**1. Introduction**

Gamma is a high photon energy electromagnetic radiation which is absorbed by material with a number of different physical consequences. Its absorption results in the generation of fast electron tracks capable of breaking chemical bonds in living tissue with the generation of reactive ionic species and free radicals. These energetic fragments can then, themselves, migrate away from the ionisation track to react with other stable molecules and ions. The overall processes result in damage to living cells, either by direct interaction with a molecule or by indirect effects from the ionised or reactive species, and this can result either in cell death or in downstream genetic and genomic effects which are harmful to the health of the exposed individual. The mechanisms of genetic and genomic biological damage which follow from gamma ray exposure and X-ray exposures are described in the literature and are accepted by all the radiation risk agencies [1–3]. In this chapter, I will write *gamma ray*, but it is to be assumed that the processes I discuss apply to X-radiation also.

It is generally accepted now that the biological effects of exposure are a consequence of either direct damage to cellular DNA or due to induction of instability in cellular DNA through a mechanism involving the detection of ionisation, expressed as an increased concentration of reactive oxygen species (ROS), generated by gamma ray interaction with water. Either way, the essential biological effective target for gamma ray (and indeed all ionising radiation) absorption is not primarily water but is the cellular DNA. Historically, the method developed for assessing exposure after 1950 involved defining quantities based on the absorption of energy per unit mass of material exposed to these high-energy photon radiations. Since the detection and quantification of gamma radiation (and X-rays) became most easily based on the ionisation of gases (Geiger Muller counters, proportional counters and ionisation chambers and, later, scintillation counters), it was a simple step to quantify absorption by living tissue in the same way. Thus, for ionising radiation, the quantity *absorbed dose* became the prime measure of risk. Since it became clear that for heavily ionising radiations, alpha and neutron radiations which have higher ionisation per unit track length, there must be allowance made, the later quantity, *equivalent dose*, was introduced whereby a weighting factor was added, based on the ionisation density or linear energy transfer of the radiation. However, for the purposes of this brief chapter, the concern is with *absorbed dose* and its calculation for the purposes of radiation protection.

Clearly, from the outline above, it is the ionisation density at the DNA which is the key factor defining radiation risk. But *absorbed dose* does not measure this. In the way it has come to be employed by the radiation risk agencies; it is a measure of mean ionisation density over significant masses of tissues and kilograms, modelled as water. The issue of anisotropy of ionisation density for *internal* radiation exposures to alpha and beta particles from incorporated radionuclides has been addressed elsewhere [4].

The calculation of absorbed dose assumes that the tissue in which the energy is dissipated is water or its tissue-equivalent substitute. Since all photon energy absorption from *external* exposure is converted ultimately to energetic electron tracks in tissue, either in the initial instance or as a result of the reabsorption of photons from other secondary sources (e.g. Compton, Bremsstrahlung), the averaging of these tracks over all tissue may seem reasonable as an approximation. But what this does (and this is the issue explored here) is it fails entirely to address or incorporate increases in absorption of photon radiations by elements of higher atomic number Z than water or tissue-equivalent material which is largely absorbed by the highest Z element in it, namely, oxygen (Z = 8). This would not matter much if any elements of higher Z were uniformly distributed in the tissue: in such a case, since gamma and X-ray absorption increases very quickly with atomic number, the overall absorption might be slightly increased, but where an incorporated elevated Z element is chemically bound to DNA, the transfer of energy into the DNA becomes very much greater than that which is assumed by conventional dosimetry. A similar enhancement of local dose occurs near high-Z nanoparticles incorporated into tissue. This is an interesting and important area of concern which has implications both for radiation safety and for the development of cancer therapy. Apart from some early work on the enhanced photoelectron density near the bone, it seems to have been entirely overlooked. The issue is also an important one for radiation protection in the nuclear industry and the military, especially in the case of uranium particle contamination, perhaps the reason why little research has been carried out on the subject. There are also other areas of interest, implications for medical prostheses and even for arguments about the development of living systems generally.

**177**

**Figure 1.**

*incorporates the density of the element.*

*The Secondary Photoelectron Effect: Gamma Ray Ionisation Enhancement in Tissues from High…*

Gamma radiation and matter interact mainly by three different mechanisms, Compton scattering, pair production and the photoelectric effect. The different contributions of these to absorption depend on the absorbing material, principally its atomic number Z and the quantum energy **E** of the incident photon, propor-

In the photoelectric effect, incident photon energy causes the emission of an electron from the absorbing element. The electron has the energy of the absorbed photon minus the binding energy of the electron. For gamma radiation the binding energies are second order, and the emission electron carries almost all the initial gamma energy. Electrons may also lose energy in secondary processes occurring within the atom. For energies below 1 MeV, the photoelectric effect largely pre-

Thus, for energies below 1 MeV, the photoelectric effect predominates. The cross section for the photoelectric effect is approximately proportional to the atomic number Z to the power of five and to the incident photon energy to the power of −7/2 [5]. The sharp dependence of photoelectron generation on Z immediately raises interest in the resulting wide variation in absorption of gamma rays by high atomic number atoms and molecules in tissue. This concern is related to the range of the photoelectrons and their deposition of ionisation effects close to the atom. For low-energy photoelectrons generated by low-energy gamma and X-ray photons, the effects will be increasingly local to the atom, and if the atom is local to DNA, there will be an enhancement of radiobiological effectiveness of the absorbed energy. This may be termed the secondary photoelectron effect. The SPE will also occur in the vicinity of internal particles of

*Relative contributions of the main different types of energy conversion in materials following the absorption of gamma ray photons. The specific curves differ considerably for different elements, driven by the electronic* 

 *g<sup>−</sup><sup>1</sup>*

 *and thus* 

*structure of the element. Note that the attenuation coefficient is normally given in cm2*

dominates. **Figure 1** illustrates the effects by incident gamma energy.

high-Z elements and in the vicinity of metal prosthetic structures.

**2. The absorption of gamma radiation by matter and the secondary** 

*DOI: http://dx.doi.org/10.5772/intechopen.86779*

**photoelectron effect**

tional to frequency **E** = **hυ**.

*The Secondary Photoelectron Effect: Gamma Ray Ionisation Enhancement in Tissues from High… DOI: http://dx.doi.org/10.5772/intechopen.86779*
