Background Systemic lupus erythematosus (SLE) is a complex chronic autoimmune disease of unknown etiology. Previous studies of beauty products as potential triggers of SLE development have shown conflicting results. Increasing awareness of parabens and estrogenic chemicals in beauty products prompted us to revisit this topic. Our study examines the relationship between hair chemical use and SLE, investigating their role in the risk of SLE development and severity of disease.

Methods Patients with SLE (n = 388) within an ongoing longitudinal registry at a single center were selected based on diagnosis of SLE, female gender, and age ≥18. Controls (total n = 178; unrelated n = 116) were from the same population-based cohort, recruited via patient family members and ‘bring a friend’ methods. All participants completed a questionnaire on hair chemical use (including dyes, permanents, straighteners) administered at one of their study visits. Disease damage, using the SLICC-Damage Index, and other SLE manifestations were obtained through in-person interviews and chart review and recorded as part of the research registry. Social vulnerability index (SVI) was calculated to identify the relative vulnerability of the participants’ communities, using US Census tract data and current addresses.

Results Patients with SLE were overall more likely to use hair chemicals than controls (OR=1.77; 95% CI=1.16–2.68), table 1. This difference did not persist when the cohort was limited to Black patients and controls (OR=1.77; 95% CI=1.16–2.68) due to low numbers of White participants. Prior use of hair chemicals was not associated with the development of SLE (OR 0.85; 95% CI 0.44–1.62).

Among the patients with SLE, lupus nephritis was more likely to develop among those who used hair chemicals prior to their diagnosis, but this difference was no longer statistically significant after controlling for covariates (OR=1.67;95% CI=0.97 – 2.94), table 2. Overall disease damage scores did not differ (p=0.64). However, when comparing SLE classification criteria, those with prior hair chemical use had a higher risk of developing cutaneous manifestations compared to non-users (p<0.01).

Cutaneous manifestations seen more frequently were malar rash (p<0.01), photosensitivity (p=0.02), and alopecia (p<0.01) and the strongest association was with use of chemical hair straighteners. This significance persisted after controlling for covariates, with increased risk of cutaneous manifestations in those who used chemical hair straighteners prior to diagnosis, (OR 2.08; 95% CI=1.27–3.41).

Conclusion Hair chemical use among females with SLE was common and did not differ significantly from population controls. There was no association between hair chemical use and development of SLE in our study, however, there was a significant increase in cutaneous manifestations if hair chemicals were used prior to SLE diagnosis. This was most significant among those using chemical hair straighteners/relaxers. Further studies delineating patterns of use and the particular chemicals used are underway to better assess these as potentially modifiable triggers of SLE manifestations.