Clinical Review

Association of Dioxin and Dioxin-like Congeners With Hypertension

Fed Pract. 2018 May;35(5):20-26

References

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Conclusion

Studies have shown an association between dioxins and endocrine disruption, reproductive and developmental problems, and certain cancers.^3,24 The Seveso Women’s Health Study of an industrial accident in Italy linked dioxins to an incidence of DM, obesity, or metabolic syndrome.²⁵ By contrast, evidence of a link between dioxins and hypertension has been limited and inconsistent. Seven of the 8 studies reviewed in this study found moderate evidence of association in patients with at least 1 chemical congener and a certain subset of the study population (Table).

Given their nature, however, these studies cannot prove a causal relationship, and their results are only suggestive and should be treated as such.

The Vietnam-Era Veterans Health Study found a higher OR of developing hypertension in herbicide sprayers than in its control group. Korean Vietnam War veterans stratified by either self-reported risk or military assignment also had significant associations. For male steelworkers in Italy, occupational exposure had a moderately higher RR in the exposure cohort. In the NHANES study, background levels of POPs were positively associated, but only in men. A nonoccupational study in urban and rural areas of Japan found a significant association between dioxins and hypertension. A nonoccupational study of elderly Swedes found a significant association with only 1 chemical congener. A study of Inuits in Greenland found no significant associations, but a study of Inuits in Canada did yield an association.Recent studies maintain the 2012 veterans update regarding a limited but suggestive association of dioxin and hypertension.⁴ Despite having high power because of the number of exposed patients, these observational studies can posit only an associative relationship, not a causal one. These studies also are limited by their categorization of dioxin exposure levels—ranging from perceived exposure to proximity and direct serum dioxin measurement. Moreover, chemical levels are measured an inconsistent number of years after exposure, and therefore, as dioxins are primarily metabolized by CYP genes, different metabolic rates could account for different susceptibility to health effects.²

In vivo animal studies could better characterize the effect of time point of exposure and effects on hypertension. Studies could also examine the synergistic effects of dioxins and other toxins, or smoking or alcohol use, on hypertension. New clinical guidelines for hypertension will have an impact on studies. Overall, clinicians who treat patients with known exposure to dioxins can suggest with moderate confidence that it is likely not a primary reason for the development of hypertension. At most, dioxin exposure is a contributing factor in the development of hypertension, with lifestyle, smoking, diet, and genetics playing more compelling roles.