Alexander, Hyman

Nathan, Arthur

English

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DePaul Law Review Volume 18 Issue 2 Issue 2 & 3 Summer 1969 Article 18 Medical-Legal Aspects of Pulmonary Disease Hyman Alexander Arthur Nathan Follow this and additional works at: https://via.library.depaul.edu/law-review Recommended Citation Hyman Alexander & Arthur Nathan, Medical-Legal Aspects of Pulmonary Disease, 18 DePaul L. Rev. 613 (1969) Available at: https://via.library.depaul.edu/law-review/vol18/iss2/18 This Article is brought to you for free and open access by the College of Law at Via Sapientiae. It has been accepted for inclusion in DePaul Law Review by an authorized editor of Via Sapientiae. For more information, please contact digitalservices@depaul.edu. MEDICAL-LEGAL ASPECTS OF PULMONARY DISEASEHYMAN ALEXANDER*ARTHUR NATHAN'1INTRODUCTIONHIS ARTICLE on the medico-legal aspects of pulmonary disease iswritten by physicians for lawyers. It is hoped that the medicalfacts and concepts presented will assist interested members ofthe legal profession in finding areas of further legal import. The fewdiseases which have been chosen are frequently involved in workmen'scompensation proceedings and lend themselvs more to legal evaluationthan many other diseases, although it is appreciated that those diseasesnot discussed have found and may again find their day in court. Beyondthe scope of this article are: the role of individual susceptibility, theresponsibility of the individual, and the responsibility of communitieswhere disease is more prevalent, all of which demand further analysisand evaluation.PNEUMOCONIOSISPneumoconiosis is a disease of the lungs caused by the inhalation ofnoxious dusts. It develops because of occupational exposure to offend-ing agents. The employer legally has certain obligations. In some states,departments of industrial hygiene attempt to keep the hazard at aminimum. Occasionally, a union group will exert pressure on an em-ployer or an industry to correct certain conditions which contribute to* DR. ALEXANDER is an Associate Attending Physician at University Hospital in NewYork and a Consulting Physician for the United States Public Health Service. He is an Asso-ciate Professor of Clinical Medicine at New York University Medical School. DR. ALEXANDERreceived his B.S. from the City College of New York and his M.D. from CreightonUniversity Medical School. He is a Fellow of the American College of Physicians,American College of Chest Physicians, and New York Academy of Medicine.t DR. NATHAN is the Assistant Chief, Pulmonary Disease Service, at the VeteransAdministration Hospital in New York City. He is an Assistant Professor of ClinicalMedicine at New York University School of Medicine. DR. NATHAN received his B.S.from the City College of New York and his M.D. from the University and BellevueHospital Medical School. He is a Fellow of the American College of Physicians and theNew York Academy of Medicine.DE PAUL LAW REVIEWthe hazard. If the employee becomes disabled because of pneumoconio-sis, state workmen's compensation laws will generally compensate himfor his disability, but, in most states, the condition must be disablingbefore compensation is awarded.Most dusts are incapable of producing significant diseases. Only afew dusts produce sufficient tissue reaction in the lungs to impair pul-monary function. A knowledge of the occupations in which causativeagents are encountered is essential in order to evaluate causally relateddisability. The materials encountered, the working conditions, the meth-ods used, the protective measures employed and the hygiene practicedmust be ascertained and evaluated. Different dusts are capable of pro-ducing varying degrees of hazard. Thus, the pneumoconiosis may bedivided into major pneumoconioses and minor pneumoconioses. Themajor pneumoconioses are silicosis, abestosis, talcosis and coal miner'spneumoconiosis. Among the minor pneumoconioses are those causedby anthracite, diatomaceous earth, silicates (mica, clays, feldspar),and the vegetable dust pneumoconioses such as mill fever, byssinosis,bagassosis, farmer's lung, weaver's cough and others. In addition, thereis a group of benign pneumoconioses such as baritosis, siderosis, stan-nosis, graphosis, and exposure to limestone, marble, cement, and otherdusts. Whether or not impaired pulmonary function ultimately resultsdepends on the development of fibrosis in the lungs or the magnitudeof the damage to the bronchioles, air sacs, and pulmonary blood vessels.SILICOSISWhether or not an individual develops disabling silicosis dependson a number of factors:1. The substances with which the employees came into contact whileat work. Quartz, quartzite, sandstone, flint, tripoli, diatomaceous earthand silica sand contain high contents of silicon dioxide which is thecausative agent in silicosis. Thus, quartz is almost pure silicon dioxide.Granite contains sixty per cent pure silicon dioxide. Silica sand hasa very high content of silicon dioxide. Mining, tunneling, quarrying,highway construction, foundry work, sand blasting, and the makingof pottery are some of the industries in which high quantities ofsilicon dioxide are encountered.2. Dust particle size. Inhaled particles over three micra in diameterdo not produce typical silicotic nodules in the lung. Particles whichrange from one to three micra in diameter generally produce nodular[Vol. XVIII: 613PULMONARY DISEASEsilicosis if inhaled in sufficient quantities for long enough periods oftime. Particles less than 0.5 micra produce a diffuse fibrosis with somenodulation in the lungs. The potency of the particles of silica increaseremarkably with the decrease in size.3. Duration of exposure. Usually, in most industries, from five tothirty years of exposure are required to produce disabling silicosis.However, exposure to dusts of extremely high silicon dioxide contentof minute particle size (I to 3 micra) and in high particle concentrationmay produce silicosis after only one and one-half or two years ofexposure. Such cases commonly occur among workers engaged in themanufacture of scouring powders where special types of extremelyfine sands in heavy concentrations are used.4. Conditions under which the employee worked. In the mining andtunneling industries it is important to know how far underground thework was being done, how confined the space was in which the em-ployee worked, whether wet or dry drilling was employed, whether aventilator was present, and what devices, types of respirators, ormasks were used. Wet drilling greatly reduces the amount of dust inthe atmosphere.5. Concentration of dust particles. This can be ascertained by in-dustrial hygienists or sanitary engineers. Less than 5,000,000 particlesper cubic foot of air of any dust will not produce disabling pneumo-coniosis even if inhaled for long periods of time.Thus it can be seen that the length of time for silicosis to developwill depend on the factors enumerated above. Inhalation of high con-centrations of dusts of extremely small particles with high silicondioxide content where no protective devices were used will producesilicosis in a much shorter period than under circumstances where theparticles were much larger, contained less silicon dioxide, were notpresent in heavy concentrations, and where the employees wore ade-quate protective devices. In addition, there is an individual suscepti-bility which renders some employees more prone to develop silicosisthan others working in the same environment.The major symptom of silicosis is shortness of breath which beginsinsidiously and progresses relentlessly to the point where the indi-vidual becomes disabled. The disease may then be complicated bytuberculosis, emphysema, or pulmonary heart disease.It remains the expert physician's task to determine not only whetherthe individual has an industrial disease, but also whether it is disabling.1969]DE PAUL LAW REVIEWAn individual with X-ray findings of simple silicosis may not be dis-abled.ASBESTOSISAsbestosis is caused by a hydrated magnesium silicate. Asbestosfibers from twenty to twenty-five microns in length are the most activein the production of a disease. Asbestos fibers are used as insulation.Exposure exists in those working with materials used for insulation,as in pipefitters, pipecoverers, and shipfitters. It also occurs in themanufacture of clutch facings, brake linings and undercoating.As in the case of silicosis, the occupational history must reveal thenature of the dust involved, the circumstances of exposure, generalventilation in the areas where the work was being done, local exhaustventilation and personal protection (masks or respirators). A detailedhistory of every job held should be taken. The types of materialhandled, operations involved, dust present, and duration of exposureshould be ascertained. Asbestosis develops after a shorter period ofexposure than silicosis. The length of exposure often is between fiveand ten years. The degree of disability is determined by medical eval-uation which may include studies of pulmonary functions.It is extremely important to know that there is an increasing inci-dence of cancer of the lung and malignant tumors of the pleura inindividuals who have asbestosis when compared with the incidence ofsuch tumors in the general population. This relationship has importantmedico-legal implications in determining causal relationships in indi-viduals with asbestosis who develop these extremely serious diseases.BERYLLIUM DISEASEThe inhalation of beryllium dusts produces systemic disease. Beryl-lium is used extensively in the atomic energy program because of itseffectiveness as a moderator and reflector of neutrons. It was used inthe manufacture of fluorescent light, but is no longer used in thisindustry. Beryllium forms an alloy with many metals such as copper,nickel and aluminum. The greatest utilization of beryllium is as aberyllium-copper alloy.Beryllium disease may be either acute or chronic. The acute form ofthe disease may be either dermal or respiratory. In the dermal type,the exposed parts of the body such as the face, neck, arms and hands[Vol. XVIII: 613PULMONARY DISEASEpresent patches of skin eruptions. The skin often is swollen, itchy andhas a burning sensation. There often is inflammation of the membranesof the eyes, nose and throat. Abrasion of the skin with implantation ofone of the beryllium salts produces a nodule which persists until sur-gically removed.Respiratory aspects vary from a mild rhinitis or tracheobronchitisto fulminating pneumonitis. The worker complains of a cough whichmay become productive of blood-streaked sputum, fatigue, anorexia,substernal discomfort and palpitation. At the onset of symptoms, X-rays disclose no specific changes. Within two to three weeks after onsetof symptoms, X-rays usually reveal a ground glass haziness followedby areas of infiltration and occasionally by discrete nodules. Thesefindings will persist for a number of weeks to several months, but oftendisappear before symptoms subside.In the chronic form of beryllium disease, the striking feature is thedelay between the last exposure and the onset of symptoms. Theinterval may vary from one month to more than ten years. The inhala-tion of irritant fumes has been cited as a stress factor initiating theonset of the symptoms of the disease. A correlation between the in-tensity and duration of exposure and the severity of the disease hasnot been demonstrated. This disease has occurred in persons residing inthe neighborhood of a beryllium plant without any established workexposure. The onset of the disease is insidious. Often the worker com-plains of frequent colds that persist, slight coughs, loss of appetite,weight loss and fatigue. This is followed by the appearance of a pro-gressive condition of shortness of breath, which increasingly limitsthe worker's activity. Often failure of the right ventricle of the heart(corpulmonale) is responsible for death.The presence of beryllium in biopsied lung tissue does not necessarilymean that the individual has had an occupational exposure to beryl-lium. Beryllium may be found in the soil in certain areas, in the atmos-phere and in certain types of coal. The findings of beryllium in theurine likewise does not justify the diagnosis of beryllium disease. Itmerely means an individual has been exposed to beryllium. The patchtest (1% solution of beryllium salt as a patch) is controversial. Somebelieve it is useful as a diagnostic tool and as a screening test. Othersbelieve that by using the patch tests, normal persons might becomesensitive to beryllium and thus made more susceptible to the disease.19691DE PAUL LAW REVIEWThe course of beryllium disease is so variable that it is not possibleto predict the degree of disability to be expected nor the outcome ofthe disease.PULMONARY TUBERCULOSISPulmonary tuberculosis is an infectious disease caused by themycobacterium tuberculosis. The tubercle bacillus enters the suscep-tible human host by inhalation of particles excreted from an infectedindividual. Previously negative, the tuberculin skin test then becomespositive a few weeks after this first infection. This primary phasebecomes inactive in most people, but the body may continue to harborlive bacilli through a latent phase.Secondary causes of tuberculosis are largely socio-economic. Theprimary phase occurs in an environment in which tubercle bacilliare present in a form that may be inhaled readily. A patient with open"tuberculosis" may spread droplets of bacillus laden sputum by coughand thus contaminate the atmosphere. This circumstance is prevalentin crowded living or working quarters (such as the crowded slums andpoorly ventilated sweat shops of a previous era), military barracks,sailors' quarters, public facilities, and hospitals. Most pulmonary tu-berculosis in the past has developed in the younger age groups, chil-dren and teenagers. Today however, the average age of the develop-ment of a positive tuberculin test is much later.The reinfection phase of tuberculosis occurs in a tuberculin positiveindividual and is currently considered to be endogenous (i.e., a focusin the body that has harbored latent or inactive tubercle bacilli ac-quired during the primary stage becomes activated, and clinicallyactive tuberculosis develops). The circumstances in which the reinfec-tion phase of pulmonary tuberculosis occurs are less well known.Activation or reactivation of a latent focus occurs more frequentlywith alcoholism, diabetes, gastrectomy, long hours of hard work,stress, dissipation and malnutrition.The steps taken to prevent disease must interrupt the transmissionof the tubercle bacilli from the patient to the person with a negativetuberculin test. The greatest effectiveness in prevention must beachieved before the primary phase. Many industrial units have in-corporated this principle into environmental control to protect theworkers from disease, and the company from negligence suits or claims[Vol. XVIII: 613PULMONARY DISEASEunder workmen's compensation laws. Adequate working space, venti-lation, and, where necessary, germicidal ultraviolet lamps are provided.Tuberculin testing and chest X-rays have become part of the requiredpre-employment physical examinations for many employers.Proof of contraction of tuberculosis in work areas requires the proofof exposure to an individual with active tuberculosis.When active clinical disease has developed, the determination of theduration and degree of disability, and the prognosis for return towork is a matter of individual assessment, although general principlesmay be described.During the acute stage of pulmonary tuberculosis, the patient maynot be able to work because of disabling symptoms. Hospitalizationmay be required because of fever, weight loss, distressing cough, bloodspitting, shortness of breath, and other related symptoms. Whenantibiotic treatment has become effective, the patient may be able toreturn to work before complete healing has occurred if the symptomshave improved. There is little risk to the patient and others on thejob with him if the cough and sputum production have been controlledby specific medicine, even though the sputum may still contain tuberclebacilli during the early phase of healing. The resultant improvement inpatient morale, the decrease in cost of hospitalization, and the reductionof wage loss is thus greatly enhanced.When pulmonary tuberculosis is in its active phase, is undiagnosed,and is unaffected by treatment, the threat of infection of the unsuspect-ing tuberculin negative bystander is great. The early detection ofdisease by physicians in industrial medical departments, by publichealth surveys, and in private practice with the use of tuberculin testsand periodic X-rays has resulted in a decrease in the number of peoplewho are sources of infection and in the number of new cases each year.Continued vigilance is still necessary.19691

Medical-Legal Aspects of Pulmonary Disease

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Medical-Legal Aspects of Pulmonary Disease

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