A case-control study of ambient heat exposure and urolithiasis among outdoor workers in a shipbuilding company, Guangzhou, China

Higher ambient temperatures will increase heat stress on workers, leading to impacts upon their individual health and productivity. In particular, research has indicated that higher ambient temperatures can increase the prevalence of urolithiasis. This thesis examines the relationship between ambient heat exposure and urolithiasis among outdoor workers in a shipbuilding company in Guangzhou, China, and makes recommendations for minimising the possible impacts of high ambient temperatures on urolithiasis. A retrospective 1:4 matched case-control study was performed to investigate the association between ambient heat exposure and urolithiasis. Ambient heat exposure was characterised by total exposure time, type of work, department and length of service. The data were obtained from the affiliated hospital of the shipbuilding company under study for the period 2003 to 2010. A conditional logistic regression model was used to estimate the association between heat exposure and urolithiasis. This study found that the odds ratio (OR) of urolithiasis for total exposure time was 1.5 (95% confidence interval (CI): 1.2–1.8). Eight types of work in the shipbuilding company were investigated, including welder, assembler, production security and quality inspector, planing machine operator, spray painter, gas-cutting worker and indoor employee. Five out of eight types of work had significantly higher risks for urolithiasis, and four of the five mainly consisted of outdoors work with ORs of 4.4 (95% CI: 1.7–11.4) for spray painter, 3.8 (95% CI: 1.9–7.2) for welder, 2.7 (95% CI: 1.4–5.0) for production security and quality inspector, and 2.2 (95% CI: 1.1–4.3) for assembler, compared to the reference group (indoor employee). Workers with abnormal blood pressure (hypertension) were more likely to have urolithiasis with an OR of 1.6 (95% CI: 1.0–2.5) compared to those without hypertension. This study contributes to the understanding of the association between ambient heat exposure and urolithiasis among outdoor workers in China. In the context of global climate change, this is particularly important because rising temperatures are expected to increase the prevalence of urolithiasis among outdoor workers, putting greater pressure on productivity, occupational health management and health care systems. The results of this study have clear implications for public health policy and planning, as they indicate that more attention is required to protect outdoor workers from heat-related urolithiasis.

Stimulation of liver tryptophan pyrrolase during heat exposure

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.

Heat exposure and hypothyroid conditions decrease hydrogen peroxide generation in liver mitochondria

Exposure of rats to heat (39 +/- 1 degree C) decreased H2O2 generation in mitochondria of the liver, but not of the kidney or the heart. The effect was obtained with three substrates, succinate, glycerol 1-phosphate and choline, with a decrease to 50% in the first 2-3 days of exposure, and a further decrease on longer exposure. The dehydrogenase activity with only glycerol 1-phosphate decreased, which is indicative of the hypothyroid condition, whereas choline dehydrogenase activity remained unchanged and that of succinate dehydrogenase decreased on long exposure. The serum concentration of thyroxine decreased in heat-exposed rats. Thyroxine treatment of rats increased H2O2 generation. Hypothyroid conditions obtained by treatment with propylthiouracil or thyroidectomy caused a decrease in H2O2 generation and changes in dehydrogenase activities similar to those with heat exposure. Treatment of heat-exposed or thyroidectomized rats with thyroxine stimulated H2O2 generation by a mechanism apparently involving fresh protein synthesis. The results indicate that H2O2 generation in mitochondria of heat-exposed animals is determined by thyroid status.

Effect of heat exposure on the thermoregulatory responses of selected naked neck chickens

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of acute heat exposure on respiratory metabolism and blood glucose in freshwater fishes, Prochilodus scrofa (curimbatá) and Cyprinus carpio (carp) acclimatized to tropical winter

1. 1. Routine oxygen consumption and blood glucose were determined from freshwater fishes, Prochilodus scrofa and Cyprinus carpio, exposed at high temperatures for 1 hr. 2. 2. Prochilodus scrofa had a significantly higher rate of oxygen consumption at 30°C than at 25°C, and carp higher at 25°C than at 30°C. 3. 3. Blood glucose was significantly higher for Cyprinus carpio than for Prochilodus scrofa at 25 and 30°C; however, after exposure to these temperatures for 1 hr blood glucose did not change significantly for both species. 4. 4. The results suggest that these interspecific variations may be linked to the differences between native and foreign fishes and their way of life. © 1985.

Heat shock protein 70 as a biomarker of heat stress in a simulated hot cockpit

Background: Fighter pilots are frequently exposed to high temperatures during high-speed low-level flight. Heat strain can result in temporary impairment of cognitive functions and when severe, loss of consciousness and consequent loss of life and equipment. Induction of stress proteins is a highly conserved stress response mechanism from bacteria to humans. induced stress protein levels are known to be cytoprotective and have been correlated with stress tolerance. Although many studies on the heat shock response mechanisms have been performed in cell culture and animal model systems, there is very limited information on stress protein induction in human subjects. Hypothesis: Heat shock proteins (Hsp), especially Hsp70, may be induced in human subjects exposed to high temperatures in a hot cockpit designed to simulate heat stress experienced in low flying sorties. Methods: Six healthy volunteers were subjected to heat stress at 55degreesC in a high temperature cockpit simulator for a period of 1 h at 30% humidity. Physiological parameters such as oral and skin temperatures, heart rate, and sweat rate were monitored regularly during this time. The level of Hsp70 in leukocytes was examined before and after the heat exposure in each subject. Conclusions: Hsp70 was found to be significantly induced in all the six subjects exposed to heat stress. The level of induced Hsp70 appears to correlate with other strain indicators such as accumulative circulatory strain and Craig's modified index. The usefulness of Hsp70 as a molecular marker of heat stress in humans is discussed.

Consequences of heat stress on reproduction of cattle

Heat stress represents one of the major environmental factors that adversely affect the reproductive performance of cattle. In this paper the behavioral adjustments, physical mechanisms and physiological responses to heat loss are described; bos indicus adaptive advantages with respect to bos Taurus, pathophysiology of heat stress and heat stress effects in animal reproduction, both the male and the female.

Performance and carcass characteristics of broiler chickens with different growth potential and submitted to heat stress

In order to evaluate the effects of broiler genotype and of heat exposure on performance, carcass characteristics, and protein and fat accretion, six hundred one-day-old male broilers were randomly assigned in a 2 x 3 factorial arrangement, according to the following factors: genetic group (selected and non-selected broilers) and pair-feeding scheme (Ad(32) - reared under heat stress and fed ad libitum; Ad(23) - reared at thermoneutrality and fed ad libitum; Pf(23) - reared at thermoneutrality and pair fed with Ad(32)), with a total of six treatments with four replicates of 25 birds each. Independent of pair-feeding scheme, selected broilers showed better feed conversion, higher carcass yield, and lower abdominal fat deposition rate. However, as compared to non-selected broilers, they reduced more intensively feed intake when heat exposed, which promoted significant breast-yield decrease, and more pronounced changes on carcass chemical composition. These findings allows concluding that, in both genetic groups, both environmental temperature and feed-intake restriction influence abdominal fat deposition rate and other carcass characteristics; however, the impact of heat exposure on broiler performance is more noticeable on the selected line.

Effect of acute heat stress on heat shock protein 70 messenger RNA and on heat shock protein expression in the liver of broilers

1. The synthesis of heat shock protein 70 (Hsp70) mRNA and the expression of Hsp70 in the liver of broiler chickens submitted to acute heat stress (35 degrees C for 5 h) was investigated.2. Hsp70 expression was detected by SDS-PAGE and Western blot analysis using a polyclonal antiserum against Hsp70 of Blastocladiella emersonii. The specific signal of Hsp70 mRNA was analysed by Northern blot using as probe a Hsp70 cDNA of B. emersonii.3. An increase in the amount of Hsp70 was detected from the first up to the fifth hour of acute heat exposure. This increase in the amount of Hsp70 was accompanied by an increase in Hsp70 mRNA which peaked at 3 h.4. This study shows that the heat induced increase in Hsp70 mRNA and protein in broiler liver, in vivo, are time dependent, similar to that in mammals.

Effect of indomethacin on hyperthermia induced by heat stress in broiler chickens

An investigation was carried out to verify whether the heat stress hyperthermia response of broilers is prostaglandin-dependent. Male broiler chickens of the Hubbard-Petterson strain, aged 35-49 days, were used. Chickens were injected with indomethacin (1 mg/kg intraperitoneally) 15 min before or 2 h after heat exposure (at 35 degrees C for 4 h), and rectal temperature was measured before injection and up to 4 h thereafter. Birds were separated into two groups with and without access to water during heat stress. The increase in rectal temperature was lower (P<0.05) in birds with access to drinking water during heat exposure. All birds injected with indomethacin exhibited an increase in rectal temperature, irrespective of whether indomethacin was administered before or in the course of the rise in temperature. The results revealed that the increase in rectal temperature during heat exposure is not prostaglandin-dependent, and that the use of cyclooxigenase inhibitors is not recommended to attenuate heat stress hyperthermia in broiler chickens.

Expression of heat shock protein in broiler embryo tissues after acute cold or heat stress

This study evaluated the expression of heat shock protein 70 kD (hsp70) in broiler chicken embryos subjected to cold (Experiment 1) or high incubation temperature (Experiment 11). In each experiment, fertile eggs were distributed in three incubators kept at 37.8degreesC. At day 13 (D13), D16, and D19 of incubation, the embryos were subjected to acute cold (32degreesC) or heat (40degreesC) for 4-6 hr. Immediately after cold or heat exposure, samples from the liver, heart, breast muscle, brain, and lungs of 40 embryos were taken per age and treatment (control or stressed embryos), A tissue pool from 10 embryos was used as 1 replication. The levels of hsp70 in each tissue sample was quantified by Western blot analysis. The data were analyzed in a 3 x 2 factorial arrangement of treatments with four replications. hsp70 was detected in all embryo tissues, and the brain contained 2- to 5-times more hsp70 protein compared to the other tissues in either cold or heat stressed embryos. hsp70 increases were observed in the heart and breast muscle of cold stressed embryos at D16 and D19, respectively. Heat stressed embryos showed an increase of hsp70 in the heart at D13 and D19, and in the lung at D19 of incubation. Younger embryos had higher hsp70 synthesis than older embryos, irrespective of the type of thermal stressor. The results indicate that the expression of hsp70 in broiler chicken embryos is affected by cold and heat distress, and is tissue- and age-dependent. (C) 2004 Wiley-Liss, Inc.

Influence of Dietary Lysine Levels and Arginine:Lysine Ratios on Performance of Broilers Exposed to Heat or Cold Stress during the Period of Three to Six Weeks of Age

Four trials of identical experimental design were conducted to determine the effects of temperature, dietary Lys level, and dietary Arg:Lys ratios on performance and carcass yield of male broilers. Birds of a commercial strain were grown from 21 to 42 d of age in wire-floored finishing batteries placed in environmental chambers. The chambers were programmed to provide either a constant thermoneutral temperature (21.1 C), a constant cold temperature (15.5 C), or a cycling hot diurnal temperature (25.5 to 33.3 C). Within each environment there was a factorial arrangement of three Lys levels (1.0, 1.1, and 1.2%) with four Arg:Lys ratios (1.1:1, 1.2:1, 1.3:1, and 1.4:1). Environmental temperature significantly influenced virtually every characteristic examined. Hot cyclic temperatures reduced weight gain, feed intake, and breast meat yield, and increased feed conversion, dressing percentage, leg quarter yield, and abdominal fat content. The cold environment promoted increased feed intake and mortality. Ascites and cardiomyopathy were the leading causes of death under cold exposure and thermoneutral conditions, whereas complications arising from heat exposure were the main cause of death under hot cyclic conditions. Levels of Lys affected leg quarter yield and abdominal fat content over all environments but increased breast meat yield only under cold conditions. Increasing Arg: Lys ratios improved feed conversion and dressing percentage and reduced abdominal fat content; it could not be determined whether these responses were consistent with Arg per se or were due to a nonspecific N response. As increasing Lys levels or Arg:Lys ratios did not improve weight gain, increase breast meat yield, or attenuate adverse effects due to heat or cold exposure, it is concluded that the levels of Lys and Arg suggested for 21 to 42 d by the NRC are adequate for birds of this age under the environmental conditions encountered.

Protein levels for heat-exposed broilers: Performance, nutrients digestibility, and energy and protein metabolism

Heat stress causes significant economic losses on broilers production due to poorer performance and carcass quality. Considering that protein has the highest heat increment among nutrients, it has been suggested that protein levels should be reduced in diets for heat-exposed broilers. Nevertheless, there are no conclusive results on the benefits of such practice, and further studies should be performed to elucidate some reported discrepancies. Thus, a trial was carried out to evaluate the effects of dietary protein levels (17, 20 and 23%) and environmental temperature (22 and 32°C) on the performance, nutrients digestibility, and energy and protein metabolism of broiler chickens from 21 to 42 days of age. Nutrients digestibility was determined by total excreta collection, and energy and protein metabolism was evaluated by comparative slaughter method. It was concluded that (1) heat exposure impairs broilers performance and increases nitrogen excretion, but do not change nutrients digestibility; (2) high-protein diets are technically feasible and promotes lower heat production for broilers reared under thermoneutral or hot environments, however, high-protein diets increases nitrogen excretion. © Asian Network for Scientific Information, 2007.

Heat stress, heat strain, and productivity in Washington State tree fruit harvesters

Thesis (Master's)--University of Washington, 2016-06

The roles of exercise-induced immune system disturbances in the pathology of heat stroke - The dual pathway model of heat stroke

Heat stroke is a life-threatening condition that can be fatal if not appropriately managed. Although heat stroke has been recognised as a medical condition for centuries, a universally accepted definition of heat stroke is lacking and the pathology of heat stroke is not fully understood. Information derived from autopsy reports and the clinical presentation of patients with heat stroke indicates that hyperthermia, septicaemia, central nervous system impairment and cardiovascular failure play important roles in the pathology of heat stroke. The current models of heat stroke advocate that heat stroke is triggered by hyperthermia but is driven by endotoxaemia. Endotoxaemia triggers the systemic inflammatory response, which can lead to systemic coagulation and haemorrhage, necrosis, cell death and multi-organ failure. However, the current heat stroke models cannot fully explain the discrepancies in high core temperature (Tc) as a trigger of heat stroke within and between individuals. Research on the concept of critical Tc: as a limitation to endurance exercise implies that a high Tc may function as a signal to trigger the protective mechanisms against heat stroke. Athletes undergoing a period of intense training are subjected to a variety of immune and gastrointestinal (GI) disturbances. The immune disturbances include the suppression of immune cells and their functions, suppression of cell-mediated immunity, translocation of lipopolysaccharide (LPS), suppression of anti-LPS antibodies, increased macrophage activity due to muscle tissue damage, and increased concentration of circulating inflammatory and pyrogenic cytokines. Common symptoms of exercise-induced GI disturbances include diarrhoea, vomiting, gastrointestinal bleeding, and cramps, which may increase gut-related LPS translocation. This article discusses the current evidence that supports the argument that these exercise-induced immune and GI disturbances may contribute to the development of endotoxaemia and heat stroke. When endotoxaemia can be tolerated or prevented, continuing exercise and heat exposure will elevate Tc to a higher level (> 42 degrees C), where heat stroke may occur through the direct thermal effects of heat on organ tissues and cells. We also discuss the evidence suggesting that heat stroke may occur through endotoxaemia (heat sepsis), the primary pathway of heat stroke, or hyperthermia, the secondary pathway of heat stroke. The existence of these two pathways of heat stroke and the contribution of exercise-induced immune and GI disturbances in the primary pathway of heat stroke are illustrated in the dual pathway model of heat stroke. This model of heat stroke suggests that prolonged intense exercise suppresses anti-LPS mechanisms, and promotes inflammatory and pyrogenic activities in the pathway of heat stroke.