Ozone (O3) is a highly reactive gas composed of three oxygen atoms. 

Ozone is both a natural and a man-made product that occurs in the Earth’s upper atmosphere

Stratospheric ozone is formed naturally through the interaction of solar ultraviolet (UV) radiation with molecular oxygen (O2).  

The ozone layer, is approximately 6-30 miles above the Earth’s surface.

The ozone layer reduces the amount of harmful UV radiation reaching the Earth’s surface.

Tropospheric or ground-level ozone is formed mainly from photochemical reactions between two major classes of air pollutants: volatile organic compounds and nitrogen oxides.

These photochemical reactions depend upon the presence of heat and sunlight.

Therefore, there is higher ambient ozone concentrations in the summer months.  

Ozone contributes smog or haze, which still occurs most frequently in the summertime, but can occur throughout the year in some southern and mountain regions.

Although some stratospheric ozone is transported into the troposphere, and some volatile organic compounds and nitrogen oxides occur naturally.

The majority of ground-level ozone is the result of reactions of man-made volatile organic compounds and nitrogen oxides.

Significant sources of volatile organic compounds are chemical plants, gasoline pumps, oil-based paints, autobody shops, and print shops. 

Nitrogen oxides result primarily from high temperature combustion, power plants, industrial furnaces and boilers, and motor vehicles.

High ambient ozone concentrations found not only in heavily urbanized areas.

Ozone formation is not limited to big cities, and is transported hundreds of miles downwind from where it is created to affect ambient air quality in other urban and rural areas. 

Its peak concentrations usually occur during afternoon hours, when sunlight is the most intense. 

The downwind areas of major sources of volatile organic acids and nitrous oxides may experience ozone peaks in the afternoon and evening, many miles from their sources: high ozone concentrations can occur in remote areas and at various times of day.

Ozone affects on health: it absorbs UV light, reducing human exposure to harmful UV radiation that causes skin cancer and cataracts;it reacts chemically with many biological molecules in the respiratory tract, leading to a number of adverse health effects. 

Ozone decreases lung function, and increases Inflammation of airways.

Respiratory symptoms can include:


Throat irritation

Pleuritic pain

Chest tightness, wheezing, or shortness of breath

Higher daily ozone concentrations are associated with increased asthma attacks, increased hospital admissions, increased daily mortality, and other morbidities.

Ozone can make asthma symptoms worse and can increase sensitivity to asthma triggers.

Ozone exposure occurs when people breathe ambient air.

The cumulative amount of exposure to ozone is a function of both the rate and duration of exposure.   

Ozone concentrations indoors typically vary between 20% and 80% of outdoor levels.

Levels  depend  on whether windows are open or closed, or air conditioning is being used

The greatest cumulative exposure occur in those heavily exercising outdoors for long periods of time when ozone concentrations are high.  

During exercise people breathe more deeply, and ozone may shift from the upper airways to deeper areas of the respiratory tract, increasing the possibility of adverse health effects.  

The least cumulative exposure to ozone occurs in people resting for most of the day in an air-conditioned building with little air turnover. 

Ozone has limited solubility in water, therefore the majority of inhaled ozone reaches the lower respiratory tract and dissolves in the thin layer of epithelial lining fluid.

In the lung ozone reacts rapidly with a number of biomolecules.

Biomolecules containing thiol or amine groups or unsaturated carbon-carbon bonds are particularly involved.

Free radicals, and oxidants in the epithelial lining fluid react to ozone exposure, and then react with underlying epithelial cells, with immune cells, and with neural receptors in the airway wall.  

Ozone may react directly with epithelial cells, with immune cells, and with neural receptors.

Ozone interacts with proteins and lipids on the surface of cells or that are present in the lung lining fluid.

Epithelial cells lining the respiratory tract are the main target of ozone and its products. 

Epithelial cell injury leads to leaks in intracellular enzymes such as lactate dehydrogenase into the airway lumen, and plasma.

Epithelial cell injury results in release of inflammatory mediators that can attract polymorphonuclear leukocytes into the lung, activate alveolar macrophages, and initiate events leading to lung inflammation. 

The short-term ozone exposure results in the inability  to inhale to total lung capacity.  

A short-term exposure of up to 8 hours, causes lung function decrements such as reductions in forced expiratory volume in one second (FEV1), and cough, 

throat irritation , pain, burning, or discomfort in the chest when taking a deep breath, chest tightness, wheezing, or shortness of breath..

Short-term effects are reversible, with improvement and recovery to baseline varying from a few hours to 48 hours after an elevated ozone exposure.

Respiratory symptoms and lung function changes are due to stimulation of airway neural receptors and transmission to the central nervous system via afferent vagal nerve pathways.  

The ozone neural inhibition of inhalation effort at high lung volumes is believed to be the primary cause of being unable to inhale to total lung capacity.

Ozone induces neurally mediated stimulation of nociceptive interepithelial nerve fibers and leads to reflex cough and a decrease in maximal inspiration.

Opioid agonists block sensory pathways.  

 and relieve these symptoms.

Ozone related mechanisms are possibly  stimulation of irritant receptors contributing  to cough and induces a vagally mediated reflex that increases airway resistance.

Ozone’s C fiber stimulation releases neurokinins such as substance P that dilate nearby capillaries, activate mucous glands, and contract airway smooth muscle via neurokinin receptors. 

Prostaglandin E2 released by 

Eithelial cells exposed to ozone or to ozone reaction causes release of prostaglandin E2 products which also sensitizes C fibers. 

These changes result in decreases in forced vital capacity (FVC), FEV1 and other spirometric measures that require a full inspiration limiting maximal exercise capability. 

Ozone-induced changes in breathing pattern to more rapid shallow breathing may also be a manifestation of C-fiber stimulation.

Ozone reduces the maximal inspiratory position and may slightly increase the residual volume.

Reduction in maximum inspiration reduces forced vital capacity (FVC), causing  a reduction in expiratory flow measurements, such as flow at 50% of FVC expired (FEF50%). 

Short-term exposure of ozone and/or its reactive intermediates cause injury to airway epithelial cells followed other effects.  

These effects can be measured by bronchoalveolar lavage (BAL), by examining cells and biochemical markers in the lavage fluid.

Following ozone exposure airway inflammation includes visible redness of the airway, and an increase in the numbers of neutrophils in the lavage fluid.  

With cellular injury there is an increase in the concentration of lactate dehydrogenase (LDH), an enzyme released from the cytoplasm of injured epithelial cells, in the extracellular fluid.

Mediators: cytokines, prostaglandins, leukotrienes are released by injured cells include a number that attract inflammatory cells resulting in a neutrophilic inflammatory response in the airway.  

Ozone-induced effects that may be related to the underlying injury and inflammatory response are:

An increase in small airway obstruction

A decrease in the integrity of the airway epithelium

An increase in nonspecific airway reactivity

A decrease in phagocytic activity of alveolar macrophages

The decrease in epithelial integrity

An  increase in the concentration of plasma proteins appearing in the extra cellular fluid,  following exposure and by more rapid clearance of inhaled radio-labeled markers from the lung to the blood.  

There is the potential for allowing increased movement of inhaled substances, such as allergens or particulate air pollution from the airway to the interstitium or the blood and could modify the known effects of inhaled allergen on asthma and particulate matter on mortality.

Increased nonspecific airway reactivity is a concern for people with asthma, as increased airway reactivity is a predictor for asthma exacerbations.   

Following a single short-term exposure, inflammation, small airway obstruction, and increased epithelial permeability resolve, and damaged ciliated airway epithelial cells are replaced by underlying cells.

Damaged type I alveolar epithelial cells are replaced by more ozone-resistant type II cells.  

Over a period of weeks, the airway appears to return to the pre-exposure state.

The responses of  acute short-term ozone exposure results in a large amount of variability among individuals: from no symptom or lung function changes while the most responsive individual may experience a 50% decrement in FEV1 and have severe coughing, shortness of breath, or pain on deep inspiration.  

A similar range of response is evident for longer exposures with 5 hours of moderate activity.  

Vitamin C and E supplements may slightly reduce the lung function effects of ozone but not the inflammatory or symptom responses.  

Pre-treatment with non-steroidal anti-inflammatory drugs (NSAID) reduces lung function and symptom responses but not the inflammatory responses in non-asthmatics.  

NSAID pretreatment do not block the restrictive lung function changes seen in nonasthmatics, but does blunt some of the changes due to airway obstruction.  

Pre-treatment with high doses of inhaled steroids reduces the neutrophil influx following ozone exposure in people with asthma, but not in those without asthma.

Genetic polymorphisms for antioxidant enzymes and for genes regulating the inflammatory response may modulate the effect of ozone exposure on pulmonary function and airway inflammation. 

Ozone is associated with increased mortality, and is considerably higher in older adults, and is most prominent during the warm season

Short-term exposure to ozone is also associated with increased daily mortality. 

A 0.5 % overall excess risk in non-accidental daily mortality occurs for each 20 parts per billion increase in the 24-hour average ozone concentration.

This ozone-mortality relationship is present even after controlling for possible effects of particulate matter and other air pollutants. 

The absolute effect of ozone on mortality is considerably higher in older adults due to their higher baseline death rates.  

A preponderance of studies supports the evidence that short-term ozone is likely to be associated with premature mortality.        

Ozone-mortality relationship is most prominent during the warm season, with few or smaller effects in the winter.  

Ozone-mortality association persists when deaths are limited to those caused by either cardiac or pulmonary disease or to those caused by cardiovascular disease alone.  

Potential effects of short-term ozone exposure:

hospital admissions 

emergency room visits for respiratory causes

school absences

The most at risk of serious respiratory morbidity are those with underlying respiratory disease.  

The concentration of ozone at which effects are first observed depends upon the level of sensitivity of the individual as well as the dose delivered to the respiratory tract.  

The ozone dose, is a function of the ambient concentration, the minute ventilation, and the duration of exposure.   

Patients with more sensitivity  experience effects at lower concentrations while less sensitive individuals will experience these effects only at higher concentrations.

Patients with pre-existing respiratory diseases are potentially at increased risk of adverse effects of ozone exposure: as ozone may interact with the pathophysiology of the underlying disease or because these patients generally have less pulmonary reserve.

People with asthma are susceptible to the effects of ozone exposure. 

COPD is the one other respiratory disease for which a relationship has been observed between ozone and hospital admission, suggesting that individuals with COPD and other chronic respiratory diseases should avoid strenuous outdoor activity on days when ambient ozone concentrations are high.

Exposure to ambient ozone is a risk factor for triggering acute and chronic health effects, including chest discomfort, cough, and shortness of breath and increases in daily mortality and hospital admissions for respiratory disease in the general population as well as those with lung disease, asthma attacks in people with asthma; and the possible development of new cases of asthma and other respiratory disease in people exposed to ozone over many years.  

Reducing exposure to ozone will reduce public health impacts. 

Ozone levels are typically highest in the warmer months and in the afternoon and early evening hours for most locations.

High ozone concentrations can occur throughout the year in some southern and mountain locations.

The Air Quality Index, is a 

 uniform index for reporting and forecasting daily air quality. 

It is used to report the five most common ambient air pollutants that are regulated under the Clean Air Act: ground-level ozone, particulate matter pollution, carbon monoxide, sulfur dioxide, and nitrogen dioxide. 

The AQI tells the public how clean or polluted the air is and how to avoid potential associated health effects.

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