Air Pollution

• A brief history of air pollution

• Types and sources of air pollutants
• Factors that affect air pollution
• Air pollution and the urban environment
• Acid deposition
 A Brief History of Air Pollution

• Disastrous London smog event of

1952
smog: smoke and fog;
5 days, nearly 4000 deaths;
Clean Air Act in 1956
• Los Angeles: photochemical smog
forms in sunny weather and
irritates the eyes
• U.S. Clean Air Act, 1970, 1990
set federal emission standards for
states to implement
and enforce
 A Brief History of Air Pollution
• Bhopal Gas tragedy

•Eyes: Chronic conjunctivitis, scars on cornea,

corneal opacities, early cataracts
•Respiratory tracts: Obstructive and/or restrictive
disease, pulmonary fibrosis, aggravation of TB
and chronic bronchitis
•Neurological system: Impairment of memory,
finer motor skills, numbness etc.
•Psychological problems: Post traumatic stress
disorder (PTSD)
•Children's health: Peri- and neonatal death
rates increased. Failure to grow, intellectual
impairment, etc.
Air pollution definitions

Air pollution: The presence of contaminants or pollutant substances in the air that
interfere with human health or welfare or produce other harmful environmental
Effects. (United States Environmental Protection Agency (2007).
Diversion from anti-Vietnam war activism
Concern of wealthy people
Poor exposed to sever pollution
Treatment and control of Infectious disease (influenza, tuberculosis, and
typhoid fever) were known
Long term effect of environmental pollution disease such as arteriosclerosis,
heart malfunctions, stroke, and cancer.

Clean air act 1970

Characterizing the cities based on pollutants load

Implementation of reasonably available control technology (RACT)

Global air pollution 1980

 Outline of clean air USA

Clean air act 1970

Characterizing the cities based on pollutants load
Implementation of reasonably available control technology (RACT)
Vehicular emission control
Controlling evaporative emissions (fugitive)
Oxyfuel (1992): Gasoline blended with alcohol sold in cities during winter with sever CO
problems
Reformulated gasoline with aromatic compounds were introduced in cities with worst ozone
problem
150 000 low emitting vehicles with emission control technology and blended gasoline were
introduced in California.
Toxic pollutants control
Sources were categorized and list provided by EPA
The Maximum Achievable Control Technology (MACT) for each category was identified
A time period to achieve set goals were given
Residual risk reduction
The health risk due to chronic exposure of pollutants after achieving NAAQS using MACT
Determined the health risk due to toxic pollutants emitted from stationary sources
Ample margin of safety
More stringent/additional norms to reduce adverse environmental effect
 Clean Air Act-1970
 Pollutants regulated by National Ambient Air Quality Standards (NAAQS) as described in
40CFR50 (as of July 1, 1998). These are called criteria pollutants because before the standards
were issued, documents called Air Quality Criteria were issued.

 Pollutants regulated by National Emission Standards for Hazardous Air Pollutants (NESHAP)
as described in 40CFR61 (as of July 1, 1998). These are called hazardous air pollutants.

criteria pollutants *Hazardous Air

Pollutants
Sulfur oxides Asbestos
Nitrogen dioxide Benzene
Carbon monoxide Beryllium
Ozone Coke oven emissions
Lead Inorganic arsenic
Fine particulate Mercury
matter
Radionuclides
Vinyl chloride
*The Clean Air Amendments of 1990 expanded this list
to 189 chemicals.
Sources of Air Pollutants and effects
 Natural: dust, volcano, forest fire, ocean waves, …
 Anthropogenic: fixed sources (power plants, homes, …)
 Anthropogenic: mobile sources (cars, ships, …)
 Health Effect
 Chronic effects: Long-term, low concentration exposures.
Example lung cancer, asthma, and chronic obstructive pulmonary disease (COPD), ischemia, stroke.

 acute effects: Short-term, high-concentration exposures industrial accidents such as the Bhopal
tragedy.

 Health studies
 Epidemiological studies
 Toxicological studies

 Local air quality

 Visibility reduction
 Heat waves
 Plant damage
 Decline in crop yield
 Plant disease
 Climate change
 Radiative forcing
 Temperature and precipitation change
 CO and health effects
• CO rapidly diffuses across alveolar, capillary and placental membranes.
Approximately 80-90% of absorbed CO binds with Hb to from
Carboxyhaemoglobin (COHb), which is a specific biomarker of exposure
in blood. The affinity of Hb for CO is 200-250 times than that of oxygen.

• In patients with hemolytic anemia (red blood cells destroyed faster than
they can be replaced), the CO production rate was 2–8 times higher and
blood COHb concentration was 2–3 times higher than in normal person
(WHO 2000).

• The initial symptoms of CO poisoning may include headache, dizziness,

drowsiness, and nausea. These initial symptoms may advance to
vomiting, loss of consciousness, and collapse if prolonged or high
exposures are encountered and may lead to Coma or death if high
exposures continue.

• A US study estimated that 6 per cent of the congestive heart failures and
hospitalizations in the cities were related to an increase in CO
concentration in ambient atmosphere (WHO 2000).

• Reduction in the ability of blood to transport oxygen leads to tissue

hypoxia (insufficient O2 at tissue level). The body compensates for this
stress by increasing cardiac output and the blood flow to specific areas,
such as the heart and brain
COHb and health effect
Health effect of NO2
The major source of NO2 is combustion processes.

On inhalation, 70–90% of NO2 can be absorbed in the

respiratory tract of humans, and physical exercise
increases the total percentage absorbed (Miller et al.,
1982).

Normal healthy people exposed at rest or with light

exercise for less than 2 hours to concentrations of more
than 4700 μg/m3 (2.5 ppm) experience pronounced
decrements in pulmonary function; generally, such people
are not affected at less than 1880 μg/m3 (1 ppm).

The overall meta estimate of the change in lung cancer

incidence or mortality per 10-μg/m3 increase in exposure
is 4% [95% confidence interval (CI): 1%, 8%] (Hamra et
al., 2015).
 Behaviour of particles and gases in the respiratory system
• Particle’s behaviour depends on aerodynamic characteristics.
• Size
• Shape
• density
• Solubility of gas governs their behaviour
• Larger particles get deposited in the nasal region
• Mechanisms
• Inertial impaction
• Sedimentation
• Diffusion due to Brownian motion

Task group on lung dynamics, health physics, 12, 173 (1966).

 Deposition/absorption of particles and gases in the respiratory system

• Removal from upper airways

𝑝𝐴 = 𝐾𝐻 𝐶𝑊
• Mucous
• Nose blowing 𝑝𝐴 = 𝑃𝑎𝑟𝑡𝑖𝑎𝑙 𝑝𝑟𝑒𝑠𝑠𝑢𝑟𝑒 𝑜𝑓 𝑔𝑎𝑠
• Sneezing 𝐾𝐻 = 𝐻𝑒𝑛𝑟𝑦 ′ 𝑠 𝑙𝑎𝑤 𝑐𝑜𝑛𝑠𝑡𝑎𝑛𝑡
• Coughing
• Swallowing 𝐶𝑊 = 𝐶𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑜𝑓 𝑔𝑎𝑠 𝑖𝑛 𝑤𝑎𝑡𝑒𝑟

• Mucociliary escalator: Fibre cilia on tracheobronchial wall 𝐾𝐻 = 𝐾𝐴𝑊 𝑅𝑇

sweeps the mucous fluid upward transporting particles to the
top of the trachea, where they are swallowed. 𝐾𝐴𝑊 = 𝑎𝑖𝑟 − 𝑤𝑎𝑡𝑒𝑟 𝑝𝑎𝑟𝑡𝑖𝑜𝑛𝑖𝑛𝑔 𝑐𝑜𝑒𝑓𝑓𝑖𝑐𝑖𝑒𝑛𝑡
• Cleaning in pulmonary region: Alveolar macrophages cell engulf
the particles and move to the mucociliary escalator for removal. 𝐶𝐴
𝐾𝐴𝑊 =
• SO2 highly soluble absorbed in the upper airways. 𝐶𝑊

• Less soluble NO2 and O3 penetrate to the pulmonary region. 𝐶𝐴 = 𝐶𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑜𝑓 𝑔𝑎𝑠 𝑖𝑛 𝑎𝑖𝑟

𝑅 = 𝑔𝑎𝑠 𝑐𝑜𝑛𝑠𝑡𝑎𝑛𝑡 = 8.21 × 10−2 𝐿 𝑎𝑡𝑚 𝑚𝑜𝑙 −1 𝐾 −1

𝐷𝑠𝑎
𝐷𝑝𝑎 = 𝐷𝑠𝑎 √𝜌𝑎 𝐷𝑝𝑎 𝑇 = 𝑇𝑒𝑚𝑝𝑒𝑟𝑎𝑡𝑢𝑟𝑒 𝑖𝑛 𝐾

𝑣𝑠 𝜌𝑠
𝑣𝑠 𝜌𝑝 𝑣𝑠 𝜌𝑤
Health effect of PM

• A HEI study, (Wichmannet al., 2000) reported that the concentration of both ultrafine
(PM<0.1) and fine particles (PM0.1-2.5) was associated with increased daily mortality.

• Lippmann et al. (2000) reported that four of five size fractions (PM40 PM10-40 PM10
PM2.5-10 PM2.5) were associated with increased in morbidity and mortality.

• An association between elevated PM10 levels and hospital admissions for pneumonia,
bronchitis, and asthma was observed by Pope (1989). Long-term particulate exposure was
associated with an increase in risk of respiratory illness in children (Dockery et al., 1989).

• FEV1, PEFR and FVC are the key lung function parameters on which the impact of air
pollution have been observed (Bates, 2002).

• The deviations found in FEV1 and FVC are: (a) FEV1 -0.30 L (at VikasNagar (VN): PM10:
300μg/m3), -0.31 (at Juhi Colony (JC): PM10: 300 μg/m3) and -0.18 L (IIT Kanpur (IITK):
PM10: 185 μg/m3 IITK) and (b) FVC -0.42 L (VN), -0.40 (JC) and -0.27 L (IITK).
Mortality in Ghaziabad and Delhi
 Photochemical Smog
• Photochemical smog is a mixture of pollutants that are formed when nitrogen oxides
and volatile organic compounds (VOCs) react to sunlight, creating a brown haze
above cities.
• It tends to occur more often in summer, because that is when we have the most
sunlight.
• Primary pollutants The two major primary pollutants, nitrogen oxides and VOCs,
combine to change in sunlight in a series of chemical reactions, to create what are
known as secondary pollutants.
• Secondary pollutants The secondary pollutant that causes the most concern is
the ozone that forms at ground level. Many other hazardous substances are also
formed, such as peroxyacetyl nitrate (PAN).

USEPA, 2004
 Effect of O3 on plants
Ozone: Ozone enters leaves through stomata during normal gas exchange. As a strong
oxidant, ozone causes several types of symptoms including chlorosis and necrosis.
 Effects of Ozone Depletion
• Higher levels of UV-radiation hitting
the earth
• Eye cataracts
• Skin cancer (right)
• Weakened immunity
• May disrupt ecosystems
• May damage crops and forests
Corrosion of metals: oxidation reaction

When metallic surfaces become contaminated with hygroscopic salts

their surface can be wetted at lower %RH.
The presence of magnesium chloride (MgCl2) on a metallic surface
can make a surface apparently wet at 34% RH.
sodium chloride (NaCl) on the same surface requires 77% RH to
create the same effect.
 Effects of pollutants through
Oxidation reduction reactions

• SO2 or SO3 reacts with CaCO3 and form CaSO4 and gypsum
(CaSO4. 2H2O) which are more soluble in water than CaCO3
resulting in deterioration of monuments and other
infrastructures.

• Indirect chemical attack: when pollutants are absorbed and

reacts with the components of absorbent. Example leather
becomes brittle after it absorbs SO2 which reacts to form
sulfuric acid because of the presence of minute quantities of
iron. The iron acts as a catalyst for the formation of H2SO4.

• Large particles and lead particles from weapons fire can cause
abrasion on surface.
How to communicate the pollution level to
public?
 Air Quality Index
• Air Quality Index (AQI): includes the
pollutants CO, SO2, NO2, particulate
matter, and O3.

• An air quality index is defined as an

overall scheme that transforms the
weighed values of individual air pollution
related parameters (for example,
pollutant concentrations) into a single
number or set of numbers (Ott, 1978).
 AQI formulation

 Formation of sub-indices (I1, I2,...., In) for n pollutant variables (X1, X2...., Xn)
is carried out using sub-index functions that are based on air quality standards
and health effects. Mathematically;
Ii=f (Xi), i=1, 2,...,n

 Each sub-index represents a relationship between pollutant concentrations and

health effect.

 Aggregation of sub-indices, Ii is carried out with some mathematical function

(described below) to obtain the overall index (I), referred to as AQI.
I=F (I1,I2,....,In)
I = Aggregated Index = ΣwiIi (For i= 1, …..,n)

Ii= sub-index for pollutant i

n = number of pollutant variables
wi = weightage of the pollutant
AQI
• Eight parameters (PM10, PM2.5, NO2, SO2, CO, O3, NH3, and Pb) having short-term
standards have been considered for near real-time dissemination of AQI.

• It is recognized that air concentrations of Pb are not known in real-time and cannot
contribute to AQI.

• In India, ~ 40 automatic monitoring stations are operated where parameters like PM10,
PM2.5, NO2, SO2, CO, O3, etc. are monitored continuously.

• In India, air quality is being monitored manually at 573 locations under National Air
Monitoring Programme (NAMP). In most of these manually operated stations, only three
criteria pollutants viz. PM10, sulphur dioxide (SO2) and nitrogen dioxide (NO2) are
measured, at some stations PM2.5 and Pb are also measured. The monitoring frequency
is twice a week.

• AQI system has been build on air quality standard and pollutant dose-response
relationships to describe air quality in simple terms which clearly relates to health impacts.
Indian National Air Quality Standard and
health criteria for AQI
Breakpoint concentration of CO
and AQI
Break point concentration of NO2
and AQI
Break point concentration of PM10 and AQI
Break point concentration of
PM2.5 and AQI
Break point concentration of Ozone
and AQI
 Break point concentration of
SO2 and AQI
 SO2 is soluble in aqueous media and affects mucous membranes of the nose
and upper respiratory tract. Reduction in mean lung function values among
groups of healthy individual have been observed for 10- minute exposures at
4000 ppb (11 440 μg/m3) (Linn et al. 1984) and at 5000 ppb (14 300 μg/m3)
(Lawther et al., 1975).
 Effect of NH3, Pb and corresponding AQI
 An association has been reported between exposure to ammonia and cough,
phlegm, wheezing, and asthma at high concentration.
 Pb is a toxic metal and its exposure through all routes result in increased blood
lead level. At lower concentrations, the blood lead level is proportional to air
concentration (after accounting for all resulting exposure routes).
 For example, 1 μg/m3 of annual lead level will result in 5μg/dL(on an average) of
blood lead level (WHO 2000). The effect of blood level above 10μg/dL is seen in
haematological changes in sensitive population, therefore, at moderate pollution
level the break point is proposed at 2μg/m3.
Break point concentrations of pollutants
AQI
calculation
Human health risk estimation
 Dose of pollutant

Dose: Amount (often as mass) of • Dose

pollutant administered to an Applied
dose
inhaled/ingested/absorbe
organism. d through skin

Internal • Enters inside

dose the organism

Absorbed •Absorbed
dose by organism

Biological • Amount that

reach a
effective particular
dose target
 How to interpret dose response curves

• Curve A
B. Nutrient curve • Precautionary principle.
ADVERSE
HEALTH
EFFET
• Curve B
OR
MORTALITY C. Non cancer curve
• Essential metals and nutrients
• Optimal range
LD5
LD50 LD9
5 • Excess leads to adverse health effect
DOSE
• Essential or toxic depends on oxidation state
1. What is the difference in steepness of curve A and C?
2. What does the steepness mean in curve A and C? • Curve C
• Non cancerous adverse health effect (e.g.
• Lethal dose (LD5, LD50, LD95) cough, cold, fever, etc.)
• 90 percentile range • Steepness of the curve: potency or severity.
Uncertainties in data extrapolation

• Reference dose (RfD): The dose at and below which there is no

adverse health effect.
𝐿𝑜𝑤 𝑎𝑑𝑣𝑒𝑟𝑠𝑒 𝑒𝑓𝑓𝑒𝑐𝑡 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 (𝐿𝑂𝐴𝐸𝐶)
• 𝑅𝑓𝐶 =
𝑈𝐹𝑖𝑛𝑡𝑒𝑟 ×𝑈𝐹𝑖𝑛𝑒𝑟𝑎 ×𝑈𝐹𝑜𝑡ℎ𝑒𝑟
Calculate the RfC of a substance with NOAEC=1.5 mgm-3, UFs
Uncertainty factors are 10, 100 and 10 for interspecies variability, intra species
variability and other respectively.
• Inter species
• Intra species What will happen to curve as
• Other uncertainties improve?
Uncertainty factor should account for
Uncertainty in extrapolating the data for
homo sapiens
Variation in susceptibility among
members
Extrapolation sub-chronic to chronic
exposure
Extrapolation from LOAEC rather than
NOAEC
Extrapolation from incomplete database
Exposure assessment

• The process of estimating or measuring the magnitude, frequency and

duration of exposure to an agent, along with the number and characteristics
of population exposed. Ideally it describes the sources, pathways, routes,
and the uncertainties in the assessment. (WHO)
• Aggregate exposure
• Cumulative exposure
• Factors that must be considered
• Concentration of the agent in the air and other media
• Human behaviour and characteristics
• Population number
• Exposure pathway (course taken by the agent from the source to the receptor)
• Exposure route (the way an agent enters a receptor after contact e.g. inhalation
ingestion, dermal)
• Exposure duration
Exposure calculations 𝑛

𝐸𝑗 = ෍ 𝐶𝑖 × 𝐼𝑅𝑖𝑗 × 𝑡𝑖𝑗
𝑖=1
• Average daily dose (ADD): used for non-cancer
risk
𝐼 𝐸𝑗 = Daily exposure for the jth group (mgday−1)
𝐴𝐷𝐷 =
𝑊×𝑡 𝑛 = 𝑠𝑒𝑡𝑡𝑖𝑛𝑔𝑠 (𝑒. 𝑔. 𝑑𝑖𝑓𝑓𝑒𝑟𝑒𝑛𝑡 𝑚𝑖𝑐𝑟𝑜𝑒𝑛𝑣𝑖𝑟𝑜𝑛𝑚𝑒𝑛𝑡𝑎𝑙 𝑎𝑛𝑑 𝑜𝑢𝑡𝑑𝑜𝑜𝑟 𝑙𝑜𝑐𝑎𝑡𝑖𝑜𝑛𝑠

• I= Intake dose=concentration (mgm-3) X 𝑗 = 𝐷𝑖𝑓𝑓𝑒𝑟𝑒𝑛𝑡 𝑎𝑔𝑒 𝑔𝑟𝑜𝑢𝑝

inhalation rate (IR) 𝐶𝑖 = 𝑃𝑜𝑙𝑙𝑢𝑡𝑎𝑛𝑡 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑖𝑛 𝑑𝑖𝑓𝑓𝑒𝑟𝑒𝑛𝑡 𝑚𝑖𝑐𝑟𝑜𝑒𝑛𝑣𝑖𝑟𝑜𝑛𝑚𝑒𝑛𝑡 (𝑚𝑔𝑚−3)
• W= body weight (kg)
𝐼𝑅𝑖𝑗 = 𝐼𝑛ℎ𝑎𝑙𝑎𝑡𝑖𝑜𝑛 𝑟𝑎𝑡𝑒 𝑖𝑛 𝑡ℎ𝑒 𝑖𝑡ℎ 𝑠𝑒𝑡𝑡𝑖𝑛𝑔 𝑜𝑓 𝑡ℎ𝑒 𝑗𝑡ℎ 𝑔𝑟𝑜𝑢𝑝 (𝑚3 ℎ−1 )
• t= Averaging time (days)
𝑡𝑖𝑗 = 𝐷𝑎𝑖𝑙𝑦 𝑒𝑥𝑝𝑜𝑠𝑢𝑟𝑒 𝑡𝑖𝑚𝑒 𝑠𝑝𝑎𝑛 𝑖𝑛 𝑡ℎ𝑒 𝑖𝑡ℎ 𝑒𝑛𝑣𝑖𝑟𝑜𝑛𝑚𝑒𝑛𝑡 𝑜𝑓 𝑡ℎ𝑒 𝑗𝑡ℎ 𝑔𝑟𝑜𝑢𝑝 (ℎ𝑑𝑎𝑦 −1 )

• Cancer risk- linear non-threshold model

• Assumes Lifetime probabilities
Parameters Setting
• Lifetime average daily doses (LADDs)
Outdoor near In car while
Indoor Other outdoor
home driving
Formaldehyde
concentration 0.5 0.4 0.2 0.7
(mgm-3)
Child mean
inhalation rate 0.4 0.5 0.4 0.5
(m3h-1)
Adult mean
inhalation rate 0.6 0.7 0.5 0.8
(m3h-1)
Time spent in
setting by child 18 4 1 1
(hday-1)
Time spent in
setting by adult 16 4 1 3
(hday-1)
Chemical Exposure or Intake

Route of exposure Lifetime average daily dose (LADD) Variable description

(mgkg-1day-1)

Inhaling aerosol 𝐶. 𝐼𝑅. 𝑅𝐹. 𝐸𝐿. 𝐴𝐹. 𝐸𝐷 𝐶 = 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑜𝑓 𝑎𝑒𝑟𝑜𝑠𝑜𝑙 𝑜𝑟 𝑐𝑜𝑛𝑡𝑎𝑚𝑖𝑛𝑎𝑛𝑡𝑠 𝑜𝑛 𝑡ℎ𝑒 𝑎𝑒𝑟𝑜𝑠𝑜𝑙 𝑚𝑔𝑚−3
=
(particulate matter) 𝐵𝑊. 𝑇𝐿 𝐼𝑅 = 𝐼𝑛ℎ𝑎𝑙𝑎𝑡𝑖𝑜𝑛 𝑟𝑎𝑡𝑒 𝑚3 ℎ−1
𝑅𝐹 = 𝑅𝑒𝑠𝑝𝑖𝑟𝑎𝑏𝑙𝑒 𝑓𝑟𝑎𝑐𝑡𝑖𝑜𝑛 𝑜𝑓 𝑡𝑜𝑡𝑎𝑙 𝑝𝑎𝑟𝑡𝑖𝑐𝑢𝑙𝑡𝑒 𝑚𝑎𝑡𝑡𝑒𝑟
𝐸𝐿 = 𝑒𝑥𝑝𝑜𝑠𝑢𝑟𝑒 𝑙𝑒𝑛𝑔𝑡ℎ (ℎ𝑑𝑎𝑦 −1 )
𝐸𝐷 = 𝑑𝑢𝑟𝑎𝑡𝑖𝑜𝑛 𝑜𝑓 𝑒𝑥𝑝𝑜𝑠𝑢𝑟𝑒 𝑑𝑎𝑦
𝐴𝐹 = 𝐴𝑏𝑠𝑜𝑟𝑝𝑡𝑖𝑜𝑛 𝑓𝑎𝑐𝑡𝑜𝑟
𝐵𝑊 = 𝐵𝑜𝑑𝑦 𝑤𝑒𝑖𝑔ℎ𝑡 (𝑘𝑔)
𝑇𝐿 = 𝑇𝑦𝑝𝑖𝑐𝑎𝑙 𝑙𝑖𝑓𝑒 𝑡𝑖𝑚𝑒 (𝑑𝑎𝑦𝑠)

Inhaling vapor 𝐶. 𝐼𝑅. 𝐸𝐿. 𝐴𝐹. 𝐸𝐷 𝐶 = 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑜𝑓 𝑔𝑎𝑠 𝑝ℎ𝑎𝑠𝑒 𝑐𝑜𝑛𝑡𝑎𝑚𝑖𝑛𝑎𝑛𝑡𝑠 𝑚𝑔𝑚−3
=
phase 𝐵𝑊. 𝑇𝐿
contaminants
 Commonly used human exposure factors

Exposure factor Adult male Female Child (3-12 years old)

Body weight 70 60 15-40

Total fluid ingested (l day-1) 2 1.4 1.0

Surface area of skin. Wearing 0.1-0.3 0.1-0.3 0.05-0.15

cloth
Respiration/ventilation rate 7.5 6.0 5.0
(lmin-1), resting
Respiration/ventilation rate 20 19 13
(lmin-1), light activity
Volume of air breathed (m3day- 23 21 15
1)

Typical life time (years) 70 70 NA

National upper-bound (90th 30 30 NA

percentile) time at one
residence (years)
NANational medium time (50th 9 9 NA
pe9rcentile) at one residence
Source: EPA
Considerations of various factors in Exposure calculation

• Predominant pathway inhalation but other routes must also be considered

especially for long term exposure.

• Body burden should be estimated for the chemicals that can bioaccumulate
• Metals Pb, Hg, Cd,
• Metalloids As
• Organic compounds from incomplete combustion e.g. PAHs
• Halogenated aromatic compounds PCBs, polybrominated biphenyls, organochlorine
pesticide such as DDT

• Toxicokinetic should be taken into account

• For particles it depends in size
Cancer risk

• Cancer risk
• 𝐶𝑎𝑛𝑐𝑒𝑟 𝑟𝑖𝑠𝑘 = 𝑐𝑎𝑛𝑐𝑒𝑟 𝑠𝑙𝑜𝑝𝑒 𝑓𝑎𝑐𝑡𝑜𝑟 ×
𝐿𝑖𝑓𝑒 𝑡𝑖𝑚𝑒 𝐴𝑣𝑒𝑟𝑎𝑔𝑒𝑑 𝐷𝑎𝑖𝑙𝑦 𝐷𝑜𝑠𝑒 (𝐿𝐴𝐷𝐷)
• Time weighted average exposure concentration for each activity in every
microenvironment should be calculated.
Problems:
If a person inhales air with 100 mgm-3 aerosol with a mean aerodynamic diameter of 5 mm
at the rate of 0.007 m3min-1, approximately how much PM will be deposited in
tracheobronchial region in an 8-hour day? How much would be trapped nasally? How much
would make to small bronchi and alveolae?