Immunotoxic Effects of Organotin Compounds in Teleost Fish

A number of field studies have provided evidence that environmental toxicants can modulate immune parameters of exposed fish (for overviews see Snieszko 1974; Dunier and Siwicki 1993; Zeeman 1994; Zelikoff 1994; Rice 2001). Also, laboratory studies demonstrated that toxicants impact the immune system of fish (e.g., Weeks et al. 1988; Thuvander and Carlstein 1991; Kaattari et al. 1994; Rice and Schlenk 1995; Sanchez-Dardon et al. 1999; Carlson et al. 2004; Quabius et al. 2005). Consequently, it has been suggested to utilize immune parameters of fish as indicators of environmental pollution (Anderson 1990; Weeks et al. 1992; Wester et al. 1994).

In fish immunotoxicological studies, emphasis has been given to the measurement of single endpoints or functions such as depressed phagocytic activity of macrophages or the alteration of oxidative burst activity of immune cells. However, the ultimate concern is that toxic exposure might increase the susceptibility of fish to pathogen infections. Thus, it is important to elucidate the consequences of changes in molecular or cellular immune parameters for the overall immune system function, since, as pointed out by Rice (2001), alterations at the molecular and cellular level do not necessarily translate into immune modulation at the system level. Rather few studies directly correlated alterations of specific molecular and cellular immune parameters with altered immune system function and/or altered susceptibility to pathogens (Palm et al. 2003; Carlson et al. 2002; Burki et al. 2008). However, some more indirect evidence is available that toxic impact on immune parameters increases the susceptibility of fish to disease. One example comes from the decline of wild Pacific salmon populations in the USA and Canada. When juvenile chinook salmon (Oncorhynchus tshawytscha) collected from estuaries in the Puget Sound area and showing suppression of various immune parameters were infected with Vibrio anguillarum in the laboratory, they were more susceptible than fish from non- or less-polluted areas (Arkoosh et al. 1998). Significant differences were seen even 2 months after removal from the contaminated areas, suggesting that the chemical exposure had a lasting effect on disease susceptibility. This assumption is supported by the study of Milston et al. (2003) who showed that short-term contaminant exposure of chinook salmon during early life-history stages resulted in long-term impairment of humoral immune competence. Under complex field conditions, as in Puget Sound, it is difficult if not impossible to provide conclusive evidence that the contaminant-induced immunosuppression is causative to the observed decline of chinook salmon populations. However, in a demographic modeling study, Spromberg and Meador (2005) could show that immune suppression acting through reduction of age-specific survival would produce pronounced changes in the population growth rate. This result highlights the potential of immunotoxicants to adversely affect organism health and population growth of aquatic wildlife.