How do you think the human body handles inhalation of fatty acids?
Not well. This can be seen by any of the Safety Data Sheets regarding the handling of fatty acids such as omega 3, omega 6 and omega 9 types of both mono and polyunsaturated oils as produced by Canola and other ‘bio-oil’ flower crops . Side effects include respiratory failure, vomiting, convulsions and suffocation.
Now ask yourself, what countries have experienced the somewhat recently-established phenomena known as “thunderstorm asthma”; a condition that produces anaphylactic responses in people that are not previously reactive allergically to rye grass or other air-borne pollen or had previously exhibited asthma? Australia, UK, US and UAE; all of which are seasonably hot climates.
Victims of “thunderstorm asthma” include healthy young men and women who live in a particular area. That is the only commonality; demographics.
In a report on Thunderstorm Asthma released by ABC Australia, a specialist University Professor mentioned that Thunderstorm Asthma is only resultant from Rye Grass Pollen. Much to the contrary and to the apparent expert’s blind omission as to any other causes, it is definitely not the case and is actually impossible to occur solely due to rye grass as there are so many types of pollen floating through the air. When looking into the weather cycle which featured prior to these storm events, there was also some commonalities; time of year, providing for hot dry spells, then cycling to a rapid change usually a summer storm as such which holds little rain.
The general consensus on the cause of Thunderstorm Asthma is when the wind picks up particle matter from the plant, being pollen, then with that pollen being smashed into microscopic particles, the air-borne pollen which is carried by the warm wind is then inhaled by various victims in a certain location. The precise amount of rain is required to initially pulverise the pollen particles in mid air, but not enough to saturate and weigh down the micro-particles so that they are no longer airborne. The result is a wind event that carries plant matter small enough to inhale.
According to the CSIRO, and to many other sources, Australia is now the world’s second largest canola crop producer. Groups such as Landcare Australia, and other ‘community groups’, in conjunction with Rotary Clubs positioned in rural areas which pool members superannuation in what they call “Self Managed Super Funds” in order to produce and profit from as large a canola crop as possible, are adding to the already flooded canola population, all of which is Genetically Modified to withstand herbicides such as round up and ailments such as “Blackleg” stem rot.
Oleic Acid, also known as monounsaturated omega-9 fatty acid, which constitutes approximately 60% of the byproduct from a canola crop. Linoleic Acid constitutes approximately 20% with the remainder being made up of an assortment of acids.
With these factors combined, and in focusing on the loss of life and effects on general health of thousands of Melbournian’s during the event back in 2016, it would be highly likely that due to the large amount of canola produced in that region, the contents of the fatty-acid laden pollen and the particle weight and size, Canola, as well as Safflower (High Oleic), are more likely to cause Asthma-related symptoms and respiratory failure in a human population living in a certain area than any other plant including, the previous scapegoat, Rye Grass.
Combined with an extraordinarily high iodine content, as studied by the CSIRO in 1977 (Queensland), Oleic Acid, as featured in canola, safflower, olives and others are also responsible for Pulmonary Edema (death) in Sheep (Julien, Hoeffel & Flick 1986). See excerpt with links:
Oleic acid lung injury in sheep
Intravenous infusion of oleic acid into experimental animals causes acute lung injury resulting in pulmonary edema. We investigated the mechanism of oleic acid lung injury in sheep. In experiments with anesthetized and unanesthetized sheep with lung lymph fistulas, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and lymph and plasma protein concentrations. We injured the lungs with intravenous infusions of oleic acid at doses ranging from 0.015 to 0.120 ml/kg. We found that oleic acid caused reproducible dose-related increases in pulmonary arterial pressure and pulmonary vascular resistance, arterial hypoxemia, and increased protein-rich lung lymph flow and extravascular lung water. The lung fluid balance changes were characteristic of increased permeability pulmonary edema. Infusion of the esterified fat triolein had no hemodynamic or lung fluid balance effects. Depletion of leukocytes with a nitrogen mustard or platelets with an antiplatelet serum had no effect on oleic acid lung injury. Treatment of sheep before injury with methylprednisolone 30 mg/kg or ibuprofen 12.5–15.0 mg/kg also had no effects. Unlike other well-characterized sheep lung injuries, injury caused by oleic acid does not require participation of leukocytes.
The responsible parties should be held accountable. It has nothing to do with allergies. Humans, and other animals, are not designed to inhale and/or ingest large amounts of fatty acids. Oleic Acid is already known for its tested effects on sheep and other animals.
Opinion piece written for the benefit of all. For further documentation, please see the following slides.
Bryan Stralow, editor-in-chief, OrganicLifestyle.blog