Time series analysis of ambient air pollution effects on daily mortality

Although the growths of ambient pollutants have been attracting public concern, the characteristic of the associations between air pollutants and mortality remains elusive. Time series analysis with a generalized additive model was performed to estimate the associations between ambient air pollutants and mortality outcomes in Shenzhen City for the period of 2012–2014. The results showed that nitrogen dioxide (NO₂)-induced excess risks (ER) of total non-accidental mortality and cardiovascular mortality were significantly increased (6.05% (95% CI 3.38%, 8.78%); 6.88% (95% CI 2.98%, 10.93%), respectively) in interquartile range (IQR) increase analysis. Also, these associations were strengthened after adjusting for other pollutants. Moreover, similar associations were estimated for sulfur dioxide (SO₂), particulate matter with an aerodynamic diameter of <10 μm (PM₁₀), and total non-accidental mortality. There were significant higher ERs of associations between PM₁₀ and mortality for men than women; while there were significant higher ERs of associations between PM₁₀/NO₂ and mortality for elders (65 or elder) than youngers (64 or younger). Season analyses showed that associations between NO₂ and total non-accidental mortality were more pronounced in hot seasons than in warm seasons. Taken together, NO₂ was positively associated with total non-accidental mortality and cardiovascular mortality in Shenzhen even when the concentrations were below the ambient air quality standard. Policy measures should aim at reducing residents’ exposure to anthropogenic NO₂ emissions.     

Effect modification of ambient particle mortality by radon: A time series analysis in 108 U.S. cities

Numerous studies have reported a positive association between ambient fine particles and daily mortality, but little is known about the particle properties or environmental factors that may contribute to these effects. This study assessed potential modification of radon on PM_2.5 (particulate matter with an aerodynamic diameter <2.5 μm)-associated daily mortality in 108 U.S. cities using a two-stage statistical approach. First, city- and season-specific PM_2.5 mortality risks were estimated using over-dispersed Poisson regression models. These PM_2.5 effect estimates were then regressed against mean city-level residential radon concentrations to estimate overall PM_2.5 effects and potential modification by radon. Radon exposure estimates based on measured short-term basement concentrations and modeled long-term living-area concentrations were both assessed. Exposure to PM_2.5 was associated with total, cardiovascular, and respiratory mortality in both the spring and the fall. In addition, higher mean city-level radon concentrations increased PM_2.5-associated mortality in the spring and fall. For example, a 10 µg/m³ increase in PM_2.5 in the spring at the 10th percentile of city-averaged short-term radon concentrations (21.1 Bq/m³) was associated with a 1.92% increase in total mortality (95% CI: 1.29, 2.55), whereas the same PM_2.5 exposure at the 90th radon percentile (234.2 Bq/m³) was associated with a 3.73% increase in total mortality (95% CI: 2.87, 4.59). Results were robust to adjustment for spatial confounders, including average planetary boundary height, population age, percent poverty and tobacco use. While additional research is necessary, this study suggests that radon enhances PM_2.5 mortality. This is of significant regulatory importance, as effective regulation should consider the increased risk for particle mortality in cities with higher radon levels.

Implications: In this large national study, city-averaged indoor radon concentration was a significant effect modifier of PM_2.5-associated total, cardiovascular, and respiratory mortality risk in the spring and fall. These results suggest that radon may enhance PM_2.5-associated mortality. In addition, local radon concentrations partially explain the significant variability in PM_2.5 effect estimates across U.S. cities, noted in this and previous studies. Although the concept of PM as a vector for radon progeny is feasible, additional research is needed on the noncancer health effects of radon and its potential interaction with PM. Future air quality regulations may need to consider the increased risk for particle mortality in cities with higher radon levels.     

Particulate Air Pollution and Health Effects for Cardiovascular and Respiratory Causes in Temuco,Chile: A Wood-Smoke-Polluted Urban Area

Abstract

Temuco is one of the most highly wood-smoke-polluted cities in the world. Its population in 2004 was 340,000 inhabitants with 1587 annual deaths, of which 24% were due to cardiovascular and 11% to respiratory causes. For hospital admissions, cardiovascular diseases represented 6% and respiratory diseases 13%. Emergency room visits for acute respiratory infections represented 28%. The objective of the study presented here was to determine the relationship between air pollution from particulate matter less than or equal to 10 µm in aerodynamic diameter (PM₁₀; mostly PM_2.5, or particulate matter <2.5 µm in aerodynamic diameter) and health effects measured as the daily number of deaths, hospital admissions, and emergency room visits for cardiovascular, respiratory, and acute respiratory infection (ARI) diseases. The Air Pollution Health Effects European Approach (APHEA2) protocol was followed, and a multivariate Poisson regression model was fitted, controlling for trend, seasonality, and confounders for Temuco during 1998–2006. The results show that PM₁₀ had a significant association with daily mortality and morbidity, with the elderly (population >65 yr of age) being the group that presented the greatest risk. The relative risk for respiratory causes, with an increase of 100 µg/m³ of PM_10, was 1.163 with a 95% confidence interval (CI) of 1.057–1.279 for mortality, 1.137 (CI 1.096–1.178) for hospital admissions, and 1.162 for ARI (CI 1.144–1.181). There is evidence in Temuco of positive relationships between ambient particulate levels and mortality, hospital admissions, and ARI for cardiovascular and respiratory diseases. These results are consistent with those of comparable studies in other similar cities where wood smoke is the most important air pollution problem.     

Cumulative effects and threshold levels in air pollution mortality: Data analysis of nine large US cities using the NMMAPS dataset

We examined the existence of thresholds, cumulative effects and the homogeneity of five air pollutants on the relative risk of three mortality outcomes using data from nine major US cities using data from NMMAPS. Overall, PM₁₀ (usually 200-day accumulation) and ozone (3-day accumulation) were the two important predictors of outcome but their effect was not uniform across the nine cities. Many models exhibited thresholds (25–45 μm g/m³ for PM₁₀, and 10–45 ppb for O₃). Our preliminary exploratory analyses suggest that the use of a linear, no threshold, model for pollution studies is not consistent with the observed data. The heterogeneity in the risk estimates across the nine cities suggests combining the local risk estimates to obtain a national risk estimate may not be justifiable and the estimate is likely to be confounded.     

The short-term effects of air pollution on adolescent lung function in Taiwan

A mass screening of lung function associated with air pollutants for children is limited. This study assessed the association between air pollutants exposure and the lung function of junior high school students in a mass screening program in Taipei city, Taiwan. Among 10,396 students with completed asthma screening questionnaires and anthropometric measures, 2919 students aged 12-16 received the spirometry test. Forced vital capacity (FVC) and forced expiratory flow in 1 s (FEV₁) in association with daily ambient concentrations of particulate matter with diameter of 10 μm or less (PM₁₀), sulfur dioxide (SO₂), carbon monoxide (CO), nitrogen dioxide (NO₂), and ozone (O₃) were assessed by regression models controlling for the age, gender, height, weight, student living districts, rainfall and temperature. FVC, had a significant negative association with short-term exposure to O₃ and PM₁₀ measured on the day of spirometry testing. FVC values also were reversely associated with means of SO₂, O₃, NO₂, PM₁₀ and CO exposed 1 d earlier. An increase of 1-ppm CO was associated with the reduction in FVC for 69.8 mL (95% CI: −115, −24.4 mL) or in FEV₁ for 73.7 mL (95% CI: −118, −29.7 mL). An increase in SO₂ for 1 ppb was associated with the reductions in FVC and FEV₁ for 12.9 mL (95% CI: −20.7, −5.09 mL) and 11.7 mL (95% CI: −19.3, −4.16 mL), respectively. In conclusion, the short-term exposure to O₃ and PM₁₀ was associated with reducing FVC and FEV₁. CO and SO₂ exposure had a strong 1-d lag effect on FVC and FEV₁.     

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.     

Meta-Analysis of Time-Series Studies of Air Pollution and Mortality: Effects of Gases and Particles and the Influence of Cause of Death,Age, and Season

Abstract

A comprehensive, systematic synthesis was conducted of daily time-series studies of air pollution and mortality from around the world. Estimates of effect sizes were extracted from 109 studies, from single- and multipollutant models, and by cause of death, age, and season. Random effects pooled estimates of excess all-cause mortality (single-pollutant models) associated with a change in pollutant concentration equal to the mean value among a representative group of cities were 2.0% (95% CI 1.5-2.4%) per 31.3 μg/m³ particulate matter (PM) of median diameter <10 μm (PM₁₀); 1.7% (1.2-2.2%) per 1.1 ppm CO; 2.8% (2.1-3.5%) per 24.0 ppb NO₂; 1.6% (1.1-2.0%) per 31.2 ppb O₃; and 0.9% (0.7-1.2%) per 9.4 ppb SO₂ (daily maximum concentration for O₃, daily average for others). Effect sizes were generally reduced in multipollutant models, but remained significantly different from zero for PM₁₀ and SO₂. Larger effect sizes were observed for respiratory mortality for all pollutants except O₃. Heterogeneity among studies was partially accounted for by differences in variability of pollutant concentrations, and results were robust to alternative approaches to selecting estimates from the pool of available candidates. This synthesis leaves little doubt that acute air pollution exposure is a significant contributor to mortality.     

Meta-analysis of time-series studies of air pollution and mortality: effects of gases and particles and the influence of cause of death,age, and season

A comprehensive, systematic synthesis was conducted of daily time-series studies of air pollution and mortality from around the world. Estimates of effect sizes were extracted from 109 studies, from single- and multipollutant models, and by cause of death, age, and season. Random effects pooled estimates of excess all-cause mortality (single-pollutant models) associated with a change in pollutant concentration equal to the mean value among a representative group of cities were 2.0% (95% CI 1.5-2.4%) per 31.3 microg/m3 particulate matter (PM) of median diameter < or = 10 microm (PM10); 1.7% (1.2-2.2%) per 1.1 ppm CO; 2.8% (2.1-3.5%) per 24.0 ppb NO2; 1.6% (1.1-2.0%) per 31.2 ppb O3; and 0.9% (0.7-1.2%) per 9.4 ppb SO2 (daily maximum concentration for O3, daily average for others). Effect sizes were generally reduced in multipollutant models, but remained significantly different from zero for PM10 and SO2. Larger effect sizes were observed for respiratory mortality for all pollutants except O3. Heterogeneity among studies was partially accounted for by differences in variability of pollutant concentrations, and results were robust to alternative approaches to selecting estimates from the pool of available candidates. This synthesis leaves little doubt that acute air pollution exposure is a significant contributor to mortality.     

Fine root dynamics of mature European beech (Fagus sylvatica L.) as influenced by elevated ozone concentrations

Fine root dynamics (diameter < 1 mm) in mature Fagus sylvatica, with the canopies exposed to ambient or twice-ambient ozone concentrations, were investigated throughout 2004. The focus was on the seasonal timing and extent of fine root dynamics (growth, mortality) in relation to the soil environment (water content, temperature). Under ambient ozone concentrations, a significant relationship was found between fine root turnover and soil environmental changes indicating accelerated fine root turnover under favourable soil conditions. In contrast, under elevated ozone, this relationship vanished as the result of an altered temporal pattern of fine root growth. Fine root survival and turnover rate did not differ significantly between the different ozone regimes, although a delay in current-year fine root shedding was found under the elevated ozone concentrations. The data indicate that increasing tropospheric ozone levels can alter the timing of fine root turnover in mature F. sylvatica but do not affect the turnover rate.     

Air pollution and hospital visits for acute upper and lower respiratory infections among children in Ningbo,China: A time-series analysis

Acute upper and lower respiratory infections are main causes of mortality and morbidity in children. Air pollution has been recognized as an important contributor to development and exacerbation of respiratory infections. However, few studies are available in China. In this study, we investigated the short-term effect of air pollution on hospital visits for acute upper and lower respiratory infections among children under 15 years in Ningbo, China. Poisson generalized models were used to estimate the associations between air pollution and hospital visits for acute upper and lower respiratory infections adjusted for temporal, seasonal, and meteorological effects. We found that four pollutants (PM_2.5, PM₁₀, NO₂, and SO₂) were significantly associated with hospital visits for acute upper and lower respiratory infections. The effect estimates for acute upper respiratory infections tended to be higher (PM_2.5 ER = 3.46, 95% CI 2.18, 4.76; PM₁₀ ER = 2.81, 95% CI 1.93, 3.69; NO₂ ER = 11.27, 95% CI 8.70, 13.89; SO₂ ER = 15.17, 95% CI 11.29, 19.19). Significant associations for gaseous pollutants (NO₂ and SO₂) were observed after adjustment for particular matter. Stronger associations were observed among older children and in the cold period. Our study suggested that short-term exposure to outdoor air pollution was associated with hospital visits for acute upper and lower respiratory infections in Ningbo.     

Association between particulate matter air pollution and cardiovascular disease mortality in Lanzhou,China

Ambient particulate matter (PM) pollution has been linked to elevated mortality, especially from cardiovascular diseases. However, evidence on the effects of particulate matter pollution on cardiovascular mortality is still limited in Lanzhou, China. This research aimed to examine the associations of daily mean concentrations of ambient air pollutants (PM_2.5, PM_C, and PM₁₀) and cardiovascular mortality due to overall and cause-specific diseases in Lanzhou. Data representing daily cardiovascular mortality rates, meteorological factors (daily average temperature, daily average humidity, and atmospheric pressure), and air pollutants (PM_2.5, PM₁₀, SO₂, NO₂) were collected from January 1, 2014, to December 31, 2017, in Lanzhou. A quasi-Poisson regression model combined with a distributed lag non-linear model (DLNM) was used to estimate the associations. Stratified analyses were also performed by different cause-specific diseases, including cerebrovascular disease (CD), ischemic heart disease (IHD), heart rhythm disturbances (HRD), and heart failure (HF). The results showed that elevated concentration of PM_2.5, PM_C, and PM₁₀ had different effects on mortality of different cardiovascular diseases. Only cerebrovascular disease showed a significant positive association with elevated PM_2.5. Positive associations were identified between PM_C and daily mortality rates from total cardiovascular diseases, cerebrovascular diseases, and ischemic heart diseases. Besides, increased concentration of PM₁₀ was correlated with increased death of cerebrovascular diseases and ischemic heart diseases. For cerebrovascular disease, each 10 μg/m³ increase in PM_2.5 at lag4 was associated with increments of 1.22% (95% CI 0.11–2.35%). The largest significant effects for PM_C on cardiovascular diseases and ischemic heart diseases were both observed at lag0, and a 10 μg/m³ increment in concentration of PM_C was associated with 0.47% (95% CI 0.06–0.88%) and 0.85% (95% CI 0.18–1.52%) increases in cardiovascular mortality and ischemic heart diseases. In addition, it exhibited a lag effect on cerebrovascular mortality as well, which was most significant at lag6d, and an increase of 10 μg/m³ in PM_C was associated with a 0.76% (95% CI 0.16–1.37%) increase in cerebrovascular mortality. The estimates of percentage change in daily mortality rates per 10 μg/m³ increase in PM₁₀ were 0.52% (95% CI 0.05–1.02%) for cerebrovascular disease at lag6 and 0.53% (95% CI 0.01–1.05%) for ischemic heart disease at lag0, respectively. Our study suggests that elevated concentration of atmospheric PM (PM_2.5, PM_C, and PM₁₀) in Lanzhou is associated with increased mortality of cardiovascular diseases and that the health effect of elevated concentration of PM_2.5 is more significant than that of PM_C and PM₁₀.

     

Association between micronuclei frequency in pollen mother cells of Tradescantia and mortality due to cancer and cardiovascular diseases: A preliminary study in Sao José dos Campos, Brazil

The present study was designed to explore the correlation between the frequency of micronuclei in Trad-MN, measured across 28 biomonitoring stations during the period comprised between 11 of May and 2 of October, 2006, and adjusted mortality rates due to cardiovascular, respiratory diseases and cancer in Sao José dos Campos, Brazil, an area with different sources of air pollution. For controlling purposes, mortality rate due to gastrointestinal diseases (an event less prone to be affected by air pollution) was also considered in the analysis. Spatial distribution of micronuclei frequency was determined using average interpolation. The association between health estimators and micronuclei frequency was determined by measures of Pearson's correlation. Higher frequencies of micronuclei were detected in areas with high traffic and close to a petrochemical pole. Significant associations were detected between micronuclei frequency and adjusted mortality rate due to cardiovascular diseases (r = 0.841, p = 0.036) and cancer (r = 0.890, p = 0.018). The association between mortality due to chronic obstructive pulmonary diseases was positive but did not reach statistical significance (r = 0.640, p = 0.172), probably because of the small number of events. Gastrointestinal mortality did not exhibit significant association with micronuclei frequency. Because the small number of observations and the nature of an ecological study, the present findings must be considered with caution and considered as preliminary. Further studies, performed in different conditions of contamination and climate should be done before considering Trad-MN in the evaluation of human health risk imposed by air pollutants.     

Assessing the relationship between global warming and mortality: lag effects of temperature fluctuations by age and mortality categories

Although interests in assessing the relationship between temperature and mortality have arisen due to climate change, relatively few data are available on lag structure of temperature-mortality relationship, particularly in the Southern Hemisphere. This study identified the lag effects of mean temperature on mortality among age groups and death categories using polynomial distributed lag models in Brisbane, Australia, a subtropical city, 1996-2004. For a 1 °C increase above the threshold, the highest percent increase in mortality on the current day occurred among people over 85 years (7.2% (95% CI: 4.3%, 10.2%)). The effect estimates among cardiovascular deaths were higher than those among all-cause mortality. For a 1 °C decrease below the threshold, the percent increases in mortality at 21 lag days were 3.9% (95% CI: 1.9%, 6.0%) and 3.4% (95% CI: 0.9%, 6.0%) for people aged over 85 years and with cardiovascular diseases, respectively. These findings may have implications for developing intervention strategies to reduce and prevent temperature-related mortality.     

Air pollutants and health outcomes: Assessment of confounding by influenza

We assessed confounding of associations between short-term effects of air pollution and health outcomes by influenza using Hong Kong mortality and hospitalization data for 1996–2002.Three measures of influenza were defined: (i) intensity: weekly proportion of positive influenza viruses, (ii) epidemic: weekly number of positive influenza viruses ≥4% of the annual number for ≥2 consecutive weeks, and (iii) predominance: an epidemic period with co-circulation of respiratory syncytial virus <2% of the annual positive isolates for ≥2 consecutive weeks. We examined effects of influenza on associations between nitrogen dioxide (NO₂), sulfur dioxide (SO₂), particulate matter with aerodynamic diameter ≤10 μm (PM₁₀) and ozone (O₃) and health outcomes including all natural causes mortality, cardiorespiratory mortality and hospitalization. Generalized additive Poisson regression model with natural cubic splines was fitted to control for time-varying covariates to estimate air pollution health effects. Confounding with influenza was assessed using an absolute difference of >0.1% between unadjusted and adjusted excess risks (ER%).Without adjustment, pollutants were associated with positive ER% for all health outcomes except asthma and stroke hospitalization with SO₂ and stroke hospitalization with O₃. Following adjustment, changes in ER% for all pollutants were <0.1% for all natural causes mortality, but >0.1% for mortality from stroke with NO₂ and SO₂, cardiac or heart disease with NO₂, PM₁₀ and O₃, lower respiratory infections with NO₂ and O₃ and mortality from chronic obstructive pulmonary disease with all pollutants. Changes >0.1% were seen for acute respiratory disease hospitalization with NO₂, SO₂ and O₃ and acute lower respiratory infections hospitalization with PM₁₀. Generally, influenza does not confound the observed associations of air pollutants with all natural causes mortality and cardiovascular hospitalization, but for some pollutants and subgroups of cardiorespiratory mortality and respiratory hospitalization there was evidence to suggest confounding by influenza.     

Health effects of PM2.5 constituents and source contributions in major metropolitan cities,South Korea

Ambient PM_2.5 is one of the major risk factors for human health, and is not fully explained solely by mass concentration. We examined the short-term associations of cause-specific mortality (i.e., all-cause, cardiovascular, and respiratory mortality) with the 15 chemical constituents and sources of PM_2.5 in four metropolitan cities of South Korea during 2014–2018. We found transition metals consistently showed significant associations with all-cause mortality, while the effects of other constituents varied across the cities and for cause of death. Carbonaceous components strongly affected the all-cause, cardiovascular, and respiratory mortality in Daejeon. Secondary inorganic aerosols, SO₄^2? and NH₄⁺, showed significant associations with respiratory mortality in Gwangju. We also found the sources from which species closely linked to mortality generally increased the relative mortality risks. Heavy metal markers from soil or industrial sources were significantly associated with mortality in all cities. However, several sources influenced mortality despite their marker species not being significantly associated with it. Secondary nitrate and secondary sulfate sources were linked to mortality in DJ. This could be attributed to the deep inland location, which might have facilitated formation of secondary inorganic aerosols. In addition, primary sources including mobile and coal combustion seemed to have acute impacts on respiratory mortality in Gwangju. Our findings suggest the necessity of positive matrix factorization (PMF)-based approaches for evaluating health effects of PM_2.5 while considering the spatial heterogeneity in the compositions and source contributions of PM_2.5.

     

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.     

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.     

Deciduous shrubs for ozone bioindication: Hibiscus syriacus as an example

Ozone-like visible injury was detected on Hibiscus syriacus plants used as ornamental hedges. Weekly spray of the antiozonant ethylenediurea (EDU, 300 ppm) confirmed that the injury was induced by ambient ozone. EDU induced a 75% reduction in visible injury. Injury was more severe on the western than on the eastern exposure of the hedge. This factor of variability should be considered in ozone biomonitoring programmes. Seeds were collected and seedlings were artificially exposed to ozone in filtered vs. not-filtered (+30 ppb) Open-Top Chambers. The level of exposure inducing visible injury in the OTC seedlings was lower than that in the ambient-grown hedge. The occurrence of visible injury in the OTC confirmed that the ozone sensitivity was heritable and suggested that symptomatic plants of this deciduous shrub population can be successfully used as ozone bioindicators. EDU is recommended as a simple tool for diagnosing ambient ozone visible injury on field vegetation.     

Simulation of a Hazardous and Noxious Substances (HNS) spill in the marine environment: Lethal and sublethal effects of acrylonitrile to the European seabass

Despite the extensive maritime transportation of Hazardous and Noxious Substances (HNS), there is a current lack of knowledge on the effects posed by HNS spills on the marine biota. Among the HNS identified as priority, acrylonitrile was selected to conduct ecotoxicological assays. We assessed the acute and subletal effects of acrylonitrile in seabass, followed by a recovery phase to simulate the conditions of a spill incident. The work aimed at testing a broad range of biological responses induced by acrylonitrile. Sublethal exposure to the highest two doses increased the fish mortality rate (8.3% and 25% mortality in 0.75 and 2 mg L⁻¹ acrylonitrile concentrations), whereas no mortality were observed in control and 0.15 mg L⁻¹ treatments. Additionally, important alterations at sub-individual level were observed. Acrylonitrile significantly induced the activities of Catalase– CAT and Glutathione S-Transferase – GST; and the levels of DNA damage were significantly increased. Conversely, Superoxide Dismutase– SOD – activity was found to be significantly inhibited and no effects were found on Lipid Peroxidation– LPO and ethoxyresorufin O-deethylase – EROD – activity. Following a 7 d recovery period, the levels of CAT, GST and EROD fell to levels at or below those in the control. In the 2 mg L⁻¹ group, SOD remained at the levels found during exposure phase. This study has gathered essential information on the acute and subletal toxicity of acrylonitrile to seabass. It also demonstrated that 7 d recovery allowed a return of most endpoints to background levels. These data will be useful to assist relevant bodies in preparedness and response to HNS spills.     

Parental phenols exposure and spontaneous abortion in Chinese population residing in the middle and lower reaches of the Yangtze River

Widespread use of phenols has led to ubiquitous exposure to phenols. In experimental animals, phenols increased resorptions, reduced live litter size and fetal body weights. However, there are limited epidemiological evidences of the relationships between exposure to phenols and pregnancy outcomes. We evaluated the associations between parental urinary levels of various phenols and spontaneous abortion in a Chinese population residing in the middle and lower reaches of the Yangtze River. A case-control study was conducted that included 70 case couples with medically unexplained spontaneous abortion and 180 control couples who did not have a history of spontaneous abortion and had at least one living child. Both parental urinary phenols were measured by ultra-high performance liquid chromatography-tandem mass spectrometry including bisphenol A (BPA), benzophenone-3 (BP-3), 2,3,4-trichlorophenol (2,3,4-TCP), pentachlorophenol (PCP), 4-n-octylphenol (4-n-OP) and 4-n-nonylphenol (4-n-NP). Compared with the low exposure group, there was an increased risk of spontaneous abortion with high paternal urinary PCP concentration [odds ratio (OR) = 2.09, 95% Confidence Interval (CI), 1.05–4.14], and maternal exposure to 4-n-OP and alkylphenol(s) also significantly increased the risk of spontaneous abortion (OR = 2.21, 95% CI, 1.02–4.80; OR = 2.81, 95% CI, 1.39–5.65, respectively). Our study firstly provides the evidence that paternal PCP exposure, maternal 4-n-OP and alkylphenol(s) exposure are associated with spontaneous abortion in humans.