Increased risk of preterm birth due to heat exposure during pregnancy: Exploring the mechanism of fetal physiology.

BACKGROUND: Heat exposure during pregnancy can increase the risk of preterm birth (PTB) through a range of potential mechanisms including pregnancy complications, hormone secretion and infections. However, current research mainly focuses on the effect of heat exposure on pathophysiological pathways of pregnant women, but ignore that that maternal heat exposure can also cause physiological changes to the fetus, which will affect the risk of PTB. OBJECTIVE: In this study, we aimed to explore the mediating role of fetal heart rate (FHR) in the relationship between maternal heat exposure and PTB incidence. METHODS: We assigned heat exposure to a multi-center birth cohort in China during 2015-2018, which included all 162,407 singleton live births with several times FHR measurements during the second and third trimesters. We examined the associations between heat exposure, FHR and PTB in the entire pregnancy, each trimester and the last gestational month. The inverse odds ratio-weighted approach applied to the Cox regression was used to identify the mediation effect of heat exposure on PTB and its clinical subtypes via FHR. FINDINGS: Exposure to heat significantly increased the risk of PTB during the third trimester and the entire pregnancy, hazard ratios and 95 % CIs were 1.266 (1.161, 1.379) and 1.328 (1.218, 1.447). Heat exposure during the third trimester and entire pregnancy increased FHR in the third trimester by 0.24 bpm and 0.14 bpm. The proportion of heat exposure mediated by FHR elevation on PTB and its subtype ranged from 3.68 % to 24.06 %, with the significant mediation effect found for both medically indicated PTB and spontaneous PTB. CONCLUSIONS: This study suggests that heat exposure during pregnancy has an important impact on fetal health, and FHR, as a surrogate marker of fetal physiology, may mediate the increased risk of PTB caused by extreme heat. Monitoring and managing physiological changes in the fetus would constitute a promising avenue to reduce adverse birth outcomes associated with maternal heat exposure.

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.

A double-edged sword: risks and benefits of heat for human health.

Extreme heat events will become more frequent and intense across the globe. In this science and society article we summarize how heat affects our body and discuss the associated health threats, but also the potential health benefits of heat exposure. Moreover, we provide practical suggestions for sustainable and health-oriented strategies to cope with heat.

Sex-specific effects of environmental temperature during gestation on fluctuating asymmetry in deciduous teeth.

OBJECTIVES: External environmental heat exposure during gestation impacts the physiology of human development in utero, but evidence for these impacts has not yet been explored in dentition. We examined deciduous teeth for fluctuating asymmetry (FA), a measure of developmental instability, together with gestational environmental temperature data drawn from historical weather statistics. MATERIALS AND METHODS: We measured dental casts from the longitudinal Burlington Growth Study, representing 172 participants (ages 3-6 years) with health records. FA was calculated from crown dimensions and intercuspal distances that develop during gestation. Multiple regression separated by sex (nfemale = 81) examined the effects of mean temperatures in each trimester, controlling for birth year. RESULTS: In females, increased temperatures during the first trimester are significantly associated with an increase in FA (p = 0.03), specifically during the second and third prenatal months (p = 0.03). There is no relationship between temperature and FA for either sex in the second or third trimesters, when enamel is formed. DISCUSSION: Dental instability may be sensitive to temperature in the first trimester in females during the scaffolding of crown shape and size in the earliest stages of tooth formation. Sexual dimorphism in growth investment strategies may explain the differences in results between males and females. Using enduring dental characteristics, these results advance our understanding of the effects of temperature on fetal physiology within a discrete period.

Early Pulmonary Fibrosis-like Changes in the Setting of Heat Exposure: DNA Damage and Cell Senescence.

It is well known that extreme heat events happen frequently due to climate change. However, studies examining the direct health impacts of increased temperature and heat waves are lacking. Previous reports revealed that heatstroke induced acute lung injury and pulmonary dysfunction. This study aimed to investigate whether heat exposure induced lung fibrosis and to explore the underlying mechanisms. Male C57BL/6 mice were exposed to an ambient temperature of 39.5 ± 0.5 °C until their core temperature reached the maximum or heat exhaustion state. Lung fibrosis was observed in the lungs of heat-exposed mice, with extensive collagen deposition and the elevated expression of fibrosis molecules, including transforming growth factor-ß1 (TGF-ß1) and Fibronectin (Fn1) (p < 0.05). Moreover, epithelial-mesenchymal transition (EMT) occurred in response to heat exposure, evidenced by E-cadherin, an epithelial marker, which was downregulated, whereas markers of EMT, such as connective tissue growth factor (CTGF) and the zinc finger transcriptional repressor protein Slug, were upregulated in the heat-exposed lung tissues of mice (p < 0.05). Subsequently, cell senescence examination revealed that the levels of both senescence-associated ß-galactosidase (SA-ß-gal) staining and the cell cycle protein kinase inhibitor p21 were significantly elevated (p < 0.05). Mechanistically, the cGAS-STING signaling pathway evoked by DNA damage was activated in response to heat exposure (p < 0.05). In summary, we reported a new finding that heat exposure contributed to the development of early pulmonary fibrosis-like changes through the DNA damage-activated cGAS-STING pathway followed by cellular senescence.

Risk factors associated with indicators of dehydration among migrant farmworkers.

OBJECTIVE: Farmworkers are at increased risk of adverse health outcomes related to occupational heat exposure and inadequate access to water, shade, or rest breaks. Presently, there is a dearth of studies examining the prevalence of dehydration and related factors in U.S. farmworkers. Our objectives were to characterize hydration status during typical workdays and to identify risk factors associated with increased dehydration in migrant farmworkers employed in Florida. METHODS: Urine samples were collected and analyzed for urine specific gravity (USG) 2-3 times per person per day over five days in May 2021 and 2022. Data collection included demographic characteristics, wet-bulb-globe-temperature (WBGT), and information on working conditions (task type, duration, and crop units harvested), fluid intake, clothing worn, and heat safety behaviors. Multivariable mixed regression models were used to evaluate risk factors associated with change in USG levels (continuous) during a work shift. RESULTS: A total of 111 farmworkers participated in this study providing 1020 cumulative USG measurements, of which 96.8% of end-of-shift USG samples were above 1.020 indicating potential dehydration. In multivariable models, dehydration assessed using change in USG levels significantly declined with age (ß = -0.078; 95%CI: 0.150, -0.006) but showed significant increase with body mass index (ß = 0.016; 95%CI: 0.003, 0.028), WGBT (ß = 0.054; 95%CI:0.044, 0.064), mean shift duration, and state of primary residence. We did not find significant associations of dehydration with type of clothing worn, intake of employer-provided water, or crop units harvested during a shift in this sample of farmworkers. CONCLUSION: Our findings underscore the need for additional research to evaluate adverse outcomes related to dehydration and to better understand recovery patterns from chronic dehydration across workweeks and harvest seasons in migrant farmworkers.

LRRK2 is involved in heat exposure-induced acute lung injury and alveolar type II epithelial cell dysfunction.

Heat exposure induces excessive hyperthermia associated with systemic inflammatory response that leads to multiple organ dysfunction including acute lung injury. However, how heat impairs the lung remains elusive so far. We aimed to explore the underlying mechanism by focusing on leucine-rich repeat kinase 2 (LRRK2), which was associated with lung homeostasis. Both in vivo and in vitro models were induced by heat exposure. Firstly, heat exposure exerted core temperature (Tc) disturbance, pulmonary dysfunction, atelectasis, inflammation, impaired energy metabolism, and reduced surfactant proteins in the lung of mice. In addition, decreased LRRK2 expression and increased heat shock proteins (HSPs) 70 were observed with heat exposure in both the lung of mice and alveolar type II epithelial cells (AT2). Furthermore, LRRK2 inhibition aggravated heat exposure-initiated Tc dysregulation, injury in the lung and AT2 cells, and enhanced HSP70 expression. In conclusion, LRRK2 is involved in heat-induced acute lung injury and AT2 cell dysfunction.

Reducing heat exposure from personal cooling strategies to green city construction in China's tropical city.

With rapid industrialization and urbanization, the risk of summer heat exposure for urban dwellers has increased. The use of air conditioners (ACs) has become the most common personal cooling strategy, but further increasing fossil fuel consumption. As sustainable and affordable cooling strategies, urban parks can reduce heat exposure and substitute a part of air conditioners use. This study evaluates the heat exposure reduction from personal cooling to urban parks based on satellite images, questionnaire surveys, and network analysis in Liuzhou, one tropical city in China. We found that residents with lower income had a higher risk of heat exposure. Among the respondents, 85 % of residents chose to use ACs to alleviate high temperatures in summer, and 81.8 % among them were willing to access park cooling area (PCA) to cool off instead of using ACs. About one third parks could serve as potential alternatives (with temperatures <28 °C) to air conditioning, reducing carbon emissions by 175.93 tons per day during the hot summer and offsetting 2.5 % of urban fossil fuel carbon emissions. The design of parks should give more consideration to elder people and provide a good cooling platform for various social income groups. Future planning should also focus on accessibility to enable residents to fully utilize the parks. Building parks within 34.10 ha would provide a more efficient use of land. This research guides sustainable, high-quality growth in industrial cities and might contribute to promotion of low-carbon cities and social equity.

Characterization of human extreme heat exposure using an outdoor thermal manikin.

Extreme heat is a current and growing global health concern. Current heat exposure models include meteorological and human factors that dictate heat stress, comfort, and risk of illness. However, radiation models simplify the human body to a cylinder, while convection ones provide conflicting predictions. To address these issues, we introduce a new method to characterize human exposure to extreme heat with unprecedented detail. We measure heat loads on 35 body surface zones using an outdoor thermal manikin ("ANDI") alongside an ultrasonic anemometer array and integral radiation measurements (IRM). We show that regardless of body orientation, IRM and ANDI agree even under high solar conditions. Further, body parts can be treated as cylinders, even in highly turbulent flow. This geometry-rooted insight yields a whole-body convection correlation that resolves prior conflicts and is valid for diverse indoor and outdoor wind flows. Results will inform decision-making around heat protection, adaptation, and mitigation.

Heat exposure as a cause of injury and illness in mine industry workers.

The objective of this study was to explore the association between ambient temperature and injuries and illnesses experienced by mine industry workers. Eleven years of de-identified data from a mine industry company in Australia was explored in regards to injuries and illnesses occurring due to outdoor exposure. Each case was filtered for reported symptoms, and meteorological data to match the location of the mine site and date reported were sourced. Of the 18 931 injuries and illnesses observed over the 11-year period, 151 cases of heat-related illness due to outdoor exposure were reported. Twenty-five conditions/symptoms of heat-illness were found, with the most prevalent being dehydration (n = 81), followed by heat rash (n = 40), dizziness (n = 24), and headache (n = 23). The mean number of symptoms reported by each worker was 2 ± 1. There was a positive correlation between ambient temperature and injuries/illnesses (r2 = 0.89, P < 0.001), where, as temperature increased so did the number of reported heat-related illnesses. Underreporting of heat-related illness and injury in the mining industry is likely, which is a risk to the health and wellbeing of employees. Workers require industry specific training about the severity of heat stress and the associated prevention strategies.

Strategies to mitigate acute kidney injury risk during physical work in hot environments.

Prolonged physical work in the heat can reduce renal function and increase the risk of acute kidney injury (AKI). This is concerning given that the latest climate change projections forecast a rise in global temperature as well as the frequency, intensity, and duration of heatwaves. This means that outdoor and indoor workers in the agriculture or construction industries will be exposed to higher heat stress in the years ahead. Several studies indicate a higher incidence of chronic kidney disease from nontraditional origins (CKDnt) in individuals exposed to high temperatures, intense physical work, and/or recurrent dehydration. It has been proposed that prolonged physical work in the heat accompanied by dehydration results in recurrent episodes of AKI that ultimately lead to permanent kidney damage and the development of CKDnt. Thus, there is a need to identify and test strategies that can alleviate AKI risk during physical work in the heat. The purpose of this review is to present strategies that might prevent and mitigate the risk of AKI induced by physical work in the heat.

Time-series transcriptome reveals inflammatory signature in monocytes and neutrophils following acute heat exposure in mine rescuers.

Occupational exposure to extreme high temperatures and the increasing global temperatures necessitates a deeper understanding of the impact of heat exposure on human health. However, the molecular mechanisms underlying the response of monocytes and neutrophils to heat exposure in occupational population remain to be fully elucidated. This study used longitudinal transcriptome to assess the impact of acute heat exposure (50°C for 30 min) in 10 subjects from a mine rescue team before acute heat exposure (baseline) and at 5 min, 30 min, 1 h, and 24 h after acute heat exposure (recovery). The time-series analysis revealed a coordinated molecular choreography of changes involving inflammation, coagulation, extracellular matrix, and energy metabolism. Importantly, the study characterized the inflammatory signature associated with heat exposure in monocytes and neutrophils, as evidenced by the rapid activation of the inflammation-related transcriptome following heat exposure. Additionally, we pinpointed potential regulators, such as NR4A1, FOSL1, EGR3, and ATF3. In summary, the study suggested that the initial response to heat stress in monocytes and neutrophils from mine rescue team member was primarily characterized by a pro-inflammatory stress response, which could potentially lead to the development of inflammation and ultimately result in a systemic inflammatory response in heatstroke.

A longitudinal assessment of heat exposure and biomarkers of kidney function on heat shock protein 70 and antibodies among agricultural workers.

Background: Exposure to extreme heat impacts millions of people worldwide and outdoor workers are among the populations most affected by high temperatures. Heat stress induces several biological responses in humans, including the production of heat shock proteins (HSP) and antibodies against HSP (anti-HSP) which may play a central role in the body's cellular response to a hot environment. Objective: This longitudinal study investigated the impact of high temperatures and humidity on the presence of HSP70 and anti-HSP70 and examined relationships with markers of kidney function in an at-risk workforce under conditions of extreme heat and exertion in Guatemala. Methods: We collected ambient temperature and relative humidity data as well as biomarkers and clinical data from 40 sugarcane workers at the start and the end of a 6-month harvest. We used generalized mixed-effects models to estimate temperature effects on HSP70 and anti-HSP70 levels. In addition, we examined trends between HSP70 and anti-HSP70 levels and markers of kidney function across the harvest. Results: At the end of the harvest, temperatures were higher, and workers had, on average, higher levels of HSP70 and anti-HSP70 compared to the beginning of the season. We observed significant increasing trends with temperature indices and HSP70 levels. Maximum temperature was associated with HSP70 increments after controlling for age, systolic and diastolic blood pressure (ß: 0.21, 95% Confidence Interval: 0.09, 0.33). Kidney function decline across the harvest was associated with both higher levels of anti-HSP70 levels at the end of the harvest as well as greater increases in anti-HSP70 levels across the harvest. Conclusions: These results suggest that workplace heat exposure may increase the production of HSP70 and anti-HSP70 levels and that there may be a relationship between increasing anti-HSP70 antibodies and the development of renal injury. HSP70 holds promise as a biomarker of heat stress in exposed populations.

Reductions in premature deaths from heat and particulate matter air pollution in South Asia, China, and the United States under decarbonization.

Following a sustainable development pathway designed to keep warming below 2 °C will benefit human health. We quantify premature deaths attributable to fine particulate matter (PM2.5) air pollution and heat exposures for China, South Asia, and the United States using projections from multiple climate models under high- and low-emission scenarios. Projected changes in premature deaths are typically dominated by population aging, primarily reflecting increased longevity leading to greater sensitivity to environmental risks. Changes in PM2.5 exposure typically have small impacts on premature deaths under a high-emission scenario but provide substantial benefits under a low-emission scenario. PM2.5-attributable deaths increase in South Asia throughout the century under both scenarios but shift to decreases by late century in China, and US values decrease throughout the century. In contrast, heat exposure increases under both scenarios and combines with population aging to drive projected increases in deaths in all countries. Despite population aging, combined PM2.5- and heat-related deaths decrease under the low-emission scenario by ~2.4 million per year by midcentury and ~2.9 million by century's end, with ~3% and ~21% of these reductions from heat, respectively. Intermodel variations in exposure projections generally lead to uncertainties of <40% except for US and China heat impacts. Health benefits of low emissions are larger from reduced heat exposure than improved air quality by the late 2090s in the United States. In contrast, in South and East Asia, the PM2.5-related benefits are largest throughout the century, and their valuation exceeds the cost of decarbonization, especially in China, over the next 30 y.

The effects of cool roofs on health, environmental, and economic outcomes in rural Africa: study protocol for a community-based cluster randomized controlled trial.

BACKGROUND: High ambient air temperatures in Africa pose significant health and behavioral challenges in populations with limited access to cooling adaptations. The built environment can exacerbate heat exposure, making passive home cooling adaptations a potential method for protecting occupants against indoor heat exposure. METHODS: We are conducting a 2-year community-based stratified cluster randomized controlled trial (cRCT) implementing sunlight-reflecting roof coatings, known as "cool roofs," as a climate change adaptation intervention for passive indoor home cooling. Our primary research objective is to investigate the effects of cool roofs on health, indoor climate, economic, and behavioral outcomes in rural Burkina Faso. This cRCT is nested in the Nouna Health and Demographic Surveillance System (HDSS), a population-based dynamic cohort study of all people living in a geographically contiguous area covering 59 villages, 14305 households and 28610 individuals. We recruited 1200 participants, one woman and one man, each in 600 households in 25 villages in the Nouna HDSS. We stratified our sample by (i) village and (ii) two prevalent roof types in this area of Burkina Faso: mud brick and tin. We randomized the same number of people (12) and homes (6) in each stratum 1:1 to receiving vs. not receiving the cool roof. We are collecting outcome data on one primary endpoint - heart rate, (a measure of heat stress) and 22 secondary outcomes encompassing indoor climate parameters, blood pressure, body temperature, heat-related outcomes, blood glucose, sleep, cognition, mental health, health facility utilization, economic and productivity outcomes, mosquito count, life satisfaction, gender-based violence, and food consumption. We followed all participants for 2 years, conducting monthly home visits to collect objective and subjective outcomes. Approximately 12% of participants (n = 152) used smartwatches to continuously measure endpoints including heart rate, sleep and activity. DISCUSSION: Our study demonstrates the potential of large-scale cRCTs to evaluate novel climate change adaptation interventions and provide evidence supporting investments in heat resilience in sub-Saharan Africa. By conducting this research, we will contribute to better policies and interventions to help climate-vulnerable populations ward off the detrimental effects of extreme indoor heat on health. TRIAL REGISTRATION: German Clinical Trials Register (DRKS) DRKS00023207. Registered on April 19, 2021.

Cyclooxygenase inhibition does not blunt thermal hyperemia in skeletal muscle of humans.

Acute heat exposure increases skeletal muscle blood flow in humans. However, the mechanisms mediating this hyperemic response remain unknown. The cyclooxygenase pathway is active in skeletal muscle, is heat sensitive, and contributes to cutaneous thermal hyperemia in young healthy humans. Therefore, the purpose of this study was to test the hypothesis that cyclooxygenase inhibition would attenuate blood flow in the vastus lateralis muscle during localized heating. Twelve participants (6 women) were studied on two separate occasions: 1) time control (i.e., no ibuprofen); and 2) ingestion of 800 mg ibuprofen, a nonselective cyclooxygenase inhibitor. Experiments were randomized, counter-balanced, and separated by at least 10 days. Pulsed short-wave diathermy was used to induce unilateral deep heating of the vastus lateralis for 90 min, whereas the contralateral leg served as a thermoneutral control. Microdialysis was utilized to bypass the cutaneous circulation and directly measure local blood flow in the vastus lateralis muscle of each leg via the ethanol washout technique. Heat exposure increased muscle temperature and local blood flow (both P < 0.01 vs. baseline). However, the thermal hyperemic response did not differ between control and ibuprofen conditions (P ≥ 0.2). Muscle temperature slightly decreased for the thermoneutral leg (P < 0.01 vs. baseline), yet local blood flow remained relatively unchanged across time for control and ibuprofen conditions (both P ≥ 0.7). Taken together, our data suggest that inhibition of cyclooxygenase-derived vasodilator prostanoids does not blunt thermal hyperemia in skeletal muscle of young healthy humans.NEW & NOTEWORTHY Acute heat exposure increases skeletal muscle blood flow in humans. However, the mechanisms mediating this hyperemic response remain unknown. Using a pharmacological approach combined with microdialysis, we found that thermal hyperemia in the vastus lateralis muscle was well maintained despite the successful inhibition of cyclooxygenase. Our results suggest that cyclooxygenase-derived vasodilator prostanoids do not contribute to thermal hyperemia in skeletal muscle of young healthy humans.

Using individual approach to examine the association between urban heat island and preterm birth: A nationwide cohort study in China.

BACKGROUND: Evidence suggests that maternal exposure to heat might increase the risk of preterm birth (PTB), but no study has investigated the effect from urban heat island (UHI) at individual level. AIMS: Our study aimed to investigate the association between individual UHI exposure and PTB. METHODS: We utilized data from the ongoing China Birth Cohort Study (CBCS), encompassing 103,040 birth records up to December 2020. UHI exposure was estimated for each participant using a novel individual assessment method based on temperature data and satellite-derived land cover data. We used generalized linear mixed-effects models to estimate the association between UHI exposure and PTB, adjusting for potential confounders including maternal characteristics and environmental factors. RESULTS: Consistent and statistically significant associations between UHI exposure and PTB were observed up to 21 days before birth. A 5 °C increment in UHI exposure was associated with 27 % higher risk (OR = 1.27, 95 % confident interval: 1.20, 1.34) of preterm birth in lagged day 1. Stratified analysis indicated that the associations were more pronounced in participants who were older, had higher pre-pregnancy body mass index level, of higher socioeconomic status and living in greener areas. CONCLUSION: Maternal exposure to UHI was associated with increased risk of PTB. These findings have implications for developing targeted interventions for susceptible subgroups of pregnant women. More research is needed to validate our findings of increased risk of preterm birth due to UHI exposure among pregnant women.

Biochemical, histological and transcriptomic analyses for the immunological organs provide insights into heat stress-induced disease susceptibility in Largemouth Bass.

Aquaculture of Largemouth Bass (LMB, Micropterus salmoides), an economically important species, is badly affected by the outbreak of bacterial diseases in summer. However, the mechanisms underlying heat-induced disease susceptibility remain largely unknown. In this study, after exposure to 34 °C for 1, 7 and 14 d, the head kidney, spleen and blood of LMB were sampled for biochemical and histological assays to explore the effects of heat exposure on the oxidative and immunological indices. Compared to the controls maintained at 28 °C, chronic heat exposure (34 °C for 14 d) induced oxidative stress, caused cell apoptosis and decreased expression of the immunological genes in the head kidney and spleen tissues; and attenuated the blood immunological indices. Consistent with the impaired immunological functions, chronic heat exposure predisposed LMB to Aeromonas hydrophila infection and significantly (p < 0.001) increased tissue bacterial load. Furthermore, the effects of chronic heat exposure (heat), A. hydrophila infection (infection) and heat exposure followed by A. hydrophila infection (heat + infection) on gene expression in the head kidney and spleen of LMB were characterized by RNA sequencing. The results indicated that chronic heat exposure facilitated the bacteria-elicited changes in expression of the genes involved in a couple of metabolic and signaling pathways in both tissues. Upon heat + infection, the pathways involved in energy production and nutrients biosynthesis were enhanced, whereas those associated with the host cell functions such as cell-cell interactions and cell signaling were depressed. Our data provide new insights into the mechanisms underlying heat-induced disease susceptibility in LMB.

Ambient heat and diabetes hospitalizations: Does the timing of heat exposure matter?

BACKGROUND: Although ambient heat exposure is linked with diabetes mortality, the impacts of heat exposure on diabetes-related hospitalizations remain controversial. Previous research did not examine the timing of heat-diabetes associations and relation with comorbidities/risk factors. OBJECTIVE: We examined the association between heat exposure and diabetes-related hospitalizations in the transitional and summer months and identified populations vulnerable to heat. METHODS: We conducted a time-stratified case-crossover study. Data on diabetes hospital admissions (primary diagnosis of type 1 and type 2 diabetes, 2013-2020) were collected by the New York State (NYS) Department of Health under the state legislative mandate. We treated temperature and air pollutants as continuous variables and defined the heat exposure as per interquartile range (IQR, a measure between the 25th and 75th percentiles) increase of daily mean temperature. Conditional logistic regressions were performed to quantify the heat-diabetes associations after controlling for air pollutants and time variant variables. Multiplicative-scale interactions between heat and demographics/comorbidities/risk factors on diabetes hospitalizations were investigated. RESULTS: Each IQR increase in temperature was associated with significantly increased risks for diabetes admissions that occurred immediately and lasted for an entire week during multi-day lags in the transitional month of May (ranges of excess risk: 3.1 %-4.8 %) but not in the summer (June-August) (ranges of excess risk: -0.3 %-1.3 %). The significant increases in the excess risk of diabetes were also found among diabetes patients with complications of neuronopathy (excess risk: 27.7 %) and hypoglycemia (excess risk: 19.1 %). Furthermore, the modification effects on the heat-diabetes association were significantly stronger in females, Medicaid enrollees, non-compliant patients, and individuals with comorbidities of atherosclerotic heart disease and old myocardial infarction. CONCLUSIONS: Ambient heat exposure significantly increased the burden of hospital admissions for diabetes in transitional rather than summer months indicating the importance of exposure timing. Vulnerability to heat varied by demographics and heart comorbidity.

The effect of heat on lung diffusing capacity for carbon monoxide (DLCO) during cycling exercise.

PURPOSE: This study aimed to quantify the combined effects of heat exposure and exercise of increasing intensity on pulmonary blood flow using lung diffusing capacity for carbon monoxide (DLCO) as an indirect measure. We hypothesized that, during exercise in the heat, the well-documented increase in skin blood flow for thermoregulation would lead to alterations in pulmonary blood flow and a subsequent fall in DLCO versus a thermoneutral condition. METHODS: Nine healthy subjects (4 F/5 M, 20-45 years, VO2max 46.7 ± 5.8 mL/kg/min) completed three 15-min stages including rest and during cycling at 20 and 40% of maximum workload (Wmax) in either thermoneutral (TN; 22.2 ± 0.6 °C) or heat (HT; 39.4 ± 0.4 °C) conditions. DLCO, minute ventilation (VE), oxygen consumption ([Formula: see text]), heart rate (HR), and core (TC) and skin temperature (Tsk) were measured. RESULTS: DLCO showed a significant interaction between exercise intensity and heat (P = 0.019); post hoc testing revealed that DLCO was higher at 40% of Wmax in HT vs. TN (53.2 ± 10.6 vs 50.0 ± 10.3 mL/min/mmHg, P = 0.003) only. VE and [Formula: see text] showed no difference in HT vs. TN. HR was higher in HT vs. TN (P < 0.001). TC and Tsk showed a significant interaction between temperature and intensity (P < 0.05). CONCLUSION: The unexpected increase in DLCO during exercise in HT vs. TN conditions suggests a larger lung surface area for gas exchange, perhaps due to increased pulmonary capillary recruitment and/or distension secondary to a higher cardiac output (Q) in the heat. This study furthers our understanding of how heat exposure might impact pulmonary blood flow, specifically as assessed via DLCO.