Publications: Peer-reviewed journal articles (by staff)

Quantitative assessment of aerosolized cyanobacterial toxins at two New Zealand lakes

1 January, 2011
CITATION

Wood SA, Dietrich DR 2011. Quantitative assessment of aerosolized cyanobacterial toxins at two New Zealand lakes. Journal of Environmental Monitoring 13(6): 1617-1624.

ABSTRACT

The cyanobacterial toxins, nodularin and microcystin, are highly efficient inhibitors of cellular protein phosphatases. Toxicity primarily evolves following ingestion of cyanobacterial material or toxins and results in liver and renal pathology. Ingestion is the main route of exposure in the World Health Organizations current risk assessment of nodularin and microcystins. Nasally applied microcystin appears to have a 10-fold higher availability and toxicity than orally ingested toxins, suggesting that aerosolized toxins could represent a major risk for human populations close to lakes with cyanobacterial blooms. In this study, nodularin and microcystin levels in aerosols were assessed using high and low volume air samplers for 4, 12 and 24 h periods at lakes Forsyth and Rotorua (South Island, New Zealand). These lakes were experiencing blooms of Nodularia spumigena and Microcystis sp., respectively. Using the high volume samplers up to 16.2 pg m(-3) of nodularin and 1.8 pg m(-3) of microcystins were detected in the air. Aerosolized nodularin and microcystins do not appear to represent an acute or chronic hazard to humans. The latter was concluded based on calculations using average human air intakes, the highest nodularin or microcystin concentrations measured in the air in this study, and assuming inhalatory toxicities comparable to toxicological data obtained following intraperitoneal applications in mice. However, as the toxin concentrations in the air were calculated over extended sampling periods, peak values may be underestimated. Aerosolized toxins should be considered when developing risk assessments particularly for lakeside populations and recreational users where inhalation of cyanotoxins may be a secondary exposure source to a primary oral exposure.