Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.
Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.
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DOI：
10.1289/ehp.02110s4573
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发表时间：
2002-08
影响因子：
10.4
通讯作者：
Delfino RJ
中科院分区：
文献类型：
--
作者：
Delfino RJ
社区室外环境空气污染物暴露与哮喘急性加重和可能发病有关。然而，污染物混合物的复杂性和哮喘的病因异质性使得很难确定这些混合物中的因果成分。与哮喘相关的职业性暴露可提供环境空气污染中因果成分的线索，因为这种暴露通常可识别为单一化学物（例如，金属化合物）。然而，将职业暴露-反应关系转化为社区暴露-反应关系是有限的。在导致职业性哮喘的空气毒性物质中，只有甲醛在室内空气过敏呼吸反应的流行病学研究中经常被调查，尽管环境暴露量较低，但总体上可以显示出一致性。与职业性哮喘相关的特定挥发性有机化合物（VOCs）通常与显示VOC混合物对非职业成人和儿童哮喘呼吸影响的研究不同。此外，实验证据表明，与柴油废气颗粒（DEPs）相关的空气中多环芳烃（PAH）暴露对气道有促炎作用，但DEPs对哮喘或肺功能的影响在职业文献中没有足够的支持证据。相反，非职业流行病学研究经常显示，过敏反应或哮喘与暴露于含有多环芳烃成分的环境空气污染物混合物（包括黑烟、高家庭或学校交通密度（特别是卡车交通）和环境烟草烟雾）之间存在关联。其他颗粒相和气体共污染物也可能是这些关联的原因。需要对哮喘发作和加重与空气污染的关系进行流行病学研究，以便将空气毒物的影响与监测的标准空气污染物（如颗粒质量）区分开来。社区研究应侧重于根据生物学机制，特别是哮喘发作和恶化的刺激物和免疫途径，预计会对呼吸系统产生不利影响的空气有毒物质。
Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.
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DOI：
10.1164/ajrccm.158.1.9710101
发表时间：
1998-07-01
影响因子：
24.7
作者：
Abbey, DE;Burchette, RJ;Enright, PL
通讯作者：
Enright, PL
DOI：
10.1080/00039896.1984.10545870
发表时间：
1984-01-01
期刊：
ARCHIVES OF ENVIRONMENTAL HEALTH
影响因子：
--
作者：
AMES, RG;REGER, RB;HALL, DS
通讯作者：
HALL, DS
影响因子：
2.8
作者：
Behrendt, H;Becker, WM;Ring, J
通讯作者：
Ring, J
影响因子：
14.2
作者：
Barnes, PJ
通讯作者：
Barnes, PJ
影响因子：
9.6
作者：
Berglund, DJ;Abbey, DE;McDonnell, WF
通讯作者：
McDonnell, WF