Abstract

Chickens were fed methyl mercury-dressed wheat (average mercury content 8 ppm) for 5–6 weeks and were then sacrificed. Muscle, and some liver, of the chickens were fed to goshawks. Three goshawks receiving chicken muscle and liver (average dietary mercury content 13 ppm) as the sole food died within 30, 38 and 47 days and one goshawk receiving only muscle (average mercury content 10 ppm) within 39 days. Main clinical symptoms, appearing after a latency period of about 2 weeks, were inappetence, muscular weakness, ataxia and loss of body weight. On autopsy, the dominating gross finding was muscular atrophy which presumably was the main cause of the weight loss. Pronounced histological changes, including demyelination and nerve cell degeneration of the cerebellum and medulla oblongata and demyelination of the peripheral nerves were in conformity with the clinical and gross observations. No lesions were found in the cerebrum. Tissue mercury levels at death were high in the liver and kidneys and also in skeletal muscle and the brain. Remarkably high levels were found in the gonads, particularly in the testicles (up to 280 ppm, fresh weight). Tissue mercury was almost exclusively methyl mercury. The fatal brain level of methyl mercury in goshawks, as well as in ferrets (Hanko et al., 1970), seems to be of the order of 30–40 ppm (as Hg). The results provide direct evidence that methyl mercury may accumulate in a food chain and without apparent loss of its toxic qualities. The ecological implications are discussed.

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