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

2003Archives of Environmental Health An International JournalJournal Article

Hypothalamic-PituitaryImmune/InnateNeurologicalRespiratory/Sinus

Indoor Mold (Stachybotrys, Aspergillus, etc.)MycotoxinsWater-Damaged Buildings (WDB)

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.

Key Biomarkers

Abnormal nerve conduction studies (mixed sensory-motor polyneuropathy, motor neuropathy, sensory neuropathy)Abnormal T and B cell subsets (CD20+, CD5+CD25+, CD3+CD26+, CD8+HLR-DR+, CD8+CD38+)Antinuclear autoantibodies (ANA)Autoantibodies against smooth muscle (ASM)Decreased CD8+CD11b+ and CD3-CD16+CD56+ NK cellsElevated IgA, IgM, IgG to neural antigensMold-specific antibodies and mycotoxin antibodiesNeural autoantibodies (anti-myelin basic protein, anti-myelin-associated glycoprotein, anti-ganglioside GM1, anti-sulfatide, anti-MOG, anti-alpha-B-crystallin, anti-chondroitin sulfate, anti-tubulin, anti-neurofilament)QEEG abnormalities (narrowed frequency bands, increased alpha and theta power in frontal areas)Trichothecene toxins in urine and serum

Symptom Clusters

Autonomic nervous system dysfunctionCognitive impairment (short-term memory loss, concentration problems, hand-eye coordination deficits)Neurobehavioral dysfunction (balance impairment, reaction time delay, color discrimination problems)Neuropsychological impairment (memory loss, executive dysfunction, visuospatial deficits, psychomotor speed reduction)Peripheral neuropathy (numbness, tingling, tremors, muscle weakness)Psychological symptoms (depression, acute stress, adjustment disorder, PTSD)Pulmonary dysfunction (reduced vital capacity, abnormal spirometry)Respiratory symptoms (rhinorrhea, sinus tenderness, wheezing, airway obstruction)

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