Outdoor air pollution and health effects in urban children with moderate to severe asthma

Particulate matter less than 2.5 μm in diameter (PM_2.5) is associated with asthma morbidity. Recent studies have begun examining the role of various constituents of PM_2.5, their potential sources, and their effects on health. We examine their role in asthmatic children. Thirty-six children 6–14 years with moderate/severe asthma from inner city areas in New York City were studied for 2-week periods (summer and winter) using diaries and lung function. Outdoor data, including PM₁₀, PM_2.5, elements, elemental/organic carbon, and criteria gases (NO₂, SO₂, and O₃) were collected at two sites. Odds ratios (ORs) relating daily pollutant concentrations to asthma indicators were calculated. During summer significant ORs>1 for symptom severity were obtained (O₃, PM_10, PM_2.5, and S); after adjustment for O₃, the ORs were no longer significant. During winter, Cu, Fe, Si, and Zn were significantly but negatively (ORs<1) associated with symptoms. Lag effects in winter suggested delayed effects (ORs>1) on symptoms (As, K, Pb, and V). Albuterol use increased during summer (O₃, PM₁₀, PM_2.5, Na, and S); after adjustment for O₃, only Na and S remained significant. Reduced pulmonary function was significantly associated with O₃ and Cl. Components of PM_2.5 are associated with asthma exacerbation in asthmatic children. Same-day pollutant associations with symptoms are seen in summer. In winter, our analysis suggests delayed adverse associations of PM_2.5 components.     

Personal and ambient air pollution exposures and lung function decrements in children with asthma

BACKGROUND: Epidemiologic studies have shown associations between asthma outcomes and outdoor air pollutants such as nitrogen dioxide and particulate matter mass < 2.5 mum in diameter (PM(2.5)). Independent effects of specific pollutants have been difficult to detect because most studies have relied on highly correlated central-site measurements. OBJECTIVES: This study was designed to evaluate the relationship of daily changes in percent-predicted forced expiratory volume in 1 sec (FEV(1)) with personal and ambient air pollutant exposures. METHODS: For 10 days each, we followed 53 subjects with asthma who were 9-18 years of age and living in the Los Angeles, California, air basin. Subjects self-administered home spirometry in themorning, afternoon, and evening. We measured personal hourly PM(2.5) mass, 24-hr PM(2.5) elemental and organic carbon (EC-OC), and 24-hr NO(2), and the same 24-hr average outdoor central-site(ambient) exposures. We analyzed data with transitional mixed models controlling for personal temperature and humidity, and as-needed beta(2)-agonist inhaler use. RESULTS: FEV(1) decrements were significantly associated with increasing hourly peak and daily average personal PM(2.5), but not ambient PM(2.5). Personal NO(2) was also inversely associated with FEV(1). Ambient NO(2) was more weakly associated. We found stronger associations among 37 subjects not taking controller bronchodilators as follows: Personal EC-OC was inversely associated with morning FEV(1); for an interquartile increase of 71 mug/m(3) 1-hr maximum personal PM(2.5), overall percent-predicted FEV(1) decreased by 1.32% [95% confidence interval (CI), -2.00 to -0.65%]; and for an interquartile increase of 16.8 ppb 2-day average personal NO(2), overall percent-predicted FEV(1) decreased by 2.45% (95% CI, -3.57 to -1.33%). Associations of both personal PM(2.5) and NO(2) with FEV(1) remained when co-regressed, and both confounded ambient NO(2). CONCLUSIONS: Independent pollutant associations with lung function might be missed using ambient data alone. Different sets of causal components are suggested by independence of FEV(1) associations with personal PM(2.5) mass from associations with personal NO(2).     

Ambient air pollution and asthma exacerbations in children: an eight-city analysis

The authors investigated the relation between ambient concentrations of five of the Environmental Protection Agency's criteria pollutants and asthma exacerbations (daily symptoms and use of rescue inhalers) among 990 children in eight North American cities during the 22-month prerandomization phase (November 1993-September 1995) of the Childhood Asthma Management Program. Short-term effects of carbon monoxide, nitrogen dioxide, particulate matter less than 10 mum in aerodynamic diameter (PM10), sulfur dioxide, and warm-season ozone were examined in both one-pollutant and two-pollutant models, using lags of up to 2 days. Lags in carbon monoxide and nitrogen dioxide were positively associated with both measures of asthma exacerbation, and the 3-day moving sum of sulfur dioxide levels was marginally related to asthma symptoms. PM10 and ozone were unrelated to exacerbations. The strongest effects tended to be seen with 2-day lags, where a 1-parts-per-million change in carbon monoxide and a 20-parts-per-billion change in nitrogen dioxide were associated with symptom odds ratios of 1.08 (95% confidence interval (CI): 1.02, 1.15) and 1.09 (95% CI: 1.03, 1.15), respectively, and with rate ratios for rescue inhaler use of 1.06 (95% CI: 1.01, 1.10) and 1.05 (95% CI: 1.01, 1.09), respectively. The authors believe that the observed carbon monoxide and nitrogen dioxide associations can probably be attributed to mobile-source emissions, though more research is required.     

Personal and ambient air pollution is associated with increased exhaled nitric oxide in children with asthma

BACKGROUND: Research has shown associations between pediatric asthma outcomes and airborne particulate matter (PM). The importance of particle components remains to be determined. METHODS: We followed a panel of 45 schoolchildren with persistent asthma living in Southern California. Subjects were monitored over 10 days with offline fractional exhaled nitric oxide (FeNO), a biomarker of airway inflammation. Personal active sampler exposures included continuous particulate matter < 2.5 microm in aerodynamic diameter (PM2.5), 24-hr PM2.5 elemental and organic carbon (EC, OC), and 24-hr nitrogen dioxide. Ambient exposures included PM2.5, PM2.5 EC and OC, and NO2. Data were analyzed with mixed models controlling for personal temperature, humidity and 10-day period. RESULTS: The strongest positive associations were between FeNO and 2-day average pollutant concentrations. Per interquartile range pollutant increase, these were: for 24 microg/m3 personal PM2.5, 1.1 ppb FeNO [95% confidence interval (CI), 0.1-1.9]; for 0.6 microg/m3 personal EC, 0.7 ppb FeNO (95% CI, 0.3-1.1); for 17 ppb personal NO2, 1.6 ppb FeNO (95% CI, 0.4-2.8). Larger associations were found for ambient EC and smaller associations for ambient NO2. Ambient PM2.5 and personal and ambient OC were significant only in subjects taking inhaled corticosteroids (ICS) alone. Subjects taking both ICS and antileukotrienes showed no significant associations. Distributed lag models showed personal PM2.5 in the preceding 5 hr was associated with FeNO. In two-pollutant models, the most robust associations were for personal and ambient EC and NO2, and for personal but not ambient PM2.5. CONCLUSION: PM associations with airway inflammation in asthmatics may be missed using ambient particle mass, which may not sufficiently represent causal pollutant components from fossil fuel combustion.     

被动吸烟与家养宠物对儿童哮喘及哮喘样症状影响

目的 探讨被动吸烟与家养宠物对儿童哮喘及哮喘样症状的交互效应。方法 采用整群随机抽样方法在广西百色市随机抽取6所小学,采用国际统一的标准问卷美国胸腔协会(ATS)调查表对所选学校的所有儿童进行有关被动吸烟、饲养宠物以及哮喘及哮喘样症状等情况调查。结果 广西百色市3 473名儿童中,持续咳嗽、持续咳痰、哮喘、哮喘现患、喘鸣现患的发生率分别为11.52%(400/3 473)、6.68%(232/3 473)、7.63%(265/3 473)、2.04%(71/3 473)、4.15%(144/3 473),17.71%(615/3 473)的儿童目前家中饲养宠物,目前暴露环境烟雾的比率高达39.48%(1 371/3 473);在调整了儿童的年龄、性别、父母文化程度等混杂因素后,多因素非条件logistic回归分析表明,与既不被动吸烟又不家养宠物的儿童比较,单纯暴露被动吸烟或家养宠物可使儿童患有持续咳嗽的风险分别增高28%(OR=1.28,95%CI=0.98~1.66)和8%(OR=1.08,95%CI=0.73~1.61),而同时暴露于这2个因素使儿童患有持续咳嗽的危险性增加155%(OR=2.55,95%CI=1.85~3.51);暴露于被动吸烟和家养宠物对儿童持续咳嗽影响的交互效应有统计学意义(χ²=5.50,P=0.019),但对哮喘及其他哮喘样症状影响的交互效应均无统计学意义(P>0.05)。结论 被动吸烟与家养宠物均可增加儿童患有哮喘及哮喘样症状的风险,且两者对儿童持续咳嗽的影响存在明显交互效应。     

Effects of air pollution on the prevalence and incidence of asthma in children

The effects of air pollution on asthmatic symptoms were assessed in a prospective cohort study of 3,049 schoolchildren in 8 different communities in Japan. Respiratory symptoms in these children were evaluated by questionnaires every year from the 1st through the 6th grades. The prevalence of asthma among the 1st graders was strongly associated with a history of allergic or respiratory diseases, but it was not associated with concentrations of air pollution. During the follow-up period, incidence rates of asthma were associated significantly with atmospheric concentrations of nitrogen dioxide. Particulate matter less than 10 microm in diameter (PM10) was also associated with a higher incidence of asthma, although the association was not significant. These findings suggest that air pollution, including nitrogen dioxide, may be an important factor in the development of asthma among children in urban districts.     

Health impact of air pollution to children

Health impact of air pollution to children was studied over the last twenty years in heavily polluted parts of the Czech Republic during. The research program (Teplice Program) analyzed these effects in the polluted district Teplice (North Bohemia) and control district Prachatice (Southern Bohemia).     

Medication use modifies the health effects of particulate sulfate air pollution in children with asthma.

Previous controlled studies have indicated that asthma medication modifies the adverse effects of sulfur dioxide (SO2) on lung function and asthma symptoms. The present report analyzed the role of medication use in a panel study of children with mild asthma. Children from Sokolov (n = 82) recorded daily peak expiratory flow (PEF) measurements, symptoms, and medication use in a diary. Linear and logistic regression analyses estimated the impact of concentrations of sulfate particles with diameters less than 2.5 microns, adjusting for linear trend, mean temperature, weekend (versus weekday), and prevalence of fever in the sample. Fifty-one children took no asthma medication, and only 31 were current medication users. Most children were treated with theophylline; only nine used sprays containing beta-agonist. For the nonmedicated children, weak associations between a 5-day mean of sulfates and respiratory symptoms were observed. Medicated children, in contrast, increased their beta-agonist use in direct association with an increase in 5-day mean of sulfates, but medication use did not prevent decreases in PEF and increases in the prevalence of cough attributable to particulate air pollution. Medication use was not a confounder but attenuated the associations between particulate air pollution and health outcomes.     

空气污染与儿童哮喘发病机制的研究进展

我国多地区雾霾严重,空气质量堪忧。大气污染成因复杂,大气颗粒物的来源更为复杂多变。常见的空气污染物种类繁多,如交通相关空气污染物、多环芳香烃、香烟烟雾、尘埃颗粒及细颗粒物 PM2.5,均与儿童哮喘密切相关,其毒性组分和致毒机制尚不明确,健康效应和毒理机制已经成为前沿的科学热点问题之一。本文就近几年来关于空气污染加重或引起儿童哮喘的机制进行综合分析。     

Impact of ambient air pollution on the prevalence of main symptoms of asthma in children

The impact of ambient air pollution on the prevalence of main symptoms of asthma was analyzed in children. A total of 3,506 children were interviewed using the ISAAC questionnaire. The prevalence of the abnormality was studied via continuous questioning in children aged 7-8 and 13-14 years, who lived in areas with varying aerogenic loads. The higher rates of main asthma-like symptoms and clinically diagnosed asthma were ascertained in the children living in higher ambient air pollution areas.     

温州儿童哮喘发作与空气污染及气象因子的相关性分析

目的探讨温州儿童哮喘发作与空气污染及气象因子的相关性,为预防儿童哮喘发作提供理论依据。方法收集2013年7月-2014年6月因哮喘发作在本科室住院治疗的患儿资料,以及同时期温州空气主要污染物浓度和气象因子数据资料,通过双变量相关性分析法、多元线性逐步回归分析法分析各月哮喘发作住院的患儿例数与各项空气污染物浓度及各气象因子的相关性。结果哮喘发作住院的患儿例数随空气污染物浓度升高呈增加趋势,其中可吸入颗粒物(pm10)浓度与哮喘住院患儿例数(尤其单纯哮喘例数)关系密切,呈显著正相关(P=0.039,r=0.601;P=0.020,r=0.660)。结论空气中pm10浓度升高能诱发儿童哮喘发作,尤其增加儿童单纯哮喘发作的发病率。故做好环境保护,降低空气污染,对减少儿童哮喘发作有重要意义。     

Outdoor air pollution, family and neighborhood environment, and asthma in LA FANS children

We examined associations between outdoor air pollution and childhood asthma, using measures of SES, neighborhood quality, and social support from the Los Angeles Family and Neighborhood Survey (LA FANS). We linked residential census tracts for 3114 children to government air monitoring stations and estimated average pollutant concentrations for the year before interview. CO and NO(2) levels increased and O(3) levels decreased as neighborhood quality decreased, yet correlations were low. Pollutant levels were not correlated with neighborhood support. Even after adjustment for social environment characteristics, LA FANS children living in high O(3), PM(10), and CO areas appeared to have worse asthma morbidity.     

宠物饲养及居住条件与学龄前儿童过敏性哮喘的关系

目的 研究宠物饲养及居住条件与学龄前儿童过敏性哮喘发生的关系.方法 选择2～5岁过敏性哮喘患者115例及相同年龄段的对照110例,采用问卷记录母亲怀孕及婴幼儿期宠物饲养和居住情况,比较病例组与对照组之间的差异.结果 与对照组相比,患者组饲养宠物的比例更低(34.8％vs70.0％,P=0.000),而居住于城镇小区的比例更高(73.9％ vs53.3％,P=0.001).母亲怀孕及婴幼儿期宠物饲养的儿童不易发生过敏性哮喘(OR =0.391,P=0.001),而居住于城镇小区的儿童更容易发生过敏性哮喘(OR =2.160,P =0.011).结论 在没有过敏性家族史的儿童中,较好的居住条件是过敏性哮喘发生的风险因素,而宠物饲养则是保护因素.     

Personal exposures to traffic-related air pollution and acute respiratory health among Bronx schoolchildren with asthma

Background

Previous studies have reported relationships between adverse respiratory health outcomes and residential proximity to traffic pollution, but have not shown this at a personal exposure level.

Objective

We compared, among inner-city children with asthma, the associations of adverse asthma outcome incidences with increased personal exposure to particulate matter mass ≤ 2.5 μm in aerodynamic diameter (PM_2.5) air pollution versus the diesel-related carbonaceous fraction of PM_2.5.

Methods

Daily 24-hr personal samples of PM_2.5, including the elemental carbon (EC) fraction, were collected for 40 fifth-grade children with asthma at four South Bronx schools (10 children per school) during approximately 1 month each. Spirometry and symptom scores were recorded several times daily during weekdays.

Results

We found elevated same-day relative risks of wheeze [1.45; 95% confidence interval (CI), 1.03–2.04)], shortness of breath (1.41; 95% CI, 1.01–1.99), and total symptoms (1.30; 95% CI, 1.04–1.62) with an increase in personal EC, but not with personal PM_2.5 mass. We found increased risk of cough, wheeze, and total symptoms with increased 1-day lag and 2-day average personal and school-site EC. We found no significant associations with school-site PM_2.5 mass or sulfur. The EC effect estimate was robust to addition of gaseous pollutants.

Conclusion

Adverse health associations were strongest with personal measures of EC exposure, suggesting that the diesel “soot” fraction of PM_2.5 is most responsible for pollution-related asthma exacerbations among children living near roadways. Studies that rely on exposure to PM mass may underestimate PM health impacts.     

Update on asthma and air pollution research in inner cities

The health impact of current ambient levels of particulate matter (PM) and ozone (O(3)) remains controversial. Exposure to both ambient O(3) and airborne PM has been shown to be related to short-term lung function deficits in children, a correlation that is greater among children with symptoms of asthma than among asymptomatic children. Day-to-day fluctuations in airborne PM also appear to be related to mortality and hospitalizations among the elderly. Despite these and other data suggesting that current ambient levels of O(3) and PM are associated with adverse health effects, there is an ongoing debate about the magnitude and clinical importance of the health effects of exposure to these pollutants.     

Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study

We observed a panel of 133 children (5-13 years of age) with asthma residing in the greater Seattle, Washington, area for an average of 58 days (range 28-112 days) during screening for enrollment in the Childhood Asthma Management Program (CAMP) study. Daily self-reports of asthma symptoms were obtained from study diaries and compared with ambient air pollution levels in marginal repeated measures logistic regression models. We defined days with asthma symptoms as any day a child reported at least one mild asthma episode. All analyses were controlled for subject-specific variables [age, race, sex, baseline height, and FEV(1) PC(20) concentration (methacholine provocative concentration required to produce a 20% decrease in forced expiratory volume in 1 sec)] and potential time-dependent confounders (day of week, season, and temperature). Because of variable observation periods for participants, we estimated both between- and within-subject air pollutant effects. Our primary interest was in the within-subject effects: the effect of air pollutant excursions from typical levels in each child's observation period on the odds of asthma symptoms. In single-pollutant models, the population average estimates indicated a 30% [95% confidence interval (CI), 11-52%] increase for a 1-ppm increment in carbon monoxide lagged 1 day, an 18% (95% CI, 5-33%) increase for a 10-microg/m(3) increment in same-day particulate matter < 1.0 microm (PM(1.0)), and an 11% (95% CI, 3-20%) increase for a 10-microg/m(3) increment in particulate matter < 10 microm (PM(10)) lagged 1 day. Conditional on the previous day's asthma symptoms, we estimated 25% (95% CI, 10-42%), 14% (95% CI, 4-26%), and 10% (95% CI, 3-16%) increases in the odds of asthma symptoms associated with increases in CO, PM(1.0), and PM(10), respectively. We did not find any association between sulfur dioxide (SO(2)) and the odds of asthma symptoms. In multipollutant models, the separate pollutant effects were smaller. The overall effect of an increase in both CO and PM(1. 0) was a 31% (95% CI, 11-55%) increase in the odds of symptoms of asthma. We conclude that there is an association between change in short-term air pollution levels, as indexed by PM and CO, and the occurrence of asthma symptoms among children in Seattle. Although PM effects on asthma have been found in other studies, it is likely that CO is a marker for vehicle exhaust and other combustion by-products that aggravate asthma.