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1.  Environmental inequality and circulatory disease mortality gradients 
Study objective: Studies in Europe and North America have reported that living in a disadvantaged neighbourhood is associated with an increased incidence of coronary heart disease. The aim of this study was to test the hypotheses that exposure to traffic and air pollution might account for some of the socioeconomic differences in mortality rates in a city where residents are covered by universal health insurance.
Design: Cohort mortality study. Individual postal codes used to derive: (1) socioeconomic status from census data; (2) mean air pollution levels from interpolation between governmental monitoring stations; (3) proximity to traffic from the geographical information system. Analysis conducted with Cox proportional hazards models.
Setting: Hamilton Census Metropolitan Area, Ontario, Canada, on the western tip of Lake Ontario (population about 480 000).
Participants: 5228 people, aged 40 years or more, identified from register of lung function laboratory at an academic respirology clinic between 1985 and 1999.
Main results: Circulatory disease (cardiovascular and stroke) mortality rates were related to measures of neighbourhood deprivation. Circulatory disease mortality rates were also associated with indices of long term ambient pollution at the subjects' residences (relative risk 1.06, 1.00 to 1.13) and with proximity to traffic (relative risk 1.40, 1.08 to 1.81). Subjects in more deprived neighbourhoods had greater exposure to ambient particulate and gaseous pollutants and to traffic.
Conclusions: At least some of the observed social gradients in circulatory mortality arise from inequalities in environmental exposure to background and traffic air pollutants.
doi:10.1136/jech.2004.026203
PMCID: PMC1757055  PMID: 15911644
2.  Relation between income, air pollution and mortality: a cohort study 
Background
Community levels of air pollution have been associated with variability in mortality rates, but previous studies have inferred exposure to pollutants on a citywide basis. We investigated mortality in relation to neighbourhood levels of income and air pollution in an urban area.
Methods
We identified 5228 people in the Hamilton–Burlington area of southern Ontario who had been referred for pulmonary function testing between 1985 and 1999. Nonaccidental deaths that occurred in this group between 1992 and 1999 were ascertained from the Ontario Mortality Registry. Mean household income was estimated by linking the subjects' postal codes with the 1996 census. Mean neighbourhood levels of total suspended particulates and sulfur dioxide were estimated by interpolation from data from a network of sampling stations. We used proportional hazards regression models to compute mortality risk in relation to income and pollutant levels, while adjusting for pulmonary function, body mass index and diagnoses of chronic disease. Household incomes and pollutant levels were each divided into 2 risk categories (low and high) at the median.
Results
Mean pollutant levels tended to be higher in lower-income neighbourhoods. Both income and pollutant levels were associated with mortality differences. Compared with people in the most favourable category (higher incomes and lower particulate levels), those with all other income–particulate combinations had a higher risk of death from nonaccidental causes (lower incomes and higher particulate levels: relative risk [RR] 2.62, 95% confidence interval [CI] 1.67–4.13; lower incomes and lower particulate levels: RR 1.82, 95% CI 1.30–2.55; higher incomes and higher particulate levels: RR 1.33, 95% CI 1.12–1.57). Similar results were observed for sulfur dioxide. The relative risk was lower at older ages.
Interpretation
Mortality rates varied by neighbourhood of residence in this cohort of people whose lung function was tested. Two of the broader determinants of health — income and air pollution levels — were important correlates of mortality in this population.
PMCID: PMC183288  PMID: 12952800
3.  Long-Term Exposure to Air Pollution and Cardiorespiratory Disease in the California Teachers Study Cohort 
Rationale: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease.
Objectives: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction and stroke, as well as all-cause and cause-specific mortality.
Methods: We estimated long-term residential air pollution exposure for more than 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals. We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident myocardial infarction and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models.
Measurements and Main Results: We found elevated hazard ratios linking long-term exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5), scaled to an increment of 10 μg/m3 with mortality from ischemic heart disease (IHD) (1.20; 95% confidence interval [CI], 1.02–1.41) and, particularly among postmenopausal women, incident stroke (1.19; 95% CI, 1.02–1.38). Long-term exposure to particulate matter less than 10 μm in aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06; 95% CI, 0.99–1.14) and incident stroke (1.06; 95% CI, 1.00–1.13), while exposure to nitrogen oxides was associated with elevated risks for IHD and all cardiovascular mortality.
Conclusions: This study provides evidence linking long-term exposure to PM2.5 and PM10 with increased risks of incident stroke as well as IHD mortality; exposure to nitrogen oxides was also related to death from cardiovascular diseases.
doi:10.1164/rccm.201012-2082OC
PMCID: PMC3208653  PMID: 21700913
particulate matter; cardiovascular diseases; air pollutants; epidemiology
4.  Air Pollution and the Microvasculature: A Cross-Sectional Assessment of In Vivo Retinal Images in the Population-Based Multi-Ethnic Study of Atherosclerosis (MESA) 
PLoS Medicine  2010;7(11):e1000372.
Sara Adar and colleagues show that residing in locations with higher air pollution concentrations and experiencing daily increases in air pollution are associated with narrower retinal arteriolar diameters in older individuals, thus providing a link between air pollution and cardiovascular disease.
Background
Long- and short-term exposures to air pollution, especially fine particulate matter (PM2.5), have been linked to cardiovascular morbidity and mortality. One hypothesized mechanism for these associations involves microvascular effects. Retinal photography provides a novel, in vivo approach to examine the association of air pollution with changes in the human microvasculature.
Methods and Findings
Chronic and acute associations between residential air pollution concentrations and retinal vessel diameters, expressed as central retinal arteriolar equivalents (CRAE) and central retinal venular equivalents (CRVE), were examined using digital retinal images taken in Multi-Ethnic Study of Atherosclerosis (MESA) participants between 2002 and 2003. Study participants (46 to 87 years of age) were without clinical cardiovascular disease at the baseline examination (2000–2002). Long-term outdoor concentrations of PM2.5 were estimated at each participant's home for the 2 years preceding the clinical exam using a spatio-temporal model. Short-term concentrations were assigned using outdoor measurements on the day preceding the clinical exam. Residential proximity to roadways was also used as an indicator of long-term traffic exposures. All associations were examined using linear regression models adjusted for subject-specific age, sex, race/ethnicity, education, income, smoking status, alcohol use, physical activity, body mass index, family history of cardiovascular disease, diabetes status, serum cholesterol, glucose, blood pressure, emphysema, C-reactive protein, medication use, and fellow vessel diameter. Short-term associations were further controlled for weather and seasonality. Among the 4,607 participants with complete data, CRAE were found to be narrower among persons residing in regions with increased long- and short-term levels of PM2.5. These relationships were observed in a joint exposure model with −0.8 µm (95% confidence interval [CI] −1.1 to −0.5) and −0.4 µm (95% CI −0.8 to 0.1) decreases in CRAE per interquartile increases in long- (3 µg/m3) and short-term (9 µg/m3) PM2.5 levels, respectively. These reductions in CRAE are equivalent to 7- and 3-year increases in age in the same cohort. Similarly, living near a major road was also associated with a −0.7 µm decrease (95% CI −1.4 to 0.1) in CRAE. Although the chronic association with CRAE was largely influenced by differences in exposure between cities, this relationship was generally robust to control for city-level covariates and no significant differences were observed between cities. Wider CRVE were associated with living in areas of higher PM2.5 concentrations, but these findings were less robust and not supported by the presence of consistent acute associations with PM2.5.
Conclusions
Residing in regions with higher air pollution concentrations and experiencing daily increases in air pollution were each associated with narrower retinal arteriolar diameters in older individuals. These findings support the hypothesis that important vascular phenomena are associated with small increases in short-term or long-term air pollution exposures, even at current exposure levels, and further corroborate reported associations between air pollution and the development and exacerbation of clinical cardiovascular disease.
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Cardiovascular disease (CVD)—disease that affects the heart and/or the blood vessels—is a common cause of illness and death among adults in developed countries. In the United States, for example, the leading cause of death is coronary heart disease, a CVD in which narrowing of the heart's arteries by atherosclerotic plaques (fatty deposits that build up with age) slows the blood supply to the heart and may eventually cause a heart attack (myocardial infarction). Other types of CVD include stroke (in which atherosclerotic plaques interrupt the brain's blood supply) and peripheral arterial disease (in which the blood supply to the limbs is blocked). Smoking, high blood pressure, high blood levels of cholesterol (a type of fat), having diabetes, being overweight, and being physically inactive all increase a person's risk of developing CVD. Treatments for CVD include lifestyle changes and taking drugs that lower blood pressure or blood cholesterol levels.
Why Was This Study Done?
Another risk factor for CVD is exposure to long-term and/or short-term air pollution. Fine particle pollution or PM2.5 is particularly strongly associated with an increased risk of CVD. PM2.5—particulate matter 2.5 µm in diameter or 1/30th the diameter of a human hair—is mainly produced by motor vehicles, power plants, and other combustion sources. Why PM2.5 increases CVD risk is not clear but one possibility is that it alters the body's microvasculature (fine blood vessels known as capillaries, arterioles, and venules), thereby impairing the blood flow through the heart and brain. In this study, the researchers use noninvasive digital retinal photography to investigate whether there is an association between air pollution and changes in the human microvasculature. The retina—a light-sensitive layer at the back of the eye that converts images into electrical messages and sends them to the brain—has a dense microvasculature. Retinal photography is used to check the retinal microvasculature for signs of potentially blinding eye diseases such as diabetic retinopathy. Previous studies have found that narrower than normal retinal arterioles and wider than normal retinal venules are associated with CVD.
What Did the Researchers Do and Find?
The researchers used digital retinal photography to measure the diameters of retinal blood vessels in the participants of the Multi-Ethnic Study of Atherosclerosis (MESA). This study is investigating CVD progression in people aged 45–84 years of various ethnic backgrounds who had no CVD symptoms when they enrolled in the study in 2000–2002. The researchers modeled the long-term outdoor concentration of PM2.5 at each participant's house for the 2-year period preceding the retinal examination (which was done between 2002 and 2003) using data on PM2.5 levels collected by regulatory monitoring stations as well as study-specific air samples collected outside of the homes and in the communities of study participants. Outdoor PM2.5 measurements taken the day before the examination provided short-term PM2.5 levels. Among the 4,607 MESA participants who had complete data, retinal arteriolar diameters were narrowed among those who lived in regions with increased long- and short-term PM2.5 levels. Specifically, an increase in long-term PM2.5 concentrations of 3 µg/m3 was associated with a 0.8 µm decrease in arteriolar diameter, a reduction equivalent to that seen for a 7-year increase in age in this group of people. Living near a major road, another indicator of long-term exposure to PM2.5 pollution, was also associated with narrowed arterioles. Finally, increased retinal venular diameters were weakly associated with long-term high PM2.5 concentrations.
What Do These Findings Mean?
These findings indicate that living in areas with long-term air pollution or being exposed to short-term air pollution is associated with narrowing of the retinal arterioles in older individuals. They also show that widening of retinal venules is associated with long-term (but not short-term) PM2.5 pollution. Together, these findings support the hypothesis that long- and short-term air pollution increases CVD risk through effects on the microvasculature. However, they do not prove that PM2.5 is the constituent of air pollution that drives microvascular changes—these findings could reflect the toxicity of another pollutant or the pollution mixture as a whole. Importantly, these findings show that microvascular changes can occur at the PM2.5 levels that commonly occur in developed countries, which are well below those seen in developing countries. Worryingly, they also suggest that the deleterious cardiovascular effects of air pollution could occur at levels below existing regulatory standards.
Additional Information
Please access these Web sites via the online version of this summary at http://dx.doi.org/ 10.1371/journal.pmed.1000372.
The American Heart Association provides information for patients and caregivers on all aspects of cardiovascular disease (in several languages), including information on air pollution, heart disease, and stroke
The US Centers for Disease Control and Prevention has information on heart disease and on stroke
Information is available from the British Heart Foundation on cardiovascular disease
The UK National Health Service Choices website provides information for patients and caregivers about cardiovascular disease
MedlinePlus provides links to other sources of information on heart disease and on vascular disease (in English and Spanish)
The AIRNow site provides information about US air quality and about air pollution and health
The Air Quality Archive has up-to-date information about air pollution in the UK and information about the health effects of air pollution
The US Environmental Protection Agency has information on PM2.5
The following Web sites contain information available on the MESA and MESA Air studies
doi:10.1371/journal.pmed.1000372
PMCID: PMC2994677  PMID: 21152417
5.  An Association Between Long-Term Exposure to Ambient Air Pollution and Mortality From Lung Cancer and Respiratory Diseases in Japan 
Journal of Epidemiology  2011;21(2):132-143.
Background
Evidence for a link between long-term exposure to air pollution and lung cancer is limited to Western populations. In this prospective cohort study, we examined this association in a Japanese population.
Methods
The study comprised 63 520 participants living in 6 areas in 3 Japanese prefectures who were enrolled between 1983 and 1985. Exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5), sulfur dioxide (SO2), and nitrogen dioxide (NO2) was assessed using data from monitoring stations located in or nearby each area. The Cox proportional hazards model was used to calculate the hazard ratios associated with the average concentrations of these air pollutants.
Results
The 10-year average concentrations of PM2.5, SO2, and NO2 before recruitment (1974–1983) were 16.8 to 41.9 µg/m3, 2.4 to 19.0 ppb, and 1.2 to 33.7 ppb, respectively (inter-area range). During an average follow-up of 8.7 years, there were 6687 deaths, including 518 deaths from lung cancer. The hazard ratios for lung cancer mortality associated with a 10-unit increase in PM2.5 (µg/m3), SO2 (ppb), and NO2 (ppb) were 1.24 (95% confidence interval: 1.12–1.37), 1.26 (1.07–1.48), and 1.17 (1.10–1.26), respectively, after adjustment for tobacco smoking and other confounding factors. In addition, a significant increase in risk was observed for male smokers and female never smokers. Respiratory diseases, particularly pneumonia, were also significantly associated with all the air pollutants.
Conclusions
Long-term exposure to air pollution is associated with lung cancer and respiratory diseases in Japan.
doi:10.2188/jea.JE20100098
PMCID: PMC3899505  PMID: 21325732
air pollution; lung neoplasms; nitrogen dioxide; particulate matter; sulfur dioxide
6.  The role of particulate size and chemistry in the association between summertime ambient air pollution and hospitalization for cardiorespiratory diseases. 
Environmental Health Perspectives  1997;105(6):614-620.
In order to address the role that the ambient air pollution mix, comprised of gaseous pollutants and various physical and chemical measures of particulate matter, plays in exacerbating cardiorespiratory disease, daily measures of fine and coarse particulate mass, aerosol chemistry (sulfates and acidity), and gaseous pollution (ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Toronto, Ontario, Canada, in the summers of 1992, 1993, and 1994. These time series were then compared with concurrent data on the number of daily admissions to hospitals for either cardiac diseases (ischemic heart disease, heart failure, and dysthymias) or respiratory diseases (tracheobronchitis, chronic obstructive long disease, asthma, and pneumonia). After adjusting the admission time series for long-term temporal trends, seasonal variations, the effects of short-term epidemics, day of the week effects, and ambient temperature and dew point temperature, positive associations were observed for all ambient air pollutants for both respiratory and cardiac diseases. Ozone was least sensitive to adjustment for the gaseous and particulate pollution measures. However, the association between the health outcomes and carbon monoxide, fine and coarse mass, sulfate levels and aerosol acidity could be explained by adjustment for exposure to gaseous pollutants. Increases in ozone, nitrogen dioxide, and sulfur dioxide equivalent to their interquartile ranges corresponded to an 11% and 13% increase in daily hospitalizations for respiratory and cardiac diseases, respectively. The inclusion of any one of the particulate air pollutants in multiple regression models did not increase these percentages. Particle mass and chemistry could not be identified as an independent risk factor for the exacerbation of cardiorespiratory diseases in this study beyond that attributable to climate and gaseous air pollution. We recommend that effects of particulate matter on health be assessed in conjunction with temporally covarying gaseous air pollutants.
Images
PMCID: PMC1470088  PMID: 9288496
7.  A Cohort Study of Traffic-Related Air Pollution Impacts on Birth Outcomes 
Environmental Health Perspectives  2008;116(5):680-686.
Background
Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.
Objectives
We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW), and preterm birth using spatiotemporal exposure metrics.
Methods
With linked administrative data, we identified 70,249 singleton births (1999–2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) μm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon), and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile), term LBW (< 2,500 g), and preterm birth.
Results
Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI), 1.07–1.49] and an 11% (95% CI, 1.01–1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02; 95% CI, 1.00–1.04; IDW: OR = 1.05; 95% CI, 1.03–1.08 per 10-μg/m3 increase in NO). For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks). No consistent patterns suggested exposure windows of greater relevance.
Conclusion
Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.
doi:10.1289/ehp.10952
PMCID: PMC2367679  PMID: 18470315
air pollution; birth weight; carbon black; carbon monoxide; nitrogen dioxide; nitric oxide; particulate matter; pregnancy; pregnancy outcome; preterm birth; soot; sulfur dioxide; vehicle emissions
8.  Epigenetic Influences on Associations between Air Pollutants and Lung Function in Elderly Men: The Normative Aging Study 
Environmental Health Perspectives  2014;122(6):566-572.
Background: Few studies have been performed on pulmonary effects of air pollution in the elderly—a vulnerable population with low reserve capacity—and mechanisms and susceptibility factors for potential effects are unclear.
Objectives: We evaluated the lag structure of air pollutant associations with lung function and potential effect modification by DNA methylation (< or ≥ median) at 26 individual CpG sites in nine candidate genes in a well-characterized cohort of elderly men.
Methods: We measured forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and blood DNA methylation one to four times between 1999 and 2009 in 776 men from the Normative Aging Study. Air pollution was measured at fixed monitors 4 hr to 28 days before lung function tests. We used linear mixed-effects models to estimate the main effects of air pollutants and effect modification by DNA methylation.
Results: An interquartile range (IQR) increase in subchronic exposure (3 to 28 days cumulated), but not in acute exposure (during the previous 4 hr, or the current or previous day), to black carbon, total and nontraffic particles with aerodynamic diameter ≤ 2.5 μm (PM2.5), carbon monoxide, and nitrogen dioxide was associated with a 1–5% decrease in FVC and FEV1 (p < 0.05). Slope estimates were greater for FVC than FEV1, and increased with cumulative exposure. The estimates slopes for air pollutants (28 days cumulated) were higher in participants with low (< median) methylation in TLR2 at position 2 and position 5 and high (≥ median) methylation in GCR.
Conclusions: Subchronic exposure to traffic-related pollutants was associated with significantly reduced lung function in the elderly; nontraffic pollutants (particles, ozone) had weaker associations. Epigenetic mechanisms related to inflammation and immunity may influence these associations.
Citation: Lepeule J, Bind MAC, Baccarelli AA, Koutrakis P, Tarantini L, Litonjua A, Sparrow D, Vokonas P, Schwartz JD. 2014. Epigenetic influences on associations between air pollutants and lung function in elderly men: the Normative Aging Study. Environ Health Perspect 122:566–572; http://dx.doi.org/10.1289/ehp.1206458
doi:10.1289/ehp.1206458
PMCID: PMC4050500  PMID: 24602767
9.  Mortality Associations with Long-Term Exposure to Outdoor Air Pollution in a National English Cohort 
Rationale: Cohort evidence linking long-term exposure to outdoor particulate air pollution and mortality has come largely from the United States. There is relatively little evidence from nationally representative cohorts in other countries.
Objectives: To investigate the relationship between long-term exposure to a range of pollutants and causes of death in a national English cohort.
Methods: A total of 835,607 patients aged 40–89 years registered with 205 general practices were followed from 2003–2007. Annual average concentrations in 2002 for particulate matter with a median aerodynamic diameter less than 10 (PM10) and less than 2.5 μm (PM2.5), nitrogen dioxide (NO2), ozone, and sulfur dioxide (SO2) at 1 km2 resolution, estimated from emission-based models, were linked to residential postcode. Deaths (n = 83,103) were ascertained from linkage to death certificates, and hazard ratios (HRs) for all- and cause-specific mortality for pollutants were estimated for interquartile pollutant changes from Cox models adjusting for age, sex, smoking, body mass index, and area-level socioeconomic status markers.
Measurements and Main Results: Residential concentrations of all pollutants except ozone were positively associated with all-cause mortality (HR, 1.02, 1.03, and 1.04 for PM2.5, NO2, and SO2, respectively). Associations for PM2.5, NO2, and SO2 were larger for respiratory deaths (HR, 1.09 each) and lung cancer (HR, 1.02, 1.06, and 1.05) but nearer unity for cardiovascular deaths (1.00, 1.00, and 1.04).
Conclusions: These results strengthen the evidence linking long-term ambient air pollution exposure to increased all-cause mortality. However, the stronger associations with respiratory mortality are not consistent with most US studies in which associations with cardiovascular causes of death tend to predominate.
doi:10.1164/rccm.201210-1758OC
PMCID: PMC3734610  PMID: 23590261
air pollution; mortality; cohort study; respiratory
10.  Cardiorespiratory Biomarker Responses in Healthy Young Adults to Drastic Air Quality Changes Surrounding the 2008 Beijing Olympics 
Associations between air pollution and cardiorespiratory mortality and morbidity have been well established, but data to support biologic mechanisms underlying these associations are limited. We designed this study to examine several prominently hypothesized mechanisms by assessing Beijing residents’ biologic responses, at the biomarker level, to drastic changes in air quality brought about by unprecedented air pollution control measures implemented during the 2008 Beijing Olympics.
To test the hypothesis that changes in air pollution levels are associated with changes in biomarker levels reflecting inflammation, hemostasis, oxidative stress, and autonomic tone, we recruited and retained 125 nonsmoking adults (19 to 33 years old) free of cardiorespiratory and other chronic diseases. Using the combination of a quasi-experimental design and a panel-study approach, we measured biomarkers of autonomic dysfunction (heart rate [HR*] and heart rate variability [HRV]), of systemic inflammation and oxidative stress (plasma C-reactive protein [CRP], fibrinogen, blood cell counts and differentials, and urinary 8-hydroxy-2′-deoxyguanosine [8-OHdG]), of pulmonary inflammation and oxidative stress (fractional exhaled nitric oxide [FeNO], exhaled breath condensate [EBC] pH, EBC nitrate, EBC nitrite, EBC nitrite+nitrate [sum of the concentrations of nitrite and nitrate], and EBC 8-isoprostane), of hemostasis (platelet activation [plasma sCD62P and sCD40L], platelet aggregation, and von Willebrand factor [vWF]), and of blood pressure (systolic blood pressure [SBP] and diastolic blood pressure [DBP]). These biomarkers were measured on each subject twice before, twice during, and twice after the Beijing Olympics. For each subject, repeated measurements were separated by at least one week to avoid potential residual effects from a prior measurement. We measured a large suite of air pollutants (PM2.5 [particulate matter ≤ 2.5 μm in aerodynamic diameter] and constituents, sulfur dioxide [SO2], carbon monoxide [CO], nitrogen dioxide [NO2], and ozone [O3]) throughout the study at a central Beijing site near the residences and workplaces of the subjects on a daily basis. Total particle number (TPN) was also measured at a separate site. We used a time-series analysis to assess changes in pollutant concentration by period (pre-, during-, and post-Olympics periods). We used mixed-effects models to assess changes in biomarker levels by period and to estimate changes associated with increases in pollutant concentrations, controlling for ambient temperature, relative humidity (RH), sex, and the day of the week of the biomarker measurements. We conducted sensitivity analyses to assess the impact of potential temporal confounding and exposure misclassification.
We observed reductions in mean concentrations for all measured pollutants except O3 from the pre-Olympics period to the during-Olympics period. On average, elemental carbon (EC) changed by −36%, TPN by −22%, SO2 by −60%, CO by −48%, and NO2 by −43% (P < 0.05 for all these pollutants). Reductions were observed in mean concentrations of PM2.5 (by −27%), sulfate (SO42−) (by −13%), and organic carbon (OC) (by −23%); however, these values were not statistically significant. Both 24-hour averages and 1-hour maximums of O3 increased (by 20% and 17%, respectively) from the pre-Olympics to the during-Olympics period. In the post-Olympics period after the pollution control measures were relaxed, mean concentrations of most pollutants (with the exception of SO42− and O3) increased to levels similar to or higher than pre-Olympics levels.
Concomitantly and consistent with the hypothesis, we observed, from the pre-Olympics to the during-Olympics period, statistically significant (P ≤ 0.05) or marginally significant (0.05 < P < 0.1) decreases in HR (−1 bpm or −1.7% [95% CI, −3.4 to −0.1]), SBP (−1.6 mmHg or − 1.8% [95% CI, −3.9 to 0.4]), 8-OHdG (−58.3% [95% CI, −72.5 to −36.7]), FeNO (−60.3% [95% CI, −66.0 to −53.6]), EBC nitrite (−30.0% [95% CI, −39.3 to −19.3]), EBC nitrate (−21.5% [95% CI, −35.5 to −4.5]), EBC nitrite+nitrate (−17.6% [95% CI, −28.4 to −5.1]), EBC hydrogen ions (−46% [calculated from EBC pH], or +3.5% in EBC pH [95% CI, 2.2 to 4.9]), sCD62P (−34% [95% CI, −38.4 to −29.2]), sCD40L (−5.7% [95% CI, −10.5 to −0.7]), and vWF (−13.1% [95% CI, −18.6 to −7.5]). Moreover, the percentages of above-detection values out of all observations were significantly lower for plasma CRP and EBC 8-isoprostane in the during-Olympics period compared with the pre-Olympics period. In the post-Olympics period, the levels of the following biomarkers reversed (increased, either with or without statistical significance) from those in the during-Olympics period: SBP (10.7% [95% CI, 2.8 to 18.6]), fibrinogen (4.3% [95% CI, −1.7 to 10.2), neutrophil count (4.7% [95% CI, −7.7 to 17.0]), 8-OHdG (315% [95% CI, 62.0 to 962]), FeNO (130% [95% CI, 62.5 to 225]), EBC nitrite (159% [95% CI, 71.8 to 292]), EBC nitrate (161% [95% CI, 48.0 to 362]), EBC nitrite+nitrate (124% [95% CI, 50.9 to 233]), EBC hydrogen ions (146% [calculated from EBC pH] or −4.8% in EBC pH [95% CI, −9.4 to −0.2]), sCD62P (33.7% [95% CI, 17.7 to 51.8]), and sCD40L (9.1% [95% CI, −3.7 to 23.5]).
Furthermore, these biomarkers also showed statistically significant associations with multiple pollutants across different lags after adjusting for meteorologic parameters. The associations were in the directions hypothesized and were consistent with the findings from the comparisons between periods, providing further evidence that the period effects were due to changes in air quality, independent of season and meteorologic conditions or other potential confounders. Contrary to our hypothesis, however, we observed increases in platelet aggregation, red blood cells (RBCs) and white blood cells (WBCs) associated with the during-Olympics period, as well as significant negative associations of these biomarkers with pollutant concentrations. We did not observe significant changes in any of the HRV indices and DBP by period. However, we observed associations between a few HRV indices and pollutant concentrations.
Changes in air pollution levels during the Beijing Olympics were associated with acute changes in biomarkers of pulmonary and systemic inflammation, oxidative stress, and hemostasis and in measures of cardiovascular physiology (HR and SBP) in healthy, young adults. These changes support the prominently hypothesized mechanistic pathways underlying the cardiorespiratory effects of air pollution.
PMCID: PMC4086245  PMID: 23646463
11.  Does respiratory health contribute to the effects of long-term air pollution exposure on cardiovascular mortality? 
Respiratory Research  2007;8(1):20.
Background
There is growing epidemiological evidence that short-term and long-term exposure to high levels of air pollution may increase cardiovascular morbidity and mortality. In addition, epidemiological studies have shown an association between air pollution exposure and respiratory health. To what extent the association between cardiovascular mortality and air pollution is driven by the impact of air pollution on respiratory health is unknown. The aim of this study was to investigate whether respiratory health at baseline contributes to the effects of long-term exposure to high levels of air pollution on cardiovascular mortality in a cohort of elderly women.
Method
We analyzed data from 4750 women, aged 55 at the baseline investigation in the years 1985–1994. 2593 of these women had their lung function tested by spirometry. Respiratory diseases and symptoms were asked by questionnaire. Ambient air pollution exposure was assessed by the concentrations of NO2 and total suspended particles at fixed monitoring sites and by the distance of residency to a major road. A mortality follow-up of these women was conducted between 2001 and 2003. For the statistical analysis, Cox' regression was used.
Results
Women with impaired lung function or pre-existing respiratory diseases had a higher risk of dying from cardiovascular causes. The impact of impaired lung function declined over time. The risk ratio (RR) of women with forced expiratory volume in one second (FEV1) of less than 80% predicted to die from cardiovascular causes was RR = 3.79 (95%CI: 1.64–8.74) at 5 years survival time and RR = 1.35 (95%CI: 0.66–2.77) at 12 years. The association between air pollution levels and cardiovascular death rate was strong and statistically significant. However, this association did only change marginally when including indicators of respiratory health into the regression analysis. Furthermore, no interaction between air pollution and respiratory health on cardiovascular mortality indicating a higher risk of those with impaired respiratory health could be detected.
Conclusion
Respiratory health is a predictor for cardiovascular mortality. In women followed about 15 years after the baseline investigation at age 55 years long-term air pollution exposure and impaired respiratory health were independently associated with increased cardiovascular mortality.
doi:10.1186/1465-9921-8-20
PMCID: PMC1821323  PMID: 17343725
12.  Adverse effects of outdoor pollution in the elderly 
Journal of Thoracic Disease  2015;7(1):34-45.
With fewer newborns and people living longer, older people are making up an increasing fraction of the total population. Epidemiological evidence shows that older-age-related health problems affect a wide and expanding proportion of the world population. One of the major epidemiological trends of this century is the rise of chronic diseases that affect more elderly than younger people. A total of 3.7 million premature deaths worldwide in 2012 are attributable to outdoor air pollution; the susceptibility to adverse effects of air pollution is expected to differ widely between people and within the same person, and also over time. Frailty history, a measure of multi-system decline, modifies cumulative associations between air pollution and lung function. Moreover, pre-existing diseases may determine susceptibility. In the elderly, due to comorbidity, exposure to air pollutants may even be fatal. Rapid and not-well-planned urbanization is associated with high level of ambient air pollution, mainly caused by vehicular exhausts. In general, there is sufficient evidence of the adverse effects related to short-term exposure, while fewer studies have addressed the longer-term health effects. Increased pollution exposures have been associated with increased mortality, hospital admissions/emergency-room visits, mainly due to exacerbations of chronic diseases or to respiratory tract infections (e.g., pneumonia). These effects may also be modulated by ambient temperature and many studies show that the elderly are mostly vulnerable to heat waves. The association between heat and mortality in the elderly is well-documented, while less is known regarding the associations with hospital admissions. Chronic exposure to elevated levels of air pollution has been related to the incidence of chronic obstructive pulmonary disease (COPD), chronic bronchitis (CB), asthma, and emphysema. There is also growing evidence suggesting adverse effects on lung function related to long-term exposure to ambient air pollution. Few studies have assessed long-term mortality in the elderly. It is still unclear what are the pollutants most damaging to the health of the elderly. It seems that elderly subjects are more vulnerable to particulate matter (PM) than to other pollutants, with particular effect on daily cardio-respiratory mortality and acute hospital admissions. Not many studies have targeted elderly people specifically, as well as specific respiratory morbidity. Most data have shown higher risks in the elderly compared to the rest of the population. Future epidemiological cohort studies need to keep investigating the health effects of air pollutants (mainly cardiopulmonary diseases) on the elderly.
doi:10.3978/j.issn.2072-1439.2014.12.10
PMCID: PMC4311079
Outdoor air pollution; elderly people; frailty elderly; respiratory disease; environmental exposure
13.  Long-Term Ozone Exposure and Mortality 
The New England journal of medicine  2009;360(11):1085-1095.
BACKGROUND
Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution–related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.
METHODS
Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are ≤2.5 μm in aerodynamic diameter [PM2.5]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.
RESULTS
In single-pollutant models, increased concentrations of either PM2.5 or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM2.5 was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.
CONCLUSIONS
In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM2.5 was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.
doi:10.1056/NEJMoa0803894
PMCID: PMC4105969  PMID: 19279340
14.  Long-Term Effects of Traffic-Related Air Pollution on Mortality in a Dutch Cohort (NLCS-AIR Study) 
Environmental Health Perspectives  2007;116(2):196-202.
Background
Several studies have found an effect on mortality of between-city contrasts in long-term exposure to air pollution. The effect of within-city contrasts is still poorly understood.
Objectives
We studied the association between long-term exposure to traffic-related air pollution and mortality in a Dutch cohort.
Methods
We used data from an ongoing cohort study on diet and cancer with 120,852 subjects who were followed from 1987 to 1996. Exposure to black smoke (BS), nitrogen dioxide, sulfur dioxide, and particulate matter ≤mu;M2.5), as well as various exposure variables related to traffic, were estimated at the home address. We conducted Cox analyses in the full cohort adjusting for age, sex, smoking, and area-level socioeconomic status.
Results
Traffic intensity on the nearest road was independently associated with mortality. Relative risks (95% confidence intervals) for a 10-μg/m3 increase in BS concentrations (difference between 5th and 95th percentile) were 1.05 (1.00–1.11) for natural cause, 1.04 (0.95–1.13) for cardiovascular, 1.22 (0.99–1.50) for respiratory, 1.03 (0.88–1.20) for lung cancer, and 1.04 (0.97–1.12) for mortality other than cardiovascular, respiratory, or lung cancer. Results were similar for NO2 and PM2.5, but no associations were found for SO2.
Conclusions
Traffic-related air pollution and several traffic exposure variables were associated with mortality in the full cohort. Relative risks were generally small. Associations between natural-cause and respiratory mortality were statistically significant for NO2 and BS. These results add to the evidence that long-term exposure to ambient air pollution is associated with increased mortality.
doi:10.1289/ehp.10767
PMCID: PMC2235230  PMID: 18288318
air pollution; cohort; mortality; traffic
15.  Impact of Covariate Models on the Assessment of the Air Pollution-Mortality Association in a Single- and Multipollutant Context 
American Journal of Epidemiology  2012;176(7):622-634.
With the advent of multicity studies, uniform statistical approaches have been developed to examine air pollution-mortality associations across cities. To assess the sensitivity of the air pollution-mortality association to different model specifications in a single and multipollutant context, the authors applied various regression models developed in previous multicity time-series studies of air pollution and mortality to data from Philadelphia, Pennsylvania (May 1992–September 1995). Single-pollutant analyses used daily cardiovascular mortality, fine particulate matter (particles with an aerodynamic diameter ≤2.5 µm; PM2.5), speciated PM2.5, and gaseous pollutant data, while multipollutant analyses used source factors identified through principal component analysis. In single-pollutant analyses, risk estimates were relatively consistent across models for most PM2.5 components and gaseous pollutants. However, risk estimates were inconsistent for ozone in all-year and warm-season analyses. Principal component analysis yielded factors with species associated with traffic, crustal material, residual oil, and coal. Risk estimates for these factors exhibited less sensitivity to alternative regression models compared with single-pollutant models. Factors associated with traffic and crustal material showed consistently positive associations in the warm season, while the coal combustion factor showed consistently positive associations in the cold season. Overall, mortality risk estimates examined using a source-oriented approach yielded more stable and precise risk estimates, compared with single-pollutant analyses.
doi:10.1093/aje/kws135
PMCID: PMC3658102  PMID: 22984096
air pollution; dimension reduction; mortality; multipollutant; time series
16.  The association between air pollution and mortality in Thailand 
Scientific Reports  2014;4:5509.
Bayesian statistical inference with a case-crossover design was used to examine the effects of air pollutants {Particulate matter <10 μm in aerodynamic diameter (PM10), sulphur dioxide (SO2), and ozone (O3)} on mortality. We found that all air pollutants had significant short-term impacts on non-accidental mortality. An increase of 10 μg/m3 in PM10, 10 ppb in O3, 1 ppb in SO2 were associated with a 0.40% (95% posterior interval (PI): 0.22, 0.59%), 0.78% (95% PI: 0.20, 1.35%) and 0.34% (95% PI: 0.17, 0.50%) increase of non-accidental mortality, respectively. O3 air pollution is significantly associated with cardiovascular mortality, while PM10 is significantly related to respiratory mortality. In general, the effects of all pollutants on all mortality types were higher in summer and winter than those in the rainy season. This study highlights the effects of exposure to air pollution on mortality risks in Thailand. Our findings support the Thailand government in aiming to reduce high levels of air pollution.
doi:10.1038/srep05509
PMCID: PMC4076679  PMID: 24981315
17.  Air Pollution and Newly Diagnostic Autism Spectrum Disorders: A Population-Based Cohort Study in Taiwan 
PLoS ONE  2013;8(9):e75510.
There is limited evidence that long-term exposure to ambient air pollution increases the risk of childhood autism spectrum disorder (ASD). The objective of the study was to investigate the associations between long-term exposure to air pollution and newly diagnostic ASD in Taiwan. We conducted a population-based cohort of 49,073 children age less than 3 years in 2000 that were retrieved from Taiwan National Insurance Research Database and followed up from 2000 through 2010. Inverse distance weighting method was used to form exposure parameter for ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particles with aerodynamic diameter less than 10 µm (PM10). Time-dependent Cox proportional hazards (PH) model was performed to evaluate the relationship between yearly average exposure air pollutants of preceding years and newly diagnostic ASD. The risk of newly diagnostic ASD increased according to increasing O3, CO, NO2, and SO2 levels. The effect estimate indicating an approximately 59% risk increase per 10 ppb increase in O3 level (95% CI 1.42–1.79), 37% risk increase per 10 ppb in CO (95% CI 1.31–1.44), 340% risk increase per 10 ppb increase in NO2 level (95% CI 3.31–5.85), and 17% risk increase per 1 ppb in SO2 level (95% CI 1.09–1.27) was stable with different combinations of air pollutants in the multi-pollutant models. Our results provide evident that children exposure to O3, CO, NO2, and SO2 in the preceding 1 year to 4 years may increase the risk of ASD diagnosis.
doi:10.1371/journal.pone.0075510
PMCID: PMC3783370  PMID: 24086549
18.  Comparing exposure assessment methods for traffic-related air pollution in an adverse pregnancy outcome study 
Environmental research  2011;111(5):685-692.
Background
Previous studies reported adverse impacts of traffic-related air pollution exposure on pregnancy outcomes. Yet, little information exists on how effect estimates are impacted by the different exposure assessment methods employed in these studies.
Objectives
To compare effect estimates for traffic-related air pollution exposure and preeclampsia, preterm birth (gestational age less than 37 weeks), and very preterm birth (gestational age less than 30 weeks) based on four commonly-used exposure assessment methods.
Methods
We identified 81,186 singleton births during 1997–2006 at four hospitals in Los Angeles and Orange Counties, California. Exposures were assigned to individual subjects based on residential address at delivery using the nearest ambient monitoring station data [carbon monoxide (CO), nitrogen dioxide (NO2), nitric oxide (NO), nitrogen oxides (NOx), ozone (O3), and particulate matter less than 2.5 (PM2.5) or less than 10 (PM10) μm in aerodynamic diameter], both unadjusted and temporally-adjusted land-use regression (LUR) model estimates (NO, NO2, and NOx), CALINE4 line-source air dispersion model estimates (NOx and PM2.5), and a simple traffic-density measure. We employed unconditional logistic regression to analyze preeclampsia in our birth cohort, while for gestational age-matched risk sets with preterm and very preterm birth we employed conditional logistic regression.
Results
We observed elevated risks for preeclampsia, preterm birth, and very preterm birth from maternal exposures to traffic air pollutants measured at ambient stations (CO, NO, NO2, and NOx) and modeled through CALINE4 (NOx and PM2.5) and LUR (NO2 and NOx). Increased risk of preterm birth and very preterm birth were also positively associated with PM10 and PM2.5 air pollution measured at ambient stations. For LUR-modeled NO2 and NOx exposures, elevated risks for all the outcomes were observed in Los Angeles only – the region for which the LUR models were initially developed. Unadjusted LUR models often produced odds ratios somewhat larger in size than temporally-adjusted models. The size of effect estimates was smaller for exposures based on simpler traffic density measures than the other exposure assessment methods.
Conclusion
We generally confirmed that traffic-related air pollution was associated with adverse reproductive outcomes regardless of the exposure assessment method employed, yet the size of the estimated effect depended on how both temporal and spatial variations were incorporated into exposure assessment. The LUR model was not transferable even between two contiguous areas within the same large metropolitan area in Southern California.
doi:10.1016/j.envres.2011.03.008
PMCID: PMC3114297  PMID: 21453913
Air monitoring; CALINE4; land-use regression; preeclampsia; preterm birth
19.  Air Pollution and Incidence of Hypertension and Diabetes in African American Women Living in Los Angeles 
Circulation  2012;125(6):767-772.
Background
Evidence suggests that longer-term exposure to air pollutants over years confers higher risks of cardiovascular morbidity and mortality than shorter term exposure. One explanation is that cumulative adverse effects that develop over longer durations lead to the genesis of chronic disease. Preliminary epidemiological and clinical evidence suggest that air pollution may contribute to the development hypertension and type 2 diabetes.
Methods and Results
We used Cox proportional hazards models to assess incidence rate ratios (IRRs) and 95% confidence intervals (CI) for incident hypertension and diabetes associated with exposure to fine particulate matter (PM2.5) and nitrogen oxides (NOx) in a cohort of African American women living in Los Angeles. Pollutant levels were estimated at participant residential addresses with land use regression models (NOx) and interpolation from monitoring station measurements (PM2.5). Over follow-up from 1995-2005, 531 incident cases of hypertension and 183 incident cases of diabetes occurred. When pollutants were analyzed separately, the IRR for hypertension for a 10 μg/m3 increase in PM2.5 was 1.48 (95% CI 0.95-2.31) and the IRR for the interquartile range (12.4 parts per billion) of NOx was 1.14 (95% CI 1.03-1.25). The corresponding IRRs for diabetes were 1.63 (95% CI 0.78-3.44) and 1.25 (95% CI 1.07-1.46). When both pollutants were included in the same model, the IRRs for PM2.5 were attenuated and the IRRs for NOx were essentially unchanged for both outcomes.
Conclusions
Our results suggest that exposure to air pollutants, especially traffic-related pollutants, may increase the risk of type 2 diabetes and possibly of hypertension.
doi:10.1161/CIRCULATIONAHA.111.052753
PMCID: PMC3326581  PMID: 22219348
air pollution; epidemiology; diabetes mellitus; hypertension
20.  Insights into the Mechanisms and Mediators of the Effects of Air Pollution Exposure on Blood Pressure and Vascular Function in Healthy Humans 
Hypertension  2009;54(3):659-667.
Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, cross-over studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 μg/m3) + ozone (120 ppb) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan 250 mg), anti-oxidant (Vitamin C 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles + ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0 and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor-alpha. In Ann Arbor, diastolic blood pressure significantly similarly increased during all exposures (2.5 - 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.
doi:10.1161/HYPERTENSIONAHA.109.130237
PMCID: PMC3706996  PMID: 19620518
hypertension; endothelium; sympathetic nervous system; inflammation; oxidative stress
21.  Lung Function and Incidence of Chronic Obstructive Pulmonary Disease after Improved Cooking Fuels and Kitchen Ventilation: A 9-Year Prospective Cohort Study 
PLoS Medicine  2014;11(3):e1001621.
Pixin Ran, Nanshan Zhong, and colleagues report that cleaner cooking fuels and improved ventilation were associated with better lung function and reduced COPD among a cohort of villagers in Southern China.
Please see later in the article for the Editors' Summary
Background
Biomass smoke is associated with the risk of chronic obstructive pulmonary disease (COPD), but few studies have elaborated approaches to reduce the risk of COPD from biomass burning. The purpose of this study was to determine whether improved cooking fuels and ventilation have effects on pulmonary function and the incidence of COPD.
Methods and Findings
A 9-y prospective cohort study was conducted among 996 eligible participants aged at least 40 y from November 1, 2002, through November 30, 2011, in 12 villages in southern China. Interventions were implemented starting in 2002 to improve kitchen ventilation (by providing support and instruction for improving biomass stoves or installing exhaust fans) and to promote the use of clean fuels (i.e., biogas) instead of biomass for cooking (by providing support and instruction for installing household biogas digesters); questionnaire interviews and spirometry tests were performed in 2005, 2008, and 2011. That the interventions improved air quality was confirmed via measurements of indoor air pollutants (i.e., SO2, CO, CO2, NO2, and particulate matter with an aerodynamic diameter of 10 µm or less) in a randomly selected subset of the participants' homes. Annual declines in lung function and COPD incidence were compared between those who took up one, both, or neither of the interventions.
Use of clean fuels and improved ventilation were associated with a reduced decline in forced expiratory volume in 1 s (FEV1): decline in FEV1 was reduced by 12 ml/y (95% CI, 4 to 20 ml/y) and 13 ml/y (95% CI, 4 to 23 ml/y) in those who used clean fuels and improved ventilation, respectively, compared to those who took up neither intervention, after adjustment for confounders. The combined improvements of use of clean fuels and improved ventilation had the greatest favorable effects on the decline in FEV1, with a slowing of 16 ml/y (95% CI, 9 to 23 ml/y). The longer the duration of improved fuel use and ventilation, the greater the benefits in slowing the decline of FEV1 (p<0.05). The reduction in the risk of COPD was unequivocal after the fuel and ventilation improvements, with an odds ratio of 0.28 (95% CI, 0.11 to 0.73) for both improvements.
Conclusions
Replacing biomass with biogas for cooking and improving kitchen ventilation are associated with a reduced decline in FEV1 and risk of COPD.
Trial Registration
Chinese Clinical Trial Register ChiCTR-OCH-12002398
Please see later in the article for the Editors' Summary
Editors' Summary
Background
Nearly 3 billion people in developing countries heat their homes and cook by burning biomass—wood, crop waste, and animal dung—in open fires and leaky stoves. Burning biomass this way releases pollutants into the home that impair lung function and that are responsible for more than a million deaths from chronic obstructive pulmonary disease (COPD) every year. COPD is a group of diseases that interfere with breathing. Normally, air is breathed in through the nose or mouth and travels down the windpipe into two bronchial tubes (airways) in the lungs. These tubes branch into smaller tubes (bronchioles) that end in bunches of tiny air sacs (alveoli). Oxygen in the air passes through the thin walls of these sacs into small blood vessels and is taken to the heart for circulation round the body. The two main types of COPD—chronic bronchitis (long-term irritation and swelling of the bronchial tubes) and emphysema (damage to the walls of the alveoli)—make it hard for people to breathe. Most people with COPD have both chronic bronchitis and emphysema, both of which are caused by long-term exposure to cigarette smoke, indoor air pollution, and other lung irritants. Symptoms of COPD include breathlessness during exercise and a persistent cough that produces large amounts of phlegm (mucus). There is no cure for COPD, but drugs and oxygen therapy can relieve its symptoms, and avoiding lung irritants can slow disease progression.
Why Was This Study Done?
Exposure to indoor air pollution has been associated with impaired lung function and COPD in several studies. However, few studies have assessed the long-term effects on lung function and on the incidence of COPD (the proportion of a population that develops COPD each year) of replacing biomass with biogas (a clean fuel produced by bacterial digestion of biodegradable materials) for cooking and heating, or of improving kitchen ventilation during cooking. Here, the researchers undertook a nine-year prospective cohort study in rural southern China to investigate whether these interventions are associated with any effects on lung function and on the incidence of COPD. A prospective cohort study enrolls a group of people, determines their characteristics at baseline, and follows them over time to see whether specific characteristic are associated with specific outcomes.
What Did the Researchers Do and Find?
The researchers offered nearly 1,000 people living in 12 villages in southern China access to biogas and to improved kitchen ventilation. All the participants, who adopted these interventions according to personal preferences, completed a questionnaire about their smoking habits and occupational exposure to pollutants and had their lung function measured using a spirometry test at the start and end of the study. Some participants also completed a questionnaire and had their lung function measured three and six years into the study. Finally, the researchers measured levels of indoor air pollution in a randomly selected subset of homes at the end of the study to confirm that the interventions had reduced indoor air pollution. Compared with non-use, the use of clean fuels and of improved ventilation were both associated with a reduction in the decline in lung function over time after adjusting for known characteristics that affect lung function, such as smoking. The use of both interventions reduced the decline in lung function more markedly than either intervention alone, and the benefits of using the interventions increased with length of use. Notably, the combined use of both interventions reduced the risk of COPD occurrence among the study participants.
What Do These Findings Mean?
These findings suggest that, among people living in rural southern China, the combined interventions of use of biogas instead of biomass and improved kitchen ventilation were associated with a reduced decline in lung function over time and with a reduced risk of COPD. Because participants were not randomly allocated to intervention groups, the people who adopted the interventions may have shared other unknown characteristics (confounders) that affected their lung function (for example, having a healthier lifestyle). Thus, it is not possible to conclude that either intervention actually caused a reduction in the decline in lung function. Nevertheless, these findings suggest that the use of biogas as a substitute for biomass for cooking and heating and improvements in kitchen ventilation might lead to a reduction in the global burden of COPD associated with biomass smoke.
Additional Information
Please access these websites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.1001621.
The US National Heart, Lung, and Blood Institute provides detailed information for the public about COPD
The US Centers for Disease Control and Prevention provides information about COPD and links to other resources (in English and Spanish)
The UK National Health Service Choices website provides information for patients and carers about COPD, personal stories, and links to other resources
The British Lung Foundation, a not-for-profit organization, provides information about COPD in several languages
The Global Initiative for Chronic Obstructive Lung Disease works to improve prevention and treatment of COPD around the world
The World Health Organization provides information about all aspects of indoor air pollution and health (in English, French, and Spanish)
MedlinePlus provides links to other information about COPD (in English and Spanish)
doi:10.1371/journal.pmed.1001621
PMCID: PMC3965383  PMID: 24667834
22.  Acute Effects of Ambient Particulate Matter on Mortality in Europe and North America: Results from the APHENA Study 
Environmental Health Perspectives  2008;116(11):1480-1486.
Background
The APHENA (Air Pollution and Health: A Combined European and North American Approach) study is a collaborative analysis of multicity time-series data on the effect of air pollution on population health, bringing together data from the European APHEA (Air Pollution and Health: A European Approach) and U.S. NMMAPS (National Morbidity, Mortality and Air Pollution Study) projects, along with Canadian data.
Objectives
The main objective of APHENA was to assess the coherence of the findings of the multicity studies carried out in Europe and North America, when analyzed with a common protocol, and to explore sources of possible heterogeneity. We present APHENA results on the effects of particulate matter (PM) ≤ 10 μm in aerodynamic diameter (PM10) on the daily number of deaths for all ages and for those < 75 and ≥ 75 years of age. We explored the impact of potential environmental and socioeconomic factors that may modify this association.
Methods
In the first stage of a two-stage analysis, we used Poisson regression models, with natural and penalized splines, to adjust for seasonality, with various degrees of freedom. In the second stage, we used meta-regression approaches to combine time-series results across cites and to assess effect modification by selected ecologic covariates.
Results
Air pollution risk estimates were relatively robust to different modeling approaches. Risk estimates from Europe and United States were similar, but those from Canada were substantially higher. The combined effect of PM10 on all-cause mortality across all ages for cities with daily air pollution data ranged from 0.2% to 0.6% for a 10-μg/m3 increase in ambient PM10 concentration. Effect modification by other pollutants and climatic variables differed in Europe and the United States. In both of these regions, a higher proportion of older people and higher unemployment were associated with increased air pollution risk.
Conclusions
Estimates of the increased mortality associated with PM air pollution based on the APHENA study were generally comparable with results of previous reports. Overall, risk estimates were similar in Europe and in the United States but higher in Canada. However, PM10 effect modification patterns were somewhat different in Europe and the United States.
doi:10.1289/ehp.11345
PMCID: PMC2592267  PMID: 19057700
air pollution; effect modification; heterogeneity; meta-regression; mortality; natural splines; particulate matter; penalized splines; time-series analysis
23.  Health Impacts of the Built Environment: Within-Urban Variability in Physical Inactivity, Air Pollution, and Ischemic Heart Disease Mortality 
Environmental Health Perspectives  2011;120(2):247-253.
Background: Physical inactivity and exposure to air pollution are important risk factors for death and disease globally. The built environment may influence exposures to these risk factors in different ways and thus differentially affect the health of urban populations.
Objective: We investigated the built environment’s association with air pollution and physical inactivity, and estimated attributable health risks.
Methods: We used a regional travel survey to estimate within-urban variability in physical inactivity and home-based air pollution exposure [particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5), nitrogen oxides (NOx), and ozone (O3)] for 30,007 individuals in southern California. We then estimated the resulting risk for ischemic heart disease (IHD) using literature-derived dose–response values. Using a cross-sectional approach, we compared estimated IHD mortality risks among neighborhoods based on “walkability” scores.
Results: The proportion of physically active individuals was higher in high- versus low-walkability neighborhoods (24.9% vs. 12.5%); however, only a small proportion of the population was physically active, and between-neighborhood variability in estimated IHD mortality attributable to physical inactivity was modest (7 fewer IHD deaths/100,000/year in high- vs. low-walkability neighborhoods). Between-neighborhood differences in estimated IHD mortality from air pollution were comparable in magnitude (9 more IHD deaths/100,000/year for PM2.5 and 3 fewer IHD deaths for O3 in high- vs. low-walkability neighborhoods), suggesting that population health benefits from increased physical activity in high-walkability neighborhoods may be offset by adverse effects of air pollution exposure.
Policy implications: Currently, planning efforts mainly focus on increasing physical activity through neighborhood design. Our results suggest that differences in population health impacts among neighborhoods are similar in magnitude for air pollution and physical activity. Thus, physical activity and exposure to air pollution are critical aspects of planning for cleaner, health-promoting cities.
doi:10.1289/ehp.1103806
PMCID: PMC3279444  PMID: 22004949
active travel; air quality; environmental planning; infill; risk assessment; urban form
24.  Traffic-Related Air Pollution and Asthma Onset in Children: A Prospective Cohort Study with Individual Exposure Measurement 
Environmental Health Perspectives  2008;116(10):1433-1438.
Background
The question of whether air pollution contributes to asthma onset remains unresolved.
Objectives
In this study, we assessed the association between asthma onset in children and traffic-related air pollution.
Methods
We selected a sample of 217 children from participants in the Southern California Children’s Health Study, a prospective cohort designed to investigate associations between air pollution and respiratory health in children 10–18 years of age. Individual covariates and new asthma incidence (30 cases) were reported annually through questionnaires during 8 years of follow-up. Children had nitrogen dioxide monitors placed outside their home for 2 weeks in the summer and 2 weeks in the fall–winter season as a marker of traffic-related air pollution. We used multilevel Cox models to test the associations between asthma and air pollution.
Results
In models controlling for confounders, incident asthma was positively associated with traffic pollution, with a hazard ratio (HR) of 1.29 [95% confidence interval (CI), 1.07–1.56] across the average within-community interquartile range of 6.2 ppb in annual residential NO2. Using the total interquartile range for all measurements of 28.9 ppb increased the HR to 3.25 (95% CI, 1.35–7.85).
Conclusions
In this cohort, markers of traffic-related air pollution were associated with the onset of asthma. The risks observed suggest that air pollution exposure contributes to new-onset asthma.
doi:10.1289/ehp.10968
PMCID: PMC2569108  PMID: 18941591
air pollution; asthma onset; children; nitrogen dioxide
25.  Modification by antioxidant supplementation of changes in human lung function associated with air pollutant exposure: A systematic review 
BMC Public Health  2011;11:532.
Background
Outdoor air pollution, given its demonstrated negative effects on the respiratory system, is a growing public health concern worldwide, particularly in urban cities. Human exposure to pollutants such as ozone, nitrogen oxides, combustion-related particulate matter and oxides of sulfur is responsible for significant cardiopulmonary morbidity and mortality in both adults and children. Several antioxidants have shown an ability to partially attenuate the negative physiological and functional impacts of air pollutants. This study systematically presents current data on the potential benefits of antioxidant supplementation on lung function outcomes associated with air pollutant exposures in intact humans.
Methods
Electronic databases (MEDLINE, EMBASE, BIOSIS Previews, Web of Sciences, Environmental Sciences & Pollution Management and TOXNET) were systematically searched for all studies published up to April 2009. Search terms relating to the concepts of respiratory tract diseases, respiratory function tests, air pollution, and antioxidants were used. Data was systematically abstracted from original articles that satisfied selection criteria for inclusion. For inclusion, the studies needed to have evaluated human subjects, given supplemental antioxidants, under conditions of known levels of air pollutants with measured lung function before and after antioxidant administration and/or air pollution exposure. Selected studies were summarized and conclusions presented.
Results
Eight studies investigated the role of antioxidant supplementation on measured lung function outcomes after subject exposure to air pollutants under controlled conditions; 5 of these studies concluded that pollutant-induced airway hyper-responsiveness and diminution in lung function measurements were attenuated by antioxidant supplementation. The remaining five studies took place under ambient (uncontrolled) exposures and unanimously concluded that antioxidant supplementations attenuate the negative effects of urban air pollution on lung function.
Conclusions
The data evaluating modification of changes in lung function associated with air pollutant exposure by antioxidant supplementation, in intact humans, is limited. Of 13 studies dedicated to this concern, ten demonstrated an attenuation of pollution-associated decrements. There is growing evidence for the benefit of anti-oxidant supplementation in moderating the effects of air pollution on lung function, but more research on human participants is needed to inform this topic.
doi:10.1186/1471-2458-11-532
PMCID: PMC3158771  PMID: 21729301

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