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1.  Blood

1. Blood (3)

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1.  Blood

Chapter Editor: Bernard D. Goldstein


Table of Contents

 

Tables

 

Haematopoietic and Lymphatic System
Bernard D. Goldstein

 

Leukaemia, Malignant Lymphomas and Multiple Myeloma
Timo Partanen, Paolo Boffetta, Elisabete Weiderpass

 

Agents or Work Conditions Affecting the Blood
Bernard D. Goldstein

 

Tables

 

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  1. Agents in environmental and occupational methaemoglobinaemia

 

 

 

 

 

 

 

 

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3. Cardiovascular System

3. Cardiovascular System (7)

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3. Cardiovascular System

Chapter Editors: Lothar Heinemann and Gerd Heuchert 


Table of Contents

Tables and Figures

Introduction
Lothar Heinemann and Gerd  Heuchert

Cardiovascular Morbidity and Mortality in the Workforce
Gottfried Enderlein and Lothar Heinemann

The Risk Factor Concept in Cardiovascular Disease
Lothar Heinemann, Gottfried Enderlein and Heide Stark

Rehabilitation and Prevention Programmes
Lothar Heinemann and Gottfried Enderlein

Physical, Chemical and Biological Hazards

Physical Factors
Heide Stark and Gerd Heuchert

Chemical Hazardous Materials
Ulrike Tittelbach and Wolfram Dietmar Schneider

Biological Hazards
Regina Jäckel, Ulrike Tittelbach and Wolfram Dietmar Schneider

Tables

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  1. Mortality from cardiovascular diseases
  2. Mortality rates, special cardiovascular diagnosis groups
  3. Rate of disease and reduced work ability
  4. Work associated with cardiovascular hazards
  5. Occupation-related infection and disease

 

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4. Digestive System

4. Digestive System (6)

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4. Digestive System

Chapter Editor: Heikki Savolainen


 

Table of Contents

Figures

Digestive system
G. Frada

Mouth and teeth
F. Gobbato

Liver
George Kazantzis

Peptic ulcer
K. S. Cho

Liver cancer
Timo Partanen, Timo Kauppinen, Paolo Boffetta and Elisabete Weiderpass

Pancreatic cancer
Timo Partanen, Timo Kauppinen, Paolo Boffetta and Elisabete Weiderpass

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5. Mental Health

5. Mental Health (8)

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5. Mental Health

Chapter Editors: Joseph J. Hurrell, Lawrence R. Murphy, Steven L. Sauter and Lennart Levi


Table of Contents

Tables and Figures

Work and Mental Health
Irene L.D. Houtman and Michiel A.J. Kompier

Work-related Psychosis
Craig Stenberg, Judith Holder and Krishna Tallur

Mood and Affect

Depression
Jay Lasser and Jeffrey P. Kahn

Work-related Anxiety
Randal D. Beaton

Post-traumatic Stress Disorder and its Relationship to Occupational Health and Injury Prevention
Mark Braverman

Stress and Burnout and their Implication in the Work Environment
Herbert J. Freudenberger

Cognitive Disorders
Catherine A. Heaney

Karoshi: Death from Overwork
Takashi Haratani

Tables

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    1. Schematic overview of management strategies & examples

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      6.  Musculoskeletal System

      6. Musculoskeletal System (14)

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      6.  Musculoskeletal System

      Chapter Editors: Hilkka Riihimäki and Eira Viikari-Juntura

       


       

      Table of Contents

      Tables and Figures

      Overview
      Hilkka Riihimäki

      Muscles
      Gisela Sjøgaard

      Tendons
      Thomas J. Armstrong

      Bones and Joints
      David Hamerman

      Intervertebral Discs
      Sally Roberts and Jill P.G. Urban

      Low-back Region
      Hilkka Riihimäki

      Thoracic Spine Region
      Jarl-Erik Michelsson

      Neck
      Åsa Kilbom

      Shoulder
      Mats Hagberg

      Elbow
      Eira Viikari-Juntura

      Forearm, Wrist and Hand
      Eira Viikari-Juntura

      Hip and Knee
      Eva Vingård

      Leg, Ankle and Foot
      Jarl-Erik Michelsson

      Other Diseases
      Marjatta Leirisalo-Repo

      Tables

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      1. Structure-function of joint components
      2. Prevalence of back disorders, in Finns over 30 years
      3. Reducing the risks for low-back pain at work
      4. Classification-low-back disorders (Quebec Task Force)
      5. Permissible motions for head in prolonged driving
      6. Incidence of epicondylitis in various populations
      7. Incidence of tenosynovitis/peritendinitis
      8. Primary osteoarthrosis of the hip in Malmö, Sweden
      9. Guidelines for the treatment of rheumatoid arthritis
      10. Infections known to trigger reactive arthritis

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      MUS050F1MUS050F2MUS050F3MUS040F1MUS020F1MUS020F2MUS020F3MUS020F4MUS020F5MUS130F1MUS130F2MUS130F3MUS080F1MUS080F4MUS080F5MUS090F1MUS090F2MUS090F3MUS090F4MUS110F1MUS140F1MUS170F1MUS170T1MUS170T2

       


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      8.  Renal-Urinary System

      8. Renal-Urinary System (2)

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      8.  Renal-Urinary System

      Chapter Editor: George P. Hemstreet


       

      Table of Contents

      Tables and Figures

      Renal-Urinary Systems
      George P. Hemstreet

      Renal-Urinary Cancers
      Timo Partanen, Harri Vainio, Paolo Boffetta and Elisabete Weiderpass

      Tables

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      1. Drug-metabolism enzymes in kidney
      2. The most common causes of haematuria, by age & sex
      3. Criteria for biomarker selection
      4. Potential biomarkers linked to cell injury
      5. Acute renal insufficiency & occupation
      6. Segments of the nephron affected by selected toxicants
      7. Applications of urinary cytology

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      10. Respiratory System

      10. Respiratory System (18)

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      10. Respiratory System

      Chapters Editors:  Alois David and Gregory R. Wagner


       

      Table of Contents

      Tables and Figures

      Structure and Function
      Morton Lippmann

      Lung Function Examination
      Ulf Ulfvarson and Monica Dahlqvist

      Diseases Caused by Respiratory Irritants and Toxic Chemicals
      David L.S. Ryon and William N. Rom

      Occupational Asthma
      George Friedman-Jimenez and Edward L. Petsonk

      Diseases Caused by Organic Dusts
      Ragnar Rylander and Richard S. F. Schilling

      Beryllium Disease
      Homayoun Kazemi

      Pneumoconioses: Definition
      Alois David

      ILO International Classification of Radiographs of Pneumoconioses
      Michel Lesage

      Aetiopathogenesis of Pneumoconioses
      Patrick Sébastien and Raymond Bégin

      Silicosis
      John E. Parker and Gregory R. Wagner

      Coal Workers’ Lung Diseases
      Michael D. Attfield, Edward L. Petsonk and Gregory R. Wagner

      Asbestos-Related Diseases
      Margaret R. Becklake

      Hard Metal Disease
      Gerolamo Chiappino

      Respiratory System: The Variety of Pneumoconioses
      Steven R. Short and Edward L. Petsonk

      Chronic Obstructive Pulmonary Disease
      Kazimierz Marek and Jan E. Zejda

      Health Effects of Man-Made Fibres
      James E. Lockey and Clara S. Ross

      Respiratory Cancer
      Paolo Boffetta and Elisabete Weiderpass

      Occupationally Acquired Infections of the Lung
      Anthony A. Marfin, Ann F. Hubbs, Karl J. Musgrave, and John E. Parker

      Tables

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      1. Respiratory tract regions & particle deposition models
      2. Inhalable, thoracic & respirable dust criteria
      3. Summary of respiratory irritants
      4. Mechanisms of lung injury by inhaled substances
      5. Compounds capable of lung toxicity
      6. Medical case definition of occupational asthma
      7. Steps in diagnostic evaluation of asthma in the workplace
      8. Sensitizing agents that can cause occupational asthma
      9. Examples of sources of hazards of exposure to organic dust
      10. Agents in organic dusts with potential biological activity
      11. Diseases induced by organic dusts & their ICD codes
      12. Diagnostic criteria for byssinosis
      13. Properties of beryllium & its compounds
      14. Description of standard radiographs
      15. ILO 1980 Classification: Radiographs of Pneumoconioses
      16. Asbestos-related diseases & conditions
      17. Main commercial sources, products & uses of asbestos
      18. Prevalence of COPD
      19. Risk factors implicated in COPD
      20. Loss of ventilatory function
      21. Diagnostic classification, chronic bronchitis & emphysema
      22. Lung function testing in COPD
      23. Synthetic fibres
      24. Established human respiratory carcinogens (IARC)
      25. Probable human respiratory carcinogens (IARC)
      26. Occupationally acquired respiratory infectious diseases

      Figures

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      RES010F1RES010F2RES010F3RES010F4RES030F1RES030F2RES030F3RES030F4RES030F5RES030F6RES070F1RES070F2RES070F3RES130F1RES130F2RES130F3RES160F1RES160F2RES160F3RES160F4RES160F5RES160F6RES160F7RES170F1RES170F2RES170F3RES170F4RES170F5RES170F6RES170F7RES200F1RES200F2RES200F5RES200F3RES200F4RES200F6


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      11. Sensory Systems

      11. Sensory Systems (8)

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      11. Sensory Systems

      Chapter Editor: Heikki Savolainen


      Table of Contents

      Tables and Figures

      The Ear
      Marcel-André Boillat   

      Chemically-Induced Hearing Disorders
      Peter Jacobsen

      Physically-Induced Hearing Disorders
      Peter L. Pelmear

      Equilibrium
      Lucy Yardley

      Vision and Work
      Paule Rey and Jean-Jacques Meyer

      Taste
      April E. Mott and Norman Mann

      Smell
      April E. Mott

      Cutaneous Receptors
      Robert Dykes and Daniel McBain

      Tables

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      1. Typical calculation of functional loss from an audiogram
      2. Visual requirements for different activities
      3. Recommended illuminance values for the lighting design
      4. Visual requirements for a driving licence in France
      5. Agents/processes reported to alter the taste system
      6. Agents/processes associated with olfactory abnormalities

      Figures

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      12. Skin Diseases

      12. Skin Diseases (7)

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      12. Skin Diseases

      Chapter Editor: Louis-Philippe Durocher


       

      Table of Contents

      Tables and Figures

      Overview: Occupational Skin Diseases
      Donald J. Birmingham

      Non-Melanocytic Skin Cancer
      Elisabete Weiderpass, Timo Partanen, Paolo Boffetta

      Malignant Melanoma
      Timo Partanen, Paolo Boffetta, Elisabete Weiderpass

      Occupational Contact Dermatitis
      Denis Sasseville

      Prevention of Occupational Dermatoses
      Louis-Phillipe Durocher

      Occupational Nail Dystrophy
      C.D. Calnan

      Stigmata
      H. Mierzecki

      Tables

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      1. Occupations at risk
      2. Types of contact dermatitis
      3. Common irritants
      4. Common skin allergens
      5. Predisposing factors for occupational dermatitis
      6. Examples of skin irritants & sensitizers with occupations
      7. Occupational dermatoses in Quebec in 1989
      8. Risk factors & their effects on the skin
      9. Collective measures (group approach) to prevention

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      13. Systemic Conditions

      13. Systemic Conditions (3)

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      13. Systemic Conditions

      Chapter Editor: Howard M. Kipen


       

      Table of Contents

      Figures

      Systemic Conditions: An Introduction
      Howard M. Kipen

      Sick Building Syndrome
      Michael J. Hodgson

      Multiple Chemical Sensitivities
      Mark R. Cullen

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      Tuesday, 25 January 2011 20:13

      Environmental Cancer

      Written by

      Cancer is a common disease in all countries of the world. The probability that a person will develop cancer by the age of 70 years, given survival to that age, varies between about 10 and 40% in both sexes. On average, in developed countries, about one person in five will die from cancer. This proportion is about one in 15 in developing countries. In this article, environmental cancer is defined as cancer caused (or prevented) by non-genetic factors, including human behaviour, habits, lifestyle and external factors over which the individual has no control. A stricter definition of environmental cancer is sometimes used, comprising only the effect of factors such as air and water pollution, and industrial waste.

      Geographical Variation

      Variation between geographical areas in the rates of particular types of cancer can be much greater than that for cancer as a whole. Known variation in the incidence of the more common cancers is summarized in table 1. The incidence of nasopharyngeal carcinoma, for example, varies some 500-fold between South East Asia and Europe. This wide variation in frequency of the various cancers has led to the view that much of human cancer is caused by factors in the environment. In particular, it has been argued that the lowest rate of a cancer observed in any population is indicative of the minimum, possibly spontaneous, rate occurring in the absence of causative factors. Thus the difference between the rate of a cancer in a given population and the minimum rate observed in any population is an estimate of the rate of the cancer in the first population which is attributable to environmental factors. On this basis it has been estimated, very approximately, that some 80 to 90% of all human cancers are environmentally determined (International Agency for Research on Cancer 1990).

      Table 1.  Variation between populations covered by cancer registration in the incidence of common cancers.1

      Cancer (ICD9 code)

      High-incidence area

      CR2

      Low-incidence area

      CR2

      Range of variation

      Mouth (143-5)

      France, Bas Rhin

      2

      Singapore (Malay)

      0.02

      80

      Nasopharynx (147)

      Hong Kong

      3

      Poland, Warsaw (rural)

      0.01

      300

      Oesophagus (150)

      France, Calvados

      3

      Israel (Israeli-born Jews)

      0.02

      160

      Stomach (151)

      Japan, Yamagata

      11

      USA, Los Angeles (Filipinos)

      0.3

      30

      Colon (153)

      USA, Hawaii (Japanese)

      5

      India, Madras

      0.2

      30

      Rectum (154)

      USA, Los Angeles (Japanese)

      3

      Kuwait (non-Kuwaiti)

      0.1

      20

      Liver (155)

      Thailand, Khon Khaen

      11

      Paraguay, Asuncion

      0.1

      110

      Pancreas (157)

      USA, Alameda County (Calif.) (Blacks)

      2

      India, Ahmedabad

      0.1

      20

      Lung (162)

      New Zealand (Maori)

      16

      Mali, Bamako

      0.5

      30

      Melanoma of skin (172)

      Australia, Capital Terr.

      3

      USA, Bay Area (Calif.)(Blacks)

      0.01

      300

      Other skin cancers (173)

      Australia, Tasmania

      25

      Spain, Basque Country

      0.05

      500

      Breast (174)

      USA, Hawaii (Hawaiian)

      12

      China, Qidong

      1.0

      10

      Cervix uteri (180)

      Peru, Trujillo

      6

      USA, Hawaii (Chinese)

      0.3

      20

      Corpus uteri (182)

      USA, Alameda County (Calif.) (Whites)

      3

      China, Qidong

      0.05

      60

      Ovary (183)

      Iceland

      2

      Mali, Bamako

      0.09

      20

      Prostate (185)

      USA, Atlanta (Blacks)

      12

      China, Qidong

      0.09

      140

      Bladder (188)

      Italy, Florence

      4

      India, Madras

      0.2

      20

      Kidney (189)

      France, Bas Rhin

      2

      China, Qidong

      0.08

      20

      1 Data from cancer registries included in IARC 1992. Only cancer sites with cumulative rate larger or equal to 2% in the high-incidence area are included. Rates refer to males except for breast, cervix uteri, corpus uteri and ovary cancers.
      2 Cumulative rate % between 0 and 74 years of age.
      Source: International Agency for Research on Cancer 1992.

      There are, of course, other explanations for geographical variation in cancer rates. Under-registration of cancer in some populations may exaggerate the range of variation, but certainly cannot explain differences of the size shown in table 1. Genetic factors also may be important. It has been observed, however, that when populations migrate along a gradient of cancer incidence they often acquire a rate of cancer which is intermediate between that of their home country and that of the host country. This suggests that a change in environment, without genetic change, has changed the cancer incidence. For example, when Japanese migrate to the United States their rates of colon and breast cancer, which are low in Japan, rise, and their rate of stomach cancer, which is high in Japan, falls, both tending more closely towards United States’ rates. These changes may be delayed until the first post-migration generation but they still occur without genetic change. For some cancers, change with migration does not occur. For example, the Southern Chinese retain their high rate of cancer of the nasopharynx wherever they live, thus suggesting that genetic factors, or some cultural habit which changes little with migration, are responsible for this disease.

      Time Trends

      Further evidence of the role of environmental factors in cancer incidence has come from the observation of time trends. The most dramatic and well-known change has been the rise in lung cancer rates in males and females in parallel with but occurring some 20 to 30 years after the adoption of cigarette use, which has been seen in many regions of the world; more recently in a few countries, such as the United States, there has been the suggestion of a fall in rates among males following a reduction in tobacco smoking. Less well understood are the substantial falls in incidence of cancers including those of the stomach, oesophagus and cervix which have paralleled economic development in many countries. It would be difficult to explain these falls, however, except in terms of reduction in exposure to causal factors in the environment or, perhaps, increasing exposure to protective factors—again environmental.

      Main Environmental Carcinogenic Agents

      The importance of environmental factors as causes of human cancer has been further demonstrated by epidemiological studies relating particular agents to particular cancers. The main agents which have been identified are summarized in table 10. This table does not contain the drugs for which a causal link with human cancer has been established (such as diethylstilboestrol and several alkylating agents) or suspected (such as cyclophosphamide) (see also Table 9). In the case of these agents, the risk of cancer has to be balanced with the benefits of the treatment. Similarly, Table 10 does not contain agents that occur primarily in the occupational setting, such as chromium, nickel and aromatic amines. For a detailed discussion of these agents see the previous article “Occupational Carcinogens.” The relative importance of the agents listed in table 8 varies widely, depending on the potency of the agent and the number of people involved. The evidence of carcinogenicity of several environmental agents has been evaluated within the IARC Monographs programme (International Agency for Research on Cancer 1995) (see again “Occupational Carcinogens” for a discussion of the Monographs programme); table 10 is based mainly on the IARC Monograph evaluations. The most important agents among those listed in table 10 are those to which a substantial proportion of the population is exposed in relatively large amounts. They include particularly: ultraviolet (solar) radiation; tobacco smoking; alcohol drinking; betel quid chewing; hepatitis B; hepatitis C and human papilloma viruses; aflatoxins; possibly dietary fat, and dietary fiber and vitamin A and C deficiency; reproductive delay; and asbestos.

      Attempts have been made to estimate numerically the relative contributions of these factors to the 80 or 90% of cancers which might be attributed to environmental factors. The pattern varies, of course, from population to population according to differences in exposures and possibly in the genetic susceptibility to various cancers. In many industrialized countries, however, tobacco smoking and dietary factors are likely to be responsible each for roughly one-third of environmentally determined cancers (Doll and Peto 1981); while in developing countries the role of biological agents is likely to be large and that of tobacco relatively small (but increasing, following the recent increase in the consumption of tobacco in these populations).

      Interactions between Carcinogens

      An additional aspect to consider is the presence of interactions between carcinogens. Thus for example, in the case of alcohol and tobacco, and cancer of the oesophagus, it has been shown that an increasing consumption of alcohol multiplies manyfold the rate of cancer produced by a given level of tobacco consumption. Alcohol by itself may facilitate transport of tobacco carcinogens, or others, into the cells of susceptible tissues. Multiplicative interaction may also be seen between initiating carcinogens, as between radon and its decay products and tobacco smoking in miners of uranium. Some environmental agents may act by promoting cancers which have been initiated by another agent—this is the most likely mechanism for an effect of dietary fat on the development of breast cancer (probably through increased production of the hormones which stimulate the breast). The reverse may also occur, as, for example, in the case of vitamin A, which probably has an anti-promoting effect on lung and possibly other cancers initiated by tobacco. Similar interactions may also occur between environmental and constitutional factors. In particular, genetic polymorphism to enzymes implicated in the metabolism of carcinogenic agents or DNA repair is probably an important requirement of individual susceptibility to the effect of environmental carcinogens.

      The significance of interactions between carcinogens, from the point of view of cancer control, is that withdrawal of exposure to one of two (or more) interacting factors may give rise to a greater reduction in cancer incidence than would be predicted from consideration of the effect of the agent when acting alone. Thus, for example, withdrawal of cigarettes may eliminate almost entirely the excess rate of lung cancer in asbestos workers (although rates of mesothelioma would be unaffected).

      Implications for Prevention

      The realization that environmental factors are responsible for a large proportion of human cancers has laid the foundation for primary prevention of cancer by modification of exposure to the factors identified. Such modification may comprise: removal of a single major carcinogen; reduction, as discussed above, in exposure to one of several interacting carcinogens; increasing exposure to protective agents; or combinations of these approaches. While some of this may be achieved by community-wide regulation of the environment through, for example, environmental legislation, the apparent importance of lifestyle factors suggests that much of primary prevention will remain the responsibility of individuals. Governments, however, may still create a climate in which individuals find it easier to take the right decision.

       

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      Tuesday, 25 January 2011 20:15

      Prevention

      Written by

      Occupational exposures account for only a minor proportion of the total number of cancers in the entire population. It has been estimated that 4% of all cancers can be attributed to occupational exposures, based on data from the United States, with a range of uncertainty from 2 to 8%. This implies that even total prevention of occupationally induced cancers would result in only a marginal reduction in national cancer rates.

      However, for several reasons, this should not discourage efforts to prevent occupationally induced cancers. First, the estimate of 4% is an average figure for the entire population, including unexposed persons. Among people actually exposed to occupational carcinogens, the proportion of tumours attributable to occupation is much larger. Second, occupational exposures are avoidable hazards to which individuals are involuntarily exposed. An individual should not have to accept an increased risk of cancer in any occupation, especially if the cause is known. Third, occupationally induced cancers can be prevented by regulation, in contrast to cancers associated with lifestyle factors.

      Prevention of occupationally induced cancer involves at least two stages: first, identification of a specific compound or occupational environment as carcinogenic; and second, imposing appropriate regulatory control. The principles and practice of regulatory control of known or suspected cancer hazards in the work environment vary considerably, not only among different parts of the developed and developing world, but also among countries of similar socio-economic development.

      The International Agency for Research on Cancer (IARC) in Lyon, France, systematically compiles and evaluates epidemiological and experimental data on suspected or known carcinogens. The evaluations are presented in a series of monographs, which provide a basis for decisions on national regulations on the production and use of carcinogenic compounds (see “Occupational Carcinogens”, above.

      Historical Background

      The history of occupational cancer dates back to at least 1775, when Sir Percivall Pott published his classical report on scrotal cancer in chimney-sweeps, linking exposure to soot to the incidence of cancer. The finding had some immediate impact in that sweeps in some countries were granted the right to bathe at the end of the working day. Current studies of sweeps indicate that scrotal and skin cancer are now under control, although sweeps are still at increased risk for several other cancers.

      In the 1890s, a cluster of bladder cancer was reported at a German dye factory by a surgeon at a nearby hospital. The causative compounds were later identified as aromatic amines, and these now appear in lists of carcinogenic substances in most countries. Later examples include skin cancer in radium-dial painters, nose and sinus cancer among woodworkers caused by inhalation of wood dust, and “mule-spinner’s disease”—that is, scrotal cancer among cotton industry workers caused by mineral oil mist. Leukaemia induced by exposure to benzene in the shoe repair and manufacturing industry also represents a hazard that has been reduced after the identification of carcinogens in the workplace.

      In the case of linking asbestos exposure to cancer, this history illustrates a situation with a considerable time-lag between risk identification and regulatory action. Epidemiological results indicating that exposure to asbestos was associated with an increased risk of lung cancer were already starting to accumulate by the 1930s. More convincing evidence appeared around 1955, but it was not until the mid-1970s that effective steps for regulatory action began.

      The identification of the hazards associated with vinyl chloride represents a different history, where prompt regulatory action followed identification of the carcinogen. In the 1960s, most countries had adopted an exposure limit value for vinyl chloride of 500 parts per million (ppm). In 1974, the first reports of an increased frequency of the rare tumour liver angiosarcoma among vinyl chloride workers were soon followed by positive animal experimental studies. After vinyl chloride was identified as carcinogenic, regulatory actions were taken for a prompt reduction of the exposure to the current limit of 1 to 5 ppm.

      Methods Used for the Identificationof Occupational Carcinogens

      The methods in the historical examples cited above range from observations of clusters of disease by astute clinicians to more formal epidemiological studies—that is, investigations of the disease rate (cancer rate) among human beings. Results from epidemiological studies are of high relevance for evaluations of the risk to humans. A major drawback of cancer epidemiological studies is that a long time period, usually at least 15 years, is necessary to demonstrate and evaluate the effects of an exposure to a potential carcinogen. This is unsatisfactory for surveillance purposes, and other methods must be applied for a quicker evaluation of recently introduced substances. Since the beginning of this century, animal carcinogenicity studies have been used for this purpose. However, the extrapolation from animals to humans introduces considerable uncertainty. The methods also have limitations in that a large number of animals must be followed for several years.

      The need for methods with a more rapid response was partly met in 1971, when the short-term mutagenicity test (Ames test) was introduced. This test uses bacteria to measure the mutagenic activity of a substance (its ability to cause irreparable changes in the cellular genetic material, DNA). A problem in the interpretation of the results of bacterial tests is that not all substances causing human cancers are mutagenic, and not all bacterial mutagens are considered to be cancer hazards for human beings. However, the finding that a substance is mutagenic is usually taken as an indication that the substance might represent a cancer hazard for humans.

      New genetic and molecular biology methods have been developed during the last 15 years, with the aim of detecting human cancer hazards. This discipline is termed “molecular epidemiology.” Genetic and molecular events are studied in order to clarify the process of cancer formation and thus develop methods for early detection of cancer, or indications of increased risk of the development of cancer. These methods include analysis of damage to the genetic material and the formation of chemical linkages (adducts) between pollutants and the genetic material. The presence of chromosomal aberrations clearly indicates effects on the genetic material which may be associated with cancer development. However, the role of molecular epidemiological findings in human cancer risk assessment remains to be settled, and research is under way to indicate more clearly exactly how results of these analyses should be interpreted.

      Surveillance and Screening

      The strategies for prevention of occupationally induced cancers differ from those applied for control of cancer associated with lifestyle or other environmental exposures. In the occupational field, the main strategy for cancer control has been reduction or total elimination of exposure to cancer-causing agents. Methods based on early detection by screening programmes, such as those applied for cervical cancer or breast cancer, have been of very limited importance in occupational health.

      Surveillance

      Information from population records on cancer rates and occupation may be used for surveillance of cancer frequencies in various occupations. Several methods to obtain such information have been applied, depending on the registries available. The limitations and possibilities depend largely on the quality of the information in the registries. Information on disease rate (cancer frequency) is typically obtained from local or national cancer registries (see below), or from death certificate data, while information on the age-composition and size of occupational groups is obtained from population registries.

      The classical example of this type of information is the “Decennial supplements on occupational mortality,” published in the UK since the end of the nineteenth century. These publications use death certificate information on cause of death and on occupation, together with census data on frequencies of occupations in the entire population, to calculate cause-specific death rates in different occupations. This type of statistic is a useful tool to monitor the cancer frequency in occupations with known risks, but its ability to detect previously unknown risks is limited. This type of approach may also suffer from problems associated with systematic differences in the coding of occupations on the death certificates and in the census data.

      The use of personal identification numbers in the Nordic countries has offered a special opportunity to link individual census data on occupations with cancer registration data, and to directly calculate cancer rates in different occupations. In Sweden, a permanent linkage of the censuses of 1960 and 1970 and the cancer incidence during subsequent years have been made available for researchers and have been used for a large number of studies. This Swedish Cancer-Environment Registry has been used for a general survey of certain cancers tabulated by occupation. The survey was initiated by a governmental committee investigating hazards in the work environment. Similar linkages have been performed in the other Nordic countries.

      Generally, statistics based on routinely collected cancer incidence and census data have the advantage of ease in providing large amounts of information. The method gives information on the cancer frequencies regarding occupation only, not in relation to certain exposures. This introduces a considerable dilution of the associations, since exposure may differ considerably among individuals in the same occupation. Epidemiological studies of the cohort type (where the cancer experience among a group of exposed workers is compared with that in unexposed workers matched for age, sex and other factors) or the case-control type (where the exposure experience of a group of persons with cancer is compared to that in a sample of the general population) give better opportunities for detailed exposure description, and thus better opportunities for investigation of the consistency of any observed risk increase, for example by examining the data for any exposure-response trends.

      The possibility of obtaining more refined exposure data together with routinely collected cancer notifications was investigated in a prospective Canadian case-control study. The study was set up in the Montreal metropolitan area in 1979. Occupational histories were obtained from males as they were added to the local cancer registry, and the histories were subsequently coded for exposure to a number of chemicals by occupational hygienists. Later, the cancer risks in relation to a number of substances were calculated and published (Siemiatycki 1991).

      In conclusion, the continuous production of surveillance data based on recorded information provides an effective and comparatively easy way to monitor cancer frequency by occupation. While the main purpose achieved is surveillance of known risk factors, the possibilities for the identification of new risks are limited. Registry-based studies should not be used for conclusions regarding the absence of risk in an occupation unless the proportion of individuals significantly exposed is more precisely known. It is quite common that only a relatively small percentage of members of an occupation actually are exposed; for these individuals the substance may represent a substantial hazard, but this will not be observable (i.e., will be statistically diluted) when the entire occupational group is analysed as a single group.

      Screening

      Screening for occupational cancer in exposed populations for purposes of early diagnosis is rarely applied, but has been tested in some settings where exposure has been difficult to eliminate. For example, much interest has focused on methods for early detection of lung cancer among people exposed to asbestos. With asbestos exposures, an increased risk persists for a long time, even after cessation of exposure. Thus, continuous evaluation of the health status of exposed individuals is justified. Chest x rays and cytological investigation of sputum have been used. Unfortunately, when tested under comparable conditions neither of these methods reduces the mortality significantly, even if some cases may be detected earlier. One of the reasons for this negative result is that the prognosis of lung cancer is little affected by early diagnosis. Another problem is that the x rays themselves represent a cancer hazard which, while small for the individual, may be significant when applied to a large number of individuals (i.e., all those screened).

      Screening also has been proposed for bladder cancer in certain occupations, such as the rubber industry. Investigations of cellular changes in, or mutagenicity of, workers’ urine have been reported. However, the value of following cytological changes for population screening has been questioned, and the value of the mutagenicity tests awaits further scientific evaluation, since the prognostic value of having increased mutagenic activity in the urine is not known.

      Judgements on the value of screening also depend on the intensity of the exposure, and thus the size of the expected cancer risk. Screening might be more justified in small groups exposed to high levels of carcinogens than among large groups exposed to low levels.

      To summarize, no routine screening methods for occupational cancers can be recommended on the basis of present knowledge. The development of new molecular epidemiological techniques may improve the prospects for early cancer detection, but more information is needed before conclusions can be drawn.

      Cancer Registration

      During this century, cancer registries have been set up at several locations throughout the world. The International Agency for Research on Cancer (IARC) (1992) has compiled data on cancer incidence in different parts of the world in a series of publications, “Cancer Incidence in Five Continents.” Volume 6 of this publication lists 131 cancer registries in 48 countries.

      Two main features determine the potential usefulness of a cancer registry: a well-defined catchment area (defining the geographical area involved), and the quality and completeness of the recorded information. Many of those registries that were set up early do not cover a geographically well-defined area, but rather are confined to the catchment area of a hospital.

      There are several potential uses of cancer registries in the prevention of occupational cancer. A complete registry with nationwide coverage and a high quality of recorded information can result in excellent opportunities for monitoring the cancer incidence in the population. This requires access to population data to calculate age-standardized cancer rates. Some registries also contain data on occupation, which therefore facilitates the monitoring of cancer risk in different occupations.

      Registries also may serve as a source for the identification of cases for epidemiological studies of both the cohort and case-control types. In the cohort study, personal identification data of the cohort is matched to the registry to obtain information on the type of cancer (i.e., as in record linkage studies). This assumes that a reliable identifying system exists (for example, personal identification numbers in the Nordic countries) and that confidentiality laws do not prohibit use of the registry in this way. For case-control studies, the registry may be used as a source for cases, although some practical problems arise. First, the cancer registries cannot, for methodological reasons, be quite up to date regarding recently diagnosed cases. The reporting system, and necessary checks and corrections of the obtained information, results in some lag time. For concurrent or prospective case-control studies, where it is desirable to contact the individuals themselves soon after a cancer diagnosis, it usually is necessary to set up an alternative way of identifying cases, for example via hospital records. Second, in some countries, confidentiality laws prohibit the identification of potential study participants who are to be contacted personally.

      Registries also provide an excellent source for calculating background cancer rates to use for comparison of the cancer frequency in cohort studies of certain occupations or industries.

      In studying cancer, cancer registries have several advantages over mortality registries commonly found in many countries. The accuracy of the cancer diagnoses is often better in cancer registries than in mortality registries, which are usually based on death certificate data. Another advantage is that the cancer registry often holds information on histological tumour type, and also permits the study of living persons with cancer, and is not limited to deceased persons. Above all, registries hold cancer morbidity data, permitting the study of cancers that are not rapidly fatal and/or not fatal at all.

      Environmental Control

      There are three main strategies for reducing workplace exposures to known or suspected carcinogens: elimination of the substance, reduced exposure by reduced emission or improved ventilation, and personal protection of the workers.

      It has long been debated whether a true threshold for carcinogen exposure exists, below which no risk is present. It is often assumed that the risk should be extrapolated linearly down to zero risk at zero exposure. If this is the case, then no exposure limit, no matter how low, would be considered entirely risk-free. Despite this, many countries have defined exposure limits for some carcinogenic substances, while, for others, no exposure limit value has been assigned.

      Elimination of a compound may give rise to problems when replacement substances are introduced and when the toxicity of the replacement substance must be lower than that of the substance replaced.

      Reducing the exposure at the source may be relatively easily accomplished for process chemicals by encapsulation of the process and ventilation. For example, when the carcinogenic properties of vinyl chloride were discovered, the exposure limit value for vinyl chloride was lowered by a factor of one hundred or more in several countries. Although this standard was at first considered impossible to achieve by industry, later techniques allowed compliance with the new limit. Reduction of exposure at the source may be difficult to apply to substances that are used under less controlled conditions, or are formed during the work operation (e.g., motor exhausts). The compliance with exposure limits requires regular monitoring of workroom air levels.

      When exposure cannot be controlled either by elimination or by reduced emissions, the use of personal protection devices is the only remaining way to minimize the exposure. These devices range from filter masks to air-supplied helmets and protective clothing. The main route of exposure must be considered in deciding appropriate protection. However, many personal protection devices cause discomfort to the user, and filter masks introduce an increased respiratory resistance which may be very significant in physically demanding jobs. The protective effect of respirators is generally unpredictable and depends on several factors, including how well the mask is fitted to the face and how often filters are changed. Personal protection must be considered as a last resort, to be attempted only when more effective ways of reducing exposure fail.

      Research Approaches

      It is striking how little research has been done to evaluate the impact of programmes or strategies to reduce the risk to workers of known occupational cancer hazards. With the possible exception of asbestos, few such evaluations have been conducted. Developing better methods for control of occupational cancer should include an evaluation of how present knowledge is actually put to use.

      Improved control of occupational carcinogens in the workplace requires the development of a number of different areas of occupational safety and health. The process of identification of risks is a basic prerequisite for reducing exposure to carcinogens in the workplace. Risk identification in the future must solve certain methodological problems. More refined epidemiological methods are required if smaller risks are to be detected. More precise data on exposure for both the substance under study and possible confounding exposures will be necessary. More refined methods for description of the exact dose of the carcinogen delivered to the specific target organ also will increase the power of exposure-response calculations. Today, it is not uncommon that very crude substitutes are used for the actual measurement of target organ dose, such as the number of years employed in the industry. It is quite clear that such estimates of dose are considerably misclassified when used as a surrogate for dose. The presence of an exposure-response relationship is usually taken as strong evidence of an aetiological relationship. However, the reverse, lack of demonstration of an exposure-response relationship, is not necessarily evidence that no risk is involved, especially when crude measures of target organ dose are used. If target organ dose could be determined, then actual dose-response trends would carry even more weight as evidence for causation.

      Molecular epidemiology is a rapidly growing area of research. Further insight into the mechanisms of cancer development can be expected, and the possibility of the early detection of carcinogenic effects will lead to earlier treatment. In addition, indicators of carcinogenic exposure will lead to improved identification of new risks.

      Development of methods for supervision and regulatory control of the work environment are as necessary as methods for the identification of risks. Methods for regulatory control differ considerably even among western countries. The systems for regulation used in each country depend largely on socio-political factors and the status of labour rights. The regulation of toxic exposures is obviously a political decision. However, objective research into the effects of different types of regulatory systems could serve as a guide for politicians and decision-makers.

      A number of specific research questions also need to be addressed. Methods to describe the expected effect of withdrawal of a carcinogenic substance or reduction of exposure to the substance need to be developed (i.e., the impact of interventions must be assessed). The calculation of the preventive effect of risk reduction raises certain problems when interacting substances are studied (e.g., asbestos and tobacco smoke). The preventive effect of removing one of two interacting substances is comparatively greater than when the two have only a simple additive effect.

      The implications of the multistage theory of carcinogenesis for the expected effect of withdrawal of a carcinogen also adds a further complication. This theory states that the development of cancer is a process involving several cellular events (stages). Carcinogenic substances may act either in early or late stages, or both. For example, ionizing radiation is believed to affect mainly early stages in inducing certain cancer types, while arsenic acts mainly at late stages in lung cancer development. Tobacco smoke affects both early and late stages in the carcinogenic process. The effect of withdrawing a substance involved in an early stage would not be reflected in a reduced cancer rate in the population for a long time, while the removal of a “late-acting” carcinogen would be reflected in a reduced cancer rate within a few years. This is an important consideration when evaluating the effects of risk-reduction intervention programmes.

      Finally, the effects of new preventive factors have recently attracted considerable interest. During the last five years, a large number of reports have been published on the preventive effect on lung cancer of consuming fruits and vegetables. The effect seems to be very consistent and strong. For example, the risk of lung cancer has been reported as double among those with a low consumption of fruits and vegetables versus those with high intake. Thus, future studies of occupational lung cancer would have greater precision and validity if individual data on fruit and vegetable consumption can be included in the analysis.

      In conclusion, improved prevention of occupational cancer involves both improved methods for risk identification and more research on the effects of regulatory control. For risk identification, developments in epidemiology should mainly be directed toward better exposure information, while in the experimental field, validation of the results of molecular epidemiological methods regarding cancer risk are needed.

       

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      Tuesday, 15 February 2011 20:21

      Introduction

      Written by

      Cardiovascular diseases (CVDs) are among the most common causes of illness and death in the working population, particularly in industrialized countries. They are also increasing in developing countries (Wielgosz 1993). In the industrialized countries, 15 to 20% of all working people will suffer from a cardiovascular dis- order sometime during their working lives and the frequency climbs sharply with age. Among those between 45 to 64 years of age, more than a third of the deaths among men and more than a quarter of deaths among women are caused by this group of diseases (see table 1). In recent years, CVDs have become the most frequent cause of death among post-menopausal women.

      Table 1. Mortality from cardiovascular diseases in 1991 and 1990 in the age groups 45-54 and 55-64 for selected countries.

      Country

      Men

      Women

       

      45-54 Years

      55-64 Years

      45-54 Years

      55-64 Years

       

      Rate

      %

      Rate

      %

      Rate

      %

      Rate

      %

      Russia**

      528

      36

      1,290

      44

      162

      33

      559

      49

      Poland**

      480

      38

      1,193

      45

      134

      31

      430

      42

      Argentina*

      317

      40

      847

      44

      131

      33

      339

      39

      Britain**

      198

      42

      665

      47

      59

      20

      267

      32

      USA*

      212

      35

      623

      40

      83

      24

      273

      31

      Germany**

      181

      29

      597

      38

      55

      18

      213

      30

      Italy*

      123

      27

      404

      30

      41

      18

      148

      25

      Mexico**

      128

      17

      346

      23

      82

      19

      230

      24

      France**

      102

      17

      311

      22

      30

      12

      94

      18

      Japan**

      111

      27

      281

      26

      48

      22

      119

      26

      *1990. **1991. Rate=Deaths per 100,000 inhabitants. % is from all causes of death in the age group.

      Because of their complex aetiology, only a very small pro- portion of the cases of cardiovascular disease are recognized as occupational. Many countries, however, recognize that occu- pational exposures contribute to CVDs (sometimes referred to as work-related diseases). Working conditions and job demands play an important role in the multifactorial process that leads to these diseases, but ascertaining the role of the individual causal com- ponents is very difficult. The components interact in close, shifting relationships and often the disease is triggered by a combination or accumulation of different causal factors, including those that are work related.

      The reader is referred to the standard cardiology texts for details of the epidemiology, pathophysiology, diagnosis and treatment of cardiovascular diseases. This chapter will focus on those aspects of cardiovascular disease that are particularly relevant in the workplace and are likely to be influenced by factors in the job and work environment.

       

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      In the following article, the term cardiovascular diseases (CVDs) refers to organic and functional disorders of the heart and circu- latory system, including the resultant damage to other organ systems, which are classified under numbers 390 to 459 in the 9th revision of the International Classification of Diseases (ICD) (World Health Organization (WHO) 1975). Based essentially on international statistics assembled by the WHO and data collected in Germany, the article discusses the prevalence of CVDs, new disease rates, and frequency of deaths, morbidity and disability.

      Definition and Prevalence in the Working-Age Population

      Coronary artery disease (ICD 410-414) resulting in ischaemia of the myocardium is probably the most significant CVD in the working population, particularly in industrialized countries. This condition results from a constriction in the vascular system that supplies the heart muscle, a problem caused primarily by arteriosclerosis. It affects 0.9 to 1.5% of working-age men and 0.5 to 1.0% of women.

      Inflammatory diseases (ICD 420-423) may involve the endo- cardium, the heart valves, the pericardium and/or the heart muscle (myocardium) itself. They are less common in industrialized countries, where their frequency is well below 0.01% of the adult population, but are seen more frequently in developing countries, perhaps reflecting the greater prevalence of nutritional disorders and infectious diseases.

      Heart rhythm disorders (ICD 427) are relatively rare, although much media attention has been given to recent instances of disability and sudden death among prominent professional athletes. Although they can have a significant impact on the ability to work, they are often asymptomatic and transitory.

      The myocardiopathies (ICD 424) are conditions which involve enlargement or thickening of the heart musculation, effectively narrowing the vessels and weakening the heart. They have attracted more attention in recent years, largely because of improved methods of diagnosis, although their pathogenesis is often obscure. They have been attributed to infections, metabolic diseases, immunologic disorders, inflammatory diseases involving the capillaries and, of particular importance in this volume, to toxic exposures in the workplace. They are divided into three types:

      • dilative—the most common form (5 to 15 cases per 100,000 people), which is associated with the functional weakening of the heart
      • hypertrophic—thickening and enlargement of the myocardium resulting in relative insufficiency of the coronary arteries
      • restrictive—a rare type in which myocardial contractions are limited.

       

      Hypertension (ICD 401-405) (increased systolic and/or diastolic blood pressure) is the most common circulatory disease, being found among 15 to 20% of working people in industrialized countries. It is discussed in greater detail below.

      Atherosclerotic changes in the major blood vessels (ICD 440), often associated with hypertension, cause disease in the organs they serve. Foremost among these is cerebrovascular disease (ICD 430-438), which may result in a stroke due to infarction and/or haemorrhage. This occurs in 0.3 to 1.0% of working people, most commonly among those aged 40 and older.

      Atherosclerotic diseases, including coronary artery disease, stroke and hypertension, by far the most common cardiovascular diseases in the working population, are multifactorial in origin and have their onset early in life. They are of importance in the workplace because:

      • so large a proportion of the workforce has an asymptomatic or unrecognized form of cardiovascular disease
      • the development of that disease may be aggravated or acute symptomatic events precipitated by working conditions and job demands
      • the acute onset of a symptomatic phase of the cardiovascular disease is often attributed to the job and/or the workplace environment
      • most individuals with an established cardiovascular disease are capable of working productively, albeit, sometimes, only after effective rehabilitation and job retraining
      • the workplace is a uniquely propitious arena for primary and secondary preventive programmes.

       

      Functional circulatory disorders in the extremities (ICD 443) include Raynaud’s disease, short-term pallor of the fingers, and are relatively rare. Some occupational conditions, such as frostbite, long-term exposure to vinyl chloride and hand-arm exposure to vibration can induce these disorders.

      Varicosities in the leg veins (ICD 454), often improperly dismissed as a cosmetic problem, are frequent among women, especially during pregnancy. While a hereditary tendency to weakness of the vein walls may be a factor, they are usually associated with long periods of standing in one position without movement, during which the static pressure within the veins is increased. The result- ant discomfort and leg oedema often dictate change or modifi- cation of the job.

      Annual incidence rates

      Among the CVDs, hypertension has the highest annual new case rate among working people aged 35 to 64. New cases develop in approximately 1% of that population every year. Next in frequency are coronary heart disease (8 to 92 new cases of acute heart attack per 10,000 men per year, and 3 to 16 new cases per 10,000 women per year) and stroke (12 to 30 cases per 10,000 men per year, and 6 to 30 cases per 10,000 women per year). As demonstrated by global data collected by the WHO-Monica project (WHO-MONICA 1994; WHO-MONICA 1988), the lowest new incidence rates for heart attack were found among men in China and women in Spain, while the highest rates were found among both men and women in Scotland. The significance of these data is that in the population of working age, 40 to 60% of heart attack victims and 30 to 40% of stroke victims do not survive their initial episodes.

      Mortality

      Within the primary working ages of 15 to 64, only 8 to 18% of deaths from CVDs occur prior to age 45. Most occur after age 45, with the annual rate increasing with age. The rates, which have been changing, vary considerably from country to country (WHO 1994b).

      Table 1 shows the death rates for men and for women aged 45 to 54 and 55 to 64 for some countries. Note that the death rates for men are consistently higher than those for women of corresponding ages. Table 2 compares the death rates for various CVDs among people aged 55 to 64 in five countries.

      Table 1. Mortality from cardiovascular diseases in 1991 and 1990 in the age groups 45-54 and 55-64 for selected countries.

      Country

      Men

      Women

      45-54 Years

      55-64 Years

      45-54 Years

      55-64 Years

      Rate

      %

      Rate

      %

      Rate

      %

      Rate

      %

      Russia**

      528

      36

      1,290

      44

      162

      33

      559

      49

      Poland**

      480

      38

      1,193

      45

      134

      31

      430

      42

      Argentina*

      317

      40

      847

      44

      131

      33

      339

      39

      Britain**

      198

      42

      665

      47

      59

      20

      267

      32

      USA*

      212

      35

      623

      40

      83

      24

      273

      31

      Germany**

      181

      29

      597

      38

      55

      18

      213

      30

      Italy*

      123

      27

      404

      30

      41

      18

      148

      25

      Mexico**

      128

      17

      346

      23

      82

      19

      230

      24

      France**

      102

      17

      311

      22

      30

      12

      94

      18

      Japan**

      111

      27

      281

      26

      48

      22

      119

      26

      *1990. **1991. Rate=Deaths per 100,000 inhabitants. % is from all causes of death in the age group.

       

      Table 2. Mortality rates from special cardiovascular diagnosis groups in the years 1991 and 1990 in the age group 55-64 for selected countries

      Diagnosis group
      (ICD 9th Rev.)

      Russia (1991)

      USA (1990)

      Germany (1991)

      France (1991)

      Japan (1991)

      M

      F

      M

      F

      M

      F

      M

      F

      M

      F

      393–398

      16.8

      21.9

      3.3

      4.6

      3.6

      4.4

      2.2

      2.3

      1.2

      1.9

      401–405

      22.2

      18.5

      23.0

      14.6

      16.9

      9.7

      9.4

      4.4

      4.0

      1.6

      410

      160.2

      48.9

      216.4

      79.9

      245.2

      61.3

      100.7

      20.5

      45.9

      13.7

      411–414

      586.3

      189.9

      159.0

      59.5

      99.2

      31.8

      35.8

      6.8

      15.2

      4.2

      415–429

      60.9

      24.0

      140.4

      64.7

      112.8

      49.2

      73.2

      27.0

      98.7

      40.9

      430–438

      385.0

      228.5

      54.4

      42.2

      84.1

      43.8

      59.1

      26.7

      107.3

      53.6

      440

      441–448


      {50.0}


      {19.2}

      4.4

      18.4

      2.1

      6.7

      11.8

      15.5

      3.8

      4.2

      1.5

      23.4

      0.3

      3.8

      0.3

      3.8

      0.1

      2.6

      Total 390–459

      1,290

      559

      623

      273

      597

      213

      311

      94

      281

      119

      Deaths per 100,000 inhabitants; M=male; F=female.

      Work Disability and Early Retirement

      Diagnosis-related statistics on time lost from work represent an important perspective on the impact of morbidity on the working population, even though the diagnostic designations are usually less precise than in cases of early retirement because of disability. The case rates, usually expressed in cases per 10,000 employees, provide an index of the frequency of the disease categories, while the average number of days lost per case indicates the relative seriousness of particular diseases. Thus, according to statistics on 10 million workers in western Germany compiled by the Allgemeinen Ortskrankenkasse, CVDs accounted for 7.7% of the total disability in 1991-92, although the number of cases for that period was only 4.6% of the total (Table 3). In some countries, where early retirement is provided when work ability is reduced due to illness, the pattern of disability mirrors the rates for different categories of CVD.

      Table 3. Rate of cardiovascular disease among early pensioners* due to reduced ability to work (N = 576,079) and diagnosis-related work disability in the western part of Germany, 1990-92

      Diagnosis group
      (ICD 9th Rev.)

      Main cause of illness

      Access to early retirement; number  per 100,000 early retirees

      Average annual work disability 1990–92

       

      Cases per 100,000 employed

      Duration (days) per case

       

      Men

      Women

      Men

      Women

      Men

      Women

      390–392

      Acute rheumatic fever

      16

      24

      49

      60

      28.1

      32.8

      393–398

      Chronic rheumatic heart disease

      604

      605

      24

      20

      67.5

      64.5

      401–405

      Hypertension, high blood pressure diseases

      4,158

      4,709

      982

      1,166

      24.5

      21.6

      410–414

      Ischaemic heart diseases

      9,635

      2,981

      1,176

      529

      51.2

      35.4

      410, 412

      Acute and existing myocardial infarction

      2,293

      621

      276

      73

      85.8

      68.4

      414

      Coronary heart disease

      6,932

      2,183

      337

      135

      50.8

      37.4

      415–417

      Pulmonary circulatory diseases

      248

      124

      23

      26

      58.5

      44.8

      420–429

      Other non-rheumatic heart diseases

      3,434

      1,947

      645

      544

      36.3

      25.7

      420–423

      Inflammatory heart diseases

      141

      118

      20

      12

      49.4

      48.5

      424

      Heart valve disorders

      108

      119

      22

      18

      45.6

      38.5

      425

      Myocardiopathy

      1,257

      402

      38

      14

      66.8

      49.2

      426

      Stimulus performance disorder

      86

      55

      12

      7

      39.6

      45.0

      427

      Cardiac rhythm disorder

      734

      470

      291

      274

      29.3

      21.8

      428

      Cardiac insufficiency

      981

      722

      82

      61

      62.4

      42.5

      430–438

      Cerebrovascular diseases

      4,415

      2,592

      172

      120

      75.6

      58.9

      440–448

      Diseases of the arteries, arterioles and capillaries

      3,785

      1,540

      238

      90

      59.9

      44.5

      440

      Arteriosclerosis

      2,453

      1,090

      27

      10

      71.7

      47.6

      443

      Raynaud’s disease and other vascular diseases

      107

      53

      63

      25

      50.6

      33.5

      444

      Arterial embolism and thrombosis

      219

      72

      113

      34

      63.3

      49.5

      451–456

      Diseases of the veins

      464

      679

      1,020

      1,427

      22.9

      20.3

      457

      Noninfectious diseases of the lymph nodes

      16

      122

      142

      132

      10.4

      14.2

      458

      Hypotension

      29

      62

      616

      1,501

      9.4

      9.5

      459

      Other circulatory diseases

      37

      41

      1,056

      2,094

      11.5

      10.2

      390–459

      Total cardiovascular diseases

      26,843

      15,426

      6,143

      7,761

      29.6

      18.9

      *Early pensioned: Statutory pensions insurance for former Federal Republic of Germany, work disability AOK-West.

       

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      Risk factors are genetic, physiological, behavioural and socioeconomic characteristics of individuals that place them in a cohort of the population that is more likely to develop a particular health problem or disease than the rest of the population. Usually applied to multifactorial diseases for which there is no single precise cause, they have been particularly useful in identifying candidates for primary preventive measures and in assessing the effectiveness of the prevention programme in controlling the risk factors being targeted. They owe their development to large-scale prospective population studies, such as the Framingham study of coronary artery disease and stroke conducted in Framingham, Massachusetts, in the United States, other epidemiological studies, intervention studies and experimental research.

      It should be emphasized that risk factors are merely expressions of probability—that is, they are not absolute nor are they diagnostic. Having one or more risk factors for a particular disease does not necessarily mean that an individual will develop the disease, nor does it mean that an individual without any risk factors will escape the disease. Risk factors are individual characteristics which affect that person’s chances of developing a particular disease or group of diseases within a defined future time period. Categories of risk factors include:

      • somatic factors, such as high blood pressure, lipid metabolism disorders, overweight and diabetes mellitus
      • behavioural factors, such as smoking, poor nutrition, lack of physical movement, type-A personality, high alcohol consumption and drug abuse
      • strains, including exposures in the occupational, social and private spheres.

       

      Naturally, genetic and dispositional factors also play a role in high blood pressure, diabetes mellitus and lipid metabolism disorders. Many of the risk factors promote the development of arteriosclerosis, which is a significant precondition for the onset of coronary heart disease.

      Some risk factors may put the individual at risk for the development of more than one disease; for example, cigarette smoking is associated with coronary artery disease, stroke and lung cancer. At the same time, an individual may have multiple risk factors for a particular disease; these may be additive but, more often, the combinations of risk factors may be multiplicative. Somatic and lifestyle factors have been identified as the main risk factors for coronary heart disease and stroke.

      Hypertension

      Hypertension (increased blood pressure), a disease in its own right, is one of the major risk factors for coronary heart disease (CHD) and stroke. As defined by the WHO, blood pressure is normal when the diastolic is below 90 mm Hg and the systolic is below 140 mm Hg. In threshold or borderline hypertension, the diastolic ranges from 90 to 94 mm Hg and the systolic from 140 to 159 mm Hg. Individuals with diastolic pressures equal to or greater than 95 mm Hg and systolic pressures equal to or greater than 160 mm Hg are designated as being hypertensive. Studies have shown, however, that such sharp criteria are not entirely correct. Some individuals have a “labile” blood pressure—the pressure fluctuates between normal and hypertensive levels depending on the circumstances of the moment. Further, without regard to the specific categories, there is a linear progression of relative risk as the pressure rises above the normal level.

      In the United States, for example, the incidence rate of CHD and stroke among men aged 55 to 61 was 1.61% per year for those whose blood pressure was normal compared to 4.6% per year for those with hypertension (National Heart, Lung and Blood Institute 1981).

      Diastolic pressures over 94 mm Hg were found in 2 to 36% of the population aged 35 to 64 years, according to the WHO-MONICA study. In many countries of Central, Northern and Eastern Europe (e.g., Russia, the Czech Republic, Finland, Scotland, Romania, France and parts of Germany, as well as Malta), hypertension was found in over 30% of the population aged 35 to 54, while in countries including Spain, Denmark, Belgium, Luxembourg, Canada and the United States, the corresponding figure was less than 20% (WHO-MONICA 1988). The rates tend to increase with age, and there are racial differences. (In the United States, at least, hypertension is more frequent among African-Americans than in the White population.)

      Risks for developing hypertension

      The important risk factors for developing hypertension are excess body weight, high salt intake, a series of other nutritional factors, high alcohol consumption, physical inactivity, and psychosocial factors, including stress (Levi 1983). Furthermore, there is a certain genetic component whose relative significance is not yet fully understood (WHO 1985). Frequent familial high blood pressure should be considered a danger and special attention paid to controlling lifestyle factors.

      There is evidence that psychosocial and psychophysical factors, in conjunction with the job, can have an influence on developing hypertension, especially for short-term blood pressure increases. Increases have been found in the concentration of certain hormones (adrenalin and noradrenalin) as well as cortisol (Levi 1972), which, alone and in combination with high salt consumption, can lead to increased blood pressure. Work stress also appears to be related to hypertension. A dose-effect relationship with intensity of air traffic was shown (Levi 1972; WHO 1985) in comparing groups of air traffic controllers with different high psychic strain.

      Treatment of hypertension

      Hypertension can and should be treated, even in the absence of any symptoms. Lifestyle changes such as weight control, reduction of sodium intake and regular physical exercise, coupled when necessary with anti-hypertensive medications, regularly evoke re- ductions in blood pressure, often to normal levels. Unfortunately, many individuals found to be hypertensive are not receiving adequate treatment. According to the WHO-MONICA study (1988), less than 20% of hypertensive women in Russia, Malta, eastern Germany, Scotland, Finland and Italy were receiving adequate treatment during the mid-1980s, while the comparable figure for men in Ireland, Germany, China, Russia, Malta, Finland, Poland, France and Italy was under 15%.

      Prevention of hypertension

      The essence of preventing hypertension is identifying individuals with blood pressure elevation through periodic screening or medical examination programmes, repeated checks to verify the extent and duration of the elevation, and the institution of an appropriate treatment regimen that will be maintained indefinitely. Those with a family history of hypertension should have their pressures checked more frequently and should be guided to elimination or control of any risk factors they may present. Control of alcohol abuse, physical training and physical fitness, normal weight maintenance and efforts to reduce psychological stress are all important elements of prevention programmes. Improvement in workplace conditions, such as reducing noise and excess heat, are other preventive measures.

      The workplace is a uniquely advantageous arena for programmes aimed at the detection, monitoring and control of hypertension in the workforce. Convenience and low or no cost make them attractive to the participants and the positive effects of peer pressure from co-workers tend to enhance their compliance and the success of the programme.

      Hyperlipidemia

      Many long-term international studies have demonstrated a convincing relationship between abnormalities in lipid metabolism and an increased risk of CHD and stroke. This is particularly true for elevated total cholesterol and LDL (low density lipoproteins) and/or low levels of HDL (high density lipoproteins). Recent research provides further evidence linking the excess risk with different lipoprotein fractions (WHO 1994a).

      The frequency of elevated total cholesterol levels >>6.5 mmol/l) was shown to vary considerably in population groups by the worldwide WHO-MONICA studies in the mid-1980s (WHO- MONICA 1988). The rate of hypercholesterolemia for popu- lations of working age (35 to 64 years of age) ranged from 1.3 to 46.5% for men and 1.7 to 48.7% for women. Although the ranges were generally similar, the mean cholesterol levels for the study groups in different countries varied significantly: in Finland, Scot- land, East Germany, the Benelux countries and Malta, a mean of over 6 mmol/l was found, while the means were lower in east Asian countries like China (4.1 mmol/l) and Japan (5.0 mmol/l). In both regions, the means were below 6.5 mmol/l (250 mg/dl), the level designated as the threshold of normal; however, as noted above for blood pressure, there is a progressive increase of risk as the level rises, rather than a sharp demarcation between normal and abnormal. Indeed, some authorities have pegged a total chol- esterol level of 180 mg/dl as the optimal level that should not be exceeded.

      It should be noted that gender is a factor, with women averaging lower levels of HDL. This may be one reason why women of working age have a lower mortality rate from CHD.

      Except for the relatively few individuals with hereditary hyper- cholesterolemia, cholesterol levels generally reflect the dietary intake of foods rich in cholesterol and saturated fats. Diets based on fruit, plant products and fish, with reduced total fat intake and substitution of poly-unsaturated fats, are generally associated with low cholesterol levels. Although their role is not yet entirely clear, intake of anti-oxidants (vitamin E, carotene, selenium and so on) is also thought to influence cholesterol levels.

      Factors associated with higher levels of HDL cholesterol, the “protective” form of lipoprotein, include race (Black), gender (female), normal weight, physical exercise and moderate alcohol intake.

      Socio-economic level also appears to play a role, at least in industrialized countries, as in West Germany, where higher cholesterol levels were found in population groups of both men and women with lower education levels (under ten years of schooling) compared to those completing 12 years of education (Heinemann 1993).

      Cigarette Smoking

      Cigarette smoking is among the most important risk factors for CVD. The risk from cigarette smoking is directly related to the number of cigarettes one smokes, the length of time one has been smoking, the age at which one began to smoke, the amount one inhales and the tar, nicotine and carbon monoxide content of the inspired smoke. Figure 1 illustrates the striking increase in CHD mortality among cigarette smokers compared to non-smokers. This increased risk is demonstrated among both men and women and in all socio-economic classes.

      The relative risk of cigarette smoking declines after tobacco use is discontinued. This is progressive; after about ten years of non-smoking, the risk is down almost to the level of those who never smoked.

      Recent evidence has demonstrated that those inhaling “second-hand smoke” (i.e., passive inhalation of smoke from cigarettes smoked by others) are also at significant risk (Wells 1994; Glantz and Parmley 1995).

      Rates of cigarette smoking vary among countries, as demonstrated by the international WHO-MONICA study (1988). The highest rates for men aged 35 to 64 were found in Russia, Poland, Scotland, Hungary, Italy, Malta, Japan and China. More women smokers were found in Scotland, Denmark, Ireland, the United States, Hungary and Poland (the recent Polish data are limited to large cities).

      Social status and occupational level are factors in the level of smoking among workers. Figure 1, for example, demonstrates that the proportions of smokers among men in East Germany increased in the lower social classes. The reverse is found in countries with relatively low numbers of smokers, where there is more smoking among those at higher social levels. In East Germany, smoking is also more frequent among shift-workers when compared with those on a “normal” work schedule.

      Figure 1. Relative mortality risk from cardiovascular diseases for smokers (including ex-smokers) and social classes compared to non-smoking, normal weight, skilled workers (male) based on occupational medical care examinations in East Germany, mortality 1985-89, N= 2.7 million person years.

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      Unbalanced Nutrition, Salt Consumption

      In most industrialized countries traditional low-fat nutrition has been replaced by high-calorie, high-fat, low carbohydrate, too sweet or too salty eating habits. This contributes to the development of overweight, high blood pressure, and high cholesterol level as elements of high cardiovascular risk. The heavy consumption of animal fats, with their high proportion of saturated fatty acids, leads to an increase in LDL cholesterol and increased risk. Fats derived from vegetables are much lower in these substances (WHO 1994a). Eating habits are also strongly associated with both socio-economic level and occupation.

      Overweight

      Overweight (excess fat or obesity rather than increased muscle mass) is a cardiovascular risk factor of lesser direct significance. There is evidence that the male pattern of excess fat distribution (abdominal obesity) is associated with a greater risk of cardiovascular and metabolic problems than the female (pelvic) type of fat distribution.

      Overweight is associated with hypertension, hypercholesterolemia and diabetes mellitus, and, to a much greater extent in women than men, tends to increase with age (Heuchert and Enderlein 1994) (Figure 2). It is also a risk factor for musculoskeletal problems and osteoarthritis, and makes physical exercise more difficult. The frequency of significant overweight varies considerably among countries. Random population surveys conducted by the WHO-MONICA project found it in more than 20% of females aged 35 to 64 in the Czech Republic, East Germany, Finland, France, Hungary, Poland, Russia, Spain and Yugoslavia, and in both sexes in Lithuania, Malta and Romania. In China, Japan, New Zealand and Sweden, fewer than 10% of both men and women in this age group were significantly overweight.

      Common causes of overweight include familial factors (these may in part be genetic but more often reflect common dietary habits), overeating, high-fat and high-carbohydrate diets and lack of physical exercise. Overweight tends to be more common among the lower socio-economic strata, particularly among women, where, among other factors, financial constraints limit the availability of a more balanced diet. Population studies in Germany demonstrated that the proportion of significant overweight among those with lower education levels is 3 to 5 times greater than that among people with more education, and that some occupations, notably food preparation, agriculture and to some extent shift work, have a high percentage of overweight people (Figure 3) (Heinemann 1993).

      Figure 2. Prevalence of hypertension by age, sex and six levels of relative body weight according tot he body-mass index (BMI) in occupational medical care examinations in East Germany (normal BMI values are underlined).

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      Figure 3. Relative risk from overweight by length of education(years of schooling) in Germay (population 25-64 years).

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      Physical Inactivity

      The close association of hypertension, overweight and diabetes mellitus with lack of exercise at work and/or off the job has made physical inactivity a significant risk factor for CHD and stroke (Briazgounov 1988; WHO 1994a). A number of studies have demonstrated that, holding all other risk factors constant, there was a lower mortality rate among persons engaging regularly in high-intensity exercises than among those with a sedentary lifestyle.

      The amount of exercise is readily measured by noting its duration and either the amount of physical work accomplished or the extent of the exercise-induced increase in heart rate and the time required for that rate to return to its resting level. The latter is also useful as an indicator of the level of cardiovascular fitness: with regular physical training, there will be less of an increase in heart rate and a more rapid return to the resting rate for a given intensity of exercise.

      Workplace physical fitness programmes have been shown to be effective in enhancing cardiovascular fitness. Participants in these tend also to give up cigarette smoking and to pay greater attention to proper diets, thus significantly reducing their risk of CHD and stroke.

      Alcohol

      High alcohol consumption, especially the drinking of high-proof spirits, has been associated with a greater risk of hypertension, stroke and myocardiopathy, while moderate alcohol use, particularly of wine, has been found to reduce the risk of CHD (WHO 1994a). This has been associated with the lower CHD mortality among the upper social strata in industrialized countries, who generally prefer wine to “hard” liquors. It should also be noted that while their alcohol intake may be similar to that of wine drinkers, beer drinkers tend to accumulate excess weight, which, as noted above, may increase their risk.

      Socio-economic Factors

      A strong correlation between socio-economic status and the risk of CVD has been demonstrated by analyses of the death register mortality studies in Britain, Scandinavia, Western Europe, the United States and Japan. For example, in eastern Germany, the cardiovascular death rate is considerably lower for the upper social classes than for the lower classes (see Figure 1) (Marmot and Theorell 1991). In England and Wales, where general mortality rates are declining, the relative gap between the upper and lower classes is widening.

      Socio-economic status is typically defined by such indicators as occupation, occupational qualifications and position, level of education and, in some instances, income level. These are readily translated into standard of living, nutritional patterns, free-time activities, family size and access to medical care. As noted above, behavioural risk factors (such as smoking and diet) and the somatic risk factors (such as overweight, hypertension and hyperlipidemia) vary considerably among social classes and occupational groups (Mielck 1994; Helmert, Shea and Maschewsky Schneider 1995).

      Occupational Psychosocial Factors and Stress

      Occupational stress

      Psychosocial factors at the workplace primarily refer to the combined effect of working environment, work content, work demands and technological-organizational conditions, and also to personal factors like capability, psychological sensitivity, and finally also to health indicators (Karasek and Theorell 1990; Siegrist 1995).

      The role of acute stress on people who already suffer from cardiovascular disease is uncontested. Stress leads to episodes of angina pectoris, rhythm disorders and heart failure; it can also precipitate a stroke and/or a heart attack. In this context stress is generally understood to mean acute physical stress. But evidence has been mounting that acute psychosocial stress can also have these effects. Studies from the 1950s showed that people who work two jobs at a time, or who work overtime for long periods, have a relatively higher risk of heart attack, even at a young age. Other studies showed that in the same job, the person with the greater work and time pressure and frequent problems on the job is at significantly greater risk (Mielck 1994).

      In the last 15 years, job stress research suggests a causal relationship between work stress and the incidence of cardiovascular disease. This is true for cardiovascular mortality as well as frequency of coronary disease and hypertension (Schnall, Landsbergis and Baker 1994). Karasek’s job strain model defined two factors that could lead to an increased incidence of cardiovascular disease:

      • extent of job demands
      • extent of decision-making latitude.

       

      Later Johnson added as a third factor the extent of social support (Kristensen 1995) which is discussed more fully elsewhere in this Encyclopaedia. The chapter Psychosocial and Organizational Factors includes discussions on individual factors, such as Type A personality, as well as social support and other mechan- isms for overcoming the effects of stress.

      The effects of factors, whether individual or situational, that lead to increased risk of cardiovascular disease can be reduced by “coping mechanisms”, that is, by recognizing the problem and overcoming it by attempting to make the best of the situation.

      Until now, measures aimed at the individual have predominated in the prevention of the negative health effects of work stress. Increasingly, improvements in organizing the work and expanding employee decision-making latitude have been used (e.g., action research and collective bargaining; in Germany, occupational quality and health circles) to achieve an improvement in productivity as well as to humanize the work by decreasing the stress load (Landsbergis et al. 1993).

      Night and Shift Work

      Numerous publications in the international literature cover the health risks posed by night and shift work. It is generally accepted that shift work is one risk factor which, together with other relev- ant (including indirect) work-related demands and expectation factors, leads to adverse effects.

      In the last decade research on shift work has increasingly dealt with the long-term effects of night and shift work on the frequency of cardiovascular disease, especially ischaemic heart disease and myocardial infarction, as well as cardiovascular risk factors. The results of epidemiological studies, especially from Scandinavia, permit a higher risk of ischemic heart disease and myocardial infarction to be presumed for shift workers (Alfredsson, Karasek and Theorell 1982; Alfredsson, Spetz and Theorell 1985; Knutsson et al. 1986; Tüchsen 1993). In Denmark it was even estimated that 7% of cardiovascular disease in men as well as women can be traced to shift work (Olsen and Kristensen 1991).

      The hypothesis that night and shift workers have a higher risk (estimated relative risk approximately 1.4) for cardiovascular disease is supported by other studies that consider cardiovascular risk factors like hypertension or fatty acid levels for shift workers as compared to day workers. Various studies have shown that night and shift work may induce increased blood pressure and hypertension as well as increased triglyceride and/or serum cholesterol (as well as normal range fluctuations for HDL-cholesterol in increased total cholesterol). These changes, together with other risk factors (like heavy cigarette smoking and overweight among shift workers), can cause increased morbidity and mortality due to atherosclerotic disease (DeBacker et al. 1984; DeBacker et al. 1987; Härenstam et al. 1987; Knutsson 1989; Lavie et al. 1989; Lennernäs, Åkerstedt and Hambraeus 1994; Orth-Gomer 1983; Romon et al. 1992).

      In all, the question of possible causal links between shift work and atherosclerosis cannot be definitively answered at present, as the pathomechanism is not sufficiently clear. Possible mechanisms discussed in the literature include changes in nutrition and smoking habits, poor sleep quality, increases in lipid level, chronic stress from social and psychological demands and disrupted circadian rhythms. Knutsson (1989) has proposed an interesting pathogenesis for the long-term effects of shift work on chronic morbidity.

      The effects of various associated attributes on risk estimation have hardly been studied, since in the occupational field other stress-inducing working conditions (noise, chemical hazardous materials, psychosocial stress, monotony and so on) are connected with shift work. From the observation that unhealthy nutritional and smoking habits are often connected with shift work, it is often concluded that an increased risk of cardiovascular disease among shift workers is more the indirect result of unhealthy behaviour (smoking, poor nutrition and so on) than directly the result of night or shift work (Rutenfranz, Knauth and Angersbach 1981). Furthermore, the obvious hypothesis of whether shift work promotes this conduct or whether the difference comes primarily from the choice of workplace and occupation must be tested. But regardless of the unanswered questions, special attention must be paid in cardiovascular prevention programmes to night and shift workers as a risk group.

      Summary

      In summary, risk factors represent a broad variety of genetic, somatic, physiological, behavioural and psychosocial characteristics which can be assessed individually for individuals and for groups of individuals. In the aggregate, they reflect the probability that CVD, or more precisely in the context of this article, CHD or stroke will develop. In addition to elucidating the causes and pathogenesis of multifactorial diseases, their chief importance is that they delineate individuals who should be targets for risk factor elimination or control, an exercise admirably suited to the workplace, while repeated risk assessments over time demonstrate the success of that preventive effort.

       

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      Tuesday, 15 February 2011 20:54

      Rehabilitation and Prevention Programmes

      Written by

      Most individuals with recognized CVD are able to work effectively and productively in most of the jobs found in the modern workplace. Just a few decades ago, individuals surviving an acute myocardial infarction were cosseted and pampered for weeks and months with close supervision and enforced inactivity. Laboratory confirmation of the diagnosis was enough to justify labelling the individual as “permanently and totally disabled”. New diagnostic technology that provides more accurate evaluation of cardiac status and the favourable experiences of those who could not or would not accept such a label, soon demonstrated that an early return to work and an optimal level of activity was not only possible but desirable (Edwards, McCallum and Taylor 1988; Theorell et al. 1991; Theorell 1993). Today, patients commence supervised physical activity as soon as the acute effects of the infarction subside, are often out of the hospital in a few days instead of the mandatory 6 to 8 weeks of yore, and are often back on the job within a few weeks. When desirable and feasible, surgical procedures such as angioplasty, by-pass operations and even cardiac transplantation can improve the coronary blood flow, while a regimen featuring diet, exercise and control of the risk factors for CHD can minimize (or even reverse) the progression of coronary atherosclerosis.

      Once the acute, often life-threatening phases of the CVD have been overcome, passive movement followed by active exercise should be initiated early during the stay in the hospital or clinic. With heart attacks, this phase is completed when the individual can climb stairs without great difficulty. At the same time, the individual is schooled in a risk-prevention regimen that includes proper diet, cardiovascular conditioning exercises, adequate rest and relaxation, and stress management. During these phases of rehabilitation, support from family members, friends and co-workers can be particularly helpful (Brusis and Weber-Falkensammer 1986). The programme can be carried out in rehabilitation facilities or in ambulatory “heart groups” under the supervision of a trained physician (Halhubar and Traencker 1986). The focus on controlling lifestyle and behavioural risk factors and controlling stress has been shown to result in a measurable reduction in the risk of re-infarction and other cardiovascular problems.

      Throughout the programme the attending physician should maintain contact with the employer (and particularly with the company doctor, if there is one) to discuss the prospects for recovery and the probable duration of the period of disability, and to explore the feasibility of any special arrangements that may be needed to permit an early return to the job. The worker’s knowledge that the job is waiting and that he or she is expected to be able to return to it is a potent motivating factor for the enhancement of recovery. Experience has amply demonstrated that the success of the rehabilitation effort diminishes as the absence from work lengthens.

      In instances where desirable adjustments in the job and/or the workplace are not possible or feasible, retraining and appropriate job placement can obviate unnecessary invalidism. Specially protected workshops are often helpful in reintegrating into the workplace people who have been absent from the job for long periods while receiving treatment for the serious effects of stroke, congestive heart failure or disabling angina pectoris.

      Following the return to work, continued surveillance by both the attending physician and the occupational physician is eminently desirable. Periodic medical evaluations, at intervals that are frequent initially but lengthen as recovery is assured, are helpful in assessing the worker’s cardiovascular status, adjusting medications and other elements in the maintenance regimen and monitoring the adherence to the lifestyle and behavioural recommendations. Satisfactory findings in these examinations may allow the gradual easing of any work limitations or restrictions until the worker is fully integrated into the workplace.

      Workplace Health Promotion and Prevention Programmes

      The prevention of occupational diseases and injuries is a prime responsibility of the organization’s occupational health and safety programme. This includes primary prevention (i.e., the identifica- tion and elimination or control of potential hazards and strains by changing the work environment or the job). It is supplemented by secondary prevention measures which protect the workers from the effects of existing hazards and strains that cannot be elim- inated (i.e., personal protective equipment and periodic medical surveillance examinations). Workplace health promotion and pre- vention (HPP) programmes go beyond these goals. They place their emphasis on health-conscious behaviour as it relates to life- style, behavioural risk factors, eliminating or coping with stress and so on. They are of great significance, particularly in pre- venting CVD. The goals of HPP, as formulated by the WHO Committee on Environmental and Health Monitoring in Occupational Health, extend beyond the mere absence of disease and injury to include well-being and functional capacity (WHO 1973).

      The design and operation of HPP programmes are discussed in more detail elsewhere in the chapter. In most countries, they have a particular focus on the prevention of CVDs. For example, in Germany, the “Have a heart for your heart” programme supplements the heart health circles organized by the health insurance companies (Murza and Laaser 1990, 1992), while the “Take Heart” movement in Britain and Australia has similar goals (Glasgow et al. 1995).

      That such programmes are effective was verified in the 1980s by the WHO Collaborative Trial in Prevention of Heart Disease, which was carried out in 40 pairs of factories in four European countries and involved approximately 61,000 men aged 40 to 59. The preventive measures largely comprised health education activities, carried out primarily by the organization’s employee health service, focused on cholesterol-lowering diets, giving up cigarette smoking, weight control, increased physical activity and controlling hypertension. A randomized screening of 10% of the eligible workers in the factories designated as controls demonstrated that during the 4 to 7 years of the study, overall risk of CVDs could be reduced by 11.1% (19.4% among those initially at high risk). In the study factories, mortality from CHDs fell by 7.4%, while overall mortality fell by 2.7%. The best results were achieved in Belgium, where the intervention was carried out continuously during the entire study period, while the poorest results were seen in Britain, where the prevention activities were sharply curtailed prior to the last follow-up examination. This disparity emphasizes the relationship of success to the duration of the health education effort; it takes time to inculcate the desired lifestyle changes. The intensity of the educational effort was also a factor: in Italy, where six full-time health educators were involved, a 28% reduction in overall risk-factor profile was achieved, whereas in Britain, where only two full-time educators served three times the number of workers, a risk factor reduction of only 4% was achieved.

      While the time required to detect reductions in CHD mortality and morbidity is a formidable limiting factor in epidemiological studies aimed at evaluating the results of company health programmes (Mannebach 1989), reductions in risk factors have been demonstrated (Janssen 1991; Gomel et al. 1993; Glasgow et al. 1995). Temporary decreases in the number of lost workdays and a decline in hospitalization rates have been reported (Harris 1994). There seems to be general agreement that HPP activities in the community and particularly in the workplace have significantly contributed to the reduction in cardiovascular mortality in the United States and other western industrialized countries.

      Conclusion

      CVDs loom large in the workplace, not so much because the cardiovascular system is particularly vulnerable to environmental and job hazards, but because they are so common in the popu- lation of working age. The workplace offers a singularly advant- ageous arena for the detection of unrecognized, asymptomatic CVDs, for the circumvention of workplace factors that might accelerate or aggravate them and for the identification of factors that increase the risk of CVDs and the mounting of programmes to eliminate or control them. When CVDs do occur, prompt attention to control of job-related circumstances that may prolong or increase their severity can minimize the extent and duration of disability, while early, professionally supervised rehabilitation efforts will facilitate the restoration of working capacity and reduce the risk of recurrences.

      Physical, Chemcial and Biological Hazards

      The intact cardiovascular system is remarkably resistant to the harmful effects of physical, chemical and biological hazards encountered on the job or in the workplace. With a very few exceptions, such hazards are rarely a direct cause of CVDs. On the other hand, once the integrity of the cardiovascular system is compromised—and this may be entirely silent and unrecognized—exposure to these hazards may contribute to the ongoing development of a disease process or precipitate symptoms reflecting functional impairment. This dictates early identification of workers with incipient CVD and modification of their jobs and/or the work environment to reduce the risk of harmful effects. The following segments will include brief discussions of some of the more commonly encountered occupational hazards that may affect the cardiovascular system. Each of the hazards presented below is discussed more fully elsewhere in the Encyclopaedia.

       

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      Tuesday, 15 February 2011 21:54

      Digestive System

      Written by

      The digestive system exerts a considerable influence on the efficiency and work capacity of the body, and acute and chronic illnesses of the digestive system are among the commonest causes of absenteeism and disablement. In this context, the occupational physician may be called upon in either of the following ways to offer suggestions concerning hygiene and nutritional requirements in relation to the particular needs of a given occupation: to assess the influence that factors inherent in the occupation may have either in producing morbid conditions of the digestive system, or in aggravating others that may pre-exist or be otherwise independent of the occupation; or to express an opinion concerning general or specific fitness for the occupation.

      Many of the factors that are harmful to the digestive system may be of occupational origin; frequently a number of factors act in concert and their action may be facilitated by individual predisposition. The following are among the most important occupational factors: industrial poisons; physical agents; and occupational stress such as tension, fatigue, abnormal postures, frequent changes in work tempo, shift work, night work and unsuitable eating habits (quantity, quality and timing of meals).

      Chemical Hazards

      The digestive system may act as a portal for the entry of toxic substances into the body, although its role here is normally much less important than that of the respiratory system which has an absorption surface area of 80-100 m2 whereas the corresponding figure for the digestive system does not exceed 20 m2. In addition, vapours and gases entering the body by inhalation reach the bloodstream and hence the brain without meeting any intermediate defence; however, a poison that is ingested is filtered and, to some degree, metabolized by the liver before reaching the vascular bed. Nevertheless, the organic and functional damage may occur both during entry into and elimination from the body or as a result of accumulation in certain organs. This damage suffered by the body may be the result of the action of the toxic substance itself, its metabolites or the fact that the body is depleted of certain essential substances. Idiosyncrasy and allergic mechanisms may also play a part. The ingestion of caustic substances is still a fairly common accidental occurrence. In a retrospective study in Denmark, the annual incidence was of 1/100,000 with an incidence of hospitalization of 0.8/100,000 adult person-years for oesophageal burns. Many household chemicals are caustic.

      Toxic mechanisms are highly complex and may vary considerably from substance to substance. Some elements and compounds used in industry cause local damage in the digestive system affecting, for example, the mouth and neighbouring area, stomach, intestine, liver or pancreas.

      Solvents have particular affinity for lipid-rich tissues. The toxic action is generally complex and different mechanisms are involved. In the case of carbon tetrachloride, liver damage is thought to be mainly due to toxic metabolites. In the case of carbon disulphide, gastrointestinal involvement is attributed to the specific neurotropic action of this substance on the intramural plexus whilst liver damage seems to be more due to the solvent’s cytotoxic action, which produces changes in lipoprotein metabolism.

      Liver damage constitutes an important part of the pathology of exogenic poisons since the liver is the prime organ in metabolizing toxic agents and acts with the kidneys in detoxication processes. The bile receives from the liver, either directly or after conjugation, various substances that can be reabsorbed in the enterohepatic cycle (for instance, cadmium, cobalt, manganese). Liver cells participate in oxidation (e.g., alcohols, phenols, toluene), reduction, (e.g., nitrocompounds), methylation (e.g., selenic acid), conjugation with sulphuric or glucuronic acid (e.g., benzene), acetylation (e.g., aromatic amines). Kupffer cells may also intervene by phagocytosing the heavy metals, for example.

      Severe gastro-intestinal syndromes, such as those due to phosphorus, mercury or arsenic are manifested by vomiting, colic, and bloody mucus and stools and may be accompanied by liver damage (hepatomegalia, jaundice). Such conditions are relatively rare nowadays and have been superseded by occupational intoxications which develop slowly and even insidiously; consequently liver damage, in particular, may often be insidious too.

      Infectious hepatitis deserves particular mention; it may be related to a number of occupational factors (hepatotoxic agents, heat or hot work, cold or cold work, intense physical activity, etc.), may have an unfavourable course (protracted or persistent chronic hepatitis) and may easily result in cirrhosis. It frequently occurs with jaundice and thus creates diagnostic difficulties; moreover, it presents difficulties of prognosis and estimation of the degree of recovery and hence of fitness for resumption of work.

      Although the gastro-intestinal tract is colonized by abundant microflora which have important physiological functions in human health, an occupational exposure may give rise to occupational infections. For example, abattoir workers may be at risk to contract a helicobacter infection. This infection may often be symptomless. Other important infections include the Salmonella and Shigella species, which must be also controlled in order to maintain product safety, such as in the food industry and in catering services.

      Smoking and alcohol consumption are the major risks for oesophageal cancer in industrialized countries, and occupational aetiology is of lesser importance. However, butchers and their spouses seem to be at elevated risk of colorectal cancer.

      Physical Factors

      Various physical agents may cause digestive system syndromes; these include direct or indirect disabling traumata, ionizing radiations, vibration, rapid acceleration, noise, very high and low temperatures or violent and repeated climatic changes. Burns, especially if extensive, may cause gastric ulceration and liver damage, perhaps with jaundice. Abnormal postures or movements may cause digestive disorders especially if there are predisposing conditions such as para-oesophageal hernia, visceroptosis or relaxatio diaphragmatica; in addition, extra-digestive reflexes such as heartburn may occur where digestive disorders are accompanied by autonomic nervous system or neuro-psychological troubles. Troubles of this type are common in modern work situations and may themselves be the cause of gastro-intestinal dysfunction.

      Occupational Stress

      Physical fatigue may also disturb digestive functions, and heavy work may cause secretomotor disorders and dystrophic changes, especially in the stomach. Persons with gastric disorders, especially those who have undergone surgery are limited in the amount of heavy work they can do, if only because heavy work requires higher levels of nutrition.

      Shift work may cause important changes in eating habits with resultant functional gastro-intestinal problems. Shift work may be associated with elevated blood cholesterol and triglyceride levels, as well as increased gamma-glutamyltransferase activity in serum.

      Nervous gastric dyspepsia (or gastric neurosis) seems to have no gastric or extragastric cause at all, nor does it result from any humoral or metabolic disorder; consequently, it is considered to be due to a primitive disorder of the autonomic nervous system, sometimes associated with excessive mental exertion or emotional or psychological stress. The gastric disorder is often manifested by neurotic hypersecretion or by hyperkinetic or atonic neurosis (the latter frequently associated with gastroptosis). Epigastric pain, regurgitation and aerophagia may also come under the heading of neurogastric dyspepsia. Elimination of the deleterious psychological factors in the work environment may lead to remission of symptoms.

      Several observations point to an increased frequency of peptic ulcers among people carrying responsibilities, such as supervisors and executives, workers engaged in very heavy work, newcomers to industry, migrant workers, seafarers and workers subject to serious socio-economic stress. However, many people suffering the same disorders lead a normal professional life, and statistical evidence is lacking. In addition to working conditions drinking, smoking and eating habits, and home and social life all play a part in the development and prolongation of dyspepsia, and it is difficult to determine what part each one plays in the aetiology of the condition.

      Digestive disorders have also been attributed to shift work as a consequence of frequent changes of eating hours and poor eating at workplaces. These factors can aggravate pre-existing digestive troubles and release a neurotic dyspepsia. Therefore, workers should be assigned to shift work only after medical examination.

      Medical Supervision

      It can be seen that the occupational health practitioner is faced with many difficulties in the diagnosis and estimation of digestive system complaints (due inter alia to the part played by deleterious non-occupational factors) and that his or her responsibility in prevention of disorders of occupational origin is considerable.

      Early diagnosis is extremely important and implies periodical medical examinations and supervision of the working environment, especially when the level of risk is high.

      Health education of the general public, and of workers in particular, is a valuable preventive measure and may yield substantial results. Attention should be paid to nutritional requirements, choice and preparation of foodstuffs, the timing and size of meals, proper chewing and moderation in the consumption of rich foods, alcohol and cold drinks, or complete elimination of these substances from the diet.

       

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      Tuesday, 15 February 2011 22:31

      Mouth and Teeth

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      The mouth is the portal of entry to the digestive system and its functions are, primarily, the chewing and swallowing of food and the partial digestion of starches by means of salivary enzymes. The mouth also participates in vocalizing and may replace or complement the nose in respiration. Due to its exposed position and the functions it fulfils, the mouth is not only a portal of entry but also an area of absorption, retention and excretion for toxic substances to which the body is exposed. Factors which lead to respiration via the mouth (nasal stenoses, emotional situations) and increased pulmonary ventilation during effort, promote either the penetration of foreign substances via this route, or their direct action on the tissues in the buccal cavity.

      Respiration through the mouth promotes:

      • greater penetration of dust into the respiratory tree since the buccal cavity has a retention quotient (impingement) of solid particles much lower than that of the nasal cavities
      • dental abrasion in workers exposed to large dust particles, dental erosion in workers exposed to strong acids, caries in workers exposed to flour or sugar dust, etc.

       

      The mouth may constitute the route of entry of toxic substances into the body either by accidental ingestion or by slow absorption. The surface area of the buccal mucous membranes is relatively small (in comparison with that of the respiratory system and gastro-intestinal system) and foreign substances will remain in contact with these membranes for only a short period. These factors considerably limit the degree of absorption even of substances which are highly soluble; nevertheless, the possibility of absorption does exist and is even exploited for therapeutic purposes (perlingual absorption of drugs).

      The tissues of the buccal cavity may often be the site of accumulation of toxic substances, not only by direct and local absorption, but also by transport via the bloodstream. Research using radioactive isotopes has shown that even the tissues which seem metabolically the most inert (such as dental enamel and dentine) have a certain accumulative capacity and a relatively active turnover for certain substances. Classical examples of storage are various discolorations of the mucous membranes (gingival lines) which often provide valuable diagnostic information (e.g. lead).

      Salivary excretion is of no value in the elimination of toxic substances from the body since the saliva is swallowed and the substances in it are once more absorbed into the system, thus forming a vicious circle. Salivary excretion has, on the other hand, a certain diagnostic value (determination of toxic substances in the saliva); it may also be of importance in the pathogenesis of certain lesions since the saliva renews and prolongs the action of toxic substances on the buccal mucous membrane. The following substances are excreted in the saliva: various heavy metals, the halogens (the concentration of iodine in the saliva may be 7-700 times greater than that in plasma), the thiocyanates (smokers, workers exposed to hydrocyanic acid and cyanogen compounds), and a wide range of organic compounds (alcohols, alkaloids, etc.).

      Aetiopathogenesis and Clinical Classification

      Lesions of the mouth and teeth (also called stomatological lesions) of occupational origin may be caused by:

      • physical agents (acute traumata and chronic microtraumata, heat, electricity, radiations, etc.)
      • chemical agents which affect the tissues of the buccal cavity directly or by means of systemic changes
      • biological agents (viruses, bacteria, mycetes).

       

      However, when dealing with mouth and teeth lesions of occupational origin, a classification based on topographical or anatomical location is preferred to one employing aetiopathogenic principles.

      Lips and cheeks. Examination of the lips and cheeks may reveal: pallor due to anaemia (benzene, lead poisoning, etc.), cyanosis due to acute respiratory insufficiency (asphyxia) or chronic respiratory insufficiency (occupational diseases of the lungs), cyanosis due to methaemoglobinaemia (nitrites and organic nitro-compounds, aromatic amines), cherry-red colouring due to acute carbon monoxide poisoning, yellow colouring in cases of acute poisoning with picric acid, dinitrocresol, or in a case of hepatotoxic jaundice (phosphorus, chlorinated hydrocarbon pesticides, etc.). In argyrosis, there is brown or grey-bluish coloration caused by the precipitation of silver or its insoluble compounds, especially in areas exposed to light.

      Occupational disorders of the lips include: dyskeratoses, fissures and ulcerations due to the direct action of caustic and corrosive substances; allergic contact dermatitis (nickel, chrome) which may also include the dermatitis found in tobacco industry workers; microbial eczemas resulting from the use of respiratory protective equipment where the elementary rules of hygiene have not been observed; lesions caused by anthrax and glanders (malignant pustules and cancroid ulcer) of workers in contact with animals; inflammation due to solar radiation and found among agricultural workers and fishermen; neoplastic lesions in persons handling carcinogenic substances; traumatic lesions; and chancre of the lip in glassblowers.

      Teeth. Discoloration caused by the deposition of inert substances or due to the impregnation of the dental enamel by soluble compounds is of almost exclusively diagnostic interest. The important colourings are as follows: brown, due to the deposition of iron, nickel and manganese compounds; greenish-brown due to vanadium; yellowish-brown due to iodine and bromine; golden-yellow, often limited to gingival lines, due to cadmium.

      Of greater importance is dental erosion of mechanical or chemical origin. Even nowadays it is possible to find dental erosions of mechanical origin in certain craftsmen (caused by holding nails or string, etc., in the teeth) which are so characteristic that they can be considered occupational stigmata. Lesions caused by abrasive dusts have been described in grinders, sandblasters, stone industry workers and precious stone workers. Prolonged exposure to organic and inorganic acids will often cause dental lesions occurring mainly on the labial surface of the incisors (rarely on the canines); these lesions are initially superficial and limited to the enamel but later become deeper and more extensive, reaching the dentine and resulting in solubilization and mobilization of calcium salts. The localization of these erosions to the anterior surface of the teeth is due to the fact that when the lips are open it is this surface which is the most exposed and which is deprived of the natural protection offered by the buffer effect of saliva.

      Dental caries is such a frequent and widespread disease that a detailed epidemiological study is required to determine whether the condition is really of occupational origin. The most typical example is that of the caries found in workers exposed to flour and sugar dust (flourmillers, bakers, confectioners, sugar industry workers). This is a soft caries which develops rapidly; it starts at the base of the tooth (rampant caries) and immediately progresses to the crown; the affected sides blacken, the tissue is softened and there is considerable loss of substance and finally the pulp is affected. These lesions begin after a few years of exposure and their severity and extent increases with the duration of this exposure. X rays may also cause rapidly developing dental caries which usually commences at the base of the tooth.

      In addition to pulpites due to dental caries and erosion, an interesting aspect of pulp pathology is barotraumatic odontalgia, i.e., pressure-induced toothache. This is caused by the rapid development of gas dissolved in the pulp tissue following sudden atmospheric decompression: this is a common symptom in the clinical manifestations observed during rapid climbing in aircrafts. In the case of persons suffering from septic-gangrenous pulpites, where gaseous material is already present, this toothache may commence at an altitude of 2,000-3,000 m.

      Occupational fluorosis does not lead to dental pathology as is the case with endemic fluorosis: fluorine causes dystrophic changes (mottled enamel) only when the period of exposure precedes the eruption of permanent teeth.

      Mucous membrane changes and stomatitis. Of definite diagnostic value are the various discolorations of the mucous membranes due to the impregnation or precipitation of metals and their insoluble compounds (lead, antimony, bismuth, copper, silver, arsenic). A typical example is Burton’s line in lead poisoning, caused by the precipitation of lead sulphide following the development in the oral cavity of hydrogen sulphide produced by the putrefaction of food residues. It has not been possible to reproduce Burton’s line experimentally in herbivorous animals.

      There is a very curious discoloration in the lingual mucous membrane of workers exposed to vanadium. This is due to impregnation by vanadium pentoxide which is subsequently reduced to trioxide; the discoloration cannot be cleaned away but disappears spontaneously a few days after termination of exposure.

      The oral mucous membrane can be the site of severe corrosive damage caused by acids, alkalis and other caustic substances. Alkalis cause maceration, suppuration and tissue necrosis with the formation of lesions which slough off easily. Ingestion of caustic or corrosive substances produces severe ulcerative and very painful lesions of the mouth, oesophagus and stomach, which may develop into perforations and frequently leave scars. Chronic exposure favours the formation of inflammation, fissures, ulcers and epithelial desquamation of the tongue, palate and other parts of the oral mucous membranes. Inorganic and organic acids have a coagulating effect on proteins and cause ulcerous, necrotic lesions which heal with contractive scarring. Mercury chloride and zinc chloride, certain copper salts, alkaline chromates, phenol and other caustic substances produce similar lesions.

      A prime example of chronic stomatitis is that caused by mercury. It commences gradually, with discreet symptoms and a prolonged course; the symptoms include excessive saliva, metallic taste in the mouth, bad breath, slight gingival reddening and swelling, and these constitute the first phase of periodontitis leading towards loss of teeth. A similar clinical picture is found in stomatitis due to bismuth, gold, arsenic, etc.

      Salivary glands. Increased salivary secretion has been observed in the following cases:

      • in a variety of acute and chronic stomatites which is due mainly to the irritant action of the toxic substances and may, in certain cases, be extremely intense. For example, in cases of chronic mercurial poisoning, this symptom is so prominent and occurs at such an early stage that English workers have called this the “salivation disease”.
      • in cases of poisoning in which there is central nervous system involvement—as is the case in manganese poisoning. However, even in the case of chronic mercurial poisoning, salivary gland hyperactivity is thought to be, at least in part, nervous in origin.
      • in cases of acute poisoning with organophosphorus pesticides which inhibit cholinesterases.

       

      There is reduction in salivary secretion in severe thermoregulation disorders (heatstroke, acute dinitrocresol poisoning), and in serious disorders of water and electrolyte balance during toxic hepatorenal insufficiency.

      In cases of acute or chronic stomatitis, the inflammatory process may, sometimes, affect the salivary glands. In the past there have been reports of “lead parotitis”, but this condition has become so rare nowadays that doubts about its actual existence seem justified.

      Maxillary bones. Degenerative, inflammatory and productive changes in the skeleton of the mouth may be caused by chemical, physical and biological agents. Probably the most important of the chemical agents is white or yellow phosphorus which causes phosphorus necrosis of the jaw or “phossy jaw”, at one time a distressing disease of match industry workers. The absorption of phosphorus is facilitated by the presence of gingival and dental lesions, and produces, initially, productive periosteal reaction followed by destructive and necrotic phenomena which are activated by bacterial infection. Arsenic also causes ulceronecrotic stomatitis which may have further bone complications. The lesions are limited to the roots in the jaw, and lead to the development of small sheets of dead bones. Once the teeth have fallen out and the dead bone eliminated, the lesions have a favourable course and nearly always heal.

      Radium was the cause of maxillary osteonecrotic processes observed during the First World War in workers handling luminous compounds. In addition, damage to the bone may also be caused by infection.

      Preventive Measures

      A programme for the prevention of mouth and teeth diseases should be based on the following four main principles:

      • application of measures of industrial hygiene and preventive medicine including monitoring of workplace environment, analysis of production processes, elimination of hazards in the environment, and, where necessary, the use of personal protective equipment
      • education of workers in the need for scrupulous oral hygiene—in many cases it has been found that lack of oral hygiene may reduce resistance to general and localized occupational diseases
      • a careful check on the mouth and teeth when workers undergo pre-employment or periodical medical examinations
      • early detection and treatment of any mouth or teeth disease, whether of an occupational nature or not.

       

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      Tuesday, 15 February 2011 22:36

      Liver

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      The liver acts as a vast chemical factory with diverse vital functions. It plays an essential role in the metabolism of protein, carbohydrate and fat, and is concerned with the absorption and storage of vitamins and with the synthesis of prothrombin and other factors concerned with blood clotting. The liver is responsible for the inactivation of hormones and the detoxification of many drugs and exogenous toxic chemical substances. It also excretes the breakdown products of haemoglobin, which are the principal constituents of the bile. These widely varying functions are performed by parenchymal cells of uniform structure which contain many complex enzyme systems.

      Pathophysiology

      An important feature of liver disease is a rise in the level of bilirubin in the blood; if of sufficient magnitude, this stains the tissues to give rise to jaundice. The mechanism of this process is shown in figure 1. Haemoglobin released from worn out red blood cells is broken down to haem and then, by removal of iron, to bilirubin before it reaches the liver (prehepatic bilirubin). In its passage through the liver cell, bilirubin is conjugated by enzymatic activity into water-soluble glucuronides (posthepatic bilirubin) and then secreted as bile into the intestine. The bulk of this pigment is eventually excreted in the stool, but some is reabsorbed through the intestinal mucosa and secreted a second time by the liver cell into the bile (enterohepatic circulation). However, a small proportion of this reabsorbed pigment is finally excreted in the urine as urobilinogen. With normal liver function there is no bilirubin in the urine, as prehepatic bilirubin is protein bound, but a small amount of urobilinogen is present.

      Figure 1. The excretion of bilirubinthrough thte liver, showing the enterohepatic circulation.

      DIG020F1

      Obstruction to the biliary system can occur in the bile ducts, or at cellular level by swelling of the hepatic cells due to injury, with resulting obstruction to the fine bile canaliculi. Posthepatic bilirubin then accumulates in the bloodstream to produce jaundice, and overflows into the urine. The secretion of bile pigment into the intestine is hindered, and urobilinogen is no longer excreted in the urine. The stools are therefore pale due to lack of pigment, the urine dark with bile, and the serum conjugated bilirubin raised above its normal value to give rise to obstructive jaundice.

      Damage to the liver cell, which may follow injection of or exposure to toxic agents, also gives rise to an accumulation of posthepatic, conjugated bilirubin (hepatocellular jaundice). This may be sufficiently severe and prolonged to give rise to a transient obstructive picture, with bilirubin but no urobilinogen in the urine. However, in the early stages of hepatocellular damage, without obstruction present, the liver is unable to re-excrete reabsorbed bilirubin, and an excessive amount of urobilinogen is excreted in the urine.

      When blood cells are broken down at an excessive rate, as in the haemolytic anaemias, the liver becomes overloaded and the unconjugated prehepatic bilirubin is raised. This again gives rise to jaundice. However, prehepatic bilirubin cannot be excreted in the urine. Excessive amounts of bilirubin are secreted into the intestine, rendering the faeces dark. More is reabsorbed via the enterohepatic circulation and an increased amount of urobilinogen excreted in the urine (haemolytic jaundice).

      Diagnosis

      Liver function tests are used to confirm suspected liver disease, to estimate progress and to assist in the differential diagnosis of jaundice. A series of tests is usually applied to screen the various functions of the liver, those of established value being:

      1. Examination of the urine for the presence of bilirubin and urobilinogen: The former is indicative of hepatocellular damage or of biliary obstruction. The presence of excessive urobilinogen can precede the onset of jaundice and forms a simple and sensitive test of minimal hepatocellular damage or of the presence of haemolysis.
      2. Estimation of total serum bilirubin: Normal value 5-17 mmol/l.
      3. Estimation of serum enzyme concentration: Hepatocellular damage is accompanied by a raised level of a number of enzymes, in particular of g-glutamyl transpeptidase, alanine amino-transferase (glutamic pyruvic transaminase) and aspartate amino-transferase (glutamic oxalo-acetic transaminase), and by a moderately raised level of alkaline phosphatase. An increasing level of alkaline phosphatase is indicative of an obstructive lesion.
      4. Determination of plasma protein concentration and electrophoretic pattern: Hepatocellular damage is accompanied by a fall in plasma albumin and a differential rise in the globulin fractions, in particular in g-globulin. These changes form the basis for the flocculation tests of liver function.
      5. Bromsulphthalein excretion test: This is a sensitive test of early cellular damage, and is of value in detecting its presence in the absence of jaundice.
      6. Immunological tests: Estimation of the levels of immunoglobulins and detection of autoantibodies is of value in the diagnosis of certain forms of chronic liver disease. The presence of hepatitis B surface antigen is indicative of serum hepatitis and the presence of alpha-fetoprotein suggests a hepatoma.
      7. Haemoglobin estimation, red cell indices and report on blood film.

       

      Other tests used in the diagnosis of liver disease include scanning by means of ultrasound or radio-isotope uptake, needle biopsy for histological examination and peritoneoscopy. Ultrasound examination provides a simple, safe, non-invasive diagnostic technique but which requires skill in application.

      Occupational disorders

      Infections. Schistosomiasis is a widespread and serious parasitic infection which may give rise to chronic hepatic disease. The ova produce inflammation in the portal zones of the liver, followed by fibrosis. The infection is occupational where workers have to be in contact with water infested with the free-swimming cercariae.

      Hydatid disease of the liver is common in sheep-raising communities with poor hygienic standards where people are in close contact with the dog, the definitive host, and sheep, the intermediate host for the parasite, Echinococcus granulosus. When a person becomes the intermediate host, a hydatid cyst may form in the liver giving rise to pain and swelling, which may be followed by infection or rupture of the cyst.

      Weil’s disease may follow contact with water or damp earth contaminated by rats harbouring the causative organism, Leptospira icterohaemorrhagiae. It is an occupational disease of sewer workers, miners, workers in rice-fields, fishmongers and butchers. The development of jaundice some days after the onset of fever forms only one stage of a disease which also involves the kidney.

      A number of viruses give rise to hepatitis, the most common being virus type A (HAV) causing acute infective hepatitis and virus type B (HBV) or serum hepatitis. The former, which is responsible for world-wide epidemics, is spread by the faecal-oral route, is characterized by febrile jaundice with liver cell injury and is usually followed by recovery. Type B hepatitis is a disease with a more serious prognosis. The virus is readily transmitted following skin or venipuncture, or transfusion with infected blood products and has been transmitted by drug addicts using the parenteral route, by sexual, especially homosexual contact or by any close personal contact, and also by blood-sucking arthropods. Epidemics have occurred in dialysis and organ transplant units, laboratories and hospital wards. Patients on haemodialysis and those in oncology units are particularly liable to become chronic carriers and hence provide a reservoir of infection. The diagnosis can be confirmed by the identification of an antigen in the serum originally called Australia antigen but now termed hepatitis B surface antigen HBsAg. Serum containing the antigen is highly infectious. Type B hepatitis is an important occupational hazard for health care personnel, especially for those working in clinical laboratories and on dialysis units. High levels of serum positivity have been found in pathologists and surgeons, but low in doctors without patient contact. There is also a hepatitis virus non-A, non-B, identified as hepatitis virus C (HCV). Other hepatitis virus types are likely to be still unidentified. The delta virus cannot cause hepatitis independently but it acts in conjunction with the hepatitis B virus. Chronic virus hepatitis is an important aetiology of liver cirrhosis and cancer (malignant hepatoma).

      Yellow fever is an acute febrile illness resulting from infection with a Group B arbovirus transmitted by culicine mosquitoes, in particular Aedes aegypti. It is endemic in many parts of West and Central Africa, in tropical South America and some parts of the West Indies. When jaundice is prominent, the clinical picture resembles infective hepatitis. Falciparum malaria and relapsing fever may also give rise to high fever and jaundice and require careful differentiation.

      Toxic conditions. Excessive red blood cell destruction giving rise to haemolytic jaundice may result from exposure to arsine gas, or the ingestion of haemolytic agents such as phenylhydrazine. In industry, arsine may be formed whenever nascent hydrogen is formed in the presence of arsenic, which may be an unsuspected contaminant in many metallurgical processes.

      Many exogenous poisons interfere with liver-cell metabolism by inhibiting enzyme systems, or may damage or even destroy the parenchymal cells, interfering with the excretion of conjugated bilirubin and giving rise to jaundice. The injury caused by carbon tetrachloride may be taken as a model for direct hepatotoxicity. In mild cases of poisoning, dyspeptic symptoms may be present without jaundice, but liver damage is indicated by the presence of excess urobilinogen in the urine, raised serum amino-transferase (transaminase) levels and impaired bromsulphthalein excretion. In more severe cases the clinical features resemble those of acute infective hepatitis. Loss of appetite, nausea, vomiting and abdominal pain are followed by a tender, enlarged liver and jaundice, with pale stools and dark urine. An important biochemical feature is the high level of serum amino-transferase (transaminase) found in these cases. Carbon tetrachloride has been widely used in dry cleaning, as a constituent of fire extinguishers and as an industrial solvent.

      Many other halogenated hydrocarbons have similar hepatotoxic properties. Those of the aliphatic series which damage the liver are methyl chloride, tetrachloroethane, and chloroform. In the aromatic series the nitrobenzenes, dinitrophenol, trinitrotoluene and rarely toluene, the chlorinated naphthalenes and chlorinated diphenyl may be hepatotoxic. These compounds are used variously as solvents, degreasers and refrigerants, and in polishes, dyes and explosives. While exposure may produce parenchymal cell damage with an illness not dissimilar to infectious hepatitis, in some cases (e.g., following exposure to trinitrotoluene or tetrachlorethane) the symptoms may become severe with high fever, rapidly increasing jaundice, mental confusion and coma with a fatal termination from massive necrosis of the liver.

      Yellow phosphorus is a highly poisonous metalloid whose ingestion gives rise to jaundice which may have a fatal termination. Arsenic, antimony and ferrous iron compounds may also give rise to liver damage.

      Exposure to vinyl chloride in the polymerization process for the production of polyvinyl chloride has been associated with the development of hepatic fibrosis of a non-cirrhotic type together with splenomegaly and portal hypertension. Angiosarcoma of the liver, a rare and highly malignant tumour developed in a small number of exposed workers. Exposure to vinyl chloride monomer, in the 40-odd years preceding the recognition of angiosarcoma in 1974, had been high, especially in men engaged in the cleaning of the reaction vessels, in whom most of the cases occurred. During that period the TLV for vinyl chloride was 500 ppm, subsequently reduced to 5 ppm (10 mg/m3). While liver damage was first reported in Russian workers in 1949, attention was not paid to the harmful effects of vinyl chloride exposure until the discovery of Raynaud’s syndrome with sclerodermatous changes and acro-osteolysis in the 1960s.

      Hepatic fibrosis in vinyl chloride workers can be occult, for as parenchymal liver function can be preserved, conventional liver function tests may show no abnormality. Cases have come to light following haematemesis from the associated portal hypertension, the discovery of thrombocytopoenia associated with splenomegaly or the development of angiosarcoma. In surveys of vinyl chloride workers, a full occupational history including information on alcohol and drug consumption should be taken, and the presence of hepatitis B surface antigen and antibody determined. Hepatosplenomegaly may be detected clinically, by radiography or more precisely by grey scale ultrasonography. The fibrosis in these cases is of a periportal type, with a mainly presinusoidal obstruction to portal flow, attributed to an abnormality of the portal vein radicles or the hepatic sinusoids and giving rise to portal hypertension. The favourable progress of workers who have undergone portocaval shunt operations following haematemesis is likely to be attributed to the sparing of the liver parenchymal cells in this condition.

      Fewer than 200 cases of angiosarcoma of the liver which fulfil current diagnostic criteria have been reported. Less than half of these have occurred in vinyl chloride workers, with an average duration of exposure of 18 years, range 4-32 years. In Britain, a register set up in 1974 has collected 34 cases with acceptable diagnostic criteria. Two of these occurred in vinyl chloride workers, with possible exposure in four others, eight were attributable to past exposure to thorotrast and one to arsenical medication. Thorium dioxide, used in the past as a diagnostic aid, is now responsible for new cases of angiosarcoma and hepatoma. Chronic arsenic intoxication, following medication or as an occupational disease among vintners in the Moselle has also been followed by angiosarcoma. Non-cirrhotic perisinusoidal fibrosis has been observed in chronic arsenic intoxication, as in vinyl chloride workers.

      Aflatoxin, derived from a group of moulds, in particular Aspergillus flavus, gives rise to liver cell damage, cirrhosis and liver cancer in experimental animals. The frequent contamination of cereal crops, particularly on storage in warm, humid conditions, with A. flavus, may explain the high incidence of hepatoma in certain parts of the world, especially in tropical Africa. In industrialized countries hepatoma is uncommon, more often developing in cirrhotic livers. In a proportion of cases HBsAg antigen has been present in the serum and some cases have followed treatment with androgens. Hepatic adenoma has been observed in women taking certain oral contraceptive formulations.

      Alcohol and cirrhosis. Chronic parenchymal liver disease may take the form of chronic hepatitis or of cirrhosis. The latter condition is characterized by cellular damage, fibrosis and nodular regeneration. While in many cases the aetiology is unknown, cirrhosis may follow viral hepatitis, or acute massive necrosis of the liver, which itself may result from drug ingestion or industrial chemical exposure. Portal cirrhosis is frequently associated with excessive alcohol consumption in industrialized countries such as France, Britain and the United States, although multiple risk factors may be involved to explain variation in susceptibility. While its mode of action is unknown, liver damage is primarily dependent on the amount and duration of drinking. Workers who have easy access to alcohol are at greatest risk of developing cirrhosis. Among the occupations with the highest mortality from cirrhosis are bartenders and publicans, restaurateurs, seafarers, company directors and medical practitioners.

      Fungi. Mushrooms of the amanita species (e.g., Amanita phalloides) are highly toxic. Ingestion is followed by gastro-intestinal symptoms with watery diarrhoea and after an interval by acute liver failure due to centrizonal necrosis of the parenchyma.

      Drugs. A careful drug history should always be taken before attributing liver damage to an industrial exposure, for a variety of drugs are not only hepatotoxic, but are capable of enzyme induction which may alter the liver’s response to other exogenous agents. Barbiturates are potent inducers of liver microsomal enzymes, as are some food additives and DDT.

      The popular analgesic acetaminophen (paracetamol) gives rise to hepatic necrosis when taken in overdose. Other drugs with a predictable dose-related direct toxic action on the liver cell are hycanthone, cytotoxic agents and tetracyclines (though much less potent). Several antituberculous drugs, in particular isoniazid and para-aminosalicylic acid, certain monoamine oxidase inhibitors and the anaesthetic gas halothane may also be hepatotoxic in some hypersensitive individuals.

      Phenacetin, sulphonamides and quinine are examples of drugs which may give rise to a mild haemolytic jaundice, but again in hypersensitive subjects. Some drugs may give rise to jaundice, not by damaging the liver cell, but by damaging the fine biliary ducts between the cells to give rise to biliary obstruction (cholestatic jaundice). The steroid hormones methyltestosterone and other C-17 alkyl-substituted compounds of testosterone are hepatotoxic in this way. It is important to determine, therefore, whether a female worker is taking an oral contraceptive in the evaluation of a case of jaundice. The epoxy resin hardener 4,4´-diamino-diphenylmethane led to an epidemic of cholestatic jaundice in England following ingestion of contaminated bread.

      Several drugs have given rise to what appears to be a hypersensitive type of intrahepatic cholestasis, as it is not dose related. The phenothiazine group, and in particular chlorpromazine are associated with this reaction.

      Preventive Measures

      Workers who have any disorder of the liver or gall bladder, or a past history of jaundice, should not handle or be exposed to potentially hepatotoxic agents. Similarly, those who are receiving any drug which is potentially injurious to the liver should not be exposed to other hepatic poisons, and those who have received chloroform or trichlorethylene as an anaesthetic should avoid exposure for a subsequent interval. The liver is particularly sensitive to injury during pregnancy, and exposure to potentially hepatotoxic agents should be avoided at this time. Workers who are exposed to potentially hepatotoxic chemicals should avoid alcohol. The general principle to be observed is the avoidance of a second potentially hepatotoxic agent where there has to be exposure to one. A balanced diet with an adequate intake of first class protein and essential food factors affords protection against the high incidence of cirrhosis seen in some tropical countries. Health education should stress the importance of moderation in the consumption of alcohol in protecting the liver from fatty infiltration and cirrhosis. The maintenance of good general hygiene is invaluable in protecting against infections of the liver like hepatitis, hydatid disease and schistosomiasis.

      Control measures for type B hepatitis in hospitals include precautions in the handling of blood samples in the ward; adequate labelling and safe transmission to the laboratory; precautions in the laboratory, with the prohibition of mouth pipetting; the wearing of protective clothing and disposable gloves; prohibition of eating, drinking or smoking in areas where infectious patients or blood samples might be handled; extreme care in the servicing of non-disposable dialysis equipment; surveillance of patients and staff for hepatitis and mandatory screening at intervals for the presence of HBsAg antigen. Vaccination against hepatitis A and B viruses is an efficient method to prevent infection in high risk occupations.

       

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      Tuesday, 15 February 2011 22:40

      Peptic Ulcer

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      Gastric and duodenal ulcers—collectively called “peptic ulcers”—are a sharply circumscribed loss of tissue, involving the mucosa, submucosa and muscular layer, occurring in areas of the stomach or duodenum exposed to acid-pepsin gastric juice. Peptic ulcer is a common cause of recurring or persistent upper abdominal distress, especially in young men. Duodenal ulcer comprises about 80% of all peptic ulcers, and is commoner in men than in women; in gastric ulcer the gender ratio is about one. It is important to distinguish between gastric ulcer and duodenal ulcer because of differences in diagnosis, treatment and prognosis. The causes of peptic ulcer have not been completely determined; many factors are believed to be involved, and in particular nervous tension, the ingestion of certain drugs (such as salicylates and corticoids) and hormonal factors may play roles.

      Persons at Risk

      Although peptic ulcer cannot be regarded as a specific occupational disease, it has a higher-than-average incidence among professional people and those working under stress. Stress, either physical or emotional, is believed to be an important factor in the aetiology of peptic ulcer; prolonged emotional stress in various occupations may increase the secretion of hydrochloric acid and the susceptibility of the gastroduodenal mucosa to injury.

      The results of many investigations of the relationship between peptic ulcer and occupation clearly reveal substantial variations in the incidence of ulcers in different occupations. Numerous studies point to the likelihood of transport workers, such as drivers, motor mechanics, tramcar conductors and railway employees, contracting ulcers. Thus, in one survey covering over 3,000 railway workers, peptic ulcers were found to be more frequent in train crew, signal operators and inspectors than in maintenance and administrative staff; shift work, hazards and responsibility being noted as contributing factors. In another large-scale survey, however, transport workers evidenced “normal” ulcer rates, the incidence being highest in doctors and a group of unskilled workers. Fishers and sea pilots also tend to suffer from peptic ulcer, predominantly of the gastric type. In a study of coal miners, the incidence of peptic ulcers was found to be proportional to the arduousness of the work, being highest in miners employed at the coal face. Reports of cases of peptic ulcer in welders and in workers in a magnesium refining plant suggest that metal fumes are capable of inducing this condition (although here the cause would appear to be not stress, but a toxic mechanism). Elevated incidences have also been found among overseers and business executives, i.e., generally in persons holding responsible posts in industry or trade; it is noteworthy that duodenal ulcers account almost exclusively for the high incidence in these groups, the incidence of gastric ulcer being average.

      On the other hand, low incidences of peptic ulcer have been found among agricultural workers, and apparently prevail among sedentary workers, students and draftsmen.

      Thus, while the evidence regarding the occupational incidence of peptic ulcer appears to be contradictory to a degree, there is agreement at least on one point, namely that the higher the stresses of the occupation, the higher the ulcer rate. This general relationship can also be observed in the developing countries, where, during the process of industrialization and modernization, many workers are coming increasingly under the influence of stress and strain, caused by such factors as congested traffic and difficult commuting conditions, introduction of complex machinery, systems and technologies, heavier workloads and longer working hours, all of which are found to be conducive to the development of peptic ulcer.

      Diagnosis

      The diagnosis of peptic ulcer depends upon obtaining a history of characteristic ulcer distress, with relief of distress on ingestion of food or alkali, or other manifestations such as gastro-intestinal bleeding; the most useful diagnostic technique is a thorough x-ray study of the upper gastro-intestinal tract.

      Attempts to gather data on the prevalence of this condition have been seriously hampered by the fact that peptic ulcer is not a reportable disease, that workers with peptic ulcer frequently put off consulting a physician about their symptoms, and that when they do so, the criteria for diagnosis are not uniform. The detection of peptic ulcer in workers is, therefore, not simple. Some excellent researchers, indeed, have had to rely on attempts to gather data from necropsy records, questionnaires to physicians, and insurance company statistics.

      Preventive Measures

      From the viewpoint of occupational medicine, the prevention of peptic ulcer—seen as a psychosomatic ailment with occupational connotations—must be based primarily on the alleviation, wherever possible, of overstress and nervous tension due to directly or indirectly work-related factors. Within the broad framework of this general principle, there is room for a wide variety of measures, including, for example, action on the collective plane towards a reduction of working hours, the introduction or improvement of facilities for rest and relaxation, improvements in financial conditions and social security, and (hand in hand with local authorities) steps to improve commuting conditions and make suitable housing available within a reasonable distance of workplaces—not to mention direct action to pinpoint and eliminate particular stress-generating situations in the working environment.

      At the personal level, successful prevention depends equally on proper medical guidance and on intelligent cooperation by the worker, who should have an opportunity of seeking advice on work-connected and other personal problems.

      The liability of individuals to contract peptic ulcers is heightened by various occupational factors and personal attributes. If these factors can be recognized and understood, and above all, if the reasons for the apparent correlation between certain occupations and high ulcer rates can be clearly demonstrated, the chances of successful prevention, and treatment of relapses, will be greatly enhanced. A possible Helicobacter infection should also be eradicated. In the meantime, as a general precaution, the implications of a past history of peptic ulcer should be borne in mind by persons conducting pre-employment or periodic examinations, and efforts should be made not to place—or to leave—the workers concerned in jobs or situations where they will be exposed to severe stresses, particularly of a nervous or psychological nature.

       

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      Contents

      Preface
      Part I. The Body
      Part II. Health Care
      Part III. Management & Policy
      Part IV. Tools and Approaches
      Part V. Psychosocial and Organizational Factors
      Part VI. General Hazards
      Part VII. The Environment
      Part VIII. Accidents and Safety Management
      Part IX. Chemicals
      Part X. Industries Based on Biological Resources
      Part XI. Industries Based on Natural Resources
      Part XII. Chemical Industries
      Part XIII. Manufacturing Industries
      Part XIV. Textile and Apparel Industries
      Part XV. Transport Industries
      Part XVI. Construction
      Part XVII. Services and Trade
      Part XVIII. Guides