Decision #04/11 - Type: Workers Compensation
Preamble
The employer is appealing a decision made by Review Office of the Workers Compensation Board ("WCB") which ultimately determined that the worker's low level exposure to respiratory irritants in the employer's workplace led to the development of bronchiolitis. A hearing was held on March 9, 2010 to consider the matter. The hearing later reconvened on October 12, 13, and 14, 2010.
Issue
Whether or not the claim is acceptable.
Decision
That the claim is not acceptable.
Background
On May 25, 2006, the worker filed a claim with the WCB for breathing difficulties which he related to his employment activities in a food processing plant.
The worker advised the WCB that he was employed with the accident employer for 18 years. He was diagnosed with constrictive bronchiolitis, a bilateral multilobar bronchial wall thickening with air trapping which caused persistent coughing and wheezing with low level exertion. The worker attributed his condition to secondary inhalation of industrial hazards in the workplace.
On May 26, 2006, the worker attended the WCB’s offices and submitted injury forms, Material Safety Data Sheets (“MSDS”) and chemical information. The worker explained that he worked on a 20 liter dispensing machine and as each bag and box was filled, a sanitizing mist was sprayed on the filler nozzle. He was also affected by three other machines in his work area that were shut down earlier than his and went through a sanitizing process which would expose him to fumes. The worker indicated that they used a chemical last year called Matrixx which was highly corrosive and that the employer had since stopped using it. He noted that a maintenance engineer suffered chemical burns from the product.
The worker filled out a WCB questionnaire on May 28, 2006 outlining his work history with the employer, the irritants to which he was exposed and the number of hours he was exposed to each irritant. The worker answered questions related to the onset and worsening of his symptoms, his smoking history and other chest related medical conditions.
On June 12, 2006, the employer’s plant manager acknowledged that the worker had a condition that was causing him difficulty with breathing but disputed that it was work related. The plant manager had concerns with the worker’s respiratory specialist’s opinion, as the specialist never attended the workplace to assess the employee’s daily exposure to chemicals nor did he have any information as to the amount and which chemicals were used. He stated that none of the chemicals used were above 4% concentration. He stated that the employer was required by law to perform meticulous cleaning and sanitizing operations of equipment and the facility in general and to adhere to proper chemical handling procedures.
The plant manager advised the WCB that the worker had breathing difficulties in September 2005 and that he applied for short term disability as his condition was not considered work related. The worker had been off work from September 28 to December 19, 2005 and he returned to modified duty work that was not in the production area. The worker continued on modified duties until May 19, 2006 when his doctor indicated that the worker’s condition was work related. The plant manager confirmed that the worker had no exposure to the production area since the end of September 2005 and that there has been no improvement in his condition. He stated that an independent, unbiased certified industrial hygienist would be performing a time-weighted average study of chemical vapors in the workplace and that the results would be shared with the WCB.
On August 17, 2006, the worker advised his WCB case manager that he had concerns in the way the employer’s air quality testing was conducted. He said it was performed during a one month period, not a 17 to 18 year period, and that some of the chemicals he was exposed to had been discontinued.
On August 4, 2006, the occupational hygienist issued a report summarizing their two day environmental sampling of the cleaning chemical emissions present in the production area where the worker worked. The results of the sampling indicated that airborne concentrations of the chemicals measured were below their respective Occupational Exposure Limits ("OEL"). The actual air monitoring measurements were included and were adjusted against American Conference of Governmental Industrial Hygienists ("ACGIH") threshold limit valves and time weighted averages.
The worker provided the WCB with a submission from the Health & Safety Committee outlining the following concerns pertaining to the recent air quality testing:
· employees were only tested to their exposure to one chemical when in fact employees would come in contact with a number of chemicals during a shift;
· the testing did not take into account the effects of repeated, long term exposure to chemicals;
· the testing was done during the summer when doors and windows were open and fans were used to help with air circulation;
· the testing was limited to a 24 hour period;
· the testing was done for only a half a normal 10 hour shift and in some cases as little as 18 minutes. The testing was done for only one chemical on an average day and did not represent a “worse case” condition.
· the report did not include the chemical Matrixx which had been in used in the plant and was discontinued due to its effects on employees.
Medical reports on file showed that the worker was seen by a specialist at the Adult Allergy/Immunology Clinic on November 25, 2005. The specialist reported that the worker presented with symptoms of shortness of breath, coughing and wheezing since last spring. The worker had pulmonary function tests (“PFT”) two months ago which showed an obstructive pattern with a significant bronchodilator response. He noted that the worker was unaware of triggers for his symptoms but wondered if exposure to chemicals and cleansing agents at his work may be the trigger. He noted that the worker worked as a machine operator for the last 18 years. The specialist indicated that the equipment and machines were washed and sanitized every day with various cleaning agents and chemicals. The worker worked Monday to Thursday and was then off for three days. The worker did not notice any significant difference in his symptoms during weekends compared to weekdays.
In a follow up report dated January 9, 2006, the above specialist reported that the worker was on an inhaler but still complained of shortness of breath and wheezing on exertion with the cold. On February 3, 2006, the specialist reported that the worker continued to experience cough and wheezing. He stated that a recent methacholine challenge and PFT showed a normal methacholine challenge.
The worker was assessed by an occupational health physician in February 2006. The specialist considered the worker’s occupational history, medical history, physical examination and laboratory evaluations. His assessment of the worker’s condition was a possible irritant induced asthma. He stated that the worker worked with a large number of irritants at work and it was possible that these may have started off his asthmatic condition. He said the worker could not identify any sensitizers amongst the chemicals he worked with, but it was possible he could have been sensitized to some of the milk products, and recommended allergy testing for whey. The specialist indicated that the worker remained quite symptomatic in spite of treatment for asthma and reasonable lung function tests. He stated that this raised the possibility that another diagnosis should be considered.
On April 11, 2006, the specialist from the Adult Allergy/Immunology Clinic reported that an uninfused CT scan of the worker’s chest showed bilateral multilobar bronchial wall thickening with air trapping. He stated that while this finding may be consistent with asthma, there was really no support for this diagnosis and so the possibility arose that this was a constrictive bronchiolitis perhaps secondary to an inhalation injury in the workplace.
In a July 5, 2006 report, a respirologist reported that he saw the worker on April 21, 2006. He reported that the worker had no previous history of asthma. He noted that worker was exposed to a number of chemicals which he utilized as washing agents for machines while at work. These included various acids such as acidic acid, hydrogen peroxide, sulfonic acid and octanoic. He was exposed to chlorine and other irritants on a regular basis. “While working on this job for many years, he developed symptoms of shortness of breath which have now progressed. He has been away from work for approximately 6 to 7 months now. There has been some improvement in his symptoms but these have not resolved." The respirologist noted that the worker continued to have significant dyspnea with activities and was barely able to perform activities of daily living. The respirologist concluded that the worker developed occupational asthma from his work in the food processing industry and that the occupational exposure could have been any of the sensitizers listed above.
The file information, which included MSDS, air quality survey and medical reports were reviewed by a WCB internal medicine consultant on September 19, 2006 at the request of primary adjudication. The consultant provided the following medical opinion:
· he suspected that the diagnosis was bronchiolitis secondary to exposure to either the chlorine gases that may have evolved in the use of nitrate acid, phosphoric acid or acetic acid. He reviewed the environmental studies and although they did not show any increase in noxious gases, he suspected there may have been instances when the gases evolved and the worker inhaled them.
· the consultant suspected that the worker will have exacerbation each time he was exposed to the noxious gases and also with other possible reasons such as respiratory infections. He suggested that the worker avoid working in an environment that exposed him to gases. This would be a permanent restriction. The worker’s PFT results on file indicated a fairly good function which would allow him to work but not involving heavy physical activity.
On September 29, 2006, a WCB case manager gathered additional information from the employer’s plant manager as to what specifically occurred in the worker’s work area regarding cleaning and sanitizing. On October 4 and 6, 2006, the case manager obtained additional information from the person who performed the air quality testing at the plant.
The worker’s file was referred back to the WCB internal medicine consultant to review the new information on file and to respond to several queries. The case manager noted that during the summer periods when production was higher, the worker, on day shift, would not usually be involved in using chemicals to clean machines because production would run into the next shift and cleaning was not done until the production was complete. He stated that the air quality testing was done during cleaning and handling of the raw chemicals to try to produce a worst case scenario under normal operations.
On October 17, 2006, the WCB internal medicine consultant outlined the causes of bronchiolitis. He stated, in part, that the diagnosis of bronchiolitis was based mainly on a CT scan of the chest done in March 2006.
Primary adjudication requested and received additional information from the family physician who saw the worker for treatment on June 6, 2005. The physician reported that the worker’s chief complaints were “1 month ago, gave allergies. At the top of the chest cavity, training for the marathon, don’t feel he has the lung capacity. Advils Tylenol, no phlegm that doesn’t want to go away”. The physical examination was normal and the physician assessed the worker with acute bacterial bronchitis.
On December 7, 2006, the WCB internal medicine consultant reviewed the information again and stated:
“…We have no medical evidence of any illnesses prior to May 2005. [the occupational health physician] in his consultation report mentions that the claimant had been previously healthy and was physically active and was a marathon runner in the past. In addition there is no history of any acute accidental chemical spill which would explain the development of some acute illness in May of 2005. He did not see [family physician] until June 6, 2005. Based on the above information, my conclusion is that [the worker] had developed a viral infection in May of 2005. The viral infections are not susceptible to antibiotic treatment and can produce damage to the lower respiratory tract resulting in bronchospasm…In summary, I suspect the physical findings by various physicians, the mild airflow limitations seen on pulmonary function tests in September of 2005 and the findings of bronchial mucosal thickening on the CT of the chest could be explained on the basis of viral infection.”
On December 15, 2006, the worker advised his case manager that there was no specific incident/event at work in early 2005. He was relating his condition to the ongoing exposure to chemicals. The worker confirmed that he had an onset of symptoms around March/April 2005 while training for the marathon.
In a decision dated December 15, 2006, the worker was advised that his claim for compensation was not accepted as the information on file did not establish that his condition was related to his employment. The case manager’s decision was based on the following factors:
· information from the employer that chemicals were used in the cleaning process; however, they were used in a solution and the concentration did not exceed 4%.
· air quality testing had been done during the cleaning process when there would be the most risk of exposure and it was shown that the concentrations were below the allowable limits and in some cases below the detectable levels.
· comments by the employer that the worker would have a lesser exposure than other workers as production from the machine he operated would frequently extend into the next shift and he would not be involved in the cleaning of the machine in those instances.
· medical information which showed that there was an onset of symptoms in early 2005 with no indication of prior problems.
· the worker’s symptoms may be caused by factors other than exposure to chemicals and the onset of symptoms appeared over a relatively short period of time in the absence of a specific exposure event at work.
On December 28, 2006, the worker’s union representative appealed the case manager’s decision to Review Office.
On January 19, 2007, Review Office outlined the opinion that there was no conclusive evidence to confirm a medical diagnosis in the worker’s case and felt that further medical investigation was required by the case manager to determine the acceptability of the claim.
A submission was received from the worker’s union representative dated May 1, 2007. He indicated that he disagreed with the some of the points outlined in the WCB’s decision of December 15, 2006 and memorandums to file dated September 29, 2006 and October 4, 2006.
He indicated that he conducted two interviews with employees who had serious and extensive injuries after coming into contact with chemical sanitizers Matrixx and Oxonia. These chemical sanitizers were sprayed in close proximity to the worker after each bag on his machine was filled, an average of 1000 bags per day. Matrixx was introduced into the plant in September 2004 and immediate problems occurred. The dangerous chemical Matrixx was removed from the work site in October 2005. He noted that the worker began having signs and symptoms of respiratory problems in the spring of 2005. Matrixx was removed from the plant in October of 2005. This was not included or even mentioned in the chemical report.
On May 17, 2007, the case manager asked the employer to provide information regarding when Matrixx was used, the dilution factor, times when the worker worked on the machine and the reason the product was discontinued. The acting plant manager advised the case manager that Matrixx was still at use in other facilities with no problems and was surprised that it was not still in use at the worker’s plant. He noted that he worked at another facility for four years and it was in use all the time and still was in use. He was not aware of any workers having problems related to the product use.
A report dated May 15, 2007 was received from the treating respirologist. The respirologist outlined the opinion that he did not think the worker suffered from viral related bronchiolitis, since viral bronchiolitis was unknown to occur in adults and only occurred in children. He stated that the history was such that the worker became sick over months to years which was against viral infections as viral infections occur fairly quickly.
On May 23, 2007, the WCB’s internal medicine consultant reviewed the file and stated, in part, “In my memo of Oct. 6, 2006 I had discussed the various causes that may result in bronchiolitis. I did not employ that the claimant’s disease process was of viral origin. More over I had stated in a later memo that it would not be possible to investigate for viral etiology on such late date. I had stated my conclusion regarding the diagnosis in my memo of September 19, 2006.”
On May 28, 2007, the acting plant manager spoke with the case manager. He noted that they switched from Matrixx to Oxonia in August 2005. The reason for the switch was because the workers did not like the smell of Matrixx. He was not aware of Matrixx damaging pipes or pumps, and that the product was still being used in other facilities. The product was diluted with water and was used at 1200 to 2600 parts per million. There was no mist and it was applied in a direct spray. The manner the Oxonia is applied was the same therefore he believed that there would not be any more airborne Matrixx than there was of the chemical used at the time of the testing.
In a second decision dated May 28, 2007, the case manager advised the worker that he was unable to change his prior decision to deny the claim based on the following factors:
· the worker’s prior history that he was healthy and active in sports with no health problems until he started training for the marathon in 2005;
· the air quality testing which did not indicate any excessive airborne concentrations of the chemicals that were in use;
· Matrixx was still in use in other plants and the decision to switch from Matrixx in the Winnipeg plant was due to concerns about odor. The product was not used in a mist application and was mixed with water and diluted to 1200 – 2600 parts per million.
On June 14, 2007, the worker’s union representative wrote to Review Office in appeal of the WCB’s decision to deny the worker’s claim. The union representative indicated in part, that the acting plant manager provided the WCB with the wrong information, ie. that Matrixx was removed from the plant not for health and safety concerns but because of odor. He noted that the WCB was provided with a written statement from an employee who had been seriously injured when a chemical line eroded shortly after Matrixx was introduced.
In a report dated July 3, 2007, the worker's family physician provided a letter in support of the worker's claim. The family physician opined that it was highly unlikely that a viral infection would continue to disable the worker two years later and that the worker's lung condition was secondary to the exposure of chemicals he suffered at work.
Prior to considering the worker’s appeal, Review Office referred the case to the WCB’s internal medicine consultant. On July 10, 2007, the consultant stated:
“…In my opinion, the claimant had suffered from some form of viral infection when he saw [the family physician] in April 2005. Although viral infections aren’t common in adults, it is still possible that the symptoms were caused by a viral infection. The reversible airway disease could be related to the viral infection, as would be the changes in the CT scanning of the thorax. The non-response to treatment would suggest a non-allergic nature of the problem.
I did consider the possibility of exposure to the chemicals, which, as I mentioned in my previous memos, are irritants to the respiratory system. Minor exposure may produce upper respiratory symptoms, but changes of bronchiolitis would indicate more severe degree of exposure. Heavy exposure would occur with accidental spills or some other form of accident. Presently, we have no indications of such occurrence. The environmental study indicates that there was no excess level of irritants present in the environment.
Considering all the facts, I have arrived at the conclusion that a viral infection fits the picture better than exposure to chemicals. Persistence of dyspnea may be related to some other organ being involved, eg., heart.”
In a decision dated July 19, 2007, Review Office determined that the claim for compensation was not acceptable. Review Office accepted the medical opinion of the WCB’s internal medicine consultant that the diagnosis was bronchiolitis caused by a viral infection. It also found no evidence to support that the air testing was not conducted in a proper manner and did not dispute the results. Review Office outlined the position that the evidence did not support that there was an identifiable factor in the workplace that would result in the development of a respiratory condition and that the file evidence did not support a causal relationship between the worker’s condition and the workplace environment.
The worker’s union representative submitted additional information to Review Office for consideration. This included additional medical information regarding bronchiolitis obliterans, comments/opinion from the family physician and readings of the sanitizer levels from January 2005 to July 2006.
On November 28, 2007, the Review Office contacted the union representative and gathered further information related to the sanitizer level reports that were submitted.
Review Office referred the case to the WCB internal medicine consultant to review the new evidence that was submitted and to ascertain whether the information changed his previous opinions. On December 11, 2007, the WCB consultant confirmed that the diagnosis of the worker’s condition was viral bronchiolitis. He did not think that viral bronchiolitis was related to the workplace exposure.
On December 18, 2007, Review Office confirmed that the claim for compensation was not acceptable. Review Office stated that the sanitizer level reports documented that at times the level of Matrixx was high (above the target concentration). However, there was no evidence to support that these levels would result in the development of a respiratory condition. Review Office accepted the WCB’s internal medicine consultant (outlined on December 11, 2007) that the reading of the FEF 25-75% is not significant given that the interpreter of the test results reported a mild air flow limitation and no comments or importance was given to the FEF 25-75% reading. Review Office concluded also that the file evidence did not support a causal relationship between the worker’s respiratory condition and the workplace environment.
On December 20, 21 and 28, 2007, a second environmental study was conducted by an environmental engineer retained by the employer. The purpose of the second study was to measure the exposure of a machine operator in the worker's position to airborne levels of Matrixx sanitizing solution vapour. The two primary components to Matrixx were determined to be acetic acid (15-40%) and hydrogen peroxide (5-10%). Based on time weighted average concentrations of acetic acid and hydrogen peroxide vapour during the standard 10 hour work shift, the study found that the exposure of the machine operator was well below permissible levels. The study concluded that operation of the machine did not represent an inhalation risk to the health of the machine operator under the operational conditions encountered during the exposure tests.
On March 7, 2008, the worker’s union representative provided the WCB with a February 12, 2008 report from an occupational health physician who provided a narrative report outlining his opinion that the cause of the worker’s bronchiolitis was due to his exposure to irritants in the workplace.
On May 12, 2008 a senior WCB medical advisor reviewed the information on file. In response to questions posed by Review Office, the medical advisor outlined the view that low level exposure to respiratory irritants could lead to the development of bronchiolitis and that the medical evidence did not support that the worker’s respiratory condition was related to a viral infection.
On May 21, 2008, Review Office determined that the worker’s claim for compensation was acceptable. Review Office concluded that Matrixx was used in the workplace when the worker became symptomatic and that the evidence on file supported that the worker had a low level exposure to a respiratory irritant in the workplace. It accepted the opinion of the medical consultant that the medical evidence supported that low level exposure to respiratory irritants could lead to the development of bronchiolitis. Review Office was of the opinion that a factor had been identified at the workplace as being the proximate cause of the condition and therefore the claim was acceptable.
On June 12, 2008, the employer’s legal representative appealed Review Office’s decision to the Appeal Commission and a hearing took place on March 9, 2010. Appearing at the hearing was legal counsel and a regional director of operations for the employer, and the worker with the assistance of his union representative/co-worker. At the hearing, in addition to a report dated November 24, 2008 by an occupational medicine specialist which was submitted prior to the hearing in accordance with the Appeal Commission Rules of Procedure, the employer sought to introduce a second medical report dated March 8, 2010 from another occupational and environmental medicine specialist. Given the short notice, the hearing was adjourned to permit the worker to respond to the second medical report. The reconvened hearing was held October 12 to 14, 2010.
On October 19, 2010, the worker's union representative was asked by the appeal panel to submit his comments in regard to an article entitled Bronchiolitis: The Pathologist's Perspective that was submitted at the October 2010 hearing. On the same day, the appeal panel also asked legal counsel representing the employer to submit additional information regarding the installation of back check valves from the plant and MSDS pertaining to two specific chemicals. Legal counsel was also advised that the appeal panel wished to visit the plant to view the worker's work station.
On October 26, 2010, legal counsel provided the Appeal Commission with the requested information concerning the back check valves and the MSDS. This information was forwarded to the union representative for comment.
On October 27, 2010, the union representative provided the Appeal Commission with a report from an occupational health physician dated October 18, 2010 which included comments regarding the bronchiolitis article as well as a curriculum vitae and further medical opinion. On November 1, 2010, legal counsel submitted argument to the appeal panel that the new report should be ruled inadmissible. On November 8, 2010, the appeal panel advised all parties that it would accept the occupational health physician's report of October 18, 2010 only as far as it related to commentary on the bronchiolitis article and that it would accept the physician's curriculum vitae.
On November 22, 2010, the appeal panel attended the job site to view the worker's work station and the equipment he worked with. On November 22 and December 8, 2010, the appeal panel met to discuss the case and render its final decision.
Reasons
Chairperson Choy and Commissioner Finkel:
Applicable Legislation
The Appeal Commission and its panels are bound by The Workers Compensation Act (the “Act”), regulations and policies of the Board of Directors.
Subsection 4(1) of the Act provides:
4(1) Where, in any industry within the scope of this Part, personal injury by accident arising out of and in the course of the employment is caused to a worker, compensation as provided by this Part shall be paid by the board out of the accident fund, subject to the following subsections. (emphasis added)
Analysis
The issue before the panel is whether or not the worker’s claim for bronchiolitis is acceptable. In order for the employer’s appeal to be successful, the panel must find on a balance of probabilities that the worker’s bronchiolitis did not arise out of and in the course of his employment.
The issue before us is one of causation. Although there was significant discussion on the WCB file and in oral submissions at the hearing as to whether the cause of the worker's breathing difficulties was viral vs. chemical exposure, we do not feel it is necessary for the panel to consider whether the cause was viral. In order for us to determine this appeal, we need only to be satisfied that workplace chemical exposure was the cause of the worker's condition. We do not need to determine an alternate cause.
After carefully reviewing the evidence on file and the evidence submitted at the hearing, the majority of the panel finds that we are not convinced on a balance of probabilities that work related exposure caused the worker's bronchiolitis and accordingly, the employer's appeal should be allowed.
Evidence of chemicals in the workplace
The first point considered by the panel was the extent to which chemical sensitizers were present in the workplace. The workplace was a food processing plant and therefore there were strict handling procedures in place. The types of chemicals being used in the workplace were closely monitored and the employer was able to provide a comprehensive list of the possible chemical exposures.
The worker's evidence was that for the last eight years he was working for the employer, he was posted at the "B & B" station. At this station, product would be deposited by a machine into a container. After each container was filled, a cleaning solution was automatically sprayed onto the filler head of the machine to sanitize it. The worker estimated that he would fill anywhere between 500 to 2000 bags per day and the chemical sanitizer solution was sprayed after every bag. His evidence was that the spray would land on his hands and upper chest area and that there was a mist in the air. He could definitely smell the chemicals in the air, although the concentration levels would vary day to day. In addition to the sanitizing spray, the worker also identified other exposures to cleaning chemicals. At the end of his shift, the worker would be required to wash down his machine. Four different cleaning solutions were used in the regular cleaning of his station. There was also a sanitation spray hose, which would be used periodically throughout his shift to spray the machine when required. Finally, clean up of other production areas would be conducted in close proximity, approximately five feet away from where the worker stood. The cleaning solutions would be heated to a temperature of between 150 to 190 degrees Fahrenheit and fumes would be produced.
Following the hearing, the panel requested an opportunity to conduct a site visit. On November 22, 2010, the panel viewed the production area. Our observations were that the sanitizing spray consisted of a visible burst of liquid which was angled away from the operator. The spray consisted of a range of droplets, mist and finer mist. The location of the spray nozzle was at approximately waist height and was to some extent shielded by the machinery. There did not appear to be much errant spray in an upwards direction and into the operator's breathing zone. Rather, the general ventilation in that area tended to dispense the spray directly away from the operator. The general environment was extremely humid and the smell of cleaning solution was detectable.
The employer commissioned two environmental surveys to measure the airborne levels of chemical exposure. The first survey conducted in August 2006 monitored the cleaning chemicals being used at that time. The occupational hygienist identified the types of chemicals present in the cleaning solutions used in the production process and monitored the following agents: sodium hydroxide, inorganic acids (nitric and phosphoric), chlorine and acetic acid. The panel notes that the environmental studies monitored both the ambient conditions in the room as well as the likely inhaled exposures for the worker, by use of devices attached to the worker's lapel. The results of the testing showed the following:
- Sodium hydroxide - none detected in production area;
- Acetic acid - between 0.034 to 0.21 ppm detected (adjusted OEL is 7 ppm);
- Chlorine - in four of six stations, none detected; at the worker's station, 0.045 ppm detected (adjusted OEL is 0.35 ppm)
- Nitric acid - none detected in production area;
- Phosphoric acid - none detected in production area
In response to the criticism that the August 2006 environmental survey did not include testing for a discontinued cleaning solution called "Matrixx", a second environmental survey was conducted in December, 2007 to specifically test for the chemical agents in this solution. This testing was also directed to the worker's station only, and not the general production area. The results of the December 2007 tests showed the following:
- Acetic acid vapour
- in the breathing zone of the machine operator, between 0.257 and 0.273 mg/m3 was detected (TWA guideline is 10 ppm or 17.2 mg/m3); this represents 1.5 to 1.6% of the 10 hour guideline;
- passive monitoring badges measured between 0.822 to 1.03 mg/m3; this represents 4.8 to 6.0% of the 10 hour guideline;
- Hydrogen peroxide
- Passive monitoring badges measured between 0.030 to 0.059 mg/m3 (TWA guideline is 0.97); this represents 3.1 to 6.1% of the 10 hour guideline.
The majority notes that while the conclusions of the environmental studies showed that the exposures were significantly below OEL guidelines, we recognize that these guidelines are just that - guidelines, and should not be considered conclusive as to whether or not there could be a harmful effect in sensitive individuals. Nevertheless, it is evident that the measured presence of chemical vapour in the workplace was very low and the majority feels that this is an important factor to consider in making our decision.
There was nothing observed during our site visit of the production area which would cause us to question the reliability of the environmental surveys conducted in August 2006 and December 2007. Further, there was no evidence that the operating conditions at the worker's station had changed much between the time he was working and the time of the environmental surveys. There were some new back-up valves installed, but we find that these modifications would not have significant impact on the dispersal of the sanitizing spray, and if anything, would have tended to increase the amount of spray. We therefore accept the environmental surveys as the best evidence as to the extent of the chemical exposure the worker experienced in the workplace.
Expert medical opinions
There was extensive medical evidence submitted at the hearing which had not previously been considered by the WCB. On behalf of the employer, two new medical expert reports addressing the issue of causation were filed and one of the experts was called as a witness. On behalf of the worker, the treating respirologist appeared at the hearing and provided evidence on causation.
The expert evidence relied upon by the employer can be summarized as follows:
- Expert report dated November 24, 2008 - this report was prepared by an occupational medicine specialist who had thirty years of experience in the field. His opinion was that the level of chemicals to which the worker had been exposed would be insufficient to cause the respiratory symptoms with which he presented at the time. While some individuals may be more susceptible to certain physical items than others, there was no evidence from the testing that the worker had any greater sensitivity to allergens or other substances than anyone else. The specialist went on to opine that the probable cause of the worker's condition was a viral infection. This expert was also called as a witness at the hearing.
- Expert report dated March 8, 2010 - this report was prepared by an occupational and environmental medicine specialist, who had experience in conducting research into dust-related and toxic-gas related diseases of the lung. In this report, the following observations are made:
- The environmental surveys show no evidence of significant inhaled exposure to any of the chemicals specified. While it is true that the OEL is not the same as a threshold for toxicity and some adverse effects can occur below the OEL in susceptible individuals, in this case levels of exposure are well below what one would expect even in that situation;
- No toxic exposures affect just one part of the lung when they are inhaled. The worker's abnormality was localized in the lower small airways but whatever caused it did not also produce the more usual upper large-airway response of irritant-induced asthma, RADS or bronchitis;
- The chemistry and physical properties of the chemical exposures identified in the workplace were not consistent with an irritative bronchiolitis. Acetic acid and chlorine are highly water soluble and so would exert their primary effects on the proximal airways, proving an asthma reaction, not an isolated bronchiolitis. Hydrogen peroxide is unstable in air and would have to be inhaled as droplets or in very high concentrations to produce pulmonary toxicity, which would then be generalized;
- A distant possibility would be allergic sensitization by one of these chemicals, resulting in an immune effect or allergy confined to the bronchioles. This would be highly implausible, as an allergic bronchiolitis would not occur in isolation. It would accompany other allergic manifestations, which the worker did not show.
- The employer also relied on December 11, 2007 opinion of the WCB internal medicine consultant, which was that the diagnosis of the worker's condition was viral bronchiolitis and that viral bronchiolitis was not related to the workplace exposure.
The worker relied on the following expert evidence:
1) The treating respirologist was called as a witness at the hearing to give his opinion on causation. The respirologist had been a specialist in respiratory medicine for over twenty years and estimated that he had treated thousands of patients in his years as a specialist. The respirologist's previous reports to the WCB showed an evolving diagnosis as the worker's condition progressed, but ultimately he was of the opinion that the worker developed bronchiolitis secondary to exposure to chlorine gases that may have been generated through the use of nitrate acid, phosphoric acid or acetic acid. It was his view that although environmental studies did not show any increase in noxious gases, there may have been instances when noxious gases evolved and the worker inhaled them. His reports expressed the opinion that chemical related injury to the lung was the only explanation for the worker's symptoms. The explanation of viral related bronchiolitis was rejected as viral bronchilitis was unknown to occur in adults and the worker's history was that he became sick over months to years, which is contrary to how viral infections develop.
At the hearing, the respirologist confirmed his opinion that the worker's condition was caused by work exposure to chemicals. With respect to analysis of the specific chemicals present in the workplace, the respirologist indicated that he viewed the environmental surveys to be of limited value as they measure only the exposure on a particular day and do not take into account repetitive exposures over the long term. For the purposes of his analysis, he would generally only inquire to see whether or not there was an exposure and if so, whether the disease process could be caused by the exposure. That would be sufficient to "connect the dots." He did not really focus on concentrations and went so far as to say that the levels of exposure were "irrelevant." In the present case, he looked only at the fact that the worker was exposed to chlorine based chemicals in a fine mist hundreds of times in a day, and this type of exposure was sufficient to cause lung injury. In his opinion, as there was no alternative explanation, the prolonged workplace exposure definitely caused the worker's disease.
The respirologist was asked to comment on the occupational and environmental specialist's opinion that the absence of damage to the upper airways essentially eliminated chemical exposure as a cause of the smaller airway damage. The respirologist's response was that it depends on the exposure. If the inhalation material is very small and fine (two to three microns), the material does not even stay in the upper airway. It goes right down into the lungs into the small bronchioles. So classically, when people are exposed to such fine particles, just the lungs become involved and there is no upper airway involvement. Chronic prolonged exposure may cause injury, and it is never detected because the upper airway is not involved. Whereas large particles lodge in the airway and cause symptoms right away, the small particles continue to cause damage slowly until about half of the small tubes are damaged, at which time the person starts to feel symptoms.
When asked why there would be no effect on the upper airways by acetic acid and chlorine which are water soluble, and hydrogen peroxide which is unstable in air and must travel on water droplets, the respirologist stated that it would depend on the quantity or concentration. If the irritant was diluted extremely low, the person may not feel any effect. So even though the particle may be lodged in the upper airway, the person may not exhibit any symptoms.
2) The worker also relied on the following medical reports already on file:
· Report dated April 11, 2006 from the treating allergist;
· Opinion of September 19, 2006 from the WCB internal medicine specialist;
· Report dated July 3, 2007 from the worker's family physician;
· Report dated February 12, 2008 from an occupational health physician; and
· Opinion of May 12, 2008 of a senior WCB medical advisor.
The panel was faced with two directly contrary medical opinions on what is essentially a very simple question: Did exposure to chemicals at work cause the worker's condition? There was agreement between all experts as to the diagnosis of bronchiolitis (albeit there was still some disagreement as to terminology). Everyone seemed to agree that the worker's breathing difficulties are based in his small airways. The problem was in determining how it was caused.
The majority notes that the fact that the employer's first expert witness consulted another expert in the field for his opinion only shortly before the initially scheduled hearing date highlights the complexity of the case and the difficulty in reaching a definitive opinion on etiology. Even though the first expert had already submitted a report on the matter, he was still sufficiently curious about the case that he sought out another opinion. The majority was impressed by the qualifications of all the experts involved in this matter and our decision should not be considered a rejection of anyone's expertise. We must, however, choose one opinion over the other, and after much deliberation, the majority is inclined to place more weight on the opinions of the experts relied upon by the employer. In particular, the majority considered the following:
· The expert report of March 8, 2010 contains a detailed consideration of the identified types of chemical exposures and analyzes the measured levels. The specific chemistry and physical properties of the exposures are discussed. This methodical analysis was more convincing to the majority than was the general approach towards causation taken by the treating physicians, particularly given the low measured presence of chemical vapour in the workplace.
· The majority found the explanation regarding the absence of upper airway damage as being indicative of a non-chemical etiology to be compelling.
It therefore follows that the worker's condition was not caused by exposure to chemicals in the workplace. As a result, the majority finds that the worker's claim is not acceptable. The employer's appeal is allowed.
Panel Members
L. Choy, Presiding Officer
A. Finkel, Commissioner
Recording Secretary, B. Kosc
L. Choy - Presiding Officer
Signed at Winnipeg this 20th day of January, 2011
Commissioner's Dissent
Commissioner Walker's dissent:
The Employer's Position
This is an employer appeal and the panel was asked to confirm the employer’s assertion that the workplace exposures were not sufficient to cause the worker's lung condition and therefore deny claim acceptability. The employer introduced an alternate diagnosis they felt was more acceptable in determining the worker's current condition. To support their position, they brought a witness to provide testimony and submitted an occupational health consultant's report.
The Worker's Position
The worker and his union advocate requested the panel support the previous acceptance of the claim. The worker relied on evidence in the file that included medical opinions that the diagnosis resulted from exposure to workplace chemicals. To support their position, they brought the treating respiratory specialist to provide testimony on the worker's medical condition including causes.
Reasons
To decide the appeal, the panel must determine whether the worker's bronchiolitis obliterans was caused by exposure in his workplace. For the reasons that follow, I find that it was.
Analysis
Presence of toxins.
According to the Workplace Hazardous Material Information System (WHMIS) records, a total number of 31 products were used in the worker's area. The worker and the employer had submitted relevant Material Safety Data Sheets (MSDS) of 5 products, plus 2 the panel later requested, used for sterilization of the equipment. According to the MSDS, hazardous components within the products were chlorine, nitrate acid, phosphoric acid, acetic acid and sodium hydroxide. The respiratory system was a target organ of all those products.
Acute health effects when inhaled were noted on all products. Three noted respiratory tract irritation, two noted severe irritation to the respiratory system and two were noted to be corrosive to the respiratory system. One MSDS noted, "May cause respiratory tract irritation, including a burning taste, sneezing, coughing and difficulty breathing." No information was provided on any of the MSDS regarding long term exposure effects.
Evidence of exposure.
Evidence confirmed the majority of the cleaning products were used during changeover of product within a closed system. The various pipes and nozzles would be completely rinsed and once a day flushed and sanitized. Some cleaning was done with a standard garden hose used to rinse away over-spill or leakage during the filling process.
At the worker's fill station, an automatic rinse and sanitization occurred after every container was filled to ensure no contaminants entered the product. After the injector was removed from one sealed container and prior to filling the next container, the injector nozzle area was sprayed with two streams, one on each side, of sanitizer/cleanser. Upon contacting the nozzle, the spray was further atomized resulting in a noticeable mist observed by panel members during their visit.
Occupational hygiene air sampling had been conducted to determine levels of worker exposures for the joint workplace safety and health committee. After corrective measures were implemented a second survey confirmed any reduction of exposure levels. The first survey monitored for the presence of chlorine, sodium hydroxide, inorganic acids (nitric and phosphoric) and acetic acid. Concentrations were recorded as parts per million (ppm) compared to the Threshold Limit Value (TLV) adjusted for the 10 hour shifts at the plant.
Monitoring of the fill station was for chlorine and acetic acid exposure and measurements of ppm were taken. The findings showed an acetic acid concentration of 0.16 ppm compared to an adjusted TLV of 7 ppm or 2% of the TLV and chlorine concentration of 0.045 ppm compared to an adjusted TLV of 0.35 ppm or 13% of the TLV.
The worker's evidence noted cleaning chemicals were used in close proximity to his station when other filling equipment had been used. The equipment was no longer in the plant during the hygiene survey or the panel's visit.
The medical condition.
The worker was diagnosed with bronchiolitis obliterans, which affects the smallest bronchi of the lungs. This diagnosis was confirmed by the worker's treating physician, a respiratory specialist, an occupational health physician, a WCB internal medicine consultant and a senior WCB medical advisor to the Review Office. This diagnosis is not in dispute.
Testimony was provided on the lung's defense mechanisms and the probability that low concentrations of the chemicals were able to enter and penetrate to the smallest bronchi of the lungs. The treating respiratory specialist noted the lung had an escalator process where cilia, in the upper airways that are 5 centimeters wide, bring up larger particles that are coughed out. Those cilia are not present in the bronchioles, less than 2 millimeters wide, but a mechanism of phagocytosis, where white blood cells and macrophages from the blood destroy or remove noxious substances. This smaller airway defense mechanism also adds to the inflammation and causes more scarring.
When asked about minute quantities of contaminants the specialist noted that, "…larger particles they lodge in the upper airway, cause a little bit of inflammation and it usually goes away." He stated that fine particles go way down in the lungs and that's where the damage occurs. When exposure is gradual or progressive and repetitive over a long term, these conditions are rarely taken into account when air quality testing is done for workers' exposures.
When asked for specific exposures regarding the worker, the specialist stated;
"Right, so I think the chemical, the chlorine based chemicals he was exposed to a fine mist, I was told hundreds of times in a day, can cause lung injury and can cause this injury."
He further noted:
"This fine mist comes out and he's repetitively, hundreds of times a day, the mist comes out, the sanitiser (sic) solution, and he will be fairly close to that with no respiratory protection and inhaling tiny small amounts of that material, which would not affect the upper airway but just go down into the small bronchioles. And I think short-term exposure may not be an issue and I mean again a lot of factors need to be plain, how close he was and so on, but prolonged exposure in this case definitely caused the disease." (emphasis added).
The treating respiratory specialist was asked to comment on prior testimony that chemical exposure was eliminated as a cause because there would be presence of damage to the upper airways before it would have filtered down into the bronchioles. He replied that when the material is fine or very small, two or three microns, it doesn’t stay in the upper airway. It just goes right down into the lungs, into the alveoli or small bronchioles.
He further noted that this chronic process of prolonged exposure causes the injury which is not detected earlier because the upper airway is not involved. The problem with the bronchioles is that they are tiny tubes and we have many millions of them, so injury to a few hundred at a time does not produce any symptoms. If people keep getting exposed then you reach a certain point, generally half of those small tubes are injured, then they start to feel symptoms. In the upper airway we only have one tube, so if the injury is to the upper airway the symptoms come much earlier and the patient will stop the exposure.
In early 2008 the occupational health specialist completed a thorough review of the worker's WCB file, his test results, recorded an occupational history, reviewed the occupational hygiene assessments and performed a physical exam of the worker. After ruling out the presence of all other potential causes, his opinion was that it is probable that low dose exposures to respiratory irritants could lead to the development of bronchiolitis. He noted in summary, "I feel the most likely cause of your development of bronchiolitis was your exposure to irritants at work."
The senior WCB medical advisor to the Review Office noted in a memo May 12, 2008 that based on his reading of the information at hand, it is true that the exposure to the sanitizer in question could have caused the worker's respiratory condition. He further noted in the same memo "I do believe the evidence would indicate that low level exposure to respiratory irritants can lead to the development of bronchiolitis."
The senior WCB medical advisor suggested that the occupational health specialist be asked for his opinion on a balance of probability whether the exposure to the sanitizer itself caused the worker's respiratory condition. I note that this question was not posed to the occupational specialist but the treating respiratory specialist did testify to that point, as noted above.
Weighting the evidence.
I have placed significant weight on the conclusions of the treating respiratory specialist, the occupational health physician who is also an internal medicine specialist and had examined the worker, and the senior WCB medical advisor to the Review Office, that the workplace exposures would have caused the condition of bronchiolitis obliterans. The WCB's internal medicine consultant in his initial file reviews had also supported this causation.
The WCB internal medicine consultant had based a later opinion, which changed significantly from his four previous opinions, on the evidence that the worker had "…sought treatment in April 2005 for some form of viral infection." He further noted that while viral infections aren't common in adults, it was possible the worker's symptoms were being caused by viral infection. I place less weight on the latter opinion as I found a greater probability that exposure to one of the chemicals would have produced the same symptoms.
To arrive at this conclusion I note the earlier noted caption from one of the sanitizing products, "May cause respiratory tract irritation, including a burning taste, sneezing, coughing and difficulty breathing." Also, information readily available regarding the potential symptoms of chlorine exposures noted the following, rhinorrhea (a thin watery discharge from the nose), coughing, nausea, vomiting, headache and dizziness. All of these symptoms could also be present with viral infections, yet were not considered.
Further, testimony by the treating respiratory specialist, when asked about possible symptom mimicry, stated, "So we see it all the time for all conditions, so asthma, for years sometimes called colds or lung disease, colds, but it's not colds. When eventually it's not going away, you do further testing….that's what I think was happening. In this case it was called colds..." This testimony adds strength to the conclusion that the probability of the worker developing his bronchiolitis obliterans from a viral infection is very low compared to the greater probability of workplace exposures.
The WCB internal medicine consultant's fifth opinion in the file was later refuted by the senior medical advisor in his response to the Review Office when he noted "...the medical evidence at this time does not indicate, in my opinion, that the worker's condition was probably related to a viral infection."
Conclusion.
Based on evidence on file I am able to conclude that materials, toxic to the worker's lung, were present in his workplace. I am also able to conclude that a chronic exposure history of low level dosage of those toxins had occurred. I find that medical opinion on file and in testimony strongly supports that the diagnosis of bronchiolitis obliterans is directly related to the workplace exposures.
I therefore find, on a balance of probabilities, that the worker's bronchiolitis obliterans arose out of and in the course of the his employment therefore, the claim is acceptable. I would therefore dismiss the employer’s appeal.
P. Walker
Commissioner
Signed at Winnipeg, this 20th day of January, 2011.