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.

We have been most fortunate in being able to attract world leaders in the field of asbestosis, mesothelioma and silicosis. These premier experts include Dr.Tee Guidotti, Dr. Michele Carbone, and Dr.
David Goldsmith. Many conferences would count it a success to have but one of these visionary scientists speaking at their conference. In Sudbury we have the distinct honour of having these three experts join
together with us in this task. The May 10th conference will employ the most advanced knowledge transfer methods as the meeting will
be held at the eDome centre at Cambrian College in Sudbury. The plan is to reach out to the widest possible audience including, but not limited to, clinical medical experts, family physicians, and other health care providers who treat these patients. The Occupational Health Clinic has partnered with unions and community business partners in this initiative. We have also taken this opportunity to increase awareness of these diseases in our medical and nursing schools in the North.

Together we can make a difference. In the not too distant future, we hope to be able to say that this group who met in Sudbury on May 10th, 2007 helped change how we understand these occupational lung diseases for future generations.

In the Sudbury Area: eDome @ Cambrian College, 1400 Barrydowne Road, Sudbury, Ontario,

Canada Parking: Available at Cambrian College at the cost of $4/day Cost: $100, which includes lunch Outside of Sudbury: With the aid of the eDome, now anyone can access this international event regardless of geographic location. All that is required is a high speed internet connection, sound, and Quicktime player, which can be downloaded free. Using this method, people will be able to join in on the event without having to leave their office. Attendees using this method will be able to ask questions through the internet to any of the presenters.

The day before the event, the website address and login password will be sent to all participants not located in Sudbury as well as the handouts for the presentations.

Cost: $50
- Media

Applicaton #: 20050266098 Class: 424682000 (USPTO)

[0001] This application claims the benefit of U.S. Provisional Application No. 60/575,397, filed Jun. 1, 2004.

FIELD OF THE INVENTION

[0002] This invention relates to a composition comprising a non-toxic calcium compound and a carrier for the treatment of a hydrofluoric acid burn. In a preferred embodiment, the invention relates to a calcium levulinate composition for treatment of a hydrofluoric acid burn.

[0003] It is well known that strong acids, especially concentrated inorganic acids, can attack skin [1]. In general, acid contact with skin results in localized irritation, but an appreciable number of acids, such as hydrofluoric acid, are absorbed through the skin and can produce systemic poisoning.

[0004] Hydrofluoric acid is an inorganic acid which may cause skin/tissue/flesh damage via two mechanisms: (1) corrosive burns due to free hydrogen ions, and (2) chemical burns from tissue penetration by fluoride ions. In the latter case, the main portals of entry for hydrofluoric acid through the skin are hair follicles, sebaceous glands, sweat glands and cuts or abrasions of the outer layers of the skin. There are numerous blood vessels immediately below the skin, which facilitate the absorption of chemicals for transport throughout the entire body.

[0005] The most deleterious injuries arise when fluoride ions from the hydrofluoric acid bind with calcium ions in human cellular materials. This scavenging of calcium ions may lead to the condition described as hypocalcaemia and/or cellular necrosis and death. This process, if untreated, can continue for several days, causing increased tissue damage. Even after thorough washing of the exposed skin with large amounts of water, the hydrofluoric acid molecules under the skin may continue to enter into other parts of the body and cause tissue destruction. Hydrofluoric acid possesses an unusual penetrating ability that requires immediate and proper treatment to prevent further damage.

[0006] In addition to washing with water, the most effective way to prevent or slow down the effects of hydrofluoric acid penetration into the tissue is to neutralize the fluoride ions as quickly as possible to prevent further reaction of the fluoride ions with tissue in/on or under the exposed area. This can be done either by complexation of the fluoride ions or by delivering a high concentration of active ions, such as Ca.sup.2+, which react with fluoride ions to form CaF.sub.2 which can then be removed from the damaged area.

[0007] Currently, the most widely used treatment of hydrofluoric acid injuries comprises a benzalkonium chloride such as [C.sub.6H.sub.5CH.sub.2N(CH.sub.3).sub.2R].sup.+Cl.sup.- where R represents a mixture of alkyls from C.sub.8H.sub.17 to C.sub.18H.sub.37) and solutions of calcium gluconate, which are applied either as a topical application or as an injection [2-10].

[0008] The major problem associated with the use of the quaternary ammonium compounds, Hyamine.RTM. and Zephiran.RTM., is their toxicity. For example, it is estimated that 1-3 g of Hyamine could be fatal [3]. This dosage is equivalent to that supplied in 50-150 mL of a 2 wt % solution. Other disadvantages of quaternary ammonium compounds are:

[0009] (i) the solutions are applied at ice-water temperature often causing patients to experience discomfort;

[0010] (ii) it is a time-consuming procedure to change compresses every few minutes for the several hours recommended; and

[0011] (iii) compresses often cause painful reaction when applied on a patient's head, neck or near the mucous membranes.

[0012] Toxicology and carcinogenesis studies of Hyamine.RTM. were conducted on rats and mice by the National Cancer Institute [11]. The research indicated that exposure of rats and mice to Hyamine.RTM. led to lesions (16 days) and ulcers (13 weeks) at the site of application.

[0013] The major disadvantages associated with the calcium gluconate treatment are:

[0014] (i) calcium gluconate is not very soluble in water (0.4 g/100 mL at 20.degree. C.) and forms unstable suspensions in the absence of an organic stabilizer and aqueous hydrochloric acid;

[0015] (ii) when applied topically, calcium gluconate solutions are often irritating especially when used for the treatment of eyes [2];

[0016] (iii) calcium gluconate injections for deep penetrating burns;

[0017] (iv) injections are often painful and there is the possibility of infection or tissue necrosis especially when used on digits [2, 3, 6-10]; and

[0018] (v) in some cases, injections are ineffective [4].

[0019] Calcium gluconate 10% (wt/wt) in dimethyl sulphoxide (DMSO) has also been used for treatment of hydrofluoric acid burns on laboratory rats [12, 13]. The efficacy of these treatments may have been limited by the low solubility of calcium gluconate.

[0020] Calcium acetate soaks were also tested as a source of calcium ions for treatment of hydrofluoric acid injury [4]. Their major disadvantage is a negative epidermal response that results from the treatment.

[0021] Additional compositions for the treatment of hydrofluoric acid burns are described in the French patent No. FR2604900 issued 15 Apr. 1988 to M. C. Blomet and entitled "Physiological Solution for Washing Parts of the Human Body Which Have Come into Contact with Hydrofluoric Acid and Concentrate for Preparing It" [14]. The active ingredients disclosed therein are ethylenediaminetetraacetate tetrasodium salt and aluminum nitrate combined in various ratios. The major disadvantage of application of these compositions arises from the fact that ethylenediaminetetraacetate tetrasodium salt is a cancer suspect and an irritant [15]. A further disadvantage of using these mixtures is that they can only be applied for decontamination (washing) of hydrofluoric acid and are not suitable for the treatment of delayed or deeper burns.

[0022] The composition called Hexafluorine.RTM., produced by laboratoire PREVOR in France, is described as an effective treatment for immediate decontamination (washing) of HF exposed eye/skin [16]. The major disadvantage of using Hexafluorine.RTM. arises from the fact that it is not suitable for the treatment of delayed or deeper burns.

SUMMARY OF THE INVENTION

[0023] The present invention provides a composition for the treatment of a hydrofluoric acid burn. The composition comprises a non-toxic calcium compound, for example a non-toxic organic calcium compound such as calcium levulinate, and a carrier, for example water, an aqueous dimethyl sulphoxide solution, or an aqueous urea solution, which is applied to an affected area. The composition provides for the delivery of calcium ions to the affected area to neutralize fluoride ions and prevent further damage to the affected area. The composition also provides for trapping of free hydrogen ions thus preventing further corrosive damage to the affected area. Consequently, the compositions described herein may be used in the treatment of corrosive burns not only from hydrofluoric acid, but also from other inorganic acids.

[0024] The composition has particular importance in the treatment of superficial and/or delayed or deeper hydrofluoric acid burns through the rapid delivery of calcium ions to the affected area.

[0025] According to one aspect of the present invention, there is provided a composition for the treatment of a hydrofluoric acid burn, comprising a non-toxic calcium compound having an aqueous solubility of at least 10 g/100 mL at room temperature and a carrier.

[0026] According to a further aspect of the present invention, the non-toxic calcium compound is an organic calcium compound. An organic calcium compound is a calcium compound having a counterion comprising carbon-hydrogen bonds.

[0027] According to another aspect of the present invention, there is provided a composition for the treatment of a hydrofluoric acid burn comprising calcium levulinate and a carrier.

[0028] According to yet another aspect of the present invention, there is provided a method of treating a hydrofluoric acid burn comprising administering a therapeutically effective amount of a composition as defined herein to a patient or subject in need thereof.

[0029] According to still another aspect of the present invention, there is provided a method of treating a hydrofluoric acid burn comprising administering a therapeutically effective amount of calcium levulinate to a patient or subject in need thereof.

[0030] According to a further aspect of the present invention, there is provided a use of a composition, as defined herein, for the treatment of a hydrofluoric acid burn.

[0031] According to another aspect of the present invention, there is provided a use of a composition, as defined herein, for the manufacture of a medicament for the treatment of a hydrofluoric acid burn.

[0032] According to yet another aspect of the present invention, there is provided a use of calcium levulinate for the treatment of a hydrofluoric acid burn.

[0033] According to still another aspect of the present invention, there is provided a use of calcium levulinate for the manufacture of a medicament for the treatment of a hydrofluoric acid burn.

[0034] According to a further another aspect of the present invention, there is provided a commercial package comprising a composition, as defined herein, together with instructions for its use in treating a hydrofluoric acid burn.

[0035] According to another aspect of the present invention, there is provided a commercial package comprising calcium levulinate together with instructions for its use in treating a hydrofluoric acid burn.

DETAILED DESCRIPTION OF THE INVENTION

[0036] There is provided a use of a non-toxic calcium compound for the treatment of a hydrofluoric acid burn. The term "non-toxic" refers to a calcium compound in which any toxic or detrimental effects of the calcium compound are outweighed by the therapeutically beneficial effects. Preferably, the non-toxic calcium compound has an aqueous solubility of at least 10 g/100 mL at room temperature, more preferably an aqueous solubility of at least 20 g/100 mL at room temperature, and most preferably an aqueous solubility of at least 30 g/100 mL at room temperature. The non-toxic calcium compound may be an organic calcium compound. An example of a non-toxic organic calcium compound is calcium levulinate.

[0037] The non-toxic calcium compound may be used together with a carrier in a composition for the treatment of a hydrofluoric acid burn. The composition comprises the non-toxic calcium compound preferably at a concentration of 10 to 40 wt %, more preferably at a concentration of 15 to 35 wt %, and most preferably at a concentration of 20 to 30 wt %.

[0038] The carrier is also non-toxic in that any toxic or detrimental effects of the carrier are outweighed by the therapeutically beneficial effects. The carrier also has the property of skin permeability, which permits the non-toxic calcium compound to penetrate the skin barrier.

[0039] The carrier may be water, an aqueous dimethyl sulfoxide solution, or an aqueous urea solution. Preferably, the aqueous dimethyl sulfoxide solution is at a concentration of 10 to 45 wt %, more preferably at a concentration of 15 to 40 wt %, and most preferably at a concentration of 20 to 35 wt %. Preferably, the aqueous urea solution is at a concentration of 5 to 25 wt % and more preferably at a concentration of 10 to 20 wt %.

[0040] A person skilled in the art would recognize that the carrier may also be selected from polyethylene glycol monolaurate, eucalyptol, a halogenated compound selected from trichloroethanol and trifluoroethanol, a lanoline derivative, a 1-substituted azacycloalkan-2-one, a urethane compound, polyvinyl-pyrrolidone, a binary composition of N-(2-hydroxyethyl)-pyrrolidone and methyl laureate or oleic acid or oleyl alcohol, and a pyrrolidone-type compound.

[0041] In various embodiments, a non-toxic calcium compound, e.g. a non-toxic organic calcium compound such as calcium levulinate may be used therapeutically in formulations or medicaments to treat a hydrofluoric acid burn. The invention provides corresponding methods of medical treatment, in which a therapeutic dose of a non-toxic calcium compound is administered in a pharmacologically acceptable formulation, e.g. to a patient or subject in need thereof. Accordingly, the invention also provides therapeutic compositions comprising a non-toxic calcium compound, e.g. a non-toxic organic calcium compound such as calcium levulinate, and a pharmacologically acceptable excipient or carrier. In one embodiment, such compositions include a non-toxic calcium compound in a therapeutically effective amount sufficient to treat a hydrofluoric acid burn.

[0042] A "therapeutically effective amount" refers to an amount effective, at dosages and for periods of time necessary, to achieve the desired therapeutic result, such as a reduction of tissue damage. A therapeutically effective amount of a non-toxic calcium compound may vary according to factors such as the disease state, age, sex, and weight of the individual, and the ability of the compound to elicit a desired response in the individual. Dosage regimens may be adjusted to provide the optimum therapeutic response. A therapeutically effective amount is also one in which any toxic or detrimental effects of the compound are outweighed by the therapeutically beneficial effects.

[0043] Therapeutic compositions typically must be sterile and stable under the conditions of manufacture and storage. The composition can be formulated as a solution. In many cases, it will be preferable to include isotonic agents, for example, sugars, polyalcohols such as mannitol, sorbitol, or sodium chloride in the composition. Prolonged absorption of the compositions can be brought about by including in the composition an agent which delays absorption, for example, monostearate salts and gelatin. Moreover, a non-toxic calcium compound can be administered in a time release formulation, for example in a composition which includes a slow release polymer. The active compounds can be prepared with carriers that will protect the compound against rapid release, such as a controlled release formulation, including implants and microencapsulated delivery systems. Biodegradable, biocompatible polymers can be used, such as ethylene vinyl acetate, polyanhydrides, polyglycolic acid, collagen, polyorthoesters, polylactic acid and polylactic, polyglycolic copolymers (PLG). Many methods for the preparation of such formulations are patented or generally known to those skilled in the art.

[0044] Sterile solutions can be prepared by incorporating the active compound (e.g. a non-toxic calcium compound) in the required amount in an appropriate solvent with one or a combination of ingredients enumerated above, as required, followed by filtered sterilization. In the case of sterile powders for the preparation of sterile solutions, the preferred methods of preparation are vacuum drying and freeze-drying which yields a powder of the active ingredient plus any additional desired ingredient from a previously sterile-filtered solution thereof. In accordance with an alternative aspect of the invention, a non-toxic calcium compound may be formulated with one or more additional compounds that enhance the solubility of the non-toxic calcium compound.

[0045] A non-toxic calcium compound, for example a non-toxic organic calcium compound such as calcium levulinate may be provided in containers or commercial packages which further comprise instructions for use of the non-toxic calcium compound for the treatment of a hydrofluoric acid burn. Further, a composition comprising a non-toxic calcium compound, for example a non-toxic organic calcium compound such as calcium levulinate and a carrier may be provided in containers or commercial packages which further comprise instructions for use of the composition for the treatment of a hydrofluoric acid burn.

[0046] In a preferred embodiment, the composition contains calcium levulinate and a carrier for the rapid delivery of calcium ions to fluoride-exposed tissue. Interpretation of the studies described below suggest that calcium ions reacted with fluoride ions to form non-toxic calcium fluoride, as in equation [a]:

(CH.sub.3COCH.sub.2CH.sub.2COO).sub.2Ca+2HF.fwdarw.CH.sub.3COCH.sub.2CH.su- b.2COOH+CaF.sub.2 [a]

[0047] The calcium fluoride product was identified by X-ray diffraction (XRD) analyses. In the experiments carried out, the calcium fluoride was precipitated as fine particles (particle size<0.2 .mu.m).

[0048] The other product of the reactions was levulinic acid, which was identified by Raman spectroscopy. Levulinic acid, a weak non-toxic acid (for 98% aqueous solution pH is 6.2 at 18.degree. C.), is found in many fruits and vegetables and is widely used as an additive in the food industry. Levulinic acid has a low dissociation constant (pK.sub.a=4.64 at 18.degree. C. [17]) and binds hydronium ions, H.sub.3O.sup.+, according to the equation [b]:

CH.sub.3COCH.sub.2CH.sub.2COOH+H.sub.2OCH.sub.3COCH.sub.2CH.sub.2COO.sup.-- +H.sub.3O.sup.+[b]

[0049] Surprisingly, Applicants have determined that a composition containing a non-toxic calcium compound having an aqueous solubility of at least 10 g/100 mL, for example a non-toxic organic calcium compound such as calcium levulinate, can be applied to an affected area and effectively remove fluoride ions to prevent further reaction of fluoride ion with skin tissue in or on the affected area. The non-toxic calcium compound, such as the calcium levulinate contained in the compositions described in the examples, binds both F.sup.- and H.sub.3O+, apparently as described previously in equations [a]and [b].

[0050] It is desirable to select a calcium compound that is non-toxic and causes less irritation to the skin than other calcium compounds [18]. Further, the non-toxic calcium compound should be soluble in aqueous solution, and preferably in aqueous solution with a carrier such as DMSO or urea. For example, calcium levulinate has been found to exhibit favourable solubility in water and in aqueous solution with a carrier such as DMSO or urea. The examples described below illustrate that calcium levulinate is more soluble, in different aqueous solvent systems at several temperatures, than the calcium gluconate used in existing commercial compositions. Therefore, a composition comprising calcium levulinate may deliver a potentially higher concentration of fluoride sequestering agent to the affected area than prior art compositions comprising calcium gluconate.

[0051] The membrane-penetrating ability of a carrier such as DMSO may enhance absorption of the non-toxic calcium compound into skin tissue. This enhanced absorption may lead to delivery of calcium ions deeper into an affected area than use of a non-toxic calcium compound without a carrier. As a result, fluoride ions that have penetrated into skin tissue may be neutralized thereby limiting or preventing extensive tissue damage due to delayed or deeper HF burns.

[0052] Preferably, the pH range during treatment of HF burns with a non-toxic calcium compound is maintained between 3.4 and 6.5, which is physiologically reasonable and acceptable [19]. The pH could be maintained closer to physiological pH 7.4, if large excess (as compared to the stoichiometric amount of a non-toxic calcium compound required for the reaction with a given amount of hydrofluoric acid) of the composition comprising the non-toxic calcium compound is applied. As illustrated in the examples, a composition comprising a non-toxic calcium compound such as calcium levulinate and a carrier maintains the pH in the range of 3.4 to 5.8 during reaction with hydrofluoric acid.

EXAMPLES

[0053] The following examples are provided to illustrate the invention. It will be understood, however, that the specific details given in each example have been selected for the purpose of illustration and are not to be construed as limiting in scope of the invention.

[0054] In Example 1, the solubility of calcium levulinate is compared to prior art calcium gluconate. The reactions of various calcium levulinate compositions with hydrofluoric acid are illustrated in Examples 2-8, in all of which concentrations are expressed in weight % (wt %).

Example 1

Solubility of Calcium Levulinate

[0055] Solubility studies of calcium gluconate and calcium levulinate in various solvent systems at temperatures 20.degree. C., 37.degree. C., 60.degree. C. and 90.degree. C. are given in Table 1. The results show calcium levulinate to be more soluble than calcium gluconate in the listed solvent systems.

1TABLE 1 Solubilities of active compounds (g/100 mL of solvent) at various temperatures T Calcium gluconate Calcium levulinate Solvent .degree. C. g/100 mL g/100 mL Water 20 0.4 38.0 37 1.0 48.1 60 2.4 55.2 90 5.6 90.0 45% DMSO in water 20 0.2 14.0 37 0.4 15.0 60 1.0 20.1 90 1.3 44.6 10% urea in water 20 0.4 38.1 37 1.0 47.1 60 1.4 55.1 90 2.2 74.3 100% DMSO 20 0.1 42.8 37 0.3 58.4 60 0.6 70.0 90 1.1 92.3

Example 2

Reaction of a Solution of 10% Calcium Levulinate in Water with an Equal Molar Solution of 48% Hydrofluoric Acid--[Calcium Levulinate]:[HF]=1:1.

[0056] 5 g of calcium levulinate powder were dissolved in 45 ml of deionized water in a 150 mL beaker and placed into a water bath maintained at 37.degree. C. The pH of the solution was 8.1.

[0057] 1.5 g of 48% hydrofluoric acid was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution taken five minutes after the start of the reaction indicated that 96% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 3.4.

Example 3

Reaction of a Solution of 20% Calcium Levulinate in Water with 48% Hydrofluoric Acid--[Calcium Levulinate]:[HF]=2:1.

[0058] 10 g of calcium levulinate powder were dissolved in 40 mL of deionized water in a 150 mL beaker and placed into a water bath maintained at 37.degree. C. The pH of the solution was 8.1.

[0059] 1.5 g of 48% hydrofluoric acid was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution taken five minutes after the start of the reaction indicated that 97% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 4.4.

Example 4

Reaction of a Solution of 30% Calcium Levulinate in Water with 48% Hydrofluoric Acid--[Calcium Levulinate]:[HF]=3:1.

[0060] 15 g of calcium levulinate powder were dissolved in 35 mL of deionized water in a 150 mL beaker and placed into a water bath maintained at 37.degree. C. The pH of the solution was 8.4.

[0061] 1.5 g of 48% hydrofluoric acid was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution taken five minutes after the start of the reaction indicated that 92% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 4.7.

Example 5

Reaction of a Solution of 10% Calcium Levulinate, 10% Urea and 80% Water with 48% Hydrofluoric Acid--[Calcium Levulinate]:[HF]=1:1.

[0062] 5 g calcium levulinate and 5 g urea were dissolved in 40 mL deionized water in a 150 mL beaker inside a water bath maintained at 37.degree. C. The pH of the solution was 8.2.

[0063] 1.5 g of 48% hydrofluoric was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution taken five minutes after the start of the reaction indicated that 92% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 4.2.

Example 6

Reaction of a Solution of 10% Calcium Levulinate in 10% Urea and 80% Water with 48% Hydrofluoric Acid--[Calcium Levulinate]:[HF]=2:1.

[0064] 5 g calcium levulinate and 5 g urea were dissolved in 40 mL of deionized water in a 150 mL beaker and placed into a water bath maintained at 37.degree. C. The pH of the solution was 8.2.

[0065] 0.75 g of 48% hydrofluoric acid was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution taken five minutes after the start of the reaction indicated that 93% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 4.6.

Example 7

Reaction of a Solution of 10% Calcium Levulinate in 45% DMSO and 45% Water with 48% Hydrofluoric Acid--[calcium levulinate]:[HF]=1:1.

[0066] 5 g calcium levulinate were dissolved in a solution of 22.5 g DMSO and 22.5 mL of deionized water in a 150 mL beaker and placed into a water bath maintained at 37.degree. C. The pH of the solution was 9.2.

[0067] 1.5 g of 48% hydrofluoric acid was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution taken five minutes after the start of the reaction indicated that 92% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 4.4.

Example 8

Reaction of a Solution of 10% Calcium Levulinate in 45% DMSO and 45% Water with 48% Hydrofluoric Acid--[Calcium Levulinate]: [HF]=2:1.

[0068] 5 g of calcium levulinate were dissolved in a solution of 22.5 g DMSO and 22.5 mL of deionized water in a 150 mL beaker and placed into a water bath maintained at 37.degree. C. The pH of the solution was 9.2.

[0069] 0.75 g of 48% hydrofluoric acid was added to the beaker and the mixture stirred by means of a magnetic stirrer. Analysis of a 5 mL sample of the reaction solution was taken five minutes after the start of the reaction indicated that 83% of the hydrofluoric acid had reacted during the first five minutes of the test and that the pH of the solution had dropped to 5.8.

[0070] While embodiments of the present invention have been described in the foregoing, it is to be understood that other embodiments are possible within the scope of the invention. The invention is to be considered limited solely by the scope of the appended claims.

REFERENCES

[0071] [1] Committee on Hazardous Substances in the Laboratory, National Research Council, "Prudent Practices for Handling Hazardous Chemicals in Laboratories", National Academy Press, Washington, D.C., U.S.A., 1981, 33.

[0072] [2] M. A. MacKinnon, "Hydrofluoric Acid Burns", Dermatologic Clinics, 1988, Vol. 6, No. 1, 67-74.

[0073] [3] J. J. R. Kirkpatrick, D. S. Enion and D. A. R. Burd, "Hydrofluoric Acid Burns: A Review", Burns, 1995, Vol. 21, No. 7, 483-493.

[0074] [4] B. J. Dunn, M. A. MacKinnon, N. F. Knowlden, D. J. Billmaier, M. J. Derelanko, G. M. Rusch, D. J. Naas and R. R. Dahlgren, "Hydrofluoric Acid Dermal Burns. An Assessment of Efficacy Using an Experimental Pig Model", J. Occup. Med., 1992, Vol. 34, No. 9, 902-909.

[0075] [5] B. J. Dunn, M. A. MacKinnon, N. F. Knowlden, D. J. Billmaier, M. J. Derelanko, G. M. Rusch, D. J. Naas and R. R. Dahlgren, "Topical Treatments for Hydrofluoric Acid Dermal Burns. Further Assessment of Efficacy Using an Experimental Pig Model", J. Occup. Environ. Med., 1996, Vol. 38, No. 5, 507-514.

[0076] [6] F. Edelman, "Hydrofluoric Acid Burns", J. Occup. Med., 1986, Vol. 1, No. 1, 89-103.

[0077] [7] D. Peters and R. Miethchen, "Symptoms and Treatments of Hydrogen Fluoride Injuries", J. Fluorine Chem., 1996, No. 79, 161-165.

[0078] [8] S. W. Shewmake and B. G. Anderson, "Hydrofluoric Acid Burns", Arch. Dermatol., 1979, Vol. 115, 593-596.

[0079] [9] M. S. El Saadi, A. H. Hall, P. K. Hall, B. S. Riggs, W. L. Augenstein and B. H. Rumack, "Hydrofluoric Acid Dermal Exposure", Vet. Hum. Toxicol., 1989, Vol. 31, No. 3, 243-247.

[0080] [10] A. T. Jones, "The Treatment of Hydrofluoric Acid Burns", J. Industrial Hygiene and Toxicology, 1939, Vol. 21, No. 6, 205-212.

[0081] [11] Toxicology and Carcinogenesis Studies of Benzethonium Chloride (Hyamine, CAS No. 121-54-0) in F344/N Rats and B6C3F1 Mice (Dermal Studies), NTIS Report No. PB96-162300, July 1995.

[0082] [12] L. S. Zachary, W. Reus, J. Gottieb, J. P. Heggers and M. C. Robson, "Treatment of Experimental Hydrofluoric Acid Burns", J. Burn Care and Rehabilitation, 1986, Vol. 7, No. 1, 35-39.

[0083] [13] S. T. Seyb, L. Noordhock, S. Botens and M. M. Mani, "A Study to Determine the Efficacy of Treatment for Hydrofluoric Acid Burns", J. Burn Care and Rehabilitation, 1995, Vol. 16, No. 3, 253-257.

[0084] [14] M. C. Blomet, "Physiological Solution for Washing Parts of the Human Body Which Have Come into Contact with Hydrofluoric Acid and Concentrate For Preparing It", French Patent No. 2604900, 15 Apr. 1988.

[0085] [15] Sigma Aldrich Fine Chemicals, Aldrich Catalogue Handbook of Fine Chemicals, 1996, 686.

[0086] [16] A. H. Hall, J. Blomet, M. Gross and J. Nehles, "Hexafluorine for Emergent Decontamination of Hydrofluoric Acid Splashes", SSA Journal, 2000, Vol. 14, 30-33.

[0087] [17] SRC Physical Properties Database, CAS No 000123 76-2.

[0088] [18] G. L. Jenkins, W. H. Hartung, K. E. Hamlin and J. B. Data, "The Chemistry of Organic Medicinal Products", New York, John Wiley & Sons, 1957, 515.

[0089] [19] Improvements in or Relating to Chymotrypsin Solutions, Great Britain Patent No. 866423, 26 Apr. 1961.

Linked from fresh patents

The new criteria can be summarized as follows:

Evidence of structural change, as demonstrated by one or more of the following:

Chest x-ray, CT or HRCT scan

Pathology samples

Evidence of plausible causation, as demonstrated by one or more of the following:

Occupational and environmental history of exposure (with plausible latency).

Markers of exposure, such as pleural plaques.

Recovery of asbestos bodies on pathology review.

Exclusion of alternative diagnoses.

Evidence of functional impairment, as demonstrated by one or more of the following:

Signs and symptoms of impairment.

Reduced ventilatory capacity evidencing restrictive and or obstructive disease.

Impaired gas exchange.

reduced diffusion capacity.

Inflammation on bronchiolar lavage.

Exercise testing impairment.

The most significant differences and what they mean

The new criteria make a point of stating that significant exposures of less than a year can cause asbestosis and that bystander exposures in the right setting may also be sufficient.

The requisite ILO profusion score for asbestosis has been lowered to 1/0. This requirement is further diluted by categorizing the 0/1 profusion score as "suggestive," and adding that 15 - 20% of individuals with no radiographic evidence of asbestosis had histo-pathologic findings of parenchymal asbestosis.

The authors also promote high resolution CT scanning as being able to find asbestosis in 34% of asbestos-exposed workers with 0/0 or 0/1 profusion scores on plain chest x-ray.

While the 2004 criteria concede that restrictive impairment is the classic finding of asbestosis on pulmonary function testing, the ATS statement adds that mixed restrictive and obstructive impairment is frequently seen, and that asbestos exposure has been associated with obstructive physiological abnormalities which may or may not be attributable to asbestos exposure.

The new criteria revisit the finding of pleural plaques as an inconsequential marker and suggest that some studies have attributed a reduction in lung function to plaques, and that plaques have been associated with both restrictive impairment and diminished diffusing capacity.

The new statement also espouses medical monitoring every 3 to 5 years for anyone with a history of exposure but no manifest disease.

Today is Chronic Obstructive Pulmonary Disease day. What better an opportunity to learn about this disease, asthma and The Asthma Society of Canada’s support of Canadians in exercising their right to breathe easily and freely?

If nothing changes, more than 500 people will die in the next 365 days from complications due to asthma. Of these avoidable deaths, 50 will be children with asthma. Adults and children with the most severe forms of asthma will miss dozens of work and school days – on average, 34 days of work for adults and 20 days of school for kids.

Many of the more than three million Canadians with asthma and the 714,000 people with COPD will also suffer “presenteeism” – a term coined to describe impaired performance and quality of life caused by lack of sleep, illness while at work or school, and the associated anxiety parents inevitably experience when their children may be in danger of a respiratory crisis.

While the human cost is incalculable, the economic toll is not: according to some estimates, in 1998, the last year for which figures are available, health-care and disability costs relating to respiratory illness in Canada reached $8.5 billion.

Perhaps the most terrible aspect of this tragedy is that it is largely avoidable. Eighty per cent of asthma-related deaths are preventable, and most symptoms can be controlled with proper treatment, allowing children and adults to live active and symptom-managed lives.

“It is the equivalent,” says Dr. Noel Kerin, president and CEO of Kerin Occupational Health Consultants, “of watching a 747 jetliner crash needlessly each year.” In his clinical practice, Dr. Kerin has treated patients with chronic respiratory conditions for years, and the emotion in his voice is clear as he speaks of avoidable deaths and those left behind; of trying to treat patients whose prescription coverage didn’t include the medications they needed and couldn’t otherwise afford. Some 20 per cent of Canadians with asthma cannot access their medications because they can not afford them.

The causes of Canada’s respiratory crisis are complex, but the solutions are within reach – through a concerted, co-operative effort from patients, the medical community, governments and industry. The primary strategy to mitigating the damage is the optimal management of the disease. “Although we’ve had the Canadian Asthma Consensus Guidelines for a number of years now, we aren’t doing very good job at treating patients,” says Dr. Oxana Latycheva, vice president for Asthma Control Programming of the . Surveys conducted by the society found that almost 60 per cent of asthma patients do not have their condition under control. “People often just think that it is normal to miss school or work, to wake up during the night, to not be able to exercise. We need to work together to tell people that they don’t need to accept a lower quality of life.” (In fact, Olympic medalist Silken Laumann has asthma, illustrating the quality of health that’s possible for others with the condition.)

Taken from: Randall Anthony, special to the Globe & Mail

If Mesothelioma is a rogue viral infection - then there is the possibility of developing a vaccine and offering vaccination to asbestos exposed people who are at heightened risk of developing future asbestos related malignancies.

Q: Is asbestos a co-carcinogen to a viral infection?
A: Needs to be studied...

Topics on the conference agenda, to be delivered by an international who’s who of occupational medicine, include Occupational Asthma, Beryllium—the ‘new’ chronic lung disease, and Mental Health in the workplace. “Economics of Occupational Health” will look at Benefits for the Workplace, The Cost of human Capital, and Examples of Best Practices in Industry.

Dr. Kerin said that the overarching purpose of the Conference was to build answers to three key questions and bring them to the front of mind of business. “How can we help our employees stay at work and be healthy? How can we help our employees return to work in a timely manner? How are we doing in this regard?” Dr. Kerin said. “If we can start to share and understand the different perspectives, Canadian Industry will be in a better position to make sound human capital management decisions—particularly in relation to chronic diseases’ huge toll on employees and industry.”

OEMAC sees the Conference as a unique opportunity to develop consensus. “We—all parties—need to learn how human capital can be better managed.” said Dr. Kerin. “And we need to learn quickly, if Canadian industry wants to continue as global competitors. The statistics are grim, and they don’t lie.”

• 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.

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.

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.

Copyright © Dr. Noel Kerin and KOHC. All rights reserved.

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