Document 8VO6y9re2R4LzxJrMQ4d17Q1a
FILE NAME Colonial Sugar Refinery CSR
DATE 1950 Nov DOC CSR027
DOCUMENT DESCRIPTION Journal Article - Occupational Factors in Pulmonary Dust Disease
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EMBER 18 1950
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AUSTRALIA THE MEDICAL JOURNAL OF
VOL 37TH YEAR
SYDNEY SATURDAY NOVEMBER 25 1950
No. 22
Table of Contents
The Whole of the Literary Hatter in THE MEDICAL JOURNAL OF AUSTRALIA is Copyright
ORIGINAL ARTICLES
Page
Occupational Factors in Pulmonary Dust Disease
by Gordon C. Smith M.B. B.S. The Changing Face of Obstetric
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OCCUPATIONAL
FACTORS IN PULMONARY DISEASE
DUST
By GORDON C. SMITH M.B. B.S. Industrial Health Unit School of Public
and Tropical Medicine Sydney
Health
THE Third International Conference of Experts on
Pneumonokoniosis held recently in Sydney under the
auspices of the International Labour Organisation 1950
adopted the following definition of pneumonokoniosis
a diagnosable disease of the lungs produced by the inhala-
tion of dust the term dust being understood to refer to
particulate matter in the solid phase but excluding living
organisms the term diagnosable indicating the presence
of signs or symptoms but not always loss of function
The implications and scope of this definition are very
wide Whilst pneumonokoniosis in the etymological sense
means dust in the lung and therefore is applicable to
the pulmonary reactions due to all types of dust and
fumes in practice it has been associated chiefly with
silicosis asbestosis and in recent years with the lung
disease due to coal diseases in which permanent
fibrosis occurs abnormalities
and
with
characteristic
radiographic
Of late it has become evident that acute semiacute and chronic pulmonary conditions may result from inhalation of a variety of dusts both organic and inorganic other than silica asbestos and coal Although the nature and
severity of the tissue reaction vary according to the type
of dust and conditions of exposure the term pneumono
koniosis can be applied to these conditions
Read at a meeting of the Section of Public Health Tuberculosis Tropical Medicine and Industrial Medicine Aus-
tralasian Medical Congress British Medical Seventh Session Brisbane June 1950
Association
The Occupational History in Pneumonokoniosis
Whilst the diagnosis of pulmonary dust disease should
never be made without proper consideration of the occupational history medical history clinical examination and
|
radiographic findings the first is of special importance Unless there has been exposure to dust of a harmful
nature matter might
there cannot be what the medical
indicate and no
a pulmonary dust disease no
history or clinical examination
matter how closely the radio-
graphic appearances of the lungs simulate those of
pneumonokoniosis
Thorough and detailed inquiries should be made about
any process in which the patient may have been exposed
to dust nature and conditions of the work the type of dust and duration of employment at the process Unless these particulars are obtained accurately the industrial history may be rendered invalid with resultant error in
diagnosis Negative evidence as to dust exposure is as important as positive pneumonokoniosis has been diagnosed in certain individuals with suspicious radiographie signs evidently on the film appearances alone for a proper inquiry as to the nature of their work would have revealed no history of industrial dust exposure in these
cases
Properties of Dust in Relation to its Disease-
Producing Capacity
Although all dusts if inhaled in sufficient quantities may be regarded as being potentially harmful some are known to be considerably more injurious than others Important information concerning the potential capacity of a dusty environment to cause disease of the lungs can be obtained from a study of the following factors i the composition and nature of the dust ii the size of the dust particles iii the intensity of exposure as determined by a the atmospheric concentrations of the dust b the
duration of exposure
778
THE MEDICAL JOURNAL OF AUSTRALIA
NOVEMBER 25 1950
The Composition of Dust
An analysis for stituents should be
the chemical carried out on
or mineralogical conany dust suspected of
causing pneumonokoniosis and preferably the borne dust should be examined
The most injurious component of an industrial dust is
crystalline free silica uncombined silicon dioxide
The pulmonary reactions from amorphous or crystalline free silica are less severe while silicates that is silica in a combined form with the notable exception of asbestos
a hydrated magnesium silicate are less harmful than
free silica
Most minerals which contain silicates also contain some proportion of free silica compounds of other elements such as iron aluminium calcium magnesium and potassium may also be present Because of the possible modifying or inhibitory Influence of certain substances on the action of free silica the analysis should be not only for free and combined silica but also where indicated for other likely constituents especially if these by themselves are capable of producing a lung reaction
In regard to metallie dust and fume even though there may be no question of the presence of silica the concentration and chemical analysis of the atmospheric contaminant should be determined in order that a proper appraisal of the suspected hazard may be made
In the case of siliceous materials as a general rule and other conditions being similar the higher the percentage of free silica in a dust the greater is its capacity to produce disease When pulmonary disease is caused by dusts which contain lower percentages of free silica than say sandstone or quartz greater exposures due to higher atmospheric concentrations of dust or to a longer working period or both are necessary Thus pneumonokoniosis has been found in men engaged in dragging bricks from continuous or patent kilns Tests in New South Wales have shown these men to be exposed to very high concentrations of dust containing about 25 of free silica
The pulmonary changes in coal miners are out of proportion to what one would expect having regard only to
the free silica content of coal dust which Smith and Whaite
1950 found averaged 1.8 in the under 10 micron
fraction of sixteen samples collected from the coal face of
five collieries in New South Wales but a long period of exposure seems necessary to produce disabling pneumono-
koniosis
Asbestos which contains no free silica produces pulmonary disease but the mode of action of the fibre differs from that of the silica particle
a severe
asbestos
The pneumonokoniosis conference agreed that an analysis
of material from which dust is derived does not of
necessity represent the composition of the dust inhaled in
in industrial process The free silica content of borne
lust may be similar or may be appreciably increased or
decreased compared with according to the nature Industrial process
that in the parent material
of the material and type of
The problems associated with exposure to mixed dusts
for example in foundries are of interest Foundry dusts
nay comprise a mixture of carbon free silica silicates
ron oxide and other metal particles as well as particles
from carborundum and other abrasive materials
Iron
xide may play some part in the production of the nodular
shadows seen in radiographs and may influence the action
of of silica in the lungs certain foundry workers apparently
affected with silicosis One may also question whether
any of the nodulation seen in films of grinders with
apparent pneumonokoniosis is due to particles from metals
or synthetic abrasives
The physical nature of substances whether hard and i
try or soft and wet influences their capacity to produce | lust Thus the fact that work is being done in sandstone loes not necessarily mean that there will be a serious dust
azard f th
on
despite the high k was wet and
free silica soft little
content of or no dust
the rock would be
breaking it up whereas if it was of a dry
tightly cemented type dust high in free silica would be
generated because more energy would be required to rupture it
The Particle Size of Inhaled Dust
The pneumonokoniosis conference concluded that in the case of fibrous dusts such as asbestos and certain vegetable
dusts the larger sizes appear to be more harmful whereas
in many mineral dusts the smaller sizes seem to be the
most injurious In general whilst particles of mineral dusts except asbestos exceeding five microns in size are
of minor importance the lower limit of the size of particles
causing pneumonokoniosis has not yet been determined
Particles of the harmful size range cannot be seen with
the naked eye and it is well to remember that a dangerous
concentration of dust of this particle size may be present
in the air without being seen contain fine harmful particles
innocuous size
A visible as well as
dust cloud may
those of larger
The actual number and size distribution of dust particles depend upon the method by which dust is produced and the nature of the parent material from which the dust is derived Experience in New South Wales like that of investigations elsewhere is that at least 70 and in some
cases over % of dust particles generated in industrial
processes are up to three microns in size About % of coal dust particles and only about % of sandstone particles are over five microns in size Thus not only is there a relatively small production of the larger particles but such particles settle out from the atmosphere more rapidly than the smaller sizes Further it is known that only a portion of inhaled dust is retained permanently in the lungs most particles of about five microns and larger being removed by the physiological mechanisms of the nasal and
upper respiratory passages
In a recent review of this subject Hatch 1950 that particles smaller than one micron in size the principal contributors to silicosis production
suggests may be Vorwald
1950 showed in animal experiments that amorphous silica of particle size down to 0.005 micron produces profound lung changes and states that the rate of tissue
reaction to dust is inversely proportional to particle size
On the other hand in regard to asbestos it appears that the larger particles are more harmful than the smaller
and that in the lungs they act as mechanical rather than
as chemical irritants Gardner 1938 Wyers 1949 states that dangerous fibres measure about 20 microns
Dust Exposure
. In general exposure is measured in terms of concentrations of borne dust and the period of time during which the individual is exposed to those concentrations the
the higher the average concentration of borne dust and
longer the period of exposure the greater will be the risk of contracting pulmonary dust disease
In the case of silicosis and related types of pneumonokoniosis including asbestosis the disease is usually of
gradual onset and slow development It does not become evident until after exposure for a period of years the actual time varying according to the type of dust and industry
Meiklejohn 1949 states that under present conditions in Great Britain silicosis in a diagnosable stage seldom
occurs in under fifteen to twenty years exposure to the risk and in regard to coal miners McVittie 1949 gives
a similar period for the development of pneumonokoniosis
My own observations on a group of 416 New South Wales
in coal miners showed that the average period of exposure
the men with disabling pneumonokoniosis was thirty years their average age being four years
Asbestosis apparently occurs after a shorter
exposure Thus Wyers 1949 who investigated 115 fatal cases of asbestosis found the average exposure had been 10-4 years
Under conditions of intermittent exposure it is
more difficult to predict the likely effect on the lungs than the exposure was continuous but the severity of any
dust dust
NOVEMBI
hazard is us however m exposures
In the cas period neces
generally m
months or w instances a reaction
The liter acute or exposures to following no
In April 1 weeks after } of his indust he was enga From 1931 to fifteen month for two year in the sub using a wa pick for six
His chest on two occ had left the 17 days befo the last exa of bilateral
At autops silicosis of Microscopica immature fit to nodular a
In October Industrial H in the baser been employ picks and a Nevertheless from 1150 t Owens's dust in 1937 were doubt that th dust inhalati
Occupati
The most dast containi commoner p
mining or qu surfacing of
and mouldin in iron foun
milling silic brick industi facture of al handling of
several of th
specially mer but still cont
Pneumonok other papers to asbestosis this country it is much m cessing and example text
In recent }
1949 and M
of the respir
silica coal ai
due to vegeta I propose b
lung disorder of them hav
industries or carried out h
80 we should
risks
:
Fould be ired to
t in the egetable whereas " be the mineral size are
particles
ined
en with Ingerous
present ud may
flarger flarger
particles ced and he dust - that of in some idustrial t % of particles there a les but ' rapidly t only a
in the er being isal and
suggests may be Vorwald rphous
ces prof tissue e size
ars that smaller
er than ) states
ncentrag which ns the and the the risk
eumono-
ually of become
ars the ust and
nditions seldom
> to the
) gives
coniosis
h Wales osure in
four
xposure cases of .4 years
is more
than if ny dust
NOVEMBER 25 1950
oa
a
THE MEDICAL JOURNAL OF AUSTRALIA
779
hazard is usually lessened in such circumstances This
however might exposures
not apply
with
very
high
intermittent
In the case of metallic and vegetable dusts the exposure
periodperiod necessary to produce a pulmonary disturbance is
* generally much shorter than with other sometimes
months or weeks or even less rather than years In some . instances a single exposure may be sufficient to cause a
reaction contains The literature contains reports of the occurrence of
acute or rapidly developing silicosis after short ~ exposures to high concentrations of silica dust and the ., following notes about a Sydney case are of interest
In April 1942 a man aged thirty years died three - weeks after he had collapsed at work The significant details
of his industrial history were as follows From 1917 to 1919 he was engaged in coal mining Cessnock for two years From 1931 to 1937 he was with the Water Board including fifteen months on rock work From 1937 to 1940 he was for two years a builder's labourer excavating in sandstone in the basement of a building Latterly he had been
using a water pick but earlier had been using a dry
pick for six months
His chest had been examined by X rays in 1937 1940 on two occasions the second being some weeks after he
had left 17 days the last
the basement excavation work and again in 1942 before his death It was only in the film from examination that the radiologist reported evidence
of bilateral nodular fibrosis At autopsy aortitis congestive
cardiac
failure
and
silicosis of the rapidly developing type were found
Microscopically the lungs showed generalized somewhat
immature fibrosis mainly diffuse but with some tendency
to nodular arrangement In October 1939 the New South Wales Division of
Industrial Hygiene had investigated the working conditions in the basement of the building where this patient had
been employed Water jets were fitted to
picks and an exhaust ventilation system Nevertheless concentrations of sandstone
the pneumatic
was installed dust ranging
from 1150 to 10,000 particles per cubic centimetre by Owens's dust counter were obtained The dust conditions in 1937 were probably worse than in 1939 there is little doubt that this patient contracted silicosis as the result of dust inhalation during the period 1937 to 1940
Occupations Dusts et cetera Associated with a Pneumonokoniosis Hazard
The most important risks are those where exposure to dust containing free silica is likely to occur Among the commoner processes involved are tunnelling excavating mining or quarrying in sandstone or quartz cutting and surfacing of sandstone or granite sandblasting dressing and moulding in foundries especially machine moulding in iron foundries if siliceous parting powders are used
milling siliceous ores certain pottery processes in the
brick industry chiefly dragging in patent kilns manufacture of abrasive soaps and powders manufacture and
handling of refractory materials and metal mining In several of these instances and in a number of others not specially mentioned here the dusts are of a mixed nature but still contain significant percentages of free silica
Pneumonokoniosis of coal miners has been discussed in
other papers and will not be further considered In regard to asbestosis which is of very infrequent occurrence in
this country all the evidence from overseas indicates that
it is much more common in workers engaged in the pro-
cessing and fabrication of asbestos in factories example textile work than in asbestos miners
for
In recent reviews of the literature Perry 1947 Doig
1949 and Middleton 1950 have described disturbances
of the respiratory organs due to mineral dusts other than
silica coal and asbestos and have discussed the reactions
due to vegetable dusts
I propose briefly to mention the more important of these lung disorders because although to my knowledge most of them have not been reported in this country the
industries or processes involved in their causation are carried out here or may be conducted in the future and
so we should be familiar with the possible occupational
;
risks
Before referring to these however I wish to make a few comments about the lung changes which have been observed in basalt workers and biograph operators in New
South Wales
Basalt Work
Basalt or blue metal is a basic igneous rock composed essentially of a bearing feldspar with smaller amounts of one or other of the magnesian minerals and a little iron oxide Free silica is typically absent but may be present up to % Thus basalt is a silicate with 40 to 50 of silica in combined form Whitworth 1947
Badham 1927 described a case of fine fibrosis of the lungs in a man aged sixty years who for twenty years had worked in a blue metal quarry and crusher house and was exposed only to the dust of orthoclase basalt which contains no free silica This man died but an
autopsy was not performed
In recent years I have seen two men aged forty years and three years respectively who as far as could be ascertained had been exposed only to basalt dust
The first man had been a crusher attendant for fifteen
years at the same quarry as Badham's patient and the second had worked chiefly on the crusher and screens for thirty years at another blue metal quarry The radio-
graphs of both men showed a marked generalized
fine type of nodulation throughout the lung fields in the film of the first man who was totally disabled there were
also large shadows suggesting consolidation
Biograph Operating
Two brothers whom I first saw in 1947 were aged
forty and forty years respectively and worked in the projection booth at the same
had both suburban
cinema elder for ten years and the younger for
twenty years There was no history of exposure to dust in other employment The elder man complained of
shortness of breath and loss of weight his brother of
pains and tightness in the chest The chest radiographs of both men were similar and showed a generalized fine
nodulation throughout both lungs Films of both men taken in 1949 showed no significant change since 1947
In 1946 the New South Wales Division of Industrial
Hygiene had found that the concentration of dust in the air of the biograph box in the cinema concerned was approximately 6000 particles per cubic centimetre of air by the Owens dust counter the dust particles were mostly about half a micron or less in size The ventilation in the box was faulty A sample of dust obtained from the biograph room in 1946 on analysis gave the following
result
Total SiO ..
..
..
Rare earth oxides ..
: Al2Os Fe
Cao
on
ignition
we
ee
ignition
Loss on ignition
.
Copper Fluorides
ve
:
:
P2O5
ee
eee
ee
SOs
tee
ee
ee
6.0 48.0 17.0
6.7 2.0 Trace Present Present Present
Following the discovery of the unusual pulmonary condition in the two brothers seventeen biograph operators
from fourteen other theatres were submitted to X ray
examination Their period of employment ranged from seven to thirty years and some had worked in badly ventilated booths However no evidence of a lung reaction resembling pneumonokoniosis was found
Several authorities have investigated gases fumes and
dusts from carbon ares and the ventilation of motion
picture booths MacQuiddy and others 1939 showed that some of the intensity carbon are ashes appear to cause mildly proliferative reactions when injected intraperitoneally in the albino rat They state that it might be deduced that if inhaled in sufficient quantities over long
enough periods of time these ashes might cause a pro-
liferative type of pneumonokoniosis
On the limited evidence at present available and in the
absence of autopsy studies it is not possible to say whe
kod
the lung condition biograph operators
present in these
is due to dust
basalt wepulmonary Furthexception the
we
780
THE MEDICAL JOURNAL OF AUSTRALIA
NOVEMBER 25 1950
responsible the question arises whether it has fibrosis or is merely present as inert deposits
caused
It seems reasonable to associate the radiographic abnor-
malities of the basalt workers with inhalation of dust at
their employment but in the case of the biograph operators whilst occupational factors cannot be ruled out indeed one of these men was compensated for silicosis as they were brothers and as examinations of other operators gave negative results a industrial ^tiology
has to be considered
Although these cases are incomplete I mention them in order to emphasize that with present advances in industrial activity and with increasing knowledge of pneumonokoniosis we must constantly be watching for lung conditions due to dust not only from new processes but also in industries and occupations where previously they have
not been suspected
is said to be caused also by fumes of other metals When
it is due to zinc there is an acute febrile reaction or chill
of short duration and with no permanent lung damage
metallic If other
oxides such as cadmium or manganese
may are involved a more serious pulmonary condition
ensue
Cadmium
Johnstone 1948 states that cadmium has probably more lethal potentialities than any other of the metals The inhalation of dust or fumes from cadmium compounds especially the oxide for example in welding on cadmiumplated surfaces from the ignition of cadmium and from the use of cadmium in solder produces irritant effects which may be severe in the respiratory tract perhaps with
pulmonary ^demaand death
Beryllium
Talc
The literature on the pulmonary and other lesions
Until comparatively recently asbestos was considered to be the only harmful silicate Now however there is
pneumonokoniosis evidence of several investigators that talc a hydrated mag-
nesium silicate which occurs in flaky and fibrous forms and
is used in a number of industries may cause significant
lung changes McLaughlin Rogers and Dunham 1948
described a case of
confirmed at autopsy
in a man aged fifty years who had worked for thirty-
seven years in a rubber tire factory where he had been
exposed to a fair concentration of talc dust and who
died primarily from rheumatic endocarditis There was
much fibrosis in the lungs and curious bodies similar to
absestosis bodies were also present These authors con-
clude that tale pneumonokoniosis and asbestosis are
similar diseases and that pneumonokoniosis is probably
caused only by the fibrous varieties of talc
Graphite
Doig 1949 and Middleton 1950 refer to recent reports by other authorities in Britain chiefly Dunner and Gloyne concerning pulmonary disease in graphite workers
According to Harding and Oliver 1949 graphite plumbago which is a crystalline form of carbon may be mixed with up to 10 of free silica and with other
affecting workers exposed to beryllium is now extensive many reports having been published during the past five years Abstracts of the various papers and articles were recently made in Australia by Taylor 1949 Two principal types of pulmonary lesion have been described an acute pneumonitis and a chronic diffuse granulomatosis A
number of fatal cases have occurred
It appears that the acute form which may follow a single exposure to toxic fumes occurs mainly among workers exposed to compounds in the extraction and refining of beryllium from the ore beryl usually within a few weeks
of the first exposure
The chronic or delayed form which resembles sarcoidosis
Howevr is more persistent A period of from several weeks or
may elapse from the time of the last exposure to the
years
This type usually
onset and recognition of the disease
occurs in persons who have been exposed to dust from
fluorescent powders containing zinc beryllium silicate
notably in the fluorescent lamp industry However eleven
cases of the chronic type were recently reported amongst
residents in the vicinity of a beryllium plant
There was no history of occupational exposure Eisenbud
and others 1949
minerals They point out that grinding of natural graphite
produces the greatest dust risk and can lead to a disabling and fatal pneumonokoniosis which they describe as resembling both radiologically and histologically that of
South Wales coal workers
Other Silicates
Abnormal reactions in the lungs of animals or man have been described following inhalation of dust from china clay mica sillimanite and fuller's earth
Cement
Cement is mentioned here because of its very widespread
use and of questions which periodically arise as to its
possible harmfulness
The raw materials from which
cement is made are chiefly limestone which has not more
than about % of free silica and shale which may contain
from 20 to 40 of free silica The finished product has
practically no free silica Gardner and others 1939
examined 2278 employees from 11 making plants in
the United States of America Only eight persons showed
evidence of nodular fibrosis attributable to dust and in
six of these exposure to silica dust in previous employment was presumably responsible Baetjer 1947 showed that in rats exposure to high concentrations of cement dust did not lower resistance to lobar pneumonia and did not produce any acute or chronic pathological changes in the
lung tissue
Manganese
pneumonitis Doig 1949 mentions that since 1921 a relationship between manganese and pneumonia has been suspected
following reports from Norway and Germany In England Lloyd Davies 1946 found that men exposed to dust of oxides of manganese experienced a high incidence of a
No condition which he called manganese
permanent lung changes were observed Three years later Lloyd Davies and Harding 1949 reported that pneu-
monitis has continued to affect manganese workers
both Firket 1950 states
follows inhalation of
that chemical nonia which
dusts of manganese vanadium
osmium and beryllium resembles virus pneuwmhoentihaer the clinically and histologically and he questionswhether they dusts themselves provoke the disease or
activate viruses
Iron Oxide
Doig
and
McLaughlin
1936
described
a
fine nodulation
in
in the lung fields of welders who wecrlienicaaplpaarnedntlryadio-
good health
Later following further
them and other investigators it became
graphic studies by evident that the pulmonary
changes
were
due to the
in welding
deposition of iron oxide dust which is present
fume and which is relatively opaque to X rays and physical
they were not associated with symptomsA asbinmoirlmaralcopnhdiytsiioncalcondition |
signs or lessened cianpaoctihteyr fwororwkeorrsk than welders exposed
has been reported
Metal Fume Fever
The
If thethe ru m formform
known example of a minor pulmonary reaction
me
in
fever due to fume rather than to dust mostly exposure to zinc oxide fumes for example in bi or from welding on galvanized iron It
to iron oxide
examination Enzer and Sander 1938 made an autopsy
of the lungs of a welder whose chest radiograph showed fine nodulation and who died following an accident there
was no fibrosis in the lung tissue
Nov
Acco due to case d
pletely
and in Dust
more
simila
Sinc
experi metalli sideral alumi
have b The
there alumi cosis i therap
-
when under indust
was e
of alu
Shu diseas engag oxide furna ture (
accort
and 8 Rid
to be that t
The
for [ alumi
The Bruns abrasi the lu
A minoi mate timbe
Cot chitis ---- -- -- work elsew The other
Ba the s
cane
the 3 respi work
were
broke
revie one litis dust
by
yett
WI to w
incre 1941 -- -- -- --
r manganese
may ndition
as probably
the probably .
i compounds
on cadmium- cadmium-
the and from
ffects which
her lesions
w extensive
he past five
rticles were Two prin-
scribed an
matosis A
How a single
ng workers refining of few weeks
sarcoidosis
1 weeks or sure to the pe usually
dust from
in silicate
ver eleven d amongst
cing plant Eisenbud
elationship suspected 1 England to dust of
ence of a itis No ears later hat pneukers
tia which vanadium onia both ether the ther they
odulation rently in nd radiot became to the
welding and that
physical
condition
exposed
mination showed
it there
NOVEMBER 25 1950
THE MEDICAL JOURNAL OF AUSTRALIA
781
_
_
According to Doig and McLaughlin 1948 the changes
to iron oxide are not necessarily permanent In one
due
case described by them the abnormal lung shadows completely disappeared some years after cessation of welding and in another the shadows became less intense Dusts from compounds of barium and tin which are more opaque than iron are believed to behave similarly to the latter in the lungs
Aluminium
Since Denny Robson and Irwin 1937 showed that
experimental animals exposed to quartz dust plus % metallic aluminium powder did not develop silicosis con-
- siderable interest has been taken in the question whether aluminium dust damages the lungs and conflicting reports have been published
The recent pneumonokoniosis conference decided that
there was no conclusive evidence that the inhalation of
aluminium in any form prevents the development of sili-
cosis in man or that aluminium powder is of value as a therapeutic agent in human silicosis or that it is harmful when used for this purpose There was some evidence that under certain conditions the inhalation of aluminium in Industrial processes may be harmful and further there was experimental evidence that in animals the inhalation of aluminium dust aggravates pulmonary tuberculosis
Synthetic Abrasives
Shaver and Riddell 1947 described an unusual lung
disease with fibrosis in some cases fatal in workers
engaged oxide
in the manufacture The process involves
of corundum aluminium treating in special electric
furnaces a mixture of bauxite iron and coke at a tempera-
ture of 2000 C. Dense white fumes are given off which
according to Jephcott 1948 consist mainly of alumina
and silica
Riddell 1948 states that the lung condition appears to be induced by an irritant of a chemical nature but that the precise agent has not been determined
These findings are of interest because artificial abrasives for example carborundum that is silicon carbide and aluminium oxide have such widespread use in industry The observations of Smith and Perina 1948 and of Bruusgaard 1948 indicate that dust from synthetic abrasives when inhaled may produce nodular shadows in
the lungs
Vegetable Dusts
A variety of respiratory disturbances some only of a minor nature have been attributed to dust from vegetable materials such as cotton flax hay grain bagasse and timbers Three examples may be cited
Cotton A condition termed byssinosis chronic bronchitis and emphysema with a tendency to asthma has been reported particularly amongst room and room workers in the spinning industry in Britain and elsewhere There are no specific ray or autopsy findings The literature has been well reviewed by Caminita and
others 1947
Bagasse This is of interest to Australians because of
the sugar industry here cane after the sugar has
Bagasse or megass is sugar been extracted and is used in
the manufacture of wall boards
Since 1941 cases of
respiratory disease bagassosis have been reported in workers handling bagasse England the persons affected
were those engaged on a machine shredder which
broke up the bales of bagasse Hunter and Perry 1946
reviewed the literature fully and described eleven cases
one of the patients subsequently died of acute bronchiolitis and pneumonia arising from the inhalation of bagasse dust They considered the disease was most likely caused by fine vegetable dust however its exact ^tiologyhas not
yet been determined
Wheat Dust Investigations have indicated that exposure to wheat dust may result in asthma Duke 1935 and an increased liability to respiratory disease Smith and others 1941 The fine hairs of the grain are believed to be responsible at least in part for these reactions
Pulmonary Carcinoma
Where an occupation which is associated with an appar ently high incidence of lung cancer has involved dust
exposure it is reasonable to consider carcinoma in a dis-
cussion of pulmonary dust disease
The problem has been reviewed briefly by both Dolg
1949 and
incidence of
Perry 1947 lung cancer in
They mention the Schneeberg
the high miners in
Saxony and in miners in the Joachimstal area in Bohemia
Arsenic and radioactive ores are both considered likely
causes in these cases
They also refer to reports by
various investigators which indicate that workers in
chromate factories and those exposed to arsenic and
asbestos have a high incidence of pulmonary cancer
In a personal communication Dr. J. H. Blakemore of Concord advises that in a chromate factory in New South Wales which has been operating since 1944 and which at present employs about 100 persons all workers engaged in the various stages of production have an ray examination of the chest before starting work and at monthly intervals thereafter To date nothing to suggest pulmonary cancer has been found In its early years this factory had a number of cases of nasal septal perforation and skin conditions due to chrome and relatively high concentrations of chromates were found in the atmosphere
Prevention of Pulmonary Dust Disease
The measures to be applied in the suppression and control of dust and for the protection of the workers are essentially the same irrespective of the industry and type of dust Briefly they include the following
1. The abolition of processes creating harmful dust If that is not possible the total enclosure of such processes in mechanically ventilated structures or their segregation from other operations in the factory Isolation can be applied either geographically or by time that is by carrying out a dusty process when no other workers are in its vicinity
2. The use of a harmless material in place of one that is dangerous
3. The removal of dust at its point of origin by local
mechanical exhaust ventilation
4. The use of water or other wetting agent to prevent dust from certain processes becoming borne
5. Electrostatic precipitation
6. The provision of adequate general ventilation to dilute
contaminated air
7. Maintenance of a high standard of plant cleanliness and housekeeping
8. Personal respiratory protection of the worker Respirators should be worn only when other methods of protection are not practicable or for jobs of short duration They should be well fitting comfortable and efficient and should be kept clean
9. Preemployment and periodical medical examinations including a radiograph of the chest of workers exposed
to a dust hazard
If these control methods or such of them as are
applicable to a particular industry or process are conscientiously applied and maintained workers would be
protected against hazardous exposures to dust
;
Summary
The term pneumonokoniosis is defined and its scope briefly outlined the need for a complete and accurate occupational history in the diagnosis of pulmonary dust
disease is stressed
The potential capacity of a dust to cause disease is discussed with special reference to its composition and nature particle size and intensity of exposure In addition to dusts containing high percentages of free silica others in which free silica is absent for example asbestos and
certain metals are capable of producing severe pulmonary damage In most dusts asbestos being an exception the
782
THE MEDICAL JOURNAL OF AUSTRALIA
NOVEMBER 25 1950
harmful particles are those less than about five
size Intensity of exposure which
microns in
dusts depends on the
varies for different
and the duration of atmospheric concentrations of dust
exposure
rapidly developing silicosis
Brief notes of a case of
are given
of The main occupations and dusts associated with a risk
pneumonokoniosis are briefly discussed diseases
In addition to
made
caused to
by
silica coal
and
asbestos
reference
is
the radiographic abnormalities of certain
workers and biograph operators and to the
basalt
effects
of
talc
graphite
cement
zinc
pulmonary cadmium beryllium
bmaagnagsaseneasned iwrhoenataluminium synthetic abrasives cotton
The occurrence of
exposed to
pulmonary carcinoma in workers
chromates arsenic and asbestos is mentioned
Measures for the control of dust and
workers are stated
protection of
Acknowledgements
I am grateful to the following for
to clinical records of
permitting me access
films the
patients and for the loan of ray
Director of Public Health New South
Wales the Chairman
of New South
Workers
Compensation
Commission
Wales mittee New South
and the
Chairman
Silicosis Com-
E. Ford for
Wales I am also grateful to Professor
helpful Director
criticism
and
to
the
Commonwealth
of Health for permission to publish this
paper
References
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of
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WRaelpeosrtfoorf tthhee YDeair ree ndc edt3o1srt DoefcePmubbleirc
other Minerals Health New South
1927 page 102
Baetjer A. M. 1947 ) The Effect of Portland
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Cement Dust
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the
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Resulting
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II
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1948
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1950
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An Investigation
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_
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M.
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MEDICAL JOURNAL OF
Pneumoconiosis THE
AUSTRALIA Volume I page 514
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1948
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Medicine and
Mosby Company St. Louis
THE CHANGING FACE OF OBSTETRIC INFECTION
By ARTHUR M. HILL M.D. D.G.O. Melbourne F.R.C.S.E. F.R.C.O.G.
Gynacologist to Patients The Women's Hospital Melbourne
THE last fifteen years of the century
have seen the greatest advances of all time vention and treatment of obstetric infection
now ending in the preThis is due
predominantly
modern
to
the
introduction
and
development
of
tant
chemotherapy and antibiotic therapy but impor-
contributory factors are improved bacteriological
knowledge and methods of investigation and a clearer
appreciation of the place of maternal resistance in com-
bating infection
It is proposed to review the major effects of these
advances on puerperal morbidity on the death
of the
main
bacterial
types
of
puerperal
and
rate
abortional
infection and on modern obstetric practice at the Women's
Hospital Melbourne over the past ten years During that period
period 41,643 women % of whom had attended our own
ante- natal clinics were confined and 18,285 cases of
abortion of which 5175 were diagnosed as septic were
dealt with The annual morbidity following the confinements
is shown in Figure I.
Sulphonamides were in use in the earliest of
general years although the compounds employed were in
general toxic and less efficient than those now avariemleamibnbfeeclrtieoend obstetric addition they were not always given in adequate
and their use was largely restricted to the
established infection However when it remembered
that less than 10 of all cases of
sulphonamide sulphonamidseulphonamide likely to be of a bacterial type responsive to sulphonamide
years
more
avilable
In
dosage dosage
of
are
sulphonamide
Gynecology Read at
Association
meeting
Section
sulphonamide a meeting of Medical Section of ObstOebtsrteitcrsics
Obstetrics Australasian Medical Congress British June Brisbane
Seventh Session Brisbane June
Obstetrics
19159050
and
Medical
therap
in pu antibi 1944 i
freely
coinci
therap tion o Routin
Gra
of penic every t followed be given figures incidenc standard morbidit patients
wh
~~
YEAR m PER fe
ws
DEATHS ww
Year #MC
D
Of consi
in
in the me main bact
during the Hospital
problem of
that of fo
cocci Stre pyogenes &
serious ty
Bacterium streptococc
will not b
four main