7092

• UCREFRP Catalog Number: 7092
• Author: Eisler, R.
• Title: Arsenic Hazards to Fish, Wildlife, and Invertebrates
• USFW Year: 1988.
• USFW - Doc Type: A Synoptic Review.
• Copyright Material: NO

10 days later, although some enrichment was noted in eyes, throat, gills, and
pyloric caeca (Pershagen and Vahter 1979). Oral administration of sodium
arsenate to estuary catfish (Cnidoglanis macrocephalus) and school whiting
(Sillago bassensis) resulted in tissue accumulations of trimethylarsine
oxide. Arsenobetaine Aevels, which occur naturally in these teleosts, were
not affected by As dosing. The toxicity of trimethylarsine oxide is
unknown, but the ease with which it can be reduced to the highly toxic
trimethylarsine is cause for concern (Edmonds and Francesconi 1987).
BIRDS
Signs of inorganic trivalent arsenite poisoning in birds (muscular
incoordination, debility, slowness, jerkiness, falling hyperactivity, fluffed
feathers, drooped eyelid, huddled position, unkempt appearance, loss of
righting reflex, immobility, seizures) were similar to those induced by many
other toxicants and did not seem to be specific for arsenosis. Signs occurred
within 1 hour and deaths within 1 to 6 days postadministration; remission took
up to 1 month (Hudson et al. 1984). Internal examination suggested that
lethal effects of acute inorganic arsenic poisoning were due to the
destruction of blood vessels lining the gut, which resulted in decreased blood
pressure and subsequent shock (Nystrom 1984). +3 Coturnix (Coturnix coturnix),
for example, exposed to acute oral doses of As showed hepatocyte damage,
i.e., swelling of granular endoplasmic reticulum; these effects were
attributed to osmotic imbalance, possibly induced by direct inhibition of the
sodium pump by arsenic (Nystrom 1984).
Western grasshoppers (Melanophis spp.) poisoned by arsenic trioxide were
fed, with essentially no deleterious effects, to nestling northern bobwhites
(Colinus virginianus), mockingbirds (Mimus polyglottos), American robins
(Turdus migratorius), and other songbirds (NAS 1977). Up to 134 poisoned
grasshoppers, containing a total of about 40 mg As, were fed to individual
nestlings without any apparent toxic effect. The species tested that were
most sensitive to various arsenicals were brown-headed cowbird (Molothrus
ater) with an LD-50 (11-day) value of 99.8 mg of copper acetoarsenite/kg diet;
California quail (Callipepla californica) with an LD-50 single oral dose value
of 47.6 mg of sodium arsenite/kg body weight; and chicken with 33 and turkey
with 17.4 mg/kg body weight of 3-nitro-4-hydroxy phenylarsonic acid as a
single oral dose (Table 5).
Chickens rapidly excrete arsenicals; only 2% of dietary sodium arsenite
remained after 60 hours (NAS 1977), and arsanilic acid was excreted largely
unchanged (Woolson 1975). Excretion of arsanilic acid by chickens was
affected by uptake route: excretion was more rapid if administeration was by
intramuscular+?njection than if it was oral (NRCC 1978). Studies with
inorganic As and chickens indicated that arsenates rap %y penetrated
mucosal and serosal surfaces of epithelial membranes; that As intestinal
absorption was essentially complete within 1 hour at 370 mg As /kg BW but
only 50% complete at 3,700 mg/kg BW; that Vitamin D3 was effective in
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