Parabens and Cancer Risk: Evaluating the Evidence

Abstract

The potential carcinogenic effects of parabens, particularly their association with breast cancer, represent one of the most contentious issues in environmental health research. As ubiquitous preservatives in consumer products, pharmaceuticals, and food, parabens function as weak xenoestrogens with demonstrated endocrine-disrupting properties. This review critically examines the epidemiological, molecular, and experimental evidence linking paraben exposure to various cancers, with emphasis on breast cancer, while addressing the significant scientific debate surrounding risk assessment, regulatory perspectives, and the challenges of establishing causality in the context of cumulative, low-dose chemical exposure. 

Introduction

Parabens are synthetic preservatives classified as endocrine-disrupting chemicals (EDCs) and xenoestrogens because of their capacity to mimic natural oestrogen and bind to oestrogen receptors [1; 2; 3]. While regulatory agencies in many jurisdictions have deemed parabens safe within specified concentration limits, ongoing research into their potential carcinogenic impacts continues to generate scientific controversy and public concern [1; 4; 5]. The most extensively studied and debated association involves breast cancer, though emerging evidence suggests potential links to thyroid, reproductive, and other malignancies. Understanding the paraben-cancer relationship requires careful consideration of detection studies, epidemiological associations, mechanistic plausibility, and the inherent limitations of current research. 

Parabens and Breast Cancer: The Primary Controversy

Detection in Tumour Tissues

The modern concern regarding parabens and breast cancer crystallised following a landmark 2004 study that detected residues of five distinct parabens in 19 out of 20 human breast tumour samples [1; 6; 7]. Critically, these compounds were identified as intact esters rather than metabolites, demonstrating that parabens can penetrate dermal barriers, accumulate in breast tissue, and resist immediate metabolisation [1; 6; 8]. Subsequent investigations found that 27% of 160 breast tissue samples contained at least one paraben at concentrations sufficient to stimulate breast cancer cell proliferation in vitro [9].

Anatomical Distribution Patterns

Research has documented particularly high paraben concentrations in the upper outer quadrant of the breast, the anatomical region proximate to the axilla (armpit) [3; 4]. This distribution pattern led investigators to hypothesize a connection with underarm cosmetic products, particularly deodorants and antiperspirants, which typically contain paraben preservatives and are applied directly to skin overlying breast tissue. However, this hypothesis faces a significant challenge: parabens have also been detected in breast tissue of women who reported never using underarm cosmetic products [7; 9], suggesting that dermal exposure from these products represents only one of multiple paraben sources contributing to breast tissue accumulation.

Epidemiological Evidence: A Mixed Picture

The epidemiological literature presents a complex and sometimes contradictory landscape of associations between paraben exposure and breast cancer risk. Several studies have identified positive correlations worthy of serious consideration. Case-control investigations found that women in the highest quintiles of urinary methylparaben (MeP) and propylparaben (PrP) concentrations demonstrated increased breast cancer risk [4]. The Sister Study, a large prospective cohort investigation, reported a 10 to 15% higher breast cancer risk among moderate-to-frequent users of beauty products, which represent primary paraben exposure sources [8].

Conversely, other substantial epidemiological studies have yielded null or inverse associations that complicate risk assessment. A multiethnic cohort study observed that breast cancer risk was weakly inversely associated with total paraben exposure [4], suggesting that higher paraben levels correlated with reduced rather than elevated cancer risk. Furthermore, a study encompassing over 1,600 women found no difference in breast cancer incidence related to underarm deodorant or antiperspirant use [9].

These conflicting findings have led regulatory bodies to adopt cautious positions. The European Commission has concluded that current evidence does not demonstrate a clear risk for breast cancer development from paraben-containing underarm cosmetics [1; 9]. However, the absence of definitive epidemiological proof does not necessarily establish safety, particularly given the methodological challenges inherent in studying low-dose, chronic chemical exposures.

Mechanistic Evidence from Cellular Studies

While epidemiological associations remain inconsistent, in vitro mechanistic studies provide compelling evidence of parabens' capacity to influence cellular processes relevant to carcinogenesis. Laboratory investigations demonstrate that parabens can promote cell proliferation, migration, and invasive properties in human breast cancer cell lines [3; 4]. These compounds appear capable of enabling several recognised "hallmarks of cancer," including evading growth suppressors, resisting programmed cell death (apoptosis), and sustaining proliferative signalling [9].

The molecular mechanisms through which parabens might contribute to breast carcinogenesis involve multiple pathways. Parabens bind to oestrogen receptors (ER-alpha and ER-beta), triggering expression of genes involved in cell cycle progression and tumour growth [3; 4]. Beyond direct receptor activation, parabens can engage in hormonal crosstalk with the human epidermal growth factor receptor 2 (HER2) pathway, synergising with oestrogen receptor signalling to increase pro-oncogenic c-Myc expression in certain breast cancer cell subtypes [4].

Parabens may also elevate local oestrogen concentrations within breast tissue through enzyme modulation. They can inhibit 17β-hydroxysteroid dehydrogenase, an enzyme that inactivates potent oestrogens, while simultaneously inducing aromatase, which synthesizes oestrogen from androgenic precursors [4; 10]. This dual enzymatic effect could amplify estrogenic signalling beyond what would be predicted from direct receptor binding alone.

Additionally, some research suggests parabens may exert genotoxic effects, causing DNA oxidative stress, generating reactive oxygen species (free radicals), and promoting genomic instability, all recognized drivers of carcinogenic transformation [2; 3; 8].

The REDUXE Study: Molecular Evidence of Reversible Effects

A particularly significant contribution to the paraben-cancer debate comes from the REDUXE (Regimen of Reduced Xenoestrogen Use) intervention study, which provided molecular-level evidence of xenoestrogen effects directly within human breast tissue. This paradigm-shifting investigation, facilitated through community-based participatory research, examined the adverse effects of persistent exposure to parabens and phthalates from personal care products on oestrogen-responsive breast tissue [11].

Study Design and Methodology: The REDUXE study enrolled healthy volunteers who discontinued use of paraben- and phthalate-containing personal care products over a 28-day intervention period. Pre- and post-intervention fine needle aspirates (FNAs) of breast tissue were collected from participants, providing direct access to the cellular environment most relevant to breast cancer development. This methodological approach represents a critical advancement over studies relying solely on urinary biomarkers or surrogate tissues, as it examines molecular changes within the target organ itself [11].

Molecular and Phenotypic Changes: Using high-dimensional gene expression analysis of matched FNA pairs, investigators documented striking reversals of cancer-associated phenotypes in breast cells of REDUXE-compliant subjects. Specifically, the study identified significant alterations in several critical signalling pathways implicated in carcinogenesis:

• PI3K-AKT/mTOR pathway: This crucial signalling cascade regulates cell growth, proliferation, survival, and metabolism. Dysregulation of PI3K-AKT/mTOR signalling represents one of the most common molecular abnormalities in breast cancer, making its modulation by xenoestrogen exposure particularly concerning. The REDUXE intervention reversed aberrant activation patterns in this pathway, suggesting that environmental xenoestrogen exposure may chronically stimulate pro-growth signalling in healthy breast tissue.
• Autophagy and apoptotic networks: Autophagy (cellular self-digestion and recycling) and apoptosis (programmed cell death) represent critical quality control mechanisms that eliminate damaged or potentially malignant cells. Cancer development often involves evasion of these protective processes. The REDUXE study documented normalisation of autophagy and apoptotic signalling networks following xenoestrogen reduction, indicating that chronic exposure may impair the breast's natural tumour suppression mechanisms.
• Oestrogen pathway normalisation: In vitro treatment of paired FNAs with 17β-oestradiol (E2) revealed a "normalising" impact of the REDUXE intervention on gene expression within known oestrogen-modulated pathways. This finding is particularly significant because it demonstrates that xenoestrogen exposure alters how breast tissue responds to natural oestrogen signalling. Functional endpoints further illustrated this normalisation:
• Oestrogen receptor alpha:beta ratio: The balance between oestrogen receptor subtypes (ERα and ERβ) influences proliferative responses to estrogenic stimulation. ERα generally promotes proliferation, while ERβ can exert anti-proliferative effects. The REDUXE intervention modified this receptor ratio, suggesting that chronic xenoestrogen exposure may skew oestrogen signalling toward pro-proliferative phenotypes.
• S-Phase fraction: The S-phase represents the DNA synthesis portion of the cell cycle when cells replicate their genetic material before division. Elevated S-phase fraction indicates increased proliferative activity, a hallmark of cancer. REDUXE compliance reduced S-phase fraction in breast cells, demonstrating decreased proliferative drive following xenoestrogen avoidance.

Biomarker validation: These molecular and cellular changes occurred concurrently with significant reductions in urinary paraben and phthalate metabolite concentrations, confirming that the intervention successfully reduced xenoestrogen exposure and that the observed biological effects temporally correlated with this reduction [11].

Implications and significance: The REDUXE findings carry several profound implications for understanding paraben-cancer relationships:

1. The study demonstrates that parabens and phthalates from everyday personal care products induce measurable pro-carcinogenic molecular programming in healthy human breast tissue, even in the absence of diagnosed disease. This suggests that carcinogenic processes may begin long before clinical detection, during a "field of injury" phase when tissue-wide molecular abnormalities precede frank malignancy.
2. The reversibility of these changes within a mere 28-day period indicates that the effects are not fixed or permanent, offering hope that exposure reduction strategies could meaningfully decrease cancer risk. This finding challenges fatalistic perspectives that damage from environmental exposures is irreversible and suggests a potential avenue for breast cancer prevention through simple lifestyle modifications.
3. By examining direct tissue effects rather than relying solely on epidemiological associations or animal models, REDUXE provides a mechanistic link between environmental exposure and biological outcomes in humans. This approach bridges the gap between laboratory studies showing cellular effects and population studies examining disease incidence, strengthening causal inference.
4. The study validates concerns about cumulative, low-dose exposures that may not produce immediate toxic effects but alter cellular phenotypes in ways that could promote carcinogenesis over extended periods. The identification of changes in fundamental processes like PI3K-AKT signalling, autophagy, and cell cycle regulation demonstrates that the biological impact extends beyond simple oestrogen receptor activation to encompass multiple cancer-relevant pathways.

The REDUXE study thus represents a methodological and conceptual advance in environmental health research, revealing unfavourable consequences from xenoestrogen exposure in daily-use personal care products and illustrating the potential for exposure reduction to suppress pro-carcinogenic phenotypes at the cellular level. While this single intervention study cannot definitively establish that paraben avoidance prevents breast cancer development, which would require decades-long follow-up of clinical outcomes, it provides compelling molecular evidence that parabens influence breast tissue biology in ways consistent with increased cancer risk, and importantly, that these effects are modifiable through behavioural change [11].

Associations with Other Cancer Types

Thyroid Cancer

Beyond breast cancer, emerging evidence suggests associations between paraben exposure and thyroid malignancy. Biomonitoring studies in China identified positive associations between urinary levels of methylparaben (MeP), ethylparaben (EtP), and propylparaben (PrP) with thyroid cancer odds [12; 13]. Among the parabens examined, ethylparaben demonstrated the strongest association with thyroid cancer [12], suggesting potential compound-specific differences in carcinogenic risk.

The biological plausibility of thyroid cancer associations relates to parabens' documented capacity to disrupt thyroid hormone signalling, a critical regulatory system for metabolism, growth, and development. Thyroid hormone receptors share structural and functional similarities with oestrogen receptors, potentially rendering them susceptible to paraben-mediated disruption.

Reproductive Cancers: Uterine and Ovarian Malignancies

The relationship between parabens and reproductive tract cancers presents a particularly complex picture. Exploratory research using National Health and Nutrition Examination Survey (NHANES) data yielded unexpected findings: while some phenolic compounds showed positive associations with ovarian cancer, ethylparaben was inversely associated with previous uterine cancer diagnosis (Oddd ratio, OR: 0.31), indicating that higher paraben levels correlated with reduced odds of this malignancy [13].

These inverse associations complicate risk interpretation and underscore the challenges of drawing conclusions from observational studies where confounding factors, selection bias, and reverse causation may influence apparent relationships. Parabens have been detected in ovarian cancer tissues [14], confirming tissue accumulation, though this detection alone does not establish causal involvement in carcinogenesis.

Skin Cancer

The potential for parabens to contribute to skin cancer has received limited investigation relative to other malignancies. Laboratory studies have demonstrated that parabens in combination with ultraviolet (UV) radiation can induce oxidative stress and DNA damage in skin cells in vitro [9; 15]. Given that parabens are common ingredients in sunscreen formulations and other topical products applied to sun-exposed skin, potential photochemical interactions warrant consideration.

However, despite mechanistic plausibility, no human epidemiological studies have confirmed a role for parabens in the development of nonmelanoma skin cancer or melanoma [8; 9]. Parabens have been detected in blood and urine samples from cancer patients, but detection does not establish causation, and current clinical evidence does not support paraben avoidance as a skin cancer prevention strategy based on available data.

The Weak Potency Argument and Cumulative Exposure

Estrogenic Potency Comparisons

A central argument in regulatory determinations of paraben safety concerns their estrogenic potency relative to endogenous oestrogens. Laboratory binding assays demonstrate that parabens exhibit estrogenic activity approximately 10,000 to 2.5 million times weaker than that of natural 17β-oestradiol [5; 9; 16]. Based on this substantial potency difference, regulatory agencies often conclude that current environmental and cosmetic exposure levels remain too low to cause significant biological harm or meaningfully contribute to cancer risk.

Challenges to the Safety Margin Perspective

Critics of the weak potency argument raise several important counterpoints that question whether potency comparisons alone provide adequate safety assessment:

1. While individual paraben potency may be weak, humans experience simultaneous exposure to multiple paraben types (methylparaben, ethylparaben, propylparaben, butylparaben) plus numerous other EDCs with potentially additive or synergistic effects [1; 3; 6; 17]. The cumulative estrogenic burden from chemical mixtures may exceed predictions based on individual compound assessments.
2. Chronic, continuous exposure from daily personal care product use, dietary intake, and environmental contamination creates a fundamentally different toxicological scenario than acute, high-dose exposures traditionally used in safety testing. Low-dose endocrine disruption may follow non-monotonic dose-response curves where effects at low concentrations differ qualitatively from those at high doses, challenging conventional toxicological assumptions.
3. Tissue-specific accumulation, as demonstrated by paraben detection in breast tissue, suggests that local concentrations in target organs may substantially exceed circulating blood levels. If parabens preferentially accumulate in adipose-rich breast tissue while also locally modulating oestrogen-metabolising enzymes, their effective estrogenic impact within the tissue microenvironment could surpass predictions based on systemic exposure metrics.
4. Timing of exposure matters profoundly in endocrine-sensitive carcinogenesis. Exposure during critical developmental windows, puberty, pregnancy, or the transition to menopause, when breast tissue undergoes rapid remodelling and demonstrates heightened sensitivity to hormonal signals, may carry disproportionate risk compared to exposure during other life stages.

Methodological Limitations and Research Challenges

Study Design Constraints

Most available evidence linking parabens to cancer derives from cross-sectional or case-control study designs, which can identify associations but cannot establish causation [9; 13]. Confounding variables, including other chemical exposures, genetic susceptibilities, reproductive histories, and lifestyle factors, complicate interpretation of observed associations. Reverse causation represents another concern in cross-sectional studies: cancer diagnosis may alter product use behaviours, creating spurious associations.

Long-term prospective cohort studies with repeated exposure biomarker measurements from before disease onset would provide stronger causal inference, but such investigations require substantial resources and extended follow-up periods spanning decades given cancer's typical latency. The Sister Study represents one of few prospective investigations in this domain, yet even large cohort studies face challenges in capturing cumulative lifetime exposure and accounting for temporal changes in product formulations and usage patterns.

Exposure Assessment Challenges

Accurately characterising paraben exposure presents significant methodological difficulties. Urinary paraben measurements, the most common biomarker approach, reflect only recent exposure (typically 24-48 hours) due to rapid metabolism and excretion, potentially missing important exposure windows, or long-term cumulative burden. Self-reported product use suffers from recall bias and cannot account for unlabelled paraben content or environmental sources beyond personal care products.

Individual susceptibility variations based on metabolic capacity, genetic polymorphisms affecting hormone metabolism, and baseline endocrine status further complicate exposure-response relationships. The same environmental exposure may produce markedly different internal doses and biological effects across individuals, reducing study power and obscuring true associations.

Mixture Effects and Chemical Interactions

Humans are not exposed to parabens in isolation but rather to complex mixtures of endocrine disruptors, many of which may act through similar or complementary mechanisms. Assessing paraben-specific cancer risk while controlling for concurrent exposures to phthalates, phenols, pesticides, and other EDCs presents formidable statistical and methodological challenges. Mixture toxicology remains an underdeveloped field, and most regulatory assessments continue to evaluate chemicals individually rather than as components of real-world exposure scenarios.

Regulatory Perspectives and Public Health Implications

Current regulatory positions on parabens reflect the uncertainty inherent in the available evidence. The European Commission, the U.S. Food and Drug Administration, and other regulatory bodies generally maintain that parabens are safe at currently permitted concentrations in cosmetics and food products. However, some jurisdictions have implemented restrictions on specific paraben variants, particularly longer-chain compounds like butylparaben and propylparaben, recognising their greater estrogenic potency and lipophilicity.

The divergence between regulatory assurances and growing public concern reflects fundamental differences in how scientific uncertainty is interpreted and managed. Regulatory frameworks typically require definitive proof of harm before restricting commercial chemicals, while the precautionary principle advocates limiting exposures to plausibly hazardous substances even in the absence of conclusive evidence, particularly when safer alternatives exist.

From a public health perspective, several considerations warrant emphasis:

1. While definitive proof of paraben-mediated carcinogenesis remains elusive, the biological plausibility is substantial: parabens demonstrate estrogenic activity, accumulate in breast tissue, can promote cancer cell proliferation in vitro, and modify gene expression patterns associated with carcinogenesis in human studies.
2. Vulnerable populations, including pregnant women, developing foetuses, and adolescent girls, may warrant protection given critical windows of hormone-sensitive development.
3. The availability of paraben-free product alternatives reduces the necessity of accepting uncertain risks when avoidance is feasible.

Conclusions and Future Directions

The relationship between paraben exposure and cancer, particularly breast cancer, remains scientifically controversial and incompletely resolved. Detection of intact parabens in tumour tissues, mechanistic evidence of oestrogenic activity and cancer-promoting cellular effects, and some epidemiological associations support biological plausibility for a causal relationship. However, inconsistent epidemiological findings, regulatory determinations of safety based on weak oestrogenic potency, and methodological limitations in existing research prevent definitive conclusions.

Several research priorities emerge from this assessment:

1. Long-term prospective cohort studies with repeated biomarker measurements from pre-diagnostic periods are needed to better establish temporal relationships and cumulative exposure effects.
2. Investigation of paraben effects during critical developmental windows, prenatal, pubertal, and perimenopausal periods, should be prioritised given potential for heightened susceptibility.
3. Mixture toxicology approaches examining parabens in combination with other EDCs would better reflect real-world exposure scenarios and potential synergistic effects.
4. Mechanistic research should further elucidate tissue-specific accumulation patterns, local enzyme modulation effects, and epigenetic modifications that may contribute to carcinogenic transformation. Fifth, intervention studies following the REDUXE model that examine molecular and cellular changes in response to exposure reduction could strengthen causal inference while evaluating risk reduction strategies.

From a precautionary perspective, individuals concerned about potential cancer risk can reduce paraben exposure by selecting paraben-free personal care products, limiting consumption of processed foods containing these preservatives, and advocating for greater transparency in product labelling. However, it is important to recognise that paraben avoidance alone addresses only one component of complex chemical exposures contributing to cancer risk in modern environments.

Ultimately, the paraben-cancer debate illustrates broader challenges in environmental health risk assessment: how to evaluate potential harms from ubiquitous, low-dose chemical exposures when definitive proof requires study designs and timeframes that may be practically infeasible. While awaiting more conclusive evidence, both continued research and prudent exposure reduction strategies merit serious consideration.

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