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Attached question

This presents key attributes of solid and hazardous waste. There are laws that an environmental professional can use to determine if a waste is solid or hazardous. Key issues are addressed in the required unit resources concerning exposure to toxicity used in hazardous waste determination as well as the interplay between industry and regulators.

Now, consider this: You are an environmentalist presenting a continuing education seminar to environmental professionals, and you want to drive home several concerns on solid and hazardous waste. Create a PowerPoint presentation. Your presentation should address the following:

· key attributes of solid and hazardous waste,

· Resource Conservation and Recovery Act (RCRA) definitions,

· the role of risk assessment, and

· the interplay of industry interests versus regulatory protections.

Feel free to be creative. You are allowed to utilize PowerPoint’s features to create charts, graphics, and images. The notes section for your presentation is not required.

Your PowerPoint presentation must be at least 12 slides in length and will include a title slide and reference slide (title and reference slides do not count toward the minimum slide requirement). You must use a minimum of four references, two of which must be the two articles listed under Required Unit Resources. The other two references must be peer-reviewed sources from the CSU Online Library.

Attached question

Chemical Risk Assessment: Traditional vs Public
Health Perspectives

Preventing adverse health ef-

fects of environmental chemical

exposure is fundamental to pro-

tecting individual and public he-

alth. When done efficiently and

properly, chemical risk assess-

ment enables risk management

actions that minimize the in-

cidence and effects of environ-

mentally induced diseases related

to chemical exposure. However,

traditional chemical risk assess-

ment is faced with multiple chal-

lenges with respect to predicting

and preventing disease in human

populations, and epidemiological

studies increasingly report obser-

vations of adverse health effects

at exposure levels predicted

from animal studies to be safe

for humans. This discordance

reinforces concerns about the

adequacy of contemporary risk

assessment practices for pro-

tecting public health.

It is becoming clear that to

protect public health more effec-

tively, future risk assessments will

need to use the full range of

available data, draw on innovative

methods to integrate diverse data

streams, and consider health

endpoints that also reflect the

range of subtle effects and mor-

bidities observed in human pop-

ulations.

Considering these factors,

there is a need to reframe

chemical risk assessment to be

more clearly aligned with the

public health goal of minimizing

environmental exposures asso-

ciated with disease. (Am J Public

Health. 2017;107:1032–1039.

doi:10.2105/AJPH.2017.303771)

Maureen R. Gwinn, PhD, Daniel A. Axelrad, MPP, Tina Bahadori, ScD, David Bussard, BA, Wayne E.
Cascio, MD, Kacee Deener, MPH, David Dix, PhD, Russell S. Thomas, PhD, Robert J. Kavlock, PhD, and
Thomas A. Burke, PhD, MPH

See also Greenberg, p. 1020.

For the past several decades,human health risk assessment
has been a pillar of environmental
health protection. In general,
the products of risk assessment
have been numerical risk values
derived from animal toxicology
studies of observable effects at
high doses of individual chem-
icals. Although this approach has
contributed to our understanding
of overt health outcomes from
chemical exposures, it does not
always match our understanding
from epidemiology studies of the
consequences of real-world ex-
posures in human populations,
which are characterized by expo-
sure to multiple pollutants, often
chronically, at concentrations that
can fluctuate over wide ranges;
susceptible populations and life
stages; potential interactions be-
tween chemicals and nonchemical
stressors and background disease
states; and lifestyle factors that
modify exposures (e.g., airtight
houses).1 Theseandotherissuesare
particularly important when de-
termining risk of complex diseases,
such as cardiovascular disease.

Ten years ago, the National
Research Council offered a new
paradigm for evaluating the safety
of chemicals on the basis of
chemical characterization, testing
using a toxicity pathway ap-
proach, and modeling and ex-
trapolating the dose–response
relationship from in vitro testing,
all embedded in a risk context

and considering population-
based data and exposure.2 Efforts
such as the Tox21 Consortium3,4

and ToxCast program5 have
helped us better understand the
biological interactions of large
numbers of chemicals using
high-throughput assay systems,
and we are witnessing early
adoption of new technologies
and approaches for screening
chemicals for integrated testing.6

Several other factors are also
changing the way environmental
health professionals think about
chemical risks and how to most
effectively protect public health,
especiallyforcomplexdiseaseslike
cardiovascular disease. It is esti-
mated that intrinsic factors (e.g.,
those that result in mutations
stemming from random errors in
DNA replication) account for
only 10% to 30% of many com-
mon cancers.7 Similarly, only 30%
to 40% of birth defects can be
attributed to known causes such as
genetics, fetal alcohol syndrome,
maternal smoking, and folate in-
sufficiency.8 Other studies have
concluded that nongenetic envi-
ronmental factors and gene by

environment interactions are the
primary causes of chronic dis-
eases.9 The ability to evaluate and
quantifytheroleofenvironmental
factors on public health is a clear
opportunity, but it is limited by
thelack ofreadilyavailablemodels
for prominent clinical outcomes.

CURRENT
CHALLENGES

Understanding public health
risk from environmental chem-
ical exposures is complicated by
many factors, such as population
variability and susceptibility,
long latencies between critical
exposures and disease manifesta-
tions, and background environ-
mental exposures. Issues of
population variability and sus-
ceptibility are poorly understood
and difficult to characterize and
incorporate into risk assessments.
For example, a person’s unique
microbiome may modulate his or
her response to environmental
exposures.10,11 Although studies
are limited in this emerging area,
knowledge about the

ABOUT THE AUTHORS
At the time of the writing of this article, all of the authors were with the US Environmental
Protection Agency, Washington, DC.

Correspondence should be sent to Maureen R. Gwinn, PhD DABT ATS, Office of Research
and Development, US Environmental Protection Agency, 1300 Pennsylvania Ave NW, Ronald
Reagan Building, Room 41205, MC 8101R, Washington, DC 20460 (e-mail: gwinn.
maureen@epa.gov). Reprints can be ordered at http://www.ajph.org by clicking the “Reprints”
link.

This article was accepted March 2, 2017.
doi: 10.2105/AJPH.2017.303771

1032 Analytic Essay Peer Reviewed Gwinn et al. AJPH July 2017, Vol 107, No. 7

AJPH RISK ASSESSMENT

microbiome may inform inter-
individual variability and un-
explained susceptibility observed
in populations. Scientists have
begun to appreciate the role of
the microbiome in the lack of
reproducibility and in-
terpretability of animal studies.12

Another example is the effects
of early life environmental
exposures on health outcomes
later in life. Advances in the field
of epigenetics have revealed that
developmental exposure to
endocrine disrupting chemicals
can alter epigenetic program-
ming of gene regulation and thus
may play a role in the risk of
obesity later in life.13 Similar to
microbiome research, studies in
this area are limited, and a better
understanding of the link
between chemical exposure,
epigenetic gene regulation, and
health outcomes through epide-
miological research can help us

better address factors that are
currently difficult to account for
in traditional risk assessment.
Finally, there are also methodo-
logical challenges in determining
attributable risks in populations
with background environmental
exposures, as these background
exposures may change the
populationhealthbaselinesoraffect
the response of the target chemical.
Other examples of important fac-
tors to incorporate in risk assess-
ments can be found in Table 1.

OPPORTUNITIES FOR
USING MULTIPLE
DATA TYPES

Concurrent with these chal-
lenges, science and technology
are advancing rapidly and in ways
that create opportunities for risk
assessment. Public health

disciplines help us understand
how baseline health status can
influence the effect of
population-level chemical ex-
posures. We also need to consider
how environmental pollutants
may contribute to overall disease
burden for endpoints not tradi-
tionally considered in chemical
risk assessment (e.g., metabolic
disorders, autism). New
methods in epidemiological re-
search help us evaluate complex
interactions among multifacto-
rial causes of disease ranging
from macro (societal, neigh-
borhood) to micro (molecular)
factors, relevance of exposures
during sensitive life stages, and
a better understanding of in-
terrelatedness of disease across
the life span.14

Advances in high-throughput
technologies and computational
modeling (e.g., ToxCast, Tox21,
and ExpoCast efforts) are

providing data on hazard and
exposure potential for a large
number of data-poor chemicals.
The increased generation of data
for both hazard and exposure
from these advances can be used
to better understand the bi-
ological pathways that lead to
adverse health effects in ways that
were not possible in the past. But
linking these observations to
specific disease endpoints is
challenging because the trans-
lation of effects across levels of
biological organization is not well
understood. One approach with
the potential to advance our
understanding of how chemical
exposures can affect health is the
use of adverse outcome path-
ways, which integrate various
types of biological information to
link molecular initiating events
to downstream key events and
ultimately unwanted health
outcomes.15,16

TABLE 1—Examples of Current Risk Assessment Challenges and Opportunities

Risk Assessment Challenge Description Impact on Risk Assessment Public Health Opportunity

Molecular initiating events and subsequent

key events in adverse outcome pathways

Earlybiologicalchangesor precursoreffects

in response to chemical exposures may be

identified by in vitro, animal, or

epidemiological studies

Useful for qualitative and quantitative

understanding of ultimate health effect of

early biological changes

Improved public health protection without

need for long-term toxicology or

epidemiology studies

Background exposures Population exposures to a myriad of

environmental chemicals at low

concentrations

Exposures to background chemicals may

affect response to target chemical

exposures and may change population

health baselines

Increased public health protection if

baseline exposures are taken into account

when determining prevention strategies

Nonchemical stressors Physical and psychosocial stressors,

including noise, temperature,

socioeconomic status, social stress, and

limited resources

Impact on baseline susceptibility and

potential effect modification

Potential role in cumulative assessment,

improved identification of vulnerable

populations, potential target for public

health interventions (e.g., stress

management)

Early life determinants of health Biological characteristics and exposures

that can determine chronic and lifelong

health outcomes

Effect of exposures during early life may

play a role in later disease states (e.g.,

endocrine disruptors, epigenetic changes)

Potential for early life interventions for

prevention and management of later

disease

Baseline health status Individual health status, with a focus on

potential health susceptibilities

Baseline health status may affect response

to additional environmental chemical

exposures

Increased public health protection if

baseline health status is taken into

account

Microbiome Microorganisms that reside within and on

our bodies and interact with the

environment

Exposure modification, susceptibility and

resilience to environmental pollutants,

important as an early life determinant of

health

Potential targets for prevention and

intervention, management of allergic

responses, and precision risk management

AJPH RISK ASSESSMENT

July 2017, Vol 107, No. 7 AJPH Gwinn et al. Peer Reviewed Analytic Essay 1033

To fully realize the potential
of adverse outcome pathway–
based approaches and to in-
tegrate biological findings across
disciplines, we must strengthen
our ability to detect precursor
events in human populations
and to identify biologically rel-
evant exposure metrics, ideally
measurable in individuals. An-
other advancement that has
a great potential to advance our

understanding of data-poor che-
micals is the use of nontesting
approaches (e.g., quantitative
structure–activity relationship)
that allow us to predict toxicity
when adequate testing data are
absent—especially when we
combine knowledge of chemical
structural features and in vitro
bioactivity determinations. Ad-
vances in the development
of chemical libraries,

cheminformatics, and
read-across predictions and in-
tegration with molecular data
and adverse outcome pathways
have significantly improved
their application and predictive
capacity, which will allow more
comprehensive assessment of the
health effects of exposures.17,18

Effectively predicting
population risk by integrating
a variety of data streams (e.g.,

epidemiology, toxicology,
high-throughput testing) and
considering multiple sources and
pathways of exposure can better
inform environmental public
health decisions. Advances in
technology and computational
capabilities have fostered new
opportunities for generating and
analyzing molecular, animal, and
human data on effects and ex-
posures, which can be integrated

TABLE 2—Data Streams and Opportunities and Challenges for Informing Risk Assessment

Data Type Description Opportunity Challenge

Nontesting

data

Nontesting approaches, such as quantitative structure–

activity relationship models and read-across allow us

to predict toxicity when adequate testing data are

absent

Advances in the field have significantly improved

their application and predictive capacity

Developing principles for acceptance, for

characterizing and incorporating uncertainties into

predictions, and for developing objective metrics of

performance

Molecular Biochemical and cell-based bioactivity data and “omics-

based” data on thousands of chemicals

Can help inform our understanding of the health

outcomes of environmental exposures, using data

that are potentially more human relevant

Lack of scientific consensus on inferring hazard from

bioactivity in vitro assay and omics-based data and

providing quantitative dose–response information

on exposure metrics

Animal Traditional animal testing provides a hazard based

point of departure for risk assessments

Targeted animal testing can be performed on the

basis of the results of bioactivity data to focus on

key health outcomes

Potential uncertainties with using traditional animal

testing to estimate human risk (e.g., extrapolating

from animal to human or high to low doses and

accounting for human population variability and

life stage susceptibility)

Human Epidemiological and other human data support holistic

assessment of the effects of chemical exposures on

public health

Newer exposure science and statistical techniques

advance the understanding of human variability

that can be obtained from epidemiology and

individual sequencing; understanding effect

modification by nonchemical stressors and baseline

health status

Often limited mechanistic and dose–response data,

and exposure misclassification can bias results to

the null; possibility of unmeasured confounders

often undermines confidence in observed

associations, and it may require multiple studies

and many years to rule out chance, bias, and

confounding as possible explanations for observed

associations

Exposure Exposure characterization that captured the variability

in time, space, and within and across populations;

better toxicokinetic data link external to internal

dosimetry and relevant environmental exposure

concentrations with biological significance

Targeted and nontargeted biomonitoring,

application of sensors, and other new technologies

are greatly advancing population exposure

characterization; high-throughput exposure

models allow exposure predictions on thousands of

chemicals with associated uncertainty

Estimating and incorporating the inter- and

intraindividual variability in exposures into current

designs of toxicity testing and risk assessments;

extrapolating relevant target tissue and organ dose

information from external exposures and in vitro

assays; accounting for multiple exposures; sample

collection, data management, and analysis; and

covering or extrapolating to a broader chemical

space

Digital data The ongoing revolution in social media use and

communication has provided a new source of data

used in exposure science and environmental

epidemiology for local and timely information about

disease and health dynamics

A significant source of untapped data The collection and application of these data have

significant ethical implications that need to be

understood and managed, particularly taking

into account personal identifiable information;

methods to evaluate the quality of the data and

build confidence in the applications are needed

AJPH RISK ASSESSMENT

1034 Analytic Essay Peer Reviewed Gwinn et al. AJPH July 2017, Vol 107, No. 7

into chemical risk assessments.
At the same time, probabilistic
and high-throughput ap-
proaches for risk assessment have
been advancing. Table 2 high-
lights various data types available
and challenges in applying these
data types to inform risk
assessment.

A PUBLIC HEALTH
PERSPECTIVE

A public health perspective for
chemical risk assessment would
approach risk assessment from
a new lens. It would address
population health with a focus on
the health and societal burden of
disease; use and integrate all
available types of data—including
traditional toxicology, human
epidemiological findings, and

newer and emerging data
streams and information, such as
digital epidemiology,19 high-
throughput and high-content
data, and adverse outcome path-
ways; and draw on public health
approaches, such as attributable
risk or relative risk. This new
perspective may be especially
important for some historically
challenging aspects of risk assess-
ment, such as understanding
cumulative risks of exposures to
multiple chemical and non-
chemical stressors. Internationally,
scientists have raised concerns
about the large number of ubiq-
uitous chemicals people are
exposed to and called for re-
thinking approaches to evalu-
ating the health effects of
chemicals.16 Figure 1 presents
a conceptual model for a public
health perspective for risk
assessment.

Although approaching assess-
ments from the perspective of
health outcomes may be chal-
lenging, it provides the oppor-
tunity to evaluate exposures and
effects across the life span that are
relevant to population health.
Advances in science and tech-
nology, such as adverse outcome
pathway development, the
broader availability of chemical
and biological data, and the
applications of statistical and
bioinformatics tools, bring this
previously aspirational approach
well within reach.20

EXAMPLE:
CARDIOVASCULAR
DISEASE

A public health approach
may inform the challenge of

cardiovascular disease. Cardio-
vascular disease is the number 1
cause of mortality worldwide and
is a major US public health
burden.21,22 Annual costs of
cardiovascular disease in the
United States were estimated to
be $317 billion in 2011 and 2012,
considering direct medical costs
and lost productivity because of
premature mortality.22 This es-
timate is likely to substantially
underestimate the social cost
of cardiovascular disease
because of limitations in the es-
timation of indirect costs associ-
ated with morbidity and
premature mortality.23

Although much is known
about the biochemical and be-
havioral risk factors associated
with cardiovascular disease, par-
ticularly compared with other
diseases and health conditions,
the traditional risk factors fail to
account for 10% to 25% of its
prevalence.24 Environmental
factors, including air pollution25

and chemical exposures26 are
thought to contribute to the
unexplained fraction. Although
mortality stemming from car-
diovascular disease has decreased
over the past few decades in the
developed world as a result of
reductions in behavioral risk
factors, the rising prevalence of
obesity and diabetes might ac-
count for the deceleration in the
rate of improvement in annual
cardiovascular mortality in the
United States over the past
few years.27

There is an urgent need to
better understand the biological
pathways through which envi-
ronmental exposures to chemical
and nonchemical stressors act to
stimulate and accelerate athero-
sclerosis and promote adverse
cardiovascular health effects.
Applying the adverse outcome
pathway framework,28 the initial
molecular response to a chemical
exposure will often be receptor

Improved

public

health

Starting Point

• Adverse health outcome of

concern

Data Sources (along with those

used in traditional assessment)

• Clinical data on baseline

population health status

• Molecular epidemiology

• Exposure information in the

population

• Behavioral data

Synthesis

• Chemical/nonchemical

stressors contributing to the

adverse outcome

• Prevention strategies

Public Health Perspective

Starting Point

In context of a statutory authority

• Chemical or class of concern

• Route(s) of exposure

Data Sources

• Epidemiology studies

• Laboratory animal studies

• Mechanistic data

Synthesis

• Multiple health outcomes of

concern

• Toxicity values for specific

chemical/endpoint

• Output/risk metric: absolute

estimate of risk in population, or

safety assessment (e.g., hazard

index)

Traditional Risk Assessment

Note. This conceptual model illustrates how the starting point in a public health–focused risk assessment would differ from
that of traditional risk assessment. In traditional risk assessment, the starting point is focused on specific chemicals or
classes of chemicals of concern, with multiple data streams saying what the critical effects from that chemical are. A
public health perspective would focus on the adverse health outcome of concern with multiple data streams, informing
our understanding of hazard and exposure in the context of public health decisions related to that outcome and not
necessarily focused on just 1 chemical or class of chemicals.

FIGURE 1—Conceptual Model for a Public Health Perspective for Chemical Risk Assessment

AJPH RISK ASSESSMENT

July 2017, Vol 107, No. 7 AJPH Gwinn et al. Peer Reviewed Analytic Essay 1035

activation and changes in meta-
bolism and, ultimately, changes
in tissue and organ function. Such
changes can be modified by
both intrinsic (e.g., gender, age,
genetic, and epigenetic back-
ground) and extrinsic factors
(e.g., coexposures to other
chemical and nonchemical
stressors; Figure 2). Over time,
these changes produce subclinical
effects, such as changes in elec-
trical and mechanical cardiac
function, vascular function, and
nonobstructive atherosclerotic

vascular changes. With the per-
sistence of metabolic changes
that stimulate the progression of
vascular disease, clinical cardio-
vascular events such as heart at-
tacks, strokes, heart failure, and
abnormal heart rhythms follow.

To date, the most compre-
hensive application of this ap-
proach has been in the study of
population-level health effects
of air pollution exposure.28

Epidemiological data at the
population level has provided
support that air pollutant

exposure (e.g., ambient particular
matter and NO2) accelerates the
development and progression
of coronary atherosclerosis.25

Xenobiotic metals such as arse-
nic, cadmium, lead, and mer-
cury are also associated with
atherosclerosis.29 Gene–
environment interaction alters
the risk of vascular disease30; for
example, the residential proximity
to highways (representing ex-
posure to a mixture of traffic-
related air pollutants) is associated
with peripheral vascular disease,

which is modified by the gene
encoding bone morphogenic
protein.7,31

Because of the complexity of
the drivers of atherosclerosis,
a medical model treating blood
pressure and high cholesterol and
advising dietary modification and
exercise will be inadequate to
fully address this disease. Like-
wise, identifying the chemicals
that increase risk on an individual
basis will be inadequate to pre-
vent vascular disease. Instead an
integrated systems approach is

Atherosclerosis

As TCDD

BaP Phthalate

PCB PM2.5

Cd

PCBs

TCDD

InflammationPlaque Growth

Chemical

Exposures

z

Oxidative Stress

Adipokine

Dysregulation

Dyslipidemia

Insulin

Resistance

Hyperglycemia

Myocardial Infarction Stroke

As

Cd

PCB

TCDD

BPA

BaP

Endothelial

Dysfunction

As

Cd

BPA

PM2.5
PCBs

TCDD

DEHP

PFOS

As

Cd

PM2.5
TCDD

Phthalates
PCBs As

TCDD Cd

PFOS BPA

PM2.5

Age

Gender

Family

History

Diet

Smoking

Physical

Inactivity

Emotional

State

High BP

High LDL

Low HDL

Diabetes

Obesity

R
is

k
F

a
c

to
rs

f
o

r
A

th
e

ro
sc

le
ro

si
s,

C
a

rd
io

v
a

sc
u

la
r

D
is

e
a

se
, a

n
d

C
a

rd
io

v
a

sc
u

la
r

E
v

e
n

ts

Clinical

Intrinsic

Behavioral

A
d

v
e

rs
e

O
u

tc
o

m
e

P
a

th
w

a
y

(
A

O
P

)

Clinical
Events (AO)

Biochemical
and Physiologic
Responses (IKE)

Cellular
Response (IKE)

Environmental
Exposure

Subclinical
and

Clinical Responses
(IKE)

Molecular
Initiating Event

Public Health
Burden Mortality – Morbidity – Disability – Frailty

As PFOS

PCBs PM2.5

Individual Health
Burden

Source. Action of specific chemicals and metals adapted from Kirkley and Sargis.26

Note. As = Arsenic; AO = adverse outcome; BaP = benzo[a]pyrene; BPA = bisphenol A; Cd = Cadmium; DEHP = di(2-ethylhexyl) phthlate; DES = diethylstilbestrol; HDL = high-
density lipoprotein; IKE = intermediate key event; LDL = low-density lipoprotein; PCB = polychlorinated biphenyl; PFOS = perfluorooctane sulfonic acid; PM2.5 = particulate
matter £ 2.5 mm; TCDD = tetrachlorodibenzo-p-dioxin.This figure illustrates the biological pathway leading from exposure to adverse cardiovascular outcomes for a variety
of chemicals. On the left-hand side of the figure these pathways are linked to the adverse outcome pathway, and on the right-hand side of the figure we see the traditional
risk factors for adverse cardiovascular outcomes.

FIGURE 2—Adverse Outcome Pathway for Cardiovascular Outcomes

AJPH RISK ASSESSMENT

1036 Analytic Essay Peer Reviewed Gwinn et al. AJPH July 2017, Vol 107, No. 7

needed to fully account for all
known risk factors and formulate
the problem to define the most
effective strategy to decrease in-
dividual risk and societal burden.
Accomplishing this will require
clinical data that fully reflect
a population under consideration
as well as exposures to traditional
risk factors, biomonitoring data
documenting exposures to mul-
tiple chemicals, and molecular
responses from in vitro and
in vivo studies indicative of
the activation of biochemical
pathways that accelerate
atherosclerosis.

Although this approach might
not be practical currently, it is not
unrealistic to think about future
states where it could become
standard practice. Our proposed
innovative approach to chemical
risk assessment is occurring
contemporaneously during the
formative stages of the National
Institutes of Health–sponsored
Precision Medicine Initiative,
which will drive integration of
genomics, data sciences, and
bioinformatics as the basis for
improved individual health care,
disease prevention, and public
health. The Affordable Care
Act has accelerated electronic
medical record adoption in
health care practices and hospital
systems, potentially offering
a valuable source of information
for population-level health
monitoring. Recent research has
used big data to study the early
stages of disease and better classify
and predict disease progression
and could be used to inform
personalized medicine to
optimize wellness in healthy
populations.32–34

Moreover, the anticipated
integration and development of
technologies and analytical tools
have the potential to improve
public health and increase the
spatial and temporal resolution of
environmental health

surveillance. The establishment
of a long-term representative
precision medicine cohort, if
integrated with the proposed
National Biomonitoring Net-
work,35 could have enormous
benefit in helping us understand
the relationship between chem-
ical exposures and disease and
in managing some of the most
challenging clinical problems
more effectively.

Applying this framework
would potentially expand our
understanding of the origins of
vascular disease and its progres-
sion, helping define strategies
for primary prevention to thwart
the initiation of the process we
ultimately call atherosclerosis.
Thus, such a framework would
provide new and ongoing
insights into the associations
between environmental expo-
sures that contribute the greatest
burden to public health. This
approach would facilitate ac-
counting for sensitive pop-
ulations and could inform
suggested individual health or
behavioral measures in which
there have been past exposures
or in which current exposure
cannot be reduced enough to
protect those most at risk.

CONCLUSIONS
The proposed conceptual

model is grounded in public
health principles and focused on
identifying the greatest oppor-
tunity to reduce environmental
exposures to improve health
outcomes. Along with traditional
risk assessment, this perspective
can better inform public health
decision-making. Although
there are clear benefits to
operating within a public health–
focused framework and moving
away from individual chemicals
and apical endpoints, there are
also challenges.

Informing Decision-
Making

Since the 1980s, the Envi-
ronmental Protection Agency’s
decision-making has been
grounded on traditional risk as-
sessments that are conducted
within the constraints of the
Environmental Protection
Agency’s statutes and programs.
Although program-targeted risk
assessments will remain an im-
portant component, the disease-
based approach draws on
information in a holistic fashion
that cuts across organizational and
legal boundaries, integrating
traditional inputs and newe

Attached question

AJPH HISTORY

September 2017, Vol 107, No. 9 AJPH Rosner and Markowitz Peer Reviewed Public Health Then and Now 1395

“Ain’t Necessarily So!”: The Brake Industry’s Impact
on Asbestos Regulation in the 1970s
David Rosner, PhD, MPH, and Gerald Markowitz, PhD

Canada is proposing a ban on asbestos, and the US Environmental Protection Agency has listed it

among the first 10 materials it is investigating under the new Toxic Substances Control Act revisions.

However, this effort is currently running up against enormous industry and political opposition.

Here, we detail the activities in the early 1970s of the Friction Materials Standards Institute, an

industry trade association, to stifle earlier attempts to regulate asbestos use in brake linings, one

of the oldest and most obvious sources of asbestos exposure to mechanics, among others. (Am J

Public Health. 2017: 1395–1399. doi: 10.2105/AJPH.2017.303901)

At the end of 2016, the US Environmental Protec-
tion Agency (EPA) proposed

asbestos, the cause of fi brotic

lung disease and cancer, as one

of the 10 industrial chemi-

cals to be evaluated under the

newly revised Toxic Substances

Control Act.1 Under the new

act, a risk evaluation of asbestos

is to be completed within three

years and, if asbestos is found

to be an “unreasonable risk to

humans and the environment,”

the EPA is required to mitigate

that risk, possibly through a

ban, within two more years.2

By 1970, asbestos was used

in some 3000 products, such as

roof shingles, fl oor tiles, house

siding, ironing boards, and

particularly in brakes, among

other consumer items. Today, this

carcinogenic material is banned

in the United States in a few

products, including corrugated

paper and fl ooring felt, but it is

still legal in brakes and clutches

and a host of construction and

industrial materials, such as vinyl

fl oor tile, roofi ng materials, and

cement pipe, among others.

Consequently, it is in millions of

homes, gas stations, and repair

shops across the country.3

Historians have documented

one major reason for the

delay in banning this known

carcinogen: private industry

trade groups stifl ed earlier eff orts

at regulation.4 Here, we look at

the specifi c eff orts of one such

group, the Friction Materials

Standards Institute (FMSI),

to forestall the regulation of

asbestos used in brakes and

clutches, one of the oldest

sources of asbestos exposure.

We examine the industry’s

reaction to the newly created

Occupational Safety and Health

Administration’s (OSHA)

dramatic reduction of the

Permissible Exposure Limit

(PEL) in the early 1970s. There

is a literature that addresses

the current medical and

epidemiological evidence of the

dangers from asbestos brakes.5

Here, however, using internal

corporate documents, most of

which have not been previously

reviewed but are now available

at https://toxicdocs.org,6 we

explore what the industry

understood about the dangers to

mechanics from asbestos.

The concern about asbestos

in brakes refl ects the broader

acknowledgment of the impact

of industrial toxins on workers

and consumers in the 20th

century.7 In the early 1930s,

E. R. A. Merewether identifi ed

the dust produced by “the

sawing, grinding and turning

in the dry state of articles

composed wholly or partly

of asbestos such as motor car

brake and clutch linings” when

inhaled as a cause of asbestosis,

the fi brotic condition that slowly

strangles aff ected workers.8

Merewether’s early observation

that any material that contained

asbestos could prove to be a

hazard was affi rmed in the

immediate postwar period, as

offi cials noted that “asbestos

has been incorporated into

… protective clothing, brake

linings, cements, … and other

forms of insulation” and that

exposure to asbestos dust caused

by “the breakdown of the native

mineral” was also associated with

cancer of the lung.9 By the mid-

1960s, asbestos was associated

with asbestosis, lung cancer,

and mesothelioma, a cancer

of the lining of the lung and

abdominal cavity, leading the

British Ford Motor Company

to host a conference in 1969 on

the possible dangers presented

to brake mechanics and those

installing or replacing brake

linings.10

In 1970, the Occupational

Safety and Health Act,

establishing OSHA and

the National Institute of

Occupational Safety and

Health (NIOSH), was passed.11

Almost immediately, the FMSI

established an Asbestos Study

Committee (ASC), which

focused on the possible impact

of OSHA regulations on brake

and clutch manufacturers.

Working with the Asbestos

AJPH September 2017, Vol 107, No. 9

AJPH HISTORY

1396 Public Health Then and Now Peer Reviewed Rosner and Markowitz

Information Association of

North America (AIA), another

trade association, it sought to

forestall any drastic regulation.12

Among the ASC’s fi rst acts was

to meet with OSHA offi cials

who had issued an emergency

PEL of 12 fi bers per cubic

centimeter in 1971 and, a year

later, reduced it further to 5

fi bers per cubic centimeter, with

an even greater reduction to 2

fi bers per cubic centimeter by

1976.13

ACKNOWLEDGING
DANGER PRIVATELY

The FMSI was aware of why

OSHA was considering this

reduction. At its meeting in June

1972, the ASC received a report

that Rohl and colleagues had

presented a paper at a meeting of

the American Industrial Hygiene

Association, which was held at

Mt Sinai School of Medicine

in New York City. According to

the ASC, the paper revealed that

“the dust concentrations during

the blowing off of brakes are in

excess of the fi ve fi bers per cc

[cubic centimeter] allowance.”14

They acknowledged that

exposure to asbestos dust was a

possibility, if not a probability, for

workers installing and replacing

brakes.15

This raised the question

for the ASC as to whether

the manufacturers, under the

new OSHA regulations, had

an obligation to warn workers

of dangers they potentially

faced.16 Hence, a new rationale

for not warning was developed:

they publically pronounced

that asbestos, when “locked

in” to fabrics, lacquers, plastics,

or other fi nished products,

was not a danger as it could

not be released into the

air.17 In private, however, the

committee members noted

that because their products

were friction materials, there

was an inherent danger in the

“handling [by employees] of

the products with supposedly

locked-in asbestos during …

drilling, grinding, inspection and

boxing.” Furthermore, there was

the potential for the release of

asbestos during “the handling of

the brake lining or clutch facing

by the customer” even far from

the shop fl oor. One member

of the ASC suggested that “a

notifi cation be put in boxes in

brake linings or clutch facings,”

but this was quickly shot down

when another member objected

because “he felt it was another

‘red fl ag’ that would bring more

harm to the industry than the

alleged good that would come

from enclosing such notices.”18

Despite public assurances

that using “locked-in” asbestos

was safe, E. W. Drislane, the

executive director of the FMSI,

wrote to the ASC about an

internal survey that revealed “the

problem [that] in many cases

subsequent operations will be

performed—cutting, grooving,

drilling and grinding [and that]

these subsequent operations

can produce concentrations of

asbestos fi bers in excess of the

current exposure limits.”19 “Most

members of the Committee”

believed that the OSHA

standard was “exceeded in many

areas such as inspection, drilling,

and grinding where there is

not adequate dust collection

machinery.”20

AIN’T NECESSARILY SO
In mid-1973, “Ike” Weaver,

an engineer with the Raybestos–

Manhattan Corporation

and chair of the ASC, gave a

major address to the entire

membership that provides a

summary of what the industry

understood about the dangers

of asbestos. He informed them

about the recent meeting of

the International Agency for

Research on Cancer at which

“the most important item

[was] the incrimination of all

major types of asbestos as causal

agents of carcinoma, particularly

mesothelioma.” He further

warned that “since most of us

[in the FMSI] use substantial

amounts of chrysotile asbestos in

our formulations association of

this material with mesothelioma

and other types of cancer is of

serious concern.”21

For an industry that

identifi ed friction as the primary

characteristic of its products,

he knew “of no way any of us

can be absolutely sure that his

friction products, regardless

of whether they are sold as

original equipment or on the

replacement market, …[would

not] result in excessive exposure

“Look What Makes the Disc Brake
Brake.” From the 1930s on, sawing,
cutting, sanding, or abrading asbestos-
containing products in any way was
identified as a major concern. Here, we
see an “asbestos-based” Johns–Manville
disk brake ad from the 1960s with no
mention of any potential danger.

September 2017, Vol 107, No. 9 AJPH Rosner and Markowitz Peer Reviewed Public Health Then and Now 1397

AJPH HISTORY

of workers or bystanders to

airborne asbestos fi bre.” He

was “appalled to learn … of

instances where this problem has

occurred.”22

He objected to those in

his industry who argued that

most workers were exposed

only “relatively intermittently”

to respirable asbestos dust: “I

say emphatically this just ain’t

necessarily so!” Not only did

“large volume replacement

users [perhaps chains such as

Midas and Meineke] present

major potential hazards,” but

“even small job shops can

needlessly expose people to

high fi bre concentrations if

operations are performed

without controls.” There was

the risk for dread disease

even when exposures were

minimal or of short duration.23

“To me,” Weaver concluded,

“labelling all containers or

packagers of asbestos-containing

friction material is the very

least the industry can do to

fulfi ll its moral obligation to

its customers, their employees

and the public and at the

same time conform with

minimum requirements of the

Occupational Safety and Health

Act.”24

Further evidence about the

potential dangers to mechanics,

including cancer, was provided

with the publication of the Rohl

paper on New York City garages

that the ASC had heard about

before. The ASC acknowledged

that “some of the housekeeping

conditions in these shops

[were] deplorable.” And they

acknowledged that conditions

in New York were “perhaps

no worse than in other shops

throughout the country.”25

COLLAPSING DEFENSES
By the mid-1970s, the FMSI

had learned that both national

and international experts,

NIOSH, the International Labor

Organization, the International

Agency for Research on Cancer,

and other researchers agreed that

the PEL was irrelevant to the

question of cancer.26 In addition,

one of the leading fi gures in

industrial medicine and the

leading asbestos researcher,

Irving Selikoff , echoed these

ideas, writing that the “only safe

concentration is zero fi ber per

cc.”27

In April 1975, as the date

for the proposed reduction of

the PEL to 2 fi bers per cubic

centimeter approached, the FMSI

faced a dilemma. They claimed

they were already “having dif-

fi culty meeting the 5 fi bers/cc

limit,” and worried that “it would

be near impossible to meet the

2 fi bers/cc limit due July 1,

1976.” Some on the ASC “sug-

gested that the industry should

oppose this change,”28 and Guy

Gabriellson, vice president of the

Asbestos Information Association,

said that the industry should

simply reject OSHA’s and

NIOSH’s position.29

GROWING PRESSURE,
GROWING EVIDENCE

The situation was becoming

dire for the FMSI as they

faced growing pressure to

acknowledge that there was

no exposure below which

workers could be protected

from asbestos-induced cancers.

The pressure came from

NIOSH, the International

Labor Organization, and others.

Selikoff predicted an “epidemic

of asbestos related death and

disease in years to come.”

The FMSI Board of Directors

was alarmed by the growing

consensus that “no known dose

level [of asbestos exposure was]

‘safe.’ ” Furthermore, Selikoff

and his colleagues were “actively

promoting” the view that the

hazards were “associated with

asbestos emissions”—specifi cally

to mechanics—“from brake

lining wear and from brake

service operations.”30

The pressures became even

greater in July 1975, after

NIOSH called a meeting in

Washington of an automobile

company, union representatives,

the major asbestos companies,

researchers, and a trade

association representative.31

They learned that the medical

literature “revealed at least

four cases of these rare tumors

[mesotheliomas] in persons who

were employed in jobs involving

automobile brake servicing.”32

The liability dimensions of the

problem facing the industry

were frightening: “It has been

reported that approximately

900,000 persons are employed

in such work in the United

This ad from Raybestos-Manhattan
emphasizes the “safety” of the asbestos
brakes, despite the fact that by this
point, it was clear that exposure to
asbestos dust could cause cancer.

AJPH September 2017, Vol 107, No. 9

AJPH HISTORY

1398 Public Health Then and Now Peer Reviewed Rosner and Markowitz

States. It is recommended that

stringent industrial hygiene

measure to control exposure

be implemented as rapidly as

possible.”33 In a separate article,

the industry learned that “during

brake-lining maintenance and

repair, workmen in garages,

service stations and brake repair

shops are exposed to asbestos

and thus may be subject to

serious cancer risk. Others, at

some distance from the repair

work, are perhaps subject to the

same hazard.”34

RESISTANCE RAMPS UP
At the same time that these

articles were being published,

OSHA proposed to reduce the

asbestos standard even lower,

which the FMSI described

as a “drastic reduction.”35

The ASC began to mobilize

committee members and the

general membership of the

FMSI to oppose OSHA’s

recommendation that the PEL

be reduced to 0.5 fi bers per

cubic centimeter instead of the

2 fi bers per cubic centimeter

standard that was scheduled to

go into eff ect July 1, 1976. In

June, they proposed a three-part

strategy. First, they intended

to educate their membership

on how to comply with the

2-fi bers per cubic centimeter

standard to go into eff ect in the

following month and further to

recognize “the impact that will

be required to cope with the

0.5 fi bre standard, should it be

imposed.” Second, they planned

to oppose the more stringent

standard with “every possible

means at our disposal,” and “to

enlighten government offi cials

of what informed members

within our industry regard as the

complete impracticality of the

[proposed] 0.5 standard.” Finally,

they planned on “cooperating

with the Asbestos Information

Association and the Institute

Offi ce in their response to

OSHA on the revised standard,”

an eff ort they believed had

already borne fruit.36 In the

end, the standard would not

be reduced until the mid-

1980s,37 and they congratulated

themselves and the AIA on

forestalling the reduction of the

standard. The FMSI thanked the

AIA for “the outstanding job

[they did] in rebutting some of

the reasons for OSHA’s stringent

proposals.”38 The committee

bragged that “we have been told

that our eff orts … have been

effi cacious.”39

The infl uence of the asbestos

industry can be observed

directly by comparing the

warnings the FMSI and AIA

recommended for gas stations

and auto repair shops with those

of the government. NIOSH in

1976 suggested that a sign be

posted at the entrance to the

work area of these garages that

specifi cally warned: “Asbestos;

Dust Hazard; Avoid Breathing

Dust; Wear Assigned Protective

Equipment; Do Not Remain

in Area Unless your Work

Requires it; Breathing Asbestos

Dust May Cause Asbestosis and

Cancer.”40 The FMSI and the

AIA adopted similar wording,

with one crucial diff erence:

they did not use the word

“cancer.” Instead, they adopted

OSHA’s wording from the 1972

standard:41 “Breathing Asbestos

Dust May be Hazardous to Your

Health.”42 As a result of the

FMSI and AIA’s opposition, the

lowering of OSHA’s PEL was

signifi cantly delayed. In addition,

they trivialized the dangers to

workers by not including cancer

in their warnings. As a result,

they belittled and undercut the

warnings of NIOSH, Irving

Selikoff , and many other

scientists that workers were

putting their lives at risk by

working with products made

with asbestos.

For policymakers, it is

important to understand the

tragic history we relate here. It

took 45 years of work on the

part of physicians, laboratory

scientists, regulators, and citizens

to achieve these monumental

victories for public health, but

all of this work can be undone

if the current administration in

Washington follows through

on its threats to undercut the

EPA and other federal agencies.

There are few materials in the

modern environment that are

documented to be as hazardous

as asbestos. It would be tragic if

all this work was to be undone

by new lobbying eff orts aimed

at a new administration and

EPA administrator particularly

receptive to industry’s siren call

to deregulate.43

ABOUT THE AUTHORS
David Rosner is with the Center for the

History and Ethics of Public Health,

Department of Sociomedical Sciences,

Mailman School of Public Health, and the

Department of History, Columbia University,

New York, NY. Gerald Markowitz is with the

Department of Interdisciplinary Studies, John

Jay College, and the Department of History,

Graduate Center, both of the City University

of New York, New York, NY.

Correspondence should be sent to David

Rosner, Center for the History and Ethics of

Public Health, Department of Sociomedical

Sciences, Columbia University, Mailman

School of Public Health, 722 West 168th St,

Room 934, New York, NY 10032 (e-mail:

dr289@columbia.edu). Reprints can be

ordered at http://www.ajph.org by clicking the

“Reprints” link.

This article was accepted May 4, 2017.

doi: 10.2105/AJPH.2017.303901

CONTRIBUTORS
The authors contributed equally to the

research, writing, and conceptualization

of this article.

ACKNOWLEDGMENTS
We acknowledge that many of the

primary source documents were gathered

in the process of litigation regarding

asbestos-related diseases. These documents

are available online at http://www.

toxicdocs.org, a Web site of corporate

memos, letters, reports, and other articles

developed through the cooperative eff orts

of the Center for the History and Ethics

of Public Health, Columbia University

and the City University of New York.

We have appeared as expert witnesses on

behalf of plaintiff s in asbestos lawsuits.

ENDNOTES
1. This revision is now known as the

Frank R. Lautenberg Chemical Safety

for the 21st Century Act.

2. Environmental Protection Agency,

“News Releases From Headquarters:

EPA Names First Chemicals for Re-

view Under New TSCA Legislation;

Agency Answers Call to Move For-

ward on Chemical Reform, Naming

Asbestos Among the First to Undergo

Risk Evaluation,” November 11, 2016.

https://www.epa.gov/newsreleases/

epa-names-first-chemicals-review-under-

new-tsca-legislation (accessed December

29, 2016).

3. Environmental Protection Agency,

“US Federal Bans on Asbestos.” https://

www.epa.gov/asbestos/us-federal-bans-

asbestos#main-content (accessed Decem-

ber 29, 2016). See also Kathleen Ruff,

“Asbestos Lobby Launches Attack to

Undermine Upcoming UN Conference

on Trade in Hazardous Substances.”

Asbestos lobby launches attack to undermine upcoming UN Conference on trade in hazardous substances

(accessed April 17, 2017).

4. See, for example, Barry Castleman,

Asbestos: Medical and Legal Aspects, 3rd

edition (Englewood, NJ: Prentice

Hall, 1990); Gerald Markowitz and

David Rosner, “ ‘Unleashed Upon an

Unsuspecting World’: The Asbestos

Information Association and Its Role

in Perpetuating a National Epidemic,”

American Journal of Public Health 106, no.

5 (2016): 834–840.

5. See Castleman, Asbestos, pp 443–479,

for one of the first reviews of the

existing scientific evidence of the dangers

of asbestos in brake linings.

6. These documents are available on the

Web site https://www.toxicdocs.org, a

collection of nearly 6 000 000 corporate

memos, studies, letters, and notes

gathered through a variety of law suits

over toxic materials.

7. David Rosner and Gerald Markowitz,

“A ‘Gift of God’? The Public Health

Controversy Over Leaded Gasoline

During the 1920s,” American Journal of

Public Health 75, no. 4 (1985): 344–352;

William Graebner, “Hegemony Through

Science: Information Engineering and

Lead Toxicology, 1925–1965,” in

David Rosner and Gerald Markowitz,

eds, Dying for Work: Workers’ Safety

and Health in Twentieth Century

America (Bloomington, IN: Indiana

University Press, 1987), 140–159;

David Egilman and Marion Billings,

“Abuse of Epidemiology: Automobile

Manufacturers Manufacture a Defense

to Asbestos Liability,” International

Journal of Occupational and Environmental

September 2017, Vol 107, No. 9 AJPH Rosner and Markowitz Peer Reviewed Public Health Then and Now 1399

AJPH HISTORY

16. Title 29, Labor, Chapter XVII—

Occupational Safety and Health

Administration, Department of Labor,

Part 1910—Occupational Safety

and Health Standards, “Standard for

Exposure to Asbestos Dust,” Federal

Register 37 (1972): 11321: “Caution

Labels shall be affixed to all raw

materials, mixtures, scrap, waste, debris,

and other products containing asbestos

fibers or to their containers, except that

no label is required where asbestos fibers

have been modified by a bonding agent,

coating, binder, or other material so

that during any reasonably foreseeable

use, handling, storage, disposal,

processing, or transportation, no airborne

concentrations of asbestos fibers in

excess of the exposure limits prescribed

in paragraph (b) of this section will be

released.”

17. Ibid, p. 11319: “Employers in

general strongly contend that finished

products that effectively entrap asbestos

fibers, so that these would not be released

in the normal use of the products, should

not be required to be labelled.”

18. FMSI, Asbestos Study Committee,

“Minutes,” August 17, 1972.

19. E. W. Drislane to Asbestos Study

Committee, “Interpretation of OSHA

Labelling Requirements,” November

6, 1972.

20. FMSI, Asbestos Study Committee,

“Minutes,” February 16, 1973.

21. FMSI, Annual Meeting, “Minutes,”

June 27–28, 1973. Weaver noted that

“risk is greatest with crocidolite, less

with amosite and apparently still less

with chrysotile.”

22. FMSI, Annual Meeting, “Minutes,”

June 27–28, 1973.

23. Ibid.

24. Ibid.

25. FMSI, Asbestos Study Committee,

“Minutes,” June 14, 1974.

26. The International Labor

Organization’s “Meeting of Experts on

Safe Use of Asbestos” stated that “the

2 fibres/ml standard should be regarded

as an interim concentration related to

fibrogenic effects and not to carcinogenic

effects, for which no standards exist at

the present time.” See Report of

International Labor Organization,

“Meeting of Experts on Safe Use of

Asbestos,” in Geneva, December 11–18,

1973, in “Asbestos Study Committee

Report,” June 1974, attached to Minutes

of Annual Meeting, June 18–19, 1975.

27. FMSI Board of Directors,

“Minutes,” June 25, 1974.

28. See also FMSI, Asbestos Study

Committee, “Minutes,” April 28, 1975.

29. See: Gerald Markowitz and David

Rosner, “Unleashed on an Unsuspecting

World,”: The Asbestos Information

Association and Its Role in Perpetuating

a National Epidemic,” AJPH, 106(May,

2016), p.838.

30. FMSI, Board of Directors, “Minutes,”

June 17, 1975; “Asbestos Study Commit-

tee Report,” June 1975.

31. Department of Health, Education

and Welfare, CDC, NIOSH, “Minutes

of Occupational Exposures to Asbestos

Dust From Brake Linings Meeting,” July

21, 1973.

32. Department of Health, Education

and Welfare, CDC, NIOSH, “Minutes

of Occupational Exposures to Asbestos

Dust From Brake Linings Meeting,”

July 21, 1973. See also J. W. Lloyd,

NIOSH, to “Dear Colleague,”

“Current Intelligence Bulleting 5:

Asbestos Exposure During Servicing

of Motor Vehicle Brake and Clutch

Assemblies,” DHHS (NIOSH),

Publication No. 78-127, August 8,

1975 (in FMSI file). At the meeting, Dr

George Wright, representing the Johns

Manville Corporation, “emphasized that

manufacturers have a responsibility to

ascertain what happens to their products

after being sold to others.” He was not

surprised about “the [high] fiber counts

reported” and expressed the belief that

one might subsequently encounter the

full spectrum of asbestos-related disease

among grinders.

33. Arthur N. Rohl, Arthur M. Langer,

Mary S. Wolff, and Irving Weisman,

“Asbestos Exposure During Brake

Lining Maintenance and Repair,” Envi-

ronmental Research 12 (1976): 110–128.

In this article, the authors describe the

work practices in repair shops and the

attendant hazards: “When a vehicle is

brought into a repair shop for brake

lining inspection or replacement, the

wheel is removed and loose dust is

removed from the drums and back plates,

generally by means of a compressed

air jet. … The cloud of dust that is

produced is visible for several minutes

afterwards. Table 3 shows that fiber

concentrations are high in the operator’s

area under these conditions (an average

concentration of 16 fibers/ml), and that

there are significant concentrations at

least 20 ft away. … It is evident that any

person 65–75 ft away can be exposed”

(p. 118). “It was generally found that

there was minimal, if any, effort to control

dust in most garages. Workmen do not

use respiratory protection. There was

little awareness of the potential hazard

of brake dust” (pp. 117–118).

34. Arthur N. Rohl, “Asbestos Exposure

During Brake Lining Maintenance

Repair,” ca. January 1976, enclosed in

Selikoff to Drislane, January 14, 1976.

Rohl says in a handwritten note, “Dr.

Selikoff has asked me to send you the

results of our asbestos fiber counts

during brake repair work.” (This reference

is to the early draft of paper published

in mid-1976).

35. Asbestos Study Committee, FMSI,

“Minutes of Annual Meeting,” June

16–17, 1976.

36. “Asbe

Attached question

AJPH HISTORY

September 2017, Vol 107, No. 9 AJPH Rosner and Markowitz Peer Reviewed Public Health Then and Now 1395

“Ain’t Necessarily So!”: The Brake Industry’s Impact
on Asbestos Regulation in the 1970s
David Rosner, PhD, MPH, and Gerald Markowitz, PhD

Canada is proposing a ban on asbestos, and the US Environmental Protection Agency has listed it

among the first 10 materials it is investigating under the new Toxic Substances Control Act revisions.

However, this effort is currently running up against enormous industry and political opposition.

Here, we detail the activities in the early 1970s of the Friction Materials Standards Institute, an

industry trade association, to stifle earlier attempts to regulate asbestos use in brake linings, one

of the oldest and most obvious sources of asbestos exposure to mechanics, among others. (Am J

Public Health. 2017: 1395–1399. doi: 10.2105/AJPH.2017.303901)

At the end of 2016, the US Environmental Protec-
tion Agency (EPA) proposed

asbestos, the cause of fi brotic

lung disease and cancer, as one

of the 10 industrial chemi-

cals to be evaluated under the

newly revised Toxic Substances

Control Act.1 Under the new

act, a risk evaluation of asbestos

is to be completed within three

years and, if asbestos is found

to be an “unreasonable risk to

humans and the environment,”

the EPA is required to mitigate

that risk, possibly through a

ban, within two more years.2

By 1970, asbestos was used

in some 3000 products, such as

roof shingles, fl oor tiles, house

siding, ironing boards, and

particularly in brakes, among

other consumer items. Today, this

carcinogenic material is banned

in the United States in a few

products, including corrugated

paper and fl ooring felt, but it is

still legal in brakes and clutches

and a host of construction and

industrial materials, such as vinyl

fl oor tile, roofi ng materials, and

cement pipe, among others.

Consequently, it is in millions of

homes, gas stations, and repair

shops across the country.3

Historians have documented

one major reason for the

delay in banning this known

carcinogen: private industry

trade groups stifl ed earlier eff orts

at regulation.4 Here, we look at

the specifi c eff orts of one such

group, the Friction Materials

Standards Institute (FMSI),

to forestall the regulation of

asbestos used in brakes and

clutches, one of the oldest

sources of asbestos exposure.

We examine the industry’s

reaction to the newly created

Occupational Safety and Health

Administration’s (OSHA)

dramatic reduction of the

Permissible Exposure Limit

(PEL) in the early 1970s. There

is a literature that addresses

the current medical and

epidemiological evidence of the

dangers from asbestos brakes.5

Here, however, using internal

corporate documents, most of

which have not been previously

reviewed but are now available

at https://toxicdocs.org,6 we

explore what the industry

understood about the dangers to

mechanics from asbestos.

The concern about asbestos

in brakes refl ects the broader

acknowledgment of the impact

of industrial toxins on workers

and consumers in the 20th

century.7 In the early 1930s,

E. R. A. Merewether identifi ed

the dust produced by “the

sawing, grinding and turning

in the dry state of articles

composed wholly or partly

of asbestos such as motor car

brake and clutch linings” when

inhaled as a cause of asbestosis,

the fi brotic condition that slowly

strangles aff ected workers.8

Merewether’s early observation

that any material that contained

asbestos could prove to be a

hazard was affi rmed in the

immediate postwar period, as

offi cials noted that “asbestos

has been incorporated into

… protective clothing, brake

linings, cements, … and other

forms of insulation” and that

exposure to asbestos dust caused

by “the breakdown of the native

mineral” was also associated with

cancer of the lung.9 By the mid-

1960s, asbestos was associated

with asbestosis, lung cancer,

and mesothelioma, a cancer

of the lining of the lung and

abdominal cavity, leading the

British Ford Motor Company

to host a conference in 1969 on

the possible dangers presented

to brake mechanics and those

installing or replacing brake

linings.10

In 1970, the Occupational

Safety and Health Act,

establishing OSHA and

the National Institute of

Occupational Safety and

Health (NIOSH), was passed.11

Almost immediately, the FMSI

established an Asbestos Study

Committee (ASC), which

focused on the possible impact

of OSHA regulations on brake

and clutch manufacturers.

Working with the Asbestos

AJPH September 2017, Vol 107, No. 9

AJPH HISTORY

1396 Public Health Then and Now Peer Reviewed Rosner and Markowitz

Information Association of

North America (AIA), another

trade association, it sought to

forestall any drastic regulation.12

Among the ASC’s fi rst acts was

to meet with OSHA offi cials

who had issued an emergency

PEL of 12 fi bers per cubic

centimeter in 1971 and, a year

later, reduced it further to 5

fi bers per cubic centimeter, with

an even greater reduction to 2

fi bers per cubic centimeter by

1976.13

ACKNOWLEDGING
DANGER PRIVATELY

The FMSI was aware of why

OSHA was considering this

reduction. At its meeting in June

1972, the ASC received a report

that Rohl and colleagues had

presented a paper at a meeting of

the American Industrial Hygiene

Association, which was held at

Mt Sinai School of Medicine

in New York City. According to

the ASC, the paper revealed that

“the dust concentrations during

the blowing off of brakes are in

excess of the fi ve fi bers per cc

[cubic centimeter] allowance.”14

They acknowledged that

exposure to asbestos dust was a

possibility, if not a probability, for

workers installing and replacing

brakes.15

This raised the question

for the ASC as to whether

the manufacturers, under the

new OSHA regulations, had

an obligation to warn workers

of dangers they potentially

faced.16 Hence, a new rationale

for not warning was developed:

they publically pronounced

that asbestos, when “locked

in” to fabrics, lacquers, plastics,

or other fi nished products,

was not a danger as it could

not be released into the

air.17 In private, however, the

committee members noted

that because their products

were friction materials, there

was an inherent danger in the

“handling [by employees] of

the products with supposedly

locked-in asbestos during …

drilling, grinding, inspection and

boxing.” Furthermore, there was

the potential for the release of

asbestos during “the handling of

the brake lining or clutch facing

by the customer” even far from

the shop fl oor. One member

of the ASC suggested that “a

notifi cation be put in boxes in

brake linings or clutch facings,”

but this was quickly shot down

when another member objected

because “he felt it was another

‘red fl ag’ that would bring more

harm to the industry than the

alleged good that would come

from enclosing such notices.”18

Despite public assurances

that using “locked-in” asbestos

was safe, E. W. Drislane, the

executive director of the FMSI,

wrote to the ASC about an

internal survey that revealed “the

problem [that] in many cases

subsequent operations will be

performed—cutting, grooving,

drilling and grinding [and that]

these subsequent operations

can produce concentrations of

asbestos fi bers in excess of the

current exposure limits.”19 “Most

members of the Committee”

believed that the OSHA

standard was “exceeded in many

areas such as inspection, drilling,

and grinding where there is

not adequate dust collection

machinery.”20

AIN’T NECESSARILY SO
In mid-1973, “Ike” Weaver,

an engineer with the Raybestos–

Manhattan Corporation

and chair of the ASC, gave a

major address to the entire

membership that provides a

summary of what the industry

understood about the dangers

of asbestos. He informed them

about the recent meeting of

the International Agency for

Research on Cancer at which

“the most important item

[was] the incrimination of all

major types of asbestos as causal

agents of carcinoma, particularly

mesothelioma.” He further

warned that “since most of us

[in the FMSI] use substantial

amounts of chrysotile asbestos in

our formulations association of

this material with mesothelioma

and other types of cancer is of

serious concern.”21

For an industry that

identifi ed friction as the primary

characteristic of its products,

he knew “of no way any of us

can be absolutely sure that his

friction products, regardless

of whether they are sold as

original equipment or on the

replacement market, …[would

not] result in excessive exposure

“Look What Makes the Disc Brake
Brake.” From the 1930s on, sawing,
cutting, sanding, or abrading asbestos-
containing products in any way was
identified as a major concern. Here, we
see an “asbestos-based” Johns–Manville
disk brake ad from the 1960s with no
mention of any potential danger.

September 2017, Vol 107, No. 9 AJPH Rosner and Markowitz Peer Reviewed Public Health Then and Now 1397

AJPH HISTORY

of workers or bystanders to

airborne asbestos fi bre.” He

was “appalled to learn … of

instances where this problem has

occurred.”22

He objected to those in

his industry who argued that

most workers were exposed

only “relatively intermittently”

to respirable asbestos dust: “I

say emphatically this just ain’t

necessarily so!” Not only did

“large volume replacement

users [perhaps chains such as

Midas and Meineke] present

major potential hazards,” but

“even small job shops can

needlessly expose people to

high fi bre concentrations if

operations are performed

without controls.” There was

the risk for dread disease

even when exposures were

minimal or of short duration.23

“To me,” Weaver concluded,

“labelling all containers or

packagers of asbestos-containing

friction material is the very

least the industry can do to

fulfi ll its moral obligation to

its customers, their employees

and the public and at the

same time conform with

minimum requirements of the

Occupational Safety and Health

Act.”24

Further evidence about the

potential dangers to mechanics,

including cancer, was provided

with the publication of the Rohl

paper on New York City garages

that the ASC had heard about

before. The ASC acknowledged

that “some of the housekeeping

conditions in these shops

[were] deplorable.” And they

acknowledged that conditions

in New York were “perhaps

no worse than in other shops

throughout the country.”25

COLLAPSING DEFENSES
By the mid-1970s, the FMSI

had learned that both national

and international experts,

NIOSH, the International Labor

Organization, the International

Agency for Research on Cancer,

and other researchers agreed that

the PEL was irrelevant to the

question of cancer.26 In addition,

one of the leading fi gures in

industrial medicine and the

leading asbestos researcher,

Irving Selikoff , echoed these

ideas, writing that the “only safe

concentration is zero fi ber per

cc.”27

In April 1975, as the date

for the proposed reduction of

the PEL to 2 fi bers per cubic

centimeter approached, the FMSI

faced a dilemma. They claimed

they were already “having dif-

fi culty meeting the 5 fi bers/cc

limit,” and worried that “it would

be near impossible to meet the

2 fi bers/cc limit due July 1,

1976.” Some on the ASC “sug-

gested that the industry should

oppose this change,”28 and Guy

Gabriellson, vice president of the

Asbestos Information Association,

said that the industry should

simply reject OSHA’s and

NIOSH’s position.29

GROWING PRESSURE,
GROWING EVIDENCE

The situation was becoming

dire for the FMSI as they

faced growing pressure to

acknowledge that there was

no exposure below which

workers could be protected

from asbestos-induced cancers.

The pressure came from

NIOSH, the International

Labor Organization, and others.

Selikoff predicted an “epidemic

of asbestos related death and

disease in years to come.”

The FMSI Board of Directors

was alarmed by the growing

consensus that “no known dose

level [of asbestos exposure was]

‘safe.’ ” Furthermore, Selikoff

and his colleagues were “actively

promoting” the view that the

hazards were “associated with

asbestos emissions”—specifi cally

to mechanics—“from brake

lining wear and from brake

service operations.”30

The pressures became even

greater in July 1975, after

NIOSH called a meeting in

Washington of an automobile

company, union representatives,

the major asbestos companies,

researchers, and a trade

association representative.31

They learned that the medical

literature “revealed at least

four cases of these rare tumors

[mesotheliomas] in persons who

were employed in jobs involving

automobile brake servicing.”32

The liability dimensions of the

problem facing the industry

were frightening: “It has been

reported that approximately

900,000 persons are employed

in such work in the United

This ad from Raybestos-Manhattan
emphasizes the “safety” of the asbestos
brakes, despite the fact that by this
point, it was clear that exposure to
asbestos dust could cause cancer.

AJPH September 2017, Vol 107, No. 9

AJPH HISTORY

1398 Public Health Then and Now Peer Reviewed Rosner and Markowitz

States. It is recommended that

stringent industrial hygiene

measure to control exposure

be implemented as rapidly as

possible.”33 In a separate article,

the industry learned that “during

brake-lining maintenance and

repair, workmen in garages,

service stations and brake repair

shops are exposed to asbestos

and thus may be subject to

serious cancer risk. Others, at

some distance from the repair

work, are perhaps subject to the

same hazard.”34

RESISTANCE RAMPS UP
At the same time that these

articles were being published,

OSHA proposed to reduce the

asbestos standard even lower,

which the FMSI described

as a “drastic reduction.”35

The ASC began to mobilize

committee members and the

general membership of the

FMSI to oppose OSHA’s

recommendation that the PEL

be reduced to 0.5 fi bers per

cubic centimeter instead of the

2 fi bers per cubic centimeter

standard that was scheduled to

go into eff ect July 1, 1976. In

June, they proposed a three-part

strategy. First, they intended

to educate their membership

on how to comply with the

2-fi bers per cubic centimeter

standard to go into eff ect in the

following month and further to

recognize “the impact that will

be required to cope with the

0.5 fi bre standard, should it be

imposed.” Second, they planned

to oppose the more stringent

standard with “every possible

means at our disposal,” and “to

enlighten government offi cials

of what informed members

within our industry regard as the

complete impracticality of the

[proposed] 0.5 standard.” Finally,

they planned on “cooperating

with the Asbestos Information

Association and the Institute

Offi ce in their response to

OSHA on the revised standard,”

an eff ort they believed had

already borne fruit.36 In the

end, the standard would not

be reduced until the mid-

1980s,37 and they congratulated

themselves and the AIA on

forestalling the reduction of the

standard. The FMSI thanked the

AIA for “the outstanding job

[they did] in rebutting some of

the reasons for OSHA’s stringent

proposals.”38 The committee

bragged that “we have been told

that our eff orts … have been

effi cacious.”39

The infl uence of the asbestos

industry can be observed

directly by comparing the

warnings the FMSI and AIA

recommended for gas stations

and auto repair shops with those

of the government. NIOSH in

1976 suggested that a sign be

posted at the entrance to the

work area of these garages that

specifi cally warned: “Asbestos;

Dust Hazard; Avoid Breathing

Dust; Wear Assigned Protective

Equipment; Do Not Remain

in Area Unless your Work

Requires it; Breathing Asbestos

Dust May Cause Asbestosis and

Cancer.”40 The FMSI and the

AIA adopted similar wording,

with one crucial diff erence:

they did not use the word

“cancer.” Instead, they adopted

OSHA’s wording from the 1972

standard:41 “Breathing Asbestos

Dust May be Hazardous to Your

Health.”42 As a result of the

FMSI and AIA’s opposition, the

lowering of OSHA’s PEL was

signifi cantly delayed. In addition,

they trivialized the dangers to

workers by not including cancer

in their warnings. As a result,

they belittled and undercut the

warnings of NIOSH, Irving

Selikoff , and many other

scientists that workers were

putting their lives at risk by

working with products made

with asbestos.

For policymakers, it is

important to understand the

tragic history we relate here. It

took 45 years of work on the

part of physicians, laboratory

scientists, regulators, and citizens

to achieve these monumental

victories for public health, but

all of this work can be undone

if the current administration in

Washington follows through

on its threats to undercut the

EPA and other federal agencies.

There are few materials in the

modern environment that are

documented to be as hazardous

as asbestos. It would be tragic if

all this work was to be undone

by new lobbying eff orts aimed

at a new administration and

EPA administrator particularly

receptive to industry’s siren call

to deregulate.43

ABOUT THE AUTHORS
David Rosner is with the Center for the

History and Ethics of Public Health,

Department of Sociomedical Sciences,

Mailman School of Public Health, and the

Department of History, Columbia University,

New York, NY. Gerald Markowitz is with the

Department of Interdisciplinary Studies, John

Jay College, and the Department of History,

Graduate Center, both of the City University

of New York, New York, NY.

Correspondence should be sent to David

Rosner, Center for the History and Ethics of

Public Health, Department of Sociomedical

Sciences, Columbia University, Mailman

School of Public Health, 722 West 168th St,

Room 934, New York, NY 10032 (e-mail:

dr289@columbia.edu). Reprints can be

ordered at http://www.ajph.org by clicking the

“Reprints” link.

This article was accepted May 4, 2017.

doi: 10.2105/AJPH.2017.303901

CONTRIBUTORS
The authors contributed equally to the

research, writing, and conceptualization

of this article.

ACKNOWLEDGMENTS
We acknowledge that many of the

primary source documents were gathered

in the process of litigation regarding

asbestos-related diseases. These documents

are available online at http://www.

toxicdocs.org, a Web site of corporate

memos, letters, reports, and other articles

developed through the cooperative eff orts

of the Center for the History and Ethics

of Public Health, Columbia University

and the City University of New York.

We have appeared as expert witnesses on

behalf of plaintiff s in asbestos lawsuits.

ENDNOTES
1. This revision is now known as the

Frank R. Lautenberg Chemical Safety

for the 21st Century Act.

2. Environmental Protection Agency,

“News Releases From Headquarters:

EPA Names First Chemicals for Re-

view Under New TSCA Legislation;

Agency Answers Call to Move For-

ward on Chemical Reform, Naming

Asbestos Among the First to Undergo

Risk Evaluation,” November 11, 2016.

https://www.epa.gov/newsreleases/

epa-names-first-chemicals-review-under-

new-tsca-legislation (accessed December

29, 2016).

3. Environmental Protection Agency,

“US Federal Bans on Asbestos.” https://

www.epa.gov/asbestos/us-federal-bans-

asbestos#main-content (accessed Decem-

ber 29, 2016). See also Kathleen Ruff,

“Asbestos Lobby Launches Attack to

Undermine Upcoming UN Conference

on Trade in Hazardous Substances.”

Asbestos lobby launches attack to undermine upcoming UN Conference on trade in hazardous substances

(accessed April 17, 2017).

4. See, for example, Barry Castleman,

Asbestos: Medical and Legal Aspects, 3rd

edition (Englewood, NJ: Prentice

Hall, 1990); Gerald Markowitz and

David Rosner, “ ‘Unleashed Upon an

Unsuspecting World’: The Asbestos

Information Association and Its Role

in Perpetuating a National Epidemic,”

American Journal of Public Health 106, no.

5 (2016): 834–840.

5. See Castleman, Asbestos, pp 443–479,

for one of the first reviews of the

existing scientific evidence of the dangers

of asbestos in brake linings.

6. These documents are available on the

Web site https://www.toxicdocs.org, a

collection of nearly 6 000 000 corporate

memos, studies, letters, and notes

gathered through a variety of law suits

over toxic materials.

7. David Rosner and Gerald Markowitz,

“A ‘Gift of God’? The Public Health

Controversy Over Leaded Gasoline

During the 1920s,” American Journal of

Public Health 75, no. 4 (1985): 344–352;

William Graebner, “Hegemony Through

Science: Information Engineering and

Lead Toxicology, 1925–1965,” in

David Rosner and Gerald Markowitz,

eds, Dying for Work: Workers’ Safety

and Health in Twentieth Century

America (Bloomington, IN: Indiana

University Press, 1987), 140–159;

David Egilman and Marion Billings,

“Abuse of Epidemiology: Automobile

Manufacturers Manufacture a Defense

to Asbestos Liability,” International

Journal of Occupational and Environmental

September 2017, Vol 107, No. 9 AJPH Rosner and Markowitz Peer Reviewed Public Health Then and Now 1399

AJPH HISTORY

16. Title 29, Labor, Chapter XVII—

Occupational Safety and Health

Administration, Department of Labor,

Part 1910—Occupational Safety

and Health Standards, “Standard for

Exposure to Asbestos Dust,” Federal

Register 37 (1972): 11321: “Caution

Labels shall be affixed to all raw

materials, mixtures, scrap, waste, debris,

and other products containing asbestos

fibers or to their containers, except that

no label is required where asbestos fibers

have been modified by a bonding agent,

coating, binder, or other material so

that during any reasonably foreseeable

use, handling, storage, disposal,

processing, or transportation, no airborne

concentrations of asbestos fibers in

excess of the exposure limits prescribed

in paragraph (b) of this section will be

released.”

17. Ibid, p. 11319: “Employers in

general strongly contend that finished

products that effectively entrap asbestos

fibers, so that these would not be released

in the normal use of the products, should

not be required to be labelled.”

18. FMSI, Asbestos Study Committee,

“Minutes,” August 17, 1972.

19. E. W. Drislane to Asbestos Study

Committee, “Interpretation of OSHA

Labelling Requirements,” November

6, 1972.

20. FMSI, Asbestos Study Committee,

“Minutes,” February 16, 1973.

21. FMSI, Annual Meeting, “Minutes,”

June 27–28, 1973. Weaver noted that

“risk is greatest with crocidolite, less

with amosite and apparently still less

with chrysotile.”

22. FMSI, Annual Meeting, “Minutes,”

June 27–28, 1973.

23. Ibid.

24. Ibid.

25. FMSI, Asbestos Study Committee,

“Minutes,” June 14, 1974.

26. The International Labor

Organization’s “Meeting of Experts on

Safe Use of Asbestos” stated that “the

2 fibres/ml standard should be regarded

as an interim concentration related to

fibrogenic effects and not to carcinogenic

effects, for which no standards exist at

the present time.” See Report of

International Labor Organization,

“Meeting of Experts on Safe Use of

Asbestos,” in Geneva, December 11–18,

1973, in “Asbestos Study Committee

Report,” June 1974, attached to Minutes

of Annual Meeting, June 18–19, 1975.

27. FMSI Board of Directors,

“Minutes,” June 25, 1974.

28. See also FMSI, Asbestos Study

Committee, “Minutes,” April 28, 1975.

29. See: Gerald Markowitz and David

Rosner, “Unleashed on an Unsuspecting

World,”: The Asbestos Information

Association and Its Role in Perpetuating

a National Epidemic,” AJPH, 106(May,

2016), p.838.

30. FMSI, Board of Directors, “Minutes,”

June 17, 1975; “Asbestos Study Commit-

tee Report,” June 1975.

31. Department of Health, Education

and Welfare, CDC, NIOSH, “Minutes

of Occupational Exposures to Asbestos

Dust From Brake Linings Meeting,” July

21, 1973.

32. Department of Health, Education

and Welfare, CDC, NIOSH, “Minutes

of Occupational Exposures to Asbestos

Dust From Brake Linings Meeting,”

July 21, 1973. See also J. W. Lloyd,

NIOSH, to “Dear Colleague,”

“Current Intelligence Bulleting 5:

Asbestos Exposure During Servicing

of Motor Vehicle Brake and Clutch

Assemblies,” DHHS (NIOSH),

Publication No. 78-127, August 8,

1975 (in FMSI file). At the meeting, Dr

George Wright, representing the Johns

Manville Corporation, “emphasized that

manufacturers have a responsibility to

ascertain what happens to their products

after being sold to others.” He was not

surprised about “the [high] fiber counts

reported” and expressed the belief that

one might subsequently encounter the

full spectrum of asbestos-related disease

among grinders.

33. Arthur N. Rohl, Arthur M. Langer,

Mary S. Wolff, and Irving Weisman,

“Asbestos Exposure During Brake

Lining Maintenance and Repair,” Envi-

ronmental Research 12 (1976): 110–128.

In this article, the authors describe the

work practices in repair shops and the

attendant hazards: “When a vehicle is

brought into a repair shop for brake

lining inspection or replacement, the

wheel is removed and loose dust is

removed from the drums and back plates,

generally by means of a compressed

air jet. … The cloud of dust that is

produced is visible for several minutes

afterwards. Table 3 shows that fiber

concentrations are high in the operator’s

area under these conditions (an average

concentration of 16 fibers/ml), and that

there are significant concentrations at

least 20 ft away. … It is evident that any

person 65–75 ft away can be exposed”

(p. 118). “It was generally found that

there was minimal, if any, effort to control

dust in most garages. Workmen do not

use respiratory protection. There was

little awareness of the potential hazard

of brake dust” (pp. 117–118).

34. Arthur N. Rohl, “Asbestos Exposure

During Brake Lining Maintenance

Repair,” ca. January 1976, enclosed in

Selikoff to Drislane, January 14, 1976.

Rohl says in a handwritten note, “Dr.

Selikoff has asked me to send you the

results of our asbestos fiber counts

during brake repair work.” (This reference

is to the early draft of paper published

in mid-1976).

35. Asbestos Study Committee, FMSI,

“Minutes of Annual Meeting,” June

16–17, 1976.

36. “Asbe