Organometallic Compounds - Organic Pollutants: An Ecotoxicological Perspective - page 170

13.3, 21, and 23.7 ppm, respectively. Thus, symptoms of neurotoxicity were observed
in individuals containing brain concentrations of Hg substantially lower than those
associated with lethal toxicity. Interestingly, the proportion of the total mercury
accounted for as organomercury declined with time, indicating that demethylation
slowly occurred in the brain.
Captive goshawks dying from methyl mercury poisoning contained 30-40 ppm
Hg in brain and 40-50 ppm Hg in muscle (Borg et al. 1970, see also Section 8.2.3).
In this study and others (Wolfe et al. 1998), it became apparent that birds, like mam-
mals, experience a range of sublethal effects before tissue levels became high enough
to cause death. The first symptoms of methyl mercury poisoning in birds are reduced
food consumption and weakness of the extremities. Muscular coordination is poor,
there is ataxia, and birds can neither walk nor fly (See Rissanen and Mietinnen
in IAEA Technical Report 137 1972). The severity of sublethal neurotoxic effects
produced by methyl mercury would have reduced the likelihood of predatory birds
acquiring lethal concentrations of methyl mercury when chronically exposed in the
field. More likely they would have died from starvation due to sublethal effects before
they could build up lethal concentrations. Predators would lose their ability to catch
prey once muscular coordination was affected. These feeding skills are not tested in
laboratory trials in which birds are presented with food and they may be expected to
tolerate relatively high levels of methyl mercury in tissues before losing their ability
to feed. This contrasts with acute exposures in the field where predators sometimes
consumed high doses of methyl mercury in poisoned prey, and a single meal might
have contained a lethal dose for the predator. More generally, impairment of ability
to fly would have adversely affected herbivores and omnivores in their ability to feed
or escape predation.
The acute toxicity of different types of organomercury compounds to mammals,
expressed as mg/kg, fall into the following ranges:

Methyl mercury compounds 16-32

Ethyl mercury compounds 16-28

Phenyl mercury compounds 5-70

Thus, there is not a great deal of difference between the three classes in acute toxic-
ity; all are highly toxic. However, methyl mercury is more persistent than the other
two types, and so has the greater potential to cause chronic toxicity. The latter point
is important when considering the possibility of sublethal effects.

8.2.5 e c o l o g i c a l e f f e c T s o f o r g a n o m e r c u r y c o m p o u n d s
Of the different forms of organomercury, methyl mercury is the one most clearly
implicated in toxic effects in the field. When methyl mercury seed dressings were
used in Sweden and other Northern European countries during the 1950s and 1960s,
many deaths of seed-eating birds, and of predatory birds feeding upon them, were
attributed to methyl mercury poisoning. There was evidence of birds experiencing
sublethal effects such as inability to fly. There may well have been local declines of
bird populations consequent upon these effects, but these were not clearly established