Hormetic effects of chemical contaminants on animal development: Mechanisms, phenotypes, and ecological implications

Emerging evidence reveals low, environmental concentrations of contaminants trigger stimulatory-hormetic responses in animals, prompting this literature synthesis to explore broader patterns and implications of contaminant-induced developmental hormesis. Findings demonstrate consistent biphasic responses across fundamental developmental endpoints. Low-dose exposures enhance key traits such as embryonic survival, hatching success, and fertilization rates while reducing developmental deformities and mortality. Hormetic stimulation further manifests in morpho-anatomical traits, including altered growth and organ size and shape, and shifts in developmental timing across life stages. These phenotypic outcomes are mechanistically linked to physiological and molecular changes, such as modified gene expression in critical developmental pathways and altered energy allocation strategies, though molecular evidence is limited. Such responses often represent interconnected adjustments across anatomical, physiological, and temporal dimensions of development. However, apparent stimulations of specific endpoints at sub-lethal (but not true hormetic) doses often involve context-dependent trade-offs and may arise from indirect contaminant interactions rather than direct biological stimulation. Consequently, low-dose developmental stimulation does not necessarily confer net fitness benefits at organismal or population levels. Future research should clarify underlying mechanisms, quantify long-term fitness and ecological consequences across developmental stages and generations, and assess prevalence under realistic multi-stressor conditions to advance ecological risk assessment beyond linear models.