JOHNNIE NEAL, Applicant
C&D TECHNOLOGIES INC, Employer
TRAVELERS PROPERTY CAS CO OF AMERICA, Insurer
An administrative law judge (ALJ) for the Worker's Compensation Division of the Department of Workforce Development issued a decision in this matter. A timely petition for review was filed.
The commission has considered the petition and the positions of the parties, and it has reviewed the evidence submitted to the ALJ. Based on its review, the commission agrees with the decision of the ALJ, and it adopts the findings and order in that decision as its own.
The findings and order of the administrative law judge are affirmed.
Dated and mailed October 30, 2006
nealjo . wsd : 101 : 9 ND § 3.42
/s/ James T. Flynn, Chairman
/s/ David B. Falstad, Commissioner
/s/ Robert Glaser, Commissioner
The applicant was born in 1947. He has worked for the employer or its predecessor (Johnson Controls) since 1978. He was a COS (cast on strap) operator, a job that involved exposure to lead oxide while handling plates used in making batteries. 2004 transcript, page 27. The applicant testified he worked well in excess of 40 hours a week. 2004 transcript, page 57.
Currently, the applicant has a number of health problems. He claims these conditions -- and the resulting disability -- were caused by his occupational exposure to lead. The employer and its insurer (collectively, the respondent) claims occupational exposure was not the cause, but instead contends the applicant's problems are caused by alcohol abuse.
The parties submit substantial expert medical opinion in this case. Treating doctor Masci opines that the applicant was exposed to lead while working for the employer and its predecessor, and that it was a material contributory causative factor in the development and onset of lead toxicity he diagnosed. Exhibit D, Masci letter dated August 11, 2003. Dr. Masci concludes:
The disabilities which were directly caused by the lead toxicities include hypertension and peripheral neuropathy. He is also suffering from congestive heart failure which is secondary to his hypertension. It is true that these conditions which he is experiencing, most prominently the hypertension and peripheral neuropathy, can also have other causes, specifically in the case of Mr. Neal. It is my opinion that the hypertension, peripheral neuropathy and congestive heart failure have been precipitated, aggravated, and accelerated beyond normal progression because of his exposure to lead at work.
Dr. Masci added that the applicant's prognosis was poor. He did not know, at that point in time, whether treatment would be effective, but he did state that the "lead exposure which [the applicant] experienced resulted in a body burden of lead that will continue to injure him until he dies."
The respondent retained Kurt Hegmann, M.D., as its medical examiner. His April 19, 2004 report is at exhibit 1. His report includes this summary of the applicant's blood pressure and blood levels:
A table, presumably a compute printout of [the applicant's] whole blood levels, from August 21, 1978 until November 6, 2003 was reviewed. His initial blood pressure was 142/90 on August 21, 1978. Subsequent blood pressure readings were systolic as high as 160 mm/Hg with several in the 150's and diastolic measures as far as 104 with multiple readings in the 90's (only 5 exceptions until June 2003). The blood lead level initially was 94 on October 9, 1979. The highest value was 67 on January 16, 1980. After April 7, 1981, when he was at 55, only two of his readings were above 40, the last of which was September 2, 1981. This is an average systolic blood pressure of 137 over the duration and an average diastolic blood pressure of 91. The average blood lead was 33.6. [Emphasis omitted.]
According to Dr. Hegmann, the applicant suffers from peripheral neuropathy, congestive heart failure, renal insufficiency, memory problems, alcoholism and possible diabetes.
Dr. Hegmann did not think the applicant's peripheral neuropathy was caused by lead exposure at work because lead exposure causes a "motor" or "pure" neuropathy, which affects the nerves to the muscles so that weakness -- and not numbness, tingling or other "sensory" symptoms -- occurs. Neuropathy from lead exposure is also usually focused in the radial nerve distribution of the posterior interosseous nerve.
By contrast, Dr. Hegmann stated, the applicant has a diffuse peripheral neuropathy, not one focused on the posterior interosseous nerve. Further, the neuropathy included both sensory and motor components. Dr. Hegmann also stated that most problems with lead poisoning occur in individuals with very high lead exposures, and suggested the applicant did not have a history of very high levels of lead exposure with a highest level of 64.
Dr. Hegmann went on to note that a mixed sensory and motor neuropathy, such as what the applicant has, is more commonly caused by diabetes or alcohol use. Dr. Hegmann also felt that the records supported a diagnosis of alcoholism, noting the varying quantities of alcohol the applicant admitted to consuming, low BUN levels consistent with malnutrition commonly seen in alcoholism, and congestive heart failure consistent with alcohol induced cardiomyopathy.
Dr. Hegmann did not think that lead exposure caused the applicant's cardiomyopathy. He noted that lead exposure generally does not cause congestive heart failure directly, and that it is speculative to say it causes it indirectly. His report suggests that the applicant's blood pressure, at an average of 137/91, "substantially lower[s] the possibility that hypertension is the main etiology for the congestive heart failure as such." Dr. Hegmann notes further that applicant's blood pressure was already elevated when he began work for the employer. He noted, too, that race, diet, lack of exercise, and alcoholism were all associated with elevated blood pressure. Dr. Hegmann opined that the extent to which lead exposure was associated with hypertension was weak, not enough to cause the applicant's problems. However, the doctor did acknowledge that it was generally thought among most researchers that there was a relationship between lead and hypertension.
Dr. Hegmann concluded:
In summary of the diagnostic issues, Mr. Neal has been diagnosed with congestive heart failure, mixed sensory motor peripheral neuropathy, renal insufficiency (which I cannot objectively support), memory problems (subjective) hypertension and alcoholism. All of these things are explained by alcohol as the root cause. Explaining these problems with a far more complex theory involving a few remote modest lead level elevates and more recent low lead levels is not probable scenario.
Thus, more likely than not, Mr. Neal's problems are not occupational in etiology.
Regardless of cause, Dr. Hegmann felt some permanent partial disability was warranted for the heart failure and neuropathy. He rated permanent partial disability on a functional basis at 20 percent. He felt the applicant's cardiomyopathy and heart failure were under good control, but nonetheless due to that condition, the applicant's weakness, and his neuropathy problems, he was not capable of unrestricted activities. Rather, a limitation to medium duty work within three months of his September 2003 hospitalization was reasonable. See exhibit 1, report of Hegmann dated April 19, 2004, page 18; exhibit 2, report of Hegmann dated June 27, 2004.
Apparently attached to Dr. Hegmann's April 19, 2004 report to the insurer are documents discussing the relationship between lead exposure and heart blood pressure, including a summary of a NIOSH (National Institute for Occupational Safety and Health) report stating that
See exhibit 10. The Interim Report of NIOSH itself states in its Discussion section:
In this study, we had the opportunity to measure left ventricular mass by echocardiogram. Evidence for a relationship between left ventricular mass and lead exposure was found in one population-based survey, even after controlling for recognized cardiovascular risk factors. Our results ... are not inconsistent. Our findings support the idea that the effects of lead on blood pressure may be related to the development of cardiovascular disease.
Exhibits E and 9.
Subsequent documents written by medical doctors criticize the NIOSH study for suggesting a link between lead exposure and elevated blood pressure or thickened heart wall. See exhibits 11 and 12. Among the criticisms -- and perhaps the most understandable from a lay view -- is that when the blood pressure testing was done, lower than average systolic numbers were noted during the NIOSH study. Since both the diastolic and systolic blood pressure numbers are usually very closely correlated, it was suggested that the higher and lower numbers in effect balanced out, meaning there really is no significant effect on blood pressure from lead exposure.
Dr. Masci then wrote a letter dated June 16, 2004 (exhibit B), in response to Dr. Hegmann's report. (1) This begins with a defense of the NIOSH report's conclusion of a positive correlation between lead exposure and elevated blood pressure. Indeed, Dr. Masci contends that by excluding the sickest and most severely affected lead workers, the NIOSH study "clearly understates the risk of lead effect on blood pressure and heart disease." Dr. Hegmann included an article which states that hypertension is among the reported cardiovascular aberrations detected in humans chronically and acutely exposed to toxic lead levels. The article also states that:
Although the threshold blood lead level that triggers cardiac involvement and symptoms of cardiotoxicity has not been determined conclusively, it is apparent that environmental and occupational lead exposures that raise the blood level above 100 μg% and 60 μg% in adults and children, respectively, are frequently associated with transient as well as permanent cardiac and vascular lesions and disturbances. ... At lower blood levels the effects of lead on the heart and vasculature have not been firmly established. The possibility exists, based on recent epidemiological findings, that lead may induce adverse cardiovascular effects (i.e., hypertension) at blood levels commonly found in the general, nonoccupationally exposed population.... The postulated causal relationship between lead and hypertension remains a subject of considerable controversy...
Exhibit B, "Cardiovascular Actions of Lead and Relationship to Hypertension: A Review," Environmental Health Perspectives, volume 78, page 92 (1988).
The article concludes:
Lead poisoning unequivocally results in significant derangements in cardiovascular function in humans.... Less certain are the effects of subclinical lead exposures on the cardiovascular system. As summarized, chronic low-level lead exposure has been shown to affect the electrical and mechanical activity of the heart and to alter vascular smooth muscle function in experimental animals. Whether lead produces similar effects in humans is unknown; however, recent studies suggest that lead may play a role in human essential hypertension. Further studies are needed....
Id., at page 98.
Dr. Masci noted that while the applicant's initial blood pressure reading was 140/90, later readings were lower, indicative of "white coat syndrome." However, Dr. Masci went on to state that still later, after years of lead exposure, the applicant's blood pressure readings steadily and progressively rose, suggesting lead exposure as a cause, at least by aggravating and accelerating a preexisting condition.
Dr. Masci also disputed Dr. Hegmann's conclusion that lead exposure caused motor-only neuropathy. Again, Dr. Masci cites medical journal articles that suggest that peripheral neuropathy, in both the ulnar and median nerves (though the clearest difference was in the median nerve) of the upper extremities may be caused by relatively lower level exposures, including exposure below 50 μg/dl. One of the articles stated directly that "[n]erve conduction velocities, especial in the arm nerves, slow down in lead exposure and this impairment is caused by really low lead exposure..." "Subclinical Lead Neuropathy," American Journal of Industrial Medicine 1:413-420 (1980).
The articles also seem to provide some support for the conclusion that lead exposure causes polyneuropathy -- that is motor and non-motor neuropathy -- as Dr. Masci stated. One article -- discussing the clinical features of polyneuropathy in connection with lead exposure, recites that "Paraestheiae and pain or impaired sensation occurred to varying severity for all 46 neuropathic lead intoxicated patients. "Peripheral neuropathy in chronic occupational inorganic lead exposure: a clinical and electrophysiolocial study," Neural Neurosurg Psychiatry 2001; 71-202. (2) More directly, the abstract of another article states in conclusion:
This study suggests ... that lead might cause sensory neuropathy with an effect threshold corresponding to a 5 year mean lead concentration of 31μ/dl.
"Vibration perception thresholds in workers with long-term exposure to lead," Occupational Environmental Medicine, 2000; 57:588. As Dr. Baltrusaitis testified, physicians other than Dr. Masci believe that lead exposure of a lower level can lead to the development of both motor and sensory neuropathies. January 2006 transcript, page 92.
Returning to Dr. Masci's report itself, the doctor goes on to note that OSHA's goal is to keep levels below 25 micrograms/dl, but that the permissible exposure limit might still be safe for only 90 percent of all workers. As workers become better protected, the doctor continued, more diseases secondary to lead exposure are discovered.
Regarding Dr. Hegmann's diagnosis of alcoholism and his opinion that that condition was the root cause of the applicant's problems, Dr. Masci stated:
...25 years of Johnson Controls' hepatic data show only trivial elevations of GGT and no significant elevations of AST or ALT, when an elevation of four to six times normal is needed to make the diagnosis of alcohol induced liver disease and abuse. ...Dr. [Hegmann] ... tries to make the preposterous suggestion that [the applicant] developed alcoholic-induced peripheral neuropathy without having experienced alcoholic liver disease. In fact, [the applicant] does not even meet the National Institute of Alcohol Abuse and Alcoholism (a division of the National Institute of Health) criteria for alcohol abuse, much less alcoholism. [Emphasis in original.]
While asserting that the 25 years of serial lack of abnormal liver function confirms alcohol played a minor role in his disease process, Dr. Masci opined that even if alcohol did play a role, the medical literature he cited "suggests to a medical degree of certainty that lead aggravated and accelerated the damage."
Dr. Masci went on to opine that the applicant reached a plateau of healing as of April 24, 2004, unless chelation treatment, which improved injection fraction in many individuals with cardiac injury by lead exposure, proved successful. He went on to rate permanent partial disability for congestive heart failure, hypertension, chronic renal insufficiency, and brain injury, at 80 percent. Regarding work restrictions, the doctor opined the applicant should have no further exposure to lead, or any metal or solvent cardiotoxin, pulmonary toxin, or neurotoxin. The doctor stated also that the applicant should "probably not work more than three hours per day, expecting he will be absent from work one to two days per week.
Dr. Hegmann makes a sur-response, by letter dated December 22, 2004 (exhibit 26). Addressing the medical journal articles cited by Dr. Masci, Dr. Hegmann suggests that (1) there are design problems with the "Peripheral neuropathy in chronic occupational inorganic lead exposure" study and (2) the "Vibration perception thresholds in workers with long-term exposure to lead" article merely proved that with sensitive testing non-motor neuropathy could be detected, but that the fact remained the presenting complaint in lead exposure cases was motor neuropathy.
Dr. Hegmann went on cite numerous articles for the clear relationship between alcohol consumption and high blood pressure, congestive heart failure, cardiomyopathy. He also cited studies that indicated hypertension, cardiomyopathy, and peripheral neuropathy could result from an "alcohol problem" from consumption of more than two drinks per day, even if there is no actual alcohol dependence. He added that he was unaware of any studies stating the one needed to drink enough to cause alcoholic liver disease to develop neuropathy from alcohol consumption. Dr. Hegmann does state that people may have problems with alcohol abuse and alcoholic liver disease with completely normal hepatic enzymes. He stated as well that the applicant's cardiac silhouette was more consistent with being caused by alcohol consumption than by hypertension.
Some of Dr. Hegmann's response on rebuttal was echoed by Dr. Baltrusaitis's testimony at the second day of hearing. Dr. Baltrusaitis, too, stated a person can be a heavy drinker and have polyneuropathy but not liver disease. January 2006, transcript, page 18. He added that historically, the exposure to lead had to be heavy, with readings in the 80s and 90s. He also made the point that a polyneuropathy, such as what the applicant has, is related to alcohol abuse but not lead exposure. Id., at 20 et seq.
Dr. Baltrusaitis also asserted that alcohol is "one and only ... cause that relates to all" of the conditions of congestive heart failure, long-term high blood pressure and peripheral neuropathy, though when asked if someone could have all those problems without consuming alcohol he declined to answer asserting that "anything is possible." Id., at 32. But he also said that if someone had all three problems and did not drink, but was exposed to lead, he still would not relate the problems to lead. Id., at 33.
The ALJ credited Dr. Masci's opinion regarding causation. He noted that the applicant was exposed to lead levels of over the 25 μ/dl limit set by OSHA, and that Dr. Hegmann at one point said that lead exposure produced primarily a motor neuropathy suggesting that lead exposure did not cause motor neuropathy exclusively. ALJ Martin also noted that the evidence of alcohol abuse did not cancel out the effect of lead exposure as a material contributory causative factor in the progression of the disabling neuropathy and cardiomyopathy, especially where the applicant was a long time employee with no indication of any alcohol related problems in his employment history. However, the ALJ declined to credit Dr. Masci on work restrictions. Rather, he awarded loss of earning capacity percent based on Dr. Hegmann's "regardless of cause" work restrictions and the vocational opinion of the respondent's vocational expert, Michael Campbell.
The respondent appealed, raising the causation issue. The respondent asserts that the lead exposures were not enough to cause any illness, that the diagnosis of renal insufficiency is not established, and that the diagnoses of polyneuropathy, congestive heart failure, and elevated blood pressure are all related to drinking rather than lead exposure. The respondent points out that the OSHA article does not state that excessive lead exposure causes hypertension, let alone congestive heart failure. The respondent also suggests that the lead exposure is only associated with "pure" or motor neuropathy, not with sensory neuropathy (such as numbness or tingling sensations).
The commission agrees with ALJ Martin's decision. Dr. Baltrusaitis's treatment note of June 5, 2003 seems to suggest that the applicant's doctors invented the applicant's symptomatic complaints for him because the applicant denied having symptoms. By that point, however, the applicant had been hospitalized for eight days for congestive heart failure. Congestive heart failure and neuropathy have been established by objective tests that nobody disputes at least at this point.
There is no question that the alcohol consumption raises a question here. However, there is no history of work attendance problems or other social problems related to alcohol consumption. The is apparently no significant evidence of alcohol-related liver disease. There is no diagnosis of alcoholism in the applicant's periodic lead level examinations by Dr. Baltrusaitis prior to his hospitalization for congestive heart failure.
The commission acknowledges that alcohol abuse affects different people differently. However, the commission finds credible Dr. Masci's suggestion that it is unlikely that the applicant's alcohol consumption would be significant to cause polyneuropathy, but not affect his liver function. In other words, the commission is not persuaded that the applicant drank enough for alcohol consumption to be essentially the cause of his congestive heart failure and polyneuropathy -- with no material contribution from his long-term lead exposure exceeding OSHA standards -- on this record.
While there is still dispute 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 the idea that the effects of lead on blood pressure may be related to the development of cardiovascular disease."
While the classic case of lead exposure is motor neuropathy characterized by loss of strength, the medical literature suggests lead exposure causes at least some degree of polyneuropathy -- that is the kind of sensory or nonmotor neuropathy shown in the applicant's EMG. Dr. Hegmann suggests that this medical literature merely establishes that a non-motor or sensory neuropathy may be detectable by testing, but still the presenting complaint is motor neuropathy or loss of strength. However, the applicant's testimony suggests his first symptomatic complaint was loss of strength -- his problems lifting the 60-pound bars of lead. The applicant testified he noticed this problem a few months before the April 2003 hospitalization, though he also told Dr. Masci in his initial visit in May 2003 he had noticed decreased strength for the past 8 or 9 years and had no sensory symptoms. The doctor who did the EMG testing noted the applicant complained to him of weakness but not sensory problems. It was only after the EMG nerve testing was done that the sensory problems -- or polyneuropathy -- began to be reported (though of course Dr. Baltrusaitis reported on June 5, 2003 that the applicant had had intermittent numbness for years.) Finally, the medical literature suggests that doctors are appreciating symptoms of lead poisoning -- particularly neuropathic symptoms in at least some individuals at lower blood levels than previously thought.
In short, the commission like the ALJ, concludes the applicant's disability in this case was caused by occupational disease: that the occupational lead exposure was at least a material contributory causative factor in the progression of the applicant's disabling conditions. As the courts have consistently held, occupational exposure need not be the sole cause or main factor for an employer to be held liable under the occupational disease theory. City of Superior v. ILHR Department, 84 Wis. 2d 663, 668 note 2 (1978); Universal Foundry Co. v. ILHR Department, 82 Wis. 2d 479, 487-88 note 5. It is sufficient to show that work exposure was a material factor in the development or progress of the disabling disease. Id; Milwaukee M. & G.I. Works v. Industrial Commission, 239 Wis. 610, 615-16 (1942). The applicant has met that burden here.
cc:
Attorney Robert T. Ward
Attorney Thomas M. Rohe
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