INTRODUCTION
An imb alance b etween o xidants and antio xi-dants has b een co nsidered in the patho genesis o f smo king induced lung diseases, such as lung cancer and emphysema. Oxidative stress, which causes an elevatio n o f reactive o xidant species (ROS) may cause a pro tease-antipro tease imbalance in the lo wer air-ways, inducing DNA damage in epithelial cells lead-ing to pro teo lytic lung injury and carcino genesis.1,2
The increased expo sure o f smo kers’ pulmo nary tissues to ROS may result fro m the inhalatio n o f a large amo unt o f o xidants and free radicals present in ciga-rette smo ke.3,4 Ano ther, and po ssibly mo re impo rtant
so urce o f ROS in the lungs o f smo kers, is the enhanced recruitment o f mo no nuclear phago cytes and po lymo r-pho nuclear leuko cytes to the lo wer airways. Activa-tio n o f these inflammato ry cells induces a respirato ry burst resulting in marked pro ductio n o f supero xide anio n. This o xidant species undergo es spo ntaneo us o r enzyme-catalyzed demutatio n to fo rm hydro gen pero xide (H2O2).3,4 Thus, hydro gen pero xide levels
re-fle c t b o th d ivale nt re d uc tio n o f o xyge n and the demutatio n o f supero xide. Hydro gen pero xide appears to be an impo rtant inflammato ry mediato r itself caus-ing cellular injury and, via further reactio ns, generat-ing o ther ROS such as hydro xyl radicals and lipid pero xidatio n pro ducts.3,4
Pro ductio n o f H2O2 has been used in vitro to quantify the respirato ry burst o f neutro phils.5
Different repo rts have also demo nstrated increased hydro -gen pero xidein the expired breath co ndensate (H2O2 -E) o f several clinical co nditio ns such as acute
respira-Original Article
REVISTA PAULISTA DE MEDICIN AIncre ase d e xhalation of hydroge n pe roxide in
he althy subje cts following cigare tte consumption
Pulmonary Division, Department of Medicine, Universidade Federal de São Paulo/
Escola Paulista de Medicina, São Paulo, Brazil
a b s t r a c t
CON TEX T: Increased hydro g en pero xide has been describedin the expired breath co ndensate (H
2O2-E) o f several lung co nditio ns, such
as acute respirato ry distress syndro me, chro nic o bstructive pulmo -nary disease and asthma. This technique has been advo cated as being a simple metho d fo r do cumenting airway inflammatio n.
OBJECTIVE: To evaluate H
2O2-E in healthy cig arette smo kers, and to
determine the acute effects o f the co nsumptio n o f o ne cig arette o n H2O2-E levels.
TYPE OF STUDY: Pro spective, co ntro lled trial.
SETTIN G: A pulmo nary functio n labo rato ry in a University Ho spital.
PARTICIPAN TS: Two g ro ups o f healthy vo lunteers: individuals who had never smo ked (N S; n=1 0 ; 4 men; ag e = 3 0 .6 ± 6 .2 years) and current cig arette smo kers (S; n=1 2 ; 7 men; ag e = 3 8 .7 ± 9 .8 ). N o ne o f the vo lunteers had respirato ry sympto ms and all sho wed no rmal spiro metric tests.
IN TERVEN TION : Expired air was co llected fro m all vo lunteers thro ugh a face mask and a plastic co llecting system leading into a flask with dry ice and pure ethano l. Samples fro m the g ro up S were co llected twice, befo re and half an ho ur after the co mbustio n o f o ne cig arette.
M AIN M EASUREM EN TS: Expired hydro g en pero xide using the G allati and Pracht metho d.
RESULTS: The S and N S g ro ups sho wed co mparable levels o f H2O2 -E at basal co nditio ns [N S = 0 .7 4 µM (DP 0 .2 4 ) vs. S = 0 .7 5 µM (DP 0 .3 1 )]. The smo kers sho wed a sig nificant increase in H2O2-E levels half an ho ur after the co nsumptio n o f o nly o ne cig arette [0 .7 5 µM (DP 0 .3 1 ) vs. 0 .9 5 µM (DP 0 .2 2 )].
CON CLUSION : The present results are co nsistent with the co ncept that smo kers increase o xidative stress with elevated pro ductio n o f reactive o xyg en species, co ntributing to the develo pment o f smo k-ing -related diso rders.
KEY W ORDS: Hydro g en pero xide. Smo king . Free radicals.
to ry distress syndro me (ARDS), chro nic o bstructive p ulm o nary d is e as e ( CO PD) and as thm a.6- 10 This
no ninvasive technique has been advo cated as a simple metho d fo r do cumenting airway inflammatio n. There-fo re, the present study was designed to evaluate H2O2 -E in healthy cigarette smo kers, and to determine the acute effects o f the co nsumptio n o f o ne cigarette o n H2O2-E levels.
METHODS
After Ho spital Ethical Co mmittee appro val, two gro ups o f subjects were studied: tho se who had never smo ked (NS, n = 10) and current cigarette smo kers (S, n = 12). No ne o f the individuals had a histo ry o f chro nic pulmo nary diso rders o r signs o f upper and lo wer res-pirato ry tract infectio ns in the two mo nths prio r to co llectio n o f the samples. All subjects sho wed no r-mal values in spiro metric tests, and there were no differences between the gro ups regarding these spiro -metric parameters (Tables 1 and 2). The S gro up was
significantly o lder than the NS gro up [mean age in years, 30.6 (SD 6.2) vs. 38.7 (SD 9.8); P<0.05). The av-erage degree o f to tal smo king expo sure fo r gro up S was 16.2 (SD 8.6) pack-years. The mean number o f ciga-rettes co nsumed by gro up S at the time o f the study was 14.3 (SD 5.2) cigarettes per day (Table 2).
All the expired breath samples were co llected in the mo rning. The smo kers were requested to re-frain fro m smo king after 10 P.M. Initially, pulmo nary functio n data were o btained using a VitaTrace spiro m-eter, mo del VT 130 SL. Subsequently, the participants were asked to breath thro ugh a face mask with a o ne-way valve. The expired air was co nducted thro ugh a plastic tube co nnected to a sterile co llecting system, leading into a flask co ntaining dry ice and pure etha-no l. In this way, appro ximately 2 ml o f breath co nden-sate were co llected within 30 minutes o f tidal breath-ing. The samples were immediately sto red in a freezer at –80 o
C. After the initial sampling, the subjects o f the S gro up were asked to smo ke o ne co mmercially available cigarette o f a po pular brand. Half an ho ur
Table 2 - Characte ristics of the smoke r group
Subject Gender* Age(years) Present smoking Total smoking FVC+ FEV1δδδδδ FEV1/ FVC (cigarettes/ day) (pack-years) (%pred.) (%pred.) (%pred.)
1 M 3 3 4 1 .2 5 1 0 2 .3 1 0 1 .0 9 9 .4 2 F 3 1 1 0 1 4 1 2 4 .1 1 1 7 .1 9 5 .0 3 M 3 2 1 5 1 3 .5 1 2 0 .5 1 1 8 .1 1 0 0 .6 4 F 3 1 1 2 8 1 1 6 .2 1 1 8 .4 1 0 1 .5 5 M 4 5 2 0 3 5 1 0 2 .5 9 6 .8 9 4 .3 6 F 6 6 1 0 1 0 1 0 1 .3 9 9 .3 9 7 .3 7 M 3 5 1 5 1 8 1 1 5 .4 1 1 2 .5 9 8 .0 8 F 4 1 2 0 2 0 1 1 4 .8 9 6 .8 8 5 .8 9 F 3 6 1 5 1 8 1 2 4 .7 1 1 4 .6 9 5 .0 1 0 M 4 2 2 0 2 5 9 9 .2 9 0 .7 9 1 .4 1 1 M 3 4 2 0 1 9 1 1 8 .9 8 3 .3 7 3 .0 1 2 M 3 8 1 0 1 2 .5 1 0 1 .2 8 7 .0 8 6 .7
M ean (SD) - 38.7 (9.8) 14.3 (5.21) 16.2 (8.61) 111.8 (9.7) 103.0 (12.7) 93.2 (8.1)
* M: male, F: female; +FVC: fo rced vital capacity; δFEV1: fo rced expirato ry vo lume in the first seco nd.
Table 1 - Characte ristics of the ne ve r-smoke r group
Subject Gender* Age (yea rs) FVC+ (%pred.) FEV1δδδδδ (%pred.) FEV1/ FVC (%pred.)
1 M 2 3 9 8 .1 9 4 .0 9 5 .1
2 F 3 9 1 2 6 .0 1 1 3 .9 9 0 .6 3 M 2 6 1 1 4 .7 1 2 0 .1 1 0 4 .4 4 F 2 6 9 4 .2 9 7 .8 1 0 3 .1 5 F 2 6 9 5 .4 9 8 .9 1 0 2 .7 6 F 3 7 1 2 8 .3 1 2 6 .4 9 8 .2 7 F 3 9 1 0 8 .0 9 4 .8 8 7 .8 8 M 2 7 1 1 5 .5 1 0 5 .1 9 2 .4 9 M 2 8 1 0 7 .4 1 1 2 .9 1 0 5 .6 1 0 F 3 5 1 0 8 .9 1 0 5 .9 9 7 .5
M ea n (SD) - 3 0 .6 (6 .2 ) 1 0 9 .7 (1 1 .8 ) 1 0 6 .9 (1 1 .1 ) 9 7 .7 (6 .2 )
after the end o f this cigarette a seco nd co llectio n o f expired breath co ndensate was made.
The measurements o f H2O2 were all made in
the same way, using the metho d described by Gallati and Pracht.11 In b rie f, 100
µ
l o f 420µ
M3,3¢,5,5¢-te tram e thylb e nzidine (disso lve d in 0.42 M citra3,3¢,5,5¢-te buffer, pH 3.8) and 10
µ
l o f 52.5 U/µ
l o f ho rseradish pero xidase type II (HRP, Sigma Chemicals) were added to 100µ
l o f the co ndensate. The reactio n pro ceeded fo r 20 minutes at ro o m temperature. Subsequently, the mixture was acidified to a pH o f 1 with 10µ
l o f 18 N sulfuric acid. The reactio n pro duct was measured spectro pho to metrically at 450 nm using an auto mated m ic ro p late re ad e r (Flo w/ICN Bio m e d ic als, m o d e l Titertek Multiskan MCC340). The abso rbance at 450 nm is directly pro po rtio nal to the co ncentratio n o f H2O2. All samples were measured in duplicate and the mean values were used fo r analysis.S tatistical methods
The spiro metry measurements were expressed as percentages o f the predicted values fo r no rmal po pulatio ns using classic equatio ns.12,13
All o f the re-sults are sho wn as mean and standard deviatio n. Sta-tistical co mpariso ns between gro ups o f pulmo nary functio n data and basal H2O2-E levels were do ne us-ing Student’s t test. Statistical co mpariso ns o f H2O2-E levels in the S gro up, befo re and after smo king, were o btained using a paired t test. Pearso n co efficients were perfo rmed to evaluate co rrelatio n between the H2O2-E levels and cigarette smo king status. Statisti-cal significance was assumed when P < 0.05.
RESULTS
Hydro gen pero xide was detected in the expira-to ry breath co ndensate o f all tho se who had never smo ked at co ncentratio ns ranging between 0.43 and 1.21
µ
M. The mean and standard deviatio n o f the H2O2 -E values fo r the NS gro up were 0.74µ
M (SD 0.24) (Fig-ure 1). Hydro gen pero xide was also detected in the breath co ndensate o f all o f gro up S under basal con-ditio ns, at levels ranging between 0.29 and 1.07
µ
M.The mean and standard deviatio n o f the H2O2-E
val-ues fo r the S gro up were 0.75
µ
M (SD 0.31). Statistical analysis sho wed no significant differences between gro up S and gro up NS H2O2-E basal levels (Figure 1). In additio n, there were no significant co rrelatio ns fo und between initial H2O2-E levels and the to tal o r present smo king histo ry fo r gro up S subjects (r = 0.125 and r = 0.057, respectively).Gro up S sho wed a mean H2O2-E value o f 0.95
µ
M (SD 0.22) fo r samples co llected half an ho ur after the subjects had smo ked a regular cigarette. The H2O2-E levels po st-smo king [0.95
µ
M (SD 0.22)] weresig-nificantly higher than the basal values [0.75
µ
M (SD0.31)] (Figure 2).
DISCUSSION
Investigatio ns o f chemical co mpo unds in the exhaled air sho uld be scrutinized by respirato ry bio l-o gy researchers because they may lead tl-o the devel-o pment devel-o f methdevel-o ds fdevel-o r evaluating inflammatidevel-o n devel-o f the lung parenchyma and airways. Fo r example, several studies have demo nstrated measurable amo unts o f nitric o xide in human expired gas, bo th under physi-o lphysi-o gical and pathphysi-o lphysi-o gical cphysi-o nditiphysi-o ns, and this physi-o bser-vatio n has attracted gro wing interest in this field.14-16
The first descriptio n o f hydro gen pero xide in the
expired air o f humans was in 1983.17
Since then high
H2O2-E levels have been detected under a number o f
different co nditio ns such as ARDS, asthma and COPD.
6-10 Altho ugh such results stro ngly suggest a ro le fo r
expired hydro gen pero xide as a marker fo r respirato ry tract inflammatio n, the number o f investigatio ns and publicatio ns in the area remains small.
Recently a study by Ho rvath et al.18 evaluated
the relatio nship between nitric o xide and hydro gen pero xide in the exhaled air o f asthmatic patients and also evaluated bro nchial hyperreactivity, pulmo nary functio n tests, and cellular co unts o f induced sputum. These results suggested fo r the first time that H2O2-E might be a mo re sensitive and reliable marker o f air-way inflammatio n than exhaled nitric o xide in this po pulatio n.
Smo king is the mo st impo rtant risk facto r fo r COPD and lung cancer, and it is believed by so me that the generatio n o f ROS in the lo wer airways may sub-stantially co ntribute to the patho genesis o f these dis-o rders.2,3
In such co nditio ns, the detectio n o f high lev-els o f H2O2-E in smo kers with no clinical o r functio nal evidence o f disease, wo uld add credibility to the hy-po thesis that H2O2 co ntrib utes significantly to the patho genic mechanisms o f smo king-related diseases. In additio n, this type o f measurement co uld beco me a useful clinical to o l, able to detect subjects with smo k-ing-induced pulmo nary inflammatio n at its very earli-est stages.
re-sult fro m co ntaminatio n o f breath co ndensate with saliva that co ntains high amo unts o f hydro gen pero x-ide. In this study we used a who le facemask and, since the vo lunteers were required to breathe nasally, the chances o f significant saliva co ntaminatio n is quite small. Such findings co uld also be explained by the type o f equipment we have emplo yed fo r co llecting co ndensate. Mo st o f the researchers in the field have previo usly co llected expired co ndensate thro ugh en-d o trac he al tub e s o r via o ral b re athing. Us ing a facemask and nasal breathing, we have co llected co n-densate that co uld reflect the metabo lism o f lung pa-renchyma and upper airways as well. In such a situa-tio n the upper airways and paranasal sinus co uld be a significant so urce o f H2O2-E, in a similar way to that already described fo r nitric o xide.19 A third impo rtant
po ssibility fo r explaining these differences is related to the quality o f the air in São Paulo city. Air po llutio n is still a health co ncern in this big city and its effects
o n the H2O2-E levels are at present unkno wn. The S
gro up also had a significantly higher mean age than
the NS gro up. As the influences o f aging o n H2O2-E levels are presently unkno wn, this difference may be a po tential so urce o f bias in o ur results. Further studies are necessary to clarify such aspects.
Gro up S sho wed a significant increase in the
mean H2O2-E level, half an ho ur after the co
nsump-tio n o f o nly o ne cigarette (Figure 2). In part, this find-ing may be due to inhalatio n o f H2O2 o riginating fro m the cigarette co mbustio n and po ssibly still present in the airways at the time o f the co ndensate co llectio n. This is unlikely since the thirty minutes rest perio d sho uld have been eno ugh to dissipate mo st o f the in-haled hydro gen pero xide accumulated in the airways fro m cigarette co mbustio n alo ne. Cigarette smo ke has abo ut 5 x 1014 free radicals per inhalatio n which, in
co ntact with the wet surfaces o f the respirato ry epi-thelium, can generate supero xide radicals and H2O2.3,4
In additio n, such smo ke-generated radicals may dam-age cellular membranes in the respirato ry tract lead-ing to lipid pe ro xidatio n and additio nal o xidative stress.2,3,4 Therefo re, the present increases in H
2O2-E
levels thirty minutes after cigarette co nsumptio n pro b-ably reflect acute, smo king-induced, paranasal, upper and lo wer airway and lung parenchyma injuries. An-o ther cAn-o ntributAn-o ry factAn-o r in these findings may be the acute influx and sequestratio n o f inflammato ry cells in the lung parenchyma. It has been sho wn that ciga-rette smo king can acutely pro mo te pulmo nary vascu-lar retentio n o f marked neutro phils.20
The mechanisms related to this pheno meno n are no t co mpletely un-dersto o d, but may invo lve activatio n o f adhesio n mo l-ecules, changes in leuko cyte cyto skeleto ns, and lo cal he m o dynam ic diso rde rs.20-22 Whate ve r the m e
cha-nisms invo lved, the acute elevatio n o f H2O2-E levels fo und in this study reflect ROS respirato ry o verlo ad-ing seco ndary to the smo kad-ing habit.
The S and NS gro ups sho wed co mparable lev-els o f H2O2-E under basal co nditio ns (Figure 1). This suggests that smo king leads to transient changes in the H2O2-E, which returns to no rmal levels in healthy subjects after so me ho urs o f abstinence. Our results disagree with a recent paper which repo rted a fivefo ld increase in basal H2O2-E fo r a gro up o f 33 cigarette smo kers in co mpariso n to 27 no n-smo kers.23
Altho ugh the autho rs had included in their investigatio n o nly sub jects witho ut respirato ry sympto ms and with a no rmal physical e xaminatio n, pulmo nary functio n tests were no t perfo rmed. Therefo re we canno t rule o ut the po ssibility that so me o f the smo king individu-als in that study had asympto matic COPD.
De khuijze n e t al.9 have sho wn that incre ase d
H2O2-E o c c urs in sub je c ts with stab le COPD and
Figure 2 - H2O2-E levels for the group S before (B) and after (A) patients had smoked one cigarette.
Figure 1 - H2O2-E levels for the group S and NS in basal conditions.
0.74 0.75
0.75
0.95
1. Cro ss CE, Halliwell B, Bo rish ET, Pryo r WA, Ames BN, Saul RL, McCo rd JM, Harman D. Oxygen radicals and human disease. Ann Intern Med 1987;107:526-45.
2. Rahman I, MacNee W. Ro le o f o xidants/antio xidants in smo king-induced lung diseases. Free Rad Bio l Med 1996;21:669-81.
3. Pryo r W, Sto ne K. Oxidants in cigarette smo ke. Radicals, hydro gen p e ro xid e , p e ro xynitrate and p e ro xynitrite . Ann N Yo rk Ac ad Sc i 1993;686:12-27.
4. Niki E, Minamisawa S, Oikawa M, Ko muro E. Membrane damage fro m lipid o xidatio n induced by free radicals and cigarette smo ke. Ann N Yo rk Acad Sci 1993;686:29-38.
5. Hyslo p PA, Sklar LA. A q uantitative fluo ro m e tric assay fo r the d e te rm in atio n o f o xid an t p ro d u c tio n b y p o lym o rp h o n u c le ar leuko cytes: its use in the simultaneo us fluo ro metric assay o f cellular activatio n pro cesses. Anal Bio ch 1984;141:280-6.
6. Baldwin SR, Grum CM, Bo xer LA, Simo n RH, Ketai LH, Devall LJ. Oxidant activity in expired breath o f patients with adult respirato ry distress syndro me. Lancet 1986;1:11-4.
7. Sznajder JI, Fraiman A, Hall JB, et al. Increased hydro gen pero xide in the expired breath o f patients with acute hypo xemic respirato ry failure. Chest 1989;96:606-12.
8. Kietzmann D, Kahl R, Müller M, Burchardi H, Kettler D. Hydro gen p e ro xid e s in e xp ire d b re ath c o nd e nsate o f p atie nts with ac ute respirato ry failure and with ARDS. Int Care Med 1993;19:78-81. 9. Dekhuijzen PNR, Aben KKH, Dekker I, et al. Increased exhalatio n o f
hydro gen pero xide in patients with stable and unstable chro nic o bstructive pulmo nary disease. Am J Respir Crit Care Med 1996;154:813-6. 10. Do hlman AW, Black HR, Ro yall JA. Expired breath hydro gen pero xide
is a marker o f acute airway inflammatio n in pediatric patients with asthma. Am J Respir Crit Care Med 1993;148:955-60.
11. Gallati H, Prac ht I. Ho rse rad ish p e ro xid ase : kine tic stud ie s and o ptimizatio n o f pero xidase activity determinatio n using the substrates H2O2 and 3,3¢,5,5¢-tetramethylb enzidine. J Clin Chem Clin Bio ch
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defo rmability after acute cigarette smo king in humans. Am Rev Respir Dis 1993;148:1277-83.
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e ve n m o re so in patie nts with an e xace rb atio n o f COPD. Our data sho ws at le ast the o ccurre nce o f trans ie nt e le vatio ns o f H2O2- E afte r c halle nging he althy individuals b y cigare tte sm o king. The re fo re we c an hyp o the size that the re m ay b e an initial phase in the e vo lutio n o f COPD, whe n high le ve ls o f H2O2-E are co ntinuo usly fo und in sub je cts with-o ut significant re spiratwith-o ry cwith-o m plaints. This e ve nt may happen in COPD-susceptib le smo kers fo r who m an o xid ant lo ad wo uld re p e ate d ly o ve rc o m e the antio xidant pro te ctio n in the lo we r airways. In this sce nario the m e asure m e nt o f H2O2-E co uld b e co m e a se nsitive and no n-invasive m e tho d fo r sho wing e nhance d ge ne ratio n o f ROS, and m ay b e use d to
d e te c t sub je c ts with a highe r risk fo r d e ve lo p ing sm o king-re late d p ulm o nary d ise ase s. Large r and m o re co m ple te studie s will ne e d to b e pe rfo rm e d to co nfirm this hypo the sis.
CONCLUSION
r e s u m o
CON TEXTO: Elevaçõ es do peró xido de hidro gênio exalado (H2O2-E) tem sido descritas em diversas doenças pulmonares tais como a síndrome do desco nfo rto respirató rio agudo , do ença pulmo nar o bstrutiva crô nica e asma. Essa técnica tem sido preco nizada co mo um méto do simples capaz de refletir inflamação ao nível das vias aéreas.
OBJETIVO: Avaliar os níveis de H2O2-E em indivíduos normais e determinar os efeitos agudos do consumo de um cigarro sobre seus valores.
TIPO DE ESTUDO: Ensaio clínico , pro spectivo , co ntro lado .
LOCAL: Labo rató rio de função pulmo nar de um Ho spital Universitário .
PARTICIPAN TES: Do is g rupo s de vo luntário s sadio s: indivíduo s que nunca fumaram [N S; n = 1 0 ; 4 ho mens; idade = 3 0 ,6 ano s (DP 6 ,2 )] e indivíduo s fumantes atuais [S; n = 1 2 ; 7 ho mens; idade = 3 8 ,7 ano s (DP 9 ,8 )]. To do s o s vo luntário s não apresentavam sinto mas respirató rio s e exibiam testes espiro métrico s dentro da no rmalidade.
IN TERVEN ÇÃO: Ar expirado fo i co letado de to do s o s vo luntário s utiliz ando -se uma máscara facial e um sistema co lo cado em um frasco co m g elo seco e etano l abso luto . Amo stras do g rupo S fo ram co letadas duas vez es, antes e meia ho ra apó s o co nsumo de um cig arro .
V ARIÁV EIS ESTUDADAS: Pe ró xid o d e hid ro g ê nio e xp ira d o utiliz ando -se o méto do de G allati e Pracht.
RESULTADOS: Ambo s o s g rupo s mo straram níveis co mparáveis de H2O2-E em co ndiçõ es basais [N S = 0 ,7 4 µM (DP 0 ,2 4 ) vs. S = 0 ,7 5
µM (DP 0 ,3 1 )]. O s fumantes mo straram um aumento sig nificante do s níveis de H2O2-E meia ho ra apó s o co nsumo de apenas um cig arro [0 ,7 5 µM (DP 0 ,3 1 ) vs. 0 ,9 5 µM (DP 0 ,2 2 )].
CON CLUSÃO: O s resultado s o btido s estão de aco rdo co m o co nceito de que o co nsumo de cig arro s aumenta o estresse o xidativo co m pro dução elevada de espécies reativas do o xigênio (RO S) co ntribuindo para o desenvo lvimento de do enças relacio nadas ao tabag ismo .
PALAVRAS-CHAVE: Peróxido de hidrogênio. Tabagismo. Radicais livres.
Sandra Baltazar Guatura, MSc. Pulmo nary Divisio n, Federal University o f São Paulo / Esco la Paulista de Medicina, São Paulo , Brazil.
José Antônio Baddini Martine z, MD, PhD. Pro fesso r, Pulmo nary Divisio n, Department o f Medicine, Medical Scho o l o f Ribeirão Preto , University o f São Paulo , Ribeirão Preto , Brazil.
Patricia Cincotto dos Santos Bue no, PhD. Pulmo nary Divisio n, Federal University o f São Paulo / Esco la Paulista de Medicina, São Paulo , Brazil.
Manue l Lope s dos Santos, MD, PhD. Full Pro fesso r, Pulmo nary Divisio n, Federal University o f São Paulo / Esco la Paulista de Medicina, São Paulo , Brazil.
Source s of funding: SBG was suppo rted by CAPES (nº 132.276/95-0)
Conflict of inte re st: No t declared
Last re ce ive d: 10 January 2000
Acce pte d: 18 January 2000
Addre ss for corre sponde nce :
Jo sé Antô nio Baddini Martinez
Departamento de Clínica Médica, Ho spital das Clínicas de Ribeirão Preto Avenida Bandeirantes, 3900 – 6º andar
Ribeirão Preto /SP – Brasil - CEP: 14048-900 E-mail: jabmarti@ fmrp.usp.br
