Common questions of professional pathology
Pneumoconiosis.
Silicosis. Silicatosis. Carboconiosis. Metaloconiosis.
Pneumoconiosis of electric welder.
Occupational disease (OD) is defined as any disease contracted as a result of an exposure to risk factors arising from work activity. Risk factors include exposure to physical, chemical, biological, ergonomic or psychosocial hazards at the workplace. Doctors have a legal responsibility to report ODs under the Workplace Safety and Health (WSH) Act. In Singapore, there are 35 ODs that are reportable under the Second Schedule of the WSH Act (see Appendix C). The three most common ODs reported in Singapore are noise-induced hearing loss, occupational skin diseases and excessive absorption of chemicals.
Professional pathology is the section of clinical medicine that studies the question of etiology, pathogenesis, clinic, diagnostics, medical treatment and prophylaxis of professional diseases. Main objectives of the occupational pathology are as follows:
· study of occupational diseases, their pathogenesis, symptomatology, progress, long-term consequences, therapy issues, medical rehabilitation, and labor ability expertise; early diagnostics of occupational diseases is gaining particular importance;
· study of non-specific action of occupational factors, their meaning for development, progress and consequences of general and non-occupational diseases.
We understand the professional illnesses as a disease that caused by professional harmfulness. Professional harmfulness – it is the factors of production environment or labor process, which cause an unfavorable action to the organism of working and at certain force and duration of their action are able to cause the pathological states or nosologic forms of diseases.
One of the basic forms of human activity is the labour that favorably affects its health and provides the welfare of society. At the same time some types of labour at certain conditions, at the non-observance of necessary sanitary-hygienic rules, can become the reason of the development of professional diseases. Professional harmfulness, as a rule, related to the industrial process, its technology and equipment.
The most popular classification of toxic matters, which reflects their practical utilization, is as follows:
1) industrial poisons used in production: organic solutions (dichlorethane), dyes (aniline), chemical reagents (methyl alcohol), etc.;
2) poisoning chemicals used against agricultural plant pests: organochloral pesticides (hexachloran, polychloropinen), organophosphorus insecticides (Trichlorfon, methylmercaptophos); organomercurous matters (granosan) and derivatives of aminoformic acid (Sevin);
3) medicinal drugs;
4) household chemicals used as food supplements (acetic acid), sanitary, personal hygiene and cosmetics means;
5) biological plant and animal poisons contained in plants and fungi, animals and insects (snakes, and bees);
6) military poisoning matters (sarin, mustard gas or yperite, and phosgene).
There are maximum possible concentrations of toxic substances and maximum possible levels of professional harmfulness’ influence, which eliminate the possibility of development of professional diseases both acute and chronic.
Professional harmfulness are not only able to cause the professional diseases, but also can show influence on the clinic course of general, etiologically unconnected with labour activity, diseases of cardio-vascular and nervous systems, breathing organs, hemopoietic organs, locomotor system, skin, causing their exacerbation, complication, relapse.
There is no internationally accepted definition for the term “occupational disease”. However, occupational diseases are usually defined as diseases arising out of or in the course of employment. For convenience, they may be grouped as under:
/. Diseases due to physical agents :
(1) Heat: Heat hyperpyrexia, heat exhaustion, heat syncope, heat cramps, burns and local effects such as prickly heat.
(2) Cold: Trench foot, frost bite, chilblains
(3) Light: Occupational cataract, miner’s nystagmus
(4)Pressure: Caisson disease, air embolism, blast (explosion)
(5) Noise: Occupational deafness
(6)Radiation: Cancer, leukaemia, aplastic anaemia, pancytopenia
(7) Mechanical: Injuries, accidents factors
(8) Electricity: Burns
II. Diseases due to chemical agents:
(1) Gases: C02, CO, HCN, CS2, NH3, N2, H2S, HCI, SO2 – these cause gas poisoning.
(2) Dusts(Pneumoconiosis)
(і)Inorganic dusts :
(a) Coal dust: Anthracosis
(b) Silica: Silicosis
(c) Asbestos: Asbestosis, cancer lung
(d) Iron: Siderosis
(ii) Organic (vegetable) Dusts :
(a) Cane fibre: Bagassosis
(b) Cotton dust: Byssinosis
(c) Tobacco: Tobacossis
(d) Hay or Farmers’ lung grain dust
(3) Metals and their compounds :
Toxic hazards from lead, mercury, cadmium, manganese, beryllium, arsenic, chromium etc.
(4) Chemicals: Acids, alkalies, pesticides
(5) Solvents: Carbon bisulphide, benzene,trichloroethylene, chloroform, etc.
III. Diseases due to biological agents:
Brucellosis, leptospirosis, anthrax, actinomycosis, hydatidosis, psittacosis, tetanus, encephalitis, fungal infections, etc.
IV Occupational cancers:
Cancer of skin, lungs, bladder
V. Occupational dermatosis:
Dermatitis, eczema
VI. Diseases of psychological origin :
Industrial neurosis, hypertension, peptic ulcer, etc.
Main Principles of Occupational and Environmental Medicine
1. The clinical and pathologic expression of most environmentally caused diseases are indistinguishable from those of non environmental origin. Most occupational diseases, such as occupational cancers, not only resemble diseases caused by other factors but are otherwise indistinguishable except by careful documentation of a history of a relevant exposure
2. Many diseases of occupational or environmental origin are multifactorial, with non-environmental factors playing a contributing role. Asbestos exposed workers who smoke have a far higher likelihood of lung cancer than individuals exposed to cigarettes or asbestos singly.
3. The effects of occupational and environmental exposures occur after a biologically predictable latent interval following exposure. Agents or chemicals capable of causing direct and acute injury to the body will typically exert their effects either immediately or soon after exposure. Other substances initiate insidious disease processes that may become clinically apparent only after a latent interval for many years.
4. The dose of an exposure to a noxious agent is the strongest predictor of the likelihood and type of effect.In general, higher exposures confer a higher likelihood of being affected (dose-response relationship) and of more serious effects (dose-effect relationship). Other harmful agents act by eliciting an immunologic or other hypersensitivity response (asthma, allergic alveolitis, dermatitis).
5. People differ substantially in their responses to noxious exposures. Human sometimes differ remarkably in their responses to environmental exposures. These differences may be due to a wide range of factors, including genetic differences in metabolism, age, gender or size, co-exposures to environmental substances that may interact with agents of interest, coexisting morbid conditions, or complex behavioral factors.
Definitions of occupational hygiene may be presented in different ways; however, they all have essentially the same meaning and aim at the same fundamental goal of protecting and promoting the health and well-being of workers, as well as protecting the general environment, through preventive actions in the workplace.
Occupational hygienist. An occupational hygienist is a professional able to:
- anticipate the health hazards that may result from work processes, operations and equipment, and accordingly advise on their planning and design
- recognize and understand, in the work environment, the occurrence (real or potential) of chemical, physical and biological agents and other stresses, and their interactions with other factors, which may affect the health and well-being of workers
- understand the possible routes of agent entry into the human body, and the effects that such agents and other factors may have on health
- assess workers’ exposure to potentially harmful agents and factors and to evaluate the results
- evaluate work processes and methods, from the point of view of the possible generation and release/propagation of potentially harmful agents and other factors, with a view to eliminating exposures, or reducing them to acceptable levels
- design, recommend for adoption, and evaluate the effectiveness of control strategies, alone or in collaboration with other professionals to ensure effective and economical control
- participate in overall risk analysis and management of an agent, process or workplace, and contribute to the establishment of priorities for risk management
- understand the legal framework for occupational hygiene practice in their own country
- educate, train, inform and advise persons at all levels, in all aspects of hazard communication
- work effectively in a multidisciplinary team involving other professionals
- recognize agents and factors that may have environmental impact, and understand the need to integrate occupational hygiene practice with environmental protection.
The Practice of Occupational Hygiene
The classical steps in occupational hygiene practice are:
· ·the recognition of the possible health hazards in the work environment
· ·the evaluation of hazards, which is the process of assessing exposure and reaching conclusions as to the level of risk to human health
· ·prevention and control of hazards, which is the process of developing and implementing strategies to eliminate, or reduce to acceptable levels, the occurrence of harmful agents and factors in the workplace, while also accounting for environmental protection.
The ideal approach to hazard prevention is “anticipated and integrated preventive action”, which should include:
· ·occupational health and environmental impact assessments, prior to the design and installation of any new workplace
· ·selection of the safest, least hazardous and least polluting technology (“cleaner production”)
· ·environmentally appropriate location
· ·proper design, with adequate layout and appropriate control technology, including for the safe handling and disposal of the resulting effluents and waste
· ·elaboration of guidelines and regulations for training on the correct operation of processes, including on safe work practices, maintenance and emergency procedures.
From: http://ilocis.org/documents/chpt30e.htm
History of professional pathology is interlinked with the history of occupational hygiene. Problem of human health, influence on it of work conditions, its harmoniousness of physical and spiritual development, was the object of attention of thinkers of human society from a deep remoteness.
The history of occupational medicine can be traced into antiquity. Observations of increased rates of illnesses and mortality among miners date back to Greek and Roman times. Specific data onto the impact of harmful conditions of work onto the human health, as well as existence of particular occupational diseases can be met in ancient documents. As an example, we can name ancient Egyptian and Chinese characters and a code of medical rules and lectures by Hippocrates, Aristotle, Lucretius, Ovid, Plutarch, Pliny, Juvenal, and Galen.
Information about the influence of work conditions to a health and about the existence of peculiarities of professional diseases meet yet in the works of Egyptian, ancient Greek and the Roman scientists (Aristotle, Hippocrates, Pleniy, Lucretsiy, Galen and others. – VI-IV century B.C.). In works of Hippocrates, that lived approximately in 577-450 B.C., described disease of miners that run with the severe breathlessness.
Bauer was born in Glauchau, Saxony, as the son of a prosperous clothier. He attended the University of Leipzig, Saxony, from 1514 to 1517, originally with the intent of becoming a priest. One of his professors, Mosellanus, a former student of the great humanist, Erasmus, may have enticed Bauer to study ancient languages and become a teacher instead. During this time, according to the scholarly tradition of his days, Bauer Latinized his name to Georgius Agricola.
His first assignment was at the public school in Zwickau, Saxony, where he advanced rapidly to vice-principal and principal. In this capacity he reformed the curriculum thoroughly, transforming the religion-oriented school into a modern educational institution.
Evidently Agricola played his cards as town physician and entrepreneur well and became the richest man in Chemnitz. In his last published work, De Re Metallica (Of Metal Matters), he disclosed some of his secrets. All the following verbatim statements are taken from the only English translation of De Re Metallica (Agricola, 1950).
De Re Metallica was completed in 1553 and published by Froben in the year following Agricola’s death. He had taken 20 years to write the book on prospecting, surveying, metallurgy, logistics, mine and smelter construction, mining tools and machinery, and mining-related health problems. It comprises 12 books (chapters), including hundreds of woodblock prints, some of which depict nothing less than the early industrial revolution! He brought forth an achievement that was beyond anything contemporary and it remained the miner’s handbook for almost 200 years.
From: http://toxsci.oxfordjournals.org/content/69/2/292.full.pdf+html
In 1530 Paracelsus wrote a clinical description of syphilis, in which he maintained that the disease could be successfully treated by carefully measured doses of mercury compounds taken internally. He stated that the “miners’ disease” (silicosis) resulted from inhaling metal vapours and was not a punishment for sin administered by mountain spirits. He was the first to declare that, if given in small doses, “what makes a man ill also cures him”—an anticipation of the modern practice ofhomeopathy. Paracelsus was the first to connect goitre with minerals, especially lead, in drinking water.
He prepared and used new chemical remedies, including those containing mercury, sulfur, iron, and copper sulfate, thus uniting medicine with chemistry, as the first London Pharmacopoeia, in 1618, indicates. Paracelsus, in fact, contributed substantially to the rise of modern medicine, including psychiatric treatment.
http://www.britannica.com/EBchecked/topic/442424/Paracelsus/5504/Career-at-Basel
However, the first work, in which systematically were laid out the questions of occupational hygiene of people of different professions with the description of the proper professional diseases, was the book of Italian scientific Bernardino Ramazzini, published in 1700 under the name “About diseases of artisans”.
In the late 1600s Ramazzini described outbreaks of lathyrism, a disease of humans and animals caused by eating legumes of the genus Lathyrus. The disease is commonly called chick-pea poisoning and is characterized by spastic paralysis, by-paresthesia and paresthesia (a prickling skin sensation). Between 1690 and 1695 he expanded his studies to outbreaks of malaria in Italy. During this study, Ramazzini used the cinchona bark (from which the alkaloid quinine is derived) to treat his malaria-stricken patients. His use of this medicine is considered a turning point in the history of medicine. It was a practice of most physicians of the time to prescribe the cinchona bark extract for all types of illnesses; it was Ramazzini, however, who realized this medicine should not be used indiscriminately, but rather be reserved for the treatment of malaria. One of his earliest investigations found that sewage workers were affected with a severe reddening of the eyes, resulting in blindness for many of them. Ramazzini studied this phenomenon, quesa result of this study, he developed the idea for his treatise on occupational diseases.
In 1700 Ramazzini wrote De Morbis Artificum Diatriba ( Diseases of Workers) Although the first recorded observations of occupational disease date back to Hippocrates (c. 460-377 B.C.), De Morbis Artificum Diatriba was the first comprehensive work on occupational disease. Ramazzini applied his approach of inspecting the workplace, questioning the workers, and advising on remedies to outline the health hazards associated with chemicals, dust, metals, as well as other abrasive agents that laborers may encounter in the daily routine of their work. In his De Morbis Artificum Diatriba, Ramazzini describes over 50 dirty or dangerous trades; among those at risk, he noted, were miners, gilders, chemists, potters, tinsmiths, glassmakers, painters, tobacco workers, lime-workers, tanners, weavers, coppersmiths, and printers.
Ramazzini’s work was soon followed by others. In 1775 Percivall Pott published a work on the diseases of chimney sweeps. Charles Turner Thackrah published an extensive study of industrial illnesses and poverty in 1831. Regardless of the proof of these various pamphlets, dissertations, and full studies, it was not until 1895 that Great Britain became the first country to introduce statutory notification of occupational diseases.
Industrial medicine, factory and safety laws, and the eventual introduction of the treatment of occupational diseases into workers’ compensation laws can surely be traced back to Ramazzini and his De Morbis Artificum Diatriba.
From (http://www.answers.com/topic/bernardino-ramazzini)
In the second half of ХІХ and in the ХХ century, in relation with development of great industry, professional morbidity grows sharply. In this period considerable development of researches in the branch of occupational hygiene and professional pathology, appearance of many books and manuals on these questions is marked.
Among the researchers that worked in the field of professional pathology and authors of the most known manuals we can mark Shevale, Tankerel de Planshet, Cussmaul, Zenker, Galfort.
In
The development of large-scale industry in the second half of the XIX – early XX century was accompanied by the appearance of new professions and new occupational hazards. This contributed to an even wider study of occupational diseases, the description of which was presented in more works. Dr. Alice Hamilton (1869-1970) was the first woman appointed to the faculty of Harvard Medical School and was a leading expert in the field of occupational health. She was a pioneer in the field of toxicology, studying occupational illnesses and the dangerous effects of industrial metals and chemical compounds on the human body.
Alice Hamilton was a pioneer in correcting the medical problems caused by industrialization, awakening the country in the early twentieth century to the dangers of industrial poisons and hazardous working conditions. Through her untiring efforts, toxic substances in the lead, mining, painting, pottery, andrayon industries were exposed and legislation passed to protect workers. She was also a champion of worker’s compensation laws, and was instrumental in bringing about this type of legislation in the state of Illinois. A medical doctor and researcher, she was the first woman of faculty status at Harvard University, and was a consultant on governmental commissions, both domestic and foreign.
Investigating a typhoid epidemic in Chicago, she was instrumental in reorganizing the city’s health department and in drawing attention to the role flies played in spreading the epidemic. After reading Dangerous Trades by Sir Thomas Oliver, Hamilton began her life-long mission to treat the excesses of industrialization. Unlike other countries such as Germany and England, the United States had no industrial safety laws at the time. During her time at Hull House, Hamilton investigated the steel industry and others for occupationally caused lead poisoning.
In 1925, she published her Industrial Poisons in the United States, the first text on the subject, and became one of the few worldwide authorities in the area of industrial toxins. At this same time, she was also instrumental in influencing the surgeon general to investigate the dangerous effects of tetraethyl lead and radium.
Hamilton demonstrated the toxicity involved in rayon processes, and these findings that led to Pennsylvania’s first compensation law for occupational diseases. In her later years, Hamilton, who never married, wrote an autobiography and continued to be active politically, advancing causes of social justiceand pacifism.
From: http://www.faqs.org/health/bios/58/Alice-Hamilton.html
The end of the 19th and beginning of the 20th are characterized by rapid development of capitalism in Europe. Valuable contribution in studying occupational pathology was made by representatives of rural medicine – F.Yerisman, Ye.Osipov, and O.Pogozhev. An original manual “Occupational Hygiene or Hygiene of Mental and Physical Work” by F.Yerisman, published in 1877, was in big demand. Scale and depth of research is well shown in the 19-volume edition “Materials on Research of Factories and Plants”, compiled based on research of 1008 factories and plants. It includes data on the health condition and physical development of 114 thousand workers. This work, completed by F.Yeresman, O.Pogozhev, Ye.Dementiev et. al., had no analogue in the world practice of that time.
F.Yerisman
Significant contribution into he development of home science on occupational hygiene and occupational pathology was made by D.Nikolsky, V.Levitsky, V.Novrotsky, G.Khlopin, M.Kavalyerov, I.Liatschenko, O.Navakatikyan, G.Yevtushenko, M.Paranko, and A.Shevchenko.
Among outstanding scientists, who had big impact onto the development of professional pathology as a science, it is necessary to mention such scientists as M.Vigdorchyk and S.Kaplun. M.Vigdorchyk published a number of important works on occupational pathology and statistics of professional diseases; he was also a director for Leningrad Institute of Occupational Hygiene and Occupational Diseases. S.Kaplun was an organizer and the first leader of the Central Institute on Labor Protection.
Together with the realization of practical activity in occupational pathology, research and development work was widely implemented as well. In 1923, Ukrainian Institute on Occupational Medicine (now, Kharkiv National Institute on Occupational Hygiene and Diseases) was created in Kharkiv; in 1924, there appeared Moscow Institute on Occupational Diseases named after Obukhov, and in 1925, Central Institute of Labor Protection, and Leningrad Institute of Occupational Hygiene. In the following years, research and development institutes in occupational hygiene and occupational diseases were formed in Kyiv, Donetsk, Dnepropetrovsk, Sverdlovsk, Krivoy Rog, and Karaganda. Almost all the medical institutions on refreshing courses conducted the work in this direction for doctors, as well as departmental institutes.
Establishment and development of industrial toxicology is connected with the names of M.Pravdin, M.Lazarev, G.Shkavera, O.Cherkes, and L.Medved; studies of production microclimate are connected with the names of A.Letavet, G.Shakhbazyan and M.Karnaukh; S.Andreyeva-Galanina, V.Artamonova and G.Balan studied impact of vibration ontot a human body and professional pathology in agriculture was studied by Yu.Kundiyev and O.Krasnyuk.
Nowadays, issues on scientific development in the sphere of professional pathology are studied at R&D Institutes on Occupational Hygiene and Diseases. The main institute among them is the institute in Kyiv. Nowadays, four institutes like that function in Kyiv, including one in Kharkiv. As one of their research directions, they all study clinics of occupational diseases. Besides, study of occupational pathology is conducted by professors at chairs of medical institutes and universities, as well as institutes on refreshing courses for doctors. These chairs conduct research either independently (Donetsk Medical University), or together with chairs on Occupational Hygiene (National Medical University), or with chairs on therapy (Dnipropetrovsk Medical Academy, Lviv State Medical University and Kharkiv State Medical University).
Creation of the first research institutes of hygienic and professional pathologic profile became the beginning of the period of coordinated study of work conditions and morbidity on enterprises, with the development of prophylactic measures of defence and approvement of sharply defined maximum possible concentrations of substances that find application in industry.
NIOSH (National Institute for Occupational Safety and Health) is an agency established to help assure safe and healthful working conditions for working men and women by providing research, information, education, and training in the field of occupational safety and health. Information pertaining to the specific responsibilities of NIOSH are found in Section 22 of the Occupational Safety and Health Act of 1970.
The mission of NIOSH is to generate new knowledge in the field of occupational safety and health and to transfer that knowledge into practice for the betterment of workers. To accomplish this mission, NIOSH conducts scientific research, develops guidance and authoritative recommendations, disseminates information, and responds to requests for workplace health hazard evaluations.
The act created the National Institute for Occupational Safety and Health (NIOSH) in 1970. The tasks of this act:
v To identify the causes of work-related diseases and injuries.
v To evaluate the hazards of new technologies and work practices.
v To study industrial hygiene and hazard control.
v To make recommendations for occupational safety and health standards.
EMPLOYER DUTIES UNDER THE
1. Each employer
v shall furnish to each of his employees employment and a place of employment which are free from recognized hazards that are causing or are likely to cause death or serious physical harm to his employees;
v shall comply with occupational safety and health standards promulgated under this Act.
2. Each employee shall comply with occupational safety and health standards and all rules, regulations, and orders issued pursuant to this Act which are applicable to his own actions and conduct
From: http://www.cdc.gov/niosh/about.html
II. PECULIARIOTIES OF DIAGNOSIS OF OCCUPATIONAL DISEASES AND PRINCIPLES OF THEIR CLASSIFICATION.
Diagnosing of occupational diseases is a responsible and often a complicated business. People with occupational diseases have a number of social advantages, including pension based on medical list, and payment for medicinal drugs. Clinical picture of the majority of occupational diseases, in particular on early stages, does not differ much from the clinical picture of similar forms of non-occupational diseases. To consider and solve issues on the presence of occupational diseases, the following documents should be present:
1. Assigning of the medicinal establishment with the purpose of medical examination.
2. Extract from an ambulatory card of the sick person (medical and sanitary part, policlinics and dispensary), put together by the doctor, who attended the patient.
3. Sanitary and hygienic characteristics of labor conditions with the description of specific unfavorable factors of the production environment, their parameters, duration of the contact of the patient with them. In case of combined impact of unfavorable factors, it is necessary to make a detailed description of the production process character. A sanitary doctor of the sanitary and epidemiological station, who carries out state sanitary supervision of the object, where the patient works, puts sanitary and hygienic characteristics of labor conditions together.
4. Extract from a Work Record Book of the patient, which would prove his/her work term at the enterprise, where occupational disease appeared. The extract should be authorized by the Human Resource Department at the enterprise where the patient works. When diagnosing occupational diseases, especially on early stages, special clinical and functional, as well as biochemical, immunology, radiological and other methods of examination are very important. Starting with the examination of the patient, first of all, it is necessary to find out what hazard production factors could have or still have unfavorable impact onto his/her health condition in the work process. It is necessary to study thoroughly the documents, the patient brought with him. The assignment for hospitalization should state the reason of hospitalization, and information on the disease progress before the hospitalization. Particular attention should be paid to the ambulatory health history record of the patient, where the following should be given:
– all diseases, which were previously encountered, including professional ones;
– time of their appearing with the consideration of work under conditions of unfavorable factor, acting of the production environment;
– information on the health state based on results of previous and periodical medical examination;
– clinical picture of the present disease;
– results of the conducted instrumental and laboratory research;
– contents of the conducted treating and its efficiency.
Sanitary and hygienic characteristics of work conditions should include the information on hazard production factors and their intensiveness, results of measured on the containing of toxic matters, dust, noise parameters, and vibration. When examining patient with occupational diseases, it is necessary to pay close attention to targeted questioning. Patients should have an opportunity to give a detailed narration on hygienic and sanitary work conditions, life conditions, and disease progress. During the examination, it is necessary to keep to requirements of medical deontology, remember about responsibility to the patient, necessity of attentive care about him/her as well
as keeping medical secrecy. Filling in the Medical History Record for a patient with an occupational disease has specific peculiarities.
Conclusions regarding the reason of the disease: After the diagnosis has been made, it is necessary to make a conclusion regarding the reason of the disease (occupational or non-occupational). To determine the ability of the patient to work: if the patient is capable to work or not at the current occupation if keeping to specific conditions; ability to work is limited – to show what types of occupation can be carried out by the patient; the patient is unable to work and needs specialized assistance. Besides, it is necessary to provide recommendations regarding rehabilitation, treatment and disease prevention.
Doctor and labor expertise. Social and clinical conclusion is the basis for decision making by Doctor Consulting Commission (DCC) or Medical Social Expert Commission regarding the type of work ability disorder, disorder level and the character of disablement of the given patient. After the patient leaves hospital, the conclusion is sent to the medical establishment that assigned the patient. The list of occupational diseases (Appendix 1), approved by the order of the Ministry of Health of Ukraine and the Ministry of Labor of Ukraine, dated February 2, 1995 (No. 23/36/9), is the main document in compliance with which, the diagnosis of the occupational disease is made, as well as the connection with completed work or profession is done, issues on work ability expertise, medical and work rehabilitation, reimbursement by enterprise owners, establishments or organizations or agencies empowered by them to employees for the caused harm when fulfilling labor obligations are carried out. The list includes occupational diseases, which appear only due to unfavorable production and professional factors (black-lung disease, vibration disease, intoxication, etc), as well as a number of diseases, the development of which is connected with the influence of specific unfavorable production and professional factor and only a clear influence of other non-occupational factors, which cause similar changes in the organism (bronchitis, allergies, cataract, etc). It is necessary to remember that in the corresponding lines of the given document only an approximate list of enterprises, manufacturing enterprises and work done there, as well as etiological factors, which can cause disease, is provided there. Occupational diseases also include closest and distant consequences of occupational diseases (e.g. stable organic changes in the central nervous system after intoxication by carbon oxide). It is necessary to consider the possibility of the development of occupational diseases in long term after termination of contact with hazard factors (late: silicosis, papilloma of urinary bladder, etc). Occupational diseases can also include such diseases, which developed based on the occupational disease (e.g. lung cancer, which appeared with the patient with black-lung disease or dust bronchitis, and should be considered as an occupational disease, which is proved by histological changes in the mucus tunic of bronchi – diffused metaplasia with elements of displasia and development of epidermoid cancer, as a rule). If occupational disease causes worsening of the development of nonoccupational disease, what led to the loss of ability to work, it can bee considered occupational (e.g. progressing of a form of arterial hypertension, which appeared on the background of vibration disease).
Diagnostics of acute poisoning include:
– clinical diagnostics based in the given anamnesis, results on examination of the event place and study of clinical picture of the disease to establish specific poisoning symptoms;
– laboratory toxicological diagnostics, quality and quantity definition of toxic matters in biological environment of the organism (in blood, urine, or cerebrospinal fluid);
– pathomorphological diagnostics, definition of specific posthumous poisoning indications.
Diagnosis of acute occupational disease (intoxication) can be stated by a physician of any medical establishment after obligatory consultation with a specialist on occupational diseases and a physician on occupational hygiene of a territorial sanitary and epidemiological station (SES). Acute occupational disease (intoxication) appears suddenly, after one time impact of relatively high concentration chemical matters (for not more than one shift), which is in the air of the work zone, or levels or dozes of other unfavorable factors. The connection of acute infectious diseases with the occupational activity of the victim in case of necessity to clarify specialized departments of hospitals, clinics of scientific and research institutes on occupational hygiene and occupational diseases after the obligatory consultation with physicians on occupational hygiene and epidemiology of the SES. Professional etiology of acute contact dermatitis can be established by a doctor of skin and venereal dispensary on the agreement with a territorial SES.
Diagnosis of chronic occupational disease (or intoxication) have the right to state first of all specialized treatment and prevention establishments of Ukraine: Donetsky R&D Center for Occupational Hygiene and Prevention of Traumatism, Institute of Medicine of Labor of the Academy of Sciences of Ukraine (Kyiv), Kryvorizky R&D Institute of Occupational Hygiene and Diseases, Kharkiv R&D Institute of Occupational Hygiene Institute on Medical Radiology, Ukrainian R&D Institute of Ecohygiene and Toxicology of Chemical Matters (in case of utilization of means of protection of agricultural plants), Donetsk Regional Specialized Clinical hospital on occupational diseases, Department on Occupational pathology of Lviv Regional Hospital, Department on Occupational Pathology of Cherkassy Regional Hospital, as well as the clinic of the Institute of Health named after Medved. Diagnosis of chronic occupational diseases should include its name, main clinical syndromes of affections, degree of affected organ function disorder.
Research and registration of professional diseases should be carried out based on the “Regulations on Research and Registration of Accidents, Occupational Diseases and Damages at Enterprises, Establishments and Organizations”, approved by the Cabinet of Ministers of Ukraine, No. 623, dated August 10,
Based on the results of investigation of appearing of occupational diseases, an owner of an enterprise should make an order with measures on prevention of occupational diseases whose fault was in violation of sanitary norms and rules, which caused occupational diseases. When realizing measures on prevention of occupational diseases, suggested by the investigation commission, an enterprise owner should inform the SES within the terms stated in the act.
Registration and records of people, who were among the first to have occupational diseases, are conducted in specialized record books in compliance with the form, approved by the Ministry of Health, which should be filled out:
– at enterprises and establishments on sanitary and epidemiological service based ootifications about occupational diseases and acts of their investigation;
– at medical institutions based on the medical record of a patient, extracts from the medical history, doctor’s conclusion on the diagnosis after examination at the hospital, as well as notification about occupational diseases. Using the data of disseminated acts on occupational diseases, the SES compiles special record cards for keeping and analyzing occupational diseases with the assistance of computers. These compiled cards should be saved for 45 years in the SES. In compliance with the documents, investigation is carried out on every acute occupation disease and poisoning. A witness, employer, who found out about each case like this, or the victim him/herself should notify the work coordinator, foreman or any other authority of the enterprise and provide first aid medical assistance. In his/her turn, the leader should do the following: organize medical aid to the victim immediately and deliver him/her to a medical establishment, also notify the enterprise owner about the accident; keep the original state of the work place and equipment until the investigation commission arrives, also take measures to prevent similar cases. A medical establishment should notify the leader of the company about each accident like this, which was registered at the company where the victim works within one day, and in case of acute occupational poisoning (disease), they also should notify a sanitary-hygienic station, by sending urgent notification on each victim. The same type of notifications is sent to the owner of the company/enterprise to take urgent measures to prevent further similar accidents. A medical establishment, which clarified or changed the diagnosis of an acute occupational poisoning (disease), compiles an urgent notification and sends it to the sanitary and hygienic station which coordinates the enterprise the victim works at with changed (clarified) diagnosis, as well as its date, within 10 hours.
Upon receiving the notification about the accident, the company owner appoints a commission on investigation, which includes a head (specialist) of the labor protection service of the company (chairman of the commission), head for structural subsection or chief specialist. The commission should also include a representative of a trade union, member of which the victim is, and in case of acute occupational poisoning (diseases) – a specialist of the SES. If the victim is not a trade union member, then an authorized representative of a work team on labor protection should be in the structure of the commission. Within three days since the moment of the event, the investigation commission is obliged to do the following:
– to examine the accident place, interrogate witnesses and those involved in the accident, and to receive explanations from the victim, if applicable;
– to consider the correspondence of labor conditions and production means on the project and passports, and also keeping to requirements of normative and technical documentation on operation of equipment and normative acts on labor protection;
– to find conditions and reasons of the accident; to determine responsible for the accident; and also to develop measures to prevent cases like this;
– to fill in an act, form H-
Organization and Conduct of Medical Inspection of Workers. Medical assistance to patients with some occupational disease is provided by clinics, parts of R&D Institutes, as well as medical and sanitary sectors (MSS). The main task of the MSS is to develop and conduct measures, targeted at improvement of labor conditions and life of the employees and officers, prevention and decrease of total and professional disease, provision of specialized medical assistance and realization of systematic dispensary care together with the administration of establishments. As until now, amount a list of doctors, there has beeo physician on occupational diseases, all the work on servicing the patients with occupational diseases were carried out by general practitioners (workshop general practitioner). Nowadays, when such speciality became officially known, occupational pathological service is at the stage of development. To prevent occupational diseases, preliminary and periodical medical examinations of workers to start their career or those who work in close contact with hazard factors of the production environment. The order of their conduct is regulated by the Order of the Ministry of Health of Ukraine No. 45 dated of March 31, 1994 “About Approving Regulations on the Order of Conduct of Medical Examinations of Workers of Specific Categories”. The order envisages that the organization and medical examinations will be
provided by:
– an owner of an enterprise, establishment, organization independently of pattern of ownership and types of activity;
– establishments and agencies of the Ministry of Health of Ukraine, treatment and prevention, sanitary and hygienic, R&D and medical institutions (universities), on the territory where enterprises, establishments, organizations, agricultural companies, agrofirms, rental, cooperative, small, joint venture companies; catering, industrial, and children’s sites, elementary schools and other objects.
The owner of the enterprise finances medical examinations, reimburses losses on care, occupational and medical rehabilitation of people with occupational diseases, examination of specific labor conditions to put together a sanitary and hygienic characteristics.
Preliminary medical examinations are dune with the purpose to state physical and psychological ability of a person to work in the specific area, speciality, position, when first admitted to work; as well as to prevent diseases and accidents, exposure of diseases (infectious and others), which threaten with contagion of workers and manufactured products, as well as admission to work for people under 21.
Periodical medical examinations are conducted in the process of labor activity for people, who are engaged in hard work, work with hazard or unsafe conditions in compliance with the list of matters, unfavorable production factors and works to implement which, obligatory medical examinations of employees should be carried out. They provide dynamic examination of the health state of workers, expose early signs of the impact of production conditions and hazards onto the body, and which do not give the opportunity to continue working on the given profession: prevent accidents, expansion of infectious and parasitic diseases. They can be conducted within the period of staying of an employee in the hospital or in cases when he/she asked for help. Results of medical examinations should be drawn up within a month in a relevant act, which is made in four copies (for a medical establishment, owner, trade union committee and sanitary and hygienic station). During the medical examination, examination in occupation pathologic centers, clinics of R&D and medical institutes (universities) to specify the diagnosis or to determine a role of production factors in the development of diseases, a job and average salary is kept for a worker.
The order of organization of medical examinations:
The enterprise shall:
– determine a contingent of people, subject to periodical medical examination; and draw up a list of them in two copies with last and first names, and then approve it at the sanitary and hygienic station. One copy is sent to the medical establishment, and the other stays at the enterprise (with the organization responsible for medical examination) together with the sanitary and hygienic station and a trade union;
– assign people, who are sent to the enterprise or to change profession and work place to take preliminary medical examination in compliance with a proper document;
– introduce a new-comer to the hazard and dangerous production factors and matters, as well as normative acts on labor protection, which are specific to the profession;
– finance medical examination, and reimburse costs on examination and treatment of workers at occupational pathologic institutes, medical institutes (universities); as well as examination of work conditions with developing sanitary and hygienic characteristics;
– make an order to conduct medical examinations within the terms, approved by the treatment and prevention establishments, appoints responsible for organization of medical examination;
– assist the creation of improvement of material and technical bases of medical sectors, and medical establishments to conduct medical examinations, clinical and other research;
– apportion premises to conduct medical examinations;
http://www.medicalcd.info, [email protected], ICQ: 359 787 262
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– assign workers to have medical examination in medical establishments and controls the term of its implementation;
– provide implementation of the recommended rehabilitation and prevention measures.
A medical establishment shall:
– make an annual order to create commission to conduct medical examinations with a fixed term, place of conduct and list of physicians, clinical and other research; the commission will be chaired by a vice chief physician of the medical establishment, which trains doctors in occupational pathology;
– develop a plan – schedule of medical examination of workers, which should be approved by an owner and sanitary and hygienic station;
– conduct medical examination of employees, as well as clinical and other types of research;
– involve other specialists to participate in the medical examination; conduct additional clinic research, necessary to assess the health state of employees if applicable;
– inquire sanitary and hygienic characteristics of labor conditions of employees at sanitary and hygienic stations;
– control keeping to the terms of medical examination;
– make conclusions on the health state of each employee, who underwent a medial examination; make a decision regarding medical contraindications as to the possibility to continue work on the profession for those who have general or occupational diseases;
– inform an employee as to the state of his/her health, as well as the possibility to continue work on the profession based on the results of medical examinations or provide conclusions regarding transfer to another job;
– based on the medical indications, send an employee to further examination at medical centers, which have the right to make a diagnosis of an occupational disease;
– assign an employee to meet medical and social expertise commission (MSEC) based on medical indications.
It conducts:
– annual medical examination of people who terminated their work at the enterprise with hazard and dangerous factors, the impact of which can cause late development of occupational diseases;
–analysis and generalizing results on medical examinations, drawing up a final act, which is sent to the territorial SES, owner and a trade union of the enterprise;
– sending out a list with names of those, who are contraindicated to work under unfavorable conditions to an owner within a month after the medical examination took place;
– carrying out dispensary supervision over patients with occupational diseases, who continue their work activity, treatment and occupational rehabilitation;
– keeping records of patients with occupational diseases and poisoning.
A sanitary and hygienic establishment shall:
– determine authenticity of the record keeping made by the owner of hazard and dangerous factors and matters, work with which require medical examinations;
– confirm lists with names of people, subject to medical examination, as well as plans – schedules of medical examinations.
It participates in the following:
– in preparing and training specialists of a medical center; and
– in compiling the final act on periodic medical examination.
– in expert evaluation of the organization and the quality of medical examinations.
It sends decisions as to elimination of exposed violations and drawbacks in the organization and conduct of medical examinations;
– considers issues on temporary termination of medical examination in case of isolation of the existing situation;
– compiles sanitary and hygienic characteristics on work conditions;
– applies with proposals as to prevention of occupational diseases to territorial state administrations.
Research and Development (R&D) institutes on labor medicine, labor hygiene and occupational diseases, as well as chairs of medical universities(institutes) shall:
– develop normative and methodical documents on scientific and organizational principles of conduct of medical examinations, expertise of their quality and evaluation of results; criteria of determination of contingent of people – subjects to medical examinations; indications of the risk of occupational disease development and criteria of determining diseases as occupational ones;
– are engaged in elaborating issues on prevention, early diagnostics and treatment of occupational diseases, medical rehabilitation of workers with the risk of development of occupational diseases and patients with occupational diseases; definition of distant consequences of the impact of hazard and dangerous production agents onto the health. They also carry out refreshening and upgrading courses on occupational diseases in the form of provision of information, training and seminars, and also make final decision as to the connection of the disease with work conditions.
III. ORGANIZATION OF PREVIOUS AND PERIODICAL MEDICAL EXAMINATION OF WORKERS OF INDUSTRIAL FACTORIES AND OF AGRICULTURE. EXAMINATION OF WORKUNG CAPACITY.
One of important questions in the clinic of professional diseases is the examination of working capacity. Early detection of initial forms of professional diseases and timely application of medical and preventive measures, rational employment, and sometimes stopping of contact with the harmful factors of industrial environment, bring to complete liquidation of pathological process. During examination of working capacity at professional diseases the primary importance has the continuation of working longevity of workers.
The measures directed on warning of the development of professional diseases and saving of capacity of working and office workers are the important section of the examination of capacity.
Previous medical examinations at the receipt on work are realized for the detection of professional fitness by the state of health and possibility of the use of working on industries with professional harmfulness. Such medical examinations allow timely revealing at starting work diseases, which are contraindication for work with the harmful factors of industrial environment.
The purpose of periodic medical examination is the early detection of initial signs of professional diseases, and also timely detection of early forms of unprofessional diseases, at which subsequent work in the conditions of influence of the proper harmful factors of industrial environment is contra-indicated.
The terms of realizing of periodic medical examinations depend on the type of industry and profession.
General medical contraindications to admittance on the work related to the dangerous harmful substances and harmful industrial factors are the following:
1. Inherent anomalies of organs with the evident insufficiency of their functions.
2. Organic diseases of the central nervous system with the stable evident dysfunction.
3. Chronic psychical diseases.
4. Diseases of the endocrine system with the expressed violations of functions.
5. Malignant neoplasm.
6. All diseases of the system of blood and hematosis.
7. Arterial hypertension of the ІІІ stage.
8. Heart diseases with heart insufficiency.
9. Chronic diseases of lungs with the evident pulmonary-cardiac insufficiency.
10.Bronchial asthma of severe form with the evident disturbance of breathing and circulation of blood.
11.Active forms of tuberculosis of any localization.
12.Stomach and duodenal ulcer with chronic recurrent course and susceptibility to complications.
13.Cirrhosis of liver and active chronic hepatitis.
14.Chronic illnesses of kidneys with the phenomena of kidney insufficiency.
15.Collagenosis.
16.Illnesses of joints with the stable dysfunction.
17.Pregnancy and period of lactation.
18.Ordinary miscarriage and anomalies of fetus in anamnesis of women, which plan child-bearing.
19.Disturbance of menstrual function that is accompanied by the uterine bleeding.
20.Decompensated glaucoma.
Except the general medical contraindications at admittance to the job related with the dangerous harmful substances and industrial factors, also exist additional contraindications for every industrial factor taking into account its influence.
Examination of working capacity at professional diseases includes three basic questions: determination of diagnosis, determination of relation of disease with the influence of professional factors, estimation of patient’s working capacity.
The diagnosis of professional disease is determined according to the generally accepted nosologic forms of pathology and must represent a stage and course of pathological process, its expressiveness and localization, degree of functional disorders, peculiarities of clinical course, presence of complications and concomitant diseases.
At the decision of question about the relation of disease with action of professional factor it is necessary to analyze industriously the data of professional route, time of origin and clinical picture of disease, results of some special additional X-rays, laboratory and other researches, to eliminate the possible role of unprofessional factors in development of the given disease. The obligatory condition for the confirmation that the disease is professional is a work of patient in the conditions of action of harmful factors of work.
Acute professional disease (intoxications) can be diagnosed by the doctor of any medical-preventive establishment after obligatory consultation with the specialist of profpatologist and doctor of occupational hygiene of the territorial sanitary-epidemiology station.
Only specialized medical-preventive establishments have a right to diagnose first a chronic professional disease (or intoxications).
The large importance at the professional diseases has social, working and medical rehabilitation of patient, the purpose of which is a renewal of health, general and professional capacity of patient by taking of medical and social measures.
In the complex of measures after the rehabilitation of patients enter: early and timely detection of initial forms of professional and unprofessional illnesses, realizing of pathogenetically founded therapy, temporal or permanent employment of patient taking into account functional possibilities, profession, age and desire of sick.
Thus the basic tasks of medical rehabilitation are the realizing of medical and prophylactic measures directed on warning of chronic course and relapses of disease; of professional rehabilitation – renewal of professional capacity, retraining and rational employment of patients; of social-working rehabilitation – social, labour and domestic security of ill people and invalids.
(Сenters for diseases control and prevention: http://www.cdc.gov/niosh/hhe/HHEprogram.html)
What is a Health Hazard Evaluation?
An HHE is a study of a workplace. It is done to learn whether workers are exposed to hazardous materials or harmful conditions. On the basis of the information you provide, NIOSH responds to an HHE request in one of the following ways:
· NIOSH staff responds in writing with helpful information or a referral to a more appropriate agency.
· NIOSH staff calls to discuss the problems and how they might be solved.
· NIOSH staff visits the workplace. When this happens, they will meet with the employer and the employee representatives to discuss the issues. They will tour the workplace. They may review records about exposure and health, interview or survey employees, measure exposures, and do medical testing. These activities may happen during one or more visits. At the end of this evaluation, NIOSH will provide a written report to the employer and to the employee representatives. This can take from a few months to a few years, depending on the type of evaluation.
Who Can Request an HHE?
Private sector and Federal workplaces
An employee can request an HHE if he or she is currently an employee at the workplace of concern and has the signatures of two other employees. If the workplace has three or fewer employees, the signature of only one employee is enough.
An officer of a labor union that represents employees for collective bargaining can request an HHE.
Any management official may request an HHE on behalf of the employer.
For anyone who submits a request, NIOSH will not reveal to the employer the names of the persons who made the request if they indicate this on the request form
State or local government workplaces
When the workplace is part of a State or local government, NIOSH authority is more limited than for the private and Federal sectors. The cooperation of the employer may be necessary before NIOSH can do an evaluation.
Should you request an HHE?
Interviewing an emergency response worker.
When there is concern about a health hazard in a workplace, you can request an HHE, file a complaint with the Occupational Safety and Health Administration (OSHA), or request help from the OSHA Consultative Service. Some things to consider for each of these options are listed below.
When to request an HHE from NIOSH
You are an employee, employee representative, or employer and the following apply:
· Employees have an illness from an unknown cause.
· Employees are exposed to an agent or working condition that is not regulated by OSHA.
· Employees experience adverse health effects from exposure to a regulated or unregulated agent or working condition, even though the permissible exposure limit is not being exceeded.
· Medical or epidemiological investigations are needed to evaluate the hazard.
· The incidence of a particular disease or injury is higher than expected in a group of employees.
· The exposure is to a new or previously unrecognized hazard.
· The hazard seems to result from the combined effects of several agents.
When to request help from the OSHA Consultation Program
(http://www.osha.gov/dcsp/smallbusiness/consult.html):
You are a small business owner and you want:
· assistance in recognizing hazards in your workplace.
· suggestions or options for correcting safety and health issues.
· assistance in developing or maintaining an effective safety and health program.
· to reduce workers compensation cost and improve employee morale.
The OSHA On-site Consultation Program:
· is a free service.
· is delivered by state (and territorial) governments using well-trained safety and health professionals.
· is separate from enforcement.
· is confidential. The company’s name, and any other identifying information provided about the workplace, plus any unsafe or unhealthful working conditions that the consultant uncovers, will not routinely be reported to OSHA enforcement personnel.
· does not issue and citations, penalties, or fines.
· will provide you a confidential, written report that summarizes the consultant’s findings.
· requires the correction of hazards identified by the consultant(s).
· under specific circumstances, employers with exemplary safety and health programs can be recommend for recognition and provided with an exclusion from general schedule inspections.
When to file a complaint with OSHA
(www.osha.gov/as/opa/worker/index.html):
You are an employee and the following situations apply*:
· Immediate enforcement by a regulatory agency is needed.
· Employees want the employer to comply with existing health and safety standards.
· The hazard is well recognized.
· An OSHA standard is known to adequately protect employees from the hazard.
* Employers in the Federal sector may wish to explore the services available through the Division of Federal Occupational Health (DFOH), which maintains an office in each Federal region. State and local government employers may be eligible for help under the OSHA Consultation Program operating in their State. The State or local health department may also be able to help with occupational safety and health issues.
How Does NIOSH Respond to an HHE Request?
Wipe sampling to evaluate dermal exposure to a chemotherapy agent.
NIOSH logs in each request for an HHE and generally sends a letter to the person making the request. Most often this happens within a few weeks.When NIOSH decides to send information or make a referral to another agency, usually a letter is sent within 4-6 weeks.
When NIOSH decides that telephone consultation or a workplace visit is needed, a project officer is assigned. Usually, within 4-6 weeks, the project officer contacts the person who sent in the request. When the request is made by an employee or union, NIOSH also contacts the employer to let them know about the request and to arrange for a site visit. Typically, NIOSH does not conduct surprise visits.
What protections are provided for employees who request and participate in HHE investigations?
Confidentiality
If desired and noted on the HHE request form, NIOSH will not reveal to the employer the names of the persons who made the request. Personal information from records, questionnaires, interviews with NIOSH investigators, and individual medical results will be safeguarded in accordance with provisions of the Privacy Act.
Anti-discrimination Provisions
The Occupational Safety and Health Act and the Federal Mine Safety and Health Act forbid employers from retaliating or punishing employees for making HHE requests or cooperating with NIOSH investigators (see Section 11(c) of the Occupational Safety and Health Act or Section 105(c) of the Mine Safety and Health Act). The enforcement of these anti-discrimination provisions is the responsibility of the U.S. Department of Labor. If discrimination is suspected, contact the nearest OSHA or MSHA office immediately.
Role of the Employee Representative
The local, national, or international union may submit an HHE request on behalf of employees it represents. Two employees may authorize a third employee to submit an HHE request on their behalf.
The employee representative has the following rights:
· To accompany NIOSH investigators on the initial inspection of the workplace.
· To convey to the NIOSH investigators, privately if requested, additional information related to the HHE request.
· To participate in the opening and closing conferences.
· To receive copies of all interim and final reports
How Are HHE Results Reported?
Collecting noise measurements in an animal shelter.
NIOSH reports its findings and recommendations to employers, employees, and employee representatives. Verbal reports are normally provided to employer and employee representatives during a closing conference at the conclusion of a site visit, and by telephone. Often, results are only preliminary or incomplete at that time. Written interim reports are sometimes provided while an investigation is still in progress.
When all the information and data have been analyzed, NIOSH issues a report of its final determination, giving findings and recommendations. Copies of this report are sent to the requestor, the employer, employee representatives, OSHA, and other appropriate agencies.
The employer is required to post the final report in a place accessible to employees from all areas evaluated (alternatively, the employer may give NIOSH names and addresses of affected employees to permit NIOSH to mail the report to each affected employee.) Although NIOSH has no authority to force the employer to adopt its recommendations, experience has shown that most employers attempt to address any problems identified in the HHE report.
PNEUMOCONIOSIS, SILICOSIS, SILICATOSIS (etiology, pathogenesis, diagnosis, differential diagnosis, treatment, preventive measures).
Occupational lung diseases are a broad group of diagnoses caused by the inhalation of dusts, chemicals, or proteins. “Pneumoconiosis” is the term used for the diseases associated with inhaling mineral dusts. The severity of the disease is related to the material inhaled and the intensity and duration of the exposure. Individuals who do not work in the industry can develop occupational disease through indirect exposure. These diseases have been documented as far back as ancient
Importance of occupational lung diseases
1. Knowledge of cause may affect patient management and prognosis and may prevent further disease progression in the affected person
2. Establishment of cause may have significant legal, financial and social implications for the patient
3. The recognition of occupational and environmental risk factors can also have important public health and policy
4. Occupational and environmental lung diseases can also serve as important disease models
Pneumoconiosis is the generic term for the inhalation of mineral dust and the resultant diffuse, usually fibrotic, reaction in the acinar part of the lung. The term excludes asthma, neoplasia, and emphysema.
Occupational lung diseases (Pneumoconiosis) can be classified according to several schemes.
1. Clinical presentation
2. Type of exposure to agent
· Organic dusts
· Inorganic dusts
· Metals
· Biological factors
3. Types of industry potentially associated with respiratory diseases
The new classification by the
1. Pneumoconiosis, which develops by influence moderately and highly fibrogenic dust (with containing free silica more than 10 %) – silicosis, antracosilicosis, silicosiderhosis, silicisilicatosis. These pneumoconiosis are wide spread among sandblasters, fettlers, miners, workers for the production of ceramic materials. They are inclined to progressive fibrotic process and complication of tuberculosis infection.
2. Pneumoconiosis, which develops by influence mild fibrogenic dust (with containing free silica less than 10 % or not containing it) – silicatosis (asbestosis, talcosis, caolinosis, olivinosis, nephelinosis, pneumoconiosis from exposure to cement dust) –carboconiosis (anthracosis, graphitosis, black-lung carbon disease etc.), polisher’s and emery’spneumoconiosis, metalloconiosis or pneumoconiosis from exposure radiopaque dusts (siderosis, includingof aerosol electric welding or gas cutting iron products, baritoz, stanioz, manganokoniozetc). They are characterized by moderate fibrosis, benign and slow-progressive duration, often complicated by the non-specific infection, chronic bronchitis, which is mainly determined by the severity of illness.
3. Pneumoconiosis, which develops by influence toxic-allergic aerosols (dust, which containing metals-allergens, plastic and other polymeric material compounds, organic dust etc) – berylliosis, aluminosis, farmer’s lung and other hypersensitivity pneumonitis. In the initial stages of the disease they are characterized by a clinical picture of chronic bronchiolitis, alveolitis progressive course with the outcome of fibrosis. Dust concentration is not critical in the development of this group of pneumoconiosis. The disease is associated with a slight, but prolonged and close contact with the allergen.
The International Labour Organization (ILO) in 2000, revised the previous version of the classification of pneumoconiosis and amounted new, based on the coding of radiographic evidence of disease. he purpose of creation International Classification of X-ray is the standardization of methods of diagnosis of pneumoconiosis.
International Labour organization,
1. Diseases caused by agents
1.1 Chemical agents ( 32 items)
1.2 Physical agents ( 8 items )
1.3 Biological agents ( infectious and parasitic diseases contracted in an occupation where there is a par contracted in an occupation where there is a particular risk of contamination )
2. Diseases by target organ systems
2.1 Occupational respiratory diseases
2.2 Occupational skin diseases
2.3 Occupational musculoskeletal disorders
3. Occupational cancer ( 15 items )
(Asbestos, Benzidineand compounds, Bischloromethylether, chromium and compounds, coal tar, beta-naphthylamine, Vinylchloride, Benzene, Toxic nitro and amino derivatives of benzene, Ionizing radiations, Tar, pitch bitumen, mineral oil, and related compounds, coke oven emission, coke oven emission, wood dust ).
4. Other diseases
4.1 Miner’s nystagmus
2.1 Occupational respiratory diseases
2.1.1 Pneumoconioses caused by sclerogenic mineral dusts
2.1.2 Bronchopulmonary disease caused by hard-metal dust
2.1.3 Bronchopulmonary disease caused by cotton, flax, hemp or sisal dust
2.1.4 Occupational asthma
2.1.5 Extrinsic allergic alveolitis
2.1.5 Siderosis
2.1.6 Chronic obstructive pulmonary diseases
2.1.7 Diseases caused by aluminium
2.1.9 Upper airways disorders
2.1.10 Any other respiratory disease not mentioned in the proceeding items caused by an agent where the casual relationship is established
Basic principles of occupational lung diseases
Certain principles apply broadly to the full range of occupational respiratory disorders
While a few environmental and occupational lung diseases may present with pathognomonic features, most are difficult to distinguish from disorders of nonenvironmental origin
A given substance in the workplace or environment can cause more than one clinical or pathologic entity
The etiology of many lung diseases may be multifactorial and occupational factors may interact with other factors
The dose of exposure is an important determinant of the proportion of people affected or the severity of disease
Individual differences in susceptibility to exposures do exist
The effects of a given occupational or environmental lung exposure occur after the exposure with a predictable latency interval
The effects of an inhaled agent depend on many factors
• its physical and chemical properties (physical state (solid particulates, mist, vapor and gases), solubility, size, shape and density, concentration, penetrability, radioactivity, alkalinity, acidity, fibrogenicity, antigenicity)
• the susceptibility of the exposed person (integrity of local defense mechanisms, immunological status ( atopy, HLA type), airway geometry)
• the site of deposition within the bronchial tree (when airborne particles come in contact with the wall of the conducting airway or a respiratory unit they do not become airborne again, governs the lung response substantially, mechanisms of dust deposition, sedimentation, Inertial impaction, diffusion, interception, electrostatic precipitation)
Particle size is important
1. particles with a size of 5-10 microns are detained in the upper airways
2. particles with a size of 3-5 microns – in the mid respiratory tract
3. particles with a size of 1-3 microns – in alveoli
Clinical approach to the patient
There are two important phases in the workup of any patient with a potential occupational or environmental lung disease.
1. General approach: To define and characterize the nature and extent of the respiratory illness, regardless of the suspected origin
A detailed history
Physical examination
Appropriate diagnostic tools
2. To determine the extent to which the disease or symptom complex is caused or exacerbated by an exposure at work or in the environment
Occupational and environmental history – single most helpful tool in the diagnostic workup. First of all it is important to find out:
1. Employment details
Job title
Type of industry and specific work
Name of employer
Years employed
2. Exposure information
General description of job process and overall hygiene
Materials used by worker and others
Specific workplace exposures
Ventilation / exhaust system
Use of respiratory protection
Industrial hygiene informations provided by the employer to the employee
3. Environmental nonoccupational factors
Smoking
Diet
Hobbies
4. Details about past employments in chronological order
5. Other details
Does the patient think symptoms / problem is related to anything at work?
Are other workers affected?
Work absenteeism
Prior pulmonary problems and medications used
ILO – International Classification of radiographs of pneumoconiosis, 1971, 2002
1. Film quality : Grades I to IV
2. Small opacities, depending on their size, identified by the letter
Ø round opacities: p (<1.5mm)
q (1.5 –3mm)
r (3 – 10mm)
Ø Irregular opacities: s (<1.5mm)
t (1.5 – 3mm)
u (3 – 10mm)
Profusion:
Category 0: small rounded opacities absent or less profuse than in category 1
Category 1: small rounded opacities definitely present but few iumber
Category 2: small rounded opacities numerous. The normal lung markings are still visible
Category 3: small rounded opacities very numerous. The lung markings are partially or totally obscured
Large opacities
Category A: one or more large opacities not exceeding a combined diameter of
Category B: large opacities with combined diameter greater than
Category C: bigger than B
Pleural Abnormalities:
Location
width
extent
degree of calcification
Other abnormal features
Silicosis is the commonest type of pneumoconiosis orldwide. It is caused by inhalation of crystalline silicon dioxide, and may affect people working in quarrying, mining, stone cutting and polishing, sandblasting, and fettling. Silicosisoccurs in several different forms depending on the level and duration of exposure. Simple nodular silicosis is the most common form, and is similar clinically and radiographically to coal worker’s pneumoconiosis. Chronic silicosis presents with increasing dyspnoea over several years and chest radiography shows upper lobe fibrosis or calcified nodules. Acute silicosis results from a brief but heavy exposure: patients become intensely breathless and may die within months. Chest radiographs show an appearance resembling pulmonary oedema. Accelerated silicosis occurs as the result of less heavy exposure and presents as slowly progressive dyspnoea caused by upper lobe fibrosis. Coal worker’s pneumoconiosis is caused by inhalation of coal dust, which is a complex mixture of coal, kaolin, mica, silica, and other minerals. Simple coal worker’s pneumoconiosis usually produces no symptoms or physical signs apart from exertional dyspnoea. The diagnosis is made by a history of exposure and the presence of characteristic opacities on chest radiographs. A small proportion of individuals with simple coal worker’s pneumoconiosis go on to develop progressive massive fibrosis which, when sufficiently advanced, causes dyspnoea, cor pulmonale, and ultimately death. Coal worker’s pneumoconiosis is disappearing in developed countries as mines close and working conditions improve; however, it remains widespread in China and India.
Fig. 1 Chest radiograph of quarry worker showing extensive simple silicosis
Silicosis
Introduction
Silicosis is an occupational lung disease caused by inhalation of silica, a ubiquitous mineral found in abundance in the earth’s crust, composed of regular molecules of silicon dioxide (SiO2). Certain occupations predispose the individual to high concentrations of silica, which is fibrogenic to the lungs, resulting in radiographic and pathological abnormalities.
The first worst incidence of silicosis was recorded in the USA in 1930-1931 on the construction of Hawk’s Nest Tunnel in Gauley Bridge, West Virginia. It was called the worst industrial accident in US history.
Full description of silicosis by Bernardino Ramazzini (1633-1714) in early 18th century. Citation: “…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)
Workers engaged in occupations such as tunneling, mining, sandblasting and quarrying are inevitably exposed to the mineral, due to its ubiquity in the earth’s crust. Other occupations, such as work with gemstones, including jade polishers, foundry and pottery workers and glass and silica bricks workers, are associated with silica exposure.
The diagnosis of silicosis is based on the typical radiographic appearance of diffuse nodules or reticulonodular pattern in the presence of a strong occupational exposure to silica. The International Labour Organization (ILO) 2000 International Classification of Radiographs of the Pneumoconiosis is the most commonly accepted classification of extent of involvement of the pneumoconiosis and one in which the presence or absence of pneumoconiosis is established in workers exposed to mineral dust including silica. Standard reference radiographs are available from the ILO office with standard nomenclature to describe the changes.
Pathogenesis
The role of macrophages in the pathogenesis of silicosis has been extensively studied. Inhaled crystalline silica smaller than 5 μm are deposited in the small airways and alveoli from which they are ingested within 48 h of deposition by alveolar macrophages or tissue macrophages, if they penetrate the interstitium. Free particulate silica that are not ingested by macrophages enter the perivascular lymphatic channels to be translocated to the draining mediastinal lymph nodes as free particles or within macrophages. In vivo and in vitro studies have shown that these silica exposed macrophages release fibroblast growth factors that facilitate the accumulation of fibroblasts and fibroblast products, which induce inflammatory and fibrogenic reaction in the interstitium, alveoli and lymph nodes. Other inflammatory cells recruited in the lung in addition to the macrophages include lymphocytes, particularly T-helper cells and neutrophils.
Pathology
Classic (Nodular) Silicosis
Nodular silicosis is characterized by the presence of small rounded nodules of 3–6 mm in the lung parenchyma. The nodules of silicosis are well defined and located in the perivascular and peribronchiolar interstitium as well as in the paraseptal and subpleural interstitium and are preferentially distributed in the upper lobes. The silicotic nodule starts as a central zone of mononuclear cells surrounded by fibroblasts and collagen tissue. With time, the central zone becomes hypocellular, with concentric laminar deposition of reticulin, proteins, phospholipids and collagen in the periphery, giving a whorled appearance. Adjacent vessels and bronchioles may become involved and destroyed by these nodules, with occlusion of their lumen. Conglomeration of the nodules frequently occurs to form large masses of progressive massive fibrosis (PMF), usually in the upper lobes where nodular profusion is highest. The lower lobes are less frequently involved. PMF lesions sometimes cross the interlobar fissure to form elongated masses from lung apex to the lower lobe. Although conglomeration usually occurs in heavily dust-laden lung with a high profusion of nodules, its development does not always parallel nodular profusion. Cavitation of PMF masses occurs as a result of ischemic necrosis and mycobacterial infection.
Hilar and mediastinal lymph nodes are enlarged and pigmented, with a whorled appearance similar to that found in the silicotic nodule. Calcification is also a frequent finding. Features characterized on imaging, particularly on computed tomography (CT), will reflect these pathological changes in the lungs and lymph nodes.
The health lung and lung of the patients with silicosis
Three types of silicosis:
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.
Mixed Dust Fibrosis
Although the radiographic characteristics of mixed dust fibrosis have not been a subject of interest in recent literature, this entity is frequently described in pathology textbooks and is of some clinical importance within the context of lung damage in silica-exposed workers. Exposure to high content (more than 18% of total dust deposited in lung) of free crystalline silica results in classic silicosis, while mixed dust fibrosis develops in the presence of low silica content (less than 18% of total dust deposited in lung), particularly with simultaneous inhalation of other minerals such as non-fibrous silicate (mica, kaolin, coal, talc, fuller’s earth, etc.).
These non-fibrous silicates augment the strong fibrotic effect of crystalline silica. Instead of a well-defined, whorled appearance found in the silicotic nodule, the lesions in mixed dust fibrosis are characterized by irregular shaped fibrotic nodules (often called stellate nodules) and a predilection of the fibrotic lesion to extend into the surrounding pulmonary interstitium (Fig. 2). The stellate nodules are less fibrotic with less collagen and are more cellular than silicotic nodules. Calcification in the nodule is rarely observed.
Fig. 2a,b. A 72-year-old retired tunnel worker with silicotic nodules and mixed dust fi brosis. a Posterior–anterior chest radiograph shows ill-defi ned multiple small nodules and reticular opacities in both upper lobes. b Photomicrograph obtained at autopsy performed 2 years after chest radiograph shows two pneumoconiotic nodules with stellate appearance.
The left nodule shows irregular shape without whorled appearance (arrows) typical of silicotic nodule. The right nodule also shows irregular shape but has a central whorled appearance of silicotic nodule. Emphysema is identified around the nodules of silicosis or fibrosis.
Depending on the proportion of crystalline silica in the inhaled dust, mixed dust fibrosis and silicotic nodules coexist in the same lung, thus forming a spectrum of pathological findings. The nodules of mixed dust fibrosis are also located within the center of the secondary pulmonary lobule and in the subpleural and paraseptal interstitium, with upper lobe predominance.
Silicoproteinosis
The principal finding in silicoproteinosis is the presence of surfactant protein filling the alveolar spaces, as is seen in acquired form of alveolar proteinosis. Silicotic nodules are sparse and poorly demarcated or absent, probably because of a short period of time after exposure. There is diffuse alveolar wall thickening and fibrosis, as is seen in acquired form of proteinosis
The three main clinical presentations of silicosis are classic silicosis, accelerated silicosis and silicoproteinosis. Classic silicosis is the most common presentation, in which patients remain asymptomatic until after an interval of 10–20 years of continuous silica exposure, by which time radiographic evidence is present. With accelerated silicosis, the exposure time after which the disease becomes clinically evident is much shorter, ranging from 5 years to 10 years of exposure, and the rate of disease progression noticeably faster.
Clinical presentation as early as 1 year after exposure and death within 5 years has been reported. High concentrations of dust in a relatively confined space are thought to predispose the individual to this form of silicosis. However, for all intents and purposes, the radiographic, clinical and pathological features of this entity are nearly indistinguishable from classic silicosis.
Silicoproteinosis is another acute and progressive form of silicosis that often results in death from respiratory failure. This variant of silicosis is also associated with high dust concentration in occupations such as sandblasting, tunneling and quartzite milling.
Radiological Evaluation
Chest Radiograph
The chest radiograph remains the most convenient imaging modality by which silicosis is diagnosed and its progression monitored (Fig. 3).
Fig. 3a,b. A 67-year-old old retired tunnel worker. a Posterior–anterior (PA) chest radiograph obtained in 2000 showing small nodules predominantly on the upper lobe. The nodule size and profusion are p/p and 1/1 respectively. b PA chest radiograph obtained in 2004 show progression in the profusion of the nodules from 1/1 to 2/2. There is also more prominent egg-shell calcifi cation of enlarged hilar lymph nodes (arrows)
In the ILO classification of radiographs, the radiographic opacities are characterized by their size and shape. Small rounded opacities are described as “p”, “q” or “r”, according to their size (
Fig. 4a,b. Chest radiographs of two retired metal ore miners illustrating different categories of profusion of “r”-size nodules. a Posterior–anterior (PA) chest radiograph shows multiple nodules in both lungs. The nodule profusion category is 2/2. b PA chest radiograph shows more severe nodular profusion of category 3/3
These can be grouped into 4 broad categories, based on the degree obscuration of vascular lung markings by the nodules: category 0 (0/0, 0/0, 0/1), when small opacities are absent or less than category 1; category 1 (1/0, 1/1, 1/2), when small opacities are present in small numbers with normal lung markings (Fig. 3); category 2 (2/1, 2/2, 2/3), wheumerous small opacities are present and when lung markings are partially obscured) (Fig. 1, Fig. 4) and category 3 (3/2, 3/3, 3/+), when very numerous small opacities totally obscure normal vascular markings (Fig. 4). less than the right upper zone and C is used when one or more opacities has a combined area greater than the area of the right upper zone.
On the chest radiograph, the nodules in simple silicosis are well defined and small, ranging from
These PMF lesions are usually found in the upper zones with smooth or irregular borders. They commonly start off at the outer two-thirds of the lung, migrating centrifugally with time towards the hilum, resulting in paracicatricial emphysema between the PMF and the pleura, with volume loss in the upper lobes. With increasing severity of PMF and shrinkage of the upper lobes, reduced nodularity in the rest of the lungs will be noted. Unilateral PMF is uncommon and, when present, can be mistaken for carcinoma of the lung.
Accelerated silicosis has similar radiographic features as the classic form of silicosis, except for its earlier onset and rapid rate of progression, which is truncated to a period of between 5 years and 10 years. Silicoproteinosis is a variant characterized by rapid and progressive involvement of the lungs with bilateral air space opacities similar to that found in alveolar proteinosis. The rate of progression ranges from a few months to a couple of years, usually culminating in death in a few years. Lymph node involvement in silicosis reflects the pathogenesis of the disease, and hilar lymphadenopathy on the chest radiograph is therefore common. “Eggshell” calcification of lymph nodes has become synonymous with silicosis, since they were first described over half a century ago and are mainly referable to the hilar lymph nodes (Fig. 3), although abdominal lymph nodes have also been described as bearing eggshell calcification. Its presence in coal and metal miners has been attributed to the concomitant exposure to silica.
Radiographic progression in silicosis is associated with the following risk factors: duration and concentration of silica exposure, initial nodular profusion on chest radiograph, simple and complicated disease, tuberculous infection, age at initial radiograph, race and time interval between radiographs. Workers who are exposed to high concentration and longer duration of dust exposure with complicated disease or tuberculous infection and who are younger at initial radiograph, are non-Caucasians and had longer duration between radiographic follow-up are reported to be more likely to have radiographic progression than their counterparts. Complicated disease on initial chest radiograph and interval of radiographic follow were independent determinants of radiographic progression in 37% of 141 granite workers with silicosis exposed to high levels of silica.
Computed Tomography/Thin-Section
Computed Tomography
The superiority of CT, and thin-section CT over the chest radiograph in evaluating interstitial and parenchymal lung disease is well established. Prior to the advent of multi-slice CT, CT evaluation of silicosis was performed using conventional or spiral CT scans comprising contiguous 7-mm or 10-mm section thickness supplemented by thin-section CT scans obtained with 1–2 mm collimation.
These CT techniques allowed clearer depiction of nodules, pleural calcification and conglomeration of nodules than the chest radiograph.
Due to superimposition of lesions,
Fig. 5a–e. Complicated silicosis in a 79-year-old retired tunnel worker. a Posterior–anterior chest radiograph shows bilateral large opacities in the upper lung zones near the pulmonary hila (arrows) compatible with the diagnosis of complicated silicosis. Note that there is bilateral hilar lymphadenopathy with reduced background nodulation. b Spiral computed tomography image (10-mm thickness) shows bilateral larger nodules with irregular shape, suggesting progressive massive fi brosis (PMF). There are paracicatricial emphysema around the PMF in the right lung. c Mediastinal window image shows punctuate calcifi cation in the PMF as well as in the mediastinal lymph nodes. d Macroscopic lung image in coronal section reveals black-pigmented PMF in the right upper lung zone adjacent to and contiguous with the right hilar lymphadenopathy. There is moderate centrilobular emphysema but sparse silicotic nodules. e Gough–Wentworth whole-lung section clearly demarcates the PMF as well as silicotic nodules with pigmentation. Note that there are advanced emphysematous changes around the PMF in both upper lobes
On CT and thin-section CT, the silicotic nodules are well defined, ranging from
Fig. 7a-c. A 56-year-old tunnel blaster with simple silicosis and lung cancer who was evaluated with multi-slice computed tomography (CT) scan of the thorax (2.5-mm slice thickness) with retrospective reconstruction into 1.25-mm thin-section CT scans. a CT scan (2.5-mm thickness) shows small centrilobular nodules in both lungs, with an irregular mass in the superior left hilum. b Thin-section CT scan (1.25-mm thickness) at the same level as a was reconstructed from the multidetector CT data set. c CT scan (2.5-mm thickness) in mediastinal window shows enlarged mediastinal lymph nodes with dense (arrowheads) and eggshell (arrows) calcifi cation
In their review of thin-section CT scans in 55 patients with type-p pneumoconiosis, Akira et al. found intralobular areas of low attenuation with a central dot, which corresponded to irregular fibrosis around and along the respiratory bronchioles and to focal areas of centrilobular emphysema in two post-mortem specimens. Nevertheless, there is still debate whether centrilobular emphysema (Fig. 5.10) found in silicosis is due to silica dust per se, exposure to other dust, such as coal and asbestos, or to concomitant smoking. Some studies have reported that emphysema in silicosis occurs independently of smoking, while other investigators believe that silicosis per se without PMF does not contribute to emphysema.
All patients had enlarged lymph nodes in at least two lymph node stations, with calcification found iearly 50% of lymph node stations. Hyperdense lymph node (Fig.8) was present in one-third of
Fig. 8a,b. A 78-year-old retired construction site worker. a Computed tomography (CT) scan (7-mm thickness) through the upper lobes shows typical silicotic nodules in a centrilobular distribution. b CT scan in mediastinal window shows densely calcifi ed (arrow) and hyperdense (arrowheads) lymph nodes in the mediastinum and hila
Fig. 9a,b. A 74-year-old retired tunnel blaster with progressive massive fi brosis (PMF) complicated by tuberculosis. a Thinsection CT scan through the lung apices shows a cavitating PMF lesion (arrowheads) in the right upper lobe secondary to mycobacterium tuberculosis infection. Note paracicatricial emphysema (arrows) surrounding the left PMF lesion and traction bronchiectasis in both lung apices. b Thin-section CT scan through the lower lobes shows a loculated pneumothorax (arrows) at the lateral aspect of the left lower lobe secondary to ruptured paracicatricial emphysema
Thin-section CT appearances of silicoproteinosis have been described only in occasional case reports. In addition to diffuse ground-glass opacities that typify idiopathic alveolar proteinosis, the presence of centrilobular poorly defined nodules and consolidation in the dorsal portion of lower lobes serve to differentiate silicoproteinosis from the former. Bilateral hilar lymphadenopathy is another discriminating feature found in silicoproteinosis. The pathological basis for the centrilobular nodules and peripheral consolidation has not been disclosed, although ground-glass opacity has been attributed to the accumulation of excess alveolar surfactant protein.
Fig.10a,b. A 68-year-old retired construction site worker. a Thin-section CT scan through the upper lobes shows bilateral progressive massive fi brosis (PMF) with surrounding paracicatricial emphysema. b Thin-section CT scan through the lower lobes shows confl uent centrilobular emphysema (asterisks) in the right lower lobes and bullae in the left lower lobe (arrows )
Complications
There are a few diseases that may complicate silicosis; these are primarily Caplan’s syndrome, tuberculosis, carcinoma and connective tissue disease. The two most serious complications, lung cancer and tuberculosis, may affect the prognosis and natural history of the underlying disease. Caplan’s syndrome, also known as rheumatoid pneumoconiosis, was initially identified in coal workers’ pneumoconiosis but is now known to occur in silicosis as.
The incidence of this disease ranges from 0.48% to 0.74%. The rheumatoid pneumoconiotic nodules are similar to necrobiotic nodules seen in rheumatoid arthritis and are described as either classic or silicotic type based on their pathological findings. The classic type corresponds to the original Caplan’s cases, showing large nodules characterized by uniform necrosis and associated with little background pneumoconiotic nodules.
On the chest radiograph, rheumatoid pneumoconiosis presents with multiple well-defined nodules ranging from
In cases of indolent nodular tuberculosis, it may be impossible to isolate the tubercle bacilli in the sputum, in which case polymerase chain reaction has been advocated as a means of identifying the organism.
The association between silicosis and lung cancer is also well documented. Silica has been recognized as a probable human carcinogen [International Agency for Research on Cancer (IARC) type 2A] since
The strength of the association between silicosis and connective tissue disease varies with the type of connective tissue disorder. The risk of developing systemic sclerosis, particularly in workers with high exposure to silica dust, is well established, although such casual associations between silicosis, rheumatoid arthritis and systemic lupus erythematosis are less widely reported.
Differential Diagnosis
A similar centrilobular and subpleural distribution of nodules may be noted in sarcoidosis and lymphangitis carcinomatosis, although a careful review of the clinical history may provide useful pointers for and against these other diseases. In addition, on thin-section CT, there are a few distinguishing features, such as beaded septa and fissures and reticular opacities, which are usually not found in silicosis. Clustering of nodules around parahilar regions and bronchi are also more commonly found with sarcoidosis.
Anthracosis
Previously it was thought that pulmonary “anthracosis” was inert. Studies indicate that there are two general phases in coal miners pneumoconiosis – (1) the first phase is labelled simple pneumoconiosis which is associated with little ventilatory impairment. This phase may require about 12 years of work exposure for its development (2) the second phase is: characterised by progressive massive fibrosis (PMF); this causes severe respiratory disability and frequently results in premature death. Once a background of simple pneumoconiosis has been attained in the coal worker, a progressive massive fibrosis may develop out of it without further exposure to it. From the point of view of epidemiology, the risk of death among coal miners has beeearly twice that of the general population. Coal-miners’ pneumoconiosis has been declared a notifiable disease in the Indian Mines Act of 1952 and also compensatable in the Workmen’s Compensation (Amendment) Act of 1959.
Byssinosis
Byssinosis is due to inhalation of cotton fibre dust over long periods of time. The symptoms are chronic cough and progressive dyspnoea, ending in chronic bronchitis and emphysema. India has a large textile industry employing nearly 35 per cent of the factory workers. Incidence of byssinosis is reported to be 7 to 8 percent in three independent surveys carried out in Mumbai, Ahmedabad and Delhi.
Organic dust toxic syndrome can be defined as a febrile illness following exposure to organic dust in individuals who do not have evidence of hypersensitivity pneumonitis. However, some investigators believe that the two abnormalities represent a spectrum of findings in the same disease rather than two separate entities. Typically, fever and influenza-like symptoms occur 4–8 hours after dust exposure; symptoms of dry cough, chest tightness, mild dyspnea, and wheezing may also be present. Organic dust toxic syndrome is thought to be much more common than farmer lung. It has been estimated that the disorder may be 50 times more common than hypersensitivity pneumonitis in farmers. Organic dust toxic syndrome encompasses diseases previously described by a variety of terms, including humidifier fever (in office and hospital workers), pulmonary mycotoxicosis, grain fever, pig fever, cotton fever (byssinosis), and wood-chip fever. The common pathogenetic link between these disorders may be the presence of a bacterial endotoxin in the dust or aerosol. The mechanisms underlying organic dust toxic syndrome and the interrelationships between this syndrome and other occupational lung diseases associated with organic dust inhalation (including asthma, chronic airway obstruction, and hypersensitivity pneumonitis) are still poorly understood. The disorder shares some features with hypersensitivity pneumonitis: Both frequently occur after exposure to moldy vegetable matter, and affected patients improve rapidly without therapy. However, it is important to distinguish between the two disease entities because organic dust toxic syndrome causes no permanent impairment of lung function.
Byssinosis occurs in textile workers exposed to the dust of cotton, flax, hemp, and jute. In its early stages, byssinosis is characterized by acute dyspnea, cough, and wheeze on Monday morning following a weekend away from the workplace; symptoms decrease during the work week, despite continued exposure. The prevalence and severity of symptoms and functional impairment are proportional to the duration and intensity of exposure. Although the pathogenesis of byssinosis is unclear, it may be related to the presence of a bacterial endotoxin rather than the textile itself. The disorder shares some features with hypersensitivity pneumonitis: Both frequently occur after exposure to dust, and affected patients improve rapidly without therapy
Byssinosis in a 56-year-old woman who had had frequent episodes of “Monday fever” and dyspnea while working in a cotton quilt factory over a 7-year period. (a) Chest radiograph shows diffuse, ill-defined haziness, predominantly in the lower lung zones. (b) High-resolution CT scan shows numerous ill-defined small nodules with ground-glass attenuation in both lungs.(c) High-resolution CT scan obtained 23 days later shows resolution of the ground-glass attenuation with fewer residual small nodules than were previously noted. No abnormality was seen at high-resolution CT performed 1 year after the patient quit her job. In spite of prolonged exposure, the patient’s respiratory symptoms and pulmonary functional impairment resolved completely.
From: http://radiographics.rsna.org/content/21/6/1371/F47.expansion.html
Bagassosis
Bagassosis is the name given to an occupational disease of the lung caused by inhalation of bagasse or sugar-cane dust. It was first reported in India by Ganguli and Pal in
Bagassosis has been shown to be due to a thermophilic actinomycete for which the name Thermoactinomyces sacchari was suggested. The symptoms consist of breathlessness, cough, haemoptysis and slight fever. Initially there is acute diffuse bronchiolitis. Skiagram may show mottling in lungs or shadow. There is impairment of pulmonary function. If treated early, there is resolution of the acute inflammatory condition of the lung. If left untreated, there is diffuse fibrosis, emphysema and bronchiectasis.
PREVENTIVE MEASURES :
(1) DUST CONTROL: Measures for the prevention and suppression of dust such as wet process, enclosed apparatus, exhaust ventilation etc., should be used. (2) PERSONAL PROTECTION: Personal protective equipment (masks or respirators with mechanical filters or with oxygen or air supply) may be necessary.
(3) MEDICAL CONTROL: Initial medical examination and periodical medical check-ups of the workers are indicated.
(4) BAGASSE CONTROL: By keeping the moisture content above 20 per cent and spraying the bagasse with 2 percent propionic acid, a widely used fungicide, bagasse can be rendered safe for manufacturing use.
Asbestosis
Asbestos is the commercial name given to certain types of fibrous materials. They are silicates of varying composition; the silica is combined with such bases as magnesium, iron, calcium, sodium and aluminium. Asbestos is of two types –serpentine or chrysolite variety and the amphibole type. Ninety per cent of the world’s production of asbestos is of the serpentine variety, which is hydrated magnesium silicate, the amphibole type contains little magnesium. The amphibole type occurs in different varieties, e.g., crocidolite (blue), amosite (brown), and anthrophyllite (white). Asbestos fibres are usually from 20 to 500 μ in length and 0.5 to 50 ц in diameter. Asbestos is used in the manufacture of asbestos cement, fire-proof textiles, roof tiling, brake lining , gaskets and several other items. Asbestos is mined in Andhra Pradesh (Cudappah), Bihar, Jharkhand, Karnataka, and Rajasthan – but most of it is imported from USSR, Canada, US and South Africa.
Asbestos enters the body by inhalation, and fine dust may be deposited in the alveoli. The fibres are insoluble. The dust deposited in the lungs causes pulmonary fibrosis leading to respiratory insufficiency and death; carcinoma of the bronchus; mesothelioma of the pleura or peritoneum; and cancer of the gastro-intestinal tract. In Great Britain, an association was reported between mesothelioma and living within
Asbestous fibres under
the electronic microscope
Fig. 12. The sputum shows “ASBESTOS BODIES” which are asbestos fibres coated with fibrin.
Fig.
Pleural plaques, diffuse pleural thickening, rounded atelectasis, and asbestosis in a 50-year-old man with asbestos exposure from working in a brake lining production plant. (a) Chest radiograph shows diffuse thickening of the left pleura and curvilinear band opacities in the left lower lung zone. (b) High-resolution CT scan (mediastinal windowing) shows pleural plaques on the right side (small white arrows) and rounded atelectasis (large white arrow) with adjacent diffuse pleural thickening (black arrows) on the left side. (c) High-resolution CT scan obtained at a lower level than b demonstrates pleural plaques along the diaphragmatic contour (black arrows) and an irregular attenuation pattern, which is typical in rounded atelectasis (white arrows). (d) High-resolution CT scan (lung windowing) obtained at the level of the liver dome shows a visceral pleural plaque in the right major fissure (arrow) and curvilinear bands of hyperattenuation in the posterior subpleural area. Note also the rounded atelectasis with posterior displacement of the left major fissure. The diagnosis of asbestosis was proved at open lung biopsy. (from
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An asbestos wart, or sometimes referred to as an asbestos corn, may develop when unprotected skin becomes irritated or damaged by asbestos fibers. Asbestos fibers, which are microscopic in size, tend to be harsh, needle-like spurs that easily penetrates the skin. If the particle remains in the skin, the area becomes inflamed and in time callus-like skin cells form around the asbestos particle. Due to the nature of asbestos, the human body has a difficult time expelling the material once in the body. Workers who directly handle asbestos may develop small, hard callus-type growth or scars on the fingers and hands where asbestos particles penetrated the skin. An asbestos wart posses a minimal risk of secondary contamination into the blood stream or other organs from skin exposure since asbestos is not likely to be absorbed through the skin.
Bronchogenic Carcinoma and Asbestos Exposure
The association between asbestos exposure and bronchogenic carcinoma is accepted as being causal iature. Bronchogenic carcinoma is estimated to develop in 20%–25% of workers who are heavily exposed to asbestos. The risk is increased in asbestos workers who smoke because smoking and asbestos exposure interact in a multiplicative manner. The risk of bronchogenic carcinoma in asbestos workers who smoke may be as much as 80–100 times that in the nonsmoking, nonexposed population. Asbestos-related tumors frequently occur in the periphery of the lungs with a lower lobe distribution, which correlates with the usual distribution of asbestosis.
MalignantMesothelioma
Diffuse malignant mesothelioma is an uncommon and fatal neoplasm of the serosal lining of the pleural cavity, peritoneum, or both. The risk of mesothelioma in an asbestos worker is approximately 10% over his or her lifetime. Persons at risk include not only the worker but other household members as well as persons who reside near asbestos mines and plants. Usually, a latency period of approximately 20–40 years occurs between exposure and tumor detection. The tumor commences as nodules on the visceral or parietal pleura that progress to a thick rind encasing and constricting the lung. Unilateral pleural effusion is the most frequent manifestation of malignant mesothelioma at initial chest radiography. At CT, the combination of mediastinal pleural involvement and thick (
The preventive measures consist of:
(1) use of safer types of asbestos (chrysolite and amosite);
(2) substitution of other insulants: glass fibre, mineral wool, calcium silicate, plastic foams, etc.;
(3) rigorous dust control;
(4) periodic examination of workers; biological monitoring (clinical, X-ray, lung function), and
(5) continuing research.
EXOGENOUS ALLERGIC ALVEOLITIS
It is a general term of the group of allergic pneumonias, which progress with involvement into a diffusive dispersed inflammatory process of some groups of alveoles.
Etiology. The reason of the development of exogenous allergic alveolitis is the allergen, which enters the organism with inhalation, together with the inhaled air. Such allergens can be weevil (wheat), extract from the dust of cacao beans (cacao beans), serum protein, antigens of bird droppings (feature and droppings of pigeons, chickens, and parrots), thermophilic actinomycetin (rotten hay), penicillin (medicinal drugs), salts of heavy metals (chemical matters), etc.
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Size and number of particles are very important in the development of alveolitis. It is considered that particles up to 5 micromicrons easily achieve alveoli and are capable to cause sensitizations.
Pathogenesis. Allergen, which gets to the organism, causes sensitization, accompanied by the creation of antibodies. These precipitant antibodies together with allergen create immune complexes, capable to deposit in the walls of alveoli, and bronchial tubes. They cause inflammation (bronchiolitis and alveolitis), increased permeability of vessel walls (due to discharges of mast cells and basophiles of vasoactive amines), formation of granulomas (granulomatous pneumonitis), which leads to the development of interstitial fibrosis and disorders of ventilation function of lungs of the restrictive type.
Clinics. Clinical pattern of the disease is characterized by general symptoms (fever, pain in muscles, reduction of body weight). Sings, connected with the affection of respiratory organs, show involvement of bronchioles and alveoli into the pathologic process.
Often the disease starts with the growing dyspnea and coughing. When using auscultative methods, it is often possible to hear crepitations, mostly in interscapular regions. Acute form can be recognized rather easily. At functional research, decrease of blood saturation with oxygen, increase of partial pressure of CO2 in the arterial blood, also clear respiratory alkalosis can be observed. Pulmonary capacity is reduced in the majority of cases, in particular, lung vital capacity.
Alveolitis can be chronic. It develops in the result of repeated less intensive influences of disease causing agents in several months after coming across them and are characterized with progressing respiratory insufficiency. Patients are bothers with dyspnea, sometimes with moderate fever and drowse. With X-ray examination, interstitial fibrosis can be observed.
One of the examples of allergic alveolitis is “farmer’s or thresher’s lung”. That is the disease when inhaling of organic dust causes the reaction of increased sensitivity on the alveolar level, connected with the production of precipitin, and which is characterized with allergic diffusive affection of alveolar interstitial structures of lungs. The disease can be met among agricultural workers, which come across damp moldy hay, grain, silo and other herbal materials. It is more often can be observed in winter and autumn period of the year, when hay stocks are used as feed for domestic animals. Mostly, the development of the “farmer’s lung” disease is caused by thermophilic actinomycetes: Micropolyspora faeni and Thermoactinnomyces vulgaris.
Acute forms are characterized by their sudden initiation. In 3 to 6 years after the exposure, temperature suddenly increases up to 39 to 40 ºC, headaches appear, as well as pain in muscles, and coughing with poor phlegm, and sometimes with the mixture of blood. Sometimes, there is nausea and vomit, voluminous hidrosis, and progressing dyspnea. During examination, cyanosis, tachycardia, frequent breathing at rest can be observed; and crepitations and single dry rales can be observed during auscultative examination. After radiological examination, intensification of pulmonary picture and small nodular types of different intensiveness can be observed. If the action of the allergen is eliminated, symptoms of the disease disappear in 7 to 10 days.
To treat exogenic allergic alveolitis (in particular of subacute and chronic forms), corticosteroids are used. Prednisolone is prescribed in the dosage of 1 mg/kg a day for 7 to 14 days, then the dose is gradually reduced.
Figures 7, 8 (7) Bird fancier’s disease. Axial high-resolution CT images show multifocal ground-glass opacities in the right lung. Spared lobules (arrow) probably represent air trapping, but expiratory high-resolution CT images were not available for confirmation. (8) Insidious onset of hypersensitivity pneumonitis in a 63-year-old man with repeated exposure to birds and mold. The results of serum testing were positive for mold precipitins, and lymphocyte predominance was found in bronchoalveolar lavage (BAL) fluid. Axial high-resolution inspiratory (a) and expiratory (b) CT images demonstrate patchy ground-glass opacities, normal regions, and air trapping. This combination of findings, known as the headcheese sign, is indicative of hypersensitivity pneumonitis. The accentuation of the attenuation difference between lobules with low or normal attenuation and those with high attenuation on expiratory images helps confirm the presence of air trapping. (from: From the Department of Medicine, VA Medical Center, Seattle, Wash (J.V.H.); and Department of Radiology, University of Washington Medical Center, Box 357115, 1959 NE Pacific St, Seattle, WA 98195 (S.N.J.P., J.D.G.). Received January 27, 2009; revision requested April 8 and received April 23; accepted May 8. All authors have no financial relationships to disclose. Address correspondence to S.N.J.P. (e-mail: [email protected])
Treatment and Prognosis. The most important recommended therapy is curtailing exposure to the causal agent by eliminating it from the environment, avoiding settings where it is present, or using a respirator in those settings. Systemic corticosteroids at doses equivalent to 40–60 mg of prednisone daily for a few days to weeks may improve symptoms of all forms of the disease, although substantial fibrosis and emphysema are less likely to respond. Indications for the use of such drugs include acute, severe, or progressive disease. The effectiveness of corticosteroid therapy lasting 12 weeks is not evidently superior to that of 4 weeks’ duration , and corticosteroid therapy apparently confers no long-term benefits.
Verification of the ability to work. Issues as to the ability to work of patients with the disease of lungs, conditioned by the impact of rottening herb dust, is solved the same way as in case of corresponding forms of dust diseases of lungs, caused by other types of dust.
Preventive measures. Main preventive measures for the patients with exogenous allergic alveolitis are in preventing the contact of the patient with corresponding allergens by the change of technological process (decrease of concentration of the allergen in the exhaled air), as well as the usage of respirators and other means of individual protection of respiratory organs.
References
1. 1. Davidson’s Principles and practice of medicine (21st revised ed.) / by Colledge N.R., Walker B.R., and Ralston S.H., eds. – Churchill Livingstone, 2010. – 1376 p.
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3. The Merck Manual of Diagnosis and TherapyRobert S. Porter., 19th Revised edition. –
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5. P. A. Gevenois and P. De Vuyst. Imaging of occupational and environmental disorders of the chest. – 2006. – 124 p.
6. Akira M. High resolution CT in the evaluation of occupational and environmental disease. Radiol Clin North Am (2002) 40:43-59.
7. K. Park. Park’s textbook of preventive and social medicine. –
8. Web -sites:
a) http://emedicine.medscape.com/
b) http://meded.ucsd.edu/clinicalmed/introduction.htm
