© All Information Copyright: Branko R Babic Invention and Innovation

Pat GB 2441526

The Use of Cement Fibre Composites in Prolonged Wet Environments
Branko R Babic 53A Middle Way Summertown OXFORD OX2 7LE UK Tel/Fax: +44 (0)1865 310772 E-mail: babic.branko@virgin.net Visit our www: http://homepage.virgin.net/babic.branko/

Abstract

Over the last twenty five years or so, studies have been conducted on a number of issues relating to cement bonded aggregate and fibre additives. Experiments with various additives to mortars made possible the incorporation of cellulose into mortars and concrete mixes and milled straw and aggregate building blocks were manufactured. The StrawCrete blocks were positioned in a shaded section of the site where the material once soaked took time to dry so that the materials remained wet for prolonged periods. The study continued for over ten years during which it become obvious that the superficial cellulose particles become degraded and supported fungal growths. Experiments with other cement bonded fibre composites demonstrated a similar fall out of fibers into the environment due to the degrading cement matrix so that fibre contamination occurs across the product range in wet environments. Where the fibers such as asbestos, known to have health concerns are involved, important legal obligations arise that reflect on the manufacturers responsibilities. Follow up experiments were conducted to reduce the rate of matrix degradation and a series of tests using mortars with increasing porosity and an integral water repellent additive which prevented prolonged wetting was assessed. The addition of the experimental additive did not interfere with the cementing properties of the portland cement used and the crushing strength of the resulting mortar reflected the properties of conventional mortar control. None critical structures were built to test the experimental mortar over a 25 year period. The paper discuses possible ways of extending the useful life span of cement composite materials to at least double the life time of manufactured cement fibre materials.

Fibre composites in prolonged wet environments. Initial efforts at manufacturing StrawCrete building blocks approximately fifteen years ago used Crete Grades 2 of wheat straw particles in a 30% by volume ration. Other cellulose concrete mixtures have been in existence for many decades and in the UK, standard sized building blocks manufactured for the medium density concrete block market, used selected imported wood that had been allowed to stand for several months before use. Cellulose additives to concrete impart a warm, delicate, pleasant color to the finished product as well as reducing the weight of the block. Such additives therefore are used for fine faced exposed block construction that, provides a visually pleasing surface which does not need additional surface treatment. These blocks were used for internal applications only and we now have a manufacturer 4 who can make any number of blocks to order. The 440x215x100mm blocks comply with UK Building Regulations. Manufactured StrawCrete building blocks. Pat. 2340125. Fig 1

In an attempt to provide a cement bonded cellulose composite that could use up the vast amounts of surplice agricultural waste generated by the UK farming industry, experiments were undertaken using wheat straw. Provided that the straw was milled to particles of 5mm to dust in size (Crete Grades), complete homogeneity was achieved between the binder, cellulose and aggregates. Large quantities of straw could be mixed with cement and concrete slurries to provide building blocks that had excellent uses for dry internal applications. The load bearing properties of these blocks met the required 3.5N/mm2 standards and had good dimensional stability. Continuing the experiments, sheet material were manufactured that contained up to 80% volume of straw and 20% by volume of high alumina cement. Materials manufactured with such high quantities of cellulose additive were found not to support fires, so that they could be used as fillers that have good insulation properties manifesting thermal conductivity of about 0.11w/m/0K.

Cement wheat straw composite board Fig2

The fire tolerance of these high cellulose and high alumina composites, stimulated interests so that other fire tolerating composites were examined and in the end a composite of high alumina cements as the binder and fibo (a baked clay manufactured material) was used to manufacture a batch (see Fig 3) of building blocks. Other heat tolerating aggregates can be useful e.g. crushed brick, crushed volcanic ash, basalt, clay, fuel ash and other suitable heat tolerating aggregate, to produce fire retardant building blocks that endure heat stress for prolonged periods. Tests in kilns over a 24 hour period at temperatures in excess of 1000 0C, showed that the given composites provide suitable fire tolerating building materials that do not collapse in prolonged high intensity fires. The same compositions using prepared grades of fines, provide suitable mortars, renders, plaster board etc to provide an entire system that tolerates fires for prolonged periods and respond to heat stress in a similar way to the prepared blocks. The advantage being that the mortar and block are made from the same material and in any given heat stress situation expand and contract at the same rate. High alumina cement/fibo 440x215x100mm 3.5N/mm2 building block at 10000C for 24hours. Pat. No 2377931 Fig 3

Follow up studies exposing StawCrete to the elements continued for the straw based composites and in particular the effect prolonged wetting had on the building blocks. Concrete blocks, 440x215x100mm in size, were manufactured with 30% by volume of wheat straw and 70% sand/cement mixture using accelerated high alumina cement. Samples were then positioned in a shaded site and left exposed. The intention was to examine the effect the wet environment had on the organic and inorganic mixture in this slow drying situation.

Wood Cement composite building block also grew fungal growth. Fungal growths (Peziza Genus) Fig 4

StrawCrete composite building block Fungal growths (Peziza Genus) Fig 5

It was of no surprise to see flora growth on these blocks. The blocks become wet and over the winter months generally remained wet for months on end, with short drying out periods, before the material was again saturated. Several plant forms were observed and of particular interest was the growth of a fungus. This was totally unexpected because although the exposed surface cellulose particulates (being specified at 5mm0mm) would no doubt attract wood feeding entities, it was expected that these would be of a diminutive size. The appearance of a complex large fungus 8 on the shaded sites of the block, induced an anxiety that certain life forms might have enzyme systems that could actually damage the concrete mixture These fungal growths remained well contained and short lived and appeared in all cellulose cement bonded composites. The same fungus was seen growing on the wood block but the surprised was the size of the fungus. On closer examination it appeared that the cement, wood, aggregate block used as a control, contained large particles of wood that were 30mm long and up to 5mm thick. The fungus died having consumed the nutrients on which it was growing. It appeared clear, that the growth of fungus in cement bonded cellulose composites was dependant on the availability of exposed cellulose, in damp conditions. In all cases, all fungal growth died, as the blocks dried out. Control blocks kept in the dry environment, did not develop or sustain any kind of visible organic life forms during the same time span, nor, did they lose the golden color of wheat straw.

Surface straw particles fall out of the StrawCrete material after prolonged exposure to British weather. Fig 6

The availability of water was concluded to be a prime factor in sustaining life forms on cement bonded cellulose composites. The end result of StrawCrete Blocks being kept in the wet environment for prolonged periods was the loss of all of the surface cellulose particles exposed to the weathering process and a 440 x 215 x 100mm block kept in the wet were seen to show an irregular surface reflecting the shape and form of the surface cellulose particles used in the original mix, see Fig 6. The weathering process is seen right across the cement bonded composite materials industry. As an example, the asbestos fiber cement bonded manufacturing sector has major problems relating to this abrasive process. Work done on wet roofing tiles demonstrates that weathering removes layers of the composites and this occurs extensively. The wet surface containing the fiber is abraded away to release fibers contained therein. Fig 7 shows a ten year old roofing tile on the right of the picture, next to a new tile manufactured by the same manufacturer, demonstrating the extent of the abrasive process which releases fine asbestos fibers into the environment 5,7,9. Fig 8 demonstrates an old corrugated roofing asbestos cement sheet and clearly shows the asbestos fibers sticking out of the cement matrix. As the weathering process continues, the asbestos fibers loosen from the cementing matrix, to move about in the wind and snap off, to be released into the environment The process of fiber release continues for the life of the asbestos cement product and accelerates

with age, so that the older the product the greater the release of asbestos.

Photograph of a new acrylic coated asbestos cement roofing tile on the left and a ten year old similar tile demonstrating fall out of asbestos from the cementing matrix on the right. Fig 7

The above mechanism extends to other asbestos fibre products and is clearly seen in cladding sheets, guttering, cowling and the many other cement bonded materials manufactured.

Asbestos cement corrugated sheeting demonstrating fall out of asbestos fiber. Fig 8

Asbestos cement cladding demonstrating asbestos fibre fallout in old materials Fig 9 The process of fiber release continues for the life of the asbestos cement product and accelerates with age, so that the older the product the greater the release of asbestos. Vast quantities of asbestos are released into the environment by this process and given that millions of acres of asbestos roofing exist in the UK, means that the population is subject to background asbestos fibre fallout. In all cases, fibers are released from cement fibre composites the dropout of fibre being related to the wetting and mechanical abrasive process imposed on the composites. In dry conditions, cement fibre composites retain their composition and fibers such as straw kept in dry conditions are documented to retain their structure for thousands of years. It is the wetting of such materials that causes the problems.

Containing fibre release . Given that wetting of materials is the cause of degradation we refer to earlier experiments with water repellant additives to mortars and the like. In the late 70s and early 80s we were involved in a project to find a way to provide a continuity of adherence across the Damp Proof Membranes (DPC), particularly in tall garden walls and stand alone structures. In the UK there are regular accidents with children in particular, climbing tall stand alone walls, resulting in the structures peeling apart at the physical DPC, to collapse and cause injury. Our brief was to find a way to continue bonding across the DPC layer to prevent this type of collapse and a series of experiments were undertaken to establish a suitable integral mortar based dpc that was the starting point for the work done with the enclosed mortars, see Graphs 1-5. After much searching one of the few water soluble chemical DPC preparations, the potassium methysiliconate 3, that Imperial Chemical Industries were manufacturing at the time, was selected and on mixing the preparation with the mortar, found that the prepared mortar behaved like conventional mortar. All initial results were promising and when the crushing strength data came back and showed no difference between the aqueous siliconate and conventional mortar mixes, the concept was subjected to further testing.

Aqueous Siliconate mortar cubes being crush tested 1982. Fig 10

Testing of an integral water repellant additive. The testing consisted of immersing brick constructions in water trays for 120 days over which time water transmission via various parameters was measured. The assembly is specified in Graph 1 and consists of test assemblies with two Hammill Multi Red facing bricks, known for their manufactured consistency and picked for the experiments because they are known to transmit rising damp rapidly. The made brick assemblies were left for 48 hours and then placed in trays which contained about 25mm of water and were left in the trays for 120 days, during which time the assemblies were periodically withdrawn, drained for about 5 minutes so that no free water dripped from the construction and weighed. The variation in water absorption was calculated and plotted. Graph 1 represents the water uptake of the reference assemblies: (a) when two dry bricks are separated by an absorbent paper tissue placed between the bricks, water is absorbed into the bottom brick across the paper tissue, to saturate the top brick. After about 20 days the water loss by evaporation from the assembly is equal to the water absorption from the tray and there was no change in the weigh of the assembly thereafter. (b) when two dry bricks are separated by a physical damp proof course (DPC) such as a piece of polythene, the immersed assembly quickly gains weight as the bottom brick becomes saturated but because no water can pass through the DPC thereafter, there is no further change in the weight of the assembly and the graph is again a straight line.

(c) when two bricks separated by a paper tissue were pre-saturated and then places in the test trays, no substantial change was observed over the test period. The unexpected apparent drying out (N.B.), was discovered to be an unplanned draught which was isolated and blocked off from the test tray wherein the measurements settled down to the expected, i.e. no change in the weight of the assembly, demonstrating again that the water evaporating in the brick assembly was equal to the water absorption and the bricks remind saturated. (d) when two saturated bricks were separated by a physical DPC the graph shows the top brick drying out demonstrating a loss in weight which settled to a steady state over the experimental period. Graph 2 represents the water uptake of the 1: 3 portland cement and sand mortar: (a) The Babic's mortar dry assembly demonstrated a similar uptake but at a slightly higher level. The flat part of the graph demonstrates that the there was no transfer of water across the chemical DPC and the steady state graph was lower than the polythene DPC, again due probably to the lower absorbancy of the bottom brick. (b) when the dry assembly with the conventional mortar layer between the two bricks was placed in the tray, there was an uptake of water which is reduced gradually so that by about the 28th day virtually no water was being transmitted through the mortar layer to the upper brick. (c) saturating the conventional mortar assembly initially retained water but the top brick dried out after about 28 days providing similar results to conventional DPC. (d) saturating the assembly with the Babic's mortar and placing into the water tray, was seen to be effective rapidly, achieving the drying out of the top brick more quickly than conventional mortar, indicating a lower transfer of water across the treated mortar layer. This assembly gave results very similar to the conventional polythene DPC Graph 3 represents test using 1: 6 portland cement and sand mortar: (a) the dry Babic's mortar assembly, produced an uptake of water to give substantially the same trace as a conventional DPC but was slightly wetter than conventional DPC. (b) the dry control, conventional mortar using a dry assembly of bricks, indicates an uptake of water which dried slightly during the first 28 days, to give a constant trace to the end of the experiment. (c) the control assembly in a saturated condition demonstrated a gradual drying out after about 25 days to provide a steady state towards the end of the experimental period. (d) the experimental chemical DPC in a saturated state demonstrated similar behavior to the conventional DPC but was about 4% wetter and attained a similar final state to the saturated control. Graph 4 represents test using 1: 9 portland cement and sand mortar mix: In this, an experimental mortar mix, we wanted to test the concept in an extreme situation. Certainly such mortars have no value in standard construction practice and the use of such mortar for structural purposes is inconceivable but it nevertheless remained a useful indicator of the effectiveness of the siliconate molecule in this extremely porous and absorbent mortar:

(a) initially the dry control demonstrated a large pick up of water which resulted in the top brick drying out by about the 20th day and thereafter leveled out at about 30 days, meaning that the top brick attained an equilibrium of water absorption and evaporation. The assembly was drawing water from the tray to remain wet for the duration of the experiment. (b) the saturated control showed a slight additional pickup of water transmitted from the tray to remain wet for the duration of the experiment again showing that the conventional 1:9 mortar mix transmitted water across the mortar layer. (c) adding the aqueous siliconate to the 1: 9 cement sand mortar mix in the dry assembly resulted in the rapid uptake of water in the lower brick to allow only a small transfer across the chemical DPC into the top brick, which then dried out to achieve a steady state that resulted in the assembly being bout 1% wetter than the conventional DPC assembly. (d) The Babic's mortar saturated assembly allowed the top brick in the water tray to dry out during the first 20 days to give a stable graph indicating that the mortar layer was acting as a DPC even though the trace did not fall to a value of 0 and was therefore not as effective as the polythene DPC.

Conclusions from water bath tests. Most usefully these experiments indicate that the 1:9 mortar mix with the chemical additive prevent the upward passage of water across the modified mortar layer. The conventional 1:9 mortar mix does not prevent the upward passage of water across the mortar layer and therefore the brick assembly remained wet. In applications using the chemical additive where saturated assemblies were placed in the water trays, it was found that the assemblies dried out at about the same rate as the assemblies with physical DPC, to prevent the upward passage of water across the modified mortar layer, during the experimental time scale. In applications using dry brick assemblies that were then placed into the water trays it was found that the conventional and the experimental mortars prevented the passage of water across the mortar layer during the experimental time scale.

Clearly conventional mortars fail during prolonged use so that long term tests were required to asses the long term effectiveness of conventional mortar mixtures as compared with identical mortar mixes to which was added the aqueous siliconate chemical DPC. Test examining the effectiveness of aqueous siliconate in old failing mortars will yield useful data. Our findings were submitted to the UK Agrement Board for independent testing and a report findings in some detail. Long Term Follow Up With that in mind we built walls using the Babic's mortar as a DPC and are delighted to be in a position to present a follow up that has lasted almost twenty five years. Example of conventional mortar "A" and chemical DPC mortar layer "B" after almost 25 years of exposure to British weather. N.B. Spalling brick "C" August 2006. Fig 11
1

presents their

Item "B" represents the water soluble aqueous siliconate additive (the Rhone-Poulenc subsequently took over the manufacture of Rhdosil Siliconate R 333 the aqueous solution of potassium methysiliconate 3, 5% w/w preparation) to the mortar layer. The mix consisted of a 1:3 portland cement builders sand mixture which was separated into the conventional and experimental mortar piles, the same procedure that was used to prepare the cubes for the crushing tests, see Fig 10. To the conventional mortar "A" was added water and the mortar was mixed until the experienced bricklayer decided that the consistency was suitable for the given job. To the second portion of the above mixture, was added the R333 solution and mixed until the same workable consistency was achieved. The wall was built using the R333 mixture at the DPC level only and above that, was used the conventional mortar. To this day the surface of the experimental mortar layer remains in an exceptionally good condition and in fact does not show any deterioration in the cementing matrix. Remarkably, the layer still shows the original brick layers finishing tooling marks as he closed off the surface. The regions of the layer that are bonded to the spalled brick "C" indicate that where the spalling was sizable the bond between the mortar and the brick was so strong that the chemically modified mortar fractured, allowing the spalled section to fall away. That indicates that the treated mortar retains its structural strength and in fact retains sharp edges and continues to adhere to the brick either side of the mortar and spalled brick sections. At "A" the conventional mortar layer is seen to have responded to the weathering process and exhibits the typical long term deterioration seen in such materials. The above astonishing finding indicates that cement bonded composites retain their structure without degradation for the nearly 25 year duration of this experimental follow up. There is every indication that no substantial change will occur in the immediate future so that if the water repellant characteristics of this mixture continue, then there will be no change in the nature of the treated mortar until the chemical structure of the formed aqueous siliconate molecular lattice established during the curing process, starts to break down and the efficacy of the water repellence starts to abate. Normal degradation over the following 25 years or so is expected to occur and follow a similar degradation pattern to the conventional mortar layer as

demonstrated at Item "A". That water is penetrating the wall below the DPC mortar layer is demonstrated by the fact that the bricks below the DPC are spalling, Item "C", so that the weathering process is clearly having a severe effect on the wet structure below but not above the DPC mortar layer. The indication is that cement bonded composites can in practice have their life time performance doubled by addition of water repellant admixtures during the production stage. The implications of these finding are enormous, right across the cement bonded fibre composite technology and a patent application has been registered. It seems that adding water repellant add-mixtures to the mix during the production process, provides a means of substantially improving material performance over time and in all weathering conditions and will in any case gives substantial advantages over current coating technology in retaining added fibers. In retrospect, it becomes obvious as to what industry needs to do to contain fibre loss in cement fibe composites and with this in mind an old cement fibre roofing tile was examined and gave a rough sweep with a wire brush. Not surprisingly, the exposed surface resulted in deep gauge marks, asbestos flying out in a dusty plume whilst the covered area of the same A single old asbestos cement roofing tile. On the left the area of tile exposed to the elements and on the right the area of tile covered by the overlapping tiles.

Fig 12

tile, barley showed scratches. This action demonstrated that the area of roofing tile that was covered by the overlapping tiles above it prevented wetting, so that the normal degradative weathering mechanisms could not take effect. This excellent example of experimental controls, wherein the single tile, made by the same methodology, of the same batch composition and at the same time, acted as the best form of control to the wet and dry condition that the material was subjected to. This tile clearly demonstrated the effect of wetting one half of the product and exposing it to the weathering process, whilst keeping the other half of the tile dry. Embarrassingly obvious but the evidence was clear for all time and indeed demonstrates the outcome of reducing wetting, on cement fibre composites.

Water repellent additives There are very many water repellent additives that the construction industry uses but for the sake of simplicity, we categorize the available preparations into basic groups. Water repellents act by a variety of means but all are directed at reducing the water ingress into the substance of the material. When mixed with cement fibre composites, mortars, concretes and the like, the admix is spread throughout the matrix of the material to achieve its effect at each site the additive is precipitated. Once cured the water repellent additives are effective for the duration of the given additive's lifespan. The many currently available water repellent additives supplied by the UK admix manufacturers provided for integral cement composites, can be classified into basic groups: 1. Chemical formulations that form electrostatic mesh constructs, which repel water to reduce the diffusion coefficients.

2. Compositions that block the pores within the formed material to configure physical barriers. Available integral water proofing formulations: 1. 2. 3. 4. 5. 6. 7. 8. 9. Silicone resins Fluoropolymers Lignosulphates and sterates Soaps and fatty acid composites Acrylic preparations Colloid silicates Styrene Butadiene Rubbers Oil based emulsions Inorganic additives

10. Other More specifically, examples of additives used: 1. Silicon resin formulations, modifications and innovations such as aqueous siliconates, silanes, siloxanes emulsions as supplied by eg. WAKER Gmbh 2. Fluoropolymers as provided by the DuPONT Group. 3. Lignosulphates and sterates as provided by DEGUSSA Gmbh. 4. Soaps and fatty acid composites such as Brunolene SP, as supplied by the WYKAMOL Group. 5. Acrylic polymers such as mixtures of vinyl chloride, ethylene, vinyl esters, and proactive colloids and copolymers, supplied by WYKAMOL Group. 6. Colloids of for example the SEKA 1 range, provided by BSF Construction Chemicals, UK. 7. 8. 9. The many SBR formulations as provided by for example, FOSROC UK. Linseed oil composites. Inorganic solid additives that increase the density by blocking up the pores of the material to reduce porosity and permeability.

10. Many other formulations mixtures and preparations are sold by the damp proof industry. Research continues and bitumen based water soluble emulsions are being experimented with. As always with admixtures, the user must assess the available additives to confirm that the proposed application is suitable for the purpose for which it is intended. The additive must be examined for compatibility of all constituents within the proposed composite. We greatly look forward to long term results with water repellent additives admixed with high alumina cement. Samples of high alumina cement and more specifically Lafarge Cement Fondu, demonstrate that provided the finished product is not exposed to water, that the product retains its properties and that there is no degradation of the cement matrix during the experimental time scale. It seems to us that adding selected integral water repellents during production of high alumina composites materials, will reduce water ingress to extend the life of such composites. The crystal structure of high alumina cement remains stable provided water is prevented from contaminating the finished product. The range of uses for such cements could be extended provided water ingress is prevented.

Discussion
Consequences of fibre release into the environment. Evidence that asbestos causes disease is extensive and this fibre above all others has been extensively studied not only because asbestos providing companies are paying out vast sums of money in compensation to damaged individuals. The main problems relate to asbestoses, cancer of the lung and mesothelioma. All types of asbestos are carcinogenic 6. Asbestoses is a condition that is seen in people who are exposed to heavy contamination of asbestos fibers i.e. 25 to30 fibers/ml over many years 16 such as miners, asbestos manufacturing, factory work processing asbestos fibers etc and is a form of silicosis . In this condition the lungs become so full of inorganic fibre that the pliability of lung tissues is lost and there is general debilitation because air transfer is incapacitated 37 across scarred lung tissues. Cancer of the lung is the disease that develops because asbestos dust changes the genetic structure of the cells 19 24 in the lungs and mesothelioma is the cancer of the mesothelial linings of for example the chest cavities whose DNA is changed to again result in uncontrolled cell replication that kills those effected. This condition is the only one that is said to be substantially caused by asbestos i.e. no other factors are currently associated with the development of mesothelioma although clearly contributory factors will no doubt be identified in time. Mesothelial tissue, is present elsewhere in the body so that mesothelial lining cancers are not limited to the linings of the pleura. It is stated that the number of lung cancer deaths due to asbestos inhalation is at least equal to the number of cases of mesothelioma 21 and both types of disease require about twenty years or so of contamination, although much longer periods of time are reported. The fact that a very long time is required for cells to undergo critical damage indicates that the causation is not likely to be due to bio solubility such as e.g. Mg++ leaching out of asbestos fibers because such soluble factors would quickly wash out of the cell environment over a given time span. Rather, bio persistence is claimed to be of importance in asbestos pathogenicity 11 i.e. the prolonged effects trapped fibers exercise on the local populations of cells. Isometric dust is said not to cause cancer whereas, fibrous dust of a given size causes scarring and disease 10. Fibers of 5 m 23 are considered particularly dangerous and those that are less than 1 m are very respirable and are to be particularly avoided since when inhaled, they are for the most part, likely to end up in the deepest areas of the lungs and remain trapped there. Excluding respirable dust therefore became an issue. The entire industrial standard relating to respirator standards was challenged in the 1980s and revolved

around the then used British Standard for filters i.e. BS 4400 which certificated filters to 0.5 microns. Smaller particles could pass through the then recognized filtering technology and that applied to all filter designs 4. Given that fibers end up trapped in lung tissues it becomes clear that such prolonged irritation produces localized inflammation and induces fluid flux. These factors increases permeability and thus make cells more susceptible to damage by associated factors leading to disease. Cigarette smoke constituents for example, increase the likelihood of damaged cells becoming diseased. Of the three diseases quoted the most puzzling is the development of mesothelioma which is seen not only in individuals who are heavily contaminated but is also manifest in individuals who have demonstrably very low levels of exposure, even cases which can barely remember ever being in contact with asbestos. This condition is particularly interesting since the presence of very small levels of contamination, hugely below the Health and Safety Executive (HSE) recommended safety levels of exposure to asbestos, also promote development of terminal illness. Over many years of studying the processes by which very low levels of contamination with asbestos results in terminal illness, we involved analyses of the standards by which the HSE guides users and handlers of asbestos. It appears that the entire HSE recommendations relating to asbestos exposure are based on mistaken parameters and indeed it seems that there are no safe levels of exposure to asbestos and all that the HSE the world over is doing is practicing precautionary principals that are designed to manage the risk. The UK HSE advice on asbestos exposure is based on the Code of Federal Regulations for Construction Asbestos Standard 29 CFR 1926.1101 and European Union Directives together with various scientific projections, all of which are working to reduce exposure to asbestos fibre. Surprisingly, the latest recommendations from the UK HSE of exposure levels to asbestos fibers of 0.1fibres per ml, are still calculated to result in substantial death numbers from mesothelioma 18. The regulatory bodies the world over are therefore recommending exposure levels to asbestos fibers in the full knowledge that disease will result from such exposure but explain the recommendations in terms of practicability rather than safety, i.e. yes it will kill people but industry has to keep going. What an absurd abrogation of duty to the population given that alternative fibers are available. In an effort to explain how it comes about that a teacher 28 who work in classrooms where asbestos display boards were used to display pupils work ended up developing mesothelioma, necessitated a new approach to the causative factor analyses and required the disregard of all previous evidence of causation in an attempt to formulate a new model of how fibers interact with cell populations. Many models were considered and the probability model consumed a very great deal of time and effort. Basically, all effort to explain causation revolves about a definitive population of cells. A model wherein a single population of cells was isolated and exposed to disease causing factors was considered and it become very complicated to contain the reasoning in living environments, which at this basic level where a population of cells was supplied by an arterial capillary that was then drained via the continuity of the same capillary network at the venous end. The volume of cells was also drained of excess liquid by the lymphatic capillary which as an independent system, drained the liquid content of the interstitial space. A model was considered wherein the population of cells was subjected to say, asbestos fibers and given that the above vessel distribution was entirely responsible for the delivery of nutrients, removal of waste products and removal of excess fluids it became obvious that the cell population encompassed by these vessels was exposed to directional flow of fluids, from the high pressure arterial capillary down a pressure gradient to the venous and lymphatic capillaries. There is therefore a pressure gradient of fluid moving directionally, to provide directional current of liquid washing over all cells in the volume encompassed by the arrangement of vessels. This arrangement forms the capillary bed. In this model, the presence of a contaminating fibre would pollute all cells downstream of the fibre. All cells in the fouled current therefore would be exposed to whatever factors were causing damage leading to disease.

The capillary bed hypotheses as we called it, became ever more complicated as complex probability factors were considered and when the fact that all capillary beds are open arrangement of cell populations where fluids migrate down pressure gradients across, interlinked populations of cells that had no physical boundary but was defined by fluid flow down paths of least resistance, the model became so complex that too many possibilities existed for a resolution. It was during one of these attempts to explain the interlinking factors in the model that a friend started writing down mathematical formulas to describe the probability of multiple influence due to adjoining cell volumes. The effort to understand the problem in terms of the probability of damaging fibers ending up in cell populations that were prone to succumb to disease, become so complex that we expired in confusion and abandoned the effort to explain causation in terms of probability. The mathematician had encompassed overlapping environments wherein the fluid volumes could migrate down an unspecified number of gradients to empty into any given capillary structure and the complexity she described made it clear that the answer to the problem was to be found elsewhere. Although papers exist that have correlated quantities of asbestos exposure to the development of disease 25 we abandoned the probability effort to concentrate on a model specifying genetic factors which predispose individuals to disease when exposed to certain materials. It seems to us that the models considering genetics is of importance where people develop disease and indeed there are many cases where individuals are heavily contaminated with asbestos fibers but never die from asbestos related illness and yet other individuals succumb to disease in minimal exposure levels. The work done on the capillary bed hypothesis demonstrated the value of examining the problem on a microanatomical level. It was on this model of reasoning that the absurdity of existing safety exposure levels become obvious. The HSE stipulates in the latest Code of Practice 15 that 0.1 asbestos fibers per cubic centimetre of inhaled air is a safe working limit for an 8 hour working day. At 0.1 fibres/cm3 i.e. 100 asbestos fibers per litre of air, are considered as tolerable working level of exposure. Given that the average resting ventilation rate is about 6-8 litres per minute or say 360 litres per hour then over an 8 hour working day, about 300,000 fibers are inhaled into the lungs every working day. There is no information on how many fibers are breathed in and how many fibers are breathed out in any given tidal volume but it can be assumed that a large number of inhaled fibers become entrapped by the mucous membranes. This has to be so because there is a build up of asbestos fibers in the lungs of people exposed to asbestos particles. A great deal of professional research work goes on relating to analyses of factors involved in fibre inhalation and a useful model of calculating risk factors has been published to allow specifies of safety levels to estimate numbers of incidence given certain parameters 17. A useful calculating facility is provided on the World Wide Web 18 by researchers, that allows participants to calculate likely death rates from given exposure to asbestos As the capillary bed hypotheses is further consolidated it needs to be pointed out that total allowed fibre numbers that are inhaled, are separated into two totally separate and independent volumes the right and the left lung. Each lung has independent blood and lymph distributions. On closer examination, each lung is further subdivided into segments which are similarly independently supplied with branched blood and lymph vessels and that this independent subdivision continues segmentation to the finest lung aggregations terminating in capillary beds. Each segment and sub-segment has an independent blood supply, blood drainage and lymphatic drainage serving finally the capillary beds. The HSE deems say, 250,000 asbestos fibers during an 8 hour day, to be a workable level of exposure but given that the disease starts somewhere in the lungs on a cellular level it immediately becomes obvious that if the mesothelioma starts in say the right lining of lung, that only half the allowed exposure of the contaminant entered the right lung and that is where the disease is initiated and therefore only half of the permitted exposure level of asbestos fibers ever played a part in disease development. The existing safety level is already twice that needed for disease to establish. From this example alone, specified safety levels are twice the necessary level of exposure that is needed to initiate disease!

Plastic cast of airways. Half inhaled air goes into the right lung and the half into the left

Fig 13 But, staying with the example, the focus of disease is at one given point in the lung tissue and therefore identifying the spot where it started, we can say that only the asbestos fibers that ended up in that segment had an effect on the development of that particular incident. The right lung has three lobes which are subdivided into ten independent segments so that the established safety levels need to be divided by ten, meaning that nine tenths of the fibers entering the right lung play no part in the development of that disease event. The safe exposures are thus further reduced and in real terms, each segment is further divided into a multitude of sub-segments and thereafter, into a vast number of capillary beds per segment on each side on the lung. Since mesothelioma starts at some cellular level, in some capillary bed, it is clear that at no point do more that a few asbestos fibers that end up in that given capillary bed, ever play a part in causation of disease. The fibers that are lodged in the adjoining segment that is physically separated from the diseased section cannot influence developments locally. Certainly, what happens in one segment has little to do with what happens in an adjoining segments and indeed what happens in the right lung has no bearing on what happens in the left. World vide, the HSE safe levels of exposure to asbestos dust, are a nonsense. Theoretically, only a small level of exposure to asbestos dust can cause mesothelioma meaning that there are no safe levels of exposure to asbestos. The capillary bed hypotheses makes understandable the means by which low level exposure to asbestos fibers causes disease and we are working on the hypothesis that what allows one individual to continue in health with vast levels of asbestos dust contamination whilst a few fibers kill another, are genetically driven mechanisms. Given that individual tolerance to given irritants exist, it becomes a matter of urgency to require the scientific community to provide reliable tests which can identify individuals susceptible to given irritants. Such individuals should be refused employment in situations where their genetic makeup predisposes them to development of disease by factors present in the given working environment. An extraordinary situation exists wherein industry acknowledges that asbestos contamination is harmful to people coming into contact with this fibre and are paying enormous sums of money in compensation and yet, the asbestos industry continues to invest vast sums of money corrupting professional people, lobby groups, the media etc to maintain production, distribution and use of asbestos containing materials 8 . Evidence is available around the world that very eminent scientists are misrepresenting statistical and scientific analyses to provide conclusions that asbestos is not responsible for the epidemic proportions of disease seen in countries around the world. In the UK, about 50 people die from occupational cancers every day and the

figure is still rising. Statement that the rise in disease is due to “lifestyle factors” 34 is banded about and such authoritative papers are used by the standards setting agencies to stipulate working levels of exposure to any given substance. Thankfully, the unions responsible for workers welfare are challenging such findings and indeed are publicly stating that the large financial inducements awarded to authors are corrupting individuals and that their work is substantially flawed, seem to have little effect on the industries push to increase sales of asbestos 27. Figures available demonstrate that use of asbestos fibre in for instance the USA and elsewhere is increasing in spite of the fact that asbestos is banned including the UK and many other countries. The continued trading in asbestos generates large profits for participating companies and considerable investment is being pored into expanding asbestos mining in India, Canada and elsewhere. Considerable pressures are being applied on Brazil, Indonesia, Zimbabwe, India and elsewhere, in a successful attempt to increase sales of asbestos. In response to the ongoing expansion of asbestos use the French government has called on the International Labour Organization to ban asbestos all over the world. It is understood that Brazil banned the use of asbestos recently and important recommendations are anticipated in the UK, by the end of 2006. Difficult to accept the stance of Canadian asbestos mining interests 9 and others, that continue to invest so much money in asbestos production when ample evidence is available as to the end effects of asbestos mining in countries such as South Africa 37 and the long term devastation resulting. The facilitators of asbestos materials are continuing to push this profitable material at the expense of the health of individuals and damage to the environment. They are confident that their lobby efforts, lawyers, paid scientists, advisory boards, front groups, industrial organizations, think tanks, the media and others, will succeed in confusing the issue so that they can continue to trade in this fibre. Indeed, occupational health doctors complain of being pressurized by asbestos industry to diagnose patients with asbestos as having tuberculosis or bronchitis 26. Figures from the US Commerce Department show that asbestos interests in the US have increased asbestos importation by over 300% during the last decade. This rise in business has resulted in such companies increasing their staff and profits. Some of these companies report to their share holders that the asbestos problem is not effecting their profit margins, even though they have gone into protective bankruptcy called “Chapter11”. Bankruptcy in these cases is a means of avoiding most of the court room penalties for asbestos related damages, protecting the profits and ensuring a healthy return on the investors shares. A scandalous situation exists where manufacturers profit from the sale of carcinogens 17 knowing that they can walk away from responsibility when the costs of paying for damaged caused becomes burdensome. Much of this problem rests on the findings of expert evidence which confuses scientific findings by stating ambiguous conclusions that muddy the waters by excluding many susceptible groups 12 and claiming other possible causative factors such as smoking and lifestyle. In an academic culture where the ethos “publish or perish” prevails, conducting industry friendly research anchors careers and guarantees a steady income for research that keeps many departments afloat. Powerful interests support research findings which suggest that their products are innocuous 9 and therefore safe to use. Implicated authors ignore the evidence that before asbestos use was widespread the level of cancers from lifestyle” factors was far smaller. Figures for the UK state that in the 1901 only 5% of deaths was from cancer and it was not until the 1940 that the disease was formerly classified by the International Classification of Disease Code. Cancer levels continue to increase so that by 1950s 15% of deaths were from cancer and figures for 2000 show that 25% of all deaths in England and Wales were from cancers 36. Today, epidemic proportions of cancer means that 1 in 4 people will develop cancers and that 1800 males and about 1000 female die of asbestos related disease in 2004. The mesothelioma epidemic is claiming large numbers per year and the death rate from this disease is expected to peak some time in the next decade 35. The Law all over the world acknowledges the damaging effects of asbestos and awards hefty compensation to injured individuals but still clever lawyers, bankruptcy practitioners et al are having a feeding frenzy during which they earn tens of millions exercising legal procedures that prevent legitimate claims against asbestos facilitators. Monies that should be available for compensation are paid over to practitioners acting

on behalf of the very people that have consciously destroyed lives and individuals often die before they see any compensation to their families. For individuals to be knowingly exposed to health damaging industrial contaminants, is a matter of great concern because these are not “lifestyle issues” that are within an individuals choice. The working man has no option but to work. He has no control over the use of industrial materials and manufacturing procedures that require him to be exposed to carcinogens during a working day nor is the control of such materials a matter of informed lifestyle choice. It is surprising to find that directors of companies continue practices knowing that the long term result will be their companies having to pay substantial sums in compensation, or go into a planned bankruptcy because large compensation claimed by damaged workers, become unmanageable. There is a case for identifying individuals who formulate policy for fast money making in the knowledge that in the long term the practice could destroy the companies that employ them. Who are the individuals in these companies that enforce the continuance of known injurious practices. It is no good taking large corporations to Law because corporations are in themselves inert entities that are responsive to the driving forces of the executives who formulated policy. If their ethos is to make as much money as they can during their tenure, fully anticipating grinding the corporation into Chapter 11 as a means of escaping culpability for decisions they made, then clearly the unions must find a way to prevent such thinking being exercised, at the expense of those the corporations serve. The immorality of continuing mining, manufacture, sale and use of known health damaging materials in underdeveloped societies where Laws governing health and safety issues at work are poorly enforced, as a means of profiteering, does not bear reflection and not only because it belittles the human spirit. It is difficult to understand why such practices are not illegal? The unions must continue their work on behalf of the working men who have no option but to take a job in order to provide. Much remains to be done and corporations in the 21st century cannot maim, mutilate and murder working men, clients and the general population, for the sake of their profit margins nor should the Law allow such practices. Disturbingly, and because medical science has successfully identified asbestos as a disease causing agent 20 38 the vast industry associated with asbestos mining and its use instead of removing this fibre from the market, is finding new uses for it. In the UK, we have identified asbestos cement fibre in drinking water. Even after presenting our work to the water companies some fifteen years ago, the pipes delivering drinking water from the Farmoor reservoir to Oxford and Swindon, remain in use. The argument by specialist epidemiologists and others for continuing to feed asbestos to populations, revolves about facts relating to the very low numbers of cases of the linings of the abdomen developing the cancerous disease called mesothelioma 2 29. Outrageously, the specialists ignore the main purpose of the alimentary system which is to absorb the contents of the lumen and distribute the material to all parts of the body5. Many such papers have been publish in relation to cities of the USA, Norway 20, Canada and elsewhere but the industry ignoring the clear link between ingesting asbestos and other gastrointestinal cancers, continue to claim no correlation between asbestos in drinking water and disease and continue to produce and supply asbestos cement products for processing drinking water. Given the overwhelming evidence against asbestos and the papers which compared geographical regions 14 where no asbestos contamination was found in the drinking water and the resultant absence of an elevated risk, it would seem obvious that damage was being done to populations subjected to ingested asbestos. Epidemiological specialists nevertheless continued to support the use of asbestos cement composites for the manufacture of water conduits of whatever type so that asbestos cement water carrying pipes were used in the UK until relatively recently. In any case, given the evidence, such services have in the Oxford and Swindon areas at least, not been dug up and removed. In many parts of the world the use of asbestos cement in drinking water utilities, continues to grow. The populations around the World, where asbestos cement pipes, bulk water storage etc continue to be used

are therefore subjected to eating and drinking asbestos because industrial specialist are of the opinion that drinking or eating asbestos is safe but breathing it and contaminating the lungs, is in their opinion, not. There was a report that a scientists in Oxford working with experimental animals in one of the university laboratories, refused to allow their experimental rats to drink tap water because it contained asbestos and would introduce an unknown variable into the experimental assay. Thankfully, the incurable cancerous disease mesothelioma is rare and the question as to why in the presence of so much asbestos contamination, is the disease seen so rarely, remains to be clarified but in an ongoing research project we are looking at the fundamental processes involving disease causing agents. With this in mind, a new concept is put forward for discussion. A model of disease causation challenging the existing wisdom relating to causal factors. Continuing the above analyses of micro-environments, it becomes clear that any given asbestos fibre finding its way into any given population of cells of lung lining tissues, can have an effect only on the given population in its proximity. To consolidate this concept, tissue drainage is considered and according to understood principals of fluid flow in capillary beds, there is directional flow of fluids from the capillaries supplying local areas of tissue, across the capillary cell populations via intercellular clefts and fenestrations or pore openings between the endothelial cells of capillaries, to emerge into the capillary bed environment. This directional fluid flow carries nutrients to the cell populations and at the same time removes cellular waste, via the venule capillary distribution and the lymphatic network serving the capillary bed. Crucially. the flow of fluid through capillary beds, exposes cells in that environment to the effects of the asbestos fibers trapped in that site and all cells downstream of the asbestos fibers will be exposed to prolonged and sustained influence from whatever constituents the presence of asbestos releases into the fluid flow. What is being considered here is that if components released from asbestos turns out to be a contributory factor in disease causation, or the presence of the fibre stimulates the releases of agents into the cell environment that make that population of cells subject to changes, then all cells in the immediate environment will be subject to such dynamics. A post mortem stained slide to demonstrate asbestos fibres trapped in a cell population. The patient died from asbestoses following many years of heavy exposure to asbestos fibres in the work place. The cell population in this volume is exposed to a tiny number of fibers. Other fibres in other cell populations play no part in the environment of the given cell population. Fig 14 Once the fluid flows into the capillaries, cells of that site are no longer influenced by the factors released in that environment. Such causative agents would then be conducted into the venous blood stream and pumped to all parts of the body, to contaminate all tissues of the body but at much lower concentrations. Clearly, any small fibers able to migrate via this arrangement would be taken up by the lymphatic capillaries and transported around the body and indeed asbestos fibers are found in various parts of the body 13 where mechanical transfer from exposed tissues is not possible.

Graphic representation of a capillary bed with arteriole, venule and lymphatic capillaries serving a population of cells. Never do more than a few fibres end up in any given cell population.

Fig 16

A difficult fact to explain is the causation of asbestos related cancers in individuals who have never been in obvious contact with asbestos. There are cases of mesothelioma in patients who have never had direct exposure to asbestos i.e. these people have never worked with asbestos, nor have they directly handled asbestos and in these cases one relates to the fall out of asbestos fibers from the many asbestos containing composites in the environment. Such examples and case histories of minimal occasional exposure to asbestos fibers present a considerable challenge to cause and effect when current exposure levels recommended by the HSE are considered. Prolonged efforts to consider disease causation in terms mathematical probability, of one fibre being deposited in a given cell population that was otherwise damaged and susceptible to cancerous changes, ended up in such perplexity and uncertainty that it become obvious that the probability approach was unworkable and the model was abandoned in favour of genetic factors. The latest effort to explain why a small number of individuals with minimal exposure to asbestos fibers develop mesothelioma and why it is that individuals who worked in asbestos manufacture or mining or other asbestos processing occupations where they were exposed to large levels of contamination of asbestos did not, led to the consideration of genetic susceptibility. Currently, an effort is being made to explain these widely differing exposures outcomes in terms of genetic disposition to changes responding to encountered mutagenic factors. Epigenetic i.e. external influences on the development of organisms have long been understood. The notion of genetic susceptibility has opened up a completely new avenue for study and what emerges is a very interesting possibility that given individuals have varied resistance to being damaged by given agents. What this means is that the scientific community will need to provide industry a means of testing individuals for susceptibility to damaged by substances they are require to work with. In time, we can look forward to selection procedures that will exclude certain individuals from handling or having to work with given materials and then, industry may substantially reduce the incidence of industrial disease. In any case, presented with the fact that changes to cells in capillary beds is a localized effect, means that at any given time or place only a tiny number of asbestos fibers have a direct effect on any given group of cells. Such arguments mean that existing safety levels to asbestos contamination cannot be correct. In real terms, given the small number of fibers that can be accommodated by any given capillary bed, means that one asbestos fibre in any given site, could be the cause of disease. If that indeed is the case then there are no safety levels of exposure to asbestos fibers and all current health and safety recommendations are based on a wrong premise.

The addition of straw fibre to building blocks requires the use of accelerated high alumina cement to overcome the retardation problem hydroxyl groups exercise in a cement slurries. It is the hydroxyl groups attached to the molecular skeletons of the many hydroxyl group compounds found in plant life that cause retardation of setting of cements. The powerful effect the dipolar group exercises in its immediate environment has an effect on the water molecules attached to the cement hydrate, preventing the cement crystal forming. To overcome this problem our research demonstrated that providing an alternative focus of crystallization allows rapid precipitation of the high alumina cement crystal, allowing the cement to set and provide a suitable cellulose cement manufactured building material. Unfortunately, all subsequent work demonstrates that because of the problem of miscibility of straw particles with aggregates, in the original trials more water had to be added than was recommended by the manufacturers of high alumina cements. Once the crystal formation starts to set, there is rapid setting of cement to provide a fast turn around from mixing to stacking the blocks. This rapid crystal formation results in poor quality crystals which when combined with extended wetting of materials and after about ten years of being moved about in the yard, resulted in an unsatisfactory block. The surface layers seem to lose their strength and could easily be dislodged by mechanical pressure. The broken up pieces of high alumina, straw cellulose building blocks, that were kept in the wet and used as a "football" about the yard, did not wear well. There appears to be a complexity that we have not been able to isolate because the research facilities needed for identification of the exact problem, requires well established facilities and know-how. A suitably equipped university department, ought to quantify the effect of an excess of water on the properties of high alumina straw fibre composites. The fast crystal formation also needs to be controlled in such applications and requires recommendations. In particular, a detailed study into the size and formation of accelerated high alumina crystal and the effect prolonged wetting has on such poorly formed crystals is awaited. The crystal structure of high alumina cement undergoes conversion to form the thermodynamically stable final form. In the process of converting from the metastable crystal forms of CAH 10 and C2AH8 to the cubic C3AH6 crystal form, there is a reduction in the volume of the crystal so that additional spaces are created

within the substance of the composite 6. These spaces increase the porosity of the material so that more water can penetrate the material. The water freezes during low temperature cycles to damage the material so that these materials fail in prolonged wet conditions. There is no information on what happens in wet situations during the reversion of molecules from the metastable crystalline phase into the ionic state in solution and how excess water effects the chemistry of CAC. The molecules forming the metastable crystals must revert into the ionic state before they can recombine to form the thermodynamically stable final crystal form. Provided water is prevented from contaminating the finished product the range of uses for calcium aluminate cements could be extended.

Conclusion Ample evidence exists to demonstrate fibre fallout from cement fibre composite materials and the ever increasing applications of fibers in such composites is forcing manufacturing industry to continue using fibers that are best avoided. Extreme health risks are associated with certain fibers, resulting in crippling legal outcomes to involved companies from consequential damage. There appear to be no safe levels of exposure to cancer causing fibers such as asbestos. All cement fibre composites release fibre into the environment because the weathering process breaks down the cement matrix to release material contents into the environment and contaminate the surrounding area so that methods of reducing the fibre fallout due to weathering become useful. Extensive effort is exercised by fibre manufacturers to continue the use of certain high profit margin fibers. The health and safety regulatory bodies are failing those they represent, by allowing the continued use of

certain fibers and in particular, by ignoring health issues, to allow industry to continue extending uses of such known harmful constituents. Analyses of the fibre contamination problem on a micro-anatomical level, demonstrates the physical limits to fibre contamination in any given locality and argues that world health and safety guidance is based on the wrong parameters and that very small numbers of fibers are the causative factor in cancer. Long term studies suggest that reducing the weathering process by adding water repellent preparations to fibre cement mixtures, extends the lifespan of cement bonded composites, to at least double the expected lifespan of conventional methodology. This patent applied for technology, has very substantial commercial and environmental implications. We are not confident about the use of accelerated high alumina cements in combination with straw fibers that are required to be kept in prolonged wet conditions. Similar materials kept in dry conditions, have to date, not shown any adverse effects.

References 1. Egilman D S, Rankin B S, 2005 Over a barrel: Corporate corruption of science and its effects on workers and the environment.: 331-337. 2. Egilman D, et al, 2003, Exposing the Myth of ABC, Anything but Chrysotile: A critique of the Canadian asbestos mining industry and the McGill University chrysotile studies, AJIM, Vol. 44,issue 5: 540-557. 3. Elmes PC 1980 Fibrous Minerals and Health, J. geol. Soc. London, Vol 137, 525-535.

4. Fasy T M, 1991, Asbestos fibers are mutagenic after all: new signs of orthodoxy for a paradoxical group of carcinogens. Ann NY Acad Sci, 643: 271-279. 5. Gennaro V, Tomatis L 2005, Business Bias: How epidemiological studiesmay underestimate or fail to detect increased risk of cancer and other diseases. International Journal of Occupational and Environmental Health, Vol II, 4: 356-359. 6. Guillemin M P, Litzistorf G, Buffat P A. Urinary fibre in occupational exposure to asbestos, 1989. Ann. Occup. Hyg.33(2):219-233. 7. Harrington JM, Craun GF, Mcigs JW, Landrigan PJ, Flanncry JT, WoodhullRS, 1978, An investigation of the use of asbestos cement pipes for public water supply and the incidence of gastrointestinal cancers in Connecticut 1935-1973 Am. J Epidemiology 107: 96-103. 8. Health and Safety Executive UK, Control of Asbestos Regulations 2006. Recommendations Following Consultations, HSE/06/56. 9. Health and Safety Guidance Notes MS13 2005.

10. Hodgson JT, McElvenny DM, Darnton AJ, Price MJ, Peto J. (2005) The expected burden of mesothelioma mortality in great Britain from 2002 to 2050. British Journal of Cancer; 92 587-593. 11. http://www.hse.gov.uk/statistics/causdis/proj6801.pdf 12. Kane A B, Boffetta P, Saracci R, Wilborne J D, 1996, Mechanism of mineral fibrecinogenesis.

IARC Scientific Publications No 140. 13. Kjaerheim K, Ulvastad B, Martinsen JI, Andersen A 2005 Cancer of the gastrointestinal tract and exposure to asbestos drinking water among lighthouse keepers (Norway), Cancer Causes and Control 16:593-598. 14. LaDou J, 2004, The asbestos cancer epidemic, Environmental Health Perspectives, vol 112, 3: 285-290. 15. Lignacite Ltd, Norfolk House, High Street, Brandon, Suffolk IP27 0AX UK. 16. Lippmann M1988. Review. Asbestos exposure indices. Environ.Res 46, 86-106. 17. Mosman B T, Craighead J E, 1981 Mechanism of asbestos carcinogenicity, Environ Res. 25(2) 269-280. 18. Magnani C, Agudo A, Gonzalez CA, Andrion A, Calleja A, Chellini, Dalmasso P, Escolar A, Hernandez S, Ivaldi C, Mirabelli D, Ramirez J, Turuguet D, Usel M, Terracini B. 2000, Multicentric study on malignant pleural mesothelioma and non-occupational exposure to asbestos. Br J Cancer 83(1): 104-111. 19. News round up. 2003, Asbestos poisoning was covered up by doctors, claims health team. BMJ, Vol. 327: 248. 20. Rankin B S, Zorabedian J, Egilman D S, 2005, Maximizing profit and endangering health: Corporate strategies to avoid litigation and regulation. International Journal of Occupational and Environmental Health, Vol II, 4,: 338-483. 21. Risks 248, 18March 2006. 22. Sadler TD, Room WN, Lyon JL, Mason JO 1984, The use of asbestos cement pipes for water supply and the incidence of cancer in selected communities in Utah, Community Health 9: 285-293. 23. Shuker L, Harrison P, Poole . 1997, Health effects of asbestos and man made mineral fibers, Institute of Environment and Health, Leicester University UK. 24. Scrivener K L, Capmas A, 1997, Calcium Aluminate Cements, Lee's Chemistry of Cement and Concrete, 4th Edition, Hewlett PC, ed, 709-778. 25. Spooner B, Roberts P 2005. Fungi. The New Naturalist Library. Collins, London UK. 26. Spurny K, Marfels H, Boose C, Weiss G, Opiela H, Wulbeck FJ. 1989 Fibre emissions from weathered asbestos cement products. 1. Fibre release in ambient air. Zentralbl Hyg Umweltmed. May;1988(1-2):127-43. German. 27. Stop Cancer before it starts campaign: 2003 Feb, How to win the loosing war against cancer. US Cancer prevention coalition. 28. Treasure T, Waller D, Swift S, Peto J, 2004, Radical surgery for mesothelioma, The epidemic is still to peak and we need more research to manage it. BMJ Vol. 328: 237-238. 29. Twentieth century mortality trend in England and Wales, 2003 Feb, 18 Health and Safety Statistics Quarterly UK.

30. Wagner JC 1980, The Pneumoconioses Due to Mineral Dust, J geol. Soc. London, Vol 137, 537545. 31. Varga C, 2000, Asbestos fibers in drinking water: are they carcinogenic or not? Medical Hypothesis 55(3); 225-226.

Master your semester with Scribd & The New York Times

Special offer for students: Only $4.99/month.

Master your semester with Scribd & The New York Times

Cancel anytime.