© 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 StrawCrete composite building block

block also grew fungal growth. Fungal growths (Peziza Genus)
Fungal growths (Peziza Genus)
Fig 5
Fig 4
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 5mm-
0mm) 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 1 presents their
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

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. Silicone resins

2. Fluoropolymers

3. Lignosulphates and sterates

4. Soaps and fatty acid composites

5. Acrylic preparations

6. Colloid silicates

7. Styrene Butadiene Rubbers

8. Oil based emulsions

9. 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. The many SBR formulations as provided by for example, FOSROC UK.

8. Linseed oil composites.

9. 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 micro-
anatomical 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.

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