31 year follow up dpc

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Fibre composites

Our work on cement bonded materials concentrated on the use of fast setting high

alumina cement which was used because these cements do not suffer from retardation

that is exerted by the multitude of hydroxyl groups1 forming the cellulose molecule.

Workpresented in an earlier paper demonstrated a mechanism that explained the waythe powerful charges on the hydroxyl group held onto the water of crystallization to

prevent cements such as portland cement from forming the cement crystal. Setting of

portland cement in the presence of hydroxyl groups responds to thermodynamic

drivers that force cement to precipitate small poorly formed cement crystals that result

in material failure over time.

We manufactured StrawCrete blocks2 that were exposed to the British elements over a

ten year period and the behaviour of these materials was recorded.

Straw, aggregate, cement blocks complying with British Standards for such materials

were manufactured using 30% by volume of wheat straw milled to produce particles

of straw that complied to the named Crete Gradesie cellulose particle sizes

encompassed by the British Standard BS EN 12620:2002 for sharp sand. Most of the

particle sizes in this grade were about 5mm and less. Other cellulose concrete mixture

materials have been available for many decades but prior to our research wood

particles were used. This technology was time consuming and the used wood that was

expensive, imported selected forestry off cuts. This timber had to stand for many

months, in an effort to dry out the timber as a means of precipitating as much of the

free sugars in the wood as possible. Free sugars were thought to be the problem

preventing portland cement from setting. At that time the total hydroxyl component of

the cellulose additives was not taken into account. The prepared wood was processedinto shavings and other particulates that were mixed with aggregate and portland

cement. Subsequent research demonstrated that cellulose fibres remaining from paper

processing also caused retardation and only about 17% cellulose3 could be used to

mix with aggregates for the manufacture of concrete materials.

A wonderful product of a medium weight facing block resulted and these materials

were generally produced for partitions and internal leaves providing a pleasing light

coloured building material. The wood shavings used imparted a warm delicate texture

that reflected in the colour of the wood used in the finished concrete block. Such

wood fibre materials were popular in use of communal structures such as sports

centres, commercial builds and the like. No surface treatment was required so the costof the wood additive was offset by the fact that cellulose concrete blocks did not need

to be surface treated.

In the UK we have millions of tons of surplice agricultural waste 4 every year and our

research was directed at finding a use for these agricultural surplices. We produced

building blocks that were of a standard size for blocks, conformed to the B. S.

Regulations but containing large quantities of milled straw, a research effort that was

granted a UK patent, GB 2340125. In our experiments we found that provided the

straw was reduced to particulates of about 5mm in size and less that there was no

problem in miscibility of the low density cellulose fraction with the heavy sands

aggregate used. Any grade of straw could be used to give excellent homogeneity withthe high alumina cement used as a binder. Aggregates and straws used produce a

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homogeneous slurry that cast well in the block forming machinery and produced a

dimensionally stable material that cured quickly and resulted in the required load

bearing 3.5N/mm2 crushing strength.

These cellulose based materials have been shown to be suitable only for internal uses.

The excellent results achieved with the building blocks and high alumina cement as a

binder led us to experiment with composites using very high quantities of cellulose

fibre but in this case using only the high alumina cement, without any additional

aggregates to set the cellulose fibres into the final board material we were making. In

one example we used 80% by volume straw fibres milled to the crete grades

(equivalent to the sand standard of the BS EN 12620) and 20% by volume high

alumina cement as the binder to produce a hard well formed board material that had

remarkable properties. We discovered that in a dry state, the finished material had

insulation properties with a thermal conductivity of 0.11watts/m/0K.Most

surprisingly, the dry board did not support fires. Very high quantities of cellulose

fibre added to cement binders produced materials that exhibited thermal propertiesclosely matching the thermal properties of solid wood and in a dry application, could

be used as fire retardant thermal insulating fillers.

Fibre release.

Fibres are very useful to the construction industry and many composite applications

are in use around the world. The best studied fibre additive to concrete is asbestos and

this fibre above all others provides the best example of the problems released fibres

create in the construction industry. Asbestos fibre is today used in greater quantities

then ever before5

but its use is spread across the world and much to thedisappointment of the health professionals asbestos fibre manufacture is transferred to

countries with poor health and safety records where enforcement of health guidelines

for industrial standards is low or non existent. Asbestos cement composites

manufacturers produce a wide range of products and as an example only samples of

asbestos fibre materials bonded with cement is discussed.

The industry does not use high alumina cement for general manufacturing purposes so

exterior quality asbestos fibre materials are bonded with portland cement. In all cases

cement bonded fibres release fibres due to normal abrasive wear and tear and this is

accelerated in materials exposed to the wetting and drying cycles. Very considerable

breakdown of the superficial layer of the cementing matrix is experienced during thefreeze thaw cycle. Work done on cement asbestos composites demonstrates extensive

abrasive effects due to weathering and as soon as the surface matrix is destroyed

asbestos fibres are seen to become free from the substance of the material to rise

above the matrix.

The flow of water in wet conditions has a grinding effect on the surface layers and

fibres released from the matrix break off to be released into the environment.

Similarly, in windy conditions the pressure exerted on exposed fibres flexes them to

eventually break off the fibres because of the compressive and tension stresses

imposed on the fibres. Released fibres are carried by air currents to any distance from

the source material. Contamination of the local environment is high6 gardens,vegetables, clothes drying in the air, inhalation by individuals in the vicinity etc are all

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recorded. Anyone living in properties clad with or covered with asbestos materials is

subject to asbestos contamination as indeed is anyone who has any asbestos fibre

composite within their environment.

Fibre release accelerates with the age of the product and the older the materials the

greater the release of fibres. The process of environmental contamination occurs fromthe moment the product arrives on site and continues for the life of the material. Vast

quantities of asbestos fibre are released by asbestos products meaning that the entire

environment is subject to asbestos contamination. In Europe for example there are

millions of hectares of asbestos roofing tiles, corrugated sheeting and sheet material

for cladding. All these materials are continually releasing fibres to contaminate the

environment.

The abrasive mechanism is mechanical and the Health and Safety Regulations

recognise that fibre fallout occurs and acknowledges that fibre fallout occurs readily7

but is powerless to impose controls other than to recommend caution and plead

Reasonable Practicality in handling asbestos materials. There are such hugequantities of asbestos in use that it is impossible to avoid contact with the material

particularly by the repair and maintenance services8 and all the HSE does is

recommend caution and Reasonable Care in their 2012 supplemented

recommendations which have to be in place by 2015.

None of the HSE recommendations are adequate because in practice no level of

exposure to asbestos fibre has a safe limit.

Fibre composites in dry conditions retain the matrix integrity to a far greater degree

than wet materials and dry asbestos cement retains its fibres for the life of the binder.

Provided such materials are kept dry straw fibres are known to stay trapped in

matrixes and remain in good condition for years. Composite materials in dry

conditions found in Egyptian tombs have retained their molecular integrity for

thousands of years and still demonstrate all the characteristics of the cellulose source.

It is the wetting of fibre composites that causes the greatest problem and accelerates

the breakdown of the cementing matrix and the release of fibres.

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Fig 3 Fig 4

Asbestos tile roof New and a 10 year old asbestos tile

On the left Fig 3 demonstrates a typical asbestos roof covering. These tiles were used

because they were about half the price of slate quarried tiles and in the 1970 these

composites were the preferred choice for all grant supported re-roofing in the UK.

The Local Authorities giving grants for re-roofing contracts specifying the use of

asbestos tiles. On the left in Fig 4 is a new roofing tile which was sprayed to seal in

asbestos fibres. In Fig 4 on the right is a ten year old asbestos roofing tile

demonstrating the loss of the coatings applied during production and showing

weathering and release of asbestos fibres into the environment.

Fig 5 Fig 6

Old corrugated roof sheeting Macro photograph of

and asbestos guttering a weathered corrugated sheet

In Fig 5 is demonstrated a widely used asbestos corrugated sheeting that was also

used for side cladding of buildings. Also seen in this picture is asbestos guttering with

a hopper section and an asbestos down pipe. In Fig 6 is seen a macro photograph of

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loose asbestos fibres working their way out of the corrugated asbestos cement sheet

composite.

Fig 7 Fig 8

Asbestos sheet Macro photograph of weathered sheets

cladding panels

Fig 9

Manufacture drinking water carrying pipes.

Asbestos cement drinking water pipes remain in use world wide9, 10, 11, 12 and as a well

documented example, the City of Oxford and the City of Swindon in the UK are

supplied by water ducted via asbestos cement pipes. There are asbestos pipes carrying

hot water, providing ventilation shafts, chimney flues, foul water ducting etc all

subject to the abrasive effects of the flowing fluids.

Our research into the use of high alumina cement13 and straw fibre required us to

subject samples of the manufactured blocks to prolonged wet exposure so sample

blocks were left in a shaded area where the drying process was slow. The blocks

were seen to be damp for extended periods of time and after a couple of years of this

weathering it was a great surprise to find large fungal growths on the surface of the

straw block. Exactly the same fungus family grew on the control block kept under the

same conditions but using wood shavings instead of straw. The fungus established a

colony on cellulose concentrations in the blocks and grew vigorously to produce

mature fungal organisms with well developed physical characteristics. We took a

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sample to the local university where the fungi were identified as belonging to the

Peziza Family14.

In all cases the fungi dried up and died very quickly as soon as the blocks dried. More

persistently we observed other micro flora that regenerated when the blocks became

wet again and in the high alumina cement bonded cellulose blocks the micro florabecame more extensive over time. It became clear that the porosity of the composites

bonded with High Alumina Cement (HAC) increased with time and the blocks under

experiment retained water much more effectively than control blocks bonded with

portland cement.

It turns out that the crystal phases of HAC13 vary in volume as one form of crystal

structure forms into another as the waters of crystallisation are removed during the

curing process. The volume of the principal crystal hydrate CaO.Al2 O3.10H2O the

CAH10, is larger than the minor hydrate (CaO)2.AL2O3.8H2O C2AH8. The final said

thermodynamically stable crystalline phase of calcium aluminate cements the cubic

crystalline phase of (CaO)3.Al2O3.6H2O and AH3 (C3AH6) has the smallest crystalvolume of the three discussed crystal phases. The reduction in volume in these crystal

changes leads to the creation of voids in the material matrix which can accommodate

free water. In time these cements fail in use when exposed to prolonged wet

environments. It is our opinion that CAC does not have a thermodynamically stable

phase and it seems to us that the cuboid crystal phase probably reverts to the earlier

crystal phases in the presence of free water.

All the blocks kept in the dry conditions retained their form and showed none of the

micro flora seen in wet blocks kept in the open. Water was the key to the biological

flora supported in the cement bonded cellulose fibre composites.

Fig 10 Fig 11

Control block

made with wood chip

Building blocks made with

High Alumina Cement and

milled straw

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Consequences of fibre release into the environment.

It is generally accepted that asbestos causes disease and a great deal of information

has become available over the last few decades. Asbestos fibre above all others has

been extensively studied and not only because providers of this fibre are in acontinuous process of paying out substantial compensation to contaminated

individuals. Problems relating to contamination with asbestos fibres reflect in the

incidence of various related diseases. The best described are asbestoses which results

in prolonged, tortured incapacitation of individuals leading to eventual death and a

great deal of suffering, cancerous changes in cells genetics leading to mesothelioma, a

progressive disease for which there is no cure. Recently, the medical profession has

acknowledged that asbestos fibres cause inflammation and exhaust the immune

system so that cancer of the lung, abdominal cancers42 and other diseases15 are being

linked to asbestos contamination.

It is now accepted that all asbestos fibres precipitate cancers and cause disease15,16,17,18,23. Asbestoses is a condition where the individual is exposed for prolonged

time19 scales with asbestos fibres in high concentrations of 25 to 30 fibres/ml and this

condition was frequently seen in workers associated with mining, manufacturing and

asbestos processing industries. Initially the condition was considered to be silicoses

but it is also referred to as pneumoconiosis. A ghastly disease associated with the loss

of lung tissue pliability in which the transfer of respiratory gases is impaired 19because

of the extensive scarring that is associated with hard inorganic materials damaging

delicate lung tissues, the scarring of which deposits a build-up of cologne. This build

up of scar tissue results in a loss of lung tissue pliability and oxygen transfer.

Development of cancers associated with asbestos dust occurs because the presence of

asbestos in cell proximity changes the genetic structure of cells20,23 to result in tumour

formations wherein cells no longer function to comply with the organ characteristics.

In human cells genotoxicity is precipitated by all asbestos fibres23. A complex set of

developments unfolds at cellular level in the presence of fibres and asbestos is known

to activate macrophages and release inflammatory mediators. Genetic damage to the

cavity linings the pleura, are an example of DNA change in cells resulting in

uncontrolled growth of cells with changed biological function of misothelial tissues.

Mesothelioma is always fatal and has been linked to the presence of asbestos although

in medical science contributory factors always emerge with better understanding.

It is suggested that cancers resulting from asbestos contamination21 are at least as

prevalent as mesotheliomaand it is recognised that decades of exposure is required

before such diseases become established22 . The length of time needed for these

cancers to establish in the body provides an indication that the causative mechanism

resulting in cancerous growths is not due to the confirmed soluble Mg++ leaching from

the asbestos molecule. It is argued that such soluble components would quickly wash

away in the continuous stream of interstitial fluid washing over cell populations. It has

been proposed that biopersistance be considered in pathogenicity22 and the divalent

iron present in all forms of asbestos, is being studied.

The half life of white (chrysotile) asbestos is said to be about 15 days whilst that ofthe brown (amosite) and blue (crocilodite) asbestos have much longer half lives and


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larger iron content. Here evidence is provided to suggest that isomeric micro

constructs do not cause cancers whereas fibrous dust23 of a given size38 of about less

than 10m and thickness of about 0,25-3m causes scarring and disease. Asbestos

fibres of 5mare thought to be particularly damaging but smaller fibres are respirable

and are to be avoided as they tend to be transported to the deepest areas of the lungs

there to be trapped in the liquid interface coating the membranes. Studies in fluiddynamics show that the smallest particulates always end up in the fastest central flow

volumes and are therefore transported to the deepest parts of the lungs.

In the 1980s the entire recommended filtration standard was challenged. The size of

specified pores in filters recommended by the British Standard 4400 prevented a

majority of fibres of 5 microns in diameter from passing through the filters. The

problem with this standard we argued was that fibres can be of 5 microns in diameter

but pores of that size cannot prevent longer fibres passing through the mesh. All filter

designs allowed fibres smaller but longer than then 5 microns, to pass through and

that applied to filters in use when working with asbestos . Fibres small enough to pass

through the pores are the very fibres that are classified as causative of disease. Thesefibres are inhaled to be trapped in lung tissue to cause inflammation. Inflamed tissues

have altered permeability of cell membranes and increased fluid flux. Such changes in

permeability to cell walls increase the absorption of contaminants which make cells

more susceptible to disease. Membrane irritation exposes cell to an increased insult

from damaging factors such as cigarette smoke which is known to cause cancer.

Of the diseases quoted above the development of mesothelioma in subjects which

have demonstrably a very low level of exposure to asbestos are known and very

challenging, even though the patients cannot recall ever being in contact with asbestos

disease events are recorded. Nonetheless in exposures to asbestos that is well within

the recommended minimum exposure level specified by the HSE cases of

mesothelioma are seen.

Over many years of creating models for analyses of these low level disease causing

exposures it became obvious that all recommendations by the HSE were based on

practicalities rather than proven scientific data. In effect, the HSE appears to be

making recommendations based on reasonable exposure that in practice hopes that

reducing exposure would also reduce incidence of disease. The World over, HSEs are

making recommendations that are specified by the Code of Federal Regulations for

Construction quoting the Asbestos Standard 29 CFR 1926.1101, the European Union

Directives and various scientific projections, all of which are working to reduceexposure to asbestos fibres. Even recommended exposure levels of 0.1fibres/ml issued

by the HSE (2012- 2015) is surprisingly, expecting substantial death statistics from

mesothelioma24.

The regulatory bodies are making recommendations about asbestos exposure in the

full knowledge that deaths will result from their recommendations but explain the

specifications on the grounds of practicality. What an extraordinary abrogation of

responsibility to the working man, given that alternative fibres are available that could

replace asbestos.

Our work involved the consideration of various models of exposure andcontamination and led to the disregarding of all previous information and the


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Statistics correlating quantitative exposure to asbestos and disease causation are

published but given the capillary bed arrangement it seems clear that quantitative

exposure is not the causative agent in the development of diseases such as

mesothelioma. There are examples of individuals exposed to heavy contamination of

asbestos fibre that do not develop cancers and examples where minute exposure to

asbestos fibres causes death. Clearly factors other than quantitative exposure 26 are atplay and we have considered genetics as the principal factor determining which

individuals will or will not develop disease when exposed to any given contaminant.

Our work on the micro anatomical arrangement providing a relatively constant

environment where asbestos and other contaminants embedded in any given

arrangement of cells suggests that cells can never be subjected to more than a few

fibres at best. The observable effects on cells are the result of minimal quantities of

contaminants that the worker is exposed to and when the micro anatomical

arrangement is taken into account, it becomes obvious that the entire Health and

Safety Industry is acting and issuing safety instructions on a total lack of

understanding as to the causative parameters precipitating asbestos diseases.

HSE specifies a working level of asbestos concentration in inhaled air at 0.1fibres/cm 3

ie 100 fibres per litre of inhaled air. If we measure the average rate of ventilation at

rest of about 6-8 litres per minute then at 360 litres per hour the individual is likely to

inhale in excess of 250000 thousand fibres each working day. There is no information

to demonstrate how many inhaled fibres are exhaled in the ventilation cycle but the

numbers of fibres the working individual is exposed to every day, far exceeds the

maximum number of fibres any given capillary bed can accommodate. Contaminants

become trapped in the mucous lining of the ventilation ducts and are from there

transported via the lymphatic vessels of the lungs, to over time result in asbestoses

and other medical conditions relating to the contamination. The lymphatic nodes of

heavily contaminated individuals are choked up with fibres.

Depressingly, the HSE has recently been issuing guidance7 that is to be implemented

by 2015, on levels of contamination to asbestos in terms of practicability ie

minimise contamination to the lowest practicable level but keep on working with

asbestos. The vast amounts of work done by researches has demonstrating the

damaging effects of asbestos but this evidence has not removed asbestos from the

market nor prevented it from being used. Safety bodies have been issuing guidelines

on statistical modelling of death rates that allows employers in asbestos industry to

calculate expected death rates from exposure given specified parameters24

Thiscalculating facility is available on the World Wide Web27 .

To better understand the argument of low level contamination we need to consider the

dynamics of the air flow entering the lungs and the fibre carrying volumetric

distribution as the air is inhaled.


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Fig 12

Cast of air passages in a human lung

The HSE is for some reason not considering asbestos contamination in practical

terms. What needs to be discussed is the actual physical behaviour of contaminating

elements and the easiest way of demonstrating levels of exposure to contaminants is

to discuss volumetric flow in any ventilation cycle. The volume of inhaled air is

divided into two flows as soon as the inhaled air reaches the bronchial bifurcation so

that one volume of air flows to the left lung and the other to the right. The left and

right lungs are two entirely separate structures which are separated one from the other

by physical structures, independent blood supply and lymphatic drainage and the

lungs are encased in layers of membranes that isolate the lung in an independent and

self contained environment. Contaminants flowing into either lung cannot for physical

reasons have any effect on the cell populations sited in the other lung.

The number of fibres in the inhaled volume is therefore halved as soon as the inhaled

air enters the lungs so that the working level of fibres contaminating a given lung is

half that specified by the HSE.

Taking this consideration further it becomes clear that each lung is further subdivided

into 3 lobes which are isolated from each other in physical and physiological terms.Each structure is supplied by an independent and specific distribution of blood vessels

and lymphatic drainage and is again wrapped in membranes to provide a complete

and isolated anatomical environment from the adjacent lobes. If we consider the right

lung we find that the lobes are further subdivided into 10 bronchopulmanory segments29 and these segments are further subdivided into sub segments which for practical

purposes means that the number of asbestos fibres inhaled into the right lung is further

divided by some fraction relating to the number of isolated sub segments. Each sub

segment continue the bifurcation until the terminal alveolar air sacs are reached where

the numbers of contaminating fibres entering the right lung is divided by whatever

fraction off the total volume these air the sacs contain.


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The segregation of structures in the body is a remarkable evolutionary step that

continues in ever decreasing anatomical constructs which finalise in the capillary bed

arrangement.

The evolutionary isolation of areas of the lungs means that these constructs are cut off

from disease manifestations in adjacent sections. An incredibly valuable safety featurethat prevents disease migrating by proximity. As mesothelioma stars in some

population of cells it means that at no time do more than a few fibres ever play a part

in disease causation. Asbestos fibres lodged in adjacent capillary beds in various sub-

segment in the same lobe cannot possibly have any influence on cell populations in

other segments of the same lobe. Even more remote is the influence of the fibres

trapped in the right lung and events taking place in the left lung.

The crucial anatomical arrangement allowing us to explain the concept of specific cell

population contamination is better understood by considering the capillary bed

construct29 as demonstrated by the below drawing. In this schematic we have made an

effort for the sake of clarity, to expand the blood vessel distribution leading from thearteriole vessel to the venule indicating a possible distribution of blood vessels

supplying the many cell populations served by these vessels. It can be seen that there

is a general movement of fluids from the capillaries into the cell bed interstitial space

where blood fluids flow from the high pressure region to the low pressure regions to

be absorbed by the venous blood vessels and removed from the capillary bed

environment. Arrows indicate roughly the direction of the fluid flow in this

arrangement and as an example only the capillary bed populations are supplied with

lymphatic capillaries to add to the removal of fluids from the capillary bed.

Fig 13

Schematic of the blood vessels supplying capillary beds

This micro environment can only accommodate a small number of asbestos fibres or

other contaminants. Movement of fibres from the capillaries to the interstitial spaces

is considered to be by migration via blood fluid flows and out of the blood vesselsthrough intercellular clefts, fenestrations and pores that are located between the


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endothelial cells forming capillaries. Once in the capillary bed the fibres are

considered fixed and remain trapped within the cell populations.

The isolated nature of the subdivided lung anatomy makes the observable low level

incidence of asbestos cancer understandable and we are working on the hypotheses

that genetic drivers are the dominant influence that explains why some individualswith asbestoses do not develop cancers whilst other with minimal exposure to

asbestos do. It becomes obvious when this anatomical segregation is considered that

the currently recommended levels of exposure to asbestos contamination are a

complete nonsense.

Our research suggests that there is no safe level of contamination with asbestos fibres.

The concept that some individuals are more sensitive to exposure to given irritants

leads us to the obvious conclusion that science needs urgently to provide industry

with tests that will allow employers to refuse work to individuals genetically

susceptible to agents that are likely to be handle in the workplace.

Industry

Extraordinarily the asbestos industry continues to pay out vast sums in damages to

individuals poisoned by asbestos and in the USA alone, it is estimated that the total

cost of litigation exceed 250 billion and still there are about a million claims in the

pipeline. Yet, the asbestos industry continues to invest large sums of money in

supporting professional researchers and employing lobby groups in order to continue

to mine and sale of asbestos30. There is evidence that leading scientists are corrupting

scientific data to confuse issues31

relating to the cause of epidemic incidence ofdisease seen around the world. Recent publications show that the incidence of

mesothelioma in the UK is still rising 32,33,43. Leading authorities in the statistical

analyses of disease epidemiology state that the incidence of such diseases are due to

lifestyle factors 34 and it is these assessments that the HSE regulatory specifications

are using to formulate policy.

Much effort is directed by the unions in challenging conclusions issuing out of

research facilities and claims are being made by unions that scientific researchers are

being corrupted by large financial inducements to muddy the waters35,41 are refusing to

go away as the asbestos mining industry does all it can to increase the availability of

asbestos. Very considerable pressures are being applied on countries such asIndonesia, Zimbabwe and others countries to increase the use of asbestos and the

mining interests in Canada, India, Russia, Kazakhstan, Brazil and elsewhere are

producing more asbestos today then ever before. As an example only there is more

asbestos being used today in the USA then in earlier times. Some 54 countries have

banned the importation and use of asbestos but the vast quantities of asbestos installed

in the infrastructure in many countries will take hundreds of years to remove and

bury.

In a desperate effort to contain the spread of asbestos use the French Government

some years ago called on the World Labour Organisations Such as the European

Agency for Safety and Health at Work, to ban the use of asbestos.


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The very considerable profit margins from the sale of asbestos has created a situation

wherein the asbestos industry management proudly reports to shareholders that the

ongoing settlements for damages is not seriously affecting profit margins30. As a last

resort, in order to protect investment returns, the companies can file for bankruptcy

under the protection of Chapter 11 which allows the bankrupt companies to avoid

most of the legal damages relating to their activities. This abusive procedure is part ofthe problem relating to deliberate and planned abuse of workers interests and in case

of damages all those profiting from the sale of known carcinogens17 should be made

responsible for the ill health their financial manoeuvres cause.

Commercial interest preside and there is pressures on scientists working in the field to

continue corrupting data31,39,40 and sidestepping definitive conclusions so that research

departments can continue to receive financial support for further research and

departmental activities. Many of these scientific studies reach unprofessional

conclusions that deliberately confuse the issues and exclude many at risk groups35 to

deflect symptoms to other causative factors such as smoking and lifestyle choices.

Pressure on academe is common in many industrial establishments and great demandsare exerted on scientists conducting research to state that the questionable product are

safe to use30,35 and doctors are encouraged to corrupted diagnoses of asbestos related

disease and report cases as bronchitis or tubecoloses31.

Statistical evidence speaks for itself36 and figures for 1901 before asbestos became

available deaths from cancers was reported to be about 5%. About 1940s an

International Classification of Disease Code classified cancer and in the 1950s death

rates from cancers rose to 15%. Statistics for deaths from cancers in 2000 showed a

rise to 25% of all deaths. In recent times incidence of cancer during an individuals life

is assessed at 1 in 3 and rising to 1 in 2 within another quarter of a Century, far

exceeding epidemic proportions. Deaths from mesothelioma has not yet peaked and is

expected to reach its maximum in not too distant a future.

It is extraordinary that in the 21st Century corrupt practices continue to be

implemented in the full knowledge that the substances working men are required to

handle will kill them or cause them physical harm. Working men have no choice but

to handle whatever the industry is manufacturing. An individual has no control over

what the manufacturer is producing and if the management knowingly exposes the

workforce to carinogens7,30,35 than there are very serious moral and legal implications

that must be enforced. Until labour Laws are seen to be effective in protecting the

interests of the workforce than there will always be those who can be persuaded tointerpret scientific evidence in dubious ways.

Those who formulate policy must be identifiable and complete transparency should be

mandatory in business practice so that all those involved in handling industrial

materials know what is being done and what precautions need to be implemented in

handling known hazardous materials. It is no good taking companies to courts of Law

because these are structures that are managed by individuals and it is the individuals

who implement injurious practices that must answer for decisions made. The

immorality of continuing the use of known hazardous materials and when challenged

to shut up shop and transfer profit making to societies where Labour Laws are less

well established, defies belief. Such practices belittle the human spirit and must


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become illegal no matter where they occur. In the 21st Century industry cannot harm,

mutilate and murder workers so that their shareholders can maintain profit margins.

Great effort is made by the asbestos providers to maintain the sue of asbestos and in

the UK we are disappointed to find that in spite of much effort and exposure in the

media about asbestos pipes being used to duct drinking water from the main reservoirat Frmore in Oxfordshire UK, the drinking water for the city of Oxford and Swindon

continues to be pumped via about 5 miles and 30 miles respectively, of asbestos

conduits. This setup, could provide excellent statistical data for Epidemiologists.

Exposure and letters to notable researchers about the use of asbestos pipes for pipe

manufacture generally results in dismissal and finger pointing at the low level of

incidence of abdominal mesotheliomas,33,36. Outrageously, specialists dismiss the

principal function of the gut which is to absorb material from the gut. Asbestos fibres

are known to clog up in lymphatic nodes and the argument that the lymphatics are a

means of transportation for fibres into the blood stream are not attracting attention

from the scientific community. There is evidence from the USA, Norway10,42Canadaand elsewhere indicating that there is a link between ingestion of asbestos and various

cancers of the gastrointestinal tract.

Comparative studies have been published wherein geographical differences21 in

disease incidence between regions where asbestos in drinking water and those where

no asbestos fibres have been identified have demonstrated that there is an absence of

elevated risk of cancers in regions with no asbestos contamination it is surprising that

the asbestos pipes currently in use have not been dug up and replaced. Regions of the

UK continue to drink water that is ducted via asbestos piping!

A report was issued in which a scientist conducting experiments on rats refused to

allow his experimental animals to drink tap water because there was asbestos. The

reason was that consumption of asbestos would have introduced an unknown variable

into his experimental assay. People continue to drink water that is stored in asbestos

cement tanks and ducts because specialist researchers say that as far as experimental

data is concerned, eating and drinking asbestos fibre is safe but inhaling such fibres is

deadly.

Thankfully, mesothelioma is rare but time factors and genetic predisposition in

succumbing to the disease appear important parameters.

We have presented models for discussion suggesting that in all cases the causal focus

of disease can only be due to very small numbers of asbestos fibres. The importance

of the microenvironments seems clear at least in as far as the entrapment of asbestos

fibres is concerned. Any trapped fibre in any given capillary bed can only have a

localised effect on that group of cells and given when capillary beds are considered in

three dimensions, there is only a localised group of capillary beds that can be

influenced by trapped contaminants.

Given the understood physiological fluid dynamics in capillary beds it is seen that

filtered blood flows into the intercellular space via the many intercellular clefts,

fenestrations or pore openings structured between the endothelial cells of thecapillaries. The fluids entering the capillary beds are mostly free of blood cells so that


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the interstitial fluid is basically a carrier responding to pressure gradient flow

mechanics. Cells in this environment are continually involved in maintaining the

physiological balance which in the presence of a foreign body causing irritation

inducing stress dynamics that over time thought to result in disease causation.

There is general consensus amongst researches in the field of fibre contamination thatmany factors are necessary for carcinogenicity but the length38 to diameter ratio seems

to be crucial for asbestos fibre diseases. When assessing fibre characteristics

sophisticated scientific methodology is used to determine biological activity.

Transmission electron microscopy, scanning electron microscopy, x-ray

crystallography, low temperature nitrogen absorption for surface area of fibres are

used amongst other methods. Research technology for assessing surface chemistry

liquid solid interface of fibres extends to analysing atomic components of fibres to

analysing the iron content which has a positive correlation to carcinogenicity wherein

amosite (brown fibres) and crocilodite (blue fibres) are seen to demonstrate larger

number of iron atoms than is found in white fibres so that redox states of ions are

being considered although taxonomic specifics remain elusive.

Biopersistance has long been recognised but fibre carcinogenicity seems to be a

multistage process. Fibres in cell populations are said to cause chronic persistent

inflammation which alters the permeability of cell membranes to result in a loss of

control over the constituents flooding in and out of the internal cell environment.

Inflammation is said to precipitates an altered state of cell proliferation, genetic

function, apoptosis and other factors which mediate proper cell function. Uncontrolled

influx of material including carcinogenic factors such as cigarette smoke components

etc can in this state of intracellular insult precipitate the sort of changes seen in

asbestos diseases.

Whatever the mechanism involved, foreign bodies stimulate exposed cells to react in

a way that changes their cell environment. This post mortem stained slide, confirm

that any given capillary bed is subject to only small numbers of contaminating fibres.

Fig 14

Post mortem slidedemonstrating asbestos fibres trapped in cell populations


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came back from testing the fact that there was no loss in load bearing due to the

addition of PMS we continued with detailed tests.

Fig 15 Fig 16

Testing crushing strength of Crush test results


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experimental mortars

Testing the water repellent additive.

There are many water repellent additives manufactured around the world and it is up

to experimental groups to decide which additive to use in their assay.

Testing the effectiveness of various experimental preparations involved the

immersion of a two brick assembly contained in a tray of about 25mm of water so that

the lower brick was immersed in a constant level of water. Evaporated water in the

tray was topped up periodically so that the lower brick was always immersed in water

and saturated. The brick used was the Hammill Multi Red which was selected because

it was known for its manufactured consistency and because it readily transmitted

rising damp.

Fig 17

Typical experimental wet tray assay

Long Term Testing

Because the 120 day study period of these experiments was not long enough give us

an indication of the long term effect of the Potassium Methylsiliconate additive to the

mortar mix we determined to establish a long term study that is still ongoing and we

include photographs of a structure put up to test the long term effect of this additive.

It is well known in construction that mortar undergoes degradation with time and as a

means of confirming the effectiveness of water repellent additives to mortars we built

a low level, stand alone garden wall that was put up in December 1982 and left

exposed to the British elements. We still retain the Invoice for the contract issued on

the 31st December 1982. Over the last thirty years we have periodically visited the siteto photograph and record the progress of the experiment.

The chemical solution we experimented with was manufactured by ICI but the

manufacture of the Potassium Methysiliconate was subsequently taken over by

Rhone-Poulenc a French company. We persisted with experiments using the French

product which had an industrial name of Rhodosil Siliconate R333 a water soluble

form of the Potassium Methysiliconate, specifying a concentration of solids at 3.5%

w/w.

The experimental assay was identical to that used in earlier experiments on DPC

mortars and consisted of a 1 : 3 portland cement : sand mix using the standard locallyavailable grades of builders sand. We mixed a batch of sand until we were satisfied


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with the miscibility and then divided the batch into two parts. To one part of this mix

we added tap water until the right brick laying consistence was obtained and used that

mortar to continue building the wall up above the DPC layer.

For the DPC experimental mortar we added the Potassium Methysiliconate solution to

the other part of the earlier prepared batch and mixed until the same workingconsistency was achieved. This mortar was used for the DPC layers only but the

working practice was the same throughout the build using standard brick laying

methodology.

We have continued to monitor the construction over the years and below present a

photographic chronicle of changes in the condition of various components of this

experiment.

Fig 17

Conventional bituminous DPC layer.

Note that the continually wet bricks below the DPC

spall due to the freeze thaw cycles.


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Fig 18

Photograph taken in 1990

some 8 years after the experimental wall was built

This area of the wall was the worst effected section. Note that conventional mortar

perpendicular between the bricks has lost its surface. The DPC mortar layer shown no

degradation whatever and remains in the original condition. The surface layer is still

present and the surface tension tooling marks can still be seen. The wet bricks below

the DPC have started to spall and the spalled sections have been pushed away from

the brick to break off at the Experimental layer. Note that the mortar is fractured here

indicating that the bond between the mortar and the brick remains strong.

Fig 18

Photograph taken in 2006 of the same walland at the most weather damaged area of the build.


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In 2006 this structure was exposed to the British elements for 24 years and at the

worse effected area of the wall there is severe damage due to the freeze thaw cycles.

Generally because the brick bellow the experimental mortar were partially belowground level the bricks were subjected to prolonged wetting and this was a design

parameter in this experiment. 24 years after the structure was put up, we were

extremely surprised to see that the experimental DPC layer was in pristine condition.

No degradation of the mortar layer made with the Potassium Methylsiliconate was

observed. The surface layer remains in the condition it was in when the wall was built

and surprisingly, the tooling marks can still be seen in the DPC layers but not in the

conventional mortar layers.

When we built the wall the final part of the build was to point the mortar between the

bricks layers with a pointing tool and brush away any surplice mortar. The fact that

the tooling marks are still obvious was exceptionally surprising. The tooling marksresult from the fine sand being dragged along by the surface tension forces of the

liquid layer and dried to remain firmly bonded to the underlying mortar bed. This fact

is a clear indication that the cementing integrity of the cement binder remains

unaffected by exposure to the weather conditions.

The brick exposed to the wet conditions for prolonged periods of time has undergone

extensive damage and spalled deeply into the brick substance. It is of very

considerable interest that the brick bonded to the experimental mortar layer retains a

firm bond and is bonded to the spalled sections of the brick. Where the expanding

action of the freezing water forced the spalled sections away from the body of the

brick the brick sections remained firmly bonded to the DPC mortar layer and the

expansive forces increased as growing water crystals grew. The bond between the

mortar and the brick was so firm that eventually the force exerted by the freezing

water broke off the mortar for the spalled brick section to fall away. No spalling of the

DPC mortar layer is seen.

Note the degradation in the conventional mortar in between the upper bricks in the

next coarse up. Here the bonding property of the portland cement has failed in the

superficial layer to result in loose spalling mortar which is at this sage porous so that

the damage to the conventional mortar layer is accelerated. Water is the cause of the

damage seen.

31 Year Report

The long term study continues and we are able to present recent photographs of the

same wall taken in June 2013, 31 years after it was built.


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Fig 20

Photograph taken in June 2013

31 year old experimental follow up.

Least damaged section of the build.

In this 31 year old wall structure we have had the opportunity to witness the progress

of weathering damage to a structure that we built to exacting standards where care

was taken to observe the best control practice available to us. In the above photograph

of the least effected area of the structure we see that the perpendicular mortar layer

made with conventional mortar has lost its surface resulting in an increase in porosity.The experimental DPC layer has remind unchanged and very much to our surprise, we

still see the tooling marks on the surface of this layer. The surface remains in a

pristine condition and the bond between the mortar and the brick is sound and we can

see no difference in the bonding property between conventional mortar and the

experimental mortar. Note that the brick below the DPC is spalling and exerting

mechanical stresses on DPC mortar layer. The surface of the brick face is separating

from the body of the brick substance.


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Fig 21



Moderate spalling damaged to bricks in this section of the wall

In a different section of the same wall brick spalling has taken place and here we see

the mechanics of the spalling forces. The bond between the brick surface and the

mortar must have been very strong for the spalled brick to break off the surfacesection of the DPC layer. It can be seen that below this surface layer the mortar is in

excellent condition. Small stones remain embedded in the mortar substance indicating

a forceful braking off of the layer immediately above it. The brick on the upper

surface of the DPC layer is also braking off under the lever effect exerted during the

mechanical stresses induced by ice crystals. There is an unplanned variable in this

experiment and that is that this construction is on the side of a hill. Additional and

unplanned mechanical stresses are imposed on this structure due to land slip.


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Fig 22



Severe weathering damage.

At yet another section of the wall the damage is more extensive and the conventional

mortar is damaged to an extent where it has become porous and absorbent to water so

that wetting will increase the rate of degradation of this layer. In the layer below the

spalled brick the DPC layer is in excellent condition with no visible change to the

surface. No change has occurred in this mortar layer over the 31 years of thisexperiment.

We needed to have a comparison between the wetting characteristics of very slightly

positive water pressure exerted on the lower DPC mortar layer and the very slightly

negative water pressure as experienced by the upper DPC layer above the ground

level. On this level of the wall there is a public footpath on the other side of this wall

just below the top DPC mortar layer. Both DPC layers remain unchanged and the

surface of these layers still show tooling marks. The conventional mortar layers have

by this stage become damaged to absorb water.

This experimental condition is of particular interest because the 3 dimensionalPotassium Methysiliconate lattice or mesh formed by the molecule within the

substance of the mortar is said to be ineffective in preventing water transportation

across its lattice in positive pressure gradients. This chemical treatment is

recommended only for negative pressure gradients ie rising damp and is specifically

precluded from use in positive water pressure exposure. The above slight positive

water pressure gradient is clearly not sufficient to allow water to permeate the

substance of the treated mortar so that the water repellent characteristics of the PMS

molecule remain effective in moving water out of its environment. The lower DPC

layer is about 50mm below ground level and the upper DPC layer is about 25mm

above the ground level.


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We do not have any scientifically assessed data on the degree of pressure exerted at

the two layers but simply observations of the practical application of this experimental

setup.

Fig 23

Extreme damage due to weathering.

This section of the build is in structural failure.

Photograph taken 31 years after the build.

The worse effected section of this wall is seen in the above photograph. The twoexperimental mortar layers remain in excellent condition even though extreme

damage is seen in bricks in this part of the structure. There is deep invasive spalling

and damage to the bricks sandwiched between the DPC layers. Interestingly, in sites

where the brick has spalled from the mortar layer the edges of the mortar remain

sharp indicating that the integrity of the mortar substance remains firm and that the

mortar layers have not undergone any change in the strength of the material. In the

centre of this photograph the brick damage is extensive and traverses deep into the

substance of the brick whilst spalled sections of brick that are bonded to the DPC

layer remain bonded to the mortar.

The bond between the DPC mortar and the brick remains strong.

Once the concept of the wetting of materials was acknowledged we looked for

examples of this variable and found many cases of weathering damage all around us.

One of the best was this roofing tile which constitutes the finest experimental

comparison and clearly exemplifies the difference between the areas of materials

exposed to weathering and those protected from it.


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Fig 24

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.

We took this old roofing asbestos tile from one of the contracts we were involved in

and gave it a rough sweep with a wire brush. The exposed area of the tile gave off a

dusty cloud of asbestos released from the degraded portland cementing matrix thatwas used to make these composite manufactured tiles. There were deep gouge marks

in the exposed surface whilst the covered section of the tile barely registered the wire

brush in effect, showing that the cementing matrix was still effective and holding the

composite firmly together. On this side of the tile the normal weathering mechanisms

could not cause damage because wetting was prevented by the overlapping tiles so

that the expanding stresses of the freezing water forming the growing water crystal in

the wetted surface of the tile, could not cause damage to the matrix.

We were embarrassed by such an obvious case in point staring us in the face but this

example was the best of experimental controls possible. This experimental material

was made of the same batch composition, at the same time using the same

methodology and experienced exactly the same conditions during the curing cycle,

storage, handling etc. When placed on the roof the tile was subjected to exactly the

same expansive and contractile stresses and exactly the same temperature changes etc

the only difference being that one half of this product was exposed to wetting and the

wind whilst the other half was protected from the elements by the covering tiles. This

example above all others demonstrated that water was the causative agent in the

destruction of the cementing matrix binding fibre composites.


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Conclusions.

There is fibre fallout in all cement bonded fibre composites.

Straw cellulose fibres in high volumes can be used to make composites bonded with

the Fondu, Calcium Aluminate Cement but the hydrated crystal formed is not stable in

prolonged wet environments. Similar products kept in dry conditions showed no

deterioration during the ten year trials.

A capillary bed model is put forward to explain why only a very small number of

fibres ever plays a part in disease causation, arguing that the world over, all Health

and Safety recommendations to asbestos fibres are arbitrary. There is no safe level to

asbestos exposure.

Industrial interests continue to provide dangerous materials because the profit marginsare high so that for example, there is more asbestos fibre in distribution today than

ever before.

The conventional and the experimental mortars prevented the passage of water across

the mortar layer during the 120 day experimental time scale for the experimental trial.

A 31 year old experiment indicates that a 1:3 conventional mortar absorbs water but

the chemical additive mortar prevents the upward passage of water and surprisingly,

no deterioration in the experimental DPC mortar layer has been observed.

Addition of water repellent additives to cement composites can at least double the

lifespan of such materials.

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