{"paper_id":"3bf2caa2-03b5-4a21-9162-95768fba1686","body_text":"Journal of Gynecology and Obstetrics \n2026, V ol. 14, No. 1, pp. 13–29 \nhttps://doi.org/10.11648/j.jgo.20261401.12  \n \n \n \nReceived: 27 November 2025; Accepted: 18 December 2025; Published: 20 January 2026 \n \nCopyright: © The Author(s), 2026. Published by Science Publishing Group. This is an Open Access article, distributed \nunder the terms of the Creative Commons Attribution 4.0 License ( http://creativecommons.org/licenses/by/4.0/), which \npermits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited. \n \nReview Article \nThe Potential Role of Vaping in the Increasing Burden of \nEndometriosis Among Women of Reproductive Age in Sub-\nSaharan Africa: A Public Health Concern \nKalala Elisee Kabuya1, * , Mukasa Charline Sangany2  \n1Department of Public Health, Africa University, Manicaland-Mutare, Zimbabwe \n2Department of Health Science, School of Laboratory of Medicine and Medical Science, University of Kwazulu-Natal, \nDurban, South Africa \n \nAbstract \nThe use of electronic nicotine delivery systems (ENDS) is increasing rapidly across Sub -Saharan Africa (SSA), particularly \namong young women, while endometriosis remains substantially underdiagnosed in the region. Emerging evidence suggests that \nvaping may influence hormonal, inflammatory, and oxidative pathways relevant to endometriosis. This scoping review followed \nPRISMA guidelines and searched PubMed, Web of Science, Scopus, African regional databases, and grey literature to identify \nstudies examining vaping exposure in relation to reproductive or hormonal outcomes and gynecologic pathology. Eligible studies \nwere appraised using the Newcastle –Ottawa Scale and STROBE criteria, and findings were narratively synthesized due to \nmethodological heterogeneity. Across epidemiologic and mechanistic domains, the evidence indicates that nicotine -product use \nis associated with higher odds of dysmenorrhea and suspected endometriosis; disrupts the hypothalamic –pituitary–gonadal axis \nand estrogen–progesterone signaling; induces oxidative stress, mitochondrial dysfunction, and NF-κB activation; and may drive \nepigenetic and immune alterations that promote endometrial adhesion, angiogenesis, and impaired fertility. Contextual \nvulnerabilities in SSA including environmental co -exposures, infectious disease burden, limited diagnostic capacity, and dual \nuse of vaping with alcohol may further amplify these risks. Although direct causal data from SSA remain limited, the convergence \nof biological plausibility and emerging epidemiologi c signals highlights vaping as a potential reproductive health concern, \nunderscoring the need to integrate vaping into sexual and reproductive health guidelines and to prioritize region-specific research. \nKeywords \nVaping, Endometriosis, Sub-Saharan Africa, Women of Reproductive Age, Public Health \n \n1. Introduction \nSub-Saharan Africa (SSA), home to the world ’s youngest \npopulation, is undergoing rapid social and behavioral \ntransitions amid persistent public health and socio -economic \nchallenges. One emerging concern is the growing popularity \nof vaping and electronic ni cotine delivery systems (ENDS), \nparticularly among urban youth and women of reproductive \n\n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n14 \nage. As traditional cigarette sales decline in high -income \ncountries, multinational tobacco companies are increasingly \ntargeting SSA as a growth market [1]. In this context, vaping \nhas evolved into a prominent lifestyle trend, often perceived \nas a safer alternative to smoking, despite insufficient evidence \nregarding its long -term health effects especially among \nwomen [2]. \nCurrently, an estimated 13 million women in SSA use \nvarious tobacco products, including snuff, chewing tobacco, \nand water pipes such as shisha and hookah. Alarmingly, the \ngender gap in tobacco and nicotine use is narrowing, with \nprevalence among girls now ranging from 4.6% to 36.6%, \ncomparable to rates among boys [3, 4] . Despite being \npreventable, tobacco -related conditions contribute to \napproximately 22,000 female deaths annually in the region [5], \nwith projections showing a doubling of such deaths in low - \nand middle-income countries by 2030 [6]. Moreover, about 64% \nof adult deaths from second-hand smoke occur among women, \nmost of whom are exposed through household contact with \nmale smokers [7]. Yet, emerging patterns of direct exposure to \nvaping and nicotine among young women warrant renewed \nscrutiny from a reproductive health perspective. \nIn parallel, endometriosis, a chronic and often debilitating \ngynecological disorder characterized by ectopic growth of \nendometrial tissue remains underdiagnosed and undertreated \nin SSA [8]. Limited access to diagnostic  tools, shortages of \ntrained healthcare personnel, financial barriers, and cultural \nstigma surrounding menstrual health significantly impede \nearly detection and effective management [9]. The condition \ncontributes to severe pelvic pain, infertility, and a d ecline in \noverall quality of life. Qualitative research in countries like \nKenya has documented the profound psychosocial and \nmedical challenges faced by women with endometriosis, \nemphasizing delayed diagnoses and fragmented care \npathways [10]. \nDespite its burden, endometriosis is still erroneously \nperceived as rare among African women, leading to an \nalarming lack of research, awareness, and targeted \ninterventions [11]. The double burden of rising nicotine \nexposure through vaping and the already inadequate response \nto endometriosis represents a neglected but urgent public \nhealth issue. Nicotine and other chemicals present in e -\ncigarettes are known to disrupt hormonal function, induce \noxidative stress, and provoke inflammatory responses, \nmechanisms also implic ated in the pathogenesis of \nendometriosis [12]. Yet, no existing studies have directly \nexplored the potential relationship between vaping and \nendometriosis in the African context. \nGiven the increasing uptake of vaping among reproductive-\naged women in SSA a nd the persistent underrecognition of \nendometriosis, this study addresses a critical gap [13]. It aims \nto systematically review the existing evidence on the health \neffects of vaping, with a particular emphasis on its potential \nrole in the development or pr ogression of endometriosis. The \nstudy also seeks to assess the prevalence and awareness of \nvaping among women in the region, explore biological \nmechanisms linking nicotine exposure to reproductive \ndysfunction, and identify research and policy gaps. Ultimately, \nthe goal is to inform comprehensive public health responses \nand policies aimed at safeguarding women ’s reproductive \nhealth amid evolving tobacco and nicotine consumption \npatterns in SSA. \n2. Literature Review \nTobacco and nicotine use among women and gi rls in SSA \nhas historically been low compared to men [14]; however, \nrecent trends indicate a growing prevalence of smoking and, \nincreasingly, vaping among young women [15]. Studies from \nNigeria and other African countries highlight that although \ncurrent sm oking rates among women of reproductive age \nremain relatively low, shifting social norms and targeted \nmarketing necessitate more women -focused prevention \nstrategies [16, 17]. In parallel, the rapid expansion of the e -\ncigarette market has facilitated increa sed adoption of vaping \nacross SSA, particularly among adolescents and young adults \n[18]. This rise is largely driven by widespread perceptions of \nreduced harm relative to traditional cigarettes, aggressive \nglobal marketing campaigns, and the growth of onli ne and \ninformal markets that bypass regulatory oversight [19, 20]. \nE-cigarettes deliver nicotine alongside heavy metals and \nvolatile organic compounds that exert multiple physiological \neffects relevant to women’s reproductive health [21]. Nicotine \nexposure is known to trigger catecholamine release, increase \nsystemic oxidative stress, and stimulate inflammatory \npathways, creating biological conditions that may negatively \naffect reproductive tissues [22, 23]. Despite persistent claims \nof reduced harm, misconceptions about the safety of vaping \nremain common among young women, particularly in urban \nsettings where targeted digital advertising and social media \nportray vaping as trendy, modern, and socially acceptable \n[24]. Regulatory frameworks in SSA are inconsistent, ranging \nfrom comprehensive restrictions in some countries to \ncomplete policy absence in others, thereby facilitating \nwidespread accessibility and unregulated marketing [25, 26]. \nEmerging evidence suggests increasing uptake among gi rls \nand young women aged 15 years and older, driven by \nmotivations such as stress relief, social acceptance in nightlife \ncontexts, and targeted online promotion [27]. \nThe potential implications of these trends for women ’s \nreproductive health are particular ly important in relation to \nendometriosis, a chronic gynecological disorder characterized \nby the presence of endometrial -like tissue outside the uterus \n[28]. Endometriosis is driven by interrelated processes such as \nhormonal dysregulation, immune dysfuncti on, oxidative \nstress, and angiogenesis, all of which contribute to lesion \nproliferation, chronic inflammation, pelvic pain, and \ninfertility [29]. [30] asserted that in SSA, endometriosis \nremains substantially underdiagnosed due to limited \ndiagnostic expert ise, insufficient specialist services, cultural \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n15 \nstigma surrounding menstrual pain and infertility, and low \npublic awareness of the condition. These factors delay care -\nseeking and contribute to severe disease presentation among \nmany women [31, 33] . Research  from countries such as \nUganda further highlights widespread misconceptions about \nreproductive disorders, with some women viewing infertility \nas more socially devastating than other health conditions, \nunderscoring the sociocultural dimensions that complica te \ndiagnosis and management [34]. \nExisting evidence suggests several plausible biological \npathways through which nicotine exposure from vaping could \ninteract with the mechanisms underlying endometriosis [35]. \nNicotine has been shown to increase oxidative s tress, alter \nestrogen receptor expression, [36] modulate immune \nresponses, and promote pro -inflammatory cytokine activity \nmechanisms that overlap significantly with endometriosis \npathophysiology and may facilitate the survival or progression \nof ectopic lesions[37]. Although animal studies suggest that e-\ncigarettes may produce fewer reproductive impacts in males \nthan combustible tobacco, the evidence base for women ’s \nreproductive health remains extremely limited and \ninconclusive [38], with virtually no studies directly examining \nvaping and endometriosis [39]. This scientific gap is \nparticularly concerning given the rapid increase in vaping \namong young women in urban African contexts. \nContextual factors in SSA may further compound the \npotential reproductive hea lth risks associated with vaping. \nHigh levels of urban air pollution, [40] environmental \nexposure to heavy metals, and poor regulation of consumer \nproducts may intensify oxidative stress pathways already \nimplicated in both vaping aerosol exposure and endometriosis \ndevelopment [41]. Cultural stigma surrounding gynecologic \npain and limited health literacy reduce early diagnosis and \ncompound women ’s vulnerability to reproductive morbidity \n[42]. Simultaneously, expanding urban nightlife, increased \nsocial media exposure, and the normalization of vaping \namong peer groups contribute to rising uptake among young \nwomen, even as policy enforcement remains weak, and health \neducation interventions are limited [43]. \nTaken together, these trends highlight an urgent and \nunderstudied intersection between rising vaping prevalence \nand the existing burden of endometriosis in SSA [44]. The \nbiological plausibility linking nicotine and vaping \nconstituents to endometriosis mechanisms, combined with \ncontextual vulnerabilities such as poor regulation, stigma, and \nenvironmental stressors, indicates that vaping may represent a \nmodifiable risk factor for exacerbating reproductive health \nchallenges [45]. This review therefore aims to synthesize \navailable evidence on vaping and its potenti al contribution to \nendometriosis among women of reproductive age in SSA, \nexamining prevalence patterns, awareness levels, biological \npathways, and regulatory gaps to inform comprehensive \npublic health policies and targeted interventions that safeguard \nwomen’s reproductive health in the region. \n3. Methodology \n3.1. Review Design \nThis study employed a systematic scoping review \nframework aligned with PRISMA guidelines to promote \ntransparency, reproducibility, and methodological rigor. Its \nprimary aim was to explore whether vaping (e -cigarette use) \nis associated with the rising burden of endometriosis among \nwomen of reproductive age in SSA. The literature search \nencompassed studies published up to 2024 that investigated \nvaping, hormonal or reproductive health outcomes, and \ngynecological conditions pertinent to endometriosis. \n3.2. Search Strategy \nA systematic search was conducted in PubMed, Scopus, and \nWeb of Science to identify studies examining vaping, nicotine \nexposure, and endometriosis among women of reprod uctive \nage, with relevance to Sub -Saharan Africa (SSA). Searches \ncombined controlled vocabulary and keywords related to: \n1) Exposure: “vaping,” “ e-cigarette,” “ electronic nicotine \ndelivery systems,” “nicotine exposure” \n2) Outcome: “endometriosis,” “ reproductive health,” \n“female fertility” \n3) Mechanisms: “oxidative stress, ” “estrogen imbalance, ” \n“inflammation” \n4) Context: “Sub-Saharan Africa,” “developing countries” \nBoolean operators such as (vaping OR e -cigarette) AND \n(endometriosis OR reproductive health) were applied . Limits \nincluded English-language, human females aged 15–49, and \npublications up to December 2024. \nTo enhance completeness, manual reference -checking and \ngrey literature searches were conducted using OpenGrey, \nWHO Global Health Library, and African Journals Online \n(AJOL). \n3.3. Inclusion and Exclusion Criteria \nPredefined inclusion and exclusion criteria ensured the \nrelevance and quality of the selected studies. \nInclusion Criteria: \n1) Were peer-reviewed and published in English \n2) Included human data or translational animal/mechanistic \ndata relevant to endometriosis \n3) Assessed vaping, nicotine exposure, or biological \nmechanisms linked to endometriosis \n4) Reported outcomes related to endometriosis or \nreproductive health \n5) Were conducted in SSA or produced findings applicable \nto SSA contexts \nExclusion Criteria \n1) Were non-English \n2) Showed no relevance to nicotine/vaping or \nendometriosis \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n16 \n3) Did not report original data (e.g., narrative reviews, \ncommentaries) \n4) Focused exclusively on non-reproductive populations or \nunrelated outcomes \n3.4. Screening Process \nAll retrieved records were imported into EndNote, and \nduplicates removed. Screening followed PRISMA guidelines: \nTitle and Abstract Screening: Two independent reviewers \nscreened records against the eligibility criteria. \nFull-Text Review: Full texts of potentially relevant studies \nwere reviewed independently by two reviewers. \nDisagreements were resolved through discussion or third -\nreviewer adjudication. \nAll screening decisions were documented to ensure \ntransparency and reproducibility. \n3.5. Data Extraction Process \nA standardized data extraction form was developed to \nensure uniformity and minimize errors. Two reviewers \nindependently extracted the following data: \nStudy characteristics: Authors, year of publication, study \ndesign, and country. \nPopulation details: Sample size, participant age range, and \nreproductive health status. \nExposure variables: Type and frequency of vaping or e -\ncigarette use, duration, and nicotine concentration. \nOutcome variables: Endometriosis diagnosis, sympt om \nseverity, hormonal levels (e.g., estrogen, progesterone), \nmenstrual cycle regularity, and fertility indicators. \nConfounding factors: Lifestyle behaviors, co -use of \ntobacco or alcohol, and occupational exposures. \nPolicy or regulatory context: Existing national or \ninstitutional frameworks addressing vaping or women ’s \nhealth. \nDisagreements were resolved by consensus or by \nconsultation with a senior reviewer. \n3.6. Risk of Bias Assessment \nThe Newcastle-Ottawa Scale (NOS) was used to assess the \nrisk of bias in observational studies. Each study was evaluated \non three domains: \nSelection of participants, \nComparability of groups, and \nAscertainment of exposure and outcomes. \nTwo reviewers conducted the assessments independently. \nStudies with high risk of bias were not excluded but were \ninterpreted cautiously in the narrative synthesis. \n3.7. Quality Assessment of Studies \nThe STROBE (Strengthening the Reporting of \nObservational Studies in Epidemiology) checklist was used to \nevaluate the methodological quality of included studies. Each \nstudy’s adherence to STROBE criteria such as clarity in \nobjectives, participant selection, data collection, and statistical \nanalysis was documented in a summary table and considered \nin the synthesis. \n3.8. Data Synthesis and Analysis \nDue to the heterogeneity in study designs, populations, and \noutcome measures, a meta-analysis was not feasible. Instead, \na narrative synthesis was conducted to summarize evidence \non: \n1. The association between vaping exposure and \nendometriosis prevalence or severity. \n2. Biological mechanisms linking nicotine, oxidative \nstress, and hormonal dysregulation to endometriosis. \n3. Regional variations and contextual factors influencing \nvaping behaviors among women in SSA. \n4. Policy implications and gaps in existing reproductive \nhealth interventions. \nWhere feasible, subgroup analyses were conducted based \non age group, duration of vaping, nicotine concentration, and \nconcurrent tobacco or alcohol use. \n3.9. PRISMA Flow Diagram \nA PRISMA flow diagram was constructed to det ail the \nliterature selection process, including the number of studies \nidentified, screened, excluded (with reasons), and included in \nthe final review. \n3.10. Summary of Evidence \nA summary table was created to present the characteristics \nof included studies: \nStudy location (country or city in SSA). \nStudy design (cross-sectional, case-control, cohort). \nSample size and participant demographics. \nType of vaping exposure (nicotine-based or nicotine-free). \nPrimary outcomes (endometriosis incidence, menstrual \npain, infertility). \n3.11. Limitations and Future Research \nThis review recognizes limitations such as limited regional \ndata, potential underreporting of vaping among women, and \nheterogeneous diagnostic criteria for endometriosis across \nstudies. Future research should focus on longitudinal and \ninterventional studies to better establish causality, \nbiochemical studies to elucidate hormonal mechanisms, and \npolicy-oriented research to assess regulatory frameworks and \nprevention strategies in SSA. \n \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n17 \n4. Pathophysiological Basis \nIn female mammals, reproduction is regulated through \ncomplex mechanisms that integrate environmental, hormonal, \nand resource -related cues, particularly suppressing \nreproductive activity during periods of resource scarcity [46]. \nDisruptions to thes e regulatory systems such as hormonal \nimbalances or adverse environmental exposures can lead to \nreproductive disorders, including endometriosis [47]. \nEndometriosis is characterized by the ectopic growth of \nendometrial tissue and is associated with chronic pelvic pain, \ninfertility, and inflammation [48]. \nThe endometrium is a dynamic tissue composed of luminal \nand glandular epithelial cells supported by stromal cells, \nforming the innermost lining of the uterus [49]. Estrogen \ndominance plays a central role in the pathophysiology of \nendometriosis, driving the proliferation of ectopic tissue, \nsustaining chronic inflammation, and contributing to pain [50]. \nElevated estrogen levels facilitate the implantation and growth \nof lesions outside the uterus, enhance inflammatory responses, \nand impair immune clearance of ectopic cells [51]. This is \noften accompanied by reduced progesterone activity, which \nfurther contributes to disease progression [52]. Therapeutic \nstrategies aimed at correcting estrogen dominance through \nlifestyle modifications, hormonal treatments (e.g., oral \ncontraceptives, GnRH agonists), and natural hormone -\nregulating interventions have demonstrated efficacy in \nsymptom management and slowing disease progression [53]. \nImmune dysfunction, oxidative stress,  and inflammation are \nint errelated contributors to endometriosis severity [54]. \nImpaired immune surveillance permits the persistence of \nectopic tissue, while oxidative stress resulting from an \nimbalance between reactive oxygen species (ROS) and \nantioxidants induces cellular damage and promotes \ninflammatory cascades. This sustained inflammatory \nenvironment drives symptom severity, adhesion formation, \nand disease persistence [55]. Hence, effective interventions \nmust target these overlapping pathways by modul ating \nimmune function, minimizing oxidative stress, and reducing \ninflammation. \nOver the past decade, the global use of ENDS, including e-\ncigarettes, has increased significantly [56]. ENDS are non -\ncombustible tobacco products that operate by heating and \naerosolizing liquids containing humectants, flavoring agents, \nand frequently nicotine [57]. Emerging research suggests that \nexposure to the chemical constituents of vaping products may \nexacerbate the underlying mechanisms of immune \ndysregulation, oxidative stress, and inflammation in \nendometriosis [58]. \nVaping aerosols commonly contain compounds such as \nnicotine, formaldehyde, acrolein, and various flavoring agents, \nall of which can gen erate ROS and overwhelm cellular \nantioxidant defenses [59]. These substances can impair \nimmune function by disrupting immune cell activity, altering \ncytokine profiles, and promoting pro-inflammatory conditions \n[60]. Moreover, direct tissue toxicity caused by these \nchemicals may contribute to further inflammation and \noxidative injury in reproductive tissues [61]. The cumulative \neffect of these exposures may amplify immune and \ninflammatory dysregulation, thereby aggravating the \nsymptoms and progression of endometriosis. \nNicotine, a principal toxic component of tobacco products, \nis known to negatively affect reproductive health in both men \nand women [62]. It can interfere with hormonal regulation by \nstimulating the adrenal glands to release stress hormones such \nas cortisol, potentially disrupting the balance of key \nreproductive hormones like estrogen and progesterone [63]. \nAdditionally, nicotine may disrupt the hypothalamic-pituitary-\novarian (HPO) axis, leading to decreased progesterone and \nrelatively elevated e strogen levels, contributing to an \nestrogen-dominant state [64]. This hormonal imbalance may \nfoster ectopic endometrial growth, intensify endometriosis \nsymptoms, and hinder normal reproductive functions. \n \nFigure 1 . Mechanism: Nicotine and Hormonal Dysregulation in \nEndometriosis. \n\n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n18 \nFurthermore, volatile organic compounds (VOCs) and \nheavy metals present in vaping aerosols can further disrupt \nimmune function. These substances promote oxidative stress \nby generating ROS, damaging immune cells, and impairin g \ntheir functionality [65]. Ebrahimi and colleagues (2020)  \nhighlight the pervasive nature of heavy metal exposure in \ndaily life, particularly from sources like cadmium, lead, and \nnickel found in vaping aerosols [66]. These metals accumulate \nin tissues, dis turb immune signaling, and enhance \ninflammatory responses, thereby diminishing the body's \nability to manage infections or eliminate aberrant tissues [67]. \nVOCs are also known to activate inflammatory pathways, \nsustaining a chronic inflammatory state that may contribute to \nthe exacerbation of endometriosis [68]. \n \nFigure 2. Mechanism: VOCs and Heavy Metals in Immune Dysregulation. \nFlavoring agents used in vaping liquids present additional \nhealth r isks. These compounds can exert cytotoxic effects \nthrough mechanisms such as membrane disruption, oxidative \ndamage, and induction of apoptosis or necrosis [69]. \nFurthermore, certain flavorants may induce epigenetic \nmodifications including changes in DNA methylation, histone \nstructure, and microRNA expression that alter gene regulation \nand cellular function [70]. These cellular and molecular \ndisruptions may contr ibute to tissue damage and immune \ndysfunction, ultimately exacerbating the development and \nseverity of endometriosis. \n \n\n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n19 \nTable 1. West Africa. \nDomain / Focus Area Mechanism or \nObservation \nKey Findings (Study Type / Evidence \nSource) \nSubgroup / Regional Relevance (SSA \nContext) \nEpidemiologic \nassociations \nVaping exposure ↔ \nendometriosis \nprevalence/severity \nCase–control & cross-sectional studies \nfrom mixed settings suggest higher odds \nof dysmenorrhea and diagnosis among \nnicotine product users; heterogeneity \nprevents meta-analysis. \nUnderdiagnosis due to limited \nlaparoscopy, stigma; rising youth e-\ncigarette uptake in urban Nigeria, Ghana; \nperi-urban mining zones (heavy metals) \nmay interact with vaping exposures. \nNicotine & hormonal \ndysregulation \nNicotine → HPG axis \ndisruption, altered \nER/PR signaling \nExperimental and human biomarker \nstudies show increased inflammatory \nmarkers and disrupted progesterone \nsignaling after nicotine exposure. \nIn West Africa, contraceptive access gaps \nand high adolescent pregnancies may \namplify hormonal vulnerability. \nOxidative stress & \ninflammation \nE-cig aerosols → \nROS, mitochondrial \ndamage \nIn vitro & animal studies show ROS, NF-\nκB activation; human studies link \nbiomarkers to vaping/alcohol co-use. \nMalnutrition and infectious comorbidities \n(e.g., malaria) could worsen oxidative \ndamage in West African populations. \nEpigenetic / miRNA \nAltered DNA \nmethylation, miR \nexpression \n(HOXA10, miR-200) \nSmoking literature robust; early vaping \nepigenetic signals emerging. \nEnvironmental pollutants (artisanal \nmining) + vaping may create cumulative \nepigenetic risk in coastal and inland \nmining communities. \nImmune & angiogenic \npathways \nFlavors → \nmacrophage \npolarization, ↑VEGF \nPreclinical pro-angiogenic findings; early \nhuman inflammatory marker elevation in \nyoung initiators. \nHigh rates of pelvic infection could mask \nor modify immune signals from vaping. \nFertility & \nimplantation \nNicotine delays \nimplantation, reduces \nreceptivity \nAnimal and limited human fertility \nstudies show implantation delays and \npoorer outcomes. \nFertility services are limited; such effects \ncould have large social impact in contexts \nwhere family size is highly valued. \nDuration & intensity \nLong-term / high-\nnicotine use → worse \nsymptoms \nObservational correlation between use \nduration and menstrual pain severity. \nYoung urban professionals and students \nincreasingly use high-nicotine pods; \noccupational exposure (mining) matters. \nConcurrent exposures \nVaping + \nalcohol/tobacco → \nsynergistic harm \nMixed-exposure studies show amplified \noxidative/hormonal disruption. \nSocial nightlife culture in cities like \nLagos/Accra increases dual exposures \namong women. \nPolicy & interventions \nWeak regulation, low \nreproductive \neducation \nWHO/AU recommend action; few \nregion-specific guidelines exist. \nNeed to integrate vaping education in \nadolescent reproductive health programs \nand mining occupational health policies. \n \nThe table presents a coherent, multidisciplinary synthesis of \nhow vaping exposure might influence endometriosis -relevant \noutcomes in SSA, with a clear focus on West Africa. It \norganizes mechanisms —from nicotine -induced hormonal \ndisruption to oxidative stre ss, epigenetic changes, and \nimmune/angiogenic pathways alongside epidemiologic \nevidence and region -specific contextual factors such as \ndiagnosis gaps, adolescent vaping trends, and mining -related \nexposures. While the narrative links are plausible and well -\nstructured, several rows would benefit from explicit study \ndesigns, standardized exposure metrics, and cautious \ninterpretation where evidence is primarily observational or \npreclinical. \nPolicy implications are appropriately foregrounded, \nhighlighting weak r egulation and the need to embed vaping \neducation within adolescent reproductive health and mining \noccupational health programs. To strengthen the table for \nsynthesis, consider adding uniform definitions of exposure, \nconcrete biomarkers or outcomes, and exp licit gaps or future \ndirections per domain. This would enhance clarity for readers \naiming to identify methodological needs and prioritize \nregionally relevant research and interventions. \n \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n20 \nTable 2. East Africa. \nDomain / Focus Area Mechanism or \nObservation \nKey Findings (Study Type / \nEvidence Source) \nSubgroup / Regional Relevance (SSA \nContext) \nEpidemiologic \nassociations \nRising urban vaping ↔ \nendometriosis symptoms \nCross-sectional surveys in tertiary \nclinics indicate associations \nbetween nicotine exposure and \npelvic pain but limited diagnostics. \nKenya/Uganda show increasing e-cig \nuptake among youth; rural healthcare \naccess gaps lead to late presentation. \nNicotine & hormones \nNicotine alters \nestrogen/progesterone \nsignaling \nLab and clinical biomarker studies \nshow upregulated inflammatory \npathways, aromatase activity. \nLimited hormone monitoring capacity and \ncontraceptive counseling in peripheral \nfacilities. \nOxidative stress \nAerosol constituents \ncause ROS and lipid \nperoxidation \nIn vitro and animal evidence; \nhuman biomarker studies show \nhigher oxidative markers in dual-\nusers. \nHigh burden of infectious diseases \n(HIV/TB) could amplify oxidative \npathways. \nEpigenetics miRNA shifts regulating \nendometrial adhesion \nEarly evidence from smokers; \nvaping epigenetic evidence \nemerging. \nUrban pollution (traffic) + vaping may have \ncombined epigenetic impacts in cities like \nNairobi and Dar es Salaam. \nImmune & \nangiogenesis \nFlavored condensates → \nVEGF, macrophage shift \nAnimal models show pro-\nangiogenic changes relevant to \nlesion growth. \nHigh STI prevalence and pelvic \ninflammation could confound diagnosis of \nendometriosis. \nFertility Reduced uterine \nreceptivity after nicotine \nMouse models + small human \ncohorts show implantation issues. \nAssisted reproduction limited; fertility \nimpacts have outsized social consequences. \nDuration/intensity Chronic use → severe \ndysmenorrhea \nObservational link between years of \nvaping and pain scores. \nUniversity students and young \nprofessionals in capital cities are an at-risk \ngroup. \nConcurrent use Alcohol/Tobacco/vaping \ninteractions \nSynergistic oxidative & endocrine \ndisruption reported. \nCultural alcohol consumption patterns at \nsocial events may increase joint exposures. \nPolicy \nFew reproductive \nguidelines referencing \nvaping \nRegional health policy lags behind \nuse trends. \nOpportunities for school-based prevention \nand adolescent SRH programming. \n \nThe table offers a context-specific synthesis of how vaping \ncould relate to endometriosis-related outcomes in East Africa, \nanchored by Kenya and Uganda. It notes tentative epidemiologic \nlinks between urban vaping and endometriosis-like symptoms, \nwhile stressing diagnostic limits in SSA. It outlines plausible \nbiological pathways, nicotine-hormone interactions, oxidative \nstress, epigenetic changes, immune/angiogenic processes, and \nfertility considerations framed by regional factors such as STI \nprevalence and healthcare access. A policy note highlights few \nreproductive health guidelines on vaping and advocates \npreventive actions in schools and adolescent SRH programs. \nOverall, it signals a plausible public health concern while \ncarefully noting the observational and preclinical nature of the \nevidence. \nTable 3. Central Africa. \nDomain / Focus \nArea Mechanism or Observation Key Findings Subgroup / Regional Relevance \nEpidemiology \nSparse data; probable \nunderestimation of vaping-related \ngynecologic disease \nClinic case series \nsuggest links but \ndiagnostic capacity \nlimited. \nDRC, CAR: few laparoscopies; artisanal mining \nexposures (lead, mercury) common — potential \nsynergists. \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n21 \nDomain / Focus \nArea Mechanism or Observation Key Findings Subgroup / Regional Relevance \nNicotine & \nhormones \nNicotine → endocrine disruption \ndemonstrated experimentally \nLimited human \nbiomarker work; animal \nstudies generalizable. \nNutritional deficiencies and anemia prevalent — \ncould worsen hormonal effects. \nOxidative stress Aerosol-induced ROS exacerbated \nby infections \nPreclinical evidence \nstrong; human data \nlimited. \nHigh infectious disease burden may amplify \noxidative/inflammatory pathways. \nEpigenetics Environmental pollutants + vaping \nmay change epigenome \nSmoking literature \nstrong; vaping not well-\nstudied. \nMining towns (Lubumbashi) are priority areas to \nstudy combined exposures. \nImmune pathways Proinflammatory shifts with \nflavored aerosols \nAnimal studies: \nmacrophage \npolarization and \nangiogenesis. \nCoexisting pelvic infections increase diagnostic \ncomplexity. \nFertility Nicotine harms implantation in \nanimal models \nRelevant but poorly \ndocumented in human \nCentral African cohorts. \nSocial importance of fertility and very limited \nART services increase impact of subfertility. \nDuration & \nintensity \nChronic users show worse \nmenstrual outcomes elsewhere; \nlocal data lacking \nNeed longitudinal \ntracking. \nYoung urban migrants to mining towns may be \nhigh-risk group. \nConcurrent \nexposures \nHigh prevalence of multi-toxin \nexposures (smoke, mining \npollutants) \nLikely synergistic but \nunder-researched. \nOccupational exposures create unique exposure \nprofiles. \nPolicy & \ninterventions \nMinimal e-cig regulation, limited \nSRH integration \nPublic health priorities \noften focus on \ninfectious disease. \nIntegrate vaping topics into maternal/occupational \nhealth guidance for mining regions. \n \nThe Central Africa tab offers a concise, mechanism-focused \noverview of how vaping might affect gynecologic and \nreproductive health within a setting marked by high infectious \ndisease burden and environmental exposures (notably  \nartisanal mining with lead and mercury). It groups evidence \ninto domains epidemiology, nicotine and hormones, oxidative \nstress, epigenetics, immune pathways, fertility, \nduration/intensity, concurrent exposures, and policy to show \nboth plausible biological links and the contextual limitations. \nA key message is the reliance on animal and preclinical data \nfor many mechanisms, coupled with significant gaps in human \nbiomarkers and region -specific longitudinal data, which \nhinders translation into public health action. \nThe text highlights several priorities: (1) the need for \nlongitudinal, human -focused research on nicotine -hormone \ninteractions and fertility, particularly in contexts with \nnutritional deficiencies and anemia that could amplify effects; \n(2) attention to synergistic exposures from mining pollutants \nand smoking, especially in mining towns and among young \nurban migrants; and (3) practical policy steps to incorporate \nvaping considerations into maternal and occupational health \nguidance despite limited regu lation and SRH integration. \nOverall, the tab offers a compact, provisional map of Central \nAfrica-specific factors and clearly identifies critical data gaps \nto support evidence-based policy and practice. \n \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n22 \nTable 4. Southern Africa. \nDomain / Focus Area Mechanism or Observation Key Findings Subgroup / Regional Relevance \nEpidemiology \nRising urban vaping (SA) with \nsome clinic data on pelvic pain \nassociations \nCase–control and hospital series \nfrom South Africa more numerous \nthan other SSA regions. \nSouth Africa leads in vaping \nprevalence and diagnostic capacity; \nneighboring countries show emerging \nuptake. \nNicotine & hormones Robust experimental evidence \nfor endocrine disruption \nHuman biomarker studies \navailable; vaping data building. \nBetter lab capacity (Cape Town, \nJohannesburg) enables mechanistic \nstudies. \nOxidative stress Aerosols cause ROS & \nmitochondrial damage \nBoth in vitro and small clinical \nstudies support this. \nIntersection with high HIV prevalence \nand TB could magnify impacts. \nEpigenetics Smoking and vaping associated \nwith methylation changes \nSouth African cohorts feasible for \nepigenetic studies. \nUrban industrial pollution + vaping → \ncumulative exposures. \nImmune & \nangiogenesis \nFlavors → angiogenic \npathways in animal models Mechanistic signals present. Pelvic infection patterns may \ncomplicate diagnosis. \nFertility Nicotine reduces implantation \nin models; limited human data \nFeasible to study at fertility clinics \nin major cities. \nFertility clinics concentrated in SA \nenable cohort studies. \nDuration & intensity Chronic, high-nicotine users \nexperience worse symptoms \nObservational data align with \nglobal findings. \nUniversity student cohorts and nightlife \ncultures are clear target groups. \nConcurrent exposures Alcohol + vaping common in \nnightlife settings \nSynergistic damage observed in \nmixed-use studies. \nStrong nightlife economy in SA \nincreases dual exposures among young \nwomen. \nPolicy & interventions Some regulatory movement but \ngaps remain \nSouth Africa has some policy \nactivity; regional harmonization \nlacking. \nOpportunity to pilot reproductive-\nhealth integration into tobacco control \nprograms. \n \nIn Southern Africa, especially South Africa, vaping \nepidemiology is rapidly evolving with potentia l links to \ngynecologic and reproductive health issues like pelvic pain \nand possibly endometriosis. South Africa ’s advanced \ndiagnostic infrastructure positions it as a regional data hub for \nmechanistic and clinical findings, showing nicotine ’s \nendocrine dis ruption, oxidative stress from aerosols, \nmitochondrial dysfunction, and epigenetic changes. These \npathways matter amid coexisting HIV , TB, and urban \npollution, and are reinforced by hospital-based case series and \nstudent cohorts that emphasize the role of duration and \nintensity of use. Socioculturally, high alcohol –vaping co-use \nin nightlife and concentrated fertility clinics offer both risk \ncontext and research opportunities, while policy progress on \nelectronic nicotine delivery systems is tempered by \nimplementation gaps and weak regional harmonisation. \nOverall, there is a clear need for region -specific research and \nintegrated public health strategies to address the unique \nexposure landscape affecting women ’s health in Southern \nAfrica. \nNarrative Interpretation \nDue to heterogeneity in study designs, populations, and \noutcome measures, quantitative synthesis was not possible. \nInstead, evidence was narratively organized across \nepidemiologic, mechanistic, and contextual domains. \n1) Epidemiologic patterns suggest a plausible but \nunderexplored association between vaping and \nendometriosis, particularly in reproductive -age women \nwith concurrent substance use. \n2) Biological evidence supports nicotine-induced oxidative \nstress, hormonal imbalance, and epigenetic \ndysregulation as mechanistic pathways linking vaping \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n23 \nexposure to lesion development and symptom severity. \n3) Regional contextual factors including regulatory \nweakness, cultural barriers, and high environmental \ntoxin exposure likely amplify risks among women in \nSub-Saharan Africa. \n4) Policy implications highlight an urgent need for \nreproductive health surveillance and targeted awareness \ncampaigns. \n5) Subgroup analyses emphasize greater vulnerability \namong younger women, chronic vapers, and dual users \n(vaping + smoking/alcohol). \n5. Implications for Public Health in SSA \nWomen’s health encompasses far more than pregnancy and \nchildbirth [71]. In SSA, menstrual health remains \nunderprioritized due to persistent stigma, inadequate access to \nmenstrual products and sanitation fac ilities, and limited \neducational outreach, with marginalized populations \ndisproportionately affected [72]. Access to essential sexual, \nreproductive, and maternal health services is further \nconstrained by gender inequality and discrimination [73]. \nPeriod po verty defined as the inability to afford or access \nmenstrual products, sanitation and hygiene facilities, and \nrelated education places preventable burdens on women and \ngirls [74]. Addressing this requires health services and \nproducts that are affordable, a ccessible, acceptable, and \ndelivered with quality, equity, and dignity. \nAccording to the WHO, adolescent health behaviors are \nalso shifting, with rising cigarette consumption and increasing \ne-cigarette use (vaping) introducing new risks for women of \nreproductive age in SSA [75]. While long -term population -\nlevel data remain limited, the WHO warns that e-cigarettes are \nharmful, addictive, and may increase uptake of combustible \ntobacco among youth, a trend that could broaden nicotine \nexposure among reproductiv e-age women if not addressed \n[76]. Nicotine and many aerosol constituents in e -cigarettes \nhave biologically plausible effects on reproductive tissues and \nsystemic inflammation, which could influence gynecological \nhealth [77]. Endometriosis, a highly preval ent and morbid \ncondition primarily affecting women in their 20s–40s, already \ncontributes substantially to disability -adjusted life years \n(DALYs) and infertility in low - and middle -income settings \n[78]. Global and regional analyses indicate that incidence and \ndisability remain concentrated in young women, with \nvariation by region [79]. Thus, any new exposure impacting \nreproductive health, such as vaping, could amplify both \nindividual suffering and the broader burden in SSA [80]. Even \nin the absence of definitive causal evidence, early findings that \ne-cigarettes influence ovarian reserve, menstrual function, and \ninflammatory pathways warrant precautionary action from a \npublic-health perspective [81]. \nThe health -system implication s are immediate and \npractical. If vaping exacerbates pelvic pain, delays \nconception, or increases healthcare utilization, SSA health \nsystems already strained by infectious disease burdens and \nlimited gynecologic capacity will face rising diagnostic and \ntreatment demands, including laparoscopy, imaging, [82] \nchronic pain management, and fertility services. Such \npressures risk worsening inequities, as women in rural or low-\nincome urban areas often have the least access to timely \ndiagnosis and evidence-based management for endometriosis \n[83]. \nSurveillance and research gaps further hinder timely \nresponse. Current data on e -cigarette prevalence in SSA are \nsparse and heterogeneous, limiting the ability to project \nreproductive-health impacts [84]. Few longitudinal or \nmechanistic studies from African populations directly link \nvaping to endometriosis or related outcomes, [85], with most \nevidence extrapolated from animal models, in vitro \nexperiments, or high -income settings. Strengthening \nsurveillance and prioritizing prospective cohort and \nmechanistic research in SSA are essential to progress from \nplausible concern to evidence-informed policy [86]. \nPolicy and prevention implications are therefore critical. In \nline with the precautionary principle and WHO guidance [87], \nSSA countries should integrate e -cigarettes into existing \ntobacco-control frameworks through measures such as age \nrestrictions, marketing and flavor bans, taxation, and \nrestrictions on public use [88]. Tailored messaging for women \nof reproductive age and adolescents is essential [89]. Public-\nhealth campaigns should concurrently address established \ndrivers of endometriosis morbidity while incorporating \ninformation on nicotine and vaping-related reproductive risks \ninto counseling and family -planning services  [90]. \nPartnerships with schools and youth programs will be crucial, \ngiven that adolescent uptake strongly predicts adult \nprevalence [91]. \nEquity considerations must remain central. Any increase in \nvaping-related reproductive harms will disproportionately \naffect marginalized populations with limited healthcare access, \nlower health literacy, and greater exposure to targeted \nmarketing [92]. Pol icy responses should therefore include \nsafeguards such as subsidized diagnostic and fertility services, \nculturally tailored risk communication, and community \nengagement to avoid further stigmatization of women seeking \ncare for chronic pelvic pain or infertility [93, 94]. \nAlthough vaping is not yet a proven cause of endometriosis, \nthe combination of biological plausibility, emerging \nreproductive-health signals, and rising use among urban youth \nin SSA justifies a public-health response [95, 96]. Immediate \nsteps including enhanced surveillance, targeted research, \nintegration of e -cigarette regulation into tobacco -control \npolicies, [97] and strengthened reproductive-health education \nare needed both to protect women ’s reproductive health and \nto generate the evide nce base required for robust causal \ninferences and policy decisions [98]. \n \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n24 \n6. Research Gaps and Recommendations \nDespite growing global attention to vaping and women ’s \nreproductive health, significant gaps persist in SSA [99]. \nCurrent evidence on the associ ation between e -cigarette use \nand endometriosis is largely extrapolated from animal studies, \nin vitro experiments, and high -income country populations, \nwith little region -specific data [100, 101] . Existing \nepidemiological studies in SSA are sparse, fragmen ted, and \noften cross -sectional, making it difficult to establish causal \npathways or quantify the potential burden of vaping -related \nreproductive health outcomes [102]. Additionally, \nsurveillance systems rarely disaggregate tobacco use by \nproduct type, gend er, or reproductive age group, thereby \nobscuring the true prevalence and patterns of vaping among \nwomen [103, 104]. \nThe biological plausibility linking nicotine and e -cigarette \naerosols to systemic inflammation, ovarian reserve depletion, \nand menstrual dys function underscores the need for region -\nspecific mechanistic studies [105, 106] . However, limited \nlaboratory capacity, underfunded reproductive-health research, \nand competing health priorities in SSA constrain progress in \nthis area [107, 108]. Moreover, few longitudinal cohort studies \nare underway to explore the temporal relationship between \nvaping, gynaecological morbidity, and fertility outcomes \n[109-110]. Without such evidence, policymakers lack the data \nrequired to develop targeted interventions or int egrate vaping \ninto reproductive-health frameworks. \n7. Recommendations \nStrengthen Surveillance: Incorporate e -cigarette use into \nnational health surveys and reproductive health surveillance \nsystems, with disaggregation by sex, age, and socioeconomic \nstatus. \nInvest in Epidemiological Research: Support longitudinal \ncohort studies and case –control investigations in SSA to \nassess the association between vaping and endometriosis \nincidence, severity, and fertility outcomes. \nAdvance Mechanistic Studies: Develop lab oratory and \nclinical research capacity to examine the biological pathways \nthrough which vaping may influence ovarian function, pelvic \npain, and inflammatory responses in African populations. \nIntegrate with Tobacco Control: Align vaping regulation \nwith exis ting tobacco -control measures (age restrictions, \ntaxation, advertising bans) while including reproductive \nhealth considerations in policy frameworks. \nEnhance Health Education: Incorporate evidence -based \ninformation on vaping ’s reproductive risks into famil y-\nplanning services, school -based health programs, and \ncommunity campaigns. \nPromote Equity in Research and Care: Ensure that \nmarginalised groups particularly women in rural and low -\nincome settings are represented in research and have access to \ndiagnostic, preventive, and therapeutic services. \nFoster Multisectoral Collaboration: Encourage partnerships \nbetween governments, academia, civil society, and \ninternational health bodies to mobilize resources, share data, \nand drive regionally tailored interventions. \nAddressing these research gaps and implementing the \nabove recommendations will generate the evidence base \nneeded to move from biological plausibility to policy action, \nultimately safeguarding the reproductive health of women of \nreproductive age in SSA. \n8. Conclusion \nThis review highlights a critical need for robust, region -\nspecific epidemiologic and mechanistic studies to clarify the \nrelationship between vaping and endometriosis in Sub -\nSaharan Africa. The convergence of biologically plausible \npathways, rapidly increasing ENDS use among reproductive -\naged women, and persistent gaps in diagnostic, menstrual, and \nreproductive health services indicates that vaping may \nrepresent an overlooked contributor to gynaecologic \nmorbidity in the region. Strengthening surve illance systems, \nintegrating ENDS into tobacco control and reproductive -\nhealth policies, and expanding targeted education for \nadolescents and young women are urgently required. \nCoordinated multisectoral action spanning public health, \nclinical services, environmental regulation, and youth-focused \ninterventions is essentially both to mitigate potential harms \nand to generate the evidence base required for informed policy \nand programmatic decisions across SSA. \nAbbreviations \nAJOL African Journals Online \nAU African Union \nCAR Central African Republic \nDRC Democratic Republic of the Congo \nENDS Electronic Nicotine Delivery Systems \nER Estrogen Receptor \nGnRH Gonadotropin-Releasing Hormone \nHPO Axis Hypothalamic–Pituitary–Ovarian Axis \nHPG Axis Hypothalamic–Pituitary–Gonadal Axis \nHIV Human Immunodeficiency Virus \nLMICs Low- and Middle-Income Countries \nNF-κB Nuclear Factor Kappa-Light-Chain-\nEnhancer of Activated B Cells \nNOS Newcastle–Ottawa Scale \nPR Progesterone Receptor \nPRISMA Preferred Reporting Items for Systematic \nReviews and Meta-Analyses \nROS Reactive Oxygen Species \nScopus Scientific Citation Index Database \n(Elsevier) \nSSA Sub-Saharan Africa \nSRH Sexual and Reproductive Health \n\nJournal of Gynecology and Obstetrics http://www.sciencepg.com/journal/jgo \n \n25 \nVEGF Vascular Endothelial Growth FactorSTI – \nSexually Transmitted Infection \nSTROBE Strengthening the Reporting of \nObservational Studies in Epidemiology \nTB Tuberculosis \nVOCs V olatile Organic Compounds \nWHO World Health Organization \nAcknowledgments \nWe give thanks to God for His provision, guidance, and \ngrace throughout the course of this research. We acknowledge \nthese blessings as gifts that sustained and enabled the \nsuccessful completion of this work, and we offer our sincere \ngratitude. \nA special acknowledgement goes to our co -author Mukasa \nCharline San gany, whose invaluable support as a scientific \nmentor and her dedication in reserving library hours \nsignificantly facilitated the progress of this work. Her \ncontributions have been instrumental in shaping the quality of \nthis research. \nAuthor Contributions \nKalala Elisee Kabuya : Conceptualization, Methodology, \nResources, Validation, Visualization, Writing – original draft, \nProject administration, Supervision \nMukasa Charline Sangany: Project administration, \nResources, Data curation, Writing – review & editing \nConflicts of Interest \nThe author declares no conflicts of interest. \nReferences \n[1] Agaku, I. T., Sulentic, R., Dragicevic, A., Njie, G., Jones, C. \nK., Odani, S.,... & Ayo -Yusuf, O. (2024). 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