Exploring Relationships Between Endocrine Disruptors & Male Reproductive Health

Exploring Relationships Between Endocrine Disruptors & Male Reproductive Health

Abstract

Over the last eight decades, a substantial increase in the production of endocrine disrupting chemicals (EDCs) has been accompanied by a marked decline in indicators of reproductive health. This study sought to investigate the relationship between these trends.

Meta-analysis data on total sperm count, as well as census data on annual global plastic and pesticide production were compiled into a correlation test using R studio software. Correlation coefficients of -0.982 for plastic production and -0.976 for pesticide production were obtained, indicating a significant inverse correlation between EDC production and sperm count.

Ample supplementary research describing the biochemical mechanisms through which EDCs disrupt the reproductive system has been discovered in the published literature, providing causation for the observed correlations.

These findings raise serious concerns regarding public health for two primary reasons. First, the continuation of humankind is contingent upon reproduction. Second, reproductive health is indicative of general health and is connected to numerous chronic diseases, which account for many of the leading causes of death in developed countries (Levine et al. 2020).

Considering the precarious state of human health and reproductive potential, as well as the alarming speed at which they have regressed, future research is urgently needed to further investigate the causes of, and potential solutions to this unprecedented situation. More importantly, definitive actions need to be taken to curtail the damage being done by EDCs and restore human well being.

Introduction

The endocrine system is a delicately balanced network of glands and organs that secrete
hormones, which are chemical messengers that bind to receptor sites to exert their effects (Wang
et al. 2017). Hormones are responsible for regulating numerous physiological processes that
operate in harmony to maintain homeostasis. Sex steroid hormones are distinct because while all the other divisions of the endocrine system are devoted to survival, the sex steroid hormones are primarily responsible for reproduction. The sex steroid hormones include estrogens, progesterone, and androgens, all of which are derived from the lipid precursor molecule cholesterol. In women, estrogen is responsible for the development and maintenance of female reproductive tissues and secondary sexual characteristics, as well as regulation of metabolism, blood lipids, cognitive function, bone health, and more (Kirtana et al. 2022). Estrogen and progesterone fluctuate biweekly as part of the menstrual cycle, which prepares the body for pregnancy.

In males, androgens drive male sexual differentiation during development (Wang et al. 2017). The principal androgen is testosterone, which is produced via steroidogenesis in the Leydig cells of the testes. The androgen receptors onto which testosterone binds are found throughout the body (Wang et al. 2017). Thus, testosterone serves many functions in human physiology, including but not limited to, facilitating proper metabolic function, maintaining optimal body composition (Herbst 2004), cognition and neuroprotection (McHenry et al. 2014), libido, maintenance of bone density (Bandeira 2022), balancing blood lipids (Tsang et al. 2007), mental health, promoting prosocial behaviors such as status attainment and leadership (Dreher et al. 2016), as well as spermatogenesis (sperm production), which occurs in the Sertoli cells of the testes (Walker 2011). Due to its physiological universality, testosterone levels make for a serviceable barometer of general virility.

Given the interconnectedness and necessity of the sex steroid axis in males and females, the fact that a growing body of literature showing evidence of declining reproductive health and fertility is highly disconcerting. The most recent and comprehensive meta-analysis tracking sperm quality, titled: Temporal trends in sperm count: a systematic review and meta-regression analysis of samples collected globally in the 20th and 21st centuries, was published by Hagai Levine and colleagues in 2022. This review compiled nearly three thousand publications tracking sperm quality. The results revealed that mean sperm concentration declined 52.4% between 1973 and 2018, and total sperm count declined 59.3% over the same timeframe, with no indications of plateauing. That equates to a decline rate of approximately -1.3% per year, which accelerated to -2.63% per year after 2000. These findings are noteworthy because strong evidence links reduced sperm count and concentration to increases in all-cause mortality and morbidity (Levine et al. 2022). Links between low sperm count and infertility are also well-recognized (Levine et al. 2022).

The decline in sperm count is paralleled by declines in testosterone levels, which is to be expected because testosterone is required to stimulate sperm production in the testes. Thus, sperm count and testosterone level make for mutually inclusive indicators of male reproductive health. The most widely referenced study tracking testosterone levels over time, titled: A Population-Level Decline in Serum Testosterone Levels in American Men, was published in 2007 by Thomas Travison and company. The study found a substantial age-independent decline in serum testosterone concentrations in the 1,400 men followed during the 20-year duration of the study (1980-2000). Age-independent means the decline was observed across different age groups and could not be attributed to declines expected with chronological aging, as it is known that testosterone levels fall off as men get older. This suggests that factors beyond chronological age contributed to the decrease in testosterone concentrations. To account for such factors, the researchers adjusted their results for a wide range of confounding variables (factors that can influence data) including obesity, smoking, alcohol consumption, pharmaceuticals, illicit drug use, chronic illness, as well as employment and marital status, all of which are known to affect testosterone levels. Although adjustment for these factors accounted for some of the decline, the total drop in testosterone concentrations was not fully explained by age and lifestyle factors, as a residual 1.3% decline per year persisted. The researchers concluded the study with a request for future research endeavors to further investigate the causal factors driving the declines in testosterone levels observed in their study.

This mysterious pattern is consistent with other studies whose results also demonstrate
declines in testosterone. A follow up study published in 2020 by Gabriel Chodik and colleagues sought to discover if the testosterone declines revealed by the Travison paper continued in the twenty years that elapsed. The study, titled: Secular trends in testosterone- findings from a large state-mandate care provider, pulled data from blood test measures on over 100,000 Israeli men between 2000-2020, the largest sample size ever conducted in a study tracking testosterone levels. The study used parameters almost identical to those used in the Travison study (age-independent & adjustment for confounding variables) and found that the decline seen in the Travison study continued almost perfectly, with an annual testosterone decline of approximately 1.1%. Twenty years later, the conclusion remained the same; mean testosterone concentration for men in developed countries is decreasing with no evident causes. Since there are a litany of publications exhibiting evidence for declining testosterone, a detailed analysis of each one would be extraneous. For the sake of brevity, figure 1 summarizes the most prominent studies related to testosterone decline.

Figure 1. Previous studies on secular trends in serum testosterone levels in men. Sourced from: Chodik et al. 2020.

The takeaway is that the markers of male reproductive health I investigated in this project, sperm counts and testosterone levels, have fallen off appreciably with no apparent explanation. Although numerous confounding variables have been considered as possible contributors to reproductive decline, endocrine disrupting chemicals (EDCs) have not.
As their name implies, endocrine disruptors are synthetic compounds that cause adverse health effects consequent to alterations in endocrine function (Kirtana 2022). There are over a thousand EDCs in circulation as of this writing, which can be found in a litany of products we come in contact with on a daily basis (Kirtana 2022). The prevalence of plastics and pesticides, the two foremost sources of EDCs, has risen exponentially since their simultaneous introduction into the market in the second half of the 20th century (Gasnier 2009). The growing ubiquity of EDCs is reflected by the fact that detectable levels of microplastics and pesticides have been repeatedly discovered in human tissue and urine samples (CDC, 2020). This is noteworthy because the timeline over which EDCs were introduced into society perfectly overlaps with the timeframe during which reproductive health has fallen off. While conclusive causation cannot be drawn from correlation alone, EDCs have been shown to directly disrupt the reproductive axis through known biochemical pathways (Vogel, 2009; Hlisníková et al. 2020). Due to their environmental omnipresence, specificity toward disrupting the reproductive system, correlation with reproductive decline, and absence in the list of confounding variables in the literature on reproductive decline, I hypothesized that EDCs may, at least in part, be contributing to the unexplained declines in male reproductive health.

Materials & Methods

Review of Primary Literature

While there are many indicators of population level reproductive health, such as infertility rates, miscarriages, ectopic pregnancies, genital abnormalities, PCOS incidence, reproductive tract cancers, early puberty, menstrual abnormalities, and more (Shanna H. Swan, 2020), I decided to concentrate on indicators of male reproductive health for several reasons. The first is that the data following sperm counts and testosterone levels are clear, consistent, and abundant, whereas the data on other measures of reproductive health are either ambiguous, sporadic or lacking. The second is that male-factor infertility rates are on the rise and contribute to over 50% of infertility cases (Agarwal et al. 2015), however the shame and emotional burden is often unjustly placed on women. I hope that more awareness on male-factor infertility will inspire men to take accountability for their reproductive health. Third, due to the current cultural shift toward male domestication and societal overreach curtailing “toxic masculinity” (which may have psychological implications on hormonal outcomes consequent to neuro-endocrine interactions), issues pertaining to male reproductive health tend to remain esoteric. Lastly, since the causes of the declines in male reproductive health remain unknown, my curiosity intrigued me to help solve this mystery.

Over fifty publications among the literature surrounding male reproductive health and endocrine disruptors were systematically reviewed to gain a comprehensive understanding of what is currently known in this field of research and to discover any noteworthy trends or gaps The first objective was to elucidate changes in population scale testosterone levels over time, with the hypothesis being that levels have declined over time. After reading nearly a dozen papers tracking testosterone levels, it became apparent that testosterone levels are on the downtrend, as all studies showed a decline to some degree.

Creating a Novel Testosterone Meta-analysis

Although all of the studies showed declines, they followed disparate populations, over different time frames, under different circumstances, and the methodologies used were not uniform. Moreover, the rate of decline varied between studies. This inspired my original goal, which was to compile the results from all of the most prominent studies tracking testosterone levels into a linear regression model which would output a trendline representative of the body of literature on testosterone levels as a whole, likened to a meta-analysis. Since no such meta-analysis currently exists, this would outline the overall trend in testosterone levels for the first time, which would be a novel publication. Collaborative efforts with two PhD statisticians, Dr. Ober and Dr. Lombardo, were met with challenges that made it clear why there is no meta-analysis on testosterone levels. Due to limitations in data availability, time, and personnel to extract and plot all the data, I realized it was not feasible as an undergraduate researcher to create a meta-analysis, and decided to pivot.

Causes of Reproductive Decline: A Missing Link

Although the research tracking testosterone levels varied in their parameters and methodologies, in addition to the fact that they all showed declines, I identified another commonality between them, which was that the causes of the declines were not entirely understood. While most papers adjusted their results for a number of confounding variables which are known to have an adverse effect on testosterone levels, including advancing age, BMI, chronic illness, and so on, the decline rates remained significant even after adjustment for these factors. This missing link indicated that there must be something else contributing to testosterone decline, which was reflected in the need for future research that nearly all the authors requested at the end of their papers. During my investigation to solve this mystery, I read about a class of chemicals called endocrine disruptors, which mimic or obstruct endogenous hormone production, leading to adverse health effects.

Correlational Time Frame Overlap

After learning that plastics and pesticides are the two foremost sources of EDCs, and that they were first synthesized halfway through the 20th century, it dawned on me that the timeframe over which plastics and pesticides have been incorporated into the market perfectly overlaps with the timeframe over which testosterone levels declined. To verify this, I found census data tracking worldwide plastic and pesticide production over time, and confirmed that both have become exponentially more pervasive. This discovery galvanized a new idea, which was to see if the growing prevalence of endocrine disruptors is correlated with reproductive decline. The problem was that in order to generate a correlation, two trend lines are needed to be compared. While the census data tracking plastic and pesticide production already existed, I could not correlate it against testosterone levels because the studies were disconnected and none were representative enough of the research body as a whole to suffice in isolation.

The Pivot From Testosterone to Sperm Count

Under the advisement of Dr. Lutton, the decision was made to use a different metric for reproductive health, that being sperm count. Sperm count made for an excellent metric for a few reasons. First, a meta-analysis compiling data from over three thousand studies tracing sperm count had been published in 2020, so a reliable trendline emblematic of the literature on sperm count as a whole was available. Second, sperm count and testosterone level are intimately related and serve as interchangeable markers of male reproductive health (Wang et al. 2017).

Creating Linear Regression Models

To disclose the correlation between endocrine disruptors and sperm count, two plots were created. One overlayed census data on plastic production over sperm count, and the other overlayed census data on pesticide production over sperm count. With the assistance of Dr. Ober, the census data on plastic and pesticide production, as well as the meta-analysis data on sperm count, were imported into R studio software and linear regression models were generated. While the meta-analysis data on sperm count and census data on plastic and pesticide production already existed, in addition to the extensive research required to discover these patterns, the novelty in my thesis lies in the fact that no publication has overlaid the data from these sources to identify the statistical significance of the relationship between them.

Results

To disclose the relationship between meta-analysis data on total sperm count (TSC) and
census data on plastic production, a correlation test was run on R studio. There was a statistically
significant inverse relationship between plastic production (metric tons per year) and average
total sperm count (million per year) (Figure 2). Plastic production has a dramatic, negative effect on total sperm count.

Figure 2. Impact of global annual plastic production on average total sperm count. Data tracking
global annual plastic production and average total sperm count between the years 1970-2020
were overlaid and the relationship between the two was elucidated using a correlation test on R
studio. White dots represent the values for total sperm count in millions and plastic production in
tons at a given year. P-value < 2.2e-16, alternative hypothesis: true correlation is not equal to 0
95 percent confidence interval: -0.9908282 -0.9659195, sample estimates correlation coefficient:
-0.9822848.

To elucidate the connection between meta-analysis data on total sperm count (TSC) and census data on pesticide production, R studio was utilized to generate a correlation test between the two. A statistically significant inverse correlation between pesticide production (metric tons per year) and average total sperm count (millions per year) was observed (Figure 3). Pesticide production exerts a considerable, detrimental impact on total sperm count.

Figure 3. Inverse correlation between annual global pesticide production (millions of gallons per year) and mean total sperm count (millions). Linear regression analysis was run using R studio, which outputted a correlation coefficient of -0.976, and a P-value of 9.446e-15. Red trend line; TSC over time, Blue trend line; pesticide production over time.

Discussion

Summary & Outcome

Sperm counts and testosterone levels are important to study for two primary reasons: first, they are indicative of human reproductive potential, and second, they serve as biomarkers for overall vitality (Levine et al. 2020). In recent decades, both sperm counts and testosterone levels have fallen appreciably, and definitive explanations continue to elude researchers. Simultaneously, the prevalence of EDCs, which adversely alter endocrine and reproductive function, has grown exponentially. The first objective of this study was to draw correlations between the two foremost sources of EDCs, plastics and pesticides, against sperm counts. The second objective was to connect the correlations with pre-published qualitative research describing the mechanisms through which EDCs disrupt male reproductive function. Our results show that there is a highly significant inverse correlation between EDC production and sperm counts, which is corroborated by copious research providing causation for these correlations. These findings may explain the residual declines in male reproductive health that are not entirely attributable to the lifestyle factors the researchers accounted for.

Evidence & Support

A correlation test overlaying plastic production with sperm count was run in R studio and showed a strong, negative association between sperm counts and plastic production plastic production, denoted by a correlation coefficient of -0.982 and an P-value < 2.2e-16 (Figure 2). The negative sign indicates that the relationship is inverse; as plastic production increases, sperm counts decrease. The p-value being less than 0.05 indicates that the observed correlation coefficient is statistically significant. In other words, it is highly unlikely that such a strong negative correlation could occur due to random chance alone. This strengthens the evidence supporting the existence of a true relationship between plastic production and sperm counts. A correlation test was run again, this time overlaying pesticide production over sperm counts. R studio outputted a correlation coefficient of -0.976 and a P-value < 9.446e-15 (Figure 3). Just like the plastic results, these values imply that as pesticide production has increased, sperm counts have decreased proportionally. While these findings are purely correlative, the following research describes the mechanisms through which three noteworthy EDCs disrupt the reproductive axis, providing causation for these correlations. It is worth reiterating that there are over a thousand synthetic chemicals classified as endocrine disruptors, so the following three are just the tip of the iceberg.

Bisphenol A (BPA) is one of the most ubiquitous and potent endocrine disrupting plastic
compounds on the market (Cariati et al. 2019). BPA has been shown to exert estrogenic and
antiandrogenic properties by way of disrupting the hypothalamic-pituitary-gonadal axis, and the
ability to alter normal epigenetic patterns with impairing consequences on the reproductive
system. In addition to mimicking estrogenic activity by binding to estrogen receptors, BPA
impairs the ability of the hypothalamus to secrete Gonadotropin Releasing Hormone (GnRh),
which triggers the release of Luteinizing Hormone (LH) and follicle stimulating hormone (FSH)
from the anterior pituitary gland. LH and FSH bind to Leydig and Sertoli cells in the testes,
initiating the processes of steroidogenesis (testosterone production) and spermatogenesis (sperm production) respectively (Cariati et al. 2019). As a result, BPA exposure significantly retards male reproductive function consequent to the combination of behaving as an estrogenic agonist and downregulating testosterone and sperm production. The ubiquity of BPA is reflected by the 2003-2004 National Health and Nutrition Examination Survey (NHANES III) conducted by the Centers for Disease Control and Prevention (CDC), which found detectable levels of BPA in 93% of urine samples they collected. The CDC NHANES data are considered representative of nationwide exposures in the United States.

Phthalates are another class of mass produced chemical plasticizers which are known to
have deleterious effects on human health. Regarding the reproductive system, in vitro studies
demonstrated that phthalate exposure at low concentrations (40-160 μM) resulted in apoptosis of
Leydig and Sertoli cells of Male Sprague-Dawley rats, which are responsible for spermatogenesis and steroidogenesis respectively (Hlisníková et al. 2020). These cytotoxic
modalities are reflected by studies conducted in Chinese and Polish infertility clinics, which
found that urinary phthalate levels were associated with decreased sperm concentration and
reduced sperm motility, and semen phthalate levels were associated with decreased sperm
concentration, motility, and spermatic DNA damage (Hlisníková et al. 2020). Moreover, the
offspring of fathers with damaged spermatic DNA have an increased risk of miscarriage, birth
defects, autism, and trisomy 21 (Shanna H. Swan 2020). Prenatal phthalate exposure can induce
testicular dysgenesis syndrome, which is characterized by retarded testicular development, as
well as necrosis of seminiferous tubules (Hlisníková et al. 2020).

Glyphosate, the most extensively used herbicide in the United States, behaves as a reproductive endocrine disruptor in several ways (Gasnier et al. 2019). One key pathway is its interference with the function of aromatase, an enzyme responsible for the conversion of androgens (male hormones) into estrogens (female hormones). Glyphosate has been shown to inhibit aromatase activity, leading to a decrease in estrogen synthesis. This disruption of estrogen production can have far-reaching effects on reproductive processes, as estrogen plays a crucial role in regulating menstrual cycles, ovarian function, and sperm production. Moreover, glyphosate has been found to interfere with the activity of estrogen receptors, which can impair normal physiological responses to estrogen, further contributing to reproductive dysfunction. Furthermore, glyphosate has been shown to disrupt the function of the hypothalamic-pituitary-gonadal (HPG) axis, a complex hormonal system that regulates reproductive function. Studies have demonstrated that glyphosate exposure can alter the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, which in turn affects the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland. These hormones play pivotal roles in the regulation of menstrual cycles, ovulation, as well as testosterone sperm production. Lastly, glyphosate has been linked to oxidative stress, which can further exacerbate its reproductive toxicity, which disrupts cellular function by causing damage to DNA, proteins, and lipids (Gasnier et al. 2019).

While the scope of this thesis prioritized male reproductive health, evidence for female reproductive decline is also abundant, and is attributable to an array of indicators, including
increasing rates of infertility, Polycystic Ovarian Syndrome (PCOS), endometriosis, hormone
dependent cancers (breast, ovarian, cervical), miscarriages, birth defects, and more (Shanna H.
Swan, 2020). Causal mechanisms through which EDCs disrupt the female reproductive system are well described (Rattan et al. 2017; Shanna H. Swan, 2020). The fact female reproductive health is also suffering provides further support for the notion that human reproductive health as a whole is plummeting, and that EDCs are a likely culprit.

To recap, the timeframe over which EDC prevalence has risen overlaps with the timeframe over which sperm counts have declined. These inverse correlations were shown to be highly significant following statistical analysis, and the mechanistic evidence described in this section provides plausible causation for these correlations. Moreover, other measures of reproductive health, including testosterone levels and indicators of female fertility, have also fallen. These findings strongly support my hypothesis that endocrine disruptors are contributing to the unexplained declines in testosterone and sperm count remaining in the scientific literature.

Assumptions & Limitations

My results, which present plastic and pesticide production as independent variables on the x axes of their respective graphs, and sperm count as the dependent variable on the Y axis, inherently assume that the observed changes in sperm count are solely attributable to changes in plastic and pesticide production. In other words, if there were other factors contributing to declining sperm counts, they were not accounted for. Thus, the relationship between EDC production and sperm count decline may not be as closely correlated as depicted by my results.

Most of the publications tracking reproductive decline adjusted their results for a number
of confounding variables that are known to adversely influence reproductive health (i.e.
advancing age, obesity, drug & alcohol consumption, and the like), however a residual,
unexplained decline remained following adjustment for these variables. Since EDCs are so
pervasive and effective at disrupting the reproductive system, my thesis hypothesizes that EDCs
are contributing to the residual dip in reproductive health that currently has no identifiable
cause. While the aforementioned evidence strongly points to the fact that EDCs are very likely
contributing to reproductive decline, due to the sensitivity of the reproductive system, it is
susceptible to influence from many factors. Therefore, the effect of further confounding
variables, which were not considered by myself or prior researchers, cannot be ruled out. For
instance, the rate of male depression is on the rise (CDC), and depression is linked to low
testosterone (McHenry et al. 2014). This highlights the complexity and interconnectedness of
human physiology, which shows that unsuspected factors could be at work. It is probable that the
declines in sperm count and testosterone are attributable to a mix of factors, not just EDCs. Thus,
this paper is limited in that it only provides evidence for one possible cause of the unexplained
reproductive decline, when more are likely contributing.

Implications and Further Directions

Before delving into the implications of these findings, a brief word on the systemic effects of EDCs is in order. As their name implies, EDCs disrupt all hormone systems including but not limited to the adrenals, thyroid, and pancreas (Shanna H. Swan, 2020). EDCs are also carcinogenic, neurotoxic, and generally inflammatory and cytotoxic by way of free radical damage and oxidative stress. Rates of obesity, diabetes, heart disease, neurodegenerative diseases, and cancer are all on the rise. EDCs could contribute to obesity through disruption of the thyroid axis, which is responsible for regulation of basal metabolic rate, a major determinant of calorie balance. EDCs may progress diabetes through pancreatic damage, which is responsible for blood sugar regulation. Lastly, EDCs exacerbate heart disease through vascular free radical damage, leading to atherosclerosis, and have the potential to initiate cancer through DNA damage (Shanna H. Swan, 2020). All of this is to say that the impacts of EDCs extend beyond the reproductive system, which adds to the panoply of effects caused by EDC induced reproductive harm.

The public health implications of my findings and those of all the supplementary research
referenced throughout this thesis are insidious and urgent. If sperm counts continue to decline at
at this rate (~2.6% per year), they are on pace to hit zero by 2050 (Shanna H. Swan, 2020). Low testosterone and sperm count are tied to obesity, diabetes, heart disease, cancer, depression, anxiety, and overall morbidity and mortality (Shanna H. Swan, 2020). Healthcare expenditures have grown from 5% of national GDP in the 1960s to over 20% in the 2020s (Chris Kresser, 2017). The American economy would be much better off if the chronic diseases that account for the majority of healthcare expenses were remediated, and since reproductive decline is connected to said diseases, more attention should be given to preserving reproductive health as part of a holistic model.

Given that the continuation of the human species and our quality of life along the way is on the line, it behooves the scientific community and policy makers alike to rapidly prioritize funding for research and policy changes to curtail the damage being done by EDCs and restore human wellbeing.

Specifically, future research should seek to discover ways in which the effects of EDCs can be neutralized and how humans can detoxify their bodies after years of inadvertent EDC exposure. Future research should also continue to seek out other possible contributors to reproductive decline, so that this challenge can be approached from as many angles as possible to maximize our chances of preserving our health, and our future.

Even if all the requisite research is conducted, nothing will change unless action is taken. As the most intelligent complex life form known in existence, we have the capacity and the obligation to address the threats to our reproductive health and overall well-being posed by endocrine disruptors. This will require the following multi-faceted approach.

Policy changes will be crucial to mitigate the impact of endocrine disruptors on human health. Regulatory agencies should strengthen restrictions on the use of EDCs in consumer products, agricultural practices, and industrial processes. Bans or restrictions on the most harmful chemicals, along with incentives for the development of safer alternatives, can help reduce human exposure to these harmful substances.

Education is key to raising awareness about the sources and effects of endocrine disruptors. Public health campaigns should be launched to educate individuals about the chemicals found in everyday products and their health risks. Consumers can make informed choices to reduce their exposure to EDCs by avoiding products containing known harmful chemicals and opting for safer alternatives.

Finally, promoting a holistic approach to health and wellness is essential for mitigating the impact of endocrine disruptors on reproductive health. This includes promoting healthy lifestyle behaviors such as regular exercise, balanced nutrition, stress management, and adequate sleep, which can help support overall hormonal balance and reproductive function, fortifying the body against inevitable EDC exposure. Additionally, healthcare providers should be trained to recognize and address the impacts of environmental exposures on reproductive health, and incorporate preventive measures into patient care.

In conclusion, the findings of this study underscore the pressing need to address the threat posed by endocrine disruptors to reproductive health. By conducting further research, implementing policy changes, raising awareness, and promoting holistic approaches to health, we can work towards safeguarding human reproductive health and ensuring a sustainable future for generations to come.

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