NATIONAL
AMBIENT AIR QUALITY STANDARD
FOR LEAD
NOTICE OF PROPOSED RULEMAKING
[40 CFR PART 50]
[FRL 821-4]
DECEMBER 14, 1977
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Air and Waste Management
Office of Air Quality Planning and Standards
Research Triangle Park, North Carolina 27711
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ENVIRONMENTAL PROTECTION AGENCY
[40 CFR Part 50]
[FRL 821-4]
Docket Number OAQPS 77-1
PROPOSED NATIONAL AMBIENT AIR QUALITY STANDARD FOR LEAD
AGENCY: Environmental Protection Agency
ACTION: Proposed Rule
SUMMARY: In response to a court order to adopt a national ambient air
quality standard for lead, EPA proposes to set a national standard
for airborne lead of 1.5 micrograms lead per cubic meter (ug Pb/m3),
monthly average. Following promulgation of the standard, States will
develop implementation plans for EPA approval which demonstrate how the
standard will be attained by 1982, and maintained thereafter. The proposed
standard for lead is based on EPA judgments about groups in the popula-
tion that are at particular risk to lead, the lowest levels of lead exposure
associated with adverse effects on health, and the relative importance
of airborne lead as a source of lead exposure. EPA believes its proposal
reflects the increasing concern from medical research about prolonged
low level exposure to lead by young children. The air standard proposed
t EPA is based on a goal for total lead exposure lower than previously
advocated by other Federal agencies. There is, however, continuing
controversy over- key areas of research underlying the standard. EPA would
welcome information and views pertaining to EPA's approach in developing
the standard and to the factors discussed in this notice. EPA also believes
that the analyses and judgments that will lead to setting the air standard
for lead will have strong implications for other regulatory programs
related to lead at the Federal and other levels of government. In the six-
month period between proposal and final promulgation, EPA will continue its
examination of these difficult issues related to setting the level of the
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ambient air quality standard for lead and will seek to involve the public and
other affected Federal agencies, both on the final decisions on this air
standard as well as planning on ways to control population exposure to
lead from non-air sources.
DATES: Comments must be received by February 17, 1978. There will be
a public hearing at EPA, 401 M Street, S.W., Washington, D.C. 20460 on
January 17, 1978. The standard will be promulgated by June, 1978.
FOR FURTHER INFORMATION AND SUBMISSION OF COMMENTS, CONTACT:
Mr. Joseph Padgett, Director
Strategies and Air Standards Division
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina 27711
Telephone: 919-541-5204
AVAILABILITY OF SUPPORTING INFORMATION: A docket (Number OAQPS-77-1) con-
taining information used by EPA in development of the proposed standard is
available for public inspection between 8:00 a.m. and 4:30 p.m. Monday
through Friday, at EPA's Public Information Reference Unit, Room 2922,
Waterside Mall, 401 M Street, S.W., Washington, D.C. 20460.
The Federal Reference Method for collecting and measuring lead and
its compounds in the ambient air is described in Appendix G to this
proposal. Regulations for development of State implementation plans for
lead are proposed under 40 CFR Part 51 elsewhere in this Federal Register.
The environmental and economic impacts of implementing this standard are
described in an Environmental Impact Statement and an Economic Impact
Assessment available upon request from Mr. Joseph Padgett at the address
shown above.
The documents "Air Quality Criteria for Lead" and "Control Techniques
for Lead Air Emissions" are being issued simultaneously with this proposal
Both documents are available upon request from Mr. Joseph Padgett at the
address shown above.
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SUPPLEMENTARY INFORMATION:
BACKGROUND
Lead is emitted to the atmosphere by vehicles burning leaded fuel
and by certain industries. Lead enters the human body principally through
ingestion and inhalation with consequent absorption into the blood stream
and distribution to all body tissues. Clinical, epidemiological, and toxi-
cological studies have demonstrated that exoosure to lead adversely affects
human health.
EPA's initial approach to controlling lead in the air was to limit
the lead emissions from automobiles, the principal source of lead air
emissions. In January of 1972, EPA proposed regulations under Section 211
of the Clean Air Act for phase-down of the lead in gasoline. Subsequently,
this action was divided into the promulgation of regulations for the
availability of lead-free gasoline for catalyst-equipped cars and other
vehicles certified for unleaded fuel and reproposal of the regulations
for lead phase-down in leaded gasoline. The regulations for lead phase-
lown in the total gasoline pool were promulgated in 1973 and, following
.itigation, modified and put into effect in 1976.
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In 1975S the Natural Resources Defense Council (NRDC) and others
brought suit against EPA to list lead under Section 108 of the Clean Air
Act as a pollutant for which air quality criteria would be developed and
a National Ambient Air Quality Standard be established under Section 109
of the Act. The Court ruled in favor of NRDC. EPA listed lead on March 31,
1976, and proceeded to develop air quality criteria and the standard.
In proposing this air standard, EPA is concerned that there are
reciprocal effects between the goals and actions taken to control the
level of lead in the air, and the parallel judgments and actions taken
under other Federal programs. These other programs include EPA's own
responsibilities to set standards for lead in drinking water and for the
disposal of hazardous waste, the authorities of the Food and Drug Administra-
tion to control lead in food, and the regulations adopted by the Consumer
Product Safety Commission to control lead in paint. EPA has raised through
the Interaqency Regulatory Liaison Group the need to coordinate the programs
of the Food and Drug Administration, Consumer Product Safety Commission,
and the Occupational Safety and Health Administration. Where appropriate,
EPA will continue to work with other Federal agencies in developing a
general Federal approach to limiting other avenues of exposure to environ-
mental lead.
In parallel with developing the proposed standard, EPA has used
information available to assess the economic impact of technological
controls necessary to reduce air emissions of lead from industrial facilities
For primary copper smelters, primary and secondary lead smelters, gray
iron foundries and battery plants, attaining the standard may require
control of fugitive lead emissions, i.e., those emissions escaping from
process steps, other than emissions from smoke stacks. Fugitive emissions
are difficult to estimate, measure, or control, and it is also difficult
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to predict their impact on air quality near the facility. From the
information available to the Agency, it does appear that non-ferrous
smelters may have great difficulty in achieving lead air quality levels
consistent with the proposed standard in areas immediately adjacent to
the smelter complex. While the possible imoact of the standard on these
facilities is of concern to EPA, and will be the subject of continuing
studies and analysis, these impacts have not entered into determination of
the level of the standard.
LEGISLATIVE REQUIREMENTS FOR NATIONAL AMBIENT AIR QUALITY STANDARDS
Two sections of the Clean Air Act govern the development of a
National Ambient Air Quality Standard. Section 108 instructs EPA to
document the scientific basis for the standard:
Sec. 108(a) "(2) The Administrator shall issue air quality criteria
for an air pollutant within 12 months after he has included such
pollutant in a list under paraqraoh (1). Air quality criteria
for an air pollutant shall accurately reflect the latest scientific
knowledge useful in indicating the kind and extent of all identifi-
able effects on public health or welfare which may be expected from
the presence of such pollutant in the ambient air, in varying quan-
tities. The criteria for an air pollutant, to the extent practicable,
shall include information on--
"(A) those variable factors (including atmospheric condi-
tions) which of themselves or in combination with other factors
may alter the effects on oublic health or welfare of such air
oollutant;
11 (B) the types of air pollutants which, when present in
the atmosphere, may interact with such pollutant to produce an
adverse effect on public health or welfare; and
"(C) any known or anticipated adverse effects on welfare."
Section 109 addresses the actual setting of the standard:
Sec. 109 "(b) (1) National primary ambient air quality standards,
prescribed under subsection (a) shall be ambient air quality
standards the attainment and maintenance of which in the judg-
ment of the Administrator, based on such criteria and allowing an
adequate margin of safety, are requisite to protect the public
health. Such primary standards may be revised in the same manner
as promulgated.
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"(2) Any national secondary ambient air quality standard
prescribed, under subsection (a) shall specify a level of air
quality the attainment and maintenance of which in the judgment
of the Administrator, based on such criteria, is requisite to
protect the public welfare from any known or anticipated adverse
effects associated with the presence of such air pollutant in the
ambient air. Such secondary standards may be revised in the same
manner as promulgated."
EPA interprets these sections of the Act to mean that the level of
the standard is to be determined from information covered in the Criteria
Document pertaining to the health and welfare implications of lead air
pollution. This is in contrast to other sections of the Act which allow
EPA to consider costs of air pollution control and availability of tech-
nological controls in determining the level of a standard. Also, EPA
should not attempt to place the standard at a level anticipated to represent
the threshold for adverse effects, but should set a more stringent level
which provides a margin of safety. EPA believes that the extent of margin
of safety represents a judgment issue in which the Agency should consider
the severity of adverse effects, the probability that the effects may occur,
and uncertainties associated with scientific knowledge about the biological
effects of lead.
DEVELOPMENT OF AIR QUALITY CRITERIA
Following the listing of lead, EPA proceeded with development of
the document, "Air Quality Criteria for Lead". In the process of
developing the Criteria Document, EPA has provided a number of opportuni-
ties for external review and comment. Three drafts of the Criteria
Document have been made available for external review and EPA has
received 60 to 80 written comments on each draft. The Criteria Document
was the subject of three meetings of the Subcommittee on Scientific
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Criteria for Environmental Lead of EPA's Science Advisory Board. Each
of these meetings has been open to the public and a number of individuals
have presented both critical review and new information for EPA's con-
sideration.
Development of the Criteria Document indicated to EPA that there are
a number of areas in which additional research could provide information
useful to determining the level for the lead standard. It is also evident
that scientific controversy exists about facts or interpretation of material
included in the Criteria Document, including two areas critical to the
setting of the standard: the health significance of abnormal biological
effects associated with blood lead levels below traditional levels of con-
cern, and the relative significance of lead air emissions as the direct
or indirect source of lead exposure, compared to other sources of exposure.
However, the provisions of the Act requiring a deadline for proposal
and promulgation of the standard, and the requirements for periodic
future review of air quality criteria and standards, indicate that Congress
intends for the Agency to proceed even where scientific knowledge is not
complete or where there is an absence of full scientific consensus. EPA
hu5: therefore, developed the proposed air standard on the basis of its
best judgment as to what the Act requires, and what information the
"Air Quality Criteria for Lead" provides. To arrive at the air standard,
EPA has attempted to use numerical estimates of key factors. In several
instances, factors which are not known precisely have a large effect on
the level of the standard. EPA invites information, views and judgments
both on its approach to setting a level for the standard and the numerical
values used for key factors described in the following sections.
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SUMMARY OF GENERAL FINDINGS FROM AIR QUALITY
CRITERIA FOR LEAD
From the extensive review of scientific information presented in the
Criteria Document, conclusions in several key areas have particular
relevance for setting the lead standard.
1. There are multiple sources of lead exposure. In addition to
air lead these sources include: lead from paint and inks, lead from
water supplies and distribution systems, lead from pesticides,.and lead
in fresh and processed food. The relative contribution to population
exposure from each source is difficult to quantify.
2. Exposure to air lead can occur directly by inhalation, or in-
directly by ingestion of lead'contaminated food, water, or non-food materials
including dust and soil.
3. There is a significant variability In response to lead exposure.
Certain subgroups within the population are more susceptible to the
effects of lead or have a greater potential for exposure. Of these,
young children represent a population of foremost concern. Even within
a particular population, group response to lead exposure may vary widely
from the average response.
4. Within the human body, three systems appear to be most sensitive
to interference by lead—the blood-forming or hematopoietic system, the
nervous system, and the renal system. In addition, lead has been shown
to affect the normal functions of the reproductive, endocrine, hepatic,
cardiovascular, immunologic, and gastrointestinal systems.
5. Effects reported in the Criteria Document range from impairment
of biochemical systems (inhibition of aminolevulinic acid dehydratase
(ALAD)) at a blood lead level of 10 micrograms lead per deciliter blood
Pb/dl) to encephalopathy at 80 to 100 ug Pb/dl.
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6. From various studies of lead exposure, estimates can be made of
the impact of exposure through inhalation and ingestion on blood lead
level. Of particular importance, are the estimates of: air lead/blood
lead ratios, the percentage of deposition and absorption of air lead,
the percentage of absorption of ingested material, estimates of the variability
of blood lead within a population exposed to uniform levels of lead, and
estimates of the contribution of air lead to blood lead.
Determination of a proposed level for the lead standard requires
the use and interpretation of specific information for each of these
areas. The approach taken is described in the following sections.
GENERAL APPROACH TO SETTING THE LEAD STANDARD
Development of the National Ambient Air Quality Standard for lead
requires certain judgments by EPA about the relationship between concen-
trations of lead in the air and possible adverse health effects experienced
by the public. This relationship is greatly complicated by the fact that
lead in the air is not the only source of lead exposure; that there is
variability of response among individuals exposed to lead; and that there
are numerous effects of lead on health, occurring at various levels of
ey -»osure which vary in public health significance.
In developing the standard, EPA has made judgments in five key
areas:
1. Determining the critically sensitive population.
2. Determining the pivotal adverse health effect.
3. Determining the mean population blood lead level which would
be consistent with protection of the sensitive population.
4. Determining the relationship between air lead exposure and
resulting blood lead level.
5. Determining the allowable blood lead increment from air.
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DETERMINING THE CRITICALLY SENSITIVE POPULATION
Certain subgroups within the general population differ in sen-
sitivity to lead exposure. Protection of populations exhibiting the
greatest sensitivity of response to lead is a major consideration in
determining the level of the lead standard. From information presented
in the Criteria Document, there are a number of populations for which
lead exposure poses a greater risk: young children, pregnant women and
the fetus; the occupationally exposed; and individuals suffering from
dietary deficiencies or exhibiting the genetic inability to produce
certain blood enzymes.
EPA believes that young children (ages 1-5 years) should be regarded
as the foremost critically sensitive population for setting the lead
standard. This is because hematologic and neurologic-effects in children
are shown to occur at lower thresholds than adults, and because children
have a greater risk of exposure to non-food material containing lead, such as
dust and soil, as the result of normal hand-to-mouth activity. The
Criteria Document also states that children may be at greater risk than adults
due to 1) greater intake of lead via inhalation and ingestion per unit
body weight; 2) greater absorption and retention of ingested lead; 3)
physiologic stresses due to rapid growth rate and dietary habits; 4) in-
complete development of metabolic defense mechanisms; and 5) greater sensi-
tivity of developing systems.
Pregnant women and the fetus are at risk because of transplacental
movement of lead to the fetus and the possibility of maternal complications
at delivery. Because there is a balance between maternal blood lead
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levels and fetal blood lead levels, concern exists that development of
the nervous system of the fetus may be impaired due to neurotoxicity of
lead. Changes in fetal heme synthesis and premature births have been
associated with prenatal exposure of the fetus to lead. However, available
evidence does not indicate that pregnant women and the fetus would
require a more stringent standard than young children.
Groups exposed to lead in the workplace also comprise a population
at greater risk. Because members of such groups are generally healthy
and do not have a greater physiological sensitivity to lead than young
children, EPA believes that the protection of such groups does not require
an air quality standard for lead more stringent than that for young children,
Other possible critically sensitive populations suggested in the
Criteria Document include individuals with genetic conditions such as
sickle cell disease. The Criteria Document cites a tentative association
between the existence of sickle cell disease in children and increased
risk of peripheral neuropathy due to lead exposure. Individuals suffering
from iron deficiency or malnutrition may also be at greater risk from
'.ead exposure. There is, however, insufficient data to determine the
ef "ects threshold for such groups or to accurately characterize such
grji.'ps within the general population.
DETERMINING THE PIVOTAL ADVERSE HEALTH EFFECT
The toxic effects of lead resulting from high levels of exposure
are well documented. Among the first effects noted historically were
the severe and sometimes fatal consequences such as colic, palsy, and
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encephalopathy which followed acute occupational exposure in the mining
and smelting industries. Exposure to high concentrations of lead in
paints, inks, pesticides, and plumbing have similarly been implicated in
cases of severe poisoning.
Recent widespread increase of lead in the environment as a result
of human activities has stimulated research on the possible effects of
the longer-term, low level exposure characteristic of the general popula-
tion. Clinical and epidemic!ogical studies have revealed that lead
accumulates in the body throughout life, to a large extent immobilized
in bone, but with a significant mobile fraction in the blood and soft
tissues. Blood lead concentrations respond predictably to changes in
the level of environmental exposure and, as a result, are generally
accepted as good indicators of that exposure as well as of the internal
dose of lead to which all body tissues are exposed. The threshold for
a particular health effect is considered to be the blood lead level
at which the effect is first detected.
The Criteria Document provides a ranking by blood lead threshold of
the health effects observed in children.
SUMMARY OF HEALTH EFFECTS IN CHILDREN
Blood Lead Threshold Effect Population Group
( Ug Pb/dl) t
10 ALAD inhibition Children and adults
15-20 Erythrocyte protoporphy- Women and children
rin elevation
40 Increased urinary ALA Children and adults
excretion
40 Anemia Children
40 Coproporphyrin elevation Adults, children
50 - 60 Central Nervous System Children
(CNS) deficits
50 - 60 Peripheral neuropathies Adults and children
80 - 100 Encephalopathic symptoms Children
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Inhibition of the enzyme aminolevulinic acid dehydratase (ALAD)
represents the lowest level effect of lead that has been detected.
The decreased activity of this enzyme, while observable, is not suf-
ficient at blood leads at and below 10 yg Pb/dl to interfere with the
step in heme synthesis which it mediates. Because no significant accumu-
lation of precursors occurs at this level of exposure, ALAD inhibition
of this degree is not regarded as a physiological impairment of the
system. This effect becomes more significant at higher lead concen-
trations (40 yg Pb/dl) which reduce the activity of ALAD sufficiently to
cause build-up of the precursor (ALA) in the urine.
Erythrocyte Protoporphyrin Elevation
Above 15-20 ^g Pb/dl, the Criteria Document notes a correlation
between blood lead levels in children and the elevation of protoporphy-
rin in red blood cells. Unlike ALAD inhibition at 10 ug Pb/dl, the
accumulation of erythrocyte protoporphyrin (EP) indicates a functional
impairment of the heme synthetic pathway.
In regard to the implications for health of EP elevation, the
Cr crria Document provides the following description:
"Accumulation of protoporphyrin in the erythrocytes is the
result of decreased efficiency of iron insertion into protoporphyrin,
the final step in heme synthesis which takes place inside the mito-
chondria. When this step is blocked by the effect of lead, large
amounts of protoporphyrin without iron accumulate in the erythrocyte,
occupying the available heme pockets in hemoglobin."
"The effect of lead on iron incorporation into protoporphyrin
is not limited to the normoblast and/or to the hematopoietic system.
Formation of the heme-containing protein, cytochrome-P450, which
is an integral part of the liver mixed-function oxidase, may also
be inhibited by lead. Accumulation of protoporphyrin in the
presence of lead has been shown to occur also in cultured cells
of chick dorsal root ganglion, indicating that inhibition of heme
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synthesis takes place in the neural tissue as well. These observa-
tions, and the fact that lead is known to disrupt the mitochondria!
structure and function, indicate that the lead effect on heme
synthesis is exerted on all body cells, possibly with different
dose/response curves holding for effects in different cell types.
On the other hand, it must be noted that increased levels of
protoporphyrin in the erythrocyte reflect an accumulation of substrate
and therefore imply a functional alteration of mitochondria! function
in the same way that the increased urinary excretion of urinary 6-
ALA implies impairment. In other words, if a "reserve" activity of
ferrochelatase exists, such as has been suggested for 6-ALAD,
accumulation of protoporphyrin in the erthrocytes indicates
that this has been hampered by the lead effect to the point that the
substrate is accumulated. For these reasons, as well as for its
implication of the impairment of mitochondria! function, accumula-
tion of protoporphyrin has been taken to indicate physiological
impairment relevant to human health."
The remaining effects listed in the table present progressively
greater health risks to susceptible individuals including anemia, the
possibility of irreversible learning deficits, and lead encephalopathy.
EPA is proposing that lead-induced elevation in children of EP
should be accepted as the pivotal adverse effect of lead. Accordingly, the
air lead standard should be designed to prevent the occurrence of EP
elevation in children. EPA bases its determination that EP elevation
due to lead should be regarded as an adverse health effect on the following
points:
1. EP elevation indicates an abnormal impairment of various
cell functions, which should not be allowed to persist as a
chronic condition.
2. The impairment of cellular function indicated by EP elevation
extends to all body cells, and may have particular implications
for the functioning of neural and hepatic tissues.
3. The air lead standard is intended to establish a level of
airborne lead which can be regarded as consistent with
protecting the health over a lifetime of exposure. The pervasive
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biological involvement of lead in the body, and its demon-
strated impairment of biological functions are a strong impetus
to the Agency in adopting the lowest threshold biological effect
which can be considered adverse to health.
4. The Center for Disease Control has also used EP elevation as
an indicator of undue lead exposure, although their guidelines
published in 1975 are oriented to establishing an individual
threshold for risk (30 ug Pb/dl) in populations of children
exposed to high-dose lead sources such as lead-based paint
rather than for establishing a safe mean population blood lead
level with a margin of safety.
5. The Act intends that the air standard be precautionary. Taking
the lowest adverse effect levels is compatible with the
scientific uncertainty about the health consequences of pro-
longed low level lead exposure, and with the downward trend in
levels of lead in the blood regarded as adverse to health by the
public health community.
As an alternative to using elevation of EP as the pivotal health
:fect, EPA could take the position that EP elevation, while of concern
to public health, is not sufficiently adverse to health, and that the
standard should be based on the more severe effects such as anemia,
or CNS deficits- EPA would welcome comments on whether what is known,
or anticipated, about EP elevation or other subclinical effects has
sufficient implications to warrant a role in determining the level of
the standard.
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DETERMINING A SAFE BLOOD LEAD LEVEL FOR PROTECTION OF THE
SENSITIVE POPULATION
The third key area for judgment in the development of the proposed
standard involves the determination of the mean population blood lead
level for children at which EP elevation does not occur. EPA is proposing
that this standard for lead be based on the judgment that the mean popula-
tion blood lead for children not exceed 15 yg Pb/dl. This is the
lowest value given in the Criteria Document as a threshold for the correla-
tion of EP with blood lead level, based on studies by Roels (1976) and
Piomelli (1977). On the basis of present knowledge, EPA believes that a
population mean of IS ug Pb/dl can be regarded as an indicator of a safe
level of total lead exposure for children.
There are two reasons why the use of a blood lead target as an
intermediate goal between air quality and EP levels is necessary. First,
most of the scientific literature covered by the Criteria Document
reports studies which link air lead with blood lead levels. Second, EP
levels can be expected to respond to all sources of lead exposure; blood
lead level serves as an indicator of total exposure.
In selecting 15 yg Pb/dl mean population blood lead as a target,
EPA wishes to stress that it is proposing a statistical measure of popula-
tion exposure. EPA is not suggesting that individual blood lead levels
in excess of 15 yg Pb/dl necessarily constitute a significant risk to
health. It can be expected that a population with a mean blood lead level of
15 iag Pb/dl will have individuals with higher and lower blood lead levels.
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There will also be a variation of EP levels for individuals with a given
blood lead level. It i^ also true that the absence of statistical correla-
tion of EP levels with blood lead levels below 15 yg Pb/dl does not
necessarily mean that these lower blood lead levels are known to be
without risk. However, the threshold of 15 ug Pb/dl does represent a
point below which the sensitive population as a group has not been seen
to show an elevation in EP due to lead and above which EP elevation has
been demonstrated to rise with increasing implications for health. While
other thresholds for EP elevation have been found (Sassa, 1973), EPA is
using the lowest level cited in the Criteria Document in order to establish
a margin of safety.
Alternatively, EPA could attempt to judge the actual level of EP
elevation which represents an adverse effect on healths and then apply
an adjustment for margin of safety. For example, in 1975, the Center
for Disease Control established as a guideline for undue or increased
lead absorption in children a blood lead level of 30 ug Pb/dl or EP
levels of 60 yg/dl. The level of 30 ug Pb/dl in the blood represents
some degree of health risk., but it is difficult to know whether any inter-
i diate levels between 30 ug Pb/dl and 15 ug Pb/dl safeguard the public
health.
EPA believes that elevations in individual blood levels and corre-
sponding changes in EP levels are reversible, and may not in a single
cycle constitute a serious physiological impairment. However, taken
as a population average, underlying an environmental standard describing
the safe limits for a lifetime of exposure, EPA. -is proposing that no
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elevation of EP associated with lead exposure should be seen as free
from risk to the health of the sensitive population.
In establishing the target mean blood lead level for the sensitive
population, EPA has used the lowest threshold for EP rather than attempt
to use statistical techniques discussed in the Criteria Document in order
to take into account the extent of individual variation in blood lead
levels for a given level of exposure. The Criteria Document points out
that data from epidemiological studies show that the log values of indi-
vidual blood lead values in a uniformly-exposed population are normally
distributed with a standard geometric deviation of 1.3 to 1.5. Using
standard statistical techniques, it is possible to calculate the mean
population blood lead level which would place a given percentage of the
population below the level of an effects threshold. For example,
a mean population blood lead level of 15 yg Pb/dl would place 99.5%
of a population of children below the Center for Disease Control guide-
line of 30 yg Pb/dl.
EPA believes that variable response within the sensitive population
should be taken into consideration in setting the level of the standard,
but recognizes a number of problems in using the log-normal distribution
in the case of the lead standard.
(1) The log-normal distribution describes the variable response
of individuals' blood lead levels to air exposure. It can be expected
that there is also a probability distribution associated with the
elevation of EP among individuals with a given blood lead level. The
parameters of this second probability distribution are not presented in
the Criteria Docurnent3 but it is reasonable to expect that only a small
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percentage of those individuals just above the threshold blood lead level
will experience EP elevation beyond what could be expected from the
normal scatter of EP values around blood lead levels just below the
threshold. The effect of using blood lead as an intermediary between
air lead exposure and EP levels is to combine two probability distributions,
one known and one unknown, between population blood values and EP elevation.
(2) There are a number of sources of variability in blood lead
levels other than individual differences of response within a population
group. These include variability from possible non-uniform exposure to
lead in the populations studied and from analytical and process techniques
used in measuring blood lead.
For these reasons, EPA believes that use of a log-normal correction
may overestimate the degree to which the population mean should be below
the threshold blood lead level. This is particularly true in dealing
with the threshold for EP where considerable margin of safety results
from selection of the target blood lead level at which slight EP elevation
is first detected, rather than a level at which lead has had a substantial
impact on EP levels.
DETERMINING THE RELATIONSHIP BETWEEN AIR LEAD EXPOSURE
AND RESULTING BLOOD LEAD LEVEL
On the basis of clinical and epidemiological studies evaluated, the
Criteria Document concludes:
"Evidence indicates that a positive relationship existi between
blood and air lead levels, although the exact functional relation-
ship has not yet been clarified. Available data indicate that in
the range of air lead exposures generally encountered by the popula-
tion, the ratio of the increase in blood lead per unit of air lead
is from 1 to 2. It appears that the ratio for children is in the
upper end of the range and that ratios for males may be higher than
those for females."
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The range of ratios for children's blood lead response to a one yg in-
crease in air lead cited in the Criteria Document is from 1.2 to 2.3.
The lower ratio comes from studies at Kellogg, Idaho, where dust levels
of lead were separately correlated with blood lead. In view of the ten-
dency of children to experience higher ratios due to greater intake and
absorption of air lead, EPA has selected a ratio of 1:2 in calculating
the impact of air lead levels on blood lead levels in children.
DETERMINING THE ALLOWABLE BLOOD LEAD INCREMENT FROM AIR
The fifth area of judgments made by EPA in developing the proposed
standard for lead is related to an aspect of lead which has not characterized
any pollutant previously addressed by EPA under Section 109 of the Clean
Air Act: that significant amounts of the pollutant result from sources
that are not subject to control by implementing an air quality standard.
Some studies reported in the Criteria Document clearly show that
levels of lead in the blood derive from non-air sources. For example,
studies in areas with minimal air lead levels still show significant
levels of lead in the blood (Johnson, Tillery 1975). A study of
children in Boston correlates blood lead levels with lead levels in
water supplies (Worth, in press).
Other studies demonstrate a strong relationship of blood lead level
with air lead. Clinical studies on adult volunteers in chamber studies
demonstrate changes of blood lead with changes of the concentration of
lead in the air (Griffin, et. al, 1975). Epidemiological studies show a
general pattern of urban-rural difference where blood lead levels are
higher in urban settings where air lead levels are also higher. Other
epidemiological studies directly correlate air lead with blood lead.
These include studies using personal dosimeters to accurately gauge lead
20
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exposure (AZAR, 1975), and the extensive population studies conducted in
the community around the smelter complex at Kellogg, Idaho (Yankel and
von Lindern, 1977).
Implications of Multiple Sources of Lead in Setting an Air Standard
The implications of multiple sources of environmental lead are difficult
to reconcile with the concept of a National Ambient Air Quality Standard.
If the air were the only source of lead, it would be a reasonably straight-
forward matter to identify a safe level and to require that, regardless
of what prevailing levels of air lead are today, the safe level be
achieved. However, since non-air sources contribute lead as well, the
level of an ambient air quality standard which will protect public health
is affected by the contribution of these non-air sources. If their
contribution is far below the allowable level of blood lead, the
air contribution can be permitted to be relatively high. However, if they
alone contribute more than the allowable blood lead level, even a zero
ambient air quality standard would not prevent EP elevation in children.
EPA believes that it should assume some level of blood lead
attributable to non-air sources in order to determine what the air lead
ontribution can be, and what the ambient air quality standard should be as
a result. This calculation is complicated, however, by the fact that
the non-air contribution to blood lead varies from time-to-time and
place to place. As a result, the level selected as the basis for determining
the allowable contribution from air and the resulting air quality standard
becomes in part a policy choice reflecting how much of the lead pollution
problem should be dealt with through control of air sources.
Because of the factors just discussed, no National Ambient Air Quality
Standard can be assured of being protective in all locations. Regardless
of what the non-air contribution is assumed to be, the air standard will
21
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be overprotective in areas where lead from non-air sources is low and
underprotective in areas where it is high. EPA does not believe, however,
that it is given the latitude to set area specific air quality standards
under Section 109. EPA has, therefore, undertaken to make a single
judgment as to what contribution to population blood lead levels derives
from non-air sources. This single numerical value represents, in fact,
what EPA proposes should be taken as a goal in limiting lead exposures
from non-air sources. The level for non-air contribution used in this
proposal is EPA's best judgment as to the appropriate level based partly
on what is known about non-air lead contribution from a limited number
of studies and partly on what EPA believes is an appropriate goal for
air pollution control, consistent with the Agency's responsibility to
protect the public health. The specific derivation of the goal for non-
air contribution to mean population blood lead levels is described in
the next section.
Basis for EPA's Estimate of Contribution to Blood Lead Levels from Non-
Air Sources
The level of the standard is very strongly influenced by judgments
made regarding the size of non-air contribution to total exposure. EPA
has encountered difficulties in attempting to estimate exposure from
various lead sources in order to determine the contribution of such
sources to blood lead levels:
(1) Studies reviewed in the Criteria Document do not provide
detailed or widespread information about relative contribution of
various sources to young children. Estimates can only be made by
inference from other empirical or theoretical studies, usually in-
volving adults.
22
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(2) It can be expected that the contribution to blood lead levels
from non-air sources can vary widely, is probably not in constant
proportion to air lead contribution, and in some cases may alone
exceed the target mean population blood lead level.
In spite of these difficulties, EPA has attempted to assess available
information in order to estimate the general contribution to population
blood lead levels from air and non-air sources. This has been done with
evaluation of evidence from general epidemiological studies, studies showing
decline of blood lead levels with decrease in air lead, studies of
blood lead levels in areas with low air lead levels, and isotopic
tracing studies.
Studies reviewed by the Criteria Document show that mean blood lead
levels for children are frequently above 15 yg Pb/dl. In studies reported,
the range of mean population blood lead levels for children was from
16.5 ug Pb/dl to 46.4 ug Pb/dl with most studies showing mean levels
greater than 25 pg Pb/dl (Fine, 1972; Landrigan, 1975; von Lindern,
1975). EPA believes that for most of these populations, the contribution
to blood lead levels from non-air sources exceeds the desired target
-nean blood lead level.
In a number of studies, it is apparent that reduction in air lead
levels results in a decline in children's blood lead levels. A study of
blood lead levels in children in New York City showed that children's mean
blood lead levels fell from 30.5 pg Pb/dl to 21.0 pg Pb/dl from 1970 to 1976,
while during the same period air lead levels at a single monitoring site
fell from 2.0 u9 Pb/dl to 0.9 yg/Pb, (Billick, 1977). Studies at Omaha,
Nebraska (Angle, 1977) and Kellogg, Idaho (Yankel, von Lindern, 1977)
also show a drop in mean blood lead levels with declines in air lead levels.
However, as air lead levels decline there appears to be a rough limit to
23
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the drop in blood lead levels. EPA has also examined epidemiological
studies in the Criteria Document where air lead exposure is low, and can
be assumed to be a minor contributor to blood lead. These studies
provide an indication of blood lead levels resulting from a situation
where non-air sources of lead are predominant.
Studies Reporting Blood Lead Levels in Children
Exposed to Moderate - Low Air Lead Levels
Investigator
Hammer, 1972
Angle, 1974
Goldsmith, 1974
Johnson, Tillery, 1975
Blood Lead
yq Pb/dl
11.6
14.4
13.7
13.8
10.2
Air Lead
yq Pb/m3
0.1
0.14
0.2 - 0.7
0.3 - 0.6
0.6
Comment
Children in Helena,
Montana
Suburban children
ages 1 to 4 in Omaha
Children in Benecia,
California
Children in Crocket,
California
Female children - me
age 9 in Lancaster,
California
The range of mean blood lead levels in those studies is from 10.2 yg Pb/dl
to 14.4 yg Pb/dl, with an average at 12.7 yg Pb/dl.
In addition to epidemiological investigations, EPA has reviewed
studies that examine the source of blood lead by detecting characteristic
lead isotopes. A study using isotopic tracing (Manton, 1977) suggests
that for several adults in Houston, Texas, 7 to 41 percent of blood lead
could be attributed to air lead sources. An earlier isotopic study
(Rabinowitz, 1974) concluded that for two adult male subjects studied,
approximately one-third of total daily intake of lead could be attributed
to exposure to air lead levels of 1-2 yg Pb/m3, While these results
-------
cannot be directly related to children, it is reasonable to assume that
children may exhibit tho same or higher percentages of air lead contri-
bution to blood lead level because of a greater potential for exposure
to indirect air sources, soil and dust.
From reviewing these areas of evidence, EPA concludes that:
1. In studies showing mean blood lead levels above 15 ug Pb/dl, it
is probable that both air and non-air sources of lead contribute
significantly to blood lead with the possibility that contributions
from non-air sources exceed 15 ug Pb/dl.
2. Studies showing a sustained drop in air lead levels show a
corresponding drop in blood lead levels, down to an apparent limit
in the range of 10.2 to 14.4 ug Pb/dl. These studies show the rough
»
range of the lowest blood lead levels that can be attributed to
non-air sources.
3. Isotopic tracing studies show air contribution to blood lead
to be 7-41 percent in one study and about 33 percent in another study.
In considering this evidence, EPA notes that if, from the isotopic
studies, approximately two-thirds of blood lead is typically derived
from non-air sources, a mean blood lead target of 15 Ug Pb/dl would
attribute 10 ^g Pb/dl to non-air sources. On the other hand, the average
blood lead level from studies EPA believes to represent the least amount
of blood lead attributable to non-air sources is 12.7 yg/Pb. In the absence
of more precise information, EPA is proposing that the lead standard be
based on the assumption that in general, 12 ug Pb/dl of the
blood lead level in children is derived from lead sources unaffected by the
lead air quality standard. EPA is aware that actual population blood lead
25
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levels, either individually or as a population mean, may exceed this
benchmark. However, if EPA were to use a larger estimate of non-air
contribution to blood lead, the result would be an exceptionally stringent
standard, which would not address the principle source of lead exposure.
Conversely, EPA believes that it should not adopt an estimate of non-air
contribution below the level shown in available studies to be the lowest
mean blood lead level documented in the Criteria Document.
Because of the strong impact that adopting this goal for non-air
sources has on the level of the standard, EPA welcomes information and
judgments about the validity of the numerical value chosen for this factor,
as well as views about alternative ways in which EPA could develop an
air standard that takes into account other routes of exposure.
CALCULATION OF THE AIR STANDARD
EPA has calculated the proposed standard based on the conclusions
reached in the previous sections:
1) Sensitive Population:
2) Health Basis (lowest detectable
adverse effect):
3) Effect Threshold in Sensitive
Population:
4) Assumed Goal for Contribution to Blood
Lead from Non-Air Sources:
5) Allowable Contribution to Blood
Lead from Air Sources:
15 yg Pb/dl - 12 ug Pb/dl =
6) Air Lead Concentration Con-
sistent with Blood Lead Con-
tribution from Air Sources:
3 ug Pb/dl x 1 yg/m3 air =
children, ages 1-5
elevation of erythrocyte
protoporphyrin (EP)
15 yg Pb/dl
12 yg Pb/dl
3 yg Pb/dl
1.5 yg Pb/m:
2 yg/dl blood
26
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SELECTION OF THE AVERAGING PERIOD FOR THE STANDARD
To be protective of human health, the averaging period for the lead
standard should be chosen such that variations in exposure which could
result in adverse effects do not occur unless the standard is exceeded.
The averaging period is the length of time over which measured concen-
trations of air lead are averaged to obtain an air quality level which
is compared to the standard level to determine if a violation of the
standard has occurred.
Moderate increases in air lead levels have been shown to produce
increases in blood lead levels in adults after seven weeks of exposure
(Griffin, 1975). Because of the slow response of blood lead levels to
increases in air lead levels, it is not. probable that short-term peaks
in air lead levels will cause adverse effects.
Based on available information, EPA has concluded that the averaging
period for the lead standard be a calendar months based on the average
of 24-hour measurements. This period is somewhat shorter than the time
observed for the adjustment of blood lead levels in adults to changes in
?ir lead concentration because of the greater risk of exposure of young
lildren.
MARGIN OF SAFETY
EPA believes that the recommended standard incorporates a
sufficient margin to protect the public health and welfare from the
adverse effects of lead exposure deriving from lead in the air. Margin
of safety considerations have entered into the development of the standard
in several key areas:
27
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1) The standard is based on protection of young children, a critically
sensitive general subgroup within the population.
2) The standard is based on the lowest threshold for the first
adverse effect occurring with increasing blood lead levels in
children: elevation of protoporphyrin in red blood cells at a
blood lead level of 15 \ig Pb/dl.
3) In estimating the change in blood lead levels resulting from the change
in air lead levels, EPA has selected a ratio at the protective end of
the range provided in the Criteria Document.
IMPACT OF LEAD DUSTFALL ON BLOOD LEAD
The significance of dust and soil lead as indirect routes of
exposure has been of particular concern in the case of young children.
Play habits and mouthing behavior between the ages of one and five
have led to the conclusion that greater potential may exist in these children
for ingestion and inhalation of the lead available in dust and soil.
Studies reviewed in the Criteria Document indicate a correlation between
soil and dust levels and childrens' blood lead levels in highly contaminated
environments (Yankel and von Lindern, 1977; Barltrop, 1974; Galke, in
press). The lead threshold for concern has been reported as 1,000 ppm
in soil (Yankel and von Lindern, 1977); at exposures of 500 and 1,000
ppm soil the Document concludes that blood lead levels begin to increase.
A two-fold increase in soil concentration in this range is predicted to
result in a 3-6 percent rise in blood lead levels. Below 500 ppm soil,
no correlation has been observed with blood lead levels.
28
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The normal background for lead -in soil is cited in the Criteria
Document as 15 ppm. Due to human activities, the average levels in most
areas of the U.S. are considerably higher. Soil studies conducted by
EPA's Office of Pesticides Programs from 1974-1976 in 17 urban areas
reported only 3 cities with arithmetic mean concentrations in excess of
200 ppm, with the highest value 537 ppm. Concentrations in the soils
surrounding large point sources of lead emissions, or heavily-travelled
roads, on the other hand, may reach several thousand ppm.
Because of the many factors involved, EPA is unable to predict the
relationship between air lead levels, dustfall rates, and resulting soil
accumulation. Complicating factors include: particle size distribution,
rain-out, other meteorological factors, topographical features affecting
deposition, and removal mechanisms.
EPA believes, however, that significant impacts on blood lead of
soil and dust lead are mainly limited to areas of high soil concentration
(in excess of 1,000 ppm) around large point sources and in major urban
areas which also experience high air lead levels. Evidence suggests that
oil lead levels in areas with air lead levejs in the range of the
proposed standard are well below the threshold for blood lead impact
(Johnson, Ttllery, 1975; Johanson, 1972; EPA, 1975 Air Quality Data and
Soil Levels).
29
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WELFARE EFFECTS
Available evidence cited in the Criteria Document indicates that
animals do not appear to be more susceptible to adverse effects from
lead than man nor do adverse effects in animals occur at lower levels of
exposure than comparable effects in humans.
There is some evidence that atmospheric sources of lead may be
injurious to plants. Lead is absorbed but not accumulated to any great
extent by plants from soil. Lead is either unavailable to plants or is
fixed in the roots and only small amounts are transported to the above
ground portions. Lead may be deposited on the leaves of plants and
present a hazard to grazing animals. Although some plants may be susceptible
to lead in the natural environment, it is generally in a form that is
largely nonavailable to them.
There is no evidence to indicate that ambient levels of lead result
in significant damage to man-made materials. Effects of lead on visibility
and climate are minimal.
Based on such datas EPA concludes that significant welfare effects
associated with exposure, to lead which would necessitate a secondary
standard more restrictive than the primary standard have not been
established. Therefore, the primary ambient air quality standard should
protect against known and anticipated adverse effects on public welfare.
A more restrictive- secondary standard will not be established at this
time.
30
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ECONOMIC IMPACT ASSESSMENT
The Agency conducted a general analysis of the economic impact
that might result from the implementation of lead emission control
measures. This analysis pointed out that the categories of sources
likely to be affected fay control of lead emissions are primary lead and
copper smelters, secondary lead smelters, gray iron foundries, gasoline
lead additive manufacturers, and lead storage battery manufacturers.
This analysis further indicates that primary and secondary lead smelters
and copper smelters may be severely strained both technically and economically
in achieving emission reductions that may be required in implementing the
proposed air quality standard.
There are, however, uncertainties associated with evaluating the
impact of attaining the standard. For smelters, foundries and battery
plants, attaining the standard may require control of fugitive.lead
emissions3 i.e., those emissions escaping from process steps, other than
emissions from smoke stacks. Fugitive emissions are difficult to estimate,
measure, or control and it is also difficult to predict their impact on
air quality near the facility. From the information available to the
Agency, it does appear that non-ferrous smelters may have great difficulty
;n achieving lead air quality levels consistent with the proposed standard
in areas immediately adjacent to the smelter complex. While the possible
impact of the standard on these facilities is of concern to EPA, and will
be the subject of continuing studies and analysis, these impacts have not
entered into determination of the level of the standard.
OTHER EPA REGULATIONS
In 1975, EPA promulgated the national interim primary drinking
water regulation for lead. The standard was aimed at protecting children
from undue lead exposure and limited lead to 0.05 milligrams per liter
(mg/1) which was considered as low a level as practicable. In 1977,
31
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the National Academy of Sciences evaluated the interim drinking water
standards and concluded that a no-observed-adverse health effect for
lead cannot be set with assurance at any value greater than 0.025 mg/1.
The Office of Water Supply is currently reviewing the need to revise
the interim drinking water standard for lead.
Based on its toxicity, EPA included lead on its 1977 list of
priority pollutants for which effluent guidelines will be developed
by early 1979. Effluent guidelines for non-ferrous smelters, the
major stationary source emitters of airborne lead, are being developed
based on achievement of best available technology.
EPA's Office of Pesticide Programs has promulgated regulations
based on toxicity of lead which require the addition of coloring agents
to the pesticide lead arsenate and specify disposal procedures for
lead pesticides. Use of lead in pesticides is a small and decreasing
proportion of total lead consumption in the U.S.
The Resource Conservation and Recovery Act of 1976 through which
EPA is to establish standards on how to treat, dispose, or store
hazardous wastes, provides a means for specifying how used crankcase
oil and other waste streams containing lead should be recycled or
safety disposed of. At the present time, no regulatory actions related
to wastes containing lead have been proposed.
EPA has regulations for reducing the lead content in gasoline to
0.5 grams/gallon by October 1, 1979, and regulations providing for lead-
free gasoline required for cars equipped with catalytic converters and
other vehicles certified for use of unleaded fuel. The former regulations
are based on reducing exposure to airborne lead to protect public health.
Other EPA actions which result in the reduction of airborne lead levels
include ambient standards and State implementation plans for other
pollutants such as particulate matter and sulfur dioxide and new source
32
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P - '"'or.?!,:ace standards liniTirtg emissions at such pollutants. Existing
asvj new sources of particu!ate matter emissions generally use control
techniques which reduce lead emissions as one component of participate
matter.
OTHER FEDERAL AGENCY REGULATIONS AND POSITIONS ON LEAD
The Occupational Safety and Health Administration proposed regulations
in 1975 to limit occupational exposure to lead to TOO yg Pb/m3, 8-hour
time weighted average. The exposure limit was based on protecting against
effects, clinical or subclinical, and the mild symptoms which may occur
below 80 yg Pb/dl, providing an adequate margin of safety. The level of
100 yg Pb/m3 is anticipated to limit blood lead levels in workers to a
mean of 40 yg Pb/dl and a maximum of 60 yg Pb/dl. OSHA is presently
reviewing the latest information on lead exposure and health effects in
preparation for promulgation of the workplace standard for lead.
The Department of Housing and Urban Development (HUD) has requirements
for reducing human exposure to lead through the prevention of lead
poisoning from ingestion of paint from buildings, especially residential
dwellings. Their activities include (1) prohibition of use of lead-based
paints on structures constructed or rehabilitated through Federal funding
i d on all HUD-associated housing; (2) notification of purchasers of HUD-
associated housing constructed prior to 1950 that such dwellings may contain
lead-based paint; and (3) research activities to develop improved methods
of detection and elimination of lead-based paint hazards.
The Consumer Product Safety Commission (CPSC) promulgated regulations
in September 1977 which ban 1) paint and other surface coating materials
containing more than 0.06 percent lead; 2) toys and other articles intended
for use by children bearing paint or other similar surface coating material
containing more than 0.06 percent lead; and 3) furniture coated with materials
containing more than 0.06 percent lead. These regulations are based on
33
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CPSC's conclusion that it is in the public interest to reduce the risk
of lead poisoning to young children from ingestion of paint and other
similar surface-coating materials.
The Food and Drug Administration adopted in 1974 a proposed
tolerance for lead of 0.3 ppm in evaporated milk and evaporated skim milk.
This tolerance is based on maintaining children's blood lead levels below
40 yg Pb/dl. FDA also has a proposed action level of 7 ng/ml for
Teachable lead in pottery and enamelware, although the exact contribution
of such exposure to total human dietary intake has not been established.
The Center for Disease Control concluded in 1975 that undue or
increased lead absorption exists when a child has confirmed blood lead
levels 30-70 vg Pb/dl or an EP elevation of 60-189 ^g Pb/dl except where
the elevated EP level is caused by iron deficiency. This guideline is
V
presently accepted by the scientific community but because of more recent
data is being reevaluated.
STATE AIR QUALITY STANDARDS
Four states currently have lead air quality standards - California,
Pennsylvania, Montana and Oregon. California has the lowest standard of
1.5 yg Pb/m , 30-day average, which is based on limiting the portion of
blood lead that is air derived to 5 percent if individual values are
held to 30 pg Pb/dl or less. California concludes that this standard is
consistent with restricting mean blood lead levels to less than 15 ug
Pb/dl. Pennsylvania based their standard of 5.0 v>g Pb/m3, 30-day average
on the health effects of absorbed lead and concluded that 50 ug/day of
lead can be safety absorbed from the air- Assiming a daily respiration
volume of 20 m and a 50 percent absorption rate, a maximum of 5 yg/m3 fs
34
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allowed in the air. Montana's standard of 5.0 pg Pb/m3, 30-day average,
was adopted as a goal based on Pennsylvania's experience. Oregon has a
standard of 3.0 yg Pb/m3,, 30-day average, which was based primarily on
health effects data with some consideration of economic implications.
THE FEDERAL REFERENCE METHOD
The Federal Reference Method for Lead describes the appropriate
techniques for determining the concentration of lead and its compounds
measured as elemental lead in ambient air. The method is based on
measuring the lead content of suspended particulate matter on glass
fiber filters using high volume sampling. The lead is then extracted
from the particulate matter using nitric acid with heat or ultrasonic
energy; finally, the lead content is measured by atomic absorption
spectrometry.
The method has received single laboratory evaluation using
samples of airborne particulates collected at a number of locations. In
addition, four other laboratories have conducted two abbreviated colla-
borative tests using particulate samples. All available precision and
"ccuracy information from these tests is included in the proposed method.
dditional methodological studies will be completed between this date
arid promulgation.
EPA does not anticipate changing the sampling method or analytical
principle involved but may amend the final Federal Reference Method
for Lead in any or all of the following weys:
35
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1. Removal of some inherent judgment processes left to the
individual analyst.
2. Inclusion of a third extraction procedure which uses aqua regia.
This perm-its the analyst to extract more metals than just lead
quantitatively thereby permitting him to analyze the same extract
for more than one metal.
3. Although the atomic absorption principle was selected as the
method of analysis, other analytical principles appear to be equally
applicable and are currently being evaluated. These methods are
fTameless atomic absorption, optical emission spectrontetry, and
anodic stripping voltametry. These analytical principles may be
included in the final method but probably will be handled via the
"equivalent method" route.
PUBLIC PARTICIPATION
All interested persons are invited to comment on all aspects of the
proposed standard and the Federal Reference Method. In particular,
data, views and arguments are solicited on the level of the standard,
and conclusions, assumptions, and calculations used by EPA in selecting
that level. Comments should be submitted in duplicate to: Mr. Joseph
Padgett, Strategies and Air Standards Division, MD-12, Research Triangle
Park, North Carolina 27711.
36
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The Agency proposes tc amend 40 CFR Part 50 by adding the following:
§50,12 National primary and secondary ambient air quality
standards for lead
The national ambient air quality standards for lead
and its compounds measured as elemental lead by a reference
method based on Appendix G to this part, or by an equivalent
method, are: 1.5 micrograms per cubic meter—monthly
arithmetic mean.
(Sections 109 and 301(a) of the Clean Air Act as Amended (42 U.S.C.
7409, 7601(a))).
37
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REFERENCES
Angle, C. R. and M. S. Mclntlre, Environmental controls and the decline
of blood lead. Arch. Environ. Hlth. (In press.) 1977.
Angle, C. R. and M. S, Mclntire. Lead in Air, Dustfall, Soil, Housedust,
Milk and Water: Correlation with Blood Lead of Urban and Suburban School
Children. _In_: Trace Substances in Environmental Health-VIII Proceedings
of the 8th Annual Conference on Trace Substances in Environmental Health.
Columbia. June 11, 1974.
Azar, A., R. D. Snee, and K. Habibi. An Epideirnologic Approach to
Conmunity Air Lead Exposure Using Personal Air Samplers. Environmental
Quality and Safety, Supplement Vol H - Lead 254-288 (1975).
Billick, I., A. Curran, and D. Shier. Presentation to the U.S. EPA
Lead Subcommittee of the Science Advisory Board, Washington, D.C.,
October 73 1977.
Fine., P. R., C. W. Thomas, R. H. Suho, R. E. Cohnberg, and B. A. Flashner.
r=>diatric Blood Lead Levels. A Study in 14 Illinois Cities of Intermediate
Population. JAMA 221:1475-1479, Sept. 25, 1372.
Goldsmith, J.R. Food chain and health implications of airborne lead.
U.S. Department of Commerce. NTTS PB-248745, 1974.
Griffen, T.B., F. Coulsten, H. Wills, J.C. Russell, and J. H. Knelson.
Clinical studies on men continuously exposed to airborne particulate
lead. Environ. Qua!. Suf., Suppl. 2_: 221-240, 1975.
38
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Hammer, D. S. et al. Trace Metals in Human Hair as a Simple Epidemiological
Monitor of Environmental Exposure. In: Trace Substances in Environmental
Health. Hemphills D. D. (ed) Columbia, Univ. of Missouri Press. 1973.
p. 25-38.
Johnson, D. E., J. B. Tillery, and R. J. Prevost. Levels of platinum,
palladium and lead in populations of Southern California. Environ.
Health Persp. 12:27-33, 1975.
Landrigan, P. J., S. H. Gehlbach, B. F. Rosenblum, J. M. Shoults, et al.
Epidemic Lead Absorption Near an Ore Smelter. The role of particulate
lead. New England J. Med. 2_92_:123-129, 1975.
Manton, W. I. Sources of Lead in Blood. Arch. Environmental Health,
32_: 149-156, 1977.
Piomelli, S., C. Seaman, D. Zullow, A. Curran» and B. Davidow. Metabolic
evidence of lead toxicity in "normal" urban children. Clin. Res. 25_:495A,
1977.
Rabinowitz, M. B. Lead contamination of the biosphere by human activity.
A stable isotope study. PhD Thesis, University of California, Los
Angeles, 1974. 120 pp.
Roels, H., J. P. Buchel, R. Lauwerys, G. Hubermont, P. Bruaux, F. Claeys-
Thoreau, A. La Fontaine, and J. Van Overschelde. Impact of air pollution
by lead on the heme biosynthetic pathway irr school-age children. Arch.
Environ. Health. 31:310-316, 1976.
39
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Sassa, 3., L, J. Granick, S, Granick, A. Kaopas, and R,, D, Levere,
Studies in lead poisoning, I, Microanalysis of erythrocyte proto-
porphyrin levels by spectrofluorometry in the detection of chronic
lead intoxication in the sub-clinical range. Biochem. Med. 8; 135-148,
1973.
von Lindern, I. and A, J. Yankel. Presentation to the Shoshone Heavy
Metals Project Committee by Idaho Department of Health and Welfare,
Boise, Idaho, Sept. 48 1975.
Worth, D., et si. Lead in drinking water, a public health problem with a
solution. J. Amer. Public Health Ass. In press.
Yankel, A. 0. and I. von Lindern. The Silver Valley lead study. The
relationship of childhood lead poisoning and environmental exposure,
J. Air Pollut, Cent. Ass., August, 1977.
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APPENDIX G
REFERENCE METHOD FOR THE DETERMINATION OF LEAD IN
SUSPENDED PARTICIPATE MATTER COLLECTED FROM AMBIENT AIR
1. Principle and Applicability
"LI Ambient air suspended participate matter is collected on a
glass-fiber filter for 24-hours using a high volume air sampler.
1.2 Lead in the participate matter is solubilized by extraction
with nitric acid (HNG.,), facilitated by heat or ultrasonication.
1.3 The lead content of the sample is analyzed by atomic absorption
spectrometry using an air-acetylene flame, the 283.3 or 217.0 nm lead absorption
line, and the optimum instrumental conditions recommended by the manufacturer.
2. Range, Sensitivity and Lower Detectable Limit
The values given below are typical of the methods capabilities. Absolute
values will vary for individual situations depending on the type of instrument
used, the lead line, and operating conditions.
2.1 Range. The typical range of the method is 0.03 to 7.5 \ig Pb/m
assuming an upper linear range of analysis of 15 uQ/ml and an air volume of
2400 T,3.
2.2 Analytical sensitivity. Typical sensitivities for a 1% change
in absorption (0.0044 absorbance units) are 0.2 and 0.5 ug Pb/ml for the 217.0
and 283.3 nm lines,, respectively.
41
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2.3 Lower Detectable Limit (LDL). A typical LDL is 0.03 ^g Pb/m .
This LDL is for the 217 nm line. The LDL for the 283.3 nm line will be somewhat
higher. The above value was calculated by doubling the between laboratory stan-
dard deviation obtained for the lowest measurable lead concentration in a colla-
15 3
borative test of the method. An air volume of 2400 m was assumed.
3. Interferences
Two types of interferences are possible: chemical, and light scattering.
3.1 Chemical. Reports on the absence 1»2»3»4»5 Of chemical inter-
ferences far outweigh those reporting their presences therefore, no
correction for chemical interferences is given here. If the analyst suspects
that the sample matrix is causing a chemical interference, the interference
can be verified and corrected for by carrying out the analysis using the method
of standard additions.
3.2 Light Scattering. Non-atomic absorption or light scattering,
produced by high concentrations of dissolved solids in the sample, can produce
2
a significant interference, especially at low lead concentrations. The
interference is greater at the 217.0 nm line than at the 283.3 nm line. No
interference was observed using the 283.3 nm line with a similar method.
Light scattering interferences can, however, be corrected for
instrumental!y. Since the dissolved solids can vary depending on the origin
of the sample, the correction may be necessary, especially when using the
217.0 nm line. Dual beam instruments with a continuum source give the most
accurate- correction. A less accurate correction can be obtained by using a.
non-absorbing lead line that is near the lead analytical line. Information on
use of these correction techniques can be obtained from instrument manufacturers
manuals.
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If instrumental correction Is not feasible, the interference
can be eliminated by use of the ammonium pyrrol ich"fiec3rbodi thioate-rnethyl isobutyl
ketone, chelation-solvent extraction technique of sample preparation.
4. Precision and Bias
4.1 The high-volume sampling procedure used to collect ambient air participate
matter has a between laboratory relative standard deviation of 3.7% over the
3 9
range 80 to 125 yg/m . The following equations give the precision of lead measure-
ments made on 3/4" x 8" strips cut from exposed glass fiber filters using the hot
extraction procedure.
x = 1.73 + 0.01C
y - 4.82 + 0.03C
where
x = within laboratory standard deviation, ug Pb/strip
y = between laboratory standard deviations yg Pb/strip
c = measured lead concentration, yg Pb/strip
Similar information is being obtained for the ultrasonic extraction procedure.
4.2 Single laboratory experiments indicate that there is no significant
difference in lead recovery between the hot and ultrasonic extraction procedures.
5. Apparatus
5.1 Sampling,
5.1.1 High volume sampler. Use and calibrate the sampler as described
in reference 10.
5,2 Analysis.
5.2.1 Atomic Absorption Spectrophotometer. Equipped with lead hollow
cathode or electrade!ess discharge lamp.
43
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5.2.1.1 Acetylene. The grade recommended by the instrument manufacturer
should be used. Change cylinder when pressure drops below 50-100 psig.
5.2.1.2 Air. Filtered to remove particulate, oil and water.
5.2.2 Glassware. Class A borosilicate glassware should be used
throughout the analysis.
5.2.2.1 Beakers. 30 and 150 ml. graduated, Pyrex.
5.2.2.2 Volumetric flasks. 100-ml.
5.2.2.3 Pipettes. To deliver SO, 30, 15, 8, 4, 2, 1 ml.
5.2.2.4 Cleaning. All glassware should be scrupulously cleaned. The
following procedure is suggested. Wash with-laboratory detergent, rinse, soak
for 4 hours in 20% (w/w) HNOj, rinse 3 times with distilled-deionized water,
and dry in a dust free manner.
5.2.3 Hot plate.
5.2.4 Ultrasonication water bath, unheated. Commercially available laboratory
ultrasonic cleaning baths of 450 watts or higher "cleaning power", i.e., actual
ultrasonic power output to the bath have been found satisfactory.
5.2.5 Template. To aid in sectioning the glass-fiber filter. See
Figure 1 for dimensions.
5.2.6 Pizza cutter. Thin wheel. Thickness -'< 1 mm.
5.2.7 Watch glass.
5.2.8 Polyethylene bottles. For storage of samples. Linear poly-
ethylene gives better storage stability than other polyethylenes and is preferred.
5.2.9 Parafilm "M".* American Can Company, Marathon Products, Nennah,
Wisconsin* or equivalent.
*Mention of commercial products does not imply endorsement by the Environmental
Protection Agency.
44
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6. Reacjents_
6.1 Sampling.,
6.1.1 Glass fiber filters. The specifications given below are intended
to aid the user in obtaining high quality filters with reproducible properties,
These specifications have been met by EPA contractors.
6.1.1.1 Lead content. The absolute lead content of filters is not critical,
but low values are, of course, desirable. EPA typically obtains filters with a
lead content of <75 pg/filter.
It is important that the variation in lead content from filter to
filter, within a given batch, be small.
6.1.1.2 Testing.
6.1.1.2.1 For large batches of filters ( a 500 filters) select at random
20 to 30 filters from a given batch. For small batches ( < 500 filters) a lesser
number of filters may be taken. Cut one 3/4" x 8" strip from each filter any-
where in the filter. Analyze all strips, separately, according to the directions
in Sections 7 and 8.
6.1.1.2.2 Calculate the total lead in each filter as
c n, , , 100 ml 12 strips
Fb= tig Pb/ml x j^j- x —-
where:
F,= Amount of lead per 72 square inches of filter,
6.1.1.2.3 Calculate the mean, F, , of the values and the relative standard
deviation (standard deviation/mean x 100)- If the relative standard deviation
is high enough so that, in the analysts opinion, subtraction of F"b, (Section 10.3)
rray result in a significant error in the ug Pb/m , the batch should be rejected.
6.1.T.2.4 For acceptable batches, use the value of Fb to correct all lead
analyses (Section 10.3) of particulate matter collected using that hatch of filters
If the analyses are below the LDL (Section 2.3) no correction is necessary.
45
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6.2 Analysis,
6.2.1 Concentrated (15.6 M_) HN03. ACS reagent grade HNO, and commer-
cially available redistilled HN03 has been found to have sufficiently low lead con-
centrations.
6.2.2 Distilled-deionized water. (D.I. water).
6.2.3 3 M_HN03. Add 192 ml of-concentrated HN03 to D.I. water in a
1 SL volumetric flask. Shake well, cool, and dilute to volume with D.I. water.
CAUTION: Nitric Acid Fumes Are Toxic. Prepare in a well ventilated fume hood.
6.2.4 0.45 M HN03- Add 29 ml of concentrated HN03 to D.I. water in
a U volumetric flask. Shake well, cool, and dilute to volume with D.I. water.
6.2.5 Lead Nitrate, Pb(N03)2. ACS reagent grade, purity 99.0%. Heat
for 4 hours at 120°C and cool in a desiccator.
6.3 Calibration standard.
6.3.1 Master standard, 1000 pg Pb/ml. Dissolve 1.598 g of Pb(N03)2
in 0.45 M^ HNO., contained in a 1 i volumetric flask and dilute to volume with
0.45 M_ HNCL. Store in a polyethylene bottle. Commercially available certified
lead standard solutions may also be used.
7. Procedure.
7.1 Sampling. Collect samples for 24 hours using the procedure described in
reference 10 with glass-fiber filters meeting the specifications in 6.1.1.
Transport collected samples to the laboratory taking care to minimize contamination
and loss of sample.
7.2 Sample Preparation.
7.2.1 Hot Extraction Procedure,
7.2.1.1 Cut a 3/4" x 8" strip from the exposed filter using a template and
a pizza cutter as described in Figures 1 and 2. Other cutting procedures may be used,
46
-------
Load in ambient participate matter collected OH glass fiber filters
has been shown to be uniformh distributed across the filter 1'3']1 suggesting that
the position of the strip is unimportant. However, other studies 12»"!7 have shown
that when sampling near a road-way lead is net uniformly distributed across the
filter. Therefore, when sampling near a road way, additional strips at different
positions within the filter should be analyzed.
7.2.1.2 Fold the strip in half twice and place in a 150-ml beaker. Add
15 ml of 3 M^ HNCL to cover the sample. The acid should completely cover the sample.
Cover the beaker with a watch glass.
7.2.L3 Place beaker on the hot-plate, contained in a fume hood, and boil gently
for 30 nrin. Do not let the sample evaporate to dryness. CAUTION: Nitric Acid
Fumes Are Toxic.
7.2.1.4 Remove beaker from hot plate and cool to near room temperature.
7.2.1.5 Quantitatively transfer the sample as follows:
7.2.1.5.1 Rinse watch glass and sides of beaker with D.I. water.
7.2.1.5.2 Decant extract and rinsings into a 100-ml volumetric flask.
7.2.1.5.3 Add D.I. water to 40 ml mark on beaker, cover with watch glass,
and set aside for a minimum of 30 minutes. This is a critical step and cannot
be omitted since it allows the HN03 trapped in the filter to diffuse into the
rinse v 'ter.
7.2.1.5.4 Decant the water from the filter into the volumetric flask.
7.2.1.5.5 Rinse filter and beaker twice with D.I. water and add rinsings
to volumetric flask until total volume is 80 to 85 ml.
7.2.1.5.6 Stopper flask and shake vigorously. Set aside for approximately
5 minutes or until foam has dissipated.
7.2.1.5.7 Bring solution to volume with D.I. water. Mix thoroughly.
47
-------
7.2.1.5.8 Allow solution to settle for one hour before proceeding with
analysis.
7.2.1.5.9 If sample is to be stored for subsequent analysis, transfer to
a linear polyethylene bottle.
7.2.2 Ultrasonic Extraction Procedure.
7.2.2.1 Cut a 3/4" x 8" strip, fold and place in a beaker as described in
Sections 7.2.1.1 and 7.2.1.2 except that a 30-ml beaker covered with Parafilm
is used instead of a 150-ml beaker covered with a watch glass. The Parafilm should
be placed over the beaker such that none of the Paraflim is in contact with water
in the ultrasonic bath. Otherwise, rinsing of the Parafilm (Section 7.2.2.3.1) may
contaminate the sample.
7.2.2.2 Place the beaker in the ultrasonication bath and operate for 30
minutes.
7.2.2.3 Quantitatively transfer the sample as follows:
7.2.2.3.1 Rinse Parafilm and sides of beaker with D.I. water.
7.2.2.3.2 Decant extract and rinsings into a 100-ml volumetric flask.
7.2.2.3.3 Add 20 ml D.I. water to cover the filter strip, cover with parafilm,
and set aside for a minimum of 30 minutes. This is a critical step and cannot be
omitted. The sample is then processed as in Sections 7.2.1.5.4 through 7.2.1.5.9.
NOTE: Samples prepared by either procedure are now in 0.45 M_ HNO,.
8. Analysis.
8.1 Set the wavelength of the monochromator at 283.3 or 217.0 nm. Set or
align other instrumental operating conditions as recommended by the manufacturer.
8.2 The sample can be analyzed directly from the volumetric flask, or an
appropriate amount of sample decanted into a sample analysis tube. In either case,
care should be taken not to disturb the settled solids.
43
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8.3 Aspirate samples, calibration standards and blanks (Section 9.2) into
the flame and record the equilibrium absorbance.
8.4 Determine the lead concentration in gg Pb/ml, from the calibration
curve, Section 9.3.
8.5 Samples that exceed the linear calibration range should be diluted with HNQ~
of the same concentration as the calibration standards and reanalyzed.
9. Calibration.
9.1 Working standard, 20 u9 Pb/ml. Prepare by diluting 2.0 ml of Master
standard (6.3.1) to 100 ml with 0.45 M_ HNOj. Prepare daily.
9.2 Calibration standards. Prepare daily by diluting the working standard
with 0.45 M_ HN03 as indicated below. Other concentrations may be used.
Volume of 20 yg/ml Final Concentration
Working Standard, ml Volume, ml yg Pb/ml
0 100 0.0
1.0 200 0.1
2.0 200 0.2
2.0 100 0.4
4.0 100 0.8
8.0 100 1.6
15.0 100 3.0
30.0 100 6.0
50.0 100 10.0
100 100 20.0
9.3 Preparation of calibration curve. Since the working range of analysis
will vary depending on which lead line is used and the type of instrument, no one
49
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set of instructions for preparation of a calibration curve can be given. Select
at least six standards (plus the reagent blank) to cover the linear absorption
range indicated by the instrument manufacturer. Measure the absorbance of the blank
and standards as in Section 8.0. Repeat until good agreement is obtained between
replicates. Plot absorbance (y-axis) versus concentration in pg Pb/ml (x-axis).
Draw (or compute) a straight line through the linear portion of the curve. Do not
force the calibration curve through zero.
To determine stability of the calibration curve, remeasure - alternately -
one of the following calibration standards for every 10th sample analyzed:
concentration < 1 pg Pb/ml; concentration < 10 pg Pb/ml. If either standard
deviates by more than 5% from the value predicted by the calibration curve,
recalibrate and repeat the previous 10 analyses.
10. Calculation.
10.1 Measured air volume. Calculate the measured air volume as
m ——* x T
where:
V = Air volume sampled (uncorrected), m
Q.J = Initial air flow rate, m /min.
2
Q.p = Final air flow rate, m /min.
T = Sampling Time, min.
The flow rates Q.. and Qf should be corrected to the temperature and pressure
conditions existing at the time of orifice calibration as directed in addendum B of
reference 10, before calculation of V
m"
50
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10.2 Air volume at STP. The measured air volume is corrected to reference
conditions of 750 mm Hg and 25'C as follows. The units are standard cubic meters,
sm .
VSTP = vmxVL^
1 X T2
VSTp = Sample volume, sm3, at 760 mm Hg and 298° K
Vm = Measured volume from 10.1
?2 ~ Atmospheric pressure at time of orifice
calibration, mm Hg
P-, = 760 mm Hg
Tp = Atmospheric temperature at time of orifice
calibration, °K
T1 = 298°K
10.3 Lead Concentration. Calculate lead concentration in the air sample.
r _ (u9 Pb/ml x 100 ml/strip x 12 strips/filter) - F.
w ~ U
VSTP
where:
C = Concentration, vg Pb/sm
ug Pb/ml = Lead concentration determined from Section 8
100 ml /strip = Total sample volume
Useable filter area, 7" x 9
- Exposed area of one stripj 3/4" x 7
" "
" "
T. = Lead concentration of blank filter, yg, from Section
6.1.1.2.3
V = Air volume from 10. 2
51
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1. Quality Control.
3/4" x 8" glass fiber filter strips containing 80 to 2000 yg Pb/strip
as lead salts) and blank strips with zero Pb content should be used to
ietermine if the method - as being used - has any bias. Quality control charts should
ie established to monitor differences between measured and true values. The frequency
if such checks will depend on the local quality control program.
To minimize the possibility of generating unreliable data, -the user should
'ollow practices established for assuring the quality of air pollution data,
ind take part in EPA's semi-annual audit program for lead analyses.
2. Trouble Shooting.
1. During extraction of lead by the hot extraction procedure, it is
mportant to keep the sample covered so that corrosion products - formed on
;ume hood surfaces which may contain lead - are not deposited in the extract.
2. The sample acid concentration of 0.45 M_ should minimize corrosion
if the nebulizer. However, different nebulizers may require lower acid '
oncentrations. Lower concentrations can be used provided samples and
tandards have the same acid concentration.
3. Ashing of particulate samples has been found, by EPA and contractor
aboratories, to be unnecessary in lead analyses by Atomic Absorption.
'herefore, this step was omitted from the method.
4. Filtration of extracted samples, to remove particulate matter, was
;pecifically excluded from sample preparation, because some analysts have observed
osses of lead due to filtration.
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13. References.
1. Scott, D. R. et al. Atomic Absorption and Optical Emission Analysis
of NASN Atmospheric Participate Samples for Lead. Envir. Sci. and
Tech. , JO., 877-880 (1976).
2. Skogerboe, R. K. et al. Monitoring for Lead in the Environment.
pp. 57-66, Department of Chemistry, Colorado State University,
Fort Collins, Colorado 80523. Submitted to National Science
Foundation for publication, 1976.
3. Zdrojewski, A. et al. The Accurate Measurement of Lead in Airborne
Particulates. Inter. J. Environ. Anal. Chem. , 2_, 63-77 (1972).
4. Slavin, W. Atomic Absorption Spectroscopy. Published by Inter-
science Company, New York, NY (1968).
5. Kirkbright, G. F., and Sargent, M. Atomic Absorption and Fluorescence
Spectroscopy. Published by Academic Press, New York, N.Y. 1974.
6. Burnham, C. D. et al. Determination of Lead in Airborne Particulates
in Chicago and Cook County, Illinois by Atomic Absorption Spectroscopy
Envir. Sci. and Tech. , 3_, 472-475 (1969)
7. Proposed Recommended Practices for Atomic Absorption Spectrometry.
ASTM Book of Standards, Part 30, pp. 1596-1608 (July 1973).
8. Koirttyohann, S. R., and Wen, J. W. Critical Study of the APCD-MIBK
Extraction System for Atomic Absorption. Anal. Chem. , 45, 1986-1989
(1973).
9. Collaborative Study of Reference Method for the Determination of
Suspended Particulates in the Atmosphere (High Volume Method).
Obtainable from National Technical Information Service, Department
of Conmerce, Port Royal Road, Springfield, Virginia 22151, as
PB-205-891.
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10. Reference Method for the Determination of Suspended Participates in
the Atmosphere (High Volume Method). Code of Federal Regulations, Title 40,
Part 50, Appendix B, pp. 12-16 (July 1, 1975).
11. Dubois, L., et al . The Metal Content of Urban Air. JAPCA, J_6_,
77-78 (1966).
12. EPA Report No. 600/4-77-034, June 1977. Los Angeles Catalyst Study
Symposium. Page 223.
13. Quality Assurance Handbook for Air Pollution Measurement Systems.
Volume 1 - Principles. EPA-600/9-76-005, March 1976.
14. Thompson, R. J. et al. Analysis of Selected Elements in Atmospheric
Particulate Matter by Atomic Absorption. Atomic Absorption Mews-
letter, 9_. No. 3, May-June 1970.
15. To be published. EPA, QAB, EX£L, RTP, N.C. 27711
16. To be published. EPA, QAB, EMSL, RTP, N.C. 27711
17. Hirschler, D. A. et al. Particulate Lead Compounds in Automobile
Exhaust Gas. Industrial and Engineering Chemistry, £9_, 1131-1142-
(1957).
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l\r V.iU A FILE F11J.BER TO PREVENT
ni in; FROM STICKING TO PLASTIC
RIGID PLASTIC
WIDTH OF
OHOOVF 1 cm ._
GLASS FIBER FILTER
FOLDED (LENGTHWISE) IN HALF
-WIDTH OF fiROOVE
fi mm
ALL GROOVES
2 mm DEEP
25mm (!") WIDE -
f i((ill f 1
-------
V.J I
a.
STRIPS FORV
OTHER ANALYSES
•%"x 8" STRIP FOR
LEAD ANALYSIS
Figure 2
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