Toxicity of cadmium to early life stages of brown trout (Salmo trutta) at multiple water hardnesses

Abstract

Abstract-Toxicity of cadmium to early life stages of brown trout (Salmo trutta) was determined at multiple water hardnesses. Increasing water hardness decreased cadmium toxicity. Postswimup fry were much more sensitive than embryos and larvae. Chronic values from early life stage tests initiated with eyed embryos were 3.52, 6.36, and 13.6 g Cd/L at water hardnesses of 30.6, 71.3, and 149 mg/L, respectively. In tests initiated with 30-d postswimup fry, chronic values were 1.02, 1.83, and 6.54 g Cd/L at water hardnesses of 29.2, 67.6, and 151 mg/L, respectively. Higher chronic values from the early life stage tests compared to tests initiated with swimup fry likely are caused by acclimation during cadmium-tolerant embryo and larval stages. Growth was not affected by cadmium in the early life stage tests but was negatively affected in tests initiated with fry at water hardnesses of 29.2 and 67.6 mg/L. Concentrations of cadmium that reduced growth were higher than those that increased mortality. Median lethal concentrations for swimup fry after 96 h were 1.23, 3.90, and 10.1 g Cd/L at water hardnesses of 29.2, 67.6, and 151 mg/L, respectively. Test results enable prediction of acute mortality of brown trout swimup fry based on cadmium concentration and water hardness.

Development and application of the adverse outcome pathway framework for understanding and predicting chronic toxicity: II. A focus on growth impairment in fish

“…3. Exposure to Cd was documented to cause growth impairment in a variety of fish species, including brook trout (Salvelinus fontinalis) (Eaton et al, 1978), Atlantic salmon (Salmo salar) (Rombaugh and Garside, 1982;Peterson et al, 1983), rainbow trout (Woodworth and Pascoe, 1982;Ricard et al, 1998;Heydarnejad et al, 2013), white sucker (Catostomus comersoni) and common shiner (Notropis cornutus) (Borgmann and Ralph, 1986), guppy (Miliou et al, 1998), bull trout (Salvelinus confluentus) (Hansen et al, 2002b), topsmelt (Atherinops affinis) (Rose et al, 2005(Rose et al, , 2006, common carp (Cyprinus carpio) (Reynders et al, 2006), brown trout (Salmo trutta) (Brinkman and Hansen, 2007), European eel (Anguilla anguilla) (Pierron et al, 2007), silver catfish (Rhamdia quelen) (Benaduce et al, 2008), red sea bream (Pagrus major) (Cao et al, 2009), Japanese flounder (Paralichthys olivaceus) (Cao et al, 2010) and ide (Leuciscus idus) (Witeska et al, 2014). In Aphanius fasciatus collected in the field, a high accumulation of Cd associated with a decreased growth rate and condition index was observed (Kessabi et al, 2013).…”

“…For example, Cd toxicity was shown to decrease in media with higher hardness (Hansen et al, 2002a,b;Brinkman and Hansen, 2007;Benaduce et al, 2008) and increase under hypoxic conditions (Hattlink et al, 2005). In regard to toxicity outcomes, environmentally relevant factors, such as food limitation, have been shown to affect the degree of Cd toxicity (Rose et al, 2005).…”

“…Interestingly, post-swim-up fry are often reported to be more sensitive to Cd compared to embryos and early larvae. Such is the case in Atlantic salmon (Peterson et al, 1983) and brown trout (Brinkman and Hansen, 2007). However, a detailed time-resolved analysis of Cd toxicity during the first day of development showed that the earliest life stages of Japanese medaka (up to morula) were the most sensitive to Cd, with sensitivity rapidly decreasing if exposure was started at later time points (Michibata et al, 1987).…”

Molecular and phenotypic responses of Japanese medaka (Oryzias latipes) early life stages to environmental concentrations of cadmium in sediment

“…In addition to its widely recognized carcinogenicity and mutagenicity, Cd was also reported as an important teratogenic and embryotoxic chemical in several fish species (Hallare et al 2005;Brinkman and Hansen, 2007;Benaduce et al 2008;Cao et al 2009; Barjhoux et al 2012) and several studies already investigated gene expression modulation…”

A toxic diet: transfer of contaminants to offspring through a parental care mechanism

“…The frequent feeding performed by fry would result in a continuous dietary exposure to Cd for this period. This exposure period coincides with the early developmental period of these fry and hence is considered a sensitive time of exposure (Brinkman and Hansen, 2007). In fish, the toxicity of dietary contaminants to early life stages (Westin et al, 1985) is not as well studied as the effects of aqueous exposures (Sloman and McNeil, 2012), most likely because of practical reasons of diet manufacture, and certainly warrants further study.…”