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Measures as amended, taking into account amendments up to National Environment Protection (Assessment of Site Contamination) Amendment Measure 2013 (No. 1)
Administered by: Agriculture, Water and the Environment
Registered 03 Jun 2013
Start Date 16 May 2013

Commonwealth Coat of Arms

National Environment Protection (Assessment of Site Contamination) Measure 1999

as amended

made under section 14(1) of the

National Environment Protection Council Act 1994 (Cwlth), the National Environment Protection Council (New South Wales) Act 1995 (NSW), the National Environment Protection Council (Victoria) Act 1995 (Vic), the National Environment Protection Council (Queensland) Act 1994 (Qld), the National Environment Protection Council (Western Australia) Act 1996 (WA), the National Environment Protection Council (South Australia) Act 1995 (SA), the National Environment Protection Council (Tasmania) Act 1995 (Tas), the National Environment Protection Council Act 1994 (ACT) and the National Environment Protection Council (Northern Territory) Act 1994 (NT)

Compilation start date:                     16 May 2013

Includes amendments up to:            National Environment Protection (Assessment of Site Contamination) Amendment Measure 2013 (No. 1)

This compilation has been split into 22 volumes

Volume 1:       sections 1–6, Schedules A and B

Volume 2:       Schedule B1

Volume 3:       Schedule B2

Volume 4:       Schedule B3

Volume 5:       Schedule B4

Volume 6:       Schedule B5a

Volume 7:       Schedule B5b

Volume 8:       Schedule B5c

Volume 9:       Schedule B6

Volume 10:     Schedule B7 - Appendix 1

Volume 11:     Schedule B7 - Appendix 2

Volume 12:     Schedule B7 - Appendix 3

Volume 13:     Schedule B7 - Appendix 4

Volume 14:     Schedule B7 - Appendix 5

Volume 15:     Schedule B7 - Appendix 6

Volume 16:     Schedule B7 - Appendix B

Volume 17:     Schedule B7 - Appendix C

Volume 18:     Schedule B7 - Appendix D

Volume 19:     Schedule B7

Volume 20:     Schedule B8

Volume 21:     Schedule B9

Volume 22:     Endnotes

 

Each volume has its own contents

 

 

 

About this compilation

The compiled instrument

This is a compilation of the National Environment Protection (Assessment of Site Contamination) Measure 1999 as amended and in force on 16 May 2013. It includes any amendment affecting the compiled instrument to that date.

This compilation was prepared on 22 May 2013.

The notes at the end of this compilation (the endnotes) include information about amending Acts and instruments and the amendment history of each amended provision.

Uncommenced provisions and amendments

If a provision of the compiled instrument is affected by an uncommenced amendment, the text of the uncommenced amendment is set out in the endnotes.

Application, saving and transitional provisions for amendments

If the operation of an amendment is affected by an application, saving or transitional provision, the provision is identified in the endnotes.

Modifications

If a provision of the compiled instrument is affected by a textual modification that is in force, the text of the modifying provision is set out in the endnotes.

Provisions ceasing to have effect

If a provision of the compiled instrument has expired or otherwise ceased to have effect in accordance with a provision of the instrument, details of the provision are set out in the endnotes.

 

 

  

  

  


 

National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of Site Contamination) Measure 1999 National Environment Protection (Assessment of

Schedule B7

APPENDIX A3

Derivation of HILs for Organochlorine Pesticides

 


Contents
The Derivation of HILs for organochlorine pesticides
                                                                                       Page

1                             DDT+DDE+DDD Review                               1

1.1             General                                                                                        1

1.2             Previous HIL                                                                               1

1.3             Significance of Exposure Pathways                                          2

1.3.1                Oral Bioavailability                                                         2

1.3.2                Dermal absorption                                                           2

1.3.3                Inhalation of Dust                                                            2

1.3.4                Plant Uptake                                                                    2

1.3.5                Intakes from Other Sources – Background                    3

1.4             Identification of Toxicity Reference Values                             3

1.4.1                Classification                                                                    3

1.4.2                Review of Available Values/Information                        3

1.4.3                Recommendation                                                             4

1.5             Calculated HILs                                                                          4

1.6             References                                                                                   5

2                             Aldrin + Dieldrin                                             7

2.1             General                                                                                        7

2.2             Previous HIL                                                                               7

2.3             Significance of Exposure Pathways                                          8

2.3.1                Oral Bioavailability                                                         8

2.3.2                Dermal absorption                                                           8

2.3.3                Inhalation of Dust                                                            8

2.3.4                Plant Uptake                                                                    8

2.3.5                Intakes from Other Sources – Background                    8

2.4             Identification of Toxicity Reference Values                             9

2.4.1                Classification                                                                    9

2.4.2                Review of Available Values/Information                        9

2.4.3                Recommendation                                                           10

2.5             Calculated HILs                                                                        11

2.6             References                                                                                 11

3                             Chlordane (total)                                           13

3.1             General                                                                                      13

3.2             Previous HIL                                                                             13

3.3             Significance of Exposure Pathways                                        13

3.3.1                Oral Bioavailability                                                       13

3.3.2                Dermal absorption                                                         13

3.3.3                Inhalation of Dust                                                          13

3.3.4                Plant Uptake                                                                  14

3.3.5                Intakes from Other Sources – Background                  14

3.4             Identification of Toxicity Reference Values                           14

3.4.1                Classification                                                                  14

3.4.2                Review of Available Values/Information                      14

3.4.3                Recommendation                                                           15

3.5             Calculated HILs                                                                        16

3.6             References                                                                                 16

4                             Endosulfan (total)                                         18

4.1             General                                                                                      18

4.2             Previous HIL                                                                             18

4.3             Significance of Exposure Pathways                                        18

4.3.1                Oral Bioavailability                                                       18

4.3.2                Dermal absorption                                                         18

4.3.3                Inhalation of Dust                                                          19

4.3.4                Plant Uptake                                                                  19

4.3.5                Intakes from Other Sources – Background                  19

4.4             Identification of Toxicity Reference Values                           19

4.4.1                Classification                                                                  19

4.4.2                Review of Available Values/Information                      19

4.4.3                Recommendation                                                           21

4.5             Calculated HILs                                                                        21

4.6             References                                                                                 21

5                             Endrin (total)                                                23

5.1             General                                                                                      23

5.2             Previous HIL                                                                             23

5.3             Significance of Exposure Pathways                                        23

5.3.1                Oral Bioavailability                                                       23

5.3.2                Dermal absorption                                                         23

5.3.3                Inhalation of Dust                                                          23

5.3.4                Plant Uptake                                                                  23

5.3.5                Intakes from Other Sources – Background                  23

5.4             Identification of Toxicity Reference Values                           24

5.4.1                Classification                                                                  24

5.4.2                Review of Available Values/Information                      24

5.4.3                Recommendation                                                           25

5.5             Calculated HILs                                                                        25

5.6             References                                                                                 25

6                             Heptachlor                                                     27

6.1             General                                                                                      27

6.2             Previous HIL                                                                             27

6.3             Significance of Exposure Pathways                                        27

6.3.1                Oral Bioavailability                                                       27

6.3.2                Dermal absorption                                                         27

6.3.3                Inhalation of Dust                                                          27

6.3.4                Plant Uptake                                                                  28

6.3.5                Intakes from Other Sources – Background                  28

6.4             Identification of Toxicity Reference Values                           28

6.4.1                Classification                                                                  28

6.4.2                Review of Available Values/Information                      28

6.4.3                Recommendation                                                           29

6.5             Calculated HILs                                                                        30

6.6             References                                                                                 31

7                             Hexachlorobenzene (HCB)                           32

7.1             General                                                                                      32

7.2             Previous HIL                                                                             32

7.3             Significance of Exposure Pathways                                        32

7.3.1                Oral Bioavailability                                                       32

7.3.2                Dermal absorption                                                         32

7.3.3                Inhalation of Dust                                                          32

7.3.4                Plant Uptake                                                                  32

7.3.5                Intakes from Other Sources – Background                  33

7.4             Identification of Toxicity Reference Values                           33

7.4.1                Classification                                                                  33

7.4.2                Review of Available Values/Information                      33

7.4.3                Recommendation                                                           34

7.5             Calculated HILs                                                                        35

7.6             References                                                                                 35

8                             Methoxychlor                                                37

8.1             General                                                                                      37

8.2             Previous HIL                                                                             37

8.3             Significance of Exposure Pathways                                        37

8.3.1                Oral Bioavailability                                                       37

8.3.2                Dermal absorption                                                         37

8.3.3                Inhalation of Dust                                                          37

8.3.4                Plant Uptake                                                                  37

8.3.5                Intakes from Other Sources – Background                  37

8.4             Identification of Toxicity Reference Values                           38

8.4.1                Classification                                                                  38

8.4.2                Review of Available Values/Information                      38

8.4.3                Recommendation                                                           39

8.5             Calculated HILs                                                                        39

8.6             References                                                                                 39

9                             Mirex                                                             41

9.1             General                                                                                      41

9.2             Previous HIL                                                                             41

9.3             Significance of Exposure Pathways                                        41

9.3.1                Oral Bioavailability                                                       41

9.3.2                Dermal absorption                                                         41

9.3.3                Inhalation of Dust                                                          41

9.3.4                Plant Uptake                                                                  41

9.3.5                Intakes from Other Sources – Background                  42

9.4             Identification of Toxicity Reference Values                           42

9.4.1                Classification                                                                  42

9.4.2                Review of Available Values/Information                      42

9.4.3                Recommendation                                                           43

9.5             Calculated HILs                                                                        43

9.6             References                                                                                 43

10                          Toxaphene                                                     45

10.1          General                                                                                      45

10.2          Previous HIL                                                                             45

10.3          Significance of Exposure Pathways                                        45

10.3.1             Oral Bioavailability                                                       45

10.3.2             Dermal absorption                                                         45

10.3.3             Inhalation of Dust                                                          45

10.3.4             Plant Uptake                                                                  45

10.3.5             Intakes from Other Sources – Background                  46

10.4          Identification of Toxicity Reference Values                           46

10.4.1             Classification                                                                  46

10.4.2             Review of Available Values/Information                      46

10.4.3             Recommendation                                                           47

10.5          Calculated HILs                                                                        47

10.6          References                                                                                 48

11                          Shortened forms                                            49

 


1                  DDT+DDE+DDD Review

1.1              General

Several comprehensive reviews of DDT, DDE and DDD in the environment and their toxicity to humans are available and should be consulted for more detailed information (ATSDR 2002, 2008; WHO 1979;1989). The following provides a summary of the key aspects of these compounds that are relevant to the derivation of a soil HIL.

 

Dichlorodiphenyltrichloroethane (DDT), dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane (DDD) are structurally similar aromatic compounds containing chlorine. Technical DDT was manufactured for broad-spectrum insecticidal usage under a number of trade names including Genitox, Anofex, Detoxan, Neocid, Gesarol, Pentachlorin, Dicophane and Chlorophenothane. Limited manufacture of DDD also occurred under the trade names Rothane, Dilene and TDE (ATSDR 2002).

 

These compounds are all white crystalline solids with relatively no odour or taste. They are relatively insoluble in water but highly soluble in animal fats and organic solvents (WHO 1979). All three compounds (DDT, DDE, DDD) can exist in different forms (congeners) based on the relative position of chlorines on the two phenyl rings, but the p,p’- congener is the most common in the environment (ATSDR 2002).

 

DDT was primarily manufactured as an insecticide for the agricultural industry. It was also used to control vector-borne diseases such as malaria and typhus and was used in a domestic setting to protect items from moth damage and to control lice (ATSDR 2002). The widespread usage of DDT reportedly began in 1939. However, it has been progressively banned in many countries since the early 1970s due to its effects on human health and the environment (ATSDR 2002). DDT is still used in some developing regions for the control of disease-bearing insects and it may also be illegally used in the agriculture industry in some countries (WHO 1979). DDT has not been registered for any use in Australia since the 1980s (NHMRC & NRMMC 2011). DDD was manufactured and used to a lesser extent to control insects and the o,p’-isomer was used to medically treat adrenal gland cancer. DDE has no commercial use (ATSDR 2002).

DDT and its metabolites are essentially immobile in soil, becoming strongly absorbed onto the surface layer of soils. Likewise, as a consequence of their extremely low water solubilities, DDT and its metabolites become absorbed onto particulates in water and settle into sediments. Because of its chemical characteristics, DDT can undergo long-range transport through the atmosphere in a process known as ‘global distillation’ where DDT migrates from warmer regions to colder regions through repeated cycles of volatilisation from soil and water surfaces followed by deposition of DDT onto surfaces through dry and wet deposition processes. Due to the persistence of DDT and its metabolites in the environment, potential for bioaccumulation and potential for long-range transport, DDT is listed under the Stockholm Convention on Persistent Organic Pollutants.

 

The following information primarily relates to DDT which has been adopted as the most appropriate indicator for the assessment of all three compounds due to the similarity of toxic effects and toxicokinetics. A larger database of data is also available for DDT.

1.2              Previous HIL

The derivation of the previous HIL (HIL A = 200 mg/kg) for DDT+DDE+DDD is presented by Beard (1993) and NEPC (1999). In summary, the HIL was derived on the basis of the following:

·         Background intakes were considered in the derivation of the current HIL (Beard 1993) with the intake from food estimated to range from 0.001 mg/kg/day for adults to 0.546 mg/kg/day for infants. Intakes from water and air were essentially negligible compared with that derived from food.

·         An ADI of 0.002 mg/kg/day was adopted as the toxicity reference value (based on the ADI from WHO and an additional uncertainty factor of 10).

·         Based on intakes derived from soil (ingestion), an HIL of 200 mg/kg was calculated.

·         It is noted that the review undertaken also considered an oral RfD of 0.0005 mg/kg/day reference from the US EPA and a LOAEL and NOAEL.

1.3              Significance of Exposure Pathways

1.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of DDT in the range of contaminated sites that may need to be considered in Australia. On this basis, a default approach of assuming 100% oral bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

1.3.2        Dermal absorption

Dermal absorption of DDT is considered to be very low and has been considered to be negligible in the derivation of the previous HIL. Review of dermal absorption of DDT by MfE (2011) indicated the following: ‘US EPA (2004) recommends a dermal absorption factor of 0.03 (3%), which is based on data from Wester et al. (1990). These authors indicate that only 1.0% of DDT from soil penetrated into human skin over a 24-hour period, and none (<0.1%) of this partitioned into human plasma. Additionally, 3.3% of DDT from soil was absorbed percutaneously following in vivo exposure of rhesus monkeys. Taking the geometric mean of these values yields an average dermal absorption factor of 0.018 (1.8%).’

 

As few other reviews are available in relation to dermal absorption of DDT, the average value estimated by Wester et al. (1990) as referenced by MfE (2011), has been adopted in the derivation of HILs.

1.3.3        Inhalation of Dust

DDT, DDE and DDD are not considered sufficiently volatile to be of significance and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the HIL derived.

1.3.4        Plant Uptake

As DDT has the potential to bioaccumulate, uptake into fruit and vegetable crops (as well as eggs and poultry where relevant) are likely to be of significance (Beard, 1993). Review by MfE (2011) noted that there are limited studies available for the assessment of plant uptake of DDT, however plant uptake has been considered. It is noted that the few studies available relate to the uptake of DDT in plants when applied in solution (as would be the case as an applied pesticide). DDT, DDE and DDD have a high Koc values (log Koc = 5.19-5.35, ATSDR 2002) suggesting that these compounds are strongly bound to the soil particulates and immobile in soil (with low solubility in water). For plant uptake to be significant, the chemicals must be able to partition to soil water. In addition there is evidence that DDT, as well as other chemicals, undergoes an ageing process in soil whereby the DDT is sequestered in the soil so decreasing its bioavailability to microorganisms, extractability with solvents, and toxicity to some organisms (ATSDR 2002).

 

ATSDR (2002) reviewed available studies associated with potential uptake of DDT that is sorbed to soil. The studies show that the potential for uptake was low and there was little or no evidence of translocation. Some uptake was noted where the DDT source was fresh and some volatilisation had occurred resulting in uptake, though this process is not consider relevant for most DDT-contaminated sites as these compounds are no longer used in Australia.

 

On the basis of the above, the potential for plant uptake of DDT, DDE and/or DDD bound to the soil is considered to be negligible.

 

It is noted, however, that should these compounds be present in other media such as groundwater (used for irrigation) or in solution then the potential for uptake into fruit and vegetable crops is likely to be of significance. These issues should be assessed on a site-specific basis

1.3.5        Intakes from Other Sources – Background

For the general population, background intakes would be expected to be primarily associated with residues in food, which appear to be slowly disappearing from the food chain (Beard 1993). Background intakes considered in the previous HIL were estimated to be 0.546 mg/kg/day for infants, predominantly derived from dietary sources.

 

More recent information from Food Standards Australia New Zealand in the 20th Australian Total Diet Survey (FSANZ 2003) indicates that dietary exposures for all age groups was less than 0.2% of the adopted ADI (0.002 mg/kg/day). DDT was not detected in the 23rd Australian Total Diet Survey (FSANZ 2011). On this basis, background intakes can be considered negligible (0%). This evaluation is consistent with that presented by RIVM (2001).

1.4              Identification of Toxicity Reference Values

1.4.1        Classification

The International Agency for Research on Cancer (IARC 1991) has classified DDT and associated compounds as 2Bpossible human carcinogens.

 

The US EPA has classified DDT as B2probable human carcinogen.

1.4.2        Review of Available Values/Information

While DDT has some carcinogenic potential, the mode of action is important in determining the most appropriate approach to the identification of quantitative toxicity values. No discussion is presented in the profile regarding mode of action and potential for genotoxicity. Review of available information (ATSDR 2002; WHO (2011); RIVM 2001; IARC 1991) suggests that while some conflicting data is available with regard to some genetic end points, DDT and derivatives are not genotoxic (or it is equivocal) and therefore it is not appropriate to consider a non-threshold (linear) dose-response approach. Hence, it is not appropriate to consider the use of the slope factor and unit risk values available from US EPA.

 

On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for DDT. The following are available from Level 1 Australian and International sources:

 

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.0025 mg/kg/day

The NHMRC derived a guideline of 0.009 mg/L based on a TDI of 0.0025 mg/kg/day. The TDI is derived on the basis of a NOEL of 0.25 mg/kg/day from a 25-year study in humans, and an uncertainty factor of 100 (includes 10 for intraspecies variation and 10 for the uncertainty arising from the lack of detail in the epidemiological study used).

OCS (2012)

TDI = 0.002 mg/kg/day

TDI was set in 2003 (same as previous ADI), based on a NOEL of 0.25 mg/kg/day from studies in humans and experimental animals, and an uncertainty factor of 100.

International

WHO (2011)

PTDI = 0.01 mg/kg/day

Provisional TDI referenced inWHO(2011) was established by JMPR in 2000 (as published by JMPR 2001) based on a NOAEL of 1 mg/kg/day for developmental toxicity in rats, and a safety factor of 100.

RIVM (2001)

TDI = 0.0005 mg/kg/day

 

TDI based on a NOAEL of 0.05 mg/kg/day associated with hepatotoxic effects in a 15 to 27-week study in female rats, and a 100-fold uncertainty factor.

ATSDR (2002)

No chronic value derived

Not derived as most sensitive non-cancer effects were observed at doses higher than doses for most sensitive acute and intermediate duration effects. The acute and intermediate MRL derived for DDT was 0.0005 mg/kg/day.

US EPA (IRIS 2012)

RfD = 0.0005 mg/kg/day

 

The US EPA review (last updated in 1987) derived an oral RfD on the basis of a NOEL of 0.05 mg/kg/day associated with liver effects in a rat study (1950 study), and uncertainty factor of 100. The US EPA has also derived an oral slope factor and inhalation unit risk, however these are not considered appropriate for the assessment of a non-genotoxic carcinogen.

 

There is a wide range of threshold values available for oral intakes of DDT. It is recommended that the oral value available from OCS (2012) ,which is consistent with the value in the ADWG (NHMRC 2011), be adopted for the derivation of an Australian HIL. The US EPA evaluation, while providing a more conservative TRV, has not been considered as it is significantly dated, using a key study from 1950. Reviews conducted by WHO and NHMRC are more current and have considered more recent studies.

 

No dermal or inhalation-specific studies or data are available. For the presence of DDT (DDE and DDD) in soil, it is considered appropriate to consider use of the available ADI for all pathways of exposures.

1.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for DDT, DDE and DDD (in total) in the derivation of HILs:

Recommendation for DDT 
Oral TRV (TRVO) = 0.002 mg/kg/day (OCS 2012) for all routes of exposure
Dermal absorption factor (DAF) = 0.018 (or 1.8%) (Wester et al. 1990)
Background intakes from other sources (as % of TRV):
BIO = 0% for oral and dermal intakes
BIi = 0% for inhalation

1.5              Calculated HILs

On the basis of the above, the following HILs have been derived for DDT+DDE+DDD (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)

Residential A

240

80

--

20

<1

Residential B

600

51

--

49

<1

Recreational C

400

67

--

33

<1

Commercial D

3600

42

--

58

<1

-- Pathway not included in derivation of HIL

 

1.6              References

ATSDR 2002, Toxicological Profile for DDT, DDE and DDD, US Department of Health and Human Services, ATSDR, available from: http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=81&tid=20.

ATSDR 2008, Addendum to the DDT/DDD/DDE Toxicological Profile. US Department of Health and Human Services, ATSDR,  available from http://www.atsdr.cdc.gov/toxprofiles/ddt_addendum.pdf.

Beard 1993, ‘The Evaluation of DDT Contaminated Soil Associated with Cattle Tick Dip Sites’, presented in the proceedings of the Second National Workshop on the Health Risk Assessment and Management of Contaminated Sites, Contaminated Sites Monograph Series, No. 2.

FSANZ 2003, The 20th Australian Total Diet Survey, A total diet survey of pesticide residues and contaminants, Food Standards Australia and New Zealand.

FSANZ 2011, The 23rd Australian Total Diet Study, Food Standards Australia and New Zealand.

IARC 1991, Summaries & Evaluations. DDT and Associated Compounds, vol. 53, (1991), p.179, International Agency for Research on Cancer.

JMPR1985, Pesticide residues in food — 1984 evaluations, Food and Agriculture Organization of the United Nations, Rome, Joint FAO/WHO Meeting on Pesticide Residues (FAO Plant Production and Protection Paper 67).

JMPR 2001, Pesticide residues in food - 2000. Evaluations - 2000. Part II - Toxicology, World Health Organization, Geneva, Joint FAO/WHO Meeting on Pesticide Residues (WHO/PCS/01.3).

MfE 2011, Toxicological intake values for priority contaminants in soil, New Zealand Ministry for the Environment, Wellington, New Zealand.

NEPC 1999, Schedule B (7a), Guideline on Health-Based Investigation Levels, National Environment Protection (Assessment of Site Contamination) Measure, National Environment Protection Council, Australia.

NHMRC & NRMMC 2011, National water quality management strategy, Australian drinking water guidelines, National Health and Medical Research Council and National Resource Management Ministerial Council, Australia.

OCS 2012, ADI List, Acceptable Daily Intakes for Agricultural and Veterinary Chemicals, Current to 31 March 2012, Australian Government, Department of Health and Ageing, Office of Chemical Safety (OCS), available from: http://www.health.gov.au/internet/main/publishing.nsf/content/E8F4D2F95D616584CA2573D700770C2A/$File/ADI-apr12.pdf.

RIVM 2001, Re-evaluation of human-toxicological Maximum Permissible Risk levels. National Institute of Public Health and the Environment, Bilthoven, Netherlands, available from: http://www.rivm.nl/bibliotheek/rapporten/711701025.html.

US EPA (IRIS 2012), Data and information available from the Integrated Risk Information System, an online database, available from http://www.epa.gov/iris/.

Weste,r RC, Maibach, HI, Bucks, DAW, Sedik, L, Melendres, J, Liao, C & DiZio, D 1990, ‘Percutaneous absorption of [14C]DDT and [14C]benzo[a]pyrene from soil’, Fundamental and Applied Toxicology, vol. 15, pp. 510–516.

WHO 1979, DDT and its Derivatives, Environmental Health Criteria 9, available from: http://www.inchem.org/documents/ehc/ehc/ehc009.htm.

WHO 1989, DDT and its Derivatives – Environmental Aspects, Environmental Health Criteria 83. available from http://www.inchem.org/documents/ehc/ehc/ehc83.htm.

WHO 2011, Guidelines for drinking-water quality, 4th edn, World Health Organization, Geneva, available from http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html.

 

2                  Aldrin + Dieldrin

2.1              General

Several comprehensive reviews of aldrin and dieldrin in the environment and their toxicity to humans are available and should be consulted for more detailed information (ATSDR 2002; WHO 1989). The following provides a summary of the key aspects of these compounds that are relevant to the derivation of a soil HIL.

 

Aldrin and dieldrin are the common names of two structurally similar compounds that were historically used as insecticides. These two chemicals are discussed together because aldrin is readily converted to dieldrin once it enters either the environment or the body, and both compounds reportedly have similar health effects. Aldrin predominantly contained the compound hexachlorohexahydrodimethanonaphthalene (HHDN) and was also produced under the following trade names; Aldrec, Aldrex, Drinox, Octalene, Seedrin, and Compound 118 (ATSDR 2002). Technical-grade aldrin contained not less than 85% aldrin with common impurities including isodrin, hexachlorobutadiene, chlordane, octachlorocyclopentene and toluene (ATSDR 2002).

 

Dieldrin was manufactured by the epoxidation of aldrin. Technical grade dieldrin, which was also produced under the trade names Alvit, Dieldrix, Octalox and Red Shields, contained no less that 85% by weight hexachloroepoxyoctahydrodimethanonaphthalene (HEOD). Pure HHDN and HEOD are structurally similar, stable white powders or crystals with a mild chemical odour. Commercial grade aldrin and dieldrin are tan coloured powders. Aldrin and dieldrin have low vapour pressure and are relatively insoluble in water (ATSDR 2002).

 

Aldrin and dieldrin, which do not occur naturally in the environment, were synthesised for commercial use as contact insecticides. Both chemicals were widely used against soil-dwelling pests in agriculture, particularly in the corn and citrus industries (ATSDR 2002). They were also used for the protection of wood structures or electrical and telecommunication cables against termites and woodborers.

 

They were used in Australia and across the world from the 1950s until their commercial distribution was restricted in the 1970s. By the end of 1980, there was a significant reduction on the number of aldrin and dieldrin products formally approved. All uses of these products were deregistered by 1985.

2.2              Previous HIL

The derivation of the previous HIL (HIL A = 10 mg/kg) for aldrin and dieldrin is presented by Di Marco (1993) and NEPC (1999). In summary, the HIL was derived on the basis of the following:

·         Background intakes were considered in the derivation of the current HIL with the intakes from food, water and ambient air considered to comprise 40% of the adopted ADI.

·         An ADI of 0.0001 mg/kg/day referenced from the JMPR (1985) was considered. An additional factor of 3 was used because of the uncertainties associated with the bioavailability estimates adopted and exposure levels in the future.

·         Dermal absorption of aldrin and dieldrin was considered to be 5%.

·         Oral bioavailability of organochlorine pesticides was considered to be 10%.

·         Based on intakes derived from soil (ingestion, dermal absorption and dust inhalation), an HIL of 10 mg/kg was calculated.


2.3              Significance of Exposure Pathways

2.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of aldrin and dieldrin in the range of contaminated sites that may need to be considered in Australia. On this basis, a default approach of assuming 100% oral bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

2.3.2        Dermal absorption

A proposed range for dermal absorption of pesticides from soil was 1%-10% (Ryan et al. 1987). The reported absorption of topically applied pesticides and herbicides in acetone to in vitro human skin was reported to be within this range for lindane, aldrin, dieldrin, malathion, parathion, and 2,4-D in Feldmann & Maibach, (1974). WHO (1989) noted that aldrin and dieldrin are readily absorbed by oral, inhalation and dermal routes. Absorption through the intact skin was about 7-8% of the applied dose in a human volunteer study. On this basis, adopting the default of 0.1 (10%) recommended by US EPA (1995) for pesticides is considered reasonable.

2.3.3        Inhalation of Dust

Aldrin and dieldrin are not considered sufficiently volatile to be of significance and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the derivation of soil HILs.

2.3.4        Plant Uptake

Aldrin and dieldrin have the potential to bioconcentrate in terrestrial ecosystems. However, the available studies show mixed results with respect to plant uptake. Some studies show potential uptake (more significantly into roots) while others have shown no plant uptake (from these compounds bound to soil) (ATSDR 2002). Both aldrin and dieldrin have high Koc values (log Koc = 6.67-7.67, ATSDR 2002), suggesting that these compounds are largely bound to soil particulates and immobile in soil. For plant uptake to be significant, the chemicals must be able to partition to soil water. With respect to aldrin and dieldrin bound to the soil, this is considered to be insignificant. Hence, the potential for plant uptake of aldrin and dieldrin from soil contamination is considered negligible.

 

It is noted, however that should these compounds be present in other media such as groundwater (used for irrigation) or solution, then the potential for uptake into fruit and vegetable crops is likely to be of significance. In addition, the mobility of these compounds in the soil environment can be enhanced by the presence of organic solvents. These organic solvents have the ability to increase the water solubility of non-polar compounds, which in turn increases their mobility in soil. The organic solvents in a sense act as a transport medium for chemicals that would normally bind strongly to soil (ATSDR 2002). These issues should be assessed on a site-specific basis.

2.3.5        Intakes from Other Sources – Background

For the general population where aldrin and dieldrin are no longer used, background intakes would be expected to be primarily associated with residues in food. Food Standards Australia and New Zealand has not detected aldrin or dieldrin in any sample in the 19th or 20th food surveys (FSANZ 2003). Dieldrin was reported (at 1.28-3.23% of the ADI adopted) in the earlier 18th survey and again in the most recent survey (FSANZ 2011) with the highest intake estimated to be 0.021 µg/kg/day for children aged 2-5 years, which comprises 20% of the adopted oral TRV. Other than the most recent food survey, intakes of aldrin and dieldrin are negligible, however the higher level of intake estimated for young children more recently suggests intakes are not negligible. For the purpose of establishing a soil HIL, an intake of 10% (assumed to represent a longer-term average of intakes from the available food surveys) of the TRV from other sources has been assumed.

2.4              Identification of Toxicity Reference Values

2.4.1        Classification

The International Agency for Research on Cancer (IARC) has classified aldrin and dieldrin as Group 3—not classifiable as to carcinogenicity to humans. It is noted that US EPA has classified both aldrin and dieldrin as Class B2—probable human carcinogens.

2.4.2        Review of Available Values/Information

There are mixed reviews of carcinogenicity with respect to aldrin and dieldrin. Based on a review by RIVM (2001) it is noted that epidemiological data remains inadequate, though some studies have shown hepatocellular carcinomas in mice, while other studies have not shown carcinogenic effects. Further evaluation of carcinogenicity by Stevenson et al. (1999) within the framework of the US EPA Proposed Guidelines for Carcinogen Risk Assessment considered that dieldrin-induced liver tumours occur through a non-genotoxic mode of action. The review also considers that a more appropriate cancer descriptor for aldrin/dieldrin is ‘not likely to be carcinogenic to humans’.

 

On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for aldrin and dieldrin. The following are available from Level 1 Australian and International sources:

Source

Value

Basis/Comments

Australian

ADWG (NHMRC & NRMMC 2011)

ADI = 0.0001 mg/kg/day

The ADI available in the ADWG (NHMRC & NRMMC 2011) is noted to be derived from JMPR evaluation (noted to be 1977).

OCS (2012)

TDI = 0.0001 mg/kg/day

This value (set in 2003) is based on the JMPR evaluation from 1994 (refer to comment below). The TDI is noted to be retained for comparison against dietary intakes only as these compounds are no longer used in agricultural practice. The ADI listed is also adopted by FSANZ.

International

WHO (2011)

PTDI = 0.0001 mg/kg/day

The ADI/PTDI has been considered in the derivation of WHO (2011) based on the JMPR evaluation where the provisional TDI is based on a NOAEL of 1 mg/kg/day in dogs and 0.5 mg/kg/day in rats (dietary studies, Fitzhugh et al. 1964; Fitzhugh & Nelson 1963), which is equivalent to 0.025 mg/kg/day in both species, and application of 250-fold uncertainty factor (10 for interspecies variation, 10 for intraspecies variation and 2.5 for concern about carcinogenicity observed in mice). It is noted that the WHO DWG evaluation has not changed since 1970.

RIVM (2001)

Adopted JMPR evaluation as noted above from WHO DWG

ATSDR (2002)

MRL = 0.00003 mg/kg/day for aldrin

MRL = 0.00005 mg/kg/day for dieldrin

Chronic oral MRLs for aldrin and dieldrin based on a LOAEL of 0.025 mg/kg/day associated with liver effects in rats and application of 100-fold uncertainty factor. Values adopted are consistent with those available from the US EPA (IRIS 2012).

US EPA (IRIS 2012)

RfD = 0.00003 mg/kg/day for aldrin

RfD = 0.00005 mg/kg/day for dieldrin

 

RfD for aldrin based on a LOAEL of 0.025 mg/kg/day associated with liver toxicity in a chronic rat study (Fitzhugh et al. 1964) and application of a 1000-fold uncertainty factor. The evaluation was last reviewed in 1988.

RfD for dieldrin based on a NOAEL of 0.005 associated with liver lesions in a 2-year rat study and a 100-fold uncertainty factor. The review was last updated in 1990.

In addition the US EPA has also derived non-threshold values for aldrin and dieldrin. It is not considered appropriate to quantify aldrin and dieldrin toxicity on the basis of a non-threshold approach.

 

All the key studies considered in the above reviews are dated (in the 1960s) and no new studies are available that suggest the evaluations provided and adopted in the Australian and WHO drinking water guidelines are not current. Hence the oral value adopted by NHMRC & NRMMC (2011) and WHO (2011) provide a suitable basis for the derivation of a soil HIL. No dermal or inhalation-specific studies or data are available. For the presence of aldrin and dieldrin in soil, it is considered appropriate to consider use of the available TRV for all pathways of exposures.

2.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for aldrin and dieldrin in the derivation of HILs:

Recommendation for Aldrin and Dieldrin
Oral TRV (TRVO) = 0.0001 mg/kg/day (NHMRC 2011 and WHO 2011) for all pathways of exposure
Dermal absorption factor (DAF) = 0.1 (or 10%) (US EPA 1995)
Background intakes from other sources (as % of TRV):
BIO = 10% for oral and dermal intakes
BIi = 10% for inhalation


 

2.5              Calculated HILs

On the basis of the above, the following HILs have been derived for aldrin and dieldrin (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)

Residential A

6

43

--

57

<1

Residential B

10

16

--

84

<1

Recreational C

10

27

--

73

<1

Commercial D

45

12

--

88

<1

-- Pathway not included in derivation of HIL

 

2.6              References

ATSDR 2002, Toxicological Profile for Aldrin/Dieldrin US Department of Health and Human Services, ATSDR, September 2002, available from http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=317&tid=56.

Di Marco, P 1993, ‘The Assessment and Management of Organochlorine Termiticides’, presented in the proceedings of the Second National Workshop on the Health Risk Assessment and Management of Contaminated Sites, Contaminated Sites Monograph Series, No. 2.

Feldmann, RJ & Maibach, HI 1974, ‘Percutaneous penetration of some pesticides and herbicides in man’, Toxicol. Appl. Pharmacol, vol. 28, pp. 126-132.

Fitzhugh, OG & Nelson, AA 1963, Unpublished data from the US Food and Drug Administration, as cited in JMPR, 1967.

Fitzhugh, OG, Nelson, AA & Quaife, ML 1964, ‘Chronic oral toxicity of aldrin and dieldrin in rats and dogs’, Food Cosmet Toxicol, vol. 2, pp. 551-562.

FSANZ 2003, The 20th Australian Total Diet Survey, A total diet survey of pesticide residues and contaminants, Food Standards Australia and New Zealand.

FSANZ 2011, The 23rd Australian Total Diet Study, Food Standards Australia and New Zealand.

IARC 1991, Summaries & Evaluations. DDT and Associated Compounds, vol. 53, (1991), p.179, International Agency for Research on Cancer.

NEPC 1999, Schedule B (7a), Guideline on Health-Based Investigation Levels, National Environment Protection (Assessment of Site Contamination) Measure, National Environment Protection Council, Australia.

NHMRC 2011, National water quality management strategy. Australian drinking water guidelines, National Health and Medical Research Council, Australia.

OCS 2012, ADI List, Acceptable Daily Intakes for Agricultural and Veterinary Chemicals, current to 31 March 2012, Australian Government, Department of Health and Ageing, Office of Chemical Safety (OCS), available from: http://www.health.gov.au/internet/main/publishing.nsf/content/E8F4D2F95D616584CA2573D700770C2A/$File/ADI-apr12.pdf.

RIVM 2001. Re-evaluation of human-toxicological Maximum Permissible Risk levels, National Institute of Public Health and the Environment, Bilthoven, Netherlands,, available from: http://www.rivm.nl/bibliotheek/rapporten/711701025.html.

Ryan, EA,  Hawkins, ET et al. 1987, ‘Assessing Risk from Dermal Exposure at Hazardous Waste Sites’, in Bennett, G & Bennett, J, (eds), Superfund '87: Proceedings of the Eighth National Conference, November 16-18, pp. 166-168, The Hazardous Materials Control Research Institute, Washington, DC.

Stevenson, DE, Walborg, .F, North, DW, Sielken Jr, RL, Ross, CE, Wright, AS, Xu, Y, Kamendulis, LM & Klaunig, JE 1999, ‘Monograph: Reassessment of human cancer risk of aldrin/dieldrin’, Toxicology Letter, vol. 109, Issues 3, October 1999, pp. 123-186.

US EPA (IRIS 2012), Data and information available from the Integrated Risk Information System, an online database, available from http://www.epa.gov/iris/.

US EPA 1995, Technical Guidance Manual, Assessing Dermal Exposure from Soil, US EPA Region 3, available from: http://www.epa.gov/reg3hwmd/risk/human/info/solabsg2.htm.

WHO 1989, Aldrin and dieldrin. Environmental Health Criteria 91, International Programme on Chemical Safety, World Health Organization Geneva.

WHO 2011, Guidelines for drinking-water quality, 4th edn, World Health Organization, Geneva, available from http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html.

3                  Chlordane (total)

3.1              General

Several comprehensive reviews of chlordane in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (ATSDR 1994). The following provides a summary of the key aspects of chlordane that are relevant to the derivation of a soil HIL.

 

Chlordane is a manufactured chemical that does not occur naturally in the environment. It is a thick liquid, and the colour ranges from colourless to amber depending on its purity. Chlordane does not dissolve in water but can be produced as an emulsion enabling it to be sprayed (ATSDR 1994). Sixty to eighty-five percent of chlordane consists of the stereo-isomers cis- and trans-chlordane, with the remainder comprising a number of impurities (ATSDR 1994).

 

Chlordane is a manufactured chemical that was used as a broad-spectrum insecticide in the United States between 1948 and 1988 (ATSDR 1994). In Australia, it was used to protect wooden structures against termites until June 1995 (NHMRC 2011). Some of its trade names are Octachlor and Velsicol 1068.

3.2              Previous HIL

The derivation of the previous HIL (HIL A = 50 mg/kg) for chlordane is presented by Di Marco (1993) and NEPC (1999). In summary, the HIL was derived on the basis of the following:

·         Background intakes were considered in the derivation of the current HIL with the intakes from food, water and ambient air considered to comprise 40% of the adopted ADI.

·         An ADI of 0.0005 mg/kg/day, referenced from the JMPR, was considered. An additional factor of 3 was used because of the uncertainties associated with the bioavailability estimates adopted and exposure levels in the future.

·         Dermal absorption of organochlorine pesticides was considered to be 5%.

·         Oral bioavailability of organochlorine pesticides was considered to be 10%.

·         Based on intakes derived from soil (ingestion, dermal absorption and dust inhalation), an HIL of 50 mg/kg was calculated.

3.3              Significance of Exposure Pathways

3.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of chlordane in the range of contaminated sites that may need to be considered in Australia. On this basis, a default approach of assuming 100% oral bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

3.3.2        Dermal absorption

US EPA (2004) has identified a dermal absorption fraction of 0.04 (4%), based on a study by Wester et al. (1992) for chlordane in soil. No additional data is available to suggest more significant dermal absorption values are relevant for chlordane.

3.3.3        Inhalation of Dust

Chlordane is not considered sufficiently volatile to be of significance and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the HIL derived.

3.3.4        Plant Uptake

Chlordane has the potential to bioconcentrate in terrestrial ecosystems. However, there are few studies available on the potential for plant uptake. Chlordane has a high Koc value (log Koc = 3.49-6.3, ATSDR 1994) suggesting that the compound is largely bound to soil particulates and immobile in soil. In addition, chlordane has a low solubility in water. For plant uptake to be significant, the chemicals must be able to partition to soil water. Information available from EFSA (2007) notes that chlordane is considered a non-systemic (not taken up by the plant) insecticide. Hence, with respect to chlordane bound to the soil, this is considered to be insignificant and negligible.

3.3.5        Intakes from Other Sources – Background

The review presented by Di Marco (1993) in the derivation of the previous HIL included a review of intakes (using available Australian data) that may be derived from water, air (including homes where termiticide treatment had occurred), soil and food. It is noted that use of chlordane was phased out in all states/territories except the Northern Territory in 1995. In 1997, chlordane was allowed to be used in the Northern Territory until stocks of the product were exhausted. Chlordane is now banned in Australia and hence background intakes estimated by Di Marco (1993) associated with product use are no longer relevant.

 

Background intakes of chlordane (where the product is not used) range from 0.1 ng/kg/day for adults to 0.46 ng/kg/day for children (where food intakes were most significant). Food Standards Australia and New Zealand has not detected chlordane in any sample in the 19th, 20th or 23rd food surveys (FSANZ 2003; FSANZ 2011). Hence, background intakes would be expected to be negligible. Assuming a negligible background intake is considered appropriate, based on current information.

3.4              Identification of Toxicity Reference Values

3.4.1        Classification

The International Agency for Research on Cancer (IARC 2001) has classified chlordane as Group 2B—possibly carcinogenic to humans.

 

It is also noted that US EPA has classified chlordane as B2—probable human carcinogen (last reviewed in 1998).

3.4.2        Review of Available Values/Information

As chlordane has been banned from use in a number of countries, there are few recent studies/reviews available. Review of chlordane by the European Food Safety Committee (EFSA 2007) provided a review of long-term toxicity studies, carcinogenicity and genotoxicity for chlordane. Long-term oral studies with the nervous system and liver were shown to be the most significant target organs. Data on genotoxicity is limited and conflicting, however overall chlordane was not mutagenic in vivo and not or only weakly mutagenic in a few tests in vitro. On the basis of the weight of evidence, chlordane is not considered to be genotoxic. Chlordane causes liver tumours in mice via a non-genotoxic mechanism and is classified by IARC as possibly carcinogenic to humans.

 

On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for chlordane. The following are available from Level 1 Australian and International sources:

 

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

ADI = 0.00045 mg/kg/day

Current ADWG (NHMRC 2011) of 0.001 mg/L based on 10% intake from drinking water, a NOEL of 0.045 mg/kg/day based on a long-term (30 week) dietary study in rats, and a 100-fold uncertainty factor. This is consistent with the PTDI used in the current WHO DWG, as well as OCS (2012).

OCS (2012)

TDI = 0.0005 mg/kg/day

TDI was set in 2003, no study referenced. This value is noted to be based on the JMPR evaluation from 1994. The TDI is noted to be retained for comparison against dietary intakes only as these compounds are no longer used in agricultural practice. The TDI listed is also adopted by FSANZ.

International

WHO (2011)

PTDI = 0.0005 mg/kg/day

Provisional TDI based on a NOAEL of 0.05 mg/kg/day for increased liver weights, serum bilirubin levels and hepatocellular swelling from a long term study in rats (same study as considered in the ADWG), and a 100-fold uncertainty factor.

ATSDR (1994)

Oral MRL = 0.0006 mg/kg/day

Inhalation MRL = 0.00002 mg/m3

Chronic oral MRL based on liver hypertrophy in a 30-month rat study.

Chronic inhalation MRL based on hepatic effects in a 90-day subchronic rat study. The study used to derive the inhalation MRL is the same as that used by the US EPA in the derivation of the RfC. The application of uncertainty factors differs between the organisations.

US EPA (IRIS 2012)

RfD = 0.0005 mg/kg/day

RfC = 0.0007 mg/m3

 

Oral RfD based on a NOAEL of 0.15 mg/kg/day associated with hepatic necrosis in a 104-week mouse study, and 300-fold uncertainty factor.

RfC based on hepatic effects in a subchronic rat inhalation study. The evaluation was last reviewed in 1998. In addition, US EPA has also derived an oral cancer slope factor and an inhalation unit risk (based on the oral evaluation). It is not considered appropriate to quantify chlordane toxicity on the basis of a non-threshold approach.

 

Based on the available data above, there is general agreement on the consideration of an oral TRV of 0.0005 mg/kg/day. Limited inhalation data is available, with the US EPA RfC essentially equivalent to the oral TRV; hence it is recommended that all intakes associated with contaminated soil be assessed on the basis of the oral TRV.

3.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for chlordane in the derivation of HILs:

Recommendation for Chlordane
Oral TRV (TRVO) = 0.0005 mg/kg/day (OCS 2012; NHMRC 2011; WHO 2011) for all pathways of exposure
Dermal absorption factor (DAF) = 0.04 (or 4%) (US EPA 2004)
Background intakes from other sources (as % of TRV):
BIO = 0% for oral and dermal intakes
BIi = 0% for inhalation

 

 

 

 

3.5              Calculated HILs

On the basis of the above, the following HILs have been derived for chlordane (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)

Residential A

50

65

--

35

<1

Residential B

90

32

--

68

<1

Recreational C

70

48

--

52

<1

Commercial D

530

25

--

75

<1

-- Pathway not included in derivation of HIL

 

3.6              References

ATSDR 1994, Toxicological Profile for Chlordane, US Department of Health and Human Services, ATSDR, available from http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=355&tid=62.

Di Marco, P 1993 ‘The Assessment and Management of Organochlorine Termiticides’, presented in the proceedings of the Second National Workshop on the Health Risk Assessment and Management of Contaminated Sites, Contaminated Sites Monograph Series, No. 2, 1993.

EFSA 2007, ‘Chlordane as undesirable substance in animal feed, Scientific Panel on contaminants in the Food Chain’, The EFSA Journal, vol. 582, pp. 1-52, European Food Safety Authority, adopted 7 November 2007.

FSANZ 2003, The 20th Australian Total Diet Survey, A total diet survey of pesticide residues and contaminants, Food Standards Australia and New Zealand.

FSANZ 2011, The 23rd Australian Total Diet Study, Food Standards Australia and New Zealand.

IARC 2001, Summaries & Evaluations, Chlordane and Heptachlor, Vol. 79, p.411, International Agency for Research on Cancer.

NEPC 1999, Schedule B (7a), Guideline on Health-Based Investigation Levels, National Environment Protection (Assessment of Site Contamination) Measure, National Environment Protection Council, Australia.

NHMRC 2011, National water quality management strategy, Australian drinking water guidelines, National Health and Medical Research Council, Australia.

OCS 2012, ADI List, Acceptable Daily Intakes for Agricultural and Veterinary Chemicals, current to 31 March 2012, Australian Government, Department of Health and Ageing, Office of Chemical Safety (OCS), available from: http://www.health.gov.au/internet/main/publishing.nsf/content/E8F4D2F95D616584CA2573D700770C2A/$File/ADI-apr12.pdf.

US EPA 2004, Risk Assessment Guidance for Superfund, Volume I: Human Health Evaluation Manual (Part E, Supplemental Guidance for Dermal Risk Assessment), Final, EPA/540/R-99/005, OSWER 9285.7-02EP.

US EPA (IRIS 2012), data and information available from the Integrated Risk Information System, an online database, available from http://www.epa.gov/iris/.

Wester, RC, Maibach, HI, Sedik, L, Melendres, J, Laio, CL, & DeZio, S 1992, ‘Percutaneous Absorption of [14C]Chlordane from Soil’, J. Toxicol. Environ. Health, vol. 35, pp. 269-277.

WHO 2011, Guidelines for drinking-water quality, 4th edn, World Health Organization, Geneva, available from http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html.

 

 

 

 

 

 

4                  Endosulfan (total)

4.1              General

Several comprehensive reviews of endosulfan in the environment and its toxicity to humans are available and should be consulted for more detailed information (ATSDR 2000; APVMA 2005; Marshall & Rutherford 2003; WHO 1984). The following provides a summary of the key aspects of endosulfan that are relevant to the derivation of a soil HIL.

 

Endosulfan is the common name for an organochlorine pesticide which predominantly contains the compound 6,7,8,9,10,10-hexachloro-1,5,5a,6,9,9a-hexahydro-6,9-methano-2,4,3-benzodioxathiepine-3-oxide. The manufacture of endosulfan yields two stereo-isomers denoted as α-endosulfan and β-endosulfan in a ratio of 7:3. Technical grade endosulfan generally comprises 94% total endosulfan (α-endosulfan and β-endosulfan) with the remainder comprising impurities and degradation products such as endosulfan ether, endosulfan alcohol and endosulfan sulfate (ATSDR 2000). Endosulfan insecticides are produced under the following trade names; Thiodan; Thionex; Thionate Malix; HOE 2671; FMC 5462; Cyclodan; Thifor; Beosit; Chlorthiepin and Endocide (ATSDR 2000).

 

Endosulfan is a cream to brown-coloured crystalline solid or waxy solid with a distinct turpentine-like odour. It has a low solubility in water, a low vapour pressure and does not burn (ATSDR 2000). The β-isomer is more chemically stable than the α-isomer, which slowly transforms to the β-isomer in the environment (ATSDR 2000).

 

Endosulfan is manufactured and used as a broad-spectrum insecticide to control insects on horticultural and agricultural products such as grains, tea, fruits, vegetables, tobacco and cotton. It is manufactured worldwide for commercial agricultural use and domestic (home gardening) use. Endosulfan is also used as a wood preservative (ATSDR 2000). Endosulfan was registered for commercial use in Australia in the 1970s until its deregistration in October 2010 with a two-year phase-out until October 2012. Prior to the late 1990s, when restrictions on its use were introduced, approximately 900 tonnes of technical grade endosulfan was imported annually into Australia. Its use significantly decreased in the years leading up to its deregistration. It was primarily used in cotton production (70%), followed by vegetables (20%) and other crops and horticultural products (10%) (APVMA 2005). Both isomers of endosulfan and endosulfan sulphate were added to the Stockholm Convention in April 2011.

4.2              Previous HIL

No previous HIL is available (NEPC 1999), though it is noted that review of endosulfan by Marshall & Rutherford (2003) suggested a soil guideline value of 160 mg/kg may be derived (assuming 20% of ADI is derived from soil, 100% bioavailability and soil ingestion is the most significant pathway of exposure).

4.3              Significance of Exposure Pathways

4.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of endosulfan in the range of contaminated sites that may need to be considered in Australia. On this basis, a default approach of assuming 100% oral bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

4.3.2        Dermal absorption

Insufficient data is available on the dermal absorption of endosulfan from soil. Hence the default values of 0.1 (10%) suggested by US EPA (1995) for pesticides has been adopted in the derivation of HILs.

4.3.3        Inhalation of Dust

Endosulfan is not considered sufficiently volatile to be of significance and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the HIL derived.

4.3.4        Plant Uptake

The few studies that are available with respect to the potential for plant uptake of endosulfan relate to the application of endosulfan in solution, rather than uptake from soil. Endosulfan has a high Koc value (log Koc = 3.5) and low solubility in water (ATSDR 2000), suggesting that the compound is largely bound to soil particulates and immobile in soil. For plant uptake to be significant, the chemicals must be able to partition to soil water. With respect to endosulfan bound to the soil, the potential for partitioning to soil water is considered to be low and hence plant uptake is considered to be negligible.

4.3.5        Intakes from Other Sources – Background

Background intakes have been assessed by Marshall & Rutherford (2003) on the basis of available Australian data. For a 2-year-old child, background intakes (from air, food and water) were estimated to contribute 7% of the ADI adopted (0.006 mg/kg/day). However, it has been noted that this evaluation was based on limited data and a default approach of considering 80% background intakes was adopted.

 

Background exposure by the general public is expected to be dominated by food residue intakes in areas away from where endosulfan products are being applied. Food Standards Australia and New Zealand has reported that intakes of endosulfan by all age groups was less than or equal to 2% of the adopted ADI in the 23rd Australian Total Diet Study (FSANZ 2011). The National Estimated Daily Intake of endosulfan was reviewed by APVMA (2005) and estimated to be equivalent to 27% of the recommended oral TRV (0.006 mg/kg/day), which is more conservative that the current dietary survey indicates. On this basis a background intake of 30% is considered appropriate for deriving a soil HIL for endosulfan.

4.4              Identification of Toxicity Reference Values

4.4.1        Classification

The International Agency for Research on Cancer (IARC) and US EPA have not classified endosulfan with respect to human carcinogenicity.

4.4.2        Review of Available Values/Information

Limited data is available to assess carcinogenicity of endosulfan. Evaluation of the WHO DWG (WHO 2011) referenced JMPR (WHO 1998), who concluded that endosulfan is not genotoxic and no carcinogenic effects have been noted in long-term studies in rats and mice. This is also noted, in the NRA (1998) review. Review by APVMA (2005) has reassessed the potential for endosulfan to be an endocrine disruptor. The review concluded that the endocrine-disrupting potential of the compound was not a significant risk to public health under the existing management controls and health standards.

 

On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for endosulfan and that no additional consideration is required to address endocrine-disrupting effects. The following are available from Level 1 Australian and International sources:


Source

Value

Basis/Comments

Australian

ADWG (NHMRC, 2011)

TDI = 0.006 mg/kg/day

The NHMRC derived a guideline of 0.02 mg/L from a TDI of 0.006 mg/kg/day that is based on a NOEL of 0.57 mg/kg/day from a 1-year dietary study in dogs, and an uncertainty factor of 100.

OCS (2012) and FSANZ (2011)

ADI = 0.006 mg/kg/day

ADI was set in May 1997 and based on a NOEL of 0.6 mg/kg/day from a 78-week dietary study in mice, 13-week dietary study in rats, 1-year dietary study in dogs and a developmental study in rats. The ADI is currently used by FSANZ in the assessment of endosulfan residues in food.

NRA (1998)

ADI – 0.006 mg/kg/day

As noted above from OCS (2012).

International

WHO (2011)

ADI = 0.006 mg/kg/day

No guideline is currently set in WHO (2011) as concentrations in drinking water occur well below those of health concern. However the review has noted that a health-based value of 0.02 mg/L can be derived on the basis of an ADI of 0.006 mg/kg/day derived from a 2-year dietary study in rats, supported by a 78-week study in mice, a 1 -ear study in dogs and a developmental study in rats.

ATSDR (2000)

Oral MRL = 0.002 mg/kg/day

Chronic oral MRL based on a NOAEL of 0.18 mg/kg/day associated with liver effects in a dog study, and an uncertainty factor of 100.

US EPA (IRIS 2012)

RfD = 0.006 mg/kg/day

 

Oral RfD (last reviewed in 1994) is based on a NOAEL of 0.6/0.7 (M/F) mg/kg/day associated with kidney effects and aneurysms in a rat study, and an uncertainty factor of 100.

 

Based on the available reviews, a consistent oral TRV of 0.006 mg/kg/day is available and considered suitable for the derivation of soil HILs. No inhalation or dermal data is available hence it is recommended that all intakes associated with contaminated soil be assessed on the basis of the oral TRV.


 

4.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for endosulfan in the derivation of HILs:

Recommendation for Endosulfan
Oral TRV (TRVO) = 0.006 mg/kg/day (OCS 2012) relevant for all pathways of exposure
Dermal absorption factor (DAF) = 0.1 (or 10%) (US EPA 1995)
Background intakes from other sources (as % of TRV):
BIO = 30% for oral and dermal intakes
BIi = 30% for inhalation

4.5              Calculated HILs

On the basis of the above the following HILs have been derived for endosulfan (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)

Residential A

270

43

--

57

<1

Residential B

400

16

--

84

<1

Recreational C

340

27

--

73

<1

Commercial D

2000

12

--

88

<1

-- Pathway not included in derivation of HIL

 

 

 

4.6              References

APVMA 2005, The Reconsideration of Approval of Active Constituent Endosulfan, Registration of Products Containing Endosulfan and their Associated Labels, Final Review Report and Regulatory Decision Review Series 2, Australian Pesticide and Veterinary Medicines Authority Canberra, Australia.

ATSDR 2000, Toxicological Profile for Endosulfan, available on website at http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=609&tid=113.

FSANZ 2003, The 20th Australian Total Diet Survey, a total diet survey of pesticide residues and contaminants, Food Standards Australia and New Zealand.

FSANZ 2011, The 23rd Australian Total Diet Study, Food Standards Australia and New Zealand.

Marshall, I & Rutherford, S 2003, ‘Health Investigation Level for Endosulfan in Soil’, presented in the proceedings of the Fifth National Workshop on the Health Risk Assessment and Management of Contaminated Sites.

NEPC 1999, Schedule B (7a), Guideline on Health-Based Investigation Levels, National Environment Protection (Assessment of Site Contamination) Measure, National Environment Protection Council, Australia.

NHMRC 2011, National water quality management strategy, Australian drinking water guidelines, National Health and Medical Research Council, Australia.

NRA 1998, The NRA Review of Endosulfan, Volume 1, Existing Chemicals Review Program, National Registration Authority for Agricultural and Veterinary Chemicals, Commonwealth of Australia, ACT, Australia.

OCS 2012, ADI List, Acceptable Daily Intakes for Agricultural and Veterinary Chemicals, current to 31 March 2012, Australian Government, Department of Health and Ageing, Office of Chemical Safety (OCS), available from: http://www.health.gov.au/internet/main/publishing.nsf/content/E8F4D2F95D616584CA2573D700770C2A/$File/ADI-apr12.pdf.

US EPA 1995, Technical Guidance Manual, Assessing Dermal Exposure from Soil, US EPA Region 3, available from: http://www.epa.gov/reg3hwmd/risk/human/info/solabsg2.htm.

US EPA (IRIS2012), data and information available from the Integrated Risk Information System, an online database, available from http://www.epa.gov/iris/.

WHO 1984, Environmental Health Criteria 40, Endosulfan, International Programme of Chemical Safety, World Health Organization, Geneva.

WHO 1998, JMPR Evaluation – Endosulfan, published under the joint sponsorship of the United Nations Environment Programme, the International Labour Organization, and the World Health Organization, and produced within the framework of the Inter-Organization Programme for the Sound Management of Chemicals.

WHO 2011, Guidelines for drinking-water quality, 4th edn, World Health Organization, Geneva, available from http://www.who.int/water_sanitation_health/dwq/chemicals/en/index.html.

 

 

 

 

5                  Endrin (total)

5.1              General

Several comprehensive reviews of endrin in the environment and its toxicity to humans are available and should be consulted for more detailed information (ATSDR 1996; WHO 1992; DEH 2006). The following provides a summary of the key aspects of endrin that are relevant to the derivation of a soil HIL.

 

The organochlorine pesticide endrin is a white to light tan, crystalline solid with a mild chemical odour. It is relatively insoluble in water and has a low vapour pressure. Endrin is the common name for 1,2,3,4,10,10-hexachloro-6,7-epoxy-1,4, 4a,5,6,7,8,8a-octahydro-1,4-endo,endo-5,8- dimethanonaphthalene but the term is also used to describe the commercial grade insecticide which typically contains 96% endrin. Endrin is the endo,endo stereoisomer of dieldrin (WHO 1992; WHO 2011).

 

Endrin was manufactured as a broad-spectrum insecticide and rodenticide, which was active against a wide range of agricultural pests. It was mainly used in the cotton industry and to a lesser extent on rice, sugar cane and maize (WHO 2011). Endrin has been widely used in agriculture since the 1950s but its manufacture and use was banned under the Stockholm Convention.

 

Endrin use was phased out in Australia in 1987 (DEH 2006).

5.2              Previous HIL

No previous HIL is available for endrin (NEPC 1999).

5.3              Significance of Exposure Pathways

5.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of endrin hence a default approach of assuming 100% oral bioavailability has been adopted in the derivation of an HIL. It is noted that a site-specific assessment of bioavailability can be undertaken where required.

5.3.2        Dermal absorption

Insufficient data is available on the dermal absorption of endrin from soil. Hence the default values of 0.1 (10%) suggested by US EPA (1995) for pesticides has been adopted in the derivation of HILs.

5.3.3        Inhalation of Dust

Endrin is not considered sufficiently volatile to be of significance and inhalation exposures associated with particulates outdoors and indoors are expected to be of less significance than ingestion of soil. While likely to be negligible, potential inhalation exposures associated with dust have been considered in the HIL derived.

5.3.4        Plant Uptake

The few studies that are available with respect to the potential for plant uptake of endrin relate to the application of the product in solution, rather than uptake from soil. Endrin has a high Koc value (log Koc = 4.53) and low solubility in water (ATSDR 1996), suggesting that the compound is largely bound to soil particulates and is immobile in soil. For plant uptake to be significant, the chemicals must be able to partition to soil water. With respect to endrin bound to the soil, the potential for partitioning to soil water is considered to be low and hence plant uptake is considered to be negligible.

5.3.5        Intakes from Other Sources – Background

WHO (1992) provides an evaluation of exposures by the general public which are dated and relate to a period when endrin was in use. The total intake of endrin from dietary, water and air sources (noted to be dominated by dietary intakes) was estimated by WHO (1992) to be ‘far below’ the ADI adopted (0.2 µg/kg/day). Use of endrin was phased out in Australia in the late 1980s with the last product registration cancelled at the end of 1990. Hence background intakes in Australia are expected to lower than estimated by WHO. Food Standards Australia and New Zealand has not detected endrin in any sample in the 19th, 20th or 23rd food surveys (FSANZ 2003; FSANZ 2011). Hence, background intakes would be expected to be negligible. Assuming a negligible background intake is considered appropriate, based on current information.

5.4              Identification of Toxicity Reference Values

5.4.1        Classification

The International Agency for Research on Cancer (IARC 1987) has classified endrin as Group 3not classifiable, on the basis of inadequate evidence in humans and experimental animals.

 

It is noted that US EPA has classified endrin as Group Dnot classifiable.

5.4.2        Review of Available Values/Information

Insufficient data is available to indicate if endrin is carcinogenic to humans. The available data does show that endrin is not genotoxic (WHO 1992; ATSDR 1996; RIVM 2001). On the basis of the available information it is considered appropriate that a threshold dose-response approach be adopted for endrin. The following are available from Level 1 Australian and International sources:

 

 

Source

Value

Basis/Comments

Australian

ADWG NHMRC (2011)

No evaluation available

 

OCS (2012)

TDI = 0.0002 mg/kg/day

TDI (changed from ADI of same value in 2003) provided as endrin no longer in use in Australia. TDI adopted derived from JMPR evaluation.

International

JMPR (1970)

ADI/PTDI =0.0002 mg/kg/day

ADI first established by JMPR in 1970 based on the level that caused no toxicological effects in dietary studies in rats and dogs (NOEL of 0.025 mg/kg/day, and uncertainty factor of 100).

WHO (2011)

PTDI =0.0002 mg/kg/day

Value available in WHO DWG based on JMPR (1970) evaluation (above).

RIVM (2001)

TDI = 0.0002 mg/kg/day

TDI derived on basis of NOAEL of 0.025 mg/kg/day associated liver and kidney effects in a rat study, and an uncertainty factor of 100.

ATSDR (1996)

Oral MRL = 0.0003 mg/kg/day

Chronic oral MRL based on a NOAEL of 0.025 mg/kg/day associated with CNS effects in a 2-year dog study, and an uncertainty factor of 100.

US EPA (IRIS 2012)

RfD = 0.0003 mg/kg/day

 

Oral RfD based on a NOAEL of 0.025 mg/kg/day associated with liver effects in a 2-year dog study, and an uncertainty factor of 100.

 

The above evaluations have identified consistent NOAEL values and oral TRVs for the assessment of endrin intakes. Hence the current Australian TRV of 0.0002 mg/kg/day has been adopted for the derivation of soil HILs. No inhalation or dermal data is available, hence it is recommended that all intakes associated with contaminated soil be assessed on the basis of the oral TRV.

5.4.3        Recommendation

On the basis of the discussion above, the following toxicity reference values (TRVs) have been adopted for endrin in the derivation of HILs:

Recommendation for Endrin
Oral TRV (TRVO) = 0.0002 mg/kg/day (OCS 2012) relevant for all pathways of exposure
Dermal absorption factor (DAF) = 0.1 (or 10%) (US EPA 1995)
Background intakes from other sources (as % of TRV):
BIO = 0% for oral and dermal intakes
BIi = 0% for inhalation

5.5              Calculated HILs

On the basis of the above, the following HILs have been derived for endrin (refer to Appendix B for equations used to calculate the HILs and Appendix C for calculations):

HIL Scenario

HIL (mg/kg)

Percentage Contribution from Exposure Pathways

Ingestion of Soil/Dust

Ingestion of Home-grown Produce

Dermal Absorption of Soil/Dust

Inhalation (dust)