Objective
We hypothesize that different sources of lung irritation may contribute to elicit an immune
reaction in the lungs and subsequently lead to multiple sclerosis (MS) in people with a genetic
susceptibility to the disease. We aimed to investigate the influence of exposure to organic
solvents on MS risk, and a potential interaction between organic solvents and MS risk human
leukocyte antigen (HLA) genes.
Methods
Using a Swedish population-based case-control study (2,042 incident cases of MS and 2,947
controls), participants with different genotypes, smoking habits, and exposures to organic
solvents were compared regarding occurrence of MS, by calculating odds ratios with 95%
confidence intervals using logistic regression. A potential interaction between exposure to
organic solvents and MS risk HLA genes was evaluated by calculating the attributable proportion due to interaction.
Results
Overall, exposure to organic solvents increased the risk of MS (odds ratio 1.5, 95% confidence
interval 1.2–1.8, p = 0.0004). Among both ever and never smokers, an interaction between
organic solvents, carriage of HLA-DRB1*15, and absence of HLA-A*02 was observed with
regard to MS risk, similar to the previously reported gene-environment interaction involving
the same MS risk HLA genes and smoke exposure.
Conclusion
The mechanism linking both smoking and exposure to organic solvents to MS risk may involve
lung inflammation with a proinflammatory profile. Their interaction with MS risk HLA genes
argues for an action of these environmental factors on adaptive immunity, perhaps through
activation of autoaggressive cells resident in the lungs subsequently attacking the CNS