Transmissible Spongiform Encephalopathy Risk Assessment: The UK experience

Abstract

Transmissible spongiform encephalopathy (TSE) risk assessments undertaken in the United Kingdom have mainly had the objective of determining the risks posed to humans from exposure to the causal agents associated with bovine spongiform encephalopathy (BSE) and variant Creutzfeld-Jakob disease (vCJD). In this article, I examine 19 of these risk assessments published to date and consider how their results might be influenced by underlying model assumptions and methodology. Three separate aspects common to all the assessments are infective load estimation, exposure pathway identification, and risk estimation. These are each discussed in detail.

Estimation of the Exposure of the UK Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake During the Period 1980 to 1996

“…It has been well recognized that a species barrier must exists [4], [39], [50] when comparing the large number of individuals who might have been exposed with the only 177 vCJD cases observed to date [1]. The hypothesis that these vCJD cases might have been exposed to a rare high infectious dose also supports this observation.…”

“…Additionally, we further justify the threshold hypothesis [4], [34]–[39] and provide a threshold estimate by comparing the observed incidence of vCJD cases. We estimate the number of exposed individuals by multiplying the population size of different birth cohorts in the UK [40] by their corresponding probability of exposure during the BSE epidemic period 1980–1996.…”

“…Among these meat products, we adopt the inclusion rates of MRM and head meat given in the DNV report [45] because of more specific information. For infectivity in consumed MRM and head meat, we adopt the estimate that 1 g of the BSE-infected brain and spinal cord contains 10 bID 50 [39] and derive the relative infectivity in infected DRG based on Arnold et al’s estimate [46].…”

“…We further estimate the number of subclinical carriers making use of the survey findings and the estimated number of exposed individuals from above. Also, we adopt the threshold hypothesis [4], [34]–[39] that an individual must consume a sufficiently high infectious dose to trigger exponential growth in the brain [35], and we estimate the threshold dose by fitting an extreme-value distribution.…”

“…We then multiply the estimated number of exposed individuals in each birth cohort by the corresponding posterior estimate of age-specific susceptibility [13], [17] using a Bayesian statistic approach and the survival probability [40] to obtain the number of susceptible exposed individuals who were alive at the end of 2013. These individuals are most likely the subclinical subpopulation, but they may not develop into a vCJD case if they were exposed to a low infectious dose [4], [36]–[39]. To further justify the threshold hypothesis, which states that an individual must be exposed to a very high dose to trigger the exponential growth of abnormal prions in the brain [35], we fit an extreme-value distribution to the susceptible exposed individuals for their exposure dose.…”