Epidemiological Evidence In Occupational Injury Cases


Daubert v. Merrell Dow Pharceuticals, Inc., 509 U.S. 579, 113 S.Ct. 2786 (1993). The “general acceptance” test for admissibility of scientific evidence was superseded by Fed. R. Evid. Rule 702. The trial judge, as gatekeeper, pursuant to Rules 104(a) and Rule 702, must make a preliminary assessment of whether the underlying reasoning or methodology of the expert’s testimony is scientifically valid and properly can be applied to the facts at issue. Standards for relevance and reliability should include: (1) whether the theory or technique has been tested; (2) whether the theory or technique has been subjected to peer review or publication; (3) whether the existence of known or potential error rates has been determined; and (4) whether standards exist for controlling the technique’s operation.  Whether the methodology is generally accepted within the scientific community should also be considered but is not controlling. Under the circumstances of this case, where infants and their guardians ad litem sued a pharmaceutical company to recover for birth defects allegedly sustained as result of mothers’ ingestion of anti-nausea drug Bendectin, proffering eight experts who sought to testify on the basis of in vitro, animal and epidemiological studies evidencing causation, the Supreme Court reversed and remanded summary judgment, and ordered that the trial court implement the new standards in determining the admissibility of the scientific evidence on causation.

Epidemiology:  The science that studies the patterns, causes and effects of health and disease conditions in defined populations. Wikipedia. “Epidemiology is the field of public health and medicine that studies the incidence, distribution and etiology of disease in human populations.” Reference Manual on Scientific Evidence, Third Edition, Federal Judicial Center, National Resource Council, The National Academic Press, p. 551 (2013); Kusnetz, S., “A Guide To The Work-Relatedness of Disease,” Rev. Ed., DHEW (NIOSH) Pub. No. 79-116, ch. 3, p. 9 (1979).

Frye v. United States, 293 F.1013, 1014 (D.C. Cir. 1923). Landmark decision relied upon by most courts until the Daubert case, holding that expert opinion based on a scientific technique is inadmissible unless the technique is “generally accepted” as reliable in the relevant scientific community. Language from the court:

Just when a scientific principle or discovery crosses the line between the experimental and demonstrable stages is difficult to define. Somewhere in this twilight zone the evidential force of the principle must be recognized, and while courts will go a long way in admitting expert testimony deduced from a well-recognized scientific principle or discovery, the thing from which the deduction is made must be sufficiently established to have gained general acceptance in the particular field in which it belongs.

Bradford Hill Criteria, The leading modern authority on the criteria for determining whether a statistical association between environmental factors constitutes a cause of disease. Factors to be considered:  (1) strength of association; (2) consistency of association; (3) specificity of association; (4) temporality of association; (5) biological gradient of association – dose response curve; (6) plausibility; (7) coherence; (8) experiment evidence; and (9) analogy. Hill, A.B., “The Environment and Disease: Association or Causation?” Proc. Royal Soc. Med. 58: 295-300 (1965); Rothman, Kenneth J., Modern Epidemiology, 3d ed., ch. 2, pp. 26-31, Lippincott, Williams & Wilkins (2008).

Confounding: An apparent association between a presumed causal variable and an outcome is in fact accounted for by a third variable, which is itself associated with both the presumed cause and the outcome.  Susser, M. ”Glossary: Causality in Public Health Science,” 55 J. Epidemiol. Com. Health 376 (2001).

General Electric Co. v. Joiner, 522 U.S. 136 (1997). A long time smoker, who suffered from lung cancer, brought an action against the manufacturer of polychlorinated biphenyls (PCBs) and manufacturers of electrical transformers and dielectric fluid, seeking to prove that his exposure caused his illness.  The Supreme Court affirmed summary judgment, holding that the district court had not abused its discretion in excluding expert testimony based on animal studies indicating that infant mice developed cancer after receiving massive doses of PCBs or in excluding expert testimony based on epidemiological studies. “. . . nothing in either Daubert or the Federal Rules of Evidence requires a district court to admit opinion evidence which is connected to existing data only by the ipse dixit of the expert.” 509 U.S. at 146.

A Guide To The Work-Relatedness of Disease, Revised Edition, Kusnetz, S. et al, U.S. Department of HEW, Public Health Service, CDC, NIOSH Publication No. 79-116 (January 1979). Available online: http://www.cdc.gov/niosh/pdfs/79-116-a.pdf This guide is designed primarily as an aide to state agencies concerned with occupational disease compensation. It suggests a protocol for collecting, organizing and appraising medical, occupational and other evidence for determining the probable work-relatedness of alleged occupational diseases. Accord, Glass, L., ed., “Work-Relatedness,” Occupational Medicine Practice Guidelines: Evaluation and Management of Common Health Problems and Functional Recovery of Workers, 2d ed, Beverly Farms, A: OEM Press, p. 55-62 (2004).

Koch’s Postulates.  Four classic criteria required for determination of causation between microbial agents and disease:

  1. the microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms;
  2. the microorganism must be isolated from a diseased organism and grown in pure culture;
  3. the cultured microorganism should cause disease when introduced into a healthy organism
  4. the microorganism must be re-isolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent. Koch, R. “Investigations Into Bacteria: V. The Etiology of Anthrax, Based on the Antogenesis of Bacillus Anthracis,” [In German: Cohns Beitrage zur Biologie der Pflanzen 2 (2): 277–310 (1876)].

Kumho Tire Co. v. Carmichael, 526 U.S. 137 (1999). Daubert rule creating gatekeeping obligation by trial court applies not only to scientific evidence but also to proffers of technical or other specialized knowledge by experts. The Supreme Court held that the trial court had properly exercised its discretion in excluding opinions of plaintiffs’ expert in tire failure analysis, who concluded on the basis of a visual inspection of a tire that a blowout causing a crash resulting in one death and several injuries, was caused by a defect in the manufacture or design of the tire.


Direct Cause – Practitioner’s Report, Box 11.   Lewellyn v. DILHR, 38 Wis.2d 43, 155 N.W.2d 678 (1968)(applying “breakage” concept). See also Lange v. LIRC, 215 Wis.2d 561, 573 N.W.2d 856 (Ct. App. 1997)(flirting with substantial factor test); Kruse v. Inter Lake Wisconsin, Inc., WC Claim No. 1999018314, (LIRC January 23, 2003)(applying substantial factor test).

Indirect Cause – Practitioner’s Report, Box 12. Precipitation, aggravation and acceleration.  Joseph Schlitz Brewing Co. v. DILHR, 67 Wis.2d 185, 226 N.W.2d 492 (1975); Semons Department Store v. DILHR, 50 Wis.2d 518, 184 N.W.2d 871 (1971); Lewellyn v. DILHR, 38 Wis.2d 43, 155 N.W.2d 678 (1968).

Work Exposure – Material contributory causative factor in onset or progression of disease. Practitioner’s Report, Box 13.  White v. LIRC, 2000 WI App 244, 239 Wis.2d 505, 620 N.W.2d 422; City of Superior v. ILHR Department, 84 Wis.2d 663, 267 N.W.2d 637 (1978); E.F. Brewer Co. v. ILHR Dept. 82 Wis.2d 634, 264 N.W.2d 322 (1978)(disability is compensable despite pre-existing or congenital condition if work exposure was a material cause); Universal Foundry Co. v. DILHR, 82 Wis.2d 479, 263 N.W.2d 172 (1978)(exposure must be material factor); Maynard Elec. Steel Casting Co. v. Industrial Comm’n, 273 Wis. 38, 76 N.W.2d 604 (1956) (exposure must either cause or further the progress of occupational disease);Clausen v. Electro Kold Corp., WC Claim No. 2012-005239 (LIRC Jan. 30, 2014)(exposure hastens progression of occupational ankle); Gilbertson v. Hormel Foods Corp., WC Claim No. 2009-013851 (LIRC Sept. 20, 2010)(occupational hip from repetitive work exposure in a food processing company, and exposure need not be the sole cause); Woelffer v. Kohler Co., 2000 WL 258590, WC Claim No. 1992017380 (LIRC Feb. 3, 2000)(material contributory causative factor may be as low as 2.5% to 5%).  The Court of Appeals and LIRC frequently reject arguments that a medical expert marked the “wrong box,”Gray v. Master Lock, WC Claim No. 94024018 (LIRC, April 30, 1996), and usually focus on the substance of narrative explanations given by doctors over the marked box in the Practitioner’s Report. Neitzel v. Northcott Hospitality International, WC claim no. 2003-039230 (LIRC, July 31, 2007. See Harnischfeger v. LIRC and Dzenzeol, Appeal No. 95-0212 (Wis. Ct. App. August 8, 1995), slip op., page 7; Lehman v. Nilsen’s Super Value, WC Claim No. 2008-011157  (LIRC July 9, 2009).

Level of Certainty to Establish Causation – Reasonable degree of medical probability or certainty. No particular words of art are necessary to express the degree of medical certainty required to remove an expert opinion from the realm of mere possibility or conjecture. The test is whether the expert’s words may be reasonably interpreted as demonstrating an expert medical opinion. Expressions such as “I felt,” “I feel,” “I believe,” “liable,” “likely,” and “probably” may be sufficient. Aurora Consol. Health Care v. LIRC, 2010 WI App 173, 330 Wis.2d 804, 794 N.W.2d 520; Drexler v. All American Life & Cas. Co., 72 Wis.2d 420, 241 N.W.2d 401 (1976).  Pucci v. Rausch, 51 Wis.2d 513, 187 N.W.2d 138 (1971); Segelken v. City of Eau Claire, WC Claim No. 2004-022842 (LIRC July 27, 2006)

Medical Cause –  a relationship between one phenomenon or event (A) and another (B) in which A precedes B and B results from A.  See Susser, M., “Glossary:  Causality in Public Health Science,” 55 J. Epidem. Comm. Health 376 (2001).  Some social scientists contend that it is impossible to prove a causal relationship. Mosby’s Medical Dictionary, 8th edition. © 2009, Elsevier. Differential etiology refers to the study of causation in disease, and is concerned with establishing or refuting causation between and external cause and a patient’s condition. See Wong, John B., “Reference Guide on Medical Testimony,” p. 691, in Reference Manual on Scientific Evidence, supra.  See also, Koch’s Postulates, supra. “General causation” involves the question whether a particular exposure can cause the outcome in the general population. “Specific causation” involves the question whether a particular exposure caused a particular outcome in a particular individual.  See Koehler, Steven A., et al, Forensic Epidemiology: A Method for Investigating and quantifying Specific Causation,” For. Sci. Med. Path., vol. 10, p. 217-222 (2014)

Musculoskeletal Disorders and Workplace Factors: A Critical Review of Epidemiological Evidence for Work-Related Musculoskeletal Disorders of the Neck, Upper Extremity and Low Back. U.S. Dept. HHS, Public Health Service, CDC, NIOSH Publication No. 97-141 (1997).  “NIOSH concludes that a large body of credible epidemiologic research exists that shows a consistent relationship between MSDs and certain physical factors, especially at higher exposure levels.” Available online:http://www.cdc.gov/niosh/pdfs/97-141.pdf

Reference Manual on Scientific Evidence. Federal Judicial Center, National Resource Council, The National Academic Press, 3d ed. (2013).  This 1034 page manual is available online: http://www.fjc.gov/public/pdf.nsf/lookup/SciMan3D01.pdf/$file/SciMan3D01.pdfIt is an authoritative treatise for use by federal judges in performing their gatekeeping role with respect to expert testimony and evidence.

Shelby Mut. Ins. Co. v. DILHR, 109 Wis.2d 655, 327 N.W.2d 178 (Ct. App. 1982). An occupational disease may result from several identifiable, recurrent traumatic injuries.

Susser, M., “What Is A Cause and How Do We Know One? A Grammar for Pragmatic

Epidemiology.” Am. J. Epidemiol., vol. 133 (7), p. 635-48 (1991). Two criteria have to be present for any association that has a claim to be causal: i.e. time order (X precedes Y); and direction (X leads to Y).  Rejection of a hypothesis can be accomplished with confidence by only three criteria: time order, consistency, factual incompatibility or incoherence.  Acceptance or affirmation can be achieved by only four, namely: strength, consistency, predictive performance, and statistical coherence in the form of regular exposure/effect relation.

Weisgram v. Marley, 528 U.S. 440 (2000).  Plaintiffs are entitled to only one chance to select experts who can withstand Daubertscrutiny. Despite winning at trial, the verdict was reversed on appeal and the epidemiological evidence found wanting.  The Supreme Court affirmed the reversal but did not grant a new trial for a second chance.

Wisconsin Ins. Sec. Fund v. LIRC, 2005 WI App 242, 288 Wis.2d 206, 707 N.W.2d 293.  An occupational disease may be compensable whether or not there were any specific, identifiable traumatic injuries.

Wis. Stat. § 907.02. 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 the testimony is based upon sufficient facts or data, the testimony is the product of reliable principles and methods, and the witness has applied the principles and methods reliably to the facts of the case.


There is a substantial difference between how scientists, including medical doctors look at the issue of causation and the way that insurance companies, state agencies lawyers, and courts look at the issue of causation.  Whether in terms of differential diagnosis or differential etiology, medical doctors consider all possible causes for a condition, attempt to rule out the least likely ones until a presumed most likely cause and diagnosis of the condition is established, and then go on to recommend treatment. See Wong, John B., “Reference Guide on Medical Testimony,” p. 691, in Reference Manual on Scientific Evidence, Federal Judicial Center, National Resource Council, The National Academic Press, 3d ed. (2013)


On the other hand, in the legal context, courts, state agencies, lawyers and insurance companies are more concerned with the admissibility and credibility of scientific and medical evidence concerning general causation and specific causation in the case at bar. Melhorn, J. Mark, “Understanding Work-Relatedness,” Ch. 2 in AMA Guides To The Evaluation of Disease and Injury Causation, 2d ed. (2013).

The remainder of this presentation will outline the criteria that most often appear in the medical, scientific and legal literature for accomplishing the task of establishing both general causation and specific causation in conformity with evolving standards.

The first step in determining the work-relatedness of an alleged occupational disease is to confirm that an occupational disease exists, and that the particular manifestation of the disease appears to be the result of exposure to a specific harmful occupational agent. Kusnetz, S., “A Guide To The Work-Relatedness of Disease,” Rev. Ed., U.S. DHEW, Pub. Health Serv., CDC, NIOSH (Jan. 1979).  According to the Guide, this process requires that the expert perform a detailed review of the background facts, including:

  • Medical History
  • Personal History
  • Family History
  • Occupational History
  • Detailed Description of Job Tasks
  • Clinical Assessment of Worker

The next step is an epidemiological assessment of the relationship between the exposure and the disease.  Id.  The traditional methodology requires an analysis of Bradford Hill’s nine criteria. See Hill, A.B., “The Environment and Disease: Association or Causation?” Proc. Royal Soc. Med. Vol. 58: 295-300 (1965).  See also Rodricks, Joseph V., “Reference Guide on Exposure Science,” p. 503, and Green, Michael D., “Reference Guide on Epidemiology,” p. 597 in Reference Manual on Scientific Evidence, supra; Freeman, M.D., “Forensic Epidemiology: A Systematic Approach to Probabilistic Determinations in Disputed Matters,” J. Forensic Legal Med. vol. 15, 5:281-290 (July 2008); Koehler, S.A., and Freeman, M.D., “Forensic Epidemiology: A Method for Investigating and Quantifying Specific Causation,” Forensic Sci. Med. Pathol., vol. 10 (2):217-22 (June 2014).

  • Strength of the association – the larger the association the more likely the causal relationship

The concept of “relative risk” has been established to measure the strength of the

association between exposure and result.  The higher the relative risk, the greater the strength of association. If the relative risk of lung cancer among smokers is about 10, that means that smokers have ten times the risk of contracting lung cancer as non-smokers.  Doll, R. and Hill, B., “Lung Cancer and Other Causes of Death in Relation to Smoking: A Second Report on the Mortality of British Doctors,” 2 Brit. Med. J. 1071 (1956). Heavy smoking is associated with a 20-fold higher rate of lung cancer, and a doubled rate of coronary artery disease. The association between smoking and lung cancer is therefore stronger than the association between smoking and coronary artery disease. Id.

  • Consistency of the association

The association must be reproducible among different samples by different investigations. Daubert, supra. If the outcome is not replicable, then the association is not consistent and causation cannot exist.

  • Specificity of the association

There must be a closeness of the causal relationship between specific exposure to a specific population. The best example is the association between asbestos exposure and mesothelioma. Reference Manual on Scientific Evidence, pp. 605-606.

  • Temporality of the association

There must be a temporal relationship between the exposure and the outcome.  A must precede B in order for A to be considered a cause of B.  The outcome must occur during the effective range of the hazard period, i.e, neither too soon nor too late.Reference Manual on Scientific Evidence, p. 601.

  • Biological gradient

The greater the exposure, the greater the incidence must follow.  The dose-response must have a positive correlation. Newman v. Motorola, Inc., 218 F. Supp. 2d 769 (D. Md. 2002).  This is a sub-category of strength of association, e.g., light smokers contract lung cancer at a rate intermediate between heavy smokers and non-smokers.

  • Biological plausibility

There must be a biologically plausible link between the exposure and the outcome, i.e., high cholesterol as a cause of coronary heart disease because cholesterols is found in atherosclerotic plaques.  Reference Manual on Scientific Evidence, p. 604.

  • Coherence of the association

There must coherence between epidemiological and laboratory findings, and there must not be any likely alternative explanations. Freeman, M.D., “Applied Forensic Epidemiology, Part 1 Medical Negligence,” OA Epidemiology, Vol. 18; 2(1): 2 (Jan. 2014). The association should be compatible with pre-existing theory, knowledge, biology and statistical findings.

  • Experimental evidence for the association

Studies on animals or fetuses, or other experimental evidence must confirm the association. Freeman, “Applied Forensic Epidemiology . . . ,” supra; Daubert.

  • Analogy

This factor assesses whether there is a reasonable analogy between an exposure and an adverse health consequence on one organ or system and exposure-effect involving another organ or system.  Freeman, “Applied Forensic Epidemiology, . . ,” supra.

In conjunction with all the factors, the investigator must consider the possibility of error due to chance, bias or confounding of association. O’Neal, Jon T., “Causation Determination in Worker’s Compensation and Toxic Tort Cases,”http://www.health.state.mn.us/divs/eh/hazardous/topics/eegrandrounds/causation.pdf

The next step in the process is identification of the causative agent. The investigator should investigate all factors thoroughly, identify all possible substances, review industrial hygiene studies, and obtain details of the worker’s exposure.

The next step is to rule out pre-existing conditions or other possible relevant causes.


The Wisconsin statutory rules of evidence do not apply in worker’s compensation cases. Wis. Stat. § 911.01; J.I. Case Co. v. LIRC, 118 Wis.2d 45, 346 N.W.2d 315 (Ct. App. 1984); Goranson v. DILHR, 94 Wis.2d 537, 289 N.W.2d 270 (1980).

In worker’s compensation cases, LIRC and the courts so far have been far more liberal in permitting the introduction of what the courts in civil cases might classify as “junk science.”

In City of Seymour v. Industrial Commission, 25 Wis.2d 482, 131 N.W.2d 323 (1964), the court affirmed LIRC’s decision that a fall had accelerated the growth of a cancerous tumor located in a worker’s spine.  The concept of traumatic tumor acceleration was controverted in the literature.  The court stated:

When scientific or medical theories or explanations have not crossed the line and become an accepted medical fact, opinions based thereon are no stronger or convincing than the theories. While this court has gone a long way in admitting expert testimony deduced from well-recognized scientific and medical principles or discoveries, nevertheless, the facts from which the opinion is made must be sufficiently established to have gained general acceptance in the particular medical field in which they belong.  Otherwise the opinion is based not on facts but conjecture.

Id. at 487. Nevertheless, three physicians had supported causation in the case at bar. The court accepted the applicant’s evidence and allowed the claim.

Even though the statutory rules of evidence that apply in circuit court do not apply in the arena of worker’s compensation, there is no reason why the parties should not attempt, to the extent possible, to make their evidence as credible as possible, or by critiquing the credibility of their opponents’ evidence as if they were both bound by the statutory rules that apply in circuit court.  Bituminous Cas. Co. v. DILHR, 97 Wis.2d 730, 295 N.W.2d 183 (Ct. App. 1980).

Wis. Stat. § 907.02 provides:

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 the testimony is based upon sufficient facts or data, the testimony is the produce of reliable principles and methods, and the witness has applied the principles and methods reliably to the facts of the case.

Section 907.02 has essentially adopted the Daubert standards for the admissibility of expert testimony. Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 582, 589-95 (1993).

The four Daubert factors to assist the trial judges in determining the reliability of expert testimony are:

  1. Whether the expert’s theory or technique can be or has been tested;
  2. Whether the expert’s theory or technique has been subject to peer review and publication;
  3. Whether the rate, or potential rate of error is known and whether there are standards controlling the technique’s operation; and
  4. Whether the expert’s methodology is “generally accepted” in the relevant scientific community.

Daubert, 509 U.S. at 593-95.

The sequelae of Daubert have involved numerous examples of expert testimony found to be wanting for non-compliance with the rigorous epidemiological standards applicable to civil courts. For an excellent summary of the legal criteria for the admissibility of epidemiological evidence, see Sinclair, Donald C., “Epidemiology in the Courtroom: An Evidence – Based Paradigm for the Determination of Causation in Compensation Environments,” 52 JOEM 456 (April 2010).

The Advisory Committee notes to Rule 702 of Fed. R. Evid. list additional factors to be considered beyond the four basic criteria found in Daubert:

  1. Whether experts are “proposing to testify about matters growing naturally and directly out of research they have conducted independent of the litigation, or whether they have developed their opinions expressly for purposes of testifying.” Daubert v. Merrell Dow Pharmaceuticals, Inc., 43 F.3d 1311, 1317 (9th Cir. 1995).
  2. Whether the expert has unjustifiably extrapolated from an accepted premise to an unfounded conclusion. See General Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997) (noting that in some cases a trial court “may conclude that there is simply too great an analytical gap between the data and the opinion proffered”).
  3. Whether the expert has adequately accounted for obvious alternative explanations. See Claar v. Burlington N.R.R., 29 F.3d 499 (9th Cir. 1994) (testimony excluded where the expert failed to consider other obvious causes for the plaintiff’s condition). Compare Ambrosini v. Labarraque, 101 F.3d 129 (D.C. Cir. 1996) (the possibility of some uneliminated causes presents a question of weight, so long as the most obvious causes have been considered and reasonably ruled out by the expert).
  4. Whether the expert “is being as careful as he would be in his regular professional work outside his paid litigation consulting.” Sheehan v. Daily Racing Form, Inc., 104 F.3d 940, 942 (7th Cir. 1997). See Kumho Tire Co. v. Carmichael, 119 S.Ct. 1167, 1176 (1999) (Daubert requires the trial court to assure itself that the expert “employs in the courtroom the same level of intellectual rigor that characterizes the practice of an expert in the relevant field”).
  5. Whether the field of expertise claimed by the expert is known to reach reliable results for the type of opinion the expert would give. See Kumho Tire Co. v. Carmichael, 119 S.Ct.1167, 1175 (1999) (Daubert’s general acceptance factor does not “help show that an expert’s testimony is reliable where the discipline itself lacks reliability, as for example, do theories grounded in any so-called generally accepted principles of astrology or necromancy.”), Moore v. Ashland Chemical, Inc., 151 F.3d 269 (5th Cir. 1998) (en banc) (clinical doctor was properly precluded from testifying to the toxicological cause of the plaintiff’s respiratory problem, where the opinion was not sufficiently grounded in scientific methodology); Sterling v. Velsicol Chem. Corp., 855 F.2d 1188 (6th Cir. 1988) (rejecting testimony based on “clinical ecology” as unfounded and unreliable).

In Woelffer v. Kohler Co., WC Claim No. 1999201380 (LIRC February 3, 2000), LIRC affirmed a decision in favor of an applicant whose contracture of lung cancer was attributed by his experts to his occupational exposure to silica dust. One of the experts admitted that tobacco was clearly the major cause of the cancer, and attributed 95% of the cause to tobacco but only 5% of the cause to silica. The expert did opine, using the magic words, that the exposure to silica was a material contributory causative factor in the onset or progression of the cancer.  An occupational exposure that contributes only 5% to the development of a disabling condition may still be a “material factor” in the development or progression of the disabling disease.

In Segelken v. City of Eau Claire, WC Claim No. 2004-022842 (LIRC July 27, 2006), the applicant claimed that he sustained a loss of olfactory sensation as a result of exposure to various chemical odors and fumes while inspecting a building.  His treating physician, an otolaryngologist, submitted a letter, not a Practitioner’s Report, indicating that the applicant’s loss of smell came on shortly following exposure at work, and that “it would seem like this was directly the cause, or at least added to the disability.”  The ALJ dismissed the case, and the dismissal was affirmed by LIRC, as the physician’s degree of certainty was held insufficient to establish the necessary medical proof. The letter did not exhibit a conviction of the mind or that degree of positiveness that his belief was to the correct reasonable degree of medical probability.

Martin v. Ashley Furniture Industries, WC Claim No. 2004-023421 (LIRC July 31, 2007), reaffirmed the rule that a reasonable degree of medical probability means more than a 50%  likelihood.  In other words, while under Woelffer an employer may be liable even if the work exposure contributes only 5% to the cause or progress of a disabling condition, Woelffer does not hold that an employer may be held liable based on the opinion of a doctor who is only 5% sure that the work exposure was a contributing cause in any degree.


Kusnetz, Stanley,A Guide to The Work – Relatedness of Disease, Rev. Ed. DHEW (NIOSH) Publ. No. 79-116, supra, suggests that the following checklist be considered by the hearing examiner following the submission of evidence that satisfies the criteria listed in the preceding materials:

  • Has a disease condition been clearly established?
  • Has it been shown that disease can result from the suspected agent?
  • Has exposure to the agent been demonstrated?
  • Has exposure to the agent been shown to be of sufficient degree to result in the disease?
  • Have non-occupational causes been ruled out?
  • Have all special circumstances been considered?
  • Has the burden of proof been met?
  • Is the expert recognized in the industry?


There is a large NIOSH database of all publications available online:

NIOSH has an authoritative 1997 treatise summarizing the epidemiological evidence of musculoskeletal disorders caused by workplace factors. See Musculoskeletal Disorders and Workplace Factors. . ., supra. http://www.cdc.gov/niosh/pdfs/97-141.pdf

The US Department of Labor, Bureau of Labor Statistics, compiles an Annual Summary of Occupational Injuries and Illnesses from a random sample of 250,000 private employers, who provide estimates of work-related injuries and illnesses on logs of reportable injuries and illnesses, pursuant to 29 C.F.R. § 1904.42. See https://www.osha.gov/recordkeeping/new-osha300form1-1-04-FormsOnly.pdf   NIOSH analyzed the literature for evidence of a relationship between workplace factors and the development of MSDs. NIOSH employed the Hill Criteria for causality. The studies were divided into four categories as follows:

  1. Strong evidence of work-relatedness;
  2. Evidence of work-relatedness;
  3. Insufficient evidence of work-relatedness; and
  4. Evidence of no effect.

The treatise consists of various chapters summarizing the evidence of work-related MSDs by body part.


The NIOSH treatise found evidence for a causal relationship between highly repetitive work and neck and neck/shoulder MSDs. The chapter 2 summary states as follows:

Most of the epidemiologic studies reviewed defined “repetitive work” for the neck as work activities, which involve continuous arm or hand movements which affect the neck/shoulder musculature and generate loads on the neck/shoulder area; fewer studies examined relationships based on actual repetitive neck movements. The two studies which measured repetitive neck movements by measuring head position (using frequency and duration of movements) fulfilled the most stringent epidemiologic criteria, showing strong associations with neck/shoulder MSDs. In those studies defining repetitive work involving continuous arm or hand movements affecting the neck/shoulder, nine studies were statistically significant and had odds ratios (ORs) greater than 3.0.; eight studies fulfilled all the epidemiologic criteria except the exposure criteria, and measured repetition for the hand/wrist and not for the neck. Of these, three were statistically significant and had ORs greater than 3, five had nonsignificant ORs, all under 2.0. There is also evidence for forceful exertion and the occurrence of neck MSDs in the epidemiologic literature. Most of the epidemiologic studies reviewed defined “forceful work” for the neck/shoulder as work activities which involve forceful arm or hand movements, which generate loads to the neck/shoulder area; no study examined a relationship based on actual forceful neck movements. Of the 17 studies addressing force as one of the exposure factors, five studies found statistically significant associations, but did not derive ORs; two studies found ORs greater than 3.0, seven studies from 1 to 3.0, and two studies with ORs less than 1.0. Many of the studies relating measured force (as workload, etc.) to MSDs are in the biomechanical and ergonomic literature. There is strong evidence that working groups with high levels of static contraction, prolonged static loads, or extreme working postures involving the neck/shoulder muscles are at increased risk for neck/shoulder MSDs.

The NIOSH findings are largely refuted by the AMA Guides to the Evaluation of Disease and Injury Causation, Second Edition, chapter 8, supra.  The AMA Guides reviewed a small sample of studies on heavy physical work and neck pain, and concluded that “there is insufficient evidence for heavy physical work as a risk factor for neck pain.” Id. at 186.  The AMA Guides also reviewed some studies on the effect of sedentary work, repetitive work and precision work, but concluded that “[t]here is insufficient evidence for neck posture, prolonged work in a sedentary position, or repetitive and precision work as risk factors for neck pain.” Id. at 187.  The AMA Guides cited various individual factors positively associated with increased neck pain in conjunction with work activities, including age, gender, body mass index, smoking and psychosocial factors.


The NIOSH treatise found in chapter 3 that there is:

. . . evidence for a positive association between highly repetitive work and shoulder MSDs. The evidence has important limitations. Only three studies specifically address the health outcome of shoulder tendinitis and these studies involve combined exposure to repetition with awkward shoulder postures or static shoulder loads. The other six studies with significant positive associations dealt primarily with symptoms. There is insufficient evidence for a positive association between force and shoulder MSDs based on currently available epidemiologic studies. There is evidence for a relationship between repeated or sustained shoulder postures with greater than 60 degrees of flexion or abduction and shoulder MSDs. There is evidence for both shoulder tendinitis and nonspecific shoulder pain. The evidence for specific shoulder postures is strongest where there is combined exposure to several physical factors like holding a tool while working overhead. The association was positive and consistent in the six studies that used diagnosed cases of shoulder tendinitis, or a constellation of symptoms and physical findings consistent with tendinitis, as the health outcome.

The AMA Guides to the Evaluation of Disease and Injury Causation, supra, found some evidence of occupational risk factors for shoulder tendinopathy, impingement, and rotator cuff tears when there was a combination of factors such as force and repetition, force and posture, but insufficient evidence of causation with respect to vibration, cold environment, length of employment or keyboard activities. Id. at 320.

In Moran v. Gateway Concrete Forming Sys., WC Claim No. 2009-015267 (LIRC June 30, 2011), a carpenter who performed mostly concrete work claimed bilateral shoulder injuries caused by years of occupational exposure. The ALJ and LIRC relied on the testimony of the treating physician, who based his causation opinion on the applicant’s detailed description of his job duties, which were not contradicted by the respondents. The commission rejected the IME’s suggested that tobacco use and alcohol consumption may have contributed to the shoulder condition.


According to the NIOSH study, chapter 4:

There is insufficient evidence for support of an association between repetitive work and elbow musculoskeletal disorders (MSDs) based on currently available epidemiologic data. No studies having repetitive work as the dominant exposure factor met the four epidemiologic criteria. There is evidence for the association with forceful work and epicondylitis. Studies that base exposure assessment on quantitative or semiquantitative data tended to show a stronger relationship for epicondylitis and force. Eight studies fulfilling at least one criteria showed statistically significant relationships. There is insufficient evidence to draw conclusions about the relationship of postural factors alone and epicondylitis at this time. There is strong evidence for a relationship between exposure to a combination of risk factors (e.g., force and repetition, force and posture) and epicondylitis. Based on the epidemiologic studies reviewed above, especially those with some quantitative evaluation of the risk factors, the evidence is clear that an exposure to a combination of exposures, especially at higher exposure levels (as can be seen in, for example, meatpacking or construction work) increases risk for epicondylitis. The one prospective study which had a combination of exposure factors had a particularly high incidence rate (IR=6.7), and illustrated a temporal relationship between physical exposure factors and epicondylitis.  The strong evidence for a combination of factors is consistent with evidence found in the sports and biomechanical literature. Studies outside the field of epidemiology also suggest that forceful and repetitive contraction of the elbow flexors or extensors (which can be caused by flexion and extension of the wrist) increases the risk of epicondylitis. Epidemiologic surveillance data, both nationally and internationally, have consistently reported that the highest incidence of epicondylitis occurs in occupations and job tasks which are manually intensive and require high work demands in dynamic environments—for example, in mechanics, butchers, construction workers, and boilermakers.

The AMA Guides to the Evaluation of Disease and Injury Causation, supra, found strong evidence of occupational risk factors for painful elbow based on a combination of risk factors (e.g., force and repetition, force and posture), but insufficient evidence with respect to vibration, highly repetitive work alone, or in combination with other factors, forceful work, awkward postures, keyboard activities, cold environment and length of employment.  Id. at 275.


NIOSH found in chapter 5a:

There is evidence of a positive association between highly repetitive work alone or in combination with other factors and CTS based on currently available epidemiologic data. There is also evidence of a positive association between forceful work and CTS. There is insufficient evidence of an association between CTS and extreme postures. Individual variability in work methods among workers in similar jobs and the influence of differing anthropometry on posture are among the difficulties noted in measuring postural characteristics of jobs in field studies. Findings from laboratory-based studies of extreme postural factors support a positive association with CTS. There is evidence of a positive association between work involving hand/wrist vibration and CTS. There is strong evidence of a positive association between exposure to a combination of risk factors (e.g., force and repetition, force and posture) and CTS. Based on the epidemiologic studies reviewed above, especially those with quantitative evaluation of the risk factors, the evidence is clear that exposure to a combination of the job factors studied (repetition, force, posture, etc.) increases the risk for CTS. This is consistent with the evidence that is found in the biomechanical, physiological, and psychosocial literature. Epidemiologic surveillance data, both nationally and internationally, have also consistently indicated that the highest rates of CTS occur in occupations and job tasks with high work demands for intensive manual exertion–for example, in meatpackers, poultry processors, and automobile assembly workers.

The AMA Guides to the Evaluation of Disease and Injury Causation, supra, basically punted on a conclusion concerning the relationship between work factors and carpal tunnel syndrome.  The Guides cited both positive and negative causation studies, but leaned toward criticizing the positive studies as being inconclusive.  Id. at p. 278-301.  There was very strong evidence of occupational risk factors for median nerve entrapment at the wrist when there was a combination of risk factors (e.g., force and repetition, force and posture), but low risk evidence with respect to vibration, awkward postures, keyboard activities, cold environment, and length of employment. Id at 282.


Occupational exposures to heavy or awkward lifting exertional activities frequently lead to low back pain, lumbar fusions, disability and potential worker’s compensation claims.  Whether the work environment was a material contributory factor in the onset or progression of lumbar disc degeneration is often hotly disputed.  On the applicants’ side of the issue, there is much epidemiological evidence, beginning with NIOSH’s Musculoskeletal Disorders and Workplace Factors, Chapter 6 Summary, which states:

The review provided evidence for a positive relationship between back disorder and heavy physical work, although risk estimates were more moderate than for lifting/forceful movements, awkward postures, and WBV. This was perhaps due to subjective and imprecise characterization of exposures. Evidence for dose response was equivocal for this risk factor. There is strong evidence that low-back disorders are associated with work-related lifting and forceful movements. Of 18 epidemiologic studies that were reviewed, 13 were consistent in demonstrating positive relationships. Those using subjective measures of exposure showed a range of risk estimates from 1.2 to 5.2, and those using more objective assessments had odds ratios (ORs) ranging from 2.2 to 11. Studies using objective measures to examine specific lifting activities generally demonstrated risk estimates above three and found dose-response relationships between exposures and outcomes. For the most part, higher ORs were observed in high-exposure populations (e.g., one high-risk group averaged 226 lifts per hour with a mean load weight of 88 newtons [N]) . Most of the investigations reviewed for this document adjusted for potential covariates in analyses; nevertheless, some of the relatively high ORs that were observed were unlikely to be caused by confounding or other effects of lifestyle covariates. Several studies suggested that both lifting and awkward postures were important contributors to the risk of low-back disorders. The observed relationships are consistent with biomechanical and other laboratory evidence regarding the effects of lifting and dynamic motion on back tissues. The review provided evidence that work-related awkward postures are associated with low-back disorders. Results were consistent in showing positive associations, with several risk estimates above three. Exposure-response relationships were demonstrated. Many of the studies adjusted for potential covariates and a few examined the simultaneous effects of other work-related physical factors. Again, it appeared that lifting and awkward postures both contribute to risk of low-back disorder. There is strong evidence of an association between exposure to WBV and low-back disorder. Of 19 studies reviewed for this document, 15 studies were consistent in demonstrating positive associations, with There is strong evidence of an association between exposure to WBV and low-back disorder. Of 19 studies reviewed for this document, 15 studies were consistent in demonstrating positive associations, with risk estimates ranging from 1.2 to 5.7 for those using subjective exposure measures, and from 1.4 to 39.5 for those using objective assessment methods. Most of the studies that examined relationships in high exposure groups using detailed quantitative exposure measures found strong positive associations and exposure-response relationships between WBV and low back disorders. These relationships were observed after adjusting for covariates. Both experimental and epidemiologic evidence suggest that WBV may act in combination with other work-related factors, such as prolonged sitting, lifting, and awkward postures, to cause increased risk of back disorder. It is possible that effects of WBV may depend on the source of exposure (type of vehicle).

A “Twin Spine Study,” which started in 1991, set out to study the causes of lumbar disc degeneration in 147 pairs of identical male twins and 153 pairs of fraternal male twins who had exposure – discordant histories. Battié, M.C., “The Twin Spine Study: Contributions To A Changing View of Disc Degeneration,” Spine J., 2009 Jan-Feb; 9(1): 47-59, available online here:http://jonathanhearseydotnet1.files.wordpress.com/2012/05/battie_the-twin-spine-study-contributions-to-a-changing-view-of-disc-degeneration_the-spine-journal_2009.pdf and Battié, M.C., “Lumbar Disc Degeneration: Epidemiology and Genetic Influences,” Spine J. 2004 Dec. 1:29(23) 2679-90.  The investigators estimated that 61% of the variance in disc degeneration in the low back region was explained by familial aggregation, while only 16% was explained by age and occupational physical loading together. They concluded that disc degeneration should now be considered a condition that is genetically determined in large part, with environmental factors also playing an important role. Id.

A well-known orthopedic forensic IME specialist, who does not perform spine surgery but is mainly focused on knee surgery in his clinical life, has written the following extremely controversial paragraph in one or more of his reports:

A lay person may argue that Mr. [Applicant’s] work performing lifting at [Employer] caused or aggravated his preexisting lumbar spondylosis.  However, there is no documentation in the orthopaedic literature that heavy labor causes or aggravates degenerative disc disease of the lumbar spine [Emphasis added].  On the contrary, degenerative disc disease is not due to workplace exposure. A lay person may argue that work as a laborer causes or aggravates degenerative disc disease of the lumbar spine however, this allegation is incorrect.  For example, Battié, et al., the recipients of the 2008 Kapa Delta Elizabeth Winston Lanier Award, have documented that twins who are involved in sedentary or manual labor have nearly identical rates of degenerative disc disease of the lumbar spine (Spine, 2004; (29) 23:2679-2690).  In other words, similar patterns of disc degeneration were noted between twin siblings, despite high discordance in lifetime physical loading exposures. In fact, Videman, Levalathi, and Battié state that, “…routine or repetitive loading may actually have a beneficial effect, delaying disc desiccation associated with aging.” (Spine, 2007; (32) 13:14-6-13).

The treating doctor in this particular case appropriately rebutted the IME’s report as follows:

I also disagree with [IME doctor’s] use of the literature to support his opinions.  I also reviewed the 2008 Kappa Delta Elizabeth Winston Lanier Award. This was a study about twins and their development of degenerative disc disease and back pain.  [The IME doctor] used the study to conclude that degenerative disc disease is not due to work place exposure. In fact, within the study are statements and figures which reveal that there are a variety of determinants that cause disc degeneration and back pain including genetics and biomechanical environmental factors.  In the L4 through S1 levels where [patient’s] injury occurred, much of the determinants of disc degeneration are unexplained in the study that [IME doctor] references.

The Twin Spine Study was roundly criticized by McLean, D., et al,” The ‘Twin Study’ and the Misunderstanding of Epidemiology That Clouds Occupational Associations and Low Back Disorder,”  Journal of the New Zealand Medical Association, Vol. 124, no. 1330, (29 July 2011). The author went on to conclude:

In fact this does not tell us anything about what percentage of cases are caused by genetic factors, or what percentage are caused by environmental factors (and could be prevented by removing these environmental causes.) In misinterpreting this study, [the agency] is confusing two completely different sets of numbers – the % of population variation that is explained by variation in the environment, and the % of cases that are caused by environmental factors.

There is ample evidence, including that from occupational epidemiological studies conducted in heterogeneous populations, of interactions between a range of factors (mechanical, traumatic, nutritional and genetic) playing a role in the disease process that results in lumbar disc degeneration and chronic low back pain. LBD, like all occupationally acquired medical conditions arises as a consequence of a multifactorial mosaic influences.

This single review by Battié et al, of their own work utilizing dated MRI scanning findings does not invalidate over a century of clinical observation and multiple quality epidemiological findings.


The AMA Guides to the Evaluation of Disease and Injury Causation, supra, acknowledged the existence of some studies positively correlating low back pain with work activities.  However, the AMA Guides are not convinced of occupational causation.  The conclusion is stated as follows:

Research to date has identified more than 100 potential risk factors for low back pain. Heavy physical loading, often associated with occupation, has historically been the primary suspected risk factor for disc degeneration, which is assumed to be, in part, explained by “wear and tear.”

In recent years, our understanding of genetic influences on the risk for disc degeneration has changed traditional views. More current research, primarily studies of twins, [Battié, M.C., “The Twin Spine Study: Contributions To A Changing View of Disc Degeneration,” Spine J., 2009 Jan-Feb; 9(1): 47-59 and Battié, M.C., “Lumbar Disc Degeneration: Epidemiology and Genetic Influences,” Spine J. 2004 Dec. 1:29(23) 2679-90] suggest that physical loading specific to occupation and sport plays a relatively minor role in disc degeneration.  Disc degeneration is now considered a condition that is determined largely by genetics.  As a result, previous interpretations of the effects of heavy physical loading on changes in the disc have been challenged and remain inconclusive.

Id. at p. 199.

The author of this presentation made a private inquiry to a local spine neurosurgeon whether the results of studies of twins demonstrating that physical exertion was less of a factor than genetics in the development of degenerative disc disease held water, and received this response:

Any spine surgeon you ask will likely tell you that lumbar spondylosis (as well as degenerative disc disease) is primarily a degenerative (wear and tear) condition.  There is no question that genetics play a role, as this study suggests, but is certainly not the primary factor.  I do not have any literature at hand on the topic, but from extensive personal experience heavy manual labor is the primary reason for progression of spondylosis.  A look at the daily schedule of any spine surgeon will confirm that the majority of our patients use their back for a living – we see many manual laborers for every office worker.

Sorry I do not have citations for you, but I can assure you that the prevailing wisdom is that the conclusion of this one study is over reaching and requires much more study.

Private correspondence from neurosurgeon, July 8, 2014.

There are innumerable publications demonstrating that NIOSH is not impressed with the AMA Guides to the Evaluation of Disease and Injury Causation, supra, or the Twin Spine Study. The studies presented below collectively show a strong link between occupational physical exertion and work-related musculoskeletal disorders. In Garg, A. et al, “The NIOSH Lifting Equation and Low-back Pain, Part 1, Association With Low-Back Pain in the Back Works Prospective Cohort Study,” Hum Factors. 2014 Feb; 56(1) 6-28 and “The NIOSH Lifting Equation and Low-Back Pain, Part 2,” Hum Factors. 2014 Feb; 56(1):44-57, it was concluded that job physical stressors are associated with increased risk of low back pain. See also Lu, Ming-Lun, “Efficacy of the Revised NIOSH Lifting Equation to Predict Risk of Low-Back Pain Associated With Manual Lifting: A One-Year Prospective Study,” Human Factors, vol. 56, no. 1, February 2014, pp. 73-85; Marras, WS, “Cumulative Spine Loading and Clinically Meaningful Declines in Low Back Function,” Human Factors 2014; 56(1): 29-43; “Musculoskeletal Disorders and the Workplace: Low Back and Upper Extremities,” Panel on Musculoskeletal Disorders and the Workplace, Commission on Behavioral and Social Sciences and Education, National Research Council and Institute of Medicine. Washington DC: National Academy Press, (2001).

A comprehensive book published in 2001 by the National Research Council and the Institute of Medicine, in response to a charge from NIOSH and the NIH to conduct a comprehensive review of the scientific literature on the relationship of work and the workplace to musculoskeletal disorders of the low back and upper extremities, authoritatively addressed this topic and concluded as follows:

The weight of the evidence justifies the identification of certain work-related risk factors for the occurrence of musculoskeletal disorders of the low back and upper extremities.

The panel concludes that there is a clear relationship between back disorders and physical load; that is, manual material handling, load moment, frequent bending and twisting, heavy physical work, repetition, force, and vibration are particularly important work-related factors.

Work-related psychosocial factors recognized by the panel to be associated with low back disorders include rapid work pace, monotonous work, low job satisfaction, low decision latitude, and job stress. High job demands and high job stress are work-related psychosocial factors that are associated with the occurrence of upper extremity disorders.

“Musculoskeletal Disorders and The Workplace: Low Back and Upper Extremities,” Panel on Musculoskeletal Disorders and the Workplace, Commission on Behavioral and Social Sciences and Education, National Research Council and Institute of Medicine, National Academy Press, Executive Summary, p. 9 (2001).

Wisconsin courts and the Department have a long history of recognizing the compensability of occupational back claims.

In Koser v. Doskocil Foods, WC Claim No. 1999009744 (LIRC August 2, 2002), LIRC characterized as an “extreme conclusion from the literature” an IME doctor’s reliance on the Twin Spine Study to disclaim causation in the case at bar, and rejected the view that the role of genetics was a more powerful influence on the development of lumbar spine disorders than occupational exposure.  LIRC pointed out that in the Battié Twin Spine Study, there is a concession that other articles cited within the study do relate degenerative disc disease to repeated lifting and bending, and that the study does not completely rule out the effects of occupational exposure in the progression of degenerative disc disease.

In Shelby Mut. Ins. Co. DILHR, 109 Wis.2d 655, 327 N.W.2d 178 (Ct. App. 1982), the court declared that a back injury resulting from working in an industry over an extended period of time is a compensable occupational disease rather than an accidental injury.

In Connell v. Lear Seating Corp., WC Claim No. 1997007805 (LIRC, November 30, 1998), LIRC said that “the law does not require a work injury caused by occupational disease be based on an ‘extended period of time,’” and found for the applicant who claimed that fifteen weeks of work exposure was sufficient to cause a lumbar herniated disc, because “whether occupational exposure is of sufficient duration to cause an occupational back injury is a medical question that will vary from case to case.” Id.

In Van Vonderen v. Miller Electric Mfg. Co., WC Claim No. 20001061234 (LIRC August 14, 2002), LIRC upheld an award for a low back injury with only one day of work exposure.  The exposure may be relatively brief, but not so sudden or traumatic as to be an accident. Accord, Gumieny v. County Concrete Corp., WC Claim No. 2004-017501 (LIRC July 11, 2006).

In Reimer v. Service Painting Corp, WC Claim No. 2010-012540 (LIRC Nov. 13, 2013), an industrial painter who had to load bags of sand weighing 80 – 100 pounds into a sandblasting pot, operate the sandblasting machine, and shovel the sand into disposal containers claimed an occupational back injury.  His treating physiatrist identified a number of identifiable work injuries, events and exposures, but the principal injury occurred over time, rather than as a result of any one event. The proof was held sufficient, despite a submission by the IME doctor that the applicant had multiple level, age-related degenerative disc disease that was entirely not work related.

In Vrana v. Maynard Steel Casting Co., 2014 WL 1234863, WC Claim No. 2004-042249 and 2010-011247 (February 6, 2014), the administrative law judge dismissed an occupational low back injury claim on the grounds that, inter alia, the one of treating physicians failed to document the details of the worker’s workplace exposure and the other treating doctor based his opinion on an inaccurate understanding of the work duties.


The NIOSH study did not address knee disorders.

The AMA Guides to the Evaluation of Disease and Injury Causation, supra, did.  The Guides found some evidence of occupational risk factors for osteoarthritis, meniscal tears or degeneration involving kneeling, squatting and bending, climbing and heavy physical demand, but insufficient evidence for such activities as standing and walking, low and moderate levels of physical activity. Id. at p. 364.

There are often studies available from private and government sources, which directly relate to specific recurring issues that appear in our cases.  As an example, if you have a case involving a potential occupational knee injury case involving a delivery driver for a bottling company, you could search the NIOSH data base and find, “Ergonomic Intervention for the Soft Drink Beverage Delivery Industry,” US Dept. HHS, Public Health Service, CDC, NIOSH publication no. 96-109 (1996), which strongly associates the work of that industry with knee injuries.

In Fuller v. M & H Industrial Service, WC Claim No. 2008-007593 and 2010-025552 (LIRC Nov. 13, 2012),  the treating orthopedic surgeon submitted a report indicating that applicant’s “rigorous work activities”  accelerated the “degenerative process beyond that which would have occurred through natural progression” of his knee condition, thereby requiring knee replacement.  Citing the proposition that work exposure need not be the sole cause or main factor resulting in the occupational disease, LIRC found the evidence sufficient to prove the case.

In Thompson, Jr. v. J & L Fiber Services, Inc., WC Claim No. 1995-032018 and 2002-039488 (LIRC May 21, 2003), LIRC upheld the findings of an ALJ that the applicant’s employment as a foundry work, performing heavy lifting, bending and twisting, were at least a material contributory causative factor in the progression of his knee condition, which eventually required knee replacement. Citing Joseph Schlitz Brewing Co. v. ILHR Department, 67 Wis.2d 185, 191, 226 N.W.2d 492 (1975), LIRC pointed out that an employer is liable for work exposure that hastens the progression of a condition to disability, even if the disability might have eventually occurred anyway from everyday living.


Established risk factors for cardiovascular disease, having nothing to do with workplace factors, include abnormal lipids, smoking, hypertension, diabetes, abdominal obesity, stress, psychosocial factors, low consumption of fruits and vegetables, alcohol use, and lack of regular physical activity.  AMA Guides to the Evaluation of Disease and Injury Causation, p. 412.  Non-occupational risk factors often confound causation analysis, because they are a joint cause with the factors in the work environment.  Occupational risk factors for cardiovascular disease include exposure to carbon monoxide, methyl chloride, cadmium carbon disulfide, lead, arsenic, beryllium, organic solvents, organophosphates and polycyclic aromatic compounds.  Id. at 417-18.

In Neal v. C & D Technologies, Inc., WC claim No. 2003-037006 (LIRC October 30, 2006), LIRC affirmed an award in a case involving occupational exposure to lead causing peripheral neuropathy, hypertension and congestive heart failure.  The treating physician’s report cited reports of a positive correlation (albeit no confirmed causation) between lead exposure,  hypertension and cardiovascular dysfunction.  LIRC stated:

While there is still disputed among the medical experts, the studies cited by Dr. Masci support the conclusion that there is a correlation between elevated blood pressure and lead exposure. There may be some question of whether, or insufficient data to support the conclusion that, lead exposure can cause heart failure by elevating blood pressure in an otherwise healthy individual, but given the NIOSH-documented relationship to elevated blood pressure and the studies/articles cited by Dr. Masci, lead exposure as a material contributory causative factor for cardiomyopathy seems reasonable. Again, the NIOSH report “support[s] the idea that the effects of lead on blood pressure may be related to the development of cardiovascular disease.


The AMA Guides to the Evaluation of Disease and Injury Causation, supra, chapter 13, describe the following generally recognized categories of occupational pulmonary disease:  occupational asthma, hypersensitivity pneumonitis, inhalational fever, fibrotic lung disorders (pneumoconiosis), mesothelioma, bronchogenic lung carcinoma and chronic obstructive pulmonary disease (COPD).

An excellent article by Martin, L., “Pitfalls in Diagnosing Occupational Lung Disease (OLD) For Purposes of Compensation,” 13 J.L. & Health 49 (1998-1999), the author lists several factors that must be avoided by testifying physicians and their attorneys:

    • Making an unsupported medical diagnosis
    • Echoing an unsupported diagnosis made by someone else
    • Inadequate clarification of “impairment” and “disability”
    • Ignoring or minimizing relevant medical history
    • Arguing against yourself
    • Ignoring the possibility of a rare or unusual diagnosis
    • Not obtaining or reviewing independent chest X-rays and reports
    • Attributing causation with certainty when it is unwarranted by the facts
    • Relying on a claimant’s own smoking history
    • Misinterpreting pulmonary function and arterial blood gas tests
    • Missing the real cause of a patient’s complaint
    • Diagnosing occupational lung disease without attempting to remove the patient from the cause
    • Confusion over basic terminology and pathophysiology
    • Using sloppy or incorrect language
  • Not saying, “I don’t know” when you don’t

Zurich General Accident & Liab. Ins. Co. Ltd. v. Industrial Commission, 203 Wis. 135,

233 N.W. 772 (1930), was a pneumoconiosis occupational injury case, involving a man who was exposed to extensive dusts and particulate matter in the chipping room of a factory. The insurance carrier that was on the risk at the time the employer received notice of partial disability from the occupational disease was held liable for the subsequent total disability and death due to the recurrence of the disease. The court said:

The deceased had been employed for eleven years in a dusty occupation. It is a matter of common knowledge that such occupations give rise to lung troubles and that a continued exposure increases the difficulty and greatly diminishes the chances of recovery. While this does not appear in the evidence, it is a matter of common knowledge.

Id. at 142, 233 N.W. at 775.

In Casta v. K-Mart Corp., WC Claim No. 2006-034342 (LIRC March 31, 2009), the applicant claimed that his exposure to mold and mildew in the store where he worked caused sarcoidosis, an immune system disease.  Other co-employees had the same complaint. A treating doctor submitted a Practitioner’s report verifying occupational causation.  Respondents submitted reports from physicians, one of which was the president of the World Association of Sarcoidosis, who opined that the cause of sarcoidosis is not known, and that the applicant’s work exposure did not directly or indirectly cause the condition, although there was an association in the literature between the disease and exposure to water damaged buildings.  LIRC stated:

The fact that there is controversy regarding the cause of the disease, does not mean that that commission must accept the opinion that there is no cause for it.  Credible, relevant, and probative evidence of record, in the form of Dr. Williams’ medical opinion and the medical literature submitted, links the type of environmental conditions to which the applicant was exposed in the employer’s store to contraction of the disease. While this evidence does not constitute unanimous scientific consensus regarding the cause of sarcoidosis, the commission finds it scientifically probative and credible.

In Rose v. Rustoleum Sales Co., Inc., WC Claim No. 2005-013428 (LIRC Sept. 11, 2007), the applicant worked as a chemist in a paint factory, and developed pulmonary disease.  His expert physician opined that the work exposure to isocyanates caused occupational asthma, rhinitis and sinusitis, and possibly also hypersensitivity pneumonitis.  The doctor described almost daily contact with isocyanates while wearing a cartridge mask, as well as spills that applicant cleaned up with towels, and spray painting in a spay booth without a mask. Despite a history of an allergic background, this evidence was held sufficient to allow the claim.

In Mueller v. Carnes Co., Inc., WC Claim No. 2001-003048 (LIRC July 8, 2003),  the applicant developed emphysema and asthma while operating as a plasma cutter to cut sheets used in ventilation systems.  Her treating physicians reported that despite her history of smoking and pre-existing lung pathology, her exposure to ultrafine particles in the arc cutting process was a material contributory cause of her occupational lung disease, and benefits were awarded.


NIOSH has published an Index of 53 Occupational Diseases, involving airway, skin, lung, other chronic conditions, metal poisoning, inhalation or dermal absorption, occupational infections and occupational cancer.  It is available online:

http://www.haz-map.com/occindex.htm NIOSH also publishes an extremely useful online pocket guide to chemical hazards:http://www.cdc.gov/niosh/npg/

The CDC publishes a list of substances considered by NIOSH to be potential occupational carcinogens:http://www.cdc.gov/niosh/topics/cancer/npotocca.html

Sometimes the diagnosis of a condition implies the industrial cause because the link between the exposure and the disease has been irrefutably established by well-established epidemiological studies: silicosis in a foundry worker, mesothelioma in an asbestos worker, or angiosarcoma in a rubber worker exposed to vinyl chloride.  AMA Guides to the Evaluation of Disease and Injury Causation, p. 577.  In other cases, the Guides recommend a three step process for analyzing exposure causation:

  • Establish or verify the diagnosis
  • Determine whether a cause-Effect Relationship [Plausibly] Exists
  • Implement the Hazard Evaluation ProcessId. at 578-79.

The hazard evaluation process requires several steps, which the Guides describe as follows:

  • Attention to the Occupational History
  • Characterization of the Latent Period
  • Identification of Toxic Agents – Material Safety Data Sheets
  • Review of Available Toxicological Information
  • Estimation of Exposure Dose
  • Development of a Dose-Response Model

Id. at 579-82.

An illustrative non-Wisconsin worker’s case employing the Vermont Rules of Evidence,

which are patterned on the  Federal Rule of Evidence and  Daubert-type analysis is Estate of George v. Vermont League of Cities and Towns, 187 Vt. 229, 993 A.2d 367 (VT 2010).  The estate of a deceased firefighter sought review of a decision that denied worker’s compensation benefits for an allegedly occupationally caused non-Hodgkin’s lymphoma. Three experts testified that the claimant’s cancer arose from his work as a firefighter and was caused by his exposures in the course of his duties. Epidemiological studies relied on by the experts quantified the degree of association between exposure to a particular substance and a particular disease by assigning a relative risk of factor of 2.0 to the general causation issue, meaning  that the risk was twice as high among the exposed group as compared to the non-exposed group.  However, the trial court found that only two of eight studies offered by the experts met the relative risk minimal standard of 2.0.  Moreover, when employing an alternative “meta-analysis” that pooled the results of multiple studies to arrive at a single figure representative of all studies reviewed, the court found that meta-analysis was not a reliable scientific method and that it was not reproducible by others. The Supreme Court of Vermont affirmed the trial court’s dismissal of the case for lack of compliance with Daubert.  Both in terms of general causation and specific causation, the claimant’s evidence was found wanting.


Obtain the complete personnel file from all relevant employers

Obtain job description and physical exertion requirements of job from target employer

Obtain the complete medical records from all relevant providers

Obtain detailed interview from applicant

After research below is completed, have applicant prepare an extremely detailed synopsis of job duties, with emphasis on the physical exertion or exposure that has been found in the literature to be a legally sufficient predicate for an occupational disease. See examples in Appendix.

Obtain relevant information from applicant’s union, if any

Obtain Material Data Safety Sheets, if relevant

Conduct a thorough literature search regarding causation from government sources


Dictionary of Occupational Titles Job Descriptions


Conduct private research

Google Scholar

Pub Med Medline

Submit applicant’s synopsis of job duties to treating physician, with a letter seeking an opinion on causation of occupational disease

Research LIRC decisions

Locate a forensically inclined outside expert who has published or is familiar with peer reviewed articles dealing with the general causation issue

Consider hiring outside expert to perform IME

Get a rebuttal from opponent’s IME from treating doctor or outside doctor

Do not rely on a check in the Practitioner’s Report, box 13!

Be prepared to contest the adverse IME opinion if it is not supported by acceptable evidence, i.e., knee specialist opining on occupational back claim by reference to Battié article