Persistent Organochlorine Pollutants and Male Fertility: A Narrative Review of Human Exposure-response Evidence
Gulshara A. Berdesheva¹, Bakhytzhan A. Duisembekov, Saulesh Seitzhanovna Kurmangaliyeva, Mukhtar S. Zhailybayev, Elmira D. Ismagulova, Dilnaz A. Aidyngaliyeva, Madina I. Yakupova, Bakhyt S. Atzhaxynova, Andrej M. Grjibovski
A
BSTRACT
Background:
Chlorinated pesticides and related persistent organochlorine pollutants (POPs), including polychlorinated biphenyls (PCBs), dioxins (2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD]), and hexachlorobenzene, are persistent environmental contaminants whose reproductive effects have been studied predominantly in women, leaving evidence for male reproductive health fragmented.
Objective:
To summarize human evidence on exposure-response relationships between chlorinated pesticides, related POPs, and male fertility outcomes.
Methods:
A structured, nonsystematic search was conducted in PubMed, OpenAlex, and Elicit, covering chlorinated pesticides (dichlorodiphenyltrichloroethane, lindane, dieldrin, aldrin, endosulfan, chlordecone, and 1,2-dibromo-3-chloropropane [DBCP]) and related POPs (PCBs/CB-153, TCDD/dioxins, hexachlorobenzene). Studies were included if they assessed human males, measured exposure, reported a fertility outcome, and provided a quantifiable exposure measure, per CINAR narrative-review guidelines.
Results:
The most consistent finding was an inverse exposure-response association with sperm motility, with formal dose-response evidence shown for compounds such as CB-153, p,p’-DDE, β-hexachlorocyclohexane (HCH), TCDD, and DBCP, while γ-HCH showed a binary exposure-response association (detectable versus non-detectable) rather than a formally tested dose-response trend. Sperm concentration and morphology showed less consistent associations, evident mainly during peripubertal exposure. A “testosterone paradox” emerged: very high chronic exposures were associated with elevated testosterone and estradiol, whereas moderate exposures showed suppression, though the mechanism remains hypothetical. Developmental timing critically modified effects, and exposure-response associations, including dose-response trends, were also documented for sperm DNA fragmentation, aneuploidy, and epigenetic alterations.
Conclusions:
Available evidence suggests exposure-response associations between chlorinated pesticides, related POPs, and impaired male fertility, most consistently sperm motility, with developmental timing as an important effect modifier. Given the largely cross-sectional evidence base, causal inference should remain cautious. Prospective cohorts assessing developmental exposure windows are needed, particularly in under-studied regions such as Central Asia.