Pneumoconiosis

Contents

Guided By

: - Prof. Debi

Prasad

Tripathy

_{By Manoranjan Sahoo}

_|

Roll no. - 111MN0087

|

TYPES OF PNEUMOCONIOSIS,

MEASURES TO PREVENT THEM,

MEDICAL EXAMINATION FOR DUST

RELATED ISSUES AND DUST

CONTROL IN MINES

1. Perspective of

pneumoconiosis………02

2. Types of

pneumoconiosis……….0

6

3. Measures to prevent

pneumoconiosis……….23

4. Medical examinations done for dust related

issues…………29

5. Methods used to control dust in

mines………37

6. References………

………..48

Perspective of pneumoconiosis:

-The pneumoconiosis are parenchymal lung diseases that arise from inhalation of (usually) inorganic dusts at work. Some such dusts are biologically inert but visible on a chest X-ray or CT scan; thus, while they are radiologically alarming they do not give rise to either clinical disease or deficits in pulmonary function. Others – notably asbestos and crystalline silica – are fibrogenic so that the damage they cause is through the fibrosis induced by the inhaled dust rather than the dust itself. Classically these give rise to characteristic radiological patterns and restrictive deficits in lung function with reductions in diffusion capacity; importantly, they may progress long after exposure to the causative mineral has finished.

It can also be described as lung condition that is caused by inhaling particles of mineral dust, usually while working in a high-risk, mineral-related industry. At first, irritating mineral dust can trigger lung inflammation, which causes areas of the lung to be temporarily damaged. Over time, these areas can progress to form tough, fibrous tissue deposits. This stage of pneumoconiosis is called fibrosis. Fibrosis stiffens the lungs and interferes with the lung's normal exchange of oxygen and carbon dioxide.

Pneumoconiosis, also known as miner's lung, is a lung condition caused by the inhalation of dust, characterized by formation of nodular fibrotic changes in lungs.

What are dusts

?

 Dust is a generic term used to describe fine particles that are suspended in the atmosphere.

 The term is non-specific with respect to the size, shape and chemical make-up of the particles. Particles as small as a few nanometers and as large as 100 microns (μm) have been measured in the atmosphere.

 Dust is formed when fine particles become entrained in the atmosphere by the turbulent action of wind, by the mechanical disturbance of fine materials, or through the release of particulate-rich gaseous emissions.

 The concentration of particles in the atmosphere can range from a few micrograms to hundreds of micrograms per cubic meter (μg/m3_{) in highly}

Dusts occurrence and its form

 Dust associated with mining activity usually occurs as a result of the disturbance of fine particles derived from soil or rock.

 Dust formation is initiated by the disturbance of particles through mechanical action, blasting, handling, transporting, in combination with air movement.  Where particles are small and light, with a high surface area relative to their

mass, the upward forces exerted on particles by air movement may exceed downward gravitational forces, leading to the formation of dust.

 Depending on the factors such as climate, geology and the method of mining, the potential exits for greatly increased dust levels in the environment surrounding a mine.

 Modern methods of open cut mining often involve the mining, transport and handling of huge tonnage of material, increasing the potential of dust to be produced.

 The consequences may include visible plumes and haze, the staining and soiling of surfaces, aesthetic or chemical contamination of water bodies or vegetation and, effects on personal comfort, amenity and health.

Classification

Toxic dusts:

It can cause chemical reactions within the respiratory system or allow toxic compounds to be absorbed into the bloodstream through the alveolar walls. Poisonous to body tissue or to specific organs. The most hazardous include compounds of arsenic, lead, uranium and other radioactive minerals, mercury, cadmium, selenium, manganese, tungsten, silver and nickel.

Carcinogenic (cancer causing) dusts:

The cell mutations that can be caused by alpha, beta and gamma radiation from decay of the uranium series make radon daughters the most hazardous of the carcinogenic particulates.

A combination of abrasion of lung tissue and surface chemical action can result in tumour formation from asbestos fibers and, to a lesser extent, freshly produced quartz particles.

Exposure to arsenic dust can also cause cancers. Diesel exhaust particulates are a causative factor in lung and other types of cancer.

Fibrogenic dusts:

Microscopic scarring of lung tissue. Over long periods this can produce a fibrous growth of tissue resulting in loss of lung elasticity and a greatly reduced area for gas exchange.

The silica and some silicate (asbestos, mica, talc) dusts are the most hazardous of the fibrogenic dusts and may also produce toxic and carcinogenic reactions.

Welding fumes and some metalliferous ores produce fibrogenic dusts. Long and excessive exposure to coal dusts also gives rise to fibrogenic effects.

Explosive dusts:

These are a concern of safety rather than health.

Ex: Coal dust becomes explosive when finely divided at high concentrations in air. Sulphide ores and many metallic dusts are also explosive.

Nuisance dusts:

Irritating to the eyes, nose and throat. In sufficiently high concentration may cause reduced visibility.

Some dusts have no well-defined effects on health but remain in the category of a nuisance dust.

Dust as a Health Issue for Mine Workers (Pneumoconiosis)

 Health risks posed by inhaled dust particles are influenced by both the penetration and deposition of particles in the various regions of the respiratory tract and the biological responses to these deposited materials.

 The smaller the particles, the further they penetrate the respiratory tract. The largest particles are deposited predominantly in the nasal passages and throat. Much smaller particles, nominally less than 2.5 μm, reach the deepest portion of the lungs.

 Silica dust has been a widespread problem in the past for workers in mining and quarrying industries.

 Silica dust refers to silicon and its compounds that are very common in the rocks forming the earth's crust. Silica is non-toxic and safe except where specific crystalline forms of silica occur in dust.



Long term inhalation of silica dust may lead to the formation of scar tissue in the lungs and can result in 'silicosis', a serious and life threatening lung disease

.

 Toxic metals include arsenic, antimony, cadmium, chromium, cobalt, lead, manganese, mercury, nickel, selenium, vanadium, zinc and their compounds.  Dusts containing mercury, arsenic or cadmium are particularly hazardous.

Lead has a much lower toxicity but is a common constituent of dust in certain locations.

 Asbestos dust, a recognized human carcinogen, is a product of the mining and processing of asbestiform minerals.

 Four minerals types are well known, namely chrysotile, amosite, crocidolite and anthophyllite.

 Serpentine bands may host asbestos minerals and are common geologic intrusions in mines and quarries.

 Asbestos is chemically inert, yet can induce a severe reaction within the lungs.

Reaction of the lung to inhaled dust depends upon:

1) The chemical nature of the dust 2) The size of the dust particles 3) Concentration of the dust particles 4) The duration of exposure

How does our body defends against dusts…

 Trapping larger particles in the nasal passages, throat, trachea, larynx

 Trapping particles in mucous and carrying them up the airways where they are coughed out or swallowed (mucociliary escalator)

Thus the lung diseases caused by dusts are called pneumoconiosis and he name of each pneumoconiosis comes from the dust that produces it.

Types of Pneumoconiosis:

-Pneumoconiosis can be divided into two types:

1) Simple Pneumoconiosis: –

Appear as small nodular shadows as on chest x-ray and can normally be detected on routine medical examination. It rarely causes any difficulty though.

2) Complicated Pneumoconiosis or progressive massive fibrosis (PMF): –

It is seen in advance stage of simple pneumoconiosis and among the persons exposed to high concentration of dust. The disease once detected is normally progressive and causes significant disability.

Pneumoconiosis may be classified as either fibrotic or nonfibrotic, according to the presence or absence of fibrosis. Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are examples of fibrotic pneumoconiosis. Siderosis, stannosis, and baritosis are nonfibrotic forms of pneumoconiosis that result from inhalation of iron oxide, tin oxide, and barium sulfate particles, respectively.

• Silicosis

• Asbestosis

• Anthracosis Fibrotic Pneumoconiosis

•

Talcosis

•

Berylliosis

•

Mixed-dust fibrosis

• Stannosis

• Baritosis Non fibrotic Pneumoconiosis

•

Siderosis

1. Silicosis:

-Silicosis results from the accumulation of respirable particles of crystalline silica in the lung. Crystalline silica is found in many types of stone, but sandstone is

approximately 70% silica and therefore stonemasons – particularly if using angle grinders which generate large quantities of respirable dust – are at high risk of developing silicosis. Other groups at risk are quarry workers and tunnellers, foundry and pottery workers, and construction workers (such as pavers, who frequently cut or break stone, concrete or brick). Classic silicosis is the most common presentation and typically follows 10-20 years of work during which time the individual often remains asymptomatic. The typical plain chest X-ray appearances are similar to those of coal worker’s pneumoconiosis, with a profusion of small nodules in the upper and mid zones. Hilar and mediastinal lymph node enlargement may be present. Non-specific findings include a peripheral blood lymphopenia and raised serum angiotension converting enzyme (ACE), which together with the chest X-ray changes may give rise to confusion with sarcoidosis.

High resolution CT (HRCT) scan (Figure 3) provides greater diagnostic confidence, showing bilateral well-defined 3-5 mm nodules in a centrilobular and subpleural distribution with a posterior bias. In addition, HRCT facilitates the identification of progressive massive fibrosis (coalescence of nodules into irregular masses) and lymph node involvement. Lung biopsy may be considered if the diagnosis remains uncertain on clinical and radiological grounds; in silicosis it shows acellular whorls of hyaline collagen and, when viewed under polarised light, the presence of bi-refringent crystals confirming the presence of silica and other Silicates.

This case illustrates that substantial lung damage, including the development of progressive massive fibrosis, may occur without symptoms in young fit workers, and highlights two potential pitfalls in the interpretation of lung function tests. First, although the FEV1 normally declines with age, it does not significantly do so until the late thirties and so any loss of lung function occurring before this should raise concern. Second, the predicted value represents the average value in healthy subjects of a given age, height and sex and it is possible to lose a significant amount of lung function yet remain within the ‘normal’ range.

Silicosis history

:

- This respiratory disease was first recognized in 1705 by Ramazzini who noticed sand-like substances in the lungs of stonecutters

 Full description by Bernardino Ramazzini (1633-1714) in early 18th _century.

“...when the bodies of such workers are dissected, they have been found to be stuffed with small stones.” Diseases of Workers (De Morbis Artificum

Diatriba, 1713).

 The name silicosis (from the Latin silex or flint) was attributed to Visconti in 1870

 First U.S. description in 19th _century.

 Prevalence increased markedly with introduction of mechanized mining.  Came to national attention 1930-1931 with construction of Hawk’s Nest

Tunnel in Gauley Bridge, West Virginia. Called “the worst industrial accident in U.S. history.” At least 764 tunnel workers died from silicosis. Hawk’s Nest disaster led to Congressional hearings in 1936, and new laws protecting workers in many states.

 Prevalence of silicosis has greatly declined in recent decades because of effective industrial hygiene measures.

 The full name for this disease when caused by the specific exposure to fine

silica dust found in volcanoes is

pneumonoultramicroscopicsilicovolcanoconiosis, and at 45 letters it is the longest word in any of the major English dictionaries.

 The prevalence of silicosis led some men to grow what is called a miner's mustache, in an attempt to intercept as much dust as possible.

Silica (Silicon Dioxide or SiO2) is found mainly as quartz in nearly all mineral

deposits. It is found in common rocks such as granite, sandstone, limestone, and is the principle component of sand.

Severity of Disease Depends on:

- Dust Concentration

 Percent of free silica

 Duration of exposure

 Size of particles

Symptoms

1st _stage

 dysponoea (inelasticity) of the lung

 Shortening of breath is noticed on exertion

 Dry cough

 Radiographs show discrete circular shadows of nodules of 2mmdia (max)

2nd _stage

Well established dysponoea & cough with impaired chest expansion. Radiograph shows diffuse nodulation with a tendency to coalescence 3rd stage

Dysponoea leads to total incapacity Radiograph shows massive consolidation

 Silicosis in advanced stage is usually associated with Tuberculosis infection which may modify the symptoms

Silicosis is an occupational hazard to mining, sandblasting, quarry, ceramics and foundry workers, as well as grinders, stonecutters and those continually exposed to silica dust.

Effect of silicosis to the body:

-Generally, the silica dust affects the lungs ability to work correctly. Each type of silicosis affects the body somewhat differently:

 In simple chronic silicosis, the silica dust causes areas of swelling in the lungs and chest lymph nodes, which causes breathing difficulty.

 In accelerated silicosis, swelling in the lungs and symptoms occur faster than in simple silicosis.

 In acute silicosis, the lungs become very inflamed and can fill with fluid, which causes severe shortness of breath and low blood oxygen levels.

Anyone with silicosis may suffer from several complications:

 Increased risk for lung infections and tuberculosis.

 Progressive massive fibrosis—severe scarring and stiffening of the lung, which makes it difficult to breathe. Progressive massive fibrosis can occur in either simple or accelerated silicosis, but is more common in the accelerated form.

 Respiratory failure.

Managing Silicosis:

-Silicosis is invariably progressive, even following complete cessation of exposure, and regular assessment should be undertaken including more detailed lung function testing and serial chest X-rays. As the condition progresses, typical symptoms include cough and shortness of breath occurring on exertion.

There are no effective pharmacological treatments for silicosis. Smoking cessation is particularly important as silica is a carcinogen, and individuals with silicosis are at increased risk of lung cancer. The development of silicosis also increases the risk of contracting pulmonary tuberculosis (TB), which is an important consideration in areas where TB is endemic, especially as the typical upper lobe chest X-ray changes of pulmonary TB may be masked by the presence of silicosis. Less common but well recognised complications include the development of connective tissue diseases such as scleroderma and SLE and, rarely, glomerulonephritis. Advanced disease may be complicated by pulmonary hypertension, cor pulmonale and respiratory failure, and any evidence of these should trigger a pulmonary transplant assessment.

The patient should be encouraged to inform the company’s occupational health team of his diagnosis. In the UK the employer is legally bound to notify the Health and Safety Executive through the Reporting of Injuries, Diseases and Dangerous Occurrences (RIDDOR) mechanism. The diagnosis of silicosis in a worker should trigger a thorough review of the occupational hygiene measures and supply of personal protective equipment in the factory.

Case Studies

:

-The Americas Silicosis Initiative

When Chilean artisans worked in the past, they used hand tools to artfully shape and cut stone. Today, craftsman working in small open-air settings with two to four workers, use power tools for the same tasks. While efficient, these contemporary tools pose a major health risk by generating dust with high levels of airborne crystalline silica. When workers breathe in this dust, it can result in silicosis, a serious but preventable lung disease. Occupational exposure to crystalline silica inhaled in the lungs is also associated with lung cancer, pulmonary tuberculosis and airway diseases, and may be related to the development of autoimmune disorders, chronic renal disease, and other adverse health effects.

Concerned about these threats, the Chilean National Institute for Public Health (ISP), invited three industrial hygienists from CDC’s National Institute for Occupational Safety and Health (NIOSH) to examine high-risk work conditions among ornamental stone carvers in Pelequén, Chile (both ISP and NIOSH are WHO Collaborating Centres in Occupational Health). A NIOSH industrial hygienist said “the silica dust levels were some of the highest I’ve seen anywhere in the world – and there were no controls to prevent silicosis.” NIOSH plans to assist ISP in implementing interventions to introduce dust control measures in these small shops. NIOSH has expertise in all aspects of silica measurement, including control of exposure, diagnosis, treatment and medical surveillance of silica-related diseases. This expertise is sought by international and national organizations to address the problems in developed and developing countries, where occupational silicosis is believed to be widespread.

For many exposed workers, prevention measures are non-existent. China recorded more than 500,000 cases of silicosis from 1991- 1995. In Brazil, more than 4,500 workers with silicosis have been cumulatively reported in the state of Minas Gerais. In India alone, millions of workers are at risk. In 1995, the World Health Organization (WHO) and the International Labour Organization (ILO) began a campaign to eliminate silicosis from the world by 2030. In 2005, WHO and its regional office, the Pan American Health Organization (PAHO), ILO, and the Chilean Health Ministry (MOH) requested that NIOSH provide technical assistance to build adequate capacity to eliminate silicosis in the Americas. In

response to this request, NIOSH initiated a program called the “Americas Silicosis Initiative” in partnership with WHO, PAHO, and ILO. It is the first regional approach to silicosis and is based upon the sharing of expertise to benefit many countries. Substantial work was accomplished in Chile in 2006 and is underway in 2007 in Chile, Brazil, and Peru, including:

 Training of physicians from Chile, Brazil, and Peru by US, Chilean and Brazilian experts

 Development of a silica laboratory at the ISP in Santiago (including training for laboratory technicians from Chile, Brazil, Peru and Uruguay)

 Training of workshop participants from Chile, Peru, Brazil and Uruguay in methods of dust control

 Development of simple guidance for employers to put controls in place

 Provision of field visits to small quarries and stone crushing and stone craft worksites to develop customized guidance sheets

The impact of NIOSH’s technical assistance was seen in July 2007, when Chilean Ministries of Health and Labour jointly hosted representatives of the Ministries of Brazil, Argentina, Uruguay, Mexico and Peru for a regional planning meeting that brought these countries into the Americas’ partnership.

The Americas Silicosis Initiative includes a cost-effective, novel educational approach called “Control Banding” to control exposures to the hazardous crystalline silica dust. NIOSH’s technical assistance to partners in Brazil, Chile, and Peru enables these countries to develop their own capacity to implement National Plans to eliminate silicosis. This partnership is a model for other countries and is helping to meet the ILO/WHO goal to eliminate silicosis by 2030. Global collaboration in silicosis benefits NIOSH in its effort to reach small business in the United States though experience and lessons learned in applying simple guidance to control silica exposures in small enterprises with partner countries in the Americas. At least 1.7 million United States’ workers are potentially exposed to respirable crystalline silica in a variety of industries and occupations, including mining and construction, and many are exposed to concentrations that exceed limits defined by current regulations and standards. OSHA is currently working on new regulations and NIOSH is developing new forms of simple guidance for employers and workers.

In October, a NIOSH technical expert visited Chile in to present the United States’ experience in controlling silicosis with the use of respirators in the workplace at the “Breath Safely” seminar. He met with the Chilean ISP on silica control topics related to respiratory protection, and proposed a joint project on developing respiratory protection programs for small and medium business enterprises. Prevention activities with the cooperation of government, labor, and industry are ongoing, and are the keys to silicosis elimination.

Compensation for silicosis:

-The diagnosis of silicosis invariably represents the end of a career. Companies are reluctant to re-employ stonemasons or others diagnosed with silicosis and doctors should be cautious in advising continued exposure to any form of dust. The implications of this, especially to younger workers, can be devastating, and finding alternative sufficiently remunerative work can be challenging. They should be encouraged to seek compensation from the Industrial

Injuries Disablement Benefit scheme (silicosis is a prescribed disease) or the appropriate equivalent in other countries, and informed that they can seek legal advice with a view to pursuing a civil claim, as described above.

2. Asbestosis:

-Asbestosis (as-bes-TOE-sis) is a chronic lung disease caused by inhaling asbestos fibers. Prolonged exposure to these fibers can cause lung tissue scarring and shortness of breath. Asbestosis symptoms can range from mild to severe, and usually don't appear until many years after continued exposure.

Asbestos is a natural mineral product that's resistant to heat and corrosion. It was used extensively in the past in products such as insulation, cement and some floor tiles. Most people with asbestosis acquired it on the job before the federal government began regulating the use of asbestos and asbestos products in the 1970s. Today, its handling is strictly regulated. Acquiring asbestosis is extremely unlikely if you follow your employer's safety procedures. Treatment focuses on relieving your symptoms. In other words it is a chronic inflammatory and fibrotic medical condition affecting the parenchymaltissue of the lungs caused by the inhalation and retention of asbestos fibers. It usually occurs after high intensity and/or long-term exposure to asbestos (particularly in those individuals working on the production or end-use of products containing asbestos) and is therefore regarded as an occupational lung disease. People with extensive occupational exposure to the mining, manufacturing, handling, or removal of asbestos are at risk of developing asbestosis. Sufferers may experience severe dyspnea (shortness of breath) and are at an increased risk for certain

malignancies, including lung cancer but especially mesothelioma. Asbestosis specifically refers to interstitial (parenchymal) fibrosis from asbestos, and not pleural fibrosis or plaguing.

All types of asbestos tend to break into very tiny fibers. These individual fibers are so small they must be identified using a microscope. Some fibers may be up to 700 times smaller than a human hair.

Because asbestos fibers are so small, once released into the air, they may stay suspended there for hours or even days.

They are resistant to chemicals and heat, and they are very stable in the environment. They do not evaporate into air or dissolve in water, and they are not broken down over time.

Asbestos is probably the best insulator known to man. Because asbestos has so many useful properties, it has been used in over 3,000 different products.

Symptoms of Asbestosis:

-The signs and symptoms of asbestosis do not manifest until after an appreciable latency (time since first exposure), often several decades under current conditions in the US.[3] _{The primary symptom of asbestosis is generally the slow onset of dyspnoea,}

especially on exertion.[4] _{Clinically advanced cases of asbestosis may lead}

to respiratory failure. On auscultation of the lungs, the physician may hear inspiratory rales.

The characteristic pulmonary function finding in asbestosis is a restrictive ventilatory defect.[5] _{This manifests as a reduction in lung volumes, particularly the vital capacity}

(VC) and total lung capacity (TLC). The TLC may be reduced through alveolar wall thickening; however this is not always the case.[6] _{Large airway function, as reflected}

by FEV1/FVC, is generally well preserved.[3] In the more severe cases, the drastic

reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale).[7][8] _{In addition to a restrictive defect,}

asbestosis may produce reduction in diffusion capacity and arterial hypoxemia.

In summary,

 Shortness of breath and a dry crackling sound in the lungs while inhaling.

 Cough, sputum & weight loss

 In its advanced stages, the disease may cause cardiac failure. However,

 Progress of fibrosis in asbestosis is more severe than silicosis  But, it makes the lung less susceptible to TB than silicosis

One of the diseases associated with asbestosis is lung cancer and this usually occurs in the asbestos worker who smokes cigarettes. In fact the risk of the asbestos worker who smokes is 90 times more likely than the non-asbestos, non-smoking worker

Pathogenesis:

-Asbestosis is the scarring of lung tissue (around terminal bronchioles and alveolar ducts) resulting from the inhalation of asbestos fibers. There are two types of fibers: amphibole (thin and straight) and serpentine (curved). The former are primarily responsible for human disease as they are able to penetrate deeply into the lungs.

When such fibers reach the alveoli (air sacs) in the lung, where oxygen is transferred into the blood, the foreign bodies (asbestos fibers) cause the activation of the lung's local immune system and provoke an inflammatory reaction. This inflammatory reaction can be described as chronic rather than acute, with a slow ongoing progression of the immune system in an attempt to eliminate the foreign fibers. Macrophagesphagocytose (ingest) the fibers and stimulate fibroblasts to deposit connective tissue. Due to the asbestos fibers' natural resistance to digestion, the macrophage dies off, releasing cytokines and attracting further lung macrophages and fibrolastic cells to lay down fibrous tissue, which eventually forms a fibrous mass. This mass can be seen microscopically, with the asbestos fiber layered by an iron-containing proteinaceous material (ferruginous body). The result is interstitial fibrosis. The fibrotic scar tissue causes alveolar walls to thicken, which reduces elasticity and gas diffusion, reducing oxygen transfer to the blood as well as the removal of carbon dioxide.

Diagnosis:

-Asbestosis is the ‘pneumoconiosis’ that arises from exposure to asbestos in the workplace. The diagnosis is made when, on the background of heavy occupational exposure to any type of asbestos, there is radiological evidence of pulmonary fibrosis. The diagnosis is not necessarily straightforward and is often a matter of judgement2 after taking the following into account:

• The radiological features of asbestosis are non-specific and closely resemble the ‘usual interstitial pneumonia’ that is characteristic of ‘idiopathic’ pulmonary fibrosis (IPF). Changes are far more readily seen on CT scan (Figure 1) than on a conventional chest X-ray. In fact, the increasing use of thoracic CT in both respiratory and cardiac care is probably responsible for some of the apparent increase in the incidence of asbestosis.

Other radiological features of asbestos exposure such as pleural thickening or plaques are often seen and can be used to help make the distinction between asbestosis and IPF.

• The ‘dose’ of asbestos required to induce fibrosis is relatively high and usually acquired over at least several years of high exposure in the workplace; these doses are generally higher than those necessary to induce pleural plaques or mesothelioma. Common occupations associated with asbestosis include boiler lagging with asbestos (as is likely in this case), work with asbestos textiles, and the manufacture of asbestos-containing building materials. In the UK these are long-abandoned industries, but because the latency of asbestosis is also long, new cases continue to be identified; indeed the incidence of, and mortality from, asbestosis in older UK men is still rising. • The ‘Helsinki criteria’ suggest that a dose of at least 25 fibre/ml.years is necessary to cause asbestosis. This cumulative exposure metric is similar to the ‘pack years’ used to measure cigarette smoking; thus, 10 years work in an average airborne concentration of 2.5 fibre/ml is equivalent to one year at 25 fibre/ml. This latter concentration is very high but may readily have been found, for example, in the

asbestos textile industry in the 1950’s and 1960’s. In practice there is rarely any information available about exposure levels in individual cases and the criterion value is used only as a guide.

• Asbestos bodies are fibres, usually of ‘blue’ or ‘brown’ asbestos (so-called ‘amphiboles’) that have become coated in an iron-rich proteinaceous material and are readily visible on light microscopy. If a lung biopsy has been taken then the presence of asbestos bodies is helpful evidence of substantial asbestos exposure; their absence, however, does not rule out a diagnosis of asbestosis.

.

Treatment:

-There is no curative treatment for asbestosis. Oxygen therapy at home is often necessary to relieve the shortness of breath and correct underlying hypoxia. Supportive treatment of symptoms includes respiratory physiotherapy to remove secretions from the lungs by postural drainage, chest percussion, and vibration. Nebulized medications may be prescribed in order to loosen secretions or treat underlying Chronic Obstructive Pulmonary Disease. Immunization against pneumococcal pneumonia and annual influenza vaccination is administered due to increased sensitivity to the diseases. Patients are at increased risk for certain malignancies. If the patient smokes, cessation reduces further damage. Periodic PFTs, chest x-rays, and clinical evaluations, including cancer screening/evaluations, are given to detect additional hazards.

Managing asbestosis:

-The diagnosis of asbestosis is particularly frightening to most people. This is not necessarily warranted, since the prognosis of mild cases is good6 and in almost all cases is better than the (dismal) prognosis of IPF. In limited disease an appropriate degree of reassurance can be very helpful.

Most patients with asbestosis will be followed-up in secondary care to monitor the radiological and functional progression of their disease; the gap between appointments may be long, for example 12 months, and an interval assessment of symptoms and spirometry can be helpful. There is no effective drug treatment for asbestosis and in most cases no pharmacological treatment is offered – in particular, neither bronchodilators nor corticosteroids (inhaled or oral) are helpful. Some patients may like to take n-acetyl cysteine which has been proven to be of some benefit in IPF and has at least the virtue of being harmless. Advanced cases may benefit from oxygen at home. Severe cases of asbestosis are sometimes treated with lung transplantation, but this is rare in the UK.

The course of the disease depends largely on its extent and on the quantity of asbestos retained in the lungs. In mild cases there is little if any evidence of progression for many years. In others with more advanced disease there is a steady decline towards respiratory failure. A precipitous deterioration, marked by increasing breathlessness

and sometime cyanosis on exercise, is usually indicative of secondary pulmonary hypertension. This requires rapid assessment by a specialist service but successful treatment is rare. A high proportion of those with asbestosis die from lung cancer, reflecting the synergistic effects of smoking and asbestos exposure. It is probably good practice to advise those with asbestosis who smoke to stop doing so, although the benefit in reducing the risk of lung cancer at that stage is uncertain. Around one in 10 patients will develop (and die from) mesothelioma – about the same proportion that will die from asbestosis itself.

Compensation for asbestosis:

-The provision of compensation for occupational lung diseases varies between different countries. In the UK, for example, patients with asbestosis can claim compensation through a number of routes:

Industrial Injuries Disablement Benefit is a statutory payment available to those who have developed a ‘prescribed’ disease (of which asbestosis is an important example) through their employment. Those who have been exposed through self-employment are ineligible. The process of claim – through the Benefits Agency – is deliberately simple and almost all claimants with asbestosis will be awarded compensation which at its lowest level is a little over £30 weekly, payable for life.

Alternatively, or in addition, patients may open a civil case against their employer, usually a previous employer given the long latency of the disease. This is best done through a trade’s union or other specialist solicitor and almost always is on a no-win-no- fee basis. Where an employer (or their insurer) cannot be discovered, other avenues for compensation are available by statute. These claims can be quite complex and it is useful to seek advice from a suitably qualified lawyer or one of the many Asbestos Support groups in the UK.

Background

:

-In the late 19th century and early 20th century, asbestos was considered an ideal material for use in the construction industry. It was known to be an excellent fire retardant, to have high electrical resistance, and was inexpensive and easy to use. The problem with asbestos arises when the fibers become airborne and are inhaled. Because of the size of the fibers, the lungs cannot expel them.[2] _{They are also sharp}

and penetrate tissues.

Health problems attributed to asbestos include

1. Asbestosis - A lung disease first found in textile workers, asbestosis is a scarring of the lung tissue from an acid produced by the body's attempt to

dissolve the fibers. The scarring may eventually become so severe that the lungs can no longer function. The latency period (meaning the time it takes for the disease to develop) is often 10–20 years.

2. Mesothelioma - A cancer of the mesothelial lining of the lungs and the chest cavity, the peritoneum (abdominal cavity) or the pericardium (a sac surrounding the heart). Unlike lung cancer, mesothelioma has no association with smoking. The only established causal factor is exposure to asbestos or similar fibers. The latency period for mesothelioma may be 20–50 years. The prognosis for mesothelioma is grim, with most patients dying within 12 months of diagnosis.

3. Cancer - Cancer of the lung, gastrointestinal tract, kidney and larynx have been linked to asbestos. The latency period for cancer is often 15–30 years. 4. Diffuse pleural thickening

Considerable international controversy exists regarding the perceived rights and wrongs associated with litigation on compensation claims related to asbestos exposure and alleged subsequent medical consequences. Some measure of the vast range of views expressed in legal and political circles can perhaps be exemplified by the two quotes below, the first [10] _{from Prof. Lester Brickman, an American legal ethicist}

writing in the Pepperdine Law Review, and second, Michael Wills, a British Member of Parliament, speaking in the House of Commons on July 13. 2006:

"A review of the scholarly literature indicates a substantial degree of indifference to the causes of this civil justice system failure. Many of the published articles on asbestos litigation focus on transactional costs and ways in which the flow of money from defendants to plaintiffs and their lawyers can be expeditiously and efficiently prioritized and routed. The failure to acknowledge, let alone analyse, the overriding reality of specious claiming and meritless claims demonstrates a disconnect between the scholarship and the reality of the litigation that is nearly as wide as the disconnect between rates of disease claiming and actual disease manifestation".

"Many of those who I see in my surgeries have worked in a number of workplaces and they could have been exposed to asbestos in each of them, but medical science is such that no one can identify which of them it is. As a result, there has been a long and complex history of legal discussion on how to apportion liability. The lawyers and the judiciary have wrestled, rightly and valiantly, with complex and difficult law, but it has created despair for the families whom we represent. Many of my constituents’ families have been riven by the consequences of litigation in trying to get some compensation for a disease that has been contracted through no fault of theirs. That is cruel and unacceptable."

3. Anthracosis:

-Coal workers' pneumoconiosis (CWP), more commonly referred to as black lung disease or just black lung, is caused by long exposure to coal dust. It is a common affliction of coal miners and others who work with coal, similar to both silicosis from inhaling silica dust, and to the long-term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and is unable to be removed by the body; this leads to inflammation, fibrosis, and in worse cases, necrosis.

Coal workers' pneumoconiosis, severe state, develops after the initial, milder form of the disease known as anthracosis (anthrac — coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, simple coal workers' pneumoconiosis and complicated coal

workers' pneumoconiosis (or Progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis,[2] _{clinically defined}

as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In non-smokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% to 17% incidence of industrial bronchitis.

Simple Form.—The radiographic pattern of simple coal worker pneumoconiosis typically consists of small round nodular opacities and occasionally includes reticular or reticulonodular opacities. The nodules in coal worker pneumoconiosis have a diameter of 1–5 mm and tend to be less well defined at the margins and more granular in appearance than those found in silicosis. Calcifications are observed on chest radiographs in 10%–20% of patients. Calcification develops as a central nodular dot in coal worker pneumoconiosis, whereas it tends to be more diffuse in silicosis. Furthermore, the eggshell calcification pattern that is pathognomonic of simple silicosis is uncommon in simple coal worker pneumoconiosis (it is observed in only 1.3% of patients) (22).

The CT features of coal worker pneumoconiosis are similar to those of silicosis. Small nodules may be observed diffusely throughout the lungs, typically with a perilymphatic distribution but sometimes with a centrilobular predominance, but they tend to be most numerous in the upper lung zone (Fig 9). At CT, calcification is observed within the nodules in 30% of patients with the disease. Moreover, hilar or mediastinal lymph

node enlargement also is reported in 30% of patients.

Complicated Form.—On chest radiographs, large opacities (progressive massive fibrosis) may be seen in complicated coal worker pneumoconiosis, as in complicated silicosis. However, the histopathologic basis of these features in complicated coal worker pneumoconiosis is different from that in complicated silicosis. In coal worker pneumoconiosis, the fibrotic mass consistsof haphazardly arranged collagen with numerous pigment-laden macrophages and with abundant free pigment especially

evident in the central region. Foci of frank necrosis, cholesterol clefts, and chronic inflammatory cellular infiltrates also are often present.

Fibrotic masses in complicated coal worker pneumoconiosis are defined according to the

regularity of the lesion border and the pattern of the surrounding parenchyma. Most such lesions have an irregular border with associated surrounding pericicatricial emphysema. However, some have a regular border without pericicatricial emphysema. It is clinically and radiologically important to differentiate progressive massive fibrosis from lung cancer. Matsumoto et al reported that magnetic resonance (MR) imaging is potentially useful for this purpose. On MR images, lung cancer appears as a high-signal-intensity lesion on T2-weighted images, whereas progressive massive fibrosis appears as a low-signal-intensity abnormality when compared with the signal intensity of muscle on both T1- and T2-weighted images. Some investigators have suggested that the most common MR characteristics of progressive massive fibrosis are signal isointensity on T1-weighted images and hypointensity on T2-weighted images, in comparison with the signal intensity in skeletal muscle. Moreover, with an intravenously administered MR contrast medium, the lesion in progressive massive fibrosis appears peripherally enhanced more frequently than not. Thus, the signal intensity manifested on T2-weighted images provides a clue for the differentiation of lung cancer from progressive massive fibrosis. When a mass lesion is depicted with high signal intensity on T2-weighted MR images, the finding is highly suggestive of lung cancer, and histopathologic analysis should be performed for diagnosis. PET is useful for distinguishing benign abnormalities from malignancies, but its role in the diagnosis of malignancy in the setting of pneumoconiosis remains unclear. Intensive uptake of FDG may occur in the fibrotic mass in progressive massive fibrosis, and the observation of resultant mass enhancement on images may

lead to confusion of progressive massive fibrosis with lung cancer.

Symptoms:

- Cough  Chest pain  Breathing problems  Breathlessness  Bronchitis  Cyanosis

 Progressive lung stiffening

 Shortness of breath

 Impaired lung functions

 Breathing difficulty

-Black lung is actually a set of conditions and until the 1950s its dangers were not well understood. The prevailing view was that silicosis was very serious but it was solely caused by silica and not coal dust. The miners' union, the United Mine Workers of America, realized that rapid mechanization meant drills that produced much more dust, but under John L. Lewis they decided not to raise the black lung issue because it might impede the mechanization that was producing higher productivity and higher wages. Union priorities were to maintain the viability of the long-fought-for welfare and retirement fund, and that required higher outputs of coal. After the death of Lewis, the union dropped its opposition to calling black lung a disease, and realized the financial advantages of a fund for its disabled members.

In the Federal Coal Mine Health and Safety Act of 1969, the US Congress set up standards to reduce dust and created the Black Lung Disability Trust. The mining companies agreed to a clause, by which a ten-year history of mine work, coupled with X-ray or autopsy evidence of severe lung damage, guaranteed compensation. Equally important was a "rate retention" clause that allowed workers with progressive lung disease to transfer to jobs with lower exposure without loss of pay, seniority, or benefits. Financed by a federal tax on coal, the Trust by 2009 had distributed over $44 billion in benefits to miners disabled by the disease and their widows. A miner who spent 25 years in underground coal mines has a 5–10% risk of contracting the disease.

Diagnosis:

-There are three basic criteria for the diagnosis of CWP: 1. Chest radiography consistent with CWP

2. An exposure history to coal dust (typically underground coal mining) of sufficient amount and latency

3. Exclusion of alternative diagnoses (mimics of CWP)

Symptoms and pulmonary function testing relate to the degree of respiratory impairment, but are not part of the diagnostic criteria. As noted above, the chest X-ray appearance for CWP can be virtually indistinguishable from silicosis. Chest CT, particularly high-resolution scanning (HRCT), are more sensitive than plain X-ray for detecting the small round opacities.

4. Stannosis

Stannosis is a condition in which tin-oxide is deposited in the lung tissue after inhalation. It was first recognised in Germany during the Second World War.

Occupational stannosis in non-mining industry may occur with earth tinning where molten tin is poured into heated iron hollow-ware or articles are dipped by hand into molten tin to coat them.

Grinding, briquet-making, smelting and casting of tin, as well as the handling of tin-oxide in industry may cause stannosis. Stannosis in tin mines is caused by the process of bagging where highly concentrated (70%-80%) tin-oxide is packaged for transport into a tin smelter and is a very dusty occupation. Cut-surface of the lungs reveals numerous tiny (1mm-3mm), grey-black dust macules, soft to touch and not raised above the cut-surface of the lung. Macrophages containing tin-oxide dust particles are present in alveolar walls and spaces, perivascular lymphatics and interlobular hilar nodes. There are no symptoms and abnormal physical signs due to the inhalation and retention of tin-oxide dust. Lung function is unaffected. Radiologically, it presents with numerous small, very dense opacities scattered evenly throughout the lung fields and may even be somewhat larger at 2mm to 4mm diameter and more fluffy or irregular in outline than those of Siderosis. Kerley’s lines are often clearly defined and dense linear opacities are seen in the upper lung zones.

5. Baritosis

Baritosis, a benign type of pneumoconiosis, is caused by long-term exposure to barium dust. It was first described by Fiori in Italy. Inhaled particulate matter remains in the lungs for years without producing symptoms, abnormal physical signs or interference with lung function. Owing to the high radio-opacity of barium, the discrete

shadows in the chest radiograph are extremely dense. The discrete opacities in baritosis clear slowly over the years.

6. Siderosis

Siderosis (buffer‘s lung or silver polisher’s lung) is a non-fibrogenic or a “benign” form of pneumoconiosis due to inhalation of iron particles. It is caused by the accumulation of iron oxide in macrophages within the lung.2 Dust or fumes of metallic iron oxide encountered in various processes like iron and steel rolling mills, steel grinding,

electric arc welding, silver polishing, mining and crushing iron ores are responsible for producing this kind of pneumoconiosis. It is observed most commonly in workers exposed to metal fumes during welding, and thus, is also known as welder siderosis or arc welder pneumoconiosis. Doig and McLaughlin first described ‘welders’ siderosis in 1936 when they carried out a prospective study examining the clinical and chest radiological characteristics of 16 electric arc welders. Though non-fibrogenic fibrosis is seen in some occasionally and is likely due to associated silica exposure causing silicosiderosis. Pathologically, the cutsurface of the lung reveals grey to brown coloured

macules from 1mm to 4mm in diameters and these do not stand up from the surface. These are evenly distributed and can regress. Microscopically, the lesion consists of a perivascular and peribronchiolar aggregation of dark pigmented iron oxide particles present in macrophages and alveolar spaces and walls. Slight reticulin proliferation may be present diseases as severe as that related to smoking. The chest radiograph

shows a variable, usually, large number of small nodular opacities varying from 0.5mm to 2mm in diameter with fine linear opacities. Kerley’s B lines may be present in some patients

caused by the accumulation of iron in interlobular septa. The hilar nodes may appear unusually radiopaque due to the concentrated iron content; but these are not enlarged. The HRCT shows widespread, ill-defined, small centrilobular nodules and, less commonly, patchy areas of ground-glass attenuation without zonal predominance. Emphysema is often seen. After cessation of exposure, the iron dust is slowly eliminated from the lungs over a period of years. This results in the partial or complete disappearance of radiographic opacities

7. Talcosis

Talc is a mineral widely used in the ceramic, paper, plastics, rubber, paint, and cosmetic industries. Talcosis, a granulomatous inflammation of the lungs caused by inhalation of talcum dust, is a rare form of silicate induced lung disease. Thorel reported the first case of talc pneumoconiosis in 1896. Talc has been recognised as a cause of pneumoconiosis in miners, millers, rubber workers.31 Talc exposure may occur as a result of inhalation or by intravenous administration. Three forms of talc pneumoconiosis by inhalation have been described in the literature: talc asbestosis, talc silicosis, and talcosis. Patients often present with isolated, non-specific symptoms of progressive exertional dyspnoea or cough. Histologically, it causes non-necrotising granulomatous inflammation characterised by the formation of foreign body granulomas of varying degree within a fibrotic stroma. These granulomas are composed of free or intracellular birefringent deposits accompanied by multinucleated giant cells. These may also appear ill defined with only few surrounding histiocytes. The distribution of these lesions is variable and these may develop in intraand peri-vascular areas as well as in the interstitium.32 Chest radiography shows micro nodular patterns of diffuse or well-defined nodules that may fuse with progression to form larger opacities in the perihilar regions. The HRCT findings of small centrilobular nodules associated with heterogeneous conglomerate masses containing high-density amorphous areas, with or without panlobular emphysema in the lower lobes, are highly suggestive of pulmonary talcosis. Interstitial thickening and lower-lobe emphysema may also be present.

8. Berylliosis

Berylliosis, or chronic beryllium disease, is a chronic allergic-type lung response and chronic lung disease caused by exposure to beryllium and its compounds. Acute beryllium disease causes nonspecific inflammatory reaction. Exposure to beryllium occurs in a variety of industries, including aerospace, ceramics, dentistry and dental supplies, nuclear weapons etc.34 Beryllium exposure can lead to an acute chemical pneumonitis and a chronic granulomatous disease. Histologically, chronic

beryllium disease may mimic sarcoidosis. The chest radiograph shows hilar lymphadenopathy and increased interstitial markings. On HRCT, the most common findings are parenchymal small nodules that are often clustered around the bronchi, interlobular septa, or in the subpleural region where the nodules may form pseudoplaques and interlobular septal thickening. Ground-glass opacities, honeycombing, conglomerate masses, bronchial wall thickening and hilar or

mediastinal lymph nodes with amorphous or eggshell calcification may also be seen. Blood beryllium lymphocyte proliferation test (BeLPT) currently is the test of choice to identify beryllium workers who develop beryllium sensitisation or chronic beryllium disease.

9. Mixed-dust Fibrosis

Clinical diagnosis of mixed-dust fibrosis requires the exclusion of other well-defined pneumoconiosis. Mixed-dust pneumoconiosis is defined as a pneumoconiosis caused by concomitant exposure to silica and less fibrogenic dusts, such as iron, silicates and carbon. The silica is usually at a lower concentration than what causes silicotic nodules to occur. Microscopically, a stellate shape characterises the mixed-dust fibrotic nodule and has a central hyalinised collagenous zone surrounded by linearly and radially arranged collagen fibers admixed with dust-containing macrophages. Generally, as the proportion of silica increases, the number of silicotic nodules increases in proportion to the mixed-dust nodules. The radiological findings of a mixed-dust pneumoconiosis include a mixture of small, rounded and irregular opacities. Honeycombing is also seen. Similar radiological changes were described earlier as ‘Transkei silicosis’ in females in Transkei region of South Africa by Palmer where maize is ground using silica containing rocks. Subsequently the term ‘hut lung’ was coined by Grobbelaar and Bateman in patients exposed to components of organic maize and biomass fuel with non-quartz containing dust for cooking in poorly ventilated room. Sundaram et al described cases of mixed-dust fibrosis that occurred in the setting of poorly ventilated flour mills where various kinds of grain, chiefly wheat, were ground using stones containing greater than 80% silica and proposed the term ‘Flour mill lung’ for this form of pneumoconiosis.

Measures to prevent Pneumoconiosis:

-It is unlikely that it is possible to entirely prevent any instance of a worker developing a pneumoconiosis condition if they happen to work in an environment with a high degree of exposure to organ or non-organic dust that is known to cause the condition, however, it is certainly possible to mitigate the possibility of it happening by taking common sense prevention measures such as

 Any worker that is in contact with dust that is known to cause pneumoconiosis conditions should be given a well-fitting facemask.

 The workplace should take whatever steps necessary to try to keep the levels of dust down to a minimum.

 It is important that the workplace environment is ventilated adequately.

 Workers should be made aware of safe procedures with regard to the washing down of dust laden areas and of the removal and washing of clothes that have been exposed to the dust.

 Any part of the body exposed should be cleaned thoroughly and the worker should be mindful that dust should not be transmitted into the mouth by e.g. dust contaminated food, smoking, drinking, taking medicine, etc.

NATIONAL ACTION PLAN FOR THE PREVENTION OF PNEUMOCONIOSES TURKEY

1. Determination of the Importance of the Problem

Pneumoconiosis is one of the most frequently faced occupational lung diseases in Turkey and is known as one of the preventable. It is possible to prevent Pneumoconiosis by the way of effective protection and prevention methods at all steps of occupational health services. Since regular and effective monitoring on occupational health and safety in our country is not be able to be applied, new Pneumoconiosis cases are determined even in coal mining enterprises which are expected to take control against Pneumoconiosis.

In addition, recently silicosis cases have been determined increasingly in the sectors that are not known until today (sandblasting of jeans by sand spraying, glass shaping works etc). Because of the troubles related to occupational diseases notification system in Turkey, diagnosis of the pneumoconiosis cases is relatively low in the records as other occupational diseases. Thus, when the non-notified pneumoconiosis cases are taken into account, the importance of the pneumoconiosis can be understood clearly for our country. Therefore, there is a need for an immediate action plan.

In the intervention process, the pilot works should be started immediately in the determined sectors. With this, in the risky sectors pneumoconiosis frequency and its effects will be presented, moreover assessment of working environment with respect to pneumoconiosis and formation of thought about the health surveillance of the workers, review of legal processes and gathering information for necessary arrangements will be possible.

2. Taking account the socio-economical situation in the country

Pneumoconiosis that causes occupational diseases and the high mortality rates results both societal problems, high costs of treatment and compensatory and the loss of the workforce, so that it generally affects manufacturing process and working peace in the country.

Therefore, by means of through serious measures which will be realized it will be primarily ensured for employees to participate to production actively and also the costs of the treatment and compensatory will be minimized.

3. Determination of employees working under risk

Some sub-sectors based on mining (rock, soil, clay, sand etc.) are very common in our country. Like the other sectors in our country, majority of the firms in this sector are small sized enterprises. Health risks caused by global problems in the small sized enterprises are shown even greater in our country. The limited numbered epidemiological studies made in this field shows that the risk of pneumoconiosis is significantly high among the workers in this sector.

The improvement of national pneumoconiosis control program will be progressed more efficiently via the assessment of the official data by Occupational Health and Safety Centre (İSGUM) to determine risk containing sectors and population working under risk in order to establish a base for national scaled activities which will be planned.

4. Determination of prevention strategies

For this purpose the following measures should be taken:

 The necessary changes should be done in the regulation of dust control,

 Determination and monitoring of the fields in which the fibrinogen minerals are used.

 Making the inspection more effective by taking the prevention culture in to account especially in the establishing phase of workplaces.

 Enabling the workplace audits by notification of the index cases to Ministry of Labour and Social Security (MoLSS).

 Enabling the participation of the social parts.

5. Determination of participants that the cooperation will be done by the

institutional frame 1

 Ministry of Labour and Social Security

 Ministry of Health

 Ministry of Energy and Natural Resources

 Ministry of Industry and Trade

 Ministry of Environment and Forestry

 Employees’ and employers’ organizations

 Universities (related departments of medicine and engineering)

 Related organizations of occupation and expertise (TTB, TMMOB, Thorax Assoc., Radiology Assoc, etc)

 Related non-governmental organizations (T.HASAK, HASUDER etc)

 ILO Turkey Office

6. Fields that have priority for implementing the program and embody the

activity

Priority having pilot working fields that are planned for the implementation of the program are predicted as follows:

 Workplaces that uses asbestos in manufacturing,

 Sandblasting and grinding workplaces in which quartz is used.

7. Criteria of implementation and evaluation of pilot working

- Determination of the workplaces and population that are under pneumoconiosis risk, - Enabling workers have chest radiography taken,

- Searching of personal and occupational histories of workers,

- Realizing inhalable dust concentration measurements in the workplaces according to standard which will be defined,

- In the scope of project, formation of regional working groups who will be responsible for examination of lung radiography and assessment of workplaces, - Assessment of lung radiography according to the Regulation for Dust Control, - Displaying the relation between dust level and personal health status statistically, - Determination of the frequency of prevalence of pneumoconiosis,

- Monitoring of hospitalization chain for suspicious pneumoconiosis facts, - Evaluation of confirmed pneumoconiosis cases from the insurance aspect, - Presentation of reports of the pilot working to related parts,

- Preparation of diagnosis guides for pneumoconiosis,

- Training of employees, employers, occupational physicians and safety experts, - Performing technical activities in order to assess and activate the methods for dust control.

8. In the guidance of the international standards reassessment of the national standards

It will be arise as an expected result of the action plan

8. Associate with the saving of the environment

1 Informing the related parts about the regulation in this field,

2 Ensuring scientific and technological information support for the waste management of the each enterprise and making the necessary arrangements

10. Monitoring the implementation

1

2 Enabling annual controls of the working environment according to standards in the pilot work,

3 Monitoring health records and radiological assessments of workers in the context of periodical examination according to the Regulation for Dust Control,

4 Monitoring the performance of the readers for evaluation of chest radiography, organizing and maintaining of certificate and re-certificate training programs.

11. Expected results

11.1. Short term (until year 2008)

 Identification of the pneumoconiosis frequency and the factors affecting this in the sectors of pilot working,

 Initiating foundation of pneumoconiosis monitoring unit under Directorate General of Occupational Health and Safety (DGOHS),

 Preparation of pneumoconiosis diagnosis guide,

 Increasing the awareness of pneumoconiosis among physicians,

 Performing the legal arrangements for authorization of health service suppliers for setting occupational diseases-pneumoconiosis diagnosis.

 Completion of establishment of the pneumoconiosis monitoring unit under DGOHS,

 Determination of the workplace environment assessment standard,

 Review of present acceptable dust concentration level via presenting the pneumoconiosis development trend,

 Realization of the occupational physician training on pneumoconiosis diagnosis guide,

 Increasing the social awareness on the subject,

 Monitoring the implementation and review of the legal arrangements for authorization of health service suppliers for setting occupational diseases-pneumoconiosis diagnosis.

 Presenting necessity of pneumoconiosis diagnosis and of update of insurance assessment processes and realization of necessary arrangements according to evidence,

 Review of disability criteria of the pneumoconiosis detected cases according to modern norms and presentation of prepared proposal to MoLSS,

 Spreading of the readers’ training according to ILO standards,

 Monitoring detected pneumoconiosis cases and searching for rehabilitation possibilities.

11.3 Long Term (until year 2015)

1

 Identification of the workplaces that have risk of pneumoconiosis in the country and assessment of the working environment in these workplaces and development of a structure for monitoring worker health surveillance,

 Foundation of the real pneumoconiosis database in Turkey,

 Increasing the number of the readers and upgrading of the reader standards to international level,

Medical examinations done for dust related

issues:

-Centre of Clinical Research Excellence into Asbestos-Related Disease

In January 2009, the Australian Government announced that from 2010, $4.5 million would be directed to support world-class research into Asbestos Related Diseases In July 2010, the National Centre for Asbestos-Related Diseases was awarded $4.5 million over five years to further the centre’s research focusing on improving diagnosis, early intervention strategies and improving treatment of asbestos-related diseases.

Existing research centres who work on asbestos related diseases will be able to apply for this funding. This funding will be part of NHMRC's Centres of Research Excellence scheme.

National Centre for Asbestos-Related Diseases (NCARD)

The National Centre for Asbestos Related Diseases (NCARD) is a collaboration of researchers across Australia, with a national and strategic focus into asbestos related diseases and cancers. NCARD provides a platform to build on Australia’s existing research expertise and encourages strong organisational linkages to ensure our research is systematic and complementary to existing research efforts in the area of asbestos related diseases.

Through NHMRC, $6.2 million was provided to set up the NCARD collaboration, with $5.8 million of this allocated in a competitive grants process to 11 research centres across Australia, including the University of Western Australia, Peter MacCallum Centre in Victoria, James Cook University in Queensland, and The Prince Charles Hospital in Queensland. The remaining $0.4 million has been used to support NCARD at the University of Western Australia to administer and coordinate the research network.

NCARD’s research projects include:

 A study of epidemiology and community consequences of asbestos exposure.  The development of sensitive serum markers for improved diagnosis,

 An investigation of the importance of specific genes in asbestos-related disorders and their relationship to environmental factors.

 The development of a national resource for mouse models, to help understand the disease in humans and provide essential data for clinical trials.

 An investigation of mechanisms to inhibit the body’s collagen production to slow growth in malignant mesothelioma tumours.

 A combination of conventional therapies with immuno/gene therapies that encourage the body’s own anti-cancer immune responses.

 An investigation of ways to improve the ability to measure patient responses to chemotherapy treatment.

 An examination of chromosomal changes in cancer cells to help improve the early detection of mesothelioma.

 The development of a sustainable community-based response to asbestos-related disease in Aboriginal communities.

 A study of people with chronic obstructive pulmonary disease who were formerly exposed to asbestos and cigarette smoke.

Research past, present, and future

Each of the occupational diseases begins with the inhalation of disease-inducing particles. Therefore, the main goals have been to identify and regulate the industries that generate these particles on one hand and to determine ways to prevent or minimize their inhalation on the other. In dealing with silica, coal, and asbestos, the significant latency period between exposure and diagnosis makes it difficult to determine dose–response relationships.

There is no treatment for any of the occupational diseases that can reverse the damage already done. However, for those who were or continue to be exposed, the search for treatments must continue. Early reports of gene therapy resulting in anti-tumor responses may hold promise for those with mesothelioma. Research in pulmonary fibrosis may be applicable to asbestosis in the future. Inthe case of HP, early research was based on observation and the discovery of the causative antigens, the removal of which improved symptoms. Studying the patient’s serum allowed the discovery of antibodies that reacted with the specific antigen (precipitins). It is still not possible to predict who will develop HP, which antigens set up the inflammation, and how or in whom the disease will progress, but there are reasons to hope. Certain genetic predispositions have been discovered, and recent studies in the mouse have shown that certain cells and their signalling cytokines are important in the pathogenesis of HP.