Worker v. Employer, 2024 CanLII 140989

APPEALS RESOLUTION OFFICER DECISION

DECISION NUMBER:

20250014

OBJECTING PARTY:

worker

REPRESENTED by:

WORKER REPRESENTATIVE

RESPONDENT PARTY:

EMPLOYER

REPRESENTED by:

EMPLOYE REPRESENTATIVE

HEARING:

HEARING IN WRITING

HEARD by:

L. Cirillo, appeals resolution officer

DATED:

NOVEMBER 20, 2024

ISSUE

The worker objects to the Adjudicator’s decision dated April 28, 2023, which denied initial entitlement for Chronic Idiopathic Axonal Sensory Neuropathy.

BACKGROUND

This claim was established in March 2022 upon receipt of a Form 6, Worker’s Report of Injury, and a report from the Occupational Health Clinics for Ontario Workers Inc. (OHCOW). The worker outlined that he had a long history of chronic idiopathic axonal sensory neuropathy dating back to before 2015, which he claimed was related to occupational exposures to solvents and heavy metals while working in the mining industry. The worker was employed from 1969 to 2003 in a variety of occupations including a Gas Station Attendant and as a Miner for the employer.

The worker’s medical and employment history was referred to the WSIB Occupational Medical Consultant (OMC). In his memo dated May 2, 2022, he opined that based on the available medical on file, the earliest date of diagnosis was June 29, 2016 and this was determined to be the date of injury. He also suggested that the worker be assessed at the Occupational Disease Specialty clinic in order to clarify if he was suffering from occupationally related peripheral neuropathy. In addition, he suggested that an Occupational Hygiene (OH) assessment be completed in order to address the worker’s potential exposure to specific agents related to this type of disease.

The worker participated in an Occupational Hygiene (OH) assessment on July 13, 2022, and

Dr. Spilchuk, of the Occupational Disease Speciality Program, completed a comprehensive assessment via file review on March 17, 2023.

It was ultimately concluded that the workplace exposures were not a significant contributing factor in the development of the worker’s chronic idiopathic axonal sensory neuropathy and therefore, initial entitlement was denied. The decision was communicated to the worker in correspondence dated

April 28, 2023.

In correspondence dated June 3, 2024, the worker’s representative objected to the denial of entitlement to chronic idiopathic axonal sensory neuropathy. She provided a claim background and argued the following in part:

• The worker worked the majority of his career as an underground miner having had exposures to multiple toxins including copper, blasting fumes, diesel exhaust fumes, welding fumes, sulphur dioxide, uranium, McIntyre Powder, to name a few;
• She acknowledges the opinions of Dr. Spilchuk and Dr. Mathew, who opined that the worker’s diagnosis was unlikely related to work and there was no cause evident as per history of bloodwork; however, she refers to the OHCOW report completed by Dr. Boyce, who concluded that there was a moderate probability that the worker’s occupational exposures contributed at least in part to the development of chronic idiopathic axonal sensory neuropathy;
• She refers to operational policy 11-01-13, Benefit of Doubt and states that although the adjudicator notes the medical reports on file, the report of Dr. Boyce was not considered in their decision. In her view, Dr. Boyce’s references were much more detailed versus those of

Dr. Spilchuk;

• For these reasons, she requested that initial entitlement be reconsidered and allowed

Following the above, the file was re-referred to the OMC in order to obtain a further opinion on whether the references from OHCOW would alter the previous opinion.

Despite the above, it was once again concluded that the workplace exposures were not a significant contributing factor in the development of the worker’s condition and entitlement remained denied. The reconsideration decision was communicated to the worker in correspondence dated July 8, 2024.

As the worker continued to object and the decision remained unchanged, the matter was referred to the Appeals Services Division for further consideration.

Worker’s Position:

The worker’s representative relies on her previous submission dated June 3, 2024.

Employer’s Position:

On the Respondent Form (RF) dated October 8, 2024, the employer’s representative agrees with the decision, which denied initial entitlement. He argues the following in part:

• He states the adjudicator undertook a comprehensive treatment [sic] of the evidence surrounding the diagnosis in question, against the worker’s occupational exposure history, inclusive of expert opinions from an OH and OMC;
• He notes that the employer agrees with the adjudicator, that the weight of evidence and opinions fail to support a relationship between the development and diagnosis of chronic idiopathic axonal sensory neuropathy and the worker’s occupational exposures, as claimed;
• For these reasons, the employer requests that the decision be affirmed

AUTHORITY

Workplace Safety & Insurance Act, 1997

Section 2 (1) & 15

Schedules 3 & 4

Operational Policy Manual

Published

11-01-01 – Adjudicative Process

November 3, 2008

ANALYSIS

I have reviewed the record and considered the information, relevant legislation and operational policy in reaching this decision. In considering all of the evidence, including the medical reporting on file, the OHCOW report and the opinions of the OH and OMC, I conclude the balance of evidence does not support that the worker’s occupational exposures as a Gas Station Attendant and as a Miner were a significant contributing factor in the development of his chronic idiopathic axonal sensory neuropathy.

The rationale for my decision is as follows.

The WSIB’s Operational Policy 11-01-01 Adjudicative Process states in part:

Five point check system

All decision-makers use the same criteria for ruling on initial entitlement to WSIB benefits. This system is known as the "five point check system.”

An allowable claim must have the following five points:

• an employer
• a worker
• personal work-related injury
• proof of accident, and
• compatibility of diagnosis to accident or disablement history.

Diagnosis

If it is not clear that the (injury or disablement) diagnosis provided is the result of the accident or disablement history described, a decision-maker may consult with the WSIB's clinical staff to assist in making this determination.

Occupational disease cases are adjudicated under s. 2 (1) and s. 15 of the WSIA and by Regulation in Schedules 3 & 4 of the Act. If the disease is not listed in the Schedules, entitlement to benefits and services, is determined based on the merits and justice of the case. It must be established that it is more probable than not that the circumstances of the worker’s employment and exposure history significantly contributed to the development of the medical condition being claimed. In this case, the worker claims that he developed chronic idiopathic axonal sensory neuropathy as a result of his workplace exposure to various solvents and heavy metals while working as a Gas Bar Attendant and as a Miner.

As is outlined above, the worker held a variety of jobs from 1969 – 2003 including Station Attendant from 1969 – 1970 and Miner (underground and above ground) from 1971 to 2003. In reviewing the record, there is no dispute with respect to the timeframe or the job descriptions on file. As outlined in the OH report dated July 13, 2022, the worker’s employment history and potential exposures were as follows:

• 1969 -1970 - Station attendant - gasoline, diesel fuel, tetraethyl lead, benzene, carbon monoxide, rubber dust, n-hexane, toluene, solvents, degreasers, asbestos, oil, transmission fluid, propylene glycol;
• 1971-1978, 1979-2003 - Mine Labourer, driller, stope miner, haulage, tool room, hoist, mine serviceman, modified worker - Nickel ore dust, cement, drill oil mists, hard metals, silica, diesel exhaust, solvents, arsenic, lead, blasting fumes, explosives, gasoline, whole body vibration, hand-transmitted vibration, noise;
• 1978 – 1979 – Driller - Uranium ore dust, cement, drill oil mists, hard metals, silica, diesel exhaust, radon, blasting fumes, explosives, aluminum powder, whole body vibration, hand-transmitted vibration, noise

The OH concluded, and I accept, the following:

• The worker may have been routinely exposed to hexacarbons such as n-Hexane when working in a service station from 1969-71 as a result of using rubber tire adhesives and handling fuel. Airborne concentrations of n-Hexane from gasoline due to routine fueling work may have been in the range of 6.25-8.5 ppm, with additional direct skin exposures from handling adhesives or using mixed solvents as a cleaner. When working on the surface in modified work or the tool room, the worker may have had some sporadic limited exposures to solvents or products containing

n-Hexane or methyl n-butyl ketone;

• When the worker worked at a service station, he may have been exposed to fugitive emissions of carbon monoxide sporadically when working in the repair garage. When the worker was an underground miner, his carbon monoxide exposures were likely in the range of 10 - 50 ppm most of the time, with short term exposures exceeding 50 ppm some of the time. After 1983, when the worker was working on the hoist or the surface, carbon monoxide exposure is not anticipated, except for rare unforeseen situations;
• There is no record of arsenic intoxications. Exposures to traces of arsenic in motor oil is not ruled out for the 2-3 years when the worker was in an auto service station and sometimes did oil changes. The worker was likely exposed to very low concentrations of arsenic when they were drilling and mining in the nickel mines for 12 years. It is unlikely they were exposed to arsenic containing dust when working on the surface;
• The worker was probably routinely exposed to tetraethyl lead during the 2 - 3 years he was pumping gasoline at a service station from 1969 - 71. He was exposed via air and skin routes. Employer reports potential for miners to have some low-level lead exposure from mining operations – total lead averaging ~0.001 mg/m3. The worker worked underground as a nickel miner for about 12 years. It is unlikely he was exposed to lead later in employment when on the surface;
• When the worker was in the nickel mines, trace exposures to gold and thallium in mineral ores is possible, but elemental metal exposure is unlikely;
• In absence of relevant exposure information specific to the workplace, it was assumed that exposure information presented in published literature for similar operations are representative of this worker’s exposures

In a follow-up memo dated October 7, 2022, the OH noted that as per the worker’s CPP history he was employed at a gasoline service station from 1966 which effectively increased his employment in the service station work to 5 - 6 years, an increase from the original history as per the OH review on file.

The OH noted that the impact of this additional exposure is that the duration of exposure to potential agents of interest including hexacarbons such as n-Hexane, tetraethyl-lead, and carbon monoxide was increased by 2 - 3 years. Thus, the worker’s total exposure to the above noted agents as identified in the conclusions of the original report is higher than was originally assessed.

The record reveals that in approximately 2012 the worker began experiencing numbness and tingling on the bottom of his feet. I note the following pertinent medical information:

• Electromyography report dated June 29, 2016, is for tingling and numbness symmetrically in both feet. Nerve conduction studies (NCS) reveal clear evidence of an axonal sensorimotor peripheral neuropathy, the underlying cause of which isn’t immediately clear;
• Dr. Mathew, Neurologist – October 3, 2016 – was seen for numbness in the pads of the toes and balls of the feet, first noted intermittently three years prior, with more or less persistence in the last year. There is no associated pain, balance is good, denied finger symptoms. Blood work included haemoglobin A1C, CBC, TSH, vitamin B12, creatinine, liver enzymes, ANA, and protein electrophoresis, all reportedly normal; Nerve Conduction Studies (NCS) in June 2016 showed changes consistent with an axonal neuropathic process. While the worker had symptoms and subtle clinical evidence as well as changes on electrophysiologic studies to indicate a mild sensory neuropathic process, there was no evident cause in his bloodwork. It was Dr. Mathew’s opinion that the worker’s condition belonged in the chronic idiopathic axonal sensory neuropathy group, which is an indolent neuropathic process with very gradual progression over years
• The OHCOW report dated November 29, 2021 – Dr. Boyce
  • History of presenting illness notes a history of chronic idiopathic axonal sensory neuropathy dating back to before 2015, with a comprehensive work up;
  • Massage therapy reportedly improved the worker’s symptoms;
  • Symptoms were stable until June 2020, when they worsened with bilateral tingling and burning of the feet which increased to two to three episodes per week. He developed sudden onset stiffness and discomfort in the shoulder, neck, hips, and lower back in December 2019 with subsequent workup revealing elevated CRP and ESR, in keeping with the diagnosis of polymyalgia rheumatica, and he was treated with a course of Prednisone. Symptoms returned with cessation of Prednisone;
  • Based on his assessment, Dr. Boyce noted medical comorbidities of alcohol use and significant traumatic injury to the lower extremities as being potential risk factors. However, he opined that based on the worker’s relatively moderate alcohol use, and significant latency between the leg injury and onset of symptoms, would argue against these as significant contributors;
  • He also notes that the worker may have had exposure to neurotoxic heavy metals, as well as solvents, which are capable of causing neurotoxicity. He notes that it is difficult to determine what specific solvents and metals the worker may have been exposed to; however, taken together it was opined that it was more probable than not that chronic low dose exposure to heavy metals or solvents may have contributed at least in part of the development of his disease
• OMC Review dated May 2, 2022
  • Based on the current information in the claim file June 29, 2016, appears to be the earliest date of diagnosis;
  • From a practical perspective, it is often difficult to prove causality when a toxic neuropathy is suspected (Morrison B, Chaudhry V. Medication, toxic and vitamin-related neuropathies. Continuum (Minneap Minn) 2012:18:139-60);
  • Many clinicians regard toxic neuropathy as a diagnosis of exclusion and it may be helpful to use quantitative measurement tools, such as the Total Neuropathy Score (TNS) to better appreciate the temporal relation of disease’s severity and a suspected toxin. (Cavaletti G, Frigeni B, Lanzani F et al., The Total Neuropathy Score as an assessment tool for grading in the course of chemotherapy-induced peripheral neurotoxicity: comparison with the National Cancer Institute-Common Toxicity Scale. J Peripher Nerv Syst. 2007; 12::210-5);
  • Most toxic neuropathies cause distal, length-dependent peripheral neuropathy, regardless of toxin. Neurotoxins affect entire length of nerve, from its cell body to terminal axon, affecting more severely in the distal portion. This “dying back” neuropathy is very common in most forms of neuropathy, difficult to diagnose;
  • Hence, other systemic features can be a clue to diagnose certain toxic neuropathies. For example, toxic neuropathy due to arsenic poisoning can show not only typical length-dependent neuropathy, but also systemic symptoms, such as GI symptoms, psychosis, and/or Mee’s line in fingernails) [my emphasis added];
  • Currently, he was unable to answer the question as to whether the information in the claim file supported the worker’s condition as being related to occupational exposures;
  • He further noted that in most cases, the condition is idiopathic (i.e., of unknown cause), but in an effort to be as thorough as possible, he suggested that the worker have an assessment with the Occupational Disease Specialty clinic to clarify if he has occupationally related peripheral neuropathy and an OH assessment of various agents of interest
• Dr. Spilchuk - Occupational Disease Specialty Program report dated March 17, 2023:
  • The clinical impression was that based on the worker’s exposure history, substances involved, and particularly the latency between onset of potential exposures (s) and onset of symptoms (up to 44 years), it was unlikely that the worker’s diagnosis was related to work and it is impossible to confidently state that they have contributed to the worker’s neurologic diagnosis;
  • Against occupational relatedness is that there are relatively few substances that might cause axonopathy (n-hexane, acrylamide, carbon disulphide organophosphate pesticides, and Tri-o-cresyl phosphate) and none would manifest with new onset of symptoms decades after exposure;
  • Lead is also associated with peripheral neuropathy, but the mechanism of neurotoxicity is not known to be exclusively axonal;
  • Of the noted substances associated with this only n-Hexane was identified as a potentially relevant exposure (associated with demyelinating sensorimotor polyneuropathy); however, the estimated exposure concentrations (up to 8.5 ppm for up to 3 years during gas station attendant work) was well below known thresholds documented to cause peripheral neuropathy (500 to 2,500 ppm);
  • In observed cases of n-hexane induced peripheral neuropathy, symptoms onset was within days or weeks (depending on the dose) and improved or resolved after cessation of exposure; this was in keeping with the short biological half-life of n-hexane, which was eliminated from the body rapidly, within 10 -120 minutes;
  • Therefore, it was opined that neither the dose nor the timing of onset was in keeping with the expected exposure-response seen in n-hexane induced peripheral neuropathy;
  • Similarly, peripheral neuropathy has been seen in individuals with acute and chronic lead poisoning, however these symptoms would occur in the context of concurrent toxicity and would not occur in isolation (e.g., lead exerts a multisystem effect, so acute toxicity manifests with abdominal colic, CNS symptoms, arthralgias and myalgias, etc). In the absence of clinical frank lead poisoning, it is difficult to ascribe the diagnosis to lead exposure that occurred decades prior;
  • Carbon monoxide is well known to cause acute central nervous system effects (with a threshold of blood level of 20%, corresponding to sustained ambient concentrations of around 150 ppm) but is not associated with peripheral nervous system effects, such as peripheral neuropathy;
  • Arsenic is also associated with peripheral neuropathy, but the evidence only supports this in cases of chronic ingestion of significant doses (such as from contaminated drinking water) and is not generalizable to this case. Such cases generally present with other well-known signs of arsenic toxicity, such as palmoplantar hyperkeratosis, hyperpigmentation, arrhythmias, and vascular effects, not reported in this case;
  • Therefore, it is most likely that the worker’s diagnosis is indeed “idiopathic” (no known cause) as per the neurologist who diagnosed the worker, which is in keeping with the medical literature, where up to 50% of polyneuropathies are of unknown cause
• OMC Review dated June 6, 2024
  • The OMC noted that he restricted his review to the agents noted by Dr. Boyce as he did not believe that the argument of 6 references versus 16 made any impact on the question asked, as it is the quality of the references not the numbers that help shape an opinion one way or the other;
  • The OMC noted that he completed a literature/toxicology search in relation to the agents in question (listed in the memo and will not be repeated).
  • He noted other resources specifically reviewed;
  • Further, he noted that he looked into the agents referenced by Dr. Boyce and what follows is a toxicology review that considered:

Agents

Symptoms

METALS

Arsenic

Chronic arsenic exposure can lead to sensory neuropathy, characterized by numbness and tingling. Other symptoms include skin lesions, pancytopenia, diarrhea, and abdominal pain.

Lead

Acute high-level exposure causes motor neuropathy with minimal sensory involvement, while chronic exposure leads to axonal dying-back neuropathies similar to those from diabetes or alcohol. Symptoms include wrist and foot drops, sensory deficits, and systemic signs like anemia and abdominal colic.

Mercury

Chronic exposure leads to sensory neuropathy, ataxia, and neuropsychiatric symptoms. Acute exposure can cause pneumonitis and systemic toxicity.

Nickel and Copper

These metals can cause contact dermatitis and respiratory issues, but their role in neuropathy is less well-documented compared to arsenic, lead, and mercury.

SOLVENTS

Solvents

Solvents like n-hexane, perchloroethylene (PERC), and trichloroethylene (TCE) are used in industries such as printing, painting, and dry cleaning.

Symptoms: Solvent exposure can lead to peripheral neuropathy characterized by altered sensation, loss of vibration perception, and impaired proprioception. Chronic exposure can result in encephalopathy with symptoms like fatigue, irritability, and neurobehavioral deficits.

• The OMC also noted the following:

Comparison of toxic neuropathy with Chronic Idiopathic Axonal Polyneuropathy (CIAP)

Characteristics: CIAP is a slowly progressive sensory or sensorimotor polyneuropathy with an unknown cause, typically affecting elderly individuals. It presents with distal sensory disturbances and sometimes distal leg weakness.

Diagnosis: CIAP is diagnosed by excluding other causes of polyneuropathy through clinical and laboratory investigations. Electrophysiological studies show axonal degeneration without demyelinating features.

Symptoms: Symptoms include sensory loss, pain, and sometimes motor deficits, but without systemic signs seen in toxic neuropathies.

• The OMC opined that the worker’s presentation is that of chronic idiopathic axonal polyneuropathy (CIAP) and not that of a toxic neuropathy in relation to heavy metals or solvents;
• The OMC noted they are of the same opinion that was provided by Dr. Spilchuk and that the references they reviewed support his line of analysis and opinion provided

It is my understanding that chronic idiopathic axonal sensory neuropathy (also known as CIAP) is a frequent disorder in the elderly where typically, the feet, lower legs and sometimes the hands slowly become numb or weak.

It is also my understanding that toxic neuropathy is nerve damage caused by toxic (harmful) substances. It is a form of peripheral neuropathy, with damage to the nerves away from the brain and spinal cord. It occurs in the nerves of one’s arms and hands or legs and feet.

While I acknowledge Dr. Boyce’s (OHCOW) opinion in that chronic low dose exposure to heavy metals or solvents may have contributed at least in part to the development of the worker’s disease, in weighing the medical evidence I am more persuaded by the opinions of the three other specialists on file including

Dr. Mathew, Neurologist, Dr. Razavi, Occupational Medicine Specialist and Dr. Spilchuk, Occupational Medicine Consultant who all opine that the workplace exposures were not a significant contributing factor in the development of the worker’s condition.

I come to this conclusion based on the following in part [with various areas of my emphasis]:

• Dr. Mathew opined there was no evident cause for the worker’s condition and that it ought to be placed in the chronic idiopathic axonal sensory neuropathy group;
• Dr. Boyce confirms that peripheral polyneuropathies can be a result of multiple etiologies including other diseases, alcohol abuse, vitamin deficiencies as well as environmental and occupational toxins; however, his opinion on work-relatedness is based on the lack of an identifiable etiology versus a definitive work-related one. Further, he states that the condition is only possibly related to neurotoxic compounds that the worker was exposed to during his career. He also notes that neuropathies resulting from neurotoxic metals most frequently occur when high levels of solvents/metals are ingested or absorbed. While he states that chronic low-level exposures specifically to lead and arsenic may result in neurotoxicity (with synergistic effect of multiple agents) he does not address/confirm other symptoms, which would be associated and indicative of these types of exposure;
• Dr. Spilchuk and Dr. Razavi both opine that the worker does not meet the latency between potential exposure and the development of symptoms; there are relatively few substances that might cause axonopathy and none would manifest with new symptoms decades after exposure. Of the noted substances associated with the condition, only n-Hexane was identified as a potentially relevant exposure and as per the OH assessment, this exposure was well below known thresholds documented to cause peripheral neuropathy. In addition, even if exposed, symptom onset would be within days or weeks and improved or resolved after cessation of exposure. Most importantly, peripheral neuropathy seen with lead, carbon monoxide and arsenic poisoning would occur in the context of concurrent toxicity and would not occur in isolation and in this case, the worker does not display any of the other concurrent symptoms;
• Further, I concur with the OMC in that it is the quality of the scientific literature, not the number of studies, that help shape an opinion one way or the other. In my view, despite the quantity of studies referred to by OHCOW, there is no evidence or argument put forth that they are statistically stronger than those referred to by the OMC

In considering all of the above, I find that the worker’s presentation is not that of a toxic neuropathy in relation to heavy metals or solvents. As a result, there is no persuasive evidence that establishes that the worker’s chronic idiopathic axonal sensory neuropathy is causally related to his employment or employment exposures. In addition, I do not consider that the overall evidence in this case establishes probable work-relatedness or that the evidence for and against entitlement is equal in weight. Instead, the medical supports that the condition is idiopathic, i.e., a condition that arises spontaneously or for which the cause is unknown.

For these reasons, on the balance of probabilities, I find that the workplace exposures were not a significant contributing factor in the development of chronic idiopathic axonal sensory neuropathy, and as a result, initial entitlement is denied.

CONCLUSION

I conclude the workplace exposures were not a significant contributing factor in the development of chronic idiopathic axonal sensory neuropathy.

The worker’s objection is therefore, denied.

DATED November 20, 2024

L. Cirillo

Appeals Resolution Officer

Appeals Services Division