Document o912e3aqD6n3ZJVGwGQYMRpj8
ST0556734
DOUJ 05837
ASBESTOSIS EDITORIALS-ACTION ON ASCESTOS
J .THE NEW ENGLAND
OF MEDICINE
VOL. 285 No 23, D ec. 2 , 1971
pps. 1317-1318
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Vol. 285 No. 23
EDITORIALS
The New England Journal of Medicine
Official Organ of The Massachusetts Medical Society
Founded in 1812 as the New England Journal of Medicine and Surgery and continued in 1828 as Vol. I of
the Boston Medical and Surgical Journal
Published Weekly by the Committee on Publications of the M assachusetts Medical Society
Claude E. Welch, M.D., Chairman
Alexander Marble, M.D.
Saul S. Radovsky, M.D.
Samuel Proger, M.D.
Leroy D. Vandam, M.D.
Joseph Garland, M.D., Editor Emeritus
Franz J. Ingellinger, M.D.. Editor
Associate Editors
Jane F. Desforges, M.D. Jan Koch-Weser, M.D.
Ronald A. Malt, M.D. Arnold L. Smith, M.D.
George S. Richardson, M.D., Book Reviews Robert O'Leary , Assistant Editor
Editorial Board
Robert E. Johnson, M.D.
John W. Littlefield, M.D.
Norman G. Levinskv, M.D.
Arthur A. Sasahara, M.D.
Francis D. Moore, M.D.
Louis Weinstein, M.D.
Charles A. Sanders, M.D.
Howard Bleich, M.D.
Jerome H. Shapiro, M.D.
John R. David, M.D.
Ronald A. Arky, M.D.
Edward A. Gaensier, M.D.
Dana L. Farnsworth, M.D.
Brian Mac.Mahon, M.D.
Isadore N. Rosenberg, M.D.
Milton C. Paige, Jr,, Business Manager
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ACTION ON ASBESTOS
Asbestos workers are unintentional victims of industrial progress. They are at risk of pulmonaryfibrosis, pleural calcification, mesotheliomas and lung cancer. Asbestos exposure is now widespread, involving not only air but also drinking water, wine and beer.1 Fibers have been found in the lungs of people without industrial asbestos ex posure. Whatever the exact nature of asbestos or ferruginous bodies may be, there is no doubt that electron microscopy of the lungs of urban dwellers has shown the presence of chrysotile asbestos.2 Al though there is no evidence of asbestos-linked dis ease in the general population at this time, the presence of asbestos in their lungs is disturbing. Asbestos is relatively resistant to destruction bymost chemical and physical means and can float freely in the atmosphere for prolonged periods. Asbestos diseases have a long latent period, 20 years or more. We therefore believe that more sweeping decisions on the control of asbestos must be made now, on the basis of "reasonable probabili ty" rather than after a delay for a precise definition of dose-response relations.
These thoughts are reinforced by the work of Murphy and associates in this issue of the Journal (p 1271). Their studies of pipe coverers involved in new ship construction include better than usual exposure data and indicate a high incidence of asbestosis (38 per cent after 20 years) at what have been previously regarded as "safe" dust concentra tions. A second study of Murphy et al.J reports two cases of pleural disease (one mesothelioma) in workers who sanded asbestos floor tiles. Since the degree of asbestos exposure was unknown, tfie au thors simulated the working conditions and found concentrations of 1.3 fibers per milliliter of room air. This concentration is less than 1/5 of currently used threshold limit values. A fiber per milliliter of room air means that a worker breathing 15 liters per minute for eight hours inhales some 107 fibers every work day. Although only a fraction of the inhaled fibers remains in the lung, these figures suggest that an alarming number will still accumulate over a 10year period.
A recent Committee report prepared by a Nation al Academy of Sciences panel4 has called for control of asbestos emissions at the source and for protec tion of those who are exposed in their occupations. The report also calls for further research on the biologic effects and the physical characteristics of asbestos fibers; such data are urgently needed "if a range of jafe exposure is to be established with confidence." Although we endorse these recommen dations, we want to underline the urgent need for technical controls based on existing knowledge. Epidemiologic monitoring, physical studies of as bestos and other fibers and analysis of their effects on cells and tissues are important and must be con-
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tinned. But there is now a clear need for more deci sive action on control measures and the Occupation al Safety and Health .V : of 1970 sets the stage for such action.
Application of the technics of industrial hygienemust be accelerated. The present threshold limit value for asbestos should be lowered far below some recent proposals. National administrative mechanisms to initiate and implement action are available -- the recently established National Insti tute for Occupational Safety and Health and the National Advisors Committee on Occupational Safe ty and Health foremost among them. The Secretary of Labor, under the aforementioned Act, is charged with the setting of standards and has the right of entry into and inspection of places of employment. Thus, enforcement and regulators- mechanisms as well as advisory' bodies have been established by law. Among the many problems that they face, as bestos should have high priority. Technologic de velopments are needed in many areas: sophisticated dust control; better and harmless asbestos substi tutes; and improved monitoring of both the workers and their environment. Adequately devised tax poli cies could provide incentives for industry to clean the air and protect the workers. Such policies, bygenerating action in each plant where a risk exists, can rapidly and considerably amplify efforts on the national scale.
Bernard Gee, M.D. Arend Bouhuys, M.D., Ph.D.
References
1. Cunningham HM. Pomefract R: Asbestos fibres in beverages and drinking water. Nature (Lond) 232:332-333. 1971
2. Langer AM. Selikoff IJ. Sastre A: Chrysolite asbestos in the lungs of persons in New York City. Arch Environ Health 22:348-361. 1971
3. Murphy RL. Levine BW. Al Bazzaz FJ, et al: Floor tile installa tion as a source of asbestos exposure. Am Rev Resp Dis 104:576580. 1971
4. Asbestos: The need for and feasibility of air pollution controls. Panel on Asbestos. Committee on Biologic Effects of Atmospheric Pollutants. Washington. DC. Division of Medical Sciences. Na tional Research Council. 1971
ONE PRICE OF ACROPHILIA
er the centu-
Vsiatics, high of the gods; home of del below, and l walks and
?red century' e overcome/ by conquest tsulted. j ive society it ers hunr, to ir acrobatics more incredible, but the speed with which ever
higher altitudes are reached is quickening. Whereas
Victorians experienced the same symptoms of
mountain sickness as had been described in the
I5th century, today's climbers have added a new
entity tA mountain sickness -- high-altitude pulmo
nary edema.1'3
This "Physiologic disease" is directly caused by
hypoxia, sand probably by hypoxia alone. The clini
cal and radiologic picture is classic and similar to
edema of other causes. High pdimonary-artery pres
sures have\ been demonstrated3 in individuals
brought to Hospital shortly after onset of severe high-
altitude pulmonary edema (HAPE). developing as
low as 11,000 feet. But why do not equally high
pressures callse edema in other persons resident at
altitude,3 or in some patients with chronic heart or
lung disease?\Pulmonary Aypertension is obviously
not the sole cause. No cnemical abnormalities have
been identified Hypovolemia and tissue dehydra
tion contrast snarply with the waterlogging of the
lungs: is the condition due to too great a shift of
blood from peripheral to pulmonary circulation,
perhaps resulting from peripheral vasoconstriction?4
Cardiac output ts reduced or normal, left atrial
and pulmonary wedge pressures are generally
low.4-* It is postulated that precapillary arteriolar
constriction4,7 in tile lungs produces the condition
-- but how? The uifluence of local humoral changes
and the contribution of the hypothalamus may be
considerable -- out Have not yet been fully defined.3
Hypoxia is known to\increase capillary permeabili
ty, as may be manifest by the occurrence of retinal
hemorrhage during hyppxia from any cause,* but the
definitive stuaies remain to be done.
Whatever /the pathogenesis, the condition has
become increasingly common among people who go
too high tofo fast, before the normal and marvelous
acclimatization process can protect. The modem
climber is usually in a hurry, flying from home to
mountam base and thence rapidly by small plane to
a landing above 10,000 fe. In the next few days
he clrnnbs -- usually with a heavy pack -- faster
than Adaptation can keep up, and trouble begins.
His iickling cough becomes productive -- often of
frotny, bloody sputum. His companions hear his
gurgles during sleep, he weakens and sinks to semi
consciousness sometimes in a Vew hours. L'nless
energetically treated early, he is likely to die.
/ Of course, not every dyspneit-.Y-oughing climber
has pulmonary edema. Pneumonitis, pericarditis,
hypertensive heart failure and ottier conditions
probably account for half or more of the cases hasti
ly called "pulmonary edema." As one\examines the
incidence among mountain climbers, one must be
careful not to confuse the record by inaacurate diag
nosis.
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HAPE is a preventable disease -- net an acci
dent. Although physical conditioning does not pre
vent, a leisurely ascent does. The climber who
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