Keywords

4.1 Introduction

Mankind has witnessed rapid urbanization and industrialization over the last 50 years. As a consequence, a wide array of toxic substances has been introduced into the atmosphere affecting the natural processes directly or indirectly (Sirohi et al. 2018). These substances are often termed as “pollutants.” Later these pollutants make their way into food chain ultimately affecting the health and well-being of humans.

Plants being sessile are continuously exposed to various types of air pollutants, which may act individually or synergistically to affect plant metabolism and growth and often leads to decline in crop yield and nutritional quality (Kulshrestha and Saxena 2016; Agrawal et al. 2003; Marshall et al. 1999). Principally, plants are not selective in gas uptake (Heagle 1989), which makes it even more challenging to recognize the stress conditions being faced by plants. This in turn adversely affects the global food security. The rate with which population is expanding, it becomes important to understand the response of plants in terms of physiology and metabolism to their external environment. Decline in crop yield in the present scenario due to any kind of stress needs to be addressed immediately for sustainable future. Therefore, understanding the impact of major air pollutants on plant physiology and metabolism will help us to look after the indirect effect of these on entire ecosystem as well as to predict the future of plant health (Saxena and Kulshrestha 2016a, b).

4.2 Air Pollutants and Their Impacts on Plant Health

It is difficult to assess the direct effect of individual pollutant on physiology and metabolism of plants because natural factors such as light, water, and mineral nutrition affects the interaction of plants with pollutants. Moreover, in a particular environment, plants are subjected to a combination of pollutants simultaneously, thereby making it more difficult to single out the causal pollutant (Kulshrestha and Saxena 2016; Mudd and Kozlowski 1975).

Some of the environmental factors that determine the rate at which morphological and physiological symptoms appear on plants are type and concentration of pollutants, duration of exposure, distance from the source of pollutant, and weather conditions. Clear, warm, still, and humid weather with high barometric pressure appears to be the perfect environmental condition when the damage caused to plants is severe (Unsworth and Ormrod 1982; Mudd and Kozlowski 1975). Injury in response to these air pollutants can occur in two forms namely chronic and acute injury. Chronic injury to plants may occur as a result of long-term exposure to pollutants at a low concentration. On the other hand, acute injury occurs when plants are fumigated with high concentration of pollutants for short duration (Saxena and Kulshrestha 2016a, b; Zeevaart 1976).

For instance, Chen et al. (2009) studied the photosynthetic response of soybean leaf toward acute (400 ppb, 6 h) and chronic (90 ppb, 8 h, 28 days) exposure to O3. Different patterns of O3 damage at the leaf level appeared. In chronic O3-exposed leaves, the areas of least photosynthetic capacity were of variable size and shapes which appeared mostly in the interveinal regions. On the other hand, acute damage to leaf was characterized by small local areas of reduced photosynthetic capacity that appeared mainly in areas near the major veins.

Plants use complex recognition and response mechanisms to combat any kind of stress (Bita and Gerats 2013). Whenever stress conditions are detected by plants, first response of plants is production of reactive oxygen species (ROS). High concentrations of ROS are toxic and affect the normal functioning of cell (Saxena et al. 2017a; Caverzan et al. 2016; Suzuki et al. 2012). Because of their highly reactive nature, ROS can damage major biomolecules such as nucleic acids, lipids, and proteins. Nucleic acids may be modified by inducing oxidation, strand breaks, deletion, and modification of nucleotides. Lipids can be damaged by inducing the chain break and increasing the fluidity of membranes or oxidation. Proteins, on the other hand, may be subjected to site-specific amino acid modification, alteration of the electric charge, and enzymes inactivation. ROS may also lead to activation of programmed cell death (PCD) that may result in death of the cells (Caverzan et al. 2016; Sharma et al. 2012).

ROS performs dual roles in cell. Under normal conditions they may act as secondary messengers involved in signal transduction networks but under oxidative stress they can potentially cause damage or even cell death. Therefore, ROS production and scavenging tightly regulates the “redox homeostasis” in cells (Sharma et al. 2012; Neill et al. 2002). ROS are by-products of aerobic metabolism and formation of various ROS such as hydrogen peroxide (H2O2), superoxide anion (•O−2), hydroxyl ion (OH−), hydroxyl radical (•OH), and singlet oxygen (1O2) is enhanced in response to the pollutants. These ROS can act as both intra- and intercellular messengers. In absence of effective ROS detoxification strategies, conditions of “oxidative stress” are created as the levels of ROS are elevated (Saxena et al. 2017b; Sharma et al. 2012). Unavoidable leakage of electrons onto O2 from the various electron transport activities of chloroplast, mitochondria, and other cellular compartments including plasma membrane leads to formation of ROS (Sharma et al. 2012; Heyno et al. 2011; Blokhina and Fagerstedt 2010). Figure 4.1 shows the abiotic stress-induced ROS-mediated changes in major biomolecules in plant cells.

Fig. 4.1
figure 1

Effect of air pollutants (abiotic stress) induced ROS on major biomolecules present in cells

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In order to survive the deleterious effects of these ROS, plants have evolved a complex defense mechanism which maintains a balance between production and removal of ROS. Antioxidant defense system of plants consists of both enzymatic and nonenzymatic components. The enzymatic components of defense system includes superoxide dismutase (SOD), catalase (CAT), guaiacol peroxidase (GPX). A set of four enzymes are involved in ascorbate-glutathione (AsA-GSH) cycle of antioxidant defense system, viz. ascorbate peroxidase (APX), monodehydroascorbate reductase (MDHAR), glutathione-dependent dehydroascorbate reductase (DHAR) and glutathione reductase (GR) (Caverzan et al. 2016; Chew et al. 2003). Successive oxidation and reduction of Ascorbate (AsA), Glutathione (GSH), and NADPH catalyzed by the enzymes APX, MDHAR, DHAR, and GR occur in AsA-GSH cycle (Caverzan et al. 2016; Pandey et al. 2015; Sharma et al. 2012). The AsA-GSH cycle acts in different subcellular compartments (chloroplast, mitochondria, peroxisomes, cytosol, and apoplast) and multiple isoforms of enzymes of this pathway exist in cell (Pandey et al. 2015). Table 4.1 shows the major ROS scavenging antioxidant enzymes and the reactions catalyzed by them.

Table 4.1 Major antioxidant enzymes of the plant antioxidant defense machinery and the reactions catalyzed by them (Caverzan et al. 2016; Das and Roy Choudhury 2014; Gill and Tuteja 2010)
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The nonenzymatic components of antioxidant defense machinery include major cellular redox buffers GSH and AsA. Others include carotenoids, flavonoids, alkaloids, and tocopherols (Sharma et al. 2012; Gill and Tuteja 2010; Mittler et al. 2004). These biomolecules can act directly to detoxify ROS and may also act by reducing the substrates for antioxidant enzymes (Caverzan et al. 2016; Mittler 2002).

The following section deals with the impact of major air pollutants on morphological, physiological, and biochemical changes within plants, and how antioxidative defense system plays a major role in acting against this abiotic stress condition.

4.3 Sulfur Dioxide (SO2)

Sulfur dioxide is one of the most common and distinguished air pollutants across the world. It is a colorless gas with pungent odor generally released upon combustion of sulfur-based fuels and from copper smelting or released during volcanic eruption. Sulfuric acid (H2SO4) is the major source of acid rain, formed as a result of hydrolysis of SO2 when dissolved in water. Over the years atmospheric level of SO2 has increased; therefore, plants are being exposed to higher levels of SO2 throughout the world (Saxena and Kulshrestha 2016a, b; Qu et al. 2016; Emberson et al. 2001; Robinson and Robin 1970).

A wide range of investigations has been carried out to assess the impact of SO2 on plants (Tiwari et al. 2006; Mehlhorn et al. 1986; Riding and Percy 1985; Olszyk and Tingey 1984; Mclaughlin and Mcconathy 1983). Chronic as well as acute SO2 exposure influences the growth of plants (Muneer et al. 2014). Sometimes small dosage of SO2 may not have any effect on plants or may promote plant growth considering the fact that  sulfur is an integral component of biomolecules such as proteins, chlorophyll, and hormones. It is also involved in efficient fixation of nitrogen by legumes (Li and Yi 2012; Mudd and Kozlowski 1975).

However, when given in large amounts, sulfur toxicity can be observed. Cereals like oats (Avena sativa), corn (Zea mays), rye (Secale cereal) and barley (Hordeum vulgare) and conifers such as Austrian pine (Pinus nigra J.F. Arnold) and Balsam fir (Abies balsamia L. Mill.) are somewhat sensitive to SO2 injury. Among dicots carrot (Daucus carota), cabbage (Brassica oleracea var. capitata), black willow (Salix nigra Marsh.), beans (Phaseolus vulgaris), and celery (Apium graveolens) are sensitive (Legge and Krupa 2002; Treshow 1971). Injury on the parallel veined plants appears as necrotic streaks between the veins near the leaf tip and extends toward the base with increase in severity of injury. Conifers needle tips are the first to show injury in form of browning which extends toward the base with increase in severity of injury. Continuous exposure to injurious levels of SO2 may then result in dark bands on the brown necrotic part of needle. Marginal or interveinal necrotic areas appear on broad leaved plants in response to acute SO2 injury (Legge and Krupa 2002; Mudd and Kozlowski 1975; Taylor 1973). Generally young leaves are more sensitive to SO2 than older leaves (Horsman and Wellburn 1977; Zeigler 1972). The susceptible areas affected by SO2 become flaccid and subsequently dried becoming white to ivory in most plant leaves. Sometimes, the dead tissue may turn red, brown, or almost black (Taylor 1973). Chronic injury including brown/red leaf spots arising from leaf edges, decline in leaf area, and crop yield are some common symptoms (Kropff 1991). In monocots, acute injury symptoms appear at the tip of leaves and advances downward as necrotic and chlorotic streaks with infrequent reddish pigmentation (Rai et al. 2011).

Reduction in chlorophyll content, biomass, photosynthetic and respiration rate are common effects of excess SO2 (Padhi et al. 2013). During the exposure to toxic levels of SO2, plants are not capable of assimilating the SO2 at the same rate as it is being absorbed (Stratigakos and Ormrod 1985) which exceeds the threshold accumulation in intercellular spaces of the leaf resulting in acute injury (Thomas 1961).

Stomatas are the main facilitators of gas exchange between plants and external environment. Plants can metabolize SO2 received in the gaseous form through stomata. Therefore, primary effect of high SO2 exposure is the alteration of stomata. Guard cells damaged by SO2 affect stomatal opening, thus plant water content (Bytnerowicz et al. 2007) and high-level SO2 decrease the stomata abundance and result in aborted stomata (Olszyk and Tibbitts 1981; Koziol and Whatley 2016). Reduction in total number of stomata by plants is a mechanism to cope with the increased concentration of SO2, preventing the entry of SO2 inside. SO2-induced erosion of the epicuticular wax structures around the stomata contributes to the damage of stomata (Unsworth and Black 1981; Taylor 1978). Once it enters the intercellular spaces, SO2 dissolves in water on the cellular surfaces causing considerable cellular K+ loss (Koziol and Whatley 2016).

SO2 is capable of inducing apoptosis and reducing the viability of guard cells in Tagetes erecta in a dose-dependent manner. ROS and NO act as facilitators of SO2-induced cell death (Wei et al. 2015). SO2, after its entry into plants via stomata, generates more toxic forms, sulfite (SO32−) and bisulfite (HSO3−), by dissolving in cellular cytoplasm. These toxic forms are capable of damaging plants (Lewandowska and Sirko 2008). Sulfite is 30 times more toxic than sulfate (Thomas et al. 1943). Therefore, prolonged exposure to high atmospheric concentration of SO2 (more than 0.3 ppm) can cause severe tissue damage (Taiz and Zeiger 2002). Stable cytoplasmic pH is an important factor for executing the important cellular activities. SO2 causes acidification of cytoplasmic pH affecting the various metabolic processes.

Detoxification process of sulfite (SO32−) and bisulfite (HSO3−) to less toxic form sulfate (SO42−) leads to enhancement of ROS, such as superoxide radical (O2−), hydrogen peroxide (H2O2), and hydroxyl radical (OH−). Increased ROS content can affect biomolecules and can cause oxidative damage to nucleic acids, proteins, and lipids. Activation of antioxidant defense machinery that consists of both enzymatic and nonenzymatic components in response to SO2 stress takes place. In Arabidopsis thaliana, O2− generation rate and H2O2 content enhances with increasing SO2 concentration and prolonged exposure duration (Li and Yi 2012). Upregulation of defense-related genes encoding antioxidant defense enzymes viz. peroxidase (POD), Glutathione peroxidase (GPX), superoxide dismutase (SOD), cytochrome P450, heat shock proteins (Hsps) and pathogenesis-related (PR) proteins in SO2-treated Arabidopsis shoots takes place (Li and Yi 2012). SO2-induced upregulation of POD and other genes involved in the phenyl propanoid pathway to synthesize protective substances depicts the defense effects of the alteration of secondary metabolism in SO2-fumigated plants (Sharma and Davis 1997).

SO2 can affect the metabolism by either accepting or donating electrons, affecting the cellular electron transport system in plants (Osmond and Avadhani 1970). Exposure to higher concentration of SO2 can also lead to lipid peroxidation in plants (Li and Yi 2012; Shimazaki et al. 1980). ROS produced in response to prolonged exposure to air pollutants can cause extensive damage to membranes and associated molecules, including the chlorophyll pigments and enzymes in chloroplast.

Chlorophyll content of plants serves as a biomarker parameter for air pollution levels (Darrall and Jager 1984). Chlorophyll content reduces significantly in tomato leaves with brief exposure to SO2 (Padhi et al. 2013). SO2 can convert chlorophyll into phaeophytin with release of Mg2+ by lowering the pH, changing the spectral properties (Rao and Leblanc 1965). It can also inactivate many enzymes by breaking the disulfide bridges (Cecil and Wake 1962) or may even activate some hydrolytic enzymes by inducing some conformational changes (Malhotra and Hocking 1976).

Photosynthetic CO2 fixation is also affected by SO2, higher concentration of SO2 can result in inhibition of Rubisco by competing with CO2 or bicarbonate for the binding sites in RuBP carboxylase (Zeigler 1972). Bisulfites also hold the capacity to inhibit the activity of phosphoenol pyruvate (PEP) carboxylase and malate dehydrogenase (MDH) in C4 plants (Osmond and Avadhani 1970). Mukerji and Yang (1974) also confirmed the inhibition of PEP carboxylase in spinach by sulfite in a competitive manner with respect to bicarbonate. According to different studies SO2 has been known to affect respiration as well (Gheorghe and Ion 2011; Kropff 1991; Gilbert 1986). Ballantyne (1973), showed evidence of decreased ATP synthesis in corn and bean mitochondria in response to sodium sulfite.

Accumulation of sulfite and bisulfite in cells can disturb the existing balance between incompletely oxidized sulfur compounds and sulfhydryl groups present in glutathione and cysteine that play central role in maintaining the structural integrity of proteins (Loughman 1964; McMullen 1960). It can convert disulfide enzymes into thiosulfonates and thiols (GSH) leading to its deactivation (Bailey and Cole 1959). SO2-damaged pine needles show 2–4 times more SH content than control leaves (Grill and Esterbauer 1973). GSH content is also greatly increased in SO2-fumigated leaves of wheat (Triticum aestivum) (Navari-Izzo and Izzo 1991) indicating the activation of defense response that helps to protect cell membrane lipids against peroxidation. GSH plays important role in the process of redox buffering. It also acts as co-substrate in reaction catalyzed by GPX and DHAR as shown in Table 4.1.

Enzymes involved in antioxidant defense system such as Glutathione reductase (GR) are shown to be expressed at higher levels when exposed to SO2. Increase in level of GR when barley plants are fumigated with SO2 shows the activation of antioxidant defense system (Navari-Izzo and Izzo 1994). Increased levels of SOD has also been observed in spinach (Spinacia oleracea) leaves and Arabidopsis exposed to SO2 (Li and Yi 2012; Tanaka and Sugahara 1980). Increased levels of catalase in Barley were reported (Navari-Izzo and Izzo 1994) but not in Arabidopsis (Li and Yi 2012). Tanaka and Sugahara (1980) stated that high level of SOD activity is correlated with increased resistance to SO2. Also SOD activity in leaves increases with long-term exposure to low concentration of SO2.Therefore, it can be said that SO2 exposure results in high levels of ROS which stimulates the antioxidant defense system as it may occur in case of any abiotic stress in plants.

4.4 Nitrogen-Containing Pollutants NOX and NHy

Nitrogen dioxide (NO2) and nitric oxide (NO) are oxides of nitrogen and generally referred as (NOx) (Mansfield and Freer-Smith 1981). Ammonia (NH3) and ammonium (NH4+) are collectively referred as “NHy.” NO2 is one of the most prevalent and harmful air pollutants in atmosphere generated by anthropogenic activities. NO2 undergoes splitting in the presence of sunlight to form ozone (O3) and NO. When nitrogen oxides react with moisture, they form nitric acid (HNO3) or nitrous acid (HNO2). Nitrate and nitrite salts are formed upon neutralization of HNO3 and HNO2, respectively. Therefore, NOx and derivatives exist and react either as gases in the air, as acids in droplets of water or as salts. These gases, acid gases and salts together contribute to pollution effects that have been recognized and attributed to acid rain (Park et al. 2018; Blaszczak 1999).

About half of NOx are discharged in atmosphere from automobiles exhausts (Blaszczak 1999). NOx emission from combustion is primarily in the form of NO. Other stationary sources such as industrial power plant boilers, incinerators, cement and glass manufacture, petroleum refineries and iron–steel mills, all contribute to atmospheric NOx. With increased industrialization, global NOx content in atmosphere has arisen quickly in past decades. Trace amounts of other nitrogen-containing compounds such as nitrous oxide (N2O), nitrous acid (HONO), and ammonia (NH3) also constitute the N-containing pollutants’ emission from vehicles (Colvile et al. 2001).

Leaves are the most vulnerable to acute injury owing to their most active status in exchanging gases with the surrounding atmosphere (Taylor 1973). NOx like other gaseous pollutants enter leaf mesophyll tissue through open stomata, and upon reaction with water NOx gets converted to nitric acid or nitrous acid (Park et al. 2018), which is toxic for plant tissue. The symptoms usually appear as wound on both sides of the leaves, which initially occurs between leaf veins or alongside leaf (Law and Mansfield 1982; Taylor and Eaton 1966). However, the foliar uptake of nitrogenous compounds in the form of wet deposition is through the cuticle (WHO 2000). Exposure to gaseous NH3 (180 μg/m3) or NH4+ in rainwater (5 mmol/L) damages the crystalline framework of the epicuticular wax layer of the needles of Pseudotsuga menziesii. But uptake of pollutants via leaf surface is slower than uptake via stomata and is significant only when the leaf surface remains wet for longer time period such as in tropical areas (Thijsse and Baas 1990).

NO2 can enter the intercellular cavities of the leaf and dissolves in the extracellular water to form nitrate (NO3−) and nitrite (NO2−) in equal amounts (Yan et al. 2007). When atmospheric concentration is high, it is rapidly absorbed, and susceptible areas on recently matured and rapidly expanding leaves are prone to death (Taylor 1973). Irregularly shaped, dark-pigmented lesions are formed when susceptible plants are exposed for several hours at lower atmospheric concentrations. Tip burn is common in conifers needles (Gheorghe and Ion 2011). Appearance of large yellow necrotic pockets and wilting on older leaves has been reported in several studies (Yan et al. 2007; Yu et al. 1988). In case of Arabidopsis, yellowing of leaves is subsequently followed by death when 18.8 mg/m3 NO2 is supplied (Liu et al. 2015). Similarly, chlorosis in spinach leaves appears starting from lower leaves and slowly develops upward when plants are fumigated with NO2 at 8 ppm in the light for 36 h (Yu et al. 1988). Long-term treatment with NO2 also leads to delay in flowering in tomato plants (Pandey and Agrawal 1994) and increased level of leaf senescence and reduced stomatal conductance in rice (Maggs and Ashmore 1998). Symptoms of acute injury on bean, tomato, and tobacco seedlings induced by exposure to high concentrations (>4.93 mg/in.3) of NO appear as necrotic lesions similar to the lesions caused by SO2 or by excessive concentration of ozone (Taylor and Eaton 1966).

Intrinsic plant properties, nutritional status, and environmental conditions determine the fate of N that appears on the leaf surface. When given in low concentration NOx may result in growth stimulation (WHO 2000). Low light or dark conditions increase the susceptibility of leaf tissue to NO2 injury. Extent of accumulation of nitrite in leaves decides the acute injury to plants by NO2 (Kato et al. 1974). Light-dependent enzyme nitrite reductase (NiR) is more or less inactive in dark; therefore, exposure of plants to NO2 in dark results in accumulation toxic levels of nitrites causing acute injury (Zeevart 1976). In light, NiR using reducing power from the photosynthetic electron transport system reduce nitrites produced from foliar absorbed NO2 to the ammonia that is assimilated further into N-containing compounds inside plant.

Free radical •N=O is a key player in the phytotoxicity of NOx (Wellburn 1990). Phytotoxic effects of nitrogen-containing compounds (NO2–, NH3, and NH4+) are due to their interference with the cellular acid/base homeostasis (Raven 1988). Noncyclic electron flow in photosynthesis, ATP formation by photophosphorylation, and nitrite reduction are all pH-dependent processes inside chloroplast. Therefore, disturbance of the stromal pH by pollutants like NOx can affect the normal operation of these processes (Wellburn et al. 1980).

NOx is known to inhibit photosynthesis, reduce chlorophyll content and biomass in a variety of plants at concentrations quite below those required to produce visible leaf injury as a function of NOx concentration (Chen et al. 2010; Yan et al. 2007; Pandey and Agrawal 1994; Okano et al. 1985; Spierings 1971; Hill and Bennett 1970). Iron-nitric oxide free radical complexes have been implicated as effective inhibitors of enzymatic activity in proteins containing SH groups or histidine residues which indicates that iron-containing redox agents such as ferredoxin and cytochromes involved in photosynthesis can form a complex with NO and interfere with photosynthetic electron transport chain (Woolum et al. 1968). However, complex formation is dependent upon the concentration of NO in the cell cytoplasm. This inhibition can also be explained by competition for nicotinamide adenine dinucleotide phosphate (NADPH) between carbon assimilation and nitrite reduction in chloroplast, also the strong radical nature of NO2 results in the generation of ROS leading to activation of antioxidant defense system (Ramge et al. 1993; Sabaratnam and Gupta 1988).

NOx being an oxidant pollutant can promote ROS formation which induces oxidative damage to biological macromolecules such as proteins, nucleic acids, and lipids, resulting in the generation of ROS (Yu et al. 1988). Upon accumulation of excess ROS, antioxidant defense system is activated to avoid oxidative damage. The induction of antioxidant enzymes is a protective action of plants against NO2 stress (Liu et al. 2015).

Increased activities of antioxidant enzyme SOD have been reported on exposure to NO2 (Liu et al. 2015). SOD, a metalloprotein catalyzes the dismutation of superoxide radical to H2O2 and molecular oxygen (O2), providing protection against superoxide radical. In Camphora seedlings and Arabidopsis shoots SOD activity increases with increasing NO2 concentration in a dose-dependent manner. Peroxidase (POD) and catalase (CAT) are H2O2 scavenging enzymes in plant cells that shows enhanced activity upon exposure to NO2 (Liu et al. 2015; Yan et al. 2007) confirming the activation of antioxidant defense system regulated by a ROS-mediated signaling pathway.

In a recent study by Sheng and Zhu (2019) on 40 different garden plants, NO2 showed significant increase in the activity of POD which may be linked with increased ROS generation. Sheng and Zhu (2019) also reports that increased POD not only helps in fighting against ROS directly but can also contribute to overall cellular resistance against NO2 stress by initiating the lignification and phenolic cross-linking of cell wall. Lipids are one of the main biomolecules susceptible to damage by ROS. Peroxidation of unsaturated fatty acids in membranes results in formation of Malondialdehyde (MDA) (Labudda 2013; Price et al. 1990). Therefore, cellular MDA content is an indicator of oxidative stress induced by NO2. Significant increase in MDA content has been reported in various species in response to NO2 (Sheng and Zhu 2019; Liu et al. 2015; Chen et al. 2010; Yan et al. 2007) supporting the increase in cellular ROS in response to NO2 that cause damage to membrane lipids thus affecting the membrane permeability.

ASA and glutathione are major players of antioxidant defense system in plants. Therefore, an increase in these confirms the activation of antioxidant defense system. Several studies reports change in AsA and glutathione levels upon fumigation with NOx (Liu et al. 2015; Chen et al. 2010; Yan et al. 2007).

In Brassica campestris, exposure to 1 μL L−1 and higher NO2 leads to decrease in ASA contents (Yan et al. 2007). Similarly Liu et al. (2015) also reported decrease in ASA content with increment in exposure to NO2. According to the study by Chen et al. (2010) in Camphora, similar pattern was observed, AsA content decreased significantly during the first 30 days of exposure to the NO2 at 0.5 μL L−1 but it showed an increase in the following 30 days supporting the fact that ascorbate-glutathione cycle worked efficiently in the second 30 days period (Yan et al. 2007).

4.5 Ozone

Ozone is an unstable but strong oxidant with triatomic form of oxygen (O3). In the stratosphere, it absorbs some of the sun’s ultraviolet radiation. However, in troposphere it is a secondary pollutant formed in the presence of sunlight by complex photochemical reactions involving its precursors such as carbon monoxide (CO), oxides of nitrogen (NOx), and volatile organic compounds (VOC). NO2 splits into NO and O in the presence of sunlight at wavelength of 430 nm. Free oxygen atom released from this reaction combines with molecular oxygen to form ozone. NO then reacts with free radicals formed as a result of action of UV on VOC. Free radicals then convert NO into NO2. Newly formed NO2 then participates in the next cycle of O3 formation. In this way whole cycle of ozone formation is continued until the VOCs are not photoreactive anymore (Ghazali et al. 2010; Price et al. 1997).

Principal source of these precursors is from industrial emission, refineries, chemical plants, fossil fuels burning, and transport sector. These precursors can be transported to long distances before they react to form ozone in the atmosphere or O3 may directly be transported from urban areas to agricultural lands (Singh and Agrawal 2017; Saxena and Ghosh 2011). Ozone from the stratosphere might also be transported to troposphere (Forster et al. 2007; Bell and Treshow 2002). Concentration of O3 might be higher in rural areas than urban areas due to long distance transport of O3 or its precursors. O3 concentration is reported to be higher on sunny, spring and summer days when enough sunlight and primary pollutants are present in troposphere (Tiwari and Agrawal 2018; Singh and Agrawal 2017).

O3 is phytotoxic because of strong reactive nature (Saxena et al. 2019; Mudd and Kozlowski 1975). Daily exposure to O3 at a concentration below 120 nmol mol−1 for days, weeks, or months are generally considered to be chronic, whereas, exposure to O3 at a concentration between 120 and 150 nmol mol−1 for even few hours is considered acute (Fiscus et al. 2005; Long and Naidu 2002). Generally O3 exposure leads to loss in yield of agriculturally important crop plants (Pell et al. 1997; Sharma and Davis 1994; Heagle 1989). In an attempt to rescue itself from O3 stress, biomass accumulation and allocation pattern adopted by plants dictates the yield loss and cultivar’s sensitivity or resistivity toward O3 (Tiwari and Agrawal 2018; Mills et al. 2018; Mishra et al. 2013).

Wide array of investigations have been carried out to assess the impact of continuously increasing O3 on morphology of plants (Moura et al. 2018; Zouzoulas et al. 2009; Heagle 1989). Various factors such as duration and concentration of O3 exposure, weather conditions, genotype, type of plants and growth stage affect the level of injury caused by O3. Some plants are more sensitive to O3 than others, for example soybean (Glycine max) is one of the most O3-sensitive agriculturally important crops while on the other hand Sorghum (Sorghum bicolor) appears to be relatively insensitive to O3. While within same plant species some cultivars/varieties maybe more sensitive than others; e.g., among two cultivars of soybean, cultivar Essex is O3 tolerant while cultivar Forrest is sensitive to O3 (Chernikova et al. 2000). In a study by Pleijel et al. (2006), old cultivar of wheat was found to be less affected by O3 than the modern cultivar. Monocots as a group (e.g., grain sorghum and tall fescue) appear to be less sensitive to O3 than dicots (cotton, peanut) (Heagle 1989).

Necrosis, interveinal chlorosis, chlorotic stippling, flecking, bronzing, and reddening of the upper leaf surface, marginal and tip burn injury are the common symptoms of O3 injury (Ueda et al. 2013; Mishra et al. 2013; Calatayud et al. 2011; Paoletti 2009; Lee et al. 1981). Following sequence of events are supposed to be responsible for these visible symptoms: (1) O3 interaction with cellular components in leaf tissue; (2) cell collapse and localized accumulation of cellular water at the site of interaction; (3) bleached chlorophyll of the injured cell; (4) followed by the breakdown of the leaf structure around the cell (Mudd and Kozlowski 1975).

Ozone injury symptoms generally appear between the veins on the upper surface of aged and middle-aged leaves, but can also be bifacial for some species. Young plants and middle-aged leaves are more susceptible to injury caused by O3 than mature leaves (Gheorghe and Ion 2011). In Arabidopsis plants, curling of leaves and 30–48% reduction in fresh and dry weights is observed with 150 and 300 ppb O3 for 2 weeks (Sharma and Davis 1994). Interveinal chlorosis and stippling is observed in various cultivars of wheat and mung bean upon fumigation with elevated O3 (Mishra and Agrawal 2014; Mishra et al. 2013). Spot like necrotic lesions appears on approximately 20% of the leaf area of older leaves of tobacco whereas young leaves do not show any symptoms at all (Camp et al. 1994). Lesion formation in leaves of sensitive plants in response to O3 exposure is comparable to the hypersensitive response against biotic stress. Rapid increase in ROS, deposition of autofluorescent phenolic compounds, and pathogenesis-related proteins (PR) expression are key plant responses against O3 stress (Overmyer et al. 2003; Schraudner et al. 1998). Grimes et al. (1983) was able to show that phenolic compounds enhance the decomposition of O3 in the aqueous solution primarily into •OH radical.

Since O3 entry through the leaf cuticle is negligible (Kerstiens and Lendzian 1989), it passes mainly through stomata and is rapidly degraded in the aqueous phase of substomatal cavity to generate various forms of ROS causing oxidative stress (Booker et al. 2009). Oxidative burst as a result of O3 decomposition exceeds the normal ROS scavenging capacity of cells leading to activation of antioxidant defense system including antioxidant enzymes and other stress-related proteins. It also affects the nitrogen metabolism, by influencing the associated enzymes, affecting the biosynthesis of amino acids (Tiwari and Agrawal 2018).

O3 stress also affects the common physiological processes by reducing photosynthetic proteins, reduction in the photosystem (PS) II efficiency (Feng et al. 2010; Singh et al. 2009) accelerating senescence (Feng et al. 2016) and impaired reproductive development. It also affects the stomatal conductance. All of these processes lead to decreased carbon assimilation and alteration in allocation of photosynthates. As biomass is utilized in protection and repair against stress instead of getting stored which results in reduced yield (Sarkar et al. 2015; Tripathi and Agrawal 2012; Heagle 1989).

Apoplastic and symplastic antioxidant defense system is activated upon O3 injury. Important apoplastic antioxidants include both protein as well as nonprotein components of antioxidant defense machinery. Pool of reduced apoplastic ascorbate has been proposed to be the first line of detoxification barrier against O3. Various studies report the correlation of total ascorbic acid (AsA) content with ozone resistance (Liu et al. 2015; Dumont et al. 2014; Conklin and Barth 2004), for instance, increased levels of apoplastic ascorbate in Sedum album leaves as a function of O3 concentration (Castillo and Greppin 1988). Similarly, soybean’s ozone-tolerant cultivar Essex had higher levels of total AsA than the sensitive-Forrest cv. (Robinson and Britz 2000) confirming the positive relation between the two. When the natural capacity of specific cell wall components to scavenge the ROS is limited by overproduced ROS under O3 stress, damage to the plasma membrane eventuates (Sanmartin et al. 2003). As mentioned earlier, increase in MDA content is an indicator of stress conditions in plants. MDA content increases up to 1.4-fold in rice leaves after 24 h of fumigation with O3 implying that increase in MDA is not caused by O3 directly, instead it is a result of other metabolic processes affected by O3 (Ueda et al. 2013). An increase of 314.3% and 65% in MDA content is observed in wheat during jointing and heading stages of growth, respectively, when treated with high concentration of O3 (120 ppb) (Liu et al. 2015). Higher MDA concentrations are also observed in two different cultivars of mung bean exposed to O3 (Mishra and Agrawal 2014). All of these findings depict the positive correlation between O3 fumigation and increase in MDA content (Feng et al. 2016; Sarkar et al. 2015; Rai et al. 2007; Iglesias et al. 2006).

Apart from nonenzymatic components of antioxidant defense machinery, the enzymatic components play a crucial role in providing resistance against the oxidative stress due to O3. Superoxide (O−2) generated as a product of O3 decomposition is scavenged effectively by SOD in apoplast. H2O2, the product of SOD activity is further decomposed into water and oxygen by POD and CAT (Lee and Bennett 1982).

Effect of O3 (300 ppb) has also been determined on the SOD levels in A. thaliana after 12 h of treatment. Cu/Zn SOD (Cytosolic/chloroplast SOD) mRNA levels increased 2-3 folds than control plants (Sharma and Davis 1994). Downregulation of organellar SOD in Japanese rice leaves is reported by Ueda et al. (2013). However, cytosolic SOD showed little sensitivity to O3 suggesting that organellar SOD are more important in response to O3 than cytosolic SOD (Ueda et al. 2013). A significant elevation in apoplastic SOD activity is observed in the wheat cultivar Y16 exposed to O3 (Wang et al. 2014) showing that SOD is a component of first line of defense against O3 stress. Similarly, an increase in activities of SOD and CAT is observed when two different cultivars of rice viz. Shivani and Malviyadhan 36 are exposed to O3 (Sarkar et al. 2015). All of these studies highlight the importance of antioxidant enzymes involved in defense against this abiotic stress.

Ozone as an air pollutant also affects the chlorophyll content of plants. Reduction in chlorophyll is an indicator of decline in photosynthetic yield. O3 can prevent the synthesis of chlorophyll or the ROS generated by O3 can attack the chloroplast leading to destruction of chlorophyll. A significant decrease of 34% in chlorophyll content of sugar beet (Beta vulgaris cv. Loretta) during exposure period of 26 days at high concentration of O3 is observed by Köllner and Krause (2003). Chlorophyll content decreases during both young stage as well as during flowering in Brassica napus (cv. Licolly). More pronounced decline is observed during flowering stage. Similarly, a decline in chlorophyll content of flag leaves of old and modern wheat varieties is observed by Pleijel et al. (2006). Total chlorophyll content of Fepagro 26 variety of Phaseolus vulgarisis is also affected by O3, with a significant reduction of approximately 50% of total Chl. However, O3 does not have any effect on the chlorophyll content of other variety, i.e., Irai (Caregnato et al. 2013). Decrease in total chlorophyll content in Aleppo pine (Pinus halepensis) indicated the potential damage to photosynthetic machinery (Pelloux et al. 2001). All of these studies suggest that sensitivity to O3 is species dependent  which also depends upon the stage of development.

Reduced RuBisCO activity in response to O3 plays an important role in reduction in photosynthetic rate. Photosynthetic rates declines in five varieties of winter wheat exposed to 1.5 times the normal concentration of O3 due to lower maximum carboxylation capacity and electron transport rates (Feng et al. 2016). Rubisco activity reduced by 40% in O3 in Aleppo pine (Pinus halepensis) (Pelloux et al. 2001). In another study, it is observed that Rubisco activity and quantity decline with chronic O3 treatment throughout the lifetime of the leaves of hybrid poplar and Raphanus sativus L. cv. Cherry Belle (Pell et al. 1992). It is indicated that O3 accelerates the normal process of senescence by declining both the quantity and activity of Rubisco in leaves and chronic exposure to O3 is necessary for continuous degradation of Rubisco (Pell et al. 1992).

4.6 Fluorides

Fluorine is the most electronegative element that belongs to halogen group of elements. It is an abundant element in earth’s crust that reacts easily with most compounds. Because of its high reactivity it combines easily with other elements such as sodium, calcium, and aluminum and occurs as stable fluoride or fluorine compounds in nature (Gheorghe and Ion 2011). Fluorides are defined as any combination of elements containing the fluorine atom in the −1 oxidation state.

The primary source of fluoride in the atmosphere is the result of numerous anthropogenic activities such as aluminum and uranium smelters and industries related to steel, brick, ceramic, and glass manufacturing. Fluoride compounds are also used in toothpastes and mouthwash as a protective agent against tooth decay. Fluorine emitted from these sources is extremely reactive and easily hydrolyzes in the atmosphere to form hydrogen fluoride (HF), most hazardous gaseous fluoride pollutant. HF thereafter may react with other compounds in atmosphere to form nonvolatile stable fluorides (Walna et al. 2013). Hexafluorosilicic acid (SiF6), tetrafluoromethane (CF4), and hydrogen fluoride (HF) are some of the gaseous fluorides. These gaseous pollutants are highly soluble and toxic in nature. HF is a hygroscopic gas which forms the clouds acidic in nature. HF being lighter than air can harm the plants far away from the source. The nonvolatile particulate fluorides pollutants include Cryolite (Na3AlF6), Calcium fluoride (CaF2), and ammonium fluoride (NH4F) (Gheorghe and Ion 2011). Solubility of these particulate fluorides is species dependent, for example, sodium fluoride is water soluble on the other hand while cryolite is insoluble in water.

Fluoride is considered as the most phytotoxic air pollutant in terms of the minimum atmospheric concentrations required to cause injury in plants which is comparable to the peroxyacetylnitrate, a nitrogen-based pollutant (Weinstein 1983). Fluoride can cause injury to sensitive plants at a concentration of 10–1000 times lesser than those of other major air pollutants (less than 1 ppb) (Unsworth and Ormrod 1982). On the other hand, the threshold concentration for O3 and SO2 to cause an irreversible injury is found to be generally above 0.05 ppm (Panda 2015).

Other HF-like air pollutants can enter the leaf tissue via stomata and dissolve in the water crossing the cell wall. Morphological symptom “tip burn” or marginal necrosis of the leaves is associated with fluorides-based pollutants (Fornasiero 2001; Mudd and Kozlowski 1975; Jacobson et al. 1966). Young and expanding leaves tend to be most susceptible to HF fumigation. Plant foliage can accumulate fluorides entering in its tissues for a long time which then translocates toward tip and margin of the leaves because the water in the leaf has a tendency to move toward the site of greatest evaporation, therefore appearing as marginal and tip injury (Baunthiyal et al. 2014). Due to the tendency of foliage to accumulate the fluoride, it can cause injury even at very low atmospheric concentration (Panda 2015; Gheorghe and Ion 2011). According to Baunthiyal et al. (2014), crucial factor that determines the severity of injury is the accumulation of fluoride at the active sites in toxic levels.

Chlorosis in response to fluoride injury in the affected area is generally followed by the desiccation, change in color, and finally necrosis. Fully grown and middle-aged leaves appear to be more sensitive to damage by fluoride, whereas younger and old leaves only show tip burns occasionally (Weinstein and Alscher-Herman 1982). Marginal yellowing appears earlier in the primary and older leaves of soybean which is followed by necrosis upon exposure to 15–20 nL/L fluoride concentration (Poovaiah and Wiebe 1973). Appearance of randomly scattered red areas on the entire lamina of fully expanded mature leaves of Hypericum perforatum is observed growing in the areas close to ceramics industry. Apparently symptoms appear on both adaxial and abaxial surface of leaves (Fornasiero 2003). Some plants are more sensitive to fluoride than others. Peach fruits, conifers, sweet corn, gladiolus, and apricot are susceptible to damage by fluoride. On the other hand, cucumber, eggplant, tobacco, and wheat show resistance to fluoride damage (Heather 2003).

All physiological and metabolic processes are affected by high internal fluoride concentration. Root–shoot length, stress tolerance index, vigor, biomass accumulation, and seed germination are all affected negatively (Baunthiyal et al. 2014). Spongy mesophyll and lower epidermis are prone to damage by fluoride upon its entry in leaf which is followed by disruption in the palisade cells (Panda 2015). According to the study of Yang and Miller (1963), fluoride fumigated leaves contain more reducing sugars and smaller amount of sucrose than the untreated leaves suggesting the inhibition of sucrose synthesis process which in turn might be related to decline in photosynthesis. Leaf necrosis can be related with various altered metabolic effects. Mcnulty and Newman (1957) report increased uptake of oxygen in beans and gladiolus exposed to HF. In a study by Hill et al. (1959), no direct effect of fluoride on the respiration is observed. However, an increase in oxygen uptake is directly correlated to leaf necrosis in gladiolus. Carbon dioxide assimilation decreases in gladiolus, barley, alfalfa, and cotton due to acute HF fumigation (Thomas 1958), indicating that destabilization of metabolic homeostasis takes place upon exposure to fluoride.

Plasma membrane and tonoplast are overly sensitive to fluoride. Plasma membrane ATPase appears to be sensitive to fluoride, thus affecting the normal metabolism (Giannini et al. 1987). Giannini studied the effects of fluoride on the plasma membrane ATPase of sugarbeet. Results indicated that fluoride inhibition of plasma membrane ATPase is at active sites of the enzyme and occurs in association with magnesium ion. Rakowski et al. (1995) studied the effect of fluoride fumigation on Eastern white pine (Pinus strobus) seedlings for 28 days. Significant decrease in activity of plasma membrane ATPase activity is observed after 28 days and it is suggested that plasma membrane might be primary target site for fluoride injury. Lipid peroxidation levels in response to fluoride stress also reflect the severity of damage caused. Sunflower (Helianthus annus) when exposed to high fluoride concentration shows increase in lipid peroxidation with increasing fluoride concentration and time of exposure (Saleh and Abdel-Kader 2003).

Concerning the activation of antioxidant machinery against fluoride stress, several studies have attempted to dissect the antioxidant defense system. But most of them focus on the fluoride received by plants via soil or hydroponics; therefore, it can be expected that plants will respond in the similar way when plants are fumigated with fluoride.

Fornasiero (2003) studied the effect of fluoride treatments on the activity of SOD in H. perforatum. SOD activity decreases after 2 h of fluoride fumigation which continues to decrease in the following hours as well. It is speculated that the antioxidant defense system is unable to efficiently remove the harmful ROS that results in the appearance of visible injuries. A decrease in SOD activity is observed in the sunflower (Helianthus annus) at the seedling growth stage (Saleh and Abdel-Kader 2003) and Li et al. (2011) showed that the activity of total SOD decreased significantly with increasing fluoride concentration in tea (Camelllia Sinensis) leaves. However, some studies also report increase in the SOD activity in response to the fluoride. For instance, Wilde and Yu (1998) observed an increase in mitochondrial SOD activity in mung bean seedlings. Similarly, Chakrabarti and Patra (2015) reported 75% increase in SOD activity in paddy grains and about 60% increase in roots and leaves. CAT enzyme also shows similar behavior in the presence of fluoride. CAT activity can also decline up to 80% with increasing fluoride concentration in rice (Oryza sativa L.) (Chakrabarti and Patra 2015). It is hypothesized that hydroxyl ions (OH−) attached to iron atoms in catalase are replaced by low molecular weight anions causing inhibition of its activity (Kumar et al. 2009). In contrast, CAT activity increases at low fluoride concentrations and starts to decrease at higher concentrations in C. sinensis (Zheng et al. 2011). Further, nonenzymatic component of defense machinery, i.e., ascorbic acid also shows a tendency to decrease because of binding of F− ion with ascorbic acid oxidase enzyme that delays the inhibition of destruction of ascorbic acid (Sharma 2018; Saleh and Abdel-Kader 2003).

4.7 Effect of Particulate Matter

Particulate matter (PM) is an air contaminant of industrial and urban areas which appears as a complex mixture of solid and liquid particles suspended in air that have different physical and chemical properties. These PMs are emitted by anthropogenic activities and natural sources. Anthropogenic activities such as coal and oil burning, motor vehicle exhaust fumes, road dust, metal and construction industrial activities are major source of introducing PM into the atmosphere. On the other hand, natural processes such as volcanic eruptions, rock weathering, forest fires, and sandstorms also release toxic PMs into the atmosphere (Prajapati 2012; Bosco et al. 2005). Another important source of PM could be nucleation, condensation, or coagulation of gaseous pollutants such as SO2, NOx, NH3, and VOCs (Sonwani and Kulshrestha 2018; Sonwani et al. 2016a, b; Dzierżanowski et al. 2011).

These atmospheric PMs have been classified based on their aerodynamic diameter as PM10 (<10 μm diameter), PM2.5 (<2.5 μm diameter), and ultrafine particles (UP) (<0.2 μm) (Dietz and Herth 2011; Prajapati et al. 2006; NEPC 1998; Beckett et al. 1998; Schwartz et al. 1996). Toxic PM, especially PM2.5 and UP, often comprises toxic components such as heavy metals, PAHs, polychlorinated biphenyls (PCBs), black carbon, and other carcinogenic compounds (Sonwani et al. 2016a; Dzierżanowski et al. 2011; Ariola et al. 2006; Yu et al. 2006). Sulfate, nitrate, ammonium, organic matter, and elemental carbon are regarded as the main PM contributors (Daresta et al. 2015).

Growth and development of plants can be affected by PM either by direct deposition on above ground biomass or indirectly via soil–root interactions (Žalud et al. 2012). These particle depositions onto vegetation surface occur via three major pathways: (1) wet deposition, (2) dry deposition, and (3) occult deposition. Wet deposition is a result of addition of atmospheric particles and gases into cloud droplets by nucleation followed by precipitation as rain and snow (Lovett 1994; Grantz et al. 2003). Precipitation amount and ambient particulate concentrations largely determine wet deposition. Magnitude of wet deposition is directly determined by rainfall and snowfall. Surface properties of leaves such as wettability, exposure, and roughness affect the contact with PM by strongly influencing liquid retention (Sonwani and Kulshrestha 2019; Grantz et al. 2003; Neinhuis and Barthlott 1998). Rate of dry deposition of atmospheric particles on plants and soil is considerably slower than wet or occult deposition; however, it acts constantly and affects all exposed surfaces of plants including those that are not currently physiologically active (Hicks 1986; U.S. EPA 1982). Steady deposits of grease films, dry dusts, elemental carbon encrustations, and heterogeneous secondary particles formed from gaseous precursors on vegetation can be observed (U.S. EPA 1982; Grantz et al. 2003). Leaf age, orientation, surface geometry, phyllotaxy roughness, and wettability of the leaf surface affect the dust interception and hence its retention (Prajapati 2012; Beckett et al. 2000; Neinhuis and Barthlott 1998). Occult deposition is driven by fog, cloud-water, and mist interception. Gaseous pollutant species can dissolve in the suspended water droplets of fog and clouds. Concentration of PM is usually manyfold higher in cloud or fog water than in precipitation or ambient air in the same location. Foliar surface receives PM in a hydrated form by fog and cloud water thus making it more bioavailable to plants (Grantz et al. 2003; Prajapati 2012).

Generally, the effect of PM on vegetation is associated with the reduced irradiation for photosynthesis, stomatal aperture blockage, reduction in leaf area and number, abrasion, altered pigment and mineral content and an increase in leaf temperature linked with change in surface optical properties (Rai 2016; Prajapati 2012; Kuki et al. 2008; Grantz et al. 2003; Hirano et al. 1995). Rough leaf surface receives more PM than leaves with smooth surface and inert particulate interact with plants in a purely physical manner (Hwang et al. 2011; Farmer 2002; Beckett et al. 2000). Alkaline dust material such as limestone can cause the leaf surface injury while other PM may cross the cuticle (Brandt and Rhoades 1972). Also the ionic form of chemicals can enter the mesophyll through the stomatal aperture or fissures in the cuticle by aerial deposition (Kuki et al. 2008; Watmough et al. 1999) which results in the accumulation of essential and nonessential elements in the plants (Pavlík et al. 2012; Lau and Luk 2001). Another possible root for metabolic uptake of PM is through the rhizosphere which is of great importance as large-scale sustained exposure of soil to PM occurs through wet and dry depositions of trace elements (Prajapati 2012; Voutsa et al. 1997).

Exposure of the lettuce plants to PM results in reduced leaves dry matter, increased concentration of trace elements in the above ground parts (Pavlík et al. 2012). Similarly, maize and soybean upon treatment with fly ash (a waste product of coal-fired electric generating plants) at the rate of 8 g m−2 day−1 for 30 days shows reduction in pigment content and dry matter production (Mishra and Shukla 1986).

Delayed seed germination, decreased chlorophyll content, root and shoot weight, inhibition of root elongation, and enhanced lateral root formation are observed when tomato plants are exposed to PM10 (Daresta et al. 2015). Tree species also show reduced biomass and chlorophyll content in response to dust accumulation (Younis et al. 2013; Prajapati and Tripathi 2008; Prusty et al. 2005). Similarly, cement dust pollution affects the growth and morphology. Significant delay in germination, reduced number of leaves, flower and fruits and visible marking on leaves such as chlorosis, necrosis and mottling appear as common symptoms of cement dust pollution (Katiyar et al. 2015; Rawat and Katiyar 2015; Ade-Ademilua and Obalola 2008; Kumar et al. 2008). Reduced growth of plants in response to PM can be attributed to the excessive uptake and accumulation of trace elements and alkalinity due to presence of excessive soluble salts on the leaf surface. Furthermore, the toxic effect of PM is augmented by the shading effect on leaf surface. Decrease in chlorophyll content can either be due to direct influence of PM on their biosynthesis or by indirect PM-induced destruction. Increased ROS levels in response to PM may also contribute to chlorophyll destruction (Daresta et al. 2015). Heavy metals such as Pb, Cd, and Cr accumulation by leafy vegetables, pine needles and grasses have been reported extensively (Žalud et al. 2012; Voutsa et al. 1997; Hovmand et al. 1983; Tjell et al. 1979). Trace elements in PM may contribute to decrease in chlorophyll content and chlorophyll a/b ratio of plants (Khudsar et al. 2004).

Presence of heavy metals may cause oxidative stress either by inducing ROS generation within subcellular compartments or by decreasing the enzymatic or nonenzymatic antioxidants because of their affinity with sulfur-containing group (-SH) hastening the senescence (Rai 2016; Gupta et al. 2011).

It is evident from various studies that exposure of plants to PM creates stressful conditions for plants which causes them to activate antioxidant defense system. A significant increase in ascorbic acid content in leaves of trees growing on the roadside in central Varanasi is observed in response to PM (Prajapati and Tripathi 2008). Being an antioxidant, as discussed in previous sections, it helps in combating the stress conditions and preventing leaf senescence. Atmospheric PM10 also triggers ROS production in tomato roots (Daresta et al. 2015).

Dust pH can also alter the pH of plants. For instance, cement dust on hydration releases calcium hydroxide which can increase the alkalinity of leaf surface up to pH 12. This alkaline environment can cause hydrolysis of lipids and wax components, penetrate the cuticle and denature proteins, leading to plasmolysis of leaf (Rai 2016; Guderian 1986; Czaja 1960, 1961, 1962).

Simulated acid rain and iron ore dust deposition in Eugenia uniflora (Surinam cherry) causes decrease in net photosynthesis, transpiration, stomatal conductance and chlorophyll a content (Neves et al. 2009). Decrease in CAT and SOD activities and injuries to membrane as depicted by high electrolyte leakage value in response to simulated acid rain in E. uniflora show the conditions of severe oxidative stress. Similarly, activity loss of CAT and SOD in leaves of Clusia hilariana (Clusia) in response to solid iron PM depicts high oxidative stress (Pereira et al. 2009) because of accumulation of toxic levels of iron that leads to inhibition of enzyme activity (Schutzendubel and Polle 2002). Decrease in total soluble protein contents in response to heavy metal toxicity in various plants such as Platanus orientalis (Oriental plane) and Acer negundo (Boxelder) can be attributed to disturbed protein synthesis mechanism and protein breakdown (Doğanlar and Atmaca 2011). Heavy metals induced lipid peroxidation and fragmentation of proteins due to highly reactive ROS may lead to reduced protein content (Solanki and Dhankhar 2011). Reduced photosynthetic rate in lettuce in response to PM has been shown to limit the supply of metabolic energy for nitrogen assimilation. Moreover, nitrate reductase activity is subjected to inhibition by trace elements (Nagajyoti et al. 2010).

PM affects the general plant growth and physiology as confirmed by extensive research from across the world. With increase in automobiles and industries plants growing near the roads and industries often face stressful conditions. Use of PM-tolerant plant species can be an effective approach to purify the ambient air. However, selection of tolerant and accumulator species depends upon the location and type of PM found in the particular area.

4.8 Summary

Implacable rise in pollutants has seriously deteriorated the quality of air and will continue to do so in coming future. This has imposed serious damaging effects on health of living organisms. In particular, plants are one of the main targets of the air pollutants causing reduction in the yield of crop plants and trees. Various air pollutants such as SO2, NOx, ozone, PM, and fluorides have direct effect on growth and development of plants. Fluoride can cause injury in plants even at very low concentrations of less than 1 ppb in sensitive plants due to its highly electronegative nature. On the other hand, O3 upon entry inside cell decomposes causing an oxidative burst. Nitrogen-containing compounds (NO2–, NH3, and NH4+) exert their phytotoxic effects by interfering with the cellular acid/base homeostasis. SO2-induced injury is a result of generation of more toxic forms such as sulfite and bisulfite in the cellular cytoplasm which causes acidification of cytoplasmic pH affecting the various metabolic processes in cell. The negative effect of these major air pollutants results in altered morphology which is a consequence of altered metabolism. Necrosis, chlorosis, and tip burns appear to be the common symptoms in plants when exposed to these air pollutants. When exposed to pollutants, ROS production takes place that has deleterious effects on plant health which includes destruction of pigments, membrane lipids and proteins, decreased photosynthetic yield, stomatal and leaf injury. In order to protect themselves from the deleterious effects of these pollutants, plants use complex antioxidant defense system which consists of protein and nonprotein components that work together actively against ROS. Variety of studies has been conducted to understand the effect of the individual air pollutants on plant health; however, in natural environment plants are constantly being exposed to combination of these pollutants. Therefore, it becomes important to dissect the underlying mechanisms involved in protection against combination of these air pollutants.