急性臭氧暴露对大鼠肺部细胞遗传毒性的影响*

目的: 探讨不同浓度臭氧急性暴露对大鼠肺部细胞的遗传毒性的影响。方法: 36只wistar大鼠随机分为对照组(过滤空气暴露)、臭氧暴露组(0.12 ppm、0.5 ppm、1.0 ppm、2.0 ppm、4.0 ppm)共6组,每组6只。以不同浓度的臭氧对大鼠进行动态染毒4 h后,取肺组织并分离单细胞,采用酶联免疫吸附法检测8-羟基脱氧鸟苷(8-OHdG),利用彗星实验、微核试验和DNA-蛋白质交联实验进行DNA和染色体损伤分析。结果: 与对照组相比,肺组织中8-OHdG含量从臭氧暴露浓度为0.12 ppm起即显著增加,在0.5 ppm时达到最高值。随着臭氧暴露浓度升高,彗星拖尾率逐渐上升,且存在明显的剂量-效应关系;DNA-蛋白质交联率有先升高后下降的趋势,且在2.0 ppm时达到最大值;而肺部细胞微核率尽管呈现出上升趋势,但与对照组相比无显著性差异。结论: 急性臭氧暴露在较低浓度(0.12 ppm)时即可导致大鼠肺部细胞的DNA损伤;而在较高浓度(4 ppm)时却未见显著的染色体损伤。     

利用~(13)C同位素示踪方法测定O_3对水稻C固定和迁移的影响

本研究设置2个臭氧浓度处理,即空气对照(CK,臭氧浓度约4～10 nL·L-1),臭氧浓度升高处理(O3,8 h平均浓度为110 nL·L-1),利用13C同位素示踪的方法,模拟研究了臭氧浓度升高对水稻碳固定和迁移的影响。结果表明:臭氧浓度升高后减少了植株对13C的固定,两次标记时臭氧处理下植株总的13C固定分别比对照处理低37.8%和20.0%;臭氧浓度升高处理1个月和2个月后叶片的13C分配相对于对照而言分别提高了47.3%和37.5%;而臭氧处理则降低了茎和根中的碳分配;臭氧浓度升高后叶的库强有明显的提高,而根的库强则明显降低,茎的库强虽有所降低但不明显;臭氧处理1个月和2个月后植株叶片的相对吸收能力分别比对照显著提高了48.5%和93.3%,臭氧处理下根的相对吸收能力则显著降低。     

臭氧熏气下春小麦叶片脂质过氧化作用的研究

 应用开顶式熏气装置,以低浓度(0.1ppm)的臭氧对春小麦(Triticum aestivum)进行了长时间的熏气,观测到：随着熏气时间的延长,叶片内叶绿素含量下降,丙二醛(MDA)积累增多,膜透性增大。在较高浓度(0.2ppm、0.3ppm、0.4ppm)臭氧熏气下,臭氧浓度越高,叶片内叶绿素降解越快,MDA含量越高,膜透性越大。低浓度和短时间的臭氧熏气可使超氧化物歧化酶(SOD)活性升高,而高浓度和长时间的臭氧熏气则导致SOD活性下降。试验结果表明,由臭氧熏气所引起的植物体内代谢紊乱与诸多伤害是由于脂质过氧化作用的结果。     

臭氧和增温对醉蝶花(Cleome spinosa)氧化伤害及抗氧化酶活的影响

采用开顶箱气室(OTCs)研究不同臭氧浓度(80和160 nmol·mol-1)及增温(比对照的大气温度增加2℃)对园林观赏植物醉蝶花(Cleome spinosa)氧化及抗氧化特性的影响。结果表明:(1)经过160 nmol·mol-1高浓度臭氧急性熏蒸7 d后,醉蝶花叶片出现了明显的伤害症状,叶片表面呈现较大面积的漂白褪绿斑块,其他处理下无明显可见伤害症状;(2)与对照相比,高浓度臭氧(160 nmol·mol-1)处理下醉蝶花叶片丙二醛(MDA)含量、相对电导率、过氧化物酶(POD)活性、超氧化物歧化酶(SOD)活性均分别显著升高175.7%、259.9%、111.4%、54.3%(P0.05),而超氧自由基(O2-·)产生速率显著降低67%(P0.05);臭氧浓度80 nmol·mol-1处理下,MDA含量显著升高65.5%(P0.05),CAT活性显著下降65.9%(P0.05),说明醉蝶花在臭氧浓度80 nmol·mol-1左右时具有较高的臭氧耐受性,而臭氧浓度160 nmol·mol-1左右时植物叶片遭受臭氧胁迫,主要通过增强POD和SOD等抗氧化酶活性来抵御氧化伤害;(3)单独增温导致醉蝶花叶片的MDA含量和相对电导率显著升高62.1%和58.1%(P0.05),但O2-·产生速率和CAT活性显著低于对照(P0.05),分别降低了28.8%和71.1%,POD和SOD活性与对照相比差别不大,可能是增温使植物自身代谢增强产生这种现象;(4)与单独臭氧处理相比(80 nmol·mol-1),臭氧(80 nmol·mol-1)增温复合处理下植物叶片CAT、POD、SOD均分别显著升高141.7%、72.1%、107.9%(P0.05); O2-·产生速率显著下降51%(P0.05),说明臭氧和增温复合处理使醉蝶花遭受的臭氧胁迫加剧。该研究结果可为我国应对高浓度臭氧污染的突发急性事件下的园林及城市绿化植物选择和栽培提供科学依据。     

不同密度下臭氧胁迫对Ⅱ优084水稻光合作用和物质生产的影响—FACE研究

依托中国稻田臭氧FACE(free air ozone concentration enrichment)技术平台,以超级稻Ⅱ优084为供试材料,臭氧设置当前大气臭氧浓度和高臭氧浓度(比前者高50%),移栽密度设置低密度(16穴·m^-2)、中密度(24穴·m^-2)和高密度(32穴·m^-2),研究不同移栽密度条件下近地层臭氧浓度升高对水稻光合作用、物质生产以及茎鞘非结构性碳水化合物浓度和含量的影响.结果表明: 臭氧浓度升高使水稻移栽后63 d、77 d和86 d剑叶SPAD值分别下降6%、11%和13%,均达显著或极显著水平.臭氧胁迫下结实期叶片净光合速率、气孔导度和蒸腾速率的降幅亦随时间推移而明显增加.高臭氧浓度使水稻抽穗至成熟期的物质生产量平均下降46%,从而使最终生物产量下降25%,均达显著水平.臭氧浓度升高使水稻拔节后茎鞘可溶性糖和淀粉的浓度和含量均显著降低,但使抽穗前茎鞘贮藏同化物的转运率大幅增加.方差分析表明,臭氧与密度间的互作对水稻所有测定参数均无显著影响.综上,近地层臭氧浓度升高使超级稻Ⅱ优084生育中后期的光合和生长均明显受抑,但这种抑制作用不受移栽密度的影响.
     

臭氧浓度升高对盆栽小麦根系和土壤微生物功能的影响

模拟研究了臭氧浓度升高（日变化熏蒸方式）对小麦根系和土壤微生物活性的影响。实验分3个处理，即空气对照（CF，臭氧浓度约4～10nl·L^-1），臭氧浓度Ⅰ（OⅠ，8h平均75nl·L^-1），臭氧浓度Ⅱ（OⅡ，8h平均110nl·L^-1）。结果表明，臭氧浓度升高后小麦茎叶、根系生物量以及根冠比都会降低，根系活力更是显著低于空气对照，可见臭氧对植物地下部分的影响是显著的。与对照相比，低浓度O3（75nl·L^-1）对根际土和非根际土的微生物生物量碳没有什么影响；而较高的O3浓度（110nl·L^-1）会造成根际土微生物生物量碳降低9．3％，非根际土微生物生物量碳降低5．3％，说明高浓度臭氧抑制土壤微生物的量。臭氧浓度升高后小麦根际土壤微生物利用单一碳源的能力（AWCD）都明显低于对照；低浓度的臭氧对土壤微生物的多样性指数和丰富度指数都没有显著影响，而浓度较高的臭氧则显著降低了根际土微生物的多样性指数，而对丰富度指数没有显著影响，且也没有发现O3浓度升高对非根际土微生物的影响。可见，臭氧主要影响根际土壤微生物而对非根际土壤微生物影响不大，且只有在高浓度的臭氧处理下才会显著降低根际土壤微生物的多样性指数。     

臭氧胁迫对水稻生长以及C、N、S元素分配的影响

采用开顶式气室(Open-top Chamber, OTC),对水稻"3694繁"(Oryza sativa L., 3694 Fan)在浙江嘉兴进行田间原位臭氧(O₃)熏气实验,研究不同臭氧浓度熏气对水稻生长以及C、N,S元素分配的影响。实验设置分4个水平:过滤大气组(CF,10 nL/L)、自然大气组(NF,40 nL/L)和两个不同浓度的臭氧处理组(O₃-1:100 nL/L; O₃-2:150 nL/L)。主要结果表明:(1)开始臭氧熏气时,各个处理组单茎水稻各组分生物量没有差异. 在熏气后期(水稻成熟期),臭氧处理使单茎水稻根、茎和穗生物量显著下降,根冠比降低,株高显著降低,表明臭氧胁迫增加水稻地上部分的干物质分配,且对株高的影响可能大于对地上生物量的影响;(2)臭氧处理使水稻根和茎C元素含量下降,叶C元素含量上升,表明臭氧胁迫提高了叶片中碳分配,而降低了根和茎的碳分配;(3)各个组分N元素含量上升和碳氮比下降;(4)茎、叶和穗S元素含量上升,可能会增强水稻抗氧化系统的作用,从而抵抗臭氧胁迫。所有实验结果表明臭氧浓度升高会对水稻生长产生严重不利影响,从而导致水稻各个组分的C、N、S元素分配格局发生改变。     

不同秧苗素质和移栽密度条件下臭氧胁迫对水稻光合作用、物质生产和产量的影响

近地层臭氧浓度升高使水稻生长受抑进而使产量下降,但这种影响是否因不同栽培条件而异尚不清楚。2011年依托先进的稻田臭氧FACE(Free Air gas Concentration Enrichment)技术平台,以汕优63为供试材料,臭氧设置大气臭氧浓度(Ambient)和高臭氧浓度(比Ambient高50%),秧苗素质设置弱苗(移栽时无分蘖)和壮苗(移栽时带两个分蘖),移栽密度设置低密度(16穴/m2)、中密度(24穴/m2)和高密度(32穴/m2),研究不同秧苗素质和移栽密度条件下臭氧胁迫对水稻生长和产量的影响。结果表明:高浓度臭氧使水稻结实期叶片SPAD值、净光合速率、气孔导度和蒸腾速率明显下降,但胞间CO2浓度和叶温无显著变化。高浓度臭氧对水稻拔节前物质生产量没有影响,但使拔节至抽穗期、抽穗至成熟期物质生产量平均分别降低13%和29%,进而使成熟期生物产量和籽粒产量均显著下降。方差分析表明,臭氧与秧苗素质间没有互作效应,但臭氧与移栽密度的互作对最终产量的影响达显著水平。以上结果表明,臭氧胁迫使水稻生长后期光合受阻,导致物质生产和产量显著下降;适当增加移栽密度可能会减少臭氧胁迫下水稻产量的损失。     

全身稳恒磁场暴露对糖尿病性动脉粥样硬化大鼠血脂和血液流变学的影响

目的:探索全身暴露强度为4.0 m T中强度稳恒磁场对于糖尿病性动脉粥样硬化的血脂和血液流变学影响,以明确稳恒磁场对糖尿病性动脉粥样硬化的潜在作用效果。方法:选择3月龄雄性SD大鼠30只,随机等分至空白对照组、糖尿病组及糖尿病磁场暴露组。糖尿病和糖尿病磁场暴露组的大鼠采用链脲佐菌素+维生素D3+高脂饮食组合作用法建立糖尿病性动脉粥样硬化大鼠模型,对糖尿病磁场暴露组施加2小时/天、强度为4.0 m T的全身稳恒磁场暴露,连续刺激8周后,检测空腹血糖、血清胰岛素、血脂四项(血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇以及低密度脂蛋白胆固醇)以及血液流变参数(低切全血粘度、中切全血粘度、高切全血粘度以及血浆粘度)。结果:稳恒磁场暴露显著抑制了糖尿病动脉粥样硬化大鼠血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇和低密度脂蛋白胆固醇的升高(P0.05),同时也显著降低了低切、中切和高切全血粘度以及血浆粘度(P0.05),但对血糖和血清胰岛素的影响不显著(P0.05)。结论:中强度稳恒磁场可显著降低糖尿病性动脉粥样硬化大鼠的血脂水平并改善其血液流变学。     

臭氧浓度升高对银杏光合作用的影响

在臭氧浓度升高条件下,采用开顶箱(OTC)方法研究了臭氧浓度升高对沈阳市主要绿化树种银杏光合生理特性的影响.结果表明,与对照相比,高浓度(80±8 nmol·mol-1)臭氧处理下,银杏叶片净光合速率显著降低.处理50 d时,降低幅度为33.90%(P＜0.01),类胡萝卜素含量显著增加(P＜0.05);叶绿素a、叶绿素b与叶绿素(a b)含量变化复杂,叶绿素a/b值则先降低后升高;可溶性糖含量无明显变化,而淀粉含量则随着处理时间的延长显著降低;可溶性蛋白含量低于对照,并随着处理时间延长下降幅度增大;叶片中丙二醛含量随着处理时间显著增加.处理80 d时,丙二醛含量增加了79.53%.光合作用的下降与叶绿素的变化无关,主要与膜脂过氧化有关.光合作用的下降导致了可溶性蛋白质和淀粉的减少,并最终导致生长缓慢.     

Ozone inhibits prostacyclin synthesis in pulmonary endothelium

The effects of ozone on lung arachidonate metabolism in-vitro were studied in cultured bovine pulmonary endothelial cells exposed for 2 hours to ozone in concentrations up to 1.0 ppm. A concentration-dependent decrease in prostacyclin synthesis was found (90% decrease at the highest ozone level of 1.0 ppm). The inhibition of prostacyclin synthesis was not due to a decreased release of arachidonic acid from membrane lipids. We also examined the hypoxic pulmonary vasoconstrictive response to 10% oxygen inhalation in anesthetized dogs in-vivo after exposure to 1.0 ppm ozone for 1 hour. Pulmonary vascular resistance was significantly increased after ozone exposure, similar to the findings in dogs given indomethacin (15 mg/kg). The percentage change in the hypoxic pulmonary pressor response was similar between the ozone exposure and indomethacin-treated groups, although due to the variance of the pulmonary vascular resistance values during hypoxia the results did not reach statistical significance. These results suggest that ozone inhalation affects pulmonary endothelial arachidonate metabolism in-vivo as well as in-vitro.     

Chromosome damage in rat pulmonary alveolar macrophages following ozone inhalation

To determine whether ozone is clastogenic at environmentally relevant exposure levels, rats were exposed for 6 h to 0.0, 0.12, 0.27, or 0.80 ppm ozone. The alveolar macrophages were isolated from animals sacrificed 28 h after the end of the exposure. The mitotic index and frequency of chromosome aberrations were determined. No change in the mitotic index was detected following 0.12 ppm ozone exposure. A significant decrease in mitotic index was observed after exposure to 0.27 ppm ozone; a significant (4-fold) increase in the frequency of dividing macrophages was detected following exposure to 0.8 ppm ozone. Only chromatid-type aberrations were observed. There was a significant increase in the frequency of cells with chromatid gaps and in the frequency of cells with chromatid deletions. Animals exposed to 0.27 ppm ozone had the highest proportion of cells with chromatid deletions (0.172) relative to background level (0.028). No exchanges or chromosome-type aberrations were detected in any of the animals. These data suggest that ozone, at relatively low levels, is clastogenic in macrophages from exposed rats.     

血清HCY、MMP-9、NT-proBNP水平与老年2型糖尿病大血管病变的相关性研究

目的:探讨血清同型半胱氨酸(HCY)、金属蛋白酶9(MMP-9)、N-端B型钠利尿肽(NT-pro BNP)变化与老年2型糖尿病大血管病变的关系。方法:选取我院2014年5月至2016年5月收治的老年2型糖尿病患者50例,依据大血管病变发生情况将其分为合并大血管病变组(A组,n=25)和未合并大血管病变组(B组,n=25),另选取同期来我院进行体检的健康人员50例作为对照组,比较三组的一般临床资料、血清HCY、MMP-9、NT-pro BNP水平。结果:A组患者的收缩压、舒张压、空腹血糖(FBG)、餐后2h血糖(2h BG)水平均显著高于B组(P0.05),高密度脂蛋白胆固醇(HDL-C)水平显著低于B组(P0.05),但三组患者的性别、年龄、体质量指数(BMI)、糖化血红蛋白(Hb A1c)、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)水平比较差异均无统计学意义(P0.05)。A组、B组患者的BMI、收缩压、舒张压、FBG、2h BG、Hb A1c、TG、TG、LDL-C水平均显著高于对照组(P0.05),LDL-C水平均显著低于对照组(P0.05),但三组人员的性别、年龄比较差异均无统计学意义(P0.05)。A组患者的血清HCY、MMP-9、NT-pro BNP水平均显著高于B组(P0.05);A组、B组患者的HCY、MMP-9、NT-pro BNP水平均显著高于对照组(P0.05)。结论:血清HCY、MMP-9、NT-pro BNP水平与老年2型糖尿病的大血管病变显著相关。     

Ozone inhibits endothelial cell cyclooxygenase activity through formation of hydrogen peroxide

We have previously demonstrated that a 2H exposure of cultured pulmonary endothelial cells to ozone (0.0-1.0 ppm) in-vitro resulted in a concentration-dependent reduction of endothelial prostacyclin production (90% decrease at the 1.0 ppm level). Ozone-exposed endothelial cells, incubated with 20 uM arachidonate, also demonstrated a significant inhibition of prostacyclin synthesis. To further examine the mechanisms of the inhibition of prostacyclin synthesis, bovine pulmonary endothelial cells were exposed to 1.0 ppm ozone for 2H. A significant decrease in prostacyclin synthesis was found within 5 min of exposure (77 +/- 36% of air-exposed control values, p less than 0.05). Endothelial prostacyclin synthesis returned to baseline levels by 12H after ozone exposure, a time point which was similar to the recovery time of unexposed endothelium treated with 0.5 uM acetylsalicylic acid. Incubation of endothelial cells, previously exposed to 1.0 ppm ozone for 2 hours, with 4 uM PGH2 resulted in restoration of essentially normal prostacyclin synthesis. When endothelial cells were co-incubated with catalase (5 U/ml) during ozone exposure, no inhibition of prostacyclin synthesis was observed. Co-incubation with either heat-inactivated catalase or superoxide dismutase (10 U/ml) did not affect the ozone-induced inhibition of prostacyclin synthesis. These data suggest that H2O2 is a major toxic species produced in endothelial cells during ozone exposure and responsible for the inhibition of endothelial cyclooxygenase activity.     

Role of interleukin-6 in murine airway responses to ozone

This study sought to examine the role of interleukin-6 (IL-6) in ozone (O(3))-induced airway injury, inflammation, and hyperresponsiveness (AHR). Subacute (72 h) exposure to 0.3 ppm O(3) significantly elevated bronchoalveolar lavage fluid (BALF) protein, neutrophils, and soluble TNF receptors (sTNFR1 and sTNFR2) in wild-type C57BL/6 (IL-6(+/+)) mice; however, all four outcome indicators were significantly reduced in IL-6-deficient (IL-6(-/-)) compared with IL-6(+/+) mice. Acute O(3) exposure (2 ppm for 3 h) increased BALF protein, KC, macrophage inflammatory protein(MIP)-2, eotaxin, sTNFR1, and sTNFR2 in IL-6(+/+) mice. However, MIP-2 and sTNFR2 were not significantly increased following O(3) exposure in IL-6(-/-) mice. Increases in BALF neutrophils induced by O(3) (2 ppm for 3 h) were also significantly reduced in IL-6(-/-) vs. IL-6(+/+) mice. Airway responsiveness to methacholine was measured by whole body plethysmography before and following acute (3 h) or subacute (72 h) exposure to 0.3 ppm O(3). Acute O(3) exposure caused AHR in both groups of mice, but there was no genotype-related difference in the magnitude of O(3)-induced AHR. AHR was absent in mice of either genotype exposed for 72 h. Our results indicate that IL-6 deficiency reduces airway neutrophilia, as well as the levels of BALF sTNFR1 and sTNFR2 following acute high dose and/or subacute low-dose O(3) exposure, but has no effect on O(3)-induced AHR.     

Ozone inhibits endothelial cell cyclooxygenase activity through formation of hydrogen peroxide

We have previously demonstrated that a 2H exposure of cultured pulmonary endothelial cells to ozone (0.0–1.0 ppm) resulted in a concentration-dependent reduction of endothelial prostacyclin production (90% decrease at the 1.0 ppm level). Ozone-exposed endothelial cells, incubated with 20 uM arachidonate, also demonstrated a significant inhibition of prostacyclin synthesis. To further examine the mechanisms of the inhibition of prostacyclin synthesis, bovine pulmonary endothelial cells were exposedto 1.0 ppm ozone for 2H. A significant decease in protacyclin synthesis was found within 5 min of exposure (77 ± 36% of air-exposed control values, p < 0.05). Endothelial prostacyclin synthesis returned to baseline levels by 12H after ozone exposure, a time point which was similar to the recovery time of unexposed endothelium treated with 0.5 uM acetylsalicylic acid. Incubation of endothelial cells, previously exposed to 1.0 ppm ozone for 2 hours, with 4 uM PGH₂ resulted in restoration of essentially normal prostacyclin synthesis. When endothelial cells were co-incubated with catalase (5U/ml) during ozone exposure, no inhibition of prostacycline synthesis was observed. Co-incubation with either heat-inactivated catalase or superoxide dismutase (10U/ml) did not affect the ozone-induced inhibition of prostacycline synthesis. These data suggest that H₂O₂ is a major toxic species produced in endothelial cells during ozone exposure and responsible for the inhibiton of endothelial cyclooxygenase activity.     

血压、血脂、血糖、同型半胱氨酸及超敏C反应蛋白水平与脑梗死发病危险性的关系

目的:探讨血压、血脂、血糖、糖化血红蛋白、同型半胱氨酸(HCY)和超敏C反应蛋白(hs-CRP)与脑梗死发病危险性的相关性,为及时防止脑梗死的发病及早期诊断脑梗死提供理论依据。方法:采用回顾性病例对照研究,用全自动生化分析仪器检测各项生化指标,并运用SPSS 20.0软件包对256例脑梗死患者和216例健康对照者的血生化指标进行统计分析。同时,将脑梗死组分为三组:单纯脑梗死组、合并高血压组、合并糖尿病组,分别与正常对照组进行血脂水平的分析比较。结果:血压、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇酯(HDL-C)、同型半胱氨酸(HCY)、血糖、hs-CRP水平和总胆固醇/高密度脂蛋白胆固醇(TC/HDL-C)比值在病例组和对照组间有显著性差异(P0.05)。同时,在三组不同的病例组中血脂(TC、TG、LDL-C、TC/HDL-C)水平和HCY水平明显高于正常对照组,而HDL-C水平则明显低于对照组。(P0.05)。结论:高血压、高血糖、HCY、hs-CRP水平增高及血脂异常均与脑梗死发病危险性相关,联合检测上述指标对预防及治疗脑梗死均有重要意义。     

Peripheral Blood Neutrophilia as a Biomarker of Ozone-Induced Pulmonary Inflammation

Background

Ozone concentrations are predicted to increase over the next 50 years due to global warming and the increased release of precursor chemicals. It is therefore urgent that good, reliable biomarkers are available to quantify the toxicity of this pollutant gas at the population level. Such a biomarker would need to be easily performed, reproducible, economically viable, and reflective of ongoing pathological processes occurring within the lung.

Methodology

We examined whether blood neutrophilia occurred following a controlled ozone challenge and addressed whether this could serve as a biomarker for ozone-induced airway inflammation. Three separate groups of healthy subjects were exposed to ozone (0.2 ppm, 2h) and filtered air (FA) on two separate occasions. Peripheral blood samples were collected and bronchoscopy with biopsy sampling and lavages was performed at 1.5h post exposures in group 1 (n=13), at 6h in group 2 (n=15) and at 18h in group 3 (n=15). Total and differential cell counts were assessed in blood, bronchial tissue and airway lavages.

Results

In peripheral blood, we observed fewer neutrophils 1.5h after ozone compared with the parallel air exposure (-1.1±1.0x10⁹ cells/L, p<0.01), at 6h neutrophil numbers were increased compared to FA (+1.2±1.3x10⁹ cells/L, p<0.01), and at 18h this response had fully attenuated. Ozone induced a peak in neutrophil numbers at 6h post exposure in all compartments examined, with a positive correlation between the response in blood and bronchial biopsies.

Conclusions

These data demonstrate a systemic neutrophilia in healthy subjects following an acute ozone exposure, which mirrors the inflammatory response in the lung mucosa and lumen. This relationship suggests that blood neutrophilia could be used as a relatively simple functional biomarker for the effect of ozone on the lung.     

Pulmonary response to threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm)

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25-75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25-75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.