Document 3QNNdRjNG4ReEx0krnr905pEO

The following papers were presented at the -1970 annual meeting of the M.A.P.A.O.'s Committee on Occupational Health held in Toronto on May 20, 1970. The papers deal with problems of improving mine working conditions in the areas of dust control and noise abatement, with special emphasis this year on methods of dust collection. fp[^j[^ppg EXHIBIT -UC-186. Health hazards of dust inhalation (pneumoconlosi* By J. E. COWLE* There are many definitions of the word pneumoconiosis but for practical purposes it may be considered to mean the deposition and retention of dust in the lungs. The term does not necessarily imply that significant structural change has occurred in the lungs or that dis ability has been produced even though extensive and abnormal shadowing may be observed on the chest x-ray film. How the lung handles inhaled dust When the dust-laden air is inspired it passes through the nose and/or mouth, down the trachea (windpipe) and through the various bronchial tubes to the alveoli (small air sacs) across whose walls the exchange of oxygen and carbon dioxide takes place. Dust particles of greater than five microns in.diameter are almost invari ably trapped in the layer of sticky mucus which coats the nose, sinuses, trachea and bronchi. Because many of the cells of this membrane are ciliated and because the waving action of these little cilia moves the mucus layer up ward toward the throat, the large dust particles are either expectorated or swallowed. Panicles of less than 0.1 micron diameter behave differently and. although some may be retained >n the iung tissue, a great many remain within the alveolar air and flow out 3Sain on expiration. Particies whose diameter is between 5 and 0.1 microns are. therefore, the important ones insofar as the various `vk.T'ior Physician. Uvc'ap.honai Chest Disease Unit hr.vironmema! Health Branch, ^spt- ci Health for Ontario. pneumoconioses are concerned, (the exception being asbestos fibres). Dust particles in this size range settle on the walls of the alveoli and many of them gain entrance to the lung tissue by passing through the alveolar walls in some manner which is not fully un derstood. They are then engulfed by phagocytes (dust cells) whose task is to remove foreign material from the lungs. It is believed that the dust laden phagocytes then enter the lymphatic system and flow to the lymph glands in the hilae (lung roots) where they are usually arrested. If the inhalation of dust continues over a period of years, the hilar lymph glands appear to be come saturated with dust and the pha gocytes then begin to be arrested in the much smaller aggregations of lyjnphoid tissue scattered throughout the lungs, predominantly at the points where the bronchial tubes bifurcate. It is in these locations that the dust if opaque (as in the case of iron) can be seen on chest x-ray and it is here that the be ginning of fibrosis of the lung (if the dust is fibrogenic) occurs. Classification of mineral dusts It is doubtful that any dust can be re garded as harmless under conditions of extreme exposure. In general, how ever, dusts may be divided into two broad groups depending on their abil ity to evoke a fibrous tissue reaction in the lungs. For practical purposes they may be classified as follows. (See Table I). Inert dusts ^ U 5 zl 0 The dusts in this group do not as a rule produce a fibrotic reaction with in the lungs. They maj as in the case of iron, barium and tin which are ra dio-opaque produce extensive shadow ing on chest x-ray. They are chiefly important because the x-ray changes which result from their retention in the lungs may be misinterpreted and con sidered to represent disabling pneumo coniosis. There is some difference of opinion as to whether pure carbon or graphite can produce significant pulmonary fi brosis but there is little evidence in the medical literature to support the oc currence of disabling pneumoconiosis due to this exposure in the absence of fibrogenic dust. Fibrogenic dusts Although the inhalation of fibrogenic dust is essential for the production of disabling pneumoconiosis, individual Dr. ]. E. Cowle was I barn in Taranto and ...I received his early education in Toronto tv. schools. In 1942 he { I I i J & /______ graduated from Uni versity of Toronto. He served in the Canadian Army from 1943 to 1946 and retired with the rank of Major. Dr. Cowle had a private practice from 1947 to 1952. In 1953 he received a U of T diploma in public health and since that time has been employed by the Ontario Department of Health where he is presently senior physician in the Occupational Chest Diseases Section. He is also secretary for the Advisory Committee on Occu pational Chest Diseases (Ontario W.C.B.). cp. *./,4.iccmi 10 pifcij* fin important part 'in determining the degree of tibresis produced. Other factors also are of prime im portance in the production of pneumo coniosis. Of these the chief ones are: a) Intensity of exposure (dust counts) b) Panicle size c) Content of the fibrogenic substance in the dust (e.g., SiO)' d) Length of exposure -- usually in years e) Age at first exposure f) Presence of other pulmonary con dition, e.g., tuberculosis Since this meeting is mainly con cerned with prevention of occupational illness and injury as it affects Onta rio miners the following remarks will be. confined to a consideration of the more important aspects of silicosis. It should be remembered that while these remarks refer in general to sili cosis regardless of industry and geogra phy they are specifically based on ex perience in the province of Ontario. Silicosis Silicosis, because of the numbers of men involved and the degree of dis ability produced, has been and prob ably still is the most important of the pneumoconioses. It results from the prolonged inhalation of dust contain ing a significant concentration of free crystalline SiO:. Dusts containing not more than 107c silica rarely produce problems. Dusts with higher concen trations of silica are. of course, more important and broadly speaking the risk of producing silicosis increases with the silica content. As previously noted the significant portion of the in haled dust embraces the particles whose diameter falls between 0.1 and 5.0 microns. The previously described manner in which the lung handles dust applies to silica. The reaction of the lung to the silica-laden dust cells is to lay down fibrous tissue in a whorled arrange ment so as to produce a nodular lesion. As previously noted these tend to fol low the distribution of the lymphatics which are intimately related to the tiny blood vessels and the bronchial airways. The earliest silicotic nodulation is found in the glands at the lung root and immeditely beneath the pleural surface of the lung. These early changes are not specific on chest x-ray and produce no disability because they do not involve the respiratory portion of the lung. When further progression has taken place, silicotic nodules occur within the lung tissue and it is at this stage that the nodules cast their sha dows on x-ray and begin to diminish the breathing capacity of the lung by causing structural change. 62 lAbLE l Ciassuicanon ot dusts according to their ability to evoke a fibrous tissue reaction in the lungs Fig. 1 Tnis section demonstrates nodular silicosis. The silicotic nodules appear as rounded black densities since they contain many carbon panicles which Inert dusts Fibrogenic dusts produce the black colorization. Silicosis of this degree usually does not Iron dust Free crystalline silica (Si0;) produce significant disability Limestone Amorphous silica if calcined Fig 2 This section demonstrates the Marble Most silicates Tin Barium Coal Asbestos (fibrous silicates) Talc Nepheline syenite (low grade fibrogenieity) presence of silicotic nodules in the lung. The main feature is that many of the nodules in the upper lobe of the lung have coalesced producing a massive lesion. This was due to superimposed tuberculous infection. Lesions of this type distort the lung architecture and While under poor environmental produce disability conditions silicosis can develop quick ly (eg., 2-5 years in an unprotected sandblaster) with effective dust control this time can be greatly lengthened and the numbers of men affected kept to a minimum. Of all men who have entered Ontario mines since 1940 only Fig. 3 Nodular silicosis with a massive conglomerate lesion in the upper lobe due to superimposed tuberculosis. The disease in this case was so severe as to cause actual breakdown of the massive lesion producing a tuberculous . cavity. Serious disability accompanied seventy-six have developed radiological this advanced type of lesion evidence of silicosis as of October 1969 and of these 789c had significant previous exposure elsewhere. This means that since 1940 of all men who have worked only in Ontario mines, only seventeen are. at this time con Fig. 4 Massive silicosis is beautifully demonstrated in this section. At least two-thirds of the lung is the site of a mass of silicotic nodules which have run together to form a solid lesion. These solid lesions, of course, contain sidered to have silicosis. no air and the patient whose other While all figures concerning men who began mining since 1940 are not yet available it appears that the mean elapsed time from first exposure to the earliest evidence of silicosis in chest film is in the order of 25-30 years. lung was equally affected was breathing with no more than one-third of h?s total lung substance. Such far advanced cases were more common previously when tuberculosis among siiicotics was more common and before we had drugs for treating this condition. Simple silicosis Fortunately, we see relatively few cases with this far advanced and crippling In the absence of complications, the condition nowadays most important of which is tuberculo sis, silicosis causes little disability. Re tained silica in the lungs produces fi brous nodules along the course of the lymphatics, the bronchioles and the blood vessels which bear an intimate on chest x-ray begins to coalesce with the development of larger conglome rate shadows. This usually, although relationship to each other. The produc not invariably, indicates that a tuber tion of fibrous nodules may progress culous infection has become superim for several years after cessation of ex posed upon the silicotic process even posure and then gradually arrive at a though the tubercle bacilli may not be state where the reparative processes of found in the sputum. the lungs successful!}' contain the fibro The most serious feature of silico genic silica particles. In most such cases sis lies in the fact that its presence the tremendous functional reserve of predisposes to tuberculous infection. In the lungs is such that the amount of some siiicotics the tuberculosis runs an lung tissue replaced by the fibrotic no acute course; more commonly, how dules is usually of minor importance ever, the combination of tubercle ba and causes little disability. If the cilli and inhaled quartz produces chro amount of nodulation is sufficient to nic fibrosis of the lungs which slowly interfere with the elasticity of the lung spreads over a period of many years. then this pliable organ becomes less Contraction of the masses of fibrosis elastic and the amount of air flowing grossly distorts the lung tissue and in and out on respiration is decreased. often results in the formation of areas At this stage of silicosis the chest x- of emphysema in the less affected por rays exhibit nodular shadowing and tions of the lung. Such a condition the workman may complain of some causes considerable shortness of breath degree of shortness of breath on exer and if severe may produce total respi tion. ratory disability. The usual symptoms Complicated silicosis of tuberculosis such as fever, night sweats, loss of weight and productive Complicated silicosis is considered to cough frequently are not present. The be present when the nodulation seen dyspnoea, (shortness of breath) and A r\'intiv \*vtvr Ini'p'-n F Fi rw uojOnii.. \vcic lormcrty Qc- lieved to be characteristic of silicosis were in most instances due to the mas sive fibrosis and secondary emphysema which .foilow the combined action of tubercle bacilli and silica. Simple sili cosis alone does not appear to cause emphysema with its resultant disability. in the 1920's and 1930's the cause of death in the overwhelming majority of silicotics was pulmonary tuberculo sis and the mean age at death was' below fifty. By the mid 1940"s silico tics were living longer and the number of tuberculosis deaths declined. Within the last few years silicotic miners are living at least as long as the average adult male in the general population and the present death rate from tuber culosis is down to about 3.9c. Most silicotics are now dying of conditions unrelated to their occupation. From time to time the question of whether there is an increased incidence of deaths from lung cancer among sili cotics has been raised. Our records as well as those from Great Britain and South Africa demonstrate that this is not the case. Lung cancer has in re cent years very greatly increased in the male population but there appears to be no statistically significant excess among silicotic miners. Prevention While a knowledge of the manner in which silicosis develops, the disability which it produces and the complica tions which may accompany it is of importance, the prime objective of all efforts in this field must be prevention. This should hold the uppermost priori ty in our approach to the problem and we must never become complacent in this respect even in the light of vast improvement in the incidence of new cases. Silicosis is preventable and the ultimate aim of all concerned should be its total extinction. The measures aimed at the prevention of silicosis are: a) The engineering control of dust in the mining environment. b) The medical measures offered by pre-employment selection and pe riodic screening. c) The inhalation of McIntyre alumi num powder. d) The hope that P.V.N.O. may be useful in prevention when inhaled and in treatment when given by injection. Engineering methods It would be presumptive for the writ er to comment seriously on the engi neering aspects of dust control. It is. however, felt in order to mention that surface workers such as those sharpen ing drills and those working in appa rently clean mills and assay offices have on occasion developed silicosis. 64 ouen occupations shouja never be over looked in any assessment of dust con ditions and where indicated should be considered in every respect on the same basis as underground workers. It would be folly to place in such work areas, `poor risk" men who are considered medically unfit to work underground. In addition, in mines and mills where the free silica content of the dust is in the order of 70-909c, extraordinary measures are indicated and constant care is essential to maintain dust con trol at a very high level. As long as men are required to work in an atmossphere containing a significant amount of free silica, the engineer must never relax his vigilance. Medical methods The injurious effects of mining on the lungs and the lives of miners have been known for over four hundred years. As early as 1556 Agricola wrote con cerning the work of mining "when the dust is corrosive it ulcerates the lungs and produces consumption". Even three hundred years before the discov ery of the tubercule bacillus, it was known that miners ran an extremely high risk of dying of this disease which was referred to as consumption. With the discovery of the tubercle bacillus in 1881 it was soon recognized that it was infection by this organism which produced virtually all of the serious chest complications in miners. It became apparent shortly after the turn of the century that persons with silicosis are extremely susceptible to tuberculosis. In addition, it was also observed that persons with tuberculosis of the lungs whether active or "healed" are poor risks for work in silica expo sure since they are likely to develop active tuberculosis or silicosis or a combination of the two. The establish ment of the miners' Phthisis Bureau in South Africa in 1916 began an era of attack on tuberculosis and silicosis which has continued to the present. As a direct result of the earlier ef forts in South Africa, steps were taken to set up a similar program of exam ining applicants and miners in Onta rio. In 1928 the Mining Act was amended to require the compulsory pre-employment and annual examina tion including chest x-ray of all per sons in Ontario mines exposed to sili ca dust for at least fifty hours per month. The legislation came into ef fect in January' 1929 and miners' chest examining stations were opened by the Workmen's Compensation Board in all mining camps. Since that time applicants found to have x-ray evidence of present or past tuberculosis of the lungs are rejected for silica exposure work. In addition compulsory annual examinations are conducted on all miners in order to regarding or move from the exposure area any men-^ silicotic who develop tuberculosis. The signih- ultimate p: cance of this action is that `poor risk" is still not men are prevented from entering ex- definite c posure in the mines and those miners made at t' developing tuberculosis are Temoved To beg from exposure as early as possible and that the ir. treated. This is of benefit not only to. in the c. the men with the infection but also to, duced ill their fellow workers who might con-, based on tract tuberculosis by working and as-, inations sociating with them. 'miners at Since compulsory examinations be- post mot gan there has been a very' significant on the 1 drop in the numbers of new cases of \ cotic mi: silicosis which have developed. Of course, it would be folly to attribute this entirely to the medical examina tions because over the same period of time much has been done to decrease dust exposure by engineering methods. In addition, tuberculosis in the general population has gradually declined due to a vigorous public health program. The improvement is due to the com bined effects of these and probably to other factors. In addition to the above, drugs for the effective treatment of tuberculosis became available about 1950 and short ly thereafter the prophylactic use of these same drugs was made available to men with silicosis. Since 1957 most silicotics have been given a course of the same drugs which are used to treat tuberculosis in an attempt to prevent this serious and often very disabling complication. A study of silicotics given these drugs as a preventive meas ure up to December 1967 revealed a dramatic drop in the development of active tuberculosis among those treat ed and an accompanying decline in the numbers of silicotics dying from tuberculosis. McIntyre aluminum powder dence to inhalatic of tubei When age goh (and th those a of elap diagnos prophv not si. If alur vent o silicosi is still be dc is no Ontar as "c pare ` inhah lactic ly de is nc a ve cone be 1 min effe wht to l riec The use of inhaled aluminum powder (McIntyre) as a prophylactic agent ide tiv< against the development of silicosis was introduced into the Ontario gold mines in 1944. It has now been dispersed in change rooms for 25 years and there Po <p T! fore is deserving of mention. To begin with it should be noted a w that its use is based on earlier experi ib mental work in animals where it was shown to prevent or retard the develop v ment of silicosis under carefully con 1 trolled conditions. It was, therefore, in > the hope that similar benefits would follow its use in humans, that its dis persal in change houses was initiated. It should further be noted that alumi num prophylaxis has never been claimed to be a substitute for good dust control and careful medical selection and regu lar examination of miners. It must be looked upon as a supplementary meas ure which may benefit miners by re- p p r\ p ^ JuS Pix'initv XtivTvr Inmvii taiding or preventing the development of silicotic lesions in the lungs. The ultimate proof of its effect in humans is still riot certain but there are some definite observations which can be made at this time. To begin with there is no evidence that the inhalation of aluminum powder in the concentrations used has pro duced ill effects. This statement is based on a great many physical exam inations of silicotic and non-silicotic .miners and on a significant number of post mortem examinations, performed on the lungs of silicotic and non-sili cotic miners. There is likewise no evi dence to suggest that aluminum powder inhalation enhances the development of tuberculosis. When one considers that the aver age gold miner who develops silicosis (and this is a very small percentage of those at risk) requires about 25 years of elapsed time from first exposure to diagnosis, it is at once obvious that the prophylactic use of aluminum has still not significantly exceeded that time. If aluminum powder does in fact pre vent or even retard the development of silicosis a further period of observation is still required before such effects can I be documented. Unfortunately, there is no specific group of gold miners in Ontario which might be looked upon as "controls" against which to com pare the experience of those who have inhaled aluminum powder as a prophy lactic. In addition, the number of new ly developed silicotics in the gold mines is now so small that it would require a a very dramatic change before a firm conclusion could be drawn. It should be kept in mind, however, that if alu \n minum pow'der has had a beneficial m effect this has occurred during a period when the engineering-medical efforts to control silicosis have also been car ried out. It may well be impossible to :er identify which has been the most effec :nt tive. vas nes Polyvinyl-pyridine-N-oxide in (PVNO or P204) ::e- The problems of disabling pneumoco niosis which motivated the research -?ted. i with aluminum powder in Ontario in :en- the 1930`s have also been vigorously was approached by a group of research iop-' workers in Western Germany since con-' 1953. The magnitude of the West Ger ;. in' man problem can be realized from the Olild fact that there are presently about dis- 700.000 men employed underground r.ed in coal mines and some 85.000 receiv ,u"ni- ing workmen's compensation payments .i-ned for disabling pneumoconiosis. ?r.ucl This research work has been carried regu- out at the state sponsored Medical Re :s: bf search Institute of Silicosis and Air Hygiene at the University of Dussel-v rc dorf. In 1960 the present director of this institute published a paper on the beneficial effects in animals of polvvinyl-pyridine-N-oxide, a highly poly meric powder which is readily soluble in water. This substance is more sim ply referred to as PVNO or by its test number P204. Professor Schlipkotcr's observations are summarized by him as follows: "1) PVNO suppresses the experiment al development of silicosis in several kinds of animals and protects the cell from quartz necrosis, ie.. it annuls the cytotoxicity of siliceous dust. 2) The highly polymeric N-oxide has not only an inhibitory effect on the development of the fibroblastic reaction to quartz, but also a genuinely thera peutic one on an existing quartz silico sis. Parenteral application, particularly the intravenous injection of 100 to 200 mg. of PVNO per kilogram of body weight, achieves the retrogression of an advanced silicosis in the animal ex periment. 3) PVNO markedly improves the bronchial clearing of the lung and also reduces the SiO: contents of the lymph nodes, i.e., it reduces the penetration of the dust through the relatively dust proof barrier between the alveoli and the interstitium. An increased elimin ation of the quartz dust and a delay in the transfer of dust into the parabronchial lymph nodes can be achieved by weekly inhalation of a highly dilut ed PVNO aerosol. These three effects of this substance could be proved by numerous animal experiments. Since no side effects of the PNVO have been observed to date and the toxicological investigations have been concluded, the clinical test ing on patients suffering from silicosis have been initiated." Professor Schlipkoter visited Can ada in April 1969 and presented a pre liminary review of this work. He warned that the results in animals should be interpreted with caution in sofar as they might be projected to hu mans. He did. however, report that in January 1969 a selected group of about sixty miners with pneumoconiosis were started on treatment with PVNO in six hospitals in West Germany and Austria. In a recent personal commu nication to Dr. John F. Paterson he in dicated that this clinical trial is con tinuing and is under the direction of Dr. Grundmann. As yet no reports concerning the results have been pub lished. In addition to the trial to ascertain the value of PVNO in treating estab1 i s h e d pneumoconiosis, Professor Schlipkoter advised that permission was granted by the West German Min istry of Economics early in 1969 to institute a prophylactic trial of PVNO among the underground workers at one coal mine. The trial is to take the form of the inhalation of the powder for one hour once a week. To date no re ports have been forthcoming regarding this trial. Much interest has been stimulated by this work and it is hoped that within the next year or two more will be known concerning the effectiveness of PVNO. Results of preventive measures It is only by a careful study of the ex perience among miners that the ef fectiveness of preventis'e measures can be assessed. The need for a statistical study designed to prepare and analyse data concerning the incidence, preva lence and progression of silicosis in the mining industry in Ontario was recognized over twenty years ago by a committee appointed by the Honorable Prime Minister in 1949. As a direct result of recommendations made at that time a Medical Statistical Unit was established under the Workmen's Compensation Board. Since that time this unit has not only reconstructed, from 'available records, the silicosis picture in Ontario from the earliest examinations in 1928-1929, but has maintained complete records on the examinations of all miners and former miners and has at appropriate intervals TABLE II Deaths-silicotics (after S. W McIntosh, March 1970) Period died 1926 -- 1929...................... 1930- 1934.................... 1935 - 1939 ................... 1940 -- 1911.................... 1915 -- 1919................... 1950 - 1S51 ............ 1955 - 1959 ... 1960 - 1961.................... 1965 - 1969...................... 1970 - 1974...................... No. 42 79 101 125 153 160 193 171 178 Due to tuberculosis Ave. age No. % Total Ave. age 43.3 47.9 50.7 52.8 58.8 62.4 65.1 67.9 MA c. 1/ Qu ^o 33 61 70 87 92 59 43 19 6 78.6 43.4 77.2 46.8 69.3 49.0 69.6 51.9 564 57.7 36.9 60.0 22.3 65.1 11.1 68.5 3.4 72.2 TABLE III Mew 5 ratings from 1927 to 1069'" by period of first Ontario exposure (excluding original examinations) (after W. C. Wheeler. B.A.) Period of First Ontario exposure Ontario Exposure Exposure Outside only Ontario Total Before 1910 1910 14 1915 -19 1920 - 24 . 1925 29 1930 34 1935 - 39 1940- 44 1945 - 49 1950 - 54 1955 - 59 1960 - 64 1965 - 69 Other (2) r 132 124 236 189 49 27 6 30) 3(1) 5(5) -- -- -- 51 71 59 107 147 57 28 12 4(1) 16(5) 25 (21) 2 0) . -- 11 128 203 183 343 336 106 55 18 7(2) 19C 6) 30(26) 2( 1) -- 11 Total 851 590 1,441 Tc September 30, 1969. <2)Meri with no exposure in Ontario. published repons. The figures referred to today are as up to date as possible and are taken from a brief report pre pared in October 1969. This has been kindly made available by W. C. Wheel er, B.A., Chief Statistician of the Workmens Compensation Board of Ontario. Figure 3, of this report (Fig. 5 here) shows the numbers of newly diagnosed cases of silicosis based on x-ray evi dence, per thousand miners in dust ex posure. It is apparent at a glance that an overall steady decline in the inci dence of new cases has occurred. The upper solid line represents all miners and the lower broken line those who have mined only in Ontario. Both lines indicate considerable improvement since 1930 but the difference between the two indicates the added risk in volved for men who have mined else where where conditions probably were less well controlled: There can be no doubt that the situation has improved tremendously and in my opinion this is the direct result of the preventive measures which have been taken. Table III from Mr. Wheeler's report shows the same data in a different form. The declining number of new silicotics is very clearly demonstrated when they are considered by period of first exposure. I draw your attention particularly to the small number of cases which have developed in men who. have begun mining since 1940. The improvement in the situation is obvious and it is hoped that it will continue but this will depend in large part on the care with which the pre ventive measures are maintained and possibly improved. Table II is a most informative tabu lation drawn up by S. W. McIntosh. It supplies further evidence of the ef fects of the preventive measures even in men who have developed silicosis. It shows dramatically how miners with silicosis are living as long as their nonsilicotic counterparts in the general population of the province. It also shows that the numbers of silicotics dying from tuberculosis of the lungs has dropped from a devastating 78 $3 to 3.49c in the years 1965-1969. While this latter figure is extremely good it should be interpreted with no compla cency when we note that the death rate for the general male population of On tario in the 60-69 age group during 1968 was only 10.3 per 100,000 and that it was considerably lower in men under 60. The continuing medical su pervision and the prophylactic use of anti-tuberculous drugs still appear to be very strongly indicated in men with silicosis. I wish to draw particular attention to Figure 5 with respect to the adverse trend in incidence since 1962. This in my opinion can be accounted for by a new and important factor. In the mid 1950's uranium mines came into ope ration in two areas of the province -- Bancroft and Elliot Lake. The native rock in the Bancroft area contains in the order of 109c free SiO: whereas in the Elliot Lake area is in the order of 70 9c. As one would expect the Ban croft area mines have not produced any cases of silicosis. On the other hand 35 of the last 58 new cases of silicosis in the prov ince have had some and a few have had all of their exposure at Elliot Lake. These men are indicated by the nura- j hers in brackets in Table III which I , have taken the liberty of superimposing 1 on Mr. Wheeler's table. j The pathological findings based on j examination of small portions of the j lungs of seven of these men have j shown a type of pathology which while | possessing some of the classical changes of silicosis also show other changes which are of a different na ture. This pathological picture is some thing not previously encountered in Ontario silicotics. It is not considered that radioactiv ity in the inhaled dust is modifying the picture as similar changes have not been observed in the lungs of silicotic miners from the radioactive dusts in haled in the mines in Joachimsthal, Czechoslovakia, St Lawrence, New- - foundland and the Colorado plateau of the United States. We do know that exposure in the Elliot Lake area can produce silicosis in 5-8 years and that, therefore, rela tively young men can be affected. We also know that in many of the cases the lesions seem to become stationary within a few years after exposure ceases. It would appear, therefore, that a modified type of silicosis results from this exposure, which requires fur ther investigation. It also is obvious that vigorous dust control measures Fig. 5 New 5 ratings per 1,000 mine employees in dust. All cases, and Ontario exposure only 1930-1967 (after W. C. Wheeler) 66 are. required to meet the problems created by this exposure. Conclusion The facts mentioned in this paper are strong evidence that a great deal has been achieved in Ontario in the pre vention of disabling silicosis and in the improved expectancy of life and the freedom from tuberculous compli cations among our miners. Only through the continued efforts using all available means will this situation con tinue. In fact renewed efforts should be put forth by all concerned in an at tempt to further protect the well being of the miners. As long as new cases of silicosis are being produced there is do reason to feel satisfied. In this respect the engineering con trol of respirable dust is of paramount importance and the engineer is obvious ly a person who must face this problem with every means at his disposal. Industrial noise control By C. H. WOOD* Noise has been with us for a long time but the question of noise control in industry has received a great deal of publicity only recently. Noise is now being classified as a type of pol lution which is to be cleared up just like other forms of pollution. Most of the information available on how noise problems are to be corrected is pre sented in the form of charts or graphs generally showing noise spectra giving decibel levels on a base of frequency. Unfortunately, this information is of little use to operating personnel who are more familiar with physical things that can be seen, touched and meas ured. Noise cannot be seen or touched so it is an intangible condition. How ever. it certainly can be heard. The purpose of this paper is to put the characteristics of noise and the means of solving noise problems into readily understandable terms. First, to define and demonstrate noise, and then to show how to get rid if it. Noise, for the purpose of this dis cussion. consists of minute fluctuations in the ambient air pressure. These pres sure pulses travel through the air and register on our ear drums. We hear this sensation as noise. The frequency at which these pressure pulses occur varies very widely, but the frequencies that the human ear can sense vary from about 50 cycles per second to about 15.000 cycles per second, or Hertz (Hz). The ear is most sensitive in the range from about 250 to 10,000 Hz. The amount of pressure fluctuation is very small ar.d is impractical to meas ure with normal pressure measuring equipment. Noise is measured on a sound level meter and the unit of meas urement is the decibel. Now most read ers have all heard this type of informa tion before, but would you know a de cibel if you heard one? And just what is frequency? Well, for those who are musical, mid- "PreiiJent, Flexmi'ter Co. Ltd. die `C' on the piano is 261 Hz and `A' is 440 Hz. The hum from small trans formers and from fluorescent lighting fixtures is 120 Hz. Some common sounds might be worth mentioning. When you just crack open the vent on your car at 60 mph, the hiss is primar ily 500 Hz. The whine of a jet engine inlet is primarily high frequency in the 5.000 cycle range, while the rumble of a freight train is mostly in the me dium to low range of 200 Hz. So much for frequency. The loudness of a sound is measured in decibels, and to give you some idea of general overall Db levels . . . That in most rooms is about 42 Db, and that hiss from your car vent is about 80 Db. A teenage daugh ter threw a party recently and the noise level in the living room was generally from 110 to 115 Db. A demonstration of sounds Various frequencies to which the ear is sensitive are readily demonstrated by means of proper sound producing and measuring equipment. Pure tones are given to acquaint the ear with sen sations produced by this or that fre quency. However, in practice pure tones rarely exist. A demonstration readily shows the difference between a pure tone of 1000 Hz and a typical power saw having its sound mostly in the 1000 Hz band. While these are similar on the frequency meter, the sound to the ear is quite different. An other useful demonstration is to re produce sounds of various decibel levels. The reason for this demonstra tion is that on occasion when discus sing a proposed enclosure with a client we comment that it would reduce the overall level from 90 to 80 Db. This has no real meaning unless he knows what 90 Db and 80 Db sound like. In addition to showing frequency and noise levels, another demonstra tion is designed to give consideration to getting rid of industrial noise prob lems. (The basic problem is that noise bothers people). The logical conclu sion then is that in any new installation try to group the noisy equipment in areas that are removed from people. Put the noisy MG set, compressor or other equipment off in a little concrete house by itself and put the people somewhere else. In those installations where this is not possible the usual ap proach is to build a house around the noise source or a house around the peo ple it is bothering. In .the case of air moving equipment, silencers can be de signed to handle most ducting noise problems and enclosures can control radiated noise. Let us first consider enclosures. To do this we must first think about the nature of sound, then select the type of enclosure construction best suited for the particular application. I already mentioned that noise consists of minute pressure fluctuations. It can be seen from demonstrations that a very stiff or a very heavy ma terial will act as a good barrier. Soft or very thin materials are not good. It is possible by laminating certain ma terials to obtain a sound barrier much superior to that which would be ob tained by the individual materials used separately. For instance, 3 inches of glass fiber has a sound transmission loss of about 3 Db at 1000 Hz, 18 gauge steel sheet has a transmission loss of about 100 Db for a total of 13 Db. If, however, these are laminated so the glass wool is under some degree of compression, the transmission loss can be as high as 30 Db. To demonstrate this we have a noise source and a vari ety' of enclosures such as those of plas tic and regular panel construction. Design of enclosures An enclosure, by its very nature restricts access to the equipment it encloses. Where access is required only for maintenance or inspection, it is usually possible to design the enclosure to provide the neces sary noise reduction and at the same time have enough doors or other open ings to provide the required access. Enclosures around fans, pumps, com- Cecil H. Wood graduated from Univer sity of Toronto in 1946 in mechanical engineering. Mr. Wood was involved in the design of the Orenda jet engine Testing of the Orenda made him fami liar with noise control equipment in the test house. He studied acoustics at U of T and has since I960 been president of Flcxinaster. His prime function with this company is the design and develop ment of special noise control equip ment for industry.