Document gak07XJo8zdRjbXZ19aMODLR3

Conference Theme Presentations EVALUATION OF RESPIRATORY HAZARDS IN THE WORKING ENVIRONMENT THROUGH ENVIRONMENTAL, EPIDEMIOLOGIC AND MEDICAL SURVEYS MARGARET R. BECKLAKE, M.D., FRCP* Pulmonary Research Laboratory, Department of Epidemiology and Biostatistics McGill University 1110 Pine Avenue West Montreal, Quebec, Canada. H3A 1A3 HISTORICAL AMD CURRENT CONTEXT Respiratory disease consequent on work in dusty trades has been recognized since ancient times when man first turned to tools to help him to exploit the riches at die earth's sur face. In die past, distinctions have been blurred between various disease processes involved (fibrotic, infectious, malignant), all of which may follow occupational ex posures.1 The term pneumoconiosis was introduced in the 19th century to describe the rather specific nature of the lung's fibrotic reaction to inorganic dusts, such as silica, coal and iron. In keeping with its Greek roots, the term is cur rently defined by the World Health Organization as the "ac cumulation of dust in the lung and tissue reactions to its presence."2 Over die past century, industrialization, the growth of populations, and die increased demands for the raw materials of die earth's crust have led to an increase in the number of workers whose jobs expose diem to mineral dusts. In consequence, the early years of this century saw an in crease in the burden of dust diseases in industrialized coun tries, and post World War n in die newly industrializing countries. There are no global estimates of die number of workers currendy at risk; Table I refers to the 1970's3*5 and is mainly based on information furnished to die International Labour Office by those countries which report on their min ing, tunnelling and quarrying operations.3 The considerable between country differences in rates are no doubt largely due to differences in methods of reporting. Nor is the coverage comprehensive. Not only the distribution but also die nature of some of the pneumoconioses may be changing. For instance, since the first International Pneumoconiosis Conference held in Johan nesburg, in 1930,6 the profile of diseases such as silicosis appears to have changed, at least in die large controlled in dustries.7*8 Whereas in die early decades of this century, these were diseases which disabled young and killed prematurely, they are now increasingly diseases ofprimari ly radiologic manifestation with littie morbidity or impact on longevity. Reasons no doubt include improved living stan dards, better medical care and tuberculosis control in addi tion to improved environmental controls at the workplace.8 Career Investigator, Medical Research Council of Canada. However, outbreaks of acute disease continue to appear, usually in new processes or small uncontrolled industries, even in the technologically advanced countries.1*8*12 The mid-century epidemic of asbestos-related disease is another example of the failure to apply known control technologies to commercial exploitation, in this instance due perhaps in part to the exigencies of World War n.13 The perspective envisaged for die Vffih International Pneumoconiosis Conference as reflected in the themes selected for discussion is considerably broader than that of the First Conference, held in Johannesburg in 1930. The players are also different. Clinical, engineering and industrial hygiene scientists were die major contributors at die First Conference, with die major contributing laboratory sciences being pathology and microbiology. Today all branches of the clinical laboratory sciences are represented, in particular, epidemiology. This is a late comer on this scene and has become increasingly important as it adapted die techniques developed for die study of epidemic infectious disease to die study of chronic noninfectious disease of multifactorial etiology. It is well accepted that environmental and medical surveys can be used to evaluate hazards in die working en vironment. However, today I wish to indicate how they may be combined using the approaches and methods of epidemiology, and statistics which together offers 3 powerfill tools: i) a basis for sampling when numbers to be studied exceed resources; ii) a means ofestimating power when sam ple size is limited (workforces are after all finite) and iii) the methods of analysis which enable the simultaneous con sideration of more than one factor in these diseases of multifactorial etiology. The examples chosen to illustrate this presentation are from my own field of endeavour. ROLE OF EPIDEMIOLOGY Epidemiology is defined as the study of the "distribution and determinants of health related states or events in specified populations and the application of this study to the control of health problems."14 I agree with those who argue that it is a discipline rather than a science, i.e., a field of learn ing or practice applicable to the study of natural phenomena (biological, sociologic or other), rather than a science, i.e., a systematized theoretical body of knowledge about a par ticular category of natural phenomena.15 As such, it is a 16 Conference Theme Presentations Table I Selected Information on Dusty Occupations in Various Countries: Number of Current Workers at Risk, Reported Prevalences of Pneumoconiosis (total cases) and Incidences (new cases each year) per 1000 Exposed Workers Continent /country Sources of exposure Europe France Germany Poland UK mines, pits, quarries coal mines. other mines, other coal mines. other America US Ontario Quebec coal mining mining Mexico* Peru mining not stated Australia NSW Queensland W Australia coal other coal other mines mines Years 1Number at risk Total cases/ 1000 New cases/y: 1000 1977 1977 1977 1978 1977 1977 89,391 111,992 c.7,000 c.90,000 252,600 5,800 51.1 228.9 116.9 34.4 119.1 103.4 5.1 7.5 2.4 3.7 2.1 9.4 1973-78 1970 1967-77 118,579 17,355 12,556 1973 1976 4,815 56,819 '20.0 na na 8.9 c.36.0 na 1.4 1.8 8.9 na 1973-76 1976-78 1968-72 1968-72 1978 15,970 4,484 1,387 3,903 6,923 28.8 10.6 na na 27.0 na 0.5 6.4 8.1 2.6 India mines,other 1973-77 c.600,000 c.25.0 Africa Kenya small mines 1977 3,359 0.0 na S Africa hard rock 1977 1977 19,504 300,357 na 11.1 na 1.6 Table shows information derived mainly 3 countries reporting to ILO on the number of subjects exposed in dusty occupations as well as pneumoconiosis rates: (ref 3): figures for Ontario, Quebec, and for S Africa were derived from ref 4. * refers to 1 company only; each company keeps its own statistics 17 Conference Theme Presentations discipline which must be of interest and of use to all par ticipants here today, whatever our branch of science. Epidemiology can be used to address in populations die same issues which a clinician addresses in the management of a single case: namely, die description and recording of its features (the history, examination and laboratory tests); the explanation contained in the diagnosis and die formulation of prognosis, and in light of the above the planning of the management and the evaluation of its success. Thus popula tion based (epidemiologic) studies may have as their objec tive, description (prevalence or incidence ofdisease) and/or explanation (who in a population is affected and why: who is not and why not). These findings can then be used to for mulate corrective measures, and once in place, their effec tiveness can be evaluated by further studies. The key in the clinical as well as the public health management of occupa tional disease is how to establish the link between the biologic outcome of interest (abnormality, dysfunction or disease) and the pertinent exposure. ESSENTIAL ELEMENTS OF AN EPIDEMIOLOGIC SURVEY These can be summarized in four interrogative adverbs: why (the objectives of the survey), how (its design), who (the target population or workforce(s)) and what is to be studied (referring to the measurements made of dependent and in dependent study variables).13 Most important is the first, what McDonald calls the "fundamental ingredient of any scientific endeavour,** namely, "an obtainable objective or answerable question ... clearly and unambiguously de fined.*'16 He also recommends that a subsidiary question be asked: "and what will I do with the answer?'* Thus an epidemiologic study is neither "a data gathering exercise with a nebulously defined purpose and no hypothesis to test;*' nor is it a study "which misses a truth because it is buried in a mass of data.*' These are both popular misconceptions which relate to the false belief that the key characteristic in epidemiological study is that it is based on large numbers of subjects.17 Indeed some of the most effective epidemiologic studies are very economical in this regard. Design At the heart of the scientific method is the experimental design. In its complete form it requires that the researcher have control of all aspects of the study including the option of testing the entire target population (or sampling at ran dom from it); control of the assignment of test units to in tervention (exposure) or not, as well as die opportunity to examine all test units before and after the intervention with no loss to follow-up.16 When study units are cells, or plants or animals, this is possible; when the subjects are human, and exposure the result of natural experiment, this is rarely so. Indeed, the definition of a survey (the word used in the title of this presentation) is "an investigation in which in formation is systematically collected but in which the ex perimental method is not used.''14 Other than randomized control trial, for instance, of tuber culosis drug therapy, most occupational health surveys must of necessity use a less-than-complete experimental design. While die strongest designs include measurements before and 18 after exposure (i.e., are longitudinal or cohort in concept), prevalence (i.e., cross-sectional) designs are often all that is feasible, and are most frequently used for chronic nonmalignant diseases such as pneumoconiosis whose onset is difficult to pinpoint. Indeed, the prevalence study has been not inappropriately dubbed the "workhorse** of chronic disease epidemiology.17 By contrast, the case control design is an elaboration of the traditional clinical case series, in which clinical case ex perience is described without reference to the population from which they were derived. The case control study also starts with identification cases of the disease under study; persons without the disease (controls) are then selected from as far, as can be determined, the same population as generated the cases, and the past of cases and controls are compared for evidence of exposure. Hybrid designs, using the case-control approach within a cohort, have been creatively exploited in establishing relationships between occupational exposure and malignant diseases,18 and they are now increasingly being used in the study of non-malignant diseases such as the pneumoconioses.17 Nor does the case series study necessari ly merit the scorn often accorded it by editors and reviewers: it was after all such a clinical case series reported by a mis sionary doctor, the surgeon to whom his cases were re ferred, and die pathologist on the surgical pathology service which first drew the attention of the medical community to the link between mesothelioma and asbestos exposure.19 In deed, it has been pointed out that shrewd clinical observa tion remains the most powerful tool in detecting new disease patterns linked to workplace exposure,20 also in identifying recognized disease patterns in workplaces or associated with exposures not previously thought to be at risk.17 Dose Response Relationships Dose response relationships form the scientific basis ofphar macology (which deals with desired responses) and tox icology (which deals with undesired responses). In both, dose refers to die amount ofthe agent delivered to the target organ and retained for a period of time sufficient to evoke a response. In occupational surveys of chronic diseases like pneumoconiosis and chronic obstructive pulmonary disease, dose-response relationships are important in establishing causality.16*17'21 However, estimates of exposure have un til recently, been die only available indicator of dose; ob viously a very poor substitute given the low deposition rates and highly efficient clearance of so much ofwhat we breathe in. What is surprising, given die impossible task of represent ing exposure over a working lifetime accurately, is that exposure-response relationships are usually demonstrable in workplace surveys even using quite simple indicators of exposure. The development of new methods, such as the quantitative measurement of lung dust residue represent a quantum ad vance in the study of the dose variable and these have already contributed to our understanding of why exposure response relationships differ between workforces. For instance, there is now evidence in support of mass rather than fiber number being the determinant of fibrosis scores for asbestosis.22 This topic is rigfady one ofthe key themes ofthis Conference. New technologies of this sort to obtain the most precise estimates of dose possible may not however always be available, and the value ofwhat is surely die simplest estimate of exposure, the worker's personal assessment, should not be overlooked. Thus several recent community-based studies have shown clear evidence of association between indicators of chronic obstructive pulmonary disease (COPD) such as FEV] and occupational exposure to dusts at work, evaluated subjectively by study participants.23'24 Subjective estimates of personal exposure have also proved as useful as objec tive dust exposure measurements in demonstrating exposure response relationships in workforce based studies, an obser vation of relevance in situations where resources for objec tive environmental control measurements do not exist, for instance in certain industrializing countries. Modelling Exposure Profiles Whether or not lung responses are influenced by exposure profiles (such as the occurrence ofpeaks or gaps in exposure versus steady level exposure) remains a matter of concern, with implications for setting control levels. However it is not an easy matter to investigate. One approach is to use mathematical modelling based on biologically plausible models.26*27 For instance, in Quebec asbestos miners, tem poral patterns of exposure appeared to influence the different respiratory responses;27 thus for asbestosis, the strongest predictor was cumulative exposure; for pleural change ex posure, peaks and residence time of dust in the lung; for air way reactivity, both with early and recent exposure, and for airflow limitation and bronchitis, dust level and dust load over time as well as smoking. MEASUREMENT TOOLS OLD AND NEW: APPLICATIONS AND EXAMPLES The effect of measurement error, whether of exposure or response, is attenuation of exposure response relationships. This has led to concerted efforts to improve standardization and reduce measurement error. In die case of die chest radiograph, the traditional health measurement tool in pneumoconiosis surveys, the ILO has taken die lead in stan dardizing techniques of film reading.28 Subsequendy, respiratory questionnaires and lung function tests have been included in most workplace surveys,1,17 originally in sup port of the diagnosis of pneumoconiosis, but subsequendy as outcome measurements in their own right to characterize among other things airway function and standardization pro cedures for their use in surveys has been developed by various professional bodies.29,30 Despite its modest status (it is cheap and despised by clinicians as inaccurate), the respiratory questionnaire has proved a surprising but power ful measurement tool. For instance, exposure-response rela tionships for the complaint of shortness of breath when hur rying on the flat are readily demonstrated in asbestos ex posed workers, consistent with the clinical conviction that shortness of breath is an early, characteristic and essential feature of asbestosis.8,13 Recently there has been a resurgence of interest in this and other symptoms such as wheezing as response variables coinciding with the increas ing appreciation of the fact that acute and chronic airway responses occur following a wide range of occupational exposures.31 Conference Theme Presentations Pulmonary Function Tests Obsession with the importance of reproducibility of lung function tests for epidemiology studies often led researchers to exclude subjects whose results failed to meet specified criteria for acceptability.29 A careful analysis by one research group of subsequent health experience in subjects with and without test failure brought to light a very interesting source of bias, namely, that test failure in itself carries a greater chance of a less unfavourable outcome.32 This observation has now been confirmed in several cohorts and the underlying mechanism(s) are under investigation. The "healthy worker effect" is a term originally coined to describe die lower mortality experience of employed workers compared to the general population,14 presumably due to their better than average health status. There may be a similar explanation for the better than average lung function often seen in workers engaged in physically demanding jobs. For instance, in a survey of Paris workers employed in a number of plants, younger workers with pollutant exposure had consistently better (not worse) values for FEV than those whose jobs did not involve exposure; in older workers the situation was reversed.33 Nor is this experience unique.34 It is also biologically plausible: dusty jobs are traditionally heavy jobs likely to attract those of above average perform ance. This potential source of bias has implications for analysis as well as for interpretation, and suggests that cross sectional studies of older workers are likely to underestimate exposure effects on lung function even when external reference values are used to take account of confounders.39 Complex Health Measurements as Tools in Epidemiologic Studies The laboratory measurements now available to characterize pulmonary abnormality, dysfunction and disease are re markable for their variety and precision, but also for their complexity and cost and their optimal integration into research into pneumoconiosis and other diseases of occupa tion can be challenging. This is often possible through the use of hybrid study designs, such as case-control within a cohort or within a prevalence study. This allows the target population to be described by low-technology measurements (e.g., questionnaire, job, and if necessary lung function or x-ray), and within this framework, stratification by exposure, or response, or both can be done prior to sampling. In this way it is possible to address well formulated objectives by comparison of selected but small groups of subjects using high technology tools. Note the population description should respect basic epidemiologic principles including a complete definition ofthe target population with an assessment of selec tion bias into and out of the workforce (respectively the "healthy worker" effect and the "survivor" effect). For ex ample, it was possible to use questionnaire, x-ray and lung function data gathered, in a cross-sectional study of the Quebec asbestos miners and millers36 to select smaller subsets of subjects in whom further measurements were car ried out to address additional questions on the early effects of exposure,37 and whether lung geometry was a risk fac tor for the development of asbestosis.38 19 Conference Theme Presentations UNRESOLVED ISSUES, FUTURE RESEARCH AND DIALOGUE A conference like this brings to light many unresolved issues, and perceptions vary as to their importance. One which deserves careful scrutiny is how best to evaluate the effec tiveness of current pneunoconiosis control measures in cluding health surveillance and environmental control levels. Most current survey research is descriptive (for instance, health hazard identification or evaluation) or etiologic (ex amining exposure response relationships), little is evaluative (determining the effectiveness of controls). Despite the prob ably billions ofchest radiographs, and the probably millions of spirometric test records carried out in health surveillance programs, it is still not clear whether medical surveillance and/or current environmental control levels for silica12 and asbestos35 if respected, do indeed protect human health. A second and related question concerns die links between pneumoconiosis and tuberculosis, an issue of great impor tance in those countries of Africa and Asia with both high tuberculosis infection rates, and extensive mining opera tions.4 Under such circumstances, mine medical services may be responsible for extensive surveillance and treatment programs which could provide the framework for important research. For instance, a recently completed study in goldminers in the Orange Free State evaluated several short tuberculosis treatment regimens, and in a subset of the data showed that continued mining exposure while on treatment did not affect the outcome unfavourably.39 This important finding went contrary to die current practice which preclud ed miners on treatment for tuberculosis from further underground service, in die belief that continued silica dust exposure diminished die chance of treatment success. Nor was outcome unfavourably influenced by the presence of silicosis. As a result of these findings, regulations now per mit miners to continue in underground service, while under treatment, without loss of income, an important considera tion in a largely migrant and rurally based workforce. A third issue is how better to exploit die many existing data banks (including case registries and health surveillance data) for research and health control purposes. For instance, the Swedish silicosis case registry,40 set up in 1933, has been used to study i) progression (shown to be greater if cases continued in ajob with exposure after die earliest radiologic manifestation); ii) die relationship to lung cancer (silicosis cases have a greater risk than non-cases); iii) tuberculosis rates (still a frequent complication in cases of silicosis, even after the introduction of drug therapy in 1931). The PATHAUT data file, another registry containing machine readable autopsy reports on some 33,000 South African miners,41 has also been used as a data base for a case con trol study which showed hard rock mining to be a risk feetor for emphysema.41 Other uses of case registries will be reported at this meeting. Finally there is the issue of dialogue, within and between disciplines, within and between researchers, and within and between professionals. Each of us tends to believe die other is ignorant of what we have to offer. Dialogue is less dif ficult in die context of a conference such as this, when par ticipants are free ofdaily tasks; dialogue is also less difficult 20 perhaps in institutes dedicated to a common theme "Dialogue" should also include user-responsiveness: those who are in the workplace on a daily basis are often die first to perceive die unexplained or the unexpected and yet their comments are often not sought or heard. Finally, research into die diseases of occupations (whether it be basic laboratory research, cellular biology, environmental or clinical research) should always and only be driven by hypotheses which have biologic credibility as well as user plausibility, in the context of good study design. In addition, ifthere is a sound answer to Dr. McDonald's question: "and what will I do with the information" before starting a survey, then the survey is likely to be one which will furnish a useful evaluation ofrespiratory hazards in the working environment. REFERENCES 1. Morgan, W.K.C., Seaton, A.: Occupational lung disease, 2nd Ed., 686p. W.B. Saunders Co., Philadelphia (1984). 2. Encyclopedia of Occupational Health and Safety, 3rd Ed., pp. 1731-1733. L. Parmeggiani, Ed. International Labour Office, Geneva (1983). 3. Becklake, M.R.: Occupational pollution. WHO/IUAT-LD Consulta tion: or Chronic airways disease: distribution and determinants, preven tion and contra/. Dubrovnik, October 3-10 (1988). 4. International Labour Office: 6th International report on the suppres sion ofdust in mining, tunnelling and quarrying. 1973-1977. Interna tional Labour Office, Geneva (1982). 5. VI International Pneumoconiosis Conference, Sept, 20-23, 1983, Bochum, Veranstaller. International Labour Office, Bochum, Federal Republic of Germany (1984). 6. Proceedings ofan International Conference, Johannesburg, Aug. 13-17, ~ 1930. International Labour Office, Geneva, series F, No. 13, (1930). 7. Sadoul, P.: Pneumoconiosis in Europe yesterday, today and tomorrow. Eur. J. Resp. Dis. 64:177-182 (1983). 8. Becklake, M.R., Chapter 67, Pneumoconioses, Text-boot ofRespiratory Medicine, pp. 1336-1592. J.F. Murray and I. Nadel Eds. W.B. Saunders, Philadelphia (1988). 9. Edstrom, H., Rice, P.M.B.: "Laboratory lung": an unusual mixed pneumoconiosis. Gan. Med. Assoc. J. 120:27-30 (1982). 10. Martin, J.R., Muir, D.C.F., Moore, E., Edwards, A.C., Becklake, M., Morgan, W.K.C., Anderson, H., Edstrom, H., Rested, L, Segovia, J. Pneumoconiosis in iron ore surface miners in Labrador. Am. J. Ind. Med. (1988) (accepted). 11. Oakes, D., Douglas, R., Knight, K., Wusterman, M., McDonald, J.C.: Respiratory effect of prolonged exposure to gypsum (hist. Ann. Occup. Hyg. 26:833-840 (1982). 12. McDonald, J.C., Oakes, D.: Exposure response in miners exposed to silica. VIInternational Pneumoconiosis Conference 1983. Bochun, pp. 114-121. International Labour Office (1984). 13. Becklake, M.R.; Asbestos related diseases ofthe lungs and other organs: epidemiology and implications for clinical practice. Am. Rev. Resp. Dis. 114:187-227 (1976). 14. ADictionary ofEpidemiology. 2nd Ed. A hand book sponsored by the International Epidemiological Association. 141p. Oxford University Press, New York (1988). 15. Mietdnen, 0. Theoretical epidemiology: principles of occurrence in medicine. John Wiley & Sons, New York (1988). 16. McDonald, J.C.: Chapter 13, Epidemiology. Occupationalkmgdiseases: research approaches andmethods, pp. 373-404. H. Weill, M. TumerWarwick, Eds. Marcel Dekker, New York (1981). 17. Becklake, M.R. Chapter 5, Epidemiology studies in human populations. Handbook ofExperimental Pharmacology. Vol. 75, pp. 115-147. H.P. Witschi and J.D. Brain, Eds. Springer-Verlag, Berlin (1985). 18. Liddell, F.D.K.L., McDonald, J.C.: Survey design and analysis. Re cent advances in occupational health, pp. 95-106. J.C. McDonald, Ed. Churchill Livingstone, Edinburg (1981). 19. Wagner, J.C., Sleggs, C.A., Marchand, P.: Diffuse pleural mesotheli oma and asbestos exposure in the North Western Cape Province. Br. J. Ind. Med. 17:260-271 (1960). 20. McDonald, J.C., Harrington, J.M.: Early detection of occupational hazards. J. Soc. Occup. Med. 31:93-98 (1981). 21. Dotl, R.: Occupational cancer problems in interpreting human evidence. Ann. Occup. Hyg. 28:291-305 (1984). 22. Timbrel], V., Ashcroft, T., Goldstein, B., Heyworth, F., Meurman, L., Rendall, R.E.G., Reynolds, J.A., Shilkin, K.B., Whitaker, D. Rela tionships between retained amphibole fibers and fibrosis in human lung specimens. Inhaled Particles VI, in press (1988). 23. Becklake, M.R. Occupational exposure: evidence for a causal associa tion with COPD- National Heart Lung and Blood Institute Workshop, The rise in chronic obstructive disease mortality. Bethesda, MD (1987). 24. Becklake, M.R-: Chronic airflow limitation: its relationship to work in dusty occupations. Chest. 88:608-617 (1985). 25. Fonn, S., Groeneveld, H., de Beer, M., Becklake, M.R. Subjective and objective assessment of exposure to grain dust in relation to lung function change over the working week (abstract) 8thInternational Symposiun on Epidemiology in Occupational Health. Stockholm, Aug. 16-18, 1988. 26. Kujawaka, A., Marek, M.: Factors influencing the development of coalworkers' poeunoconiosis in the light of epidemiologic investiga tions. pp. 156-163. Vlth Internationa} Pneumoconiosis Conference. Bochum. Office, Geneva (1984). Bochum. 27. Copes, R., Thomas, D., Becklake, M.R. Temporal patterns ofexposure and non malignant pilmonary abnormality in ehiyanlite worker* Arrh Environ. Health. 40:80-87 (1985). 28. Gukfcfines forthe useofiLOinternationalClassification ofRadiographs ofPneumoconiosis. Revised edition 1980,48pp. International Labour Office, Geneva (1980). 29. Ferris, B.G.: Ed. Epidemiology standardization project. Am. Rev. Respir. Dis. 118:6 (part 2): 1-120 (1978). 30. Quanjer, Ph.H. Ed. Standardized lung function testing. Bull. Europ. Pbysiopath. Reap. 19 (supp. 5): 1-95 1983). 31. Becklake, M.R., Bourbeau, I., Menzies, R., Ernst, p.: The relation ship between acute and chronic airway responses to occupational ex Conference Theme Presentations posures. Current Pnevnonology, Vol. 9, pp. 25-66. D.H. Simmons Ed. Year Book Medical Publishers Inc., Chicago (1988). 32. Eisen, E.A., Robins, J.M., Greaves, I.A., Wegman, D.: Selection ef fects of repeatability criteria applied to lung spirometry. Am. J. Epidemiol. 120:734-742 (1984). 33. Kaufltnann, F., Drouet, D., Lellouch, I., Brille, D.: Twelve year spirometric changes among Paris area workers, fir. /. Ind. Med. 39:221-232 (1982). 34. Ernst, P., Dales, R.E., Nunes, F., Becklake, M.R.: Health selection may be determined by airway reactivity in a dusty environment. Thorax. accepted (1988). 35. Becklake, M.R.: Concepts of normality applied to the measurement of lung function. Am. J. Med. 80:1158-1164 (1984). 36. McDonald, J.C., Becklake, M.R., Gibbs, G.W., McDonald, A.D., Rossiter, C.E.: The health of chrysolite mine and mill workers of Quebec. Arch. Environ. Health. 28:61-68 (1974). 37. Jodoin, G., Gibbs, G.W., Macklem, P.T., McDonald, J.G., Becklake. M.R.: Early effects of asbestos exposure on hutg function. Am. Rev. Respir. Dis. 104:525-535 (1971). 38. Becklake, M.R., Toyota, B., Stewart, M., Hanson, R., Hanley, J.: Lung structure as a risk factor in adverse pulmonary responses to asbestos exposures: a case-referent study in Quebec chrysotile miners and millers. Am. Rev. Respir. Dis. 128:385-388 (1983). 39. Cowie, R.L., Langton, M.E., Becklake, M.R. Pulmonary tuberculosis in South African goldminers (submitted). 40. Westerbolm, P., Silicosis: observations on a case registry. Scand. J. Work Environ. Health. 6 (supp. 2):l-86 (1980). 41. Hessel, P. A., Hnizdo, E., Goldstein, B., Sluis-Cremer, G.K.: Pathological findings in mine workers. 1. Description ofthe PATHAUT database. Am. J. Ind. Med. 12:71-80 (1987). 42. Becklake, M.R., Irwig, L., Kielkowski, D., Webster, I., deBeer, M., freeman, S.: The predictors ofemphysema in South African goldminers. Am. Rev. Respir. Dis. 135:1234-1241. 21 Conference Tberae Presentations PROGRESS IN ETIOPATHOGENESIS OF RESPIRATORY DISORDERS DUE TO OCCUPATIONAL EXPOSURES TO MINERAL AND ORGANIC DUSTS J.C. WAGNER, M.D., FRCPath MRC External Staff Team on Occupational Lung Diseases Llandough Hospital, Penarth, South Wales INTRODUCTION Thank you for giving me die honour ofintroducing the theme on progress of Etiopathogenesis of Respiratory Disorders due to Occupational Exposures to Mineral and Organic Dusts. In the first place, I would like to say how pleased I am to follow Margaret Becklake in the setting ofthese themes. We both did our Graduate and Postgrauate training in Johan nesburg which was the scene of the first of these conferences in 1930. Of course, we were both too young to attend. Secondly, I have been given a vast field to cover in a very short time. I will paint with a very thick brush on a large canvas. I will concentrate on my personal experiences and views to offer a provocative base to the further sessions of this conference. I trust this will stir up sufficient controver sy to satisfy our sponsors. I note that my remit covers both mineral and organic dusts. On organic dusts my experience is brief--I do not believe that there is such a disease as byssinosis. The biological ef fects of cotton dust are part of die vast new field of study covered by the term "Industrial Asthmas," which is now a separate field from pneumoconiosis. SILICOSIS There are two facets of silicosis research in which we have developed new ideas since the 1930 conference. One is positive and requires explanation, the other I feel is a false lead which requires most serious scrutiny. Although historical evidence goes back to neolithic times, it was in the industrial revolution that it was realized that exposure to mineral dust could have fatal consequences. By 1912 South African workers had shown that quartz was responsible for these lesions and by the Johannesburg con ference it was proved that tuberculosis was the main killer of silicotics. The problem is how does silica do the damage and why is there this promotion of tuberculosis? My views are now considered simplistic and I hope that at a later stage of this conference someone will produce a more scientific hypothesis. I believe that silicosis is a disease ofthe monocyte macrophage system and the destruction of numerous macrophages by the inhaled quartz crystals produces a local milieu promoting infection from the mycobacteria when they 22 are present. As far as I will go in explaining this are the studies of Tony Allison and Jack Harington. Briefly die quartz crystal is taken up by the macrophage forming phagosomes with the relevant lyzosomes which are re leased, but fail to digest either the quartz crystal or the wax coat surrounding the tubercle bacillus. The quartz crystal then by some means disrupts die membrane of the phagosome releasing the "enzyme soup" which destroys the macrophage: die unscathed quartz crystal is freed to destroy further macrophages and the bacillus to reproduce. The other facet which disturbs me is die suggestion that quartz is an important carcinogen. We have as pathologists studied numerous cases of silicosis and exposed a vast number of animals to quartz dust. In all the human cases I know ofwhere carcinoma does occur in silicotics it is either associated with cigarette smoking or much more rarely with radon release. In the experimental evidence only two series of experiments are quoted in which malignancy occurs. I am responsible for one of these studies and our results have been incorrectly interpreted. In 19601 inoculated quartz into the pleural cavity ofWistar rats. Some ofthese rats subsequently died of tumour which were not mesotheliomas. In 1962 the experiment was repeated with two further strains of Wistar rats in which a much higher incidence of these tumours oc curred. These tumours were subsequently studied by my wife who showed that these tumours were in fact histiocytic lym phomas of macrophage origin. She was unable to produce a significant number of these tumours by using different routes ofexposure. It is unlikely in human exposure that silica would reach the pleural cavity. The other study was carried out by Dave Smith at Los Alamos where Fischer rats were exposed to very heavy clouds of quartz and developed severe pulmonary fibrosis. Some of these animals subsequently died of peripheral car cinomata. These peripheral tumours occur in the animals with severe pulmonary fibrosis and these lesions are not specific for silica exposure. COAL WORKERS PNEUMOCONIOSIS When I first became involved in the study of coal workers pneumoconiosis I was informed that the disease could be divided into simple and complicated forms. The simple form did not cause disability; the complicated form did because of the production of massive pulmonary lesions consisting of vast chunks of fibrous tissue. All these facts have been disproved. The majority of coalworkers do not develop any pathological change apart from having excessive coal dust blackening their lungs. About 10% of these then develop pulmonary nodulation, so at this stage the disease becomes "complicated," and with further exposure, these nodules tend to form vast coalescent masses ifexposure is sufficient. The main disease in these men is not the nodulation per se, but the associated emphysema and interstitial fibrosis in some cases. In the massive lesions, the lumps are not fibrous tissue. In fact, die amount of collagen and pre-collagen amino-acids present in them is the same as in the non-involved lung tissues. Working with Dr. F. Wusterman ofthe Biochemistry Department of die University College of Wales in Cardiff and Professor P. McGee at Oxford, we were able to show that the main constituent of these lesions is fibronectin, a glycoprotein which occurs as 3% of the normal serum proteins. ASBESTOS AND ASSOCIATED DISEASES There are as we all know, a group of fibrous minerals that can be split longitudinally and have commercial uses. These are chrysodle, crocidolite, amosite, tremolite / actinolite and anthophyllite. The term "asbestos" was originally used for chrysodle. If this had been maintained and the other materials referred to as the amphibole fibres, die present confusion in assessing the risk hazard would not have occurred. In the amphiboles die risk hazard depends on the ultimate length diameter ratio of the fibre and this has been clarified with the studies ofthe biological effects of tremolite, an amphibole with a widespread occurrence in the earth's crust, usually as a contaminant of chrysodle, talc, anthophyllite, and other minerals. It also occurs in small deposits and is frequendy used all over the world as a soil conditioner in agriculture. The physical features of tremolite vary in all forms from thick flakes to very fine fibres. The electron microscopic ap pearance of some fibres is shown. Under the transmission electron microscope it can be seen that the finest and straightest of the fibres is crocidolite followed by amosite and the coarse anthophyllite. Now tremolite covers this whole spectrum. By far the finest of all fibres are chrysodle fibres particularly when they break up into fibrils, one chrysodle fibre having the equivalent diameter of at least 100 chrysodle fibrils. However, due to the coiled wave-like configuration the aerodynamic efficiency of chrysodle depends upon that of the full coil. Before venturing into an account of die biological effects of these different fibres, it is necessary to state the hypothesis of selective retention of fibres in the lungs. This contends that it is the fibres retained in the lung parenchyma which are significant in the causation of the disease. Now I will briefly state our belief in die correlation of disease with fibre type. I am sure this will be contended and defended during this conference. Asbestos Bodies Asbestos bodies develop around amphibole and other straight mineral fibres and are seldom on chrysodle fibres. Conference Theme Presentations Pleural Plaques All types of asbestos are associated with development of pleural plaques particularly tremolite, amosite and an thophyllite. The incidence of environmental plaques is ex tremely high in agricultural situations and these are usually associated with tremolite. Asbestosis All forms of asbestos dust if inhaled in excessive quantities will cause asbestosis. Carcinoma of the Lung Initially carcinoma of die lung occurred in people with severe asbestosis with long term survival. Since the 1950's the in cidence of carcinoma of the lung has greatly increased due to the association with cigarette smoking. We still contend, and will present supporting evidence, that the association is between cases of definite asbestosis and carcinoma. Diffuse Pleural Mesotheliomas Diffuse pleural mesotheliomas are associated with exposure to crocidolite, very fine tremolite, very fine amosite; and if associated with pure chrysodle this must be an extremely rare occurrence. These associations have been occupational, para-occupational or familial. In 30% of cases of diffuse mesotheliomas in adults, there is no evidence of an association with actual asbestos exposure as defined above. The amount of asbestos in the lungs of these cases is similar to that seen in the the general popula tion living in the same environment. Diffuse Peritoneal Mesotheliomas These tumours are not as common as those originating in the pleural cavity. Experimental Mesotheliomas We have produced these tumours by the intrapleural inocula tion of various types of asbestos dust, including chrysodle. In the majority of the chrysotiles used there was tremolite contamination. The exception to this was the chrysodle that gave the highest rate of experimental tumours. This was a specially prepared preparation containing numerous long straight fibrils and the actual dosage was at least one thou sand million times greater than occurs in human exposures. When we used this dust in an inhalation study the tumour rate was similar to that seen in the controls. Significance of Fibre Body Burden Chrysotfle Chrysodle fibres are difficult to count as they tend to form clumps, and fibres break up into a myriad of fibrils, so that amphibole fibre is equivalent to about 100 chrysodle fibrils. The present opinion is that exposure to chrysodle has a much milder effect than the amphiboles, and that the association with mesotheliomas is minimal. Amphiboles The total amphibole count, a mixture of fibre types, with different length and diameter, can be used in the assessment 23 Conference Theme Presentations of effect, taking 5 x 106 fibres per gram dried weight of lung as the absolute upper limit of non-occupational exposure. In significant asbestosis there are 100 X 106 fibres and in severe asbestosis 1000 x 106 fibres. Significant Fibre Size Mesotheliomas Diameter <0.25 pm, length >8.0 pm Pulmonary Fibrosis Diameter <3.0 pm, length >8.0 pm Diffuse Mesotheliomas Crocidolite--1 million fibres probably minimal but there have been familial cases with counts of 500,000. Other Amphibole Fibres Again, only fibres in the size range of less than 0.25 pm and greater than 8.0 pm in length are regarded as signifi cant. The tremolite and amosite are probably equivalent to crocidolite. It must be borne in mind that these studies are in a developmental stage and die criteria recorded above are those ofour present state of knowledge. Further modifications will be reported as the studies continue. The number of fibres recorded as millions per gram weight of dried tissue depend on die technique developed by Fred Pooley in Wales in collaboration with Patrick Sebastien in France. There have been modifications of their methods which I understand can be made comparable in some circumstances. MAN-MADE MINERAL FIBRES (VITREOQS) I have used die above tide deliberately as we have only under taken extensive studies on samples of rockwool, dag wool, glass wool and sub-micronic glass fibre. I am not in die posi tion to report cm detailed studies ofthe other synthetic fibres such as the ceramic fibres; but hope that later in the con ference others will give reports. In our extensive studies with fibres given to us by both Euro pean and American industries, we were only able to pro duce significant tumour incidents following the intrapleural inoculation of die sub-micron glass fibre. No increased in cidence of tumours or significant fibrosis was seen follow ing inhalation experiments. It should be recorded that in the numerous specimens of lung extracts from tumours that Professor Pooley has studied, only a handful have contained commercially prepared man-made mineral fibre. If the material does not get retained in die lung it is unlikely to cause disease. ABSORBENT CLAYS These clays are part of the palygorskite group and are used for cat litter and containing spills on factory floors. Another use is in the preparation of drilling mud for die oil industry. Our detailed studies have been confined to the attapulgite and sepiotite produced in Spain. In our experimental studies only fibres from a small deposit in western Spain were shown to be of a length/diameter ratio to be regarded with suspi cion. These fibres produce mesothelioma following in trapleural inoculation into rats. On our advice, the produc tion of this fibre has been discontinued. Other attapulgite fibres and sepiotite fibres did not produce tumours follow ing both intrapleural and inhalation studies. Later in this con ference Dr. Kathryn McConnochie will report on a clinical and radiological study of the workers who produce die sepiotite. ERIONITE The most fascinating new development in the fibre studies are those on erionite. We all know of Professor Baris' fascinating studies in which erionite was shown to produce a higher incidence of mesotheliomas than any other fibre. From our experimental studies we obtained fibres from one ofthe houses in Karain and also from other sources in Oregon State and following intrapleural inoculation it was shown that die sample from Oregon produced 100% tumours and only a slightly lower rate was found in the dust from Karain although it had a lower fibre content. In inhalation studies the Oregon fibre produced mesotheliomas in 27 out of the 28 animals exposed, 1 animal dying of leukaemia. In repeated experiments tumours rose to 100%. In comparison to this in our much larger experiments in which animals inhaled asbestos dust, we were only able to produce a very low incidence of mesotheliomas. Therefore, as I retire from this field, I leave you with a fibre which is a very potent carcinogen and must be of value in unraveling the mineral fibre mesothelioma mystery. . .oOo . ADIEU! 24 Conference Theme Presentations PROGRESS IN PREVENTION: EARLY DIAGNOSIS AND MEDICAL CONTROL OF OCCUPATIONAL LUNG DISEASE W. T. ULMER, M.a University Clinic and Out-Patient-Clinic, Bergbau-Berufsgenossenschaft Krankenstalten "Bergmannsheil Bochum,*' Gilsingstr. 14 4630 Bochum 1/FRG 1 would like to touch the old--nevertheless very interestinghistory ofdust-related lung diseases very briefly. I will con centrate more on later results and on data available for fur ther research and strategies for dust-exposed persons, especially miners. PARACELSUS already mentioned the miners' disease, and he called it consumption of miners ("Bergsucht"). In this term, the relationship to tuberculosis is obvious. At this time and till the early fifties of this century, silico-tuberculosis was one of the main problems of complications of miners' dust-related lung disease. This is more or less history but not in all parts of the world. RAMAZZINI of Padua (1780) described bakers' asthma for the first time which was caused by the organic flour dust as an asthma-like disease. The term "pneumoconiosis" was introduced by ZENKER (1867) for the first time, and at this time pathologists showed us all the changes of the structures in the lungs caused by dust, mainly by quartz and coal mine dust. In Germany, mostly the term "silicosis" was used for "coal workers' pneumoconiosis" as it is called in English speaking coun tries. At present, coal workers' pneumoconiosis is still the most important dust-related disease from the sociomedical point of view. Many of us may remember the tremendous basic contribution given by pathologists and some may remember that for physicians' better understanding of this disease radiology was the key to a new era. These different pictures led to different X-ray classifications. The first in ternationally used classification was that of Johannesburg (1928) followed by the classification of the International Labour Office (ILO 1980/81). With one set of standard films edited by ILO we have an instrument world-wide available to control the development of pneumoconiosis by the X-rays and for comparative studies. We leave history now and we move on to the present time. The development during the last 30 years has shown tremen dous progress not only on behalf of our knowledge. Our im proved understanding ofthis disease "coal workers' pneumo coniosis" and very similarly of pneumoconiosis caused by organic dusts like bakers' asthma have had important pro gress for the expectation of life as well as for the quality of life of dust-exposed and disabled persons due to exposure to harmful dust. The development of new methods in basic research work was followed by much better insights in the etiology and pathogenesis ofthese diseases. At the same time, new drugs, very efficient drugs, were developed which could not pre vent these diseases till now, but could control the complica tions responsible for disablement and early death. Both ear ly disablement and early death were terrible facts connected with most of the pneumoconiotic disorders and with the com plications related to the different forms of pneumoconiosis. To remember some of these steps, it may be useful to under stand our plans and projects for the future. There is no doubt that the improvement of dust control at all levels is a very important step for the control of dustrelated diseases, but besides the improved dust control tremendous medical progress took place. All the coal workers who really develop problems in relation to coal workers' pneumoconiosis have obstructive airway diseases. This kind of airway obstruction starts on the basis of chronic bronchitis and is followed by obstructive bronchitis. In case of less strong X-ray changes, the obstructive airway disease is not more frequent than in non-dust-exposed men (REICHEL et al., 1969). In categories B and C of the ILO classification this means large massive fibrotic lesions die incidence of which is twice as high as in non-dust-exposed men (the smoking habits of miners agree with the control group of non-dust-exposed men) (Figure 1). Like patients with idiopathic obstructive bronchitis, the obstructive bronchitis of coal miners dictates the clinical situation of these patients. Fortunately, the obstructive bron chitis of coal workers with coal workers' pneumoconiosis can be treated in the same way with the same success as the idiopathic form of chronic obstructive bronchitis (Figure 2). We control our coal workers with coal workers' pneumo coniosis very carefully. This means, coal workers with coal workers' related obstructive bronchitis stay under a con trolled regime of treatment. Under the long-term treatment the expectation of like of our miners with large opacities and fibrotic lesions on the X-ray is now at least as long as that of the general population (Figure 3). 25 Conference Theme Presentations Frequency Rt >3.5 V. Figure 1. Age dependency of patients with obstructive airway diseases at different stages of coal workers* pneumoconiosis and of non-dust-exposed men (obstructive airway disease = R,,w >3.5). At first glance, the situation may give satisfaction, but we have to realize that the age at which the coal workers develop obstructive bronchitis is nearly the same as 20 years ago. The mean age of the manifestation of obstructive bronchitis is 57 years. In the fifties the expectation of life after airway obstruction was 3.5 years on the average, and now die ex pectation of life is 16 years on die average. But during this time, coal workers with coal workers* pneumoconiosis and obstructive bronchitis are disabled and have more or less dyspnea, and some even develop cor pulmonale. Therefore, for the future we have to avoid die development of coal workers* pneumoconiosis and we have to learn to avoid manifestations of chronic obstructive airway diseases. First the development of coal workers' pneumoconiosis on the X-ray: The correlation between the ILO12 step classifica tion (from --/0 to 3/+) is relatively linear. Figure 4 shows the results of one mine in W.-Germany as mean value and also die progression ofthe worst and the best case (Figure 4). From these curves we can calculate the ILO classification step time: it is the time in years necessary to get from one classification step to the next one (e.g., 0/1--1/0). In the ex ample in Figure 4, die ILO classification step time is $ years on the average. These curves allow an extrapolation at a relatively early time. From such curves we may learn more about the causes ofthe different ILO classification step times for different individuals as well as for different mines. There are clear differences between different mines as Figure 5 shows (Figure 5). We proposed that: a) the X-ray development of coal workers' pneumo coniosis should be documented for each coal worker on ILO classification step times/exposure times curves; b) an interval of 4 years for X-ray examination of coal miners is adequate and without any risk for coal miners at present exposure levels. In order to prevent the pneumoconiosis due to obstructive airway disease die prevention of airway obstruction is the most important factor as already mentioned above. Today, we dispose of sensitive methods to detect early signs of lung function changes related to airway obstruction. In W.Germany, we examined in 4 mines the miners by careful lung 26 IGV in % (normal value s 100) Conference Theme Presentations I 1 | i i i { i i i | i ' i i l i i i i \ i 1 i'"l 0 100 200 300 MO 500 600 Rfin% of normal value Figure 2. Decrease of airway resistance (RJ and of intrathoracid gas volume (IGV) under typical treatment with bronchodilators and glucocorticoids in patients with pneumoconiosis-related obstructive bronchitis (n = 21) and of patients with idiopathic obstructive bronchitis (n = 19). function tests. Among the miners is a relatively high percent age still at work who has obstructive airway disease, and there is quite a number ofminers with oversensitivity (hyperreagibility) of die airways. It is very important to detect persons with signs of obstruc tive airway disease as early as possible to control the develop ment of die lung function of these persons: 1. to start with an adequate treatment at adequate time and 2. to avoid progression of this disease. It is very likely that an early treatment can control this disease and can avoid progression. We have to control the lung function of dust-exposed per sons with adequate methods. Time intervals for re-examina tion could be 4 years but not longer. Dust concentration decreases in the inhaled air are most im portant for prevention. The very effective dust masks are normally worn for short times only. The acceptance of nor mal light masks depends on the isolation, and therefore on the development of sweat under the mask. The loss of the possibility of communication is also important and problems of increased airflow resistance may be a factor, too. The light masks (Figure 6) comparable to those masks worn in hospitals, have in this respect many advantages, although they decrease die dust concentration only for about 70%. 1. They allow communication with other persons without effort; 2. They soak up the sweat around the mask; 3. The decrease of dust concentration in the inhaled air is about 70%, and therefore the ILO classification step time increases so that during the life time coal workers* pneumoconiosis responsible for dust-related obstructive airway disease will not develop (Figure 7). CONCLUSION In addition to the best available dust suppression we should emphasize that the light (one-way) masks will be used con tinuously. With this strategy, coal workers' pneumoconiosis could be controlled so that dust related obstructive airway diseases never will occur. These results shown mostly for coal miners and coal workers' pneumoconiosis can be transferred more or less to other types of pneumoconiosis. Our knowledge about the development of pneumoconiosis increased tremendously. During the last decades we could dispose of strategies which are able to slow down the development of coal workers' pneumoconiosis suddenly and which can avoid the coal workers' pneumoconiosis-related obstructive airway diseases. Furthermore, we can improve the health situation of the miners we are responsible for. 27 Conference Theme Presentations 1951 T 1954 y. --------^------- 1960 - 1963 -------- ^-------- 1969 - 1972 % AGE Figure 3. Expectation of life of coal workers with obstructive bronchitis and of miners without coal workers' pneumoconiosis and of non-dust-exposed men in fee years 1951-1954, 1960-1965, 1969-1972. 28 ILO-Classification Density of shadows worst case Conference Theme Presentations Figure 4. Correlation between ILO classification and exposure time (mean values of S3 miners and the best as well as the worst individual case). 29 Conference Theme Presentations focus density 110 Figure 5. Correlation between ILO classification steps and exposure time on 3 different mines in W.-Germany (mine In 616, mine 2 n = 604, mine 3 n = 596). 30 Conference Theme Presentations Figure 6. Light mask with very good acceptance and many advantages protecting against the develop ment of coal workers' pneumoconiosis (decrease of dust concentration in the inhaled air--70%). 31 Conference Theme Presentations Oust concentration reduction in per cent in 1970 5 9 61 63 65 67 69 71 73 75 77 79 81 83 85 87 89 91 93 95 97 99 101 Obtained age up to the manifestation of functional coal worker's pneumoconiosis Figure 7. Relationship between decrease of dust concentration in percent of the values from 1970 and the age at which X-ray changes take place which could be responsible for coal workersrelated obstructive airway diseases (a decrease of about 35 % would be enough to pro long the manifestation time to the values of the normal expectation of life). REFERENCES 1. HjO 1980/81: Richtlinien for die Anwendung der intemationalen Klassifikation des IAA von PneunKjkoriiose-RbntgenfUroen. Internal. Arbeitsamt, Genf 1980. 2. Paracelsus, T. von Hohenheim, gen. Paracelsus: Von der Bergsucht und anderen Bergkrankbeiten. Bearb. von Franz Koelsch. Schriften aus dem Gesamtgebiet der Gewerbebygiene N.F.H. 12 V, 69 S. Berlin: Springer 1925. 3. Ramazzxni, B.: Abhandlung von den Krankbeiten der IQinstler und Handwerker. "De morbis artificum deatriba". "Neu bearbeitet und Vennehret" von J. Chr. G. Ackermann, Stendal 1760, S. 124-135. 4. Reicbel, G., W.T. Ulmer, H. Buckup, G. Stempel, U. Werner Die chronisch obstruktiven Atemwegserkrankungen des Bergmannes. Dtsch. med. Wschr. 94, 2375 (1969). 32 Conference Theme Presentations REFLECTIONS ON PROGRESS WITH MINE DUST CONTROL AND DUST CONTROL TECHNOLOGY MORTON CORN, Ph.D. Professor and Director, Division of Environmental Health Engineering Department of Environmental Health Sciences, School of Hygiene and Public Health Johns Hopkins University, 615 North Wolfe Street, Baltimore, MD 21205 INTRODUCTION It is obviously impossible to provide a detailed historical or even present-day account of die control ofdust in mines and dust control technology in the brief time allotted to me. Therefore, as a compromise this theme paper highlights ma jor selected subject areas of scientific and technical knowledge that have culminated in the current degree of dust control and control technology in U.S. mines. What were the historical understandings and emphases; what types of knowledge were gained through laboratory and applied research that permitted us to effectively implement dust con trol strategies through either voluntary or regulatory societal mechanisms? hi different nations there has been a shared con cern with this occupational problem, and die contributions to understanding have been multinational. Bear with me if I tend to oversimplify; it is my belief that at times we must sit back and take a long look at what has been called the "drum roll of history." This enables us to discern "the big picture" from the many necessary and essential details that punctuate progress in any field of human endeavor. It also enables us to better consider where we are at present and to define further, needed progress. CONTROL OF MINE DUST Recognition of Coal Workers Pneumoconiosis as a Disease State The report by Bedford and Warner1 in Great Britain in 1943 must be regarded as a major turning point in our understand ing of die impact of inhaled coal dust and of dust control in mines in Great Britain. This report stimulated the adop tion of airborne dust standards for "approved dust condi tions" in conjunction with employment underground. No specific dust concentration limits or standards were set by law, but the adopted standards in the attainment ofdust sup pression continued for almost 30 years. The standards were die result of extensive studies of pulmonary disease in South Wales coal miners conducted by the Medical Research Coun cil. These studies were conducted in five mines; they associated dust with x-ray abnormalities. The British later extended these studies to a larger number of mines, i.e., the so-called 25 Pit Studies. The proposal for a standard was that not more than 10 milligrams per cubic meter of anthracite dust or 1 milligram per cubic meter of minerals other than coal for particles 5 microns or less in size, should be achieved. Note that the particle number standards for approved mine dust conditions introduced in Britain in 1949, remained basically the same until 1970, when gravimetric standards were introduced, again resulting from epidemiologic studies relating dust and pneumoconiosis. Thus, in Great Britain there was recogni tion of the disease state and adoption of standards for ap proved dust conditions. In the United States, a major 1936 report by die Public Health Service3 indicated that the term anthracosilicosis, as used, was a descriptive title for the form of pneumoconiosis com monly called miners' asthma. It was diagnosed by occupa tional histories, clinical examination and x-ray exams. The report indicated that die correlations "between exposure to dust and the evidence of constitutional changes left little doubt as to the etiological significance of the dust in the air breathed. ' ' Similar correlations were found between the silica exposure and the extent ofpulmonary changes. Investigators concluded that employment in an atmosphere containing less than 50 million dust particles per cubic foot would produce a negligible number of cases of anthracosilicosis when the quartz content ofthe dust was less than 5 %. This report was also an extraordinarily important one in that it lead to adop tion ofthe standards for free silica in die United States, which are in effect to this day under our Occupational Safety and Health Act, if die user chooses to utilize midget impinger sampling and dust counting methods to evaluate dustiness. My point in citing these two reports is to indicate that acknowledgement ofthe correlation between the disease state and the etiological agent is essential before control efforts can take place. In the 1950s the Commonwealth of Penn sylvania pioneered in studies of coal miners that lead to the recognition of the disease state of coal workers pneumoconiosis in bituminous coal miners, as contrasted to anthracite miners. Urns, the 1930's U.S. investigations resulted in differentiation between free silica in die dust caus ing silicosis, and miners' asthma occurring in hard coal mines. We spent another 25 years in the United States 33 Conference Theme Presentations debating legitimacy of the disease state of coal workers pneumoconiosis, which seriously hampered efforts at dust control. In this regard, the British reached consensus on this point before we did. The Physics of Dust In order to control die dust associated with a disease, one must know a great deal about dust physical and chemical properties. Although there were scientific treatises on dust properties as early as 1934,2>37 these volumes were very limited in the technical information provided that could be translated to die measurement and control of mine dust. The dust measurement techniques in effect during die 1930's were the midget impinger16 developed in the United States, and the Kotze' Konimeter,26 developed in South Africa. Gravimetric techniques were not extensively utilized to assess airborne dust for disease prevention until die late 1940's and 1950's. In fact, calibration ofdie impinger for coal dust par ticles (the only particles for which, to my knowledge, the instrument was ever calibrated) was reported by C.N. Davies in 1951.9 The concept of aerodynamic particle size re mained to be elucidated. However, even without these understandings enormous progress in mine dust reduction could be, and was made, as evidenced in South Africa in the 1930's through the 1950's. The ability to advance beyond die qualitative understanding that inhalation of dust is dangerous to your health and that dust concentrations measured as described correlate with disease prevalence in exposed workers, also depends upon insights into the hygienically significant sizes of inhaled par ticles. The development of this area of understanding is my third selected critical area of knowledge for effective dust control. Dust Deposition in the Human Respiratory Tract Drinker and Hatch11 traced the examination of particles in exhaled air to studies by Tyndall in 1882, and also cite a hy gienic study by Saito in K.B. Lehmann's laboratory in 1912. Studies in the 1930*s on nasal filtration by normal men were performed by Lehmann and by Torangeau and Drinker. The studies by Brown in 1931 were the first major studies on dust retention in man.3 Experimental investigations by Davies,8 I^ndahl and Hermann,23 Van Wijk and Patterson36 and Wilson and LaMer,38 supplemented by theoretical calcula tions by Findeisen,13 all advanced the state-of-the-art of par ticle size deposition in the human respiratory tract. The par ticle inhalation study that dictated U.S. views on deposition for two decades was that by Brown, et al., in 1950.6 It was the major source ofdefinitions for respirable dust in die U.S. and Europe, and for the very important report on dust deposi tion and retention in the human respiratory tract by the In ternational Congress on Radiological Protection in 1966.35 These were the first ofa long series ofexperiments, still con tinuing, to define die particle sizes of significance for chronic disease developing in the pulmonary compartment of die respiratory tract. The studies have been refined and there has been international agreement on the deposition curves in healthy men after inhalation at standard volume. The sub ject was reviewed by lippman24 and the new definitions of 34 compartmental deposition in the human respiratory tract have been published.27 The significance of this work was that it provided a target in terms of the spectrum ofparticle sizes ofhygienic impor tance in dusty environments, and enabled those interested in control to take aim at that target. It should be noted that during all of this work the characteristic "size" of a particle was the projected area diameter, because die predominant instrument for viewing collected dust particles was the light microscope. In the light microscope one observes a silhouette, a two dimensional representation of a three dimensional object, die dust parti cle. Work performed at a later date would differentiate be tween die aerodynamic size of a particle and die silhouette size of die particle that one observes in die microscope. While this may appear to be a minor physical differentiation, it is of the utmost significance. It explains why we observe fibers 200 microns in length in the human pulmonary compartment; their aerodynamic size is equivalent to a less than 10 pm diameter sphere of unit density which could penetrate to that region of the respiratory tract. It took many years for the significance of the aerodynamic size to be recognized. The understanding ofdust aerodynamic behavior and deposi tion in the lung required decades to crystallize. The control ofdust could progress, but there was great uncertainty ifone was capturing the sizes appropriate to the disease state. An analogy is use of a shotgun versus a target rifle. The stan dardization of so called "respirable dust" and the develop ment of an instrument to simulate that dust size waited until 1954 when B.M. Wright in England introduced the horizontal elutriator.39 Dust control efforts were proceeding in all in dustrialized nations, but it is fair to say that permissible dustiness was far above the concentrations we have today in mines of industrialized nations. There was also great uncertainty in the long term benefits associated with the con trol efforts, because the largest particles have the greatest weight associated with them. There could be extensive reduc tions in dust measured in terms of weight per unit volume; there could, however, still be only conjectural impact on the disease state, because the smallest particles reaching the pulmonary compartment are associated with the least weight per particle. West Germany began a series of epidemiologic studies in their mines in the search for the dust parameter that would best correlate with disease. They concluded that die surface area ofthe dust was an appropriate parameter and developed their dust measurement techniques accordingly. At a later date, they too would recognize the respirable dust concept with cyclone precollector sampling to determine respirable dust weight. During all the years ofthe 1950s and 1960s the British counted particles using a thermal precipitator instru ment and reported their dust concentrations in numbers of appropriately sized particles per cubic centimeter of air. Instruments to Measure Respirable Dust It is interesting to peruse the first volume of air sampling instruments entitled "The Encyclopedia of Instrumentation for Industrial Hygiene."40 The volume is concerned with many different types of air sampling instruments. The cas cade impactor, the midget impinger, and the electrostatic precipitator were the major instruments available for par ticulate sampling in 1956. Indeed, at a Governor's Con ference in die Commonwealth of Pennsylvania in 1964 a leading U.S. industrial hygienist who was director of in dustrial hygiene for our major steel firm, and a previous President of the American Industrial Hygiene Association, stated publicly that the respirable dust concept then in vogue in England and Germany was not applicable to United States mines. Thus, one reason that efforts to develop instruments that would apppropriately sample respirable dust in coal mines did not rapidly progress in the U.S. was because the respirable dust concept was not readily accepted. Subsequently, appropriate instruments were developed in the 1960s, utilizing a United States Atomic Energy Commission cyclone preseparator and the definition of die United States Atomic Energy Commission for respirable dust. It approx imates the BMRC respirable dust acceptance curve defined by die horizontal elutriator.20 These instruments approx imated die accepted pulmonary deposition curve at that time, mainly based on the data of Brown et al.5 The dust standards in mines enforced in Great Britain dur ing the period 1949 to 1970 were summarized by Chamberlain et al.7 The British abandoned the particle counting standards in 1970 and adopted gravimetric stan dards. The introduction ofgravimetric standards in the United States accompanied the Coal Mine Health and Safety Act of 1969. The Mine Health and Safety Act of 1969 required that begin ning June 30,1970 die operator of each coal mine was re quired to maintain the average concentration of respirable dust in the active working at or below 3.0 milligrams per cubic meter. The standard was reduced to 2 milligrams per cubic meter after December 30, 1972 and has remained at this level.32 Because of the difficulty of adapting to this standard an Interim Compliance Panel was authorized to issue a permit for non-compliance for a dust concentration as high as 4.5 milligrams per cubic meter while the standard was 3 milligrams per cubic meter, and for 3 milligrams per cubic meter when the standard was 2 milligrams per cubic meter. However, by December 30, 1975 the 2 milligrams per cubic meter was to be met. In the U.S. we are still not meeting that standard in all mines. The Mine Safety and Health Ad ministration has developed an elaborate sampling procedure to insure compliance with this standard. The procedure in volves sampling key occupations or key locations in toe mine. The progress in duk control in mines has been achieved with a regulatory inspectorate for approximately 275,000 miners that equals the inspectorate of toe U.S. Occupational Safety and Health Administration, which has responsibility for over 75 million workers at all types of worksites. Mine Safety and Health Administration inspectors in the United States visit every mine many times in a given year; toe probability for a visit by an OSHA inspector to a workplace are, on the average, less than one in 50 for most businesses. RISK LEVEL OF PRESENT STANDARD Since 1982, there has been major emphasis on risk assess ment in toe regulatory process in the U.S.30 The 1969 U.S. Conference Theme Presentations standard for permissible dustiness in mines was keyed to toe British standard. It is interesting to review toe risk level estimated to be associated with that standard. The interpreta tion of risk level can be derived from the British and the Ger man epidemiological studies, hi England the 25 pit study pro vided toe data base.22 In the British studies toe quartz in toe coal dust varied from 0.8% to 7.8% (respirable dust), with an average of 4.1 %. The progression of the disease seemed to be associated with the quartz content of toe respirable dust. Nonetheless, the probability of occurrence of 0/1 ILO classification x-ray for mean dust concentration of 2 milligrams per cubic meter for 35 years of exposure, is ap proximately 4%. The probability that a man starting with no pneumoconiosis (category 0/0) will be classified into 2/1 or higher after 35 years exposure to 2 milligrams per cubic meter is about 1 1/2% for low rank coal; 3% for high rank coal.31 The U.S. estimate of CWP category 1 at 2 mg/m3 is 9%; category 2 is 1-2%. In terms of current risk levels being discussed in toe United States for other airborne con taminants, this is a somewhat high risk level. For example, the current estimate of risk at 0.2 fibers per cc for 35 years asbestos exposure is 0.7 % for lung cancer and mesothelioma, with virtually zero risk of asbestosis. The 35 year time base for estimate oftoe risk is the same as that for respirable coal mine dust. The German epidemiological studies occurred in 10 coal mines over a 10 year period.29 A cumulative dust index was utilized based on light scattering measurement of toe dust. Thus, the dust measurement was dependent cm some func tion of toe dust surface area. The German investigators related toe Tyndallometric fine dust concentrations to the gravimetric fine dust concentrations measured with a cyclone/filter collecting device. They concluded that the ratio varied with coal rank; therefore, there was considerable uncertainty in a general correlation, but they did correlate by high, medium and low ranks of coal. Using the index developed, a cumulative dust value of50,000 was associated with definite pulmonary change. The parameters influenc ing the conversion from light scattering to gravimetric measurements were a dirt concentration factor and the fineness factor of the dust, which influences the degree of forward scattering of light in the instrument. The concen tration range of 0.9 to 1.5 milligrams per cubic meter as measured by the cyclone, was estimated to correspond to a cumulative fine dust concentration measured by light scat tering of about 125,000. If I correctly interpret the publica tion describing these results, there would be a risk of about 5 % oflight to medium pulmonary changes with a 6,000 shift exposure to approximately 1.5 milligrams per cubic meter, indicating a risk level about that encountered in Great Bri tain and the U.S. These estimates are very intimately associated with the rank of coal and my conversions are therefore a rough estimate. Chemical Composition of Dust and Coal Miners* Pneumoconiosis The pathophysiology of coal miners pneumoconiosis is still not well understood. The presence of quartz in the dust is a confounding factor. The present tools for disease diagnoses, namely x-ray and pulmonary function testing, cannot dif 35 Conference Theme Presentations ferentiate in the living miner between silicosis and coal workers pneumoconiosis. There is considerable disagreement at die lowest ILO classifications re: die disease state. Prom ising efforts to understand the disease state, as reflected in the present research emphasis, appears to be correlation of residual dust components for dust retained in the lungs and analyzed post mortem, with components of die exposure dust.94 In particular, there seems to be increasing emphasis in the United States on free silica content of mine dust. MSHA is increasingly stressing the silica content ofthe dust. The classification in 1986 by the International Agency for Research on Cancer of crystalline free silica as Class 2A gives further impetus to die emphasis on free silica.33 The inability to estimate the free silica of die airborne dust on the basis of settled dust has long been known.12 It is now possible to measure free silica in respirable dust samples with a sensitivity of 1-10 micrograms, depending on technique, and it is anticipated that with die IARC classification there will be a change of the current U.S. silica standard, which is presendy stated as a sliding scale for permissible dustiness based on free silica content. In summary, the control ofdust in mining has witnessed enor mous progress during die past 20 years, stimulated by in creased regulation in many countries, including the U.S., and innovative development of standards in South Africa, Germany and England, standards preceded by extensive epidemiological investigations that provided an estimate of die risk levels associated with adopted numbers. Areas of knowledge that required development to efficiently imple ment dust reduction in mines were the deposition of dust in the respiratory tract and the physics of dust, die latter re quired for instrument development and sensitive analytical techniques to measure the dust collected. Different nations took different approaches to the evaluation of dustiness but almost all now utilize gravimetric methods, for both feasibili ty and for scientific reasons. When compared to risk levels associated with standards now being adopted for other air borne contaminants in die United States, there is need to fur ther consider the airborne respirable mine dust standard. Re cent classification by IARC ofcrystalline free silica as a Class 2A carcinogen strongly suggests die need to better under stand the exposure to and impact of free silica in coal mine dust, in particular. Having discussed selected topics in die control of mine dust, I will now briefly look at the progres sion of dust control techniques in mines. What are the technologies that have brought about this progress and bow much further can we exploit these technologies, or are other "understandings" needed to make further progress? DOST CONTROL TECHNOLOGY Ventilation The Office ofTechnology Assessment in its 1984 report Con trolling Hazards in the Workplace27 introduced the ter minology of the "hierarchy of controls," with engineering controls at die top of die hierarchy and administrative pro cedures and work practices following; personal protective equipment is the last intervention to control exposure. Among the engineering controls are control at die source and con trol by substitution. The seven engineering controls listed by OTA are shown in Table I. In 1950 in a review of 36 literature on dusts,14 die authors quote Harrington, a 1934 reference18 with regard to die control of dust in mines. Har rington indicates that ventilation, fire protection and preven tion, health, safety and efficiency are very closely interlocked in mines. He indicates that ventilation is perhaps die major route for control ofhazards in mining, both in metal and non metal mines, permitting the worker to exert himself in com fort at maximum physical capacity without endangering his health. He focuses very heavily on "die best remedy for the dust menace in mines, other than preventing its formation, is the universal coursing ofcurrents ofair to remove the dust, as it has been proved that die very fine, most dangerous dust in metal mines remains suspended..." Harrington indicates that spraying devices available to reduce dust while drilling may be effective if used intelligently. However, they may even intensify the air dustiness if used without intelligence and, unfortunately, the latter is generally die case. He points to die availability of efficient water drills. Harrington also indicates that while finely divided dust "in mines is probably the chiefcause ofminers consumption, it is now recognized that there may be other factors of almost equal influence, such as high temperatures and humidities, harmful gases, and lack of air movement; all of these defects are readily remedied by ventilation." Table II is a summary of ap proaches or "lines of attack" for dust control in mines, as presented by Hamilton in 1972.17 It differs little from Har rington's approach. Table I OTA Hierarchy of Controls: Engineering Controls Elimination Substitution Isolation Enclosure Ventilation Process Change Product Change Table U "Lines of Attack" for Dust Control in Mines17 1 2 3 4 1. Removal and dilution of dust by ventilation. 2. Contol of the formation and dispersion of dust by atten tion to the method of mining and the way in which machines are operated. 3. Application of water, either to limit the dispersion ofdust into the air, or to suppress airborne particles. 4. Use of exhaust ventilation to contain dust sources, fol lowed either by ducting the dusting air to unoccupied parts ofthe mine, or by filtration before returning it to foe mam ventilation current. The use ofwater in drilling and in mining has a long history. The British Coal Mines Act of 1911 required that a drill worked by mechanical power` `shall not be used for drilling in ganister, hard sandstone, or other highly siliceous rock, the dust from which is liable to give rise to fibroid phthisis, unless a water jet or spray or other means equally efficient is used to prevent foe escape of dust into the air."21 Water Water has also been used, particularly in Western Europe to infuse the coal seam prior to drilling. Coal piles have been wetted after blasting and after cutting. Permanent use ofwater is not possible because moisture can be detrimental to cer tain processes in minerals and in some mines limited quan tities of liquid must be used ifthe product is to be marketed. Wetting agents have been added to water and in recent years droplets have been electrified during spraying to increase contact with die dust. Foams has also been utilized, the theory being that dust particles will be trapped in the individual cells of the foam and subsequendy wetted by the liquid as the cells collapsed. The development of our understanding of aerosols and par ticles owes much to the concerns of mining. In particular, the work of the Safety in Mines Research Establishment in Sheffield, England and die Bergbaustaubsverein and the Silicosisforscungs Institut in the Ruhr were major con tributors to the pool of knowledge of the physical properties of dust as reflected in compendium volumes such as that by Green and Lane.15 Other summaries of particulate knowledge also reflect the contributions of investigators at these institutes who, although they were pursuing applied research, recognized the necessity for basic contributions on the physics and chemistry of dust. The names of Cartwright, Hodkinson, Davies, Robock, Hamilton and Timbrell im mediately come to mind. It is not my purpose here to dwell on the specific research investigations that lead to progress in the control of mine dust. Rather, I believe it is possible to discern the trends in this area, as reflected in comparing a 1980's review published in die United States with the earlier literature on dust control in mines. The review by Breslin and Niewiadomski4 of the United States Bureau of Mines was published in 1984 and reviews progress in dust control technologies for U.S. mines from 1969 to 1982. In this report die authors stressed the control of dust formation, primarily. The relationship of coal cut ting to the generation of airborne dust is highest on the priori ty list of the Bureau's dust control "understandings" for con trol technology. This is an extension of the innovative work by Hamilton in England.17 The type of cutting bit, the depth of cut, the possibility for injecting water through the bit, the number of bits used, are all aspects ofthis research program. Because the mining methodology in the U.S. is shifting very rapidly to longwall production the applications of these techniques to the longwall operation both at the cutting site and upstream are focused upon. As indicated in the earlier statements by Harrington, the dust movement caused by the application of water is of great concern in these investiga tions. Ventilation is still our major workhorse in die dilu tion and removal of dust through both blowing and exhaust, but a substantial gain is achieved through the use of water injection and control of cutting. The Bureau also focuses upon the use of dust collectors for trapping die dust; these operate both on scrubbing and filtra tion principles. The trapping of the dust after generation per mits the use of the air without its burden of respirable mine dust. The largest fraction of work performed by the Bureau in these years was for in situ testing ofthese techniques after Conference Theme Presentations laboratory evaluation. A great deal has been learned about the equivalent volume of air cleaned versus water pressure as a function of different types of spray nozzles in the wet type scrubbers. Wetting agents have also been tested and there is some reported incremental gain due to their use. In the course ofadvancement ofthis technology die Bureau lists the following basic "understandings" which have come from this work. Laboratory studies showing the relationship between dust generation and the specific energy used to cut coal. Studies of deposition of aerosol on electrostatically charged surfaces. Experimental research on the dynamics of water drops impacted on surfaces. Development oflaboratory apparatus for generating water drops of uniform size and for measuring drop size. Measurement of the adhesion force between dust particles and surfaces. Characterization of the physical and chemical properties in mine dust. Development of technology for automatic measurement of particle size, shape and composition using a scanning electron microscope. Studies of the efficiency of dust sampling inlets. Development of apparatus for generation of laboratory aerosols. Studies on the effect of water sprays on air movement and dust suppression. The Bureau indicates that fundamental research was done with the ultimate long term goal of improving technology for control of dust in mines and that meant many of these areas of knowledge have applications in areas other than min ing. The National Academy of Sciences in 1980 issued a report25 in which the Academy directed the Bureau towards research which "should be directed more toward obtaining fundamental understanding of the origin, transport and characteristics of respirable coal mine dust. ' ' One could say this is expected from an Academy report, but I prefer to think that there is finally broad recognition of the need to under stand fundamentals in order to develop technology. The future goals ofthe dust control technology in the Bureau are also of interest. They are stated as: Optimization and in mine application of the new water spray system ("Shearer/Clearer") for longwall dust control. In-mine evaluation of new and emerging longwall dust control technology. Determination of the applicability and effectiveness of water powered scrubbers at longwall operations and on continuous miners. Completion of field evaluation and application of a mine worthy twin scrubber system for continuous miners. 37 Conference Theme Presentations Development and testing of optimal ventilation systems for dust control during continuous miner operations. Redesign, testing, and application ofan improved canopyair curtain system in underground as well as surface operations. Development of a basic understanding of die formation of transport of dust during the cutting cycle for develop ment of more effective controls. Development and testing of improved bagging machine dust controls, bag ceiling, cleaning and disposal techniques for the mineral processing industry. Development of dust suppression systems for cutter machines and other equipment used in conventional min ing operations. Development of improved dust controls for conveyors, transfer points and stage loaders. Determination of cutting force in coal seam for use in development of deep cutting machines. Development and testing of improved personal dust exposure. It would be interesting to compare these research goals for control of dust in mines with those of other nations commit ting significant expenditures to development of dust control technology at the national level. As one reviews progress in this field over die past 50 years, it is striking that die im petus for sharing of information has come from die profes sionals and the professional associations and not through their governments. Thus, die first International Pneumoconiosis Conference was held in South Africa, very much due to the efforts of Dr. Beadle, who was preeminent in development of a dust control and medical surveillance program in South Africa. The inhaled particles and vapors series of con ferences, a major stage for sharing of information by in vestigators and practitioners, was sponsored by the British Occupational Hygiene Society. The overlapping of many research program areas is apparent in die past. One wonders if we can become more efficient in our approaches to development ofthese new technologies. The scientific com munity will always sham results, but the planning of research could greatly benefit by such an international effort. It is impossible to not be struck by our utilization ofthe same workhorses for making progress with dust control in mines. We have reached die limit for bringing air to the face and diluting the generated dust. We are probably on the asymp totic portion of die curve for extracting greater efficiency from the application of water, either through the cutting tool or after the cut. We are in need of some new, innovative approaches. In view of the enormous progress over the last 2-3 decades with our understanding of disperse systems and aerosols, it would appear there is opportunity for introduc ing new and innovative ideas into dust control technology. There are analogies in other fields to this need. The treat ment of hazardous waste is receiving major impetus because the major workhorse heretofore has been burial and storage in the ground, which has run its course and is associated with great risks for the future. New technologies are appearing 38 and will undoubtedly have a major impact on die quantities of materials disposed of to ground by 1995. The Superfund Act and its recent renewal have stimulated this work. While the impression in England and perhaps also in die United States is that we have4 `solved* ' die problem of coal workers pneumoconiosis and dust in mines, in general, it is incum bent upon us to make clear that this is by no means true. We have made enormous progress, but it remains to bring our risk levels in concordance with those accepted for other work environments. Doing this efficiendy requires knowl edge and knowledge requires investment of funds. On this note I would like to end. The story of dust control in mines has some logical development. It is troubling that die current perception is that die job is done, and that diver sification of scientific effort and funds from this subject area is occurring in many countries. We must correct this er roneous perception in order to maintain and continue the hard won gains to date. REFERENCES 1. Bedford, T. and Warner, C.G.: Chronic Pulmonary Disease in South Wales Coal Miners. M.R.C. Special Report Series, No. 244, H.M.S.O. London (1944). 2. Blacktin, S.C.: Dust. Chapman and Hall, Ltd. London (1934). 3. Bloomfield, JJ., Dallavalle, J.M., Jones, R.R., Dieessen, W.C., Bnm- dage, D.K. and Britten, R.H.: Anthraco-silicosis Among Hard Coal Miners. Public Health Bulletin Number 221. U.S. Government Print ing Office Washington, DC (1936). 4. Breslin, J.A. and Niewiadomsld, G.E.: Improving Dust Control Technology for U.S. Mines; The Bureau of Mines Respirable Dust Research Program, 1969--1982. Bureau of Mines U.S. Department of the Interior. Washington, DC (1982). 5. Brown, C.E.: Quantitative Measurements of the Inhalation, Retention and Exhalation ofDusts and Fumes. B.Y.Moui.J. lod. Hyg. 13:285-301 (1931). 6. Brown, J.H., Cook, K.M., Ney, F.G. and Hatch, T.: Influence ofPar ticle Size Upon the Retention of Particulate Matter in the Human Long. Am. J. Pub. Health, 40:450 (1950). 7. Chamberlain, E.A.C., Makower, A.D. and Walton, W.H.: New Gravimetric Dust Standards and Sampling Procedures for British Coal Mines, Inhaled Particles m, 1015-1030. W.H. Walton, Ed. The Gresham Press, Old Woking, Surrey, England, (1971). 8. Davies, C.N.: Filtration of Droplets in the Nose of the Rabbit. Pro. Roy. Soc., London, B., 133:282 (1946). 9. Davies, C.N., Aytward, M. and Leacey, D.: Impingement ofDust from Jets. Arch. Industrial Hygiene and Occupational Medicine, 4:354 (1951). 10. Disperse Systems in Gases: Dust, Smoke and Fog. Transactions ofthe Faraday Society, Gurney and Jackson, London (1936). 11. Drinker, P. and Hatch, T.: Industrial Dust, McGraw Hill Book Com pany, Inc., New York (1936). 12. Drinker, P. and Hatch, T.: (1954). Op. Cit. p. 202. 13. Findeisen, W.: Uber das Absetzen Kleiner in der Luft Suspeodierter Teilchen in der Menschlicean Langer bei der Atmung. Pfliiggeis Arcb. Fid. ges Physiol. 236:367 (1935). 14. Forbes, JJ., Davenport, SJ. and Morgis, G.G.: Review ofLiterature on Dust. U.S. Department of the Interior Bureau of Mines, Bulletin 478. U.S. Government Printing Office, Washington, DC (1950). 15. Green, H.L. and Lane, W.R.: Particulate Clouds: Dust, Smoke and Mi^s. D. Van Nostrand Company, Inc., New York (1964). 16. Greenburg, L. and Smith, G.W.: A New Instrument forSamplingAerial Dust. U.S. Bureau of Mines Rept. Invest. 2392, (1922). 17. Hamilton, RJ.: Control of Dust in Mining. Chapter 8 in Medicine in tbe MiningIndustries, pp. 128-144. Rogan, J.M., Ed. W. Heinemann Medical Bodes, Ltd., London (1972). 18. Harrington, D.: Ventilation. Joum. Cbem. MET. and MIN. SOC. South Africa, 35:131-134 (1934). 19. Hatch, T.: Permissible Dustiness. Am. Iod. Hyg. Assoc. J. 16:1 (1955). 20. Hatch, T.F. and P. Gross: Pulmonary Deposition andRetention ofInbaled Aerosols, p. 149. Academic Press, New York (1964). 21. Hay, P.S.: A Method of Trapping tbe Dust Produced by Pneumatic Rock Drills. Safety in Mines Resboard Paper Number 23, London (1926). 22. Jacobson, M.,Rae, S., Walton, W.H., Rogan, J.M.: The Relation Be tween Pneumoconiosis and Dust Exposure in British Coal Mines, In haled Particles ZZZ, 903-920. Gresham Press, Oki Woking, Surrey, England (1971). 23. Landahl, H.D. and Herrmann, R.G.: On the Retention ofAirborne Par ticulates in the Human Lung. /. Indust. Hyg. A Toxicol. 30:181 (1948). 24. Lippman, M.: ''Regional Deposition of Particles in the Human Respiratory Tract." In Handbook ofPhysiology. Sec. 9. Reactions to Environmental Agents, Lee, D.H.K., Ed. American Physiology Society, Bethesda, MD (1977). 25. Measurement and Control of Respirable Dust in Mines. National Academy of Science Report NMAB-363. Washington, D.C. (1980). 26. Miners Phthisis Prevention Cotnmitttee: Pinal Report, Union ofSouth Africa, Johannesburg, January 10, 1919. 27. Preventing Injury and Illness in the Workplace. Office ofTechnology Assessment. U.S. Congress, Washington, D.C. (1985). 28. Phalen, R.E., et al.: Rationale and Recommendations for Particle Size Selective Sampling in the Workplace. Appl. tod. Hyg. 1:3-14 (1986). 29. Reisner, M.T.R.: Results ofEpidemiological Studies offtieumocuniosis in West German Coal Mines. InhaledParticles W, pp. 921-931. W.H. Walton, Ed. Gresham Press, Old Woking, Surrey, England (1976). 30. Risk Assessment in the Federal Government: Managing the Process. National Academy of Sciences. Washington, D.C. (1983). Conference Theme Presentations 31. Seaton, A.: Presentation at Special Meeting, VII International Pneumoconiosis Conference, Pittsburgh, PA, August 22, 1988. 32. Schlick, D.P.: Respirable Coal Mine Dust Standards InhaledParticles IB, 1007-1013. Gresham Press, Old Woking, Surety, England (1971). 33. Silica and Some Silicates. IARC Monographs on the Evaluation of the Carcinogenic Risk ofChemicals to Humans. Volume 42. IARC, WHO, Lyon, France (1987). 34. Sweet, D.V. et al.: The Relationship of Total Dust, Free Silica and Trace Metals Concentration to the Occupational Respiratory Disease ofBituminous Coal Mines. Am. tod. Hyg. Assoc. J. 35:479-488 (1974). 35. Task Group on Lung Dynamics: Deposition and Retention Models for Internal Dosimetry ofthe Human Respiratory Tract Health Pbys. 12:173 (1966). 36. Van Wijk, A.M. and Patterson, H.S.: The Percentage of Particles of Different Sizes Removed from Dust-Laden Air by Breathing. /. Industr. Hyg. A Toxicol. 22:31 (1940). 37. Whydaw-Gray, R. A Patterson, H.S.: Smoke: A Study of Aerial Disperse Systems. Edward Arnold and Company, London (1932). 38. Wilson, l.B. and LaMer, V.K.: The Retention of Aerosol Particles in the Human Respiratory Tract as a Function of Particle Radius. J. In dustr. Hyg. A Toxicol. 30:265 (1948). 39. Wright, B.M.: A Size-Selecting Sampler for Airborne Dust. Brit. J. tod. Med. 11:284 (1954). 40. Yaffee, C.D., Byers, D.H. and Hosey, A.D.: Encyclopedia of In strumentation forIndustrialHygiene. University of Michigan. Ann Ar bor, Ml (1956). 39