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1.  Oral Cleft Defects and Maternal Exposure to Ambient Air Pollutants in New Jersey 
Evidence links exposure to ambient air pollution during pregnancy, particularly gaseous pollutants and particulate matter, to an increased risk of adverse reproductive outcomes but the results for birth defects have been inconsistent.
We compared estimated exposure to ambient air pollutants during early pregnancy among mothers of children with oral cleft defects (cases) to that among mothers of controls, adjusting for available risk factors from birth certificates. We obtained ambient air pollutant data from air monitoring sites in New Jersey for carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), particulate matter less than 10 µm in aerodynamic diameter (PM10) and particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5). We used values from the nearest monitor (within 40 km of the residence at birth) for controls, cleft lip with or without cleft palate (CLP) and cleft palate only (CPO).
Based on logistic regression analyses for each contaminant and all contaminants together, there were no consistent elevated associations between selected air pollutants and cleft malformations. Quartile of CO concentration showed a consistent protective association with CPO (p<.01). For other contaminants, confidence intervals (95%) of the odds ratios for some quartiles excluded one. CLP showed limited evidence of an association with increasing SO2 exposure while CPO showed weak associations with increasing O3 exposure.
There was little consistent evidence associating cleft malformations with maternal exposure to ambient air pollutants. Evaluating particular pollutants or disease subgroups would require more detailed measurement of exposure and classification of cleft defects.
PMCID: PMC2862481  PMID: 20146378
2.  Short-term effect of ozone on the pulmonary function of children in primary school. 
Environmental Health Perspectives  1999;107(11):921-925.
The objective of this study was to evaluate the short-term effect of ambient air pollution on the pulmonary function of schoolchildren. We sampled 941 children in primary school in three communities in Taiwan (Sanchun, Taihsi, and Linyuan). The nearby stations of the Taiwan air quality monitoring network provided the hourly ambient concentrations of sulfur dioxide, carbon monoxide, ozone, particulate matter < or = to 10 microm in aerodynamic diameter, and nitrogen dioxide. Spirometry was performed once for each sampled child. We also obtained the status of indoor air pollution and chronic respiratory disease history by using a structured questionnaire. Multivariate linear model analysis was used to evaluate pulmonary function effects of each pollutant in addition to determinants of indoor air pollution and meteorologic conditions. We found a significantly negative association of peak O(3) concentration on the day before spirometry with individual forced vital capacity and forced expiratory volume in 1 sec. The decrease in children's lung function can occur at peak hourly O(3) concentrations < 80 ppb. The slope of lung function decrease for Taiwanese children is approximately 1 mL/ppb for peak hourly O(3) exposure.
PMCID: PMC1566719  PMID: 10544161
3.  Airborne pollutants and lacunar stroke: a case cross-over analysis on stroke unit admissions 
Neurology International  2012;4(2):e11.
Particulate air pollution is known to be associated with cardiovascular disease. The relation of particulate air pollution with cerebrovascular disease (CVD) has not been extensively studied, particularly in relation to different subtypes of stroke. A time-series study was conducted to evaluate the association between daily air pollution and acute stroke unit hospitalizations in Mantua, Italy. We analyzed 781 CVD consecutive patients living in Mantua county admitted between 2006–08. Data on stroke types, demographic variables, risk factors were available from the Lombardia Stroke Registry. Daily mean value of particulate matter with a diameter <10 µm (PM10), carbon monoxide, nitric oxide, nitrogen dioxide, sulphur dioxide, benzene and ozone were used in the analysis. The association between CVD, ischemic strokes subtypes and pollutants was investigated with a case-crossover design, using conditional logistic regression analysis, adjusting for temperature, humidity, barometric pressure and holidays. Among the 781 subjects admitted 75.7% had ischemic stroke, 11.7% haemorrhagic stroke 12.6% transient ischemic attack. In men admission for stroke was associated with PM10 [odds ratio (OR) 1.01, 95%; confidence interval (CI) 1.00–1.02; P<0.05]. According to the clinical classification, lacunar anterior circulation syndrome stroke type was related to PM10 level registered on the day of admission for both genders (OR: 1.01, 95%; CI: 1.00–1.02; P<0.05) while for total anterior circulation syndrome stroke only in men (OR: 1.04, 95%; CI 1.01–1.07; P<0.05).
In conclusion, our study confirms that air pollution peaks may contribute to increase the risk of hospitalization for stroke and particulate matter seems to be a significant risk factor, especially for lacunar stroke.
PMCID: PMC3490470  PMID: 23139849
lacunar stroke; air pollution; stroke registry.
4.  Temperature, air pollution, and hospitalization for cardiovascular diseases among elderly people in Denver. 
Environmental Health Perspectives  2003;111(10):1312-1317.
Daily measures of maximum temperature, particulate matter less than or equal to 10 micro m in aerodynamic diameter (PM10), and gaseous pollution (ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide) were collected in Denver, Colorado, in July and August between 1993 and 1997. We then compared these exposures with concurrent data on the number of daily hospital admissions for cardiovascular diseases in men and women > 65 years of age. Generalized linear models, assuming a Poisson error structure for the selected cardiovascular disease hospital admissions, were constructed to evaluate the associations with air pollution and temperature. After adjusting the admission data for yearly trends, day-of-week effects, ambient maximum temperature, and dew point temperature, we studied the associations of the pollutants in single-pollutant models with lag times of 0-4 days. The results suggest that O3 is associated with an increase in the risk of hospitalization for acute myocardial infarction, coronary atherosclerosis, and pulmonary heart disease. SO2 appears to be related to increased hospital stays for cardiac dysrhythmias, and CO is significantly associated with congestive heart failure. No association was found between particulate matter or NO2 and any of the health outcomes. Males tend to have higher numbers of hospital admissions than do females for all of the selected cardiovascular diseases, except for congestive heart failure. Higher temperatures appear to be an important factor in increasing the frequency of hospitalization for acute myocardial infarction and congestive heart failure, and are associated with a decrease in the frequency of visits for coronary atherosclerosis and pulmonary heart disease.
PMCID: PMC1241612  PMID: 12896852
5.  Air pollution and daily mortality in Inchon, Korea. 
Journal of Korean Medical Science  1999;14(3):239-244.
The association between total daily mortality and air pollution was investigated for a 1-year period (January 1995 to December 1995) in Inchon, Korea. The purpose of this study was to evaluate the relative importance of particulate and gaseous air pollution as predictors of daily mortality. Concentration of total suspended particulates (TSP), inhalable particles (PM10), and gaseous pollutants, such as sulfur dioxide, nitrogen dioxide, ozone, carbon monoxide, were measured daily during the study period. A generalized additive model was used to regress daily death counts on each air pollutant, controlling for time trend and meteorologic influences such as temperature or relative humidity. Total mortality was found to increase 1.2% (95% CI: 0.2 to 2.2%) for each 10 microg/m3 increase in 6-day moving average of TSP, and 1.2% (95% CI 0.2 to 2.1%) for each 10 microg/m3 increase in 5-day moving average of PM10. The association is similar in magnitude to associations between particulate air pollution and mortality found in several other communities in America and Europe. Associations with gaseous pollutants were all statistically insignificant in the generalized additive model. The relative risk of death increased at particulate levels that were well below the current Korean Ambient Air Quality Standard.
PMCID: PMC3054386  PMID: 10402164
6.  Asthma symptoms in Hispanic children and daily ambient exposures to toxic and criteria air pollutants. 
Environmental Health Perspectives  2003;111(4):647-656.
PMCID: PMC1241459  PMID: 12676630
7.  Ambient air pollution and term birth weight in Texas from 1998 to 2004 
Previous studies have explored the association between air pollution levels and adverse birth outcomes such as lower birth weight. Existing literature suggests an association, although results across studies are not consistent. Additional research is needed to confirm the effect, investigate the exposure window of importance, and distinguish which pollutants cause harm.
We assessed the association between ambient pollutant concentrations and term birth weight for 1,548,904 births in TX from 1998 to 2004. Assignment of prenatal exposure to air pollutants was based on maternal county of residence at the time of delivery. Pollutants examined included particulate matter with aerodynamic diameter ≤10 and ≤2.5 μm (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3). We applied a linear model with birth weight as a continuous variable. The model was adjusted for known risk factors and region. We assessed pollutant effects by trimester to identify biological exposure window of concern, and explored interaction due to race/ethnicity.
An interquartile increase in ambient pollutant concentrations of SO2 and O3 was associated with a 4.99-g (95% confidence interval [CI], 1.87–8.11) and 2.72-g (95% CI, 1.11–4.33) decrease in birth weight, respectively. Lower birth weight was associated with exposure to O3 in the first and second trimester, whereas results were not significant for other pollutants by trimester. A positive association was exhibited for PM2.5 in the first trimester. Effects estimates for PM10 and PM2.5 were inconsistent across race/ethnic groups.
Current ambient air pollution levels may be increasing the risk of lower birth weight for some pollutants. These risks may be increased for certain racial/ethnic groups. Additional research including consideration of improved methodology is needed to investigate these findings. Future studies should examine the influence of residual confounding.
PMCID: PMC3536032  PMID: 23210220
8.  Use of an index to reflect the aggregate burden of long-term exposure to criteria air pollutants in the United States. 
Environmental Health Perspectives  2002;110(Suppl 1):95-102.
Air pollution control in the United States for five common pollutants--particulate matter, ground-level ozone, sulfur dioxide, nitrogen dioxide, and carbon monoxide--is based partly on the attainment of ambient air quality standards that represent a level of air pollution regarded as safe. Regulatory and health agencies often focus on whether standards for short periods are attained; the number of days that standards are exceeded is used to track progress. Efforts to explain air pollution to the public often incorporate an air quality index that represents daily concentrations of pollutants. While effects of short-term exposures have been emphasized, research shows that long-term exposures to lower concentrations of air pollutants can also result in adverse health effects. We developed an aggregate index that represents long-term exposure to these pollutants, using 1995 monitoring data for metropolitan areas obtained from the U.S. Environmental Protection Agency's Aerometric Information Retrieval System. We compared the ranking of metropolitan areas under the proposed aggregate index with the ranking of areas by the number of days that short-term standards were exceeded. The geographic areas with the highest burden of long-term exposures are not, in all cases, the same as those with the most days that exceeded a short-term standard. We believe that an aggregate index of long-term air pollution offers an informative addition to the principal approaches currently used to describe air pollution exposures; further work on an aggregate index representing long-term exposure to air pollutants is warranted.
PMCID: PMC1241151  PMID: 11834467
9.  Effects of Air Pollution on Heart Rate Variability: The VA Normative Aging Study 
Environmental Health Perspectives  2004;113(3):304-309.
Reduced heart rate variability (HRV), a marker of poor cardiac autonomic function, has been associated with air pollution, especially fine particulate matter [< 2.5 μm in aerodynamic diameter (PM2.5)]. We examined the relationship between HRV [standard deviation of normal-to-normal intervals (SDNN), power in high frequency (HF) and low frequency (LF), and LF:HF ratio] and ambient air pollutants in 497 men from the Normative Aging Study in greater Boston, Massachusetts, seen between November 2000 and October 2003. We examined 4-hr, 24-hr, and 48-hr moving averages of air pollution (PM2.5, particle number concentration, black carbon, ozone, nitrogen dioxide, sulfur dioxide, carbon monoxide). Controlling for potential confounders, HF decreased 20.8% [95% confidence interval (CI), 4.6–34.2%] and LF:HF ratio increased 18.6% (95% CI, 4.1–35.2%) per SD (8 μg/m3) increase in 48-hr PM2.5. LF was reduced by 11.5% (95% CI, 0.4–21.3%) per SD (13 ppb) increment in 4-hr O3. The associations between HRV and PM2.5 and O3 were stronger in people with ischemic heart disease (IHD) and hypertension. The associations observed between SDNN and LF and PM2.5 were stronger in people with diabetes. People using calcium-channel blockers and beta-blockers had lower associations between O3 and PM2.5 with LF. No effect modification by other cardiac medications was found. Exposures to PM2.5 and O3 are associated with decreased HRV, and history of IHD, hypertension, and diabetes may confer susceptibility to autonomic dysfunction by air pollution.
PMCID: PMC1253756  PMID: 15743719
air pollution; diabetes; heart rate variability; hypertension; ischemic heart disease; ozone; PM2.5
10.  Baseline Repeated Measures from Controlled Human Exposure Studies: Associations between Ambient Air Pollution Exposure and the Systemic Inflammatory Biomarkers IL-6 and Fibrinogen 
Environmental Health Perspectives  2009;118(1):120-124.
Systemic inflammation may be one of the mechanisms mediating the association between ambient air pollution and cardiovascular morbidity and mortality. Interleukin-6 (IL-6) and fibrinogen are biomarkers of systemic inflammation that are independent risk factors for cardiovascular disease.
We investigated the association between ambient air pollution and systemic inflammation using baseline measurements of IL-6 and fibrinogen from controlled human exposure studies.
In this retrospective analysis we used repeated-measures data in 45 nonsmoking subjects. Hourly and daily moving averages were calculated for ozone, nitrogen dioxide, sulfur dioxide, and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5). Linear mixed-model regression determined the effects of the pollutants on systemic IL-6 and fibrinogen. Effect modification by season was considered.
We observed a positive association between IL-6 and O3 [0.31 SD per O3 interquartile range (IQR); 95% confidence interval (CI), 0.08–0.54] and between IL-6 and SO2 (0.25 SD per SO2 IQR; 95% CI, 0.06–0.43). We observed the strongest effects using 4-day moving averages. Responses to pollutants varied by season and tended to be higher in the summer, particularly for O3 and PM2.5. Fibrinogen was not associated with pollution.
This study demonstrates a significant association between ambient pollutant levels and baseline levels of systemic IL-6. These findings have potential implications for controlled human exposure studies. Future research should consider whether ambient pollution exposure before chamber exposure modifies IL-6 response.
PMCID: PMC2831955  PMID: 20056584
air pollution; epidemiology; fibrinogen; inflammation; interleukin-6
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.
PMCID: PMC1470088  PMID: 9288496
Environmental Health Perspectives  2004;112(5):557-561.
Although particulate air pollution has been associated with increased numbers of daily deaths in dozens of cities around the world, issues still remain about the association. Some have questioned the complex modeling used to control for season in Poisson regression or the role of gaseous air pollutants as potential confounders of the association. I examined the association between deaths and particulate matter with an aerodynamic diameter less than or equal to 10 microm (PM10) using a case-crossover design. In this approach, the pollution on the day of each death is contrasted with the pollution level on control days when the subject did not die. Season and gaseous air pollutants were controlled by matching. Control days were chosen within the same month of the same year to control for season, and matched on either sulfur dioxide (SO2; within 1 ppb), nitrogen dioxide (within 1 ppb), maximum ozone (within 2 ppb), or carbon monoxide (within 0.03 ppm). The analysis was conducted in 14 U.S. cities that have daily PM10 monitoring. After matching, there were about 400,000 deaths in each analysis. Results were combined across cities using a maximum likelihood method. PM10 was a significant predictor of mortality when controlling for gaseous air pollutants, with effect sizes ranging from a 0.45% increase per 10 microg/m3 increment of PM10 [95% confidence interval (CI), 0.12-0.79%] when matched on maximum hourly ozone levels, to a 0.81% increase per 10 microg/m3 increment of PM10 (95% CI, 0.47-1.16%) when matched on 24-hr average SO2.
PMCID: PMC1241921  PMID: 15064161
Environmental Health  2010;9:57.
PMCID: PMC2972268  PMID: 20920362
14.  Ozone and Other Air Pollutants and the Risk of Oral Clefts 
Environmental Health Perspectives  2008;116(10):1411-1415.
Our goal in this study was to assess the relations between exposure to ambient air pollution and the risk of cleft lip with or without cleft palate (CL/P).
We conducted a population-based case–control study of all 653 cases of CL/P and a random sample of 6,530 control subjects from 721,289 Taiwanese newborns in 2001–2003. We used geographic information systems to form exposure parameters for sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with an aerodynamic diameter ≤ 10 μm (PM10) during the first 3 months of pregnancy using inverse distance weighting method. We present the effect estimates as odds ratios (ORs) per 10-ppb change for SO2, NOx, and O3, 100-ppb change for CO, and 10-μg/m3 change for PM10.
The risk of CL/P was increased in relation to O3 levels in the first gestational month [adjusted OR = 1.20; 95% confidence interval (CI), 1.02–1.39] and second gestational month (adjusted OR = 1.25; 95% CI, 1.03–1.52) in the range from 16.7 ppb to 45.1 ppb, but was not related to CO, NOx, SO2, or PM10.
The study provides new evidence that exposure to outdoor air O3 during the first and second month of pregnancy may increase the risk of CL/P. Similar levels of O3 are encountered globally by large numbers of pregnant women.
PMCID: PMC2569104  PMID: 18941587
air pollution; cleft lip; ozone; traffic
15.  Urban air pollution and emergency room admissions for respiratory symptoms: a case-crossover study in Palermo, Italy 
Environmental Health  2011;10:31.
PMCID: PMC3096899  PMID: 21489245
16.  Evaluating the health significance of hazardous air pollutants using monitoring data. 
Public Health Reports  2001;116(1):32-44.
PMCID: PMC1497289  PMID: 11571406
17.  The Association between Fatal Coronary Heart Disease and Ambient Particulate Air Pollution: Are Females at Greater Risk? 
Environmental Health Perspectives  2005;113(12):1723-1729.
The purpose of this study was to assess the effect of long-term ambient particulate matter (PM) on risk of fatal coronary heart disease (CHD). A cohort of 3,239 nonsmoking, non-Hispanic white adults was followed for 22 years. Monthly concentrations of ambient air pollutants were obtained from monitoring stations [PM < 10 μm in aerodynamic diameter (PM10), ozone, sulfur dioxide, nitrogen dioxide] or airport visibility data [PM < 2.5 μm in aerodynamic diameter (PM2.5)] and interpolated to ZIP code centroids of work and residence locations. All participants had completed a detailed lifestyle questionnaire at baseline (1976), and follow-up information on environmental tobacco smoke and other personal sources of air pollution were available from four subsequent questionnaires from 1977 through 2000. Persons with prevalent CHD, stroke, or diabetes at baseline (1976) were excluded, and analyses were controlled for a number of potential confounders, including lifestyle. In females, the relative risk (RR) for fatal CHD with each 10-μg/m3 increase in PM2.5 was 1.42 [95% confidence interval (CI), 1.06–1.90] in the single-pollutant model and 2.00 (95% CI, 1.51–2.64) in the two-pollutant model with O3. Corresponding RRs for a 10-μg/m3 increase in PM10-2.5 and PM10 were 1.62 and 1.45, respectively, in all females and 1.85 and 1.52 in postmenopausal females. No associations were found in males. A positive association with fatal CHD was found with all three PM fractions in females but not in males. The risk estimates were strengthened when adjusting for gaseous pollutants, especially O3, and were highest for PM2.5. These findings could have great implications for policy regulations.
PMCID: PMC1314912  PMID: 16330354
air pollution; coronary disease; ischemic heart disease; long-term exposure; mortality; particulate matter
Lancet  2013;382(9897):1039-1048.
Acute exposure to air pollution has been linked to myocardial infarction, but its effect on heart failure is uncertain. We did a systematic review and meta-analysis to assess the association between air pollution and acute decompensated heart failure including hospitalisation and heart failure mortality.
Five databases were searched for studies investigating the association between daily increases in gaseous (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate (diameter <2·5 μm [PM2·5] or <10 μm [PM10]) air pollutants, and heart failure hospitalisations or heart failure mortality. We used a random-effects model to derive overall risk estimates per pollutant.
Of 1146 identified articles, 195 were reviewed in-depth with 35 satisfying inclusion criteria. Heart failure hospitalisation or death was associated with increases in carbon monoxide (3·52% per 1 part per million; 95% CI 2·52–4·54), sulphur dioxide (2·36% per 10 parts per billion; 1·35–3·38), and nitrogen dioxide (1·70% per 10 parts per billion; 1·25–2·16), but not ozone (0·46% per 10 parts per billion; −0·10 to 1·02) concentrations. Increases in particulate matter concentration were associated with heart failure hospitalisation or death (PM2·5 2·12% per 10 μg/m3, 95% CI 1·42–2·82; PM10 1·63% per 10 μg/m3, 95% CI 1·20–2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM2·5. In the USA, we estimate that a mean reduction in PM2·5 of 3·9 μg/m3 would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year.
Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy.
British Heart Foundation.
PMCID: PMC3809511  PMID: 23849322
19.  Gaseous Air Pollutants and Hospitalization for Respiratory Disease in the Neonatal Period 
Environmental Health Perspectives  2006;114(11):1751-1754.
Current levels of ambient air pollution are associated with morbidity and mortality in the general population. To determine the influence of gaseous air pollutants on neonatal respiratory morbidity, we tested the association between daily respiratory hospitalizations and daily concentrations of ambient air pollution gases: ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide, in 11 large Canadian cities.
Study Design
Daily time-series analyses were employed and results were adjusted for day of the week, temperature, barometric pressure, and relative humidity.
The percent increases in hospitalization associated with an increase in air pollution equivalent to its interquartile range were 3.35 [95% confidence interval (CI), 1.73–4.77] for O3, 2.85 (95% CI, 1.68–4.02) for NO2, 1.66 (95% CI, 0.63–2.69) for SO2, and 1.75 (95% CI, 0.48–3.02) for CO. The independent effect of all pollutants combined was 9.61% (95% CI, 4.52–14.7%).
Our results suggest that neonates are experiencing adverse effects of air pollution at current levels in Canada, and that accounts for a significant proportion of hospitalizations in this subgroup.
PMCID: PMC1665436  PMID: 17107863
carbon monoxide; hospital admission; infants; ozone; sulfur dioxide
20.  Climate, traffic-related air pollutants, and asthma prevalence in middle-school children in taiwan. 
Environmental Health Perspectives  1999;107(12):1001-1006.
PMCID: PMC1566819  PMID: 10585904
21.  Effect of air pollution on daily mortality in Hong Kong. 
Environmental Health Perspectives  2001;109(4):335-340.
In different weather conditions, constituents and concentrations of pollutants, personal exposure, and biologic responses to air pollution may vary. In this study we assessed the effects of four air pollutants on mortality in both cool and warm seasons in Hong Kong, a subtropical city. Daily counts of mortality, due to all nonaccidental causes, and cardiovascular and respiratory diseases were modeled with daily pollutant concentrations [24-hr means for nitrogen dioxide, sulfur dioxide, and particulate matter < 10 microm in aerodynamic diameter (PM(10)); 8-hr mean for ozone]. using Poisson regression. We controlled for confounding factors by fitting the terms in models, in line with those recommended by the APHEA (Air Pollution and Health: a European Approach) protocol. Exposure-response relationships in warm and cool seasons were examined using generalized additive modeling. During the cool season, for a linear extrapolation of 10th-90th percentiles in the pollutant concentrations of all oxidant pollutants, NO(2), SO(2), and O(3), we found significant effects on all the mortality outcomes under study, with relative risks (RR) of 1.04-1.10 (p < 0.038, except p = 0.079 for SO(2) on respiratory mortality). We observed consistent positive exposure-response relationships during the cool season but not during the warm season. The effects of PM(10) were marginally significant (RR = 1.06; p = 0.054) for respiratory mortality but not for the other outcomes (p > 0.135). In this subtropical city, local air quality objectives should take into account that air pollution has stronger health effects during the cool rather than warm season and that oxidant pollutants are more important indicators of health effects than particulates.
PMCID: PMC1240272  PMID: 11335180
22.  Air Pollution, Aeroallergens, and Emergency Room Visits for Acute Respiratory Diseases and Gastroenteric Disorders among Young Children in Six Italian Cities 
Environmental Health Perspectives  2009;117(11):1780-1785.
Past studies reported evidence of associations between air pollution and respiratory symptoms and morbidity for children. Few studies examined associations between air pollution and emergency room (ER) visits for wheezing, and even fewer for gastroenteric illness. We conducted a multicity analysis of the relationship between air pollution and ER visits for wheezing and gastroenteric disorder in children 0–2 years of age.
We obtained ER visit records for wheezing and gastroenteric disorder from six Italian cities. A city-specific case–crossover analysis was applied to estimate effects of particulate matter (PM), nitrogen dioxide, sulfur dioxide, ozone, and carbon monoxide, adjusting for immediate and delayed effects of temperature. Lagged effects of air pollutants up to 6 prior days were examined. The city-specific results were combined using a random-effect meta-analysis.
CO and SO2 were most strongly associated with wheezing, with a 2.7% increase [95% confidence interval (CI), 0.5–4.9] for a 1.04-μg/m3 increase in 7-day average CO and a 3.4% (95% CI, 1.5–5.3) increase for an 8.0-μg/m3 increase in SO2. Positive associations were also found for PM with aerodynamic diameter ≤ 10 μg and NO2. We found a significant association between the 3-day moving average CO and gastroenteric disorders [3.8% increase (95% CI, 1.0–6.8)]. When data were stratified by season, the associations were stronger in summer for wheezing and in winter for gastroenteric disorders.
Air pollution is associated with triggering of wheezing and gastroenteric disorders in children 0–2 years of age; more work is needed to understand the mechanisms to help prevent wheezing in children.
PMCID: PMC2801171  PMID: 20049132
air pollution; asthma in children; epidemiology of asthma; children’s health
23.  PM(10) exposure, gaseous pollutants, and daily mortality in Inchon, South Korea. 
Environmental Health Perspectives  1999;107(11):873-878.
To evaluate the relative importance of various measures of particulate and gaseous air pollution as predictors of daily mortality in Inchon, South Korea, the association between total daily mortality and air pollution was investigated for a 20-month period (January 1995 through August 1996). Poisson regression was used to regress daily death counts on each air pollutant, controlling for time trends, season, and meteorologic influences such as temperature and relative humidity. Regression coefficients of a 5-day moving average of particulate matter less than or = to 10 microm in aerodynamic diameter (PM(10)) on total mortality were positively significant when considered separately and simultaneously with other pollutants in the model. PM(10) remained significant when the models were confined to cardiovascular or respiratory mortality. Sulfur dioxide (SO(2)) and carbon monoxide (CO) were significantly related to respiratory mortality in the single-pollutant model. Ozone exposure was not statistically significant with regard to mortality in the above models, and graphic analysis showed that the relationship was nonlinear. A combined index of PM(10), nitrogen dioxide, SO(2), and CO seemed to better explain the exposure-response relationship with total mortality than an individual air pollutant. Pollutants should be considered together in the risk assessment of air pollution, as opposed to measuring the risk of individual pollutants.
PMCID: PMC1566699  PMID: 10544154
24.  Air pollution and case fatality of SARS in the People's Republic of China: an ecologic study 
Environmental Health  2003;2:15.
Severe acute respiratory syndrome (SARS) has claimed 349 lives with 5,327 probable cases reported in mainland China since November 2002. SARS case fatality has varied across geographical areas, which might be partially explained by air pollution level.
Publicly accessible data on SARS morbidity and mortality were utilized in the data analysis. Air pollution was evaluated by air pollution index (API) derived from the concentrations of particulate matter, sulfur dioxide, nitrogen dioxide, carbon monoxide and ground-level ozone. Ecologic analysis was conducted to explore the association and correlation between air pollution and SARS case fatality via model fitting. Partially ecologic studies were performed to assess the effects of long-term and short-term exposures on the risk of dying from SARS.
Ecologic analysis conducted among 5 regions with 100 or more SARS cases showed that case fatality rate increased with the increment of API (case fatality = - 0.063 + 0.001 * API). Partially ecologic study based on short-term exposure demonstrated that SARS patients from regions with moderate APIs had an 84% increased risk of dying from SARS compared to those from regions with low APIs (RR = 1.84, 95% CI: 1.41–2.40). Similarly, SARS patients from regions with high APIs were twice as likely to die from SARS compared to those from regions with low APIs. (RR = 2.18, 95% CI: 1.31–3.65). Partially ecologic analysis based on long-term exposure to ambient air pollution showed the similar association.
PMCID: PMC293432  PMID: 14629774
Over the past two decades there has been increasing interest in studies regarding effects on human health of climate changes and urban air pollution. Climate change induced by anthropogenic warming of the earth's atmosphere is a daunting problem and there are several observations about the role of urbanization, with its high levels of vehicle emissions and other pollutants, and westernized lifestyle with respect to the rising frequency of respiratory allergic diseases observed in most industrialized countries.
There is also evidence that asthmatic subjects are at increased risk of developing exacerbations of bronchial obstruction with exposure to gaseous (ozone, nitrogen dioxide, sulfur dioxide) and particulate inhalable components of air pollution.
A change in the genetic predisposition is an unlikely cause of the increasing frequency in allergic diseases because genetic changes in a population require several generations. Consequently, environmental factors such as climate change and indoor and outdoor air pollution may contribute to explain the increasing frequency of respiratory allergy and asthma. Since concentrations of airborne allergens and air pollutants are frequently increased contemporaneously, an enhanced IgE-mediated response to aeroallergens and enhanced airway inflammation could account for the increasing frequency of allergic respiratory diseases and bronchial asthma.
Scientific societies such as the European Academy of Allergy and Clinical Immunology, European Respiratory Society and the World Allergy Organization have set up committees and task forces to produce documents to focalize attention on this topic, calling for prevention measures.
PMCID: PMC3463061  PMID: 22958620
Air pollution; airway hyperreactivity; bronchial asthma; pollen allergy; respiratory allergy; thunderstorm-associated asthma; urban air pollution

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