***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVES : To identify whether acute lung function effects of ozone can be modulated by antioxidant vitamin supplementation . METHODS : Amateur cyclists ( n = 26 ) were studied in the summer of 1994 in The Netherl and s. Repeated lung function measurements were performed with a rolling seal spirometer after training sessions or competitive races on four to 14 occasions . The cyclists were assigned to two study groups . The supplementation group ( n = 12 ) received antioxidant supplements ( 15 mg beta-carotene , 75 mg vitamin E , and 650 mg vitamin C ) once a day for three months . The control group did not receive supplementation . For each subject , lung function after exercise was regressed on the previous eight hour mean ozone concentration . The individual regression coefficients were pooled for each study group and weighted with the inverse of the variance . RESULTS : The eight hour mean ozone concentration was 101 micrograms/m3 ( 30 to 205 micrograms/m3 ) . For the supplementation group , there was no effect of ozone on FVC , FEV1 , peak expiratory flow ( PEF ) , and maximal mid-expiratory flow ( MMEF ) . For the control group the mean coefficients were negative , except for MMEF . The difference between the groups was 2.08 ( 95 % confidence interval ( 95 % CI ) 1.31 to 2.85 ) ml/microgram/m3 for FVC , 1.66 ( 95 % CI 0.62 to 2.70 ) for FEV1 , 6.83 ( 95 % CI 3.17 to 10.49 ) for PEF , and 0.42 ( 95 % CI -1.38 to 2.22 ) for MMEF . CONCLUSION : The results suggest that antioxidant vitamin supplementation protects against acute effects of ozone on lung function in heavily exercising amateur cyclists The aim of this study was to investigate whether the acute effects of ozone on lung function could be modulated by antioxidant vitamin supplementation in a placebo-controlled study . Lung function was measured in Dutch bicyclists ( n = 38 ) before and after each training session on a number of occasions ( n = 380 ) during the summer of 1996 . The vitamin group ( n = 20 ) received 100 mg of vitamin E and 500 mg of vitamin C daily for 15 weeks . The average ozone concentration during exercise was 77 microg/m3 ( range , 14 - 186 microg/m3 ) . After exclusion of subjects with insufficient compliance from the analysis , a difference in ozone exposure of 100 microg/m3 decreased forced expiratory volume in 1 second ( FEV1 ) 95 ml ( 95 % confidence interval ( CI ) -265 to -53 ) in the placebo group and 1 ml ( 95 % CI -94 to 132 ) in the vitamin group ; for forced vital capacity , the change was -125 ml ( 95 % CI -384 to -36 ) in the placebo group and -42 ml ( 95 % CI -130 to 35 ) in the vitamin group . The differences in ozone effect on lung function between the groups were statistically significant . The results suggest that supplementation with the antioxidant vitamins C and E confers partial protection against the acute effects of ozone on FEV1 and forced vital capacity in cyclists To determine whether antioxidants can influence human susceptibility to ozone ( O(3))-induced changes in lung function and airway inflammation , we placed 31 healthy nonsmoking adults ( 18 to 35 yr old ) on a diet low in ascorbate for 3 wk . At 1 wk , subjects were exposed to filtered air for 2 h while exercising ( 20 L/min/m(2 ) ) , and then underwent bronchoalveolar lavage ( BAL ) and were r and omly assigned to receive either a placebo or 250 mg of vitamin C , 50 IU of alpha-tocopherol , and 12 oz of vegetable cocktail daily for 2 wk . Subjects were then exposed to 0.4 ppm O(3 ) for 2 h and underwent a second BAL . On the day of the O(3 ) exposure , supplemented subjects were found to have significantly increased levels of plasma ascorbate , tocopherols , and carotenoids as compared with those of the placebo group . Pulmonary function testing showed that O(3)-induced reductions in FEV(1 ) and FVC were 30 % and 24 % smaller , respectively , in the supplemented cohort . In contrast , the inflammatory response to O(3 ) inhalation , as represented by the percent neutrophils and the concentration of interleukin-6 recovered in the BAL fluid at 1 h after O(3 ) exposure was not different for the two groups . These data suggest that dietary antioxidants protect against O(3)-induced pulmonary function decrements in humans The air pollutant ozone induces both airway inflammation and restrictions in lung function . These responses have been proposed to arise as a consequence of the oxidizing nature of ozone , depleting endogenous antioxidant defenses with ensuing tissue injury . In this study we examined the impact of an environmentally relevant ozone challenge on the antioxidant defenses present at the surface of the lung in two groups known to have profound differences in their antioxidant defense network : healthy control ( HC ) and mild asthmatic ( MA ) subjects . We hypothesized that baseline differences in antioxidant concentrations within the respiratory tract lining fluid ( RTLF ) , as well as induced responses , would predict the magnitude of individual responsiveness . We observed a significant loss of ascorbate ( ASC ) from proximal ( -45.1 % , p < .01 ) and distal RTLFs ( -11.7 % , p < .05 ) in healthy subjects 6 h after the end of the ozone challenge . This was associated ( Rs , -0.71 , p < .01 ) with increased glutathione disulphide ( GSSG ) in these compartments ( p = .01 and p < .05 ) . Corresponding responses were not seen in asthmatics , where basal ASC concentrations were significantly lower ( p < .01 ) and associated with elevated concentrations of GSSG ( p < .05 ) . In neither group was any evidence of lipid oxidation seen following ozone . Despite differences in antioxidant levels and response , the magnitude of ozone-induced  neutrophilia ( + 20.6 % , p < .01 [ HC ] vs. + 15.2 % , p = .01 [ MA ] ) and decrements in FEV(1 ) ( -8.0 % , p < .01 [ HC ] vs. -3.2 % , p < .05 [ MA ] ) did not differ between the two groups . These data demonstrate significant differences between the interaction of ozone with RTLF antioxidants in MA and HC subjects . These responses and variations in basal antioxidant defense were not , however , useful predictive markers of group or individual responsiveness to ozone Pulmonary cells exposed to diesel exhaust ( DE ) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations . In the present study , the authors examined whether similar responses occurred in vivo , specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly . A total of 15 volunteers were exposed to  DE ( 100 µg·m−3 airborne particulate matter with a diameter of < 10 µm for 2 h ) and air in a double-blinded , r and omised fashion . At 18 h post-exposure , bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status . Following DE exposure , the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers , as well as increased neutrophil numbers , interleukin-8 and myeloperoxidase concentrations in bronchial lavage . No inflammatory responses were seen in the alveolar compartment , but both reduced glutathione and urate concentrations were increased following diesel exposure . In conclusion , the lung inflammatory response to diesel exhaust is compartmentalised , related to differing antioxidant responses in the conducting airway and alveolar regions Vitamin supplements have been reported to reduce the magnitude of symptoms in subjects exposed to oxidant air pollution . To confirm whether supplementation with vitamins C and E could reduce lung function decrements , airway inflammation , and epithelial injury in subjects sensitive to ozone , a double-blinded , crossover control study was performed . Fourteen ozone-responsive subjects were r and omly exposed to both air and ozone ( 0.2 ppm for 2 h ) after 7 days of either placebo treatment or supplementation with vitamin C ( 500 mg/day ) and E ( 100 mg/day ) . Lung function was assessed pre- and immediately postexposure and blood sample s were taken at set intervals . Inflammatory , tissue injury , and antioxidant responses were examined in lavage fluid obtained by bronchoscopy 6 h postexposure . Exposure to ozone result ed in significant ( P < 0.01 ) decrements in FEV1 with no protection observed following vitamin supplementation ( -8.5 % ) versus placebo ( -7.3 % ) treatment . Similarly , ozone-induced neutrophilia were of a similar magnitude after both treatments ( P < 0.05 ) . This lack of protection was observed despite elevated plasma vitamin C ( + 60.1 % ) and vitamin E ( + 51.4 % ) concentrations following supplementation , and increased vitamin C concentrations in the airways after supplementation following ozone exposure . These data do not therefore support the contention that acute ozone-induced symptoms can be attenuated through the use of dietary antioxidants in well-nourished individuals To evaluate whether acute effects of ozone , nitrogen dioxide , and particulates with mass median diameter less than 10 micro m could be attenuated by antioxidant vitamin supplementation , we conducted a r and omized trial using a double-blinded design . Children with asthma ( n = 158 ) who were residents of Mexico City were r and omly given a daily supplement of vitamins ( 50 mg/day of vitamin E and 250 mg/day of vitamin C ) or a placebo and were followed from October 1998 to April 2000 . Pulmonary function tests were carried out twice a week in the morning . During the follow-up observation period , the mean 1-hour maximum ozone level was 102 ppb ( SD = 47 ) , and the mean 24-hour average PM(10 ) level was 56.7 micro g/m(3 ) ( SD = 27.4 ) . In children with moderate and severe asthma , ozone levels 1 day before spirometry were inversely associated significantly with forced expiratory flow ( FEF(25 - 75 ) ) ( -13.32 ml/second/10 ppb ; p = 0.000 ) , FEV(1 ) ( -4.59 ml/10 ppb ; p = 0.036 ) , and peak expiratory flow ( PEF ) ( -15.01 ml/second/10 ppb ; p = 0.04 ) in the placebo group after adjusting for potential confounding factors . No association between ozone and lung functions was observed in the supplement group . We observed significant differences in lung function decrements between groups for FEF(25 - 75 ) and PEF . Our results suggest that supplementation with antioxidants might modulate the impact of ozone exposure on the small airways of children with moderate to severe asthma We conducted a double-blind r and omized study to determine the effect of vitamin C on  NO2-induced airway hyperresponsiveness in normal subjects . Eleven normal subjects were r and omly assigned an order for 4 experimental exposures . For each exposure , subjects took either vitamin C ( 500 mg 4 times a day for 3 days ) or placebo followed by exposure either to clean air or to 2.0 ppm NO2 .  Measurements of lung mechanics and airway responsiveness to methacholine aerosol were obtained . Serum level of ascorbic acid was determined before each exposure . NO2 exposure with placebo result ed in significant enhancement of airway responsiveness to methacholine aerosol ( air-placebo 64 + /- 7 to NO2-placebo 53 + /- 8 mg/ml ) . Pretreatment with ascorbic acid prevented the significant alteration in airway responsiveness to methacholine aerosol ( 65 + /- 13 mg/ml , p less than 0.04 ) . These results suggest that airway hyperresponsiveness induced by NO2 in normal subjects is completely prevented by pretreatment with ascorbic acid To determine whether vitamin E ( di-alpha-tocopherol ) supplementation could protect against short-term respiratory responses to O3 exposure its effects were investigated in young healthy adult volunteers . Experimental groups received 800 or 1600 IU vitamin E per day for 9 or more wk , while control groups received placebo . Subjects were then exposed for 2-h periods to 0.5 ppm O3 , with secondary stresses of heat and intermittent light exercise . Responses to O3 exposure , evaluated in terms of symptoms , forced expiratory performance , and single-breath nitrogen washout , were not significantly different between vitamin E and placebo groups 
    Output:
    
The remaining five studies took place under ambient ( uncontrolled ) exposures and unanimously concluded that antioxidant supplementations attenuate the negative effects of urban air pollution on lung function .