Workplace Health & Medicine Blog

May 2014

by Dr. Noel Kerin - May 25, 2014

Over the past 25 years there have been widespread improvements to both the design and delivery of Employee and Family Assistance Programs (EFAP). There does however, remain, significant concern among occupational medical personnel as to the measured effectiveness of these programs in helping to identify and manage, in particular, mental health issues.

Scenario One

  • A 32-year-old woman, struggling with work-life balance, trying to maintain a household with two young children, a demanding job, and a husband who travels with his job.

  • Final diagnosis in this case was uni-polar depression, for which she did not receive appropriate therapy for approximately 13 weeks. By the time she received therapy she had been disciplined at work for absenteeism and poor quality of work produced while at work.

  • Appropriate management in her case would have been delivery of a recognized diagnostic questionnaire for depression at an intake clinic, to be followed by prompt referral to a treating professional with the capability of prescribing anti-depressants as indicated.

  • Financial cost to the company – 14 lost days and probably twice as many when her performance at work was poor (presenteeism).

Scenario Two

  • A 33-year-old male, accounts manager, received a written warning from management as to his work performance and chronic lateness

  • Intake clinic did not administer a substance abuse questionnaire

  • Two months after first contact with EFAP this employee was found to have uni-polar depression with a co-morbid condition (alcohol dependency)

  • Proper treatment consisted of 28-day in-patient program to address his alcohol dependency issues and an anti-depressant with cognitive behavioural therapy to address his depression issues

  • Cost to company – approximately 38 working days

  • Cost to individual – near loss of employment and lost promotional opportunities

Both of the above cases are from my files and illustrate the serious nature of these illnesses and the impact on both employee and employer when critical mental health and addiction issues are not addressed promptly.

By being able to administer a bonded, confidential clinical audit system, one could hold the EFAP provider to a standard of enquiry and disposition of cases, which would be appropriate and in the best interest of the employee and the company. Performance incentives could be written into contracts so that, should the EFAP provider meet the agreed-upon standard in 95% of cases, a bonus would be paid. Likewise, if the EFAP provider did not meet the standard in 95% of cases, then a financial penalty would be applied against the EFAP carrier, along with a review of their contract.

As we can see, both in attendance management and disability management, the EFAP Program is central and essential to the useful and smooth functioning of modern workplace employee support programs.

EFAP providers, to date, have been reluctant to allow their confidential medical files to be reviewed. However, I would counter that hospital patient medical files (which include as much confidential personal information as one would find in an EFAP file), are regularly audited by independent, external, bonded, confidential reviewer(s); therefore, there is clear precedent to have auditing measures applied against any clinical program. I believe it is past time that this take place with EFAP programs in general.

by Dr. Noel Kerin - May 23, 2014

Occupational asthma (OA) is a serious and sometimes fatal illness; it is a growing problem in many Canadian workplaces. A very wide range of chemicals, and agents of biological origin, has been described as causes of OA. The costs to the worker and the employer are significant but preventable. Advances in effective management of asthma bring new hope to the employer when attempting to handle this chronic disease effects on their workers and the workplace. About 10% (5-15%) of asthma cases are occupationally caused. The proportion of asthma cases attributable to workplace factors may be as great as 28% (US National Institute for Occupational Health and Safety, 1996).

Half of all asthma cases are said to be not controlled properly.

What is Occupational Asthma?
Occupational asthma is a breathing (respiratory) disease caused by exposure to a trigger in the workplace. It is a chronic (long-term, ongoing) inflammation of the breathing passages (bronchi) of the lungs and often also involves the nasal passages. The inflammation irritates the airway, causing breathing problems.

• Most people with asthma have sudden attacks or periods of bothersome or severe symptoms separated by periods of mild symptoms or no symptoms at all.
• Asthma is an inflammatory reaction that is triggered by external factors or specific situations.
• When a person with asthma is exposed to one of his or her triggers, the inflammation worsens and symptoms ensue.

Occupational Asthma Facts
OA has become the most prevalent occupational lung disease in developed countries. Asthma, both occupational and non-occupational kills approximately 500 people in Canada each year (Health Canada) and according to the Workers Safety and Insurance Board of Ontario (WSIB) OA causes approximately two cases of lost time claims per working day in Ontario (400 per year). These are likely but the tip of the iceberg of actual OA cases.

OA is a common disorder that may be caused by several hundred agents (250+ and counting). The key to diagnosis is a high index of suspicion for the condition. Several readily available tests can be used to confirm the diagnosis. Many patients suffer from continued asthma despite cessation of exposure; early diagnosis and early removal from exposure are the most important factors for improving the long-term outcome.

OA can be either induced (caused by agents in the workplace or aggravated by agents in the workplace). Level of exposure is an important risk factor, and reduction of exposure is the only certain method of prevention. Atopy (hay fever, allergies) and smoking are further risk factors.

Asthma, whether it be caused by the workplace or not, is the same condition and causes a group of symptoms, which range from stuffy nose and cough to full-blown, life-threatening shortness of breath. Some people are ‘born with asthma’, and this is described as a genetic tendency to asthma. Studies now show that people born with asthma or who developed asthma in childhood, are more likely to develop allergic type asthmatic symptoms when exposed to asthmogenic agents in the workplace.

How is Occupationally-Induced Asthma caused?
Researchers have shown that a specific type of white cell (T-lymphocyte) becomes sensitized to a foreign agent, so that when this agent is again introduced to the person, a reaction occurs in the nasal passages and bronchial tree, which we understand to be asthma. This hyper-sensitivity reaction is, at present, a chronic disease with no cure. There are, however, very successful management systems for this condition.

Agents that cause asthma in the workplace do so in one of two ways:

1. Direct irritation of the respiratory tract tissues which is called reactive airways dysfunction syndrome (RADS) or irritant asthma, e.g. Chlorine gas, from mixing janitorial agents incorrectly or releases in the pulp and paper industry; and
2. Through an allergic pathway. This is the commonest type of occupationally-induced asthma. The asthma agents vary from very small molecules (Isocyanates), to very large molecules (red western cedar dust), as well as all sorts of various chemical agents in between. More recently researchers, including Dr. Susan Tarlo and her group in Toronto, recognized that some of the smaller molecules, such as Isocyanates, may actually sensitize a worker through the skin. This could explain why some workers develop an asthma response when coming in contact with chemicals while wearing appropriate respiratory protection.

Economic Burden of Occupational Asthma
The economic cost of asthma is very significant. Because it can be a life-threatening illness, parents become extremely concerned when a child has an asthmatic attack. This affects the workplace as both a problem with presenteeism (at work but not producing the usual amount and/or quality of work) and unavoidable parental absenteeism. When a child is admitted to hospital the average length of stay is five days, removing the child from school for at least one week at a time. This can have long-lasting effects as children who have chronic illnesses are known to perform less-well academically than those who are not afflicted with a chronic illness, such as asthma.

The cost of OA, likewise, has very serious implications. Firstly, for the life and health of the worker; as OA too, can be fatal. When a worker cannot breathe freely, their productivity suffers and, from various studies we know that approximately half of all asthmatics are poorly controlled. This, in turn, creates a significant presenteeism effect. When the disease becomes more difficult to manage, the employee loses time from work, creating further economic loss for both employee and employer. A quick calculation for the cost of absenteeism is: base pay x 2-5 times x days lost due to lost production/replacement costs. Presenteeism is not easily measured but in the USA it is commonly assigned a value of 2 times absenteeism!

How does an Employer Suspect an Employee is Suffering from Occupational Asthma?
A high index of suspicion is required to monitor for the development of OA in a worker. In the employee, frequent bouts of sneezing, stuffy nose, coughing, wheezing or shortness of breath when exposed to the workplace may be symptoms of an asthma problem developing. Conversely, workers may in fact develop early morning (e.g. 3-4 am) symptoms of asthma, making the connection between an asthma agent exposure in the workplace and the asthma condition difficult to connect. In other workers there may be a definite week-to-weekend variation in symptoms, so that a person may feel completely free of symptoms of nasal stuffiness, wheezing and coughing towards the end of a weekend and, in particular, a long weekend, than they do after being exposed day-by-day during the working week. Approximately half of all OA cases present first as an allergic rhinitis or hay-fever (recurrent sinus infection, nasal stuffiness and sneezing).

Finally, some workers will explain how they can reduce or withdraw all asthmatic medications when on an extended leave from the workplace, such as annual vacations.

All of these presentations of asthma in the workplace require careful consideration, vis-à-vis placement of the worker and various accommodation requirements under law. When faced with these difficult decisions, employers are well advised to seek counsel from an occupational health practitioner familiar with their work-type practices and the management of OA. In spite of the enormous amount of research that has gone into understanding asthma, including OA, much remains to be learned.

Specific Causes of Occupational Asthma
No job is immune from OA. We cannot mention all the causes here but we can highlight some of the commonest. In Ontario Isocyanate exposure from the automotive parts manufacturing and painting industries are the most common cause. In British Columbia western red cedar dust is a major problem, while the East Coast struggles with ‘crab asthma’ from working with crabs and other similar fish. Baker’s asthma is a problem wherever there is exposure to flour dust. Welders’ smoke and metal cutting fluids, colophony fume, from soldering especially in the electronics industry, cause frequent cases of the illness. Laboratory workers who handle animals and health care workers who use latex gloves are at risk of developing allergic asthma.

Indoor air quality is a growing issue when dealing with OA. Indoor air quality is influenced by poor air exchanges/unit of time (stale air), house mite droppings and other dust; by off-gassing of volatile organic chemicals (VOCs) from carpets, furniture, fragrances, perfumes and mould growth. Mould is a form of fungal growth that gives off a ‘perfume’ or toxin (mycotxin) when growing. Some toxins are known to cause allergic reactions in humans including asthma, e.g. Stachybotrys Chartarum, Penicillium Marneffei and Aspergillus Fumigatus. Mould needs three conditions to grow: moisture, warmth and food, e.g. cellulose such as found in ceiling tiles, paper and wood. Workplace floods, roof leaks, toilets and damp basements are typical breeding grounds for this type of mould problem.

How Can Employers Manage Asthma in the Workplace?
There have been several excellent management models developed by the Asthma Society of Canada, which show a very sound return on investment by an employer, of between three and seven times the invested dollar. In manufacturing, every effort at engineering out asthmogenic agents from the workplace has been shown to be beneficial. Where not possible, then strict engineering and administrative controls have been shown to effectively reduce the attack rate of asthma in the workforce.

In manufacturing plants where chemicals, such as chlorine and sulphur oxide products are used or manufactured, careful attention should be given to personal protective equipment (PPE) so that sudden high-dose exposure to these chemicals does not occur.

Today’s work environment is a challenge to both the worker and employer. We have new chemicals coming on stream that have not been tested for human safety. What about nanoparticles’ lung effects and how they carry other chemicals? What about combined effects of low dose chemical exposures which individually register under legislative chemical exposure guidelines in the workplace? What about the long term lung effects of OA. At this time, OA has been studied for about 30 years. It may take longer yet to see an evolving pattern of permanent lung damage.

Occupational Asthma Management
The most effective means of control is to prevent exposure altogether, either by not doing the task in question or by substituting the sensitizer agent for a less harmful material, although this is not always feasible. For example if a di-isocyanate based paint or varnish is being used, one should question whether a much less hazardous paint which simply dries out without curing can be applied instead.

Early removal from exposure increases the likelihood of recovery.
Continuous exposure in affected workers is associated with worsening of asthma.

Unfortunately, well-established asthma in many patients progresses in the absence of known further exposure, or perhaps does so because of increased sensitivity (reactivity) to undetected low-level exposure to the causative agent. Low level exposures at the workplace still may not allow affected employees to return to work because people with occupational asthma tend to react to extremely low concentrations of an agent.

The duration of symptoms before removal from exposure is a prognostic indicator irrespective of the agent.

Pulmonary function testing is a cornerstone in diagnosing occupational asthma. In cases where there is early or poorly defined symptoms a Methacholine ChallangeTest may help better define, if in fact, a workers’ lungs have become sensitized to a chemical. At this time there is no reliable blood test for OA. For the worker who in being investigated for OA or who is being reintroduced (accommodated) into the workplace, serial peak flow meter reading can help in emonstrating success or recurrence of the asthmatic condition.

As a large number of asthma suffers, including occupational asthma, achieve, at best, fair control of their condition, education is now considered to be an essential component of a successful management program. Also, newer understanding of the underlying mechanisms of causation and more effective medications has brightened the outlook for those who are unfortunate enough to have contracted asthma.

by Dr. Noel Kerin - May 23, 2014

Asbestos was recognized for centuries before scientists and industrialists saw it as the dream answer to acid and heat resistance. Asbestos did not conduct electricity and was resistant to the massive heating/cooling cycles that were the basis of the industrial revolution. No wonder the great industrial corporations of the late-19th and 20th centuries embraced asbestos with such fervor.

It was not until the early 1960s that the first warnings of a wolf in sheep’s clothing appeared in medical literature, with Wagner describing several cases of a rare lung cancer (mesothelioma) in asbestos miners in South Africa. Other researchers of that time also claimed evidence of asbestos’ capability to cause cancer and other illnesses – primarily of the respiratory tract.

Predictably, these early findings triggered fierce debate between two camps: the asbestos industry defending itself, and the scientific community drawing attention to the now-obvious damaging health effects of asbestos. Sadly, the debate lasted decades, and the issues were often muddied or misdirected by inadequate knowledge.

For example, as recently as 2000, in our own city of Toronto, a prominent occupational medical physician could write in full belief that “…the train carrying asbestos diseases has arrived at the train station and the burden of asbestos diseases has been unloaded, and now the train has left the station.” This seemingly authoritative statement has since been proven horribly wrong.

Most of the burden of correcting this type of opinion has fallen to the trade union movement in Canada – as it did in the United States, when the great Selikoff was employed to review worker asbestos damages in New York City. Here in Ontario, the CAW has led the fight, forcing the Workplace Safety and Insurance Board (WSIB) of Ontario to accept the huge health damage brought about by the now-defunct Holmes Foundry in Sarnia, where literally hundreds of ex-workers have developed asbestos-related diseases from mesothelioma to lung cancers, bowel cancers and lung fibrosis (asbestosis).

More recently, CAW has tackled the asbestos problem in another huge manufacturing company in Ontario, where hundreds of asbestos-related cancers and respiratory diseases have been discovered.

In both communities, the cause of the various cancers often went unrecognized or unreported. We know that mesothelioma is caused almost exclusively by asbestos exposure, yet in the majority of these cases we found that no compensation claim had been launched on the workers’ behalf.

To grasp the extent of the lack of reporting, and the lack of acceptance of occupationally induced lung cancers, we need only look at the total claims accepted by Workplace Safety and Insurance Board of Ontario in the years 2002/2003. Seven. Seven lung cancers for the Province of Ontario. Contrast that total with today’s reality, where one occupational medical physician alone has seven times that total number of asbestos-related lung cancers currently launched before WSIB.

Does this mean there are seven times the 2002/3 number of (either declared or accepted) lung cancers than had been previously accepted? Yes. At least that many. I’m convinced the estimated numbers will prove hopelessly conservative.

Four decades after the first warnings, we’re only now lifting the veil from a great tragedy. All the mounting knowledge indicates that asbestos exposure’s full impact on cancers and other occupational diseases will be massive. This unhappy prognosis is not helped by the reality that belated acceptance of the medical evidence has left no overall plan in place to deal with this huge, unfunded liability in our province.

Occupational diseases are the price society pays for industry’s past willingness to accept health risks as a justifiable cost of doing business. More correctly stated, it is the price that workers are paying. And now – like the old Ontario Hydro stranded debit – it falls to the public of Ontario in the 21st century to pick up the cost of the past’s excessive ways. How did it come to this?

The old adage “Out of sight, out of mind” is nowhere more relevant than in the field of occupational diseases. With a latency period of up to 50 years between exposure to workplace hazards and expression of a disease such as asbestosis (scarring of the lungs or lung cancer), industry could view the risks as a problem for a distant tomorrow.

But tomorrow always comes. As the earlier “train station” quote indicates, asbestos-related diseases were considered to be issues of the 20th century. However, in examining the asbestos exposure file of one regional town, we found ten times the national average rate of occurrence for mesothelioma – with most cases identified in the 21st century! There is now broad consensus in the field of epidemiology that the appearance of diseases resulting from old exposures to asbestos will not peak until 2015 to 2020 at the earliest.

What does this all mean? If we think of it as a crime story, it means we’ve caught and convicted the perpetrator – but we’re still actively gathering evidence to learn the true scope of its legacy. It means that new knowledge imposes on us the need for new vigilance and new thinking.

For example, lung cancer. We can no longer make the automatic assumptive link between lung cancers and cigarette smoking. Other known primary cancer exposures must now be taken into account – and particularly the huge lung-cancer impact of asbestos.

Evidence of the emerging shift in thinking can be found in the new “asbestos” guidelines developed by the American Thoracic Society ATS document (in PDF format), the leading international experts on respiratory disease. Published in 2004, the guidelines were developed over several years, under the chairmanship of Prof. Tee Goidotti. They set out new criteria for addressing diagnoses and assessing the damages brought about by asbestos exposures (functional impairment).

We have posted our KOHC synopsis of this very-detailed publication on our site. We have also posted a quick asbestos decision-making algorithm for the health-care practitioner who is faced with a potentially asbestos-exposed worker.

So far, we have not discussed any other systems damaged by asbestos, but it is now clear that many of the so-called cigarette smoking laryngeal (throat) cancers are, in fact, partially or totally caused by asbestos-fiber damage. Similarly, stomach and colon cancer are, in some cases, caused by old asbestos-fiber exposure.

However, when a surgeon looks at a pre-malignant or malignant polyp in a patient’s colon, there is no reliable indicator to determine if pre-cancer or cancerous changes were caused by asbestos. As we know, with most cancers the causes are multi-factorial. Diet has something to do with the appearance of bowel cancer, as have genetics and, unfortunately, asbestos. There is strong epidemiological evidence supporting the notion that these cancers appear more frequently in asbestos-exposed than non-exposed workers.

Finally, when we felt we knew all about asbestos, and the ten-year exposure to asbestos was the standard for accepting asbestos-related diseases, research by Erlich out of the United Kingdom crumpled our comfort zone – with a clear statement that one month of heavy asbestos fibre-dust exposure is sufficient to induce asbestos-caused pulmonary fibrosis (asbestosis) in 20% of cases.

I’ll end with this thought. For well over a century, asbestos exposure has been a deadly, silent killer. The toll across the generations can only have been horrific. The evidence is indisputable. To ignore it is unconscionable.

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