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  • br Table br Associations between breast

    2020-07-06


    Table 3
    Associations between breast and prostate cancer and occupational exposure to alkylphenolic compounds.
    Breast cancer
    Prostate cancer
    Never exposed to alkylphenolic compounds 1233 1101 Ref Ref 1103 764 Ref Ref
    Occasional and/or low intensity (scores 1 and 2d)
    Duration (years)e
    Tertile 1
    Ptrend
    Tertile 1
    Ptrend
    Tertile 1
    Ptrend
    Tertile 1
    Ptrend
    Tertile 1
    Ptrend
    OR = odds ratio, CI = confidence interval. Numbers do not add up to the totals due to missing values.
    a Adjusted for region, age and educational level.
    b Adjusted for age, region, educational level, BMI, smoking, alcohol consumption, occupational shift, exposure to pesticides, exposure to solvents, hormonal contraception, postmenopausal hormone therapy, menopausal status and parity.
    c Adjusted for age, region, educational level, BMI, smoking, alcohol consumption, occupational shift, exposure to pesticides and exposure to solvents.
    In general, we found no associations between prostate cancer and exposure to alkylphenolic compounds. Previous studies suggested a possible relationship between exposure to endocrine disrupting com-pounds with estrogenic activity, other than alkylphenols, and an in-creased prostate cancer risk (Hess-Wilson and Knudsen, 2006). How-ever, no epidemiologic study has ever evaluated the relationship between alkylphenolic compounds and prostate cancer. Besides their estrogenic activity, alkylphenolic compounds may also have weak anti-androgenic effects, as they can act as partial agonists Spectinomycin of androgenic receptors thus inhibiting the effect of full agonists (Weiss et al., 2009). Androgens are necessary for cancer prostate development, and an-drogen receptor signaling has been well characterized in the develop-ment of prostate cancer metastasis (Zhou et al., 2014). Although they have been less studied in cancer prostate risk compared with breast cancer, there is evidence that high doses of estrogens also have direct effects on the development of the prostate gland and also indirect ef-fects through the suppression of the hypothalamic pituitary gonadal axis (Jarred et al., 2000). Metabolism of these sex Spectinomycin is complex and correlated and conversion of androgens to estrogens is mediated by an enzyme encoded by CYP19A1 (Risbridger et al., 2010; Rothenberger et al., 2018). Given the complexity of the hormonal metabolism, and the estrogenic and anti-androgenic effects of alkylphenolic compounds, further research is needed to disentangle whether and how these compounds could influence prostate cancer risk.
    JEMs for occupational exposure assessment are useful and cost-ef-ficient tool in large scale studies (Kauppinen, 1996; Kim et al., 2011; Le Moual et al., 2000; Martín-Bustamante et al., 2017), but they can lead to substantial misclassification of exposures (Rothman et al., 2007). In the present analysis, this misclassification would be non-differential as the exposure assessment was blind to the case-control status. In case of truly positive associations, it would result in the attenuation of the estimates for binary and continuous exposures (Pearce et al., 2007; Steenland et al., 2000). The JEM used in the present analyses was de-veloped undertaking several strategies to minimize potential sources of misclassification. Among others, it considered relevant changes over time in use and manufacture of alkylphenolic compounds in the same population that it is applied, which probably results in better estimates of the exposure. However, we could not validate the JEM using biologic measurements given the short life of these compounds, and the changes in use over time. Evaluating levels among workers may help better understanding current exposures, but the scores in our JEM reflect lifetime exposures which have greatly varied over time. We had the opportunity to adjust for many potential confounders, including well-established and other potential risk factors for breast and prostate cancer. We did not observe clear evidence of confounding by any of them, although residual confounding cannot be completely discarded in explaining some of our results. Non-occupational sources of exposure, such as diet, use of personal care and household cleaning products, could be relevant sources of alkylphenolic compounds. The JEM ex-posure scores reflect the probability that occupational exposure con-tributes significantly to an individual's body burden in comparison to other sources of exposure. Although we do not expect big differences in background levels, we were not able to assess non-occupational sources of these compounds and therefore certain misclassification of the ex-posure cannot be ruled out. The relatively large sample size of the study, allowed us to perform several subgroup analysis. Nevertheless, some of the analyses by scenarios and compound subtypes were based on small sample sizes. Some of the job titles involving alkylphenols actually involved a mixture of alkylphenols and alkylphenolic ethox-ylates, and therefore the JEM that we used did not assign a more spe-cific category of compound. Some of the reported associations could be spurious as multiple comparisons were performed in our analysis.