching
of hair, loss of hair, greatly thickened skin, hyperplastic
muscular coats in terminal and respiratory bronchioles,
buds of fibrotic tissue scattered in the lungs, patchy areas of
atelectasis intermingled with emphysematous areas
Respiratory tract irritation at the two higher doses, necrosis
and inflammation of the epithelium in the anterior regions
of the nasal cavity
Study designed
for range finding
purposes
CEFIC
Peroxygen
Sector Group*
*unpublished industry studies cited by the EU-RAR
9
5.6
Mutagenicity
Hydrogen peroxide is not classed as a mutagen according to EU principles. Hydrogen
peroxide is a mutagen and genotoxicant in a variety of in vitro test systems but gives
negative results in a range of in vivo assays.
5.7
Carcinogenicity
There are no human data on the potential carcinogenicity of hydrogen peroxide.
A drinking water study in a catalase-deficient mouse strain showed a dose dependent
increase in duodenal carcinomas (at low frequency). These lesions showed a marked
tendency to regress and even disappear after the cessation of treatment. The lowest
concentration of H2O2 in drinking water at which tumours were observed was 0.1% (Ito
et al, 1981). A subsequent study with different strains of mice found a strong negative
correlation between the incidence of duodenal tumours and catalase activities in duodenal
mucosa, blood and liver (Ito et al, 1984). No gastrointestinal tumours were found in a
similar study in rats exposed to up to 0.6% H2O2 in drinking water for 18 months
(Takayama, 1980 – unpublished industry study). Squamous cell papillomas of the
forestomach were reported in a later drinking water study in which rats were exposed to
1% H2O2 in drinking water for 32 weeks (Takahashi et al, 1986). Several studies have
demonstrated that hydrogen peroxide had a promoting effect on the carcinogenicity of
other substances whereas other studies have failed to identify a promoting effect.
The EU-RAR concluded that there was insufficient evidence to classify hydrogen
peroxide as a carcinogen.
5.8
Reproductive toxicity
There are no human reproductive toxicity data available.
There are a number of animal studies, but the EU-RAR did not consider any to be
appropriate for a complete evaluation of reproductive and developmental toxicity. No
adverse effects on fertility in mice were observed in two drinking water experiments
reviewed by the EU-RAR at drinking water concentrations of up to 1% H2O2. In a
feeding experiment in rats, some adverse effects on the foetus were observed with an
H2O2 feed content of 10%, but this dose level was associated with substantial maternal
toxicity. It was presumed that conventional study protocols were unlikely to show
specific embryonic or foetal effects because it is doubtful whether hydrogen peroxide
rather than its degradation products would reach the foetus and also because maternal
toxicity would be expected.
10
6
Recommendation
Hydrogen peroxide is a widely used industrial chemical but relatively few studies have
been undertaken of exposed workers and there are few case reports describing adverse
effects arising from hydrogen peroxide exposure.
Exposure to hydrogen peroxide vapours is associated with irritation of the nose, eyes and
respiratory tract. As for data available on humans occupationally exposed (summarized in
table 1), the evidences reported by CEFIC (1996), Degussa-Huls (1999) and Mastrangelo
et al (2005, 2009) appear to be adequate in order to derive an OEL.
According to a CEFIC (1996) report, very briefly described in the EU-RAR (2003),
repeated lung function testing on all employees of a hydrogen peroxide production
facility for a period of 3-5 y showed no evidence of adverse effects attibutable to
occupational exposure. Typical exposure levels ranged from non-detectable to 0.6 ppm.
In another health surveillance program, no effects on lung function were seen in two
plants with mean shift levels of below 1.1 ppm hydrogen peroxide (Degussa-Huls, 1999,
briefly described in EU-RAR 2003).
Further, no lung function impairment was seen in workers at a beverage processing plant
with average exposures between 0.1 and 0.4 ppm (Mastrangelo et al, 2005).
In a more recent study in the same beverage factory, the severity of self-reported
irritation correlated with the number of entrances in sterile chambers with mean exposure
levels of 0.6 (upper 95%CI 1.8) ppm. No increased ratings were reported by workers
engaged only at the bottling lines with mean levels of 0.1 (upper 95%CI 0.5) ppm
(Mastrangelo et al, 2009).
On the basis of these four studies, although each study has limited information on
exposure levels, a NOAEL for impaired lung function in the upper end of the range 0.10.6 ppm may be assumed. Hence, an 8-h OEL of 0.2 ppm is recommended for hydrogen
peroxide. A 15-min STEL of 0.5 ppm is recommended based on increased self-reported
irritation at mean levels of 0.6 ppm. These values are further supported by the NOAEL
for irritation of 2.2 ppm in a 28-day rat inhalation study (unpublished report cited by
CEFIC 1996).
No "skin" notation was considered to be necessary.
At the level recommended, no measurement difficulties are foreseen.
11
References
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healthy human volunteers. Solvay Duphar BV. Environmental Research
Department, Weesp, CEFIC Peroxygen Sector Group.
Comstock CC, Hackley EB, Oberst FW. (1954). The inhalation toxicity of 90% hydrogen
peroxide vapour for acute, subacute, and chronic exposures to laboratory animals.
Edgewood: Army Chemical Center. (Chemical Corps Medical Laboratories
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Degussa-Huls AG. (1999). Draft report of hydrogen peroxide production workers health
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peroxide of Degussa-Huls AG.
Dickson KF, Caravati EM. (1994). Hydrogen peroxide exposure – 325 exposures
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El Chemaly S, Salathe M, Baier S, Conner GE, Forteza R (2003). Hydrogen peroxidescaveging properties of normal human airway secretions. Am J Respir Crit Care
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Ito A, Naito M, Naito M. (1981). Induction and characterization of gastro-duodenal
lesions in mice given continuous oral administration of hydrogen peroxide.
Japanese Journal of Cancer Research: Gann; 73: 315-322 (cited by EU-RAR).
Ito A, Watanabe H, Naito M, Naito Y and Kawashima K (1984). Correlation between
induction of duodenal tumor by hydrogen peroxide and catalase activity in mice.
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with hydrogen peroxide inhalation in a dairy worker. Annual. Review of
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Kondrashov VA. (1977). Evaluation of the toxicity of hydrogen peroxide vapours for
inhalation and percutaneous exposures. Gigiena Truda Professional’nye
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ANNEX. Classification and hazard statements following Regulation (EC)
No 1272/2008 Annex VI table 3.1 arising from translation of classifications
listed in Annex I to directive 67/548/EEC for hydrogen peroxide 3.1ation
(EC) No 1272/2008 Annex VI Table 3.1
Regulation (EC) No 1272/2008 Annex VI Table 3.1
Ox. Liq. 1
Acute Tox. 4 *
Acute Tox. 4 *
Skin Corr. 1A
H271 May cause fire or explosion; strong oxidiser.
H332 Harmful if inhaled.
H302 Harmful if swallowed.
H314 Causes severe skin burns and eye damage.
C ≥ 70 %****
50 % ≤ C < 70 % ****
*
C ≥ 70 %
50 % ≤ C < 70 %
35 % ≤ C < 50 %
8 % ≤ C < 50 %
5%≤C<8%
STOT SE 3; H335; C ≥ 35 %
(May cause respiratory irritation)
Ox. Liq. 1; H271 May cause fire or explosion; strong oxidiser
Ox. Liq. 2; H272 May increase fire
Skin Corr. 1A; H314 Causes severe skin burns and eye damage
Skin Corr. 1B; H314 Causes severe skin burns and eye damage
Skin Irrit. 2; H315 Causes skin irritation.
Eye Dam. 1; H318 Causes serious eye damage
Eye Irrit. 2; H319 Causes serious eye irritation
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