Endocrine Disruption by Diesel Exhaust Components

Summary

Diesel exhaust is a complex mixture containing particulate matter, nitrophenols, polycyclic aromatic hydrocarbons and other organic compounds. Several of these constituents act as endocrine disruptors by interfering with hormone synthesis, transport and receptor signalling across species, with implications for reproduction, development and metabolic regulation. Experimental and observational evidence indicates that nitrophenol derivatives, such as p-nitrophenol and 3-methyl-4-nitrophenol, impair oocyte maturation, perturb spermatogenesis and compromise early embryonic development through effects on spindle integrity, mitochondrial function and steroid hormone balance. Other diesel-derived substances modulate the hypothalamic–pituitary–gonadal axis, altering gonadotrophin release and the expression of steroidogenic enzymes. Emerging studies are beginning to quantify real-world exposure levels and long-term reproductive outcomes, emphasising the need for refined risk assessment and targeted mitigation in both occupational and urban settings.

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Endocrine Disruption by Diesel Exhaust Components publication trend

The graph below shows the total number of articles in endocrine disruption by diesel exhaust components across all publications each year (not limited to Nature Index journals).

Technical terms

Endocrine disruptor: A chemical that interferes with hormone synthesis, secretion, transport or receptor interaction, leading to altered physiological function.

Oocyte maturation: The process by which an immature egg undergoes meiotic divisions to become capable of fertilisation.

Spindle apparatus: A dynamic microtubule structure responsible for segregating chromosomes during cell division.

Mitochondrial membrane potential: The electrochemical gradient across the mitochondrial membrane essential for ATP synthesis and cellular energy metabolism.

Apoptosis: Programmed cell death characterised by specific biochemical and morphological changes.

References

  1. 3-Methyl-4-nitrophenol Exposure Deteriorates Oocyte Maturation by Inducing Spindle Instability and Mitochondrial Dysfunction. International Journal of Molecular Sciences (2024).
  2. Suppressive effects of long-term exposure to P-nitrophenol on gonadal development, hormonal profile with disruption of tissue integrity, and activation of caspase-3 in male Japanese quail (Coturnix japonica). Environmental Science and Pollution Research (2015).
  3. 3-methyl-4-nitrophenol disturbs the maternal-to-zygotic transition of early embryos by damaging mitochondrial function and histone modification. Ecotoxicology and Environmental Safety (2025).

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