What does this research mean for the field?

Exposure to mercury-contaminated effluent from the chlor-alkali industry causes severe, irreversible physiological damage and significant mercury bioaccumulation in the vital organs of the fish Tilapia mossambica. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research aims to evaluate the toxic effects of chlor-alkali industry effluent on the fish species Tilapia mossambica under controlled conditions.

May 30, 2026Open Access

Eco-Toxicological Changes Induced By Effluent Of A Chlor-Alkali Industry On A Fish, Tilapia mossambica, Peters Under Laboratory Controlled Conditions.

Key Points

This research aims to evaluate the toxic effects of chlor-alkali industry effluent on the fish species Tilapia mossambica under controlled conditions.
Collected effluent samples from contaminated sites for analysis.
Conducted a 30-day toxicity experiment using maximum allowable concentration (MAC) for fish exposure.
Monitored physiological changes and mercury accumulation in exposed fishes compared to controls.
Exposed fishes displayed lethargy, erratic swimming, and increased ventilation rates initially, followed by depression.
Significant accumulation of mercury was found in organs, affecting fish physiological parameters.
No recovery was observed in exposed fish after transfer to effluent-free medium, indicating permanent organ damage.

Abstract

Effluent collected from the effluent dumping site and other contaminated sites in and around the industry at different time periods indicated significant difference in chemical composition and mercury concentration. Hence, it was planned to collect the effluent from the effluent soaking pond where the discharged effluent is stocked for aerial drying and soaking. The effluent of the Chlor-alkali industry contained 0.38mg of Hg l -1 which is significantly high when compared to the values prescribed by Pollution Control Boards. The toxicity study indicated that the effluent is deadly toxic. The maximum allowable concentration (MAC) for 30d experiment was deduced and the long term experiments were conducted at MAC value. The exposed fishes appeared lethargic after introduction of the effluent. Initial symptoms like erratic swimming, ataxia, in appetence were marked in the effluent exposed fishes. Initial higher ventilation rate followed by depression was due to initial over excitation followed by impact leading to stress impact was clear in exposed fishes. Control fishes remained clinically healthy through the experimental period. Depression in BSI and LSI values in effluent exposed fishes compared to control fish values were noted. The residual mercury accumulation was significant and residual mercury enrichment increased with the increase in exposure period indicating a positive correlation. It was also noted that all the tested values were probably linked to residual mercury. It seems the body enrichment of mercury in different organs impacted the physiological parameters of the effluent exposed fishes. The exposed fishes did not recover when transferred to effluent free medium. The exposed fish could not recover during recovery period indicating permanent damage caused to the vital organs by the mercury contained effluent. Little variations during recovery period were not statistically significant and it was not possible to attribute this insignificant recovery in the parameters to be an asset for stress physiology.

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