Association between urinary perchlorate and malignancies of endocrine-related tissues in U.S. adults: analysis of National Health and Nutrition Examination Survey (NHANES) data

Introduction

Malignancies of endocrine-related tissues are an important public health concern. They include cancers arising from classical endocrine glands such as the thyroid and adrenal glands, as well as those from organs with endocrine functions such as the pancreas. Despite their heterogeneity, these tumors share a common feature in that the involved tissues contribute to systemic homeostasis through hormonal regulation (1). Although their overall incidence is lower than that of malignancies in other organ systems, abnormal hormone secretion and rapid disease progression can cause substantial morbidity and mortality. Among malignancies of endocrine-related tissues, thyroid cancer is the most common, with papillary thyroid carcinoma (PTC) accounting for approximately 80% of cases (2,3). In 2022, more than 821,000 new cases of thyroid cancer were reported worldwide, ranking seventh among all cancers and fifth among women (4). In the United States, about 44,000 new cases are diagnosed annually, and the 5-year relative survival rate is 98.5% (5). In China, thyroid cancer ranked third in cancer incidence in 2022 with 466,100 new cases (6), representing more than half of the global burden, and its incidence continues to increase in both sexes.

Pancreatic cancer, predominantly pancreatic ductal adenocarcinoma (PDAC), arises from ductal epithelium or acinar cells. According to the Global Cancer Statistics 2022, 511,000 new cases occurred worldwide, ranking 12th in incidence but sixth in mortality, with an incidence-to-mortality ratio close to one to one (4,7). The highest rates are observed in North America, Europe, and Australia (8), and PDAC is projected to become the second leading cause of cancer-related death in the United States by 2030 (9). In China, approximately 130,000 new cases are reported annually, with a 5-year survival rate of only 7.2%, giving PDAC the reputation of the “king of cancers”.

The development of both thyroid and pancreatic cancers involves complex interactions among genetic predisposition, lifestyle factors, and environmental exposures. Rapid industrialization has led to substantial increases in industrial emissions and wastewater discharge, raising concerns about the carcinogenic potential of environmental pollutants (10). Perchlorate is a common and persistent endocrine-disrupting chemical that occurs naturally and is also produced through human activities such as propellant manufacturing, fireworks production, and fertilizer use (11,12). It is highly stable, readily soluble in water, and a strong oxidizing agent, which contributes to its persistence in the environment. Human exposure occurs mainly through contaminated groundwater and surface water (13). Perchlorate disrupts thyroid hormone synthesis by competitively inhibiting iodine uptake via the sodium-iodide symporter (NIS), leading to endocrine and metabolic disturbances (14). Beyond its effects on thyroid function, perchlorate may also exert direct tumorigenic effects on endocrine cells through the induction of oxidative stress. Excessive reactive oxygen species production can cause DNA damage, lipid peroxidation, and genomic instability, providing a molecular basis for tumor initiation (15). Chronic perchlorate exposure has been associated with follicular cell hypertrophy, apoptosis, and compensatory proliferation in the thyroid, changes that may increase susceptibility to neoplastic transformation. Moreover, systemic hormonal disruption induced by perchlorate may indirectly affect pancreatic endocrine cells and glucose metabolism, both of which are involved in endocrine-related tumorigenesis (16). Experimental studies also suggest its potential effects on the reproductive, immune, nervous and cardiovascular systems, and may also affect the growth and development of children (17-21).

Although perchlorate exposure has been associated with thyroid dysfunction and other endocrine abnormalities, its relationship with malignancies of endocrine-related tissues, particularly thyroid and pancreatic cancers, remains insufficiently characterized.

To address this knowledge gap, we conducted a cross-sectional analysis of National Health and Nutrition Examination Survey (NHANES) data to examine the association between urinary perchlorate levels and the prevalence of malignancies in endocrine-related tissues, thereby generating hypotheses for future longitudinal and mechanistic studies. We present this article in accordance with the STROBE reporting checklist (available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-1785/rc).

Methods

Study population

NHANES is a continuous, nationally representative survey of the non-institutionalized U.S. population, conducted by the National Center for Health Statistics (NCHS). It combines interviews, physical examinations, and laboratory tests to collect data on demographic characteristics, health status, diet, and environmental exposures.

We analyzed NHANES cycles from 2003 to 2018. Of 82,498 participants, 46,976 were adults aged ≥20 years. We excluded 26,622 participants without urinary perchlorate measurements and 38 with missing covariates, leaving 20,316 participants for analysis (Figure 1). The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Figure 1 Selection process for the study sample based on the 2003–2018 NHANES. NHANES, National Health and Nutrition Examination Survey.

Urinary perchlorate measurement

Urinary perchlorate was quantified using ion chromatography coupled with electrospray tandem mass spectrometry. Chromatographic separation employed an IonPac AS16 column with 100 mM sodium hydroxide as the eluent. An electrospray interface generated negative ions for mass spectrometric detection. Analyte concentrations (ng/mL) were determined from calibration curves using stable isotope-labeled internal standards. Perchlorate concentrations were corrected for urinary creatinine to account for urine dilution and expressed as ng/mg creatinine. Exposure was analyzed as both a continuous variable and by quartiles based on the distribution of creatinine-corrected values.

Evaluation of malignancies of endocrine-related tissues

Data on physician-diagnosed thyroid cancer and pancreatic cancer were obtained from the NHANES medical conditions questionnaire.

Covariates

We adjusted for demographic, socioeconomic, lifestyle, clinical, and laboratory variables. Demographic factors included sex, age (20–44, 45–64, and ≥65 years), and race/ethnicity (Mexican American, other Hispanic, non-Hispanic White, non-Hispanic Black, and other). Socioeconomic indicators comprised education level (<high school, high school, and >high school) and ratio of family income to poverty (PIR; <1.3, 1.3–3.5, and >3.5). Lifestyle factors included smoking status (≥100 cigarettes in a lifetime) and alcohol use (≥12 drinks per year). Clinical variables encompassed body mass index (BMI; <18.5, 18.5–24.9, 25.0–29.9, and ≥30 kg/m²), hypertension (systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or antihypertensive medication use), and diabetes (fasting blood glucose ≥126 mg/dL, HbA1c ≥6.5%, or glucose-lowering medication use). Laboratory parameters included direct high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and total cholesterol (TC).

Statistical analysis

Continuous variables were tested for normality using the Kolmogorov-Smirnov test and expressed as mean ± standard deviation for normally distributed data or median (interquartile range) for skewed data, while categorical variables were summarized as percentages. Weighted multivariable logistic regression was performed to evaluate associations between urinary perchlorate and each cancer outcome across three models: model 1, unadjusted; model 2, adjusted for age, sex, race, education, and PIR; and model 3, further adjusted for BMI, smoking status, alcohol use, hypertension, and diabetes. Pearson correlation analysis was conducted, and Bayesian correlation methods were applied to address the limited number of pancreatic and thyroid cancer cases. Dose-response relationships were assessed using restricted cubic spline models. All analyses were performed using R version 4.5.1 and SPSS version 27.0, with statistical significance set at P<0.05.

Results

Baseline characteristics of participants

Individuals aged 20 to 44 years accounted for 43.3%, and those aged 65 years or older accounted for 23.8%. Males comprised 49.0% of the sample, non-Hispanic White participants accounted for 44.4%, and 49.8% had an education level higher than high school. Participants with a medium PIR (1.3 to 3.5) represented 35.5%. Most participants (70.3%) were classified as overweight or obese. Current smokers accounted for 46.0% of the sample, and current drinkers accounted for 66.7%. A total of 14.9% had a confirmed diagnosis of diabetes, and 39.0% had hypertension. Corrected urinary perchlorate concentrations were not normally distributed, with a median of 3.09 and a range from 0.0381 to 494. HDL-C, TG, and TC also showed non-normal distributions, whereas LDL-C followed a normal distribution, with a mean of 2.96±0.930 (Table S1).

Distribution of malignancies of endocrine-related tissues

From a gender perspective, thyroid cancer was more common in females, who accounted for 66.44% of cases, whereas the incidence of pancreatic cancer mainly affects male patients, accounting for 85.79%. Thyroid cancer occurred predominantly in middle-aged individuals (58.68%) but was also observed in younger and older adults. In contrast, all pancreatic cancer cases in this study were among elderly individuals. For both cancer types, a higher proportion of patients were non-Hispanic White, had attained education beyond high school, and belonged to high-income families. Overall, patients with thyroid or pancreatic cancer were most often overweight or obese and frequently had comorbid hypertension and diabetes (Tables 1,2).

Weighted multiple linear regression analysis of malignancies of endocrine-related tissues

Corrected urinary perchlorate concentration showed a significant association with pancreatic cancer (P<0.001). Pancreatic cancer prevalence was also correlated with age, PIR, HDL-C, LDL-C, TG, TC, and smoking status. Moreover, a significant association was observed between creatinine-corrected urinary perchlorate and thyroid cancer (P<0.05). In addition, it was correlated with age and LDL-C levels.

Relationship between corrected urinary perchlorate and malignancies of endocrine-related tissues

Weighted multiple linear regression was used to evaluate the relationship between corrected urinary perchlorate and the two malignancies after adjusting for potential confounders in three models (Tables S2,S3). For thyroid cancer, when creatinine-corrected urinary perchlorate was analyzed as a categorical variable based on quartiles, a significant association was found in quartile 3 of model 1 [odds ratio (OR) =3.81; 95% confidence interval (CI): 1.26–11.5; P=0.02]. Similarly, model 3 also showed a significant association (P<0.001). Likewise, for pancreatic cancer, a significant association was observed in quartile 3 of model 1 (OR =13.4; 95% CI: 1.13–159; P=0.04) (Figure S1,S2).

Bayesian correlation analysis

Given the small number of thyroid and pancreatic cancer cases, a Bayesian approach was applied. As shown in Table 3, the Bayes factor for the association between corrected urinary perchlorate and thyroid cancer was 139.525, providing extremely strong evidence for a correlation. The Pearson correlation coefficient was 0.005, suggesting an almost negligible linear relationship. As shown in Table 4, the Bayes factor for the association between corrected urinary perchlorate and pancreatic cancer was 176.853, also providing extremely strong evidence for a correlation. The Pearson correlation coefficient was −0.001, indicating a very weak but stable negative relationship. Using the Jeffreys prior (C =0) and the available data (Tables S4,S5), the posterior probability distribution of the correlation parameter was obtained. The posterior mean and mode were consistent with the Pearson coefficient, with a variance approaching zero. Due to the large overall sample size, the posterior distribution was highly concentrated.

Dose-response relationship

Corrected urinary perchlorate concentrations in patients with thyroid cancer and pancreatic cancer were predominantly concentrated in the lowest quintile, and no clear dose-response relationship was observed (Figures 2,3).

Figure 2 The relationship between corrected perchlorate and pancreatic cancer. 0/1 indicates no/yes.

Figure 3 The relationship between corrected perchlorate and thyroid cancer. 0/1 indicates no/yes.

Discussion

This study provides nationally representative evidence on the relationship between urinary perchlorate and malignancies of endocrine-related tissues, focusing on thyroid cancer and pancreatic cancer. Using NHANES data, we observed a significant association between corrected perchlorate and both thyroid and pancreatic cancer. No linear dose-response pattern was found for either cancer type. The absence of a clear dose-response relationship may be partly attributable to the limited sample size. Moreover, the biological effects of environmental endocrine-disrupting chemicals are often non-linear and may follow threshold or non-monotonic dose–response patterns. Complex interactions between perchlorate and other dietary or environmental factors could also obscure a straightforward dose-response gradient (22,23). To our knowledge, few population-based studies have examined the potential link between perchlorate exposure and pancreatic cancer, making these findings relevant for environmental health risk assessment.

Perchlorate is a competitive inhibitor of the NIS, reducing iodine uptake and impairing thyroid hormone synthesis (14). Multiple studies using data from NHANES have found that there is a certain association between perchlorate and thyroid hormone T4, independent of other variables (24-26). Through feedback regulation of the hypothalamic-pituitary-thyroid axis, reduced thyroid hormone levels increase thyroid-stimulating hormone (TSH) secretion, potentially inducing thyroid cell hyperplasia and, in the presence of genetic instability, carcinogenesis. Some studies, including a 2018 case–control study from the Cancer Hospital of the Chinese Academy of Medical Sciences and another from southeastern China (21), reported that perchlorate may increase the risk of PTC, sometimes in a non-linear manner (22). In contrast, studies conducted in California and Nevada found no elevated thyroid cancer risk associated with perchlorate-containing drinking water (27,28). These inconsistencies may arise from population differences, regional variations in exposure sensitivity, covariate adjustment strategies, and the influence of strong risk factors such as genetic mutations and radiation, which could mask the weaker effects of perchlorate. This lack of correlation may reflect synergistic interactions between perchlorate and co-exposures. Elevated urinary perchlorate combined with thiocyanate has been linked to increased central thyroid hormone sensitivity in U.S. adults (29).

Our observation of an association between perchlorate and pancreatic cancer aligns with several recent findings. A 2024 study by Rodriguez et al. (30) reported higher perchlorate levels in patients with PDAC. Experimental studies have demonstrated perchlorate-related effects on pancreatic tumor cell lines and NIS-mediated iodide uptake in PDAC models, supporting the biological plausibility of our results (31,32).

Two pathways may explain the link between perchlorate and pancreatic cancer. First, a direct toxic effect: perchlorate can reach the pancreas through the bloodstream or bile reflux, where NIS expression in ductal epithelial cells facilitates iodine uptake for antioxidant defense (30). Inhibition of this uptake may cause reactive oxygen species accumulation and DNA damage. Second, an indirect metabolic pathway: pancreatic cancer is often accompanied by insulin resistance, and some studies have shown that dracorhodin perchlorate can modulate endoplasmic reticulum stress and mitochondrial pathways, affecting β-cell survival and insulin secretion, potentially influencing carcinogenesis (33).

Differences in the research results for thyroid cancer and pancreatic cancer may be related to tissue-specific variations in NIS regulation. NIS is a natural transmembrane glycoprotein predominantly expressed in the thyroid (34). However, NIS has also been explored as a therapeutic target for PDAC in numerous clinical studies (35-37). While thyroid NIS activity is tightly regulated by TSH, pancreatic NIS expression is influenced by local inflammatory signals and oncogenic mutations, which may alter the sensitivity of cancerous and normal pancreatic tissues to perchlorate.

Traditionally, research on perchlorate toxicity has focused on the thyroid. However, our results suggest a possible link to pancreatic cancer, highlighting the need to include pancreatic health in perchlorate risk assessments. In etiological research on pancreatic cancer, alongside established factors such as smoking, alcohol consumption, and high-fat diet, more attention should be given to environmental pollutants. For individuals with occupational exposure to perchlorate, personal protective measures, reduced workplace exposure, and regular health monitoring are advisable. At the community level, treatment of drinking water in perchlorate-contaminated areas, such as those near fireworks factories and military facilities, should be strengthened, alongside enhanced environmental monitoring. Policymakers should consider implementing stricter environmental emission standards for perchlorate.

There are some limitations in this study. The small number of cancer cases may have limited statistical power, and cancer status based on self-report could introduce misclassification. The cross-sectional design precludes causal inference, and reverse causation due to impaired renal clearance cannot be excluded. Co-exposures to other environmental toxins were unmeasured, covariate data were limited, and findings from U.S. adults may not generalize globally. Perchlorate exposure was estimated from a single spot urine sample, which may not reflect long-term exposure relevant to carcinogenesis, possibly leading to underestimation of true associations. Future research should employ prospective cohort designs with repeated exposure measurements, larger case numbers, and integrated environmental and biomarker analyses to better elucidate causal pathways and underlying mechanisms.

Conclusions

Our study demonstrates a significant association between perchlorate exposure and both thyroid and pancreatic cancer. These findings suggest that perchlorate may pose a potential risk to endocrine health and highlight the need for further investigation into its role in malignancies of endocrine-related tissues and for strengthened measures to reduce exposure. Public awareness of perchlorate pollution and its potential health impacts should be increased.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-1785/rc

Peer Review File: Available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-1785/prf

Funding: This study was supported by Shandong Provincial Natural Science Foundation (Nos. ZR2024QH098 and ZR2024MH306), and Taishan Scholars Project of Shandong Province (No. tsqn202211365).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tcr.amegroups.com/article/view/10.21037/tcr-2025-1785/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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