Fine particulate matter (PM2.5) air pollution and selected causes of postneonatal infant mortality in California

Studies suggest that airborne particulate matter (PM) may be associated with postneonatal infant mortality, particularly with respiratory causes and sudden infant death syndrome (SIDS). To further explore this issue, we examined the relationship between long-term exposure to fine PM air pollution and postneonatal infant mortality in California. We linked monitoring data for PM相似文献   

空气污染物与绿化环境暴露水平对心肌梗塞死亡交互作用的病例交叉研究

目的 探索空气污染物与绿化暴露水平对心梗死亡的发生所产生的交互作用。方法 主要收集天津市2017—2019年因心梗死亡的个案病例,估计每名病例环境因素的暴露水平,采用条件logistic回归模型,分析空气污染物与绿化暴露水平对心梗死亡的发生所产生的交互作用。结果 在不同的季节,空气污染物浓度、气象因素和绿化环境暴露水平存在着差异（P＜0.001）。在单污染物模型中,每升高10 μg/m3的NO2（lag2期）,可使心梗死亡发生的风险升高0.4%（OR = 1.004,95%CI:1.000～1.008）。在多污染物模型中,每升高10 μg/m3的NO2（lag2期）、PM2.5（lag2期）和PM10（lag6期）,可使心梗死亡发生的风险升高1.1%（OR = 1.011,95%CI:1.005～1.018）、0.4%（OR = 1.004,95%CI:1～1.008）和0.3%（OR = 1.003,95%CI: 1.000～1.006）。对于滞后期lag1、lag2、lag6和lag7的暴露水平来说,颗粒污染物［可入肺颗粒物（PM1）、PM2.5 和PM10］与绿化环境暴露水平对心梗死亡的发生具有拮抗作用。结论 绿化环境可以起到降低颗粒污染物升高心梗死亡风险的作用,为指导人们有效的防护空气污染的危害,减轻颗粒污染物对心梗以及其他心血管疾病的发生和死亡提供依据。     

Air pollution and postneonatal infant mortality in the United States, 1999-2002

OBJECTIVE: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States. METHODS: We linked county-specific monitoring data for particles with aerodiameter of < or = 2.5 microm (PM2.5) and < or = 10 microm (PM10), ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS), and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity), percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths. RESULTS: After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI), 1.06-1.27] for a 10-mug/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09-1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category). CONCLUSIONS: This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.     

Acute effects of the breathing of industrial waste and of sulfur dioxide on the respiratory health of children living in the industrial area of Puchuncaví, Chile]

This study investigated the acute effect of air pollution on the respiratory health of children living in the industrial area of Puchuncaví, in Region V of Chile. The 114 children studied were from 6 to 12 years old; 57 of them had chronic respiratory symptoms and 57 did not. Each day for 66 days the air was checked for levels of sulfur dioxide (SO2) and of breathable particles that were < 10 microns (PM10). The children were selected and classified according to their susceptibility to chronic respiratory disease by means of a questionnaire used with 882 children living within the area of the emissions from a copper foundry and a thermoelectric plant. Each day, each studied child's peak expiratory flow (PEF) and incidence of respiratory symptoms were checked and recorded. Using regression models (generalized estimation equations), estimates were made of the association of SO2 and PM10 levels with PEF and the incidence of cough, expectoration, episodes of wheezing, dyspnea, and use of bronchodilators. Among the children who were initially symptomatic, an increase of 50 micrograms/m3 in the daily mean level of SO2 caused a reduction of -1.42 L/min (95% confidence interval (95% CI): -2.84 to -0.71) in the PEF of the following day. An increase of 30 micrograms/m3 in the cumulative concentration of PM10 over three days produced a PEF reduction of -2.84 L/min (95% CI: -4.26 to 0.00). With respect to symptoms, an increase of 30 micrograms/m3 in the weekly mean level of PM10 was related with a 26% increase (odds ratio (OR) = 1.26; 95% CI: 1.01 to 1.57) in the incidence of cough and of 23% (OR = 1.23; 95% CI: 1.00 to 1.50) in the incidence of expectoration. An increase of 50 micrograms/m3 in the mean level of SO2 for three days was associated with a 5% increase (OR = 1.05; 95% CI: 1.00 to 1.10) in the incidence of expectoration. An increase of 30 micrograms/m3 in the daily average of PM10 increased the use of bronchodilators two days later by 10% (OR = 1.10; 95% CI: 1.03 to 1.18). Among the initially asymptomatic children, a significant effect from PM10 exposure was found after an increase of 30 micrograms/m3 in the mean daily PM10 level, with a reduction of -1.34 L/min (95% CI: -2.68 to -0.67) in the PEF of the following day. A similar increase in the cumulative exposure over three days was associated with an increase of 9% in the incidence of episodes of wheezing (OR = 1.09; 95% CI: 1.01 to 1.31). It is concluded that high levels of PM10 and SO2 affect the respiratory health of children living in the industrial area of Puchuncaví.     

Risk factors for early infant mortality in Sarlahi district, Nepal

OBJECTIVES: Early infant mortality has not declined as rapidly as child mortality in many countries. Identification of risk factors for early infant mortality may help inform the design of intervention strategies. METHODS: Over the period 1994-97, 15,469 live-born, singleton infants in rural Nepal were followed to 24 weeks of age to identify risk factors for mortality within 0-7 days, 8-28 days, and 4-24 weeks after the birth. FINDINGS: In multivariate models, maternal and paternal education reduced mortality between 4 and 24 weeks only: odds ratios (OR) 0.28 (95% confidence interval (CI) = 0.12-0.66) and 0.63 (95% CI = 0.44-0.88), respectively. Miscarriage in the previous pregnancy predicted mortality in the first week of life (OR = 1.98, 95% CI = 1.37-2.87), whereas prior child deaths increased the risk of post-neonatal death (OR = 1.85, 95% CI 1.24-2.75). A larger maternal mid-upper arm circumference reduced the risk of infant death during the first week of life (OR = 0.88, 95% CI = 0.81-0.95). Infants of women who did not receive any tetanus vaccinations during pregnancy or who had severe illness during the third trimester were more likely to die in the neonatal period. Maternal mortality was strongly associated with infant mortality (OR = 6.43, 95% CI = 2.35-17.56 at 0-7 days; OR = 11.73, 95% CI = 3.82-36.00 at 8-28 days; and OR = 51.68, 95% CI = 20.26-131.80 at 4-24 weeks). CONCLUSION: Risk factors for early infant mortality varied with the age of the infant. Factors amenable to intervention included efforts aimed at maternal morbidity and mortality and increased arm circumference during pregnancy.     

Association between maternal exposure to ambient air pollutants during pregnancy and fetal growth restriction

Previous research demonstrated consistent associations between ambient air pollution and emergency room visits, hospitalizations, and mortality. Effect of air pollution on perinatal outcomes has recently drawn more attention. We examined the association between intrauterine growth restriction (IUGR) among singleton term live births and sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and fine particles (PM2.5) present in ambient air in the Canadian cities of Calgary, Edmonton, and Montreal for the period 1985-2000. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for IUGR, based on average daily levels of individual pollutants over each month and trimester of pregnancy after adjustment for maternal age, parity, infant gender, season, and city of residence. A 1 ppm increase in CO was associated with an increased risk of IUGR in the first (OR=1.18; 95% CI 1.14-1.23), second (OR=1.15; 95% CI 1.10-1.19) and third (OR=1.19; 95% CI 1.14-1.24) trimesters of pregnancy, respectively. A 20 ppb increase in NO2 (OR=1.16; 95% CI 1.09-1.24; OR=1.14; 95% CI 1.06--1.21; and OR=1.16; 95% CI 1.09-1.24 in the first, second, and third trimesters) and a 10 mug/m3 increase in PM2.5 (OR=1.07; 95% CI 1.03-1.10; OR=1.06; 95% CI 1.03-1.10; and OR=1.06; 95% CI 1.03-1.10) were also associated with an increased risk of IUGR. Consistent results were found when ORs were calculated by month rather than trimester of pregnancy. Our findings add to the emerging body of evidence that exposure to relatively low levels of ambient air pollutants in urban areas during pregnancy is associated with adverse effects on fetal growth.     

The temporal pattern of respiratory and heart disease mortality in response to air pollution

Short-term changes in ambient particulate matter with aerodynamic diameters < 10 micro m (PM10) have been associated with short-term fluctuations in mortality or morbidity in many studies. In this study, we tested whether those deaths are just advanced by a few days or weeks using a multicity hierarchical modeling approach for all-cause, respiratory, and cardiovascular deaths, for all ages and stratifying by age groups, within the APHEA-2 (Air Pollution and Health: A European Approach) project. We fit a Poisson regression and used an unconstrained distributed lag to model the effect of PM10 exposure on deaths up to 40 days after the exposure. In baseline models using PM10 the day of and day before the death, we found that the overall PM10 effect (per 10 micro g/m3) was 0.74% [95% confidence interval (95% CI), -0.17 to 1.66] for respiratory deaths and 0.69% (95% CI, 0.31-1.08) for cardiovascular deaths. In unrestricted distributed lag models, the effect estimates increased to 4.2% (95% CI, 1.08-7.42) for respiratory deaths and to 1.97% (95% CI, 1.38-2.55) for cardiovascular deaths. Our study confirms that most of the effect of air pollution is not simply advanced by a few weeks and that effects persist for more than a month after exposure. The effect size estimate for PM10 doubles when we considered longer-term effects for all deaths and for cardiovascular deaths and becomes five times higher for respiratory deaths. We found similar effects when stratifying by age groups. These larger effects are important for risk assessment.     

The relationship between selected causes of postneonatal infant mortality and particulate air pollution in the United States.

Recent studies have found associations between particulate air pollution and total and adult mortality. The relationship between particulate air pollution and mortality among infants has not been examined in the United States. This study evaluates the relationship between postneonatal infant mortality and particulate matter in the United States. Our study involved analysis of cohorts consisting of approximately 4 million infants born between 1989 and 1991 in states that report relevant covariates; this included 86 metropolitan statistical areas (MSAs) in the United States. Data from the National Center for Health Statistics-linked birth/infant death records were combined at the MSA level with measurements of particulate matter 10 microns or less (PM10) from the EPA's Aerometric Database. Infants were categorized as having high, medium, or low exposures based on tertiles of PM10. Total and cause-specific postneonatal mortality rates were examined using logistic regression to control for demographic and environmental factors. Overall postneonatal mortality rates were 3.1 among infants with low PM10 exposures, 3.5 among infants with medium PM10 exposures, and 3.7 among highly exposed infants. After adjustment for other covariates, the odds ratio (OR) and 95% confidence intervals (CI) for total postneonatal mortality for the high exposure versus the low exposure group was 1.10 (1.04, 1.16). In normal birth weight infants, high PM10 exposure was associated with respiratory causes [OR = 1.40, (1.05, 1.85)] and sudden infant death syndrome [OR = 1.26, (1.14, 1.39)]. For low birth weight babies, high PM10 exposure was associated, but not significantly, with mortality from respiratory causes [OR = 1.18, (0.86, 1.61)]. This study suggests that particulate matter is associated with risk of postneonatal mortality. Continued attention should be paid to air quality to ensure optimal health of infants in the United States.     

The lag structure between particulate air pollution and respiratory and cardiovascular deaths in 10 US cities.

To assess differences in the lag structure pattern between particulate matter < 10 microns/100 microns in diameter (PM10) and cause-specific mortality, we performed a time-series analysis in 10 US cities using generalized additive Poisson regressions in each city; nonparametric smooth functions were used to control for long time trend, weather, and day of the week. The PM10 effect was estimated based on its daily mean, 2-day moving average, and the cumulative 7-day effect by means of an unconstrained distributed lag model. A 10-microgram/m3 increase in the 7-day mean of PM10 was associated with increases in deaths due to pneumonia (2.7%, 95% confidence interval [CI]: 1.5, 3.9), chronic obstructive pulmonary disease (1.7%, 95% CI: 0.1, 3.3), and all cardiovascular diseases (1.0%, 95% CI: 0.6, 1.4). A 10-microgram/m3 increase in the 2-day mean of PM10 was associated with a 0.7% (95% CI: 0.3, 1.1) increase in deaths from myocardial infarction. When the distributed lag was assessed, two different patterns could be observed: respiratory deaths were more affected by air pollution levels on the previous days, whereas cardiovascular deaths were more affected by same-day pollution. These results contribute to the overall efforts so far in understanding how exposure to air pollution promotes adverse health effects.     

Surveillance of acute health effects of air pollution in Mexico City

BACKGROUND: A unique, active, timely, low-cost surveillance system for the metropolitan area of Mexico City was established in the mid-1990s. METHODS: The system obtained upper and lower respiratory tract symptoms and eye symptoms from daily interviews for a systematic sample of the general nonhospitalized population living within a 2-km radius of air pollution monitors during 1996-1997. RESULTS: Ozone increments (10 ppb) were associated with upper respiratory symptoms (odds ratio [OR] = 1.003; 95% confidence interval [CI] = 1.002-1.004) and ocular symptoms indicators (OR = 1.005; CI = 1.004-1.007), and with a higher risk of lower respiratory symptoms indicator among nonsmokers (OR = 1.003; CI = 1.002-1.005). Increases in relative humidity reduced the risk of increments of sulfur dioxide on the 3 acute health indicators. Association of PM10 with health indicators varied among the 5 regions. During emergency episodes, symptoms increased sharply when ozone reached 281 ppb, a finding that resulted in a change in the ozone criteria for emergency declaration from 294 to 281 ppb. CONCLUSIONS: This system has been low cost, timely, and useful for local decision making.     

Effects of air pollutants on acute stroke mortality

The relationship between stroke and air pollution has not been adequately studied. We conducted a time-series study to examine the evidence of an association between air pollutants and stroke over 4 years (January 1995-December 1998) in Seoul, Korea. We used a generalized additive model to regress daily stroke death counts for each pollutant, controlling for seasonal and long-term trends and meteorologic influences, such as temperature, relative humidity, and barometric pressure. We observed an estimated increase of 1.5% [95% confidence interval (CI), 1.3-1.8%] and 2.9% (95% CI, 0.3-5.5%) in stroke mortality for each interquartile range increase in particulate matter < 10 microm aerodynamic diameter (PM(10)) and ozone concentrations in the same day. Stroke mortality also increased 3.1% (95% CI, 1.1-5.1%) for nitrogen dioxide, 2.9% (95% CI, 0.8-5.0%) for sulfur dioxide, and 4.1% (95% CI, 1.1-7.2%) for carbon monoxide in a 2-day lag for each interquartile range increase in single-pollutant models. When we examined the associations among PM(10) levels stratified by the level of gaseous pollutants and vice versa, we found that these pollutants are interactive with respect to their effects on the risk of stroke mortality. We also observed that the effects of PM(10) on stroke mortality differ significantly in subgroups by age and sex. We conclude that PM(10) and gaseous pollutants are significant risk factors for acute stroke death and that the elderly and women are more susceptible to the effect of particulate pollutants.     

Paternal smoking and increased risk of infant and under-5 child mortality in Indonesia

We examined the relationship between paternal smoking and child mortality. Among 361,021 rural and urban families in Indonesia, paternal smoking was associated with increased infant mortality (rural, odds ratio [OR] = 1.30; 95% confidence interval [CI] = 1.24, 1.35; urban, OR = 1.10; 95% CI = 1.01, 1.20), and under-5 child mortality (rural, OR = 1.32; 95% CI = 1.26, 1.37; urban, OR = 1.14; 95% CI = 1.05, 1.23). Paternal smoking diverts money from basic necessities to cigarettes and adversely affects child health; tobacco control should therefore be considered among strategies to improve child survival.     

Effects of air pollution on adults with chronic obstructive pulmonary disease

Few studies have been conducted on the effects of air pollution on patients with chronic obstructive pulmonary disease (COPD). During a 14-mo period, 39 Parisian adults with severe COPD were monitored by their physicians. Daily levels of 4 air pollutants were provided by an urban air-quality network. Exacerbation of COPD was associated only with ozone (O3) (odds ratio [OR] = 1.44 for a 10-microg/m3 increase in O3; 95% confidence interval [CI] = 1.14, 1.82), with a lag of 2-3 days. The effect of O3 was greater in patients whose carbon dioxide pressure (PaCO2) was higher than 43 mm Hg (OR = 1.83; 95% CI = 1.36, 2.47) vs. those with a lower PaCO2 (OR = 1.26; 95% CI = 0.90, 1.77). The effect of O3 was unchanged, regardless of the maintenance medications used. The only air pollutant to which patients with severe COPD were particularly sensitive was O3.     

Does Air Pollution Trigger Infant Mortality in Western Europe? A Case-Crossover Study

Background: Numerous studies show associations between fine particulate air pollutants [particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀)] and mortality in adults.Objectives: We investigated short-term effects of elevated PM₁₀ levels on infant mortality in Flanders, Belgium, and studied whether the European Union (EU) limit value protects infants from the air pollution trigger.Methods: In a case-crossover analysis, we estimated the risk of dying from nontraumatic causes before 1 year of age in relation to outdoor PM₁₀ concentrations on the day of death. We matched control days on temperature to exclude confounding by variations in daily temperature.Results: During the study period (1998–2006), PM₁₀ concentration averaged 31.9 ± 13.8 μg/m³. In the entire study population (n = 2,382), the risk of death increased by 4% [95% confidence interval (CI), 0–8%; p = 0.045] for a 10-μg/m³ increase in daily mean PM₁₀. However, this association was significant only for late neonates (2–4 weeks of age; n = 372), in whom the risk of death increased by 11% (95% CI, 1–22%; p = 0.028) per 10-μg/m³ increase in PM₁₀. In this age class, infants were 1.74 (95% CI, 1.18–2.58; p = 0.006) times more likely to die on days with a mean PM₁₀ above the EU limit value of 50 μg/m³ than on days below this cutoff.Conclusions: Even in an affluent region in Western Europe, where infant mortality is low, days with higher PM air pollution are associated with an increased risk of infant mortality. Assuming causality, the current EU limit value for PM₁₀, which may be exceeded on 35 days/year, does not prevent PM₁₀ from triggering mortality in late neonates.     

Effects of air pollution on postneonatal infant mortality among firstborn infants in Seoul, Korea: case-crossover and time-series analyses

Infants are known to be susceptible to the adverse health effects of ambient air pollution. The authors examined the relationship between air pollution and postneonatal mortality from all causes among firstborn infants in Seoul, Korea, during 1999-2003, using both case-crossover and time-series analyses. Using a bidirectional control-sampling approach, the authors compared the effects of various types of air pollution on postneonatal mortality. The relative risk of postneonatal mortality from all causes was 1.000 (95% confidence interval [CI] = 0.998-1.002) for particulate matter with a diameter <10 mum, 1.002 (95% CI = 0.994-1.009) for nitrogen dioxide, 1.015 (95% CI = 0.973-1.058) for sulfur dioxide, 1.029 (95% CI = 0.833-1.271) for carbon monoxide, and 0.984 (95% CI = 0.977-0.992) for ozone for each 1-unit increase of air pollution level in the 1:6 control selection scheme. The authors observed a positive association between air pollution and infant daily mortality except for the studied particulate matter and ozone, although it was not statistically significant. They obtained similar results in the time-series analysis. The risk of postneonatal infant death from all causes was positively associated with all studied air pollutants except ozone. The authors also confirmed that the bidirectional method with many controls will give a more efficient estimator than will a method with fewer controls.     

Saharan dust and associations between particulate matter and daily mortality in Rome, Italy

Background: Outbreaks of Saharan-Sahel dust over Euro-Mediterranean areas frequently induce exceedances of the Europen Union''s 24-hr standard of 50 μg/m³ for particulate matter (PM) with aerodynamic diameter ≤ than 10 μm (PM₁₀).Objectives: We evaluated the effect of Saharan dust on the association between different PM fractions and daily mortality in Rome, Italy.Methods: In a study of 80,423 adult residents who died in Rome between 2001 and 2004, we performed a time-series analysis to explore the effects of PM_2.5, PM_2.5–10, and PM₁₀ on natural, cardiac, cerebrovascular, and respiratory mortality. We defined Saharan dust days by combining light detection and ranging (LIDAR) observations and analyses from operational models. We tested a Saharan dust–PM interaction term to evaluate the hypothesis that the effects of PM, especially coarse PM (PM_2.5–10), on mortality would be enhanced on dust days.Results: Interquartile range increases in PM_2.5–10 (10.8 μg/m³) and PM₁₀ (19.8 μg/m³) were associated with increased mortality due to natural, cardiac, cerebrovascular, and respiratory causes, with estimated effects ranging from 2.64% to 12.65% [95% confidence interval (CI), 1.18–25.42%] for the association between PM_2.5–10 and respiratory mortality (0- to 5-day lag). Associations of PM_2.5–10 with cardiac mortality were stronger on Saharan dust days (9.73%; 95% CI, 4.25–15.49%) than on dust-free days (0.86%; 95% CI, –2.47% to 4.31%; p = 0.005). Saharan dust days also modified associations between PM₁₀ and cardiac mortality (9.55% increase; 95% CI, 3.81–15.61%; vs. dust-free days: 2.09%; 95% CI, –0.76% to 5.02%; p = 0.02).Conclusions: We found evidence of effects of PM_2.5–10 and PM₁₀ on natural and cause-specific mortality, with stronger estimated effects on cardiac mortality during Saharan dust outbreaks. Toxicological and biological effects of particles from desert sources need to be further investigated and taken into account in air quality standards.     

Influence of exposure error and effect modification by socioeconomic status on the association of acute cardiovascular mortality with particulate matter in Phoenix

Using ZIP code-level mortality data, the association of cardiovascular mortality with PM(2.5) and PM(10-2.5), measured at a central monitoring site, was determined for three populations at different distances from the monitoring site but with similar numbers of deaths and therefore similar statistical power. The % risk and statistical significance for the association of mortality with PM(2.5) fell off with distance from the monitor, as would be expected if exposure error increased with distance. However, the % risk for PM(10-2.5) increased in going from the population in Central Phoenix, where the monitoring site was located, to a population in a Middle Ring around Phoenix and fell off in an Outer Ring population. The % risks for the Outer Ring were low for each of the six lag days (0-5) and for the 6-day moving average. The lag structures for PM(2.5) and PM(10-2.5) also differed for the Central Phoenix and Middle Ring populations. These differences led us to examine the socioeconomic status (SES) of the populations. On the basis of education and income, the population in Central Phoenix had a lower SES than the Middle Ring. Thus, the differences between Central Phoenix and the Middle Ring may be due to effect modification by SES and differences in exposure error. However, the effect modification by SES may be different for thoracic coarse particulate matter (PM) than for fine PM. This study provides new information on the association of PM(10-2.5) with cardiovascular mortality. In the Middle Ring, the % risk per 10 microg/m3 increase in PM(10-2.5) concentration (lower and upper 95% confidence levels) for lag day 1 was 3.4 (1.0, 5.8) and for the 6-day distributed-lag was 3.8 (0.3, 7.5). The differences in lag structure for PM(2.5) and PM(10-2.5) provide evidence that the two particle size classes have health effects that are different and independent. This study also helps explain the high % risks for PM(2.5) found for Central Phoenix, 6.6 (1.1, 12.5) for lag day 1, and 11.5 (2.8, 20.9) for the 6-day moving average. The smaller area may have a lower exposure error, and the lower SES population may be more susceptible to fine PM as compared to the larger areas and more heterogeneous populations used in many studies.     

Air pollution and exacerbation of asthma in African-American children in Los Angeles

Significant increases in asthma morbidity and mortality in the United States have occurred since the 1970s, particularly among African-Americans. Exposure to various environmental factors, including air pollutants and allergens, has been suggested as a partial explanation of these trends. To examine relations between several air pollutants and asthma exacerbation in African-Americans, we recruited a panel of 138 children in central Los Angeles. We recorded daily data on respiratory symptoms and medication use for 13 weeks and examined these data in conjunction with data on ozone (O3) nitrogen dioxide (NO2), particulate matter (PM10 and PM2.5), meteorological variables, pollens, and molds. Using generalized estimating equations, we found associations between respiratory symptom occurrence and several environmental factors. For example, new episodes of cough were associated with exposure to PM10 (OR = 1.25; 95% CI = 1.12-1.39; interquartile range [IQR] = 17 microg/m3, 24-hour average), PM2.5 (OR = 1.10; 95% CI = 1.03-1.18; IQR = 30 microg/m3, 12-hour average), NO2, and the molds Cladosporium and Alternaria, but not with exposure to O3 or pollen. The factors PM10 and O3 were associated with the use of extra asthma medication. For this population several bioaerosols and air pollutants had effects that may be clinically significant.     

Socioeconomic status, particulate air pollution, and daily mortality: differential exposure or differential susceptibility

BACKGROUND: Short-term increases in particulate air pollution are linked with increased daily mortality and morbidity. Socioeconomic status (SES) is a determinant of overall health. We investigated whether social class is an effect modifier of the PM(10) (particulate matter with diameter <10 micron)-daily mortality association, and possible mechanisms for this effect modification. METHODS: Area-based traffic emissions, income, and SES were available for each resident in Rome. All natural deaths (83,253 subjects) occurring in Rome among city residents (aged 35+ years) during the period 1998-2001 were identified. For each deceased individual, all the previous hospitalizations within 2 years before death were available via a record linkage procedure. PM(10) daily data were available from two urban monitoring sites. A case-crossover analysis was utilized in which control days were selected according to the time stratified approach (same day of the week during the same month). Conditional logistic regression was used. RESULTS: Due to the social class distribution in the city, exposure to traffic emissions was higher among those with higher area-based income and SES. Meanwhile, people of lower social class had suffered to a larger extent from chronic diseases before death than more affluent residents, especially diabetes mellitus, hypertension, heart failure, and chronic obstructive pulmonary diseases. Overall, PM(10) (lag 0-1) was strongly associated with mortality (1.1% increase, 95%CI = 0.7-1.6%, per 10 microg/m(3)). The effect was more pronounced among persons with lower income and SES (1.9% and 1.4% per 10 microg/m(3), respectively) compared to those in the upper income and SES levels (0.0% and 0.1%, respectively). CONCLUSIONS: The results confirm previous suggestions of a stronger effect of particulate air pollution among people in low social class. Given the uneven geographical distributions of social deprivation and traffic emissions in Rome, the most likely explanation is a differential burden of chronic health conditions conferring a greater susceptibility to less advantaged people.     

Air pollution and daily mortality in Shanghai: a time-series study

In this study, the authors assessed the relationship between air pollution and daily mortality from June 2000 to December 2001 in Shanghai, the largest city in China. They used the generalized additive model to allow for the highly flexible long-term and seasonable trends, and for nonlinear weather variables. In the single-pollutant models, the authors found significant associations between concentrations of air pollutants (particulate matter less than 10 microm in aerodynamic diameter [PM10], sulfur dioxide [SO2], and nitrogen dioxide [NO2]) and daily mortality. An increase of 10 microg/m3 in PM10, SO2, and NO2 corresponded to a respective increase in relative risk of mortality from all causes of 1.003 (95% confidence interval [CI] = 1.001, 1.005), 1.014 (95% CI = 1.008, 1.020), and 1.015 (95% CI = 1.008, 1.022). In the multiple-pollutant models, the association between SO2 and daily mortality was not affected by the inclusion of other pollutants; for PM10 and NO2, however, the inclusion of other pollutants possibly weakened the effects between these 2 pollutants and mortality. This finding suggests that gaseous pollutants may be more important than particulate matter as indicators of health in Shanghai. The authors' analyses provided evidence that the current amounts of air pollution in Shanghai continue to adversely affect population health, and strengthen the rationale for limiting the quantities of pollutants in outdoor air.