Environmental Chemicals

Author: laura bucchino
Date: 14/01/2013


Ozone: our enemy or our ally - that is the question

Since we are children we hear about the so called ozone hole .
Every day we read on sprays : "It contains only ozone friendly substances".
Everybody is aware to be breathing ozone.
But actually...

What is it?

Ozone called trioxygen, is a molecule, consisting of three oxygen atoms. It is much less stable than the diatomic allotrope (O2), its half life is about 30 minutes in the lower atmosphere, it means that it breaks down rapidly to the normal dioxygen.

Ozone was proposed as a new substance in air in 1840, and its name comes from the Greek verb ozein (ὄζειν, to smell), because of the peculiar odor after lightning storms. Ozone's odor is sharp, reminiscent of chlorine, and detectable by many people at very little concentrations in air.

Where is it?

In nature ozone can be found at high altitude (15-60 km high) in the stratosphere , that for this reason could be also called "Ozonosphere", it forms a layer protecting the Earth from the sun's ultraviolet rays.

Even if in the lower atmosphere layers, i.e. the so-called troposphere (less than 15 km high from the ground), ozone is less concentrated, it is still present because of the natural interchange with the stratosphere. Its concentration may vary between 20 and 80 µg/m 3, however, it can rise in some areas because of the so-called photochemical smog . It is the chemical reaction of sunlight, nitrogen oxides and volatile organic compounds (VOCs) in the atmosphere, which leaves airborne particles and ground-level ozone. This noxious mixture of air pollutants can include the following:
- Aldehydes
- VOCs
- Nitrogen oxides, such as nitrogen dioxide
- Peroxyacil nitrates
- Tropospheric ozone

Unlike "primary" pollutants, which are directly emitted by specific sources such as carbone monoxyde, ozone is a "secondary" pollutant, so it is difficult to determine the correlation with its precursor. The sources of ozone precursor pollutants are both anthropic (motor vehicles, combustion processes, thermoelectric plants, chemical solvents) and natural (woods and forests emit highly reactive VOCs, like terpens).
Others metereological variables that can affect ozone concentrations are sun radiation intensity and temperature, in fact they trigger photochemical reactions, which are responsible for ozone formation. Moreover the particular concentrations like high pressure, low humidity, high temperature and scarce ventilation can facilitate pollutant stagnation and accumulation. Therefore the presence of ozone varies during the day, from 12 to 6 pm, then decreasing during night hours. On the other hand, the lowest concentrations are recorded in winter, mainly because of the reduced sun radiation.

Industrial application

Because of his oxydant properties, ozone is able to damage the bacterial cell wall, in fact it is used for a lot of purposes :
• Disinfect laundry in hospitals, food factories, care homes etc.;
• Disinfect water in place of chlorine, i.e. sanitize swimming pools and spas
• Kill bacteria on food or on contact surfaces;
• Kill insects in stored grain
• Scrub yeast and mold spores from the air in food processing plants;
• Wash fresh fruits and vegetables to kill yeast, mold and bacteria;
• Eradicate water borne parasites such as Giardia lamblia and Cryptosporidium in surface water treatment plants.

Ozone effects on human physiology

Everyday, we inhale a variable amount of ozone that can affect human physiology in many different ways: positive and negative effects can be detected.


Special attention has been focused on the respiratory system which is the first point of contact with air pollutants in humans and various studies have been performed to evaluate the effects of air pollution on health status demonstrating that the level of environmental pollution has a role in human health as well as temporal exposure. In particular ozone can affect lungs and respiratory system in several ways. These are all short-term health effects:
• It can irritate respiratory system and immediately onset of coughing can occur. Symptoms may last a few hours after exposure.
• It can impair ability to breathe and can make breathing more rapid and shallow.
It can inflame and damage the epithelium that lines lungs. The damaged cells could be replaced, but repeated damage may result in permanent problems.
It can aggravate asthma: a case- crossover study in Milan demonstrated that increases in ozone levels corresponde to a 78% increases in ERAs ( emergency room admission in hospital) for asthma especially during the warm season.
Asthma is the common chronic inflammatory disease of the airways characterized by variable and recurring symptoms, reversible airflow obstruction, and bronchospasm. Symptoms include wheezing, coughing, chest tightness, and shortness of breath.
Interleukin-17 ( IL-17 ), secreted by Th17 cells, has been caught lurking in lung tissue and in the blood of asthmatic patient and it can cause airway constriction in different ways:
- It stimulates Type 2 helper T cells (Th2 cells) to secrete other cytokines (IL-4, IL-5, IL-13) and an excessive amount of mucus that inflame the lungs, irritate the chest and cause asthma's characteristic wheezing;
- IL-17 drawns eosinophils and neutrophils into the lung which make asthma attacks worse;
- IL-17 lures NKTcells into the lung and they produce IL-13 and IFNγ .In a study carried out on mices was found that they had difficulty breathing after inhaling ozone at concentrations equivalent to ozone-polluted air, in fact the mices produced more IL-17 and they had plenty of NKT cells.

Viruses, allergens, cigarette smoke and airborne pollutants have all been fingered as potential culprits. In 2010 in a specific study was discovered that allergens provoke Th17 cells, and thereby exacerbate asthma. In fact house dust mites activate the C3 of the Complement system , a molecular cascade that causes the number of Th17 cells to rise. And IL-17A, produced by Th17 cells, reactivated the C3 system and perpetuated the response.

ozone-the symptoms.

Asthma: Breathing new life into research.2011.

How air pollution influences clinical management of respiratory diseases. A case-crossover study in Milan.2012.

Health Effects of Ozone in Patients with Asthma and Other Chronic Respiratory Disease.



A Randomized, double-blind, crossover chamber study proved that ozone can influence macrovascular diameter and tone. The brachial artery narrowing resulting from short term inhalation (2 hours) of fine particulate air pollution (150 μg/m³) and ozone at urban environments level rendered it reasonable to suspect that, since brachial and coronary reactivity are correlated, the coronary vasculature may respond similarly to air pollution exposure.
Despite the impact of this reduction in coronary diameter on healthy adults is minimal, it must be kept in mind that-according to epidemiological findings-the instability of susceptible plaques can be triggered and the cardiac ischemia can be promoted by sudden coronary vasoconstriction in people with underlying flow-limiting obstructive lesions.
Even if further investigation upon coronary circulation in high-risk individual must be done, it seems reasonable that susceptibility for acute cardiac events can be increased after air pollution exposure, by the hyper-reaction of the vasculature of patients with coronary risk factors to a variety of vasoconstrictors.


Another aspect of cardiac morbidity in the genesis of which ozone seems to play a main role, is hypertension . As has been demonstrated by Zanobetti and al. air pollution (120 hours averages of ozone) may contribute in increasing peripheral blood pressure by means of increase in sympathetic nervous system activity. This can be achieved mainly via an acute increase in vascular endothelin release.
This mechanism can be explained as follows:
- When ET (a family of short peptides of 21 aa) is released(by vascular endothelial cells), after inducing a short-term and short –lasting vasodilatation, triggers long-lasting vasoconstriction. This particular behavior depends on the type of receptor that reacts with ET.
- When Eta receptor –present on smooth muscle cells- links ET1, it activates the PLC-pathway, thus leading to increased intracellular calcium-levels both by allowing:
entrance of the ion from outside the cell (see DAG)
release of it from intracellular storage (see IP₃)
- This increased quantity of calcium inside the muscle cell leads to vasoconstriction both:
Peripheral, thus increasing AFTERLOAD
Coronary, thus decreasing contraction
These two combined effects lead to heart failure

Ambient pollution and blood pressure in cardiac rehabilitation patients.2004


Ozone is one of the most reactive compounds and can be both inhaled or produced during physiologic processes within the body. Particularly it has been appointed as a responsible of the pathogenesis of atherosclerotic plaques. These plaques are mainly composed of cholesterol as the lipid component, which, when present in very high concentrations, can crystallize within the lipid core of the diseased artery.
It has been found out that among a group of oxidant (triplet oxygen, superoxide anion, etc..)only ozone can cleave serum cholesterol's double bond. This ozonolysis results in the production of 5,6 secosterol, categorized into a class of compound called atheronals.
The atheronals are cytotoxic through the following pathways:
• Coadministration with LDL
• Oxydation of LDL by ozone
• Phagocytosys of ox- LDL by tissue macrophages
• Transformation of these cells in foam cells releasing cytokines
• Luring of smooth muscle cells from media to intima tunica of the vessels
• Production of ECM by modified muscle cells
• Adhesion of platelets upon ECM newly synthesized
Formation atheronal plaque and obstruction of the vessel

Evidence for Ozone Formation in Human Atherosclerotic Arteries.2003.

Ozone and cardiovascular injury.2009.


In works published by Science is reported evidence that all antibodies, regardless of source or antigenic specificity , can catalyze redox reactions that are independent of antibody binding. When provided with singlet molecular oxygen (O2*), immunoglobulines oxidize water (H2O) to produce hydrogen peroxide (H2O2) via the postulated intermediacy of H2O3 (Trioxidane, hydrogen trioxide or dihydrogen trioxide).
Hydrogen peroxide is one of the reactive oxygen species ( ROS ) that can kill bacteria producing holes in the bacterial cell wall at the sites of antigen-antibody union that lead to an increased permeability of the plasma membrane to water, thus pathogens die for osmotic shock.
However experiments demonstrated that antibodies don’t generate enough hydrogen peroxide to account for all the cell killing. That suggested that some other, more powerful bactericidal agent is also involved . In the course of exploring has been observed that one of the antibody-generated oxidants possesses the chemical signature of ozone (O3). For example, the researchers found that antibodies provided with singlet oxygen produce an oxidizing agent that splits the dye indigo carmine (a pH and redox indicator) , just as ozone does.

Although ozone itself is highly bactericidal, there also exists a reaction between H2O2 and O3 that is termed the peroxone process. Has been reported that a combination of H2O2 and O3 is far more toxic to bacteria than either H2O2 or ozone alone.
Moreover ozone is short-lived substance and this property makes it an ideal effector molecule, because any damage would be localized to the site of inflammation.
Ozone synthesis in vivo is triggered by antigen-antibody union that occurs when activated neutrophils at the site of an infection generate O2*, which is the substrate for the antibody-catalyzed water oxidation process.

Furthermore ozone not only kills but also functions as a signaling device that serves to amplify the inflammatory response by the production of nuclear factor kappa B NF-kB , interleukin-6 IL-6 , and tumor necrosis factor TNFa .

The discovery of the bactericidal activity of antibodies in the presence of O2* is the first direct evidence that they can destroy their antigenic targets in the absence of complement or phagocytes.

Antibodies Kill by Producing Ozone.2002.

Evidence for Antibody-Catalyzed Ozone Formation in Bacterial Killing and Inflammation.2002.


The studies we reported state and demonstrate that ozone has a pathogenetic role affecting both cardiovascular and respiratory system. However, since everyday we inhale lots of air pollutants together and not only ozone, it isn’t possible to build up studies testing the effects of ozone itself. In fact biological effects of atmospheric pollution cannot be attributed to a single pollutant, but to the atmospheric complex mix of different substances that, through common or different processes, determine the above mentioned negative effects on human physiology.

Silvana Giachero & Laura Bucchino

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