In recent years, fertility clinics have begun observing a contradiction that routine investigations fail to adequately explain, says Dr Radhika Sheth, Medical Director, Luma Fertility. Women with predictable cycles, acceptable ovarian reserve for their age, and no obvious gynaecological pathology are producing poor-quality embryos, experiencing repeated implantation failure, or showing an unexpectedly rapid decline in reproductive potential. “The question is no longer whether this is coincidental,” she notes, “but why our diagnostic frameworks have been so slow to account for it.”
Hormonal function does not deteriorate suddenly. It erodes. And, as Dr Sheth explains, environmental exposure accelerates this erosion in ways that standard fertility
testing simply does not capture.
Endocrine-disrupting chemicals do not behave like classic hormonal disorders. They rarely stop ovulation or eliminate menstruation. Instead, Dr Sheth points out, they interfere at a cellular and receptor level. Estrogen signalling becomes exaggerated or erratic, progesterone response weakens, inflammatory pathways remain chronically activated, and mitochondrial function within eggs and sperm deteriorates. “The menstrual cycle continues,” she says, “but its biological efficiency declines.”
Clinically, this disruption presents subtly. Progesterone levels may fall within ‘normal’ laboratory ranges yet fail to adequately sustain implantation. Ovarian stimulation may yield eggs, but a disproportionate number arrest early or develop into embryos with limited competence. Miscarriages occur despite apparently reassuring reports. “These are not random failures,” emphasises Dr Sheth. “They reflect cumulative exposure over time.”
Air pollution is one of the most consistent contributors to this pattern. According to Dr. Sheth, fine particulate matter induces oxidative stress that directly affects ovarian follicles and sperm DNA. “The impact is rarely dramatic enough to alter menstrual timing,” she explains, “but it is sufficient to compromise gamete quality.” In cities with persistently high pollution levels, fertility clinics are increasingly seeing younger patients requiring higher stimulation doses for poorer outcomes, a trend that cannot be explained by age or lifestyle factors alone.
Plastic exposure further compounds the problem. Chemicals such as bisphenols and phthalates exert estrogen-mimicking effects while simultaneously impairing progesterone receptor sensitivity. Clinically, Dr. Sheth notes, this often presents as adequate follicle development followed by poor luteal support, recurrent biochemical pregnancies, or embryos that implant briefly and fail. In men, sperm counts may appear acceptable while DNA fragmentation remains high, a factor often overlooked until multiple IVF failures occur.
What makes environmental hormonal disruption particularly difficult to address, says Dr Sheth, is that it operates below the threshold of routine diagnosis. Menstruation continues. Ultrasounds appear reassuring. Standard hormone panels offer comfort rather than clarity. “By the time infertility is recognised,” she explains, “the biological environment may have been compromised for years.”
In the Indian context, these effects are further amplified. High ambient pollution, widespread plastic use, agricultural chemical exposure, and limited regulation of endocrine disruptors coexist with delayed fertility planning. Patients often arrive at clinics expecting technology to compensate for biology that has been under chronic strain. “Assisted reproduction can work around many barriers,” Dr Sheth clarifies, “but it cannot fully reverse cellular damage.”
This is not an argument against IVF. It is, as Dr. Sheth describes, an argument for realism. Reproductive medicine must expand its understanding of risk beyond ovaries, sperm counts, and cycle charts. Environmental load, metabolic health, and inflammatory status are not peripheral concerns, they directly influence outcomes.
The implications extend beyond fertility. Hormonal disruption during reproductive years is linked to long-term metabolic dysfunction, cardiovascular risk, bone density loss, and mood disorders. “Fertility challenges are often the first visible sign,” says Dr. Sheth, “not the final consequence.”
Pollution and plastic exposure do not announce themselves as disease. They present instead as declining efficiency, inconsistent outcomes, and unexplained failure. The danger lies precisely in their subtlety. If reproductive care continues to focus only on cycle regularity and isolated hormone values, interventions will remain delayed and explanations incomplete.
“A regular cycle is not evidence of hormonal resilience,” Dr. Sheth concludes. “It is merely evidence of adaptation. The cost of that adaptation becomes visible only when the system is pushed often when fertility is already compromised.”
