Comparison of Ambient PM Risk with Risks Estimated from PM Components of Smoking and Occupational Exposures

ABSTRACT

Air pollution studies are based on individual-level health response data and group-level exposure data. Therefore, exposure misclassification occurs, and the results may be biased to an unknown magnitude and direction. Testing the validity of such associations requires a study design using individual-level data for both exposure and response. One can test the plausibility of group-level PM risk estimates by comparing them to individual-level estimates of risk from constituents of ambient air. The twofold purpose of this review is to consider the internal consistency of risks estimated from the three major PM cohort studies and to determine individual-level mortality risks associated with ambient concentrations of tobacco smoke and occupational exposures and compare them with risks associated with ambient PM.

The paper demonstrates the risks are not consistent within and between the PM cohort studies. Higher ambient concentration risks (ACRs) from the ambient PM cohort studies are not coherent with ACRs derived from individual-level smoking and occupational risks for total, cardiopulmonary, and lung cancer mortality. Individual-level studies suggest increased risk of mortality cannot be measured with reliability at concentrations found in ambient air.     

Comparison of ambient PM risk with risks estimated from PM components of smoking and occupational exposures

Air pollution studies are based on individual-level health response data and group-level exposure data. Therefore, exposure misclassification occurs, and the results may be biased to an unknown magnitude and direction. Testing the validity of such associations requires a study design using individual-level data for both exposure and response. One can test the plausibility of group-level PM risk estimates by comparing them to individual-level estimates of risk from constituents of ambient air. The twofold purpose of this review is to consider the internal consistency of risks estimated from the three major PM cohort studies and to determine individual-level mortality risks associated with ambient concentrations of tobacco smoke and occupational exposures and compare them with risks associated with ambient PM. The paper demonstrates the risks are not consistent within and between the PM cohort studies. Higher ambient concentration risks (ACRs) from the ambient PM cohort studies are not coherent with ACRs derived from individual-level smoking and occupational risks for total, cardiopulmonary, and lung cancer mortality. Individual-level studies suggest increased risk of mortality cannot be measured with reliability at concentrations found in ambient air.     

Long-term associations of morbidity with air pollution: A catalog and synthesis

I searched the National Institutes of Health MEDLINE database through January 2017 for long-term studies of morbidity and air pollution and cataloged them with respect to cardiovascular, respiratory, cancer, diabetes, hospitalization, neurological, and pregnancy-birth endpoints. The catalog is presented as an online appendix. Associations with PM_2.5 (particulate matter with an aerodynamic diameter <2.5 μm), PM₁₀ (PM with an aerodynamic diameter <10 μm), and nitrogen dioxide (NO₂) were evaluated most frequently among the 417 ambient air quality studies identified. Associations with total suspended particles (TSP), carbon, ozone, sulfur, vehicular traffic, radon, and indoor air quality were also reported. I evaluated each study in terms of pollutant significance (yes, no), duration of exposure, and publication date. I found statistically significant pollutant relationships (P < 0.05) in 224 studies; 220 studies indicated adverse effects. Among 795 individual pollutant effect estimates, 396 are statistically significant. Pollutant associations with cardiovascular indicators, lung function, respiratory symptoms, and low birth weight are more likely to be significant than with disease incidence, heart attacks, diabetes, or neurological endpoints. Elemental carbon (EC), traffic, and PM_2.5 are most likely to be significant for cardiovascular outcomes; TSP, EC, and ozone (O₃) for respiratory outcomes; NO₂ for neurological outcomes; and PM₁₀ for birth/pregnancy outcomes. Durations of exposure range from 60 days to 35 yr, but I found no consistent relationships with the likelihood of statistical significance. Respiratory studies began ca. 1975; studies of diabetes, cardiovascular, and neurological effects increased after about 2005. I found 72 studies of occupational air pollution exposures; 40 reported statistically significant adverse health effects, especially for respiratory conditions. I conclude that the aggregate of these studies supports the existence of nonlethal physiological effects of various pollutants, more so for non–life-threatening endpoints and for noncriteria pollutants (TSP, EC, PM_2.5 metals). However, most studies were cross-sectional analyses over limited time spans with no consideration of lag or disease latency. Further longitudinal studies are thus needed to investigate the progress of disease incidence in association with air pollution exposure.

Implications: Relationships of air pollution with excess mortality are better known than with long-term antecedent morbidity. I cataloged 489 studies of cardiovascular, respiratory, cancer, and neurological effects, diabetes, and birth outcomes with respect to 12 air pollutants. About half of the studies reported statistically significant relationships, more frequently with noncriteria than with criteria pollutants. Indoor and cumulative exposures, coarse or ultrafine particles, and organic carbon were seldom considered. Significant relationships were more likely with less-severe endpoints such as blood pressure, lung function, or respiratory symptoms than with incidence of cancer, chronic obstructive pulmonary disease (COPD), heart failure, or diabetes. Most long-term studies are based on spatial relationships; longitudinal studies are needed to link the progression of pollution-related morbidity to mortality, especially for the cardiovascular system.     

Determinants of perceived air pollution annoyance and association between annoyance scores and air pollution (PM2.5, NO2) concentrations in the European EXPOLIS study

Apart from its traditionally considered objective impacts on health, air pollution can also have perceived effects, such as annoyance. The psychological effects of air pollution may often be more important to well-being than the biophysical effects. Health effects of perceived annoyance from air pollution are so far unknown. More knowledge of air pollution annoyance levels, determinants and also associations with different air pollution components is needed. In the European air pollution exposure study, EXPOLIS, the air pollution annoyance as perceived at home, workplace and in traffic were surveyed among other study objectives. Overall 1736 randomly drawn 25–55-yr-old subjects participated in six cities (Athens, Basel, Milan, Oxford, Prague and Helsinki). Levels and predictors of individual perceived annoyances from air pollution were assessed. Instead of the usual air pollution concentrations at fixed monitoring sites, this paper compares the measured microenvironment concentrations and personal exposures of PM_2.5 and NO₂ to the perceived annoyance levels. A considerable proportion of the adults surveyed was annoyed by air pollution. Female gender, self-reported respiratory symptoms, downtown living and self-reported sensitivity to air pollution were directly associated with high air pollution annoyance score while in traffic, but smoking status, age or education level were not significantly associated. Population level annoyance averages correlated with the city average exposure levels of PM_2.5 and NO₂. A high correlation was observed between the personal 48-h PM_2.5 exposure and perceived annoyance at home as well as between the mean annoyance at work and both the average work indoor PM_2.5 and the personal work time PM_2.5 exposure. With the other significant determinants (gender, city code, home location) and home outdoor levels the model explained 14% (PM_2.5) and 19% (NO₂) of the variation in perceived air pollution annoyance in traffic. Compared to Helsinki, in Basel and Prague the adult participants were more annoyed by air pollution while in traffic even after taking the current home outdoor PM_2.5 and NO₂ levels into account.     

Infant mortality and air pollution: a comprehensive analysis of U.S. data for 1990

This paper uses U.S. linked birth and death records to explore associations between infant mortality and environmental factors, based on spatial relationships. The analysis considers a range of infant mortality end points, regression models, and environmental and socioeconomic variables. The basic analysis involves logistic regression modeling of individuals; the cohort comprises all infants born in the United States in 1990 for whom the required data are available from the matched birth and death records. These individual data include sex, race, month of birth, and birth weight of the infant, and personal data on the mother, including age, adequacy of prenatal care, and smoking and education in most instances. Ecological variables from Census and other sources are matched on the county of usual residence and include ambient air quality, elevation above sea level, climate, number of physicians per capita, median income, racial and ethnic distribution, unemployment, and population density. The air quality variables considered were 1990 annual averages of PM10, CO, SO2, SO4(2-), and "non-sulfate PM10" (NSPM10--obtained by subtracting the estimated SO4(2-) mass from PM10). Because all variables were not available for all counties (especially maternal smoking), it was necessary to consider various subsets of the total cohort. We examined all infant deaths and deaths by age (neonatal and postneonatal), by birth weight (normal and low [< 2500 g]), and by specific causes within these categories. Special attention was given to sudden infant death syndrome (SIDS). For comparable modeling assumptions, the results for PM10 agreed with previously published estimates; however, the associations with PM10 were not specific to probable exposures or causes of death and were not robust to changes in the model and/or the locations considered. Significant negative mortality associations were found for SO4(2-). There was no indication of a role for outdoor PM2.5, but possible contributions from indoor air pollution sources cannot be ruled out, given higher SIDS rates in winter, in the north and west, and outside of large cities.     

The Impact of Migration on Air Quality Dose-Response Functions: A Case Study of Jacksonville,Florida

The purpose of this study was to analyze quantitative relationships between air pollution and mortality, and to examine the impact of migration on pollution-related mortality functions. Dose-response functions were estimated for intra-urban variations in ambient air quality for the city of Jacksonville, Florida. Indices of air pollution used in this study were sulfur dioxide (SO₂) and total suspended particulates (TSP). Ambient air quality was measured by the dispersion of TSP and SO₂ across census tracts using the SYMAP dispersion model in conjunction with air quality monitoring stations.

Holding other things constant, TSP apeared to have no statistically significant association with mortality rates. By contrast, the significance of the estimated coefficient for the pollution variable, SO₂, supported the contention that there is a positive and statistically significant relationship between air pollution and mortality rates. However, after making a limited test of the impact of migration on dose-response functions, the SO₂ pollution variable was no longer statistically significant. That is, recent migrants may have limited exposure to the existing level of SO₂ in Jacksonville, Florida, but carry with them long term exposure to more heavily polluted areas in the Northern United States. The results of this study suggest that further epidemiological studies and economic analysis of the health effects on air pollution should make some attempt to control the migration effect.     

Significant Relationships Concerning Exponential Transmission or Penetration

This paper reviews the statistical evidence linking human mortality with air pollution due to sulfur oxides and particulates. Three types of analyses are discussed: episodic increases in mortality coincident with high pollution, perturbations in mortality in a given city as a time-series in relation to perturbations in air quality, and comparisons of geographic differentials in both pollution and mortality rates. The paper concludes that there are no reliable statistical associations between SO _x and mortality, but that particulates are in some cases associated with excess mortality. Establishing whether the association is in fact causal would require elimination of potential confounding effects such as occupational exposures.     

Validity of Ambient Levels of Fine Particles as Surrogate for Personal Exposure to Outdoor Air Pollution—Results of the European EXPOLIS-EAS Study (Swiss Center Basel)

ABSTRACT

To evaluate the validity of fixed-site fine particle levels as exposure surrogates in air pollution epidemiology, we considered four indicator groups: (1) PM₂₅ total mass concentrations, (2) sulfur and potassium for regional air pollution, (3) lead and bromine for traffic-related particles, and (4) calcium for crustal particles. Using data from the European EXPOLIS (Air Pollution Exposure Distribution within Adult Urban Populations in Europe) study, we assessed the associations between 48-hr personal exposures and home outdoor levels of the indicators. Furthermore, within-city variability of fine particle levels was evaluated.

Personal exposures to PM_2.5 mass were not correlated to corresponding home outdoor levels (n = 44, r_{S (S)} =r o v ' Spearman (Sp) 0.07). In the group reporting neither relevant indoor sources nor relevant activities, personal exposures and home outdoor levels of sulfur were highly correlated (n = 40, r_Sp = 0.85). In contrast, the associations were weaker for traffic (Pb: n = 44, r_Sp = 0.53; Br: n = 44, r_Sp = 0.21) and crustal (Ca: n = 44, r_Sp = 0.12) indicators. This contrast is consistent with spatially homogeneous regional pollution and higher spatial variability of traffic and crustal indicators observed in Basel, Switzerland.

We conclude that for regional air pollution, fixed-site fine particle levels are valid exposure surrogates. For source-specific exposures, however, fixed-site data are probably not the optimal measure. Still, in air pollution epidemiology, ambient PM_2.5 levels may be more appropriate exposure estimates than total personal PM_2.5 exposure, since the latter reflects a mixture of indoor and outdoor sources.     

Validity of ambient levels of fine particles as surrogate for personal exposure to outdoor air pollution--results of the European EXPOLIS-EAS Study (Swiss Center Basel)

To evaluate the validity of fixed-site fine particle levels as exposure surrogates in air pollution epidemiology, we considered four indicator groups: (1) PM2.5 total mass concentrations, (2) sulfur and potassium for regional air pollution, (3) lead and bromine for traffic-related particles, and (4) calcium for crustal particles. Using data from the European EXPOLIS (Air Pollution Exposure Distribution within Adult Urban Populations in Europe) study, we assessed the associations between 48-hr personal exposures and home outdoor levels of the indicators. Furthermore, within-city variability of fine particle levels was evaluated. Personal exposures to PM2.5 mass were not correlated to corresponding home outdoor levels (n = 44, rSpearman (Sp) = 0.07). In the group reporting neither relevant indoor sources nor relevant activities, personal exposures and home outdoor levels of sulfur were highly correlated (n = 40, rSp = 0.85). In contrast, the associations were weaker for traffic (Pb: n = 44, rSp = 0.53; Br: n = 44, rSp = 0.21) and crustal (Ca: n = 44, rSp = 0.12) indicators. This contrast is consistent with spatially homogeneous regional pollution and higher spatial variability of traffic and crustal indicators observed in Basel, Switzerland. We conclude that for regional air pollution, fixed-site fine particle levels are valid exposure surrogates. For source-specific exposures, however, fixed-site data are probably not the optimal measure. Still, in air pollution epidemiology, ambient PM2.5 levels may be more appropriate exposure estimates than total personal PM2.5 exposure, since the latter reflects a mixture of indoor and outdoor sources.     

Estimated long-term outdoor air pollution concentrations in a cohort study

Several recent studies associated long-term exposure to air pollution with increased mortality. An ongoing cohort study, the Netherlands Cohort Study on Diet and Cancer (NLCS), was used to study the association between long-term exposure to traffic-related air pollution and mortality. Following on a previous exposure assessment study in the NLCS, we improved the exposure assessment methods.Long-term exposure to nitrogen dioxide (NO₂), nitrogen oxide (NO), black smoke (BS), and sulphur dioxide (SO₂) was estimated. Exposure at each home address (N=21 868) was considered as a function of a regional, an urban and a local component. The regional component was estimated using inverse distance weighed interpolation of measurement data from regional background sites in a national monitoring network. Regression models with urban concentrations as dependent variables, and number of inhabitants in different buffers and land use variables, derived with a Geographic Information System (GIS), as predictor variables were used to estimate the urban component. The local component was assessed using a GIS and a digital road network with linked traffic intensities. Traffic intensity on the nearest road and on the nearest major road, and the sum of traffic intensity in a buffer of 100 m around each home address were assessed. Further, a quantitative estimate of the local component was estimated.The regression models to estimate the urban component explained 67%, 46%, 49% and 35% of the variances of NO₂, NO, BS, and SO₂ concentrations, respectively. Overall regression models which incorporated the regional, urban and local component explained 84%, 44%, 59% and 56% of the variability in concentrations for NO₂, NO, BS and SO₂, respectively.We were able to develop an exposure assessment model using GIS methods and traffic intensities that explained a large part of the variations in outdoor air pollution concentrations.     

PM2.5 Assessment in 21 European Study Centers of ECRHS II: Method and First Winter Results

Abstract

The follow-up of a cohort of adults from 29 European centers of the former European Community Respiratory Health Survey (ECRHS) I (1989–1992) will examine the long-term effects of exposure to ambient air pollution on the incidence, course, and prognosis of respiratory diseases, in particular asthma and decline in lung function. The purpose of this article is to describe the methodology and the European-wide quality control program for the collection of particles with 50% cut-off size of 2.5 µm aerodynamic diameter (PM_2.5 ) in the ECRHS II and to present the PM_2.5 results from the winter period 2000–2001.

Because PM_2.5 is not routinely monitored in Europe, we measured PM_2.5 mass concentrations in 21 participating centers to estimate background exposure in these cities. A standardized protocol was developed using identical equipment in each center (U.S. Environmental Protection Agency Well Impactor Ninety-Six [WINS] and PQ167 from BGI, Inc.). Filters were weighed in a single central laboratory. Sampling was conducted for 7 days per month for a year.

Winter mean PM_2.5 mass concentrations (November 2000–February 2001) varied substantially, with Iceland reporting the lowest value (5 µg/m³) and northern Italy the highest (69 µg/m³). A standardized procedure appropriate for PM_2.5 exposure assessmnt in a multicenter study was developed. We expect ECRHS II to have sufficient variation in exposure to assess long-term effects of air pollution in this cohort. Any bias caused by variation in the characteristics of the chosen monitoring location (e.g., proximity to traffic sources) will be addressed in later analyses. Given the homogenous spatial distribution of PM_2.5 , however, concentrations measured near traffic are not expected to differ substantially from those measured at urban background sites.     

Infant Mortality and Air Pollution: A Comprehensive Analysis of U.S. Data for 1990

ABSTRACT

This paper uses U.S. linked birth and death records to explore associations between infant mortality and environmental factors, based on spatial relationships. The analysis considers a range of infant mortality end points, regression models, and environmental and socioeconomic variables. The basic analysis involves logistic regression modeling of individuals; the cohort comprises all infants born in the United States in 1990 for whom the required data are available from the matched birth and death records. These individual data include sex, race, month of birth, and birth weight of the infant, and personal data on the mother, including age, adequacy of prenatal care, and smoking and education in most instances. Ecological variables from Census and other sources are matched on the county of usual residence and include ambient air quality, elevation above sea level, climate, number of physicians per capita, median income, racial and ethnic distribution, unemployment, and population density. The air quality variables considered were 1990 annual averages of PM₁₀, CO, SO₂, SO₄ ^2-, and “non-sulfate PM₁₀” (NSPM₁₀—obtained by subtracting the estimated SO₄ ^2-mass from PM₁₀). Because all variables were not available for all counties (especially maternal smoking), it was necessary to consider various subsets of the total cohort.

We examined all infant deaths and deaths by age (neonatal and postneonatal), by birth weight (normal and low [<2500 g]), and by specific causes within these categories. Special attention was given to sudden infant death syndrome (SIDS). For comparable modeling assumptions, the results for PM₁₀ agreed with previously published estimates; however, the associations with PM₁₀ were not specific to probable exposures or causes of death and were not robust to changes in the model and/or the locations considered. Significant negative mortality associations were found for SO₄ ^2-. There was no indication of a role for outdoor PM_2.5, but possible contributions from indoor air pollution sources cannot be ruled out, given higher SIDS rates in winter, in the north and west, and outside of large cities.     

Short-Term Effects of Gaseous Pollutants on Cause-Specific Mortality in Wuhan,China

Abstract

In Asia, limited studies have been published on the association between daily mortality and gaseous pollutants of nitrogen dioxide (NO₂), ozone (O₃), and sulfur dioxide (SO₂). Our previous studies in Wuhan, China, demonstrated long-term air pollution effects. However, no study has been conducted to determine mortality effects of air pollution in this region. This study was to determine the acute mortality effects of the gaseous pollutants in Wuhan, a city with 7.5 million permanent residents during the period from 2000 to 2004. There are approximately 4.5 million residents in Wuhan who live in the city’s core area of 201 km², where air pollution levels are highest, and pollution ranges are wider than the majority of the cities in the published literature. We used the generalized additive model to analyze pollution, mortality, and covariate data. We found consistent NO₂effects on mortality with the strongest effects on the same day. Every 10-μg/m³increase in NO₂daily concentration on the same day was associated with an increase in nonaccidental (1.43%; 95% confidence interval [CI]: 0.87–1.99%), cardiovascular (1.65%; 95% CI: 0.87–2.45%), stroke (1.49%; 95% CI: 0.56–2.43%), cardiac (1.77%; 95% CI: 0.44–3.12%), respiratory (2.23%; 95% CI: 0.52–3.96%), and cardiopulmonary mortality (1.60%; 95% CI: 0.85– 2.35%). These effects were stronger among the elderly than among the young. Formal examination of exposure-response curves suggests no-threshold linear relationships between daily mortality and NO₂, where the NO₂concentrations ranged from 19.2 to 127.4 μg/m³. SO₂and O₃were not associated with daily mortality. The exposure-response relationships demonstrated heterogeneity, with some curves showing nonlinear relationships for SO₂and O₃. We conclude that there is consistent evidence of acute effects of NO₂on mortality and suggest that a no-threshold linear relationship exists between NO₂and mortality.     

1987 APCA Govermenet Agencies Directory

A method for setting air quality standards for long-term cumulative exposures of a population based on epidemiological studies has been developed. It uses exposure estimates interpolated from monitoring stations to zip code centroids, each month applied to zip code by month residence histories of the population. Two alternative cumulative exposure indices are used—hours in excess of a threshold, and the sum of concentrations above a threshold. The indices are then used with multiple logistic regression models for the health outcome data to form dose response curves for relative risk, adjusting for covariates. These curves are useful for determination of at what exposure amounts and threshold levels, effects which have both statistical and public health significance begin to occur. The method is applied to a ten year follow-up of a sub cohort of 7,343 members of the National Cancer Institute-funded Adventist Health Study. Up to 20 years of residence history was available. Analysis for prevalence of symptoms was conducted for four air pollutants— total oxidants, sulfur dioxide, nitrogen dioxide, and total suspended particulates. For each pollutant, cumulated exposures were calculated above each of five different thresholds. Statistically significant effects were noted for total suspended particulates, total oxidants, sulfur dioxide, past and passive smoking.     

PM2.5 assessment in 21 European study centers of ECRHS II: Method and first winter results

The follow-up of a cohort of adults from 29 European centers of the former European Community Respiratory Health Survey (ECRHS) I (1989-1992) will examine the long-term effects of exposure to ambient air pollution on the incidence, course, and prognosis of respiratory diseases, in particular asthma and decline in lung function. The purpose of this article is to describe the methodology and the European-wide quality control program for the collection of particles with 50% cut-off size of 2.5 microm aerodynamic diameter (PM2.5) in the ECRHS II and to present the PM2.5 results from the winter period 2000-2001. Because PM2.5 is not routinely monitored in Europe, we measured PM2.5 mass concentrations in 21 participating centers to estimate background exposure in these cities. A standardized protocol was developed using identical equipment in each center (U.S. Environmental Protection Agency Well Impactor Ninety-Six [WINS] and PQ167 from BGI, Inc.). Filters were weighed in a single central laboratory. Sampling was conducted for 7 days per month for a year. Winter mean PM2.5 mass concentrations (November 2000-February 2001) varied substantially, with Iceland reporting the lowest value (5 microg/m3) and northern Italy the highest (69 microg/m3). A standardized procedure appropriate for PM2.5 exposure assessment in a multicenter study was developed. We expect ECRHS II to have sufficient variation in exposure to assess long-term effects of air pollution in this cohort. Any bias caused by variation in the characteristics of the chosen monitoring location (e.g., proximity to traffic sources) will be addressed in later analyses. Given the homogenous spatial distribution of PM2.5, however, concentrations measured near traffic are not expected to differ substantially from those measured at urban background sites.     

Development of an individual exposure model for application to the Southern California children's health study

The Southern California Children's Health Study (CHS) investigated the relationship between air pollution and children's chronic respiratory health outcomes. Ambient air pollutant measurements from a single CHS monitoring station in each community were used as surrogates for personal exposures of all children in that community. To improve exposure estimates for the CHS children, we developed an Individual Exposure Model (IEM) to retrospectively estimate the long-term average exposure of the individual CHS children to CO, NO₂, PM₁₀, PM_2.5, and elemental carbon (EC) of ambient origin. In the IEM, pollutant concentrations due to both local mobile source emissions (LMSE) and meteorologically transported pollutants were taken into account by combining a line source model (CALINE4) with a regional air quality model (SMOG). To avoid double counting, local mobile sources were removed from SMOG and added back by CALINE4. Limited information from the CHS survey was used to group each child into a specific time-activity category, for which corresponding Consolidated Human Activity Database (CHAD) time-activity profiles were sampled. We found local traffic significantly increased within-community variability of exposure to vehicle-related pollutants. PM-associated exposures were influenced more by meteorologically transported pollutants and local non-mobile source emissions than by LMSE. The overall within-community variability of personal exposures was highest for NO₂ (±20–40%), followed by EC (±17–27%), PM₁₀ (±15–25%), PM_2.5 (±15–20%), and CO (±9–14%). Between-community exposure differences were affected by community location, traffic density, and locations of residences and schools in each community. Proper siting of air monitoring stations relative to emission sources is important to capture community mean exposures.     

Short-term effects of gaseous pollutants on cause-specific mortality in Wuhan, China

In Asia, limited studies have been published on the association between daily mortality and gaseous pollutants of nitrogen dioxide (NO2), ozone (O3), and sulfur dioxide (SO2). Our previous studies in Wuhan, China, demonstrated long-term air pollution effects. However, no study has been conducted to determine mortality effects of air pollution in this region. This study was to determine the acute mortality effects of the gaseous pollutants in Wuhan, a city with 7.5 million permanent residents during the period from 2000 to 2004. There are approximately 4.5 million residents in Wuhan who live in the city's core area of 201 km2, where air pollution levels are highest, and pollution ranges are wider than the majority of the cities in the published literature. We used the generalized additive model to analyze pollution, mortality, and covariate data. We found consistent NO2 effects on mortality with the strongest effects on the same day. Every 10-microg/m3 increase in NO2 daily concentration on the same day was associated with an increase in nonaccidental (1.43%; 95% confidence interval [CI]: 0.87-1.99%), cardiovascular (1.65%; 95% CI: 0.87-2.45%), stroke (1.49%; 95% CI: 0.56-2.43%), cardiac (1.77%; 95% CI: 0.44-3.12%), respiratory (2.23%; 95% CI: 0.52-3.96%), and cardiopulmonary mortality (1.60%; 95% CI: 0.85-2.35%). These effects were stronger among the elderly than among the young. Formal examination of exposure-response curves suggests no-threshold linear relationships between daily mortality and NO2, where the NO2 concentrations ranged from 19.2 to 127.4 microg/m3. SO2 and O3 were not associated with daily mortality. The exposure-response relationships demonstrated heterogeneity, with some curves showing nonlinear relationships for SO2 and O3. We conclude that there is consistent evidence of acute effects of NO2 on mortality and suggest that a no-threshold linear relationship exists between NO2 and mortality.     

Predicting residential indoor concentrations of nitrogen dioxide,fine particulate matter,and elemental carbon using questionnaire and geographic information system based data

Previous studies have identified associations between traffic-related air pollution and adverse health effects. Most have used measurements from a few central ambient monitors and/or some measure of traffic as indicators of exposure, disregarding spatial variability and factors influencing personal exposure-ambient concentration relationships. This study seeks to utilize publicly available data (i.e., central site monitors, geographic information system, and property assessment data) and questionnaire responses to predict residential indoor concentrations of traffic-related air pollutants for lower socioeconomic status (SES) urban households.As part of a prospective birth cohort study in urban Boston, we collected indoor and outdoor 3–4 day samples of nitrogen dioxide (NO₂) and fine particulate matter (PM_2.5) in 43 low SES residences across multiple seasons from 2003 to 2005. Elemental carbon (EC) concentrations were determined via reflectance analysis. Multiple traffic indicators were derived using Massachusetts Highway Department data and traffic counts collected outside sampling homes. Home characteristics and occupant behaviors were collected via a standardized questionnaire. Additional housing information was collected through property tax records, and ambient concentrations were collected from a centrally located ambient monitor.The contributions of ambient concentrations, local traffic and indoor sources to indoor concentrations were quantified with regression analyses. PM_2.5 was influenced less by local traffic but had significant indoor sources, while EC was associated with traffic and NO₂ with both traffic and indoor sources. Comparing models based on covariate selection using p-values or a Bayesian approach yielded similar results, with traffic density within a 50 m buffer of a home and distance from a truck route as important contributors to indoor levels of NO₂ and EC, respectively. The Bayesian approach also highlighted the uncertanity in the models. We conclude that by utilizing public databases and focused questionnaire data we can identify important predictors of indoor concentrations for multiple air pollutants in a high-risk population.     

Screening-level ecological risk assessment of polychlorinated dibenzo-p-dioxins and dibenzofurans in sediments and aquatic biota from the Venice Lagoon, Italy

Recent monitoring data indicate that portions of Italy's Venice Lagoon ecosystem have been degraded due to biological and chemical pollution from a variety of potential sources. Using polychlorinated dibenzo-p-dioxin (PCDD) and dibenzofuran (PCDF) data collected from sediment, fish and shellfish in the Lagoon, a screening-level ecological risk assessment (ERA) was performed to evaluate the risks to representative aquatic biota and wildlife receptors. Risks to aquatic invertebrates posed by PCDD/Fs in sediment were evaluated by comparing measured tissue concentrations in fish and shellfish to appropriate ecotoxicological reference values. For mammalian and avian receptors, risks posed by theoretical exposures to PCDD/Fs through the food chain were calculated using conservative wildlife exposure models. Results of the screening-level approach indicate that the potential for adverse effects to fish and aquatic invertebrate receptors from PCDD/Fs in surficial sediments are unlikely. Adverse effects to wildlife are possible but highly uncertain, and warrants further investigation in a more comprehensive ERA.