The value of repeating studies and multiple controls: replicated 28-day growth studies of rainbow trout exposed to clofibric acid

Two studies to examine the effect of waterborne clofibric acid (CA) on growth‐rate and condition of rainbow trout were conducted using accepted regulatory tests (Organisation for Economic Co‐operation and Development [OECD] 215). The first study (in 2005) showed significant reductions after 21 d of...

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Published in:Environmental toxicology and chemistry 2010-12, Vol.29 (12), p.2831-2839
Main Authors: Owen, Stewart F., Huggett, Duane B., Hutchinson, Thomas H., Hetheridge, Malcolm J., McCormack, Paul, Kinter, Lewis B., Ericson, Jon F., Constantine, Lisa A., Sumpter, John P.
Format: Article
Language:English
Subjects:
Animals
Anticholesteremic Agents - blood
Anticholesteremic Agents - toxicity
Aquatic ecosystems
Body Composition - drug effects
Body Weight - drug effects
Clofibric acid
Clofibric Acid - blood
Clofibric Acid - toxicity
Control equipment
Dose-Response Relationship, Drug
Economics
Environmental risk assessment
Female
Fish
Growth
Herbicides
Liver
Oncorhynchus mykiss
Oncorhynchus mykiss - blood
Oncorhynchus mykiss - growth & development
Organ Size - drug effects
Pharmaceuticals
Physical growth
Rainbow trout
Replication
Stands
Tanks
Toxicity
Toxicity Tests, Chronic - methods
Toxicology
Trout
Water Pollutants, Chemical - blood
Water Pollutants, Chemical - toxicity
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Summary:Two studies to examine the effect of waterborne clofibric acid (CA) on growth‐rate and condition of rainbow trout were conducted using accepted regulatory tests (Organisation for Economic Co‐operation and Development [OECD] 215). The first study (in 2005) showed significant reductions after 21 d of exposure (21‐d growth lowest‐observed‐effect concentration [LOEC] = 0.1 µg/L, 21‐d condition LOEC = 0.1 µg/L) that continued to 28 d. Growth rate was reduced by approximately 50% (from 5.27 to 2.67% per day), while the condition of the fish reduced in a concentration‐dependant manner. Additionally, in a concentration‐dependent manner, significant changes in relative liver size were observed, such that increasing concentrations of CA resulted in smaller livers after 28‐d exposure. A no‐observed‐effect concentration (NOEC) was not achieved in the 2005 study. An expanded second study (in 2006) that included a robust bridge to the 2005 study, with four replicate tanks of eight individual fish per concentration, did not repeat the 2005 findings. In the 2006 study, no significant effect on growth rate, condition, or liver biometry was observed after 21 or 28 d (28‐d growth NOEC = 10 µg/L, 28‐d condition NOEC = 10 µg/L), contrary to the 2005 findings. We do not dismiss either of these findings and suggest both are relevant and stand for comparison. However, the larger 2006 study carries more statistical power and multiple‐tank replication, so probably produced the more robust findings. Despite sufficient statistical power in each study, interpretation of these and similar studies should be conducted with caution, because much significance is placed on the role of limited numbers of individual and tank replicates and the influence of control animals. Environ. Toxicol. Chem. 2010;29:2831–2839. © 2010 SETAC
ISSN:0730-7268
1552-8618
1552-8618
DOI:10.1002/etc.351