• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文OA文献 >Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.
【2h】

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

机译：哮喘和空气中毒暴露的流行病学证据：职业，室内和社区空气污染研究之间的联系。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

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.
机译：社区中室外空气污染物的暴露与急性加重和哮喘的发作有关。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。与哮喘相关的职业暴露可能会为环境空气污染中的因果关系提供线索，因为这种暴露通常可以识别为单一化学试剂（例如金属化合物）。但是，将职业转化为社区暴露-反应关系是有限的。在发现引起职业性哮喘的空气毒性中，在对室内空气的过敏性呼吸反应的流行病学研究中，经常仅对甲醛进行研究，尽管环境暴露水平较低，但仍显示出总体一致性。与职业性哮喘相关的特定挥发性有机化合物（VOC）通常与研究表明挥发性有机化合物对非职业性成人和小儿哮喘有呼吸作用的研究不同。此外，实验证据表明，与柴油机排气颗粒（DEP）关联的机载多环芳烃（PAH）暴露对呼吸道具有促炎作用，但从职业文献中没有足够的支持证据表明DEP对哮喘或肺功能有影响。相比之下，非职业流行病学研究经常表明，过敏反应或哮喘与暴露于含有PAH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（尤其是卡车交通）和环境烟草烟雾）之间的关联。在这些关联中，其他粒子相和气态共同污染物也可能是因果关系。需要对哮喘发作和恶化与空气污染之间的关系进行流行病学研究，以消除空气中毒物与受监测标准空气污染物（如颗粒质量）的影响。社区研究应基于生物学机制，尤其是哮喘发作和加重的刺激性和免疫学途径，着重研究预期会对呼吸系统产生不利影响的空气毒性。

著录项

  • 作者

    Delfino, Ralph J;

  • 作者单位
  • 年度 2001
  • 总页数
  • 原文格式 PDF
  • 正文语种 {"code":"en","name":"English","id":9}
  • 中图分类

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号