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 monoxideSulfur dioxideNitrogen dioxide Lead

Smog and lung injurySmog 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 hyperesponsiveness

1 hr@120ppb asthmatics specific bronchial hypresposiveness

Pulmonary Function Response to Various Ozone Exposures

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


PM 3-30 - SIZE MATTERS ! Determines deposition site and resultant effect (bronchitis,chronic cough, resp. illness, COPD exacerbation, longevity

A 10mcg/m3 increase in PM10 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 O2 for hemoglobin with an 4 -fold

greater affinity

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


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


-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

Biomarkers and degree of response - evaluation of biologically effective dose

Limitations of Biomarkers

to date are not adequate assessment factors of clinical status or physiological impairment

unclear indicators of ongoing injury or merely transient effect on exposure.

interpretation of their significance remains to be determined

Am. J. Respir. Crit. Care Med., Volume 161, Number 2, February 2000, 665-673

AMERICAN THORACIC SOCIETYWhat Constitutes an Adverse Health Effect of Air Pollution? THIS OFFICIAL STATEMENT OF THE AMERICAN THORACIC

SOCIETY WAS ADOPTED BY THE ATS BOARD OF DIRECTORS, JULY 1999

• New scientific findings recorded since previous statement• Reassessment of adverse vs. nonadverse health effects.• Improved sensitivity of research approaches (biomarker detection

of even subtle disturbances of biological systems ).• Epidemiological research designs are more refined• New statistical approaches (software and hardware)• Improved design of clinical studies to include specimen sampling• Medical outcomes research now recognizes that patient well-being

should be broadly conceptualized and measured rigorously

(REVISION OF THE 1985 STATEMENT )

What constitutes and adverse respiratory health effect ?

Definition: a medically significant physiologic or pathologic change evidenced

by one or more of the following:a. interference with normal activity of the affected person or persons.b. episodic respiratory illnessc. incapacitating illnessd. permanent respiratory injury and/or

e. progressive respiratory dysfunction

Finally,

- it distinguishes between reversible and nonreversible effects.

- Healthy persons may sustain transient reductions in pulmonary function associated with air pollution.

Acute Effects of Ambient Inhalable Particles in Asthmatic and Nonasthmatic Children

SVERRE VEDAL, JOHN PETKAU, RICK WHITE, and JIM BLAIR

Increases in inhalable particle (PM10)concentration have been associated with acute reduction in the level of lung function and increased symptom reporting in children. It is unclear whether asthmatic children are more likely to experience these effects than children without asthma

CONCLUSION: Children experience reduction in PEF and increase symptoms after increases in relatively low ambient PM10 concentrations, and children with diagnosed asthma are more susceptible

Acute Effects of Particulate Air Pollution on Respiratory Admissions

Results from APHEA 2 Project

RICHARD W. ATKINSON, H. ROSS ANDERSON, JORDI SUNYER, JON AYRES, MICHELA BACCINI, JUDITH M. VONK, AZZEDINE BOUMGHAR, FRANCESCO FORASTIERE, BERTIL FORSBERG, GIOTA TOULOUMI,

JOELSCHWARTZ, and KLEA KATSOUYANNI • Investigated short-term health effects of particles (<PM10) in eight European

cities and black smoke and daily counts of emergency hospital admissions for asthma (0-64yr.), COPD, and all respiratory disease (65+yr) controlling for environmental factors and temporal patterns.

• CONCLUSION: Confirmed that particle air pollution was associated with daily admissions for respiratory disease in a selection of European cities and average daily ozone levels explaine a proportion of between city variability.

What is the physiological impact?

INDIVIDUAL POPULATION –BASED QUALITY OF LIFE

PHYSICAL

-Functioning

-Symptoms

- cough

- wheeze

- pain

- nausea

- headache

- Cognitive function

- Exercise

PSYCHOSOCIAL

- Well-being

- Anxiety, worry, fear

- Depression

SOCIAL

-Relationships (friends, family)

-Opportunity for social interaction

-Community interaction

-Work, School

-Recreation

-Work performance (concentration and productivity

Acute Effects of Ambient Inhalable Particles in Asthmatic and Nonasthmatic Children

SVERRE VEDAL, JOHN PETKAU, RICK WHITE, and JIM BLAIR

Long-Term Inhalable Particles and Other Air Pollutants Related to Mortality in Nonsmokers

DAVID E. ABBEY, NAOMI NISHINO, WILLIAM F. MCDONNELL, RAOUL J. BURCHETTE, SYNNØVE F. KNUTSEN, W. LAWRENCE BEESON, and JIE X. YANG

Cytokines Involved in the Systemic Inflammatory Response Indused by Exposure to Particulate Matter (PM(10))

VAN EEDEN SF, TAN WC, SUWA T, MUKAE H, TERASHIMA T, FUJII T, QUI D, VINCENT R, HOGG JC.

Exacerbation of COPD Environmental Mechanisms

WILLIAM MACNEE, MD AND KENNETH DONALDSON, DSC

Where we live and breathe

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