An airborne concentration, t is time (duration) of

An exposure assessment examines the exposure to the hazard over a particular period of time in foods that are actually consumed,taking into account the food consumption patterns of the target population and levels of hazard in all steps of the production process. The assessment should also account for varying levels of hazard throughout production to estimate the likely hazard level at point of consumption.1The application of transcriptomic technology to chemical risk assessment has been proposed due to its sensitivity and the ability to examine more comprehensively the molecular changes resulting from chemical exposure 3. In most cases, toxicity is not expected to occur without alterations at the transcriptional level.4 These transcriptional alterations include both the direct and indirect e ects on the cell or tissue. The direct effects include potential key events in the mode of action for a chemical while the indirect effects include secondary processes that are activated following the initial damage. When performed in dose{response format, the transcriptionalchanges can provide both quantitative and qualitative information on the dose atwhich cellular processes are a ected. This information can then be used to identify a transcriptional point-of-departure for chemical risk assessment 5. “Risk” is being used to mean the probability of the detrimental effect of interest. Risk is typically zero when dose is zero,for acute or short-term exposures, and it is commonly assumed that risk is determined from cumulative exposure, de ned as dose duration. Habers Rule usually stated as Ct 14 k, where C is an airborne concentration, t is time (duration) of exposure, and k is a constant.11 Toxicological response measurements generally can be classi ed into two distinct types: nominal(quantal) scale and continuous (quantitative) scale. Quantal responses characterize the effect by the presence or absence of a condition on a toxicity endpoint while Quantitative responses measure the effect in quantitative terms such as a change in weight, survival time, or some hematology or clinical chemistry measurements. Although the use of mathematical models in risk assessment for quantal response data has been widely developed for carcinogenic effects and to a lesser extent for reproductive/developmental effects, the use of dose response models in risk assessment for quantitative response data has been slow to develop.16