Pharmaceuticals in water: read biomarkers cautiously

Pharmaceuticals in water: read biomarkers cautiously

Four pharmaceuticals altered several biomarkers in experimentally exposed carp. These early biological signals are not yet a field diagnosis of ecological risk.

Content type
Scientific news
Sector
Environment
Animal group
FishCyprinids
Theme
Ecology and environmentDiagnostics

Pharmaceuticals reach aquatic environments through municipal and hospital effluent, livestock and aquaculture discharges, runoff, poor disposal and incomplete removal during wastewater treatment. A 2025 study exposed common carp to four compounds—bromazepam, naproxen, metoprolol and sotalol—at nominal concentrations selected from values reported in effluent. After two weeks, several blood, biochemical, antioxidant and genotoxicity markers differed from controls. The experiment demonstrates biological responses; it does not provide a stand-alone diagnosis for a river.

A controlled experiment with four compounds

The researchers divided 150 juvenile carp averaging 40.5 g into five groups of 30 fish, with three tanks per group. One group served as the unexposed control. Each of the other groups received one substance: 15.54 µg/L bromazepam, 14.40 µg/L naproxen, 5.76 µg/L metoprolol or 3.33 µg/L sotalol. Fish were held for two weeks at approximately 28.5°C, mean pH 7.4 and dissolved oxygen near 6.9 mg/L.

This design compares each compound with a control under stable conditions. It does not recreate a catchment where concentrations fluctuate, substances occur as mixtures, organisms have different exposure histories and temperature, food or other pollutants modify responses.

Six fish per group were selected for final sampling. Analyses included haematology, biochemical variables, antioxidant enzymes, apoptosis and DNA damage assessed using the comet assay. The endpoints are therefore sublethal biological signals, not direct measurements of population survival.

Multiple responses, but no unique signature

Exposed groups showed changes in red and white blood cells, glucose, tissue-associated enzymes and antioxidant defences. All four compounds increased several oxidative-stress markers. Naproxen, metoprolol and sotalol were also associated with a greater comet-assay tail moment, interpreted as a DNA-damage signal; naproxen produced the largest response in this experiment.

These differences matter for ecotoxicology because they demonstrate that compounds designed to act on biological systems can affect conserved functions in fish. They are not, however, a fingerprint specific to pharmaceuticals. Hypoxia, infection, capture stress and other contaminants may alter some of the same variables.

A biomarker should therefore be treated as one part of the evidence. Interpretation becomes stronger when biology is linked to chemical measurement, spatial or temporal gradients, appropriate reference sites, multiple levels of organisation and habitat information. Without that structure, an altered blood value identifies neither the responsible compound nor the ecological consequence.

Limits that prevent direct field extrapolation

The study tested each pharmaceutical separately, while environmental exposure involves mixtures. It used nominal concentrations redosed into tanks; actual concentrations and internal exposure may change through adsorption, degradation and water renewal. Two weeks cannot represent intermittent releases or chronic effects on growth, reproduction, behaviour and survival.

Species and life stage also matter. Common carp are a useful experimental model and widespread fish, but their response does not automatically represent salmonids, amphibians or invertebrates. Results in juveniles at 28.5°C do not establish a universal safe concentration.

Some biochemical interpretations in the paper, particularly those concerning plasma proteins, require additional caution. The analytical result should be distinguished from the proposed mechanism. Independent replication, better protein characterisation and measured concentrations in water and tissues would strengthen causal interpretation.

The findings also cannot distinguish source categories. A compound detected downstream may originate from household use, healthcare, manufacturing, animal treatment or several pathways. Source attribution requires catchment evidence, not pharmacological labels alone.

Build monitoring around a decision

A field campaign should begin with a defined question: detect a source, follow a trend, compare sites or evaluate an impact? The design then combines water and possibly sediment sampling, hydrology, catchment use, sentinel species and biological endpoints. Blanks, replicates, quantification limits, timing and storage conditions need to be documented.

Bioaccumulation cannot be inferred merely because an effect is present. It requires measurements in water, tissue or exposed organisms over an appropriate timeline. Equally, a lack of visible mortality does not rule out sublethal effects, while an altered biomarker does not prove a population-level consequence.

Managers can reduce inputs through take-back schemes for unused medicines, improved control of discharges and evaluation of effluent treatment. Monitoring should remain proportionate. Ordering a very long analytical list without an interpretation plan can consume resources while producing few actionable conclusions.

The carp study provides a coherent experimental signal: several pharmaceuticals can alter biological variables over a short exposure at low concentrations. Its professional value is to inform integrated investigation, not to offer a universal blood test for rivers. Vetofish can support question definition, matrix and species selection, sampling, biomarker interpretation and integration with chemical and ecological evidence.

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