Overview

Reduction of adverse health and environmental effects related to air quality has been the primary driving force for tightening the exhaust emission limits of transport sector for decades. While struggling with the emission regulations and challenging targets for engine efficiency, ever even cleaner cars and engines equipped with dedicated emission control technologies have been introduced.  At the same time, concerns on energy security and global warming are driving towards new liquid and gaseous fuel alternatives. All new technologies should meet the “no harm to health and environment” principle, however, verification of this is challenging for a variety of technologies with potential presence of new, unknown species in the exhaust gases.

Air pollution is world’s largest single environmental health risk. WHO (2014) estimated that approximately 7 million premature deaths are attributable to air pollution exposure. Air pollution also increases respiratory and cardiovascular diseases and cancer. In addition to health effects, air pollution deteriorates vegetation, water and soil. Air pollution causes substantial adverse economic impacts (EEA 2015).

Table 1. Classification of emissions based on their adverse effects on health, environment and global warming.

 

	Health	Environmental effects			Global
	effects	Vege-tation	Acidifi-cation	Eutrophi-cation	warming
CO	x	x
NOx/NO2	x	x	x	x
PM and SOA	x
PN	x
BC	x				x
SO2	x		x
Priority PAHs	x
Aldehydes: formaldehyde, acetaldehyde, acrolein	x	x
1,3-Butadiene	x	x
Aromatics: benzenes, toluene, xylenes	x	x
Methane					x
NH3	x		x	x
N2O					x
Ozone in troposphere caused by VOCs a, CO and NOx	x	x			x
Ozone depletion in stratosphere caused by N2O					x
CO2					x

^a Light olefins, aromatics, aldehydes
 

Legislative limits are rare for the emissions species other than carbon monoxide (CO), total hydrocarbons (HC), nitrogen oxides (NO_x) and particulate matter (PM) for the transport applications. However, a number of unregulated exhaust species are harmful to human health and to the environment, and some of them are also strong greenhouse gases. Moreover, transformation of primary (tailpipe) emissions into secondary products is an important aspect when transport emissions are assessed.

There are several lists of “priority air toxics” that define the most harmful compounds to be taken into account when evaluating exhaust gases from the transport sector. These lists have been defined from various starting points, and consequently, outcomes are not uniform. Diesel engine exhaust itself has been classified as carcinogenic  to humans, Group 1, while gasoline engine exhaust is classified as possibly carcinogenic to humans, Group 2B (IARC, 2013).

The U.S. Environmental Protection Agency (EPA) has defined key mobile-source air toxics (MSATs). The US EPA (2001) MSAT list included 21 compounds, among them acetaldehyde, acrolein, benzene, 1,3‑butadiene, dioxin/furans, diesel exhaust, ethylbenzene, formaldehyde, n-hexane, six metals, MTBE, naphthalene, styrene, toluene and xylene. The US EPA (2007) includes eight key MSATs and gasoline particulate matter. The emission species in this MSAT group are listed below (US EPA 2007).

• Benzene, formaldehyde and 1,3-butadiene are classified as human carcinogens (IARC, 2010, 2012). The lifetime of 1,3-butadiene is short, but it is highly reactive and may also form formaldehyde, acetaldehyde, and acrolein in atmospheric reactions.
• Acetaldehyde has been classified as possible carcinogen by IARC (1999). It may also produce peroxyacetyl nitrate (PAN), a phytotoxicant and mutagen, through reactions with NO_x.
• Acrolein is highly irritating, and long-term inhalation results in chronic inflammation.
• Polycyclic organic matter is found in the gaseous exhaust, particles, or both. It contains a mixture of compounds, for example benzo(a)pyrene, which is classified as a human carcinogen. Many other polyaromatic hydrocarbons (PAHs) and nitro-PAHs have been classified as proven, probable or possible carcinogens to humans.
• Naphthalene is the most abundant PAH in ambient air. There is evidence in rodents that exposure to naphthalene leads to inflammation of the nasal tract and tumors of the nasal epithelium, for example. However, there are no data on carcinogenicity in humans. Case reports suggest that exposure may cause effects in blood cells, such as haemolysis and haemolytic anaemia. (HEI 2007).
• Diesel exhaust has been classified as carcinogenic to humans (Group 1, IARC),
• Gasoline PM: Gasoline engine exhaust is classified as possibly carcinogenic to humans (Group 2B, IARC).

Review of HEI (2007) concluded that the contribution of mobile sources is greatest for 1,3‑butadiene, followed by benzene, formaldehyde, acetaldehyde and acrolein.

In addition to the defined MSAT species, number of particles (PN), especially number of nanoparticles in the lowest size classes below 50 nm, is addressed with potential adverse health impacts. In addition, reduction of mass-based PM emissions does not necessarily reduce PN emissions. (HEI 2002, Kittelson et al. 2002, IARC 2016).

Ozone is harmful to both human health and the environment. It causes irritation of the respiratory system, reduction of lung function and induced asthma, and there is also evidence of induced cardiovascular related morbidity. Ozone contributes to the damage of plants and ecosystems, which may lead to shifts and losses of species (US EPA 2007). Many volatile organic compounds (VOCs) contribute to the formation of ground-level ozone together with nitrogen oxides (NO_x) in the presence of heat and sunlight through complex atmospheric chemistry. (Gaffney and Marley 2011, Carter 2001).

NO_x, sulphur dioxide (SO₂) and ammonia (NH₃) contribute to the acidification causing the loss of animal and plant life. In addition, NH₃ and NO_x bring nutrients in land and water disrupting these ecosystems and leading to eutrophication and changes in species. NH₃ is associated with harmful effects on health and vegetation, and can form ammonium aerosols that affect climate and visibility. SO_x, NO_x and CO₂ can damage materials and buildings by corrosion, biodegradation and soiling caused by particles and by acidifying compounds. (EEA 2015). NH₃ is a catalyst induced emission, both from the three-way catalysts (TWC) and urea-based selective catalytic reduction (SCR) systems for NO_x control for diesel vehicles, though it mainly originates from agricultural sources. (Meija-Centeno 2007, EEA 2012b). 

Besides CO₂, methane (CH₄), black carbon (BC, a constituent of PM), nitrous oxide (N₂O) and ozone precursors increase global warming. (EEA 2015). In the opposite, the PM associated organic carbon, ammonium (NH₄⁺), sulphate (SO₄^2–) and nitrate (NO₃^–) have a cooling effect on climate (Myhre et al. 2013 in IPCC AR5). Methane is emitted from engines and vehicles, particularly when fuelled with natural gas or biomethane. N₂O is induced by catalyst chemistry of (TWC) of the spark-ignited gasoline cars. (Meija-Centeno 2007).

Overall cancer potency of the exhaust gases can be calculated using risk factors (OEHHA 2009, US EPA IRIS, the Nordic Ecolabelling 2008). There are also methodologies to evaluate ozone forming potential, acidification potential, photochemical oxidation creation potential, particulate matter formation potential and marine eutrophication potential of exhaust gases (Querini et al. 2011). Individual VOC species contribute differently to formation of ozone and oxidants, which is evaluated by using a maximum incremental reactivity (MIR) scale to assess the ozone-forming potential (OFP) of any emitted molecule (Carter and Atkinson 1987). These methods do not take into account possible presence of “super-toxics”, which can be harmful at concentrations below detection limits of the analysis methods (for example some nitro-PAHs), or previously unknown exhaust species that are not characterized at all. Thus comprehensive methods and tests are desired. Screening of biological activity of exhaust gases can be conducted by using different tests, for example Ames test for mutagenicity, which is a term related to genotoxicity and carcinogenesis. However, the bacterial test does not reflect in vivo mutagenic activity, nor it is capable to accurately predict the risk of carcinogenicity in mammals. Reactive oxygen and nitrogen species are thought to be related to oxidative stress associated with inflammation and tissue damage in the cells and lungs. Many test methods are available for monitoring oxidative stress or oxidative potential of exhaust gases. IEA-AMF Task 42 studied toxicity of exhaust gases (Czerwinski 2014 link).

Exhaust emissions from new cars and heavy-duty vehicles have been reduced drastically with tightening emission legislations. For example, HEI (2015) reported that the 2007 compliant diesel engines equipped with exhaust gas recirculation (EGR), diesel oxidation catalyst (DOC) and diesel particulate filter (DPF) reduced levels of PM by 90% and those of VOCs and semivolatile organic compounds (SVOCs) by over 90% compared with emissions from old engines. Emissions for new-technology engines were not carcinogenic in in-vivo studies (rats), though a few effects in rat lungs were observed resembling changes seen in earlier studies after long-term exposures to gaseous oxidant pollutants, in particular nitrogen dioxide (NO₂). Low emission level of new cars and heavy-duty vehicles is compensated to some extent by their increasing numbers on road, and by  emission species attached with the emission control technologies, e.g. nitrous oxide (N₂O) and ammonia (NH₃), or with alternative fuels e.g. methane and aldehydes. (Meija-Centeno 2007, IEA-AMF Task 35-2: Rosenblatt et al. 2014, IEA-AMF Task 22: Aakko and Nylund 2003). Many emission species are significant even at low concentrations. In addition, engine-out emissions from internal combustion engines are still high, which is immediately reflected in the tailpipe emissions when emission control technologies are not working properly. All in all, exhaust emissions from on-road transport are still a relevant, particularly when new technologies and alternative fuels are introduced.

Composition of exhaust gas

Complete combustion of fuels produces only carbon dioxide (CO₂) and water, while constituents called traditional “emissions” represent only a small share of the total exhaust gas, below 0.5%(V/V). The major constituents of diesel exhaust are nitrogen, oxygen, water and CO₂. Exhaust gas from gasoline fuelled cars does not contain oxygen, because it is consumed in stoichiometric combustion.

Figure 1. Examples of compositions of the exhaust gases from “diesel” combustion using excess air and stoichiometric spark-ignited “gasoline” combustion. Concentrations are shown as %(V/V).

Air to fuel ratio (AFR) is one of the parameters affecting the exhaust emissions from internal combustion engines (Figure 2). Diesel engines use excess air (lean, AFR>1), while spark-ignited otto engines typically operate close to the stoichiometric air to fuel ratio (AFR~1). In diesel combustion, NO_x and PM emissions tend to be elevated, while emissions of THC and CO are typically at low level. Spark-ignited gasoline cars operating close to stoichiometric air to fuel ratio can use TWC, which efficiently reduces CO, HC and NO_x emissions. Complicated emission control systems consisting of SCR and diesel particulate filter (DPF) are required for diesel engines to achieve similar emission level as for stoichiometric spark-ignited otto engines. Alternative fuels can be used in both diesel and otto engines. Some alternative fuels can assist performance of existing emission control systems (paraffinic diesel), while others may require development/adjustment of aftertreatment technologies (ethanol, methane).

Figure 2. Engine-out emissions from internal combustion engines at different air to fuel ratios (Windawi 1992).

“Emissions”, representing less than 0.5 %(V/V) of the exhaust, include for example the following constituents:

• Carbon monoxide
• Nitrogen oxides and other nitrogen containing compounds, such as NH₃ and N₂O
• PM consisting of elemental carbon, organic compounds, anions (sulphates, nitrates) and metals
• Hydrocarbons, hundreds of compounds, some of them toxic, for example benzene and 1,3-butadiene, or greenhouse gases, such as methane
• Carbonyls, for example formaldehyde, acetaldehyde and acrolein
• Polycyclic aromatic compounds (PAC), for example PAHs, nitro-PAHs and oxy-PAHs

Most of these emission species are fuel- and engine-dependent, but some of them are formed in emission control devices (NH₃, N₂O). Methane is emitted from engines and vehicles, particularly when fuelled with methane containing fuels, natural gas or biomethane. N₂O is induced by catalyst chemistry of TWC of the spark-ignited gasoline cars. Another catalyst induced emission is NH₃, which is associated with harmful effects on health and vegetation, and can form ammonium aerosols that affect climate, and visibility. NH₃ originates mainly from agricultural sources, but also from catalytic reactions in TWCs and the urea-based SCR systems for NO_x control for diesel vehicles. (Meija-Centeno 2007, EEA 2012b).

IARC classification of diesel engine exhaust is carcinogenic to humans (Group 1), and classification of gasoline exhaust is possibly carcinogenic to humans (Group 2B) (IARC 2013). These classifications are assumedly based on studies with old engines. HEI (2015) found emissions from a 2007 new-technology engine to be not carcinogenic in the rat. A few effects in rat lungs were observed resembling changes seen in earlier studies after long-term exposures to gaseous oxidant pollutants, in particular NO₂. The results showed that the 2007 compliant diesel engines equipped with EGR, DOC and DPF significantly reduced levels of PM (90%), VOCs and SVOCs (> 90%) compared with emissions from old engines. The NO_x emissions from the 2007 engines were reduced, however, the full extent of NO_x reduction was seen for 2010 engines equipped with urea-SCR (>90% reduction compared with 2007 engines).

Emission regulations

CO, THC, NO_x and PM emissions from transport applications are typically limited by legislation. In addition to these “regulated” emission species, the following emission regulations are implemented:

• In addition to the mass-based PM limits, a limit to solid particulate number emissions (SPN) was introduced in 2011 for diesel engines (Euro 5b) and in 2014 for petrol engines (Euro 6).
• An NH₃ concentration limit of 10 ppm applies in Europe to Euro VI diesel and gas engines, but not to cars.
• Formaldehyde emissions are regulated in the US.
• Greenhouse gas emissions are regulated in the US.
• NO₂ is limited for retrofitted heavy-duty engines in the US.
• Sulphur oxide (SO_x) emissions are limited through regulations on the sulphur content of fuel. For example, sulphur content of diesel fuel and gasoline is limited to 10 mg/kg in Europe and to 15 mg/kg in the U.S.

The most stringent emission regulations are implemented in California, such as LEV III emission categories in Table 2. Formaldehyde emission from cars has been regulated in the United States for decades.

Table 2. LEV III emission standards in California phased-in over the 2015-2025 (FTP-75 test). Durability 150,000 miles, FTP-75. (www.dieselnet.com 5.7.2016).

		NMOG a +NOx g/mi	CO g/mi	HCHO mg/mi	PM b g/mi
Passenger cars LD trucks ≤ 8500 lbs GVWa Medium-duty passenger vehicles		0.160	4.2	4	0.01
	LEV160	0.160	4.2	4	0.01
	ULEV125	0.125	2.1	4	0.01
	ULEV70	0.070	1.7	4	0.01
	ULEV50	0.050	1.7	4	0.01
	SULEV30	0.030	1.0	4	0.01
	SULEV20	0.020	1.0	4	0.01

^a Non-methane organic gases ^b PM standards will be tightened to 3 mg/mi with phase-in from 2017 to 2021.

The United States has limits for greenhouse gas emissions (Table 3). The CO₂-equivalent in this rule is calculated by using CO₂ equivalence factors of 298 for N₂O and of 25 for CH₄. In addition, the rule includes limits for tailpipe N₂O and CH₄ emissions to prevent increase in these emissions in the future vehicles (www.dieselnet.com 5.7.2016):

• N₂O: 0.010 g/mile
• CH₄: 0.030 g/mile

Table 3. Projected 2012-2016 Fleet-Wide CO₂ and Fuel Economy Compliance Levels in the US. (www.dieselnet.com 5.7.2016).

		Model Year
		2012	2013	2014	2015	2016
Passenger cars	CO2, g/mi	263	256	247	236	225
	CO2 equiv. mpg a	33.8	34.7	36.0	37.7	39.5
	CAFE mpg	33.3	34.2	34.9	36.2	37.8

^a In the CO₂-equivalent standard, the N₂O and CH₄ emissions are added to the CO₂ emissions using a CO₂ equivalence factor of 298 for N₂O and of 25 for CH₄.

Regulations on the exhaust emissions are in some respects less demanding in Europe than in the US. In Europe, greenhouse gases are not regulated, while targets for CO₂ emissions are defined. Progress of the NO_x standards have been slower in Europe than in the US leading to high levels of NO₂ in urban areas in Europe. The EURO 6/VI regulations are expected to alleviate this situation by wider use of the SCR technology (Health Effects Institute 2015). Limits for formaldehyde, N₂O or CH₄ emissions are not implemented in Europe, while they are limited in the US. On the other hand, PN limit is not included in the US regulation, while it is in place in Europe. PN limit in Europe takes into account only solid particles (SPN), while health effects are assumedly related in total particles (wet-PN). Development of the regulated emissions in Europe over the past decades is shown in Figure 3. HC and NO_x emissions are below 20%, PM emissions below 10% and CO emissions below 40 of the level of 1992.

Figure 3. Schematic figure of tightening emission regulations in Europe.

Carbon monoxide (CO)

CO is a colorless, odorless gas, which reduces oxygen delivery to the body's tissues by binding and interfering with heme proteins. The health threat from lower levels of CO is most serious for e.g. persons with impaired cardiovascular systems. Potential effects include damage to the central nervous system, reproduction and prenatal development, and the respiratory system. At sufficient levels, CO is poisonous and can be fatal. (Vallero 2014)

CO contributes to the formation of ground-level ozone, which is harmful to human health and environment.

Nitrogen oxides (NO_x)

The sum of nitric oxide (NO) and nitrogen dioxide (NO₂), both calculated as NO₂, is called nitrogen oxides (NO_x). NO is reactive compound, which oxidizes to NO₂ in atmosphere, rate of oxidation depends on the conditions and on the other compounds present.

Health - NO₂ can irritate the lungs and is addressed with adverse respiratory effects including airway inflammation and increased number and severity of asthma episodes. Inhalation of elevated short-term NO₂ concentrations has been associated with increased hospital emergency room visits for respiratory distress (Vallero, 2014). NO_x reacts in the atmosphere with various compounds to form toxic products, for example organic nitrates, nitroarenes, nitrosamines and peroxyacetyl nitrate (PAN, a phytotoxicant and mutagen).

Ozone - NO_x contribute to formation of ground-level ozone when NO_x and VOC_s react in the presence of heat and sunlight (see Chapter 3.13).

Acidification, eutrophication - NO_x can have adverse effects on terrestrial and aquatic ecosystems through acid rain and eutrophication of waters due to increase in nitrogen containing nutrients. NO₂ is a strong oxidizing agent that can form nitric acid (HNO₃), which falls to earth as acid rain. Acid rain also deteriorates materials, such as historical buildings and monuments.

PM - NO_x and its oxidation products can form small particles in reactions with ammonia, moisture, and other compounds (see PM).

Visibility Impairment - Nitrate particles and NO₂ can reduce visibility.

(Websites as in August 2016)

Nitrous oxide (N₂O)

N₂O is a nonflammable, colorless gas commonly called “laughing gas”. N₂O is used for example as an anesthetic agent. Adverse effects are associated with N₂O abuse, such as breathing difficulty.

N₂O is a strong greenhouse gas with a global warming potential (GWP, 100-year) 265 relative to CO₂. Lifetime of N₂O is 121 years. (Myhre et al. 2013 in IPCC AR5).

The N₂O probably plays the dominant role in the depletion of stratospheric ozone layer when concentrations of halocarbons reach the pre-industrial concentrations. (Portmann 2012).

Ammonia (NH₃)

NH₃ is corrosive and can cause permanent injury in the eye. Dermal exposure to NH₃ or its solutions may result in irritation and alkali burns at sufficient concentrations. Ingestion of NH₃ solution causes rapid signs and symptoms and extensive alkali burns to the aerodigestive tract. In severe cases perforation of the stomach or oesophagus may occur. Aspiration of ammonia following ingestion may also lead to respiratory complications. Chronic oral exposure to NH₃ may lead to osteoporosis secondary to chronic metabolic acidosis. Exposure to a massive concentration of NH₃ gas may be fatal within minutes. (Public Health England 2015).

Sulfur dioxide (SO₂)

SO₂ is a precursor for compounds that are harmful to people and the environment. SO₂ is a respiratory irritant, damages crops, and causes visibility problems. SO₂ and other sulphur oxides form acids in the atmosphere, particularly sulfuric acid (H₂SO₄), a key component of acid rain. SO₂ also causes crop and material damage when acidic liquid and solid aerosols are deposited. (Vallero 2014).

Volatile organic compounds (VOCs)

In Europe, VOCs are defined as organic compounds having an initial boiling point less than or equal to 250 °C at 101.3 kPa (Directive 2004/42/CE). Examples of VOCs are hydrocarbons, alcohols, ethers, esters and aldehydes. Some of the VOCs are toxic and some contribute to the ozone formation (see ozone). Adverse health effects are identified for example for the following mobile-source VOCs:

• Benzene increases the risks of acute myeloid leukaemia. Benzene seems to affect haematologic indices at exposure concentrations lower than those reported previously. (HEI 2007). IARC (2012) has defined benzene as carcinogenic to humans, Group 1.
• 1,3‑Butadiene has a short lifetime, but it is reactive forming other MSATs, such as formaldehyde, acetaldehyde and acrolein. Concentrations may be elevated in the tobacco smoke. 1,3‑Butadiene may cause lymphohaematopoietic cancers in high-exposures.(HEI 2007). IARC (2012) has defined 1,3-butadiene as carcinogenic to humans, Group 1.
• Formaldehyde is present predominantly indoors, but transport is a source of ambient concentrations, both directly and through photochemical activity. In Brazil, ambient formaldehyde concentrations increased along with increased use of natural gas vehicles. Formaldehyde is an irritant to the eyes, skin and respiratory tract in humans with possible increase in asthma. (HEI 2007). IARC (2012) has defined formaldehyde as carcinogenic to humans, Group 1.
• Acetaldehyde is present in for example in some foods, but it originates also from mobile sources. The use of ethanol as fuel may increase acetaldehyde emissions in air. Acetaldehyde causes irritation to the eyes, skin and respiratory tract and induces cellular inflammation. Acetaldehyde is a carcinogen in rodents, but the data on its carcinogenicity in humans are inadequate. (HEI 2007) IARC has defined acetaldehyde as Group 1 carcinogen when associated with consumption of alcoholic beverages (IARC 2012) Indirect effect of acetaldehyde is through reaction with NO_x in the atmospheric photochemical system producing peroxyacetyl nitrate (PAN), which is a phytotoxicant and mutagen.(ref)
• Acrolein is formed from 1,3‑butadiene in atmosphere in addition to the direct sources, such as tobacco smoke. Environmental concentrations have been close to those causing irritation. Acrolein is irritant to the respiratory tract. Chronic inhalation results in inflammation. (HEI 2007). IARC (1995) defined acrolein as “not classifiable as to its carcinogenicity to humans (Group 3 carcinogen).

Particulate mass (PM) and number (PN), black carbon (BC)

PM from internal combustion engines consists of elemental carbon, organic compounds, metals, sulphates, nitrates and other constituents originating from fuel and lube oil in the combustion process and in the aftertreatment devices. Primary PM forms secondary organic aerosols (SOA) in the atmospheric reactions. Outdoor PM consists also of other species, such as dust and dirt.

Human health concerns of PM include effects on breathing and the respiratory system, damage to lung tissue, and premature death. BC associated in particles increase the global warming potential, while other constituents of PM mainly have a cooling effect on climate.

Figure 4. Deposition of particles into human body (Altshuler 2002).

Effects of PM on human health depend on their size and composition. The primary mechanisms for deposition of particles in the respiratory tract are sedimentation, impaction, and diffusion, which depend on the diameter of the particle. Coarse particles are removed e.g. by swallowing or coughing (Figure 4). Particles below 0.1 μm can reach the surface of the lung. These particles can be removed by scavenging cells (macrophages), but they may also drift into lymphatic vessels, and possibly further into the blood. (DEFRA 2001). Small particles penetrate deeply into the lungs and can cause or worsen respiratory disease such as emphysema and bronchitis, and aggravate existing heart disease.

More than 90% of diesel particles are in the size class below 0.1 μm, ultrafine particles (UPs), and nanoparticles below 50 nm may occur (Figure 5). Diesel particles have a large surface area, which may adsorb various compounds that can be toxic, mutagenic and carcinogenic (e.g., PAHs). (HEI 2002, Kittelson 2002, IARC vol 109, 2016).

Li et al. (2016) found that UPs have detrimental effects on both the cardiovascular and respiratory systems, including a higher incidence of atherosclerosis and exacerbation rate of asthma. UPs can also play a role in allergen sensitization. The inflammatory properties of UPs can be mediated by reactive oxygen species, leading to the generation of proinflammatory cytokines and airway inflammation. In addition, UPs might be able to alter cellular function, penetrate intracellularly and potentially cause DNA damage. (Li et al. 2016).

The toxicological and epidemiological data suggest that the chemical composition of particles may be important contributor to the health effects (Jalava et al. 2009, 2010a).

IARC (Vol 109, 2016) has defined particulate matter of outdoor air pollution as carcinogenic to humans, Group 1.

 

Figure 5. Major features of particle-size distributions from diesel exhaust  (IARC vol 109, 2016).

 

Polyaromatic hydrocarbons (PAHs), and their derivatives

Polycyclic organic matter, POM, defined by the US EPA as “Priority Air Toxic”, consists of hundreds of different compounds, for example PAH and PAHs containing heteroatoms (N, S, O). PAHs are neutral, nonpolar aromatic molecules found in fossil fuels and formed also in incomplete combustion of organic matter (e.g. in engines). Mobile sources may be significant contributors to the ambient PAH concentrations in urban areas. Diesel vehicles are known PAHs emitters, however, gasoline vehicles may also emit high PAH concentrations at cold temperatures (Aakko-Saksa et al. 2011). Cigarette-smoking and food-derived sources, may lead to exposure to PAHs. (HEI 2007).

Naphthalene is the most abundant PAH in ambient air. There is evidence in rodents that exposure to naphthalene leads to inflammation of the nasal tract and tumors of the nasal epithelium. However, there are no data on carcinogenicity in humans. Case reports suggest that exposure may cause effects in blood cells, such as haemolysis and haemolytic anaemia. (HEI 2007).

A few PAHs are potent carcinogens, for example, benzo(a)pyrene is a PAH compound whose metabolites are mutagenic and highly carcinogenic. In general PAHs have been identified as carcinogenic and mutagenic and are considered therefore pollutants of concern with potential health impacts.

The US EPA (1998) defined 16 priority PAHs, many of which are classified as carcinogenic, Group 1, probably carcinogenic, Group 2A or possibly carcinogenic, Group 2B, according to the IARC classification (IARC 2008, 2011). In a list of mobile-source air toxics defined by the US EPA (2007), 7 priority PAHs are included. European directive 2004/107/EC relating to arsenic, cadmium, mercury, nickel and polycyclic aromatic hydrocarbons in ambient air, defines seven priority PAHs: benzo(a)pyrene, benzo(a)anthracene, benzo(b)fluoranthene, benzo(j)fluoranthene, benzo(k)fluoranthene, indeno(1,2,3-cd)pyrene, and dibenz(a,h)anthracene.” These PAHs are classified in Group 2A and Group 2B by IARC. In addition to these definitions, there are several other lists of “Priority PAHs” to describe the cancer-related risks of substances. For example, (Kokko et al. 2000) presented a sum of 14 PAHs based on the US EPA priority list of 16 PAHs, from which naphthalene, acenaphthene and acenaphthylene were excluded, because these low-molecular weight PAHs significantly decrease the repeatability of the results. On the other hand, benzo(e)pyrene was included as it is listed by NIOSH and VDI 3872, for example. Substitued nitro-PAHs and oxy-PAHs may be present in the exhaust gases. For example, the IARC classification for 2-nitropyrene is Group 2A and for 1,8-dinitropyrene Group 2B.

A Working Group of the European Commission prepared a position paper to review knowledge of PAHs in ambient air (EU 2001). As part of the study, toxic equivalency factors (TEFs) relative to benzo(a)pyrene were reviewed. Table 4 summarizes the selected lists for priority PAHs and the TEFs relative to benzo(a)pyrene. Supplementary TEFs are shown for fluorene (Flu) and 7,12-dimethylbenz(a)anthracene (DMBA) (Collins et al. 1998). A total cancer potency for PAHs can be evaluated by calculating the BaP equivalent using Equation (1).

                                            (1)

BaP_eq = Benzo(a)pyrene equivalent (µg/km)

TEF_x  = Relative toxic equivalency factor for individual PAH compounds in Table 4.

PAH_x  = Mass emissions (µg/km) of PAH compound

Table 4 summarizes the selected lists for priority PAHs and the toxic equivalency factors relative to benzo(a)pyrene.

Table 4. a) 16 PAHs defined by the US EPA (1998) b) 7 PAHs defined by the US EPA (2007) and c) 7 PAHs defined in European Directive 2004/107/EC. TEF represents toxic equivalency factors relative to benzo(a)pyrene.

N

Ace

Acy

Flu

Phe

An

F

P

BaA

DMBA

Chr

BbF

BjF

BkF

BaP

BeP

IP

DBahA

BghiP

IARC*

2B

3

3

3

3

3

3

2B

2B

2B

2B

2B

1

3

2B

2A

3

Ring **

2/2

3/2

3/2

3/2

3/3

3/3

4/3

4/4

4/4

4/4

4/4

5/4

5/4

5/4

5/5

5/5

6/5

5/5

6/5

TEF

***

0.0005– 0.01

0– 0.01

0– 0.06

0– 0.081

0.005– 0.145

0.001– 0.89

0.06– 0.14

0.045– 0.061

0.03– 0.1

1

0– 0.004

0– 0.232

0.69– 5

0.01– 0.03

a (16)

x

x

x

x

x

x

x

x

X

X

X

X

X

X

X

x

c (US 7)

X

X

X

X

X

X

X

d (EU7)

X

X

X

X

 * No. of rings/aromatic rings    ** Group 1: carcinogenic; Group 2A: probably carcinogenic; Group 2B: possibly carcinogenic; Group 3: not classifiable with regard to carcinogenicity; Group 4: probably non-carcinogenic.
N= Naphthalene, Ace = Acenaphthene, Acy = Acenaphthylene, Flu = Fluorene, Phe = Phenanthrene, An = Anthracene, F = Fluoranthene, P = Pyrene, BaA = Benz(a)anthracene, DMBA = 7,12-dimethylbenz(a)anthracene, Chr = Chrysene, BbF = Benzo(b)fluoranthene, BkF = Benzo(k)fluoranthene, BjF = Benzo(j)fluoranthene, BaP = Benzo(a)pyrene, IP = Indeno(1,2,3-cd)pyrene, ZBahA = Dibenz(ah)anthracene, BghiP = Benzo(ghi)perylene.

Toxical effects

Screening of biological activity of exhaust gases can be conducted by using different tests, for example Ames test for mutagenicity, which is a term related to genotoxicity and carcinogenesis. However, the bacterial test does not reflect in vivo mutagenic activity, nor it is capable to accurately predict the risk of carcinogenicity in mammals. Reactive oxygen and nitrogen species are thought to be related to oxidative stress associated with inflammation and tissue damage in the cells and lungs. Many test methods are available for monitoring biological activity of the exhaust gases.

Biological tests are often carried out on the PM of the exhaust gases. However, a comprehensive view on the toxical effects of the exhaust gases would require exposure of the living cells or cell cultures to the exhaust aerosol as a whole (i.e. gaseous components and particles). IEA-AMF Annex 42 gathered information on the studies on toxicity of exhaust gases. Research activities on toxicology have been conducted in several countries with focus on different emission sources using epidemiological or cohort studies, exposures in vivo (humans or animals) and exposures in vitro. Harmonized international biological test method with a holistic approach of the exposure of human lung cells to the exhaust aerosol as emitted is not established. Further efforts are needed to develop reliable methodology (IEA-AMF Task 42: Czerwinski, J. 2014).

Ozone, tropospheric and stratospheric

Ground-level, tropospheric ozone

Ground-level ozone (O₃) causes adverse health effects, for example irritation of the respiratory system, coughing and reduction of lung function. Ozone may aggravate asthma. There is also evidence of the effect of ozone on, for example, cardiovascular-related morbidity. Potential interactions between ozone and PM have been suggested. Ozone contributes to damage to plants and ecosystems. The adverse effects of ozone on forest and other natural vegetation may lead to species shifts and loss from the affected ecosystems, resulting in the loss or reduction of related goods and services (US EPA 2007). The tropospheric ozone (lifetime ~12 years) increases global warming. Ozone is not an emitted as such, while it is formed by the precursor emissions of CO, VOCs and NO_x (Akimoto et al. 2011).

Formation of ozone

Ground-level tropospheric ozone is created in the presence of NO₂, VOCs, heat and sunlight (i.e. photochemical reactions). Ozone precursors arise from both natural and anthropogenic sources. Urban areas may have high ozone levels on warm, sunny days, but even rural areas may experience elevated ozone levels due to transported emissions with the movement of an air mass from one region to another (Vallero 2014).

The simplified summary of complex formation of ozone in the troposphere is presented here based on Drechsler (2004). Ozone is formed in the troposphere by addition of atomic oxygen to molecular oxygen (2).

                      (2)

The atomic oxygen needed for this reaction is produced from photolysis of NO₂ (3).

              (3)

The reaction ends by reaction of ozone and NO back to NO₂ and O₂, forming a nitrogen cycle. When these reactions are in balance, the net ozone concentration does not increase or decrease.

When ratio of the NO₂ to NO is low, ozone is not accumulated by the nitrogen cycle. Ozone accumulates only when excessive NO₂ is formed and ozone is not destroyed. The photochemical oxidation of VOCs, such as hydrocarbons and aldehydes, provides the pathway to formation of excessive NO₂.

VOCs are oxidized in the atmosphere typically driven by hydroxyl radical (OH^.) attack (4) to form peroxy radical. R can be hydrogen or any organic fragment. Hundreds of VOC species participate in thousands of similar reactions.

      (4)

The key reaction in the VOC oxidation cycle is the conversion of NO to NO₂ by the radical transfer reaction (5). This production of NO₂ is necessary to generate atomic oxygen (3) and further ozone (2).

(5)

Ozone is consumed in the presence of for example water vapor, nitrous acid (HONO) and hydrogen peroxide (formed by hydroxyl radical). Reaction of NO₂ with OH produces nitric acid, HNO₃, which is a sink of NO₂ and radical thus inhibiting the net ozone formation. However, in some conditions HNO₃ may regenerate to NO₂. (Drechsler 2004).

In the early morning, the urban NO_x is mainly in a form of NO, because free radicals are not sufficiently present to convert of NO to NO₂. When photolysis of VOCs starts, NO₂ becomes dominant and ozone builds up. VOC reactions are relatively slow and thus the highest ozone concentrations may be observed many kilometres from the emission sources. During the night, NO and ozone combine to form NO₂ and oxygen until either of the reactants is consumed. HONO may assists ozone formation when sunlight breaks it down to NO and OH, which further reacts with VOCs (4, 5). (Drechsler 2004).

VOCs are necessary to generate high concentrations of ozone, but NO_x emissions can be the limiting factor for the high ozone concentrations. When the NO_x concentration is high and the VOC concentration low (VOC/ NO_x ratio low, "VOC-limited", NO_x tends to inhibit ozone formation. When the VOC concentration is high relative to NO_x (VOC/ NO_x ratio high, " NO_x -limited"), NO_x tends to generate ozone (Drechsler 2004).

Photochemical reactivity of VOCs

Photochemical reactivity describes a VOC's ability to participate in photochemical reactions to form ozone in the atmosphere. Examples of the reactive VOCs in California include propene, m-xylene, ethene, and formaldehyde. (Drechsler et al. 2004).

Individual VOC species contribute very differently to formation of oxidants and ozone. Carter and Atkinson (1987) developed a maximum incremental reactivity (MIR) scale to assess the ozone-forming potential (OFP) of any emitted molecule (Equation 6).

OFP = S (MIR x mass emissions)          (6)

The MIR values for selected individual hydrocarbons and oxygen-containing compounds are shown in Table 5 (Carter 2010).

Table 5. Maximum incremental reactivity (MIR) values of selected compounds (Carter 2010).
 

	MIR g ozone/g VOC			MIR g ozone/g VOC
carbon monoxide	0.056		ethanol	1.53
methane	0.0144		isobutanol	2.51
ethane	0.28		n-butanol	2.88
ethene	9.00		ETBE	2.01
propane	0.49		formaldehyde	9.46
propene	11.66		acetaldehyde	6.54
acetylene	0.95		acrolein	7.45
isobutene	6.29		propionaldehyde	7.08
1,3‑butadiene	12.61		crotonaldehyde	9.39
benzene	0.72		methacrolein	6.01
toluene	4.00		butyraldehyde	5.97
ethyl benzene	3.04		benzaldehyde	-0.67
m-xylene	9.75		valeraldehyde	5.08
p-xylene	5.84		m-tolualdehyde	-0.59
o-xylene	7.64		hexanal	4.35

Stratospheric ozone

Ozone occurs naturally in the stratosphere approximately 10 to 30 miles above the earth’s surface and forms a layer that protects life on earth from the sun’s harmful rays. The major ozone losses have been due to the halocarbons gases. The N₂O probably plays the dominant role in the depletion of stratospheric ozone layer when concentrations of halocarbons reach the pre-industrial concentrations. (Portmann 2012).

Risk factors and external costs for emissions

Emissions impose indirect, external costs on society related to impacts in health and environment and climate change. The monetary values of these impacts have been evaluated to determine the lifetime costs of, for example, exhaust emissions from transport vehicles. Directive 2009/33/EC defines the following external costs for CO2, NMHC, NO_x and PM:

o   CO₂                                                        €30–40/tonne

o   NMHC (without methane)                     €1000/tonne

o   NO_x                                                        €4400/tonne

o   PM                                                         €87 000/tonne.

There are also published external costs for CO and HC emissions in addition to those for NO_x, PM_2.5 and CO₂ emissions, for example defined by Tiehallinto (2001) in Finland:

o   CO                                                         €29/tonne

o   HC (with methane)                                €62/tonne.

Risk factors for calculating the cancer potency of exhaust gas, as defined by OEHHA (2009), US EPA IRIS (2010) and The Nordic Ecolablelling (2008), are shown in Table 6. OEHHA (2009) defines cancer unit risks and potency factors for 107 carcinogenic substances or groups of substances. The US EPA IRIS, Integrated Risk Information System, is a human health-assessment program that evaluates quantitative and qualitative risk information for effects that may result from exposure to environmental contaminants. The Nordic Swan labelling criteria for biofuels define substances, which are measured in accordance with a particular protocol, and calculate the cancer potency of exhaust gas using risk factors (Nordic Ecolabelling 2008).

The most significant differences in the risk factors defined by different organizations concern ethene and propene emissions, which are included in Nordic Ecolabelling but not in the other definitions. Törnqvist et al. (1994) reported that ethene is metabolized in animals and in humans to a probable human carcinogen, ethylene oxide. Similarly, propene is metabolized to propylene oxide.

Table 6. Substances and risk factors for calculating the cancer potency of exhaust gas according to OEHHA (2009), US EPA IRIS (2010) and Nordic Ecolabelling (2008).

Substance	Unit Risk Factor (µg/m3)-1			Normalized a
	Nordic Ecolabelling	OEHHA 2009	US EPA IRIS 2010
Particulate matter	7 x 10-5	30 x 10-5	insuff. Data	177
Benzene	0.8 x 10-5	2.9 x 10-5	(0.22-0.78) x 10-5	17
Formaldehyde	10 x 10-5	0.6 x 10-5	1.3 x 10-5	4
Acetaldehyde	0.2 x 10-5	0.27 x 10-5	0.22 x 10-5	2
Ethene	5 x 10-5			17
Propene	1 x 10-5			3
1,3‑Butadiene	30 x 10-5	17 x 10-5	3 x 10-5	100
PAH (including benzo(a)pyrene) b	2800 x 10-5			9333

^a In the normalization, 1,3-Butadiene = 100. OEHHA 2009 factors are used for substances other than ethene, propene and PAH, for which factors of Nordic Ecolabelling are used. ^b Toxic equivalence factors are presented in PAH Chapter.

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