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This chapter summarizes the current understanding of the health risks associated with employment in various industries where exposure is alleged to occur. Topics discussed include textile mill workers, shipbuilders and navy/merchant marine personnel, insulators, plumbers and pipe fitters, construction workers, building interior workmen, floor tile and linoleum installers and removers, asbestos-cement manufacturers and end-product users, occupants of public and commercial buildings, electricians, automotive mechanics, railroad workers, and thermoelectric power and chemical plant workers.

This chapter considers the magnitudes of risk for the development of asbestosis, malignant mesothelioma (MM), and lung cancer (LC) resulting from exposure to different airborne concentrations of asbestos. Information on risk is obtained from epidemiological studies. The risk analysis requires three components: (i) the level of exposure, (ii) cases that have occurred, and (iii) factors that might confound or modify the exposure-response relationship.

This chapter reviews the history of asbestos-related lung cancer (LC) together with the prevailing theories of lung carcinogenesis in asbestos-exposed subjects. The synergism between tobacco smoke and asbestos, clinical, pathological, and mineralogical evidence for ascription of LC to asbestos exposure is assessed together with a review of the recent consensus document, the so-called “Helsinki criteria.”.

This chapter discusses the historical development of asbestos litigation and the current state of relevant legal affairs in the United States. Depending on one's vantage point, the history of asbestos-related lawsuits reveals either a series of unwitting failures to understand the gravity of the problem, or a knowing disregard and avoidance of the health concerns faced by workers and their families. Whether it is lack of knowledge or reckless disregard, responsibility for fault has become the paramount issue for assigning blame during American trials involving asbestos exposure and disease.

This chapter focuses on malignant mesothelioma (MM) and other mesothelial lesions and conditions that mimic MM. MM is now, alongside lung cancer, the most important occupational cancer among industrial populations worldwide. MM is a diffuse tumor that arises in the serosal surfaces of the pleura, peritoneum, pericardium, ovary, and tunica vaginalis of the testis. The most frequent location is the pleura followed by the peritoneum. As a result of serosal effusion and diffuse serosal thickening by tumor, patients with pleural tumors typically present with chest pain and shortness of breath and abdominal pain with distension in the peritoneal cases.

This chapter reviews the clinical manifestations of asbestos-associated lung problems, with particular emphasis on the milder forms of the diseases, which are now more common. Topics discussed include lung parenchymal disease, malignant mesothelioma, and benign asbestos-associated pleural diseases.

This chapter discusses mineral fiber analysis in asbestos-related diseases. Mineral fiber analysis can provide valuable information for both research and the assessment of exposure. Studies of tissues pleural plaques, diffuse pleural fibrosis and rounded atelectasis, malignant mesothelioma, asbestosis, asbestos miners, end-product users, and paraoccupational and environmental exposures are reviewed.

This chapter considers the historical evolution of society's efforts to protect workers and the members of the general public in the United States in the context of the existing regulations in major industrial countries of Europe and North America. The elimination of occupational and environmental asbestos-related disease rarely satisfies all interested parties. The outcome proves to be a compromise, in part, dictated by the technical inadequacies of industrial control measures for dust in the workplace, and the shortcomings of the available scientific information, particularly data on the long-term outcome of asbestos exposures in humans. Regulators are faced with an impossible task juxtaposed between the pleas of industry for economic “sanity” and members of the general population often influenced by inflammatory predictions of the media, worker groups, and environmental activists.

This chapter describes the radiological appearances of benign and malignant asbestos-related chest diseases and the utility of the various imaging modalities for the assessment of each manifestation. Topics covered include ILO classification of radiographs of the pneumoconioses, pleural effusion, diffuse pleural thickening, rounded atelectasis, malignant mesothelioma, asbestosis, and lung cancer.

This chapter discusses how asbestos interacts with cell-signaling pathways to modulate cell functions, including induction of proliferation and cell death, either by necrosis or by apoptosis (programmed cell death). Activation of extracellular signal-regulated kinase (ERK) and other signaling pathways by asbestos, or reactive oxygen species/reactive nitrogen species (ROS/RNS) elaborated by asbestos, may be critical to elicitation of injury and proliferation in mesothelial and epithelial cells during carcinogenesis. The responses to asbestos are dose-related, and represent a dynamic balance between the induction of cell injury and cell death and promotion of cell proliferation. Chronic cell injury coupled with inflammatory responses also may promote compensatory hyperplasia over time. Because of its durability and capability to produce or modulate ROS/RNS, asbestos may have a unique ability to perturb cell signaling pathways.

This chapter focuses on malignant mesothelioma (MM). Topics discussed include prognostic indicators, staging, treatment, surgery, radiotherapy, prevention of recurrences of MM in chest scars, multimodality treatment, novel intrapleural approaches, and chemotherapy and newer agents.

Two often confused statistical techniques are the odds ratio and relative risk ratio. These basic statistics are discussed and illustrated by contrasting risks from an analysis of breast cancer incidence among military women who served in Vietnam.

EPA was only five weeks old on January 7, 1971, when the Court of Appeals ordered the agency to cancel all DDT registrations. The situation was fluid, to say the least. EPA did not know how the cancellation process was to be carried out, since USDA before them had never executed a cancellation procedure. There was no precedent to follow, and the parties did not agree on the rules for cancellation. The cancellation process for DDT clearly would be adversarial, with the pesticide industry already objecting. Represented by Bill Butler, EDF insisted on judicial rules of evidence with qualification of expert witnesses, testimony to be relevant to the topics at issue, and full rights of cross-examination for all parties. That was a bottom line for EDF, and EPA lawyers agreed. If a witness was qualified as expert on topic A and not on topic B, he or she could testify on A but not on B. We had learned from experience that we did not want industry representatives and salesmen or lobbyists making opinion statements and then walking away, leaving a muddy record that would be little more than a popular vote open to varied interpretations. Industry wanted that. EDF wanted competent scientists to build an accurate record, and after months of haggling, EDF and EPA ultimately prevailed. There would be judicial rules of evidence. It was a triumph for Bill Butler and EDF. Little did we know then that this procedure would influence pesticide regulation by EPA far into the future. Judicial rules of evidence proved critically important in the litigation and eventual banning of aldrin, dieldrin, chlordane, heptachlor, and mirex, as we will describe in Chapter 12. Qualified scientists and experts testified in those proceedings, and some previously vocal advocates never appeared. Since EPA had been ordered by the court to consider cancellation of all registrations of DDT, it was the DDT proponents who were bringing the appeal. They were known as the Group Petitioners. It had become the burden of industry to prove DDT safe, whereas before it had been our burden to prove hazard.