Proposed Rule2024-14824
Heat Injury and Illness Prevention in Outdoor and Indoor Work Settings
Primary source
Metadata and text below are from the Federal Register, a public-domain U.S. government work. Always verify the official published version before relying on it for any legal matter.
Published
August 30, 2024
Issuing agencies
Labor DepartmentOccupational Safety and Health Administration
Abstract
OSHA is proposing to issue a new standard, titled Heat Injury and Illness Prevention in Outdoor and Indoor Work Settings. The standard would apply to all employers conducting outdoor and indoor work in all general industry, construction, maritime, and agriculture sectors where OSHA has jurisdiction, with some exceptions. It would be a programmatic standard that would require employers to create a plan to evaluate and control heat hazards in their workplace. It would more clearly set forth employer obligations and the measures necessary to effectively protect employees from hazardous heat. OSHA requests comments on all aspects of the proposed rule.
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[Federal Register Volume 89, Number 169 (Friday, August 30, 2024)]
[Proposed Rules]
[Pages 70698-71073]
From the Federal Register Online via the Government Publishing Office [<a href="http://www.gpo.gov">www.gpo.gov</a>]
[FR Doc No: 2024-14824]
[[Page 70697]]
Vol. 89
Friday,
No. 169
August 30, 2024
Part II
Department of Labor
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Occupational Safety and Health Administration
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29 CFR Part 1910, 1915, 1917, et al.
Heat Injury and Illness Prevention in Outdoor and Indoor Work Settings;
Proposed Rule
Federal Register / Vol. 89, No. 169 / Friday, August 30, 2024 /
Proposed Rules
[[Page 70698]]
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DEPARTMENT OF LABOR
Occupational Safety and Health Administration
29 CFR Part 1910, 1915, 1917, 1918, 1926, and 1928
[Docket No. OSHA-2021-0009]
RIN 1218-AD39
Heat Injury and Illness Prevention in Outdoor and Indoor Work
Settings
AGENCY: Occupational Safety and Health Administration (OSHA), Labor.
ACTION: Notice of proposed rulemaking (NPRM); request for comments.
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SUMMARY: OSHA is proposing to issue a new standard, titled Heat Injury
and Illness Prevention in Outdoor and Indoor Work Settings. The
standard would apply to all employers conducting outdoor and indoor
work in all general industry, construction, maritime, and agriculture
sectors where OSHA has jurisdiction, with some exceptions. It would be
a programmatic standard that would require employers to create a plan
to evaluate and control heat hazards in their workplace. It would more
clearly set forth employer obligations and the measures necessary to
effectively protect employees from hazardous heat. OSHA requests
comments on all aspects of the proposed rule.
DATES: Comments to this NPRM (including requests for a hearing) and
other information must be submitted by December 30, 2024.
Informal public hearing: OSHA will schedule an informal public
hearing on the proposed rule if requested during the comment period. If
a hearing is requested, the location and date of the hearing,
procedures for interested parties to notify the agency of their
intention to participate, and procedures for participants to submit
their testimony and documentary evidence will be announced in the
Federal Register.
ADDRESSES:
Written comments: You may submit comments and attachments,
identified by Docket No. OSHA-2021-0009, electronically at <a href="https://www.regulations.gov">https://www.regulations.gov</a>, which is the Federal e-Rulemaking Portal. Follow
the instructions online for making electronic submissions. After
accessing ``all documents and comments'' in the docket (Docket No.
OSHA-2021-0009), check the ``proposed rule'' box in the column headed
``Document Type,'' find the document posted on the date of publication
of this document, and click the ``Comment Now'' link. When uploading
multiple attachments to <a href="http://regulations.gov">regulations.gov</a>, please number all of your
attachments because <a href="http://regulations.gov">regulations.gov</a> will not automatically number the
attachments. This will be very useful in identifying all attachments.
For example, Attachment 1--title of your document, Attachment 2--title
of your document, Attachment 3--title of your document. For assistance
with commenting and uploading documents, please see the Frequently
Asked Questions on <a href="http://regulations.gov">regulations.gov</a>.
Instructions: All submissions must include the agency's name and
the docket number for this rulemaking (Docket No. OSHA-2021-0009). All
comments, including any personal information you provide, are placed in
the public docket without change and may be made available online at
<a href="https://www.regulations.gov">https://www.regulations.gov</a>. Therefore, OSHA cautions commenters about
submitting information they do not want made available to the public,
or submitting materials that contain personal information (either about
themselves or others), such as Social Security Numbers and birthdates.
Docket citations: This Federal Register document references
material in Docket No. OSHA-2021-0009, which is the docket for this
rulemaking.
Citations to documents: The docket referenced most frequently in
this document is the docket for this rulemaking, docket number OSHA-
2021-0009, cited as Document ID OSHA-2021-0009. Documents in the docket
get an individual document identification number, for example ``OSHA-
2021-0009-0047.'' Because this is the most frequently cited docket, the
citation is shortened to indicate only the document number. The example
is cited in the NPRM as ``Document ID 0047.''
Documents cited in this NPRM are available in the rulemaking docket
(Docket ID OSHA-2021-0009). They are available to read and download by
searching the docket number or document ID number at <a href="https://www.regulations.gov">https://www.regulations.gov</a>. Each docket index lists all documents in that
docket, including public comments, supporting materials, meeting
transcripts, and other documents. However, some documents (e.g.,
copyrighted material) in the dockets are not available to read or
download from that website. All documents in the dockets are available
for inspection at the OSHA Docket Office. This information can be used
to search for a supporting document in the docket at
<a href="http://www.regulations.gov">www.regulations.gov</a>. Contact the OSHA Docket Office at (202) 693-2350
(TTY number: 877-889-5627) for assistance in locating docket
submissions.
FOR FURTHER INFORMATION CONTACT:
For press inquiries: Contact Frank Meilinger, Director, OSHA Office
of Communications, Occupational Safety and Health Administration;
telephone: (202) 693-1999; email: <a href="/cdn-cgi/l/email-protection#b8d5ddd1d4d1d6dfddca96decad9d6dbd1cb8af8dcd7d496dfd7ce"><span class="__cf_email__" data-cfemail="cca1a9a5a0a5a2aba9bee2aabeada2afa5bffe8ca8a3a0e2aba3ba">[email protected]</span></a>.
General information and technical inquiries: Contact Stephen
Schayer, Director, Office of Physical Hazards and Others, OSHA
Directorate of Standards and Guidance; telephone: (202) 693-1950;
email: <a href="/cdn-cgi/l/email-protection#95fae6fdf4bbf1e6f2d5f1faf9bbf2fae3"><span class="__cf_email__" data-cfemail="f49b879c95da908793b4909b98da939b82">[email protected]</span></a>.
Copies of this Federal Register notice: Electronic copies are
available at <a href="https://www.regulations.gov">https://www.regulations.gov</a>. This Federal Register notice,
as well as news releases and other relevant information, also are
available at OSHA's web page at <a href="https://www.osha.gov">https://www.osha.gov</a>.
The docket is available at <a href="https://www.regulations.gov">https://www.regulations.gov</a>, the Federal
eRulemaking Portal. A ``100-word summary'' is also available on <a href="https://www.regulations.gov">https://www.regulations.gov</a>. For additional information on submitting items
to, or accessing items in, the docket, please refer to the ADDRESSES
section of this NPRM. Most exhibits are available at <a href="https://www.regulations.gov">https://www.regulations.gov</a>; some exhibits (e.g., copyrighted material) are not
available to download from that web page. However, all materials in the
dockets are available for inspection and copying at the OSHA Docket
Office.
SUPPLEMENTARY INFORMATION:
Table of Contents
I. Executive Summary
II. Pertinent Legal Authority
A. Introduction
B. Significant Risk
C. Feasibility
D. High Degree of Employee Protection
III. Background
A. Introduction
B. Need for Proposal
C. Events Leading to Proposal
D. Other Standards
IV. Health Effects
A. Introduction
B. General Mechanisms of Heat-Related Health Effects
C. Identifying Cases of Heat-Related Health Effects
D. Heat-Related Deaths
E. Heat Stroke
F. Heat Exhaustion
G. Heat Syncope
H. Rhabdomyolysis
I. Hyponatremia
J. Heat Cramps
K. Heat Rash
L. Heat Edema
M. Kidney Health Effects
N. Other Health Effects
O. Factors That Affect Risk for Heat-Related Health Effects
P. Heat-Related Injuries
[[Page 70699]]
V. Risk Assessment
A. Risk Assessment
B. Basis for Initial and High Heat Triggers
C. Risk Reduction
VI. Significance of Risk
A. Material Harm
B. Significant Risk
C. Preliminary Conclusions
VII. Explanation of Proposed Requirements
A. Paragraph (a) Scope and Application
B. Paragraph (b) Definitions
C. Paragraph (c) Heat Injury and Illness Prevention Plan
D. Paragraph (d) Identifying Heat Hazards
E. Paragraph (e) Requirements at or Above the Initial Heat
Trigger
F. Paragraph (f) Requirements at or Above the High Heat Trigger
G. Paragraph (g) Heat Illness and Emergency Response and
Planning
H. Paragraph (h) Training
I. Paragraph (i) Recordkeeping
J. Paragraph (j) Requirements Implemented at no Cost to
Employees
K. Paragraph (k) Dates
L. Paragraph (l) Severability
VIII. Preliminary Economic Analysis and Initial Regulatory
Flexibility Analysis
A. Market Failure and Need for Regulation
B. Profile of Affected Industries
C. Costs of Compliance
D. Economic Feasibility
E. Benefits
F. Initial Regulatory Flexibility Analysis
G. Distributional Analysis
H. Appendix A. Description of the Cost Savings Approach
I. Appendix B. Review of Literature on Effects of Heat Exposure
on Non-Health Outcomes
J. Appendix C. Heat Exposure Methodology Used in Distributional
Analysis
K. Appendix D. Definitions of Core Industry Categories Used in
Cost Analysis
IX. Technological Feasibility
X. Additional Requirements
A. Unfunded Mandates Reform Act, 2 U.S.C. 1501 et seq.
B. Consultation and Coordination With Indian Tribal Governments/
Executive Order 13175
C. Consultation With the Advisory Committee on Construction
Safety and Health
D. Environmental Impacts
E. Consensus Standards
F. Incorporation by Reference
G. Protection of Children From Environmental Health Risks and
Safety Risks
H. Federalism
I. Requirements for States With OSHA-Approved State Plans
J. OMB Review Under the Paperwork Reduction Act of 1995
XI. Authority and Signature
I. Executive Summary
Heat is the leading cause of death among all weather-related
phenomena in the United States. Excessive heat in the workplace can
cause a number of adverse health effects, including heat stroke and
even death, if not treated properly. Yet, there is currently no Federal
OSHA standard that regulates heat stress hazards in the workplace.
Although several governmental and non-governmental organizations have
published regulations and guidance to help protect workers from heat
hazards, OSHA believes that a mandatory Federal standard specific to
heat-related injury and illness prevention is necessary to address the
hazards posed by occupational heat exposure. OSHA has preliminarily
determined that this proposed rule would substantially reduce the risk
posed by occupational exposure to hazardous heat by clearly setting
forth employer obligations and the measures necessary to effectively
protect exposed workers.
OSHA is proposing this standard pursuant to the Occupational Safety
and Health Act of 1970, 29 U.S.C. 651 et seq. (OSH Act or Act). The Act
authorizes the agency to issue safety or health standards that are
``reasonably necessary or appropriate'' to provide safe or healthful
employment and places of employment (29 U.S.C. 652(8)). A standard is
reasonably necessary or appropriate when a significant risk of material
harm exists in the workplace and the standard would substantially
reduce or eliminate that workplace risk. Applicable legal requirements
are more fully discussed in Section II., Pertinent Legal Authority.
Workers in both outdoor and indoor work settings without adequate
climate controls are at risk of hazardous heat exposure. Certain heat-
generating processes, machinery, and equipment (e.g., hot tar ovens,
furnaces) can also cause heat hazards when cooling measures are not in
place. Based on the best available evidence, as discussed in this
preamble, OSHA has preliminarily determined that exposure to hazardous
heat in the workplace poses a significant risk of serious injury and
illness. This finding of a significant risk of material harm is based
on the health consequences associated with exposure to heat (see
Section IV., Health Effects) as well as the risk assessment (see
Section V., Risk Assessment and Section VI., Significance of Risk). In
Section V.C., Risk Reduction, OSHA demonstrates the efficacy of the
controls relied on in this proposed rule to reduce the risk of heat-
related injury and illness in the workplace. Employees working in
workplaces without these controls are at higher risk of severe health
outcomes from exposure to hazardous heat.
On October 27, 2021, OSHA published in the Federal Register an
advance notice of proposed rulemaking (ANPRM) for Heat Injury and
Illness Prevention in Outdoor and Indoor Work Settings (86 FR 59309).
The ANPRM outlined key issues and challenges in occupational heat-
related injury and illness prevention and aimed to collect evidence,
data, and information critical to informing how OSHA proceeds in the
rulemaking process. The ANPRM included background information on
injuries, illnesses, and fatalities due to heat, underreporting, scope,
geographic region, and inequality in exposures and outcomes. The ANPRM
also covered existing heat injury and illness prevention efforts
including OSHA's efforts, the National Institute for Occupational
Safety and Health (NIOSH) criteria documents, State standards, and
other standards.
OSHA received 965 unique public comments, which largely supported
the need for continued rulemaking. The agency then worked with the
National Advisory Committee on Occupational Safety and Health (NACOSH)
to assemble a Heat Injury and Illness Prevention Work Group. The Work
Group was tasked with evaluating stakeholder input to the ANPRM and
developing recommendations on potential elements of a proposed heat
injury and illness prevention standard. The Work Group presented its
recommendations on potential elements of a proposed heat injury and
illness prevention standard for consideration by the full NACOSH
committee. On May 31, 2023, NACOSH amended the report to ask OSHA to
include a model written plan and then unanimously voted to submit the
Work Group's recommendations to the Secretary of Labor.
In accordance with the requirements of the Small Business
Regulatory Enforcement Fairness Act (SBREFA), OSHA next convened a
Small Business Advocacy Review (SBAR) Panel in August 2023. The Panel,
comprised of members from the Small Business Administration's (SBA)
Office of Advocacy, OSHA, and OMB's Office of Information and
Regulatory Affairs, heard comments directly from Small Entity
Representatives (SERs) on the potential impacts of a heat-specific
standard. The Panel received advice and recommendations from the SERs
and reported its findings and recommendations to OSHA. OSHA has taken
the SER's comments and the Panel's findings and recommendations into
consideration in the development of this proposed rule (see Section
VIII.F., Initial Regulatory Flexibility Analysis).
In accordance with 29 CFR parts 1911 and 1912, OSHA also consulted
with and considered feedback from the Advisory Committee on
Construction
[[Page 70700]]
Safety and Health (ACCSH). On April 24, 2024, the Committee unanimously
passed a motion recommending that OSHA proceed expeditiously with
proposing a standard on heat injury and illness prevention. In
addition, in accordance with Executive Order 13175, Consultation and
Coordination with Indian Tribal Governments, 65 FR 67249 (Nov. 6,
2000), OSHA held a listening session on May 15, 2024, with Tribal
representatives regarding this Heat Injury and Illness Prevention in
Outdoor and Indoor Work Settings rulemaking and provided an opportunity
for the representatives to offer feedback.
The proposed rule is a programmatic standard that requires
employers to create a heat injury and illness prevention plan to
evaluate and control heat hazards in their workplace. It establishes
requirements for identifying heat hazards, implementing engineering and
work practice control measures at or above two heat trigger levels
(i.e., an initial heat trigger and a high heat trigger), developing and
implementing a heat illness and emergency response plan, providing
training to employees and supervisors, and retaining records. The
proposed rule would apply to all employers conducting outdoor and
indoor work in all general industry, construction, maritime, and
agriculture sectors, with some exceptions (see Section VII.A.,
Paragraph (a) Scope and Application). Throughout this document, OSHA
seeks input on alternatives and potential exclusions.
Organizations affected by heat hazards vary significantly in size
and workplace activities. Accordingly, many of the provisions of the
proposed standard provide flexibility for affected employers to choose
the control measures most suited to their workplace. The flexible
nature of the proposed rule may be particularly beneficial to small
organizations with limited resources.
Additionally, to determine whether the proposed rule is feasible
for affected employers, and in accordance with Executive Orders 12866
and 13563, the Regulatory Flexibility Act (RFA), and the Unfunded
Mandates Reform Act (2 U.S.C 1501 et seq.), OSHA has prepared a
Preliminary Economic Analysis (PEA), including an Initial Regulatory
Flexibility Analysis (see Section VIII., Preliminary Economic Analysis
and Initial Regulatory Flexibility Analysis). Supporting materials
prepared by OSHA are available in the public docket for this
rulemaking, Document ID OSHA-2021-0009, through <a href="http://regulations.gov">regulations.gov</a>.
II. Pertinent Legal Authority
A. Introduction
In the Occupational Safety and Health Act, 29 U.S.C. 651 et seq.,
Congress authorized the Secretary of Labor (``the Secretary'') ``to set
mandatory occupational safety and health standards applicable to
businesses affecting interstate commerce'' (29 U.S.C. 651(b)(3); see
Nat'l Fed'n of Indep. Bus. v. Dep't of Labor, 595 U.S. 109, 117 (2022)
(per curiam); see also 29 U.S.C. 654(a)(2) (requiring employers to
comply with OSHA standards)). Section 6(b) of the Act authorizes the
promulgation, modification or revocation of occupational safety or
health standards pursuant to detailed notice and comment procedures (29
U.S.C. 655(b)).
Section 3(8) of the Act defines a safety or health standard as a
standard which requires conditions, or the adoption or use of one or
more practices, means, methods, operations, or processes ``reasonably
necessary or appropriate'' to provide safe or healthful employment and
places of employment (29 U.S.C. 652(8)). A standard is reasonably
necessary or appropriate within the meaning of section 3(8) when a
significant risk of material harm exists in the workplace and the
standard would substantially reduce or eliminate that workplace risk
(see Indus. Union Dep't, AFL-CIO v. Am. Petroleum Inst., 448 U.S. 607
(1980) (``Benzene'')). OSHA's authority extends to, for example,
removing workers from environments where workplace hazards exist (see,
e.g., United Steelworkers of America v. Marshall, 647 F.2d 1189, 1228-
38 (D.C. Cir. 1981); 29 CFR 1910.1028(i)(8); 29 CFR 1910.1024(l); cf.
Whirlpool Corp. v. Marshall, 445 U.S. 1, 12 (1980) (upholding
regulation allowing employees to refuse dangerous work in certain
circumstances because ``[t]he Act does not wait for an employee to die
or become injured.'').
In addition to the requirement that each standard address a
significant risk, standards must also be technologically feasible (see
UAW v. OSHA, 37 F.3d 665, 668 (D.C. Cir. 1994)). A standard is
technologically feasible when the protective measures it requires
already exist, when available technology can bring the protective
measures into existence, or when that technology is reasonably likely
to develop (see Am. Iron and Steel Inst. v. OSHA, 939 F.2d 975, 980
(D.C. Cir. 1991)).
Finally, a standard must be economically feasible (see Forging
Indus. Ass'n v. Secretary of Labor, 773 F.2d 1436, 1453 (4th Cir.
1985)). A standard is economically feasible if industry can absorb or
pass on the costs of compliance without threatening its long-term
profitability or competitive structure (see American Textile Mfrs.
Inst., Inc., 452 U.S. 490, 530 n.55 (``Cotton Dust'')). Each of these
requirements is discussed further below.
B. Significant Risk
As noted above, OSHA's workplace safety and health standards must
address a significant risk of material harm that exists in the
workplace (see Benzene, 448 U.S. at 614-15). The agency's risk
assessments are based on the best available evidence, and its final
conclusions are made only after considering all information in the
rulemaking record. Reviewing courts have upheld the Secretary's
significant risk determinations where supported by substantial evidence
and ``a reasoned explanation for [their] policy assumptions and
conclusions'' (Bldg & Constr. Trades Dep't v. Brock, 838 F.2d 1258,
1266 (D.C. Cir. 1988) (``Asbestos II'')).
The Supreme Court in Benzene explained that ``[i]t is the agency's
responsibility to determine, in the first instance, what it considers
to be a `significant' risk'' (Benzene, 448 U.S. at 655). The Court
declined to ``express any opinion on the . . . difficult question of
what factual determinations would warrant a conclusion that significant
risks are present which make promulgation of a new standard reasonably
necessary or appropriate'' (Benzene, 448 U.S. at 659). The Court
stated, however, that the substantial evidence standard applicable to
OSHA's significant risk determination (see 29 U.S.C. 655(b)(f)) does
not require the agency ``to support its finding that a significant risk
exists with anything approaching scientific certainty'' (Benzene, 448
U.S. at 656). Rather, OSHA may rely on ``a body of reputable scientific
thought'' to which ``conservative assumptions in interpreting the
data'' may be applied, ``risking error on the side of overprotection''
(Benzene, 448 U.S. at 656). The D.C. Circuit has further explained that
OSHA may thus act with a pronounced bias towards worker safety in
making its risk determinations (Asbestos II, 838 F.2d at 1266). The
Supreme Court also recognized that the determination of what
constitutes ``significant risk'' is ``not a mathematical straitjacket''
and will be ``based largely on policy considerations'' (Benzene, 448
U.S. at 655 & n.62).
Once OSHA makes its significant risk finding, the standard it
promulgates must be ``reasonably necessary or appropriate'' to reduce
or eliminate that
[[Page 70701]]
risk (29 U.S.C. 652(8)). In choosing among regulatory alternatives,
however, ``[t]he determination that [one standard] is appropriate, as
opposed to a marginally [more or less protective] standard, is a
technical decision entrusted to the expertise of the agency'' (Nat'l
Mining Ass'n v. Mine Safety and Health Admin., 116 F.3d 520, 528 (D.C.
Cir. 1997) (analyzing a Mine Safety and Health Administration standard
under the Benzene significant risk standard)).
C. Feasibility
The statutory mandate to consider the feasibility of the standard
encompasses both technological and economic feasibility; OSHA has
performed these analyses primarily on an industry-by-industry basis
(United Steelworkers of Am., AFL-CIO-CLC v. Marshall, 647 F.2d 1189,
1264, 1301 (D.C. Cir. 1980) (``Lead I'')). The agency has also used
application groups, defined by common tasks, as the structure for its
feasibility analyses (Pub. Citizen Health Research Grp. v. OSHA, 557
F.3d 165, 177-79 (3d Cir. 2009)). The Supreme Court has broadly defined
feasible as ``capable of being done'' (Cotton Dust, 452 U.S. at 509-
10).
I. Technological Feasibility
A standard is technologically feasible if the protective measures
it requires already exist, can be brought into existence with available
technology, or can be created with technology that can reasonably be
expected to be developed (Lead I, 647 F.2d at 1272; Amer. Iron & Steel
Inst. v. OSHA, 939 F.2d 975, 980 (D.C. Cir. 1991) (``Lead II'')).
Courts have also interpreted technological feasibility to mean that a
typical firm in each affected industry or application group will
reasonably be able to implement the requirements of the standard in
most operations most of the time (see Public Citizen v. OSHA, 557 F.3d
165, 170-71 (3d Cir. 2009); Lead I, 647 F.2d at 1272; Lead II, 939 F.2d
at 990)). OSHA's standards may be ``technology forcing,'' so long as
the agency gives an industry a reasonable amount of time to develop new
technologies to comply with the standard. Thus, OSHA is not bound by
the ``technological status quo'' (Lead I, 647 F.2d at 1264).
II. Economic Feasibility
In addition to technological feasibility, OSHA is required to
demonstrate that its standards are economically feasible. A reviewing
court will examine the cost of compliance with an OSHA standard ``in
relation to the financial health and profitability of the industry and
the likely effect of such costs on unit consumer prices'' (Lead I, 647
F.2d at 1265 (citation omitted)). As articulated by the D.C. Circuit in
Lead I, ``OSHA must construct a reasonable estimate of compliance costs
and demonstrate a reasonable likelihood that these costs will not
threaten the existence or competitive structure of an industry, even if
it does portend disaster for some marginal firms'' (Lead I, 647 F.2d at
1272). A reasonable estimate entails assessing ``the likely range of
costs and the likely effects of those costs on the industry'' (Lead I,
647 F.2d at 1266). As with OSHA's consideration of scientific data and
control technology, however, the estimates need not be precise (Cotton
Dust, 452 U.S. at 528-29 & n.54), as long as they are adequately
explained.
OSHA standards satisfy the economic feasibility criterion even if
they impose significant costs on regulated industries so long as they
do not cause massive economic dislocations within a particular industry
or imperil the very existence of the industry (Lead II, 939 F.2d at
980; see also Lead I, 647 F.2d at 1272; Asbestos I, 499 F.2d. at 478).
As with its other legal findings, OSHA ``is not required to prove
economic feasibility with certainty, but is required to use the best
available evidence and to support its conclusions with substantial
evidence'' (Lead II, 939 F.2d at 980-81 (citing Lead I, 647 F.2d at
1267)).
In addition to determining economic feasibility, OSHA estimates the
costs and benefits of its proposed and final rules to ensure compliance
with other requirements such as those in Executive Orders 12866 and
13563.
D. High Degree of Employee Protection
Safety standards must provide a high degree of employee protection
to be consistent with the purpose of the Act (see Control of Hazardous
Energy Sources (Lockout/Tagout) Final Rule, Supplemental Statement of
Reasons, 58 FR 16612, 16614-15 (March 30, 1993)). OSHA has
preliminarily determined that this proposed standard is a safety
standard because the health effects associated with exposure to
occupational heat are generally acute. As explained in Section IV.,
Health Effects, the proposed standard aims to address the numerous
acute health effects of occupational exposure to hazardous heat. These
include, among other things, heat stroke, heat exhaustion, heat
syncope, and physical injuries (e.g., falls) due to fatigue or other
heat-related impairments. These harms occur after relatively short-term
exposures to hazardous heat and are typically apparent at the time of
the exposure or shortly thereafter. Consequently, the link between
these harms and heat exposures is also often apparent and they do not
implicate the concerns about latent, hidden harms that underly health
standards (see Benzene, 448 U.S. at 649 n. 54; UAW v. OSHA, 938 F.2d
1310, 1313 (D.C. Cir. 1991) (``Lockout/Tagout I''); National Grain &
Feed Ass'n v. OSHA, 866 F.2d 717, 733 (5th Cir. 1989) (``Grain
Dust'')).
Finally, although OSHA acknowledges that there is growing evidence
occupational exposure to hazardous heat may lead to some chronic
adverse health outcomes like chronic kidney disease, much of the
science in this area is still developing (see Section IV., Health
Effects). In any event, the agency expects that addressing the acute
hazards posed by heat would also protect workers from potential chronic
health outcomes by reducing workers' overall heat strain.
III. Background
A. Introduction
The Occupational Safety and Health Administration (OSHA) is
proposing a new standard to protect outdoor and indoor workers from
hazardous heat in the workplace. OSHA promulgates and enforces
occupational safety and health standards under authority granted by the
Occupational Safety and Health (OSH) Act of 1970 (29 U.S.C. 651 et
seq.).
In the absence of a Federal occupational heat standard, five States
have issued heat injury and illness prevention regulations to protect
employees exposed to heat hazards in the workplace: Minnesota (Minn. R.
5205.0110 (1997)); California (Cal. Code of Regs. tit. 8, section 3395
(2005)); Oregon (Or. Admin. R. 437-002-0156 (2022); Or. Admin. R. 437-
004-1131 (2022)); Colorado (7 Colo. Code Regs. section 1103-15 (2022));
and Washington (Wash. Admin. Code sections 296-62-095 through 296-62-
09560; 296-307-097 through 296-307-09760 (2023)). Although Minnesota
was the first State to adopt a standard covering employees exposed to
indoor environmental heat conditions, California was the first State to
adopt a standard covering employees exposed to outdoor environmental
heat conditions. Washington, Oregon, and Colorado have since enacted
similar regulations to California's, requiring employers to implement
controls and monitor for signs and symptoms of heat-related injury or
illness, among other requirements. In 2023, California proposed a new
standard that would cover indoor work environments (California, 2023).
In 2024, Maryland
[[Page 70702]]
published a proposed standard that would cover both outdoor and indoor
work environments (Maryland, 2024).
Workers in many industries are at risk for heat-related injury and
illness stemming from hazardous heat exposure (see Section V.A., Risk
Assessment). While the general population may be able to avoid and
limit prolonged heat exposure, workers across a wide range of indoor
and outdoor settings often are required to work through shifts with
prolonged heat exposure. Some workplaces have heat generation from
industrial processes and expose workers to sources of radiant heat,
such as ovens and furnaces. Additionally, employers may not take
adequate steps to protect their employees from exposure to hazardous
heat (e.g., not providing rest breaks in cool areas). Many work
operations also require the use of personal protective equipment (PPE)
that can reduce the worker's heat tolerance because it can decrease the
body's ability to cool down. Workers may also face pressure, or
incentivization through pay structures, to push through and continue
working despite high heat exposure, which can increase the risk of
heat-related injury and illness (Billikopf and Norton, 1992; Johansson
et al., 2010; Spector et al., 2015; Pan et al., 2021).
OSHA uses several terms related to excessive heat exposure
throughout this proposal. Heat stress is the combined load of heat that
a person experiences from sources of heat (i.e., metabolic heat and the
environment) and heat retention (e.g., from clothing or personal
protective equipment). Heat strain refers to the body's response to
heat stress (American Conference of Governmental Industrial Hygienists
(ACGIH), 2023). Heat-related illness means adverse clinical health
outcomes that occur due to heat exposure, such as heat exhaustion or
heat stroke. Heat-related injury means an injury linked to heat
exposure, such as a fall or cut. OSHA sometimes refers to these
collectively as ``heat-related injuries and illnesses.''
B. Need for Proposal
Occupational heat exposure affects millions of workers in the
United States. Each year, thousands of workers experience heat-related
injuries and illnesses, and some of these cases result in fatalities
(BLS, 2023b; BLS, 2024c). OSHA has relied on the General Duty Clause of
the OSH Act (discussed further below), as well as enforcement emphasis
programs and hazard alerts and other guidance, to protect workers and
inform employers of their legal obligations. However, a standard
specific to heat-related injury and illness prevention would more
clearly set forth enforceable employer obligations and the measures
necessary to effectively protect employees from hazardous heat.
Workers in both outdoor and indoor work settings without adequate
climate controls are at risk of hazardous heat exposure. In addition to
weather-related heat, certain heat-generating processes, machinery, and
equipment (e.g., hot tar ovens, furnaces) can cause hazardous heat
exposure when cooling measures are not in place. An evaluation of 66
heat-related illness enforcement investigations from 2011-2016 found
heat-related injuries and illnesses, including fatalities, occurring in
both outdoor (n=34) and indoor (n=29) work environments (Tustin et al.,
2018a). Excessive heat exacerbates existing health conditions like
asthma, diabetes, kidney failure, and heart disease, and can cause heat
stroke and death if not treated properly and promptly. Some groups may
be more likely to experience adverse health effects from heat, such as
pregnant workers (NIOSH, 2024), while others are disproportionately
exposed to hazardous levels of heat, such as workers of color in
essential jobs, who are more often employed in work settings with a
high risk of hazardous heat exposure (Gubernot et al., 2015).
The Bureau of Labor Statistics (BLS), in its Census of Fatal
Occupational Injuries, documented 1,042 U.S. worker deaths due to
occupational exposure to environmental heat from 1992-2022, with an
average of 34 fatalities per year during that period (BLS, 2024c). In
2022 alone, BLS reported 43 work-related deaths due to environmental
heat exposure (BLS, 2024c). The BLS Annual Survey of Occupational
Injuries and Illnesses (SOII) estimates 33,890 work-related heat
injuries and illnesses involving days away from work from 2011-2020,
which is an average of 3,389 injuries and illnesses occurring each year
during this period (BLS, 2023b).
Workers across hundreds of industries are at risk for hazardous
heat exposure and resulting heat-related injuries and illnesses. From
January 1, 2017, to December 31, 2022, 1,054 heat-related injuries,
illnesses, and fatalities were reported to and investigated by OSHA,
including 625 heat-related hospitalizations and 211 heat-related
fatalities, as well as 218 heat-related injuries and illnesses that did
not result in hospitalization. During this time, hospitalizations
occurred most frequently in construction, manufacturing, and postal and
delivery service. Fatalities were most frequently reported in
construction, landscaping, agriculture, manufacturing, and postal and
delivery service (as identified by 2-digit NAICS codes).
However, as explained in Section V.A., Risk Assessment, these
statistics likely do not capture the true magnitude and prevalence of
heat-related injuries, illnesses, and fatalities. Recent studies
demonstrate significant undercounting of occupational injuries and
illnesses by both the BLS SOII and OSHA's enforcement data. One reason
for this undercounting is that the BLS SOII only reports the number of
heat-related injuries and illnesses involving days away from work and
thus does not capture the full picture of heat-related injuries and
illnesses. An examination of workers' compensation claims in
California, which include more than only cases involving days away from
work, identified 3 to 6 times the number of annual heat-related illness
and injury cases than reported by BLS SOII (Heinzerling et al., 2020).
In addition, evidence has shown significant underreporting as employers
and employees are disincentivized from reporting injuries and illnesses
due to several factors, including potential increases in workers'
compensation costs or impacts on the employer's reputation, or an
employee's fear of retaliation or lack of awareness of their right to
speak out about workplace conditions (BLS, 2020b).
Heat-related injuries and illnesses may present unique challenges
to surveillance efforts. As the nature of heat-related symptoms (e.g.,
headache, fatigue) vary, some cases may be attributed to other
illnesses rather than heat (as discussed in Section IV., Health
Effects). Furthermore, heat is not always identified as a contributing
factor to fatality, as heat exposure may exacerbate existing medical
conditions and medical professionals may not witness the symptoms and
events preceding death (Luber et al., 2006).
Finally, exposure to heat can interfere with routine occupational
tasks and impact workers' psychomotor and mental performance, which can
lead to workplace injuries. Particularly, heat can impair performance
of job tasks related to complex cognitive function (Hancock and
Vasmatzidis, 2003; Piil et al., 2017) and reduce decision making
abilities (Ramsey et al., 1983; Xiang et al., 2014a) and productivity
(Foster et al., 2021). A growing body of evidence has demonstrated that
heat-induced impairments may result in significant occupational
injuries that are not currently factored into official statistics for
heat-related cases (Spector et al., 2016; Calkins et al., 2019;
Dillender, 2021; Park et al., 2021). See Section V.A., Risk Assessment,
for further
[[Page 70703]]
discussion on underreporting of heat-related injuries, illnesses, and
fatalities.
While a significant percentage of heat-related incidents are
unreported, OSHA's investigations of reported heat-related fatalities
point to many gaps in employee protections. OSHA has identified the
following circumstances in its review of 211 heat-related fatality
investigations from 2017-2022: employees left alone by employers after
symptoms started; employers not providing adequate medical attention to
employees with symptoms; employers preventing employees from taking
rest breaks; employers not providing water on-site; employers not
providing on-site access to shade; employers not providing cooling
measures on-site; and employers not having programs to acclimatize
employees to hot work environments (<a href="https://www.osha.gov/fatalities">https://www.osha.gov/fatalities</a>).
OSHA has relied on multiple mechanisms to protect employees from
hazardous heat, however, OSHA's efforts to prevent the aforementioned
circumstances have been met with challenges without a heat-specific
standard (as discussed in Section III.C.III., OSHA's Heat-Related
Enforcement).
Many U.S. States run their own OSHA-approved State Plans (e.g.,
State heat standards, voluntary consensus standards) (see Section
III.D., Other Standards), however OSHA has preliminarily determined
that this standard is still needed to protect workers from the
persistent and serious hazards posed by occupational heat exposure. As
explained in Section VI., Significance of Risk, OSHA has preliminarily
determined that a significant risk of material harm from occupational
exposure to hazardous heat exists, and issuance of this standard would
substantially reduce that risk. Therefore, to more clearly set forth
employer obligations and the measures necessary to more effectively
protect employees from hazardous heat, and reduce the number and
frequency of occupational injuries, illness, and fatalities caused by
exposure to hazardous heat, OSHA is proposing a Federal standard for
Heat Injury and Illness Prevention for Outdoor and Indoor Work
Settings.
C. Events Leading to the Proposal
I. History of Heat as a Recognized Occupational Hazard
Heat exposure has long been recognized as an occupational hazard.
For example, in the United States, the occupational hazards associated
with the construction of the Hoover Dam between 1931 and 1935 brought
attention to the effects of heat on worker health. The Bureau of
Reclamation reported that 14 dam workers and two others residing in the
work area died from ``heat prostration'' in 1931 (Bureau of
Reclamation, 2015). According to a local newspaper, temperatures at the
dam site that summer reached 140 [deg]F in the sun and 120 [deg]F in
the shade (Turk, 2018; Rogers, 2012). In response to the extreme heat
of the summer and other unsafe working conditions, the Industrial
Workers of the World convinced Hoover Dam workers to strike over safety
concerns (Turk, 2018; Rogers, 2012). Six Companies, the conglomerate of
companies hired by the Bureau of Reclamation to construct most of the
dam, was forced to make concessions, including protections against HRI
such as providing potable water in dormitories, bringing ice water to
workers at their work sites, and adding first aid stations closer to
the job site (Rogers, 2012). The heat-related deaths that occurred
during 1931 also prompted Harvard University researchers from the
Harvard Fatigue Laboratory to travel to the Hoover Dam and study the
relationship between hot, dry temperatures, physical performance, and
heart rate (Turk, 2018).
Heat-related illnesses were identified as a major concern for the
U.S. military in the 1940s and 1950s. Between 1942 and 1944, 198
soldiers died of heat stroke at U.S.-based training camps, 157 of which
did not have a known history of cardiac diseases or other conditions
that may predispose them to heat illness (Schickele, 1947, p. 236).
This led to investigations of the environmental conditions at the time
of these deaths, and eventually to the development of wet bulb globe
temperature (WBGT) to measure heat stress (Yaglou and Minard, 1957;
Minard, 1961; Department of the Army, 2022; Department of the Navy,
2023).
Research on the effects of occupational heat exposure continued in
the 1960s, as researchers conducted trials examining the physiological
effects of work at various temperatures (e.g., Lind, 1963). Findings
from these trials would eventually underpin the American Conference of
Governmental Industrial Hygienists (ACGIH) Threshold Limit Value (TLV),
as well as the National Institute of Occupational Safety and Health
(NIOSH) Recommended Exposure Limit (REL) (Dukes-Dobos and Henschel,
1973). ACGIH first proposed guidelines for a TLV in 1971, which were
later adopted in 1974.
Heat was recognized as a preventable workplace hazard in the
legislative history of the OSH Act. Senator Edmund Muskie submitted a
letter in support of the OSH Act into the Congressional record on
behalf of ``a distinguished group of citizens, including a former
Secretary of Labor and several noted scientists.'' (Senate Debate on S.
2193, Nov. 16, 1970), reprinted in Legislative History of the
Occupational Safety and Health Act of 1970, pp. 513-14 (1971)
(Committee Print) (``Leg. Hist.''). The letter states, ``Most
industrial diseases and accidents are preventable. Modern technological
and medical sciences are capable of solving the problems of noise,
dust, heat, fumes, and toxic substances in the plants. However,
existing legislation in this area does not begin to meet the problems''
(Leg. Hist., pp. 513-14).
In 1972, just two years after promulgation of the OSH Act, NIOSH
first recommended a potential OSHA heat standard in its Criteria for a
Recommended Standard (NIOSH, 1972). This criteria document, issued
under the authority of section 20(a) of the OSH Act, recommended an
OSHA standard based on a critical review of scientific and technical
information. In response, an OSHA Standards Advisory Committee on Heat
Stress was appointed in 1973 and presented recommendations for a
standard for work in hot environments in 1974. At the time, 12 of 15
members of the advisory committee agreed that occupational heat stress
warranted a standard (Ramsey, 1975).
NIOSH's criteria document for a recommended standard has since been
updated in 1986 (NIOSH, 1986) and again in 2016 (NIOSH, 2016). The 2016
criteria document recommends various provisions to protect workers from
heat stress, including rest breaks, hydration, shade, acclimatization
plans, and worker training (NIOSH, 2016). The 2016 criteria document
also recommends that no worker be ``exposed to combinations of
metabolic and environmental heat greater than'' the recommended alert
limit (RAL) for unacclimatized workers or the recommended exposure
limit (REL) for acclimatized workers). The document recommends that
environmental heat be assessed with measurements of WBGT (NIOSH, 2016).
A detailed report of the history of heat as a recognized
occupational hazard is available in the docket (ERG, 2024a). The report
summarizes historical documentation of occupational heat-related
illness beginning in ancient times and from the eighteenth century
through the regulatory interest in the twentieth century.
[[Page 70704]]
II. OSHA's Heat Injury and Illness Prevention Efforts
In 2011, OSHA issued a memorandum to inform regional administrators
and State Plan designees of inspection guidance for heat-related
illnesses (OSHA, 2011). That same year, OSHA launched the Heat Illness
Prevention Campaign (<a href="https://www.osha.gov/heat">https://www.osha.gov/heat</a>) to build awareness of
prevention strategies and tools for employers and workers to reduce
occupational heat-related illness. In its original form, the Campaign
delivered a message of ``Water. Rest. Shade.'' The agency updated
Campaign materials in 2021 to recognize both indoor and outdoor heat
hazards, as well as the importance of protecting new and returning
workers from hazardous heat with an acclimatization period.
In addition, OSHA maintains on its website a Heat Topics page on
workplace heat exposure (<a href="https://www.osha.gov/heat">https://www.osha.gov/heat</a>-exposure/), which
provides additional information and resources. The page provides
information on planning and supervision in hot work environments,
identification of heat-related illness and first aid, information on
prevention such as training, calculating heat stress and controls,
personal risk factors, descriptions of other heat standards and case
study examples of situations where workers developed heat-related
illness. OSHA and NIOSH also co-developed a Heat Safety Tool Smartphone
App for both Android and iPhone devices (see <a href="http://www.osha.gov/heat/heat-app">www.osha.gov/heat/heat-app</a>). The app provides outdoor, location-specific temperature,
humidity, and heat index (HI) readings. Measurements for indoor work
sites must be collected and manually entered into the app by the user
for accurate calculations. The app also provides relevant information
on identifying signs and symptoms of heat-related illness and steps to
prevent heat-related injuries and illnesses. Despite the strengths and
reach of the Campaign, Heat Topics page, and Heat Safety Tool App,
these guidance and communication materials are not legally enforceable
requirements.
III. OSHA's Heat-Related Enforcement
Without a specific standard governing hazardous heat conditions at
workplaces, the agency currently enforces section 5(a)(1) (the General
Duty Clause) of the OSH Act against employers that expose their workers
to this recognized hazard. Section 5(a)(1) states that employers have a
general duty to furnish to each of their employees ``employment and a
place of employment which are free from recognized hazards that are
causing or are likely to cause death or serious physical harm'' to
employees (29 U.S.C. 654(a)(1)). To prove a violation of the General
Duty Clause, OSHA must establish--in each individual case--that: (1)
the employer failed to keep the workplace free of a hazard to which its
employees were exposed; (2) the hazard was recognized; (3) the hazard
was causing or likely to cause death or serious injury; and (4) a
feasible means to eliminate or materially reduce the hazard existed
(see, e.g., A.H. Sturgill Roofing, Inc., 2019 O.S.H. Dec. (CCH) ]
[thinsp]33712, 2019 WL 1099857 (No. 13-0224, 2019)).
OSHA has relied on the General Duty Clause to cite employers for
heat-related hazards for decades (see, e.g., Duriron Co., 11 BNA OSHC
1405, 1983 WL 23869 (No. 77-2847, 1983), aff'd, 750 F.2d 28 (6th Cir.
1984)). According to available OSHA enforcement data, between 1986 and
2023, Federal OSHA issued at least 348 hazardous heat-related citations
under the General Duty Clause. Of these citations, 85 were issued
between 1986-2000 (OSHA, 2024b). Citations were identified using
multiple queries of OSHA enforcement data and then manually reviewed to
ensure the inclusion of only citations due to heat exposure and no
other exposures (e.g., burns or explosions). Several keywords were
utilized to filter the data for inclusion (e.g., ``heat,'' ``heat
stress,'' ``heat illness,'' ``WBGT'') and exclusion (e.g.,
``explosion,'' ``flash,'' ``electrical burn,'' ``fire''). Due to
limitations of the data set on which OSHA relied, OSHA did not have
access to violation text descriptions of citations issued before the
mid-1980s and thus did not determine how many are related to heat
exposure prior to this time period. Additionally, over half of the
citations from 1986-1989 are missing violation text descriptions, which
likely resulted in an undercount of heat-related citations.
OSHA has used its general inspection authority (29 U.S.C. 657) to
target heat-related injuries and illnesses in various Regional Emphasis
Programs (REPs). OSHA enforcement emphasis programs focus the agency's
resources on particular hazards or high-hazard industries (see Marshall
v. Barlow's, Inc., 436 U.S. 307, 321 (1978) (affirming OSHA's use of an
administrative plan containing specific neutral criteria to focus
inspections)). OSHA's Region VI regional office, located in Dallas, TX,
has a heat-related special REP (OSHA, 2019). This region covers Texas,
New Mexico, Oklahoma, Arkansas, and Louisiana. OSHA's Region IX
regional office, located in San Francisco, CA, also has a heat-related
REP (OSHA, 2022). This region covers American Samoa, Arizona,
California, Guam, Hawaii, Nevada, and the Northern Mariana Islands.
These REPs allow field staff to conduct heat illness inspections of
outdoor work activities on days when the high temperature is forecasted
to be above 80 [deg]F.
On September 1, 2021, OSHA issued updated Inspection Guidance for
Heat-Related Hazards, which established a new enforcement initiative to
protect employees from heat-related injuries and illnesses while
working in hazardous hot indoor and outdoor environments (OSHA, 2021).
The guidance provided that days when the heat index exceeds 80 [deg]F
would be considered heat priority days. It announced that enforcement
efforts would be increased on heat priority days for a variety of
indoor and outdoor industries, with the aim of identifying and
mitigating potential hazards and preventing heat-illnesses before they
occur.
In April 2022, OSHA launched a National Emphasis Program (NEP) to
protect employees from heat-related hazards and resulting injuries and
illnesses in outdoor and indoor workplaces. The NEP expanded the
agency's ongoing heat-related injury and illness prevention initiatives
and campaign by setting forth a targeted enforcement component and
reiterating its compliance assistance and outreach efforts. The NEP
targets specific industries expected to have the highest exposures to
heat-related hazards and resulting illnesses and deaths. This approach
is intended to encourage early interventions by employers to prevent
illnesses and deaths among workers during high heat conditions (CPL 03-
00-024). As of June 26, 2024, OSHA has conducted 5,038 Heat NEP Federal
inspections. More than 1,229 of these were initiated by complaints and
117 were due to the occurrence of a fatality or catastrophe. As a
result of these inspections, OSHA issued 56 General Duty Clause
citations and 736 Hazard Alert Letters (HALs). Inspections occurred
across various industries (as identified by 2-digit NAICS codes)
including construction, which had the highest number of inspections, as
well as manufacturing, maritime, agriculture, transportation,
warehousing, food services, waste management, and remediation services.
On July 27, 2023, OSHA issued a heat hazard alert to remind
employers of their obligation to protect workers against heat injury
and illness in outdoor and indoor workplaces. The alert highlights what
employers can and
[[Page 70705]]
should be doing to protect employees. It also serves to remind
employees of their rights, including protections against retaliation.
In addition, the alert highlights steps OSHA is currently taking to
protect workers and directs employers, employees, and the public to
OSHA resources, including guidance and fact sheets on heat.
OSHA's efforts to protect employees from hazardous heat conditions
using the General Duty Clause, although important, have limitations
leaving many workers vulnerable to heat-related hazards. For example,
the Commission has struggled to determine exactly what conditions
create a recognized heat hazard under the General Duty Clause, and has
therefore suggested the necessity of a standard (see, A.H. Sturgill
Roofing, Inc., 2019 OSHD (CCH) ] [thinsp]33712, 2019 WL 1099857, at *2-
5 and n.8 (No. 13-0224, 2019) (``The Secretary's failure to establish
the existence of an excessive heat hazard here illustrates the
difficulty in addressing this issue in the absence of an OSHA
standard.''); U.S. Postal Service, 2023 OSHD (CCH) ] 33908, 2023 WL
2263313, at *3 n.7 (Nos. 16-1713, 16-1872, 17-0023,17-0279, 2023)
(noting Commissioner Laihow's opinion that ``A myriad of factors, such
as the geographical area where the work is being performed and the
nature of the tasks involved, can impact'' whether excessive heat is
present, and indicating that a standard is therefore necessary to
define the hazard).
Under the General Duty Clause, OSHA cannot require abatement before
proving in an enforcement proceeding that specific workplace conditions
are hazardous; whereas a standard would establish the existence of the
hazard at the rulemaking stage, thus allowing OSHA to identify and
require specific abatement measures without having to prove the
existence of a hazard in each case (see Sanderson Farms, Inc. v. Perez,
811 F.3d 730, 735 (5th Cir. 2016) (``Since OSHA is required to
determine that there is a hazard before issuing a standard, the
Secretary is not ordinarily required to prove the existence of a hazard
each time a standard is enforced.'')). Given OSHA's burden under the
General Duty Clause, it is currently difficult for OSHA to ensure
necessary abatement before employee lives and health are unnecessarily
endangered. Further, under the General Duty Clause OSHA must largely
rely on expert witness testimony to prove both the existence of a
hazard and the availability of feasible abatement measures that will
materially reduce or eliminate the hazard in each individual case (see,
e.g., Industrial Glass, 15 BNA OSHC 1594, 1992 WL 88787, at *4-7 (No.
88-348, 1992)).
Moreover, as OSHA has noted in similar contexts, standards have the
advantage of providing greater clarity to employers and employees of
the measures required to protect employees and are developed with the
benefit of information gathered in the notice and comment process (see
86 FR 32376, 32418 (Jun. 21, 2021) (COVID-19 Healthcare ETS); 56 FR
64004, 64007 (Dec. 6, 1991) (Bloodborne Pathogens Standard)).
OSHA currently has other existing standards that, while applicable
to some issues related to hazardous heat, have not proven to be
adequate in protecting workers from exposure to hazardous heat. For
example, OSHA's Recordkeeping standard (29 CFR 1904.7) requires
employers to record and report injuries and illnesses that meet
recording criteria. Additionally, the agency's Sanitation standards (29
CFR 1910.141, 1915.88, 1917.127, 1926.51, and 1928.110) require
employers to provide potable water readily accessible to workers. While
these standards require that drinking water be made available in
``sufficient amounts,'' they do not specify quantities, and employers
are not required to encourage workers to frequently hydrate on hot
days.
OSHA's Safety Training and Education standard (29 CFR 1926.21)
requires employers in the construction industry to train employees in
the recognition, avoidance, and prevention of unsafe conditions in
their workplaces. OSHA's PPE standards (29 CFR 1910.132, 1915.152,
1917.95, and 1926.28) require employers to conduct a hazard assessment
to determine the appropriate PPE to be used to protect employees from
the hazards identified in the assessment. However, hazardous heat is
not specifically identified as a hazard for which workers need training
or PPE, complicating the application of these requirements to hazardous
heat.
IV. Rulemaking Activities Leading to This Proposal
OSHA has received multiple petitions to promulgate a heat injury
and illness prevention standard, including in 2018 from Public Citizen,
on behalf of approximately 130 organizations (Public Citizen et al.,
2018). OSHA has also been urged by members of Congress to initiate
rulemaking for a Federal heat standard, as well as by the Attorneys
General of several States in 2023.
On October 27, 2021, OSHA published an advance notice of proposed
rulemaking (ANPRM) for Heat Injury and Illness Prevention in Outdoor
and Indoor Work Settings in the Federal Register (86 FR 59309)
(referred to as ``the ANPRM'' hereafter). The ANPRM outlined key issues
and challenges in occupational heat-related injury and illness
prevention and aimed to collect evidence, data, and information
critical to informing how OSHA proceeds in the rulemaking process. The
ANPRM included background information on injuries, illnesses, and
fatalities due to heat, underreporting, scope, geographic region, and
inequality in exposures and outcomes. The ANPRM also covered existing
heat injury and illness prevention efforts, including OSHA's efforts,
the NIOSH criteria documents, State standards, and other standards. The
initial public comment period was extended and closed on January 26,
2022. In response to the ANPRM, OSHA received 965 unique comments. The
comments covered several topics, including the scope of a standard,
heat stress thresholds for workers across various industries, heat
acclimatization planning, and heat exposure monitoring, as well as the
nature, types, and effectiveness of controls that may be required as
part of a standard.
Following the publication of the ANPRM, OSHA presented topics from
the ANPRM and updates on the heat rulemaking to several stakeholders,
including several trade associations, the Office of Advocacy of the
Small Business Administration's (SBA's Office of Advocacy) Labor Safety
Roundtable (November 19, 2021), and NIOSH National Occupational
Research Agenda (NORA) councils, including the Construction Sector
Council (November 17, 2021), Landscaping Safety Workgroup (January 12,
2022), and Oil and Gas Extraction Sector (April 7, 2022).
On May 3, 2022, OSHA held a virtual public stakeholder meeting on
the agency's ``Initiatives to Protect Workers from Heat-Related
Hazards.'' A total of over 1,300 people attended the virtual meeting,
and the recorded video has been viewed over 3,500 times (see
<a href="http://www.youtube.com/watch?v=Ud29WsnsOw8">www.youtube.com/watch?v=Ud29WsnsOw8</a>) as of June 2024. The six-hour
meeting provided stakeholders an opportunity to learn about and comment
on efforts OSHA is taking to protect workers from heat-related hazards
and ways the public can participate in the agency's rulemaking process.
OSHA also established a Heat Injury and Illness Prevention Work
Group of the National Advisory Committee on Occupational Safety and
Health (NACOSH) to support the agency's rulemaking and outreach
efforts. The Work Group was tasked with reviewing
[[Page 70706]]
and developing recommendations on OSHA's heat illness prevention
guidance materials, evaluating stakeholder input, and developing
recommendations on potential elements of any proposed heat injury and
illness prevention standard. On May 31, 2023, the Work Group presented
its recommendations on potential elements of a proposed heat injury and
illness prevention standard for consideration by the full NACOSH
committee. The Work Group recommended that any proposed heat injury and
illness prevention standard include: a written exposure control plan/
heat illness prevention plan; training; environmental monitoring;
workplace control measures; acclimatization; worker participation; and
emergency response (Document ID OSHA-2023-0003-0007). After
deliberations, NACOSH amended the report to ask OSHA to include a model
written plan and then submitted its recommendations to the Secretary of
Labor (Document ID OSHA-2023-0003-0012).
As an initial rulemaking step, OSHA convened a Small Business
Advocacy Review Panel (SBAR Panel) on August 25, 2023, in accordance
with the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et seq.), as
amended by the Small Business Regulatory Enforcement Act (SBREFA) of
1996. This SBAR Panel consisted of members from OSHA, SBA's Office of
Advocacy, and the Office of Information and Regulatory Affairs (OIRA)
in the White House Office of Management and Budget (OMB). The SBAR
Panel identifies individual representatives of affected small entities,
termed small entity representatives (SERs), which includes small
businesses, small local government entities, and non-profits. This
process enabled OSHA, with the assistance of SBA's Office of Advocacy
and OIRA, to obtain advice and recommendations from SERs about the
potential impacts of the regulatory options outlined in the regulatory
framework and about additional options or alternatives to the
regulatory framework that may alleviate those impacts while still
meeting the objectives and requirements of the OSH Act.
The SBAR Panel hosted six online meetings on September 9, 12, 13,
14, 18, and 19, 2023, with participation from a total of 82 SERs from a
wide range of industries. A final report containing the findings,
advice, and recommendations of the SBAR Panel was submitted to the
Assistant Secretary of Labor for Occupational Safety and Health on
November 3, 2023, to help inform the agency's decision making with
respect to this rulemaking (Document ID OSHA-2021-0009-1059).
In accordance with 29 CFR parts 1911 and 1912, OSHA presented to
the Advisory Committee on Construction Safety and Health (ACCSH) on its
framework for a proposed rule for heat injury and illness prevention in
outdoor and indoor work settings on April 24, 2024. The Committee then
passed unanimously a motion recommending that OSHA proceed
expeditiously with proposing a standard on heat injury and illness
prevention. The Committee also recommended that OSHA consider the
feedback and questions discussed by Committee members during the
meeting in formulating the proposed rule (see the minutes from the
meeting, Docket No. 2024-0002). OSHA has considered the Committee's
feedback in the development of this proposal.
In accordance with Executive Order 13175, Consultation and
Coordination with Indian Tribal Governments, 65 FR 67249 (Nov. 6,
2000), OSHA held a listening session with Tribal representatives
regarding this Heat Injury and Illness Prevention in Outdoor and Indoor
Work Settings rulemaking on May 15, 2024. OSHA provided an overview of
the rulemaking effort and sought comment on what, if any, tribal
implications would result from the rulemaking. A summary of the meeting
and list of attendees can be viewed in the docket (DOL, 2024a).
D. Other Standards
Various other organizations have also either identified the need
for standards to prevent occupational heat-related injury and illness
or published their own standards. In 2024, the American National
Standards Institute/American Society of Safety Professionals A10
Committee (ANSI/ASSP) published a consensus standard on heat stress
management in construction and demolition operations. The International
Organization for Standardization (ISO) also has a standard for
evaluating heat stress: ISO 7243: Ergonomics of the thermal
environments--Assessment of heat stress using the WBGT (wet bulb globe
temperature) index (ISO, 2017). ISO 7243 uses WBGT values, along with
metabolic rate, to assess hot environments, similar to ACGIH and NIOSH
recommendations. Additional ISO standards address predicting sweat rate
and core temperature (ISO 7933), and determining metabolic rate (ISO
8996), physiological strain (ISO 9886), and thermal characteristics for
clothing (ISO 9920). In 2021, the American Society for Testing and
Materials (ASTM) finalized its Standard Guide for Managing Heat Stress
and Heat Strain in Foundries (E3279-21) which establishes ``best
practices for recognizing and managing occupational heat stress and
heat strain in foundry environments.'' The standard outlines employer
responsibilities and recommends elements for a ``Heat Stress and Heat
Strain Management Program'' (ASTM, 2021).
ACGIH has identified TLVs for heat stress (ACGIH, 2023). The TLVs
utilize WBGT and take into consideration metabolic rate or workload
categories. Additionally, ACGIH provides clothing adjustment factors
which are added to the measured WBGT for certain types of work clothing
to account for the impaired thermal regulation.
The U.S. Armed Forces has developed extensive heat-related illness
prevention and management strategies. The Warrior Heat and Exertion
Related Events Collaborative is a tri-service group of military leaders
focused on clinical, educational, and research efforts related to
exercise and exertional heat-related illnesses and medical emergencies
(HPRC, 2023). The U.S. Army has a Heat Center at Fort Benning which
focuses on management, research, and prevention of heat-related illness
and death (Galer, 2019). In 2023, the U.S. Army updated its Training
and Doctrine Command (TRADOC) Regulation 350-29 addressing heat and
cold casualties. The regulation includes requirements for rest and
water consumption according to specific WBGT levels and work intensity
(Department of the Army, 2023). The U.S. Navy has developed
Physiological Heat Exposure Limit curves that are based on metabolic
and environmental heat loads and represent the maximum allowable heat
exposure limits, which were most recently updated in 2023. The Navy
monitors WBGT and has guidelines based on these measurements, with
physical training diminishing as WBGTs increase and all nonessential
outdoor activity stopped when WBGTs exceed 90 [deg]F (Department of the
Navy, 2023). The U.S. Marine Corps follows the Navy's guidelines for
implementation of the Marine Corps Heat Injury Prevention Program
(Commandant of the Marine Corps, 2002). In 2022, the U.S. Army and U.S.
Air Force issued an update to their technical heat stress bulletin,
which outlines measures to prevent indoor and outdoor heat-related
illness in soldiers. The bulletin includes recommended acclimatization
planning, work-rest cycles, fluid and electrolyte replacement, and
limitations on work based on WBGT (Department of the Army, 2022).
[[Page 70707]]
As of April 2024, five States have promulgated heat standards
requiring employers in various industries and workplace settings to
implement protections to reduce the risk of heat-related injuries and
illnesses for their employees: California, Minnesota, Oregon,
Washington, and Colorado. In addition, Maryland and California are
currently engaged in rulemaking. State standards differ in the scope of
coverage (see tables III-1 and 2). For example, Minnesota's standard
covers only indoor workplaces. California and Washington standards
cover only outdoor workplaces, although California's proposal would
include coverage of indoor workplaces. Oregon's rule covers both indoor
and outdoor workplaces. State rules also differ in the methods used for
triggering protections against hazardous heat. Minnesota's standard
considers the type of work being performed (light, moderate, or heavy)
and provides WBGT trigger levels based on the type of work activity.
California's heat-illness prevention protections go into effect at an
ambient temperature of 80 [deg]F. Washington's rule also relies on
ambient temperature readings combined with considerations for the
breathability of workers' clothing. Oregon's rule uses a heat index 80
[deg]F as a trigger.
California, Washington, Colorado, and Oregon all have additional
protections that are triggered by high heat. However, they differ as to
the trigger for these additional protections. In California, high heat
protections are triggered at an ambient temperature reading of 95
[deg]F (and only apply in certain industries). In Washington, high heat
protections are triggered at an ambient temperature reading of 90
[deg]F. In Colorado, additional protections are triggered at an ambient
temperature reading of 95 [deg]F or by other factors such as unhealthy
air quality, length of workday, heaviness of clothing or gear, and
acclimatization status. These additional protections only apply to the
agricultural industry. Finally, in Oregon, high heat protections are
triggered at a heat index of 90 [deg]F.
All the State standards require training for employees and
supervisors. All the State standards, except for Minnesota, require
employers to provide at least one quart of water per hour for each
employee, require some form of emergency response plan, include
provisions related to acclimatization for workers, and require access
to shaded break areas. Washington and Oregon require that employers
provide training in a language that the workers understand. Similarly,
California's standard requires that employers create a written heat-
illness prevention plan in English as well as in whatever other
language is understood by the majority of workers at a given workplace.
California also requires close monitoring of new employees for the
first fourteen days and monitoring of all employees during a heat wave.
Table III-1 below provides an overview of the provisions included in
the existing and proposed State standards on heat injury and illness
prevention. Table III-2 provides an overview of the additional
provisions required when the high heat trigger is met or exceeded.
Table III-1--Initial Heat Triggers and Provisions in State Heat Standards
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
Shade or
Threshold Provision of cool-down Rest breaks Emergency Acclimatization Training Heat illness prevention Observation/
water means if needed response plan supervision
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
General
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
California: Outdoor................... 80 [deg]F (Ambient) \1\.. <bullet> <bullet> <bullet> <bullet> <bullet> <bullet> <bullet>................ ............
Washington: Outdoor................... 80 [deg]F (Ambient), All <bullet> <bullet> <bullet> <bullet> <bullet> <bullet> <bullet> (accident ............
other clothing; 52 prevention).
[deg]F, Non-breathable
clothes.
Colorado: Agriculture................. 80 [deg]F (Ambient)...... <bullet> <bullet> <bullet> <bullet> <bullet> <bullet> ........................ <bullet>
California (proposal): Indoor......... 82 [deg]F (Ambient)...... <bullet> <bullet> <bullet> <bullet> <bullet> <bullet> <bullet>................ ............
Maryland (proposal): Indoor & Outdoor. 80 [deg]F (Heat Index)... <bullet> <bullet> ............ <bullet> <bullet> <bullet> <bullet>................ ............
Minnesota: \2\ Indoor................. 86 [deg]F (WBGT), Light ............ ............ ............ ............ ............... <bullet> ........................ ............
work; 80 [deg]F,
Moderate work; 77
[deg]F, Heavy work.
Oregon: Indoor & Outdoor.............. 80 [deg]F (Heat Index)... <bullet> <bullet> ............ <bullet> <bullet> <bullet> <bullet>................ ............
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Some provisions, including water, emergency response, training, and heat illness prevention plan, apply to covered employers regardless of the temperature threshold.
\2\ Minnesota uses a 2-hour time-weighted average permissible exposure limit rather than a trigger.
Table III-2--High Heat Triggers and Additional Provisions in State Heat Standards
----------------------------------------------------------------------------------------------------------------
Assessment
Threshold Work-rest Observation/ Pre-shift and control
schedule supervision meetings measures \1\
----------------------------------------------------------------------------------------------------------------
Additional High Heat Provisions
----------------------------------------------------------------------------------------------------------------
California: Outdoor \2\....... 95 [deg]F <bullet> (only <bullet>........ <bullet> ............
(Ambient). agriculture).
Washington: Outdoor........... 90 [deg]F <bullet>........ <bullet>........ ............ ............
(Ambient).
Colorado: Agriculture......... 95 [deg]F <bullet>........ covered in <bullet> ............
(Ambient) or general
other condition provisions
\3\. above.
California (proposal): Indoor. 87 [deg]F ................ ................ ............ <bullet>
(Ambient or
Heat Index) or
other
conditions \4\.
Maryland (proposal): Indoor & 90 [deg]F (Heat <bullet>........ <bullet>........ ............ ............
Outdoor. Index).
Oregon: Indoor & Outdoor...... 90 [deg]F (Heat <bullet>........ <bullet>........ ............ ............
Index).
----------------------------------------------------------------------------------------------------------------
\1\ Assessment and control measures include measuring temperature and heat index, identifying and evaluating all
other environmental risk factors for heat illness, and using specified control measures to minimize the risk
of heat illness.
[[Page 70708]]
\2\ High heat procedures apply in agriculture; construction; landscaping; oil and gas extraction; transportation
or delivery of agricultural products, construction materials or other heavy materials, except for employment
that consists of operating an air-conditioned vehicle and does not include loading or unloading.
\3\ Other conditions include unhealthy air quality, shifts over 12 hours, heavy clothing or gear required, or
the employee is new or returning from absence.
\4\ Other conditions include wearing clothing that restricts heat removal, or working in a high radiant heat
area, when the ambient temperature is at or above 82 [deg]F.
IV. Health Effects
A. Introduction
I. Health Effects of Occupational Heat Exposure
Exposure to workplace heat can be seriously detrimental to workers'
health and safety and, in some cases, can be fatal. Workplace heat
contributes to heat stress, which is a person's total heat load (NIOSH,
2016) from the following sources combined: (1) heat from the
environment, including heat generated by equipment or machinery; (2)
metabolic heat generated through body movement, which is proportional
to one's relative level of exertion (Sawka et al., 1993; Astrand 1960);
and (3) heat retained due to clothing or personal protective equipment
(PPE), which is highly dependent on the breathability of the clothing
and PPE worn (Bernard et al., 2017). Heat is routinely an occupation-
specific risk because, for example, workers may experience greater heat
stress than non-workers, particularly when they are required to work
through shifts with prolonged heat exposure, complete tasks that
require physical exertion, and/or their employers do not take adequate
steps to protect them from exposure to hazardous heat. In addition,
many work operations require the use of PPE. PPE can increase heat
stress and can reduce workers' heat tolerance by decreasing the body's
ability to cool down. Workers may also face pressure, or
incentivization through pay structures (e.g., piece-rate, bonuses), to
work through hazardous heat. Pressure to produce results and be seen as
a good worker can have a direct impact on worker self-care choices that
impact health (Wadsworth et al., 2019). Pay structures and production
quotas intended to motivate workers may also compromise worker safety
(Iglesias-Rios et al., 2023). These pressures can increase their risk
of heat-related injury and illness (Billikopf and Norton, 1992;
Johansson et al., 2010; Spector et al., 2015; Pan et al., 2021). The
body's response to heat stress is called heat strain (NIOSH, 2016). As
the heat stress a person experiences increases, the body attempts to
cool itself by releasing heat into the surrounding environment. If the
body begins to acquire heat faster than it can release it, the body
will store heat. As stored heat accumulates, the body can show signs of
excessive heat strain, such as increased core temperature and heart
rate, as well as symptoms of heat strain, such as sweating, dizziness,
or nausea.
Two large meta-analyses (n=2,409 and n=11,582) \1\ have confirmed
that occupational heat exposure is associated with both signs and
symptoms of heat strain (Ioannou et al., 2022; Flouris et al., 2018).
In one, the authors found a high prevalence of heat strain (35%) among
workers in hot conditions, defined by the authors as WBGT greater than
26 [deg]C (78.8 [deg]F); they also found that workers in hot conditions
were four times more likely to experience signs and symptoms of heat
strain than workers in more moderate conditions (Flouris et al., 2018).
---------------------------------------------------------------------------
\1\ In the Health Effects section, OSHA refers to statistics
that were reported by authors when describing results from their
research studies. These include the sample size (n), the odds ratio
(OR), the confidence interval (CI), and the p-value (p). These
statistics provide information about effect size, error, and
statistical significance.
---------------------------------------------------------------------------
II. Literature Review for Health Effects Section
OSHA conducted a non-systematic review of the medical and
scientific literature to identify evidence on the relationship between
heat exposure and illnesses and death. OSHA's literature review focused
on meta-analyses, systematic reviews, and studies cited in NIOSH's
Criteria for a Recommended Standard: Occupational Exposure to Heat and
Hot Environments, published in 2016. OSHA separately searched for
additional meta-analyses and systematic reviews that were not cited in
the NIOSH Criteria document, including those that were published after
the document was released (i.e., 2016 and on).
OSHA also reviewed sentinel epidemiological evidence including
observational, experimental, and randomized controlled studies. OSHA
primarily reviewed epidemiological studies focusing on worker
populations, athletes, and military members, but also included studies
in non-worker populations where appropriate. For example, when there
was limited occupation-specific research or data for some heat-related
health effects, OSHA sometimes considered general population studies as
they relate to understanding physiological mechanisms of heat-related
illness, severity of an illness, and prognosis. In addition to the
evidence of heat-related illnesses and deaths, OSHA reviewed a large
body of evidence that evaluated the association of occupational heat
exposure with workplace injuries such as falls, collisions, and other
accidents. OSHA also reviewed evidence regarding individual factors
such as age, medication use, and certain medical conditions that may
affect one's risk for heat-related health effects.
III. Summary
The best available evidence in the scientific and medical
literature, as summarized in this Health Effects section, demonstrates
that occupational heat exposure can result in death; illnesses,
including heat stroke, heat exhaustion, heat syncope, rhabdomyolysis,
heat cramps, hyponatremia, heat edema, and heat rash; and heat-related
injuries, including falls, collisions, and other workplace accidents.
B. General Mechanisms of Heat-Related Health Effects
This section briefly describes the mechanisms of heat-related
health effects, i.e., how the body's physiological responses to heat
exposure can lead to the heat-related health effects identified in
OSHA's literature review. More detailed information about the
mechanisms underpinning each specific heat-related health effect is
described in the relevant subsections that follow.
As explained above, occupational heat exposure contributes to heat
stress. The resulting bodily responses are collectively referred to as
heat strain (Cramer and Jay, 2016). The bodily responses included in
heat strain serve to decrease stored heat by increasing heat loss to
the environment to maintain a stable body temperature (NIOSH, 2016).
When the brain recognizes that the body is storing heat, it activates
the autonomic nervous system to initiate cooling (Kellogg et al., 1995;
Wyss et al., 1974). Blood is shunted towards the skin and vasodilation
begins, meaning that the blood vessels near the skin's surface become
wider, thereby increasing blood flow near the surface of the skin
(Kamijo et al., 2005; Hough and Ballantyne, 1899). The autonomic
nervous system also triggers the body's sweat response, in which sweat
glands release water to wet the skin (Roddie et al., 1957; Grant and
Holling, 1938). These processes allow the body to cool in four ways:
(1) radiation, i.e., when heat is released directly into the
[[Page 70709]]
surrounding air; (2) convection, i.e., when there is air movement that
moves heat away from the body; (3) evaporation, i.e., when sweat on the
skin diffuses into surrounding air (as clothing/PPE permits) and (4)
conduction, i.e., when heat is directly transferred through contact
with a cooler surface (e.g., wearing an ice-containing vest (Cramer and
Jay, 2016; Leon and Kenefick, 2012)).
Importantly, the extent of heat release through radiation,
convection, and evaporation depends on environmental conditions such as
the speed of air flow, temperature, and relative humidity (Clifford et
al., 1959; Brebner et al., 1958). For example, when relative humidity
is high, sweat is less likely to evaporate off the skin, which
significantly reduces the cooling effect of evaporation. Additionally,
when sweat remains on the skin and irritates the sweat glands, it can
cause a condition known as heat rash, whereby itchy red clusters of
pimples or blisters develop on the skin (DiBeneditto and Worobec, 1985;
Sulzberger and Griffin, 1968).
While the purpose of the sweat response is to cool the body, in
doing so, it can deplete the body's stores of water and electrolytes
(e.g., sodium [Na], potassium [K], chloride [Cl], calcium [Ca], and
magnesium [Mg]) that are essential for normal bodily function
(Shirreffs and Maughan, 1997). The condition resulting from abnormally
low sodium levels is known as hyponatremia. When stores of electrolytes
are depleted, painful muscle spasms known as heat cramps can occur
(Kamijo and Nose, 2006). Additionally, depletion of the body's stored
water causes dehydration, which is known to reduce the body's
circulating blood volume (Trangmar and Gonzalez-Alonso, 2017; Dill and
Costill, 1974).
During vasodilation that happens as the body attempts to cool,
blood can pool in areas of the body that are most subject to gravity,
and fluid can seep from blood vessels causing noticeable swelling under
the skin (known as heat edema). Upright standing would further
encourage blood to pool in the legs, and thus, the heart has an even
lower blood volume available for circulation (Smit et al., 1999). A
large reduction in circulating blood volume will lead to (1) a
continued rise in core body temperature, and (2) reduced blood flow to
the brain, muscles, and organs. A rise in core body temperature and
reduced blood flow to the brain can cause neurological disturbances,
such as loss of consciousness, which are characteristic of heat stroke
and heat syncope (Wilson et al., 2006; Van Lieshout et al., 2003). A
rise in core body temperature and reduced blood flow to muscles can
also cause extreme muscle fatigue (to the point of collapse) and muscle
cell damage during exertion, which are characteristic of heat
exhaustion and rhabdomyolysis, respectively (Torres et al., 2015; Nybo
et al., 2014). Finally, a rise in core body temperature and reduced
blood flow to organs can damage multiple vital organs (such as the
heart, liver, and kidneys), which is often observed in heat stroke
(Crandall et al., 2008; O'Donnell and Clowes, 1972). Heat stroke and
rhabdomyolysis can lead to death if not treated properly and promptly.
C. Identifying Cases of Heat-Related Health Effects
In its review of the scientific and medical literature on the
health effects of occupational heat exposure, OSHA found several
studies that relied upon coding systems, in which medical providers or
other public health professionals identify fatalities and non-fatal
cases of various illnesses and injuries, including heat-related
illnesses and injuries (HRIs). The medical and scientific communities
use data from these coding systems to study the incidence and
prevalence of illnesses and injuries, including HRIs. In both this
Health Effects section and Section V., Risk Assessment, OSHA relied on
several studies that make use of data from these coding systems. A
brief summary of each of the major coding systems is provided below.
I. International Statistical Classification of Diseases and Related
Health Problems (ICD) Codes
The International Statistical Classification of Diseases and
Related Health Problems (ICD) System is under the purview of the World
Health Organization (WHO), an international agency that, as the leading
authority on health and disease, regularly publishes evidence-based
guidelines to advance clinical practice and public health policy. The
ICD System harmonizes the diagnosis of disease across many countries,
and ICD codes are used routinely in the U.S. healthcare system by
medical personnel to record diagnoses in patients' medical records, as
well as to identify cause of death. These codes are utilized as part of
a standardized system for recording diagnoses, as well as organizing
and collecting data into public health surveillance systems. Each ICD
code is a series of letters and/or numbers that corresponds to a highly
specific medical diagnosis. Healthcare providers may record multiple
ICD codes if an individual presents with multiple diagnoses. The ICD
system has multiple codes that medical personnel can use when
diagnosing HRIs.
The ICD system was first developed in the 18th century and was
adopted under the purview of the World Health Organization (WHO) in
1948 (Hirsch et al., 2016). Since then, the ICD system has been revised
11 times--ICD-11 was released in 2022. However, because the ICD-11
system has not yet been implemented in the United States, many of the
epidemiological studies cited throughout this Health Effects section
used the ICD-9 and ICD-10 systems to survey heat-related deaths and
HRIs. Table IV-1 provides a list of heat-related ICD-9 and ICD-10
codes.
Table IV--1--ICD-9 and ICD-10 Codes for Heat-Related Health Effects *
------------------------------------------------------------------------
ICD-9 code ICD-10 code equivalent
------------------------------------------------------------------------
992 Effects of heat and light.......... T67 Effects of heat and light.
992.0 Heatstroke and sunstroke......... T67.0 Heatstroke and sunstroke.
992.1 Heat syncope..................... T67.1 Heat syncope.
992.2 Heat cramps...................... T67.2 Heat cramp.
992.3 Heat exhaustion, anhydrotic...... T67.3 Heat exhaustion,
anhydrotic.
992.4 Heat exhaustion due to salt T67.4 Heat exhaustion due to
depletion. salt depletion.
992.5 Heat exhaustion, unspecified..... T67.5 Heat exhaustion,
unspecified.
992.6 Heat fatigue, transient.......... T67.6 Heat fatigue, transient.
992.7 Heat edema....................... T67.7 Heat edema.
992.8 Other effects of heat and light.. T67.8 Other effects of heat and
light.
992.9 Effects of heat and light, T67.9 Effects of heat and
unspecified. light, unspecified.
E900 Accident caused by excessive heat. NA.
[[Page 70710]]
E900.0 Accident caused by excessive X30 Exposure to excessive
heat due to weather conditions. natural heat.
E900.1 Accidents due to excessive heat W92 Exposure to excessive heat
of man-made origin. of man-made origin.
E900.9 Accidents due to excessive heat X30 Exposure to excessive
of unspecified origin. natural heat.
------------------------------------------------------------------------
Note: The above heat-related codes exclude X32 Exposure to sunlight and
W89 Exposure to man-made radiation, among others.
* These ICD codes are specific to heat as indicated by the names of the
codes. There are additional codes that can be associated with
diagnosed heat illness but may not be specific to heat-related illness
which are not included here but may be included in text where relevant
(e.g., M62.82 for rhabdomyolysis and E87.1 for hypo-osmolality and
hyponatremia).
Various surveillance systems exist to track documentation of ICD
codes. For example, the CDC leverages ICD-10 codes to collect nearly
real-time data on heat-related deaths and HRIs through the National
Syndromic Surveillance System (NSSP). The CDC also uses ICD-10 codes to
collect annual data on heat-related deaths and HRIs, then reports these
data via the National Vital Statistics System (NVSS) and National
Center for Health Statistics (NCHS). Additionally, all branches of the
U.S. Armed Forces (i.e., Army, Navy, Air Force, and Marine Corps) use
ICD-10 codes to document HRIs among service members in the Defense
Medical Surveillance System (DMSS). The US Army also uses ICD-10 codes
to document HRIs in the Total Army Injury and Health Outcomes Database
(TAIHOD) (Bell et al., 2004).
II. Occupational Illness and Injury Classification System (OIICS) Codes
The U.S. Bureau of Labor Statistics (BLS) is a Federal agency,
housed in the Department of Labor, that collects and analyzes data on
the U.S. economy and workforce. In 1992, BLS developed the Occupational
Illness and Injury Classification System (OIICS) to harmonize reporting
of injuries and illnesses that affect U.S. workers. The OIICS is
similar to the ICD system. Each OIICS code is a series of numbers that
specifies a diagnosis (referred to as the nature of an illness or
injury, or a ``nature code'') and event(s) leading to an illness or
injury (referred to as an ``event code''). OIICS was updated in 2010
(Version 2.0), and again in 2022 (Version 3.0); Version 3.0 is the most
up to date version (<a href="https://www.bls.gov/iif/definitions/occupational-injuries-and-illnesses-classification-manual.htm">https://www.bls.gov/iif/definitions/occupational-injuries-and-illnesses-classification-manual.htm</a>; BLS, 2023e). The
OIICS system has multiple codes that can be used when identifying
occupational HRIs. Table IV-2 provides a list of heat-related OIICS
codes (nature and event codes).
Table IV--2--OIICS Codes (Version 3.0) for Heat-Related Health Effects
[dagger]
------------------------------------------------------------------------
-------------------------------------------------------------------------
Nature Codes:
172 Effects of heat and light.
1720 Effects of heat--unspecified.
1721 Heat stroke, syncope.
1722 Heat exhaustion, fatigue.
1729 Effects of heat--not elsewhere classified.
2893 Prickly heat, heat rash, and other disorders of the sweat
glands including ``miliaria rubra''.
Event Codes:
53 Exposure to temperature extremes.
530 Exposure to temperature extremes--unspecified.
531 Exposure to environmental heat.
5310 Exposure to environmental heat--unspecified.
5311 Exposure to environmental heat--indoor.
5312 Exposure to environmental heat--outdoor.
------------------------------------------------------------------------
[dagger] Some of the data OSHA relies on uses older versions of OIICS
codes (Versions 1 and 2) but the major categories for heat-related
incidents did not change significantly between versions.
Through a combination of survey staff and a specialized automated
coding system, BLS applies OIICS codes to data collected through their
worker safety and health surveillance systems, the Census of Fatal
Occupational Injuries (CFOI) and the Survey of Occupational Injuries
and Illnesses (SOII), to identify and document occupational heat-
related deaths and occupational HRIs, respectively. Researchers have
also relied on this system for identifying occupational HRIs (e.g.,
Spector et al., 2016). However, BLS data does not currently specify
discrete codes for all HRIs described in this health effects section.
The CFOI is a cooperative program between the Federal Government and
the States that relies on various administrative records, including
death certificates, to accurately produce counts of fatal work injuries
(BLS, 2012). The CFOI examines all cases marked ``At work'' on the
death certificate, and the CFOI database relies on the death
certificate (among other sources) to ascertain the cause(s) of death.
Further details about BLS reporting using OIICS codes, as well as rates
of HRIs, can be found in Section V., Risk Assessment.
III. Limitations
A limitation to relying on these coding systems to identify heat-
related fatalities and HRIs is underreporting. Numerous studies have
found that HRIs are likely vastly underreported (see Section V., Risk
Assessment). Reasons for the likely underreporting include
underreporting of illness and injuries by workers to their employers
(Kyung et al., 2023), underreporting of injuries and illnesses by
employers to BLS and OSHA (Wuellner and Phipps, 2018; Fagan and
Hodgson, 2017), underutilization of workers' compensation insurance
(Fan et al., 2006; Bonauto et al., 2010), influence of structural
factors and work culture on workers perceptions about seeking help
(Wadsworth et al., 2019; Iglesias-Rios, 2023), and difficulties with
determining heat-related causes of death (e.g., Luber et al., 2006;
Pradhan et al., 2019). As a result, there are likely many heat-related
fatalities and cases of HRIs that are not
[[Page 70711]]
captured in these coding systems. For a more detailed discussion of
underreporting, see Section V., Risk Assessment.
IV. Summary
As demonstrated by these coding systems, in which medical providers
or other public health professionals assign one or more codes to
identify a heat-related fatality or HRI, it is well accepted in the
medical and scientific communities that heat exposure, including
occupational heat exposure, can result in death and HRIs. Indeed, in
its review of the best available scientific and medical literature on
the health effects of occupational heat exposure, OSHA identified
several studies that relied upon data from these coding systems to
determine the incidence or prevalence of heat-related deaths and HRIs
in workers. OSHA relies on these studies in both this Health Effects
section and Section V., Risk Assessment, of this preamble to the
proposed rule.
D. Heat-Related Deaths
I. Introduction
Heat is the deadliest weather phenomenon in the United States (NWS,
2022). Heat as a cause of death is widely recognized in the medical and
scientific communities. Studies investigating relationships between
heat and mortality have long demonstrated positive associations between
heat exposure and increased all-cause mortality (e.g., Weinberger et
al., 2020; Basu and Samet, 2002; Whitman et al., 1997). As explained
below, the connection between heat exposure, the body's physiological
responses, and death (i.e., heat-related death mechanisms) is clearly
established. Exposure to occupational heat can be fatal. According to
BLS's CFOI, occupational heat exposure has killed 1,042 U.S. workers
between 1992-2022 (BLS, 2024c).
II. Physiological Mechanisms
Death caused by exposure to heat can occur in occupational settings
if the worker's body is not able to adequately cool in response to heat
exposure or if treatment for symptoms of heat-related illness is not
provided promptly. Nearly all body systems can be negatively affected
by heat exposure. Mora et al. (2017) systematically reviewed
mechanistic studies on heat-related deaths and identified five harmful
physiological mechanisms triggered by heat exposure that can lead to
death: ischemia (inadequate blood flow), heat cytotoxicity (damage to
and breakdown of cells), inflammatory response (inflammation that
disrupts cell and organ function), disseminated intravascular
coagulation (widespread dysfunction of blood clotting mechanisms), and
rhabdomyolysis (breakdown of muscle tissue). These mechanisms, with the
exception of rhabdomyolysis, are associated with the development of
heat stroke. Rhabdomyolysis, which is a potentially fatal illness
resulting from the breakdown of muscle tissue, can also occur in
conjunction with or in the absence of heat stroke. For a more detailed
discussion on rhabdomyolysis, see Section IV.H., Rhabdomyolysis. Mora
et al. (2017) also identified seven vital organs that can be critically
impacted by heat exposure--the brain, heart, kidneys, lungs, pancreas,
intestines, and liver. Across the five identified mechanisms and seven
vital organs, Mora et al. (2017) found medical evidence for twenty-
seven pathways whereby physiological mechanisms triggered by heat
exposure could lead to organ failure and fatality.
The most common cause of heat-related occupational deaths is heat
stroke. Heat stroke is a potentially fatal dysregulation of multiple
physiological processes and organ systems resulting in widespread organ
damage. Heat stroke is typically marked by significant elevation in
core body temperature and cognitive impairment due to central nervous
system damage. The physiological mechanisms involved in the development
and progression of heat stroke are discussed in more detail in Section
IV.E., Heat Stroke.
III. Determining Heat as a Cause of Death
The identification of deaths caused by heat exposure can take place
in a few different ways. Healthcare professionals may identify heat-
related deaths in medical settings. For example, a heat-related death
may be identified if an individual experiencing heat stroke presents to
an emergency room and then later dies. The heat-related nature of the
death should be documented by the healthcare professional in the chief
complaint field during medical history taking and selection of relevant
ICD diagnosis codes. The ICD system allows for identification of heat
as either an underlying cause of death or a significant contributing
condition. The ICD-10 instruction manual defines underlying cause as
``(a) the disease or injury which initiated the train of morbid events
leading directly to death, or (b) the circumstances of the accident or
violence which produced the fatal injury'' (WHO, 2016, p. 31). A
significant contributing condition is defined as a condition that
``contributed to the fatal outcome, but was not related to the disease
or condition directly causing death'' (WHO, 2004, p. 24).
Medical examiners or coroners can also identify heat as a cause of
death or significant condition contributing to death during death
investigations, which should be noted on the deceased individual's
death certificate. The National Association of Medical Examiners
(NAME), a professional organization for medical examiners, forensic
pathologists, and medicolegal affiliates and administrators, defines
``heat-related death'' as ``a death in which exposure to high ambient
temperature either caused the death or significantly contributed to
it'' (Donoghue et al., 1997). This definition was developed in an
effort to standardize the way in which heat-related deaths were
identified and documented on death certificates. According to the NAME
definition, cause is ascertained based on circumstances of the death,
investigative reports of high environmental temperature (e.g., a known
heat wave), or a pre-death temperature >=105 [deg]F. Cause is also
indicated in cases where the person may have a lower body temperature
due to attempted cooling measures, but where the individual had a
history of mental status changes and specific toxicological findings of
elevated muscle and liver enzymes. Heat may be designated as a
``significant contributing condition'' if: (1) ``antemortem body
temperature cannot be established but the environmental temperature at
the time of collapse was high''; and/or (2) heat stress exacerbated a
pre-existing disease, in which case heat and the pre-existing disease
would be listed as the cause and significant contributing condition,
respectively, or vice versa. Importantly, Donoghue et al. note ``The
diagnosis of heat-related death is based principally on investigative
information; autopsy findings are nonspecific.'' (Donoghue et al.,
1997). While this definition is the official definition of this
professional organization, other definitions or processes for
determining whether or not a death is heat-related may be used.
Additionally, there are processes in place to identify and document
deaths that are work-related. Death certificates include a field that
can be checked for ``injury at work'' (Russell and Conroy, 1991).
Further, work-related fatalities due to heat are identified and
documented through the CFOI (for more details, see Section IV.C.,
Overview of ICD and OIICS Codes for Heat-Related Health Effects).
[[Page 70712]]
IV. Occupational Heat-Related Deaths
Occupational heat exposure has led to worker fatalities in both
indoor and outdoor work settings and across a variety of industries,
occupations, and job tasks (Petitti et al., 2013; Arbury et al., 2014;
Gubernot et al., 2015; NIOSH, 2016; Harduar Morano and Watkins, 2017).
BLS's CFOI identified 1,042 U.S. worker deaths due to heat exposure
between 1992 and 2022, with an average of 34 fatalities per year during
that period (BLS, 2024c). Between 2011 and 2022, BLS reports 479 worker
deaths (BLS, 2024c). During the latest three years for which BLS
reports data (2020-2022), there was an average of 45 work-related
deaths due to exposure to environmental heat per year (BLS, 2024c).
However, for the reasons explained in Section V., Risk Assessment,
these statistics likely do not capture the true magnitude and
prevalence of heat-related fatalities because of underreporting.
There are numerous case studies documenting the circumstances under
which occupational heat exposure led to death among workers. For
example, in three NIOSH Fatality Assessment and Control Evaluations
(FACE) investigations of worker fatalities, workers died of heat stroke
after not receiving prompt treatment upon symptom onset (NIOSH, 2004;
NIOSH, 2007; NIOSH, 2015). Another case report of a farmworker who died
due to heat stroke indicates that confusion the worker experienced as a
result of heat exposure may have played a role in his ability to seek
help (Luginbuhl et al., 2008). Additional case reports show workers
have collapsed and later died while working alone, such as in mail
delivery (Shaikh, 2023), and that worker distress has been interpreted
as drug use as opposed to symptoms of heat illness (Alsharif, 2023).
V. Summary
OSHA's review of the scientific and medical literature indicates
that occupational heat exposure can and does cause death. The
physiological mechanisms by which heat exposure can result in death are
clearly established in the literature, and heat exposure being a cause
of death is widely recognized in the medical and scientific
communities. Indeed, occupational surveillance data demonstrates that
numerous work-related deaths from occupational heat exposure occur
every year.
E. Heat Stroke
I. Introduction
Among HRIs, the most serious and deadly illness from occupational
heat exposure is heat stroke. NIOSH (2016) defines heat stroke as ``an
acute medical emergency caused by exposure to heat from an excessive
rise in body temperature [above 41.1 [deg]C (106 [deg]F)] and failure
of the [body's] temperature-regulating mechanism.'' When this happens,
an individual's central nervous system is affected, which can result in
a sudden and sustained loss of consciousness preceded by symptoms
including vertigo, nausea, headache, cerebral dysfunction, bizarre
behavior, and excessive body temperature (NIOSH 2016).
Because progression of symptoms varies and involves central nervous
system function, it may be difficult for individuals, or those they are
with, to know when they are experiencing serious heat illness or to
understand that they need urgent medical care (Alsharif, 2023). If not
treated promptly, early symptoms of heat stroke may progress to
seizures, coma, and death (Bouchama et al., 2022). Thus, heat stroke is
often referred to as a life-threatening form of hyperthermia (i.e.,
elevated core body temperature) because it can cause damage to multiple
organs such as the liver and kidneys. Of note, the term ``stroke'' in
``heat stroke'' is a misnomer in that it does not involve a blockage or
hemorrhage of blood flow to the brain.
There are two types of heat stroke: classic heat stroke (CHS) and
exertional heat stroke (EHS). CHS can occur without any activity or
physical exertion, whereas EHS occurs as a result of physical activity.
CHS typically occurs in environmental conditions where ambient
temperature and humidity are high and is most often reported during
heat waves (Bouchama et al., 2022). It is most likely to affect young
children and the elderly (Laitano et al., 2019). Studies have found
that EHS can occur with any amount of physical exertion, even within
the first 60 minutes of exertion (Epstein and Yanovich, 2019; Garcia et
al., 2022). Additionally, EHS can occur in healthy individuals who
would otherwise be considered low risk performing physical activity,
regardless of hot or cool environmental conditions (Periard et al.,
2022; Epstein et al., 1999).
Cases of heat stroke can be identified in a few ways. Medical
personnel who make a formal diagnosis of heat stroke record the
corresponding ICD code in the patient's medical record. Medical
examiners also identify heat stroke as a cause of death or significant
condition contributing to death and note it on the deceased
individual's death certificate.
II. Physiological Mechanisms
Heat stroke happens when the body is under severe heat stress and
is unable to dissipate excessive heat to keep the body temperature at
37 [deg]C (98.6 [deg]F), resulting in an elevated core body temperature
(Epstein and Yanovich, 2019). The hallmark characteristics of heat
stroke are: (1) central nervous system (CNS) dysfunction, including
encephalopathy (i.e., brain dysfunction manifesting as irrational
behavior, confusion, coma, or convulsions); and (2) damage to multiple
organs, including the kidneys, liver, heart, pancreas, gastrointestinal
tract, as well as the circulatory system. There are three accepted
mechanisms through which heat exposure can cause CNS dysfunction and/or
multi-organ damage (Bouchama et al., 2022; Garcia et al., 2022; Iba et
al., 2022). All three mechanisms share a common origin: heat exposure
contributes to excessive heat stress, which results in hyperthermia.
One mechanism of heat stroke is reduced cerebral blood velocity
(CBV) (an indicator of blood flow to the brain) that results in
orthostatic intolerance (i.e., the inability to remain upright without
symptoms) (Wilson et al., 2006). As individuals experience whole body
heating, CBV is reduced and cerebral vascular resistance (the ratio of
carbon dioxide stimulus to cerebral blood flow) increases. These
changes ultimately contribute to reduced cerebral perfusion (flow of
blood from the circulatory system to cerebral tissue) and blood flow,
as well as orthostatic intolerance (Wilson et al., 2006).
Another mechanism is damage to the vascular endothelium.
Hyperthermia can damage or kill cells in the lining of blood vessels,
known as the vascular endothelium. The body responds to vascular
endothelium damage through a process called disseminated intravascular
coagulation (DIC). DIC is characterized by two processes: (1) tiny
clots form in the tissues of multiple organs, and (2) bleeding occurs
at the sites of those tiny clots. DIC is extremely damaging and results
in injury to organs (Bouchama and Knochel, 2002). Namely, DIC limits
the delivery of oxygen and nutrients to several organs including the
brain, heart, kidneys, and liver. Thus, DIC can result in both CNS
dysfunction and multi-organ damage. Additionally, damage to the
vascular endothelium makes it more permeable and creates an imbalance
in the substances that control blood clotting,
[[Page 70713]]
which promotes abnormal and increased blood clotting (Bouchama and
Knochel, 2002; Wang et al., 2022).
A third mechanism is damage to the cells in the lining of the gut,
known as the gut epithelium. Hyperthermia can alter the cell membranes'
permeability (Roti Roti et al., 2008), or directly cause cells to die
(Bynum et al., 1978). In either case, cells in the gut epithelium will
leak endotoxins into the blood, a process known as endotoxemia. When
these endotoxins circulate throughout the body, the immune system
aggressively responds by activating cells to fight infection and
inflammation, known as systemic inflammatory response syndrome (SIRS)
(Leon and Helwig, 2010). The presence of endotoxins, as well as the
body's aggressive immune response, can cause serious multi-organ damage
(Epstein and Yanovich, 2019; Wang et al., 2022). In particular, the
liver is usually one of the first organs to be damaged and is often
what causes a heat stroke death (Wang et al., 2022).
III. Occupational Heat Stroke
Heat stroke is life-threatening and can severely impair workers'
safety and health (Lucas et al., 2014). A study of work-related HRIs in
Florida using hospital data reported that, during the warm seasons from
May through October between 2005 through 2012, heat stroke was the
primary diagnosis in 91% (21 of 23) of deaths. In total, they reported
160 cases of work-related heat stroke (Harduar Morano and Watkins,
2017). Analyses of heat stroke among military members indicate that
roughly 73% of EHS patients require hospitalization for at least two
days (Carter et al., 2007).
IV. Treatment and Recovery
Heat stroke is a serious medical emergency that requires immediate
rest, cooling, and usually hospitalization. Prognosis for heat stroke
is highly dependent on how quickly heat stroke is recognized and how
quickly an affected worker can be cooled. When an affected person can
be diagnosed early and cooled rapidly, the prognosis is generally good.
For example, rapid cooling within one hour of presentation of symptoms
of CHS was found to reduce the mortality rate from 33% to 15% (Vicario
et al., 1986). For EHS, cooling the body below 104 [deg]F within 30
minutes of collapse is associated with very good outcomes (Casa et al.,
2012; Casa et al., 2015). The authors also reported that they were
unaware of any cases of fatalities among EHS victims where it was
recorded that the body was cooled below 104 [deg]F within 30 minutes of
collapse (Casa et al., 2012).
Comparably, others have found that the risk of morbidity and
mortality from heat stroke increases as treatment is delayed (Demartini
et al., 2015; Schlader et al., 2022). Schlader et al. (2022) found that
a delay in cooling can result in tissue damage, multi-organ
dysfunction, and eventually death. Similarly, Zeller et al. (2011)
found in their retrospective cohort study that patients who did not
receive early or immediate cooling had worse outcomes, such as more
severe forms of disease or death, although their study design does not
allow for conclusions regarding causality (Zeller et al., 2011).
Khogali and Weiner's (1980) case study report on 18 cases of heat
stroke found that 72% of the patients took between 30-90 minutes to
cool, whereas the other 28% were resistant to cooling, taking two to
five hours to reach 38 [deg]C (100.4 [deg]F). This means that there is
variation in how individuals respond to heat stroke treatment and that
some individuals will respond quicker to treatment than others. Prompt
treatment is likely even more critical for the individuals who take
longer to cool.
Data from the general population also demonstrate the serious
nature of heat stroke. One analysis of nationwide data estimated that
nearly 55% of emergency department visits for heat stroke required
hospitalization and roughly 3.5% of patients died in the emergency
department or at the hospital (Wu et al., 2014). This study also found
that heat stroke medical emergencies are more severe than other non-
heat-related emergencies, with a 2.6-fold increase in admission rate
and a 4.8-fold increase in case fatality compared to those other
conditions (Wu et al., 2014).
Complete recovery for individuals who are affected by heat stroke
may require time away from work. Some research suggests the length of
recovery time and the need for time away from work is based on how long
a person was at or above the critical core body temperature of 41
[deg]C (105.8 [deg]F), and how long it takes for biomarkers in blood to
normalize (McDermott et al., 2007). Relevant biomarkers include those
for acute liver dysfunction, myolysis (the breakdown of muscle tissue),
and other organ system biomarkers (Ward et al., 2020; Schlader et al.,
2022).
Guidelines for military personnel and athletes suggest that it may
be weeks or months before a worker who has suffered heat stroke can
safely return to work or perform the same level of work they did before
suffering heat stroke. U.S. military members have clear return-to-work
protocols post-heat stroke where members are assigned grades of
functional capacity in six areas: physical capacity or stamina, upper
extremities, lower extremities, hearing and ears, eyes, and psychiatric
functioning (O'Connor et al., 2007). For example, when a soldier/airman
experiences heat stroke, they automatically receive a reduced function
capacity grade status in physical capacity. This also results in an
automatic referral to a medical examination board. Soldiers and airmen
are not cleared to return to duty until their laboratory results
normalize, and even then, their status remains a trial of duty. If the
individual has not exhibited any heat intolerance after three months,
they are returned to a normal work schedule. However, maximal exertion
and significant heat exposure remains prohibited for these individuals.
If a military member experiences any heat intolerance during the period
of restriction, or subsequent resumption to normal duty, a referral to
the physical examination board for a hearing regarding their health
status is required (O'Connor et al., 2007).
The U.S. Navy has its own set of guidelines, which does not
distinguish between heat exhaustion and heat stroke, but uses
laboratory tests, especially liver function tests, to determine when
sailors are allowed to return to duty. For those who have suffered heat
stroke, full return to duty is usually not granted until somewhere
between two days to three weeks later (O'Connor et al., 2007).
In 2023, the American College of Sports Medicine (ACSM) published
their consensus statement which provides evidence-based strategies to
reduce and eliminate HRIs, including a return to activity protocol for
athletes recovering from EHS (Roberts et al., 2023). Of note, ACSM
names athletes (whether elite, recreational, or tactical) and
occupational laborers as groups who are active and regularly perform
exertional activities that could lead to EHS. Specifically, ACSM
recommendations include refraining from exercise for at least seven
days following release from the initial medical care for EHS treatment.
Once all laboratory results and vital signs have normalized, ACSM
recommends an individual can exercise in cool environments and
gradually increase duration, intensity, and heat exposure over a two to
four-week period to initiate environmental acclimatization (Roberts et
al., 2023). If the affected athlete does not return to pre-EHS activity
levels within four to six weeks, further medical evaluation is needed.
ACSM recommends a full return to
[[Page 70714]]
activity between two to four weeks after the individual has
demonstrated exercise acclimatization and heat tolerance with no
abnormal symptoms or test results during the re-acclimatization period
(Roberts et al., 2023). Similarly, the National Athletic Trainer's
Association proposes that individuals who experience EHS should
complete a 7 to 21-day rest period, be asymptomatic, have normal blood-
work values, and obtain a physician's clearance prior to beginning a
gradual return to activity (Casa et al., 2015).
In the military setting it is accepted that returning to work too
early and/or without adequate work restrictions can result in
incomplete recovery from heat stroke, which may necessitate a prolonged
restricted work status (McDermott et al., 2007). About 10-20% of people
who have had heat stroke have been shown to experience heat intolerance
roughly two months after having the heat stroke (Binkley et al., 2002).
In some instances, this has lasted for five years and has increased the
risk for another heat stroke (Binkley et al., 2002; McDermott et al.,
2007). Similarly, a case study report of EHS cases amongst the U.S.
Army found that in one of the ten cases examined, the person was heat
intolerant for 11.5 months post-EHS (Armstrong et al., 1989).
Only a limited number of studies have focused on the long-term
effects of heat stroke. This includes research by Wallace et al.
(2007), whose retrospective review of military service members found
that those who suffered an EHS event earlier in life were more likely
to die due to cardiovascular disease and ischemic heart disease.
Similarly, Wang et al. (2019) report that prior exertional heat illness
was associated with a higher prevalence of acute ischemic stroke, acute
myocardial infarction, and an almost three-fold higher prevalence of
chronic kidney disease. Other research in mice support these claims and
indicate that epigenetic effects post-EHS result in immunosuppression
and an altered heat shock protein response as well as development of
metabolic disorders that could negatively impact long-term
cardiovascular health (Murray et al., 2020; Laitano et al., 2020).
V. Summary
OSHA's review of the scientific and medical literature indicates
that occupational heat exposure can cause heat stroke, a medical
emergency. The physiological mechanisms by which heat exposure can
result in heat stroke are well-established in the literature, and heat
exposure as a cause of heat stroke is well-recognized in the medical
and scientific communities. The best available research demonstrates
that heat stroke must be treated as soon as possible and that prolonged
time between experiencing heat stroke and seeking treatment increases
the likelihood of death and may result in long-term health effects.
F. Heat Exhaustion
I. Introduction
NIOSH defines heat exhaustion as ``[a] heat-related illness
characterized by elevation of core body temperature above 38 [deg]C
(100.4 [deg]F) and abnormal performance of one or more organ systems,
without injury to the central nervous system'' (NIOSH, 2016). Heat
exhaustion can progress to heat stroke if not treated properly and
promptly, and may require time away from work for a full recovery.
Signs and symptoms of heat exhaustion typically include profuse
sweating, changes in mental status, dizziness, nausea, headache,
irritability, weakness, decreased urine output and elevated core body
temperature up to 40 [deg]C (104 [deg]F) (NIOSH, 2016; Kenny et al.,
2018). Collapse may or may not occur. Significant injury to the central
nervous system, and significant inflammatory response do not occur
during heat exhaustion. However, there appears to be a fine line
between heat exhaustion and heat stroke. Kenny et al. 2018 state that
it can be difficult to clinically differentiate between heat exhaustion
and early heat stroke. NIOSH also states that heat exhaustion ``may
signal impending heat stroke'' (NIOSH, 2016). Armstrong et al. (2007)
recommend that rectal temperature be taken to distinguish between heat
exhaustion and heat stroke.
II. Physiological Mechanisms
Heat exhaustion occurs when heat stress results in elevated body
temperature between 98.6 [deg]F and 104 [deg]F (37 [deg]C and 40
[deg]C) and physiological changes occur (Kenny et al., 2018). Under
these significant heat stress conditions, heavy sweating occurs, tissue
perfusion is reduced, and inflammatory mediators are released.
Electrolyte imbalances can occur due to fluid and electrolyte losses
through sweating paired with inadequate replenishment. Voluntary and
involuntary dehydration can exacerbate this process (Hendrie et al.,
1997; Brake and Bates, 2003). ``Voluntary dehydration,'' as used by
Brake and Bates, refers to the circumstance where a dehydrated worker
does not adequately rehydrate, despite the availability of water. Upon
review of several studies, Kenny et al. (2018) report that dehydration
among workers is common, even when water is readily available. There is
also evidence that even when water intake increases, as sweat rate and
dehydration increase, intake may not be adequate to fully replace
losses (Hendrie et al., 1997).
Brake and Bates (2003) summarized various hypothesized reasons for
voluntary and involuntary dehydration. One hypothesized reason for
voluntary dehydration is a delayed or decreased thirst response (Brake
and Bates, 2003). Other reasons include mechanisms that affect fluid
retention, such as the dependence of fluid retention on solutes such as
sodium, which may be in imbalance under heat stress (Brake and Bates,
2003). Lack of adequate hydration could also be due to workplace
pressures or concerns about sanitation (Rao, 2007; Iglesias-Rios,
2023).
The combination of heat stress, upright posture, and low vascular
fluid volume (hypovolemia) can further dysregulate the circulatory
system and affect clotting mechanisms (Kenny et al., 2018). Heat stress
reduces blood flow to the abdominal organs, kidneys, muscles, and brain
and increases blood flow to the skin to aid in cooling. These changes
in the circulatory system and blood flow to the brain can potentially
lead to dizziness or faintness upon standing (orthostatic intolerance),
or collapse. Other factors that affect the development of heat
exhaustion include individual health status, preparedness (such as
acclimatization level), individual characteristics, knowledge, access
to fluids, environmental factors, personal protective equipment use and
work pacing and intensity (Kenny, 2018).
III. Occupational Heat Exhaustion
Heat exhaustion is one of the more common heat-related illnesses
(Armstrong et al., 2007; Harduar Morano and Watkins, 2017; Lewandowski
and Shaman, 2022). In their study of heat-illness hospitalizations in
Florida during May to October from 2005-2012, Harduar Morano and
Watkins (2017) reported that there were 2,659 cases of work-related
heat exhaustion that resulted in emergency department visits or
hospitalization, versus 181 cases of work-related heat stroke that
resulted in emergency department visits, hospitalization, or death.
Similar results have been reported in studies of heat-related illness
among the United States Armed Forces and miners showing the frequency
of heat exhaustion (Dickinson, 1994; Armed Forces Health Surveillance
Division, 2022b;
[[Page 70715]]
Lewandowski and Shaman, 2022; Donoghue et al., 2000; Donoghue, 2004).
While in some studies heat exhaustion is not specifically diagnosed,
several qualitative studies describe self-reported symptoms in workers
that may be indicative of heat exhaustion (e.g., Mirabelli et al.,
2010; Fleischer et al., 2013; Kearney et al., 2016; Mutic et al.,
2018). These symptoms included headache, nausea, vomiting, feeling
faint, and heavy sweating.
IV. Treatment and Recovery
Heat exhaustion may require treatment beyond basic first aid to
prevent progression to heat stroke (Kenny et al., 2018). In cases where
the degree of severity of heat illness is unclear, the individual
should be treated as if they have heat stroke (Armstrong, 1989). For a
worker experiencing heat exhaustion, NIOSH recommends the following
steps to ensure the worker receives proper and adequate treatment:
``Take worker to a clinic or emergency room for medical evaluation and
treatment; If medical care is unavailable, call 911; Someone should
stay with worker until help arrives; Remove worker from hot area and
give liquids to drink; Remove unnecessary clothing, including shoes and
socks; Cool the worker with cold compresses or have the worker wash
head, face, and neck with cold water; Encourage frequent sips of cool
water'' (NIOSH, 2016).
Complete recovery from heat exhaustion may require a restricted
work status (or limited work duties). Donoghue et al. (2000) reported
that following heat exhaustion, 29% (22 of 77) of miners included in
the study required a restricted work status for at least one shift. The
military has specific protocols for return to duty following heat
exhaustion. For example, the U.S. Army and Air Force follow the
protocol outlines in AR 40-501 (O'Connor et al., 2007). Three instances
of heat exhaustion in less than 24 months can result in referral to a
Medical Evaluation Board before a full return to service. Some military
units have additional or more specific guidelines. For example, one
military unit, at Womack Army Medical Center in North Carolina, has
guidelines that allow individuals who are considered to have mild
illness, fully recovered in the emergency room, and have no abnormal
laboratory findings to return to light duty the following day and
limited duty the day after that. However, they also indicate that some
effects of heat illness may be subtle or delayed and recommend
individuals avoid strenuous exercise for several days and remain under
observation (O'Connor et al., 2007).
V. Summary
The scientific and medical literature presented here clearly
demonstrate that heat exhaustion is a recognized health effect of
occupational heat exposure. The best available evidence on the
symptoms, treatment, and recovery of heat exhaustion demonstrates that
heat exhaustion can progress to heat stroke, a medical emergency, if
not treated promptly and that heat exhaustion may require time away
from work for a full recovery.
G. Heat Syncope
I. Introduction
Occupational heat exposure can result in heat syncope. Syncope is
the medical term for ``fainting,'' and heat syncope is defined as
``fainting, dizziness, or light-headedness after standing or suddenly
rising from a sitting/lying position'' due to heat exposure (NIOSH,
2023a). Heat syncope may sometimes be referred to as ``exercise-
associated collapse'' (EAC), but heat syncope can happen without
significant levels of exertion (Asplund et al., 2011; Pearson et al.,
2014). As explained below, heat syncope is an acknowledged and
documented health effect of occupational heat exposure.
II. Physiological Mechanisms
There are two mechanisms for how heat exposure can cause heat
syncope (Schlader et al., 2016; Jimenez et al., 1999). One mechanism
for heat syncope is reduced blood flow to the brain. Elevated core
temperature induces vasodilation, sweating, and may result in blood
pooling in certain areas of the body (see Section IV.B., General
Mechanisms of Heat-Related Health Effects). Thus, there is a lower
circulating blood volume, which can reduce blood flow to the brain and
cause loss of consciousness (Wilson et al., 2006; Van Lieshout et al.,
2003).
A second mechanism for heat syncope is reduced cerebral blood
velocity (CBV) (indicative of reduced blood flow to the brain) that
results in orthostatic intolerance (the inability to remain upright
without symptoms) during a heat stress episode (Wilson et al., 2006).
As individuals experience whole body heating, CBV is reduced and
cerebral vascular resistance (the ratio of carbon dioxide stimulus to
cerebral blood flow) increases. These changes ultimately contribute to
reduced cerebral perfusion and blood flow, as well as orthostatic
intolerance (Wilson et al., 2006). The orthostatic response to heat
stress during ``rest'' (i.e., standing/sitting) is essentially
equivalent to the orthostatic response to heat stress after exercise if
skin temperature is similarly elevated (Pearson et al., 2014). While
core temperature is not always elevated in cases of heat syncope, skin
temperature typically is (Department of the Army, 2022; Noakes et al.,
2008).
Differentiating between heat syncope, heat exhaustion, and heat
stroke is a critical step in proper diagnosis (Santelli et al., 2014;
Coris et al., 2004). As stated above, heat syncope always involves loss
of consciousness, but it does not require elevated core body
temperature (Santelli et al., 2014; Holtzhausen et al., 1994).
Conversely, heat exhaustion and stroke do not require loss of
consciousness. Though central nervous system (CNS) disturbances are
possible in heat stroke and heat stroke is always characterized by
significantly elevated core temperature. Further, recovery of mental
status is faster in heat syncope than in exhaustion and heat stroke,
since cooling may not be required for treatment of heat syncope (Howe
and Boden, 2007).
III. Occupational Heat Syncope
Workers have experienced heat syncope when exposed to heat. A
survey-based study in southern Georgia found that 4% of 405 farmworkers
experienced fainting within the previous week (Fleischer et al., 2013).
Another survey-based study in North Carolina asked 281 farmworkers if
they had ever experienced heat-related illness and found that 3% of
workers had fainted (Mirabelli et al., 2010). While these cases were
not formally diagnosed as heat syncope, Fleischer reported temperatures
ranging from 34-40 [deg]C (94-104 [deg]F) and a heat index of 37-42
[deg]C (100-108 [deg]F) at the time workers fainted, and Mirabelli
described the working conditions at the time of fainting as being in
``extreme heat.''
IV. Treatment and Recovery
NIOSH recommends treating heat syncope by having the worker sit
down in a cool environment and hydrate with either water, juice, or a
sports drink (NIOSH, 2016). The Department of the Army recommends that
``victims of heat/parade syncope will recover rapidly once they sit or
lay supine, though complete recovery of stable blood pressure and heart
rate (resolution of orthostasis or ability to stand without fainting)
in some individuals may take 1 to 2 hours'' (Department of the Army,
2022). Treatment recommendations for athletes consist of moving the
athlete to a cool area and laying them supine with elevated legs to
assist in venous return,
[[Page 70716]]
possibly with oral or intravenous rehydration (Peterkin et al., 2016;
Howe and Boden, 2007; Seto et al., 2005; Lugo-Amador et al., 2004).
An episode of heat syncope may require time away from work for a
thorough evaluation to ascertain one's risk for recurrent/future
episodes of heat syncope. No studies have evaluated recurring episodes
of syncope among workers specifically, but a study found that, for the
general population, 1-year syncope recurrence (any type) was 14% in
working-age people (18-65 years) (Barbic et al., 2019). The U.S. Army
has a requirement to ``obtain a complete history to rule out other
causes of syncope, including an exertional heat illness or other
medical diagnosis (for example, cardiac disorder)'' (Department of the
Army, 2022). Recommendations for athletes include thorough evaluation
``for injury resulting from a fall, and all cardiac, neurologic, or
other potentially serious causes for syncope'' (Howe and Boden, 2007;
Lugo-Amador et al., 2004; Binkley et al., 2002). Indeed, if an injury
(e.g., fall, collision) is sustained because of heat syncope, treatment
beyond first aid (including hospitalization) may be necessary.
Supporting this point, more general syncope has been linked to
occupational accidents requiring hospitalizations (Nume et al., 2017).
V. Summary
The scientific and medical literature presented in this section
demonstrate that heat syncope is a recognized health effect of
occupational heat exposure. Studies suggest that heat syncope may
require time away from work for further evaluation. Additionally, heat
syncope can lead to injuries (e.g., injury from a fall), some of which
may require hospitalization.
H. Rhabdomyolysis
I. Introduction
Rhabdomyolysis is a life-threatening illness that can affect
workers exposed to occupational heat. NIOSH defines rhabdomyolysis as
``a medical condition associated with heat stress and prolonged
physical exertion, resulting in the rapid breakdown of muscle and the
rupture and necrosis of the affected muscles'' (NIOSH, 2016). This
definition is specific to exertional rhabdomyolysis. Another form of
rhabdomyolysis, called traumatic rhabdomyolysis, is caused by direct
muscle trauma (e.g., from a fall or crush injury). Workers can
experience such injuries, and consequently suffer from traumatic
rhabdomyolysis, because of occupational heat exposure (see Section
IV.P., Heat-Related Injuries). However, this section will focus only on
exertional rhabdomyolysis. Unless otherwise specified, all references
to rhabdomyolysis are shorthand for exertional rhabdomyolysis.
Signs and symptoms of rhabdomyolysis include myalgia (muscle pain),
muscle weakness, muscle tenderness, muscle swelling, and/or dark-
colored urine (Armed Forces Health Surveillance Division, 2023b; Dantas
et al., 2022; O'Connor et al., 2008; Cervellin et al., 2010). Notably,
the onset of these symptoms may be delayed by 24-72 hours (Kim et al.,
2016). Rhabdomyolysis commonly affects individuals who are exposed to
heat during physical exertion. For example, the Centers for Disease
Control and Prevention (CDC) investigated an incident in which an
entire cohort of 50 police trainees were diagnosed with rhabdomyolysis
after the first 3 days of a 14-week training program; the trainees had
engaged in heavy physical exertion outdoors with limited access to
water. The CDC concluded that adequate hydration is particularly
important when the HI approaches 80 [deg]F (Goodman et al., 1990).
Rhabdomyolysis has long been recognized as a heat-related illness
by NIOSH, the U.S. Armed Forces, and national athletic organizations
such as the American College of Sports Medicine (Armstrong et al.,
2007). Specifically, NIOSH lists rhabdomyolysis as an ``acute heat
disorder'' in its Criteria for a Recommended Standard (2016) and
provides detailed recommendations for recognition and treatment of
rhabdomyolysis. NIOSH also conducted case studies and retrospective
analyses to identify cases of rhabdomyolysis among workers exposed to
heat, including firefighter cadets and instructors, as well as park
rangers (Eisenberg et al., 2019; Eisenberg J et al., 2015; Eisenberg
and Methner, 2014).
Similarly, the U.S. Armed Forces developed a case definition that
specifies rhabdomyolysis can be heat-related (Armed Forces Health
Surveillance Board, 2017), and this definition is applied in their
annual surveillance reports of HRIs. From 2018 to 2022, most
rhabdomyolysis cases (75.9%) occurred during warmer months (i.e., May
to October) (Armed Forces Health Surveillance Division, 2023b). In a
retrospective study of hospital admissions for rhabdomyolysis in
military members (2010-2013), 60.1% (193 out of 321) cases were deemed
to be associated with exertion and exposure to heat (Oh et al., 2022).
Many studies have also found that rhabdomyolysis often coincides
with exertional heat stroke and other HRIs such as heat exhaustion,
heat cramps, hyponatremia, and dehydration. The frequent co-occurrence
of rhabdomyolysis and other HRIs has been reported among workers,
including police and firefighters (Eisenberg et al., 2019; Goodman et
al., 1990), workers included in OSHA enforcement investigations (Tustin
et al., 2018a), military members (Oh et al., 2022; Carter et al.,
2005), athletes (Thompson et al., 2018), and in the general population
(Thongprayoon et al., 2020).
II. Physiological Mechanisms
Studies have identified two interrelated mechanisms through which
heat exposure, combined with exertion, can cause rhabdomyolysis. Both
mechanisms share a common origin: occupational heat exposure and
exertion both contribute to excessive heat stress, which in turn causes
an elevated core temperature. Both mechanisms also share a common
outcome: the breakdown and death of muscle tissue, which is the
hallmark characteristic of rhabdomyolysis. The first mechanism is
thermal injury to muscle cells. When the body's core temperature is
elevated, it creates a toxic environment that can directly injure or
kill muscle cells. The temperature at which this occurs, known as the
thermal maximum, is estimated to be about 107.6 [deg]F (42 [deg]C)
(Bynum et al., 1978). At the thermal maximum, the structural components
of the cells' membranes are liquified and the membrane breaks down.
Proteins in the cells' mitochondria, which are key to energy
production, change shape and no longer function properly. Calcium,
which is normally maintained at a low level inside muscle cells, will
rush into the cells and activate inflammatory processes that accelerate
the death of those cells (Torres et al., 2015; Khan, 2009).
The second mechanism is lack of oxygen to muscle cells. When the
body attempts to cool itself, it can lose high volumes of sweat. Sweat
loss can deplete the body's stores of water and electrolytes, leading
to low blood volume (see Section IV.B., General Mechanisms of Heat-
Related Health Effects). Low blood volume, and low potassium in the
blood (known as hypokalemia), can both contribute to muscle cell death.
An adequate supply of blood is necessary to deliver oxygen to muscles,
and an adequate supply of potassium is needed to support vasodilation
(to support increased blood flow to the muscles during exertion). When
neither blood volume nor
[[Page 70717]]
potassium are sufficient, the muscle cells do not receive enough oxygen
(known as ischemia). When this occurs, the muscle cells produce less
energy and eventually will die if exertion continues (Knochel and
Schlein, 1972).
III. Occupational Rhabdomyolysis
While OSHA is not aware of surveillance data on the incidence of
rhabdomyolysis in the worker population in the United States, there are
surveillance data on the incidence of rhabdomyolysis among active
military members in the Army, Navy, Air Force, and Marine Corps. These
data have been reported for the U.S. Army from 2004 to 2006 (Hill et
al., 2012) and for all military branches from 2008 through 2022 (Armed
Forces Health Surveillance Division, 2023b; Armed Forces Health
Surveillance Division, 2018; U.S. Armed Forces, 2013). These
surveillance data and the studies described above by NIOSH and others
indicate that workers performing strenuous tasks in the heat are at
risk of developing rhabdomyolysis. The U.S. Armed Forces has
successfully identified many cases of heat-related rhabdomyolysis by
searching medical records for the presence of either the ICD-10 code
for rhabdomyolysis and/or the ICD-10 code for myoglobinuria, along with
any other heat-related codes (table IV-1) (Armed Forces Health
Surveillance Division, 2023b; Oh et al., 2022).
IV. Treatment and Recovery
Rhabdomyolysis is a serious heat-related illness that can cause
life-threatening complications. Many cases of rhabdomyolysis may
require hospitalization. For example, A CDC investigation into a police
training program in Massachusetts found that 26% of police trainees (13
out of 50) were hospitalized for rhabdomyolysis only three days into
their training (Goodman et al., 1990). The mean length of
hospitalization was 6 days, with a range of 1 to 20 days (Goodman et
al., 1990). Similarly, a military surveillance study identified 473
rhabdomyolysis cases among military members in 2022, with 35.3% of
cases (167 out of 473) requiring hospitalization (Armed Forces Health
Surveillance Division, 2023b). In a retrospective study of 193 military
trainees hospitalized for rhabdomyolysis, the mean length of
hospitalization was 2.6 days, with a range of 0 to 25 days (Oh et al.,
2022).
The focus of treatment for rhabdomyolysis during hospitalization is
to reduce levels of creatine kinase (CK) and myoglobin in the blood, as
well as correct electrolyte imbalances, through aggressive
administration of intravenous fluids (generally normal saline)
(O'Connor et al., 2020; Luetmer et al., 2020; Manspeaker et al., 2016;
Torres et al., 2015). Monitoring is used to repeatedly measure CK
levels until a peak concentration is reached (often within 1-3 days),
and then to ensure that CK levels are consistently trending downwards
before discharge from the hospital (Kodadek et al., 2022; Oh et al.,
2022).
Complications of rhabdomyolysis are also possible. When muscle
cells die, they release several electrolytes and proteins into the
bloodstream that can cause severe health complications. For example,
the release of potassium from muscle cells can cause hyperkalemia (high
level of potassium in the blood), which then leads to heart arrhythmias
(abnormal heart rhythms) (Mora et al., 2017; Sauret et al., 2002).
Also, the release of myoglobin into the bloodstream can be toxic for
the kidneys. When blood is filtered by nephrons (functional units of
the kidneys) to produce urine, the presence of even small amounts of
myoglobin can obstruct and damage the nephrons (Mora et al., 2017;
Sauret et al., 2002). In some cases, these complications from
rhabdomyolysis can be life-threatening (Wesdock and Donoghue, 2019) and
in fact fatalities have been reported (Gardner and Kark, 1994; Goodman
et al., 1990). A more detailed discussion of how rhabdomyolysis can
cause acute kidney injury or other kidney damage can be found in
Section IV.M., Kidney Health Effects.
Guidelines for return to work among workers diagnosed with
rhabdomyolysis are limited. In the U.S. military, soldiers deemed to be
at low risk for recurrence of rhabdomyolysis are restricted to light,
indoor duty and encouraged to rehydrate for at least 72 hours to allow
for normalization of CK levels. If CK levels do not normalize, they
must continue indoor, light duty; if CK levels do normalize, they can
proceed to light, outdoor duty for at least 1 week and must show no
return of clinical symptoms before they can gradually return to full
duty. In contrast, soldiers deemed to be at high risk for recurrence of
rhabdomyolysis must undergo additional diagnostic tests, with
consultation from experts, and can be given an individualized,
restricted exercise program while they await clearance for full return
to duty (O'Connor et al., 2020; O'Connor et al., 2008). These
guidelines have been adopted by the Armed Forces and restated in their
surveillance reports of rhabdomyolysis (Armed Forces Health
Surveillance Division, 2023b).
V. Summary
The available scientific literature indicates that rhabdomyolysis
can result from physical exertion in the heat. Based on plausible
mechanistic data, studies by NIOSH and others, and surveillance data
indicating incidence of rhabdomyolysis among active military members,
OSHA preliminarily determines that workers performing strenuous tasks
in the heat are at risk of rhabdomyolysis.
I. Hyponatremia
I. Introduction
Workers in hot environments may experience hyponatremia, a
condition that occurs when the level of sodium in the blood falls below
normal levels (<135 milliequivalents per liter (mEq/L)) (NIOSH, 2016).
Hyponatremia is often caused by drinking too much water or hypotonic
fluids, such as sports drinks, over a prolonged period of time. Without
sodium replacement, the high water intake can result in losses of
sodium in the blood as more sodium is lost due to increased sweating
from heat exposure and urination (Korey Stringer Institute (KSI),
n.d.). Mild forms of hyponatremia may not produce any signs or
symptoms, or may present with symptoms including muscle weakness and/or
twitching, dizziness, lightheadedness, headache, nausea and/or
vomiting, weight gain, and swelling of the hands or feet (KSI, n.d.;
NIOSH, 2016). In severe cases, hyponatremia may cause altered mental
status, seizures, cerebral edema, pulmonary edema, and coma, which may
be fatal (KSI, n.d.; NIOSH, 2016; Rosner and Kirven, 2007). NIOSH and
the U.S. Army classify hyponatremia as a heat-related illness (NIOSH,
2016; Department of the Army, 2022).
II. Physiological Mechanisms
When exposed to heat, the autonomic nervous system triggers the
body's sweat response, in which sweat glands release water to wet the
skin (Roddie et al., 1957; Grant and Holling, 1938). The purpose of the
sweat response is to cool the body. However, in doing so, it can
deplete the body's stores of water and electrolytes (e.g., sodium,
potassium, chloride, calcium, and magnesium) that are essential for
normal bodily function (Shirreffs and Maughan, 1997). As the body's
store of sodium is lessening and high quantities of water are consumed,
hyponatremia may develop as sodium in the blood becomes diluted (<135
mEq/L). In some cases, this dilution may cause an osmotic
disequilibrium--an imbalance in the amount of sodium inside and outside
the cell resulting in
[[Page 70718]]
cellular swelling--which can lead to the serious and fatal health
outcomes discussed above.
III. Occupational Hyponatremia
Surveillance of hyponatremia among workers is limited. However, a
recent case study demonstrates the potential severity and life-
threatening nature of hyponatremia. After a seven-day planned absence
from work, a 34-year-old male process control operator in an aluminum
smelter pot room was hospitalized due to a variety of HRI symptoms
including hyponatremia, with serum (the liquid portion of blood
collected without clotting factors) sodium level of 114 millimoles per
liter (mmol/L) (reference range: 136-145 mmol/L) (Wesdock and Donoghue,
2019). After 13 days in the hospital, the patient was discharged with a
diagnosis of ``severe hyponatremia likely triggered by heat exposure''
(Wesdock and Donoghue, 2019). The patient was still out of work 32
weeks after the incident. While no temperature data for the pot room
were available, an exposure assessment used outdoor temperatures that
day and pot room temperatures from the literature to estimate that the
WBGT could have been as high as 33 [deg]C, which the authors state
exceeds the ACGIH TLV for light work for acclimatized workers (Wesdock
and Donoghue, 2019).
The relationship of heat exposure and hyponatremia was examined
among male dockyard workers in Dubai, United Arab Emirates (Holmes et
al., 2011). This population performed long periods of manual work in
the heat and consumed a diet low in sodium. A first round of plasma
(i.e., the liquid part of blood collected that contains water,
nutrients and clotting factors) samples were taken at the end of the
summer (n=44), with a second round taken at the end of the winter among
volunteers still willing to participate (n=38). In the summer, 55% of
participants were found to be hyponatremic (<135 millimolar (mM)),
whereas only 8% were hyponatremic in the winter. Although ambient
temperature conditions were not reported, the authors indicate that
hyponatremia was highest during the summer because of sodium losses
through sweat and inadequate sodium replacement (Holmes et al., 2011).
Hyponatremia among the military population has been well documented
by the Annual Armed Forces Health Surveillance Division, which releases
annual reports on exertional hyponatremia among active duty component
services members, each with surveillance data for the previous 15 years
(e.g., Armed Forces Health Surveillance Division, 2023a; Armed Forces
Health Surveillance Division, 2022a; Armed Forces Health Surveillance
Division, 2021; Armed Forces Health Surveillance Division, 2020). Cases
come from the Defense Medical Surveillance System and include both
ambulatory medical visits and hospitalizations in both military and
civilian facilities. During the period of 2004 through 2022, the number
of cases of hyponatremia among U.S. Armed Forces peaked in 2010 with
180 cases. The lowest number during that time period was 2013, when 72
cases were reported. During the last 15 years in which data were
reported (2007-2022), 1,690 cases of hyponatremia occurred. Of these
1,690 cases, 86.8% (1,467) were diagnosed and treated during an
ambulatory care visit (Armed Forces Health Surveillance Division,
2023a). As the diagnostic code for hyponatremia may include cases that
are not heat-related, these data may be overestimates. However, such
overestimation is reduced in this study as the authors controlled for
many other related diagnoses (e.g., kidney diseases, endocrine
disorders, alcohol/illicit drug abuse), which can cause hyponatremia.
IV. Treatment and Recovery
Treatment and recovery for hyponatremia can vary depending on
severity and symptoms. Workers presenting with mild symptoms should
increase salt intake by consuming salty foods or oral hypertonic saline
and restrict fluid until symptoms resolve or sodium levels return to
within normal limits (KSI, n.d.). Medical attention may be required in
severe cases, which may be life-threating, and may be sought to address
symptoms and personal risk factors (e.g., history of heart conditions,
on a low sodium diet) (NIOSH, 2016).
V. Summary
The available evidence in the scientific literature indicates that
hyponatremia can result from occupational heat exposure. The evidence
on treatment and recovery demonstrates that hyponatremia can require
medical attention and, in some cases, may be life-threatening.
J. Heat Cramps
I. Introduction
Workers exposed to environmental or radiant heat can experience
sudden muscle cramps known as ``heat cramps.'' NIOSH defines heat
cramps as ``a heat-related illness characterized by spastic
contractions of the voluntary muscles (mainly arms, hands, legs, and
feet), usually associated with restricted salt intake and profuse
sweating without significant body dehydration'' (NIOSH, 2016). Someone
can experience heat cramps even if they are frequently hydrating with
water, but they are not replenishing electrolytes. Heat cramps are
recognized as a ``heat-related illness'' by numerous organizations,
including NIOSH, U.S. Army, U.S. Navy, National Athletic Trainers'
Association (NATA), American College of Sports Medicine (ACSM), and
World Medicine (formerly known as IAAF).
II. Physiological Mechanisms
It is recognized in the medical and scientific communities that
heat cramps result from heat exposure. However, the exact physiological
mechanism is not known. In an early study of heat cramps, investigators
included the following as the diagnostic criteria for heat cramps:
exposure to high temperatures at work; painful muscle cramps; rapid
loss of salt in the sweat that is not replaced (which may cause
hyponatremia); diminished concentration of chloride in the blood and in
the body tissues (also known as hypochloremia); and rapid amelioration
of symptoms after appropriate treatment (Talbott and Michelsen, 1933).
The following mechanism has been proposed for the development of
heat cramps: profuse sweating can deplete electrolyte stores (e.g.,
sodium (Na), potassium (K), calcium (Ca)), which exacerbates muscle
fatigue and can cause heat cramps (Bergeron, 2003; Horswill et al.,
2009; Schallig et al., 2017; Derrick, 1934). The U.S. Army further
posits that ``intracellular calcium is increased via a reduction in the
sodium concentration gradient across the cell membrane. The increased
intracellular calcium accumulation then stimulates actin-myosin
interactions (that is, filaments propelling muscle filaments) causing
the muscle contractions'' (Department of the Army, 2022). Heat cramps
are sometimes referred to, more broadly, as exercise-associated muscle
cramps (EAMCs) (Bergeron et al., 2008). However, heat cramps are
distinct in that they only occur in hot conditions, which exacerbate
electrolyte depletion, and may or may not be associated with exercise.
III. Occupational Heat Cramps
Surveillance data and survey study data demonstrate that workers
exposed to environmental or radiant heat frequently experience heat
cramps in the United States. In a study of heat-related illness
hospitalizations and deaths for the U.S. Army from 1980-
[[Page 70719]]
2002, 8% of heat-related illness hospitalizations recorded were due to
heat cramps (Carter et al., 2005). Similarly, in studies of self-
reported heat-related illness, workers frequently cite heat cramps as a
common symptom of heat exposure. Specifically, in several studies of
self-reported heat-related symptoms among farmworkers in multiple
States, participants reported experiencing sudden muscle cramps in the
prior week in Georgia (33.7% of 405 respondents) (Fleischer et al.,
2013), North Carolina (35.7% of 158 respondents) (Kearney et al.,
2016), and Florida (30% of 198 respondents) (Mutic et al., 2018). In
another study of self-reported symptoms among 60 migrant farmworkers in
Georgia, heat-related muscle cramps were reported by 25% of
participants, the second most frequently reported HRI symptom (Smith et
al., 2021). In a study examining exertional heat illness and
corresponding wet bulb globe temperatures in football players at five
southeastern U.S. colleges from August to October 2003, the authors
found that the highest incidences of exertional heat illness (EHI)
occurred in August (88%, EHI rate= 8.95/1000 athlete-exposures (Aes))
and consisted of 70% heat cramps (6.13/1000 Aes) (Cooper et al., 2016).
IV. Treatment and Recovery
Treatment for heat cramps includes electrolyte-containing fluid
replacement (also known as isotonic fluid replacement), stretching, and
massage (Gauer and Meyers, 2019; Peterkin et al., 2016). In some cases,
sodium replacement may be a treatment for heat cramps (Talbott and
Michelsen, 1933; Sandor, 1997; Jansen et al., 2002). In severe cases,
it is recommended that magnesium levels of the patient are obtained and
if necessary, magnesium replacement through IV therapy is provided
(O'Brien et al., 2012). The ACSM recommends rest, prolonged stretching
in targeted muscle groups, oral sodium chloride ingestion in fluids or
foods, or intravenous normal saline fluids in severe cases (ACSM,
2007). NIOSH recommends that medical attention is needed if the worker
has heart problems, is on a low sodium diet, or if cramps do not
subside within 1 hour (NIOSH, 2016). If treated early and effectively,
individuals may return to activity after heat cramps have subsided
(Bergeron, 2007; Savioli et al., 2022; Gauer and Meyers, 2019).
However, severe heat cramps may require an emergency department visit
or hospitalization (Harduar Morano and Waller, 2017; Carter et al.,
2005). While most cases of heat cramps do not require restricted work
status or time away from work, guidelines for military personnel
suggest some cases may require light workload the next day and limited
workload the following day, with observation of the affected patient
because some additional deficits may be delayed or subtle (O'Connor et
al., 2007). In addition, guidelines for military personnel advise that
strenuous exercise be avoided for several days in some cases of heat
cramps (O'Connor et al., 2007). Severe heat cramps may also elicit
soreness for several days which can lead to a longer recovery period
(Casa et al., 2015).
V. Summary
OSHA's review of the scientific and medical literature indicates
that heat cramps are a recognized health effect of occupational heat
exposure. Indeed, several studies of self-reported symptoms of HRI
among farmworkers in multiple States have indicated that heat cramps
are quite common. The best available evidence on treatment and recovery
indicates that heat cramps can, in some cases, require medical
attention and may require time away from work or an adjusted workload.
K. Heat Rash
I. Introduction
Workers in hot environments may experience heat rash. Heat rash is
defined by NIOSH as ``a skin irritation caused by excessive sweating
during hot, humid weather'' (NIOSH, 2022). NIOSH, the U.S. Army, and
the U.S. Navy classify heat rash as a heat-related illness (NIOSH,
2016; Department of the Army, 2022; Department of the Navy, 2023). Also
known as miliaria rubra or prickly heat, workers with heat rash develop
red clusters of pimples or small blisters, which can produce itchy or
prickly sensations that become more irritating as sweating persists in
the affected area. Heat rash can last for several days and tends to
form in areas where clothing is restrictive and rubs against the skin,
most commonly on the neck, upper chest, groin, under the breasts, and
in elbow creases (OSHA, 2011; NIOSH, 2022; OSHA, 2024a). If left
untreated, heat rash can become infected, and more severe cases can
lead to high fevers and heat exhaustion (Wenzel and Horn, 1998). In
some cases, heat rash can lead to hypohidrosis (i.e., the reduced
ability to sweat) in the affected area, even weeks after the heat rash
is no longer visible, which impairs thermoregulation and can cause
predisposition for heat stress (Sulzberger and Griffin, 1969; Pandolf
et al., 1980; DiBeneditto and Worobec, 1985). This can impair an
employee's ability to work and prevent resumption of normal work
activities in hot environments to allow for the area to heal, which in
some cases can take 3-4 weeks for heat intolerance to subside (Pandolf
et al., 1980).
II. Physiological Mechanisms
The development of heat rash has been studied for centuries
(Renbourn, 1958). While working in hot environments with a high
relative humidity, the body's ability to cool itself is greatly
reduced, as sweat is less likely to evaporate from the skin (Sulzberger
and Griffin, 1969; DiBeneditto and Worobec, 1985). Heat rash occurs
when sweat remains on the skin and causes a blockage of sweat (eccrine)
glands and ducts (Wenzel and Horn, 1998). Since the sweat ducts are
blocked, sweat secretions can leak and accumulate beneath the skin,
causing an inflammatory response and resulting in clusters of red bumps
or pimples (Dibeneditto and Worobec, 1985). If left untreated, heat
rash may become infected (Holzle and Kligman, 1978). Depending on the
level of blockage, this can manifest as various types of miliaria, with
miliaria rubra being the most common form of heat rash (Wenzel and
Horn, 1998).
III. Occupational Heat Rash
Surveillance of heat rash in worker populations is limited.
However, farmworkers have reported cases of skin rash or skin bumps
while working in summer months (Bethel and Harger, 2014; Kearney et
al., 2016; Luque et al., 2020). From these studies, the percentage of
participants surveyed or interviewed that report experiencing skin rash
or skin bumps in the previous week were 10% (n=100, Beth and Harger,
2014), 12.1% (n=158, Kearney et al., 2016) and 5% (n=101, Luque et al.,
2020). Although these studies do not purport a diagnosis, presentation
of skin rash or skin bumps while working in hot environments with
reported average high temperatures ranging to the mid-90s [deg]F
indicates respondents may have developed heat rash.
Similar findings with diagnosis of heat rash or related symptoms
have been recorded outside of the U.S. among workers in the following
professions: 17% of indoor electronics store employees in air-
conditioned (4%) and non-air-conditioned (13%) areas in Singapore
(n=52, Koh, 1995); 2% of underground miners at a site in Australia
(n=1,252, Donoghue and Sinclair, 2000); 34% of maize farmers in Nigeria
(n=396, Sadiq et al., 2019); 68% of sugarcane cutters and 23% of
[[Page 70720]]
sugarcane factory workers in Thailand (n=183, Boonruksa et al., 2020);
41% of sugarcane farmers in Thailand (n=200, Kiatkitroj et al., 2021);
17% of autorickshaw drivers (n=78), 23% of outdoor street vendors
(n=75), 16% of street sweepers (n=75) in India (n=228, Barthwal et al.,
2022); and 13% of underground and open pit miners across Australia
(n=515, Taggart et al., 2024). Although these studies illustrate the
prevalence of heat rash in various worker populations, OSHA notes that
differences in study methodologies and the populations studied mean
that the results of these studies are not necessarily directly
comparable to each other or to similar industries or worker populations
in the United States.
The type of clothing worn may also contribute to formation of heat
rash while working in higher temperatures. Heat rash was formally
diagnosed among U.S. military personnel wearing flame resistant army
combat uniforms in hot and arid environments (102.2 [deg]F to 122
[deg]F (39 [deg]C to 50 [deg]C), 5% to 25% relative humidity) (Carter
et al., 2011). In this case series, 18 patients with heat rash
presented with moderate to severe skin irritation, which was worsened
by reactions to chemical additives not removed from the laundering
process and increased heat retention from sweat-soaked clothing, as
well as the friction from the fabric and the occlusive effect of the
clothing, which allowed sweat to accumulate on the skin despite the
lower humidity (Carter et al., 2011). This study calls attention to the
effect of clothing on the development of heat rash and factors that may
influence its severity.
IV. Treatment and Recovery
Although most cases of heat rash can be self-treated without
seeking medical attention, symptoms typically last for several days
(Wenzel and Horn, 1998). It is important that heat rash is kept dry and
cool to avoid possible infection. Workers experiencing heat rash should
move to a cooler and less humid work environment and avoid tight-
fitting clothing, when possible (NIOSH, 2022). The affected area should
be kept dry, and ointments and creams, especially if oil-based, should
not be used (NIOSH, 2022). However, powder may be used for relief.
V. Summary
The available evidence in the scientific literature indicates that
heat rash can result from occupational heat exposure. Although heat
rash usually resolves on its own without medical attention, symptoms
often persist for several days and more severe cases can impair an
employee's ability to work and lead to infection if left untreated.
L. Heat Edema
I. Introduction
Workers in hot environments may experience heat edema. Heat edema
is the swelling of soft tissues, typically in the lower extremities
(feet, ankles, and legs) and hands, and may be accompanied by facial
flushing (Gauer and Meyers, 2019). Surveillance systems and the U.S.
Army classify heat edema as a heat-related illness (Department of the
Army, 2022). Workers who are sitting or standing for prolonged periods
may be at higher risk for heat edema (Barrow and Clark, 1998). Workers
who are not fully acclimatized to the work site may be more prone to
developing heat edema as the body adjusts to hotter temperatures (Howe
and Boden, 2007).
II. Physiological Mechanism
When exposed to heat, the body increases blood flow and induces
vasodilation to cool itself and thermoregulate. This means, as blood is
shunted towards the skin and vasodilation begins, the blood vessels
near the skin's surface become wider (Hough and Ballantyne, 1899;
Kamijo et al., 2005). However, blood can pool in areas of the body that
are most subject to gravity (e.g., legs), and fluid can seep from blood
vessels causing noticeable swelling under the skin--this is known as
heat edema (Gauer and Meyers, 2019).
III. Occupational Heat Edema
Surveillance of heat edema is limited. Many studies include heat
edema as one of many HRIs that contributed to an aggregate measure of
HRI in worker, military, or general populations, but very few were
found to quantify heat edema alone.
Multiple studies outside of the U.S. have examined HRIs among farm
and factory workers in the sugarcane industry through surveys and
interviews (Crowe et al., 2015; Boonruksa et al., 2020; Kiatkitroj et
al., 2021; Debela et al., 2023). Respondents in the studies were asked
if they experienced swelling of the feet or hands (with varying degrees
of frequency) during periods of heat exposure, which could indicate
presentation of heat edema. In different samples of sugarcane workers
in two provinces of Thailand, two studies found incidence of swelling
of the hands and feet. Among sugarcane cutters, 16.7% self-reported
ever experiencing swelling of the hands or feet and 5.6% self-reported
experiencing these symptoms (mean 30.6 [deg]C WBGT) (n=90, Boonruksa et
al., 2020). In another province, 10.5% self-reported swelling of the
hands/feet while working one summer (n=200, Kiatkitroj et al., 2021).
While comparing HRI symptoms among sugarcane harvesters and non-
harvesters in Costa Rica, 15.1% of harvesters (n=106) and 7.9% of non-
harvesters (n=63) self-reported having ever experienced swelling of
hands/feet (p=0.173) (n=169, Crowe et al., 2015). While 7.5% of
harvesters, who worked outdoors in the field, self-reported
experiencing this symptom at least once per week, no non-harvesters
self-reported swelling with this level of frequency (p=0.026) (Crowe et
al., 2015). The sample of non-harvesters included both workers that
were intermediately exposed to heat (e.g., in the processing plant or
machinery shop) and workers not exposed to heat (e.g., in offices).
In a sample of sugarcane factory workers (n=1,524) in Ethiopia,
72.4% (1,104) were considered exposed to heat defined as conditions
exceeding the ACGIH's TLV (Debela et al., 2023). Of the total sample
(including workers considered exposed to heat and not), 78% (1,189)
self-reported having experienced swelling of hands and feet at least
once per week, which was the most commonly reported HRI symptom (Debela
et al., 2023). Although these studies do not purport a diagnosis,
presentation of swelling of the hands and feet while working in hot
environments suggests respondents may have developed heat edema.
IV. Treatment and Recovery
Although most cases of heat edema can be self-treated without
seeking medical attention, symptoms can last for days and reoccurrence
is less likely if individuals are properly acclimatized (Howe and
Boden, 2007; Department of the Army, 2023). It is important that the
affected individual moves out of the heat and elevates the swollen
area. Diuretics are not typically recommended for treatment (Howe and
Boden, 2007; Gauer and Meyers, 2019; CDC, 2024a).
V. Summary
The available evidence in the scientific literature indicates that
heat edema can result from occupational heat exposure, causing swelling
of the lower extremities (feet, ankles, and legs) and hands. It may be
difficult to move swollen body parts, thereby impeding an employee's
ability to perform their job. The need for medical attention can
typically be avoided if the condition is properly treated.
[[Page 70721]]
M. Kidney Health Effects
I. Introduction
The kidneys perform many functions in the body, including filtering
toxins out of the blood and balancing the body's water and electrolyte
levels (NIDDK, 2018). Working in the heat places a lot of demand on the
kidneys to conserve water and regulate electrolytes, like sodium, lost
through sweat. A growing body of experimental and observational
literature suggests that intense heat strain can cause damage to the
kidneys in the form of acute kidney injury (AKI), even independent of
conditions like heat stroke and rhabdomyolysis. An epidemic of chronic
kidney disease in Central America and other regions around the world
has placed additional attention on the potential of recurrent heat
stress-related AKI to cause chronic kidney disease (CKD) over time
(Johnson et al., 2019; Schlader et al., 2019). Working in the heat has
also been associated with the development of kidney stones among
workers outside the U.S., likely a result of decreased urine volume
leading to increased concentration of minerals in the urine that
crystallize into stones.
Each kidney is comprised of hundreds of thousands of functional
units called nephrons. Each nephron has multiple parts, including the
glomerulus (a cluster of blood vessels that conduct the initial
filtering of large molecules) and the tubules (tubes that reabsorb
needed water and minerals and secrete waste products). The fluid that
remains after traveling through the glomeruli and tubules becomes urine
and is eliminated from the body (NIDDK, 2018).
This section will discuss three kidney-related health effects
associated with heat exposure: kidney stones, AKI, and CKD.
II. Kidney Stones
A. Introduction
Kidney stones are hard objects that form in the kidney from the
accumulation of minerals. They range in size from a grain of sand to a
pea (NIDDK, 2017a). Symptoms include sharp pain in the back, side,
lower abdomen, or groin; pink, red, or brown blood in the urine; a
constant need to urinate; pain while urinating; inability to urinate or
only able to urinate a small amount; and cloudy or foul-smelling urine
(NIDDK, 2017b). Nausea, vomiting, fever, and chills are also possible,
and symptoms may be brief, prolonged, or come in waves (NIDDK, 2017b).
In rare cases or when medical care is delayed, kidney stones can lead
to complications including severe pain, urinary tract infections (UTI),
and loss of kidney function (NIDDK, 2017a). Risk factors for kidney
stones include being male, a family history of kidney stones, having
previously had kidney stones, not drinking enough liquids, other
medical conditions (e.g., chronic inflammation of the bowel, digestive
problems, hyperparathyroidism, recurrent UTIs), drinking sugary
beverages, and working in the heat, especially if unacclimatized
(NIDDK, 2017a; Maline and Goldfarb, 2024). NIOSH has also cautioned
workers that experiencing chronic dehydration can increase the risk of
developing kidney stones (NIOSH, 2017a).
B. Physiological Mechanisms
Kidney stones form when concentrations of minerals are high enough
to the point of forming crystals, which then aggregate into a stone in
either the renal tubular or interstitial fluid (Ratkalkar and Kleinman,
2011). Reduced urine volume, altered urine pH, diet, genetics, or many
other factors may cause this concentration of minerals (Ratkalker and
Kleinman, 2011). Heat exposure has the potential to cause kidney stones
through heat-induced sweating and dehydration. Loss of extracellular
fluid increases osmolality (i.e., increased concentration of solutes,
like sodium and glucose) which leads to increased secretion of
vasopressin, an antidiuretic hormone. Vasopressin signals to the
kidneys to conserve water by reducing urine volume, leading to
increased concentration of relatively insoluble salts, like calcium
oxalate, in the urine. These salts can eventually form crystals which
can develop into stones (Fakheri and Goldfarb, 2011).
C. Occupational Heat Exposure and Kidney Stones
Epidemiological studies conducted outside the U.S. have documented
the association between working in heat and developing kidney stones.
One of the earliest publications on occupational heat and kidney stones
was a small study of beach lifeguards in Israel (Better et al., 1980).
Eleven of 45 randomly selected lifeguards (24%) were found to have had
kidney stones, which Better et al. noted was approximately 20 times the
incidence rate of the general Israeli population at the time. The
authors attributed this finding to low urine output due to dehydration,
hyperuricemia (elevated levels of uric acid in the blood), and
absorptive hypercalciuria (elevated levels of calcium in the urine),
among other factors. In 1992, Pin et al. compared outdoor workers
exposed to hot environmental conditions to indoor workers exposed to
cooler conditions (Pin et al., 1992). This study of 406 men in Taiwan
included quarry, postal, and hospital engineering support workers. The
prevalence of kidney stones was found to be significantly higher in the
outdoor workers than the indoor workers (5.2% versus 0.85%, p<0.05).
The authors posited that chronic dehydration from working outdoors in a
tropical environment might explain the higher prevalence of kidney
stones among outdoor workers (Pin et al., 1992).
Several studies have also considered occupational exposure to
indoor heat sources. Borghi et al. studied machinists who had been
working in the blast furnaces of a glass plant in Parma, Italy for five
or more years, excluding those who had kidney stones before working at
the plant (Borghi et al., 1993). The prevalence of kidney stones was
significantly higher among machinists exposed to heat (n=236) than
among those working in cooler temperatures (n=165) (8.5% vs. 2.4%,
p=0.03) (Borghi et al., 1993). An analysis of risk factors revealed
that workers in the heat lost substantially more water to sweat and
that their urine had higher concentrations of uric acid, higher
specific gravity, and lower pH than workers in normal temperatures
(Borghi et al., 1993).
In a large study in Brazil, the prevalence of at least one episode
of kidney stones was 8.0% among the 1,289 workers in hot areas, which
was significantly higher than the 1.75% prevalence found among the
9,037 people working in room temperature conditions (p<0.001) (Atan et
al., 2005). An analysis of a subset of workers demonstrated that
workers in hot temperatures had significantly less citrate in their
urine (p=0.03) and lower urinary volume (p=0.01) compared to room-
temperature workers.
Venugopal et al. studied 340 steel workers in southern India
engaged in moderate to heavy labor with three or more years of heat
exposure (Venugopal et al., 2020). Of the 340 participants, 91 workers
without other risk factors for kidney disease, but who had reported a
symptom of kidney or urethral issues, underwent renal ultrasounds,
which revealed that 27% had kidney stones. 84% of the participants with
kidney stones were occupationally exposed to heat, as defined as
working in conditions above the ACGIH TLV. Having five or more years of
heat exposure was significantly associated with risk of kidney stones,
while
[[Page 70722]]
controlling for smoking (OR: 3.6, 95% CI: 1.2, 10.7).
Most recently, Lu et al. studied 1,681 steel workers in Taiwan, 12%
of whom had kidney stones, compared to the age-adjusted prevalence
among men in Taiwan of 9% (Lu et al., 2022). Heat exposure was found to
be positively associated with prevalence of stones, particularly among
workers <=35 years old (OR: 2.7, 95% CI: 1.2, 6.0) (Lu et al., 2022).
Overall, the peer-reviewed literature supports occupational heat
exposure as a risk factor for kidney stones, in both indoor and outdoor
environments, across multiple countries, and in several industries.
D. Treatment and Recovery
Treatment of kidney stones depends on their size, location, and
type. Someone with a small kidney stone may be able to pass it by
drinking plenty of water and taking pain medications as prescribed by a
doctor (NIDDK, 2017c). Larger kidney stones can block the urinary
tract, cause intense pain, and may require medical intervention such as
shock wave lithotripsy, cystoscopy, ureteroscopy, or percutaneous
nephrolithotomy to remove or break up the stone (NIDDK, 2017c).
Percutaneous nephrolithotomy, whereby kidney stones are removed through
a surgical incision in the skin, requires several days of
hospitalization, but the other interventions typically do not require
an overnight hospital stay (NIDDK, 2017c). One study found that among
working aged adults, approximately one third of people treated for
kidney stones miss work and that they miss, on average, 19 hours of
work per person (Saigal et al., 2005). With monitoring or treatment,
people typically recover from kidney stones. However, over the long
term, individuals who develop kidney stones are at increased risk of
chronic kidney disease and end-stage renal disease, particularly if
kidney stones are recurrent (Uribarri, 2020).
E. Summary
The available peer-reviewed scientific literature demonstrates
occupational heat exposure as a risk factor for kidney stones, in both
indoor and outdoor environments. Kidney stones may require medical
treatment and in some cases hospitalization. Finally, individuals who
develop kidney stones are at increased risk of other kidney diseases.
III. Acute Kidney Injury
A. Introduction
Acute kidney injury (AKI) can affect workers exposed to
occupational heat. AKI is an abrupt decline in kidney function in a
short period (e.g., a few days). As normally functioning kidneys filter
blood and maintain fluid balance in the body, AKI events can disrupt
this fluid balance, which can impact major organs like the heart. AKI
can also have metabolic consequences, like a build-up of too much
potassium in the blood (hyperkalemia) (Goyal et al., 2023). AKI is not
always accompanied by symptoms and is typically diagnosed with blood
and/or urine tests (e.g., increase in serum creatinine). While damage
to the kidneys is one potential consequence of heat stroke (such as in
the context of multi-organ failure, as mentioned in Section IV.E., Heat
Stroke), this section is focused on AKI that is not necessarily
preceded by clinical heat stroke.
B. Physiological Mechanisms
There are three categories of AKI used to distinguish the location
of the cause(s) of AKI--prerenal, intrarenal, and postrenal (Goyal et
al., 2023). Prerenal AKI represents a reduction in blood volume being
delivered to the kidneys (i.e., renal hypoperfusion). This can be the
result of heat-induced sweating that leads to reduced circulating blood
volume. Prerenal AKI that is reversed (e.g., dehydration is quickly
reversed) is typically not associated with impairment to the kidney
glomeruli or tubules, however prolonged exposure can lead to direct
injury to renal cells through ischemia (inadequate blood and oxygen
supply to cells). Intrarenal AKI is when the function of the glomeruli,
tubules, or interstitium are affected, such as in the case of
nephrotoxic exposures (e.g., heavy metals) or prolonged ischemia.
Rhabdomyolysis, which was previously discussed in Section IV.H.,
Rhabdomyolysis, is one potential cause of necrosis of tubular cells
resulting from myoglobin precipitation and direct iron toxicity (Sauret
et al., 2002, Patel et al., 2009). Postrenal AKI is when there is an
obstruction to the flow of urine, such as kidney stones, pelvic masses,
or prostate enlargement. Postrenal AKI is less relevant to a discussion
of heat-related health effects, apart from kidney stones, which is
discussed in Section IV.M.II., Kidney Stones.
Researchers have written specifically about potential mechanisms
leading from occupational heat exposure to AKI (Roncal-Jim[eacute]nez
et al., 2015; Johnson et al., 2019; Schlader et al., 2019; Hansson et
al., 2020), often in the context of chronic kidney disease. As
previously discussed in Section IV.B., General Mechanisms of Heat-
Related Health Effects, working in the heat can lead to increases in
core temperature and reductions in circulating blood volume.
Researchers hypothesize that elevated core temperature could directly
injure renal tissue or that injury could be mediated through
subclinical (mild and asymptomatic) rhabdomyolysis or increases in
intestinal permeability that can cause inflammation. Reductions in
blood volume could inflame or injure the kidneys through reduced renal
blood flow that leads to ischemia and/or local reductions in adenosine
triphosphate (ATP) availability. Reduced blood flow and increased blood
osmolality also trigger physiologic pathways (e.g., renin-angiotensin-
aldosterone system, polyol-fructokinase pathway) which are energy-
intensive and may lead to oxidative stress and inflammation. Other
mechanistic pathways under investigation include urate crystal-induced
injury (Roncal-Jim[eacute]nez et al., 2015) and increased reabsorption
of nephrotoxicants (Johnson et al., 2019).
C. Identifying Cases of Acute Kidney Injury
Serum creatinine levels are used in clinical settings to estimate
kidney function (glomerular filtration rate, or GFR), as it is
typically produced in the body at a relatively stable rate and is
removed from circulation by the kidneys. Multiple criteria exist for
defining AKI based on increases in serum creatinine over hours or days,
such as the KDIGO criteria published by a non-profit organization that
produces recommendations on kidney disease (KDIGO, 2012). There are
multiple factors that could affect the reliability of using serum
creatinine to estimate GFR, including the increased production of
creatinine during exercise. As a result of the limitations of serum
creatinine, there is growing use of alternative biomarkers to identify
cases of AKI, which may be more reliable and specific to AKI, such as
neutrophil gelatinase-associated lipocalin, or NGAL.
D. Experimental Evidence
Researchers have documented an association between heat strain and
biomarkers of AKI in controlled experimental conditions. In 2013,
Junglee et al. documented elevations in urine and plasma NGAL and
reductions in urine flow rate in participants after a heat stress trial
that induced elevations in core temperature and reductions in body mass
(an indication of hydration status) (Junglee et al., 2013). These
increases in NGAL were higher in an experimental group that underwent a
muscle damaging, downhill (-10% gradient) run (compared to a non-
[[Page 70723]]
muscle damaging run on a 1% gradient) prior to the heat stress trial,
providing support for the argument that subclinical rhabdomyolysis may
be a pathway from heat stress to kidney injury. Schlader et al.
conducted a trial in which participants wearing firefighting gear
completed two separate exercise trials in hot conditions of different
durations. The longer duration trial was intended to induce higher
levels of heat strain, while the shorter duration was intended to
induce lower levels (Schlader et al., 2017). The researchers found that
the longer trial was associated with elevated core temperature and
reduced blood volume, as well as increases in serum creatinine and
plasma NGAL, suggesting the magnitude of kidney injury may be
proportional to the magnitude of heat strain. McDermott et al. tested
longer durations of exercise in the heat (5.7 <plus-minus> 1.2 hours)
and similarly found elevations in serum creatinine and serum NGAL from
before the trial to after (McDermott et al., 2018). To determine
whether it is elevated core temperature or reduced blood volume that
primarily drives heat-induced AKI, Chapman et al. conducted four trials
in which subjects exercised for two hours in the same conditions, but
received different interventions (water, cooling, water plus cooling,
and no intervention) (Chapman et al., 2020). The group with no
intervention had the highest levels of urinary AKI biomarkers in the
recovery period, whereas the water and cooling groups each experienced
reductions in AKI biomarker levels relative to the control group. The
researchers concluded that limiting hyperthermia and/or dehydration
reduces the risk of AKI.
The relationship between AKI and hyperthermia and/or dehydration
has also been demonstrated in animal models (Hope and Tyssebotn 1983;
Miyamoto 1994; Roncal-Jim[eacute]nez et al., 2014; Sato et al., 2019).
E. Cases of Occupational Heat-Related AKI
In addition to experimental evidence, heat-related AKI has also
been observed in ``real world'' conditions going back to the 1960s. In
1967, Schrier et al. documented evidence of military recruits
developing AKI (referred to as ``acute renal failure'') following
training exercises in the heat (Schrier et al., 1967). It was soon
after reported that AKI cases linked to exercise in the heat
represented a sizeable portion (approximately 10%) of all AKI cases
treated at Walter Reed General Hospital in the early 1960s (Schrier et
al., 1970).
More recently, serum creatinine-defined AKI has been observed in
agricultural workers in both Florida and California. Among a cohort of
field workers from the Central Valley of California, Moyce et al.
report a post-work shift incidence of AKI of 12.3% (35 of 283 workers)
(Moyce et al., 2017). Workers with heat strain, characterized by
increased core temperature and heart rate, were significantly more
likely to have AKI (OR: 1.34, 95% CI: 1.04, 1.74). Among a cohort of
agricultural workers in Florida, Mix et al. found that heat index
(based on nearest weather monitor) was positively associated with the
risk of AKI--47% increase in the odds of AKI for every 5 [deg]F
increase in heat index. The authors reported an incidence of AKI of 33%
(i.e., 33% of workers had AKI on at least one day of monitoring) in
this study (Mix et al., 2018).
OSHA researchers have also identified cases of heat-related AKI
among workers in the agency's own databases: the Severe Injury Reports
(SIR) database and case files from consultations by the Office of
Occupational Medicine and Nursing (OOMN) (Shi et al., 2022). Shi et al.
identified 22 cases of heat-related AKI between 2010 and 2020 in the
OOMN consultation records (based on serum creatine elevations meeting
the KDIGO requirements) after excluding cases related to severe
hyperthermia, multi-organ failure, or death. Using inclusion criteria
of a heat-related OIICS code (172*) and a mention of AKI in the
narrative, they also identified 57 cases of probable heat-related AKI
between 2015 and 2020 in the SIR database.
Studies conducted among workers outside the U.S. have also reported
a relationship between working in the heat and acute elevations in
serum creatinine or increased risk of AKI (Garc[iacute]a-Trabanino et
al., 2015; Wegman et al., 2018; Nerbass et al., 2019; Sorensen et al.,
2019).
There are a few limitations to these observational studies, such as
the use of serum creatinine to characterize AKI, as described above. An
additional limitation is the inability to determine from these studies
whether the AKI observed is due to prerenal or intrarenal causes. As
discussed in Physiological Mechanisms, prerenal AKI may be due to
reductions in renal blood flow (which would be expected in cases of
dehydration) and is not necessarily indicative of clinically
significant structural injury. Another limitation may be the use of
serum creatinine measures taken over relatively short spans of time,
which may be too short to see true reductions in GFR (Waikar and
Bonventre, 2009). However, there are a growing number of studies that
find a relationship between short-term fluctuations in serum creatinine
and longer-term declines in kidney function among outdoor workers (see
discussion in Section IV.M.IV., Chronic Kidney Disease).
F. Treatment and Recovery
There is a spectrum of severity for AKI. For example, some
individuals may not know they are experiencing AKI without a serum or
urine test. There is also a spectrum of time and medical treatment
needed for recovery, dependent on whether the AKI is quickly reversed
or sustained for longer periods of time. In Schlader et al. 2017,
researchers noted that the biomarkers of AKI for participants in their
trial returned to baseline the following day. However, intrarenal
causes of AKI may require longer periods of time for recovery and may
potentially require the need for medication or dialysis (Goyal et al.,
2023). AKI can be severe, which can be the case when resulting from
heat stroke, where it may represent irreversible damage to the kidneys
and can be fatal (Roberts et al., 2008; King et al., 2015; Wu et al.,
2021). Recurrent AKI may also lead to chronic kidney disease (as
discussed in Section IV.M.IV., Chronic Kidney Disease).
G. Summary
The available peer-reviewed scientific literature, both
experimental and observational studies, suggests that occupational heat
exposure causes AKI among workers. However, there are limitations in
the case definitions used to define AKI in observational settings.
IV. Chronic Kidney Disease
A. Introduction
Chronic kidney disease (CKD) is a progressive disease characterized
by a gradual decline in kidney function over months to years. It is
typically asymptomatic or mildly symptomatic until later stages of the
disease, when symptoms such as edema, weight loss, nausea, and vomiting
can occur (NIDDK 2017d). People with CKD can be at a greater risk for
other health conditions, like AKI, heart attacks, hypertension, and
stroke. The diagnosis typically requires multiple blood and urine tests
taken over time (NIDDK 2016). Typical risk factors for CKD include
hypertension and diabetes.
Epidemics of CKD in Central America and other pockets of the world,
such as India and Sri Lanka, that appear to be afflicting mostly young,
outdoor workers with no history of hypertension or diabetes have raised
questions about
[[Page 70724]]
whether working in hot conditions can cause the development of CKD
(Johnson et al., 2019). Researchers have been investigating this
question and the cause of the epidemic over the past 20 years,
including other potential exposures, such as heavy metals,
agrichemicals, silica, and infectious agents (Crowe et al., 2020).
B. Physiological Mechanisms
Researchers have proposed that working in the heat could lead to
the development of CKD through repetitive AKI events (see discussion of
heat-related mechanisms in Section IV.M.III., Acute Kidney Injury).
However, some researchers acknowledge the possibility that the
unexplained CKD cases observed in Central America and elsewhere may
instead represent a chronic disease process that begins earlier in life
which places workers at increased risk of AKI (Johnson et al., 2019;
Schlader et al., 2019). Additionally, as discussed above in Section
IV.M.III., Acute Kidney Injury, some occupational cases of AKI could be
transient, the result of prerenal causes, and possibly unrelated to the
development of CKD.
Independent of the epidemic of unexplained CKD, frequent and/or
severe AKI has been identified as a risk factor for developing CKD
(Ishani et al., 2009; Coca et al., 2012; Chawla et al., 2014; Hsu and
Hsu 2016; Heung et al., 2016). The relationship between heat-related
AKI and risk of developing CKD is untested in the experimental
literature because of the ethical implications (Schlader et al., 2019;
Hansson et al., 2020).
As discussed in Section IV.E., Heat Stroke, there is also evidence
that experiencing heat stroke may increase an individual's risk of
developing CKD (Wang et al., 2019; Tseng et al., 2020).
C. Identifying Cases of Chronic Kidney Disease
As discussed previously in the context of AKI, serum creatinine is
commonly used to estimate glomerular filtration rate (GFR), the
indicator of kidney function. When measures of serum creatinine (and
therefore estimates of GFR) are taken over periods of months to years,
medical professionals can determine if an individual's kidney function
is declining. CKD is typically diagnosed when the estimated GFR is
below a rate of 60 mL/min/1.73m\2\ for at least 3 months, although
there are other indicators, like a high albumin-to-creatinine ratio.
There are various stages of CKD; the final stage is called end-stage
renal disease (ESRD) and represents a point at which the kidneys can no
longer function on their own and require dialysis or transplant.
D. Observational Evidence
There is a growing body of evidence that suggests that heat-exposed
workers who experience AKI (or short-term fluctuations in serum
creatinine) are at greater risk of experiencing declines in kidney
function over a period of months to years. For instance, sugarcane
workers in Nicaragua who experienced cross-shift increases (i.e.,
increase from pre-shift to post-shift) in serum creatinine at the
beginning of the harvest season were more likely to experience declines
in estimate GFR nine weeks later (Wesseling et al., 2016). Another
study conducted among Nicaraguan sugarcane workers found that
approximately one third of workers who experienced AKI during the
harvest season had newly decreased kidney function (greater than 30%
decline) and a measure of estimated GFR of less than 60 mL/min/1.73m2
one year later (Kupferman et al., 2018). In an analysis among
Guatemalan sugarcane workers, Dally et al. found that workers with
severe fluctuations in serum creatinine over a period of 6 workdays had
greater declines in estimated GFR (-20% on average) (Dally et al.,
2020). In a separate study conducted in Northwest Mexico, researchers
observed declines in estimated GFR among migrant and seasonal farm
workers from March to July that were not observed in a reference group
of office workers in the same region (L[oacute]pez-G[aacute]lvez et
al., 2021).
Further support for the hypothesis that working in the heat may
lead to declines in GFR and increased risk of CKD comes from
intervention studies in Central America, in which workers were given
water-rest-shade interventions and observed longitudinally for kidney
outcomes. In these stu
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