hypothesize how air pollution like smog affects photosynthesis

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How Does Pollution Affect Photosynthesis?

The Effect of Black Light on Plants

​ Photosynthesis ​ is the process of converting the inorganic molecules water, carbon dioxide and light into energy in the form of glucose. Plants, algae and some bacteria, known as ​ primary producers ​ in the food web, rely on their photosynthetic capabilities to fuel their cellular processes. Pollution affects photosynthesis and damages overall plant health in many ways. Primary producers' photosynthetic efficiency is not only crucial for their survival, but also vital for all life on Earth as other organisms eat them and breathe the oxygen they produce as a byproduct of photosynthesis.

Types of Air Pollution

The most damaging air pollutants to plants are ​ persistent organic pollutants ​. These types of contaminants stay in the environment for long periods before they degrade. The worst organic pollutants may even last centuries. Organic pollutants come in many forms, including pesticides, antibiotics, bisphenols used to make plastics and polycyclic aromatic hydrocarbons, produced by burning coal, wood, tobacco, gas, oil and garbage.

Because persistent organic pollutants contaminate the air, they can travel great distances with the wind, impacting vast areas of land away from the initial contamination zone. Once these pollutants settle, they enter waterways, giving them the potential of spreading even further. Air pollution's ability to disperse and remain active in ecosystems for long periods makes it particularly dangerous to the health of all life on Earth.

Does Air Pollution Affect Plants?

Exposure to air pollution impacts both plants' leaves and roots. Plants leaves contain ​ chlorophyll ​, a pigment made in ​ chloroplasts ​, which are cellular organelles responsible for photosynthesis. Initially, photosynthesis is directly affected as the cellular metabolic functions of chloroplasts exposed to air pollution have a lowered ability to fix carbon.

Though the vertical position of many plants' leaves is adapted to shed dust, large volumes of dust particles from air pollution can accumulate on their surfaces. Dust buildup has many effects on plants, including increasing their temperature, killing leaf sections and plugging stomata openings. Accumulation of dust on leaves damages chloroplasts and minimizes their overall number within the leaf, so the plant has a lower photosynthetic rate.

Later, once air pollution settles, it contaminates the soil. In the ground, a plant's roots are once again exposed to these pollutants, damaging their ability to uptake vital nutrients and water. As water is a critical component of photosynthesis, this further restricts a plant's energy production and growth.

Effects of Haze on Plants

A significant effect haze has on plants is that it blocks light, which reduces a plant's rate of photosynthesis. Lower photosynthetic ability, in turn, reduces plants' ability to grow. Haze also minimizes ​ stomatal conductance ​, which is the carbon dioxide and water vapor exchange in and out of the plant leaves through the stomata.

Ultimately, the more haze a plant is exposed to, the lower its growth rates and less productive its fruit yield. The broader implication of haze on human society is that farmers would produce fewer crops in the same area of land. Therefore, the more haze, the less efficient a plant's physiological processes are, resulting in poorer growth.

Pollution and Environmental Stressors

Plants have different adaptive strategies for coping with stressors to maintain efficient rates of photosynthesis. For example, plants growing in low-light conditions tend to have a higher chlorophyll percentage in their leaf tissues to maintain a healthy rate of photosynthesis than leaves in high-light environments. Similarly, due to water limitations in the desert, cacti have evolved large stems to store water and have thick cuticles to prevent water loss so they can continue to photosynthesize even when water is unavailable.

However, despite their adaptations, all organisms have limited thresholds for dealing with stress. As a result, pollution has more significant effects on photosynthesis when an organism is faced with multiple environmental stressors. For example, under abnormal drought conditions, photosynthetic capabilities are reduced. Adding pollution into the mix during times of stress further weakens or kills plants and can potentially change the natural balance of organisms in a community.

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• United States Environmental Protection Agency: Plant Response to Air Pollution
• United States Environmental Protection Agency: Persistent Organic Pollutants: A Global Issue, a Global Response
• BBC Bitesize: Plant Organisation
• Marine Biology: Pigment Content and Photosynthetic Rate of the Fronds of Macrocystis Pyrifera
• Horticulture International Journal: Responses in Plants Exposed to Dust Pollution

About the Author

Adrianne Elizabeth is a freelance writer and editor. She has a Bachelor of Science in Ecology and Biodiversity, and Marine Biology from Victoria University of Wellington in New Zealand. Driven by her love and fascination with all animals behavior and care, she also gained a Certificate in Captive Wild Animal Management from UNITEC in Auckland, New Zealand, with work experience at Wellington Zoo. Before becoming a freelance writer, Adrianne worked for many years as a Marine Aquaculture Research Technician with Plant & Food Research in New Zealand. Now Adrianne's freelance writing career focuses on helping people achieve happier, healthier lives by using scientifically proven health and wellness techniques. Adrianne is also focused on helping people better understand ecosystem functions, their importance, and how we can each help to look after them.

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• Published: 02 December 1982

Effects of aerosols on photosynthesis

• Siegfried A. W. Gerstl 1 &
• Andrew Zardecki 1  

Nature volume  300 ,  pages 436–437 ( 1982 ) Cite this article

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Air pollution can cause various problems to agriculture through its direct or indirect effects on plants 1,2 . The net effects of air pollution on agricultural crop yields are very difficult to estimate quantitatively, and are generally considered secondary to the effects of fertilizers or chemical disease control measures. However, continually increasing air pollution may represent a persistent and largely irreversible threat to agriculture in the future. Here we have examined only one indirect aerosol effect on agricultural plant life—the reduction in photosynthetically active radiation (PAR) reaching the ground in the presence of significant air pollution. This effect can be quantified confidently from results of detailed model calculations of the transfer of solar radiation through the atmosphere with varying levels of air pollution. For the biologically effective wavelength region between 0.35 and 0.72 µm, the reductions in PAR due to increasing tropospheric aerosol loads have been determined for rural and urban pollution scenarios. For example, for the northeastern United States during the summer months, a reduction in PAR of about 20% and 33% was obtained when the visual range due to rural and urbtn aerosols, respectively, was decreased from clear air conditions to 10 km.

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Erickson, P. A. Environmental Impact Assessment , 85–204 (Academic, New York, 1979); Airborne Particles 199 (University Park Press, 1979).

Google Scholar  

Gerstl, S. A. W., Zardecki, A. & Wiser, H. L. Nature 294 , 352–354 (1981).

Article   ADS   CAS   Google Scholar  

Bach, W., Pankrath, J. & Williams, J. (eds) Interaction of Energy and Climate , 107–361 (Reidel, Dordrecht, 1980).

Jaenicke, R. J. Aerosol Sci. 11 , 577–588 (1980).

Article   ADS   Google Scholar  

Shettle, E. P. & Fenn, R. W. Air Force Geophys. Lab. Rep. AFGL-TR-79-0214 (US National Technical Information Service (NTIS accession no. ADA-085-951) (1979); Proc. AGARD Conf. No 183, Denmark (NTIS accession no. ADA-028-615) (1975).

McClatchey, R. A., Fenn, R. W., Selby, J. E. A., Garing, J. S. & Volz, F. E. Air Force Cambridge Res. Laboratories, Envir. Res. Pap. 331 AFCRL-70-0527 (NTIS AD-715270) (1970).

Volz, F. E. J. geophys. Res. 77 , 1017–1031 (1972).

Unsworth, M. H. & Monteith, J. L. Q. Jl R. met. Soc. 98 , 778–787 (1972).

Hill, T. R. Los Alamos nat. Lab. Rep. LA-5990-MS (1975).

Gerstl, S. A. W. Int. Radiat. Symp. , Fort Collins, Colorado (1980); Los Alamos nat. Lab. Preprint LA-UR-80-1403 (1980).

Zardecki, A. & Gerstl, S. A. W. Los Alamos nat. Lab. Rep. LA-9010-MS (1981).

McCree, K. Agric. Met. 10 , 443–453 (1972).

Article   Google Scholar  

McCree, K. Agric. Met. 9 , 191–216 (1971).

Trijonis, J. & Yuan, K. US Envir. Protection Agency Rep. EPA-600/3-78-075 (1978).

McCartney, H. A. Q. Jl R. met. Soc. 104 , 911–926 (1978).

Emerson, R. A. Rev. Pl. Physiol. 3 , 1–24 (1958).

Lawlor, D. W. in Stress Physiology in Crop Plants 303–325 (Wiley-Interscience, New York, 1979).

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The Effects of Air Pollutants on Vegetation and the Role of Vegetation in Reducing Atmospheric Pollution

Submitted: 21 October 2010 Published: 26 September 2011

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Author Information

Iuliana florentina gheorghe.

• Ecological University of Bucharest, Faculty of Ecology and Environmental Protection, Romania
• Forest Research and Management Institute, Romania

*Address all correspondence to:

1. Introduction

The main air pollutants are represented by gases forms, particles in suspension, different ionizing radiation and noise.

The gases forms are: oxidized and reduced forms of carbon (CO 2 , CO, CH 4 ), of nitrogen (NO 2 , NO, N 2 O 4 , NH 3 , NH 4+ ), SO 2 , O 3 , C 6 H 6 vapours, Hg, volatile phenols, Cl 2 , etc.

The particulate forms are: PM10 and PM2.5 particulate matter, heavy metals with toxic effect (Pb, Ni, Cd, As), polycyclic aromatic hydrocarbons PAHs, etc.

Atmospheric pollutants have a negative effect on the plants; they can have direct toxic effects, or indirectly by changing soil pH followed by solubilization of toxic salts of metals like aluminum. The particulate matters have a negative mechanical effect. They cover the leaf blade reducing light penetration and blocking the opening of stomata. These impediments influence strongly the process of photosynthesis which rate declines sharply.

Also the leaves of the trees have an important role in retention of the particulate matters; they are mostly affected when the wet and dry atmospheric deposition increase.

The vegetation plays an important positive role in atmospheric purification and air pollutants reduction.

The primary producers represented by plants are an important component in biogeochemical cycles. The vegetation made exchanges with a part of the atmospheric gases by photosynthesis, respiration processes, and the final stage of litter decomposition which mineralization.

The plants play an important role in reducing atmospheric CO 2 content, by photosynthesis. This reduction of atmospheric CO 2 content has an important role in reducing of greenhouse gases, participating in reducing greenhouse effect and its consequences on climatic changes. The carbon stored in plants is the result of balance between carbon fixed by photosynthesis and carbon released in the atmosphere by respiration.

As the structure of vegetation is more complex, the carbon stock in plants biomass is higher and the period of storage is longer. The most efficient type of vegetation in storing carbon in terms of carbon stored in plants alive is the temperate-continental forest; and in terms of carbon stored in dead organic matter are peat lands.

Trees have also been planted to reduce the intensity of ionizing radiation and noise in different urban and industrial areas. The existence of vegetation in an area creates a microclimate where the temperature differentials between day and night are buffered.

This prevents the occurrence of warmer temperatures which stimulate the production of volatile pollutants into the atmosphere.

2. General information about air pollution

Environmental pollution is any discharge of material or energy into water, land, or air that causes or may cause acute (short-term) or chronic (long-term) detriment to the Earth's ecological balance or that lowers the quality of life. Pollutants may cause primary damage, with direct identifiable impact on the environment, or secondary damage in the form of minor perturbations in the delicate balance of the biological food web that are detectable only over long time periods.

Air pollution is the process which the substances and the energy forms are not present in normal atmospheric composition reach the atmosphere, or are present but in much lower concentrations.Air pollution is the introduction of chemicals, particulate matter, or biological materials that cause harm or discomfort to humans or other living organisms, or cause damage to the natural environment or built environment, into the atmosphere.

More than 3,000 substances that are not part of the atmospheric composition, falling in the atmosphere can be considered air pollutants.

Some substances that are normally present in the atmosphere in a certain concentration can be considerate pollutants because their concentration is much higher than usual concentration.

Also certain substances that are normally present in certain layers of the atmosphere (e.g. ozone in the stratosphere), once arrived in the troposphere is pollutant.

Some gases, such as oxides of nitrogen may have beneficial effect on vegetation, after hydration may affect the leaf fertilizer.

The air pollutants factors can be chemical (chemicals), mechanics (particles in suspension) physical (ionizing radiation) and acoustic (noise).

Global polluants circuit ( http://www.cleartheair.nsw.gov.au , 2011)

Pollutants describe a global circuit; they are produced by different sources, are transported and transformed into atmosphere, some of them being removed, another part is reaching the earth having different effects on different biocoenosis of ecosystems ( fig. 1) .

An analysis done at the global level revealed a diversification of pollutants agents and sources of air pollution. This diversification and increasing concentrations are in strict correlation with industrialization and the increasing of amounts use as fossil energy (non-renewable sources).

At the beginning, the pollution has been felt in urban areas and the forms of relief that favored the accumulation of pollutants and long stay (depressions, closed valleys, etc.). Currently, air pollution has become a larger area, sometimes to disperse across multiple continents.

Air pollution can be analyzed on three spatial scales: global pollution, regional pollution and local pollutants.

The global pollution is the result of cumulative effects of various sources, located on the entire surface of the globe, manifested by global effects: the stratospheric ozone depletion; greenhouse effect - emission of greenhouse gases (CO 2 , methane, CFCs, etc.); formation of aerosols (pollutant clouds which suspended particles and chemical compounds).

The regional pollution is in part the result of local air pollution--including that produced by individual sources, such as automobiles - that has spread out to encompass areas of many thousands of square kilometers. Meteorological conditions and landforms can greatly influence air-pollution concentrations at any given place, especially locally and regionally. For example, cities located in bowls or valleys over which atmospheric inversions form and act as imperfect lids are especially likely to suffer from incidences of severe smog. Oxides of sulfur and nitrogen carried long distances by the atmosphere and then precipitated in solution as acid rain, can cause serious damage to vegetation, waterways, and buildings.

The local pollutants (smog) can be loosely defined as a multi-source, widespread air pollution that occurs in the air of cities. Smog, a contraction of the words smoke and fog, has been caused throughout recorded history by water condensing on smoke particles, usually from burning coal.

In terms of the effects of pollutants can be acidifying agents - sulphur dioxide (SO 2 ), nitrogen oxides (NOx) ammonia (NH 3 ) fluoride and Cl 2 , hydrogen chloride (HCl) - and oxidizing agents - carbon monoxide (CO), PAN (peroxyacetylnitrate-CH 3 CO.O 2 .NO 2 ), ozone (O 3 ).

3. Sources of pollutants

Air pollution comes from natural and anthropic sources; these sources generate pollutants with different effects at global level or on individuals of plants and animals ( tab. 1) .

Natural processes that affect air quality include volcanoes, which produce sulfur, chlorine, and ash particulates. Wildfires produce smoke and carbon monoxide. Cattle and other animals emit methane as part of their digestive process. Even pine trees emit volatile organic compounds (VOCs).

Many forms of air pollution are human-made. Industrial plants, power plants and vehicles with internal combustion engines produce nitrogen oxides, VOCs, carbon monoxide, carbon dioxide, sulfur dioxide and particulates. In most mega-cities, cars are the main source of these pollutants. Stoves, incinerators, and farmers burning their crop waste produce carbon monoxide, carbon dioxide, as well as particulates. Other human-made sources include aerosol sprays and leaky refrigerators, as well as fumes from paint, varnish, and other solvents. One important thing to remember about air pollution is that it doesn’t say in one place. Winds and weather play an important part in transport of pollution locally,

Type of pollutants, origin and effect at global level or on plants end animals individuals

regionally, and even around the world, where it affects everything it comes in contact with. The major anthropic sources of air pollution are:

industry and conventional energies (the mining industry, the energy industry based on fossil fuels - coal, oil, natural gas, central heating, chemical and metallurgical industry, engineering internal combustion machinery industry, industrial waste, noises, etc);

agriculture (the vegetation fire, denitrification in soils excessively fertilized, paddy field, intensive husbandry, deforestation, etc)

transportation (motor vehicle pollution, noises, etc)

and urbanization (sewage plans, authorized landfill site, etc) ( fig. 2)

The major anthropic sources of air pollution ( http://www.cleartheair.nsw.gov.au , 2011)

4. The most important atmospheric pollutants

The air pollutants are represented by gases forms, particles in suspension, different ionizing radiation and noise.

5. Major gaseous pollutants

Sulphur dioxide (SO 2 ) is the most important and common air pollutant produced in huge amounts in combustion of coal and other fuels in industrial and domestic use. It is also produced during smelting of sulphide ores. Sulphur dioxide concentrations in air have decreased in the past two decades, mainly because we use more non-sulphur-containing fuels for the generation of energy. Sulphur dioxide is a stinging gas and as a result it can cause breathing problems with humans. In moist environments, sulphur dioxide may be transferred to sulphuric acid. This acid causes acidification and winter smog.

Nitrogen oxides (NO x ) and nitrous oxide (N 2 O) Using catalysers in car exhausts can prevent emissions of nitrogen oxides. Nitrogen oxides are gasses that react with other air pollutants when they are present in air. For example, nitrogen oxides play an important rolein the formation of ozone in the lower atmosphere, and in acidification and eutrophication processes. They can deeply penetrate the lungs and damage human lung functions.

Fluorides Common gaseous fluoride pollutants are HF, SiF 6 , CF 4 and F 2 . Particulate fluoride pollutants include Ca 3 AlF 6 (Cryolite), CaF 2 , NH 3 F, AlF 6 , CaSiF, NaF and Na 2 SiF 6 . Aerosols are often formed from NaF, NaAlF 6 and AlF 6 . Chief sources of fluoride pollutants are brickworks, aluminium factories, glassworks, steelworks, ceramic factories, phosphate fertilizer plants and uranium smelters. Some fluorine pollution also occurs during combustion of coal. Most injurious fluoride pollutant is gaseous hydrogen fluoride (HF).

Fluoride is released into the air in large quantities by aluminum reduction plants, phosphate processors, steel mills, coal burning operations, brick and tile manufacturers, and various less significant sources[ 1 ]. It can cause adverse effects when ingested by domestic animals or absorbed by plants. There are also reports that fluoride air pollution can adversely affect human health, though these are less well documented than those concerning sensitive animals and plants. Fluorides are released into the air in both a gaseous state (as hydrogen fluoride and silicon tetra-fluoride) and in solid particles. The particles fall on, and the gases are absorbed by, vegetation near the polluting industry. If this vegetation includes forage crops which are fed to cattle, sheep, horses, or pigs, serious problems may ensue, since these animals, particularly the cattle are vulnerable to fluoride [ 2 ]. In fact, according to the U.S. Ninety-six percent of the ingested fluoride that accumulates in the bodies of animals is incorporated into the crystal structure of bone and tooth mineral [ 3 ], [ 4 ]. When fluoride is ingested with food or water, most of that which is not deposited in the bones, teeth, and other calcified tissue is excreted in the urine within hours of ingestion [ 5 ]. Thus it is not surprising that fluoride mainly affects the bones and teeth. Teeth are more markedly affected by ingested fluoride than are bones, but their high sensitivity is limited to the period of their formation. Thus a cow that has not been exposed to excessive fluoride before the age of two and one-half to three years will not develop the severe dental lesions which would occur in the same animal exposed at a younger age [ 6 ]. The developing tooth exposed to small amounts of fluoride may experience color variations ("mottling") that have little or no effect on the animal's ability to eat. Higher levels of fluoride result in more serious dental abnormalities, ranging from small, brittle, chalky areas on the tooth surface to pitting of enamel and easily eroded teeth [ 2 ]. Even more serious effects, including severe pain and the wearing down of the tooth right to the gum, can prevent the cattle from drinking cold water or eating. Localized or generalized enlargement of certain bones in the legs (metacarpals and metatarsals) and the lower jaw (mandible) of cattle are common symptoms of excessive fluoride ingestion [ 7 ]. As highly abnormal bone tissue replaces normal bone, [ 8 ] overall enlargement occurs, and the normally smooth bone surfaces take on a chalky, white, irregular appearance [ 2 ]. Hard ground can cause fluorotic hoof (pedal) bones to fracture, resulting in severe lameness [ 6 ]. Cattle with advanced fluorosis may also be crippled by mineralization of ligaments, tendons, and the structures surrounding the joints [ 9 ]. Enlargement of the joints themselves may also contribute to lameness. Fluoride-induced tooth destruction, lameness, and stiff joints affect the animal’s ability to stand, eat, and graze, and all tend to lower the milk yield of dairy cattle or the weight of beef cattle.

Chlorine (Cl 2 ) Although chlorine concentrations change very rapidly in the atmosphere due to atmospheric chemistry and light rain can remove all the chlorine from the air in a very short time, chlorine injury can occur to plants near the source of pollution.

The impact of chlorine pollution increases in bright sunlight and decreases in drought and low temperature.

Many particulate and gaseous fluorides are produced when ores containing fluorine are processed and used in industries. Common gaseous fluoride pollutants are HF, SiF 6 , CF 4 and F 2 . Particulate fluoride pollutants include Ca 3 AlF 6 (Cryolite), CaF 2 , NH 3 F, AlF 6 , CaSiF, NaF and Na 2 SiF 6 . Aerosols are often formed from NaF, NaAlF 6 and AlF 6 . Chief sources of fluoride pollutants are brickworks, aluminium factories, glassworks, steelworks, ceramic factories, phosphate fertilizer plants and uranium smelters. Some fluorine pollution also occurs during combustion of coal. Most injurious fluoride pollutant is gaseous hydrogen fluoride (HF).

Hydrogen chloride (HCl) HCl gas is released in large quantities in combustion of PVC and all chlorinated hydrocarbon material in large fires or incinerators. The HCl gas is very hygroscopic and quickly changes to hydrochloric acid by reacting with atmospheric moisture and forms aerosol droplets.

Ammonia (NH 3 ) Continuous releases of ammonia from the sources are rarely high enough to cause acute injury but occasional high release or spillage may cause ammonia pollution. High concentrations of ammonia are sometimes found around intensive farm units e.g. chicken batteries. Extent of injury reduces rapidly with increase in distance form the source. Under certain conditions the ammonia may remain as a cloud above ground level causing more injury to trees than to the ground flora. Injury symptoms may take up to 9 days to develop. In most plant species, recovery may occur in about 2 weeks after exposure is stopped.

Ammonia forms during agricultural activities. EEA-32 emissions of NH 3 have declined by 24% between the years 1990 and 2008. Agriculture was responsible for 94% of NH 3 emissions in 2008. The reduction in emissions within the agricultural sector is primarily due to a reduction in livestock numbers (especially cattle) since 1990, changes in the handling and management of organic manures and from the decreased use of nitrogenous fertilizers. The reductions achieved in the agricultural sector have been marginally offset by the increased emissions which have occurred during this period in sectors such as transport and to a lesser extent the energy industry and other (non-energy) sectors.

Environmental context: NH 3 contributes to acid deposition (plays an important role in acidification) and eutrophication. The subsequent impacts of acid deposition can be significant, including adverse effects on aquatic ecosystems in rivers and lakes and damage to forests, crops and other vegetation. Eutrophication can lead to severe reductions in water quality with subsequent impacts including decreased biodiversity, changes in species composition and dominance, and toxicity effects. NH 3 also contributes to the formation of secondary particulate aerosols, an important air pollutant due to its adverse impacts on human health.

VOC (Volatile Organic Compounds) VOC can be a range of different contaminants, such as carbohydrates, organic compounds and solvents. These compounds usually derive from petrol and gasoline reservoirs, industrial processes and fuel combustion, paint and cleanser use, or agricultural activities. VOC play an important role in ozone shaping in the lower atmospheric layer, the main cause of smog. VOC can cause various health effects, depending on the kind of compounds that are present and their concentrations. Effects can vary from smell nuisance to decreases in lung capacity, and even cancer.

Organic gases (Ethylene) and Methane (CH 4 ) Among organic gaseous pollutants, ethylene is most common. Other organic gases are propylene, butylenes and acetylene. Ethylene is continuously emitted from many sources involving combustion or processing of petroleum or its products or burning of organic materials e.g. straw burning. Other organic gases are also produced in various chemical industrial processes.

Ethylene is a natural plant growth substance so the injury effects produced by it on plants are very similar to growth abnormality symptoms. Other organic gases also produce symptoms similar to those of ethylene pollution. However, the sensitivities of species to different gases are variable.

Ethylene is a byproduct of automobile exhaust and can be a noticeable problem in urban environments.

Chlorofluorocarbons (or CFCs) is an organic compound that contains carbon, chlorine, and fluorine, produced as a volatile derivative of methane and ethane. A common subclass is the hydro-chlorofluorocarbons (HCFCs), which contain hydrogen, as well. They are also commonly known by the DuPont trade name Freon. The most common representative is dichlorodifluoromethane (R-12 or Freon-12). Many CFCs have been widely used as refrigerants, propellants (in aerosol applications), and solvents. The manufacture of such compounds is being phased out by the Montreal Protocol because they contribute to ozone depletion.

Minor gaseous pollutants Many other air pollutants which are highly injurious to animals and human beings also cause damage to plants. However, plants are affected by these gases at quite higher concentrations than the animals. Common such gaseous pollutants are CO, H 2 S, Br 2 , I 2 and Hg - vapors.

Hydrogen sulphide (H 2 S) It is a colorless, very poisonous, flammable gas with the characteristic foul odor of rotten eggs at concentrations up to 100 parts per million. It often results from the bacterial breakdown of organic matter in the absence of oxygen, such as in swamps and sewers (anaerobic digestion). It also occurs in volcanic gases, natural gas, and some well waters. The human body produces small amounts of H 2 S and uses it as a signaling molecule.

Carbon monoxide (CO) carbon dioxide in excess (CO 2 ), this gas consists during incomplete combustion of fuels. When we let a car engine run in a closed room, carbon monoxide concentrations in the air will rise extensively. Carbon monoxide contributes to the greenhouse effect, smog and acidification. The gas can bind to hemoglobin in blood, preventing oxygen transport through the body. This results in oxygen depletion of the heart, brains and blood vessels, eventually causing death.

It is highly toxic to humans and animals in higher quantities, although it is also produced in normal animal metabolism in low quantities, and is thought to have some normal biological functions.

Carbon monoxide consists of one carbon atom and one oxygen atom, connected by a triple bond which consists of two covalent bonds as well as one dative covalent bond. It is the simplest ox-carbon. In coordination complexes the carbon monoxide ligand is called carbonyl.

Carbon monoxide is produced from the partial oxidation of carbon-containing compounds; it forms when there is not enough oxygen to produce carbon dioxide (CO 2 ), such as when operating a stove or an internal combustion engine in an enclosed space. In the presence of oxygen, carbon monoxide burns with a blue flame, producing carbon dioxide [ 10 ]. Coal gas, which was widely used before the 1960s for domestic lighting, cooking and heating, had carbon monoxide as a significant constituent. Some processes in modern technology, such as iron smelting, still produce carbon monoxide as a byproduct [ 11 ]. Worldwide, the largest source of carbon monoxide is natural in origin; due to photochemical reactions in the troposphere which generate about 5 x 10 12 kilograms per year [ 12 ], other natural sources of CO include volcanoes, forest fires, and other forms of combustion.

In biology, carbon monoxide is naturally produced by the action of heme oxygenase 1 and 2 on the heme from hemoglobin breakdown. This process produces a certain amount of carboxyhemoglobin in normal persons, even if they do not breathe any carbon monoxide. Following the first report that carbon monoxide is a normal neurotransmitter in 1993, as well as one of three gases that naturally modulate inflammatory responses in the body (the other two being nitric oxide and hydrogen sulfide), carbon monoxide has received a great deal of clinical attention as a biological regulator. In many tissues, all three gases are known to act as anti- inflammatory, vasodilators and promoters of neo-vascular growth [ 13 ]. Clinical trials of small amounts of carbon monoxide as a drug are on-going.

Bromine (Br 2 ) and Iodine (I 2 )

At high temperatures, organo-bromine compounds are easily converted to free bromine atoms, a process which acts to terminate free radical chemical chain reactions. This makes such compounds useful fire retardants and this is bromine's primary industrial use, consuming more than half of world production of the element. The same property allows volatile organo-bromine compounds, under the action of sunlight, to form free bromine atoms in the atmosphere which are highly effective in ozone depletion. This unwanted side-effect has caused many common volatile brominated organics like methyl bromide, a pesticide that was formerly a large industrial bromine consumer, to be abandoned. Remaining uses of bromine compounds are in well-drilling fluids, as an intermediate in manufacture of organic chemicals, and in film photography.

Iodine and its compounds are primarily used in nutrition, the production of acetic acid and polymers. Iodine's relatively high atomic number, low toxicity, and ease of attachment to organic compounds have made it a part of many X-ray contrast materials in modern medicine.

Like the other halogens, iodine occurs mainly as a diatomic molecule I 2 , not the atom. In nature, iodine is a relatively rare element, ranking 47th in abundance. It is the heaviest essential element utilized in biological functions. Its rarity in many soils has led to many deficiency problems in land animals and inland human populations, with iodine deficiency affecting about two billion people and being the leading preventable cause of mental retardation [ 14 ]. As a component of thyroid hormones, iodine is required by higher animals. Radioisotopes of iodine are concentrated in the thyroid gland. This property of thyroid-concentration, along with its mode of beta decay, makes iodine-131 one of the most carcinogenic nuclear fission products.

Hg and Mercury vapors Pre-industrial deposition rates of mercury from the atmosphere may be about 4 ng/ (1 l of ice deposit). Although that can be considered a natural level of exposure, regional or global sources have significant effects. Volcanic eruptions can increase the atmospheric source by 4–6 times [ 15 ]. Natural sources, such as volcanoes, are responsible for approximately half of atmospheric mercury emissions. The human-generated half can be divided into the following estimated percentages:

65% from stationary combustion, of which coal-fired power plants are the largest aggregate source (40% of U.S. mercury emissions in 1999). This includes power plants fueled with gas where the mercury has not been removed. Emissions from coal combustion are between one and two orders of magnitude higher than emissions from oil combustion, depending on the country [ 15 ].

11% from gold production. The three largest point sources for mercury emissions in the U.S. are the three largest gold mines. Hydro-geochemical release of mercury from gold-mine tailings has been accounted as a significant source of atmospheric mercury in eastern Canada [ 16 ]

6.8% from non-ferrous metal production, typically smelters.

6.4% from cement production.

3.0% from waste disposal, including municipal and hazardous waste, crematoria, and sewage sludge incineration. This is a significant underestimate due to limited information, and is likely to be off by a factor of two to five.

3.0% from caustic soda production.

1.4% from pig iron and steel production.

1.1% from mercury production, mainly for batteries.

2.0% from other sources [ 15 ], (EPA report, 2007).

The above percentages are estimates of the global human-caused mercury emissions in 2000, excluding biomass burning, an important source in some regions [ 15 ]. Current atmospheric mercury contamination in outdoor urban air is (0.01–0.02 µg/m 3 ) indoor concentrations are significantly elevated over outdoor concentrations, in the range 0.0065–0.523 µg/m 3 (average 0.069 µg/m 3 ) [ 17 ]. Mercury also enters into the environment through the improper disposal (e.g., land filling, incineration) of certain products.

6. Particulate pollutants

Particles in suspension

Dust particles. Dust particles form a complex of organic compounds and minerals. These can derive from natural sources, such as volcanoes, or human activities, such as industrial combustion processes or traffic. Particles are categorized according to particle size. The smallest particles have the ability to transport toxic compounds into the respiratory tract. Some of these compounds are carcinogenic. The upper respiratory tract stops the larger dust particles. When they are released into the environment, dust particles can cause acidification and winter smog.

Cement-kiln dust Cement factories are the chief source of cement dust pollution. The composition of such dust varies with the source. Main component of cement dust is CaO and varying amounts of K 2 O, Na 2 O and KCl and traces of Al, Fe, Mn, Mg, S and silica. Dust with more than 24% CaO is more injurious to plants. Fine particles cause more damage than larger particles. Cement-kiln dust is alkaline in nature and dissolves in atmospheric moisture forming a solution of pH 10-12.

Lime and gypsum Lime and gypsum processing industries and mining deposits are chief sources from where fine particles of these substances are blown away to great distances.

Soot Burning of fossil fuels, organic matter or natural forest fires produce huge quantities of fine carbon particles which form the soot pollution. Soot can be dispersed over a quite wide area and transported to great distances by blowing winds.

Magnesium oxide Magnesium roasters are the chief sources of such pollution. The magnesium oxide dust may be carried by winds and deposited even at a distance of 5 km from the source. In the atmosphere, magnesium sulphate (MgSO 4 ) combines with carbon dioxide and water to form Mg(CO 3 ) 2 . Both these compounds are alkaline and slightly soluble in water.

Boron Boric acid and borax are common raw materials in many industries. Oven and refrigerator manufacturing industries are chief sources of boron pollution.

Chlorides of sodium, potassium and calcium Sodium and calcium chlorides are commonly used in cold countries on the roads during winters to melt ice and snow. Potash industry produces aerial emission of KCl and NaCl in ratio of 3:1. All such chlorides are carried away by winds and deposited on the soil and plants.

Sodium sulphate , with an annual production of 6 million tones, it is a major commodity chemical and one of the most damaging salts in structure conservation: when it grows in the pores of stones it can achieve high levels of pressure, causing structures to crack.

Sodium sulfate is mainly used for the manufacture of detergents and in the Kraft process of paper pulping. About two-thirds of the world's production is from mirabilite, the natural mineral form of the decahydrate, and the remainder from by-products of chemical processes such as hydrochloric acid production.

Pesticides, insecticides and herbicides Pesticide use in the agricultural industry began in earnest in the early 1940s. Although pesticide use had been quite popular for more than twenty years, government officials first became aware of the potential danger of pesticide runoff to humans in the early 1960s when Rachel Carson’s famous and influential Silent Spring was published. Though this book warned mainly of the detrimental effects of DDT (a popular insecticide developed in the early 1940s) for birds and other non-human victims, Carson’s work inspired health officials to speculate about the effects of pesticide runoff on humans. Recently, exposure to DDT was linked to Parkinson’s disease. Because of concern over DDT’s adverse effects on the environment and on people, this pesticide was banned in 1972. Despite the ban of DDT, pesticide use continues, and the effects of some modern insecticides and herbicides can be just as debilitating. Even through careful use, runoff from pesticides continues to makes its way into drinking water sources.

7. Secondary pollutants

Photo-oxidants In presence of strong sunlight and in hot weather a series of complex chemical reactions involving nitrogen oxides and hydrocarbons may produce certain photo-oxidant chemicals. These chemicals do not have any specific anthropogenic source but are formed over wide areas in which suitable environmental conditions are prevailing. Two such photo-oxidants that can reach ambient concentrations toxic to plants are PAN (Peroxyacetylnitrate) and ozone.

PAN (Peroxyacetylnitrate-CH 3 CO.O 2 .NO 2 ) Impact of this secondary pollutant is not affected by humidity. However, the impact decreases with lowering of temperature and increasing drought conditions. The impact also increases in the morning and in bright sunlight. Young plants and young rapidly expanding leaves are more sensitive to this pollutant. PAN interacts with SO 2 and O 3 in complex manner producing variable impact conditions.

Ozone (O 3 ) is the main pollutant in the oxidant smog complex.

Ozone is formed in the troposphere when sunlight causes complex photochemical reactions involving oxides of nitrogen (NOx), volatile organic hydrocarbons (VOC) and carbon monoxide that originate chiefly from gasoline engines and burning of other fossil fuels. Woody vegetation is another major source of VOCs. NOx and VOCs can be transported long distances by regional weather patterns before they react to create ozone in the atmosphere, where it can persist for several weeks. Seasonal exposures at low elevations consist of days when ozone concentrations are relatively low or average, punctuated by days when concentrations are high. Concentrations of ozone are highest during calm, sunny, spring and summer days when primary pollutants from urban areas are present. Ozone concentrations in rural areas can be higher than in urban areas while ozone levels at high elevations can be relatively constant throughout the day and night.

Middle aged leaves and young plants are more sensitive to ozone. This pollutant interacts with SO 2 , NO 2 , PAN and heavy metals in complex manner.

Ozone is created through photochemical transfer of oxygen. This process takes place under the influence of ultra violet sunlight (UV), aided by pollutants in the outside air ( fig. 2) . Ozone causes smog and contributes to acidification and climate change. Ozone is an aggressive gas. This can easily penetrate the respiratory tract, deeply. When humans are exposed to ozone, the consequences may be irritation of the eyes and the respiratory tract.

Acid deposition Various acid gases, aerosols and other acidic substances released into the atmosphere from the industrial or domestic sources of combustion of fossil fuels eventually come down to the ground. These substances are deposited directly on the water bodies. In addition, these substances also reach the water bodies along with run-off rainwater from the polluted soil. Deposition of acidic substances causes acidification of water by lowering its pH below 6.0. The sulphates, nitrates and chlorides have been reported to make water bodies like lakes, rivers and ponds acidic in many countries.

Acid deposition is not merely characterized as acid rain; it can also be snow and fog or gas and dust. Acid deposition mainly forms during fossil fuel combustion. When emissions of sulphur dioxide and nitrogen oxides come in contact with water, they will become sulphuric acid and nitric acid.

When acidifying agents, such as sulphur dioxide, nitrogen oxides and ammonia, end up in plants, surface water and soils, this has a number of consequences:

availability of nutrients and metal spores is likely to decrease

when acidity is high more metals will dissolve in water. This can cause surface water to become polluted, which has serious health effects on aquatic plants and animals. For example, high aluminum (Al) concentrations can complicate nutrients uptake by plants. This makes aluminum one of the prior causes of forest decay. Mercury can be dispersed by transport through surface water, causing it to accumulate in fish. Mercury can bio magnify up the food chain, to be taken up by humans eventually

Buildings and monuments may be damaged through erosion. Sulphur dioxide breaks down limestone by reacting with calcium carbonate, causing limestone to absorb water during rainfall. Limestone will than fragment

Noise pollution has a relatively recent origin. It is a composite of sounds generated by human activities ranging from blasting stereo systems to the roar of supersonic transport jets. Although the frequency (pitch) of noise may be of major importance, most noise sources are measured in terms of intensity, or strength of the sound field. The standard unit, one decibel (dB), is the amount of sound that is just audible to the average human. The decibel scale is somewhat misleading because it is logarithmic rather than linear; for example, a noise source measuring 70 dB is 10 times as loud as a source measuring 60 dB and 100 times as loud as a source reading 50 dB. Noise may be generally associated with industrial society, where heavy machinery, motor vehicles, and aircraft have become everyday items. Noise pollution is more intense in the work environment than in the general environment, although ambient noise increased an average of one dB per year during the 1980s. The average background noise in a typical home today is between 40 and 50 decibels. Some examples of high-level sources in the environment are heavy trucks (90 dB at 15 m/50 ft), freight trains (75 dB at 15 m/50 ft), and air conditioning (60 dB at 6 m/20 ft).

Radiation pollution is any form of ionizing or no ionizing radiation that results from human activities. The most well-known radiation results from the detonation of nuclear devices and the controlled release of energy by nuclear-power generating plants (see nuclear energy). Other sources of radiation include spent-fuel reprocessing plants, by-products of mining operations, and experimental research laboratories. Increased exposure to medical x rays and to radiation emissions from microwave ovens and other household appliances, although of considerably less magnitude, all constitute sources of environmental radiation.

Radioactive radiation . Radioactive radiation and radioactive particles are naturally present in the environment. During power plant incidents or treatments of nuclear waste from a war where nuclear weapons are used, radioactive radiation can enter the air on account of humans. When humans are exposed to high levels of radioactive radiation, the chances of serious health effects are very high. Radioactive radiation can cause DNA alteration and cancer.

8. Flow of atmospheric pollutants at global level

The air pollutants are produced by different sectors of the economy like: industry, agriculture, transports and urbanization. The burning of hydrocarbons in motor vehicle engines gives rise to CO 2 , CO, SO 2 (sulfur dioxide), NO x (NO [nitrogen monoxide]) and NO 2 – - in varying proportions-and C 2 H 4 (ethylene), as well as a variety of other hydrocarbons. Additional SO 2 originates from domestic and industrial burning of fossil fuels. Industrial plants, such as chemical works and metal-smelting plants, release SO 2 , H 2 S, NO 2 , and HF (hydrogen fluoride) into the atmosphere. Tall chimney stacks may be used to carry gases and particles to a high altitude and thus avoid local pollution, but the pollutants return to Earth, sometimes hundreds of kilometers from the original source.

Photochemical smog is the product of chemical reactions driven by sunlight and involving NO x of urban and industrial origin and volatile organic compounds from either vegetation ( biogenic hydrocarbons) or human activities ( anthropogenic hydrocarbons). Ozone (O 3 ) and peroxyacetylnitrate (PAN) produced in these complex reactions can become injurious to plants and other life forms, depending on concentration and duration of exposure. Hydrogen peroxide, another potentially injurious molecule, can form by the reaction between O 3 and naturally released volatiles (terpenes) from forest trees.

The concentrations of polluting gases, or their solutions, to which plants are exposed are thus highly variable, depending on location, wind direction, rainfall, and sunlight. Experiments aimed at determining the impact of chronic exposure to low concentrations of gases should allow plants to grow under near-natural conditions. One method is to grow the plants in open-top chambers into which gases are carefully metered, or where plants receiving ambient, polluted air are compared with controls receiving air that has been scrubbed of pollutants.

These pollutants emitted into the atmosphere can react with components of the atmosphere and transform into more or less aggressive or toxic compounds. The air pollutants can accumulate and manifest directly effects in the atmosphere (greenhouse effect, ozone layer depletion, etc) or can to transform in other pollutants and manifest indirectly effects on ecosystem biocoenosis, plants, animals and human health ( fig. 3)

9. Effect of pollutants on vegetation, direct effects, and indirect effect, gas toxicity, wet and dry deposition, and deposition mixtures

Dust pollution is of localized importance near roads, quarries, cement works, and other industrial areas. Apart from screening out sunlight, dust on leaves blocks stomata and lowers their conductance to CO 2 , simultaneously interfering with photosystem II. Polluting gases such as SO 2 and NO x enter leaves through stomata, following the same diffusion pathway as CO 2 . NO x dissolves in cells and gives rise to nitrite ions (NO 2 – , which are toxic at high concentrations) and nitrate ions (NO 3 – ) that enter into nitrogen metabolism as if they had been absorbed through the roots. In some cases, exposure to pollutant gases,

The air pollutants flow diagram

particularly SO 2 , causes stomatal closure, which protects the leaf against further entry of the pollutant but also curtails photosynthesis. In the cells, SO 2 dissolves to give bisulfite and sulfite ions; sulfite is toxic, but at low concentrations it is metabolized by chloroplasts to sulfate, which is not toxic. At sufficiently low concentrations, bisulfite and sulfite are effectively detoxified by plants, and SO 2 air pollution then provides a sulfur source for the plant. In urban areas these polluting gases may be present in such high concentrations that they cannot be detoxified rapidly enough to avoid injury. Ozone is presently considered to be the most damaging phytotoxic air pollutant in North America [ 18 ], [ 19 ]. It has been estimated that wherever the mean daily O 3 concentration reaches 40, 50, or 60 ppb (parts per billion or per 10 9 ), the combined yields of soybean, maize, winter wheat, and cotton would be decreased by 5, 10, and 16%, respectively. Ozone is highly reactive: It binds to plasma membranes and it alters metabolism. As a result, stomatal apertures are poorly regulated, chloroplast thylakoid membranes are damaged, rubisco is degraded, and photosynthesis is inhibited. Ozone reacts with O 2 and produces reactive oxygen species, including hydrogen peroxide (H 2 O 2 ), superoxide (O 2 – ), singlet oxygen ( 1 O 2 *), and the hydroxyl radical ( - OH). These denature proteins and damage nucleic acids (thereby giving rise to mutations), and cause lipid peroxidation, which breaks down lipids in membranes. Reactive oxygen species form also in the absence of O 3 , particularly in electron transport in the mitochondria and chloroplasts, when electrons can be donated to O 2 . Cells are protected, at least in part, from reactive oxygen species by enzymatic and nonenzymatic defense mechanisms [ 20 ], [ 21 ]. Defense against reactive oxygen species is provided by the scavenging properties of molecules, such as ascorbic acid, α-tocopherol, phenolic compounds, and glutathione. Superoxide dismutases (SODs) catalyze the reduction of superoxide to hydrogen peroxide. Hydrogen peroxide is then converted to H 2 O by the action of catalases and peroxidases. Of particular importance is the ascorbate-specific peroxidase localized in the chloroplast. Acting in concert, ascorbate peroxidase, dehydroascorbate reductase, and glutathione reductase remove H 2 O 2 in a series of reactions called the Halliwell–Asada pathway , named after its discoverers. Glutathione is a sulfur-containing tripeptide that, in its reduced form, reacts rapidly with dehydroascorbate and becomes oxidized in the process. Glutathione reductase catalyzes the regeneration of reduced glutathione (GSH) from its oxidized form (GSSG) in the following reaction:

Exposure of plants to reactive oxygen species stimulates the transcription and translation of genes that encode enzymes involved in protection mechanisms. In Arabidopsis, exposure for 6 hours per day to low levels of O 3 induces the expression of several genes that encode enzymes associated with protection from reactive oxygen species, including SOD, glutathione S-transferase (which catalyzes detoxification reactions involving glutathione), and phenylalanine ammonia lyase (an important enzyme at the start of the phenylpropanoid pathway that leads to the synthesis of flavonoids and other phenolics) [ 22 ].

In transgenic tobacco transformed with a gene from Escherichia coli to give additional glutathione reductase activity in the chloroplast, short-term exposure to high levels of SO 2 is much less damaging than for wild-type tobacco [ 23 ]. Environmental extremes may either accelerate the production of reactive oxygen species or impair the normal defense mechanisms that protect cells from reactive oxygen species. In water-deficient leaves, for example, greater oxygen photoreduction by photosystems I and II increases superoxide production, and the pool of glutathione, as well as the activity of glutathione reductase, increase-presumably as part of the cell defense mechanism. In contrast, levels of ascorbate, another antioxidant, generally decline with mild water stress. Transgenic plants overexpressing mitochondrion superoxide dismutase (Mn-SOD), the isozyme localized in the mitochondrial matrix, show less water-deficit damage and, significantly, improved survival and yield under field conditions [ 24 ]. In other experiments, transgenic alfalfa overexpressing Mn-SOD was found to be more tolerant of freezing. Conversely, winter rye, wheat, and barley acclimated at 2 °C for several weeks, were found to have developed resistance to the herbicides, paraquat and acifluorfen, which generate reactive oxygen species. Such investigations support the hypothesis that tolerance of oxidative stress is an important factor in tolerance to a wide range of environmental extremes. Many deleterious changes in metabolism caused by air pollution precede external symptoms of injury, which appear only at much higher concentrations. For example, when plants are exposed to air containing NO x , lesions on leaves appear at a NO x concentration of 5 ml/l, but photosynthesis starts to be inhibited at a concentration of only 0.1 ml/l. These low, threshold concentrations refer to the effects of a single pollutant. However, two or more pollutants acting together can have a synergistic effect, producing damage at lower concentrations than if they were acting separately. In addition, vegetation weakened by air pollution can become more susceptible to invasion by pathogens and pests. Unpolluted rain is slightly acidic, with a pH close to 5.6, because the CO 2 dissolved in it produces the weak acid, H 2 CO 3 . Dissolution of NO x and SO 2 in water droplets in the atmosphere causes the pH of rain to decrease to 3 to 4, and in southern California polluted droplets in fog can be as acidic as pH 1.7. Dilute acidic solution can remove mineral nutrients from leaves, depending on the age of the leaf and the integrity of the cuticle and surface waxes. The total annual

contributions to the soil of acid from acid rain ( wet deposition ) and from particulate matter falling on the soil plus direct absorption from the atmosphere ( dry deposition ) may reach 1.0 to 3.0 kg H + per hectare in parts of Europe and the northeastern United States [ 25 ]. In soils that lack free calcium carbonate, and therefore are not strongly buffered, such additions of acid can be harmful to plants. Furthermore, the added acid can result in the release of aluminum ions from soil minerals, causing aluminum toxicity. Air pollution is considered to be a major factor in the decline of forests in heavily polluted areas of Europe and North America. There are indications that fast-growing pioneer species are better able to tolerate an acidifying atmosphere than are climax forest trees, possibly because they have a greater potential for assimilation of dissolved NO x , and more effective acid buffering of the leaf tissue cell sap. Air pollution injury to plants can be evident in several ways. Injury to foliage may be visible in a short time and appear as necrotic lesions (dead tissue), or it can develop slowly as a yellowing or chlorosis of the leaf. There may be a reduction in growth of various portions of a plant. Plants may be killed outright, but they usually do not succumb until they have suffered recurrent injury.

Major primary air pollutants gases are sulphur dioxide, oxides of nitrogen particularly NO 2 , HF, HCl, chlorine, ammonia, ethylene and other organic substances. Particulate air pollutants are soot, dust, fine particles of cement and various other substances. Various fertilizers, pesticides and insecticides used in aerial spray are also important air pollutants. The common sources of the pollutants, factors affecting the effect of pollutant and the injury symptoms produced in plants are discussed below.

10. Major gaseous pollutants

Sulphur dioxide (SO 2 )

Sulfur dioxide is a major component in acid rain. One of the byproducts of sulfur dioxide is sulfuric acid, and both can be extremely damaging to plants that are exposed to these chemicals. Exposed leaves can begin to lose their color in irregular, blotchy white spots. Some leaves can develop red, brown or black spots. When the pigments in enough tissue are damaged or killed, plants can begin to lose their leaves. Crop output is greatly reduced and growth can be stunted. This is especially noticeable in young plants.

It is the most important and common air pollutant produced in huge amounts in combustion of coal and other fuels in industrial and domestic use. It is also produced during smelting of sulphide ores. Major sources of sulfur dioxide are coal-burning operations, especially those providing electric power and space heating. Sulfur dioxide emissions can also result from the burning of petroleum and the smelting of sulfur containing ores.

SO 2 effects increase in high humidity, windy conditions, in the early morning, in the deficiency of K and Cl 2 and excess of sulphur in the soil. It interacts with ozone, NO 2 and HF. The nature of interaction depends on the relative proportion of gases. The impact of SO 2 decreases in low soil moisture, low temperature, deficiency of nitrogen, sulphur and phosphorus and sometimes in excess of nitrogen also.

In angiosperms, young leaves and in conifers, needles are most sensitive to SO 2 pollution. In general, seedlings are more sensitive than older plants. The effect of the gas usually decreases with age of the plant and lesser morphological and physiological symptoms appear in older plants.

Injury symptoms: The gas is a strong reducing agent. In low concentration, it is oxidized and used in protein synthesis of the plant. However, in high concentration, it causes swelling of thylakoids and interferes with electron transport chain. In SO 2 pollution, plants show initial reduction of photosynthesis and increased respiration. The gas reduces stomatal opening and thus causes general water stress in plants. SO 2 replaces oxygen in cellular materials and changes their nature. It affects structural proteins in the cell membrane and thus changes the membrane permeability. High concentration of the gas causes accumulation of sulphydril and decrease of sulphides in plants. SO 2 interferes with amino acid metabolism and reduces the synthesis of proteins and enzymes. It stimulates the oxidation of PGA and increases the pentose phosphate cycle activity. It reduces the level of keto acids, ATP, sucrose and glutamate in plants and increases the level of glucose, fructose and glycolate. It inactivates many enzymes either by breaking their S-S bonds or by changing their stereo structure. In lichens, the gas induces photooxidation in the phycobiont part. Most common visible symptom of SO 2 injury is water-soaked appearance of leaves which later become necrotic changing into brown spots. Color and shape of necrotic spots is characteristic in different species and NO 2 concentrations. In some species, characteristic intraveinal chlorosis is caused. In general, SO 2 pollution results in abscission of older leaves and tip necrosis in flower and sepals.

Sulfur dioxide enters the leaves mainly through the stomata (microscopic openings) and the resultant injury is classified as either acute or chronic. Acute injury ( fig. 4) is caused by absorption of high concentrations of sulfur dioxide in a relatively short time. The symptoms appear as 2-sided (bifacial) lesions that usually occur between the veins and occasionally along the margins of the leaves. The colors of the necrotic area can vary from a light tan or near white to an orange-red or brown depending on the time of year, the plant species affected and weather conditions. Recently expanded leaves usually are the most sensitive to acute sulfur dioxide injury, the very youngest and oldest being somewhat more resistant.

Acute sulfur dioxide injuries to raspberry [ 26 ].

Chronic injury is caused by long-term absorption of sulfur dioxide at sub-lethal concentrations. The symptoms appear as a yellowing or chlorosis of the leaf, and occasionally as a bronzing on the under surface of the leaves. Different plant species and varieties and even individuals of the same species may vary considerably in their sensitivity to sulfur dioxide. These variations occur because of the differences in geographical location, climate, stage of growth and maturation. The following crop plants are generally considered susceptible to sulfur dioxide: alfalfa, barley, buckwheat, clover, oats, pumpkin, radish, rhubarb, spinach, squash, Swiss chard and tobacco. Resistant crop plants include asparagus, cabbage, celery, corn, onion and potato. Plants damaged by sulfur dioxide can be as far as 30 miles from its source, but the most severe damage, defoliation and discoloring is typically found within five miles. For some plants, it can take exposure of only four hours to suffer damage. A wide variety of plants are vulnerable, from alfalfa and carrots to crab apple and fir trees.

Nitrogen dioxide (NO 2 )

NO 2 mostly affects the leaves and seedlings. Its effects decrease with increasing age of the plant and tissue. Conifers are found to be more sensitive to this gas during spring and summer than in winters. Older needles are more sensitive to the gas than young ones.

Injury symptoms: The gas causes formation of crystalloid structures in the stroma of chloroplasts and swelling of thylakoid membrane. As a result the photosynthetic activity of the plant is reduced.

Most common visible injury symptoms are chlorosis in angiospermic leaves and tip burn in conifer needles. In angiosperms, most of the species produce water-soaked intraveinal areas that later become necrotic. Tip burn is common symptom in bracts, sepals and awns.

Fluirides in general, are accumulated in the plant tissues over long times. They are first accumulated in the leaves and then are translocated towards tips and margins of the leaves. The injury symptoms are produced only after a critical level of fluoride is attained. Due to such accumulation over long times, flurides generally and HF particularly can induce injury at very low atmospheric concentrations. Critical concentration for fluoride injury is 0.1 ppm for several days. Toxicity of particulate fluorides depends upon the particle size, their solubility and humidity of the atmosphere.

HF gas is much lighter than air and so can cause damage in plants even at a distance of 30 km from the source. It is a hygroscopic gas and forms acidic cloud near the source. Generally the impact of HF pollution increases with humidity and excess of P in soil while decreases in low temperature, drought and deficiency of N and Ca in the soil. In some species, impact of HF has been reported to decrease with excess of N and Ca in the soil.

In most of the species, recovery from moderate fluoride injury can occur within few days if exposure to pollutant stops. However, some highly sensitive species e.g. pine and spruce can never recover fully. HF generally affects immature leaves in angiosperms and needles in conifers.

Injury symptoms: Fluorides combine with metal components of proteins or inhibit them otherwise and thus interfere with the activity of many enzymes. As a result the cell wall composition, photosynthesis, respiration, carbohydrate synthesis, synthesis of nucleic acids and nucleotides and energy balance of the cell are affected. In the leaves subjected to HF exposure, endoplasmic reticulum is reduced, ribosomes are detached from ER, number of ribosomes is reduced and mitochondria become swollen. Chlorophyll synthesis and cellulose synthesis are inhibited. Activities of UDP-glucose-fructose transglucosylase, phosphoglucomutase, enolase and polyphenol oxidase are reduced. On the other hand activities of catalase, peroxidase, pyruvate kinase, PEP-carboxylase, glucose-6-phosphate dehydrogenase, cytochrome oxidase and pentose phosphate pathway are stimulated.In conifer needles common visible injury symptoms are chlorosis later turning into red/brown discolouration, tip burn later turning into necrosis of whole needle, formation of sharply defined red/purple bands between healthy and injured tissue. Similar symptoms are common in angiospermic leaves also. In addition, the angiospermic leaves in many species also show zonation of necrotic areas, leaf cupping, curling of leaf edges and ragged leaf margins. In sepals, petals, bracts and awns, water-soaked margins and later tip and marginal necrosis are observed. Fluorides absorbed by leaves are conducted towards the margins of broad leaves (grapes) and to the tips of monocotyledonous leaves (gladiolus). Little injury takes place at the site of absorption, whereas the margins or the tips of the leaves build up injurious concentrations. The injury ( fig. 5) starts as a gray or light-green water-soaked lesion, which turns tan to reddish-brown. With continued exposure the necrotic areas increase in size, spreading inward to the midrib on broad leaves and downward on monocotyledonous leaves.

Fluoride injuries to plum foliage [ 26 ].

The fluoride enters the leaf through the stomata and is moved to the margins where it accumulates and causes tissue injury. Note, the characteristic dark band separating the healthy (green) and injured (brown) tissues of affected leaves. Studies of susceptibility of plant species to fluorides show that apricot, barley (young), blueberry, peach (fruit), gladiolus, grape, plum, prune, sweet corn and tulip are most sensitive. Resistant plants include alfalfa, asparagus, bean (snap), cabbage, carrot, cauliflower, celery, cucumber, eggplant, pea, pear, pepper, potato, squash, tobacco and wheat.

Chlorine (Cl 2 )

Older plants are more sensitive to chlorine than seedlings. The age of tissue has little effect on the sensitivity and older as well as young tissues are almost equally afected by chlorine pollution.

Injury symptoms: Chlorine injury symptoms can appear from 18 hours to 8 days after exposure. In most plant species, recovery from chlorine injury can occur 3 to 4 days after exposure is stopped. Chlorine injury symptoms are quite variable in different species. Most common visible symptoms in conifers are chlorosis, tip burn and necrosis is needles. In angiosperm leaves, marginal or intraveinal necrosis, water-soaked appearance, leaf cupping and abscission are common.

Hydrogen chloride (HCl)

The HCl injury can be caused to plants even at a distance of 800 meter from the source. Like fluorides, the chloride from HCl is accumulated in the leaves and translocated towards their margins and tips. Symptoms of HCl injury appear after a critical concentration is reached, usually between 24 and 72 hours after the exposure.

Impact of HCl pollution decreases with increase in humidity, deficiency of Mg and excess of Ca. Mature plants are more sensitive to HCl than seedlings. Similarly, young fully expanded leaves are more sensitive than immature unexpanded leaves.

Injury symptoms: Most common visible injury symptoms in conifer needles are red or brown discolouration and tip burn. In angiosperm leaves, common symptoms are intraveinal water-soaked streaks, yellow or brown necrosis, tip necrosis, bleached areas around the necrosis and shot-holing. Tip burn, necrotic stipple and discolouration in sepals and petals are also observed.

Ammonia (NH 3 )

Impact of ammonia on plants generally increases with humidity and decreases with drought. Effect of darkness on ammonia sensitivity is highly variable among species. Some species are more sensitive to low concentrations of ammonia than to its high concentration. Age of tissue has little effect on sensitivity and both young and old tissues are equally sensitive to ammonia.

Injury symptoms: Most common visible symptoms in conifers are black discolouration, usually sharply bordered tip burn and abscission of needles. In angiosperm leaves, common symptoms are water-soaked appearance later turning black, intercostal necrosis, slight marginal and upper surface injury, glazong/bronzing of upper surface, desiccation and abscission. Ammonia injury to vegetation has been observed frequently in Ontario in recent years following accidents involving the storage, transportation or application of anhydrous and aqua ammonia fertilizers. These episodes usually release large quantities of ammonia into the atmosphere for brief periods of time and cause severe injury to vegetation in the immediate vicinity. Complete system expression on affected vegetation usually takes several days to develop, and appears as irregular, bleached, bifacial, necrotic lesions. Grasses often show reddish, interveinal necrotic streaking or dark upper surface discolouration. Flowers, fruit and woody tissues usually are not affected, and in the case of severe injury to fruit trees, recovery through the production of new leaves can occur ( fig. 6) . Sensitive species include apple, barley, beans, clover, radish, raspberry and soybean. Resistant species include alfalfa, beet, carrot, corn, cucumber, eggplant, onion, peach, rhubarb and tomato.

Severe ammonia injuries to apple foliage and subsequent recovery through the production of new leaves following the fumigation [ 26 ].

Organic gases (Ethylene)

Ethylene injury symptoms develop in plants only in exposure to high concentrations and take several days to develop. After exposure to the gas is stopped, level of recovery is variable in different species. Generally, younger plant parts recover but older parts do not. Much ‘acute’ damage to plants is caused on the fringes of polluted area or by a steady leakage of gas in low concentration.

Injury symptoms: In injuriously high concentrations of ethylene, growth of plants is stopped. In low concentrations, growth abnormalities appear. In conifers, yellow tips in needles and abscission of branches and cones are common. In angiosperms, common symptoms are epinasty or hyponasty, loss of bark, abscission of leaves and flowers, premature flower opening and fruit ripening. Ethylene affects the growth hormones and regulatory process that takes place in the plant and results in a number of outward manifestations of infection. Leaves can begin to curl and die; ethylene causes the leaves of plants to curl down and fold under as they shrivel and are stuck with necrosis. On flowering plants, buds can stop opening or flowers can begin to show signs of discoloration or die and drop sooner than expected. Even in more resistant plants like evergreen conifers, growth of the plant will be stunted, needles will be small and few pine cones will be produced. Plants such as peach trees, marigolds, blackberries and tomatoes are extremely vulnerable to damage from exposure to ethylene.

11. Minor gaseous pollutants

Hydrogen sulphide (H 2 S)

Plants show wilting on exposure to this gas but the symptoms develop after about 48 hours. No injury occurs below the exposure of 40 ppm for 4 hours.

Carbon monoxide (CO)

Like ethylene this gas produces epinasty, chlorosis and abscission. However, concentration of over 1000 times that of ethylene is needed to produce same degree of damage. No injury to plants occurs below exposure of 100 ppm for 1 week.

Studies show these gases are highly toxic to plants. HI and I 2 are readily absorbed and accumulated by plants producing visible injury symptoms similar to those of SO 2 . Injury occurs at exposure of 0.1 ppm for 18 hours.

Common injury symptoms of bromine in angiosperms are necrosis of leaf margins, leaf tips and tendrils; brown discoloration and black spots later spreading to entire leaf. In conifers, yellow/white needle tips or red/brown discoloration later becoming grey/brown are common symptoms.

Mercury vapors (Hg)

Unlike other pollutants, flowers are more sensitive to Hg than leaves. Injury symptoms usually appear within 24 hours of Hg exposure but often go on increasing up to 5 days.

Common injury symptoms due to Hg-vapors pollution are abscission of oldest leaves, interveinal necrosis, chlorosis around veins, flower abscission, loss of petal colors, buds remaining closed and later becoming necrotic, blackening of stamens, pistils and peduncles.

Particulate pollutants

Different types of solid particulate materials are also important air pollutants. Each of these affects the plants in characteristic manner. Some common particulate air pollutants have been discussed below.

Cement-kiln dust

In generals, plants having hairy surface of leaves trap more dust and are, therefore, damaged more than the plants with shiny leaf surface. The cement dust forms crusts on the surface of leaves, twigs and flowers. This inhibits gaseous exchange from the surfaces of plant parts. Such crust on the leaves also inhibits light penetration and consequently reduces photosynthesis. Such crusts are especially thicker in conditions of dew, mist or light rains. In dry conditions, dust blowing with wind is highly abrasive and damages the cuticle of leaves. Cuticle is also damaged due to alkalinity of cement dust. Due to damaged cuticle plants become more susceptible to infection by pathogens.

Lime and gypsum

Lime and gypsum deposited on the soil from the air, these change the pH of the soil and thus affect the nutrient availability to plants. Such deposition usually causes appearance of various nutrient deficiency symptoms in the plants. Lime and gypsum are less adhering as compared to cement-kiln dust. However, these are also trapped and deposited on the surface of plant parts particularly the leaves with hairy surfaces and produce injury symptoms similar to cement dust. Lime and gypsum particles blowing with wind are also highly abrasive for cuticle.

Soot deposited on the surface of leaves may be washed away by rains so its damage may be reduced. However, in bright sunlight and high temperature, the damage is increased.

Soot deposited on the surface of leaves inhibits light penetration, increased surface temperature due to absorption of heat and clogging of stomata. The result of these is reduced gaseous exchange, reduced photosynthesis and general weakening of the plant growth. Necrotic spots also develop in many species due to soot deposition.

Magnesium oxide

Deposited on the soil these compounds can soon increase the soil pH to levels injurious to plants. Deposition of these substances on the soil prevents germination of seedlings. The seedlings that are able to emerge usually have yellow/brown tips of leaves and their roots are stunted. In areas of heavy pollution, composition of the vegetation changes completely.

Severe injury to plants is observed even at a distance of 200 meters from the source and mild injury may be observed up to 500 meters in all the directions from the source.

Impact of boron pollution is more severe on older leaves than on younger leaves. Boron is also accumulated in the leaves and produces injury symptoms quite similar to fluoride pollution.

Chlorides of sodium, potassium and calcium Injury symptoms produced by these chlorides in plants are very similar to those produced by SO 2 and fluoride pollution.

Sodium sulphate dust can cause necrosis of leaves of the plants. The damage increases in moist condition.

Pesticides, insecticides and herbicides

A large variety of such chemicals are sprayed on the crops these days. These substances may drift with wind to nearby areas. Generally, these chemicals are deposited on the soil and form important soil pollutants. However, in frosty conditions when crops and other plants damaged by early frost are quite susceptible to foliar spray of these chemicals, these may also be injurious air pollutants. Injury symptoms vary with the plant species and the type of chemical. Generally, the symptoms are produced on foliage and are quite similar to those produced when these substances act as soil pollutants.

12. Secondary pollutants and plants

Many of the primary pollutants under specific environmental conditions may interact with each other and produce secondary environmental pollutants or certain complex environmental conditions that are injurious to plants. Such secondary pollutants and pollution conditions are discussed below.

Photo-oxidants

PAN (Peroxyacetylnitrate-CH 3 CO.O 2 .NO 2 )

The common visible symptoms of exposure to PAN are chlorosis and necrosis in leaves. It also interferes with photosynthesis, respiration and absorption and synthesis of carbohydrates and proteins. It inhibits photorespiration, NADP reduction, carbon dioxide fixation, cellulose synthesis and the enzymes associated with photosynthesis and respiration.

Ozone (O 3 ) is released into the atmosphere from the burning of fossil fuels and is one of the most harmful pollutants to plants. It can be carried for long distances and is readily absorbed as a part of the photosynthetic process. Plants exposed to large amounts of ozone can develop spots on their leaves. These spots are irregular and often tan, brown or black. Some leaves can take on a bronze or red appearance, usually as a precursor to necrosis. Depending on the concentration of ozone in the environment, plants can show different amounts of discoloration before the leaves begin to die.

Studies by the National Crop Loss Assessment Network show that ozone in the environment also has a detrimental effect on crop production. While crops such as cotton, soybeans and other dicots are more sensitive than monocot crops, all crops sampled over the decades-long studies show significant loss of productivity when exposed to ozone. Cotton crops show significantly less yield when exposed to levels of ozone in the atmosphere. Middle aged leaves and young plants are more sensitive to ozone. This pollutant interacts with SO 2 , NO 2 , PAN and heavy metals in complex manner.

Common symptoms of ozone pollution are yellowing, flecking and blotching in leaves, premature senescence and early maturity. It interferes with pollen formation, pollination, pollen germination and growth of pollen tubes. Increase in the level of RNA, starch, polysaccharides and number of polysomes is observed in ozone pollution. Ozone stimulates respiration, inhibits oxidative phosphorylation and changes membrane permeability. In some species, it inhibits the synthesis of glucon and cellulose and reduces the level of reducing sugars, ascorbic acid and ATP while in other species the effect is opposite to it. The impact of ozone on plants increases with humidity and decreases with drought, darkness, low temperature, high soil salinity, deficiency of soil phosphorus and excess of soil sulphur. Throughout the growing season, particularly July and August, ozone levels vary significantly. Periods of high ozone are associated with regional southerly air flows that are carried across the lower. Localized, domestic ozone levels also contribute to the already high background levels. Injury levels vary annually and white bean, which are particularly sensitive, are often used as an indicator of damage. Other sensitive species include cucumber, grape, green bean, lettuce, onion, potato, radish, rutabagas, spinach, sweet corn, tobacco and tomato. Resistant species include endive, pear and apricot.

Ozone injuries to soybean foliage [ 26 ].

Ozone symptoms ( fig. 7) characteristically occur on the upper surface of affected leaves and appear as a flecking, bronzing or bleaching of the leaf tissues. Although yield reductions are usually with visible foliar injury, crop loss can also occur without any sign of pollutant stress. Conversely, some crops can sustain visible foliar injury without any adverse effect on yield. Susceptibility to ozone injury is influenced by many environmental and plant growth factors. High relative humidity, optimum soil-nitrogen levels and water availability increase susceptibility. Injury development on broad leaves also is influenced by the stage of maturity. The youngest leaves are resistant. With expansion, they become successively susceptible at middle and basal portions. The leaves become resistant again at complete maturation

Ground-level ozone causes more damage to plants than all other air pollutants combined. This web page describes the ozone pollution situation, shows classical symptoms of ozone injury and shows how ozone affects yield of several major crops.

Ozone enters leaves through stomata during normal gas exchange. As a strong oxidant, ozone (or secondary products resulting from oxidation by ozone such as reactive oxygen species) causes several types of symptoms including chlorosis and necrosis. It is almost impossible to tell whether foliar chlorosis or necrosis in the field is caused by ozone or normal senescence. Several additional symptom types are commonly associated with ozone exposure, however. These include flecks (tiny light-tan irregular spots less than 1 mm diameter), stipples (small darkly pigmented areas approximately 2-4 mm diameter), bronzing, and reddening.

Ozone symptoms usually occur between the veins on the upper leaf surface of older and middle-aged leaves, but may also involve both leaf surfaces (bifacial) for some species. The type and severity of injury is dependent on several factors including duration and concentration of ozone exposure, weather conditions and plant genetics. One or all of these symptoms can occur on some species under some conditions, and specific symptoms on one species can differ from symptoms on another. With continuing daily ozone exposure, classical symptoms (stippling, flecking, bronzing, and reddening) are gradually obscured by chlorosis and necrosis.

Studies in open-top field chambers have repeatedly verified that flecking, stippling, bronzing and reddening on plant leaves are classical responses to ambient levels of ozone. Plants grown in chambers receiving air filtered with activated charcoal (CF) to reduce ozone concentrations do not develop symptoms that occur on plants grown in non-filtered air (NF) at ambient ozone concentrations. Foliar symptoms shown on this web site mainly occurred on plants exposed to ambient concentrations of ozone (either in NF chambers or in ambient air).

Yield Loss Caused by Ozone

Field research to measure effects of seasonal exposure to ozone on crop yield has been in progress for more than 40 years. Most of this research utilized open-top field chambers in which growth conditions are similar to outside conditions. The most extensive research on crop loss was performed from 1980 to 1987 at five locations in the USA as part of the National Crop Loss Assessment Network (NCLAN). At each location, numerous chambers were used to expose plants to ozone treatments spanning the range of concentrations that occur in different areas of the world. The NCLAN focused on the most important agronomic crops nationally

The strongest evidence for significant effects of ozone on crop yield comes from NCLAN studies [ 18 ] ( fig. 8) . The results show that dicotyledonous species (soybean, cotton and peanut) are more sensitive to yield loss caused by ozone than monocot species (sorghum, field corn and winter wheat).

Particulate Matter

Particulate matter such as cement dust, magnesium-lime dust and carbon soot deposited on vegetation can inhibit the normal respiration and photosynthesis mechanisms within the leaf. Cement dust may cause chlorosis and death of leaf tissue by the combination of a thick crust and alkaline toxicity produced in wet weather. The dust coating ( fig. 9) also may affect the normal action of pesticides and other agricultural chemicals applied as sprays to foliage. In addition, accumulation of alkaline dusts in the soil can increase soil pH to levels adverse to crop growth.

Effect of ozone on yield of crops [ 18 ]. cotton image by arklite06 from

Cement-dust coating on apple leaves and fruit. The dust had no injurious effect on the foliage, but inhibited the action of a pre-harvest crop spray [ 26 ].

13. Effect of atmospheric pollutants on vegetation monitoring system, why forestry monitoring system?

Because the crop plants are mostly annual plants they can not show the long-term effects produced by air pollutants. Therefore to monitor the effects of air pollution are recommended the trees, the changes in forest structure highlight the harmful effects of different air pollutants.

The evident decline of the health state of the forest in Europe since the beginning of the 1980 due to the negative impact of air pollution were illustrated by numerous publication from this period (see litt.). In the efforts to obtain objective and comparable data concerning the health of the European forests were developed a common methodology for the assessment of the forest state under the influence of air pollution. This network is known under the short term ICP- Forest (International Cooperative Programme for the investigation of the trans-boundary Pollution Influence on the Forests).

The poor health status of the forests in Central Europe concerns all the Europe. The pictures of the forests on large area were dominated by tree with defoliated crowns and an increasing rate of the death trees ( fig 10) . The assessment of the causes of the “new damages“- neuartiges waldschaden, in germ– is not easy because the symptoms of the decline were different from the symptoms of the damages caused by natural (biotic and abiotic) and anthropic causes.

Under the umbrella of ICP Forest Programme, were developed and implemented an European network of plots for the assessment of the parameters of the trees crowns condition known as Level I plots. The grid of the European Level I plots were established at 16 * 16 km, arranged on a transnational unified grid over Europe. In comparison with the national grids used by each country the obtained data were relevant for the evaluation of the forest health state at European level.

After 1996 were put in function the Level II monitoring plots used for the intensive monitoring and collection of comparable data related to the changes in forest ecosystems which are directly connected to specific environment at factors such as atmosphere pollution and acid deposition. Such data can help in a better understanding at the relation causes and effects in the forests decline.

General aspects of silver fir crowns affected by decline in the border of the northern Carpathians (Forest District Solca)

The monitoring results contribute to the scientific basis of air pollution control policies of UN/ECE and the European Commission (EC). Fifteen years of monitoring forest condition and two decades of forest damage research have shown, however, that the discussion of recent forest damage must not be confined to the effects of air pollution alone. The comprehensive monitoring programme corresponds to the complex interrelations between natural and anthropogenic factors in forest ecosystems. Infrastructure and data of the programme are thought to be relevant for other processes of international forest policies, e.g. those on biodiversity, climate change and sustainable forest management. In this respect the monitoring pursues the objectives of Resolution SI of the Strasbourg, Resolution HI of the Helsinki and Resolution, L2 of the Lisbon Ministerial Conference on the Protection of Forests in Europe, and contributes to global forest policies such as the United Nations Forum on Forests (ICP- Report 2007).

The monitoring results obtained each year are summarized in annual Executive Reports. The methodological background and detailed results of the individual surveys are described in Technical Reports ( http://www.icp-forests.org ).

Methodology for the crown health condition assessment of forests

The state of health of forest trees can be determined by assessing the foliage loss. With a little practice, this can be accurately estimated by the foresters or other trained personnel. The development of forest damage can be traced through repeated assessments of the same trees.

Loss of needles or leaves should be assessed after sprouting in spring or early summer and before broadleaves and larch display autumn coloration, at best in July and August. Evergreen conifers ( fig. 11 - 18 ) may also be assessed in their winter state as long as they are free of snow. Assessments should be made under good light conditions in good weather: rain and fog render assessments inaccurate. Leaf or needle loss is estimated for the entire crown.

The crown is considered to reach from the peak of the tree to, the lowest strong green branch forming part of the crown as such; epicormic shoots on the stem are not considered, while those in the crown are.

Figure 11-14.

Defoliation in % of Oak crowns [ 27 ].

Figure 15-18.

Defoliation in % of Beech crowns [ 27 ]

A forest tree can spread its crown to a greater or lesser extent depending on the room available within the stand. Consequently, spatial conditions must be considered in crown assessment; that is, the maximum foliage that each tree could possibly produce must be taken as a basis. The photo series ( fig. 19 - 26 ) depicts trees of the upper storey with well developed crowns enjoying optimum light conditions. It is therefore applicable to trees of the middle and lower strata only to a limited extent. Foliage loss may be determined by comparing the tree under consideration with the corresponding photo series. The appearance of the crown is matched with one of the photos and the foliage loss estimated to a degree of 5 percent accuracy. Assessments should be made with field-glasses from a distance of at least one tree-length. Field-glasses permit precise identification of bare branches and twigs and discoloration. In subsequent surveys it is important that the tree always be observed from the same side; this should either be marked on the tree itself or noted in terms of compass direction. Leaf or needle loss due to known causes, e.g., hail, lightning, whipping, insect attack, etc., should not be included but separately inventoried [ 27 ].

14. Political background and objectives of ICP forests

The objectives and the strategy of ICP Forests are based on the draft long-term strategy and the work plan for the effects-oriented activities of the Working Group on Effects (WGE) of

Figure 19-22.

Figure 23-26.

Defoliation in % of Beech crowns [ 27 ].

CLRTAP (Convention on Long-range Transboundary Air Pollution). The draft long-term strategy of WGE specifies the following long-term aims to which all ICP are expected to contribute:

Assessment of knowledge on

The present status, long-term trends and dynamics, and the degree and geographical extent of the impact of air pollution, particularly, but not exclusively, its long range trans-boundary impact

Exposure-response relationships for agreed air pollutants;

Critical loads, levels and limits for agreed air pollutants;

Interactive effects of air pollution and climate change on forest ecosystems

Moreover, the long-term strategy of WGE specifies the following long-term priorities of special relevance to ICP Forests:

Derivation of exposure-response functions for chemical and biological effects of air pollutants including investigation of nutrient nitrogen, acidifying compounds and ozone effects on ecosystem functions and on biodiversity, including combinations with other stresses (e.g. climate change and land use practices);

Further development of models and mapping procedures, particularly for effects of nitrogen and ozone on the environment and for the description of dynamic processes of damage and recovery (acidification, eutrophication, heavy metal accumulation) by including to a larger extent biological effects;

Evaluation of environmental benefits of air pollution control policies.

In order to meet the information needs of the Working Group on Effects of Atmospheric Pollution (WGE), ICP Forests pursues the following two main objectives:

Objective 1: A periodic overview on the spatial and temporal variation of forest condition in relation to anthropogenic and natural stress factors (in particular air pollution) by means of European-wide and national large-scale representative monitoring on a systematic network.

Objective 2: A better understanding of the cause-effect relationships between the condition of forest ecosystems and anthropogenic as well as natural stress factors (in particular air pollution) by means of intensive monitoring on a number of selected permanent observation plots spread over Europe and to study the development of important forest ecosystems in Europe.

These objectives imply in accordance with the long-term priorities of WGE contributions to calculations of critical loads and levels and the assessment of their exceedances. They imply also dynamic modeling of the response of forest ecosystems to deposition scenarios expected for the future. Additional insight is gained by compiling available studies from the National Focal Centers (NFCs) and from related programmes inside and outside of Convention on Long-range Trans-boundary Air Pollution.

15. Strategy of ICP forests

Monitoring activities

In order to meet its data generation and reporting obligations, ICP Forests employs data collection at two levels.

Large-scale monitoring (Level I) provides a periodic overview of the spatial and temporal variation in a range of attributes related to forest condition. Level I plots, national forest inventory (NFI) plots, and other related inventory plots may be combined when appropriate, feasible and necessary, according to defined and agreed procedures.

Intensive monitoring (Level II) is carried out on plots installed in important forest ecosystems.

These plots are dedicated to in-depth investigation of the interactive effects of anthropogenic and natural stress factors on the condition of forest ecosystems.

Quality assurance and control

All monitoring activities are harmonized by ICP Forests among the participating countries and are laid down in this Manual. This ensures a standard approach for data collection and evaluation and can form the nucleus for a future common European forest monitoring programme. A consistent quality assurance approach is applied within the programme covering the set up of methods, data collection, submission and investigation as well as reporting. Quality assurance and control is supervised by the Programme Coordinating Group through its Quality Assurance Committee. A set of Expert Panels cares for data quality assurance within the specific surveys and for the further development of monitoring methods and standards. This includes field checks, inter-calibration courses, laboratory ring tests, and data validation.

Data evaluation and reporting

A range of monitoring variables is required to meet the information requirements of Convention on Long-range Trans-boundary Air Pollution and other international institutions. The Programme Coordinating Group and the Expert Panels are responsible for a data evaluation and reporting approach which takes the medium term work-plan of Working Group on Effects of Atmospheric Pollution into account. International and national data from other programmes and institutions should be included in combined analysis. The main topics for data analysis are:

Forest condition

Effects on forest ecosystems from

Acidity and nitrogen

Contributions in the fields of

Climate change

Biodiversity

Trends in deposition and their interactive effects on the adaptation and vulnerability of forest ecosystems are evaluated. This includes spatial and temporal changes and cause-effect relationships with special emphasis on critical loads and their exceedances. Dynamic models and transfer functions derived from suitably selected intensive monitoring plots are used to investigate the effects of climatic factors and greenhouse gases on forest ecosystems and applied to the large scale monitoring plots. These models are validated against measured data collected at the plots. Furthermore, data gathered at the plots are used in an integrated manner to investigate the carbon sequestration potential of forests, ozone fluxes to forests and contribute to assess status and trends of forest biodiversity at the pan-European level.

The integrative monitoring approach of ICP Forests using the Level I and Level II networks provides robust data on the health and stability of forests. This facilitates an understanding of the effects of deposition on the role and functioning of forest ecosystems in protecting soils and water. Furthermore the programme surveys can contribute to the understanding and forecast of climate change effects on forests and can be used to supply information on the sequestration of carbon and are going to provide information on forest biodiversity as an integral part of forest ecosystems. Results are published via reports and a website ( http://www.icp-forests.org ).

ICP Forests aims to provide periodic overviews on the spatial and temporal variation of forest condition in relation to man-made and natural stress factors (particularly air pollution); to contribute to a better understanding of the cause-effect relationships between the condition of forest ecosystems and man-made and natural stress factors (particularly air pollution); and to study the development of important forest ecosystems in Europe.

More specifically, to support harmonized forest monitoring by linking existing and new monitoring mechanisms at the national, regional and EU level ( tab. 2) ; to collect quantitative and qualitative forest data related to climate change, air pollution, biodiversity, and forest condition; and to contribute information on sustainable forest management to the Ministerial Conference on the Protection of Forests in Europe.

Surveys and number of plots for Level II monitoring. The variation in assessment frequency results in different numbers of plots with data submission for the different surveys (after http://www.icp-forests.org )

Conclusions after 25 years of forest monitoring at European level

For 25 years, forest condition has been monitored by ICP Forests in close cooperation with the European Commission. The system combines an inventory approach with intensive monitoring. It provides reliable and representative data on forest ecosystem health and vitality and helps to detect responses of forest ecosystems to the changing environment. The data collected so far provide a major input for several international programmes and initiatives, such as the Convention on Long-range Trans-boundary Air Pollution and the Ministerial Conference for the Protection of Forests in Europe.

Forest surveys and defoliation classes for all tree species in European countries (2009). Results of national surveys as submitted by National Focal Centres (after www.icp-forests.org)

In the early 1980s, a dramatic deterioration in forest condition was observed in Europe and this initiated the implementation of forest condition monitoring under Convention on Long-range Trans-boundary Air Pollution. Today, the monitoring results indicate that, at the large scale, forest condition has deteriorated far less severely than was feared at that time. Stress factors like insects, fungi and weather effects have been shown to affect tree health. The drought in the Mediterranean region in the mid-1990s and the extremely warm and dry summer across large parts of Europe in 2003 led to increased levels of defoliation as a natural reaction of trees to this type of stress. The programme has also reported on acidifying deposition which is regionally correlated with defoliation and on atmospheric inputs that are accentuating other stress factors. In the past three years there has been little change in the mean levels of defoliation for the main European tree species. However, long-term trends show more deterioration than improvement ( tab. 3) .

The health status of forest trees in Europe is monitored over large areas by surveys of tree crown condition. Trees that are fully foliated are regarded as healthy. The Ministerial Conference on the Protection of Forests in Europe uses defoliation as one of four indicators for forest health and vitality.

In 2009, crown condition data were submitted for 7193 plots in 30 countries. In total, 136 778 trees were assessed. This constitutes the programmer’s largest number of plots for which annual data were submitted.

In 2009, 20.2 % of all trees assessed had a needle or leaf loss of more than 25 % and were thus classified as either damaged or dead ( fig. 27 ). This represents no change relative to 2008.

Of the main tree species, European and sessile oak had the highest levels of damaged and dead trees, at 31.8 %.

There were no significant changes in crown condition over the past ten years on two-thirds of the plots, but deterioration prevailed on the remaining third.

In 2009, a fifth of the 136 778 trees studied were considered damaged or dead

Trends vary between species, with European and sessile oak the most frequently damaged species. However, both have shown some recovery over the past five years. The health of Norway spruce and Scots pine has improved over the past 18 years. Defoliation in common beech, Holm oak and maritime pine has increased.

There has been no significant change in tree health on most plots monitored over the past ten years. Defoliation increased on 24.4 % of plots monitored and decreased, indicating an improvement in crown condition, on only 14.9 % ( fig. 28 ).

Over the past 18 years there has been a clear improvement in crown condition for Scots pine and a slight improvement for Norway spruce. European and sessile oak have shown the highest mean defoliation over the past decade.

Defoliation peaked after the extremely dry and warm summer in 2003 and has been slowly recovering since 2007. Defoliation of common beech peaked in 2004, while Holm oak showed a sharp deterioration in crown condition in the mid-1990s and again in 2005. Unfavorable weather conditions are thought to be responsible for these trends. There was a reasonably consistent increase in defoliation of maritime pine up to 2005, followed by a short period of recovery after which crown condition again deteriorated in 2009 [ 28 ], [ 29 ], [ 30 ].

Extent of defoliation for the main European tree species. Total Europe and EU, 2009. (after http://www.icpforests.org )

Mean percentage defoliation for the most frequent tree species in European forests (after http://www.icpforests.org )

Defoliation is an indicator of tree health and vitality that can be easily monitored over large areas and which reacts to many different factors, including climatic conditions and weather extremes as well as insect and fungal infestations.

Defoliation represents a valuable early warning system for the response of the forest ecosystems to change – this is particularly relevant as climatic extremes are predicted to occur more frequently in the relatively near future.

Deposition of pollutants from the air can affect soil and site conditions and thus the condition of forest trees.

The status and trends in forest condition vary regionally and for different species. Local conditions may differ from the European average.

Conclusions concerning the dynamic of atmospheric deposition

ICP Forests began deposition measurements on intensive (Level II) monitoring plots in the latter half of the 1990s. Measurements are carried out within the forest stands (through fall deposition) and in nearby open fields (bulk deposition). In the forest canopy, some elements can be leached from the foliage and increase the measured deposition load, whereas others are taken up by leaves and needles and are so not detected in through fall. Bulk deposition is mostly lower than through fall deposition because of the additional deposition loads filtered from the air by the forest canopy. Thus, neither through fall deposition nor bulk deposition is equal to the total deposition received by the forest stands. However, through fall deposition is presented here as this reflects the inputs reaching the forest floor and so these measurements are of greater ecological relevance to forest ecosystems than open field measurements. On the plots, samples are collected weekly, fortnightly or monthly and are analyzed by national experts.

After intensive quality checks, annual mean deposition for the years 1998 to 2007 was calculated for plots with complete data sets. Slopes of plot wise linear regressions of deposition over time were tested for significance. Plot-specific means were calculated for the period 2005 to 2007.

The most relevant trends cam is formulated as follows:

Mean annual sulphur inputs decreased by 30 % between 1998 and 2007, with significant reductions measured on half of the plots. These findings are based on deposition measurements made under the forest canopy on 157 plots located mostly in central Europe. Mean nitrogen inputs showed little change or only a very small decrease.

The downward trend in sulphur deposition reflects the success of the clean air policies under the UNECE and the EU for sulphur emissions. In contrast, the nitrogen deposition data indicate a clear need for further reductions in nitrogen emissions.

Deposition is generally higher on central European plots than on plots in northern and southern Europe.

On average, through fall deposition in forests is higher than deposition on open field sites because trees filter dust and other dry deposition from the air which is then washed from the foliage to the forest floor by rain. Between 1998 and 2007, sulphate deposition on the open field sites fell by 26 %; from 6.1 to 4.5 kg per hectare per year.

The decrease in sulphate through fall deposition (measured below the forest canopy) was higher at 34 %; from 10.0 to 6.6 kg per hectare per year ( fig. 29 ).

About half the plots showed a significant reduction in sulphur inputs over the 10-year study period. The data are mean values from around 150 measurement stations located mainly in central Europe.

Mean nitrogen deposition within the forest stands fluctuated (for nitrogen measured as nitrate and ammonium) and few plots showed significant changes in through fall deposition.

Slight decreases in mean nitrogen deposition at the open field plots were observed ( fig. 30 ). The deposition data show the success of the clean air policies in Europe for sulphur emissions, and show the need for further reductions in nitrogen emissions [ 31 ], [ 32 ], [ 33 ].

Development of mean deposition of sulphate from 1998 to 2007. The forest canopy alters pollutants from the air. Inputs within the forest stands are higher than in the open field. In 2003 there was less precipitation and thus less deposition. (after http://www.icpforests.org )

Development of mean plot deposition of nitrogen compounds plots) from 1998 to 2007. Some reduction are visible in open field measurements. There was little change in deposition for the forest stands over the10 years of observation. (after http://www.icpforests.org )

Atmospheric deposition has been the specific focus of the programme since its inception. Current evaluations show decreasing sulphur inputs on about 50% of around 150 intensive monitoring plots since 1998, which is a result of clean air policies under the LRTAP Convention and EU legislation. However, critical limits in the soil water are still substantially exceeded on a quarter of the plots and indicate a potential threat to forest vegetation. Earlier studies conducted under the programme have shown that the risk of storm damage is higher on acidic soils. Nitrogen inputs have hardly changed over the past ten years and the data sets now show shifts in the composition of forest ground vegetation towards more nitrogen tolerant species. Atmospheric deposition is a driver for these changes in biodiversity. Another effect of nitrogen deposition is increased tree growth which was found on intensive monitoring plots across Europe [ 34 ].

© 2011 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike-3.0 License , which permits use, distribution and reproduction for non-commercial purposes, provided the original is properly cited and derivative works building on this content are distributed under the same license.

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Air pollution induced changes in the photosynthetic pigments of selected plant species

Affiliation.

• 1 Department of Zoology and Environmental Sciences, Gurukul Kangri University, Haridwar, India. [email protected]
• PMID: 20121034

Changes in the concentration of different photosynthetic pigments (Chlorophyll and carotenoids) were determined in the leaves of six tree species exposed to air pollution due to vehicular emissions. The six tree species, which are all economically important because of their being fruit bearers, used for timber fodder and as road side trees on the basis of their air pollution tolerance index. These included Mangifera indica L., Tectona grandis Linn.f , Shorea robusta Gaertn.f., Holoptelea integrifolia (Roxb.) Planch, Eucalyptus citridora Hook. Syn. and Mallotus philippinensis Muell-Arg. Reduction in chlorophyll 'a', 'b' and carotenoid was recorded in the leaf samples collected from polluted areas when compared with samples from control areas. The highest reduction in total chlorophyll was observed in Holoptelea integrifolia (Roxb.) (48.73%) Planch whereas, the lowest reduction (17.84 %) was recorded in Mallotus philippinensis Muell-Arg. Similarly in case of carotenoid contents, highest reduction (43.02%) was observed in Eucalyptus citridora, and lowest in Mallotus philippinensis Muell-Arg (19.31%). The data obtained were further analyzed using one-way ANOVA and a significant change was recorded in the studied parameters. These studies clearly indicate that the vehicular induced air pollution reduces the concentration of photosynthetic pigments in the trees exposed to road side pollution.

Publication types

• Research Support, Non-U.S. Gov't
• Air Pollutants / toxicity*
• Photosynthesis*
• Pigments, Biological / metabolism*
• Plants / drug effects*
• Plants / metabolism
• Species Specificity
• Air Pollutants
• Pigments, Biological

• Environmental Topics
• Laws & Regulations

Science Inventory

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PLANT RESPONSE TO AIR POLLUTION

Weber, J., D. Tingey, AND C. Andersen. PLANT RESPONSE TO AIR POLLUTION. U.S. Environmental Protection Agency, Washington, DC, EPA/600/A-93/050 (NTIS PB93167260).

Impact/Purpose:

Description:.

Air pollutants have a negative impact on plant growth, primarily through interfering with resource accumulation. Once leaves are in close contact with the atmosphere, many air pollutants, such as O3 and NOx, affect the metabolic function of the leaves and interfere with net carbon fixation by the plant canopy. Air pollutants that are first deposited on the soil, such as heavy metals, first affect the functioning of roots and interfere with soil resource capture by the plant. These reductions in resource capture (production of carbohydrate through photosynthesis, mineral nutrient uptake and water uptake from the soil) will affect plant growth through changes in resource allocation to the various plant structures. When air pollution stress co-occurs with other stresses, e.g. water stress, the outcome on growth will depend on a complex interaction of processes within the plant. At the ecosystem level, air pollution can shift the competitive balance among the species present and may lead to changes in the composition of the plant community. In agroecosystems, these changes may be manifest in reduced economic yield.

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Air Pollution and Climate Change: Their Impact Today and in the Future

• Environment
• Global Warming
• Sustainable
• Climate Change

While the concern with air pollution may seem relatively novel to some people, it’s been considered a threat to human health since about 400 BCE . But as industrialization took hold worldwide, pollution levels soared, resulting in many health issues for humans, animals, and plants.  

In recent decades, humans have become more aware of air pollution and climate change and have tried to slow and even reverse both. While we’ve made strides in these efforts, we still need to do more work to help preserve our world.  

Below, we look at air pollution and climate change to see just how they’re correlated as well as pollution’s impact on humans, plants, and animals.  

How Does Air Pollution Affect Our Climate?

Air pollutants have a broad-reaching impact on our climate, but it’s not always the same impact. Some can make the climate warmer, while others can make it cooler, according to the Environmental Protection Agency ( EPA ) . This can lead to some confusion. Let’s review how the various pollutants impact the climate and what larger-scale effect this can have on the world.  

Pollutants Can Cause the Climate to Warm

Most people hear about how air pollutants can cause global warming, which means they cause the global temperature to rise, leading to warmer climates worldwide. Greenhouse gases (GHGs), such as carbon dioxide or nitrogen oxide, are among the pollutants responsible for this warming effect.  

GHGs naturally occur in the Earth’s atmosphere and help regulate the temperature so our planet is habitable. However, since the early 1900s , the GHG levels in the atmosphere have steadily risen due to fossil fuel burning in automobiles, factories, power plants, agriculture, and more. Wildfire smoke also contributes to GHG emission levels.  

These GHGs are causing warming in the Arctic regions , and when you warm these regions too much, the abundant snow and ice there can melt in the spring and summer months. This not only drastically changes the ecosystems in the Arctic regions but also can dramatically change the Earth’s surface and lead to even more warming.  

The burning of fossil fuels also releases fine particulate matter into the atmosphere, known as aerosols . While aerosols all act differently and have varying effects on the global climate, one form of particle pollution known as black carbon or soot absorbs the sun’s heat and warms the atmosphere.  

Pollutants Can Cause the Climate to Cool

As mentioned above, aerosols don’t all act the same, and some actually cool the Earth’s surface by reflecting the sun’s rays. They also aid in cloud production, so the more aerosols in the atmosphere, the higher the potential for cloudy, sunlight-blocking skies. This can result in an overall cooling effect.  

These aerosols occur naturally in the atmosphere due to volcano eruptions, sea spray, and other events, but they also come from fossil fuel emissions .  

It’s easy to assume that the cooling effect of aerosols could offset the warming effect of GHGs, but that’s not the case. The fact is, GHGs can remain in the atmosphere far longer than aerosols can, meaning their warming effect is longer-lasting, resulting in a net increase in global temperatures.  

Simulations and models show these fine particles cause about half as much cooling as GHGs cause warming.  

Does Air Pollution Worsen Climate Change?

Yes, high air pollution levels worsen our changing climate — specifically, excessive greenhouse gas emissions into the atmosphere from human activities, such as cars, factories, power plants, and more. These GHGs remain in high concentrations in the atmosphere for decades or even centuries, steadily increasing the amount of heat retained on the Earth’s surface.  

As we continue emitting these GHGs, the impact of air pollution can be even higher global temperatures and more snow and ice melting in the Arctic regions. This can lead to a wide range of worldwide issues that we’ll cover below.  

What Are the Main Effects of Air Pollution on Humans?

Air pollution has many effects on top of the impacts of climate change that we all witness today. Let’s review the main effects of air pollutants on humans.  

Health Impact

Outdoor air pollution , such as smog or ground-level ozone , has various long- and short-term negative health effects on humans. Sensitive groups — such as children, the elderly, and those with existing illnesses — are particularly susceptible to these health risks.  

Short-term exposure to poor air quality , especially in crowded cities like New York or San Francisco , can result in mild symptoms , including:   

• Eye, nose and throat irritation  
• Headaches  
• Dizziness  

While these can go away on their own by getting into an area with clean air , the long-term impacts are far more serious. These long-term public health impacts include:   

• Respiratory diseases like asthma or COPD  
• Cardiovascular harm  
• H eart attacks  
• Harm to the liver, spleen, and blood  
• Damage to the nervous system  
• Lung cancer and other cancers  
• Birth defects  
• Premature death  

Food Production Impact

Air pollution can also impact food production and lead to scarcity of certain staple foods. Among the most sensitive crops to ground-level ozone are soybeans, wheat, potatoes, rice, and corn . A study showed ozone created an estimated 6% to 16% decrease in soy, a 7% to 12% decrease in wheat, and a 3% to 5% decrease in corn.  

On a grander scale, this could eventually result in food shortages and leave many people in the world struggling to find sufficient food. With acute food insecurity affecting 135 million to 345 million people worldwide and 49 million people being near famine, this is not something the world can afford to ignore.  

What Are the Main Effects of Air Pollution on the Environment?

Air pollution and climate change ’s potential impact on humans is alarming, but there is also significant environmental risk associated with air pollution — ranging from harm to wildlife to extreme weather conditions, such as flooding and powerful hurricanes. Let’s explore these environmental risks.  

Harms Animals and Plant Life

Like humans, plants and animals can experience severe harm from air pollution and climate change .  

Animals can experience many of the same physical ailments as humans when exposed to harmful air pollution like smog , soot, and other particles. Similarly, when enduring short-term exposure, their symptoms can include:   

Long-term exposure can cause lung disease and cardiovascular damage and disease, harm to internal organs, and cancer — just like in humans.  

Plants also suffer from excessive air pollution , as long-term exposure to airborne toxins can lead to reduced growth. Ozone pollution damages plants’ stomata, which are what allow the plants to essentially breathe the air around them.   

Air pollution can also lead to reduced sunlight from the smog and heavy cloud coverage, preventing plants from performing photosynthesis and further reducing their ability to grow.  

Air pollution can also lead to toxins in the soil, such as nitrogen dioxide , gaseous ammonia, and lead, robbing the plants of the nutrients they need. Plus, all these toxins in the soil can run off into the lakes, streams, and other bodies of water and seriously affect fish and other marine animals.  

On top of all this, air pollution can negatively impact plant and animal populations, thereby limiting the natural food supplies in the food chain. This can cause worldwide food shortages for animals, leading to lower populations across the entire food chain.  

Creates Acid Rain

When you burn fossil fuels , sulfur dioxide and nitrogen oxides are emitted into the atmosphere. When these two mix with the water droplets in the air, they can create extreme weather known as acid rain, which is a mixture of sulfuric and nitric acid. The wind can then carry these acid-rain-filled clouds thousands of miles and dump it on the Earth below.  

Acid rain impacts vegetation by damaging it physically and increases the acidity in the water and soil in the area.  

On top of damaging plant life, acid rain is also associated with over 500 deaths annually and can dissolve buildings and other structures, causing upward of $5 billion in damage annually.  

Harms the Ozone Layer

While the hole in the ozone layer is showing signs of shrinking , it remains a key symptom of air pollution , specifically refrigerants, such as chlorofluorocarbons (CFCs). CFCs contain chlorine atoms that can destroy ozone atoms. In fact, one chlorine atom can destroy thousands of ozone molecules.  

The ozone layer blocks the sun’s harmful ultraviolet-B (UVB) radiation. A hole in this layer puts all life on Earth at risk by increasing risk of skin cancer in humans and animals, restricting plant growth, and slowing fish and amphibian growth.  

Creates Extreme Weather Conditions

The hole in the ozone layer and GHG emissions retaining more heat at the Earth’s surface also can result in extreme weather conditions. These can include drought, catastrophic storms, extreme heat, and extreme cold. All these conditions can lead to various related issues , such as wildfires , water scarcity, rising sea levels, flooding, and more.  

Where Will We Be in 20 to 30 Years?

If we can manage to continue reducing our carbon emissions , experts predict the global temperature will rise 1.5 to 2 degrees Celsius by 2050 . This seems low, but keep in mind this is the average. In the sensitive Arctic regions, the temperature will increase by an estimated 5.5 to 8 degrees Celsius, which is far more dramatic and can lead to accelerated melting of snow and ice.  

In turn, that will result in increased solar radiation absorption as well as severe ocean conditions and 37% more heatwaves.  

Even if we successfully reduce GHG emissions and other air pollution , things will continue to worsen through 2050. That’s the sad truth. We’ll continue seeing more droughts and wildfires , more flooding and extreme weather, more ice cap melting, and rising sea levels.  

While that may sound like a gloomy future, the power is still in our hands to slow this change and start the road back to recovery.  

Air Pollution and Climate Change Go Hand in Hand

Air pollution generally includes various GHG emissions and aerosols that can impact the ozone layer and the ability for the atmosphere to regulate the global temperature. This leads directly to climate change , meaning air pollution and climate change are correlated. If we focus on air pollution mitigation, we can help fight climate change and keep our planet habitable for generations.  

Everyone can do their part, from switching to alternative fuel cars or public transportation to focusing on renewable energy that pulls us away from fossil fuels. We can also further help by funding initiatives that help lower GHG emissions through carbon offsets. These carbon credits fund carbon reduction or carbon sequestering — those focusing on absorbing carbon, such as planting trees — programs and offset your carbon footprint.    

Check out the carbon removal products Terrapass offers for both individuals and businesses .   

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Human Actions and the Atmosphere

Effects of air pollution, lesson objectives.

• Describe the damage that is being done by smog.
• Discuss how acid rain is formed and the damage it does.
• Discuss how chlorofluorocarbons destroy the ozone layer.
• bioaccumulation
• polar stratospheric clouds (PSC)

Introduction

People in developing countries often do not have laws to protect the air that they breathe. The World Health Organization estimates that 22 million people die each year from complications caused by air pollution. Even in the United States, more than 120 million Americans live in areas where the air is considered unhealthy. This lesson looks at the human health and environmental problems caused by different types of air pollution.

Smog Effects on the Environment

All air pollutants cause some damage to living creatures and the environment. Different types of pollutants cause different types of harm.

Particulates

Particulates reduce visibility. In the western United States, people can now ordinarily see only about 100 to 150 kilometers (60 to 90 miles), which is one-half to two-thirds the natural (pre-pollution) range on a clear day. In the East, people can only see about 40 to 60 kilometers (25-35 miles), about one-fifth the distance they could see without any air pollution ( Figure below ).

This NASA video discusses the ingredients of ozone depletion of Antarctica and the future of the ozone hole, including the effect of climate change (8c) : http://www.youtube.com/watch?v=qUfVMogIdr8 (2:20).

Effects of Ozone Loss

Ozone losses on human health and environment include:

• Increases in sunburns, cataracts (clouding of the lens of the eye), and skin cancers. A loss of ozone of only 1% is estimated to increase skin cancer cases by 5% to 6%.
• Decreases in the human immune system’s ability to fight off infectious diseases.
• Reduction in crop yields because many plants are sensitive to ultraviolet light.
• Decreases in phytoplankton productivity. A decrease of 6% to 12% has been measured around Antarctica, which may be at least partly related to the ozone hole. The effects of excess UV on other organisms is not known.
• Whales in the Gulf of California have been found to have sunburn cells in their lowest skin layers, indicating very severe sunburns. The problem is greatest with light colored species or species that spend more time near the sea surface.

When the problem with ozone depletion was recognized, world leaders took action. CFCs were banned in spray cans in some nations in 1978. The greatest production of CFCs was in 1986, but it has declined since then. This will be discussed more in the next lesson.

Lesson Summary

• Air pollutants damage human health and the environment. Particulates reduce visibility, alter the weather, and cause lung problems such as asthma attacks.
• Ozone damages plants and can also cause lung disease. Acid rain damages forests, crops, buildings, and statues.
• The ozone hole, caused by ozone-destroying chemicals, allows more UV radiation to strike the Earth.
• UV radiation can cause plankton populations to decline and skin cancers in humans to increase, along with other effects.

Review Questions

1. Why is visibility so reduced in the United States?

2. Why do health recommendations suggest that people limit the amount of tuna they eat?

3. Why might ozone pollution or acid rain change an entire ecosystem?

4. Why does air pollution cause problems in developing nations more than in developed ones?

5. Why are children more vulnerable to the effects of air pollutants than adults?

6. Describe bioaccumulation.

7. How does pollution indirectly kill or harm plants?

8. What do you think the effect is of jet airplanes on global warming?

9. Why is air pollution a local, regional, and global problem?

10. How do CFCs deplete the ozone layer?

Points to Consider

• Since mercury bioaccumulates and coal-fired power plants continue to emit mercury into the atmosphere, what will be the consequence for people who like to eat tuna and other large predatory fish?
• What are the possible causes of rising asthma rates in children?
• A ban has been imposed on CFCs and some other ozone-depleting substances. How will the ozone hole change in response to this ban?
• Earth Science for High School. Provided by : CK-12. Located at : http://www.ck12.org/book/CK-12-Earth-Science-For-High-School/ . License : CC BY-NC: Attribution-NonCommercial

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Air pollution, metabolites and respiratory health across the life-course

Olena gruzieva.

1 Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

2 Centre for Occupational and Environmental Medicine, Region Stockholm, Stockholm, Sweden

16 Both authors contributed equally to this article

Ayoung Jeong

3 Swiss Tropical and Public Health Institute, Basel, Switzerland

4 University of Basel, Basel, Switzerland

Jeroen de Bont

Maria g.m. pinho.

5 Dept of Epidemiology and Data Science, Amsterdam Public Health, Amsterdam UMC, location VUmc, Amsterdam, The Netherlands

Ikenna C. Eze

6 IUF-Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany

Craig E. Wheelock

7 Unit of Integrative Metabolomics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

8 Dept of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Sweden

9 Gunma University Initiative for Advanced Research (GIAR), Gunma University, Maebashi, Japan

Annette Peters

10 Institute of Epidemiology, Helmholz Zentrum München – German Research Center for Environmental Health, Neuherberg, Germany

Jelle Vlaanderen

11 Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands

Kees de Hoogh

Augustin scalbert.

12 Nutrition and Metabolism Branch, International Agency for Research on Cancer (IARC/WHO), Lyon, France

Marc Chadeau-Hyam

13 Imperial College London, London, UK

Roel C.H. Vermeulen

Ulrike gehring.

17 These authors contributed equally to this article

Nicole Probst-Hensch

Erik melén.

14 Dept of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden

15 Sachs Children's Hospital, Stockholm, Sweden

Associated Data

Please note: supplementary material is not edited by the Editorial Office, and is uploaded as it has been supplied by the author.

Table S1 ERR-0038-2022.SUPPLEMENT1

Table S2 ERR-0038-2022.SUPPLEMENT2

Previous studies have explored the relationships of air pollution and metabolic profiles with lung function. However, the metabolites linking air pollution and lung function and the associated mechanisms have not been reviewed from a life-course perspective. Here, we provide a narrative review summarising recent evidence on the associations of metabolic profiles with air pollution exposure and lung function in children and adults. Twenty-six studies identified through a systematic PubMed search were included with 10 studies analysing air pollution-related metabolic profiles and 16 studies analysing lung function-related metabolic profiles. A wide range of metabolites were associated with short- and long-term exposure, partly overlapping with those linked to lung function in the general population and with respiratory diseases such as asthma and COPD. The existing studies show that metabolomics offers the potential to identify biomarkers linked to both environmental exposures and respiratory outcomes, but many studies suffer from small sample sizes, cross-sectional designs, a preponderance on adult lung function, heterogeneity in exposure assessment, lack of confounding control and omics integration. The ongoing EXposome Powered tools for healthy living in urbAN Settings (EXPANSE) project aims to address some of these shortcomings by combining biospecimens from large European cohorts and harmonised air pollution exposure and exposome data.

Short abstract

Metabolomics offers the potential to identify biomarkers linked to both environmental exposures and respiratory health. Studies with prospectively collected biosamples and harmonised exposure assessment are needed for insights into mechanisms and causality. https://bit.ly/3MRF2iq

Introduction

The exposome concept encompasses measures of both external and internal exposures and is thought to reflect the sum of all nongenetic influences on health and disease [ 1 – 3 ]. Typically, the external exposome domains include factors related to ambient environmental exposures, such as air pollution; temperature; built, social and food environments; and behaviour-related and psychosocial factors, whereas the internal exposome refers to internalised exogenous exposures that comprise the fraction of dietary and nondietary environmental molecules that have entered the organism. The internal exposome also includes the gut microbiota and the associated metabolites, arising directly from the biotransformation of environmental and endogenous metabolites and endogenous metabolites reflecting responses to exposures ( e.g. lipid peroxidation products from oxidative stress) [ 3 ].

In recent years, it has been widely acknowledged that both environmental exposures and host characteristics influence respiratory health and disease in both children and adults [ 4 – 6 ]. However, little is known about the life-course perspective of exposure and disease, the critical windows of exposure, the early biomarkers of exposure and disease mechanisms, and disease progression and prognosis. Accordingly, causal inference regarding the health effects of single exposures or mixtures remains limited, in particular regarding chronic effects.

The life-course perspective is of particular relevance for lung function-related respiratory diseases. Lung function progresses over the life-course, going through growth, plateau and decline phases [ 7 ]. Timing and duration of the phases, and lung function levels at each phase, differ between individuals, shaping distinct lung function trajectories [ 8 ]. Genetic and environmental factors have been associated with these trajectories. Today, it is well accepted that lung function attained in the growth phase and maintained in the plateau phase affects respiratory (and cardiovascular) health in later life [ 8 , 9 ]. COPD incidence is attributed not only to accelerated decline in lung function in later life but also to impaired attainment of lung function in earlier life [ 10 , 11 ]. Early life exposures ( e.g. maternal smoking) and diseases such as childhood asthma can alter lung development, affecting the trajectories in the growth phase. Factors in later life, such as personal smoking and adult asthma, may affect lung function decline or aggravate the effects of early life exposures. The individual effects of environmental exposures on respiratory health may differ across the life-course, potentially with distinct aetiologies at susceptible time windows [ 12 – 14 ], thereby complicating the understanding of the causality of effects.

Identifying metabolic profiles in different phases of life may inform us about the distinctive aetiology in each phase. Untargeted metabolomics analysis has emerged as a potentially powerful approach to investigate the biological responses of exposure to environmental pollutants. The metabolome reflects the end products of genetic and endogenous processes in response to environmental exposures and, therefore, offers the potential to investigate the aetiology of diseases arising from exposome impact, and also reflects genetic susceptibility to exposures. Metabolites identified as intermediate biomarkers between environmental exposures and respiratory health in the context of prospective cohort studies with biomaterials obtained at multiple time points can strengthen causal interpretation, conceptualised as the meet-in-the-middle (MITM) approach; namely, starting with separate investigations of the metabolites or metabolic pathways that are associated with exposures and health outcomes, respectively, followed by the identification of the overlapping pathways [ 15 ].

In addition to tobacco smoking, long-term exposure to ambient air pollution is considered to be the top-ranking environmental risk factor for respiratory diseases; for example, COPD and asthma, cardiovascular diseases, premature mortality, and other noncommunicable diseases [ 16 – 18 ]. Following the new World Health Organization (WHO) Air Quality Guidelines 2021, an urgent call for global action has been announced by the European Respiratory Society (ERS) Environmental Health Committee [ 19 ]. A recent comprehensive overview of studies on air pollution and nontargeted metabolomics suggests that air pollution exposure is associated with metabolic pathways primarily related to oxidative stress, inflammation and steroid metabolism [ 20 ]. This is in line with findings from earlier air pollution research on candidate biomarkers [ 21 – 24 ] and from epigenome-wide association studies [ 25 – 27 ]. Yet, in recent years, the links between air pollution, metabolites as mediators, and respiratory diseases have not been reviewed from a life-course perspective. The present narrative review summarises current knowledge on the associations of metabolic profiles with air pollution exposure and respiratory health outcomes, taking different stages of life into consideration.

This work was undertaken within the framework of the EU-funded EXPANSE (EXposome Powered tools for healthy living in urbAN Settings) project on the urban exposome and cardiometabolic and pulmonary health across the life-course [ 28 ].

Air pollution-related metabolic profiles

A recently published review on air pollution and metabolomics by J in et al . [ 20 ] included articles published up until 9 June 2020. As many as 23 out of 315 identified studies were included, of which 13 focused on short-term air pollution exposure, two focused on sub-chronic ( i.e. multiple months) and eight on long-term effects ( i.e. ≥1 year). Two of these 23 studies investigated metabolic profiles in relation to both air pollution exposure and pulmonary function [ 29 , 30 ]. As this is a rapidly evolving field, we conducted complementary searches of articles published in PubMed ( https://pubmed.ncbi.nlm.nih.gov/ ) up to 30 September 2021 in the English language using the search terms “metabolomics” OR “metabolic profiling” AND “air pollution” (which were also included in the search by J in et al. [ 20 ]). This resulted in an additional 10 articles being included in this review ( figure 1 ). More details on the selected studies are provided in table S1 .

Flowchart of the selection of eligible metabolomics studies on air pollution and lung function or COPD related metabolic profiles. The PubMed literature search was performed following the search strategy by J in et al . [20], extending the search period up to 30 September 2021.

Lung function-related metabolic profiles

We searched for articles in PubMed published in the English language with the search term “metabolomics” OR “metabolomic profiling”, “lung function” OR “pulmonary function” OR “respiratory function” restricted to human studies only (performed on 30 September 2021). We first narrowed down the articles identified by the PubMed search criteria (n=101) by screening the titles and abstracts to assess eligibility. We supplemented the results of this search with three additional studies related to the topic that did not arise from the PubMed search but were cited in the articles identified by the search ( figure 1 ). We did not search separately for metabolic profiles associated with COPD or asthma per se , since these topics were recently presented in separate reviews [ 31 – 34 ] and our focus of interest for this review was lung function, and not clinical respiratory disease. Because cystic fibrosis (CF) is a monogenic disease with very different underlying pathophysiology, compared with other respiratory diseases such as asthma and COPD, we chose to exclude the CF papers from this review. Articles were excluded if they did not contain original research ( i.e. reviews, n=12), did not report quantitative data on associations of metabolites with lung function parameters (n=68), or employed targeted metabolomics analysis (n=6), resulting in a total of 16 original articles included in the present review. None of these 16 studies investigated metabolites or metabolic pathways related to both air pollution exposures and lung function. More details on selected studies are provided in table S2 . Figure 2 is a word cloud of the weighted list of the words extracted from the abstracts of all articles included.

The word cloud of the weighted list of the words extracted from the abstracts of included articles. This word cloud mainly highlights the clinical outcomes “asthma”, “COPD” and “lung function” and general exposure terms such as “air pollution”. Apart from the broad term “pathway”, few specific metabolomic pathways are highlighted, which is likely to be because of the issues with the studies included, such as small sample size, cross-sectional design, heterogeneity in exposure assessment, lack of confounding control and omics integration.

Life-course perspective in the exposome research of respiratory health

Here, we relied mostly on our experience and judgement, supported by selected references. In addition, we searched for articles in PubMed with the search term “lung function trajectories” AND (“metabolomics” OR “metabolomics profiling”), restricted to the English language and human studies (performed on 30 September 2021).

Air pollution exposure and metabolic profiles

Previous review.

A recent literature review by J in et al . [ 20 ] reported a wide range of metabolites linked to air pollution exposure, the majority of which were endogenous ( i.e. lipids, amino acids, steroids, nucleotides, carbohydrates and vitamins). Several of the included studies also found xenobiotics, such as polycyclic aromatic hydrocarbon metabolites; for example, catechol, 3-(2-hydroxyphenyl) propanoate, naphthylamine, nicotine metabolites and benzoate. Pathway analyses identified that most detected metabolites were related to oxidative stress or inflammatory responses. Metabolites with pro-inflammatory effects ( e.g. leukotrienes) generally tended to be upregulated, while anti-inflammatory metabolites ( e.g. histidine, linolenic acid) appeared to be downregulated following air pollution exposure. Furthermore, differential perturbations of air pollution-related metabolites and pathways by asthma status [ 35 ], age [ 36 ] and sex [ 37 , 38 ] have been detected, providing evidence on mechanisms for susceptible subpopulations. Of note, the vast majority of studies included in the review by J in et al . [ 20 ] were based on adults aged 18 or older, while only two studies focused on children.

New studies

Studies on short-term air pollution exposure.

In a series of newly published studies employing plasma untargeted metabolomics in elderly males from the US Normative Aging Study (NAS), the authors identified 19 metabolites that were significantly associated with short-term exposure to nitrogen dioxide (NO 2 ), mainly lipids ( e.g. dihomolinoleoylcarnitine (C20:2), palmitoloelycholine, oleoylcholine, 8-hydroxyoctanoate, linolenate, phosphoethanolamine and choline phosphate), and hypotaurine, maltotriose and 3-phosphoglycerate [ 39 ]. In the pathway analysis, short-term exposure to NO 2 was associated with sphingolipid and butanoate metabolism. In a subsequent study looking at the relative contribution of the different PM 2.5 species (particulate matter with a diameter of 2.5 µm or smaller), the authors revealed 12 metabolic pathways that were significantly associated with short-term exposure to ultrafine particles and PM 2.5 elemental composition (nickel, vanadium, potassium, silicon and lead), including glycerophospholipid, sphingolipid, glutathione, β-alanine, pyrimidine, propanoate, purine, arginine and butanoate metabolism [ 40 ]. Another US study of 180 adults from an Emory University-based employee cohort identified several thousands of metabolic features significantly associated with traffic-related air pollutants. Further, the authors reported 21 biological pathways enriched by metabolic features linked to short-term air pollution exposure, including nucleic acids damage and repair (pyrimidine and purine metabolism), nutrient metabolism ( e.g. fatty acid β-oxidation, tryptophan and vitamin A metabolism) and acute inflammation ( e.g. histidine, tyrosine, alanine and aspartate metabolism) [ 41 ]. Higher levels of exposure to PM 2.5 , black carbon (BC) and SO 2 in healthy adults living in Beijing, China, were also related to reductions in plasma levels of alanine, threonine and glutamic acid [ 42 ]. The authors also identified several metabolic pathways affected by high levels of air pollution, most of them involved in amino acid metabolism. In the US prospective cohort of women undergoing assisted reproduction, the top identified metabolic pathways associated with short-term exposure to NO 2 , ozone, PM 2.5 and BC, comprised butanoate, β-alanine, tryptophan, linolenic acid, urea cycle/amino group and vitamin B3 metabolism [ 43 ]. Several studies based on personal exposure measurements reported a number of metabolites found to be significantly associated with traffic-related air pollution (TRAP) exposure, mainly involved in amino acid, glucose and fatty acid metabolism [ 44 ], and metabolites involved in haem, energy, oxidative stress, phospholipid and tryptophan metabolism related to PM 2.5 exposure levels [ 45 ]. In the latter study, sex-specific analysis revealed males to be more susceptible to PM 2.5 exposure than females. D u et al . [ 44 ] also reported novel pathways activated in response to air pollution, including growth hormone signalling, adrenomedullin signalling and arachidonic acid metabolism. Importantly, there is limited existing evidence on the short-term effects in children and, therefore, on life-course perspective.

Studies on long-term air pollution exposure

A study based on plasma untargeted metabolomic profiling of the NAS cohort of men revealed several metabolites perturbed by long-term exposure to PM 2.5 , belonging to glycerophospholipids, sphingolipids, glutathione, β-alanine, propanoate, purine, taurine and hypotaurine, and unsaturated fatty acids [ 46 ]. In addition, 18 pathways related to the elemental composition of long-term exposure to PM 2.5 (BC, nickel, vanadium, zinc, iron, copper, selenium), including glycerophospholipid, sphingolipid, purine and glutathione metabolism, were identified [ 40 ]. These pathways are involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair. In a Chinese prospective cohort study of college students, long-term exposure to PM 2.5 , but not particulate matter with a diameter of less than 10 µm (PM 10 ), was associated with 25 plasma metabolic markers, most of which were phospholipids [ 47 ]. Further, prenatal exposure to PM 2.5 , particularly during the third trimester of pregnancy, has been shown to influence the newborn metabolome, contributing to alterations of fatty acid, glycerophospholipid, methionine and cysteine metabolism [ 48 ]. Thus, for long-term exposure, the present studies cover a broad age range that suggest effects across the whole life-course.

Metabolomics and respiratory health

In the present review, we identified 16 studies of metabolic profiles in relation to lung function measures. Only two of the included studies were performed in children, while the remaining ones were predominantly conducted in adults with existing lung diseases such as COPD. Most of the studies performed metabolic profiling of blood samples (n=11), followed by urine (n=2), bronchoalveolar lavage fluid (BALF) (n=2) and exhaled breath (n=1). The studies are presented in the following sections stratified by paediatric, adult and population-based studies. Studies are not further stratified by short- and long-term associations, given the fact that many studies were cross-sectional case–control studies and given that acute impacts on physiology are in part thought to be at the heart of subsequent chronic changes ( i.e. disentangling short- and long-term effects is challenging).

Studies on paediatric patient cohorts (lung function in the presence of asthma)

In a cohort of Costa-Rican children with asthma (6–14 years, n=380), the researchers identified plasma metabolic profiles that distinguish children with and without asthma by their phenotypic aspects of lung function, i.e. the ratio of forced expiratory volume in 1 s (FEV 1 ) to forced vital capacity (FVC) (FEV 1 /FVC) and airway hyperresponsiveness (AHR) [ 49 ]. Pre- and post-bronchodilator FEV 1 /FVC were associated with 102 and 155 metabolites, respectively, with a large overlap (97 common metabolites). The majority of these were amines, a metabolite class consistently linked with asthma [ 50 ]. The metabolic profile for AHR (measured as a 20% decrement in FEV 1 after methacholine administration) included metabolites different from the FEV 1 /FVC-related ones, largely polar and nonpolar lipids. Further downstream, metabolite-set enrichment analysis revealed several significantly enriched pathways, namely glycerophospholipid, linoleic acid and pyrimidine metabolism. Two other pathways, sphingolipid metabolism and D-glutamine/glutamate metabolism, were exclusive for AHR, while pantothenate and CoA biosynthesis was enriched only among the FEV 1 /FVC post-bronchodilator (post-BD) metabolites. In subsequent integrated omics analyses, this research group interrogated blood transcriptomic and metabolomic data, and discovered associations of ORMDL3 and dysregulated sphingolipid metabolism with impaired lung function [ 51 ]. ORMDL3 is known to be one of the key genes associated with childhood asthma along with other genes at the chromosome 17q12–21 locus [ 52 , 53 ].

Of note, in all the abovementioned studies, biospecimens for metabolomics profiling were collected after asthma occurrence, thus limiting the opportunities to gain insights into disease aetiology from a clearly time-resolved longitudinal perspective.

Studies on adult patient cohorts (lung function in the presence of COPD and/or asthma)

In a US cohort of individuals with and without COPD, proton nuclear magnetic resonance ( 1 H NMR) spectroscopy-based metabolomics revealed three particular urinary metabolites that correlated with lung function (trigonelline, hippurate and formate), with trigonelline evidencing the strongest correlation with baseline FEV 1 measurements [ 54 ]. Hippurate and formate originate from production by the gut microbiome and dietary sources [ 55 ]. Therefore, the differential urine levels of these compounds might be indicative of the differences in microbiome composition or functionalities between individuals with different lung function. In the same study, no significant associations with lung function or lung function decline were observed for plasma metabolites.

By integrating plasma proteomic and metabolomic data from 1008 former and current smokers of the US COPD Gene study, M astej et al . [ 56 ] found a protein–metabolite network consisting of 13 proteins and seven metabolites that negatively correlated with FEV 1 % predicted. Troponin T, phosphocholine and ergothioneine metabolites demonstrated high connectivity ( i.e. number of edges linked to a metabolite node) and strong edges in the FEV 1 network, where edges represent associations between metabolite–protein pairs relative to FEV 1 . Further, enrichment analysis found metabolites in the diacylglycerol and branched-chain amino acids (leucine, isoleucine and valine) sub-pathways to be enriched for associations with FEV 1 /FVC [ 57 ]. For FEV 1 % pred, 79 metabolites, including lipid phosphocholine, ergothioneine and carbohydrate N6-carboxymethyllysine, were most significantly associated. By combining blood metabolomics and transcriptomics data within the same cohort, the authors identified glycerophospholipids, an important component of lung surfactant, along with the lipid classes lysophosphatidylethanolamine (LysoPE) and phosphatidylglycerol (PG) as highly significant in relation to FEV 1 % pred, and sphingolipids to be associated with FEV 1 /FVC [ 58 ].

Similarly, examination of the serum metabolome in a large UK cohort of women with lymphangioleiomyomatosis revealed a link between sphingolipid, fatty acid and phospholipid metabolites and FEV 1 [ 59 ]. H alper -S tromberg et al . [ 60 ] showed that the concentrations of lipid metabolites were negatively correlated with FEV 1 /FVC in BALF from patients with COPD.

In a US study, metabolic profiling of BALF in patients with COPD demonstrated a significant increase in peptides compared with healthy controls that was strongly associated with lung function [ 61 ]. The detected associations were strongest for lung function tests associated with airflow obstruction (FEV 1 and FEV 1 /FVC).

Several studies have examined metabolomics of lung function in the context of asthma-COPD overlap. They report significant positive correlations between lung function parameters ( i.e. FEV 1 and FEV 1 /FVC) and urinary L-histidine [ 62 ], serum valine, citrate and glutamate metabolites [ 63 ], serine, threonine, glucose, cholesterol, D-mannose and succinic acid [ 64 ], and fatty acid, propionate, isopropanol, lactate, acetone, valine, methanol and formate in exhaled breath condensate [ 65 ]. Of note, in the abovementioned studies, biosamples for metabolomics analysis have mostly been collected at the time of lung function measurements, whereas studies with prospectively assessed metabolic profiles are scarce.

Population-based studies on metabolic profiles and lung function

Metabolic profiling of fasting blood from 6055 individuals from the population-based UK twins study identified C-glycosyl tryptophan (C-glyTrp) to be strongly correlated with FEV 1 [ 66 ]. This finding was further replicated in the independent German KORA cohort (also cross-sectional). Further, by comparing metabolite levels of C-glyTrp with genome-wide DNA methylation profiles, the authors found three differentially methylated CpG sites, annotated to the WDR85, EDN2 and GLB1L3 genes, respectively, that have previously been implicated in human early development and age-related phenotypes, such as retinal degeneration, renal inflammation and hypertension.

By combining data from over 4700 individuals across two population-based studies, Y u et al . [ 67 ] identified 95 serum metabolites associated with FEV 1 and 100 with FVC (73 overlapping), including inverse associations with branched-chain amino acids and positive associations with glutamine. More metabolites were found to be associated with FEV 1 and FVC than with FEV 1 /FVC, suggesting better abilities to detect lung and airway size as opposed to obstructive airflow associations with serum compounds. Subsequent pathway analysis revealed enriched pathways of amino acid metabolism. Several of the lung function-related metabolic pathways overlapped with those reported in studies on air pollution-related metabolic profiles, including the metabolism of glycerophospholipid, pyrimidine, sphingolipid, purine, glutamate, histidine and tryptophan. More detailed descriptions of study-specific findings, including identified metabolites and metabolic pathways, are provided in tables S1 and S2 . However, since none of the included studies investigated both sets of metabolites (associated with air pollution exposure and with lung function) measured in the same population and with the same analytical platform, inference regarding overlapping findings is limited.

So far, only a limited number of studies investigated correlated metabolites or pathways for the association between air pollution exposure and respiratory conditions. Most of these studies applied the MITM concept, starting with separate investigations of the metabolites or pathways that are associated with air pollution and health outcomes, followed by identification of the overlapping pathways [ 68 ]. J in et al . [ 20 ] found, in their recent review, eight studies examining air pollution-related metabolites that are also perturbed by health outcomes, such as COPD and lung function, ischaemic heart disease, as well as biomarkers of oxidative stress, or inflammation, all but one of which collected biological samples after or at the same time of the assessment of health outcomes. Only two out of these eight studies applied metabolomic analyses to investigate molecular and biochemical pathways that link environmental exposures to pulmonary function. In a Dutch experimental study based on a panel of 31 volunteers exposed to ambient air pollution, a causal mediation analysis of the effects of air pollutants on lung function parameters through a change in blood metabolic features demonstrated metabolic perturbations within eight pathways, including tyrosine metabolism, urea cycle/amino group metabolism and N-glycan degradation [ 29 ]. A cross-sectional study conducted within the TwinsUK cohort found eight metabolites, i.e. asparagine, glycine, N-acetylglycine, serine, glycerate, threonate, α-tocopherol and benzoate, associated with both long-term particulate matter air pollution exposure and lung function [ 30 ]. Some of these ( i.e. tyrosine, guanosine, glycine, α-tocopherol, benzoate, and urea cycle/amino group metabolism) were also reported in the studies on air pollution-related metabolic profiles included in the present review [ 41 – 43 , 46 ]. Also, the studies on lung function-related metabolic profiles included in the present review showed associations with tyrosine [ 58 , 67 ], glycine [ 58 , 67 ], N-acetylglycine [ 66 , 69 ], serine [ 58 , 66 ], glycerate [ 67 ] and urea cycle/amino group metabolism [ 57 , 66 ].

These results highlight the promising role of metabolomics for identification of biomarkers both linked to environmental exposures and to intermediate respiratory health end-points and of the MITM concept.

Conclusions and recommendations for future research

Metabolomics offers the potential to fill the gap in the exposome research of respiratory health, from exposure assessment, and the improved causal understanding and identification of individuals at risk. There is accumulating evidence for distinct variations in circulating metabolites related to both air pollution exposure and lung function, including compounds of amino acid and lipid metabolism. Identifying subtle alterations in metabolic profiles related to lung function in the general population holds the potential to identify biomarkers of the early stages of asthma and COPD pathogenesis that precede diagnostic reductions in lung function. However, our review of the literature identified several shortcomings that need to be addressed in future studies ( table 1 ), as listed below.

• Most reports were based on a small number of subjects recruited from clinical settings for COPD or other respiratory pathology. Studies of metabolic profiles and quantitative lung function traits in the general population ( e.g. trajectories) are still limited.
• Very few studies have investigated the overlap between markers of exposure and predictive markers of disease outcomes within the same study. Implementation of the MITM and/or other causal mediation analytical approaches may facilitate identification of intermediate biomarkers involved in health effects related to air pollution.
• It is difficult to fully benefit from increasingly available metabolomics findings because of heterogeneities in the analyses, i.e. the choice of biological matrix analysed, the type of analytical platform employed and the technical variabilities in how data are processed and annotated. There is a need for large-scale data acquisition, including replication, from the same analytical platform and with uniform metabolite annotation protocols (and exposure assessment).
• Many of the reviewed studies measured metabolic profiles at the same time as health markers were evaluated ( i.e. cross-sectional studies), thus making it challenging to draw conclusions on whether these overlapping metabolites mediate the impact of air pollution on lung function, or whether impaired lung function is exacerbated through these shared metabolic features. This temporal disconnect between sampling and exposure and/or health marker renders it difficult to identify causality. Therefore, future studies should prospectively assess air pollution exposures, metabolic profiles and health outcomes to effectively identify such intermediate metabolites in the causal pathway linking exposure to the outcome.
• A lack of long-term longitudinal data with information on respiratory health and air pollution exposure, and the heterogeneity of air pollution metrics and sources across studies poses major challenges in the interrogation of latency. Also, to which extent the metabolome may aid in characterising exposure history (including the stability of biomarkers) needs to be explored. The latency may vary widely from days to decades depending on which respiratory outcome is involved. While some studies of the short-term effects of air pollution incorporated a priori determined lag periods into their analysis, very few studies conducted a systematic search for latency of air pollution effects on respiratory health.
• Many potential confounders and effect modifiers remain unaccounted for; for example, noise, heat, diet, physical activity, socioeconomic factors and detailed smoking histories. For a complete understanding of how exposures influence health, a full exposome perspective will be needed.
• Susceptibility factors are often ignored, such as genetics and other host factors. Given that gene–air pollution interactions are well described for respiratory outcomes [ 70 ], genetics are likely to also influence associations between exposure, metabolic profiles and respiratory disease. In this context, the use of polygenic risk scores offers an attractive analytical approach, as exemplified in recent COPD studies [ 71 ].
• The integration of metabolomics with other types of omics data, such as epigenetics and transcriptomics [ 72 ], will improve the interrogation and understanding of pathophysiological pathways mediating air pollution effects on lung function across the life-course [ 9 ].

Limitations of current air pollution, metabolomics and respiratory health studies and directions for future research

In addition to the above shortcomings, the challenges of the life-course perspective in exposome research for respiratory health need to be acknowledged, discussed and considered to optimise the use of the metabolome as a mediator.

Metabolic profiling at different time points can shed light on the biological mechanisms through which environmental exposures affect respiratory health in different growth phases. Causal mediation analysis [ 73 ] is a widely used epidemiological method to assess the role of intermediate variables ( i.e. metabolites) that lie along causal pathways from exposure ( i.e. air pollution) to outcome ( i.e. lung function trajectories). This method has several advantages, including allowing for nonlinearity, interactions, as well as multiple mediators with path-specific effects [ 74 – 76 ]. Ideally, this approach would require long-term follow-up of the same subjects, not only with information on their respiratory health, but also with prospectively collected biological samples and air pollution exposure estimates. Such long-term longitudinal data are unfortunately scarce and to our best knowledge there has been no study that has investigated metabolic profiles as mediators across a broad age spectrum. However, many studies of different age groups have applied the MITM concept (as described in the Population-based studies on metabolic profiles and lung function section). However, combining findings across studies is challenging because of the heterogeneity in the biological matrices and in the analytical technologies used. More detailed methodological issues of adopting the metabolome as the mediator between air pollution exposure and adverse health outcomes have been reviewed elsewhere [ 77 ]. Furthermore, by comparing metabolic profiles related to air pollution and lung function between different age groups, we ignore the fact that older people have different childhood air pollution-related metabolic profiles than the current childhood/adolescent group. In the absence of biosamples collected prospectively decades ago and in the absence of exposures back-extrapolated many decades back in long-term studies with repeat lung function measures from childhood to late adulthood, we cannot learn about the long-term health effects of specific metabolic profiles arising from childhood exposure to air pollution. Yet, if we do find that air pollution affects overlapping metabolic profiles in all age groups and that these are associated with lung function irrespective of age, this strengthens our causal and biological understanding of life-long respiratory effects of air pollution.

In the EXPANSE project, we aim to address several of the abovementioned challenges [ 28 ]. We will: 1) bring together large datasets including individual adult and matured birth cohorts with prospectively obtained biosamples, longitudinal high-quality lung function measurements and incident respiratory diagnoses covering different age groups towards a life-course perspective; 2) model back-extrapolated air pollution exposure as well as exposure to potential confounders ( e.g. noise, temperature) and the external exposome in a harmonised manner to participating cohorts; 3) systematically analyse metabolic profiles using prospectively collected biosamples from several cohorts on a same analytical platform for both untargeted liquid- and gas-chromatography coupled with high-resolution mass spectrometry; and 4) link both exposures and metabolomics to respiratory health outcomes using a life-course perspective and gain insights into mediating biological mechanisms and causality by applying an MITM approach.

Supplementary material

Provenance: Submitted article, peer reviewed.

Disclaimer: Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization.

Conflict of interest: M.G.M. Pinho reports a Leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid as an Associate editor at the journal Public Health Nutrition . C.E. Wheelock has received support for the present manuscript from Swedish Heart Lung Foundation. M. Chadeau-Hyam has shares in the OSMOSE consulting company; work performed in the company has no link with the present work. N. Probst-Hensch reports salary support from Swiss TPH Core Funds. The remaining authors have nothing to disclose.

Support statement: This work was conducted within the EXPANSE project that has received funding from the European Union's Horizon 2020 research and innovation programme under grant agreement No 874627. E. Melén has received funding from the European Research Council (TRIBAL, No 757919), Region Stockholm (ALF) and the Swedish Research Council. O. Gruzieva has received funding from the Swedish Research Council (No 2020-01886) and the Swedish Research Council for Health, Working life and Welfare (FORTE No 2017-01146). Funding information for this article has been deposited with the Crossref Funder Registry .

Vital Signs

Carbon dioxide, key takeaway:.

Carbon dioxide in the atmosphere warms the planet, causing climate change. Human activities have raised the atmosphere’s carbon dioxide content by 50% in less than 200 years.

Carbon dioxide (CO 2 ) is an important heat-trapping gas, also known as a greenhouse gas, that comes from the extraction and burning of fossil fuels (such as coal, oil, and natural gas), from wildfires, and natural processes like volcanic eruptions. The first graph shows atmospheric CO 2 levels measured by NOAA at Mauna Loa Observatory, Hawaii, since 1958. The second graph shows CO 2 levels during Earth’s last three glacial cycles, as captured by air bubbles trapped in ice sheets and glaciers.

Since the onset of industrial times in the 18th century, human activities have raised atmospheric CO 2 by 50% – meaning the amount of CO 2 is now 150% of its value in 1750. This human-induced rise is greater than the natural increase observed at the end of the last ice age 20,000 years ago.

The animated map shows how the historical changes in global carbon dioxide over time. Note the colors change as the amount of CO 2 rises from 365 parts per million (ppm) in 2002 to over 420 ppm currently. It's important to understand that “parts per million” refers to the number of carbon dioxide molecules per million molecules of dry air. These measurements are from the mid-troposphere, the layer of Earth's atmosphere that is 8 to 12 kilometers (about 5 to 7 miles) above the ground. This data provides insights into the significant rise in atmospheric CO2 concentrations, highlighting the impact of human activities on Earth's climate.

CO 2 Through the Seasons

A closer look at the carbon dioxide measurements at Mauna Loa shows a series of wiggles in the data. Although total CO 2 is increasing each year, there is also a short-term cycle visible within the larger trend.

This annual rise and fall of CO 2 levels is caused by seasonal cycles in photosynthesis on a massive scale. In Northern Hemisphere spring, plants come to life and draw in CO 2 to fuel their growth. This begins the process of lowering the amount of CO 2 in the atmosphere. In northern autumn, plant growth stops or slows down, and the whole process reverses itself. Much of the plant matter decomposes, releasing CO 2 back to the atmosphere.

A similar but less intense pattern repeats in the Southern Hemisphere in opposite seasons. Spring growth starts in September and winter decomposition begins in March, so CO 2 records in the Southern Hemisphere show the opposite pattern of that seen in Mauna Loa. However, because there is a lot more land and vegetation in the Northern Hemisphere than the southern, the global seasonal cycle more closely aligns with the northern pattern.

See the cycle in action in the visualization Watching Earth Breathe: The Seasonal Vegetation Cycle and Atmospheric Carbon Dioxide .

This boom-and-bust cycle of plant growth gives the graph of CO 2 a sawtooth pattern of ups and downs from year to year. At a larger scale, the upward climb of the trend line over the decades is caused by CO 2 emissions, primarily from burning fossil fuels. Thus, the data illustrate both natural factors and human additions of CO 2 .

Learn more:

NASA's Climate Kids: Why is Carbon Important?

Missions That Observe CO 2

Atmospheric Infrared Sounder (AIRS)

Orbiting Carbon Observatory (OCO-2)

Orbiting Carbon Observatory (OCO-3)

DIRECT MEASUREMENTS: 1958-PRESENT

Proxy (indirect) measurements, time series: 2002-2022.

Effects of Air Pollution

Air pollution affects all things. It is harmful to our health, and it impacts the environment by reducing visibility and blocking sunlight, causing acid rain, and harming forests, wildlife, and agriculture. Greenhouse gas pollution, the cause of climate change, affects the entire planet.

Harming Human Health

According to the World Health Organization , an estimated seven million people die each year from air pollution. More than 4,000 people died in just a few months due to a severe smog event that occurred in London in 1952. Ground-level ozone causes muscles in the lungs to contract, making it difficult to breathe. Exposure to high ozone levels can cause sore throat, coughing, lung inflammation, and permanent lung damage.

Ozone pollution affects our lungs, making it difficult to breathe. UCAR

Symptoms from short-term exposure typically resolve quickly, but long term exposure is linked to serious illness and disease in multiple body systems. Children, the elderly, and people with ongoing illnesses are more vulnerable to air pollution than other groups. Urban populations are also at greater risk due to high concentrations of pollution within cities. Check the current air quality in your area to determine if you should take precautions such as reducing or avoiding outdoor activity.

Harming Animals and Plants

Brown patches on these potato leaves are evidence of moderate ozone damage.

Danica Lombardozzi/NCAR

Wildlife can experience many of the same negative health effects of air pollution that humans do. Damage to respiratory systems is the most common effect on animals, but neurological problems and skin irritations are also common.

Plants and crops grow less when exposed to long-term air pollution. Ozone pollution harms plants by damaging structures called stomata, which are tiny pores on the underside of leaves that allow the plant to "breathe." Some types of plants can protect themselves by temporarily closing their stomata or producing antioxidants, but others are particularly sensitive to damage. Between 1980 and 2011, nine billion dollars-worth of soybeans and corn were lost in the US as a result of ozone pollution. When acid rain, lead toxicity, and exposure to nitrogen oxides change the chemical nature of the soil, plants are robbed of the nutrients that they need to grow and survive. This impacts agriculture, forests, and grasslands.

There are many other ways that air pollution affects living things, such as damaging the habitat, water, and food sources that plants and animals need to survive.

Causing Acid Rain

Acid rain damages buildings. UCAR/NAME

Burning fossil fuels releases sulfur and nitrogen oxides into the atmosphere. Acid rain forms when sulfur dioxide and nitrogen dioxide mix with water droplets in the atmosphere to make sulfuric acid and nitric acid. Winds can carry these pollutants for thousands of miles, until they fall to the Earth's surface as acid rain, which damages the leaves of vegetation, increases the acidity of soils and water, and is linked to over 500 deaths each year. Buildings and other structures are also impacted by acid rain, which causes an estimated five billion dollars of property damage each year. Acid rain dissolves mortar between bricks, causes stone foundations to become unstable, and is destroying ancient buildings and statues carved from marble and limestone.

Reducing Sunlight

High levels of particulate pollution from all types of burning reduces the amount of sunlight that reaches the surface and even changes  the appearance of the sky . When less sunlight is available for photosynthesis, forests grow at a slower rate and crops are less productive. Hazy skies not only reduce visibility, but also impact the weather and even the climate .

Making a Hole in the Ozone Layer

In 2019 the ozone hole over Antarctica (shown in blue) was the smallest it has been since the hole was discovered. Since the banning of CFCs, the ozone hole continues to shrink, but scientists warn that complete recovery is still uncertain.

The hole in the ozone layer is caused by air pollutants . Chemicals used as refrigerants, such as chlorofluorocarbons (CFCs), contain chlorine atoms. Releasing chlorine atoms into the atmosphere destroys ozone. A single chlorine atom can destroy thousands of ozone molecules. The ozone layer blocks harmful ultraviolet-C (UVC) and ultraviolet-B (UVB) radiation from the Sun — it protects us in a way that is similar to putting sunscreen on your skin to prevent sunburn. The ozone hole puts all living things at risk by increasing the amount of ultraviolet radiation that reaches the surface. Exposure to this radiation increases the risk of skin cancer in humans, restricts growth and development in plants, slows the development of fish and amphibians, and reduces the number of phytoplankton in marine ecosystems. It also causes natural and synthetic materials to breakdown at an accelerated rate.

Adding Too Much Nitrogen to the Land

Gaseous ammonia (NH3) from agriculture and nitrogen dioxide (NO2) from car, truck, and airplane emissions increase the amount of nitrogen in soils. Plants need nitrogen to grow, but too much nitrogen can limit the growth of some plants and increase the growth of others, disrupting the balance of species within an ecosystem. This disruption is negatively impacting grasslands and other fragile environments around the world.

This map shows global ammonia hotspots identified over a 14-year period. Warm colors represent an increase in ammonia, while cool colors represent a decrease in ammonia. NASA

Effects of Greenhouse Gas Pollution

Greenhouse gas pollution is causing climate change. As a result, ecosystems are changing faster than plants and animals can adapt, and many species are going extinct. Marine ecosystems are vulnerable to ocean acidification caused when carbon dioxide emitted into the atmosphere is dissolved in seawater. Ocean acidification makes it difficult for many marine species to grow shells and skeletons.

Melting ice sheets, warming oceans, and extreme weather conditions are examples of how climate changes caused by greenhouse gas pollution threaten ecosystems across the Earth. In many cases, the decline of one or a few species due to air pollution can topple the balance of entire ecosystems.

• Air Quality Activities
• How Does Ozone Damage Plants?
• Ozone in the Troposphere
• The Changing Nitrogen Cycle
• The Greenhouse Effect