EXCRETION OF LEAD
=Symptomatology and Diagnosis= (_Continued_)--=Excretion of Lead.=--The
two chief channels for excretion of lead are the urine and the fæces,
while some include the saliva and the sweat.
In the case of the sweat there is not much evidence, but a few
observers, mainly French, claim to have discovered traces of lead in
the skin of lead-workers. In such a case, however, it is exceedingly
difficult to eliminate the question of surface contamination; and
although brisk peripheral circulation and transudation may possibly
carry off a certain amount of lead, the chance of this is highly
improbable.
There seems rather more evidence that the salivary glands may eliminate
lead, as a number of other substances are undoubtedly passed in this
way. Mercury certainly undergoes excretion through the salivary
glands and the mucous glands of the mouth, and it is therefore not
improbable that a metal so closely related in its chemical, and
perhaps physiological, relations may be excreted in a similar fashion.
Meillère[1] cites three instances of parotitis which were considered to
be of lead origin, and further quotes an instance where, in chemical
examination of the salivary glands after death, lead was found in small
quantities.
Chronic parotitis is not infrequently cited as a symptom in cases
of reported industrial lead poisoning, and may owe its origin to
impairment of the salivary gland by the passage of the metal. Chronic
parotitis, or even tenderness of the parotid glands, does not occur
frequently among lead-workers with symptoms of lead absorption.
Excretion, however, of lead through the salivary glands is not of
great importance, except from the occasional complaint of a metallic
taste in the mouth in chronic lead poisoning, and in such instances
possibly definite excretion of lead is taking place through the parotid
glands. A case may be cited which rather supports the view that lead
may be excreted through the salivary glands. A certain worker engaged
in a dangerous lead process from time to time, but never as a constant
symptom, showed distinct pigmentation in the internal surfaces of
both cheeks in the region of the buccal papillæ of the parotid duct.
The pigmentation was intermittent; at times a large patch of deep
blue-black pigmentation was found in the situation on both sides,
with no staining of the cheeks around or of the gum margins, although
his teeth in these regions were coated with foul tartar. If the lead
in this instance gained access through the mouth, why should it have
been deposited merely upon the cheek in this one situation, despite
the fact that several other situations in the mouth exhibited the
same conditions of bacterial decomposition for the production of
sulphuretted hydrogen? We have not observed this pigmentation in the
neighbourhood of the ducts of the submaxillary and sublingual glands,
but only in the parotid.
By far the most important organ in the excretion of lead, from the
point of view of symptomatology and diagnosis, is the kidney. Lead is
not uncommonly found in the urine of lead-workers and in the urine of
those suffering from lead poisoning. The quantity present is usually
small and in a form in which it is exceedingly difficult to detect.
Yet very pronounced changes in the kidneys may take place, with little
evidence in the urine itself that pathological changes are taking place.
The urine of workers in lead factories is frequently high-coloured; in
fact, as a general rule the degree of pigmentation is greater than is
normal, and in those persons who show some degree of icterus, with the
curious yellowish-brown colour of the conjunctivæ, hæmatoporphyrin may
be detected on applying suitable tests.
In well-established cases of chronic poisoning, albuminuria as a rule
is found, together with certain alterations in the other constituents
of the urine, such alteration frequently making its appearance before
the definite onset of albuminuria. Further, the changes in the eye,
referred to under a special heading, have been frequently described as
albuminuric retinitis of lead origin, it being true that eye changes
are often associated with chronic changes in the kidney.
In acute poisoning lead is generally found in the urine, but in chronic
poisoning it is by no means a common occurrence. From time to time
small quantities are excreted, and in the chemical analysis made of
the kidneys in cases of fatal lead poisoning a certain amount of lead
has frequently been noted. Wynter Blyth[2] found in the kidneys of two
white lead workers a total of 0·003 gramme. Peyrusson and Pillault[3],
quoted by Meillère, found a similar quantity, 0·003 gramme, while in
experimental animals Meillère himself found considerably less, only
0·0001 gramme; Stevenson, in a case reported by Newton Pitt[4], 0·0086
per cent. of lead in the cæcum and colon. Notwithstanding a small
quantity of lead which may be determined by chemical methods as present
in the urine or the kidney, very definite nephritis is set up in these
organs, obviously due to the irritative effect of the metallic poison.
=The Kidneys.=--Kidney disease of several types has been described
as associated with poisoning by lead, particularly with chronic lead
poisoning, where large quantities of a soluble lead salt have been
ingested. Very considerable strain is thrown upon the kidney, with the
result that the lead salts themselves are passed through; but, as has
been pointed out when dealing with acute poisoning, the passage of lead
through the kidneys does not continue for any considerable time, and in
lead poisoning of an industrial and chronic nature no lead at all has
been found in the urine in undoubted cases. Even when present, it may
be difficult to detect unless the electrolytic method is used (see p.
174). At the same time kidney disease undoubtedly does occur in a very
large number of workers.
All heavy metals, of which silver, mercury, iron, zinc, and finally
lead, may be quoted as examples, appear to be eliminated by the kidney
when they are present in the body in toxic doses, and often when in
small non-toxic doses, but in the latter case to a greater extent
through the bowel than through the kidney. The lead circulating in the
blood, in common with other heavy metals, may be found chemically in
the kidney, but the quantity recovered is not as large as one would
expect from the considerable amount of inflammation often present.
In the experiments on animals, subjected to poisoning over considerable
periods, the condition of the kidney in every instance showed distinct
histological changes; and the longer such animals had been subjected
to the poisonous effects of the metal, the more advanced were the
signs of degeneration in its structure. In the earliest cases the
disease partook much more of the nature of an interstitial nephritis,
and it was in the later and more chronic stages only that changes
in the glomeruli and fibroid degeneration were to be found, but in
even these earliest cases of poisoning definite minute interstitial
hæmorrhages were to be found scattered about the kidney. These minute
hæmorrhages did not cause symptoms of hæmaturia, as in none of the
experimental animals was bloody urine observed. On the other hand,
besides definite small areas of hæmorrhage, patches were discoverable,
indicative of hæmorrhage which had undergone fibroid change. Even in
the illustrations given by Glibert[5], there appears to be evidence
that hæmorrhage had taken place and had undergone fibroid degeneration,
and there is very little doubt that in cases of kidney disease, the
preliminary action of the poison determines small local yieldings
of the vessel walls, with leakage, often hardly amounting to true
hæmorrhage, at such spots. There is nothing opposed to the theory in
the findings of other observers; in fact, if the preliminary gross
effect be leakage of the description given, all the other lesions
described by various observers follow as a corollary.
In the kidney, as in the other regions of the body, the venioles rather
than the arterioles appear to be the preliminary site of destruction,
and microscopical observation of the sections leads to the view that
the intima of the vessels and not the media or the muscular coat is
the one affected in the first place. Capillary hæmorrhages under
these conditions are easier to understand than if the arterioles
themselves or their muscular or middle coats were primarily affected.
As degenerative changes progress, the whole of the vessel--external and
middle coats and intima--undergoes change, ultimately resulting in the
extreme narrowing and consequent blocking of the vessels themselves.
Further shrinkage taking place in this area produces the shrunken
sclerosed kidney.
Zinc in the form of oxide behaves in very much the same way upon the
kidney as does lead. An experimental animal, which was given 0·2 gramme
of zinc oxide per kilogramme body weight by hypodermic injection in
the muscles of the back, died in fifteen days, and the kidneys showed
extensive hæmorrhages--not merely the minute and capillary hæmorrhages
found in lead poisoning, but hæmorrhages extending right through from
the cortex.
Clinically, kidney disease, unless albumin be detected in the urine,
is not a prominent symptom during the progress of an attack of chronic
lead poisoning, and is to be regarded as a late symptom, developing as
the result of long-continued irritation. The difficulty of eliminating
alcoholic complication has been discussed, and there are no specific
symptoms or post-mortem signs which enable one to distinguish alcoholic
nephritis from the nephritis of lead poisoning.
In the chapter on Pathology, the effect of alcohol on the kidney was
cited as a common predisposing cause of kidney disease in lead-workers,
and the effect of alcoholic excess in the case of a person who is
already the subject of chronic lead absorption may determine the change
from absorption to definite poisoning, because of alteration in the
excreting-power of the kidney. So long as the ratio between ingestion
and excretion is maintained the balance is kept up, and, although the
tissues of the body may show signs of a certain amount of degeneration,
no definite disease is produced; but the gastric irritation and the
work thrown upon the kidney in removing from the blood large quantities
of alcohol may be sufficient to alter this absorption-excretory balance
and determine the attack of poisoning.
Acute nephritis is rare, and cannot be regarded as a sequela of chronic
lead poisoning. Acute nephritis occurring in a lead-worker, with the
associated symptoms of general œdema of the face, eyes, hands, feet,
is of the gravest possible moment, and such a sudden appearance of
nephritis is almost invariably fatal. In chronic nephritis, to which
most of the lead cases belong, the usual signs are to be found in
the urine. Pain is rarely a symptom; and although pain in the back
is often complained of by lead-workers, examination rarely suggests
that the backache is of kidney origin, but rather the lumbago type
associated with chronic constipation. Care, however, must be taken,
when backache is complained of, in eliminating kidney disease as a
possible origin of the pain. A quantitative examination of the urine,
with reference to the total acidity and phosphate excretion, may
assist; and although this is not possible in a routine examination
of cases of lead absorption, it may be useful in cases of suspected
poisoning, especially where there are evidences of a good deal of
blood-destruction.
For convenience of description, it is better to consider the action of
lead upon the blood under two headings:
1. That of the corpuscular and other changes.
2. The action on the vessel walls, and pathological changes secondary
to disease of the vessels.
=The Anæmia of Lead Poisoning and Saturnine Anæmia.=--From the early
days of medicine it has been known that lead produces poverty of the
blood, and the white or yellowish-white appearance of persons who have
been subjected to long-continued inhalation of lead dust or fumes
constitutes striking evidence of blood-alteration. At the same time
it is a common fact that the facial pallor does not always go hand in
hand with diminution in the hæmoglobin. The conjunctiva may be observed
as a test for colour, and here may be seen the curious vaso-motor
disturbances which are partially responsible for the facial pallor.
Facial pallor in some forms of lead cachexia owes its origin to
interference with the nerve-supply to the vessel walls, and it is
a noticeable fact that a lead-worker whose face shows unmistakable
signs of pallor rapidly flushes when spoken to suddenly or if mentally
disturbed. The anæmia of lead poisoning is, however, a very definite
fact. All observers are agreed that a marked diminution in the
hæmoglobin of the blood takes place, to as low, often, as 35 per cent.,
without necessitating abstention from work, and without any serious
interference with respiration, even when performing heavy manual labour.
In persons in whom the hæmoglobin is diminished there is frequently a
yellowish or icterous hue of the skin, particularly the conjunctiva,
due to staining of the tissues with altered blood-pigment. The
hæmoglobin derivative--hæmatoporphyrin--can also be found in the
urine of persons suffering from a marked degree of reduction in the
blood-pigment, and may be taken as confirmatory evidence of destructive
or hæmolytic anæmia. The symptom is, however, a later one than is
frequently stated by the French observers, and can only be regarded as
a later and confirmatory symptom, and not as an early one of diagnostic
importance.
As would be expected from the destruction of blood-pigment, the
morbid process leaves its imprint upon the individual red cells, and
basophile staining of a number of the red corpuscles is to be found in
a very large proportion of persons poisoned by lead. Moritz[6] first
pointed out that these alterations in the red cells were present in
lead poisoning. The basophile granules are by no means confined to
lead anæmia, but are to be found in any severe secondary anæmia where
hæmolysis has taken place, as in nitrobenzene and aniline poisoning,
carbon bisulphide, etc. In addition to the basophile-staining granules
in the blood-cells, the whole corpuscle may take on a bluish-grey tint
when stained. The best stain to demonstrate these bodies is Leishman’s
modification of Romanowski’s, and there is no occasion to stain the
blood in the fresh condition, as the presence of the granules may be
demonstrated easily, even after two or three months. Schmidt[7] thinks
that if the basophile corpuscles reach 100 per million red cells the
cause is undoubtedly lead poisoning.
Alterations are also to be observed in the structure of the red
blood-cells in addition to the basophile staining. Distinct vacuoles
appear, but as a general observation--first noted by Glibert[8]--the
blood appears to be more resistant to damage when making the films,
and the red corpuscles themselves seem to be more elastic than normal
(increased viscosity). Alteration in the shapes of the corpuscles also
takes place, and not only small varieties--microcytes--but also the
large macrocytes are to be found. Nucleated red cells are rare.
The diminution in the number of the red cells is not so pronounced as
would be supposed from the diminution in the quantity of hæmoglobin;
but in the later stages, as in other secondary anæmias of toxic origin,
the total quantity of red cells sinks to a count of a million or less
per cubic millimetre.
According to Garrod, etc., the alkalinity of the blood is decreased in
lead absorption.
The white blood-corpuscles do not show any change in their structure
by the ordinary methods of staining, but they apparently show, as do
the red cells, more resistance to injury in spreading blood-films--that
is to say, the viscosity of the blood, which is apparently increased
in lead poisoning, is also exhibited by the white cells. In the
early stages of lead poisoning, more especially in acute lead
poisoning, distinct leucocytosis may be observed, such a leucocytosis
showing itself rather in relation to the lymphocytes than to the
polymorphonuclear cells. In addition, the large mononuclear cells are
also greatly increased, and a differential blood-count from a case of
lead poisoning which also shows the presence of basophile granules
in the cells invariably brings to light a definite increase in the
percentage number of lymphocytes, and a decrease in the number of
polymorphonuclears, and this even when the total leucocyte count is
not outside the ordinary limit of normal variation. On the whole, the
number of leucocytes present in the blood of persons suffering from
lead absorption will always be found to tend rather towards the higher
than the lower limit of normal variation.
At times a considerable increase in the number of eosinophile cells
is found in films made from persons suffering from lead poisoning,
particularly when there has been prolonged obstinate constipation. The
count is never high, and is rarely more than 5 or 6 per cent. It is not
usual to find any of the other forms of white cells in the blood, and
in this way the anæmia of lead poisoning may be easily differentiated
from the other forms, such as pernicious anæmia, lymphatic leucæmia,
spleno-medullary lymphocythæmia. By examining a number of blood-films
derived from persons subjected to lead absorption, and shuffled with a
number of films from normal persons, one of us (K. W. G.) has been able
to separate out, by the above method, the blood-films taken from the
suspected persons. The criteria in the determination were--
1. The presence of basophile granules.
2. Total basophile staining and size of corpuscles--poikilocytosis.
3. Differential count, showing increase in a number of lymphocytes and
large mononuclear cells.
Determination of the presence of lead poisoning from the examination of
the blood, therefore, receives considerable support; but at the same
time it is open to some objection from the fact that it is not in lead
poisoning alone that basophile granules make their appearance in the
blood. Any cause producing destruction of the red blood-cells, and even
their depletion by prolonged hæmorrhage, is followed by an increase in
the output of the red cells from the bone-marrow[9]. During this output
of extra blood-cells from the bone-marrow, numerous cells gain entrance
to the blood, in which the nuclei are not entirely degenerated; and
it is these particular cells which give the phenomena of basophile
staining, and their presence is rather indicative of the increased
blood-formation that is progressing, following blood-destruction,
rather than direct evidence of blood-destruction itself.
In a number of forms of anæmia--in fact, in almost all forms of severe
secondary anæmia, and certainly all forms of anæmia associated with
hæmolysis--the presence of basophile granules may be demonstrated.
They are commonly found in pernicious anæmia, secondary septic anæmia,
and the anæmia of malaria. Practically, the use of basophile granules
in the presence of the blood of lead-workers is being utilized in
Leipzig for the early detection of lead poisoning. By means of the
Zeiss eyepiece enumeration disc the relative number of basophile
granule cells to normal red cells is determined; and when the number
of red cells containing basophile granules exceeds 100 per million red
cells, the individual from whom the blood is derived is regarded as in
a presaturnine condition, and given proper treatment. By this means
it has been found possible to diminish the number of persons actually
suffering from lead poisoning.
The adoption of such a method has some drawbacks, especially in view of
the fact that substances other than lead may cause the basophilia. At
the same time there is no doubt that, if all persons employed in lead
trades who showed basophilia were suspended from their employment at
the present time, a very large number of persons would be dealt with.
Yet the practical application of this method is by no means impossible
under industrial conditions, and would at any rate give a definite test
upon which diagnosis could be made, though it would be quite impossible
to expect the general practitioner or the certifying surgeon to
estimate the basophilic content. All such estimations would necessarily
have to be performed at some properly equipped pathological laboratory,
such as at the present time many municipal authorities possess.
These facts are of importance, as a differential count of the white
cells, together with a careful inspection of a blood-film for basophile
staining and alteration in the red cells, as well as other phenomena
noted, together with an estimation of the hæmoglobin contained in the
blood, are to our mind of considerably more value in the diagnosis of
lead poisoning than is the quantitative estimation of the red or white
cells. The following tables give a certain number of enumerations,
etc., made from the blood of lead-poisoned persons:
BLOOD-EXAMINATION OF LEAD ANÆMIA--DIFFERENTIAL COUNT PER CENT.
+---+-----+---------+------+------+--+--+--+--+--+--+--+--+--+--+--+
|No.| Hb. | R.B.C. |W.B.C.|Index.|A.|B.|C.|D.|E.|F.|G.|H.|I.|J.|K.|
+---+-----+---------+------+------+--+--+--+--+--+--+--+--+--+--+--+
| | Per | | | | | | | | | | | | | | |
| |Cent.| | | | | | | | | | | | | | |
| 1| 60 |3,460,000| 7,000| 0·7 |63|20| 6| 3| 8| 0| +| -| +| -| +|
| 2| 45 |1,707,000| 9,000| 1·4 |46|38| 8| 1| 7| 0| +| +| +| +| +|
| 3| 55 |2,620,000|20,000| 1·0 |58|32| 4| 2| 4| 0| +| -| +| -| +|
| 4| 60 |1,334,000|10,000| 3·0 |55|35| 8| 0| 5| 0| +| -| +| +| +|
| 5| 54 |3,210,000| 8,000| 0·9 |52|41| 4| 2| 1| 0| +| +| +| -| +|
| 6| 60 |1,347,000|10,000| 3·0 |59|32| 3| 2| 3| 1| +| +| +| +| +|
| 7| 65 |3,760,000| 9,000| 0·9 | | | | | | | | | | | |
| 8| 65 |2,200,000|10,000| 0·7 | | | | | | | | | +| | +|
| 9| 50 |3,860,000| 8,000| 0·6 | | | | | | -| | | +| | +|
| 10| 60 |3,420,000| 9,000| 1·0 |76|16|13| 3| 0| 0| | | +| | +|
+---+-----+---------+------+------+--+--+--+--+--+--+--+--+--+--+--+
+---+-----------------------+------------------------------------+
|No.| Work. | Notes. |
+---+-----------------------+------------------------------------+
| | | |
| | | |
| 1|Paint mill | 5 years. |
| 2|Paint mill |10 years. |
| 3|Paint mill | 7 years. |
| 4|Packer white lead | 5 years. |
| 5|Grinder | 6 years. |
| 6|White lead | 8 years. |
| 7|Press and stoves | 8 years. |
| 8|Zinc distillation still|20 years; double wrist-drop 2 years.|
| 9|White lead beds |10 years. |
| 10|Packer | |
+---+-----------------------+------------------------------------+
A = Polymorphonuclears.
B = Lymphocytes.
C = Large hyaline.
D = Eosinophile.
E = Transitional.
F = Basophile.
G = Microcytes.
H = Megalocytes.
I = Poikilocytes.
J = Nucleated red.
K = Plehn’s bodies.
Corpuscles, Thoma-Zeiss.
Hæmaglobin, Haldane’s instrument.
Films, stained Leishman.
The form of lead inhaled is immaterial, and definite poisoning with
alteration in the blood may be occasioned, not only with white lead and
lead fume, but also even with lead sulphate and lead silicate.
The following table gives the result of blood-counts performed upon the
blood of persons employed in the manufacture of a paint erroneously
supposed to be innocuous, as the base consisted of lead sulphate and
oxysulphate:
DIFFERENTIAL COUNTS PER CENT. OF BLOOD-FILMS FROM LEAD SULPHATE WORKERS.
+---+-----+--+--+--+--+--+--+--+--+--+--+
|No.|A.[A]|B.|C.|D.|E.|F.|G.|H.|I.|J.|K.|
+---+-----+--+--+--+--+--+--+--+--+--+--+
| 1 | 55 |16| 5| 1| 0| +| +| -| +| +| +|
| 3 | 57 |16|26| 1| 0| +| +| -| -| +| -|
| 6 | 67 |23| 9| 1| 0| +| +| +| +| +| +|
| 7 | 72 |18| 5| 5| 0| +| -| -| -| +| +|
| 8 | 65 |26| 7| 2| 0| +| +| -| -| +| +|
+---+-----+--+--+--+--+--+--+--+--+--+--+
[A]
A = Polymorphonuclears.
B = Lymphocytes.
C = Mononuclears.
D = Eosinophiles.
E = Myelocytes.
F = Basophiles.
G = Microcytes.
H = Megalocytes.
I = Poikilocytes.
J = Vacuolated red cells.
K = Normoblasts.
Sand-papering surfaces of painted objects, walls, coaches, etc.,
also throws a definite amount of lead dust into the air whenever
the sand-papered paint contains lead. The following table gives
the differential counts of the blood of persons employed in the
furniture-painting trades:
DIFFERENTIAL COUNTS PER CENT. OF BLOOD-FILMS FROM FURNITURE-MAKERS
(SAND-PAPERERS).
+---+-----+--+--+--+--+--+--+--+--+--+--+
|No.|A.[A]|B.|C.|D.|E.|F.|G.|H.|I.|J.|K.|
+---+-----+--+--+--+--+--+--+--+--+--+--+
| 10| 48 |39|11| 1| 1| +| +| +| +| +| +|
| 13| 54 |35| 9| 2| 0| +| +| +| +| +| -|
| 15| 53 |32|13| 1| 1| +| -| -| -| -| -|
| 16| 58 |30| 9| 3| 0| +| -| -| +| -| -|
| 19| 56 |31|12| 0| 1| +| -| -| +| +| -|
+---+-----+--+--+--+--+--+--+--+--+--+--+
[A]
A = Polymorphonuclears.
B = Lymphocytes.
C = Mononuclears.
D = Eosinophiles.
E = Myelocytes.
F = Basophiles.
G = Microcytes.
H = Megalocytes.
I = Poikilocytes.
J = Vacuolated red cells.
K = Normoblasts.
=Circulatory System.=--A very large number of the symptoms referable to
chronic and well-defined lead poisoning are referable to circulatory
lesions, and, as has been elsewhere pointed out, the ultimate nerve
degeneration occurring in various parts of the body is probably but
a final symptom of the earlier hæmorrhage which has taken place.
Certain symptoms are, however, more closely related to the circulation
than others, and may therefore be more conveniently grouped together
under the present heading. The smaller changes, many of them connected
with special organs (such, for instance, as the eye) or particular
regions (as the mesenteric vessels), have been already referred to in
dealing with colic and eye changes. Vaso-motor changes precede the
actual change in the vessel walls themselves. On the other hand, the
alterations in the structure of the liver, lung, spleen, and more
especially the kidney, are secondary to change in the structure of the
walls of the vessels themselves.
Vaso-motor disturbances may or may not be of nervous origin, although
the former view is probably correct, and it is also equally possible
that the direct affection of the vessels is associated with the nerve
irritation. On the other hand, direct inflammation of the vessel
walls, resulting in obliterative arteritis, in arterio-sclerosis,
and degeneration and exudation in the kidney, lung, and liver,
are practically due to degenerative changes either in the intima
or the middle coats of the finer vessels. The common symptoms of
arterio-sclerosis, vertigo, headache, and pulsation in the vessels, and
of the persistent headache already referred to, all suggest changes
taking place in the vessels complicated by œdema. In the early stages
of kidney degeneration, however, it is common to find an interstitial
nephritis due apparently to exudation from the vessel walls. Such an
hypothesis is to some extent supported by the somewhat allied condition
of engorgement and fibroid change in the liver and lung, and to a
lesser extent in the spleen. In the lung, even in persons not exposed
to inhalation of lead, and in animals, as pointed out by Glibert,
secondary changes in the lung follow lead intoxication, such changes
taking the form of emphysema and generalized fibrosis; whilst the
liver is engorged with blood, and later undergoes similar degenerative
changes. The bloodvessels in these organs are found to have lost a
considerable amount of their elasticity, to have yielded here and
there, and in other places to be completely closed by obliterative
arteritis. Microscopical hæmorrhages are to be found mainly in the
veins leading from the capillaries. In the kidney such vessel changes
as are outlined are the precursors of disease, and albumin is found
in the urine, but the quantity is rarely very large. Casts are not
common, and the amount of lead present in the urine may be exceedingly
small, difficult to trace, and in many cases entirely absent.
In the later stages of chronic saturnism the heart may show
degenerative changes. Microscopical examination of the heart muscle
shows that alteration of the fibres of the muscles takes place in a
manner similar to that of the voluntary muscles. Disease of the heart
valves is uncommon; alterations in the heart sounds are infrequent; the
clinical picture of the cardiac condition is that of a “flabby” heart.
REFERENCES.
[1] MEILLÈRE, G.: Le Saturnisme. Paris, 1903.
[2] BLYTH, WYNTER: Proc. Chem. Soc, 1887-88.
[3] PEYRUSSON AND PILLAULT: Meillère’s Le Saturnisme, chap. iv.
[4] NEWTON PITT: Trans. Path. Soc, No. 42, 1891.
[5] GLIBERT: Le Saturnisme Expérimental: Extrait des Rapports Ann. de
l’Inspect. du Travail, Brussels, 1906.
[6] MORITZ: Mediz. Woch., St. Petersburg, 1901.
[7] SCHMIDT: Arch. für Hygiene, vol. lxiii., p. 1, 1907.
[8] GLIBERT: _Ibid._
[9] BOYCOTT: Journal of Hygiene, 1910.