BackgroundAll forms of asbestos are now banned in 52 countries. Safer products have replaced many materials that once were made with it. Nonetheless, many countries still use, import, and export asbestos and asbestos-containing products, and in those that have banned other forms of asbestos, the so-called “controlled use” of chrysotile asbestos is often exempted from the ban. In fact, chrysotile has accounted for > 95% of all the asbestos used globally.ObjectiveWe examined and evaluated the literature used to support the exemption of chrysotile asbestos from the ban and how its exemption reflects the political and economic influence of the asbestos mining and manufacturing industry.DiscussionAll forms of asbestos, including chrysotile, are proven human carcinogens. All forms cause malignant mesothelioma and lung and laryngeal cancers, and may cause ovarian, gastrointestinal, and other cancers. No exposure to asbestos is without risk. Illnesses and deaths from asbestos exposure are entirely preventable.ConclusionsAll countries of the world have an obligation to their citizens to join in the international endeavor to ban the mining, manufacture, and use of all forms of asbestos. An international ban is urgently needed. There is no medical or scientific basis to exempt chrysotile from the worldwide ban of asbestos.

No abstract

Greenberg, M., and Lloyd Davies, T. A. (1974).British Journal of Industrial Medicine,31, 91-104. Mesothelioma Register 1967-68. A register of mesothelioma cases is maintained by the Department of Employment, Medical Services Division (now Employment Medical Advisory Service). This paper describes an investigation of 413 notifications to the Register in 1967-68 from England and Wales and Scotland. Cases were regarded as `definite' when histological confirmation of diagnosis had been obtained, either by hospital pathologists, or by the UICC Panel of Pathologists, to whom pathological material was submitted whenever possible. Two hundred and forty-six cases were accepted as `definite' and 76 cases were regarded as `definitely not' mesothelioma. The remainder were classified as `undecided' or `insufficient pathological material'. Thirty-five of the 76 cases definitely not mesothelioma had nevertheless been so described on death certificates. The investigation carried out covers clinical aspects, survival, and evidence of exposure to asbestos. Twelve per cent of definite mesotheliomata were of peritoneal origin. The age range was 21 to 87 years, but, in general, mesothelioma occured at an earlier age than `carcinoma of bronchus and lung' or `all malignant tumours' in the Registrar General's statistical mortality tables. Concomitant asbestosis and the finding of asbestos bodies or pleural plaques occured as frequently in those cases classified as definitely not mesothelioma as in confirmed cases. Occupational exposure to asbestos was found in 68% of definite cases, apparently significantly more frequently than in those definitely not mesothelioma, but there was observer bias. The interval between the first exposure and death from mesothelioma exceeded 25 years in 85% of cases but was only three and a half years in one case. The duration of exposure varied widely: in 12% of cases it was under five years. The type of asbestos could be ascertained in so few cases that it was impossible to asses the rôle of crocidolite in aetiology. There were 38 definite cases in which no history of any exposure to asbestos could be obtained. Definite mesotheliomata showed marked clustering in areas where there is substantial industrial use of asbestos. Whether this should be interpreted as evidence of causation or an effect of heightened awareness in these areas cannot be deduced from this study. Evidence is quoted suggesting that the observed annual incidence of approximately 120 definite mesotheliomata in England, Scotland, and Wales may considerably understate the true prevalence.

1 PCDDs and PCDFs are ubiquitous and persistent in the environment. They are to be found in body tissues of both humans and animals. 2 The most extensively studied PCDD is 2,3,7,8-TCDD. It has been shown to produce a wide range of effects and is considered to be a (non-genotoxic) carcinogen in animals. 3 Studies into the mechanisms of toxicity so far reveal that there is involvement of a specific receptor (Ah), however further work is required to elucidate the mechanisms of the various effects. 4 Reports on a number of human exposures to PCDDs and PCDFs are described. Results from human epidemiological studies are difficult to interpret: there have been problems in methodology; there has been inadequate information on intake, and exposures have often been to mixtures of PCDDs and/or PCDFs together with other related compounds. 5 Many regulatory authorities faced with the problem of providing an index of risk from exposure to mixtures of PCDDs and PCDFs have employed the concept of 'TCDD equivalents'. 6 Whether or not PCDDs and PCDFs pose a significant human health risk at current levels of exposure they remain of considerable interest to the toxicologist.

Summary Skin (prick) and serological tests were made with enzyme preparations of Bacillus subtilis in exposed factory workers and potential ‘consumers’. Prick tests with these materials at 10 mg/ml gave positive immediate reactions in twenty‐six out of sixty‐five factory workers. Eighteen of the factory workers were classified as atopic because of allergy to common allergens and fifteen gave positive reactions to the enzymes compared with eleven out of forty‐seven non‐atopic workers. A group of eleven of the factory workers had consistent ventilatory impairment on repeated examination; all were prick test positive and seven were atopic, and four non‐atopic. Of 2500 patients attending for investigation of respiratory allergy, 40% were highly atopic, 40% moderately atopic and 20% non‐atopic. 80% were consumers of biological detergents. Only two gave weak, not clinically relevant, prick test reactions to the enzyme preparations. In radioallergosorbent (RAST) tests for specific IgE antibody against the enzyme preparations, counts in the present investigation of 600/30 sec or more corresponded best with prick test positivity, such values being found in twelve of the fifteen prick test positive atopics and in eight of the eleven workers with ventilatory impairment. Comparison of the RAST counts on sera from cord blood and from the patients who included non, light and heavy consumers showed increasingly higher specific IgE counts in these groups, although these counts were almost all below the level of 600/30 sec, which corresponded with skin test reactions and clinical relevance. Radioimmunodiffusion (RID) and radioimmunoelectrophoretic (RIEP) tests with enzyme preparations gave positive reactions only in the factory workers, of whom forty‐three had IgG and twenty‐one IgA antibody, none having only IgE antibody.