The Editors are sorry that the production of this volume was delayed by the ill health of one of them and we hope that this does not detract from the value of the con tents. For once this delay is not the fault of any of the authors only the editors are to blame. Many of the workers in the field of fibre toxicology became convinced by the middle 1980's that the worst of the furore over asbestos was over although we were left with an intriguing problem - how does asbestos cause disease? It was expected that the future impact of fibres on human health would be very small since asbestos exposure would be controlled and there was little chance that man-made fibres would prove haz ardous. These man-made fibres are much thicker than asbestos and, in most cases, they are less durable in the body. Both of these properties are believed to make them much less likely to cause disease. However many of us had fallen into the habit of calling these materials "asbestos substitutes" and thus they have acquired a little of the notoriety at tached to the natural fibrous minerals. Very few of these man-made fibres are actually used as replacements for asbestos. Asbestos was not suitable for the uses to which the insulation wools are usually put and the ceramic fibres are replacements for fire brick not asbestos which is destroyed at the temperatures at which these materials are used.

but also the possibility of intervention in specific stages. In Human behavior, including stress and other factors, plays an important role in neoplasia, although too little is known addition, variables which affect cancer development as well on the reasons for such development. Carcinogens, which as some endogenous factors can be better delineated help initiate the neoplastic process, may be either synthetic through such investigations. The topics of this volume encompass premalignant non or naturally-occurring. Cancer causation may be ascribed to invasive lesions, species-specific aspects of carcinogenicity, certain chemicals, physical agents, radioactive materials, viruses, parasites, the genetic make-up of the organism, and radiation, viruses, a quantum theory of carinogenesis, onco bacteria. Humans, eumetazoan animals and vascular plants genes, and selected environmental carcinogens. are susceptible to the first six groups of cancer causes, whe reas the last group, bacteria, seems to affect only vascular plants. Neoplastic development may begin with impairment ofJmdy defenses by a toxic material (carcinogen) which acts as an initiator, followed by promotion and progression to an overt neoplastic state. Investigation of these processes Series Editor Volume Editor allows not only a better insight into the mechanism of action Hans E. Kaiser Elizabeth K. Weisburger vii ACKNOWLEDGEMENT Inspiration and encouragement for this wide ranging project on cancer distribution and dissemination from a comparative biological and clinical point of view, was given by my late friend E. H. Krokowski.

The result of a meeting held at IARC early in 1996, this volume provides a thorough and up-to-date synthesis of the mechanisms of fibre carcinogenesis. A consensus document assesses the strengths, weaknesses and gaps in the data concerning fibre characterization and genotoxicity, fibre-related cell proliferation and activation, gene expression, animal models, mixed dust exposure and interactions with other carcinogens. The relevance of mechanistic data from in vitro and in vivo assays to the evaluation of fibre carcinogenicity are also discussed. Authored review papers, also published in this volume, provide the background material for much of the discussion.

"This publication represents the views and expert opinions of an IARC working group on the evaluation of carcinogenic risks to humans, which met in Lyon, 9-16 October 2001."

This work has been selected by scholars as being culturally important, and is part of the knowledge base of civilization as we know it. This work is in the "public domain in the United States of America, and possibly other nations. Within the United States, you may freely copy and distribute this work, as no entity (individual or corporate) has a copyright on the body of the work. Scholars believe, and we concur, that this work is important enough to be preserved, reproduced, and made generally available to the public. We appreciate your support of the preservation process, and thank you for being an important part of keeping this knowledge alive and relevant.

This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.

Provides the most current information and research available for performing risk assessments on exposed individuals and populations, giving guidance to public health authorities, primary care physicians, and industrial managers Reviews current knowledge on human exposure to selected chemical agents and physical factors in the ambient environment Updates and revises the previous edition, in light of current scientific literature and its significance to public health concerns Includes new chapters on: airline cabin exposures, arsenic, endocrine disruptors, and nanoparticles