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

Gases
COx SOx NOx PAH

Solid and liquid

Smoke (from combustion) Coastal aerosols

Liquid Aggregate gases (sulfate, nitrate)

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

respirable

Chemical reactivity Shape (fibers) Water content

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 (H2SO3), 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
(sulfite, bisulfite)

continued

Absorption at upper respiratory tract 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
Oxidant, less potent than O3

NAAQS: 0.05ppm, annual

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

Health effects - starting at 1.5-2ppm

Gas pollutants - CO
Properties
Sources
Incomplete combustion Traffic (inside the car, parking garages, tunnels is highest) Inside cars = 3x urban streets, and = 5x residential streets Odorless, heavier than air, stronger binder to Hb than O2

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

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 Properties
Short lived, highly reactive, water soluble Scrubbed in nasopharynx Reaches terminal bronchioles and alveoli NAAQS: 0.12ppm, 1h 0.08ppm, 8h

Sources
Photochemical reactions

Health effects
Degenerative lung disease Loss of lung function

Photochemical pollution
NO2 O2 + O O3 + NO Twist: In absence of HC- the reaction reaches equilibrium uv NO + O O3 O2 + NO2

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 build-up!!

O3

Photochemical pollution
NO2 O2 Hydrocarbons

uv

O3
The O3 molecule is highly reactive . O
2

O3
O

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

H2O

Effects of Ozone on lung function

FEV
0.5ml

1 0.12 - 0.4 ppm for 2-3 h FVC and FEV1

ppb

(Kinney et.al, 1996)

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

Ozone levels

ppm 0.30 LA, until 1998 0.24 0.20 LA, 1h-ave 0.18 EU 1h ave US-EPA 1h ave 0.12 Italy study (low exposure) 0.10 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 Alcoxyl radical Alkoperoxyl radical Nitrous acid Nitric acid Hydroxyl radical Hydroperoxy radical R C H

RO (RO ) . . RO2 (ROO ) HONO HONO2 . (HO.) 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 compartments

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 aldehydes H2 O

Hydroxyhydroperoxy compound . HO H2 O 2 Lipid peroxidation cascade Malondialdehyde (MDA) Lipid fragmentation 8-isoprostane LTB4 (PMN chemotractant)

Lipid peroxidation cascade

Effects on nucleic acids

Electrophiles react with strong nucleophilic atoms of nucleic acids 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 responsiveness 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
H+

L-arginine + O2

NO

.
Fenton

NO2

NAD(P)H + O2

Oxidase
NAD(P)+ H+

. O
2

HO O2 Cl-

H20

HOOH + H+ +Cl-

MPO

HOCl

The lungs defenses:

Antioxidant molecules:
ascorbic acid (vit. C) a-tocopherol (vit. E) uric acid glutathione (GSH)

Metabolic enzymes:
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. 9 ppm (10 mg/m3) 35 ppm (40 mg/m3) 1.5 g/m3 0.053 ppm Nitrogen Dioxide Particulate Matter (PM10) Particulate Matter (PM2.5) Ozone (100 g/m3) Revoked(2) 150 g/m3 15.0 g/m3 35 g/m3 0.08 ppm 0.12 ppm * 0.03 ppm 0.14 ppm ------Annual (Arithmetic Mean) Annual(2) (Arith. Mean) 24-hour(3) Annual(4) (Arith. Mean) 24-hour(5) 8-hour(6) 1-hour(7) Annual (Arith. Mean) 24-hour(1) 3-hour(1) Same as Primary Same as Primary Same as Primary ------------0.5 ppm (1300 g/m3) Same as Primary Averaging Times 8-hour(1) 1-hour(1) Quarterly Average Secondary Stds. None None Same as Primary Carbon Monoxide

Lead

Sulfur Oxides
*Applies only in limited areas

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