Risk, logically defined, is nothing more than the likelihood of an adverse outcome. Globally, the term is used synonymously with hazard, although in the United States, hazards have traditionally been associated with toxins, their inherent properties, and possible effects on susceptible hosts.1 The concept of risk, nonetheless, would be limited to aspects of assessments and the challenges of risk communication, thus negating the need to differentiate between the nuances of risk and hazard.
Risk assessment is a subset of risk and is a continuous organized objective of all industrialized countries of the world, and defined as, “the systematic characterization of potential adverse health effects resulting from human exposures to hazardous agents or situations.”2
It is a primary responsibility of public health agencies and government officials to communicate the varying aspects/concepts of risks, and the prevailing ways to reduce the prevalence and consequences associated with them. The actions have to be broad and have to be actively modified dependent on the degree(s) of perceived risk, but generally include environmental controls such as the protection of air, water, and food from microbiological and chemical contamination. Therefore, the principles of risk communication are an integral part of managing risk, regardless of the inciting cause. It is a tool that can be used in effect to provide important updates during the different phases of any exposure to risk.
Barriers/Challenges in Risk Communication
Communicating the risk of a disease outbreak could be a frustrating and arduous undertaking. It is often complicated by the existing scientific/medical unknowns, people’s perceptions, lack of accurate estimates, the prevailing policies and politics, what actions or options are possible, or what are the best goals to pursue based on current information.3 In the case of bovine spongiform encephalopathy (BSE), there were uncertain barriers to hurdle from the inception of the outbreak of the disease in the United Kingdom (UK) in 1986. It included the realization that effective decision-making requires a lot more than knowledge, albeit limited, and also the humbling recognition of the tentative nature of the disease, including the debate (still ongoing) on the cause or the genesis of the disease. In essence, BSE started as a challenge that was overwhelming, and continues to mock our ingenuity to this day.
A troubling aspect of risk communication developed early in the process and shortly after it was determined by British epidemiologists in 1987 that BSE was a new disease and the likelihood that the first clinical case probably occurred in the spring of 1985. The speculation based on the epidemiological features of the outbreak was that the feeding of meat and bone meal of ruminant origin was the most likely contributing cause.4 This was followed by both professional concern and public anxiety that transmission from cattle to the human population through consumption of potentially contaminated beef may occur.5 The concurrent widespread media coverage heightened the subject to varying degrees of emotionalism. This was due to the limited knowledge of the disease and the prevailing fear of the unknown, plus government’s inability in their public policy pronouncements to clearly articulate with confidence, the responses needed to satisfy the wide range of consumer anxiety.
This element of uncertainty was complicated by the fact that it is difficult for people to discern what experts or government authorities mean when a risk is defined in nebulous terms like “very likely” or “rare.”3 This form of ambiguity often means different things to different people, even within the professional community. The resulting variability of the interpretations of risk created doubts and contributed to stresses in communication. The media saw an opportunity to identify inconsistencies in many of the official pronouncements and capitalized on the chance to highlight them to advantage, thus amplifying feelings of doubt, and, to a degree, fear.
Dimensions of risk and how they are judged, therefore, are not limited to uncertainty and catastrophic potential, but must consider exposure contextual to the number of people at risk to the threat in present or future generations, and this has to be factored as a correlate with attitudes, the infra-structural limitations, and the regulatory considerations needed to effectually minimize or eliminate the risk.3
The BSE Dilemma Contextual to Risk Communication
Throughout the early history of medicine, there were empirical suggestions that transmissible agents could be causally associated with certain diseases. These early concepts were later validated by work done much later by bacteriologists in the 19th century, exemplified by Pasteur and Koch in Europe, affirming the “germ theory” of disease. This advancement of knowledge pertaining to the relevance of infectious agents contributed to the later identification and description of a broad range of new agents and some novel mechanisms of disease transmission.6
Doubtless, these rapid advances in the field of microbiology and infectious diseases contributed to the continuing considerable progress being made in the field that subsequently generated the characterization of unconventional agents by Prusiner, et. al., termed prions, as the cause of disease in animals and man, known as the transmissible spongiform encephalopathies (TSEs). Prusiner’s prion hypothesis was a direct challenge to the established dogma of infectious diseases, namely that the “informational molecule” for replicating organisms is nucleic acid.7 This newly defined pathogen (the prion) with the unusual characteristics of not eliciting an immune reaction, highly resistant to heat and chemicals that normally inactivate other known infectious agents, was itself a barrier to effective communication of risk because what may seem quite straightforward and logical to research scientists was extraordinary and enigmatic to those outside of the mainstream of neuropathology. The reality is that prion diseases in animals and man are complex, and defy ready answers.
The public was also challenged from every conceivable dogma of communication and was obligated to consider the acceptance that BSE was indeed a novel disease, first diagnosed in the UK in 1986, caused by an “unconventional” agent still to be fully characterized, transmitted through feed based on an epidemiological theory yet to be finitely validated, and the later hypothesis that BSE was related to another new disease in humans first described in 1996 as a variant of Creutzfeldt-Jakob disease (v-CJD) and linked to the “likely” consumption of beef products that were possibly contaminated by the infectious agent of BSE. In essence, the entire issue started as an affront to good communication that continues to this day, thus complicating the principles of defining risk and articulating with confidence to a public that was saturated by the media’s interpretation of the disease and the concurrent risks associated with it.
Therefore, in spite of government’s many concerted efforts to put the entire issue in perspective and correct the varied misconceptions, doubts continue to prevail. In general, what the public remembered most was the picture of a cow displaying “strange” symptoms and falling with an accompanying caption asking whether the meat supply was safe. All of this happens in a country without any evidence of BSE and government announcements of that status in all official communiqués. (During this writing, reports from both television news network CNN and the print media have indicated a diagnosis of v-CJD in a 22-year-old British female patient, a current resident of Florida, who is believed to have caught the disease in Britain at the height of that country’s BSE epidemic. In the CNN report, the same picture of BSE affected cattle in the UK were shown with the accompanying caption, should you worry about mad cow disease in the United States.)
The entire subject of the challenges of risk communication circumvents BSE and is further complicated by recent media reports of chronic wasting disease (CWD) and scrapie in sheep. The recent spread of CWD in Wisconsin was heightened to question what if the disease can be transmitted to cattle, and the accompanying inference that nobody knows what we are dealing with including the suggestion of a potential link to humans.8
This was followed by an announcement from the U.S. Department of Agriculture that tests conducted on a flock of sheep confiscated from a farm in Vermont confirm that “two of the 125 sheep tested positive for an atypical undifferentiated transmissible spongiform encephalopathy (TSE) of foreign origin.”9 The latter announcement has a definite need for a translation into an easily understood statement, with an accompanying explanation, even considering the difficulty associated with it. When that is not done, interpretations become loose and not truly representative of the findings, and, thus, a challenge to good communication of risk.
Unlike BSE, there is no evidence that CWD, which affects mule deer and elk, has a feed origin. The disease was first reported in Colorado in 1967, and although the transmission of the disease remains unknown, consideration should be given to the possibility of maternal or horizontal transmission. Other species susceptible to TSEs, including cattle, have for years been in contact (direct or indirect) with CWD cases, but none has succumbed.10 The disease, like scrapie, has no apparent known human health implications, but safety precautions are issued by public health departments to sensitize hunters and others of the “unknowns” associated with the disease.
Discussion
Effective risk communication can assist government and help people (and livestock producers) to reduce health risks by gaining an appreciation and understanding of the factors associated with exposure and likely outbreaks of diseases like BSE in cattle and v-CJD in humans. Misdirected communications, however, can result in wrong decisions by either the omission of key information or a failure to contradict misconceptions. This results in confusion and misplaced assumptions and could erode public confidence in the government’s communicators as was evident during many of the early BSE pronouncements in the UK. In reality, poor communications, by either causing complacency or unnecessary alarm, can have a greater public health impact than the risks that are described.3
Since the United States is free of BSE, risk communicators have an obligation to highlight that fact without reservation, while policy decision-makers have the concurrent obligation to ascertain that the disease-free status is maintained through the continuing appropriate preventive controls.11 The findings of the Harvard Risk Analysis team describing risk contextual to BSE and the inferences for the United States should serve as an exemplar for risk communicators and should be used by government to the fullest extent in efforts to explain the currency of the issues.
While the complexity of the pathology associated with BSE and v-CJD must be accepted, and the necessity to be cautious should prevail, it should be evident, nonetheless, that either the risk factors do not exist for an outbreak of BSE in the United States, or the control measures instituted since 1986 have worked well to preclude the disease and the likely consequence of v-CJD in humans.
Summary
The TSEs, as a group, exemplified by BSE and v-CJD, are complicated and enigmatic diseases that defy easy answers or responses, and, as such, tend to complicate and make risk communication challenging and difficult. The many current unknowns and unanswered questions relating to these diseases also contribute to the existing dilemma. This, however, should not deter from a responsible communication of risk based on our knowledge, albeit limited, of these diseases.
The record clearly indicates that 16 years after the initial outbreak of BSE in the UK, and seven years after the first reference of v-CJD in the same country, the United States (and Canada) remains free of both diseases. This should be heightened as an accomplishment of disease surveillance and the institution of control measures that have precluded an outbreak of either disease.
While this status should not lead to a cavalier reaction, it could, nonetheless, assist risk communicators (and decision-makers) in describing the elements/factors associated with the United States in a clear and concise manner, instead of the ongoing tentative statements that continue to predominate, including additional regulatory measures for more controls.
Our control system has worked well. Let science continue to be the only logical arbiter for disease preven-tion and control, and keep politics out of disease related policies.
References:
1. National Research Council. 1983. Risk assessment in the federal government: managing the process. Washington, DC: National Academy Press.
2. Omenn, G.S. and E.M. Faustmann. 1997. Risk assessment, risk communication, and risk management. In Oxford Textbook of Public Health, 3d ed., vol. 2, eds. R. Detels, W.W. Holland, J. Mc Ewen, and G.S. Omenn: 969-986. New York: Oxford University Press.
3. Fischhoff, B., A. Bostrom, and M.J. Quadrel. 1997. Risk perception and communication. In Oxford Textbook of Public Health, 3d ed., vol. 2, eds. R. Detels, W.W. Holland, J. Mc Ewen, and G.S. Omenn: 988-1002. New York: Oxford University Press.
4. Wilesmith, J.W., G.A.H. Wells, M.P. Cranwell, and J.B.M. Ryan. 1988. Bovine spongiform encephalopathy: epidemiological studies: 123, 638-644.
5. Will, R.G. 1990. Is there a potential risk of transmission of BSE to the human population and how may this be assessed? In Sub-acute Spongiform Encephalopathies, eds. R. Bradley, M. Savey, and B. Marchant: 179-186. Dordrecht, The Netherlands: Kluwer Academic Publishers.
6. Monto, A.S., C.F. Marrs. 1997. Infectious Agents. In Oxford Textbook of Public Health, 3d ed., vol. 1, eds. R. Detels, W.W. Holland, J. Mc Ewen, and G.S. Omenn: 175-198. New York: Oxford University Press.
7. Palmer, M.S. and J. Collinge. Prion diseases: an introduction. In Prion Diseases, eds. J. Collinge and M.S. Palmer: 1-17. New York: Oxford University Press.
8. Zaleski, R. “Deer disease is a nasty problem.” Madison (Wisconsin) Capital Times, 8 April 2002, sec. B, p.1.
9. Anon. “Testing shows TSE in confiscated sheep.” Feedstuffs, 15 April 2002, p. 4.
10. Bradley, R. 1997. Animal prion diseases. In Prion Diseases, eds. J. Collinge and M.S. Palmer: 89-129. New York: Oxford University Press.
11. Franco, D.A. “Inferences made for U.S. rendering, feed industries.” Feedstuffs, August 2001.
Tech Topics - June 2002 Render