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Microsoft word - appendix 5 - picrite ecotox report.doc

Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. Appendix 5; Eco-toxicity of Nitroguanidine (Picrite) and its Degradation
Products
1.0 Background
Nitroguanidine is a constituent of some gun propellants. This substance was manufactured at the now decommissioned Royal Ordnance Factory, Bishopton. Relatively high concentrations of this substance have been discovered previously in the effluent disposal lagoons situated approximately 1km southwest from the main site. These lagoons were used until 1993 for the disposal of lime neutralised sulphuric acid effluent, a by-product of picrite manufacture. The slurry was pumped to the lagoons, the solids allowed to settle out and the supernatant left to drain away from the unlined lagoons and/or evaporate to the atmosphere. Periodically, when the material had dried sufficiently, solids were excavated and mounded on adjacent land Analysis of samples from the lagoons suggests that the lagoon solids are rich in calcium and sulphate1. The concentration (%w/w) of Ca in the samples was approximately 20.3±5%, whilst the concentration of SO 2- This raises t2he possibility of the formation of a range of calcium sulphate like minerals in varying mass ratios of calcium and sulphate. The pH of the lagoon solids was in the range 4.1-12.7, with a decrease in value as the depth of the lagoons increased. The average total nitroguanidine concentration in the lagoon samples was in the range <0.05 – 1320 mg L-1. The average leachable nitroguanidine concentration in water samples collected at varying lagoon depths was in the range The effluent discharge lagoons at the former Royal Ordnance Factory, Bishopton known as the ‘picrite lagoons’ contain traces of nitroguanidine (picrite). Picrite has also been detected over the years in groundwater and surface water at up to 32mg/l. However, concentrations have decreased significantly since the factory ceased production in 2002 and decommissioning of the section took place. Surface water samples have recorded less than 5mg/l picrite since January 2004 and the majority of groundwaters were found to contain less than 1mg/l picrite, except from one borehole where a maximum of 12mg/l has been detected. Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. Ecological Toxicity of Nitroguanidine
Invertebrates

Van der Schalie3 has studied the acute toxicity of nitroguanidine to several
invertebrates. No 48 hour LD50 were obtained by van der Schalie3 for the following invertebrates exposed to saturated solutions of nitroguanidine: water flea (P. magna) at 2838mg L-1, amphipods Gammarus minus and Hyallela azteca at 2720 and 2730mg L-1 respectively; midge larva (P. dissimilis) at 3395 mg L-1 and aquatic oligochaete (L. variegates) at 2868mg L-1. Warner (1978) found that nitroguanidine was not acutely toxic to D. magna (20°C) at a nominal concentration of 1175 mg L-1. Fish
Various studies have shown that no mortality occurred to the rainbow trout or fathead minnow in 96h at the solubility limits of the compound, which were 1550mg L-1 for rainbow trout at 12°C and 3320mg L-1 for fathead minnow at 25°C. In a study conducted by Burton et al (1993)4 it was observed that there was no mortality to 17d old rainbow trout exposed to 1550mg L-1 nitroguanidine at 25°C. Similarly there was no mortality to 37d old fathead minnow exposed to 1550mg L-1 at 12°C or in the van der Schalie3 study (63d old; 22°C) at 2634 mg L-1. Therefore, it can be concluded that the acute toxicity of nitroguanidine to freshwater invertebrates and fish is quite low. With the exception of the hydra and cladoceran in which the 48h LD50s were 2061 and 2698mg L-1 respectively, the toxicity of nitriguanidine does not appear to be an acute hazard to freshwater invertebrates and fish except at concentrations approaching the solubility limit of the compound in water. Toxicity of Photolyzed Nitrogaunidine
Several authors have reported that photolyzed nitroguanidine was approximately two orders of magnitude more toxic to the cladoceran than the parent compound under the same test conditions. Van der Schalie (1985)3 exposed green algae (S. capricornutum), water flea (D. magna), and fathead minnow to photolyzed nitroguanidine and found it to be more toxic. The 120h LD50 concentration of the parent compound was 2146mg L-1 whilst the 120h LD50 concentration of the photolyzed compound was 32mg L-1 for the algae exposed to these compounds. The 48h and 96h LD50s of the water flea and fathead minnow were >2838mg L-1 and >2714mg L-1 respectively, when the organisms were exposed to the parent Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. compound. The 48h and 96h LD50s of the water flea and fathead minnow exposed to photolyzed nitroguanidine were 25mg L-1 and 35mg L-1 of the compound respectively. A number of products are formed in aqueous solution when nitroguanidine is photolyzed in distilled water or surface waters by UV radiation or natural light. Studies of the UV photolysis of nitroguanidine in unbuffered distilled water have shown that the products are primarily guanidine, urea, and nitrite, with lesser quantities of cyanoguanidine, ammonia, and nitrate5,6. Nitrosoguanidine has been observed as a transient intermediate which appears to be photolyzed to guanidinium nitrate7. Several of the above products have also been observed in surface waters photolyzed by sunlight although the yields were different in most cases. Burrows et al (1988)6 conducted a literature survey of the toxicity of photolyzed nitroguanidine products to aquatic organisms. They concluded that of the five photolysis products for which data were available, four are more toxic to aquatic organisms than the parent compound. They pointed out, however, that only nitrite ion is present at a concentration high enough to account for the greatly enhanced toxicity of photolyzed nitroguanidine observed in the Van der Schalie (1985)3 study. Burrows et al. (1988)6 also made the point that synergistic effects may be involved in the observed toxicity. The cladoceran in the current study was approximately an order of magnitude more sensitive to photolyzed nitroguanidine than the organisms in the Van der Schalie study. Similar data on the chronic toxicity of the photolyzed products to the cladoceran are not available. Clearly, one or more of the photolyzed products is quite toxic to the cladoceran. The environmental fate of nitroguanidine in surface waters has been shown to be dominated by photolysis. The half life of nitroguanidine at 40°N latitude ranges from 0.6 days in summer to 2.3 days in winter. Although nitroguanidine is very soluble in water, it is not toxic to several aquatic organisms at its solubility limit. However, photolyzed nitroguanidine is about two orders of magnitude more toxic than the parent compound. It is clear that photolysis should be considered during hazard evaluation of nitroguanidine discharged to the aquatic environment. Toxicity of Chemical and Biodegraded Nitroguanidine
Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. Kaplan et al. (1982)8 and Haag et al. (1990)9 have evaluated the susceptibility of nitroguanidine to microbial degradation and the potential hazards associated with the degradation products. They observed that nitroguanidine did not biodegrade until the anaerobic cultures had a sufficient period of acclimatisation. Once acclimated, anaerobic cultures readily reduced nitroguanidine cometabolically. This transformation did not occur under aerobic conditions. No evidence was found for further microbiological reduction of nitrosoguanidine. Unlike nitroguanidine, Kaplan et al (1982) were unable to acclimatise cells to completely metabolise nitrosoguanidine by further reduction. Probable reduction products would have been hydrazine and urea or aminoguanidine and guanidine. Hydrazine, urea and aminoguanidine were never detected during these studies, and guanidine, although present in trace amounts, can be postulated to arise by an alternative pathway. Figure 1: Scheme for chemical and biological degradation of nitroguanidine.
Step 1 is biologically mediated; step 2 and beyond are chemically mediated
(Kaplan et al., 1982).

It is probable that under these conditions nitrosoguanidine decomposes
nonbiologically. Significant quantities of cyanamide, cyanoguanidine and melamine were identified in the culture effluents. These products were reported to be among the products of the chemical decomposition of nitrosoguanidine (Figure 1). Nitrosoguanidine decomposes to cyanamide and nitrosamide. The cyanamide Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. polymerises to its dimer, cyanoguanidine, and finally to its trimer, cyclic melamine. Cyanamide can also react with ammonia to form guanidine. The nitrosamide formed is transitory and decomposes to nitrogen gas and water. Kaplan et al., (1982) observed that in sterile broth batch culture controls, under anaerobic conditions with a reducing agent present, there was no change in the concentration of nitroguanidine, and there was no evidence for nonbiological reduction to nitrosoguanidine. Sterile broth controls with nitrosoguanidine revealed similar patterns of substrate disappearance and product formation, supporting the notion that the decomposition steps from nitrosoguanidine are nonbiologically mediated. Under more harsh chemical conditions, Davis and Rosenquist (1937)10 reported that nitrosoguanidine reacts chemically with ammonia to give cyanamide and nitrosamide. With excess ammonia this reaction proceeds to guanidine, melamine, ammeline, ammelide and a trace of urea. Presumably, under the milder conditions of biological studies, the hydroxylated analogues of melamine are not Nitrosoguanidine and nitroguanidine gave negative results in the Ames screening test for mutagenicity. Nitrosoguanidine, however, was reported to be a carcinogen in screening tests with Chinese hamster cells for detection of chromosomal aberrations11. Cyanamide is metabolised by plants to arginine through various guanidino compounds12. Calcium cyanamide is used as a plant fertiliser13 and root stimulator and is not carcinogenic14. Cyanamide is bacteriostatic at 1000mg L-1 and toxic to mammals. Melamine presents a low toxicity hazard. Aquatic Fate of Nitroguanidine
The high water solubility and the low values of the Henry’s constant, soil sorption coefficient, and biouptake coefficient all indicate that nitroguanidine exists predominantly in the aqueous phase of the environment9. In oligotrophic streams and lakes, the fate of nitroguanidine will be dominated by photolysis, with surface half-lives at 40°N ranging from 0.6d in summer to 2.3d in winter. Photolysis products include nitrite, nitrate, hydroxyguanidine and unknown products of hydroxyguanidine Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. In coloured, eutrophic surface waters, photolysis will be inhibited and biotransformation promoted, resulting in photolysis half-lives of several days and biotransformation half-lives as short as one day. Cyanamide was the only significant biotransformation product observed. In ground waters, anaerobic biotransformation is expected to be the dominant fate process, having a half-life of 4 days. Abiotic, sediment mediated reduction is a possibly important process that has not yet been investigated. Similar environmental fate parameters are found for water-soluble nitro compounds such as diethylene glycol dintrate. 1.6 Conclusions

The effluent discharge lagoons at the former Royal Ordnance Factory, Bishopton
known as the ‘picrite lagoons’ contain traces of nitroguanidine (picrite). Picrite has also been detected over the years in groundwater and surface water at up to 32mg/l. However, concentrations have decreased significantly since the factory ceased production in 2002 and decommissioning of the section took place. Surface water samples have recorded less than 5mg/l picrite since January 2004 and the majority of groundwaters were found to contain less than 1mg/l picrite, except from one borehole where a maximum of 12mg/l has been detected. Picrite on its own is a non-toxic substance with a toxicity threshold as high as 2200mg L-1. Various authors have experimentally shown that although picrite is a non-toxic substance, in the presence of light and/or microorganisms it degrades to nitrosoguanidine, guandine, cyanoguanidine, melamine, urea and ammonia. Each of these degradation products has varying degrees of toxicity, with the overall toxicity of nitroguanidine being approximately two orders of magnitude more when compared with the toxicity of the parent compound. The threshold toxicity level of photolyzed nitroguanidine is approximately 32mg L-1. Published literature to date suggests that nitroguanidine cannot be successfully metabolised by microbial activity to completely innocuous compounds. Nitrosoguanidine, a nitrosamine, is the primary reduction product, and no evidence was found for further microbial action on this compound. Residual levels of nitrosoguanidine persist because of the slow rates of chemical reaction under biological conditions. More stringent chemical conditions would presumably enhance the rate of decomposition and change the number and the types products found in Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. It is therefore recommended that the threshold toxicity level of phytolyzed nitroguanidine of 32mg/l is used as the Tier 1 assessment criteria for assessing the
REFERENCES
1 BAE SYSTEMS Environmental Services (2003). Preliminary Ground Investigation: Picrite Lagoons, RO Bishopton. Prepared for BAE SYSTEMS Properties Ltd. BAE SYSTEMS, Westcott Venture Park, Westcott, Aylesbury, UK. 2 BAE Systems Environmental (2006). Generic Quanititative Risk Assessment Report, Bishopton A385-00-R5-A. 3 Van der Schalie, W.H. (1985). The toxicity of nitroguanidine and photolyzed nitroguanidine to freshwater aquatic organisms. Technical Report 8404, AD A153045. U.S. Army Medical Bioengineering Research and Development Laboratory, Fort Detrick, Fredrick, MD. 4 Burton, D. T., Turley, S. D., Peters, G. T. (1993). Toxicity of nitroguanidine, nitroglycerin, hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX), and 2,4,6-trinitrotoluene (TNT) to selected freshwater aquatic organisms. US Army Medical Research and Development Command, Fort 5 Noss, C. I and Chyrek, R. H. (1984). Nitroguanidine wastewater pollution control technology: Phase III. Treatment with ultraviolet radiation, ozone and hydrogen peroxide. Technical Report 8309, AD A139389. U.S. Army Medical Bioengineering Research and Development Laboratory, Fort Detrick, Frederick, MD. 6 Burrows, W. D., Schmidt, M.O, Chyrek, R. H. and Noss, C.I. (1988). Photochemistry of aqueous nitroguanidine. Technical Report 8803, AD A203200. U.S. Army Medical Research and Development Laboratory, Ft. Detrick, Detrick, Fredrick, MD. 7 Burrows, E.P., Rosenblatt, D.H., Mitchell, W. R., and Parmer, D. L. (1989). Organic explosives and related compounds: Environmental and health considerations. Technical Report 8901, AD A210554. U.S. Army Biomedical Research and Development Laboratory, 8 Kaplan, D. L., Cornell, J.H. and Kaplan, A. M. (1982). Decomposition of Nitroguanidine. Generic Quantitative Risk Assessment Report, Bishopton Redrow Group & BAE Systems Property Investments Ltd. 9 Haag, W. R., Spanggord, R., Mill, T. (1990). Aquatic environmental fate of nitroguanidine. 10 Davis, T. L., Rosenquist, E.N. (1937). J. Am. Chem. Soc. 15, 2112-2115. 11 Ishidate, M., Odashima, S. (1977). S. Mut. Res., 48, 337-354. 12 Wvensch, A., Amberger, A.A. (1974). Z. Pfalzenphysiol. 72, 359-366. 13 Iwasaki, K., Weaver, R. J. (1977). J. Am. Soc. Hort. Sci. 102, 584-587. 14 Sax, M. I. (1975). Dangerous Properties of Industrial Materials. Van Nostrand Reinhold,

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