EVALUATION OF A POSSIBLE ASSOCIATION OF URBAN AIR TOXICS AND ASTHMA
EVALUATION OF A POSSIBLE ASSOCIATION OF URBAN AIR TOXICS AND ASTHMA
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DOI：
10.2307/3432382
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发表时间：
1995-09-01
影响因子：
10.4
通讯作者：
BUNCHER, CR
中科院分区：
文献类型：
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作者：
LEIKAUF, GD;KLINE, S;BUNCHER, CR
哮喘的患病率，无论是住院的频率或归因于哮喘的死亡人数，在过去的15至20年增加。疾病流行率的迅速增加更可能归因于环境因素而不是遗传因素。从过去空气污染和哮喘之间的联系推断。周围环境的变化可能导致发病率和死亡率的增加。然而，对空气污染和哮喘恶化之间联系的科学评估还不完整。目前，标准污染物[SOx，NOx，O-3，CO，Pb，颗粒物（PM（10））]和其他风险因素（暴露于环境烟草烟雾。挥发性有机化合物等）正在不断评估他们对这种情况可能作出的贡献。这些研究的数据表明，呼吸道疾病的增加与暴露于环境中的颗粒和气体污染物浓度有关。同样。暴露于环境烟草烟雾，也是一种颗粒和气体空气毒物的混合物，与儿童哮喘的增加有关。此外，目前的有害健康影响与现有污染测量的关联，往往是在浓度低于那些产生影响的控制动物和人类接触到每一种污染物单独。这些发现意味着，当人们暴露于颗粒和气体的刺激性混合物时，不良反应会增加，并且目前对空气污染的测量部分是间接的，因为标准污染物的浓度是我们暴露于复杂混合物的替代品。其他刺激性空气污染物。包括某些城市空气毒物，与职业环境中的哮喘有关，并可能与环境空气中的标准污染物相互作用，加剧哮喘。因此，需要对城市空气毒物的剂量反应信息和作为哮喘可能贡献者的生物学可行性进行评估。然而，由于缺乏关于这些化合物在环境空气中的浓度及其对哮喘发病率和死亡率的影响的信息，这一评价变得更加复杂。通过对目前毒理学文献的初步审查，我们提出了一个可能对哮喘和呼吸系统健康产生最大影响的30种化合物的暂定清单。这些化合物的选择是基于它们在职业和非职业环境中诱导或加重哮喘的能力，它们的过敏潜力和与生物大分子反应的能力，以及它们刺激呼吸道的能力。我们建议通过常规空气采样和总暴露评估更好地记录这些化合物的暴露情况，并通过专门针对这些物质在哮喘诱导和加重中所起作用的实验室和流行病学研究进一步评估生物学机制。
The prevalence of asthma, measured either as the frequency of hospital admissions or number of deaths attributed to asthma, has increased over the last 15 to 20 years. Rapid increases in disease prevalence are more likely to be attributable to environmental than genetic factors. inferring from past associations between air pollution and asthma. it is feasible that changes in the ambient environment could contribute to this increase in morbidity and mortality. Scientific evaluation of the links between air pollution and the exacerbation of asthma is incomplete, however. Currently, criteria pollutants [SOx, NOx, O-3, CO, Pb, particulate matter (PM(10))] and other risk factors (exposure to environmental tobacco smoke. volatile organic compounds, etc.) are constantly being evaluated as to their possible contributions to this situation. Data from these studies suggest that increases in respiratory disease are associated with exposures to ambient concentrations of particulate and gaseous pollutants. Similarly. exposure to environmental tobacco smoke, also a mixture of particulate and gaseous air toxics, has been associated with an increase in asthma among children. In addition, current associations of adverse health effects with existing pollution measurements are often noted at concentrations below those that produce effects in controlled animal and human exposures to each pollutant alone. These findings imply that adverse responses are augmented when persons are exposed to irritant mixtures of particles and gases and that current measurements of air pollution are, in part, indirect in that the concentrations of criteria pollutants are acting as surrogates of our exposure to a complex mixture. Other irritant air pollutants. including certain urban air toxics, are associated with asthma in occupational settings and may interact with criteria pollutants in ambient air to exacerbate asthma. An evaluation of dose-response information for urban air toxics and biological feasibility as possible contributors to asthma is therefore needed. However, this evaluation is compounded by a lack of information on the concentrations of these compounds in the ambient air and their effects on asthma morbidity and mortality. Through an initial review of the current toxicological literature, we propose a tentative list of 30 compounds that could have the highest impact on asthma and respiratory health. These compounds were selected based on their ability to induce or exacerbate asthma in occupational and nonoccupational settings, their allergic potential and ability to react with biological macromolecules, and lastly, their ability to irritate the respiratory passages. We recommend better documentation of exposure to these compounds through routine air sampling and evaluation of total exposure and further evaluation of biological mechanisms through laboratory and epidemiological studies directed specifically at the role these substances play in the induction and exacerbation of asthma.