Epidemiologist Fired for Reporting Politically Incorrect Results

James Enstrom, an epidemiologist who has worked at the UCLA School of Public Health for 34 years, was recently fired, supposedly because his research "is not aligned with the academic mission of the Department [of Environmental Health Sciences]." As Michael Siegel notes, this rationale is patently false. The department's official mission is to "explore the fundamental relationship between human health and the environment," and that is exactly what Enstrom has done.

The problem is not that he tackled the wrong questions; it's that he came up with the "wrong" answers. Specifically, he has failed to find a connection between exposure to fine particulate matter and disease. Worse, he is a prominent critic of the view that such a connection is established well enough to justify new regulations by the California Air Resources Board (CARB).

He has not only criticized the evidence underlying the proposed regulations but has made trouble by pointing out that a key CARB staffer, Hien Tran, had falsified his academic credentials and that a UCLA colleague who supports regulation of fine particulate matter, John Froines, had served on a scientific panel that advises CARB for 25 years without being reappointed every three years, as required by law.

Froines, who has publicly ridiculed Enstrom, participated in the faculty vote recommending his dismissal. Enstrom's popularity among his colleagues was not enhanced by his work on secondhand smoke, which also failed to generate politically correct results.

These circumstances have led observers such as Siegel, Sacramento Bee columnist Dan Walters, Bakersfield Californian columnist Lois Henry, epidemiologist Carl Phillips, and Jeff Stier of the American Council on Science and Health (where Enstrom is a trustee) to conclude that Enstrom's sacking was politically motivated.

Siegel reviews Enstrom's impressive body of work dating back to 1975, which includes studies reporting positive as well as negative results (among them important research on the lifestyle factors that make Mormons less prone to cancer). Siegel concludes that Enstrom "has not been afraid to report the results of his research as they unfold," an openness to evidence that clashes with what appears to be the true mission of his former department:

The mission of the Department of Environmental Health Sciences is not to "explore the fundamental relationship between human health and the environment." Instead, its mission is to show that fine particulate matter pollution and other environmental exposures adversely affect human health.

If your research fails to show an adverse effect of an environmental exposure on human health, then your research is apparently no longer "aligned" with the mission of the Department and School....As soon as you obtain negative findings and report them, you have deviated from the School's mission and you are at risk of being fired....

Is there no room for a difference of opinion in a public health institution? Must all faculty members [toe] a certain party line, regardless of what their research shows?

You can supply the answers yourself after considering the weak case against Enstrom as a scientist. I have interviewed him several times over the years, and he impresses me as an honest and conscientious investigator who is genuinely dismayed by the extent to which science has been politicized since he began his career. It is sadly unsurprising that his long stint at UCLA has ended this way.

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Promising malaria breakthrough

THE race to subvert the drug resistance of malaria parasites has been hotly contested by scientific teams across the world. Rowena Martin leads the team that solved the problem, which is why she has been awarded the inaugural Macquarie University Eureka Prize for Early Career Research. She is among 19 winners of the Australian Museum's Eurekas, worth $190,000 and now in their 21st year, announced last night in Sydney.

After establishing how the drug resistance works, Martin and her team are now collaborating on drugs to overcome it.

At 36, Martin is a National Health and Medical Research Council Australian Biomedical Fellow and shuttles between the Australian National University and the University of Melbourne. Last year her paper describing her breakthrough work in the field was published in Science.

Malaria causes untold human suffering; there are 300 million cases annually and a million deaths, mostly of children, and mostly in developing countries.

The parasite has now developed resistance to one of the most effective drugs ever used against it, chloroquine, that works by accumulating in large quantities inside the parasite's "stomach", or digestive vacuole. Resistant parasites thwart that accumulation, leaking the drug out of the vacuole and rendering it harmless.

"It was during my PhD that I began developing a hypothesis that led to this work," she says, harking back to 2002.

By then, scientists had discovered the culprit was a protein called the chloroquine resistance transporter (PfCRT), that sits in the membrane enclosing the digestive vacuole. "But they didn't know exactly what it did, or what similarities it had to other proteins, so they had no strong direction to follow in research.

"There were a lot of teams trying to produce enough of it to experiment on, or understand it, but they were not finding anything conclusive. It was all very unclear and that's when I began thinking of this as an interesting field.

"I had had some experience in doing some expression of malaria proteins and had some ideas for what might be causing the problem and a hypothesis on a way of getting around the problem. When I began my postdoctoral work I put it into practice."

She turned to a common lab animal, the South African claw-toed frog, whose eggs are large and therefore easy to inject with genetic material encoding the protein of interest. The egg acts as "a little factory, producing many copies of the protein and targets them to the egg surface, where they can be studied".

By getting the eggs to produce and send to their surface the copies of the protein, the team was able to introduce chloroquine and observe how the resistant parasites dealt with it. Now the way is open for the development of drugs that can inhibit the function of the mutant protein.

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