Assessing exposure to air toxics relative to asthma

Asthma is a respiratory disease whose prevalence has been increasing since the mid 1970s and that affects more than 14.6 million residents of the United States. Environmental triggers of asthma include air pollutants that are respiratory irritants. Air toxics emitted into the ambient air are listed in the 1990 Clean Air Act Amendments as hazardous air pollutants (HAPs) if they can adversely affect human health, including the respiratory tract. HAPs include particulate and gaseous-phase pollutants, individual organic compounds and metals, and mixtures. Associations between asthma exacerbation and both particles and indoor volatile organic compounds (VOCs), often referred to as indoor air quality, have been reported. Studies conducted in the United States, Canada, and Europe over the past two decades have shown that most people living in the developed countries spend the majority of their time indoors and that the air concentrations of many air toxics or HAPs are higher indoors than in the ambient air in urban, suburban, and rural settings. Elevated indoor air concentrations result from emissions of air toxics from consumer products, household furnishings, and personal activities. The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to oversample homes in close proximity to ambient sources, excluding residences where smokers lived, to determine the contribution of ambient emissions to air toxics exposure. The ratios of indoor to outdoor air concentrations of some VOCs in homes measured during RIOPA were much greater than one, and for most other VOCs that had indoor-to-outdoor ratios close to unity in the majority of homes, elevated ratios were found in the paired samples with the highest concentration. Thus, although ambient emissions contribute to exposure of some air toxics indoors as well as outdoors, this was not true for all of the air toxics and especially for the higher end of exposures to most volatile organic air toxics examined. It is therefore critical, when evaluating potential effects of air toxics on asthma or other adverse health end points, to determine where the exposure occurs and the source contributions for each air toxic and target population separately and not to rely solely on ambient air concentration measurements.     

Addressing community concerns about asthma and air toxics

People with asthma who live near or downwind from a source of toxic emissions commonly express concerns about the possible impact of hazardous air pollution on their health, especially when these emissions are visible or odorous. Citizens frequently turn to their local and state health departments for answers, but health departments face many challenges in addressing these concerns. These challenges include a lack of asthma statistics at the local level, limited exposure information, and a paucity of scientific knowledge about the contributions of hazardous air pollutants to asthma induction or exacerbation. Health agencies are creatively developing methods to address these challenges while working toward improving asthma surveillance data at the state and local levels. Recent community health investigations suggest that hazardous air pollutants that are occupational asthmagens or associated with odors may deserve more attention. In seeking to address community concerns about hazardous air pollution and asthma, community health investigations may also help to fill gaps in our scientific knowledge and identify areas for further research or environmental intervention. The solutions to community problems associated with environmental contamination and asthma, however, require sustained, coordinated efforts by public and private groups and citizens. Public health agencies can make a unique contribution to this effort, but additional resources and support will be required to develop information systems and epidemiologic capacity at the state and local levels.     

室内甲醛与成人过敏性哮喘关系的研究

目的　探讨室内甲醛暴露与成人过敏性哮喘之间的关系。方法　采用病例 -对照流行病学研究设计 ,通过问卷收集 30例成人过敏性哮喘患者及 81例健康对照相关信息并测定 111户研究对象室内空气中甲醛浓度。结果　病例组室内甲醛浓度总体分布高于对照组 ,且具有显著性差异 (P <0 0 0 0 1)。将甲醛浓度从低到高分为 4个等级 ,以等级 1作为参考组 ,可见其余各等级在病例组和对照组中的OR值不断增大 ;调整了年龄、性别、目前吸烟及慢支 /哮喘家族史后其相应的OR值也不断增大 ;同时总趋势OR值表明在调整混杂因素前后 ,甲醛浓度平均升高一个等级可以使哮喘的危险性分别增加 2 5 1倍和 2 36倍。结果表明 ,室内甲醛每升高 1个单位 (μg/m3 ) ,可以使成人过敏性哮喘的危险性提高 0 0 2倍。同时本研究也表明 ,装修可以使家庭室内甲醛浓度平均升高 30 6 5 μg/m3 。结论　随着室内甲醛浓度的升高 ,哮喘及其发作的危险性逐渐增加 ,两者之间具有一定的剂量 -反应关系 ,但只有当室内甲醛达到一定的高浓度水平时 ,其对哮喘的危险性才会显现出来。     

Pollutants and asthma: role of air toxics

Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway reactivity to both allergic and nonallergic stimuli. Most asthma exacerbations that result in hospitalization are associated with viral upper respiratory tract infections. Such infections typically induce T-helper type 1 (T(H)1) responses in the airway, involving activation of nuclear factor-kappaB (NF-Kappa B). However, a more recently appreciated cause of asthma exacerbation is exposure to pollutants, including ozone and various components of particulate matter (PM), including transition metals, diesel exhaust, and biologicals such as endotoxin. Although the role of air toxics in asthma pathogenesis remains incompletely examined, many components of PM that are active exacerbants of asthma are also prominent air toxics (metal ions and organic residues). These agents have been observed to activate NF-Kappa B. Reviewed in this article are the actions of specific air pollutants on airway inflammation in humans and potential common response pathways for ozone, PM, and several air toxics.     

六个国家室内空气污染和吸烟对≥50岁人群哮喘的交互作用研究

目的 探讨室内空气污染和吸烟之间的交互作用对≥50岁人群哮喘的影响,为哮喘的防控提供科学依据。方法 随机抽取中国、加纳、印度、墨西哥、俄罗斯和南非6个中低收入国家的居民家庭户进行家庭问卷调查和对所有≥50岁的成员进行个人问卷调查。运用logistic回归模型分别分析室内空气污染（做饭燃料、烟囱设施）和吸烟（是否吸烟、吸烟频率、烟龄）与人群哮喘患病的关系,利用乘法模型和加法模型评价空气污染和吸烟对人群哮喘的交互作用影响。结果 共有33 327名调查对象纳入分析,≥50岁人群哮喘的总患病率为3.89%（1 296/33 327）。调整国家、年龄、性别、婚姻状况、居住地、教育程度、体力活动、家庭收入等混杂因素后,吸烟人群相对于从不吸烟人群患哮喘风险增加（OR=1.18,95% CI：1.01~1.45）;在不同吸烟频率的人群中,偶尔吸烟人群患哮喘的风险最高（OR=1.75,95% CI：1.33~2.30）。交互作用分析结果显示,除烟龄和做饭燃料外,室内空气污染和吸烟之间对≥50岁人群哮喘存在相加交互作用;是否吸烟（交互项OR=1.60,95% CI：1.26~2.02）、吸烟频率（交互项OR=1.61,95% CI：1.28~2.04）、吸烟烟龄（交互项OR=1.69,95% CI：1.39~2.21）均与做饭燃料之间在≥50岁人群哮喘患病风险中存在相乘交互作用。当2种危险因素同时存在时,患哮喘的风险最高。吸烟和做饭燃料为柴/煤/炭人群患哮喘的风险是不吸烟和燃料为电/燃气的1.43倍（95% CI：1.17~1.75）。结论 室内空气污染和吸烟均与≥50岁人群哮喘患病有关,并对≥50岁人群哮喘患病存在交互作用。     

Association between indoor and outdoor air pollution and adolescent asthma from 1995 to 1996 in Taiwan

The study aim was to estimate the contribution of indoor and outdoor air pollution to the 1-year prevalence of adolescent asthma after personal susceptibility and other potential risk factors were taken into account. A large-scaled cross-sectional study was conducted among 165,173 high school students aged 11 to 16 years in the different communities of Kaohsiung and Pintong in Taiwan, from October 1995 to June 1996. Each student and his/her parents participating in the study completed a video and a written International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire about symptoms of wheezing and allergies, passive smoking, and demographic variables. After adjustment for potential confounders, adolescents exposed to cigarette smoking (odds ratio = 1.29, 95% confidence interval (CI), 1.17-1.42) and environmental tobacco smoke (odds ratio = 1.08, 95% CI, 1.05-1.12) were found to suffer from asthma at an increased frequency. We observed a statistically significant association between outdoor air pollution and asthma, after controlling for potential confound variables. Total suspended particulate, nitrogen dioxide, carbon monoxide, ozone, and airborne dust particles all displayed an independent association with asthma, respectively. There were no selection biases in this community-based study, which provides evidence that passive smoking and long-term, high average outdoor air pollution are independent risk factors of asthma.     

Effect of insurance coverage on the relationship between asthma hospitalizations and exposure to air pollution

OBJECTIVE: Based on the assumption that people without health insurance have limited access to the primary care services needed to prevent unnecessary hospitalizations for asthma, the authors hypothesized that insurance is a factor in the strength of the association between hospital admissions for asthma and exposure to air pollution. They tested this hypothesis with 1991-1994 data from central Los Angeles. METHODS: The authors analyzed the effect of insurance status on the association between asthma-related hospital admissions and exposure to atmospheric particulates (PM10) and ozone (O3) using hospital discharge and air quality data for 1991-1994 for central Los Angeles. They used regression techniques with weighted moving averages (simulating distributed lag structures) to measure the effects of exposure on overall hospital admissions, admissions of uninsured patients, admissions for which MediCal (California Medicaid) was the primary payer, and admissions for which the primary payer was another government or private health insurance program. RESULTS: No associations were found between asthma admissions and O3 exposure. An estimated increase from 1991 to 1994 of 50 micrograms per cubic meter in PM10 concentrations averaged over eight days was associated with an increase of 21.0% in the number of asthma admissions. An even stronger increase--27.4%--was noted among MediCal asthma admissions. CONCLUSIONS: The authors conclude that low family income, as indicated by MediCal coverage, is a better predictor of asthma exacerbations associated with air pollution than lack of insurance and, by implication, a better predictor of insufficient access to primary care.     

Testing selected behaviors to reduce indoor air pollution exposure in young children

Indoor air pollution is responsible for the deaths and illness of millions of young children in developing countries. This study investigated the acceptability (willingness to try) and feasibility (ability to perform) of four indoor air pollution reduction behaviors (improve stove maintenance practices, child location practices, ventilation practices and reduce the duration of solid fuel burning). The study further aimed to identify the motivations for and barriers against modifying the behaviors, the perceived impact of the behaviors on children's respiratory health, and families intention to continue with the behaviors. Thirty families in a rural village of South Africa tried out one or more of the behaviors over a 4-week trial period during winter 2002. Improving stove maintenance and reducing the duration of solid fuel burning proved to be very difficult for most families. It is recommended that the main intervention should focus on improving child location and ventilation practices.     

Long-term exposure to air pollution and the incidence of asthma: meta-analysis of cohort studies

We quantified the association between long-term exposure to air pollution and the incidence of asthma by conducting a systematic review and meta-analysis of cohort studies. Incidence was defined as the incidence of diagnosed asthma or of new wheeze symptom between two assessments or, in birth cohorts followed up to 10 years of age, a lifetime prevalence estimate of asthma or wheeze symptom. We identified 17 cohorts (eight birth cohorts and nine child/adult cohorts) with a total of 99 population-based risk estimates. The studies were heterogeneous in their design and methods of measurement. Follow-up ranged from 3 to 23 years. Most studies were based on within-community exposure contrasts dominated by traffic pollution. Twelve of the cohorts reported at least one positive statistically significant association between air pollution and a measure of incidence. Of the total of 99 estimates, only a minority (29) were positive and statistically significant. Estimates for meta-analysis were chosen a priori using a protocol. For the 13 studies with estimates for nitrogen dioxide (NO₂), the random effects odds ratio was 1.07 (95% CI 1.02 to 1.13) per 10 μg/m³. For five studies with estimates for particulate matter with aerodynamic diameter <2.5 μm (PM_2.5), the random effects estimate was 1.16 (95% CI 0.98 to 1.37) per 10 μg/m³. These estimates were reduced in size and statistical significance by adjustment for publication bias but remained positive. The results are consistent with an effect of outdoor air pollution on asthma incidence. Future meta-analyses would benefit from greater standardisation of cohort methods.     

Improving the linkages between air pollution epidemiology and quantitative risk assessment

Background: Air pollution epidemiology plays an integral role in both identifying the hazards of air pollution as well as supplying the risk coefficients that are used in quantitative risk assessments. Evidence from both epidemiology and risk assessments has historically supported critical environmental policy decisions. The extent to which risk assessors can properly specify a quantitative risk assessment and characterize key sources of uncertainty depends in part on the availability, and clarity, of data and assumptions in the epidemiological studies.Objectives: We discuss the interests shared by air pollution epidemiology and risk assessment communities in ensuring that the findings of epidemiological studies are appropriately characterized and applied correctly in risk assessments. We highlight the key input parameters for risk assessments and consider how modest changes in the characterization of these data might enable more accurate risk assessments that better represent the findings of epidemiological studies.Discussion: We argue that more complete information regarding the methodological choices and input data used in epidemiological studies would support more accurate risk assessments—to the benefit of both disciplines. In particular, we suggest including additional details regarding air quality, demographic, and health data, as well as certain types of data-rich graphics.Conclusions: Relatively modest changes to the data reported in epidemiological studies will improve the quality of risk assessments and help prevent the misinterpretation and mischaracterization of the results of epidemiological studies. Such changes may also benefit epidemiologists undertaking meta-analyses. We suggest workshops as a way to improve the dialogue between the two communities.     

A behavioral intervention to reduce child exposure to indoor air pollution: identifying possible target behaviors.

Indoor air pollution has been causally linked to acute lower respiratory infections in children younger than 5. The aim of this study was to identify target behaviors for a behavioral intervention to reduce child exposure to indoor air pollution by attempting to answer two research questions: Which behaviors are protective of child respiratory health in the study context? and Which behaviors do mothers recommend to reduce their children's exposure to indoor air pollution? Observations and interviews were conducted with 67 mother-child combinations. The authors recommend that four behavioral clusters should be considered for the main intervention. These are to improve stove maintenance practices, to increase the duration that two ventilation sources are opened while a fire is burning, to reduce the time that children spend close to burning fires, and to reduce the duration of solid fuel burning.     

室内颗粒物污染对儿童哮喘的影响

目的探讨室内大气PM_(10)、PM_(2.5)、PM1污染对儿童哮喘的影响。方法采用1∶1成组病例-对照研究,于2015年10月—2016年5月对石河子市80名哮喘儿童和80名健康对照儿童进行问卷调查与室内颗粒物浓度检测,分析儿童哮喘的危险因素。结果两组合计160名儿童的室内PM_(10)、PM_(2.5)、PM1浓度范围分别为26.57~507.30、12.66~159.00、4.53~77.08μg/m~3,其中PM_(10)超标率为61.9%,PM_(2.5)超标率为6.9%。病例组室内空气中的PM_(10)、PM_(2.5)、PM1浓度中位数均高于对照组,差异有统计学意义(P0.01)。多因素logistic回归分析结果显示,儿童有过敏史(OR=5.171)、有环境烟草烟雾(ETS)暴露(OR=2.429)、PM_(2.5)浓度高于中位数(OR=3.459)是儿童哮喘的危险因素,母乳喂养(OR=0.454)是儿童哮喘的保护因素,均有统计学意义(P0.05)。结论儿童有过敏史、ETS暴露和PM_(2.5)暴露可能增加儿童哮喘风险,同时应提倡母乳喂养,以保护儿童呼吸系统健康。     

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.     

Epidemiologic evidence on the relationship between formaldehyde exposure and cancer

Over 30 epidemiologic studies have evaluated cancer risks associated with formaldehyde exposure. Excesses were reported for several sites, leukemia and cancers of the nasal cavities, nasopharynx, lung, and brain generating the greatest interest. The excesses of leukemia and brain and colon cancer found among professionals may not be related to formaldehyde exposure, since similar excesses were not observed among industrial workers. Inconsistencies among and within studies impede assigning formaldehyde a convincing causal role for the excesses of lung cancer found among industrial workers. A causal role for formaldehyde is the most probable for cancers of the nasopharynx and, to a less extent, the nasal cavities. Evidence of exposure-response relationships, the fact that direct contact with formaldehyde may occur at these upper respiratory sites, and the consistency of these findings with experimental studies make this assumption highly probable.     

Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology

BACKGROUND: Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated. OBJECTIVES: We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology. METHODS: We developed geographic information systems (GIS)-based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology. RESULTS: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO(2) exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14-2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48-3.88). Of multiple exposure periods, year-of-diagnosis NO(2) was most predictive of asthma outcomes. CONCLUSIONS: We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.     

Association between hospital emergency visits for asthma and air pollution in Valencia,Spain

OBJECTIVE: To assess the short term effect of concentrations of black smoke, sulphur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O3) in ambient air on emergency room visits for asthma in the city of Valencia, Spain during the period 1994-5. METHODS: Ecological study with time series data and application of Poisson regression. Associations between number of daily emergency visits in a city''s hospital and concentrations of air pollutants were analysed taking into account potential confounding factors by the standardised protocol of the air pollution and health: a European approach (APHEA) project. RESULTS: Mean (range) daily number of emergency room visits for asthma was 1 (0-5). Concentrations of all pollutants studied remained within current air quality standards. The association between an increase of 10 micrograms/m3 in ambient air pollution and asthma, measured as a relative risk (RR) of emergency visits, was significant for NO2 24 hour mean (lag 0, RR 1.076, 95% confidence interval (95% CI) 1.020 to 1.134), NO2 hour maximum (lag 0, RR 1.037, 95% CI 1.008 to 1.066), and O3 hour maximum (lag 1, RR 1.063, CI 95% 1.014 to 1.114). The association was not significant for SO2 or for black smoke during the period analysed. The effects were not significantly different for the time of year, cold months (November to April), or warm months (May to October). CONCLUSIONS: Current concentrations of ambient air pollution in Valencia are significantly associated with emergency room visits for asthma. This association is high and more consistent for NO2 and O3 than for particulate matter and SO2 (classic pollutants).       

Segregation and black/white differences in exposure to air toxics in 1990

I examined non-Hispanic Black and non-Hispanic White differences in exposure to noncriteria air pollutants in 44 U.S. Census Bureau-defined metropolitan areas with populations greater than one million, using data on air toxics concentrations prepared for the U.S. Environmental Protection Agency as part of its Cumulative Exposure Project combined with U.S. census data. I measured differences in exposure to air toxics through the calculation of a net difference score, which is a statistical measure used in income inequality analysis to measure inequality over the whole range of exposures. The scores ranged from 11.52 to 83.60. In every metropolitan area, non-Hispanic Blacks are more likely than non-Hispanic Whites to be living in tracts with higher total modeled air toxics concentrations. To assess potential reasons for such a wide variation in exposure differences, I performed a multiple regression analysis with the net difference score as the dependent variable. Independent variables initially included were as follows: the dissimilarity index (to measure segregation), Black poverty/White poverty (to control for Black/White economic differences), population density and percentage of persons traveling to work who drive to work (alone and in car pools), and percentage of workforce employed in manufacturing (factors affecting air quality). After an initial analysis I eliminated from the model the measures of density and the persons driving to work because they were statistically insignificant, they did not add to the predictive power of the model, and their deletion did not affect the other variables. The final model had an R(2) of 0.56. Increased segregation is associated with increased disparity in potential exposure to air pollution.