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Occupational trichloroethylene exposure and antinuclear antibodies: a cross-sectional study in China
  1. Mark Purdue1,
  2. Luoping Zhang2,
  3. Roel Vermeulen3,
  4. Martyn T Smith2,
  5. Wei Hu1,
  6. Jongeun Rhee1,
  7. Cuiju Wen4,
  8. Yongshun Huang4,
  9. Xiaojiang Tang4,5,
  10. Sonja I Berndt1,
  11. Ashley A Frazer-Abel6,
  12. Kevin D Deane6,
  13. Nathaniel Rothman1,
  14. Qing Lan1
  1. 1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA
  2. 2 School of Public Health, University of California Berkeley, Berkeley, California, USA
  3. 3 Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
  4. 4 Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou, Guangdong, China
  5. 5 Zhuhau BesTest Biotechnology Co. Ltd, Zhuhai, Guangdong, China
  6. 6 Department of Medicine, University of Colorado Anschutz Medical Campus, Denver, Colorado, USA
  1. Correspondence to Dr Mark Purdue, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, USA; purduem{at}


Objectives There has been concern over the possible risk of autoimmune diseases from exposure to trichloroethylene (TCE), an industrial solvent and common pollutant near hazardous waste sites. Studies of TCE-exposed lupus-prone mouse strains have reported increases in serum antinuclear antibodies (ANAs), a marker of autoimmunity, and autoimmune pathologic changes, while epidemiologic studies have provided limited support for an association between TCE exposure and scleroderma. To investigate exposure-related biologic evidence of autoimmunity in humans, we measured ANA levels in sera from a cross-sectional study of TCE-exposed (n=80) and TCE-unexposed (n=96) workers in Guangdong, China.

Methods Full-shift personal air exposure measurements for TCE were taken prior to blood collection. Serum ANAs were detected by immunofluorescence on HEp-2 cells. We calculated ORs and 95% CI relating levels of TCE exposure (categorised using tertiles as cut-points) and ANA positivity (1+ intensity at 1:320 dilution) using multivariable logistic regression.

Results Samples from 16 of 176 participants were ANA-positive. We found higher levels of TCE exposure (concentrations>17.27 ppm) to be associated with an elevated odds of ANA positivity (OR 4.7, 95% CI 1.3 to 16.8) compared with unexposed controls. This association remained after excluding two subjects with diagnosed autoimmune disease (OR 4.5, 95% CI 1.2 to 16.2). We did not observe an association with ANAs at lower exposure levels.

Conclusions Our findings, to our knowledge the first direct human evidence of an association between TCE exposure and systemic autoimmunity, provide biologic plausibility to epidemiologic evidence relating TCE and autoimmune disease.

  • Epidemiology
  • Solvents
  • Autoimmune Diseases
  • Cross-Sectional Studies

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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  • KDD, NR and QL contributed equally.

  • Contributors MP conceptualised the antinuclear antibody (ANA) investigation, conducted the data analysis and wrote the first draft of the paper. QL, NR, LZ and MTS designed the cross-sectional study. RV, CW, YH and XT conducted the study fieldwork and exposure assessment. WH and SIB organised study logistics for the ANA analysis. AAF-A and KDD oversaw the ANA laboratory analysis. JR contributed to the data analysis. All authors critically revised and approved the final version of this manuscript. QL, NR and KDD contributed equally to this paper.

  • Funding This project was supported by Intramural Research Program funding from the National Cancer Institute (Bethesda, Maryland, USA) and funding from the Department of Science and Technology of Guangdong Province, China (2007A050100004 to XT).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.