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.

 I:\MEPC\60\2-9.doc 

INTERNATIONAL MARITIME ORGANIZATION

IMO 

E

MARINE ENVIRONMENT PROTECTION 

COMMITTEE 

60th session 

Agenda item 2 

MEPC 60/2/9

 28 August 2009

 Original: ENGLISH

HARMFUL AQUATIC ORGANISMS IN BALLAST WATER 

Application for Basic Approval of the Severn Trent DeNora BalPure®

Ballast Water Management System 

Submitted by Germany 

SUMMARY

Executive summary: This document contains the non-confidential information related to 

the application for Basic Approval of the Severn Trent DeNora 

(STDN) BalPure® Ballast Water Management System under the 

“Procedure for approval of ballast water management systems that 

make use of Active Substances (G9)” adopted by 

resolution MEPC.169(57) 

Strategic direction: 7.1 

High-level action: 7.1.2 

Planned output: 7.1.2.4 

Action to be taken: Paragraph 5 

Related documents: BWM/CONF/36; MEPC 57/21; BWM.2/Circ.13 and BWM.2/Circ.18 

Introduction 

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

of Ships’ Ballast Water and Sediments stipulates that ballast water management systems that 

make use of Active Substances to comply with the Convention shall be approved by 

the Organization. 

2 The “Procedure for approval of ballast water management systems that make use 

of Active Substances (G9)” stipulates the required information (MEPC 57/21, annex 1, 

paragraph 4.2.1) and provisions for risk characterization and analysis (MEPC 57/21, annex 1, 

section 5), which, according to section 6 of Procedure (G9), should be evaluated by 

the Organization. 
MEPC 60/2/9 - 2 - 

I:\MEPC\60\2-9.doc 

3 The receiving competent authority in Germany has verified the application dossier 

and believes it to satisfy the data requirements of Procedure (G9) adopted by 

resolution MEPC.169(57). 

4 In accordance with BWM.2/Circ.18, Germany therefore submits the non-confidential part 

of the manufacturer’s application dossier in the annex. The complete dossier will be made 

available to the experts of the GESAMP-BWWG with the understanding of confidential 

treatment. 

Action requested of the Committee 

5 The Committee is invited to consider the proposal for approval and decide as appropriate. 

***
MEPC 60/2/9 

I:\MEPC\60\2-9.doc 

ANNEX 

NON-CONFIDENTIAL INFORMATION ON THE BALPURE®

BALLAST WATER MANAGEMENT SYSTEM 

Contents 

1 INTRODUCTION 

1.1 Overview of the BalPure® Technology 

2 IDENTIFICATION OF THE SUBSTANCE OR PREPARATION (G9: 4.1) 

2.1 Introduction to the chemical basis of BalPure® Ballast Water Management System 

2.2 Active Substances 

2.3 Relevant Chemicals 

2.4 Other chemicals

3 DATA ON EFFECTS ON AQUATIC PLANTS, INVERTEBRATES AND FISH, 

AND OTHER BIOTA, INCLUDING SENSITIVE AND REPRESENTATIVE 

ORGANISMS (G9: 4.2.1.1) 

3.1 Acute aquatic toxicity 

3.2 Chronic aquatic toxicity 

3.3 Endocrine disruption 

3.4 Sediment toxicity 

3.5 Bioavailability/biomagnification/bioconcentration 

3.6 Food web/population effects 

4 DATA ON MAMMALIAN TOXICITY (G9: 4.2.1.2) 

4.1 Acute toxicity 

4.2 Effects on skin and eye 

4.3 Repeated-dose toxicity 

4.4 Chronic toxicity 

4.5 Developmental and reproductive toxicity 

4.6 Carcinogenicity 

4.7 Mutagenicity/genotoxicity 

4.8 Toxicokinetics 

5 DATA ON ENVIRONMENTAL FATE AND EFFECT UNDER AEROBIC AND 

ANAEROBIC CONDITIONS (G9: 4.2.1.3) 

5.1 Modes of degradation (biotic; abiotic) 

5.2 Bioaccumulation, partition coefficient, octanol/water partition coefficient 

5.3 Persistence and identification of the main metabolites in the relevant media 

5.4 Reaction with organic matter 

5.5 Potential physical effects on wildlife and benthic habitats 

5.6 Potential residues in seafood 

5.7 Any known interactive effects
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6 PHYSICAL AND CHEMICAL PROPERTIES OF THE ACTIVE SUBSTANCES, 

RELEVANT CHEMICALS AND TREATED BALLAST WATER (G9: 4.2.1.4) 

7 ANALYTICAL METHODS AT ENVIRONMENTALLY RELEVANT 

CONCENTRATIONS (G9: 4.2.1.5) 

7.1 Analysis of Total Residual Oxidant (TRO) 

7.2 Analysis of Disinfection By-Products (DBPs)

8 USE OF ACTIVE SUBSTANCE 

8.1 The manner of application 

9 MATERIAL SAFETY DATA SHEETS (G9: 4.2.7) 

9.1 Active Substances hazard classification 

9.2 Hazard classification of Relevant Chemicals 

9.3 Hazard classification of other chemicals 

10 RISK CHARACTERIZATION AND ANALYSIS 

10.1 Screening for persistence, bioaccumulation and toxicity (G9: 5.1) 

11 EVALUATION OF THE TREATED BALLAST WATER (G9: 5.2) 

11.1 Total Residual Oxidants 

11.2 Water quality parameters 

11.3 Disinfection By-Products (DBPs) in treated ballast water 

11.4 Toxicity testing of treated ballast water 

11.5 Determination of holding time 

11.6 Reaction with organic matter 

11.7 Characterization of degradation route and rate (G9: 5.3.5) 

11.8 Prediction of discharge and environmental concentrations 

11.9 Assessment of potential for bioaccumulation 

11.10 Effects assessment 

11.11 Effects on aquatic organisms 

11.12 Effects on sediment 

11.13 Comparison of effect assessment with discharge toxicity 

12 RISK ASSESSMENT 

12.1 Risk to Safety of Ship 

12.2 Risks to Human Health 

12.3 Risks to the Aquatic Environment

13 ASSESSMENT REPORT 

13.1 Overview of the Data and Endpoints 

14 REFERENCES 
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LIST OF TABLES 

Table 1 - Overview of chemical identification 

Table 2 - Acute aquatic toxicity data 

Table 3 - Acute aquatic toxicity-treated ballast water 

Table 4 - Overview of chronic aquatic toxicity 

Table 5 - Chronic aquatic toxicity-treated ballast water 

Table 6 - KOCs for Active Substances and Relevant Chemicals 

Table 7 - BCFs for Active Substances and Relevant Chemicals 

Table 8 - Acute mammalian toxicity data 

Table 9 - Skin, eye, and dermal effects 

Table 10 - Repeated-dose toxicity 

Table 11 - Chronic mammalian toxicity 

Table 12 - Summary of developmental and reproductive toxicity data 

Table 13 - Summary of data on carcinogenicity 

Table 14 - Summary of data on mutagenicity and genotoxicity 

Table 15 - Summary of uptake, absorption, and excretion of chemicals 

Table 16 - Modes of degradation 

Table 17 - Physical and chemical properties of Active Substances 

Table 18 - Physical and chemical properties of Relevant Chemicals-THMs 

Table 19 - Physical and chemical properties of Relevant Chemicals-HAAs 

Table 20 - Physical and chemical properties of Relevant Chemicals and other chemicals 

Table 21 - Physical and chemical properties of treated ballast water 

Table 22 - Analytical methods 

Table 23 - Overview of BalPure® system alarms 

Table 24 - PBT criteria evaluation 

Table 25 - Total Residual Oxidant (TRO) measured as Total Chlorine 

Table 26 - Summary of water quality parameters 

Table 27 - Levels of Trihalomethanes (THMs) and Haloacetic acids (HAAs) in treated 

fresh water 

Table 28 - Levels of Trihalomethanes (THMs) and Haloacetic acids (HAAs) in treated 

brackish water 

Table 29 - Levels of Trihalomethanes (THMs) and Haloacetic acids (HAAs) in treated 

seawater 

Table 30 - PNEC value summary 

Table 31 - Summary of COPC exposure point concentrations 

Table 32 - Summary of dermal intake factors 

Table 33 - Summary of oral intake factors 

Table 34 - Summary of toxicity criteria 

Table 35 - Summary of cancer risks and non-cancer hazards for BalPure® technicians 

Table 36 - Summary of cancer risks and non-cancer hazards for ship’s crew/dock workers 

Table 37 - Summary of cancer risks for the general public 

Table 38 - Summary of non-cancer hazards for general public 

Table 39 - Estimated concentrations of THMs in vent air and comparisons to PELs 
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LIST OF FIGURES 

Figure 1 - Distribution of chlorine species at different pH values 

Figure 2 - Distribution of bromine species at different pH values 

Figure 3 - Example of chlorine demand/decay at three different TRO (measured as Cl2/L) 

Figure 4 - TRO concentration and effect of sodium bisulfite addition to treated water 

Figure 5 - Overview of the BalPure® ballasting process 

Figure 6 - Overview of the BalPure® de-ballasting process 

Figure 7 - Conceptual exposure model, BalPure® System 

LIST OF ABBREVIATIONS 

Abbreviation Description Abbreviation Description 

AIS Aquatic Invasive Species L/kg Liters per kilogram 

ATSDR Agency for Toxic Substances and 

Disease Registry 

LD50 Lethal Dose for 50% of test 

population 

AWWA American Water Works 

Association LEL Lower Explosive Limit 

BDCM Dichlorobromomethane LOAEL Lowest Observable Adverse 

Effect Level 

BCF Bioconcentration Factor m Meters 

BMD Benchmark dose-response method MCA Monochloroacetic acid 

Br2 Bromine MEPC Marine Environment Protection 

Committee 

BWMS Ballast Water Management System mmHg Millimeters of Mercury 

CAS Chemical Abstract Service mV Millivolts 

CCOHS Canada’s National Centre for 

Occupational Health and Safety μg/L micrograms per liter 

CEM Conceptual Exposure Model μg/ml micrograms per milliliter 

CFR Code of Federal Regulations 

(United States) μS/cm microsiemens per centimeter 

Cl- Chloride ion mA Milliamp 

Cl2 Chlorine mg/kg bw milligrams per kilogram body 

weight 

CO2 Carbon dioxide mg/kg-d milligrams per kilogram per day 

CO Carbon monoxide mg/L Milligrams per liter 

COPC Chemical(s) of Potential Concern MSDS Material Safety Data Sheet 

CSF Cancer Slope Factor NaHSO3 Sodium bisulfite 

C x t Concentration x time NaOCl Sodium hypochlorite 

DC Direct Current NIOZ Netherlands Institute for Sea 

Research 

DBAA Dibromoacetic acid NOAEL No Observed Adverse Effect 

Level 

DBPs Disinfection By-products NOEC No Observed Effect 

Concentration 

DCA Dichloroacetic acid NOEL No Observed Effect Level (used 

interchangeably with NOAEL) 
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Abbreviation Description Abbreviation Description 

DOC Dissolved Organic Carbon OBr- Hypobromite ion 

DPD N,N-diethyl-p-phenylenediamine OCl- Hypochlorite ion 

EC50 Effective concentration of 

substance that causes 50% of 

maximum response 

OECD Organization for Economic 

Co-operation and Development 

EDCs Endocrine Disrupting Chemicals OIT Operator Interface Terminal 

EEC European Economic Community O&M Operational/Maintenance 

EPI Estimation Programs Interface OSHA Occupational Safety and Health 

Administration 

ETV Environmental Technology 

Verification 

OPPTS Office of Prevention, Pesticides, 

and Toxic Substances 

FAC Free Available Chlorine ORP Oxidation Reduction Potential 

FAB Free Available Bromine PBT Persistence, Bioaccumulation, 

Toxicity 

FDA Food and Drug Administration 

(United States) PEL Permissible Exposure Limit 

FHSA Federal Hazardous Substance Act 

(United States) PFD Process Flow Diagram 

GESAMPBWWG 

Joint Group of Experts on the 

Scientific Aspects of Marine 

Environmental Protection – Ballast 

Water Working Group 

pKa Dissociation Constant 

H+ Hydrogen ion PLC Programmable Logic Controller 

H2 Hydrogen gas PNEC Probable no Effect 

Concentration 

H2O2 Hydrogen peroxide POC Particulate Organic Carbon 

HSDB Hazardous Substances Data Bank PPE Personal Protective Equipment 

HSO3 Bisulfite ion ppm Parts per million 

HSO4 Bisulfate ion PM Phase Rotation Monitor 

HAA Haloacetic acid PSU Practical Salinity Units 

HOBr Hypobromous acid RfD Reference Dose 

HOCl Hypochlorous acid SIDS Screening Information Data Set 

IARC International Agency for Research 

on Cancer SCR Silicon Controlled Rectifier 

IC Ion chromatography SGPT Serum Glutamate-Pyruvate 

Transaminase 

ILCR Incremental Lifetime Cancer Risk STDN Severn Trent De Nora 

IMDG International Maritime Dangerous 

Goods Code TCA Trichloroacetic acid 

IMO International Maritime 

Organization THMs Trihalomethanes 

ICSC International Chemical Safety Card TOC Total Organic Carbon 

IPCS International Programme on 

Chemical Safety TOXNET Toxicology Data Network 

IRIS Integrated Risk Information System TRO Total Residual Oxidant 
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Abbreviation Description Abbreviation Description 

IUPAC International Union of Pure and 

Applied Chemistry TSS Total Suspended Solids 

Koc Organic Carbon Partition 

Coefficient UCL Upper Confidence Level 

Kow Octanol/Water Partition Coefficient US EPA United States Environmental 

Protection Agency 

Kpa Kilopascal vdc Volts of continuing current 

L/min Liters per minute WHO World Health Organization 

wt % Weight Percent 
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1 INTRODUCTION 

Severn Trent De Nora (STDN), LLC, www.severntrentdenora.com, is a joint venture subsidiary 

of Severn Trent Services and Gruppo De Nora. STDN is the world leader in the supply of on-site 

generation of biocide solutions to the power, marine, offshore industrial water disinfection 

markets. Over the past 30 years, STDN organizations have supplied 65% of the worldwide 

installed base of on-site generated hypochlorite. STDN draws upon the strength and global 

resources of Severn Trent Services and Gruppo De Nora. The joint venture was formed in 2001 

by the combination of their respective subsidiaries, Exceltec International Corporation 

and DeNora SeaClor, S.r.l. The history of STDN includes: 1974 – Diamond Shamrock 

Corporation, Electrolytic Systems Division formed; 1986 – Acquisition of OMNIPURE by 

Diamond Shamrock Corporation; 1987 – Formation of Eltech International Corporation (Sugar 

Land, TX); 1997 – Eltech International Corporation name changed to Exceltec International 

Corporation; 1998 – Exceltec International Corporation acquired by Severn Trent Services; 2001 

– Severn Trent Services enters into joint venture with Gruppo De Nora; and 2002 – Severn Trent 

De Nora is formed. Established in 1923 by Oronzio De Nora, Gruppo De Nora is recognized 

worldwide as a leading supplier of electrochemical technologies for the production of chlorine, 

caustic soda and derivatives, as well as the largest worldwide supplier of noble metal-coated 

electrodes for the chlor-alkali industry and for the electrochemical industry in general. Energy 

saving and environmental protection are the Group's distinguishing technologies. Gruppo De 

Nora has built more than 500 plants for the production of chlorine, caustic soda and for the 

electrochlorination of industrial waters in 60 different countries. 

The BalPure® system and the testing for the installation on board the S/R American Progress

has been acknowledged/approved by the states of Florida, Texas, and Louisiana (United States). 

Additionally, all requirements for acceptance of the BalPure® system on the 

S/R American Progress into the United States Coast Guard Shipboard Technology Evaluation 

Program (STEP) have been completed, with issuance of the acceptance certificate anticipated by 

the third quarter of 2009. 

STDN is submitting this dossier to obtain the International Maritime Organization’s 

Basic Approval under Procedure (G9) (MEPC 57/21, resolution MEPC.169(57)) for 

the BalPure® Ballast Water Management System (BWMS). 

1.1 Overview of the BalPure® technology 

The BalPure® system provides a safe and economic electrolytic process for the on-site generation 

of a biocide solution from seawater to disinfect aquatic invasive species (AIS) in ballast water. 

Ballast water treatment is accomplished using a simple three-step process of filtration, injection 

of a biocide solution, and residual oxidant neutralization. The first phase is filtration using 

a 40 micron stainless steel mesh filter to remove large particles and sediment. The second phase 

of the treatment process is electrochemical generation of the biocide solution. This involves 

passing a small supply (1/100 of total ballast flow) of seawater, either from the incoming ballast 

water line or sea cooling water, through electrolytic cells. The resulting disinfectant solution is 

injected directly into the incoming ballast water line where it will oxidize potential AIS. The 

third and final treatment process phase is residual oxidant neutralization to ensure environmental 

acceptability. When the treated ballast water is ready to be discharged, sodium bisulfite is 

injected directly into the ballast water discharge line. 
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The BalPure® system is designed to require minimal input from the ship’s crew, with the system 

starting and stopping the necessary treatment steps based on electronic signals. This minimizes 

added duties to ship’s crew and ensures proper ballast water treatment. 

STDN’s experience with electrochlorination in a variety of industrial and maritime settings has 

proven the effectiveness of the technology. As discussed further in section 2.2.1, the 

concentration of the biocide solution needed for effective ballast water treatment is related to the 

total organic carbon (TOC) present in the water. Efficacy of the BalPure® system has been tested 

in both pilot-scale and full-scale scenarios. A pilot-scale efficacy study was conducted by 

the University of Washington. Results indicated that a residual chlorine concentration 

of 2.95 mg/L-3.71 mg/L with ballast seawater containing <2 mg/L TOC was sufficient to 

inactivate 98%–100% mesozooplankton, 99%–99.9% phytoplankton and 99%–100% bacteria 

in 5 hours (Herwig et al., 2006). Within 24 hours of treatment, the residual chlorine was 

neutralized with the addition of sodium bisulfite. Testing of the treated water was shown to be 

non-toxic to aquatic organisms following the sodium bisulfite neutralization step. 

A full-scale study was conducted at the Naval Research Laboratory (NRL) in Key West, Florida 

(United States). The tests were part of the Environmental Technology Verification (ETV) 

Program instituted by the United States Environmental Protection Agency (US EPA) to verify 

environmental treatment performance as well as operational performance. The test protocol 

evaluated biological treatment performance based on IMO Guidelines (G8) and ETV test 

criteria, operation and maintenance, reliability, cost factors, environmental acceptability, and 

safety. Examination of these factors was accomplished through two types of 

tests: Operational/maintenance (O&M) tests and challenge water tests. Based on the test results, 

it was found that a residual chlorine concentration of 14 mg/L-16 mg/L treating ballast seawater 

containing 10 mg/L TOC effectively inactivated >99% zooplankton, phytoplankton and bacteria 

after a 24-hour treatment period (NRL, 2007). 

During 2009, efficacy of the BalPure® system will be tested according to IMO Guidelines (G8) at 

the Royal Netherlands Institute for Sea Research (NIOZ) land-based testing facility under the 

direction of Dr. Marcel Veldhuis. Land-based testing of a commercial BalPure® system will also 

be conducted at the Maritime Environmental Resource Center in Maryland, USA during the fall 

of 2009. 

2 IDENTIFICATION OF THE SUBSTANCE OR PREPARATION (G9: 4.1) 

2.1 Introduction to the chemical basis of BalPure® Ballast Water Management System 

Chlorine, often in the form of sodium hypochlorite, has been used for many years in a wide 

variety of water treatment applications. A few examples include drinking/potable water 

disinfection, biofouling control, recreational water (swimming pools/spa) treatment, and 

wastewater treatment. When chlorine is used for water treatment, hypochlorous acid is instantly 

produced over the pH 4-8 range. Therefore, regardless of what form of chlorine (gaseous or 

sodium hypochlorite) is being used to treat ballast water, effective disinfection is largely the 

result of the properties of hypochlorous acid. 

The BalPure® system uses electrolysis of seawater to safely generate sodium hypochlorite 

on board, and immediately injects the solution directly into ballast water while it is pumped on 

board. Seawater is passed through electrolytic cells (electrolyzers) where it is subjected to 

medium amperage, low voltage direct current. Electrolytic cells are comprised of a cathode and 

an anode. At the outlet of the electrochemical generator, the seawater contains a mixture of 
MEPC 60/2/9 

ANNEX 

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chemicals produced at both the anode and cathode. Because seawater contains bromide ions, the 

electrochemical process results in the formation of hypochlorous acid (HOCl) in equilibrium with 

hypochlorite ion (OCl-

), hyprobromous acid (HOBr) in equilibrium with hypobromite ion (OBr-), 

and hydrogen gas (H2) produced as a by-product. During the electrochemical process a small 

amount of caustic (OH-) is also produced, which is effectively neutralized within the cell and 

causes no apparent increase in the pH of treated ballast water. 

Further, chlorine and bromine can undergo reactions with ammonia naturally present in seawater 

and may result in the formation of low concentrations of chloramines and bromamines. 

Chloramine and bromamine are important to discuss in disinfection chemistry because these 

species are also considered disinfectants. However, they are less effective disinfectants 

(i.e. weak oxidants) and the amount of disinfection attributed to chloramine and bromamine is 

not considered relevant. The amount of chloramine and/or bromamine potentially formed is 

related to the amount of ammonia present, amount of oxidant present, reaction time, and pH of 

the water treated. The amount of chloramine and bromamine formed during use of the BalPure®

system is expected to be insignificant because of the neutral pH at which treatment is occurring 

and the long reaction time required for their formation. In treated discharge, chloramines and 

bromamines have not been determined analytically for several reasons. First, the methods 

capable of measuring combined halogen species are not readily available, thereby making 

individual quantification of chloramine and bromamine difficult. Second, combined chlorine and 

bromine species are included in the TRO measurement. Lastly, the BalPure® system applies a 

dechlorination/dechloamination process upon discharge of the treated ballast water. The use of 

sodium bisulfite or sodium metabisulfite is an effective means of removal for any combined 

chlorine or bromine species according to the following reactions: 

NaHSO3 + NH2Cl + H2O → NaHSO4 + NH4Cl 

Na2S2O5 + NH2Cl → 2NaHSO4 + NH4Cl 

The measurable oxidant species present during chlorine-based water disinfection, and the 

terminology used, is often a point of confusion. By industry standards and convention, all 

chlorine present in a water sample, regardless of form, is referred to as Free Available Chlorine 

(FAC). FAC includes Cl2, HOCl, and OCl-. When including chloramines, the term Combined 

(or Total) Chlorine is used. Similarly, all bromine species present in a water sample are referred to 

as Free Available Bromine (FAB). When including bromamine, the term used is Combined (or 

Total) Bromine. The common factor in all of these chemical species is that they are considered 

oxidants, and due to the difficulty in measuring each chemical species individually in a complex 

water sample, the term Total Residual Oxidants (TRO) is used to include all of these oxidants when 

present in a sample. To clarify: 

Free Available Chlorine (FAC) = Cl2 +HOCl + OClCombine (or Total) Chlorine = FAC + chloramine 

Free Available Bromine (FAB) = Br2 + HOBr + OBrCombine (or Total) Bromine = FAB + bromamine 

Total Residual Oxidants (TRO) = FAC + chloramine + FAB + bromamine 

Therefore, in this dossier, TRO is used to describe the total of all oxidants present in treated water. 

The chemical methods used for analysing TRO often state that the measurement is calculated 

as mg Cl2/L. However, these methods include all of the oxidants present in a water sample as 

mentioned above, not just Cl2. 
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Using the definitions of Active Substances, Relevant Chemicals, and other components as 

provided in the Methodology for information gathering and the conduct of work of 

the GESAMP-BWWG (23 May 2008), Severn Trent De Nora classifies the substances associated 

with the BalPure® system as follows: 

Active Substances: As described above, the electrochemical process generates a mixture 

of chemicals. Of these, hypochlorous acid (HOCl) in equilibrium with hypochlorite ion 

(OCl-) and hyprobromous acid (HOBr) in equilibrium with hypobromite ion (OBr-) are 

the actual disinfecting agents. These Active Substances are discussed in detail in 

section 2.2. In this dossier, these Active Substances are considered together and 

referenced as Total Residual Oxidants (TRO). 

Relevant Chemicals: Disinfection of water with chlorine-based disinfectants can result 

in the formation of trihalomethanes (THMs), haloacetic acids (HAAs), and bromate that 

may be present at detectable levels in treated ballast water. THMs and HAAs are 

discussed as Relevant Chemicals in section 2.3.1, while bromate is discussed in 

section 2.3.2. 

During the electrolysis process, hydrogen gas is produced. For this reason, H2 gas is 

classified as a Relevant Chemical, however, the hydrogen gas produced is immediately 

separated from the solution and removed from the system via ventilation to the 

atmosphere. Though it is not present in treated ballast water, but needs to be considered 

when evaluating the BalPure® system, hydrogen gas is considered a Relevant Chemical 

and is discussed in more detail in section 2.3.3. 

Other chemicals (i.e. Other components): Sodium bisulfite is used with the BalPure® 

system to neutralize residual oxidants that may be present in treated ballast water 

discharge. Because sodium bisulfite is not an Active Substance, and is not produced 

during or after employment of the treatment system (Relevant Chemical), it is considered 

to fall under the ‘other chemicals’ category. Sodium bisulfite is discussed in more detail 

in section 2.4.1. 

Table 1 below provides a summary of the substances associated with the BalPure® treatment 

system. 

Table 1 : Overview of Chemical Identification 

Ingredient 

(IUPAC Name) 

Identification 

Numbers 

Chemical 

Formula 

Structural 

Formula 

Molecular 

Weight 

Percentage 

(by weight) 

Active Substances in Ballast Water 

Hypochlorous acid CAS # 7681-

52-9 HOCl 52.46 <25 mg/L 

TRO 

Hypobromous acid CAS # 

13824-96-9 HOBr 96.91 <25 mg/L TRO 

Relevant Chemicals 

Bromate (as sodium 

bromate) 

CAS #7789-

38-0 NaBrO3 150.89 By-product 

Hydrogen CAS #133-

74-0 H2 H---H 2.016 By-product 
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Ingredient 

(IUPAC Name) 

Identification 

Numbers 

Chemical 

Formula 

Structural 

Formula 

Molecular 

Weight 

Percentage 

(by weight) 

THMs 

Chlorodibromomet

hane 

CAS #124-

48-1 CHBr2Cl 208.29 By-product 

Dichlorobromomet

hane 

CAS #75-27-

4 CHBrCl2 163.8 By-product 

Tribromomethane 

(bromoform) 

CAS #75-25-

2 CHBr3 252.77 By-product 

Trichloromethane 

(chloroform) 

CAS # 67-

66-3 CHCl3 119.38 By-product 

HAAs 

Bromochloroacetic 

acid 

CAS # 5589-

96-8 

C2H2BrCl

O2

173.39 By-product 

Monochloroacetic 

acid 

CAS #79-11-

8 C2H3ClO2 94.50 By-product 

Dibromoacetic acid CAS #631-

64-1 

Br2CHCO

OH 217.84 By-product 

Dichloroacetic acid CAS # 79-

43-6 

CHCl2CO

OH 128.9 By-product 

Trichloroacetic acid CAS # 76-

03-9 

CCl3COO

H 163.4 By-product 

Monobromoacetic 

acid 

CAS # 79-

08-3 C2H3BrO2 138.95 By-product 

Other Chemicals 

Sodium Bisulfite CAS # 7631-

90-5 NaHSO3 104.06 Neutralizing agent 
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2.2 Active Substances 

2.2.1 Hypochlorous acid and hypobromous acid 

To avoid storing Active Substances on board, the BalPure® system safely generates sodium 

hypochlorite by electrolysis of seawater. Seawater is passed through electrolytic cells 

(electrolyzers) where it is subjected to medium amperage, low voltage direct current. 

Electrolytic cells are comprised of a cathode and an anode. The primary cell reactions occurring 

in the electrochemical generation process in seawater are as follows: 

Reaction 1 (at the cathode): 2H2O + 2e-

 → H2 + 2OHReaction 2 (at the anode): 2Cl-

 + 2H2O → Cl2 + 2e-

 --------------------------------------- 

Reaction 3 (overall reaction): 2Cl-

 + 2H2O → Cl2 + H2 + 2OHWhen the chlorine is produced, it is rapidly hydrolyzed and forms hypochlorous acid: 

Reaction 4: Cl2 + H2O ↔ HOCl + H+ + ClHypochlorous acid (HOCl) undergoes a pH-dependent dissociation to form hypochlorite ion (OCl-

): 

 Reaction 5: HOCl ↔ OCl- + H+

Thus, depending on pH, one observes a distribution of chlorine species as shown in figure 1 below. 

Figure 1 : Distribution of Chlorine Species at Different pH Values 

As discussed in section 2.1, the combination of Cl2, HOCl, and OCl-

 are commonly referred to as 

free available chlorine (FAC). As figure 1 depicts, at the pH of seawater (typically ranges 

from 7.5-8.4), the solution generated by the BalPure® system will consist of a near equal mixture 

of hypochlorous acid (HOCl) and hypochlorite ion (OCl-). 
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Because seawater also contains bromide ion, it is important to note that reactions similar to those 

occurring with chloride ion can also be occurring with bromide ion in the electrolytic cell. For 

example, bromide ion will form Br2: 

Reaction 6 (at the anode): 2Br- + 2H2O → Br2 + 2eWhen bromine is produced, it is rapidly hydrolyzed and forms hypobromous acid: 

Reaction 7: Br2 + H2O ↔ HOBr + H+ + BrHypobromous acid (HOBr) undergoes a pH-dependent dissociation to form hypobromite ion (OBr-

): 

 Reaction 8: HOBr ↔ OBr-

 + H+

Thus, depending on pH, one observes a distribution of bromine species as shown in figure 2 below. 

Figure 2 : Distribution of Bromine Species at Different pH Values 

As figure 2 depicts, at the pH of seawater, the solution generated by the BalPure® system will 

also consist of a mixture of hypobromous acid (HOBr) and hypobromite ion (OBr-), with a 

slightly greater proportion of the mixture existing as HOBr. As discussed in section 2.1, the 

combination of Br2, HOBr, and OBr-

 are commonly referred to as free available bromine (FAB). 

When using chlorine-based water disinfection, it is important to discuss the concept of oxidant 

demand and decay. Oxidant demand is defined simply as the difference between the amount of 

oxidant added to the water and the amount of oxidant remaining at the end of a specified contact 

period (i.e. total residual oxidant (TRO)). When an oxidant is added to natural waters, it will react 

(oxidize) with organisms and other components (e.g., natural minerals, organic matter) normally 

present in natural waters. These components, often measured as total organic carbon (TOC), 

determine the oxidant demand of the water. As such, for effective treatment, an oxidant needs to 

be applied at a concentration that exceeds the demand of the water source and also maintain a 

residual concentration within the ballast tanks. This allows for sufficient concentration and 

contact time (C x t) to ensure complete and effective inactivation of AIS. 
MEPC 60/2/9 

ANNEX 

Page 14 

I:\MEPC\60\2-9.doc 

Regardless of the initial oxidant dose, the residual oxidant concentration will decay over time. 

Studies on the demand/decay of TRO (measured as mg Cl2/L) produced by the BalPure® system 

have been performed by the University of Washington. Figure 3 provides an example of the 

decay of TRO observed over time for varying concentrations of hypochlorite treatment. 

 

Figure 3 : Example of Chlorine Demand/Decay at three different TRO 

(measured as Cl2/L) treatments over time. (Treatment 4.A, 3.6 mg/L; 

Treatment 4.B, 3.6 mg/L with immediate neutralization; Treatment 4.C, 

6.0 mg/L) (Herwig, et al., 2006). 

Because water qualities where ballast water uptake may occur can vary by location and season, 

this can impact the oxidant demand. This in turn can affect the hypochlorite dose needed to 

adequately inactivate AIS. Therefore, the effective concentration generated by the BalPure®

system is adjusted based on the TOC concentration. Low TOC concentrations require a lower 

hypochlorite dose, while higher TOC concentrations require a higher hypochlorite dose to meet 

the oxidant demand of the incoming ballast water and also maintain a residual concentration. 

Empirical studies with pilot and full-scale systems over a wide range of water qualities and TOC 

levels have shown that an applied concentration of <20 mg/L of hypochlorite solution results in 

effective ballast water treatment. This relationship can be seen in the brief summary of the 

efficacy results presented above in section 1.1 regarding testing conducted at the University of 

Washington and the Naval Research Laboratory. 

The BalPure® system is designed to control the amount of Active Substances produced to 

effectively treat AIS, yet avoid over-production of the biocide to control the level of potential 

DBPs. This is accomplished using oxidation-reduction potential (ORP) technology. Although 

ORP technology does not directly measure the amount of Active Substances present in the water 

the way a chlorine residual measurement would, ORP allows for an in-line rapid determination of 

the amount of oxidation (or reduction) potential of the water. ORP is measured in millivolts 

(mV) and increases or decreases in direct relation with the oxidant residual in the water 

(Kelley, 2004). For example, natural waters have an ORP reading in the range of 100 mV–150 mV. 

When hypochlorite is added to water, the ORP reading increases with an increase in hypochlorite 

dosage. Similarly, when a de-chlorinating agent such as sodium bisulfite is added to the water, 

the ORP reading will drop to a low mV level (Kelley, 2004). In this way, ORP measurements 

provide a practical and efficient method of controlling biocide dosage and ensure optimized 

water disinfection. More discussion of how the BalPure® system incorporates ORP technology is 

presented in section 8.1.1. 
MEPC 60/2/9 

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I:\MEPC\60\2-9.doc 

2.3 Relevant Chemicals 

2.3.1 Trihalomethanes (THMs) and Haloacetic Acids (HAAs) 

During the disinfection process, reactions with organic materials present in water may result in 

the formation of THMs and HAAs. The amount of THMs and/or HAAs formed as disinfection 

by-products (DBPs) will vary depending on water quality. During pilot scale testing of 

the BalPure® system at the University of Washington, the following THMs have been measured 

in treated ballast water: chloroform, dichlorobromomethane, chlorodibromomethane, and 

bromoform. The following HAAs have been measured in treated ballast 

water: bromochloroacetic acid, monochloroacetic acid, dichloroacetic acid, trichloroacetic acid, 

monobromoacetic acid, and dibromoacetic acid. The presence of tribromoacetic acid was not 

determined analytically during pilot studies and is not anticipated to be present at 

environmentally relevant concentrations. However, tribromoacetic acid will be evaluated during 

land-based testing and reported in a subsequent application for Procedure (G9) Final Approval. 

The existing data for Relevant Chemicals in treated ballast water is presented in section 11, 

“Evaluation of Treated Ballast Water”. 

2.3.2 Bromate 

Formation of bromate may occur during the electrochemical treatment process. The following 

equation shows the reaction occurring at the electrode: 

 Reaction 9: Br-

 + 3H2O → BrO3

-

 + 6eThe amount of bromate formed will vary based on the amount of bromide ion present in the 

incoming seawater and the overall production rate of the treatment system. The concentration of 

bromate in brackish water and seawater treated with the BalPure® system has been analysed and 

this data is presented in Tables 28 and 29, respectively. This constituent will be evaluated further 

during land-based testing. 

Other potential mechanisms for bromate ion formation include the secondary reaction of HOCl 

with bromide ion to form hypobromite ion, which can further react to form bromate ion. 

 Reaction 10: HOCl + Br- → HOBr + ClOnce formed either by the generation of bromine at the anode or from a subsequent secondary 

reaction, hypobromous acid (HOBr) dissociates and depending on the pH of the media, will react 

to form a low level intermediate species (bromite ion, BrO2

-

), and eventually bromate ion 

(BrO3

-

). The reactions of this secondary pathway of bromate formation are: 

 Reaction 11: HOBr ↔ OBr- + H+ 

 Reaction 12: OBr- + OBr- → BrO2

-

 + Br-

 Reaction 13: BrO2

-

 + OBr- → BrO3

-

 + BrAs mentioned previously, reactions 10-13 are dependent on the concentration of available 

bromide ion and pH. At the concentrations of oxidant produced in the electrolytic cell, the 

formation of bromate ion through these secondary pathways is expected to be minimal. 
MEPC 60/2/9 

ANNEX 

Page 16 

I:\MEPC\60\2-9.doc 

2.3.3 Hydrogen gas 

Hydrogen (H2) is formed as a by-product of seawater electrolysis, as can be seen in Reaction 3 

above. Due to the explosive properties of hydrogen gas, allowing it to accumulate in the ballast 

tanks would create an unsafe situation. Therefore, the hydrogen produced during the 

electrochlorination process is separated immediately upon exit from the electrolytic cell using 

a patented cyclone separation device and is not allowed to enter the ballast water piping. 

The separated hydrogen gas is diluted to less than 1% hydrogen by forced air blowers and vented 

to the atmosphere outside of the ship. The lower explosive limit (LEL) for hydrogen is 4% and 

the operating limitations of the system provide a four-fold safety factor. 

As an atmospheric gas that will not be present in treated ballast discharge it is not evaluated in 

regards to aquatic toxicity. Further, exposure to atmospheric gases typically are not included in 

risk assessment, and the safety features inherent in the BalPure® BWMS as well as the physical 

properties of hydrogen gas suggest it is unlikely to accumulate to levels of concern (e.g., above 

the LEL). Therefore, hydrogen gas is not considered relevant for the assessment of human health 

risks. 

2.4 Other chemicals 

2.4.1 Sodium bisulfite 

During discharge of treated water (de-ballasting), sodium bisulfite (NaHSO3) is injected into the 

ballast water discharge line to neutralize residual oxidants that may be present. Bisulfite addition 

is monitored and controlled to apply a small excess (<2 mg/L) to ensure that no residual oxidants 

(HOCl/HOBr) are present in the effluent water. The bisulfite chemically reduces any free 

chlorine and/or hypochlorous acid to chloride ion, the bromine and/or hypobromous acid to 

bromide ion. 

Reaction 14: HSO3

-

+ Cl2 + H2O → HSO4

-

+ 2HCl 

Reaction 15: HSO3

-

+ Br2 + H2O → HSO4

-

+ 2HBr 

Because the pKa for the bisulfate ion/sulfate ion equilibrium is approximately 2, any residual 

bisulfate ion is expected to be in the form of sulfate ion and not contribute to a measurable 

change in the residual sulfate ion concentration. 

Reaction 16: HSO4

-

 ↔ SO4

2- + H+

Seawater typically contains approximately 3 g/L (or 3,000 mg/L) of sulfate ion. On a theoretical 

basis the reaction of the residual oxidant will require 1.77 parts of sodium bisulfite by weight to 

remove one part of halogen (present at mg/L concentrations). Thus, the concentration of sodium 

bisulfite that might be added to the discharged ballast water is negligible and by definition the 

increased sulfate ion concentration in the seawater will also be negligible. The reaction might 

produce up to 5 mg/L of acid, which in the highly buffered ballast water will not lower the 

apparent pH of the treated water. 
MEPC 60/2/9 

ANNEX 

Page 17 

I:\MEPC\60\2-9.doc 

Sodium bisulfite is a very effective oxidant neutralizing agent and an example of TRO 

concentrations after addition to water treated with the BalPure® system is presented in figure 4. 

 

 

Figure 4 : TRO concentration and effect of sodium bisulfite addition to treated water 

(Herwig et al., 2006) 

Because sodium bisulfite is added to treated ballast water discharge in slight excess, Severn Trent 

has evaluated the aquatic toxicity to confirm that the discharge is environmentally acceptable. 

Toxicity data is presented in Tables 2 through 5 and discussed further in section 11.4. 

3 DATA ON EFFECTS ON AQUATIC PLANTS; INVERTEBRATES AND FISH, 

AND OTHER BIOTA, INCLUDING SENSITIVE AND REPRESENTATIVE 

ORGANISMS (G9: 4.2.1.1) 

A literature search was conducted to locate existing aquatic toxicity data for the substances 

associated with the BalPure® system. The data summarized in Tables 2 and 4 present the acute 

and chronic toxicity data that was identified. A complete base-set for fish, crustaceans, and algae 

was not located for all substances and in some cases, the data do not meet validity criteria. 

However, the data has been provided as supporting information and is discussed in relation 

to PNEC derivation in section 11.11. 

Aquatic toxicity data on whole effluent from treated ballast water studies of the BalPure® system 

is presented in Tables 3 and 5. 
MEPC 60/2/9 

ANNEX 

Page 18 

I:\MEPC\60\2-9.doc 

3.1 Acute aquatic toxicity 

Table 2 : Acute Aquatic Toxicity Data 

Test Substance 

F

C

A

Species Test Type E(L)C50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

F Oncorhynchus 

mykiss 15-d survival 0.059 N/A Fisher et al. (1999) 

C Daphnia magna 48-h survival 0.032 N/A Fisher et al. (1999) TRO 

(Freshwater) 

A Natural 

phytoplankton 

47-h change in 

Chla

<0.1 N/A Brooks and Liptak 

(1978) 

F Menidia 

beryllina 96-h survival 0.143 N/A Fisher et al. (1999) 

C Mysidopsis 

bahia 96-h survival 0.062 N/A Fisher et al. (1999) TRO 

(Saltwater) 

A Dunaliella 

primolecta 24-h growth 0.075 N/A Videau et al. (1979)

Active Substance 

F Oncorhynchus 

mykiss 96-h survival 0.032 N/A 

Thatcher (1978) 

(Taken from US 

EPA ECOTOX 

database) 

C Americanmysis 

bahia 7-d survival 0.144 N/A Fisher et al. (1994) 

Hypochlorous 

acid 

A Porphyra 

yezoensis 10-d growth 1.4 N/A Maruyama et al.

(1988) 

Hypobromous 

acid No Data found in literature 

Relevant Chemicals 

F Morone saxatilis 96-h survival 31 N/A Richardson et al. 

(1981) 

C Neomysis 

awatschensis 24-h survival 176 N/A 

Crecelius (1979) 

(Taken from 

US EPA ECOTOX 

database) 

Bromate 

A Glenodinium 

halli Not specified 13.6 N/A Hutchinson, et al. 

(1997) 

THMs 

F Lepomis 

macrochirus 96-h survival 14 N/A 

Anderson & Lusty

(1979) (Taken from 

US EPA ECOTOX 

database) 

Chloroform 

C Artemia salina 24-h survival 30 N/A 

Foster and Tullis 

(1984) 

(Taken from US 

EPA ECOTOX 

database) 
MEPC 60/2/9 

ANNEX 

Page 19 

I:\MEPC\60\2-9.doc 

Test Substance 

F

C

A

Species Test Type E(L)C50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

A Scenedesmus 

subspicatus 48-h growth 950 N/A 

Kuhn and Pattard 

(1990) 

(Taken from US 

EPA ECOTOX 

database) 

F Cyprinodon 

variegates 96-h survival 18 2.9 

Heitmueller et al. 

(1981) 

(Taken from US 

EPA ECOTOX 

database) 

C Daphnia magna 48-h 

immobilization 46 N/A 

LeBlanc, G.A. 

(1980) 

(Taken from US 

EPA ECOTOX 

database) 

Bromoform 

A Skeletonema 

costatum 

96-h growth 

inhibition 12.3 N/A 

US EPA (1978) 

(Taken from US 

EPA ECOTOX 

database) 

Chlorodibromomethane F Cyprinus carpio 

72-120-h egg 

fertilization to 

hatch 

34 N/A Mattice et al.

(1981) 

Dichlorobromomethane F Oryzias latipes 96 h survival 72 N/A Toussaint, et al.

(2000) 

HAAs 

Dichloroacetic 

acid C Daphnia magna 24-h immobilization 106 N/A 

Trenel and Kuhn 

(1982) 

(Taken from US 

EPA ECOTOX 

database) 

F Pimephales 

promelas 96-h survival 2000 N/A 

Dennis et al. (1979) 

(Taken from US 

EPA ECOTOX 

database) 

C Daphnia magna 48-h 

immobilization 2000 N/A 

Dennis et al. (1979) 

(Taken from US 

EPA ECOTOX 

database) 

Trichloroacetic 

acid 

A Chlorella 

pyrenoidosa 72-h growth N/A 500 

Huang and Gloyna 

(1968) (Taken from 

US EPA ECOTOX 

databases) 

Dibromo-acetic 

acid F Pimephales 

promelas 24-h survival 160 N/A 

Mayes (1985) 

(Taken from US 

EPA ECOTOX 

database) 
MEPC 60/2/9 

ANNEX 

Page 20 

I:\MEPC\60\2-9.doc 

Test Substance 

F

C

A

Species Test Type E(L)C50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

F Pimephales 

promelas 48-h survival 107 N/A 

Mayes (1985) 

(Taken from US 

EPA ECOTOX 

database) 

F Pimephales 

promelas 72-h survival 81 N/A 

Mayes (1985) 

(Taken from US 

EPA ECOTOX 

database) 

F Pimephales 

promelas 96-h survival 69 N/A 

Mayes (1985) 

(Taken from US 

EPA ECOTOX 

database) 

Bromochloroacetic acid No data found in 

literature 

F Cyprinus carpio 5-h survival 222 N/A 

Loeb & Kelly 

(1963) (Taken from 

US EPA Ecotox 

Databases) 

C Daphnia magna 24-h survival 34 N/A 

Kuhn (1988) 

(Taken from US 

EPA Ecotox 

Databases) 

Monobromoacetic acid 

A Scenedesmus 

subspicatus 48-h survival 0.34 N/A 

Kuhn & Pattard 

(1990) (Taken from 

US EPA Ecotox 

Databases) 

F No data found in 

literature 

C Daphnia magna 48-h mobility 96 N/A 

Kuhn & Pattard 

1990 

(Taken from US 

EPA Ecotox 

Databases) 

A Scenedesmus 

subspicatus 48-h growth 0.028 N/A 

Kuhn & Pattard 

(1990) 

(Taken from US 

EPA Ecotox 

Databases) 

Monochloroacetic acid 

A Scenedesmus 

subspicatus 48-h growth 0.07 N/A 

Kuhn & Pattard, 

(1990) 

(Taken from US 

EPA Ecotox 

Databases) 

Other Chemicals 

Sodium bisulfite F Carassius 

gibelio 96-h survival 100 N/A MSDS Solvay 

Chemicals (2007) 
MEPC 60/2/9 

ANNEX 

Page 21 

I:\MEPC\60\2-9.doc 

Test Substance 

F

C

A

Species Test Type E(L)C50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

F Gambusia affinis 96-h survival 240 N/A 

Wallen & Lasater 

1957 

(Taken from US 

EPA Ecotox 

databases) 

C Daphnia magna 72-h survival 102 N/A 

Dowden & Bennett 

(1965) 

(Taken from US 

EPA Ecotox 

databases) 

C Daphnia magna 96-h survival 102 N/A 

Freeman L. and 

Fowler I. (1953) 

(Taken from US 

EPA Ecotox 

databases) 

C Daphnia magna 24-h survival 171 N/A 

Dowden B.F. and 

H. Bennett 1965 

(Taken from US 

EPA Ecotox 

databases) 

F= Fish, C = Crustacean, A = Algae 

Table 3 summarizes acute aquatic toxicity tests performed by Nautilus Environmental 

(Nautilus, 2009) on the BalPure® system at differing hypochlorite concentrations. These tests 

were done in conjunction with studies performed at the University of Washington and were not 

intended for evaluation of efficacy. Rather, the tests were to evaluate aquatic toxicity and 

disinfection by-products, and the applied hypochlorite concentrations were based on the organic 

matter present in the test water. Tests were conducted using algae, invertebrates, and fish in 

fresh water, brackish water, and saltwater. All tests followed OECD or US EPA OPPTS testing 

protocols. The samples were collected for toxicity testing on Day 0 (immediately after addition 

of hypochlorite), and on Day 2 and Day 5 after treatment. Following the collection of Day 5 

samples, residual chlorine was neutralized with sodium bisulfite and a second Day 5 

post-neutralization sample was collected for toxicity testing. The neutralized water was then held 

an additional 5 days (i.e. 10 days after hypochlorite treatment) and then evaluated for aquatic 

toxicity. With the exception of the marine algae, Skeletonema, results indicated that the 

neutralization step removed toxicity. The water quality data associated with the samples 

collected for toxicity testing and the testing results are discussed further in section 11 “Evaluation 

of Treated Ballast Water”. 

Documentation of the quality assurance program for toxicity testing at Nautilus Environmental is 

included in appendix A.7.1

 

1

 Appendix A.7 is provided in the confidential dossier of the proposal for approval. 
MEPC 60/2/9 

ANNEX 

Page 22 

I:\MEPC\60\2-9.doc 

Table 3 : Acute Aquatic Toxicity-Treated Ballast Water 

Test 

Substance 

F 

C 

A 

Species 

Days after 

treatment, 

Pre/Post 

neutralization 

Test 

Type 

E(L)C50 

% 

sample 

NOEC 

% 

sample 

References/ 

comments 

Freshwater (average conductivity 1002 μS/cm)

0 

72h 

growth 

(OECD 

201) 

7.76 <6.25 

Nautilus 

Environmental, 

2009 

2 

72h 

growth 

(OECD 

201) 

11.5 <6.25 

Nautilus 

Environmental, 

2009 

5-pre 

72h 

growth 

(OECD 

201) 

>100 25 

Nautilus 

Environmental, 

2009 

5-post* 

72h 

growth 

(OECD 

201) 

>100 100 

Nautilus 

Environmental, 

2009 

A Selenastrum 

capriconutum 

5+* 

72h 

growth 

(OECD 

201) 

>100 100 

Nautilus 

Environmental, 

2009 

0 

48h 

survival 

(OECD 

202) 

3.13 <6.25 

Nautilus 

Environmental, 

2009 

2 

48h 

survival 

(OECD 

202) 

3.13 <6.25 

Nautilus 

Environmental, 

2009 

5-pre 

48h 

survival 

(OECD 

202) 

41.4 25 

Nautilus 

Environmental, 

2009 

5-post* 

48h 

survival 

(OECD 

202) 

>100 100 

Nautilus 

Environmental, 

2009 

6.7 

mg/L 

HOCl 

C Daphnia 

magna 

5+* 

48h 

survival 

(OECD 

202) 

>100 100 

Nautilus 

Environmental, 

2009 
MEPC 60/2/9 

ANNEX 

Page 23 

I:\MEPC\60\2-9.doc 

Test 

Substance 

F 

C 

A 

Species 

Days after 

treatment, 

Pre/Post 

neutralization 

Test 

Type 

E(L)C50 

% 

sample 

NOEC 

% 

sample 

References/ 

comments 

0 

96h 

survival 

(OECD 

203) 

4.03 <6.25 

Nautilus 

Environmental, 

2009 

2 

96h 

survival 

(OECD 

203) 

43.8 25 

Nautilus 

Environmental, 

2009 

5-pre 

96h 

survival 

(OECD 

203) 

>100 100 

Nautilus 

Environmental, 

2009 

5-post* 

96h 

survival 

(OECD 

203) 

>100 100 

Nautilus 

Environmental, 

2009 

F Pimephalus 

promelas 

5+* 

96h 

survival 

(OECD 

203) 

>100 100 

Nautilus 

Environmental, 

2009 

Brackish water (average salinity 22.14 PSU)

0 

96h 

survival 

(EPA 

OPPTS 

850.5400)

8.61 <6.25 

Nautilus 

Environmental, 

2009 

2 

96h 

survival 

(EPA 

OPPTS 

850.5400)

15.9 12.5 

Nautilus 

Environmental, 

2009 

5-pre 

96h 

survival 

(EPA 

OPPTS 

850.5400)

16.4 12.5 

Nautilus 

Environmental, 

2009 

5-post* 

96h 

survival 

(EPA 

OPPTS 

850.5400)

66.1 50 

Nautilus 

Environmental, 

2009 

9.1 

mg/L 

HOCl 

A Skeletonema 

costatum 

5+* 

96h 

survival 

(EPA 

OPPTS 

850.5400)

>100 100 

Nautilus 

Environmental, 

2009 
MEPC 60/2/9 

ANNEX 

Page 24 

I:\MEPC\60\2-9.doc 

Test 

Substance 

F 

C 

A 

Species 

Days after 

treatment, 

Pre/Post 

neutralization 

Test 

Type 

E(L)C50 

% 

sample 

NOEC 

% 

sample 

References/ 

comments 

0 

96h 

survival 

(EPA 

OPPTS 

850.1035)

5.94 6.25 

Nautilus 

Environmental, 

2009 

2 

96h 

survival 

(EPA 

OPPTS 

850.1035)

17.7 12.5 

Nautilus 

Environmental, 

2009 

5-pre 

96h 

survival 

(EPA 

OPPTS 

850.1035)

17.5 12.5 

Nautilus 

Environmental, 

2009 

5-post* 

96h 

survival 

(EPA 

OPPTS 

850.1035)

>100 100 

Nautilus 

Environmental, 

2009 

C Americamysis 

bahia 

5+* 

96h 

survival 

(EPA 

OPPTS 

850.1035)

>100 100 

Nautilus 

Environmental, 

2009 

0 

96h 

survival 

(EPA 

OPPTS 

850.1075)

11.7 6.25 

Nautilus 

Environmental, 

2009 

2 

96h 

survival 

(EPA 

OPPTS 

850.1075)

28.4 25 

Nautilus 

Environmental, 

2009 

5-pre 

96h 

survival 

(EPA 

OPPTS 

850.1075)

22.6 12.5 

Nautilus 

Environmental, 

2009 

F Cyprinodon 

variegatus 

5-post* 

96h 

survival 

(EPA 

OPPTS 

850.1075)

>100 100 

Nautilus 

Environmental, 

2009 
MEPC 60/2/9 

ANNEX 

Page 25 

I:\MEPC\60\2-9.doc 

Test 

Substance 

F 

C 

A 

Species 

Days after 

treatment, 

Pre/Post 

neutralization 

Test 

Type 

E(L)C50 

% 

sample 

NOEC 

% 

sample 

References/ 

comments 

 

5+* 

96h 

survival 

(EPA 

OPPTS 

850.1075)

>100 100 

Nautilus 

Environmental, 

2009 

Saltwater (average salinity 31 PSU)

0 

96h 

survival 

(EPA 

OPPTS 

850.5400)

33.4 25 

Nautilus 

Environmental, 

2009 

2 

96h 

survival 

(EPA 

OPPTS 

850.5400)

34.5 25 

Nautilus 

Environmental, 

2009 

5-pre 

96h 

survival 

(EPA 

OPPTS 

850.5400)

38 25 

Nautilus 

Environmental, 

2009 

5-post* 

96h 

survival 

(EPA 

OPPTS 

850.5400)

>100 100 

Nautilus 

Environmental, 

2009 

A Skeletonema 

costatum 

5+* 

96h 

survival 

(EPA 

OPPTS 

850.5400)

>100 100 

Nautilus 

Environmental, 

2009 

0 

96h 

survival 

(EPA 

OPPTS 

850.1075)

10.5 6.25 

Nautilus 

Environmental, 

2009 

2 

96h 

survival 

(EPA 

OPPTS 

850.1075)

16.7 12.5 

Nautilus 

Environmental, 

2009 

4.3 

mg/L 

HOCl 

C Americamysis 

bahia 

5-pre 

96h 

survival 

(EPA 

OPPTS 

850.1075)

16.8 12.5 

Nautilus 

Environmental, 

2009 
MEPC 60/2/9 

ANNEX 

Page 26 

I:\MEPC\60\2-9.doc 

Test 

Substance 

F 

C 

A 

Species 

Days after 

treatment, 

Pre/Post 

neutralization 

Test 

Type 

E(L)C50 

% 

sample 

NOEC 

% 

sample 

References/ 

comments 

5-post* 

96h 

survival 

(EPA 

OPPTS 

850.1075)

>100 100 

Nautilus 

Environmental, 

2009 

 

5+* 

96h 

survival 

(EPA 

OPPTS 

850.1075)

>100 100 

Nautilus 

Environmental, 

2009 

0 

96h 

survival 

(EPA 

OPPTS 

850.1075)

24.3 25 

Nautilus 

Environmental, 

2009 

2.5-pre 

96h 

survival 

(EPA 

OPPTS 

850.1075)

28.3 12.5 

Nautilus 

Environmental, 

2009 

5-pre 

96h 

survival 

(EPA 

OPPTS 

850.1075)

35 25 

Nautilus 

Environmental, 

2009 

5-post* 

96h 

survival 

(EPA 

OPPTS 

850.1075)

>100 100 

Nautilus 

Environmental, 

2009 

4.3 

mg/L 

HOCl 

F Cyprinodon 

variegatus 

5+* 

96h 

survival 

(EPA 

OPPTS 

850.1075)

>100 100 

Nautilus 

Environmental, 

2009 

F= Fish, C = Crustacean, A = Algae; *Samples neutralized with sodium bisulfite. 
MEPC 60/2/9 

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Page 27 

I:\MEPC\60\2-9.doc 

3.2 Chronic aquatic toxicity 

The following table summarizes data found in literature concerning chronic aquatic toxicity for 

the substances associated with the BalPure® system. The available chronic data was limited for 

some chemicals. Chronic toxicity data for treated ballast water is presented in Table 5 below. 

Table 4 : Overview of Chronic Aquatic Toxicity 

Test 

Substance 

F

C

A

Species Test Type EC50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

Active Substance 

F Ictalurus 

punctatus 134-d growth N/A 0.005 Hermanutz et 

al. (1990) 

C Gammarus 

pseudolimnaeus 70-d fecundity N/A 0.012 Arthur et al. 

(1975) 

TRO 

(Freshwater) 

A Natural algae 24-d inhibition of 

biomass N/A 0.079 Pratt et al(1988) 

F Menidia 

peninsula

32-d egg to posthatch N/A 0.04 Goodman et al. 

(1983) 

C Panaeus 

kerathurus 

7-d 

growth/molting N/A 0.079 Saroglia and Scarano (1979) 

TRO 

(Saltwater) 

A Natural 

phytoplankton 

21-d reduction in 

cell density N/A 0.001 Sanders et al.(1981) 

F Oncorhynchus 

kisutch 23-d survival N/A 0.101 Holland 

Hypochlorous et al.(1960) 

acid C Americamysis 

bahia 7-d reproduction N/A 0.048 Fisher et al. 

(1994) 

Hypobromous 

acid No data found in literature 

Relevant Chemicals 

F Morone 

saxatilis 10-d survival 93 50 Richardson et 

al. (1981) 

Bromate 

A Isochrysis 

galbana 

7-d growth 

inhibition N/A 8 

Erickson & 

Freeman (1978) 

(taken from US 

EPA Ecotox 

databases) 

THMs 

F Oryzias 

latipes 9- month growth N/A 1.5 Toussaint et al. 

(2001) 

C Daphnia 

magna 21-d reproduction N/A 13 

Kuhn et. al 

(1988) (Taken 

from US EPA 

Ecotox 

databases) 

Chloroform 

A Skeletonema 

costatum 

5-d reduction in 

cell volume 477 216 Cowgill et al. (1989) 
MEPC 60/2/9 

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Page 28 

I:\MEPC\60\2-9.doc 

Test 

Substance 

F

C

A

Species Test Type EC50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

F Cyprinodon 

variegates 28d- growth N/A 8.5 

Ward et al.

1981(Taken 

from US EPA 

from Ecotox 

databases) Bromoform 

A

Pseudokirchne

riella 

subcapitata 

96-h biochemistry 

change N/A 26.1 

U.S. EPA 

(1978) 

(Taken from US 

EPA Ecotox 

databases) 

Dichlorobromomethane No data found 

in literature 

Chlorodibromomethane No data found 

in literature 

HAAs 

Dichloroacetic 

acid A Scenedesmus 

subspicatus 

7-d cell 

proliferation 

1485 

(EC0

3) 

N/A 

Trenel and 

Kuhn (1982) 

(from ECOTOX 

databases) 

Dibromoacetic 

acid No data found in literature 

A Scenedesmus 

quadricauda 

7-d growth 

threshold N/A 200 OECD SIDS (2008) 

Trichloroacetic 

acid A Chlorella 

vulgaris 

4d-population 

change N/A 100 

Garten (1990) 

(taken from US 

EPA Ecotox 

databases) 

Bromochloroacetic acid No data found 

in literature 

C Daphnia 

magna 

21d-NOEC N/A 3.2 

Kuhn (1988) 

(Taken from US 

EPA Ecotox 

databases) Monobromoacetic acid 

A Scenedesmus 

subspicatus 

3d-population 

change N/A 1.4 

Kuhn & Pattard 

(1990) 

(Taken from US 

EPA Ecotox 

databases) 

Monochloroacetic acid C Daphnia 

magna 

21d-reproduction 

change N/A 32 

Kuhn & Pattard 

(1990) (Taken 

from US EPA 

Ecotox 

databases) 
MEPC 60/2/9 

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Page 29 

I:\MEPC\60\2-9.doc 

Test 

Substance 

F

C

A

Species Test Type EC50 

mg/L 

NOEC 

mg/L 

Reference/ 

comments 

A Scenedesmus 

subspicatus 7d-histology 

(EC0

3) 

0.13 

N/A 

Trenel and 

Kuhn (1982) 

(Taken from US 

EPA Ecotox 

databases) 

Other Chemicals 

Sodium 

bisulfite No data found in literature 

 F= Fish, C = Crustacean, A = Algae 

Chronic toxicity tests were conducted by Nautilus Environmental (Nautilus, 2007) using treated 

ballast water samples collected during the full-scale study at the Naval Research Facility in Key 

West, Florida (United States). The applied hypochlorite concentration was based on the level of 

organic matter present in the test water. Samples were collected from challenge tests in which 

organism and organic enriched ballast water was treated with hypochlorite to a 15 mg/L total 

residual oxidant (TRO) concentration and then held for 48 hours (2 days). After 48 hours the 

treated water was neutralized with an excess concentration of ~ 2 mg/L sodium bisulfite. Five 

concentrations of treated sample using a 0.5X dilution series were tested. Bioassays were 

conducted using 7-day tests with a mysid (Americamysis bahia) and a larval fish (Menidia 

beryllina), a 48-hour larval development test using a mussel (Mytilus galloprovincialis), and 

a 48-hour germination and germ tube length test using the giant kelp (Macrocystis pyrifera). 

Chronic toxicity tests using mysid shrimp and silverside minnows were conducted according 

to US EPA (2002) methods. Chronic toxicity tests using mussels and giant kelp were conducted 

according to US EPA (1995) methods. Documentation of the quality assurance program for 

toxicity testing at Nautilus Environmental is included in appendix A.72

. 

Results for the chronic toxicity tests are summarized in Table 5 below and discussed further in 

section 11 “Evaluation of Treated Ballast Water”. No toxicity was observed with the treated 

water samples for any species tested. The highest concentration with no observed effect (NOEC) 

was 100 percent sample (Nautilus, 2007). 

 

2

 Appendix A.7 is provided in confidential dosier of the proposal for approval. 
MEPC 60/2/9 

ANNEX 

Page 30 

I:\MEPC\60\2-9.doc 

Table 5 : Chronic Aquatic Toxicity-Treated Ballast Water 

Test 

Substance 

F

C

A 

Species 

Days after 

hypochlorite 

treatment, plus 

neutralization 

Test Type 

E(L)C50 

% 

Sample 

NOEC 

% 

Sample 

References/ 

comments 

Seawater (average salinity 36 PSU)

F Menidia 

beryllina 2 days 

7 day 

survival 

(EPA R821-02-

014) 

>100 100 

Nautilus 

Environmental, 

2007 

F Menidia 

beryllina 2 days 

7 day 

survival 

(EPA R821-02-

014) 

>100 100 

Nautilus 

Environmental, 

2007 

C Americamysis 

bahia 2 days 

7 day 

survival 

(EPA R821-02-

014) 

>100 100 

Nautilus 

Environmental, 

2007 

C Americamysis 

bahia 2 days 

7 day 

survival 

(EPA R821-02-

014) 

>100 100 

Nautilus 

Environmental, 

2007 

B Mytilus 

galloprovincialis 2 days 

48 hour 

larval 

developme

nt (EPA 

600-R-95-

136) 

>100 100 

Nautilus 

Environmental, 

2007 

A Macrocystis 

pyrifera 2 days 

48 hour 

germination

(EPA 600-

R-95-136) 

>100 100 

Nautilus 

Environmental, 

2007 

15.0 

mg/L 

HOCl 

A Macrocystis 

pyrifera 2 days 

48 hour 

germ tube 

length 

(EPA 600-

R-95-136) 

>100 100 

Nautilus 

Environmental, 2007 

F = Fish, C = Crustacean, B = Bivalve, A = Algae 
MEPC 60/2/9 

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Page 31 

I:\MEPC\60\2-9.doc 

3.3 Endocrine disruption 

Endocrine disrupting chemicals (EDCs) are defined as “exogenous substances that cause adverse 

effects in an organism or its progeny, consequent to changes in endocrine functions”. 

In a recently conducted study to investigate whether chlorinated by-products formed through 

wastewater disinfection were estrogenic, no relationship was found between the formation 

of THMs and estrogenic activity (Schiliro 2009). In fact, chlorination of surface water and 

effluents was found to decrease estrogenic activity, which is thought to be due to the oxidation 

effects of chlorine (Lee, 2004). A thorough review of the literature found no indications that 

either of the Active Substances in the TRO (HOCl/HOBr) or the chemically more 

complex THMs/HAAs were EDCs. 

3.4 Sediment toxicity 

The sediment toxicity of a chemical is a function of the ability of the chemical to be adsorbed to 

sediment as well as its persistence and toxicity. The organic carbon partition coefficient (Koc) is 

a measure of the tendency of an organic substance to be adsorbed by soil or sediment. 

The TRO Active Substances are all inorganic substances and therefore have a very low 

calculated Koc as presented in Table 6 below. None of the organic Relevant Chemicals 

(THMs/HAAs) appear to have the potential to be absorbed to sediments to a significant extent 

based on their low Kocs (<500 L/kg) and other information in the literature (HSDB/TOXNET). 

The low Kocs for all of the chemicals in Table 6 indicate that the chemicals would not readily 

partition to sediment and therefore be of concern to benthic organisms residing in the sediment. 

Table 6 : KOCs for Active Substances and Relevant Chemicals 

Chemical Koc(L/kg) Reference 

Active Substances 

TRO NA 

Hypochlorous acid 13.2 As calculated − EPI Suite 

(2009c)

Hypobromous acid 13.2 As calculated − EPI Suite 

(2009b)

Relevant Chemicals 

Bromate 31.8 As calculated − EPI Suite 

(2009a)

THMs 

Chloroform 153-196 HSDB/TOXNET (2009f)

Bromoform 35 HSDB/TOXNET (2009l)

Dichlorobromomethane 9 HSDB/TOXNET (2009c)

Chlorodibromomethane 84 HSDB/TOXNET (2009e)

HAAs 

Bromochloroacetic 

acid 1.9 HSDB/TOXNET (2009b)

Monochloroacetic acid 31 HSDB/TOXNET (2009d)

Monobromoacetic acid 1.9 HSDB/TOXNET (2009a)

Dichloroacetic acid 75 HSDB/TOXNET (2009h)

Trichloroacetic acid 130 HSDB/TOXNET 

(2009m)
MEPC 60/2/9 

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Chemical Koc(L/kg) Reference 

Dibromoacetic acid 1.5 HSDB/TOXNET (2009g)

Other Chemicals 

Sodium bisulfite 2.2 As calculated − EPI Suite 

(2009d) 

3.5 Bioavailability/biomagnification/bioconcentration 

The bioconcentration factor (BCF) is the concentration of a particular chemical in a tissue per 

concentration of chemical in water (reported as L/kg). This physical property characterizes the 

accumulation of pollutants through chemical partitioning from the aqueous phase into an organic 

phase, such as fish or other aquatic organism tissues. The BCF is the best measure of 

bioavailability, biomagnification, and bioconcentration. Typical BCFs for organic chemicals in 

fish and most aquatic invertebrates are in the 500 – 1000 range. The BCFs summarized 

in Table 7 below are all much lower indicating a low potential for significant 

bioconcentration/bioaccumulation in aquatic organisms (HSDB/TOXNET). Little 

biomagnification should occur in a food web since the chemicals are not readily bioconcentrated 

or bioaccumulated. 

Table 7 : BCFs for Active Substances and Relevant Chemicals 

Chemical BCF (L/kg) Reference 

Active Substances

TRO NA

Hypochlorous acid 3.2 As calculated − EPI Suite 

Hypobromous acid 3.2 As calculated − EPI Suite 

Relevant Chemicals

Bromate 3.2 As calculated − EPI Suite 

THMs 

Chloroform 2.9-10.35 HSDB/TOXNET (2009f) 

Bromoform 14 HSDB/TOXNET (2009l) 

Dichlorobromomethane 7 HSDB/TOXNET (2009c)

Chlorodibromomethane 9 HSDB/TOXNET (2009e) 

HAAs 

Bromochloroacetic acid 3.2 HSDB/TOXNET (2009b)

Monochloroacetic acid 3.1 HSDB/TOXNET (2009d)

Monobromoacetic acid 3.2 HSDB/TOXNET (2009a)

Dichloroacetic acid 0.3 HSDB/TOXNET (2009h) 

Dibromoacetic acid 0.17 HSDB/TOXNET (2009g) 

Trichloroacetic acid 0.1-1.7 HSDB/TOXNET (2009m) 

Other Chemicals

Sodium Bisulfite 3.2 As calculated − EPI Suite 
MEPC 60/2/9 

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I:\MEPC\60\2-9.doc 

3.6 Food web/population effects 

Population and food web effects can occur if substances have properties that tend to 

bioaccumulate and/or persist in the environment. Little biomagnification and persistence in 

aquatic and mammalian food webs is anticipated from the Active Substances 

or Relevant Chemicals. This conclusion is based on the low Kocs of the chemicals. All of the 

Kocs for the Active Substances and Relevant Chemicals (section 3.4) are <500 L/kg which 

indicate that the chemicals would not readily absorb to sediment and therefore be a concern to 

benthic populations and their food webs. Similarly, the BCFs also show that little 

bioconcentration/bioaccumulation will occur in aquatic organisms (section 3.5). 

4 DATA ON MAMMALIAN TOXICITY (G9: 4.2.1.2) 

The Tables 8 through 14 below present data on mammalian toxicity for different endpoints and 

effects. The information was located through literature reviews of existing data from a variety of 

governmental organizations such as the World Health Organization, the International Programme 

on Chemical Safety, and the United States Environmental Protection Agency. In some cases, 

data was gathered from Material Safety Data Sheets (MSDS). 

In the studies reviewed, the chemicals were tested for various exposure routes (oral, dermal, etc.) 

and/or chemical forms, which do not necessarily reflect the actual potential exposure routes or 

chemical forms associated with the BalPure® system. Potential for human exposure to the 

substances associated with the BalPure® system is discussed in detail in section 12.2. 

4.1 Acute toxicity 

Table 8 : Acute Mammalian Toxicity Data 

Test Substance Exposure 

Route Species Value range Reference/ Comments 

Active Substance 

Hypochlorous acid (test 

concentration not 

specified) 

a. Oral 

LD50 

b. Oral 

LD50 

a. Rat 

b. Mouse 

a. 8900 mg/kg 

b. 5800 mg/kg 

HSDB/TOXNET 

(2009i)

Hypobromous acid 

No data found in 

literature. 

Thought to have 

similar toxicity to 

chlorinated 

analogue. 

Relevant Chemicals 

Bromate Oral 

LD50 

Rats, mice and 

hamsters 280-495 mg/kg IPCS (2000a) 

HAAs 

Bromochloro-acetic 

acid 

2-Week 

Oral 

Drinking 

Water 

Study 

a. Rat 

b. Mice 

a. NOEL = 140 

mg/kg/day 

b. NOEL = 170 

mg/kg/day 

NTP (2009) 
MEPC 60/2/9 

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Page 34 

I:\MEPC\60\2-9.doc 

Test Substance Exposure 

Route Species Value range Reference/ Comments 

Monochloro-acetic acid 

a. Oral 

LD50 

b. Skin 

LD50 

c. Oral 

LD50 

 

a. Mouse 

b. Rabbit 

c. Mice, male 

rats, and male 

guinea pigs 

a. 260 mg/kg 

b. 230 mg/kg 

c. 255, 76, and 80 

mg/kg respectively 

a,b. IPCS (2000a) 

c. WHO (2004b) 

Monobromo-acetic 

acid 

Oral 

LD50 a. Rat 177 mg/kg ICPS (2000a) 

Dichloroacetic acid 

a. Oral 

LD50 

b. Oral 

LD50 

a. Rat 

b. Mouse 

a. 4500 mg/kg 

b. 5500 mg/kg IPCS (2000a) 

Dibromoacetic Acid Oral 

LD50 a. Rat 1737 mg/kg WHO (2004a) 

Trichloroacetic acid 

a. Oral 

LD50 

b. Oral 

LD50 

a. Rat 

b. Mouse 

a. 3300 mg/kg 

b. 4900 mg/kg IPCS (2000a) 

THMs 

Chloroform 

a. Oral 

LD50 

b. Oral 

LD50 

c. 

Inhalation 

LC50, 6 h 

exposure 

a. Rat 

b. Mice 

c. Rats 

a. 450-2000 mg/kg 

b. 36-1366 mg/kg 

c. 9.2 g/m3

IPCS (2004) 

Bromoform 

a. Oral 

LD50 

b. Oral 

LD50 

a. Male 

rats/female rats 

b. Male 

mice/female 

mice 

a. 1388 

mg/kg/1147 mg/kg 

b. 1400 

mg/kg/1550 mg/kg 

IPCS (2000a) 

Dichlorobromomethane Oral 

LD50 

Male 

rats/female rats 

430 mg/kg/510 

mg/kg 

ATSDR & US 

EPA 

(1989) 

Chlorodibromomethane 

a. Oral 

LD50 

b. Oral 

LD50 

a. Male 

Rats/female rats 

b. Male 

mice/female 

mice 

a. 1186 mg/kg/848 

mg/kg 

b.800 

mg/kg/1200mg/kg 

IPCS (2000a) 

Other Chemicals 

Sodium bisulfite Oral 

LD50 Rat 2000 mg/kg 

Health Council of 

the Netherlands 

(2005) 
MEPC 60/2/9 

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4.2 Effects on skin and eye 

Table 9 : Skin, Eye and Dermal Effects 

Test 

Substance Skin Eye Sensitization Reference/ comments 

Active Substance 

Hypochlorous 

acid 

Irritant at 

concentrations 

≥5% 

Irritant at 

concentrations 

≥5%; 

concentrations 

≥12.5% 

corrosive to 

eye 

Low potential for 

sensitization after 

chronic exposure to 

damaged skin; in 

Patch tests on 

humans show 

positive results for 

concentrations 

ranging from 0.3-2% 

HSDB/TOXNET 

(2009i), 

EU (2007b)

Hypobromous 

acid 

No data found in 

literature. 

Thought to have 

similar toxicity 

to chlorinated 

analogue. 

Relevant Chemicals 

Bromate (as 

sodium 

bromate) 

Causes 

irritation 

Causes 

irritation 

No data found in 

literature 

HSDB/TOXNET 

(2009k)

THMs 

Chloroform 

Causes 

irritation 

(redness and 

pain) 

(10μg/m3

) 

Causes 

irritation 

Possible damage to 

nervous system, 

heart, liver, and 

kidneys; Possible 

dermatitis 

IPCS (2004) 

Bromoform Causes 

irritation 

Causes 

irritation 

Greater risk 

sensitization for 

those with preexisting 

skin/respiratory 

problems 

U.S. Dept. 

Health and 

Human Services 

& ATSDR 

(2005) 

Dichlorobromomethane 

Causes 

irritation; 

Levels of 13-34 

μg/L show a 

measurable 

body burden 

for humans 

(from 

chlorinated 

swimming 

pools) 

Causes 

irritation 

No data found in 

literature 

HSDB/TOXNET 

(2009c), NTP 

1991 
MEPC 60/2/9 

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Page 36 

I:\MEPC\60\2-9.doc 

Test 

Substance Skin Eye Sensitization Reference/ comments 

Chlorodibromomethane Causes 

irritation 

Causes 

irritation 

No data found in 

literature 

U.S. Dept. 

Health and 

Human Services 

& ATSDR 

(2005) 

HAAs 

Bromochloroacetic acid Causes skin 

burns 

Causes eye 

burns 

No data found in 

literature 

HSDB/TOXNET 

(2009b)

Monochloroacetic acid 

Corrosive, 

causes skin 

burns; 

concentrations 

above 40% are 

toxic to dermal 

tissue 

Corrosive, 

causes eye 

burns and 

blurred vision; 

0.9% solution 

causes severe 

eye irritation 

Liver and kidney 

damage after chronic 

exposure 

Mallinckrodt 

Baker MSDS 

(2006a), 

EU (2005) 

Monobromoacetic acid Causes skin 

burns 

Causes eye 

burns 

Liver, kidney, and 

muscle damage after 

chronic exposure 

HSDB/TOXNET 

(2009a)

Dichloroacetic 

acid 

Redness, 

blisters, serious 

skin burns 

Redness, 

severe burns 

No data found in 

literature IPCS (2000c) 

Dibromoacetic 

acid 

Causes skin 

burns 

Causes eye 

burns 

No data found in 

literature 

Sigma Aldrich 

MSDS 

(2009) 

Trichloroacetic 

acid 

Corrosive, 

causes 

irritation, and 

moderate burns 

Corrosive, 

causes 

irritation and 

moderate 

burns 

No data found in 

literature 

ATSDR & 

OSHA (1989) 

Other Chemicals 

Sodium 

bisulfite 

NOAEL 0.5% 

solution 

Causes 

irritation 

No data found in 

literature 

Mallinckrodt 

Baker MSDS 

(2006b), 

EU (2000) 

 Note: Test concentrations are provided when specified in the reference document. 
MEPC 60/2/9 

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4.3 Repeated-dose toxicity 

Table 10 : Repeated-dose toxicity 

Chemical Exposure Route Species Value Range Reference/ 

Comments 

Active Substances

Hypochlorous 

acid 

a. Oral, 90-day, 

drinking water 

b. Oral, 90-day, 

drinking water 

a. Rats 

b. Mice 

a. NOAEL, 10 mg/kg-day 

b. Spleen/liver weights 

depressed in males, but 

not females at the higher 

doses* 

IPCS (2000a) 

Hypobromous 

acid 

 

No data found 

in literature. 

Thought to 

have similar 

toxicity to 

chlorinated 

analogue. 

Relevant Chemicals

Bromate 

 Oral, drinking 

water, 13 weeks, 

doses 0-10,00-

mg/L 

Rats 

b. LOAEL=63 mg/kg 

bw/d (body weight gain, 

serum parameters, kidney 

effects) 

IPCS (2000a) 

US EPA 

(2001a) 

THMs 

Chloroform 

a. Oral, gavage, 

90 d, 0-270 

mg/kg/d 

b. Oral, drinking 

water, 1-6 

months, 0-1,800 

mg/L (0-263 

mg/kg) 

Mice 

a. LOAEL 60 mg/kg 

(liver effects) 

b. NOAEL 34 mg/kg 

a. IPCS 

(2000a) 

b. US EPA 

(2001b) 

Bromoform Gavage, 13 

weeks 

Rats and 

mice 

NOAEL, 25 mg/kg/day 

(rats) & 100 mg/kg/day 

(mice) 

IPCS (2000a) 

Dichlorobromomethane 

Oral, gavage, 13 

weeks, 

a. 0-300 mg/kg/d 

b. 0-400 mg/kg/d 

a. Rats 

b. Mice 

a. NOAEL 75 mg/kg/d 

(decrease in body weight) 

b. NOAEL 50 mg/kg/d 

(kidney lesions) 

NTP (1987) 

Chlorodibromomethane 

a. gavage, 13 

weeks 

b. gavage, 90 

days 

a. Rats and 

mice 

b. Rats 

a. NOAEL 30 mg/kg/day 

b. kidney damage at 50 & 

100mg/kg/day* 

IPCS (2000a) 

HAAs

Bromochloroacetic acid 

Drinking water, 

3 months, 0-1000 

mg/L 

a. 0-85 mg/kg 

b. 0-140 mg/kg 

a. Rats 

b. Mice 

a. NOAEL 20 mg/kg/d 

(increased liver weight) 

b. LOAEL 8 mg/kg/d 

(hematopoietic cell 

proliferation in the spleen) 

NTP (2009) 
MEPC 60/2/9 

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Page 38 

I:\MEPC\60\2-9.doc 

Chemical Exposure Route Species Value Range Reference/ 

Comments 

Monochloro

-acetic acid 

Oral gavage, 13 

weeks 

a. 0-150 mg/kg/d 

b. 0-200 mg/kg/d 

a. Rats 

b. Mice 

a. LOAEL 30 mg/kg/d 

(changes in heart, liver, 

and kidney weights, 

clinical chemistry values) 

b. NOAEL 100/LOAEL 

150 mg/kg/s (increased 

liver weight) 

NTP (1992b), 

EU (2005) 

Monobromoacetic acid 

 No data 

available 

Dichloroacetic acid 

a. Oral, 90 days, 

doses up to 72 

mg/kg/d 

b. oral, 30 days 

c. oral, 90 days 

a. Dogs 

b. Mice 

c. Rats 

a. LOAEL 12.5 mg/kg/d 

(liver effects, testicular 

degeneration) 

b. LOAEL 

70-100 mg/kg/day 

c. LOAEL 125 mg/kg/day 

IPCS (2000a) 

Dibromoacetic acid 

Oral, drinking 

water, 3 months, 

0-2000 mg/L 

a. Rats 

b. Mice 

Increased liver weights 

a. LOAEL 10 mg/kg/d 

b. LOAEL 56 mg/kg/d, 

NOAEL 30 mg/kg/d 

NTP 2007 

Trichlor 

acetic acid 

a. Oral, 90 days, 

0-355 mg/kg/day 

b. Oral, 90 days, 

785 mg/kg/day 

a. Rats 

b. Rats 

a. decrease in body 

weight, NOAEL 

36.5 mg/kg/d 

b. minimal evidences of 

liver damage* 

IPCS (2000a) 

Other Chemicals

Sodium 

bisulfite 

Oral, drinking 

water, 5-8 week 

study 

Rats NOAEL 70 mg/kg bw/day 

Health 

Council of the 

Netherlands 

(2005) 

 *No NOAEL/LOAEL reported 
MEPC 60/2/9 

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I:\MEPC\60\2-9.doc 

4.4 Chronic toxicity 

The data located in a literature search for chronic mammalian studies (six months or longer) is 

presented below. 

Table 11 : Chronic Mammalian Toxicity 

Test Substance Exposure Route Species Value range Reference/ 

comments 

Active Substance 

Hypochlorous 

acid 

Oral, drinking water, 

2-year 

Mice 

and 

rats 

NOAEL= 14 mg/kg/d 

Dilation of renal 

tubules in male mice 

IPCS (2000a) & 

NTP (1992a) 

Hypobromous 

acid 

No data found in 

literature. 

Thought to have 

similar toxicity 

to chlorinated 

analogue. 

Relevant Chemicals 

Bromate 

Oral, drinking water, 

100 weeks 

a. 0-400 mg/L 

b. 0-800 mg/L 

a. Rats 

b. Mice

a. kidney effects, 

NOAEL 1.1 mg/kg/d 

b. no effects, NOAEL 

>60 mg/kg/d 

US EPA (2001a) 

THMs

Chloroform 

a. Oral, gavage, 

2-years 

b. Oral, 7.5 years, 

toothpaste 

a. Mice 

and 

rats 

b. Dogs

a. liver effects noted, 

including tumors* 

b. LOAEL, 

15 mg/kg/day 

(6 days/week) 

a. IPCS (2004) 

b. US Dept. of 

Health and 

Human Services 

in ATSDR 

(1997) 

Bromoform Gavage, 2-year, doses 

up to 200 mg/kg/day 

Mice 

and 

rats 

LOAEL 100 mg/kg/d 

(liver effects) 

IPCS (2000a) 

US Dept. Health 

and ATSDR 

(2005) 

Dichlorobromomethane 

a. Gavage, 104 week 

study, doses 5 

days/week 

b. Gavage, 104 week 

study, doses 5 

days/week 

a. Rats 

b. Mice

a. NOAEL 

100 mg/kg/day 

b. LOAEL 

25 mg/kg/day (renal 

cytomegaly) 

a. ATSDR & US 

EPA (1989) 

b. US EPA 

(1991c) 

Chlorodibromomethane 

Oral gavage, 2-years 

a. 0/40/80 mg/kg/d 

b. 0/50/100 mg/kg/d 

a. Rats 

b. Mice

Kidney and liver effects 

noted at all doses* IPCS (2000a) 
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Test Substance Exposure Route Species Value range Reference/ 

comments 

HAAs

Bromochloroacetic acid 

Oral, drinking water, 

2 years, 0-1000 mg/L 

a. 0-50 mg/kg 

b. 0-90 mg/kg 

a. Rats 

b. Mice

a. NOAEL 13 mg/kg/d 

(non-neoplastic lesions 

in the liver) 

b. LOAEL 15 mg/kg/d 

(non-neoplastic and 

neoplastic liver effects) 

NTP (2009) 

Monochloroacetic acid 

Oral, drinking water, 

104 weeks, 

0-60 mg/kg/d 

Rats 

NOAEL 3.5/LOAEL 

26 mg/kg/d (changes in 

body weight) 

EU (2005)

Monobromoacetic acid No long-term toxicity studies for any exposure route were 

identified WHO (2004a) 

Dichloroacetic 

acid 

Oral, drinking water, 

2 years, doses up to 

2 g/L 

a. Rats 

b. Mice

a. Dose dependent 

increase in liver tumor 

incidence, LOAEL 

40 mg/kg/d, NOAEL 

4 mg/kg/d 

b. 80% increase in liver 

tumor incidence at 

95 mg/kg/d 

IPCS (2000a) 

Dibromoacetic 

acid 

Oral, drinking water, 

2 years, 0-1000mg/L 

a. Rats 

b. Mice 

a. LOAEL 2mg/kg/d 

(liver effects in males, 

kidney effects in 

females) 

b. liver tumors, male: 

LOAEL 4/mg/kg/d, 

female: LOAEL 

35/NOAEL 4 mg/kg/d 

NTP (2007) 

Trichloroacetic 

acid 

Oral, 2-year, doses up 

to 5g/L 

a. Rats 

b. Mice 

a. liver effects, NOAEL 

32.5 mg/kg/d 

b. dose-dependent 

increase in liver tumors, 

NOAEL 40 mg/kg/d 

IPCS (2000a) 

Health Canada 

(2009) 

Other Chemicals 

Sodium 

bisulfite 

a. Oral, 3 generation 

study, doses from 

0.125-20 g/L 

a. Oral, doses from 

0.1%-2% conc. for 

2 years 

a. Rats 

b. Rats 

a. No evidence of 

systemic toxicity at 

levels of 10 g/L or 

20 g/L; calculated 

NOAEL 72/kg/day 

b. LOAEL 0.1%. 

Reduced survival and 

body weight, 

myocardial fibrosis, and 

renal calcification at 

doses of 0.25% and 

higher 

a. Health 

Council of the 

Netherlands 

(2005) 

b. 

HSDB/TOXNET

(2009j)

 *No NOEAEL/LOAEL reported
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4.5 Developmental and reproductive toxicity 

Table 12 : Summary of Developmental and Reproductive Toxicity Data 

Chemical Exposure 

Route Species Effects Reference/ 

Comments 

Active substances 

Hypochlorous acid 

Oral, 

chlorinated 

drinking water, 

10 mg/kg/day 

for 7 

generations 

Rats No effects on fertility, 

growth, or survival IPCS (2000a) 

Hypobromous acid 

No data found in 

literature. 

Thought to have 

similar toxicity to 

chlorinated 

analogue. 

Relevant chemicals

Bromate (as 

sodium bromate) 

Oral, drinking 

water, 35d, 

doses up to 

250 mg/L 

Rats 

Male fertility: decreased 

sperm density, NOAEL 7.7 

mg/kg/d, female fertility: 

no effects, NOAEL >22 

mg/kg/d 

US EPA (2001a)

THMs

Chloroform Doses up to 

41 mg/kg/day Mice No effect on fertility or fetal development IPCS (2004) 

Bromoform 

Gavage, doses 

ranging from 

0-200 mg/kg/day 

Mice 

postnatal survival 

significantly decreased at 

doses of 200 mg/kg/day. 

No other reproductive 

effects seen in F1 or F2 

generations* 

US EPA (1991b) 

Dichlorobromomethane 

Oral, 10 day 

study, doses 

from 

50-200 mg/kg/d

ay on days 6-15 

of gestation 

Rats Doses of 50 mg/kg/day 

show fetotoxic effects* 

ATSDR and 

US EPA (1989) 

Chlorodibromomethane 

Oral, 2-

generation 

study, doses up 

to 

685 mg/kg/day 

Mice 

Decrease in fertility in high 

dose groups. No lethal or 

teratogenic effects* 

IPCS (2000a) 

HAAs

Bromochloroacetic 

acid 

Oral, gavage, 14 

days, 0/8/24/72 

mg/kg/d 

Rats Decreased sperm fertility at 

all doses 

Klinefelter et.al. 

(2002)
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Chemical Exposure 

Route Species Effects Reference/ Comments 

Monochloroacetic 

acid 

Gavage, doses 

of 0 or 

193 mg/kg/day 

on gestation 

days 1-22 

Rats 

Significant decrease in 

body weight but no adverse 

reproductive, 

developmental, or 

teratogenic effects 

reported. LOAEL of 

193 mg/kg/day for 

maternal toxicity 

WHO (2004b)

Monobromoacetic 

acid 

Oral intubation, 

doses ranging 

from 

0-100mg/kg/day 

on gestation 

days 6-15 

Rats 

Maternal weight changes, 

decrease in fetal weight, 

LOAEL of 100 mg/kg/day 

HSDB/TOXNET 

(2009a)

Dichloroacetic acid 

a. Gavage, 

10 weeks, doses 

up to 

125 mg/kg/day 

b. Gavage, days 

6-15 of 

gestation 

a. Rats 

b. Rats 

a. dose-dependent effect on 

male reproductive function, 

LOAEL 31 mg/kg/d 

(reduced weights of 

accessory organs) 

b. soft tissue abnormalities 

in fetal rats, LOAEL 

140 mg/kg/d, NOAEL 

14 mg/kg/d 

IPCS (2000a) 

Dibromoacetic acid 

Gavage, doses 

up to 

250 mg/kg/day 

Rats 

Effects noted on male 

reproductive behavior 

>10 mg/kg/d), sperm 

morphology 

(>50 mg/kg/d), fertility 

(>250 mg/kg/d) 

IPCS (2000a) 

Trichloroacetic 

acid 

Gavage, doses 

up to 1800 

mg/kg/day, 

gestation day 

6-15 

Rats 

Reduced pup weights 

≥800 mg/kg/d, soft tissue 

malformations 

≥330 mg/kg/d (LOAEL) 

IPCS (2000a) 

Other Chemicals

Sodium bisulfite 

a. Topical 

treatment 2 

mL/kg on 

gestational days 

1-19 

b. Gavage, 

doses of 100-

120 mg/kg bw 

during 

organogenesis 

a. 

Female 

rats 

b. Rats, 

mice, 

rabbits, 

hamsters 

a. mean number of corpora 

lutea, implantation sites, 

live fetuses, and resorptions 

per pregnancy and number 

of litters w/ resorptions not 

significantly affected* 

b. Did not induce 

maternal/reproduction 

toxicity* 

Health Council for 

the Netherlands 

(2005) 

*No NOEAL/LOAEL reported
MEPC 60/2/9 

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4.6 Carcinogenicity 

Table 13 below summarizes the carcinogenic classification for the chemicals related to 

the BalPure® system. The majority of the classifications are mandated by the International Agency 

for Research on Cancer (IARC) and the US EPA, while some come from other governmental 

organizations such as Health Canada. Some chemicals have not been classified by the IARC or 

other governmental organizations due to a lack of sufficient research and data. Most of the 

chemicals that are classified are characterized as possibly or unlikely to be carcinogenic to humans. 

Table 13 : Summary of Data on Carcinogenicity 

Chemical Carcinogen 

Classification Description Reference/ Comments 

Active substances

Hypochlorous acid 

a. IARC group 3-not 

classifiable as 

carcinogenic to humans 

b. Not classified by NTP 

a. Inadequate evidence in 

experimental animals 

b. Oral exposure in drinking 

water, 2 years, at doses a) 0-

14.4 mg/kg bw/d and b) 0-

24.2 mg/kg bw/d; Species: 

a) rats and b) mice; Value 

Range: a) equivocal 

evidence of increased 

leukaemia incidence in 

female rats ≥7 mg/kg bw/d 

and b) no evidence of 

carcinogenic effects in male 

rats and in mice 

a. IARC (2009) 

b. NTP (1992a) 

Hypobromous acid Not classified No information 

available 

Relevant chemicals

Bromate 

a. IARC Group 2Bpossibly carcinogenic to 

humans 

b. US EPA Group B2-

probable human 

carcinogen based on 

sufficient evidence of 

carcinogenicity in animal 

a. Inadequate evidence in 

humans and sufficient 

evidence in experimental 

animals 

b. Oral exposure in drinking 

water: a) 104 weeks, 0 – 

500 mg/L (0 – 33 mg/kg) 

and b) 100 weeks, 0 – 

400 mg/L (0 – 28.7 mg/kg); 

Species: a) and b) rats; 

Value Range: a) dysplastic 

foci ≥1.3 mg/kg, kidney 

tumours ≥5.6 mg/kg, 

thyroid tumours, 

mesotheliomas at 33 mg/kg; 

b) mesotheliomas ≥6.1 

mg/kg, thyroid tumours 

≥12.9 mg/kg, kidney 

tumours at 28.7 mg/kg 

a. IARC (1999a) 

b. US EPA 

(2001a) 
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Chemical Carcinogen 

Classification Description Reference/ Comments 

THMs 

Chloroform 

a. IARC Group 2Bpossibly carcinogenic to 

humans 

b. US EPA Group B2-

probable human 

carcinogen based on 

sufficient evidence of 

carcinogenicity in animal 

a. Inadequate evidence in 

humans and sufficient 

evidence in experimental 

animals 

b. Likely to be 

carcinogenic to humans 

by all routes of exposure 

under high-dose 

conditions that lead to 

cytotoxicity and 

regenerative hyperplasia 

in susceptible tissues but 

is not likely to be 

carcinogenic by any 

exposure route under 

exposure conditions that 

do not cause cytotoxicity 

and cell regeneration 

a. IARC (1999) 

b. US EPA 

(2001b) 

Bromoform 

a. IARC Group 3-not 

classifiable as to 

carcinogenicity to 

humans 

b. US EPA Group B2-

probable human 

carcinogen based on 

sufficient evidence of 

carcinogenicity in animal 

a. Inadequate evidence in 

humans and limited 

evidence in experimental 

animals 

b. Oral exposure, gavage, 

2 years, 0 – 200 mg/kg/d; 

Species: a) rats and 

b) mice; Value Range: 

a) increased incidence of 

intestinal tumours at 

200 mg/kg/d and b) no 

neoplastic effects 

a. IARC (1991) 

b. NTP (1989), 

US EPA (1991a), 

IPCS (2000a) and 

US Dept. Health 

(2005) 
MEPC 60/2/9 

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Chemical Carcinogen 

Classification Description Reference/ Comments 

Dichlorobromomethane 

a. IARC Group 2Bpossibly carcinogenic to 

humans 

b. Recommendation for 

EU Classification 2–

Substances which should 

be regarded as if they are 

carcinogenic to man 

c. US EPA Group B2-

probable human 

carcinogen based on 

sufficient evidence of 

carcinogenicity in animal 

d. Not classified by NTP 

a. No epidemiological 

evidence available; 

sufficient evidence in 

experimental animals 

b. No data in humans 

available; conflicting 

results in experimental 

animals. Sufficient 

indications that 

carcinogenic effect may 

be exerted by a stochastic 

genotoxic mechanism 

c. Oral exposure, gavage, 

102 weeks: a) 0 – 

100 mg/kg/d and b) 0 – 

150 mg/kg/d Species: 

a) rats and b) mice; Value 

Range: a) increased 

incidence of kidney 

(100 mg/kg/d) and 

intestinal tumours (males 

dose dependent; females 

100 mg/kg/d) and 

b) increased incidence of 

kidney (males, 

50 mg/kg/d) and liver 

tumours (females, 75 and 

150 mg/kg/d) 

d. Oral exposure, 

drinking water, 2 years: 

a) 0/6/12/25 mg/kg/d and 

b) 0/9/18/36 mg/kg/d; 

Species: a) rats and 

b) mice; Value Range: 

a) and b) no tumours 

observed 

a. IARC (1999c); 

b. Health Council 

of the Netherlands 

(2007) 

c. NTP (1987), 

IPCS (2000a) and 

US EPA (1991d) 

d. NTP (2006) 
MEPC 60/2/9 

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Chemical Carcinogen 

Classification Description Reference/ Comments 

Chlorodibromomet

hane 

a. IARC Group 3-not 

classifiable as 

carcinogenic to humans 

b. US EPA Group C - 

possible human 

carcinogen based on 

limited evidence of 

carcinogenicity in animal 

a. Inadequate evidence in 

humans and limited 

evidence in experimental 

animals 

b. Oral exposure, gavage, 

2 years: 

a) 0/40/80 mg/kg/d and 

b) 0/50/100 mg/kg/d; 

Species: a) rats and 

b) mice; Value Range: 

a) no carcinogenic effects 

and b) increased 

incidence of liver 

tumours at 100 mg/kg/d 

a. IARC (1999b) 

b. NTP (1985), US 

EPA (1991c) and 

IPCS (2000a)

HAAs 

Bromochloroacetic 

acid 

a. Not Classified by 

IARC 

b. Not Classified by NTP 

a. Not Classified by 

IARC 

b. Oral exposure in 

drinking water, 2 years, 

0 – 1000 mg/L: (a) 0 – 50 

mg/kg and b) 0 – 90 

mg/kg); Species: a) rats 

and b) mice; Value 

Range: Clear evidence of 

carcinogenic activity a) 

NOAEL, male: 

10 mg/kg/d (malignant 

mesothelioma), NOAEL, 

female: 13 mg/kg/d 

(mammary gland 

fibroadenomas), 

b) LOAEL, male: 

25 mg/kg/d, LOAEL, 

female: 15 mg/kg/d 

(hepatocellular 

adenomas) 

a. IARC (2009) 

b. NTP (2009)

Monobromoacetic 

acid 

a. Not classified by IARC 

b. Health Canada Group 

IV–unclassifiable with 

respect to carcinogenicity 

in humans 

a. Inadequate evidence 

for assessment of human 

carcinogenic potential 

b. Inadequate data from 

animal studies 

a. IARC (2009) 

b. Health Canada 

(2009) 
MEPC 60/2/9 

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Chemical Carcinogen 

Classification Description Reference/ Comments 

Monochloroacetic 

acid 

a. Not classified by IARC 

b. Health Canada Group 

IV.D–unlikely to be 

carcinogenic to humans 

a. Not Classified by 

IARC 

b. Oral exposure, gavage, 

2 years: a) 0/15/30 mg/kg 

and b) 0/50/100 mg/kg; 

Species: a) rats and 

b) mice; Value Range: 

a) and b): No evidence of 

carcinogenicity in mice 

or rats in a lifetime study; 

inadequate evidence for 

assessment of human 

carcinogenic potential 

a. IARC (2009) 

b. NTP (1992b) 

and Health 

Canada (2009) 

Dichloroacetic acid 

a. IARC Group 2B – 

possibly carcinogenic to 

humans 

b. US EPA Group B2-

probable human 

carcinogen based on 

sufficient evidence of 

carcinogenicity in animal 

a. Inadequate evidence in 

humans and sufficient 

evidence in experimental 

animals 

b. Oral exposure in 

drinking water, 2 years, 

0 – 3,500 mg/L 

(0 – 429 mg/kg); 

Species: mice; Value 

Range/Effects: 

hepatoclellular adenoma 

at 84 mg/kg/d and higher, 

clear evidence of 

carcinogenicity 

a. IARC (2004a) 

b. US EPA (2003) 
MEPC 60/2/9 

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Chemical Carcinogen 

Classification Description Reference/ Comments 

Dibromoacetic acid 

a. Not classified by IARC 

b. Health Canada Group 

II–probably carcinogenic 

to humans 

a. Not Classified by 

IARC 

b. Inadequate evidence in 

humans and sufficient 

evidence in animals, 

specifically oral exposure 

in drinking water, 

2 years, 0 – 1,000 mg/L: 

a) 0 – 45 mg/kg and b) 0 

– 87 mg/kg); Species: 

a) rats and b) mice; Value 

Range/Effects: 

a) malignant 

mesothelioma at 

40 mg/kg/d (males), 

mononuclear cell 

leukemia at 45 mg/kg/d 

(females) and b) liver 

tumours ≥4 mg/kg/d 

(males), ≥35 mg/kg/d 

(females), lung tumours 

≥45 mg/kg/d (males) 

a. IARC (2009) 

b. NTP (2007) and 

Health Canada 

(2009) 

Trichloroacetic 

acid 

a. IARC Group-3-not 

classifiable as 

carcinogenic to humans 

b. Health Canada Group 

III–possibly carcinogenic 

to humans 

c. US EPA Group C - 

possible human 

carcinogen based on 

limited evidence of 

carcinogenicity in animal 

a. Inadequate evidence in 

humans and limited 

evidence in experimental 

animals 

b. Inadequate evidence in 

humans and limited 

evidence (one species) in 

animals 

c. Oral exposure in 

drinking water, 2 years, 

0- 5,000 mg/L; a) 0 – 284 

mg/kg and b) 0 – 595 

mg/kg); Species: a) rats 

and b) mice; 

Effects/Value Range: 

a) no carcinogenic effects 

and b) dose-dependent 

increase in liver tumours 

> 71 mg/kg/d 

a. IARC (2004b ) 

b. Health Canada 

(2009) 

c. US EPA (1996) 

and IPCS (2000a) 
MEPC 60/2/9 

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Chemical Carcinogen 

Classification Description Reference/ Comments 

Other Chemicals

Sodium bisulfite 

a. IARC Group 3-not 

classifiable as 

carcinogenic to humans 

b. American Conference 

of Governmental 

Industrial Hygienists 

TLVs and BEIs Group 

A4-not classifiable as a 

human carcinogen 

a. Inadequate evidence 

for carcinogenicity in 

humans for sulfur 

compounds and limited 

evidence in experimental 

animals. 

IARC 1992 and 

IPCS (2000a) 

4.7 Mutagenicity/genotoxicity 

Table 14 below summarizes data on mutagenicity and genotoxicity for the chemicals involved in 

STDN’s BalPure® treatment system. 

Table 14 : Summary of Data on Mutagenicity and Genotoxicity 

Chemical Study Results Reference/ 

Comments 

Active Substances

Hypochlorous acid 

Some studies show that sodium chlorite causes 

mutagenic responses in bacteria and mammalian cells 

in vitro. There is no evidence of mutagenic response 

in mammalian systems in vivo.

IPCS (2000a) 

Hypobromous acid No information 

available 

Relevant Chemicals

Bromate Some studies show positive results for genotoxic 

activity in several in vitro and in vivo systems. 

IPCS (2000a), 

IARC (1999a), 

US EPA (2001a) 

THMs

Chloroform Studies show negative results for mutagenicity in 

several in vitro and in vivo assays. IPCS (2000a) 

Bromoform 

Studies show positive results for mutagenicity in 

several in vitro and in vivo assays. In vivo studies with 

rodents bromoform did not cause chromosomal 

aberrations 

 IARC (1991), 

 IPCS (2000a) 

Dichlorobromomethane Increased frequency of sister chromatid exchange in 

mice dosed with 50 or 100 mg/kg/day for 4 days. 

ATSDR & US 

EPA (1989) 

Chlorodibromomethane 

Studies show positive results for mutagenicity in 

several bacterial and eukaryotic in vitro systems; 

equivocal results are reported from in vivo studies in 

rodents. 

IPCS (2000a) 
MEPC 60/2/9 

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Chemical Study Results Reference/ 

Comments 

HAAs

Bromochloroacetic 

acid 

Some positive results for Salmonella typhimurim for 

genotoxicity. Negative genotoxic results for male and 

female mice exposed to BCAA for 3 months in 

drinking water. 

HSDB/TOXNET 

(2009b)

Monochloroacetic 

acid 

Data is conflicting; most evidence suggests no 

significant mutagenic potential WHO (2004b) 

Monobromoacetic 

acid 

Mutagenic in Salmonella typhimurium. Chromosomal 

damage not observed in newt micronucleus test. WHO (2004a) 

Dichloroacetic acid 

Conflicting results are reported from several in vitro 

and in vivo studies; the overall dataset indicated that 

DCA induces mutations and chromosomal effects. 

IARC (2004a) 

Dibromoacetic 

acid 

Studies show positive results for mutagenicity in 

several in vitro and in vivo assays. IPCS (2000a) 

Trichloroacetic 

acid 

Weakly mutagenic. Did not induce chromosomal 

aberrations or DNA strand breaks in single studies, 

and no effect observed in a DNA strand-break assay or 

single-cell gel assay. 

IARC (2004b) 

Other Chemicals

Sodium bisulfite 

Not mutagenic in rats at doses up to 150 mg/kg. No 

mutagenic activity in human tissue cells in vitro up to 

200 μg/mL. 

WHO/IPCS 

(2008) 

4.8 Toxicokinetics 

 

Table 15 below characterizes the existing data concerning the uptake, absorption, and excretion 

of the chemicals. 

Table 15 : Summary of Uptake, Absorption, and Excretion of Chemicals 

Chemical Study Results Reference/ 

comments 

Active Substances 

Hypochlorous 

acid 

Hypochlorous acid breaks down into several different 

chemicals in the gut such as trichloroacetic acid, 

dichloroacetic acid, and dichloroacetonitrile 

HSDB/TOXNET 

(2009i) 

Hypobromous 

acid 

No data found in 

literature 

Relevant chemicals 

Bromate (as 

sodium bromate) 

After a dose of 230-460 mg BrO3

-

/kg in a 2 year old 

child (13 kg), 60-70% was recovered from dialysate and 

urine as bromide (1,850mg). Bromate is rapidly 

absorbed from gastrointestinal tract, partially converted 

to bromide in tissues and excreted rapidly 

HSDB/TOXNET 

(2009k) 

Health Canada 

(1998)
MEPC 60/2/9 

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Chemical Study Results Reference/ 

comments 

THMs

Chloroform 

Well absorbed, metabolized, and eliminated rapidly by 

mammals after oral, inhalation, or dermal exposure. 

After dose of 0.5 g chloroform, 50-52% of dose 

absorbed and approx. 100% of dose metabolized to 

carbon dioxide 

IPCS (1994) 

Bromoform After administered to mice and rats, 3-6% and 5-14% 

remains in body tissues after 36 or 48 hrs, respectively. 

HSDB/TOXNET 

(2009l)

Dichlorobromom

ethane 

Moves from stomach/intestines into the blood. Leaves 

body mostly through exhalation and less through urine 

and feces. Removal fairly rapid (95% in 8 hours) 

ATSDR & US 

EPA 

(1989) 

Chlorodibromom

ethane 

Rats administered with 100 mg/kg bw absorbed and 

eliminated as expired air as BDCM or CO2 in 8 hours. 

1% eliminated in urine and 1% retained in body tissues. 

Metabolized to CO in vitro and in vivo 

HSDB/TOXNET 

(2009e)

HAAs

Bromochloroacetic 

acid 

Rapidly cleared from blood following single intravenous 

dose. Urine and feces minimal contributors-suggests 

elimination via conversion to CO2 

WHO (2004b) 

Monochloroacetic 

acid 

In mice, 80-90% of administered MCA excreted in urine 

within 24 hours; 8 % was exhaled as CO2

IPCS (2000b) 

Monobromoacetic 

acid No studies have been found in literature WHO (2004a) 

Dichloroacetic 

acid 

Both humans and rodents metabolize DCA to glyoxylate 

by oxidative de-chlorination; the plasma half-life of the 

parent compound Is 0.5-2 hours 

HSDB/TOXNET 

(2009h)

Dibromoacetic 

acid 

Limited in vitro data suggests rapid excretion and 

minimal bioaccumulation. Urine and feces minimal 

contributors to blood clearance, suggesting 

biotransformation 

WHO (2004a) 

Trichloroacetic 

acid 

After administration of single oral dose of 3 mg/kg bw to 

volunteers, mean plasma half life was ~50 hrs and 

volume of distribution was ~115 mL/kg bw. TCA is 

absorbed rapidly and expelled in urine as TCA or 

oxalic/thiodiacetic acids 

HSDB/TOXNET 

(2009m)

Other Chemicals

Sodium bisulfite 

Rats given a 0.2% solution eliminated 55% of 

administered sulfur as sulfate in urine within first four 

hours. Rapid elimination of sulfites as sulfate observed 

in man and dog. 

WHO /IPCS 

(2008) 
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5 DATA ON ENVIRONMENTAL FATE AND EFFECT UNDER AEROBIC AND 

ANAEROBIC CONDITIONS (G9: 4.2.1.3) 

5.1 Modes of degradation (biotic; abiotic) 

As shown in Table 16 below, the Active Substances (hypochlorous and hypobromous acid) decay 

in seconds to hours; this is after all their mechanism of action and how they produce an oxidizing 

environment. As a consequence of this oxidizing environment, along with the presence of 

organic matter, THMs and HAAs are also produced as described in section 2.3. For THMs 

and HAAs, both the biotic and abiotic degradation data are shown in Table 16. Biotic 

degradation for all of these simple halogenated organic compounds is on the order of days to 

weeks. Abiotic degradation of these compounds is longer. 

5.2 Bioaccumulation, partition coefficient, octanol/water partition coefficient 

The bioconcentration factor (BCF) is the concentration of a particular chemical in a tissue per 

concentration of chemical in water (reported as L/kg). This physical property characterizes the 

accumulation of pollutants through chemical partitioning from the aqueous phase into an organic 

phase, such as the gill of a fish. Generally, a high potential BCF is greater than 1000, a moderate 

potential BCF is less than a 1000 but greater than 250, and a low potential BCF is less than 250. 

The literature reported and/or estimated BCFs are shown for the Active Substances and Relevant 

Chemicals in Table 7. 

The organic carbon adsorption coefficient (Koc) is the chemical adsorption coefficient 

normalized to the organic carbon content of soil or sediment. This parameter describes the 

tendency of a substance to bind to organic matter in the soil or sediment. 

The octanol/water partition coefficient (Kow) is defined as the ratio of a chemical’s 

concentration in the octanol phase to its concentration in the aqueous phase of a two-phase 

octanol/water system. Measured values of log Kow for organic chemicals range from -3 to 7. 

Generally, chemicals with low Log Kow values can be considered relatively hydrophilic 

(i.e. tendency for high water solubility, low potential for sediment adsorption), while chemicals 

with high Log Kow values are considered hydrophobic (i.e. low water solubility, high potential 

for sediment adsorption). The literature reported and/or estimated log Kows are shown for 

the Active Substances and Relevant Chemicals in Table 16. 

Based on the data shown in Table 7 for both Active Substances and Relevant Chemicals all of 

these substances have very low BCFs, indicating that they are unlikely to bioaccumulate in 

aquatic organisms or present a significant food chain risk. With the exception of the THMs, all 

of the Active Substances and Relevant Chemicals have very low log Kow’s, which indicates the 

compounds are hydrophilic. The THMs, as would be expected, are moderately hydrophobic. 

However, none of the log Kow values located in the literature and/or estimated are ≥ 3. 

The log Kow and BCF are related to each other with the BCF being the more relevant parameter 

to determine the likelihood of impacts of a chemical to aquatic organisms. The Koc’s for all 

chemicals in Table 16 are all at or below 250 indicating a low likelihood of partitioning into the 

sediment compartment of aquatic systems. 
MEPC 60/2/9 

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Table 16 : Modes of Degradation 

Chemical Information on Modes of Degradation BCF/Koc/ 

Log Kow 

Comments/

References 

Active Substances 

Hypochlorous 

acid Decays within seconds to hours, no rate specified 

BCF: 3.2 

Koc: 13.2 

Log Kow: 

-0.87 

Echigo & 

Minear 

(2006)/EPI 

Suite (2009c)

Hypobromous 

acid Decays within seconds to hours, no rate specified 

BCF: 3.2 

Koc: 13.2 

Log Kow: 

-0.78 

Echigo & 

Minear 

(2006)/EPI 

Suite (2009b)

Relevant Chemicals 

Bromate (as 

sodium 

bromate) 

No information located. 

BCF:3.2 

Koc: 31.8 

Log Kow: 

-4.6 

HSDB/ 

TOXNET 

(2009k)/EPI 

Suite (2009a)

THMs 

Chloroform 

BIOTIC: Estimated volatilization half-lives for 

model river and lake are 1.3 hrs and 4.4 days, 

respectively. No marine biodegradation reported. 

Can be biodegraded under anaerobic conditions by 

methanogenic bacteria. 

ABIOTIC: Atmospheric half life of ~151 days at 

atmospheric concentration of 5X105 hydroxyl 

radicals/cm3. Avg. degradation rate of 0.8%/hr. 

BCF: 

2.9-10.35 

Koc:153-

196 

HSDB/ 

TOXNET 

(2009f)

Bromoform 

BIOTIC: In anoxic groundwater environments: 

20% degradation after 6 hours, 99% degradation 

after ~2.5 days. Volatilization from water surface 

expected. Estimated volatilization half lives for 

model river and lake are 7.3 hours and 7.1 days, 

respectively. 

ABIOTIC: Atmospheric half life of ~325 days at 

an atmospheric concentration of 5X105

 hydroxyl 

radicals/cm3. Hydrolysis is not expected. 

BCF: 14 

Koc: 35 

Log Kow: 

2.4 

HSDB/ 

TOXNET 

(2009l) 

Chlorodibro

mo-methane 

BIOTIC: Volatilization from water surfaces is 

expected. Volatilization half-lives for model river 

and lake are 2.6 hrs and 6 days, respectively. 

Resistant to aerobic biodegradation; degrades 

anaerobically within 2 to 8 weeks. 

ABIOTIC: Atmospheric half life of ~280 days at 

an atmospheric concentration of 5X105 hydroxyl 

radicals/cm3

. Direct photolysis or aquatic oxidation 

not relevant processes. 

BCF: 9 

Koc: 84 

HSDB/ 

TOXNET 

(2009e)
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Chemical Information on Modes of Degradation BCF/Koc/ 

Log Kow 

Comments/

References 

Dichlorobro

mo-methane 

BIOTIC: 51-59% biodegradation over 28 days in 

aerobic conditions using static flask screening 

procedures. 100% biodegradation in anaerobic 

conditions after 2 weeks using methanogenic 

bacteria from sewage. (No degradation in control 

without bacteria). 

ABIOTIC: Atmospheric half life of 205 days at 

atmospheric concentration of 5X105 hydroxyl 

radicals/cm3. Direct photolysis not expected. 

Aqueous hydrolysis half life estimated at 137 years 

(25  ̊C and pH 7)

BCF: 7 

Koc: 35-

251 

Log Kow: 2 

HSDB/ 

TOXNET 

(2009c)

HAAs 

Bromochloroacetic acid 

BIOTIC: Volatilization from water surfaces not 

expected. (No biodegradation data available) 

ABIOTIC: Atmospheric half life of ~23.8 days at 

atmospheric concentration of 5X105

 hydroxyl 

radicals/cm3. Not expected to undergo hydrolysis 

or direct photolysis by sunlight. 

BCF: 3.2 

Koc: 1.9 

Log Kow: 

0.61 

HSDB/ 

TOXNET 

(2009b) 

Monochloroacetic acid 

BIOTIC: Volatilization from water surfaces not 

expected. In aerobic conditions CAA reaches 65% 

of theoretical BOD in 3 weeks at 100 mg/L. No 

biodegradability in seawater after 3 days using 

cultivation method at 10 mg/L. Difficult to 

degrade. 

ABIOTIC: Atmospheric half life of ~ 20 days at 

atmospheric concentration of 5X105 hydroxyl 

radicals/cm3. Hydrolysis and direct photolysis by 

sunlight not expected. 

BCF: 3.2 

Koc: 31 

Log Kow: 

0.22 

HSDB/ 

TOXNET 

(2009d)

Monobromoacetic acid 

BIOTIC: Volatilization from water surfaces not 

expected. In biodegradation screening tests, 

reached 82% of theoretic BOD when using 

acclimated inoculums. (not readily biodegradable 

w/out un-acclimated inoculums). 

ABIOTIC: Atmospheric half life of ~22.4 days at 

an atmospheric concentration of 5X105

 hydroxyl 

radicals/cm3

. Not expected to undergo hydrolysis 

or direct photolysis from sunlight. 

BCF: 3.2 

Koc: 39.8 

Log Kow: 

0.41 

HSDB/ 

TOXNET 

(2009a)

Dichloroacetic 

acid 

BIOTIC: Biodegradability reported to be 14 and 

8% after 3 days of incubation for river and 

seawater, respectively. Volatilization from water is 

not expected due to pKa values. 

ABIOTIC: Atmospheric half life of ~22 days at 

atmospheric concentration of 5X105

 hydroxyl 

radicals/cm3. Not expected to undergo hydrolysis 

or direct photolysis by sunlight. 

BCF: 0.3 

Koc: 75 

Log Kow: 

0.92 

HSDB/ 

TOXNET 

(2009h) 
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Chemical Information on Modes of Degradation BCF/Koc/ 

Log Kow 

Comments/

References 

Dibromoacetic 

acid 

BIOTIC: Limited data available. Volatilization 

from water surface is not expected due to pKa 

values. 

ABIOTIC: Atmospheric half life of ~ 25.3 days at 

atmospheric concentration of 5X105 hydroxyls 

radicals/cm3. Not expected to undergo hydrolysis 

or direct photolysis by sunlight. 

BCF: 0.17 

Koc: 1.5 

HSDB/ 

TOXNET 

(2009g)

Trichloroacetic 

acid 

BIOTIC: Volatilization from water surfaces is not 

expected due to pKa values. At concentrations of 

100 mg/L reaches 7% of theoretical BOD in 

4 weeks using activated sludge. 

ABIOTIC: Atmospheric half life of ~31 days at 

atmospheric concentration of 5X105 hydroxyl 

radicals/cm3. 

BCF: 0.1-

1.7 

Koc: 130 

Log Kow: 

1.33 

HSDB/ 

TOXNET 

(2009m)

Other Chemicals

Sodium 

bisulfite No information located. 

BCF: 3.2 

Koc: 2.21 

Log Kow: 

-6.85 

EPI Suite 

(2009d) 

5.3 Persistence and identification of the main metabolites in the relevant media 

Higher tier simulation tests not required; section not applicable. 

5.4 Reaction with organic matter 

The formation of disinfection by-products (DBPs) when using chlorine-based water disinfection 

methods is well known. Two major classes of DBPs that are commonly formed in chlorine 

treated water include THMs and HAAs (Westerhoff, et al., 2003). Both of these DBP classes 

have been measured in water treated with the BalPure® system. DBP formation is a result of 

disinfectant reactions with natural organic matter, often measured as total organic carbon (TOC), 

which serves as the organic precursor, and/or bromide ion, which serves as the inorganic 

precursor (IPCS, 2000a). Reactions between disinfectant halogens (e.g., chlorine and bromine) 

and DBP precursors include substitution reactions and carbon bond oxidation reactions 

(Westerhoff, et al., 2003). Water quality (e.g., pH, temperature, bromide level, TOC) and 

treatment conditions (e.g., hypochlorite dose, contact time, removal of organic matter prior to 

treatment) influences the formation of DBPs. Further, the distribution of DBP species (four 

THM species, up to nine HAA species) is affected by the amounts of TOC, bromide and chlorine 

present (IPCS, 2000a). 

Analysis for DBP concentrations has been conducted during pilot scale testing of the BalPure®

system. Different water types (freshwater, brackish, seawater) were treated and then evaluated 

for DBPs. The data are presented in section 11 “Evaluation of Treated Ballast Water”. 

Additional evaluation of DBP concentrations in treated ballast water will be performed during 

land-based testing at NIOZ and the results will be reported in the Final Approval dossier. 
MEPC 60/2/9 

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5.5 Potential physical effects on wildlife and benthic habitats 

When evaluated using GESAMP Reports and Studies No. 64, the chemical and physical 

properties of the Active Substances and Relevant Chemicals associated with the BalPure® system 

(Tables 17, 18, 19, 20, and 21) indicate that physical effects on wildlife and benthic habitats as 

described are not expected to occur. 

5.6 Potential residues in seafood 

Chemicals detected in treated ballast water that is discharged may pose a threat to seafood 

consumers only if they tend to bioaccumulate (within a trophic level, an increase in concentration 

of a substance in tissues due to uptake from food and sediments) or biomagnify (an increase in 

the concentration of a substance in the food web). The bioaccumulation criteria per 

the Methodology for information gathering and the conduct of work of the GESAMP-BWWG 

(MEPC 58/2/7, annex 4) include an octanol-water partition coefficient (Log Kow) of ≥3 or a 

bioconcentration factor (BCF) >2000. The chemicals identified in this risk assessment all 

have Log Kows less than 3 and BCFs less than 2000, and therefore are not expected to persist in 

the food web. 

5.7 Any known interactive effects 

No other interactive effects are known. 

6 PHYSICAL AND CHEMICAL PROPERTIES OF THE ACTIVE SUBSTANCES, 

RELEVANT CHEMICALS AND TREATED BALLAST WATER (G9: 4.2.1.4) 

Table 17 : Physical and Chemical Properties of Active Substances 

Physical/Chemical Property Active Substance −

Hypochlorous Acid 

Active Substance −

Hyprobromous Acid 

Melting point (oC) 194.89oC 208.57oC 

Boiling point (oC) 507.1oC 527.32oC 

Flammability 

(flash point for liquids; oC) Not flammable Not flammable 

Density (20oC; kg/m3) 1.21 Not located. 

Vapor pressure/Vapor density 

(air=1) 1.85 x10-12mm Hg 3.06 x10-13 mm Hg 

Water solubility (temp; effect 

of pH; mg/L)/ Dissociation 

constant (pKa) 

1x106 (25oC) 1x106 mg/L (25oC) 

Oxidation/Reduction 

potential 700-800 mv* 700-800 mv* 

Corrosivity to materials Corrosive Data not located 

Auto-ignition temperature 

(oC) Data not located Data not located 

Explosive properties In ballast water – not 

applicable 

In ballast water – not 

applicable 

Oxidizing properties Strong oxidizing agent Oxidizing agent 

Surface tension Same as ballast water Same as ballast water 

Viscosity (20oC) Same as ballast water Same as ballast water 
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I:\MEPC\60\2-9.doc 

Physical/Chemical Property Active Substance −

Hypochlorous Acid 

Active Substance −

Hyprobromous Acid 

Thermal stability 

Very stable in aqueous 

solutions between 15-

18oC 

Data not located 

Reactivity to container 

material 

Not stored; produced in 

situ 

Not stored; produced 

in situ 

Other known’s May have slight 

chlorine-like odor None 

*ORP as measured in ballast water after treatment with hypochlorite. 

Note: All data from HSDB/TOXNET unless otherwise specified.

Table 18 : Physical and Chemical Properties of Relevant Chemicals-THMs 

Physical/Chemical 

Property 

THMs 

Chloroform 

THMs 

Bromoform 

THMs 

Chlorodibrom

omethane 

THMs 

Dichlorobromo

-methane 

Flammability 

(flash point for 

liquids; oC) 

Non-flammable Non-flammable 

Non-flammable 

(US Dept. of 

Health and 

Human 

Services and 

ATDSR, 2005) 

Non-flammable 

Vapor 

pressure/Vapor 

density (air=1) 

197 mmHg 

(25oC) 1 Kpa (30 ̊C)/8.7 5.54 mm Hg (25oC) 

50 mm Hg 

(20oC) 

Water solubility 

(temp; effect of pH; 

mg/L)/ Dissociation 

constant (pKa) 

7,710 mg/L 

(25oC) 

3,100 mg/L 

(25oC) 

2,700 mg/L 

(20oC) 

4,700 mg/L 

(22oC) 

Oxidation/Reduction 

potential 700-800 mv* 700-800 mv* 700-800 mv* 700-800 mv* 

Corrosivity to 

materials 

Aqueous form 

corrosive to 

some forms of 

plastics, rubber, 

and coatings 

(CCOHS, 2007)

Aqueous form 

corrosive to steel 

and gray cast iron, 

and some plastics 

(CCOHS, 2007) 

Data not 

located Data not located 

Auto-ignition 

temperature (oC) NA NA 

NA 

(US Dept. of 

Health and 

Human 

Services and 

ATSDR, 2005) 

NA 
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Physical/Chemical 

Property 

THMs 

Chloroform 

THMs 

Bromoform 

THMs 

Chlorodibrom

omethane 

THMs 

Dichlorobromo

-methane 

Explosive properties 

Explosive in 

presence of 

some alkali 

metals and 

strong mineral 

acids 

Explosive in 

presence of crown 

ethers or 

potassium 

hydroxide 

Incompatible 

with strong 

bases, strong 

oxidizing 

agents, and 

magnesium 

Incompatible 

with strong 

bases and strong 

mineral acids 

Oxidizing properties Strong 

oxidizing agent No data available No data available 

No data 

available 

Reactivity to 

container material 

Not stored; 

produced in situ 

Not stored; 

produced in situ 

Not stored; 

produced in 

situ 

Not stored; 

produced in situ 

Other known’s None None None None 

 NA=Not applicable 

 *ORP as measured in ballast water after treatment with hypochlorite. 

 Note: All data from HSDB/TOXNET unless specified otherwise 

Table 19 : Physical and Chemical Properties of Relevant Chemicals-HAAs 

Physical/ 

Chemical 

Property 

HAAs 

Bromochloroacetic acid 

HAAs 

Monochloroacetic acid 

HAAs 

Monobromoacetic acid 

HAAs 

Dichloroacetic acid 

HAAs 

Dibromoacetic 

acid 

HAAs 

Trichloroacetic acid

Flammability 

(flash point for 

liquids; oC) 

110oC 

(closed 

cup) 

126oC 

(closed 

cup) 

113oC 

(closed 

cup) 

113oC 

113oC 

(closed 

cup) 

198oC 

Vapor 

pressure/ 

Vapor density 

(air=1) 

0.14 mm 

Hg (25oC) 

0.065 

mmHg 

(25oC)/3.26 

0.119 mm 

Hg (25oC) 

0.179 mm 

Hg 

(25oC)/4.45 

0.023 mm 

Hg 

(25oC) 

0.06 mm 

Hg (25oC) 

Water 

solubility 

(temp; effect 

of pH; 

mg/L)/ 

Dissociation 

constant (pKa) 

2.5 X105

mg/L 

(25oC)/ 

pka=1.4 

8.58105

mg/

L(25oC)/ 

Pka=2.87 

1.75X106mg

/L(25oC)/ 

pka=2.89 

Miscible 

with water/ 

pka=1.26 

2.1X106

mg/L 

(25oC)/ 

pka=1.48 

5.4X104

mg/L 

(25oC)/ 

pka=0.51 

Oxidation/ 

Reduction 

potential 

700-800 

mv* 

700-800 

mv* 

700-800 

mv* 

700-800 

mv* 

700-800 

mv* 

700-800 

mv* 

Corrosivity to 

materials 

Data not 

located 

Data not 

located 

Data not 

located 

Data not 

located 

Data not 

located 

Corrosive 

to iron, 

zinc, 

aluminium 
MEPC 60/2/9 

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Physical/ 

Chemical 

Property 

HAAs 

Bromochloroacetic acid 

HAAs 

Monochloroacetic acid 

HAAs 

Monobromoacetic acid 

HAAs 

Dichloroacetic acid 

HAAs 

Dibromoacetic 

acid 

HAAs 

Trichloroacetic acid

Auto-ignition 

temperature 

(oC) 

Data not 

located >500oC Data not located 

Data not 

located 

Data not 

located 

Data not 

located 

Explosive 

properties 

Incompatible 

with strong 

oxidizing 

agents 

 Explosive 

in presence 

of strong 

oxidizers, 

strong 

bases, and 

strong 

reducing 

agents 

Closed 

containers 

may explode 

when heated 

or 

contaminated 

with water) 

Vapors in 

confined 

area may 

explode in 

fire. 

Data not 

located 

Data not 

located 

Oxidizing 

properties 

Data not 

located 

Data not 

located 

Data not 

located 

Data not 

located 

Data not 

located 

Data not 

located 

Reactivity to 

container 

material 

Not stored; 

produced 

in situ 

Not stored; 

produced in 

situ 

Not stored; 

produced in 

situ 

Not stored; 

produced in 

situ 

Not 

stored; 

produced 

in situ 

Not stored; 

produced 

in situ 

Other known’s None None None None None None 

*ORP as measured in ballast water after treatment with hypochlorite. 

Note: All data from HSDB/TOXNET unless otherwise specified. 

Table 20 : Physical and Chemical Properties of Relevant Chemicals and Other Chemicals 

 Relevant Chemicals Other 

Chemicals 

Physical/Chemical 

Property 

Bromate Hydrogen Gas Sodium 

Bisulfite 

Flammability 

(flash point for liquids; 

oC) 

Data not located Extremely 

flammable (ICSC) 

Non-flammable 

Vapor pressure/Vapor 

density (air=1) 

Data not located 0.07 (ICSC) 1.48 

Water solubility (temp; 

effect of pH; 

mg/L)/Dissociation 

constant (pKa) 

3.64 g/L (20oC) Not applicable Very soluble in 

water 

Oxidation/Reduction 

potential 

700-800 mv* 700-800 mv* 700-800 mv* 

Corrosivity to materials Data not located NA Data not located 

Auto-ignition 

temperature (oC) 

Data not located 500-571 ̊C (ICSC) Data not located 
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Explosive properties Prolonged 

exposure to heat 

may result in 

explosion 

Gas/air mixtures 

are explosive; 

LEL: 4-76% 

volume in air 

(ICSC) 

Not considered 

explosive 

Oxidizing properties Oxidizing agent Not Applicable None 

Reactivity to container 

material 

Not stored; 

produced in situ 

Not stored; 

produced in situ 

Not stored; 

produced in situ 

Other known’s None None None 

NA=Not applicable 

*ORP as measured in ballast water after treatment with hypochlorite. 

Note: All data from HSDB/TOXNET unless otherwise specified. 

Table 21 : Physical and Chemical Properties of Treated Ballast Water 

Physical/Chemical Property Treated Ballast Water 

Density (20oC; kg/m3) Same as seawater 

Oxidation/Reduction potential <200 mV* 

Corrosivity to materials 

Similar to untreated ballast 

water 

Reactivity to container material 

Similar to untreated ballast 

water 

pH See Table 26 

Salinity See Table 26 

TOC See Table 26 

DOC See Table 26 

Other known’s None 

 *ORP as measured in ballast water after neutralization with sodium bisulfite. 

7 ANALYTICAL METHODS AT ENVIRONMENTALLY RELEVANT 

CONCENTRATIONS (G9: 4.2.1.5) 

7.1 Analysis of Total Residual Oxidant (TRO) 

TRO is measured at two concentration ranges (high and low) using two different analytical 

procedures. An iodometric titration procedure is used to measure higher range TRO in the 

product stream exiting the BalPure® unit. Concentrations are typically 1,000 mg/L and this 

procedure is accepted by the American Water Works Association (AWWA) for examination of 

water and wastewater. The procedure is only used if needed to perform diagnostics on the 

BalPure® system, and is included in appendix A.53

. A second method is typically used for 

measuring lower range TRO in potable water and waste water streams. A Hach colorimeter can 

be used to measure the TRO in ballast tanks and in the de-ballast stream prior to neutralization. 

The TRO oxidizes triiodide ion (I3-) to iodine (I2). The iodine and free chlorine react with DPD 

(N,N-diethyl-p-phenylenediamine) to form a red solution. The color intensity is proportional to 

the TRO concentration. This method is also provided in appendix A.53

. 

 

3 Appendix A.5 is provided in the confidential dossier of the proposal for approval. 
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During system testing at the University of Washington, TRO measurements were performed 

internally by the researchers using a Hach DR/820 colorimeter and the Hach DPD powder pillow 

Method 10070 in appendix A.51

 (equivalent to EPA Method 330.5). 

7.2 Analysis of Disinfection By-Products (DBPs) 

During the pilot scale studies of the BalPure® system, qualified and accredited laboratories were 

utilized for analysis of treated water samples. The methods used to determine 

DBP concentrations are listed in Table 22 below. 

Table 22 : Analytical Methods 

Chemical/ 

Parameter 

US EPA 

Method Description 

Method 

Detection 

Limit (MDL) 

TRO 

(Range: 

0.1-10 

mg/L) 

Hach Method 

10070 

(Equivalent to 

EPA Method 

330.5) 

DPD, colorimetric 0.1 mg/L 

THMs 524.2 Capillary column gas 

chromatography/mass spectrometry 

0.02 - 1.6 

μg/L* 

HAAs 552.1 

Ion-exchange liquid-solid extraction 

and gas chromatography 

with an electron capture detector 

0.07 – 0.45 

μg/L* 

Bromate 300.1 Ion chromatography 1.28 – 1.44 

μg/L* 

*MDL as determined by the analytical method. MDL is compound, instrument and especially 

matrix dependent. 

8 USE OF ACTIVE SUBSTANCE 

8.1 The manner of application 

The BalPure® system can service ships with ballast water flow requirements from 100 to 10,000 

cubic metres per hour. The BalPure® system size (electrolytic cell size) is defined by the ship’s 

designed ballast water flow rate, but because the system has a 100% turn down capability the 

hypochlorite production rate is matched to the actual measured ballast flow rate. Treatment is 

done during ballasting operations allowing the biocide solution to be generated anywhere on the 

ship and injected as needed. This would apply to ships with one or multiple ballast systems or 

ships with multiple ballast pumps mounted within separate ballast tanks. The system can be 

delivered as a complete system on one skid or divided into seven separate smaller skids based on 

specific unit operation (pumping, hypochlorite generation, hydrogen-hypochlorite separation, 

bisulfite storage, bisulfite metered addition, instrument and controls, and power rectification). 

This allows multiple skid locations as space is available throughout the vessel. The multiple skid 

design is perfect for retrofit applications and the one skid system is best for new builds. 
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Operational control of the BalPure® system is accomplished by the main control panel or by the 

remote panel located in the cargo control room. Together, the control panel and the 

transformer/rectifier unit comprise the main Programmable Logic Controller (PLC) control and 

rectification components. The control panel provides a visual display of the status of the 

rectifier DC voltage, current, and can alert the operator of any system alarms via the operator 

interface terminal (OIT). The main control panel also has a local emergency stop push button. 

All major equipment such as booster pumps, bisulfite metering pumps, and hydrogen blowers 

can be controlled from the main control panel. All monitoring equipment such as flow meters 

and ORP probes send the output in the form of 4-20 mA signals. All system control screens are 

password protected to limit operator modification to existing control logic. Only properly trained 

ship’s crew members and BalPure® technicians will be allowed to access password-protected 

portions of the PLC. 

Other system monitoring and control devices include a magnetic flow transmitter to monitor the 

flow of seawater at the electrolyzer inlet, transformer temperature switches that monitor the 

internal temperature of the rectifier, and airflow switches that monitor the hydrogen gas dilution 

blowers. 

8.1.1 Process flow description 

The BalPure® system is designed to operate automatically and has two modes of 

operation: ballasting and de-ballasting. During ballasting, the biocide solution is produced and 

injected into the ballast water intake piping; during de-ballasting sodium bisulfite is added 

directly to the ballast water discharge piping. The ballasting mode is discussed first, followed by 

the de-ballasting mode. A complete process flow diagram (PFD) of the system is included in 

appendix A.34. Figures 5 and 6 presented below provide a simplified overview of each phase of 

the treatment process. 

Very generally, during the automatic ballasting mode, the system will sense that adequate 

seawater flow is available using a flow meter in the main ballast line. Once the system is primed 

with sufficient water (an approximate 1 minute cycle), the transformer/rectifier will supply 

DC current to the electrolyzer and initiate the electrochemical generation process. 

The hypochlorite production rate is primarily tied to the ballast flow rate and achieves the pre-set 

required oxidant concentration by modulating the rectifier output amperage to coincide with the 

ballast flow rate. This is considered the large or gross adjustment. The produced oxidants are 

then injected into the main ballast line. If necessary, the system may also be operated in manual 

mode. Figure 5 below provides an overview of the BalPure® ballasting process. 

 

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Figure 5 : Overview of the BalPure® Ballasting Process 

The BalPure® system remains in a stand-by mode until the flow meter in the main ballast line 

detects ballast water flow and activates the BalPure® system. In the ballasting mode, seawater 

from the sea chest will be filtered with a 40 micron stainless steel mesh filtration unit. If an 

installation requires that seawater be taken from a source other than filtered ballast water 

(e.g., seawater cooling), a duplex strainer filters the seawater to remove any particles larger 

than 800 microns. Using an inline booster pump, the BalPure® system typically receives <1% of 

the total incoming ballast water flow as a side-stream off the main ballast intake line. An inlet 

flow transmitter, designed to protect the treatment system, will shut down the electrical current to 

the electrolyzer should seawater flow through the electrolyzer drop below 80% of the design flow 

rate. The filtered seawater passes through a heat sink where it absorbs excess heat generated by 

the silicon-controlled rectifiers. The seawater then passes through a series of electrolytic cells, 

which are connected to the transformer/rectifier. The electrolyzer units then generate 

the Active Substance along with hydrogen gas as a by-product. 

Immediately after exit from the electrolytic cells, the combined seawater/biocide solution (liquid) 

and hydrogen (gas) is delivered to a patented cyclone separation device where the hydrogen is 

separated from the biocide/seawater solution. Hydrogen gas does not enter the ballast water 

piping or tanks. The hydrogen gas is directed to a vent stack where it is diluted by forced air 

blowers and vented to the atmosphere outside of the ship. To ensure proper ventilation, the vent 

line is serviced by two redundant blowers coupled to sail switches. The sail switches ensure 

proper air flow to dilute the air stream to <1% hydrogen. The LEL for hydrogen is 4% and the 

operating limitations on the system provide a four-fold safety factor. The PLC monitors proper 

air flow and will shut down the system, resulting in an alarm condition if proper ventilation air 

flow is not maintained. Both blower motors and sail switches are tied to an emergency shutdown 
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for the production unit in the unlikely event all four devices fail. For additional safety, 

a hydrogen sensor with alarm will be provided in the general work area. 

For optimum hypochlorite generator performance (i.e. to produce 90% of theoretical values), the 

inlet seawater temperature should be at least 15°C and have a chloride concentration of 

at 19,000 mg/L (19 PSU). However, the BalPure® system can operate at temperatures as low 

as 5°C and salinities of 10,000 mg/L (10 PSU). Less optimal conditions result in a slightly 

decreased hypochlorite production rate to 20% less than optimum. The hypochlorite production 

rate of the electrolytic cells is directly related to chloride ion availability and mobility. 

The salinity (PSU) of the source water determines the chloride ion availability, while temperature 

affects chloride ion mobility. These parameters impact the operating voltage of the electrolytic 

cells. For instance, when chloride ions are abundantly available and mobile, the operating 

voltage and hypochlorite production within the electrolytic cells will be optimum. If chloride 

ions and/or temperature are low, the operating voltage increases proportionally and hypochlorite 

production will be reduced. The BalPure® system is designed to adjust the hypochlorite 

production rate by monitoring the operating voltage of the electrolytic cells and increasing the 

rectifier operating amperage to sustain the TRO concentration required to treat incoming ballast 

water. These adjustments are small and used to control the hypochlorite production rate to 

a narrow range (fine tuning). 

The BalPure® system can also operate at higher salinities, such as ≥30,000 mg/L (≥30 PSU). 

In this case where chloride ions are highly abundant, the generator will only produce the design 

hypochlorite concentration. This is because higher salinity does not increase the efficiency or the 

production rate of the electrolytic cell beyond the optimum. 

By monitoring the operating voltage of the electrolytic cells and adjusting the amperage applied, 

the PLC programming of the BalPure® system guarantees effective operation over a wide 

temperature and/or PSU range. 

In the de-ballast mode of operation, the last phase of the treatment process, residual chlorine 

present in the ballast tank is neutralized (de-chlorinated) with sodium bisulfite just prior to 

discharge from the ship. This is accomplished using ORP technology and bisulfite metering 

pumps. Two ORP probes are used; one confirms the presence of residual oxidant exiting the 

ballast tanks, while the second probe monitors and controls the addition of sodium bisulfite to 

neutralize TRO during ballast water discharge. The first ORP probe is located upstream of the 

bisulfite injection point, and the second ORP probe is located downstream of the bisulfite 

injection point. 
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Figure 6 : Overview of the BalPure® De-ballasting Process 

ORP technology is based on the potential measurement between two dissimilar metals within 

the ORP probe. ORP is not a quantitative measure of oxidant or bisulfite concentration but rather 

a qualitative measure that confirms the presence of oxidizing or reducing agents in the water. 

ORP technology allows for an in-line rapid determination of the amount of oxidation (or 

reduction) potential of the water. ORP is measured in millivolts (mV) and increases or decreases 

in direct relation with the oxidant residual in the water (Kelley, 2004). For example, natural 

waters have an ORP reading in the range of 100 – 150 mV. When hypochlorite is added to water, 

the ORP reading increases with an increase in hypochlorite dosage. Similarly, when a 

de-chlorinating agent such as sodium bisulfite is added to the water, the ORP reading will drop to 

a low mV level (Kelley, 2004). In this way, ORP measurements provide a practical and efficient 

method of optimizing water disinfection and controlling neutralizing agent dosage. 

The first BalPure® ORP probe confirms that there are residual oxidants in the treated water being 

discharged from the ballast tank. In principle, this confirmation of oxidants translates to 

affirmation that there are no living organisms in the discharge. The ORP reading at the first probe 

is typically between 700 and 800 mV. The second ORP probe measures the ORP value of the 

de-ballast stream after bisulfite has been added to the discharge piping. This ORP value is 

typically <200 mV and is used to control the addition of bisulfite solution to ensure complete 

neutralization of residual oxidants. With the mixing effect of the de-ballast water pump and the 

discharge pipe, the bisulfite will easily react with any free oxidants that may be present. As a 

fail-safe measure, the BalPure® system is fitted with two redundant bisulfite metering pumps; 

one pump is the primary dosing pump and the second is an on-line ready spare. 
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Design and engineering of the BalPure® system has considered a variety of safety measures to 

protect the ship’s ballasting system, the BalPure® system, as well as the health and safety of 

crew and technicians. Table 23 below lists some of the primary system alarms to aid the operator 

in proper system function and maintenance. 

Table 23 : Overview of BalPure® System Alarms 

(Table 23 is provided in the complete confidential dossier.) 

It is important to note that because of the redundant engineering of the BalPure® system, an 

alarm condition will not result in the system being non-operational or unsafe. For instance, if 

hydrogen blower ‘A’ were to fail, an alarm would be displayed on the OIT to notify the operator, 

but hydrogen blower ‘B’ would automatically begin operating. This redundancy in system 

components ensures that the system continues to operate effectively and safely even if an alarm 

condition indicates that a system component requires maintenance. 

8.1.2 Chemical storage and handling 

The only chemical that will require onboard storage and handling is the neutralizing agent, 

sodium bisulfite. With the BalPure® system, sodium bisulfite is stored in stainless steel tanks 

designed for installation in a marine setting. Stainless steel is an appropriate material for storage 

of this chemical. Each storage tank is properly vented with a common vent line to an alkaline 

‘scrubber’, then to the atmosphere. Exact tank specifications such as size and location will be 

determined according to the specifics of each ship, and as approved by the ship’s classification 

society. The amount of bisulfite stored on board will depend upon the ballasting operations of 

the vessel such as total ballast capacity and frequency, and be sized to minimize the frequency of 

chemical re-supply. 

The only potential activities that may require ‘handling’ of bisulfite is either system maintenance 

or chemical re-supply operations. The BalPure® system can be installed to include a flush cycle 

after a de-ballasting operation is completed to clear bisulfite from the chemical delivery piping, 

when needed to enhance the safety of the installation or if required by the ship’s classification 

society. This greatly reduces the potential for chemical handling during maintenance activities. 

Normal operation of the BalPure® system involves automatic chemical dosing and does not 

require contact with any chemicals. The bisulfite fill and vent station will be located on the 

weather deck of the vessel; this ensures adequate ventilation. The chemical will be transferred 

only using hose(s) exclusive to bisulfite chemical operations. Proper personal protective 

equipment (PPE) will be worn and only properly trained STDN technicians or representatives 

will be allowed to perform sodium bisulfite re-supply. 
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8.1.3 Various procedures and management measures 

8.1.3.1 Fire 

Sodium bisulfite solution, the only chemical stored on board, is non-flammable and poses no fire 

hazard. As such, it is highly unlikely that sodium bisulfite would be a direct cause of a fire on 

board. If a fire occurred on board in an area surrounding the bisulfite storage tanks, excessive 

heat may result in liberation of harmful fumes (sulfur dioxide). Because the storage tanks are 

properly vented to the atmosphere, this does not pose any direct hazard. As a fire mitigation 

measure, the bisulfite storage tanks can be cooled by applying water spray to the exterior. 

In any fire situation, regardless of source or location, human exposure to fire, smoke, fumes or 

combustion products will be prevented by utilization of proper personal protective equipment 

(PPE). Also, non-essential personnel should be evacuated from the fire area. 

During the in situ electrochemical generation of the Active Substance, hydrogen gas is created as 

a by-product. At concentrations >4% volume in air, hydrogen gas is flammable/explosive. 

The BalPure® system removes hydrogen gas immediately and continuously during the 

electrochemical process via a degassing unit and blowers that vent to the atmosphere at a 

concentration of <1% vol. in air. 

 

8.1.3.2 Accidental release measures

Technicians and ship’s crew will be sufficiently trained to respond to a sodium bisulfite spill 

situation. Training will include, but may not be limited to, familiarization of the chemical 

properties and reactivity, exposure hazards, and correct donning of PPE. Proper PPE will include 

respiratory protection equipment, eye and face protection (goggles and/or face shield), chemical 

resistant gloves and boots (or boot covers), and chemical resistant clothing. 

In the unlikely event there is an accidental release of sodium bisulfite, the spill should be 

contained and neutralized with an alkali such as sodium carbonate, sodium bicarbonate, soda ash, 

lime or limestone granules. All spilled material and neutralization residues must be disposed of 

in accordance with applicable regulations. Decomposition of sodium bisulfite may liberate sulfur 

dioxide, which can be harmful when inhaled. Adequate ventilation and respiratory protection are 

required in any area of accidental release. 

 

8.1.3.3 Marine environment release

Sodium bisulfite (38% solution) is slightly acidic and should not be allowed to freely enter the 

marine environment as a concentrated solution. In the unlikely event of a marine environment 

release, sodium bisulfite is water soluble and will not cause surface impacts such as slicks or 

thick sludge. Spills should be reported as required by the appropriate agency. Storage in tanks 

constructed of appropriate materials and proper handling of bisulfite during chemical supply 

operations are the primary measures that reduce the potential risk of marine environment 

release. 
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 8.1.3.4 Conditions for controlled release

In the unlikely event that sodium bisulfite needs to be removed from the onboard storage tanks, a 

controlled removal utilizing the appropriate chemical transfer pumps, discharge piping and 

vessel-specific safety protocols will be conducted. 

8.1.4 Evaluation of management measures 

The BalPure® system has been properly designed and constructed for use on board ships. 

The risk management measures consider safe placement of the system on board, proper crew and 

technician training, and substance storage/handling that will prevent emergency situations such 

as accidental release and chemical exposure situations. The management measures discussed in 

section 8.1.3 above are considered adequate to properly manage the chemicals used with the 

BalPure® system and reduce hazards to the ship, personnel, and the environment. 

9 MATERIAL SAFETY DATA SHEETS (G9: 4.2.7) 

The hazard classifications presented in this section reflect reported hazards only and do not 

consider the actual potential for exposure to the substances or hazards associated with the 

BalPure® system. Safety mechanisms in the BalPure® system and proper safety practices 

mitigate potential hazards identified. Material Data Safety Sheet (MSDS) and/or International 

Chemical Safety Card (ICSC) information is provided in appendix A.45. 

9.1 Active Substances hazard classification 

Also known as bleach, sodium hypochlorite will be generated at a concentration of ~0.1 wt % 

before being injected into the ballasting system. As the sodium hypochlorite enters the ballast 

system it is diluted to ~10 mg/L. Common household bleach is often sold in a 5% (50,000 mg/L) 

concentration, which is many times greater than the concentration used with the ballast treatment 

system. An MSDS is not available for the chemical composition being produced inside the 

BalPure®. However, ICSC #0482 (<10% solution) has been used for hazard classification. 

R-Phrases: R31, R36/38 S-Phrases: S1/2, S28, S45, S50, S61 

Sodium hypochlorite is not stored on board, but is generated in situ and injected directly into the 

ballast piping. When the system has completed a treated ballasting operation and is shut down, 

an automatic flush cycle clears any residual chemical from the piping. The only storage of 

sodium hypochlorite on board the vessel is in the ballast tanks at a concentration of < 20 mg/L. 

9.2 Hazard classification of Relevant Chemicals 

9.2.1 Trihalomethanes (THMs), Haloacetic Acids (HAAs), Bromate 

THMs, HAAs and bromate disinfection by-products may be formed at varying low-level 

concentrations in ballast water during the BalPure® treatment process. Concentrated solutions of 

these substances will never be transported or utilized on board ship. As such, typical MSDSs for 

these low-level substances (parts per billion range) do not accurately represent the potential 

 

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hazards that may be presented by these chemicals in treated ballast water. Determining the 

hazards for these substances at part per billion levels is not feasible when the MSDSs reflect 

hazards for much higher concentrations. 

Paragraph 5.3 of the Methodology seems to allow for this justification based on the above 

information. As such, the R-phrases and S-phrases are not detailed for these disinfection 

by-products; however, the MSDSs are included in appendix A.46

. 

9.2.2 Hydrogen gas 

While producing sodium hypochlorite, the BalPure® system produces hydrogen gas as 

a by-product. As discussed in section 8.1.1, hydrogen is removed from the sodium hypochlorite 

solution stream in a degassing unit as part of the BalPure® system and vented to the atmosphere. 

Non-compressed hydrogen is not considered a hazardous material in the table 

in 49 CFR 172.101. A non-sparking blower in the degasser unit dilutes the hydrogen to 

a concentration of less than 1% (well below the 4% Lower Explosive Limit) before reaching the 

atmosphere. Hazard classifications according to ICSC #0001 are as follows: 

R-Phrases: R12 S-Phrases: S2, S9, S16, S33 F+ symbol 

9.3 Hazard classification of other chemicals 

9.3.1 Sodium bisulfite 

Sodium bisulfite 38% solution is added to hypochlorite treated ballast water as it is being 

discharged from the ship. This is the only substance stored on board. The quantity stored will 

vary depending on the amount of ballast water treated and will be specific to each installation. 

Sodium bisulfite is stored in vented stainless steel tanks. Hazards according to the MSDS are as 

follows: 

 R-Phrases: R20, R22, R36, R37, R38 S-Phrases: S26, S36 

 

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10 RISK CHARACTERIZATION AND ANALYSIS 

10.1 Screening for persistence, bioaccumulation and toxicity (G9: 5.1) 

Table 24 : PBT Criteria Evaluation 

Substance 

Persistence (P) Half-life: 

>60 days in marine water (MW), or 

>40 days in freshwater (FW) , or 

>180 days in marine sediment (MS), 

or 

>120 days in freshwater sediment 

(FWS) 

 (YES or NO) 

Bioaccumulation (B) 

BCF >2,000 

or Log Kow 

≥3 

(YES or 

NO) 

Toxicity (T) 

Chronic 

NOEC 

<0.01mg/L 

(YES or NO) 

Active substances

Hypochlorous 

acid 

No 

FW: 15 days (EPI Suite, 2009c) 

No 

Log Kow = -

0.87 

No 

Lowest NOEC 

= 0.042 mg/L 

(Fish) 

Hypobromous 

acid 

No 

FW: 15 days (EPI Suite, 2009b)

No 

Log Kow = -

0.78 

No 

based on 

hypochlorous 

acid 

Relevant Chemicals

Bromate No 

FW: 15 days (EPI Suite, 2009a) 

No 

Log Kow = -

4.6 

No 

Lowest NOEC 

= 8 mg/L 

(Crustacean) 

THMs

Chloroform 

No 

FW: 4.4 days; Not expected to adsorb 

to sediment. (HSDB/TOXNET 2009f)

No 

BCF = 2.9-

10.35 

No 

Lowest NOEC 

= 1.5 mg/L 

(Fish) 

Bromoform 

No 

FW: 7.1 days; Not expected to adsorb 

to sediment. (HSDB/TOXNET 2009l)

No 

BCF = 14 

No 

Lowest NOEC 

= 8.5 mg/L 

(Fish) 

Dichlorobromomethane 

No 

FW: 5 days; Not expected to adsorb to 

sediment. (HSDB/TOXNET 2009c)

No 

BCF = 7 

No 

LC50 = 

72 mg/L (Fish) 

Chlorodibromomethane 

No 

FW: 6 days; Not expected to adsorb to 

sediment. (HSDB/TOXNET 2009e)

No 

BCF = 9 

No 

LC50 = 

34 mg/L (Fish) 

HAAs

Bromochloroacetic 

acid 

No biodegradation data available. Not 

expected to adsorb to suspended 

solids or sediment. (HSDB/TOXNET 

2009b)

No 

Log Kow = 

0.61 

Data not 

located. 
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Substance 

Persistence (P) Half-life: 

>60 days in marine water (MW), or 

>40 days in freshwater (FW) , or 

>180 days in marine sediment (MS), 

or 

>120 days in freshwater sediment 

(FWS) 

 (YES or NO) 

Bioaccumulation (B) 

BCF >2,000 

or Log Kow 

≥3 

(YES or 

NO) 

Toxicity (T) 

Chronic 

NOEC 

<0.01mg/L 

(YES or NO) 

Monochloroacetic 

acid 

No 

FW: 14 days (Ellis, et al. 2001); Not 

expected to adsorb to sediment. 

(HSDB/TOXNET 2009d)

No 

Log Kow = 

0.22 

No 

Lowest NOEC 

= 0.13 mg/L 

(Algae) 

Monobromoacetic 

acid 

No half life data available; Not 

expected to adsorb to sediment. In 

aqueous biodegradation screening 

tests, reached 82% of its theoretical 

BOD when using pre-acclimatized 

inoculums (HSDB/TOXNET 2009a)

No 

Log Kow = 

0.41 

No 

NOEC = 

3.2 mg/L 

(Crustacean) 

Dichloroacetic 

acid 

No 

FW: 4 days (Ellis et al.2001); Not 

expected to adsorb to sediment. 

(HSDB/TOXNET 2009h)

No 

Log Kow = 

0.92 

No 

EC03 = 

1485 mg/L 

(Algae) 

Dibromoacetic 

Acid 

No 

FW: 14 days (HSDB/TOXNET 

2009g)

No 

BCF = 0.17 

No 

Lowest LC50 = 

69 mg/L (Fish) 

Trichloroacetic 

acid 

No 

FW: 40 days (Ellis et al 2001); Not 

expected to adsorb to sediment. 

(HSDB/TOXNET 2009m)

No 

BCF = 0.1-

1.7 

No 

Lowest NOEC 

= 100 mg/L 

(Algae) 

Other Chemicals

Sodium bisulfite 

No 

FW: 15 days (HSDB/TOXNET 2009-

j)

No 

BCF = 3.2 

No 

Lowest LC50 = 

100 mg/L 

(Fish) 

Note: Based on an evaluation of the data presented in Table 24 above, none of the substance 

meet all three criteria to be considered as PBT substances. 

10.1.1 Persistence (G9: 5.1.1.1) 

Using the half-life criteria of >40 days in fresh water or sediment persistence, an evaluation of 

the environmental persistence data for Active Substances, Relevant Chemicals, and other 

chemicals indicates that none of the substances are likely to be persistent in the environment. 

See Tables 16 and 24 above. 
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10.1.2 Bioaccumulation (G9: 5.1.1.2) 

Using the criteria of either BCF >2000 or Log Kow ≥ 3, an evaluation of the data 

for Active Substances, Relevant Chemicals, and other chemicals indicates that the substances 

have low potential for bioaccumulation. See Table 7 above. 

10.1.3 Toxicity tests (G9: 5.1.2.3) 

Chronic aquatic toxicity data was not located for hypobromous acid but toxicity is thought to be 

less than or similar to the chlorinated analog, hypochlorous acid. Chronic aquatic toxicity data 

was not located for two THMs (bromodichloromethane, and dibromochloromethane). Therefore, 

the lowest acute aquatic toxicity data points were considered. Chronic aquatic toxicity was not 

located for two HAAs (bromochloroacetic acid and dibromoacetic acid), and limited chronic data 

was located for the other HAAs. Acute toxicity data was also not located for bromochloroacetic 

acid and could not be considered. In the case of dichloroacetic acid and dibromoacetic acid, the 

lowest acute toxicity data points available were considered. 

With the exception of the substances noted above where chronic toxicity data was limited, all 

other substances did not have chronic NOEC values <0.01 mg/L. 

11 EVALUATION OF THE TREATED BALLAST WATER (G9: 5.2) 

Numerous studies have been conducted on the BalPure® system to evaluate many aspects of 

treated water. In addition to the aquatic toxicity data presented in section 3, data on TRO, water 

quality parameters (e.g., salinity, pH, particulate organic carbon (POC), dissolved organic carbon 

(DOC), total suspended solids (TSS), and disinfection by-products (DBPs) have been measured 

and recorded, and is provided in this section. 

11.1 Total Residual Oxidants 

During testing of the BalPure® treatment system conducted at the University of Washington 

in 2008, varying hypochlorite concentrations were applied and TRO levels were measured at 

different time intervals after treatment. Table 25 below presents TRO data from three different 

water types that were treated. The Day 0 value represents the applied concentration of 

the Active Substance. As expected, the TRO concentration decayed quickly immediately after 

treatment, and then more slowly after the demand of the water was met. Regardless of water 

type, decay of TRO follows a predictable and consistent pattern. Also see figure 3. 
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Table 25 : Total Residual Oxidant (TRO) measured as Total Chlorine 

Day 

Treatment 

Tank 1* 

TRO (mg/L) 

Treatment 

 Tank 2 

TRO (mg/L) Reference

Freshwater

5-Dec (Day 0) 6.7 5.7 Sosik & Herwig, 2009 

7-Dec (Day 2) 2.3 1.5 Sosik & Herwig, 2009 

10-Dec (Day 5) 1 0.5 Sosik & Herwig, 2009 

15-Dec (Day 10) 0 0 Sosik & Herwig, 2009 

Brackish Water 

9-Dec (Day 0) 9.1 10.5 Sosik & Herwig, 2009 

11-Dec (Day 2) 6.3 N/A Sosik & Herwig, 2009 

14-Dec (Day 5) 4.8 3.9 Sosik & Herwig, 2009 

19-Dec (Day 10) 0 0 Sosik & Herwig, 2009 

Saltwater 

9-Dec (Day 0) 4.3 4.5 Sosik & Herwig, 2009 

11-Dec (Day 2) 3.6 N/A Sosik & Herwig, 2009 

14-Dec (Day 5) 3.1 N/A Sosik & Herwig, 2009 

19-Dec (Day 10) 0 N/A Sosik & Herwig, 2009 

*Samples from Tank 1 were collected for DBP and toxicity evaluation and correspond 

to the data presented below. 
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11.2 Water quality parameters 

During the University of Washington studies in 2008, water quality parameters of the treated 

water were measured. These included salinity, pH, POC, DOC ad TSS. In the case of fresh 

water and brackish water treatments, amendments were made to increase the organic and 

suspended solids loads. Table 26 summarizes the data. 

Table 26 : Summary of Water Quality Parameters 

Parameter Fresh 

water 

Brackish 

Water 

Seawater Reference 

Initial POC (mg/L) 2.81 2.72 1.37 Sosik & Herwig, 2009 

Initial DOC (mg/L) 3.72 5.69 4.23 Sosik & Herwig, 2009 

Initial TSS (mg/L) 34.46 76.09 3.75 Sosik & Herwig, 2009 

Salinity range 

(PSU) 

0.62 -0.64 21.54 – 21.75 30.48 – 

30.57 

Sosik & Herwig, 2009 

pH range 7.23 - 7.74 7.15 – 8.26 7.46 – 7.97 Sosik & Herwig, 2009 

Temperature range 

(°C) 

10.9 – 

13.16 

6.72 – 9.75 6.43 – 9.36 Sosik & Herwig, 2009 

11.3 Disinfection By-Products (DBPs) in treated ballast water 

The studies of the BalPure® system conducted by the University of Washington in 2008 also 

evaluated treated water samples collected at different time intervals for THMs and HAAs. 

The concentrations of THMs and HAAs after treatment with the BalPure® system of three 

different water types (freshwater, brackish water, and seawater) were evaluated. As stated in 

section 2.3.1, the presence of tribromoacetic acid was not determined analytically during pilot 

studies and is not anticipated to be present at environmentally relevant concentrations. However, 

tribromoacetic acid will be evaluated during land-based testing and reported in a subsequent 

application for Procedure (G9) Final Approval. Tables 27, 28 and 29 present data from samples 

collected immediately after treatment (Day 0), two days after treatment (Day 2), five days after 

treatment (Day 5), and ten days after treatment (Day 10). The samples collected on Day 0 

and Day 2 were analysed prior to the neutralization step. The samples collected on Day 5 

and Day 10 were analysed after neutralization with sodium bisulfite. 

Bromate was also evaluated for in the brackish water and seawater testing cycles. The results for 

bromate are presented in Tables 28 and 29. 
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Table 27 : Levels of Trihalomethanes (THMs) and Haloacetic acids (HAAs) 

in Treated Fresh water 

FRESHWATER 

Day 0 Day 2 Day 

5* 

Day 

10* Reference 

THM (EPA Method 

524.2) μg/L μg/L μg/L μg/L 

chloroform 21.6 42.2 52.9 43.1 Sosik & Herwig, 

2009 

dichlorobromomethane 33.2 70.8 90.2 73.6 Sosik & Herwig, 

2009 

chlorodibromomethane 71.8 127 157 123.7 Sosik & Herwig, 

2009 

bromoform 69.7 92.1 100 95 Sosik & Herwig, 

2009 

Total THM 196.3 332 400 335.4 Sosik & Herwig, 

2009 

HAA (EPA Method 

552.1) 

bromochloroacetic acid 23.4 49.7 38.3 44.2 Sosik & Herwig, 

2009 

monochloroacetic acid 3.9 2.5 2.7 2.8 Sosik & Herwig, 

2009 

dichloroacetic acid 18.4 38.8 33.7 39.5 Sosik & Herwig, 

2009 

trichloroacetic acid 33 42.2 47.7 56.3 Sosik & Herwig, 

2009 

monobromoacetic acid 2.4 3.3 3.3 2.1 Sosik & Herwig, 

2009 

dibromoacetic acid 36 51.1 47.4 54 Sosik & Herwig, 

2009 

Total HAA (6) 93.7 137.9 134.8 154.7 Sosik & Herwig, 

2009 

 “*” = Experimental tanks were neutralized with sodium bisulfite. 
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Table 28 : Levels of Trihalomethanes (THMs) and Haloacetic acids (HAAs) 

in Treated Brackish Water 

BRACKISH WATER 

 Day 0 Day 2 Day 

5* 

Day 

10* Reference 

THM μg/L μg/L μg/L μg/L 

chloroform 0 0.5 0.6 0.5 Sosik & Herwig, 

2009 

dichlorobromomethane 2.4 6.4 6.3 4.6 Sosik & Herwig, 

2009 

chlorodibromomethane 13.4 42.8 45.7 34.1 Sosik & Herwig, 

2009 

bromoform 209 854 1046 782.8 Sosik & Herwig, 

2009 

Total THM 225 904 1099 822 Sosik & Herwig, 

2009 

HAA 

bromochloroacetic acid 11.2 7.8 9.4 7.1 Sosik & Herwig, 

2009 

monochloroacetic acid 7.4 12.1 15.3 0 Sosik & Herwig, 

2009 

dichloroacetic acid 2.9 1.2 2.4 3.7 Sosik & Herwig, 

2009 

trichloroacetic acid 0 1.5 1.5 0.7 Sosik & Herwig, 

2009 

monobromoacetic acid 8.4 8.4 6.1 3.5 Sosik & Herwig, 

2009 

dibromoacetic acid 117.9 219 156.3 193 Sosik & Herwig, 

2009 

Total HAA (6) 136.6 242.2 181.6 200.9 Sosik & Herwig, 

2009 

Bromate 0 33 23 42 Sosik & Herwig, 

2009 

“0” = Level below detectable limits, <2 μg/L. 

“*” = Experimental tanks were neutralized with sodium bisulfite. 

 
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Table 29 : Levels of Trihalomethanes (THMs) and Haloacetic acids (HAAs) 

in Treated Seawater 

SEAWATER 

 Day 0 Day 2 Day 

5* 

Day 

10* Reference 

THM μg/L μg/L μg/L μg/L 

chloroform 0 0 0 0 Sosik & Herwig, 

2009 

dichlorobromomethane 0 0 0 0 Sosik & Herwig, 

2009 

chlorodibromomethane 0.7 2.7 3.4 2.2 Sosik & Herwig, 

2009 

bromoform 32.6 106.9 117.9 90.1 Sosik & Herwig, 

2009 

Total THM 33.3 109.6 121.3 92.3 Sosik & Herwig, 

2009 

HAA 

bromochloroacetic acid 0 0 0 0 Sosik & Herwig, 

2009 

monochloroacetic acid 5.3 12.8 9.9 0 Sosik & Herwig, 

2009 

dichloroacetic acid 0 0 0 0 Sosik & Herwig, 

2009 

trichloroacetic acid 0 0 0 0 Sosik & Herwig, 

2009 

monobromoacetic acid 0 1.4 2.2 0 Sosik & Herwig, 

2009 

dibromoacetic acid 12.5 19.6 24.7 19.3 Sosik & Herwig, 

2009 

Total HAA (6) 17.8 33.8 36.8 19.3 Sosik & Herwig, 

2009 

Bromate 0 13 23 14 Sosik & Herwig, 

2009 

“0” = Level below detectable limits, <2 μg/L. 

“*” = Experimental tanks were neutralized with sodium bisulfite. 

The data in Tables 27 and 28 show unexpected levels of brominated by-products, particularly 

bromoform, in fresh water and brackish water treatments. During these University 

of Washington (Sosik and Herwig, 2009) studies amendments were added to the fresh water and 

brackish water test runs to increase the organic matter and suspended solids. Amendments 

included were unsweetened tea, humate and test dust. These amendments were not added to the 

salt water test run. Although definitive analytical data of a potential bromide source in these 

amendments is not available, their addition to test waters appears to have unintentionally 

increased the production of disinfection by-products. Because the amendments may have been 

processed using unknown chemicals or may contain other unknown contaminants, it is difficult 

to compare the observed disinfection by-product levels to those that may occur as a result of 

treating waters with naturally present organic matter. 
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For the brackish water test run, where higher levels of bromoform were measured, there is an 

additional factor likely contributing to the levels of brominated organic by-products observed. 

To reach the desired brackish water salinity, natural seawater was diluted with tap water from a 

municipal water source. This water had been previously chlorinated using chlorine gas. 

The researchers aerated the water to remove pre-existing chlorine; however, at the pH of the test 

water most of the residual chlorine present in the tap water would exist as HOCl/OCl- and 

some HOBr/OBr-

 if the chlorine had a small bromine impurity. Therefore, use of local 

chlorinated tap water potentially increased the level of hypochlorite ion in treated water and may 

also be a source of bromine. Additionally, the tap water source likely had pre-existing levels of 

disinfection by-products. Disinfection by-product data for the specific date the tap water was 

used by the researchers is not known, but the annual report from the municipal water treatment 

facility indicates that levels of THM’s and HAA’s detected during 2008 were 23.2 μg/L 

and 15.5 μg/L, respectively, (City of Port Townsend, 2008). 

Due to the addition of amendments, the potential presence of bromine present in the chlorine 

source prior to treatment with the STDN system, along with the presence of pre-existing 

disinfection by-products, it can be reasonably deduced that these factors influenced the levels of 

brominated by-products in the fresh water and brackish water studies. Further analysis of 

disinfection by-products will be conducted during land-based testing. 

11.4 Toxicity testing of treated ballast water 

11.4.1 University of Washington studies 

Toxicity testing of water treated with the BalPure® system has been conducted 

by Nautilus Environmental (Nautilus, 2009). In conjunction with BalPure® system mesocosm 

studies undertaken at the University of Washington (Sosik and Herwig, 2009), Nautilus evaluated 

treated water collected at differing time intervals after treatment and after neutralization with 

bisulfite. The mesocosm studies were done with three different water types: fresh water, 

brackish, and seawater. Acute aquatic toxicity testing was performed with algae, invertebrates, 

and fish for water samples collected immediately after treatment with hypochlorite (Day 0), 2 

days after hypochlorite treatment, and 5 days after hypochlorite treatment. These samples were 

collected and tested prior to the neutralization step (i.e. pre-neutralization). After the Day 5 

samples were collected, residual oxidants in the mesocosms were neutralized with bisulfite and a 

second Day 5 sample was collected for testing. Finally, 5 days after neutralization (i.e. 10 days 

after hypochlorite treatment) additional samples were collected for toxicity testing. The toxicity 

data is presented in section 3. Water from the mesocosm studies was also evaluated for TRO, 

water quality parameters, and disinfection by-products (DBPs). The data are presented 

in Tables 25, 26, 27, 28 and 29. 

As expected, toxicity was observed for all species in the samples collected immediately after 

hypochlorite treatment (Day 0). Some toxicity was observed in the Day 2 and Day 5 

pre-neutralization samples, with the exception of freshwater fish. With the exception of one data 

point for the marine diatom (Skeletonema) in brackish water, toxicity was not observed in the Day 5 

post-neutralization samples. Although the sensitivity between the taxonomic groups (algae, 

invertebrate, and fish) varied with the water type (freshwater, brackish, and seawater) tested, fish 

were the most tolerant species and invertebrates were generally the least tolerant species. Overall, the 

most sensitive species tested was Daphnia magna (Nautilus, 2009). In all species tested, no toxicity 

was observed in the samples tested 5 days after neutralization (Day 5+). 
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Because sodium bisulfite is injected into the ballast water discharge line at a slight excess to 

ensure that all residual oxidants are neutralized, Nautilus Environmental performed toxicity 

testing using a very large excess of bisulfite (Nautilus, 2005). Seawater samples treated with 

sodium hypochlorite generated with the BalPure® system were provided to Nautilus by 

the University of Washington on behalf of STDN. Test solutions were prepared by diluting the 

chlorinated sample with laboratory seawater to a total chlorine concentration of 3 mg/L, and then 

neutralizing with a 22 mg/L solution of sodium bisulfite. Although only 6 mg/L of bisulfite 

would be needed to neutralize a 3 mg/L hypochlorite treatment, the substantially higher bisulfite 

addition was evaluated to determine a safety margin for the neutralization process 

(Nautilus, 2005). A 0.5X dilution series was used to obtain a definitive toxicity threshold. 

Toxicity tests were conducted using 7-day chronic (sub-lethal endpoints) tests with a mysid 

(Mysidopsis bahia) and a fish (Menidia beryllina), a 48-hour larval development test using a 

mussel (Mytilus edulis), a 48-hour germination and germ tube length test using giant kelp 

(Macrocystis pyrifera), and a 16-day embryo development test using Pacific herring 

(Clupea pallasi). Results were that none of the test endpoints exhibited a 25% reduction relative 

to the control. These data suggest that a 3 mg/L treatment of hypochlorite in seawater with up 

to 22 mg/L of sodium bisulfite would not be expected to exhibit an adverse effect, defined as 

resulting in a 25% performance reduction for the endpoint tested. Based on this study, the safety 

factor = 22 /application rate (mg/L sodium bisulfite) was determined. This safety factor is 

considered conservative because no effects were observed at this treatment level 

(Nautilus, 2005). 

Evaluating toxicity to aquatic organisms at various holding times after treatment (without 

neutralization) demonstrates that the residual chlorine remains effective after treatment. Additionally, 

performing toxicity testing pre- and post- neutralization verifies that the bisulfite treatment is effectively 

removing residual oxidants making treated water discharge environmentally safe. Lastly, dosing with 

excessive neutralizing agent, as well as holding neutralized water for an additional 5 days and then 

performing toxicity testing, demonstrates that the neutralizing agent is not itself toxic or otherwise 

making the neutralized discharge toxic to aquatic organisms. 

Documentation of the quality assurance program for toxicity testing at Nautilus Environmental is 

included in appendix A.77

. 

11.4.2 Naval Research Laboratory studies 

Chronic toxicity tests were conducted by Nautilus Environmental (Nautilus, 2007) using treated 

ballast water samples collected during the full-scale study at the Naval Research Facility in Key 

West, Florida (United States). Samples were collected from challenge tests in which organism 

and organic enriched ballast water was treated with hypochlorite to a 15 mg/L total residual 

oxidant (TRO) concentration and then held for 48 hours (2 days). After 48 hours the treated 

water was neutralized with an excess concentration of ~ 2 mg/L sodium bisulfite. Five 

concentrations of treated sample using a 0.5X dilution series were tested. Bioassays were 

conducted using 7-day tests with a mysid (Americamysis bahia) and a larval fish (Menidia 

beryllina), a 48-hour larval development test using a mussel (Mytilus galloprovincialis), and a 

48-hour germination and germ tube length test using the giant kelp (Macrocystis pyrifera). 

Chronic toxicity tests using mysid shrimp and silverside minnows were conducted according 

to US EPA (2002) methods. Chronic toxicity tests using mussels and giant kelp were conducted 

according to US EPA (1995). 

 

7

 Appendix A.7 is provided in the confidential dossier of the proposal for approval. 
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Results for the chronic toxicity tests are summarized in Table 5. No toxicity was observed with 

the treated water samples for any species tested. The highest concentration with no observed 

effect (NOEC) was 100 percent sample (Nautilus, 2007). 

11.5 Determination of holding time 

Because the BalPure® system employs an oxidant neutralization step at discharge, there is no 

specified holding time required before treated water can be safely discharged to the environment. 

Using ORP technology (discussed in section 8.1.1) sodium bisulfite can be added to the ballast 

water discharge line at the concentration needed to ensure that all residual oxidants are 

neutralized. Aquatic toxicity testing performed with treated water samples pre- and 

post-neutralization with sodium bisulfite demonstrates that the discharge has no adverse effect 

after the neutralization process. Toxicity testing results with excessive treatment of sodium 

bisulfite also indicate that there is no adverse effect from sodium bisulfite. The data is presented 

in Tables 3 and 5. 

Therefore, the holding time that treated ballast water needs to be retained is determined by the 

amount of contact time required to properly disinfect and inactive AIS. Studies performed at 

the University of Washington determined that at low (<2 mg/L) TOC concentrations 98%-100% 

of organisms were inactivated 5 hours after hypochlorite treatments of 2.95 mg/L–3.71 mg/L 

(Herwig et al., 2006). Studies performed at the Naval Research Laboratory determined BalPure®

hypochlorite treatments of 14 mg/L–16 mg/L effectively inactivated >99% of organisms 24 hours 

after treatment in seawater with 10 mg/L TOC (NRL, 2007). These studies indicate that even if a 

ship had to discharge treated ballast water shortly after hypochlorite treatment, the number of live 

organisms would be very limited and no aquatic toxicity could be expected from neutralized 

discharge. 

11.6 Reaction with organic matter 

As discussed in section 2, chlorine-based water disinfection can result in the formation of THMs 

and HAAs. The concentration of these DBPs that will result from disinfection is based on 

the Active Substance dose as well as the parameters of the water being treated (e.g., TOC, pH, 

temperature), with the amount of TOC being of significant influence. Lower TOC levels reduces 

the amount of DBPs formed. The BalPure® system filters incoming ballast water, which will 

reduce the amount of TOC, and thereby, the DBPs formed during disinfection. The levels 

of THMs and HAAs in treated ballast water at various doses of Active Substance in different 

water types and water quality conditions is presented in section 11.3. The concentrations 

of THMs and HAAs in treated water discharge will be monitored further during land-based 

testing at NIOZ. Results of this testing will be reported in the future dossier for Final Approval. 

11.7 Characterization of degradation route and rate (G9: 5.3.5) 

For all substances related to use of the BalPure® system, both the biotic and abiotic degradation 

data are shown in Table 16. For THMs and HAAs, biotic degradation for all of these simple 

halogenated organic compounds is on the order of days to weeks. Abiotic degradation of these 

compounds is longer. In the case of bromate and sodium bisulfite, no specific degradation 

information was located in the existing literature. However, for these inorganic substances, the 

BCF, Koc, and Log Kow values indicate low potential for bioaccumulation, low adsorption to 

sediment, and high water solubility. 
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11.8 Prediction of discharge and environmental concentrations 

Due to the oxidant neutralization step during ballast water discharge, the TRO in treated water 

discharge will be non-detectable. Therefore, the discharge and predicted environmental 

concentration (PEC) for TRO is 0 mg/L. 

Sodium bisulfite is added to ballast water discharge at a slight excess to ensure that any residual 

oxidants have been reacted. As such, treated water discharge may contain sodium bisulfite. 

In seawater bisulfite is reduced to bisulfate, and ultimately to sulfate ion as shown 

in Reactions 14-16 in section 2.4. In the marine environment, sulfate ion is ubiquitous and does 

not pose unacceptable environmental risks. Therefore, discharge or environmental 

concentrations are not considered relevant. 

During the pilot studies of the BalPure® system, the amounts of DBPs in treated water discharge 

were evaluated in three different water types (fresh water, brackish water and seawater), at 

different Active Substance treatments and organic matter levels. The data is presented in 

sections 11.1 to 11.3 above. In fresh water, total THMs in treated water ranged 

from 196.3 μg/L – 400 μg/L and total HAAs ranged from 93.7μg/L–154.7 μg/L. In brackish 

water, total THMs ranged from 225 μg/L–1099 μg/L and total HAAs ranged 

from 136.6 μg/L–242.2 μg/L. In seawater, total THMs ranged from 33.3 – 121.3 μg/L and 

total HAAs ranged from 17.8 – 36.8 μg/L. The DBP bromate was also measured in the brackish 

and seawater studies. In brackish water, bromate concentrations ranged from <2 – 42 μg/L. 

In seawater, bromate concentrations ranged from <2 μg/L–23 μg/L. 

As discussed in section 5.4, formation of DBPs is dependent upon several variables such 

as Active Substance dose, contact time, pH, organic matter, etc. Data from the BalPure®

discharge reflects those trends. For instance, the highest THM and HAA formation occurred in 

the brackish water treatment where the hypochlorite dose, organic matter, and suspended solids 

were the highest. Similarly, the lowest THM and HAA formation occurred in the seawater study 

where the hypochlorite dose, organic matter and suspended solids were at lower levels. 

Additional contributing factors to the levels of brominated by-products observed are discussed 

above in section 11.3. 

The DBP concentrations from the pilot studies noted above consider analysis of the whole 

effluent (i.e. discharge concentration) only and do not reflect actual environmental concentrations 

when treated ballast water is released in a harbour where dilution and mixing will occur. 

Meaningful PEC values will be derived using appropriate emission scenario modelling based on 

analysis of treated ballast water samples drawn from the full-scale land-based test setup of 

the-BalPure® system and will be presented in a future dossier for Final Approval. 

Regardless of the Relevant Chemical discharge concentrations, it is important to note that acute 

and chronic (sub-lethal endpoint) toxicity testing of the neutralized whole effluent from 

the BalPure® system was not toxic to aquatic organisms, with the only exception 

being Skeletonema (EC50 66.1%, Table 3) in one fresh water study. 
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11.9 Assessment of potential for bioaccumulation 

Based on the data shown in Table 7 for both Active Substances and Relevant Chemicals, all of 

these substances have very low BCFs, indicating that they are unlikely to bioaccumulate in 

aquatic organisms or present a significant food chain risk. With the exception of the THMs, all 

of the Active Substances and Relevant Chemicals have very low log Kow’s, which indicates the 

compounds are hydrophilic. The THMs, as would be expected, are moderately hydrophobic. 

However, none of the log Kow values estimated and/or located in the literature are ≥ 3. 

11.10 Effects assessment 

The data for the substances associated with use of the BalPure® system indicate that there is a 

low potential for bioaccumulation, sediment adsorption, and persistence in the aquatic 

environment. No effects or risks in the form of secondary (food chain) poisoning or to sediment 

species are anticipated. As such, aquatic toxicity presents the only likely potential risk for 

aquatic organisms. 

Whole effluent toxicity testing (acute and sub-lethal endpoints) of neutralized ballast water 

discharge suggests no apparent toxicity for all species and endpoints tested (E(L)C50 and/or 

NOEC values of ≥100% ballast water sample) with the exception of one marine diatom, 

Skeletonema costatum (96-hour exposure EC50 of 66.1% sample) (Nautilus, 2009). In light of 

these results, although aquatic toxicity is identified as having the most potential for risk to 

aquatic organisms, toxicity testing results suggest the potential risk is low. 

11.11 Effects on aquatic organisms 

A thorough literature review of available acute and chronic toxicity data for the substances 

associated with the STDN system was conducted; the data are presented in Tables 2 and 4. 

However, the data set is limited for many of the substances. Even where data was located in 

literature studies did not meet validity criteria, it could only be used as supporting information. 

This resulted in incomplete data sets for fish, crustaceans, and algae that prevented individual 

PNEC derivation for all substances based on the guidance in the Methodology (MEPC 58/2/7) as 

well as the Technical Guidance Document on Risk Assessment (2004). Similar data gaps are 

also noted in other dossiers submitted for Procedure (G9) approval, suggesting that other 

literature searches have had similar findings. 

When a complete valid data set was located in literature, and/or any supporting data could be 

identified, the reported toxicity values have been used for PNEC derivation. Where the available 

data is limited, the PNEC derivation approach used in the EU RAR for Sodium Hypochlorite 

(2007) was utilized. 

Two valid acute aquatic toxicity data points (one fish, one crustacean) were located for TRO 

(saltwater), with one additional acute data point for algae used as supporting information. 

Additionally, one valid chronic fish test was located, while one chronic endpoint for crustacean 

and one chronic endpoint for algae were located as supporting information. The lowest acute 

effect concentration reported was 0.062 mg/L. Using a higher assessment factor (1000) because 

the data is based on acute endpoints and the algae exposure period was only 24 hours, results in a 

PNEC for TRO (saltwater) of 0.062 μg/L. This corresponds directly with the PNECsaltwater value 

derived in the sodium hypochlorite RAR; also 0.06 μg/L (as TRC). 
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For hypochlorous acid (HOCl), a complete data set of acute toxicity end points was located. One 

valid chronic end point for fish was also located, and one sub-lethal data point for a crustacean 

was available as supporting information. Using the lowest acute effect concentration 

(0.032 mg/L) and an assessment factor of 1000, a PNEC value of 0.032 μg/L was derived. 

No data for hypobromous acid was located in the literature; however, the aquatic toxicity is 

expected to be similar or less than that of the chlorinated analogue, hypochlorous acid. 

Therefore, a PNEC value of 0.032 μg/L hypobromous acid is proposed. 

For bromate, acute aquatic toxicity endpoints were located for the three basic taxonomic groups, 

and two chronic endpoints were located (one fish, one alga). Although not all of the data met 

validity criteria, a conservative PNEC of 13.6 μg/L was derived using the lowest acute endpoint 

(13.6 mg/L) and an assessment factor of 1000. Using the available data and a conservative 

assessment factor allows for PNEC derivation and avoids performing unnecessary toxicity 

testing, particularly for vertebrate species. 

For THM’s, the data sets for dibromochloromethane (DBCM) and dichlorobromomethane 

(DCBM) were incomplete, while chloroform and bromoform had complete data sets that would 

allow for direct PNEC calculation. Complete, valid acute and chronic toxicity data sets for fish, 

crustacean, and algae were available for chloroform. Using the lowest chronic effect 

concentration of 1.5 mg/L and an assessment factor of 100 results in a chloroform PNEC 

of 15 μg/L. A complete, valid acute toxicity data set was available for bromoform, and two 

chronic endpoints (one fish, one alga) were available as supporting information. Using the 

lowest acute effect concentration (12.3 mg/L) and an assessment factor of 1000, results in a 

bromoform PNEC of 12.3 μg/L. 

As mentioned above, the data sets for DBCM and DCBM are incomplete. Only one valid acute 

endpoint for fish was located for both DBCM and DCBM. It seems beyond the scope of 

Procedure (G9) application process to conduct chemical-specific testing with these substances on 

a variety of organisms to complete the data set available in open literature. This is particularly 

true considering that whole effluent toxicity testing results of the treated ballast water discharge 

are available. Therefore, as an alternative to having PNEC values that are non-derivable for 

DBCM and DCBM, the PNEC derivation approach for THMs used in the EU RAR for sodium 

hypochlorite was utilized. For chloroform, the RAR references an aquatic PNEC of 146 μg/L, 

which is higher than that calculated from the chronic end point data located during the literature 

search (chloroform PNEC 15 μg/L). However, the RAR presents that the data collected in 

connection with an assessment for seawater chlorination “...suggest that the ecotoxicities of the 

brominated THMs are not markedly different from chloroform”. (EU RAR for sodium 

hypochlorite, 2007). The RAR concludes that for the purposes of a broad assessment, THMs can 

be regarded as having similar toxicities and applies the chloroform PNEC to total 

trihalomethanes. Therefore, utilizing the RAR suggested PNEC value of 146 μg/L for total

THMs ensures that all THMs are considered, even in cases where toxicity data is limited. To 

maintain a conservative approach, the lower PNEC values for chloroform (15 μg/L) and 

bromoform (12.3 μg/L) derived from the available data can be used for PEC/PNEC ratio 

evaluation for these two THMs using the chemical analysis data collected during land-based 

testing. This evaluation will be presented in a future dossier for Procedure (G9) Final Approval. 

With the exception of one HAA, trichloroacetic acid (TCA), the aquatic toxicity database is 

incomplete and did not allow for direct PNEC calculation for each individual HAA. For TCA, 

the literature search located two valid acute endpoints (one fish, one crustacean), and one acute 

endpoint for an algae that was reported as a NOEC rather than an EC50. Additionally, two 

chronic endpoints were located for algae as supporting information. Using the lowest acute 
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effect concentration of 500 mg/L and an assessment factor of 1000, a PNEC of 500 μg/L was 

calculated for TCA. 

Again, it is beyond the scope of Procedure (G9) application process to conduct the extensive 

amount of toxicity testing that would be required to complete the HAA data set. This is 

particularly true considering that whole effluent toxicity testing results of the treated ballast water 

discharge are available. Therefore, the approach utilized in the sodium hypochlorite RAR for 

PNEC derivation of HAA’s was utilized. That is, the RAR considered it “...conservative to treat 

all haloacetic acids simplistically as being TCA...” in regards to PNECs and all HAA’s could be 

considered to have a PNEC of 0.85 μg/L. Since this PNEC is far lower than the PNEC 

of 500 μg/L based on the data found in literature, this seems to be a very protective and 

reasonable approach to this assessment. 

For sodium bisulfite, the available aquatic toxicity data was also limited. Two acute endpoints 

for fish were located along with three acute endpoints for crustaceans. The lowest acute effect 

occurred at 100 mg/L. No chronic aquatic toxicity data was located. Therefore, a PNEC value 

appears to be non-derivable. However, based on the chemical properties (high solubility, 

low BCF value, low Koc value), and also considering that <2 mg/L of sodium bisulfite may be 

present in treated ballast water discharge, it is highly unlikely that this substance will cause 

unacceptable environmental risks during use of the STDN system. This has been demonstrated 

in whole effluent toxicity testing treated with sodium bisulfite (see Tables 3 and 5 and 

section 11.4.1). Should further information or testing results become available to derive a PNEC 

for sodium bisulfite, this will be reflected in a subsequent application for Procedure (G9) 

Final Approval. 

Table 30 : PNEC Value Summary 

Substance 

Lowest Effect 

Concentration 

(mg/L) 

Assessment 

Factor 

PNEC Value 

(μg/L) Reference/Comments 

Active Substances

TRO (Freshwater) Insufficient 

Data Located -- 0.06 (as TRC) 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

TRC in freshwater 

TRO (Saltwater) 0.062 1000 0.062 

HOCl 0.032 1000 0.032 

HOBr Data Not 

Located -- 0.032 Estimated based on HOCl toxicity data 

Relevant Chemicals

Bromate 13.6 1000 13.6 

THMs 

Chloroform 1.5 100 15 / 146 146 μg/L to be used as 

PNEC for Total THMs 

Bromoform 12.3 1000 12.3 / 146 146 μg/L to be used as 

PNEC for Total THMs 

Dibromochlorometh

ane (DBCM) 

Data Not 

Located -- Not Derivable 

Use EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

Total THMs 
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Substance 

Lowest Effect 

Concentration 

(mg/L) 

Assessment 

Factor 

PNEC Value 

(μg/L) Reference/Comments 

Dichlorobromometh

ane (DCBM) 

Data Not 

Located -- Not Derivable 

Use EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

Total THMs 

Total THMs -- -- 146 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

Total THMs 

HAAs 

Bromochloroacetic 

acid 

Data Not 

Located -- 0.85 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

HAAs 

Monochloroacetic 

acid 

Insufficient 

Data Located -- 0.85 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

HAAs 

Dichloroacetic acid Insufficient 

Data Located -- 0.85 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

HAAs 

Trichloroacetic acid 500 1000 500 

Monobromoacetic 

acid 

Insufficient 

Data Located -- 0.85 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

HAAs 

Dibromoacetic acid Insufficient 

Data Located -- 0.85 

Based on EU Sodium 

Hypochlorite RAR 

suggested PNEC for 

HAAs 

Other Chemicals 

Sodium bisulfite Insufficient 

Data Located -- Not Derivable 

11.12 Effects on sediment 

Based on the chemical and physical properties of the substances associated with the BalPure®

system, no effects on sediment are anticipated. See sections 3.4 and 5.2. 

11.13 Comparison of effect assessment with discharge toxicity 

The information reviewed for degradation and bioaccumulation of the substances related to use 

of the BalPure® system suggest that potential effects from these mechanisms cannot be 

reasonably anticipated. The effects assessment establishes that there is potential for reaction of 

the Active Substances with organic matter and formation of DBPs. This has been confirmed by 

data from ballast water discharge samples analysed for DBPs. The presence of DBPs in 

disinfected water can potentially result in toxic effects to aquatic organisms. With the exception 

of testing with one species (Skeletonema), all toxicity tests after neutralization with bisulfite 
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resulted in E(L)C50 and/or NOEC values ≥100% ballast water sample (see data in Tables 3 and 5, 

discussion in section 11.4). Testing using a 96-hour exposure with Skeletonema resulted in 

an EC50 of 66.1% sample. Thus, to reach a concentration lower than the EC50 would require 

less than a two-fold dilution. This level of dilution will be readily achieved when treated water is 

discharged. 

Discharge toxicity testing results are consistent with the overall effects assessment that the 

potential effects are related to aquatic toxicity, rather than bioaccumulation or persistence in the 

environment. Further, the toxicity observed with neutralized discharge samples was limited to 

only one of the nine species tested. 

12 RISK ASSESSMENT 

The risks presented by having the BalPure® Ballast Water Management System on board are 

discussed in section 12.1 and the risks to human health presented in section 12.2. Section 12.3 

addresses risks to the aquatic environment. 

12.1 Risk to Safety of Ship 

A risk analysis was conducted by The Glosten Associates and approved by American Bureau 

of Shipping (ABS) to demonstrate that the BalPure® Ballast Water Management System is 

acceptable for installation on tankers, and specifically on the S/R American Progress. 

A qualitative comparative analysis was conducted for the chemical dosing and ballast water 

sampling systems involved in the installation. Results indicated that these systems do not pose 

greater risk than comparative systems currently allowed by the ABS Steel Vessel Rules 

(Glosten Associates, Inc., 2006). 

12.1.1 Corrosion 

Corrosion of steel and other metallic parts is of significant concern to the shipping industry. This 

is why a majority of the surfaces internal to the ship and in contact with seawater such as piping 

and tanks are coated with protective paints and coatings. Tests of how well these coatings 

protect metal surfaces are completed by various organizations and coating vendors themselves. 

One study prepared test samples from standard ship building steels with fully intact coatings 

applied to manufacturer’s specifications (BMT 2004). Four different coatings and solutions 

containing 0, 10 mg/L, and 40 mg/L Total Residual Chlorine (TRC, as added hypochlorite) were 

tested to determine weight gain as a measure of permeability. All samples showed the same rate 

and minimal amount of water uptake, indicating the coated parts were not permeable and did not 

corrode when in contact with solutions containing up to 40 mg/L TRC. Other tests were 

conducted applying ASTM Standard “Test Method for Evaluation of Painted or Coated 

Specimens Subjected to corrosive Environments D 1654-92”. Four different coating systems 

using five identical test coupons per coating were exposed to two levels of hypochlorite. 

Scribed and unscribed test coupons were subjected to four different environments to replicate 

conditions in a ballast tank being: (1) buried in inert sand to replicate the under sediment 

condition at the bottom of the silt filled tanks; (2) in damp humid space replicating an empty 

ballast tank; (3) fully submerged to replicate a full ballast tank; and 4) rotating on a wheel with 

cyclic immersion into the test solution to replicate the splash zone in the top of a partially full 

tank. Results show: (1) no accelerated failures in any unscribed coating system; (2) other 

samples exposed to hypochlorite tend to experience slightly more damage than the control 

samples; and (3) there is a trend in the level of damage realized relative to the tank location with 

more aggressive locations provides more damage. But a statistical analysis of the data shows that 
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at the 95% confidence level only the 40 mg/L exposure on the wheel showed significantly more 

damage (BMT 2004). 

There also have been studies with uncoated steel to determine the effects of fresh water and 

saltwater with and without the presence of chlorine. One report contains corrosion experiments 

again simulating the four conditions observed in a ballast tank: submerged in sediment, 

submerged in liquid, exposed to damp humid space above the liquid, and alternating between 

submerged liquid and humid air. TRC levels in the liquids were maintained at 10 mg/L 

and 40 mg/L and the tests were conducted for up to 90 days (BMT 2004). Results indicate that 

the condition had more of an impact on the corrosion rate than the addition of hypochlorite. 

As an example, the corrosion rate submerged in seawater was approximately 0.75 mm/year over 

90 days. However, another sample tested in a cyclic manner showed corrosion rates 

of 2.8 mm/year over 90 days. Similar samples exposed to 10 mg/L TRC (an expected maximum 

instantaneous threshold for the BalPure® system in a ballast tank) showed corrosion rates 

of 0.80 mm/year and 3.25 mm/year, respectively. 

Paik developed a time dependent corrosion wastage model for tankers and Offshore Floating 

Production and Storage Vessels (FPSO’s) in which corrosion loss is calculated from the 

following equation: 

tr = C1 (T – Tc – Tt)

C

2 

where the thickness of the steel tr at time T after construction is dependent on the time to coating 

breakdown Tc and the transition time Tt and coefficients C1 and C2 (Paik 2004, as referenced 

in BMT 2004). Paik investigated 34 different components within the typical ship structure and 

completed a statistical review of ships up to 32 years old. The study determined that the time to 

coating breakdown and corrosion is generally 7.5 years after construction. The rate of corrosion 

is linear, however this is dependent on location within the tank. After applying the corrosion rates 

given in the test above to the Paik model it was concluded that hypochlorite in levels 

commensurate with ballast water treatment will reduce the time for steel replacement on a ship 

by less than 5% (Paik 2004, as referenced in BMT 2004). 

12.1.2 Fire and explosion 

Potential fire and explosion risks associated with the BalPure® system are related to the hydrogen 

gas generated during the electrochemical process, the sodium sulfite (neutralizing agent) stored 

on board or electrical components of the system. 

While producing sodium hypochlorite, the BalPure® produces hydrogen gas as a by-product. 

Hydrogen gas can be explosive at concentrations >4% volume in air. The hydrogen is removed 

from the sodium hypochlorite solution stream in a degassing unit as part of the BalPure® system. 

Non-compressed hydrogen is not considered a hazardous material in the table 

in 49 CFR 172.101. A non-sparking blower in the degasser unit dilutes the hydrogen to a 

concentration of less than 1% (well below the 4% Lower Explosive Limit) before reaching the 

atmosphere. 

The BalPure® system has several safety mechanisms that are engineered into the system to ensure 

that hydrogen gas is effectively removed from the ship. These include a patented cyclone 

separator device that removes the hydrogen gas from the biocide solution (see section 8.1.1) and 

redundant blowers to reduce the concentration of hydrogen gas to <1% within a vent line to the 

atmosphere outside the ship. Additionally, a hydrogen gas detector is located in the space(s) 
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Exposure

Assessment

Review &

Assessment of

Toxicological

Data

Risk

Quantification

Uncertainties

Evaluation

Risk Assessment

Conclusions

Hazard

Identification

(Data Review/

COPC

Selection )

where hydrogen gas may enter should a BalPure® system failure occur. The PLC monitors and 

controls all of these safety features and will result in an alarm condition should the system 

require maintenance. 

Sodium bisulfite is a non-flammable, stable liquid. Excessive heating and/or contact with acids 

can liberate sulfur dioxide fumes, but does not create a fire hazard. 

All electrical components and hardware associated with a BalPure® unit have been tested and 

certified to meet established safety guidelines by groups such as UL, IEC, IEEE, and FM. These 

same components have been approved for use aboard ship by classification societies such 

as ABS, USCG, Lloyd’s, and BV. 

With the inclusion of the above safety measures, the fire/explosion risk associated with having 

the BalPure® system installed on board is low. 

12.1.3 Storage of chemicals 

As presented in section 2, the only chemical stored on board is sodium bisulfite. As discussed 

above, sodium bisulfite is non-flammable and does not present any onboard fire risk. Because 

the BalPure® system is engineered and constructed to ensure proper chemical storage, and will be 

installed per approval of the ship’s classification society, the potential risks to the ship from 

chemical storage are very minimal. 

12.2 Risks to human health 

12.2.1 Introduction 

Quantitative human health risk assessments generally follow the process outlined below: 

Step 1 Step 2 Step 4 Step 5 Step 6 

 Step 3 

With respect to the potential human health risks associated with the BalPure® BWMS, Step 1 is 

the hazard identification process. The BalPure® operational system is reviewed, and chemicals 

stored on the ship and added to the system or produced in situ at concentrations potentially 

harmful to human health are carried forward in the quantitative risk assessment as the chemicals 

of potential concern (COPCs). In Step 2, COPC-specific toxicity values for use in the 

quantitative risk analysis are compiled via an exhaustive literature search. If no toxicity data 

exists, information from appropriate surrogates and/or structurally similar chemicals may be 

used. For COPCs without toxicity information, quantitative risk evaluation is not possible. 
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In Step 3, exposure scenarios are developed: (1) to describe the potential exposures on board 

during routine vessel operations including operation, monitoring and maintenance of 

the BalPure® BWMS; and (2) to describe the potential exposures on and off board during 

equipment failure/and or accidental release of the COPCs; and (3) to provide a basis for 

quantifying those exposures. Each exposure scenario addresses the COPCs, the potential route or 

mechanism of exposure, and potentially exposed human populations (known as “receptors”). 

When operation-specific data for scenario development are unavailable, conservative values 

found in the appropriate regulatory guidance are used. 

In Step 4, the toxicity and exposure assessments are integrated into quantitative expressions of 

risks. This includes COPC-specific, multi-pathway risks for each of the potential receptors. 

The risk values presented in a risk assessment are conditional estimates derived from a 

considerable number of conservative, health-protective assumptions about exposure and toxicity. 

Thus, to place the risk estimates in proper perspective, it is important to specify the assumptions 

and uncertainties inherent in the risk assessment. This process is conducted in Step 5. This step 

may also involve the re-evaluation of data or the identification of additional data requirements to 

decrease uncertainty. Step 6 involves the development and presentation of conclusions that can 

be inferred from the findings of the risk assessment. This step provides risk managers with 

insight into the interpretation of the risk assessment results. 

12.2.2 Hazard identification/chemical of potential concern selection 

The chemicals of potential concern (COPCs) associated with the use of BalPure® BWMS are 

selected by determining which chemicals, either stored and added to the system or formed in situ, 

have the potential to adversely impact human health under either routine operating conditions, 

maintenance operations, or during an emergency resulting in an unexpected release. 

As described in sections 1 and 2, the BalPure® system is a nearly closed system that produces the 

disinfection agent, sodium hypochlorite (as a mixture of hypochlorous acid/hypobromous acid), 

via electrolysis of seawater. Hydrogen gas, a secondary by-product of the in situ electrochemical 

process, is vented to the atmosphere (using blowers) at concentrations of less than 1%. However, 

exposure to atmospheric gases typically are not included in risk assessment, and the safety 

features inherent in the BalPure® system as well as the physical properties of hydrogen gas 

suggest it is unlikely to accumulate to levels of concern (e.g., above the LEL). Therefore, as 

indicated in section 2.3.3, hydrogen gas is not considered relevant for the assessment of human 

health risks. Sodium bisulfite is added to de-chlorinate the ballast water as it is discharged from 

the ship. As identified in section 2, the following chemicals associated with the BalPure® system 

were evaluated as possible COPCs, and the rational for their selection or exclusion as COPCs is 

provided. 

The final list of COPCs carried forward in this risk assessment includes hypochlorous acid, 

THMs, HAAs, bromate and sodium bisulfite. 

12.2.2.1 Chemicals produced in situ on vessel

.1 Active Substance: Sodium hypochlorite (NaOCl) is generated at a 

concentration of ~0.1 wt % (1,000 mg/L) prior to injection into the ballast 

tanks. As sodium hypochlorite enters the ballast system, it is diluted to no 

more than 20 mg/L (See section 2.2.1 for discussion of determination of 

applied hypochlorite concentration). Because sodium hypochlorite is 
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generated in situ, it is not stored on board the vessel except in the ballast tanks 

at concentrations <20 mg/L. At the pH of seawater, and because seawater 

contains bromide ion, the actual disinfecting agents are hypochlorous acid 

(HOCl) and hypobromous acid (HOBr). These two chemicals, along with 

chloramines and bromamines, are referred to as the total residual oxidant 

(TRO) and are evaluated in this risk assessment as a single COPC – 

hypochlorous acid. 

.2 Trihalomethanes and haloacetic acids: Once mixed with ballast water, 

sodium hypochlorite can react with organic materials to form trihalomethanes 

(THMs) and haloacetic acids (HAAs). BalPure® -associated concentrations of 

these chemical groups have been generated for treatment of fresh-, brackish, 

and seawater (Sosik and Herwig, 2009). THMs detected include chloroform, 

bromoform, bromodichloromethane, and chlorodibromomethane, at a 

maximum total THM concentration of 1.1 mg/L (in brackish water following 

neutralization on Day 5). Six HAAs were detected, at a maximum total HAA 

concentration of 0.24 mg/L (in brackish water pre-neutralization on Day 2). 

Refer to section 11.3, Tables 27-29. 

.3 Bromate: Bromate has been measured as a DBP in BalPure® treatment of 

brackish water and seawater (Sosik and Herwig, 2009). The maximum 

concentration, 0.042 mg/L, occurred in brackish water tested on Day 10. 

Refer to section 11.3, Tables 28-29. 

12.2.2.2 Chemicals stored on board 

.1 Sodium Bisulfite: Sodium bisulfite (NaHSO3), as a 38% aqueous solution, is 

loaded aboard from a filling station and stored in holding tanks which are 

vented to the atmosphere. The sodium bisulfite is injected into the ballast line 

during de-ballasting operations to neutralize any residual TRO. Sodium 

bisulfite is added in excess (<2 mg/L) to ensure complete neutralization of 

the TRO. Given that sodium bisulfite is stored on the ship and residual 

remains in the ballast water, it is included as a COPC in the risk assessment. 

12.2.3 Human Exposure Scenario 

The US EPA (1989) defines an exposure pathway as “the course a chemical or pollutant takes 

from the source to the organism exposed”. An exposure route is “the way a chemical or pollutant 

enters an organism after contact” (US EPA 1989). A complete exposure pathway requires four 

key elements: chemical sources; migration routes (i.e. environmental transport); potentially 

exposed human receptors; and routes of exposure to impacted media (e.g., ingestion of chemicals 

in water). All four factors are required for a complete exposure pathway; if any one factor is 

missing, the pathway is considered incomplete. Because an incomplete pathway does not pose a 

potential health hazard, incomplete exposure pathways are not included in this health risk 

assessment. Potential human receptor groups and exposure routes are described below. 

12.2.3.1 Potential exposure pathways 

The conceptual exposure model (CEM) provides the basis for a comprehensive evaluation of the 

risks to human health by identifying the mechanisms through which people may be exposed to 

COPCs. The CEM traces the COPCs in a logical migration from their sources through various 
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release mechanisms and exposure routes to potentially affected receptor groups. The CEM 

identifies the exposure routes that are potentially complete under the given use(s). These 

pathways are evaluated in the quantitative risk assessment for each receptor. The CEM also 

facilitates the analysis and screening of exposure pathways not likely to pose significant risks. 

Primary, secondary, and tertiary sources of COPCs associated with the BalPure® system are listed 

in the CEM (figure 7). The primary sources of COPCs include the in situ production of sodium 

hypochlorite, the sodium bisulfite storage tanks and associated pipelines, and the treated ballast 

water itself. Chemicals associated with the BalPure® system are expected to remain contained, 

unless a storage or pipeline failure occurs. Such a release would allow COPCs to migrate to 

secondary and tertiary sources. For example, accidental spills and pipe or tank failure could 

result in the release of COPCs on board the vessel or to seawater. From these secondary sources, 

the COPCs may migrate to tertiary sources such as volatizing into air within enclosed spaces on 

the vessel or in outdoor air, or migration to shorelines and/or docking areas. 

As shown in figure 7, only exposure to COPCs resulting from leaks of storage tanks, pipelines 

and ballast tank discharges are evaluated quantitatively in this risk assessment. This is because 

no exposure is anticipated during normal operating conditions, because chemicals used in 

the BalPure® system are contained within a closed system (hypochlorous acid is produced in situ

and is injected directly into the ballast system; sodium bisulfite is injected into the ballast water 

as it is discharged from the ship), While both the chemical storage tanks and ballast tanks are 

vented, vent lines are directed to the atmosphere or to spaces within the ship with proper 

ventilation. Significant volatilization of COPCs from solution (from either storage tanks or 

treated ballast water) into indoor or outdoor air is extremely unlikely, and is not evaluated 

quantitatively. It is noted, however, that the trihalomethanes produced as disinfectant byproducts are volatile and hydrophobic, and as such, could be inhaled near ballast water or vent air 

outlets. While this inhalation pathway is not evaluated in the quantitative risk assessment, 

potential exposures and risks associated with vent air during ballasting and de-ballasting are 

discussed in section 12.2.5.5. 

SOURCES

Primary Secondary Tertiary

Vessel Surface

Seawater

Dock/Shoreline

• Pathway is or might be complete; sufficient data available for quantitative evaluation

X Pathway is or might be complete, but judged to be minor; not evaluated quantitatively

1

STDN Technician exposure considered worst-case scenario for anyone working onboard vessel.

2

Not evaluated quantiatively in risk assessment; semi-qualitatively evaluation provided.

Pathway is not complete; no evaluation required

General 

Public

Off Board

Dock 

Workers

•

X

Spills/Leaks from 

Storage Tanks, 

Pipelines or BWTS

Vapors/Indoor Air

Vapors/Outdoor Air

•

STDN 

Technician

X1

X

•

Release from

Ballast Tanks

Dermal Contact/

Incidental Ingestion X

Inhalation X

On Board

X

Dermal Contact/

Incidental Ingestion

Inhalation

X

Exposure Routes

•

X2

Ship's Crew

Figure 7 : Conceptual Exposure Model, BalPure® System 
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12.2.3.2 Identification of potentially exposed populations 

As described in sections 1.1 and 8.1.1, the BalPure® system is designed to operate automatically, 

with the system processes during ballasting and de-ballasting started and stopped based on 

electronic signals. Therefore, under normal operating conditions, neither STDN BalPure®

technicians nor the ship’s crew is expected to have contact with the system-related COPCs. 

Because the BalPure® system is closed system, exposure to the Active Substance, disinfection 

by-products, or sodium bisulfite is highly unlikely. 

As shown in figure 7, people with the greatest potential for exposure to BalPure® BWMS-related 

COPCs are STDN BalPure® technicians involved in routine maintenance and repair, or chemical 

resupply activities. Although unlikely, ship’s crew on board and in the spaces where the system 

components are present could also be exposed to COPCs during a pipeline or chemical tank 

failure; it is anticipated that these potential exposures would be less than those for STDN 

technicians conducting routine maintenance or chemical resupply. Because ballast water tanks 

remain closed at all times (with the exception of planned inspections/repairs of empty tanks), 

STDN technicians and the ship’s crew are not expected to have direct contact with treated ballast 

water. However, either the ship’s crew or dock workers could have dermal contact with released 

ballast water as a result of spray drift. As shown in figure 7, while STDN technicians, ship’s 

crew, or dock workers potentially could inhale chemicals volatilizing from solution, these 

source-exposure pathways are considered highly unlikely and are not evaluated quantitatively. 

Others with potential for COPC contact include the general public recreating at beaches near 

areas where treated ballast water has been discharged from the ship, although this exposure 

scenario is highly unlikely. 

These receptors and the potential exposure pathways are summarized below: 

.1 STDN BalPure® system technicians: STDN technicians or properly 

trained BalPure® personnel are the only receptors who would work directly with 

the system, including routine maintenance and chemical resupply of sodium 

bisulfite, and therefore have the greatest potential for actual exposure. Although 

proper chemical storage and handling, safety training, and use of appropriate PPE 

would prevent direct contact with COPCs, technicians could be exposed to 

hypochlorous acid, sodium bisulfite, or treated ballast water during maintenance 

activities via: 

- incidental ingestion of COPCs during routine maintenance and chemical 

resupply activities; 

- dermal contact with COPCs during routine maintenance and chemical 

resupply activities; and 

- inhalation of COPC vapors or mists in air during routine maintenance and 

chemical resupply activities. 

The potentially complete and quantifiable exposure pathways for STDN BalPure®

technicians include: (1) incidental ingestion of and dermal contact with 

hypochlorous acid at maximum concentrations of 1,000 mg/L, and (2) incidental 

ingestion of and dermal contact with sodium bisulfite during chemical resupply at 

maximum concentrations of 380,000 mg/L. 
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For hypochlorous acid, potential exposure is further mitigated by a pipeline 

flushing cycle that is engineered into the system. For instance, after generation of 

the Active Substances and the ballasting operation is complete, a 10-minute cycle 

is initiated by the PLC to the electrolyzer cells and injection pipelines with 

seawater. The same can be done for the sodium bisulfite delivery piping when a 

de-ballasting operation is complete, if needed to enhance the safety of an 

installation. These flush cycles ensure that pipelines do not remain filled with 

chemicals when the system is not in operation. 

.2 Ship’s crew: Under normal operating conditions, the ship’s crew has limited to 

no interaction with the BalPure® system. The system and piping are located in 

areas where the crew may be present, but normal ballasting and de-ballasting 

modes of the BalPure® system are controlled automatically and do not require 

chemical contact. However, this group has the potential to be exposed to sodium 

bisulfite while chemical-resupply activities take place, or if a pipeline or storage 

tank fails, or to any COPCs during a failure of the BalPure® system. Exposure to 

treated ballast water is highly unlikely, since the tanks are opened for required 

inspections only when empty, although the potential for exposure to ballast water 

spray drift exists. The actual exposure potential for this group is extremely low, 

but the possible exposure routes include: 

- incidental ingestion of the COPCs during an accidental release; 

- dermal contact with COPCs during an accidental release; and 

- inhalation of COPC vapors or mists in air during an accidental release. 

As previously indicated, accidental release of hypochlorous acid and/or sodium 

bisulfite are expected to result in exposures smaller than those for STDN BalPure®

technicians engaged in routine maintenance and chemical resupply. Moreover, as 

described in section 8.1.3.2, STDN technicians and ship’s crew will be trained to 

respond to sodium bisulfite spills; therefore these exposure scenarios are not 

included in the quantitative risk assessment. The only potentially complete and 

quantifiable exposure pathway for ship’s crew is dermal contact with COPCs in 

discharged ballast water, including hypochlorous acid, bromate, THMs, HAAs, 

and sodium bisulfite at the maximum residual ballast water concentrations 

– <20, 0.042, 1.1, 0.242, and <2.0 mg/L, respectively (see section 11.3). It is also 

important to note that treated ballast water discharge will be neutralized with 

sodium bisulfite, so the maximum residual ballast water concentration for 

hypochlorous acid is overly conservative because it does not consider 

neutralization. 

.3 Dock workers: Under normal operating conditions, dock workers will have no 

interaction with the BalPure® system or chemical resupply activities. While 

exposure to treated ballast water is highly unlikely, the potential for exposure to 

ballast water spray drift exists. The actual exposure potential for this group is 

extremely low, but the possible exposure routes include: 

- dermal contact with COPCs in ballast water spray drift. 
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The only potentially complete and quantifiable exposure pathway for dock 

workers is dermal contact with COPCs in discharged ballast water, including 

hypochlorous acid, bromate, THMs, HAAs, and sodium bisulfite at the maximum 

residual ballast water concentrations. This quantitative evaluation is identical to that 

for ship’s crew. 

.4 General public: Although it is unlikely that the general public would recreate 

near docked ships, it is possible that recreation areas could be located downstream 

of shipping docks. While any COPC releases from the ship would be immediately 

diluted into surrounding seawater, the general public (adults or children) could be 

exposed to COPCs via: 

- incidental ingestion of ballast water COPCs discharged to seawater near the 

shoreline; 

- dermal contact with ballast water COPCs discharged to seawater near the 

shoreline; and 

- inhalation of ballast water COPC vapors or mists in outdoor air near the 

shoreline. 

The potentially complete and quantifiable exposure pathways for swimmers 

include: incidental ingestion of and dermal contact with hypochlorous acid, 

bromate, THMs, HAAs, sodium bisulfite, and recently discharged ballast water. It 

is conservatively assumed that maximum residual ballast water COPC 

concentrations are diluted 100-fold prior to contact with beachgoers. 

Table 31 provides a summary of the exposure point concentrations discussed above and used in 

the risk assessment. 

Table 31 : Summary of COPC Exposure Point Concentrations 

STDN 

Technicians: 

Maximum 

Concentration in 

System 

Ship’s Crew/Dock 

Workers: 

Maximum Residual 

Ballast Water 

Concentrations 

General Public: 

Diluted 

Residual 

Ballast Water 

Concentration 

COPC mg/L mg/L mg/L 

Hypochlorous 

Acid 1.00E+03 2.00E+01 2.00E-01 

Bromate 4.20E-02 4.20E-04 

THMs 1.10E+00 1.10E-02 

HAAs 2.42E-01 2.42E-03 

Sodium bisulfite 3.80E+05 2.00E+00 2.00E-02 

12.2.3.3 Quantitative exposure assessment 

As described above, although highly unlikely, STDN BalPure® technicians could have direct 

contact (ingestion and dermal contact) with COPCs within the system during maintenance 

activities and to sodium bisulfite during chemical resupply activities. Ship’s crew or dock 

workers could have dermal exposure to ballast water spray drift, and beachgoers may recreate in 
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the vicinity of ballast water discharges. Intake factors are used to determine the amount of 

COPC that each receptor is potentially exposed to via each exposure route, and are used to 

evaluate both cancer risk and non-cancer hazard. 

The following equation was used to quantify intake from the dermal contact pathway: 

Iw = (Cw)(SA)(PC)(CF)(ET)(EF)(ED) / (BW)(AT) 

Where 

Iw = intake from dermal contact with COPC in ballast water/solution (mg/kg-d) 

Cw = maximum concentration of a COPC in ballast water/solution (mg/L) 

SA = skin surface area in contact with ballast water/solution (cm2

/d) 

PC = dermal permeability coefficient (cm/hr), chemical-specific 

CF = conversion factor 10-3 (L/cm3) 

ET = exposure time (h/d) 

EF = event frequency (d/y) 

ED = exposure duration (y) 

BW = body weight (kg) 

AT = averaging time (d), ED x 365d/y (noncarcinogens), 

 70y x 365d/y (carcinogens) 

The following equation was used to quantify intake from the incidental ingestion pathway: 

Iw = (Cw)(IngR)(EF)(ED) / (BW)(AT) 

Where 

Iw = intake from incidental ingestion of COPC in ballast water/solution 

(mg/kg-d) 

Cw = maximum concentration of COPC in ballast water/solution (mg/L) 

IngR = ingestion rate (L/day) 

EF = event frequency (d/y) 

ED = exposure duration (y) 

BW = body weight (kg) 

AT = averaging time (d) - ED x 365d/y (noncarcinogens), 

70y x 365d/y (carcinogens) 

The receptor-specific exposure parameters used to estimate COPC intake based on the equations 

above are summarized below and the resulting intake factors summarized in Tables 32 and 33. 

As shown in Tables 32 and 33, the intake equations described above for the general public are 

age-adjusted to account for six years of exposure as a child and 24 years of exposure as an adult. 

This approach is consistent with guidance (US EPA 1989 and 1991e), and accounts for any 

differences in exposure assumptions between children and adults. 

.1 STDN technicians 

The adult exposure factors used to quantify potential exposure to hypochlorous 

acid during maintenance of the BalPure® system or to sodium bisulfite during 

chemical resupply are: 
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- Ingestion rate: While incidental ingestion is likely to be only a fraction of the 

ingestion rate for swimming, 0.05 L/hour is conservative and therefore used 

(US EPA 1989); 

- Skin surface area available for contact: During an accidental spill, 

technicians or workers may have significant contact with hands and arms, 

which results in a skin surface area of 3,300 cm2

 (US EPA 2004); 

- Permeability constant: Chemical-specific; for inorganics without a 

permeability coefficient, and especially for ionized chemicals, guidance 

recommends using 0.001 cm/hour (US EPA 2004); 

- Body weight: The adult body weight typically applied in risk assessment 

is 70 kg (US EPA 2002); 

- Exposure time: The exposure time is assumed to be 0.25 hours per event, is 

based on best professional judgment; 

- Event frequency: Based on best professional judgment, an exposure 

frequency of 1 spill event per year is used; 

- Exposure duration: Based best professional judgment, the exposure duration 

is 10 years; and 

- Averaging time: The life expectancy of 70 years (25,550 days) was used as 

the averaging time for exposure to carcinogenic contaminants (US EPA 2002). 

The averaging time for non-carcinogenic effects is equal to the exposure 

duration of 10 years (3,650 days). 

.2 Ship’s crew/dock workers 

The adult exposure factors used to quantify potential exposure to discharged 

ballast water spray drift are: 

- Skin surface area available for contact: During a spray drift incident, crew 

or workers may have limited contact with hands, arms, and face, which results 

in a skin surface area of 1,800 cm2

 which is based on best professional 

judgment (10% of total body; US EPA 2004). 

- Permeability constant: Chemical-specific; for inorganics without a 

permeability coefficient, and especially for ionized chemicals, guidance 

recommends using 0.001 cm/hour (US EPA 2004). The value for 

chloroform, 0.0068 cm/hour, is used as a surrogate for THMs and HAAs 

(US EPA 2004). 

- Body weight: The adult body weight typically applied in risk 

assessment 70 kg (US EPA 2002); 

- Exposure time: The exposure time is assumed to be 0.25 hours per event, is 

based on best professional judgment; 
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- Event frequency: Based on best professional judgment, an exposure 

frequency of 1 spray drift event per year is used; 

- Exposure duration: Based on best professional judgment, the exposure 

duration is 10 years. 

- Averaging time: The life expectancy of 70 years (25,550 days) was used as 

the averaging time for exposure to carcinogenic contaminants (US EPA 2002). 

The averaging time for non-carcinogenic effects is equal to the exposure 

duration of 10 years (3,650 days). 

.3 General public (beachgoers) 

The exposure factors used to quantify potential exposure to COPCs in discharged 

ballast water to swimming beachgoers (adults and children) are described below. 

As discussed above and shown in Tables 32 and 33, the intake factors used to 

evaluate cancer risk for beachgoers are age-adjusted to account for differences in 

exposure assumptions between children and adults. 

- Ingestion rate: The ingestion rate for swimming, 0.05 L/hour, is used 

(US EPA 1989). 

- Skin surface area available for contact: The average of the 50th percentile 

total skin surface area for adults is 18,000 cm2

 and for children is 6,600 cm2

(US EPA 2004). 

- Permeability constant: Chemical-specific; for inorganics (hypochlorous acid 

and sodium bisulfite) without a permeability coefficient, and especially for 

ionized chemicals, guidance recommends using 0.001 cm/hour 

(US EPA 2004). The largest value for organics evaluated in this risk 

assessment is for chloroform, at 0.0068 cm/hour (US EPA 2004). 

- Body weight: The adult and child body weights typically applied in risk 

assessment are 70 and 15 kg, respectively (US EPA 2002). 

- Exposure time: The US EPA’s recommended swimming duration of 60 

minutes per event, based on the 50th percentile value (US EPA 1997). 

- Event frequency: Based on best professional judgment, an upper-end 

exposure frequency of 10 events per year is used. 

- Exposure duration: Based on US EPA guidance, the exposure duration is 30 

years, which includes six years as a child and 24 years as an adult 

(US EPA 2002). 

- Averaging time: The life expectancy of 70 years (25,550 days) was used as 

the averaging time for exposure to carcinogenic contaminants (US EPA 2002). 

The averaging time for non-carcinogenic effects is equal to the exposure 

duration; 24 years as an adult (8,760 days) and 6 years as a child (2,190 days). 
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Table 32 : Summary of Dermal Intake Factors 

IFdermal =

IFdermal/adj =

IFdermal = Dermal Intake Factor, L water/kg body weight-day

SA = Surface Area, cm2

PC = Dermal Permeability Constant, cm/hour

CF = Volumetric Conversion Factor, 1 Liter/1000 cm3

ET = Exposure Time, hours/day

EF = Exposure Frequency, days/year

ED = Exposure Duration, years

BW = Body Weight, kg

AT = Averaging Time, days

Child

Adult (0-6 years)

SA 3300 1800 18000 6600

CF 0.001 0.001 0.001 0.001

ET 0.25 0.25 1 1

EF 1 1 10 10

ED 10 10 24 6

BW 70 70 70 15

ATcarcinogens 25550 25550 25550 25550

ATnonarcinogens 3650 3650 8760 2190

PATHWAY-SPECIFIC INTAKE FACTORS:

Chemical-Specific Intake Factors via Dermal Contact (IFdermal), L water/kg body weight-day

Carcinogens x PC 4.61E-06 2.52E-06 3.45E-03 NA

Noncarcinogens x PC 3.23E-05 1.76E-05 7.05E-03 1.21E-02

Exposure Variable

General Public

STDN 

Technician

Ship's Crew/

Dock Worker

SA x PC x CF x ET x EF x ED

BW x AT

SAchild x PC x CF x ETchild x EFchild x Edchild

BWchild x AT + SAdult x PC x CF x ETadult x EFadult x EDadult

BWadult x AT
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Table 33 : Summary of Oral Intake Factors 

IForal =

IForal/adj =

IForal = Oral Intake Factor, L water/kg body weight-day

IR = Ingestion Rate, L/hour

ET = Exposure Time, hours/day

EF = Exposure Frequency, days/year

ED = Exposure Duration, years

BW = Body Weight, kg

AT = Averaging Time, days

Child

Adult (0-6 years)

IngR 0.05 NA 0.05 0.05

ET 0.25 NA 1 1

EF 1 NA 10 10

ED 10 NA 24 6

BW 70 NA 70 15

ATcarcinogens 25550 NA 25550 25550

ATnonarcinogens 3650 NA 8760 2190

PATHWAY-SPECIFIC INTAKE FACTORS:

Chemical-Specific Intake Factors via Oral Ingestion (IForal), L water/kg body weight-day

Carcinogens 6.99E-08 NA 1.45E-05 NA

Noncarcinogens 4.89E-07 NA 1.96E-05 9.13E-05

Exposure 

Variable

General Public

STDN 

Technician

Ship's Crew/

Dock Worker

IngR x ET x EF x ED

BW x AT

IngRchild x ETchild xEFchild x EDchild

BWchild x AT

+ IngRadult x ETadultx EFadult x EDadu

BWadult x AT

12.2.4 Health effects in humans 

The objective of this section is to provide information regarding the potential for health risks 

from exposure to chemicals potentially present in treated ballast water. Specifically, this section 

describes how dose-response, or toxicity values, are established and used for non-carcinogenic 

and carcinogenic COPCs. Because only the ingestion and dermal exposure routes are evaluated 

quantitatively, this section focuses exclusively on oral toxicity values (which are commonly used 

as surrogates for evaluation of dermal exposure). 

12.2.4.1 Acute health effects 

All of the COPCs identified can be skin and eye irritants as described in Table 9. With the 

exception of sodium bisulfite, all of the COPCs identified are generated in situ at aqueous 

concentrations in the μg/L to mg/L range. These in situ generated COPCs are at concentrations 

too low to cause serious eye and skin irritation. There may be some limited potential for minor 

eye irritation if there is direct contact with ballast water, due to a combination of the COPCs, 

salts, and other compounds which may be in the ballast/seawater prior to treatment. Skin 

irritation is considered unlikely given the very low concentrations of the COPCs. THMs, with 

chloroform an example of a solvent known to de-fat the skin, are known to cause both skin and 
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eye irritation when present at much high concentrations than those present in situ in ballast water 

(IPCS 2004). 

The one COP, which could represent an acute eye and skin hazard, is the sodium bisulfite 

solution stored on the vessel. The MSDS (Table 9) clearly states that contact with 

the 38% solution can cause eye and skin irritation. Appropriate PPE should be used when 

working with this solution to minimize the potential for these acute health effects, and only 

trained personnel should be handling the concentrated solution (Mallinckrodt 2006a). 

The potential for acute irritation of the nose and throat upon inhalation is unlikely. The THMs 

are the most likely COPCs to volatize and are considered in a separate inhalation assessment in 

Table 39. The safe levels used in the inhalation assessment (section 12.2.5.5) are considered 

protective of irritation of mucous membranes caused by volatile THMs (OSHA 2009). 

The more critical endpoint for potential exposure to ballast water COPCs at low concentrations 

are chronic health issues such as liver disease and cancer. These chronic effects are fully 

addressed in the risk assessment. 

12.2.4.2 Non-carcinogenic adverse health effects 

For the non-carcinogenic effects of specific constituents, most regulatory agencies assume a dose 

exists below, which no adverse health effects will be seen (US EPA 1989). Below this 

“threshold” it is believed that exposure to a chemical can be tolerated without adverse effects. 

Adverse effects manifest only when physiologic protective mechanisms are overcome by 

exposure to doses above the threshold. The reference dose (RfD), expressed in units of 

milligrams per kilogram-day (mg/kg-d), represents the daily intake of a constituent 

(averaged over a year) per kilogram of body weight that is below the effect threshold for the 

constituent. It is assumed that non-carcinogenic exposure doses are not cumulative from age 

group to age group over a lifetime of exposure (US EPA 1989). An RfD is specific to the 

constituent, route of exposure, and duration over which the exposure occurs. 

Agencies, most notably the US EPA, review all relevant human and animal studies for each 

constituent and select the studies pertinent to the derivation of specific RfDs. Each study is 

evaluated to determine the no-observable-adverse-effect level (NOAEL) or, if data are 

inadequate for such a determination, the lowest-observable-adverse-effect level (LOAEL). 

The NOAEL corresponds to the dose (mg/kg-d) that can be administered over a lifetime without 

inducing observable adverse effects. The LOAEL corresponds to the lowest daily dose 

(mg/kg-d) that can be administered over a lifetime that induces an observable adverse effect. The 

toxic effect characterized by the LOAEL is referred to as the “critical effect” (US EPA 1989). 

To derive an RfD, the NOAEL (or LOAEL) is divided by uncertainty factors (alternatively 

known as safety factors) to ensure protection of human health. Uncertainty factors are applied to 

account for: (1) extrapolation of data from laboratory animals to humans (interspecies 

extrapolation); (2) variation in human sensitivity to the toxic effects of a constituent (intraspecies 

differences); (3) derivation of a chronic RfD based on a subchronic rather than a chronic study; 

and (4) derivation of an RfD from the LOAEL rather than the NOAEL. A safety factor of 10 is 

typically applied for each of these uncertainties during the development of the RfD. Thus, the 

safety factor for an individual COPC could be as high as 10,000. In addition to these uncertainty 

factors, modifying factors between 0 and 10 may be applied to reflect additional qualitative 

considerations (US EPA 1989). 
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12.2.4.3 Carcinogenic adverse health effects 

The incremental lifetime cancer risk (ILCR) attributed to a carcinogen is calculated as a product 

of the daily intake (mg/kg-d) and the cancer slope factor (CSF). The US EPA’s model of 

carcinogenesis assumes the relationship between exposure to a carcinogen and cancer risk is 

linear over the entire dose range, except at very high doses (US EPA 1989). This linearity 

assumes there is no threshold-of-exposure dose below which harmful effects will not occur. 

Because of this, carcinogenic effects are considered to be cumulative across age groups when 

considering lifetime exposures. 

CSFs are upper-bound (95% upper confidence limit (UCL)) estimates of the increased cancer 

risk per unit dose, in which risk is expressed as the probability that an individual will develop 

cancer within his or her lifetime as the result of exposure to a given level of a carcinogen. 

All cancers or tumors are considered whether or not death results. This approach is inherently 

conservative because of the no-threshold assumption and the use of the 95% UCL of the 

estimated slope of dose versus cancer risk. 

To identify oral RfDs and slope factors, the studies and approaches described by the US EPA in 

its Integrated Risk Information System (IRIS) were compared to the toxicological information 

reported in section 4 (Tables 11 through 13). When no toxicity values are reported in IRIS, best 

professional judgment was used to develop values based on the data reported in Tables 11 

through 13. 

12.2.4.4 Hypochlorous acid and hypobromous acid 

The health effects associated with hypochlorite (salts of hypochlorous acids) have been studied 

primarily as it relates to its use as a disinfectant in drinking water. While various drinking water 

goals for disinfectants have been established by the US EPA, the World Health Organization 

(WHO), and the European Union (EEC), only the US EPA has identified an oral reference dose 

for chlorine: 0.1 mg/kg-day (US EPA 1994). This value, as reported in IRIS, is based on the 

NOAEL of 14 mg/kg-day for rats exposed to chlorine in drinking water for two years 

(NTP 1992a), as reported in Table 11 (Chronic Mammalian Toxicity). The US EPA (1994) 

applies a composite uncertainty factor of 100: 10 to account for interspecies extrapolation and 10 

to account for the protection of sensitive subpopulations. 

No toxicological information was found for hypobromous acid, or the associated hypobromite 

salts. As previously reported, hypobromous acid is believed to be similar in toxicity to its 

chlorinated analogue, hypochlorous acid. Therefore, as indicated in the COPC selection 

section 12.2.2, the Active Substance in the BalPure® system is evaluated qualitatively as 

hypochlorous acid. 

 12.2.4.5 Bromate 

The US EPA has identified an oral reference dose for bromate in IRIS: 0.004 mg/kg-day 

(US EPA 2001a). This value is based on the NOAEL of 1.1 mg/kg-day for rats exposed to 

potassium bromate in drinking water for 100 weeks (US EPA 2001a), as reported in Table 11 

(Chronic Mammalian Toxicity). The oral reference dose includes a composite uncertainty factor 

of 300: 10 to account for extrapolation from animal data to humans, 10 to protect sensitive 

subpopulations and account for potential differences between adults and children, and 3 to 

account for some deficiencies in the database (US EPA 2001a). 
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As summarized in Table 13 (Summary of Data on Carcinogenicity), IARC has concluded that 

bromate is a possible human carcinogen, while the US EPA classifies it as a probable human 

carcinogen. Based on the same study of rats exposed to potassium bromate in drinking water 

for 100 weeks (and also summarized in Table 13), the US EPA (2001a) includes an oral slope 

factor of 0.7 per mg/kg-day in IRIS, based on the incidence of renal tubular tumors, thyroid 

follicular tumors, and testicular mesotheliomas. 

12.2.4.6 Total Trihalomethanes 

As discussed in section 2, trihalomethane (THM) by-products in ballast water may include 

chloroform (trichloromethane), bromoform (tribromomethane), dichlorobromomethane, and 

chlorodibromomethane. The US EPA has identified oral reference doses for all four compounds 

in IRIS with values ranging from 0.01 mg/kg-day (chloroform; US EPA 2001b) 

to 0.02 mg/kg-day (bromoform [US EPA 1991a], dichlorobromomethane [US EPA 1991b], and 

chlorodibromomethane [US EPA 1991c]). The lowest (and therefore most conservative) value is 

from the study of beagles administered oral doses (15 or 30 mg/kg-day) of chloroform in 

capsules for 5 days/week over 7.5 years for which a LOAEL of 15 mg/kg/day for liver effects, as 

is reported in Table 11 (Chronic Mammalian Toxicity).8 The US EPA (2001b) derived the oral 

reference dose based on a modeled low benchmark dose (BMDL10) of 1.0 mg/kg-day, and 

included a composite uncertainty factor of 100: 10 to account for extrapolation from animal data 

to humans and 10 to account for intrahuman variability (US EPA 2009).9

As reported in Table 13 (Summary of Data on Carcinogenicity) either IARC or the US EPA has 

classified each of the four THMs as “probable” or “possible” human carcinogens. Based on the 

studies identified in Table 13, US EPA, in IRIS, has derived oral slope factors for bromoform 

(7.3 x 10-3 per mg/kg-day; US EPA 1991a), dichlorobromomethane (6.2 x 10-2 per mg/kg-day; 

US EPA 1991b), and chlorodibromomethane (8.4 x 10-2 per mg/kg-day; 1991c)10. The highest 

value is the most conservative, therefore the oral slope factor for chlorodibromomethane is used 

to evaluate carcinogenic risks from THMs. 

12.2.4.7 Total Haloacetic Acids 

As described in section 2, haloacetic acid (HAA) by-products in ballast water may include 

bromochloracetic acid, mono-, di- and trichloroacetic acids, and mono- and dibromoacetic acids. 

Of these, the US EPA (2003) has identified an oral reference dose in IRIS for only dichloroacetic 

acid, however, this value is based on a subchronic (90 day study), which is not optimal for the 

evaluation of chronic effects. As described above, a chronic effects level can be developed based 

on the NOAELs or LOAELs reported for chronic toxicity studies in Table 11. The NOAELs 

identified for HAAs in Table 11 range from 3.5 mg/kg/day for monochloroacetic acid (EU 2005) 

to 40 mg/kg/day for trichloroacetic acid (IPCS 2000a); all studies are based on effects on rodents, 

therefore a composite uncertainty factor of 100 (10 to account for extrapolation from animal data 

to humans and 10 to account for intrahuman variability) is appropriate for the determination of a 

reference dose from any of these studies. The lowest (and therefore most conservative) 

NOAEL-based calculated value is for monochloroacetic acid – 0.034 mg/kg/day. The LOAELs 

 

8 IRIS reference doses for bromoform and chlorodibromomethane are based on subchronic studies associated with 

the same NTP studies (1989 and 1985, respectively) cited in Table 11. The IRIS reference dose for 

dichlorobromomethane is based on the NTP (1987) chronic LOAEL of 25 mg/kg/d cited in Table 11. 

9 A similar oral reference dose resulted from the NOAEL/LOAEL approach. 

10 US EPA has determined that while oral exposure to chloroform may cause cancer, the reference dose of 0.01 

mg/kg-day is considered to be protective against cancer risk. 
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identified for HAAs in Table 11 range from 2 mg/kg/day for dibromoacetic acid (NTP 2007) 

to 40 mg/kg/day for dichloroacetic acid (IPCS 2000a); all studies are based on effects on rodents, 

therefore, a composite uncertainty factor of 1000 (10 to account for the use of a LOAEL instead 

of a NOAEL, 10 to account for extrapolation from animal data to humans, and 10 to account for 

intrahuman variability) is appropriate for the determination of a reference dose from any of these 

studies. The lowest (and therefore most conservative) LOAEL-based value is for dibromoacetic 

acid – 0.002 mg/kg/day. Because the LOAEL-based value results in the lowest reference dose, it 

is used to evaluate non-carcinogenic risks from HAAs. 

As reported in Table 13 (Summary of Data on Carcinogenicity) only dichloroacetic acid, 

dibromoacetic acid, and trichloroacetic acid have been classified as either “probable” or 

“possible” human carcinogens.11 However, IRIS includes oral slope factors for only 

dichloroacetic acid (0.05 per mg/kg-day; US EPA 2003), therefore this value is used to evaluate 

carcinogenic risks from HAAs. It is noted that while no cancer slope factor has been developed 

for the remaining HAAs, the effects levels reported in Table 13 are up to 20 times lower for 

dibromoacetic acid (≥ 4 mg/kg/day) than those reported for dichloroacetic acid (84 mg/kg/day). 

Therefore, some uncertainty exists in the carcinogenic evaluation of HAAs; specifically 

carcinogenic risks associated with dibromoacetic acid, the dominant residual HAA measured in 

ballast water (see Tables 27 to 29) may be underestimated. 

 12.2.4.8 Sodium bisulfite 

The US EPA has not developed an oral reference dose for sodium bisulfite inclusion in IRIS. 

However, as reported in Table 11 (Chronic Mammalian Toxicity), The Health Council of 

the Netherlands identified a NOAEL of 72 mg/kg-day for rats fed up to 20,000 mg/L sodium 

bisulfite, based on local effects (blood in feces; hyperplastic changes of gastric epithelium) 

(2005). In the absence of other information, an oral RfD can be calculated by applying a 

composite uncertainty factor of 100, 10 to account for interspecies extrapolation and 10 to 

account for intrahuman variability, to the NOAEL (72 mg/kg-day). This results in an oral RfD 

of 0.72 mg/kg-day. 

As reported in Table 13 (Summary of Data on Carcinogenicity), sodium bisulfite is not 

classifiable as to its carcinogenicity, therefore, no oral cancer slope factor is available. 

As shown in Table 34, reference doses were identified for all COPCs. Cancer slope factors are 

available for only bromate, THMs, and HAAs; therefore, carcinogenic effects can be evaluated 

for only these three COPCs. 

 

11 As indicated in Table 13, NTP (2009) reports “Clear evidence of carcinogenic activity” in animals for 

bromochloroacetic acid. 
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Table 34 : Summary of Toxicity Criteria 

Chemical 

Oral Reference Dose

(mg/kg/day) 

Oral Cancer Slope Factor (per 

mg/kg-day) 

Hypochlorous 

Acid 1.00E-01 (chlorine) NC 

Bromate 4.00E-03 7.00E-01 

THMs 1.00E-02 (chloroform) 8.40E-02 (chlorodibromomethane) 

HAAs 2.00E-03 (dibromoacetic acid) 5.00E-02 (dichloroacetic acid) 

Sodium bisulfite 7.20E-01 NC 

 NC – No criteria 

12.2.5 Risk characterization 

Risk characterization, the final step in the risk assessment process, combines data from the 

hazard identification, health effects assessment, and exposure assessment to estimate the 

potential carcinogenic and non-carcinogenic effects of COPCs over the applicable duration of 

exposure. Despite quantification, it is believed that the actual potential health risks are very low 

because of the low potential of exposure to chemicals associated with the BalPure® system. 

Risks presented below should be considered worst-case estimates. 

12.2.5.1 Acceptable risk levels 

The risk that is acceptable is very much dependent on site-specific characteristics that 

include: the number of people potentially exposed, the likelihood of exposure, the chemicals 

driving the risk, and the decisions of risk managers. The incremental lifetime cancer risk (ILCR) 

is compared to a range of acceptable probabilities to determine whether the potential risk poses 

an unacceptable health threat. The US EPA directive, Role of the Baseline Risk Evaluation in 

Superfund Remedy Selection Decisions (US EPA 1991a), states that action is generally not 

warranted at a site when the cumulative carcinogenic risk for current and future land use is less 

than 1 x 10-4 and the cumulative non-carcinogenic hazard index (HI) is less than 1.0. The level 

of non-cancer hazard concern increases as the HI increases above unity, although the two are not 

linearly related (US EPA 1989). The US EPA uses a potential excess individual lifetime cancer 

risk of 1 x 10-6 (1 in 1,000,000) as a point of departure for risk management actions. 

12.2.5.2 Quantitative estimate of potential risks to STDN BalPure® technicians 

Table 35 summarizes the risks quantified for the BalPure® Technician who may be exposed to 

concentrated hypochlorous acid (generated concentration of 0.1%) during maintenance activities 

or to the 38% sodium bisulfite solution during chemical resupply. Neither hypochlorous acid nor 

sodium bisulfite is classifiable with respect to carcinogenicity, therefore cancer risks are not 

reported below. The non-cancer hazard of 0.3 is well below the level of concern (1.0); use of 

personal protective equipment (PPE) and safe chemical handling procedures will further reduce 

any potential exposures and associated effects. 
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Table 35 : Summary of Cancer Risks and Non-cancer Hazards for BalPure® Technicians 

Cancer Risk Non-cancer Hazard 

Chemical 

Ingestio

n 

Derma

l Total Ingestion Dermal Total 

Hypochlorous Acid NC NC NA 0.0049 0.00032 0.0052 

Sodium Bisulfite NC NC NA 0.26 0.017 0.28 

TOTAL NA 0.3 

 NA = not applicable, NC = no criteria 

12.2.5.3 Quantitative estimate of potential risks to ship’s crew or dock workers 

Table 36 summarizes the risks quantified for ship’s crew or dock workers who may be exposed 

to COPCs in ballast water from spray drift. Neither hypochlorous acid nor sodium bisulfite is 

classifiable with respect to carcinogenicity, therefore cancer risks are reported for only bromate, 

THMs, and HAAs. The total estimated cancer risk of 2 x 10-9 (2 in 1,000,000,000) is far below 

the US EPA point of departure of 1 x 10-6 (1 in 1,000,000). The total non-cancer 

hazard, 0.00002, is many orders of magnitude below the target level of 1.0. 

Table 36 : Summary of Cancer Risks and Non-cancer Hazards 

for Ship’s Crew/Dock Workers 

Cancer Risk Non-cancer Hazard 

Chemical 

Ingestio

n 

Derma

l Total Ingestion Dermal Total 

Hypochlorous Acid NA NC NA NA 0.0000035 0.0000035 

Bromate NA 7.4E11 7.4E-11 NA 0.0000001

8 

0.0000001

8 

THMs NA 1.6E09 1.6E-09 NA 0.000013 0.000013 

HAAs NA 2.0E10 2.0E-10 NA 0.000012 0.000012 

Sodium Bisulfite NA NC NA NA 0.0000000

49 

0.0000000

49 

TOTAL 2E-09 0.00003 

 NC = no criteria, NA = not applicable 

12.2.5.4 Quantitative estimate of potential risks to the general public (beachgoers) 

Table 37 shows cancer risks to beachgoers who may swim in the vicinity of recently discharged 

ballast water associated with the BalPure® system. Neither hypochlorous acid nor sodium 

bisulfite is classifiable with respect to carcinogenicity, therefore cancer risks are reported for only 

bromate, THMs, and HAAs. The total estimated cancer risk is very low, at 4 x 10-8 

(4 in 100,000,000). 
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Table 37 : Summary of Cancer Risks for the General Public 

Cancer Risk*

Chemical 

Ingestio

n 

Derma

l Total 

Hypochlorous Acid NC NC NA 

Bromate 4.3E-09 1.0E09 5.3E-09 

THMs 1.3E-08 2.2E08 3.5E-08 

HAAs 1.8E-09 2.9E09 4.6E-09 

Sodium Bisulfite NC NC NA 

TOTAL 4E-08 

* Cancer risk is age-adjusted, assuming 6 years of exposure as a child 

and 24 years as an adult. 

NC = No criteria, NA = not applicable. 

Non-cancer hazards for the general public, which are summarized in 

Table 38, also are very low; 0.0004 for children and 0.0001 for adults. 

Table 38 : Summary of Non-cancer Hazards for General Public 

Adult Non-cancer Hazard Child Non-cancer Hazard 

Chemical Ingestion Dermal Total Ingestion Dermal Total 

Hypochlorous 

Acid 0.000039 0.000014 0.000053 0.00018 0.000024 0.00021 

Bromate 0.0000021 0.000000

74 

0.000002

8 

0.000009

6 0.0000013 0.000011 

THMs 0.000022 0.000053 0.000075 0.00010 0.000090 0.00019 

HAAs 0.000020 0.000048 0.000068 0.000092 0.000082 0.00017 

Sodium Bisulfite 0.0000005

4 

0.000000

2 

0.000000

74 

0.000002

5 

0.0000003

3 0.0000029 

TOTAL 0.0002 0.0006 

12.2.5.5 Semi-quantitative evaluation of potential risks from inhalation 

The risk estimates reported in Tables 35 through 38 do not include inhalation of COPCs in indoor 

or outdoor air. While significant volatilization of COPCs from ballast water into indoor or 

outdoor air is not anticipated, some exposure to COPCs in air could occur. The most likely 

operation that could result in exposure to COPCs in air is during ballasting, when air in the 

ballast tanks is vented to the atmosphere as water is brought into the tanks. If the ship’s crew is 

present during this operation, they could be exposed to residual THMs in vent air, since these 

disinfection by-products are both volatile and hydrophobic. Although concentrations of THMs in 

vent air have not been measured, worst-case estimates of air concentrations can be made 

based on maximum ballast water THM concentrations (see section 11.3) and the 

appropriate Henry’s Law constants (the ratio of the aqueous-phase concentration of a chemical to 
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its equilibrium partial pressure in the gas phase). Because vent air will be immediately mixed 

into the surrounding atmosphere, the air concentration estimates are also adjusted for dilution 

into ambient air by dividing by a factor 10. As a conservative evaluation of the inhalation 

exposure pathway, Table 39 summarizes these data, and compares the estimated air 

concentrations to U.S. OSHA Permissible Exposure Levels (PELs). 

Table 39 : Estimated Concentrations of THMs in Vent Air and Comparisons to PELs 

Chemical 

Maximum 

Residual 

Ballast Water 

Conc. 

(ug/L) 

Henry’s 

Law 

Constant 

(unitless) 

Conc. in 

Air 

(mg/m3

)* 

Air 

Exposure 

Limit 

(mg/m3)** 

Air 

Concentratio

n Exceeds 

Exposure 

Limit? 

THM 

Bromoform 1050 0.0218 2.3 5 No 

Chloroform 53 0.150 0.8 240 No 

Chlorodibromometh

ane 

157 0.0320 0.5 NA NA 

Dichlorobromometh

ane 

90 0.0654 0.6 NA NA 

 NA = Not Available 

 * Estimated based on Henry’s Law constant at 25C, and divided by a factor of 10 for dilution 

into ambient air. 

** U.S. Department of Labor, 2009. Occupational Health and Safety Administration, 

Permissible Exposure Limits (PEL). 

Actual air exposures will depend on proximity to vent outlets, atmospheric conditions (wind), as 

well as the duration of ballasting. Because the THMs in vent air would quickly dissipate into the 

atmosphere, it is anticipated that air exposures will decrease as distance to the ballast water 

increases; therefore potential air exposures for dock workers and the general public would be 

even less than those for the ship’s crew. Based on this assessment of THMs in vent air as a result 

of concentrations in ballast water, there is no evidence for the potential of adverse health effects 

to the ship’s crew, dock workers, or the general public. 

12.2.5.6 Potential risks to consumers of seafood 

Chemicals detected in treated ballast water that is discharged may pose a threat to seafood 

consumers only if they tend to bioaccumulate (within a trophic level, an increase in concentration 

of a substance in tissues due to uptake from food and sediments) or biomagnify (an increase in 

the concentration of a substance in the food web). As indicated in section 10.1, the 

bioaccumulation criteria per document MEPC 53/2/1 (or Procedure (G9)) include an 

octanol-water partition coefficient (Log Kow) of greater than 3 or a bioconcentration factor 

greater than 2000. The COPCs identified in this risk assessment all have Log Kows less than 3 

(Table 16), and therefore are not expected to persist in the food web. 
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12.2.6 Risk assessment conclusions 

The health risks to all receptors from the BalPure® system under normal operating conditions are 

very small and well within acceptable levels. Even an STDN technician, exposed to concentrated 

sodium bisulfite during a spill during chemical resupply, and who is wearing no PPE – an 

unlikely scenario – would have low health risk. Cancer risk and non-cancer hazards for the 

general public/beachgoers are well below levels of concern; actual risks to these receptors are 

expected to be even lower, as they are unlikely to be repeatedly exposed to treated ballast water 

as assumed in this risk evaluation. Since the risk assessment only evaluated direct exposure via 

ingestion and dermal contact with chemicals or ballast water, as these were considered the most 

relevant pathways, further semi-qualitative evaluation of the inhalation pathway was performed 

for the volatile THMs. This assessment demonstrated that conservative concentrations of 

airborne THMs generated by a release of ballast water were well below occupational exposure 

limits. 

12.3 Risks to the aquatic environment 

The data for the substances associated with use of the BalPure® system indicate that there is a 

low potential for bioaccumulation, sediment adsorption, and persistence in the aquatic 

environment. No effects or risks in the form of secondary (food chain) poisoning or to sediment 

species are anticipated. As such, toxicity presents the only likely potential risk for aquatic 

organisms. 

Whole effluent toxicity testing (acute and sub-lethal endpoints) of neutralized ballast water 

discharge indicates no apparent toxicity for all species and endpoints tested (E(L)C50 

and/or NOEC values of ≥100% ballast water sample) with the exception of the marine diatom, 

Skeletonema (96-hour exposure EC50 of 66.1% sample) (Nautilus, 2009). Less than a two-fold 

dilution would be required to reach a concentration less than the EC50 for Skeletonema. 

Certainly, when treated water is discharged to a harbour, the dilution would be much greater than 

two-fold. 

To ensure that no risks can be expected from the oxidant neutralizing agent, further testing was 

conducted on ballast water neutralized with a large excess of sodium bisulfite (22 mg/L). Testing 

results were that none of the test acute and/or chronic endpoints exhibited a 25% reduction 

relative to the control. These data suggest that a 3 mg/L treatment of hypochlorite in seawater 

with up to 22 mg/L of sodium bisulfite, which is much larger than would normally be applied, 

would not be expected to exhibit an adverse effect (Nautilus, 2005). 

Therefore, the toxicity testing of the treated ballast discharge indicates that unacceptable risks to 

the aquatic environment are not expected from use of the BalPure® system. 
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13 ASSESSMENT REPORT 

13.1 Overview of the data and endpoints 

The constituents associated with the BalPure® system were evaluated for a variety of endpoints, 

including toxicity, bioaccumulation, and persistence in the environment. The physical and 

chemical properties were evaluated to assess proper chemical handling and/or storage in a 

shipboard setting, and risks such as fire/explosion. Treated ballast water discharge and the risks 

of the COPCs to human health were also evaluated. 

Because TRO is neutralized prior to discharge, the DBPs potentially present in treated ballast 

water discharge are the most important to consider for this evaluation. In regards to aquatic 

toxicity, the existing database for chronic endpoints is limited for many of the THMs and HAAs. 

As such, the acute database, which is more complete, indicates the lowest EC50 was 0.028 mg/L 

for monochloracetic acid. The evaluation of the chemical and physical properties of all 

chemicals relevant to the BalPure® system suggests that bioaccumulation, sediment adsorption, 

or persistence is not expected to occur. Further, none of the chemicals met all three PBT 

substance criteria. 

Whole effluent discharge toxicity testing has been conducted for different water types 

(fresh water, brackish, and seawater) at various Active Substance treatment and TOC levels, and 

at different holding times. During the most recent studies, and with the exception of one sample 

for the marine diatom (Skeletonema) in brackish water, toxicity was not observed in the Day 5 

post-neutralization samples. Although the sensitivity between the taxonomic groups 

(algae, invertebrate, and fish) varied with the water type (freshwater, brackish, and seawater) 

tested, fish were the most tolerant species and invertebrates were generally the least tolerant 

species. Overall, the most sensitive species tested was Daphnia magna (Nautilus, 2009). In all 

species tested, no toxicity was observed in the samples tested 5 days after neutralization 

(Day 5+). 

Toxicity tests of treated water discharge from studies being done at the Naval Research 

Laboratory were also conducted. Results for the chronic toxicity tests are summarized in 

Table 5, and show that no toxicity was observed with the treated water samples for any species 

tested. The highest concentration with no observed effect (NOEC) was 100 percent sample 

(Nautilus, 2007). 

Because the BalPure® process uses an oxidant neutralization step during ballast water discharge, 

the TRO in the discharge will be non-detectable. Therefore, the discharge and predicted 

environmental concentration (PEC) for TRO is 0 mg/L. 

During pilot studies of the BalPure® system, the amount of DBPs in treated water discharge were 

evaluated in three different water types (freshwater, brackish water and seawater), at different 

Active Substance treatments and organic matter levels. The data is presented in sections 11.1 

to 11.3 above. In freshwater, total THMs in treated water ranged from 196.3 μg/L–400 μg/L and 

total HAAs ranged from 93.7 μg/L–154.7 μg/L. In brackish water, total THMs ranged 

from 225 μg/L–1099 μg/L and total HAAs ranged from 136.6μg/L–242.2 μg/L. In seawater, 

total THMs ranged from 33.3 – 121.3 μg/L and total HAAs ranged from 17.8 μg/L–36.8 μg/L. 

The DBP bromate was also measured in the brackish and seawater studies. In brackish water, 

bromate concentrations ranged from <2 μg/L–42 μg/L. In seawater, bromate concentrations 

ranged from <2 μg/L–23 μg/L. 
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The DBP concentrations from the studies noted above consider analysis of the whole effluent 

(i.e. discharge concentration) only and do not reflect actual environmental concentrations when 

treated ballast water is released in a harbour where dilution and mixing will occur. Meaningful 

PEC values will be derived using appropriate emission scenario modelling based on analysis of 

treated ballast water samples drawn from the full-scale land-based test set-up of the BalPure®

system and will be presented in a future dossier for Final Approval. 

Potential human exposures and health effects were evaluated qualitatively and quantitatively, 

when possible. Overall, the risk assessment determined risks to all receptors from the BalPure® 

system under normal operating conditions are very small and well within acceptable levels. 

A variety of reputable sources were consulted to gather test data and conduct the assessments 

required. These sources include, but are not limited to WHO, IPCS, OECD and US EPA. 

Information was also gathered from published independent research, which in most cases is 

peer-reviewed by others with similar levels of expertise. In some cases the test method used was 

not specified; however if the data set was limited, this data was included to provide at least some 

information. Due to the primary sources relied upon during the evaluation the level of 

uncertainty with this assessment is low. 

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