Impact of heat stress on health-related symptoms and physiological changes among workers at a palm oil mill in Mukah, Sarawak, Malaysia.

INTRODUCTION: The palm oil (PO) industry is one of the most important sectors in the Malaysian economy. Workers at PO mills are, however, at risk for a number of health and safety issues, including heat stress, as the PO is one of the industries with high heat exposure. Heat stress occurs when a person's body cannot get rid of excess heat. Heat stress can result in heat cramps, heat exhaustion, heat rash, and heat stroke. It also results in physiological and psychological changes that can have an impact on a worker's performance. Therefore, this study aimed to evaluate the impact of heat stress on health-related symptoms and physiological changes among workers in a PO mill. MATERIALS AND METHODS: This cross-sectional study was conducted in a PO mill located in Mukah, Sarawak, Malaysia. Thirty-one workers from the four workstations (sterilizer, boiler, oil, and engine rooms) were selected as the respondents in this study. Wet Bulb Globe Thermometer was used in this study to measure the environmental temperature (WBGTin). Body core temperature (BCT), blood pressure (BP), and heart rate (HR) were recorded both before and after working in order to assess the physiological effects of heat stress on workers. A set of questionnaires were used to determine sociodemographic characteristics of the respondents and their symptoms related to heat stress. Data were then analyzed using SPSS Ver28. RESULTS: The WBGTin was found to be above the ACGIH threshold limit value of heat stress exposure in the engine room, sterilizer, and boiler workstations (>28.0°C). Additionally, there was a significant difference in the worker's BCT in these three workstations before and after work (p<0.05). Only the systolic BP and HR of those working at the boiler workstation showed significant difference between before and after work (p<0.05). The most typical symptoms that workers experience as a result of being exposed to heat at work include headache and fatigue. However, statistical analysis using Spearman Rho's test showed that there is no correlation between heat stress level with physiological changes and health-related symptoms among study respondents (p>0.05). CONCLUSION: Results of the present study confirmed that workers in PO mill were exposed to high temperatures while at work. Although the evidence indicates the physiological parameters in general are not significantly affected while working, it also demonstrated that worker's body adapts and acclimates to the level of heat. Even so, precautions should still be taken to reduce future heat exposure. It is recommended that a physiological study be carried out that focuses on cognitive function impairment to support the evidence regarding the effects of heat stress on PO mill workers.

Experimental heat stress nephropathy and liver injury are improved by allopurinol.

An epidemic of chronic kidney disease (CKD) has been observed in Central America among workers in the sugarcane fields. One hypothesis is that the CKD may be caused by recurrent heat stress and dehydration, and potentially by hyperuricemia. Accordingly, we developed a murine model of kidney injury associated with recurrent heat stress. In the current experiment, we tested whether treatment with allopurinol (a xanthine oxidase inhibitor that reduces serum urate) provides renal protection against recurrent heat stress and dehydration. Eight-week-old male C57BL/6 mice were subjected to recurrent heat stress (39.5°C for 30 min, 7 times daily, for 5 wk) with or without allopurinol treatment and were compared with control animals with or without allopurinol treatment. Mice were allowed ad libitum access to normal laboratory chow (Harlan Teklad). Kidney histology, liver histology, and renal function were examined. Heat stress conferred both kidney and liver injury. Kidneys showed loss of proximal tubules, infiltration of monocyte/macrophages, and interstitial collagen deposition, while livers of heat-stressed mice displayed an increase in macrophages, collagen deposition, and myofibroblasts. Allopurinol provided significant protection and improved renal function in the heat-stressed mice. The renal protection was associated with reduction in intrarenal uric acid concentration and heat shock protein 70 expression. Heat stress-induced renal and liver injury can be protected with allopurinol treatment. We recommend a clinical trial of allopurinol for individuals developing renal injury in rural areas of Central America where the epidemic of chronic kidney disease is occurring.

Reconsidering betaine as a natural anti-heat stress agent in poultry industry: a review.

Betaine is found ubiquitously in plants, animals, microorganisms, and rich dietary sources including seafood, spinach, and wheat bran. The chief physiological role of betaine is to function as a methyl donor and an osmolyte. Betaine also acts as an osmolyte, to maintain the avian's cellular water and ion balance to improve the avian's capacity against heat stress via preventing dehydration and osmotic inactivation. It helps in maintaining the protective osmolytic activity, especially in heat-stressed birds. Betaine may promote various intestinal microbes against osmotic variations and thus improve microbial fermentation activity. Previous studies showed that dietary supplementation of betaine in poultry diets could positively affect nutrients' digestibility, reduce abdominal fat weight, and increase breast meat yield. In addition, betaine has been reported to protect internal organs and boost their performance. Its inclusion in poultry diet is sparing essential amino acids like choline and methionine. In addition, it may play an important role in lean meat production by positively affecting the lipid metabolism with increased fatty acids catabolism and thus reducing carcass fat deposition. The aim of this review article was to broaden the knowledge regarding betaine and its importance in the poultry industry to cope with the heat stress problem. Moreover, it should be added to the diet as a natural anti-stressor through different routes (water/feed) to overcome the heat stress problem. However, further studies need to be conducted at the genetic and molecular basis to elucidate the mechanism behind the betaine as a natural anti-heat agent to decrease the heat stress problem in the poultry industry.

Role of the Red Ginseng in Defense against the Environmental Heat Stress in Sprague Dawley Rats.

Global temperature change causes heat stress related disorders in humans. A constituent of red ginseng has been known the beneficial effect on the resistance to many diseases. However, the mechanism of red ginseng (RG) against heat stress still remains unclear. To determine the effect of RG on heat stress, we examined the effect of the RG on the gene expression profiles in rats subjected to environmental heat stress. We evaluated the transcripts associated with hepatic lipid accumulation and oxidative stress in rats subjected to heat stress. We also analyzed the reactive oxygen species (ROS) contents. Our results suggested RG inhibited heat stress mediated altering mRNA expressions include HSPA1, DEAF1, HMGCR, and FMO1. We also determined RG attenuated fat accumulation in the liver by altering C/EBPß expression. RG promoted to repress the heat stress mediated hepatic cell death by inhibiting of Bcl-2 expression in rats subjected to heat stress. Moreover, RG administered group during heat stress dramatically decreased the malondialdehyde (MDA) contents and ROS associated genes compared with the control group. Thus, we suggest that RG might influence inhibitory effect on environmental heat stress induced abnormal conditions in humans.

Heat: not black, not white. It's gray!!!

Heat-related illness (HRI) is a broad term that includes clinical conditions ranging from heat cramps and syncope to heat exhaustion and heatstroke, which may result in death. HRIs are one of the major causes of death worldwide and continue to increase in severity with the rise in global temperature. The identification and estimation of heat-related morbidity and mortality is a major challenge. Heat stress manifests itself into respiratory, cardiovascular, and cerebrovascular disorders, leading to the attribution of the deaths caused by heat stress to these disorders. Although HRIs affect mankind in general, certain occupational workers such as soldiers and athletes are more prone. Various pharmacological and nonpharmacological strategies have been employed to combat HRIs. Despite this, heat exposure results in significant morbidity and mortality. Hence, complete understanding of HRIs at physiological as well as molecular level is required to facilitate design of more efficient preventive and treatment strategies. The impact of heat on mankind is not just restricted to HRIs. Heat treatment, i.e., thermotherapy, has been used extensively since ancient times for relieving pain, making heat a two-edged sword. This review attempts to summarize various HRIs, their physiological and molecular basis, and the state-of-the-art techniques/research initiatives to combat the same. It also illustrates the application of thermotherapy as a means for improving quality of life and morbidity associated with several disease conditions such as fibromyalgia syndrome, heart diseases, cancer, chronic pain, and depression.

Hypohydration and acute thermal stress affect mood state but not cognition or dynamic postural balance.

Equivocal findings have been reported in the few studies that examined the impact of ambient temperature (T a) and hypohydration on cognition and dynamic balance. The purpose of this study was to determine the impact of acute exposure to a range of ambient temperatures (T(a) 10-40 °C) in euhydration (EUH) and hypohydration (HYP) states on cognition, mood and dynamic balance. Thirty-two men (age 22 ± 4 years, height 1.80 ± 0.05 m, body mass 85.4 ± 10.8 kg) were grouped into four matched cohorts (n = 8), and tested in one of the four T(a) (10, 20, 30, 40 °C) when EUH and HYP (-4 % body mass via exercise-heat exposure). Cognition was assessed using psychomotor vigilance, 4-choice reaction time, matching to sample, and grammatical reasoning. Mood was evaluated by profile of mood states and dynamic postural balance was tested using a Biodex Balance System. Thermal sensation (TS), core (T core) and skin temperature (T(sk)) were obtained throughout testing. Volunteers lost -4.1 ± 0.4 % body mass during HYP. T sk and TS increased with increasing T(a), with no effect of hydration. Cognitive performance was not altered by HYP or thermal stress. Total mood disturbance (TMD), fatigue, confusion, anger, and depression increased during HYP at all T(a). Dynamic balance was unaffected by HYP, but 10 °C exposure impaired balance compared to all other T(a). Despite an increase in TMD during HYP, cognitive function was maintained in all testing environments, demonstrating cognitive resiliency in response to body fluid deficits. Dynamic postural stability at 10 °C appeared to be hampered by low-grade shivering, but was otherwise maintained during HYP and thermal stress.

[Effects of heat and cool-producing needling manipulations on rectal temperature and serum endotoxin content in endotoxin-induced heat syndrome rabbits].

OBJECTIVE: To observe the effect of traditional manipulations of "Shaoshanhuo" (heat-producing needling) and "Toutianliang"(cool-producing needling) on body temperature and serum endotoxin level in heat syndrome rabbits. METHODS: Twenty-four Japanese rabbits were randomly divided into control, model, Shaoshanhuo and Toutianliang groups. Heat-syndrome model was established by subcutaneous injection of bacterium coli endotoxin solution (40 microg/mL, 2 mL/kg). Heat-producing and cool-producing needling was applied to bilateral "Quchi" (LI 11) for 5 min, respectively. Rectal temperature was detected by using a thermometer, and serum endotoxin content assayed by using Limulus Ameboyte Lysate kit (luminescence measuring). RESULTS: In comparison with the control group, both rectal temperature and serum endotoxin levels were increased significantly in the model group (P < 0.01). While compared to the model group, the rectal temperature and serum endotoxin levels were down-regulated considerably in both Shaoshanhuo and Toutianliang groups (P < 0.05, P < 0.01). The effect of the Toutianliang group was obviously superior to that of the Shaoshanhuo group in reducing serum endotoxin content (P < 0.01). CONCLUSION: Both heat-producing needling and cool-producing needling can lower rectal temperature and serum endotoxin levels in heat-syndrome rabbits, and the effect of cool-producing needling is relatively better in reducing endotoxin content.

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow.

For decades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positron-emission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 ± 1.0°C to 37.4 ± 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 ± 0.5 to 2.3 ± 1.2 ml·100 g⁻¹·min⁻¹ (P < 0.05), whereas skin blood flow under the heating source increased from 0.7 ± 0.3 to 5.5 ± 1.5 ml·100 g⁻¹·min⁻¹ (P < 0.01). While whole body heat stress increased intestinal temperature by ∼1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 ± 0.5 ml·100 g⁻¹·min⁻¹; heat stress: 1.7 ± 0.3 ml·100 g⁻¹·min⁻¹; P = 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 ± 1.5 ml·100 g⁻¹·min⁻¹) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress.

Palm cooling does not reduce heat strain during exercise in a hot, dry environment.

To compare the effectiveness of the rapid thermal exchange device (RTX) in slowing the development of hyperthermia and associated symptoms among hand immersed in water bath (WB), water-perfused vest (WPV), and no cooling condition (NC). Ten subjects performed 4 heat stress trials. The protocol consisted of 2 bouts of treadmill walking, separated by a cooling-rehydration period. The times to reach the predetermined rectal temperature in the first (38.5 degrees C) and second bouts (39 degrees C) were not different among RTX, NC, and WB, but was longer for the WPV in both bouts (p<0.05). Heat storage was significantly lower for WPV only in the first bout vs. the other conditions (p<0.05). Heart rate (HR) was not different at 10, 20, and 30 min during the first bout among RTX, NC, and WB, but was lower for WPV (p<0.05). HR was not different among conditions during the second bout. The RTX was not effective in slowing the development of hyperthermia.

Chronic hypertension aggravates heat stress-induced brain damage: possible neuroprotection by cerebrolysin.

Whole body hyperthermia (WBH) aggravates brain edema formation and cell damage in chronic hypertensive rats compared with normotensive animals. In this investigation, we examined the influence of cerebrolysin on WBH-induced edema formation and brain pathology in hypertensive and normotensive rats. Rats subjected to 4 h WBH at 38 degrees C in a biological oxygen demand (BOD) incubator showed breakdown of the blood-brain barrier (BBB), reduced cerebral blood flow (CBF), edema formation and cell injuries in several parts of the brain. These effects were further aggravated in chronic hypertensive rats (two-kidney one clip model (2K1C), for 4 weeks) subjected to WBH. Pretreatment with cerebrolysin (5 mL/kg, 24 h and 30 min before heat stress) markedly attenuated the BBB dysfunction and brain pathology in normal animals. However, in hypertensive animals, a high dose of cerebrolysin (10 mL/kg, 24 h and 30 min before heat stress) was needed to attenuate WBH-induced BBB dysfunction and brain pathology. These observations indicate that heat stress could affect differently in normal and hypertensive conditions. Furthermore, our results suggest that patients suffering from various chronic cardiovascular diseases may respond differently to hyperthermia and to neuroprotective drugs, e.g., cerebrolysin not reported earlier.

Dysregulation of hepatic iron with aging: implications for heat stress-induced oxidative liver injury.

Environmental heat stress is associated with an age-related increase in hepatic oxidative damage and an exaggerated state of oxidative stress. The purpose of this investigation was to evaluate the regulation of hepatic iron after heat stress. A secondary aim was to determine a potential role for iron in heat stress-induced liver injury. Hyperthermia-induced alterations in hepatic iron were evaluated in young (6 mo) and old (24 mo) Fischer 344 rats by exposing them to a two-heat stress protocol. Livers were harvested at several time points after the second heating and assayed for labile and nonheme iron. In the control condition, there was no difference in labile iron between age groups. Both labile iron and storage iron were not altered by hyperthermia in young rats, but both were increased immediately after heating in old rats. To evaluate a role for iron in liver injury, hepatic iron content was manipulated in young and old rats, and then both groups were exposed to heat stress. Iron administration to young rats significantly increased hepatic iron content and ferritin but did not affect markers of lipid peroxidation under control conditions or after heat stress. In old rats, iron chelation with deferoxamine prevented the increase in nonheme iron, labile iron, ferritin, and lipid peroxidation after heat stress. These results suggest that iron may play a role in hepatic injury after hyperthermia. Thus, dysregulation of iron may contribute to the gradual decline in cellular and physiological function that occurs with aging.

Caffeine, carbohydrate, and cooling use during prolonged simulated tennis.

PURPOSE: To determine the effects of prolonged simulated tennis on performance and the ergogenic potential of caffeine, carbohydrates, and cooling. METHODS: Twelve highly trained male tennis players (age 18.3 +/- 3.0 y, height 178.8 +/- 8.5 cm, body mass 73.95 +/- 12.30 kg, mean +/- SD) performed 4 simulated matches (2 h 40 min) against a ball machine on an indoor hard court. The counterbalanced experimental trials involved caffeine supplementation (3 mg/kg), carbohydrate supplementation (6% solution), precooling and intermittent cooling, and placebo control. Physiological markers (core temperature, heart rate, blood lactate, and blood glucose), subjective responses (ratings of perceived exertion and thermal sensation), stroke velocity and accuracy, serve kinematics, and tennis-specific perceptual skill quantified the efficacy of interventions. RESULTS: Significant effects of time (P < .01) reflected increased physiological demand, reduced serve velocity and ground-stroke velocity and accuracy, and a slowing of the serve racket-arm acceleration phase. Caffeine increased serve velocity (165 +/- 15 km/h) in the final set of the match (P = .014) compared with placebo (159 +/- 15 km/h, P = .008) and carbohydrate (158 +/- 13 km/h, P = .001) conditions. Carbohydrate and cooling conditions afforded physiological advantage (increased blood glucose, P < .01, and reduced preexercise thermal sensation, P < .01) but did not affect performance relative to the placebo condition. CONCLUSIONS: Prolonged simulated tennis induced significant decrements in tennis skills. Caffeine supplementation partly attenuated the effects of fatigue and increased serve velocity. In contrast, carbohydrate and cooling strategies had little ergogenic effect on tennis performance.

Cross validation of USARIEM heat strain prediction models. U.S. ARMY Research Institute of Environmental Medicine.

HYPOTHESIS: This study was a cross validation of three heat strain prediction models developed at the U.S. Army Research Institute of Environmental Medicine: the ARIEM, HSDA, and ARIEM-EXP models ability to predict core temperature. METHODS: Seven heat-acclimated subjects completed twelve experimental tests, six in each of two hot climates, at three exercise intensities and two uniform configurations in each climate. RESULTS: Experimental results showed physiological responses as expected with heat strain increasing with work load and level of protective clothing, but with similar heat strain between the two environments matched for wet bulb, globe index. Neither the ARIEM or HSDA model closely predicted core temperatures over the course of the experiment, due mostly to an abrupt initial rise in core temperature in both models. A proportionality constant in the ARIEM-EXP buffered some of this abrupt rise. CONCLUSIONS: Comparisons of the core temperature and tolerance times data with the three models led to the conclusions that for healthy males: 1) the ARIEM and HSDA models provide conservative safety limits as a result of predicting rapid initial increases in core temperature; 2) the ARIEM-EXP most closely represents core temperature responses; 3) the ARIEM-EXP requires modifications with an alternate proportionality coefficient to increase accuracy for low metabolic cost exercise; 4) all of the models require additional input from existing research on tolerance to heat strain to better predict tolerance times; and 5) additional models should be examined to investigate the transient state of the body as it is affected by environment, clothing and exercise.

Appropriateness of international heat stress standards for use in tropical agricultural environments.

Where a danger to health from heat stress is identified, standards allow decisions for implementing measures to reduce the heat stress to be made. These standards, specifically ISO 7243 (Wet Bulb Globe Temperature Index, WBGT) and ISO 7933 (Sweat Required, SWreq) were designed with European and American subjects, primarily for use in those countries. While the scope of the standards is international, little consideration has been made about how valid and usable they are in industrially developing countries. This investigation evaluated ISO 7933 and ISO 7243 in terms of validity and usability. A tropical agricultural task was simulated; 16 subjects plucking tea leaves for 2 h, (ta = tr = 37.18 degrees C; va = 0.16 m/s; rh = 70.17%). While ISO 7243 was valid (if slightly over protective) and usable, ISO 7933 was over protective and underestimated sweat and evaporation rates in its predictions. The discrepancies between predicted and observed results were attributed primarily to the calculations related to clothing in the standard. Furthermore, ISO 7933 was unusable without a computer; in regions where access to such technology may be limited, a simpler method of presentation is required.

[The effect of phenazepam on the pancreatic excretory function in thermal stress]. / Vliianie fenazepama na vneshnesekretornuiu funktsiiu podzheludochnoi zhelezy pri teplovom stresse.

The excretory function of the pancreas was studied on albino rats during thermal stress and ACTH (corticotropine) administration. Stress inhibited the enzyme-synthesizing and enzyme-secreting functions of the gland. The tranquilizer phenazepam influencing the GABA-ergic brain systems exerted a protective effect on pancreatic exosecretion in stress and its strength depended on the administration regimen of the drug. Experiments with corticotropine have shown that the antistress effect of phenazepam, to a certain extent is related to its action on the level of ACTH production in the hypophysis.

[The protective effect of a NO-synthase inhibitor in heat shock]. / Zashchitnyi éffekt ingibitora NO-sintazy pri teplovom shoke.

Acute hypotension related to the excessive production of a potent endogenous vasodilator nitric oxide (NO) is a most important link of heat shock pathogenesis. It was shown that inhibition of inducible NO-synthase by N(W)-nitro-L-arginine (L-NNA) at 10 mg/kg reduces the mortality of animals due to heat shock, prevents the fall of arterial blood pressure and abnormal inhibition of constriction and stimulation of dilation reactions related to NO hyperproduction. A total blockade of NO synthesis by L-NNA at 300 mg/kg did not exert a protective effect from heat shock. The data obtained suggest the importance of inducible NO-synthase in heat shock pathogenesis and show promise for the application of selective inhibition of inducible NO-synthase at pathological states related to NO hyperproduction.

Factors affecting heat illness when working in conditions of thermal stress.

In hot working conditions, high sweat rates with excessive loss of body fluids may result in dehydration and electrolyte imbalance. It is well established that dehydration and/or electrolyte disturbances will impair work performance, and, if prolonged or severe, can pose a serious risk to health. The lesser condition of hypohydration is undoubtedly widespread in the workplace, and may be indirectly responsible for less than optimal performance and workplace accidents. With the aid of a new sweat collection method, fluid and electrolyte loss from a population of male workers with varying fitness and body composition has been documented. This has provided the basis for prescribing guidelines of fluid replacement when working in the heat. In addition, the minimum duration of heat exposure required to trigger heat acclimmatization was sought using sweat sodium as an indicator. Rehydration at the rate of 500 ml/h (250 ml every 30 min) is recommended for people working in all but extreme heat (> 45 degrees C). Electrolyte supplements (sodium and potassium) are not generally required in the workplace, but may be warranted in certain circumstances to avoid hyponatremia (> 3 h). The ability to predict the susceptibility of an individual to fluid and electrolyte disturbances cannot be made from age, body composition, ethnicity or VO2max, although a high VO2max appears to enhance heat tolerance. Sodium loss in sweat varies greatly and is not significantly related to sweat rate. Acclimatization results in a significant decrease in sweat sodium and increased sweat rate during summer compared with winter. This advantageous physiological adaptation requires a minimum of 9 h of heat exposure to initiate.

Heat illness--a review of military experience (Part 1).

This paper is the first part of a two part review of the published literature reporting the military experience of heat illness. It summarises current concepts of the mechanisms for the development of heat illness. The reports of heat illness in the military medical literature from pre-World War 1 to the end of World War 2 are discussed. The second part will consider reports from the end of the Second World War to the present day. Epidemiological evidence for the factors causing heat illness will be summarised and finally the current areas of uncertainty will be identified with proposals for future research.