The subject of silicate induced neoplasms is discussed at length. Topics include silicate structural chemistry; silica (silca solubility, silicosis solubility theories, intracellular silicon, antigen antibody theory, piezo electric theory; clinical silicosis and lung cancer, experimental tumorigenesis); glass; asbestos (asbestos dust and human cancer, mesothelioma arising at human serous membranes, experimental carcinogenesis); iron (experimental carcinogenesis in rodents, carcinogenic mechanisms, human neoplasms); silicone (chemistry, experimental tests, silicone implantation effects, human considerations); pneumoconiosis as a prelude to carcinogenesis (role of free silica and of bacteria in pneumoconiosis, degree of pneumoconiosis correlated with dust type, pulmonary dust distribution, diatomaceous earth pneumoconiosis, dust deposition and fibrosis related to carcinogenesis); carcinogenic mechanisms (scar cancers and solid state carcinogenesis, role of cholesterol crystals in silicate induced neoplasms, subcutaneously implanted cholesterol hydrate and needle disks in the rat, origin and occurrence of primary pleural fibrosarcoma, mesothelioma and carcinoma of the lung, nonspecific irritation). Although a causal relationship between silicosis and cancer was not universally accepted by early researchers, a survey of evidence based on recent animal experimentation and statistical studies on humans indicates that such a relationship can exist. Since silica is a normal body constituent, etiology of cancer production would be nonspecific and would involve a fibrogenic response. No completely satisfactory explanation has been offered for the unique fibrogenic response to quartz and other crystalline forms of silica. The solid state glass surface as an etiologic experimental carcinogenic agent in the gallbladder substantiates the role of the cholesterol crystal surface in gallbladder carcinoma. Statistical studies correlating pulmonary, pleural, and peritoneal carcinomas and mesotheliomas of humans with asbestosis or asbestos dust exposure, together with experimental studies, conclusively implicate asbestos as a carcinogenic agent. Animal experiment and statistical study results do not indicate a correlation of asbestos induced neoplasms with iron or carcinogenic hydrocarbon components of the various asbestoses. The fibrogenic character of dusts is evaluated in terms of physical and chemical properties leading directly to solid state carcinogenesis. Since iron-dextrans in human therapeutic doses produce a minimal fibrotic reaction and are nontumorigenic, the possible factor of scar cancer etiology must be eliminated in rodent studies with iron-dextran before high sarcoma yield may be ascribed to the action of iron-dextran as a carcinogen.