Delaying aging while prolonging health and lifespan is a major goal in aging research. One promising strategy is to focus on reducing negative interventions such as pollution and their accelerating effect on age-related degeneration and disease. Here, we used the short-lived model organism C. elegans to analyze whether two candidate pollutants corrupt general aging pathways. We show that the emergent pollutant silica nanoparticles (NPs) and the classic xenobiotic inorganic mercury reduce lifespan and cause a premature protein aggregation phenotype. Comparative mass spectrometry revealed that increased insolubility of proteins with important functions in proteostasis is a shared phenotype of intrinsic- and pollution-induced aging supporting the hypothesis that proteostasis is a central resilience pathway controlling lifespan and aging. The presented data demonstrate that pollutants corrupt intrinsic aging pathways. Reducing pollution is, therefore, an important step to increasing healthy aging and prolonging life expectancies on a population level in humans and animals.


Biological Sciences


National Institutes of Health, Grant P40 OD010440

Keywords and Phrases

Animal physiology; Biological sciences; Environmental science; Physiology; Toxicology

International Standard Serial Number (ISSN)


Document Type

Article - Journal

Document Version

Final Version

File Type





© 2023 The Authors, All rights reserved.

Publication Date

16 Sep 2022

Included in

Biology Commons