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Metabolic balance studies show that germfree and conventional Sprague-Dawley rats synthesize nitrate. Equivalent results for germfree and conventional rats eliminate the microflora as obligatory components of nitrate production. Nitrate synthesis appears to be a mammalian process.

Whether and to what extent contaminated sites harm ecologic and human health are topics of considerable interest, but also considerable uncertainty. Several federal and state agencies have approved the use of some or many aspects of probabilistic risk assessment (PRA), but its site-specific application has often been limited to high-profile sites and large projects. Nonetheless, times are changing: newly developed software tools, and recent federal and state guidance documents formalizing PRA procedures, now make PRA a readily available method of analysis for even small-scale projects. This article presents and discusses a broad review of PRA literature published since 2000.

Objectives-To obtain summary measures of the relation between cumulative exposure to asbestos and relative risk of lung cancer from published studies of exposed cohorts, and to explore the sources of heterogeneity in the doseresponse coefficient with data available in these publications. cohorts in which the doseresponse relation between cumulative exposure to asbestos and relative risk of lung cancer has been reported were identified. Linear dose-response models were applied, with intercepts either specific to the cohort or constrained by a random effects model; and with slopes specific to the cohort, constrained to be identical between cohorts (fixed effect), or constrained by a random effects model. A meta-analysis of the relation between cumulative exposure to asbestos and relative risk of lung cancer Cumulative exposure strata were usually defined by a range, often with an open end for the highest exposure stratum-for example, > 100 fibre-year/mnl (f-y/ml). We assigned fixed exposures to these ranges as the midpoint of the range, unless a mean or median was reported. For open ended categories, we assigned a fixed exposure by repeating the pattern found at lower exposures. We calculated 95% confidence intervals (95% CIs) about the SMR for each cumulative exposure with an approximation to a Poisson distribution. For each study reporting SMRs for more than one cumulative exposure category, we fitted the following dose-response model:where Ejj is the number of deaths from lung cancers expected under the model in study i at dose j, Ai is the fitted intercept corresponding to the relative risk of lung cancer among the cohort at zero exposure, kl,, (a measure of potency) is the coefficient relating cumulative exposure to asbestos to relative risk of lung cancer in study i under the linear dose-response model,7 djj is the dose of asbestos assigned to cumulative exposure category j of study i, and ej is the population based expected number of deaths from lung cancer. The number of observed deaths from lung cancer in study i at dose j, which we denote Oj, was assumed to be a Poisson random variable with expectation Ej.To obtain estimates of Ai and kl,,, we maximised the likelihood (2i) for each study:We estimated the 95% CI about each k,i with the profile likelihood method.We obtained a maximum likelihood summary measure of the dose-response coefficient (K,)

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