Abstract

The acute and chronic effects of secondary-treated effluent from a New Zealand pulp and paper mill were assessed using both long-term adult and early life stage (ELS) laboratory exposures of rainbow trout. The relative impact of maternal exposure versus ELS exposure was assessed by a comparison of directly exposed eggs and larvae with the eggs and larvae of exposed adult trout that were reared in reference water. Rainbow trout were exposed to a secondary-treated mixed thermomechanical/bleached kraft mill effluent at a concentration of 15% or to reference water from the egg through to 320-d-old juveniles. The 2 adult rainbow trout exposures were undertaken with nominal concentrations of 10% and 12% treated effluent, respectively. There was no marked effect of water hardening with 15% effluent on fertility or survival of eggs to 16 d. In a subsequent exposure (with hardening in reference water), no significant effects were found on mortality to hatch, time to hatch, length at hatch, mortality to swim-up, mortality to 320 d, or deformity rate at hatch. At experimental termination (320 d), direct-exposed juveniles had smaller livers and reduced condition factor, likely due to differences in food consumption. In 2 subsequent consecutive experiments, exposure of adult trout to 10% and 12% effluent for 2 mo, followed by incubation of the fertilized eggs in reference water, produced no impact on fertility, survival to hatch, survival to swim-up, or length and weight of fry at swim-up. Exposure of adult trout to 12% treated effluent for 8 mo prior to egg fertilization also did not result in differing rates of fertility, mortality to hatch or mortality to swim-up. However, the 8-mo maternal exposure did result in swim-up fry that were significantly shorter and weighed less than the reference swim-up fry. This difference was directly attributable to smaller eggs in the 8-mo-exposed female trout. These results demonstrate that this pulp and paper mill effluent is more likely to elicit indirect impacts on progeny size through chronic exposure of adults to effluent during gonadal recrudescence rather than through direct exposure of early life stages to effluent. Funding for this research was provided by the Arthur and Aenne Feindt Foundation of Germany, The Foundation for Research Science and Technology of New Zealand and by the Norske-Skog/Carter Holt Harvey Tasman Mill. The authors acknowledge the assistance of Megan Harris, Luca Chiaroni, Suzanne Lambie, Murray Smith, Nicola Marvin, Rob Hunter, Robert Donald, and Errol Cudby.

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