Itchy , irritated throat, cough bc of that, low fever starting (once back at home) offen stuffiness etc etc, some time ago pleuritis like pain: pain with breathing, nausea, headache, general malaise etc. I remembered the repeated cough of Tim Rifat in some of his videos and his comment; "because of ozone". (ozone=a gas)
So I started to investigate a bit: the causes of increase of low ground ozone, like sun radiation (= electromagnetic spectrum radiation), 'space weather' and local low ground ozone: the operation of electrical devices; high power lines, cell towers etc.
Fact seems to be that being exposed to a higher level of ( low ground) ozone (short-term and higher- term) can cause immense health problems ; like specifically respiratory system- lung problems; asthma etc. cardiovasculair, neurodegenerative diseases ( Alzheimer etc.), which can lead a.o. to death.
I simply will copy and past some articles; everyone who wants to read them, could analyse and deduce some possible causes , effects and correlations themselves...
I want to repeat as well this article about EMF and health effects;Covid-19, which I put on a former blog:
https://www.electricsense.com/5g-covid-19/
I want to repeat as well this article about EMF and health effects;Covid-19, which I put on a former blog:
https://www.electricsense.com/5g-covid-19/
Ozone
Ozone (O3) is an allotrope of oxygen, the molecule consisting of three oxygen atoms instead of the more stable diatomic O2.
Ozone is a powerful oxidizing agent.
It is present in low concentrations throughout the Earth's atmosphere.
It has many industrial and consumer applications as well as being used in ozone therapy.
Ozone may be formed from O2 by electrical discharges and by action of high energy electromagnetic radiation.
Certain electrical equipment generate significant levels of ozone.
The highest levels of ozone in the atmosphere are in the stratosphere, in a region also known as the ozone layer between about 10 km and 50 km above the surface.
Here it filters out the shorter wavelengths (less than 320 nm) of ultraviolet light (270 to 400 nm) from the Sun that would be harmful to most forms of life in large doses.
excerpt:
3.4. Ozone
Ozone is a powerful oxidizing agent mainly produced by photochemical reactions of O2, NOx, and VOCs in the atmosphere. However, it cannot be used to eliminate other indoor chemical pollutants, due to its slow reaction with most airborne pollutants [50,51]. Ozone enables rapid reaction with several indoor pollutants, but the reaction products can irritate humans and damage materials. The main sources of indoor ozone mainly come from the outdoor atmosphere and the operation of electrical devices [52]. The machines commonly emitting indoor ozone gas include photocopiers, disinfecting devices, air-purifying devices, and other office devices [53,54,55,56]. The ozone emission mechanisms of these devices can be divided into two categories : Corona discharge and photochemical mechanisms. It has been shown that indoor ozone levels depend on various factors: (i) The outdoor ozone level; (ii) indoor emission rates; (iii) air-exchange rates; (iv) surface-removal rates, and (v) reactions between other chemicals and ozone in the air [50]. Indoor ozone levels generally fluctuate between 20% and 80% of the outdoor ozone level according to the air-exchange rate [57]. Humans are exposed to ozone primarily by inhalation, but skin exposure is also a recognized vector [58]
and:
Health Effects of Ozone Pollution
Ozone is a powerful oxidant that can irritate the airways.
Ozone in the air we breathe can harm our health, especially on hot sunny days when ozone can reach unhealthy levels. Even relatively low levels of ozone can cause health effects.
Who is at risk?
People most at risk from breathing air containing ozone include people with asthma, children, older adults, and people who are active outdoors, especially outdoor workers. In addition, people with certain genetic characteristics, and people with reduced intake of certain nutrients, such as vitamins C and E, are at greater risk from ozone exposure.
Children are at greatest risk from exposure to ozone because their lungs are still developing and they are more likely to be active outdoors when ozone levels are high, which increases their exposure. Children are also more likely than adults to have asthma.
What health problems can ozone cause?
Ozone can cause the muscles in the airways to constrict, trapping air in the alveoli. This leads to wheezing and shortness of breath.
Ozone can cause the muscles in the airways to constrict, trapping air in the alveoli. This leads to wheezing and shortness of breath.
Ozone can:
- Make it more difficult to breathe deeply and vigorously.
- Cause shortness of breath, and pain when taking a deep breath.
- Cause coughing and sore or scratchy throat.
- Inflame and damage the airways.
- Aggravate lung diseases such as asthma, emphysema, and chronic bronchitis.
- Increase the frequency of asthma attacks.
- Make the lungs more susceptible to infection.
- Continue to damage the lungs even when the symptoms have disappeared.
- Cause chronic obstructive pulmonary disease (COPD).
These effects have been found even in healthy people, but can be more serious in people with lung diseases such as asthma. They may lead to increased school absences, medication use, visits to doctors and emergency rooms, and hospital admissions.
Long-term exposure to ozone is linked to aggravation of asthma, and is likely to be one of many causes of asthma development. Long-term exposures to higher concentrations of ozone may also be linked to permanent lung damage, such as abnormal lung development in children.
Recent studies consistently report associations between short-term ozone exposures and total non-accidental mortality, which includes deaths from respiratory causes. Studies suggest that long-term exposure to ozone also may increase the risk of death from respiratory causes, but the evidence is not as strong as the evidence for short-term exposure.
An excerpt of another article:
Immune-inflammatory Responses and Emerging Effects
As a potent oxidizing gas, ambient ozone is well-known to cause oxidative damages to the cells and the lining fluids of the airways, thereby inducing immune-inflammatory responses in the lung. Recent findings have shown that innate immunity is implicated in ozone-induced airway inflammation, such as the involvement of innate lymphoid cells (ILCs) in mice (33, 34). Ozone exposure contributes to the increased expression of mRNA of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-lβ), interleukin-6 (IL-6), and interleukin-8 (IL-8) in human alveolar macrophages (35) and increased concentrations of IL-6, IL-8, and fibrinogenic proteins in human airway epithelial cells (36). A seminal work by Koren et al. demonstrated that an acute exposure to ozone (0.4 ppm for 2 h) resulted in 8.2-fold increase of polymorphonuclear leukocytes (PMN) in bronchial alveolar lavage (BAL) fluid and enhanced level of inflammatory mediators in the lower airways of humans (37). Krishna et al. further confirmed that ozone-induced neutrophil influx in human peripheral airways was partly mediated by IL-8 (38). Ozone exposure resulted in significant neutrophilic inflammation, reflected with increased levels of myeloperoxidase (MPO) in the supernatant of induced sputum samples from healthy subjects (39, 40).
These immune-inflammatory responses to ozone may “spill over” to the circulatory system, which may help explain emerging evidence on the cardiovascular and neuronal effects of ozone. Since the 2013 EPA assessment was released, several studies conducted in North America further confirmed significant positive associations, robust to controlling for co-pollutants, between short-term ozone exposure and one or more of the following mortality classifications: cardiovascular, dysrhythmia, cardiometabolic, and ischemic heart disease. A meta-analysis of 53 studies showed a weak but significant association between ozone and hospital admission and mortality from stroke (41). Significant associations of ozone were found with ischemic stroke occurrence in Seoul (42) and with non-myocardial infarction out-of-hospital cardiac arrests in Helsinki (43). Although Jerrett et al. (44) in the original analysis of an American Cancer Society cohort found that ozone exposure was associated with respiratory but not cardiovascular mortality, in the follow-up study using the same cohort, Turner et al. (14) found a significant association of long-term exposure to ozone with cardiovascular mortality. A recent cohort study by Lim et al. further confirmed this association between long-term exposure to ozone and increased cardiovascular mortality (45). However, there have also been epidemiological studies reporting null findings between long-term ozone exposure and cardiovascular mortality in Europe (46, 47).
Initiated in the lung, the immune-inflammatory responses to ozone may ultimately contribute to increased cardiovascular mortality and morbidity via two major pathways affecting hemostasis and autonomic tone. Increased exposure to ambient ozone has been associated with increased levels of hemostatic markers, including fibrinogen (48–50), von Willebrand factor (49), and plasminogen activator inhibitor-1 (48). Xia et al. revealed that short-term exposure to ambient ozone can elevate serum levels of ACE and ET-1, decrease their DNA methylation, and alter the lipid metabolism, which may be partly responsible for increased blood pressure and vascular endothelial disfunction (51). Day et al. found that an increase in 24-h or 2-week average exposure to ozone was associated with increased p-selectin (a soluble plasma marker of platelet activation), suggesting that ozone exposure increases the risk of thrombosis (21). Wang et al. found that increased ambient ozone exposure was associated with increased rate of carotid wall thickness progression and risk of new plaque formation in healthy adults (52). Jia et al. showed that ambient ozone exposure within several minutes can decrease heart rate variability in the healthy elderly subjects, suggesting that a dysfunction of cardiac autonomic nervous system may be involved (53). In controlled human exposure studies, a few hours of ozone exposure resulted in changes in markers of inflammation and fibrinolysis at 300 ppb and changes in cardiac autonomic function at 110–300 ppb (54, 55). Although one study found a blunting of exercise-induced blood pressure increases (56) and another found increased systolic blood pressure in response to ozone exposure (57), other such studies found increases in diastolic blood pressure to a co-exposure of ozone and concentrated ambient PM but not to ozone alone (58, 59). In contrast, animal studies with high ozone exposures have generated more consistent findings on cardiovascular effects of ozone through altering vascular tone (60–62), mRNA for genes encoding thrombogenic factors (63), and atherogenesis (60).
Additionally, deleterious effects of ozone exposure on the central nervous system (CNS) are emerging (64, 65). Neurodegenerative disorders, such as Alzheimer's disease (AD) and Parkinson's disease, have been linked to ozone exposures in recent epidemiologic studies (66, 67). The following toxicological studies in rodents have demonstrated the CNS effects of ozone, shedding light on biological mechanisms to support the link between ozone exposure and outcomes related to CNS. Rodríguez et al. showed that ozone exposure resulted in the activation of apoptotic death in rat hippocampus mediated by endoplasmic reticulum stress (68). Bello-Medina et al. found that rats chronically exposed to ozone exhibited deficits in learning and memory loss associated with deafferentation in hippocampus-related neurons (69). Chronic exposure to low-dose ozone, on the other hand, could enhance systemic and hippocampal Th17/IL-17A immune responses, which may be partly responsible for neurodegenerative effects in rats (70).
AND THIS PDF; IMPACT OF CABINE OZONE CONCENTRATIONS PASSENGER REPORTED SYMPTOMS IN COMMERCIAL AIRCRAFT!!
AIRCLINE CREW ARE CLASSIFIED AS RADIATION WORKERS...
