ReviewEpidemiology of environmental exposures and human autoimmune diseases: Findings from a National Institute of Environmental Health Sciences Expert Panel Workshop
Highlights
► We review the epidemiologic evidence for environmental factors in development of AID. ► We also define critical knowledge gaps, and research needed to fill these gaps. ► We suggest more studies are needed of phenotypes, genotypes, and multiple exposures.
Section snippets
Introduction and approaches
Autoimmune diseases (AID) are characterized by an inflammatory reaction caused by the body's own immune system attacking self-tissues. There are over 80 different AID, and collectively they are among the most prevalent diseases in the U.S., affecting at least 7% of the population. Because most AID are chronic and incurable, from a public health perspective they constitute a major health problem that, besides causing individual suffering, has high societal costs (Autoimmune Coordinating
Silica
This field of research began with the initial description of SSc among Scottish stonemasons in 1914 [2] and became more fully developed through studies of miners and granite workers in the 1950s through 1980s. Freshly fractured particulate silica (crystalline silica or quartz) is released typically in mining but also in the so-called dusty trades, including sandblasting, rock drilling, sand factory work, granite cutting, construction work, brick laying, tilling, and cement work. Variable levels
Ionizing radiation
The thyroid is a target organ for radiation-related damage in that ionizing radiation is a known cause of thyroid cancer; therefore, other thyroid abnormalities have also been assessed as potential outcomes of exposure. There is convincing evidence that external radiation treatment for cancer increases the risk of autoimmune thyroiditis and GD, especially in treatment for cancers of the neck region (e.g., Hodgkin disease, thyroid cancer, head and neck cancers) [61], [62]. Radioiodine therapy
Infections
The concept that infections play a role in the development of AID has a long history, and many infectious agents, including viruses, bacteria, and parasites, have been proposed as triggers for particular AID. A common pattern, however, is that after initial positive reports, subsequent studies have not been able to reproduce the initial finding.
The database of epidemiologic studies of Epstein–Barr virus (EBV) and MS is relatively strong [85] such that, in aggregate, the data support the
Chemical factors
- 1)
Crystalline silica exposure contributes to the development of several AID, including RA, SSc, SLE, and ANCA-related vasculitis.
- 2)
Solvent exposure contributes to the development SSc.
- 3)
Smoking contributes to the development of ACPA-positive and anti-RF-positive RA, and there is an interaction with the shared epitope.
Physical factors
- 1)
An inverse association exists between UVR exposure and risk of development of MS.
Biological factors
- 1)
Ingestion of gluten contributes to the development of GSE.
- 2)
Ingestion of certain lots of l-tryptophan
Discussion
Many recent advances have helped to decipher the factors that contribute to the development of AID. The development of efficient and reliable high-throughput genotyping techniques has resulted in many studies designed to discover genetic risk factors for AID. Frequent findings from these studies are strong associations with different alleles of genes within the HLA region, and multiple, weaker associations with non-major histocompatibility genes. Several years into the era of genome-wide
Acknowledgements
The authors gratefully acknowledge expertise and input from Elizabeth Arkema of Harvard School of Public Health, Ryan Gan of the University of Colorado, Brandi Stevens of the Medical University of South Carolina, and Christine Parks and Michael C. Humble, NIEHS. We also appreciate the useful discussions and suggestions of Glinda Cooper of the U.S. Environmental Protection Agency.
This review was prepared in conjunction with the NIEHS Environmental Autoimmunity Conference, Durham, NC, September
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