1. Physics of Living Systems
Download icon

Upper bound on the biological effects of 50/60 Hz magnetic fields mediated by radical pairs

  1. Peter J Hore  Is a corresponding author
  1. University of Oxford, United Kingdom
Research Article
  • Cited 9
  • Views 1,487
  • Annotations
Cite this article as: eLife 2019;8:e44179 doi: 10.7554/eLife.44179

Abstract

Prolonged exposure to weak (~1 µT) extremely-low-frequency (ELF, 50/60 Hz) magnetic fields has been associated with an increased risk of childhood leukaemia. One of the few biophysical mechanisms that might account for this link involves short-lived chemical reaction intermediates known as radical pairs. In this report, we use spin dynamics simulations to derive an upper bound of 10 parts per million on the effect of a 1 µT ELF magnetic field on the yield of a radical pair reaction. By comparing this figure with the corresponding effects of changes in the strength of the Earth's magnetic field, we conclude that if exposure to such weak 50/60 Hz magnetic fields has any effect on human biology, and results from a radical pair mechanism, then the risk should be no greater than travelling a few kilometres towards or away from the geomagnetic north or south pole.

Article and author information

Author details

  1. Peter J Hore

    Department of Chemistry, University of Oxford, Oxford, United Kingdom
    For correspondence
    peter.hore@chem.ox.ac.uk
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-8863-570X

Funding

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Anant Paravastu, Georgia Institute of Technology, United States

Publication history

  1. Received: December 6, 2018
  2. Accepted: February 2, 2019
  3. Accepted Manuscript published: February 25, 2019 (version 1)
  4. Version of Record published: March 14, 2019 (version 2)

Copyright

© 2019, Hore

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 1,487
    Page views
  • 191
    Downloads
  • 9
    Citations

Article citation count generated by polling the highest count across the following sources: Crossref, PubMed Central, Scopus.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Download citations (links to download the citations from this article in formats compatible with various reference manager tools)

Open citations (links to open the citations from this article in various online reference manager services)

Further reading

    1. Computational and Systems Biology
    2. Physics of Living Systems
    Lakshya Chauhan et al.
    Research Article Updated

    Phenotypic (non-genetic) heterogeneity has significant implications for the development and evolution of organs, organisms, and populations. Recent observations in multiple cancers have unraveled the role of phenotypic heterogeneity in driving metastasis and therapy recalcitrance. However, the origins of such phenotypic heterogeneity are poorly understood in most cancers. Here, we investigate a regulatory network underlying phenotypic heterogeneity in small cell lung cancer, a devastating disease with no molecular targeted therapy. Discrete and continuous dynamical simulations of this network reveal its multistable behavior that can explain co-existence of four experimentally observed phenotypes. Analysis of the network topology uncovers that multistability emerges from two teams of players that mutually inhibit each other, but members of a team activate one another, forming a ‘toggle switch’ between the two teams. Deciphering these topological signatures in cancer-related regulatory networks can unravel their ‘latent’ design principles and offer a rational approach to characterize phenotypic heterogeneity in a tumor.

    1. Evolutionary Biology
    2. Physics of Living Systems
    Gautam Reddy, Michael M Desai
    Research Article

    Epistasis between mutations makes adaptation contingent on evolutionary history. Yet despite widespread 'microscopic' epistasis between the mutations involved, microbial evolution experiments show consistent patterns of fitness increase between replicate lines. Recent work shows that this consistency is driven in part by global patterns of diminishing-returns and increasing-costs epistasis, which make mutations systematically less beneficial (or more deleterious) on fitter genetic backgrounds. However, the origin of this 'global' epistasis remains unknown. Here we show that diminishing-returns and increasing-costs epistasis emerge generically as a consequence of pervasive microscopic epistasis. Our model predicts a specific quantitative relationship between the magnitude of global epistasis and the stochastic effects of microscopic epistasis, which we confirm by re-analyzing existing data. We further show that the distribution of fitness effects has a universal form when epistasis is widespread, and introduce a novel fitness landscape model to show how phenotypic evolution can be repeatable despite sequence-level stochasticity.