INT J TUBERC LUNG DIS 12(2):115127 2008 The Union

Outdoor and indoor air pollution and COPD-related diseases in high- and low-income countries

Y. Liu,* K. Lee,* R. Perez-Padilla, N. L. Hudson,* D. M. Mannino*

* Department of Preventive Medicine and Environmental Health, University of Kentucky College of Public Health, Lexington, Kentucky, USA; School of Public Health, Seoul National University, Korea; National Institute of

S U M M A R Y

Respiratory Diseases, Mexico City, Mexico

Chronic obstructive pulmonary disease (COPD) is animportant cause of morbidity and mortality in bothhigh- and low-income countries. While active cigarettesmoking is the most important preventable risk factorglobally, outdoor and indoor air pollutants can cause orexacerbate COPD. In high-income countries, historic airpollution events provide clear evidence that exposure tohigh levels of outdoor air pollutants is associated withincreased mortality and morbidity due to COPD and re-lated cardiorespiratory diseases. Studies in the last 20years continue to show increased risk associated mainlywith particulate matters, even at much lower levels. Pop-

ulations in low-income countries are largely exposed toindoor air pollutants from the combustion of solid fuels,which contributes significantly to the burden of COPD-related diseases, particularly in non-smoking women.Effective preventive strategies for COPD may vary be-tween countries, and include continued improvements inair cleaning technology, air quality legislation and dis-semination of improved cooking stoves. A joint effortfrom both society and governments is needed for theseendeavors.KEY WORDS: COPD; outdoor air pollution; indoor bio-mass pollution; environmental exposures

AIR POLLUTION has been recognized for its relation-ship with cardiorespiratory illnesses, including chronicobstructive pulmonary diseases (COPD), since the early1900s. Sharp increases in fatalities and hospital admis-sion rates, particularly in the elderly, were well docu-mented in air pollution events in the 1940s and 1950s.This led to rapid developments in technology and airpollution legislation in the 1960s and 1970s that even-tually improved outdoor air quality in the United Statesand many other high-income countries.1 However, therelative increase in motor vehicle traffic in the pastdecades13 has now presented as a more worrying airpollution problem in many metropolitan cities around

the world. In low-income countries where more house-holds use traditional cooking fuels and stoves, indoorair pollution from biomass combustion has been foundto contribute to COPD and other cardiorespiratorydiseases, particularly in non-smoking women.

The health effects of air pollution are a spectrum ofresponses that includes sensory response to odors, ir-ritation of the upper respiratory systems, increasedprevalence of respiratory infections, symptoms suchas cough, phlegm production, chest tightness andwheezing, chronically reduced pulmonary function inforced vital capacity (FVC), forced expiratory volumein one second (FEV1) together with symptoms, andincreased incidence in exacerbation of cardiopulmo-nary diseases, asthma attacks, cancer and mortality.4While air pollution may affect all ages of the popula-tion, the elderly, particularly those with pre-existingcardiopulmonary diseases such as COPD, are the mostsusceptible group. This review will therefore focus onthe more serious adverse health effects of COPD

Correspondence to: Youcheng Liu, Department of Preventive Medicine and Environmental Health, University of KentuckyCollege of Public Health, 121 Washington Ave, Lexington, KY 40536, USA. Tel: (1) 859 218 2234. Fax: (1) 859 2579862. e-mail: youcheng.liu@uky.eduArticle submitted 28 September 2007. Final version accepted 19 November 2007.

STATE OF THE ART

STATE OF THE ART SERIESChronic obstructive pulmonary disease in high- and low-income countries

Edited by G. Marks and M. Chan-YeungNUMBER 2 IN THE SERIES

Previous articles in this series Editorial: Marks G, Chan-Yeung M.COPD: a new global challenge to lung health. Int J Tuberc Lung Dis2008; 12(1): 2. No. 1: Slama K. Global perspective on tobacco con-trol. Part I. The global state of the tobacco epidemic. Int J TubercLung Dis 2008; 12(1): 37. Chapman S. Global perspective on to-bacco control. Part II. The future of tobacco control: making smok-ing history? Int J Tuberc Lung Dis 2008; 12(1): 812.

116 The International Journal of Tuberculosis and Lung Disease

(mortality, morbidity and health care utilization) aloneor in the context of cardiorespiratory diseases.

COPD remains a major public health problemworldwide, and is one of the leading causes of mor-tality and morbidity in both high- and low-incomecountries.59 According to World Health Organiza-tion (WHO) estimates, about 80 million people havemoderate to severe COPD and 3 million died of COPDin 2005, which corresponds to 5% of all deaths glo-bally.5 Total deaths due to COPD are projected to in-crease by more than 30% in the next 10 years. Mor-tality and morbidity rates vary across countries andregions, and are affected by the COPD definitionsused, the accuracy of local reporting systems and thesurvey methods used.8 Dramatic increases in the nexttwo decades are expected in Asian and African coun-tries due to increasing tobacco use.10

COPD has profound effects on the quality of life ofpatients, and places an enormous economic burdenon society. In high-income countries, exacerbations ofCOPD account for the greatest burden on the healthcare system. In the US in 2002, for example, the directcosts of COPD were $18 billion and the indirect coststotalled $14.1 billion.11 In the European Union, thetotal direct costs of respiratory diseases are estimatedto be about 6% of the total health care budget, withCOPD accounting for 56% (38.6 billion) of thetotal.9 Although data are lacking for low-incomecountries, it is projected to increase along with the in-crease in tobacco use, based on estimates from per pa-tient cost in high-income countries.12

COPD results from interaction between individualgenetic factors and environmental exposures to toxicagents, such as tobacco smoking, outdoor and indoorair pollution, occupational exposure to organic andmineral dusts, gases and fumes and lower respiratoryinfections in early childhood.13 Most genetic factorsare unknown, except for alpha 1-antitrypsin deficiency,present in 13% of COPD patients. Nutrition mayalso be a predisposing factor, and interacts with envi-ronmental exposures.14 Tobacco smoke is well estab-lished as the most important risk factor for COPD,particularly in high- and middle-income countries;15,16however, in low-income countries, exposure to indoorair pollution, such as the use of biomass fuels for cook-ing and heating, increases the burden of COPD in ad-dition to tobacco smoking.5 This suggests that differ-ent specific public health measures and strategies needto be used to target priority risk factors in the preven-tion of COPD in different parts of the world, althoughall involve breathing clean air.

This article will review the most recent develop-ments in outdoor and indoor air pollution that con-tribute to the burden of COPD and other relatedcardiorespiratory diseases in high- and low-incomecountries. Our focus is the risk of COPD and relatedmortality and morbidity from epidemiological studies.No controlled human exposure studies or laboratory

animal studies are included. The review does not ad-dress smoking, active or passive, the role of infectionsin COPD or the relationship between occupationalexposures and the risk of COPD, nor will it includeelaborations on the environmental mechanisms forasthma in producing irreversible airflow obstruction.Readers are advised to refer to previous reviews pub-lished on traffic air pollution and health,1,3 air pollu-tion and respiratory risk in low-income countries,17,18indoor air pollution and respiratory health,19 as wellas review articles on air pollution and health in gen-eral,20 and on COPD.21,22

METHODS

We conducted systematic searches of the literature inEnglish or articles with English abstracts using biblio-graphic databases of PubMed/Medline (National Li-brary of Medicine and National Institutes of Health)and Web of Science (Science Citation Index Expanded,Thomson Corporation). We used the keywords COPDor emphysema or chronic bronchitis AND outdoorair pollution or indoor biomass and coal pollutionto search articles up to October 2007. We were par-ticularly interested in epidemiological studies pub-lished within the last 10 years, although some impor-tant previous studies were also cited as background.Articles were also found from the reference lists ofselected articles and systemic searches on specific jour-nals such as Thorax and the American Journal of Res-piratory and Critical Care Medicine. In addition,extensive searches using Google (google.com) wereperformed on the Internet. We did not intend to in-clude all articles in our review; instead we selected themost recent studies that evaluated mortality, morbid-ity or hospital admissions/emergency room visits intypical regions (North America, Europe, Oceania andlow-income countries) for summary. Large multi-country studies were selected over reports from indi-vidual countries in the same study.

Outdoor air pollutionMost epidemiological air pollution studies conductedin high-income countries on short-term exposure andeffects on the general population or patients sufferingfrom COPD used the time series method to evaluatethe risk of mortality due to cardiorespiratory dis-eases, or COPD hospital admissions temporally re-lated to air pollution levels, i.e., these studies measureddaily variations in the number of health events in acity in relation to daily variations in air pollutants andconfounding variables, such as temperature. Comparedwith short-term exposure studies, few studies havebeen conducted prospectively to evaluate the long-termeffects of air pollution on COPD. Although outdoorair pollutant levels tend to be higher in low-incomecountries than in high-income countries, fewer studieswere conducted.

Air pollution and COPD burden 117

MortalityHistorical reports of dramatic air pollution episodesin the early 1950s have provided clear evidence of mor-tality associated with high levels of particulate matter(PM), measured as black smoke in Europe, sulfur di-oxide (SO2), and acid aerosols. During the Londonsmog of 59 December 1952, there was a more than2-fold increase in the daily death rate, resulting inaround 4000 extra deaths. Between 80% and 90% ofthe deaths were from cardiorespiratory causes, andthe greatest relative increase was in deaths due to bron-chitis, which rose 9-fold.2 In the December 1991 airpollution episode in London, all-cause mortality, ex-cluding accidents, increased (relative risk [RR] 1.10).Although not statistically significant, increases wereobserved for all respiratory diseases (RR 1.22) andobstructive lung diseases (RR 1.23).23

While improved technology and legislation havereduced air pollution levels in high-income countries,studies in the past 20 years continue to show in-creased mortality related to air pollution. Overall, a50 g/m3 increase in 24 h PM with aerodynamic di-ameter 10 m (PM10) is associated with a 2.55%increase in premature non-accident mortality for thegeneral population, with higher risks for the elderlyand those with pre-existing cardiopulmonary condi-tions (Table 1).2429 Most studies evaluated total mor-tality due to cardiorespiratory diseases or respiratorydiseases, although some looked specifically at COPD.For example, Schwartz and Dockery found that a100 g/m3 increase in total suspended particles (TSP)would lead to a 10% (95% confidence interval [CI]614) increase in COPD mortality.28

One of the largest studies conducted in the US wasthe National Morbidity, Mortality and Air PollutionStudy (NMMAPS) sponsored by the Health EffectsInstitute, which examined the effect of short-term ex-posure to PM on mortality in 20 US cities, which waslater extended to include 90 US cities.24,30,37,38 The percent increase for cardiorespiratory mortality was0.68 (95%CI 0.201.16) in the 20-city study.30 Thisstudy addressed various important issues in air pollu-tion and mortality studies, such as measurement er-ror, confounding, and effects of multiple gaseous co-pollutants on the influence of PM.

In Europe, the Air Pollution and Health: a Europeanapproach (APHEA) study showed that an increase of50 g/m3 in SO2 or black smoke was associated witha 3% (95%CI 24) increase in daily mortality; the cor-responding value for PM10 was 2% (95%CI 13). Incentral eastern European cities, the increase in mor-tality associated with a 50 g/m3 change in SO2 was0.8% (95%CI 0.12.4) and in black smoke 0.6%(95%CI 0.11.1).31 Later, the APHEA II study showedthat a 10 g/m3 increase in daily PM10 or black smokeconcentrations increased mortality by 0.6% (95%CI0.40.8), with a slightly higher increase among the el-derly. The concentration of nitrogen dioxide (NO2)

modified the relationship between PM and mortality(mortality at 0.80%, 95%CI 0.670.93 at high NO2levels).32 Similar excesses in total and respiratorymortality were also observed in nine French cities.39

The relationship between daily exposure to air pol-lutants and daily mortality is linear, with no clearthreshold for PM10.17,40 The short-term effect be-tween exposure and mortality is affected by lag days.For example, Zeka et al. found that all-cause mortal-ity increased with PM10 exposures occurring both 1and 2 days prior to the event, and deaths from heartdisease were primarily associated with PM10 on 2 daysbefore the event, while respiratory deaths were asso-ciated with PM10 exposure on all 3 days.34

While many time series studies have shown an in-crease in mortality related to short-term air pollution,prospective cohort studies have also found increasedmortality due to long-term exposure to low-level airpollution. Pope et al. evaluated exposures to multipleair pollutants in metropolitan areas of all 50 states inthe US, and found the RR of mortality due to cardio-respiratory causes at respectively 1.06 (95%CI 1.021.60), 1.08 (95%CI 1.021.14) and 1.09 (95%CI1.081.16) for the periods 19791983 and 19992000 and the average of all periods.33

Similar results in mortality have also been found incities in low-income countries. In Mexico, Tellez-Rojo et al. found that an increase of 10 g/m3 PM10was related to a 2.9% (95%CI 0.94.9) and 4.1%(95%CI 1.36.9) increase in total respiratory andCOPD deaths, respectively.35 In Shanghai, China, anincrease of 10 g/m3 in PM10, SO2 and NO2 corre-sponded to an RR increase in mortality of COPD in allages of respectively 1.005 (95%CI 0.9991.011), 1.035(95%CI 1.0151.054) and 1.032 (95%CI 1.0091.056) (Table 1).36 As summarized by Nejjari et al., aglobal excess risk of total mortality varied from 3%to 4%, with 1% to 6% for respiratory mortality, foran increase of 50 g/m in the pollution indicators.17

The mechanisms of deaths triggered by increasedair pollution have recently been clarified, and includecardiovascular mechanisms: alteration in coagula-tion, in the autonomic control or pollutant inflamma-tion enhancing atherogenesis.4143 These mechanismsare relevant to patients with COPD who frequentlyhave comorbid diseases.8 Increased susceptibilities torespiratory infections, increased airflow obstructionand deranged gas exchange are also important. Pa-tients who die during air pollution episodes include notonly those with a very short life expectancy (this mech-anism has been called harvesting), but also patientsand subjects with much longer life expectancy.44

Hospital admissions and emergency room visitsCOPD patients are particularly vulnerable to additionalstress on the respiratory system caused by the toxiceffects of inhaled pollutants.45 Exposure to air pollut-ants has been associated with respiratory morbidity,

Tab

le 1

Out

door

air

pollu

tion

and

CO

PD-r

elat

ed m

orta

lity

in b

oth

high

-inco

me

and

low

-inco

me

coun

trie

s

Firs

t au

thor

,ye

ar, r

efer

ence

City

/cou

ntry

Subj

ects

Stud

y pe

riod

Pollu

tant

s m

easu

red

Lag

days

ana

lyze

dRi

sk t

ype

and

per

unit

incr

ease

Risk

leve

l (95

%C

I)

Hig

h-in

com

e co

untr

ies

Sam

et 2

0003

0 *20

larg

est

citie

s, U

SA

65, 6

574

,

74 y

ears

7 ye

ars

(198

719

94)

24-h

mea

n: P

M10

, g/

m3 ;

SO2,

ppb

; NO

2, p

pb;

CO

, ppb

; O3,

ppb

8-h

mea

n: O

3, p

pb

03

days

lag

Per

cent

incr

ease

in t

otal

mor

talit

y an

d ca

rdio

resp

irato

ry m

orta

lity

per

10

g/m

3 in

PM

10

1 da

y la

g:

All

caus

es 0

.51

(0.0

70.

93)

Car

dior

espi

rato

ry 0

.68

(0.2

01.

16)

Kat

souy

anni

19

9731

*12

citi

es, E

urop

e,A

PHEA

IA

ll ag

es10

yea

rs(1

977

1987

)24

-h m

ean:

PM

10,

g/m

3 ;bl

ack

smok

e,

g/m

3 ;SO

2,

g/m

3

03

days

lag

Per

cent

incr

ease

in t

otal

mor

talit

y pe

r 50

g/

m3

incr

ease

in P

M10

, bl

ack

smok

e or

SO

2

Wes

tern

Eur

ope:

SO

2 3

(24

)Bl

ack

smok

e 3

(24

)PM

10 2

(13

)C

entr

al-E

aste

rn E

urop

e: S

O2

0.8

(-0.

12.

4)Bl

ack

smok

e 0.

6 (0

.11

.1)

Kat

souy

anni

20

0132

*29

citi

es, E

urop

e,A

PHEA

IIA

ll ag

es10

yea

rs(1

977

1987

)24

-h m

ean:

PM

10,

g/m

3 ;bl

ack

smok

e,

g/m

3 ;SO

2,

g/m

3 ; N

O2,

g/

m3 ;

O3,

g/

m3

02

days

lag

Per

cent

incr

ease

in t

otal

mor

talit

y pe

r 10

g/

m3

incr

ease

in P

M10

and

blac

k sm

oke

PM10

and

bla

ck s

mok

e:A

ll ag

es 0

.6 (0

.40

.8)

65

yea

rs 0

.7 (0

.51

.0)

Pope

200

233

Met

ropo

litan

are

a,50

sta

tes,

USA

30

yea

rs21

yea

rs(1

979

2000

)24

-h m

ean:

TSP

, g/

m3 ;

PM15

, g/

m3 ;

PM

10,

g/m

3 ;PM

2.5,

g/

m3 ;

PM

152

.5,

g/m

3 ;SO

2, p

pb; N

O2,

ppb

; O3,

ppb

;C

O, p

pm; S

O4,

ppb

1 h

max

: O3,

ppb

Mod

ified

Cox

-pro

port

iona

lha

zard

s m

odel

with

spa

tial

rand

om e

ffec

tco

mpo

nent

RR in

crea

se in

car

dior

espi

rato

rym

orta

lity

per

10

g/m

3

incr

ease

in P

M2.

5

1979

198

3 tim

e pe

riod

1

.06

(1.0

21.

60)

1999

200

0 tim

e pe

riod

1

.08

(1.0

21.

14)

Ave

rage

1

.09

(1.0

81.

16)

Zeka

200

534 *

20 U

S ci

ties

All

ages

12 y

ears

(198

920

00)

24 h

mea

n: P

M10

, g/

m3

03

days

lag

Per

cent

incr

ease

in C

OPD

mor

talit

y pe

r 10

g/

m3

incr

ease

in P

M10

Sing

le la

g m

odel

: Lag

0

-0.

06 (-

0.63

0.5

1)La

g 1

0

.43

(-0.

141

.00)

Lag

2

0.3

9 (-

0.16

0.9

4)3

day

cum

ulat

ive

0

.43

(-0.

351

.21)

Low

-inco

me

coun

trie

sTe

llez-

Rojo

200

035

Mex

ico

City

, Mex

ico

65

yea

rs1

year

(199

4)24

h m

ean:

PM

10 (

g/m

3 )1

h m

ax: O

3, p

pb;

SO2,

ppm

; NO

2, p

pm

07

days

lag;

Cum

ulat

ive

lags

by 3

, 5 a

nd

7 da

ys a

naly

zed

Per

cent

incr

ease

in C

OPD

m

orta

lity

per

10

g/m

3

incr

ease

in P

M10

and

per

40 p

pb in

crea

se in

O3

Out

side

med

ical

uni

tTo

tal r

espi

rato

ry:

PM10

2

.9 (0

.94

.9),

3 da

y la

gO

3

5.6

(0.5

10.

9), 2

day

lag

CO

PD:

PM10

3

.0 (0

.15

.9),

1 da

y la

gPM

10

6.1

(2.4

9.9

), 5

day

mea

nO

3

8.3

(1.0

16.

1), 3

day

lag

Kan

& C

hen

2003

36Sh

angh

ai, C

hina

All

ages

1.

5 ye

ars

(200

020

01)

24 h

mea

n: P

M10

, g/

m3 ;

SO2,

g/

m3 ;

NO

2,

g/m

30

5 da

ys la

gRR

incr

ease

in C

OPD

mor

talit

ype

r 10

g/

m3

incr

ease

in

pol

luta

nts

All

ages

: PM

10

1.0

05 (0

.999

1.0

11)

SO2

1

.035

(1.0

151

.054

)N

O2

1

.032

(1.0

091

.056

)A

ge 6

575

yea

rs:

PM10

0

.996

(0.9

861

.007

)SO

2

1.0

10 (0

.977

1.0

43)

NO

2

1.0

07 (0

.967

1.0

47)

*Ti

me

serie

s st

udie

s to

eva

luat

e sh

ort-

term

exp

osur

e, in

whi

ch v

aria

bles

of

long

-ter

m t

rend

s, d

ay o

f th

e w

eek,

tem

pera

ture

, hum

idity

, dew

poi

nt t

empe

ratu

re, a

nd in

fluen

za e

pide

mic

wer

e co

ntro

lled.

Pr

ospe

ctiv

e co

hort

stu

dy t

o ev

alua

te lo

ng-t

erm

exp

osur

e, in

whi

ch t

he C

ox p

ropo

rtio

nal h

azar

d su

rviv

al m

odel

was

use

d an

d pe

rson

al c

hara

cter

istic

s su

ch a

s sm

okin

g, e

duca

tion,

mar

ital s

tatu

s, b

ody

mas

s in

dex,

occ

upat

iona

l exp

osur

es, d

iet

and

alco

hol u

se w

ere

cont

rolle

d.Pe

r ce

nt in

crea

se

(RR

1

) 1

00.

CO

PD

chr

onic

obs

truc

tive

pulm

onar

y di

seas

e; C

I c

onfid

ence

inte

rval

; PM

10

par

ticul

ate

mat

ter

with

aer

odyn

amic

dia

met

er

10

m; P

M15

p

artic

ulat

e m

atte

r w

ith a

erod

ynam

ic d

iam

eter

15

m

; PM

2.5

p

artic

ulat

e m

atte

r w

ith a

erod

y-na

mic

dia

met

er

2.5

m

; PM

1.5

2.5

p

artic

ulat

e m

atte

r w

ith a

erod

ynam

ic d

iam

eter

1.5

2.5

m

; RR

r

elat

ive

risk;

SO

2

sul

fur

diox

ide;

ppb

p

arts

per

bill

ion;

NO

2

nitr

ogen

dio

xide

; CO

c

arbo

n m

onox

ide;

O3

o

zone

; SO

4

aer

osol

sul

-fa

te; A

PHEA

A

ir Po

llutio

n an

d H

ealth

: a E

urop

ean

App

roac

h; T

SP

tot

al s

uspe

nded

par

ticle

s w

ith a

erod

ynam

ic d

iam

eter

40

m

.

Air pollution and COPD burden 119

including acute respiratory symptoms,46 decreasedpulmonary function and exacerbation of COPD condi-tions that may be severe enough to require an emer-gency room visit or hospitalization.2,47 In the well-known London smog incident in 59 December 1952,black smoke levels rose to 1600 g/m3, four timeshigher than normal levels at that time. This air pollu-tion episode caused total hospital admissions to riseby 50% and respiratory admissions by 160%.2 Morerecent episodes, with more modest effects, in 1991 inLondon23 and from 1985 to 1989 in Utah in the US,have been studied.48

Since the early 1990s, many epidemiological studieshave evaluated hospital admissions for COPD result-ing from short-term exposure to outdoor air pollu-tion. Statistical models have been used to evaluate theeffects of PM and co-pollutants on COPD events atdifferent lag times, while controlling for the effect ofother variables such as long-term trends, meteorolog-ical parameters or city characteristics (Table 2). Theseresearch results have provided scientific evidence andbasis for air quality regulations in the US56 and othercountries.

In the US, Schwartz conducted separate studies inMinneapolis, St. Paul, MN,47 Birmingham, AL,29 De-troit, MI57 and Spokane, WA.58 In each city, he eval-uated the change in daily average concentrations ofPM10 and ozone (O3) on the risk of hospital admis-sion for COPD among elderly persons aged 65years. Both PM10 and O3 were found to be associatedwith increased risk of hospital admissions for COPD.The RR for PM10 (per 10 g/m3 increase) ranged from1.02 to 1.57, with the 95%CI ranging from 0.76 to2.06; similar effects were noted for ozone.47 Similarresults were found in Reno-Sparks, NV, where a26.6 g/m3 increase in PM10 resulted in an RR of 1.049(95%CI 1.0111.087) for COPD hospitalizations.51

While earlier studies focused on PM10, Burnett etal. extended the studies to include the analysis of bothfine particles (FP) and coarse particles (CP), the con-tent of aerosol sulfate (SO4) and acidity (H) in par-ticles and multiple gaseous co-pollutants (O3, NO2,SO2 and CO) in Toronto, Canada, in three consec-utive summers from 1992 to 1994. These exposuredata were compared with concurrent data on respira-tory hospital admissions that included COPD. TheRR from single pollutant models was 1.022 for CO,1.023 for CP, 1.030 for SO4, 1.036 for PM10, 1.040for FP and SO2, 1.048 for NO2 and 1.068 for O3. In-creases in O3, NO2 and SO2 were associated with an11% increase in daily admissions.49 In Vancouver, O3and NO2 were found to be significantly associatedwith COPD admission, and the combined RR for allgases was 1.21.53 A similar multi-pollutant study inthree US counties also found that gases other thanozone were more strongly associated with COPD ad-missions than PM.59

In Montreal, Canada, Delfino et al. similarly eval-

uated multiple pollutants and their effect on emer-gency room (ER) visits from 1992 to 1993. For 1993,1 h maximum O3, PM10, PM2.5 and SO4 were all pos-itively associated with respiratory visits for patientsaged 64 years. An increase in the mean level of 1 hmaximum O3 (36 parts per billion [ppb]) was associ-ated with a 21% (RR 1.21) increase over the meannumber of daily ER visits (95%CI 834). The effectsof PM and SO4 were smaller, with mean increases of16% (95%CI 428), 12% (95%CI 221) and 6%(95%CI 112) for PM10, PM2.5 and SO4, respectively.60The O3 and PM10 levels were all well below the cur-rent US National Ambient Air Quality Standards,which are 80 ppb 8 h average and 120 ppb 1 h max-imum for O3 and 150 g/m3 24 h average for PM10.56

In Europe, a six-city multi-pollutant study evalu-ated air pollution and hospital admissions for COPDas part of the APHEA project. For all ages, the RR fora 50 g/m3 increase in the daily mean level of pollut-ant (lagged 13 days) was 1.02 (95%CI 0.981.06)for SO2, 1.04 (95%CI 1.011.06) for black smoke,1.02 (95%CI 1.001.05) for TSP with aerodynamicdiameter 40 m, 1.02 (95%CI 1.001.05) forNO2 and 1.04 (95%CI 1.021.07) for O3 (8 h). Theseresults for particles and O3 are generally consistentwith those from North America, although the coeffi-cients for particles are substantially smaller.45

In Sydney, Australia, a similar study with multipleair pollutants found a 4.6% increase in COPD hospi-tal admissions for a 50 g/m3 increase in daily meanlevel of PM0.012.0, consistent with previous studies.50

Most recently, Medina-Ramon et al. conducted acase-crossover study in 36 US cities in which theyevaluated the effect of daily mean concentrations ofPM10 and O3 on hospital admissions for COPD. Theyfound that during the warm season, the 2-day cumu-lative effect of a 5-ppb increase in O3 resulted in a0.27% (95%CI 0.080.47) increase in COPD admis-sions, and a 10 g/m3 increase in PM10 on a previousday increased the COPD admissions of the followingday by 1.47% (95%CI 0.932.01). In this study, theuse of a central air-conditioning system reduced theeffect of air pollution.55

Table 3 summarizes some studies in air pollutionand COPD hospitalizations in urban areas in low-income countries. In Delhi, India, a time series studyin one hospital found a 24.9% increase in emergencyroom visits related to air pollution.61 In Sao Paulo,Brazil, all measured pollutants, PM10, SO2, NO2, O3and carbon monoxide (CO), were significantly asso-ciated with increased hospital admissions, with an in-crease of 10 g/m3 in fine particulate matter associ-ated with a 4.3% increase in admissions for COPD inthe elderly.62 In Taipei City, Taiwan, during warmdays (20C), all pollutants except SO2 were associ-ated with an increased risk of hospital admissions,but on cold days (20C) only SO2 was associatedwith increased risk.63

Tab

le 2

Out

door

air

pollu

tion

and

CO

PDr

elat

ed h

ospi

taliz

atio

ns o

r em

erge

ncy

room

vis

its in

hig

h-in

com

e co

untr

ies

Firs

t au

thor

,ye

ar, r

efer

ence

City

/cou

ntry

Subj

ects

Stud

y pe

riod

Pollu

tant

s m

easu

red

Lag

days

ana

lyze

dRi

sk t

ype

and

per

unit

incr

ease

Risk

leve

l (95

%C

I)

Burn

ett

1997

49To

ront

o, C

anad

aPo

pula

tion:

2.

36 m

illio

nA

ll ag

es

3 su

mm

ers

(199

219

94)

24h

mea

nD

aytim

e m

ean

Dai

ly 1

h m

ax5-

day

mea

n: T

P,

g/m

3 ;Fi

ne p

artic

les,

g/

m3 ;

Coa

rse

part

icle

s,

g/m

3 ;H

, n

mol

/m3 ;

SO

4, n

mol

/m3 ;

NO

2, p

pb; C

O, p

pb;

SO2,

ppb

; O3,

ppb

04

days

lag

RR in

crea

se in

all

resp

irato

ry d

isea

ses

incl

udin

g C

OPD

per

incr

ease

inTP

1

4.25

g/

m3 ;

Fine

par

ticle

s

11

g/

m3 ;

Coa

rse

part

icle

s

4.7

5

g/m

3 ;N

O2

5

.75

ppb;

CO

0

.75

ppb;

SO2

4

.00

ppb;

O3

1

1.50

ppb

RR s

igni

fican

t fo

r al

l sin

gle

pollu

tant

sRR

for

par

ticle

s ad

just

ed f

or a

ll ga

seou

s po

lluta

nts:

TP

1.1

10Fi

ne p

artic

les

1

.109

Coa

rse

part

icle

s

1.1

09H

1.1

09SO

4

1.1

09

And

erso

n 19

9745

Six

Euro

pean

citi

es(A

mst

erda

m, B

arce

lona

,Lo

ndon

, Mila

n, P

aris

, Ro

tter

dam

)

All

ages

15 y

ears

(1

977

1992

)24

-h m

ean:

TSP

, g/

m3 ;

Blac

k sm

oke,

g/

m3 ;

SO

2,

g/m

3 ; N

O2,

g/

m3 ;

8-

h m

ean:

O3,

g/

m3

1-h

max

imum

: SO

2,

g/m

3 ;N

O2,

g/

m3 ;

O3,

g/

m3

Best

1 d

ay la

gou

t of

3 d

ays

Cum

ulat

ive

lag

(mea

n)

RR in

crea

se in

CO

PD p

er 5

0

g/m

3

incr

ease

in a

ll po

lluta

nts

13

days

lag:

TS

P

1.0

22 (0

.998

1.0

47)

Blac

k sm

oke

1

.035

(1.0

101

.060

)SO

2

1.0

22 (0

.981

1.0

55)

NO

2

1.0

19 (1

.002

1.0

47)

O3

1

.043

(1.0

221

.065

)

Mor

gan

1998

50Sy

dney

, Aus

tral

ia

65 y

ears

5 ye

ars

(199

019

94)

24-h

mea

n:

PM0.

012

.0, b

scat

/104

m;

NO

2, p

pb;

1-h

max

imum

: PM

0.01

2.0, b

scat

/104

m;

NO

2, p

pb; O

3, p

pb

02

days

lag

Cum

ulat

ive

lag

RR in

crea

se in

CO

PD p

er 1

0th

to

90th

per

cent

ile in

crea

se in

al

l pol

luta

nts

Lag

0:

PM24

h

2.4

1 (

0.90

5.8

4)PM

1h

3.0

1 (

0.38

6.5

2)La

g 1:

N

O2

24h

4

.30

(0.

759

.61)

NO

21h

4

.60

(0.

179

.61)

Che

n 20

0051

Reno

-Spa

rks,

NV

, USA

65

yea

rs4

year

s (1

990

1994

)24

-h m

ean:

PM

10,

g/m

30

day

lag

RR in

crea

se in

CO

PD p

er 2

6.6

(g/

m3 )

incr

ease

in P

M10

PM10

1

.049

(1.0

111

.087

)

Fusc

o 20

0152

Rom

e, It

aly

Popu

latio

n:

3 m

illio

nA

ll ag

es

3 ye

ars

(199

519

97)

24-h

mea

n: P

M13

, g/

m3 ;

SO2,

g/

m3 ;

NO

2,

g/m

3 ;C

O, m

g/m

3 ; O

3,

g/m

3 ;8-

h m

ean:

O3,

g/

m3

04

days

lag

Per

cent

incr

ease

in t

otal

res

pira

tory

dise

ases

incl

udin

g C

OPD

per

in

crea

se in

PM

13

23.

0

g/m

3 ;

SO2

6

.9

g/m

3 ; N

O2

2

2.3

g/

m3 ;

CO

1

.5 m

g/m

3 ; O

3

3.9

g/

m3

Lag

0:

Tota

l res

pira

tory

dis

ease

s:N

O2

2

.5 (0

.94

.2);

CO

2

.8 (1

.34

.3);

CO

PD: C

O

4.3

(1.6

7.1

)

Yan

g 20

0553

Van

couv

er, C

anad

aPo

pula

tion:

2

mill

ion

65

yea

rs w

ithac

ute

CO

PD

5 ye

ars

(199

419

98)

24-h

mea

n: P

M10

, g/

m3 ;

SO

2, p

pb; N

O2,

ppb

; C

O, p

pm; O

3, p

pb

06

days

lag

Ave

rage

use

dRR

incr

ease

in a

cute

CO

PD p

er in

crea

sein

PM

10

8.3

g/

m3 ;

SO

2

2.8

ppb

;N

O2

5

.5 p

pb; C

O

0.3

ppm

; O

3

9.3

ppb

Sing

le p

ollu

tant

mod

el:

PM10

1

.13

(1.0

51.

21)

NO

2

1.1

1 (1

.04

1.20

)C

O

1.0

8 (1

.02

1.13

)

Schi

kow

ski 2

0055

48

area

s (5

pol

lute

d,2

clea

n), R

hine

-Ruh

rBa

sin,

Ger

man

yPr

ospe

ctiv

e co

hort

stu

dy

4757

wom

enag

ed 5

455

year

s

9 ye

ars

(198

519

94)

Ann

ual m

ean:

PM

10,

g/m

3 ;N

O2,

g/

m3

5-ye

ar m

ean:

PM

10,

g/m

3 ;N

O2,

g/

m3 ;

Dis

tanc

e to

traf

fic r

oad

OR

incr

ease

in C

OPD

per

incr

ease

in

PM10

7

g/

m3 ;

NO

2

16

g/

m3

CO

PD p

reva

lenc

e 4.

5%A

nnua

l mea

n:

PM10

1

.37

(0.9

81.

92)

NO

2

1.3

9 (1

.20

1.63

)5

year

mea

n:PM

10

1.3

3 (1

.03

1.72

)N

O2

1

.43

(1.2

31.

66)

Med

ina-

Ram

on20

0555

36 c

ities

, USA

Cas

e-cr

osso

ver

desi

gn

65 y

ears

13 y

ears

(1

986

1999

)24

-h m

ean:

PM

10,

g/m

3

8-h

mea

n: O

3, p

pb;

Dis

tanc

e to

tra

ffic

roa

d

01

day

lag

Per

cent

incr

ease

in C

OPD

per

incr

ease

in P

M10

1

0

g/m

3 ; O

3

5 p

pb

1 da

y la

g: P

M10

1

.47

(0.9

32.

01)

2 da

y la

g: O

3

0.2

5 (0

.08

0.47

)

Not

e: T

he c

ross

-sec

tiona

l tim

e-se

ries

stud

ies

eval

uate

d sh

ort-

term

eff

ects

and

mos

tly u

sed

Pois

son

regr

essi

on w

ith g

ener

aliz

ed a

dditi

ve m

odel

s fo

r da

ta a

naly

sis

and

cont

rolle

d fo

r lo

ng-t

erm

tre

nds,

day

of

the

wee

k, t

empe

ratu

re,

hum

idity

, de

wpo

int

tem

pera

ture

, infl

uenz

a ep

idem

ic a

nd o

ther

fac

tors

. Bot

h si

ngle

pol

luta

nt a

nd m

ultip

le p

ollu

tant

mod

els

wer

e us

ed in

mos

t st

udie

s. P

er c

ent

incr

ease

(R

R

1)

100

. Con

vers

ion:

PM

2.5

g/

m3

3

0

bsc

at/1

04 m

.C

OPD

c

hron

ic o

bstr

uctiv

e pu

lmon

ary

dise

ase;

CI

con

fiden

ce in

terv

al;

TP

tho

raci

c pa

rtic

les,

equ

ival

ent

of P

M10

; H

aci

dity

; SO

4

aer

osol

sul

fate

; N

O2

n

itrog

en d

ioxi

de;

ppb

p

arts

per

bill

ion;

CO

c

arbo

n m

onox

ide;

SO

2

sul

fur

diox

ide;

O3

o

zone

; RR

r

elat

ive

risk,

obs

erve

d ov

er e

xpec

ted;

TSP

t

otal

sus

pend

ed p

artic

les

with

aer

odyn

amic

dia

met

er

40

m; P

M0.

012

.0

par

ticul

ate

mat

ter

with

aer

odyn

amic

dia

met

er 0

.01

2.0

m

; bsc

at/1

04 m

n

ephe

lom

eter

par

tic-

ulat

e co

ncen

trat

ion

scal

e; O

R

odd

s ra

tio.

Air pollution and COPD burden 121

Tab

le 3

Out

door

air

pollu

tion

and

CO

PD-r

elat

ed h

ospi

taliz

atio

ns o

r em

erge

ncy

room

vis

its in

low

-inco

me

coun

trie

s

Firs

t au

thor

,ye

ar, r

efer

ence

City

/cou

ntry

Subj

ects

Stud

y pe

riod

Pollu

tant

s m

easu

red

Lag

days

ana

lyze

dRi

sk t

ype

Risk

leve

l (95

%C

I)

Pand

e 20

0261

Del

hi, I

ndia

All

ages

2 ye

ars

(199

719

98)

24-h

mea

n: T

SP,

g/m

3 ;

SO2,

g/

m3 ;

NO

x,

g/m

3 ;C

O,

g/m

3

07

days

lag

Per

cent

incr

ease

in C

OPD

base

d on

upp

er p

erm

issi

ble

leve

l of

TSP

and

SO2

24.9

Gou

veia

200

662

Sao

Paul

o, B

razi

l

65 y

ears

4 ye

ars

(199

620

00)

24-h

mea

n: P

M10

, g/

m3 ;

SO

2,

g/m

3 ; N

O2,

g/

m3 ;

CO

, ppm

; O3,

g/

m3

02

days

lag

RR in

crea

se in

CO

PDpe

r 10

g/

m3

incr

ease

in

PM10

, SO

2, N

O2,

O3 or

pe

r 1

ppm

incr

ease

in C

O

PM10

1

.043

(1.0

281

.058

)SO

2

1.1

79 (1

.126

1.2

35)

NO

2

1.0

24 (1

.015

1.0

34)

CO

1

.049

(1.0

231

.076

)O

3

1.0

15 (1

.005

1.0

25)

Yan

g 20

0763

Ta

ipei

, Tai

wan

All

ages

8 ye

ars

(199

620

03)

24-h

mea

n: P

M10

, g/

m3 ;

SO

2, p

pb; N

O2,

ppb

; C

O, p

pm; O

3, p

pb

02

days

lag

OR

incr

ease

in C

OPD

per

incr

ease

inPM

10

26.

41

g/m

3

SO2

2

.79

ppb

NO

2

10.

05 p

pbC

O

0.5

3 pp

mO

3

11.

29 p

pb

20

oC

: PM

10

1.1

33 (1

.098

1.1

68)

SO2

1

.006

(0.9

701

.043

)N

O2

1

.193

(1.1

581

.230

)C

O

1.2

27 (1

.178

1.2

77)

O3

1

.157

(1.1

181

.197

)

20 o

C:

PM10

1

.035

(0.9

941

.077

)SO

2

1.0

71 (1

.015

1.1

29)

NO

2

0.9

72 (0

.922

1.0

24)

CO

0

.975

(0.9

211

.033

)O

3

0.9

36 (0

.974

1.0

03)

Ko

2007

64H

ong

Kon

g, C

hina

65

yea

rs6

year

s(2

000

2005

)24

-h m

ean:

PM

10,

g/m

3 ;

PM2.

5,

g/m

3 ; S

O2,

g/

m3 ;

NO

2,

g/m

3

8-h

mea

n: O

3,

g/m

3

05

days

lag;

Cum

ulat

ive

lags

by

2, 3

and

6

days

ana

lyze

d

RR in

crea

se in

CO

PD p

er

10

g/m

3 in

crea

se in

al

l pol

luta

nts

Lag

05:

PM10

1

.024

(1.0

211

.028

)PM

2.5

1

.031

(1.0

261

.036

)SO

2

1.0

07 (1

.001

1.0

14)

NO

2

1.0

26 (1

.022

1.0

31)

O3

1

.034

(1.0

301

.040

)

CO

PD

chr

onic

obs

truc

tive

pulm

onar

y di

seas

e; C

I c

onfid

ence

inte

rval

; TSP

t

otal

sus

pend

ed p

artic

les

with

aer

odyn

amic

dia

met

er

40

m; S

O2

s

ulfu

r di

oxid

e; N

Ox

nitr

ogen

oxi

de; C

O

car

bon

mon

oxid

e; P

M10

p

artic

ulat

em

atte

r w

ith a

erod

ynam

ic d

iam

eter

10

m

; NO

2

nitr

ogen

dio

xide

; ppm

p

arts

per

mill

ion;

O3

o

zone

; RR

r

elat

ive

risk;

ppb

p

arts

per

bill

ion;

OR

o

dds

ratio

; PM

2.5

p

artic

ulat

e m

atte

r w

ith a

erod

ynam

ic d

iam

eter

2.

5

m.

122 The International Journal of Tuberculosis and Lung Disease

In a similar study performed in warmer Kaohsiungcity, all pollutants were associated with increasedhospital admissions of COPD, except for SO2, onwarm days.65 In Hong Kong, significant associationswere found for all measured pollutants with increasedemergency hospitalizations of COPD and respiratorysymptoms.64,66

COPD prevalenceIn addition to exacerbations of the diseases of COPDpatients, there are also questions about to what extentair pollution is a risk factor for new cases of COPD.This is usually done by cross-sectional comparisonsof the prevalence of COPD (symptoms and reducedlung function) among subjects who lived in environ-ments with varying degrees of outdoor air pollution.21

A recent study by Schikowski in Rhine-Ruhr Basin,Germany, focused on the effects of air pollution onlung function in women living near major traffic roads.They followed 4757 women longitudinally from 1985to 1994 and found that chronic exposure to PM10,NO2 and living near a major road increased the riskof developing COPD and could have a detrimental ef-fect on lung function (Table 2). The overall preva-lence of COPD was 4.5%. A 7 g/m3 increase in 5-year means of PM10 (interquartile range) was associ-ated with a 5.1% (95%CI 2.57.7) decrease in FEV1,a 3.7% (95%CI 1.85.5) decrease in FVC and an oddsratio (OR) of 1.33 (95%CI 1.031.72) for COPD.Women living less than 100 m from a busy road alsohad significantly reduced lung function, and COPDwas 1.79 times more likely (95%CI 1.063.02) thanfor those living farther away.54

A large cross-sectional population-based study onair pollution and lung diseases in adults (SAPALDIA)evaluated 9651 subjects aged 1860 years residing ineight different areas in Switzerland. Significant andconsistent effects on FVC and FEV1 were found forNO2, SO2 and PM10 in all subgroups and in the totalpopulation, with PM10 showing the most consistenteffect of a 3.4% change in FVC per 10 g/m3.67

A prospective cohort study in Los Angeles, Cali-fornia, found that mean declines in FEV1 in maleswere significantly lower in Lancaster and Glendoracompared with Long Beach (where residents were ex-posed to high levels of sulfates, oxides of nitrogen andhydrocarbons), in each category of smoking. The meandecline in FEV1 attributable to living in Long Beachcompared with living in Lancaster was 23.6 ml/year.68

The number of recent studies on the prevalence ofsymptoms is limited. In addition to reduced lung func-tion, the SAPALDIA study in Switzerland also foundincreased risk for respiratory symptoms associated withannual mean concentrations of NO2, TSP and PM10.Among never-smokers, the OR for a 10 g/m3 increasein PM10 was 1.35 (95%CI 1.111.65) for chronicphlegm production, 1.27 (95%CI 1.081.50) forchronic cough or phlegm production, 1.48 (95%CI

1.231.78) for breathlessness during the day, 1.33(95%CI 1.141.55) for breathlessness during the dayor at night and 1.32 (95%CI 1.181.46) for dyspneaon exertion.69 In Hong Kong, a prospective cohortstudy found that the prevalence of most respiratorysymptoms increased over a 12-year period after ad-justing the data for age, sex, social status and smok-ing habits. The prevalence of self-reported physician-diagnosed emphysema increased from 2.4% to 3.1%,with adjusted OR at 1.78 (95%CI 1.122.86).66 Theauthors suggested that this might be related to envi-ronmental factors, and especially increasing air pollu-tion, in Hong Kong.

Several studies have now found that chronic expo-sure to urban or traffic air pollution reduces the rateof lung function growth in children.7072

Indoor air pollutionHuman beings spend a large proportion of their timein indoor environments such as homes, workplaces,libraries, school classrooms, shopping malls, daycarecenters and vehicles. Important indoor pollutants in-clude PM, SO2, NO2 and CO generated from cookingand heating activities, volatile organic compounds(VOCs) from paints, carpets and furniture, molds andallergens from dampness and pets and environmentaltobacco smoke (ETS).19 According to the WHO, in-door air pollution is responsible for the death of 1.6million people annually.73

Indoor air pollutant exposure varies dramaticallybetween high-income and low-income countries, withbiomass fuels being a much more common source ofexposure in the developing world. Although globalenergy consumption from biomass fuels or biofuels isonly a small part of the total (12%), their use is muchmore prevalent in low-income countries than in high-income countries (33% vs. 3%).74 It is estimated thatalmost 3 billion people, or 50% of households world-wide, use biomass and coal as their main source of en-ergy for cooking, heating and other householdneeds.75,76 Biofuels have higher emission factors forPM and other pollutants, especially during incompletecombustion at lower temperatures,77 which generateindoor airborne particles at levels much higher thanthose of cleaner fuels78 or outdoors,76 and well abovelevels in most polluted cities.79 Such particles also havesmall aerodynamic diameters (ranging from 0.05 to1 m for woodsmoke, for example)74 and can penetratedeep into the alveolar region to induce adverse pul-monary effects. The body of work focusing on indoorair pollution and COPD is much smaller than that onoutdoor air pollution. The majority of studies on in-door air pollution have focused on disease incidenceor prevalence rather than on outcomes such as hospi-talization or death.

Some of the early work concerning biomass smokeand respiratory health was done in Papua NewGuinea74,80,81 and Nepal.82,83 In Saudi Arabia, Dossing

Tab

le 4

Indo

or a

ir po

llutio

n an

d C

OPD

inci

denc

e/pr

eval

ence

in lo

w-in

com

e co

untr

ies

Firs

t au

thor

,ye

ar, r

efer

ence

Stud

y de

sign

City

/cou

ntry

Subj

ects

Stud

y pe

riod

Expo

sure

mea

sure

dH

ealth

mea

sure

dRi

sk t

ype

Risk

leve

l (95

%C

I)

Kira

z 20

0387

C

ross

-sec

tiona

l sur

vey

3 vi

llage

s; 1

city

dis

tric

tK

aser

i, Tu

rkey

242

rura

l; 10

2 ci

tyw

omen

25

yea

rs19

99Q

uest

ionn

aire

for

fuel

typ

e, y

ears

of

use

and

st

ove

type

ATS

and

BM

RCsy

mpt

omqu

estio

nnai

res

Phys

ical

exa

min

atio

nLu

ng f

unct

ion

test

ing

OR

for

CB

and

CO

PDRu

ral v

s. u

rban

wom

en:

Smok

ing

rate

, %: C

urre

nt: 4

.5 v

s. 1

4.7

Past

: 1.2

vs.

11.

8C

B, %

: 20.

7 vs

. 10.

8C

OPD

, %: 1

2.4

vs. 3

.9O

R fo

r C

B

28.

7 (8

.79

5.9)

Ekic

i 200

588

Cro

ss-s

ectio

nal s

urve

y10

vill

ages

Kiri

kkal

e,

Turk

eyBi

omas

s ex

posu

re

397

LPG

con

trol

19

9Ru

ral w

omen

40

yea

rs

2002

Que

stio

nnai

re f

or

h an

d ye

ars

doin

gbi

omas

s co

okin

g:

68.6

h-y

ear

68.8

152

.4 h

-yea

r

152.

4 h-

year

BMRC

sym

ptom

ques

tionn

aire

Phys

ical

exa

min

atio

nLu

ng f

unct

ion

test

ing

OR

and

AP

for

CO

PDC

rude

:G

roup

A

1.7

(1.0

3.1

)G

roup

B

2.5

(1.4

4.4

)G

roup

C

3.3

(1.9

5.7

)A

djus

ted:

Gro

up A

2

.0 (0

.94

.5)

Gro

up B

2

.3 (1

.14

.5)

Gro

up C

2

.2 (1

.14

.4)

Com

bine

d

2.5

(1.5

4.0

)A

djus

ted

1

.4 (1

.21

.7)

AP

2

3.1

(13.

433

.2)

Shre

stha

&Sh

rest

ha,

2005

78

Cro

ss-s

ectio

nal s

urve

y4

mun

icip

aliti

es98

hou

seho

lds

Kat

hman

duva

lley,

Nep

al16

8 su

bjec

ts94

% w

omen

2003

win

ter

PM10

, g/

m3

CO

, g/

m3

BMRC

res

pira

tory

sym

ptom

ques

tionn

aire

Phys

ical

exa

min

atio

nPe

ak f

low

m

easu

rem

ent

OR

for

CO

PD,

asth

ma

and

resp

irato

rysy

mpt

oms

CO

PD p

reva

lenc

e, %

: Sol

id f

uels

1

6.8

Cle

an f

uels

7

.0O

R fo

r C

OPD

/ast

hma:

Una

djus

ted

3

.85

(1.1

113

.38)

Smok

ing

adju

sted

3

.13

(0.8

311

.76)

Age

adj

uste

d

4.1

8 (1

.14

15.2

7)

Peab

ody

2005

89C

ross

-sec

tiona

l sur

vey

3 pr

ovin

ces

103.

4 m

illio

n pe

ople

3476

hou

seho

lds

Shan

xi, H

ubei

,Zh

ejia

ng,

Chi

na

4638

adu

lts22

85 c

hild

ren

Fuel

typ

eSt

ove

type

Dur

atio

n in

coo

king

CO

in e

xhal

ed a

ir

Adu

lt an

d ch

ildre

nqu

estio

nnai

res

Hea

rt r

ate

Resp

irato

ry r

ate

Bloo

d pr

essu

reLu

ng f

unct

ion

test

ing

(FV

C)

OR

and

prev

alen

cefo

r C

OPD

CO

PD p

reva

lenc

e, %

: 3.8

Prev

alen

ce h

ighe

r in

coa

l use

rsO

R co

mpa

red

to c

oal:

Woo

d

0.4

8 (0

.28

0.87

)C

rop

0

.57

(0.3

40.

96)

Cle

an f

uel

0.4

3 (0

.05

0.36

)O

R fo

r st

ove:

Tra

ditio

n vs

. im

prov

ed

1.8

7 (1

.30

2.69

)

Cha

pman

2005

90Re

tros

pect

ive

coho

rt s

tudy

Larg

e ru

ral

com

mun

ity

Xua

nwei

, C

hina

2045

3 pe

ople

with

trad

ition

al s

tove

s16

606

peop

le c

hang

edto

impr

oved

sto

ves

16 y

ears

(197

619

92)

Que

stio

nnai

reSt

ove

type

Fuel

typ

e

Stan

dard

qu

estio

nnai

reBr

onch

itis

Emph

ysem

aD

eath

RR f

or C

OPD

in

impr

oved

vs. u

nven

ted

stov

es

CO

PD p

reva

lenc

e, %

: 7.3

CO

PD in

cide

nce,

% r

educ

ed: M

en

42

Wom

en

25

RR: M

en

0.5

8 (0

.49

0.70

)W

omen

0

.75

(0.6

20.

92)

Liu

2007

91Po

pula

tion-

base

d,cr

oss-

sect

iona

l sur

vey

1 ru

ral c

omm

unity

with

14

000

peop

le1

urba

n co

mm

unity

with

520

000

peop

le

Gua

ngzh

ou,

Chi

naRu

ral

146

8U

rban

1

818

40

yea

rs

0.5

year

(200

220

03)

15 m

in a

vera

ge:

PM10

mg/

m3 ;

SO

mg/

m3 ;

N

O2

mg/

m3 ;

C

O 1

0 m

g/m

3

Stan

dard

qu

estio

nnai

rePh

ysic

al e

xam

inat

ion

Lung

fun

ctio

n te

stin

g

OR

for

CO

PDan

d re

spira

tory

sym

ptom

s

CO

PD p

reva

lenc

e, %

: Rur

al

12;

Urb

an

7.4

OR

for

fuel

typ

e: B

iom

ass

1

.72

(1.2

72.

35)

Coa

l 1

.55

(0.7

43.

22)

CO

PD p

reva

lenc

e, %

, for

non

-sm

okin

g w

omen

:Ru

ral

7.2

; Urb

an

2.5

OR

for

fuel

typ

e: B

iom

ass

3

.11

(1.6

35.

94)

Coa

l 2

.77

(0.8

39.

26)

OR

for

SO2

1

.80

(1.0

43.

11)

Not

e: C

ase-

cont

rol a

nd c

ross

-sec

tiona

l pre

vale

nce

stud

ies

used

2

test

, Man

tel

Hae

nsze

l met

hod,

logi

stic

reg

ress

ion

or m

ultiv

aria

te r

egre

ssio

n fo

r da

ta a

naly

sis

on O

R an

d tr

ends

, adj

ustin

g fo

r va

riabl

es s

uch

as a

ge, s

ex, m

arita

l sta

tus,

edu

catio

n,bo

dy m

ass

inde

x, a

lcoh

ol u

se, a

ctiv

e an

d pa

ssiv

e sm

okin

g, o

ccup

atio

nal e

xpos

ures

, ato

py a

nd f

amily

his

tory

of

CO

PD, p

lace

of

birt

h an

d re

side

nce

and

fam

ily in

com

e. T

he r

etro

spec

tive

coho

rt s

tudy

use

d C

ox p

ropo

rtio

nal h

azar

d su

rviv

al m

odel

.Po

lluta

nt n

ames

are

the

sam

e as

in p

revi

ous

tabl

es.

CO

PD

chr

onic

obs

truc

tive

pulm

onar

y di

seas

e; C

I c

onfid

ence

inte

rval

; ATS

A

mer

ican

Tho

raci

c So

ciet

y; B

MRC

B

ritis

h M

edic

al R

esea

rch

Cou

ncil;

OR

o

dds

ratio

; CB

c

hron

ic b

ronc

hitis

; LPG

li

quefi

ed p

etro

leum

gas

; AP

a

ttrib

utab

lepr

opor

tion

(O

R

1)

P/O

R; P

M10

p

artic

ulat

e m

atte

r w

ith a

erod

ynam

ic d

iam

eter

10

m

; CO

c

arbo

n m

onox

ide;

FV

C

for

ced

vita

l cap

acity

; P

pre

vale

nce

of e

xpos

ure

amon

g ca

ses.

124 The International Journal of Tuberculosis and Lung Disease

et al. found that two thirds of women with COPDand only 1/20 of the control women had been ex-posed to indoor open fires for 20 years (P 0.05).84In a case-control study conducted in Bogota, Colom-bia, wood burning was associated with a higher riskof COPD (adjusted OR 3.92, 95%CI 1.29.1).85 InMexico City, the OR for cooking with traditionalcook stoves was 3.9 (95%CI 2.07.6) for bronchitis,1.8 (95%CI 0.74.7) for COPD and 9.7 (95%CI 3.727) for bronchitis and COPD combined.86 In the pastdecade, several more studies have evaluated the burn-ing of solid fuels as a risk factor for COPD (Table 4).In a cross-sectional study in Turkey, Kiraz et al.found that chronic bronchitis symptoms were twotimes as high in rural women than their city counter-parts, despite a lower prevalence of smoking (20.7%vs. 11.8%, P 0.01).87 In another cross-sectionalstudy in Turkey, Ekici et al. found that women exposedto biomass smoke had a higher risk of COPD andchronic bronchitis (adjusted OR 2.5, 95%CI 1.54.0).88 More recently, in Nepal, Shrestha and Shresthafound a higher COPD prevalence among women usingunprocessed fuels (16.7% vs. 7.8%).78 No longitudi-nal data on biomass exposure and COPD have beenreported to date.

Several studies have also been published fromChina. Peabody et al. found an increased prevalenceof COPD among women in homes that burned coal.89In a recent study with 20 245 subjects in seven prov-inces/cities in China, the overall prevalence of COPDwas found to be 8.4% (men 12.4%, women 5.1%).The prevalence of COPD was significantly higher inrural residents.92 Looking further at the high preva-lence in rural areas, Liu et al. found that that COPDprevalence was significantly higher in non-smokingwomen exposed to biomass fuels in a rural commu-nity compared to an urban community (prevalence7.2% vs. 2.5%, adjusted OR 3.11, 95%CI 1.635.94).Concentrations of CO, PM10, SO2 and NO2 in thekitchen during biomass fuel combustion were signifi-cantly higher than those during liquefied petroleumgas combustion, and SO2 was significantly associatedwith the prevalence of COPD in non-smoking women(OR 1.80, 95%CI 1.043.11).91

Zhou et al. found that in Xuanwei County, Yun-nan Province, China, rates of COPD were over twicethe national average.93 In Xuanwei, 90% of resi-dents are farmers. For cooking and heating, residentsusually burnt smoky coal (bituminous coal), smoke-less coal (anthracite) or wood in unvented stoves.94,95A retrospective cohort study followed up from 1976to 1992 to compare the COPD rates between users ofthe unvented and improved coal stoves with chimneygroups. A reduction was observed for COPD inci-dence among households with improved stoves (Cox-modeled RR 0.58, 95%CI 0.490.70 in men and0.75, 95%CI 0.620.92, in women). This study sug-gests that the COPD burden associated with tradi-

tional coal stoves in low-income countries can be re-duced by using improved stoves that reduce pollutantemissions.90 The potential for improved biomass stovesto reduce adverse health effects is currently beingstudied in Guatemala and Mexico.

In high-income countries, exposure to biomasssmoke may also be a risk factor for COPD, as shownin a recent study from Spain.96 In addition, higherlevels of indoor PM2.5 were found to be associatedwith worse health status among patients with severeCOPD.97

CONCLUSIONS

Historical reports of air pollution episodes have pro-vided clear evidence that COPD-related cardiorespi-ratory mortality and morbidity are associated withhigh levels of outdoor air pollutants, particularly PM.More recent time series studies show that acute in-creases in outdoor air pollutants at much lower levelscontinue to cause health effects (i.e., mortality andhospital admissions) among patients with COPD andin the general population. Limited prospective cohortstudies have also shown an increased risk of COPDfrom long-term exposure to low levels of air pollut-ants. Indoor air pollution due to solid fuel combustionis an important risk factor for COPD in low-incomecountries, particularly in non-smoking women. Moreprospective cohort studies are needed to evaluate therisk of COPD associated with exposures to both long-term low-level outdoor air pollution and indoor bio-mass combustion. Tailored strategies and preventiveefforts at national and local levels are needed to targetthe different risk factors of COPD in different coun-tries, as well as reduction of traffic air pollution in ur-ban environments and increased dissemination of im-proved cooking stoves in low-income countries.

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