STUDENT CASE STUDY—STANFORD
CELL PHONES AND CANCER: EVALUATING THE EVIDENCE TO ASSESS POTENTIAL ASSOCIATION
CASE STUDY FOR AAC&U STIRS PROJECT
Jennifer S. Stanford, Assistant Professor of Biology, Drexel University, Philadelphia, PA
STUDENT CASE
Learning Objectives
Through their participation in this case study, students should be able to:
Part One
1. Explain how an external factor could affect cells to cause cancer development.
2. Describe the type of radiation emitted by cell phones.
Part Two
3. Describe an experiment that could be done to assess whether the radiofrequency waves from cell phones are sufficient to allow cells to become cancerous.
4. Explain why sample size is important in data analysis and extrapolation.
5. Predict results that would allow you to suggest that cell phone use and cancer are correlated.
6. Explain why causation can be difficult to establish in studies involving humans.
Part Three
7. Identify limitations of existing epidemiologic studies of cell phone use and cancer.
8. Examine data from epidemiologic and experimental studies and analyze whether there is an association between cell phone use and cancer.
9. Conduct a risk/benefit analysis regarding cell phone use and cancer.
10. Design a novel, ethical, properly controlled study to evaluate any link between cell phone use and brain cancer (optional).
Part Four
11. Consider costs and benefits and make an evidence-based recommendation about whether to fund additional research studying the association of cell phone use with brain cancer.
Preparatory Materials
Before coming to class, please:
· Read about the International Agency for Research on Cancer categorization of agents (http://monographs.iarc.fr/ENG/Preamble/currentb6evalrationale0706.php). Start at: Group 1: The agent is carcinogenic to humans (International Agency for Research on Cancer 2011).
· Read Part One of the case.
· Optional:
o Read “I don’t know what to believe. . .” Making sense of science stories. This can be found on the Sense About Science website, on their resources page: http://www.senseaboutscience.org/resources.php (select the “I don’t know what to believe” reference).
§ To evaluate claims in an article, it is really important to understand which information is valid. This pamphlet will help you think about how to know what to believe when you are reading about science (Sense About Science 2006).
o Find one article from the popular media (i.e., newspaper, magazine, website, etc.) that supports your current view of whether cell phones cause cancer.
Introduction
Cell phones truly are everywhere. As of 2013, the number of cell phone subscriptions worldwide (6.8 billion) nearly equaled the number of people in the world (7.1 billion) (Sanou 2013). As a result, understanding the health implications of cell phone use is important to ensure global public health and safety. One of the biggest health concerns with regard to cell phone use is whether it contributes to cancer development. In fact, in 2011 the International Agency for Research on Cancer (IARC), part of the World Health Organization (WHO), designated cell phones as “Group 2B possibly carcinogenic to humans” (International Agency for Research on Cancer 2011). With that said, other major US organizations including the Food and Drug Administration (FDA), National Institute of Environmental Health Sciences (NIEHS), and the Centers for Disease Control and Prevention (CDC) have indicated that there is not sufficient evidence supporting an association between cell phone use and cancer (National Cancer Institute 2013). What should we believe about cell phone use and cancer? Do additional studies need to be done to allow us to conclusively determine whether cell phones cause cancer? Would such studies be worth funding? These are questions that you will explore through this case as you learn more about the relationship between cell phones and cancer.
Part One. Cancer Development and the Possible Link to Cell Phones
What Is Cancer?
From a biological perspective, cancer is the abnormal, unregulated growth of cells (Figure 1). Our bodies are made up of cells (National Cancer Institute 2014). Some of these cells can undergo a process that allows them to divide to make two cells. This process is necessary for the growth and development of organisms, and to replace damaged or dead cells. Most of the cells in our body do not normally divide unless they receive signals within the body that indicate that more cells of that type are needed (National Cancer Institute 2014). Cancer cells no longer respond properly to signals that tell them to divide or to stop dividing (National Cancer Institute 2014). As a result, these cells divide rapidly leading to the development of an inappropriate mass of cells, called a tumor (National Cancer Institute 2014). Importantly, cells begin to divide inappropriately due to multiple, specific, alterations in cellular DNA (Almeida and Barry 2011). These alterations, or mutations, can be inherited and/or acquired (Almeida and Barry 2011). The changes to cellular DNA can affect the behavior and appearance of the cell leading to the loss of certain cellular properties and the acquisition of others (Almeida and Barry 2011). In other words, cancer is a disease caused by cells that are more apt to divide quickly and grow in inappropriate locations due to DNA mutations (Almeida and Barry 2011; National Cancer Institute 2014).
What Is DNA and How Is it Relevant to Cancer?
Our genetic information is contained within our DNA, or deoxyribonucleic acid (Figure 2). DNA is a double stranded, helical macromolecule that is made up of nucleotides. Genes are made up of DNA, and specific genes provide the information to make specific proteins within our cells (Almeida and Barry 2011). Proteins are the molecules that carry out many of the functional roles in our cells. As a result, a mutation, or change to the sequence, in DNA could lead to the production of proteins that are abnormal in terms of their shape and function (Almeida and Barry 2011). Proteins that have abnormal functions can affect the behavior of our cells.
DNA mutations, or alterations in the DNA sequence, can either be inherited or spontaneous. Inherited mutations are acquired from an individual’s parents (Almeida and Barry 2011). Spontaneous mutations can happen throughout the life of a cell (Almeida and Barry 2011). A spontaneous mutation can arise as a result of DNA damage. DNA damage, and thus spontaneous mutations, can occur because of cellular exposure to carcinogens or infectious agents, though there are also other reasons why spontaneous mutations can occur (Almeida and Barry 2011). Interestingly, approximately 90% of all diagnosed cancers are the result of the acquisition of spontaneous mutations (Almeida and Barry 2011). In other words, the vast majority of cancers arise due to DNA mutations that are acquired in response to cellular exposure to environmental factors such as carcinogens, as opposed to being caused by inherited factors.
Does a Mutation in any Gene Cause Cancer?
Not every mutation in a DNA molecule within a cell will lead to cancer development. It has been suggested that of all of the human genes, mutations in only about one percent of these genes are relevant to causing cancer development (Futreal et al. 2004). To become cancerous, cells must contain or acquire mutations in genes that are relevant to processes related to cancer development, such as cell division, cell migration, and/or DNA repair (Almeida and Barry 2011). Two classes of genes that are commonly mutated in cancer are proto-oncogenes and tumor suppressor genes (Almeida and Barry 2011).
A common analogy when discussing proto-oncogenes is to think of the cell as a car (CancerQuest 2012). In this analogy, proto-oncogenes encode proteins that function similarly to a gas pedal on a car. In response to the proper signals, such as a green light, the gas pedal can be depressed to tell the car to go. Similarly, proto-oncogenes function to tell a cell to grow and divide in response to proper conditions both within and outside the cell (Almeida and Barry 2011). If proto-oncogenes are mutated to form oncogenes, this can lead to an increase in the rate of cell division, which is abnormal. While proto-oncogenes only promote cell division if the proper signals or conditions are present, oncogenes promote cell division all of the time (Almeida and Barry 2011). This means that oncogenes promote cell division whether or not signals are present that tell the cell to divide. In the analogy, this would be similar to permanently putting a brick on the gas pedal. In that case, the car would be pushed to move forward, regardless of environmental signals.
Tumor suppressor genes are another class of genes mutated in cancer. The products of these genes prevent cells from dividing until the internal and/or external conditions are appropriate for cell division (Almeida and Barry 2011). To continue with the car analogy, these gene products function similarly to a brake pedal. In response to proper signals, such as stop signs or red lights, the brake pedal can be activated to prevent the car from moving. Similarly, tumor suppressor genes can be activated in response to the proper signals to prevent the cell from dividing (Almeida and Barry 2011). Mutations that inactivate these genes are problematic because the products are no longer able to stop cell growth and division in response to environmental factors. Just like if the brake line in a car is cut, a cell without a functional copy of a tumor suppressor gene will have a hard time with inhibiting cell division in response to relevant environmental signals.
Importantly, a mutation in one gene alone is not sufficient to cause cancer (Figure 3). The development of cancer is a multi-step process that requires acquisition of multiple mutations within cells (Hanahan and Weinberg 2000). This is because there are systems of checks and balances within the cell to keep the cell functioning properly. For example, if a cell contains an oncogene, the products of functional tumor suppressor genes could still prevent cell division until conditions are appropriate for cell division to occur.
Why Is there Concern that Cell Phones Are Dangerous?
Cell phones have been brought under scrutiny because they emit radio waves, which are a form of electromagnetic radiation (Linet and Inskip 2010; National Cancer Institute 2013). Not all electromagnetic radiation is problematic for human health. Electromagnetic radiation can be classified into two general categories: ionizing and non-ionizing (Figure 4). While ionizing radiation can directly damage DNA, non-ionizing radiation cannot (Linet and Inskip 2010; National Cancer Institute 2013). For example, X-rays are a form of ionizing radiation that has been shown to be detrimental to human health at certain levels. Visible light is a form of non-ionizing electromagnetic radiation, as are the radio waves emitted by cell phones (Linet and Inskip 2010; National Cancer Institute 2013). Although radio waves do not damage DNA, they can heat biological tissue, though at a level that is insufficient to increase body temperature (Linet and Inskip 2010; National Cancer Institute 2013) or alter biological materials (Moulder et al. 1999).
To assess the health risks of cell phones, experiments have been conducted using radiofrequency radiation at levels equivalent to those emitted by cell phones. These experiments will be described later in this case. To better understand these experiments, it is useful to learn some of the terminology used to describe electromagnetic energy. The frequency of electromagnetic energy is the number of cycles of an electromagnetic wave that occur in a second (World Health Organization 2013). Frequency is measured using Hertz (Hz) as the unit, where 1 Hz is equivalent to one cycle per second (World Health Organization 2013). Cell phones typically have frequencies ranging from 450 MHz to 2.7 GHz (World Health Organization 2011). The power of electromagnetic radiation is typically measured in watts (World Health Organization 2013). A watt (W) is a unit that is used to describe the amount of energy consumed per second, where 1W is equivalent to the consumption of one joule per second. The peak powers of cell phones range from 0.1 to 2 watts (World Health Organization 2011). To measure radiofrequency energy in the human body, Specific Absorption Rate (SAR) can be used as a way to determine exposure strength (Federal Communications Commission 2013). SAR is the power of RF wave absorbed per unit mass of tissue, and is typically measured in units of watts/kg. Currently the limit set by the US Federal Communications Commission is 1.6 W/kg (Federal Communications Commission 2013).
Question 1: Does the IARC categorization of cell phones into Group 2B indicate that cell phones cause cancer? Why or why not?
Question 2: Carcinomas are the most common type of cancer. Lung cancer, prostate cancer, breast cancer, and colon cancer are examples of carcinomas. Carcinomas are cancers that are derived from epithelial cells. These are the cells that line the walls and cavities of the body and outside of the body. Based on the information you’ve learned thus far, why do you think that the majority of diagnosed cancers are carcinomas?
Question 3: Considering what you have learned about cancer, what would a cell phone have to do in order to cause cancer?
Question 4: Do you think that radiofrequency waves are likely to cause cancer? Why or why not?