Chemtrails KILL!!!

How far could you see today?
Aviation emissions containing particulate matter (PM) create widespread cloud cover daily over populations worldwide.
PARTICULATE MATTER, MORTALITY AND VISIBILITY
Increases in the amount of particulate matter in the air have been proven beyond a doubt to directly cause corresponding increases in the death rate of the exposed population. Increased particulate matter also decreases visibility. This interesting chart clearly shows the relationship between visibility and mortality. A decrease in visibility from 60 miles to 28 miles results in an increase in the death rate of nearly 25 percent!! Chemtrails Kill. Even without the added toxic chemicals and bio matter in the chemtrails the particulates alone are deadly.

[link to i102.photobucket.com]


[link to en.wikipedia.org]
[link to curriculum.toxicology.wikispaces.net]

At a cellular level barium induces hypokalemia by two synergistic mechanisms. Barium is a competitive blocker of the potassium rectifier channel which is responsible for the efflux of intracellular potassium out of the cell. It may also directly increase cell membrane permeability to sodium. This causes a secondary increase Na+-K+ pump electrogenesis leading to a shift of extracellular potassium into the cell. Intracellular trapping of potassium leads to depolarization and paralysis. (14) Additionally, the inhibition of potassium channels increases vascular resistance and reduces blood flow (2)(4) and is the likely mechanism for hypertension and lactic acidosis (see below).

High level contamination by natural and industrial sources of the alkali earth metal, barium (Ba) has been identified in the ecosystems/ workplaces that are associated with high incidence clustering of multiple sclerosis (MS) and other neurodegenerative diseases such as the transmissible spongiform encephalopathies (TSEs) and amyotrophic lateral sclerosis (ALS). Analyses of ecosystems supporting the most renowned MS clusters in Saskatchewan, Sardinia, Massachusetts, Colorado, Guam, NE Scotland demonstrated consistently elevated levels of Ba in soils (mean: 1428 ppm) and vegetation (mean: 74 ppm) in relation to mean levels of 345 and 19 ppm recorded in MS-free regions adjoining. The high levels of Ba stemmed from local quarrying for Ba ores and/or use of Ba in paper/foundry/ welding/textile/oil and gas well related industries, as well as from the use of Ba as an ASTMOSPHERIC AEROSOL spray for enhancing/refracting the signalling of radio/radar waves along military jet flight paths, missile test ranges, etc. It is proposed that chronic contamination of the biosystem with the reactive types of Ba salts can initiate the pathogenesis of MS; due to the conjugation of Ba with free sulphate, which subsequently deprives the endogenous sulphated proteoglycan molecules (heparan sulfates) of their sulphate co partner, thereby disrupting synthesis of S-proteoglycans and their crucial role in the fibroblast growth factor (FGF) signalling which induces oligodendrocyte progenitors to maintain the growth and structural integrity of the myelin sheath. Loss of S-proteoglycan activity explains other key facets of MS pathogenesis; such as the aggregation of platelets and the proliferation of superoxide generated oxidative stress. Ba intoxications disturb the sodium-potassium ion pump--another key feature of the MS profile. The co-clustering of various neurodegenerative diseases in these Ba-contaminated ecosystems suggests that the pathogenesis of all of these diseases could pivot upon a common disruption of the sulphated proteoglycan-growth factor mediated signalling systems. Individual genetics dictates which specific disease...

Strontium has been found in atmospheric aerosols.

Due to the fact that strontium is located above barium in the group 2, potential for similar complications, such as hypokalemia, is considered during administration [4]. Acute toxicity of strontium has not been described in humans [3, 5]. In animals, high-dose strontium causes hypocalcaemia, rickets, dental caries, endocrine abnormalities, in-coordination and phosphorus deficiency [3, 6, 7]. Chronic exposure of humans is associated with elevated levels of this element, but documented toxicity is lacking. Neither delayed toxicity nor chronic toxicity can be excluded in patients treated with SrR. Metallothioneins (MT) were discovered in 1957 by Margoshes and Vallee as cadmium binding cysteine rich proteins.
Previously, we investigated interactions of MT with heavy metals (cadmium, zinc, platinum, palladium) by using hanging mercury drop electrode (HMDE) and differential pulse voltammetry [25, 36, 38]. We used these results to suggest new heavy metal biosensors based on metal-protein interactions. In this work, we studied the influence of strontium(II) ions on catalytic signals evolving due to presence of free ĀSH moieties of MT and cobalt(III) complex as supporting electrolyte. MT (100nM) was accumulated onto HMDE under open circuit. Optimal time of MT accumulation onto HMDE was verified in several papers.

Arsenic can exacerbate hypokalemia.
"Still yet, (Mari, et al, 2004) have hypothesized that the combination of arsenic, quinine, and calomel, induced hypokalemia, and ultimately caused the fatal torsades de pointes."

Arsenic has been found in atmospheric aerosols.
[link to uncensored.co.nz]
[link to aircrap.org]

2010 Air Particulates (This is only a preliminary overview of Arizona air particulates.) These figures indicate how many times they are over the “allowable” toxic limit: Aluminum: 15.8 Antimony: 63.3 [This is not a typo] Arsenic: 418 [This is not a typo] Barium: 5.3 Cadmium: 6 Chromium: 6.4 Copper: 9 Iron: 43.5 [This is not a typo] Lead: 15.7 Manganese: 513.8 [This is not a typo] Nickel: 10.7 Zinc: 7.5

[link to www.ncbi.nlm.nih.gov]

Worldwide, approximately three million people suffer sudden cardiac death annually. These deaths often emerge from a complex interplay of substrates and triggers. Disturbed potassium homeostasis among heart cells is an example of such a trigger. Thus, hypokalemia and, also, more transient reductions in plasma potassium concentration are of importance. Hypokalemia is present in 7% to 17% of patients with cardiovascular disease. Furthermore, up to 20% of hospitalized patients and up to 40% of patients on diuretics suffer from hypokalemia. Importantly, inadequate management of hypokalemia was found in 24% of hospitalized patients. Hypokalemia is associated with increased risk of arrhythmia in patients with cardiovascular disease, as well as increased all-cause mortality, cardiovascular mortality and heart failure mortality by up to 10-fold. Long-term potassium homeostasis depends on renal potassium excretion. However, skeletal muscles play an important role in short-term potassium homeostasis, primarily because skeletal muscles contain the largest single pool of potassium in the body. Moreover, due to the large number of Na /K pumps and K channels, the skeletal muscles possess a huge capacity for potassium exchange. In cardiovascular patients, hypokalemia is often caused by nonpotassium-sparing diuretics, insufficient potassium intake and a shift of potassium into stores by increased potassium uptake stimulated by catecholamines, beta-adrenoceptor agonists and insulin. Interestingly, drugs with a proven significant positive effect on mortality and morbidity rates in heart failure patients all increase plasma potassium concentration. Thus, it may prove beneficial to pay more attention to hypokalemia and to maintain plasma potassium levels in the upper normal range. The more at risk of fatal arrhythmia and sudden cardiac death a patient is, the more attention should be given to the potassium homeostasis.