Heat-related illness and dementia: a study integrating epidemiological and experimental evidence.

BACKGROUND: Heat-related illness (HRI) is commonly considered an acute condition, and its potential long-term consequences are not well understood. We conducted a population-based cohort study and an animal experiment to evaluate whether HRI is associated with dementia later in life. METHODS: The Taiwan National Health Insurance Research Database was used in the epidemiological study. We identified newly diagnosed HRI patients between 2001 and 2015, but excluded those with any pre-existing dementia, as the study cohort. Through matching by age, sex, and the index date with the study cohort, we selected individuals without HRI and without any pre-existing dementia as a comparison cohort at a 1:4 ratio. We followed each cohort member until the end of 2018 and compared the risk between the two cohorts using Cox proportional hazards regression models. In the animal experiment, we used a rat model to assess cognitive functions and the histopathological changes in the hippocampus after a heat stroke event. RESULTS: In the epidemiological study, the study cohort consisted of 70,721 HRI patients and the comparison cohort consisted of 282,884 individuals without HRI. After adjusting for potential confounders, the HRI patients had a higher risk of dementia (adjusted hazard ratio [AHR] = 1.24; 95% confidence interval [CI]: 1.19-1.29). Patients with heat stroke had a higher risk of dementia compared with individuals without HRI (AHR = 1.26; 95% CI: 1.18-1.34). In the animal experiment, we found cognitive dysfunction evidenced by animal behavioral tests and observed remarkable neuronal damage, degeneration, apoptosis, and amyloid plaque deposition in the hippocampus after a heat stroke event. CONCLUSIONS: Our epidemiological study indicated that HRI elevated the risk of dementia. This finding was substantiated by the histopathological features observed in the hippocampus, along with the cognitive impairments detected, in the experimental heat stroke rat model.

Understanding the physiological and biological response to ambient heat exposure in pregnancy: protocol for a systematic review and meta-analysis.

INTRODUCTION: Climate change increases not only the frequency, intensity and duration of extreme heat events but also annual temperatures globally, resulting in many negative health effects, including harmful effects on pregnancy and pregnancy outcomes. As temperatures continue to increase precipitously, there is a growing need to understand the underlying biological pathways of this association. This systematic review will focus on maternal, placental and fetal changes that occur in pregnancy due to environmental heat stress exposure, in order to identify the evidence-based pathways that play a role in this association. METHODS AND ANALYSIS: We will follow the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We will search PubMed and Ovid Embase databases from inception using tested and validated search algorithms. Inclusion of any studies that involve pregnant women and have measured environmental heat stress exposure and either maternal, placental or fetal physiological or biochemical changes and are available in English. Modelling studies or those with only animals will be excluded. The risk of bias will be assessed using the Office of Health Assessment and Translation tool. Abstract screening, data extraction and risk of bias assessment will be conducted by two independent reviewers.Environmental parameters will be reported for each study and where possible these will be combined to calculate a heat stress indicator to allow comparison of exposure between studies. A narrative synthesis will be presented following standard guidelines. Where outcome measures have at least two levels of exposure, we will conduct a dose-response meta-analysis should there be at least three studies with the same outcome. A random effects meta-analysis will be conducted where at least three studies give the same outcome. ETHICS AND DISSEMINATION: This systematic review and meta-analysis does not require ethical approval. Dissemination will be through peer-reviewed journal publication and presentation at international conferences/interest groups. PROSPERO REGISTRATION NUMBER: CRD42024511153.

BHBA attenuates endoplasmic reticulum stress-dependent neuroinflammation via the gut-brain axis in a mouse model of heat stress.

BACKGROUND: Heat stress (HS) commonly occurs as a severe pathological response when the body's sensible temperature exceeds its thermoregulatory capacity, leading to the development of chronic brain inflammation, known as neuroinflammation. Emerging evidence suggests that HS leads to the disruption of the gut microbiota, whereas abnormalities in the gut microbiota have been demonstrated to affect neuroinflammation. However, the mechanisms underlying the effects of HS on neuroinflammation are poorly studied. Meanwhile, effective interventions have been unclear. ß-Hydroxybutyric acid (BHBA) has been found to have neuroprotective and anti-inflammatory properties in previous studies. This study aims to explore the modulatory effects of BHBA on neuroinflammation induced by HS and elucidate the underlying molecular mechanisms. METHODS: An in vivo and in vitro model of HS was constructed under the precondition of BHBA pretreatment. The modulatory effects of BHBA on HS-induced neuroinflammation were explored and the underlying molecular mechanisms were elucidated by flow cytometry, WB, qPCR, immunofluorescence staining, DCFH-DA fluorescent probe assay, and 16S rRNA gene sequencing of colonic contents. RESULTS: Heat stress was found to cause gut microbiota disruption in HS mouse models, and TM7 and [Previotella] spp. may be the best potential biomarkers for assessing the occurrence of HS. Fecal microbiota transplantation associated with BHBA effectively reversed the disruption of gut microbiota in HS mice. Moreover, BHBA may inhibit microglia hyperactivation, suppress neuroinflammation (TNF-α, IL-1ß, and IL-6), and reduce the expression of cortical endoplasmic reticulum stress (ERS) markers (GRP78 and CHOP) mainly through its modulatory effects on the gut microbiota (TM7, Lactobacillus spp., Ruminalococcus spp., and Prevotella spp.). In vitro experiments revealed that BHBA (1 mM) raised the expression of the ERS marker GRP78, enhanced cellular activity, and increased the generation of reactive oxygen species (ROS) and anti-inflammatory cytokines (IL-10), while also inhibiting HS-induced apoptosis, ROS production, and excessive release of inflammatory cytokines (TNF-α and IL-1ß) in mouse BV2 cells. CONCLUSION: ß-Hydroxybutyric acid may be an effective agent for preventing neuroinflammation in HS mice, possibly due to its ability to inhibit ERS and subsequent microglia neuroinflammation via the gut-brain axis. These findings lay the groundwork for future research and development of BHBA as a preventive drug for HS and provide fresh insights into techniques for treating neurological illnesses by modifying the gut microbiota.

Therapeutic effects of mitoquinol during an acute heat stress challenge in growing barrows.

Study objectives were to determine the effects of mitoquinol (MitoQ, a mitochondrial-targeted antioxidant) on biomarkers of metabolism and inflammation during acute heat stress (HS). Crossbred barrows [n = 32; 59.0 ±â€…5.6 kg body weight (BW)] were blocked by BW and randomly assigned to 1 of 4 environmental-therapeutic treatments: 1) thermoneutral (TN) control (n = 8; TNCon), 2) TN and MitoQ (n = 8; TNMitoQ), 3) HS control (n = 8; HSCon), or 4) HS and MitoQ (n = 8; HSMitoQ). Pigs were acclimated for 6 d to individual pens before study initiation. The trial consisted of two experimental periods (P). During P1 (2 d), pigs were fed ad libitum and housed in TN conditions (20.6 ±â€…0.8 °C). During P2 (24 h), HSCon and HSMitoQ pigs were exposed to continuous HS (35.2 ±â€…0.2 °C), while TNCon and TNMitoQ remained in TN conditions. MitoQ (40 mg/d) was orally administered twice daily (0700 and 1800 hours) during P1 and P2. Pigs exposed to HS had increased rectal temperature, skin temperature, and respiration rate (+1.5 °C, +6.8 °C, and +101 breaths per minute, respectively; P < 0.01) compared to their TN counterparts. Acute HS markedly decreased feed intake (FI; 67%; P < 0.01); however, FI tended to be increased in HSMitoQ relative to HSCon pigs (1.5 kg vs. 0.9 kg, respectively; P = 0.08). Heat-stressed pigs lost BW compared to their TN counterparts (-4.7 kg vs. +1.6 kg, respectively; P < 0.01); however, the reduction in BW was attenuated in HSMitoQ compared to HSCon pigs (-3.9 kg vs. -5.5 kg, respectively; P < 0.01). Total gastrointestinal tract weight (empty tissue and luminal contents) was decreased in HS pigs relative to their TN counterparts (6.2 kg vs. 8.6 kg, respectively; P < 0.01). Blood glucose increased in HSMitoQ relative to HSCon pigs (15%; P = 0.04). Circulating non-esterified fatty acids (NEFA) increased in HS compared to TN pigs (P < 0.01), although this difference was disproportionately influenced by elevated NEFA in HSCon relative to HSMitoQ pigs (251 µEq/L vs. 142 µEq/L; P < 0.01). Heat-stressed pigs had decreased circulating insulin relative to their TN counterparts (47%; P = 0.04); however, the insulin:FI ratio tended to increase in HS relative to TN pigs (P = 0.09). Overall, circulating leukocytes were similar across treatments (P > 0.10). Plasma C-reactive protein remained similar among treatments; however, haptoglobin increased in HS relative to TN pigs (48%; P = 0.03). In conclusion, acute HS exposure negatively altered animal performance, inflammation, and metabolism, which were partially ameliorated by MitoQ.

Heat stress (HS) compromises animal health and productivity, and this causes major economic losses in almost every livestock sector. The negative consequences of HS are thought to originate from intestinal barrier dysfunction and subsequent immune activation. The underlying causes of lost intestinal integrity during HS are likely multifactorial; however, intestinal ischemia, increased accumulation of reactive oxygen species, and the ensuing epithelial oxidative damage might be potential causes. Mitochondria-targeted antioxidants, such as mitoquinol (MitoQ), are probably more effective than traditional dietary antioxidants (i.e., selenium, vitamin E) at alleviating oxidative stress, as they localize and accumulate within the mitochondria, potentiating their antioxidant activity. Thus, the present study aimed to investigate MitoQ's role during a thermal event in growing pigs. Herein, HS increased all body temperature indices, decreased feed intake (FI), and induced substantial body weight (BW) loss. Interestingly, the reduction in FI and BW was less dramatic in pigs receiving MitoQ. Changes in circulating metabolism and the acute phase response were observed due to the HS challenge; however, contrary to our expectations, these changes were not offset by MitoQ administration. Although our results suggest a positive MitoQ effect on growth performance, future studies are needed to corroborate the replicability of this response during HS.

Climate change and heat stress resilient outdoor workers: findings from systematic literature review.

PURPOSE: Global warming has led to an increase in the number and intensity of extreme heat events, posing a significant threat to the health and safety of workers, especially those working outdoors, as they often have limited access to cooling strategies. The present systematic literature review (a) summarizes the current knowledge on the impacts of climate change on outdoor workers, (b) provides historical background on this issue, (c) explores factors that reduce and increase thermal stress resilience, (d) discusses the heat mitigation strategies, and (e) provides an overview of existing policy and legal frameworks on occupational heat exposure among outdoor workers. MATERIALS AND METHODS: In this systematic review, we searched scientific databases including Scopus (N = 855), Web of Science (N = 828), and PubMed (N = 202). Additionally, we identified relevant studies on climate change and heat-stress control measures through Google Scholar (N = 116) using specific search terms. In total, we monitored 2001 articles pertaining to worker populations (men = 2921; women = 627) in various outdoor climate conditions across 14 countries. After full-text assessment, 55 studies were selected for inclusion, and finally, 29 eligible papers were included for data extraction. RESULTS: Failure to implement effective control strategies for outdoor workers will result in decreased resilience to thermal stress. The findings underscore a lack of awareness regarding certain adaptation strategies and interventions aimed at preventing and enhancing resilience to the impact of climate change on heat stress prevalence among workers in outdoor tropical and subtropical environments. However, attractive alternative solutions from the aspects of economic and ecological sustainability in the overall assessment of heat stress resilience can be referred to acclimatization, shading, optimized clothing properties and planned breaks. CONCLUSION: The integration of climate change adaptation strategies into occupational health programs can enhance occupational heat resilience among outdoor workers. Conducting cost-benefit evaluations of health and safety measures for thermal stress adaptation strategies among outdoor workers is crucial for professionals and policymakers in low- and middle-income tropical and subtropical countries. In this respect, complementary measures targeting hydration, work-rest regimes, ventilated garments, self-pacing, and mechanization can be adopted to protect outdoor workers. Risk management strategies, adaptive measures, heat risk awareness, practical interventions, training programs, and protective policies should be implemented in hot-dry and hot-humid climates to boost the tolerance and resilience of outdoor workers.

Sex differences in the association of long-term exposure to heat stress on kidney function in a large Taiwanese population study.

The incidence and prevalence of dialysis in Taiwan are high compared to other regions. Consequently, mitigating chronic kidney disease (CKD) and the worsening of kidney function have emerged as critical healthcare priorities in Taiwan. Heat stress is known to be a significant risk factor for CKD and kidney function impairment. However, differences in the impact of heat stress between males and females remains unexplored. We conducted this retrospective cross-sectional analysis using data from the Taiwan Biobank (TWB), incorporating records of the wet bulb globe temperature (WBGT) during midday (11 AM-2 PM) and working hours (8 AM-5 PM) periods based on the participants' residential address. Average 1-, 3-, and 5-year WBGT values prior to the survey year were calculated and analyzed using a geospatial artificial intelligence-based ensemble mixed spatial model, covering the period from 2010 to 2020. A total of 114,483 participants from the TWB were included in this study, of whom 35.9% were male and 1053 had impaired kidney function (defined as estimated glomerular filtration rate < 60 ml/min/1.73 m2). Multivariable analysis revealed that in the male participants, during the midday period, the 1-, 3-, and 5-year average WBGT values per 1 â„ƒ increase were significantly positively associated with eGFR < 60 ml/min/1.73 m2 (odds ratio [OR], 1.096, 95% confidence interval [CI] = 1.002-1.199, p = 0.044 for 1 year; OR, 1.093, 95% CI = 1.000-1.196, p = 0.005 for 3 years; OR, 1.094, 95% CI = 1.002-1.195, p = 0.045 for 5 years). However, significant associations were not found for the working hours period. In the female participants, during the midday period, the 1-, 3-, and 5-year average WBGT values per 1 â„ƒ increase were significantly negatively associated with eGFR < 60 ml/min/1.73 m2 (OR, 0.872, 95% CI = 0.778-0.976, p = 0.018 for 1 year; OR, 0.874, 95% CI = 0.780-0.978, p = 0.019 for 3 years; OR, 0.875, 95% CI = 0.784-0.977, p = 0.018 for 5 years). In addition, during the working hours period, the 1-, 3-, and 5-year average WBGT values per 1 â„ƒ increase were also significantly negatively associated with eGFR < 60 ml/min/1.73 m2 (OR, 0.856, 95% CI = 0.774-0.946, p = 0.002 for 1 year; OR, 0.856, 95% CI = 0.774-0.948, p = 0.003 for 3 years; OR, 0.853, 95% CI = 0.772-0.943, p = 0.002 for 5 years). In conclusion, our results revealed that increased WBGT was associated with impaired kidney function in males, whereas increased WBGT was associated with a protective effect against impaired kidney function in females. Further studies are needed to elucidate the exact mechanisms underlying these sex-specific differences.

Establishment and risk factor assessment of the abnormal body temperature probability prediction model (ABTP) for dairy cattle.

The study aims to develop an abnormal body temperature probability (ABTP) model for dairy cattle, utilizing environmental and physiological data. This model is designed to enhance the management of heat stress impacts, providing an early warning system for farm managers to improve dairy cattle welfare and farm productivity in response to climate change. The study employs the Least Absolute Shrinkage and Selection Operator (LASSO) algorithm to analyze environmental and physiological data from 320 dairy cattle, identifying key factors influencing body temperature anomalies. This method supports the development of various models, including the Lyman Kutcher-Burman (LKB), Logistic, Schultheiss, and Poisson models, which are evaluated for their ability to predict abnormal body temperatures in dairy cattle effectively. The study successfully validated multiple models to predict abnormal body temperatures in dairy cattle, with a focus on the temperature-humidity index (THI) as a critical determinant. These models, including LKB, Logistic, Schultheiss, and Poisson, demonstrated high accuracy, as measured by the AUC and other performance metrics such as the Brier score and Hosmer-Lemeshow (HL) test. The results highlight the robustness of the models in capturing the nuances of heat stress impacts on dairy cattle. The research develops innovative models for managing heat stress in dairy cattle, effectively enhancing detection and intervention strategies. By integrating advanced technologies and novel predictive models, the study offers effective measures for early detection and management of abnormal body temperatures, improving cattle welfare and farm productivity in changing climatic conditions. This approach highlights the importance of using multiple models to accurately predict and address heat stress in livestock, making significant contributions to enhancing farm management practices.

Heat-related illness.

ABSTRACT: This article concisely overviews heat-related illnesses, emphasizing their significant impact on public health. It explores the pathophysiology of conditions ranging from mild heat cramps to life-threatening heat stroke, highlighting key heat transfer mechanisms and the importance of environmental factors. Differential diagnosis considerations, prevention strategies, and nursing implications are discussed, underscoring the need for prompt recognition and intervention in managing these conditions.

Feeling hot is being hot? Comparing the mapping and the surveying paradigm for urban heat vulnerability in Vienna.

With rising global temperatures, cities increasingly need to identify populations or areas that are vulnerable to urban heat waves; however, vulnerability assessments may run into ecological fallacy if data from different scales are misconstrued as equivalent. We assess the heat vulnerability of 1983 residents in Vienna by measuring heat impacts, exposure, sensitivity and adaptive capacity with mirrored indicators in the mapping paradigm (i.e. census tract data referring to the geographic regions where these residents live) and the surveying paradigm (i.e. survey data referring to the residents' individual households). Results obtained in both paradigms diverge substantially: meteorological indicators of hot days and tropical nights are virtually unrelated to self-reported heat strain. Meteorological indicators are explained by mapping indicators (R2 of 15-40 %), but mostly not by surveying indicators. Vice versa, experienced heat stress and subjective heat burden are mostly unassociated with mapping indicators but are partially explained by surveying indicators (R2 of 2-4 %). The results suggest that the two paradigms do not capture the same components of vulnerability; this challenges whether studies conducted in the respective paradigms can complement and cross-validate each other. Policy interventions should first define which heat vulnerability outcome they target and then apply the paradigm that best captures the specific drivers of this outcome.

Potential of exogenous melatonin administration to mitigate heat stress induce pathophysiology of chicken.

Melatonin (MT) is an amine hormone secreted by the body that has antioxidant and anti-inflammatory properties. The aim of this study was to investigate pathophysiological protection of MT in heat-stressed chickens. By modelling heat-stressed chickens and treating them with MT. After 21 days of administration, serum antioxidant enzymes, biochemical indices, inflammatory cytokine and heat-stress indices were detected, along with cardiopulmonary function indices and histological observations in chickens. The results show heat-stress induced a decrease (P < 0.05) in body weight and an increase in body temperature, which was reversed after MT intervention. Treatment with MT inhibited (P < 0.05) the secretion of pro-inflammatory factors interleukin-1ß, interleukin-6, tumor necrosis factor α, serum heat shock protein 70, corticosterone, and elevated (P < 0.05) the levels of biochemical factors total protein, albumin, globulin, and increased (P < 0.05) the activities of antioxidant enzymes superoxide dismutase, glutathione peroxidase and catalase in chicken serum caused by heat stress, and the best effect was observed with the medium dose of MT. The heat-stress caused cardiac atrophy and pulmonary congestion, decreased (P < 0.05) the cardiac function indices creatine kinase isoenzyme, cardiac troponin I, angiotensin receptor I, creatine kinase and lung function indices myeloperoxidase, angiotensin-II, heat shock factor I, and increased (P < 0.05) the lung vascular endothelial growth factor II. Sections of the heart and lungs after administration of MT were observed to be more complete with more normal tissue indices. At the same time, compared with heat stress, heart and lung function indices of grade chickens after MT administration were significantly (P < 0.05)reduced and tended to normal levels, and the best effect was observed in the medium-dose MT. In conclusion, heat stress can cause pathophysiological damage in chickens, and 1 mg/kg/d of exogenous melatonin can attenuate this adverse effect.