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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 A4

The Derivation of HILs
for Herbicides and Other Pesticides

 

 

 


Contents
The derivation of HILs for herbicides and other pesticides
                                                                                       Page

1                             2,4,5-T                                                             1

1.1             General                                                                                        1

1.2             Previous HIL                                                                               1

1.3             Significance of Exposure Pathways                                          1

1.3.1                Oral Bioavailability                                                         1

1.3.2                Dermal absorption                                                           1

1.3.3                Inhalation of Dust                                                            1

1.3.4                Plant Uptake                                                                    1

1.3.5                Intakes from Other Sources – Background                    2

1.4             Identification of Toxicity Reference Values                             2

1.4.1                Classification                                                                    2

1.4.2                Review of Available Values/Information                        2

1.4.3                Recommendation                                                             3

1.5             Calculated HILs                                                                          4

1.6             References                                                                                   4

2                             2,4-D                                                                6

2.1             General                                                                                        6

2.2             Previous HIL                                                                               6

2.3             Significance of Exposure Pathways                                          6

2.3.1                Oral Bioavailability                                                         6

2.3.2                Dermal absorption                                                           6

2.3.3                Inhalation of Dust                                                            7

2.3.4                Plant Uptake                                                                    7

2.3.5                Intakes from Other Sources – Background                    7

2.4             Identification of Toxicity Reference Values                             7

2.4.1                Classification                                                                    7

2.4.2                Review of Available Values/Information                        7

2.4.3                Recommendation                                                             8

2.5             Calculated HILs                                                                          9

2.6             References                                                                                   9

3                             MCPA, MCPB and Mecoprop                      11

3.1             General                                                                                      11

3.2             Previous HIL                                                                             11

3.3             Significance of Exposure Pathways                                        11

3.3.1                Oral Bioavailability                                                       11

3.3.2                Dermal absorption                                                         11

3.3.3                Inhalation of Dust                                                          11

3.3.4                Plant Uptake                                                                  11

3.3.5                Intakes from Other Sources – Background                  12

3.4             Identification of Toxicity Reference Values                           12

3.4.1                Classification                                                                  12

3.4.2                Review of Available Values/Information                      12

3.4.2.1                 MCPA                                                                                            12

3.4.2.2                 MCPB                                                                                            13

3.4.2.3                 Mecoprop (MCPP)                                                                     13

3.4.3                Recommendation                                                           14

3.5             Calculated HILs                                                                        14

3.6             References                                                                                 14

4                             Picloram                                                        16

4.1             General                                                                                      16

4.2             Previous HIL                                                                             16

4.3             Significance of Exposure Pathways                                        16

4.3.1                Oral Bioavailability                                                       16

4.3.2                Dermal absorption                                                         16

4.3.3                Inhalation of Dust                                                          16

4.3.4                Plant Uptake                                                                  16

4.3.5                Intakes from Other Sources – Background                  17

4.4             Identification of Toxicity Reference Values                           17

4.4.1                Classification                                                                  17

4.4.2                Review of Available Values/Information                      17

4.4.3                Recommendation                                                           18

4.5             Calculated HILs                                                                        18

4.6             References                                                                                 19

5                             Atrazine                                                         20

5.1             General                                                                                      20

5.2             Previous HIL                                                                             21

5.3             Significance of Exposure Pathways                                        21

5.3.1                Oral Bioavailability                                                       21

5.3.2                Dermal absorption                                                         21

5.3.3                Inhalation of Dust                                                          21

5.3.4                Plant Uptake                                                                  21

5.3.5                Intakes from Other Sources – Background                  21

5.4             Identification of Toxicity Reference Values                           22

5.4.1                Classification                                                                  22

5.4.2                Review of Available Values/Information                      22

5.4.3                Recommendation                                                           23

5.5             Calculated HILs                                                                        24

5.6             References                                                                                 24

6                             Chlorpyrifos                                                  26

6.1             General                                                                                      26

6.2             Previous HIL                                                                             26

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                                                                  27

6.3.5                Intakes from Other Sources – Background                  27

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                                                           30

6.5             Calculated HILs                                                                        30

6.6             References                                                                                 31

7                             Bifenthrin                                                      33

7.1             General                                                                                      33

7.2             Previous HIL                                                                             33

7.3             Significance of Exposure Pathways                                        33

7.3.1                Oral Bioavailability                                                       33

7.3.2                Dermal absorption                                                         33

7.3.3                Inhalation of Dust                                                          33

7.3.4                Plant Uptake                                                                  33

7.3.5                Intakes from Other Sources – Background                  34

7.4             Identification of Toxicity Reference Values                           34

7.4.1                Classification                                                                  34

7.4.2                Review of Available Values/Information                      34

7.4.3                Recommendation                                                           35

7.5             Calculated HILs                                                                        35

7.6             References                                                                                 36

8                             Shortened forms                                            37


1                  2,4,5-T

1.1              General

2,4,5-T is the common name for 2,4,5-trichlorophenoxyacetic acid (or 2,4,5-triphenoxyacetic acid), a chlorophenoxy herbicide.

 

Several comprehensive reviews of 2,4,5-T in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary ( OCS 2004; HSDB 2010). The following provides a summary of the key aspects of 2,4,5-T that are relevant to the derivation of a soil HIL.

 

The herbicide was also commercially produced as an amine salt, alkali metal salt and ester derivative of 2,4,5-T. Pure 2,4,5-T is a white to light tan solid. It is slightly soluble in water whereas the amine and alkali metal salt derivatives are highly soluble. The ester, however, is insoluble in water. 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD), a known human carcinogen, was a common contaminant in the manufacture of 2,4,5-T and its derivatives and was typically present in the low mg/kg to high mg/kg level (OCS 2004). 2,4,5-T with TCDD contamination is now controlled in international trade through the 'Rotterdam Convention’ (Joint FAO/UNEP 2005). It is noted that 2,4,5-T is not expected to persist in the environment for any significant period of time but TCDD will remain and should be considered in a site-specific assessment where a 2,4,5-T source may have been present.

 

2,4,5-T and its derivatives were introduced in the 1960s and were used as herbicides for broad-leaved wood plants such as blackberries. 2,4,5-T was also combined with the compound 2,4-D to form the ‘agent orange’ herbicide which was widely used by the US military in the Vietnam war (OCS 2004). 2,4,5-T and its derivatives were withdrawn from use in the late 1980s and are no longer approved for use or marketed in Australia.

1.2              Previous HIL

No previous HIL is available for 2,4,5-T (NEPC 1999).

1.3              Significance of Exposure Pathways

1.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of 2,4,5-T, 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.

1.3.2        Dermal absorption

Insufficient data is available on the dermal absorption of 2,4,5-T from soil. Hence the default value of 0.1 (10%) suggested by US EPA (1995) for pesticides has been adopted in the derivation of HILs.

1.3.3        Inhalation of Dust

2,4,5-T 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.

1.3.4        Plant Uptake

Most chlorophenoxy herbicides are toxic to plants and, as such, will be phytotoxic to almost all broadleaf crops including tomatoes, grapes and fruit trees, well before plant uptake into edible portions of fruit and vegetable crops is of significance. Hence the uptake of these compounds into home-grown produce has not been considered in the derivation of HIL A.

 

Note that the phytotoxic effects of these compounds may need to be addressed on a site-specific basis if detected in soil.

1.3.5        Intakes from Other Sources – Background

Review of available publications suggests that very little data is available for Australia. Based on the available information on 2,4,5-T and 2,4-D in the environment, it is likely that background intakes by the general public will be similar to those considered for 2,4-D, which can be considered to be essentially negligible (0%).

1.4              Identification of Toxicity Reference Values

1.4.1        Classification

The International Agency for Research on Cancer (IARC 1987) has classified chlorophenoxy herbicides as Group 2B—possibly carcinogenic to humans.

 

US EPA has not classified 2,4,5-T.

1.4.2        Review of Available Values/Information

Limited data is available on the assessment of carcinogenicity and genotoxicity for 2,4,5-T. Available information on 2,4,5-T is often confounded with the presence of dioxin (TCDD) which was a common contaminant in 2,4,5-T herbicides. 2,4,5-T alone has not been found to be carcinogenic (Joint FAO/UNEP 2005).

 

On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for 2,4-5-T. The following are available from Level 1 Australian and International sources:

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.03 mg/kg/day

Current drinking water guideline of 0.1 mg/L based on 10% intake from drinking water. Based on equations presented in the ADWG (NHMRC 2011), the TDI considered in this derivation is equal to 0.029 mg/kg/day, essentially equivalent to the ADI available from the Joint FAO/WHO. No further information on the basis for this value is available.

OCS (2012)

Deleted from current list in 2003. Prior to this, the ADI was listed as 0.03 mg/kg/day.

Previous ADI referenced from Joint FAO/WHO evaluation from 1981.

International

WHO (1981)

Temporary ADI of 0-0.03 mg/kg/day

Temporary ADI based on a NOEL of 3 mg/kg/day from a rat carcinogenicity study with 2,4,5-T containing 0.05 ppm TCDD.

WHO (2011)

TDI = 0.003 mg/kg/day

2,4,5-T has been reviewed in the WHO DWG (originally reviewed and established in 1996,) with a TDI of 0.003 mg/kg/day derived based on a NOAEL for reduced body weight gain, increased liver and kidney weights and renal toxicity in a 2 -year rat study. The same NOAEL was derived for reproductive effects from a three-generation rat study. It is noted that the derivation of the TDI included an additional 10 fold factor to address a suggested association between 2,4,5-T and soft-tissue sarcoma and non-Hodgkin lymphoma (not noted in other reviews available).

 

2,4,5-T is included in the WHO plan for rolling revisions to the drinking water guidelines. No reviews with respect to this chemical are currently available.

ATSDR

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.01 mg/kg/day

 

The US EPA evaluation was established in 1982 and last reviewed in 1988 and provides an oral RfD of 0.01 mg/kg/day, based on a NOAEL of 3 mg/kg/day based on kidney effects in rats, and a 300-fold uncertainty factor.

 

The value derived is considered protective of reproductive end points.

 

The available information from all the above sources is dated. There are some issues with the temporary ADI derived by the Joint FAO/WHO (1981) in that the study considered for the derivation of the ADI included the dioxin (TCDD) contaminant and addressed an end point not associated with 2,4,5-T alone. This value has subsequently been adopted in the derivation of the current ADWG without further review.

 

The value has been deleted from the current ADI list (OCS 2012). The TDI available in the current WHO DWG (2011) is based on the same studies as considered in 1981, though an additional uncertainty factor has been incorporated to address uncertainties in the database, including potential carcinogenic effects. The basis for this additional factor is not clear, as the carcinogenic effects noted have not been identified in other studies. On this basis, the most appropriate threshold reference value for 2,4,5-T is from US EPA, which is similar to the previous ADI from WHO (and is considered in the current ADWG (NHMRC 2011)).

 

No dermal or inhalation specific studies or data are available. For the presence of 2,4,5-T in soil, it is considered appropriate to consider use of the available US EPA RfD as a TRV 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 2,4,5-T in the derivation of HILs:

Recommendation for 2,4,5-T
Oral TRV (TRVO) = 0.01 mg/kg/day (RfD from US EPA (IRIS 2012) relevant to 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

1.5              Calculated HILs

On the basis of the above, the following HILs have been derived for 2,4,5-T (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

600

43

--

57

<1

Residential B

900

16

--

84

<1

Recreational C

800

27

--

73

<1

Commercial D

5000

12

--

88

<1

-- Pathway not included in derivation of HIL

1.6              References

HSDB 2010, Hazardous Substances Data Bank, online database available from: http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB.

IARC 1987, Summaries and Evaluations, Chlorophenoxy herbicides, Supplement 7: (1987), p.256, 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 2004, Human Health Risk Assessment of Dioxins in Australia, National Dioxins Program, Technical Report No. 12, Department of the Environment and Heritage, Australian Government, Canberra, 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.

Joint FAO/UNEP 2005, Rotterdam Convention on the Prior Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International Trade, 2005, Decision Guidance Document: 2,4,5-T and its Salts and Esters, Joint Food and Agriculture Organisation of the United Nations and United Nations Environment Programme for the Operation of the Operation of the Prior Informed Consent, Geneva.

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

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

WHO 1981, Pesticide Residues in Food, Evaluations 1981, FAO Plant Production and Protection Paper 42, Joint FAO/WHO review.

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                  2,4-D

2.1              General

2,4-D is the common name for the chlorophenoxy herbicide 2,4-dichlophenoxy acetic acid.

 

Several comprehensive reviews of 2,4-D in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (APVMA 2006; WHO 1984; WHO 1987). The following provides a summary of the key aspects of 2,4-D that are relevant to the derivation of a soil HIL.

 

The herbicide is also formulated as an amine salt, alkali metal salt and ester derivative of 2,4-D (WHO 1984). Pure 2,4-D is a white to off-white crystalline powder with a slight phenolic odour (APVMA 2006). The commercial grade herbicide is often combined with solvents or surfactants and sold as granules, dust, emulsions and liquid concentrates (WHO 1984). 2,4-D is slightly soluble in water whereas the amine and alkali metal salt derivatives are highly soluble. The ester derivate is insoluble in water (WHO 1984). 2,4-D esters with short chain alcohols are highly volatile whereas 2,4-D and its salt and amine derivatives have a low volatility (APVMA 2006).

 

Some chlorinated by-products produced during manufacture of 2,4-D and its derivatives such as 2,7- dichlorodibenzo-p-dioxin, 1,3,6,8- and 1,3,7,9-tetrachlorodibenzo-p-dioxins and 1,3,7-trichlorodibenzo-p-dioxin have been associated with enhanced toxicity findings (WHO 1984).

 

2,4-D and its derivatives are systemic herbicides commonly used in Australia to control broadleaf and aquatic weeds (NHMRC 2004). At least 122 separate products containing these compounds were registered in Australia in 2003 (APVMA 2006). They were registered to control weeds in agricultural crops such as cereals, sugar cane and rice and in pastures and turf. 2,4-D herbicides were also applied at very low application rates to citrus and pears to reduce premature fruit drop and increase fruit storage life (WHO 1984; APVMA 2006). In addition, 2,4-D is used to increase the proportion of medium-sized potato tubers and the intensity of colour in red-skinned varieties (APVMA 2006). In 2006, the Australian Pesticides and Veterinary Medicines Authority conducted a review of the environmental fate and ecotoxicity of volatile 2,4-D esters and concluded that the registration of these compounds should be suspended (APVMA 2006). This review process is ongoing and the APVMA website (www.apvma.gov.au) should be checked for any updates on which products are currently registered.

2.2              Previous HIL

No previous HIL is available for 2,4-D (NEPC 1999).

2.3              Significance of Exposure Pathways

2.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of 2,4-D, 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.

2.3.2        Dermal absorption

A dermal absorption value of 0.05 (5%) is available from US EPA (2004) based on a study by Wester et al. (1996). This study evaluated potential dermal absorption of 2,4-D from soil, where absorption over time changed over time (noted to be not-linear). Data from the study showed low absorption over 8 hours (0.03-0.05%) with slightly higher absorption over 16 hours (2.2%). Limited other data is available on the dermal absorption of 2,4-D from soil, hence the value of 0.05 (5%) has been adopted.

2.3.3        Inhalation of Dust

2,4-D 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.

2.3.4        Plant Uptake

Most chlorophenoxy herbicides are toxic to plants and, as such, will be phytotoxic to almost all broadleaf crops including tomatoes, grapes and fruit trees well before plant uptake into edible portions of fruit and vegetable crops is of significance. Hence the uptake of these compounds into home-grown produce has not been considered in the derivation of an HIL A.

 

Note that the phytotoxic effects of these compounds may need to be addressed on a site-specific basis if detected in soil.

2.3.5        Intakes from Other Sources – Background

Exposure concentrations provided by WHO (1984, 1987) (as well as noted in APVMA (2006)) are derived from areas where 2,4-D is used and is not expected from the presence of 2,4-D contamination in soil. The intakes, however, may be of concern if the HILs were being applied to an area where products containing 2,4-D are used (or have been used in the recent past).

 

With respect to background intakes of 2,4-D, the following is noted from WHO (1987):

·         It is expected background intakes for the general population will be associated with the presence of residues in food and water.

·         Intakes from air is considered negligible.

·         Where 2,4-D is not used, intakes by the general population are considered negligible.

·         In areas where 2,4-D is used, background intakes from air, food and water are estimated to be 0.3–2 µg/kg/day.

FSANZ (2011) has estimated that the 90th percentile intake of 2,4-D by young children aged 2-5 years (most sensitive) is 0.014 µg/kg/day or 0.000014 mg/kg/day. This intake is negligible in comparison with the adopted TRV of 0.01 mg/kg/day.

 

On the basis of the above, background intakes of 2,4-D have been assumed to be essentially negligible (where 2,4-D is not used).

2.4              Identification of Toxicity Reference Values

2.4.1        Classification

The International Agency for Research on Cancer (IARC 1987) has classified chlorophenoxy herbicides as Group 2B—possibly carcinogenic to humans.

 

US EPA has not classified 2,4-D.

2.4.2        Review of Available Values/Information

There is limited information on the assessment of carcinogenicity and genotoxicity for 2,4-D from IARC and US EPA. Ibrahim et al. (1991) provided a summary of a review of carcinogenicity of 2,4-D following review by a panel of 13 scientists. Based on a weight-of-evidence approach 2,4-D was considered unlikely to be a genotoxic carcinogen because it has not been shown to be mutagenic in most in vitro and in vivo systems. The predominant opinion from the panel was that the weight of evidence indicates that it is possible that exposure to 2,4-D may cause cancer in humans.

 

On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for 2,4-D. The following are available from Level 1 Australian and International sources:

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.01 mg/kg/day

Current ADWG (NHMRC 2011) of 0.03 mg/L based on 10% intake from drinking water. Based on equations presented in the ADWG, the TDI considered in this derivation is equal to 0.009 mg/kg/day, which can be rounded to 0.01 mg/kg/day, essentially equivalent to the ADI available from the OCS.

OCS (2012)

ADI = 0.01 mg/kg/day

The ADI is noted to have been last reviewed in June 2006 and is based on a NOEL of 1 mg/kg/day associated with abnormal renal morphology in a 2-year rat study, supported by the same NOELs (based on kidney effects) in a 2-year mouse and 1-year dog study.

International

WHO (2011)

ADI = 0.01 mg/kg/day

ADI, used in the derivation of the current WHO DWG (2011), was established by JMPR (FAO/WHO 1997) for 2,4-D and its salts and esters on the basis of a NOAEL of 1 mg/kg/day in a 1-year toxicity study in dogs and 2-year study in rats, and an uncertainty factor of 100-fold.

ATSDR

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.01 mg/kg/day

 

US EPA has derived an oral RfD of 0.01 mg/kg/day. The value was last reviewed in 1986 and is derived based on a LOAEL of 1 mg/kg/day associated with abnormal renal morphology from a 90-day rat bioassay and a 1-year interim report from a 2 year rat study, and an uncertainty factor of 100.

 

Based on the available data above, there is general agreement from Australian and international sources on the consideration of an oral toxicity reference value of 0.01 mg/kg/day.

 

No dermal or inhalation specific studies or data are available. For the presence of 2,4-D in soil (not during use), it is considered appropriate to consider the use of the available ADI 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 2,4-D in the derivation of HILs:

Recommendation for 2,4-D
Oral TRV (TRVO) = 0.01 mg/kg/day (OCS 2012) for all pathways of exposure
Dermal absorption factor (DAF) = 0.05 (or 5%) (US EPA 2004)
Background intakes from other sources (as % of TRV):
BIO = 0% for oral and dermal intakes
BIi = 0% for inhalation

 

2.5              Calculated HILs

On the basis of the above, the following HILs have been derived for 2,4-D (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

900

59

--

41

<1

Residential B

1600

27

--

73

<1

Recreational C

1300

43

--

57

<1

Commercial D

9000

21

--

79

<1

-- Pathway not included in derivation of HIL

2.6              References

APVMA 2006, Preliminary Review Finding (Environment) Part 1: 2,4-D Esters. The Reconsideration of Approvals of the Active Constituents 2,4-D, Registrations of Products Containing 2,4-D and their Associated Labels, Australian Pesticides and Veterinary Medicines Authority, Canberra, Australia.

IARC 1987, Summaries and Evaluations, Chlorophenoxy herbicides, Supplement 7: (1987), p.256, International Agency for Research on Cancer.

Ibrahim ,MA, Bond, GG, Burke, TA, Cole, P, Dost, FN, Enterline, PE, Gough, M, Greenberg, RS, Halperin, WE, McConnell, E, Munro, IC, Swenberg, JA, Zahm, SH & Graham, JD 1991, ‘Weight of the Evidence on the Human Carcinogenicity of 2,4-D’, Environmental Health Perspectives, vol. 96, pp. 213-222.

FAO/WHO (1997), Pesticide residues in food — 1996, Evaluations 1996, Part II — Toxicological, World Health Organization, International Programme on Chemical Safety, Joint FAO/WHO Meeting on Pesticide Residues (WHO/PCS/97.1), Geneva.

FSANZ 2011, The 23rd Australian Total Diet Study, Food Standards Australia and 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 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, July 2004.

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, Melendres, J, Logan, F, Hui, X, & Maibach, HI 1996, ‘Percutaneous Absorption of 2,4-Dichlorophenoxyacetic Acid from Soil with Respect to the Soil Load and Skin Contact Time: In-vivo Absorption in Rhesus Monkey and in Vitro Absorption in Human Skin’, J. Toxicol. Environ. Health, vol. 47, pp. 335-344.

WHO 1984, Environmental Health Criteria No 29 2,4- Dichlorophenoxy Acetic Acid (2,4-D), World Health Organization, Geneva.

WHO 1987, Health and Safety Guide No. 5, 2,4-Dichlorophenoxyacetic (2,4-D), IPCS International Programme on Chemical Safety.

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                  MCPA, MCPB and Mecoprop

3.1              General

The following information on MCPA (4-chloro-2-methylphenoxyacetic acid), MCPB (4-(2-methyl-4-chlorophenoxy)butyric acid) and mecoprop (also referenced as MCPP) are grouped together as they are structurally similar chlorophenoxy herbicides.

 

While limited data is available, reviews of these compounds in the environment and their toxicity to humans are available and should be consulted for more detailed information not presented in this summary (WHO 2011; HSDB 2010). The following provides a summary of the key aspects of these compounds that are relevant to the derivation of a soil HIL.

 

In their pure form the three compounds are white crystalline solids, though technical grade products can be white to light brown crystal powders or liquids. The compounds are often formulated as salts (e.g. potassium or diethylamine salts) or esters (e.g. iso-octyl esters). The three compounds are the active ingredients in post emergence herbicides used to control annual and perennial weeds in agricultural, commercial/industrial and domestic environments. In Australia all three compounds are registered for agricultural application on wheat, barley, oats, sorghum, rice, linseed, peas, grass pastures, turf, clover, corn/maize and oilseed poppies, and for the home garden to control broadleaf weeds (WHO 2011).

3.2              Previous HIL

No previous HIL is available for MCPA, MCPB or mecoprop (NEPC 1999).

3.3              Significance of Exposure Pathways

3.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of MCPA, MCPB or mecoprop, 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.

3.3.2        Dermal absorption

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

3.3.3        Inhalation of Dust

MCPA, MCPB and mecoprop 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.

3.3.4        Plant Uptake

Most chlorophenoxy herbicides are toxic to plants and, as such, will be phytotoxic to almost all broadleaf crops including tomatoes, grapes and fruit trees well before plant uptake into edible portions of fruit and vegetable crops is of significance. Hence the uptake of these compounds into home-grown produce has not been considered in the derivation of HIL A.

 

Note that the phytotoxic effects of these compounds may need to be addressed on a site-specific basis if detected in soil.

3.3.5        Intakes from Other Sources – Background

Limited data is available for the assessment of background intakes of MCPA, MCPB and mecoprop. These compounds are currently registered for use in Australia (while some areas are only allowed controlled use of MCPA) and they are generally not considered persistent in the environment. The compounds are not included in the Australian Total Diet Surveys (FSANZ 2003; FSANZ 2011) and there is no data regarding concentrations in drinking water or air in Australia. Away from areas where these herbicides are used, exposure by the general public is expected to be low. In the USA, MCPA was detected up to 0.54 µg/L in surface waters and up to 5.5 µg/L in groundwater (WHO 2011). Background intakes may be similar to those considered for 2,4-D, which is essentially negligible (where these products are not used).

3.4              Identification of Toxicity Reference Values

3.4.1        Classification

The International Agency for Research on Cancer (IARC 1987) has classified chlorophenoxy herbicides as Group 2B—possibly carcinogenic to humans. Information provided in the IARC evaluation relates more specifically to MCPA and mecoprop. No evaluation is available for MCPB.

 

US EPA has not classified MCPA, MCPB or mecoprop.

3.4.2        Review of Available Values/Information

There is limited information on the assessment of carcinogenicity and genotoxicity for these compounds. WHO (2011) notes that recent studies on rats and mice do not indicate that MCPA was carcinogenic and there is only limited and inconclusive data on the genotoxicity of MCPA. Limited studies available on MCPB and mecoprop were negative with respect to genotoxicity. On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for these herbicides. The following are available from Level 1 Australian and International sources:

3.4.2.1       MCPA

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.011 mg/kg/day

MCPA has been assessed with a health-based guideline of 0.04 mg/L based on a TDI of 0.011 mg/kg/day based on a NOEL of 1.1 mg/kg/day from a 2-year study in rats, and an uncertainty factor of 100

OCS (2012)

ADI = 0.01 mg/kg/day

The ADI is noted to have been set in April 1994 and is based on a NOEL of 1.1 mg/kg/day (as considered in the ADWG (NHMRC 2011)).

International

WHO (2011)

TDI = 0.0005 mg/kg/day

The TDI was derived on the basis of a NOAEL of 0.15 mg/kg/day associated with renal and liver toxicity observed in a 1-year feeding study in dogs, and an uncertainty factor of 300. It is noted that the current guideline has remained unchanged since first derived in 1993. MCPA is included in the rolling revisions to the WHO DWG (2011) with no significant revisions issued to date.

ATSDR

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.0005 mg/kg/day

 

The RfD (last reviewed in 1987) is derived based on the same study and evaluation provided in the WHO DWG (2011).

3.4.2.2       MCPB

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

No evaluation available

 

OCS (2012)

ADI = 0.01 mg/kg/day

The ADI is noted to have been set in May 1994 and is based on a NOEL of 1.1 mg/kg/day.

International

WHO (2011)

No quantitative value available

Insufficient data was available to establish a guideline value for MCPB in drinking water.

ATSDR

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.01 mg/kg/day

 

The RfD (last reviewed in 1991) is derived based on a NOEL of 12 mg/kg/day associated with reproductive effects in a 13-week feeding study with dogs, and an uncertainty factor of 1000.

3.4.2.3       Mecoprop (MCPP)

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

No evaluation available

 

OCS (2012)

ADI = 0.01 mg/kg/day

The ADI is noted to have been set in July 1998 and is based on a NOEL of 1 mg/kg/day, and an uncertainty factor of 100.

International

WHO (2011)

TDI = 0.0033 mg/kg/day

The TDI was derived on the basis of a NOAEL of 1 mg/kg/day associated with kidney effects in 1- and 2-year studies in rats, and an uncertainty factor of 300. It is noted that the current guideline has remained unchanged since first published in 1996. Mecoprop is included in the rolling revisions to the WHO DWG (2011) with no significant revisions issued to date.

ATSDR

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.001 mg/kg/day

 

The RfD (last reviewed in 1990) is derived based on a NOEL of 3 mg/kg/day associated with kidney effects in a 90-day rat feeding study, and an uncertainty factor of 3000.

 

The available evaluations in relation to MCPA, MCPB and mecoprop are all dated (none more recent than 1996) and are based on limited databases of studies. In relation to MCPB, the evaluations available from OCS (2012) and US EPA are consistent. In relation to MCPA and mecoprop, the critical studies identified for the determination of the point of departure differ between the OCS and WHO/US EPA evaluations. The subsequent application of uncertainty factors (with WHO/US EPA more conservative) also differs. Insufficient data is available to support any one evaluation, hence preference has been given to the Australian values adopted by OCS (2012), which have also been adopted in the derivation of the Australian Drinking Water Guidelines (NHMRC 2011). On this basis, the current Australian ADIs (as presented by OCS (2012)) have been adopted for the derivation of soil HILs.

 

No dermal or inhalation-specific studies or data are available. For the presence of MCPA, MCPB and mecoprop in soil (not during use) it is considered appropriate to consider use of the available ADI for all pathways of exposures.

3.4.3        Recommendation

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

Recommendation for MCPA, MCPB and Mecoprop
Oral TRV (TRVO) = 0.01 mg/kg/day (OCS 2012) for each compound, 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 
Note that background intakes in areas where herbicides are used need to be considered on a site-specific basis.

 

3.5              Calculated HILs

On the basis of the above, the following HILs have been derived for MCPA, MCPB and mecoprop (as individual compounds) (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

600

43

--

57

<1

Residential B

900

16

--

84

<1

Recreational C

800

27

--

73

<1

Commercial D

5000

12

--

88

<1

-- Pathway not included in derivation of HIL

 

3.6              References

FSANZ 2003, The 20th Australian Total Diet Survey, a total diet survey of pesticide residues and contaminants, website: http://www.anzfa.gov.au/.

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

HSDB (2010), Hazardous Substances Data Bank, online database available from: http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB.

IARC 1987, Summaries and Evaluations, Chlorophenoxy herbicides, Supplement 7, (1987), p.256, 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 1995, Technical Guidance Manual, Assessing Dermal Exposure from Soil, US EPA Region 3, December 1995, available from: http://www.epa.gov/reg3hwmd/risk/human/info/solabsg2.htm.

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

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

4                  Picloram

4.1              General

Limited data is available on picloram, however reviews of this compound in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (Health Canada 1988; US EPA 1995a; OEHHA 1997). The following provides a summary of the key aspects of picloram that are relevant to the derivation of a soil HIL.

 

Picloram is a member of the pyridine carboxylic acid group and is manufactured in a number of forms. Picloram acid is only manufactured as an intermediate product in the production of herbicides whereas the amine salt, potassium salt and ester derivatives of picloram are produced as commercial herbicides. Technical grade picloram acid is an off-white to brown powder. It is slightly soluble in water and the amine and potassium salt derivatives are highly soluble. The ester derivative, however, is insoluble in water (US EPA 1995a).

 

Picloram acid and its derivatives have been used since the 1960s as a systemic herbicide to control woody plants and broadleaf weeds in rights of way, forestry, rangeland and pasture. In Australia, picloram derivatives are used to control weeds in winter cereals and linseed crops and to control a number of environmental and noxious weeds (APVMA 2009).

 

Picloram products are commonly contaminated with hexachlorobenzene (HCB). The presence of HCB in picloram affects the assessment of toxicity in a number of studies. Limited data is available for picloram alone. Available data also show that picloram is synergistic with several common herbicides (in particular 2,4-D, atrazine and alachlor) with respect to its toxicity to mammals and fish (NCAP 1998).

4.2              Previous HIL

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

4.3              Significance of Exposure Pathways

4.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of picloram, 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.

4.3.2        Dermal absorption

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

4.3.3        Inhalation of Dust

Picloram 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

Most carboxylic herbicides are toxic to plants and, as such, will be phytotoxic to almost all broadleaf crops including tomatoes, grapes and fruit trees well before plant uptake into edible portions of fruit and vegetable crops is of significance. Hence the uptake of these compounds into home-grown produce has not been considered in the derivation of HIL A.

 

Note that the phytotoxic effects of these compounds may need to be addressed on a site-specific basis if detected in soil.

4.3.5        Intakes from Other Sources – Background

Limited data is available for the assessment of background intakes of picloram. Picloram products are currently registered for use in Australia and the compound is considered persistent in the environment. Picloram is not included in the Australian Total Diet Surveys (FSANZ 2003; FSANZ 2011) and there is no data regarding concentrations in drinking water or air in Australia. Away from areas where picloram products are used, exposure by the general public is expected to be low. Review by US EPA (1995b) suggests that dietary intakes comprise only 0.5% of the threshold reference value (RfD) adopted (0.2 mg/kg/day) for most of the US population, with intakes from non-nursing infants highest at 1.9% of the RfD adopted. Review by Health Canada (1988) also noted the maximum dietary intake of picloram is estimated to be negligible, based on available data in Canada and the USA. On this basis, intakes from other sources have been assumed to be negligible in the derivation of HILs.

4.4              Identification of Toxicity Reference Values

4.4.1        Classification

The International Agency for Research on Cancer (IARC 1991) has classified picloram as Group 3not classifiable.

 

US EPA has not classified picloram.

4.4.2        Review of Available Values/Information

Studies associated with the assessment of carcinogenicity of picloram are noted to be affected by the presence of HCB as a contaminant/impurity. Hence a number of reviews of carcinogenicity are conflicting. The review by IARC noted limited evidence of carcinogenicity for technical grade picloram in experimental animals. In general, the available data suggests the picloram is not genotoxic (Health Canada 1988; US EPA 1995) or at most weakly mutagenic (OEHHA 1997). On the basis of the limited available information, it is considered appropriate that a threshold dose-response approach be adopted for picloram. The following are available from Level 1 Australian and International sources:

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

TDI = 0.07 mg/kg/day

The current ADWG (NHMRC 2011) derive a guideline of 0.3 mg/L derived from a NOEL of 7 mg/kg/day associated with increased liver weights in a short-term dietary study in rats, and an uncertainty factor of 100.

OCS (2012)

ADI = 0.07 mg/kg/day

The ADI is noted to have been set in February 1987 and is based on a NOEL of 7 mg/kg/day (as considered in the ADWG, noted above).

International

WHO(2011)

No evaluation available

 

ATSDR

No evaluation available

 

Health Canada (1988)

NDI = 0.02 mg/kg/day

Negligible daily intake (NDI) derived on the basis of a NOAEL of 20 mg/kg/day associated with liver and kidney changes in rat and mouse studies, and an uncertainty factor of 1000.

US EPA (IRIS 2012)

RfD = 0.07 mg/kg/day

 

The RfD (last reviewed in 1987) is derived based on the same study and evaluation provided in the ADWG (NHMRC 2004). Value also derived by OEHHA (1997).

US EPA (1995)

RfD = 0.2 mg/kg/day

RfD calculated based on a NOEL of 20 mg/kg/day from a 2-year chronic rat feeding study, and an uncertainty factor of 100.

 

Limited quantitative data is available for picloram, however it is recommended that the current Australian ADI/TDI be adopted for the derivation of a soil HIL.

 

No dermal or inhalation-specific studies or data are available. For the presence of picloram in soil (not during use), it is considered appropriate to consider use of the available ADI for all pathways of exposures.

4.4.3        Recommendation

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

Recommendation for Picloram
Oral TRV (TRVO) = 0.07 mg/kg/day (OCS 2008; NHMRC 2004; NHMRC 2009) 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 
Note that background intakes in areas where herbicides are used need to be considered on a site-specific basis.

 

4.5              Calculated HILs

On the basis of the above, the following HILs have been derived for picloram (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

4500

43

--

57

<1

Residential B

6600

16

--

84

<1

Recreational C

5700

27

--

73

<1

Commercial D

35 000

12

--

88

<1

-- Pathway not included in derivation of HIL

 


 

4.6              References

APVMA 2009, Chemicals Nominated for Review, last update unknown, accessed July 2009, Australian Pesticides and Veterinary Medicines Authority (APVMA), http://www.apvma.gov.au/chemrev/ChemRevProgram.shtml.

FSANZ 2003, The 20th Australian Total Diet Survey, a total diet survey of pesticide residues and contaminants. website: http://www.anzfa.gov.au/.

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

Health Canada 1988, Picloram, Environmental and Workplace Health, reviewed in 1990, available from: http://www.hc-sc.gc.ca/ewh-semt/pubs/water-eau/picloram-piclorame/index-eng.php.

IARC 1991, Summaries and Evaluations, Picloram, vol. 53 (1991), p,481, 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.

NCAP 1998, ‘Picloram, Herbicide Fact Sheet’, Northwest Coalition for Alternatives to Pesticides, Journal of Pesticide Reform, Spring 1998, vol. 18, No.1.

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.

OEHHA 1997, Public Health Goal for Picloram in Drinking Water, prepared by Pesticide and Environmental Toxicology Section, Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, December 1997.

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 1995a, Reregistration Eligibility Decision (RED) Office of Prevention, Pesticides and Toxic Substances, United States Environment Protection Agency, Washington, DC.

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

 

 

 

 

 

 

5                  Atrazine

5.1              General

Several comprehensive reviews of atrazine in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (ATSDR 2003; NRA 1997; APVMA 2008; IARC 1999). The following provides a summary of the key aspects of atrazine that are relevant to the derivation of a soil HIL.

 

Atrazine is the common name for the compound 6-chloro-N2-ethyl-N4-isopropyl-1,3,5-triazine-2,4-diamine which is an odourless white powder or colourless crystal (ATSDR 2003). Commercially manufactured atrazine is typically greater that 90% pure. Common impurities include dichlorotriazines, hydroxytriazines, tris(alkyl)aminotriazines, simazine, propazine and sodium chloride (ATSDR 2003). Atrazine is manufactured as a liquid, granules or wettable powder and can also be formulated in combination with other herbicides such as ametryn, amitrole, hexazinone, metalochlor, glyphosate and dicamba (NRA 1997).

 

Atrazine is one of the most widely used herbicides in Australian agriculture and has been used since the 1960s (NRA 1997). It is primarily used to control broadleaf weeds and some grasses between crops such as sorghum, maize, lupins, sugar cane and triazine-tolerant canola. Atrazine is also widely used to control weeds and some grasses by the forestry industry in pine and eucalyptus plantations (NRA 1997; NHMRC 2011). Non-agricultural uses in Australia such as the spraying of weeds along fence lines, irrigation channels, drains, driveways and footpaths were discontinued in 1995 (NRA 1997).

 

Regulatory actions (by the National Registration Authority for Agricultural and Veterinary Chemicals [APVMA]) undertaken in 1997 included cancellation of industrial and non-agricultural uses of atrazine (home garden uses and all commercial turf uses), deletion of use patterns and maximum residue limits (MRLs) for label claims for which there were no current use patterns (citrus, grapes and pineapples) and the introduction of a range of label instructions to reduce the risk of atrazine entering waterways. In addition, registrants were required to provide additional residue and monitoring data.

 

The APVMA has initiated a project to re-examine the possibility that the triazines (atrazine and related chemicals with a similar MoA) may have unintended harmful effects on humans, taking into account ongoing research into a newly hypothesised endocrine MoA. This project will take into account international reports, such as the work of the Joint Meeting on Pesticide Residues (JMPR).

 

Registrants who have a product whose label specifies a claim for weed control on triazine-tolerant canola will be required to either generate additional data or include an additional label restraint that specifies that atrazine must not be used post-emergence on triazine-tolerant canola grown on raised beds.

 

After consideration of the additional assessments completed after 1997, APVMA accepts the recommendations of OCS and the 2004 recommendations of DEWHA, and the following regulatory actions have been applied:

1.      Active constituent approvals have been affirmed.

2.      Existing label instructions have been deemed to be inadequate and the most recently approved labels have been amended as follows:

·         Labels have been amended to specify additional restraints to further reduce the risk of contamination of waterways.

·         Withholding period instructions have been amended.

·         Herbicide resistance reporting details have been added to labels.

These variations to label instructions satisfy the requirements for continued registration of products; and so

3.                  Product registrations have been affirmed.

4.                  To ensure that all labels are in line with the recommendations of the 2008 report, any previously approved labels that do not contain the amended instructions have been cancelled.

As an associated outcome of the review, changes will be made to the MRL Standard to align entries in the standard with existing approved use patterns.

5.2              Previous HIL

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

5.3              Significance of Exposure Pathways

5.3.1        Oral Bioavailability

Insufficient data is available to adequately define the bioavailability of atrazine 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 atrazine from soil. Hence the default value 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

Atrazine 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

Atrazine is used as a herbicide and, as such, is phytotoxic to almost all broadleaf weeds and plants. Some plants are more sensitive than others to residues of atrazine in the soil, however in general, phytotoxicity will occur well before plant uptake into edible portions of fruit and vegetable crops is of significance. Hence the uptake of these compounds into home-grown produce has not been considered in the derivation of an HIL A.

 

Note that the persistence of atrazine in soil and potential for phytotoxic effects may need to be addressed on a site-specific basis if detected in soil.

5.3.5        Intakes from Other Sources – Background

Reviews of potential intakes from sources other than soil (primarily food) by NRA (1997), NHMRC (2011) and RIVM (2001) suggested these intakes were essentially negligible. Further review of residue data by APVMA (2008) noted that, when atrazine was used in accordance with the revised label directions, residues were unlikely to pose a risk to human health. Potential exposures during application of atrazine products may require further consideration on a site-specific basis; however exposures by the general public (in areas away from application) are negligible.

5.4              Identification of Toxicity Reference Values

5.4.1        Classification

The International Agency for Research on Cancer (IARC 1999) has classified atrazine as Group 3not classifiable. US EPA has not classified atrazine.

5.4.2        Review of Available Values/Information

The available data reviewed by JMPR (2007) and APVMA (2008) suggested that atrazine was not likely to pose a carcinogenic risk to humans. Review by JMPR (2007) and RIVM (2001) suggested that based on the weight of evidence, atrazine was not genotoxic. There is some evidence that it can induce mammary tumours in rats as a result of hormonal changes, but the mechanism is believed to be non-genotoxic. On the basis of the available information, it is considered appropriate that a threshold dose-response approach be adopted for atrazine.

 

The following are available from Level 1 Australian and International sources:

Source

Value

Basis/Comments

Australian

ADWG (NHMRC 2011)

ADI = 0.005 mg/kg/day

Current ADWG (NHMRC 11) of 0.04 mg/L based on 50% intake from drinking water and an ADI of 0.005 mg/kg/day as referenced from the TGA (NRA 1997).

OCS (2012)

ADI = 0.005 mg/kg/day

The ADI of 0.005 mg/kg/day is noted to be based on a NOEL of 10ppm associated with mammary tumours from a 24-month female rat study, and a 100-fold safety factor. This value was set in December 1996.

NRA (1997)

ADI = 0.005 mg/kg/day

The NRA (1997) review identified the relevance of adopting an ADI of 0.005 mg/kg/day for atrazine. This value has been reconfirmed in the update provided by APVMA (2008). However the review noted that APVMA has initiated a project to re-examine the possibility that the triazines may have harmful endocrine effects, including updates available from JMPR. APVMA also note that US EPA is currently reviewing atrazine.

International

JMPR (2007)

ADI = 0.02 mg/kg/day

Review of atrazines by the Joint FAO/WHO Meeting on Pesticides Residues (JPMR, 2007) identified a group ADI (for atrazine, diethyl-atrazine, di-isopropyl-atrazine and diaminochlorotriazine) of 0-0.02 mg/kg/day based on oestrous cycle disruption.

WHO (2011)

ADI = 0.02 mg/kg/day

Group ADI for atrazine and its chloro-s-triazine metabolites (reviewed in 2011) is based on a NOAEL of 1.8 mg/kg/day identified on the basis of luteinizing hormone surge suppression and subsequent disruption of the oestrous cycle seen at

3.6 mg/kg body weight per day in a 6-month study in rats, using a safety factor of 100

RIVM (2001)

TDI = 0.005 mg/kg/day

TDI based on a NOAEL of 0.5 mg/kg/day associated with reproductive effects in rats, and a 100-fold uncertainty factor.

ATSDR

No evaluation available

 

US EPA (IRIS 2012)

RfD = 0.035 mg/kg/day

 

The US EPA (available from IRIS) have derived an oral RfD of 0.035 mg/kg/day. The value was last reviewed in 1993 and is based on a NOAEL of 3.5 mg/kg/day associated with decreased body weight gain from a 2-year rat study, and an uncertainty factor of 100.

 

While the most recent review by WHO (2011) provides a less conservative ADI, the current Australian ADI of 0.005 mg/kg/day is considered relevant and appropriate for consideration in the derivation of a soil HIL.

 

No dermal or inhalation-specific studies or data are available. For the presence of atrazine in soil (not during use in herbicide products), it is considered appropriate to consider use of the available threshold ADI for all pathways of exposures.

5.4.3        Recommendation

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

Recommendation for Atrazine
Oral TRV (TRVO) = 0.005 mg/kg/day (NHMRC 2011; OCS 2008; APVMA 2008) 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 
Note that background intakes in areas where herbicides are used need to be considered on a site-specific basis.

 

5.5              Calculated HILs

On the basis of the above, the following HILs have been derived for atrazine (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

320

43

--

57

<1

Residential B

470

16

--

84

<1

Recreational C

400

27

--

73

<1

Commercial D

2500

12

--

88

<1

-- Pathway not included in derivation of HIL

 

5.6              References

APVMA 2008, Atrazine, Final Review Report and Regulatory Decision, Australian Pesticides & Veterinary Medicines Authority, March 2008.

ATSDR 2003, Toxicological Profile for Atrazine, US Department of Health and Human Services, ATSDR, September 2003, available from http://www.atsdr.cdc.gov/ToxProfiles/tp.asp?id=338&tid=59.

IARC 1999, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Some Chemicals That Cause Tumors of the Lungs or Urinary Bladder in Rodents and Some Other Substances, World Health Organization, International Agency for Research on Cancer, Lyon, France.

JMPR 2007, Pesticide Residues in Food, 2007, Joint FAO/WHO Meeting on Pesticide Residues, FAO Plant Production Paper 191, 2007.

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 1997, Review Summary on the NRA Review of Atrazine, Existing Chemicals Review Program, National Registration Authority for Agricultural and Veterinary Chemicals 1997, National Registration Authority for Agricultural and Veterinary Chemicals, Commonwealth of Australia, Canberra, 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 1995, Technical Guidance Manual, Assessing Dermal Exposure from Soil, US EPA Region 3, December 1995, available from: http://www.epa.gov/reg3hwmd/risk/human/info/solabsg2.htm.

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

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.

 

 

 

 

 

6                  Chlorpyrifos

6.1              General

Several reviews of chlorpyrifos in the environment and its toxicity to humans are available and should be consulted for more detailed information not presented in this summary (ATSDR 1997; WHO 2004; NRAAVC 2000; APVMA 2009; Taylor & Di Marco 2003). The following provides a summary of the key aspects of chlorpyrifos that are relevant to the derivation of a soil HIL.

 

Chlorpyrifos is the common name for the organophosphorous insecticide O,O-diethyl O-3,5,6-trichloro-2-pyridyl phophorothioate. Pure chlorpyrifos is an odourless, white to colourless crystalline solid. The compound is non-polar and therefore has a low solubility in water and an affinity for organic substances. It is also thermally sensitive at temperatures over 50 °C and decomposes at 130 °C (NRAAVC 2000; WHO 2004).

 

Technical grade chlorpyrifos has a minimum purity of 940 to 990 g/kg. It is a white to light yellowish brown crystalline solid with a mild mercaptan odour. Commercial formulations of chlorpyrifos are generally produced as a concentrated emulsion, liquid, wettable powder, dust, solid bait or granules (NRAAVC 2000).

 

Chlorpyrifos has been widely used in the Australian agricultural industry since the mid-1960s as it is reportedly less harmful to beneficial insects and is a useful tool in insecticide resistance management programs (NRAAVC 2000). It is used to control insects in soil and on crop foliage including fruit (pome, stone and citrus fruit, strawberries, figs, pineapples, kiwifruit and bananas), nuts, vines, vegetables (potatoes, asparagus), grains (rice, cereals, maize, sorghum), cotton, mushrooms, sugar cane, turf and ornamental plants (NRAAVC 2000). In industrial/commercial and domestic buildings chlorpyrifos is used to control termites, cockroaches, spiders, ants, mosquitoes and fleas and is generally sprayed in the sub-floor region during construction or applied around the building. It is also registered for use in dog and cat flea collars, sprays and shampoos. While the number of products containing chlorpyrifos changes on a yearly basis[1], in 2000 there were 164 products registered in Australia that contained chlorpyrifos (NRAAVC 2000).

 

In contrast to Australia, the US banned all domestic use of chlorpyrifos in 2001.