7091

• UCREFRP Catalog Number: 7091
• Author: Eisler, R.
• Title: Tin Hazards to Fish, Wildlife, and Invertebrates
• USFW Year: 1989.
• USFW - Doc Type: A Synoptic Review.
• Copyright Material: NO

and triphenyltin compounds is shown in Figure 1.
The tendency of an organotin compound to be concentrated by an organism
depends on its partition behavior between lipid and aqueous phases. In
general, compounds highly soluble in octanol and only slightly soluble in
water have high Kow values. Kow values of organotins increase with number and
molecular weight of organic groups attached to the tin atom, with significant
bioaccumulation potential for organotins with R groups of butyl and larger
(Thompson et al. 1985). Kow values for tributyltins in seawater vary from
5,500 to 7,000, but can be significantly modified by salinity and speciation
products (Laughlin et al. 1986b). Thus, organotins would be expected to
accumulate in lipid-rich surface microlayers of natural waters (Cardwell and
Sheldon 1986) and in biota (as discussed later). However, the ability of
microorganisms, algae, and higher organisms to reduce various organotins into
less toxic metabolites that can be rapidly excreted seems to preclude food
chain biomagnification and to lessen the potential hazards to natural
resources from consumption of organisms with elevated organotin residues
(Table 1; Cardwell and Sheldon 1986).
Most authorities now agree on five points: (1) information concerning the
mechanism of the toxic action of organotin compounds is inadequate; (2)
results of all studies with various organotins for possible carcinogenicity
are negative; (3) triorganotin compounds are the most toxic group of
organotins; (4) large inter- and intraspecies differences exist in resistance
to organotin compounds; and (5) organotins can alter enzyme activity levels in
many organs and tissues including brain, liver, and kidney (Piver 1973; Duncan
1980; WHO 1980; Davies and Smith 1982; Maguire et al. 1982; Arakawa and Wada
1984; Dwivedi et al. 1985b; Blunden and Chapman 1986).
The monoorganotin compounds, RSnX 1 have a generally low toxicity and do
not seem to have any important biological action in mammals (Duncan 1980;
Davies and Smith 1982; Krigman and Silverman 1984; Blunden and Chapman 1986).
Dialkylorganotins, R SnX2, are associated with hepatotoxicity (ethyl,
propyl, butyl, and pentylt?ns), immunotoxic effects to T-cells (butyl and
octyltins), and skin and eye irritation (methyl, ethyl, propyl, butyl, and
octyltins; Watanabe 1980; Krigman and Silverman 1984). The diorganotins
combine with coenzymes or enzymes possessing dithiol groups and exert their
toxic action by inhibiting alpha-keto acid oxidation and blocking
mitochondrial respiration (Duncan 1980; WHO 1980; Davies and Smith 1982).
Resistance to diorganotin toxicity varies widely among species. For example,
dibutyltins and dioutyltins--unlike other organotins tested--were toxic to rat
thymocytes, but did not induce similar effects on lymphoid atrophy in mice,
guinea pigs, or Japanese quail (Seinen et al. 1977b). Selected dibutyltins
are effective as antihelminthics and are used to kill parasitic worms in
chickens and turkeys without harm to host birds (Davies and Smith 1982).
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