13.1 Introduction

Most scholarly writing about radiation and procedures focuses on the dose to the patient. However, patients have episodic and rare exposure in the millisievert (mSv) range. We as a profession have daily, career-long, low-dose exposure and amass over years an accumulate dose that in a busy interventionalist practice can be in the therapeutic range and measured in gray (Gy). Familiarity with current guidelines and radiation protection devices is a vital prerequisite to working with radiation. However, these preventive measures are often less than rigorously adhered to, leading to continuous everyday exposure to low-rate doses of radiation. This results in a significant accumulated exposure over a lifetime. Certain procedures in particular, including aortic intervention, cardiac electrophysiology, and neurointervention can, result in large doses to the operators. Rationalization of the inherent risk by interventionalists is common, as are ready excuses such as not wearing their radiation protection badge because it was misplaced badges or not wearing the appropriate radiation protection because of an estimated short duration of the procedure, significant muscular strain and spasm caused by the heaviness of lead aprons, decreased dexterity with lead gloves, or discomfort in wearing lead protective glasses. Most of this dismissive and cavalier attitude, however, is most likely due to the innate inability to feel threatened by something they cannot see or feel, a duty to the patient at any cost, and a workplace culture that supports and encourages their actions.

In recent years, many notable interventionalists have broadcasted their own personal stories on the detrimental consequences of chronic radiation exposure to their long-term health. In a documentary produced by the Organization for Occupational Radiation Safety in Interventional Fluoroscopy (ORSIF), Dr. Ted Diethrich, world renowned cardiovascular surgeon, revealed he had previously felt invincible to the effects of radiation, before being diagnosed with radiation-induced cataracts, premature left carotid artery atherosclerosis, and a left brain oligodendroglioma. ¹ Dr. Lindsay Machan, inventor of the drug-eluting coronary stent, has warned his colleagues for years that there is no safe level of radiation exposure and of the need to fully protect oneself against it, having himself suffered from bilateral radiation-induced cataracts. ²

There is recent, substantial evidence on the increased risk of radiation-induced cataracts even at low doses of radiation. The ICRP modified its eye lens dose thresholds in 2011, to a lifetime limit of 0.5 Gy and a yearly limit of 20 mSv/y, with no single year to surpass 50 mSv. ³ This is a far stricter reduction of the previous annual average level, which allowed 150 mSv/y to the lens. ⁴

Moreover, chronic radiation exposure and the advancement of radiation-induced tumors have been suggested by new peer-reviewed data to have a causal relationship. A recent case study recorded 31 individual cases of interventionists diagnosed with various brain and neck tumors, showing 17 professionals affected with glioblastoma multiforme, 5 with meningiomas, and 2 with astrocytomas. ⁵ These three types of primary tumors are well known for their potential to be radiation induced. Furthermore, a striking finding in this report was that there was 85% left-sided predominance of the lesions, hypothesized to be secondary to the X-ray beam being on the interventionalist’s left during the procedures. Reeves et al also reported that radiation received to the left side of the head was 16 times higher than that to the right. ⁶

13.2 Gene Mutation and Radiation Effects on DNA Leading to the Development of Cancer

The mutation of one or more genes within a cell is the origin of all cancers. This alteration in the sequence of DNA, if not corrected, can result in the production of proteins with different or lost amino acid sequences, drastically affecting protein function. In some cases, it can result in a complete lack of protein being produced at all. Genetic mutations fall under two categories: acquired and germ line. Acquired mutations are the most common cause of cancer and arise from direct or indirect damage to the DNA of somatic cells and are acquired over the course of a person’s life. Acquired mutations are found in a group(s) of somatic cells all arising from the same progenitor, rather than in sex cells, and are thus not heritable mutations. Germ line mutations are less regular, heritable, and arise from mutations in reproductive cells. This can result in the possibly cancer-inducing mutations being present throughout every cell in the organism, including those reproductive cells of the ensuing progeny.

Our DNA is consistently being attacked by the products of cellular metabolism, viral infections, ultraviolet (UV) radiation, chemical exposure, and replication errors, all of which frequently cause genetic mutations. Of course, there exists a multitude of cellular repair mechanisms to rectify these DNA-induced mutations. It is the failure of these systems to recognize or repair DNA damage, or to trigger apoptosis where the damage may not be mended. This can result in the accumulation of mutations, which can lead to cancer and other genetic diseases. Cancer is therefore unlikely to be caused by a single mutation; rather, it will take numerous mutations acquired over a lifetime for a cancer to form. Ionizing radiation is a confirmed and long-standing mutagen, producing mutation through a variety of molecular mechanisms including single-stranded DNA breaks, double-stranded DNA breaks, nucleotide substitution, and sugar ribose alterations. ^{7 , 8}

Many of the genes central to the development of cancer can be grouped into three categories: tumor suppressor genes, oncogenes, and DNA repair genes. Tumor suppressor genes are responsible for restricting cell growth by modulating cell mitosis, repairing certain kinds of DNA mismatch, or inducing apoptosis if the damage cannot be fixed. Tumor suppressor mutations tend to be loss of function, which allows cells to grow and undergo mitosis at an unchecked rate, resulting in tumor formation. Oncogenes can be defined as any gene that when mutated or expressed at suitably high levels contributes to the transformation of a normal cell into a cancer cell. Oncogenic mutations are not heritable and are acquired over time. Finally, DNA repair genes fix any mistakes and replication errors before cell division takes place. Mutations in repair genes lead to repair failure and ensuing accumulation of potentially cancer-causing mutations.

A considerable amount of peer-reviewed literature exists that focuses on the effects of solar and cosmic radiation on the long-term health of airline crew members. The ICRP has set them an occupational limit of 20 mSv/y, and they routinely aggregate between 3 and 7 mSv/y. ⁹ However, in comparison to ground crew and the normal population, their risk of cancer has been increased by between 1 in 130 and 1 in 4,800 for specific tumor types, depending on the number of hours worked and the altitudes reached on the airline routes taken. The higher the altitude, the greater the radiation received. The relationship between flight distance and altitude is well associated with the risk of chromosomal translocations that could manifest into cancer. ¹⁰ Comparatively, Canadian radiation workers are exposed to a cumulative dose of 6.3 mSv/y, ¹¹ and thus incur a significant level of risk of developing mutations that contribute to cancer. A small proportion of Danish radiation workers even managed to exceed 50 mSv/y, ¹² again increasing the risk of developing cancerous mutations. Interventionalists and technologists alike are known to routinely far surpass these radiation levels.

Propagation of radiation-induced mutation is prevented by efficient DNA damage repair mechanisms operating within the cell. Any form of inherited impairment of these repair mechanisms will potentially increase risk of cancer induction by radiation-induced mutation, especially in those health care professionals working with various forms of ionizing radiation. One approach that could feasibly minimize risk to interventionalists and technologists is to make available, when requested, and only with the appropriate ethical and genetic support, screening for genetic mutations that impair radiation-induced DNA damage repair. Screening for specific mutations or alleles of genes is already a well-established practice in breast cancer and colorectal cancer, and is a useful way to reveal someone’s genetic predisposition to cancer development. In theory, the screening process would take place before a graduate enters their residency, or fellowship, with an intent to provide an objective assessment of the individual risk incurred by pursuing a medical career in interventional radiology, interventional cardiology, vascular surgery, interventional pain management, or neuroradiology. Germline mutations to be screened for would include mutation types in BRCA1, BRCA2, MLH1, MSH2, MSH6, PMS2, APC, MYH, TP53, PTEN, CDKN2A, and RET. However, this is by no means a comprehensive list, as there are a myriad of potential alleles and mutations that could be screened for. This would have to be done in the appropriate ethical context with a focus centered on the well-being of the trainee.

Chronic low-dose radiation exposure is not benign. As interventionalists and surgeons, it is our collective responsibility to establish radiation protection awareness and promote stricter adherence to guidelines created to ensure our safety. The vast increase in demand for interventional services has increased our professional exposure. Our institutions and health care systems need to acknowledge our inherent risk of working with radiation and we should act as our own regulators so that every professional can safely practice without compromising their health.