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Short-term toxicity to fish

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Description of key information

Key studies indicate LC50 data (96hr) for saltwater fish of 0.23 mg/l and LC50 of 2.2 mg/l for freshwater fish.  These are the lowest LC50 values reported.  Other supporting studies can indicate higher values but  the reasons for such discrepancies have been discussed e.g. the differences in values can be attributed to the hardness of the water and the subsequent solubility of the test substance in the water

Key value for chemical safety assessment

LC50 for freshwater fish:
2.2 mg/L
LC50 for marine water fish:
0.23 mg/L

Additional information

The key value from the short-term toxicity in marine fish (Pleuronectes platessa) studies is a 96 h LC50 of 0.23 mg/L (Maddock et al. 1976).

One study in sea bass (Marchetti, 1978a) found a 48 h (marine water fish) LC50 of 0.065 mg/L. Although this value was lower than that reported by Maddock et al. (1976), this study was designated supporting rather than key, as the study was undertaken using TEL-CB compound containing 61.49% TEL and the dibromoethane/dichlorethane present are known to be toxic in themselves so could have affected the results.

The key study for freshwater fish (Morone labrax)by Turnbull et al. (1954) demonstrates the different toxicity compared to marine water with the effects of TEL in freshwater fish reported as LC50 of 3.1 mg/L over 24 hours & LC50 of 2.2 mg/L over 48 hours.

Studies show that the order of toxicity of the materials tested is as follows: - R4 (ethyl) » R3 (ethyl) > Inorganic lead.

The toxicity of inorganic lead compounds to aquatic animals was originally thought to be due to coagulation film anoxia (Westfall, 1945). This phenomena, which was first reported for lead by Carpenter in 1949 involves the formation, by the action of the toxicant, of a veil like film of coagulated mucus on the body surface of the fish. If this film of mucous affects the gill tissues, the fish suffers acute respiratory distress and dies from lack of oxygen. It was thought that this process was a common cause of metal toxicity. This type of mucous film was not detected during this study and we conclude that the mechanism of acute toxicity for alkyl lead compounds cannot be due to this cause.

More recently, other workers (Jackim, 1970) have indicated that direct action of the metal on enzyme systems may be responsible for their toxic effects, and such enzymatic responses may be involved in the case of the alkyl lead compounds.

The difference between the toxicity of the trialkyl lead compounds which are lipophobic materials and the tetra alkyl lead compounds which are lipophilic materials seems to support the view of Cassels and Dodds (1946) who state, in relation to mammalian toxicity, that "the fat-soluble character (of the tetra alkyl lead compounds) allows selective localisation in the nervous tissue of the body and for this reason poisoning is essentially a central nervous system intoxication".

Extrapolation of the median survival period curves, gives a tentative safe level for the marine environment of 0.001 mg/L for the R4 compounds. These levels would not be expected to cause significant mortality.

The toxic effect of lead on freshwater animals is strongly affected by the hardness of the water. Lead has a low solubility in soft water and an even lower solubility in hard water, although considerably higher concentrations of suspended and colloidal lead may remain in the water. Several workers have demonstrated the extreme effects of water hardness on the toxicity of lead.

                                                                                          96 Hr LC50 (mg/L)

Reference                                Species                              Soft       Hard

                                           Water      Water

1. Pickering and                 Fathead Minnow

Henderson (1966)          (Pimephales promelas)                       6         482

                                    (Lepomis macrochirus)                     23        442

2. Davies -et al (1976)           Rainbow Trout                           1.2        500

                                        (Salmo gairdnerii)

The reason for this massive difference in toxicity is due to the chemical form in which the lead is present in the two media. In the hard water, the lead will be mainly present as carbonate and sulphate salts and the amount of "free ionic lead" i.e. uncomplexed, which is thought to be the toxic species, will be relatively small. This has been confirmed by Davies et al (1976). They were able to measure, by electrochemical means the level of "free ionic lead" in the test solutions, as well as the total lead levels. They report that on the basis of "free ionic lead" concentrations there was no difference in toxicity between hard and soft waters.

Studies by other workers have produced values for the toxicity of lead in reasonable agreement to those in the table e. g. Brown (1968) reports a 96 hour LC50 value for Rainbow Trout of 1 mg/L in soft water. As is the case with many materials, juveniles are more sensitive than adults. McKim et al (1975) report that the 96 hour LC50 for juvenile Rainbow Trout is 0.14 mg/L i.e. 1/10th the value recorded for adults by Brown (1968).

Value used for CSA:

LC50 for freshwater fish: 2.2 mg/L

LC50 for marine water fish: 0.23 mg/L