Peer reviewers of EPA’s TCE report must affirm that the key risk is fetal heart damage

Richard Denison, Ph.D., is a Lead Senior Scientist.

Last week, the EPA Science Advisory Committee on Chemicals (SACC) conducted a virtual peer review meeting for the Agency’s draft risk evaluation of trichloroethylene (TCE). As expected, there was substantial discussion on the appropriateness of EPA’s decision to make risk determinations based on immune endpoints rather than fetal cardiac malformations (FCMs). Unfortunately, the review panel lacked anyone with specific expertise in cardiac development.

During the meeting, many of the peer review panelists signaled an initial inclination toward supporting EPA’s decision to use immune endpoints for risk determinations. However, panel members also noted with serious concern the recent investigations that have uncovered political influence exerted on EPA that led it to base the risk determinations in the draft risk evaluation on immune endpoints instead of FCMs.

Stepping back from the specifics of the discussions last week, it is important to understand the longstanding basis and support for EPA’s reliance on FCMs, the unprecedented nature of EPA’s decision to now move away from it, and the adverse implications of the decision for EPA’s ability to adequately manage the risks of TCE to all relevant subpopulations.

This decision is a major departure from thoroughly peer-reviewed science, fails to protect the most sensitive populations as mandated by TSCA, and deviates dramatically from existing Agency guidance. These concerns, discussed at length in EDF’s comments in the TCE Docket, are briefly summarized below: 

  • Setting-aside of extensive peer-reviewed science

There is strong scientific support for TCE-induced FCMs not only from the Johnson et al. 2003 study but from epidemiological, in vivo, and in vitro studies.

EPA and other scientific authorities – including the EPA Scientific Advisory Board (SAB) – have repeatedly examined and affirmed the importance of the FCM endpoint:

Any decision by the current peer review panel, lacking direct and specific expertise in cardiac development and based on discussions at a virtual meeting missing key members who could not participate, to discount years of robust scientific review that have upheld the database on fetal cardiac malformations must be made extremely carefully.

  • Failure to protect sensitive populations

EPA acknowledges that “congenital heart defects were the most sensitive endpoint for TCE” (p. 377; Table 4-5 on p. 280). This endpoint is directly relevant to the potentially exposed or susceptible subpopulations of pregnant women, infants, and children identified under TSCA.

By instead using the immune endpoint for risk determinations, EPA fails to ensure that it is protecting “potentially exposed or susceptible subpopulations,” as called for under TSCA.  EPA cannot adequately identify or protect against risks specific to pregnant women and their developing fetuses by selecting immune effects as the basis for its risk determinations.

In other words, it is not simply a matter of choosing between two endpoints for the same population; these endpoints are relevant to distinct, if overlapping, subpopulations. The SACC should ensure that its advice to EPA is consistent with EPA’s mandate to protect the most sensitive subpopulations.

  • Deviation from Agency policies

EPA’s choice to dismiss FCMs contradicts previous agency assessments of TCE and existing agency guidance to use the most sensitive endpoint and protect the most sensitive group, including:

The National Academy of Sciences (NAS) has also reiterated the need to protect the most sensitive subpopulations and to protect against the most sensitive endpoints:

These documents make clear that if EPA protects against the most sensitive endpoint, it will also generally protect against other effects.  In contrast, EPA asserts without providing supporting evidence that “it is expected that addressing risks for these [immune system] effects would address other identified risks.” (p. 377)  EPA’s “expectation” contravenes its own scientific guidance.

In summary, a recommendation by the SACC supporting EPA’s profoundly problematic decision to use immune rather than fetal cardiac endpoints for risk determinations on TCE is directly counter to the weight of evidence and years of peer review; ignores TSCA’s mandate to protect sensitive subpopulations; and disregards extensive Agency policies on the selection of the most sensitive endpoints for risk modeling.

The public health consequences of this choice will be substantial. Risk determinations based on immune endpoints rather than fetal cardiac malformations would allow EPA to develop regulations that are on the order of 500-fold less protective of acute risks and 10-fold less protective of chronic risks.


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