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Health and Safety IssuesRelating to Use of Cement

Cement “Burns”

Branko R Babic53A Middle Way

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Abstract.

Health and safety issues at work continue to achieve a low level of prominence in many sectors of the construction industry and in the UK, every year, there are serious cases of injury by cement. It is estimated that 25% of all work related skin problems worldwide are linked to Portland cement contamination. This paper examines the anatomy and biochemistry of skin and proposes a detailed chemical mechanism by which wet cement interacts with skin layers to cause injury.

Only at high pH, does the cement slurry react with the superficial keratin layer of skin to denature, the highly complex, coiled keratin protein structure. The damage process is progressive and time dependant, in effect liquefying the proteins of the protective stratum corneum to expose the reproductive cell layers to the supersaturated constituents of cement slurries. Cation concentrations are thought to damage repair mechanisms in the reproductive cell layers which replenish and maintain skin integrity. Healing takes a long time, preventing the injured person from returning to work for many months. Prolonged exposure to cement slurries is thought to affect sensory nerves innervating skin so that several hours can pass before awareness of injury become obvious.

Cement burns are easily avoided by observing good practice and current advice by professional bodies with a summary of the damage process is provided, for display on notice boards.

IntroductionDamaging effects of cement in contact with skin were reported as early as 1700 Ramazzini 14 and were attributed to contact dermatitis as late as 1960 6. Subsequent

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analyses of an actual example of a cement burn case, led to the classification of such tissue damage to be specified as a reaction to cement in 1963 51 and further consolidated in the 1970s 63, 1980s 52,53 and 1990s 29,31,32. Surprisingly little attention has been devoted to this subject, given that the damaging effects of wet mortar on skin, must have been known about since Roman times (lime kilns) 12,3. As late as 1988, the UK construction industry and the Health and Safety organisations, specified the condition as a “Concrete Burn” 59.

Since then, it has successfully been argued that as cement was the causative agent of such injury, that the condition should be referred to as a “Cement Burn” 2 and not “Concrete Burn”. All cement products cause damage to skin and literature currently published, refers to the damaging process as a “Cement Burn”.

The cement bonded fiber composite industry, construction industry 10,24,63 cement manufacturing, cement blending facilities and others 17,39,28 continue to report a steady stream of cement burn events. The hospitalised accidents tend to be severe, debilitating and even life threatening, forcing industrial compensation tribunals and the courts to award hefty damages in favor of the injured party. Most countries in the world use millions of tons of cement each year and yet, the number of cement burns reported remains relatively small 54. Little information is available to demonstrate the detailed mechanism by which cement damages skin and in an effort to provide understanding, the enclosed paper proposes a step-by-step mechanism by which skin components are dissolved by the highly alkaline cement solution.

Cement damage to skin starts when the cement slurry interacts with the oily coating covering the superficial layers of skin. The caustic reaction of calcium hydroxide at high pH, strips the skin of its protective oily coating to expose the keratinised layer of the skin epidermis. This layer of dead skin cell debris, is mostly keratin and it is the arrangement of this protein and its various levels of structural complexity that need to be unraveled, in order to understand how the cement solutions causes damage to skin.

In all cases of cement burns, the clear fact that emerges is that damage is seen only after relatively prolonged exposure to the highly alkaline solution and that only cement slurries cause damage to skin. Cement powder in contact with dry skin does not cause cement lesions. From examples of injured workmen, it can be seen that in areas of the body where the epidermis is thick, such as the skin above the kneecap 2,6,14, or the soles of feet, no damage is observed but in areas where thinner less calloused skin comes into contact with the slurry, severe damaged can result. This observation is further consolidated by the rapid and severe damage done to the non-keratinised cell coating of the cornea 38,14,50,65.

The thickness of the keratinised epidermis is therefore relevant, to the severity of damage to skin by cement slurries. Examination of damaged skin in workers who handled wet cement for several hours without protective clothing, demonstrate that provided the stratum corneum remained intact, no lasting injury to skin is seen. Cement burns, only occurs when the protective layer of skin is opened up to allow the caustic elements to come into contact with the live, reproductive layers of skin. The wounding effect takes place at the delicate stratum germinativum, the reproductive layer of the skin. Once destroyed the damaged areas are repaired by the formation of scar tissue.

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This paper considers the histology of the epidermis and the composition of the Portland cement are described in an effort to explain how slurries i.e. solvated cement solutions damage skin. This information is then used to make recommendations regarding ways of minimizing the severity of damage to skin in the working environment. The important findings of this paper include the length of time of contact with cement and the high pH of the slurry solutions which is needed to cause damage to skin. This paper concludes that the terminology of cement burns needs to be reclassified since the process that occurs is not one of “burning” but rather “chemical solvation”.

Histology of the EpidermisA step by step analyses of cement burns requires an understanding of the structure of skin and its chemical make-up. In Fig 1 the various layers that make up skin are demonstrated.

Keratinized Surface Cells

Stratum Corneum Stratum Lucidum Stratum Granulosum Stratum Spinosum

Stratum Germinativum

Dermis Fig 1

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The obvious structure in this cross section of thick skin is the superficial dead cell layer called the Stratum Corneum (SC). This layer of cells is the protective shield that provides the barrier between the external and the internal environment of the living tissues that compose the body. The nature and structure of this layer allows the body to perform all the many activities that an individual undertakes and it is this layer that prevents mechanical damage to living tissues, invasion of microbes, loss of fluids and the many other functions that the SC performs. Lipids are secreted by cells of the epithelium. These glycolipid deposits between the cells form the very important epidermal permeability barrier that helps to make skin water repellant. During all activity, the dead layers of the corneum are continuously shed by abrasive forces, to be replaced by cells from the deeper reproductive layers of the epithelium.

The principal protein of the corneum is keratin, so that the mechanism outlined in this paper will relate to keratin chemistry. Keratin is classified as an insoluble structural protein that on a primary structural level is composed of amide linked amino acids (A-A). These A-A are bonded into long chains via peptide bonds which are formed when an amino group of one A-A, combines to make a covalent chemical bond with the carboxylic group of another A-A, by elimination of water. At one end of this chain of A-A is found an uncoiled length of A-A sequence that is terminated in a carboxylic group, referred to as the tail and at the other, the amino group, referred to as the head of the monomer.

Fig 2

Amino acid sequence of polypeptide primary monomer

The reactive sites of A-A protrude into space in a specific and directional arrangement so that the electrostatic effects of the positive and negative charges interact with other

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groups, to shape the resultant protein into a regular, thermodynamically stable form 1,7,9,54. A single chain of A-A keratin results in a helical form that was researched and its three dimensional structure proposed 47 in the early 1950s. The coiling of the primary protein sequence thus establishes a secondary keratin structure that forms an -helix, which has elastomeric properties and is further stabilised by hydrogen bonds. The regular helical structure is interrupted by non-helical domains, whose function is not as yet clear but recent research suggests that these areas are sites of attachment for other proteins to chemically bond with keratin.

Fig 3

Alpha helix secondary structure of keratinproposed by Pauling and his team. Hydrogen bonds

within the chain give additional support. There are 3.6 residues per turn.

There is to date no clear picture of exactly how the above coiled helixes assemble to form keratin filaments and it may be that the difficulty in unraveling the exact structure, arises because there are different constructional parameters for different A-A sequences. There are about 30 different keratins that are identified to date, the difference arising because of variance in the A-A residues. Secondary structures of keratin are further shaped and formed by forces exerted by adjacent keratin molecules and other proteins that assemble to form a tertiary structure. In addition to keratin, coiled coil structures are well established in nature and are found in a large family of proteins 8,16,28,29,36. Any one given type of epithelial tissue contain more then one type of keratin, the exact composition reflecting the function skin has to perform in any given area of the body.

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Secondary coils interact to form parallel dimers See Fig 4.

Fig 4Parallel dimer coiled coils

The dimmer assemblies interact further to form anti-parallel tetramers that link up along their lengths to form protofilaments. These protofilaments contain long chains of linked monomers that form super helixes 10, along the length of these slow twisting filaments. Along these filaments protrude the heads and tails of the monomer terminal ends to act as bonding sites for the protofilaments.

Fig 5

Protofilaments

Pairs of protofilament structures associate laterally, to form a protofibril.

The component structures of keratin are stabilised by the formation of a multitude of hydrogen bonds that are established between the C=O and N-H groups, protruding into space from the A-A residues assembled in a monomer.

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Fig 6

Schematic representation of hydrogen bonds formed between the negativecharge of the oxygen atoms and the positive charge of the hydrogen atom

on helix strands

Further chemical bonds are formed between the side chain groups (R) 27, the nature of this group being determined by the A-A residue. Covalent chemical bonds are formed across the -helical strands when inter-helix cysteine residues form a sulphur-sulphur (S-S) bond to make inter-helix cystine, see Fig 10. The composited structure is further stabilised by the interaction of the protonated amino group of one helix residue bonding with the de-protonated carboxyl group of an adjacent helix residue, to form an ionic bond. This strong bond, is crucial to the stability of Keratin. Keratin of skin demonstrates parallel coiled coils that are flanked by regions or domains that are not coiled and these regions can be found in subunits of keratin that associate as filaments 13,19,27,42,44,62,70. Such regions are well suited to intermingling and combining with other proteins that may play a part in the complex helical assembly of the cellular cytoskeleton. That keratin interacts with other non keratin proteins is demonstrated by the bond the cytoskeleton makes with the desmosomal proteins.

The three dimensional assembly of keratin tertiary structure, form an intermediate filaments 46. This assembly of monomers is stabilised by ionic, covalent, hydrogen bonds and Wan der Waals forces that establish a thermodynamically stable cylindrical filament, as shown schematically in Fig 7. Four protofibrils associate to make the tertiary cylindrical keratin structure that forms the intermediate filament.

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Fig 7Intermediate keratin filament

Keratin in it’s final form, is an assemblage of super helixes bonded together to form an oligomeric protein complex. This complex quaternary arrangement is demonstrated in Fig 8, which illustrates a number of specially treated epidermal keratinocytes 32,67. These extraordinarily clearly verified quaternary structures of keratin, were demonstrated by Sun et al 57, using very sophisticated immunolocalisation, monoclonal antibody technique. Keratin producing cells can be observed and identified under a light microscope in the stratum spinosum and demonstrate well, the quaternary structure of keratin 66,58,67.

The quaternary arrangement within cells, link desmosomes and plasma membranes to provide the cytoskeleton that supports the cell volume and transmits tensile forces across cells, to the entire epithelial layer. The keratin “scaffolding”, is the structural element in the epidermis that contains mechanical stresses imposed on skin. In the cell cytoplasm, are found soluble keratin stores that can be assembled into the keratin network as prevailing conditions demand. An extremely sophisticated keratin maintenance system appears to exist wherein as the stresses on the keratin cytoskeleton are increased, the cell responds by assimilation of the soluble keratin into the quaternary network, to fortify the structure or conversely, to remove keratin from the structure in positions where it is combined in excess. Although the mechanism of this process is not as yet understood Kinases and Phosphates are identified and are said to provide a rapid mechanism for controlling the assembly state of keratin. Maintenance of keratin in cells is therefore a dynamic business that responds to enduring conditions. The non-helical units of the monomers are well suited to intermingling with chains of the cytoplasmic plaque attachment proteins, to anchor keratin to desmosomes. Keratin is thought to be chemically bonded to the desmosomal structures thus providing continuity of keratin from one cell to another, and in essence, forming a continuous exoskeleton that envelopes the body.

As cells migrate towards the stratum corneum they dehydrate and die, leaving the cytoplasmic keratin and other cell contents sandwiched as debris of dead cells. The surface layers of skin are made up of dead keratinocytes that are termed “squames”. The stratum corneum is thus a layer of dead cells that form a bonded network of cells across the surface of the body. Individual cells migrating to the surface are joined together via desmosomes to provide a continuity of cover to skin. It is this pliable exoskeleton layer that forms the vital “impermeable” barrier between the delicate reproductive living tissues and external elements 18.

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Fig 8

Elaborate quaternary keratin protein network as seen in human epidermal keratinocytes.

Many details of the keratin fine structure remain poorly understood.

Composition of Portland cementPortland cement slurries as found in concrete mixes, screeds, renders, mortars, manufactured products such as building blocks etc are mixtures whose solution has a pH of 12-14 21. This alkalinity is generated by the hydration of cement powder that results in a supersaturated solution of mainly, calcium hydroxide, sodium and potassium hydroxides. The pH is not substantially affected by the variance in composition as found amongst the manufacturers of portland cement so that, the typical composition of portland cement can be tabulated:

% Calcium oxide (CaO) 64.0

Silicon oxide (SiO2) 21.0 Aluminium oxide (Al2O3) 6.0Iron oxide (Fe2O3) 2.8Magnesium oxide (MgO) 2.6Potassium oxide (K2O) 0.9Sulphur oxide (SO3) 2.5Sodium oxide (Na2O) 0.2

Table 1

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Composition of portland cement

Although there has been discussion in the literature 15,20,48,64 about the chemical constituents in cement slurries it is generally accepted that no CaO (free calcium oxide) is present, although, there may be a very small amount (less than 2%), in un-hydrated cement. Most of the CaO is locked up in the complex molecule that is formed when the cement clinker is manufactured by fusing the constituents at temperatures of about 14000C. Calcium Hydroxide (Ca(OH)2) constitutes some 64% of portland cement slurries.

The amount of calcium hydroxide in hardened cement based materials 64 is represented in Table 2. The prospect of being injured by handling manufactured good because of the high alkalinity that remains in set cement, means that manufacturers need to make provisions for protection of the work force handling finished articles. Even after the concrete has set, there is content in the product that can solvate to result in high pH solutions and there are cases in the literature describing injury from handling set portland cement products. A study following admission of two workers to hospital for “dermatitis” 12, turned out to be cement burn injuries caused by caustic factors solvated by rain. By crushing newly manufactured concrete blocks and testing the crushed block material in the laboratory, it was possible using distilled water to elute, a solution of pH 11.2 56.

Ready mix concrete 3.75 Road based concrete 1.25

Floor screeds 5.50 Grouts 12.50

Table 2

Calcium hydroxide % content of set composites

Given the quantities of constituents in cement, the study of the cement burn will discuss the mechanisms involved in the process of denaturation of keratin, in terms of the chemistry of calcium hydroxide and keratin.

The Mechanism of Cement “Burns”The “burning” of skin by cement solutions starts by the saponification reaction between the fatty layers (glycolipids) and the caustic effects of the hydroxyl groups at the high pH of the slurry 40. This aggressive assault on the “epidermal permeability barrier”, damages the forward defences of skin, to initiate a cascade of homeostatic responses that are associated with barrier function. The dead cornified layer of the SC is only considered dead because there are no dividing cells within it but the epithelium is a highly organized, responsive, multi-layered organ. Damage to the barrier initiates a movement of water within the SC which make possible molecular flux, within the space created by the flow. Associated with the water movement is the flow of Ca++ and K+ ions that have an initiating effect, on the complex homeostatic mechanisms of the epithelium.

In particular, the Ca++ and K+ ions are related to the control of the releasing mechanism for fatty content of keratinocytes, located at the SG-SC border and coupled to the repair

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of the barrier, by secreting preformed lamella bodies from the outermost cells of the SG 38,41. Associated with this mechanism is a host of activities that constitutes the homeostatic environment. Such activities controls fatty acids, epidermal cholesterol and sphingolipid synthesis formation 11 and further secretion of nascent lamella bodies 37 , extracellular processing of lipids 22, phospholipids 25, non polar ceramides and increased DNA synthesis 49, to name but a few of the constituents referred to in the literature. As the Ca++ and K+ ions permeate the homeostatic domain of the epidermis, environmental stresses are superimposed on the repair mechanisms that slow down the above processes 38,41,33,34,37. Influx of cement slurry constituents into the epidermal space therefore destroy the permeability barrier and have an extremely dilatory effect on the homeostatic repair response. The shutting down of the repair process results in the multitude of symptoms that are associated with damage to the epithelium.

As the barrier is destroyed and the cement solution permeates the SC, the acid content of t2 8u[he SC is neutralized 45 and the lipid content in the extracellular domains is destroyed, to expose the quaternary structures of the keratin skeleton. The gross keratin structures are linked by chemical bonds that are reactive in an alkali environment. As the hydroxyl ion comes into proximity to the sulphur-sulphur bond the covalent bond is broken to facilitate access of the slurry constituents to the ionic bonds. Here, the hydroxyl ions react to break the ionic bond anchoring quaternary structures. Every reaction opens up the interkeratin space to a further influx of slurry constituents. At every step of the process incursion of water occurs to establish hydrogen bonding to water and thus further weaken the established construction. It is the water carrier that facilitates ingress of slurry constituents and tends to permeate all available space within the SC. The process continues to loosen up the quaternary connections and expose the tertiary keratin assemblies.

The Role of Water in the Mechanism.

Water is essential to the mechanism of the cement burn.

The bonds holding the tertiary “ropes” in skin are broken to release the various assemblies characterising keratin superhelixes. By this stage of degradation severe damage is done to the structure of keratin. The superhelix of the keratin assemblies is damaged by continued attack on the ionic interactions, the S-S cystine bonds and the hydrogen bonds, to break the “rungs” of the superhelixes and release the -helix conformations from the dimer arrangements. Irreversible damage to superficial layers of keratin result. The breakup of the superhelix releases secondary keratin coils, to be further damaged by the influx of the water solvated slurry, by forming hydrogen bonds to water. This preferential energy manoeuvre is thermodynamically driven and results in the denaturation of the keratin molecule. Keratin looses all it’s structural integrity and is easily abraded by mechanical factors.

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Fig 9

Schematic drawing of water breaking the hydrogen bonds holding polypeptide chains together to form hydrogen bonds to water.

The multitude of hydrogen bonds makes an important contribution to the stability of keratin. The bond is electrostatic in nature, in that, the positive charge of the proton of the hydrogen atom is attracted to the unshared electron on the oxygen atom. This electrostatic attraction holds the two charged particles in close proximity to establish a bond across the hydrogen atom.

As the infusing water opens up the inter-keratin structures the hydroxyl groups are able to reach reactive proximity of the protonated amino group of the ionic bond. The proton is removed from the amino group to break this powerful ionic interaction that is crucial to the stability of keratin. Until this bond is broken, no permanent damage can occur to keratin and because of that crucial fact, this reaction is taken as the first step in the process of keratin denaturation. All other reactions to this point are reversible so that as wetted keratin dries out, all the hydrogen bonds between the charged groups are re-established, as are in time, any broken S-S bonds. The breaking of the ionic bond therefore signals the beginning of permanent damage to keratin and occurs only when the pH conditions are severe enough to cause a cement burn.

Acidic and basic residues exist in most A-A and when these polar groups on adjacent A-A come into reactive proximity, ionic bonds are formed. The stronger basic group is the amino group which removes a proton from the carboxylic acid side chain, to form a protonated amino group that is positively charged, leaving an electron rich negatively charged carboxylate site. An ionic bond is formed between these dipolar groups. This bond defines the concentration of hydroxyl ions that is needed to break it and is therefore a limiting factor to reactivity of alkaline solutions with keratin. Unless the concentration of hydroxyl ions is at a high enough level to remove a proton from the protonated amino group, then no permanent damage to keratin proteins occur.

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Braking of inter-chain ionic bonds releases the superhelixes from the cable structures. The proton is removed by the strongly basic action of the hydroxyl ions to form water and the cations in cement solution react with the carboxylate ion to form salts. The superhelix structure is irreversibly damaged.

Fig 10

A schematic representation of the ionic bond between

two side chains of a superhelix

The breaking of the dipolar bond signals the collapse of the keratin structure and opens up the arrangement to further attack. All subsequent reactions take place at a substantially lower pH and proceed unchecked.

Ionic bonds between dipolar groups of amino acids are well understood and require alkali conditions to shift the equilibrium to the right of the equation:

AddAlkali

AddAcid

Fig 11

In titration terms a typical titration curve for a dipolar Amino Acid, in this example Arginine:

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Fig 12

As the stratum corneum is damaged the Sulphur-Sulphur (S-S) bonds are exposed to attack. In this case the reaction is somewhat indirect in its approach, in that the S-S bond is not attacked directly but rather via a distant carbon atom termed the carbon. This carbon atom is part of the backbone of the polypeptide chain but also has attached to it the hydrogen atom that is attacked as the first step in the process. The side chain group R, carrying the sulphur atom that forms the S-S bond with an adjacent cysteine A-A, forms a bond with the -carbon atom of the cysteine molecule. The removal of the hydrogen atom from the -carbon, forces an electron shift that cleaves the bond between the carbon atom and sulphur, to release one polypeptide chain from another. A sulphur atom is subsequently liberated to complete the reaction. See Fig 13.

The S-S covalent chemical bond, forms an important part of the structure of keratin and it is the disulphide bonds of the inter-chain cystine that impart the essential properties to native keratin. Indeed, it is the S-S bond in it’s 3 dimensional physical, stereochemical relationship of the superhelix, that imparts to keratin, it’s insoluble properties and resistance to enzyme hydrolyses.

This electrophilic cleavage is reversible and is extensively used in the cosmetic industry to form “permanent” waves in hair. The keratin structure is further opened up to the influx of the cement slurry component.

After Tarbell and Harnish 1951

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Fig 13

The breaking of the S-S bond occurs via attack on the carbon atom

Continued hydration of the keratin molecule completely solubilises the structure of the damaged stratum corneum which is by this stage of denaturation, soluble proteins. These solvated proteins are easily rubbed off by frictional forces. The damaging process continues to damage the living cell layer, where a permanent wounding effect occurs and continue to full thickness burns when the very important superficial vascular plexus 61 is destroyed. Minimizing disability in such cases may require surgical intervention.

Although histological evidence is vague as to the extent of keratinized protein in skin it nevertheless is clear that keratin as a structural protein, extends well into the stratum spinosum. If desmosomes are directly linked into the intra cellular keratin distribution, them damage to keratin by the above processes, will release whole cell debris into the traumatized area. As no collagen or reticular fibres pass through the stratum germinativum the discussion of high pH damage to skin can be restricted to the reactions of the hydroxyl ions with keratin proteins. Damage to hydrogen bonds, cystine S-S bonds and the dipolar bonds loosens the remaining epidermis to mechanical stresses that rupture the epidermis. All protective functions of the skin are lost.

Discussion.A cement burn is a time dependant process and the length of time it takes for the highly alkaline reactants to cause damage, is long enough to allow most workers to wash off the contamination in between rest periods. In most cases, as the slurry falls onto exposed skin or clothing it dries out so that the water carrier is no longer available to support the reaction mechanism. In all cases, individuals contaminated by cement should be encouraged to remove the contamination at the earliest possible time. Cement damage to skin at this stage does not go on to cause cement burns but damages the epithelial barrier

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to allow drying out of skin. Small cracks and other minor discomfort in the distressed SC does not require hospitalization or treatment by the medical profession and as such, these early stages of cement burns are not reported and therefore are not taken into account when figures for cement burns are compiled 54. It is estimated that 25% of all work related skin problems worldwide are linked to Portland cement contamination 23. When individuals actually present themselves to doctors or hospitals, it remains important to specifically point out to medical staff that they have been in contact with cement because the nature of this condition, is not all that well understood by doctors 14,4,12. Unless the pH of any given slurry is high enough, no progressive, deep dermal, deep partial thickness or full thickness burns occur under conditions similar to those when portland cement is used. The requirement for a pH that is high enough to dissolve the ionic bond, is taken as an indication that this bond is the crucial first step in the denaturation of keratin proteins. All other reactions to that point are reversible. This bond defines the concentration of hydroxyl ions that is needed to break it and is therefore taken as the limiting factor to reactivity, of alkaline solutions with keratin.

No permanent damage is done to the corneum at a pH of 11.5. Experience with Calcium Aluminate Cement (CAC) and more specifically the Ciment Fondu, manufactured by Lafarge Aluminates, which has a pH of about 11.0–11.5 5, demonstrates that progressive, full thickness burns do not occur, when similar conditions to portland cement use are experienced.

Studies in the laboratory show that at a pH of 11-12, keratin at room temperatures (with three dimensional access to reactants) takes about three hours to dissolve in vitro 18. This slow rate of reaction is reflected on site, where individuals contaminated by wet cement continue normal activity for many hours without awareness that they are being damaged 54. It is a surprising fact that no obvious reaction to damage is initiated by the bodies sensory system in these early hours of injury. If for instance an individual is stung by a bee, or comes into contact with a hot surface or any of the many sensory input situations that are met in everyday life, the individual recognizes the signal from this peripheral sensory network and responds accordingly. With cement burns, this is not the case. A workman can be kneeling in wet cement for many hours and only later on, or even during the night or the following day, does the damage done by earlier activities become clear 63.

As there is no evidence of any kind in the literature for the mechanistic processes leading to sensual perception of damaged SC, it is of considerable interest to speculate on the mechanism by which cement slurry damages tissues without causing pain. Clearly, the sensory pain input from the peripheral nervous tissues is absent and as there is no reference on this topic, one might suggest that given that pain becomes apparent within hours of exposure to the wet cement, that the absence of nervous response is due to a block in nerve activity. In this case anesthetic effects are envisaged, wherein an osmotic imbalance occurs, preventing neuronal ion exchange in axonal membranes.

Cement slurries are supersaturated solutions of Na, K, Ca, OH, and other ions which if present in the proximity of axons would create a severe imbalance between the inner and outer concentrations of Na and K ions so that the mechanisms controlling the exchange of these ions across the bilipid axonal layers, becomes ineffective, due to excessive concentration gradients. No nerve impulse is propagated under such circumstances

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Similarly, as water is the essential carrier for all cellular processes than any significant variation in the water content of nerves, must have an effect on the conduct of intra-cellular transport mechanisms. Given the excess concentrations of the ions in the slurry, the water equilibrium in the exposed tissues must be severely disrupted. Further, given that neuropeptides are linked by sulphur to sulphur bonds than the already described mechanism for the time dependent permanent damage to the sulphur bonds, would be relevant in disrupting the peptide structure of neurons. Such changes would explain long term sensory loss of the damaged nerve tissues.

Other possibilities exist namely, that the innervation of the epidermis is by non pain sensory nerve fibres that are associated to biosensor functions wherein, the terminal endings seen in the stratum corneum are associated with the sensory network that is related to the mechanical stresses and strains imposed on the SC. It is obvious that the stratum corneum on the palms of manual workers hands is substantially thicker than that of office workers and that stressed areas of skin develop calluses and as an example only, floor tillers who spend a great deal of their time on their knees, develop thick SC over their kneecaps. The mechanism which precipitates keratin proteins in cells must have a mechanical component because the keratin network linked via desmosomal proteins interacts to essentially contain the body contents within the keratin “exoskeleton” so formed, see Fig 8, and would need to have a sensory mechanism to consolidate areas of skin that were subject to additional stresses.

Extensive scar tissue is always formed in such damage and it is impossible to test the hypotheses without sophisticated facilities and expertise in neurophysiology.

Mechanical stress and abrasive factors should be reduced when dealing with exposure to high pH solutions and in particular when treating damaged areas of skin. No information is available from the medical profession, on the effect of mechanical stresses relating to scar development in patients with cement burns.

In hospitalized cases it is reported that wounded areas weep serum, the patient is in considerable discomfort and pain and in much need of medical attention. This condition persists for many days and worsens with time. The progressive nature of damage is not understood but the continuity of injury would suggest that the offending constituents are not being removed from injured tissues by current treatment plans. If the hydroxyl ions were the only factor in the equation it would be expected that in the presence of so much fluid flux, the considerable buffering capacity of serum, would negate the effect of the alkaline solution but in practice, the body is clearly not able to cope with the assault. When the slurry contents reach living tissue, many complex reactions occur by a variety of mechanisms including reduction, oxidation, salt formations, corrosion, protoplasmic poisoning, metabolic competition, competitive inhibition, desiccation and the like.

No papers are available to demonstrate the outcome of encapsulating wounded areas with acidic pH buffered solutions that would leach out any hydroxyl contaminants from damaged tissues. Recent work demonstrates that acidic environments are useful to the repair of SC permeability barrier 40. Further research is needed to establish the consequence of contaminating living tissues with supersaturated cation concentrations found in cement slurry solutions. Damaged skin eventually heals, with the formation of at times, extensive scar tissue that may require surgical intervention. Skin grafting is not uncommon in such cases.

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All cement products cause damage to skin and literature currently being published, refer to the damaging process as a “Cement Burn”. We propose that the terminology used to describe injury caused by supersaturated high pH cement slurries should be re-classified as ‘chemical solvation’ rather than ‘burn’. The Oxford English Dictionary refers to a “Burn”, as a state of combustion, to be on fire, to be enveloped in flames, a process giving off a great deal of heat energy, a state of oxidation etc. The chemical reactions occurring in the cement burn, are not entirely oxidative so do not qualify as a burn process. Even on oxidative grounds, the action of cement slurries on skin is not a burn because temperature related damage, coagulate proteins whereas the chemical attack of cement constituents, liquefy tissue. Cases of cement burns in the conventional “burn” terminology, have been reported 26,60,68,69,43,65 and may make a useful contribution to the discussion on the terminology of cement injury.

Good practice is the key to minimizing injuries when handling cement containing products. Cement burns are easily avoidable by wearing proper, impermeable, clothing as a barrier to wet cement. Washing off any slurry contamination sooner rather than later, with copious quantities of clean water, prevents severe damage that can result. No lasting damage to skin occurs unless the caustic solution achieves access to the reproductive layer of the epidermis. Access to this layer is enhanced by abrasive mechanical forces and prolonged exposure to highly alkaline solutions. Clear warning and advice on all cement packaging is essential not only because most of the severe cases are seen amongst the inexperienced, occasional users of cement. With this in mind, the latest Health and Safety advice Relating to Use of Cement from the UK Workers Union is attached, as is a Brief Description of Cement Burns; for display in the work place.

SummaryA BRIEF DISCREPTION OF

CEMENT BURNS

Health & Safety IssuesRelating to Use of Cement

“Cement Burn”

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Abstract for the Workplace

Health and safety issues at work continue to achieve a low level of prominence in many sectors of the construction industry and in the UK, every year, there are serious cases of injury by cement. The anatomy and biochemistry of skin are considered in an effort to presents a detailed chemical mechanism by which wet cement interacts with skin layers, to cause injury.

Only at high pH, does the cement slurry react with the superficial layer of skin to denature, the highly complex, coiled keratin protein structure. By solubelizing this protective layer and exposing the deeper delicate, reproductive layers that replenish and maintain the skin integrity, severe and debilitating injuries can result that may require plastic surgery. Several hours can pass before any signs of injury become obvious. “Cement Burns” are only reported to doctors and hospitals when sever damage occurs. Most minor cases never come to light so that the number of burn cases appears small, when correlated to the millions of tons of cement used. Wet cement slurries come into contact with skin and the abrasive forces between the aggregates, clothing and the superficial layers of skin cause deep, debilitating injuries, that may take weeks to heal and prevent the injured individual from returning to work for several months. Most of the damage occurs in areas of the body directly exposed to wet cement so that hands, knees, the lower leg and feet injuries are seen most often:

Fig 1. Demonstrating the sort of damage seen when wet cement flows over the top of the boot or wellington. NB. The superficial areas of skin are dissolved where mechanical stress occurs between cement slurry and skin.

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Keretinized Surface Cell (KSC) Stratum Corneum (SC)Stratum Lucidum (SL) Stratum Granulosum (SG) Stratum Spinosum (SS)Stratum Germinativum (SGr) Dermis (D)

KSC

SC

SL

SG

SS

SGr

D

OH+

Cystine covalent sulphur-sulphur bond reduced by the hydroxyl attack to further denature thekeratin protein.

H O

H

Hydrogen bonds to water form extensively throughout the entire structure of keratin.In the final stage of solvation keratin loses most of its characteristics

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Ingress of the highly alkaline water solvated components of the cement slurry permeate the Stratum Corneum. At a pH of about 11, the destruction of the ionic bonds commences the breakdown of the keratin structure to dissolve the bonds that hold the quaternary structures in place and thereby release the tertiary protein conformations. In all cases, the ionic bonds must be broken down before the secondary reactions can take place so that only at the high pH of about 13, does serious damage to skin occur. The reduction of the disulphide cystine bonds, is a slow process that can occur at a pH of about 9. As these primary reactions go to completion, water molecules infuse the keratin inter-space to form hydrogen bond to water and occupy the multitude of hydrogen bonding sites. Every reaction, weakens the corneum. The cement slurry continues to break down the ionic, sulphur to sulphur and hydrogen bonds, destroying the tertiary structure of keratin. Hydration of the secondary structure completely denature the conformation of the protein and keratin loses all its structural properties. Mechanical forces rub off detritus to expose the delicate reproductive cells of the stratum germinativum. Extensive permanent damage can be caused to this unprotected layer of living cells that regenerate skin and lead to permanent damage.

Union Information

HEALTH & SAFETY ISSUESRELATING TO USE OF CEMENT

Summary

CONCRETE BURNS

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