Carbon Monoxide and Automobile Exhaust Gases


Hayhurst, E.R.

American Journal of Public Health 16(3): 218-223

1926


There are many problems involved in the prevention of poisoning by carbon monoxide and automobile gases, one of the most important of which is the problem of diagnosis of carbon monoxide poisoning. We are not concerned about the cases where exposure is evident and severe symptoms or death follows. However, when exposure to limited amounts is possible we are much concerned whether such symptoms as the common ones of headache, weariness, weakness, dizziness, nausea, vomiting, loss of strength and muscular control, increased pulse and respiratory rates, loss of reflexes, and even coma with intermittent convulsions, cessation of respiration, and death' are due to carbon monoxide poisoning or any of the many other possible factors connected with the environment or the condition of the victim.

CARBON
MONOXIDE
AND
AUTOMOBILE
EXHAUST
GASES*
-
E.
R.
HAYHURST,
M.D.,
PH.D.,
FELLOW
A.P.H.A.
Ohio
State
University
and
Ohio
State
Department
of
Health,
Columbus,
Ohio
T
HERE
ARE
MANY
problems
in-
volved
in
the
prevention
of
poisoning
by
carbon
monoxide
and
automobile
gases,
one
of
the
most
important
of
which
is
the
problem
of
diagnosis
of
carbon
monoxide
poisoning.
We
are
not
con-
cerned
about
the
cases
where
exposure
is
evident
and
severe
symptoms
or
death
follows.
However,
when
exposure
to
limited
amounts
is
possible
we
are
much
concerned
whether
such
symptoms
as
the
common
ones
of
headache,
weariness,
weakness,
dizziness,
nausea,
vomiting,
loss
of
strength
and
muscular
control,
in-
creased
pulse
and
respiratory
rates,
loss
of
reflexes,
and
even
coma
with
intermit-
tent
convulsions,
cessation
of
respiration,
and
death'
are
due
to
carbon
monoxide
poisoning
or
any
of
the
many
other
pos-
sible
factors
connected
with
the
environ-
ment
or
the
condition
of
the
victim.
The
presence
of
pallor
and
symptoms
of
anemia,
but
with
a
high
hemoglobin
reading,
associated
with
polycythemia
is
said
to
constitute
a
characteristic
diagnos-
tic
combination.
2
Direct
blood
tests
for
carbon
monoxide
may
or
may
not
have
significance.
Norris
and
Gettler
fi
nd
that
64
per
cent
of
post-mortems
of
"
normal
cases
"
so
far
as
carbon
monoxide
has
been
a
factor
in
the
cause
of
death
show
CO
present
to
as
much
as
5
per
cent
sat-
uration
in
the
blood,
in
New
York
City,
upon
delicate
tests
such
as
that
of
Van
Slyke
as
modified
by
O'Brien
and
Parker.
3
They
found
this
test
sensitive
to
*
Read
at
the
Joint
Session
of
the
Industrial
Hygiene
and
Sanitary
Engineering
Sections
of
the
American
Public
Health
Association
at
the
Fifty-fourth
Annual
Meeting
at
St.
Louis,
Mo.,
October
19,
1925.
within
about
1
per
cent.
In
deaths
due
to
carbon
monoxide,
in
victims
found
after
varying
periods
after
exposure,
the
CO
present
ranged
from
10
to
92
per
cent.
This
raises
the
question
of
the
utility
of
delicate
tests.
Sayers
and
Yant
4
have
perfected
the
pyrotannic
acid
method
for
practical
utility
purposes
with
a
delicacy
which
appears
to
be
sufficient,
they
con-
sider,
for
all
practical
purposes.
One
of
the
most
characteristic
post-
mortem
fi
ndings,
when
present,
is
the
loosening
of
the
epidermis
and
perhaps
blisters,
located
usually
on
the
extremi-
ties
and
about
the
face
and
neck.
Death
from
no
other
cause
appears
to
show
such
phenomena.
Associated
with
this
is
the
occasional
appearance,
in
those
who
survive
a
serious
exposure,
of
gan-
grenous
areas
which
may
later
take
life
through
depletion
or
secondary
infection.
We
have
been
accustomed
to
lay
great
stress
upon
red
discolorations
of
the
body
and
blood
just
preceding
and
following
death,
but
recently
Banham,
Haldane
and
Savage
have
pointed
out
the
possibility
of
confusion
with
nitric
-oxide
hemoglo-
bin,
not
from
the
administration
of
this
compound
as
nitrites,
etc.,
but
from
the
presence
of
a
nitrifying
organism
which
may
cause
the
body
to
have
a
red
color
similar
to
that
often
found
in
carbon
monoxide
poisoning.
Such
symptoms
and
causative
organism
were
found
in
a
case
dying
of
broncho-pneumonia.
These
authors
insist
that
CO
-hemoglobin
may
be
differentiated
from
NO
-hemoglobin
by
the
fact
that
on
great
dilution
with
water
the
former
stays
pink
while
the
latter
is
[218]
CARBON
MONOXIDE
AND
AUTOMOBILE
EXHAUST
GASES
219
not
so
pink,
while
boiling
gives
a
grey
coagulum
with
CO
-hemoglobin
but
a
pink
coagulum
with
NO
-hemoglobin.
They
regard
this
as
the
simplest
and
most
delicate
means
of
detecting
the
presence
of
CO
in
the
blood
and
of
dif-
ferentiating
it
from
other
colored
blood
solutions.
DELAYED
TYPE
Our
second
problem
concerns
the
ques-
tion
of
serious
or
fatal
consequences
of
delayed
type
following
soon
after
an
alleged
exposure
in
which
the
victim
has
been
able
to
extricate
himself
from
the
CO
environment
of
his
own
volition.
For
example,
he
leaves
the
mine,
furnace
room,
garage
or
similar
place
experienc-
ing
a
shortness
of
breath;
goes
home,
utilizing
a
period
of
20
minutes
to
an
hour
;
gets
gradually
more
dyspneic
and
dies
with
evidences
of
acute
cardiac
dilation
within
1
to
4
days
;
or
develops
a
severe
form
of
broncho-pneumonia
which
is
usually
fatal.
A
typical
case
is
pre-
sented
by
Dr.
J.
M.
Thorne.°
Does
this
constitute
delayed
carbon
monoxide
poisoning?
If
other
workers
under
simi-
lar
circumstances
experience
no
such
symptoms,
or
allowing
that
they
have
symptoms
of
headache
and
a
little
slow-
ing
up
of
activity,
may
the
fatality
still
be
due
to
carbon
monoxide
poisoning?
Are
we
justified
in
labeling
a
death
as
due
to
carbon
monoxide
poisoning
when
the
individual
is
not
prostrated
or
rendered
unconscious
at
the
place
of
exposure?
These
are
all
important
practical
ques-
tions
in
compensation
matters
regarding
exposures
to
carbon
monoxide.
POSSIBLE
LATE
SEQUELAE
Four
prominent
afflictions
alleged
to
be
due
to
breathing
carbon
monoxide
in
amounts
producing
semi
-consciousness
to
just
short
of
death,
and
either
in
one
or
multiple
exposures,
present
themselves.
Usually
there
has
remained
a
degree
of
ill
health
perhaps
not
affecting
work
ability
in
the
interim
before
the
alleged
sequelae
develop.
These
sequelae
are
(a)
the
development
of
serious
pul-
monary
complications
like
pneumonia
some
weeks
or
months
afterwards;
(b)
the
development
of
multiple
sclerosis
usually
some
years
afterwards;
(c)
the
question
of
pernicious
anemia,
recently
reemphasized
by
Beck
and
Fort,
2
follow-
ing
in
due
course
of
time
and
usually
after
repeated
exposures;
and
(d)
the
question
of
psychoses
or,
simply,
psych
-
asthenia
and
neurasthenia
developing
months
or
years
after
exposure.
May
these
afflictions
really
occur
as
late
sequelae
of
carbon
monoxide
inhalations
?
Remember,
we
are
not
considering
im-
mediate
or
early
sequelae
here
following
exposures,
nor
situations
in
which
vari-
ous
disabling
complications
continue
to
exist
after
rescue
until
one
or
another
of
these
sequelae
eventuates.
ASPHYXIA
Does
asphyxia
explain
all
of
the
phe-
nomena
of
carbon
monoxide
poisoning?
If
carbon
monoxide
poisoning
simulates
the
gradual
withdrawal
of
oxygen
from
the
blood,
or
the
tenuity
of
the
atmos-
phere
as
one
ascends
to
great
heights
in
aviation
or
in
mountain
climbing.
as
is
claimed
by
most
authorities,
how
do
we
explain
the
fact
that
in
acute
cases
of
poisoning,
such
as
occur
within
a
few
minutes'
exposure
in
a
closed
garage
or
a
few
hours'
exposure
to
the
fumes
of
a
maladjusted
gas
heating
stove,
nervous
symptonts
such
as
weak-
ness
of
the
knees,
faintness,
and
loss
of
consciousness
invariably
occur
before
respiratory
symptoms
such
as
shortness
of
breath,
rapid
breathing,
cyanosis,
and
similar
phenomena
usually
associated
with
asphyxia
or
air
hunger?
In
this
connection
we
are
much
inter-
ested
in
a
recent
paper
by
Barcroft
to
the
effect
that
in
death
by
carbon
monoxide
in
animals,
although
the
blood
in
the
general
circulation
contains
a
very
high
percentage,
that
in
the
spleen
contains
practically
none.
When
carbon
monoxide
eventually
reaches
the
spleen
it
is
re-
tained
much
longer
than
in
the
general
circulation.
(Note
here
the
value
of
220
THE
AMERICAN
JOURNAL
OF
PUBLIC
HEALTH
examining
the
spleen
for
CO
in
post-
mortems.)
Barcroft
states
that
unless
CO
reaches
more
than
20
per
cent
satura-
tion
in
the
resting
animal
it
may
not
pene-
trate
the
spleen
pulp,
which
remains
en-
tirely
free
from
the
gas
for
as
much
as
4
hours.
This
discovery
has
offered
one
of
the
best
explanations
for
the
function
of
this
mysterious
organ
—that
of
a
store-
house
for
surplus
blood
corpuscles
which
are
called
into
use
only
on
extra
demands.
In
active
animals
the
CO
-hemoglobin
penetrates
at
once
into
the
spleen
pulp
so
as
to
be
noticeable
within
5
minutes.
Splenectomized
animals
die
markedly
sooner
under
carbon
monoxide
than
do
controls.
Thus
the
spleen
appears
to
be
a
reservoir
for
blood
corpuscles
to
be
put
into
the
circulation
as
required,
and
the
old
saying
"
to
vent
one's
spleen
"
has
an
intelligible
meaning.?
A
DISEASE
OR
AN
ACCIDENT
Is
carbon
monoxide
poisoning
a
disease
or
an
accident
?
Do
small
amounts
pro-
duce
any
disease?
If
acclimation
takes
place
in
those
who
do
not
show
very
noticeable
symptoms,
may
gradual
disease
nevertheless
take
place?
(Obviously
where
complications
or
sequelae
imme-
diately
follow
a
given
exposure,
the
case
is
an
accident,
that
is,
an
event
fi
xed
in
time
as
well
as
in
place.)
Our
general
belief
is
that
any
disability
consequent
upon
the
breathing
of
carbon
monoxide
has
followed
an
exposure
producing
com-
plete
inertia
if
not
unconsciousness
and
therefore
can
be
fi
xed
in
time
of
occur-
rence.
Hence
such
a
disability
does
not
constitute
a
disease
but
the
result
of
an
accident.
Therefore
chronic
poisoning
from
a
single
exposure
to
carbon
mon-
oxide
does
not
exist
;
persons
who
have
not
been
noticeably
damaged
by
a
single
exposure
(unconsciousness,
paralysis,
acute
cardiac
dilation,
etc.)
recover
from
all
symptoms
within
a
few
moments
and
no
disease
is
known
to
follow.
We
may
be
wrong
in
this,
but
if
not,
then
carbon
monoxide
poisoning
should
be
removed
from
occupational
disease
schedules
and
put
into
accident
schedules.
The
same
should
be
said
for
caisson
disease
(com-
pressed
air
illness)
which
is
apparently
always
an
injury
and
not
a
disease.
Is
our
nomenclature
garbled?
CARBON
MONOXIDE
-HEMOGLOBIN
DURING
SMOKING
Numerous
investigators
have
found
CO
-hemoglobin
present
in
one's
blood
during
the
smoking
of
an
ordinary
cig-
arette,
pipe,
or
cigar.
Incomplete
com-
bustion,
i.e.,
carbon
monoxide,
results
from
pulling
air
down
through
the
fuel
bed
of
the
burning
tobacco,
because
of
poor
aeration
there.
Several
per
cent
of
CO
may
occur
in
'undiluted
smoke
from
cigars.
8
Naturally,
those
who
inhale
show
the
most
in
the
blood.
Quantities
ranging
from
5
per
cent
to
22
per
cent
CO
-hemoglobin
have
been
reported
in
smokers.
The
question
arises
whether
this
produces
any
chronic
disease,
whether
acclimatization
does
not
take
place
in
the
habitual
smoker,
and
whether,
in
the
end,
smoking
is
not
a
form
of
exercise
similar
to
walking
at
3
to
4
miles
per
hour,
so
far
as
the
CO
factor
in
burning
tobacco
is
concerned.
If
it
is
true
that
these
rather
significant
amounts
which
occur
in
smokers
do
no
harm,
do
similar
amounts
which
occur
in
garage
workers
or
perhaps
traffic
policemen,
etc.?
A
PROBLEM
IN
MINES
We
fi
nd
that
many
are
under
a
misap-
prehension
as
to
carbon
monoxide
as
a
mine
problem.
It
should
be
emphasized
that
carbon
monoxide
is
not
a
normal
or
natural
gas
in
subterranean
spaces.
It
is
always
the
more
or
less
immediate
result
of
a
fi
re,
and
that
fi
re
has
burned
with-
out
sufficient
oxygen
;
so
that
whenever
carbon
monoxide
occurs
in
a
mine,
it
is
necessarily
the
result
of
blasting
in
poorly
ventilated
quarters,
or
of
fi
res,
usually
of
smoldering
type
located
about
the
pas-
sageways.
Carbon
monoxide
does
not
occur
naturally
anywhere,
volcanoes
and
fumaroles
excepted.
For
this
reason
it
should
be
pointed
out
that
some
other
gas,
CARBON
MONOXIDE
AND
AUTOMOBILE
EXHAUST
GASES
221
usually
carbon
dioxide,
or
a
plain
want
of
oxygen,
has
been
the
"
gas
"
respon-
sible
for
the
mishap
in
a
sudden
asphyxi-
ation
in
a
closed
or
deep
space,
rather
than
carbon
monoxide.
This
item
should
not
be
closed
without
calling
attention
to
the
perfection
of
the
"carbon
monoxide
self
rescuer
"
devised
by
Fieldner,
Katz
and
Reynolds
9
which
may
be
held
in
the
rescuer's
teeth
and
provides
protection
from
this
gas
for
at
least
one-half
hour
while
helping
miners
to
escape
from
places
in
which
fi
res
are
burning
or
ex-
plosions
have
occurred.
GAS
-FIRED
HEATERS
We
present
herewith
a
table
showing
the
carbon
monoxide
fatalities
which
have
occurred
in
Ohio
during
the
past
three
winters,
due
to
gas
-fired
heating
appliances
used
in
occupied
rooms,
al-
though
those
of
the
fi
rst
winter,
1922-23,
were
not
recorded
systematically
until
January,
1923.
We
believe
that
the
con-
siderable
falling
off
in
deaths
from
gas
-
fi
red
room
heaters
last
winter
(1924-
1925)
is
the
result
of
the
vigorous
cam-
paign
of
publicity
instituted,
in
which
all
were
strongly
advised
to
see
that
such
heaters
were
connected
to
effective
chim-
ney
fl
ues.
It
will
be
noted
that
gas
-fired
water
heaters,
usually
used
in
bathrooms
and
much
more
difficult
to
connect
with
fl
ues,
have
taken
a
small
but
constant
toll
each
winter.
There
is
also
a
surprising in-
crease
in
asphyxiations
from
automobile
exhausts.
CARBON
MONOXIDE
FATALITIES
Three
-Year
Comparative
Record
in
Ohio
(Compiled
by
Ohio
Dept.
of
Health)
Winter
Winter
Winter
1922-23
1923-24
1924-25
Deaths
Deaths
Deaths
Gas
-fired
room
heaters
41
43
23
Gas
-fired
cooking
stoves
2
3
8
Gas
-fired
water
heaters
5
4
5
Hotplates
1
1
0
Furnaces
(gas
and
coal)
and
stoves
(coal)
6
6
2
Automobile
exhaust
5
7
20
Total
60
64
58
As
a
considerable
part
of
the
gas
used
in
Ohio
is
natural
gas
and
contains
no
carbon
monoxide,
it
is
easy
to
see
that
carbon
monoxide
poisoning
has
occurred
as
the
result
of
the
burning
of
the
gas.
This
sometimes
occurs
from
improperly
constructed
heaters,
which
are
constant
carbon
monoxide
generators
from
the
moment
they
are
lighted,
sometimes
from
burning
the
heaters
too
high,
and
some-
times
from
a
rise
in
the
gas
pressure,
particularly
over
night
while
one
is
asleep
and
while
less
gas
is
being
used
in
the
neighborhood
—which
allows
a
certain
amount
of
the
gas
to
slip
through
the
heater
only
partially
burned
(i.e.,
as
car-
bon
monoxide)
and
without
reaching
a
temperature
of
1100°
F.,
which
our
metallurgists
claim
is
the
temperature
necessary
to
burn
or
oxidize
carbon
mon-
oxide
completely
to
carbon
dioxide."
,
11
'
12
The
chief
problem
here
is
the
creation
of
city
ordinances
and
of
state
laws
pro-
hibiting
the
fl
ueless
heater
as
well
as
the
abolition
of
leaky
gas
tubing
and
the
con-
trol
of
leaky
connections.
OTHER
DANGEROUS
COMBUSTION
PRODUCTS
The
question
arises
whether
other
in-
jurious
products
are
given
off
than
car-
bon
monoxide
from
carboniferous
fuels
in
heating
stoves.
One
set
of
chemical
analyses
made
at
Ohio
State
University
shows
that
under
ideal
combustion,
over
6
per
cent
carbon
dioxide
and
less
than
10
per
cent
of
oxygen
constitute
the
com-
bustion
products
of
a
high
class
gas
-stove
heater.
This
is
a
chemical
condition
in-
compatible
with
life
for
the
average
human
being.
In
addition
to
this,
we
strongly
suspect
that
other
sharp
and
offensive
substances
may
gradually
de-
bilitate
human
beings,
i.e.,
lower
their
resistance,
especially
to
diseases
of
the
respiratory
tract.
The
other
substances
found
are
said
to
be
formaldehyde,
acrolein,
ammonia,
and
sulphurous
prod-
ucts.
13
All
carbon
fuel
appliances
should
be
effectively
vented
to
the
exterior
and
so
constructed
as
not
to
endanger
life
or
health.
The
U.
S.
Bureau
of
Standards
has
laid
down
the
principles
which
should
be
followed
in
the
construction
of
air
-gas
burners
to
insure
complete
combustion
and
thereby
avoid
carbon
monoxide
and
other
menacing
by-products.1°
222
THE
AMERICAN
JOURNAL
OF
PUBLIC
HEALTH
AUTOMOBILE
EXHAUSTS
It
has
been
pointed
out
that
statistics
on
fatalities
from
inhaling
carbon
mon-
oxide
in
automobile
exhausts,
while
limited
in
absolute
fi
gures,
show
an
ap-
parent
decided
increase
in
the
state
of
Ohio.
The
question
has
been
raised
by
a
certain
motor
corporation
in
New
York
City
whether
this
may
not
be
due
to
the
use
of
wet
rather
than
dry
mixtures
said
to
obtain
in
Ford,
Maxwell,
Chevrolet,
Dodge
and
other
makes
of
cars,
usually
the
cheaper
ones,
and
not
in
dry
mixtures
which
commonly
obtain
in
the
higher
priced
cars.
So
much
insistence
has
been
made
upon
this
point
to
public
health
officials
by
this
corporation
that
we
ad-
dressed
a
letter
upon
the
subject
to
the
U.
S.
Bureau
of
Mines
Experiment
Sta-
tion,
Pittsburgh,
Pa.,
some
of
whose
sta-
tistics
are
quoted
by
Mr.
Deppe,
and
we
received
the
information
following:
"
From
the
same
101
automobile
tests
which
were
made
under
my
direction
at
Pittsburgh
and
which
Mr.
Deppe
quotes
in
his
letter
of
August
6
to
the
Society
of
Automotive
Engi-
neers
we
found
no
appreciable
difference
in
the
relative
amount
of
CO
traceable
to
using
easily
vaporized
or
difficultly'
vaporized
gasoline.
We
found
that
the
amount
of
CO
was
directly
pro-
portional
to
the
richness
of
the
mixture.
If
we
adjusted
the
carbureter
so
as
to
give
a
lean
mixture
the
CO
was
low
—in
the
neighborhood
of
1
per
cent;
if
the
carbureter
was
adjusted
rich
it
was
in
the
neighborhood
of
10
per
cent.
We
could
get
just
as
low
CO
in
a
Ford
as
in
any
other
car.
There
seemed
to
be
little
prac-
tical
advantage
on
this
score
in
any
one
make
of
car
or
any
one
time
of
mixture."
Whether
wet
or
dry,
"
if
the
mixture
is
rich
it
is
bound
to
contain
large
quantities
of
CO."
Hence
we
have
not
considered
it
worth
while
to
collect
statistics
on
the
types
of
automobiles
associated
with
CO
fatalities
in
Ohio.
We
have
been
struck,
of
late,
by
the
evidently
successful
attempts
at
suicide
reported
to
us
by
means
of
the
automobile
exhaust
method.
It
is
only
necessary
to
mention
furthermore
the
rather
frequent
occurrence
of
narrow
escapes
and
fatali-
ties
due
to
exhaust
gases
permeating
en-
closed
cars
and,
in
some
instances,
auto
-
buses,
so
that
ordinances
have
already
been
passed
by
a
number
of
cities
cover-
ing
the
proper
ventilation
of
automobile
vehicles
used
by
the
public.
TETRA
-ETHYL
LEAD
POISONING
FROM
AUTOMOBILE
EXHAUSTS
The
title
of
this
paper
does
not
permit
a
discussion
of
the
subject
of
poisoning
by
ethyl
gasoline
in
its
manufacture
or
distribution.
The
public
is
quite
familiar
with
the
mishaps
which
have
occurred
in
New
Jersey
and
Ohio
in
connection
with
the
manufacture
and
blending,
respec-
tively,
of
tetra
-ethyl
lead.
Contrary,
to
popular
opinion,
there
have
been
no
re-
ports
of
fatalities
and,
so
far
as
we
have
been
able
to
learn,
of
mishaps
of
moment
which
have
occurred,
outside
of
the
lab-
oratory,
due
to
the
handling
of
this
sub-
stance
dissolved
in
gasoline,
i.e.,
in
hand-
ling
"
ethyl
gasoline."
While
a
possible
hazard
may
still
exist
for
auto
fi
lling
station
employes
in
dispensing
ethyl
gasoline,
although
it
is
no
longer
made
by
them,
but
at
the
bulk
distributing
centers
—and
perhaps
to
indi-
viduals
careless
in
its
use
—the
big
prob-
lem
of
interest
to
the
public
is
the
ques-
tion
of
the
possibility
of
chronic
lead
poisoning
from
the
inhalation
of
automo-
bile
exhaust
fumes
from
burning
"
ethyl
gasoline."
As
you
well
know
a
general
conference
was
called
on
this
subject
by
the
Surgeon
General
of
the
Public
Health
Service
on
May
20,
1925,
where
it
was
decided
that
not
enough
evidence
was
presented
on
either
side
of
the
question
and
that
a
special.
Committee
of
Seven
should
be
ap-
pointed
by
the
Surgeon
General
to
in-
vestigate
the
subject
further,
a
report
to
be
made
during
January,
1926.
In
the
meantime
the
Ethyl
Gasoline
Corporation
voluntarily
stopped
the
sale
of
the
sub-
stance,
which
has
later
been
modified
in
that
the
Surgeon
General's
Committee
has
authorized
its
sale
under
careful
supervision
by
the
Public
Health
Service
in
order
to
gain
experience,
as
we
under-
CARBON
MONOXIDE
AND
AUTOMOBILE
EXHAUST
GASES
stand
it,
through
the
observation
of
gaso-
line
fi
lling
station
employes
in
certain
states
and
limited
territories.
This
super-
vised
investigation
is
now
going
on
in
Ohio
and
perhaps
elsewhere.
At
the
Washington
conference
it
was
pointed
out
by
prominent
public
health
leaders
that
authorities
could
not
proceed
to
ban
a
substance
alleged
to
be
dangerous
without
sufficient
evidence
of
danger
to
the
public
and
that
the
results
of
animal
experiments
alone
would
never
satisfy
them;
also
that
the
feasibility
of
close
ob-
servation
on
exposed
human
beings
was
entirely
practical.
At
this
date
it
is
truly
remarkable,
when
we
consider
all
of
the
complaints
which
come
to
the
notice
of
health
de-
partments,
particularly
following
the
publicity
of
an
alleged
hazard
to
the
pub-
lic,
that
not
a
single
one
concerning
gaso-
line
treated
with
tetra
-ethyl
lead
or
alleged
lead
poisoning
from
motor
ex-
hausts
using
the
same
has
been
reported
in
Ohio.
An
invitation
to
the
public
to
make
such
reports
began
immediately
upon
the
occurrence
of
the
mishaps
at
the
Bayway
plant
of
the
Standard
Oil
Cor-
poration
in
New
Jersey
approximately
a
year
ago.
In
view
of
the
extensive
experiments
with
automobile
exhausts
carried
out
upon
animals
by
Dr.
Sayers
and
his
asso-
ciates
at
the
U.
S.
Bureau
of
Mines
Ex-
periment
Station
in
Pittsburgh
for
ap-
proximately
a
year
and
a
half,
i.e.,
ending
May
20,
1925,
it
is
not
likely
that
lead
poisoning
may
be
feared
by
the
public.
Dr.
Sayers
reported
at
the
Surgeon
Gen-
eral's
conference
that
where
the
ethyl
gasoline
contained
the
regular
or
normal
amount
of
tetra
-ethyl
lead,
animals
ex-
posed
188
times
to
exhaust
gases
from
an
engine
during
a
period
of
about
8
months
and
for
3
-hour
and
6
-hour
periods
each
day,
no
symptoms
usually
associated
with
lead
poisoning
occurred
and
that
chemical
analyses
of
animals
gave
no
evidence
of
lead
storage
in
their
bodies.
Where
the
amounts
of
gasoline
contained
5
times
223
the
normal
or
commercial
amount
of
ethyl
fl
uid,
a
large
group
of
animals,
many
of
which
had
been
used
in
the
previous
188
days'
experiment,
still
showed
no
symp-
toms
usually
associated
with
lead
poison-
ing,
but
some
of
them
showed
storage
in
their
tissues.
Thus
this
situation
stands
until
more
information
appears.
We
know
of
no
other
experiments
upon
this
phase
of
the
subject.
Final
reports
of
experiments
conducted
by
the
Bureau
of
Mines
Experiment
Station
have
not
yet
come
to
hand.
We
understand
that
the
question
of
possible
lowered
resistance
from
the
inhalation
of
such
fumes
in
motor
exhausts
may
be
a
part
of
the
fi
nal
report.
It
is
safe
to
say
that
none
of
us
prefer
to
hazard
lead
in
our
systems
if
it
is
pos-
sible
to
prevent
same.
If,
however,
there
is
a
certain
negotiable
amount
which
can
be
handled
without
accumulation
and
subsequent
ill
effects
on
health,
and
such
an
amount
is
absolutely
indispensable
if
the
economics
of
automotive
transporta-
tion
is
to
progress,
we
may
have
to
tol-
erate
the
situation
very
much
the
same
as
we
have
to
tolerate
the
automobile
situation
in
general,
and
in
spite
of
its
manifold
evils.
The
rational
attitude
of
the
present
day
is
complete
publicity
and
education
regarding
our
manifold
hazards
so
that
legislative
and
official
bodies
may
perfect
and
administer
regulations
for
safety.
REFERENCES
1.
Sayers
and
Davenport.
Bull.
150,
U.
S.
Public
Health
Service,
1925.
2.
Beck
and
Fort.
Ann.
Clin.
Med.,
III,
6:437-
443
(Dec.
1),
1924.
3.
O'Brien
and
Parker.
Ind.
Hyg.
Bull.,
N.
Y.
State
Dept.
of
Labor,
11,
2
(Aug.),
1925.
4.
Sayers
and
Yant.
Tech.
Paper,
373,
U.
S.
Bur.
of
Mines,
1925.
5.
Banham,
Haldane
and
Savage.
Brit.
M.
J.,
3370:187
(Aug.
1),
1925.
6.
Thorne.
Pittsburgh
Med.
Bulk,
March
7,
1925.
7.
Lancet,
Feb.
14,
1925,
pp.
319-322.
8.
Serial
2539,
U.
S.
Bur.
of
Mines,
Oct.,
1923.
9.
Fieldner,
Katz
and
Reynolds.
Serial
2591,
U.
S.
Bur.
of
Mines,
Apr.,
1924.
10.
Tech.
Paper,
212,
U.
S.
Bur.
of
Standards.
11.
Tech.
Paper,
325,
U.
S.
Bur.
of
Mines.
12.
Bull.
102,
Part
8,
Smithsonian
Institution.
13.
Tech.
Paper,
337.
U.
S.
Bur.
of
Mines.