Addendum for PCP

Prepared by:

BiPRO GmbH

Mai 2010

Table of Content

1 Introduction........................................................................................................2

2 Short risk profile of PCA...................................................................................3

3 Transformation of PCP to PCA.......................................................................16

4 Potential sources of PCA in remote regions.................................................19

4.1 PCP......................................................................................................194.2 HCB and HCH (α-HCH and γ-HCH).....................................................20

5 Impurities of dioxins and furans during the production of PCP.................23

6 Link between PCP and the occurrence of dioxins and furans in the environment.....................................................................................................28

7 References.......................................................................................................34

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1 Introduction

This report is an addendum to the report “Pentachlorophenol, Dossier prepared in support of a proposal of pentachlorophenol to be considered as a candidate for inclusion in the Annex I to the Protocol to the 1979 Convention on Long-Range Transboundary Air Pollution on Persistent Organic Pollutants (LRTAP Protocol on POPs)” [LRAT dossier, 2008].

The original report for pentachlorophenol (PCP) was finalized by Poland in May 2008. Based on the information provided in the report it was concluded that PCP fulfils the indicative values for long range transport and toxicity. The fulfilment of the indicate value for bioaccumulation was considered to be doubtful and the indicative value for persistence not to be met. In this respect, it was stated that PCP does not meet the indicative value for persistence for water, sediment and soil. The authors mentioned that the metabolites (e.g. pentachloroanisole (PCA)) should be considered as well to provide a complete picture of the risks of PCP and that consideration of the impurities in technical PCP (e.g. dioxins (PCDDs), furans (PCDFs) and hexachlorobenzene (HCB)) may lead to another conclusion in meeting the indicative values.

Within the subsequent “Lead Reviewer’s Track A Summary of Expert Reviews of PCP”, the reviewers concluded that the POPs characteristics of PCA have been described in the PCP dossier (May 2008) but not really evaluated against the criteria [Summary of reviews, 2009]. All reviewers had concerns about PCA. PCA was considered one of the major metabolites in the environment and in biological systems. Based on available and scientific information, all reviewers concluded that PCA may fulfil some and/or all of the POPs indicative numerical values in Executive Body Decision 1998/2. The POPs indicative numerical values for the biological and environmental degradation products of PCP are not clearly addressed in the PCP dossier (May 2008). Therefore, based on available information, there were some different opinions about the fate and biological effects resulting from PCP long-range transboundary atmospheric transport between the reviewers. As a consequence, it has to be clarified whether PCA fulfils the POP criteria. Furthermore, manufacturers of PCP expressed doubts whether PCA detected in remote areas results from PCP metabolism or other precursors like HCB and hexachlorohexanes (HCH) [Letter PCP task force, 2009]. Therefore, there exists an information need regarding the conditions and the rates of transformation of PCP to PCA.

Except from one reviewer, who stated that dioxins and furans are outside the scope of the review, the other reviewers were quite unanimous in their judgement that the use of PCP is inseparably coupled to the emission of dioxins and furans, due to the impurities as a result of all known production processes, due to burning of treated wood and due to degradation in the environment . In chapter 4 of this addendum information regarding the PCDD and PCDF impurities in PCP products resulting from the production processes is provided. The purpose of chapter 5 is to answer the question whether a causal connection between the use of PCP products and the occurrence of PCDDs and PCDFs in the environment can be established.

To ensure that the POP dossier on PCP contains the latest relevant information on the POP characteristics of its metabolite PCA, this addendum with an update on the available literature and an assessment of PCA including an evaluation against the criteria in Executive Body Decision 1998/2, has been elaborated. A database literature research as well as online information was used to gather new information on toxicological and ecotoxicological data of PCA, transformation of PCP to PCA and connections between PCDD/F content of PCP products and occurring of PCDDs and PCDFs in the environment.

2 Short risk profile of PCA

Identity

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Chemical structure:

Formula: C7H3Cl5O

CAS registry number: 1825-21-4

CAS chemical name: Pentachloroanisole

IUPAC name: 1,2,3,4,5-Pentachloro-6-methoxybenzene

SMILES notation: COC1=C(C(=C(C(=C1Cl)Cl)Cl)Cl)Cl

Synonyms: 1,2,3,4,5-Pentachloro-6-methoxy-benzene; 2,3,4,5,6-pentachloro-anisol; Benzene, pentachloromethoxy-; ether,methylpentachlorophenyl; Methyl pentachlorophenate; Methyl pentachlorophenyl ester; Methyl pentachlorophenyl ether, PCA

Molecular weight: 280.362 g/mol

Vapour pressure (25 °C): 0.0459 Pa at 25 °C (Calculation (MPBWIN v1.42) according to modified grain method) [LRAT dossier 2008]. 0.0458 Pa (Modeled via EPIWIN) [Summary of reviews, 2009]0.0933 Pa [Dobbs and Grant, 1980]

Log Kow: 5.30 (KOWWIN v1.67) [LRAT dossier 2008]5.45 Experimentally by [Opperhuizen and Voors, 1987]

Henry’s law constant: 1.94x 10-3 atm-m3/mole (1/H = 12.7 Estimated using HENRYWIN v 3.10) [LRAT dossier 2008]

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Toxicity and Ecotoxicity

As a result of the literature review which was carried out to gather information on the POP characteristics of PCA, it must be noted that literature data concerning the toxicity of PCA is limited to this date. The metabolism of PCA has been taken into consideration when assessing the toxicological and ecotoxicological potential of PCA.

Metabolism of PCA:

Male Sprague-Dawley rats and New Zealand White rabbits were administered 14C-labelled PCA in corn oil by gavages as single doses of 25 mg/kg and were then placed in individual metabolism cages for as long as 4 days. Peak blood level of radioactivity occurred 6 hr after administration of the dose to rats and between 3 and 4 hr in rabbits; the blood elimination half-life ranged from 8 to 15 hr in rats and averaged 6 hr in rabbits. Rats excreted an average of 54.2% of the administered radiolabel in the urine and 32.4% in the faeces during the 96 hr following the dose; rabbits excreted an average of 84.2 and 13.1% of the radiolabel in the urine and faeces, respectively, during this time. Examination of the metabolites in the rat showed that 60% of the urinary radioactivity was attributable to tetrachlorohydroquinone (TCH), 3% to free PCP and 29% to conjugated PCP. Faecal metabolites were PCP (85.7%), TCH (4.3%) and polar metabolite(s) (10%). In the rabbit, 58% of the urinary radioactivity was attributable to TCH, 8% to free PCP and 34% to conjugated PCP. Faecal metabolites consisted of PCP and conjugated material [Ikeda et al., 1994].

Yuan J.H. et al. (1993) presented results from a “Toxicology and Carcinogenesis Study of PCA in F344 Rats and B6C3F Mice” within the US National Toxicology Program [U.S. Department of Health and Human Services, 1993]. They studied toxicokinetics of PCA in F344 rat and B6C3F1 mouse of both sexes by gavages at doses of 10, 20 and 40 mg/kg and by i.v. at 10 mg/kg. PCA was rapidly demethylated to PCP in both rat and mouse and the resulting PCP plasma concentrations were much higher than that of parent PCA due to the much smaller apparent volume of distribution of PCP. Peak plasma concentrations of PCA and PCP increased with dose in both rat and mouse. Bioavailability of PCA was low in both rat and mouse and was sex independent. The high plasma concentrations and relatively long biological half-life of PCP in both species after both i.v. and oral dosing with PCA indicate possible bioaccumulation of PCP upon multiple oral administrations of PCA [Yuan et al., 1993].

PCP and PCA were rapidly taken up by rainbow trout exposed to these compounds at 0.025 mg/l in water. After exposure of trout to PCP for 24 hr, the liver, blood, fat, and muscle contained 16, 6.5, 6.0, and 1.0 μg/g, respectively. The concentrations of PCA in the same tissues after an exposure to [ 14C] PCA were of the same order of magnitude as was found with PCP except that fat contained as much as 80 μg/g. Elimination rates for 14C from the blood, muscle, fat, and liver after a similar exposure were different for PCA and PCP. The half-lives for PCP residues in the blood, liver, fat, and muscle were 6.2, 9.8, 23 and 6.9 hr, respectively, while PCA was more persistent having half-lives in these same tissues of 6.3, 6.9, 23, and 6.3 days. Thin-layer chromatographic and GC-MS analyses of the tissues of the PCP-exposed trout indicated that there was no methylation of PCP in any of the tissues studied. Bile from PCP-exposed trout contained high concentrations (250 μg/g) of PCP, mostly as the glucuronide conjugate, but no other metabolites were detected. However, bile from PCA-exposed trout contained PCP glucuronide (10 μg/g) as well as PCA, indicating demethylation of this compound in vivo by rainbow trout [Glickman et al., 1977].

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Toxicity of PCA

PCP and PCA were investigated for their acute toxicity in male (m) and female (f) mice. The substances were administered orally and intraperitoneally, respectively. The oral LD50 values were: 129±9 (m) and 134±9 (f) mg/kg for PCP, 318±22 (m) and 331±22 (f) mg/kg for PCA. The intraperitoneal LD50 values were: 59±4 (m) and 61±4 (f) mg/kg for PCP, 281 ±20 (m) and 293±20 (f) mg/kg for PCA [Renner et al., 1986]. Oral toxicity GHS categories are determined by Oral LD50 per mg/kg bodyweight. GHS Category 4 Acute-Toxicity Oral is fulfilled for LD50 values between 300 and 2000 mg/kg, category 3 for LD50 values >50 - <300 mg/kg. According to the data of Renner et al. (1986) PCP would be classified as toxic cat.3 and PCA as cat. 4.

The relative toxicity of PCP and 25 of its identified intermediates of microbial transformation have been evaluated in the static Tetrahymena pyriformis population growth assay by Bryant et al. (1994).It was observed that methylation of the hydroxy group modestly increased hydrophobicity. Since there was a decrease in reactivity, methylation of chlorophenols resulted in a decrease in toxicity. Toxicity of anisole and its chloro-derivatives was correlated with hydrophobicity. The reduction in toxicity of these aromatic ethers in comparison to phenols is a reflection of the change in molecular reactivity and mechanism of toxic action. It was noted that for most chemicals, toxicity is a combination of hydrophobicity and reactivity. While phenols act as weak acid respiratory uncouplers or polar narcotics, ethers act as nonpolar narcotics [Bryant et al., 1994]. Cserjesi et al. (1972) also reported that PCA was less toxic than PCP to Trichoderma viirgatum, Cephaloascus frgrans and Penicillium sp, as well as to fish in laboratory toxicity tests [Cserjesi et al., 1972]. However, even if PCA might not be as toxic as PCP the increased hydrophobicity resulting in longer body half-lives and higher potential to bioaccumulate should be considered when evaluating potential risks to environmental and human health.

PCA was evaluated for its mutagenic potential in the L5178Y TK+/TK- mouse lymphoma forward mutation assay using established procedures [McGregor et al., 1987]. Six experiments were conducted: two without metabolic activation and four with metabolic activation. The dose levels tested in these experiments ranged from 0-500 ug/ml. The two experiments without metabolic activation were discarded because no clear mutagenic response was obtained at dose levels where PCA did not precipitate. Significant mutagenic responses were obtained in the remaining four experiments. Thus, PCA was positive in these tests and the lowest effective dose tested was 31.25 ug/ml. It was concluded that there was sufficient evidence to suggest that pentachloroanisole can induce increases in mutant fraction in the presence of S9 mix. It is further reported that in the Salmonella test, positive responses were obtained with PCA by Mortelmans et al. (1986). It was also reported that according to NTP data PCA was positive in the SCE test, but negative in the chromosomal aberrations test [NTP 1989]. Based on the results of the study and the cited further evidence in other test systems it can be concluded that PCA has to be considered as having mutagenic properties.

Toxicology and Carcinogenesis Studies of PCA in F344 Rats and B6C3F Mice (Feed Studies) were performed in the scope of the National Toxicology Program. Under the conditions of these 2 year gavage studies there was some evidence of carcinogenic activity of PCA in male F344/Nrats based on increased incidences of benign pheochromocytomas of the adrenal medulla. There was equivocal evidence of carcinogenic activity of PCA in female F344/N rats based on marginally increased incidences of benign pheochromocytomas of the adrenal medulla. There was some evidence of carcinogenic activity of PCA in male B6C3F1 mice based on increased incidences of benign pheochromocytomas of the adrenal medulla and hemangiosarcomas of the liver. There was no evidence of carcinogenic activity of PCA in female B6C3F1 mice given doses of 20 or 40 mg/kg. PCA administration was associated with increased incidences of adrenal medulla hyperplasia in female rats and increased incidences of pigmentation in the renal tubule epithelium, olfactory epithelium, and hepatocytes

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of male and female rats. In addition, decreased incidences of pancreatic adenomas and focal hyperplasia in male rats and decreased incidences of mammary gland fibroadenomas and uterine stromal polyps and sarcomas (combined) in female rats were observed. Hyperthermia-related lesions in male rats receiving 20 or 40 mg/kg were considered indirectly related to PCA administration. PCA administration was associated with increased incidences of adrenal medulla hyperplasia and hypertrophy and hepatocellular mixed cell foci in male mice. In male and female mice, non neoplastic liver lesions associated with PCA administration included hepatocellular cytologicalteration, Kupffer cell pigmentation, biliary tract hyperplasia, and subacuteinflammation [U.S. Department of Health and Human Services, 1993]. The results show that PCA should be considered as a potential carcinogen. However, the present knowledge is not sufficient for a definite assessment. Nevertheless, it can be concluded that there is some evidence that PCA possesses carcinogenic properties.

Male and female Sprague-Dawley (Spartan) rats were exposed to dietary levels of 60, 200 or 600 ppm PCA for 181 days, through mating and pregnancy. The daily intakes of PCA were 0, 4, 12 or 41 mg/kg body weight. An intake of 41 mg PCA/kg/day was associated with a decrease in the number of corpora lutea and increase in embryolethality. PCA exposure also resulted in reductions in fetal body weight and crown-rump lengths of males at 4 and 41 mg/kg/day. Female fetuses were unaffected [Welsh et al., 1987]. The results presented by Welsh et al. (1987) indicate that PCP might be toxic to reproduction.

The toxicity of water from three rivers in the Santee-Cooper drainage of South Carolina was evaluated in a series of on-site studies with larval striped bass Morone saxatilis. Mortality and swimming behaviour were assessed daily for larvae exposed to serial dilutions of water collected from the Santee, Congaree, and Wateree rivers. After 96 h, cumulative mortality was 90% in the Wateree River, and a dose-response pattern was evident in serial dilutions of the water. Larvae exposed to water from the Santee and Congaree rivers swam lethargically, but no appreciable mortality was observed. Acutely toxic concentrations of inorganic contaminants were not detected in the rivers; however, PCA was twice as high in the Wateree River as it was in the other two rivers. Phenolic compounds may have contributed to larval mortality in the Wateree River and to lethargic activity of larvae in the Santee and Congaree rivers [Finger et al., 1988].

An overview on the results of different further studies presenting data on acute toxicity of PCA to animals is provided in Table 1 These results also support the findings of the above mentioned studies and show that PCA can induce adverse effects in the environment.

Table 1: Toxicity values of PCA. MAC = Minimum affective concentration.

Species Scientific Name

Species Common Name Endpoint Exposure Duration Concentration Reference

Daphnia magna Water flea EC50 2 (days) 27.2 (ug/L) Brooke, L.T., 1991

Cladocera Water flea LC50 n.a. 27 (µg/L) Sanchez-Bayo, 2006

Pimephales promelas Fathead minnow LC50 4 (days) 650 (ug/L) Brooke, L.T., 1991

Pimephales promelas Fathead minnow LC50 4 (days) > 1190 (ug/L) Brooke, L.T., 1991

Hydra attenuate MAC 96 (hours) 10 (µg/ml) Mayura et al., 1991

Mice EC50 n.a. 318 (m) (mg/kg)331 (f) (mg/kg) Renner et al., 1986

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Human exposure to PCA:

The general population is exposed to PCA in food, especially oils and fats, and in ambient air. Dietary exposure may occur by eating contaminated fish and fish products such as fish liver oil. Occupational expose, as well as general population exposure, may occur via dermal contact with soil or wood products that had been treated with PCP. Proposed daily intake rates are 0.56 ng regarding air intake (assume mean conc. 28 pg/m3 [Hoff et al., 1992]) and 0.07 µg (adults), 0.018 µg (infants) and 0.040 µg (toddlers) [Gartrellet al., 1986 b] for food intake (assume conc. of 0.001 µg/kg [Gartrell et al., 1986 a], 70 kg for adults; 0.002 µg/kg (Gartrell et al., 1986 b], 9.2 kg for infants; and 0.003 µg/kg [Gartrell et al., 1986 b], 13.4 kg for toddlers).

Conclusion

The criterion from Executive Body Decision 1998/2 for information on Toxicity and Ecotoxicity to be submitted for the procedure for adding substances to annexes I, II or III to the Protocol on Persistent Organic Pollutants are as follows:

Potential to adversely affect human health and/or the environment

PCA is not industrially produced. Thus, there is only limited data available dealing with its toxicity. Nevertheless, the existing studies and information lead to the conclusion that PCA can be regarded as causing adverse effects on human and environmental health. It seems that PCA has the potential to fulfil the three CMR criteria. The existing data is not sufficient to allow a final assessment of CMR properties. In addition there is some evidence that PCA has the potential to adversely affect the environment. Furthermore, a substance with BCF values as high as PCA can be expected to cause toxicity in aquatic organisms at very low concentrations, only on the basis of narcotic effects [Summary of reviews, 2009]. When assessing the toxicological potential of PCA it also has to be considered that PCA may be rapidly and effective degraded to PCP in living organisms. PCA is demethylated back to PCP. If demethylation within the organism occurs, this may lead to effects equivalent to those of PCP, but at lower external concentrations, because of the higher bioaccumulation potential of PCA. Therefore PCP can be regarded as the effective metabolite of PCA. It has been shown that PCP is highly toxic for human when ingested by humans, moderate to highly toxic to many species of fish, non mutagenic or weakly mutagenic and possibly carcinogenic to humans.

Therefore, PCA on its own and due to the toxicity of its main metabolite (PCP) should be considered to fulfil the criterion from Executive Body Decision 1998/2 for Toxicity and Ecotoxicity.

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Persistence

All the relevant available information on persistence of PCA is included in the Risk Profile UNECE May 2008 [LRAT dossier 2008].

PCA can be photo-oxidized in the atmosphere through reactions with hydroxyl (OH) radicals. The calculated half-life for PCA based on this reaction is 9.8 days, with an atmospheric (OH) concentration of 1.5E6 OH/cm 3

(AopWin v1.92).

In soil PCA is product from methylation of PCP. Several bacteria and fungi may enhance this process (Walter et al. (2004), Okeke et al. (1997), Lamar et al. (1990 a), Lamar et al. (1990 b), Haggblom et al. (1988)). The estimated soil adsorption coefficient (PCKOCWIN v1.66) is 1485. In a laboratory experiment with PCA-contaminated soil concentrations of PCA have been measured over a period of 20 weeks. The PCA concentration of 0.38 μg/g at the beginning was reduced in 5 weeks to 0.18 μg/g and after 20 weeks only of 0.05 μg/g PCA remained. A t1/2 of approximately 5 weeks can be obtained from this study (Haimi et al., (1993)). Under anaerobic conditions PCA is known to be demethylated to PCP (Murthy et al. (1979)). Some fungi are found to enhance mineralization of PCA [Lamar et al., 1990b]. Volatilisation of PCA is also observed in some studies (Walter et al. (2004), Lamar et al. (1990b)) [LRAT dossier 2008].

There are no data on the persistence of PCA in water. The Henry’s Law constant for PCA is estimated as 1.94E-3 atm-m3/mole, using a group estimation method (HENRYWIN v 3.10). This value indicates that PCAwill volatize rapidly from water. Based on this Henry's Law constant, the volatilisation half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 5 m/sec) is estimated at 2.2 hours. The volatilisation half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec) is estimated as 6.9 days. Volatilisation of PCA from water has been argued to be the source of PCA concentrations measured in the air (Atlas et al. (1986)) [LRAT dossier 2008].

Conclusion

The criteria from Executive Body Decision 1998/2 for information on persistence to be submitted for the procedure for adding substances to annexes I, II or III to the Protocol on Persistent Organic Pollutants are as follows:

1. Evidence that the substance's half-life in water is greater than two months, or that its half-life in soils is greater than six months, or that its half-life in sediments is greater than six months.

2. Alternatively, evidence that the substance is otherwise sufficiently persistent to be of concern within the scope of the protocol.

The data on persistence presented in the report and available elsewhere show that PCA can be expected not to be persistent in water, soil or sediment. Nevertheless, it has to be noted that only few data is available which makes it difficult to make a clear statement on persistency of PCA based on scientific facts. However, it should be noted that under anaerobic conditions PCA is known to be demethylated to PCP. In addition, the presence and widely distribution of PCA in the environment, including remote area, clearly demonstrated its persistence in the environment. Therefore, PCA should be considered to fulfil the criteria from Executive Body Decision 1998/2 for persistency.

Bioaccumulation8

PCA is highly hydrophobic. The estimated log Kow (KOWWIN v1.67) is 5.30. Opperhuizen and Voors (1987) experimentally assessed a log Kow value of 5.45 [Opperhuizen and Voors, 1987]. It can be assumed that the compound has a high bioaccumulation potential. From the many studies on polychlorinated aromatic ethers, only few address bioaccumulation of PCA [LRAT dossier 2008]. The results of BCF studies are summarized in Table 2.

Table 2: BCF values for PCA [LRAT dossier 2008].

Exp time Exp BCF kgww/L Reference

Fish

Oncorhynchus mykiss 35 d 0,9 ng/L 16000 Oliver and Niimi (1985)

Oncorhynchus mykiss 50 d 0,9 ng/L 14000 Oliver and Niimi (1985)

Oncorhynchus mykiss 75 d 0,9 ng/L 12000 Oliver and Niimi (1985)

Oncorhynchus mykiss 96 d 0,9 ng/L 17000 Oliver and Niimi (1985)

Oncorhynchus mykiss 35 d 10 ng/L 11000 Oliver and Niimi (1985)

Oncorhynchus mykiss 50 d 10 ng/L 20000 Oliver and Niimi (1985)

Oncorhynchus mykiss 75 d 10 ng/L 15000 Oliver and Niimi (1985)

Oncorhynchus mykiss 96 d 10 ng/L 24000 Oliver and Niimi (1985)

Poecilia reticulata 7 d* 40 ng/L 9120 Opperhuizen and Voors (1987)

Earthworm 5 - 40 Haimi et al. (1992) and (1993)

* steady-state not reached

In two studies on the bioaccumulation of organochlorine compounds in earthworms, concentrations of PCA in the soil and earthworms were measured at a sawmill that was abandoned 28 years ago. In the soil PCA concentrations were found from 0.06-1 μg/g dry soil. PCA concentrations in earthworms varied from 0.09 – 8 μg/g fat [Haimi et al., 1992 and Haimi et al., 1993]. Estimated BCF’s from these studies range from 5-40 kg fat/kg dry soil [LRAT dossier 2008].

PCA has been detected in several biotic matrices at significant levels (see Table 3) confirming the suggestion of a high bioaccumulation potential. As shown in Table 3, a study from Greenland shows bioaccumulation of PCA in range of species varying from aquatic invertebrates to fish, birds and mammals (Vorkamp et al., (2004)).

Table 3: Concentrations of PCA in biotic matrices [LRAT dossier 2008].

Year Location Species Tissue Concentration ng/kg Reference

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2006 Baltic Sea herring muscle 170 fresh weight Stiehl et al., 2008

2006 Baltic Sea herring fat 5000 lipid weight Stiehl et al., 2008

2004 North Sea herring muscle 100 fresh weight Stiehl et al., 2008

2004 North Sea herring fat 900 lipid weight Stiehl et al., 2008

2004 North Atlantic herring muscle 60 fresh weight Stiehl et al., 2008

2004 North Atlantic herring fat 500 lipid weight Stiehl et al., 2008

2004 Greenland caribou muscle 200 lipid weight Vorkamp et al., 2004

2004 Greenland capelin; cod mussle;liver 2300 lw Vorkamp et al., 2004

2004 Greenland snow crab muscle;liver 660;450 lw Vorkamp et al., 2004

2004 Greenland King eider; thick billed murre liver 360;220 lw. Vorkamp et al., 2004

2004 Greenland Harp seal; Narwhal;Beluga muscle 80;540; 1,100 lw Vorkamp et al., 2004

1980-1984 Rivers US fish Whole body 100,000 ww Schmitt et al., 1990

2006 Tanzania cassave Roots;leaves 600;2,100 fresh weight Marco et al., 2006

1988 Siskiwit Lake US Lake trout; white fish Whole body 360;650 lw Swackhamer et al.,1988

1987 Finland mussels Whole body 25 ng/g lw Herve et al., 1988

2002 Tanzania Mango Leaves <0.5 to 3,900 fw Marco and Kishimba, 2007

USA costal waters Oysters/Mussels Whole body <0.25-8.99 ng/g dw Wade et al., 1998

2004 USA, Mobile River Basin

BassCarp Whole Body 0.06-0.38 ng/g ww

0.72-3.18 ng/g ww Hinck et al., 2008

2003 Colorado River and tributaries

CarpCatfish Whole body >0.1 ng/g in 46 of 48

carp had >10 ng/g Hinck et al., 2007

2000 Yellow Sea

Pseudosciaena crocea

Collichthys niveatus

Muscle

Liver

ND-0.95 ng/g dwND-0.02 ng/g dwND-0.27 ng/g dwND-0.04 ng/g dw

Oh et al., 2005

2003 Beaufort Sea Coast, Alaska Polar Bears Fat <0.1-27 ng/g ww

<0.1-42 ng/g lw Bentzen et al., 2008

Salton Sea, Calif. Fish Muscle 0.15-0.20 ng/g fw Riedel et al., 2002

The U.S. Fish and Wildlife Service periodically determines concentrations of organochlorine chemicals in freshwater fish collected from a nationwide network of 112 stations as part of the National Contaminant Biomonitoring Program. Schmitt et al. (1990) analyses samples taken from 1970 up to 1985. PCA was detected in 1980 and 1984 in fish samples from 30 % of the stations [Schmitt et al., 1990].

The National Lake Fish Tissue Study in the US, published in 2009, is the first national freshwater fish tissue survey to be based on a probabilistic sampling design, and it includes data on the largest set of PBT chemicals ever studied in fish. The USEPA worked with partner agencies in states, tribes, and other federal organizations over a four-year period (2000–2003) to collect fish from 500 lakes and reservoirs in the conterminous United States (i.e., lower 48 states). The information provided in the report documents the national distribution of 268 PBT chemicals in predator fish species (e.g., bass and trout) and in bottom-

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dwelling fish species (e.g., carp and catfish) from lakes and reservoirs in the lower 48 states. PCA occurred in the bottom-dweller samples of 27 % of the sites and predator samples of 12 % of the sites [USEPA 2009].

Table 4: Results National Lake Fish Tissue Study MDL: method detection limit, ML: minimum level. [USEPA 2009].

Tissue Concentration Estimates for Predators (Fillets)

Number ofSamples

Number ofDetects

MaximumConc.

Units

5 thPercentile

10 thPercentile

25 thPercentile

50 thPercentile

75 thPercentile

90 thPercentile

95 thPercentile

486 57 4 ppb < MDL < MDL < MDL < MDL < MDL 1.45 2.16

Tissue Concentration Estimates for Bottom Dweller (Whole Bodies)

395 92 9 ppb < MDL < MDL < MDL < MDL 1.37 4.02 4.63

Results for Predators

MDL μg/kg (ppb) ML μg/kg (ppb) < MDL ≥ MDL & < ML ≥ ML Total

1.312 4.0 429 56 1 486

Results for Bottom Dwellers

1.312 4.0 303 67 25 395

Conclusion

The criteria from Executive Body Decision 1998/2 for information on bioaccumulation to be submitted for the procedure for adding substances to annexes I, II or III to the Protocol on Persistent Organic Pollutants are as follows:

1. Evidence that the BCF or BAF for the substance is greater than 5,000 or the log Kow is greater than 5; or

2. Alternatively, if the bio-accumulative potential is significantly lower than (1) above, other factors, such as the high toxicity of the substance, that make it of concern within the scope of the protocol.

The experimental BCF values are above the indicative value limit of 5000. Furthermore, PCA was found in biotic matrices like fish indicating the potential to bioaccumulate. It can be concluded that the criterion from Executive Body Decision 1998/2 for bioaccumulation is fulfilled.

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Potential for long-range atmospheric transport

Data of PCA concentrations in snow in the Canadian Arctic regions from Welch et al. (1991) and in animals in Greenland from Vorkamp et al. (2004) (see chapter on bioaccumulation) strongly suggest that PCA is subject to long range environmental transport. [LRAT dossier 2008]

Air concentrations of organochlorine pesticides (OCPs) were measured on a weekly basis in 2000-2003 at six Arctic stations, which include Alert, Kinngait, and Little Fox Lake in Canada; Point Barrow in the USA; Valkarkai in Russia; and Zeppelin in Norway. These stations cover a large region in the Arctic, providing a comprehensive perspective on OCPs in the circumpolar atmosphere. Air concentrations of PCA showed strong seasonal/spatial variations with median values of 3.8 pg/m3 (n=245) [Suet al., 2008].

Halsall et al. (1998) reported the presence of the current-use pesticides endosulfan, methoxychlor, and trifluralin, as well as PCA, in air at Tagish (Yukon, Canada; mean 3.28 pg/m3 min 0.04 pg/m3 max 73.4 pg/m3), Alert (Nunavut, Canada; mean 3.03 pg/m3 min 0.1 pg/m3 max 20.5 pg/m3) and Dunai (eastern Russia; mean 2.92 pg/m3 min 0.95 pg/m3 max 6.93 pg/m3) during 1993-94. PCA and endosulfan were among the top five pesticide-related compounds at all three sites, exceeded in concentration only by total PCBs, HCB, and HCH (itself a current-use pesticide) [Halsall et al., 1998].

Levels of PCA in the South pacific ocean (American Samoa) in the northern hemisphere were on average 9 pg/m3, while those in the southern hemisphere, New Zealand were 2.1 pg/m 3 [Atlas et al., 1986]. Air samples collected on a cruise on the Atlantic Ocean between 50 °N and 50 °S had a mean concentration of 8.079 pg/m3 [Schreitmüller and Ballschschmiter, 1995]. The presence of PCA in the remote marine troposphere indicates that PCA is subject to long range transport.

Hung et al. (2005) reported annual average levels of PCA in air at Tagish, Kinngait and Dunai ranging from 2.6 to 4.0 pg/m3 [Hung et al., 2005]. Welch et al. reported methoxychlor, PCA and trifluralin in snow from the Canadian arctic. The snow was associated with a “brown snow” event whose clay mineral composition, soot particles, and visible organic remains point to an Asian source, probably western China [Welch et al., 1991].

Muir et al. (2007) analyzed large volume water samples from Lake Hazen in northern Ellesmere Island and from Char Lake on Cornwallis Island, collected in 2005 and 2006. Chloropyrifos, dacthal, trifluralin, PCA, and pentachloronitrobenzole (PCNB) were among the currently used pesticides (CUPs) detected in all samples at low pg/L concentrations [Muir et al., 2007]. Muir and Zheng (2007) reported detection of 7 CUPs in the Devon Island ice cap in the Canadian arctic. Samples were obtained in a snow pit dug in 2005. The 7 CUPs detected in almost all recent horizons were dacthal, lindane, PCA, methoxychlor, metolachlor, metribuzin, phorate, and trifluralin. Fluxes of PCA at the Devon ice cap in Canada were reported to be 0.4 – 0.6 ng/m 2/y [Muir and Zheng., 2007].

Concentrations of PCA have also been found in fish in Siskiwit Lake, a remote lake on Isle Royale in Lake Superior [Swackhamer et al., 1988]. It is argued that the atmosphere is the source of the found contaminants because Siskiwit Lake is remote and far from point sources.

In a study on distribution and transport of several anthropogenic lipophilic organic compounds associated with Mississippi River suspended sediment samples of sediment were taken from than 12 sites along the Mississippi River, and from some connected rivers. None of the sediment samples contained PCP, but in almost all of the samples PCA was detected. The PCA bound to the organic compounds of suspended river sediments results in transported amounts of PCA of 350 g/day to the Gulf of Mexico [Rostad et al., 1999].

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This result could be an indication for transportation of sediment bound PCA, resulting from metabolisation of PCP, along rivers to the sea.

An overview on concentrations of PCA in abiotic matrices is presented in Table 5.

Table 5: Concentrations of PCA in abiotic matrices [LRAT dossier 2008].

Year Location Compartment Concentration Reference

1998-1999 Mississipi river, US Sediment Up to2,700 ng/kg Rostad et al., 1999

1988 Canadian Arctic Snow 1,230 pico gr/L Welch et al., 1991

1998 Yangtze river China water 0,6 ng/l Jiang et al., 2000

1998 Yangtze river China Sediment Up to 4,800 ng/kg Jiang et al., 2000

1989 Finland Soil Up to 1,000,000 ng/kg Haimi et al., 1993

1985 South pacific ocean Air 9 pg/m3 Atlas et al., 1986

1985 New Zeeland Air 2.1 pg/m3 Atlas et al., 1986

2000-2003 Arctic Air Mean: 4.9 pg/m3 Su et al., 2008

n.a. Canadian and Russian Arctic Air 2.56 – 3.99 pg/m3 Hung et al., 2005

n.a. Egypt Sediment “Near or below det. limits” Barakat et al., 2002

2004-2005 Durban, South Africa Air “detected in all samples” max: 20±13 pg/m3 Batterman et al., 2008

2000 Yellow Sea Sediment ND-0.04 ng/g dw Oh et al., 2005

1992-1995 Seven Yukon Lakes Sediment Max values 0.33-4.52 ng/g dw with lower conc. in surface sediment Rawn et al., 2001

2005 Devon Ice-Cap, Canada Snow Flux = 0.4-0.6 ng.m2/yr Muir and Zheng, 2007

1993-1994 Can. Arctic Air 2.3-3.1 pg/m3 Macdonald et al., 2000

Calculation of the vapor pressure of PCA resulted in a vapour pressure for PCA of 0.0459 Pa at 25 °C (MPBWIN v1.42 according to the modified grain method) and 0.0459 Pa at 25 °C (EPWIN) indicating high volatility [LRAT dossier 2008][Summary of reviews, 2009]. Comparable results were reported by Dobbs and Grant (1980) with 0.0933 Pa at 25 °C [Dobbs and Grant., 1980]. PCA can be photo-oxidized in the atmosphere through reactions with hydroxyl (OH) radicals. The calculated half-life for PCA based on this reaction is 9.8 days, with an atmospheric (OH) concentration of 1.5E6 OH/cm3 (AopWin v1.92) [LRAT dossier 2008]. The characteristic travel distance (CDT) for PCA calculated with the OECD LRT tool is 2,110 km [Hoferkamp et al., 2009].

Conclusion

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The criteria from Executive Body Decision 1998/2 for information on potential for long-range atmospheric transport to be submitted for the procedure for adding substances to annexes I, II or III to the Protocol on Persistent Organic Pollutants are as follows:

1. Evidence that the substance has a vapor pressure below 1,000 Pa and an atmospheric half-life greater than two days.

2. Alternatively, monitoring data showing that the substance is found in remote regions.

The calculated vapour pressure of PCA is well below the numerical limit of a vapour pressure of 1,000 Pa. The calculated atmospheric half-live of PCA according to Atlas et al. 1986 is at least 9.8 days, which is far longer compared to the atmospheric half-live of two days required to fulfil the POP criterion.

Furthermore, PCA has been detected in remote areas far from point sources e.g. in the northern and southern hemisphere, in arctic snow and in fish in a remote lake. However, since PCA is a biodegradation product of PCP, its formation after transport of PCP cannot be excluded. However, the physical-chemical properties of PCA suggest that it could be transported directly.

Based on its physical-chemical properties and the available field data, PCA fulfils the POP criterion on potential for long-range atmospheric transport.

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Conclusion on POP characteristics of PCA

Criterion Criterion fulfilled

Reasons for decision

Toxicity/ecotoxicity Yes Very toxic to the aquatic organisms

Some evidence of carcinogenic activity in male rats and mice

Some evidence for mutagenicity in mouse

Some evidence for reproductive toxicity in rats

Metabolization to PCP/high toxicity of PCP

Bioaccumulation Yes BCF values > 5,000

Found in different biotic matrices

Persistence Yes Persistency of its degradation product in anaerobic condition

Presence and widely distribution in the environment, including remote area

Long-range atmospheric transport

Yes Vapour pressure < 1,000 Pa

Atmospheric half-life greater than two days

Found in remote areas

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3 Transformation of PCP to PCA

PCA is not commercially produced but it is a widespread hydrocarbon in the atmosphere. One probable source of PCA is the biotic transformation of the formerly widely used biocide, PCP. There exist two possibilities for the breakdown of PCP, namely photo degradation and biological degradation. Biological transformation, both aerobic and anaerobic has been demonstrated for PCP. Primary transformation as well as mineralisation has been observed under natural conditions. The major metabolic pathways are:

a. methylation to yield the methylether of PCP (PCA);

b. acetylation of the hydroxyl group (PCP-acetate);

c. dechlorination to tetrachlorophenols;

d. hydroxylation to tetrachlorodihydroxybenzens.

Biotransformation is the process where PCA is generated. While PCA may be formed from PCP in soil, sediment or wood chips, according to Murthy et al. (1979) its conversion is favored by anaerobic conditions. In soil PCA is product from methylation of PCP. Several bacteria and fungi may enhance this process (Walter et al. (2004), Okeke et al. (1997), Lamar et al. (1990 a), Lamar et al. (1990 b), Haggblom et al. (1988) [LRAT dossier 2008].

Under anaerobic conditions PCA is known to be demethylated to PCP. Murthy et al. (1979) investigated the biodegradation of PCP in aerobic and anaerobic soils and made the general conclusions that under anaerobic conditions methylation to PCA was a limited reaction, whereas the principle degradation pathway was by progressive reductive dechlorination. In aerobic soils there is more interconversion between PCP and PCA and the principle degradative reactions are oxidative. These results show that PCP could be biologically methylated to form PCA in aerobic soils, possibly as a means of reducing the concentration of toxic PCP. [Murthy et al., 1979].

Strategies to enhance biotransformation of PCP in a spectrum of wetland soils were investigated under laboratory conditions, which included manipulations of electron acceptors and donors, and PCP concentrations. For this purpose, D’Angelo et al. (2000) performed a study on PCP loss in 10 different soils and found that seven of the soils showed production of PCA during the first week of incubation. Between day 4 and day 20 five of these soils showed a loss of PCA. Maximum transformation rates were found at PCP concentrations < 10 μM (methanogenic conditions) and > 6 μM to > 23 μM (aerobic conditions). Aerobic PCP transformation initially produced small amounts of PCA. However, >75% of both chemicals disappeared in 30 d from five soils (100% of the produced PCA was lost in these five soils). Results demonstrated the widespread occurrence of PCP transforming microorganisms in soils, which may be promoted by manipulating environmental conditions [D'Angelo et al., 2000]. Furthermore, it can be concluded that PCA is produced by Biotransformation of PCP in soil. Because of its physical-chemical properties PCA volatilizes from the soil compartiment to air. This was also shown in a laboratory experiment with PCA-contaminated soil. Concentrations of PCA have been measured over a period of 20 weeks. The PCA concentration of 0.38 μg/g, at the beginning was reduced in 5 weeks to 0.18 μg/g and after 20 weeks only of 0.05 μg/g PCA remained. A t1/2 of approximately 5 weeks is obtained from this study [Haimi et al. 1993].

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Badkoubi et al (1996) performed experiments to quantify the mineralization and distribution of PCP by the white rot fungus Phanerochaete chrysosporium, and distribution of its transformation products into water-soluble, solvent soluble, sorbed, and volatile fractions in liquid cultures. Water-soluble and solvent-soluble products from 14C-PCP transformation were first measured under oxygen limited conditions. A rapid reduction in the percent of 14C in the aqueous phase and the fungal mat was observed in all experiments. Results indicated that after 12 days, 15% of 14C was recovered in methylene chloride, and less than 1% was water soluble. Sorption to the fungal mat reached a maximum of 16% 14C after 9 days incubation and declined to 5% at day 12. However, recovery of 14C within the system was only 30% at day 12. To improve the mass balance of the system, polyurethane foam was placed inside the culture flask to trap volatile products of PCP transformation. Results showed that after 12 days incubation of 14C-PCP with the fungus, 82% of the 14C added was volatilized. The percent 14C on the fungal mat decreased over time, while the formation of volatile intermediates increased. GC/MS analysis demonstrated that PCA was the only volatile product of PCP transformation. Sorption of 14C to the fungal mat was reversible to some extent. Chemical mass balance results in this experiment were near 100%. In the final experiment, the polyurethane volatile trap was placed outside the culture flask to assess the impact of the continuous removal of volatiles from the flask head space on mineralization. Increased 14CO2 production was observed when the polyurethane volatile trap was placed out-side the culture flask compared with placement inside the flask.These results showed that if the fungus is oxygen-limited for lignin peroxidase production, it will convert most of the PCP to the volatile PCA, the only volatile compound detected in the presence of P. chrysosporium in this experiment. When sufficient oxygen was available, the extent of mineralization was much greater, up to 32%. Higher mineralization was observed when the volatile transformation products had a chance to equilibrate between the solution and headspace. Immediate removal of the volatile transformation products reduced PCP mineralization [Badkoubi et al., 1996]. The results demonstrate that there are funghi which are able to convert PCP to PCA under anaerobic conditions. Furthermore, it is shown that if produced PCA is able to volatilize from soil an exceeded transformation rate can be observed. This indicates that in the environment PCP is transformed to PCA which volatilizes from soil to air.

The fate of PCP in autoclaved soil supplemented with straw and inoculated with the white-rot fungus Trametes versicolor was investigated. Inoculated flasks were incubated for 0 to 42 d and control flasks for 0 to 28 d. Mineralization and volatilisation of PCP and its transformation products were measured using 14C-labelled PCP for radiorespirometry and extraction analysis, and non-labeled PCP to monitor by use of gas chromatography transformation products of PCP. During 42 d of incubation T. versicolor mineralized 29% of the PCP. Only trace amounts of anisoles such as PCA and 2,3,4,6-tetrachloroanisole (2,3,4,6-TeCA) were formed during incubation. It is possible that laccase produced by T. versicolor enhances the degradation of PCP to other compounds than PCA. It was noted that crude laccase purified from T. versicolor could degrade PCP signifcantly [Tuomela et al., 1999]. On the other hand, LesÏtan et al. (1996) found a negative correlation between manganese peroxidase and PCA production by T. versicolor indicating that this enzyme may be involved in desirable PCP removal from contaminated soil. These findings demonstrate that PCA is produced from PCP by particular species. Evidence of the occurrence of these species e.g. in remote areas can be an indication of possible metabolisation of PCP to PCA in these environments.

Mardones et al. (2009) presented a study of the uptake of 2,4,6-tribromophenol (TBP), PCP, and its metabolite PCA from contaminated sawdust from the forest industry in horticultural products such as apples, raspberries, and fodder maize for cattle feed. No trace of PCP was detected in plants cultivated in presence of PCP, although PCP was detected in the soil after the culture. Additionally, PCA was found in the soil of these treatments after the culture, although it was not detected before the crop. This fact is indicative

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of PCP degradation to PCA, which could reduce the availability of PCP for its uptake by the plant. This interpretation also explains why PCA was found in maize samples from this zone [Mardones et al., 2009].

Evidence for transformation of PCP to PCA in other matrices like water or air could not be identified. Based on literature data microbial metabolism is the major degradation process in aerobic soils and sediment and the main source for PCA from PCP.

Conclusion

PCP is readily transformed to PCA in the environment.

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4 Potential sources of PCA in remote regions1

Manufacturers of PCP (The PCP Task Force) expressed doubts whether PCA detected in remote areas results from PCP metabolism or other precursors like HCB and HCH [Letter PCP task force, 2009]. Besides transformation of the above mentioned precursors, pentachloronitrobenzene (PCNB) transformation to PCA in onions has also been observed by Begum et al. (1979) as well as biotransformation in soil by micromycetes by Torres et al. (1996). The question of potential sources of PCA in remote areas has been discussed in a paper called “Risk Profile of Pentachloroanisole” which was provided by Canada together with answers to the UNECE questionnaire 2010. Therefore, the following discussion is in parts quoted from this document.

4.1 PCP

In the PCP dossier [LRAT dossier 2008] it is stated that PCP could be the source of PCA in the environment, however, the PCP Task Force indicate that the phys-chemical properties and rapid degradation of PCP would indicate that it could not be the source.

Transformation of PCP to PCA has already been discussed in the previous chapter. The PCP dossier describes PCP transport distances of 1500-3000 km. It is further noted that measurements of PCP in remote regions are complicated by the fact that PCP is transformed into other molecules and therefore, its absence in animal tissue is not indicative of its earlier presence.

The PCP task force indicates that PCP cannot be the source of PCA in remote sites because even when PCA is detected in biota or abiotic compartments PCP was never found in the Mississippi River (Rostad et al. (1999)). However, in a laboratory study that used PCP to determine plant metabolism performed by Casterline et al. (1985) only 5% of added PCP was found 90 days after addition to soil. Similar results were obtained by Mardones et al. (2009) (see previous chapter). D’Angelo et al. (2000) also found that 75% of added PCP and 100% of produced PCA was lost under aerobic conditions over 30 days in eight soils (see also previous chapter). These studies show that even though PCP was not found in some remote areas where PCA was found, PCP or other organochlorine compounds (HCB and HCH, etc.) could be the precursors of PCA because PCP may have been completely transformed.

OSPAR (1999) attributes the decreased concentrations of PCP in the European environment to the use restrictions that were implemented in the early 1990’s. Consequently, if time trend information is available for PCA it might be possible to correlate the changes in various environmental compartments.

Environmental Fate and Transport of PCP

PCP is hydrolytically stable under abiotic conditions at pHs 5, 7, and 9. There are multiple transformation pathways for PCP. It phototransforms in water with a half-life of about 20 min. PCP metabolizes aerobically in aqueous medium and in soils with a half-life of 14 days. Anaerobic aquatic soil transformation is slower with an observed half-life of 1-2 months. It is moderately mobile in sandy loam soil and appears immobile in clay soils and has slight mobility in silt loam soils.

Biotransformation of PCP to PCA in soil has already been discussed in the previous chapter. PCP had a half-life of 7-14 days (calculated first-order t1/2 of 63 days) in sandy loam soil (USEPA 2008). In aerobic soil metabolism studies, various isomers of tetrachlorophenol and trichlorophenol were detected as minor products (<10%), no major transformation products were present other than CO2. Minor transformation products were various isomers of tetrachlorophenol and trichlorophenol (individual isomers were not

1 Canada „Risk Profile of Pentachloroanisole“ February 5. 2010 provided by Canada together with answers to the UNECE questionnaire 2010.

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identified). Bound residues accounted for 64% of the applied radioactivity. Other literature indicates that major transformation products of PCP are the tetra and tri-chlorophenols, and dichlorophenols. PCA was a major product in aerobic soils, but was only present in minor amounts in anaerobic soils (USEPA 2008). Lamar and Dietrich (1990) found that 9-14% of applied PCP was transformed to PCA in soils that were inoculated with fungi. They concluded that methylation of PCP was not the major route of PCP loss.

PCP had a t1/2 of 1-2 months (calculated first-order t1/2 of 34 days (USEPA 2008) in flooded sandy loam soil under nitrogen. Transformation was initially slow but accelerated after an acclimation period. Various isomers of tetrachlorophenol and trichlorophenol were the major products, however, individual isomers were not identified [USEPA 2008].

The EPA (USEPA 2008) concluded that “Based on data from both the guideline studies and literature, microbial metabolism is a major degradation process for PCP in both aerobic and anaerobic (flooded) soils and sediments. However, in water (surface or ground), PCP may not be significantly degraded without the presence of a soil/sediment phase (except by photolysis at the upper layers of surface water). The degradation or removal of PCP in such systems is also partially due to adsorption of the compound to soil particles and organic matter.

Conclusion

Based on available data microbial metabolism is a major degradation process in both aerobic and anaerobic soils and sediment. In water PCP may not be significantly transformed without the presence of a soil/sediment phase, except by photolysis on surface water. Biotransformation usually requires an acclimation period or lag phase. PCP is also adsorbed to soil particles and organic matter.

Formation of PCP from PCA

Demethylation of PCA to PCP has been in observed in biotic compartments (fish, earthworms and mice) as described in the paragraph „ toxicity and ecotoxicity“ in chapter 2.

The PCP Task Force also states that PCA can be demethylated to PCP in soils and listed four references as evidence (Badkoubi et al. (1996), Lamar and Dietrich (1995), D’Angelo et al. (2000) and Murthy et al. (1979)). According to the Canadian authors no such process was described in Lamar and Dietrich (1990) or D’Angelo et al. (2000).

Haimi et al. (1993) also observed the demethylation of PCA to PCP in soils, but concentrations of PCP remained low for the whole experimental period ranging from 0.001 to 0.3 µg/g (0.5 µg PCA/g soil was added).

4.2 HCB and HCH (α-HCH and γ-HCH)1

The PCP Task Force promotes HCB and HCHs as the most likely sources of PCA. One reason for this is the recognized and documented long-range transport of these compounds and the fact that they transform to PCP and then to PCA. They cite Schreitmüller and Ballschmiter (1995), Hoekstra et al. (2003), Van Raaij et al. (1993), To_Figueras et al. (1997) Debets et al. (1981), Koss et al. (1976) and van Ommen et al. (1985 and 1986) as providing evidence for transformation of HCB and HCHs to PCA.

According to Schreitmüller and Ballschmiter (1995) the reaction pathway and the rate of formation of the chlorinated methoxybenzenes, especially of tetrachloro-1,4-dimethoxybenzene (TCDMB) is only poorly known. Previously Schreitmüller (PhD Dissertation 1994, in Schreitmüller and Ballschmiter (1995)) found that the sum of atmospheric concentrations of the two HCHs correlated nearly linearly to the sum of the chlorinated methoxybenzenes (r2 = 0.97) which indicated a common input.

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Although Schreitmüller and Ballschmiter (1995) found a linear relationship between concentrations of HCHs and the sum of chlorinated methoxybenzenes in air, they do not emphatically state that the HCHs are the source of PCA in the environment. They did not indicate that they tried to make correlations with other compounds so to specifically say that this correlation indicates that HCHs are the source of PCA would be misleading. In addition, they correlated the sum of the methoxybenzenes not just PCA to the HCHs so to reiterate it would be misleading to assume that the correlation would still hold true only taking PCA into consideration. Therefore, Schreitmüller and Ballschmiter (1995) do not provide conclusive evidence that the HCHs are the primary source of PCA in the environment or that it is a more important source compared to PCP.

Hoekstra et al. (2003) noted the presence of HCB and HCHs in the plasma of bowhead whales. The authors found that PCP was the most abundant halogenated phenolic compound found in bowhead plasma and assumed that the PCP in biota could be a result of the biotransformation of HCB because “PCP does not readily bioaccumulate and has a limited potential for long-range transport due to rapid photolysis and reaction with photochemically produced OH radicals”. However, Hoekstra et al. (2003) do not provide evidence for their hypothesis. It is assumed as one possible explanation. The potential for accumulation of transported PCA with methylation to PCP in the bowhead whales is not taken into consideration by the PCP Task Force. In contrast, Hoekstra et al. (2003) go on to say that “The relatively high proportion of PCP in bowhead whale plasma may also be the direct result of the biotransformation of pentachloroanisole, an abundant OC contaminant found in arctic air.” A significant omission which the PCP Task Force deemed unimportant to mention. It is not possible to conclude from Hoekstra et al. (2003) whether HCB or PCA is the more important source of PCP in bowhead whale plasma.

The PCP Task Force cites several examples of PCP as transformation product of HCB. Van Raaij et al. (1993) observed a dose-response relationship between HCB and serum levels of PCP in rats after dosing with HCB, however, after 4 weeks of dosing at 3.5 mmol HCB/kg, PCP concentrations in blood serum were only 0.01 mmol/L. The authors state that this PCP serum level would be equivalent to a dose of 0.0044 mmol PCP/kg. Therefore, the amount of HCB transformed to PCP in rats would be 0.13% of the total applied.

Figueras et al. (1997) observed HCB transformation to PCP in humans, but found that this pathway was a very minor route of HCB transformation. The study showed that elevated human serum HCB concentrations were not reflected in notable increases in PCP excretion via urine. These observations “show that HCB hydroxylation leading to the formation of PCP in humans is very small in comparison with HCB accumulation.” (Figueras et al. (1997)).Sandau et al. (2002) discussed several possible relevant reasons for PCP concentrations determined in human umbilical cord plasma samples from three different regions of Québec. The authors mention the use of PCP and state that main non-occupationally exposure to PCP is through the diet. Furthermore, the authors mention “Another significant source of PCP may occur through the metabolism of hexachlorobenzene” (Sandau et al. (2002)). Evidence on the relative importance of the sources contributing to occurrence of PCP in human blood on the basis of the study is not provided.

Other studies such as Koss et al. (1976) and Van Ommen et al. (1985 and 1986) also found the transformation of HCB to PCP in rats and rat livers, respectively. Koss et al. (1976) found that PCP was the major transformation product of HCB in rats. 7.2% of the total applied radioactivity as HCB was transformed via this route.

According to van Ommen et al. (1985) PCP was the major metabolite of HCB in rat liver microsomes (approximately 90% of all eluted metabolites), however, <2.2% of the eluted radioactivity was actually transformed. Of the total HCB added, only 0.23 and 0.77% of the applied HCB was actually metabolized to PCP in female and male rats, respectively. Similarly van Ommen et al. (1986) found that of the 25 µmol of

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added HCB to rat liver microsomes, between 35 and 265 pmol was converted (metabolized), approximately 0.01%.

The literature data show that HCB/HCH is metabolised to PCP. The observed relevance of the metabolism of HCB to PCP is species dependent and is usually very low (e.g. very low in humans; see Figueras et al. (1997)) or low in rats (see Van Raaij et al. (1993), Van Ommen et al. (1985), Van Ommen et al. 1986). According to one single study from the 1970ies a moderate transformation rate was observed; 7.2% of the applied HCB amount was transformed to PCP (see Koss et al. (1976)). These literature data could be taken as an indication that the metabolic transformation from HCB to PCP may only be a minor pathway leading to the occurrence of PCA in biota.

These and other relevant studies (Schreitmüller and Ballschmiter (1995), Hoekstra et al. (2003), Sandau et al. (2002)) do not provide evidence whether HCB/H or the use of PCP is the more important source of PCP in biota in general or in arctic biota.

Conclusions

Under environmental conditions PCP is metabolised to PCA and vice versa. PCA is subject to long range transport (see chapter 2). Also HCB/H are metabolised to PCP and are present in biota in remote areas. As a consequence both, PCA (resulting from the use of PCP) and HCH/B may contribute to the occurrence of PCA/PCP in biota remote areas. In all likelihood it is the combination of all potential precursors that contribute to the occurrence of PCA in remote areas and it would be very challenging to determine the relative importance of the different sources Literature data do not provide evidence that HCB/H are the more important precursors for PCA in the arctic compared to PCP.

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5 Impurities of dioxins and furans during the production of PCP

The use of PCP is inseparably coupled to the emission of dioxins and furans, due to the impurities as a result of all known production processes, due to burning of treated wood and due to degradation in the environment. In this chapter information regarding the dioxin (PCDD) and furan (PCDF) impurities in PCP products resulting from the production processes is provided.

Production of PCP

PCP is produced by direct chlorination of phenols and hydrolysis of HCB. The direct chlorination is carried out in two steps. First, liquid phenol, chlorophenol, or a polychlorophenol is bubbled with chlorine gas at 30 - 40 °C to produce 2,4,6-trichlorophenol, which is then converted to PCP by further chlorination at progressively higher temperatures in the presence of catalysts (aluminium, antimony, their chlorides, and others). The second method involves an alkaline hydrolysis of HCB in methanol and dihydric alcohols, in water and mixtures of different solvents in an autoclave at 130 - 170 °C [LRAT dossier 2008].

Impurities in PCP

In addition to the formation of PCP, numerous by-products/impurities are generated, as reflected by analytical profiles in tables 4 and 5. The chlorination procedure yields a technical product that usually contains a considerable amount of tetrachlorophenols (4 - 12%) due to incomplete chlorination reactions. The formation of microcontaminants is favoured by elevated temperatures and pressure. As microcontaminants, mainly polychlorodibenzodioxins (PCDDs), polychlorodibenzofurans (PCDFs), polychlorodiphenylethers, polychlorophenoxyphenols, chlorinated cyclohexenons and cyclohexadienons, hexachlorobenzene, and polychlorinated biphenyls (PCBs) are formed. Technical grade PCP is typically about 86% pure. With both manufacturing methods, these toxic by-products are formed. In addition, the alkaline HCB hydrolysis-method can result in the presence of HCB in the resulting PCP [LRAT dossier 2008]. The possible presence of PCDDs and PCDFs in commercial products is of special significance because of their extraordinary persistence and other POP properties. A scientific criteria document for chlorophenols and their impurities in the Canadian environment has been prepared by Jones (1981, 1984). According to Sheffield (1985) PCP was estimated to be one of the major chemical sources of PCDDs and PCDFs in the Canadian environment [IPCS, 88].

Masunaga et al. (2001a) studied the PCDD/F content of a number of Japanese agrochemicals. Three batches of PCP were produced between 1967 and 1971, whereas the production date from one batch was unknown. The total amount of PCDD/Fs varied between 14,000 and 24,000,000 ng/g a.i. Masunaga et al. (2001a) indicated that OCDD was the most common impurity formed during PCP production. From the congener profile it was deduced that dioxins were formed during the production of PCP through combination of two PCP molecules or between PCP and the most abundant secondary product 2,3,4,6-TeCP. This process is also described by Ballschmiter & Bacher (1996) as cited by Isosaari (2004). Kakimoto (2004) indicate that dioxins with high chlorine content, HpCDD and OCDD and HpCDFs are indicators of PCP contamination [LRAT dossier 2008].

In 1987 the US EPA established rules limiting the HxDD concentration per batch to a maximum of 4 ppm with a monthly average of 2 ppm (2,000 ng/g). In 1991 the EU restricted the use of PCP to formulations with a HxDD concentration below 4 ppm (EU directive 91/173/EEC). Due to these regulations PCDD/F concentrations have decreased considerably. Eduljee (1999) provide the results from measurements on the dioxin content in batches of PCP taken in 1992 and manufactured by Vulcan Chemicals. The HxCDD

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concentrations in these batches are roughly between 1000 and 2,300 ng/g. Eduljee (1999) citing Bingham et al. (1991) mentions a total HxDD concentration of 9,700 ng/g in one sample of NaPCP and concentrations below 2,500 ng/g in three other samples. Eduljee (1999) citing data from the Penta Task Force (1996) provided yearly average concentrations of 1,700 ng/g. These are also cited on the Eurochlor website [LRAT dossier 2008].

Buser and Bosshardt (1976) reported on the results of a survey of the PCDD and PCDF contents of PCP and PCP-Na from commercial sources in Switzerland. From the results, a grouping of the samples into two series can be observed: a first series with generally low levels (hexaCDD <1 µg/g) and a second series with much higher levels (hexaCDD >1 µg/g) of PCDDs and PCDFs. Samples with high PCDD values had also high PCDF values. For most samples, the contents of the PCDF contaminants were in the order:

tetra- = penta- < hexa- < hepta- < octaCDD/CDF.

The ranges of the combined levels of PCDDs and PCDFs were 2-16 and 1-26 µg/g, respectively, for the first series of samples, and 120-500 and 85-570 µg/g, respectively, for the second series of samples. The levels of octaCDD and octaCDF were as high as 370 and 300 µg/g, respectively. Some PCP-Na samples analyzed showed the unexpected presence of tetraCDD (0.05-0.25 µg/g), which was later identified by Buser and Rappe (1978) as the unusual 1,2,3,4-substituted isomer. Table 6 collects a number of relevant analyses of these chlorophenol formulations. The levels of PCDDs and PCDFs are higher than for the phenoxy-acetic acid herbicides [IPCS, 88].

Table 6: Levels of PCDDs and PCDFs in commercial chlorophenols (µg/g) [IPCS, 88].

Substance PCP sample 1 PCP sample 2

TetraCDDs < 0.1 < 0.1

PentaCDDs < 0.1 < 0.1

HexaCDDs < 1 2.5

HeptaCDDs 0.5 175

OctaCDD 4.3 500

TetraCDFs < 0.1 < 0.1

PentaCDFs < 0.1 < 0.1

HexaCDFs 0.03 <0.3

HeptaCDFs 0.5 19

OctaCDF 1.1 25

Miles et al. (1985) have analyzed Canadian PCP samples for hexaCDDs from five different manufacturers using an isomer-specific analytical method. The study included both free PCPs as well as the sodium salts. Total hexaCDDs in PCPs ranged from 0.66 to 38.5 mg/kg, while in the sodium salts levels of hexaCDDs between 1.55 and 16.3 mg/kg were found. The most abundant hexaCDD isomer found in the free PCPs was the 1,2,3,6,7,8 isomer; however, in the sodium salts the 1,2,3,6,7,9- and 1,2,3,6,8,9-hexaCDD pair was the most abundant. Hagenmaier and Brunner (1987) has reported that 2,3,7,8-tetraCDD can be found in European commercial PCP formulation at levels of 0.21-0.56 ng/g, while Hagenmeyer et al., (1986) report that 1,2,3,7,8-pentaCDD was found in PCP and Na-PCP in concentrations of 0.9-18 ng/g. [IPCS, 88].

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According to Crosby et al., (1981), the quality of PCP depends on the source and date of manufacture. Furthermore, analytical results may be extremely variable, particularly with regard to earlier results, which should be considered with caution. Jensen and Renberg (1972) detected chlorinated 2-hydroxydiphenyl ethers, which obviously may transform to dioxins during gas chromatography, thus giving a false indication of a higher level of PCDDs. Unlike these "predioxins", other isomers are not direct precursors of dioxins, and are labeled "isopredioxins". Table 7 presents analyses of PCP formulations taken from several publications [IPCS, 71].

Table 7: Impurities (mg/kg PCP) in different technical PCP products. aFrom: Goldstein et al. (1977); bFrom: Schwetz et al. (1974); cFrom: Schwetz et al. (1978); dFrom: Buser (1975); eFrom: Umweltbundesamt (1985); fFrom: Anon (1983); gPurified; hDowicide EC-7; IDowicide 7; ns = not specified; k < = below detection limit. Source: [IPCS, 71].

Component Specification, producer, PCP content (%)

Technical Monsantoa

(84.6%)

Technical Dowb

(88.4%)

Technical Dowb,e

(98%)

Technical Dowc,g,h

(90.4%)

Technical Dowd,i

n.a.

Technical Dyn. Nobele

(87%)

Technical Rhône-

Poulencf

(86%)PhenolsTetrachloro- 30 000 44 000 2700 10 4000 ns 50 000 70 000

Trichloro- ns < 1000 500 < 1000 ns 20 ns

Higher chlorinatedphenoxyphenols

ns 62 000 5000 ns ns ns 70 000

Dibenzo-p-dioxinsTetrachloro- < 0.1 < 0.05 < 0.05 < 0.05 < 0.2k < 0.001 < 0.01

Pentachloro- < 0.1 ns ns ns < 0.2 ns ns

Hexachloro- 8 4 < 0.5 1 9 3.5 5

Heptachloro- 520 125 < 0.5 6.5 235 130 150

Octachloro- 1380 2500 < 1.0 15 250 600 600

Dibenzofurans

Tetrachloro- < 4 ns ns ns < 0.2 ns ns

Pentachloro- 40 ns ns ns < 0.2 0.2 ns

Hexachloro- 90 30 < 0.5 3.4 39 10 ns

Heptachloro- 400 80 < 0.5 1.8 280 60 ns

Octachloro- 260 80 < 0.5 < 1.0 230 150 ns

Hexachlorobenzene ns ns ns 400 ns ns ns

Since the toxicity of PCDDs and PCDFs depends not only on the number but also on the position of chlorine substituents, a precise characterisation of PCP impurities is essential. The presence of highly toxic 2,3,7,8-tetrachlorodibenzo- p-dioxin (2,3,7,8-T4CDD) has only been confirmed once in commercial PCP samples. In the course of a collaborative survey, one out of five laboratories detected 2,3,7,8-T4CDD in technical PCP and Na-PCP samples at concentrations of 250 - 260 and 890 - 1100 ng/kg, respectively (Umweltbundesamt (1985)). Buser and Bosshardt (1976b) found detectable amounts of T4CDD (0.05 - 0.23 mg/kg) in some samples of different technical PCP products, but on re-analysis were unable to confirm the compound's identity. In other cases, T4CDD has not been identified at detection limits of 0.2 - 0.001 mg/kg [IPCS, 71].

The higher PCDDs and PCDFs are more characteristic of PCP formulations (Table 7). Hexachlorodibenzo- p-dioxin (H6CDD), which is also considered highly toxic and carcinogenic, was found at levels of 0.03 - 35 mg/kg

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(Firestone et al., (1972)), 9 - 27 mg/kg (Johnson et al., (1973)), and < 0.03 - 10 mg/kg (Buser & Bosshardt, (1976b)). According to Fielder et al. (1982), the 1,2,3,6,7,9-, 1,2,3,6,8,9-, 1,2,3,6,7,8-, and 1,2,3,7,8,9-isomers of H6CDD have been detected in technical PCP. The 1,2,3,6,7,8 and 1,2,3,7,8,9-H6CDDs predominated in commercial samples of technical PCP (Dowicide 7) and Na-PCP. Octachloro-dibenzo- p-dioxin (OCDD) is present in relatively high amounts in unpurified technical PCP [IPCS, 71].

The identification of 2-bromo-3,4,5,6-tetrachlorophenol as a major contaminant in three commercial PCP samples (ca. 0.1%) has been reported. This manufacturing by- product has probably not been detected in other analyses because it is not resolved from the PCP peak by traditional chromatographic methods (Timmons et al., (1984)) [IPCS, 71].

In 1986, an agreement was made between the industry and the U.S. EPA concerning the dioxin impurities in PCP: (1) Maximum HxCDD per batch released for shipment should not exceed 4 mg/kg. (2) Maximum average HxCDD of all batches sold during the month should not exceed 2 mg/kg. (3) Any detectable levels of 2,3,7,8-TCDD at a limit of detection should not exceed 1 pgkg. It has been noted by the Agency that between 1987 and 1999, the average total PCDD/PCDF levels in PCP manufactured in the U.S. have dropped between three to six-fold as compared to the period prior to 1987. In 2005 the USEPA presented a study which compared concentrations of the various congeners in PCP products reported to EPA by the manufacturers, KMG-Bernuth and Vulcan Chemicals, on a monthly basis between 1987 and 1999 with respective data of the time period 2000 to 2004. The data of this analysis is shown in Table 8. The summarized findings were as follows: There was no consistent trend between pre-and post-2000 data sets between dioxin and furan concentrations. Only one congener group, HxCDD, had a statistically lower mean concentration in the post-2000 data set. This finding applied to both manufacturers. There was no difference in mean concentrations for the other dioxin congeners. The furan congener data from Vulcan showed a statistically significant increase in concentration between the two time periods. For the KMG furan data, only OcCDF was significantly higher in the post-2000 data set; there was no difference in mean concentration for the other congener groups [USEPA, 1999 and 2005].

Table 8: Summary of results for comparison of pre- and post 2000 data of dioxin and furan impurities in PCP

[USEPA, 1999 and 2005].

Company Congener Pre-2000 mean (sd) N Post-2000 mean (sd) NStatistically significant different

KMG HxCDD 1.75 (1.71) 142 1.26 (0.42) 49 Yes

HpCDD 58.51 (59.05) 142 43.69 (37.01 49 No

OcCDD 224.31 (228.38) 142 186.48 (100.37) 49 No

HxCDF 15.11(16.43) 142 13.33 (9.20) 50 No

HpCDF 94.91 (97.13) 142 89.16 (46.03) 50 No

OcCDF 168.45 (197.22) 142 237.91 (135.78) 50 Yes

Vulcan HxCDD (GC) 1.53 (0.46) 147 9.65 (8.74) 49 Yes

HxCDD (HPLC) 1.48 (0.33 147 90.28 (35.83) 49 Yes

HpCDD 56.42 (69.46) 147 45.34 (11.69) 49 No

HxCDF 3.53 (6.04) 147 9.65 (8.74) 49 Yes

HpCDF 40.01 (40.67) 147 90.28 (35.83) 49 Yes

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Occupational health effects of PCP impurities

Collins et al (2009) sought to determine if workers exposed to dioxins in PCP manufacturing were at increased risk of death from specific causes. They examined death rates among 773 workers exposed to chlorinated dioxins during PCP manufacturing from 1937 to 1980 using serum dioxin evaluations to estimate exposures to five dioxins. Deaths from all causes combined, all cancers combined, lung cancer, diabetes, and ischemic heart diseases were near expected levels. No trend of increasing risk for any cause of death with increasing dioxin exposure was observed. However, the highest rates of non-Hodgkin lymphoma were found in the highest exposure group (standardized mortality ratios = 4.5, 95% CI = 1.2 to 11.5). Other than possibly an increased risk of non-Hodgkin lymphoma, no other cause of death related to the mixture of the dioxin contaminants found in PCP was detected [Collins et al., 2009].

Conclusion

Among experts it is well known and accepted, that technical PCP and PCP products contain a large number of unavoidable impurities, depending on the manufacturing method. These consist of other chlorophenols, particularly isomeric tetrachlorophenols, and several microcontaminants, mainly PCDDs, PCDFs, polychlorodiphenyl ethers, polychlorophenoxyphenols, chlorinated cyclohexenons and cyclohexadienons, hexachlorobenzene, and polychlorinated biphenyls (PCBs). Against this background, in 1986 an agreement was made between the industry and the U.S. EPA concerning the dioxin impurities in PCP: (1) Maximum HxCDD per batch released for shipment should not exceed 4 mg/kg. (2) Maximum average HxCDD of all batches sold during the month should not exceed 2 mg/kg. (3) Any detectable levels of 2,3,7,8-TCDD at a limit of detection should not exceed 1 pg/kg. From 1 September 2000 the concentration of hexachlorodibenzoparadioxin (HCDD) in PCP or in its derivatives shall not exceed 2 ppm according to Commission Directive 1999/51/EC. The former limit value for dioxin was 4 ppm. It should be noted that the available data regarding impurities in PCP is not up-to-date. Technical improvements and optimization of processes may have reduced the amount of impurities in PCP products over the last decades. The US EPA does not consider emissions from PCP treated wood a relevant source to be included in the “Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States” (see US EPA (2006)). Nevertheless, dioxins and furans are of special interest in relation with human health and pollution control. Alternatives should be considered seriously in order to prevent environmental release of dioxins and furans from products containing PCP, e.g. utility poles.

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6 Link between PCP and the occurrence of dioxins and furans in the environment

As described in the previous chapter, dioxins (i.e. PCDDs) and furans (i.e. PCDFs) are formed as by-products during the manufacture of chlorinated phenols. Therefore PCP and its derivatives usually contain dioxins and furans at parts per million level, which possibly could be released in the environment. The contribution of PCP and its derivatives to the PCDD/F loading to the aquatic environment is higher than to the atmospheric and terrestrial environment. PCP and its derivatives contain and emit the higher chlorinated PCDD/F congeners to the environment and do not contribute significantly to the burden of more toxic TCDD/F and PeCDD/F isomers; the contribution of PCP to the total I-TEQ (International Toxic Equivalents) of aquatic environmental samples is estimated to be in the order of 10% [LRAT dossier 2008].

Production of PCP

Some data are available concerning the loss of phenolic and nonphenolic compounds into the environment during the normal production of PCP or Na-PCP [Umweltbundesamt, 1985]. The following air emission concentrations (mg/m3) and mass flow values (g/h) were reported: PCP 0.7 mg/m3, 9 g/h; tetrachlorophenols 0.2 mg/m3, 0.8 g/h; trichlorophenols 0.02 mg/m3, 0.04 g/h; hexachlorobenzene 23.9 mg/m3, 12 g/h; pentachlorobenzene 2 mg/m3, 15.5 g/h; tetrachlorobenzene 2.8 mg/m3, 66.5 g/h; OCDD 0.05 mg/m3, 0.04 g/h; OCDF 0.02 mg/m3, 0.002 g/h. The annual air emission values resulting from the production of approximately 2,000 tonnes of PCP or Na-PCP, respectively, per annum are given in Table 9 [LRAT dossier 2008].

Table 9: Air emissions of phenolic and non-phenolic compounds during production (maximum values as reported in BUA (1986)) [LRAT dossier 2008].

Chemical compoundAnnual air emissions (kg/year) during production of:

2000 tonnes PCP/year 2000 tonnes Na-PCP/year

PCP 18 65

Other chlorophenols 9 5

Hexachlorobenzene - 105

Other chlorobenzenes 1 700

OCDD 0.2 0.2

While no waste water occurs during the production of PCP, the annual loss of various compounds resulting from Na-PCP production into the waste water was as follows: PCP, 60 kg; OCDD, 0.34 g; H7CDDs, 0.1 g; H6CDDs, 0.001 g; OCDF, 0.1 g; H7CDFs, 0.026 g; H6CDFs, 0.002 g (BUAS, 1986]) The volume of contaminated wastewater generated during the production of Na-PCP is small, because manufacturers and regulatory agencies have emphasized efficient process design. During the production of approximately 2000 tonnes PCP/year, about 8 tonnes of washing methanol, 4 tonnes of activated charcoal, and 2 tonnes of other wastes occur. These wastes, as well as the filtration sludge resulting from Na-PCP production, contain considerable amounts of hazardous chemicals (Table 10). They are generally disposed of by either storage in underground disposal sites (filtration sludge) or incineration at temperatures above 1200 °C (BUAS, 1986) [LRAT dossier 2008].

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Table 10: Phenolic and non-phenolic compounds in the combined wastes (PCP production) and filtration sludge (Na-PCP production) [BUAS 1986].

Compound Combined wastes (kg/year) Filtration sludge (kg/year)

PCP 1350 900

Other chlorophenols 0.7 ns

Hexachlorobenzene ns 6000

Decachlorobiphenyl ns 3400

Decachlorophenoxybenzene ns 44

OCDD (OCDF) 0.98 0.67 (0.67)

H7CDDs (H7CDFs) 0.13 0.17 (0.045)

H6CDDs (H6CDFs) 0.013 0.092 (0.015)

P5CDDs (P5CDFs) 0.003 x 10-3 0.016 (0.005)

T4CDDs (T4CDFs) 0.002 x 10-3 0.007 (0.001)

2,3,7,8-T4CDD ns 0.001

Transformation of PCP to dioxins

Baker and Hites (2000a) carried out experiments in which PCP is converted to PCDDs under varying irradiation conditions. Their data suggest that available sunlight in the troposphere may convert environmental levels of PCP in the atmosphere to PCDD/F. The authors also cite a number of other experimental studies in which OCDD and in lesser amounts HpCDD were formed through photodegradation of PCP. More recent studies confirm the formation of PCDDs through photolysis of PCP (Liu et al. (2002)) [LRAT dossier 2008].

Use of PCP

A connection between PCP and the occurrence of dioxins and furans in the environment can be found in the past and actual use of PCP and its derivatives. The main advantages of PCP and its derivatives are that they are effective biocides and soluble in oil (PCP) or water (Na-PCP). Few pesticides show a similarly broad efficiency spectrum at low cost. Therefore, PCP and its salts have a variety of applications in industry, agriculture, and in domestic fields, where they have been used as algaecides, bactericides, fungicides, herbicides, insecticides, molluscicides, defoliant, and germicide [LRAT dossier 2008].

Major uses:

− in the preservation of starches, dextrins, glues;− to inhibit fermentation in various materials;− maintenance of boats, trailers, station wagons, siding, fences, outdoor furniture and similar articles;− in construction of boats and buildings;− to mold control in petroleum drilling and production;− in treatment of cable coverings, canvas belting, nets, construction lumber and poles;− in paints, pulp stock, in pulp and paper, cooling tower water, hardboard and particle board;− as wood preservative (applied as a 0.1% solution in mineral spirits, NO2 fuel oil, or kerosene);− in pressure treatment of lumber (at 5% concentration).

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In the past, although PCP and its derivatives had many uses, the major application in the commercial sector was wood preservation (USA 80%, Canada 95%, Germany 61%, 1983). Large quantities of PCP or its sodium salt were used for agricultural application, e.g. as herbicide, insecticide etc., as well as for domestic use mainly related to the outdoor and indoor treatment of wood. With Directive 91/173/EEC of 21 March 1991, the Council had prohibited the marketing and use of PCP throughout the European Union. Voting by qualified majority on the basis of paragraph 1 of Article 100a, it had, however, provided for four exceptions authorizing the use of PCP for the treatment of wood, the impregnation of fibers and textiles, as a synthesizing agent in industrial processes and for the treatment of historical buildings. By contrast, German laws allows no exceptions to the ban on PCP. Today the predominant use of PCP containing chemicals is the treatment of wood as a sapstain control agent for freshly cut timber as well as preservation of textiles, which are subject to attack by fungi and bacteria during storage and use [LRAT dossier 2008].

There is some evidence that PCDD/Fs leaches from treated poles into the surrounding soils, but these studies do not allow for the calculation of a rate of release from this mechanism. Possible release mechanism is the volatilization of dioxins into the atmosphere. Bremmer et al. (1994) estimated an annual release of 15-125 g of TEQ from PCP-treated wood in the Netherlands, based on estimates of dioxin in treated wood and a range of half-lives of dioxin in treated wood from 15 years to 150 years. In 1996, the United States (US) Environmental Protection Agency (EPA) estimated that the use of technical grade PCP over the previous 25 years to treat wood was approximately 336,000 metric tons in the US and an associated 672 kg of dioxin toxic equivalents (TEQs; calculated using the international TEF scheme). Assuming a 3% replacement rate for treated wood, EPA estimated that 468 kg of TEQ could be present in service PCP-treated wood in 1996, and that most of it, about 80%, was in treated utility poles. If the above release assumptions were applied to the 468 kg estimate, the potential annual release in the US in 1996 would be 3 to 19 kg. If actual releases were of this magnitude, they would constitute a significant contemporary source. For these quantities of dioxin to be released to the environment from in-use poles requires that dioxin be able to migrate from the interior of a pole to a pole’s surface [Bremmer et al., 1994].

Lorber et al. (2002) designed a study to examine the potential for PCDD/Fs release from PCP-treated utility poles. The general approach taken was to collect PCP-treated poles of varying ages, to remove and analyze multiple samples from each pole cross-section, and to compare the spatial distribution of PCDD/F congeners among poles of different ages. Evidence of concentration–depth profile changes over time may provide insight into the potential for dioxins to migrate through and then out of PCP-treated utility poles. It was found that the PCDD/F concentrations were consistently higher in the outer portions of the poles than the center. This trend tends to be most marked in older poles and for the lower chlorinated congeners. The trend for dioxins to concentrate in the outer portions of the pole over time suggests migration within the poles, and this migration may result in some environmental release [Lorber et al., 1994].

A study of the Swedish EPA has investigated the importance of pentachlorophenol-treated wood in emissions of dioxins into the environment. A thorough inventory of the use of different products treated by different methods has been carried out, in addition to chemical analyses of four different treated wood products. Between 1956 and 1978 between 1900 and 2400 tonnes of pentachlorophenol were used in Sweden for different pentachlorophenol-treated wood products. The estimated amount of dioxins (I-TEQ) in the environment today due to the use of these chlorophenol-treated wood products was estimated to be between 0.4 and 3.7 kg. This estimate was based on the following assumptions: that the main sources are pressure impregnated wood and do-it-yoursel (DIY)-treated products. Of the pressure impregnated material, about 50 % of the above ground material is still in use (equivalent to about 225 tonnes of pentachlorophenol, 0.4-2.0 kg I-TEQ), while about 40 % of the DIY products are still in use, equivalent to

30

about 55 tonnes of pentachlorophenol and 0.0-0.6 kg I-TEQ.The considerable uncertainty is due to the wide variation in analytical data. In addition, a quite high figure has been used to approximate the amount of wooden products still in use, in order to avoid underestimation. Dioxin sources resulting from the use of chlorophenol-treated wood products are diffuse and scattered, and thus difficult to clean up efficiently. The most efficient method of reducing dioxin emissions is to ensure that all demolition wood is destroyed in a modern incinerator with efficient air pollution control systems [SWEPA 2009].

Eduljee (1999) states that it is likely that the presence of higher chlorinated PCDDs in the atmosphere, such as HxCDD, HpCDD and OCDD may primarily be due to the use of PCP in the past. Baker & Hites (2000b) cites US EPA who observed a 75% decrease in PCDD/F emissions from combustion sources between 1987 and 1995. However, sediment concentrations only decreased by 20%. The authors suggest that de novo synthesis of PCDD/Fs from PCP in the atmosphere explains these data. High concentrations of dioxins in sediment were also observed by various other authors. Several studies were carried out in Japan where PCP was widely used as paddy field herbicides in the past. Masunaga et al (2001b) estimated the contribution of PCP in the dioxin content of Lake Shinji Basin sediment to be 68%. Chloronitrophenol (CNP), and combustion contributed for 16 an 16% in recent surface sediment. In Tokyo bay contributions of PCP, CNP and combustion were estimated to be 76%, 15%, and 9%, respectively (Yao et al. (2002)). Uchimiya et al (2007) estimated the contribution of PCP in the Ichihara Anchorage to be more than 90%. PCP use in Japan peaked around 1967 and levelled out until 1986 (Yao et al. (2002)). Masunaga et al (2001b) indicated that PCP and CNP were used extensively nationwide in Japan, and thus the situation described for the Lake Shinji Basin is expected to be ubiquitous throughout Japan. From the decreasing trend of dioxin deposition in Lake Shinji after phasing out these herbicides, the amount of dioxins that accumulated in the agricultural soil in the basin was estimated to have decreased by about 2%/yr or a half-life of about 35 yr, indicating that dioxin runoff from agricultural fields would continue for a long time [LRAT dossier 2008].

Production and use of PCP as direct source for dioxins and furans

Dioxins in six river and three marine sediments at Nagoya City were determined, and an estimation of their sources was performed. The average concentration was found to be from 230 pg g -1 to 59 × 103 pg g-1, and the average TEQ concentration was from 0.34 to 56 pg-TEQ g -1. In the distribution of polychlorinated PCDDs and PCDFs, the percentage of OCDD was especially high (35-72%), and the order of HpCDDs was (9-13%), TeCDFs (3-11%) and TeCDDs (5-9%). From a factor analysis, it was considered that three components, such as combustion, commercial PCB and chlorinated pesticides (PCP and CNP), were sources of dioxins in the sediments. Furthermore, the contributions of the sources were estimated from multiple regression analysis. The percentages of TEQ contribution from combustion, commercial PCB, and pesticides were 61-90%, 6-39% and trace level, respectively [Ohba et al, 2009].

Although concentrations of PCDD/Fs in majority of Japanese river and ocean sediments decreased below the national environmental quality standard of 150 pg-TEQ· (g-dry sediment) -1 by 2004, localized contamination in as much as 100-fold excess of the environmental quality standard has been reported at various locations including Ichihara Anchorage in northeastern Tokyo Bay. Uchimiya et al (2007) analyzed all mono- to OCDD in 12 surface sediments from Ichihara Anchorage and applied positive matrix factorization (PMF) to quantitatively fingerprint the congener pattern and geographical distribution of a factor causing the localized contamination. A PMF-derived fingerprint attributable to dioxin impurities in PCP exerted more than 90% contribution to total dioxin concentrations in Ichihara Anchorage surface sediments. Although majority of Ichihara Anchorage-born dioxins were trapped at the origin, contribution of the PCP-derived dioxins in overall Tokyo Bay gradually increased toward Ichihara Anchorage, indicating the impact of localized dioxin

31

contamination on a large proportion of Tokyo Bay. It was suggested that, in addition to runoff from rice paddies (to which PCP had long been applied as herbicide) at the basin, Ichihara Anchorage serves as a significant source of PCP-derived dioxins especially in eastern Tokyo Bay [Uchimia et al, 2007].

Isomer-specific data were investigated by Xu, et al (2008) in order to identify the sources of PCDD/Fs in agricultural soils, including Fluvo-aquic and paddy soils, in the vicinity of a Chinese municipal solid waste incineration (MSWI) plant. Homologue and isomer profiles of PCDD/Fs in soils were compared with those of potential sources, including combustion sources, i.e., MSWI flue gas and fly ash; and the impurities in agrochemicals, such as the PCP, sodium PCP-Na and 1,3,5-trichloro-2-(4-nitrophenoxy) benzene (CNP). The results showed that the PCDD/F isomer profiles of combustion sources and agricultural soils were very similar, especially for PCDFs, although their homologue profiles varied, indicating that all the isomers within each homologue behave identically in the air and soil. Moreover, factor analysis of the isomer compositions among 33 soil samples revealed that the contamination of PCDD/Fs in agricultural soils near the MSWI plant were primarily influenced by the combustion sources, followed by the PCP/PCP-Na and CNP sources. This implication is consistent with our previous findings based on chemometric analysis of homologue profiles of soil and flue gas samples, and identifies PCP/PCP-Na as an additional important source of PCDD/Fs in the local area [Xu et al, 2008].

An as yet unidentified origin of elevated concentrations of PCDDs in soil and sediment has repeatedly been described from different locations around the world, including Australia. The present study investigated whether OCDD formation via anthropogenically derived precursors represents a possible source in such samples. Soil and sediment from Australia and Hawaii were screened for known pesticide derived dioxin precursors. Two pesticide formulations containing PCP, which are well-known to contain predominantly OCDD impurities, were also analyzed. Polychlorinated phenoxyphenols (PCPPs), common byproducts of pesticide production, were detected at parts-per-billion (ppb) levels in two PCP formulations and in five environmental samples. The evidence from this study indicates that pesticides and their impurities play an important role in the dioxin contamination of Australian soils and sediments, as well as other locations with similar PCDD/F patterns. The results further suggest that formation of OCDD from pesticide derived precursors may be a possible past, present, and future pathway for contamination of environmental samples [Holt et al, 2008].

Waste containing PCP

Besides the emission of dioxins and furans during production of PCP as well as the emissions resulting from the use of PCP as wood preservative, incineration of wastes is known to be leading to a formation of PCDD/F (dioxins and furans). Especially in the presence of corresponding chlorinated precursors (such as PCBs, PCPs) incineration of waste causes formation of dioxins and furans by a homogenous gas phase reaction at temperatures between 300 and 800°C.

Model studies were performed by Dickson (1992) to determine quantitatively the predominance of two proposed pathways of PCDD formation during municipal refuse incineration. Surface-catalyzed reactions of precursors occurring on fly ash and de novo synthesis of PCDD and related compounds from reactions of particulate carbon were investigated. The relative yields of PCDD formed from the model precursor compound PCP were 72-99000 times higher than PCDD formed from the reactions of activated charcoal, air, inorganic chloride, and Cu(II) as catalyst under identical reaction conditions [LRAT dossier 2008].

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Dioxins and furans emissions have reported to be high when PCP contaminated wood is burned. IPCS (1987) cited a few older studies on dioxin formation. A wide range of PCDD concentrations was observed in form of smoke burning wood chips impregnated with a technical PCP formulation. Temperatures below 500 °C, oxygen deficit and lower gas retention time favoured the formation of PCDDs (Jansson et al. (1978). Vikelsoe and Johansen (2000) studied the dioxin emissions from fires with various chlorinated substances (e.g. dichlorprop, chlorthalonil) and found extremely high yields of the congeners 1,2,3,4,6,7,8-HpCDD and OCDF and OCDD during burning of PCP. The precise pathways through which dioxins are formed have not yet been elucidated. In dioxin emission inventories PCP treated wood is generally taken into account. However, estimations are hampered by highly uncertain or lacking emission factors and corresponding activity rates (Quaß et al. (2000) [LRAT dossier 2008].

Conclusion

Summarising the above it can be concluded, that production and use of PCP present substantial contribution to the total burden of environmental pollution with PCDD/F. Taking into account that besides the emission of dioxins and furans during production of PCP as well as the emission resulting from the use of PCP as wood preservative incineration of wastes containing PCP is an important source of PCDD/F, it must be assumed that a considerable proportion of detectable dioxin and furan levels in environmental samples result from PCP sources. In some studies direct linkage between environmental contamination with dioxins and the use of PCP as origin has been established on the basis of selective measurements and calculations.

At the moment, contribution of earlier and actual use of PCP around the world to the total dioxin burden seems to be relatively low compared with other sources of dioxin releases like combustion processes. Given the fact, that serious efforts are made to reduce PCDD/F emissions from combustion processes, the importance of other emission sources, like the use of PCP products, will become more important in the future. Therefore, keeping in mind the potential of dioxins and furans to cause adverse effects on environmental and human health, it does make sense to undertake every effort to reduce environmental releases.

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