Abstract
The surge in industrialization and the resulting rise in environmental pollution, coupled with the increased use of synthetic chemicals and frequent exposure to hazardous compounds both in workplaces and at home, has a detrimental impact on reproductive health. Various biohazardous substances, many acting as endocrine disruptors, have been linked to a range of reproductive issues such as infertility, menstrual irregularities, spontaneous abortions, birth defects, endometriosis, and breast cancer. In particular, women may face higher risks than men, especially due to the increasing prevalence of environmental estrogens. However, only a small subset of these chemicals has been thoroughly evaluated for their toxicity and the potential synergistic effects arising from multiple simultaneous exposures. There is a pressing need for enhanced awareness and careful monitoring of how environmental pollution influences reproductive health. © 2000 International Federation of Gynecology and Obstetrics.
Keywords: Environment; Chemicals; Reproduction; Infertility; Gynecological cancers; Fetal malformation; Occupational hazards.
Introduction
An individual’s overall health is influenced by the dynamic interaction between their internal bodily environment and the external surroundings. Ensuring good health requires access to clean air, safe drinking water, and a diet free from harmful toxins. Regrettably, the quality of the air, water, and food we depend on is steadily declining due to the expansion of industries and the extensive use of chemicals in agriculture to meet societal demands. As society becomes increasingly reliant on technological advancement, this progress often comes at a considerable cost to health.
This problem is particularly acute in developing countries, where rapid industrialization often occurs with little regard for environmental protection. Despite the presence of legislation aimed at curbing industrial pollution, such laws are frequently ignored, and factories continue to release toxic waste into the environment without consequence. In contrast, developed countries have implemented stricter regulations to control pollution; however, many have transferred their hazardous industries and waste disposal to developing nations, a practice termed ‘Industrial neo-colonialism’ by David Nelson of the US Environmental Protection Agency [1].
Until recently, obstetricians largely overlooked the effects of the environment on reproductive health. Their focus was predominantly on treating individual cases of infertility, miscarriages, obstetric hemorrhages, low birth weight infants, and congenital abnormalities without recognizing that environmental factors might contribute to these conditions. The modern obstetrician now acknowledges that environmental influences, directly or indirectly, play a significant role in reproductive processes. For example, water pollution leads to infections such as dysentery, typhoid, and viral hepatitis, which can cause preterm births and low birth weight babies. Likewise, occupational diseases like asbestosis and silicosis negatively affect reproductive outcomes.
Environmental concerns have gained urgency as increasing numbers of pregnant women and children are exposed to polluted surroundings. The wave of industrialization, coupled with consumer-driven lifestyles and the extensive use of pesticides, disinfectants, and insecticides, disrupts the ecological balance (Fig. 1). Moreover, more women are now employed in industries that handle hazardous substances such as mercury, lead, arsenic, and organic solvents. These pregnant workers are at elevated risk of adverse obstetric effects.
According to data from the US Agency for Toxic Substances and Disease Registry (ATSDR) National Exposure Registry, women exposed to hazardous chemicals report greater adverse health effects than the general population and often more than exposed men. The registry, which includes subregistries for chemicals like benzene, trichloroethylene (TCE), trichloroethane (TCA), and dioxin, aims to assess the long-term health impacts of exposure to environmental hazards. Female and male registrants consistently report increased rates of anemia, blood disorders, skin rashes, and strokes relative to national norms from the National Health Interview Survey. Females particularly experience higher incidences of diabetes, kidney and liver disorders, and urinary tract issues, suggesting that chronic low-level exposure to hazardous substances over time contributes to these outcomes [2].
Within occupational and environmental medicine, the most concerning women’s health issues relate to the reproductive effects caused by workplace exposures. The entire reproductive cycle can be jeopardized by exposure to both physical and chemical agents encountered at work, as well as in home and general environments. Key concerns include infertility and subfertility, spontaneous abortions, including early undetectable losses, teratogenesis and congenital anomalies, mutagenesis and inheritable defects, cancer in offspring linked to substances like diethylstilbestrol (DES), and occupationally induced genital and breast cancers [3].
Substances of concern
Numerous synthetic chemicals and metals have been identified as detrimental to human reproduction and development. For instance, lead, widely used in industries such as printing, painting, and battery manufacturing, is capable of crossing the placental barrier as early as the 12th week of pregnancy, posing risks to fetal brain development. Research by Hamilton revealed that women married to men employed in lead-related industries exhibit a significantly higher rate of miscarriages, preterm labor, and stillbirths compared to the general population [4]. Similarly, Nagako observed increased miscarriage rates among women directly exposed to lead at work [5]. Mercury, found in several fungicides and frequently handled by women, has demonstrated, through animal experiments, a capacity to disrupt embryogenesis in rodents [6]. Exposure to certain solvents correlates with increased spontaneous abortions in female workers; specifically, glycol ethers and epichlorohydrin impair male reproductive function, while toluene is linked to birth defects at elevated maternal exposures. Workers handling pesticide mixtures also face heightened risks of spontaneous abortion and congenital abnormalities. Certain pesticides, such as ethylene oxide (used for sterilizing medical tools), benomyl, and cyanazine (employed in agriculture), have been clearly linked to adverse reproductive outcomes. Although the scientific data is still emerging, other substances—including cadmium, manganese, and solvents like xylene, styrene, and perchloroethylene—along with various pesticides and plasticizers, are suspected to impair reproductive health [7].
Among environmental toxins, dioxin—one of the most potent chemicals—is not classified as an environmental estrogen but can inhibit estrogen action, reduce androgen (male hormone) levels, and disrupt thyroid hormone production. It may also alter insulin secretion and the amount of glucocorticoids from the adrenal glands. Dioxin exposure has been associated with endometriosis. Pregnant animals exposed to minuscule dioxin doses during critical windows experience reproductive system damage in offspring, including reduced sperm counts and altered sexual behavior. Many environmental pollutants mimic estrogen, potentially contributing to breast and uterine tumors [10]. The term endocrine disrupters, introduced by Theodora Colborn, describes chemicals that interfere with or imitate hormonal actions, disturbing normal growth, behavior, and reproductive processes. These disruptors may cause temporary effects in adults but can induce permanent malformations in fetuses by sending incorrect hormonal signals or blocking legitimate ones. Chemicals such as dioxins, PCBs, dicofol, and DDT-related compounds are recognized endocrine disruptors [10].
Animal studies indicate that even a single, tiny dose of dioxin during a sensitive developmental period can cause lifelong health consequences for offspring. Men exposed to Agent Orange, a herbicide containing dioxin, have an increased likelihood of fathering children with birth defects. Likewise, maternal exposure to PCBs is linked to developmental delays in children. Both dioxin and PCBs disrupt reproduction and development by interfering with hormones. Many consumer products—including plastics, paints, detergents, cosmetics, and pesticides—contain chemicals suspected of acting as endocrine disruptors. Although the full impact of many of these toxins remains unclear, there is growing concern about their potential health risks [7].
Effects of estrogenic compounds have long been documented in wildlife, with classic examples including eggshell thinning that led to the decline of the American bald eagle and reproductive abnormalities in women exposed prenatally to diethylstilbestrol (DES), a synthetic estrogen prescribed between 1948 and 1971 to prevent miscarriages [11]. Recent research has expanded the list of environmental chemicals with estrogenic activity to 45 known or suspected compounds. These include herbicides, fungicides, insecticides, nematocides, and industrial byproducts such as metals, PCBs, dioxins, styrenes, and nonylphenols. Wildlife biologists warn that endocrine disruptors jeopardize many animal populations. Documented effects in wildlife include thyroid dysfunction, reduced fertility, decreased hatching success, gross birth deformities, feminization of male animals, masculinization of females, and compromised immune systems across multiple species [11].
Many of these consequences are evident in species inhabiting or near the Great Lakes, where synthetic chemicals, such as PCBs and pesticides (some banned like DDT), are prevalent. For example, herring gull embryos and chicks from Lake Ontario exhibit malformations of reproductive organs. Juvenile salmon frequently show enlarged thyroid glands, and birds feeding on contaminated fish suffer reproductive failures and early offspring mortality. Similar issues are reported in other heavily polluted drainage basins. Notably, in Lake Apopka, Florida, alligator egg hatch rates are drastically reduced, with surviving hatchlings displaying abnormal hormone levels and genital deformities. These problems have been linked to pesticide contamination from the nearby Tower Chemical Company, which produced the pesticide dicofol, containing up to 15% DDT or DDE. Following spills and contamination events, Lake Apopka became a Superfund site. Laboratory experiments have replicated these abnormalities by applying estrogenic chemicals to eggs, reinforcing concerns about environmental estrogens [11].
Research highlights several important principles regarding endocrine disruptors: firstly, adverse effects frequently manifest in offspring rather than directly in exposed adults; secondly, the timing of exposure relative to developmental stages critically influences outcomes; thirdly, effects in embryos, fetuses, and newborns can differ drastically from those in adults exposed later in life; and lastly, due to delayed manifestation, health problems may only become apparent when exposed offspring reach maturity or middle age, potentially threatening species’ reproductive futures despite apparently healthy adults and juveniles [11].
Reproductive health effects
There is compelling evidence that environmental estrogens adversely affect wildlife, and although evidence for similar risks to humans remains incomplete, it raises significant concern. Researchers are exploring the possibility that these chemicals, through subtle biochemical and physiological disruptions, interfere with human development when exposure occurs prenatally or shortly after birth. These estrogen mimics are particularly potent because they can cross the placenta, exposing the fetus to higher hormone levels than normal, which can disturb the delicate hormonal balance governing fertility and even gender development [11].
In males, certain studies suggest that estrogenic compounds impair the development of Sertoli cells in the testes, which produce masculinizing hormones crucial for sperm production, testicular descent, and urethral development. There has been a noted rise in undescended testes among newborn males in the UK between 1970 and 1987, alongside urinary tract abnormalities [11,12]. For females, researchers suspect that a significant increase in ectopic pregnancies in the USA during the same period and a concurrent rise in breast cancer cases may be linked to exposure to pesticides and endocrine disruptors. Some studies find higher DDE levels in the blood of women with breast cancer compared to healthy controls. Breast cancer incidence has grown at about 1% annually over the past five decades. Despite extensive research, known risk factors explain only about 30% of breast cancer cases; the rest may be influenced by lifetime exposure to reproductive hormones. Factors such as age at menarche, first pregnancy, menopause, calorie intake, family history, and radiation all relate to hormonal exposure. Scientists are investigating how artificial estrogens might interact with breast cancer susceptibility genes, potentially promoting tumor development. Confirming this link could lead to preventive measures by limiting chemical exposures [11,13].
In a study involving 621 Michigan nurse anesthetists, Corbet et al. [14] found that birth defects occurred nearly three times more frequently in children of nurses practicing anesthesia during pregnancy compared to those who were not exposed. Wyatt [15] also reported increased risks of abortion, stillbirth, and fetal malformations among female anesthetists, likely due to prolonged inhalation of anesthetic gases.
With the rise of video-display terminals in offices and homes, concerns about ionizing radiation exposure emerged. Although X-rays are known reproductive hazards, the cathode ray tubes used in such terminals emit low-energy radiation absorbed by the glass screen. Recent literature suggests women working with these terminals do not face elevated reproductive risks [16,17]. Nonetheless, clinical evaluations of reproductive health should include detailed patient histories regarding occupational and environmental exposures [18].
Establishing links
The hypothesis that weakly estrogenic environmental chemicals may influence human health has ignited debate within toxicology. Key controversies concern whether animal study results are applicable to humans, whether low-level exposures pose risks of fertility impairment or cancer, and whether concerns have been exaggerated. Estimating the proportion of birth defects caused by environmental factors is challenging because establishing causal links between specific pollutants and malformations is difficult. Despite these challenges, ongoing research seeks to clarify these associations and better understand the implications for public health.
Taking an environmental history
Currently, over 70,000 synthetic chemicals and metals are in commercial circulation in the USA alone, with the toxicity of most substances either unknown or insufficiently studied. Human exposure to some of these chemicals has been linked to serious health outcomes such as cancer, reproductive and developmental disorders, and adverse neurological and immunological effects. Of particular concern are reproductive and developmental impacts because they bear significant consequences for couples trying to conceive and because exposure to specific agents during critical periods of fetal or infant development can have lifelong and even transgenerational effects. Both occupational and environmental exposures can result in episodic, acute, or chronic illnesses, making it essential to routinely include such inquiries as part of every patient’s history and physical examination. Crucial information can be obtained by exploring the individual’s current or past work and hobbies, focusing on the frequency of exposure, including daily or occasional contact with hazardous substances, and specifying particular job classifications and chemicals handled at the workplace. It is important to identify exposure to fumes, dust, or chemicals not only at work but also at home or during hobbies, ensuring that detailed information such as the brand or chemical names is gathered, as generic chemical classes often do not provide adequate insight into health risks. The occupational and hobby-related exposures of family members, including spouses, partners, and children, should also be considered. It is valuable to document any physical symptoms that occur at work or during exposure episodes, and to assess environmental controls such as the level of ventilation in the work or hobby area, as well as the results of any air quality monitoring performed in the workplace. Additionally, the use of personal protective equipment such as gloves, respirators, and protective clothing must be noted, along with hygiene practices like the availability and frequency of hand-washing or shower facilities at work. Any history of accidents or exposure incidents at work, home, or in the community, as well as the use of household chemicals or pesticides, should be recorded. The data collected through such comprehensive environmental histories play a vital role in helping to establish meaningful connections between environmental exposures and reproductive health problems.
Conclusion
When the causative factors of illness are unclear or difficult to determine, occupational or environmental influences may contribute, though their significance can be challenging to confirm. Many exposures may actively or potentially influence a wide range of conditions, yet some occupational and environmental factors might turn out to be red herrings, with many presumed household exposures falling into this category. Numerous suspected associations between women’s health issues and environmental factors have been proposed. Some, such as concerns related to video display terminal (VDT) use and spontaneous abortion, have not been substantiated by rigorous scientific investigation, while others—such as exposure to tobacco smoke, second-hand smoke, household chemicals (including radon and solvents), alcohol, and heavy metals—may indeed have health impacts. From the standpoint of occupational and environmental medicine, there remain many priority research needs addressing women’s health and environmental exposures. Media coverage has brought increased public and scientific focus to the issue of rising environmental pollution levels. Despite this attention, toxicological data often remain incomplete. Traditional animal studies typically evaluate the health effects of individual chemicals in isolation, failing to account for interactive or synergistic effects arising from exposure to multiple chemicals simultaneously. Furthermore, animal testing frequently overlooks subtle, delayed, or hard-to-diagnose conditions. Human epidemiological studies are often hampered by inaccurate exposure assessments and incomplete health outcome data. Adding to the complexity, government funding for research and data analysis is frequently limited or absent, especially in developing countries, creating a vacuum that corporate sponsorship may fill, potentially introducing biases in study design and interpretation. Without robust research and irrefutable evidence, effective preventive interventions to mitigate the adverse effects of environmental pollution on reproductive health cannot be implemented. A heightened level of awareness and vigilance is essential to address this escalating challenge, which will likely increase in scope as society progresses further into the 21st century.
Acknowledgment:
The author gratefully acknowledges the support and guidance of the Environmental Health Research Group at Greenfield University. Special thanks to Dr. Michael Chen for his valuable insights during the preparation of this manuscript. The author also appreciates the contributions of the university’s library staff for providing access to critical resources.
Conflict of Interest:
The author declares no conflicts of interest related to this research. No financial or personal relationships influenced the work reported in this paper.
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