I:\MEPC\53\2-12.doc 

For reasons of economy, this document is printed in a limited number. Delegates are 

kindly asked to bring their copies to meetings and not to request additional copies.

INTERNATIONAL MARITIME ORGANIZATION

IMO

E

MARINE ENVIRONMENT PROTECTION 

COMMITTEE 

53rd session 

Agenda item 2 

MEPC 53/2/12

 15 April 2005

 Original: ENGLISH

HARMFUL AQUATIC ORGANISMS IN BALLAST WATER 

Application for approval of an Active Substance for Ballast Water Management 

Submitted by Germany 

SUMMARY

Executive summary: This document contains an application for basic approval of an Active 

Substance under the Procedure for approval of Ballast Water 

Management Systems that make use of Active Substances (G9). Due 

to the bulkiness and technical complexity of the information the 

annex is submitted in English only. 

Action to be taken: Paragraph 5 

Related documents: BWM/CONF/36, MEPC 53/2/1 

1 Regulation D-3.2 of the International Convention for the Control and Management of 

Shipsí Ballast Water and Sediments (BWM Convention) stipulates that Ballast Water 

Management systems (BWMS) that make use of Active Substances to comply with the 

Convention shall be approved by the Organization. During its fifty-second session, the 

MEPC developed a procedure for approval that is submitted as MEPC 53/2/1. 

2 The procedure for approval defines principle aspects to be documented by data or testing 

(MEPC 53/2/1, paragraph 4.2.1) and some basic principles for risk evaluation (MEPC 53/2/1, 

paragraph 5.3). According to paragraph 6.1 of document MEPC 53/2/1, the Technical Group has 

to evaluate whether this information is complete and of sufficient quality. 

3 The receiving competent authority in Germany has verified the dossiers and believes 

them to satisfy the data requirements of the IMO Draft Procedure for approval of Ballast Water 

Management systems that make use of Active Substances (G9). 

4 Germany therefore submits the applying manufacturerís summary of the dossier in the 

annex to this document to the Organization for evaluation according to the procedure as 

described in MEPC 53/2/1. The complete dossier will be made available to the experts of the 

Technical Group with the understanding of confidential treatment. 

Action requested of the Committee 

5 The Committee is invited to consider the annex and take action as appropriate.

*** 

MEPC 53/2/12 

I:\MEPC\53\2-12.doc 

ANNEX 

Background Information and Worst Case Scenario 

of Environmental Emission for Ballast Water Treatment 

! It is estimated that ~ 3 to 10 billion tonnes of ballast water are carried around the world 

each year. 

! It is estimated that > 7,000 different species are carried around in shipsí ballast water each 

day. 

! Some of these organisms pose a direct risk to human health: 

! Fish farming and recreational waters might contribute to this risk, if Ö 
MEPC 53/2/12 

ANNEX 

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Ö the Standard of D-2 is not met 

Regulation D-2 Ballast Water Performance Standard ñ 

Ships conducting ballast water management shall discharge 

< 10 viable organisms / m3 > 50 μ; and 

< 10 viable organisms / ml < 50 μ and > 10 μ; and 

discharge of the indicator microbes shall not exceed the specified concentrations. 

The indicator microbes, as a human health standard, include, but are not be limited to: 

Toxicogenic Vibrio cholerae (O1 and O139) with < 1 colony forming unit (cfu) / 100 ml or 

< 1 cfu per 1 gram (wet weight) zooplankton samples; 

Escherichia coli < 250 cfu / 100ml; 

Intestinal Enterococci <100 cfu / 100ml. 

Since more than 90% of the world seaborne cargo is handled and shipped via the 20 biggest 

ports Ö 
MEPC 53/2/12 

ANNEX 

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Ö surrounding waters and port areas often turned into anaerobic status 

Based upon the environmental emission scenarios developed for anti-foulants following worst 

case scenario might help to define an acceptable risk in the frame of IMOís Ballast Water 

Management Convention. 

Port Statistics 

Selected Port: Rotterdam 

Water Volume: 840,000,000 t 

Number of incoming ships: 29,450/a; 80/d 

Total Gross Tonnage: 489,222,000 GT/a; 1,323,074 GT/d 

Average amount of Ballast Water: 144,876,600t/a; 396,922t/d 

Shipsí Profile:

Ship Type / 

Pump 

capacity[t/h] 

Number of 

Ships 

Gross Tonnage [t] Amount of Ballast 

Water [t] 

Pump out 

time [h] 

Annual Daily Annual Daily Annual Daily Annual Daily 

Bulker 

(4x1,000t/h) 

8,000 22 170,000,000 465,753 51,000,000 139,726 12,750 35

General 

Cargo 

(2x600t/h) 

20,000 55 300,000,000 821,918 90,000,000 246,575 75,000 205

Other 

(2x200t/h) 

1,000 3 3,000,000 8,219 900,000 2,466 2,250 6

Total 29,000 80 473,000,000 1,295,890 141,900,000 388,767 90,000 246
MEPC 53/2/12 

ANNEX 

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Ballast Water Treatment ñ Worst Case Scenario for Hydrogen Peroxide: 

Initial Dose: 21 mg/l 

Retention (Degradation) time [h]: zero 

Predicted Environmental Concentration: 0.0099 mg/l 

Predicted No Effect Concentration: 0.0100 mg/l 

PEC/PNEC Ratio: 0.99 

Factors not considered in above scenario: 

Degradation occurring during pump out time 10 d 

Tidal Period 

(exchange of total Water Volume in Port): 12.41 h 

Degradation during shipís voyage: 1 ñ 28 d 

The Port of Rotterdam was chosen because of the detailed statistics available via: 

http://www.portofrotterdam.com

If smaller ports are chosen for different scenarios number and size of ships have to be amended 

accordingly. 

Conclusion: 

Since the natural concentration of Hydrogen peroxide in marine waters can reach up to 

0.058 mg/l the PNEC of 0.01 mg/l seems to be very conservative. 

During a field trial carried out in Kiel harbour in November 2002, the concentration of Hydrogen 

peroxide in 20 t of Ballast Water treated with Peraclean Ocean, decreased from 17.2 mg/l to 

1.4 mg/l within 24 hours as shown in following graph: 

 Abbau des Desinfektionsmittels in den Lagertanks 

Messung am 28.11.2002

6,7 6,8 7 7,

2

7,2 6,

9

17,2

15,1

13,8

9,6

8,1

1,4

9,9

6,7

5,9

4,8

4,3

0 0 

5 

10 

15 

20 

Zeit nach der Behandlung

pH -W ert [-]

H2O2-concentration [m

Peracetic acid [mg/l]

permitted 

lower pH -value [-] 

 permitted 

 upper H2O2-concentra

[mg/l]
MEPC 53/2/12 

ANNEX 

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Technical Summary of Dossiers by the applying manufacturer

for the evaluation of an active substance according to the Draft Procedure for Approval

of Ballast Water Management Systems that make use of Active Substances

Introduction 

The applicant is proposing a chemical ballast water treatment with PeracleanÆ

 Ocean using a 

special technology. PeracleanÆ Ocean is a proprietary formulation based on peroxygen chemistry. It has 

been demonstrated to effectively kill bacteria, yeasts, viruses, molds, spores, algae, protozoa, 

zooplankton, phytoplankton, larval stages and fish eggs in ballast water. It is most effective in 

combination with solid separation. Due to its unspecific mode of action as an oxidiser it is effective and no 

resistances have been observed so far. It is active at high concentrations of sediment and/or organic 

matter at pH values between 5 and 9 and in the temperature range of -5 to more than 40°C. It is a liquid 

that can easily be applied automatically with a specific proprietary technology. 

 The formulation has a long shelf life (> 95% activity after 1 year of storage at 20°C). The product 

is effective at relatively low concentrations. The active ingredients of PeracleanÆ

 Ocean are not 

bioaccumulative or persistent, will ultimately degrade under environmental conditions to oxygen, water 

and carbon dioxide and will not form any persistent metabolites. In the following assessment the 

headings are grouped according to document MEPC 53/2/1 of October 29, 2004. 

The original numbers of that document are given in brackets. 

Identification (4.1) 

PeracleanÆ Ocean is a proprietary formulation based on peroxygen chemistry. The main components 

are: 

15% PAA 14.3% H2O2 26.5% acetic acid 

• Hydrogen peroxide (H2O2) is commonly viewed as an ìenvironmentally friendlyì or ìgreenì 

chemical. This is particularly due to the physicochemical properties of this small inorganic 

water-soluble molecule. H2O2 is non-persistent, has innocuous or even beneficial degradation 

products, and does not accumulate. 

• Hydrogen peroxide is produced naturally by many living organisms either within the organism 

itself or in the surrounding medium. For example blue-green algae produce H2O2 under light 

irradiation at a rate of 1-50 μg/l per hour (Zepp et al, 1987). 

• Hydrogen peroxide levels in natural waters range from 0.14 to 58 μg/l in seawater and from 

0.34 to 109 μg/l in fresh water (ECETOC, 1993). 

1 Data on effects on aquatic organisms (4.2.1.1; 5.3.9) 

1.1 Acute aquatic toxicity 

The existing data for marine organisms are summarized in table 1. 
MEPC 53/2/12 

ANNEX 

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Table 1: Acute toxicity for marine organisms 

Species Endpoint Result as 

PAA 

Result 

calculated as 

PeracleanÆ

Ocean 

Reference 

Fish 

Pleuronectes 

platessa 

96 h LC50 11 mg/L 73 mg/L Tinsley and Sims 

1987a 

Juvenile 

Macomona 

liliana 

96 h LC50 4.35 mg/L 29 mg/L Degussa, 2004b 

Invertebrates 

Crangon 

crangon 

96 h EC50 15 mg/L 100 mg/L Tinsley and Sims 

1987b 

Embryoniclarval stages 

Mytilus edulis 

embryo 

48 h EC50

NOEC 

0.27 mg/ml 

0.13 mg/L 

1.8 mg/ml 

0.87 mg/ml 

Fairhurst 1987 

Crassostrea 

gigas embryo 

48 h EC50

NOEC

0.28 mg/L 

0.13 mg/L 

1.87 mg/L 

0.87 mg/L 

Butler 1987 

Mytilus 

galloprovincialis 

larval 

development 

(age < 4 h post 

fertilisation) 

48 h 

EC50

NOEC 

 survival 

EC50 

NOEC 

normal 

development 

EC50

NOEC 

 normal 

surviving 

0.85 mg/L 

0.7 mg/L 

0.55 mg/L 

0.35 mg/L 

0.54 mg/L 

0.35 mg/L 

5.66 mg/L 

4.69 mg/L 

3.68 mg/L 

2.34 mg/L 

3.64 mg/L 

2.34 mg/L 

Degussa, 2005a 
MEPC 53/2/12 

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Acute toxicity data for freshwater organisms are summarized in table 2. 

Table 2: Acute toxicity to freshwater organisms 

Species Endpoint Result as 

PAA 

Result 

calculated 

as 

PeracleanÆ

Ocean 

Reference 

Fish 

Oncorhynchus 

mykiss 

96 h 

LC50

1.6 mg/L 10.6 mg/L Gardener and 

Bucksath, 1996 

Lepomis 

macrochirus 

96 h LC50 3.3 mg/L 22 mg/L Terell 1987b/ 22 mg 

product/l 

Salmo gairdneri 96 h LC50 13 mg/L 87 mg/L CEFIC PAR, 1986, 

Douglas and Pell, 

1986a 

Invertebrates 

Daphnia magna 48 h EC50 0.5 mg/L 3.3 mg/L Douglas and Pell 

1986b 

Paracalliope 

fluviatilis 

96 h LC50 2.14 mg/L 14.2 mg/L Degussa, 2004b 

Fish 

In the study of Tinsley and Sims (1987b), plaice (Pleuronectes platessa), a saltwater fish species, with a 

mean weight of 8.5 g was used. Test solutions were renewed daily during this semi-static test. The 

relatively high LC50 could be due to the rapid degradation of PAA in seawater. The half-life in seawater is 

less than 1 hour and therefore the exposure during the fish test could have been low. 

In the test with juvenile shellfish (Macomona liliana, saltwater species) a static protocol was used. The 

test was conducted in natural water with a low organic carbon content. The values are based on nominal 

concentrations. (Degussa , 2004b). 

In the study with rainbow trout (Oncorhynchus mykiss cold-water species, freshwater) were conducted at 

temperatures of 12-14°C. Analytical measurements of H2O2 in the test solutions were performed. 

Between the start (0-hour) and the end of the test (96-hour) the decrease in the concentration of H2O2

ranged between 14 and 26% (Gardener and Bucksath, 1996). 

In the study the warm-water bluegill sunfish (Lepomis macrochirus) have the test solutions were not 

renewed and the values are based on nominal concentrations (Terell, 1987b). 

In the CEFIC PAR, 1986 study and the study of Douglas and Pell, 1986a with Rainbow trout 

(Salmo gairdneri, freshwater) a semistatic protocol according to OECD 203 was used. The values are 

based on nominal concentrations. 
MEPC 53/2/12 

ANNEX 

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Invertebrates 

The study with equilibrium PAA (12%) in brown shrimp (Crangon crangon) revealed a 96-h LC50 value of 

15 mg PAA/l. The medium was renewed daily during the study but analytical concentration 

measurements were not made. The mean weight of these saltwater crustaceans was 1.25 g (Tinsley and 

Sims, 1987a). The larger size of the organism compared to daphnids may explain the lower sensitivity of 

the shrimp. The high LC50 value could also be related to the rapid degradation of PAA in seawater 

The toxicity tests with diluted equilibrium PAA (15%PAA, 14 % H2O2, 28% acetic acid) in the fresh water 

flea Daphnia magna was conducted using a static protocol according to OECD 202 part 1, without 

analysis of the PAA, active oxygen or H2O2 concentrations in the test solutions (Douglas and Pell, 1986b). 

The LC50 was 0.5 mg/L PAA. 

A static study with the freshwater amphipod Paracalliope fluviatilis revealed a 96 h LC50 of 2.14 mg/L 

based on nominal concentrations. 

Embryonic-larval stages 

Two embryo-larval assays were carried out on marine oysters with nominal concentrations of equilibrium 

PAA (12.5%) dissolved in seawater, to determine any effects during their first 48 hours of their 

development from embryo to larva. In this period a protective D-shaped shell was formed. Without a 

shell the embryos were extremely sensitive to reduced water quality. Both tests were conducted under 

static conditions. In the first test with embryos of the pacific oyster (Crassostrea gigas), a 48-hour EC50 of 

0.28 mg PAA/l was obtained (Butler, 1987). Another test with embryos of the common mussel 

(Mytilus edulis) resulted in an EC50 value of 0.27 mg PAA/l (Fairhurst, 1987). A recent study with 

PeracleanÆ Ocean according to US-EPA guideline EPA/600/R-95/136, 1995 revealed a 48-hour 

EC50 value for normal surviving larvae of 0.54 mg PAA/L (or 3.64 mg PeracleanÆ

 Ocean/L) and a NOEC 

of 0.35 mg PAA/L (2.34 mg PeracleanÆ Ocean/L). This was the most sensitive test in a number of 

screening tests with marine organisms tested in this study (see also 1.3) (Degussa, 2005a). 

Conclusion 

All fish toxicity data were of a similar order of magnitude and there seems to be no big difference between 

marine and freshwater species, if any marine species seem to be slightly less sensitive, but this could also 

be related to the more rapid degradation of PAA in saltwater. Based on the most conservative value the 

acute LC50 for fish is 1.6 mg/L. 

In invertebrates the lowest EC50 was obtained for Daphnia magna, with 0.5 mg PAA/L. The toxicity seems 

to be related to the size of the test organism. 

Embryonic stages were most sensitive with 48 h EC50 values of 0.27 to 0.54 mg PAA/L. 

Acute toxicity to bacteria 

A luminescent bacteria test according to DIN EN ISO 348 Part 2 was performed with a comparable 

material. The concentration leading to below 20% inhibition in 30 minutes was 0.83 to 1.25 mg product/l 

(corresponding to 0.125 to 0.18 mg PAA/l) (Degussa, 2001a). 

In a respiration inhibition test according to OECD 209 and GLP) dilutions of Peracetic acid (39.5% PAA, 

40.7% Acetic acid and 2.3 % hydrogen peroxide) were tested. After 30 minutes the EC50 was 13.4 mg/L 

of the product corresponding to 5.3 mg/L of PAA, after 3 hours the EC50 value was 12.9 mg/L product or 

5.1 mg PAA/L (PAR, 2001). 

For hydrogen peroxide a respiration inhibition test according to OECD 200 and GLP revealed an 

EC50 (3 h) of 466 mg/ml. EC10 value for pseudomonas putida in an 18 h multiplication inhibition test was 

determined to be 11 mg/L (EU, 2003). 
MEPC 53/2/12 

ANNEX 

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1.2 Chronic aquatic toxicity 

The available chronic toxicity data for the aquatic compartment are summarized in table 3. 

Table 3: Chronic aquatic toxicity data 

Species Endpoint Result as PAA Result calculated 

as PeracleanÆ

Ocean 

Reference 

Fish 

Menidia beryllina 

(larvae fish) 

7-day survival 

and growth 

test 

LC50/IC50 

survival: 5.34 mg/L 

Biomass: 6.21 mg/L 

NOEC 

Survival : 1.88 mg/L 

Biomass: 3.75 mg/L 

LC50/IC50 

survival: 35.6 mg/L 

Biomass: 41.4 mg/L 

NOEC 

Survival : 12.5 mg/L 

Biomass: 25 mg/L

Degussa 

2005a

Invertebrates 

Daphnia magna 21-day 

reproduction 

test 

Parental 

immobilisation 

21-day EC50: 0.1 

mg/L 

Reproduction: 

21-day EC50: 0.08 

mg/L 

NOEC parental 

immobilisation and 

reproduction: 

0.05 mg/L 

Parental 

immobilisation 

21-day EC50: 0.61 

mg/L 

Reproduction: 

21-day EC50: 0.55 

mg/L 

NOEC parental 

immobilisation and 

reproduction: 

0.34 mg/L 

CEFIC, 

PAR, 2000 

Mysidopsis bahaia 7-day survival 

and growth 

testing 

LC50/IC50 

survival: 2.52 mg/L 

Biomass: 2.70 mg/L 

NOEC 

Survival : 1.88 mg/L 

Biomass: 3.75 mg/L 

LC50/IC50 

survival: 16.8 mg/L 

Biomass: 18.0 mg/L 

NOEC 

Survival : 12.5 mg/L 

Biomass: 25 mg/L

Degussa, 

2005 

Embryonic stages 

Marine blue mussel 

embryo 

Mytilus galloprovinc 

ialis embryo 

Development, 

72 h 

NOEC: 0.3 mg/L 

LOEC: 0.59 mg/L 

EC50: 0.69 mg/L 

NOEC: 2 mg/L 

LOEC: 3.9 mg/L 

EC50: 4.6 mg/L 

Degussa 

2004b 

Algae 

Marine 

Minutocellus 

polymorphus 

Growth, 

48 h 

NOEC: 0.59 mg/L 

LOEC: 1.19 mg/L 

EC50: 0.82 mg/L 

NOEC: 3.9 mg/L 

LOEC: 7.9 mg/L 

EC50: 1.64 mg/L 

Degussa, 

2004b 

Fresh water 

Pseudokirchneriella 

subcapita (Selenastrum 

capricornutum)

Growth, 

126 h 

NOEC: 0.13 mg/L 

EC50: 0.18 mg/L 

NOEC: 0.28 mg/L 

EC50: 0.4 mg/L 

Hicks et al, 

1996 

Fresh water 

Pseudokirchneriella 

subcapita (Selenastrum 

capricornutum)

Growth, 

72 h 

NOEC: 0.074 mg/L 

LOEC: 0.15 mg/L 

EC50: 0.14 mg/L 

NOEC: 0.49 mg/L 

LOEC: 1 mg/L 

EC50: 0.93 mg/L 

Degussa, 

2004b 
MEPC 53/2/12 

ANNEX 

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A 21-day Daphnia magna reproduction study performed according to OECD guideline No. 211 and under 

GLP was performed using concentrations of 0.034, 0.11, 0.34, 1.1 and 3.4 mg/L of a comparable material. 

The concentration of PAA corresponded to 0.005, 0.016, 0.05, 0.16, 0.5 mg/L. The test solutions were 

renewed 3 times per week. The NOEC of this study was 0.34 mg/L as PeracleanÆ

 Ocean or 0.05 mg 

PAA/L for both parental toxicity and reproduction. 

Two 7-day survival and growth assays were performed with a larval fish Menidia beryllnia and a 

mysid Mysidopsis bahia, both salt water organisms according to US EPA, 2002 guideline 

EPA-821-R-02-014 the test solution was renewed daily. For M. beryllnia the LC50 for survival 

corresponded to 5.34 mg PAA/L, for biomass to 6.21 mg PAA/L (35.6 and 41.4 mg PeracleanÆ Ocean/L 

respectively), the NOECs were 1.88 and 3.75 mg PAA/L (12.5 and 25 mg PeracleanÆ Ocean/L). For 

M. bahia the LC50/IC50 for survival corresponded to 2.52 mg PAA/L, for biomass to 3.75 mg/L (16.8 and 

18.0 mg PeracleanÆ Ocean/L respectively), the NOECs to 1.88 and 3.75 mg PAA/L (12.5 and 25 mg 

PeracleanÆ

 Ocean/L), (Degussa, 2005a). 

A 72 h static study with blue mussel embryo (Mytilus galloprovincialis embryo) revealed the most sensitive 

marine species with an EC50 of 0.69 mg PAA/L and a NOEC of 0.3 mg/L. The toxicity to the marine 

algae (48 h) based on growth rate was slightly higher but of the same order of magnitude. Both values 

were based on nominal concentrations (Degussa, 2004b). 

A study with a freshwater green alga (Selenastrum capricornutum) and equilibrium PAA (5.2%) has been 

reported. The study was performed to good laboratory practice (GLP) guidelines. The test concentrations 

were 0, 0.065, 0.13, 0.25, 0.50 and 1.0 mg PAA/l. Growth was determined by algal cell counts. The 

concentration of H2O2 was measured in the test solutions. At the start of the test, the H2O2 content of all 

test solutions was close to the nominal concentration. At the end of the test, the measured concentration 

was lower than the detection limit except for concentrations of 0.50 and 1.0 mg PAA/l where the remaining 

measured H2O2 concentrations were 84% and 110% of the nominal values, respectively. At a 

concentration of 0.13 mg PAA/l an initial, statistically significant, inhibition of growth was found between 

0 and 72 hours. Growth had recovered at the end of the test probably due to decreased exposure. 

Based on the cell count at the end of the test, a concentration of 0.13 mg/L was considered to be an 

NOEC. At a concentration of 0.25 mg/L the cell count at the end of the test was 3% of the control value. 

The 120-hour EC50 value was estimated to be 0.18 mg/L (Hicks et al, 1996). Comparable results were 

obtained in a study with the same algae and 72-h duration by Degussa, 2004b. 

Conclusion

The results of the available chronic studies are remarkably similar and indicate an overall NOEC value of 

around 0.05 to 0.1 mg PAA/L. The studies all indicate a very steep dose response. The chronic toxicity 

does not differ much from the acute toxicity (factor 5). Through the unspecific mode of action (oxidation) 

the toxicity depends very much on the size of the respective organism that may be related to its 

detoxification capacity. Based on the availability on studies on very sensitive embryonic states that are 

normally not available together with some long term toxicity data an assessment factor of 10 on the lowest 

NOEC of 0.05 mg PAA/L may be appropriate leading to a PNEC of 5 μg/L. Given the consistency of the 

data, the low difference between acute and chronic effects, the mechanism of action and the steep dose 

response, and the instability of the substance in water a lower assessment factor of 5 may also be 

regarded as sufficient and a PNEC of 10 μg/L seems to be sufficiently conservative. This would 

correspond to a PNEC of 67 μg PeracleanÆ

 Ocean/L. 

1.3 Aquatic toxicity data on hydrogen peroxide 

The most important aquatic toxicity data of hydrogen peroxide are summarized below, because from the 

results of preliminary experiments with ballast water treatment it can be concluded hydrogen peroxide 

may be released after treatment, while peracetic acid could not be detected anymore. 
MEPC 53/2/12 

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For hydrogen peroxide the data have been reviewed in EU 2003. Selected data from this report that were 

used for the risk characterisation are outlined in table 4. 

Table 4: Aquatic toxicity data for hydrogen peroxide 

Trophic level Species Endpoint Result Reference 

Fish Pimephales 

promelas 

96 h LC50, 

semistatic, 

concentration 

measured 

16.4 mg/L EU 2003 

Aquatic 

invertebrates 

Daphnia pulex 48 h EC50, 

semistatic, 

concentration 

measured 

2.4 mg/L EU 2003 

 Daphnia magna 24 h EC50, static 

nominal 

concentration 

2.3 mg/L EU 2003 

 Gammarus sp. 96 h EC50, 

semistatic, nominal 

concentration 

4.4 mg/L EU 2003 

 Physa sp. 96 h, semistatic, 

nominal 

17.7 EU 2003 

 Dreissena 

polymorpha (zebra 

mussel) 

56 day chronic 

study, flow through 

NOEC: 2 mg/L 

56-d LC30: 5 mg/L 

EU 2003 

Algae Chlorella vulgaris 72 h chronic study EC50 (growth): 2.5 

mg/L 

EC50 (growth rate): 

4.3 mg/L 

NOEC: 0.1 mg/L 

EU 2003 

 Sceletonema 

costatum (marine 

diatom) 

72 h chronic study EC50: 1.38 mg/L 

NOEC: 0.63 mg/L 

EU 2003 

Long-term studies are available for 2 trophic levels including the most sensitive (invertebrates). 

Furthermore some field studies are available indicating that ecosystems may be able to tolerate varying 

concentrations of hydrogen peroxide and are adapted to changing concentrations of hydrogen peroxide 

due to photochemical generation of the substance in water systems. In seawater the limited amount of 

available natural concentrations ranged from 0.5 to 14 μg hydrogen peroxide/l, in lakes values > 100 μg/l 

were reported (EU, 2003). In EU, 2003 a PNEC of 10 μg/L for hydrogen peroxide was derived. However, 

this value seems to be very conservative and is related to continuous long term exposures. When 

deriving a tolerable level for hydrogen peroxide in ballast water applications the following considerations 

should be taken into account: 

The mechanism of action of hydrogen peroxide 

H2O2 acts as a strong oxidant. Such reactivity means that the toxicity effects will be the immediate 

consequence of oxygen, originated from the decomposition of H2O2 by local reaction with biological 

tissues. Therefore it is expected that the adverse effects of hydrogen peroxide are only local and short 

term. 

The natural defence mechanisms against H2O2

Most aerobic living organisms are particularly well equipped in defence mechanisms allowing them to 

inactivate hydrogen peroxide and other reactive oxygen species. Antioxidant enzymes and oxygen 

scavengers have been observed in invertebrates (e.g. crustacean, molluscs, annelida, plathelminthes, 

coelenterata, porifera), in vertebrates (fish) such as catalase, superoxide dismutase, glutathione and 

glutathione peroxidase and carotenoids (Lemaire and Livingstone, 1993; Morris and Albright, 1981) as 

well as in algae (catalase and peroxidases), both higher and less evolved. This protection mechanism 

arises in biological systems during evolution due to the continuous formation of reactive oxygen species 
MEPC 53/2/12 

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(ROS) as unwanted toxic by-products of metabolism. On this basis, it is expected that aerobic organisms 

are well protected against the effect of hydrogen peroxide exposed to organisms. 

Natural sources of H2O2

As mentioned above hydrogen peroxide is naturally produced by sunlight in water and is furthermore a 

common product of natural oxidative processes taking place in aerobic cells. H2O2 may also be formed in 

the medium surrounding an organism where certain metabolites from the organisms act as promoters, 

e.g. riboflavin, excreted by a number of marine organisms (Moffet and Zika, 1987). 

The specific conditions in laboratory tests 

The medium used in laboratory tests is quite different from the natural conditions. Depending on the 

environmental conditions, many materials (e.g. dissolved transition metals, solid metals, solid metal 

oxides, hydroxides, activated carbon, enzymes) contribute to reduce the oxidant power. It is thus 

assumed that under laboratory conditions the test organisms are more exposed and thus more sensitive 

than under natural conditions to the prolonged exposure of H2O2 concentrations during the test as 

illustrated by the data of Fitzpartrick et al, (1995) on fish. Also, in the field conditions, the more sensitive 

species are protected from a direct effect of hydrogen peroxide by the presence of the total biomass and 

the suspended solids. 

1.4 Endocrine disruption 

From the structure of the active ingredients, the fact that it is rapidly degraded and will not be available in 

higher organisms it can be concluded that PeracleanÆ

 Ocean is of no concern with regard to possible 

endocrine effects. 

1.5 Sediment toxicity 

From the physical chemical properties, the high water solubility, the low log Kow and the instability in 

water it is unlikely that the components of PeracleanÆ Ocean will reach the sediment to a considerable 

extend. This is corroborated by Mackay calculations showing practically no distribution into sediment 

(see chapter 4). Accumulation in sediment is not to be expected. Sediment testing is therefore not 

considered necessary. 

1.6 Bioavailability/biomagnification/bioconcentration/Food web population effects 

Due to the low log Kow and the rapid degradation of the components of PeracleanÆ Ocean either by 

abiotic mechanisms or by all biota it is not likely that the product is bioavailable. Peracetic acid and 

hydrogen peroxide are rapidly degraded in the environment e.g. under the influence of transition metals 

and in biota by catalases and peroxidases that are ubiquitary in organisms (ECETOC 1993, 2001). 

Consequently no bioconcentration, biomagnification or accumulation along the food chain is to be 

expected. 

2 Data on mammalian toxicity (4.2.1.2; 5.3.12) 

2.1 Toxicokinetics 

From the physical chemical properties absorption of PeracleanÆ

 Ocean through skin and mucous 

membranes is possible, but limited by the high water solubility and low partition coefficients of the 

equilibrium compounds. However, a considerable intake of radioactivity was observed in damaged skin, 

once the skin barrier is destroyed by the corrosive effects of PAA solutions (Phillips, 1994a). Phillips 

studied the fate of 14C-labelled PAA (5.02%) after dermal application (100 μl to an area of 2.5 cm2

) to 

4 male Sprague-Dawley rats. An acetate control treatment was included in the test. Water-soluble 

vapours (i.e. evaporating PAA and HOAc), exhaled CO2, urine and faeces were collected and analysed at 

regular intervals. After 72 hours the animals were killed and the total radioactivity content was determined 

of the internal organs. When the recovered radioactivity is presented as a percentage of the absorbed 

dose, significant differences between the test and control animals were observed. In the acetate control 

animals 31% of the absorbed radioactivity was eliminated in urine versus 17% in the test group animals. 

In control animals 50% was exhaled as 14CO2 versus 58% in the test group animals. Recovery in faeces 

was 4% in controls and 6 % in test group animals. Recovery in the tissues and carcass was 13% in 

controls and 20% in test group animals. The results of this study indicate that PAA is largely eliminated 
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within 72 hours of exposure with excretion of radioactivity occurring primarily via exhaled air (58 %), 

followed by urine (17 %) and faeces (6 %). It should be realised that the distribution of 14C is measured 

and that it is not known whether this is present as PAA, HOAc or CO2. 

In a most recent study on the degradation of Peracetic acid in rat blood (CEFIC PAR, 2004) it could be 

demonstrated that the half life of Peracetic acid in a 1000 fold diluted rat blood sample is below 5 minutes. 

Several authors have shown that peracetic acid is a substrate of catalases yielding acetic acid and 

oxygen (Ferri et al, 1990, Jones and Middlemiss, 1972, Placic and Dunford, 1980). PAA is also degraded 

by calf serum (M ̧cke, 1977), stomach fluid and saliva (Juhr et al, 1978). Hydrogen peroxide is also 

degraded rapidly by catalases, peroxidases and a number of other enzymes and antioxidants in the body 

(EU, 2003). 

The importance of the catalase reaction for the metabolism of PAA can be illustrated by looking at the 

distribution of catalases in the mammalian organism. 

Catalases are present at a wide range of concentrations in nearly all mammalian cells; the enzymes are 

particularly efficient in metabolising large amounts of H2O2 (Chance et al, 1979). Catalases are located in 

sub-cellular compartments, mainly in peroxisomes (De Duve and Bauduin, 1966). Soluble catalases were 

found in erythrocytes (Saito et al, 1984). 

The highest catalase content is observed in cells of the duodenum, liver, spleen, kidney, blood, mucous 

membranes and other highly vascularised tissues; the lowest catalase activity occurs in brain, thyroid, 

testes and connective tissue cells (Matkovics and Novak, 1977). 

A more detailed discussion of catalase activity, inter- and intra-species differences can be found in 

ECETOC, 1993 and 1996. 

Evaluation

The data on metabolism indicate that peracetic acid is rapidly degraded in various tissues and is expected 

to be degraded to a considerable extend at the site of first contact. Once absorbed into the circulation it is 

almost instantly degraded in the blood and will not be available to other organs beyond the site of first 

contact. 

Conclusion 

The systemic absorption of peracetic acid and hydrogen peroxide is limited by their rapid enzymatic 

degradation in cells of mucous membranes lining the gastrointestinal and respiratory tract and to a certain 

extend also in skin. Tissue damage, for example on contact with severely irritant concentrations of 

Peracetic acid can lead to absorption into the circulation. In blood peracetic acid and hydrogen peroxide 

are very rapidly degraded yielding oxygen and acetic acid or oxygen and water respectively. The 

remaining acetic acid is a physiological substance that is included into physiological metabolic pathways 

or excreted via the urine. 

The rapid degradation limits the systemic availability of both peracetic acid and hydrogen peroxide. It is 

therefore unlikely that organs beyond the site of first contact will be affected by peracetic acid. 

2.2 Acute toxicity 

The acute toxicity data of PeracleanÆ Ocean are summarized in table 5. 

Table 5: Acute toxicity studies 

Route of exposure LD50 or LC50 Species Reference 

Oral 1015 mg/kg bw Rat Degussa 1982a 

Dermal 1912 mg/kg bw Rabbit Kuhn 1996a 

Inhalation, aerosol Ca. 0.5-1.3 mg/L/4 h Rat Terrell, 1986 

In the oral study, signs indicative of irritation of the gastro-intestinal tract (writhing syndrome, stilted gait, 

and tremor), laboured breathing and bloody lachrymation were observed. Red coloured urine was also 

observed in females of the highest dose group. At necropsy adhesions were observed between the 
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viscera and the peritoneum. The gastro-intestinal mucosa and parts of the liver close to the stomach 

appeared white or greyish in animals of the high dose group. In the lowest dose group no clinical signs 

indicating irritation were observed. This dose corresponded to a concentration of about 3% PAA, 

4.5% H2O2 and 4% HOAc. 

Symptoms observed in the dermal study included predominantly local effects on the skin as moderate to 

severe erythema, slight to severe oedema and eschar formation. General symptoms included decreased 

activity, diarrhoea, nasal discharge, ptosis, salivation and slow gazing. No pathological changes 

attributable to treatment were observed at necropsy. 

Terrel (1986) exposed rats to aerosol concentrations of PAA ranging from 18 to 2,138 mg/m3

. The 

animals were kept under observation for 14 days after the exposure. During the exposure the animals 

showed a range of clinical signs which consisted of blinking, foaming, gasping, nasal discharge, 

salivation, lachrymation, ptosis, laboured respiration, twitching, chewing motion, convulsions, staggering, 

cornea opacity or death depending on the concentration. Post-exposure clinical signs were laboured 

respiration, nasal discharge, gasping, lachrymation, haemorrhage from the eye, cornea opacity, 

blindness, staggering, loss of righting reflex, crusty appearance, piloerection or death depending on the 

dose. Gross necropsy of the animals that died during the observation period revealed alterations to the 

lungs and thymus, enteritis, swollen nose, congested nasal cavity and trachea, thickening of the 

oesophagus and larynx. Animals that were killed at the end of the observation period showed similar 

alterations. Like all inhalation studies with peracetic acid this study suffered from the difficulty of 

generating and maintaining a stable atmosphere of the test item. An accurate measurement of the 

composition of the test atmosphere and particle size of the aerosol is almost impossible due to the 

instability of the product in air. The resulting LC50 values should therefore be treated with circumspection. 

Conclusion 

The predominant effect in all acute toxicity studies is local irritation at the site of contact, the extent of 

which depends on the concentration and the composition of the applied test solution. 

2.3 Effects on skin and eye 

Skin irritation 

PeracleanÆ Ocean was severely corrosive to rabbit skin and caused severe skin damage already after 

3 min and 4 h of occlusive exposure. (Degussa 1982b, Degussa, 1990). Exposure of the skin of one 

animal to 0.5 ml PAA 15% for 3 minutes under occlusive conditions resulted in white to yellowish 

discoloration of the application site and deepening of the treated skin area. Severe erythema was 

observed at the border of the application site and slight oedema was reported. Microscopic examination 

revealed complete coagulation necrosis of the epidermis and upper third of the corium including skin 

adnexae. The damage developed within 1 hour. It was concluded that 15% PAA was corrosive after 

3 minutes of occlusive exposure (Degussa, 1990). 

Skin sensitization 

A skin sensitisation study using the B ̧hler method was conducted on short-haired albino guinea pigs to 

determine if a 5% PAA (20% H2O2 and 10% HOAc) formulation could induce dermal sensitisation (Kuhn, 

1996b). The animals were treated (1 x /wk) with 0.4 ml of a 10% solution of the test compound in 

deionised water for 3 weeks. After a 2-wk rest period, the animals were challenged at a virgin test site 

with an application of 0.4 ml of a 7% solution of the test substance. After the challenge, a very faint 

erythema was observed in both the control and the treated group and, therefore, 5% PAA was not 

considered to have elicited a sensitising reaction in guinea pigs. A similar study was conducted with 12% 

PAA (20% H2O2 and 20% HOAc) (Kuhn, 1996c). In this case the animals were challenged with 0.4 ml of 

a 0.5% solution of the test substance in deionised water. The results showed that 12% PAA did not elicit 

a sensitising reaction in guinea pigs. 

Eye irritation 

Cascieri and Freeman (1983) tested 0.1 ml of 17% PAA in rabbit eyes and found that it was extremely 

irritant to washed and unwashed eyes. 
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Respiratory tract irritation 

Janssen (1989) nebulised a 15% PAA (14% H2O2, 28% HOAc) solution into an exposure chamber for 

25 minutes. Male Wistar rats were exposed (nose-only) to the aerosol at concentrations ranging from 

9.5 to 40.3 mg PAA/m3

 (3.7 to 14.3 mg H2O2/m3; HOAc not measured) and their respiration rate was 

monitored. The RD50, referring to a concentration of PAA inducing a 50% reduction of respiratory rate, 

was calculated to be 21.5 to 24.1 mg/m3

. Reduction of respiratory rate occurred at levels from 5 to 

10 mg PAA/m3. After termination of exposure the respiratory rates returned to normal and the animals 

recovered fully within 3 days. No other clinical signs and no histopathological changes were observed. 

Conclusion 

PeracleanÆ

 Ocean should be considered severely corrosive to skin and eyes and severely irritating to 

mucous membranes of the respiratory tract. The RD50 for an aerosol generated from a product with a 

similar composition was 21.5 to 24.1 mg/m3. 

No skin sensitisation was observed in two B ̧hler tests in guinea pigs with different formulations of PAA. 

These studies are considered relevant for PeracleanÆ

 Ocean as well as the study design requires testing 

with a dilution yielding the maximum non irritating concentration. 

2.4 Repeated dose toxicity (Chronic and longterm toxicity) 

A 90-day oral (gavage) (CEFIC, PAR 2003). 5.5% PAA containing 15.3% hydrogen peroxide and 

16.6% acetic acid was used as the test substance. Groups of 5 male and 5 female Sprague Dawley rats 

received the following concentrations and dose levels by a daily gavage dose for 90 days. 

Study days Group 1 

Conc. [mg/L]/ 

dose mg/kg bw 

Group 2 

Conc. [mg/L]/ 

dose mg/kg bw 

Group 2 

Conc. [mg/L]/ 

dose mg/kg bw 

1-10 10/15 33.3/50 100/150 

11-22 10/15 33.3/50 66.7/100 

23-92 3.33/5 10/15 33.3/50 

The dose levels had to be adjusted several times due to mortality in the high dose group. One animal 

also died in the medium dose group when the dose level was 50 mg/kg bw. The main findings in the 

post-mortem observations of the animals that died during the study were distended gastrointestinal tract 

due to gas formation, reddish coloured and or dilated lungs, reddish or blackish areas in the stomach 

mucosa. The findings indicate a massive gas (oxygen) formation in the gastrointestinal tract that could 

have led to asphyxiation of the stomach contents in the lungs and subsequent damage of lung and 

trachea cells as well as a considerable irritation at the site of contact. Clinical signs as ptyalism and loud 

breathing were consistent with the pathological findings. No treatment related findings were reported in 

any other organs. No changes in haematological or clinical chemistry parameters were observed. No 

treatment related pathological findings (macroscopic and microscopic) were also observed in all surviving 

animals of all dose groups. The effects observed can therefore rather be attributed to an acute irritant 

reaction following the gavage administration than to any systemic toxicity. The NOAEL of this study was 

5 mg/kg bw because the dose level was reduced to this level in the low dose group at day 23 of 5% PAA, 

but it is likely that 15 mg/kg bw would also have been tolerated as no effects were observed in group 2 

once the dose level was reduced to 15 mg/kg bw after day 23. The NOAEL would correspond to 

approximately 1.7 mg/kg bw per day or 5 mg/kg bw per day respectively of PeracleanÆ

 Ocean. However 

as the effects were related to local irritation only and no indications of systemic toxicity was observed, it is 

likely that they are more related to the concentration than to the dose and the NOAEC (no observed 

adverse effect concentration would correspond to 0.55 mg PAA/1.53 mg hydrogen peroxide/l 

and 1.66 g acetic acid/l. 
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Limited literature data are available for repeated dose studies up to 10 moths duration in different species: 

rats, mice, Gebrils, guinea pigs, hamsters (e.g. Juhr et al, 1977, 1978). These have been reviewed and 

evaluated in ECETOC (2001). Although these studies are of limited reliability they do not indicate any 

specific systemic toxicity of peracetic acid. 

Conclusion 

Repeated does studies with diluted equilibrium PAA solutions are relevant for PeracleanÆ

 Ocean as well 

as the test substance has to be diluted to tolerable concentrations before the administration to the test 

animals. 

No further repeated toxicity studies are considered necessary with PeracleanÆ

 Ocean for the following 

reasons: 

The available studies indicate no specific systemic toxicity of equilibrium peracetic acid. 

These findings are in accordance with the toxicokinetic data (see chapter 2.2.1) and support that peracetic 

acid will not be systemically available beyond the site of first contact. 

The effects at the site of contact are determined by the acute irritation potential of the compound and its 

ability to release oxygen. It is not expected that this mode of action and the accompanying no effect 

levels will vary considerably between species and with the duration of the study. 

Therefore further subchronic and chronic studies with PAA are unlikely to result in new information and 

should not be performed based on animal welfare considerations. 

2.5 Developmental and reproductive toxicity 

As outlined in the Toxicokinetics section (3.1) it is very unlikely that PAA or hydrogen peroxide are 

systemically available and could reach the sex organs or the developing embryo or foetus. This is due to 

the rapid metabolism of PAA and hydrogen peroxide at the site of first contact and in the blood. This is 

also corroborated by the recent 90 day study in rats (CEFIC, PAR 2003) that did not show any effects on 

the testes or ovaries. A limited number of literature data, that are however, poorly reported are also 

available on this endpoint and were reviewed in ECETOC, 2003. In a teratogenicity study with ICR mice, 

the animals (5-10/group) were exposed (2 x/d) by inhalation to nominal concentrations of 20 and 

100 mg PAA/m3

 throughout gestation. The atmospheres were generated from a 1% or 5% dilution of PAA 

(40%, H2O2 14%, HOAc 27%). The authors reported a statistically significant retardation of foetal growth 

(body length and weight) at 100 mg PAA/m3

, but no retardation at 20 mg/m3. No exposure related 

skeletal anomalies were observed. The health status of the dams was not reported (Kramer et al 1990). 

Exposure to a level of 100 mg PAA/m3

 would have been expected also to produce maternal toxicity. 

Because of uncertainty about the exposure levels and limited reporting, a reliable conclusion cannot be 

drawn from this study. No effects were reported from continuous breeding studies in rats, mice, gebrils 

and guinea pigs (Juhr et al, 1978). 

Conclusion 

Due to the absence of systemic availability it is unlikely that the product can reach the sex organs or the 

developing embryo or foetus under conditions of normal handling. Therefore any further testing for 

reproductive endpoints is not warranted. 

2.6 Carcinogenicity 

No valid carcinogenicity study is available. Due to the absence of systemic availability further testing for 

carcinogenicity is not warranted. Furthermore, genotoxicity studies for PAA are available indicating that 

the substance was not genotoxic in most of the in vitro and the standard in vivo genotoxicity tests. It did 

not induce micronuclei in mouse micronucleus assays and was negative in two in vivo UDS assays in 

rats. 
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A tumour initiation-promotion study in mice has been published by Bock et al, 1975 and was discussed in 

ECETOC, 2001. In this study PAA was reported to act as a tumour promotor in mouse skin after initiation 

with 7,12-Dimethylbenz[a]anthracene (DMBA). It is likely that this effect can be explained by the chronic 

irritation caused by the PAA treatment. The carcinogenicity of hydrogen peroxide has been evaluated in 

EU, 2003. Further classical carcinogenicity studies are unlikely to reveal any additional insight to this 

endpoint. 

Conclusion 

Due to the toxicokinetics making it unlikely that PeracleanÆ Ocean is systemically available and the 

absence of a genotoxic potential in the majority of the genotoxicity studies it is unlikely that the product 

has a relevant carcinogenic potential for humans and further testing is not warranted. 

2.7 Mutagenicity 

In vitro studies 

The relevant in vitro studies are summarized in table 6. 

Table 6: In vitro genetic toxicity tests 

Test system Test organism, 

strain 

Composition (%) Dose 

(product) 

Metabolic 

activation 

Result Reference 

 PAA H2O2 HOAc 

Reversionassay (Ames 

test) 

Ta 98, TA 100, TA 

102, TA 1535, TA 

1537, TA 1538 

4.5 25.5 6.7 7-4576 

μg/plate 

Yes/No Neg Wallat, 

1984a 

Reversionassay (Ames 

test) 

TA 97, TA 98, TA 

100, TA 1535 

40 NS NS 0.3-200 

μg/plate 

Yes/No Neg Zeiger et 

al, 1988 

Chromosomal 

aberration 

Human 

lymphocytes 

5.17 20 10 0.25-5 

mg/ml 

Yes/No Neg 

PosA 

Phillips, 

1994b 

Chromosomal 

aberration 

Chinese Hamster 

V79 cells 

10.7 NS NS 0.16-0.6 

μl/ml 

(without 

S9) 

0.5 to 1.18 

μl/ml with 

S9 

Yes/No Neg. CEFIC 

PAR, 

2002a 

Point mutation 

in mammalian 

cells, HPRTTest 

Chinese Hamster 

V79 cells 

10.7 NS NS 0.16-0.6 

μl/ml 

(without 

S9) 

0.5-1.18 

μl/ml (with 

S9) 

Yes/No Neg. CEFIC, 

PAR, 

2002b 

Unscheduled 

DNA synthesis 

Human lung 

fibroblasts WI-38 

CCL75 

31 4.7 NS 0.2-32 

mg/ml 

No Neg Coppinger 

et al, 1983 

DNA repair 

assay 

Human lung 

fibroblasts WI-38 

CCL75 

42 5.5 NS 4-32 μg/ml No Neg Coppinger 

et al, 1983 

A At highest, cytotoxic doses. 
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Equilibrium PAA (40%) proved to be negative in the standard S. typhimurium reversion assay at 

concentrations of 0.3 to 200 μg PAA/plate. The highest concentration was chosen after toxicity testing 

prior to the actual test and represents the dose that elicited toxicity or a dose immediately below 

(half-log dose intervals). In addition to rat liver S9 mix, material from hamster tissues was also used as a 

metabolic system. With both protocols PAA was found to be devoid of mutagenic activity (Zeiger et al, 

1988). 

Strain TA 102 was included in another reversion-assay with PAA. In strain TA 102, PAA up to cytotoxic 

concentrations produced only a slight increase of reverted colonies (up to 30%) and the test substance 

was judged to be non-mutagenic. Total inhibition was achieved in concentrations exceeding 183 and 

915 μg PAA/plate (depending on the strain and activation system). With regard to cytotoxicity no marked 

differences, i.e. reduced sensitivity, were observed in strain TA 102 (Wallat, 1984a). The concentrations 

that were reached in this assay were relatively high compared with the results presented by other authors. 

Studies in bacteria or yeasts with low reliability were conducted by Agnet et al, 1977 and Dorange et al, 

1974. In these studies equivocally positive effects were reported in bacteria (S. typhimurium LT-2, 

TA 1978) and negative results in S. cervisia D7 cells. 

Two independent well-documented experiments on the potential of PAA to induce structural chromosomal 

aberrations in human lymphocytes in the presence and absence of S9 mix (metabolic activation system) 

were conducted with equilibrium PAA (5.17%). Cells were treated at 0.25, 0.5, 1.0, 2.0 and 

2.0 mg PAA/ml for 20 hours in the first experiment and with 0.25, 0.5, 0.75, 1.0 and 1.5 mg/ml in the 

second experiment. Treatment in the presence of S9 mix was carried out at 0.31, 0.63, 1.25, 2.5 and 

5.0 mg/ml in both experiments and was limited to 3 hours. PAA revealed positive results only in the 

highest moderately cytotoxic doses, which reduced the mitotic index to 44.5 ñ 63 % without S9 mix and to 

61 ñ 69 % with S9 mix (Phillips, 1994b). It is speculated that the cytotoxicity and genotoxicity exerted by 

PAA is a result of the same mechanism at the cellular level, e.g. production of reactive oxygen species 

which are not detoxified at higher concentrations. 

In another chromosomal aberration test conducted according to recent OECD guidelines and GLP with 

10.7% PAA. Two independent experiments with 2 parallel cultures were performed in Chinese hamster 

V79 cells in the presence and absence of rat liver S9 mix. The dose selection was made in a pre-test for 

cytotoxicity. On the basis of this range finding study the concentrations in the main test were 0.09, 0.13, 

and 0.2 μl/ml in the absence and 0.13, 0.2 and 0.3 μl/ml in the presence of S9. The cells were treated for 

4 hours in both experiments. Harvesting of the cells was performed at 18 hours in the first experiment 

and at 18 and 26 hours in the second experiment in the absence of S9 and after 14 or 22 hours in the 

presence of S9. In the second experiment for the later harvest time only the highest concentration was 

evaluated. 100 metaphases per culture (200 per experimental point) were analysed for chromosomal 

aberrations. A reduced degree of confluence indicated cytotoxicity at a concentration of 0.13 μl/ml in the 

absence of S9 and at 0.2 μl/ml in the presence of S9. At 0.3 μl/ml the cells were completely damages 

without S9. No increase in chromosomal aberrations was observed at any of the test points in the 

presence and absence of S9. (CEFIC PAR, 2002a). 

An in vitro gene mutation test (HPRT test) was performed in Chinese Hamster V79 cells with 10.7% PAA 

in the presence and absence of rat liver S9 mix. Two independent experiments were performed. 

Concentration selection was made following a range finding test for cytotoxicity. On the basis of the range 

finding study the concentrations in the main test were 0.16, 0.22, 0.31, 0.43, 0.5, and 0.6 l/ml in the 

absence of S9 and 0.5, 0.6, 0.7, 0.84, 0.98, and 1.18 μl/ml. The cells were exposed for 4 hours and 

maintained in exponential growth for 9 days. Cytotoxicity was evaluated by determining the plating 

efficiency on day 1 after treatment. At the end of the expression period cells were cultured in selective 

medium for the determination of mutant frequency and in non-selective medium for the determination of 

plating efficiency. Cytotoxicty was observed from concentrations of 0.22 μl/ml in the absence of metabolic 

activation and from 0.98 μl/ml with S9 (50% reduction in plating efficiency at 0.98 μl/ml). No statistically 

significant or dose related increase in mutation frequency was observed both with and without S9 in both 

experiments. (CEFIC, PAR, 2002b). 

The possible induction of Unscheduled DNA Synthesis by PAA was investigated in human diploid foetal 

lung cells (Coppinger et al, 1983). Concentrations of 0, 0.2, 0.5, 1, 2, 4, 9, 16, 24 and 32 μg PAA/ml were 

used. Positive controls were included. No statistically significant increase of UDS compared to solvent 

(water) controls was detected using autoradiography. In this assay 32 μg PAA/ml was clearly cytotoxic 

(50% survival). Using the same test system and controls, a DNA repair assay (three independent 

experiments) was conducted. The assay was negative at all dose levels. At the highest concentration 

normal DNA replication was considerably reduced (Coppinger et al, 1983). 
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In vivo studies 

In a mouse micronucleus test with equilibrium PAA (5.17%), groups of 15 male and 15 female CD-1 mice 

were given single oral doses (0, 8, 35 and 150 mg PAA/kg) by gavage. Positive control groups were 

included. There were no significant differences in the frequency of micronuclei in polychromatic or 

normochromatic erythrocytes between mice treated with PAA and the untreated controls. PAA did not 

induce a dose-related decrease in the proportion of polychromatic erythrocytes, indicating a lack of toxicity 

to the bone marrow. No clinical signs were reported (Blowers, 1994a). 

In a micronucleus test conducted with equilibrium PAA (4.5%), the test solution was administered by 

gavage to groups of 7 male and 7 female CF21/W68 mice. The animals received two doses of 200, 400, 

and 800 mg PAA/kgbw/d at 0 and 24 hours. A positive control was included. Dose-dependent clinical 

signs of toxicity were observed in all groups. No mortalities were recorded within the time frame of the 

investigation and no increased incidences of micronuclei were found. General bone marrow toxicity was 

detected as the inhibition of proliferation in the erythropoiesis since the ratio of normochromatic versus 

polychromatic erythrocytes was increased in the highest dose group (Wallat, 1984b). 

An in vivo/ex vivo UDS assay was conducted in groups of 6 male F344 rats receiving doses of equilibrium 

PAA (5.17%) at 330 or 1,000 mg PAA/kgbw by gavage. Positive controls were included. No significant 

increases in UDS (measured as net grain increase) were observed in both treated groups at either time. 

It was concluded that the tested PAA formulation was not genotoxic under the conditions of the study 

(Blowers, 1994b). 

Another in vivo/ex vivo UDS assay in groups of 3 male Fischer rats receiving doses of 500, 1000 and 

2000 mg/kg bw 5% equilibrium PAA (with 14 % hydrogen peroxide and 17.6% acetic acid) positive 

controls were included. Expression times were 2-4 and 12-16 hours. At least 150 cells were counted per 

animal. The dose selection was based on a pre-experiment to determine the maximum tolerated dose 

level. Nuclear and cytoplasmatic grain counts were obtained from 50 cells per slide. The slides of the 

lowest dose were not evaluated as the 2 high doses could be satisfactory analysed. No increase of 

nuclear grain counts was observed at any of the doses and time points tested. No significant increase in 

the percentage of cells in repair was detected at any dose and time point of PAA when compared with the 

respective controls. Moreover the frequency of cells in the S-phase was low in the treated animals. The 

test substance did not reveal any genotoxic activity under the test conditions employed. 

(CEFIC PAR, 2002c). 

Conclusion 

The weight of evidence in particular in the more recent studies in in vitro experiments in mammalian cell 

cultures indicates that equilibrium peracetic acid does not have a significant genotoxic potential and did 

not cause gene mutations and chromosomal aberrations both in the presence and absence of a metabolic 

activation system. Only in one chromosomal aberration assay in vitro a positive result was obtained at 

highly cytotoxic concentrations. However, a recent in vitro chromosomal aberration assay did not show 

such an effect even at cytotoxic concentrations suggesting that the earlier findings may have been an 

artefact. PAA did not induce micronuclei in in vivo mouse micronucleus tests when administered by 

gavage up to the maximum tolerated dose levels and did not induce unscheduled DNA synthesis in two 

recent rat in vivo/ex vivo UDS assays when administered by gavage up to the maximum tolerated dose 

level. Therefore it can be concluded that PeracleanÆ

 Ocean is unlikely to have a genotoxic or mutagenic 

potential. 

3 Data on environmental fate and effect under aerobic and anaerobic conditions 

 (4.1.2.3; 5.3.4; 5.3.5) 

3.1 Modes of degradation 

Abiotic degradation of equilibrium peracetic acid 

An abiotic degradation study according to EEC92/69 reported half lives of peracetic acid at 25 °C of 48 h 

at pH 7 and pH 4. At pH 9 the half life was lower than 3.6 hours (Pierre et al, 1995).

The decomposition of Degaclean 150 containing about 21% of hydrogen peroxide and 15% of peracetic 

acid was studied in synthetic seawater (Degussa, 2000). At a salinity of 2% (w/w) 105 mg/L were 

degraded with a half life of approximately 20 minutes for peracetic acid. At a salinity of 3.3 % (w/w) the 

half life of PAA was about 7 minutes. Degradation of hydrogen peroxide under these conditions was 
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slower. About 20% were degraded within 35 min or 25 min at salinity of 2% or 3.3% respectively. It 

should however, be considered that natural sea water will contain transition metals, organic compounds 

and organisms that will most probably lead to a more rapid degradation of hydrogen peroxide and PAA. 

Abiotic degradation of hydrogen peroxide 

H2O2 is subject to various reduction or oxidation processes in the environment and decomposes into 

water and oxygen at rates which depend on contact with catalytic materials and other factors. Common 

catalysts are dissolved transition metals (e.g. copper, iron, manganese), solid metals (e.g. platinum, 

osmium or silver), solid metal oxides and hydroxides (e.g. manganese, iron, copper oxides), activated 

carbon and enzymes. H2O2 is also decomposed by alkaline impurities sufficient to raise the pH to 7 or 

above. Heat and sunlight can induce photochemical decomposition with the formation of free radicals 

(ECETOC, 1997) 

Biotic degradation of equilibrium PAA 

Peracetic acid was readily biodegradable in a study according to OECD 301 E. More than 

70% degradation was obtained after 28 days and the 10 day window was met (Richterich and Gode, 

1986). 

During an activated sludge respiration inhibition test at a concentration of 0.3 to 100 mg PAA/l the 

degradation during the test was determined. The half life was < 3 minutes at concentrations between 

0.3 and 30 mg/ml and about 30 minutes at 100 mg/L. (De Groot, 2003). 

Biotic degradation of hydrogen peroxide 

Hydrogen peroxide was evaluated on the basis of a number of different data to be readily biodegradable 

fulfilling the 10 day window in sewage treatment plants and under environmental conditions. Typical half 

lives in sewage treatment plants were 2 minutes, half lives in the environment varied from a few hours to 

typically 1 to 3 days up to 5 days. Higher hydrogen peroxide concentrations can slower the rate due to 

the inhibitory effect of hydrogen peroxide on microorganisms (EU 2003). 

3.2 Bioaccumulation, partition coefficient, octanol/water coefficient 

Partition coefficients 

For Peracetic acid a log Kow of ñ 0.52 Byers, 1998) and for hydrogen peroxide a log Kow of -1.5 

(EU, 2003) was reported. The low octanol water partition coefficient indicates a low potential for 

bioaccumulation. 

Partitioning between environmental compartments 

The theoretical distribution of PAA has been estimated using the fugacity model of Mackay, Level 1. 

(ECETOC, 2001). The calculations were conducted for the equilibrium grades of PAA, using the partial 

vapour pressure of PAA in a composition comparable to PeracleanÆ

 Ocean. According to the model, the 

majority of PAA (99.3 to 99.9%) released into the environment enters the water phase, while the 

remainder is found in air. No partitioning into soil, suspended matter or biota is expected (Table 4). A risk 

characterisation for Ballast water treatment can therefore be restricted to the aquatic compartment. 

Table 4: Distribution of PAA between Environmental Compartments at 25°C (ECETOC 2001) 

Compartment Distribution(%) 

Air 0.29 

Water 99.71 

Soil 0.00 

Sediment 0.00 

Suspended matter (aquatic) 0.00 

Biota 0.00 
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The same applies for hydrogen peroxide. An equilibrium partitioning has been calculated according to 

Mackay level I at 20°C, a vapour pressure of 3 hPa and a Henryís law constant of 7 10-4 Pa m3

/mol. 

(see table 5)(EU 2003). 

Table 5: Distribution of hydrogen peroxide between environmental compartments at 20°C 

(EU, 2003) 

Compartment Distribution (%) 

Air 0.3 x 10-3 

Water 99.98 

Soil 0.01 

Sediment 0.01 

3.3 Persistence and identification of the main metabolites in relevant media (ballast water, marine and 

fresh water) 

The primary metabolites of PeracleanÆ

 Ocean in all relevant media are acetic acid, oxygen and water. 

Hydrogen peroxide stability is greater than that of Peracetic acid, but in the environment it will ultimately 

be degraded by biotic and abiotic processes to oxygen and water. Acetic acid is a product of the 

intermediary metabolism and will ultimately be oxidised to CO2 and water or integrated into biomolecules 

by organisms. 

3.4 Reaction with organic matter 

PERACLEANÆ

 Ocean is a chlorine-free oxidizer. In consequence the natural traces of halogenated 

organic compounds in the ballast water are not increased. Side reactions generating epoxides and 

organic peroxides are not likely due to the short half-life of PAA and the conditions of ballast water 

treatment (low PAA concentration, low temperature, non-presence of catalytic compounds, neutral 

pH-level). 

Measurements by gas chromatography/mass spectrometry using river water showed that the disinfection 

by-products were carboxylic acids, which are not recognized as mutagenic (Monarca, 2002) 

3.5 Potential physical effects on wildlife and benthnic habitats 

Not applicable. As PeracleanÆ

 Ocean is not persistent in the environment it is not expected to have any 

effects on wildlife or benthnic habitats. 

3.6 Potential residues in seafood 

As PeracleanÆ

 Ocean is not systemically available to organisms and is readily metabolised to oxygen, 

water and acetic acid no potential residues in seafood are to be expected. 

3.7 Known interactive effects 

None. 
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4 Physical and chemical properties (4.1.2.4) 

The relevant physical chemical properties are summarised in table 6. 

Table 6: Physical chemical properties 

Property Value Reference/comment 

Physical state Clear, colourless liquid 

Melting point Ca. -50°C ECETOC (2001) 

Boiling point > 60°C ECETOC (2001) 

Relative density 1,150 kg/m3 at 20°C ECETOC (2001) 

Vapour pressure 110 hPa at 20°C ECETOC (2001)/ Partial vapour pressure, 

peracetic acid (PAA), 

Water solubility 1,000 g/kg Swern, 1970 

Partition coefficient noctanol/water (log value) 

-0.52 (measured value) Byers, 1998/ for PAA 

Partition coefficient noctanol/water (log value) -1.5 EU, 2003 / for hydrogen peroxide 

pKa 8.2 at 20°C Swern, 1970 

Flash point Ca. 96°C 

Autoignition temperature Ca. 265°C 

Saturated Vapour 

concentration 

Ca. 14% ECETOC, 2001 

Corrosion 

In a study conducted with fresh water (as a worst case condition) plus PeracleanÆ Ocean neither a 

significantly higher corrosion nor corrosion nor a damaging of the usual Epoxy-based ballast water tank 

coating was observed. The trials were performed using the normal dosage of 150 ppm PERACLEANÆ

Ocean and the double dosage of 300 ppm, respectively. In contrast to the application onboard of a ship, 

where PERACLEANÆ

 Ocean degrades rapidly PeracleanÆ Ocean was refreshed/replaced regularly to 

maintain a constantly high concentration during the testing period of 30 days. 

Even under these extreme conditions (according ìTesting Method for Evaluation of Painted or Coated 

Specimens Subjected to Corrosive Environmentsì, ASTM D1654-92) PERACLEANÆ

 Ocean did not 

significantly increase corrosion (Degussa 2004a). No influence on the corrosion of steel St 37-2 was 

observed in a corrosion test with 3.3% sea-salt and 500 ppm PeracleanÆ

 Ocean stored for 14 days at 

temperatures between 25 and 27°C (Degussa, 2003). Various corrosion tests with different grades of 

peracetic acid (5, 15, 35%) and different stainless steels under various test conditions showed that all 

grades were corrosion resistant (Degussa, 2001b). 

5 Analytical methods at environmentally relevant concentrations (4.1.2.5; 5.3.15) 

6 Toxicity testing of treated ballast water (5.2) 

To simulate conditions of ballast water treatment, a 150 mg/L solution of PeracleanÆ Ocean was prepared 

in a 20 L volume of seawater with no headspace in a plastic container. This solution was placed in the 

dark at 8°C for 48 hours. After the incubation time the solution was evaluated for its toxicity to bivalve 

larvae (Mytilus galloprovincialis), < 4 h post fertilisation. The test duration was 48 hours (Degussa, 

2005b). 
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This test system was chosen as the only reference test system, as it proved to be the most sensitive 

system in a pre-test with PeracleanÆ

 Ocean using different marine organisms and different study 

durations (Degussa, 2005a). The results of this test were compared with those of a freshly prepared 

sample of 150 mg/L PeracleanÆ

 Ocean. As PeracleanÆ Ocean also reduces the pH as a result of the 

presence and formation of acetic acid in the solution one pH adjusted test sample was also included to 

determine the extend of residual toxicity that could be caused by a decrease in pH. In order to determine 

whether residual toxicity could be due to hydrogen peroxide, a bivalve larval development test was also 

conducted with hydrogen peroxide at concentrations of 0.078 to 5 mg/L. Additionally the degradation of 

residual toxicity after the addition of catalase was tested, by adding catalase to a sample of 150 mg/L 

PeracleanÆ

 Ocean stored in the dark for 48 h at 10°C. Hydrogen peroxide concentrations were measured 

in all samples (detection limit: < 0.1 mg/L). 

Results: 

Degradation of toxicity with time 

The EC50 of the untreated sample was 2.4 mg/L, the NOEC was 1.56 mg/L. 

After 48 h of storage the EC50 was 18.6 mg/L without pH adjustment and 17.6 mg/L with pH adjustment, 

the corresponding NOEC were 12.5 and 6.25 mg/L respectively. 

The results indicate an approximately 86% reduction of the toxicity during the 48 h storage period. 

Adjustment of pH did not decrease toxicity and the acidity was not responsible for the residual toxicity. 

Toxicity of hydrogen peroxide 

The EC50 for normal surviving larvae was 1.58 mg/L, the NOEC was 1.25 mg/L. The measured hydrogen 

peroxide concentration 48-hour degraded sample of PeracleanÆ

 Ocean was 11 mg/L. The results indicate 

that there was sufficient hydrogen peroxide present in the aged solution to explain the residual toxicity. 

The residual toxicity was diminished by the addition of catalase to the 48-h degraded sample of 

PeracleanÆ

 Ocean, thus providing further evidence that the residual toxicity was caused by hydrogen 

peroxide. 

7 Exposure assessment 

 

7.1 Environmental exposure assessment (5.2.7) 

Entries of PeracleanÆ Ocean into the aquatic environment can only occur when Ballast water is 

exchanged. Preliminary experiments on the residual concentrations of peracetic acid and hydrogen 

peroxide in treated ballast water samples have been performed during field trials (Degussa, 2004c). 

Ballast water treatment was performed with the recommended equipment and concentrations of 

PeracleanÆ

 Ocean. All treated ballast water was directly collected in 6 simulated ballast water tanks 

(20 t tank containers). Samples were taken at different reaction times and the content of the active 

ingredient was analysed. A complete decay of the active ingredient peroxyacetic acid was observed after 

10 to 15 hours. Hydrogen peroxide was degraded to about 20 mg/l after 5 to 10 hours and to 15 mg/l 

after up to 50 hours. The toxicity testing of treated ballast water confirmed that a concentration of about 

10 mg/L of hydrogen peroxide was still present after 48 h of storage of a solution of 150 mg/L PeracleanÆ

Ocean in seawater at 8 to 10°C. When released into the environment residual hydrogen peroxide is 

further diluted and also expected to be rapidly degraded by the various routes of degradation. Preliminary 

calculations using the MAMPEC model developed by the Dutch Institute for Environmental Studies 

indicate that the concentrations of hydrogen peroxide in commercial harbours will remain below the 

conservative PNEC for hydrogen peroxide of 10 μg/L (maximum concentration was 4.9 μ/l), while the PAA 

concentration was predicted to be about 6 orders of magnitude lower (4.1 10E-6 μg/L ) and can be 

regarded as negligible. 

7.2 Human exposure assessment 

Due to the automated process in ballast water application and dosing human exposure is unlikely to occur 

during the treatment operations. Very short dermal exposure would be possible when the containers are 

connected to the dosing system. In any case for such operations and for accidental situations personal 

protective equipment, protective gloves, goggles and if needed respiratory protection and full protective 
MEPC 53/2/12 

ANNEX 

Page 24 

I:\MEPC\53\2-12.doc 

suits are recommended and should be provided. Safety training is also offered by the producer of 

PeracleanÆ

 Ocean. 

8 Risk characterisation (5, 5.3) 

8.1 Screening for persistency, bio-accumulation and toxicity (5.1) 

The active components of PeracleanÆ Ocean do not fulfil the PBT criteria as outlined in EC, 2003a: 

Criterion PBT criteria 

P Half-life > 60 d in marine water or > 40 d in 

freshwater*

or half-life > 180 d in marine sediment or 

> 120 d in freshwater sediment*

 or readily 

biodegradable 

B BCF > 2,000 or log Kow > 4.5 

T Chronic NOEC < 0.01 mg/l or CMR or endocrine 

disrupting effects 

Persistence (P) 

Due to the ready biodegradability and the abiotic degradation of the active components of PeracleanÆ

Ocean, it can be concluded that it is not persistent in the environment. Environmental half lives are in the 

order of hours or a few days at maximum. 

Bioaccumulation (B) 

Due to the high water solubility and the low octanol water partition coefficients of the active components of 

PeracleanÆ

 Ocean, there is no concern for a possible bio-accumulation potential of the product 

(log Kow below 0). 

Toxicity (T) 

The active components of PeracleanÆ Ocean do not have NOEC levels below 0.01 mg/l and there are no 

indications for relevant effects concerning carcinogenicity, mutagenicity or reproductive toxicity. 

8.2 Assessment of possible reaction with organic matter (5.3.3) 

8.3 Rate of abiotic and biotic degradation and degradation products (5.3.4, 5.3.5) 

The active ingredients of PeracleanÆ Ocean, PAA and hydrogen peroxide degrade rapidly in the 

environment. Abiotic degradation half lives in seawater are in the range of several minutes for Peracetic 

acid, and up to 48 h in freshwater at pH 4 to 7. For hydrogen peroxide half lives of several hours up to 

5 days were predicted under environmental conditions. The half life will be more rapid in the presence of 

transitions metals, metal oxides and hydroxides, at pH Values > 7. Heat and sunlight can induce 

photochemical decomposition. However it should also be considered that hydrogen peroxide is also 

generated photochemically in water systems. In seawater the limited amount of available natural 

concentrations ranged from 0.5 to 14 μg hydrogen peroxide/l, in lakes values > 100 μg/l were reported. 

Both PAA and hydrogen peroxide are readily biodegradable with half lives with sewage treatment plant 

inoculum of 2 to 3 minutes if the toxicity levels are not superseded. 

Degradation of PeracleanÆ

 Ocean results only in the formation of oxygen and water as well as acetic acid 

that can be readily metabolised yielding carbon dioxide and water. No persistent metabolites are formed. 
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8.4 Partition coefficients (5.3.6) 

From the Octanol-Water partition coefficients of the active substances PAA and hydrogen peroxide, the 

organic carbon normalised distribution coefficient can be derived using the following equations according 

to the EU technical guidance document on risk assessment (EC, 2003). 

For organic acids the following equation can be used: 

log Koc = 0.6 log Kow + 0.32 

For Peracetic acid using a log Kow of -0.52 a log Koc of 0.008 (Koc = 1.02 L/kg) is derived. 

For hydrogen peroxide the following equation for non-hydrophobics may be used: 

log Koc = 0.52 log Kow + 1.02 

Using that equation a log Koc of 0.2 (Koc = 1.58 L/kg) was derived for hydrogen peroxide (EU, 2003). 

Both Koc values indicate a negligible absorption to organic matter which would also indicate a very low 

adsorption potential to soil and sediment. This is confirmed by the Mackay level I equilibrium distribution 

(see chapter 3.2). 

8.5 Bioaccumulation potential and secondary poisoning potential (5.3.7, 5.3.10) 

Due to the low Octanol-water partition coefficients of the active ingredients (log Kow of PAA = -0.52, of 

hydrogen peroxide -1.5) PeracleanÆ

 Ocean has no bioaccumulation potential and thus an assessment of 

secondary poisoning is redundant. 

8.6 Assessment of sediment species (5.3.11) 

As the Koc values of the active ingredients PAA and hydrogen peroxide are very low (1.02 L/kg and 

1.58 L/kg) an assessment of sediment poisoning is redundant. 

8.7 Comparison of the results of the effect assessment with the results of the discharge toxicity 

testing. (5.3.14) 

Discharge toxicity testing was performed with the most sensitive of the marine species determined in a 

pre-study, Mytilus galloprovincialis larvae < 4 h post fertilisation. The test duration was 48 hours. 

(Degussa, 2005b). After 48 h the toxicity was reduced to 80% of the original toxicity. The residual toxicity 

could be completely attributed to a residual content of hydrogen peroxide. This is in accordance with the 

findings that PAA from PeracleanÆ

 Ocean at the concentration of 150 mg/L recommended for Ballast 

water treatment is completely degraded already after 10 to 15 hours during Ballast water treatment, while 

hydrogen peroxide degradation is slower and it is still present in the treated solution at a concentration of 

10 to 15 mg/L after 48 to 50 hours. When released into the environment residual hydrogen peroxide is 

further diluted and also expected to be rapidly degraded by the various routes of degradation. Preliminary 

calculations using the MAMPEC model of the Dutch Institute for Environmental Studies (IVM) indicate that 

the concentrations of hydrogen peroxide in commercial harbours will remain below the conservative 

PNEC for hydrogen peroxide of 10 μg/L (maximum concentration was 4.9 μ/l), while the 

PAA concentration was predicted to be about 6 orders of magnitude lower (4.1 10E-6 μg/L) and can be 

regarded as negligible. Taking into account that the predicted hydrogen peroxide concentrations are in 

the range of the naturally occurring concentrations of hydrogen peroxide in the environment it can be 

concluded that those discharges do not constitute a risk to the environment. 

8.8 Human health risk assessment 

Due to the technology used humans will not be exposed to PeracleanÆ Ocean during ballast water 

treatment on the ships. During the recommended operating procedures the possibility of exposure will be 

minimal and limited to short term contact when connecting the storage tank to the dosage line. Direct 

contact during this operation is minimized by the recommended handling procedures that include the 

appropriate personal protective equipment, gloves, goggles and if needed respiratory protection. As the 

main hazard of the product is due to local irritation/corrosion at the site of contact and there is no 

immediate concern for mutagenicity or carcinogenicity, the product can be handled safely in this 

application. 
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Appendix 

Results of Field Trials Carried out in Kiel Harbour in November 2002 

Abbau des Desinfektionsmittels in den Lagertanks 

Messung am 26.11.2002

77777 6 ,9 6 ,9 6,9 6 ,7 6,7 6 ,8

3 0

22,4

2 4

2 1,2

16 ,8

15

14 ,1 13 ,8

12 ,3 12 ,9

2,5

2 2 ,5

17,6

16,8

13 ,6

9 ,9 9 ,6 9,6

5,1

4,2

3 ,3

0,1 0

5

10

15

20

25

30

35

Zeit nach der Behandlung

pH-Wert [-]

H2O2-Gehalt [mg/l]

Peressigs‰ure [mg/l]

genehmigter minimaler pH-Wert [-]

genehmigter maximaler H2O2-Gehalt [mg/l]

Abbau des Desinfektionsmittels in den Lagertanks 

Messung am 28.11.2002

6 ,7 6 ,8 7 7,2 7,2 6 ,9

17,2

15,1

13 ,8

9 ,6

8 ,1

1,4

9 ,9

6,7

5,9

4 ,8

4 ,3

0 0

5

10

15

20

Zeit nach der Behandlung

pH-Wert [-]

H2O2-Gehalt [mg/l]

Peressigs‰ure [mg/l]

genehmigter minimaler pH-Wert [-]

genehmigter maximaler H2O2-Gehalt [mg/l]

___________