Thursday, September 29, 2011

Real Life's a Beach (cont'd)

[fixed some typos and missing words]

It appears then, that the decision to buy Times Beach was motivated in part by the Reagan administration's concern about the EPA's image of inaction. Furthermore, the action was in part necessitated by the need to aid utterly destitute flood victims. The question remains then of assessing the danger of dioxin exposure.

How dangerous is dioxin to humans? The answer seems to be that nobody really knows. The claim that dioxin is one of the deadliest substances known to man is based on its extreme toxicity in guinea pigs. [16] No human deaths have yet been reported. Other animal tests, particularly in rats, clearly show that dioxin is a potent "carcinogen," but scientific opinion is divided as to whether it can cause cancer by itself or whether its only action is to promote cancer in cells that are already cancerous. Evidence for cancer in humans is far from conclusive. The American Medical Association's Advisory panel on toxic substances summed up these findings in an October, 1981, report:
There is little substantive evidence for the many claims that have been made against dioxin and related compounds. While suggestive, the data from animal toxicity studies are not necessarily applicable to man. [17]
Yet the Times Beach exposure may represent the greatest long term exposure to dioxins in history and as such will be looked at closely. The government is trying to resolve the uncertainties with a wide variety of epidemiological studies that will cost more the $100 million. If dioxin is the hazard that some believe it is, the costs of moving entire towns probably are not greater than the risks of letting people continue to live there.
[16] Rebecca L. Rawis, "Dioxin's Human toxicity is most difficult problem," Chemical and Engineering News, 6 June, 1983, p. 37.

[17] Robert Signor, "Dioxin effect on humans seems mild so far," St. Louis Post-Dispatch, 5 Dec., 1982, sec A, p. 1.


  1. Findings more recent than what was available in 1983 exist:

    The Seveso, Italy accident in 1976 caused the contamination of a large population by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Possible long-term effects have been examined through mortality and cancer incidence studies. We have updated the cancer incidence study which now covers the period 1977-96.

    The study population includes subjects resident at the time of the accident in three contaminated zones with decreasing TCDD soil levels (zone A, very high; zone B, high; zone R, low) and in a surrounding non-contaminated reference territory. Gender-, age-, and period-adjusted rate ratios (RR) and 95% confidence intervals (95% CI) were calculated by using Poisson regression for subjects aged 0-74 years.

    All cancer incidence did not differ from expectations in any of the contaminated zones. An excess of lymphatic and hematopoietic tissue neoplasms was observed in zones A (four cases; RR, 1.39; 95% CI, 0.52-3.71) and B (29 cases; RR, 1.56; 95% CI, 1.07-2.27) consistent with the findings of the concurrent mortality study. An increased risk of breast cancer was detected in zone A females after 15 years since the accident (five cases, RR, 2.57; 95% CI, 1.07-6.20). No cases of soft tissue sarcomas occurred in the most exposed zones (A and B, 1.17 expected). No cancer cases were observed among subjects diagnosed with chloracne early after the accident.

    The extension of the Seveso cancer incidence study confirmed an excess risk of lymphatic and hematopoietic tissue neoplasms in the most exposed zones. No clear pattern by time since the accident and zones was evident partly because of the low number of cases. The elevated risk of breast cancer in zone A females after 15 years since the accident deserves further and thorough investigation. The follow-up is continuing in order to cover the long time period (even decades) usually elapsing from exposure to carcinogenic chemicals and disease occurrence.

  2. Keep in mind that chemical cancer epidemiology requires a long time for follow-up.

  3. It might be more fun to tickle your chemical funny bone and look into mechanisms of DNA intercalation with planar aromatic hydrocarbons.

    That's a pretty easily understood and well accepted mechanism of genotoxicity.

    The current skinny is that dioxins might not intercalate directly (which would explain some of what you describe in your 2nd paragraph), but interact with an enzyme responsible for modifying the genotoxicity of intercalating agents.

    The shape of planar aromatic hydrocarbons also helps explain the role that similar compounds play in endocrine disruption and dysfunction.

    Let's hope you keep your current fight limited to dioxins and don't extend it to PCBs.

  4. PCBs resemble dioxin but for the rotational degree of freedom about the biphenyl carbon-carbon bond. This extra flexibility must translate into enhanced binding, or perhaps binding to a different enzyme.

    Chlorine substituents are relatively large (about the size of a methyl) and so I can see why a dioxin would fit where say a naked benzene would.

  5. and so I can see why a dioxin would not fit where say a naked benzene would.