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Water Quality Ambient Water Quality Guidelines for Chlorophenols 8. AQUATIC LIFE Chlorophenol toxicity, especially that of PCP, increases with higher temperatures (5, 156, 311) and lower dissolved oxygen levels (310) due to higher metabolic and respiration rates under these conditions, which in turn require increased food and oxygen uptake. Chlorophenol toxicity, especially that of PCP, is pH dependent, especially near the pKa value since pH controls the ionization status of the chlorophenol and thus its lipophilicity and uptake rate (6). Based on published EC50 and LC50 test data for marine and freshwater molluscs, worms, crustaceans, fish and algae, the majority of the EC50 or LC50 values are in the 0.1 to 1.0 mg/L PCP range. More sensitive species and life stages have lower values (91). Generally speaking, fish, molluscs, worms and crustaceans are acutely affected by PCP below 1 mg/L and chronically affected in the low µg/L range. Algae are affected below 1 µg/L (199).
8.1.1 COMMUNITIES PCP The species compositions of estuarine plankton communities were altered at 76 µg/L of PCP for most species and at a level as low as 7 µg/L for molluscan larvae (202). Marine benthos community structure was altered at 141 µg/L, but not at 1.8 µg/L, in an estuary (117). Based on laboratory tests the NOEL for PCP in marine benthic communities is 13 to 14 µg/L (91). Experiments by the Institute of Ocean Sciences in 1981, in enclosures in Saanich Inlet, started with 10 µg/L and 100 µg/L PCP. Levels were reduced by 67% in 25 days, mostly by photolysis. Effects included a shift in the centric diatom balance, reduced phytoplankton numbers, reduced sedimentation, and decimation of a major diatom population. Bacterial populations were reduced initially but recovered, as did phytoplankton, but with a shift in species ratios (689).
3-MCP and 4-MCP In Table 8.1.2 there are a number of reports of growth inhibition by 3-MCP and 4-MCP on the diatom, Skeletonema costatum at 2.5 to 5.0 mg/L (369, 372), Dunsbella tertiolecta, a green alga, and Porphridium sp., a red alga, at 10 to 15 mg/L (369), and marine plankton assemblages at 0.3 to 1.0 mg/L (354). PCP Table 8.1.2 gives some effects of PCP on marine algae. The lowest reported effect is 0.2 mg /L for C14 uptake rates in Isochrysis galbana. Reduced photosynthesis, as measured by C14 uptake rates, were caused by 0.5 mg/L in Thalassiosira pseudonana, 1.0 mg/L in Glenodinium hallii and Skeletonema costatum, a diatom, and 0.5 mg/L in an estuarine species assemblage (562). In laboratory cultures of the red alga, Champsia parvula, nominal concentrations of PCP at 465 and 280 µg/L caused decreases, 95% and 50% respectively, in fertilization and sporocarp development. These were 2-day exposure tests followed by a week in clean water to allow development of any sporocarps to visible size (2). Kelp, Macrocystis pyrifera, suffered 50% reduction in photosynthesis in 4 days by 0.3 mg/L NaPCP (331). To eliminate all photosynthesis in 4 days took 2.66 mg/L of PCP; in 2 days the required dose was 1 mg/L (174, 218).
Table 8.1.3.1 gives some effects of chlorophenols on marine molluscs, Tables 8.1.3.2 and 8.1.3.4 give effects on marine worms, Tables 8.1.3.3 and 8.1.3.6 give effects on marine crustaceans and Table 8.1.3.5 gives effects on miscellaneous marine invertebrates. Molluscs Table 8.1.3.1 gives some effects on marine molluscs. Studies on the clam, Mya arenaria, were done with a series of chlorophenols. A static bioassay with 4-MCP at pH 8.0 showed 37 mg/L to be the 96-h LC100value; this was 2.4 mg/L for 2,4,5-TCP, 3.9 mg/L for 2,4,6-TCP, and 11.8 mg/L for 2,3,4,6-TTCP, in laboratory static bioassays at 10C. For 3,5-DCP, 9.8 mg/L was the 35-h LC50 value in a laboratory study (386). PCP The eastern oyster, Crassostrea virginica, takes up PCP to an accumulation level which is inversely dependent upon the ambient level. At 25 µg/L the accumulation was 41 fold and at 2.5 µg/L the accumulation was 78 fold. However, 4 days after the exposures ceased the oysters were fully purged of PCP (119). The 96-h LC50 for larvae was found to be 40 µg/L (78). Abnormal growth of embryos, recorded as 48-h EC50 values, also occurred at 40 µg/L of NaPCP (118, 555). The numbers of molluscs in estuarine benthic communities were reduced at 15.8 µg/L of PCP, but not at 1.8 µg/L (117). Reported 96-h LC50 values for this oyster in PCP are 40 µg/L in a static bioassay and 77 µg/L in a flow-through bioassay (205). The related oyster, C. gigas, shows chronic problems with larval development and embryology at NaPCP and PCP levels from 7 to 110 µg/L (120, 257). The Bajanus Organ of clams accumulates high levels of PCP (30). The larval development of Bursatella leachi is completely suppressed at 26C and 17 ppt salinity over a 9- week period by only 7 µg/L of PCP; and 76 µg/L PCP has chronic effects on the development and maturation of miscellaneous planktonic larvae under the same conditions (202). Studies with NaPCP, either as the pure material or as the commercial product "Santobrite", on the bay mussel, Mytilus edulis, showed a NOEL level of 100 µg/L, increasing percentages of abnormal embryology as the concentration increased to 400 µg/L, and 1 to 4 -day EC100 and LC100 responses at 1 mg/L (164, 680).
Barnacles and Anemones In laboratory flow-through bioassays using NaPCP, there were no effects at 0.1 mg/L, but at 1 mg/L attachment, growth, and survival were affected; for attachment and growth 1 mg/L is the 1-d EC100 level and for survival 1 mg/L is the 3-d LC100 level (164). Tunicates and Bryozoans The tunicate, Molgula, and the bryozoan, Bugula, showed a 1-d LC100 response to 1 mg/L of NaPCP (164). Urchins Table 8.1.3.5 gives effects on sea urchin embryos. The sea urchin, Arbacia punctata, was affected by PCP at 0.3 mg/L in early embryo stages and 0.9 mg/L at 20C affected the sperm. These effects are 4-h EC50 and 1-h EC50, respectively (182). Worms Tables 8.1.3.2 and 8.1.3.4 give some effects of chlorophenols on marine worms. Nematode biomass and density were not affected by PCP concentrations of 1.8, 7.0, or 15.8 µg/L, but 161 and 622 µg/L decreased biomass and caused species composition shifts (95). The polychaete worm, Ophryotrochea diadema, was tested at pH 8.1, 21C, 70% dissolved oxygen saturation and 33% salinity. The larval forms were more sensitive to PCP than the adults. The ratio of the 96-h LC50 to the NOEL ranged from 76 to 1 up to 333 to 1 for PCP. Table 8.1.3.4 gives some experimental results for PCP levels down to 3 µg/L. The larvae are more sensitive to PCP than the adults; there are significantly more deaths in PCP concentrations at and below 100 µg/L. The polychaete, Neanthes succinea, had reduced planktonic larval development and survival at 26C and 17 ppt salinity when exposed to 0.076 mg/L of PCP. In a static bioassay the related N. arenaceodentata responded with a 3-d LC100 to 0.435 mg/L of NaPCP.
Crustaceans There are two very obviously different life-stages in marine crustaceans as far as sensitivity to chlorophenols is concerned. When the animals are in inter-molt stages and have a hard, relatively impervious carapace, they are only about one-half as sensitive to chlorophenols as when they are in ecdysis, and uptake rates are maximum. Guidelines for chlorophenols has to take this more sensitive life-stage into account (65, 66). Table 8.1.3.6 gives comparisons of molt and intermolt toxicity in the grass shrimp, Palaemonetes pugio. There is a 30 fold increase in NaPCP uptake at ecdysis over intermolt stages. At 1 mg/L NaPCP, 76% of the deaths occurred within 48 hours of first ecdysis. At 500 µg/L 66% died 24 to 48 hours after second ecdysis but only a few died after the first ecdysis. There was no effect at 100 µg/L. The 96-h EC50 was 0.436 mg/L of NaPCP (68). Table 8.1.3.3 has a great deal of data on the effects of chlorophenols on shrimp: Crangon crangon, C. septemspinosa, Leander japonicus, Penaeus aztecus, P. duorum, Palaemonetes varians., P. elegans, and P. pugio. The lowest 96-h LC50 is 84 µg/L for P. elegans exposed to PCP (73). For PCP, 100 µg/L is reported as an NOEL level in P. pugio (68),while the lowest reported EC50 is 473 µg/L for limb regeneration in the same species (74). There are also data on other chlorophenol congeners, particularly for Crangon septemspinosa (386, 419), and P. pugio (521). In P. pugio O2 consumption was not affected by 1.5 or 5 mg/L NaPCP during intermolt and pro-ecdysial portions of the molt cycle. Late pro-ecdysial stages showed increased O2 consumption at 5 mg/L and early post-ecdysial shrimp died in 3 hours due to greatly increased PCP uptake rates. Intermolt shrimp only increased O2 uptake or died at 10 to 20 mg/L NaPCP (65). In the grass shrimp, 1 mg/L causes ultrastructural changes in the gills, mitochondria, gut, and hepatopancreas, during late ecdysis; these changes may lead to death. The new cuticle is very permeable and allows NaPCP into the hemolymph for transport throughout the organism (67). The rates of regrowth of lost limbs, or initiation of limb buds, have EC50 values ranging from 0.306 to 0.852 mg/L in grass shrimp exposed to NaPCP (74). The blue crab, Callinectes sapidus, clears PCP within hours from the hemolymph to the hepatopancreatic tissues where it remains, some of it conjugated as esters (77). Hepatopancreatic enzymes such as fumarase, malate dehydrogenase, and succinic dehydrogenase are inhibited by PCP. Cytoplasmic enzymes affected are pyruvate kinase, glucose-6-phosphate dehydrogenase, and glutamate-pyruvate transaminase. Mitochondrial enzymes are more sensitive than those in the cytoplasm. Carbohydrate, protein, and lipid metabolism are affected, as is energy production and ion transport. Membrane bound enzymes are also affected (59). Planktonic larval development is affected by 76 µg/L of PCP at 26C in brackish water (202). For the copepod, Pseudodiaptomus coronatus, the 96-h EC50of NaPCP is 68.0 µg/L (78). Another copepod, Nitocra spinipes, had 96-h LC50 values of 21 mg/L for 4-MCP, and 270 µg/L for PCP, in static bioassays at pH 7.8 and brackish water (385). The isopod, Mesidotea entomon, subjected to 4-MCP in brackish water at pH 7.7, had 4 to 7 day LC50 values of 23 to 40.3 mg/L (373).
Table 8.1.4 gives some effects of chlorophenols on marine fish. There is about a one order-of-magnitude difference between the toxicity of PCP to young sockeye salmon, Oncorhynchus nerka, and the lesser toxicity of the unchlorinated parent phenol. The growth rate and food conversion efficiencies of sockeye salmon fry are affected by PCP at 2 µg/L (94). For sockeye salmon the 24-h EC50 is 1.7 mg/L for 2,4-DCP, 900 µg/L for 2,4,5-TCP, 1.1 mg/L for 2,4,6-TCP, 500 µg/L for 2,3,4,6-TTCP, and 300 µg/L for PCP (90). In static bioassays, the 96-h LC50 values for 4-MCP, 2,4,5-TCP, and 2,3,5,6,-TTCP are 5.35, 1.66, and 1.9 mg/L, respectively, when tested with the sheepshead minnow, Cyprinodon variegatus (372, 393). With PCP there is a 60-day survival reduction in a continuous-flow bioassay at 88 µg/L (556). The lowest 96-h LC50 is 223 µg/L (118). Pro-larvae of the pinfish, Lagodon rhomboides, have a 96-h LC50 of 38 µg/L to PCP (119, 205, 555). The eel, Anguilla anguilla, was exposed to 0.1 mg/L PCP for 8 days in pH 8.1 seawater and 4 days in pH 7.1 freshwater. The observed changes in both cases indicated a hypermetabolic state with accelerated utilization of tissue energy reserves (667). The killifish, Fundulus similis, has a 96-h LC50 of >0.306 to NaPCP, and the 96-h LC50 for NaPCP and PCP is 0.112 mg/L in the mullet, Mugil cephalis.
Seaweeds are relatively insensitive to PCP, while the larval stages of molluscs, worms, and crustaceans are relatively sensitive. In crustaceans, the most sensitive stage is at ecdysis when there is no hard carapace and uptake is maximal but, even so crustaceans are not very sensitive. Mollusc larvae are among the most sensitive organisms in marine waters, with LC50 values in the 10s of micrograms range. Sockeye salmon show some chronic effects at concentrations as low as 2 µg/L of PCP where growth is affected.
8.2.1 COMMUNITIES PCP Biological structure and ecosystem processes were affected in outdoor streams at 48 µg/L of Na-PCP (206). Periphyton species ratios and growth responses were affected by 48 µg/L of PCP in streams (116). Ponds with higher primary productivity, especially those with high macrophyte densities, degraded PCP more readily than other less productive ponds, and afforded more protection for fish and other organisms than less productive ponds. These productive ponds had increased levels of TTCPs indicating PCP breakdown; however, the TTCPs were found in sediments, plant tissues and fish tissues, rather than in the water column (208).
Table 8.2.2 gives some effects of chlorophenols on freshwater algae. For the unchlorinated parent compound, phenol, Chlorella pyrenoidosa was able to grow in 200 mg/L, but not in 500 mg/L (3). The equivalent concentrations are much lower for most chlorinated phenols. 2-MCP The only reported NOEL response to 2-MCP is 10 mg/L with Chlorella pyrenoidosa. Photosynthesis suppression, as measured by oxygen production, occurred in C. pyrenoidosa; reduction was to 88% at 100 mg/L and 74% at 500 mg/L. These were steady state tests at 25C, 5% CO2, 72 hours, constant light and 1 g/L dry weight of algal cells (284). The lowest 96-h EC50 value is 70 mg/L in Selenastrum capricornutum (399); no LC50 values were found. 3-MCP The only reported NOEL response to 3-MCP is 10 mg/L with Chlorella pyrenoidosa. Photosynthesis suppression, as measured by oxygen production, occurred in C. pyrenoidosa; reduction was to 82% at 100 mg/L but did not occur at 500 mg/L. The NOEL was estimated to be 10 mg/L. These were steady state tests at 25C, 5% CO2, 72 hours, constant light and 1 g/L (dry weight) of algal cells (284). The lowest 96-h EC50 value is 29 mg/L in Selenastrum capricornutum (399); no LC50 values were found.
4-MCP The suppression of photosynthesis in Chlorella pyrenoidosa, as measured by oxygen production, was down to 84% at 100 mg/L and 27.4% at 500 mg/L. Test conditions were steady state, 25C, 5% CO2, 72 hours, constant light and 1 g/L dry weight of algal cells (284). NOEL values of 0.32 mg/L and 3.2 mg/L were reported for Phaeodactylum tricornutum and Scenedesmus pannonicus, respectively (371). The lowest 96-h EC50 value is 4.79 mg/L for growth in Selenastrum capricornutum (372); and the lowest 96-h LC50 is 9.6 mg/L in P. tricornutum (371). 2,4-DCP The green alga, Chlorella pyrenoidosa, was able to grow in 8 mg/L 2,4-DCP, but not in 10 mg/L (3). At 100 mg/L there was complete destruction of chlorophyll in C. pyrenoidosa, and oxygen evolution dropped to 42%. At 50 mg/L the oxygen evolution was 56% of control (284). At 163 mg/L, nitrate and nitrite assimilation in C. pyrenoidosa is completely inhibited (500). The lowest EC value is 2 mg/L over 8 days in the green alga, Microcystis aeruginosa (383); no LC50 values were found. 2,3,4-TCP There is one 96-h EC50 value reported; 2.0 mg/L for Selenastrum capricornutum (399); no other data were found. 2,3,5-TCP The only datum found was an EC value of 10 mg/L for an unspecified green alga (220). 2,4,5-TCP The trichal blue alga, Phormidium, was completely inhibited from spreading in culture by a 100 µg spot of 2,4,5-TCP applied to the culture medium (485). The only NOEL value is 1 mg/L for chlorophyll destruction in Chlorella pyrenoidosa (284); this was very close to the lowest 96-h EC50 of 1.22 for chlorophyll production in Selenastrum capricornutum ( 399). 2,4,6-TCP Chlorella pyrenoidosa, a green alga, was able to grow in 100 µg/L of 2,4,6-TCP, but not in 1 mg/L according to one source (3); however, another source (284) indicates that 1 mg/L is the NOEL level for photosynthesis. Reported 72 to 96-h EC50 values are 3.5 mg/L in Selenastrum capricornutum (399) and 10 mg/L in Chlorella vulgaris (399 ) and C. pyrenoidosa (284 ). No EC50 data were found.
2,3,5,6-TTCP The only data are reports of 96-h EC50 values in the 2.66 to 2.72 mg/L range for Selenastrum capricornutum (220, 451). PCP The algal community structure is disrupted, and some sensitive species are affected, at 1 µg/L of PCP (199). Chlorella pyrenoidosa has a 96-h EC50 for growth of 7 mg/L (85) but a 72-h EC100 of 7.5 µg/L for photosynthesis (284). Other species are affected at 2 µg/L (330). NaPCP at 15 mg/L prevents initiation of algal growth and stops existing algae after about 7 days; 20 mg/L stops existing algal growth immediately (163). NaPCP was initially toxic at 2.0 mg/L for 3 to 7 days for different algal species but by the end of a 21 day period any initial toxicity was overcome (330). In stable ponds in Rhodesia, 5 mg/L NaPCP had the most effect within 24 hours and Spirogyra recovered quickly, within 3 weeks (666). The 48-h LC65 for Ankistrodesmus braunii in laboratory culture was 6 to 7 mg/L NaPCP. After an 8-day recovery period the remaining cells multiplied normally again (8). There is an NOEL report of 2 mg/L for Gomphonema parvulum, a diatom, (330), but more data to indicate that there are effects below this level at 1.8 mg/L, 80 µg/L, 290 µg/L, 410 µg/L, and 7.5 µg/L for several different species of fresh water algae (330, 85, 284). See Table 8.2.2 for details.
The yeast, Saccharomyces cerevisiae, is used for mutagenicity tests and is dealt with in Section 5.6. The fungi are dealt with in Section 7.1.1 in the Chapter on Terrestrial Life, rather than here under freshwater aquatic life.
Bacteria are dealt with specifically in Section 7.1.2 under terrestrial life. Section 5.6 gives the results of mutagenicity tests which are often carried out on bacteria. The standard Ames assay uses Salmonella typhimurium, but many other bacteria are also used. Further data on the responses of bacteria to chlorophenols may be found in this section of the report and in Table 7.1.2. which lists many effects of chlorophenols on bacteria, including Photobacterium phosphoreum, which is commonly used in the Microtox assay.
The free-floating small duckweeds, Lemna sp., are common experimental aquatic plants since they are easily cultured. Their identification to the species level is difficult and most specific epithets found in non-taxonomic literature should be accepted tentatively. They appear to be relatively insensitive to chlorophenols compared to other aquatic organisms. Table 8.2.5.1 gives some effects of chlorophenols on aquatic plants. 4-MCP The only effects are on Lemna sp. and the lowest EC value is 4.79 mg/L (220); other data indicate much higher 48-h EC50 values of 282 mg/L for chlorosis (372, 381). 2,4-DCP The only data are short term or multi-week EC values for growth and chlorosis; the values are in the 5 to 283 mg/L range (3, 381). 2,3,6-TCP There is one EC value of 5.92 mg/L for duckweed (220). 2,4,5-TCP The 72-h EC50 for chlorosis in duckweed is 1.66 mg/L (372, 381). 2,4,6-TCP The 2-week NOEL is reported as 100 µg/L for duckweed (3); chlorosis and growth effects are reported at 5 to 5.92 mg/L for duckweeds (3, 372, 381). 2,3,4,6-TTCP In duckweeds, 2 to 3-day EC50 values of 603 to 1400 µg/L are reported for growth and chlorosis (220, 381). PCP When Lemna minor is exposed to 6 mg/L of PCP for 60 hours, the alanine aminotransferase activity drops to 10% of its starting value. The chlorophyll concentration begins to drop at 1 mg/L and plants are pale by 3 mg/L. Dark respiration increases up to 3 mg/L, then decreases to background at 6 mg/L. Table 8.2.5.2 gives the effects at various PCP concentrations (4). In another study the 48-h EC50 value for L. minor is found to be 189 µg/L for chlorosis (381). The water Hyacinth, Eichhornia crassipes, is tolerant of PCP or NaPCP. The appearance of the plant is affected at 4.6 or 5 mg/L, but 74 or 80 mg/L is required for a complete kill (332). The contact of NaPCP with Myriophyllum and Phragmites results in heavy localized damage to the foliage but after 6 to 8 weeks new shoots are formed and the plants recover (674). Canadian waterweed, Elodea canadensis, has a NOEL value of 230 µg/L, but 1 to 3-week EC values range from 380 to 1440 µg/L as measured by growth reduction (113).
Some effects of chlorophenols on aquatic invertebrates are given in the following series of tables: Table 2.4-QSAR analyses on Daphnia magna Communities In a stable Rhodesian pond, 5 mg/L NaPCP caused the heaviest reduction in microfauna in the first 24 hours and the total population dropped from about 30 000 to 80/L after 10 days. Cladocera disappeared quickly and came back only slowly. Copepods and ostracods recovered quickly; the original population levels were back within 3 weeks (666). Protozoans Chronic data are available for several chlorophenols and the lowest ones are 68 mg/L for 2-MCP when tested with Tetrahymena pyriformis (244), 0.5 mg/L for 2,4-DCP using Enterosiphon sulcatum (42), and 0.68 mg/L for 2,4,5-TCP (237), 119 mg/L for 2,3,4,5-TTCP (260), 1.01 mg/L for 2,3,5,6-TTCP (244), and 0.15 mg/L for PCP (237), using T. pyriformis, a ciliate. Coelenterates The only datum is a 48-h LC50 value of 0.73 mg/L for PCP at 17C and 20C using Hydra oligactis (112, 197). There is one 21-day NOEL value of 0.032 mg/L NaPCP also using Hydra oligactis (333). Leeches Leeches bioconcentrate chlorophenols efficiently and, since they do not excrete it regularly, they are good integrators of fluctuating and sporadic chlorophenol levels over a period of time. The uptake rate is pH and temperature dependent (86). Worms Twenty-four hour chronic data of 10 mg/L for 2,4-DCP, 5 mg/L for 2,4,5-TCP, and 10 mg/L for 2,3,4,6-TTCP are available on liver flukes (388). The lowest 96-h LC50 NaPCP datum is 0.11 mg/L for the oligochaete worm, Nais communis (92); for PCP the lowest 96-h LC50 datum is 0.259 mg/L in the oligochaete, Branchiura sowerbyi (618), and the lowest 48-h LC50 datum is 0.13 mg/L in the planarian, Dugesia lugubris (197). Insects Insects are relatively insensitive to chlorophenols. The 48-h LC50 for 2,4,6-TCP is >13.5 mg/L for the chironomid, Tanytarsus dissimilis (245). The lowest PCP concentration having a 48-h LC50 effect is 0.11 mg/L in the midge, Chironomus thummi (197). Table 8.2.6.1 displays all the available data on the effects of chlorophenols, mostly PCP, on aquatic insects.
Crustaceans The sensitivity of crustaceans varies with the stage in the molt cycle; maximum sensitivity occurs at, and just after, ecdysis, before the carapace has hardened (67, 68, 76). A concentration above 1 mg/L PCP affects the nerve impulse transmission in the abdominal motor axon of the Crayfish, Astacus fluviatilis (307). For 2,4-DCP the lowest 48-h chronic effects were found at 0.1 mg/L ; the lowest acute effects were 10-day LC14 values of 1 mg/L. The test organisms were crayfish, Orconectes propinquus and O. immunis (387). For 2,3,6-TCP, using the crayfish Astacus fluviatilis, the lowest 8-day LC50 value was 5.4 mg/L at pH 6.5; this rose to 19 mg/L at pH 7.5 (71). The lowest chronic PCP datum is 0.023 mg/L for survival of young Gammarus fasciatus (416). The lowest 96-h LC50 datum is 0.092 mg/L for Gammarus pseudolimnaeus, using Dowicide EC7 which was 88% PCP (79); for pure PCP the lowest 96-h LC50 datum is 0.22 mg/L using the shrimp, Crangonyx pseudogracilis (113). Molluscs Molluscs are particularly sensitive, especially to PCP, and the larval stages are the most susceptible; this is also true for other invertebrates with larval development (311). In the snail, Australorbis glabratus, 2 mg/L PCP causes an accumulation of acetate, pyruvate, lactate, and inorganic phosphate, indications that the Kreb cycle has been shut down. This results from poisoning of the oxidative phosphorylation system by PCP (62) A useful set of data by Gupta et al., 1982 (97) is presented in Table 8.2.6.8, showing the effects of PCP on the snail, Lymnaea acuminata. Both Na-PCP and PCP were used and LC16, LC50 and LC84 calculations were made, for 12-, 24-, 48-, 72-, and 96-hour exposure periods. In any time series block of data, the toxicity rises with increasing exposure time. Also, as expected, LC16 values are lower than LC50 and LC84 data, respectively, for any identical time period. Thirdly, with the exception of the 48- and 72-hour LC16 values, PCP was more toxic than Na-PCP. At the pH of 7.9, where this experiment was carried out, ionization of PCP should have been essentially complete and the availability of the two compounds equal. Correcting the doses to reflect the actual amount of active ingredient, PCP, by subtracting the weight of the sodium, only gives better agreement for the 72- and 96-hour values. Shorter exposure periods still indicate much less toxicity when given as Na-PCP. In this snail the ratios of the LC50s of phenol to PCP vary from 802 to 923, over exposure periods of 12 to 96 hours. This is almost two orders-of-magnitude greater sensitivity to PCP than to phenol, which is greater than the one order-of-magnitude difference noted in section 8.2.4 for bacteria and section 8.1.4 for salmon. This verifies other work by VanDijk et al. (311) indicating the high relative sensitivity of molluscs to PCP. Table 8.2.6.9 shows the effects of pH and temperature on the 96-h LC50 of PCP in the snail, Physa gyrina (113). The maximum effect of the PCP is at the optimum growth conditions tested of 24C and pH 8.1. Snails need high pH values in order for dissolved calcium to be readily available for shell growth, and higher temperatures promote high growth rates in these poikilotherms. Due to the mode of action of PCP on terminal respiration, effects will be more marked as growth rates increase. The lowest 96-h LC50 was 0.22 mg/L ; at pH 7.8, and a temperature of 4.2C, the 96-h LC50 rose to 1.38 mg/L. Table 8.2.6.2 gives the effects of several chlorophenols on various species of molluscs. For 2-MCP, 4-MCP, 2,4-DCP, 2,4,5-TCP, and 2,3,4,6-TTCP, only 24-h LC100 data are available: the values are 10 mg/L, 10 mg/L, 10 mg/L, and 1.51 mg/L, respectively, for the limnaeid snails, Pseudosuccinea columella and Fossaria cubensis (388). There is one 96-h LC50 value of 5.5 mg/L for 2,4,6-TCP in the snail, Aplexia hypnorum (245). There are more data for PCP. NOEL values of 0.05 mg/L, 0.111 mg/L, and 0.2 mg/L are reported, generally for reproductive effects in relatively hard water (85, 102, 112). The lowest chronic effects are reported at 0.05 and 0.09 mg/L (85, 215). The lowest acute effects reported are 96-h LC50 values of 0.16 to 0.18 mg/L PCP at 18C and pH 7.9 in hard water (97).
Cladocerans There are abundant data on the cladocerans, mostly Daphnia magna. They are primarily IC50 or EC50 data; few are LC50 data. The ratio of acute to chronic toxicity endpoints varies widely, even within this relatively uniform group of organisms. It is 37 for Ceriodaphnia reticulata and 1 for Sinocephalus vetulus (113). Table 2.4 gives the results of an experiment on Daphnia magna by Devillers et al. in 1986 (57), testing all but two of the different congeners of chlorophenols under identical conditions; only 2,5-DCP and 2,3,4,6-TTCP were not included in this test series. A series of tests with PCP using the cladoceran, Sinocephalus vetulus, at 25C and at a series of different pH levels shows that, as the pH rises from 7.3 to 8.3, the 48-h LC50 also rises from 160 µg/L to 364 µg/L (113). For several species of amphipods the toxicity of PCP is clearly shown to vary by about a factor of ten, over the range pH 6.5 to pH 8.5; acidic pH levels are more toxic (79). The PCP used was a commercial mixture, Dowicide EC7, which contained 88% PCP. The experimental conditions were a temperature of 22C, a hardness of 42 to 47 mg/L, alkalinity of 10 to 52 mg/L, a free CO2 level of 0.32 to 6.32 mg/L, dissolved oxygen >60% saturation at 6.6 to 8.7 mg/L, and 16 hours of light per day. Few experiments control, or report, this many experimental variables. The series of experiments conducted by Adema et al. (85) illustrate the increase in toxicity as exposures increase from 24 hours to 21 days. Another series of experiments under identical conditions by Le Blanc (56) allow further comparisons of toxicities of the different chlorophenol congeners; however, fewer congeners were tested than in the experiment by Devillers (57). The same relatively non-toxic status for 2,4,6-TCP was found by both experiments. A much closer agreement between the ratios is found between the two experiments if the 24-h EC50 data of Le Blanc are compared to the 24-h IC50 data of Devillers (57). This shows that the length of exposure is a critical piece of data when comparing results between experiments. A series of experiments were done by Lewis and Horning on D. magna and D. pulex which illustrate the variation between experimental runs, the effect of temperature differences, and the effect of the duration of the experiment when calculating the LC50 for NaPCP. These data are given in Tables 8.2.6.11 and 8.2.6.12 and show variation of up to 2.2 between the lowest and highest calculated LC50. Tables 2.4, 8.2.6.6, 8.2.6.7, 8.2.6.11 and 8.2.6.12 give data on the effects of chlorophenols on cladocerans. All of this information has been summarized in Table 8.2.6.10 which gives the lowest chronic, acute and NOEL data for cladocerans. The acute data are usually given as the 24-h or 48-h LC50, and chronic data are usually the level which causes immobility. The lowest chronic effect level reported for PCP was 4.1 µg/L (113).
Very little work has been reported on aquatic vertebrate animals other than fish. What data there are indicate that the most sensitive organisms are the tadpole life-stages of amphibians. This is not surprising since they are small, fully submerged, growing and metamorphosing rapidly, have no impervious scales or exoskeleton, and have extensive gill surfaces exposed to the water for efficient uptake. Table 8.2.7 gives what few data there are available on amphibians. Tadpoles of the common frog, Rana pipiens, were tested with NaPCP. No tadpoles died at 0.6 mg/L over a three day period but there was a 6.3-h LC100 of 1 mg/L and a 1.3-h LC100of 5 mg/L (69). No chronic data were reported. but one would expect such values to be less than 1 mg/L. Other reported 48-h LC50 data for amphibians are in the 0.2 to 0.3 mg/L range (112, 114, 323, 551), but no deaths were reported at 0.13 to 0.21 mg/L (112, 551).
The main uptake route for chlorophenols in fish is from the water via the gills, not from the diet (131). Toxicity of NaPCP in fish increases as the pH drops and the temperature rises (19, 168); water hardness has little effect on chlorophenol toxicity (19). Using goldfish, Carassius auratus, and bluegill sunfish, Lepomis macrochirus, the effects of water hardness on the toxicity of PCP was investigated. Hardness levels of 13.0, 52.2, 208.7 and 365.2 mg/L as CaCO3 were tested at Ca/Mg ratios of 1 : 1 and 5 : 1. The tests were 96-h static bioassays and no significant effect of hardness was found (124). Yolk sac edema and skull deformations are common chronic effects with technical grade PCP, which contains dioxins and other impurities, but are rare with purified grades of PCP (259). The breakdown-product, pentachloroanisole (PCA) is much less toxic to fish, fungi, and bacteria than PCP (17). However, PCA is rapidly taken up by organisms and has a longer 1/2 life than PCP. Salmonids are especially sensitive to PCP (311). Fish mortality
is rapid at acutely toxic levels of PCP; thus 24-hour and 96-hour
LC50s are usually similar (251). When exposed to chlorinated
effluents, the fathead minnow, Pimephales promelas, accumulated
DCPs and TCPs (186). There are a series of tables showing the effects of chlorophenols to fish: Table 8.2.8.1-carp, Alburnus, Aplocheilus, Cyprinus, Rutilus,
Carassius. The lowest acute response by a fish to PCP was 0.018 mg/L or 18 µg/L, while in frogs the lowest value was 0.207 mg/L. In the frog this was a 48-h LC50 value as compared to a 96-h LC50 value for the fish. One would expect the frog value to be lower if it had been tested and reported as a 96-h LC50 . The lowest fish chronic response to PCP was 0.66 µg/L. Using the more soluble Na or K salt of PCP results in a lower acute response level of 9.8 µg/L and a slightly higher chronic response level of 1.74 µg/L (69, 94, 126, 142, 148). Salmon and trout fry are quite sensitive to chlorophenols, more so than most other fish and animals, and more sensitive than frog tadpoles. In fish, PCP concentrations are generally highest in liver, gills, gall bladder, and digestive tract, and lowest in muscle tissue (296, 143, 121). PCP absorbed by fish accumulates in various organs, but eventually ends up in the gall bladder and is ultimately secreted, as the beta-glucuronide or as the sulphate conjugate, by the liver (143). Pre- or simultaneous treatment of rainbow trout with carbaryl,
and then 0.25 or 0.50 mg/L PCP, produces a synergistic effect,
and the 2-h LC50 for the trout and PCP decreases significantly
(553). Using goldfish, Carassius auratus, and taking the product of concentration and survival time, the relative toxicities of the MCPs, compared to phenol were 1.15 for 2-MCP, 1.51 for 3-MCP and 1.89 for 4-MCP (392).
2-MCP A group of fish species were exposed to 2-MCP for 48 hours and examined to determine the metabolites. These metabolites were 50 to 60% chlorophenylsulphate and 10 to 30% chlorophenylglucuronide in the aquarium water, as a result of urinary excretions. The bile contained 70 to 80% chlorophenylglucuronide and 10% chlorophenylsulphate. No dechlorination took place, as is common in mammals (158, 135). The fish species used were: Rhodeus
serviceus amarus -bitterling These fish showed a sub-lethal response to 2-MCP at 3, 3, 10, 2, 3, 4, 4, 5, 7, 5, and 3 mg/L, respectively (158). The lowest reported acute response for 2-MCP is 2.1 mg/L in rainbow trout, Oncorhynchus mykiss (611). This is a 96-h LC50 value at pH 7.7, 12C, in water with a hardness of 280 mg/L. The lowest chronic response is 3.0 mg/L in guppies, Poecilia reticulata. In the guppy, the LC50 rose from 7.1 to 13.5 mg/L, a ratio of 1.9, as the pH rose from 6.1 to 7.8, due to better uptake of the undissociated 2-MCP at the lower pH levels (363). See Tables 8.2.8.8 and 4.2.3.7 for pH effects on chlorophenol toxicity in the guppy. Fathead minnows, Pimephales promelas, in the embryo to larvae developmental stages, were reported not to be affected at concentrations up to 3.9 mg/L during long-term exposures (364). In fish the reported NOEL and no lethal effect values range from 3 to 10 mg/L, but no Oncorhynchus or Salmo species were tested.
3-MCP The lowest reported acute response for 3-MCP is 2.9 mg/L at pH 7.7, 12C, in water with a hardness of 280 mg/L (611). The test fish was the rainbow trout, Oncorhynchus mykiss. The lowest chronic response was 10.0 mg/L in the common carp, Cyprinus carpio, where it caused malformed embryos (368). In fish the reported NOEL and no lethal effect values range from 1 to 1000 µg/L, but no Oncorhynchus or Salmo species were tested. In the guppy the LC50 rose from 6.4 to 7.9 mg/L, a ratio of 1.2, as the pH rose from 6.1 to 7.8, due to better uptake of the undissociated 2-MCP at the lower pH levels (363). See Tables 8.2.8.8 and 4.2.3.7 for pH effects on chlorophenol toxicity in the guppy. Data on 3-MCP are rare as it is not a commonly used chemical. 4-MCP As shown in Tables 8.2.8.8 and 4.2.3.7 for the guppy, Poecilia reticulata, the toxicity of 4-MCP decreases from 6.3 to 9.0 mg/L as the pH rises from pH 5 to pH 8. The ratio of the toxicity at pH 8 to the toxicity at pH 5, is 1.4 for 4-MCP, and the toxicity of 4-MCP at pH 8 is 1/10 the toxicity of PCP at pH 8 (144). The lowest reported acute toxicity to 4-MCP is a 96-h LC50 of 3.8 mg/L at pH 7.6 to 8.3 in a static bioassay using juvenile fathead minnows, Pimephales promelas (394). The lowest chronic response is a 48-h EC50 of 3.0 mg/L at pH 7 to 8, using the golden orfe, Idus idus melanotis (366). In fish the reported NOEL and no lethal effect values range from 2 to 3.2 mg/L, but no Oncorhynchus or Salmo species were tested. 2,3-DCP No data were found on the effects of 2,3-DCP on fish. 2,4-DCP The toxicity of 2,4-DCP to the guppy, Poecilia reticulata, decreases from 3.5 to 7.6 mg/L as the pH rises from pH 6 to pH 8. The ratio of the LC50 at pH 8 over that at pH 6 is 2.2, as shown in Tables 8.2.8.8 and 4.2.3.7 (144). The lowest reported chronic and acute toxicities to 2,4-DCP are both 0.07 mg/L in the rainbow trout, Oncorhynchus mykiss. The chronic response was an EC100 (220), and the acute response was a 23 to 27-d LC50 at 14C, pH 7.8, and water hardness of 200 mg/L; embryos and larvae were used (376). Several experiments were done on a number of Oncorhynchus sp. at different hardness levels, but pH was directly related to hardness so no clear distinction could be made between them and it is known that lower pH leads to greater toxicity (376).
2,5-DCP No data were found on the effects of 2,5-DCP on fish. 2,6-DCP The toxicity of 2,6-DCP to the guppy, Poecilia reticulata, decreases from 3.9 to 17.9 mg/L as the pH rises from pH 6 to pH 8. The ratio of the LC50 at pH 8 over that at pH 6 is 4.6; these data are given in Tables 8.2.8.8 and 4.2.3.7 (144). The lowest reported acute toxicity response to 2,6-DCP is a 96-h LC50 of 3.9 mg/L using the guppy, Poecilia reticulata; this was carried out at 26C, pH 6.0, and a water hardness of 90 mg/L (144). The lowest chronic response found was 5.0 mg/L in a 12-h static bioassay using larval lamprey, Petromyzon marinus (614). 3,4-DCP There are few data on the effects of 3,4-DCP on fish. No chronic data were found but the lowest acute response, an LC100 of 5.0 mg/L, was reported for three species of fish in static bioassays (614). The conditions were 2.8C for 3 hours using the rainbow trout, Oncorhynchus mykiss, 17C for 3 hours using the bluegill sunfish, Lepomis macrochirus, and 12.8C for 11 hours using larval lamprey, Petromyzon marinus. 3,5-DCP No data were found on the effects of 3,5-DCP on fish. 2,3,4-TCP No data were found on the effects of 2,3,4-TCP on fish. 2,3,5-TCP There were no chronic data found on the effects of 2,3,5-TCP on fish and acute data were rare, but the lowest effect was a 24-h LC50 value of 0.8 mg/L in Salmo trutta. The lethal concentration to the bluegill sunfish, Lepomis macrochirus, was reported to be 0.45 mg/L (220). The toxicity of 2,3,5-DCP to the guppy, Poecilia reticulata, decreases from 0.882 to 4.74 mg/L as the pH rises from pH 6.1 to pH 7.8. The ratio of the LC50 at pH 7.8 over that at pH 6.1 is 5.4; these data are given in Tables 8.2.8.8 and 4.2.3.7 (144).
2,3,6-TCP There were few data on the effects of 2,3,6-TCP on fish. The lethal concentration to the bluegill sunfish, Lepomis macrochirus, was reported to be 0.32 mg/L . The lowest chronic effect, to the fathead minnow, Pimephales promelas, was reported at 0.72 mg/L (220). No good LC50 data were available to estimate acute effects. 2,4,5-TCP The toxicity of 2,4,5-TCP to the guppy, Poecilia reticulata, decreases from 0.987 to 3.060 mg/L as the pH rises from pH 6 to pH 8 ( see Tables 4.2.3.7 and 8.2.8.8). The ratio of the LC50 at pH 8 over that at pH 6 is 3.1 (144). The lowest reported acute effect level of 2,4,5-TCP to fish was a 96-h LC50 of 0.45 mg/L at pH 7.2, 22C and a water hardness of 40 mg/L using the bluegill sunfish, Lepomis macrochirus (390). The lowest chronic response reported occurred at 1.0 mg/L of Dowicide-2 as a source of 2,4,5-TCP. This was a 4-h static bioassay at 12.8C using rainbow trout, Oncorhynchus mykiss (614). 2,4,6-TCP Rainbow trout, Oncorhynchus mykiss, were exposed to bleached kraft mill effluents for 2 weeks at pH 7 ± 0.5, 8 to 10C, 7 ppt salinity and 2.5% effluent in Baltic Sea Water. There was a 10-day half-life for clearance of the 2,4,6-TCP found in the livers once the exposure ended. Wild fish were caught near the discharge from the mill and the 2,4,6-TCP in the fatty portion of their livers was assayed. A 200 g perch, Perca fluviatilis, contained 2.7 µg/g ; 370 g and 600 g northern pike, Esox lucius, contained 0.4 µg /g and 0.5 µg/g (187). The toxicity of 2,4,6-TCP to the guppy, Poecilia reticulata, decreases from 0.61 to 7.859 mg/L as the pH rises from pH 5 to pH 8. The ratio of the LC50 at pH 8 over that at pH 5 is 12.9 (see Tables 4.2.3.7 and 8.2.8.8) (144). The lowest reported chronic effects, on enzyme function occurred at 0.2 mg/L in a 96-h test using rainbow trout, Oncorhynchus mykiss ( 245). The lowest reported acute effect, a 96-h LC50 of 0.32 mg/L, was found at pH 7.2, 22C, and a water hardness of 40 mg/L using the bluegill sunfish, Lepomis macrochirus (390). 3,4,5-TCP There are few data on the effects of 3,4,5-TCP on fish. No chronic data were found and the lowest acute value was a 7-d LC50 value of 1.14 mg/L for the guppy, Poecilia reticulata (419). TCPs (unspecified) There is a report on various salmon species, Oncorhynchus, and the northern squawfish, Ptychocheilus oreganensis, indicating that values of 1, 5, or 10 mg/L of TCP are the 0.5 to 4-h EC100 and LC100 level at 10C to 20C in a static bioassay (615). The chronic effect noted was equilibrium loss.
2,3,4,5-TTCP The lowest reported acute effect of 2,3,4,5-TTCP on fish is a 96-h LC50 of 0.205 mg/L in a flow -through bioassay at pH 6.9 to 7.7 using 10 g rainbow trout, Oncorhynchus mykiss (261). The lowest chronic effect reported is a 96-h EC50 of 0.75 mg/L using fathead minnow fry, Pimephales promelas, in a static bioassay at pH 6.5 to 7.9, 22C, and water with a hardness of 32 to 99 mg/L (261). As shown in Tables 4.2.3.7 and 8.2.8.8, the toxicity of 2,3,4,5-TTCP to the guppy, Poecilia reticulata, decreases from 0.442 to 2.32 mg/L as the pH rises from pH 6.1 to pH 7.8. The ratio of the LC50 at pH 7.8 over that at pH 6.1 is 5.2 (144). 2,3,4,6-TTCP As shown in Tables 4.2.3.7 and 8.2.8.8, the toxicity of 2,3,4,6-TTCP to the guppy, Poecilia reticulata, decreases from 0.348 to 3.665 mg/L as the pH rises from pH 6 to pH 8. The ratio of the LC50 at pH 8 over that at pH 6 is 10.53 (144). Juvenile trout exposed to 2% bleached kraft mill effluent at pH 6.7 and hardness 20 mg/L accumulated 2,3,4,6-TTCP in the bile. In one 30-day trial, 99% was conjugated. In a 10-day trial with 0.6% effluent, 69% of the 2,3,4,6-TTCP was conjugated as gluconurides in the bile. In a third trial with larger fish for 6 days, the bile conjugates were 81% gluconurides and 25% sulphates; plasma had 63% conjugated and the rest free (422). The lowest reported acute effect on fish is a 96-h LC50 of 0.085 mg/L in a static bioassay using 74% technical grade 2,3,4,6-TTCP on rainbow trout, Oncorhynchus mykiss (236). The conditions included pH 7.2, 12C, and a water hardness of 44 mg/L. If one suspects the contaminants in the 74% purity material of having an effect, then the next lowest effect reported for pure 2,3,4,6-TTCP is a 96-h LC50 of 0.14 mg/L in a static bioassay using bluegill sunfish fry, Lepomis macrochirus (390). The conditions included pH 6.5 to 7.9, 22C, and a water hardness of 32 to 99 mg/L. No chronic effects data were found. 2,3,5,6-TTCP There were no chronic data on fish for 2,3,5,6-TTCP and acute data were rare. The lowest acute value reported was a 96-h LC50 of 0.17 mg/L for young bluegill sunfish, Lepomis macrochirus (390, 459). The conditions were pH 6.7 to 7.8, 22C, and water hardness of 32 to 48 mg/L. As shown in Tables 4.2.3.7 and 8.2.8.8, the toxicity of 2,3,5,6-TTCP to the guppy, Poecilia reticulata, decreases from 0.39 to 3.94 mg/L as the pH rises from pH 6.1 to pH 7.8. The ratio of the LC50 at pH 7.8 over that at pH 6.1 is 10.1 (144).
PCP The lowest reported acute response to PCP by fish is a 96-h LC50 of 0.018 mg/L using rainbow trout fry, Oncorhynchus mykiss (148). The fry were 77 days old and the conditions were pH 7.2, 10C, and water hardness of 50 mg/L. The lowest chronic response, a reduced growth rate in rainbow trout fry at 15C, occurred at 0.66 µg/L (126). There is some difficulty with interpreting the data in this paper and it has been classed as a secondary reference and not used to set the guidelines. The next lowest value is a chronic growth effect in Sockeye salmon at 15ºC and pH 6.8 (94). The estimated threshold NOEL is 1.74 µg/L and the LOEL is 3.49 µg/L. This is the data used to set the PCP guideline. As shown in Tables 4.2.3.7 and 8.2.8.8, the toxicity of PCP to the guppy, Poecilia reticulata, decreases from 0.107 to 0.906 mg/L as the pH rises from pH 6 to pH 8. The ratio of the LC50 at pH 8 over that at pH 6 is 8.5 (144). In Cichlids there is an increased feeding rate, but decreased growth rate, when exposed to 200 µg/L of PCP (150). This reduction in conversion efficiency is quantified at 30% in largemouth bass exposed to 50 µg/L of PCP (151). Shiners, Notropis cornutus, had feeding rates up 57% at 56 µg/L PCP and 65% at 180 µg/L. Simultaneously the conversion efficiencies dropped about 50% at 180 µg/L due to uncoupled oxidation and hence reduced ATP formation (149). Growth rates dropped 25% at the 180 µg/L rate and 320 µg/L was fatal. Puntius ticto ate as much, but gained less weight, under sub-lethal levels of NaPCP. Food conversion efficiencies began to drop at levels as low as 1.5 µg/L (133). Sockeye salmon, Oncorhynchus nerka, had reduced growth rate and food conversion efficiency at 15C when PCP levels exceeded 2 µg/L (94). Rainbow trout, Oncorhynchus mykiss, at 15C, suffer growth effects at 0.66 µg/L PCP, but not at 0.035 µg/L (203). Rainbow also accumulate PCP up to 5 times over controls on the same diet, when exposed for 115 days to 0.035 µg/L. There was no effect seen on growth or weight of the fish (126). Female rainbow exposed to 22 or 49 µg/L of 99% PCP for 18 days had lower oocyte viability (146). In laboratory fish, the bluegill, Lepomis macrochirus, has the highest concentration of PCP in the bile, followed by liver, gills, and muscle (13). Experiments on Notopterus notopterus for 10, 20 or 30 days, at 13.6, 20.4, 40.8 and 60.2 µg/L of PCP, all showed effects on hepatic acid phosphatase, alkaline phosphatase, and succinic acid dehydrogenase. Liver activity was reduced over that in controls, mostly in hepatic acid phosphatase over 30 days (1). The 1/2 life of PCP in gold fish, Carassius auratus, is 10 hours, while that of the unchlorinated parent compound, phenol, is less than 1 hour. In Notopterus notopterus, 15- and 30-day exposures to 8, 6 and 4 µg/L of NaPCP caused significant reductions in 5-nucleotidase activity, which is indicative of uncoupled oxidative phosphorylation. Kidney enzyme activity was not significantly different due to stimulation of the kidneys as they tried to compensate for lost efficiency elsewhere (145). In the mullet-Rhinomugil corsula, carp-Cyprinus carpio, and cichlid-Tilapia mossambica, the metabolic rate rose at 100 µg/L of NaPCP in the water (138). As shown in Table 8.2.8.8 for the guppy, Poecilia reticulata, the toxicity of PCP decreases as the pH rises from pH 6 to pH 8. The ratio of the LC50 at pH 8 over that at pH 6 is 8.4 and the toxicity of PCP at pH 8 is 10 times that of 4-MCP at pH 8 (144). There is a block of data by Mayer et al. in 1986 (111) on the bluegill, Lepomis macrochirus, in Table 8.2.8.3, which shows that 96-hour LC50s for PCP are lower than 24 -hour LC50s, and that harder water does afford some protection against PCP toxicity. In Table 8.2.8.4 there are data by Gupta (107), on Rasbora daniconius neilgeriensis showing that, for PCP, LC16 values are smaller than LC50 values, which are in turn smaller than LC84 values for any given exposure time; this is expected and indicates internal consistency in the data set. Furthermore, as exposure times increase the LC50 decreases, also an expected result. The no-effect level is about 1/7 of the 96-h LC16, 1/15 of the 96-h LC50, and 1/33 of the 96-h LC84; this is approximately the same change, a factor of two, each time, and represents internal consistency in the data set. Since the LC16 and LC84 limits represent 1 standard deviation about the mean value of LC50, and 1 standard deviation is 68% of the animals, there are 34% of the animals between the LC16 and the LC50 and between the LC50 and the LC84 . A standard factor for estimating no chronic effects from LC50 data is 1/20 or 0.05; these data indicate that 0.010/0.148 or 0.067 is an appropriate value for PCP. In Table 8.2.8.5 there is a block of data on Pimephales promelas, the fathead minnow, from Hedtke et al., 1986 (113), which indicates that rising temperatures increase the toxicity of PCP. Data from Spelar et al., 1985 (79) show the increasing toxicity of PCP with decreasing pH. In Table 8.2.8.6 a block of data on Notopterus notopterus from Gupta et al., 1982 (132) show that increasing fish size reduces toxicity to NaPCP and that with increasing exposure times the toxicity increases. More data from Gupta et al., 1983 (142) show that higher temperatures increase toxicity and that increasing exposure time increases toxicity. The mean of 6 NOEL levels is 0.037 (range 0.032 to 0.043) of the 96-h LC50; the values vary slightly for fish from different size classes and temperatures. In goldfish, Carassius auratus, ambient PCP and pH levels affect the rate of uptake of PCP and the bioaccumulation factor, but ultimately, however long it takes, or under whatever conditions, fish begin to die when the body load reaches about 90 µg/g (547). Trout tissues do not methylate PCP, but the bile contains 250 µg/g of PCP glucuronide conjugate when the trout are subject to 26 µg/L PCP in the water (134, 141). Guppies, Lebistes reticulatus, previously acclimated to 1.0 and 0.1 mg/L NaPCP for 10 days, can survive 3 to 8 h in 5.0 mg/L NaPCP, which would be immediately lethal to un-acclimated fish (670). Campostoma anomalum, (silver-mouthed and blunt-nosed minnows), were able to detect and avoid NaPCP above 10 mg/L but not below 5 mg/L. Eggs of lake trout, Cristivomen namaycush, were more resistant than mature fish, but yolk sac fry were the most sensitive stage (69). Steelhead trout, Oncorhynchus mykiss, were exposed to NaPCP at various life stages. When exposed to 0.3 mg/L post-fertilization, 100% mortality occurred within 1 week of fertilization; at 0.05 mg/L 100% mortality occurred within 24 hours of hatch. Alevin weight at hatch decreased and hatch was delayed. In 5-day tests, alevins died within 24 hours at 0.2 mg/L. Exposure between fertilization and yolk sac absorption caused 100% mortality at 0.04 mg/L, but little at 0.02 mg/L or 0.01 mg/L. However, if the dissolved oxygen was dropped to 5 mg O2/L, then 0.02 mg/L NaPCP was 100% lethal and at 3 mg O2/L, 0.01 mg/L NaPCP was 100% lethal. These NaPCP levels caused little mortality at normal O2 levels or if NaPCP was not present; the combination of NaPCP and low O2 was lethal.
NPCP and KPCP The sodium salt is most commonly used but the potassium salt is used occasionally. The lowest reported acute effect is a 96-h LC50 of 9.8 µg/L using 9 cm long Notopterus notopterus (142). The experiment was carried out at 36C, pH 7.2, and 6.5 mg/L of dissolved oxygen. For chronic effects the lowest reported value is an EC50 of 1.74 µg/L for reduced growth rates of sockeye salmon, Oncorhynchus nerka (94).
Table 8.3.1 gives some taste threshold levels for chlorophenols in fish muscle. Values are expressed as µg/g wet weight in the flesh which result in unacceptable taste of the fish. Another concern, which is not addressed in this document, is that breakdown products of chlorophenols, such as chloroanisoles and their biodegradation products, may cause flavor problems in meat at levels well below those at which chlorophenols cause a problem (716, 717, 718). Chlorophenols enter fish and cause taste problems by 4 different routes: across gill membranes, across gut membranes, absorption through skin, and adsorption to the mucosa (676). Gill uptake is likely the most important. Table 8.3.2 gives some literature guidelines for water which are designed to prevent fish taking up enough chlorophenols to suffer from flavour impairment. For the MCPs and DCPs, the water levels necessary to prevent taste impairment in fish muscle may be below the aquatic life toxicity guidelines levels, especially at high pH and low temperature; for the other chlorophenols, the aquatic life toxicity guidelines are below the levels necessary to prevent flavour impairment in fish at any pH or temperature. One way to generate such guidelines is to divide the taste threshold by the bioconcentration factor for fish muscle to determine the maximum water level which would not result in flavour impairment. These bioconcentration factors vary considerably depending on species and environmental variables. Tables 4.2.3.1, 4.2.3.4 and 4.2.3.5 give some calculated and experimental, or observed, bioconcentration factors. The geometric mean calculated BCF values, from Table 4.2.3.1, range from 4 with 2-MCP to 3700 with PCP; arithmetic mean values range from 12 with 2-MCP to 4700 with PCP. The variability is quite large, however, with the PCP values ranging from 876 to 7590. Measured values of the PCP bioconcentration factor for salmon and trout muscle range from 4 to 39 (134, 141, 577); if fat is included then the range goes to 231 (134, 141). Liver and bile factors are much higher. If one compares the values in Tables 8.3.1 and 8.3.2 for taste thresholds and existing guidelines, it is apparent that a BCF of 1000 is being used for 2,4-DCP and 2,4,6-TCP, but for the MCPs the factors are much higher, 3000, 1600, and 7500 for 4-MCP, 3-MCP, and 2-MCP, respectively. Neither calculated nor measured BCFs for the MCPs and DCPs are near these high values; they are rarely over 100. Most taste and odour problems are caused by the MCPs and DCPs and it appears that the only reliable way to determine water guidelines is to carry out experiments using taste panels to rate the fish.
2-MCP Fish raised in water with 2 mg/L of 2-MCP will cause nausea when eaten (360); flavour impairment occurs in the µg/L range (183, 190, 360, 361). Bluegill sunfish, Lepomis macrochirus, were exposed to 2 mg/L of 2-MCP for 1 to 4 weeks; eating these fish caused mild to severe nausea (364). Rainbow trout, Oncorhynchus mykiss, exposed to 2-MCP and then cooked and eaten, tasted bad when the water was over 60 µg/L (364). In a 3-day flow-through exposure test, 15 µg/L of 2-MCP caused tainting of carp flesh. 2-MCP, at 0.1 µg/L, imparted a bad flavour to eels in 10-day exposure trials at 16C in brackish water; oyster flavour was impaired in 4 days (675). Fish from Michigan had taste problems when waters reached 15 µg/L (676). The US EPA guideline for prevention of taste problems is 2 µg/L and the lowest acute response is at 2.1 mg/L (611) as shown in Table 8.2.8.12. 3-MCP Flavour impairment in fish occurs at levels below the LC50 for the fish (335), the lowest value found being 2.9 mg/L (611) as shown in Table 8.2.8.12. Thresholds for fish-flesh taste-impairment occur at water levels of 0.05 and 0.06 mg/L (361, 370) and at 25 µg/kg in rainbow trout flesh (190). 4-MCP Fish from Michigan waters had taste problems when 4-MCP levels reached 5 µg/L (676). The Ontario guideline is 15 µg/L (220) to prevent taste problems. The lowest chronic effect level, as shown in Table 8.2.8.12, is 3.0 mg/L (366). 2,4-DCP The flavour of fish is affected by 2,4-DCP at water levels below those causing fish toxicity (335). As shown in Table 8.3.2, the water guidelines of Ontario and US EPA are 0.4 µg/L, while the lowest chronic effect level found for a fish is 70 µg/L (220), as given in Table 8.2.8.12. 2,3,6-DCP and 2,4,6-DCP Guidelines for these chlorophenols, as set by Ontario and US EPA, are 52 µg/L in the water to prevent tainting the flesh (105, 220). The lowest chronic effects levels for these chlorophenols are 720 and 200 µg/L, respectively (220, 245), as shown in Table 8.2.8.12. The MCPs and DCPs may cause flavour impairment below the aquatic life toxicity guidelines at low temperatures so flavour guidelines are set for these groups; for the other chlorophenols, tainting would only occur above the aquatic life toxicity guidelines, thus no organoleptic guidelines are necessary.
Table 8.4.1 lists some non-organoleptic literature guidelines for chlorophenols with respect to aquatic life. It is evident that not all congeners have had guidelines set, that the reasons for setting guidelines vary, and that the guidelines levels vary markedly. Acute and chronic effects have both been used as end points. Time periods vary from instantaneous maxima to 96-h means. Some agencies set guidelines for specific congeners and others group the chlorophenols into homologues of the same number of chlorine atoms, isomers, and set a guideline for the homologous group. The 1987 CCREM and 1984 Ontario guidelines are for sums of chlorophenol isomers and not for individual chlorophenols. As is evident from Figure 2.4 there is considerable variation in toxicity within a group of isomers and we feel that individual chlorophenol guidelines should be set to reflect this variability. The alternative is to set guidelines for each isomer group low enough to protect against the most toxic member of the group; this would be excessively overprotective for some congeners. The BC Ministry of Environment has established site specific objectives for the sum of tri-, tetra-, and pentachlorophenols in fish, of 0.1 µg/g wet weight in the muscle tissue (536). In the EPA-1986 criteria document, a recurring phrase is "toxicity occurs at concentrations as low as...and would occur at lower concentrations among species that are more sensitive than those tested". To get around this lack of data on more sensitive species, we have used the ratio of toxicity of PCP to that of the other congeners for Daphnia. This provides an estimate of the toxicity of the other congeners to the most sensitive species. There are no suitable data in the literature on which to base guidelines for most congeners, only calculated ratios between existing PCP data and the other congeners as determined by an experiment on Daphnia. There are also ratios inherent in the equations of Saarikoski et al. (144) derived from work on guppies and chlorophenols. The literature water levels and guidelines needed to prevent taste problems in fish muscle are given in Table 8.3.2. and some reported taste thresholds in fish muscle are given in Table 8.3.1. Guidelines needed to prevent taste problems in the fat and liver of fish would be much lower.
TOXICITY CRITERIA Raw toxicity guidelines for the chlorophenols, calculated using the equations of Saarikoski et al. (144), are given in Table 8.5.1, in µg/L at 10 C between pH 5.6 and pH 8.4 . The guidelines at pH 7.2 and 10C are shown graphically in Figure 8.5.1. Table 8.5.1.1 gives the constants and variables needed to calculate these numbers. Considering the inherent variability of the values in Table 8.5.1, based on how they were generated, the implied precision does not seem warranted. In addition, application of the guidelines would be unnecessarily complex with little if any concomitant increase in environmental protection. Guidelines were also calculated based on rainbow trout LC50 data. These guidelines are both based on acute data and are found in Table 8.6.6. The recommended maximum guidelines, given below and in Table 1.1.2 and Table 8.6.6 were derived from the chronic data of Webb and Brett (94) by calculating an NOEL from the LOEL. The derivation process is outlined in section 8.6. All these derivation processes lead to the same values for the guidelines. Interim Aquatic Life Toxicity Guidelines ** for Chlorophenols.
The recommended guidelines for the prevention of flavour impairment in fish muscle are given in Table 8.5.2; both a tissue level and a water level generally necessary to achieve this tissue level are given. These guidelines are only for flavour impairment to human consumers. Consideration has been given to other animal consumers, with a lower taste threshold than man, that might be affected by tainted fish. Effects could be a loss of desire to eat their only, or preferred, food source due to impaired flavour, or to flavour impairment of the milk in lactating females which might prevent the young from nursing. Except for the monochlorophenols and dichlorophenols, the recommended guidelines for human taste are low enough to protect such animals providing that their taste sensitivity is no better than that of man. Since no data are available on this subject, no further downward adjustment of the guidelines is warranted at this time. Food preference trials with predators of fish, and other aquatic prey organisms, are required to justify any lower guidelines. Guidelines were not set for all the congeners since appropriate data were not found.
The level of MCPs in the water should not exceed 0.1 µg/L. The level of DCPs in the water should not exceed 0.2 µg/L. The levels of TCPs, TTCPs and PCP in the water should not exceed the aquatic life toxicity guidelines as given above.
The level of 2-MCP in fish muscle should not exceed 10 µg/g The level of 3-MCP in fish muscle should not exceed 20 µg/g The level of 4-MCP in fish muscle should not exceed 40 µg/g The level of 2,3-DCP in fish muscle should not exceed 80 µg/g The level of 2,4-DCP in fish muscle should not exceed 0.2 µg/g The level of 2,5-DCP in fish muscle should not exceed 20 µg/g The level of 2,6-DCP in fish muscle should not exceed 30 µg/g The level of 2,4,6-TCP in fish muscle should not exceed 50 µg/g The level of 2,3,4,5,6-PCP in fish muscle should not exceed 20 µg/g
TOXICITY CRITERIA To help analyze the vast amount of data found in Tables 8.1.2 through 8.2.8.12, four summary tables were constructed. These tables, 8.6.2 to 8.6.5, list, for each chlorophenol congener, the lowest literature value found for freshwater and marine organisms and for chronic effects or acute LC50s. There are gaps in these tables, especially for marine life, where no experimental data exist for any life form for a given congener. As discussed elsewhere in this document, in section 5.8.1, the action of chlorophenols on all eukaryotic life is the same and the site of action is the mitochondrion. The ratios of the toxicity of the chlorophenols to the toxicity of PCP is primarily a function of their Ko/w values, but some QSAR relationships modify this response, as does the pKa value.
Fish, generally salmonids, are usually the most sensitive aquatic organisms reported; however, few data are available on tadpoles, newts and salamanders which are also intimately exposed to the water, especially in their juvenile stages. In Table 8.6.2 most of the lowest reported LC50s are for fish and only one is for a crayfish. For the tadpole of the frog, Rana catesbiana, the datum given was a 48-h LC50 of 0.207 mg/L. There is more reliable LC50 rainbow trout datum by Leeuwen et al. of 18 µg/L (148) found in Table 8.2.8.7. Niimi et al. (126) reported chronic effects of PCP on rainbow trout at 0.66 µg/L and an NOEL of 0.035 µg/L. This was determined to be secondary data and therefore not used to set the final guidelines. A paper by Webb and Brett (94) gives an LOEL of 3.49 µg/L for growth effects of PCP on young sockeye salmon and this was the value on which the final guidelines were set. Table 8.6.1 is a collection of calculated or experimental no observed effect levels, (NOEL) and non-lethal levels of chlorophenols for aquatic life. It indicates the level at which no toxic effects were found for each congener and also indicates the range of values found by different authors for different species. There are no other toxicity data on other more sensitive species, and only incomplete data for many other species, for the other chlorophenol congeners. The toxicities of the other congeners would have to be estimated by using the ratio of toxicity between PCP and the other congeners in those few cases where complete, or near complete studies, were carried out. This process is outlined below.
1-Estimating the 96-h LC50 to NOEL conversion factor CCME has used 0.01 but a standard factor for estimating no chronic effects from 96-h LC50 data is 1/20 or 0.05. Only paired NOEL and 96-h LC50 data from the same PCP experiment are used in the calculations below. Table 8.2.8.6 contains a block of PCP data on the fish Notopterus notopterus from Gupta et al., 1982 (132) and 1983 (142). In µg/L, the paired NOEL and 96-h LC50 data are: 0.0011/0.032, 0.003/0.093, 0.0035/0.083, 0.0037/0.107, 0.0045/0.131, and 0.00043/0.0098. The mean of these 6 ratios, NOEL levels/ the 96-h LC50 levels, is 0.037; the individual ratios are 0.034, 0.032,0.042,0.034,0.034 and 0.043, respectively. The values vary slightly for fish of different size classes and different experimental temperatures. In Table 8.2.8.4 there are PCP data by Gupta in 1983 (107), on Rasbora daniconius neilgeriensis . These data indicate that 0.010/0.148 or 0.067 is an appropriate ratio for PCP. The mean of these 7 NOEL /96-h LC50 ratios is 0.041. These data were also discussed above in section 8.2.8 under PCP.
To set guidelines for each of the chlorophenol congeners, starting from data sets with gaps in them and data of variable quality, the following procedures were followed. The most complete data set, that of Devilliers et al., 1986 (57) in Table 2.4 on Daphnia magna, was used as a starting point. It was used to establish the ratio of the guideline for any congener to that of PCP. The two gaps in this data set were filled by extrapolation using QSAR arguments from the data set itself, and by using calculated ratios from Saarikoski et al., 1982 (144). This process was documented, step-by-step, in Table 8.6.6 and is described below. In Table 8.6.6, Column 1 gives the ratios of the toxicity of PCP to other chlorophenols for Daphnia, as determined from experiments by Devillers et al. (57). The most complete set of data on chlorophenol toxicity exists for PCP, so the lowest reported 96-h LC50 datum for PCP was chosen as the starting point for calculations. This was the 18 µg/L value for the rainbow trout as indicated above. This value was multiplied by the appropriate ratios to derive 96-h LC50 values for the other chlorophenols and the values given in Column 2. Data from Tables 8.2.8.4 and 8.2.8.6, as discussed above, indicate that for pentachlorophenol, the mean no-effect level appears to be about 0.041 of the 96-h LC50 value. This correction is made to Column 2 to yield Column 3, which should, in the absence of good experimental data, provide an adequate estimate of the lowest no-effect level of chlorophenols to rainbow trout. The guidelines developed by this method are only good at the pH of the experiment, 7.8 to 8.2, and can not be readily converted to other pH values; thus they are of limited value.
Using a series of equations developed by Saarikoski et al. (144) for guppies, one can derive guidelines for any given pH. When this is done at pH 8.0 and the results, column 6, Table 8.6.6, compared to the results, column 3, Table 8.6.6, generated using the data of Devilliers et al. (57) for Daphnia magna, it can be seen that there is reasonably good correspondence. The data of Saarikoski et al. (144) were developed using guppies, which are less sensitive than rainbow trout. Experiments indicated that rainbow trout, Oncorhynchus mykiss, were about fifty times more sensitive to chlorophenols than guppies, Poecilia reticulata, for which the above pH relationships were determined (144). The lowest LC50 value for rainbow trout is 18 µg/L at 10C and a pH of 7.2. The water hardness was 50 mg/L and the animals were 77-d old fry. A correction factor is needed to convert the results of the equations, which are guppy LC50 values, to rainbow trout LC50 values. The procedure therefore was to calculate the guppy LC50 value at 26C and pH 7.2 using the equations in Saarikoski et al. (144). This value was 1.38 mg/L. Converting it to a guppy LC50 value at 10C and pH 7.2 results in a value of 4.18 mg/L. Since the lowest rainbow trout LC50 value at 10C and pH 7.2 is 0.018 mg/L (148), a conversion factor of 0.00431 (0.018/4.18) needs to be applied to the equations derived from guppy data.
Temperature and pH corrections need to be applied to the base guidelines calculated at 10C and a pH of 7.2. The temperature correction factor is not difficult to apply; the raw guidelines in Table 8.5.1 and interim guidelines in Table 8.6.6 are given for 10C which can be converted to any other desired temperature. However, the pH can not be simply converted. It has to be recalculated using an inconvenient equation and thus Table 8.5.1 was generated for the Saarikoski guidelines in the range pH 5.6 to pH 8.4 ; the equation is not valid outside this range, and tends to under and over estimate toxicity at low and high pH values, respectively.
Calculated raw toxicity guidelines for the chlorophenols, as given in Table 8.5.1, are in µg/L at 10 C for pHs between 5.6 and 8.4 . The Saarikoski guidelines at pH 7.2 and 10C are shown graphically in Figure 8.5.1. The temperature effects were estimated using the data in Table 8.2.8.6 taken from Gupta et al., 1983 (142) using the fish, Notopterus notopterus. The ratio of toxicity at 16C to that at 36C was 11 at 24 hours, 9 at 48 hours, 7 at 72 hours and 6 at 96 hours. It declines with length of exposure and one assumes it would equilibrate at some value not far below 6 for long-term exposures. The normally accepted temperature effect on metabolic rates is a factor of 2 for a 10C change. Thus if the temperature rose from 10C to 20C the values would be divided by 2. This temperature dependence rate is one that is well established in physiological studies and should need no further substantiation. Thus for the 20C difference in this experiment one would expect a change of 2 x 2 = 4, which is close to the 6 found at 96 hours, and 4 is probably a good estimate for long-term equilibrium conditions. Graphing these data indicate that a value of 4 should be reached within a week. For fish, Mayer et al. (111) found the following relationship for a 10C temperature change with all pollutants, except organophosphates: log 96-hour LC50 (@T)= log 96-hour LC50 + 0.4956 (@T+10). This change is about a factor of 3 for a 96-hour period and is not far off the expected long-term value of 2 for a change of 10C. The temperature correction equation is given below: Guideline at YC = (Guideline at 10C) . ( 2 - x ) where Y = the new temperature, and x = ( Y- 10) / 10.
Correction for different pH levels is more complex and guidelines at 10C for pHs in the pH 5.6 to pH 8.4 range are given in Table 8.5.1 for the raw Saarikoski guidelines. These would have to be considered interim guidelines until properly controlled experiments could provide a unified temperature and pH dependent regression equation for each chlorophenol. Table 8.5.1.1 gives the constants and variables needed to calculate these numbers. The full equation for calculating guidelines in µg/L, at any pH between about 5.6 and 8.4, and for any reasonable physiological temperature (1C to 36C), is given below : the guideline = (GMW) (0.054) (1 / ( antilog ( (0.67 log P + 0.19 (10.05 - pKa) - 0.67) - (log (4 (pH - pKa)+1) ) ) ) (1/2 ( (T - 10) /10) ) . Values for the variables, GMW, logP, and pKa are given in Table 8.5.1.1 . T and pH are the desired temperature in C and pH, respectively. GMW is the molecular weight of the chlorophenol, logP is the logarithm (base 10) of the octanol/water partition coefficient, and pKa is the acid dissociation constant. There is another pH conversion equation for PCP developed by the EPA which is easier to use and gives nearly the same results, the pH slope factor is very similar. It is probably the formula of choice for PCP but not necessarily for the other chlorophenols. newconc. = eY where Y = (ln (givenconc.) - 1.005 (given pH -new pH)) and newconc. is the concentration at the new pH and givenconc. is the concentration at the given pH. Hardness does not seem to have a consistent, predictable effect on the toxicity of chlorophenols; however, in natural waters pH and hardness would normally be well correlated. There are some data for 4-MCP, 2,4,6-TCP and PCP over the range pH 5 to pH 8 in Table 8.2.8.8. There are also data on many of the other congeners over the pH range 6 to 8. The best set of data to determine the effects of pH on chlorophenol toxicity is that of Saarikoski et al., 1982 (144) for guppies which is found in Table 8.2.8.8. The Ko/w and the pKa of the chlorophenols are factors which affect pH-related toxicity, since it is the effect of pH on lipophilicity which is important. Toxicity is generally a function of how readily the chlorophenol molecule can gain access to the interior of the organism and this is determined primarily by the amount of dissociation of the chlorophenol molecule. At pH levels below the pKa, dissociation is almost nil and uptake is rapid; at higher pH levels, dissociation is virtually complete, uptake and toxicity are relatively low, and changes in uptake with a change in pH are relatively small. Most existing regression equations are only good in the approximate range pH 6.0 to pH 8.0. A regression equation was derived by Saarikoski et al. (144) using 8 of the 19 chlorophenols, which predicted toxicity at pH 7.0 as a function of the Ko/w. To find the toxicity at some other pH, in the range pH 6.0 to pH 8.0, the pKa is required.
Niimi et al. (126) indicate, as shown in Table 8.2.8.7, that there are chronic effects of PCP on rainbow trout fry growth rates at 0.66 µg/L . This level is almost identical to the calculated chronic toxicity threshold of 0.7 µg/L as given in column 3 of Table 8.6.6. Whether one uses NOEL data from the literature, applies a 0.1 safety factor to the lowest literature chronic effect, or applies an acute-to-chronic ratio factor to the lowest LC50 data from the literature, the result is nearly the same. Inspection of Tables 8.6.2 to 8.6.5 indicates that the calculated guidelines in Column 5 are below any reported toxic effect on any organism for any chlorophenol congener. In addition, these guidelines are below guidelines set by other agencies (Table 8.4.1) for all chlorophenols. In Table 8.6.6, Column 6, calculated guidelines using the equations of Saarikoski et al. (144 ), based on guppies, are given and it is evident that there is reasonably good correspondence between these values and those in columns 3 and 5 which are derived from work by Devillers et al. (57) on Daphnia and Webb and Brett (94) on Sockeye Salmon. The values in columns 3, 5 and 6 were calculated for 10C and a pH of 7.2, since these were the conditions under which the rainbow trout LC50 data were generated. Since the guidelines derived using Daphnia data from Devillers et al. (57) can not be applied to other pH values, while the guppy data from Saarikoski et al. (144 ) can be recalculated for any desired pH, and since there is good agreement between these two methods, the equations of Saarikoski et al. (144 ) would be better to generate guidelines from acute data.
Inspection of Table 8.5.1 shows that for some chlorophenols, mostly lower molecular weight ones, there is relatively little difference in the raw guidelines at low and high pH values. For other chlorophenols the change is quite small at low pH levels but becomes larger at higher pH levels. When one considers the inherent variability of the numbers in this table, based on how they were generated, such precision does not seem to be warranted. In addition, application of the guidelines would be unnecessarily complex with no concomitant increase in environmental protection. Guidelines were derived from the numbers in Table 8.5.1 by the following procedure. The lowest value, at pH 5.6, was multiplied by 4 to establish an upper limit to a pH range:
No temperature corrections were made since the change from the guideline derived for 10C, would be less than a factor of two for any ambient temperatures encountered in BC.
To determine the base value for PCP, from which the other chlorophenols are determined by ratio, the preferred CCME protocol is followed, using sockeye salmon growth data. The LOEL is 3.49 and a factor of 0.1 is applied to this to get an estimate of the NOEL of 0.35 at a pH of 6.8 and a temperature of 15ºC. These values were converted to 10ºC and a pH of 7.2 and are found in Table 8.6.6 in columns 4 (LOEL) and 5 (NOEL). The marine guideline is simply the same data calculated at a pH of 8.2.
For flavor impairment of fish muscle, the existing taste panel data, Table 8.3.1, have been rounded down and accepted as the guidelines and are given in Table 8.5.2 as Recommended Fish Muscle Concentrations in µg/g wet weight. There does not appear to be a better way to determine these values other than a taste panel, with a safety factor to account for more sensitive individuals who were not on the panel. The existing water guidelines for aquatic life, from CCREM and Ontario for MCPs and DCPs, have been accepted as giving adequate protection for the effects of bioaccumulation in open water sport-fish with respect to flavor impairment and are given in Table 8.5.2, Recommended Water Guidelines in µg/L. For the TCPs, TTCPs and PCP the aquatic life toxicity guidelines are low enough to give protection against flavor impairment of fish muscle. Using these guidelines, fish that are not primarily bottom-feeders should remain edible; bottom feeders may accumulate a higher concentration of chlorophenols and have unacceptable taste under some circumstances. These guidelines assume consumption of the fish muscle; fat and liver tissues, which have much higher bioaccumulation ratios, would not necessarily have acceptable taste at these levels of chlorophenols.
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