| Common Commercial Cosmetic Products Induce Arthritis in the DA Rat B. Sverdrup,
1
L. Klareskog,
1
and S. Kleinau
1,2
1
Department of Medicine, Rheumatology Unit, Karolinska Institute, Stockholm, Sweden
2
Department of Pathology, University Hospital, Uppsala, Sweden Abstract
Many different agents, including mineral oil and silicone, have the capacity to act as immunological adjuvants, i.e., they can contribute to the activation of the immune system. Some adjuvants, including mineral oil, are known to induce arthritis in certain strains of rats after intradermal injection or percutaneous application. The aim of this study was to determine if common commercial cosmetic products containing mineral oil could induce arthritis in the highly susceptible DA (Dark Agouti) rat. Intradermal injection of five out of eight assayed cosmetic products without further additives resulted in arthritis with synovitis. One of the products induced a very aggressive arthritis, which had declined after 5-9 weeks. When this product was also assayed for arthritogenicity upon percutaneous administration, it induced a mild and transient arthritis in 5 out of 10 DA rats, whereas control animals showed no clinical signs of joint involvement. No arthritic reaction was seen in rats after peroral feeding with the most arthritogenic product or by intravaginal application of Freund's adjuvants. Silicone gel implants in DA rats did not cause arthritis. We conclude that mineral oils included in common commercially available products retain their adjuvant properties and are arthritogenic in the presently investigated arthritis-prone rat strain. There is yet no evidence that mineral oils present in cosmetics may contribute to arthritis in humans, but we suggest that this question should be subject to further investigation. Key words : adjuvants, arthritis, cosmetic products, mineral oil, rats, silicone gel. Environ Health Perspect 106:27-32 (1998) . [Online 2 January 1998]
http://ehpnet1.niehs.nih.gov/docs/1998/106p27-32sverdrup/ abstract.html Address correspondence to B. Sverdrup, Department of Medicine, Rheumatology Unit, Karolinska Institute, 171 76 Stockholm, Sweden. This study was supported by grants from the Swedish Workhealthfund. We thank R.A. Harris for critical reading of the manuscript. Received 18 November 1996 ; accepted 17 July 1997.
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