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Gene-environment interactions increase the risk of paediatric-onset multiple sclerosis associated with household

Zahra Nasr1, Vinicius Andreoli Schoeps1, Amin Ziaei1

  • 1UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California, USA.

Journal of Neurology, Neurosurgery, and Psychiatry
|February 1, 2023
PubMed

Insights

Household chemical exposures, like weed control products, are linked to increased pediatric multiple sclerosis risk. Gene-environment interactions, particularly with NFKB1, suggest a causal role for these toxins.

Area of Science:

  • Environmental Health
  • Genetics
  • Neurology

Background:

  • Previous research indicated a link between household chemical exposure and increased risk of pediatric-onset multiple sclerosis (MS).
  • This study investigates gene-environment interactions in the context of pediatric MS and household chemical exposures.

Purpose of the Study:

  • To examine gene-environment interactions between household chemical exposures and specific genetic risk factors for pediatric-onset MS.
  • To identify specific household chemicals and genetic variants that interact to influence MS risk in children.

Main Methods:

  • A case-control study design was employed, including 490 cases of pediatric-onset MS and 716 controls.
  • Genetic factors analyzed included HLA variants (DRB1*15, A*02) and SNPs in metabolic pathway genes (IL-6, BCL-2, NFKB1).
  • Statistical analyses estimated odds ratios (OR) for chemical exposures and interactions (additive and multiplicative) with genetic variants.

Main Results:

  • Exposure to insect repellent, weed control products, and plant/tree control products were associated with increased odds of pediatric MS.
  • Significant additive gene-environment interaction was found between weed control products and NFKB1 (rs7665090) genotype (AP=0.48).
  • A significant multiplicative interaction was observed between weed control products and NFKB1 SNP GG genotype (OR=2.30).
  • Interaction was also noted between plant/disease control products and absence of HLA-A*02 (AP=0.56).

Conclusions:

  • The identified gene-environment interactions support a potential causal role for household toxins in the development of pediatric-onset MS.
  • These findings highlight the importance of considering both genetic predisposition and environmental exposures in pediatric MS etiology.
Abstract

Keywords:
geneticsmultiple sclerosispaediatric neurology

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