Difficult to clean up

Several Sierra trails are toxic, group says

June 23, 2010|By Kelly Zito, Chronicle Staff Writer


A mountain biker cruises from the Sierra Buttes to Downieville, a hub for bikers. Although the Sierra Fund points to problems in Downieville, the Mountain Bike and Big Boulder trails were fine. Credit: Al Seib / Los Angeles Times 2007.

The thousands of mine shafts that pockmark the Sierra Nevada and testify to California's Gold Rush riches have also left a legacy of toxic contamination in some of the state's popular recreation areas, according to a new study.

The Worldwide Campaign

Stop an invisible mass killing

The worldwide campaign

Millions of people worldwide are becoming ill or dying every day, without it being known that the cause of this mass killing is chronic arsenic poisoning.

Arsenic occurs naturally all over the world, but some human activities such as hard rock mining for gold, as well as burning coal and oil and using contaminated groundwater for drinking and irrigation have largely surpassed the natural sources of arsenic, with modern gold mining being by far the most important man-made source of arsenic [1].

In addition, arsenic is still used as an ingredient in various industries, in the production of feed additives, drugs, pesticides, wood preservatives and glass, among others.

Atmospheric stability of arsines and the determination of their oxidative products in atmospheric aerosols (PM10): evidence of the widespread phenomena of biovolatilization of arsenic.

J Environ Monit, 2010, 12(2):409-16.
Jakob R, Roth A, Hass K, Krupp EM, Raab A, Smichowski P, Gómez D, Feldmann J.
Trace Element Speciation Laboratory Aberdeen, Department of Chemistry, University of Aberdeen, Meston Building, Meston Walk, Aberdeen, Scotland, UK.
Abstract - Biovolatilisation of arsenic as their arsines in the form of AsH(3), and mono-, di and trimethylarsine has often been determined under laboratory conditions. Although environmental point sources such as landfill sites or hot springs have been characterised, only limited knowledge is available on how widespread the formation of volatile methylated arsenic compounds are in the environment. Here we studied the atmospheric stability of the different arsines and quantified their oxidation products in atmospheric particulate matter (PM(10)) in two locations in Argentina. The atmospheric half-life of the arsines range from 19 weeks for AsH(3) to 2 d for trimethylarsine (TMAs) at 20 degrees C in the dark, while during simulated daytime conditions the stability is reduced for all arsines and in particular for the methylated arsines by three orders of magnitude which suggests that TMAs can only be dispersed at night. At both locations the arsenic concentration was in all samples below 1 ng As m(-3), which is considered as rural background for arsenic. The oxidation products, i.e. methylarsonate (MA), dimethylarsinate (DMA) and trimethylarsine oxide (TMAO) were identified by using HPLC-ICP-MS/ES-MS in more than 90% of the 49 PM(10) samples taken from 8 sampling points at the two geographically different locations. TMAO was the predominate organoarsenicals in both locations (66 and 69%, respectively) while DMA was determined to be between 13 and 19% of all organoarsenicals at the two locations. The concentration of the organoarsenicals ranged from 4 to 60 pg As as TMAO m(-3), while the maximum concentration for DMA and MA were 16 and 6 pg As m(-3), respectively. No difference in terms of the concentration or distribution of the organoarsenicals in the PM(10) samples was identified as significant. Since the two locations were different in climate and industrial impact and sampled in different seasons, these data suggest that methylated arsenicals do occur as background chemicals in the environment. Due to the low atmospheric stability of the methylated arsines, it is suggested that biovolatilization of arsenic as methylated arsines is a widespread phenomenon. More studies however are necessary to identify the major sources and determine the flux of the volatilization process in order to determine whether or not the process has environmental significance.

One in five deaths linked to arsenic in water

New study links 1 in 5 deaths in Bangladesh to arsenic in the drinking water

Increased mortality is linked to chronic diseases with a 70 percent increased mortality risk among those with the highest level of exposure

Source: EurekAlert (*)

June 23, 2010 – Between 33 and 77 million people in Bangladesh have been exposed to arsenic in the drinking water—a catastrophe that the World Health Organization has called "the largest mass poisoning in history." A new study published in the current issue of the medical journal The Lancet provides the most complete and detailed picture to date of the high mortality rates associated with this exposure, which began with the widespread installation of tube wells throughout the country 30 years ago—a measure intended to control water-bourne diseases.

The arsenic exposure hypothesis for Alzheimer disease

Alzheimer Disease and Associated Disorders, 2010 May 13 [Epub ahead of print].
Gong G, O'Bryant SE 
F. Marie Hall Institute for Rural and Community Health Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX.
Abstract - Prior research has shown that arsenic exposure induces changes that coincide with most of the developmental, biochemical, pathologic, and clinical features of Alzheimer disease (AD) and associated disorders. On the basis of this literature, we propose the Arsenic Exposure Hypothesis for AD that is inclusive of and cooperative with the existing hypotheses. Arsenic toxicity induces hyperphosphorylation of protein tau and overtranscription of the amyloid precursor protein, which are involved in the formation of neurofibrillary tangles and brain amyloid plaques, consistent with the amyloid hypothesis of AD. Arsenic exposure has been associated with cardiovascular diseases and associated risk factors, which is in agreement with the vascular hypothesis of AD. Arsenic exposure invokes brain inflammatory responses, which resonates with the inflammatory hypotheses of AD. Arsenic exposure has been linked to reduced memory and intellectual abilities in children and adolescents, which provides a biologic basis for the developmental origin of health and disease hypothesis for AD. Arsenic and its metabolites generate free radicals causing oxidative stress and neuronal death, which fits the existing oxidative stress hypothesis. Taken together, the arsenic exposure hypothesis for AD provides a parsimonious testable hypothesis for the development and progression of this devastating disease at least for some subsets of individuals.