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Re: Wing: Descriptive Epidemiology by Any Other Name...
> From: "Sandy Perle" <sandyfl@ix.netcom.com>
>
> John Moulder stated:
>
> > January copy of the EHP has not yet reached subscribers. It has
> > only been in the last 24-48 hours that a copy has appeared on the
> > NIEHS website.
>
> The news media printed the details of the allegations from Wing
> and colleagues... Again, WHY haven't there been
> any comments from HPS, or other organizations?
What was in the media was nothing more (and often less) than what was in the
press release. As a scientist, I cannot critique a study when I haven't seen
it.
To critque a study on the basis of a press release is as irresponsible as
publishing by press release in the first place.
I had actually meant to append the following to the previous message, but it
appears that I did not.
---From the NIEHS website-------
http://ehpnet1.niehs.nih.gov/docs/1997/105(1)/wing.html
Steve Wing, David Richardson, Donna Armstrong, and Douglas Crawford- Brown: A
Reevaluation of Cancer Incidence Near the Three Mile Island Nuclear Plant: The
Collision of Evidence and Assumptions. Environ Health Perspect 105:52-57
(1997)
Author Abstract
Previous studies concluded that there was no evidence that the 1979 nuclear
accident at Three Mile Island (TMI) affected cancer incidence in the
surrounding area; however, there were logical and methodological problems in
earlier reports that led us to reconsider data previously collected. A 10-mile
area around TMI was divided into 69 study tracts, which were assigned
radiation dose estimates based on radiation readings and models of atmospheric
dispersion. Incident cancers from 1975 to 1985 were ascertained from hospital
records and assigned to study tracts. Associations between accident doses and
incidence rates of leukemia, lung cancer, and all cancer were assessed using
relative dose estimates calculated by the earlier investigators. Adjustments
were made for age, sex, socioeconomic characteristics, and preaccident
variation in incidence. Considering a 2-year latency, the estimated percent
increase per dose unit +/- standard error was 0.020 +/- 0.012 for all cancer,
0.082 +/- 0.032 for lung cancer, and 0.116 +/- 0.067 for leukemia. Adjustment
for socioeconomic variables increased the estimates to 0.034 +/- 0.013, 0.103
+/- 0.035, and 0.139 +/- 0.073 for all cancer, lung cancer, and leukemia,
respectively. Associations were generally larger considering a 5-year latency,
but were based on smaller numbers of cases. Results support the hypothesis
that radiation doses are related to increased cancer incidence around TMI. The
analysis avoids medical detection bias, but suffers from inaccurate dose
classification; therefore, results may underestimate the magnitude of the
association between radiation and cancer incidence. These associations would
not be expected, based on previous estimates of near-background levels of
radiation exposure following the accident. Key words: dose-response
relationships, ecologic studies, environmental epidemiology, ionizing
radiation, methodology, neoplasms, nuclear power.
---------
Some comments based on my first reading of the article.
1) This is standard ecological-design risk-detection epidemiology. It looks
for associations without any real consideration of plausibility or any serious
consideration of what else is known about the agent or the disease. The fact
that it is "standard" does not make it good science; but stuff like this
appears in the epidemiological literature all the time (e.g., "hot dogs cause
childhood leukemia", which appeared in 1994 in a major epidemiological
journal)
2) This is re-analysis of the Hatch et al data (Amer J Epidem 132:397-412).
No new information appears to have been added.
3) The authors use the dose estimates previously made by Hatch et al (Amer J
Epidem 132:397-412), but assume that while the Hatch et al data is relatively
correct, it is absolutely wrong. That is, they assume that the pattern is
correct but that the absolute dose estimates are wrong. The authors' grounds
for disputing the absolute dose estimates are largely anecdotal (e.g.,
testimony to the NRC about acute radiation sickness).
4) The authors use "relative dose estimates". How these units correspond to
"dose" is not stated.
5) The results assume a two- or five-year latency.
6) Only cancers appearing between 1981 and 1985 are considered. The
explanation appears to be that this is the only data available (i.e., it's
okay to use inappropriate data if that's all that is handy). Since the latent
period for radiation induction of lung cancer is generally believed to be 20+
years, this time period makes no sense.
7) Errors are in "standard errors", multiply these by 1.96 to get 95%
confidence intervals and to assess statistical significance.
8) Cases are assigned "doses" based on their place of residence at the time
of diagnosis. It is not known where these people lived at the time of their
"exposure".
9) If anyone moved post-accident, or was treated in an out-of-area hospital,
the case would be lost.
9) Cancer rates are adjusted for age, sex and socioeconomic status, but not
for smoking history.
10) Two different "models" are used to calculate "expected" cancer rates; one
uses socioeconomic status as a variable, the other does not.
11) The authors make the point that their relative risks are highest for
leukemia, without mentioning that these relative risks are also not
significantly different from one.
12) While exposure-response data is presented, no trend analysis appears to
have been done, and the data presentation is such that it would be difficult
for someone else to do. Any attempt to seriously look at the trend analysis
would also have to deal with the fact that less cancer was observed than was
expected at the lower "doses".
Quick Hill criteria analysis:
- Strength of association: Weak, relative risks are generally below 2 for the
groups with the highest exposures.
- Consistency: None, results are inconsistent with all other epidemiological
studies of radiation induced cancer.
- Specificity: Little relevance, as we know that radiation can induce a
number of different types of cancer.
- Temporality: Okay, the reported increase was after exposure.
- Biological gradient: Unknown, no analysis of exposure-response done.
- Plausibility: None. There is no other epidemiological or experimental
evidence to support relative risks this high at this dose. With the possible
exception of leukemia, there is also no data to support latency periods this
short.
- Coherence: None. Interpretation of the results is incompatible with
essentially everything else that is known about radiation-induced cancer.
- Experiment: None. The experimental data on radiation-induced leukemia and
lung cancer does not support effects at this dose, or in the cancer of lung
cancer, a latency period this short.
- Analogy. None that I can think of. That is, I know of other cases where a
low level environmental exposure has produced an effect that is incompatible
with the results of higher dose exposures and incompatible with substantial
experimental evidence.
- Overall: The observed associations, but themselves, add little or nothing
to our knowledge of the effects of low level radiation exposure.
John Moulder (jmoulder@its.mcw.edu)