What is kaolin
Kaolin is also called bentone, China clay, porcelain clay or white bole, is a mixture of different minerals. The name “kaolin” is derived from the word Kau-Ling, or high ridge, the name given to a hill near Jau-chau Fu, China, where kaolin was first mined 1). Kaolin, commonly referred to as China clay, is a clay that contains 10–95% of the mineral kaolinite and usually consists mainly of kaolinite (85–95%). In addition to kaolinite, kaolin usually contains quartz and mica and also, less frequently, feldspar, illite, montmorillonite, ilmenite, anastase, haematite, bauxite, zircon, rutile, kyanite, silliminate, graphite, attapulgite, and halloysite 2). The structure of kaolinite is a tetrahedral silica sheet alternating with an octahedral alumina sheet. Kaolinite, the main constituent of kaolin, is formed by rock weathering. It is white, greyish-white, or slightly colored. It is made up of tiny, thin, pseudohexagonal, flexible sheets of triclinic crystal with a diameter of 0.2–12 µm. It has a density of 2.1–2.6 g/cm³. Kaolinite adsorbs small molecular substances such as lecithin, quinoline, paraquat, and diquat, but also proteins, polyacrylonitrile, bacteria, and viruses 3).
Kaolin is used in paper production, in paints, rubber, plastic, ceramic, chemical, pharmaceutical and cosmetic industries 4). Some clays used for purposes similar to those for which kaolin is used may contain substantial amounts of quartz: “kaolin-like” clays used in South African pottery contained 23–58% quartz and, as the other major constituent, 20–36% kaolinite 5).
Kaolin is a natural component in soil and found in ambient air. Kaolin and other clays are natural components of the soil and occur widely in ambient air as floating dust. Accordingly, exposure of the general population to them must be universal, albeit at low concentrations. In the vicinity of mines and industrial projects, kaolinite is likely to be present at high concentrations in air; however, no data are available. Stobbe et al. 6) analysed mine dusts of West Virginia, USA. Respirable dust samples collected in three locations in the mines contained 64% illite, 21% calcite, 8.5% kaolinite, and 6.7% quartz on average. Kaolin mining and refining involve considerable exposure and significant exposure is expected in paper, rubber and plastics production 7). Long term exposure to kaolin causes the development of radiologically diagnosed pneumoconiosis known as kaolinosis in an exposure related fashion 8). Occupationally inhaled kaolin produced chronic pulmonary fibrosis. Reduced lung function and related symptoms been reported. Kaolin contains quartz and exposure to quartz is casually related to silicosis and lung cancer 9). Significant increases in the incidence of mortality from chronic bronchitis and pulmonary emphysema have been reported after exposure to quartz 10).
No report on local or systemic adverse effects has been identified from the extensive use of kaolin in cosmetics.
A study reported in detail on six workers who had been working in the drying and bagging of kaolin from Cornwall mines, in England 11). Medical and radiological examinations /were performed/ of those occupationally exposed to kaolin. All had radiological pneumoconiosis, and two were further studied in autopsy. In one case, characteristic silicotic-type nodulation together with progressive tuberculosis were found. Large quantities of kaolinite and amorphous quartz were found in the lung. In another case, large quantities of pure kaolinite (as much as 20-40 g) were found in the lung without tuberculosis but with severe fibrosis. The disease was like the pneumoconiosis of coal miners and differed from classic silicosis. In the upper part of the lung, greyish or blue-greyish massive confluent lesions were described, which were not as hard on palpation as the silicotic conglomerates.
In animal studies, Kaolin instilled intratracheally (into the trachea) produces storage foci, foreign body reaction and diffuse exudative reaction. After high doses of kaolin containing 8-65% quartz, fibrosis was noted. Kaolin has a low toxicity to aquatic species. Intratracheal instillation of kaolin to a guinea pig, stopped lung collagen production after a long exposure period. Nonsignificant LDH, protein or phospholipid leakage to the supernatant fraction observed in bronchioalveolar fluid 15-60 days after intratracheal instillation of kaolin in rats. Rats given ip administration of kaolin developed after 1-3 months reticulin fibers. Kaolin intratracheal administration has provided data indicating rats and guinea pigs were more susceptible to bacterial infections.
Kaolin and Pectin
Pectin is a complex polysaccharide found in the cell walls of a variety of vegetables and fruits, which is mainly composed of d-galacturonic acid (GalA) with α-(1-4) glycosidic linkages 12). Pectin is a structurally complex polymer with at least 17 different monosaccharides interconnected through more than 20 different linkages 13). Pectin exists particularly in the middle lamella and the primary cell walls of dicotyledonous plants, where it plays a fundamental role in cell growth 14), mechanical strength 15) and defence mechanisms 16). In industrial extraction processes pectin is mainly derived from citrus peel.
Pectin is used as a gelling, thickening and emulsifying agent in a wide range of applications, from food to pharmaceutical products 17). Pectin is also used as a complex dietary fiber and a prebiotic 18). Pectin when eaten is completely degraded by the gut microbiota at 6, 12, and 18 hours, and Lachnospira and Faecalibacterium, which can utilize pectin, were increased. Pectin-induced changes in the gut microbiota increased the formation of associated short chain fatty acids from 6 hours on, when pectin was decomposed.
Current industrial pectin extraction processes are based on fruit peel, a waste product from the juicing industry, in which thousands of tons of citrus (orange, lemon and lime) are processed worldwide every year. As a pre-treatment before pectin extraction, washing and drying of the peel provides necessary preservation for storage and/or transport. Afterwards, commercial pectin is extracted at high temperature by acid hydrolysis. The final product has a wide range of applications related to its 1,4-linked-α-d-galacturonic acid and neutral sugar content, the degree and pattern of methylesterification, molecular weight and intrinsic viscosity. The length of homogalacturonan and the proportions of homogalacturonan, Rhamnogalacturonan I and Rhamnogalacturonan II in the molecule may also influence pectin properties 19).
Kaolin and pectin preparations have essentially no adverse effects 20). Constipation may occur but is usually mild and transient; however, constipation may rarely lead to fecal impaction, especially in infants or debilitated geriatric patients.
Use of kaolin dates back to the third century BC in China. Today it is mined and used in significant quantities for numerous industrial uses. Its most important use is in paper production, where it is used as a coating material. In addition, it is used in great quantities in the paint, rubber, plastic, ceramic, chemical, pharmaceutical, and cosmetics industries.
Kaolin is an important industrial mineral that has an enormous variety of uses. Uses of kaolin mined in the USA for the years 1995, 1999, and 2002 are summarized in Table 1.
Use of kaolin as a coating for paper accounted for almost half of the total domestic consumption and for roughly 80% of the exported kaolin. Widespread use of kaolin-coated papers in the manufacture of cigarettes 21) may expose smokers to kaolinite particles by inhalation. Other important uses of kaolin were as a filler in the production of paint, paper, and rubber, as a component of fibreglass and mineral wool, as a landfill liner, and as a catalyst in oil and gas refining. The usage historically associated with kaolin, manufacture of porcelain and chinaware, accounted for less than 1% of the domestic consumption in the USA. In China, 80–85% of the total production in 2003 was used for ceramics, 5% for paper, 3% for rubber, and 2% for paint. In India, 290 000 tonnes were used for ceramics, 84 000 tonnes for paints, 68 000 tonnes for paper/paperboard, 29 000 tonnes for detergents, and 27 500 tonnes for rubber 22).
Kaolinite has a number of properties relevant to medicine. It is an excellent adsorbent and will adsorb not only lipids and proteins 23) but also viruses and bacteria 24). Kaolinite can be used to induce aggregation of platelets 25), to initiate coagulation of plasma by activation of factor XII 26), and to remove non-specific hemaglutinin inhibitors from serum 27). Kaolin is used in medical therapy as a local and gastrointestinal adsorbent (Kaopectate, bolus alba).
Table 1. Kaolin sold or used by producers in the USA, by use
|Use||Amount sold or used (kilotonnes)b,c|
|– Catalyst (oil and gas refining)||93.2||208||210|
|– Electrical porcelain||7.6||12.7||8.3|
|– Fine china and dinnerware||26.4||23.5||27.4|
|– Floor and wall tile||38.3||39.8||63.1|
|– Roofing granules||24.9||43.2||36.5|
|– Sanitary ware||67.9||75.6||85.2|
|Fibreglass, mineral wool||402||329||288|
|Fillers, extenders, binders|
|– Medical, pharmaceutical, cosmetic||W||W||0.754|
|– Paper coating||2800||3000||2540|
|– Paper filling||853||791||450|
|Heavy clay products|
|– Brick, common and face||230||126||70.9|
|– Portland cement||W||54.2||W|
|– Firebrick, block and shapes||26.8||13.8|
|– Grogs and calcines||190||135|
|– High-alumina brick and specialties, kiln furniture||885||W|
|– Foundry sand, mortar, cement, miscellaneous refractories||145||621|
b: Data are rounded to no more than three significant digits and may not add to the totals shown.
c: W = Withheld to avoid disclosing company proprietary data; included with “Miscellaneous” or “Miscellaneous applications.”
d: Includes firebrick (blocks and shapes), grogs and calcines, high-alumina brick and specialties, kiln furniture, and miscellaneous refractories.
e: Includes 145 000 tonnes of foundry sand, mortar, cement, and miscellaneous refractories in 1995.[Source 28)]
Kaolin for skin and cosmetics
Kaolin is used in a large number of different cosmetic products, such as eyeshadows, blushers, face powders, “powders,” mascaras, foundations, makeup bases, and others. In 1998, kaolin was reported to be used in 509 different cosmetics in the USA, usually at concentrations between 5% and 30%, but reaching 84% in some paste masks 29). Medical, pharmaceutical, and cosmetic uses, however, accounted for roughly 0.01% of the total US consumption of kaolin (see Table 1).
Kaolin effects on laboratory mammals and in vitro tests
In the landmark paper in which intratracheal instillation as a means of studying the effects of dust on lungs was described, no collagen production was detected in the lung of a guinea-pig 336 days after the administration (whereas fibrosis was observed after similar injection of quartz) 30). Similarly, intratracheal instillation of kaolin from South Wales or untreated or ignited Cornish kaolin did not induce fibrosis in rats 31) (see Table 2).
After the instillation of a single dose of commercial acid-washed kaolin containing 8% hydrated free silica and 12% mica, grade 2–3 fibrosis was observed in rats after 8 months (grade 1 = minimal reticulin fibrosis, grade 4 = maximal fibrosis, as induced by quartz) 32) (Table 2).
Following intratracheal dust treatment in rats, the histological reaction was found to depend on the composition of the dust 33). Foreign body reaction as an effect of kaolinite was observed in all cases where the crystalline quartz content of the dust was less than or equal to 30%. The sample containing 65% quartz and 35% kaolinite caused progressive fibrosis. In addition to the composition, particle size also played a role in the development of the tissue reaction. Kaolin samples containing particles less than 2 µm caused storage foci 34), while the kaolin samples containing bigger particles (particle size between 2 and 5 µm) caused mainly storage foci but also, to a smaller extent, foreign body reaction (Table 2).
Goldstein & Rendall 35) observed cellular reaction with minimal fibrosis: some loose reticulin with either no collagen in some animals or a few collagen fibres in other rats 4 months after an intratracheal instillation of kaolin (Table 2).
Martin et al. 36) observed an increase in the collagen content in the lungs of rats 3 months after an intratracheal instillation of non-specified kaolin; the reaction was considerably weaker than after a similar treatment with quartz (Table 2).
Sahu et al. 37) described the development of grade 2 fibrosis in mice after 7 months of exposure to non-specified kaolin (Table 2).
Rosmanith et al. 38) compared the fibrogenicity of four kaolinite samples with that of quartz in rats using intratracheal instillation. The fibrogenicity of kaolinites, as measured by the increase in hydroxyproline content in relation to the amount of dust retained, was approximately 1/10 that of quartz, but the inflammatory reaction was considerably less (Table 2).
No significant LDH, protein, or phospholipid leakage to the supernate fraction was observed in bronchoalveolar fluid 15–60 days after an intratracheal instillation of kaolin to rats. In this system, effects of quartz became apparent towards the end of the observation period 39) (Table 2).
Table 2. Effects of intratracheal instillation of kaolin and illite on the respiratory tract
|Species/gendera / number||Treatment||Findings|
|Guinea-pig /2||Intratracheal instillation of an unstated amount of kaolin, follow-up for 14 and 336 days||No collagen production in 336 days; in animals treated similarly with quartz, fibrosis observed.|
|Rat/12||Intratracheal instillation of a single dose of commercial acid-washed kaolin containing 8% hydrated free silica and 12% mica; two animals killed between days 3 and 6; the rest kept for life (up until 8 months)||Grade 2-3 fibrosis observed in rats after 8 months (grade 1 = minimal reticulin fibrosis, 4 = maximal fibrosis, as induced by quartz).|
|Rat / 6 or 10 per group||A single intratracheal instillation (50-60 mg) of washed South Wales kaolin, untreated Cornish kaolin, ignited Cornish kaolin, quartz; follow-up up to 6 months||South Wales kaolin (10 rats): Up to 60 days, no fibrous reaction; thereafter, local reticulinosis, no fibrosis or emphysema.|
|Cornish kaolin (10): Eight animals died within 10 days; the remaining two showed no fibrous reaction.|
|Ignited Cornish kaolin (6): Only four rats available for study; their survival was 14, 28, 73, and 140 days; in the last-mentioned, there was local reticulinosis.|
|Quartz (6): Severe nodular silicosis in all five animals available for study; survival 68, 121, 130, 207, and 240 days.|
|Rat||Intratracheal administration of kaolin, kaolin baked for 1 h at 900 or 1200 °C||Active phagocytosis, local storage of the dust without reticular fibres, and nodules were observed. In the case of heat-treated kaolin samples, the reaction was somewhat stronger, although fibrosis reached grade 1 in only a few cases (Belt-King scale). Histological signs resembling silicosis did not develop.|
|Rat / 25 per group||A single intratracheal administration of kaolin containing kaolinite and quartz in ratios 82/18, 70/30, or 35/65; follow-up to 1 year||Foreign body reaction with the two samples containing 82 or 70% kaolinite, productive fibrosis with the sample containing 65% quartz.|
|Rat/10-15 per group||Single intratracheal instillation of kaolin (sericite and quartz as main impurities, 1 % quartz), particle size <5 µm; histological analysis of lungs after 4 months||Cellular lesions, some loose reticulin, with either no collagen or a few collagen fibres.|
|Rat/10 per group||Intratracheal instillation of 50 mg non-specified kaolin, 3-month follow-up||Amount of collagen / amount of dust in lung after kaolin exposure 3 times higher than in titanium dioxide-treated control and 2.4 times more than in coal-treated animals, but only 15% of that in the quartz-treated animals.|
|Rat, strain not specified / number and gender not specified||40 mg of illite clay F, nominal composition 100% illite (diameter <2 or 2-5 µm), kaolin S (82% kaolinite, 18% quartz; diameter <3 µm), or kaolin Sz (95% kaolinite, 5% quartz; diameter <2 or 2-5 µm), instilled to rats; animals killed after 5, 15, 40, and 365 days and histological analysis performed||Illite F and kaolin Sz <2 µm caused “storage foci,” kaolin S, “foreign body” reaction, and kaolin Sz 2-5 µm, mainly storage foci, rarely foreign body reaction.|
|Rat, strain not specified /10||60 mg of illite (not described) instilled intratracheally and followed for 6 months; lung weight, lipid, phospholipid, and hydroxyproline were analysed, and histological and histochemical studies on collagen performed||“Storage foci” observed in lungs of illite-treated rats.|
|Rat, Sprague-Dawley / female /10 per group||30 or 50b mg non-specified kaolin or illite clay injected intratracheally, followed for 3 and 12 months||Kaolin increased the lung weight 9 and 4 mg and collagen formed <26 and <7 mg/mg of injected dust at 3 and 12 months (all normalized to quartz = 100).|
|Illite clay induced alveolar proteinosis and thus increased the lung weight 17 and 6 mg, and collagen formed <26 and 11 mg/mg of injected dust at 3 and 12 months (all normalized to quartz = 100).|
|Rat, Sprague-Dawley / female /10 per group||30 or 50b mg non-specified kaolin or illite clay injected intratracheally, followed for 3 and 12 months||Correlation to haemolysis (rat erythrocytes) and release of LDHc and alkaline phosphatase from rabbit alveolar macrophages (see Table 17) weak.|
|Rat, Fischer F344 / 10 per group||5 mg kaolin (non-specified), MMADd 2.1 µm, instilled intratracheally, killed 1 day, 3 days, 7 days, 3 months, and 6 months later||Acute inflammatory reaction on day 1; thereafter, a slight interstitial cell thickening. At 3 and 6 months, lungs were normal.|
|Rat / male / 5 per group||Intratracheal injection of 10 mg of a kaolin containing 67% kaolinite and 23% quartz; bronchopulmonary lavage after 15 days, LDH activity and protein content and, after 15, 30, and 60 days, phospholipid content of supernatant measured||Kaolin did not induce significant LDH, protein, or phospholipid leakage to the supernate fraction. No change in the LDH or protein leakage was observed after similar exposure to eight other minerals, including two quartz samples. The quartz samples, however, increased the phospholipid content at 30 and 60 days.|
|Rat, SD/male||Intratracheal injection of 10 mg of a kaolin containing 86% kaolinite, 4% quartz, 5% illite, and 5% amorphous silica; bronchopulmonary lavage after 14, 30, and 90 days, number of cells, activities, LDH activity, protein and phospholipid content of supernatant measured||Kaolinite caused a statistically significant increase in the protein content at 14 days, which returned to control level thereafter. No changes were observed in the other parameters studied.|
|Mouse / 70 per group||Intratracheal instillation of 5 mg of kaolin, 91% >3.62 µm in diameter; follow-up 210 days||Fibroblast reaction from 60 days post-exposure, prominent from day 120. Grade 2 fibrosis by day 210 (Belt-King scale).|
|Rat, Wistar/female/ 20 per group||Kaolinite 1 (K1) contained 2% muscovite; K2, 1% quartz and 9% muscovite; K3, <1% quartz and anatase and 1 % muscovite; and K4, 1 % quartz and anatase and 2% muscovite; mean value for volume distribution was 3.6 and 2.6 µm for K3 and K4, not analysed for K1 or K2; instilled once intratracheally at 50 mg/kg of body weight; autopsy after 7 months; lung weight, histology, amount of dust, hydroxyproline, and total lipid content analysed; two samples of quartz also investigated, dose given 5 mg/kg of body weight||All kaolinite samples fibrogenic. Absolute amount of hydroxyproline roughly similar after exposure to kaolinites and quartz, hydroxyproline / retained dust in kaolinite-treated animals 1/10 that in quartz-treated animals. Absolute increase of lung weight one-sixth and of total lipids roughly 10% of that in quartz-treated animals.|
|Rats, SD(SD)BR/ male / 6 per group||Exposed by intratracheal instillation to 50 mg dust from the town Mexicali (see above), mean diameter 3.2 µm; lung analysis after 30 days||Multifocal interstitial lung disease. Mononuclear cell accumulation and presence of collagen fibres.|
a Where available.
b Composition or particle size not given.
c LDH = lactate dehydrogenase.
d MMAD = mass median aerodynamic diameter.[Source 40)]
Table 3. Toxicity of kaolin and illite clay in vitro
|System / species / gender||Dose (mg/ml)/ treatmenta||Findingsa|
|Rat (Sprague-Dawley CFY)||Two types of kaolin (90% kaolinite, 4% quartz; or 93% kaolinite, 4% quartz; diameter not given) incubated with cells for 24 h either as such or after dry milling for 32 h||Dry milling decreased the methylene blue adsorption to a third and the inhibition of TTC reduction by one-half to two-thirds.|
|Mouse (Swiss T.O.)||Kaolin (non-specified), 100 µg/ml, incubation for 18 h||Approximately 25% release of LDH and beta-glucuronidase release with native kaolin; one-half to two-thirds of the activity lost upon calcination.|
|Rat (Sprague-Dawley CFY), male||Six different kaolins, kaolinite content 51-95%, quartz content 5-20%; 1.0 mg/ml (<5 µm diameter, median 1-2 µm) incubated in cell suspension for 1 h||All samples considered cytotoxic based on TTC reduction, except one (30%), which had 71% kaolinite and 22% quartz. All considered inert based on small LDH release, except the one with the highest quartz concentration (29%); the kaolinite concentration in this specimen was 67%.|
|One sample of an illite clay (28% illite, 28% quartz); 1.0 mg/ml (<5 µm diameter, median 1-2 µm) incubated in cell suspension for 1 h||Cytotoxic based on TTC reduction, but not cytotoxic based on small LDH release.|
|Rat (Sprague-Dawley CFY), male||Four different kaolins (from Hungary, silica content 4, 5, 18, and 30%, <5 µm diameter, otherwise not specified) incubated in cell suspension for 24 h; similar experiment with a non-specified illite clay||Three out of four kaolins and illite considered cytotoxic based on TTC reduction; no relationship between quartz concentration and cytotoxicity. The clays studied did not induce release of LDH, but illite decreased intracellular LDH activity.|
|Mouse (T.O.), female||Culture of unstimulated macrophages with Cornwall kaolinite (not specified) for 18 h||Kaolinite induced LDH release from macrophages; this was prevented by polyvinylpyridine-N-oxide.|
|Mouse (T.O.), female||Cornwall kaolin (98% kaolinite, 2% mica), 98% <5 µm in diameter, incubated with cells at 40 µg/ml for 18 h||Kaolinite induced a 70% LDH release to the medium; the release was partly prevented by treatment of kaolin with polyvinylpyridine-N-oxide and fully prevented by additional treatment with polyacrylicacid.|
|Rat (Wistar, SPF), both sexes||Kaolin (composition not specified, diameter 0.2-25 µm), 0.5 mg/106 cells incubated for 2h||Of all cells with particles, 0.6% and 1.6% dead cells with particles at 1 and 2 h (lowest toxicity group of three).|
|Mouse||Fifteen respirable dust samples from kaolin drying and calcining plants in England (kaolinite content 84-96%, mica 3-6%, quartz 1 %, feldspar 0-7%), a sample of Cornish kaolin (K1, 98% kaolinite, no quartz or feldspar, 2% mica), and a sample of Georgia kaolin (K2, 99% kaolinite, no quartz, mica, or feldspar, and reference quartz DQ12, mica, gibbsite, and titanium dioxide as controls; incubation for 18 h with macrophages, LDH release measured||All dust samples were cytotoxic. The quartz content could not explain the cytotoxicity. The kaolinite samples showed a dose-dependent cytotoxicity, which could not be explained by their content of ancillary materials.|
|Polyacrylic acid treatment of kaolin has only a small effect on its cytotoxicity, indicating that the positive charge at the edge of the mineral (blocked by acrylic acid) is not a major determinant of the toxicity.|
|Rat (Wistar, SPF), both sexes||Kaolin (composition not specified, diameter 0.2-25 µm), 0.5 mg/106 cells incubated for 2h||Of all cells with particles, 3.7% and 4.2% dead cells with particles at 1 and 2 h (lowest toxicity group of three).|
|Rabbit (New Zealand)||Kaolinite (>99% pure), >99% respirable size, incubated with cells at 0.25-2.5 mg/ml||Kaolinite caused an inhibition of amino acid incorporation into protein in a dose-dependent manner, 65% inhibition at 1 mg/ml. Inhibition reversed by addition of serum.|
|Guinea-pig||Kaolin (non-specified), 100 µg/ml, incubation for 18 h||Approximately 30% release of LDH and beta-glucuronidase release with native kaolin; >90% of the activity lost upon calcination.|
|Rabbit (New Zealand)||Kaolin (unspecified) and illite clay (unspecified) (<5 µm diameter), 0.5 mg/ml incubated in cell suspension for 24 h||Kaolin induced a 15.3% release of LDH and a 7% release of alkaline phosphatase.|
Illite clay induced a 2% release of LDH and a 1.3% release of alkaline phosphatase. For quartz, the figures were 51 % and 16%.
|Rat (Sprague-Dawley), male||Georgia kaolin (>96% kaolinite, no quartz, >95% >5 µm in diameter), incubated with cells for 1 h at 0.1-1 mg/litre||Kaolin induced a dose-dependent release of LDH, beta-glucuronidase, and beta–N-acetylglucosaminidase of 60-80%. The effect was largely (9-15% release) abolished by lecithin.|
|Rat (strain not specified)||Kaolin, 1.0 mg/ml (<5 µm diameter, MMAD 2.1 µm) incubated in cell suspension for 2 h||Kaolin induced an 80% release of LDH and a 60% release of beta-glucuronidase and beta–N-acetylglucosaminidase, being most cytotoxic of all minerals studied, quartz included.|
|Rat (Wistar), male||Alveolar macrophages incubated with Mexicali dust (see Table 13); LDH release measured||Concentration- and time-dependent release of LDH, which reacted 50% at 0.5 mg/ml and was much more pronounced than with quartz.|
|Human phagocytic cells from one donor||Well crystallized standard kaolinite KGa-1, no quartz, cristobalite, or mica, particle size 3.2 µm median volume diameter||Kaolinite at concentrations of approximately 1 mg/ml induced luminol-dependent chemilumi-nescence as an expression of generation of reactive oxygen species in both monocytes and neutrophils when opsonized and when not opsonized.|
|Human washed erythrocytes||Erythrocytes incubated with Hungarian water-cleaned kaolin (composition not indicated; <5 µm in diameter), as such or after heat treatment at 290-900 °C for 90 min||Kaolin was strongly haemolytic; heating for 90 min to 200 or 350 °C increased, but heating to 500 or 650 °C practically abolished, the haemolytic potency. Kaolin heated at 800 or 950 °C was at least as potent a haemolyser as non-treated kaolin.|
|Sheep, plasma-free erythrocytes||Kaolin (source and composition unspecified), <5 µm in diameter, incubated with cells at 1 mg/ml for 2 h||Kaolin caused 40% haemolysis; acid and alkali treatments of the clay decreased its haemolytic potency.|
|Rat (strain not specified)||Kaolin (unspecified) and illite clay (unspecified) (<5 µm in diameter) 1.0 mg/ml incubated in cell suspension for 1 h||Kaolin caused 98% haemolysis, illite 24% (quartz 48%).|
|Rabbit||Kaolin (non-specified), incubation for 50 min||Twenty per cent haemolysis caused by 1.3 mg kaolin in a total volume of 4 ml; 11.6 mg of calcined kaolin was needed for the same effect.|
|Sheep (citrated blood)||Kaolin (median volume diameter 4.7 µm) incubated in cell suspension||Haemolysis 60% in 30 min; haemolytic potency similar to that of quartz.|
|Sheep||Kaolin, 1.0 mg/ml (<5 µm diameter, MMAD 2.1 µm) at five concentrations, 0.1-1 mg/ ml, incubated in cell suspension for 50 min||Linear, dose-dependent haemolysis; about 20% haemolysis with 0.5 mg/ml; 35% with 1 mg/ml; approximately 2 times as potent as quartz.|
|Sheep (citrated blood, single donor)||Kaolinite 90% <2 µm in diameter at six concentrations, 0.005-0.25 mg/ml, incubated in cell suspension for 1 h||More haemolytic per mg than silica or talc; 20% haemolysis with 0.25 mg/ml; 95% with 25 mg/ml.|
|Sheep||Georgia kaolin (>96% kaolinite, no quartz, >95% >5 µm in diameter), incubated with cells for 1 h||Kaolin induced a dose-dependent haemolysis, which reached 42% at 1 mg/ml. The effect was completely abolished by lecithin.|
|Bovine erythrocytes washed with buffered saline||South Carolina kaolinite (composition not specified) incubated in cell suspension for 1 h||A concentration of 0.6 mg/ml induced 50% haemolysis of erythrocytes. Polyvinylpyridine-N-oxide, a hydrogen-bonding material, partly inhibited the haemolysis.|
|Bovine erythrocytes washed with buffered saline||South Carolina kaolinite (composition not specified) at several concentrations of different particle sizes incubated in cell suspension for 1 h||A concentration of 0.6 mg/ml induced 50% haemolysis of erythrocytes. Of the minerals studied, kaolinite was least haemolytic, the potency being 1/20 that of silica. Particles of 0.2-2 µm diameter were most active; particles <0.2 µm or >20 diameter had no or little haemolytic activity; reduction of surface charge and cation exchange capacity by coating particles with an aluminium-hydroxy polymer largely eliminated haemolytic capacity.|
|Human (citrated blood)||Six different kaolins, kaolinite content 51-95%, quartz content 5-20%; 1.0 mg/ml (<5 µm diameter, median 1-2 µm) incubated in cell suspension for 1 h||Haemolysis 60-90% for all samples except one (30%), which had 71% kaolinite and 22% quartz.|
|One sample of an illite clay (28% illite, 28% quartz); 1.0 mg/ml (<5 µm diameter, median 1-2 µm) incubated in cell suspension for 1 h||Haemolysis 95%.|
|Human||One “bentonite,” containing 50% illite, 25% montmorillonite, 25% quartz; two undefined illite clays, one kaolinite with dickite and nakrite as main components and quartz as a minor component, one kaolin with kaolinite as the main component, and two unspecified kaolins ground in a ball mill to diameter <5 µm, incubated in cell suspension for 1 h||Fifty per cent haemolysis caused by 1.5-4 mg/ml kaolinites (0.06-0.115 m2/ml); and 1.0-4.0 mg/ml (0.039-0.12 m2/ml) illites. Haemolytic activity roughly proportionate to surface area of mineral powder; haemolytic activity largely lost after heating to over 500 °C.|
|Human red blood cells from normal donors||Dust from the town Mexicali (see Table 14)||Concentration of 2 mg/ml produced a 95 ± 3% haemolysis in 1 h; the haemolysis was stronger than with quartz.|
|Neuroblastoma (N1E-115) cells with differentiation induced by dimethylsulfoxide||Standard kaolinite KGa-1 0.1-1.0 mg/ml incubated in cell suspension||Within minutes, resting potential depolarized and ability to maintain action potentials in response to stimulation was lost; within 30 min, severe morphological deterioration of cells.|
|Neuroblastoma (N1E-115) cells and oligodendroglial (ROC-1) cells||South Carolina kaolinite (non-specified, mainly 1-2 µm diameter) incubated at 0.1 mg/ml in cell suspension for 24 h||No alteration of LDH activity in medium for either cell type; no decrease of the viability (assessed by trypan blue exclusion) of N1E-115 cells after 24 h.|
|Other cell types and in vitro systems|
|Tracheal epithelial (cloned cell line from Syrian hamster, strain 87.20) in log growth phase in monolayer||Kaolinite 90% <2 µm in diameter at four concentrations, 0.003-0.1 mg/ml, incubated in cell suspension for 24 h||Cells phagocytized clay particles; dose-dependent damage to plasma membrane as evidenced by loss of 51Cr from cells; loss of 51Cr after 24 h approximately 40% with 0.1 mg/ml, twice that of quartz.|
|Human umbilical vein endothelial cells||South Carolina kaolinite (non-specified, mainly 1-2 µm diameter) incubated at 0.1 mg/ml in cell suspension for 24 h||Kaolinite induced a statistically significant 50% increase in LDH activity in the medium and killed 90% of the cells in 24 h.|
|Macrophage-like cell line P338D1||Three kaolinites, 1 with “high crystallinity,” 1 with “medium crystallinity,” and 1 with “low crystallinity,” diameter <5 µm, incubated at 80 µg/ml for 48 h||Kaolinites caused a 78-91 % decrease in the viability of the cells and induced leakage of LDH and beta–N-acetylglucosaminidase. Adsorption of nitrous oxide on the minerals slightly decreased the effect on viability.|
|V79-4 Chinese hamster lung cell line||Non-specified kaolin incubated with the cells for 6-7 days||LD50 20 mg/ml for kaolin, which was the most toxic of the 21 particulate and fibrous materials tested.|
|Macrophage-like cell line P338D1||Thirty respirable dust specimens from coal mines in United Kingdom; cytotoxicity index developed from effects on trypan blue exclusion, release of LDH, glucos-aminidase, and lactic acid production||A positive correlation between ash content and cytotoxicity of the dusts. In dusts with >90% coal, there was also a correlation between kaolin + mica content and cytotoxicity.|
|Macrophage-like cell line P338D1||Two kaolinites (KGa-1, KGa-2) from Source Clays repository, particle sizes 3.2 and 3.9 µm, with no cristobalite or quartz, incubated for 48 h||Cell viability not changed at 20 µg/ml, and 60-70% at 80 µg/ml.|
|Isolated human leukocyte elastase||Cornwall kaolinite and four different illite clays (composition and particle size not specified), 5 µg/ml or 20 µg/ml||Kaolinite (5 µg/ml) caused 90% inhibition of the enzyme, illites (20 µg/ml), 10-53% inhibition.|
|Liposomes (artificial phospholipid membrane vesiclesb 0.1-2 µm diameter) entrapping dissolved chromate|
|Kaolinite, 90% <2 µm in diameter, at five concentrations, 0.1-10 mg/ml, incubated in cell suspension for 1 h||Dose-dependent loss of chromate from vesicles; loss of chromate after 1 h (in excess of spontaneous rate) approximately 20% with 10 mg/ml; spontaneous rate was 4-6%.|
a: LD50 = median lethal dose; LDH = lactate dehydrogenase; MMAD = mass median aerodynamic diameter; TTC = 2,3,5-triphenyltetrazolium chloride.
b: Prepared from dipalmitoyl phosphatidylcholine, sphingomyelin, cholesterol, and dicetylphosphate.[Source 41)]
Kaolin parenteral administration
Policard & Collet 42) demonstrated the development of reticulin fibres in rats 1–3 months after intraperitoneal administration of kaolin (90% <2 µm in diameter). The dust sample contained 1.2% free silica, an amount that the authors considered not to cause the effects observed.
Intraperitoneal administration of kaolinite (<3 µm or ~10 µm particle size; no quartz detectable with X-ray analysis) was fibrogenic in mice; the smaller particle size was just as active as quartz and led to fibrosis in 35 days, whereas fibrosis became evident only after 200 days for the larger size particles 43).
Intraperitoneally instilled kaolin and kaolin baked for 1 h at 900 or 1200 °C caused marked fibrosis. The degree of the reaction was only slightly smaller than that caused by quartz 44).
In a study of a large number of organic and inorganic particulates, kaolin (composition not specified, particle size 0.25–25 µm) injected intraperitoneally into rats produced a granulomatous reaction at 1 and 3 months, but no fibrosis. In vitro, it had low toxicity: it killed less than 2% of peritoneal macrophages and approximately 4% of alveolar macrophages 45). For the group of some 20 particulate materials, the authors considered that there was a good correlation between toxicity to macrophages and fibrogenicity after intraperitoneal injection.
Kaolin by inhalation
Carleton 46) studied the effects of kaolin by inhalation in guinea-pigs. Until 3 months after the exposure, mild alveolar proliferation only was observed. Thereafter, patchy bronchopneumonia occurred, with massive eosinophil infiltration. By 6 months, plaque formation and capillary bronchitis were observed.
Wagner and co-workers (1987) studied the carcinogenicity of palygorskite and attapulgite in an inhalation study and used “coating grade” kaolin as a negative control: 20 male and 20 female Fischer rats were exposed by inhalation (10 mg/m3, 91.4% of the particles <4.6 µm in diameter) for 6 h/day, 5 days/week, until they died. However, at 3, 6, and 12 months, four rats were killed from each group for ancillary studies (leaving only 28 animals for the carcinogenicity study). At the end of the study, full autopsy and microscopic analysis of the lungs, liver, kidney, spleen, and other organs were performed. In two kaolin-exposed rats, bronchoalveolar hyperplasia but no benign or malignant tumours of the lungs or pleura were observed. However, the number of tumours in the positive control group (crocidolite treatment at the same exposure level) was also low (one adenocarcinoma only). The mean fibrosis grading in the rats at interim sacrifices and at the end of the experiment was between 2.1 and 2.8 on a scale of 1–8 (1 being normal; 2, dust in macrophages; 3, early interstitial reaction; 4, first signs of fibrosis; 5, 6, 7, increasing fibrosis; 8, severe fibrosis).
As another part of the study on the carcinogenicity of mineral fibres, Wagner et al. 47) injected a single dose (amount not given) of kaolin intrapleurally into 20 male and 20 female Fischer rats and followed the animals until moribund or dead (survival of animals in different groups not given). None of the kaolin-treated rats developed mesothelioma, whereas 34 of 40 of those given crocidolite did.
Mossman & Craighead 48) treated cultured tracheas from hamsters with Georgia kaolin (composition not indicated; diameter 3–5 µm) and kaolin coated with 3-methylcholanthrene, implanted the tracheas after 4 weeks into syngeneic hamsters, and followed the animals until moribund at 105–110 weeks. Animals treated with kaolin did not develop tumours, but a high incidence of pulmonary tumours, often fatal, was observed in animals treated with kaolin coated with 3-methylcholanthrene. Animals treated with 3-methylcholanthrene-coated haematite or carbon particles also developed a similar spectrum of tumors (carcinomas, sarcomas, undifferentiated tumors).
Kaolin reproductive effects
In a study that provided limited details, Sprague-Dawley rats were administered calcium or sodium montmorillonite orally on pregnancy days 1–15. No effects were observed on the litter weight, implantation rates, or resorptions 49).
Thirty-six Sprague-Dawley rats were fed a control diet, 20% kaolin (air-floated Georgia kaolin) diet, and iron-supplemented 20% kaolin diet 37–117 days before mating and during pregnancy 50). Dams receiving kaolin diet developed anaemia, whereas anaemia was not observed in dams receiving iron supplementation. The birth weight of the pups of the dams receiving kaolin was 9% smaller than that of the control dams; again, iron supplementation prevented this decrease. There was no effect on the litter size or macroscopic malformations.
Kaolin and quartz
Schmidt & Lüchtrath 51) studied the effects of intratracheal administration of a 2:3 mixture of kaolin and quartz. Kaolin alone did not cause significant reaction in the lung. The mixture of kaolin and quartz caused significant changes in the lung; after 9 months, the fibrosis was grade 5. (Using pure quartz, the development of silicosis was somewhat quicker, but after 9 months, the difference compared with the kaolin–quartz mixture was insignificant.)
Kaolin effects on humans
Many case reports and case series have suggested that exposure to kaolin causes pneumoconiosis 52). In several cases, however, it was not clear whether kaolinite and quartz or quartz alone was responsible for the resulting pneumoconiosis 53).
Kaolin workers, United Kingdom
In England, a number of papers have dealt with the effects of kaolin originating from Cornwall mines (Table 4). Hale et al. 54) performed medical and radiological examinations of those occupationally exposed to kaolin and reported in detail on six workers who had been working in the drying and bagging of kaolin. All had radiological pneumoconiosis, and two were further studied in autopsy. In one case, characteristic silicotic-type nodulation together with progressive tuberculosis were found. Large quantities of kaolinite and amorphous quartz were found in the lung. In another case, large quantities of pure kaolinite (as much as 20–40 g) were found in the lung without tuberculosis but with severe fibrosis. The disease was like the pneumoconiosis of coal miners and differed from classic silicosis. In the upper part of the lung, greyish or blue-greyish massive confluent lesions were described, which were not as hard on palpation as the silicotic conglomerates. Hale and co-workers 55) also studied the lung of a kaolin worker from Georgia, USA, and observed that the dust in the lungs consisted entirely of kaolinite; no trace of quartz could be seen.
Kaolin workers, USA
Kaolin workers in Georgia have been studied extensively (Table 4). Edenfield 56) found pneumoconiosis in 44 (3.9%) of 1130 persons working with kaolin. All these had worked for a number of years in the loading area or some other area of the plant that in earlier years had been very dusty. Only 2 had worked in the kaolin industry less than 10 years, and 19 had been employed for more than 20 years. All of those classed as having severe pneumoconiosis (stage III) had worked more than 20 years, and all had worked in heavy dust in the car loading and bagging areas. Thirty-one of the 44 had a stage I pneumoconiosis; they had no symptoms or signs of respiratory dysfunction. Similarly, the seven workers with stage II pneumoconiosis exhibited no respiratory symptoms. The six cases with stage III pneumoconiosis also had emphysema, had complaints of cough and dyspnoea, and had been placed in jobs requiring minimal activity.
Lapenas & Gale 57) found diffuse reticulonodular lung infiltration and a nodule in the upper lung lobe in a 35-year-old worker of a Georgia kaolin processing factory who had been occupationally exposed to kaolin aerosol for 17 years. Exploratory thoracotomy revealed an 8 × 12 × 10 cm conglomerate pneumoconiotic lesion containing large amounts of kaolinite. Quartz could not be demonstrated by scanning electron microscopy or X-ray diffraction.
Lapenas et al. 58) performed a pathological study on biopsy or autopsy specimens from five patients admitted to the Medical Center Hospital of central Georgia between 1976 and 1981, who were estimated to represent some of the most advanced cases of kaolin pneumoconiosis seen in that hospital. Respiratory failure was a contributing factor to death in two of the three autopsy cases. Chest X-ray demonstrated small irregular shadows and large obscure patches typical of kaolin pneumoconiosis. Histological examinations revealed significant kaolinite deposits and peribronchial nodules. The nodules differed from those in silicotic patients and consisted mainly of kaolinite aggregates traversed by fibrous tissue trabecules. The presence of kaolinite in the lungs was confirmed by mineralogical examinations, while quartz could not be demonstrated.
Sepulveda et al. 59) examined 39 current and 16 ex-workers of a Georgia kaolin mine and mill. Average respirable dust levels were approximately 0.2 mg/m3 in the mine and between 1 and 2 mg/m3 for other work stations. Samples of respirable dust contained 96% kaolinite, 4% titanium dioxide, and no silica. Pneumoconiosis was found in 15% of the workers and ex-workers with 5 years or more of exposure. Kaolin workers had a decreased forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and mean adjusted peak flow when the values were adjusted for age, height, race, and pack-years of smoking.
Kennedy et al. 60) examined 459 kaolinite workers from central Georgia with a mean duration of employment of 12 years. Pneumoconiosis occurred in 9.2% of the workers and, among employees older than 54 years, was associated with high dust exposure. Among black workers with “complicated pneumoconiosis,” the FVC was 81.6%, indicating borderline restriction, and the FEV1/FVC was significantly lowered. The raw material from the mine contained 0.25% free crystalline silica. At the time of the study, the airborne concentrations of kaolin dust were below 5 mg/m3 and the dust contained less than 1% free silica, but dust concentrations up to 377 mg/m3 had been recorded in the past.
In a cross-sectional study of a Georgia kaolin mine and processing plant, Altekruse et al. 61) examined the pulmonary function and lung radiography of all 65 employees. The respirable dust concentration at the time of the study was 0.14 mg/m3 in the mine area and 1.74 mg/m3 in the kaolinite processing area, but had been higher earlier (see Table 9). About 94–98% of the particles were kaolinite and 2–6% anastase (titanium dioxide). Asbestiform fibres and crystalline silica were not present in the samples. Five workers, all of whom worked in the kaolinite processing area with highest exposure, showed radiological evidence of pneumoconiosis; they had worked for the company for 7–36 years. There was a slight, exposure duration-dependent decrease in the FVC and FEV1 among the workers, those with radiological pneumoconiosis having lower lung function than the others.
In a cross-sectional study of pulmonary function and radiology among workers of 12 kaolin companies in Georgia 62), an increased prevalence of pneumoconiosis and decreased lung function (FEV1, but not FVC) were observed among the workers working with calcined clay. Among workers with more than a 3-year tenure, the adjusted prevalence of simple and complicated pneumoconiosis was 3.2% and 0.63%, respectively. Smoking did not explain the presence of decreased FEV, nor was there a relationship between pneumoconiosis and lung function. The authors stated that the workers were not exposed to quartz 63).
Kaolin workers, other countries
Warraki & Herant 64) examined radiologically 914 china clay workers of Ayyat, United Arab Republic; 264 of them had been exposed for less than 10 years, 133 for 10–15 years, 326 for 15– 20 years, and 191 for more than 20 years. Pneumoconiosis was diagnosed in six workers, all with exposures longer than 15 years. In two cases, confluent masses were found in the lungs; during a 2.5-year follow-up, one of these died with cor pulmonale. No measurements of dust were reported; a sample of airborne dust contained 1–2% free silica (Table 4).
Uragoda & Fernando 65) examined workers in kaolinite processing in Sri Lanka. No individuals working with wet clay were examined because their risk of disease from dust exposure was considered low. Among the 11 persons working with dry materials (sacking and weighing), X-rays showed no sign of disease. The most frequent complaints were skin irritation and dermatitis, probably due to the tropical climate (high temperature and humidity). Lack of pneumoconiosis was to be expected because of the short exposure time (average 6 years, range 3–9 years).
Table 4. Effects of occupational exposure to kaolin and other clays on health
|Study design, studied population||Exposure measurement||Exposure||Findingsa||References|
|Cross-sectional; 533 Cornish china clay workers||Occupational history from records for everyone. Millers, baggers, loaders considered to be continuously exposed, kiln workers and drymen intermittently exposed||Exposure to china clay; industrial hygiene expertise used to group occupations based on the intensity of exposure; no quantitative data or qualitative assessment of the dust||Exposure time-dependent increase in the prevalence of radiologically diagnosed kaolinosis, from 4% in those with less than 15 years of exposure to 19% among those with more than 25 years of exposure. Among 526 workers with less than 5 years of exposure, no kaolinosis was observed. Among the workers who were more heavily exposed (milling and bagging), the prevalence was 6% for those with a work history of 5-15 years and 23% for those with an exposure of >15 years. Confluent lesions were found in 12 workers, and 30 workers had ILO categories 2-3 lesions. There was little evidence of disability related to kaolinosis; only one worker with massive fibrosis had become disabled and changed to a lighter job.||66)|
|Cross-sectional; 1728 Cornish china clay workers in 1977||Occupational group and history of work in each group for all workers||Exposure to china clay; industrial hygiene expertise used to group occupations based on the intensity of exposure; no quantitative data or qualitative assessment of the dust||77.4% of workers in pneumoconiosis category 0, 17.9% in category 1, 4.7% in category 2 or 3. Advanced pneumoconiosis in 19 workers. Every dusty job contributed to the amount of simple pneumoconiosis. Smoking unrelated to radiographic appearance. Vital capacity deteriorated with advancing pneumoconiosis; for “FEV,” the association was not statistically significant. Subjective symptoms not related to past exposure as assessed by years worked in different jobs.||67)|
|Cross-sectional; 3831 employees and 336 pensioners in china clay industry in United Kingdom in 1985||Analysis by job classification||Average exposures at the time of the study 0.5-2.7 mg/m3 (see Table 9)||3374 workers in pneumoconiosis category 0, 271 in category 1, 39 in category 2, and 5 in category 3. Employment in mills had strongest effect on pneumoconiosis category, followed by dryers (in keeping with the exposure levels). In kilns, the exposure was also high, but pneumoconiosis was not equally prevalent; kaolin there is no longer crystalline. Work in mills or as dryer before 1971 had twice the effect on pneumoconiosis prevalence as work there after 1971. Ventilatory capacity related to radiological status, no consistent independent relation with occupational history was observed. Respiratory symptoms were related to ventilatory function.||68)|
|Cross-sectional; 4401 current and retired china clay workers in United Kingdom in 1990||Dust measurements from 1978, estimated exposure before 1978; detailed occupational history for each participant||Average respirable dust exposure 1.2-4.7 mg/m3 (see Table 9)||Small opacity profusion related to work dustiness and total occupational dust dose; to reach category 1 by age 60, the estimated total dose for non-smokers was 85 mg/m3years, for smokers, 65 mg/m3years. The major determinant of respiratory symptoms was smoking; total dust exposure had a minor effect.||69)|
|Cross-sectional; 4401 current and retired china clay workers in United Kingdom in 1990||Dust measurements from 1978, estimated exposure before 1978; detailed occupational history for each participant||Average respirable dust exposure 1.2-4.7 mg/m3 (see Table 9)||Univariate analysis showed relationships between lung function and age, X-ray score, smoking class, occupational history, and total occupational dust dose. In multiple regression analysis, when the effects of age, X-ray score, and smoking class had been accounted for, there was no independent additional effect from total occupational dust dose or occupational history.||70)|
|Cross-sectional; 39 current and 16 ex-kaolin workers at a kaolin mine and mill in Georgia, USA||Respirable and total dust analysed at the time of study (see Table 9)||Dust composed of 96% kaolinite, 4% titanium dioxide, no free silica, no asbestiform fibres; average respirable dust in all job categories <2 mg/m3||Of current and ex-workers with >5 years of exposure (n = 55), 4 had simple pneumoconiosis and 4 complicated pneumoconiosis. Mean adjusted FVC, FEV1, peak flow lower (P < 0.05) among kaolin workers than among 189 non-kaolin-exposed referents.||71)|
|Cross-sectional; 459 workers in three Georgia kaolin mining and processing facilities with >1 year work history; mean duration of employment 12 years||Details on measurements not given||At the time of study, US Mine Safety and Health Administration documented exposure to kaolin dust <5 mg/m3 with less than 1% free silica; survey in one of the plants in 1951 and 1960 showed kaolin dust concentrations of 377 and 361 mg/m3; in 1951, the raw material had 0.25% free silica||417 workers had pneumoconiosis category 0, 29 category 1, 8 category 2, and 5 category 3. Of the blacks, 13.6%, and of the whites, 7.6% had pneumoconiosis. Pneumoconiosis was significantly related to age, >15 years of exposure, and greatest dust exposure. Complicated pneumoconiosis (large opacities) related to decreased respiratory function, but otherwise there was no correlation between pneumoconiosis and respiratory function.||72)|
|Cross-sectional; all 65 men employed in a Georgia kaolin mine studied||During 5-year period, 157 measurements of respirable dust (see Table 9)||Dust composed of 94-98% kaolinite and 2-6% anastase (TiO2); no asbestiform fibres of crystalline silica; mean respirable dust in processing area 1.74 mg/m3, 0.14 mg/m3 in the mine||Five of the workers had radiological pneumoconiosis. All had worked in the processing area. For the whole group, FVC and FEV1 were within the normal range, but they were lower for the workers with pneumoconiosis. FVC and FEV1 decreased with years of employment in the processing area. Pneumoconiosis was not related to smoking.||73)|
|Cross-sectional; 2379 current kaolin workers in Georgia, USA||No measurements; occupational title as proxy||The authors state that the free silica exposure is negligible because of washing out of impurities in the process||4.4% prevalence of category >1 simple pneumoconiosis, 0.89% prevalence of complicated pneumoconiosis; 7.1% of white and 19% of black dry processors and 4.1% of white and 9.1% of white wet processors had pneumoconiosis. FEV1 was <80% of the expected among 7.5, 12.8, and 33.3% and FVC was <80% among 8.0, 10.5, and 33.3% of those with normal chest radiograph and those with simple and complicated pneumoconiosis. Similarly, among lifelong non-smokers, the frequency of lowered FEV1 and FVC was elevated among those with complicated pneumoconiosis.||74)|
|Cross-sectional: workers of two Georgia, USA, kaolin plants||Reanalysis of data from two of the three plants studied by Kennedy et al. (1983); no measurements||19/162 and 21/223 workers in the two plants had pneumoconiosis. The adjusted prevalence of pneumoconiosis increased 1.1 % for each year in production. Workers in plant 1 had a 2.7 times higher prevalence than workers in plant 2. In plant 1, 15-20% of production had been calcined kaolin, while plant 2 had produced hydrous clay only.||75)|
|Cross-sectional; 914 workers in earthenware industry, United Arab Republic||No quantitative measurements||83-86% of respirable dust potassium aluminium silicate, 1-2% free silica||264 workers has worked for <10 years, 133 for 10-15 years; no pneumoconiosis cases were observed in these groups. 326 workers had worked 15-20 years and included 4 cases with pneumoconiosis, and 191 workers had worked >20 years and included 2 with pneumoconiosis. 2 of the pneumoconiosis cases were classified as progressive massive fibrosis; 4 had dyspnoea on exertion.||76)|
|Cross-sectional, 11 workers in the bagging section of a kaolin refinery in Sri Lanka, average age 35.2 years, duration of employment 3-9 years (average 6 years)||No measurements available||Kaolinite content of kaolin >99%, 76.8% <3 µm in diameter||No radiological abnormalities observed. The absence of pneumoconiosis most likely due to short duration of employment and young age of the workers studied.||77)|
|Cross-sectional; 18 factories in heavy clay industry in United Kingdom; 1934 current employees||1465 personal dust samples collected at the time of the study and analysed for respirable dust and quartz||Cumulative exposure <40 mg/m3years respirable dust for 94% and <4 mg/m3years quartz for 93%; for details, see Table 10||1.4% had radiographic small opacities in ILO category >1/0, 0.4% had small opacities in ILO category >2/1. Risk dependent on lifetime exposure to quartz and respirable dust. Anamnestic chronic bronchitis, wheezing, and breathlessness related to dust exposure. Dust and quartz exposure strongly correlated.||78)|
|Cross-sectional; 268 current brick workers in South Africa||97 respirable, 78 total dust, and 29 silica analyses from three of the five participating factories at the time of the study||Mean respirable dust and total dust exposure 2.22 and 15.6 mg/m3; mean free silica 2.1%; for exposure in different groups, see Table 10||4.2% had profusion score >1/0; profusion score significantly related to cumulative respirable dust exposure. Anamnestic respiratory symptoms and FVC and FEV1 significantly related to exposure to respirable dust.||79)|
a: FEV = forced expiratory volume; FEV1 = forced expiratory volume in 1 s; FVC = forced vital capacity; ILO = International Labour Organization.[Source 80)]
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