Volume 164 Issue 5

Passive smoking and respiratory function in very low birthweight children Lex W Doyle, Geoffrey W Ford, Anthony Olinsky, Annette M L Knoches and Catherine Callanan For editorial comment see Woodward & Jamrozik Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au/>". Abstract - Introduction - Methods - Results - Discussion - Acknowledgement - References - Authors' details - ©MJA1997 Abstract Aim: To determine if an adverse relationship exists between passive smoking and respiratory function in very low birthweight (VLBW) children at 11 years of age. Setting: The Royal Women's Hospital, Melbourne. Patients: 154 consecutive surviving children of less than 1501 g birthweight born during the 18 months from 1 October 1980. Methods: Respiratory function of 120 of the 154 children (77.9%) at 11 years of age was measured. Exposure to passive smoking was established by history; no children were known to be actively smoking. The relationships between various respiratory function variables and the estimated number of cigarettes smoked by household members per day were analysed by linear regression. Results: Most respiratory function variables reflecting airflow were significantly diminished with increasing exposure to passive smoking. In addition, variables indicative of air-trapping rose significantly with increasing exposure to passive smoking. Conclusions: Passive smoking is associated with adverse respiratory function in surviving VLBW children at 11 years of age. Continued exposure to passive smoking, or active smoking, beyond 11 years may lead to further deterioration in respiratory function in these children. MJA 1996; 164: 266-269 Introduction Passive smoking is associated with several adverse health outcomes in children, including higher rates of asthma,1 and infections of the upper2 and lower3 respiratory tract. Further, respiratory function is reduced with passive smoking in children who have no lung disease,4 as well as those with lung diseases such as asthma5 and cystic fibrosis.6 To survive the neonatal period, many very low birthweight (VLBW) children (less than 1500 g at birth) require prolonged periods of assisted ventilation, and some may develop bronchopulmonary dysplasia (BPD) and suffer from ongoing respiratory problems as a consequence. We have previously reported the respiratory health to eight years of age of cohorts of children of birthweight 500-999 g (n = 83), 1000-1500 g (n = 114) and > > 2500 g (n = 51).7 Passive smoking was significantly related to the duration of hospitalisation for respiratory problems up to two years of age for all children in that study, but was not associated with changes in respiratory function at eight years of age. In contrast, in another recent cohort study of respiratory function at seven years of age in children of birthweight less than 2000 g Chan et al.8 reported reduced air-flow rates with maternal smoking, but not with smoking by other household members. Because the effects of passive smoking could increase with increasing duration of exposure, the aim of this study was to determine if an adverse relationship exists between passive smoking and respiratory function at 11 years of age in VLBW children. Methods We studied 154 consecutive surviving children of less than 1501 g birthweight born during the 18 months from 1 October 1980 at the Royal Women's Hospital, Melbourne, the largest of the three tertiary-level perinatal centres in Victoria. Details of the survival rate and early neonatal care of this cohort have been described.9,10 Bronchopulmonary dysplasia (BPD) was diagnosed in children who had required intermittent positive pressure ventilation in the neonatal period, who had respiratory distress and were still having oxygen therapy at 28 days of age, and who had an abnormal chest x-ray consistent with stage III or IV disease (as defined by Northway et al.11 ) at or after 28 days. A previous report of the respiratory function of this cohort at eight years of age7 included data for some children with birthweights of less than 1000 g born before 1 October 1980. We did not have the resources to measure respiratory function at 11 years of age of the children born before October 1980. Respiratory health was determined by history and examination, and measurement of respiratory function. Children who had required bronchodilators within the previous year for attacks of wheezing were considered to have asthma. Data on passive smoking were obtained by asking the parents about the daily consumption of cigarettes by members of the household. We did not distinguish between mothers and other smokers, or between smoking inside or outside the home. Some data on maternal smoking in pregnancy had been collected in the perinatal period, but were obtained for only one-third of mothers. Children were questioned about active smoking in their parents' absence. As some children had changed households in their lifetimes, we considered those who had lived in any household with smokers over the 11-year period to have been passively smoking during childhood. Two categories of social class were determined -- unskilled or unemployed, and other (professional, skilled or semi-skilled) -- based on the occupation of the family breadwinner. Respiratory function was measured in the Department of Thoracic Medicine at the Royal Children's Hospital, Melbourne, as described previously,7 by personnel blinded to the exposure of individual children to passive smoking. Maximum expiratory flow rates were recorded with a pneumotachograph (Fleisch No. 3, Switzerland) and plotted against volume by integrating flow on an X-Y recorder to obtain flow-volume loops. Maximum flow rates at 75% (VEmax75%), 50% (VEmax50%) and 25% (VEmax25%) of forced vital capacity (FVC), and forced expiratory flow between 25% and 75% of FVC (FEF25%-75%), were measured from the loops. Flow rates were corrected for body size by dividing by vital capacity (VC). Vital capacity, FVC and forced expiratory volume in one second (FEV1) were measured with a water-filled spirometer (Godart Expirograph, Bilthoven, Netherlands) in accordance with standard guidelines, and results at body temperature and pressure saturated with water vapour were expressed as a percentage of the predicted value for age, height and sex.12 Total lung capacity (TLC) and residual volume (RV) were measured in a body plethysmograph (Jaeger Bodyscreen 2, Wurzburg, Germany). Children were not subjected to bronchial provocation tests as these are poorly tolerated, and we were eager to maintain a high degree of cooperation with these and with future respiratory function tests. Not all children could complete all respiratory function tests, either because of poor cooperation, or unavailability or malfunction of equipment on the day of testing. Data were edited and analysed using SPSS.13 Dichotomous variables were contrasted by chi-squared analysis, and continuous variables by t test, or Mann-Whitney U test if the data were skewed. The dose-response relationship between the estimated daily number of cigarettes consumed by members of the household and various respiratory function variables was established by linear regression; linear and quadratic relationships were tested. Data were then analysed by linear regression to adjust for the potentially confounding variables of birthweight, gestational age, birthweight ratio (child's birthweight divided by median birthweight for gestational age14 ), sex, BPD, and asthma; all variables were entered simultaneously, even if they were not statistically significant. Durations of intermittent positive pressure ventilation and oxygen therapy were not included as they were strongly related to BPD. For all analyses, P values of less than 0.05 for any test were regarded as statistically significant. Results We measured the respiratory function of 120 of the 154 (77.9%) children at 11 years of age. Of the 34 children not tested, 15 lived in another State, four lived in another country, 10 refused the tests, three were lost to follow-up, and two were too disabled to complete the tests. There were no substantial differences in perinatal variables between children who did and did not have respiratory function tests at 11 years of age. Eighty of the 120 children (66.7%) had been exposed to passive smoking in the household. The only substantial differences in perinatal or subsequent variables between children who were and were not exposed to passive smoking were a significantly longer duration of oxygen therapy and a lower proportion of unskilled or unemployed families in the group not exposed (Table 1). For children exposed to passive smoking, the median number of cigarettes consumed in the household per day was 21 (interquartile range, 15-25). Of the 15 children tested who had developed BPD in the newborn period, three (20%) had asthma at 11 years of age; this proportion was similar for children with asthma at 11 who did not have BPD (22 of 105; 21%). For variables expressed as a percentage of predicted values (FEV1, FVC, RV, TLC), the means of the measured values were all close to their expected values of 100% (Table 2). For all respiratory function variables significantly associated with the dose of passive smoking, a quadratic relationship was more significant than a linear relationship (Table 2, Figures 1 and 2). Most respiratory function variables reflecting airflow (VEmax75%/VC, VEmax50%/VC, FEF25%-75%/VC, FEV1 and FEV1/FVC) were significantly diminished by increasing exposure to passive smoking (Table 2 [below], Figures 1a and 1b). In addition, RV, TLC and RV/TLC rose significantly (consistent with progressive air trapping) with increasing exposure to passive smoking (Table 2 [below], Figure 1c). One child was exposed to 115 cigarettes per day, and the next highest exposure was only 70 cigarettes per day. When the child exposed to 115 cigarettes per day was excluded, most of the statistically significant relationships disappeared, except for the increases in RV and RV/TLC (Figure 2). From the multiple linear regression analyses, some variables reflecting flow (VEmax75%/VC, VEmax50%/VC, VEmax25%/VC, FEF25%-75%/VC and FEV1/FVC) were significantly higher in girls. BPD was significantly associated with reductions in some variables reflecting air-flow (VEmax50%/VC, FEF25%-75%/VC, FEV1 and FEV1/FVC), as was asthma (with significant reductions in FEF25%-75%/VC, FEV1 and FEV1/FVC). FVC was significantly lower and VEmax25%/VC significantly higher with lower social class. Birthweight ratio, birthweight and gestational age were not significantly associated with any lung function variable. None of the statistical conclusions relating respiratory function variables with passive smoking were altered by adjusting for all potentially confounding variables, except that the reduction in VEmax50%/VC was no longer statistically significant. Discussion Passive smoking was associated with reduced airflow and air-trapping in VLBW children at 11 years of age, which is consistent with observations in non-preterm children free of lung disease.4 However, this finding was different from our observations of these children at eight years of age,7 when passive smoking was unassociated with any lung function variable. Chan et al.8 reported reduced flow rates with smoking by mothers in children of less than 2000 g birthweight at seven years of age, but they did not measure variables reflecting air-trapping. We did not distinguish between mothers and other smokers in the household. The association between passive smoking and adverse respiratory function in our VLBW children at 11, but not at eight, years of age suggests that the harmful effects of passive smoking take time to become obvious in VLBW children. Moreover, the adverse response seems to accelerate with increasing dose of passive smoking (Figures 1 and 2). We are concerned that continued exposure to passive smoking, or, even worse, active smoking, beyond 11 years will lead to not only further, but also to an accelerating rate of, deterioration in respiratory function. Our results should not be overinterpreted. They were not substantially altered by adjusting for potentially confounding perinatal or other variables, but we did not have data on a wide range of confounding variables. Moreover, they were heavily influenced by one child who lived in a household whose members consumed 115 cigarettes per day. Excluding this child from the analysis, the only remaining statistically significant associations indicated air-trapping with increasing exposure to passive smoking. However, we consider that this child's data should not be excluded just on the basis of heavier-than-average exposure to passive smoking. To remove any doubt about the association between passive smoking and adverse lung function in VLBW children, lung function could be measured in another cohort of VLBW children, or the same cohort when they are older. Parents of VLBW children, particularly those of children who have received assisted ventilation, frequently ask about long-term lung problems. Many variables, such as family history or duration of assisted ventilation and oxygen therapy, may be related to long-term lung problems, but most cannot be altered by the parents. Exposure to passive smoking is one variable associated with poorer respiratory function in VLBW children they can influence. Until there is evidence to the contrary, families of VLBW children should be encouraged to stop exposing their children to cigarette smoke in the household. As there appears to be a dose-response relationship, those who cannot stop smoking should at least reduce their children's exposure to passive smoking. Acknowledgement This study was supported in part by a grant from the Royal Women's Hospital-3AW Community Services Trust. References Landau L. Smoking and childhood asthma. Med J Aust 1991; 154: 715-716. Wright AL, Holberg C, Martinez FD, et al. Relationship of parental smoking to wheezing and nonwheezing lower respiratory tract illnesses in infancy. J Pediatr 1991; 118: 207-214. Etzel RA, Pattishall EN, Haley NJ, et al. Passive smoking and middle ear effusion among children in day care. Pediatrics 1992; 90: 228-232. Cook DG, Whincup PH, Papacosta O, et al. Relation of passive smoking as assessed by salivary cotinine concentration and questionnaire to spirometric indices in children. Thorax 1993; 48: 14-20. Chilmonczyk BA, Salmon LM, Megathlin KN, et al. Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. N Engl J Med 1993; 328: 1665-1669. Smyth A, O'Hea U, Williams G, et al. Passive smoking and impaired lung function in cystic fibrosis. Arch Dis Child 1994; 71: 353-354. Kitchen WH, Olinsky A, Doyle LW, et al. Respiratory health and lung function in 8-year-old children of very low birth weight: a cohort study. Pediatrics 1992; 89: 1151-1158. Chan KN, Noble-Jamieson CM, Elliman A, et al. Lung function in children of low birth weight. Arch Dis Child 1989; 64: 1284-1293. Kitchen WH, Ford GW, Murton LJ, et al. Mortality and two year outcome of infants of birthweight 500-1500 g: relationship with neonatal cerebral ultrasound data. Aust Paediatr J 1985; 21: 253-259. Kitchen WH, Yu VYH, Lissenden JV, Bajuk B. Collaborative study of very-low-birthweight infants: techniques of perinatal care and mortality. Lancet 1982; i: 1 454-1457. Northway WH Jr, Rosan RC, Porter DY. Pulmonary disease following respirator therapy of hyaline-membrane disease: bronchopulmonary dysplasia. N Engl J Med 1967; 276: 357-368. Hibbert ME, Lanigan A, Landau LI, Phelan PD. Lung function values from a longitudinal study of healthy children and adolescents. Pediatr Pulmonol 1989; 7: 101-109. SPSS for Windows [computer program]. Version 6.1. Chicago, Ill: SPSS Inc, 1994. Kitchen WH, Robinson H, Dickinson AJ. Revised intrauterine growth curves for an Australian hospital population. Aust Paediatr J 1983; 19: 157-161. (Received 8 Jun, accepted 18 Nov 1995) Authors' details Division of Paediatrics, the Royal Women's Hospital, Melbourne, VIC. Lex W Doyle, MD, FRACP, Paediatrician; and Associate Professor, Departments of Obstetrics and Gynaecology, and Paediatrics, the University of Melbourne. Geoffrey W Ford, MB BS, FRACP, Paediatrician. Annette M L Knoches, MB BS, FRCP(C), Paediatrician. Catherine Callanan, RN, Research Nurse. Department of Thoracic Medicine, the Royal Children's Hospital, Melbourne, VIC. Anthony Olinsky, FRACP, Respiratory Physician. No reprints will be available. Correspondence: Associate Professor L W Doyle, Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, VIC 3052. ©MJA 1997 <URL: http://www.mja.com.au/> © 1997 Medical Journal of Australia.

Lex W Doyle · Geoffery W Ford · Anthony Olinsky · Catherine Callanan

Clinical Practice Clinical exercise stress testing -- Safety and performance guidelines* The Cardiac Society of Australia and New Zealand Clinical exercise testing has wide application in medicine, including the assessment of functional capacity, ventilatory function, gas exchange, muscle function, and endocrine and metabolic function, and as a test for claudication in peripheral vascular disease. The major use of exercise testing, however, is as a stress test in patients with known or suspected coronary artery disease. This article outlines the minimum safety and performance guidelines for exercise stress testing with electrocardiography, although many of the safety guidelines are common to other types of exercise tests, particularly exercise stress scintigraphy and echocardiography. MJA 1996; 164: 282-284 Introduction - Exercise equipment - Electrocardiograph (ECG) - Blood pressure measurement - Documentation - Postexercise period - Resuscitation equipment - Personnel - References - Authors' details - - Articles on similar material Introduction Clinical exercise stress testing with exercise electrocardiography is usually performed in patients with known or suspected coronary artery disease (see Box 1). It is thus not without risk: one in 10 000 people will die, and two to three in 10 000 will have a major morbid event such as myocardial infarction, a major arrhythmia requiring resuscitation, severe hypotension, severe heart failure or unstable angina pectoris. (The complication rates may be higher in some laboratories because of the mix of referred patients.) Those who perform exercise stress testing must thus be able to recognise and exclude patients at high risk, and have the clinical skills and equipment to recognise and deal effectively with complications. They should also obtain informed consent from the patient before performing the test. Exercise equipment Energy expenditure is best quantified by measurement of oxygen consumption (Vo2), expressed in METS, during exercise. A MET unit is the energy expenditure at rest, equivalent to an oxygen uptake of approximately 3.5 mL O2 per kilogram bodyweight per minute. This is the most precise measurement of metabolic load, and therefore cardiovascular load, and can vary considerably between individuals with differing exercise efficiency working at the same treadmill or cycle ergometer setting. Vo2 is not usually measured directly; energy expenditure in METS can be estimated from nomograms1 which assume that energy expenditure can be quantified as watts (cycle ergometer) or as speed and grade (treadmill). Treadmills must be motorised and calibrated, and should be capable of providing measured increases in speed and gradient. The treadmill speed can be easily checked by measuring the visible length of belt, multiplying by two, and multiplying this by manually counted belt revolutions/ minute to give km/hour. Treadmill inclination can be checked by a protractor. Cycle ergometers must be able to vary the external workload and quantify it in watts. Preference is for electrical or mechanical braking, although wind-braking is probably adequate. Thumb-screw braking is not adequate as the load cannot be quantified and is not reproducible. Simple step devices (including "Masters two-step"), or any other form of non-quantified and unmonitored exercise, are not adequate for clinical exercise stress testing. Equipment should be serviced on a regular basis to ensure performance within specifications. Electrocardiograph (ECG) Use 12-lead ECG equipment, recording on a 3-channel device with adequate low frequency and phase response. Devices which record only one or three ECG leads, even if these are bipolar chest leads, are not adequate. If the device provides computer-averaged complexes, raw ECG traces should also be inspected at each stage of exercise, or at least every three minutes, to avoid incorrect interpretation resulting from noise or artefact. Electrodes must be firmly fixed to the patient's skin with adhesive or continuous suction, and have good contact with the ECG lead, to prevent movement artefact in the ECG trace. Use an alcohol solution to remove oil from the patient's skin and abrade the horny layer of the epidermis with fine sandpaper or a disposable abrasive device. Record a standard supine ECG (with limb leads on the limbs) for each patient, and an additional supine ECG with the limb electrodes on the torso if this is where they will be placed during exercise. Monitor the ECG continuously during the exercise period and for five minutes after the cessation of exercise on a video display of two or three leads, preferably selected to be semiorthogonal (i.e., an inferior lead, V5, and V1 or V2). Monitoring a single lead is suboptimal for detecting arrhythmias and ischaemic patterns during exercise. Monitoring devices should have a memory loop capable of providing hard copy or storing rhythm traces on request by the operator. Record further ECGs with the patient upright; during each stage of exercise (or at least every three minutes); at peak exercise; immediately upon cessation of exercise; and at least twice during the post- exercise period. Blood pressure measurement Measure blood pressure before, during (ideally every minute but at least every three minutes, coinciding with each stage of exercise) and after exercise (at least two measurements). If possible, a measurement should be made at peak exercise. Additional measurements may be required depending on clinical circumstances. Documentation Document the resting and peak heart rate and blood pressure, and any abnormalities of these or the ECG. The peak rate-pressure product (heart rate x systolic blood pressure) should be calculated as this provides the best estimate of myocardial load. Question the patient about symptoms such as angina, anginal equivalents, shortness of breath, presyncope and claudication during and after exercise. Identify the major symptom which limits exercise and record its intensity, at least descriptively, but ideally with a quantitative measure such as the Borg scale2 (see Box 2). Also record the duration of exercise and the maximum workload achieved. Postexercise period Patients should be observed for at least 10 minutes after cessation of exercise. Continue ECG monitoring for at least five minutes, or longer if clinically indicated. The duration of ECG monitoring may be abbreviated to three minutes in special circumstances, such as thallium scintigraphy, when imaging must commence as soon as possible after exercise. In such cases, the patient should be closely observed for the first 10 minutes after exercise. Resuscitation equipment Exercise stress test laboratories must be adequately equipped to provide advanced life support in the event of a cardiac arrest (see Box 3). The exercise room must be sufficiently large to allow the patient to be removed from the treadmill or cycle and be placed on the ground for resuscitation if complications occur. All resuscitation equipment must be easily accessible and maintained and tested on a regular basis. Personnel Two people (at least one of whom is a registered medical practitioner, see Box 4) should be present in the exercise room at all times during exercise stress testing and the immediate postexercise period. Both should be trained in cardiopulmonary resuscitation and in the recognition of the major arrhythmias and ischaemic patterns on the ECG. No regular specific courses are currently available in exercise stress testing. The assistant for exercise stress testing should be a professional person with training in an area related to health (e.g., ECG technician, graduate of a course approved by the Australian Association for Exercise and Sports Sciences, coronary care-trained nurse, physiotherapist, occupational therapist). He or she must be able to perform cardiopulmonary resuscitation, obtain a high quality ECG trace, and recognise the major arrhythmic and ischaemic ECG and clinical manifestations likely to occur during exercise stress testing. He or she should also have observed exercise stress tests under the supervision of a cardiologist and performed tests under supervision of an experienced assistant. A retraining program in cardiopulmonary resuscitation should be undertaken every two years. References The Committee on Exercise, American Heart Association. Exercise testing and training of apparently healthy individuals: a handbook for physicians. Dallas, TX: American Heart Association, 1972: 13. Noble BJ, Borg GAV, Jacobs I, et al. A category-ratio perceived exertion scale: relationship to blood and muscle lactates and heart rate. Med Sci Sports Exerc 1983; 15: 523-528. * Adapted from a Cardiac Society guideline document, copies of which are available from Professor Freedman. Authors' details 145 Macquarie Street, Sydney, NSW 2000. The Cardiac Society of Australia and New Zealand. No reprints will be available. Correspondence: Professor Ben Freedman, Honorary Secretary. ©MJA 1998 Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <http://www.mja.com.au>". <URL: http://www.mja.com.au/> © 1998 Medical Journal of Australia. 1: Indications for exercise stress testing* As a diagnostic test in patients with suspected coronary artery disease (e.g., men with symptoms that are atypical for myocardial ischaemia, patients with symptoms consistent with recurrent exercise-induced cardiac arrhythmias). To assist in identifying patients with documented coronary artery disease who are at high risk (e.g., due to advanced disease and/or left ventricular dysfunction). To evaluate patients after coronary artery bypass surgery or angioplasty. To quantify a patient's functional capacity, prognosis or response to therapies, and to follow the natural course of disease at appropriate intervals (e.g., after uncomplicated myocardial infarction, in selected patients with congenital heart disease). General contraindications Unstable angina prior to a period of stabilisation Untreated life-threatening arrhythmias Uncompensated severe congestive heart failure Advanced atrioventricular heart block Acute myocarditis Critical aortic stenosis * Adapted from: Guidelines for exercise testing. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Cardiovascular Procedures (Subcommittee on Exercise Testing). J Am Coll Cardiol 1986; 8: 725-738. Back to text 2: Borg scale2 for ratings of perceived exertion 0Nothing at all0.5 Very, very weak1 Very weak2 Weak3 Moderate4 Somewhat strong5 Strong67 Very strong8910 Very, very strong(maximal)Back to text 3: Essential resuscitation equipment Defibrillator with electrogel or electrode pads Suction (motor driven or gas cylinder [Venturi] device with appropriate plastic or metal suckers) Airway plus self-inflating ventilation bag Oxygen and appropriate masks Drugs, intravenous cannulas and giving sets, including atropine, lignocaine, adrenaline, and sotalol or amiodarone for intravenous use, a β2-agonist inhaler (e.g., salbutamol), and short-acting nitrates (e.g., sublingual glyceryl trinitrate or isosorbide dinitrate, or glyceryl trinitrate spray) Alarm to summon nearby personnel and a telephone to call an intensive care ambulance in the event of an emergency Back to text 4: Medical practitioners supervising exercise stress tests should be able to: Evaluate indications for exercise stress testing and recognise contraindications. Interpret all the major abnormalities that can be detected on 12-lead electrocardiography, particularly those associated with ischaemic heart disease; those likely to preclude interpretation of the exercise ECG; those which might indicate deferral of the exercise test; and the tachy- and bradyarrhythmias that may occur during exercise. Differentiate ischaemic from non-ischaemic symptoms during exercise. Perform basic and advanced life support with skill in an emergency situation, and show evidence of continuing competence by, for example, attending retraining courses at two-yearly intervals. Demonstate previous experience in exercise stress testing supervised by a cardiologist, including determination of the most appropriate protocol for individual patients. Back to text

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