Abstract
Dietary or aerosol exposure to the environmental neurotoxin β-N-methylamino-l-alanine (BMAA) is a putative risk factor for the development of sporadic neurodegenerative disease. There are many potential sources of BMAA in the environment, but BMAA presence and quantities are highly variable. It has been suggested that BMAA in human hair may serve as an indicator of exposure. We sought to evaluate the use of the BMAA content of human scalp hair as an indicator of exposure, as well as the correlation between specific lifestyle or dietary habits, reported as hypothesised exposure risk factors, and BMAA in hair. Scalp hair samples and questionnaires were collected from participants in a small residential village surrounding a freshwater impoundment renowned for toxic cyanobacterial blooms. Data suggested a positive correlation between hair BMAA content and consumption of shellfish, and possibly pork. No statistically significant correlations were observed between hair BMAA content and residential proximity to the water or any other variable. Hair BMAA content was highly variable, and in terms of exposure, probably reflects primarily dietary exposure. However, the BMAA content of human hair may be affected to a great extent by several other factors, and as such, should be used with caution when evaluating human BMAA exposure, or correlating exposure to neurodegenerative disease incidence.
Highlights
The aetiology of sporadic neurodegenerative disease remains poorly understood, and with more than 95% of all neurodegenerative disease (ND) cases being of non-genetic or unknown cause, identifying risk factors has been the focus of many studies
All hair samples in this experiment were determined to be free of BMAA prior to exposure to BMAA
Other factors that may affect the structure of the hair fibre, like UV-radiation, heat, and weathering with age, can have a considerable effect on the binding of exogenous BMAA
Summary
The aetiology of sporadic neurodegenerative disease (sND) remains poorly understood, and with more than 95% of all neurodegenerative disease (ND) cases being of non-genetic or unknown cause, identifying risk factors has been the focus of many studies (reviewed in [1,2]). A recurring trend is the link between place of birth and the development of sND [6], which supports an environmental aetiology, as well as the importance of exposure to a causative agent during early-life development [1,2,5]. To directly link exposure to an environmental toxicant to the development of ALS, AD or PD is extremely difficult, due to the long latencies of these diseases and the natural migration of people from their place of birth or early childhood years. BMAA is produced by cyanobacteria [7], and its presence has recently been reported in diatoms [8,9] and dinoflagellates [10]
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