Full text of New Test for Industrial Lead Poisoning : The Presence of Basophilic Red Cells in Lead Poisoning and Lead Absorption : Bulletin of the United States Bureau of Labor Statistics, No. 460

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U. S. DEPARTMENT OF LABOR
JAMES J. DAVIS, Secretary

BUREAU OF LABOR STATISTICS
ETHELBERT STEWART, Commissioner

BULLETIN OF THE UNITED S T A T E S)
B UREAU OF L A B O R S T A T IS T IC S )
INDUSTRIAL

ACCIDENTS

AND

* * ’

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HYGIENE

SERIES

A NEW TEST FOR
INDUSTRIAL LEAD POISONING
THE PRESENCE OF BASOPHILIC RED CELLS
IN LEAD POISONING AND LEAD ABSORPTION

By CAREY P. McCORD, M . D.
INDUSTRIAL HEALTH CONSERVANCY LABORATORIES
CINCINNATI, OHIO




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APRIL, 1928

UNITED STATES
GOVERNMENT PRINTING OFFICE
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1928

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CONTENTS
Page

A nontechnical statement of the problem and a summary of principal
1,2
findings!------------------------------------------------------------------------ «_____________
Importance of lead poisoning___________________________________________
2-5
Immature red cells_____________________________________________________
5,6
Characteristics of young erythrocytes___________________________________
6,7
Basophilic substance in immature red cells------------------------------------------- 7-10
Methods of detecting basophilic material________________________________ 10-13
Wright’s stain---------------------------------------------------------------------------------10
Robertson’s method for the counting of reticulated cells_____________ 10,11
Cunningham’s method for the counting of reticulated Cells__________
11
Friedlander-Wiedemer method of enumeration of basophilic red cells. 11,12
The basophilic aggregation test---------------------------------------------------- 12,13
Clinical and laboratory materials utilized in this work__________________ 13-17
Basophilic red cells in normal persons___________________________________ 17-19
Basophilic red cells as an index of exposure to lead_____________________ 19-26
Basophilic red cells in clinical lead poisoning____________________________26-32
Summary---------------------------------------------------------------------------------------------- 32,33




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BULLETIN OF THE

U. S. BUREAU OF LABOR STATISTICS
NO. 460

WASHINGTON

APRIL, 1928

A NEW TEST FOR INDUSTRIAL LEAD POISONING1
A Nontechnical Statement of the Problem and a Summary of
Principal Findings
The danger of lead poisoning is so widespread in industry and the
action of lead as an intoxicant is so insidious that any method by
which the early effects following lead exposure may be detected prior
to any disability would be of the greatest worth wherever lead is a
hazard.
In the past the diagnosis of lead poisoning has generally depended
upon the presence of definite and easily recognizable symptoms, with
the result that the disease has become well established before meas­
ures to correct the condition are instituted. Therefore the incidence
of lead poisoning remains high, notwithstanding the fact that the
mode of entry of this toxic substance into the body is well known,
that the distribution of lead after absorption is well established, and
that the factors influencing the absorption, deposition, and excretion
of lead are fairly well understood. This is due to the fact that there
has been lacking any suitable index of lead absorption among workers
who are exposed to the hazard but who have not developed obvious
manifestations of the disease.
A simple laboratory method which would reveal the degree of lead
absorption in the individual and thus permit the institution of pre­
ventive measures before actual lead poisoning has taken place would
be of great value in the prevention and control of the disease. Such
a test was proposed in a preliminary report by McCord, Minster,
and Eehm in 1924,2 the proposed test being based on the appearance
in the blood stream of immature red cells. The present report is
based upon a continuation of the preliminary study, and the purpose
of the investigation is to determine the extent of usefulness of this
test in detecting lead absorption and lead poisoning in workers and
others, arid as a measure of the extent of the lead hazard in different
occupations and industries.
1 Collaborating in this work are Dorothy K. Minster, A. B .; William Paul, B. S .:
Elizabeth M. Schwebel, Ch. E .; H. G. Higginbotham, M. D .; Alfred Friedlander, M. D .;
Charlotte Wiedemer, M. D .; Susie Friedlander, A. B .; all members of or consultants to the
Industrial Health Conservancy Laboratories.
2 “ Basophilic aggregation test in lead poisoning,” by C. P. McCord, D. K. Minster, and
M. Kehm, in Journal o f the American Medical Association, May 31, 1924, vol. 82, p. 1759.




1

2

NEW TEST FOR INDUSTRIAL LEAD POISONING

The report includes a technical description of the production of
the immature red cells, of the technique followed in making the blood
counts, and an account of the clinical and laboratory materials
utilized. The study includes the examination of more than a thou­
sand persons, some of whom were exposed to lead while other groups
were used as controls in checking the results of the tests.
Following is a brief summary of the conclusions reached as a
result of the study, a more complete statement of the results being
carried at the end of the report.
The number of immature red cells in the blood which contain
basophilic substance—that is, substance which is stainable by certain
dyes—is increased above normal limits in various pathologic states,
including lead intoxication, benzol and arsenic poisoning, certain
types of anemias, at times in acute infections, and in many other
conditions; but in a person exposed to lead and in the absence of
other conditions presenting high basophilic red cell counts such a
condition may be accepted as indicative of lead absorption or lead
poisoning.
Cases of definite lead poisoning ordinarily present basophilic red
cell counts ranging from 7,000 to 50,000 per cubic millimeter of blood,
although the counts, rarely, may fall below 7,000 or may exceed
100,000. It is possible that very high basophilic red cell counts—that
is, in excess of 50,000—may be present without symptoms of clinical
lead poisoning, but cases of poisoning are prone to develop among a
group presenting such high basophilic red cell; counts.
Workers exposed to lead who present basophilic red cell counts in
excess of 6,000 to 7,000 should be regarded, in the absence of other
conditions productive of such increased counts, as potential leadpoisoning cases and as such should be subjected to treatment.
The use of this test has revealed not only an extensive absorption
of lead among workers in those industries and those departments
with a known lead hazard, but also among office workers, clerks, etc.,
in these industries who in the past have commonly been considered as
unexposed. This is especially true if the lead hazard is present in
the form of lead dust.
The basophilic red cell counts do not, however, stand in any con­
stant relation to the hemoglobin percentage, to the total red or white
count, or to the late effects of lead poisoning, such as wrist drop.

IMPORTANCE OF LEAD POISONING
Lead poisoning continues to be the outstanding severe occupa­
tional disease in the United States. Although the report of Hoff­
man3 indicates a diminishing death rate from lead poisoning, it
should not be maintained that the incidence of this disease has
reached negligible numbers. For many reasons mortality statistics
are of little value in a study of lead-poisoning incidence. One
outstanding reason is that rarely does a lead-exposed worker die
of lead poisoning which is uncomplicated and typical. The im­
* U. S. Bureau of Labor Statistics Bui. No. 426: Deaths from lead poisoning, by F. L.
Hoffman. Washington, 1927.




NEW TEST FOR INDUSTRIAL LEAD POISONING

3

mediate cause of d< 1 *
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1 ’onic lesion to which
contributed, but the
lead absorbed over
physician in making out the death certificate is prone to place em­
phasis on the apparent cause of death, such as the nephritis, the
cardio-vascular diseases, etc., without associating lead as a primary
producing factor.4 Lead mortality rates are so low as to serve only
remotely as an index of lead morbidity. For every single death from
lead not fewer than 50 cases of nonfatal Jiead poisoning are believed
to occur. On this basis, Hoffman’s 3 figure of 142 deaths in the
United States registration area in 1924 (the latest figures available)
would indicate a yearly minimum of 7,100 lead-poisoning cases in
this same area. In Ohio alone, since the application of the occupa­
tional disease act (July 1, 1921) up to January 1, 1927, 907 cases of
industrial lead poisoning have been reported, including 37 deaths.
Eight hundred and forty-two of these claims entailed awards from
the State fund for compensation and medical care of $287,760, to­
gether with a loss of 277,112 days.5 To this number of cases of
clinical lead poisoning occurring in Ohio, and those estimated for
other portions of the registration area, must be added the larger
number of cases of “ lead absorption ” common to both industry and
the general population.
A circumstance favorable to the perpetuation of a high lead poi­
soning morbidity rate grows out of the fact that most diagnoses are
dependent upon the actuality of plumbism, rather than upon the
detection of the lead-absorption stage preceding lead poisoning.
Much confusion now exists as to the relation between “ lead absorp­
tion 55 and “ lead poisoning.” “ Lead absorption ” has come to be
accepted by some as synonymous with “ mild lead poisoning,” reserv­
ing the term “ lead poisoning ” for the profound lead episodes, such
as encephalitis. This interpretation has led to evasion in reporting
such cases in some States requiring the reporting of “ lead poison­
ing,” but not specifying66lead absorption.” More nearly exact defini­
tions of several commonly used terms are as follows:
I. Lead ingestion without absorption.
Lead may enter the alimentary tract without concomitant absorp­
tion and leave the body in the feces in the same amounts. No absorp­
tion, no symptoms, no lead in the urine, no blood changes.
II. Lead absorption.
Lead may enter the body through any portal and be retained for
indefinite periods without subjective manifestations. The quantity
of lead so absorbed may be sufficient to produce lead poisoning under
conditions favoring its development, such as acidosis. Obviously,
lead poisoning is always preceded by a stage of lead absorption, but
lead absorption is not always followed by lead poisoning. In this
stage lead may be demonstrated in feces and urine. Blood changes
inay occur. A lead line may be present in lead absorption.
* U. S. Bureau of Labor Statistics Bui. No. 426: Deaths from lead poisoning, by
F. L. Hoffman. Washington, 1927.
4 U. S. Bureau of Labor Statistics Bui. 120: Hygiene o f the painters’ trade, by Alice
Hamilton, M. D. Washington, 1913.
6 Industrial Commission of Ohio. Division of Safety and Hygiene. Special Bulletin
No. 1. Columbus, Ohio, 1927.




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NEW TEST FOR INDUSTRIAL LEAD POISONING

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equally absorbed by all persons equally exposed and equal absorption
of lead by a group of workers does not lead to similar responses,
either as to severity or as to the time of manifestations among the
different individuals. Because of these circumstances it becomes
highly desirable to have available some simple laboratory procedure
through the application of which lead absorption and the fluctuation
of the rate of lead absorption in the individual may be detected.
Such a test was proposed in a preliminary report by McCord,
Minster, and Rehm, in 1924.2 This proposed test is based on the
appearance of immature red cells in the blood stream. This present
report is based upon a continuation of the preliminary study. Tbe
purpose of this investigation is to determine the extent of usefulness
of this test as previously employed and as subsequently modified, as:
(as) A quantitative index of lead absorption, (6) an index of immi­
nent plumbism, (c) an index of actual lead poisoning, (d) a measure
indicative of the extent of the lead hazard in particular processes or
industries.
IMMATURE RED CELLS
The production of red blood corpuscles (erythrocytes) is, in nor­
mal adult human life, a bone marrow function. The endothelium
lining the sinuses of bone marrow is the tissue from which the
primitive red cells spring. Prior to their entry into the blood stream,
these cells undergo a series of modifications such as the acquiring of
hemoglobin and the loss of nuclei. The bone marrow remains the
site of this maturation. Under normal conditions, the blood stream,
though intimately in contact with these developing erythrocytes does
not dislodge them until maturity is attained. It is improbable that
the delivery of developed red cells is in anywise dependent upon any
activity of the cells themselves, such as ameboid movement, although
the quality of adhesion of immature red cells as described by K ey6
may be a factor of red cell retention in bone marrow. The growth
pressure arising from a growing tissue confined in an unyielding
environment finds least resistance in the blood stream and thus leads
to extrusion of the more mature red cells lying at the periphery of
developing masses. These erythrogenetic centers commonly present
the least mature cells at the center with movement outward as
maturation progresses. Through such controlled processes as here
briefly described, an orderly steady flow of formed red cells is secured
for normal life.7
When, however, the bone marrow or other portions of the body
are subjected to abnormal circumstances this well-balanced delivery
of red cells into the peripheral circulation is upset and cells not yet
mature may find their way, in large numbers, into the general cir­
culation. A stimulation of the bone marrow only slightly in excess
2 “ Basophilic aggregation test in lead poisoning,” by C. P. McCord, D. K. Minster, and
M. Rehm, in Journal of the American Medical Association, May 31, 1924, vol. 82, p. 1759.
6 “ Studies of erythrocytes, with special reference to reticulum, polychromatopliilia,
and mitochondria,” by J. A. Key, in Archives o f Internal Medicine, November, 1921, vol.
28, p. 511.
7 “ The pathological physiology of blood cell formation and blood cell destruction,” by
C. K. Drinker, in Oxford Medical Looseleaf, Vol. II, p. 509; “ Studies of living human
blood cells,” by F. R. Sabin, in Bui. of the Johns Hopkins Hospital, September, 1928,
vol. 34, No. 391, p. 277; “ Experimental bone marrow reactions: III, Polycythemia,
normoblasts, and erythrocytic hyperplasia of the bone marrow produced by gum shellac,”
by G. L. Muller, in Journal of Experimental Medicine, May, 1927, vol. 45, No. 5, p. 753.

82758°—28------ 2



6

NEW TEST FOR INDUSTRIAL LEAD POISONING

of normal may be met by an increased delivery of red cells in a state
of essential maturity. An increased stimulus, however, leads to a
delivery of cells progressively less mature, until under the most dire­
ful conditions if any cells at all enter the blood stream they may be
so little removed from the endothelium as to possess no hemoglobin.
The stimuli to which bone marrow responds are numerous, but the
mechanism through which response is secured is uncertain in some
circumstances. When hemorrhage occurs, immature red cells are
immediately found to be in the blood stream and continue to appear
until the emergency no longer exists. In divers anemias, immature
cells commonly are detectable. The absence of immature cells under
such conditions is an unfavorable aspect.
Ultra-violet irradiation induces a similar response. Neoplasms
involving the bone marrow majr effect an abnormal blood picture
through pressure. Rarely, a quickly generated leucocytosis has as
a concomitant immature red cells in the blood stream.8 Elvidge9
has secured an outpouring of immature red cells following intra­
venous injections of quartz particles. Lehmann10 produced similar
results with calcium carbonate, coal, and cement dust administered
through inhalations. Paul, Friedlander, and McCord11 found that
benzol, long known to exert an action on bone marrow, led to altered
blood pictures because of the extrusion of unripened blood cells from
the bone marrow. Similar results were obtained by Muller8 with
colloidal silver, india ink, shellac. Lead is also capable of inducing
a marked increase in the numbers of immature cells in the peripheral
blood (McCord, Minster, and Rehm 2). It thus appears that among
other stimuli, bone marrow may respond to (a) physiologic stimula­
tion, (&) pressure stimulation, and (o) toxic stimulation.
CHARACTERISTICS OF YOUNG ERYTHROCYTES
Such young red cells as may be found in the peripheral circulation
have qualities or markings that serve to distinguish them from
mature cells.
The nucleated red cell is characteristic of marked immaturity.12
The immature cell is more resistant to heat distortion than mature
cells.13
The young cells are usually larger than the older cells in the same
preparation.14
2 “ Basophilic aggregation test in lead poisoning,” by C. P. McCord, D. K. Minster, and
M. Rehm, in Journal of the American Medical Association, May 31, 1924, vol. 82, pp.
1759-1763.
8 “ Experimental bone marrow reactions: III, Polycythemia, normoblasts, and erythro­
cytic hyperplasia of the bone marrow produced by gum shellac,” by G. L. Muller, in Jour­
nal of Experimental Medicine, May, 1927, vol. 45, No. 5, p. 753.
9 “ Foreign particles, the reticulo-endothelial system and anemia,” by A. R. Elvidge, in
Journal o f Pathology and Bacteriology, 1926, vol. 29, No. 4, p. 325.
10“ New experimental investigations on the value of basophilic granulated erythrocytes
in the early diagnosis of lead poisoning,” by H. Lehmann, in Archives of Hygiene, 1926,
vol. 96, p. 321, abstract in Journal of Industrial Hygiene, February, 1927, vol. 9, No. 2,
p. 34.
u “ Basophilic material in benzol poisoning,” a preliminary report, by W. D. Paul, A.
Friedlander, and C. P. McCord, in Journal of Industrial Hygiene, May, 1927, vol. 9,
No. 5, p. 193.
12 “ Properties of young erythrocytes in relation to agglutination and their behavior in
hemorrhage and transfusion, by R. Isaacs, in Archives of Internal Medicine, February,
1924, vol. 33, p. 193.
18 “ Resistance of immature erythrocytes to heat,” by R. Isaacs, B. Brock, and G. R.
Minot, in Journal of Clinical Investigation, June, 1925, vol. 1, p. 425.
14Biffi. H .: In Bui. Soc. Med. Ann., 1908, vol. 79, p. 8. (Quoted from Key.)




NEW TEST FOR INDUSTRIAL LEAD POISONING

7

The immature cells are more resistant to crenation than more
mature cells.6
The hemoglobin content is less in developing cells.6
A tendency appears to exist among premature cells to adhere one
to another, and to white cells.6
The incompletely developed cell consumes oxygen, while the adult
erythrocyte consumes none or much less oxygen.15
The specific gravity of immature red cells is less than that of adult
cells.16
Seyfarth16 believes that immature red cells are given to poikilocytosis more readily than mature cells.
Immature red cells contain basophilic material.6
BASOPHILIC SUBSTANCE IN IMMATURE RED CELLS
With any cells having so many distinguishing markings as indi­
cated above, it should prove readily possible to devise some test to
detect their occurrence.
Of all these characteristics of young cells, the presence of basophilic
substance appears to be most constant, and the one that lends itself
best to the demonstration of immature cells.
The exact nature of basophilic material is not known. It is
vaguelv described as a lipoidal derivative of the cell nucleus, as a
rest 01 the primary protoplasm, as a product of nuclear pyknosis.
Earlier it was thought that this substance was peculiar to blood cor­
puscles. Subsequently, it has been shown to have a wide distribution
in body tissues. In the case of red blood cells, it is a constituent only
of immature cells and of the pathologic, misbuilt types o f cell such as
is found in hemolytic jaundice.16 Prior to birth, a period exists in
which all red blood corpuscles in the fetal circulation are basophilic.17
At birth the percentage of basophilic substance in the red cells of
human beings is still far above the normal for adults. This number
quickly falls during the first 10 to 15 days of post-uterine life and
by the end of the first month of life the basophilic containing cells
in the peripheral circulation are scant.
Seyfarth,16 who describes basophilic material under the term “ sub­
stantia granulo filamentosa,” outlines the morphology of basophiliccontaining cells as follows:
Vital stained bone marrow of the embryo and the newborn and smears made
during life (by sternum puncture) of the marrow of man and animals show
that the earliest form of red cell, the hematocytoblast, which contains abso­
lutely no hemoglobin, shows no perceptible substantia granulo filamentosa. As
soon as the slightest amount of hemoglobin is perceivable in the protoplasm
of the cell one can see the first appearance of the vital granules always situ­
ated very close to the nucleus. Other erythroblasts show larger or smaller
vital granules, but always in close proximity to the nucleus. Again in other

6“ Studies on erythrocytes, with special reference to reticulum, polychromatophilia,
and mitochondria,” by J. A. Key, in Archives of Internal Medicine, November, 1921,
vol. 28, p. 511.
15“ Oxygen consumption of human erythrocytes,” by G. A. Harrop, in Archives of
Internal Medicine, June, 1919, vol. 23, p.745. (Quoted from Key.)
16“ Experimentelle und klinische untersuchungen iiber die vitalfarbbaren erythrozyten,”
by C. Seyfarth, in Folia Haematologica, Band 34, Heft 1 zu 7. April, 1927 (Archiv).
17 “ Reticulation and age of red blood corpuscles in normal and anaemic mice,” by S. B.
De Aberle, in Anatomical Record, March, 1927, vol. 35, No. 1, p. 30 (ab a ). See also
footnote 16.




8

NEW TEST FOR INDUSTRIAL LEAD POISONING

cells having a smaller nucleus it is not possible to see any protoplasm as
usually seen in these early forms. This protoplasm is obscured by a heavy
wall of substantia granule filamentosa clothing the nucleus. In some of these
cells it is possible to notice a slight excrescence of hemoglobin from the sub­
stantia. Other erythroblasts that have smaller nuclei and, therefore, are
older forms, show a zone of hemoglobin about the wall of the substantia. In
the riper erythroblasts and in the normoblasts the zone of hemoglobin is
broader while the wall of substantia about the nucleus becomes a little lighter,
broader and less compact. At this time the granules and threads are discern­
ible. Most of the normoblasts show a smaller nucleus surrounded by a
wall of substantia that shows many gapsi. And, later, one sees forms that
look like the serrations of a broken crown sitting on the nucleus * * *. As
the cell ripens, this wall of substantia becomes lighter, smaller granules are
seen and also thread forms. These break up to small granules spread mostly
at the margin of the cell, and when most of the substantia has disappeared
there are left only these fine granules at the margins. The end result is a red
cell fully ripe and free from all vitally staining substance.18

When basophilic material is present it may be observed in a
variety of forms, some of which are undoubtedly the result of
physico-chemical manipulation and do not represent native states of
this substance. Polychromasia, reticulated cells, punctate stippling,
substantia granulo filamentosa, basophilic aggregations, mossy cells,
etc., are but different stages or phases or modifications of the same
mother substance. It is very difficult to determine which of these
forms, if any, represents the native form. Seyfarth maintains that
the unstained blood as seen in the dark field presents reticulation, and
that the diffuse polychromasic granulation is a solution product
brought about in the fixation and staining. This author further
maintains that so rigid are these reticulo-granular formations that
after cellular disruption by hypotonic stains these networks may
float away intact, and that manually these networks may be un­
coiled under the microscope.
For the purpose of this work, the terms commonly used in con­
nection with the basophilic content of red cells are employed as
defined hereinafter.
Polychromotaphilia) or Polychromasia as applied to red cells is
descriptive of a diffuse but discrete distribution of basophilic ma­
terial throughout the greater portion of the red cell. When such
cells are stained with Wright’s type of stain these cells appear
grayish, bluish, or purplish, and are commonly less translucent than
other red cells in the same preparation. Between the origin of the
primitive red cell in the endothelium, after the first appearance
of hemoglobin, and the nonnucleated adult cell, practically any
stage of development may be accompanied by polychromatophilia.
There are some reasons to believe that every red cell passes through
a stage in which polychromasia may be exhibited. There are other
reasons to believe that polychromasia is present only when the ma­
turation is speeded up beyond natural rates. Polychromasia is evi­
dence of regeneration of red cells and commonly is regarded as
a beneficent phenomenon.19 When this polychromatophilia results
from a toxic irritation of the bone marrow in the absence of a phys­
iologic need for additional cells in the blood stream, this beneficence
may be questioned.
18Our translation ; for exact language see original text.
19««The pathological physiology of blood cell formation and blood cell destruction,” by
C. K. Drinker, in Oxford Medical Looseleaf, vol. 2, p. 509.




NEW TEST FOR INDUSTRIAL LEAD POISONING

9

Basophilic reticulation is that intracellular arrangement of baso­
philic substance in which a network or skein exists. This network
may occupy the entire cell or be limited to the periphery or the
central position of the cell. This form has given rise to the term
“ reticulocyte ” and the condition in which it exists is termed “ reticu­
losis.” Some doubt is justified as to the existence in a native state
of reticulation. When a stain of the Wright type is applied to a
fixed blood smear, polychromasia, if such exists, is brought into
visibility. No reticulocytes, however, are thus brought into view*
Since this stain is capable of staining basophilic substance as shown
by the polychromasia, and since basophilic reticulation is of the
same origin, the absence of the latter suggests that this condition
does not exist. When, however, a slide preparation is stained by
any of the well-known suitable vital or semivital methods, especially
if the red cells become hemolyzed in the process, reticulation is
readily observable and polychromasia is then not in evidence. It
appears tenable that reticulation at times at least may be a creation
rather than a native state of basophilic substance. We have on this
account avoided the terms “ reticulocyte ” and “ reticulosis.” Of this,
K ey20 states—
polychromatophilia and reticulum occur normally in all young red blood ceUs.

In the next paragraph, however, in referring to his earlier publi­
cations, he states—
* * * the reticulum is formed by the union of this basophilic substance
(polychromatophilia) with a supra vital stain.

Cupp21 has shown that in the animals studied by him all red cells
in the peripheral circulation are reticulated. Cupp’s reticulation is,
however, probably not composed of basophilic material. It is possi­
ble that the basophilic reticulation is but a rearrangement of polychromatophilic granules around the elements of the network of
Cupp’s reticulation.
Punctate stippling is a third form of basophilic material in red
cells. This form is probably never seen in bone marrow cells,
although chemical manipulation may create a picture simulating
this condition. In the peripheral circulation it is characterized by
the presence within the red cell of multiple minute discrete clumps
of a material having the staining reactions of basophilic material.
That punctate stippling is not a result of staining, as is believed to
be true for reticulation, may be demonstrated by the examination of
fresh untreated blood.6 Punctate stippling is to be associated with
young red cells, and represents a young cell that has been harmed.
The source of the stipples is probably the polychromatophilic cell.
It is thus a preformed condition denoting degeneration, or at least
representing a pathologic state. Punctate stippling is thus not an
6 “ Studies on erythrocytes, with special reference to reticulum, polychromatophilia, and
mitochondria,” by J. A. Key, in. Archives o f Internal Medicine, November, 1921, vol. 28,
p. 511.
20 “ Lead studies: Blood changes in lead poisoning in rabbits with especial reference to
stippled cells,” by J. A. Key, in American Journal o f Physiology, September, 1924, vol. 70,
p. 86.
21 “ On the structure of the erythrocyte,” by C. D. Cupp, in Anatomical Record, 1915,
vol. 9, p. 259.




10

NEW TEST FOR INDUSTRIAL LEAD POISONING

index as to numbers of immature cells, but possibly of numbers of
pathologic or degenerating immature cells.
Basophilic aggregations is a term introduced by McCord, Min­
ster, and Rehm2 descriptive of the various forms of basophilic
material as found in red cells that have been laked, thus removing
the hemoglobin and bringing the basophilic material into greater
visibility. Through variations in technical procedures as to tonic­
ity, time, and acidity it has proven possible to produce divers
forms of basophilic substance within the cells from the same blood
specimen. These include fragmentation, combined reticulation
and granulation, coarse stippling and fine stippling, wreaths or
bands at the periphery, balls of clumped basophilic substance at the
center of the cell, cedematous red cells with distended reticulum, etc.
These are not artifacts in the common use of that term, but are
artifactitious so far as geometric form is concerned.
Whatever be the significance of the various geometric forms o f
basophilic substance, its presence in red cells in numbers above nor­
mal is the surest and earliest indication of bone marrow response
to toxic or physiologic stimulation.
METHODS OF DETECTING BASOPHILIC MATERIAL
Consideration of the relative merits of the many procedures avail­
able for the demonstration of basophilic material can not be included
in this publication. Reference is made again to the work of K ey22
for a comprehensive presentation of methods and literature. Our
data in this respect are limited to a description of the methods we
have used most satisfactorily, and others in common use,
WRIGHT’S STAIN

This widely known method of staining is suitable for the demon­
stration of punctate stippling and polychromatophilia. Reticulation
is not brought out by this procedure. The technique of staining,
and the characteristics of cells so stained, are too well known to call
for additional comment.
ROBERTSON’S METHOD FOR THE COUNTING OF RETICULATED
CELLS23
A saturated solution of brilliant cresyl blue was made up in normal salt
solution. This was kept as a stock solution. When a count was to be made,
a small quantity of it was diluted eighty times24 with normal salt solution and
2 “ Basophilic aggregation test in lead poisoning/* by C. P. McCord, D. K. Minster,
and M. Rehm, in Journal of the American Medical Association, May 31, 1924, vol. 82,
pp. 1759.
" “ Studies on erythrocytes, with special reference to reticulum, polychromatophilia, and
mitochondria,” by J. A. Key, in Archives of Internal Medicine, November, 1921, vol. 28,
p. 511; “ Lead studies: Blood changes in lead poisoning in rabbits with especial reference
to stippled cells,” by J. A. Key, in American Journal o f Physiology, September, 1924, vol.
70, p. 86.
28 “ The effects o f experimental plethora on blood production,’’ by O. H. Robertson, in
Journal of Experimental Medicine, August, 1917, vol. 26, No. 2, p. 221.
24 “ Since doing this work, a second saturated solution of cresyl blue has been made up,
using a different stock of the dye, which went into solution to a considerably greater
extent than the first. The result was that a 1 :8 0 dilution of this saturated solution was
much too strong a staining fluid. It was found necessary to dilute to 180 for satisfactory
staining. It is apparent, therefore, that each saturated solution of cresyl blue has to be
tested beforehand for its optimum staining dilution. This is a very simple matter and
needs to be done only once.”




NEW TEST FOR INDUSTRIAL LEAD POISONING

11

mixed with blood in a pipette for counting white cells in the proportion of one
part of blood to twenty parts of cresyl-blue solution. The mixture was shaken
in the pipette for 5 minutes. The cells were thus equally distributed as well as
stained. They were counted at once in fresh preparations, which were sealed
with vaseline to prevent disturbances due to drying. At least 1,000 red cells
were counted at each test. When the numbers of reticulated cells were less
than one in a thousand, 10,000 red cells were counted. In the latter case, only
the first 1,000 were counted individually, the field being the unit of count for
the remaining 9,000.

CUNNINGHAM’S METHOD FOR THE COUNTING OF RETICULATED
CELLS25
In this study it was found that permanent preparations could be made by
combining a vital with a Wright’s stain. The reticulation is as clear, if not
clearer, than by the older methods, and the Wright’s stain retains all its
differential qualities, except the poiychromatophilia, which is not present. The
ease and simplicity of this method brings the study of reticulated erythrocytes
within the scope of routine blood examination.
The technique is divided into two stages, first, a small drop of a 0.3 or 0.5
per cent aqueous or alcoholic solution of brilliant cresyl blue is placed on the
end of a clean slide or the center of a cover glass, smeared around over an
area 1.5 centimeters in diameter with the aid of a match or glass rod and
permitted to dry. After this is dry there may be a narrow margin of thick
stain which should be wiped off with a damp cloth, leaving a central, uniform
area. These slides or cover glasses may be prepared in large quantities, and if
stacked side by side in a box and kept dry the stain will not deteriorate. The
second stage consists of taking a drop of fresh blood on a clean cover slip and
dropping it face down on one of the areas of dried stain. If the cover slip is
clean the blood will quickly spread to the edges. The stain goes into solution
almost instantly. (This preparation may be observed as a vital stain.) The
cover glasses, or slide and cover glass, are now pulled apart as in making an
ordinary blood smear and are permitted to dry. Smears may also be made
by placing the drop of blood directly on the dried stain and spreading it with
a cigarette paper or another slide. On drying, the blood turns a dirty greenish
blue color. The slide cover glass is then stained with Wright’s blood stain.
Too vigorous washing causes the reticulum to lose some of its stain. The
preparation is dried in the usual manner and when mounted in Canada balsam
keeps at least four months and probably much longer.
The reticulum is stained a deep or light blue, depending on its density, and
gives a striking picture in its contrast with the pink protoplasm of the cell as
shown in the accompanying illustrations. Various types of reticulation are easily
seen from the heavy skeinlike material to knotted granular particles connected
by delicate blue threads and finally the separate granules which resemble
stippling seen with Wright’s stain alone. The nucleated erythrocytes in human
blood usually have many fine threadlike blue staining filaments around or
radiating from the nucleus. There is no poiychromatophilia seen. Whether the
reticulation has replaced the poiychromatophilia or not is a question requiring
further investigation. The examination of many smears certainly suggests
this as a possibility.

FRIEDLANDER-WIEDEMER METHOD OF ENUMERATION OF
BASOPHILIC RED CELLS26

Two collaborators in this present study have previously published
a counting method, as follows:
After cleansing the finger or the ear of the subject in the usual manner, and
pricking, blood was drawn into the leukocyte tube of any good hemocytometer
up to 0.5. Brilliant cresyl blue solution (0.25 per cent) in normal saline solu­
tion was then drawn in until the mixture of blood and stain reached point 11
25 “ A method for the permanent staining o f reticulated red cells,” by T. D. Cunningham,
in Archives of Internal Medicine, October, 1920, vol. 26, No. 4, p. 405.
26 “ Basophilic aggregation in the newborn,” by A. Friedlander and C. Wiedemer, in
American Journal of Diseases of Children, December, 1925, vol. 30, pp. 804-809.




12

NEW TEST FOR INDUSTRIAL LEAD POISONING

on the counting tube. The tube was shaken for about three minutes; then a
drop was expressed on the ruled counting slide. With .a D D Zeiss high dry lens,
counts and computations were made as for leukocytes, the figure derived repre­
senting the total number of basophilic red cells per cubic millimeter.
In such a preparation the basophilic substance commonly presents itself as
two or three coarse granules, with or without a few reticulating strands
interwoven.
THE BASOPHILIC AGGREGATION TEST

The simple method used by McCord, Minster, and Rehm 2 in testing
for imminent lead poisoning or lead absorption permits the collection
of large numbers of blood specimens without difficulty, and without

f ig

. i — d ia g r a m m a t ic R e p r e s e n t a t io n o f a F r es h Blo o d S m e a r

the necessity for any apparatus. In this procedure a blood smear,
approximately three times the thickness of that in common use for
differential counts, is made on a glass slide. This smear is unfixed
and is air dried. Staining is secured by a dilute, acidulated methy­
lene blue or by hypotonic saline methylene blue, or through the use
of dilute Manson’s methylene blue. Staining is carried out for 10
minutes. Overstaining does not occur. The excess stain is dashed off
and the slide is dipped in distilled water as few times as are necessary
to remove the remaining stain. The slide is allowed to dry in air.
Examination is made with an oil immersion lens, without any cover
slip.
2 “ Basophilic aggregation test in lead poisoning," by C. P. McCord, D. K. Minster, and
M. Rehm, in Journal o f American Medical Association, May 31, 1924, vol. 82, pp. 17591763.




13

N E W TEST FOR IN D U STRIAL LEAD POISONIN G

Microscopic examination presents the usual red cells only as faint
shadows (Fig. I I ), except for the periphery which may be distinct.
The white cells stain deeply and the various types may be differen­
tiated. I f there are red cells containing basophilic material, this
material stands out sharply as coarse granules or as combined
granules and network. (Figs. IV and V.) This staining method
appears to bring into greater visibility the very diffuse basophilic
material seen in polychromatophilic cells.
I f the blood smears so stained are of approximately the same thick­
ness, a counting, for several fields, of the cells showing basophilic
aggregation affords a rough quantitative estimate as to the excess

F i g . I I . — d i a g r a m m a t i c r e p r e s e n t a t i o n o f a F r e s h Bl o o d S m e a r w i t h
C e l l s L a k e d w i t h H y p o t o n i c S a l in e

A ll red cells are enlarged and delineated only by periphery.
basophilic substance in cells. Characteristic o f normal blood.

No

over normal. The normal person may, by this method, show only
one or two basophilic cells in an entire slide, while in lead poisoning
every microscopic field may present 10 or more basophilic red cells.
CLINICAL AND LABORATORY MATERIALS UTILIZED IN
THIS WORK
The conclusions reached in this investigation are derived from the
results of the examinations of over a thousand persons (1,045) to
determine the number of basophilic-containing red cells found in the
blood stream under a variety of conditions. The actual number of
tests made are far in excess of 1,000, for in some instances as many as

82758°—28-----3



14

N E W TEST FOE IN D U STRIAL LEAD POISONING

30 tests were made on a single person. These persons may be divided
into the following groups:
Control I .— One hundred and forty-five persons without any ex­
posure to lead were tested to establish the range of normal numbers
of basophilic red cells. This group included no persons known to
be abnormal in any way. It included persons of all ages, both sexes,
several races. The tests were made over a period of months em­
bracing all seasons and at such times as were likely to detect the
influences of physiologic processes, such as eating, sweating, etc. The
range of normal limits accepted by us is stated and discussed in a
subsequent section.

F ig . H I — d ia g r a m m a t ic r e p r e s e n t a t io n o f a F r es h Bl o o d S m e a r w it h
C e l l s l a k e d w i t h h y p o t o n i c S a l in e

Many cells contain basophilic substance. Characteristic o f blood
in lead poisoning, severe antemias, hemolytic icterus, etc.

Control I I .—A second control group was made up o f more than
100 patients found in a general hospital. In this phase of the work
emphasis was placed on a study of anemias, leukemias, pregnancy,
the newly born, premature births, the influence of ultra-violet irra­
diation, infections, acute and chronic. The data derived are far too
diversified and extensive to permit of inclusion here in detail. The
trend o f the entire results establishes that there are many physiologic
and pathologic conditions besides lead intoxication in which numbers
of basophilic red cells far exceed normal limits. These conditions
are such that with one exception little conflict is to be anticipated in
the application of these methods to the early detection of lead absorp­
tion. The one exception is benzol poisoning, which is closely asso­



N E W TEST FOR IN D U STRIAL LEAD POISONIN G

15

ciated with lead poisoning through the extensive use of both of these
toxic substances in the painting industry.
Control I I I .—A third control group of 200 persons were patients
in a tuberculosis sanatorium. This group was selected because the
preliminary study suggested that this common infectious disease
might so often be positive as to jeopardize the worth of this method
in the control of lead poisoning. The results show that only after

hemorrhage (possibly also tuberculous peritonitis) do counts ap­
proximate the high counts seen in rarer diseases, such as pernicious
anemia or lead poisoning.
IY . Lead exposed.—This study included various groups of lead
workers in seven industrial plants, representing divers types and
different degrees of lead hazards. The total number of workers,
including persons subsequently reappearing as lead poisoning cases,
was 550. The group included white lead manufacture, lead found­
ing, storage battery manufacture, red lead manufacture, newspaper



16

N E W TEST FOR IN D U STRIAL LEAD POISONIN G

composition, spray painting, brush painting, and soldering,
various occupations represented in these groups were:
House painters.
Spray painters.
Solderers.
Linotypers.
Hand composition workers.
Stereotypers.
Pasters.
Battery chargers.
Battery assemblers.
Battery-grid molders.
Lead-oxide mixers.
Corrosion workers.
Water grinders.

The

Oil grinders.
Lead packers.
Lead-pipe makers.
Solder makers.
Office workers in lead industries.
Maintenance groups in lead in­
dustries, including crane oper­
ators.
Buckle molders.
Red-lead workers.
Tanbark workers.
Dry-kiln tenders.

F ig . V — M ic r o p h o t o g r a p h o f L a k e d B a s o p h ilic R ed C e l l s in B lo o d o f Le a d P o is o n in g Case

Laked normal red cells seen faintly as shadows

A subsequent section is given over to the discussion of findings
from this group.
A listing of the articles manufactured from lead or utilizing lead
in the process of manufacture (with the exception o f organic lead
compounds) is shown in Chart I.



NEW TEST FOR INDUSTRIAL LEAD POISONING

17

Y. Lead-poisoning cases.—Fifty cases of clinical lead poisoning
were included in this study. The significant findings are discussed in
a separate section.
VI. Animal experiments.—In addition to studies made on human
beings, experimental observations have been carried out on rabbits,
dogs, cats, monkeys, guinea pigs, chickens, goldfish, etc. A portion
of this animal study has already been published in connection with
a study on the influence of benzol and its homologues on basophilic
red cell production.11 These animal studies establish precisely that
an intake of lead is quickly followed by the appearance in the blood
stream of abnormal numbers of basophilic red cells.
BASOPHILIC RED CELLS IN NORMAL PERSONS
A traditional figure of 0.8 per cent is widely accepted as represent­
ing the basophilic cell incidence among normal adults. Isaacs27
states—
In health, while the number of these corpuscles in the peripheral blood vary
around 1 per cent, increases to 2 or 3 per cent may take place without evidence
of disease.

Vogel and McCurdy28 suggest as normal figures for basophilic
cells 5 to 10 per cent for infants and 0.5 to 2 per cent for adults.
Krumbhaar29 furnishes a table of normal reticulated cells for man
and other animals, as follows:
Species

Range (per cent)

Man_____________________________________________________ 0.1-0.8
Monkey_________________________________________________ .0 - .8
Dog______________________ ______________________________ .1 -1 .4
Cat_____________________________________________________ .0 - .4
Guinea pig---------------------------------------------------------------------- 1.0-4.0
Rabbit____________ ______________________________________ . 6-2.8
Mouse__________________________________________________ 1.0-6.0

This author cites Cathola and Dannay as finding in children, after
the fourth day of life less than one cell per thousand. Stitt30 records
not more than 1 reticulated cell per 500 as the normal limit for
healthy adults.
Some authors in commenting on the normal occurrence of baso­
philic cells use the word “ rare.” If, however, we extend Isaacs’ upper
normal figure of 3 per cent to a person presenting a total red count
of 5,000,000 per cubic millimeter, we derive 150,000 reticulated cells
per cubic millimeter, which is far from 64rare.” At best it is to be
recognized that the normal basophilic count is not standardized. The
slide methods (usually Cunningham’s or Robertson’s) such as have
led to these enumerations offer many sources of error. Few persons
11 “ Basophilic material in benzol poisoning,” a preliminary report, by W. D. Paul, A.
Friedlander, and C. P. McCord, in Journal of Industrial Hygiene, May, 1927, vol. 9,
No. 5, p. 193.
27 “ Effect of Rontgen ray irradiation on red blood cell production in cancer and leuke­
mia,” by R. Isaacs, in American Journal of Medical Science, January, 1926, vol. 171, No. 1,
p. 20.
28 “ Blood transfusion and regeneration in pernicious anemia,” by K. M. Vogel and U. F
McCurdy, in Archives of Internal Medicine, 1913, vol. 12, p. 707.
a “ Reticulosis— increased percentage of reticulated erythrocytes in the peripheral
blood,” by E. B. Krumbhaar, in Journal of Laboratory and Clinical Medicine, October,
1922, vol. 8, No. 1, p. 11.
80 “ Practical bacteriology, blood work, and animal parasitology,” by E. R. Stitt. Phila­
delphia, P. Blakiston’s Son & Co., 7th ed.




18

n e w TEST FOR INDUSTRIAL LEAD POISONING

would attempt to derive the total white-blood count by counting in
relation to 1,000 red cells and expressing the total in relation to the
total or normal red count. Nicholson81 has questioned the accuracy
of differential counts made by slide methods because of uneven dis­
tribution. In the case of immature cells. Key,6 has pointed out a
tendency to cohesion and adhesion to white cells thus jeopardizing
any even distribution throughout the slide surface. Seyfarth16
states:
In the grown, healthy person there are from 0.1 per cent to about 0.2 per cent
of vitality stained erythrocytes; in the peripheral blood. This count is also given
as normal by Naegeli, Morawitz, and others. Higher figures, as some of the
previous workers have stated, could not be substantiated in counting 50 healthy,
rested, abstinent men. Cunningham stated in 1919 that he obtained counts
about 0.8 per cent in normal persons. Roessingh’s counts of 30 healthy indi­
viduals were from 0.4 per cent to 1.8 per cent, but these figures are too high.
He used the Widal and Abrami method of centrifuging his blood, but did not
realize that the vitally stained cells are found mostly in the upper layers.
In full grown animals I have found the following average figures of vitally
stained erythrocytes in the peripheral blood; these were counted at the Leip­
zig abattoir. In the horses, cattle, sheep, and hogs there were hardly any
vitally stained cells to be seen. The cat showed 0.1 to 0.2 per cent; the dog,
0.2 to 0.5 per cent; the guinea pig, 0.5 to 5 per cent; rats, 3 to 5 per cent;
mice, 4 to 6 per cent; rabbits, 3 to 8 per cent. In the younger animals we
obtained the highest counts.

Our own examinations of normal persons for basophilic red cells
have yielded results better in keeping with Seyfarth,16 Naegeli,
Moravitz, Stitt, Cathola, and Dannay.
In 145 normal persons, repeated counts rarely exceeded 5,000
basophilic cells per cubic millimeter of blood. By far the greater
number were below 1,000 such cells. In the spring months in some
persons considerably exposed to sunlight the normal count mounts
to a maximum of 20,000 per cubic millimeter and may remain high
during the summer. We believe this is due to additional ultra­
violet irradiation from sunlight. Artificially produced ultra-violet
rays stimulate a prompt formation of basophilic red cells far in
excess of normal. According to Krumbhaar 29 the usual oil immer­
sion lens field contains approximately 200 red cells. In our thicker
slide preparations about 600 cells are then present. I f our figures
were in accord with Isaacs’ concept of from 1 to 3 per cent as normal,
we would, assuming only 1 per cent of such cells, expect to find six
basophilic cells in an average field. This has been true in no
instance for normal adults.
As utilized by us the chamber counting method has yielded as
a normal basophilic count a maximum of 5,000 per cubic millimeter,
with some temporary increases up to 20,000 per cubic millimeter as
a spring and summer seasonal variation. By the slide method of
basophilic aggregation normal persons have never presented (except
6 “ Studies of erythrocytes, with special reference to reticulum, polychromatophilia, and
mitochondria,” by J. A. Key, in Archives of Internal Medicine, November, 1921, vol. 28,
p. 511.
16 Experimentelle und klinische untersuchungen iiber die vitalfarbbaren erythrozyten,”
by C. Seyfarth, in Folia Haematologica, Band 34, Heft 1 zu 7. April, 1927 (Archiv).
29 “ Reticulosis— increased percentage of reticulated erythrocytes in the peripheral blood,”
by E. B. Krumbhaar, in Journal of Laboratory and Clinical Medicine, October, 1922, vol.
8, No. 1, p. 11.
81 “ A combined diluting and staining fluid for differential leucocyte counts in the count­
ing chamber,” by D. Nicholson, in Journal of Laboratory and Clinical Medicine, March,
1927, vol. 12, No. 6, p. 548.




NEW TEST FOR INDUSTEIAIj LEAD POISONIKG

19

in the seasonal variation) more than 1 cell per average field, The
average count for normal individuals is approximately 500 per cubic
millimeter. Although counts up to 5,000 may be accepted as within
normal limits for a particular individual, this may be indicative of
a pathologic condition for an individual who when normal would
not exceed the average of 500. As possible exceptions to our state­
ments as to normal counts we record the following physiologic or
near-physiologic states in which higher counts have been observed
by us or by others: Pregnancy, newborn, profuse sweating, after
arsenic or iron medication, high altitudes, exposure to ultra-violet
rays or X rays; possibly also the intake of foods effect slight
variations.
BASOPHILIC RED CELLS AS AN INDEX OF EXPOSURE
TO LEAD
Five hundred and fifty lead workers have been examined from one
to thirty times for the presence of basophilic red cells in the blood.
The types of industry and the divers trades presenting the lead
hazards have been mentioned in a foregoing section. Wherever
a lead hazard exists some but not all the exposed workers exhibit
basophilic red cells in excess of normal. This is shown in Table I,
in which the results from the testing of groups of workmen selected
at random are arranged in the order of previously accepted degree
of hazard.
In this table the types of processes have been divided into eight
zones according to the degree of exposure to lead. In Zone I fall
the workers without known exposure. In Zone II fall the workers
whose exposure is remote, such as automatic solder machine tenders,
etc., through the increasing severities of exposure to Zone V III,
where workers are exposed directly and grossly to lead dusts. It
will be noted that the average number of basophilic red cells for
each zone increases as the severity increases—863 per cubic milli­
meter in Zone I, 1,233 per cubic millimeter in Zone II, to 24,800 per
cubic millimeter in Zone V III.




T a b le

I.— Number

of basophilic red cells in workers, arranged according to an already established degree of hazard, by zone
Zone III

Z o n e ll
Remote exposure to
lead, such as in
tin-can manufac­
ture




2.400
2,600
1.400
400
800

1,200

1,2

1,376

2,150

1.000

800
4,400
1,200

800

Red-lead makers,
painters

Wet or oil lead
grinding

White-lead corrosion
workers; battery
pasters

Workers exposed to
lead dust; whitelead packers

Number
Number
of baso­
of baso­
philic
philic
of
of red
cells Period
red cells Period
exposure
exposure
per
per
cmm. of
cmm. of
blood
blood
400 24 years...
1,600 20 years...
200 10 years...
2,000 20 years...
600 20 years...
400 2 years__
1,200 18 years...
200 20 years...
1,200 18 years...
1.400 15 months.
800 14 years...
400 25 years...
400 15 years...
1.400 20 years...
600 27 months.
6,600 15 years...
4,000 21 years...
7 years__
1 year......
13 years...
5 months..
7 years__
7 months..
17 years...

22 years__
600 23 years__
400 6 years___
200 16 years__
1,600 16 years__
200 21 years__
1,200 39 years__
200 7 years___
200 3 years___
4.600 5 years___
1,800 8 years___
800 9 years___
2.600 1 year.......
3.000 1 month...
600 6 years___
400 17 months.
200 15 years—
600

Zone VIII

1,200
1,200

400
1,000
600
800
600
1,000
1,200

4.800
2.400
3,000
3.800
1,600
1.800
3.600
4.200
4.200
6.600

2 months..
6 months..
8 years__
20 years...
19 years...
3 years__
2 months..
3 months..
7 years___
7 years___
30 years...
3.5 years..
19 months.
19 years...
6 years—
1 year......
2.5 years..
9 years__
21 years...
13 years...
3 months..
1 month...
1 month...

Number
Number
of baso­
of baso­
philic
philic
of red
cells
red cells Period
exposure
per
per
cmm. of
cmm. of
blood
blood

Period of
exposure

3.600 30 years__
3.200 13 years...
600 1 week___
800 8 months..
3.400 1 week___
2,000 5 months..
4.800 11 years__
4.600 12 years...
800 21 years__
4.000 1 year___
5.800 5 years___
6.200 29 months.
8.600 2 years___
29,000 8 years___
4.200 5 years___ 10,000 2 years___
5.400 3.5 years. _
3.200 8 months..
600 14 years__
1,800 24 years...
7.000 13 years__
1.600 5 months..
1.000 6 years___
3.200 16 years...
200 6 years___
2.200 2.5 years. _
800 18 months.
3.000 2 months..
3,200 3 months..
800 3 months..
4.800 8 months. _
200 5 months..
9.600 3 years___
5.000 4 months..
200 7 years___ 44,800 4 years----600 7 months..
1.000 1 month...
2.800 1 year.......
6,800 23 years...
600 10 years...
600 3 days......
2.600 2 years___
1,400 1 year......
2 weeks__
1,200
3 years___
3,747

5,527

Number
of baso­
philic
red cells
per
cmm. of
blood
1,200

4.000
600
2.400
1,800
3.800
1,200

9.200
9.200
18,200
6.800
26,200
15,800
54,600

Period of
exposure

9 years----8 years___
17 years...
4 years___
21 years...
12 years...
4 years___
4 months..
12 months.
1.5 years..
1 year.......
8 years___
8 years___
5 weeks.. .

Number
of baso­
philic
red cells
per
cmm. of
blood
68,600
1,200

2,800
4.400
4.800
12.400
18,000
92,000
3,200
1.400
1.800
61,600
70.400
4,600

6.000

7,600
9.200
20.400
22.400
2.400
800
4.200
3,800
12.400
10,175 ....................

24,800

POISONING

Average.

1,000

Zone VII

LEAD

800 33 years...
2.400 8 months..
400 1 year.......
200 10 months.
400 8 months..
200 8 months..
400 10 months.
200 8 months..
1,800 1 year.......
2,200 11 years...
3.400 6 months..
600 1 year.......
800 8 months..
600 4 years___
600 1 year.......
400 8 months..
200 8 months..
400 10 months.
600 1 year.......
200 9 months..
600 6 years__
1,600 3 years__
21 years...
30 years...

Period of
exposure

Zone VI

FOR INDUSTRIAL

3 years....
8 years....
2 months.
6 months.
I month..
8 months.
II years...
11 years...
7 years....
3 months.
36 years...
1 month..
31 years...
25 years...
12 years...
7 years....
26 years...
5 years....
4.5 years..
3 years....
24 years..
18 years..

Period of
exposure

Number
of baso­
philic
red cells
•per
cmm. of
blood

Exposure such as of­
fice workers in lead Molten lead workers
industry.

Zone V

TEST

Period of
exposure

Number
of baso­
philic
red cells
per
cmm. of
blood

Zone IV

NEW

Zone I
Industrial workers
without known ex­
posure to lead (con­
trol)

NEW TEST FOB INDUSTRIAL LEAD POISONING

21

From this specimen table, which is characteristic of the entire
group2 it appears also that the length of exposure to the hazard has
very little to do with the percentages of basophilic red cells present.
Only during the first few days of exposure in cases of marked suscep­
tibility is time an essence. It may not be maintained that a year’s
service in a work place having a minor lead hazard is equal in danger
to 20 days in a work place having a severe lead hazard. In our
experience many workers exposed to minor lead hazards may work
over periods of years without presenting either signs or symptoms of
lead absorption or lead poisoning. Gradual accumulation of lead may
take place to the threshold of lead poisoning, but this is far from
being a regular occurrence. The extent of the lead hazard to which
the worker is exposed, rather than the duration of exposure, deter­
mines the probability of lead poisoning.
It is from the individuals who present basophilic red cells in excess
of 6,000 per cubic millimeter that clinical cases of lead poisoning are
apt to arise, regardless of the hazard zone into which they have been
arbitrarily placed.
The total harm produced by lead upon exposed workers is not
represented by the number of clinical cases of lead poisoning. It is
believable that small quantities of lead repeatedly absorbed exact
a toll from the health and length of life of the workers even in the
absence throughout life of any clinical lead poisoning. Preven­
tion of frank lead poisoning is not sufficient. Control should be
extended to embrace lead absorption. I f positive tests for an excess
of basophilic red cells be accepted as evidence of lead absorption,
then any abnormally high basophilic red count in a lead worker
should command attention without waiting for actual complaints.
All data have been analyzed to determine the influence of the age
of the worker on the numbers of basophilic red cells. No such rela­
tion was established.
Many of the persons presenting high basophilic red-cell counts,
while remaining at work, were none the less cases of lead poisoning.
Commonly, these persons present some of the following lesser charac­
teristics of plumbism—anemia, low hemoglobin, Burtonian line, joint
pains, muscle cramps, headaches, constipation, anorexia, etc. Under
treatment and supervision there is no necessity for the removal of
these mildly involved workers from all employment. On the other
hand, others may evince no signs of lead absorption other than the
presence of basophilic cells in large numbers until without warning
they suddenly become acutely and severely ill with lead poisoning.
Undoubtedly, quantitative determinations of lead in urine under such
circumstances would lead to the recognition of imminent poisoning,
but no dependable methods of urinalysis are available for quick
routine application in lead industries. Given sufficient exposure
while at work, enough lead may be absorbed in one day to provoke
lead poisoning. This necessitates in some industries examinations
at such short intervals as two weeks. Since urinalysis for lead
routinely requires a period represented by days, this otherwise excel­
lent procedure is at present impractical.
At the time of counting basophilic red cells other blood examina­
tions were carried out as follows: Total red count, hemoglobin, total
white count, differential white count, Cunningham count of reticu­




22

NEW TEST FOR INDUSTRIAL LEAD POISONING

lated cells, basophilic aggregation tests. No constant relation was
established between the percentages of basophilic red cells and the
total red count, total differential white count or hemoglobin. A
basophilic count far in excess of normal (e. g., 50,000 per cubic milli­
meter) is compatible with a hemoglobin of 110 per cent and a red
count of 5,500,000. A relative lymphocytosis is frequently associated
with a high basophilic count but either may occur without the other.
Punctate stippling stands in no regular quantitative relation to the
basophilic material brought out by the methods that we have
employed.
In those industries utilizing lead in some of its various forms, some
departments will obviously present a greater lead hazard than others.
In newspaper composition the linotype room, if equipped with elec­
tric heating devices and completely inclosed heating chambers, mani­
festly affords less opportunity for plumbism than the stereotype
room. In white-lead manufacture the corrosion room work is far
more hazardous than, for example, “ buckle casting” ; kiln drying
and emptying is commonly more dangerous than pulp grinding. In
storage-battery manufacture the pasting of grids represents the out­
standing danger point, while the lead hazard is almost negligible in
the electric charging room.
At present the accepted test as to the extent of the hazard or as to
the efficacy of protective measures is found in the number of leadpoisoning cases that arise. Since the number of actual cases does
not represent the totality of harm from lead, this test, which is ac­
cepted as a measure of the hazard, is fallacious, for in departments
in which no cases arise the inference is that no hazard exists, yet
appropriate tests may show that every worker is absorbing lead
The data of Table I suggest that a relation exists between the num­
ber of basophilic red cells in the blood of workers and the severity
of the hazard. I f this is true, a procedure becomes available for the
testing of the efficacy of devices protecting the worker against lead
poisoning and will permit the grading, with relative certainty, of
various types of work as to the extent of the lead hazard. Further,
to prove this method of graduation we have applied these tests to
specific departments in two lead-usmg industries. The results are
shown in Table II.
T a b le II.—Basophilic red cell counts in the ivorkers in two lead-using industries,

by department
Basophilic red cell count for
individual workers

Estimate of hazard

Type of work

D aily new spaper p la n t: Linotype departm ent—Linotypers w ith ou t
previous hand work; w ith in 20 years
400 Electrically heated inclosed lead
400
pots. Exposure to metallic lead
200
but little evidence of dust.
200
600
400
1,200
Average for group...........




485

Linotype work.

N E W TEST FOR IN D U STRIAL LEAD PO ISONIN G

23

T a b le II.—Basophilic red cell counts in the workers in two lead-using industries,

by department—Continued
Basophilic red cell count for
individual workers

Estimate of hazard

Type of work

D aily new spaper p lan t: Iiinotype departm ent—Linotypers w ith previous
hand w o rk w ith in 20 years
1,400
1,600
1,600
2,000
600
400
400
200

Similar to above, except for previ­
ous greater exposure in hand
work. No cases.

Linotype work.

Average for group______ 1,025
D aily n ew spaper p la n t: Composing: room —Hand com position
2,800
1,200
1,000

600
800
600

This work involves direct handl­
ing of type, and some open cast­
ing of type. No cases.

Usual hand composition.

1,000

400

1,200

1,200

200

Average for group______ 1,000
D a ily new spaper p la n t: Stereotype departm ent—Stereotyping
1,200

4.800
2,400
3,000
3.800
1,600
1.800
3,600
4,200

Molten lead hazard with small
quantities of dust present. No

Stereotype composition work, with
additional hazard of heated print­
ing inks.

Average for group--------- 2,933
W h ite -le a d fa c to r y : Office w orkers
600 Low. No cases............................. Office work in white-lead factory,
800
well isolated from factory. Little
1,200
communication between this
1,400
buildiDg and adjacent factory
800
building.
400
400
1,400
Average for group...........

875

W h ite -le a d fa c to ry : Corrosion room—T a k e-o u t
2,600 Hazardous. Many workers pre­
sented signs of lead poisoning.
11,000
7,800
4,600
12,400
3,800
Average for group............7,033




Work involves emptying of cor­
rosion pots. Hazard from dust.
Hazard from pulp lead.

24

NEW TEST FOR INDUSTRIAL LEAD POISONING

T a b le II. — Basophilic red cell counts in the workers in two lead-using industries,

by department— Continued
Basophilic red cell count for
individual workers

Estimate of hazard

Type of work

W h ite -le a d fa c to r y : Corrosion room —Setting; group
3,400 Some hazard. Handling of buckle
7.200
lead. Source of known cases of
plumbism.
4.800
2.800
4,600
1,000
800
1,000
200
600
4.200

Some lead dust from repeatedly
used tanbark. Some shifting of
this group to other jobs.

Average for group........... 2,616

W h it e-le a d fa c to r y : M olten m etallic lead departm ent
2,400 No known cases of lead poisoning
from this department.
200
6,200
600
1,800
800
1,000
1,800
5.200
1,000
1.200
2,600
3.800
1.800
1,800
2,200
3.000
200
2.000
4,000
400
Average for group.........

Lead pipe molding. Solder mold­
ing. Lead at low temperatures
only.

2,095

W h ite -le a d fa c to r y : D ry k iln room —D ry lead packing:
61,600
68,600
1,800
1,400
70.400
22.400
4,600

Extremely hazardous. Clinical
evidence of lead poisoning.

Hopper tending. Barreling dry
white lead. Kiln-room work.
Dust everywhere.

Average for group.......... 32,971
W h it e-le a d fa c to r y : Shipping departm ent
600 Some exposure from pulp lead,
outside containers. Shipping
3,800
room near molten-lead room.
2,600
2,200
2,200
1,400
Average for group..........




2,133

Much handling of metallic lead
and containers of white lead.

NEW TEST FOR INDUSTRIAL LEAD POISONING

25

T a b le II.—Basophilic red cell counts in the workers in two lead-using industries,

by department— Continued
Basophilic red cell count for
individual workers

Estimate of hazard

Type of work

W h.ite-le a d fa c to r y : W a te r g rin d in g
2,600
600
2,800
600
44,800

Few cases of lead poisoning origi­
nate in this department or in
the oil grinding department.
Carelessness a considerable fac­
tor.

Grinding of lead pulp after corro­
sion, prior to drying in kiln room.

Average for group.......... 10,280
W liite -le a d fa c to ry : R ecovery room
9,600
4.800
3,200
1.800
Average for group..........

Workroom very foggy. Brass
pouring in this department.
High temperatures of molten
lead.

Reclaiming work. Handling of
dross and metallic lead. Some
blow-torch work.

4,850

Although no cases of clinical lead poisoning have appeared in any
department of the newspaper plant referred to in Table II, the
results from the examination of workers in various departments for
basophilic material in the blood suggest that stereotype work is more
hazardous than hand-composition work and that hand-composition
work affords a greater hazard than linotype composition with in­
closed electrical heating devices. This classification based on blood
examination alone confirms the commonly accepted opinion as to
the relative hazard in the newspaper plant departments.
In the white and molded lead factory a number of danger points
or dangerous departments are apparent from our examination as
well as from actual experience as to the source of clinical lead cases.
It is obvious that corrosion work constitutes a greater hazard than
work in the molten-lead department. Our figures here show an aver­
age of 2,095 basophilic red cells for the molten lead group as against
7,033 for the corrosion room “ take-out” group. This again bears
out the belief as to the relative hazards of these two departments.
White lead in dry form, such as found in barrel packing and in
kiln-room work, affords a high degree of lead hazard as again shown
by our figure of 32,971 basophilic red cells.
In this same factory it was also possible to locate through routine
blood examination for basophilic material unsuspected danger points;
for example, the office boy in the works manager’s office, which is set
apart from factory work, proved to have a high count of basophilic
red cells. Observation established the fact that foremen and work­
ers from the factory daily tracked lead into this office, and this was
stirred up by the office boy’s ineffectual daily sweeping.
For the best application of this method of grading the hazards,
tests on a considerable number of workers in any department are
desirable. The larger the number of workers examined, the more
accurately will the average number of basophilic red cells show the
true magnitude of the hazard. In determining the degree of hazard



26

NEW TEST FOR INDUSTRIAL LEAD POISONING

by this method, known ambulatory cases of plumbism should not be
included. In Table II, under “ Water grinding ” the count from one
known case of plumbism is included. As a result this type of work
is made to appear more hazardous than the “ take-out ” work in the
corrosion room. This is not true.
In Table II, under “ Shipping department,” it appears that an
average of 2,133 cells per cubic millimeter obtained. This suggests
that this work is as hazardous as “ molten-lead work,” which depart­
ment averaged 2,095. In this particular factory this, undoubtedly,
is a true representation of the facts, because the shipping department
and the molten-lead department are adjacent, without separating
walls. The lead hazard is therefore about the same in these two
departments.
In “ corrosion work” those men who place buckles of lead into
corroding jars and later build up the tiers of such jars on beds of
tanbark are far less exposed than the group who later tear down
these stacks and empty out the corroded lead. The relative hazards
are shown by comparison of the “ setting group,” which averaged
2,616 basophilic red cells per cubic millimeter, as against the figure
of 7,033 for the “ take-out ” group.
In the newspaper plant the older linotypers presented a slightly
higher count than the younger men. All previous work had prompted
the belief that in adult years age alone was not a factor in the baso­
philic red-cell count. Further inquiry established that nearly all of
these older men had in previous years performed “ hand typesetting,”
which is known to be a more hazardous type of lead work.
Our total results, of which the tables presented are but specimens,
suggest that through the routine examination of lead-exposed workers
the degree of hazard and unsuspected danger points may be estab­
lished. This method affords a simple procedure for the recognition
of lead absorption by groups. Although not infallible, this method
promotes the hygienic control of the lead hazard in the absorption
stage.
BASOPHILIC RED CELLS IN CLINICAL LEAD POISONING
From fifty cases of lead poisoning under our supervision we have
made the following observations with reference to the occurrence,
duration, and significance of basophilic red cells:
Clear-cut clinical cases of lead poisoning almost invariably pre­
sent large numbers of basophilic red cells. The range more often
encountered was from 7,000 to 50,000 per cubic millimeter. (See
Case Group X .) However, counts up to 96,000 were not unusual.
The higher counts may not be interpreted as an index of greater
severity of the disease.
Long standing sequelae of lead poisoning, such as wrist drop or
other neuro-muscular lesions, need not necessarily be associated with
an increase of basophilic red cells, although one case of double wrist
drop, following lead poisoning about 10 years previous, did present
a high count. We are not certain that this is evidence of retained
lead from his earlier known involvement, owing to the fact that he
is still employed in a lead industry, although in a department apart
from any definite lead hazard. (See Case 18, P.)



NEW TEST FOR INDUSTRIAL LEAD POISONING

27

Clinical lead poisoning habitually arises in industry among those
workers who on previous examinations have presented high baso­
philic counts or counts that show increases on successive tests, al­
though within the range of normal. (See Cases 39, B. and 12, R.)
We have observed two patients who within a three-year period have
suffered from lead poisoning of severe character four or more differ­
ent times. During the first portion of this mentioned period we were
utilizing only the slide method. The oft-repeated tests revealed a
high basophilic aggregation count of from 4 to 6 per microscopic
field. Whenever for any reason, such as infection or overwork, the
normal regime of either of these two men was upset clinical lead
poisoning was prone to appear; but at the time of the disabling epi­
sodes the basophilic red cells did not apparently increase. In other
words, the amount of lead harbored by these men over periods of
months was sufficient to provoke lead poisoning—given a condition of
reduced alkalinity or comparable changes in the blood and tissues.
Many of our cases were treated with alkalies following the treat­
ment outlined by Aub.32 Although symptoms and some signs readily
disappeared, the number of basophilic red cells remained high. This
we feel is explicable inasmuch as alkali treatments lead to a deposi­
tion of lead primarily in bony tissues where the contact with bone
marrow may not be terminated. (See Cases 20, C. C.; 36, F. G. H.)
There its restricted toxic action may lead to a continued outpouring
of premature red blood cells, even though no other lead action is
manifest. The use of milk in a lead industry as a preventive measure
in part limits the absorption of lead from the intestinal tract; in
part leads to the deposition of lead in a relative harmless form in bony
tissues, because of its calcium content. However efficacious milk may
be in warding off clinical plumbism through this latter action, it
does not prevent the appearance of basophilic red cells.
Alkali treatment resulting in apparent cures without subsequent
deleading treatment will lead to the appearance of basophilic red
cells for an indefinite period. This evidence of retained lead sug­
gests that in the termination of treatment with only an apparent
cure the way is paved for a recurrence of clinical plumbism at a
subsequent time. Our experience with basophilic cells as an evi­
dence of retained lead suggests in some instances that in the course
of months these cells may gradually disappear in the absence of
further exposure. This may mean that the retained lead slowly has
been eliminated. On the other hand, in a few ancient cases of lead
poisoning we have administered acids in the hope of liberating
residual lead. Under such circumstances we have been able to detect
at times increased numbers of basophilic cells. In Table II we noted
that linotype operators who earlier had engaged in the more hazard­
ous occupation of hand typesetting averaged higher as to basophilic
cells than did operators who had done no handwork previously.
This suggests that some lead may be stored indefinitely in the
absence of deleading treatment. The use of such medicaments as
K I or NH4C1 in the treatment of acute lead poisoning appears to
increase the basophilic count transiently; but eventually such treat­
80 “ Lead poisoning,” by J. C. Aub, L. T, Fairhall, A. S. Minot, and P, Rezinkoff.
more, Williams & Wilkins Co., 1926.




Balti­

28

N E W TEST FOR INDUSTRIAL LEAD POISONING

ment will lead to the essential disappearance of basophilic red cells
from the blood stream. (See Case 39, B.)
A number of cases are now excerpted pertinent to one or more
assertions made in the preceding paragraphs.
CASE 36, F. G. H.

First seen October 14, 1926; white; age, 57; house painter for 30
years. Came to us on account of loss of strength, beginning eight
weeks previously; loss of 18 pounds weight in 7 weeks. Suffers
from nausea and dizziness. Additional questioning established fur­
ther pertinent information as follows: The vomiting of practically
all food, constipation, copper taste in mouth, low-grade intermit­
tent abdominal pain, sleeplessness, very severe cramps in calves of
legs with some cramps in other muscle groups, joint pains in knees,
wrists, and fingers, and continuous thirst.
Our examination led to these findings: Body generally flabby as
to musculature, except over abdomen which was rigid; stooped as
to posture; unsteady as to gait; tremors in all parts of the body.
Patient easily exhausted. Temperature, 98.8. Pulse, 116; after
exercise, 140; irregular. Respirations, 36; blood pressure, 148/86.
Extremities emaciated, with muscles apparently atrophic. Reflexes
diminished; marked weakness in extensor group of muscles of both
hands. Hand grips without force. Skin flabby but not colored.
Pallor.
Eyes present an arcus senilis. Pupils react to light but not to
accommodation. An ulcer was present on nasal septum. The
mouth presented many missing teeth, gross pyorrhea, calcareous
deposits with purple areas in diseased gums, suggesting exaggerated
lead lines. The less diseased gums exhibited a definite lead line.
Cobbler’s chest. Heart examination revealed a systolic murmur,
tachycardia, slightly irregular. The abdomen was rigid, particu­
larly over epigastrium. Tenderness on pressure over stomach.
Routine urinalysis was negative, save for a trace of sugar. Gas­
tric lavage and analysis established a free HC1 of 48 and a total acid­
ity of 66.
The examination of the blood when first seen established hemo­
globin, 75 per cent; red blood count, 3,960,000; white blood count,
7,600; differential—polymorphonuclears, 59; small lymphocytes, 34;
large lymphocytes, 6; eosinophils, 1. Marked polychromasia and
punctate stippling. Basophilic red cell count, 28,600 per cubic mil­
limeter of blood. Basophilic aggregations averaged 8 per micro­
scopic field. A diagnosis of lead poisoning was made and alkali
treament instituted at his home. On November 5, 1926, basophilic
red cells were 19,200. His basophilic aggregation test averaged 5.7
per microscopic field.
By December 29,1926 (two and one-half months after first exami­
nation), this patient was entirely free from complaints. His teeth
had been removed or repaired; weight and strength regained. He
was certified for work on January 3, 1927. His basophilic red count
was then 42,000 per cubic millimeter; the white blood count, 8,600:
Hemoglobin, 85 per cent: the basophilic aggregation test averaged
6 cells per field.




N E W TEST FOR INDUSTRIAL LEAD POISONING

29

On April 8, 1927, after patient had been discharged for four
months, another examination of the blood was made with results as
follows: Hemoglobin, 85 per cent; red blood count, 4,700,000; white
blood count, 10,000; differential—polymorphonuclears, 67; small
lymphocytes, 24; large lymphocytes, 8; transitional, 1. Basophilic
red count, 40,000. Basophilic aggregation test, 11 per field. Patient
declined deleading treatment. In the ensuing months no symptoms
have reappeared.
This case is cited for three purposes— (a) to point out the usual
range of basophilic red cell counts in lead poisoning; (6) to point out
the perpetuation of such cells after apparent cure by alkalinization;
(c) to show the limitation of the slide method (b. a.) for quan­
titative purposes. Although unreliable for precision work, any such
high numbers per average microscopic field should always be re­
garded as significant.
CASE 18, P.

White; Hungarian; white-lead worker; age, 47. Presents ancient
double wrist drop, which originated in 1917 as a result of lead poison­
ing when working in corrosion department. Now engaged in outside
work on tanbark pile. No complaints beyond partial Toss of use of
hands. Examination of blood shows: Hemoglobin, 75 per cent;
white blood count, 13,600; differential—polymorphonuclears, 55;
small lymphocytes, 45; eosinophils, 0; transitionals, 0; basophilic red
cell count, 18,200. Basophilic aggregations, 4.8 per average field.
This case suggests the possibility of retained lead throughout a period
of 10 years.
CASE 20, D. C.

White; male; age, 60. Janitor in storage battery factory. Began
work at the factory in September, 1926. At first was placed on lead
grid piling. Later mixed lead oxides and still later did janitor
work with gross exposure to lead oxide dusts. After these months
of hazardous work, patient suddenly developed typical lead colic,
with unusually severe constipation, muscle cramps, pallor, nausea,
with a slight degree of meningeal irritation. In a hospital he was
given alkali treatment, together with appropriate measures for pain,
constipation, etc. At this time patient’s blood findings were: Hemo­
globin, 65 per cent; red blood count, 4,240,000; white blood count,
14,200. Basophilic red cell count was 28,000. Basophilic aggrega­
tion averaged 6 per field.
After six weeks patient was ambulatory and free from complaints.
His blood at that time contained: Red blood count, 4,700,000; white
blood count, 8,500; differentials—polymorphonuclears, 65; small
lymphocytes, 26; large lymphocytes, 4; transitionals, 4; eosinophils, 1.
The basophilic red count was then 20,000, with basophilic aggrega­
tions 6 per average field. Ten days later this patient was at work
(not lead work). At that time his basophilic red count was 28,000.
Two months later patient’s blood was again examined. The baso­
philic count remained the same, 28,000. Patient agreed to deleading
treatment, but before this could be carried out he developed an acute
infection involving the respiratory tract and various joints. After
this passed his basophilic red cell count was within normal limits
and has so remained.



30

N E W TEST FOR INDUSTRIAL LEAD POISONING

This case is cited because of the persistence of basophilic cells after
the disappearance of symptoms and the disappearance of these cells
after an infectious process.
CASE 12, R.

White; male; age, 20. After working for three months as a
paster in the manufacture of storage battery plates, he developed
characteristic lead poisoning and was sent to a local hospital. Be­
tween two and three weeks after entering upon this employment
this man’s blood presented 1 basophilic aggregation per average
microscopic field. Three weeks later this average had increased to
6 per field. During the intervening period patient suffered from
mild manifestations suggestive of lead poisoning, such as nausea,
vomiting, slight pallor. He continued to work although taking
alkalis. Two weeks later the routine testing revealed about the
same number of basophilic red cells. The routine test for the next
two-week period again established an excess of basophilic red cells.
These warning prodromata continued until at the end of the third
month of exposure this patient developed a mild respiratory infec­
tion. Immediately an acute lead poisoning in severe form was
precipitated. At that time the basophilic aggregation test averaged
12 to 15 cells per microscopic field. Tests were made at one week
intervals for three weeks, all of which ranged from 5 to 8 cells per
average field. Patient fully recovered and left this type of em­
ployment.
This case is cited to point out our recognition of the imminence of
lead poisoning as evidenced in increasing numbers of basophilic red
cells, and its precipitation at the time of a respiratory infection.
This patient should have been removed from hazardous work at
the end of his sixth week of employment.
CASE 39, B.

White; male; age, 25; worked with molten lead. In August,
1925, this man suffered from acute lead poisoning. He lost but one
week from work, although the evident lead poisoning was note­
worthy for a much longer period. Beginning with September we
noted an increasing amount of basophilic material on successive tests:
October 7, 1925________________________________ + + + +
November 5, 1925______________________________ + + + + +
November 19, 1925_____________________________+ + + + 4 - + + + + +

Patient, by this time, was suffering from disabling lead poisoning,
calling for treatment. However, by January 5, 1926, patient had
become deleaded through the use of ammonium chloride, so that for
a period his routine tests showed:
January 25, 1926-------------------------------------------------------- + +
February 12, 1926_____________________________ -j- +
March 5, 1926----------------------------------------------------------- Poor slide.
March 30, 1926______________________________________ + +
April 16, 1926_______________________________________ + +
May 6, 1926_________________________________________ + + +
May 20, 1926_________________________________________ + + + +
June 4, 1926_________________________________________ + + . + +

Thus again reaching the danger zone for clinical lead poisoning.




N E W TEST FOR INDUSTRIAL LEAD POISONING

31

This case is cited to show the mounting numbers of basophilic
cells following exposure.
CASE 48, T. A.

Male; white; age, 66. Suffered from lead poisoning in January,
1924. At that time he was a mixer of lead oxides. He lost two
weeks’ time from work. His condition was complicated by pre­
existing chronic bronchitis, myocarditis, and hypertrophic arthritis.
He was completely deleaded through the use of ammonium chloride.
On resumption of work he was given the job of plant carpenter
and plumber, which was without severe exposure to lead. One day,
while at work, patient became thoroughly drenched while repairing
a broken pipe and worked throughout the day with wet clothing.
He developed pneumonia or some severe respiratory infection. He
was treated at a general hospital and completely recovered. In
May of the same year patient again became disabled, suffering from
myocarditis, bronchitis, arthritis, senility, etc., but without evidence
o f lead poisoning. Nevertheless he filed a claim for compensation.
Various examinations at hospitals failed to disclose any proper
reason for the acceptance of this condition as directly attributable to
lead. In this instance no basophilic red cells beyond normal num­
bers were detectable.
This case is cited to bring out the possible field of usefulness of
these described tests in the discrimination between lead poisoning
and conditions simulating this disease.
CASE GROUP, X

We made the following test as to the efficacy of basophilic red cell
counts as an index of lead poison or imminent lead poisoning.
Eighty-five examinations were made on 85 workers in a white-lead
and metallic-lead products factory. In this number 11 workers pre­
sented basophilic red cell counts in excess of 7,000 cells per cubic
millimeter of blood. The exact figures were:
Corrosion worker--------------------------------------------------------------- 7,800
Do___________________________________________________ 11,000
Do___________________________________________________ 12,400
Do___________________________________________________ 7,200
Kiln-room worker________________________________________ 61,600
Do_____________________________ ._____________________ 68,600
Dry white lead packer------------------------------------------------------- 70,400
Do____________________________________________ ______ 22,400
Scrap-lead furnace tender------------------------------------------------ 18,400'
Furnace dross skimmer----------------------------------------------------- 32,000
Water grinder___________________________________________ 44,800

With this evidence alone, the names of these workers were pre­
sented to the plant industrial physician (who had not participated
in our examinations) with the request that these men be carefully
examined for lead poisoning. This physician reported that 9 of
these 11 men were either previously known ambulatory cases or else
proved to have clinical evidence of lead poisoning. Our own clinical
examinations established evidence of lead poisoning in 9 of these 11
workers. In 1 of this group of 9 the patient was free of complaints
at this time but had suffered from severe lead poisoning about two
years previously.




32

N E W TEST FOR INDUSTRIAL LEAD POISONING

This group is cited in the belief that in basophilic i*ed cell counts
alone, made on lead-exposed workers, there is suggestive evidence
of lead intoxication or marked lead absorption whenever the count
is in excess of 6,000 to 7,000 per cubic millimeter of blood.
SUMMARY
Examinations as to the occurrence of basophilic red cells in the
blood have been carried out on more than 1,000 persons (1,045),
representing (a) normal persons, (b) pathologic states other than
lead poisoning, (e) lead-exposed workers, and (d) clinical lead
poisoning.
The results derived and conclusions formed are now summarized:
(1) The number of basophilic red cells found in 145 normal adults
was commonly less than 1,000 per cubic millimeter of blood. In a
few persons believed to be normal the count exceeded 1,000, but was
less than 5,000. Possible exceptions are to be found in several
physiologic states, viz, in the newborn, in pregnancy, when in high
altitudes, after considerable exposure to sunlight, especially in spring­
time, after X-ray exposure, after profuse sweating, after iron or
arsenic medication, and possibly slight variations are to be associated
with food intake. In the physiologic states to which the worker is
likely to be subjected the basophilic red cell count does not exceed
20,000 per cubic millimeter.
(2) The number of basophilic red cells is increased above normal
numbers in the following pathologic states: Lead intoxication, ben­
zol poisoning, arsenic poisoning, in all types of anemia in which
there is regeneration, hemolytic icterus, following hemorrhage, leukemias, at times in acute infections, in neoplasms involving the bone
marrow, and in polycythemia.
(3) In the absence of other conditions presenting high basophilic
red cell counts a high basophilic red cell count in a person exposed to
lead is accepted as indicative of lead absorption or lead poisoning.
(4) Mounting numbers of basophilic red cells in workers exposed
to lead is indicative of imminent clinical lead poisoning.
(5) Frank cases of lead poisoning almost invariably present baso­
philic red cell counts in excess of 7,000 such cells per cubic millimeter
of blood. Earely do the counts exceed 100,000. The usual range is
from 7,000 to 50,000.
(6) Treatment with alkalies leading to a cessation of symptoms is
not necessarily followed by the disappearance of basophilic red cells.
(7) Treatment with substances leading to the excretion of lead is
followed by the diminution and disappearance of excessive numbers
of basophilic cells.
(8) The number of basophilic red cells present in lead poisoning
or lead absorption does not stand in any constant relation to hemo­
globin percentage, total red or white count, differential white count,
or preformed punctate stippling.
(9) Sequelae of lead poisoning, such as wrist drop, do not stand in
any constant relation to basophilic red cell counts.
(10) Very high basophilic red cell counts, such as 60,000 to 80,000,
may be present without the actual signs or symptoms of clinical lead
poisoning. From the members of any group presenting such high




N E W TEST FOR IN D U STRIAL LEAD PO ISONIN G

33

basophilic red cell counts, clinical cases of lead poisoning are prone to
arise.
(11) Lead-exposed workers presenting basophilic red cell counts
in excess of 6,000 to 7,000 should be accepted, in the. absence of other
conditions productive of such increased counts, as lead poisoning
prospects and should be subjected to lead eliminating treatment or
alkali treatment with subsequent lead eliminating treatment. This
is especially desirable if successive examinations reveal progressive
increases in the number of basophilic cells.
(12) The counting method utilized in this work for the enumera­
tion of basophilic red cells is more accurate than the slide method for
basophilic aggregations.
(13) The slide method as utilized for the approximation of the
numbers of basophilic red cells is not sufficiently accurate to permit
of calculation in terms of numbers of basophilic red cells per cubic
millimeter of blood. This method, however, is a dependable method
for the recognition of small numbers or large numbers of basophilic
red cells. By this method the examining physician may recognize
workmen who are approaching dangerous degrees of lead absorption.
(14) The application of these methods suggests that in lead indus­
tries many workers commonly regarded as unexposed, such as office
workers, clerks, etc., actually may also absorb much lead and thus
become potential cases of lead intoxication. This is especially true
if the hazard of lead is in the form of dust.
(15) Basophilic red cell counts made on all workers in various
large departments of an industry with a lead hazard, afford a pos­
sible index of the degree of the lead hazard of the departments and
permits of comparison of the degree of hazard between several







LIST OF BULLETINS OF THE BUREAU OF LABOR STATISTICS
The following is a list of all bulletins of the Bureau of Labor Statistics published since
July, 1912, except that in the case of bulletins giving the results of periodic surveys of the
bureau only the latest bulletin on any one subject is here listed.
A complete list of the reports and bulletins issued prior to July, 1912, as well as the bulle­
tins published since that date, will be furnished on application. Bulletins marked thus (*)
are out of print.
Conciliation and Arbitration (including strikes and lockouts).
♦No. 124. Conciliation and arbitration in tlie building trades of Greater New York.
[1913.]
♦No. 133. Report of the industrial council of the British Board of Trade on its inquiry
into industrial agreements. [1913.]
No. 139. Michigan copper district strike. [1914.]
No. 144. Industrial court of the cloak, suit, and skirt industry of New York City.
[1914.]
No. 145. Conciliation, arbitration, and sanitation in the dress and waist industry of
New York City. [1914.]
No. 191. Collective bargaining in the anthracite coal industry. [1916.]
♦No. 198. Collective agreements in the men’s clothing industry. [1916.]
No. 233. Operation of the industrial disputes investigation act of Canada. [1918.]
No. 255. Joint industrial councils in Great Britain. [1919.]
No. 283. History of the Shipbuilding Labor Adjustment Board, 1917 to 1919.
No. 287. National War Labor B oard: History o f its formation, activities, etc.
[1921.]
No. 303. Use of Federal power in settlement of railway labor disputes. [1922.]
No. 341. Trade agreement in the silk-ribbon industry of New York City. [1923.]
No. 402. Collective bargaining by actors. [1926.]
No. 448. Trade agreements, 1926.
Cooperation.
No. 313. Consumers’ cooperative societies in the United States in 1920.
No. 314. Cooperative credit societies in America and in foreign countries. [1922.]
No. 437. Cooperative movement in the United States in 1925 (other than agricul­
tural).
Employment aiid Unemployment.
♦No. 109. Statistics of unemployment and the work of employment offices in the
United States. [1913.]
No. 172. Unemployment in New York City, N. Y. [1915.]
♦No. 183. Regularity of employment in the women’s ready-to-wear garment industries.
[1915.]
♦No. 195. Unemployment in the United States. [1916.]
No. 196. Proceedings of the Employment Managers’ Conference held at Minneapolis,
Minn., January 19 and 20, 1916.
♦No. 202. Proceedings o f the conference of Employment Managers’ Association of
Boston, Mass., held May 10, 1916.
No. 206. The British system of labor exchanges. [1916.]
♦No. 227. Proceedings of the Employment Managers’ Conference, Philadelphia, Pa.,
April 2 and 3, 1917.
No. 235. Employment system of the Lake Carriers* Association. [1918.]
♦No. 241. Public employment offices in the United States. [1918.]
No. 247. Proceedings of Employment Managers’ Conference, Rochester, N. Y., May
9-11, 1918.
No. 310. Industrial unemployment: A statistical study of its extent and causes.
[1922.]
No. 409. Unemployment in Columbus, Ohio, 1921 to 1925.
Foreign Labor Laws.
♦No. 142. Administration of labor laws and factory inspection in certain European
countries. [1914.]




(i)

Housing.
♦No. 158. Government aid to home owning and housing of working people in foreign
countries. [1914.]
No. 263. Housing by employers in the United States. [1920.]
No. 295. Building operations in representative cities in 1920.
No. 368. Building permits in the principal cities of the United States in [1921 to]
1923.
No. 424. Building permits in the principal cities of the United States in [1924 and]
1925.
No. 449. Building permits in the principal cities of the United States in [ 1925
and] 1926.
Industrial Accidents and Hygiene.
♦No. 104. Lead poisoning in potteries, tile works, and porcelain enameled sanitary
ware factories. [1912.]
No. 120. Hygiene of the painters’ trade. [1913.]
♦No. 127. Dangers to workers from dust and fumes, and methods of protection.
[1913.]
♦No. 141. Lead poisoning in the smelting and refining o f lead. [1914.]
♦No. 157. Industrial accident statistics. [1915.]
♦No. 165. Lead poisoning in the manufacture of storage batteries. [1914.]
♦No. 179. Industrial poisons used in the rubber industry. [1915.]
No. 188. Report of British departmental committee on the danger in the use of lead
in the painting of buildings. [1916.]
♦No. 201. Report of committee on statistics and compensation-insurance cost of the
International Association of Industrial Accident Boards and Commis­
sions. [1916.]
♦No. 207. Causes of death, by occupation. [1917.]
♦No. 209. Hygiene of the printing trades. [1917.]
No. 219. Industrial poisons used or produced in the manufacture of explosives.
[1917.]
No. 221. Hours, fatigue, and health in British munition factories. [1917.]
No. 230. Industrial efficiency and fatigue in British munition factories. [1917.]
♦No. 231. Mortality from respiratory diseases in dusty trades (inorganic dusts).
[1918.]
No. 234. Safety movement in the iron and steel industry, 1907 to 1917.
No. 236. Effect of the air hammer on the hands of stonecutters. [1918.]
No. 249. Industrial health and efficiency. Final report of British Health of
Munitions Workers Committee. [1919.]
♦No. 251. Preventable death in the cotton-manufacturing industry. [1919.]
No. 256. Accidents and accident prevention in machine building. [1919.]
No. 267. Anthrax as an occupational disease. [1920.]
No. 276. Standardizatiom of industrial acqident statistics. [1920.]
No. 280. Industrial poisoning in making coal-tar dye3 and dye intermediates.
[1921.]
No. 291. Carbon-monoxide poisoning. [1921.]
No. 293. The problem of dust phthisis in the granite-stone industry. [1922.]
No. 298. Causes and prevention of accidents in the iron and steel industry, 1916 to
1919.
No. 306. Occupational hazards and diagnostic sign s: A guide to impairments to be
looked for in hazardous occupations.
[1922.]
No. 339. Statistics of industrial accidents in the United States. [1923.]
No. 392. Survey of hygienic conditions In the printing trades. [1925.]
No. 405. Phosphorus necrosis in the manufacture of fireworks and in the preparation
of phosphorus. [1926.]
No. 425. Record of industrial accidents in the United States to 1925.
No. 426. Deaths from lead poisoning. [1927.]
No. 427. Health survey of the printing trades, 1922 to 1925.
No. 428. Proceedings of the Industrial Accident Prevention Conference, held at
Washington, D. C., July 14-16, 1926.
Industrial Relations and Labor Conditions.
No. 237. Industrial unrest in Great Britain. [1917.]
No. 340. Chinese migrations, with special reference to labor conditions. [1923.]
No. 349. Industrial relations in the West Coast lumber industry, [1923.]
No. 361. Labor relations in the Fairmont (W. Va.) bituminous-coal field. [1924.]




(n y

Industrial Relations and Labor Conditions— Continued.
No. 380. Postwar labor conditions in Germany. [1925.]
No. 383. Works council movement in Germany. [1925.]
No. 384. Labor conditions in the shoe industry in Massachusetts, 1920-1924.
No. 399. Labor relations in the lace and lace-curtain industries in the United States.
[1925.]
Labor Laws of
No. 211.
No. 229.
No. 285.
No.
No.
No.
No.

321.
322.
343.
370.

No. 408.
No. 434.
No. 444.

the United States (including decisions of courts relating to labor).
Labor laws and their administration in the Pacific States. [1917.]
Wage-payment legislation in the United States. [1917.]
Minimum wage laws of the United States: Construction and operation.
[1921.]
Labor laws that have been, declared unconstitutonal. [1922.]
Kansas Court of Industrial Relations. [1923.]
Laws providing for bureaus of labor statistics, etc. [1923.]
Labor laws of the United States, with decisions of courts relating thereto.
[1925.]
Laws relating to payment of wages. [1926.]
Labor legislation of 1926.
Decisions o f courts and opinions affecting labor, 1926.

Proceedings of Annual Conventions of the Association of Governmental Labor Officials of the
United States and Canada.
♦No. 266. Seventh, Seattle, Wash., July 12-15, 1920.
No. 307. Eighth, New Orleans, La., May 2-6, 1921.
No. 323. Ninth, Harrisburg, Pa., M&y 22-26, 1922.
No. 352. Tenth, Richmond, Va., May 1-4, 1923.
No. 389. Eleventh, Chicago, 111., May 19-23, 1924.
No. 411. Twelfth, Salt Lake City, Utah, August 13-15, 1925.
No. 429. Thirteenth, Columbus, Ohio, June 7-10, 1926.
No. 455. Fourteenth, Paterson, N. J., May 31 to June 3, 1927.
Proceedings of Annual Meetings of the International Association of Industrial Accident Boards
and Commissions.
No. 210. Third, Columbus, Ohio, April 25-28, 1916.
No. 248. Fourth, Boston, Mass., August 21-25, 1917.
No. 264. Fifth, Madison, Wis., September 24-27, 1918.
♦No. 273. Sixth, Toronto, Canada, September 23-26, 1919.
No. 281. Seventh, San Francisco, Calif., September 20-24, 1920.
No. 304. Eighth, Chicago, 111., September 19-23, 1921.
No. 333. Ninth, Baltimore, Md., October 9-13, 1922.
No. 359. Tenth, St. Paul, Minn., September 24-26, 1923.
No. 385. Eleventh, Halifax, Nova Scotia, August 26-28, 1924.
No. 395. Index to proceedings, 1914-1924.
No. 406. Twelfth, Salt Lake City, Utah, August 17-20, 1925.
No. 432. Thirteenth, Hartford, Conn., September 14-17, 1926.
No. 456. Fourteenth, Atlanta, Ga., September 27-29, 1927.
Proceedings of Annual Meetings of International Association of Public Employment Services.
No. 192. First, Chicago, December 19 and 20, 1913; Second, Indianapolis, Septembef
24 and 25, 1914; Third, Detroit, July 1 and 2, 1915.
No. 220. Fourth, Buffalo, N. Y., July 20 and 21, 1916.
No. 311. Ninth, Buffalo, N. Y., September 7-9, 1921.
No. 337. Tenth, Washington, D. C., September 11-13, 1922.
No. 335. Eleventh, Toronto, Canada, September 4-7, 1923.
No. 400. Twelfth, Chicago, 111., May 19-23, 1924.
No. 414. Thirteenth, Rochester, N. Y*, September 15-17, 1925.
Productivity of Labor.
No. 356. Productivity costs in the common-brick industry. [1924.]
No. 360. Time and labor costs in manufacturing 100 pairs o f shoes, 1923.
No. 407. Labor cost of production and wages and hours of labor in the paper boxboard industry. [1925.]
No. 412. Wages, hours, and productivity in the pottery industry, 1925.
No. 441. Productivity o f labor in the glass industry. [1927.]




(HI)

Retail Prices and Cost of Living.
*No. 121. Sugar prices, from refiner to consumer. [1913.]
♦No. 130. Wheat and flour prices, from farmer to consumer. [1913.]
No. 164. Butter prices, from producer to consumer. [1914.]
No. 170. Foreign food prices as affected by the war. [1915.]
No. 357. Cost of living in the United States. [1924.]
No. 369. The use of cost-of-living figures in wage adjustments. [1925.]
No. 445. Retail prices, 1890 to 1926.
Safety Codes.
♦No. 331. Code o f lighting: Factories, mills, and other work places.
No. 336. Safety code for the protection of industrial workers in foundries.
No. 350. Specifications of laboratory tests for approval of electric headlighting
devices for motor vehicles.
No. 351. Safety code for the construction, care, and use of ladders.
No. 364. Safety code for mechanical power-transmission apparatus.
No. 375. Safety code for laundry machinery and operation.
No. 378. Safety code for woodworking plants.
No. 382. Code of lighting school buildings.
No. 410. Safety code for paper and pulp mills.
No: 430. Safety code for power presses and foot and hand presses.
No. 433. Safety codes for the prevention of dust explosions.
No. 436. Safety code for the use, care, and protection of abrasive wheels.
No. 447. Safety code for rubber mills and calenders.
No. 451. Safety code for forging and hot-metal stamping.
Vocational and Workers* Education.
♦No. 159. Short-unit courses for wage earners, and a factory school experiment.
[1915.]
♦No. 162. Vocational education survey of Richmond, Va. [1915.]
No. 199. Vocational education survey of Minneapolis, Minn. [1916.]
No. 271. Adult working-class education in Great Britain and the United States.
[1920.]
Wages and Hours of Labor.
♦No. 146. Wages and regularity o f employment and standardization of piece rates in
the dress and waist industry o f New York City. [1914.]
♦No. 147. Wages and regularity of employment in the cloak, suit, and skirt industry.
[1914.]
No. 161. Wages and hours o f labor in the clothing and cigar industries, 1911 to
1913.
No. 163. Wages and hours of labor in the building and repairing of steam railroad
cars, 1907 to 1913.
♦No. 190. Wages and hours of labor in the cotton, woolen, and silk industries, 1907
to 1914.
No. 204. Street-railway employment in the United States. [1917.]
No. 225. Wages and hours of labor in the lumber, millwork, and furniture indus­
tries, 1911.
No. 265. Industrial survey in selected industries in the United States, 1919.
♦No. 297. Wages and hours of labor in the petroleum industry, 1920.
No. 356. Productivity costs in the common-brick industry. [1924.]
No. 358. Wages and hours of labor in the automobile-tire industry, 1923.
No. 360. Time and labor costs in manufacturing 100 pairs of shoes, 1923.
No. 365. Wages and hours o f labor in the paper and pulp industry, 1923.
No. 394. Wages and hours of labor in metalliferous mines, 1924.
No. 407. Labor cost of production, and wages and hours of labor in the paper boxboard industry. [1925.]
No. 412. Wages, hours, and productivity in the pottery industry, 1925.
No. 413. Wages and hours of labor in the lumber industry in the United States,
1925.
No. 416. Hours and earnings in anthracite and bituminousi coal mining, 1923 and
1924.
No. 421. Wages and hours o f labor in the slaughtering and meat-packing industry,
1925.
No. 422. Wages and hours of labor in foundries and machine shops, 1925.
No. 435. Wages and hours of labor in the men’s clothing industry, 1911 to 1926.




(IV)

Wages and Hours of Labor— Continued.
No. 438. Wages and hours of labor In the motor-vehicle industry, 1925.
No. 442. Wages and hours o f labor in the iron and steel industry, 1907 to 1925.
No. 443. Wages and hours of labor in woolen and worsted goods manufacturing,
1910 to 1926.
No. 446. Wages and hours o f labor in cotton-goods manufacturing, 1910 to 1926.
No. 450. Wages and hours of labor in the boot and shoe industry, 1907 to 1926.
No. 452. Wages and hours o f labor in the hosiery and underwear industries, 1907.
No. 454. Hours and earnings in bituminous-coal mining, 1922, 1924, and 1926.
No. 457. Union scales of wages and hours o f labor, May 15, 1927.
Welfare Work.
*No. 123. Employers’ welfare work. [1913.]
No. 222. Welfare work in British munitions factories. [1917.]
♦No. 250. Welfare work for employees in industrial establishments in the United
States. [1919.]
No. 458. Health and recreation activities in industrial establishments, 1926. (In
press.)
Wholesale Prices.
No. 284. Index numbers o f wholesale prices in the United States and foreign
countries. [1921.]
No. 440. Wholesale prices, 1890 to 1926.
No. 453. Revised index numbers o f wholesale prices, 1923 to July, 1927.
Women and Children in Industry.
No. 116. Hours, earnings, and duration of employment of wage-earning women in
selected industries in the District of Columbia. [1913.]
♦No. 117. Prohibition o f night work of young persons. [1913.]
No. 118. Ten-hour maximum working-day for women and young persons. [1913.]
No. 119. Working hours o f women in the pea canneriesi of Wisconsin. [1913.]
♦No. 122. Employment o f women in power laundries in Milwaukee. [1913.]
No. 160. Hours, earnings, and conditions of labor of women in Indiana mercantile
establishments and garment factories. [1914.]
♦No. 167. Minimum-wage legislation in the United States and foreign countries.
[1915.]
♦No. 175. Summary of the report on conditions of woman and child wage earners
in the United States. [1915.]
♦No. 176. Effect of minimum-wage determinations in Oregon. [1915.]
*No. 180. The boot and shoe industry in Massachusetts as a vocation for women.
[1915J
♦No. 182. Unemployment among women in department and other retail stores of
Boston, Mass. [1916.]
No. 193. Dressmaking as a trade for women in Massachusetts. [1916.]
No. 215. Industrial experience of trade-school girls in Massachusetts. [1917.]
♦No. 217. Effect of workmen’s compensation laws in diminishing the necessity of
industrial employment of women and children. [1918.]
No. 223. Employment of women and juveniles in Great Britain during the war.
[1917.]
No. 253. Women in the lead industries. [1919.]
Workmen’s Insurance and Compensation (Including: laws relating thereto).
No. 101. Care of tuberculous wage earners in Germany. [1912.]
♦No. 102. British national insurance act, 1911.
No. 103. Sickness and accident insurance law of Switzerland. [1912.]
No. 107. Law relating to insurance of salaried employees in Germany. [1913.]
♦No. 155. Compensation for accidents to employees of the United States. [1914.]
No. 212. Proceedings of the conference on social insurance called by the Interna­
tional Association of Industrial Accident Boards and Commissions, Wash­
ington, D. C., December 5-9, 1916.
No. 243. Workmen’s compensation legislation in the United States and foreign
countries, 1917 and 1918.
No. 301. Comparison of workmen’s compensation insurance and administration.
[1922.]
No. 312. National health insurance in Great Britain, 1911 to 1921.
No. 379. Comparison o f workmen’s compensation laws of the United States as of
January 1, 1925.
No. 423. Workmen’s compensation legislation o f the United States and Canada as
of July 1, 1926.




(V )

Miscellaneous Series.
♦No. 174. Subject index o f the publications of the United States Bureau of Labor
Statistics up to May 1, 1915.
No. 208. Profit sharing in the United States. [1916.]
No. 242. Food situation in central Europe, 1917.
No. 254. International labor legislation and the society of nations. [1919.]
No. 268. Historical survey o f international action affecting labor.
[1920.]
No. 282. Mutual relief associations among Government employees in Washington,
D. C. [1921.]
♦No. 299. Personnel research agencies: A guide to organized research in employ­
ment management, industrial relations, training, and. working condi­
tions. [1921.]
No. 319. The Bureau of Labor Statistics: Its history, activities, and organiza­
tion. [1922]
No. 326. Methods of procuring and computing statistical information of the
Bureau of Labor Statistics. [1923.]
No. 342. International Seamen’s Union o f America: A study of its history and
problems. [1923.]
No. 346. Humanity in government. [1923.]
No. 372. Convict labor in 1923.
No. 386. Cost of American almhouses. [1925.]
No. 398. Growth of legal-aid work in the United States. [1926.]
No. 401. Family allowances in foreign countries. [1926.]
No. 420. Handbook of American trade-unions. [1926.]
No. 439. Handbook of labor statistics, 1924 to 1926.
No. 459. Apprenticeship in building construction.




(VI)