The pathophysiology of heat exposure.
Ontology highlight
ABSTRACT:
SUBMITTER: Szekely M
PROVIDER: S-EPMC4843928 | biostudies-literature | 2015 Oct-Dec
REPOSITORIES: biostudies-literature
Publications
The pathophysiology of heat exposure.
Székely Miklós M Carletto Luís L Garami András A
Temperature (Austin, Tex.) 20150527 4
Similar Datasets
Project description:The goal of this study is to investigate the wage differential between groups of workers who are exposed to heat and those who are not. Workers in the heat-exposure risk group are defined as workers who work in conditions that cause them to spend more than 25% of their work hours at high temperatures. To analyze the wage differential, the Blinder-Oaxaca and Juhn-Murphy-Pierce methods were applied to Korea Working Condition Survey data. The results show that the no heat-exposure risk group received higher wages. In most cases, this can be interpreted as the endowment effect of human capital. As a price effect that lowers the endowment effect, the compensating differential for the heat-exposure risk group was found to be 1%. Moreover, education level, work experience, and employment status counteracted the compensating differentials for heat-exposure risks. A comparison of data sets from 2011 and 2014 shows that the increasing wage gap between the two groups was not caused by systematic social discrimination factors. This study suggests that wage differential factors can be modified for thermal environmental risks that will change working conditions as the impact of climate change increases.
| S-EPMC5551123 | biostudies-other
Project description:Increased heat-related morbidity and mortality are expected direct consequences of global warming. In the developed world, most fatal heat exposures occur in the indoor home environment, yet little is known of the correspondence between outdoor and indoor heat. Here we show how summertime indoor heat and humidity measurements from 285 low- and middle-income New York City homes vary as a function of concurrent local outdoor conditions. Indoor temperatures and heat index levels were both found to have strong positive linear associations with their outdoor counterparts; however, among the sampled homes a broad range of indoor conditions manifested for the same outdoor conditions. Using these models, we simulated indoor conditions for two extreme events: the 10-day 2006 NYC heat wave and a 9-day event analogous to the more extreme 2003 Paris heat wave. These simulations indicate that many homes in New York City would experience dangerously high indoor heat index levels during extreme heat events. These findings also suggest that increasing numbers of NYC low- and middle-income households will be exposed to heat index conditions above important thresholds should the severity of heat waves increase with global climate change. The study highlights the urgent need for improved indoor temperature and humidity management.
| S-EPMC4121079 | biostudies-literature
Project description:Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.
| S-EPMC7071449 | biostudies-literature
Project description:The effects of early heat conditioning on the acute heat stress response in broilers were investigated via the growth performance, dopamine, serotonin, and corticosterone and the expression of heat shock proteins (HSP) and heat shock factors. One-day-old chicks (n = 144) were divided into 3 groups in a 35-d experiment (48 chicks per each group). Group 1 (C) was treated with an optimum temperature, group 2 (CH) was treated with 40°C ± 1°C on day 35 (5 h), and group 3 (HH) was treated with 40°C ± 1°C on day 5 (24 h) and day 35 (5 h). On day 7, the body weight gain was lower (P < 0.05) in HH than in C and CH. On day 35, the heat-treated groups (CH and HH) had lower weight gains than the C group (P < 0.05), whereas the feed conversion ratio was lower in HH (P < 0.05). Serum corticosterone was higher in CH than in C, but HH and C did not differ (P < 0.05). Liver HSP70 protein expression was higher in CH than HH and C (P < 0.05), which did not differ, and HSP40 protein expression was higher in CH than C (P < 0.05). These results suggest that early heat conditioning may reduce acute heat stress on broiler.
| S-EPMC7936181 | biostudies-literature
Project description:Adequate water intake, supporting both cardiovascular function and evaporative cooling, is a critical factor in mitigating the effects of heat waves, which are expected to increase with global warming. However, the regulation of water intake during periods of intermittent heat exposure is not well understood. In this study, the effects of access to water or no access during intermittent heat exposure were assessed using male Sprague-Dawley rats exposed to 37.5°C for 4 h/day. After 7 days of intermittent heat exposure, reductions in evaporative water loss were observed in all animals and reductions in water intake following heat exposure occurred as the days of heat exposure increased. Rats that were not allowed water during the 7 days of exposure had decreased rehydration levels, however, rats allowed access to water increased water intake during exposure and exhibited higher overall rehydration levels over the same time period. Peripheral administration of angiotensinII, mimicking activation of volemic thirst, or hypertonic saline solution, activating intracellular thirst, did not result in alteration of water intake in rats exposed to heat with access to water compared to control rats. In contrast, rats exposed to heat without access to water had reduced water intake after administration of hypertonic saline and increased water intake after administration of angiotensinIIcompared to control rats. These experiments demonstrate that thirst responses to intermittent heat exposure are altered by providing water during heat exposure and that intermittent heat exposure without access to water alters drinking responses to both intracellular and extracellular thirst challenges.
| S-EPMC4848724 | biostudies-other
Project description:Heat stroke is a perilous condition marked by severe hyperthermia and extensive multiorgan dysfunction, posing a considerable risk of mortality if not promptly identified and treated. Furthermore, the complex biological mechanisms underlying heat stroke-induced tissue and cell damage across organ systems remain incompletely understood. This knowledge gap has hindered the advancement of effective preventive and therapeutic strategies against this condition. In this narrative review, we synthesize key insights gained over a decade using a translational baboon model of heat stroke. By replicating heat stroke pathology in a non-human primate species that closely resembles humans, we have unveiled novel insights into the pathways of organ injury and cell death elicited by this condition. Here, we contextualize and integrate the lessons learned concerning heat stroke pathophysiology and recovery, areas that are inherently challenging to investigate directly in human subjects. We suggest novel research directions to advance the understanding of the complex mechanisms underlying cell death and organ injury. This may lead to precise therapeutic strategies that benefit individuals suffering from this debilitating condition.
| S-EPMC10988686 | biostudies-literature
Project description:Increased exposure to extreme heat from both climate change and the urban heat island effect-total urban warming-threatens the sustainability of rapidly growing urban settlements worldwide. Extreme heat exposure is highly unequal and severely impacts the urban poor. While previous studies have quantified global exposure to extreme heat, the lack of a globally accurate, fine-resolution temporal analysis of urban exposure crucially limits our ability to deploy adaptations. Here, we estimate daily urban population exposure to extreme heat for 13,115 urban settlements from 1983 to 2016. We harmonize global, fine-resolution (0.05°), daily temperature maxima and relative humidity estimates with geolocated and longitudinal global urban population data. We measure the average annual rate of increase in exposure (person-days/year-1) at the global, regional, national, and municipality levels, separating the contribution to exposure trajectories from urban population growth versus total urban warming. Using a daily maximum wet bulb globe temperature threshold of 30 °C, global exposure increased nearly 200% from 1983 to 2016. Total urban warming elevated the annual increase in exposure by 52% compared to urban population growth alone. Exposure trajectories increased for 46% of urban settlements, which together in 2016 comprised 23% of the planet's population (1.7 billion people). However, how total urban warming and population growth drove exposure trajectories is spatially heterogeneous. This study reinforces the importance of employing multiple extreme heat exposure metrics to identify local patterns and compare exposure trends across geographies. Our results suggest that previous research underestimates extreme heat exposure, highlighting the urgency for targeted adaptations and early warning systems to reduce harm from urban extreme heat exposure.
| S-EPMC8521713 | biostudies-literature
Project description:ImportancePrevious studies have demonstrated the associations of daily high temperature with hospitalizations and mortality from ischemic stroke, but the hourly association of ambient heat and acute ischemic stroke (AIS) onset has been rarely examined.ObjectivesTo evaluate the association between hourly high ambient temperature and the onset of AIS.Design, setting, and participantsThis time-stratified case-crossover study was conducted using a nationwide registry that collects data from more than 200 stroke centers in China. Participants were adult patients with AIS who were hospitalized in the warm seasons between January 1, 2019, and December 31, 2021.ExposuresHourly temperature and single-hour temperature exposure lag up to 24 hours before the AIS onset (lag 0 hours to lag 24 hours).Main outcomes and measuresThe main outcome was onset of AIS. Associations between hourly mean temperatures and AIS onset were analyzed using conditional logistic regression integrated with the distributed lag nonlinear model. Stratification analyses were applied to examine potential association modifiers. Several sensitivity analyses were conducted to examine the robustness of the results.ResultsA total of 82 455 patients with AIS (mean [SD] age, 65.8 [11.9] years; 52 267 males [63.4%]) were included in the final analysis. A monotonically increasing risk of AIS onset was associated with higher temperatures. The excess AIS risk occurred immediately at lag 0 hours and persisted for 10 hours. Compared with the reference temperature (12.1 °C), the cumulative odds ratio (OR) over lag 0 to 10 hours of AIS onset associated with extremely high temperature (33.3 °C) was 1.88 (95% CI, 1.65-2.13) nationwide. The exposure-response curve was steeper in the north than in the south (OR, 1.80 [95% CI, 1.53-2.11] vs 1.57 [95% CI, 1.31-1.87]). The ORs were greater for males and patients with a history of dyslipidemia or atrial fibrillation, but the differences were not significant.Conclusions and relevanceResults of this study suggest that hourly heat exposure is associated with increased risk of AIS onset. This finding may benefit the formulation of public health strategies to reduce cerebrovascular risk associated with high ambient temperature under global warming.
| S-EPMC10902723 | biostudies-literature
Project description:ObjectiveNeuropathic pain due to small-fiber sensory neuropathy in type 2 diabetes can be diagnosed by skin biopsy with quantification of intra-epidermal nerve fiber (IENF) density. There is, however, a lack of noninvasive physiological assessment. Contact heat-evoked potential (CHEP) is a newly developed approach to record cerebral responses of A? fiber-mediated thermonociceptive stimuli. We investigated the diagnostic role of CHEP.Research design and methodsFrom 2006 to 2009, there were 32 type 2 diabetic patients (20 males and 12 females, aged 51.63 ± 10.93 years) with skin denervation and neuropathic pain. CHEPs were recorded with heat stimulations at the distal leg, where skin biopsy was performed.ResultsCHEP amplitude was reduced in patients compared with age- and sex-matched control subjects (14.8 ± 15.6 vs. 33.7 ± 10.1 ?V, P < 0.001). Abnormal CHEP patterns (reduced amplitude or prolonged latency) were noted in 81.3% of these patients. The CHEP amplitude was the most significant parameter correlated with IENF density (P = 0.003) and pain perception to contact heat stimuli (P = 0.019) on multiple linear regression models. An excitability index was derived by calculating the ratio of the CHEP amplitude over the IENF density. This excitability index was higher in diabetic patients than in control subjects (P = 0.023), indicating enhanced brain activities in neuropathic pain. Among different neuropathic pain symptoms, the subgroup with evoked pain had higher CHEP amplitudes than the subgroup without evoked pain (P = 0.011).ConclusionsCHEP offers a noninvasive approach to evaluate the degeneration of thermonociceptive nerves in diabetic neuropathy by providing physiological correlates of skin denervation and neuropathic pain.
| S-EPMC2992207 | biostudies-literature
Project description:Exposure of rats to heat (39 +/- 1 degree C) stimulated liver tryptophan pyrrolase 2-fold between 3 and 48 h. Plasma corticosterone increased 2-fold after 1 h of heat exposure and decreased to a low value of 50% by 16 h. The effect of heat exposure on the enzyme was obtained in adrenalectomized animals. Stimulation by cortisol and tryptophan of the enzyme was also obtained in heat exposure, and the effects seemed to be additive. The concentration of tryptophan in the liver remained unchanged, and that in the plasma decreased to about 50% at 8 h exposure to heat and reverted to normal by 46 h. Simultaneous administration of noradrenaline to heat-exposed rats had no effect, whereas that of thyroxine partly prevented the stimulation of the enzyme activity. Hypothyroid conditions obtained by thyroidectomy or treatment with propylthiouracil significantly stimulated the enzyme activity. Cycloheximide treatment of heat-exposed rats did not prevent the stimulation of the enzyme activity. The results indicate that the effect of heat exposure on liver tryptophan pyrrolase is obtained, due to the accompanying hypothyroid condition, by increasing the activity of the existing protein by a mechanism possibly different from those known at present.
| S-EPMC1144725 | biostudies-other