PROCEDIMIENTOS ESPECIFICOS RELATIVOS AL COVID-19

FIG URE 1.1: R o y a l Naval D o c k y a rd s .

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Consequently in this century, the work of the Royal Dockyards has been mostly in refit and repair rather than shipbuilding, this last activity now being commonly undertaken in civilian contract yards. When civilian/commercial yards undertake refits, the extent of these can differ from the naval version. Naval refits are more frequent and extensive than merchant refits, routinely involving the complete removal and replacement of all insulating material in machinery spaces and both the environmental and structural insulation. As the removal of this material produces more dust than its application these should be considered very important differences.

When combined with the many engineering, construction, and workplace differences between naval and merchant ships, naval shipping containing much more machinery in smaller compartments and having no portholes, it is likely that the overall exposure to asbestos dust was higher in Naval Dockyards than in their commercial counterparts. It should be noted that asbestos has no respect for frontiers or nationalities and that in this respect the shipbuilding risk of asbestos exposure has been worldwide, from the UK to the USA to Japan.

1.2 Asbestos Materials in Shipbuilding.

The asbestos materials used in Royal Navy ships are largely the same as those used in Merchant ships only the amount applied differs. The various types of asbestos fibre used, have included chrysotile (white serpentine asbestos) and the iron silicates, crocidolite (blue asbestos) and amosite. Changes in the amount and type of material used may explain the emergence of asbestos-related diseases in dockyards, in particular asbestosis, lung cancer and mesothelioma.

Until the early 1950s most of the machinery insulation aboard naval ships was in the form of asbestos mattresses, that is, magnesia sections containing an amount of amosite asbestos (commonly 15-30% amosite), and asbestos cloth made entirely of chrysotile asbestos. These materials provided adequate insulation to the operating steam temperatures of below 750°F that existed until the 1950s. A

certain amount of crocidolite asbestos would have been used in asbestos board and in magnesia sections as an available replacement for amosite. Crocidolite was also used in a sprayed asbestos process from the end of the war until the mid 1960s when this process was stopped.

Over the 1950s steam temperatures rose to 850°F and more efficient insulation was required. Magnesia sections were replaced by amosite sections (containing 90-95% amosite). A decreasing stock of amosite lagging was still used through the early 1960s with calcium silicate sections (containing 10-15% amosite) introduced as its replacement in this period. Operating temperatures aboard ship had by this time reached 950°F.

From 1968, only materials containing chrysotile asbestos were used in naval dockyards. Presently shipping worldwide contains little asbestos insulation, man­

made mineral fibres are now used as its substitute. Obviously, the use of large amounts of amosite section and crocidolite in spraying processes up to the mid 1960s implies a corresponding increase in potential asbestos exposure from insulation removal, over the preceding decades.

There have been many uses of asbestos containing materials in ships, apart from heat insulation. Table 1.1 lists some of these other materials. This table has been arranged into those uses producing dust in their handling and those not. The non- dusty uses are those that would not usually produce dust unless the materials were ground, polished or sawn. We see from table 1.1, that although most of the asbestos aboard ship has been used for heat insulation it could also be found in sound and electrical insulating materials.

T A B L E 1.1*: Asbestos materials used in Naval Dockyards. Dockyards: Asbestos spraying, lagging and sound insulation.

Asbestos spraying was used for environmental insulation, the sealing of outer wall and bulkhead surfaces; the spray consisted of a mixture of asbestos fibre and cement applied to a thickness of 2-4 ins. From the mid 1960s, the existing crocidolite material has been extensively removed during refits and replaced by glass fibre and other forms of man-made mineral fibre. The dust concentrations during application and removal have been established as being very high (for removal, many thousands of times higher than the current UK standards).[1,2]* **

Workers employed as asbestos sprayers and painters were responsible for the application and removal of this ‘sprayed asbestos’.

« Adapted from: Harries PG (1967) "Asbestos Hazards in Naval Dockyards"

Ann Occup Hyg 11:135-145.

** The referencing throughout this work is unique to each chapter, each

In the past, laggers were employed to insulate all hot surfaces in machinery spaces aboard ship with preformed ‘asbestos’ sections, covering them with asbestos cloth.

The application and removal of these heat insulating materials would involve both cutting and fixing of the sections and cloth by hand and would produce high localized dust concentrations.

As with lagging, the application and removal of sound insulation involved the cutting and fitting by hand of asbestos boards of various types and thicknesses with again high localized dust concentrations. Sound insulation work would have been undertaken by joiners not laggers.

Other dockyard ‘asbestos trades’ have included shipwrights, sailmakers, boilermakers, masons, mattress makers, labourers and storemen. Of these, shipwrights and boilermakers cut and fitted asbestos boards in either bulkheads or boiler casings. Masons applied asbestos cement over sprayed asbestos.

Sailmakers carried out water pipe and ventilation duct insulation with asbestos cloth. Mattress makers produced mattresses filled with amosite fibre and made from asbestos cloth. Labourers were employed to clear up asbestos debris and storemen issued asbestos materials to all the ‘asbestos workers’.

In all of the above trades and processes there would have been a potential asbestos exposure hazard, but the main hazard would occur during what has been termed the vigorous tearing down of old m a t e r i a l . T h e very nature of Royal Navy ships, with long thin watertight corridors, confined machinery spaces and a maze of pipes and fitments would only augment this problem.

1.4 Project Introduction.

The origin of the asbestos disease problem associated with shipbuilding and repair can, therefore, be traced, in part, to the enormous quantities of asbestos materials used by the industry from the start of World War II. During this war period the concern was to build and repair enough ships to win the war; health problems from materials used in construction took second place.

However, along with increased ship production came the requirement to reduce accidents and health hazards that might slow manufacturing. The known hazards then included silica dust, welding fumes, solvents, lead, mercury and asbestos, with asbestos being considered the least dangerous. The risks associated with lead, silica dust and welding received far more attention in the 1940s, they were better understood by the medical and industrial health community and were believed to be more dangerous and widespread.t3,4,5,61 The stage was set, therefore, for future asbestos-related health problems to surface as the other diseases were controlled.

The work of Sheers and Templeton at Devonport Dockyard reported in 1968, highlighted this problem and acted as the catalyst for many Royal Naval research projects. These projects were all undertaken with the aim of improving the health of dockyard workers and settling the asbestos problem (they are reviewed extensively in chapter 2).

In the Devonport study 1,414 men, representing a 10% random sample of the dockyard workforce was drawn.171 From this sample it was seen that laggers and sprayers with up to 20 years of continuous asbestos exposure had the highest prevalence of asbestos-related disease, asbestosis. Asbestosis was also seen in a variety of intermittently exposed trades. It was also noted that 10 cases of mesothelioma had occurred among the workforce in the 3 years prior to this study.

By 1980 Sheers was reporting on 96 mesothelioma cases in Devonport Dockyard; the incidence o f mesothelioma correlating with time from first exposure and dockyard occupation.181

Also in 1980, Rossiter and Coles reported on the striking finding of an elevated mortality risk of mesothelioma and pulmonary fibrosis among Devonport dockyard workers, but with no obvious accompanying increased risk for lung c a n c e r.^ In this study 6,292 male workers were identified from dockyard records and their mortality experience followed from January 1947 to the end of 1978. Of these workers 1,043 (16.6%) had died; 31 from mesothelioma, 9 from pulmonary fibrosis and 84 from lung cancer. The number of expected deaths, obtained using estimated South West England mortality rates, was: 998, 0.4, 0.03 and 100 respectively, with associated standardised mortality ratios (SMRs) of 104 for all causes, 7700 (P < 0.0001) for mesothelioma, 32000 (P < 0.0001) for pulmonary fibrosis and 84 for lung cancer. These results were striking since much higher lung cancer death rates, along with increased mesothelioma rates, had previously been observed in Belfast shipyards and among American insulation workers; occupational groups which were considered to have similar levels of asbestos dust exposure as dockyard w o rk e rs.0,111 However, these results were not completely unexpected. A proportional mortality study for the period 1958-1967 comparing Devonport dockyard workers with other Plymouth males showed only a slight (but not statistically significant) excess of lung cancer cases.[ 121 Nevertheless, the question remains, why in this Royal Naval Dockyard was the risk of lung cancer, a known asbestos-related disease, not significantly different from that observed in the general population when elevated risks were observed for the other known asbestos-related diseases? Was this an artefact, a result produced simply by statistical chance, or does it imply that the asbestos exposures were somehow not high enough to allow lung cancer to develop, but could generate mesothelioma and asbestosis?

Rossiter and Coles commented in this report that the pattern of dockyard asbestos use was such, reaching its peak between 1950 and 1960, that the effect of mesothelioma

American shipyard workers might die of asbestos-related disease because of exposures in the 1940s.t13^ They suggested that mesothelioma now occurs exclusively in shipyard/dockyard workers and will probably continue to do so into the 1990s.

Over the period 1972-1973 all workers of the four Royal Naval Dockyards Devonport, Chatham, Portsmouth and Rosyth were invited to have a chest x-ray taken and complete a respiratory questionnaire. The results of these with employment history information will be used in this thesis to examine the relationship between dockyard occupation, exposure to asbestos, smoking habits and cause of death. A particular emphasis will be given to lung cancer and mesothelioma in an attempt to answer the questions produced in the work of Rossiter and Coles.

Presented here is an exact 17 year follow-up of the civilian workforce employed in the Royal Naval dockyards during the period 1972-1973.

1.5 Project Aims.

The general aims of this work are twofold:

1. To identify dockyard mortality patterns, across time, and relate these to dockyard occupation, personal medical history, dockyard asbestos exposure, the prevalence of x-ray abnormalities and smoking habits.

2. To assess the relationship between asbestosis, lung cancer and mesothelioma mortality and dockyard employment, and place this relationship into the content of the ‘asbestos’ literature.

The specific question addressed in this thesis, its null hypothesis, arises directly from the work presented in 1980 by Charles Rossiter and Ruth Coles.[9] Simply stated it is: that there is no excess lung cancer risk in Royal Naval dockyard workers.

Subsidiary questions concerning the level of this risk in relation to the mesothelioma risk (i.e. why was the lung cancer risk much lower than the mesothelioma risk) will also be considered.

C hapter 2: LITERATURE REVIEW OF ASBESTOS RELATED DISEASE IN SHIPBUILDING AND REPAIR.

2.1 Introduction.

Asbestos is the collective name given to a group of minerals that are fibrous silicates sharing the common property of high resistance to destruction by physical or chemical means. These minerals include chrysotile and the amphibole group of amosite, crocidolite, anthophyllite, tremolite and actinolite. Chrysotile is the softest type of asbestos and is used in most woven asbestos products (figure 2.1).

Amphiboles are harsher, with more bulk, and are more readily used in asbestos- cement and insulation products (figures 2.2 and 2.3). There are three diseases that may commonly develop because of exposure to these minerals: asbestosis, mesothelioma and bronchial carcinoma.

The risk of mesothelioma appears to be greatest in those exposed to crocidolite, slightly less after exposure to amosite, and much less after exposure to chrysotile.

Brief exposure to amosite and crocidolite seems to carry a high risk of lung cancer, while prolonged exposure to chrysotile and anthophyllite much less of a risk. Asbestosis may develop from exposure to any type of asbestos, however, amosite appears more fibrogenic than chrysotile and tremolite.[1,2,3,4 ]

The study of asbestos-related disease has generated a vast amount of literature.

It would not be practicable to provide here an exhaustive analysis of this literature;

this review will concentrate on setting the scene for the asbestos-related health problems observed in naval dockyards. It will initially consider a historical overview of asbestos-related disease, then more specifically these problems in relation to shipbuilding and repair (with an emphasis on Royal Naval Dockyards studies), and will finally consider the very broad prevailing asbestos health related issues of present day concern. In most of the early reports no differentiation of

asbestos fibre type was made. Where feasible, such differentiation is made in this work.

In 1965 Wagner gave a good description of the etiology of asbestosis.[5] He described how due to its fibrous nature asbestos dust does not follow the same physical laws as other dusts, and that its characteristics allow long fibres to be inhaled and retained in lung tissue. The primary lodging site is in the alveoli arising directly from the respiratory bronchioles. The diameter and length of the fibre are factors resulting in aggregation on this site. He described how the fibrosis later spreads down into the alveolar ducts and atria, resulting in a linkage of the lesions to form a widespread fibrotic network in the lung. Wagner stated that asbestosis is not a sudden explosive diathesis following a dormant period, rather a slow insidious disease. This description can be equally applied to the other asbestos diseases, lung cancer and mesothelioma.

FIGURE 2.1: C h r y s o t il e - w h i t e a s b e s t o s

F IG U R E 2.2: A m o s i t e - v aries f r o m w h ite t o yellowish bro w n in c olour.

2.2 Historical Overview.

The Lady Inspectors of Factories in their 1898 report to the Chief Inspector of Factories and Workshops expressed the first concern about the hazards of asbestos d u s t/61 To quote: "three occupations can easily be demonstrated as a danger to the health of the workers, ascertained through injury to the bronchial tubes and lungs: asbestos sifting and carding, silk opening and counting, and hemp spinning".

The first reported case of disease associated with the inhalation of asbestos dust was that of pulmonary fibrosis in an asbestos textile worker described by Montague Murray to the Departmental Committee on Compensation for Industrial Diseases in 1906/71 This worker had been employed for 10 years in the carding room of a textile factory and was the last survivor of a team of 10, all working in the carding room, each having died at around the age of thirty. This man first came to the attention of Murray in 1899 and died, aged 34, in 1900. No evidence was found at postmortem of pulmonary tuberculosis.

The second case, reported by Cooke in 1924, was of a woman aged 33 who died in 1924 having worked with asbestos for 18 y e a rs /81 Postmortem here revealed extensive fibrosis of the lungs, with pulmonary tuberculosis. Both these cases were important, since their publication directed attention to the possibility that inorganic dusts containing little or no free silica might be productive of extensive pulmonary fibrosis. Until then only the opposite view point had been considered, with silicosis occupying the attention of researchers. Cooke’s case, though slightly weakened by the presence of a tuberculous infection, was of greater importance, however, as it described the discovery of ‘curious’ bodies resembling asbestos fibre in the lung tissue. In 1927 Cooke was to call the disease "pulmonary asb esto s"/91

In 1928 Seiler reported the case of an asbestos worker with pulmonary fibrosis for which no other obvious infectious or occupational cause, other than asbestos dust, was found.1101 This report resulted in the Home Office (Factory Department) undertaking investigations into the effects of asbestos dust on the lungs. This case had the four vital conditions necessary to establish a relationship between the inhalation of asbestos dust and the development of fibrosis, namely:

1. Work involving exposure to asbestos dust.

2. The existence, demonstrable clinically and radiologically, of definite pulmonary fibrosis.

3. The absence of previous or present infections known to cause pulmonary fibrosis (for example, tuberculosis, influenza, or pneumonia).

4. The absence of previous or present work involving exposure to other dusts, which might cause pulmonary fibrosis.

By 1930 Merewether and Price, as a result of these Home Office investigations, had found a correlation between the incidence of the disease and the duration and intensity of dust exposure.(111 From this study, 95 of the 363 asbestos textile workers examined clinically showed definite pulmonary fibrosis and a further 21 precursive signs. Of 133 workers examined radiologically, 52 showed signs of diffuse fibrosis and 22 early signs of fibrosis. The authors did not find any evidence of excess pulmonary tuberculosis among the asbestos workers (including those with asbestosis). A dose-response relationship in the development of asbestosis was suggested: fibrosis taking less than 10 years to develop with high exposure to asbestos, and between 15 to 25 years with low dust exposure.

Merewether and Price, in the same report, also reviewed the dust concentrations in textile factories, making numerous recommendations for dust suppression that formed the foundations o f the Asbestos Industry Regulations of 1931.[ 121 Before these regulations were enforced, asbestosis was also recognised as a compensable disease under the 1930 Workmen’s Compensation Act (Silicosis and Asbestosis).

Again in 1930, Merewether gave a more detailed account of the clinical findings of the Home office investigations carried out over 1928-29.1131 He described impairment of percussion note and reduced chest expansion as important physical signs of asbestosis, together with scattered fine rales (dry crackling sounds) at the bases and axillae. He also mentioned cyanosis, dyspnoea, finger clubbing, cough and sputum. The radiological changes were described as occurring in four stages:

Stage I increased linear striations;

II fairly definite fine dusty stippling;

III coarser mottling with increased linear striations;

IV gross lesions with pleural changes and displacements due to the pull of fibrosing lesions.

To sum up developments, by 1930 it may be said that:

The signs, symptoms, x-ray appearances, and pathological aspects of asbestosis were well recognised.

The disease had been found to be fatal in a number of reported cases.

The disease was capable of progressing after exposure to asbestos dust had ceased.

People still actively employed in asbestos mining, milling and manufacturing showed a high prevalence of asbestosis. Approximately half of those with 10 or more years in the industry were diagnosed as having asbestosis.

In reviewing the pathology and histopathology of asbestosis in 1933 Gloyne described the finding of tough, old, pleural adhesions and reported a ‘ground glass’ effect to the pleura as thickening increased, with the pleura becoming stiff, yellow and horn like.[14) He noted that ‘asbestos’ bodies and fibres were found in the lungs of persons with asbestosis and that fibres were commonly found in the upper respiratory tract of asbestos workers. He also reported having seen a case of ‘squamous carcinoma of the pleura’ with asbestosis.