Where we live and

breathe

500ml/breath x 15 breaths/min x

60 min/hr x 24hr/day

>10,000 LITERS

>10,000 LITERS

Of air pass through our

lungs every day of our

lives.

Air pollution

• Of the many components of air pollution, those

thought to pose the greatest threat to the lungs
include:

Ozone
Particulate matter
Carbon monoxide
Sulfur dioxide
Nitrogen dioxide
Lead

Smog and lung injury

Smog and lung injury

• In London, December of 1952, smog (i.e smoke,

fog and air pollution), coupled with unusually low
temperatures and a 5- day temperature inversion
conspired to produce a calamitous excess of
respiratory illness and death.

• The major pollutants came primarily from

industrial and domestic discharges of smoke
probably with a prominence of acidic aerosols
among them.

Risk groups include the elderly and the
young as well those with underlying
respiratory and cardiac illness

• CHILDREN:

– Particularly vulnerable
– Smaller and narrower airways
– > breaths/min than adults
– needs for oxygen
– More time outdoors
– The longer the duration of exposure the greater the effect

concern about chronic effects since

the effect outlasts the

exposure

Acute Effects

• Given a threshold dose, the first effects are

seen in the trachea and bronchi.

• Symptoms will include a reflex-mediated

cough

• An acute inflammatory response will ensue

the magnitude of which will depend on
various intrinsic as well as extrinsic
factors.

(cellular infiltration, edema, exudation,

ulceration, bleeding and sloughing of the mucosa)

Airway hyperesponsiveness

(inflammatory processes)

Bronchoconstriction

(obstructive derangement of the

airways)

Symptoms

(cough – productive or dry,

dyspnea, wheezing, chest

tightness, activity restriction)

OZONE: bronchial hyperesponsiveness, decline
in lung function (with time delay) -symptoms
include:substernal chest pain, tearing, burning

2 hrs @ 120

ppb

10-20% of

population

12% decline

FEV1

8 hrs @120ppb

Population

average

20%decline

FEV1

6.6 hrs

@120ppb

Asthmatics and

nonasthmatics

Non-specific

Bronchial

hyperesponsive

ness

1 hr@120ppb

asthmatics

specific

bronchial

hypresposivene

ss

Pulmonary Function Response to Various

Ozone Exposures

pollutants: Ozone, PM, CO, SO

2

,

NO

2

,

pollutants: Ozone, PM, CO, SO

2

,

NO

2

,

PM

3-30

- SIZE MATTERS !

Determines

deposition

site and resultant effect

(bronchitis,chronic cough, resp.

illness, COPD exacerbation,

longevity

A 10mcg/m

3

increase in PM

10

lead to a

rise in:

- total mortality 1%

- CVS mortality 1.4%

- Respiratory mortality 3.4%

- Asthma hospitalization 1.9%

- Asthma ED visits 3.4%

- Asthma exacerbation and increased use
of bronchodilator use 3%.

 

                                                      

                                                                                            

      

Normal gas

exchange

at the

alveolar

level.

CO competes with O

2

for hemoglobin with an

4 -fold greater affinity

CO - interferes with
normal gas exchange and
is directly responsible for
hypoxemia

pollutants: Ozone, PM, CO, SO2, NO2,

SO2 -

mucosal irritation of

upper respiratory tract. Level
of exposure is important level
may be lethal causing mucosal
sloughing and alveolar
hemorrhage

-0.5ppm = odor threshold
-6-10 ppm – irritation of eyes, nose and
throat

-0.25 ppm – can provoke asthma
exacerbation in exercising asthmatics

pollutants: Ozone, PM, CO, SO2, NO2,

-15ppb: stuffy nose and cough
->30 ppb: airway hypereactivity
-80ppb: associated with and inc. in
acute resp. infection, sore throat,
colds

-2-5ppm for 3 hrs.: airway
inflammation

(IgE, local IgA, IgG )

NO2- low concentrations:
impaired mucociliary clearance,
impaired local and cellular immunity.

Air pollution exacerbates

existing respiratory illness and

provokes asthmatic reaction

• Demonstrated by decrements in pulmonary

function testing ( flow rates, lung volumes,

impaired diffusion).

(

spirometry and body plethysmography indices

including FEV1, PEF, DLCO, TLC, IC, RV)

• Elevated levels of

biomarkers

detected in

exhaled air, blood, urine, sputum and

broncoalveolar lavage correlate with the above

(NO (exhaled nitric oxide), cell type and number,

cytokines, arachidonic acid metabolites, oxygen

radicals, fibronectin, protein, interleukins, TNF-α and

various enzymes