The study, , shows that chronic exposure to the insecticide chlorpyrifos at concentrations too low to cause immediate toxicity causes fish to age faster at the cellular level.
The research began with field studies in China where collaborators examined thousands of fish collected over several years from lakes with differing levels of pesticide contamination. Rohr and colleagues observed that fish living in contaminated lakes lacked older individuals, while populations in relatively uncontaminated lakes included many older fish. This pattern suggested that fish were not failing to add to their populations, but rather were dying earlier in life.
“When we examined telomere length and deposition of lipofuscin in the livers of the fish, well-established biological markers of aging, we found that fish of the same chronological age were aging faster in the contaminated than clean lakes,†said Rohr, the Ludmilla F., Stephen J. and Robert T. Galla Professor and Chair in the Department of Biology.
Chemical analyses revealed that chlorpyrifos was the only compound found in the fish tissues that was consistently associated with signs of aging. These include shortened telomeres, which act like the plastic caps shoelaces and decrease fraying in chromosomes, and lipofuscin deposition, a build-up of “junk†like old proteins and metals within long-lived cells. However, to determine whether chlorpyrifos was the direct cause, researchers needed to conduct controlled laboratory experiments with concentrations matching those measured in the wild, Rohr said.
In this laboratory experiment, chronic low-dose exposure to chlorpyrifos caused progressive telomere shortening, increased cellular aging and reduced survival, particularly in fish from the contaminated lakes that were already physiologically older.
“Although the laboratory results closely matched the field observations, it was possible that a missed high-dose exposure event in the field, rather than chronic low-dose exposures, caused the reduced lifespan,†said Rohr, who is affiliated with 91³Ô¹Ï’s , and
To rule out this driver, Rohr and colleagues conducted another laboratory experiment demonstrating that short-term exposure to much higher doses caused rapid toxicity and death but did not accelerate aging through shortened telomeres and increased lipofuscin. This demonstrated that long-term accumulation of exposure to extremely common low concentrations — not brief high-dose spikes — was responsible for the observed aging, Rohr said.
The loss of older individuals can have serious ecological consequences, as older fish often contribute disproportionately to reproduction, genetic diversity and population stability, Rohr said.
“These findings also raise broader concerns because telomere biology and aging mechanisms are highly conserved across vertebrates, including humans,†Rohr said. Potential future research will explore how widespread the phenomenon may be across species and chemicals.
While the European Union has largely banned chlorpyrifos, it remains in use throughout China, parts of the United States and in many other countries. However, the aging effects observed in this study occurred at concentrations below current U.S. freshwater safety standards, Rohr said.
“Our results challenge the assumption that chemicals are safe if they do not cause immediate harm,†he said. “Low-level exposures can silently accumulate damage over time by accelerating biological aging, highlighting that chemical safety assessments must move beyond short-term toxicity tests to adequately protect environmental and human health.â€
The research was funded by the National Science Foundations in both the United States and China, the Illinois-Indiana Sea Grant and the Frontiers Research Foundation.
Contact: Brandi Wampler, associate director of media relations, 574-631-2632, brandiwampler@nd.edu
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