Multiple variables impact prostate and breast cancer incidence, including genetic heredity in addition to environmental and societal influences. Endogenous steroids and thyroid hormones are required for hormone-mediated malignancies equivalent to ovarian, endometrial, testicular, thyroid, and melanoma. Identifying environmental toxins that influence these hormone levels might result in latest cancer prevention and mitigation strategies.

In a recent study published within the Journal of Exposure Science & Environmental Epidemiology, researchers determined the relationships between perfluoroalkyl and polyfluoroalkyl substances (PFAS), parabens, and phenols, and self-documented prior cancer diagnoses using the National Health and Nutrition Examination Survey (NHANES) data.

Study: Exploratory profiles of phenols, parabens, and per- and poly-fluoroalkyl substances amongst NHANES study participants in association with previous cancer diagnoses. Image Credit: Sibirian sun / Shutterstock.com

Concerning the study

In the current cross-sectional epidemiological study, researchers examine the connection between phenol exposure and past cancer diagnoses, in addition to racial and ethnic differences within the connections between ambient phenol, paraben, and PFAS exposures and the history of cancer diagnosis.

The researchers aimed to find out whether there was a link between phenol, paraben, and PFAS chemical exposure and former endocrine-active cancer diagnoses in men and ladies 20 years and older. The medical conditions questionnaire was used to extract concentrations of seven PFAS compounds and 12 parabens/phenols, demographic data, and self-documented diagnoses of malignancies of the breast, thyroid, uterus, ovary, prostate, and melanoma.

Five PFAS compounds, including 2-(N-methyl-PFOSA)acetic acid (MPAH), perfluorohexane sulfonic acid (PFHS), perfluoroundecanoic acid (PFUA), perfluorononanoic acid (PFNA), and perfluorodecanoic acid (PFDE) were measured in all cycles from 2005 to 2018. PFAS levels were quantified from serological samples using turbo ion spray ionization, high-performance-type liquid chromatography-tandem mass spectrometry (HPLC-MS)

Between 2013 and 2016, the degrees of 5 additional phenols and parabens were measured, of which included bisphenol-S (BPS), bisphenol-F (BPF), 2,4-dichlorophenol (DCP24), 2,5-dichlorophenol (DCP25), and triclocarban (TCC).

Between 2005 and 2016, seven phenols/parabens, including benzophenone-3 (BP3), bisphenol-A (BPA), methyl-paraben (MPB), triclosan (TCS), propyl-paraben (PPB), butyl-paraben (BPB), and ethyl-paraben (EPB) were measured. Five additional phenols and parabens were tested between 2013 and 2016.

Logistic regression models were used and adjusted for covariates equivalent to age, body mass index (BMI), education, race, serum concentrations of the tobacco smoke metabolite cotinine, creatinine, and the poverty-income ratio to find out odds ratios (ORs) for the relationships between prior tumor diagnoses and a rise within the interquartile range (IQR) range in exposure biological markers. Race was considered a social proxy for structural social determinants, and correlations were studied amongst Mexican-Americans, non-Hispanic blacks, and other Hispanics individually from whites.

The goal of the study was to look at gender differences in environmental exposure to PFAS, phenols, and parabens and past cancer diagnoses. To evaluate sex-specific malignancies, each datasets were divided into women and men, which yielded final sample sizes of 8,010 males and eight,686 females within the PFAS evaluation and 5,084 males and 5,344 females within the phenol/paraben study.

Study findings

PFAS and phenol/paraben exposure were linked to a rise in cancer risk in white women. Women with a history of melanoma had higher levels of PFDE, PFNA, PFUA, BP3, DCP25, and DCP24.

Prior ovarian tumor was linked to greater DCP25, BPA, and BP3 levels, whereas a history of uterine cancer was linked to higher PFNA levels. Various PFAS chemicals were linked to prior uterine and ovarian malignancies amongst white females, whereas BPF or MPAH were linked to prior breast tumors amongst non-white females.

Racial differences within the relationships between environmental exposures and past cancer diagnoses were observed, thus highlighting racial disparities in inherent cancer risk and exposure to environmental toxins. Greater PFAS exposure was related to an increased risk of prior cancer diagnosis in white women, whereas increased phenol/paraben exposure was attributed to a better risk of previous cancer diagnosis in black and Mexican-American women.

Increased PFOA and PFOS exposure was related to a significantly increased risk of previous uterine cancer diagnosis in other Hispanic women as in comparison with white women, whereas increased PFDE, PFNA, and PFUA exposure was linked to a significantly increased risk of previous uterine cancer diagnosis in each white and other Hispanic women.

Women with a history of melanoma had greater PFDE, PFNA, PFUA, BP3, DCP25, and DCP24 levels, with OR values of two.1, 1.7, 1.8, 1.8, 2.4, and 1.9, respectively. Previous ovarian cancer diagnoses were related to increased DCP25, BPA, and BP3 levels with OR values of two.8, 1.9, and 1.8, respectively. Previous uterine tumor was linked with greater PFNA, whereas higher EPB was related to lower PFNA, with OR values of 1.6 and 0.3, respectively.

Conclusions

PFAS chemicals, including PFDE, PFNA, and PFUA, were related to an increased risk of prior melanoma diagnosis amongst women. Likewise, concentrations of BPA, BP3, and two dichlorophenols were related to an increased risk of ovarian cancer. The present study highlights a sexually dimorphic nature of melanoma risk and a possible estrogen-dependent mechanism for each cancer types.

These findings could help discover the potential role of environmental toxins in prospective studies of cancer. Future studies are needed to raised characterize endocrine disruptor associations with thyroid cancer, discover environmental exposures that increase individuals’ risk of developing ovarian cancer, and explore the roles of estrogenic chemicals and estrogen disruption within the pathology of melanoma and ovarian cancer.