Neural autoantibodies and neurophysiologic abnormalities in patients exposed to molds in water-damaged buildings

Arch Environ Health. 2003 Aug;58(8):464-74. doi: 10.3200/AEOH.58.8.464-474.

Abstract

Adverse health effects of fungal bioaerosols on occupants of water-damaged homes and other buildings have been reported. Recently, it has been suggested that mold exposure causes neurological injury. The authors investigated neurological antibodies and neurophysiological abnormalities in patients exposed to molds at home who developed symptoms of peripheral neuropathy (i.e., numbness, tingling, tremors, and muscle weakness in the extremities). Serum samples were collected and analyzed with the enzyme-linked immunosorbent assay (ELISA) technique for antibodies to myelin basic protein, myelin-associated glycoprotein, ganglioside GM1, sulfatide, myelin oligodendrocyte glycoprotein, alpha-B-crystallin, chondroitin sulfate, tubulin, and neurofilament. Antibodies to molds and mycotoxins were also determined with ELISA, as reported previously. Neurophysiologic evaluations for latency, amplitude, and velocity were performed on 4 motor nerves (median, ulnar, peroneal, and tibial), and for latency and amplitude on 3 sensory nerves (median, ulnar, and sural). Patients with documented, measured exposure to molds had elevated titers of antibodies (immunoglobulin [Ig]A, IgM, and IgG) to neural-specific antigens. Nerve conduction studies revealed 4 patient groupings: (1) mixed sensory-motor polyneuropathy (n = 55, abnormal), (2) motor neuropathy (n = 17, abnormal), (3) sensory neuropathy (n = 27, abnormal), and (4) those with symptoms but no neurophysiological abnormalities (n = 20, normal controls). All groups showed significantly increased autoantibody titers for all isotypes (IgA, IgM, and IgG) of antibodies to neural antigens when compared with 500 healthy controls. Groups 1 through 3 also exhibited abnormal neurophysiologic findings. The authors concluded that exposure to molds in water-damaged buildings increased the risk for development of neural autoantibodies, peripheral neuropathy, and neurophysiologic abnormalities in exposed individuals.

MeSH terms

  • Adult
  • Autoantibodies / blood*
  • Autoantibodies / immunology
  • Case-Control Studies
  • Chondroitin Sulfates / immunology
  • Environmental Exposure / adverse effects*
  • Environmental Exposure / analysis
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Fungi* / immunology
  • G(M1) Ganglioside / immunology
  • Humans
  • Immunoglobulin A / blood
  • Immunoglobulin G / blood
  • Immunoglobulin M / blood
  • Male
  • Middle Aged
  • Mycotoxins / immunology
  • Myelin Proteins / immunology
  • Nerve Tissue Proteins / immunology*
  • Neural Conduction
  • Neurofilament Proteins / immunology
  • Neuropsychological Tests
  • Peripheral Nervous System Diseases* / diagnosis
  • Peripheral Nervous System Diseases* / etiology
  • Peripheral Nervous System Diseases* / immunology
  • Sick Building Syndrome* / diagnosis
  • Sick Building Syndrome* / etiology
  • Sick Building Syndrome* / immunology
  • Sulfoglycosphingolipids / immunology
  • Surveys and Questionnaires
  • Tubulin / immunology
  • Water Microbiology*

Substances

  • Autoantibodies
  • Immunoglobulin A
  • Immunoglobulin G
  • Immunoglobulin M
  • Mycotoxins
  • Myelin Proteins
  • Nerve Tissue Proteins
  • Neurofilament Proteins
  • Sulfoglycosphingolipids
  • Tubulin
  • G(M1) Ganglioside
  • Chondroitin Sulfates