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Perspective

Endocrine Parameters and Climate Change

1
Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, University Hospital of the University of Marburg UKGM, Philipps University Marburg, Baldingerstrasse, 35043 Marburg, Germany
2
Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, University Hospital of the University of Giessen UKGM, Justus Liebig University Giessen, Feulgenstr. 12, 35392 Giessen, Germany
Endocrines 2025, 6(1), 5; https://doi.org/10.3390/endocrines6010005
Submission received: 8 November 2024 / Revised: 27 January 2025 / Accepted: 5 February 2025 / Published: 7 February 2025

Abstract

The endocrine system relies on complex cell signaling and epigenetic processes to adjust to the body’s needs. However, stressors such as climate change and heat can disrupt the endocrine system. This study aims to collect and systematically review evidence from publications exploring how climate change impacts endocrine laboratory parameters. The review process included developing research questions, defining inclusion and exclusion criteria, conducting database searches, screening and selecting relevant publications, collecting and analyzing data, interpreting the findings, and drawing conclusions. This review identified multiple endocrine parameters linked to climate change and the mechanisms by which various stressors disrupt endocrine function. Climate change, especially heat stress, affects the production and levels of key hormones. The mechanisms underlying the disruption of key hormones are also explored in this paper. This review provides a clear overview of how climate change influences endocrine parameters and outlines the processes underlying stress-triggered endocrine disruption.

1. Introduction

The endocrine system is a versatile and resilient system that promotes and maintains reproduction and survival processes in humans and animals [1]. The endocrine system is responsive to and controlled by various cell signaling networks and epigenetic events that continually adapt to organismal demands and the environment. However, the networks within and function of the endocrine system can become overwhelmed when stressful events accrue too rapidly, especially in metropolitan settings [2]. Some studies have indicated that climate change may negatively affect the development of the endocrine system and pose significant threats to the survival of humans and animals [1,2,3,4]. In view of this, the impact of climate change on the endocrine system has been a focus of numerous recent scientific investigations [5]. Although past studies have examined the adverse effects of climate change on the exacerbation of diseases and the impairment of endocrine system function, there is inadequate data from empirical investigations to support the correlation between changes in endocrine laboratory parameters and climate change [6,7]. Nevertheless, some studies have applied endocrine laboratory parameters to examine the consequences of extreme heat stress on the endocrine system in animal models and healthy individuals [1,8]. Although the applicability of such studies to people exposed to prolonged variations in temperature caused by climate change is unknown, this prior research provides scientific evidence of the impact of climate change on the endocrine system [8]. Similarly, other researchers have provided compelling evidence of the implications of climate change on endocrine laboratory parameters [8,9,10,11]. Therefore, this systematic review aims to collate evidence from research studies to assess the influence of climate change on endocrine laboratory parameters.

2. Materials and Methods

This section outlines the research approach, data collection procedures, and analysis tools utilized to meet the study’s goals and objectives [12,13]. Certain steps were critical to avoid bias in data selection for this systematic review, include framing the research questions, determining the inclusion and exclusion criteria, searching and screening diverse publications, selecting studies, gathering data, combining outcomes, evaluating data, interpreting results, and drawing conclusions [12,14,15]. The ability to develop a detailed, well-researched topic for study is based on the researcher’s knowledge, which also helps with other aspects of the review, such as determining eligibility (inclusion/exclusion) criteria and conducting literature searches [14,16]. As a result, the study questions for this systematic review are “What is the current knowledge about endocrine laboratory parameters and climate change?” and “What are the effects of climate change on the mechanisms of action of the endocrine system?” Before commencing a review, a concise, structured, and unambiguous question related to the research problem must be created [14]. The other procedures used to conduct this systematic review are explained in the next subsections.

2.1. Summary of Inclusion and Exclusion Criteria

The study inclusion and exclusion criteria were developed to effectively identify studies relevant to the research topic [12,14]. The inclusion criteria focused on previous research relevant to this review, whereas the exclusion criteria centered on work unrelated to this study. The inclusion and exclusion criteria frequently mirror one another [14]. The inclusion criteria for this systematic review included the following:
  • Primary research investigations;
  • Studies published in English;
  • Research investigations on endocrine laboratory parameters, climate change, and/or heat;
  • Research investigations published in 2014 or thereafter (i.e., the past 10 years);
  • Primary studies that employed experimental research methods.
The exclusion criteria for this systematic review included the following:
  • Nonprimary research investigations;
  • Research investigations that were not published in English;
  • Research investigations that did not discuss endocrine laboratory parameters, climate change, and/or heat;
  • Research investigations published before 2014;
  • Primary studies that did not employ experimental research methods.

2.2. Search Strategy

The search approach entailed finding relevant literature that met the inclusion and exclusion criteria. A detailed search strategy was employed to ensure a comprehensive systematic review. In this light, specific keywords and Boolean operators were utilized to identify relevant studies addressing the research question. Keywords and Boolean combinations that were applied to produce results include “climate change” AND “endocrine parameters”, “heat” AND “endocrine parameters”, and “climatic change” OR “heat stress” AND “endocrine disruption”. Moreover, “climate variability” AND “hormonal changes” OR “endocrine axes” were also used to search for relevant articles. Fundamentally, terms were identified through a preliminary search and refined to ensure that relevant studies on the topic were obtained. Some of the filters were applied only using the studies published in English and articles published within the last 10 years (2014 onwards). Moreover, the primary research articles must be based on experimental methodologies.
Preliminary searches in Google Scholar and PubMed, the most comprehensive research databases for experimental research studies in medicine, were conducted to help design a suitable search strategy for this systematic review. Specifically, PubMed was chosen because this widely used database includes peer-reviewed publications of medical research. This preliminary search was essential for identifying key terms and phrases relevant to the research topic that could be successfully employed in the final search [14,17]. Other databases searched to find relevant papers on the topic of interest for this research included Scopus, Medline, and PsycINFO [14], which are often used for researching public health papers. In particular, the Scopus database was searched because it covers almost all aspects of public health at the global and local levels without excluding the biomedical and life sciences domains. Similarly, Medline was chosen for this evaluation because it contains peer-reviewed studies in the medical field, whereas PsycINFO is a well-known peer-reviewed resource for behavioral science and mental health research. Boolean operators were used to save time and eliminate unnecessary study search results.

2.3. Study Selection

Study selection, the second and most important stage of the search strategy for identifying relevant publications, was divided into two tasks: title/abstract screening and full-text screening. The title/abstract screening ensures that identified studies meet the inclusion criteria. After confirming that the articles/journals are relevant, the more extensive full-text screening of papers that fulfilled the inclusion criteria on the basis of title/abstract screening was performed. Studies that did not meet the inclusion criteria were excluded from the review. Although the double-screen strategy is recognized as the most successful option for systematic reviews owing to its openness and robustness, it was not applicable to this study because the research was conducted independently [17]. Therefore, a single-screen strategy was used in this review. EndNote was used to organize and categorize the search results and to filter duplicates.

2.4. Data Extraction

The data in the identified literature were compiled in Microsoft Excel under the following headings: author(s), year of publication, complete text or abstract, title of journal, purpose of study, study design, sampling procedure, method of data collection, important findings, limitations, recommendations, and conclusions [18]. The data extraction form adopted for this review was customized on the basis of previous publications [15,18].

2.5. Data Synthesis

The data synthesis involved compiling all studies that met the inclusion criteria. The primary strategies for data synthesis are meta-analysis and narrative synthesis [14,19]. Meta-analysis is the process of merging the obtained data regarding essential aspects such as quality, effects, study features, and the application of statistical methods [19]. In contrast, narrative synthesis uses words to evaluate the relationship between and within different investigations and provides a thorough appraisal of the strength of the evidence supporting the usefulness of a certain intervention [14]. Moreover, a meta-analysis uses statistical techniques to evaluate a hypothesis, whereas a narrative synthesis creates a new theory on the basis of data from numerous investigations [14,19].
This systematic review employed narrative synthesis because the use of textual approaches to examine cause-and-effect linkages provides robust information about dependent variables from numerous study designs, which reduces the requirement for meta-analysis. The narrative synthesis framework is also deemed excellent since it considers the nature of the study issue and the presentation of evidence-based results [14,20]. When the narrative synthesis strategy is used, it is critical to group, classify, and thoroughly evaluate the process before deducing findings and drawing conclusions. In this way, this review followed the previously stated recommendations for narrative synthesis in systematic reviews [14]. Tables were utilized to illustrate study information and outcomes and thus to discover trends within or between research investigations and interventions.

3. Limitations of the Study and Risk of Bias (ROB) Analysis

3.1. Limitations of the Study

The systematic review has certain limitations that can influence how the findings regarding the effects of climate change on endocrine parameters are interpreted, as well as how the results can be applied in different environmental setups. One of the limitations of this study is that the studies that were included in the research focused on different endocrine axes, hormones, and climatic stressors, particularly heat and seasonal changes. Because of this diverse selection, it is difficult to draw uniform conclusions about specific mechanisms or pathways of endocrine disruption. Subsequently, studies reviewed in this study contained data from both human and animal populations from different experimental and real-world settings. Although animal models can be important in understanding how the environment and its factors affect endocrine parameters, their findings may not be applied fully in the human context. Nevertheless, it is important to acknowledge that most of the research articles included in this study involved research that was conducted in a controlled experimental setting. The controlled laboratory conditions may not be a true reflection of the complex, multi-factorial nature of real-world climate change impacts.
Additionally, another limitation of the study is that the research primarily focused on specific regions or particular climatic zones. Thus, the studies may not be generalizable to regions with differing environmental conditions or adaptive capacities. Relevant research published in other languages or grey literature may have been excluded since this review only included peer-reviewed studies published in English. In addition, while the inclusion of data published in the last 10 years is vital in ensuring that recent and relevant data are used, foundational research that could provide additional context may have been excluded in the process.

3.2. Risk of Bias (ROB) Analysis

Different approaches were taken to minimize bias that may have occurred in the systematic review. For instance, a single-screen strategy was used to identify studies that could meet the inclusion and exclusion criteria originally defined in the research process. Although this approach is efficient, there is a possibility that it can increase the risk of selection bias compared to when a double screening strategy is utilized. Additionally, selecting studies with different designs, particularly cross-sectional studies and experimental trials, as well as diverse outcome measures, specifically hormonal concentrations and physiological parameters, led to some challenges when synthesizing the results. In this light, the Cochrane Risk of Bias (ROB) tool was adapted to evaluate randomization and blinding of experimental procedures, as well as to assess the completeness and consistency in reporting outcomes. Moreover, ROB was also used to assess potential confounders, particularly seasonal variability, changes in diet, and the difference in genetics within the study population. Notably, there is a possibility that studies whose findings are statistically significant were overrepresented, as research articles whose results are null or inclusive are less likely to be considered for publication.
Although there are certain existing limitations, consistent patterns in endocrine disruption mechanisms due to climate change, such as heat-induced alterations in hypothalamic–pituitary–adrenal axis function and hormonal imbalances, are clearly highlighted in the review. Therefore, there is a need to focus on longitudinal studies and to standardize outcome measures in future studies. Nevertheless, future research should also explore the relationship between multiple stressors for a comprehensive understanding of how climate change affects endocrine health.

4. Results

This study examined the current knowledge about endocrine laboratory parameters and climate change by evaluating several studies on the effects of climate change on endocrine system function and the underlying mechanisms.

4.1. Overview of Search Outcomes

Using the Boolean operator, the search within this study produced 715 distinct entries, 556 of which were duplicates. In total, 396 items were excluded from the review because they did not meet the screening criteria. The inclusion and exclusion criteria were utilized to filter 105 publications, and 65 of the papers that passed the title/abstract screening were subjected to full-text screening. However, 70 papers were excluded from the full-text review, and five articles were excluded for not meeting the eligibility requirements. As a result, this systematic review contains 30 studies. Figure 1 depicts the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow chart, which describes the search results and studies, as well as the rationale for excluding specific publications.

4.2. Characteristics of the Included Articles

This systematic review includes 30 experimental research papers on endocrine laboratory parameters and climate change. All of the selected publications met the inclusion criteria for this systematic review. Most of the articles chosen for this investigation sought to explore how climate change affects endocrine responses in different animals [21,22,23,24,25,26,27,28,29,30,31,32,33]. Two of the publications documented the effects of acute hypobaric hypoxia and seasonal fluctuations on human study participants [21,28]. In contrast, other publications reported the effects of heat, summer, and winter stress on endocrine system function in different animals [22,23,24,25,26,27,29,30,31,32,33]. To study the effects of climate change on endocrine laboratory parameters, scholars have used various animals, including female calves [22], dry cows [23], French bulldogs [24], thoroughbred colts and fillies [25,31], young Assamese macaques [26], whooper swans [27,28], male Shiba goats [29], trained thoroughbred yearling horses [30,31], Holstein dairy cows [32], and Holstein–Friesian cows [33]. Table 1 summarizes the aforementioned characteristics of the publications covered in this review.

4.3. Impact of Climate Change on Endocrine Parameters

4.3.1. Human Studies

A study by Nishimura et al. [21] explored individual differences during acute hypobaric hypoxia. The results of this study revealed that 75 min of exposure to settings mimicking 3500 m led to declines in aldosterone and cortisol levels in healthy lowlanders [21]. This finding highlights how the adrenal cortex is sensitive to rapid environmental changes. Fu et al. [28] reported that 11 months of winter stress caused increases in thyrotropin, free triiodothyronine and thyroxine levels, and the thyrotropin index in women of reproductive maturity. Subsequently, the authors further indicated that exposure to summer stress resulted in decreases in thyrotropin, free triiodothyronine, and thyroxine levels, and the thyrotropin index in the same study population [28]. Endocrine response during summer suggests a reduced metabolic demand for heat generation. Fundamentally, the findings reveal that seasonal temperature fluctuations significantly influenced thyroid hormone levels in women aged 20–49 [28]. Glucocorticoid levels in migratory birds were also explored, and this was necessary to compare the results with those of humans. In this light, Yang et al. [27] explored the effects of winter stress on migratory whooper swans and noted elevated levels of fecal glucocorticoid metabolites, reflecting an activation of the hypothalamic–pituitary–adrenal (HPA) axis in response to prolonged cold exposure. The results of this study indicate the difference between human and animal endocrine responses to climatic stressors.

4.3.2. Animal Studies

Animals also respond differently to climate change. In particular, research studies revealed decreases in plasma cortisol [23], insulin-like growth factor-I [30], and triiodothyronine concentrations [33] in different animals exposed to heat stress. Some authors have also reported increases in plasma triiodothyronine and growth hormone levels [23], increases in prolactin, progesterone, and total thyroxine concentrations [30], and high concentrations of cortisol and insulin [32,33]. In contrast, Lyrio et al. [24] reported no difference in testosterone levels in the semen of French bulldogs after exposure to heat stress.
In particular, Chen et al. [23] indicate that prolonged heat stress in dry seasons was found to lead to a reduction in plasma cortisol levels, potentially due to a downregulation of the HPA axis under chronic thermal conditions. Similarly, a decline in cortisol levels in heat-stressed cows, alongside increased insulin and decreased triiodothyronine concentrations, was also reported [33,34,35,36,37,38,39]. The results of these studies are an indication of metabolic adaptations to help the animal conserve energy during thermal stress [23,33]. Moreover, Mizukami et al. [25] found that thoroughbred horses exposed to summer stress exhibited elevated prolactin, luteinizing hormone (LH), and estradiol levels. Results by Samir et al. [29] also indicate that male Shiba goats exposed to summer stress demonstrated increased salivary cortisol levels. However, there were no significant changes in testosterone or estradiol levels, suggesting a species-specific variation in endocrine responses to heat stress [29].
Subsequently, a study on oxidative damage and testosterone levels found that prolonged heat stress in male rats caused oxidative damage in testicular tissues, leading to decreased testosterone production [40]. The reduction was associated with the impaired activity of enzymes critical for steroidogenesis, such as 17β-hydroxysteroid dehydrogenase-3, because of the heat stress [40]. Moreover, Behringer et al. [26] found that young Assamese macaques exposed to seasonal stress demonstrated increased levels of fecal triiodothyronine, especially in immature individuals and females. Ishimaru et al. [31] found that while winter stress alone did not significantly alter cortisol and thyroxine levels when added to exercise, there was a significant increase in these hormones, along with prolactin and insulin-like growth factor-1.

4.4. Mechanisms of Endocrine Disruption

The possible mechanisms by which climate change causes endocrine disruption were obtained from the articles selected for this review [34,35,36,37,38,39,40,41,42,43]. These mechanisms include changes in metabolic processes and animal physiology [34,36], defects in the function of the hypothalamic–pituitary–adrenal axis [35,37,38,42], and fluctuations in protein expression [39,40,41,42,43]. Pragna et al. [34] reported that metabolic processes shift under heat stress toward increased plasma triiodothyronine production at the expense of thyroid-stimulating hormone synthesis. Similarly, Bruzzio et al. [36] demonstrated how ocean acidification and hypoxia modified metabolic pathways, thereby leading to increased circulation of cortisol and lower production of insulin-like growth factor 1.
Shilja et al. [35] documented how activation of the hypothalamic–pituitary–adrenal axis caused increased protein and mRNA levels of adrenal and hepatic heat shock protein 70 in goats. As a result, the release of plasma cortisol and aldosterone was found to increase in these animals. Hadinia et al. [37] attributed hypothalamic–pituitary–adrenal axis malfunction to the accumulation of lipids in the body and the concomitant formation of reproductive hormones in broiler breeder pullets. This malfunction was also supported by the increased serum levels of gonadotropin-releasing hormone 1, luteinizing hormone, follicle-stimulating hormone, and 17β-estradiol in the study animals. Studies by Lane et al. [38] and Dovolou et al. [42] further highlighted how increased or decreased activity of the hypothalamic–pituitary–adrenal axis may cause decreases in corticosterone levels, glucocorticoid synthesis, and luteinizing hormone and gonadotropin secretion.
Li et al. [39], Halder et al. [40], and Kim et al. [43] reported similar mechanisms of endocrine disruption in response to heat stress. Specifically, study participants showed high serum levels of testosterone and corticosteroids [39,40]. However, Halder et al. [40] and Kim et al. [43] reported that heat stress might also be attributed to low circulating levels of testosterone, estrogen, and gonadotropin in animals. In contrast, de Souza et al. [41] reported that climate change amplifies the impact of pollutants on zebrafish, which impairs the expression of testicular genes, thereby impeding the formation of 11–ketotestosterone and 17β-estradiol. The aforementioned mechanisms of endocrine disruption are documented in Table 2.
The papers selected for this review provide conclusive evidence that changes in the climate can affect the production of some hormones [43,44,45,46,47] but do not offer conclusive insight into the mechanism or ultimate consequence. The hormones involved are prolactin, progesterone, cortisol, estradiol, follicle-stimulating hormone, and luteinizing hormone. The authors of the articles selected for this review agreed on similar mechanisms of endocrine disruption, including the dysregulation of gene and protein expression and the suppression of hypothalamus–pituitary–gonadal axis activity. Heat shock conditions caused by stressors may decrease or increase hormone production. Figure 2 shows a schematical illustration of the impact of climate change on the main affected endocrinological axes.

5. Discussion

This systematic review focuses on the assessment of the significant impact of climate change on endocrine parameters. In particular, endocrine parameters related to climate change were obtained from previously published articles [21,23,25,26]. The findings indicate how climatic stressors such as heat, seasonal changes, and hypoxia can alter endocrine regulation across humans and animals. The impacted endocrine hormones are prolactin, progesterone, aldosterone, cortisol, estradiol, gonadotropins such as follicle-stimulating hormone and luteinizing hormone, free triiodothyronine, and thyroxine [27,28,29,30,31,32]. Some general processes of endocrine disruption that result from climate change include the inhibition of protein expression, the modification of metabolic activities, the suppressed or absent production of hormones, and the impairment of hypothalamus–pituitary–gonadal axis activity and neuronal interactions [38,39,40,42]. Fundamentally, results on both humans and animals were obtained from various articles used in the study.
In humans, the findings indicate that acute hypobaric hypoxia resulted in decreased aldosterone and cortisol levels [21]. These results are an indication that there is a direct impact of sudden environmental changes on adrenal hormone regulation. The changes in adrenal hormone regulation could be due to impaired stimulation of the hypothalamic–pituitary–adrenal (HPA) axis because of reduced oxygen conditions. Such findings are critical for understanding how populations exposed to extreme altitudes or rapid atmospheric changes may experience compromised stress responses. Moreover, the study by Fu et al. [28] found that there are seasonal influences on thyroid hormones, leading to an increase in the level of thyrotropin, triiodothyronine, and thyroxine during winter, but declining in summer, especially among women in the reproductive age of 20–49 years. From the results, it can be argued that adaptive thermogenic mechanisms, such as elevated thyroid hormone levels during the winter months, are helpful in generating body heat. However, the level of this hormone decreases in the summer because of the body’s energy conservation strategy.
In animals, it was found that heat stress is one of the most predominant environmental factors affecting endocrine function. For instance, there were reduced cortisol levels in cows exposed to prolonged heat, a pattern suggesting that chronic thermal exposure may downregulate the HPA axis to avoid overstimulation, potentially impairing the animal’s ability to handle additional stressors [23,33]. Furthermore, the findings of this review explain the influence of high body temperature on endocrine gland function [35,39,40]. Heat stress may indirectly cause a decrease in dietary intake by inhibiting the release of gonadotropin-releasing hormone and luteinizing hormone [47,48,49,50,51,52,53,54,55,56]; this may change the uterine environment, causing harm to the embryo and infertility [50,56,57]. In this light, it is important to note that physiological problems lead to challenges in maintaining homeostasis because of persistent climatic pressures.
In light of the mechanism of endocrine disruption, evidence reveals that altered cortisol levels under both acute hypoxia and prolonged cold stress [21,27]. These results emphasize how climate factors can modify stress hormone regulation. Moreover, several studies have suggested that low doses of cortisol during follicular maturation decrease pituitary luteinizing hormone secretion [50,51,52]; these effects may circumvent the synthesis of gonadotropin at other levels, such as the hypothalamus [42,49,50,53]. Moreover, it is also evident that there can be a shift in metabolic priorities, such as increased triiodothyronine production in goats under heat stress [34]. The adaptation of these animals is linked to the need to optimize energy utilization for survival. Moreover, oxidative damage is also linked to reduced testosterone production in rats, an indication that environmental challenges lead to the vulnerability of reproductive processes [40].
Concisely, the results of these studies indicate that climate change leads to vulnerabilities in endocrine regulation. For instance, it was found that in humans, hormonal disruptions could compromise stress resilience, thermoregulation, and reproductive health, particularly among people subjected to extreme climates. However, in animals, endocrine disruption was found to lead to reduced productivity in agriculture, altered reproductive patterns, and challenges in wildlife conservation. Even though the findings of this study suggest that endocrine laboratory parameters may be useful indicators of the effects of climate change on endocrine glands, there is a lack of information on how such endocrine disruption affects endocrine health [50]. In this light, subsequent studies must be conducted to establish the underlying mechanism(s) by which climate change negatively impacts endocrine health [58,59,60,61]. Moreover, there is a need for longitudinal research to assess the cumulative impacts of climate stressors on endocrine function, as well as to explore the combined effects of climate change with pollutants, dietary changes, and other anthropogenic factors.

6. Conclusions

This review of the literature focuses on how climate change affects endocrine laboratory parameters. Changes in endocrine system function caused by climate change were derived from eligible articles selected for this review. The results of this study demonstrate how the serum levels of prolactin, progesterone, cortisol, estradiol, follicle-stimulating hormone, luteinizing hormone, and other hormones in animals are impacted by climate change. The mechanisms of endocrine system disruption caused by various stresses include interference with the function of the hypothalamic–pituitary–gonadal axis as well as impaired gene and protein expression. The findings of this review provide evidence that endocrine laboratory parameters are potentially suitable hormonal markers to study the effects of climate change on the endocrine system. However, further research should be conducted to determine the relationship between the consequences of climate change and the function of the endocrine system.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflict of interest.

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Figure 1. PRISMA flow chart for selecting publications from various databases.
Figure 1. PRISMA flow chart for selecting publications from various databases.
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Figure 2. A schematic illustration of the impact of climate change on the main affected endocrinological axes.
Figure 2. A schematic illustration of the impact of climate change on the main affected endocrinological axes.
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Table 1. Characteristics of the articles chosen for this systematic review.
Table 1. Characteristics of the articles chosen for this systematic review.
Author(s) (Year)Research ObjectiveTest SubjectsType of ExposureExposure ConditionsEffect on Endocrine Laboratory Parameters
Nishimura et al. [21]To explore endocrine, inflammatory, and immunological responses. Healthy male studentsChronic (climatic chamber)Hypobaric hypoxia, 75 min of exposure to settings mimicking 3500 m.Decrease in aldosterone and cortisol levels.
Tang et al. [22]To investigate how seasonal heat stress during late gestation affects calf development, metabolism, and the functions of the immune and endocrine systems. Female calves Acute, seasonal33 days of summer and winter stress, respectivelyDecrease in adrenocorticotropin
Chen et al. [23]The purpose of this study was to look into the effects of heat stress on endocrine, thermoregulatory, and lactation parameters in heat-tolerant and heat-sensitive dry cows.Dry cowsAcute, seasonal40 days of heat stressReduction in plasma cortisol.
Increase in plasma triiodothyronine and growth hormone levels.
Lyrio et al. [24]To assess the implications of heat stress on the quality of semen in French Bulldogs, as well as the time frame of these impacts. French BulldogsAcute (electrical heat pad)11 min of exposure to 40 °C for 60 days.No difference in testosterone levels in the semen.
Mizukami et al. [25]To evaluate the growth and hormonal changes in Thoroughbred colts and fillies raised at two Racing. Thoroughbred colts and filliesAcute (seasonal). 7 months of summer and winter stress.
Behringer et al. [26]To explore the influence of demographic and environmental variables on immunoreactive fecal total triiodothyronine levels in young Assamese macaques.Young Assamese macaquesAcute (seasonal).7 months of summer and winter stressIncrease in the concentrations of immunoreactive fecal total triiodothyronine in immature and female Assamese macaques.
Rise in immunoreactive fecal glucocorticoid levels in developing immature Assamese macaques.
Yang et al. [27]To explore the impact of two extrinsic stimuli (day length data and daily extrinsic temperatures) on the endocrine metabolism and behavior of whooper swans before their spring migration.Whooper swansAcute (seasonal).5 months of winter stressHigh levels of fecal glucocorticoid metabolite
Fu et al. [28]To assess the seasonal fluctuations in the quantities of thyrotropin, free triiodothyronine, free thyroxine, and thyrotropin index in women of reproductive maturity.Women aged 20 to 49 years. Acute (seasonal).11 months of summer and winter stressIncrease in thyrotropin, free triiodothyronine, free thyroxine, and thyrotropin index in the winter months.
Samir et al. [29]To ascertain if the quantities of steroids (T, E2, and cortisol) in male goat saliva correspond to their levels in the bloodstream. 7 male Shiba goatsAcute (seasonal).6 months of spring and summer stressHigher concentrations of salivary cortisols in summer compared to spring.
No significant difference in the levels of testosterone, estradiol, and plasma cortisol between spring and summer.
Tangyuenyong et al. [30]To examine the effects of artificial light supplementation on the concentrations of thyroxine, body growth hormone, and reproductive hormones in trained thoroughbred yearling horses from Hokkaido and Miyazaki.Trained thoroughbred yearling horsesAcute (artificial light supplementation).7 months of summer stress (14.5 h of daylight and 9.5 h of darkness).In natural settings, Hokkaido yearlings had higher total thyroxine concentrations but lower insulin-like growth factor-I (colt) and prolactin levels compared to Miyazaki yearlings.
Under light supplementation, the quantities of prolactin and progesterone increased in Hokkaido and Miyazaki, resulting in early ovarian activity compared to controls.
Ishimaru et al. [31]To compare the physiological, endocrine, and developmental parameters of thoroughbred weanlings and yearlings in Hokkaido, Japan, to those kept outdoors for 22 h in the paddock (22 h group) and 7 h in the daytime with walking exercise for 1 h using a horse-walker (7 h + W group). Thoroughbred colts and filliesAcute (seasonal)3 months of winter stress only (22 h outdoors)
3 months of winter stress and walking exercise (7 h outdoors in the daytime with walking exercise)
No significant change in the levels of circulating cortisol and thyroxine in the 22 h group.
Increase in the concentrations of circulating cortisol, thyroxine, prolactin, and insulin-like growth factor in the 7 h + W group.
Shi et al. [32]To examine the relationships between three hair cortisol features (hair cortisol concentration, protein concentration, and the ratio of hair cortisol concentration to protein concentration) with the sampling year and season and hair color in dairy cows.Holstein dairy cowsChronic stress18 months of heat stressRise in the concentration of hair cortisol.
Blond et al. [33]To determine if heat stress influences the values of metabolic, endocrinological, and inflammatory markers, as well as body surface temperature in cows throughout the early and middle phases of lactation. Holstein-Friesian breed of cowsAcute (seasonal)3 months of heat stress. Increased levels of cortisol and insulin.

Decrease in triiodothyronine (T3) concentration.
Table 2. Mechanisms of endocrine disruption documented in the articles chosen for this systematic review.
Table 2. Mechanisms of endocrine disruption documented in the articles chosen for this systematic review.
Author(s) (Year)Type of ExposureMechanism of Endocrine DisruptionEffect on Endocrine Laboratory Parameters
Pragna et al. [34]Heat stressAlterations in the metabolic activities of the Osmanabadi, Malabari and Salem black goats.An increase in the production of plasma triiodothyronine, and a decline in the synthesis of thyroid stimulating hormone.
Shilja et al. [35]Heat stress The activation of the hypothalamic–pituitary–adrenal axis, which resulted in an increase in the expression of adrenal and hepatic Heat Shock Protein 70, and messenger ribonucleic acid (mRNA) in goats. Rise in the release of plasma cortisol and aldosterone in goats.
Bruzzio et al. [36]Acidification of the ocean and hypoxia.The acidification of the ocean affected hormonal stress physiology in juvenile blue rockfish. The dissolved oxygen levels also led to differences in metabolic processes, physiological state, and behavioral stress in juvenile blue rockfish.Increase in the circulation of cortisol and decrease in the production of insulin-like growth factor 1.
Hadinia et al. [37]Artificial lightActivation of the hypothalamic–pituitary–gonadal axis, which resulted in increased body lipid accumulation, and enhanced levels of reproductive hormones in broiler breeder pullets.Rise in the circulation of gonadotropin releasing hormone 1, luteinizing hormone, follicle stimulating-hormone, and 17-beta-estradiol.
Lane et al. [38]Lack of nature The stimulation of the hypothalamic–pituitary–gonadal axis leads to a glucocorticoid stress response.
This response is stopped by a negative feedback mechanism, which occurs predominantly via the attachment of receptors in the hippocampus and hypothalamus, resulting in lowered production and release of hormones from the adrenal gland.
Decline in corticosterone levels and synthesis of glucocorticoids.
Li et al. [39]Heat stress Exposure to heat elevated blood testosterone levels and the expression of glucocorticoid receptors in the nuclei of primary and basal cells from Bama miniature pigs.Rise in the level of testosterone in the serum of Bama miniature pigs.
Halder et al. [40]Heat stressProlonged exposure to high temperatures in male rats resulted in oxidative stress and a substantial reduction in superoxide dismutase, catalase, and glutathione in the testicles. However, there was a significant increase in the synthesis of testicular lipid peroxidase, enzyme caspase-3, and expressions of testicular heat shock protein 72 and heat shock factor 1. In addition, extended exposure to high temperatures also led to a drop in the formation of 17β-hydroxysteroid dehydrogenase-3.Low serum testosterone levels.
Increase in the concentration of corticosteroids in the serum
de Souza et al. [41]Climate changeAmplification of the impact of pollutants on fish, which impairs the expression of testicular genes. Over time, the aforementioned disorder leads to serious testicular injury and subfertility in zebrafish.Impedes the formation of 11-ketotestosterone and 17β-estradiol in zebrafish.
Dovolou et al. [42]Heat stressThe hypothalamus–pituitary–gonadal axis communication is disrupted, leading to an endless cycle of decreased gonadotrophic support and inefficient biosynthesis of steroid hormones in the ovary. Inhibits the secretion of luteinizing hormone and gonadotropin.
Kim et al. [43]Heat stressSummer heat stress lowered the expression of kisspeptin and neuronal activity in the hypothalamus, thereby suppressing the activation of the hypothalamus–pituitary–gonadal axis. Low levels of circulatory estrogen and gonadotropin.
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