Associations of urinary polycyclic aromatic hydrocarbon metabolites with fractional exhaled nitric oxide and exhaled carbon monoxide: A cross-sectional study.

来自 PUBMED

作者:

Zhou YLiu YSun HMa JXiao LCao LLi WWang BYuan JChen W

展开

摘要:

Exposure to Polycyclic aromatic hydrocarbons (PAHs) has been associated with inflammatory responses. Fractional exhaled nitric oxide (FeNO) and exhaled carbon monoxide (eCO) are both important inflammatory mediators especially in airways. However, few studies have investigated associations of PAH exposures with FeNO or eCO. Therefore, we aimed to quantify the associations of urinary PAH metabolites with FeNO and eCO levels, and investigate their potential effect modifiers by linear mixed models among 4133 participants from the Wuhan-Zhuhai cohort in China. We further performed stratified analyses to estimate effect modification. We found significant associations of increased urinary PAH metabolites with elevated eCO and FeNO. Among all participants, each 1% increase of 1-hydroxynaphthalene, 2-hydroxynaphthalene, 2-hydroxyfluorene, 4-hydroxyphenanthrene, 3-hydroxyphenanthrene, and total PAH metabolites was significantly associated with a 12.6% (95% confidence interval: 9.3%, 15.9%), 9.7% (6.5%, 12.9%), 7.5% (4.1%, 10.9%), 3.2% (0.2%, 6.2%), 2.7% (0.1%, 5.3%), and 6.5% (2.7%, 10.4%) increased eCO level, respectively; while each 1% increase of urinary 1-hydroxynaphthalene, 9-hydroxyphenanthrene, 3-hydroxyphenanthrene, and 2-hydroxyphenanthrene was associated with a -3.0% (-5.8%, -0.2%), 2.9% (0.3%, 5.6%), 3.2% (1.0%, 5.4%), and 4.5% (2.2%, 6.9%) change of FeNO level, respectively. Positive associations between certain urinary PAH metabolites and eCO were observed among both ever-smokers and non-smokers, and the associations were stronger among ever-smokers than that among non-smokers. Increased urinary PAH metabolites were associated with decreased FeNO among ever-smokers and elevated FeNO levels among non-smokers. Our findings suggest that PAH exposures may impair airway through inducing inflammatory response, especially among ever-smokers.

收起

展开

DOI:

10.1016/j.scitotenv.2017.10.294

被引量:

5

年份:

1970

SCI-Hub (全网免费下载) 发表链接

通过 文献互助 平台发起求助,成功后即可免费获取论文全文。

查看求助

求助方法1:

知识发现用户

每天可免费求助50篇

求助

求助方法1:

关注微信公众号

每天可免费求助2篇

求助方法2:

求助需要支付5个财富值

您现在财富值不足

您可以通过 应助全文 获取财富值

求助方法2:

完成求助需要支付5财富值

您目前有 1000 财富值

求助

我们已与文献出版商建立了直接购买合作。

你可以通过身份认证进行实名认证,认证成功后本次下载的费用将由您所在的图书馆支付

您可以直接购买此文献,1~5分钟即可下载全文,部分资源由于网络原因可能需要更长时间,请您耐心等待哦~

身份认证 全文购买

相似文献(255)

参考文献(0)

引证文献(5)

来源期刊

-

影响因子:暂无数据

JCR分区: 暂无

中科院分区:暂无

研究点推荐

关于我们

zlive学术集成海量学术资源,融合人工智能、深度学习、大数据分析等技术,为科研工作者提供全面快捷的学术服务。在这里我们不忘初心,砥砺前行。

友情链接

联系我们

合作与服务

©2024 zlive学术声明使用前必读