Environmental Health

Air pollution
Week 8
C&D Chapters 15, 24 and 28

What is air pollution

The result of emission into the air of
hazardous substances at a rate that
exceeds the capacity of natural
processes in the atmosphere to
convert, deposit, or dilute them

Factors that affect air pollution

Emissions (traffic, industrial, domestic)

Geography (terrain)
Weather conditions (rain, winds, humidity)
Season
Time of day
Population density
Indoor vs outdoor

Types of air pollution

Aerosols
Particulates solid phase
Dust
Ash
Fumes

Solid and liquid

Smoke (from combustion)
Coastal aerosols

Liquid
Aggregate gases (sulfate, nitrate)

Gases
COx
SOx
NOx
PAH

Six primary or criteria air pollutants

Carbon monoxide (CO)
Ozone (O3)
Nitrogen dioxide (NO2)
Sulfur oxides (SOx)
PM2.5 and PM10
Lead (Pb)

Types of air pollution

Individual pollutants
Reducing pollution (SO2)
Acid rain (fog)
Corrosive, eroding

Photochemical pollution
Aldehydes, electrophilic HCs
Oxidative, carcinogenic?

Mixtures and complex patterns

Types of Exposures:
Continuous
Repeated
Low
High (acute)

Respiratory response (endpoints):

Macroscopic (e.g. coughing, FEV)
Histological

Marked variability in responses - susceptibility

Combustion pollutants

VOCs
NOx
N-organics
Halo-organics
Metals
CO

Sources of combustion

Tobacco
Power plants
Incinerators
Automobiles
Industry

Diesel pollutants
Particulate matter
C + PAHs + N-aromatics

Gases
NOx, CO, SOx

VOCs
formaldehyde, acrolein, aldehydes

Respiratory inflammation
Cytotoxicity to airway cells

Outdoor air pollution

Beijing
Delhi

Outdoor air pollution

Santiago

Mexico City

Indoor pollutants
Non-specific symptoms
Household vs work space
Sick building syndrome (20% exposed)

Cigarette smoke, combustion products

Organic offgasing (glue, fabrics, furnishings)
Biological agents (infections, allergens)
Additional factors (stress, fatigue, diet,
alcohol)

Indoor air pollution: Poor countries

In the lungs

Site of deposition along tract

Solubility in respiratory fluids
Reactivity with membranes
Infiltration (alveolar gas exchange)
Level of exposure
Duration of exposure
Respiratory rate
Pre existing conditions (heart, lung)

Absorption in lungs
As gas, directly into blood stream
As particles, deposited onto bronchiolar and
alveolar surface

Uptake by phagocytosis
Trigger of inflammatory response
Trigger of allergic response
Lung tissue scaring

Basic structure of respiratory tract

Measurements of lung volume

Typical lung volume measurements from normal

lung, obstructive airway disease, and restrictive lung
disease

Normal, Obstructive and Restrictive Patterns

of Forced Expiration

FVC
= forced vital capacity
FEV1 = forced expiratory volume at 1st second of active exhalation
FEF25-75 = maximal mid-expiratory flow rate
FEF75 = forced expiratory flow after 75% of expelled volume

Particulate matter pollution

Properties - varied
Mixture of solid phase and absorbed materials (organic, inorganic
and biological)
Carbonaceous core 40-60%, C 7%

Sources
Combustion - oil and coal
Industry
Automobiles

Tobacco smoke
Biomass burning
Metal smelters

NAAQS:
PM10: 50ug/m3, annual
150ug/m3, 24h
PM2.5 15ug/m3, annual
65ug/m3, 24h

Particulates - features
Physical size
Large
Small ~10um
Fine ~2.5um

Aerodynamic diameter (size equivalent of density=1)

Large - local irritation
(>100um)
Inhalable
(<100um)
Thoracic fraction
(<20um)
Coarse PM10
Fine PM2.5
Ultrafine

Chemical reactivity
Shape (fibers)
Water content

(<10um)
(<2.5um)
(<0.1um)

respirable

Deposition of particles in humans

Parameters
influencing
particle
deposition

Alveolar injury
and responses

Urban Particulates
In the <2.5um range
Large water content, trace metals,
acid gases, organic chemicals,
biological
Rather uniform distribution
Include diesel

Health effects of particulate pollutants

- starting at 10ug/m3
Eye irritation
Respiratory tract infection
Exacerbation of asthma
Bronchial irritation
Heart disease
Possibly cancer (controversial) (diesel, TiO2, talc,
carbon black, toner black)

Elevated hospital admissions, mortality

Causation(s) not fully understood

Gaseous pollutant features

Chemical reactivity (ozone)
Solubility in water
Soluble
Ambient (NOx, SOx)
Occupational (Hydrochloric acid, Ammonia)

Less soluble
H2S, ozone

Gas pollutants - SO2

Properties

NAAQS: 0.03ppm, annual

0.14ppm, 24h

Reacts with H2O and forms sulfurous acid (H 2SO3), which oxidizes to
sulfuric acid (H2SO4)
Chemical transformation of other pollutants
Responsible for acid rain effect

Sources
Biomass and fossil fuel combustion
Industrial emissions, smelters

Controls
Low-S fossil fuels (clean coal)
Emission control devices

London fog episode (acute)

SO2 continued
Absorption at upper respiratory tract
(sulfite, bisulfite)

Health effects (starting at <1ppm)

Respiratory tract irritation, bronchoconstriction

Pulmonary function impairment
Increased air flow resistance
Bronchitis
Exacerbation of heart diseases

Short acute: 2min 0.4-1ppm in asthmatics

Long term, low levels
Impairs immune pulmonary defenses
Susceptibility to infections

Gas pollutants - H2SO4

Product of SO2
With metals and water --> sulf. Fly ash and acid rain

Protonates biomolecules - membrane damage

Bronchoconstriction
Increased air flow resistance
Mucus secretion protects (buffer) - nose inhalation
Asthmatics are more sensitive
Acidity interferes with mucociliary clearance

Chronic exposure to 100g/m3 : lower respiratory damage, macrophage

mediated

Gas pollutants -NO2

Properties

NAAQS: 0.05ppm, annual

Oxidant, less potent than O3

Sources

NO oxidation
High To combustion (automobiles, power plants)
Indoor - kerosene, gas stoves, ETS
Silos in farming (75-100ppm)

Health effects - starting at 1.5-2ppm

Deep lung irritant - terminal bronchioles

Alveolar cells, ciliated epithelia, Clara cells
Similar to ozone but less inflammatory (if < 2-5ppm)
Enhanced infection, suppression of macrophage action
Peaks more

Gas pollutants - CO
Properties

NAAQS: 9ppm, 8h
35ppm, 1h

Odorless, heavier than air, stronger binder to Hb than O 2

Sources
Incomplete combustion
Traffic (inside the car, parking garages, tunnels is highest)
Inside cars = 3x urban streets, and = 5x residential streets

Health effects
Asphyxiant
Fatigue, confusion, headaches, dizziness, cardiac function (arrhythmias, angina)
Start at 2.5% COHb (0.5% baseline) (air level 50ppm for 90min)
2ppm COHb, no effect
>5ppm COHb, cardiovascular effects
40ppm COHb, is fatal

Gas pollutants - O3
Good O3 - stratosphere
Bad O3 - troposphere

NAAQS: 0.12ppm, 1h
0.08ppm, 8h

Properties
Short lived, highly reactive, water soluble
Scrubbed in nasopharynx
Reaches terminal bronchioles and alveoli

Sources
Photochemical reactions

Health effects
Degenerative lung disease
Loss of lung function

Photochemical pollution
NO2
O2 + O
O3 + NO

uv

NO + O
O3
O2 + NO2

Twist:
In absence of HC- the reaction reaches equilibrium

Car emitted HC- (PAH) react with O .

Hydrocarbons shift photochemical reaction

HC- + O

Oxidized free radicals

NO
NO2
+ Aldehydes

Balance of photochemical reaction shifts toward O3 buil

O3

Photochemical pollution
uv
NO2
O2
Hydrocarbons

O3

The O3 molecule is highly reactiv

O2

O3

O
H2O

2 (HO )
Ultimate toxicant:
No enzyme can
detoxify it
Only protection:
prevention of its

FEV

Effects of Ozone on lung function

0.5ml

1
0.12 - 0.4 ppm for 2-3 h

FVC and FEV1

ppb

(Kinney et.al, 1996

Ozone levels

ppb
300
240
200
180
LA, 8h-ave
120
Effects on lung 100
function observed 90
80
US-EPA 8h ave
70
60
WHO 8h ave
50
40
20

ppm
0.30
LA, until 1998
0.24
0.20
LA, 1h-ave
0.18 EU 1h ave
US-EPA 1h ave
0.12
0.10 Italy study (low exposu
0.09
0.08 WHO 1h ave
0.07
0.06
0.05
0.04
Baseline
0.02

Ambient O3, TSP and SO2

Some nomenclature of oxidative species

O
Aldehydes

R C

Alcoxyl radical

RO

Alkoperoxyl radical
Nitrous acid
Nitric acid

RO2 (ROO )
HONO
HONO2

Hydroxyl radical

HO

Hydroperoxy radical

(RO )

(HO )
HO2

(HOO )

Effects of O3 on proteins:
Oxidation of:
sulphydryls
amines
alcohols
aldehydes

Aminoacids targets:
cystein
methionine
tryptophan
tyrosine

Inactivation/inhibition of enzymes in cellular compartme

Effects of O3 on lipids:
Polyunsaturated fatty acids (PUFA):
primary target of O3 peroxidation of membrane lipids
Most important mechanism of O3-induced injury
O3 + PUFA

carbonyl oxide
H2O
aldehydes
Hydroxyhydroperoxy compound

Lipid peroxidation cascade

Lipid fragmentation

HO
H2O2
Malondialdehyde (MDA
8-isoprostane
LTB4 (PMN chemotractant)

Lipid peroxidation
cascade

Effects on nucleic acids

Electrophiles react with strong nucleophilic atoms of nucle

DNA + HO

Imidazole ring-opened purines or

ring-contracted pyrimidines

Strand breaks
Blocked DNA replication
Formation of adducts

depurination (apurinic sites: mutagenic

Effects of O3 on lung function

Decrement of lung function (FEV1 and FVC1)
Increased airway responsiveness (non specific)
Increased epithelial permeability, injury and loss

May influence allergic sensitization and responsiv

May increase sensitivity to infections
Induces inflammatory reactions following injury
Exercise increases air flow and penetration

Inflammatory oxidative burst

.

Three pathways of HO generation:

NAD(P)H oxidase
Nitric oxide synthase (NOS)
Myeloperoxidase (MPO)
L-citruline
NOS

L-arginine + O2

NAD(P)+
H+

HOOH + H+ +Cl-

NO2

NO
Oxidase

NAD(P)H + O2

H+

MPO

O2

H20

HOCl

Fenton

HO
O2
Cl-

The lungs defenses:

Antioxidant molecules:

Metabolic enzymes:

ascorbic acid (vit. C)

a-tocopherol (vit. E)
uric acid
glutathione (GSH)

SOD
Catalase
GPX
GSTs

Other air pollutants - HAPs

Hazardous air pollutants
Not included in the 6 criteria air pollutants

Include

Organic chemicals (acrolein, benzene)

Minerals (asbestos)
PAH (benzo[a]pyrene)
Metals (Hg, Be)
Pesticides (carbaryl, parathion)

Some are carcinogenic

Volatile Organic Pollutants

(VOCs)
Sources: Petroleum emissions, fuel combustion, incineration,
biomass burning
Account for ~14% of all air pollution
Important factor of indoor air pollution
Types

Aliphatic
Alcohols (ethylene glycol, MTBE)
Aldehydes (formaldehyde)
Aromatic (benzene, toluene, xylene)
Halogenated (TCE, PERC, Methylene Chloride)
Polycyclic (PAHs)
Other (Carbon disulfide)

VOCs Health Effects

Alkanes (solvents, varnishes, lacquers)
Irritants, lung and skin
CNS depressants, neuron degeneration,
paralysis
Pulmonary edema
React with OH radical in photochemical
pollution

VOCs Health Effects

Alkenes (gasoline and aviation fuel) more
reactive than alkanes - chains, oxides,
halogenated HC
CNS effects - cramps, tremor
GI tract - nausea, vomiting

Aldehydes
Formaldehyde

H2C=O

50% of total aldehydes

Water soluble
Steep dose-effect:
0.5-1ppm: odor
2-3ppm: mild irritation
4-5ppm: intolerable
Scrubbed in upper respiratory tract, but can also reach
deeper
Nasal cancer? (rodents but not humans)

Acrolein

H2C=CHCH=O

5% of total but more irritating

VOCs Health Effects

Aromatic hydrocarbons (stable, persistent) - Low water
solubility, volatile, flammable - Priority pollutants (EPA)

Benzene - most basic

Carcinogen (epoxide, phenol metabolites)
CNS toxicity - narcosis
Irritation (skin, lung)
Toluene (more lipophilic, but faster metabolism)
CNS depressant (narcosis, impaired coordination,
headaches)
Xylene (o-, p-, m-) (very lipophilic)
CNS depressant (as above)
Blood cell damage, anemia
Irritant (skin)

VOCs Health Effects

Polycyclic aromatic hydrocarbons (PAH) incomplete

combustion of organic materials, incineration, industry, natural processes

16 of 126 priority pollutants
Environmental transport, accumulation
Photo - bio- degradation

Carcinogens exposure* (metabolic activation)

Air exposure
Cigarette smoke
Unfiltered cigarettes
Vegetarian diet
Drinking water
Soil (urban)

0.02-3ug/day
0.1-0.25ug/cig
2-5ug/day
3-9ug/day
0.2-120ng/day
0.003-0.4ug/day

* Menzie et.al. 1992, Env. Sci and Technol. Vol. 26: p.1278

NAAQS - CAA 1990

National Ambient Air Quality Standards
ug/m3 or ppm

National Air Quality and Emissions Trends

Report

NAAQ Standards for

six criteria pollutants
Pollutant

Primary Stds.

Carbon Monoxide

9 ppm
(10 mg/m3)
35 ppm
(40 mg/m3)

Lead

1.5 g/m3

Averaging Times

Secondary Stds.

8-hour(1)

None

1-hour(1)

None

Quarterly Average

Same as Primary

Annual (Arithmetic Mean)

Same as Primary

0.053 ppm
Nitrogen Dioxide
Particulate Matter
(PM10)
Particulate Matter
(PM2.5)
Ozone

Sulfur Oxides

*Applies only in limited areas

(100 g/m3)
Revoked(2)

Annual(2) (Arith. Mean)

150 g/m3

24-hour(3)

15.0 g/m3

Annual(4) (Arith. Mean)

35 g/m3

24-hour(5)

0.08 ppm

8-hour(6)

Same as Primary

0.12 ppm *

1-hour(7)

Same as Primary

0.03 ppm
0.14 ppm
-------

Annual (Arith. Mean)

24-hour(1)
3-hour(1)

------------0.5 ppm
(1300 g/m3)

Same as Primary

http://www.epa.gov/air/criteria.html

US Regulation history

1947 CA - Air pollution control Act

1955 - Trumans Air pollution control Act
1963 Federal - Clean Air Act (1967 am)
1965 Federal - Motor vehicle Air pollution control Act
1970 The Clean Air Act: national level (EPA)
O3, SO2, NO2, CO, PM, Pb, total hydrocarbons (dropped)

1970 Lead is banned as fuel additive

1990 CCA amendment: 118 chemicals, some carcinogenic
Maximum achievable control technology
Additional risk assessment if health effects beyond the MACT level
Emission standards for motor vehicles (CO solution - MTBE new problem)

1997 New standard for PM2.5

Clean Air Mercury and Interstate rules

On March 15, 2005, EPA issued the Clean Air Mercury Rule to permanently
cap and reduce mercury emissions from coal-fired power plants for the first
time ever. This rule makes the United States the first country in the world to
regulate mercury emissions from utilities.

On March 10, 2005, in a separate but related action, EPA issued the Clean Air
Interstate Rule (CAIR), a rule that will dramatically reduce air pollution that
moves across state boundaries.

Together the Clean Air Mercury Rule and the Clean Air Interstate Rule create
a multi-pollutant strategy to reduce emissions throughout the United States.

http://www.epa.gov/air/mercuryrule/

Epi studies of air pollution

Outdoor studies predominantly
Cohort studies (Harvard six cities; American Cancer Society;
Adventist Health Study of Smog)
Biomarkers (breath, BAL, blood)
Lung function (FEV1, FVC, FEF25-75)
Symptoms (coughing wheezing, shortness of breath, cardiac
function)
Long-term/chronic (confounders)
Retrospective
Prospective

Time series
National Morbidity, Mortality and Air Pollution Study (NMMAPS)
Air Pollution and Health, a European Approach (APHEA)

Chronic effects of air pollution

Los Angeles basin: aging-like effect on lung function

Netherlands: 12y, SO2 and PM
Rural PA: higher incidence of respiratory symptoms
Harvard Six Cities Study: >15y, 20,000 people SO2 and
PM
Overall reduced lung function, bronchitis
Cancer risk: 2000/year vs 100,000/year from smoking associated with PM/VOC combinations

Relative contribution of individual air pollutants to

lung cancer rates after removing tobacco smoke
cancer (~85%)

PIC: products of
incomplete combustion

US emissions trend for VOCs, NOx, SO2,

and PM10, 1900-1990