The scale of the exposure problem is difficult to overstate. Pharmaceuticals such as antibiotics, anti-inflammatory drugs, antidepressants, antiepileptics, and hormones are deliberately engineered to trigger biological responses at vanishingly small doses, and they retain that potency once they reach rivers, estuaries, and coastal waters. Personal care products—antimicrobials, preservatives, fragrances, surfactants, and ultraviolet filters—pour continuously into domestic and industrial wastewater. Endocrine-disrupting compounds such as bisphenol A, nonylphenol, estradiol, and 17-ethinylestradiol can interfere with hormonal and cell-signaling pathways even at environmental concentrations. Because wastewater treatment plants were never designed to strip out these molecules, effluent-dominated waters carry a chronic chemical burden. In the Red Sea’s sewage-influenced coastal zones, for example, caffeine has been measured at 62 to over 3000 nanograms per liter, with total pharmaceutical and personal care product concentrations exceeding 10 micrograms per liter at the most contaminated sites.

What makes microalgae such powerful sentinels is their biology. With short generation times, enormous surface area-to-volume ratios, and constant immersion in the surrounding water, they absorb and respond to dissolved contaminants faster than almost any other organism. The review’s quantitative tables reveal just how variable—and how alarming—the toxicity can be. In the standard freshwater test species Pseudokirchneriella subcapitata, the antibacterial agent triclosan produced 72-hour growth inhibition at concentrations as low as 0.0018 micromolar, among the lowest thresholds recorded for any contaminant class. Yet in a mixed microalgal consortium, triclosan’s 72-hour toxicity value was 8 milligrams per liter, a difference of several orders of magnitude. Nonylphenol proved dramatically more toxic to the estuarine alga Tetraselmis sp. than chemically related endocrine disruptors, with inhibition concentrations of 0.190 to 0.313 milligrams per liter compared with more than 2 milligrams per liter for bisphenol A and 17-ethinylestradiol.

Perhaps the most technically consequential finding concerns photosynthesis, the machinery that converts light into the chemical energy driving the entire cell. Chlorophyll a emerges as the earliest and most consistent biochemical casualty: antibiotics, non-steroidal anti-inflammatory drugs, antidepressants, and endocrine disruptors all deplete it across a wide range of species. In Microcystis flos-aquae, exposure to the antibiotics florfenicol and thiamphenicol cut chlorophyll content by roughly 46 and 56 percent respectively, signaling profound disruption of the photosynthetic apparatus. The damage extends deep into Photosystem II, the oxygen-producing reaction center most vulnerable to photo-oxidative attack. The antidepressant fluoxetine slashed the maximum quantum yield of Photosystem II—measured as the Fv/Fm ratio—by approximately 81 percent in Raphidocelis subcapitata at just 15 to 30 micrograms per liter. Mechanistically, many of these compounds block electron transfer between the quinone acceptors QA and QB, destabilize the oxygen-evolving complex, and dismantle thylakoid membranes, choking the flow of energy before any visible growth decline appears.

Beneath the photosynthetic damage lies what the review identifies as the central toxicity hub: oxidative stress. Contaminants as structurally different as ibuprofen, clarithromycin, bisphenol A, and nonylphenol converge on the same endpoint—overproduction of reactive oxygen species, including superoxide radicals, hydrogen peroxide, hydroxyl radicals, and singlet oxygen. When electron transport is jammed, absorbed light energy has nowhere to go and leaks into the formation of these destructive molecules. They attack polyunsaturated fatty acids in cell membranes, triggering lipid peroxidation that is tracked by rising levels of malondialdehyde, a standard biomarker. In Scenedesmus obliquus, non-steroidal anti-inflammatory drugs induced exactly this cascade, degrading membranes, bleaching pigments, and collapsing photosynthetic efficiency. Under the microscope, exposed cells show chloroplast swelling, thylakoid disorganization, vacuolization, and mitochondrial abnormalities. At the molecular level, reactive oxygen species oxidize DNA—producing strand breaks and mutations—and oxidize amino acid residues in proteins, including the Photosystem II reaction-center proteins sitting closest to the sites of radical generation.

Microalgae are not passive victims, however. The review catalogs a sophisticated defensive arsenal: enzymatic antioxidants such as superoxide dismutase, catalase, peroxidase, ascorbate peroxidase, and glutathione reductase surge into action upon exposure; non-enzymatic scavengers including carotenoids, glutathione, and phenolic compounds mop up radicals; non-photochemical quenching dissipates excess light energy as heat before it can damage reaction centers; and extracellular polymeric substances bind contaminants before they reach the cell surface. Some species even display hormesis—low doses of ethinylestradiol, ciprofloxacin, sulfamethoxazole, amoxicillin, bezafibrate, tamoxifen, and certain anti-inflammatory drugs actually stimulated growth, apparently by providing an auxiliary carbon source or priming stress-response pathways. But the defenses have hard limits. Under chronic exposure or high concentrations, antioxidant enzymes themselves become oxidized and inactivated, and the cell tips from adaptation into irreversible injury. Repeated dosing with clarithromycin, for instance, produced greater reactive oxygen species accumulation than a single pulse, revealing cumulative damage that standard 72-hour assays completely miss.

That gap between acute testing and chronic reality is one of the review’s sharpest criticisms of the field. A ten-day exposure to carbamazepine at 200 milligrams per liter inhibited growth by 97 percent in Scenedesmus obliquus, yet the same concentration suppressed Chlamydomonas mexicana by only 30 percent, and Spirulina platensis showed just 34 percent inhibition at 100 milligrams per liter. Species identity, exposure duration, and endpoint selection all reshape toxicity rankings, which is why the authors warn against generalizing results from the handful of freshwater chlorophytes—Chlorella vulgaris, Scenedesmus species, and Pseudokirchneriella subcapitata—that dominate the literature. Marine and estuarine microalgae, cyanobacteria, and natural biofilms remain drastically understudied, even though stream biofilm experiments showed diphenhydramine suppressing algal biomass by 18 to 81 percent and photosynthetic performance by up to 99 percent. Single-compound tests compound the problem, since real waters carry mixtures that can act synergistically; co-exposure to pharmaceuticals and microplastics, for example, generates more oxidative damage than either contaminant alone.

The biotechnological implications cut in two directions at once. Contaminant stress often forces microalgae to redirect carbon from cell division into storage lipids, carotenoids, and protective secondary metabolites, creating a growth–metabolite trade-off: biomass yield falls while the content of commercially valuable compounds such as beta-carotene, astaxanthin, lutein, and zeaxanthin rises. Mild stress could therefore be exploited as a production strategy, provided contaminant accumulation in the harvested biomass is carefully monitored, since pharmaceuticals and their transformation products may lodge in cells destined for food, feed, or nutraceutical markets. At the same time, microalgae’s capacity to uptake, biotransform, and degrade these pollutants—mediated partly by cytochrome P450 enzymes—positions them as workhorses for phycoremediation. Pilot thin-layer reactors fed real wastewater laced with antibiotics and analgesics maintained biomass productivity and chlorophyll fluorescence without measurable harm, hinting that resilient algal communities could simultaneously clean water and generate feedstock for biofuels, biofertilizers, and bioplastics within a circular bioeconomy.

The review closes with a three-pronged roadmap for the decade ahead. First, ecotoxicology must embrace ecological realism: chronic multigenerational exposures, environmentally relevant mixtures, and a much broader taxonomic spread that includes marine and estuarine species. Second, omics technologies—genomics, transcriptomics, proteomics, and metabolomics—should be deployed to map the genes and networks governing contaminant uptake, detoxification, and hormesis, enabling the design of tolerant strains through synthetic biology and adaptive laboratory evolution. Third, algal biorefineries should be engineered around circular bioeconomy principles, coupling contaminant removal with nutrient recovery, carbon capture, and biomass valorization, backed by rigorous life-cycle assessments and techno-economic analysis. If those priorities are met, the very organisms now serving as early-warning indicators of chemical pollution could become the foundation of a sustainable technology that turns wastewater from an environmental liability into a resource stream.

Subject of Research: Ecotoxicological effects of pharmaceuticals, personal care products, and endocrine-disrupting compounds on microalgae

Article Title: Ecotoxicological effects of pharmaceuticals, personal care products, and endocrine disruptors on microalgae: a comprehensive review

Article References: Ecotoxicological effects of pharmaceuticals, personal care products, and endocrine disruptors on microalgae: a comprehensive review. (n.d.). https://doi.org/10.1186/s44315-026-00064-y

Image Credits: AI Generated

DOI: 10.1186/s44315-026-00064-y

Keywords: microalgae, emerging contaminants, pharmaceuticals, personal care products, endocrine disruptors, oxidative stress, photosynthesis, ecotoxicology, phycoremediation, reactive oxygen species, algal biotechnology, wastewater treatment