Preceptors: Prof. Randeep Guleria Dr. Anant Mohan Speaker: Dr. Prajwol Shrestha.

Preceptors: Prof. Randeep Guleria Dr. Anant Mohan Speaker: Dr. Prajwol Shrestha

Seminar Outline Introduction Outdoor and Indoor air pollution Lung disease associated with air pollution Classification of occupational and environmental lung diseases Highlights on environmental and occupational lung diseases Prevention of environmental and occupational lung disease Summary/Conclusion

 Lung represent the major interface between humans and their environment  Consequently, the lungs are a common site of environmentally induced disease.

Thousands of environmental toxins and commercials are in use in the form of fibers,fumes,mist or dust. Inhabitants of major metropolitan areas inhale more than 2 mg of dust each day and workers in dusty occupations inhale up to 100 times that amount.

Air pollution Sulfur Dioxide Particulate matter Carbon monoxide Ozone Nitrogen dioxide and other nitrous oxide Lead Hydrocarbon

Classification of Ambient Air pollutants: Suspended particulate Matter: -SPM, PM 10, PM 2.5, PM 1.0 - Diesel Exhaust -Coal fly ash -Mineral dust -Metal dust and fumes -Acid mists -Paint pigments -Pesticide mist -Oil smoke Gaseous pollutants: -Sulphur dioxide SO 2 -Carbon monoxide CO -Nitrogen oxides NO 2 -Ammonia NH 3 -Hydrocarbons HC -Volatile organic compounds VOC -Polycyclic Aromatic Hydro compounds PAH -Halogen compounds HF,HC

Sources of Air pollution: Stationary: Public power production Small combustion Industrial Combustion Production processes Fossil fuel extraction/distribution Solvent production/use Waste treatment/disposal Agriculture Mobile: Road transport ( Automobile, vehicles)

Air Pollution levels and trends in developed countries: SO 2,SPM, PM 10 : decreasing or often below WHO AQG NO X and O 3 : constant or increasing often above WHO AQG Air pollution and environmental health ; Mark D. Sobsey ENVR890 spring 2007, WHO Geneva

Air Pollution levels and Trends in developing countries: SO 2,SPM,PM 10 : Constant or increasing NOx,O 3 : Increasing by 5-10% annually High SO 2 and PM concentrations in Indian and Chinese cities, and in dry season in Kathmandu, Nepal; High levels of O 3 in New Delhi and Mexico city. Air pollution and environmental health ; Mark D. Sobsey ENVR890 spring 2007, WHO Geneva

Air pollution and human health 1200 million people are globally exposed to excessive level of SO 2 SO 2 and SPM outdoor concentrations cause about 500000 excess death SPM indoor concentrations cause about2.5 million excess death Excessive levels of CO levels in half of the World’s cities. Air pollution and environmental health ; Mark D. Sobsey ENVR890 spring 2007, WHO Geneva

Major Air pollutants and their effects in Respiratory system: Agents Acute effects from high exposure Chronic effects from low exposure Nitrogen Oxide Cough, Dyspnea, Pulmonary edema, Bronchiolitis obliterans Emphysema, chronic bronchitis, reduced lung function OzoneMucous membrane irritation, pulmonary hemorrhage and edema, Among children: Increased hospitalization during summer haze Chronic eye irritation and cardiopulmonary morbidity/ mortality SO 2 Mucus membrane irritation, Epistaxis Chronic bronchitis Environmental tobacco smoke and Diesel exhaust Mucus membrane irritation, Cough, Dyspnea Chronic bronchitis, COPD, fibrosis and 3-10% of all the lung cancers.

Indoor Air Pollution

Air pollution not only the contamination of urban air from automobile exhausts and industrial effluents. In developing countries, the problem of indoor air pollution far outweighs the ambient air pollution. There are four principal sources of pollutants of indoor air : (i) Combustion, (ii) Building material, (iii) The ground under the building, and (iv) Bioaerosols.

Trends of Indoor air pollution Developed countries: - Radon, asbestos, volatile organic compounds, pesticides, heavy metals, animal dander, mites and moulds, and environmental smoke. Developing countries: - unprocessed solid biomass fuels used by the poor urban and rural folk for cooking and heating.

Indoor Air Pollution Half the world’s population and 90% of rural households in developing countries rely on unprocessed biomass fuels like wood, dung and crop residues. World Health Organization (WHO) rule of 1000 - a pollutant released indoors is one thousand times more likely to reach people’s lung than a pollutant released outdoors.

Half a million women and children die each year from indoor air pollution in India. India has among the largest burden of disease due to the use of dirty household fuels and 28% of all deaths due to indoor air pollution in developing countries occur in India. World Resources Institute, United Nations Environment Programme, United Nations Development Programme and World Bank,. 1998-99 World Resources: A Guide to the Global Environment. Oxford University Press, Oxford, 1998-99. Health and Environment in Sustainable Development. Five Years After the Earth Summit. World Health Organization, Geneva,p.84, 1997. Smith, K.R. Indoor air pollution implicated in alarming health problems. In: Indoor Air Pollution – Energy and Health for the Poor. Newsletter published by World Bank, p.1, 2000.

Energy ladder The type of fuels used by a household is determined mainly by its economic status.

What is the problem? Some 3 billion people rely on solid fuels (e.g. dung, wood, agricultural residues, charcoal, coal). Cooking and heating with solid fuels leads to high levels of indoor smoke that contains small particles, carbon monoxide, nitrogen oxides.

In India Use of traditional biomass fuels- Wood, dung, and crop residues—is widespread in rural India. 86 percent of rural households and 24 percent of urban households rely on biomass as their primary cooking fuel. NSS 2000:India

Major Air Pollutants Released From Biomass Combustion Cooking food on the unprocessed solid fuels release at least 50 times more noxious pollutants than gas. The stoves or chullah used for cooking are not energy efficient- The fuels are not burned completely. The incomplete combustion of biomass releases complex mixture of suspended particulate matter, carbon monoxide, poly organic material (POM), poly aromatic hydrocarbons (PAH), formaldehyde, etc. Smith, K.R. Indoor air quality and the population transition. In: Indoor Air Quality. Ed. H. Kasuga. Springer Verlag, Berlin, p.448, 1990.

Toxic pollutants from biomass combustion and their toxicological characteristics

Health effects of exposure to smoke from solid fuel use: Health Outcome Population affected Relative Risk (Low) Relative Risk (High) Strength of evidence Acute lower respiratory infections (ALRI) <5 years 2.0 3.0Strong Asthma Females ≥15 years 1.4 2.5Intermediate/ moderate Chronic obstructive pulmonary disease (COPD) Females ≥15 years 2.0 4.0Strong Lung cancer (coal only) Females ≥15 years 3.0 5.0Strong Tuberculosis Females ≥15 years 1.5 3.0Intermediate/ moderate Source: Adapted from Smith 2000

Lung diseases associated with Air Pollution Acute lower respiratory tract infections Chronic Obstructive pulmonary Disease Pneumoconiosis Lung Cancer Pulmonary Tuberculosis

Acute lower Respiratory Tract Infection Acute respiratory infections (ARIs) are the single most important cause of mortality in children aged less than 5 years, accounting for around 3-5 million deaths annually in this age group. Many studies in developing countries have reported on the association between exposure to indoor air pollution and acute lower respiratory infections. Stansfield, S. and Shepherd, D. Acute respiratory infection. In: Disease Control Priorities in Developing Countries. Eds. D. Jameson, W. Mosle, A. Mesham and J. Bobadilla. Oxford University Press, Oxford, p.67, 1993. Robin, L.F. Less, P.S.J. Winger, M., Steinhoff, M., Moulten, L.H., Santoshom, M. and Correa, A. Wood- burning stoves and lower respiratory illness in Navajo children. Paediatr Infect Dis J 15: 859, 1996.

The studies on indoor air pollution from household biomass fuel show a significant increase in risk for exposed young children compared with those living in households using cleaner fuels or being otherwise less exposed. Younger children (<5 years) are affected more because they spend more time in indoor with their mother. Smith, K., Samet, J.M., Romieu, I. and Bruce, N. Indoor air pollution in developing countries and acute respiratory infections in children. Thorax 55: 518, 2000.

Chronic obstructive pulmonary disease In developed countries, smoking is responsible for over 80% of cases of chronic bronchitis and for most cases of emphysema and chronic obstructive pulmonary disease. In developing country like India the incidence of COPD is similar in men and women despite the fact that 75% of the men and only 10% women are smokers. COPD is more common in younger women COPD develops 10-15 years earlier in women. Padmavati, S. and Pathak, S.N. Chronic cor pulmonale in Delhi. Circulation 20: 343, 1959. Padmavati, S. and Joshi, B. Incidence and etiology of chronic cor pulmonale in Delhi: A necropsy study. Dis Chest 46: 457, 1964.

The prevalence of chronic cor pulmonale was lower in the southern states than the northern states of India. This is attributed to domestic air pollution as a result of the burning of solid biomass fuels leading to chronic bronchitis and emphysema which result in chronic cor pulmonale. Malik, S.K. Exposure to domestic cooking fuels and chronic bronchitis. Indian J Chest Dis Allied Sci 27: 171, 1985. Behera, D., Jindal, S.K. and Malhotra, H.S. Ventilatory function in nonsmoking rural Indian women using different cookingfuels. Respiration 61: 89, 1994.

Numerous studies from other countries like Saudi Arabia, Columbia, Mexico and Nepal have reported on the association between exposure to biomass smoke and chronic bronchitis or chronic obstructive pulmonary disease. Master, K.M. Air pollution in New Guinea. Cause of chronic pulmonary disease among stone-age natives in the highlands. J Am Med Assoc 228: 1635, 1974. Pandey, M.R. Prevalence of chronic bronchitis in rural community of the hill region of Nepal. Thorax 39: 331, 1984. Pandey, M.R. Domestic smoke pollution and chronic bronchitis in a rural community of the hill region of Nepal. Thorax 39: 337, 1984. Norboo, T. Domestic pollution and respiratory illness in a Himalayan village. Int J Epidemiol 20: 749, 1991.

Pneumoconiosis Pneumoconiosis is a disease of industrial workers occupationally exposed to fine mineral dust particles over a long time. Pneumoconiosis has been seen in people who are not occupationally exposed to the mineral dust particles and people who live far away from the industries and mines. Cases of respiratory morbidity whose radiological picture resembled pneumoconiosis have been reported in Ladakh.

Two factors considered responsible for the development of this respiratory morbidity: (i) Exposure to dust from dust storms. (ii) Exposure to soot – due to the severe cold in Ladakh, ventilation in the houses is kept at a minimum. Saiyed, H.N., Shrma, Y.K., Sadhu, H.G., Norboo, T., Patel, P.D., Venkaiah, K. and Kashyap, S.K. Non-occupational pneumoconiosis at high altitude villages in central Ladakh. Br J Industr Med 48: 825, 1991. Saiyed, H.N., Sharma, Y.K., Norboo, T., Sadhu, H.G., Majumdar, P.K. and Kashyap, S.K. Clincio- radiological and PFT profile in non-occupational pneumoconiosis. Indian J Industr Med 38: 148, 1992.

Lung Cancers Smoking is a major risk factor for lung cancer. About two-thirds of the lung cancers were reported in nonsmoking women in China, India and Mexico. The link between lung cancer in Chinese women and cooking on an open coal stove has been well established.

The smoke from biomass fuels contain a large number of compounds such as poly aromatic hydrocarbons, formaldehyde, etc. known for their mutagenic and carcinogenic activities. Smith, K.R. and Liu, Y. Indoor air pollution in developing countries In: Epidemiology of Lung Cancer. Lung Biology in Health and Disease. Ed. J Samet. Marcel Dekker, New York, p.151,1993. Mumford J.L. Human exposure and dosimetry of polycyclic aromatic hydrocarbons in urine from Xuan Wei, China with high lung cancer mortality associated with exposure to unvented coal smoke. Carcinogenesis 16: 3031, 1995. Gupta, R.C. Primary bronchogenic carcinoma: Clinical profile of 279 cases from mid-west Rajasthan. Indian J Chest Dis Allied Sci 40: 109, 1998.

Tuberculosis Exposure to smoke interferes- (i) mucociliary defences of the lungs and (ii) decreases several antibacterial properties of lung macrophages, such as adherence to glass, phagocytic rate and the number of bacteria phagocytosed. Chronic exposure to tobacco smoke also decreases cellular immunity, antibody production and local bronchial immunity, and there is increased susceptibility to infection and cancer.

Mishra et al reported the association between use of biomass fuels and pulmonary tuberculosis on the basis of analysis of data collected on 260,000 Indian adults interviewed during the 1992-93 National Family Health Survey. Persons living in households burning biomass fuels were reported to have odd ratio of 2.58 (1.98-3.37) compared to the persons using cleaner fuel. smoking has been identified as a risk factor in causation of tuberculosis. Mishra, V.K., Retherford, R.D. and Smith K.R. Biomass cooking fuels and prevalence of tuberculosis in India. Int J Infect Dis 3: 119, 1999. Gajalaxmi et al. Lancet 2003; 362:507-15

Occupational Lung Disease

Introduction Occupational lung diseases may arise from a vast array of exposures, representing every major category of toxins (natural) and toxicants (synthetic). They fall along a continuum of several pathological processes. Severity and onset of symptoms dependent on length and types of exposures and associated with individual risk factors.

Classification of Occupational and Environmental lung Disease: Airway Disease Occupational Asthma Industrial Bronchitis Byssinosis Reactive airway dysfunction syndrome Parenchymal Lung Disease Asbestosis Silicosis Coal worker’s pneumonia Mixed Airway and Parenchymal Disease Hypersensitivity pneumonitis Bronchiolitis Berylliosis Neoplastic Disease Bronchogenic Carcinoma Mesothelioma

Categories of Occupational exposure and Respiratory conditions Inorganic DustsRespiratory Responses Asbestos: Mining, construction, ship-repair Fibrosis(Asbestosis), Pleural disease, Cancer, Mesothelioma Silica: Mining, Stone cutting, Sand blasting, quarrying Fibrosis(Silicosis), PMF, Cancer, Silicotuberculosis, COPD Coal Dust: MiningFibrosis(Coal worker pneumoconiosis), PMF, COPD Beryllium: processing alloys for high-tech industries Acute pneumonitis, chronic granulomatous disease, lung cancer Others metals: Al, Cr, Co, Ni etc Acute pneumonitis to asthma and lung cancer.

Organic DustsRespiratory Responses Cotton dust: Milling, processingByssinosis, Chronic bronchitis, COPD Grain Dust: Dock workers, milling and bakers Asthma, chronic bronchitis, COPD Agricultural dust: Fungal spores, vegetable products, insect fragments, animal dander, bird droppings, pollens etc. Hypersensitivity pneumonitis (farmer’s lung), Asthma and chronic bronchitis Toxic chemicals: Acid fumes, ammonia, formaldehyde, hydrogen sulfide, Isocyanides, Phosgene Mucous membrane irritation, Cough, dyspnea, pulmonary edema, COPD, hypersensitivity pneumonitis and cancer Other: Uranium and radon, Environmental tobacco smoke, PHC, biomass fuels and diesel exhaust. Chronic bronchitis, COPD, fibrosis and 3-10% of all lung cancers. In-door exposure important in developing countries

Pathophysiology Factors for Development of Environmentally induced lung disease Physical state and Toxicity of Inhaled Substance Intensity and duration of exposure Susceptibility of Host

Physical state and Toxicity of Inhaled Substance Physical State: Solid (Silica, Asbestos) Fume (Toxic Gases) Mixture

Solubility Water Soluble - Ammonia - SO 2 Absorbed in the lining fluid of the upper airway Upper airway irritation Bronchoconstriction Water Insoluble -Phosgene -NO 2 Penetrate to the bronchioles and alveoli Acute Chemical pneumonitis ARDS Pulmonary edema

Particle size >10-15µm<10µm Do not penetrate the upper air way Deposited below the Larynx 2.5-10µm0.1-2.5µm<0.1µm Silica, Aluminum, Iron Deposit high in tracheo bronchial tree Most of the toxic agents Carried to the lower airways Ultrafine fraction Largest No. of particles Remain in the airstream Deposited in Alveolar walls

Individual risk factors Genetic tendencies to inflammation and fibrosis Ability to clear substances from the lower respiratory tract Co-existing pulmonary disease Smoking

Intensity and Duration of exposure Diseases are more likely to develop if: - Exposure to highly concentrated environment. - During Strenuous labor - When mouth breathing is more likely - Exposure in closed rather than open working environment

Duration Acute Edema and inflammation in respiratory tract Chronic Fibrosis and Granuloma formation

General principles of Diagnosis A relevant exposure History Definitive Diagnosis of a specific type of lung Disease Reported evidence supporting an association between the exposure and the disease process

Exposure Assessment Job process Known toxic exposures Degree of exposure Temporal relationship between exposure and symptoms Use of respiratory protective equipment The Goal of the exposure history is to establish a list of agents that could potentially cause or exacerbate lung disease

Identification Of Specific Disease Pulmonary Function test: - Essential for characterizing the functional correlates of lung disease - Non-specific in regard to etiologic diagnosis Chest X-ray: - Cornerstone of diagnostic testing for the pneumoconiosis - Neither sensitive nor specific - 15-20% of patients with pathologic evidence of asbestosis, the chest x-ray appears normal. Epler GR, Mcloud TC, Gaensler EA,et al: Normal Chest roentgenograms in chronic diffuse infiltrative Lung disease. N Engl J Med 298:934, 1978

International Labour Organization (ILO) Classification of Radiographs of Pneumoconiosis: Small rounded opacities - Silicosis - Coal worker’s Pneumonia Small linear opacities - Asbestosis

Conventional CT and High resolution CT: - High sensitivity of identifying diffuse Parenchymal abnormalities as well as pleural thickening. AsbestosisPleural plaque in AsbestosisAdvanced coal worker’s Pneumoconiosis

Other Important Tests Urine Test: Cadmium in battery plant workers Skin prick test or specific IgE titers: Occupational Asthma in (flour antigen in bakery workers) Specific IgG precipitating antibody titers: Hypersensitivity Pneumonitis (Pigeon antigen in bird handlers)

Bronchoscopy with bronchoalveolar lavage and transbronchial biopsy for histological diagnosis: Chronic beryllium disease Video-assited thoracoscopic surgery for a larger sample of lung tissue: Hypersensitivity pneumonitis or Giant cell interstitial pneumonitis due to Cobalt exposure.

Occupational Airway Disease Occupational Asthma Industrial Bronchitis Byssinosis Reactive airway dysfunction syndrome

Asthma Increased responsiveness of the tracheobronchial tree to multiple stimuli. Widespread narrowing of the air passages; relieved spontaneously or as a result of therapy- Reversible. Dyspnea, cough, and wheezing. Acute exacerbations interspersed with symptom-free periods.

Spirometry patterns Normal Obstruction Restriction

How much adult asthma is occupationally related? Attributable risk estimates (median) ◦ All studies 9%(IQI: 5%-19%) ◦ Published AR 9% ◦ Derived AR25% ◦ Highest scores (n=12)15% ◦ Conclusion: "About 1 in 10 cases" Blanc PD. Am J Med 1999; 107: 580

Occupational Asthma Physician diagnosis of asthma. Onset of asthma after entering the workplace. Association between symptoms and work. One or more of the following: ◦ (Workplace exposure to agent known to give rise to OA). ◦ Work-related changes in FEV1, PEF, or bronchial responsiveness.(15% change) ◦ Positive response to specific inhalation challenge. ◦ Onset of asthma clearly associated with symptomatic exposure to an inhaled irritant agent in the workplace.

Occupational Asthma: Management Standards medical Treatment: - Inhaled β- agonist - Inhaled or oral corticosteroids - Anticholinergic - Cromolyn sodium - Leukotriene antagonist Emphasis should be placed on Complete avoidance or minimizing further exposure

Industrial Bronchitis Dyspnea and productive cough for at least 3 months each year. Occupational exposure to high concentrations of airborne dust, mixed dust and fumes. Construction and demolition, mining and smelting, fire fighters, food processing and animal confinement. Confounding factor: Cigarette smoking.

Industrial Bronchitis: Minimize exposure to airway irritants. Cessation of smoking Antibiotics Postural drainage.

Byssinosis A form of occupational asthma Related to textile dust ◦ Particularly cotton; also flax, hemp, Jute ◦ Not synthetic fibers Range of respiratory symptoms ◦ Acute, reversible  Chronic obstructive asthma-like symptoms, lung disease 1+ days / week. No characteristic pathologic findings. No characteristic X-ray findings Latency usually 5+ years.

Byssinosis PFT: Less than 60% of expected FEV1 Distinct from other forms of occupational asthma ◦N◦N ot all cases have hyper reactive airways, on non-specific challenge test (eg, methacholine) ◦H◦H igh prevalence ◦S◦S ymptoms commonly worst on first day of work week; and improve during course of week: Monday morning fever Causative agent uncertain ◦E◦E ndotoxin? ◦T◦T annins? ◦O◦O ther biochemical constituent of textile dust?

Reactive Airway Dysfunction Syndrome ◦ No preceding complaints ◦ Onset after a single exposure incident ◦ Exposure to a gas, smoke, fume or vapor with irritant properties; in very high concentrations ◦ Persistent symptoms of asthma: cough, wheeze, dyspnea ◦ Airflow obstruction on PFTs ◦ Nonspecific bronchial hyper-responsiveness ◦ Other pulmonary diseases ruled out

Pathophysiology: - Exact mechanism unknown - May be associated with altered neural tone and vagal reflexes, modified beta-adrenergic sympathetic tone and influences of a number of inflammatory mediators. Management: Inhaled or oral corticosteroids Inhaled bronchodilators Despite the treatment, many patient left with persistent asthma like symptoms and non specific bronchial hyper reactivity.

Occupational Parenchymal Disease Pneumoconioses: Most Important Class of occupational lung disease. Result from Inhalation of and tissue reaction to various naturally occurring or synthetic mineral dust. Account for approximately 14% of the incident cases of Interstitial lung Disease. Coultas DB, Zumwalt RE, Black WC, et al: Am J Respir Crit Care Med 150: 967,1994

Occupational Parenchymal Disease Asbestosis Silicosis Coal worker’s pneumonia

Asbestosis: Exposure to asbestos (Occupational and environmental) constitute the most pervasive of the mineral dust exposure. Worldwide, about 125 million persons are exposed to asbestos at their work place. Many million more have environmental exposure to asbestos from insulation, building products in home, brake and clutch facings and demolition of asbestos containing buildings in urban areas. WHO, Geneva, 2004

Asbestos- what is it ? Asbestos is a group of six separate fibrous mineral silicates. Occurs naturally in many parts of the world. 3 main types: Chrysotile - White Asbestos Amosite – Brown Asbestos Crocidolite – Blue Asbestos Other form: Anthrophyllite, Tremolite, Actinolite Asbestos

Asbestos Products ASBESTOS CEMENT SHEETS - Flat or Corrugated Used in: Roofing, Walls, Ceiling panels/partitioning, bath panels, under stairs, door-linings FLUES - Boilers / Water heaters Rainwater pipes / Guttering, Water storage tanks Decorative plaster finishes (ARTEX) Floor tiles/ Roof tiles/ Car parts(Brake and clutch linings)

Asbestos Floor tiles

Asbestos Ceiling Tiles

Asbestos Insulating board: used in ceiling panels/ Tiles, Internal and external door linings, Heating unit, Cup boards. Asbestos lagging: Used in Broilers, pipes Asbestos spray coatings in insulation, gaskets and ropes. Asbestos siding Asbestos insulation

Asbestos brake pad Dust from brake pad that contain asbestos Asbestos brake lining

Diseases due to Asbestos o Asbestosis :parenchyma fibrosis o Pleural fibrosis o Lung ca o Pleural effusion o Localized plaques o Mesothelioma o Laryngeal ca

Asbestosis and asbestosis induced pleural fibrosis Clinical presentation: - progressive dyspnea - dry cough - Pleuritic chest pain Clubbing and cyanosis may be present in advanced cases. Physical findings: Rales best heard laterally over the lower thoracic wall. In Most cases exposure has occurred at least 15 years before the onset of disease. Cigarette smoking enhances the risk of developing asbestosis.

Asbestosis: Diagnosis Based on objective evidence of past exposure and current disease. History of past exposure with clinical presentation and typical radiographic features on a chest radiographs. Laboratory Studies: - Asbestos fibers in BAL or lung parenchyma. - PFT: Restrictive lung function with reduced diffusing capacity. - Characteristic findings in Chest X-ray or HRCT- Chest.

Asbestosis: Linear lung infiltrates with pleural plaques Small linear opacities in Asbestosis

HRCT: Pleural plaque in Asbestosis

Asbestos body in BAL Asbestos body in lung tissue Photo micrographic picture of Asbestos Body

Treatment and prevention No effective treatment. Only supportive therapy for those who develop respiratory compromise. Cessation of smoking. Avoidance of use of asbestos containing materials.

Silica and Silicosis: Definitions Silica is silicon dioxide, the oxide of silicon, chemical formula SiO 2. SiO 2 is the most abundant mineral on earth; comprises large part of granite, sandstone and slate. Silicosis is lung disease caused by inhalation of fine silica dust; the dust causes inflammation and then scarring of the lungs. Scarring shows up on chest x-ray. There is no effective treatment for any pneumoconiosis, including silicosis

Chest x-rays – silicosis Normal X-raySilicosis: Upper lobeSilicosis: Diffuse

Silicosis: Types Simple chronic silicosis From long-term exposure (10-20 years) to low amounts of silica dust. Nodules of chronic inflammation and scarring, provoked by the silica dust, form in the lungs and chest lymph nodes. Patients often asymptomatic, seen for other reasons. Accelerated silicosis (= PMF, progressive massive fibrosis) Occurs after exposure to larger amounts of silica over a shorter period of time (5-10 years). Inflammation, scarring, and symptoms progress faster in accelerated silicosis than in simple silicosis. Patients have symptoms, especially shortness of breath.

Acute silicosis From short-term exposure to very large amounts of silica dust. The lungs become very inflamed, causing severe shortness of breath and low blood oxygen level.

Simple Silicosis Simple Silicosis Normal Chest X-ray Simple Silicosis

Accelerated Silicosis (= Progressive Massive Fibrosis) Normal Chest X-ray Progressive massive fibrosis

Accelerated Silicosis (PMF) X-rayCT-Chest

Eggshell calcification – almost exclusively silicosis

Silica Dust Exposure – Risk Factors Any work that exposes you to silica dust: ◦ mining ◦ stone cutting ◦ quarrying ◦ road and building construction ◦ work with abrasives ◦ glass manufacturing ◦ sand blasting ◦ Also, some hobbies can involve exposure to silica (sculptor, glass blower)

Silica: Stone Cutting

Exposure to sand particlesSand blasting Foundry work Children exposed to silica

Silicosis: Diagnosis Abnormal chest X-ray (or chest CT scan) consistent with silicosis. History of significant exposure to silica dust. Medical evaluation to exclude other possible causes of abnormal chest x-ray. Pulmonary function tests are helpful to gauge severity of impairment, but NOT for diagnosis. Lung biopsy rarely indicated (since no effective treatment, biopsy is done only when other diagnoses are being considered).

Silicosis – associated risks Having silicosis increases risk of contracting tuberculosis & lung cancer. Degree of increased risk is highly variable; depends on several OTHER factors, including immune system & exposure history (for TB), and amount of lung scarring, age & smoking history (for cancer). PMF Tuberculosis Silicosis also strongly associated with scleroderma and rheumatoid arthritis. Other associations less well established: lupus, systemic vasculitis, end-stage kidney disease. Cowie R: Am J Respir Crit Care Med 150: 1460,1994

X-ray of SilicotuberculosisCT: Silicotuberculosis

Tuberculosis is an important consideration in diagnosis and management of silicosis. The life time risk of tuberculosis is about 20–25% in patients of silicosis. Free silica impairs macrophage and microphage functions leading to increased chances of mycobacterial infections. Positive tuberculin test and cavitatory nodule are usually indicative of tuberculosis. CT scan of chest is also helpful in detection of concurrent tubercular infection. The treatment for concurrent tubercular infection in patients of silicosis requires prolonged duration J Bras Pneumol. 2008 Nov;34(11):959-66. Review. Morgan EJ. Silicosis and tuberculosis. Chest. 1979;75:202–3

Coal Worker’s Pneumoconiosis (CWP) Radio graphically indistinguishable from chronic silicosis but pathologically quite different. Two Types: (i) Simple CWP (II) Advanced form – PMF Agent: Coal dust or graphite Seen in Coal miners

Coal Worker’s Pneumoconiosis CWP is indistinguishable from Silicosis Normal CWP

CWP Asymptomatic anthracosis Simple CWP : no lung dysfunction with accumulation of macrophages Complicated CWP (PMF): <10% of simple cases lead to PMF, pulmonary HTN & Cor pulmonale No increased risk of T.B or lung ca

CWP: Diagnosis Seen in Coal miners Occupation History and history of exposure Dyspnea, cough with expectoration. PFT: May have restrictive impairment but obstructive and mixed pattern more common Radio graphically indistinguishable from silicosis Pathologically two forms: Classic coal macule Nodular CWP-Micro <7mm - Macro >7mm Rapidly developing Nodular CWP with rheumatoid arthritis- Caplan syndrome (also seen in Asbetos and Silica)

Mixed Airway and Parenchymal Disease Hypersensitivity Pneumonitis Also known as extrinsic allergic alveolitis. Hypersensitivity reaction in the lung occurs in response to inhaled organic dust. Example is farmer’s lung. The exposure may be occupational or environmental. The disease occurs from type III and type IV hypersensitivity reactions. Farmer’s lung is due to thermophilic actinomyces in moldy hay. Bird fancier’s lung is caused by avian antigen.

Pathology There is infiltration of alveolar walls with lymphocytes, plasma cells and histiocytes. There are loosely formed granulomas. Fibrotic changes occur in advanced disease.

Clinical Features The disease may occur in acute or chronic forms. Acute HP Dyspnea, fever, malaise and cough appear 4-6 hours after exposure. These symptoms continue for 24-48 hours. Physical examination shows fine crackles throughout the lungs. These patients present with progressive dyspnea over a period of years. Chest radiograph may be normal, but may show reticular nodular infiltration.

Chronic HP These patients present with progressive dyspnea. Physical examination shows bilateral inspiratory crackles. Chest x-ray shows reticular nodular infiltration and fibrosis predominantly in upper lobes. Pulmonary function tests – restrictive pattern. Gas exchange shows hypoxemia which worsens on exercise.

Management Absolute avoidance of inciting antigen is the main stay of therapy. Corticosteroids and supplemental oxygen for Acute attacks.

Occupational Neoplastic Disease of the Lung Bronchogenic Carcinoma Malignant Mesothelioma

Bronchogenic Carcinoma Leading cause of cancer deaths in both men and women through out the world. Occupational exposure may involve any one of the four major cell types of the Bronchogenic carcinoma- large cell, small cell, sqamous cell and adenocarcinoma. Minino Am, heron MP, Smith BL: National vital statistics report, vol 54, no 19,Maryland 2006

Agents Indoor Air Pollution: - Passive exposure to cigarette smoke. - Smoke from biomass fuel combustion - Radon used for building material.

Occupational exposure: - Asbestos inhalation- highest carcinogenic risk in the work place. - Risk is 6-8 th fold higher in nonsmoking workers who are exposed to asbestos and 50-100 th fold higher in heavy smoking workers. - Lung cancer accounts for up to 25% of all deaths in asbestos-exposed workers. - Other occupational exposure : Uranium miners, chloromethyl ethers, Radon, cadmium, Nickel, Chromium and Beryllium. Seikoff IJ, Churg J, Hammond FC: Asbestos exposure and neoplasia. JAMA 188:22, 1974 Samet JM, Kutvirt DM, Waxweiler RJ,et al: Uranium mining and lung cancer. N Engl J Med 310:1481,1984

Malignant Mesothelioma Epidemiology: - First reported in 1940s. - In the 1960s, the first evidence of a link btw MM and both occupational as well as incidental asbestos exposure was reported in S. Africa - Incidence of Malignant Mesothelioma is rising worldwide due to exposure to asbestos especially in developing countries

Pathogenesis Latency period more then 30 years. Crocidolite: Most carcinogenic Asbestos. Appear grossly as multiple gray or white nodules or granules on the visceral or parietal pleura. Affected pleura becomes thicker and may encase the entire hemithorax. Local Spread: Diaphragm, liver, parietal pleura of the opposite side or pericardium. Hematological spread occurs in nearly half of the affected patients.

Clinical Features The incidence in men ranges from 7–13 per million per year. In population unexposed to asbestos, incidence of 1–2 per million per year. Unexplained pleural effusions with dyspnea, as well as chest wall pain About 80% of patients with pleural malignant mesothelioma are male. Cancer Syndrome: wt loss, fever, night sweats, cachexia, fatigue, thrombocytosis, high ESR, low albumin, and anemia. Are usually manifested in the later stages. Miller BH, Rosado-de-Christenson, Mason AC, Fleming MV, White CC, Krasna MJ: Radiographics. 1996;16:613–44. Hansen J, Klerk NH, Musk AW, Hobbs MS. Am J Respir Crit Care Med. 1998;157:69– 75.

Malignant Mesiothelioma: Gross

Malignant Mesiothelioma:X-ray Malignant Mesothelioma: CT

Prognostic Factors Median survival of patients with MM from time of diagnosis is approx 12 months. Worse prognosis in the following pts: 1. Male 2. Those with extensive diseases 3. Poor performance status 4. Elevated white-cell counts, Anemia, Thrombocytosis 5. Sarcomatoid histologic findings 6. Expresssion of certain biochemical markers(VEGF), evidence of SV40 virus in the tumor

Treatment Surgery: Palliation only. Radical resection (extrapleural pneumonectomy) or debulking surgery or VATS. Chemotherapy: Gemcitabine with cisplatin are common chemo-regimen used currently. Radiotherapy: MM is resistant to radiotherapy. Prevent seeding of tumor, and provide palliative relief of somatic chest-wall pain. Immunotherapy: Response to trials of IFN-alpha, intrapleural IL-2, GM-CSF

Indian Scenario: High SO2 and PM concentrations in Indian cities. High levels of O3 in New Delhi Use of traditional biomass fuels- Wood, dung, and crop residues—is widespread in rural India. 86 percent of rural households and 24 percent of urban households rely on biomass as their primary cooking fuel. Biomass contributes to 3.5% of morbidity/mortality and 400,000 deaths in children due to acute lower respiratory tract infections, COPD in women, and lung cancer primarily in women in India.

Indoor smoke ranks 3rd among the top ten risk factors in Indian burden of diseases. About half a million women and children die each year from indoor air pollution in India. It is estimated that 28% of all deaths due to indoor air pollution in developing countries occur in India.

The common respiratory diseases which have a proven association with air pollution are tuberculosis, pneumonia, COPD, asthma, lung cancer and pneumoconiosis. It is estimated that 3% of cases of TB in India can be attributed to poor AQ. The prevalence of chronic bronchitis in those that use biomass fuel (wood and cow dung) as the principal source of energy varies from 2.9 – 5% in India.

Occupational lung disease in India Industrial Health 2004, 42, 141–148

At present in India more than thirty mines are in operation. It produces 2800 tones of asbestos per month (mainly chrysotile and tremolite) In India, asbestos occurs in the states of Andra Pradesh, Rajastan, Bihar, Karnataka, Tamilnadu and Manipur Direct and indirect employment in asbestos mine is around 100,000 workers. AL. RAMANATHAN* and V. SUBRAMANIAN:Industrial Health 2001, 39, 309–315

Coal is prime source of energy in India. There are 5.5 lakhs of employees engaged in about 500 coalmines in different parts if India. The prevalence rate of C.W.P. in this study comes to 3.03%, ranging from 1.52% to 4.76% in different areas. Ashit Kumar Mukharjee, Sanat K. Bhattacharya: Industrial Health 2005,43,277-284 Yogender singh Parihar, Subrata Adhikary: Industrial Health 1997, 35,467-473

Silicosis in India Prevalence of 55% in group of workers engaged in the quarrying of shale sedimentary rock. The mean age at death was 35 years and the mean duration of the exposure was 12 years. International organizations have estimated work-related deaths of around 150,000 each year in India along with 2 million new cases of occupational diseases. Seaton A, Seaton D, Leitch AG. Reprint. 5th ed. Blackwell Scientific Publications; 2008. Crofton and Douglas’s Respiratory Diseases; pp. 1461–24 Morgan EJ. Silicosis and tuberculosis. Chest. 1979;75:202–3

Prevention of Environmental Lung Disease Indoor Air pollution (i) Public awareness (ii) Change in pattern of fuel use (iii) Modification in stove design (iv) Improvement in the ventilation (v) Multisectoral approach.

Public Awareness: -The first and the most important step -Educate the public, administrators and politicians to ensure their commitment and promoting awareness of the long-term health effects on the part of users. -This may lead to people finding ways of minimizing exposure through better kitchen management and infant protection.

Change in Pattern of Fuel Use The use of solar energy for cooking Switching from biomass fuel to kerosene and LPG.

Modification in Stove Design Use of cleaner fuels should be the long-term goal Mechanism (eg chimney) to remove pollutants from the indoor environment Use of smokeless stoves in comparison with traditional cooking stoves. NIOH study 2001

Improvement in Ventilation Ventilation in the kitchen should be given due priority in the design of the houses Measures such as putting a window above the cooking stove and providing cross ventilation through the door help in diluting the pollution load.

Multisectoral Approach Effective tackling of indoor air pollution requires collaboration and commitment between agencies responsible for health, energy, environment, housing and rural development.

Others Measures: Urban planning: Designing traffic patterns to flow outside of populated areas, working with the design of roadways to prevent congestion. Technology : The creation of new vehicles and fuels that produce less pollution is a major step towards clean air. Legal regulations : All possible measures are taken to prevent air pollution, regulations that prevent individuals and businesses from doing anything that can cause air pollution if it is not absolutely necessary.

Alternative Energy Source: alternative energy sources such as solar energy, hydroelectric energy and wind energy.alternative energy sourcessolar energywind energy Social awareness: The most essential step to be taken for the prevention of air pollution. Awareness programs and/or advertisements should be encouraged

Prevention of Occupational lung Disease Industrial Hygiene: Recognizing and testing for hazards and modifying the work environment if hazards exist. Measurement of specific exposures and comparison with existing standards. Substitution of toxic substance with non toxic products. Improved ventilation in work place. Personal respiratory protection. In Summary: well-supervised control program for substitution of the inciting agent is the first line of prevention. If substitution is unrealistic or unfeasible then isolating the substance from the majority of the workers through administrative Controls, local exhaust ventilation or personal protection.

You can not always get what you want, but if you try for sometime you will get what you need.