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Metastases from bronchioloalveolar carcinomas associated with long‐standing type 1 congenital cystic adenomatoid malformations. A report of two cases

has approximately 80–85% of cases attributable to asbestos exposure. Erionite exposure, radiotherapy, plombage, SV40 virus exposure and chronic chest sepsis have also been linked tomesothelioma but are probably not aetiologically important risks in the UK. The threshold issue really centres on cases that have low ⁄ undetectable fibre loads. Those affecting young patients or with minimal latency might be described as ‘spontaneous’ mesothelioma. However, this subgroup could equally well reflect a genetic susceptibility to mesothelial asbestos-related mutational events, thereby explaining why not all asbestos workers develop mesothelioma, as well as the variation in mesothelioma case fibre loads. It has been suggested that a significant parenchymal fibre load should be present for attribution of occupational mesothelioma. The European Respiratory Society guidelines suggest amphiboles in the range of > 10 ⁄ g dLt. The Helsinki Consensus suggested more latitude, with occupational history and latency being relevant. Returning to our results, if 80–85% of mesotheliomas may be attributed to asbestos, we could draw a significance line at approximately 80 000 fibres ⁄ g dLt. Interestingly, this is similar to our mean from the controls. However, this significance value might be unfair ⁄ arbitrary since, if lung cancer risk reflects a ‘pack-year tobacco consumption’, no one is suggesting that lung cancer risk has a threshold tobacco consumption. We conclude that the significance level for an individual case is open to interpretation. Fibre assay, whilst possible, cannot establish medicolegal causation for malignant mesothelioma without a balanced viewpoint of an occupational history ⁄ health records. We consequently have similar doubts with regard to significance levels and other asbestos-related diseases.