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

STATE OF THE ART

STATE OF THE ART SERIES Chronic obstructive pulmonary disease in high- and low-income countries Edited by G. Marks and M. Chan-Yeung NUMBER 2 IN THE SERIES

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 Respiratory Diseases, Mexico City, Mexico SUMMARY

Chronic obstructive pulmonary disease (COPD) is an important cause of morbidity and mortality in both high- and low-income countries. While active cigarette smoking is the most important preventable risk factor globally, outdoor and indoor air pollutants can cause or exacerbate COPD. In high-income countries, historic air pollution events provide clear evidence that exposure to high levels of outdoor air pollutants is associated with increased mortality and morbidity due to COPD and related cardiorespiratory diseases. Studies in the last 20 years continue to show increased risk associated mainly with particulate matters, even at much lower levels. Pop-

ulations in low-income countries are largely exposed to indoor air pollutants from the combustion of solid fuels, which contributes signicantly to the burden of COPDrelated diseases, particularly in non-smoking women. Effective preventive strategies for COPD may vary between countries, and include continued improvements in air cleaning technology, air quality legislation and dissemination of improved cooking stoves. A joint effort from both society and governments is needed for these endeavors. K E Y W O R D S : COPD; outdoor air pollution; indoor biomass pollution; environmental exposures

AIR POLLUTION has been recognized for its relationship with cardiorespiratory illnesses, including chronic obstructive pulmonary diseases (COPD), since the early 1900s. Sharp increases in fatalities and hospital admission rates, particularly in the elderly, were well documented in air pollution events in the 1940s and 1950s. This led to rapid developments in technology and air pollution legislation in the 1960s and 1970s that eventually improved outdoor air quality in the United States and many other high-income countries.1 However, the relative increase in motor vehicle trafc in the past decades13 has now presented as a more worrying air pollution problem in many metropolitan cities around

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

the world. In low-income countries where more households use traditional cooking fuels and stoves, indoor air pollution from biomass combustion has been found to contribute to COPD and other cardiorespiratory diseases, particularly in non-smoking women. The health effects of air pollution are a spectrum of responses that includes sensory response to odors, irritation of the upper respiratory systems, increased prevalence of respiratory infections, symptoms such as cough, phlegm production, chest tightness and wheezing, chronically reduced pulmonary function in forced vital capacity (FVC), forced expiratory volume in one second (FEV1) together with symptoms, and increased incidence in exacerbation of cardiopulmonary diseases, asthma attacks, cancer and mortality.4 While air pollution may affect all ages of the population, the elderly, particularly those with pre-existing cardiopulmonary diseases such as COPD, are the most susceptible group. This review will therefore focus on the more serious adverse health effects of COPD

Correspondence to: Youcheng Liu, Department of Preventive Medicine and Environmental Health, University of Kentucky College of Public Health, 121 Washington Ave, Lexington, KY 40536, USA. Tel: (1) 859 218 2234. Fax: (1) 859 257 9862. e-mail: youcheng.liu@uky.edu Article submitted 28 September 2007. Final version accepted 19 November 2007.

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The International Journal of Tuberculosis and Lung Disease

(mortality, morbidity and health care utilization) alone or in the context of cardiorespiratory diseases. COPD remains a major public health problem worldwide, and is one of the leading causes of mortality and morbidity in both high- and low-income countries.59 According to World Health Organization (WHO) estimates, about 80 million people have moderate to severe COPD and 3 million died of COPD in 2005, which corresponds to 5% of all deaths globally.5 Total deaths due to COPD are projected to increase by more than 30% in the next 10 years. Mortality and morbidity rates vary across countries and regions, and are affected by the COPD denitions used, the accuracy of local reporting systems and the survey methods used.8 Dramatic increases in the next two decades are expected in Asian and African countries due to increasing tobacco use.10 COPD has profound effects on the quality of life of patients, and places an enormous economic burden on society. In high-income countries, exacerbations of COPD account for the greatest burden on the health care system. In the US in 2002, for example, the direct costs of COPD were $18 billion and the indirect costs totalled $14.1 billion.11 In the European Union, the total direct costs of respiratory diseases are estimated to be about 6% of the total health care budget, with COPD accounting for 56% (38.6 billion) of the total.9 Although data are lacking for low-income countries, it is projected to increase along with the increase in tobacco use, based on estimates from per patient cost in high-income countries.12 COPD results from interaction between individual genetic factors and environmental exposures to toxic agents, such as tobacco smoking, outdoor and indoor air pollution, occupational exposure to organic and mineral dusts, gases and fumes and lower respiratory infections in early childhood.13 Most genetic factors are unknown, except for alpha 1-antitrypsin deciency, present in 13% of COPD patients. Nutrition may also be a predisposing factor, and interacts with environmental exposures.14 Tobacco smoke is well established as the most important risk factor for COPD, particularly in high- and middle-income countries;15,16 however, in low-income countries, exposure to indoor air pollution, such as the use of biomass fuels for cooking and heating, increases the burden of COPD in addition to tobacco smoking.5 This suggests that different specic public health measures and strategies need to be used to target priority risk factors in the prevention of COPD in different parts of the world, although all involve breathing clean air. This article will review the most recent developments in outdoor and indoor air pollution that contribute to the burden of COPD and other related cardiorespiratory diseases in high- and low-income countries. Our focus is the risk of COPD and related mortality and morbidity from epidemiological studies. No controlled human exposure studies or laboratory

animal studies are included. The review does not address smoking, active or passive, the role of infections in COPD or the relationship between occupational exposures and the risk of COPD, nor will it include elaborations on the environmental mechanisms for asthma in producing irreversible airow obstruction. Readers are advised to refer to previous reviews published on trafc air pollution and health,1,3 air pollution and respiratory risk in low-income countries,17,18 indoor air pollution and respiratory health,19 as well as review articles on air pollution and health in general,20 and on COPD.21,22

METHODS
We conducted systematic searches of the literature in English or articles with English abstracts using bibliographic databases of PubMed/Medline (National Library of Medicine and National Institutes of Health) and Web of Science (Science Citation Index Expanded, Thomson Corporation). We used the keywords COPD or emphysema or chronic bronchitis AND outdoor air pollution or indoor biomass and coal pollution to search articles up to October 2007. We were particularly interested in epidemiological studies published within the last 10 years, although some important previous studies were also cited as background. Articles were also found from the reference lists of selected articles and systemic searches on specic journals such as Thorax and the American Journal of Respiratory and Critical Care Medicine. In addition, extensive searches using Google (google.com) were performed on the Internet. We did not intend to include all articles in our review; instead we selected the most recent studies that evaluated mortality, morbidity or hospital admissions/emergency room visits in typical regions (North America, Europe, Oceania and low-income countries) for summary. Large multicountry studies were selected over reports from individual countries in the same study. Outdoor air pollution Most epidemiological air pollution studies conducted in high-income countries on short-term exposure and effects on the general population or patients suffering from COPD used the time series method to evaluate the risk of mortality due to cardiorespiratory diseases, or COPD hospital admissions temporally related to air pollution levels, i.e., these studies measured daily variations in the number of health events in a city in relation to daily variations in air pollutants and confounding variables, such as temperature. Compared with short-term exposure studies, few studies have been conducted prospectively to evaluate the long-term effects of air pollution on COPD. Although outdoor air pollutant levels tend to be higher in low-income countries than in high-income countries, fewer studies were conducted.

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117

Mortality Historical reports of dramatic air pollution episodes in the early 1950s have provided clear evidence of mortality associated with high levels of particulate matter (PM), measured as black smoke in Europe, sulfur dioxide (SO2), and acid aerosols. During the London smog of 59 December 1952, there was a more than 2-fold increase in the daily death rate, resulting in around 4000 extra deaths. Between 80% and 90% of the deaths were from cardiorespiratory causes, and the greatest relative increase was in deaths due to bronchitis, which rose 9-fold.2 In the December 1991 air pollution episode in London, all-cause mortality, excluding accidents, increased (relative risk [RR] 1.10). Although not statistically signicant, increases were observed for all respiratory diseases (RR 1.22) and obstructive lung diseases (RR 1.23).23 While improved technology and legislation have reduced air pollution levels in high-income countries, studies in the past 20 years continue to show increased mortality related to air pollution. Overall, a 50 g/m3 increase in 24 h PM with aerodynamic diameter 10 m (PM10) is associated with a 2.55% increase in premature non-accident mortality for the general population, with higher risks for the elderly and those with pre-existing cardiopulmonary conditions (Table 1).2429 Most studies evaluated total mortality due to cardiorespiratory diseases or respiratory diseases, although some looked specically at COPD. For example, Schwartz and Dockery found that a 100 g/m3 increase in total suspended particles (TSP) would lead to a 10% (95% condence interval [CI] 614) increase in COPD mortality.28 One of the largest studies conducted in the US was the National Morbidity, Mortality and Air Pollution Study (NMMAPS) sponsored by the Health Effects Institute, which examined the effect of short-term exposure to PM on mortality in 20 US cities, which was later extended to include 90 US cities.24,30,37,38 The per cent increase for cardiorespiratory mortality was 0.68 (95%CI 0.201.16) in the 20-city study.30 This study addressed various important issues in air pollution and mortality studies, such as measurement error, confounding, and effects of multiple gaseous copollutants on the inuence of PM. In Europe, the Air Pollution and Health: a European approach (APHEA) study showed that an increase of 50 g/m3 in SO2 or black smoke was associated with a 3% (95%CI 24) increase in daily mortality; the corresponding value for PM10 was 2% (95%CI 13). In central eastern European cities, the increase in mortality associated with a 50 g/m3 change in SO2 was 0.8% (95%CI 0.12.4) and in black smoke 0.6% (95%CI 0.11.1).31 Later, the APHEA II study showed that a 10 g/m3 increase in daily PM10 or black smoke concentrations increased mortality by 0.6% (95%CI 0.40.8), with a slightly higher increase among the elderly. The concentration of nitrogen dioxide (NO2)

modied the relationship between PM and mortality (mortality at 0.80%, 95%CI 0.670.93 at high NO2 levels).32 Similar excesses in total and respiratory mortality were also observed in nine French cities.39 The relationship between daily exposure to air pollutants and daily mortality is linear, with no clear threshold for PM10.17,40 The short-term effect between exposure and mortality is affected by lag days. For example, Zeka et al. found that all-cause mortality increased with PM10 exposures occurring both 1 and 2 days prior to the event, and deaths from heart disease were primarily associated with PM10 on 2 days before the event, while respiratory deaths were associated with PM10 exposure on all 3 days.34 While many time series studies have shown an increase in mortality related to short-term air pollution, prospective cohort studies have also found increased mortality due to long-term exposure to low-level air pollution. Pope et al. evaluated exposures to multiple air pollutants in metropolitan areas of all 50 states in the US, and found the RR of mortality due to cardiorespiratory causes at respectively 1.06 (95%CI 1.02 1.60), 1.08 (95%CI 1.021.14) and 1.09 (95%CI 1.081.16) for the periods 19791983 and 1999 2000 and the average of all periods.33 Similar results in mortality have also been found in cities in low-income countries. In Mexico, TellezRojo et al. found that an increase of 10 g/m3 PM10 was related to a 2.9% (95%CI 0.94.9) and 4.1% (95%CI 1.36.9) increase in total respiratory and COPD deaths, respectively.35 In Shanghai, China, an increase of 10 g/m3 in PM10, SO2 and NO2 corresponded to an RR increase in mortality of COPD in all ages of respectively 1.005 (95%CI 0.9991.011), 1.035 (95%CI 1.0151.054) and 1.032 (95%CI 1.009 1.056) (Table 1).36 As summarized by Nejjari et al., a global excess risk of total mortality varied from 3% to 4%, with 1% to 6% for respiratory mortality, for an increase of 50 g/m in the pollution indicators.17 The mechanisms of deaths triggered by increased air pollution have recently been claried, and include cardiovascular mechanisms: alteration in coagulation, in the autonomic control or pollutant inammation enhancing atherogenesis.4143 These mechanisms are relevant to patients with COPD who frequently have comorbid diseases.8 Increased susceptibilities to respiratory infections, increased airow obstruction and deranged gas exchange are also important. Patients who die during air pollution episodes include not only those with a very short life expectancy (this mechanism has been called harvesting), but also patients and subjects with much longer life expectancy.44 Hospital admissions and emergency room visits COPD patients are particularly vulnerable to additional stress on the respiratory system caused by the toxic effects of inhaled pollutants.45 Exposure to air pollutants has been associated with respiratory morbidity,

Table 1
Study period 03 days lag Pollutants measured Lag days analyzed Risk type and per unit increase Risk level (95%CI) 1 day lag: All causes 0.51 (0.070.93) Cardiorespiratory 0.68 (0.201.16)

Outdoor air pollution and COPD-related mortality in both high-income and low-income countries

First author, year, reference

City/country

Subjects

High-income countries 20 largest cities, USA Samet 200030*

65, 6574, 7 years 74 years (19871994)

Katsouyanni 199731*

12 cities, Europe, APHEA I

All ages

10 years (19771987)

24-h mean: PM10, g/m3; SO2, ppb; NO2, ppb; CO, ppb; O3, ppb 8-h mean: O3, ppb 24-h mean: PM10, g/m3; black smoke, g/m3; SO2, g/m3 03 days lag Per cent increase in total mortality and cardiorespiratory mortality per 10 g/m3 in PM10 Per cent increase in total mortality per 50 g/m3 increase in PM10, black smoke or SO2

Katsouyanni 200132*

29 cities, Europe, APHEA II

All ages

10 years (19771987)

Western Europe: SO2 3 (24) Black smoke 3 (24) PM10 2 (13) Central-Eastern Europe: SO2 0.8 (-0.12.4) Black smoke 0.6 (0.11.1) PM10 and black smoke: All ages 0.6 (0.40.8) 65 years 0.7 (0.51.0) 19791983 time period 1.06 (1.021.60) 19992000 time period 1.08 (1.021.14) Average 1.09 (1.081.16)

Pope 200233

Metropolitan area, 50 states, USA

30 years 21 years (19792000)

Zeka 200534*

20 US cities

All ages

12 years (19892000)

24-h mean: PM10, g/m3; 02 days lag Per cent increase in total black smoke, g/m3; mortality per 10 g/m3 SO2, g/m3; NO2, g/m3; increase in PM10 and O3, g/m3 black smoke Modified RR increase in cardiorespiratory 24-h mean: TSP, g/m3; Cox-proportional mortality per 10 g/m3 PM15, g/m3; PM10, g/m3; hazards model PM2.5, g/m3; PM152.5, g/m3; increase in PM2.5 with spatial SO2, ppb; NO2, ppb; O3, ppb; CO, ppm; SO4, ppb random effect 1 h max: O3, ppb component 24 h mean: PM10, g/m3 03 days lag Per cent increase in COPD mortality per 10 g/m3 increase in PM10

Single lag model: Lag 0 -0.06 (-0.630.51) Lag 1 0.43 (-0.141.00) Lag 2 0.39 (-0.160.94) 3 day cumulative 0.43 (-0.351.21) Per cent increase in COPD mortality per 10 g/m3 increase in PM10 and per 40 ppb increase in O3

Low-income countries Tellez-Rojo 200035 1 year (1994) 24 h mean: PM10 (g/m3) 1 h max: O3, ppb; SO2, ppm; NO2, ppm 07 days lag; Cumulative lags by 3, 5 and 7 days analyzed

Mexico City, Mexico

65 years

Kan & Chen 200336

Shanghai, China

All ages

1.5 years (20002001)

24 h mean: PM10, g/m3; SO2, g/m3; NO2, g/m3

05 days lag

RR increase in COPD mortality per 10 g/m3 increase in pollutants

Outside medical unit Total respiratory: PM10 2.9 (0.94.9), 3 day lag O3 5.6 (0.510.9), 2 day lag COPD: PM10 3.0 (0.15.9), 1 day lag PM10 6.1 (2.49.9), 5 day mean O3 8.3 (1.016.1), 3 day lag All ages: PM10 1.005 (0.9991.011) SO2 1.035 (1.0151.054) NO2 1.032 (1.0091.056) Age 6575 years: PM10 0.996 (0.9861.007) SO2 1.010 (0.9771.043) NO2 1.007 (0.9671.047)

* Time series studies to evaluate short-term exposure, in which variables of long-term trends, day of the week, temperature, humidity, dew point temperature, and inuenza epidemic were controlled. Prospective cohort study to evaluate long-term exposure, in which the Cox proportional hazard survival model was used and personal characteristics such as smoking, education, marital status, body mass index, occupational exposures, diet and alcohol use were controlled. Per cent increase (RR 1) 100. COPD chronic obstructive pulmonary disease; CI condence interval; PM10 particulate matter with aerodynamic diameter 10 m; PM15 particulate matter with aerodynamic diameter 15 m; PM2.5 particulate matter with aerodynamic diameter 2.5 m; PM1.52.5 particulate matter with aerodynamic diameter 1.52.5 m; RR relative risk; SO2 sulfur dioxide; ppb parts per billion; NO2 nitrogen dioxide; CO carbon monoxide; O3 ozone; SO4 aerosol sulfate; APHEA Air Pollution and Health: a European Approach; TSP total suspended particles with aerodynamic diameter 40 m.

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including acute respiratory symptoms,46 decreased pulmonary function and exacerbation of COPD conditions that may be severe enough to require an emergency room visit or hospitalization.2,47 In the wellknown London smog incident in 59 December 1952, black smoke levels rose to 1600 g/m3, four times higher than normal levels at that time. This air pollution episode caused total hospital admissions to rise by 50% and respiratory admissions by 160%.2 More recent episodes, with more modest effects, in 1991 in London23 and from 1985 to 1989 in Utah in the US, have been studied.48 Since the early 1990s, many epidemiological studies have evaluated hospital admissions for COPD resulting from short-term exposure to outdoor air pollution. Statistical models have been used to evaluate the effects of PM and co-pollutants on COPD events at different lag times, while controlling for the effect of other variables such as long-term trends, meteorological parameters or city characteristics (Table 2). These research results have provided scientic evidence and basis for air quality regulations in the US56 and other countries. In the US, Schwartz conducted separate studies in Minneapolis, St. Paul, MN,47 Birmingham, AL,29 Detroit, MI57 and Spokane, WA.58 In each city, he evaluated the change in daily average concentrations of PM10 and ozone (O3) on the risk of hospital admission for COPD among elderly persons aged 65 years. Both PM10 and O3 were found to be associated with increased risk of hospital admissions for COPD. The RR for PM10 (per 10 g/m3 increase) ranged from 1.02 to 1.57, with the 95%CI ranging from 0.76 to 2.06; similar effects were noted for ozone.47 Similar results were found in Reno-Sparks, NV, where a 26.6 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 et al. extended the studies to include the analysis of both ne particles (FP) and coarse particles (CP), the content of aerosol sulfate (SO4) and acidity (H) in particles and multiple gaseous co-pollutants (O3, NO2, SO2 and CO) in Toronto, Canada, in three consecutive summers from 1992 to 1994. These exposure data were compared with concurrent data on respiratory hospital admissions that included COPD. The RR from single pollutant models was 1.022 for CO, 1.023 for CP, 1.030 for SO4, 1.036 for PM10, 1.040 for FP and SO2, 1.048 for NO2 and 1.068 for O3. Increases in O3, NO2 and SO2 were associated with an 11% increase in daily admissions.49 In Vancouver, O3 and NO2 were found to be signicantly associated with COPD admission, and the combined RR for all gases was 1.21.53 A similar multi-pollutant study in three US counties also found that gases other than ozone were more strongly associated with COPD admissions than PM.59 In Montreal, Canada, Delno et al. similarly eval-

uated multiple pollutants and their effect on emergency room (ER) visits from 1992 to 1993. For 1993, 1 h maximum O3, PM10, PM2.5 and SO4 were all positively associated with respiratory visits for patients aged 64 years. An increase in the mean level of 1 h maximum O3 (36 parts per billion [ppb]) was associated with a 21% (RR 1.21) increase over the mean number of daily ER visits (95%CI 834). The effects of PM and SO4 were smaller, with mean increases of 16% (95%CI 428), 12% (95%CI 221) and 6% (95%CI 112) for PM10, PM2.5 and SO4, respectively.60 The O3 and PM10 levels were all well below the current US National Ambient Air Quality Standards, which are 80 ppb 8 h average and 120 ppb 1 h maximum for O3 and 150 g/m3 24 h average for PM10.56 In Europe, a six-city multi-pollutant study evaluated air pollution and hospital admissions for COPD as part of the APHEA project. For all ages, the RR for a 50 g/m3 increase in the daily mean level of pollutant (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 aerodynamic diameter 40 m, 1.02 (95%CI 1.001.05) for NO2 and 1.04 (95%CI 1.021.07) for O3 (8 h). These results for particles and O3 are generally consistent with those from North America, although the coefcients for particles are substantially smaller.45 In Sydney, Australia, a similar study with multiple air pollutants found a 4.6% increase in COPD hospital admissions for a 50 g/m3 increase in daily mean level of PM0.012.0, consistent with previous studies.50 Most recently, Medina-Ramon et al. conducted a case-crossover study in 36 US cities in which they evaluated the effect of daily mean concentrations of PM10 and O3 on hospital admissions for COPD. They found that during the warm season, the 2-day cumulative effect of a 5-ppb increase in O3 resulted in a 0.27% (95%CI 0.080.47) increase in COPD admissions, and a 10 g/m3 increase in PM10 on a previous day increased the COPD admissions of the following day by 1.47% (95%CI 0.932.01). In this study, the use of a central air-conditioning system reduced the effect of air pollution.55 Table 3 summarizes some studies in air pollution and COPD hospitalizations in urban areas in lowincome countries. In Delhi, India, a time series study in one hospital found a 24.9% increase in emergency room visits related to air pollution.61 In Sao Paulo, Brazil, all measured pollutants, PM10, SO2, NO2, O3 and carbon monoxide (CO), were signicantly associated with increased hospital admissions, with an increase of 10 g/m3 in ne particulate matter associated with a 4.3% increase in admissions for COPD in the elderly.62 In Taipei City, Taiwan, during warm days (20C), all pollutants except SO2 were associated with an increased risk of hospital admissions, but on cold days (20C) only SO2 was associated with increased risk.63

Table 2
Study period 04 days lag RR increase in all respiratory diseases including COPD per increase in TP 14.25 g/m3; Fine particles 11 g/m3; Coarse particles 4.75 g/m3; NO2 5.75 ppb; CO 0.75 ppb; SO2 4.00 ppb; O3 11.50 ppb Pollutants measured Lag days analyzed Risk type and per unit increase Risk level (95%CI) RR significant for all single pollutants RR for particles adjusted for all gaseous pollutants: TP 1.110 Fine particles 1.109 Coarse particles 1.109 H 1.109 SO4 1.109

Outdoor air pollution and COPDrelated hospitalizations or emergency room visits in high-income countries

First author, year, reference

City/country

Subjects

Burnett 199749

Toronto, Canada

Population: 2.36 million All ages

Anderson 199745

Six European cities All ages (Amsterdam, Barcelona, London, Milan, Paris, Rotterdam)

Best 1 day lag out of 3 days Cumulative lag (mean)

RR increase in COPD per 50 g/m3 increase in all pollutants

Morgan 199850

Sydney, Australia

65 years 02 days lag Cumulative lag

RR increase in COPD per 10th to 90th percentile increase in all pollutants

Chen 200051 04 days lag

Reno-Sparks, NV, USA

65 years 0 day lag

13 days lag: TSP 1.022 (0.9981.047) Black smoke 1.035 (1.0101.060) SO2 1.022 (0.9811.055) NO2 1.019 (1.0021.047) O3 1.043 (1.0221.065) Lag 0: PM24h 2.41 (0.905.84) PM1h 3.01 (0.386.52) Lag 1: NO224h 4.30 (0.759.61) NO21h 4.60 (0.179.61) PM10 1.049 (1.0111.087)

Fusco 200152

Rome, Italy

Population: 3 million All ages

3 summers 24h mean (19921994) Daytime mean Daily 1 h max 5-day mean: TP, g/m3; Fine particles, g/m3; Coarse particles, g/m3; H, nmol/m3; SO4, nmol/m3; NO2, ppb; CO, ppb; SO2, ppb; O3, ppb 15 years 24-h mean: TSP, g/m3; (19771992) Black smoke, g/m3; SO2, g/m3; NO2,g/m3; 8-h mean: O3, g/m3 1-h maximum: SO2, g/m3; NO2, g/m3; O3, g/m3 5 years 24-h mean: (19901994) PM0.012.0, bscat/104 m; NO2, ppb; 1-h maximum: PM0.012.0, bscat/104 m; NO2, ppb; O3, ppb 4 years 24-h mean: PM10, g/m3 (19901994) 3 years 24-h mean: PM13, g/m3; (19951997) SO2, g/m3; NO2, g/m3; CO, mg/m3; O3, g/m3; 8-h mean: O3, g/m3 5 years 24-h mean: PM10, g/m3; (19941998) SO2, ppb; NO2, ppb; CO, ppm; O3, ppb 9 years Annual mean: PM10, g/m3; (19851994) NO2, g/m3 5-year mean: PM10, g/m3; NO2, g/m3; Distance to traffic road 06 days lag Average used

Yang 200553

Vancouver, Canada

Schikowski 200554

8 areas (5 polluted, 2 clean), Rhine-Ruhr Basin, Germany Prospective cohort study

Population: 2 million 65 years with acute COPD 4757 women aged 5455 years

RR increase in COPD per 26.6 (g/m3) increase in PM10 Per cent increase in total respiratory diseases including COPD per increase in PM13 23.0 g/m3; SO2 6.9 g/m3; NO2 22.3 g/m3; CO 1.5 mg/m3; O3 3.9 g/m3 RR increase in acute COPD per increase in PM10 8.3 g/m3; SO2 2.8 ppb; NO2 5.5 ppb; CO 0.3 ppm; O3 9.3 ppb OR increase in COPD per increase in PM10 7 g/m3; NO2 16 g/m3

Medina-Ramon 200555

36 cities, USA Case-crossover design

65 years

13 years 24-h mean: PM10, g/m3 (19861999) 8-h mean: O3, ppb; Distance to traffic road

01 day lag

Per cent increase in COPD per increase in PM10 10 g/m3; O3 5 ppb

Lag 0: Total respiratory diseases: NO2 2.5 (0.94.2); CO 2.8 (1.34.3); COPD: CO 4.3 (1.67.1) Single pollutant model: PM10 1.13 (1.051.21) NO2 1.11 (1.041.20) CO 1.08 (1.021.13) COPD prevalence 4.5% Annual mean: PM10 1.37 (0.981.92) NO2 1.39 (1.201.63) 5 year mean: PM10 1.33 (1.031.72) NO2 1.43 (1.231.66) 1 day lag: PM10 1.47 (0.932.01) 2 day lag: O3 0.25 (0.080.47)

Note: The cross-sectional time-series studies evaluated short-term effects and mostly used Poisson regression with generalized additive models for data analysis and controlled for long-term trends, day of the week, temperature, humidity, dew point temperature, inuenza epidemic and other factors. Both single pollutant and multiple pollutant models were used in most studies. Per cent increase (RR 1) 100. Conversion: PM2.5 g/m3 30 bscat/104 m. COPD chronic obstructive pulmonary disease; CI condence interval; TP thoracic particles, equivalent of PM10; H acidity; SO4 aerosol sulfate; NO2 nitrogen dioxide; ppb parts per billion; CO carbon monoxide; SO2 sulfur dioxide; O3 ozone; RR relative risk, observed over expected; TSP total suspended particles with aerodynamic diameter 40 m; PM0.012.0 particulate matter with aerodynamic diameter 0.012.0 m; bscat/104 m nephelometer particulate concentration scale; OR odds ratio.

Table 3
Study period 2 years (19971998) 4 years (19962000) 02 days lag g/m3; 07 days lag 24.9 Pollutants measured Lag days analyzed Risk type

Outdoor air pollution and COPD-related hospitalizations or emergency room visits in low-income countries
Risk level (95%CI)

First author, year, reference

City/country

Subjects

Pande

200261

Delhi, India

All ages

Gouveia 200662

Sao Paulo, Brazil

65 years

24-h mean: TSP, SO2, g/m3; NOx, g/m3; CO, g/m3 24-h mean: PM10, g/m3; SO2, g/m3; NO2, g/m3; CO, ppm; O3, g/m3

Per cent increase in COPD based on upper permissible level of TSP and SO2 RR increase in COPD per 10 g/m3 increase in PM10, SO2, NO2, O3 or per 1 ppm increase in CO OR increase in COPD per increase in PM10 26.41 g/m3 SO2 2.79 ppb NO2 10.05 ppb CO 0.53 ppm O3 11.29 ppb

Yang 200763

Taipei, Taiwan

All ages

8 years (19962003)

24-h mean: PM10, g/m3; SO2, ppb; NO2, ppb; CO, ppm; O3, ppb 02 days lag

Ko 200764

Hong Kong, China

65 years 6 years (20002005)

24-h mean: PM10, g/m3; PM2.5, g/m3; SO2, g/m3; NO2, g/m3 8-h mean: O3, g/m3

05 days lag; Cumulative lags by 2, 3 and 6 days analyzed

RR increase in COPD per 10 g/m3 increase in all pollutants

PM10 1.043 (1.0281.058) SO2 1.179 (1.1261.235) NO2 1.024 (1.0151.034) CO 1.049 (1.0231.076) O3 1.015 (1.0051.025) 20 oC: PM10 1.133 (1.0981.168) SO2 1.006 (0.9701.043) NO2 1.193 (1.1581.230) CO 1.227 (1.1781.277) O3 1.157 (1.1181.197) 20 oC: PM10 1.035 (0.9941.077) SO2 1.071 (1.0151.129) NO2 0.972 (0.9221.024) CO 0.975 (0.9211.033) O3 0.936 (0.9741.003) Lag 05: PM10 1.024 (1.0211.028) PM2.5 1.031 (1.0261.036) SO2 1.007 (1.0011.014) NO2 1.026 (1.0221.031) O3 1.034 (1.0301.040)

Air pollution and COPD burden

COPD chronic obstructive pulmonary disease; CI condence interval; TSP total suspended particles with aerodynamic diameter 40 m; SO2 sulfur dioxide; NOx nitrogen oxide; CO carbon monoxide; PM10 particulate matter with aerodynamic diameter 10 m; NO2 nitrogen dioxide; ppm parts per million; O3 ozone; RR relative risk; ppb parts per billion; OR odds ratio; PM2.5 particulate matter with aerodynamic diameter 2.5 m.

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In a similar study performed in warmer Kaohsiung city, all pollutants were associated with increased hospital admissions of COPD, except for SO2, on warm days.65 In Hong Kong, signicant associations were found for all measured pollutants with increased emergency hospitalizations of COPD and respiratory symptoms.64,66 COPD prevalence In addition to exacerbations of the diseases of COPD patients, there are also questions about to what extent air pollution is a risk factor for new cases of COPD. This is usually done by cross-sectional comparisons of the prevalence of COPD (symptoms and reduced lung function) among subjects who lived in environments 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 on lung function in women living near major trafc roads. They followed 4757 women longitudinally from 1985 to 1994 and found that chronic exposure to PM10, NO2 and living near a major road increased the risk of developing COPD and could have a detrimental effect on lung function (Table 2). The overall prevalence of COPD was 4.5%. A 7 g/m3 increase in 5year means of PM10 (interquartile range) was associated 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 odds ratio (OR) of 1.33 (95%CI 1.031.72) for COPD. Women living less than 100 m from a busy road also had signicantly reduced lung function, and COPD was 1.79 times more likely (95%CI 1.063.02) than for those living farther away.54 A large cross-sectional population-based study on air pollution and lung diseases in adults (SAPALDIA) evaluated 9651 subjects aged 1860 years residing in eight different areas in Switzerland. Signicant and consistent effects on FVC and FEV1 were found for NO2, SO2 and PM10 in all subgroups and in the total population, with PM10 showing the most consistent effect of a 3.4% change in FVC per 10 g/m3.67 A prospective cohort study in Los Angeles, California, found that mean declines in FEV1 in males were signicantly lower in Lancaster and Glendora compared with Long Beach (where residents were exposed to high levels of sulfates, oxides of nitrogen and hydrocarbons), in each category of smoking. The mean decline in FEV1 attributable to living in Long Beach compared with living in Lancaster was 23.6 ml/year.68 The number of recent studies on the prevalence of symptoms is limited. In addition to reduced lung function, the SAPALDIA study in Switzerland also found increased risk for respiratory symptoms associated with annual mean concentrations of NO2, TSP and PM10. Among never-smokers, the OR for a 10 g/m3 increase in PM10 was 1.35 (95%CI 1.111.65) for chronic phlegm production, 1.27 (95%CI 1.081.50) for chronic 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 day or at night and 1.32 (95%CI 1.181.46) for dyspnea on exertion.69 In Hong Kong, a prospective cohort study found that the prevalence of most respiratory symptoms increased over a 12-year period after adjusting the data for age, sex, social status and smoking habits. The prevalence of self-reported physiciandiagnosed emphysema increased from 2.4% to 3.1%, with adjusted OR at 1.78 (95%CI 1.122.86).66 The authors suggested that this might be related to environmental factors, and especially increasing air pollution, in Hong Kong. Several studies have now found that chronic exposure to urban or trafc air pollution reduces the rate of lung function growth in children.7072 Indoor air pollution Human beings spend a large proportion of their time in indoor environments such as homes, workplaces, libraries, school classrooms, shopping malls, daycare centers and vehicles. Important indoor pollutants include PM, SO2, NO2 and CO generated from cooking and heating activities, volatile organic compounds (VOCs) from paints, carpets and furniture, molds and allergens from dampness and pets and environmental tobacco smoke (ETS).19 According to the WHO, indoor air pollution is responsible for the death of 1.6 million people annually.73 Indoor air pollutant exposure varies dramatically between high-income and low-income countries, with biomass fuels being a much more common source of exposure in the developing world. Although global energy consumption from biomass fuels or biofuels is only a small part of the total (12%), their use is much more prevalent in low-income countries than in highincome countries (33% vs. 3%).74 It is estimated that almost 3 billion people, or 50% of households worldwide, use biomass and coal as their main source of energy for cooking, heating and other household needs.75,76 Biofuels have higher emission factors for PM and other pollutants, especially during incomplete combustion at lower temperatures,77 which generate indoor airborne particles at levels much higher than those of cleaner fuels78 or outdoors,76 and well above levels in most polluted cities.79 Such particles also have small aerodynamic diameters (ranging from 0.05 to 1 m for woodsmoke, for example)74 and can penetrate deep into the alveolar region to induce adverse pulmonary effects. The body of work focusing on indoor air pollution and COPD is much smaller than that on outdoor air pollution. The majority of studies on indoor air pollution have focused on disease incidence or prevalence rather than on outcomes such as hospitalization or death. Some of the early work concerning biomass smoke and respiratory health was done in Papua New Guinea74,80,81 and Nepal.82,83 In Saudi Arabia, Dossing

Table 4
Subjects 242 rural; 102 city women 25 years 1999 Questionnaire for fuel type, years of use and stove type ATS and BMRC OR for CB symptom and COPD questionnaires Physical examination Lung function testing Study period Exposure measured Health measured Risk type Risk level (95%CI)

Indoor air pollution and COPD incidence/prevalence in low-income countries

First author, year, reference

Study design

City/country

Kiraz

200387

Cross-sectional survey 3 villages; 1 city district

Kaseri, Turkey

Ekici 200588

Shrestha & Shrestha, 200578

Peabody 200589

Chapman 200590

Liu 200791

Rural vs. urban women: Smoking rate, %: Current: 4.5 vs. 14.7 Past: 1.2 vs. 11.8 CB, %: 20.7 vs. 10.8 COPD, %: 12.4 vs. 3.9 OR for CB 28.7 (8.795.9) Cross-sectional survey Kirikkale, Biomass exposure 397 2002 Questionnaire for BMRC symptom OR and AP Crude: 10 villages Turkey LPG control 199 h and years doing questionnaire for COPD Group A 1.7 (1.03.1) Rural women 40 years biomass cooking: Physical examination Group B 2.5 (1.44.4) 68.6 h-year Lung function testing Group C 3.3 (1.95.7) 68.8152.4 h-year Adjusted: 152.4 h-year Group A 2.0 (0.94.5) Group B 2.3 (1.14.5) Group C 2.2 (1.14.4) Combined 2.5 (1.54.0) Adjusted 1.4 (1.21.7) AP 23.1 (13.433.2) Cross-sectional survey Kathmandu 168 subjects 2003 winter PM10, g/m3 BMRC respiratory OR for COPD, COPD prevalence, %: Solid fuels 16.8 4 municipalities valley, Nepal 94% women CO, g/m3 symptom asthma and Clean fuels 7.0 98 households questionnaire respiratory OR for COPD/asthma: Physical examination symptoms Unadjusted 3.85 (1.1113.38) Peak flow Smoking adjusted 3.13 (0.8311.76) measurement Age adjusted 4.18 (1.1415.27) Cross-sectional survey Shanxi, Hubei, 4638 adults Fuel type Adult and children OR and COPD prevalence, %: 3.8 3 provinces Zhejiang, 2285 children Stove type questionnaires prevalence Prevalence higher in coal users 103.4 million people China Duration in cooking Heart rate for COPD OR compared to coal: 3476 households CO in exhaled air Respiratory rate Wood 0.48 (0.280.87) Blood pressure Crop 0.57 (0.340.96) Lung function Clean fuel 0.43 (0.050.36) testing (FVC) OR for stove: Tradition vs. improved 1.87 (1.302.69) Retrospective Xuanwei, 20 453 people with 16 years Questionnaire Standard RR for COPD COPD prevalence, %: 7.3 cohort study China traditional stoves (19761992) Stove type questionnaire in improved COPD incidence, % reduced: Men 42 Large rural 16 606 people changed Fuel type Bronchitis vs. unvented Women 25 community to improved stoves Emphysema stoves RR: Men 0.58 (0.490.70) Death Women 0.75 (0.620.92) Population-based, Guangzhou, Rural 1468 0.5 year 15 min average: Standard OR for COPD COPD prevalence, %: Rural 12; Urban 7.4 cross-sectional survey China Urban 1818 (20022003) PM10 mg/m3; questionnaire and OR for fuel type: Biomass 1.72 (1.272.35) 1 rural community 40 years SO mg/m3; Physical examination respiratory Coal 1.55 (0.743.22) with 14 000 people NO2 mg/m3; Lung function testing symptoms COPD prevalence, %, for non-smoking women: 1 urban community CO 10 mg/m3 Rural 7.2; Urban 2.5 with 520 000 people OR for fuel type: Biomass 3.11 (1.635.94) Coal 2.77 (0.839.26) OR for SO2 1.80 (1.043.11)

Note: Case-control and cross-sectional prevalence studies used 2 test, MantelHaenszel method, logistic regression or multivariate regression for data analysis on OR and trends, adjusting for variables such as age, sex, marital status, education, body mass index, alcohol use, active and passive smoking, occupational exposures, atopy and family history of COPD, place of birth and residence and family income. The retrospective cohort study used Cox proportional hazard survival model. Pollutant names are the same as in previous tables. COPD chronic obstructive pulmonary disease; CI condence interval; ATS American Thoracic Society; BMRC British Medical Research Council; OR odds ratio; CB chronic bronchitis; LPG liqueed petroleum gas; AP attributable proportion (OR 1) P/OR; PM10 particulate matter with aerodynamic diameter 10 m; CO carbon monoxide; FVC forced vital capacity; P prevalence of exposure among cases.

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et al. found that two thirds of women with COPD and only 1/20 of the control women had been exposed to indoor open res for 20 years (P 0.05).84 In a case-control study conducted in Bogota, Colombia, wood burning was associated with a higher risk of COPD (adjusted OR 3.92, 95%CI 1.29.1).85 In Mexico City, the OR for cooking with traditional cook 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 3.7 27) for bronchitis and COPD combined.86 In the past decade, several more studies have evaluated the burning 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 two times as high in rural women than their city counterparts, despite a lower prevalence of smoking (20.7% vs. 11.8%, P 0.01).87 In another cross-sectional study in Turkey, Ekici et al. found that women exposed to biomass smoke had a higher risk of COPD and chronic bronchitis (adjusted OR 2.5, 95%CI 1.5 4.0).88 More recently, in Nepal, Shrestha and Shrestha found a higher COPD prevalence among women using unprocessed fuels (16.7% vs. 7.8%).78 No longitudinal data on biomass exposure and COPD have been reported to date. Several studies have also been published from China. Peabody et al. found an increased prevalence of COPD among women in homes that burned coal.89 In a recent study with 20 245 subjects in seven provinces/cities in China, the overall prevalence of COPD was found to be 8.4% (men 12.4%, women 5.1%). The prevalence of COPD was signicantly higher in rural residents.92 Looking further at the high prevalence in rural areas, Liu et al. found that that COPD prevalence was signicantly higher in non-smoking women exposed to biomass fuels in a rural community compared to an urban community (prevalence 7.2% vs. 2.5%, adjusted OR 3.11, 95%CI 1.635.94). Concentrations of CO, PM10, SO2 and NO2 in the kitchen during biomass fuel combustion were signicantly higher than those during liqueed petroleum gas combustion, and SO2 was signicantly associated with 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, Yunnan Province, China, rates of COPD were over twice the national average.93 In Xuanwei, 90% of residents are farmers. For cooking and heating, residents usually burnt smoky coal (bituminous coal), smokeless coal (anthracite) or wood in unvented stoves.94,95 A retrospective cohort study followed up from 1976 to 1992 to compare the COPD rates between users of the unvented and improved coal stoves with chimney groups. A reduction was observed for COPD incidence among households with improved stoves (Coxmodeled RR 0.58, 95%CI 0.490.70 in men and 0.75, 95%CI 0.620.92, in women). This study suggests that the COPD burden associated with tradi-

tional coal stoves in low-income countries can be reduced by using improved stoves that reduce pollutant emissions.90 The potential for improved biomass stoves to reduce adverse health effects is currently being studied in Guatemala and Mexico. In high-income countries, exposure to biomass smoke may also be a risk factor for COPD, as shown in a recent study from Spain.96 In addition, higher levels of indoor PM2.5 were found to be associated with worse health status among patients with severe COPD.97

CONCLUSIONS
Historical reports of air pollution episodes have provided clear evidence that COPD-related cardiorespiratory mortality and morbidity are associated with high levels of outdoor air pollutants, particularly PM. More recent time series studies show that acute increases in outdoor air pollutants at much lower levels continue to cause health effects (i.e., mortality and hospital admissions) among patients with COPD and in the general population. Limited prospective cohort studies have also shown an increased risk of COPD from long-term exposure to low levels of air pollutants. Indoor air pollution due to solid fuel combustion is an important risk factor for COPD in low-income countries, particularly in non-smoking women. More prospective cohort studies are needed to evaluate the risk of COPD associated with exposures to both longterm low-level outdoor air pollution and indoor biomass combustion. Tailored strategies and preventive efforts at national and local levels are needed to target the different risk factors of COPD in different countries, as well as reduction of trafc air pollution in urban environments and increased dissemination of improved cooking stoves in low-income countries. References
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RSUM

La maladie broncho-pulmonaire obstructive chronique (BPCO) est une cause importante de morbidit et de mortalit tant dans les pays industrialiss que dans les pays en dveloppement. Alors quau niveau mondial la consommation active de cigarettes est le plus important facteur de risque vitable, les polluants de lair extrieur et intrieur peuvent provoquer ou exacerber la BPCO. Dans les pays industrialiss, des accidents historiques de pollution de lair dmontrent clairement que lexposition des niveaux levs de polluants de lair extrieur est associe une mortalit et une morbidit accrues par BPCO et par les maladies cardiorespiratoires qui y sont lies. Des tudes des 20 dernires annes continuent dmontrer un accroissement de risques associs princi-

palement avec des lments particulaires mme des niveaux beaucoup plus faibles. Dans les pays en dveloppement, les populations sont largement exposes aux polluants de lair interne provenant de la combustion des combustibles solides qui contribuent de manire significative au fardeau des maladies en liaison avec la BPCO, particulirement chez les femmes non-fumeuses. Des stratgies de prvention efficace de la BPCO peuvent varier de pays pays, et comportent une amlioration continue de la technologie dpuration de lair, une lgislation sur la qualit de lair et la dissmination de cuisinires de meilleure qualit. Ces dfis ncessitent un effort conjoint de la socit et des gouvernements.

RESUMEN

La enfermedad pulmonar obstructiva crnica (EPOC) representa una causa frecuente de morbilidad y mortalidad en pases industrializados y en pases en va de desarrollo. Si bien el tabaquismo activo constituye el ms importante factor de riesgo a escala mundial, la contaminacin ambiental exterior y en interiores puede provocar exacerbacin de los sntomas de la EPOC. En los pases industrializados, los acontecimientos importantes de contaminacin ambiental ofrecen pruebas concluyentes de que la exposicin a altos niveles de contaminacin exterior se relaciona con una mayor morbilidad y mortalidad por EPOC y por enfermedades cardiorrespiratorias asociadas. Estudios de los ltimos 20 aos continan poniendo en evidencia un aumento de los riesgos, asociados sobre todo con los elementos slidos, an en

concentraciones muy inferiores. Las poblaciones de los pases en va de desarrollo se encuentran considerablemente expuestas a la contaminacin ambiental en interiores, proveniente de la combustin de combustibles slidos, lo cual contribuye en forma significativa a la carga de morbilidad por enfermedades relacionadas con la EPOC, en particular en mujeres no fumadoras. Las estrategias eficaces de prevencin de la EPOC difieren entre los diferentes pases y comprenden un perfeccionamiento continuo de las tcnicas de purificacin del aire, legislacin en materia de calidad del aire y difusin de estufas de caractersticas mejoradas. Se precisa un esfuerzo conjunto por parte de la sociedad en general y los gobiernos a fin de cumplir con estas iniciativas.