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AB0306 Caplan's syndrome, cadmium and china clay: could occupational kaolin inhalation enhance cadmium exposure to explain the sixty year conundrum of caplan's syndrome first reported in coal miners?
  1. D Murphy1,2,
  2. K Bellis1,
  3. D Hutchinson1,2
  1. 1Rheumatology, Royal Cornwall Hospital
  2. 2University of Exeter Medical School, Cornwall Campus, Truro, United Kingdom

Abstract

Background Caplan's syndrome was first described in the coal miners of South Wales (UK). The specific cause for rheumatoid pulmonary nodules associated with coal dust exposure remains unknown. Coal dust exposure alone does not appear to explain Caplan's syndrome as almost all of these men were also smokers. Cigarette smoke is the most important environmental cause of cadmium exposure. We describe Caplan's syndrome in an ex-smoking kaolin worker associated with a significantly raised urinary cadmium level.

Objectives A 65 year old Cornish kaolin worker and ex-smoker of 20 pack years with life limiting nodular erosive rheumatoid arthritis (RA), developed extra-articular manifestations including pulmonary nodules suggestive of Caplan's syndrome. We review the literature on kaolin, with respect to inhalation and mechanism of action for heavy metal adsorption and nodular disease development.

Methods Pubmed searches were undertaken using the keywords “kaolinosis”, “kaolin”, “cadmium” “nodules”, “adsorption”, “coal”. First pass mid-stream urine was analysed for cadmium using inductively coupled plasma–mass spectrometry (ICP-MS).1

Results Urinary cadmium was significantly raised at 0.66 μmol/mol creatinine (non-occupationally exposed UK male median 0.17μmol/mol creatinine1), 20 years post-industrial exposure and 35 years post-smoking cessation. Contemporary serology levels demonstrated a rheumatoid factor of 481.7 iu/ml (0–10 normal range) and an anti-cyclic citrullinated peptide of >500 u/ml (0–17 normal range). CT scan of the chest demonstrated multiple pulmonary nodules consistent with Caplan's syndrome.

The prevalence of Caplan's syndrome in kaolin workers is the highest of any occupation ever reported.2 Elevated cadmium levels of 11.2–15.9 mg/kg have been observed in kaolin,3 fifty- fold higher than those reported in coal.4 Coal contains variable amounts of clays and minerals such as kaolinite. Cadmium content in coal is strongly associated with levels of kaolinite contamination.4 Cadmium nanoparticles have been observed to cause lung parenchyma inflammation and granuloma formation in an animal model.5

Conclusions Kaolinite mineral capacity for adsorption of heavy metals, in particular cadmium, could explain the scale and pattern of Caplan's syndrome incidence seen in Welsh coal miners and Cornish kaolin workers, and further explains the interactive risk seen in sequential dust and cigarette smoke exposure.

References

  1. Morton J, Tan E, Leese E, Cocker J. Determination of 61 elements in urine samples collected from a non-occupationally exposed UK adult population. Toxicol Lett. 2014;231(2):179–93.

  2. Wells IP, Bhatt RC, Flanagan M. Kaolinosis: a radiological review. Clin Radiol. 1985;36(6):579–82.

  3. Bonglaisin JN, Mbofung CMF, Lantum DN. Intake of Lead, Cadmium and Mercury in Kaolin-eating: A Quality Assessment. J Med Sci 2011;11(7):267–273.

  4. Song D, Wang M, Zhang J, Zheng C. Contents and occurrence of cadmium in the coals from Guizhou province, China. Ann N Y Acad Sci. 2008;1140:274–81.

  5. Coccini T, Barni S, Vaccarone R, et al. Pulmonary toxicity of instilled cadmium-doped silica nanoparticles during acute and subacute stages in rats. Histol Histopathol. 2013 1;28(2):195–209.

References

Acknowledgements Cornwall Arthritis Trust.

Disclosure of Interest None declared

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