Goebel v. Denver & Rio Grande Western Railroad

F I L E D
United States Court of Appeals
Tenth Circuit
PUBLISH
OCT 9 2003
UNITED STATES COURT OF APPEALS
PATRICK FISHER
Clerk
TENTH CIRCUIT

RICHARD W. GOEBEL,

Plaintiff - Appellee,
vs. No. 02-1391

THE DENVER AND RIO GRANDE
WESTERN RAILROAD COMPANY,
a Delaware corporation,

Defendant - Appellant.

APPEAL FROM THE UNITED STATES DISTRICT COURT
FOR THE DISTRICT OF COLORADO
(D.C. No. 94-N-2206 (BNB))

Lawrence M. Mann, Alper & Mann, P.C., Washington, D.C., (and Christopher B.
Little, Montgomery, Little & McGrew, P.C., Englewood, Colorado, with him on
the brief), for Plaintiff - Appellee.

James W. Erwin (and Thomas R. Jayne, Thompson, Coburn, L.L.P., St. Louis,
Missouri, and Steven E. Napper, Denver, Colorado, on the briefs), for Defendant -
Appellant.

Before KELLY, HENRY, and HARTZ, Circuit Judges.

KELLY, Circuit Judge.
 In June 1999, Plaintiff-Appellee Richard W. Goebel obtained a $755,000

jury verdict against his employer, Defendant-Appellant The Denver and Rio

Grande Western Railroad Company (“Railroad”), for injuries suffered on the job.

The Railroad appealed and we concluded that the district court failed to perform

its gatekeeper function and thus abused its discretion by admitting the testimony

of plaintiff expert Dr. Daniel Teitelbaum. Goebel v. Denver and Rio Grande W.

R.R. Co., 215 F.3d 1083, 1088 (10th Cir. 2000) (“Goebel I”). Accordingly, we

reversed and remanded for a new trial. Id. at 1089.

On remand, the Railroad renewed its motion to exclude Dr. Teitelbaum’s

testimony under Daubert v. Merrell Dow Pharms., Inc., 509 U.S. 579 (1993).

After denying the Railroad’s request for an evidentiary hearing, the district court

denied the Railroad’s Daubert motion in a thorough written order. To expedite

appeal on the core issue, the parties stipulated to a judgment in Mr. Goebel’s

favor in an amount equal to the initial jury award, with the Railroad reserving its

right to appeal the district court’s Daubert decision. After the court entered

judgment, the Railroad filed this appeal arguing that the district court abused its

discretion in admitting Dr. Teitelbaum’s testimony. We exercise jurisdiction

pursuant to 28 U.S.C. § 1291 and affirm.

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 Background

Mr. Goebel claims that in January 1994, he was injured on the job during a

mishap in the Moffat Tunnel in Colorado which involved exposure to high

elevations and diesel fumes. Details of the mishap as described in Goebel I are

incorporated by reference. 215 F.3d at 1085-87. As we noted then, Mr. Goebel

sued the Railroad under the Federal Employers’ Liability Act alleging personal

injuries resulting from the tunnel incident. The district court granted summary

judgment to Mr. Goebel on the question of liability and limited the trial to issues

of causation and damages. At trial, Dr. Teitelbaum testified as to the causation of

Mr. Goebel’s injuries:

I believe that the cause of Mr. Goebel’s injury was his
exposure to a unique environment, deficient in oxygen at low
barometric pressure, contaminated with pulmonary irritants, which
combined with the unique physiologic setting which takes place at
high altitude produced an oxygen lack syndrome, which produced
swelling in his brain, called cerebral edema, which resulted in small
diffuse pressure injuries which resulted in his cognitive defect.
It’s a complicated chain of events, but one which is relatively
simple to explain on the basis of the fundamental physiology. All of
these pieces have been looked at in separate events. In this
gentleman, they occurred at the same time and produced this result.

I R. at 50. The jury found in favor of Mr. Goebel and awarded him $755,000 in

damages.

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 Discussion

I. Standard of Review

As we stated in Goebel I, we review de novo the question of whether the

district court performed its gatekeeper role and applied the proper legal standard

in admitting an expert’s testimony. 215 F.3d at 1087; see also Dodge v. Cotter

Corp., 328 F.3d 1212, 1223 (10th Cir. 2003). We then review for abuse of

discretion the trial court’s actual application of the gatekeeper standard in

deciding whether to admit or exclude an expert’s testimony. General Elec. Co. v.

Joiner, 522 U.S. 136, 142 (1997). The trial court’s broad discretion applies both

in deciding how to assess an expert’s reliability, including what procedures to

utilize in making that assessment, as well as in making the ultimate determination

of reliability. Kumho Tire Co. v. Carmichael, 526 U.S. 137, 152 (1999); Dodge,

328 F.3d at 1223. Accordingly, we will not disturb the district court’s ruling

unless it is “arbitrary, capricious, whimsical or manifestly unreasonable” or when

we are convinced that the district court “made a clear error of judgment or

exceeded the bounds of permissible choice in the circumstances.” Dodge, 328

F.3d at 1223 (quoting Atlantic Richfield Co. v. Farm Credit Bank of Wichita, 226

F.3d 1138, 1163-64 (10th Cir. 2000)).

Neither party argues that the district court has again failed to perform its

gatekeeper function. In fact, as we required on remand, when faced with the

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Railroad’s renewed Daubert objection, the district court took pains to

“demonstrate by specific findings on the record that it ha[d] performed its duty as

gatekeeper.” Goebel I, 215 F.3d at 1088.

Furthermore, although the district court denied the Railroad’s request for a

Daubert hearing, III R. at 661, the Railroad has not appealed that ruling. As a

result, our task here is simply to review the district court’s detailed findings in

light of the record and to apply the deferential abuse of discretion standard to its

decision to admit Dr. Teitelbaum’s testimony. The Railroad’s decision not to

appeal the denial of an evidentiary hearing prompts us to note that our review is

appropriately constrained by the record developed by the parties. In cases such as

this one, where one party alleges that an expert’s conclusions do not follow from

a given data set, the responsibility ultimately falls on that challenging party to

inform (via the record) those of us who are not experts on the subject with an

understanding of precisely how and why the expert’s conclusions fail to follow

from the data set. Any failure by the challenging party to satisfy this

responsibility is at that party’s peril.

II. An Overview of the Railroad’s Arguments

Because it provides a convenient means of analyzing the district court’s

ruling, we believe Dr. Teitelbaum’s opinion is best viewed as a conclusion that

two separate aspects of causation existed in this case: (1) general causation,

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meaning that the particular circumstances in the tunnel could have caused Mr.

Goebel’s injury, and (2) specific causation, meaning that those circumstances did

in fact cause Mr. Goebel’s injury. See, e.g., Soldo v. Sandoz Pharms. Corp., 244

F.Supp.2d 434, 524-25 (W.D. Pa. 2003) (discussing these concepts and collecting

cases). To arrive at general causation, Dr. Teitelbaum reviewed scientific

literature, drew general propositions therefrom, and then combined those

propositions to conclude that the conditions in the tunnel could have caused high

altitude cerebral edema (“HACE”) in Mr. Goebel. III R. at 664-65. To arrive at

specific causation, Dr. Teitelbaum performed a differential diagnosis in which,

after examining and testing Mr. Goebel, he ruled in all scientifically plausible

causes of the injury and then ruled out the least plausible causes until only the

most likely cause remained, i.e., that the tunnel conditions did in fact cause Mr.

Goeble to suffer HACE-induced cognitive deficits. Id. at 668-70.

The Railroad contends that the district court abused its discretion by

admitting Dr. Teitelbaum’s testimony because (1) his general causation opinion

was not supported by the medical literature he relied upon and (2) his differential

diagnosis was unreliable because he failed to account for alternative explanations

of Mr. Goebel’s condition. Aplt. Br. at 15-16. Because the Railroad’s arguments

on appeal are the same as those made before the district court, the district court’s

order and memorandum addresses each of these claims in significant detail.

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III. The Standard for Admitting Expert Testimony

The admissibility of expert testimony is governed by Rule 702 of the

Federal Rules of Evidence:

If scientific, technical, or other specialized knowledge will assist
the trier of fact to understand the evidence or to determine a fact in
issue, a witness qualified as an expert by knowledge, skill,
experience, training, or education, may testify thereto in the form of
an opinion or otherwise, if (1) the testimony is based upon sufficient
facts or data, (2) the testimony is the product of reliable principles
and methods, and (3) the witness has applied the principles and
methods reliably to the facts of the case.

Fed. R. Evid. 702 (2003). Rule 702 imposes on a district court a gatekeeper

obligation to “ensure that any and all scientific testimony or evidence admitted is

not only relevant, but reliable.” Daubert, 509 U.S. at 589. Fulfilling the

gatekeeper duty requires the judge to assess the reasoning and methodology

underlying the expert’s opinion and determine whether it is both scientifically

valid and applicable to a particular set of facts. Id. at 592-93. The Supreme

Court has made clear that “where [expert] testimony’s factual basis, data,

principles, methods, or their application are called sufficiently into question . . .

the trial judge must determine whether the testimony has ‘a reliable basis in the

knowledge and experience of [the relevant] discipline.’” Kumho Tire, 526 U.S. at

149 (quoting Daubert, 509 U.S. at 592).

To be reliable under Daubert, an expert’s scientific testimony must be

based on scientific knowledge, which “implies a grounding in the methods and

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procedures of science” based on actual knowledge, not mere “subjective belief or

unsupported speculation.” 509 U.S. at 590. In other words, “an inference or

assertion must be derived by the scientific method . . . [and] must be supported by

appropriate validation--i.e. ‘good grounds,’ based on what is known.” Id. While

expert opinions “must be based on facts which enable [the expert] to express a

reasonably accurate conclusion as opposed to conjecture or speculation, . . .

absolute certainty is not required.” Gomez v. Martin Marietta Corp., 50 F.3d

1511, 1519 (10th Cir. 1995) (quotation omitted). “The plaintiff need not prove

that the expert is undisputably correct or that the expert’s theory is ‘generally

accepted’ in the scientific community.” Mitchell v. Gencorp Inc., 165 F.3d 778,

781 (10th Cir. 1999). Instead, the plaintiff must show that the method employed

by the expert in reaching the conclusion is scientifically sound and that the

opinion is based on facts that satisfy Rule 702’s reliability requirements. Id.

To assist in the assessment of reliability, the Supreme Court in Daubert

listed four nonexclusive factors that the trial court may consider: (1) whether the

opinion at issue is susceptible to testing and has been subjected to such testing;

(2) whether the opinion has been subjected to peer review; (3) whether there is a

known or potential rate of error associated with the methodology used and

whether there are standards controlling the technique’s operation; and (4) whether

the theory has been accepted in the scientific community. 509 U.S. at 593-94. As

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noted, the list is not exclusive, and district courts applying Daubert have broad

discretion to consider a variety of other factors. Kumho Tire, 526 U.S at 150

(“[W]e can neither rule out, nor rule in, for all cases and for all time the

applicability of the factors mentioned in Daubert . . . . Too much depends upon

the particular circumstances of the particular case at issue.”).

Generally, the district court should focus on an expert’s methodology rather

than the conclusions it generates. Daubert, 509 U.S. at 595. However, an

expert’s conclusions are not immune from scrutiny: “A court may conclude that

there is simply too great an analytical gap between the data and the opinion

proffered.” Joiner, 522 U.S. at 146 (“[N]othing in either Daubert or the Federal

Rules of Evidence requires a district court to admit opinion evidence that is

connected to existing data only by the ipse dixit of the expert.”). In Joiner, when

faced with a claim that the experts in question relied on studies that did not

support their conclusions, the Supreme Court reviewed each study and concluded

that the district court did not abuse its discretion in excluding the testimony. Id.

at 145-46 (“[I]t was within the District Court’s discretion to conclude that the

studies upon which the experts relied were not sufficient, whether individually or

in combination, to support their conclusions . . . .”).

Under Daubert, “any step that renders the analysis unreliable . . . renders

the expert’s testimony inadmissible. This is true whether the step completely

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changes a reliable methodology or merely misapplies that methodology.”

Mitchell, 165 F.3d at 782 (quoting In re Paoli R.R. Yard PCB Litigation, 35 F.3d

717, 745 (3d Cir. 1994)). It is critical that the district court determine “whether

the evidence is genuinely scientific, as distinct from being unscientific

speculation offered by a genuine scientist.” Id. at 783 (quoting Rosen v.

Ciba-Geigy Corp., 78 F.3d 316, 318 (7th Cir. 1996)). Regardless of the specific

factors at issue, the purpose of the Daubert inquiry is always “to make certain that

an expert, whether basing testimony upon professional studies or personal

experience, employs in the courtroom the same level of intellectual rigor that

characterizes the practice of an expert in the relevant field.” Kumho Tire, 526

U.S. at 152.

IV. Did the Medical Literature Support the General Causation Opinion?

A. The Railroad’s Argument

The Railroad first argues that the district court abused its discretion

because Dr. Teitelbaum’s general causation opinion was not supported by the

medical literature he cited. The district court specifically found that Dr.

Teitelbaum’s methodology--i.e., surveying medical literature, drawing general

propositions and then applying them to arrive at a conclusion of general

causation--was reliable. III R. at 664. The Railroad does not contend that this

methodology is per se unreliable, Aplt. Br. at 29, but instead argues that an

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otherwise reliable method was applied to the facts of this case in an unreliable

manner. First, the Railroad suggests that Dr. Teitelbaum erroneously reached

certain “generally accepted propositions” regarding the symptoms, causes and

typical occurrences of HACE only by selecting and relying on portions of the

literature that were favorable to his ultimate conclusion without explaining or

even considering unfavorable portions. Second, it argues that Dr. Teitelbaum

then unjustifiably extrapolated from these erroneously drawn general propositions

to conclude that general causation existed here. Aplt. Br. at 21, 30-38.

B. What the District Court Found

After conducting a “thorough review of the articles,” the district court

found that Dr. Teitelbaum’s reliance on them for various general propositions was

proper and that his conclusions were “adequately supported by the scientific

literature.” III R. at 664. The court emphasized that “[a]nalyzing each individual

article and requiring that each article fully support Dr. Teitelbaum’s theory,

instead of focusing on the cumulative weight of the evidence, would be

overemphasizing [his] conclusions, as opposed to his methodology.” Id. at 665.

The court found that “this is not [a] case” where “too great an analytical gap”

existed between the data and the opinion. Id. After noting that the effects of

each component of Mr. Goebel’s injury--high altitude, oxygen deficiency and

diesel fume exposure--had been individually studied and widely accepted in the

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medical community and that neither the court nor the Railroad had uncovered

evidence suggesting an opposite conclusion, the court concluded that Dr.

Teitelbaum’s opinion was reliable: “Dr. Teitelbaum’s methodology is

scientifically sound, and . . . his opinion reasonably flows from the data upon

which he purportedly relies.” Id. at 667.

C. Did the District Court Abuse its Discretion?

In arguing that the district court’s review of the literature was insufficient,

the Railroad directs us to specific passages in the articles that, in its view,

undercut Dr. Teitelbaum’s general propositions and his ultimate conclusions.

Aplt. Br. at 30-38. As expected, Mr. Goebel reviews the same articles and, like

the district court, reaches a conclusion in direct opposition to the Railroad.

Aplee. Br. at 38-52. Notable, however, is that the Railroad apparently agrees with

the district court that there is no requirement that each individual article must

fully support Dr. Teitelbaum’s precise theory. Aplt. Br. at 29; see also Joiner,

522 U.S. at 146-47 (noting that studies may support a conclusion either

“individually or in combination”) (emphasis added); III R. at 665-66 (collecting

cases).

The Railroad’s core argument is that the district court incorrectly concluded

that “this is not [a] case” where “too great an analytical gap” existed between the

data and the opinion. III R. at 665. When faced with such a claim, we must, as

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did the Supreme Court in Joiner, review the literature to determine whether the

district court was within its discretion in finding an adequate link between the

existing data and the conclusions. 522 U.S. at 145-46. Given the lack of

scientific literature directly addressing the confluence of all of the factors at issue

in the tunnel, such a review is all the more important here.

As we stated above, our review is deferential--only if we are convinced that

the district court “made a clear error of judgment or exceeded the bounds of

permissible choice in the circumstances” will we disturb its ruling. Dodge, 328

F.3d at 1223 (quoting Atlantic Richfield Co. v. Farm Credit Bank of Wichita, 226

F.3d 1138, 1163-64 (10th Cir. 2000)). Despite our expertise on the law, our role

as judges is not to second-guess well qualified and highly trained medical experts

on difficult judgment calls within their field of expertise; our role is merely to

ensure that the district court did not abuse its discretion by concluding that the

expert testimony in this case was admissible under the standards outlined above.

Neither the district court nor this court is in a position to declare or even to know

with any degree of certainty whether otherwise admissible expert testimony is, in

fact, correct. See, e.g., Daubert, 509 U.S. at 596 (“Vigorous cross-examination,

presentation of contrary evidence, and careful instruction on the burden of proof

are the traditional and appropriate means of attacking shaky but admissible

evidence.”). We also approach our review mindful that the district court here had

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the added benefit of the Railroad’s voir dire of Dr. Teitelbaum and its cross

examination of him at trial.

After a careful review of the Railroad’s arguments, Dr. Teitelbaum’s

affidavits, the underlying medical literature and the record as a whole, we

perceive no basis to conclude that the district court abused its discretion by ruling

that Dr. Teitelbaum’s opinion was adequately supported by the scientific

literature. Given the record before us, we too are unpersuaded that this is a case

where too great a gap exists between the proffered expert opinion and the

underlying data.

(1) The Symptoms of HACE

The Railroad first argues that Dr. Teitelbaum’s basic contention--that Mr.

Goebel exhibited symptoms classically associated with HACE--is not supported

by the cited literature. Aplt. Br. at 30. Among the many symptoms exhibited by

Mr. Goebel were a severe headache, tightness in his chest, significant aches and

soreness, shortness of breath, nausea and disorientation that rendered him unable

to read. In the Railroad’s view, the studies cited by Dr. Teitelbaum do not

support a diagnosis of HACE based on these symptoms. After reviewing the

Railroad’s citations to various studies and uncovering no significant support for

its position, we conclude that the district court did not abuse its discretion.

Dr. Teitelbaum’s opinion--that Mr. Goebel suffered from acute mountain

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sickness (“AMS”) which developed into non-acute HACE, see II R. at 356, ¶ 8--

was supported by The Lake Louise Consensus on the Definition of Altitude

Illness, available in Thomas E. Dietz, High Altitude Medicine Guide (2000), II R.

at 398. That study indicates that in the setting of a recent altitude gain, a

headache plus nausea is alone sufficient to support a diagnosis of AMS. Id. Mr.

Goebel clearly satisfied this criteria. The study also states that in such a setting,

the presence of a “change in mental status” in a person with AMS is sufficient to

support a diagnosis of HACE. Id. The included Lake Louise Consensus

worksheet makes it clear that Mr. Goebel’s disorientation is also sufficient to

constitute a change in mental status. Id. at 400. Thus, contrary to the Railroad’s

suggestion, the Lake Louise Consensus supports Dr. Teitelbaum’s conclusions.

In support of its argument, the Railroad also directs us to an isolated

statement in Thomas E. Dietz, Altitude Illness Clinical Guide for Physicians,

High Altitude Medicine Guide (2000), II R. at 403-12, where the author notes that

“I have not yet seen a case of HACE in which the patient didn’t ascend with AMS

symptoms.” Id. at 408. The Clinical Guide admittedly relies on the Lake Louise

Consensus guidelines relating to symptoms and diagnosis of altitude illnesses. Id.

at 403, 407. Because under those guidelines Mr. Goebel exhibited symptoms of

AMS and HACE, the quoted statement relied upon by the Railroad is utterly

irrelevant. When read as a whole, the portions of the High Altitude Medicine

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Guide contained in the record support Dr. Teitelbaum’s opinion. See id. at 416-

18 (discussing the symptoms associated with AMS and HACE and essentially

echoing the conclusions of the Lake Louise Consensus).

Another of the Railroad’s contentions is that the chapter in Michael P.

Ward et al., High Altitude Medicine and Physiology 412-18 (2d ed. 1995),

entitled “High Altitude Cerebral Edema and Retinal Haemorrhage,” II R. at 333,

contradicts Dr. Teitelbaum’s opinion. In fact, in discussing the typical symptoms

associated with AMS and HACE, this chapter once again echoes the conclusions

of the Lake Louise Consensus. Id. (symptoms of AMS include headache and

nausea; clouding of consciousness indicates HACE). Contrary to the Railroad’s

suggestion, Aplt. Br. at 31, this chapter at no point states that “loss of

consciousness” is among the “classic symptoms of HACE.” Id. (emphasis in

original). Although the chapter states that “[o]ften there is also an element of

pulmonary edema” exhibited in HACE sufferers, II R. at 334, it is undisputed that

Mr. Goebel did not exhibit signs of that condition. Nonetheless, this quite

general and self-limited statement is insufficient to render Dr. Teitelbaum’s

conclusion unreliable given the obvious corollary that cases must exist where no

signs of pulmonary edema are exhibited by a HACE sufferer.

A similar issue arises from the Railroad ’s citation to the Statement on High

Altitude Illnesses, Canada Communicable Disease Report (Nov. 15, 1998), II R.

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at 424, which states that HACE “rarely occurs” without high altitude pulmonary

edema. Id. at 430. Although this is a stronger statement than that made in the

High Altitude Medicine and Physiology chapter just discussed, it still fails to

contradict materially Dr. Teitelbaum’s opinion. Once again, this statement is

limited by its own terms, i.e., “rarely.” Id. In addition, the Statement continues

by stating that HACE is characterized by symptoms including an “altered level of

consciousness in the form of confusion [and] impaired thinking.” Id. at 431. Its

discussion of AMS again relies on the parameters listed in the Lake Louise

Consensus. Id. at 427. Therefore, when read as a whole, the Report does not cast

serious doubt on Dr. Teitelbaum’s opinion and is certainly insufficient as a basis

for finding that the district court abused its discretion by concluding otherwise.

The Railroad’s attempted reliance on isolated passages and concepts in the

following sources is similarly unavailing: Peter H. Hackett, The Cerebral Etiology

of High-Altitude Cerebral Edema and Acute Mountain Sickness, 10 Wilderness

and Envtl. Med. 97 (1999), II R. at 446; M. Jay Porcelli & Gary M. Gugelchuk, A

Trek to the Top: A Review of Acute Mountain Sickness, 95 J. Am. Osteopath

Ass’n. 718 (1996), II R. at 309; and Phillip R. Yarnell et al., High-Altitude

Cerebral Edema (HACE): The Denver/Front Range Experience, 20 Seminars in

Neurology 209 (2000), II R. at 535. When read as a whole, none of these articles

calls Dr. Teitelbaum’s opinion into question. In fact, our review of them

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substantially buttressed Dr. Teitelbaum’s analysis given their consistency with the

Lake Louise Consensus parameters. Our review of Railroad expert Dr. Neil

Rosenberg’s affidavit, III R. at 599-609, likewise provides no additional evidence

that Dr. Teitelbaum’s opinion is not supported by the cited studies; Dr.

Rosenberg’s affidavit falls well short of a showing that would allow us to

conclude that the district court abused its discretion.

(2) Developing HACE at or near 9,200 feet

The Railroad also apparently argues that the studies cited by Dr.

Teitelbaum do not support a conclusion that it is even possible for a person to

develop HACE at altitudes at or near 9,200 feet. Aplt. Br. at 35-36; id. at 35

(reiterating Dr. Rosenberg’s opinion that the altitudes attained by Mr. Goebel are

not capable of causing HACE). In the Railroad’s view, the studies demonstrate

that “HACE is very rare and occurs at altitudes well above the 9,200 feet of

Moffat Tunnel.” Id. at 36. While subtle inconsistencies might well exist across

the various studies noted by the Railroad, we are unable to conclude that the

district court abused its discretion by finding that the studies as a whole supported

Dr. Teitelbaum’s opinion.

It is worthwhile to note first that none of the studies pointed to by the

Railroad state that a person cannot develop HACE at altitudes of 9,200 feet. On

the contrary, the studies in the record largely agree that it is possible to suffer

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from altitude illnesses such as AMS and HACE at such elevations. The consensus

appears to be that high-altitude illnesses are an issue to be considered for humans

at altitudes of only 5,280 feet, the beginning of what is commonly referred to as

“high altitude” elevation. M. Jay Porcelli & Gary M. Gugelchuk, A Trek to the

Top: A Review of Acute Mountain Sickness, 95 J. Am. Osteopath Ass’n. 718, 718

(1996), II R. at 309; All About Altitude Illness, High Altitude Medicine Guide, II

R. at 415 (noting that high altitude begins at or near 5,000 feet).

The studies also agree that although high altitude illnesses can affect

people at altitudes around only 5,000 feet, such illnesses are rare below 8,000

feet. All About Altitude Illness, II R. at 415, 417; Statement on High Altitude

Illnesses, Canada Communicable Disease Report, II R. at 424 (noting that “some

susceptible individuals may experience symptoms of altitude-related illness

beginning as low as 2,500 m[eters].”); Altitude Illness Clinical Guide for

Physicians, High Altitude Medicine Guide, II R. at 405. However, the studies

make it clear that above the 8,000 foot line, high altitude illnesses are a real

concern and become much more likely to cause people problems. E.g. American

Academy of Family Physicians, High-Altitude Illness: How to Avoid It and How

to Treat It (1998), II R. at 499. Therefore, the medical literature in the record

lends ample support to the conclusion that Mr. Goebel could suffer from high

altitude illnesses at elevations of 9,200 feet.

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 What is even more critical, however, is that Dr. Teitelbaum’s opinion is not

that Mr. Goebel developed HACE solely from the altitude exposure; rather, he

opined that other factors contributed to the onset, including the oxygen context of

the air, the heavy diesel-fume pollution, the counterproductive use of the

respirator, Mr. Goebel’s increased activity during the incident, and Mr. Goebel’s

individual physiologic response. II R. at 245. No individual study in the record

attempts to account for and control additional factors such as those relied upon by

Dr. Teitelbaum. The Railroad’s argument based on studies relying solely on

altitude as the cause of a given high altitude illness therefore misses the point.

See Aplt. Br. at 35 (citing N. A. Lassen, Increase of Cerebral Blood Flow at High

Altitude: Its Possible Relation to AMS, 13 Int’l J. Sports Med. S47 (1992)

(dealing with altitudes of 12,000 to 15,000 feet), II R. at 298). The district court

did not abuse its discretion by concluding that the studies supported Dr.

Teitelbaum’s opinion that Mr. Goebel could have developed AMS and HACE at

an elevation near 9,200 feet.

(3) Onset of HACE in One Hour

The Railroad’s final argument relating to the studies is that “[n]othing in

the medical or scientific literature suggests that HACE can be developed in an

exposure of less than one hour.” Aplt. Br. at 37. In the Railroad’s view, although

HACE would ordinarily require one to three days to develop, onset might possibly

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occur after 12 hours but is simply not going to manifest in the span of one hour.

Id. We perceive more than one error in the Railroad’s argument.

First, we disagree with the Railroad’s characterization of the facts.

According to its own statement of facts, on the night of the incident Mr. Goebel

started work at 7:30 p.m. at an altitude of approximately 5,198 feet (i.e., in

Denver). Aplt. Br. at 3-4; I R. at 99. He was directed to operate his helper

locomotives through the Moffat Tunnel at elevations near 9,200 feet and to wait

on the other side at Tabernash, elevation 8,318 feet. Id. The Railroad states that

five hours (i.e., around 12:30 am) after he started work in Denver, Mr. Goebel

had traversed the tunnel and sat waiting on a siding at Winter Park, elevation

approximately 9,100 feet. Aplt. Br. at 4; I R. at 99. After meeting the train he

was assigned to assist and experiencing the tunnel incident, Mr. Goebel

descended to Rollinsville, elevation 8,367 feet, to await an ambulance. Aplt. Br.

at 8; I R. at 99. At 2:50 a.m., more than seven hours after he began the ascent in

Denver, Mr. Goebel was placed on pure oxygen en route to the hospital. Aplt. Br.

at 8.

Consistent with our earlier observation from the studies, Mr. Goebel was

technically at “high altitude” elevations from the moment he began his ascent

from Denver. Although it is not clear precisely how long Mr. Goebel spent at

elevations over 8,000 feet, it is absolutely clear that he was exposed for far longer

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than one hour to elevations where altitude illnesses are a real concern. The

Railroad confuses two important timelines. The first is Mr. Goebel’s exposure

only to high altitudes in excess of 8,000 feet, which was clearly well over one

hour. The second is his exposure to various added factors inside the tunnel,

including the diesel-fume polluted atmosphere and his counterproductive use of

an ineffective respirator. This second window of time was indeed approximately

one hour.

This important distinction focuses us on the second and most critical error

in the Railroad’s argument. Once again, the Railroad fails to address directly the

substance of Dr. Teitelbaum’s opinion. Dr. Teitelbaum has never claimed that

Mr. Goebel developed HACE solely from the altitude exposure; instead, Dr.

Teitelbaum has repeatedly averred that the high altitude and the other factors

combined to produce the onset of HACE. II R. at 245. The Railroad’s failure to

recognize and address this fact renders unpersuasive its citation to studies for the

proposition that altitude exposure alone does not usually lead to HACE in under

12 hours. Aplt. Br. at 36-37. It is clear that Mr. Goebel was exposed to altitudes

exceeding 8,000 feet for much longer than one hour. More importantly, he was

inside the tunnel at altitudes exceeding 9,000 feet for approximately one hour and

was subjected to a variety of other factors that, in Dr. Teitelbaum’s view,

significantly worsened his condition. The studies cited by the Railroad do not

- 22 -
render Dr. Teitelbaum’s opinion unreliable and do not give us reason to conclude

that the district court abused its discretion.

V. Was the Differential Diagnosis Reliable?

A. The Railroad’s Argument

The Railroad’s second major contention is that the district court abused its

discretion because Dr. Teitelbaum’s specific causation testimony was based upon

an unreliable differential diagnosis that failed to account for obvious alternative

explanations. The Railroad’s theory is that Mr. Goebel’s cognitive deficits were

the result not of brain damage caused by HACE, but were merely symptoms of

depression or emotional distress. Therefore, the symptoms Mr. Goebel suffered

during and after the tunnel incident--i.e., dizziness, headache, abdominal pain,

back pain, and disorientation--were not sufficient to rule in HACE as a possible

diagnosis; instead, the obvious alternative was that Mr. Goebel suffered only from

overexposure to diesel fumes, which in the Railroad’s view is a diagnosis more in

line with the symptoms, but one which it acknowledges would not account for

lasting cognitive deficits from brain damage. Aplt. Br. at 41-42 (citing

overexposure to diesel smoke as an example of something “not capable of causing

brain damage”).

Upon closer inspection, much of the Railroad’s differential diagnosis

argument is largely a reiteration of its first argument. Recognizing that a reliable

- 23 -
differential diagnosis is admissible in this circuit given a valid showing of general

causation, see Hollander v. Sandoz Pharms. Corp., 289 F.3d 1193, 1210-11 (10th

Cir. 2002), the Railroad spends considerable effort rehashing its view that the

scientific literature does not support Dr. Teitelbaum’s conclusions. See Aplt Br.

at 43-44, 47, 49, 51. In the alternative, the Railroad argues that even if general

causation were established, Dr. Teitelbaum’s differential diagnosis was unreliable

for failing to account for obvious alternative explanations, i.e., overexposure to

diesel fumes and depression. Id. at 47-48.

B. What the District Court Found

Citing Hollander and its ruling in favor of Mr. Goebel on the general

causation issue, the district court first dismissed the Railroad’s argument that the

differential diagnosis was automatically insufficient because no general causation

was shown. III R. at 669. Then, noting that Dr. Teitelbaum reviewed Mr.

Goebel’s medical history, conducted a physical exam, reviewed outside

information, considered medical studies and theories in accepted medical

literature, relied on further testing performed by other specialists, and eliminated

other possible diagnoses, the district court found that Dr. Teitelbaum followed

“standard medical procedure in evaluating and diagnosing” Mr. Goebel and that

this methodology was based on valid scientific method. Id. at 670.

Addressing the Railroad’s contention that Mr. Goebel did not exhibit

- 24 -
certain classic symptoms of HACE, the court found that Dr. Teitelbaum

nonetheless reached a reliable differential diagnosis in concluding that Mr.

Goebel’s symptoms correlated both with HACE and overexposure to diesel fumes.

Id. at 672. The court relied on Dr. Teitelbaum’s reasoning that, because Mr.

Goebel suffered a less than acute form of HACE, certain symptoms associated

with acute HACE would not have necessarily manifested in Mr. Goebel. Id.

Having concluded that Dr. Teitelbaum reliably applied a sound methodology, the

court held that Mr. Goebel’s failure to exhibit certain symptoms of acute HACE

was simply a matter for the trier of fact to consider when assigning weight to the

testimony.

Regarding the Railroad’s argument that Dr. Teitelbaum failed to rule out

depression as an obvious alternative cause, the district court first noted that

several circuits have held that the failure to rule out all possible alternative causes

of an illness does not automatically render an expert’s testimony inadmissible. Id.

at 674. After again noting that Dr. Teitelbaum followed sound scientific method

in making his diagnosis, the district court held that his failure to exclude

explicitly one alternative (depression) did not affect the admissibility of the

testimony, although it was an issue the fact finder could consider when assigning

weight. Id. at 675. The court buttressed its conclusion by pointing to the

temporal relationship between the incident and Mr. Goebel’s symptoms and by

- 25 -
noting the fact that even the Railroad’s experts could not definitively opine that

Mr. Goebel’s cognitive deficits were caused by depression. Id. at 676.

C. Did the District Court Abuse its Discretion?

Whatever the merits of differential diagnosis in the abstract, the district

court correctly determined, based on our precedent in Hollander, that it can admit

a differential diagnosis that it concludes is reliable if general causation has been

established. Hollander, 289 F.3d at 1210 (declining to decide if differential

diagnosis is reliable in general but stating that such a diagnosis is admissible in

certain circumstances if determined to be reliable). We have already concluded

that the district court did not abuse its discretion by concluding that Dr.

Teitelbaum’s general causation opinion was admissible. Therefore, as in

Hollander, the only issue that remains is whether the district court abused its

discretion by concluding that Dr. Teitelbaum’s specific differential diagnosis was

reliable. In Hollander, we recognized that a differential diagnosis is most useful

when “the party relying on the diagnosis has offered independently reliable

evidence that the allegedly dangerous drug or substance had harmful effects,” i.e.,

when a reliable general causation opinion has been offered to rule the substance

in as a potential cause. Id.

Having determined that Dr. Teitelbaum’s general causation opinion was

reliable and therefore admissible, we now conclude that the district court

- 26 -
correctly ruled that Dr. Teitelbaum’s differential diagnosis was also reliable

because he followed a standard and accepted methodology in arriving at the

diagnosis, he adequately explained why Mr. Goebel might not exhibit every

symptom of acute HACE, and he adequately considered and ruled out some

alternative explanations even if he did not explicitly rule out depression.

The district court correctly relied on the temporal relationship between the

tunnel incident and Mr. Goebel’s symptoms as just one factor that supported Dr.

Teitelbaum’s conclusion. The court is not permitted to, and did not, rely on the

temporal relationship by itself as evidence of causation. See, e.g., Heller v. Shaw

Indus., Inc., 167 F.3d 146, 154 (3d. Cir. 1999) (“The temporal relationship will

often be (only) one factor, and how much weight it provides for the overall

determination of whether an expert has ‘good grounds’ for his or her conclusion

will differ depending on the strength of that relationship.”); Westberry v.

Gislaved Gummi AB, 178 F.3d 257, 265 (4th Cir. 1999). Given Mr. Goebel’s

testimony about his symptoms both during and after the incident that are entirely

consistent both with Dr. Teitelbaum’s conclusions and with a diagnosis unrelated

to depression, we agree with the district court that Dr. Teitelbaum’s failure

explicitly to rule out depression as one possible alternative cause is not

unreasonable. Furthermore, given that the Railroad’s experts could not definitely

testify that depression was a valid possible alternative, Dr. Teitelbaum’s failure to

- 27 -
specifically rule it out does little to render his diagnosis unreliable.

Finally, Dr. Teitelbaum’s explanation of why Mr. Goebel might not have

exhibited all the symptoms of acute HACE is reasonable. As noted above, the

medical studies make it clear that Mr. Goebel exhibited symptoms sufficient to

justify a HACE diagnosis. In effect, Mr. Goebel exhibited some, but not all, of

the symptoms associated with HACE. He also exhibited effects of lasting

cognitive deficits, a finding confirmed by outside specialists. Given this

combination of symptoms, it was reasonable that Dr. Teitelbaum did not diagnose

Mr. Goebel with overexposure to diesel fumes because such a diagnosis would

not account for lasting cognitive deficits. For these reasons, and in light of our

deferential standard of review, we conclude that the district court did not abuse

its discretion by ruling that Dr. Teitelbaum’s differential diagnosis was reliable

and therefore admissible. As the district court correctly noted, although Dr.

Teitelbaum’s opinion was properly admissible, any weaknesses should have been

diligently pursued and exposed on cross examination.

After a careful review the district court’s decision, the Railroad’s

arguments, and the underlying medical literature, we cannot conclude that the

district court, in admitting Dr. Teitelbaum’s general causation opinion and

differential diagnosis, “made a clear error of judgment or exceeded the bounds of

permissible choice in the circumstances.” Dodge, 328 F.3d at 1223 (quoting

- 28 -
Atlantic Richfield Co. v. Farm Credit Bank of Wichita, 226 F.3d 1138, 1163-64

(10th Cir. 2000)).

VI. Appellate Review of Adequate Scientific Support.

The dissent contends that this court has failed to take the correct approach

by not considering whether adequate scientific support exists for Dr. Teitelbaum’s

opinion. The dissent concludes that the scientific support is inadequate to

demonstrate that the HACE experienced by Mr. Goebel could cause permanent

brain damage and that the episode in the Moffat Tunnel could have caused

HACE. The trial court, having been alerted to these gaps, should have insisted

that Dr. Teitelbaum explain these gaps, or excluded his testimony.

The key to this case is the deferential standard of review–under the abuse

of discretion standard, the district court’s decision to admit the evidence must be

characterized as manifestly erroneous to warrant reversal. See Joiner, 522 U.S. at

142-43. T he lack of scientific literature directly addressing the confluence of all

of the factors at issue in the tunnel is hardly surprising because such tests could

not be run with human subjects. Though the review was for plain error due to a

belated Daubert objection, in Mascenti v. Becker, 237 F.3d 1223 (10th Cir. 2001),

this court upheld the use of an expert’s opinion of brain injury from diffusion

hypoxia where the plaintiff had been administered multiple drugs in combination

with nitrous oxide. 237 F.3d at 1231. Just as here, the defendant challenged “the

- 29 -
absence of professional literature to support [the expert’s] opinion and asserted

conflicts between portions of [the expert’s] reasoning and principles which do

find support in the professional literature.” Id. We concluded that admission of

the expert’s “opinion on the specifics of the case, in the absence of published

studies on this precise combination of medications and prolonged use of nitrous

oxide,” was not plain error. Id. at 1234.

In Mascenti, the “[d]efendant’s positions disputing [the expert’s] opinions

were energetically developed at trial through cross-examination of [the expert]

and through the testimony of defendant’s own experts, inter alia.” Id. at 1231.

Contrast that with this case where the Railroad did not appeal the lack of an

evidentiary hearing on remand, it never deposed Dr. Teitelbaum, and at trial it

did not put on its own expert to directly refute Dr. Teitelbaum’s testimony. The

Railroad’s theory is that exposure to diesel smoke and depression accounted for

Mr. Goebel’s condition, and that we as lawyers and judges on appeal can

determine what the medical literature says and its import as well as any expert, let

alone the trial court. Joiner did not go that far, nor did it invest this court with

plenary review that would displace the discretion of the district court.

Here, adequate support for the HACE diagnosis exists, based upon the

disorientation and the AMS diagnosis. Even the dissent’s review of the literature

contains self-limiting terms about symptoms, and quotes statements that support

- 30 -
Dr. Teitelbaum’s conclusions. Dissent at 6-7. Though the dissent faults the

supporting literature as not being verifiable, it is a little far afield for this court

(not the experts) to refute the validity of the underlying data in support.

The dissent also contends that Dr. Teitelbaum did not adequately prove the

onset of HACE given a one-hour exposure to the tunnel episode. Nothing in this

record is categorical about the amount of time it takes for HACE to develop,

particularly given that “medical science is unsure how HACE develops.” Dissent

at 10 n.2. Mr. Goebel spent more than one hour at elevations above 8,000 feet,

and as noted above Dr. Teitelbaum is claiming that a combination of factors,

some not present in the studies, resulted in the onset of HACE. True, these

factors result in hypoxia, but a permissible reading of Dr. Teitelbaum’s position

is that the entire transition from Denver’s altitude to the Moffat Tunnel apex was

sufficient to cause AMS and HACE in combination with the other factors.

Conclusion

For the foregoing reasons, we conclude that the district court did not abuse

its discretion by ruling that Dr. Teitelbaum’s testimony was admissible under the

standards of Rule 702 and Daubert. Accordingly, we AFFIRM the district court’s

judgment.

- 31 -
No. 02-1391 - Goebel v. The Denver and Rio Grande Western Railroad Company
HARTZ, Circuit Judge, dissenting:

I respectfully dissent. Dr. Teitelbaum’s theory of the causation of

Plaintiff’s injury lacks the scientific support necessary for it to be admissible at

trial.

My conclusion is not a reflection on Dr. Teitelbaum’s expertise as a

toxicologist. He has an impressive resume. But science is no respecter of

resumes. An author’s resume may cause the scientist-reader to pay attention to

the author’s theory; but it does quite little to cause the scientist to agree with the

theory. Agreement depends upon trustworthy supporting data. Dr. Teitelbaum’s

resume has not prevented his opinions from being properly excluded in other

litigation. See General Electric Co. v. Joiner, 522 U.S. 136 (1997) (affirming the

district court’s refusal to admit into evidence Dr. Teitelbaum’s opinion regarding

the cause of Mr. Joiner’s lung cancer).

Dr. Teitelbaum’s theory is that Plaintiff has suffered “mild diffuse

[permanent brain] damage,” Aplt.’s App. at 356 ¶ 8, caused by high altitude

cerebral edema (HACE) “of a mild nature.” Id. Dr. Teitelbaum does not purport

to be an expert on HACE itself. He has conducted no personal research on

HACE, and apparently had not even had prior patients with the condition.

Moreover, he admits that if Plaintiff had HACE, his case was quite unusual,

perhaps unique. One of his affidavits states: “I must point out that there will
never be any epidemiological study which duplicates this extraordinary event

which led to [Plaintiff’s] injury. If we write a case report of this event it likely

will be the only one in the literature . . . .” Id. at 345 ¶ 5. To justify his

conclusions, Dr. Teitelbaum asserts that he is relying on well-established general

principles and refers to numerous articles in the medical literature.

The majority opinion fails to take the correct approach. It makes good

arguments that the medical literature cited by Defendant does not prove

Dr. Teitelbaum’s opinion to be wrong. The test is not, however, whether

Defendant can prove Dr. Teitelbaum’s opinion is wrong. The test is whether

there is adequate scientific support for Dr. Teitelbaum’s opinion.

Dr. Teitelbaum’s opinion may in fact be correct. It may be an inspired insight.

But a courthouse is not the proper forum to present inspiration. Only when the

insight is properly supported by research is it admissible at trial. See Rosen v.

Ciba Geigy Corp., 78 F.3d 316, 319 (7th Cir. 1996) (“[T]he courtroom is not the

place for scientific guesswork, even of the inspired sort. Law lags science; it

does not lead it.”)

Determining whether an expert’s opinion rests on adequate scientific

support can be a daunting task for a judge. Judges are not, and should not be,

scientists. But neither must judges be passive aiders and abettors of hired guns

who can pronounce their “wisdom” with such self-appointed authority that a

-2-
layperson has little chance of resolving the muddle. The solution, albeit just a

partial one, is to rely on opposing experts to point to the gaps in each other’s

chain of reasoning. As the majority opinion properly states, “[T]he responsibility

ultimately falls on th[e] challenging party to inform (via the record) those of us

who are not experts on the subject with an understanding of precisely how and

why the expert’s conclusions fail to follow from the data set.” Op. at 5. But

when the challenging party satisfies this requirement and points out that the data

set does not support the expert’s conclusion, the expert must then present a

reasonable argument to the contrary. Otherwise, the court has no choice but to

“conclude that there is simply too great an analytical gap between the data and the

opinion proffered.” Joiner, 522 U.S. at 146. The majority of this panel believes

that Defendant failed to satisfy its obligation to point out how the data fail to

support Dr. Teitelbaum’s conclusion. My view, however, is that Defendant

satisfied this obligation and Dr. Teitelbaum failed to respond adequately.

There are at least two major gaps in Dr. Teitelbaum’s analysis. As pointed

out by Defendant’s experts, Dr. Teitelbaum has not produced adequate scientific

support for the proposition that HACE of the nature allegedly experienced by

Plaintiff can cause permanent brain damage of the type allegedly suffered by

Plaintiff. And he has not produced adequate scientific support for the proposition

that the episode in Moffat Tunnel could have caused HACE.

-3-
 First, assuming that Plaintiff indeed suffered HACE, could his HACE have

caused the brain damage allegedly present? Dr. Teitelbaum asserts that Plaintiff

has mild diffuse permanent brain damage. But Dr. Neal L. Rosenberg,

Defendant’s expert, stated in his affidavit that if Plaintiff “had suffered a

permanent injury to the brain from [the tunnel] event, he would almost certainly

have been rendered unconscious (or resulting in a coma), immediately at the time

of the alleged exposure.” Aplt.’s App. at 581. Of course, the district court was

not bound to reject Dr. Teitelbaum’s opinion just because another expert

disagreed. Nevertheless, once the trial court was alerted to the potential gap in

Dr. Teitelbaum’s chain of reasoning, it should not have admitted the expert’s

opinion into evidence unless the record before the court—other than a bald ipse

dixit from the expert, see Joiner, 522 U.S. at 146—filled that gap.

Dr. Teitelbaum’s testimony and affidavits contain no support for the

proposition that Plaintiff could have suffered permanent brain injury from HACE

without having lost consciousness during the episode. Indeed, Dr. Teitelbaum

fails to address the issue. The closest he comes is in the following passage from

one of his affidavits:

In Ward’s textbook, High Altitude Medicine and Physiology,
Chapter 19 deals with high altitude cerebral edema. Defendants have
confused increased intracranial pressure which results in local diffuse
damage with malignant high altitude cerebral edema which causes
ataxia, irrationality, hallucinations, clouding of consciousness and
death. The syndrome suffered by Mr. Goebel was more severe than

-4-
 that suffered by the usual skier or tourist who reaches altitude, and
less severe than that suffered by mountain climbers who have acute
major irreversible damage. He suffered mild diffuse damage which in
some individuals would be of little consequence and might not even
be detected.

However, in a railroad engineer who is required to carry out
complex mechanical and intellectual tasks, these residua are
disabling. The failure of the defendants to review Ward’s textbook to
which I referred in my affidavit and which deals with the fundamental
physiology of oxygen and hemoglobin at high altitude has contributed
substantially to the confusion set forth in their motion for new trial
and in the course of their cross-examination of me.

Aplt.’s App. at 356. Chapter 19 of Ward’s text, however, says nothing about

permanent brain damage, whether mild diffuse damage or otherwise. See Michael

P. Ward, et al., High Altitude Medicine & Physiology, 412-17 (2d ed. 1995)

(Ward). The three “[t]ypical cases” it describes resulted in either death or

complete recovery. Id. at 413-14.

In an abundance of caution, I have reviewed the literature cited by

Dr. Teitelbaum (as best I can as a layman, without the assistance of any references

by Dr. Teitelbaum to specific pages or passages in the literature) to see whether it

fills the gap. It does not. The literature reports that death is a common

consequence of untreated HACE. Victims who survive, however, generally exhibit

no signs of permanent injury. The case reports in Dr. Teitelbaum’s cited literature

typically refer to full recovery of the victim. See Thomas E. Dietz, All About

Altitude Illness, in High Altitude Medicine Guide 4, at http://www.high-altitude-

-5-
medicine.com/AMS.html (Dietz I) (“People with HACE . . . usually recover

completely”); Peter H. Hackett, et al., High-altitude Cerebral Edema Evaluated

with Magnetic Resonance Imaging, 280 JAMA 1920, 1920 (1998) (Hackett I) (“all

[nine] patients [with HACE] completely recovered”); Mark D. Harris, et al., High-

Altitude Medicine, 57 Am. Fam. Physician 1907, 1911 (1998) (Harris) (“usually

recover completely”); Phillip R. Yarnell, et al., High-Altitude Cerebral Edema

(HACE): The Denver/Front Range Experience, 20 Seminars in Neurology 209,

216 (2000) (Yarnell) (HACE “is completely reversible with expeditious

treatment”).

To be sure, one article cited by Dr. Teitelbaum says that persistence of

“neurologic deficits,” while “extremely rare,” has been reported, Thomas E. Dietz,

Altitude Illness Clinical Guide for Physicians, in High Altitude Medicine Guide 7,

at http://www.high-altitude-medicine.com/AMS-medical.html (Dietz II); and

another article, contrary to every other statement on the subject in the cited

articles, states that HACE “often resolves with longlasting neurologic and

psychiatric deficits,” Michael Weidman & Geoffrey C. Tabin, High-Altitude

Retinopathy and Altitude Sickness, 106 Ophthalmology 1924, 1926 (1999)

(emphasis added). But neither of these two assertions (which, by the way, were

not specifically referred to in Dr. Teitelbaum’s testimony or affidavits) is

accompanied by any reference to authority, such as a journal article, for its truth.

-6-
As a result, it is impossible to verify the assertions. More importantly, even

assuming the truth of the assertions, the absence of supporting references makes it

impossible to compare those victims’ experiences with HACE to Plaintiff’s

experience, to see whether, for example, the victims suffered permanent brain

damage without having been rendered unconscious by HACE.

In sum, Dr. Teitelbaum’s literature provides no support for any person’s

having suffered permanent brain injury—much less “mild diffuse damage”—from

a case of HACE that had not resulted in symptoms (such as coma) significantly

more severe than those experienced by Plaintiff. We have no basis for assuming

that the reports of permanent neurological damage referred to in Dr. Teitelbaum’s

literature were related to cases of “mild HACE” (as Dr. Teitelbaum describes what

happened to Plaintiff). On this ground alone, Dr. Teitelbaum’s opinion of the

cause of Plaintiff’s alleged brain injury has no business in a court of law.

The second gap in Dr. Teitelbaum’s opinion relates to the cause of HACE.

Dr. Teitelbaum asserts that the tunnel episode, which lasted less than 60 minutes,

caused Plaintiff to suffer HACE. Dr. Rosenberg, however, said in his affidavit:

“HACE typically requires 1 to 3 days to develop . . ., and I am unaware of a single

case of HACE developed in less than 12 hours.” Aplt.’s App. at 608. Again,

Dr. Teitelbaum does not confront this challenge. The closest he comes on this

issue is the following passage in an affidavit:

-7-
 Mr. Goebel’s transition in a short period of time from Denver’s
altitude of approximately 5,280 feet to the Moffat Tunnel apex
altitude of 9,200 feet is more than sufficient to produce both acute
mountain sickness (AMS) and high altitude cerebral edema (HACE)
in an individual who is both sensitive to the development of the
disease and is exposed to factors in addition to the altitude stresses
which contribute to the problem. I have discussed all of these
stressors and toxicity issues in my prior declarations.

Aplt.’s App. at 251. He cites no literature to support the proposition that HACE

could be caused during the brief period in the tunnel.

Again, in an abundance of caution I read the various articles attached to his

affidavits. None of the articles comes close to suggesting that HACE can arise

during a 60-minute episode of high-altitude hypoxia. In one article cited by

Dr. Teitelbaum all nine reported cases of HACE occurred after the victim had

spent two or more days at high altitude. Hackett I, supra, at 1922. In another, all

13 reported cases involved patients who had spent at least three days at high

altitude. Yarnell, supra, at 212. Other articles cited by Dr. Teitelbaum contain the

following statements: 1

1. “The 6-to-96-hour delay between the arrival at a high
altitude and the onset of symptoms . . . .” George H. Sands, et al.,
Cough, Exertional & Other Miscellaneous Headaches, 75 Med.

1
The articles often speak of the more general ailment AMS—acute
mountain sickness—which can progress to the more severe ailment HACE. See
Ward, supra, at 412 (“The malignant form of AMS we call . . . HACE”); The Lake
Louise Consensus on the Definition of Altitude Illness, in High Altitude Medicine
Guide, at http://www.high-altitude-medicine.com/AMS-LakeLouise.html (“HACE
[c]an be considered ‘end stage’ or severe AMS”); Dietz I, supra, at 4 (HACE is at
the “severely ill” end of AMS spectrum).

-8-
 Clinics 733, 742 (1991) (Sands).

2. “Progression to HACE from mild AMS varies from 12 hours
to the more common duration of between 1 and 3 days.” Committee
to Advise on Tropical Medicine and Travel, Statement on High-
Altitude Illnesses, 24 Can. Communicable Disease Rep. 1, 8 (1998)
(Canada Statement).

3. “AMS affects climbers 6 h[ours] to several days after an
ascent to an altitude greater than 3,000 m [9800 feet].” Sarper
Karakücük & G. Erutgral Mizra, Ophthalmological Effects of High
Altitude, 2000 Ophthalmic Res. 30, 31(1999).

4. HACE is assumed to occur with “severe prolonged
hypoxia.” John W. Severinghaus, Hypothetical roles of angiogenesis,
osmotic swelling, and ischemia in high-altitude cerebral edema, 79 J.
Applied Physiology 375, 375 (1995) (Severinghaus I).

5. “Is the increase of CBF [cerebral blood flow] [from acute
hypoxia] a causative factor in acute mountain sickness[?] This is
highly unlikely. The increase in blood flow is almost instantaneous,
while AMS, more specifically the headache, sets on only after hours.”
N. A. Lassen, Increase of Cerebral Blood Flow at High Altitude: Its
Possible Relation to AMS, 13 Int. J. Sports Med. 47, 48 (1992).

6. “[V]asogenic edema develops in humans (and sheep) who
become moderately ill with AMS/HACE during 24 hr or more of
hypoxic exposure.” Peter H. Hackett, The cerebral etiology of high-
altitude cerebral edema and acute mountain sickness, 10 Wilderness &
Envtl. Med. 97, 106 (1999).

Dr. Teitelbaum may have been assuming that the severity of the hypoxia

suffered by Plaintiff accounts for the quick onset. But the literature does not

support such an assumption. According to the literature cited by Dr. Teitelbaum,

HACE appears to be an indirect effect of prolonged hypoxia, which can be

distinguished from direct effects of oxygen deprivation on the brain. See, e.g.,

-9-
Canada Statement, supra, at 2-3 (describing acute hypoxia and AMS as distinct

ailments). Unlike what happens in AMS or HACE, “Acute severe hypoxia may,

within minutes, induce headaches, nausea, and vomiting.” Severinghaus I, supra, at

377. As explained in another article, “AMS is now considered to be primarily due

to the body’s response to modest hypoxia and has a different pathophysiology from

simple acute hypoxia, being associated with fluid shifts not seen with hypoxia

alone.” Canada Statement, supra, at 3. In noting the difference between HACE and

the direct effects of oxygen deprivation, a third article said that “attempts to

correlate AMS/HACE . . . with the degree of hypoxemia[] has been relatively

fruitless . . . .” Peter H. Hackett, Hypoxia: Into the Next Millennium 25 (1999).

And a fourth article concluded that “[t]he 6-to 96-hour delay between the arrival at a

high altitude and the onset of symptoms suggests that hypoxia is not the immediate

cause of AMS.” Sands, supra, at 742. 2

2
Medical science is unsure how HACE develops, see John W. Severinghaus,
Uses of High Altitude for Studies of Effects of Hypoxia, in Oxygen Transport to
Tissue XX 17, 24 (1998) (“[t]he underlying pathophysiology of HACE . . . is still
poorly understood”). (This in itself renders unacceptably speculative Dr.
Teitelbaum’s theory that HACE could be caused by a combination of factors
never before reported or, as far as one can tell, observed to accompany HACE.)
Nevertheless, a brief description of one of the theories may help to understand
how HACE can differ from the direct effects of hypoxia. One expert suggests
that HACE is caused by angiogenesis—“[t]he process by which growing ischemic
or hypoxic tissues stimulate the in-growth of capillaries.” Severinghaus I, supra,
at 377. This expert theorizes that HACE is observed upon the “onset of
angiogenesis after hours or days [of hypoxia].” Id. at 378. “Angiogenic capillary
breakdown and the resulting edema,” he says, “presumably occur only after many
hours of sustained hypoxia.” Id. at 377; see Yarnell, supra, at 216

-10-
 Despite Dr. Teitelbaum’s failure to explain the uniquely rapid onset of

Plaintiff’s alleged HACE, the majority opinion makes an attempt. It asserts that we

should look not just at the time in the tunnel but also should consider the entire train

trip from Denver, which began at the high altitude of 5,280 feet. Op. at 20-22. This

assertion, however, ignores the medical literature. The articles say, for example,

that “[p]ractically speaking . . . , we generally don’t worry about elevations below

about 2500 m (8000 ft) since altitude sickness [much less HACE] rarely occurs

lower than this.” Dietz I, supra, at 1. When one article says that “some susceptible

individuals may experience symptoms of altitude-related illness beginning as low as

2500 m [8200 feet],” Canada Statement, supra, at 1 (emphasis added), I infer that

conditions below 8200 feet simply do not induce AMS (much less HACE) in

anyone. See also Yarnell, supra, at 211 (“In general, . . . high-altitude illness [is]

associated with rapid ascent above 8202 feet (2500 m).”). According to the

literature, the mean altitude at which HACE develops is 15,500 feet in cases where,

as here, the person does not also suffer high altitude pulmonary edema (HAPE).

(For those who suffer HAPE, the mean altitude is 12,850 feet. Id. at 214.)

Furthermore, the cited articles report that acclimation to high altitude is the

key to avoiding AMS and HACE. See Dietz II, supra, at 3 (“continued ascent is

acceptable” once one is free of AMS symptoms); Harris, supra, at 1907 (to avoid

(“Angiogenesis is stimulated within hours of hypoxia.” (emphasis added.))

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AMS, ascend only 1,000 feet per day after reaching 8,000 feet); Dietz I, supra, at 3

(above 10,000 feet one’s sleeping elevation should not increase more than 1,000 feet

per night); Canada Statement, supra, at 6 (safest method to prevent AMS is “graded

ascent”). And the higher one’s home altitude, the better one can adjust. See

Yarnell, supra, at 211 (odds of getting AMS are 3.5 times greater if usual residence

is below 3,000 feet). Here, the first four hours of the trip were below 8,300 feet

elevation and unlikely to create the conditions for HACE, or even AMS. Also,

Plaintiff would be less likely than most people to develop AMS at such an altitude

because he was acclimated to the mile-high elevation of Denver, where he lived.

Nor did Plaintiff experience any conditions before entering the tunnel that

Dr. Teitelbaum said would exacerbate the hypoxia—exposure to thick diesel smoke,

physical exertion, or use of a counterproductive respirator. In short, the majority

opinion expands the time during which Plaintiff was exposed to high-altitude

hypoxia by speculation not supported by, indeed contradicted by, the medical

literature.

More importantly, the majority opinion’s speculation is not even supported by

Dr. Teitelbaum’s own assertions. None of his opinions regarding the cause of

Plaintiff’s alleged HACE relies on Plaintiff’s train trip up to the tunnel. Instead he

focuses on the events in the tunnel. For example, his final affidavit states:

2. . . . The[] elements of causation are the altitude of the tunnel,
the oxygen content of air at that altitude, the physiologic principles

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 which govern the partial pressure of oxygen in the blood at that
altitude, the presence of diesel fuel in [Plaintiff’s] environment, the use
of an inappropriate respirator, and the duration of the event.

3. In my opinion, the injury to [Plaintiff] was caused by an
increase in intracranial pressure due to cerebral edema and a decreased
oxygen supply to the brain which in turn were the result of the altitude
of the tunnel, the oxygen content of the air, and the partial pressure of
oxygen in the blood, combined with the exercise involved in his escape,
the polluted atmosphere, and individual physiologic response of the
patient.”

Aplt.’s App. at 344 (emphasis added). Dr. Teitelbaum makes no reference to the

altitudes encountered by Plaintiff on the trip to the tunnel. I do not think we can

rescue his opinion from the HACE-causation gap by relying on a highly suspect

theory that not even he has embraced.

As Defendant put the matter in its opening brief: “Selecting only favorable

factoids out of articles, without considering their overall conclusions, and without

confronting or explaining why the unfavorable parts of the article have been

rejected, is not science—it is simply advocacy. And that is exactly what

Dr. Teitelbaum did.” Aplt.’s Br. at 29. I am afraid that description is accurate. I

would reverse the district court’s decision to admit Dr. Teitelbaum’s testimony and

order entry of judgment in favor of Defendant.

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