Columbia University Medical Center, PH 9 East, Room 105, 630 West 168th Street, New York, NY 10032, USA.
Ann Intern Med. 2010 Feb 16;152(4):201-10. doi: 10.7326/0003-4819-152-4-201002160-00004.
Cigarette smoking is the major cause of chronic obstructive pulmonary disease, but studies on the contribution of other smoking techniques are sparse.
To determine whether pipe and cigar smoking was associated with elevated cotinine levels, decrements in lung function, and increased odds of airflow obstruction.
Cross-sectional study.
Population-based sample from 6 U.S. communities.
Men and women aged 48 to 90 years without clinical cardiovascular disease at enrollment who were part of MESA (Multi-Ethnic Study of Atherosclerosis).
The MESA Lung Study measured spirometry according to American Thoracic Society guidelines and urine cotinine levels by immunoassay on a subsample of MESA. Pipe-years and cigar-years were calculated as years from self-reported age of starting to age of quitting (or to current age in current users) multiplied by pipe-bowls or cigars per day.
Of 3528 participants, 9% reported pipe smoking (median, 15 pipe-years), 11% reported cigar smoking (median, 6 cigar-years), and 52% reported cigarette smoking (median, 18 pack-years). Self-reported current pipe and cigar smokers had elevated urine cotinine levels compared with never-smokers. Pipe-years were associated with decrements in FEV(1), and cigar-years were associated with decrements in the FEV(1)-FVC ratio. Participants who smoked pipes or cigars had increased odds of airflow obstruction whether they had also smoked cigarettes (odds ratio, 3.43 [95% CI, 1.75 to 6.71]; P < 0.001) or not (odds ratio, 2.31 [CI, 1.04 to 5.11]; P = 0.039) compared with participants with no smoking history.
Cross-sectional design.
Pipe and cigar smoking increased urine cotinine levels and was associated with decreased lung function and increased odds of airflow obstruction, even in participants who had never smoked cigarettes.
National Heart, Lung, and Blood Institute, National Institutes of Health.
吸烟是慢性阻塞性肺疾病的主要原因，但关于其他吸烟方式的研究却很少。
确定烟斗和雪茄烟是否与更高的可替宁水平、肺功能下降以及气流阻塞几率增加有关。
横断面研究。
来自美国 6 个社区的基于人群的样本。
在 MESA（动脉粥样硬化多民族研究）入组时无临床心血管疾病的 48 至 90 岁男性和女性。
MESA 肺研究根据美国胸科学会指南测量肺活量，并在 MESA 的一个子样本中通过免疫测定测量尿液可替宁水平。烟斗年和雪茄年的计算方法是从自我报告的开始吸烟年龄到戒烟年龄（或当前使用者的当前年龄）乘以每天的烟斗碗数或雪茄数。
在 3528 名参与者中，9%报告吸烟斗（中位数为 15 年烟斗年），11%报告吸雪茄（中位数为 6 年雪茄年），52%报告吸烟卷烟（中位数为 18 包年）。与从不吸烟者相比，自我报告的当前烟斗和雪茄吸烟者尿液中的可替宁水平升高。烟斗年与 FEV1 的下降有关，而雪茄年与 FEV1/FVC 比值的下降有关。无论是否还吸烟，吸烟斗或雪茄的参与者气流阻塞的几率都高于没有吸烟史的参与者（比值比，3.43[95%CI，1.75 至 6.71]；P<0.001）或不吸烟者（比值比，2.31[CI，1.04 至 5.11]；P=0.039）。
横断面设计。
烟斗和雪茄烟吸烟增加了尿液中的可替宁水平，并与肺功能下降和气流阻塞几率增加有关，即使在从未吸烟的参与者中也是如此。
美国国立卫生研究院国家心肺血液研究所。
