Figure 6.—Epidermis of control fish (a) and of fish exposed to 48 ppm (b). Note nuclear hypertrophy and paucity of mucus secreting 
cells in 6b. The separation of the epidermis from the deeper layers is probably sectioning artifact. 120; PAS-hematoxylin stain. 
the cunners exposed to 48 ppm cadmium may be 
caused by the metal’s effect on the hemopoietic 
system. Friberg (1950) found no effects in human bone 
marrow after respiratory exposure. Wilson, DeKds, 
and Cox (1941) found that rats fed a diet containing as 
low as 31 ppm cadmium would be anemic. By ad- 
ministering iron to rats receiving cadmium in their 
diet, anemias were reduced (Friberg, 1955). This in- 
dicated that cadmium was not directly blocking 
hemoglobin synthesis, but might be interfering with 
the uptake of iron by the intestine. If a reduction of 
iron absorption was occurring in the cunner, this, 
along with the observed decrease in erythrophagocytic 
activity, might account for the observed reduction in 
hemosiderin in exposed animals. 
Gill 
The lack of correlation between exposure level and 
observed pathologic changes in the gill tissue can be 
explained by Gardner and Yevich’s observations on 
mummichogs. They noted that gill lesions were focal 
in that all gill filaments were not involved, and the 
lesions were of a random nature, not limited to 
specific areas of the branchial arches. 
The importance of the effects of heavy metals on 
the respiratory epithelium of fishes is not clear. Skid- 
more (1964) believed that death of rainbow trout, 
Salmo gairdneri, exposed to acutely toxic solution of 
zinc sulphate was caused by tissue hypoxia, resulting 
from the damaging effect of the metal on gill 
epithelium. Subsequent experimental studies seem to 
confirm this hypothesis (Skidmore, 1970). Burton, 
_ Morgan, and Cairns (1972) studied levels of lactic and 
_ pyruvic acid in muscle and liver of rainbow trout ex- 
. posed to acute zinc toxicity and reached conclusions 
! similar to Skidmore. Schweiger, cited in Eisler (1971), 
concluded that the toxic action of cadmium on several 
3] 
freshwater fish and invertebrates was due to suffoca- 
tion. Friberg et al. (1971) cite examples of respiratory 
exposure to cadmium producing lung damage in 
mammals at levels which were insufficient to cause 
kidney damage. Doudoroff and Katz (1953) are cited 
by Mount and Stephan (1967) as listing nine 
references attributing the death of fish in solutions 
containing heavy metal salts to coagulation of mucus 
on the gill or damage to gill tissue. Bilinski and Jonas 
(1973) found that exposure of rainbow trout to 11.2 
ppm Cd’** for 72 hr resulted in a 66% mortality, but 
there was no significant change in the ability of the 
gill tissue to oxidise lactate. 
Evidence from the present study implicates renal 
failure as a cause of death in cunner after acute ex- 
posure to cadmium. Although pathological changes 
were observed in gill tissue and gills exposed to even 
low levels of cadmium seemed to sustain some 
physiological damage (Thurberg and Dawson, this 
report, Part III), these changes do not seem to be 
asociated with mortality. On the other hand, those 
fish exposed to 48 ppm cadmium for 96 hr all died 
within a few days after being returned to clean 
seawater (Calabrese, Collier, and Miller this report, 
Part I). Therefore, as regards the effects of cadmium 
on the cunner, mortality seems to be associated with 
severe pathological changes of an apparently irreversi- 
ble nature taking place in the kidney. 
Epidermis 
The destruction of the mucus cells of the epidermis 
could have important consequences as it would 
eliminate the fish’s first line of defense against infec- 
tious microorganisms. The possibility that heavy 
metals would destroy mucus cells with exposures too 
short to cause renal damage should be investigated. In 
the present study, the fish had already received a 
