Daily Archives: March 14, 2016

Cyanobacteria, Cyanotoxins in Desert Water Impoundments and Wells

Chatziefthimiou AD, Metcalf JS, Glover WB, Banack SA, Dargham SR, Richer RA. Cyanobacteria and cyanotoxins are present in drinking water impoundments and groundwater wells in desert environments. Toxicon 2016 Feb 24;114:75-84. doi: 10.1016/j.toxicon.2016.02.016.

Desert environments and drylands experience a drastic scarcity of water resources. To alleviate dependence on freshwater for drinking water needs, countries have invested in infrastructure development of desalination plants. Collectively, the countries of the Arabian Gulf produce 45% of the world’s desalinated water, which is stored in dams, mega-reservoirs and secondary house water tanks to secure drinking water beyond daily needs. Improper storage practices of drinking water in impoundments concomitant with increased temperatures and light penetration may promote the growth of cyanobacteria and accumulation of cyanotoxins. To shed light on this previously unexplored research area in desert environments, we examined drinking and irrigation water of urban and rural environments to determine whether cyanobacteria and cyanotoxins are present, and what are the storage and transportation practices as well as the environmental parameters that best predict their presence. Cyanobacteria were present in 80% of the urban and 33% of the rural water impoundments. Neurotoxins BMAA, DAB and anatoxin-a(S) were not detected in any of the water samples, although they have been found to accumulate in the desert soils, which suggests a bioaccumulation potential if they are leached into the aquifer. A toxic BMAA isomer, AEG, was found in 91.7% of rural but none of the urban water samples and correlated with water-truck transportation, light exposure and chloride ions. The hepatotoxic cyanotoxin microcystin-LR was present in the majority of all sampled impoundments, surpassing the WHO provisional guideline of 1 μg/l in 30% of the urban water tanks. Finally, we discuss possible management strategies to improve storage and transportation practices in order to minimize exposure to cyanobacteria and cyanotoxins, and actions to promote sustainable use of limited water resources.

How Messaging Forced the 97% “Consensus”

“The point of this book is not to disprove the “consensus” on global warming, and it doesn’t attempt to examine whether or not there is one. Instead, it shows the tactics and dangers of consensus messaging, and how these have hurt our ability to have any real discussion.” click here and here

NASA Temperature Adjustments are Arbitrary

“Nothing about climate science reeks more of confirmation bias, than the changes scientists make to their own data sets over time. They all show exactly the same pattern of monotonically cooling the past and warming the present, regardless of the instrumentation.” click here

PFAS Exposure via Water, Inhalation, Diet, and House Dust, Korea

Tian Z, Kim SK, Shoeib M, Oh JE, Park JE. Human exposure to per- and polyfluoroalkyl substances (PFASs) via house dust in Korea: Implication to exposure pathway. The Science of the total environment. 2016 Feb 27;553:266-275. doi: 10.1016/j.scitotenv.2016.02.087.

A wide range of per- and polyfluoroalkyl substances (PFASs), including fluorotelomer alcohols (FTOHs), perfluorooctane sulfonamidoethanols (FOSEs), perfluoroalkyl carboxylic acids (PFCAs), and perfluoroalkane sulfonic acids (PFSAs), were measured in fifteen house dust and two nonresidential indoor dust of Korea. Total concentrations of PFASs in house dust ranged from 29.9 to 97.6ngg-1, with a dominance of perfluorooctane sulfonic acid (PFOS), followed by 8:2 FTOH, N-Ethyl perfluorooctane sulfonamidoethanol (EtFOSE), perfluoroctanoic acid (PFOA). In a typical exposure scenario, the estimated daily intakes (EDIs) of total PFASs via house dust ingestion were 2.83ngd-1 for toddlers and 1.13ngd-1 for adults, which were within the range of the mean EDIs reported from several countries. For PFOA and PFOS exposure via house dust ingestion, indirect exposure (via precursors) was a minor contributor, accounting for 5% and 12%, respectively. An aggregated exposure (hereafter, overall-EDIs) of PFOA and PFOS occurring via all pathways, estimated using data compiled from the literature, were 53.6 and 14.8ngd-1 for toddlers, and 20.5 and 40.6ngd-1 for adults, respectively, in a typical scenario. These overall-EDIs corresponded to 82% (PFOA) and 92% (PFOS) of a pharmacokinetic model-based EDIs estimated from adults’ serum data. Direct dietary exposure was a major contributor (>89% of overall-EDI) to PFOS in both toddlers and adults, and PFOA in toddlers. As for PFOA exposure of adults, however direct exposure via tap water drinking (37%) and indirect exposure via inhalation (22%) were as important as direct dietary exposure (41%). House dust-ingested exposure (direct+indirect) was responsible for 5% (PFOS in toddlers) and <1% (PFOS in adults, and PFOA in both toddlers and adults) of the overall-EDIs. In conclusion, house-dust ingestion was a minor contributor in this study, but should not be ignored for toddlers’ PFOS exposure due to its significance in the worst-case scenario.