An exploratory survey of on-site heat stress management practices in the Canadian mining industry.

With climate change fueling more frequent and intense periods of hot weather, heat stress management programs are becoming increasingly important for protecting the health and safety of workers in the Canadian mining industry. While the inclusion of heat-mitigation measures such as those provided by the American College of Governmental Industrial Hygienists (ACGIH) Threshold Limit Values (TLVs) are commonly employed by industry, there is a need to develop more comprehensive industry-specific measures for heat stress prevention and management. To better understand current heat management practices and identify opportunities for improvement, an exploratory survey of 51 employees responsible for health and safety at underground mining (n = 35), and surface operations (n = 16) (e.g., open-pit mining, milling, smelting, and exploration site) was conducted in Canada. The respondents answered 50 questions related to workplace heat stress management, including descriptors of the workplace environment, perceived heat stress hazard, administration of heat stress management programming, heat stress emergency procedures, environmental monitoring strategies, and knowledge of mining-specific regulations related to heat stress. Twenty-four managers (47%) reported that heat-related illnesses led to restricted duty or lost time claims at their site, with a median of 5 [IQR: 2-10, max: 30] reportable heat-related illnesses occurring per site annually. Many also felt that heat-related illnesses are under-reported by their workforce (n = 36, 71%). Most sites reported established heat stress management programs to prevent heat illness (n = 43, 84%), typically based on the TLVs (n = 38, 75%). Although some organizations do conduct pre-task evaluations for heat stress (n = 30, 59%), more than half do not conduct post-job evaluations (n = 28, 55%) or pre-employment screening for heat stress vulnerability (n = 3, 6%). While our findings indicate that the health and safety managers recognize the hazard posed by heat and have stated practices to help address the hazard, we also observed inconsistencies in heat stress management programming across the sample. Developing and adopting a standard heat stress management and reporting system would be an important step toward protecting workers from existing and emerging threats from extreme heat and climate change.

Markers of enterocyte damage, microbial translocation and systemic inflammation following 9 hours of heat exposure in young and older adults.

Heat stress induced damage to the gastrointestinal barrier can induce local and systemic inflammatory reactions implicated in heat-stroke. Gastrointestinal barrier damage has been shown to be greater in older relative to young adults following hyperthermia. However, comparisons between young and older adults have been limited to brief exposures (3-h), which may not reflect the duration of heat stress experienced during heat waves. We therefore evaluated markers of intestinal epithelial damage (Log transformed intestinal fatty acid binding protein, IFABPLOG), microbial translocation (soluble cluster of differentiation 14, sCD14LOG), and systemic inflammation (tumour necrosis factor alpha, TNF-αLOG; interleukin 6, IL-6LOG; C-reactive protein, CRP) in 19 young (interquartile range: 21-27 yr; 10 females) and 37 older (68-73 yr; 10 females) adults before and after 9-h of rest in 40°C (9% relative humidity). The magnitude of the increase in IFABPLOG was 0.38 log pg/mL (95% CI, 0.10, 0.65 log pg/mL) greater in the older relative to young cohort (P=0.049) after 9-h heat exposure. At baseline both IL-6LOG and CRP concentrations were higher in the older (IL-6: 2.67 (1.5) log pg/mL, CRP: 0.28 (1.5) mg/mL) relative to the young (IL-6: 1.59 log pg/mL, SD 1.2; CRP: 0.11 mg/mL, SD 1.7) group (both P<0.001). The change in IL-6 and CRP was similar between groups following 9-h heat exposure (IL-6: P=0.053; CRP: P=0.24). Neither sCD14LOG and TNF-αLOG were different between groups at baseline nor altered after 9-h heat exposure. Our data indicate that age may modify intestinal epithelial injury following 9 h of passive heat exposure.

Exercise intensity- and body region-specific differences in sweating in middle-aged-to-older men with and without type 2 diabetes.

Type 2 diabetes is associated with reduced whole-body sweating during exercise-heat stress. However, it is unclear if this impairment is related to exercise intensity and whether it occurs uniformly across body regions. We evaluated whole-body (direct calorimetry) and local (ventilated-capsule technique; chest, back, forearm, thigh) sweat rates in physically active men with type 2 diabetes (T2D; aged 59 (7) years; V̇O2peak 32.3 (7.6) mL·kg-1·min-1; n=26; HbA1c 5.1-9.1%) and without diabetes (Control; aged 61 (5) years; V̇O2peak 37.5 (5.4) mL·kg-1·min-1; n=26) during light (~40%V̇O2peak), moderate (~50%V̇O2peak), and vigorous (~65%V̇O2peak) intensity exercise (elicited by fixing metabolic heat production at ~150, 200, 250 W·m-2, respectively) in 40°C, ~17% relative humidity. Whole-body sweating was ~11% (T2D-Control mean difference [95% confidence interval]: -37 [-63, -12] g·m-2·h-1) and ~13% (-50 [-76, -25] g·m-2·h-1) lower in the T2D compared to the Control group during moderate- and vigorous- (p≤0.001), but not light-intensity exercise (-21 [-47, 4] g·m-2·h-1; p=0.128). Consequently, the diabetes-related reductions in whole-body sweat rate were 2.3 [1.6, 3.1] times greater during vigorous relative to light exercise (p<0.001). Further, these diabetes-related impairments in local sweating were region-specific during vigorous-intensity exercise (group × region interaction: p=0.024), such that the diabetes-related reduction in local sweat rate at the trunk (chest, back) was 2.4 [1.2, 3.7] times greater than that at the limbs (thigh, arm). In summary, when assessed under hot, dry conditions, diabetes-related impairments in sweating are exercise intensity-dependent and greater at the trunk compared to the limbs.

A critical review of the effectiveness of electric fans as a personal cooling intervention in hot weather and heatwaves.

Health agencies worldwide have historically cautioned that electric fans accelerate body-heat gain during hot weather and heatwaves (typically in air temperatures ≥35°C). However, guidance published since 2021 has suggested that fans can still cool the body in air temperatures up to 40°C by facilitating sweat evaporation, and therefore are an inexpensive yet sustainable alternative to air conditioning. In a critical analysis of the reports cited to support this claim, we found that although fan use improves sweat evaporation, these benefits are of insufficient magnitude to exert meaningful reductions in body core temperature in air temperatures exceeding 35°C. Health agencies should continue to advise against fan use in air temperatures higher than 35°C, especially for people with compromised sweating capacity (eg, adults aged 65 years or older). Improving access to ambient cooling strategies (eg, air conditioning or evaporative coolers) and minimising their economic and environmental costs through policy initiatives, efficient cooling technology, and combined use of low-cost personal interventions (eg, skin wetting or fan use) are crucial for climate adaptation.

Experimental research in environmentally induced hyperthermic older persons: A systematic quantitative literature review mapping the available evidence.

The heat-related health burden is expected to persist and worsen in the coming years due to an aging global population and climate change. Defining the breadth and depth of our understanding of age-related changes in thermoregulation can identify underlying causes and strategies to protect vulnerable individuals from heat. We conducted the first systematic quantitative literature review to provide context to the historical experimental research of healthy older adults - compared to younger adults or unhealthy age matched cases - during exogenous heat strain, focusing on factors that influence thermoregulatory function (e.g. co-morbidities). We identified 4,455 articles, with 147 meeting eligibility criteria. Most studies were conducted in the US (39%), Canada (29%), or Japan (12%), with 71% of the 3,411 participants being male. About 71% of the studies compared younger and older adults, while 34% compared two groups of older adults with and without factors influencing thermoregulation. Key factors included age combined with another factor (23%), underlying biological mechanisms (18%), age independently (15%), influencing health conditions (15%), adaptation potential (12%), environmental conditions (9%), and therapeutic/pharmacological interventions (7%). Our results suggest that controlled experimental research should focus on the age-related changes in thermoregulation in the very old, females, those with overlooked chronic heat-sensitive health conditions (e.g. pulmonary, renal, mental disorders), the impact of multimorbidity, prolonged and cumulative effects of extreme heat, evidence-based policy of control measures (e.g. personal cooling strategies), pharmaceutical interactions, and interventions stimulating protective physiological adaptation. These controlled studies will inform the directions and use of limited resources in ecologically valid fieldwork studies.

Agreement between measured and self-reported physiological strain in males and females during simulated occupational heat stress.

RATIONALE: Monitoring physiological strain is recommended to safeguard workers during heat exposure, but is logistically challenging. The perceptual strain index (PeSI) is a subjective estimate thought to reflect the physiological strain index (PSI) that requires no physiological monitoring. However, sex is known to influence perceptions of heat stress, potentially limiting the utility of the PeSI. OBJECTIVES: The objective of this study was to assess whether sex modifies the relationship between PeSI and PSI. METHODS: Thirty-four adults (15 females) walked on a treadmill (moderate intensity; ~200 W/m2) for 180 min or until termination (volitional fatigue, rectal temperature ≥39.5°C) in 16°C, 24°C, 28°C, and 32°C wet-bulb globe temperatures. Rectal temperature and heart rate were recorded to calculate PSI (0-10 scale). Rating of perceived exertion and thermal sensation were recorded to calculate PeSI (0-10 scale). Relationships between PSI and PeSI were evaluated via linear mixed models. Mean bias (95% limits of agreement [LoA]) between PSI and PeSI was assessed via Bland-Altman analysis. Mean absolute error between measures was calculated by summing absolute errors between the PeSI and the PSI and dividing by the sample size. FINDINGS: PSI increased with PeSI (p < 0.01) but the slope of this relation was not different between males and females (p = 0.83). Mean bias between PSI and PeSI was small (-0.4 points), but the 95% LoA (-3.5 to 2.7 points) and mean absolute error were wide (1.3 points). IMPACT: Our findings indicate that sex does not appreciably impact the agreement between the PeSI and PSI during simulated occupational heat stress. The PeSI is not a suitable surrogate for the PSI in either male or female workers.

Hormonal intrauterine devices and heat exchange during exercise.

Synthetic progestins in oral contraceptives are thought to blunt heat dissipation by reducing skin blood flow and sweating. However, whether progestin-releasing intrauterine devices (IUDs) modulate heat loss during exercise-heat stress is unknown. We used direct calorimetry to measure whole-body total (dry + evaporative) heat loss in young, physically active women (mean (SD); aged 24 (4) years, V ̇ O 2 peak ${\dot V_{{{\mathrm{O}}_{\mathrm{2}}}{\mathrm{peak}}}}$ 39.3 (5.3) ml/kg/min) with (IUD; n = 19) and without (Control; n = 17) IUDs in the follicular and luteal phases of the menstrual cycle during light- and moderate-intensity exercise at fixed rates of heat production (∼175 and ∼275 W/m2 ) in 30°C, ∼21% relative humidity. Between-group and -phase differences were evaluated using traditional hypothesis testing and statistical equivalence testing within pre-determined bounds (±11 W/m2 ; difference required to elicit a ±0.3°C difference in core temperature over 1 h) in each exercise bout. Whole-body total heat loss was statistically equivalent between groups within ±11 W m-2 (IUD-Control [90% CIs]; Light: -2 [-8, 5] W/m2 , P = 0.007; Moderate: 0 [-6, 6] W/m2 , P = 0.002), as were dry and evaporative heat loss (P ≤ 0.023), except for evaporative heat loss during moderate-intensity exercise (equivalence: P = 0.063, difference: P = 0.647). Whole-body total and evaporative heat loss were not different between phases (P ≥ 0.267), but dry heat loss was 3 [95% CIs: 1, 5] W/m2 greater in the luteal phase (P ≤ 0.022). Despite this, all whole-body heat loss outcomes were equivalent between phases (P ≤ 0.003). These findings expand our understanding of the factors that modulate heat exchange in women and provide valuable mechanistic insight of the role of endogenous and exogenous female sex hormones in thermoregulation. KEY POINTS: Progestin released by hormonal intrauterine devices (IUDs) may negatively impact heat dissipation during exercise by blunting skin blood flow and sweating. However, the influence of IUDs on thermoregulation has not previously been assessed. We used direct calorimetry to show that IUD users and non-users display statistically equivalent whole-body dry and evaporative heat loss, body heat storage and oesophageal temperature during moderate- and high-intensity exercise in a warm, dry environment, indicating that IUDs do not appear to compromise exercise thermoregulation. However, within IUD users and non-users, dry heat loss was increased and body heat storage and oesophageal temperature were reduced in the luteal compared to the follicular phase of the menstrual cycle, though these effects were small and unlikely to be practically meaningful. Together, these findings expand our understanding of the factors that modulate heat exchange in women and have important practical implications for the design of future studies of exercise thermoregulation.

Effects of Daylong Exposure to Indoor Overheating on Thermal and Cardiovascular Strain in Older Adults: A Randomized Crossover Trial.

BACKGROUND: Health agencies recommend that homes of heat-vulnerable occupants (e.g., older adults) be maintained below 24-28°C to prevent heat-related mortality and morbidity. However, there is limited experimental evidence to support these recommendations. OBJECTIVE: To aid in the development of evidence-based guidance on safe indoor temperatures for temperate continental climates, we evaluated surrogate physiological outcomes linked with heat-related mortality and morbidity in older adults during simulated indoor overheating. METHODS: Sixteen older adults [six women; median age: 72 y, interquartile range (IQR): 70-73 y; body mass index: 24.6 (IQR: 22.1-27.0) kg/m2] from the Ottawa, Ontario, Canada, region (warm summer continental climate) completed four randomized, 8-h exposures to conditions experienced indoors during hot weather in continental climates (e.g., Ontario, Canada; 64 participant exposures). Ambient conditions simulated an air-conditioned environment (22°C; control), proposed indoor temperature upper limits (26°C), and temperatures experienced in homes without air-conditioning (31°C and 36°C). Core temperature (rectal) was monitored as the primary outcome; based on previous recommendations, between-condition differences >0.3°C were considered clinically meaningful. RESULTS: Compared with 22°C, core temperature was elevated to a meaningful extent in 31°C [+0.7°C; 95% confidence interval (CI): 0.5, 0.8] and 36°C (+0.9°C; 95% CI: 0.8, 1.1), but not 26°C (+0.2°C, 95% CI: 0.0, 0.3). Increasing ambient temperatures were also associated with elevated heart rate and reduced arterial blood pressure and heart rate variability at rest, as well as progressive impairments in cardiac and blood pressure responses to standing from supine. DISCUSSION: Core temperature and cardiovascular strain were not appreciably altered following 8-h exposure to 26°C but increased progressively in conditions above this threshold. These data support proposals for the establishment of a 26°C indoor temperature upper limit for protecting vulnerable occupants residing in temperate continental climates from indoor overheating. https://doi.org/10.1289/EHP13159.

Effect of daylong exposure to indoor overheating on autophagy and the cellular stress response in older adults.

To protect vulnerable populations during heat waves, public health agencies recommend maintaining indoor air temperature below ∼24-28 °C. While we recently demonstrated that maintaining indoor temperatures ≤26 °C mitigates the development of hyperthermia and cardiovascular strain in older adults, the cellular consequences of prolonged indoor heat stress are poorly understood. We therefore evaluated the cellular stress response in 16 adults (six females) aged 66-78 years during 8 h rest in ambient conditions simulating homes maintained at 22 °C (control) and 26 °C (indoor temperature upper limit proposed by health agencies), as well as non-air-conditioned domiciles during hot weather and heat waves (31 and 36 °C, respectively; all 45% relative humidity). Western blot analysis was used to assess changes in proteins associated with the cellular stress response (autophagy, apoptosis, acute inflammation, and heat shock proteins) in peripheral blood mononuclear cells harvested prior to and following exposure. Following 8 h exposure, no cellular stress response-related proteins differed significantly between the 26 and 22 °C conditions (all, P ≥ 0.056). By contrast, autophagy-related proteins were elevated following exposure to 31 °C (p62: 1.5-fold; P = 0.003) and 36 °C (LC3-II, LC3-II/I, p62; all ≥2.0-fold; P ≤ 0.002) compared to 22 °C. These responses were accompanied by elevations in apoptotic signaling in the 31 and 36 °C conditions (cleaved-caspase-3: 1.8-fold and 3.7-fold, respectively; P ≤ 0.002). Furthermore, HSP90 was significantly reduced in the 36 °C compared to 22 °C condition (0.7-fold; P = 0.014). Our findings show that older adults experience considerable cellular stress during prolonged exposure to elevated ambient temperatures and support recommendations to maintain indoor temperatures ≤26 °C to prevent physiological strain in heat-vulnerable persons.

The utility of heart rate and heart rate variability to identify limits of tolerance to moderate-intensity work in the heat: a secondary analysis.

We investigated the utility of heart rate (HR) and heart rate variability (HRV) for identifying individuals who may terminate work early due to excessive heat strain. Forty-eight men and women (median = 36 years; Q1 = 20 years; Q3 = 54 years) attempted 180 min of moderate-intensity work at a fixed metabolic rate (∼200 W/m2; ∼3.5 METs) in a hot environment (wet-bulb globe temperature: 32 °C). Receiver operating characteristics (ROC) curves were used to identify the ability of indices of HR (absolute HR, percentage of maximum HR, percentage of HR reserve) and HRV (root-mean-square of successive differences (RMSSD), high-frequency power, and detrended fluctuation analysis component alpha 1 (DFA α1)) to discriminate between participants who completed the 180 min work bout or terminated prematurely. Participants who terminated work prematurely (n = 26) exhibited higher HR and percentage of HR measures, as well as reduced RMSSD and DFA α1 after the first hour of work compared to participants who completed the bout. The discriminative utility of HR and HRV indices was strongest within the first hour of work, with percentage of HR reserve demonstrating excellent discriminative power (ROC area under curve (AUC) of 0.8). Stratifying participants by age and sex improved ROC AUC point estimates for most indices, particularly in female participants. The study provides preliminary evidence supporting the use of noninvasive cardiac monitoring for predicting work tolerance in healthy individuals exposed to occupational heat stress. HR and percentage of HR reserve were suggested to discriminate work termination most effectively. Further investigations are warranted to explore the influence of individual factors and refine the discriminative thresholds for early identification of excessive occupational heat strain.

Hot Topic: A Systematic Review and Content Analysis of Heat-Related Messages During the 2021 Heat Dome in Canada.

CONTEXT: During the summer of 2021, western Canada experienced a deadly heat event. From the first heat alert to postevent reporting, thousands of media articles were published that reference the heat event. However, a gap remains in understanding how this communication chain-from the release of a public heat alert to information shared through media outlets to the public-currently operates to disseminate heat-related messaging across Canada. OBJECTIVE: To understand the role of digital media in delivering heat-health messaging during an extreme heat event in Canada. DESIGN: A qualitative content analysis was conducted using Canadian news articles published on the 2021 Heat Dome between June 2021 and February 2022 (n = 2909). The coding frame was designed to align with the basic framework for information gathering used in journalism (who, what, where, when, and how) and included both concept-driven and data-driven codes. RESULTS: Overall, 2909 unique media articles discussing the 2021 Heat Dome were identified, with the majority (74%) published by online news agencies (how). The highest article count was on June 29, 2021 (n = 159), representing 5% of the total data set (n = 2909) spanning 260 days (when); 57% of the identified locations were in British Columbia (where). Although we found that the top voices providing media-based heat-health messages are government officials (who), only 23% of articles included heat-health messaging that aligns with the government health alert bulletins released during extreme heat. In addition, heat-health messaging frequently included contradictory content, inconsistent language, or incorrect advice (what). CONCLUSION: The findings demonstrate clear opportunities to improve health communication related to extreme heat, perhaps most importantly, including updates to mass media messaging educating the public on heat-protective behaviors.

Dose-dependent nonthermal modulation of whole body heat exchange during dynamic exercise in humans.

To maintain heat balance during exercise, humans rely on skin blood flow and sweating to facilitate whole body dry and evaporative heat exchange. These responses are modulated by the rise in body temperature (thermal factors), as well as several nonthermal factors implicated in the cardiovascular response to exercise (i.e., central command, mechanoreceptors, and metaboreceptors). However, the way these nonthermal factors interact with thermal factors to maintain heat balance remains poorly understood. We therefore used direct calorimetry to quantify the effects of dose-dependent increases in the activation of these nonthermal stimuli on whole body dry and evaporative heat exchange during dynamic exercise. In a randomized crossover design, eight participants performed 45-min cycling at a fixed metabolic heat production (200 W/m2) in warm, dry conditions (30°C, 20% relative humidity) on four separate occasions, differing only in the level of lower-limb compression applied via bilateral thigh cuffs pressurized to 0, 30, 60, or 90 mmHg. This model provoked increments in nonthermal activation while ensuring the heat loss required to balance heat production was matched across trials. At end-exercise, dry heat loss was 2 W/m2 [1, 3] lower per 30-mmHg pressure increment (P = 0.006), whereas evaporative heat loss was elevated 5 W/m2 [3, 7] with each pressure increment (P < 0.001). Body heat storage and esophageal temperature did not differ across conditions (both P ≥ 0.600). Our findings indicate that the nonthermal factors engaged during exercise exert dose-dependent, opposing effects on whole body dry and evaporative heat exchange, which do not significantly alter heat balance.NEW & NOTEWORTHY To maintain heat balance during exercise, humans rely on skin blood flow and sweating to facilitate dry and evaporative heat exchange. These responses are modulated by body temperatures (thermal factors) and several nonthermal factors (e.g., central command, metaboreceptors), although the way thermal and nonthermal factors interact to regulate body temperature is poorly understood. We demonstrate that nonthermal factors exert dose-dependent, opposing effects on dry and evaporative heat loss, without altering heat storage during dynamic exercise.

Body Core Temperature After Foot Immersion and Neck Cooling in Older Adults Exposed to Extreme Heat.

This randomized study evaluates the hypothesis that foot immersion in cool water alone or with supplemental neck cooling mitigates increases in core temperature in older adults exposed to environmental conditions simulating deadly heat waves in North America.

Physiological responses to 9 hours of heat exposure in young and older adults. Part III: Association with self-reported symptoms and mood state.

Older adults are at greater risk of heat-related morbidity and mortality during heat waves, which is commonly linked to impaired thermoregulation. However, little is known about the influence of increasing age on the relation between thermal strain and perceptual responses during daylong heat exposure. We evaluated thermal and perceptual responses in 20 young (19-31 yr) and 39 older adults (20 with hypertension and/or type 2 diabetes; 61-78 yr) resting in the heat for 9 h (heat index: 37°C). Body core and mean skin temperature areas under the curve (AUC, hours 0-9) were assessed as indicators of cumulative thermal strain. Self-reported symptoms (68-item environmental symptoms questionnaire) and mood disturbance (40-item profile of mood states questionnaire) were assessed at end-heating (adjusted for prescores). Body core temperature AUC was 2.4°C·h [1.0, 3.7] higher in older relative to young adults (P < 0.001), whereas mean skin temperature AUC was not different (-0.5°C·h [-4.1, 3.2] P = 0.799). At end-heating, self-reported symptoms were not different between age groups (0.99-fold [0.80, 1.23], P = 0.923), with or without adjustment for body core or mean skin temperature AUC (both P ≥ 0.824). Mood disturbance was 0.93-fold [0.88, 0.99] lower in older, relative to young adults (P = 0.031). Older adults with and without chronic health conditions experienced similar thermal strain, yet those with these conditions reported lower symptom scores and mood disturbance compared with young adults and their age-matched counterparts (all P ≤ 0.026). Although older adults experienced heightened thermal strain during the 9-h heat exposure, they did not experience greater self-reported symptoms or mood disturbance relative to young adults.NEW & NOTEWORTHY Despite experiencing greater cumulative thermal strain during 9 h of passive heat exposure, older adults reported similar heat-related symptoms and lower mood disturbance than young adults. Furthermore, self-reported symptoms and mood disturbance were lower in older adults with common age-associated health conditions than young adults and healthy age-matched counterparts. Perceptual responses to heat in older adults can underestimate their level of thermal strain compared with young adults, which may contribute to their increased heat vulnerability.

Brief ambient cooling preserves autophagy in peripheral blood mononuclear cells from older adults during 9 h of heat exposure.

Heat waves can cause dangerous elevations in body temperature that can compromise cellular function and increase the risk of heat stroke and major cardiovascular events. Visiting a cooling center or other air-conditioned location is commonly recommended by health agencies to protect heat-vulnerable older persons but the associated cellular effects remain underexplored. We evaluated cellular stress responses in peripheral blood mononuclear cells (PBMC) from 19 older adults [71 (SD 2) yr; 9 females] before and after a 9-h heat exposure [40.3°C and 9.3% relative humidity (RH)], with participants moved to a cool room (∼23°C) for hours 5 and 6 (cooling group). Responses were compared with 17 older adults [72 (4) yr; 7 females] who remained in the heat for the entire 9 h (control group). Changes in proteins associated with autophagy, apoptotic signaling, acute inflammation, and the heat shock response (HSR) were assessed via Western blot. Although both groups experienced similar elevations in physiological strain before the cooling center intervention, brief cooling resulted in stark albeit transient reductions in core temperature and heart rate. At end-exposure, autophagy proteins LC3-II and p62 were elevated 1.9-fold [95% CI: 1.2, 2.8] and 2.3-fold [1.4, 3.8], respectively, in the control group relative to cooling group. This was paired with a 2.8-fold [1.6, 4.7] greater rise in apoptotic protein cleaved-caspase-3 in the control group compared with the cooling group. Our findings indicate that 2 h of ambient cooling midway through a 9-h simulated heat wave may preserve autophagy and mitigate heat-induced cellular stress in older adults.NEW & NOTEWORTHY Heat waves can lead to dangerous elevations in body temperature, increasing the risk of life-threatening health conditions. Visiting a cooling center or other air-conditioned location is commonly recommended to protect heat-vulnerable older persons, although the effects on the cellular stress response remain unknown. We found that 2 h of ambient cooling midway through a 9 h simulated heat wave preserves autophagy, a vital cellular survival mechanism, and mitigates accompanying pathways of cellular stress in older adults.

Indoor overheating influences self-reported symptoms and mood-state in older adults during a simulated heatwave: Effects of mid-day cooling centre use.

Public health agencies recommend that older adults without home air-conditioning visit cooling centres to mitigate physiological strain from high ambient temperatures during heat waves. However, there is little evidence regarding their influence on self-reported environmental symptoms and mood-state after returning to the heat. METHODS: Forty adults (64-79 years) underwent a daylong laboratory-based indoor overheating simulation (9-hours, heat index: 37 °C) with (cooling, n = 20) or without (control, n = 20) a 2-hour air-conditioning intervention (hours 5-6). Mean skin and core temperature areas under the curve (AUC, hours 0-9) were used to assess cumulative thermal strain. Group differences in total symptom scores and subjective heat illness (68-item environmental symptoms questionnaire) as well as total mood disturbance and energy index (40-item profile of mood states questionnaire) were evaluated at end-heating (adjusted for pre-exposure scores). RESULTS: Cooling reduced mean skin and core temperature AUCs by 4.0 [0.1, 0.8] and 1.6 [0.4, 2.8] °C·hour compared to control (both p < 0.048). However, at end-heating neither mean skin nor core temperatures differed between groups (both p > 0.999). Total symptom scores and subjective heat illness were 0.58-fold [0.44, 0.77] and 0.56-fold [0.40, 0.78] lower in the cooling compared to control group (both p < 0.001). Mood disturbance was 0.91-fold [0.83, 0.99] lower for cooling than control (p = 0.036), although energy index was not different between groups (p = 0.141). CONCLUSION: Cooling centres can have sustained positive effects on perceived thermal strain and mood-state in older adults after returning to the heat. However, continued vigilance and use of appropriate countermeasures to mitigate physiological strain from indoor overheating should be encouraged as body temperatures can rapidly return to pre-cooling levels.

Physiological responses to 9 hours of heat exposure in young and older adults. Part I: Body temperature and hemodynamic regulation.

Aging is associated with an elevated risk of heat-related mortality and morbidity, attributed, in part, to declines in thermoregulation. However, comparisons between young and older adults have been limited to brief exposures (1-4 h), which may not adequately reflect the duration or severity of the heat stress experienced during heat waves. We therefore evaluated physiological responses in 20 young (19-31 yr; 10 females) and 39 older (61-78 yr; 11 females) adults during 9 h of rest at 40°C and 9% relative humidity. Whole body heat exchange and storage were measured with direct calorimetry during the first 3 h and final 3 h. Core temperature (rectal) was monitored continuously. The older adults stored 88 kJ [95% confidence interval (CI): 29, 147] more heat over the first 3 h of exposure (P = 0.006). Although no between-group differences were observed after 3 h [young: 37.6°C (SD 0.2°C) vs. older: 37.7°C (0.3°C); P = 0.216], core temperature was elevated by 0.3°C [0.1, 0.4] (adjusted for baseline) in the older group at hour 6 [37.6°C (0.2°C) vs. 37.9°C (0.2°C); P < 0.001] and by 0.2°C [0.0, 0.3] at hour 9 [37.7°C (0.3°C) vs. 37.8°C (0.3°C)], although the latter comparison was not significant after multiplicity correction (P = 0.061). Our findings indicate that older adults sustain greater increases in heat storage and core temperature during daylong exposure to hot dry conditions compared with their younger counterparts. This study represents an important step in the use of ecologically relevant, prolonged exposures for translational research aimed at quantifying the physiological and health impacts of hot weather and heat waves on heat-vulnerable populations.NEW & NOTEWORTHY We found greater increases in body heat storage and core temperature in older adults than in their younger counterparts during 9 h of resting exposure to hot dry conditions. Furthermore, the age-related increase in core temperature was exacerbated in older adults with common heat-vulnerability-linked health conditions (type 2 diabetes and hypertension). Impairments in thermoregulatory function likely contribute to the increased risk of heat-related illness and injury seen in older adults during hot weather and heat waves.

Physiological responses to 9 hours of heat exposure in young and older adults. Part II: Autophagy and the acute cellular stress response.

With rising global temperatures, heat-related mortality is increasing, particularly among older adults. Although this is often attributed to declines in thermoregulatory function, little is known regarding the effect of age on the cellular processes associated with mitigating heat-induced cytotoxicity. We compared key components of the cellular stress response in 19 young (19-31 yr; 10 female) and 37 older adults (61-78 yr; 10 female) during 9 h of heat exposure (40°C, 9% relative humidity). Mean body temperature (Tbody) was calculated from core and skin temperatures. Changes in proteins associated with autophagy, apoptotic signaling, acute inflammation, and the heat shock response were assessed via Western blot in peripheral blood mononuclear cells harvested before and after exposure. Tbody increased by 1.5 (SD 0.3)°C and 1.7 (0.3)°C in the young and older adults, respectively. We observed similar elevations in autophagy-related proteins (LC3-II and LC3-II/I) in young and older adults (both P ≥ 0.121). However, the older adults displayed signs of autophagic dysfunction, evidenced by a 3.7-fold [95% CI: 2.4, 5.6] greater elevation in the selective autophagy receptor p62 (P < 0.001). This was paired with elevations in apoptotic responses, with a 1.7-fold [1.3, 2.3] increase in cleaved caspase-3 in the older relative to young adults (P < 0.001). Older adults also exhibited diminished heat shock protein 90 responses (0.7-fold [0.5, 0.9] vs. young, P = 0.011) and, at any given level of thermal strain (Tbody area under the curve), elevated tumor necrosis factor-α (1.5-fold [1.0, 2.5] vs. young, P = 0.008). Attenuated autophagic responses may underlie greater vulnerability to heat-induced cellular injury in older adults.NEW & NOTEWORTHY We demonstrate for the first time that peripheral blood mononuclear cells from older adults exhibit signs of autophagic impairments during daylong (9 h) heat exposure relative to their younger counterparts. This was paired with greater apoptotic signaling and inflammatory responses, and an inability to stimulate components of the heat shock response. Thus, autophagic dysregulation during prolonged heat exposure may contribute to age-related heat vulnerability during hot weather and heat waves.

Efficacy of Cooling Centers for Mitigating Physiological Strain in Older Adults during Daylong Heat Exposure: A Laboratory-Based Heat Wave Simulation.

BACKGROUND: Health agencies, including the U.S. Centers for Disease Control and Prevention and the World Health Organization, recommend that heat-vulnerable older adults without home air-conditioning should visit cooling centers or other air-conditioned locations (e.g., a shopping mall) during heat waves. However, experimental evidence supporting the effectiveness of brief air-conditioning is lacking. OBJECTIVE: We evaluated whether brief exposure to an air-conditioned environment, as experienced in a cooling center, was effective for limiting physiological strain in older adults during a daylong laboratory-based heat wave simulation. METHODS: Forty adults 64-79 years of age underwent a 9-h simulated heat wave (heat index: 37°C) with (cooling group, n=20) or without (control group, n=20) a cooling intervention consisting of 2-h rest in an air-conditioned room (∼23°C, hours 5-6). Core and skin temperatures, whole-body heat exchange and storage, cardiovascular function, and circulating markers of acute inflammation were assessed. RESULTS: Core temperature was 0.8°C (95% CI: 0.6, 0.9) lower in the cooling group compared with the control group at the end of the cooling intervention (p<0.001; hour 6), and it remained 0.3°C (95% CI: 0.2, 0.4) lower an hour after returning to the heat (p<0.001; hour 7). Despite this, core temperatures in each group were statistically equivalent at hours 8 and 9, within ±0.3°C (p≤0.005). Cooling also acutely reduced demand on the heart and improved indices of cardiovascular autonomic function (p≤0.021); however, these outcomes were not different between groups at the end of exposure (p≥0.58). DISCUSSION: Brief air-conditioning exposure during a simulated heat wave caused a robust but transient reduction in core temperature and cardiovascular strain. These findings provide important experimental support for national and international guidance that cooling centers are effective for limiting physiological strain during heat waves. However, they also show that the physiological impacts of brief cooling are temporary, a factor that has not been considered in guidance issued by health agencies. https://doi.org/10.1289/EHP11651.

Association between haemoglobin A1c and whole-body heat loss during exercise-heat stress in physically active men with type 2 diabetes.

NEW FINDINGS: What is the central question of this study? Is the impairment in heat dissipation during exercise observed in men with type 2 diabetes related to glycaemic control (indexed by glycated haemoglobin; haemoglobin A1c )? What is the main finding and its importance? No association was found between haemoglobin A1c (range: 5.1-9.1%) and whole-body heat loss in men with type 2 diabetes during exercise in the heat. However, individuals with elevated haemoglobin A1c exhibited higher body core temperature and heart rate responses. Thus, while haemoglobin A1c is not associated with heat loss per se, it may still have important implications for physiological strain during exercise. ABSTRACT: Type 2 diabetes is associated with a reduced capacity to dissipate heat. It is unknown whether this impairment is related to glycaemic control (indexed by glycated haemoglobin; haemoglobin A1c ) is unknown. We evaluated the association between haemoglobin A1c and whole-body heat loss (via direct calorimetry), body core temperature, and heart rate in 26 physically active men with type 2 diabetes (43-73 years; HbA1c 5.1-9.1%) during exercise at increasing rates of metabolic heat production (∼150, 200, 250 W m-2 ) in the heat (40°C, ∼17% relative humidity). Haemoglobin A1c was not associated with whole-body heat loss (P = 0.617), nor the increase in core temperature from pre-exercise (P = 0.347). However, absolute core temperature and heart rate were elevated ∼0.2°C (P = 0.014) and ∼6 beats min-1 (P = 0.049), respectively, with every percentage point increase in haemoglobin A1c . Thus, while haemoglobin A1c does not appear to modify diabetes-related reductions in capacity for heat dissipation, it may still have important implications for physiological strain during exercise-heat stress.