Ultman James S, Ben-Jebria Abdellaziz, Arnold Steven F
Department of Chemical Engineering, Pennsylvania State University, University Park, Pennsylvania, USA.
Res Rep Health Eff Inst. 2004 Nov(125):1-23; discussion 25-30.
The primary hypothesis of this study was that intersubject variation in uptake of inhaled ozone causes corresponding variation in the resulting physiologic response. The second hypothesis was that differences in breathing pattern and lung anatomy induce differences in ozone uptake. Sixty healthy nonsmokers participated in three exposure protocols during which their minute ventilation was 30 L/min, corresponding to moderate exercise. For the intermittent bolus exposure to ozone (BO3*), we measured the penetration volume at which 50% of the bolus was taken up (VP50%). Before and after continuous clean air exposure (Ca) and continuous ozone exposure (CO3: 0.25 ppm ozone), we measured forced expiratory volume in 1 second (FEV1), calculated as the percent change after exposure relative to start of exposure [%FEV1]). We also measured the cross-sectional area of the peripheral lung (Ap) for carbon dioxide (CO2) diffusion, calculated as the percent change after exposure relative to start of exposure (%Ap). After the CO3 session, we also measured ozone uptake (as ozone uptake rate) and fractional ozone uptake efficiency. Uptake efficiency ranged from 0.70 to 0.98 among all subjects. It was inversely correlated with breathing frequency (P = 0.000) but was not correlated with conducting airways volume (P = 0.333). VP50% ranged from 67 to 135 mL among all subjects and was directly correlated with conducting airways volume (P = 0.000). These results indicate that overall ozone uptake was related to breathing frequency but not to airway size, whereas internal distribution of ozone shifted distally as airway size increased. Values of %FEV1 (mean +/- SD: -13.71 +/- 12.99) and %Ap (-7.80 +/- 9.34) were both significantly more negative (P = 0.000) in the CO3 session than in the Ca (control) session (-0.055 +/- 4.57 and 0.40 +/- 11.03, respectively). Ozone uptake rate correlated with individual %Ap (P = 0.008) but not with individual %FEV1 (P = 0.575). Nor were individual %Ap or %FEV1 correlated with VP50%. Therefore, ozone uptake did not explain intersubject differences in forced expiratory responses in this study, but it did partially explain differences in the cross-sectional area available for gas diffusion in the peripheral lung.
本研究的主要假设是,吸入臭氧摄取的个体间差异会导致相应的生理反应差异。第二个假设是,呼吸模式和肺部解剖结构的差异会导致臭氧摄取的差异。60名健康非吸烟者参与了三个暴露方案,在此期间他们的分钟通气量为30升/分钟,相当于适度运动。对于间歇性推注臭氧暴露(BO3*),我们测量了50%推注量被摄取时的渗透体积(VP50%)。在连续清洁空气暴露(Ca)和连续臭氧暴露(CO3:0.25 ppm臭氧)之前和之后,我们测量了1秒用力呼气量(FEV1),计算为暴露后相对于暴露开始时的变化百分比[%FEV1])。我们还测量了用于二氧化碳(CO2)扩散的外周肺横截面积(Ap),计算为暴露后相对于暴露开始时的变化百分比(%Ap)。在CO3阶段之后,我们还测量了臭氧摄取(作为臭氧摄取率)和分数臭氧摄取效率。所有受试者的摄取效率范围为0.70至0.98。它与呼吸频率呈负相关(P = 0.000),但与传导气道容积无关(P = 0.333)。所有受试者的VP50%范围为67至135毫升,与传导气道容积呈正相关(P = 0.000)。这些结果表明,总体臭氧摄取与呼吸频率有关,而与气道大小无关,而随着气道大小增加,臭氧的内部分布向远端转移。CO3阶段的%FEV1值(平均值±标准差:-13.71±12.99)和%Ap值(-7.80±9.34)均比Ca(对照)阶段(分别为-0.055±4.57和0.40±11.03)显著更负(P = 0.000)。臭氧摄取率与个体%Ap相关(P = 0.008),但与个体%FEV1无关(P = 0.575)。个体%Ap或%FEV1也与VP50%无关。因此,在本研究中,臭氧摄取并不能解释受试者间用力呼气反应的差异,但它确实部分解释了外周肺中可用于气体扩散的横截面积的差异。