This section reviews linkages between pollutants and human health in a little more detail. It will beuseful to have an understanding of these linkages when, later in the document, we examinepollutant emission levels from a range of fuels in the most significant energy-intensive applications.
Table 7.1, from a 2009 report published by the Victoria Transport Policy Institute, Canada (VPI 2009)summarises the key health effects of some common pollutants.
7.1 Regulated (Criteria) Pollutants
7.1.1 Particulates (PM)
"Particulate matter," also known as particle pollution or PM, is a complex mixture of extremely small particles and liquid droplets. Particle pollution is made up of a number of components, including acids (such as nitrates and sulphates), organic chemicals, metals, and soil or dust particles.
he size of particles is directly linked to their potential for causing health problems. The main health concerns relate to particles that are 10 micrometers in diameter or smaller because those are the particles that generally pass through the throat and nose and enter the lungs. Once inhaled, these particles can affect the heart and lungs and cause serious health effects. EPA groups particle pollution into two categories: "Inhalable coarse particles," such as those found near roadways and dusty industries, are larger than 2.5 micrometers and smaller than 10 micrometers in diameter. "Fine particles," such as those found in smoke and haze, are 2.5 micrometers in diameter and smaller. These particles can be directly emitted from sources such as forest fires, or they can form when gases emitted from power plants, industries and automobiles react in the air.
7.1.2 Oxides of Nitrogen (NOx)
The term "Oxides of Nitrogen" covers several gaseous compounds, the most significant of which are nitric oxide (NO), nitrogen dioxide (NO2) and nitrous oxide (N2O).
These compounds are formed by a reaction between oxygen and nitrogen during high-temperature combustion, such as in an internal combustion engine or a high-temperature flame. Although these compounds are chemically different, they are often referred to collectively as NOx. NOx affects human health in two ways. Firstly, in their own right they irritate the eyes and the lungs and are believed to lower the body's resistance to infection. These symptoms are most severely experienced by those people who already have asthma. Nitrogen dioxide has also been proved to also adversely affect plant life.
Clinical studies have shown a relationship between hospital admissions and ambient NOx levels for respiratory problems experienced by otherwise healthy people. But the strongest reactions are encountered by patients who have pre-existing respiratory illnesses. Table 7.2 below provides some
examples.
Table 7.2: Examples of Dose Response to Excess Levels of Nitrous Oxide (NAS 1997)
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In a second health-related environmental impact, NOx reacts with volatile organic compounds (VOCs)
in the presence of sunlight to form ozone (O3). Ozone is a precursor of photochemical smog, and is discussed separately in this section.
The temperatures and pressures found in the combustion of internal combustion engines are ideal for the formation of NOx, and in some American cities over 60% of all ambient NOx is attributed to motor vehicle sources.
But motor vehicles are not the only source. Industrial engines, furnaces and many industrial
processes also generate these compounds. Even nature is a source, with lightning strikes and even the decomposition of micro-bacteria in the soil making a contribution. From a climate change perspective nitrous oxide is of some significance. Although it is generally emitted in relatively low amounts, it is an extremely powerful greenhouse gas with a CO2 equivalence
of around 410. This number means that one tonne of nitrous oxide has the same impact on climate
change as 410 tonnes of CO2.
7.1.3 Volatile Organic Compounds (VOCs), including Hydrocarbons (HC)
Volatile Organic Compounds (VOCs) are compounds containing at least one carbon atom, excluding carbon monoxide and carbon dioxide, which evaporate readily to the atmosphere. VOCs include a wide range of individual substances from many substance classes such as hydrocarbons, halocarbons and oxygenates.
Major VOC emission sources are the organic solvents used in many consumer and commercial
products such as cleaning products, paints, commercial printing inks; transportation sector activities such as the exhaust emissions from cars and trucks; various industrial processes such as chemical manufacturing; and combustion of fossil and biomass fuels. Not all VOCs originate from man-made sources, however, in more populated and industrial areas man made emissions predominate. When VOCs are released to the atmosphere, they can react with other chemicals, notably oxides of nitrogen, in photochemical reactions to form ground-level ozone and particulate matter. These two air pollutants are the main ingredients of smog and cause serious health effects for humans, including many thousands of premature deaths, hospital admissions and emergency room visits every year.
Almost all ground-level ozone and in the order of two-thirds of particulate matter are formed in the atmosphere through the reactions of precursor substances, with VOCs being one of the most
significant. Consequently, reduction of atmospheric levels of particulate matter and ozone must be accomplished through reductions of precursors, such as VOCs. A number of hydrocarbon compounds, classified as “air toxics” are extremely hazardous to humans,
but many are only generated in very small quantities. Some air toxics are known to be carcinogenic and this group of chemicals is also suspected to play a role in the rapid growth of a number of “20th century” illnesses, including asthma. However, because their ambient concentrations are extremely low, it has not yet been possible to reliably establish dose response characteristics, nor to place a direct monetary cost on their exposure effects. Air toxics are discussed in some detail in Section 7.2.
7.1.4 Ozone (O3) Ozone is a gas simply composed of three oxygen atoms.
It is not usually emitted directly into the air, but at ground-level is created by a chemical reaction between oxides of nitrogen (NOx) and volatile organic compounds
(VOCs) in the presence of sunlight. Ozone has the same (Picture courtesy of US EPA)
53 chemical structure whether it occurs high above the earth or at ground-level, and can be "good" or "bad," depending on its location in the atmosphere. In the earth's lower atmosphere, ground-level ozone is considered "bad."
Motor vehicle exhaust and industrial emissions, gasoline vapours, and chemical solvents as well as natural sources emit NOx and VOCs that help form ozone, which is the primary constituent of
photochemical smog.
Many urban areas tend to have high levels of ground level ozone and its attendant smog haze, but even rural areas are also subject to increased levels when wind carries ozone and pollutants that form it long distances from their original sources.
Health Effects
People with lung disease, children, older adults, and people who are active can be affected when
ozone levels are unhealthy. Numerous scientific studies have linked ground-level ozone exposure to a variety of problems, including:
• airway irritation, coughing, and pain when taking a deep breath;
• wheezing and breathing difficulties during exercise or outdoor activities;
• inflammation, which is much like a sunburn on the skin;
• aggravation of asthma and increased susceptibility to respiratory illnesses like pneumonia
and bronchitis; and,
• permanent lung damage with repeated exposures.
Environmental Effects
Ground-level ozone can have detrimental effects on plants and ecosystems. These effects include:
• interfering with the ability of sensitive plants to produce and store food, making them more
susceptible to certain diseases, insects, other pollutants, competition and harsh weather;
• damaging the leaves of trees and other plants, negatively impacting the appearance of
urban vegetation, as well as vegetation in national parks and recreation areas; and
• reducing forest growth and crop yields, potentially impacting species diversity in
ecosystems.
Ozone also damages vegetation and ecosystems. In the United States alone, it is responsible for an estimated US$500 million in reduced crop production each year.
7.1.5 Carbon Monoxide (CO)
Carbon Monoxide (CO) is a colourless, odourless, poisonous gas composed of one atom each of
carbon and oxygen. It is formed when carbon-based fuel is not burned completely.
Motor vehicle exhaust is the most significant source of carbon monoxide in most developed
countries, and in highly urbanised areas, motor vehicles can account for up to 95% of the total.
Other non-road engines and vehicles (such as construction equipment) can account for the remaining engine-generated carbon monoxide emissions. Other sources include industrial processes (such as metals processing and chemical manufacturing), residential wood burning, and natural sources such as forest fires.
Exposure to indoor carbon monoxide can often be more dangerous than breathing outdoor
concentrations. Woodstoves, solid fuel heaters and hearths, cigarette smoke, gas and kerosene
space heaters are sources of carbon monoxide indoors and concentrations can rise to dangerous
levels if there is insufficient ventilation. Most LP Gas heaters are equipped with an oxygen depletion sensor which automatically turns off the heater if there is insufficient ventilation to sustain complete combustion.
54 Carbon monoxide can cause harmful health effects by reducing oxygen delivery to the body's organs (like the heart and brain) and tissues. Oxygen is transported around the body via the red blood cells by binding to a substance within the red blood cells called haemoglobin, which is also responsible for their red colour.
Haemoglobin takes up oxygen as blood passes through the lungs, and at the same time carbon
dioxide, produced by the body's metabolism, is released from the blood into the exhaled breath. The combination of oxygen with haemoglobin is called oxyhaemoglobin and this 'oxygenated' blood is carried away from the lungs through the bloodstream to all the tissues of the body.
Carbon monoxide can also bind to haemoglobin but does so about 240 times more tightly than
oxygen, forming a compound called carboxyhaemoglobin. This means that if both carbon monoxide and oxygen are inhaled, carbon monoxide will preferentially bind to haemoglobin. This reduces the amount of haemoglobin available to bind to oxygen, so the body and tissues become starved of oxygen.
Carboxyhaemoglobin also has direct effects on the blood vessels of the body - causing them to
become 'leaky'. This is seen especially in the brain, causing the brain to swell, leading to
unconsciousness and neurological damage.
The health threat from lower levels of carbon monoxide is most serious for those who suffer from heart disease, like angina, clogged arteries, or congestive heart failure. For a person with heart disease, a single exposure to carbon monoxide at low levels may cause chest pain and reduce that person's ability to exercise; repeated exposures may contribute to other cardiovascular effects.
But even healthy people can be affected by high levels of CO. People who breathe high levels of
carbon monoxide can develop vision problems, reduced ability to work or learn, reduced manual
dexterity, and difficulty performing complex tasks. At extremely high levels, carbon monoxide is poisonous and can cause death.
Carbon monoxide also contributes to the formation of ground level ozone, which can trigger serious
respiratory problems (see Section 7.1.4).
7.1.6 Fuel Sulphur Content and Sulphur Dioxide (SO2)
Sulphur dioxide causes a wide variety of health and environmental impacts because of the way it
reacts with other substances in the air. Particularly sensitive groups include people with asthma who are active outdoors and children, the elderly, and people with heart or lung disease. Peak levels of sulphur dioxide can cause temporary breathing difficulty for people with asthma who are active outdoors. Longer-term exposures to high levels of sulphur dioxide gas and particles cause respiratory illness and aggravate existing heart disease.
Sulphur dioxide also reacts with other chemicals in the air to form tiny sulphate particles. When
these are inhaled, they gather in the lungs and are associated with increased respiratory symptoms and disease, difficulty in breathing, and even premature death.
When sulphur dioxide and nitrogen oxides react with other substances in the air they can form acids, which fall to earth as rain, fog, snow, or dry particles – this phenomenon is commonly described as “acid rain”, which may be carried by the wind for hundreds of kilometres.
Acid rain damages forests and crops, changes the makeup of soil, and makes lakes and streams acidic and unsuitable for fish. Continued exposure over a long time changes the natural variety of plants and animals in an ecosystem.
Sulphur dioxide is generated in huge quantities, as Figure 7.3 below illustrates. (US EPA 2002)
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Figure 7.3: Annual Sulphur Dioxide Emissions in the USA (2002), note logarithmic scale
Given the extensive human health impacts and acid rain damage to crops, ecology, buildings and
infrastructure, there is clearly a strong imperative to minimise emissions of this pollutant.
Although considerable progress has already been made through the mandating of low sulphur
gasoline and diesel fuels, and the introduction of emission reduction measures for power stations,
the chart shows that there is considerable scope for further reductions in other areas.
Particle emission rates from diesel engines have a linear relationship with sulphur content in the fuel.
The following chart illustrates this relationship.
Figure 7.4: Diesel Fuel Sulphur Content Versus Particle Emissions
Testing commissioned by the Australian Government (EA, 2003), summarised in Figure 7.4, utilised six fuels, with sulphur content ranging from 24ppm to 1700ppm. Testing was performed in an independent heavy-duty emission testing facility (Parsons Australia), using the transient “real world” composite urban emissions drive cycle (CUEDC). Two medium-duty diesel vehicles were tested, and the chart represents the averaged emission rates on each fuel. The high sulphur fuel effectively increased PM emissions by 300mg/km, to double the “base” emissions for these vehicles (no particle filter installed).
Relationship between Sulfur Content and Particle Emissions (Australian Testing)
0
100
200
300
400
500
600
700
0 500 1000 1500 2000
Sulfur (ppm)
PM (mg/km)
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High sulphur fuels also inhibit the use of modern pollution control technologies, including exhaust
catalyst systems and diesel particle filters. Sulphur “poisons” the active surfaces of these devices and can seriously degrade their effectiveness.
LP Gas contains only very small concentrations of sulphur, and consequently emits little or no sulphur dioxide. It is the ideal energy source to replace many of the sulphur-bearing fuels still in use, particularly coal heaters and many industrial process heat sources.
7.1.7 Lead (Pb)
Lead is a widely used metal that, once released to the environment, can contaminate air, food,
water, or soil. Exposures to even small amounts of lead over a long time can accumulate to reach
harmful levels. Short-term exposure to high levels of lead may also cause harm. Lead can adversely affect the nervous, reproductive, digestive, cardiovascular blood-forming systems, and the kidney. In men, adverse reproductive effects include reduced sperm count and abnormal sperm. In women, adverse reproductive effects include reduced fertility, still-birth, or miscarriage. Children are a sensitive population as they absorb lead more readily and their developing nervous system puts them at increased risk for lead-related harm, including learning disabilities.
Lead additives were frequently used to raise the octane rating of gasoline and were a major source of airborne lead pollution. Most developed countries now ban the use of these additives. LP Gas contains no lead.
7.2 Air Toxic Compounds
Toxic air pollutants, also known as hazardous air pollutants (HAP), are those pollutants that are
known or suspected to cause cancer or other serious health effects, such as reproductive effects or
birth defects, or adverse environmental effects.
The US EPA is lists 187 pollutants as “Air Toxics”.
Although these chemicals are known to be
extremely hazardous to humans, many of them
exist in only extremely low concentrations in
ambient air, making it extremely difficult to
characterise their toxicity with any degree of
certainty. Figure 7.5 compares typical motor
vehicle engine-out emissions of some key air
toxics for the most widely available commercial
fuels (Anyon, 2002), based on data from an
Argonne National Laboratory report (Winebrake
J., 2000).
Note: CURE = Cancer Unit Risk Estimate, defined
as “the upper-bound excess lifetime cancer risk
estimated to result from continuous exposure to
and agent (e.g. chemical) at a concentration of 1 microgram per cubic metre in air or 1 microgram
per litre in water”. Hence the higher the CURE number, the higher the human cancer risk.
This document reviews the health effects of five air toxics - benzene, 1,3-butadiene, toluene, xylenes
and Polycyclic Aromatic Hydrocarbons (PAH). These five air toxics are ranked by the WHO as having
the greatest health damaging potential, based on a combination of their inherent toxicity and typical
human exposure levels.
Table 7.6, based on Australian Government data (NPI 2000) also highlights the extremely low air toxic
emission levels from LP Gas fuelled vehicles, compared with gasoline and diesel equivalents.
Figure 7.5: Comparison of Transport Sector Air
Toxic Emissions by Fuel Type
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Air Toxic Emissions, Passenger Car Exhaust (g/km)
By Road Type
Road Type: Arterial Freeway Residential
Benzene
Gasoline 0.08291 0.08817 0.09541
Diesel 0.00334 0.00313 0.00518
LP Gas 0.00001 0.00001 0.00002
1,3-butadiene
Gasoline 0.01064 0.00993 0.01642
Diesel 0.00064 0.00059 0.00099
LP Gas 0.00010 0.00009 0.00015
PAHs
Gasoline 0.00668 0.00625 0.01035
Diesel 0.00674 0.00628 0.01041
LP Gas 0.00000 0.00000 0.00000
Toluene
Gasoline 0.05618 0.02531 0.05618
Diesel 0.01573 0.00710 0.01573
LP Gas 0.00000 0.00000 0.00000
Xylenes
Gasoline 0.08880 0.04175 0.08880
Diesel 0.03405 0.02516 0.03405
LP Gas 0.00000 0.00000 0.00000
Table 7.6: Passenger Car Air Toxic Emissions by Fuel and Road Type (NPI 2000)
People exposed to toxic air pollutants at sufficient concentrations and durations may have an
increased chance of getting cancer or experiencing other serious health effects. These health effects
can include damage to the immune system, as well as neurological, reproductive (e.g., reduced
fertility), developmental, respiratory and other health problems.
In addition to exposure from breathing air toxics, some toxic air pollutants such as mercury can
deposit onto soils or surface waters, where they are taken up by plants and ingested by animals and
are eventually magnified up through the food chain. Like humans, animals may experience health
problems if exposed to sufficient quantities of air toxics over time.
Once toxic air pollutants enter the body, some persistent toxic air pollutants accumulate in body
tissues. Predators typically accumulate even greater pollutant concentrations than their
contaminated prey. As a result, people and other animals at the top of the food chain that eat
contaminated fish or meat are exposed to concentrations that are much higher than the
concentrations in the water, air, or soil.
Humans are exposed to toxic air pollutants in many ways that can pose health risks, such as by:
• Breathing contaminated air.
• Eating contaminated food products, such as fish from contaminated waters; meat, milk, or
eggs from animals that fed on contaminated plants; and fruits and vegetables grown in
contaminated soil on which air toxics have been deposited.
• Drinking water contaminated by toxic air pollutants.
• Ingesting contaminated soil. Young children are especially vulnerable because they often
ingest soil from their hands or from objects they place in their mouths.
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• Touching (making skin contact with) contaminated soil, dust, or water (for example, during
recreational use of contaminated water bodies).
PAHs are compounds that contain only hydrocarbon and carbon and are a group of over several
hundred organic chemicals with two or more fused aromatic rings. Two ring PAHs are found in the
vapour phase, two to five ring PAHs can be found in both the vapour and particulate phases and
PAHs consisting of five or more rings tend to be solids adsorbed onto other particles in the
atmosphere. Benzo-a-pyrene (B[a]P) is a five-ring compound and probably the most well known
PAH. B[a]P is often used a marker for PAHs.
PAHs are formed mainly as a result of incomplete combustion of organic materials during industrial
and other human activities, such as processing of coal and crude oil, combustion of natural gas,
combustion of refuse, wood burning stoves, motor vehicle exhaust, cooking, tobacco smoke, and
natural processes such as carbonisation.
7.2.1 Benzene
Benzene is a natural component of crude oil. Almost all benzene found at ground level comes from
human activities. It is emitted from industrial sources and a range of combustion sources including
motor vehicle exhaust and solid fuel combustion. Benzene is also emitted from tobacco smoke. The
major outdoor source is evaporative emissions and evaporation losses from motor vehicles, and
evaporation losses during the handling, distribution and storage of gasoline. Workers in industries
exposed to motor vehicle exhaust are at risk of exposure.
Benzene is naturally broken down by chemical reactions within the atmosphere. The length of time
that benzene vapour remains in the air varies between a few hours and a few days depending on
environmental factors, climate and the concentration of other chemicals in the air, such as nitrogen
and sulphur dioxide. It does not bio-accumulate in aquatic or terrestrial systems.
Inhalation is the dominant pathway for benzene exposure in humans. Smoking is an important
source of personal exposure. Extended travel in motorcars also produces exposures that are second
only to smoking as contributors to the intensity of overall exposure.
Current understanding of health effects of benzene are mainly derived from animal studies and
human health studies in the occupational setting.
Acute effects of benzene include skin and eye irritations, drowsiness, dizziness, headaches, and
vomiting. The most significant adverse effects of chronic benzene exposure are haematotoxicity,
genotoxicity, carcinogenicity and can also lead to birth defects in humans and animals. There
appears to be a dose-response relationship without any threshold effect. The mechanisms of
benzene toxicity are not well understood.
Benzene is carcinogenic and long term exposure can affect normal blood production and can be
harmful to the immune system. It can cause cancers and leukaemia (cancer of the tissues that form
white blood cells) in laboratory animals and human populations exposed for long periods, and has
been linked with birth defects in animals and humans.
Both the International Agency for Research and Cancer (IARC) and the US EPA have classified
benzene as known human carcinogens.
Although all in the population are susceptible to the adverse health effects of benzene, it is thought
that at levels occurring in the ambient atmosphere, benzene does not have short-term or acute
effects.
Even though adverse health effects have been documented with both acute and chronic exposures
to benzene, for the purposes of the derivation of exposure-response functions, the main health
endpoint that has been utilized is leukaemia.
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7.2.2 1,3-Butadiene
1,3-butadiene is emitted from oil refineries and chemical manufacturing plants. The major source of
1,3-butadiene is incomplete combustion of gasoline and diesel fuel. 1,3-Butadiene is highly reactive
and can oxidise to form formaldehyde and acrolin, two toxic substances in their own right. 1,3-
Butadiene is emitted from industrial facilities, tobacco smoke and motor vehicle emissions. Workers
in industries that use or produce 1,3-butadiene or are exposed to motor vehicle exhaust are at risk of
exposure. The probable route of human exposure to 1,3-butadiene is through inhalation.
Exposure to 1,3-butadiene can irritate the eyes, nose and throat. Acute exposure to 1,3-butadiene
can cause central nervous system damage, blurred vision, nausea, fatigue, headache, decreased
pulse rate and pressure, and unconsciousness. Long term exposure to lower levels has shown
increases in heart and lung damage. There are inadequate human data (based on only a few
occupational studies) but sufficient animal data to suggest that 1,3-butadiene is a human carcinogen.
Chemical compounds closely related to 1,3-butadiene are known human carcinogens.
The US EPA classified 1,3-butadiene in Group B2: probable human carcinogen. IARC classifies 1,3
Butadiene as a probable human carcinogen. The recent WHO revision of air quality guidelines
concluded that 1,3-butadiene is probably carcinogenic to humans (Group 2A).
7.2.3 Polycyclic Aromatic Hydrocarbons
PAHs contain only hydrocarbon and carbon and are a group of over several hundred organic
chemicals with two or more fused aromatic rings. Benzo-a-Pyrene (B[a]P) is probably the most well
known PAH carcinogen and is found in the exhaust of engines (especially diesels) as well as being one
of many carcinogens found in cigarette smoke.
PAHs are formed mainly as a result of pyrolitic processes, especially the incomplete combustion of
organic materials during industrial and other human activities, such as processing of coal and crude
oil, combustion of natural gas, combustion of refuse, vehicle traffic, cooking, tobacco smoke, and
natural processes such as carbonisation.
Occupational PAH exposure can occur in petroleum manufacture and use, or where coal, wood or
other plant materials are burned. Most PAHs in air they are generally found attached to particulate
matter. Occupational exposure to PAH may occur in coal production plants, coking plants and coalgasification
sites.
Data from animal studies indicate that several PAH may induce a number of adverse effects including
carcinogenicity and reproductive toxicity. B[a]P is by far the most intensively studied PAH in
animals. The lung carcinogenicity of B[a]P is enhanced by co-exposure to other substances such as
cigarette smoke and probably airborne particulates. Results from epidemiological studies indicate an
increase in lung cancer occurs in humans exposed to coke oven emissions, roofing tar emissions, and
cigarette smoke. Each of these contains a number of PAH.
7.2.4 Toluene
Toluene is widespread in the environment due to its use in a variety of commercial and household
products and it is found in tobacco smoke. Indoor toluene levels can be higher than outdoor levels
during non-occupational exposure to paints and thinners, and also where tobacco smoke is present.
Sniffing glue or paint can lead to high exposures. Air pollution from vehicles is a major source of
exposure. Toluene is emitted during crude petroleum and natural gas extraction, and petroleum
refining. Workers in industries exposed to motor vehicle exhaust are at risk of exposure.
The central nervous system (CNS) is the primary target organ for toluene toxicity in both animals and
humans for acute and chronic exposure. CNS dysfunction (often reversible) and narcosis are
observed in humans exposed to low or moderate levels. Short term exposure to high levels of
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toluene can result in light-headedness and euphoria. CNS depression occurs in chronic abusers
exposed to high levels.
Symptoms include cerebral atrophy, and impaired speech hearing and vision. Irritation of the upper
respiratory tract is associated with chronic inhalation. Toluene does not appear to be carcinogenic.
The US EPA has classified toluene in Group D, not classifiable as carcinogenic to human.
7.2.5 Xylenes
Xylenes are emitted during petroleum refining, solid fuel combustion, and are a component of
vehicle exhaust. They are also embodied in numerous domestic products.
Acute exposure to xylenes results in irritation of the respiratory tract, transient eye irritation and
neurological effects. Chronic inhalation exposure results in Central Nervous System (CNS) effects
such as headaches, dizziness, fatigue, tremors and un-coordination. Other effects of chronic
exposure include impaired pulmonary function, and possible affects on the blood and kidneys.
The evidence of developmental or reproductive effects on humans in inconclusive. Xylenes do not
appear to be carcinogenic.
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