Active Chlorine Released - Assessment - Report

Regulation (EU) No 528/2012 concerning
the making available on the market and

use of biocidal products
Evaluation of active substances
Assessment Report
Active chlorine
released from sodium hypochlorite
Product-type 1
(Human hygiene)
January 2017
IT
Active chlorine released
Product-type 1 January 2017
from sodium hypochlorite
CONTENTS
1. STATEMENT OF SUBJECT MATTER AND PURPOSE ............................................... 3
1.1. Procedure followed .............................................................................................................................. 3
1.2. Purpose of the assessment report ................................................................................................ 3
2. OVERALL SUMMARY AND CONCLUSIONS ................................................................... 3
2.1. Presentation of the Active Substance ......................................................................................... 3

2.1.1. Identity, Physico-Chemical Properties & Methods of Analysis ................................................... 3
2.1.2. Intended Uses and Efficacy................................................................................................................... 10
2.1.3. Classification and Labelling ................................................................................................................... 12
2.2. Summary of the Risk Assessment ............................................................................................... 12

2.2.1. Human Health Risk Assessment.......................................................................................................... 14
2.2.1.1. Hazard identification and effects assessment ........................................................................ 14
2.2.1.2. Exposure assessment and risk characterisation ................................................................... 25
2.2.2. Environmental Risk Assessment ......................................................................................................... 25
2.2.2.1. Hazard identification and effects assessment ........................................................................ 32
2.2.2.2. Exposure assessment and risk characterisation ................................................................... 35
2.2.2.3. Fate and distribution in the environment ................................................................................ 39
2.2.2.4. PBT and POP assessment .............................................................................................................. 40
2.2.3. Assessment of endocrine disruptor properties .............................................................................. 41
2.3. Overall conclusions ............................................................................................................................ 41
2.4. Requirement for further information related to the reference biocidal product ... 41
2.5. List of endpoints.................................................................................................................................. 41
APPENDIX I: LIST OF ENDPOINTS ..................................................................................... 42
Chapter 1: Identity, Physical and Chemical Properties, Classification and Labelling ... 42
Chapter 2: Methods of Analysis .............................................................................................................. 46
Chapter 3: Impact on Human Health ................................................................................................... 46
Chapter 4: Fate and Behaviour in the Environment..................................................................... 55
Chapter 5: Effects on Non-target Species ......................................................................................... 56
Chapter 6: Other End Points ................................................................................................................... 57
APPENDIX II: LIST OF INTENDED USES ........................................................................ 58
APPENDIX III: LIST OF STUDIES ........................................................................................ 59
2
1. STATEMENT OF SUBJECT MATTER AND PURPOSE
1.1. Procedure followed
This assessment report has been established as a result of the evaluation of the active
substance active chlorine released from sodium hypochlorite as product-type 1 (Human
hygiene), carried out in the context of the work programme for the review of existing active
substances provided for in Article 89 of Regulation (EU) No 528/20121, with a view to the
possible approval of this substance.
Active chlorine released from sodium hypochlorite (releaser CAS no.: 7681-52-9) was notified
as an existing active substance, by the Euro Chlor Sodium Hypochlorite Registration Group at
Euro Chlor, hereafter referred to as the applicant, in product-type 1.
Commission Regulation (EC) No 1062/2014 of 4 August 20142 lays down the detailed rules for
the evaluation of dossiers and for the decision-making process.
On 31st July 2007, Italian competent authorities received a dossier from the Euro Chlor Sodium
Hypochlorite Registration Group at Euro Chlor. The Rapporteur Member State accepted the
dossier as complete for the purpose of the evaluation on 2nd April 2008.
On 17th May 2010, the Rapporteur Member State submitted to the Commission and the
applicant a copy of the evaluation report, hereafter referred to as the competent authority
report.
In order to review the competent authority report and the comments received on it,
consultations of technical experts from all Member States (peer review) were organised by the
"Agency” (ECHA). Revisions agreed upon were presented at the Biocidal Products Committee
and its Working Groups meetings and the competent authority report was amended
accordingly.
1.2. Purpose of the assessment report
The aim of the assessment report is to support the opinion of the Biocidal Products Committee
and a decision on the approval of active chlorine released from sodium hypochlorite for
product-type 1, and, should it be approved, to facilitate the authorisation of individual biocidal
products. In the evaluation of applications for product-authorisation, the provisions of
Regulation (EU) No 528/2012 shall be applied, in particular the provisions of Chapter IV, as
well as the common principles laid down in Annex VI.
For the implementation of the common principles of Annex VI, the content and conclusions of
this assessment report, which is available from the Agency web-site shall be taken into
account.
However, where conclusions of this assessment report are based on data protected under the
provisions of Regulation (EU) No 528/2012, such conclusions may not be used to the benefit of
another applicant, unless access to these data for that purpose has been granted to that
applicant.
2. OVERALL SUMMARY AND CONCLUSIONS
2.1. Presentation of the Active Substance
2.1.1. Identity, Physico-Chemical Properties & Methods of Analysis
The active substance covered by this assessment is ‘active chlorine released from sodium
1 Replace by Article 90(2) for a new active substance submitted under Article 11 of the BPD
2
COMMISSION DELEGATED REGULATION (EU) No 1062/2014 of 4 August 2014 on the work programme for the
systematic examination of all existing active substances contained in biocidal products referred to in Regulation (EU)
No 528/2012 of the European Parliament and of the Council. OJ L 294, 10.10.2014, p. 1
3
hypochlorite’ (3).
Upon use for MAIN GROUP 1 – Disinfectants (PT1), sodium hypochlorite aqueous solutions
release ‘active chlorine’, i.e. efficacious chlorine or available/releasable chlorine that is
disinfectant, algaecide, fungicide and microbiocide.
Namely, in water sodium hypochlorite (NaClO) hydrolyzes to hypochlorous acid (HClO)
according to:
NaClO + H2O ↔ Na+ + HClO + OH─ (4)
Furthermore, hypochlorous acid participates in the following equilibrium with chlorine (Cl2):
HClO + H3O+ + Cl─ ↔ Cl2 + 2H2O (5)
The ratio of Cl2/HClO/ClO─ is pH and temperature dependent. The pH-dependence is displayed
in the following figure, where the percentage of the different species at the equilibrium is
showed as a function of pH. Hypochlorous acid is predominant in the pH range 4 to 5.5,
whereas the hypochlorite anion predominates at pH >10. Chlorine can be present at pH < 4
only.
(3) As in CA-March15-Doc.5.1-Final, Revised on 23 June 2015, Annex II – Releasers

(4) Khydrolysis(ClO─) = Kw/Ka, where Ka(HClO)= 3.5 x 10-8 mol/dm3 at 20°C (Solvay, International Research
Document, 1979)
(5) Khydrolysis(Cl2) = 3.2 x 10-4 mol/dm3 at 20°C (Solvay, International Research Document, 1979)
4
Identification of the active substance releaser

The following infor mation attains to the active subst ance releaser, i.e. sodi um hy pochlorit e
Active substance releaser

CAS-No. 7681-52-9
EINECS-No. 231-668- 3
Other No. 0 17-011-00-1 (Index number)
IUPAC Name Sodi um hypoch lorite
CAS name Hypochlorous acid, sod ium sa lt
Common name, synonyma Sodium hypoch lorit e
Molecular formula CIHO.Na
Structural formula Na+ Cl - O-
Molecular weight 74.44 g/ mol
Purity Aqueous solut ion with an available (active) chlor ine

concentration ::; 18% w/w ( 6 ) , in compliance wit h t he EN
901: 2013
Additives Sodium hydroxide
Impurities One relevant im purity is present : sodium ch lorat e ( ::;5.4% of

the active ch lorine)
Non-relevant impurities are considered as confidential
information and , hence, descr ibed in t he Annex of Confidential
Data
Two manufacturing processes are described in the Euro Ch lor dossier and can be found in the
Annex of Confidential Data . Due to its instability as a pure salt, sod ium hypoch lorite is
manufactured and hand led on ly as an aqueous solution with a pH va lue greater than 11 at
20°C. Solut ions are kept alkaline in order to decrease the degradat ion rate of t he hypochlorite
to chloride and chlorate.
Identification of the biocidal product

The theoretical biocidal products described in the dossier are 14% (w/w) and 5% (w/ w)
avai lable chlor ine-containing solut ions (SL, i.e. soluble concentrate) . Sod ium hypoch lorite as
manufactured is adj usted with water to t he respective concentration of avai lable chlorine.
Since an end-use concentration of 0 .1 % ava ilable chlorine is intended under PT1 for skin
disinfection in healt hcare ( professiona l use) and skin disinfection ( non -professional use), for
convenience reasons a dispenser can be delivered t o the customer wit h t he in-use solution
already adj usted, apply ing the so-called ' ready-to-use' concept.
The HH RA and the ENV RA as detai led in th is document for PT1 are focused on a ready-to-use
product (Sodium hypochlorite 0.1°/o). Nevertheless, no specific data/ infor mation on identity
( 6)Sodium hypochlorit e is determ ined by a t it rimetric met hod. Results are t ipica lly expressed as available
(active) chlorine using by convention the molecular weight of elemental chlorine in ca lculat ions, but they
can be con verted into sodium hy pochlorite by applying a con version factor of 1.05 (MWNaoc1 / MWc12 =
74 .44/ 70.91 ) .
5
and physico-chemical properties of such a ready-to-use product have been provided by the
applicant in the original dossier (to be provided at product authorization).
6
Physical-chemical properties of the active substance releaser (sodium hypochlorite)

Due to its instability as a pure salt, sodium hypochlorite is manufactured and handled
exclusively as an aqueous solution with a pH value greater than 11 at 20°C.
In compliance with EN 901:2013, sodium hypochlorite aqueous solutions with an active
chlorine concentration up to 18% w/w are considered for the purpose of the approval.
However, sodium hypochlorite aqueous solutions with an active chlorine concentration up to
25% w/w are manufactured for industrial use.
A sodium hypochlorite aqueous solution with an active chlorine concentration of 24.3% w/w
was considered for physical-chemical testing as the highest available concentration. The tested
solution is a yellow limpid liquid, with faint chlorinous odour and freezing point of -28.9 ±
0.5 °C; relative density (D21.24) is 1.300 ± 0.001.
The vapour pressure of sodium hypochlorite solutions is reported by EN 901:2013 to be
approximately 2.5 kPa at 20°C, due to water (7). At pH >11 the hypochlorite anion is the
predominant species, whereas none of the volatile species at equilibrium (hypochlorous acid
and chlorine) are virtually present. As an ionic species, the hypochlorite anion has high water
solubility and is unlikely to evaporate to the gaseous phase. Thus, it can be assumed that the
hypochlorite anion has a negligible vapour pressure. No Henry’s law constant is derived, either.
However, for the purpose of risk assessment only, the Henry’s law constant of hypochlorous
acid is also reported in the LoEPs as determined experimentally by Blatchley et al. (1992) (8)
by the air stripping method, being hypochlorous acid the only volatile chlorine species present
at the equilibrium at in-use pH values under PT1.
The CRC Handbook of Chemistry and Physics (9) indicates for sodium hypochlorite a solubility
in water of 26 g/100 g H2O at 0°C, whereas a solubility of 79.9 g/100 g H2O at 25°C is given
by the Perry’s Chemical Engineers’ Handbook (10). The latter value is not from a peer-reviewed
handbook and will not be included in the LoEPs. The high solubility in water of sodium
hypochlorite is confirmed by a calculation provided by the applicant using WSKOW v1.41,
though the result (1 kg/L at 25°C) is out of the validation domain of the model and therefore
will not be included in the LoEPs, either.
Sodium hypochlorite is not used in organic solvents due to its nature as a strong oxidiser.
Sodium hypochlorite hydrolyzes in water according to:
NaClO + H2O ↔ Na+ + HClO + OH─
Khydrolysis(NaClO) = Kw/Ka, where Ka(HClO) is 3.5 x 10-8 mol/dm3 at 20°C (11).
In water sodium hypochlorite degrades to chlorate and chloride. The degradation rate is a
function of the active chlorine concentration and of temperature. For a sodium hypochlorite
aqueous solution with an active chlorine concentration of 10% w/w, the half-life is reported to
be 800 days at 15 °C; 220 days at 25 °C; 3.5 days at 60 °C; 0.079 days at 100 °C. Whereas,
for an active chlorine concentration of 5% w/w, the half-life is reported to be 5000 days at 15
°C; 790 days at 25 °C; 13.5 days at 60 °C; 0.25 days at 100 °C.
The surface tension of the tested solution (sodium hypochlorite aqueous solution with an active
chlorine concentration of 24.3% w/w) is 82.4 ± 0.8 mN/m at 20.2-20.3 °C. Dynamic viscosity
is 6.2-6.6 mPa s at 20 ± 0.2 °C; 4.0 mPa s at 40 ± 0.2 °C. A flash-point higher than 110 °C is
considered. At 110 °C, the test item boiled and overflowed from the cup just after the
presentation of flame; then the test stopped. Furthermore, sodium hypochlorite solutions are
not known to spontaneously ignite when exposed to air or to emit flammable gases.
(7) The vapour pressure of pure water, as given in different handbooks, is 2.34 kPa at 20°C.
(8) Blatchley, E. R., III, R. W. Johnson, J. E. Alleman, and W. F. McCoy. Effective Henry’s law constants
for free chlorine and free bromine. Wat. Res., 26 , 99–106, 1992.
(9) Internet Version 2005, David R. Lide, ed., <http://www.hbcpnetbase.com>, CRC Press, Boca Raton,
FL, 2005.
(10) 7th Ed., Robert H. Perry, Don W. Green, James O’Hara Maloney, eds., McGraw-Hill, New York, 1997.
Not peer-reviewed.
(9) Solvay, International Research Document, 1979.
7
Active chlorine relea sed
Product-type 1 Janua ry 2017
Harmonized classification was approved by EU for 'sodium hypoch lorite, solution ... % Cl
active', which was inserted into Annex VI of CLP under I ndex number 0 17-011-00-1. No
classification for physical hazards applies. Nevertheless, no evidence was provided by the
applicant as regards either oxidizing and explosive properties of sodium hypoch lorite aqueous
solutions. New tests accord ing to the UN Recommendation on the Transport of Dangerous
Goods, Manua l of Tests and Criteria need to be provided (at the maximum available
concentration of sod ium hypochlorite in water), at the latest six months before the date of
approval.
Common metals shou ld never be used for the storage and hand ling of sodium hypochlorite
aqueous solutions . Su itable materials are listed in the embedded fi le below :
Packaging rraterials
for NaCIO.docx
Ana lytical methods for detection a nd identification

Sodium hypochlorite a s m a nufacture d (aqueous solutions)
An analytical method is available for the determination of sodium hypochlorite in sod ium
hypoch lorite aqueous solutions 1 % w/w . Upon appropriate dilution, the method is applicable
also to higher sodium hypochlorite concentrations. Sodium hypochlorite reacts with potassium
iodide to release iod ine in the presence of acetic acid . The iodine is titrated with a sodium
th iosu lphate solution in the presence of starch ind icator. Alternatively, titration can be carried
out potentiometrically by means of titration automates, in wh ich case the add it ion of soluble
starch is unnecessary.
Linearity was investigated over the range 0.5 - 1.5 % w/w as NaCIO (corresponding to 0.48 -
1.43 % w/w as active chlorine) :
R 0 .9999
Slope 2 .7492
I ntercept 0.4040
The prec1s1on of the method was satisfactory . The % RSDn=6 proved to be 0.51, below the
acceptance criteria according the modified Horwitz equation (2 .67) . Specificity was tested
against the blank on ly (i.e. water) . A LOQ of 0.5% w/w as NaCIO (corresponding to 0.48%
w/w as active chlorine) is proposed .
Apart from sodium ch lorate, wh ich is a relevant impurity, impurities of sod ium hypoch lorite are
regarded as confidentia l information . Therefore, information on the analytical methods for their
identification/quantification can be found in the Annex of Confidential Data .
The analytical methods available in the origina l dossier lacked validation data. The WGII2016
conclusion was that fully-validated ana lytica l methods (in compliance w ith Gu idance on the
BPR Volume I : I dentity I physico-chem ical properties I analytical methodology - Part A :
I nformation Requ irements) are required for the identification/quantification of impurit ies in
sodium hypochlorite and shou ld be provided to the eCA-IT six months before the date of
approval.
Formulation analysis
I n principle, the same ana lytica l method described above will apply .
Residues analysis
The active substance is "active ch lorine released from sodium hypoch lorite", wh ich is thought
to consist of ch lorine {Clz), hypochlorous acid {HCIO) and hypochlorite an ion {Clo- ) in
equi librium. The predominant species will depend on pH va lue (ch lorine is ava ilable only at pH
< 4, hypochlorous acid is predominant in the range 4 to 5.5, whereas on ly the hypoch lorite
8
anion is present at pH >10).

At the in-use pH values in PT1, chlorine is virtually non-present at the equilibrium, whereas the
predominant species are the hypochlorous acid and the hypochlorite anion or (at higher pH
values) the hypochlorite anion only.
Analytical method for residues in air

Residue definition: Cl2/HClO/ClO─
Hypochlorite is a non-volatile species. Hypochlorous acid is volatile, but according to literature
data, the Henry’s Law constant is ≈ 0.1 Pa m³ mol-1, i.e. volatilization from the aqueous phase
is expected to be slow. Furthermore, there are indications that the half-life is only a few hours,
i.e. much shorter than the value derived by Atkinson calculation. So occurrence in air is not
probable for this species, either.
In PT1, no spray applications are envisaged.
At the in-use pH values under PT1, exposure to gaseous chlorine is not expected, but through
accidental events (chlorine can be formed and released when the active chlorine equilibrium is
shifted to low pHs by strong acids, e.g. by mixing hypochlorite-based solutions with acidic
cleaning agents).
In case of an accidental release of chlorine, two analytical methods (12,13) for the monitoring of
chlorine in workplace air are available in the CAR, which allow the determination of chlorine in
workplace air in the range 0.3-7.0 mg Cl2/m3. In principle, the range can be expanded. Though
not validated, the two available methods are published methods, so they can still be concluded
to be acceptable for the purpose (determination of chlorine in workplace air.
Analytical method for residues in soil

Residue definition: HClO/ClO─
Not required. For none of the intended uses, soil is the first receiving compartment.
Environmental exposure is expected via the facility drain into the STP. Active chlorine
(HClO/ClO─) can reach the soil compartment only indirectly, via sewage sludge: rapid
degradation occurs already with organic matter therein. In the event of contamination of soil,
e.g. due to direct application of chlorinated water, hypochlorous acid/hypochlorite anion would
react rapidly with organic matter in soil, anyway.
Analytical method for residues in drinking water

Residue definition: HClO/ClO─ and relevant metabolite chlorate ClO3─
The analytical methods for active chlorine (HClO/ClO─) as available in the original Euro Chlor
dossier are not acceptable, since validation is not in accordance with the Additional Guidance
on TNsG on analytical methods.
Therefore, a fully-validated analytical method for active chlorine residues in drinking water is
requested. A fully validated analytical method is also requested for the relevant metabolite
chlorate (ClO3─). Methods, which are necessary for monitoring purposes, should be submitted
at the latest six months before the date of approval of the active substance.
Analytical method for residues in surface water

Not required. Environmental exposure is expected via the facility drain into the STP, but rapid
degradation occurs with organic matter therein. Rapid degradation occurs also with the organic
matter in surface water (DT50surface water = 56 min at environmental temperature).
12 Reference: OSHA Method «Chlorine in Work place Atmosphere» 05.01.83; Smith & Cochran
Spectrophotometric determination of Free Chlorine in Air using Sulphamic acid/Tri-iodide procedure -
Anal Chem 1986 Vol 58 pp 1591-1592
13 Reference: OSHA Method «Chlorine in Work place Atmosphere» 05.01.83; NIOSH free chlorine in air
01.01.75; ISO 7392/2 Water quality – Determination of free and total chlorine Part 2 Colorimetric
method using DPD for routine control purposes 15.10.85
9
Analytical method for residues in body fluids and tissues

Not required. Hypochlorous acid/ hypochlorite anion are oxidizing agents and degrade rapidly
with organic matter. Besides, due to corrosive properties, systemic toxicity would be secondary
to local effects.
Nevertheless, in case of an accidental release of chlorine, the analytical methods available for
the monitoring of chlorine in workplace air are meaningful for monitoring human exposure.
Analytical method for residues in food and feed
Not required under PT1.
2.1.2. Intended Uses and Efficacy
Sodium hypochlorite, as active chlorine releaser, has strong bactericidal, fungicidal, sporicidal
and virucidal activity. It has also been reported to inactivates prions (Block 5th edition, Ch. 33
page 659 − S. Prusiner et al. Decontamination procedures). However, as for mycobacteria,
such activity has not been supported by targeted tests for the purpose of this dossier.
Field of use envisaged

The uses assessed belong to the product-type 1:
 Skin disinfection of the hands and lower forearms
The “organism to be protected” is man, by preventing the spreading of infections (1000 mg/L
available chlorine).
Professional and non-professional use is envisaged.
The active substance released from either chlorine, sodium hypochlorite or calcium
hypochlorite in aqueous solutions is active chlorine. The hypochlorite ion is in equilibrium with
hypochlorous acid and chlorine. The equilibrium depends on the pH value: chlorine is available
only below pH 4, in the neutral pH range hypochlorous acid is the predominant species and at
pH values higher than 10 the only species present is the hypochlorite ion (please, refer to the
beginning of para. 2.1.1 of this document).
For the chemical reactivity in aqueous solution with the same active chlorine concentrations
and the same pH conditions, it is irrelevant whether active chlorine is generated from chlorine
gas, calcium hypochlorite or sodium hypochlorite. Therefore, all studies investigating
hypochlorite aqueous solutions can be used for the evaluation and assessment of active
chlorine released from any of the three releasers.
The disinfecting efficiency of hypochlorite aqueous solution is dependent on the active chlorine
concentration and decreases with an increase in pH and vice versa, which is parallel to the
concentration of un-dissociated hypochlorous acid.
It has to be stressed that the activity is strongly reduced by the presence of organic load and
in general by the presence of particles. The chlorination and the oxidation reaction of
hypochlorite are unspecific.
For bacteria it is shown that inactivation of spores need more drastic conditions than
inactivation of viable forms. Biofilms consisting of bacteria are characterized by a high
resistance against active chlorine and other biocides. Mycobacteria and fungi are more difficult
to inactivate by active chlorine in comparison with bacteria. For viruses a wide range of
inactivation conditions can be found. Prions can be inactivated by applying high concentrations
10
and longer treatment times. In general higher temperatures and lower pH increase the
efficiency of inactivation.
Efficacy studies from literature have been reported in Doc. IIIA using numerous different
organisms, concentrations and test conditions. At low concentrations, active chlorine is still
able to maintain the concentration of pathogens below a critical level. In these conditions, the
proteins of the membrane are partly destroyed and the bacteria are not able to multiply.
A very large list of studies done by different methods in different conditions and on different
groups of organisms have been reported in Doc. IIIA, but the key studies used for the
evaluation are those presented in Doc. IIIB and IIB, correctly performed following EN Norms in
which the disinfectant activity was correctly demonstrated using Eau de Javel 12°Cl (about 3.6
% available chlorine) and a product containing 2.74% available chlorine as product tests.
Concentration of available chlorine showing bactericidal, fungicidal, sporicidal and virucidal
action ranged between 3.6 and 3600 mg/L, depending on the organisms tested, conditions of
the tests, etc. (studies IIIB 05.10.01 to 05.10.12). Although known to be effective also against
mycobacteria and prions, such activity has not been demonstrated by targeted tests performed
for the purpose of this dossier.
Acceptable studies from the literature have been provided that support the efficacy of the a.s.
also at much lower concentrations, specifically those indicated for PT2 and PT5 applications.
As in-use conditions tests are not required for a.s. approval, the efficacy data package will
have to be implemented at product authorization stage, and more information should be
provided to demonstrate full efficacy against all claimed target organisms of the products.
Although different species vary in their sensitivity to active chlorine, development of acquired
resistance is not expected since its multiple molecular sites of attack on the surface and within
the microbial cells. Active chlorine is in fact regarded by experts [see IFH (International
Scientific Forum on Home Hygiene) review October 2003 and Submission to SCENIHR,
February 2008)] as one of the biocides where acquired resistance is least likely to develop. For
the same reasons cross-resistance is not to be expected, nor has it been observed. Despite its
use for almost a century in purifying drinking water, where very low (sub ppm) concentrations
are continuously maintained, the development of acquired resistance has not been observed.
Adaptation of organisms to hypochlorite can be determined by comparison of the Minimum
Inhibitory Concentration (MIC) but this is not relevant in practice as the actual use
concentrations are much higher and thus a sufficient margin of safety is provided.
No management strategies are necessary as acquired resistance to active chlorine has not
developed nor will develop due to its reactive nature and unspecific mode of action. Some
temporary adaptation giving modestly reduced susceptibility is sometimes observed in
organisms exposed continuously at low concentrations (e.g. in water pipes through formation
of biofilms), but this is readily managed e.g. by control/removal of the biofilm.
The assessment of the biocidal activity of the active substance demonstrates that active
chlorine released from sodium hypochlorite t has a sufficient level of efficacy against the target
organism(s) and the evaluation of the summary data provided in support of the efficacy of the
accompanying product, establishes that the product may be expected to be efficacious.
In addition, in order to facilitate the work of Member States in granting or reviewing

authorisations, the intended uses of the substance, as identified during the evaluation process,
are listed in Appendix II.
11
Active chlorine relea sed
2.1.3. Classification and Labelling
Active chlorine is released from sod ium hypoch lorite to give an equilibrium of ch lorine,
hypoch lorous acid and hypoch lorite anion in aqueous solution . The ratio of Cli/ HCIO/ CIO- is pH
and temperature dependent and, therefore, classification for active ch lorine is not feasible.
Current cla ssification

Sod ium hypoch lorite is listed on Annex VI, Table 3. 1 of Regu lation (EC) 1272/ 2008 (CLP
Regulation, Index No 017-011- 00- 1) with the following classification and labell ing:
Ha rmonized classification of "sodium hypochlorite, solution ... 0/o Cl" active a ccording
to Annex VI, Table 3.1 of Re gulation (EC) 1272/ 2008 ( CLP)
Classification
Hazard Class and Skin Corr. 18
Cateqorv Aquatic Acute 1
Hazard Statement H314 : Causes severe skin burns and eye damage.
Codes H400 : Verv toxic to aquatic life.
Suppl. Hazard EUH031 : Contact with acids liberates toxic gas.
Statement Code
Labellinq
GHS Pictogram GHSOS, GHS09
Signa l Word Danger (Dgr)
( Code)
H400 : Verv toxic to aquatic life.
Statement Code
Specific EUH031 : C;;::: 5 %
concentration
lim its
As precautionary statements are not included in Annex VI of Regulation EC 1272/ 2008,
no proposal is made.
Proposed classification
Based on the resu lts from toxicity and ecotoxicity stud ies performed for sod ium hypochlorite
solution according to Regu lation EC 1272/ 2008 ( CLP) :
Proposed classification of "sodium hypochlorite, solution ... 0/o Cl a ctive "
Classification
Hazard Class and Skin Corr. 18
Category Aquatic Acute 1
Aquatic Chronic 1
Codes H400 : Very toxic to aquatic life.
H410 : Verv toxic to aquatic life with long-lasting effects .
Statement Code
Labelling
GHS Pictoaram GHSOS GHS09
Signa l Word Danger (Dgr)
( Code)
H400 : Very toxic to aquatic life.
H410 : Verv toxic to aquatic life with long-lasting effects .
12
Suppl. Hazard EUH031: Contact with acids liberates toxic gas.

Statement Code
Specific EUH031: C ≥ 5 %
concentration M=10 (H400)
limits, M factor M=1 (H410)
As precautionary statements are not included in Annex VI of Regulation EC 1272/2008,
no proposal is made.
In June 2016, RAC decided to change the harmonized classification (acc. to Annex VI to CLP)
with respect to the aquatic endpoints:
 for Aquatic Acute 1 (H400), an M-factor of 10 was assigned;

 classification as Aquatic Chronic 1 (H410) with M-factor of 1 was added.
13
2.2. Summary of the Risk Assessment
2.2.1. Human Health Risk Assessment
2.2.1.1. Hazard identification and effects assessment
The active substance covered by this assessment is “active chlorine released from sodium
hypochlorite”.
In water, sodium hypochlorite dissociates into the sodium cation (Na+) and hypochlorite anion
(ClO-), which is characterised by its well-known irritating/corrosive effects. Further,
hypochlorite is in equilibrium with hypochlorous acid (HClO) and chlorine (Cl2). The remaining
sodium cation is a physiologically-essential element and required in the intermediary
metabolism. Hence, it cannot be regarded as a typical xenobiotic when entering the body.
Since in aqueous solutions, sodium hypochlorite (NaOCl) and chlorine share the same anion
(ClO-) and, thus, release the very same active substance (i.e. active chlorine, thought to
consist of hypochlorite, hypochlorous acid and chlorine in equilibrium), read-across is possible
for all the toxicological end-points.
Therefore, whenever specific data obtained with sodium hypochlorite are not available,
reference is made to the respective Euro Chlor data obtained with chlorine. It shall be noted
that the same approach was adopted for the physical-chemical properties determined in
aqueous solution, as well as for the mode of action.
During BPC TOX-WGIII-2016, the members agreed that human health effects are primarily due
to the local mode of action of sodium hypochlorite and potential systemic effects are secondary
to its direct irritating reactivity.
Absorption, distribution, metabolism and excretion

Oral administration of sodium hypochlorite
Two studies on the absorption, distribution, metabolism and excretion were conducted with
[36Cl]-radio-labelled test substance in rats (Abdel-Rahman, 1982). These studies suggest that
after exposure via oral route, HClO is absorbed and excreted mainly through urine as chloride
(36.43% + 5.67 of the administered dose after 96 h); a lesser extent of HO36Cl-derived
radioactivity not necessarily associated with absorption was detectable in the faeces 96h after
exposure (14.8% + 3.7). The oral absorption is therefore considered around 35%.
Oral absorption is considered as not relevant because chlorine-related toxicity is based on local
effects only (with secondary systemic effects at high doses).
During BPC TOX-WGIII-2016, the members considered that the oral absorption values should
be removed from the CAR due to the lack of systemic effects.
Dermal and inhalation administration

No data on ADME are available for dermal and inhalation exposure for the active chlorine
releaser sodium hypochlorite.
Regarding dermal exposure, the potential of hypochlorite solutions to penetrate the skin is low
given its reactivity to proteinaceous material at the site of first contact. In addition, the
investigation of the dermal penetration using sodium hypochlorite at non-irritant
concentrations would be poorly informative, since concentrations in the physiological range
would have to be applied.
Dermal absorption is considered as not relevant because chlorine-related toxicity is based on

local effects only (with secondary systemic effects at high doses).
In the absence of clear systemic effects, the BPC TOX-WGIII-2016 concluded that dermal
absorption values are not deemed necessary.
For consistency, the WG members also considered that the inhalation absorption values are
not relevant due to the lack of systemic effects.
14
Acute Toxicity
Sodium hypochlorite has been demonstrated to be of low toxicity in acute studies in the rat by
the oral and dermal route of exposure (Anonymous, 1970). In the acute oral and dermal
studies, the LD50 was determined to be greater than 2000 mg avCl/kg bw. Signs of toxicity
were evident in the oral study characterised by hypoactivity, muscular weakness,
haemorrhagic rhinitis and emaciation and in the dermal study by moderate to severe
erythema.
These data on NaOCl are supported by many data found in the literature, as described in the
EU-RAR on sodium hypochlorite (2007).
In the acute inhalation toxicity study (Anonymous, 1970), inactivity and lacrimation were
evident at the dose of 10.5 mg avCl/L (1 h exposure). No deaths occurred (LC0 >10.5
mg avCl/L). Thus, the LC50 was determined to be greater than 10.5 mg avCl/L.
Formally, Regulation (EC) 1272/2008 (CLP) requires conversion of existing inhalation toxicity
data which have been generated using a 1-hour testing exposure to 4-hour exposures (division
by a factor of 4 for dusts and mists according to Annex I, notes to Table 1.1, paragraph c).
However, in the case of sodium hypochlorite which only exerts local effects at the side of first
contact, it is expected that local irritative effects are rather concentration than time
dependent. Hence, findings for 4-h exposure durations are expected to be similar to those
observed after 1-h exposures.
Consequently, due to the lack of systemic effects, time extrapolation is not considered relevant
and the 4-h LC50 be expected in the same range as the 1-h LC50, i.e. >10.5 mg avCl/L.
Conclusion on acute toxicity

Based on the results of the studies performed with sodium hypochlorite solutions, sodium
hypochlorite does not warrant classification for acute oral, dermal and inhalation toxicity.
Sodium hypochlorite is not legally classified with respect to acute oral, dermal and inhalation
toxicity according to Regulation (EC) No 1272/2008 (CLP).
Irritation and Corrosivity

Skin irritation
A study to investigate the skin irritating potential of sodium hypochlorite (Nixon, 1975) was
performed. The results indicate that sodium hypochlorite, 5.25%, was slightly irritant in rabbits
and guinea pigs under the conditions described in the study. The mean score obtained from
intact skin (sum of mean erythema and edema scores at 4, 24 and 48 hours) was 1.0 for
rabbits and 0.3 for guinea pigs. All findings were reversible.
Eye irritation
Two eye irritation studies in rabbits and monkeys are available (Pashley, 1985; Carter, 1965)
indicating eye irritating properties for concentrations of 5.25 and 5.5% avCl respectively.
Conclusion on skin and eye irritation

The harmonized classification of “sodium hypochlorite, solution …% Cl active” is Skin Corr. 1B,
H314.
Data on animal skin clearly indicate an irritating effect at 5% avCl and above. Animal studies
showed eye irritation potential of sodium hypochlorite solutions. In addition to the available
studies, the EU-RAR (2007), DAR (2009) and the REACh dossier provide a variety of animal
and human studies which investigated the skin and eye irritation potential of hypochlorite
bleaches at different concentrations.
These results may support the former Specific Concentration Limits (SCL) obtained for
sodium hypochlorite under Council Directive 67/548/EEC (DSD):
15
Concentration NaOCl (as avCl) Classification (DSD)

Concentration ≥ 25% C; corrosive; R34
10% ≤ Concentration < 25% C ; corrosive; R34
5% ≤ Concentration < 10% Xi; irritant; R36/38
However, these SCLs have not been transferred to Annex VI, Table 3.1 or 3.2 of
Regulation (EC) 1272/2008 (CLP Regulation, Index No 017-011-00-1) and only Skin
Corrosion 1B was assigned to “sodium hypochlorite, solution …% Cl active”. For the
purpose of classifying sodium hypochlorite mixtures/dilutions, it is generally assumed that
the harmonized classification as Skin Corrosion 1B applies to a hypothetical 100% pure
substance. Consequently, the generic concentration limits of the CLP triggering
classification of the mixture as corrosive/irritant to the skin/eye apply to NaOCl mixtures.
In addition, sodium hypochlorite aerosols may be irritant to the respiratory tract.

According to the Guidance on the Application of the CLP Criteria (Version 4.1, 2015,
Chapter 3.8.2.5), a classification for corrosivity is considered to implicitly cover the
potential to cause respiratory tract irritation. Consequently, no additional classification is
required.
Sensitisation
Three skin sensitisation studies were conducted in guinea pigs with sodium hypochlorite
( 1982; 1985a and 1985b). The studies showed no sensitising effects.
Conclusion on skin sensitisation

On the basis of the data available it can be considered that sodium hypochlorite is not a skin
sensitizer.
Sodium hypochlorite aerosols are not expected to be sensitizer to the respiratory tract.
Sodium hypochlorite is not legally classified with respect to skin or respiratory tract
sensitisation according to Regulation (EC) No 1272/2008 (CLP).
Repeated dose toxicity

Oral administration of sodium hypochlorite
The subacute oral repeated dose toxicity of sodium hypochlorite has been investigated in a
28 day rat study (Anonymous, 1970). A NOAEC of >7500 ppm avCl was determined.
Three subchronic repeated dose toxicity drinking water studies of sodium hypochlorite are
available for rats and mice (Hasegawa, 1986; Daniel, 1990; Daniel, 1991). NOAECs derived
were 0.1% avCl, ≥0.025% avCl (highest dose tested) and ≥0.02% avCl (highest dose tested),
respectively.
Data on chronic repeated dose toxicity is available from four chronic toxicity/carcinogenicity
drinking water studies in rats and mice (Hasegawa, 1986; NTP, 1992; Soffritti, 1997;
Kurokawa, 1986). The NOAECs derived lay between >0.0275% and 0.1% avCl.
Overall, no systemic effects or morphological changes on microscopic examination could be

observed with the exception of body weight and liver effects. As a consequence of these
results, the eCA presented before BPC TOX-WGIII-2016 the statement “Chlorine-related
toxicity is based on local effects (with few secondary systemic effects at high doses)” detailing
that based on the weight of evidence, sodium hypochlorite acts via a pure local mode of action
(with secondary systemic effects at high doses only). In particular, effects on body and liver
weight observed in the 90-day and 104-week studies were discussed in detail and considered
as secondary to the local toxicity of sodium hypochlorite.
A potential mode of action underlying the reduced body and liver weights could be that the gut
mucosa and microflora may be destroyed even below irritant concentrations since it is more
sensitive than e.g. skin.
16
Since sodium hypochlorite decomposes rapidly after “port of entry” contact, only sodium or
chloride will become systemically available. Taking into account that sodium as well as chloride
are broadly distributed nutrients no toxicological hazard arises.
Dermal administration of sodium hypochlorite

No repeated dermal toxicity studies on the active chlorine releaser sodium hypochlorite are
available. The conduction of a dermal repeated dose toxicity study is considered to be not
necessary for the following reasons:
1) Due to its oxidative and corrosive nature sodium hypochlorite will cause skin
destructions. These effects are considered to be of local nature due to the reaction of
the substance with the surrounding tissue. Systemic toxicity would therefore occur only
secondary to locally irritating effects. In the available studies there are no indications
for any other mechanism of toxicity.
2) The irritant effect of sodium hypochlorite is caused by its oxidative property and basic
nature of hypochlorite and its solutions, which create a high-pH environment on
exposed body tissues. According to OECD 404 no tests should be performed with
substances having a pH of 11.5 or higher which is the case for 5% and 14%
concentrated sodium hypochlorite solutions. The testing of more diluted solutions will
not yield other results as those obtained from the oral studies.
Consequently based on information available on effects following other routes of exposure, a
repeated dermal toxicity test is not required for animal welfare reasons. In addition, some
human data exist (see in the following) from which it is possible to derive a NOAEC.
Administration of sodium hypochlorite via inhalation

There is no repeated dose inhalation toxicity study on sodium hypochlorite available. An
inhalation study is considered to be not necessary due to the following reasons:
1) Due to the intrinsic properties of the test substance and to its high reactivity the
mechanism of action of sodium hypochlorite is restricted to primary local effects like
irritation, corrosion and oxidation after contact with surrounding tissue which are shown
by the acute dermal irritation and eye irritation study.
2) Systemic toxicity after inhalation exposure towards sodium hypochlorite would
therefore occur only secondary to locally irritating effects mainly caused by the local
oxidation and basic nature of hypochlorite and its solutions. The remaining sodium and
chloride ions are physiologically essential elements and are required in the intermediary
metabolism and can therefore not be regarded as typical xenobiotics when entering the
body. In the available studies there are no indications for any other mechanism of
toxicity.
For the evaluation of local effects of repeated inhalation exposure to sodium hypochlorite
aerosols, the EU-RAR (2007) proposed to use data from chlorine gas. The NOAEC for repeated
exposure was derived at 0.5 ppm available chlorine (1.5 mg/m3) based on human studies.
Given the similar chemical reactivity based on the same active principle (i.e. the reactions of
the hypochlorite ion), use of chlorine data is also justified for evaluating local effects of sodium
hypochlorite after inhalation exposure. Therefore, relevant studies performed with chlorine gas
are summarized in the following.
In a subacute inhalation repeated dose toxicity study (Barrow, 1979) Fischer 344 rats were
exposed to chlorine gas for 6 h a day for 6 weeks. The results of this study indicated that
unequivocal upper and lower respiratory tract changes were produced in rats exposed to 9
ppm of chlorine. The respiratory tract effects found in animals exposed to 3 or 1 ppm chlorine
were very similar and much less severe than those seen at 9 ppm. The result of the current
study may have been affected by the presence of chloramines (generated from reaction of
chlorine with ammonia from urine and faeces). The NOAEC in this study was set at 1.0 ppm
equivalent to 3.0 mg/m3.
17
A subchronic study in Rhesus monkeys was performed with exposures of 6 h per day for 52
weeks towards nominal concentrations of 0, 0.1, 0.5 and 2.5 ppm Cl2 ( 1987). In this
study, treatment-related responses were confined to ocular and respiratory tract irritation.
Histopathological examinations revealed that treatment-induced lesions were limited to the
respiratory epithelium of the nose and trachea. Nasal and tracheal lesions were induced by
exposure to 2.3 ppm chlorine, while less distinct but similar changes were also present in the
nasal passages of some animals in the 0.5 and 0.1 ppm groups in the absence of tracheal
lesions, indicating a concentration-related response relationship for chlorine-induced airway
toxicity. No histological lesions were observed in this study at sites other than the nasal cavity
and trachea. The NOAEC was considered to be 0.5 ppm equivalent to 1.5 mg/m3.
In a chronic toxicity/carcinogenicity study with mice and rats (Wolf, 1995), it could be
demonstrated that chlorine is non-carcinogenic. Regarding non-cancer endpoints, Chlorine was
clearly a nasal toxicant that affected all airway epithelial types in the nose, but no response
was observed in the larynx or lower respiratory tract. The NOAEC of <0.4 ppm (<1.2 mg/m³)
was determined for both species.
Conclusion on repeated dose toxicity

Overall, no systemic effects or morphological changes on microscopic examination could be
observed after oral administration of sodium hypochlorite solutions to rats and mice, with the
exception of body weight and liver effects. However, these changes were considered secondary
to the local toxicity of sodium hypochlorite. The NOAECs derived in chronic studies lay between
>0.0275% and 0.1% avCl.
For the dermal route of exposure, no repeated dose toxicity studies are available, and are not
deemed necessary, based on information available on effects following other routes of
exposure as well as for animal welfare reasons. In addition, some human data exist (for
sodium hypochlorite, see in the following) from which it is possible to derive a dermal NOAEC.
The repeated dose toxicity studies performed with chlorine gas indicated respiratory tract
irritation due to the local chemical reactivity of chlorine (i.e. corrosion/irritation at first site of
contact). NOAECs in the range of <0.4 ppm to 1.0 ppm (<1.2 mg/m³ to 3.0 mg/m3) were
derived from the rat and mice studies, whereas a NOAEC 0.5 ppm (1.5 mg/m³) was derived
from the monkey study.
Genotoxicity
In vitro
Three Ames test studies are available for sodium hypochlorite (Ishidate, 1984; Kawachi, 1980;
LeCurieux, 1993). These studies showed sporadic positive results when sodium hypochlorite
was applied with metabolic activation.
One in vitro cytogenetic assay in mammalian cells (Ishidate, 1984) is available showing
positive results only at a toxic dosage of sodium hypochlorite applied without metabolic
activation.
In vivo
Two micronucleus tests (Hayashi, 1988; Meier, 1985) reported no mutagenic potential of
sodium hypochlorite in vivo. An in vivo bone marrow aberration assay and a non-standard DNA
damage assay in renal tissue (Meier, 1985; Kasai 1987) showed likewise negative results.
Germ cell effects were studied in male mice (Meier, 1985), showing sporadically increased
sperm-head abnormalities, however, with a non-guideline assay. Therefore, its biological
significance is unclear. In four out of the five in vivo tests, no information on bone marrow
toxicity was reported.
However, due to the local mode of action, the biological relevance of any result from an in vivo
study is questionable in view of uncertainty of the availability of the test substance at the
target organ.
18
Conclusion on genotoxicity
Overall, the results of the in vitro assays are consistent with the ability of hypochlorite to
generate reactive oxygen species. Reactive oxygen species have the ability to induce
sporadically DNA damage through an indirect mechanism, dependently on the ability of the cell
to cope with oxidative stress. Negative results in the in vivo studies are considered sufficient to
reassure about the absence of a mutagenic potential of hypochlorite in vivo.
Based on the available data, no genotoxic potential of sodium hypochlorite is expected.
Carcinogenicity
Sodium hypochlorite was tested for carcinogenicity by the oral route in several studies
(Hasegawa, 1986; NTP, 1992; Soffritti, 1997; Kurokawa, 1986). The NOAECs derived lay
between >0.0275% and 0.1% avCl.
There were no treatment-related increases in non-neoplastic lesions or tumour incidence

observed in the studies by Hasegawa, NTP and Kurokawa. In the Soffritti study, increased
incidence of lymphomas and leukaemias were observed in females which were, however,
within the historical control data.
Based on the available data, no carcinogenic potential of sodium hypochlorite is expected.
Reproductive toxicity
Prenatal developmental toxicity
In a prenatal developmental toxicity study (Abdel-Rahman, 1982), rats were exposed to
concentrations of 0, 1, 10 and 100 mg/L hypochlorite in drinking water for 2½ months prior to
and throughout gestation. There were no signs of maternal toxicity nor treatment-related
changes in viability, foetal weights and external appearance of all foetuses in all dose groups.
The NOAEC for prenatal developmental effects was considered to be greater than 100 mg/L.
However, the rat study provided has been performed at too low concentration levels (1/10 of
relevant NOAEC) and its statistical power is impaired by limited group size; therefore the study
cannot be used to draw any firm conclusion on prenatal developmental hazard.
Nevertheless, it has been shown that sodium hypochlorite is rapidly degraded in the body to
physiological metabolites (sodium, chloride and hydroxide ions). Therefore, it can be predicted
that the embryo/foetus will not be exposed due to the fast degradation of sodium hypochlorite
in blood and other body fluids before becoming systemically available.
Based on the available data, no prenatal developmental toxicity potential of sodium

hypochlorite is expected.
Due to the local mechanism of action of sodium hypochlorite it can be assumed that the same
results as seen in the rat prenatal developmental toxicity study would also be observed in the
second study performed with another mammalian species (rabbit). Therefore, performance of
a prenatal developmental toxicity study in rabbits is not considered justified for animal welfare
reasons.
The reproductive effects of chlorinated water have been examined in a one-generation gavage
study in rats (Carlton, 1986). No differences were observed between control rats and those
rats exposed to up to 5 mg avCl/kg bw/d of the test material when fertility, viability, litter size,
day of eye opening or day of vaginal patency were evaluated. No alterations in sperm count,
sperm direct progressive movement, percent motility or sperm morphology were observed
among adult male rats. In addition, male and female reproductive organ weights were
comparable to the control groups and no significant histopathological changes were observed
19
among treated male and female rats. No NOAEC could be determined since concentrations of
aqueous chlorine solutions were not indicated in the study report.
In a multi-generation study (Druckrey, 1968) highly chlorinated water, containing available

chlorine at a level of 100 mg/L was administered daily as drinking water to rats over seven
consecutive generations. There were no significant differences between control and treated
animals with respect to lifetime, fertility, breeding outcome, clinical signs, organ weights,
haematological parameters, histopathology, and neoplastic lesions. Based on this finding the
parental, reproductive and developmental NOAEC is considered to be ≥0.01% avCl (only dose
tested).
To examine the effects on the reproductive performance, mice were treated with chlorinated
water at 10 ppm acidified with hydrochloric acid (pH 2.5) over a period of 6 months (Les,
1968). There was no detrimental effect on the reproduction of treated mice; on the contrary,
reproductive performance in treated animals was statistically significantly increased when
compared to control. The NOAEC is considered to be ≥10 ppm avCl (only dose tested).
Based on the available data, no reproductive toxicity potential of sodium hypochlorite is

expected.
Conclusion on prenatal developmental and reproductive toxicity

Prenatal developmental toxicity and reproductive toxicity studies performed did not show any
effect on the prenatal development and reproductive cycle of both rats and mice.
However, these studies have been performed at too low concentration levels (1/10 of relevant
NOAEC); therefore the studies cannot be used to draw any firm conclusion on prenatal
developmental and reproductive toxicity hazard.
Nevertheless, in the absence of primary systemic effects and based on the available data, no
prenatal developmental and reproductive toxicity potential of sodium hypochlorite is expected.
Neurotoxicity
Special neurotoxicity studies were not performed with the active chlorine releaser sodium
hypochlorite. There is no evidence of a neurotoxic effect from other acute, subacute,
subchronic and chronic studies with sodium hypochlorite.
Studies investigating delayed neurotoxicity are not required as the structure of chlorine,
hypochlorite or hypochlorous acid is not related to known neurotoxic substances as
organophosphates.
Human data
A huge set of human data on “hypochlorite bleaches” and chlorine gas is available and is
shortly summarized in the following:
Oral exposure towards hypochlorite solutions
Accidental human data are reported for ingestion and parenteral route: it can be concluded
that the effects of accidental ingestion of domestic sodium hypochlorite bleaches are not
expected to lead to severe or permanent damage of the gastro intestinal tract as recovery is
rapid and without any permanent health consequences.
No indications of chronic toxicity in humans following exposure to sodium hypochlorite are
reported in the literature. Although some studies reported small relative risks for colon and
bladder cancer incidence for population consuming chlorinated drinking water for long periods
of time, they refer to DBPs, are equivocal or insufficient to establish a causal relationship,
considering the quality and the completeness of the studies and the interpretation of the
available data and of the confounding factors.
Dermal exposure towards hypochlorite solutions
The human skin irritation potential of hypochlorite bleaches has been investigated under
occluded patch test conditions and/ or prolonged contact times. These studies have been used
20
to derive reference values for local effects, when animal data were not sufficiently reliable.
Nixon et al. (1975) reported that a hypochlorite solution at 5-5.25% available chlorine (pH
10.7) was found to be severely irritating to intact human skin after 4 h exposure under
occluded patch conditions. In this study a clear evidence of irritating effects above 5% is
identified.
Weak to moderate irritation was observed in 15 of 69 dermatitis patients patch tested (48 h,
patch conditions not specified, reported as “covered contact”) with 2% NaOCl. No irritation was
observed in 20 persons from the same group after additional patch testing (48 h “covered
contact”) with 1% NaOCl (Habets 1986).
Accidental spillage of hypochlorite bleach into the eyes is expected to cause slight, temporary
discomfort, which subsides within a short period of time or after rinsing with water. The
available data from human exposure (Poison Control Centers) support Pashley’s observation
(1985), in which irritant effects in the human eye are less severe than in rabbits. Rinsing with
water shows a reduction in the irritant effects both in animals and humans.
Reports from dermatological case studies indicate that there have been a few isolated cases of
allergic contact sensitization. However, these isolated cases are poorly reported and not fully
conclusive. Based on the systematic animal and human study data as well as on the scarcity of
alleged sensitization cases reported from the market it is concluded that sodium hypochlorite
does not pose a skin sensitization hazard.
Inhalation of chlorine gas

Several reports on accidental exposure to chlorine are available (Shroff, 1988; Mryos, 1991;
Charan, 1985; Agabiti, 2001; Weill, 1969). Depending on chlorine concentrations, signs of
toxicity ranged from dyspnea and coughing, irritation of the throat and eyes, headache, to
temporary changes in lung function, cytopathological features and tracheobronchial
congestions.
There are two relevant studies reported in which human volunteers have been exposed to
chlorine:
A group of 8 volunteers were exposed on a single occasion to either 0.5 or 1.0 ppm (1.5 or 3.0
mg/m3) chlorine gas for either 4 or 8 hours. Sensory irritation and a transient impairment in
lung function were seen in those exposed to 1 ppm (3 mg/m3), resolving within 1 day.
Exposure to 0.5 ppm (1.5 mg/m3) chlorine gas resulted in only trivial changes of lung function
parameters, therefore the NOAEC was derived at 0.5 ppm (1.5 mg/m3) (Rotman, 1983).
A group of 8 male volunteers were exposed to 0, 0.1, 0.3 or 0.5 ppm (0, 0.3. 0.9 or 1.5
mg/m3) chlorine gas for 6 h/d on 3 consecutive days. Each individual was exposed to each of
the four exposure scenarios in a double-blind fashion. A range of respiratory function
parameters was measured and, in addition, nasal lavage fluid was analysed for a number of
indicators of inflammatory cell damage. No significant effects were seen in parameters
measured, and a NOAEC of 0.5 ppm (1.5 mg/m3) was derived in the study (Schins, 2000).
Other tests related to exposure

Tissue toxicity of sodium hypochlorite solutions was analysed in female guinea pigs (Cotter,
1985). On the shaved skin of the upper dorsum, a gauze pad was placed and soaked at 8-hour
intervals with 0.1 or 0.5 % sodium hypochlorite solution freshly prepared each day by dilution
of Clorox bleach. Animals were sacrificed on day 1, 4, 7 or 14. A 15 % decrease in basal cell
viabilities was observed after 2 weeks of treatment with the high concentration, i.e. 0.5 %
sodium hypochlorite. Morphological changes in cells were observed after 7 and 14 days of
treatment with the 0.5 % solution and 14 days with the 0.1 % solution. It was concluded that
a 0.1 % solution of sodium hypochlorite could be used for long-term maintenance of the
wound due to the relatively low toxicity.
Female SENCAR mice (Robinson, 1986) were treated with aqueous solutions of hypochlorous
acid (1, 10, 100, 300, 1000 ppm) and sodium hypochlorite (1000 ppm) by whole body
exposure (except head) for 10 minutes daily on 4 consecutive days. There was a dose-related
21
response to hypochlorous acid (pH 6.5) treatment, the minimally effective dose being 100
ppm. Skin thickness (interfollicular epidermis) and the number of cells (total and basal) were
increased. The sodium hypochlorite solution (pH 8.5) showed similar effects at 1000 ppm (the
only concentration tested). The NOAEL was derived at 10 ppm sodium hypochlorite.
In a non-standard study (Wohlrab, Wozniak 1982) for the effect of sodium hypochlorite
solutions on skin, 10 male and 10 female guinea-pigs per group were exposed to a 0.125 %
sodium hypochlorite solution on the dorsal side of their ears. This was done daily for 1, 2, 4
and 8 weeks. There were no treatment related effects on the parameters measured (e.g.
number of epidermal cells, area of epidermis, area of papillary layer).
Summary
The active substance covered by this assessment is “active chlorine released from sodium
hypochlorite”.
(ClO─), which is characterised by its well-known irritating/corrosive effects. Further,
(ClO─) and, thus, release the very same active substance (i.e. active chlorine, thought to
As outlined above, the primary effect of sodium hypochlorite is driven by the corrosive/irritant
properties caused by the local reaction of the hypochlorite ion. Studies on the acute toxicity,
irritation and sensitization potential as well as repeated dose toxicity, reproductive/prenatal
developmental toxicity, genotoxicity and carcinogenicity are available on sodium hypochlorite;
missing data for inhalation exposure in chronic studies relevant for the derivation of the
reference values can be replaced by data obtained from chlorine, by applying the read-across
principles.
On the basis of acute toxicity data, sodium hypochlorite is not toxic via the oral, dermal or
inhalation route.
Concerning the dermal route, sodium hypochlorite has to be classified as corrosive (Skin Corr.
1B, “Causes severe skin burns and eye damage”; H314) according to Annex VI, Regulation
(EC) No 1272/2008 (CLP; harmonized classification).
Sodium hypochlorite has no potential to be a skin sensitizer.
It is not genotoxic/mutagenic in vitro or clastogenic in vivo and has no carcinogenic potential.
It shows no potential for developmental or reproductive toxicity.
Deduction of reference values for NaOCl, HClO and chlorate

The mode of action of NaOCl was extensively discussed at Technical Meeting (TOX TMI-2012,
19 March 2012) and BPC Working Group level (TOX WGII-2016, 16 March 2016 and TOX
WGIII-2016, 26 May 2016).
Before WGIII-2016, the eCA presented the statement “Chlorine-related toxicity is based on
local effects (with few secondary systemic effects at high doses)” detailing that based on the
weight of evidence, sodium hypochlorite acts via a local mode of action (with secondary
systemic effects at high doses only). In particular, effects on body and liver weight observed in
the 90-day and 104-week studies were discussed in detail and considered as secondary to the
local toxicity of sodium hypochlorite.
The BPC WG members finally supported that an assessment for systemic effects should not be
performed and only a local risk assessment should be included. In addition, the WG agreed
that AEL values should not be derived.
22
In addition, before WGIII-2016, the eCA presented the statement “Deduction of reference
values for NaOCl, Ca(OCl)2, Cl2 and HOCl”, including a proposal for a set of local reference
values for chlorine species and routes of exposure relevant for performing a local exposure and
risk assessment.
It should be noted that for NaOCl or HClO, all (in-use) concentrations are expressed as
available chlorine (avCl; w/w) and not as NaOCl (w/w) or HClO (w/w). Hence, exposure
towards NaOCl or HClO should be compared with the relevant AECs for available chlorine and
not with the AECs for NaOCl of HClO itself.
NaOCl: NOAECdermal
During TMI-2012 meeting, a dermal NOAEC of 1% was discussed, however, not formally
agreed upon according to the meeting minutes. Although not explicitly stated in the meeting
minutes it is assumed that the concentration refers to aqueous solutions of NaOCl containing
1% available chlorine.
Data on human skin clearly indicate an irritating effect at 5% and above (Nixon, 1975). Lower
values (around 2%) for irritating concentration have been reported in dermatitis patients,
which represent a specific susceptible population, not suitable for setting limits for the general
population (Habets, 1986,). In the same study, no reaction was observed at concentrations of
1% and 0.5% NaOCl.
As a conservative approach, it was decided during the TMI-2012 that sodium hypochlorite (and
hence chlorine) shows irritant properties at concentration >1%, which was agreed by the
WGII-2016 meeting.
NOAECdermal to be used for risk characterization of NaOCl:
NOAECdermal = 1% avCl
NaOCl: AECinhalation
The BPC TOX WGIII-2016 finally agreed to derive the AECinhalation for NaOCl based on chlorine
data, namely the NOAEC of 0.5 ppm avCl (1.5 mg avCl/m3) as derived based on the rhesus
monkey ( 1987) and human studies (Rotman 1983; Schins 2000).
SCOEL has also based the deduction of the STEL for chlorine on these three studies and
disregarded the 6-week rat study (Barrow, 1979) and the 104-day rat and mice study (Wolf,
1995).
It is anticipated that the use of data on chlorine gas is likely to be a conservative assessment
of the potential effects of NaOCl aerosol as under real case conditions only a low proportion of
the product is in the respirable range. This is in line with the conclusions of the EU RAR on
NaOCl (2007, p. 217f).
Since the NOAEC of 0.5 ppm avCl (1.5 mg avCl/m3) has been derived based on the rhesus
monkey and human studies, there is no need to consider an inter-species toxicodynamic and -
kinetic assessment factor (AF).
An intra-species toxicokinetic assessment factor is not considered relevant based on the local
mode of action of NaOCl which is characterized by primary local effects, namely irritation,
corrosion and oxidation at the port of entry (skin, eye, upper respiratory or GI tract) without
influence of local metabolism (kinetics). However, the WGIII-2016 agreed on an intra-species
toxicodynamic AF of 3.2 for precautionary reasons.
The WG members further agreed that the lack of reproductive toxicity studies did not raise
additional concern or the need for an extra AF, as NaOCl was not considered to have systemic
effects.
Based on these considerations, the AECinhalat on for NaOCl is derived as follows (inter-species AF
(toxicodynamics x -kinetics): 1 x 1, intra-species AF (toxicodynamics x -kinetics): 3.2 x 1, AF
for duration: 1, AF for other uncertainties: 1):
23
AECinhalation to be used for risk characterization of NaOCl:

AECinhalation (NaOCl as avCl) = 1.5 mg avCl/m3 / 3.2 ≈ 0.5 mg avCl/m3
NaOCl: NOAECoral
Sodium hypochlorite is not classified as acutely toxic by the oral route. Moreover, ARfD and/or
ADI are only relevant for substances with a systemic mode of action. Since local effects are the
only relevant effects for NaOCl, deduction of an ARfD and/or ADI is considered to be not
relevant. In line with the approach for local dermal effects, an oral NOAEC should be derived
instead.
During TMI-2012, deduction of an oral NOAEC has already been discussed and the NTP study
as well as the studies of Hasegawa (rat, 1986) and Daniel (rat, 1990 and mouse, 1991) were
proposed as point of departure to derive an oral NOAEC.
Taking into account the complete data package of repeated dose toxicity and carcinogenicity
studies, an oral NOAEC of 1000 ppm (0.1%) available chlorine (avCl) can be derived based on
the Hasegawa (1986) study.
NOAECoral to be used for risk characterization of NaOCl:
NOAECoral = 0.1% avCl
HClO: AECinhalation
Hypochlorous acid (HClO) is a gas at room temperature and pressure and one of the three
chlorine species at equilibrium in water (i.e. Cl2, HClO, ClO- as a function of pH, please also
refer to chapter 2.4 “Transformation” of the EU RAR on NaOCl, 2007).
At pH values > 10, the hypochlorite anion (ClO-) is the predominant species which does not
evaporate. The minute fraction of volatile hypochlorous acid (HClO) is considered negligible.
At pH values of about 4-6, hypochlorous acid (HClO) is the predominant species and exposure
to HClO vapour is considered relevant.
In the EU RAR on NaOCl (2007), the chlorine species HClO has only been addressed in a
qualitative manner and no exposure and risk assessment has been performed for HClO.
There is no repeated dose/subchronic inhalation toxicity study on HClO available since HClO
does not exist as such but is only formed in aqueous solutions of NaOCl.
In the absence of data, the BPC TOX-WGIII-2016 agreed to derive the AECinhalation for HClO
based on chlorine data, namely the NOAEC of 0.5 ppm avCl (1.5 mg avCl/m3) as derived based
on the rhesus monkey ( 1987) and human studies (Rotman 1983, Schins 2000). It is
anticipated that the use of data on chlorine gas is likely to be a realistic assessment of the
potential effects of HClO gas under real case conditions.
It should be noted that in this CAR on NaOCl, all (in-use) concentrations are expressed as
available chlorine (avCl; w/w) and not as NaOCl (w/w) or HClO (w/w). Hence, HClO
concentrations should also be expressed as available chlorine and exposure towards HClO be
compared with the AECinhalat on for (available) chlorine (and not with an AECinhalat on for HClO).
Based on the NOAEC of 0.5 ppm avCl (1.5 mg avCl/m3) and applying the same consideration
as for deriving the AECinhalation for NaOCl, the AECinhalation for HClO is derived as follows (inter-
species AF (toxicodynamics x -kinetics): 1 x 1, intra-species AF (toxicodynamics x -kinetics):
3.2 x 1, AF for duration: 1, AF for other uncertainties: 1):
AECinhalation to be used for risk characterization of HClO:
AECinhalation (HClO as avCl) = 1.5 mg avCl/m3 / 3.2 ≈ 0.5 mg avCl/m3
24
Active chlorine re lea sed
fro m sodium hypochlorite
Chlorate
Due to the high reactivity of ch lorine species, residues on surfaces degrade very rapid ly
(decomposition to physiolog ica l sod ium and ch loride) . Hence, residue formation is assu med to
be neg ligible for aq ueous solutions of NaOCI. This conclusion is fu rther supported by the
concl usions drawn in the ENV part of t he dossier. Finally, no systemic assessment is req uired
for substances such as NaOCI which act by a loca l mode of action on ly.
The BPC APCP-WGII-20 16 concl uded that chlorate residues may still be relevant as chlorate is
considered a stable metabolite. Sod ium chlorate is a by-product of the man ufacturing process
and can be formed during storage. Th us, ch lorate may represent a worst-case for NaOCI
residues.
I n t he absence of data, the WGIII -20 16 agreed on the ADI and ARfD values proposed by the
EFSA Panel on Contaminants in the Food Chain {Scientific Opinion on risks for public hea lt h
related to the presence of chlorate in food . EFSA Journa l 2015; 13(6) :4 135, 103 pp) .
ARfD and ADI to be used for risk character ization of ch lorate :
ARfD = 36 µg chlorate/ kg bw
ADI = 3 µg chlorate/ kg bw
I n add ition to t he EFSA Opin ion, the follow ing data sou rces are ava ilable including but not
lim ited to the " Ch lorite and Chlorate in Drinking-water" background docu ment of the WHO
{ 2005) in which a TOI (equ ivalent to ADI ) of 30 µg/ kg bw and a provisiona l guideline val ue of
0 .7 mg/ lit re was derived for chlorate.
The provisional guideline va lue WHO for dr inking water of 0 .7 mg ch lorate/ L is also mentioned
in the draft Guidance on
Disinfection By-Products (vers. 1, April 2016) wh ich is cu r rent ly undergoing a PEG process .
Table 2 .2 . 1.1- 1 : Summary of reference values

Substance Exposure route Refe rence value
Oral NOAECora1 = 0 . 1% available chlorine
NaOCI Derma l NOAECdermal = 1 % available chlor ine
I nhalation AECinhal = 0 .5 ma/ m 3 ava ilable chlorine
HCIO I nhalation AECinhal = 0 .5 mg/ m 3 ava ilable chlorine
Oral ARfD = 36 ua ch lorate/ ka bw
Ch lorate
Oral ADI = 3 ua chlorate/ ka bw
To be noted that the reference values for local r isk assessment, i.e. AEC inhalation and NOAEC
derma l, have not been intended to protect hyper responsive and/ or sensitised subj ect s since
both values were derived from observations in healthy volunteers, while data in the CAR
clear ly ind icates higher sensitivity in subpopulations.
2 .2 .1. 2 . Exposure assessment and r isk character isation
Sod ium hypochlor ite is used in professional and non-prof essional settings in PTl. I ntended
uses are sum marised in t he table below.
25
Table 2.2. 1.2-1 I ntended uses of sodium hypoch lorit e in PT1
Likely concentration at
which sodium
Field of use envisaged hypochlorite (calculated
as available chlorine) will
MG1/PT1
be used
Skin disinfection in hea lthcare - professional use 1000 mg/ L
Skin disinfection - non-professional use 1000 mg/ L
General considerations on exposure and risk assessment

Pr imary exposu re
The pr imary mode of action of NaOCI is characterised by local ir r itation/corrosion and oxidation
at the site of first contact triggered by direct chemica l reactivity without prior metabolism .
NaOCI does not become system ically availa ble upon derma l contact, ingestion or inhalation .
Any system ic effects seen in animal studies (at high doses) are considered to be secondary to
local irrit at ion/corrosion . Consequently, on ly a loca l exposure and risk assessment was
performed for all relevant routes of exposure (i.e . der mal, inhalat ion) wh ich is considered to
also cover t he r isk result ing from potentia l syst em ic effect s. For all intended uses with in PT1 ,
the Gu idance on t he BPR, Volume III Human Hea lth - Part B Risk Assessment (vers. 2.0, Oct.
201S) was followed for the loca l assessment of the ready-to-use products used by
professiona ls and non -professiona ls.
Derma l exposure : For the dermal route of exposu re, a sem i-quantitative {Tier-1) assessment
was performed .
I nhalat ion exposu re: For the inha lation route of exposure, a quantitat ive assessment {Tier-1
and Tier-2) was performed. Exposure towards aerosol and va pou r is conceivable .
According to Doc. IllB, Section 83, a S.4% NaOCI (as avai lable ch lorine) product has a pH of
12 .S. The respective 1% (in-use) solution (corresponding to O.OS% avCI) has a pH of 10.3 .
Hence, the 0.1 % ready- to-use product is expect ed to have a pH > 10 . Human skin is expected
to have a pH of about S.S.
At pH values > 10, t he hypoch lorite anion {Clo-) is the predom inant species and on ly exposure
to aerosols of NaOCI (as ava ilable ch lor ine) is considered relevant. The m inute fraction of
volatile hypoch lorous acid {HCIO) is considered neg ligible.
At pH values of about 4 -6, hypoch lorous acid {HCIO) is the predominant species and exposure
to vapours of HCIO (as avai lable chlor ine) is considered relevant.
Oral. dermal and inhalation absorption : I n the absence of clear system ic effects, the BPC TOX-
WGIII-20 16 {26 May 20 16) concl uded that oral, der mal and inhalat ion absorption values are
not deemed necessary.
Secondary exposure
I ndirect exposu re includes exposure of persons (bystanders/general public) who are present
during or following the use of biocidal prod uct.
Secondary exposu re of professional or non-professional bystanders/non-users upon der ma l
cont act with treat ed hands is considered t o be non-relevant. Due to the high reactivit y of
ch lor ine species such as NaOCI, residues degrade very ra pidly . Decomposit ion to physiolog ica l
sodi um and chloride ions takes place which are not expected to arise any health risk.
Furthermore, the applied solutions are of a low concentration .
Hence, residue formation and chron ic secondary exposu re is assumed to be negligible for
aq ueous solutions of NaOCI.
26
Therefore, only inhalation exposure after application of NaOCl solutions is considered to be

relevant for the assessment of secondary exposure.
Dietary risk assessment

Due to the high reactivity of chlorine species, residues on surfaces degrade very rapidly
(decomposition to physiological sodium and chloride). Hence, residue formation is assumed to
be negligible for aqueous solutions of NaOCl. This conclusion is further supported by the
conclusions drawn in the ENV part of the dossier. Finally, no systemic assessment is required
for substances such as NaOCl which act by a local mode of action only.
The BPC APCP-WGII-2016 concluded that chlorate residues may still be relevant as chlorate is
considered a stable metabolite. Sodium chlorate is a by-product of the manufacturing process
and can be formed during storage. Thus, chlorate may represent a worst-case for NaOCl
residues.
Furthermore, the BPC TOX-WGII-2016 agreed that exposure via food should be assessed
during active substance approval so this is available at product authorisation.
In the BPC TOX-WGII-2016 it was finally discussed that only chlorate is relevant for the dietary
risk assessment.
A preliminary dietary exposure and risk assessment was performed for intended uses in PT3,
PT4 and PT5, however was not considered relevant for PT1.
The relevant reference value for chlorate as agreed during BPC WGIII-2016 is the ADI of
0.003 mg/kg bw (according to EFSA CONTAM Panel, 2015. Scientific Opinion on risks for public
health related to the presence of chlorate in food. EFSA Journal 2015; 13:4135).
Primary exposure assessment and risk characterisation – professionals

Taking into account the considerations as outlined above, exposure and risk of professionals
handling sodium hypochlorite for skin disinfection were assessed and are summarised in Table
2.2.1.2-2.
Skin disinfection in healthcare – professional use
A ready-to-use solution in a dispenser with a concentration of 0.1% available chlorine is used,
thus no mixing and loading has to be taken into account.
The product is applied directly onto hands or is poured on sterile gauze and then applied to the
skin. For the direct application, three wipes of the disinfection solution (in total about 2 mL of
the solution) are applied on the palm of the hands and are then dispersed on the front, the
back of both hands and the lower forearms. The hands are not washed after the disinfection
process, the product remains on the skin of the hands until next hand wash. Semi-quantitative
assessment for dermal exposure results in 10% of the NOAECdermal.
Inhalation exposure towards HClO vapour was assessed according to HEAdHoc
Recommendation No.9. Tier-1 assessment results in 93% AECinhal. A Tier-2 assessment was
performed as suggested in the same recommendation. However, as local effects of NaOCl (i.e.
irritation/corrosion at the site of first contact) are rather concentration than time-dependent,
the time weighted approach proposed by Recommendation No. 9 was considered to be not
reasonable. Instead, constant rate evaporation was calculated for 3 successive hand
disinfections in one room (according to the recommendation), but in contrast to guidance not
repeated in successive rooms and not averaged over an 8-hour shift. This Tier-2 assessment
results in 6.7% AECinhal.
For evaporation estimation, the vapour pressure of HClO was calculated as outlined in the list
of endpoint, chapter 3. The evaporation time was calculated as outlined in HEAdHoc
Recommendation No. 9.
After application, empty containers are handled and disposed of. As only minor amounts
remain in the containers, exposure to sodium hypochlorite from empty containers is negligible,
and thus considered not relevant.
27
Error! Reference source not found . Product-type 1 Version (2)
chlorine released January
from sodium hypoc hlorite
Table 2.2. 1.2-2: Resu lts of exposure assessment and risk characterisation for the primary exposure of professiona ls
Oral Dermal Inhalation

0/ oAEC 0/ oAEC 0/ oAEC
Exposure Exposure Exposure Acceptable
Intended u se Task NOAECoral NOAECdermal NOAECinhal
( NaOCI as (NaOCI as (total as mg yes/no
0.1°/o avCI 1010 avCI 0.5 mg/m 3 avCI
avCI ) avCI) avCl/m 3 )
Mixing &
n.r. n.r. n.r. n.r. n.r. n.r. yes
PT1: loading
0.465 (Tier-1 ) * 94% (Tier- 1)*
Application n.r. n.r. 0 . 1% 10 yes
Skin 0 .034 (Tier-2) * 6 .7% (Tier-2) *
disinfection in Post-
healthca re - Application
professional (Hand ling of n.r. n.r. neglig ible n.r. negligible n.r. yes
use empty
containers)
* Tier- 1 and Tier-2 refer to the tiered approach as detailed in HEAdHoc Recommendation No. 9
Qualitative local risk assessment for derma l route of exposu re

According to the Guidance on BPR, Vol. III B - Risk Assessment (Vers. 2, October 2015), risk characterization for local effects is not required when
the active substance and/ or co-form ulants in a product are classified for local effects but are present at concentrations that do not trigger
classification of the product according to t he CLP criter ia. The concentration of NaOCI in the RTU prod uct is below t he classification t r igger of 1% for
loca l irritant effects (skin and eyes), and moreover below the NOAECcierma1of 1% avCI.
28
Error! Reference source not found. Product-type 1 Version (2)
chlorine released January
Primary exposure assessment and risk characterisation – non-professionals

Skin disinfection – non-professional use
As non-professional users are expected to apply skin disinfection products less frequently than
professional users, the exposure of non-professionals is considered covered by the exposure
assessment for the professional user.
Indirect exposure assessment and risk characterisation

Due to the high reactivity of chlorine species such as hypochlorite, residues on hands degrade
rapidly. Moreover, in-use dilutions are of low concentration. Thus, secondary exposure via
dermal route is considered negligible, and only indirect inhalation exposure is assessed. Due to
the rapid chemical degradation and the local mode of action, only acute secondary scenarios
are considered relevant.
Indirect exposure of professionals and non-professionals

Indirect exposure of professionals and non-professionals is summarised in Table 2.2.1.2-3.
Secondary inhalation exposure of professional and non-professional bystanders during

application
Professional and non-professional bystanders may be exposed to sodium hypochlorite when
they are present during skin disinfection in healthcare or at home. Inhalation exposure is
expected to be in the same range as for the professional/non-professional directly performing
skin disinfection.
Quantitative assessment for inhalation exposure of professional and non-professional

bystanders during skin disinfection results in 93% AECinhal (Tier-1) and in 6.7% AECinhal (Tier-
2), respectively. It has to be noted that Tier-1 and Tier-2 refer to the tiered approach as
detailed in HEAdhoc Recommendation No. 9, 2016.
29
Active chlorine released Product-type 1 Version (2)
from sodium hypochlorite January
Table 2.2.1. 2-3: Results of exposu re assessment and risk characterisat ion for t he secondary exposu re of professionals and non-professiona ls
Oral Dermal Inhalation

0/oAEC
0/oAEC 0/oAEC
Intended Exposure Exposure Exposure AECinhal Acceptable
Task NOAECoral NOAECdermal
use ( NaOCI as (NaOCI as (total as mg 0.5 mg/m 3 yes/no
0.1010 avCI 1°/o avCI
avCI) avCI) avCl/m 3 ) avCI
PT1:
Secondary
inha lation
exposure of
0.465 (Tier-1)* 94 % (Tier-1)*
professional Application n.r. n.r . n .r . n.r . yes
0 .034 (Tier-2)* 6 .7% (Tier-2) *
and non-
professional
bystanders
du ring skin
disinfection
30
Combined exposure
Combined exposure is not relevant based on the absence of systemic effects after exposure
towards sodium hypochlorite. The primary mode of action of NaOCl is characterised by local
irritation/corrosion and oxidation at the site of first contact; thus effects triggered by NaOCl
are rather concentration than time-dependent.
For this reason, only the highest exposure level (concentration as % avCl or mg avCl/m3) is
relevant for risk characterisation and the addition of exposure levels and the calculation of a
combined exposure during the different tasks (e.g. M&L, application and post-application/
maintenance) is not relevant.
Conclusion
Based on the results obtained in the (semi-)quantitative and qualitative exposure and risk
assessments, exposure of professional and non-professional users in the intended uses within
PT1 results in no unacceptable risk.
The same conclusion applies to secondary exposure of professional and non-professional
bystanders/non-users.
31
Active c hlorine r e lea sed Product-type 1 V e rsion ( 2)
fro m sodium hypoc hlorite January
2.2.2. Environmental Risk Assessm ent

The active substance released from sod ium hypoch lorite in water is active ch lorine (please,
refer to the beg inn ing of para 2. 1.1). The hypoch lorite acid (HCIO) is in equi librium with
hypoch lorite anion (Clo-) and ch lorine. The equ ilibrium depends on the pH value : ch lorine is
avai lable below pH 4, in the neutra l pH range hypoch lorous acid is the predominant species,
and at pH va lues higher than 10, the on ly species present is the hypoch lorite ion, see figure
below.
100
@:
1: 80
~
a.
.!!!
l!!
.i5 60
:i.i.,
:a I
.lll
..
.!j
ti
40
\ Ct2
\
j I
.!: 20 \
\
g \
"-
0
' '- -
2 4 6 8 10
pH
The sum of these species (hypoch lorite ion + hypoch lorous acid + chlorine) is defined as active
ch lorine or available chlorine. For the chemical reactivity in aqueous solution with the same
active ch lorine concentrations and the same pH cond it ions, it is irrelevant whether active
ch lorine is generated from either ch lorine gas, ca lcium hypoch lorite or sod ium hypochlorite.
Therefore, all stud ies investigating hypochlorite aqueous solutions can be used for eva luation
and assessment of active ch lorine released from any of the three substances. The follow ing
estimated half-lives of hypoch lorite were used in the exposure assessment to consider the
degradation of hypoch lorite based on processes related to the specific uses of the active
substance and degradation in the relevant compartments . The DTso va lues were transferred to
an environmental temperature of 12°C using the Arrhen ius equation :
DTso (X° C) =DTso (t) e(o.os ( T-x))
Table 2 .2 .2 : Estimated half-lives of hypoch lorite in the environment

DTso of
hypoc hlorite
DTso of hypochlorite tra nsferred to a n
Compartment Ref e r e n ce
m easured in t est s environme ntal
tempe rature of
12° C (by Arrhenius)
Sewer system
Due to sim ilar high

Vandepitte and
content of organ ic
20 sec( * ) 56 sec Schowanek ( 1997),
substance, also
Doc. IIIA, Sec. A7 .1.2
transferable to the
aeration tank of the
STP
Worst case
Surface water/ assumption, based on
20 min( * ) 56 min the kinetic model of
Sediment
Vandepitte and
Schowanek ( 1997),
32
DTso of
hypochlorite
DTso of hypochlorite transferred to an
Compartment Reference
measured in tests environmental
temperature of
12° C (by Arrhenius)
Doc. IIIA, Sec. A7 .1. 2,
assum ing slower
degradat ion due to
lower content of Corg
in surface water and
sediment when
com pared to raw
sewer
Worst case
assum ption, based on
t he kinetic model of
Vandepitte and
Schowanek { 1997),
Soi l 20 sec( * ) 56 sec Doc. IIIA, Sec. A7 .1. 2,
assuming slower
degradation due to
lower content of Corg
in soil when compared
t o raw sewer
Garg, J, Glockner, T
Air 114.6 days --(2007), Sec. A7 .3.1
* No temperature was indicated; a temperature of 25°C was assumed as worst case
2 .2 .2 .1. Hazard ident ification and effects assessment
Short and long term toxicity dat a from literature are ava ilable for fish, invertebrates, algae and
m icro- organisms . Only flow-through tests or st at ic t est with a relia ble ana lytica l mon itoring of
the test concentration over the test duration shou ld be used for the effects assessment and as
a basis for the environmental risk assessments . Most tests with a static test design resu lt in by
a factor of 100 - 500 higher end-points {NOEC, LCso) than stud ies performed accord ing to a
flow-through design . Due to t he very fast hypoch lorit e decay, the static t est system is not
exposed during the complet e test duration to the same hypochlorite concentration . When data
from lit erature were considered not valid or incomplete for the risk assessment, new toxicity
laboratory studies were performed and included in the CAR.
The eva luation and comparison of toxicity data is complicated by the complexity of the active
ch lorine chemistry in water and by the different analytical methods used in the tests performed
for the monitoring of t he t est it em concentration in t he t est med ium. TRC (tot al residua l
ch lorine) is a measurement of bot h free and com bined ch lorine (such as ch loram ines). I t is
difficu lt to separate the contr ibution t o toxicity of the FAC (free ava ilable chlorine) such as
HCIO/CIO- from t hat of the combined ch lorine species . In addition, t he relat ive amount s of the
different chlorine species vary from test to test, depending on test duration, pH and other
medium related effects such as ammonium level and others. For those studies where the
percentage of FAC (free availa ble chlorine) from TRC (total residual ch lorine) was measured,
the t oxicit y endpoints were expressed also as FAC/L. I n t he tests with chlorinat ed seawat er,
test - item concentrations were expressed as TRO (tota l residua l oxidant ) or CPO (ch lorine
produced oxidants), wh ich include, in addition to free and combined chlorine, also other
oxidative species, such as bromine species .
33
Aquatic compartment
Acute toxicity studies were submitted for three aquatic trophic levels. Acute toxicity studies are
available in freshwater and seawater fish and invertebrates, freshwater algae, microorganisms.
In short term tests, fish, invertebrates and algae show a similar sensitivity: 48h LC50 = 32 g
TRO/L, 48h EC50 = 35 g active Cl/L and ErC50 = 36.5 µg available chlorine/L, respectively.
For molluscs and fish, long-term toxicity studies have also been performed. Molluscs (15d
NOEC = 7 g TRO/L) were shown to be more sensitive than fish fry (28d NOEC (fry survival) =
40 g CPO/L). A multispecies microcosm study performed in a periphytic community was
submitted too and the endpoint considered for the risk assessment is the 7d NOEC (toxicity to
algae) = 2.1 µg FAC/L.
NOEC values were defined for each trophic level: fish, invertebrates (molluscs) and algae.
From the available NOEC dataset, the lowest endpoint is derived from algae with a NOEC =
2.1 g FAC/L, which was selected as reference value for the risk assessment.
For the deduction of the aquatic PNEC an Assessment Factor (AF) of 50 is used. This is justified
because, according to the TGD on Risk Assessment, an AF of 50 can be used when two long-
term NOECs from fresh- or saltwater species representing two trophic levels and one long-term
NOEC from an additional marine taxonomic group (molluscs) are available.
After WGII2016 an Ad hoc follow-up was launched: comments from FR, NL and DE were
received. NL pointed out that differences in water characteristics will influence the chemical
equilibria. The presence of bromide in seawater will lead to a shift towards bromine species
instead of chlorine, and HBrO will be formed. It is noted that in the EU RAR on hypochlorite,
the datasets for freshwater and marine species have been kept separately, but in the CAR for
fish a comparison between freshwater and marine tests is not possible due to lack of reliable
data. For now, the lack of data makes a proper comparison of data impossible. Therefore it is
considered appropriate to keep the AF of 50 as proposed by the eCA. If, at product
authorisation additional information is provided it could become possible to lower the
assessment factor.
In addition comments from the applicant were received. The applicant still holds the opinion
that an AF of 10 is justified since a complete data set for acute and chronic effects covering
species from three trophic levels are available. The acute as well as the chronic data
demonstrate that there is no species sensitivity against the active substances. According to the
BPR guidance (Guidance on the BPR: Volume IV, Part B; Version 1.0 April 2015) “pooling of
available marine and freshwater ecotoxicity data for derivation of the freshwater PNEC is
possible as long as the species sensitivity between freshwater and marine organisms is within
a factor of 10”. This requirement is fulfilled and data on freshwater or marine fish, crustacea
and algae can be used interchangeably for evaluation of the risks to either compartment.
PNECaquatic = 2.1 g FAC/L : 50 = 0.042 g FAC/L
Sediment
The PNECsediment was calculated to be 0.045 µg FAC/kg ww on the basis of the PNECaquatic,
using the equilibrium partitioning method according to the TGD.
Microbial activity in STP

The lowest available EC50 and NOEC value for micro-organisms in the activated sludge is
77.1 mg available chlorine/L and 41.1 mg available chlorine/L, respectively. The WGII2016
agreed that the PNECSTP should be derived in accordance to previous agreements (TAB entry
ENV-4) and that an AF 10 to the NOEC (or EC10) should be applied. An assessment factor of 10
was applied to the NOEC value (lowest available endpoint), resulting in a PNECSTP of 4.11 mg
available chlorine/L. The fate of HClO and ClO─ in the environment, in the sewer and during
sewage treatment is modelled by Vandepitte and Schowanek and is estimated to drop down to
“zero” within a few minutes after release into the sewer.
34
Atmosphere
At environmental pH values (6.5-8.5) half of the active chlorine is in the un-dissociated form of
hypochlorous acid and half is dissociated to the hypochlorite anion. Only the hypochlorous acid
fraction is volatile. The measured Henry’s Law constant for hypochlorous acid of 0.11 Pa m³
mol-1 indicates that concentration in air is very low. Consequently, air is not an environmental
compartment of concern.
Terrestrial compartment
The risk assessment for the terrestrial compartment was performed on the basis of the
PNECaquatic using the equilibrium partitioning method. The PNECsoil was calculated to be
0.015 µg FAC/kg ww on the basis of the PNECaquatic, using the equilibrium partitioning
method according to the TGD. At the WGII2016 it was agreed that in accordance with the BPR
guidance (Guidance on the BPR: Volume IV, Part A; Version 1.1 November 2014) toxicity tests
on terrestrial organisms are not required for the uses assessed in the active substance dossier
since there is no direct exposure to soil.
Soil is only being exposed to hypochlorite via the STP pathway by the application of sewage
sludge or by the application of slurry/manure from PT3 uses. The active chlorine is highly
reactive and reacts rapidly with organic matter in the sewer systems, STP and also during
storage of slurry/manure. The fast degradation in these systems results in PECsoil values which
are very low indicating that the emission to soil can be regarded to be negligible (see Doc IIB).
However, it was decided at the WGII2016 meeting that PEC/PNEC values for the soil
compartment should be provided in the CAR and the PNECsoil value should be calculated by
using the equilibrium partitioning method (EPM) based on the PNECaquat c value according to the
Guidance on the BPR (Volume IV, Part B; Version 1.0 April 2015). The calculation is based on a
theoretical Koc value of 13.22 L/kg. The PNECsoil for the risk assessment for the terrestrial
compartment was calculated to be 0.015 µg FAC/kg ww.
The WGII2016 acknowledged that the use of a theoretical Koc value is not the most
appropriate value for inorganic substances for the equilibrium partitioning calculation since for
inorganic substances Kd values would be more appropriate.
Nevertheless, for the assessed uses it is justified to use the theoretical Koc values for the
calculation of the PNECsoil value since there is no direct release to soil and there is a high
degradation rate of the substance in the preceding compartments (e.g. sewer system, STP)
which results in a very low emission to soil. Furthermore, measured Kd values are not
available and by considering the low PECsoil values further data would not have an impact on
the general outcome of the environmental exposure and risk assessment.
2.2.2.2. Exposure assessment and risk characterisation
Emission and exposure resulting from all stages of the life-cycle of active chlorine released
from sodium hypochlorite have to be assessed in the exposure and risk assessments. The
calculated PEC values, according to the ESD PT 1, and the corresponding PEC/PNEC ratios are
reported in the tables below.
Aquatic compartment (incl. sediment)

Surface water
An overview on the results of the surface water risk assessment for active chlorine released
from sodium hypochlorite is provided in Table 2.2.2.2-01 and Table 2.2.2.2-02.
35
Table 2 .2 .2 .2-01: Overview on the ca lculat ed PEC/ PNEC for the aquat ic compartment not
taking into account degradation in sewer system
PNECsw =4.2 x 10-s ma/L
Exposure scenario PECsw PEC/PNECsw
PT1
rma/Ll I
PT1a - Skin disinfection - non-professional use in healt hcare i.01 x 10-3 I 24.0
PT1 b - Skin disinfection - professional use in healthcare 2 .08 x 10-4 I 4.9
Table 2 .2 .2 .2- 02 : Overview on the calculated PEC/ PNEC for the aquatic compartment taking
into account degradation in sewer system
PNECsw =4.2 x 10-s mg/L
Exposure scenario PECsw PEC/PNECsw
PT1
[mg/L] I
PT1a - Skin disinfection - non-professional use in healthcare 4.48 x 10-2 3 I 1.07 X 10-1 8
PT1b - Skin disinfection - professional use in healthcare 9 .25 x 10-24 I 2.20 x 10-19
The above results show that for all relevant applications of active ch lorine released from
sodi um hypoch lor ite in PT1 the requirements for acceptable r isk according t o t he TGD on Risk
Assessment are met when the degradation in sewer syst em has been considered : the
PEC/ PNEC va lues are below the tr igger va lue of 1.
Freshwater sediment
An overview on the resu lts of the freshwater sediment r isk assessment for active ch lorine
released from sodium hypochlorit e is provided in Table 2 .2 .2 .2-03 and Table 2.2.2.2-04 .
Table 2.2.2.2-03 : Overview on the calculated PEC/ PNEC for the sediment compartment not
=
PNECsed 4.5 x 10-s mg/kg
Exposure scenario PECsed PEC/PNECsed
rma/kal
PT1
PT1a - Skin disinfection - non-professional use in
1.08 x 10-0 3 24.0
healt hca re
PT1b - Skin disinfection - professional use in
2. 22 x 10-0 4 4.9
healt hca re
Table 2.2.2.2- 04 : Overview on the ca lcu lat ed PEC/ PNEC for the sed iment com partment t aking
int o account degradat ion in sewer system
=
PNECsed 4.5 x 10-s ma/ka
Exposure scenario PECsed PEC/PNECsed
rma/kal
PT1
PT1a - Skin disinfection - non-professional use in
4. 79 x 10-2 3 1.07 X 10-1 8
healthca re
PT1 b - Skin disinfection - professional use in
9 .89 x 10-24 2 .20 x 10-19
healthca re
sodi um hypoch lor ite in PT1 the requirements for acceptable r isk according to the TGD on Risk
Assessment are met when degradation in sewer syst em has been considered : t he PEC/ PNEC
values are below t he t r igger value of 1.
36
Sewage treatment plant

An overview on the results of the STP r isk assessment for active ch lorine released from sod ium
hypochlor ite is provided in Table 2 .2 .2 .2-05 and Table 2 .2 .2 .2-06.
Table 2 .2 .2.2-0 5: Overview on the calculated PEC/ PNEC for sewage treatment plant (STP) not
PNECsTP =4.11 mg/L
Exposure Scenario PECsTP PEC/PNECsTP
[mg/L]
PTl
PTla - Skin disinfection - non-professional use in
healthca re 1.0 1 x 10-02 2 .45 x 10-03
PT l b - Skin disinfection - professional use in healthcare 2.08 x 10-03 5 .06 x 10-04
Table 2 .2 .2 .2-06 : Overview on t he ca lcu lat ed PEC/ PNEC for sewage treatment plant (STP)
PNECsTP =4.11 ma/L
Exposure Scenario PECsTP PEC/PNECsTP
fma/Ll
PTl
PTla - Skin disinfection - non-professional use in
healt hca re 4.48 x 10-22 1.09 x 10-22
PTl b - Skin disinfection - professional use in healthcare 9 .25 x 10-23 2 .25 x 10-23
sodi um hypoch lorite in PTl the req uirements for acceptable r isk are met according to the TG D
on Risk Assessment when degradation in sewer syst em has been considered : t he PEC/ PNEC
Atmosphere
Hypoch lorite might enter the atmosphere due to volatilisation from the sewage treatment
plant.
The exposu re assessment showed that the emission to air v ia these pathways is neglig ible. T he
highest annual average PEC in air after use of active ch lorine released from sod ium
hypochlor ite in PTl was ca lcu lat ed to be 5 .96 x 10- 28 mg/ m 3 for PTl a - Skin disinfection -
non-professional use in healt hcare.
I n addition, in Doc. IIA, chapter 4 .1.2 it was outlined, that the adsorption of hy pochlorite to
aerosol particles, the volatilisation from water into air and the adsorpt ion of hypochlor ite onto
soil are very low . Thus, hypoch lorite will remain in the aqueous phase and degrade very
rapidly.
Terrestrial com partment

An overview on t he results of the soil r isk assessment for active ch lorine released from sod ium
hypochlor ite is provided in Table 2 .2 .2 .2-07 and Table 2 .2 .2 .2-08.
Table 2 .2 .2 .2-07: Overview on t he ca lculated PEC/ PNEC for the soil compartment not taking
into account degradation in sewer system
PNECsoil =
1.5 x 10-s mg/kg
Exposure scenario PECsoil
[mg/kal
I
PEC/PNECsoil
PTl
PT l a - Skin disinfection - non-professional use in healt hcare 1.29 X 10-os I 8 .6 1 x 10-04
PT l b - Skin disinfection - Professional use in healthcare 2 .66 x 10-09 I 1.78 x 10-04
37
Table 2.2.2.2-08 : Overview on the calcu lated PEC/PNEC for the soil compartment taking into
account degradation in sewer syst em
PNECsoil = 1.5 x 10-s mg/kg
Exposure scenario PECsoil
[mg/kal
I
PEC/PNECsoil
PT1
PT1a - Skin disinfection - non-professional use in healt hcare 5 .74 x 10-28 I 3.83 x 10-23
PT1b - Skin disinfection - professional use in healthcare 1.18 x 10-28 I 7 .90 x 10-24
The above results show that for all relevant applications of active chlor ine released from
sodi um hypoch lorit e in PT1 the requi rements for accepta ble r isk are met according t o the TGD
on Risk Assessment when degradation in sewer system has been considered the PEC/PNEC
Groundwater
The hypochlorite concentration in the pore water of agricult ural soi l (after application of
sewage sludge) is taken as an indication of potentia l groundwater levels. According to the
TGD, this is a worst-case assu m pt ion, because deg radation in soil, t ransformation and di lut ion
in deeper soil layers are not t aken int o account. Under real life cond it ions, it is very unl ikely
that any hypochlorite will reach t he groundwat er because hypochlor ite rapidly degrades in
sewage sludge and soil.
Table 2.2.2 .2- 09 : Overview on t he ca lcu lated PEC/Limit value for groundwater not taking into
account degradation in sewer system
Limit value= 0.1 µg/L
Exposure scenario PEC/Limit
PEC9 w
value
[µg/L]
PT1
PT1a - Skin disinfection - non-orofessional use in healt hcare 1.6 X 10-s << 1
PT1 b - Skin disinfection - professional use in healthcare 3.3 x 10-4 << 1
Table 2 .2 .2 .2-10 : Overview on t he calcu lated PEC/Li mit value for groundwater taking into
account degradation in sewer system
Limit value= 0.1 µg/L
Exposure scenario
PT1
PEC9 w
fua/Ll I
PEC/Limit
value
PT1a - Skin disinfection - non-professional use in healthcare 7.0 X 10-25 I << 1

PT1 b - Skin disinfection - professional use in healthcare 1.4 X 10-25 I << 1
The r isk for groundwater is acceptable for all relevant applications of act ive ch lorine released
from sodium hypoch lor ite in PT1.
Aggregate risk assessment

Biocidal active substances are used in various applications and are often contained in many
different products. The exposure assessment of sing le uses may t herefore underest imate the
act ua l concentrat ions of the active substance to be found in the environment.
Article 19(2 ) of the new Biocidal Products Regu lation ( BPR, 528/2012 EU) states t hat " t he
evaluation [ ... ] shall take into account t he following factors : [ ...] (d) cumu lative effects, (e)
synergistic effect s." This is fu rther elaborated in Annex VI (com mon pr inci ples for the
evaluation of biocidal products) wh ich states t hat the risks associated with the relevant
individual com ponents of the biocidal product shall be assessed, taking into account any
cumulative and synergistic effects.
38
This refers to the environmental risk assessment of an active substance contained in different
products of the same Product Type (PT) or of different PTs. Sodium hypochlorite, calcium
hypochlorite and chlorine were notified as active chlorine releasers in PTs 1 to 5, in PTs 2 to 5,
and in PTs 2 and 5, respectively. The main entry pathways into the environment are equal for
all applications mentioned above (via STP), thus a combination of exposures to active chlorine
released from sodium hypochlorite, active chlorine released from calcium hypochlorite and
active chlorine released from chlorine for all affected environmental compartments is both
possible and realistic.
Aggregate risk assessment for surface water considering all PTs

Σ PEC/PNEC sw [mg/L]
PT 1 1.3 x 10-18
PT 2 2.3 x 10-15
PT 3 2.3 x 10-17
PT 4 1.9 x 10-17
PT 5 2.0 x 10-17
Σ PEC/PNECsw PT 1-5 = 2.4 10-15 mg/L
Aggregate risk assessment for sediment considering all PTs

Σ PEC/PNEC sed [mg/kg]
PT 1 1.3 x 10-18
PT 2 2.3x 10-15
PT 3 2.3 x 10-17
PT 4 1.9 x 10-17
PT 5 2.0 x 10-17
Σ PEC/PNECsed PT 1-5 = 2.4 10-15 mg/kg
Aggregate risk assessment for STP considering all PTs

Σ PEC/PNEC STP [mg/L]
PT 1 1.3 x 10-22
PT 2 2.4 x 10-19
PT 3 2.3 x 10-21
PT 4 1.9 x 10-21
PT 5 2.0 x 10-21
Σ PEC/PNECSTP PT 1-5 = 2.5 10-19 mg/L
Aggregate risk assessment for soil considering all PTs

Σ PEC/PNEC soil [mg/kg]
PT 1 4.6 x 10-23
PT 2 8.4 x 10-20
PT 3 8.1 x 10-22
PT 4 6.7 x 10-22
PT 5 7.2 x 10-22
Σ PEC/PNECsoil PT 1-5 = 8.6 10-20 mg/kg
The aggregate risk assessment is acceptable for all PTs in all environmental compartments.
2.2.2.3. Fate and distribution in the environment
Active chlorine is highly reactive: it reacts rapidly with organic matter in the sewer, STP,
surface water and soil. Where organic and nitrogenous materials are present, it acts as a
highly reactive oxidizing agent. It reacts rapidly with organic matter and most (≈ 99%) of the
active chlorine is converted to inorganic chloride (Jolley and Carpenter, 1975).
The kinetic model of Vandepitte and Schowanek shows that hypochlorite is eliminated during
transport in the sewer within the first minutes. The abundance of reaction partners allows a
very quick reaction. The HClO/ClO─ (expressed as FAC) concentration estimated at the end of
39
the sewer, drops below 1 x 10-32 µg/L. The drop in FAC is parallel to a sharp increase of the
chloramine concentration, which can be explained by the high availability of ammonia in the
sewer. Chloramine further reacts like an oxidant during additional transport in the sewer, the
STP and in the river. The extensive degradation of chloramine in the activated sludge can be
explained by the presence of reduced organic material. Chloramine is estimated to fall below
5 x 10-10 µg/L in the river.
The Vandepit and Schowanek kinetic model is also applicable to the soil (TMI 12).
Contamination of soils due to direct application of chlorinated water will not be of permanent
origin. The high content of organic matter in a soil will allow a quick (order of seconds)
reduction of HClO, too. Hypochlorite reacts rapidly in soil with soil organics. The ultimate fate
of hypochlorite in soil is a reduction to chloride.
At environmental pH values (6.5-8.5) half of the active chlorine is present in the un-
dissociated form of hypochlorous acid and half is dissociated to the hypochlorite anion. Only
the hypochlorous acid fraction is volatile, but the amount of hypochlorous acid that could
volatilise from water into air is expected to be very low. The calculated half-life (Atkinson
calculation) for hypochlorous acid in the atmosphere is 114.6 days (2750 hours), but there are
indications that the half-life is shorter, i.e. only a few hours.
Active chlorine does not bioaccumulate or bioconcentrate due to its high water solubility and
high reactivity.
The concentration of hypochlorite in the environment is modelled by Vandepitte and
Schowanek and is estimated to drop down to “zero” within the first minutes after release in the
sewer.
2.2.2.4. PBT and POP assessment
PBT assessment
P criterion: Half-life > 40 d in freshwater (> 60 d in marine water) or > 120 d in freshwater
sediment (> 180 d in marine sediment) or > 120 d in soil.
Active chlorine reacts rapidly in soil and in the sewer with organic matter.
The photolysis half-life of aqueous chlorine in clear sky, summer noon sunlit (47°N) water of
pH 8 is 12 min when measured at the surface. It increases with decreasing pH due to the
decreasing ratio of ClO−/HClO to 37 min at pH 7 and to 60 min at pH 5.
Therefore, the P criterion is not fulfilled.
B criterion: measured BCF >2000. If measured BCF values are not available, a substance is
considered to potentially fulfil the B criterion if log Kow exceeds a value of 4.5.
Active chlorine is inorganic (Kow is not required) and degrades rapidly in the environment, so
no bioaccumulation is expected. Therefore, the B criterion is not fulfilled.
T criterion: Long term NOEC or EC10 < 0.01 mg/L for marine or freshwater organisms or CMR,
or other evidence of chronic toxicity
As regards the human health, active chlorine is not CMR. There is no evidence for chronic
toxicity, either.
Regarding the toxicity to aquatic organisms, algae is the most sensitive species (periphytic
community) for which a NOEC of 0.0021 mg FAC/L has been derived from a microcosm study.
Therefore, the T criterion is fulfilled.
Conclusion for the risk characterisation: active chlorine does not meet the PBT criteria.
POP assessment
Not applicable to inorganic substances, such as active chlorine released from sodium
hypochlorite.
40
2.2.3. Assessment of endocrine disruptor properties
Based on the available experimental results, there is no indication that active chlorine released
from sodium hypochlorite affects the endocrine system. Structural characteristics and SAR do
not hint to possible effects of active chlorine released from sodium hypochlorite as endocrine
disruptor.
2.3. Overall conclusions
The outcome of the assessment for active chlorine released from sodium hypochlorite in
product-type 1 is specified in the BPC opinion following discussions at the BPC-18 meeting of
the Biocidal Products Committee (BPC). The BPC opinion is available from the ECHA website.
2.4. Requirement for further information related to the reference biocidal

product3
At product authorization, physical-chemical data and technical characteristics which are

relevant for the product should be addressed. Moreover, a long-term storage stability study
needs to be provided in support of the shelf-life claim, including the determination prior to and
after storage of sodium chlorate (relevant impurity) by a validated method of analysis. Also the
effect of temperature, the effect of light, the low temperature stability and the reactivity
towards the container material need to be addressed.
2.5. List of endpoints
The most important endpoints, as identified during the evaluation process, are listed in
Appendix I.
41
Appendix I: List of endpoints
Chapter 1: Identity, Physical and Chemical Properties, Classification and

Labelling
Active substance (ISO Name) Active chlorine released from sodium

hypochlorite
When diluted in water upon use, sodium
hypochlorite releases active chlorine, which
consists of chlorine (Cl2), hypochlorous acid
(HClO) and hypochlorite anion (ClO-) in
equilibrium. The predominant species will
depend on pH value (chlorine is available
only at pH < 4, hypochlorous acid is
predominant in the range 4 to 5.5, whereas
only hypochlorite anion is present at pH >10
Product-type 1
Identity of the releaser, i.e. sodium hypochlorite

Chemical name (IUPAC) Sodium hypochlorite
Chemical name (CA) Hypochlorous acid, sodium salt
CAS No 7681-52-9
EC No 231-668-3
Other substance No. 017-011-00-1 (Index number)
Purity of the active substance as Aqueous solution with an active chlorine
manufactured (g/kg or g/l) concentration ≤180 g/kg (14), in compliance
with the EN 901:2013
Identity of relevant impurities and Sodium chlorate (relevant impurity): ≤5.4%
additives (substances of concern) in the of the active chlorine
active substance as manufactured (g/kg) Sodium hydroxide (additive)
Molecular formula ClHO.Na
Molecular mass Na+ Cl  O─
Structural formula 74.44 g/mol
(14) Due to its instability as a pure salt, sodium hypochlorite is manufactured and handled only as
aqueous solution, with a pH value greater than 11 at 20°C. Solutions are kept alkaline in order to
decrease the degradation rate of the hypochlorite to chloride and chlorate.
Sodium hypochlorite is determined by a titrimetric method. Results are tipically expressed as available
(active) chlorine using by convention the molecular weight of elemental chlorine in calculations, but they
can be converted into sodium hypochlorite by applying a conversion factor of 1.05 (MWNaOCl /MWCl2 =
74.44/70.91).
42
Physical and chemical properties of the releaser, i.e. sodium hypochlorite
Freezing point (state purity) -28.9±0.5 °C (24.3% w/w active chlorine)

Boiling point (state purity) Water evaporated when heating the sodium
hypochlorite aqueous solution (24.3% w/w
active chlorine), white crystals were
observed on the bottom of the test vessel
Thermal stability / Temperature of Not determined, since sodium hypochlorite in
decomposition its pure form is highly unstable
Appearance (state purity) Yellow limpid liquid (24.3% w/w active
chlorine), with faint chlorinous odour
(according to EN 901:2013)
Relative density (state purity) D21.24 = 1.300 ± 0.001 (24.3% w/w active
chlorine)
Surface tension (state temperature and 82.4 ± 0.8 mN/m at 20.2-20.3 °C (24.3%
concentration of the test solution) w/w active chlorine)
Vapour pressure (in Pa, state ca. 2.5 x 103 Pa at 20°C for sodium
temperature) hypochlorite aqueous solutions (according to
EN 901:2003)
At pH >11 the hypochlorite anion is the
predominant species. As an ionic species, the
hypochlorite anion has high water solubility
and is unlikely to evaporate from the
aqueous solution. Thus, it can be assumed
that the hypochlorite anion has a vapour
pressure significantly less than 10-5 Pa
Henry’s law constant (Pa m3 mol -1
) Not derived for sodium hypochlorite
(expected to be negligible, based on vapour
pressure and solubility in water)
For the purpose of risk assessment only, a
HLC of 0.11 Pa m3 mol-1 at 20 °C is
considered for hypochlorous acid, which is
the only volatile chlorine species present at
the equilibrium at in-use pH values under
PT1
Solubility in water (g/l or mg/l, state 26 g sodium hypochlorite/100 g H2O at 0°C
temperature) (CRC Handbook of Chemistry and Physics)
Solubility in organic solvents (in g/l or Not relevant. Sodium hypochlorite is not
mg/l, state temperature) used in organic solvents, due to its nature as
a strong oxidant
Stability in organic solvents used in Not relevant. Sodium hypochlorite is not
biocidal products including relevant used in organic solvents, due to its nature as
breakdown products a strong oxidant
Partition coefficient (log POW) (state Not required for inorganic substances such
temperature) as sodium hypochlorite
43
Dissociation constant In water, sodium hypochlorite hydrolyses

according to:
NaClO + H2O ↔ Na+ + HClO + OH─
Khydrolysis(ClO─) = Kw/Ka
where Ka(HClO)= 3.5 x 10-8 mol/dm3 at 20°C
Further, the hypochlorous acid (HClO)
participates in the following equilibrium:
HClO + H3O+ + Cl─ ↔ Cl2 + 2H2O
Khydrolysis(Cl2) = 3.2 x 10-4 mol/dm3 at 20°C
UV/VIS absorption (max.) (if absorption Not determined, since sodium hypochlorite in
> 290 nm state  at wavelength) its pure form is highly unstable
Flammability or flash point Flash-point > 110°C (24.3% w/w active
chlorine)
Sodium hypochlorite solutions are not known
to spontaneously ignite when exposed to air
or to emit flammable gases
Explosive properties New test for explosives according to the UN
Recommendation on the Transport of
Dangerous Goods, Manual of Tests and
Criteria needs to be provided (at the
maximum available concentration of sodium
hypochlorite in water), at the latest six
months before the date of approval
Oxidising properties New test for oxidising liquids according to the
UN Recommendation on the Transport of
Dangerous Goods, Manual of Tests and
Criteria needs to be provided (at the
maximum available concentration of sodium
hypochlorite in water), at the latest six
Auto-ignition or relative self ignition Not required for liquids non flammable in air
temperature such as sodium hypochlorite aqueous
solutions
Classification and proposed labelling of the releaser, i.e. sodium hypochlorite

In June 2016, RAC decided to change the harmonized classification (acc. to Annex VI to CLP)
with respect to the aquatic endpoints:
 for Aquatic Acute 1 (H400), an M-factor of 10 was assigned;
 classification as Aquatic Chronic 1 (H410) with M-factor of 1 was added.
with regard to physical hazards No classification

with regard to human health hazards Danger
GHS05
H314: Causes severe skin burns and eye
damage
EUH031: Contact with acids liberates toxic
gas
C≥5%
44
with regard to environmental hazards Danger

GHS09
H400: Very toxic to aquatic life
H410: Very toxic to aquatic life with long-
lasting effects
M=10 (H400)
M=1 (H410)
45
Chapter 2: Methods of Analysis
Analytical methods for the active substance and the releaser, i.e. sodium
hypochlorite
Active substance and releaser (principle Active chlorine (a.s.): Iodometric titration
of method) LOQ = 0.5% w/w as sodium hypochlorite
(corresponding to 0.48% w/w as active
chlorine).Results expressed as active chlorine
can be converted into sodium hypochlorite by
applying a conversion factor of 1.05
Impurities in the releaser (principle of Fully-validated analytical methods are to be
method) provided to the eCA-IT at the latest six
Analytical methods for residues

Soil (principle of method and LOQ) Not required. Active chlorine (HClO/ClO─)
reacts rapidly with organic matter
Air (principle of method and LOQ) Not required.
In case of accidental release of chlorine,
analytical methods for the monitoring of
chlorine in workplace air (a, b) are available:
a) OSHA Method «Chlorine in Work place Atmosphere»
05.01.83; Smith & Cochran Spectrophotometric
determination of Free Chlorine in Air using
Sulphamic acid/Tri-iodide procedure - Anal Chem
1986 Vol 58 pp 1591-1592
b) OSHA Method «Chlorine in Work place Atmosphere»
05.01.83; NIOSH free chlorine in air 01.01.75; ISO
7392/2 Water quality – Determination of free and
total chlorine Part 2 Colorimetric method using DPD
for routine control purposes 15.10.85
Water (principle of method and LOQ) Drinking water: fully-validated analytical

methods need to be provided for monitoring
purposes for both the active chlorine
(HClO/ClO─) and the relevant metabolite
chlorate (ClO3─), at the latest six months
before the date of approval
Surface water: Not required. Active chlorine
(HClO/ClO─) reacts rapidly with organic
matter
Body fluids and tissues (principle of Not required. Active chlorine (HClO/ClO─)
method and LOQ) reacts rapidly with organic matter
In case of accidental release of gaseous
chlorine, analytical methods available for the
monitoring of chlorine in workplace air are
meaningful for monitoring human exposure
(see “Air” above).
Food/feed of plant origin (principle of Not required under PT1
method and LOQ for methods for
monitoring purposes)
Food/feed of animal origin (principle of Not required under PT1
method and LOQ for methods for
monitoring purposes)
46
Chapter 3: Impact on Human Health
(ClO-), which is characterised by its well-known irritating/corrosive effects. Further,
(ClO-) and, thus, release the very same active substance (i.e. active chlorine, thought to
Absorption, distribution, metabolism and excretion in mammals

Rate and extent of oral absorption: The BPC TOX-WGIII-2016 agreed that
human health effects are primarily due to the
local mode of action of hypochlorite and
potential systemic effects are secondary to
its direct irritating reactivity
Consequently, oral absorption of sodium
hypochlorite is not relevant
Regarding oral absorption of sodium ions,
high sodium intakes are not expected to be
associated with severe health effects as
sodium ions are natural physiological
metabolites
Rate and extent of dermal absorption*: The BPC TOX-WGIII-2016 agreed that
Consequently, dermal absorption of sodium
hypochlorite is not relevant
Distribution: The BPC TOX-WGIII-2016 agreed that
In water, different chlorine species are
available. The final metabolites in
physiological systems are most likely the
sodium and chloride ion, which are
physiologically essential metabolites
Potential for accumulation: The BPC TOX-WGIII-2016 agreed that
Due to the high reactivity of chlorine species,
no potential for accumulation is expected
47
Rate and extent of excretion: After exposure towards [36Cl]-hypochlorous

acid, no radioactivity was detected in expired
air throughout the 96 h study
Excretion mainly through urine as chloride
(36.43% + 5.67 of the administered dose
after 96 h)
Excretion through faeces 96h after exposure
(14.8% + 3.7 of the administered dose after
96 h)
The total recovery was slightly higher than
50%
The final metabolites in physiological
systems are the sodium and chloride ion,
which are physiologically essential
metabolites
Toxicologically significant metabolite(s) None
*the dermal absorption value is applicable for the active substance and might not be usable in product
authorization
Acute toxicity
Rat LD50 oral LD50>2000 mg avCl/kg bw
No classification for acute toxicity (oral)
warranted
Rat LD50 dermal LD50>2000 mg avCl/kg bw
No classification for acute toxicity (dermal)
warranted
Rat LC50 inhalation LC50(1h)>10.5 mg avCl/L
Regulation (EC) 1272/2008 (CLP) requires
conversion of existing inhalation toxicity data
which have been generated using a 1-hour
testing exposure to 4-hour exposures. As
hypochlorite exerts only local effects at the
side of first contact, such conversion is not
considered necessary
No classification for acute toxicity
(inhalation) warranted
Skin corrosion/irritation With sodium hypochlorite solutions ≥5%

avCl, skin irritating properties were shown
Sodium hypochlorite is classified as Skin
Corr. 1B, H314, according to Annex VI,
Regulation (EC) 1272/2008 (harmonised
classification)
Eye irritation With sodium hypochlorite solutions ≥5%

avCl, eye irritation properties were shown
Sodium hypochlorite is classified as Skin
Corr. 1B, H314, according to Annex VI,
Regulation (EC) 1272/2008 (harmonised
48
classification), covering also eye irritation

effects
Respiratory tract irritation Sodium hypochlorite can be expected to be

irritant to the respiratory tract due to the
corrosive character of the substance.
According to the Guidance on the Application
of the CLP Criteria (Version 4.1, 2015,
Chapter 3.8.2.5), a classification for
corrosivity is considered to implicitly cover
the potential to cause RTI. Consequently, no
additional classification is required
Skin sensitisation (test method used Three skin sensitisation studies in guinea
and result) pigs (Buehler test) with sodium hypochlorite
showed no sensitising properties
No classification for skin sensitisation
warranted
Respiratory sensitisation (test As there are no indications for skin

method used and result) sensitising potential of sodium hypochlorite,
no potential for respiratory sensitisation is
expected
Repeated dose toxicity
Short term
Species / target / critical effect Rats (oral, inhalation)/local irritation at site
of first contact, no systemic effects
Relevant oral NOAEC / LOAEC LOAEC: not detected
NOAEC: >7500 ppm avCl
Relevant dermal NOAEC / LOAEC No dermal repeated dose studies are
available for sodium hypochlorite
Human data is available for sodium
hypochlorite (see below)
Relevant inhalation NOAEC / LOAEC No inhalation repeated dose study is
Read-across to chlorine: LOAEC: 3.0 ppm
equivalent to 9.0 mg/m3
NOAEC: 1.0 ppm equivalent to 3.0 mg/m3
Subchronic
Species/ target / critical effect Rats, mice and monkeys (oral, inhalation)/local
irritation at site of first contact, no systemic
effects
Relevant oral NOAEC / LOAEC LOAEC: 0.2% avCl
NOAEC: between 0.02% avCl (highest dose
tested) and 0.1 % avCl
49
Relevant dermal NOAEC / LOAEC No dermal repeated dose studies are available
for sodium hypochlorite
Relevant inhalation NOAEC / LOAEC No inhalation repeated dose studies are
Read-across to chlorine:
LOAEC: 2.3 ppm avCl (6.9 mg/m³ avCl)
NOAEC: 0.5 ppm avCl (1.5 mg/m³ avCl)
Long term
Species/ target / critical effect Rats and mice (oral, inhalation)/local
irritation at site of first contact, no systemic
effects
Relevant oral NOAEC / LOAEC LOAEC: 0.2% avCl
NOAEC: between 0.0275 % avCl (highest
dose tested) and 0.1 % avCl
Relevant dermal NOAEC / LOAEC No dermal repeated dose studies are
Relevant inhalation NOAEC / LOAEC No inhalation repeated dose studies are
Read-across to chlorine:
LOAEC: 0.4 ppm avCl (1.2 mg/m³)
NOAEC: <0.4 ppm avCl (<1.2 mg/m³)
Genotoxicity Hypochlorite solutions show sporadic

equivocal/positive results in in vitro assays
(three Ames tests, cytogenetic assay in
mammalian cells) which is due to the ability
to generate reactive oxygen species and to
induce DNA damage.
Standard in vivo studies (two micronucleus
tests, bone marrow aberration assay, DNA
damage in renal tissue) were negative. A
non-standard germ cell assay was equivocal.
The biological relevance of any result from
an in vivo study is questionable in view of
uncertainty of the availability of the test
substance at the target organ
Weight of evidence indicates no concern of
mutagenic/genotoxic potential in vivo
Carcinogenicity
Species/type of tumour Rat and mouse; there were no treatment
related increases in non-neoplastic lesions or
tumour incidence
50
Relevant NOAEC/LOAEC Studies performed with sodium hypochlorite

(oral):
LOAEC: 0.2% avCl
NOAEC: between 0.0275 % avCl (highest
dose tested) and 0.1 % avCl
Read-across to chlorine (inhalation):
LOAEC: 0.4 ppm avCl (1.2 mg/m³)
NOAEC: <0.4 ppm avCl (<1.2 mg/m³)
Developmental toxicity
Species/ Developmental target / critical No indication of prenatal developmental
effect toxicity, however test concentration too low
Relevant maternal NOAEC NOAEC: >100 mg/L avCl
Relevant developmental NOAEC NOAEC: ≥100 mg/L avCl
Fertility
Species/critical effect No indication for influence on fertility,
however test concentration too low
Relevant parental NOAEL NOAEL: ≥5 mg/kg/bw/d
Relevant offspring NOAEL NOAEL: ≥5 mg/kg/bw/d
Relevant fertility NOAEL NOAEL: ≥5 mg/kg/bw/d
Neurotoxicity
Species/ target/critical effect No neurotoxicity studies available; studies
are waived due to lack of evidence of a
neurotoxic effect from other acute, subacute,
subchronic and chronic studies
Developmental Neurotoxicity
Species/ target/critical effect No developmental neurotoxicity studies
available; studies are waived as the structure
of sodium hypochlorite is not related to
known neurotoxic substances
Immunotoxicity
Species/ target/critical effect No immunotoxicity studies available
Developmental Immunotoxicity
Species/ target/critical effect No developmental immunotoxicity studies
available
51
Other toxicological studies

Tissue toxicity of sodium hypochlorite solutions in female guinea pigs after dermal
exposure towards 0.1 or 0.5% sodium hypochlorite solution: 15% decrease in basal cell
viabilities after 2 weeks of treatment at 0.5%, morphological changes in cells after 7 and
14 days of treatment at 0.5% and 14 days at 0.1%. It was concluded that a 0.1%
solution of sodium hypochlorite could be used for long-term maintenance of the wound
due to the relatively low toxicity
Whole body exposure of mice (except head) with aqueous solutions of hypochlorous acid
(1, 10, 100, 300, 1000 ppm) and sodium hypochlorite (1000 ppm) for 10 minutes daily
on 4 consecutive days: dose-related response to hypochlorous acid (pH 6.5) treatment,
the minimally effective dose being 100 ppm, skin thickness (interfollicular epidermis)
and the number of cells (total and basal) increased, sodium hypochlorite solution (pH
8.5) showed similar effects at 1000 ppm. NOAEL at 10 ppm sodium hypochlorite
Effect of sodium hypochlorite solutions on skin of guinea-pigs) at 0.125% daily for 1, 2,
4 and 8 weeks: no treatment related effects on the parameters measured (e.g. number
of epidermal cells, area of epidermis, area of papillary layer)
Medical/human data
A huge set of human data on “hypochlorite bleaches” and chlorine gas is available
Oral exposure towards hypochlorite solutions
Accidental human data reported for ingestion and parenteral route; recovery is expected
rapid and without any permanent health consequences
No indications of chronic toxicity in humans following exposure to sodium hypochlorite
reported in the literature
Some studies reported small relative risks for colon and bladder cancer incidence for
population consuming chlorinated drinking water for long periods of time, however,
studies refer to DBPs, are equivocal or insufficient to establish a causal relationship, are
of poor quality, incomplete and prone to confounding factors
Dermal exposure towards hypochlorite solutions
Patch test on intact human skin: solutions ≥5% avCl irritant
Patch test on human skin in dermatitis patients: weak to moderate irritation with 2%
NaOCl; no irritation with 1 % NaOCl
Accidental spillage of hypochlorite bleach into the eyes expected to cause slight,
temporary discomfort, which subsides within a short period of time or after rinsing with
water
Dermatological case studies (poorly reported and not fully conclusive) indicate a few
isolated cases of allergic contact sensitization
Inhalation of chlorine gas
Human volunteer repeated dose study: Sensory irritation and a transient impairment in
lung function at 1.0 ppm corresponding to 3.0 mg/m3 chlorine (LOAEC), only trivial
changes of lung function parameters at 0.5 ppm corresponding to 1.5 mg/m3 chlorine
(NOAEC)
Human volunteer repeated dose study: No significant effects in respiratory function
nasal lavage fluid parameters at 0.5 ppm corresponding to 1.5 mg/m3 chlorine (NOAEC)
Several reports on accidental exposure to chlorine are available. Depending on chlorine
concentrations signs of toxicity: dyspnea and coughing, irritation of the throat and eyes,
headache, temporary changes in lung function, cytopathological features and
tracheobronchial congestions
52
Summary
Value Study Safety
factor
*ADI (chlorate) 3 µg chlorate/kg bw based on the TDI for -
perchlorate (derived from
human observations)
according to EFSA CONTAM
Panel (EFSA Journal
2015;13(6):4135)
*ARfD (chlorate) 36 µg chlorate/kg bw based on human 12-wks -
repeated dose oral
(drinking water) clinical
study according to EFSA
CONTAM Panel (EFSA
Journal 2015;13(6):4135
NOAECoral 1000 ppm avCl (0.1 % rat 90-d subchronic 1
avCl) repeated dose oral
(drinking water) study
rat 104-wks chronic
repeated dose oral
(drinking water) study
NOAECdermal 1% avCl human (dermatitis patients) 1
48 h-patch test study
NOAECinhalation 0.5 ppm avCl monkey 52-wks subchronic 3.2 (intra-
(chlorine) (1.5 mg avCl/m³) repeated dose inhalation species
study toxicodynamic
human volunteer single factor)
dose inhalation study
(4-8 h)
human volunteer repeated
dose inhalation study (3 d,
6 h/d)
AEC inhalat on No repeated dose inhalation toxicity study on NaOCl is available. In the
(NaOCl) absence of data, the BPC TOX-WGIII-2016 agreed to derive an
AECinhalat on based on chlorine data (please see above)
AECinhalat on (NaOCl) = 0.5 mg avCl/m³
AEC inhalat on No repeated dose inhalation toxicity study on HClO is available since
(HClO) HClO does not exist as such but is only formed in aqueous solutions of
chlorine. In the absence of data, the BPC TOX-WGIII-2016 agreed to
derive an AECinhalation based on chlorine data (please see above)
AECinhalat on (HClO) = 0.5 mg avCl/m³
*ADI and ARrD are not relevant for PT1
MRLs
Relevant commodities Not relevant for substances such as NaOCl

which act by a local mode of action only
For chlorate (stable relevant metabolite), no
MRL was set
53
Reference value for groundwater
According to BPR Annex VI, point 68 0.1 μg/L
Dermal absorption
Study (in vitro/vivo), species tested Dermal absorption is considered as not

relevant because chlorine-related toxicity is
based on local effects only (with secondary
systemic effects at high doses)
In the absence of clear systemic effects, the
BPC TOX-WGIII-2016 concluded that dermal
absorption values are not deemed necessary
Formulation (formulation type and -
including concentration(s) tested,
vehicle)
Dermal absorption values used in risk -
assessment
54
Chapter 4: Fate and Behaviour in the Environment
Route and rate of degradation in water

Hydrolysis of active substance and Very rapid degradation (~ 300 s) in the
relevant metabolites (DT50) (state pH presence of organic matter
and temperature)
pH 5
pH 9
Other pH: [indicate the value]
Photolytic / photo-oxidative degradation The photolysis half-life of aqueous chlorine in
of active substance and resulting clear sky, summer noon sunlit (47°N) water
relevant metabolites of pH 8 is 12 min (ClO─) when measured at
the surface. It increases with decreasing pH
due to the decreasing ratio of ClO─/HClO to
37 min at pH 7 and to 60 min at pH 5
Readily biodegradable (yes/no) Not applicable to inorganic substances
Inherent biodegradable (yes/no) Not applicable to inorganic substances
Biodegradation in freshwater Not applicable to inorganic substances
Biodegradation in seawater Not applicable to inorganic substances
Non-extractable residues Not relevant
Distribution in water / sediment systems No distribution in the sediment is expected
(active substance)
Distribution in water / sediment systems Not relevant
(metabolites)
Route and rate of degradation in soil

Mineralization (aerobic) Not relevant, active chlorine degrades to
chloride
Laboratory studies (range or median, Not relevant due to very rapid degradation
with number of measurements, with
regression coefficient)
DT50lab (20C, aerobic):
DT50lab (20C, anaerobic):
degradation in the saturated zone:
Field studies (state location, range or Not relevant, see above
median with number of measurements)
DT50f:
DT90f:
Anaerobic degradation Not relevant, see above
Soil photolysis Not relevant, see above
55
Non-extractable residues Not relevant, active chlorine degrades to

chloride
Relevant metabolites - name and/or Not relevant, active chlorine degrades to
code, % of applied a.i. (range and chloride
maximum)
Soil accumulation and plateau Not relevant, see above
concentration
Adsorption/desorption
Ka , Kd Not relevant, active chlorine degrades to
Kaoc , Kdoc chloride
pH dependence (yes / no) (if yes type of
dependence)
Fate and behaviour in air

Direct photolysis in air 2–4 hours (during day light)
main reaction product is atomic chlorine
which could react with saturated and
unsaturated hydrocarbons and ozone
Tropospherical DT50 for hypochlorous acid is
estimated to be 114.6 days (24-hr day),
corresponding to 2750 hours
Quantum yield of direct photolysis No data available
Photo-oxidative degradation in air Latitude: ............. Season:
................. DT50 ..............
Volatilization As the concentration of chlorine gas in water
is low at environmentally relevant pH, the
amount of chlorine that could volatilise from
water into air is expected to be very low
Reference value for groundwater
According to BPR Annex VI, point 68 0.1 μg/L
Monitoring data, if available

Soil (indicate location and type of study) No data available
Surface water (indicate location and type No data available
of study)
Ground water (indicate location and type No data available
of study)
Air (indicate location and type of study) No data available
56
Chapter 5: Effects on Non-target Species
Toxicity data for aquatic species (most sensitive species of each group)
Species Time- Endpoint Toxicity1, 2
scale
Fish
Coho salmon Not Mortality LC50(96 hours) =
(Oncorhynchus reported 0.032 mg TRO/L (mm)
kisutch)
Sea water
Tidewater Silverside 28 days Mortality LOEC (28 days) =
fry 0.210 mg CPO/L (mm)
(Menidia peninsulae) NOEC (28 days)=
Sea water 0.040 mg CPO/L (mm)
Invertebrates
Ceriodaphnia dubia 48 hours Immobilisation EC50( 48 hours) =
Fresh water 0.035 active Cl/L (nc)
Crassostrea virginica 15 -19 Mortality and NOEC (15 days) =
(Molluscs) Oysters, days growth 0.007 mg TRO/L
Sea water (shell deposition) (mm)
Algae
Periphytic community 7 days Inhibition IC80 (7 days) =
concentration 0.358 mg FAC/L (mm)
Fresh water IC50 (7 days) =
0.023 mg FAC/L (mm)
NOEC (7 days) =
0.0021 mg FAC/L (mm)
Pseudokirchneriella 72 hours Inhibition of cell ErC50 = 0.0365 mg available
subcapitata growth chlorine/L (ic)
Freshwater EbC50 = 0.0183 mg available
chlorine/L (ic)
Microorganisms
Activated sludge 3 hours Respiration EC50 = 77.1 mg available
inhibition chlorine/L (nc)
1TRC= total residual chlorine, TRO= total residual oxidant, FAC= free available chlorine, CPO= chlorine
produced oxidant
2mm= mean measured concentration, nc=nominal concentration, ic= initial measured concentrations
Effects on earthworms or other soil non-target organisms

Not necessary due to the very rapid
Acute toxicity to ………………………………….. degradation in soil
Not necessary due to the very rapid

Reproductive toxicity to ………………………… degradation in soil
57
Effects on soil micro-organisms

Nitrogen mineralization Not applicable
Carbon mineralization Not applicable
Effects on terrestrial vertebrates

Acute toxicity to mammals No data available and no data required
Acute toxicity to birds No data available and no data required
Dietary toxicity to birds No data available and no data required
Reproductive toxicity to birds No data available and no data required
Effects on honeybees
Acute oral toxicity No data available and no data required
Acute contact toxicity No data available and no data required
Effects on other beneficial arthropods

Acute oral toxicity No data available and no data required
Acute contact toxicity No data available and no data required
Acute toxicity to ………………………………….. No data available and no data required
Bioconcentration
Bioconcentration factor (BCF) Not applicable (inorganic substance, very
rapid degradation in the environment)
Depration time (DT50) Not applicable: no test performed
Depration time (DT90) Uptake into the organism of fish can be
excluded, due to the instantaneous
degradation of active chlorine in contact with
organic material
Level of metabolites (%) in organisms Not applicable
accounting for > 10 % of residues
Chapter 6: Other End Points
None.
58
Appendix II: List of Intended Uses
Object and/or Product Organisms Applied amount per

Formulation Application Remarks
situation Name controlled treatment
Type Conc. of method number interval g a.s./L water g
a.s. kind min between min L/m2 a.s./m2
max applications max min min
(min) max max
Skin disinfection Sodium Bacteria, Aqueous 0.1% Directly on -- The product 1000 -- -- approximately
in healthcare hypochlorite fungi solution w/w skin remains on skin mg/L 2 mL of
(professional 0.1% until next wash product are
use) applied
Skin disinfection Sodium Bacteria, Aqueous 0.1% Directly on -- The product 1000 -- -- approximately
(non- hypochlorite fungi solution w/w skin remains on skin mg/L 2 mL of
professional use) 0.1% until next wash product are
applied
59
Appendix III: List of studies
Data protection is claimed by the applicant in accordance with Article 60 of Regulation (EU)
No 528/2012.
Section Author(s) Year Title Data Owner

No / Source (where different Protection
Reference from company) Claimed
No Company (Yes/No)
Report No.
GLP (where relevant)
(Un)Published
III-A Tieche A 2007 Melting point and boiling Yes Euro Chlor
3.1.1/01 point of liquids (bs dsc) on (Data on
NaOCl the sodium hypochlorite existing
24% a.s.
Source: Defitraces Defitraces submitted
Report No.: 07-905015-001 for the
GLP; (unpublished) first time
Doc. No.: 112-004 for entry
into
Annex I)
III-A Tieche A 2007 Relative density of liquids on Yes Euro Chlor
3.1.3/01 the sodium hypochlorite (Data on
NaOCl 24% existing
Source: DefitracesDefitraces a.s.
Report No.: 07-905015-002 submitted
GLP; (unpublished) for the
Doc. No.: 113-003 first time
for entry
into
Annex I)
III-A Holzwarth G, 1984 The fate of chlorine and No N.R.
3.2.1/01 Balmer RG, chloramines in cooling
(ALL) Soni L towers
Source: Water Res. Vol. 18,
No. 11, (1984), pp. 1421-
1427
Report No.: Not applicable
Not GLP; (published)
Doc. No.: 792-002
III-A Anonymous 1999 Nf en 901 european No N.R.
3.2/01 standard chemicals used for
NaOCl treatment of water intended
for human consumption
sodium hypochlorite
Source: Associoation
Francaise de Normalisation
Not GLP; (unpublished)
Doc. No.: 031-004
III-A Pinto G, 2003 Use of chloroisocyanuarates No N.R.
3.6/01 Rohrig B for disinfection of water
60

No Company (Yes/No)
Report No.
(Un)Published
NaOCl + Source:
CaOCl JChemEd.chem.wisc.edu,
January 2003, 80, 1, 41-44
Doc. No.: 192-003
III-A Anonymous 2007 Log kow calculation Yes Euro Chlor
3.9/01 hypochlorus acid (Data on
(ALL) Source: Not indicated existing
Report No.: Not indicated a.s.
Not GLP; (unpublished) submitted
Doc. No.: 114-002 for the
first time
for entry
into
Annex I)
III-A White GC 1972 Handbook of chlorination No N.R.
3.10/01 Source: Handbook of
NaOCl Chlorination , pp. 627-675
Doc. No.: 031-001
III-A Ferron N 2007 Flash point on the sodium Yes Euro Chlor
3.12/01 hypochlorite 24% (Data on
NaOCl existing
Source: Defitraces a.s.
for entry
into
Annex I)
III-A Ferron N 2007 Surface tension on the Yes Euro Chlor
3.13/01 sodium hypochlorite 5% (Data on
(ALL) Source: Defitraces existing
Report No.: 07-905015-012 a.s.
GLP; (unpublished) submitted
first time
for entry
into
Annex I)
III-A Ferron N 2007 Surface tension on the Yes Euro Chlor
NaOCl Source: Defitraces existing
Report No.: 07-905015-004 a.s.
61

No Company (Yes/No)
Report No.
(Un)Published
first time
for entry
into
Annex I)
III-A Tieche A 2007 Viscosity on the sodium Yes Euro Chlor
Report No.: 07-905015-005 a.s.
first time
for entry
into
Annex I)
III-A Anonymous 1999 Nf en 901 european No N.R.
III-A for human consumption
4.1/02 sodium hypochlorite
Ca(OCl)2 Source: Associoation
Doc. No.: 031-004
III-A Anonymous N.I. Free alkali in sodium No N.R.
4.1/02 hypochlorite
NaOCl Source: Not indicated
III-A Report No.: Not indicated
4.1/07 Not GLP; (published)
Ca(OCl)2 Doc. No.: 492-007
III-A USP 24 N.I. Sodium chloride No N.R.
4.1/03 Source: Official Monographs
NaOCl+ USP 24, 1528-1529
Ca(OCl)2 Report No.: Not applicable
Doc. No.: 492-008
III-A Anonymous 2007 Chemicals used for No N.R.
4.1/05 treatment of water intended
NaOCl for human consumption -
sodium hypochlorite
Doc. No.: 031-006
III-A Anonymous 2000 German standard methods No N.R.
62

No Company (Yes/No)
Report No.
(Un)Published
4.1/06 for the examination of water,
NaOCl waste water and sludge
cations (group e) -
determination of iron by
atomic absorption
spectrometry (AAS) (E32)
Source: Deutsche Norm,
May 2000, DIN 38406-32 :
2000-05
Report No.: DIN 38406-32 :
2000-05
Doc. No.: 492-009
III-A Anonymous 1998 Standardization of methods No Euro Chlor
4.1/07 for the determination of
NaOCl traces of mercury
Source: Euro Chlor
Report No.: Analytical 3-7
Doc. No.: 412-005
III-A Anonymous 1988 Determination of chlorine in No Euro Chlor
4.2b workplace air - analytical 8
(ALL) Source: Euro Chlor
Publication, Analytical 8, 1st
Edition, 1988
Report No.: Anal 8, 1st
Edition
Doc. No.: 436-001
III-A Anonymous 2000 Water quality - No N.R.
4.2c determination of free
(ALL) chlorine and total chlorine -
part 1 - titimetric method
using N,N-diethyl-
1,4phenylenediamine
Source: Deutsche Norm,
April 2000, DIN EN ISO
7393-1
Report No.: Not indicated
Doc. No.: 435-001
III-A Gutiérrez CB 1995 Efficacy of a variety of No N.R.
5.3.1/01 et al. disinfectants against
(ALL) actinobacillus
pleuropneumoniae serotype
1
Source: Am J Vet Res, 1995,
63

No Company (Yes/No)
Report No.
(Un)Published
56 (8), 1025-1029
Doc. No.: 392-044
III-A Babb JR, 1980 Sporicidal activity of No N.R.
5.3.1/02 Bradley CR, glutaraldehydes and
(ALL) Ayliffe GA hypochlorites and other
factors influencing their
selection for the treatment
of medical equipment
Source: Journal of Hospital
Infection, 1980, 1, 63-75
Doc. No.: 392-014
III-A Bloomfield 1985 The antibacterial properties No N.R.
5.3.1/03 SF of sodium hypochlorite and
(ALL) Uso EE sodium dichloroisocyanurate
as hospital disinfectants
Source: Journal of Hospital
Infection, 1985, 6, 20-30
Doc. No.: 392-023
A Bloomfield 1992 Interaction of bacillus subtilis No N.R.
5.3.1/04 SF & spores with sodium
(ALL) Arthur M hypochlorite, sodium
dichloroisocyanuruate and
chloramine-T
Source: Journal of Applied
Bacteriology, 1992, 72, 166-
172
Doc. No.: 392-022
III-A Best M et al. 1994 Feasibility of a combined No N.R.
5.3.1/05 carrier test for desinfectants
(ALL) - studies with a mixture of
five types of microorganisms
Source: AJIC AM J Infect
Control, 1994, 22, 152-162
Doc. No.: 392-018
III-A Sagripanti J- 1996 Comparative sporicidal No N.R.
5.3.1/06 L, effects of liquid chemical
(ALL) Bonifacino A agents
64

No Company (Yes/No)
Report No.
(Un)Published
Source: Applied and
Environmental Microbiology,
1996, 62 (2), 545-551
Doc. No.: 392-059
III-A Grönholm L 1999 Screening of antimicrobial No N.R.
5.3.1/07 et al. activities of disinfectants and
(ALL) cleaning agents against
foodborne spoilage microbes
Source: Z Lebensm. Unters
Forsch A, 1999, 289-298
Doc. No.: 392-041
III-A Wirtanen G & 1982 Removal of foodborne No N.R.
5.3.1/08 Martilla- biofilms - comparison of
(ALL) Sandholm T surface ans suspension
tests. Part I
Source: Lebensm. Wiss. U.
Technol, 1992, 25, 43-49
Doc. No.: 392-066
III-A Blaser MJ 1986 Inactivation of No N.R.
5.3.1/09 etal. Campylobacter jejuni by
(ALL) chlorine and
monochloramine
Source: Applied and
1986, 51 (2), 307-311
Doc. No.: 392-019
III-A Orth R& 1989 Is the control of listeria, No N.R.
5.3.1/10 Mrozek H Campylobacter and yersinia
(ALL) a disinfection problem
Source: Fleischwirtsch.
1989, 69 (10), 1575-1578
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III-A Berman D, 1988 Inactivation of particle- No N.R.
5.3.1/11 Rice EW, associated coliforms by
(ALL) Hoff JC chlorine and
monochloramine
Source: Applied and
65

No Company (Yes/No)
Report No.
(Un)Published
1988, 54 (2), 507-512
Doc. No.: 392-016
III-A Bloomfield SF 1993 Comparative testing of No N.R.
5.3.1/12 et al. disinfectants using proposed
(ALL) european surface test
methods
Source: Letters in Applied
Microbiology, 1993, 17, 119-
125
Doc. No.: 392-021
III-A Maris P 1992 Biofilms and disinfection - No N.R.
5.3.1/13 development of a
(ALL) microorganism carrier-
surface method
Source: Science des
Alments, 1992, 12, 721-728
Doc. No.: 392-050
III-A Parnes CA 1997 Efficacy of sodium No N.R.
5.3.1/14 hypochlorite bleach and
(ALL) "alternative" products
Source: Environmental
Health 1997, 14-19
Doc. No.: 392-053
A5.3.1/15 Jones MV, 1992 Comparative sensitivity of No N.R.
(ALL) Wood MA, Vibrio cholerae 01 el tor and
Herd TM Escherichia coli to
disinfectants
Source: Letters in Applied
53
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III-A Kempter J 1986 Clorox vol II, epa No Euro Chlor
5.3.1/16 registration no. 5813-1, your
(ALL) amendment application
dated february 1, 1985
Source: Not applicable
66

No Company (Yes/No)
Report No.
(Un)Published
Doc. No.: 962-003
III-A Kuchta JM 1985 Enhanced chlorine resistance No N.R.
5.3.1/17 et al. of tap water-adapted
(ALL) Legionella pneumophila as
compared with agar
medium-passaged strains
Source: Applied and
1985, 50 (1), 21-26
Doc. No.: 392-047
III-A Muraca P, 1987 Comparative assessment of No N.R.
5.3.1/18 Stout JE, chlorine, heat, ozone, and
(ALL) Yu VL UV light for killing legionella
pneumophila within a model
plumbing system
Source: Applied and
1987, 52 (2), 447-453
Doc. No.: 392-051
III-A Lopes JA 1986 Evaluation of dairy and food No N.R.
5.3.1/19 plant sanitizers against -
(ALL) salmonella typhimurium and
listeria monocytogenes
Source: Not indicated
Doc. No.: 392-049
III-A El-Kest SE 1988 Inactivation of listeria No N.R.
5.3.1/20 Marth EH monocytogenes by chlorine
(ALL) Source: Journal of Food
Protection, 1988, 51, 520-
524
Doc. No.: 392-038
III-A EPA- List- 2006 List b - epa registered No Euro Chlor
5.3.1/21 December tuberculocide products
(ALL) effective against
mycobactererium
tuberculosis
67

No Company (Yes/No)
Report No.
(Un)Published
Protection Acency, USA
Report No.: Not indicated
Doc. No.: 962-002
III-A Rutala WA 1991 Inactivation of No N.R.
5.3.1/22 et al. Mycobacterium tuberculosis
(ALL) and mycobacterium bovis by
14 hospital disinfectants
Source: The American
Journal of Medicine, 1991,
91, (38),
267-271
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III-A Best M et al. 1990 Efficacies of selected No N.R.
5.3.1/23 disinfectants against
(ALL) mycobacterium tuberculosis
Source: Journal of Clinical
Microbiology, 1990, 28 (10),
2234-2239
Doc. No.: 392-017
III-A Anderson RL 1990 Effect of disinfectants on No N.R.
5.3.1/24 et al. pseudomonads colonized on
(ALL) the interior surface of PVC
pipes
Source: AJPH, 1990, 80 (1),
17-21
Doc. No.: 392-013
III-A Tanner RS 1989 Comparative testing and No N.R.
5.3.1/25 evaluation of hard-surface
(ALL) disinfectants
Source: Journal of Industrial
154
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III-A Peter J & 1998 Model tests for the efficacy No N.R.
5.3.1/26 Spicher G of disinfectants on surfaces
(ALL) IV. Communication -
dependence of test results
on the amount of
68

No Company (Yes/No)
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(Un)Published
contamination and the kind
of active substance
Source: Zent. Bl. Hyg.
Umweltmed. 1998, 201,
311-323
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III-A Bungaard- 1995 Fungicidal effect of 15 No N.R.
5.3.1/27 Nielsen K, disinfectants against 25
(ALL) Nielsen V fungal contaminants
commonly found in bread
and cheese manufacturing
Source: Journal of Food
Protection, 1995, 59 (3),
268-275
Doc. No.: 392-029
III-A Shaheen EA, 1996 Public health benefits of No N.R.
5.3.1/28 Ikawa JY bleach - a critical review
(ALL) Source: The Clorox
Company, 1996, 23-71
Doc. No.: 392-063
III-A Sattar SA 1989 Chemical disinfection of non- No N.R.
5.3.1/29 et al. porous inanimate surfaces
(ALL) experimentally contaminated
with four human pathogenic
viruses
Source: Epidem. Inf., 1989,
102, 492-505
Doc. No.: 392-060
III-A Brown P 1982 Chemical disinfection of No N.R.
5.3.1/30 et al. Creutzfeldt-Jakob disease
(ALL) virus
Source: The new England
Journal of Medicine, 1982,
306 (21), 1297-1282
Doc. No.: 392-027
III-A Centers for 2006 Interim guidance about No N.R.
5.3.1/31 Disease ebola virus infection for
69

No Company (Yes/No)
Report No.
(Un)Published
(ALL) Control airline flight crews, cargo
and cleaning personnel, and
personnel interacting with
arriving passengers
Source: CDS, 2006, 1-4
Doc. No.: 992-002
III-A Grabow WOK 1983 Inactivation of hepatitis a No N.R.
5.3.1/32 et al. virus and indicator
(ALL) organisms in water by free
chlorine residuals
Source: Applied and
1993, 46 (3), 619-624
Doc. No.: 392-040
III-A Bond WW 1983 Inactivation of hepatitis b No N.R.
5.3.1/33 et al. virus by intermediate-to-
(ALL) high-level disinfectant
chemicals
Source: Journal of Clinical
Microbiology, 1983, 18 (3),
535-538
Doc. No.: 392-024
III-A Prince HN, 1991 Principles of viral control and No N.R.
5.3.1/34 Prince DL, transmission
(ALL) Prince RN Source: Disinfactants and
Antiseptics. B. by Type of
Microorganisms, Chapter 25,
1991, 25, 411-444
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III-A Prince DL, 1990 Inactivation of human No N.R.
5.3.1/35 Prince RN, immunodeficiency virus type
(ALL) Prince HN 1 and herpes simplex virus
type 2 by commercial
hospital disinfectants
Source: Chemical Times &
Trends, 1990, 14-16, 54,
Doc. No.: 392-055
70

No Company (Yes/No)
Report No.
(Un)Published
III-A Grouse L 1985 HTLV-III transmission No N.R.
5.3.1/36 Source: JAMA, 1985, 254
(ALL) (15), 2130-2131
Doc. No.: 392-042
III-A Gustafson 1986 Precautions for health care No N.R.
5.3.1/37 PR, workers of aids patients
(ALL) Andres N Source: Supplied by the
British Library-The world´s
knowledge, 1986, 82, 28-31
Doc. No.: 392-043
III-A Centers for 1987 Recommendations for No N.R.
5.3.1/38 Disease prevention of HIV
(ALL) Control transmission in health-care
settings
Source: MMWR,
Supplements, 1987, 36, 1-
11
Doc. No.: 391-001
III-A Sattar SA 1991 Survival and disinfectant No N.R.
5.3.1/39 Springthorpe inactivation of the Human
(ALL) VS Immonudeficiency Virus - a
critical review
Source: Reviews of
Infectious Diseases, 1991
(May-June), 13, 430-447
Doc. No.: 392-061
III-A Brown TT 1981 Laboratory evaluation of No N.R.
5.3.1/40 selected disinfectants as
(ALL) virucidal agents against
porcine parvovirus,
pseudorabies virus, and
transmissible gastroenteritis
virus
Source: Am J Vet Res, 1981,
42 (6), 1033-1036
Doc. No.: 392-028
III-A Lloyd-Evans 1986 Chemical disinfection of No N.R.
71

No Company (Yes/No)
Report No.
(Un)Published
5.3.1/41 N, human rotavirus-
(ALL) Springthorpe contaminated inanimate
S, surfaces
Sattar SA Source: J. Hyg. Camb, 1986,
91, 163-173
Doc. No.: 392-048
III-A Saby S, 1999 Escherichia coli resistance to No N.R.
5.7.1/01 Leroy P, chlorine and glutathione
Block J-C synthesis in response to
oxygenation and starvation
Source: Applied and
Dec. 1999, 65, 12, 5600-
5603
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III-A Bloomfield S 2008 Submission to scenihr - No N.R.
5.7.1/02 February 2008 - assessment
of the antibiotic resistance
effects of biocides
Source: www.ifh-
homehygiene.org
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III-A Beumer R 2003 Biocide usage and No N.R.
5.7.2/01 et al. antimicrobial resistance in
home settings: an update - a
review by the international
scientific forum on home
hygiene (IFH)
Source: International
Scientific Forum on Home
Hygiene (IFH), October 2003
Doc. No.: 392-070
III-A 1975 Acute oral LD 50 in rats Yes Euro Chlor
6.1.1/01 using calcium hypochlorite (Data on
III-A existing
6.1.2/01 a.s.
III-A submitted
6.1.3/02 Not GLP; (unpublished) for the
III-A Doc. No.: 521-004 first time
72

No Company (Yes/No)
Report No.
(Un)Published
6.1.4/01 for entry
III-A into
6.1.4/02 Annex I)
Ca(OCl)2
III-A BioFax 1970 Bio - fax - sodium Yes Euro Chlor
6.1.1/01 hypochlorite (Data on
NaOCl Source: Industrial Bio-Test existing
Laboratories Inc. a.s.
Report No.: Not applicable submitted
Not GLP; (unpublished) for the
for entry
into
Annex I)
for entry
into
Annex I)
III-A BioFax 1970 Bio - fax -sodium Yes Euro Chlor
for entry
into
Annex I)
III-A Pashley EL 1985 Cytotoxic effects of naoci on No N.R.
6.1.4/01 et al. vital tissue efecto citotoxico
(ALL) del naoci en el tejido vital
Source: Journal of
Endodontists Vol. 11, No.
12, December 1985, pp.
525-528
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III-A Carter RO 1965 Experimental bases for the No N.R.
6.1.4/02 Griffin JF realistic assessment of
(ALL) safety of tropical agents
73

No Company (Yes/No)
Report No.
(Un)Published
Source: Toxicology and
Applied Pharmacology, 7,
(1965), pp. 60-73
Doc. No.: 592-013
III-A Nixon GA 1975 Interspecies comparisons of No N.R.
6.1.4/03 Tyson CA skin irritancy
(ALL) Wertz WC Source: Toxicology and
Applied Pharmacology 31,
(1975) pp. 481-490
Doc. No.: 592-035
III-A 1982 ECM BTS 730 e2050.01 Yes Euro Chlor
6.1.5/01 delayed contact (Data on
NaOCl hypersensivity in guinea pigs existing
a.s.
submitted
for the
Not GLP; (unpublished) first time
into Annex
I)
III-A 2000 Delayed contact dermal Yes Euro Chlor
6.1.5/01 sensitization test - buehler (Data on
Ca(OCl)2 method existing
a.s.
submitted
for the
first time
GLP; (unpublished) for entry
Doc. No.: 567-004 into Annex
I)
III-A 1985 Guinea pig sensitiation Yes Euro Chlor
6.1.5/02 testing by ritz, h.l. and (Data on
NaOCl buchler, E.V. on existing
E-2707.01 a.s.
submitted
for the
first time
Not GLP; (unpublished) for entry
Doc. No.: 567-003 into
Annex I)
III-A 1985 Guinea pig sensitiation Yes Euro Chlor
6.1.5/03 testing by ritz, h.l. and (Data on
NaOCl buchler, E.V. on E-2707.01 existing
74

No Company (Yes/No)
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a.s.
submitted
for the
Not GLP; (unpublished) first time
into
Annex I)
III-A Abdel - 1982 Metabolism and No N.R.
6.2/01 Rahman MS, pharmacokinetics of
NaOCl Couri D, alternate drinking water
Bull RJ disinfectants
Health Perspectives o. 46,
(1982), pp. 19-23
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III-A Abdel - 1983 A comparative kinetics study No N.R.
6.2/02 Rahman MS, of monochloramine and
NaOCl Waldron DM, hypochchlorous acid in rat
Bull RJ Source: Journal of Applied
Toxicology, Vol. 3, No. 4,
(1983), pp. 175-179
Doc. No.: 592-071
(ALL) Source: Industrial Bio-Test existing
for entry
into
Annex I)
III-A Barrows CS 1979 An inhalation toxicity study No N.R.
6.3.3/01 et al. of chlorine in fischer 344 rats
Cl2 following 30 days of
exposure
Source: Toxicology and
(1979), pp. 77-88
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III-A Hasegawa R 1986 Carcinogenicity study of No N.R.
75

No Company (Yes/No)
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6.4.1/01 et al. sodium hypochlorite in F344
(ALL) rats
Source: Fd. Chem. Toxic.
Vol. 24, No. 12 (1986), pp.
1295-1302
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III-A Daniel FB 1990 Comparative subchronic No N.R.
6.4.1/02 et al. toxicity studies of three
(ALL) disinfectants
Source: Resarch und
Technology, Journal AWWA,
October 1990,pp. 61-69
Doc. No.: 592-139
III-A Daniel FB 1991 Comparative subchronic No N.R.
6.4.1/03 et al. toxicity of chlorine and
(ALL) monochloramine in the
b6c3f1 mouse
Source: Research and
Technology Journal AWWA,
November 1991, pp. 68-75
Doc. No.: 592-144
III-A 1987 One-year inhalation toxicity Yes Euro Chlor
6.4.3/01 et al. study of chlorine in rhesus (Data on
Cl2 monkeys (macaca mulatta) existing
a.s.
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Annex I)
III-A Wolf DC et al. 1995 Chlorine gas induces nasal No N.R.
6.5/01 lesions but does not cause
Cl2 cancer in mice or rats
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Institute of Toxicology (CIT),
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Doc. No.: 592-159
III-A Hasegawa R 1986 Carcinogenicity study of No N.R.
76

No Company (Yes/No)
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6.5/01 et al. sodium hypochlorite in F344
NaOCl rats
Source: Fd. Chem. Toxic.
Vol. 24, No. 12 (1986), pp.
1295-1302
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A6.5/02 NTP-TR 1992 Toxicology and No N.R.
(ALL) carcinogenesis studies of
chlorinated water (CAS NOS.
7782-50-5 and 7681-52-9)
and chloraminated water
(CAS NO. 10599-90-3)
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Program, Technical report
Series, No. 392, March 1992
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III-A Wolf DC et al. 1995 Two-year inhalation No N.R.
6.5/03 exposure of female and male
(ALL) B6C3F1 mice and F344 rats
to chlorine gas induces
lesions confined to the nose
Source: Fundamental and
Applied Toxicology 24,
(1995), pp. 111-131
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III-A Ishidate M 1994 Primary mutagenicity No N.R.
6.6.1/01 et al. screening of food additives
(ALL) currently used in japan
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Vol. 22, No. 8 (1984), pp.
623-636
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III-A Kawachi T 1980 Results of recent studies on No N.R.
6.6.1/02 et al. the relevance of various
(ALL) short-term screening tests in
Japan
Source: Applied Methods in
Oncology, Bd. 3, 1980, pp.
253-267
77

No Company (Yes/No)
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Doc. No.: 592-054
III-A Le Curieux F, 1993 Comparison of three short- No N.R.
6.6.1/03 Marzin D, term assays - results on
(ALL) Erb F seven chemicals - potential
contribution to the control of
water genotoxicity
Source: Mutation Research,
Vol. 319, 1993, pp. 223-236
Doc. No.: 592-153
III-A Ishidate M 1994 Primary mutagenicity No N.R.
6.6.2/01 et al. screening of food additives
(ALL) currently used in Japan
Vol. 22, No. 8 (1984), pp.
623-636
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III-A Matsuoka A, 1979 Chromosomal aberration No N.R.
6.6.2/02 Hayashi M, tests on 29 chemicals
(ALL) Ishidate M combined with s9 mix in
vitro
Source: Mutation Resarch,
66 (1979), pp. 277-290
Doc. No.: 592-051
III-A Sasaki M 1980 Cytogenetic effects of 60 No N.R.
6.6.2/03 et al. chemicals on cultured
(ALL) human and chinese hamster
cells
Source: La Kromosomo II-
20, 31.12.1980, pp. 574-584
Doc. No.: 592-057
III-A Hayashi M 1988 Micronucleus tests in mice No N.R.
6.6.4/01 et al. on 39 food additives and
(ALL) eight miscellaneous
chemicals
Vol. 26, No. 6, (1988), pp.
487-500
78

No Company (Yes/No)
Report No.
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Doc. No.: 592-114
III-A Meier JR 1985 Evaluation of chemicals used No N.R.
6.6.4/02 et al. for drinking water
(ALL) disinfection for production of
chromosomal damage and
sperm-head abnormalities in
mice
Mutagenesis 7, (1985), pp.
201-211
Doc. No.: 592-091
III-A Kasai Y et al. 1987 Oral administration of the No N.R.
6.6.5/01 renal carcinogen, potassium
(ALL) bromate, specifically
produces 8-
hydroxydeoxyguanosine in
rat target organ dann
Source: Carcinogenesis Vol.
8, No. 12, (1987), pp. 1959-
1961
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III-A Meier JR 1985 Evaluation of chemicals used No N.R.
6.6.6/01 et al. for drinking water
(ALL) disinfection for production of
chromosomal damage and
sperm-head abnormalities in
mice
Mutagenesis 7, (1985), pp.
201-211
Doc. No.: 592-091
III-A Soffritti M 1997 Results of long-term No N.R.
6.7/01 et al. carcinogenicity studies of
(ALL) chlorine in rats
Source: Annals New York
Academy of Sciences, pp.
189-208
79

No Company (Yes/No)
Report No.
(Un)Published
Doc. No.: 592-003
III-A Kurokawa Y 1986 Long-term in vivo No N.R.
6.7/02 et al. carcinogenicity tests of
(ALL) potassium bromate, sodium
hypochloite and sodium
chlorite conducted in Japan
Health Perspectives Vol. 69,
(1986), pp. 221-235
Doc. No.: 592-099
III-A Abdel - 1982 Effect of chlorine and No N.R.
6.8.1/01 Rahman MS, monochloramine in drinking
(ALL) Berardi MR, water on the developing rat
Bull RJ fetus
Source: Journal of Applied
Toxicology, Vol. 2, No. 3,
(1982), pp. 156-159
Doc. No.: 592-064
III-A Carlton BD 1986 Reproductive effects of No N.R.
6.8.2/01 et al. alternative disinfectants
(ALL) Source: Environmental
Health, Vol. 69, (1986), pp.
237-241
Doc. No.: 592-097
III-A Druckrey H 1968 Chloriertes trinkwasser, No N.R.
6.8.2/02 toxizitäts-prüfungen an
(ALL) ratten über sieben
generationen
Source: Fd. Cosmet. Toxicol.
Vol. 6, pp. 147-154 (1968),
pp. 147-154
Doc. No.: 592-016
III-A Les EP 1968 Effects of acidified No N.R.
6.8.2/03 chlorinated water on
(ALL) reproduction in C3H/HEJ and
C57BL/6J mice
Source: Laboratory Animal
Care, Vol. 18, No. 2, pp.
210-213
80

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Doc. No.: 592-017
III-A Mrvos R et al. 1991 Home exposures to No N.R.
6.12.2/01 chlorine/chloramine gas - a
CI2 review of 216 cases
Source: Vet. Hum Toxicol 33
(4), August 1991, page 1
Doc. No.: 592-146
III-A Becker GL 1974 The sequelae of accidentally No N.R.
6.12.2/01 injecting sodium
NaOCl hypochlorite beyond the root
apex
Source: Oral Surg, Oral Med,
Oral Pathol. 38, (1974), pp.
633-638
Doc. No.: 592-030
III-A Charan NB 1985 Effects of accidental chlorine No N.R.
6.12.2/02 etal. inhalation on pulmonary
Cl2 function
Source: The Western Journal
of Medicine Clinical
Investigation, September
1985, 143, 3, 333-336
Doc. No.: 592-207
III-A Dedhia NM 1989 Long-term increase in No N.R.
6.12.2/02 et al. peritoneal membrane
NaOCl transport rates following
incidental intraperitoneal
sodium hypochlorite infusion
Source: The Journal of
Artificial Organs, Vol. 12, No.
11, (1989), pp. 711-714
Doc. No.: 592-134
III-A Agabiti N 2001 Short term respiratory No N.R.
612.2/03 et al. effects of acute exposure to
Cl2 chlorine due to a swimming
pool accident
Source: Occup Environ Med
81

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58, (2001), pp. 399-404
Doc. No.: 592-178
III-A Grant WM 1974 Toxicology of the eye No N.R.
6.12.2/03 Source: Charles C Thomas
NaOCl Publishers, (1974), pp. 222-
259, 571-573, 852 and 932-
934
Doc. No.: 592-031
III-A Shroff CP 1988 Respiratory cytopathology in No N.R.
6.12.2/04 chlorine gas toxicity - a
Cl2 study in 28 subjects
Source: Diagnostic
Cytopathology, March 1988,
4, 1, 28-32
Doc. No.: 592-208
III-A Bibra 1990 Toxicity profile - sodium No N.R.
6.12.2/04 hypochlorite
NaOCl Source: Bibra Toxicology
International, 1990, pp. 1-
11
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III-A Weill H et al. 1969 Late evaluation of pulmonary No N.R.
6.12.2/05 function after acute
Cl2 exposure to chlorine gas
Source: American Review of
Respiratory Disease, 1969,
99, 374-379
Doc. No.: 592-209
III-A Habets JMW 1986 Sensitization to sodium No N.R.
6.12.2/05 et al. hypochlorite causing hand
NaOCl dermatitis
Contact Dermatitis 15, Vol.
1986, pp. 140-142
Report No.: na
Not GLP, published
Doc. No.: 592-101
III-A Rotman HH 1983 Effects of low concentrations No N.R.
82

No Company (Yes/No)
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(Un)Published
6.12.2/06 et al. of chlorine on pulmonary
NaOCl function in humans
American Physiological
Society, (1983), pp. 1120-
1124
Report No.: na
Not GLP, published
Doc. No.: 592-077
III-A Schins RPF 2000 Nasal inflammatory and No N.R.
6.12.2/07 et al. respiratory parameters in
NaOCl human volunteers during
and after repeated exposure
to chlorine
ERS Journal 16, (2000), pp.
626-632
Report No.: na
Not GLP, published
Doc. No.: 592-174
III-A Coskey RJ 1974 Onycholysis from sodium No N.R.
NaOCl Source: Arch Dermatol, Vol.
109, Januar 1974, page 96
Doc. No.: 592-033
III-A Maddy KT 1990 Illnes injuries and death No N.R.
6.12.3/02 from pesticide exposure in
NaOCl California 1949-1988
Source: Reviews of
Environmental
Contamination and
Toxicology, Vol. 114, (1990),
pp. 57-124
Doc. No.: 592-141
III-A Pike DG et al. 1963 A re-evaluation of the No N.R.
6.12.5/01 dangers of clorox ingestion
NaOCl Source: The Joournal of
Pediatrics Volume 63,
Number 2, (1963), pp. 303-
305
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III-A Tanyel FC, 1988 Chlorine bleach ingestion in No N.R.
6.12.5/02 Büyükpamuk children - a review of 80
83

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Report No.
(Un)Published
NaOCl cu N, cases
Hicsönmez A Source: Inc. Türkish Journal
of Pediatrics 30, (1988), pp.
105-106
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III-A Strange DC 1951 Corrosive injury of the No N.R.
6.12.5/03 et al. stomach
NaOCl Source: A.M.A. Archives of
Surgery 62, (1951) pp. 350-
357
Doc. No.: 592-009
III-A Mühlendahl 1978 Local injuries by accidental No N.R.
6.12.5/04 KE, ingestion of corrosive
NaOCl Oberdisse U, substances by children
Krienke EG Source: Arch. Toxicol. 39,
(1978), pp. 299-314
Doc. No.: 592-050
III-A Grant WM 1974 Toxicology of the eye No N.R.
6.12.2/03 Source: Charles C Thomas
NaOCl Publishers, (1974), pp. 222-
259, 571-573, 852 and 932-
934
Doc. No.: 592-031
III-A Shroff CP 1988 Respiratory cytopathology in No N.R.
6.12.2/04 chlorine gas toxicity - a
Cl2 study in 28 subjects
Source: Diagnostic
Cytopathology, March 1988,
4, 1, 28-32
Doc. No.: 592-208
III-A Bibra 1990 Toxicity profile - sodium No N.R.
NaOCl Source: Bibra Toxicology
International, 1990, pp. 1-
11
84

No Company (Yes/No)
Report No.
(Un)Published
Doc. No.: 592-135
III-A Weill H et al. 1969 Late evaluation of pulmonary No N.R.
6.12.2/05 function after acute
Cl2 exposure to chlorine gas
Source: American Review of
Respiratory Disease, 1969,
99, 374-379
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III-A Maddy KT 1990 Illnes injuries and death No N.R.
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III-A Pike DG et al. 1963 A re-evaluation of the No N.R.
6.12.5/01 dangers of clorox ingestion
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III-A Tanyel FC, 1988 Chlorine bleach ingestion in No N.R.
6.12.5/02 Büyükpamuk children - a review of 80
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III-A Strange DC 1951 Corrosive injury of the No N.R.
85

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III-A Mühlendahl 1978 Local injuries by accidental No N.R.
6.12.5/04 KE, ingestion of corrosive
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Krienke EG Source: Arch. Toxicol. 39,
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III-A Ward MJ & 1988 Hypernatraemia No N.R.
6.12.5/05 Routledge PA hypechloraemic acidosis
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III-A Eun HC, 1984 Sodium hypochlorite No N.R.
6.12.6/01 Lee AY, dermatitis
NaOCl Lee YS Source: Cont. Derm. 11,
(1984), page 45
Doc. No.: 592-081
III-A Nixon GA 1975 Interspecies comparisons of No N.R.
6.12.6/02 Tyson CA & skin irritancy
NaOCl Wertz WC Source: Toxicology and
(1975) pp. 481-490
Doc. No.: 592-035
III-A Hostynek JJ 1990 Irritation factors of sodium No N.R.
6.12.6/03 et al. hypochlorite solutions in
NaOCl human skin
Source: Contact Dermatitis
1990, pp. 316-324
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III-A Cotter JL 1985 Chemical parameters, No N.R.
86

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6.16/01 et al. antimicrobial activities, and
NaOCl tissue toxicity of 0.1 and
0.5% sodium hypochchlorite
solutions
Source: Antimicrobial Agents
and Chemotherapy,Vol. 28,
No.1, Juily 1985, pp. 118-
122
Doc. No.: 592-095
III-A Robinson M 1986 Epidermal hyperplasia in No N.R.
6.16/02 et al. mouse skin following
NaOCl treatment with alternative
drinking water disinfectants
Health Perspectives Vol. 69,
(1986), pp. 293-300
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III-A Wohlrab W, 1982 Untersuchungen zu wirkung No N.R.
6.16/03 Wozniak KD von natriumhypochlorit als
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und verschiedene
zellsysteme
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III-A Vandepitte V, 1997 Sodiumhypochlorite - kinetic Yes Euro Chlor
7.1.2/01 Schowanek D model on the long term (Data on
(ALL) hypochlorite decay in the existing
environment - a specific a.s.
model for use in the hoci risk submitted
assessment for the
Source: Not indicated first time
Report No.: Not indicated for entry
Not GLP; (unpublished) into Annex
Doc. No.: 989-003 I)
III-A Görg J & 2007 Estimation of the Yes Euro Chlor
7.3.1/01 Glöckner T atmospheric residence time (Data on
NaOCl + of sodium hypochlorite using existing
Ca(OCl)2 the atkinson method a.s.
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III-A Heath J 1977 Toxicity of intermittent No N.R.
7.4.1.1/0 chlorination to freshwater
1 (ALL) fish - influence of
temperature and chlorine for
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56, 1, (1977), pp. 39-47
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III-A Bellanca MA, 1977 Effects of chlorinated No N.R.
7.4.1.1/0 Bailey DS effluents on aquatic
2 (ALL) ecosystem in the lower
James river
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1977, pp. 639-645
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III-A 1978 The relative sensitivity of No N.R.
7.4.1.1/0 pacific northwest fishes and
3 (ALL) invertebrates to chlorination
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III-A Heath AG 1978 Influence of chlorine from No N.R.
7.4.1.1/1 and ambient temperature on
b (ALL) the toxicity of intermittent
chlorination to freshwater
fish
Effects in Freshwater
Systems, (1978), pp. 123-
133
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III-A Roberts jr. 1978 Acute toxicity of No N.R.
7.4.1.2/0 MH, bromochlorinated seawater
2 (ALL) Gleeson RA to selected estuarine species
with a comparison to
chlorinated seawater toxicity
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Source: Marine Environ.
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III-A Gallagher, 2009 Sodium hypochloride: a 48- Yes Euro Chlor
7.4.1.2/0 S.P. et al. hour flow-through acute (Data on
3 (ALL) toxicity test with the existing
cladoceran (Daphnia magna) a.s.
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Report N.: 676A-101; 2009- first time
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III-A Gallagher, 2011 Sodium hypochloride: Yes Euro Chlor
7.4.1.2/0 S.P. et al. a 48-hour flow-through (Data on
4 (ALL) acute toxicity test with the existing
cladoceran (Ceriodaphnia a.s.
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III-A Cairns J, 1990 Evaluation of joint toxicity of No N.R.
7.4.1.3/0 Niederlehner chlorine and ammonia to
1 (ALL) BR, aquatic communities
Pratt JR Source: Aquatic Toxicology,
16, (1990), pp. 87-100
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III-A Liedtke, A 2013 Toxicity to Yes Euro Chlor
7.4.1.3/0 Pseudokirchneriella (Data on
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Algal Growth Inhibition Test a.s.
Source: Harlan Laboratories submitted
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III-A Eisner, G 2013 Toxicity to Activated Sludge Yes Euro Chlor
7.4.1.4/0 in a Respiration Inhibition (Data on
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III-A Goodman LR 1983 Early life-stage toxicity test No N.R.
7.4.3.2/0 et al. with tidewater silversides
1 (ALL) (menidia peninsulae) and
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7.4.3.4/0 Burton DT and chlorinated cooling
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III-B Ferron N 2007 Determination of ph values Yes Euro Chlor
3.5/01 on the sodium hypochlorite (Data on
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III-B White GC 1972 HANDBOOK OF chlorination No Euro Chlor
3.7/01 Source: Handbook of
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III-B Anonymous 1999 Nf en 901 european No Euro Chlor
for human consumption
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Active Chlorine Released - Assessment - Report

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Regulation (EU) No 528/2012 concerning

the making available on the market and

Evaluation of active substances

1. STATEMENT OF SUBJECT MATTER AND PURPOSE ............................................... 3

1.1. Procedure followed .............................................................................................................................. 3

1.2. Purpose of the assessment report ................................................................................................ 3

2. OVERALL SUMMARY AND CONCLUSIONS ................................................................... 3

2.1. Presentation of the Active Substance ......................................................................................... 3

2.2. Summary of the Risk Assessment ............................................................................................... 12

2.3. Overall conclusions ............................................................................................................................ 41

2.5. List of endpoints.................................................................................................................................. 41

APPENDIX I: LIST OF ENDPOINTS ..................................................................................... 42

Chapter 2: Methods of Analysis .............................................................................................................. 46

Chapter 3: Impact on Human Health ................................................................................................... 46

Chapter 4: Fate and Behaviour in the Environment..................................................................... 55

Chapter 5: Effects on Non-target Species ......................................................................................... 56

Chapter 6: Other End Points ................................................................................................................... 57

APPENDIX II: LIST OF INTENDED USES ........................................................................ 58

APPENDIX III: LIST OF STUDIES ........................................................................................ 59

1.1. Procedure followed

1.2. Purpose of the assessment report

2. OVERALL SUMMARY AND CONCLUSIONS

2.1. Presentation of the Active Substance

2.1.1. Identity, Physico-Chemical Properties & Methods of Analysis

(3) As in CA-March15-Doc.5.1-Final, Revised on 23 June 2015, Annex II – Releasers

Identification of the active substance releaser

Active substance releaser

Other No. 0 17-011-00-1 (Index number)

IUPAC Name Sodi um hypoch lorite

CAS name Hypochlorous acid, sod ium sa lt

Common name, synonyma Sodium hypoch lorit e

Molecular formula CIHO.Na

Structural formula Na+ Cl - O-

Molecular weight 74.44 g/ mol

Purity Aqueous solut ion with an available (active) chlor ine

Additives Sodium hydroxide

Impurities One relevant im purity is present : sodium ch lorat e ( ::;5.4% of

Identification of the biocidal product

Physical-chemical properties of the active substance releaser (sodium hypochlorite)

Ana lytical methods for detection a nd identification

anion is present at pH >10).

Analytical method for residues in air

Analytical method for residues in soil

Analytical method for residues in drinking water

Analytical method for residues in surface water

Analytical method for residues in body fluids and tissues

2.1.2. Intended Uses and Efficacy

Field of use envisaged

 Skin disinfection of the hands and lower forearms

Professional and non-professional use is envisaged.

In addition, in order to facilitate the work of Member States in granting or reviewing

2.1.3. Classification and Labelling

Current cla ssification

Suppl. Hazard EUH031: Contact with acids liberates toxic gas.

 for Aquatic Acute 1 (H400), an M-factor of 10 was assigned;

2.2.1. Human Health Risk Assessment

2.2.1.1. Hazard identification and effects assessment

Absorption, distribution, metabolism and excretion