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Philip Morris

Secondhand Cigarette Smoke Worsens Symptoms in Children

Date: 19860815/P
Length: 3 pages
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David, M.F.
Freigang, B.
Luciuk, G.H.
Murray, A.B.
Zimmerman, B.
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SCIENTIFIC AFFAIRS/BLACK LATERAL OLD S&T
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PSCI, PUBLICATION SCIENTIFIC
BIBL, BIBLIOGRAPHY
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R529
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Cancer Pediatric Society
Childrens Hospital of Eastern Ontario Ot
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2025816943/2025817075/Missing
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2025817015/7022

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Health Sciences Centre Winipeg
Hospital for Sick Children Toronto
Alberta Childrens Hospital Calgary
Cancer Pediatric Society
Childrens Hospital Vancouver
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MARG, MARGINALIA
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05 Jun 1998
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rno85e00

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1II I From the Canadian Paediatric Society Secondhand cigarette smoke V/ worsens symptoms in children with asthma Section on Allergy,• Canadian Paediatric Society T he physician who fails to ask the parents of a child with asthma whether they smoke is taking an incomplete history. And if they do smoke, the treatment of the child is likely to be optimal only if the physician persuades them not to sntioke, at least when at home. Cigarette smoke contains high concentrations of irritants, such as formaldehyde, acrolein, ammo- nia and nitrogen oxides. Pulmonary damage re- sults not only from mainstream smoke (that in- haled by the smoker) but also from sidestrearn smoke, the visible smoke that comes from the tip of a burning cigarette and is inhaled involuntarily by nonsmokers who are nearby.' Adverse effects of cigarette smoke have been shown both in controlled laboratory settings and under everyday conditions. When adults with asthma are placed in an environmental chamber and exposed to sidestream smoke for I hour, there is a significant decrease in forced expiratory vol- ume in 1 second (FEV,) and forced expiratory flow at 25% to 75% of forced vital capacity (FEPzsti.n%).2 Under the natural, conditions of a typical work environment, nonsmokers also absorb a considerable amount of tobacco smoke, the amount being comparable to that taken in by 'light" smokers.3 As in those exposed to smoke under experimental conditions, there is a decrease in FEFn,w,n.1 As well, cigarette smoke appears to i 'INelneeir t3rs. And,ew e. Mu,»y (pinei,Wi auM,o.X eb;!- dien's HospitaL Vancouver, AlirL F. David fcAanmanA Health Scieetnes Centn:. YVwripea; Divno FreiRang, AlEeru Children's HospitaL Ca)aary,• Gearge H Luciuh. C?+ildren s Haspital, Yanciovrer, and Darry Timmernun, HosRital lor Siclt Childnm, Taonto Reprint requests to; Section on Allerglr, Canadian Paediatric Society, Qtildnn's Hospital ol Eastern Onuria, 401 Smyth Rd., Ottawa, Ont. X1HBL1 increase bronchial responsiveness. Adults who smoke have bronchial hyperirritability s•• and hy- perirritable bronchi' more readily go into spasm when exposed to irritants such as cold air, exercise and smoke.' Some of the effects of tobacco smoke are known. It may cause increased respiratory epitheli- al permeability'•' as well as altered structure and function of pulmonary macrophages.10 But the exact way in which tobacco smoke increases bron- chial irritability and decreases airflow rates is unclear. Immunologic mechanisms are suspected since tobacco components can stimulate the pro- duction of igE antibodies in the mouse" and since IgE levels are higher in people who smoke than in those who do not." However, evidence that tobac- co smoke is antigenic in humans is scanty.13 Results of epidemiologic surveys on the effects of parents' cigarette smoke on their children were initially equivocal but have become more consis- tent since the appropriate questions have been asked. When workers inquired simply whether the parents smoked'"_'y or whether one or both smoked,'6 they were unable to show a significant difference in the prevalence of wheezing or a difference in pulmonary function between two groups of children. Only when the mother's and father's smoking habits were considered separately did it become evident that the mother's smoking was more important. In a large sample of schoolchildren, Hassel- blad and colleaguest' found a dose-response rela- tion between the amount smoked by the mother and the decrease in the child's FEYp.s. No effect due to the father's smoking habits was observed. Gortmaker and associates" conducted two random surveys in which they telephoned a total of 3966 households with children aged 17 years or less. In 18% of the children who were said to have - For prespibinp inlormation see page 405 CMAI, VOL 135, AUCUST 15, 1986 121
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wheezing in one survey and in 34% in the other survey, the wheezing was attributable to maternal smoking. Tashkin and coworkers" studied' 971 nonsmoking schoolchildren and found that flow rates were significantly lower in younger boys and older girls whose mothers were smokers. Ekwo and collaboratols" had 1355 children inhale iso- proterenol and found a small but highly significant increase in flow rates in children whose parents were smokers but not in those whose parents were nonsmokers. Veda1 and colleagues" performed spirometric tests in all students at 14 primary schools. They found that parental smoking, partic- uiarly by the mother, was associated with lower flow rates. However, although the difference in mean values between children of smokers and children of nonsmokers was statistically signifi- cant, it was small, being no greater than 5% for any mean measurement. The small difference may have been due to the fact that only a minority of children in a representative population are prone to asthma and liable to have bronchospasm. To determine whether the differences in pul- monary function between children of smokers and children of nonsmokers in a more susceptible population would be greater, Murray and Morri- son22 examined 94 children aged 7 to 17 years who had been consecutively referred to an allergy clinic and who had a history of wheezing. The asthmatic symptoms were 47% more severe in the group whose mother were smokers than in those whose mothers did not smoke, the FEV, was 13% lower, the FEFi,ti.,s,, was 23% lower and the mean degree of bronchial irritability was four times higher. There was a highly significant correlation between each of these indications of asthma sever- ity and the logarithm of the number of cigarettes that the mother smoked in the house, which suggests a dose response to cigarette smoke. There was also evidence that the length of exposure had' an effect. The older children, who had presumably been exposed to cigarette smoke for more years than the younger ones, were more severely.affect- ed. In contrast, the father's smoking habits ap- peared to have little effect on the child's asthma, probably because he smokes significantly fewer cigarettes at home than the mother does22 and spends less time with the children, and perhaps because the estimates of number of cigarettes smoked were more accurate for the mother than for the father, as the mother usually provided the history. In addition, given that over 50% of mothers now work outside the home, the smoking habits of private day-care givers may affect children's health. Infants admitted to hospital for chest prob- lems have been found to have significantly more day-care givers who smoked than did control infants (A. Cherian and W. Feldman: personal communication, 1986). Active smoking in ehildnert is also thought to impair pulmonary function: it is associated with a significant decrease in the rate of increase of the FEV, and FEF=,...,,,,?1 There is littte doubt that cigarette smoke worsens asthma, but it is uncertain whether the damage to the child!'s lungs is permanent. Avail- able evidence suggests that the changes that aggra- vate asthma are reversible. Vedal and colleagues2l reported that the pulmonary function of children whose mothers were ex-smokers was not signifi- cantly different from that of children whose moth- ers were nonsmokers. If, as seems to be the case, passive smoking results in changes that obstruct airflow, and if these changes are revenible, the parents of chil- dren with asthma should be persuaded not to smoke in their children's presence. This can be achieved easily with some concerned parents, who will stop smoking as soon as they learn that! it is harming their child. Those who are less anxious about their child's health may reject the idea that their smoke is harming the child and will' continue to smoke as much as ever. In between these two extremes are parents who will smoke fewer ciga- rettes, try not to smoke in the house, smoke only when standing by an open window, or install various filtering mechanisms, such as electrostatic air cleaners. The efficacy of these devices is not known, but they are unlikely to be beneficial. Standard filtration systems do not remove the toxic substances in the gaseous phase of tobacco smoke?' Whether the parents stop smoking depends not only on their personal motivation but also on the advice and help given by the physician. He or she can recommend a self-help smoking cessation program, such as that developed by the Canadian Lung Association, or attendance at an organized smoking cessation clinic. Success rates of these programs vary from 40% to 97%, though some of those who quit have resumed smoking by 1 year.'S Physicians who are consulted about the care of children with asthma have the duty to inquire about the smoking habits of the family and of day-care givers and to advise those who smoke to refrain from doing so, at least while in the house or in the car with the child. Needless to say, the chiidren should be questioned, in private, as to whether they smoke. References 1. rAe Health eonsrquences of Smoking: Cincer. A Report of tlie Suraeon Genera/(DHHS (RHSI pub) no 82-50179), US Dept of Health and Human Services, Rockvilk. Md. 1982 2: Dahms TE. Bolin Jt=, Slavin RG: Passive smoking - effects on bronchial asthma. Chest 1981; 80: 530-534 3. Feyerbend C, Higginbonam 7, Russell MAH: Nicotine concentrations in urine and saliva of smokers and' non- smokers. Br Med J 1902; 284: 1002-1004 4. White JR. Froeb HF: Small-airways dysfunction in non- smokers chronically exposed to tobacco smoke. N' fngl I Med 1960; 302: 720-723 5. Genard JW, Cockcrofi DW, Cotton D) et al: IncTeased N C 13J' Lrl CO 0 C N J 322 CMA), VOL 135, AUGUST 15. 1986
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non-specific bronchial rractivtty in cigarette cm,+ken with normal lung function. Am Rev Respir Dt• 1yN0: 122: 577- 5K1 6. Bucrkn GD. Day A. Vandordo.•Irn )1. M al: Lffrcts oI cigarette smoking and short term smoking n•ssation on airway responsivencss to inhaled methacholinc. Am Rrv. Reslrir Dis 1984; 129: 12-14 7. Cockcroft DW: Mechanism of perennial asthma. Gancrr 1983; 2: 253-255 R. Kennedy SM•, Elwexxi RK, Wiggc JR et al: Increased airway muco.wl permeability of smokers:, relationship to airway reactivity. Am Rev Respir Dis 1984; 129: 143-148 9. Huchon CJ, Russcll JA, Baritault LG et al: Chronic air flow limitation does not increase respiratory epithelial perme- ability by aerosol'v.ed solute, but smaking does. Am, Rev Rr%pfr Di.c 1984; 130: 457-460 10. Harris JO, Gonzalez-Rothi RJ: Abnormal phal;ntvso.omc fusion in pulmonary alveolar macrophaFcs of ratc exposed chronically to cigarette smoke. lhid: 467-471 11. Justus DE, Adams DA; Evaluation of tobacco hypcrsensitiv- ity responses in the mouse. A potential animal model for critical study of tobacco allergy. Int Arch Allergy Al+pl' Immunol 1976: ; 51: 687-695 12: Gerrard JW. Heiner DC, Ko CC et al:, Irnmunoglol+ulin kvel's in smokers and non-smokers. Ann Allergy 1980; 44:. 261-262 13. Sogn DD, Goldstein RA, Cohen SC: Toliacco - its Role in ANergv and Immunity in Smoking and Health: a Report of rhe Surgeon General (DHEW puhl no PHS79-50066). US Dept of Health, Education, and Welfare, Public Health Service, Rockville, Md, 1979: 5-32 14. Schilling RSF, Letail AD. Hui SL et, al: Lung function, respiratory disease, and smoking in families. Am JEridemi- nl'1977; 106. 274• 283, IS. Li•hoa•itr MD, Btrcrnwc B: Rrr. Piratl+rr .t•mPu.m• n•latrd u. .milking hahit• r+ffamh• adult4 Chralo7h: nu. 48 , Stl ln tAxil;e R: The effccts ofl indiwor poIlunon c.n Anr.rn.t children. Arch Environ Health 19ti2: 37. 151-155 17. Haa.elhlad V, Humble CC, Gnham MG ct ali, Indcx+r environmental determinants of lung function in children. Am Rev Respir Dis 1981; 123: 479-485 18. Gortmaker SG Walker DK, Jacot+s FH et al , Parental smoking and risk of childhood asthma.,Am J ruhlie Hvalth 1982c 72: 574-579 14:, Tachkin DP, Clark VA. Simmonr. M et al: The UCLA population studies of chronic obstructive respiratory dis- caae: 7. Relationship between parental smoking and chil- dren's lung function. Am Rev Rrsl+ir Dis 1984; 129: 891- 897 20. Ekwo EE, Weinberger MhL.Lachcnhruch PA et al: Relation- ship of parental smoking and gas cooking to respiratory disease in children. Chest 19B3: 84: 662-b68'. 21: Vedal 5, Schenker MB, Samet JM et al: Risk factors for childhood respiratory disease. Analysis of pulmonary func- tion. Am Rev Respir DisJ984; 130: 167-192 22. Murray AB, Morrison BJ:;The effect of cigarette smoke from mothers on bronchial readivity, and severity of symptoms in asthmatic children. I Allergy Clin Immunol 1986: 77: 575-581 23. Tager 1B, Munoz A, Rosner B et al: Effect of cigarette smoking on the pulmonary function of children and adoles- cents. Am Rev Respir Dis 1985; 131: 752-759 24: Collishaw NE. Kirkhride J, Wigle DT: Tobacco smoke in the workplace: an occupational health hazard: Can Med Acco,, / 1984; 131: 1199-1204 25. Bailey WC: Smoking cessation. Chr•st 1985;,88: 322-323 Pfizer Hospital Products Group Award for Innovation Pfizer Hospital Products Group is oftering a S50 000 award to recognize recent, promising inventions in the field of hospital products, Intensive care technology and new modalities of treatment made possible by medical devices. Eligibility Any person active in a health-care-related field is eligible for the award. The submitted invention or discovery must not be subject to exclusive development rights by the applicant or any for-profit organization. Full-lime employees of companies who produce or sell health care products are not eligible. FullLtime employees of Pfizer or its subsidiaries are not eligible. Criteria for selection Applications for the Hospital: Products Group Award will be reviewed by an independent advisory board consisting of distinguished academics and leaders in biomedical!research. Each application will be evaluated for scientificc merit of the invention, discovery or innovation, practical applicability of the proposed devtce• potential benefit to the patient and impact on the quality of health care. A compWete dossier must include: A completed Pfizer Hospital Products Group application and checklist form. The curriculum vitae and bibliography of the appiicant~. A list of scientific publications• relevant articles and patents. The name and address of two persons who are prepared to submit a letter of reference on behalf~of the applicant. A signed confidentiality agreement. The award recipient will receive a plaque and a cheque for $50 000 in May 1987. The applications must be received by Pfizer Hospital Products Group no later than Jan. 31. 1987. Applications will not be accepted after this date. For further inforrtnation relating to the Pfizer Hospital Products Group Award for Innovation program contact: George Ftouty, MD Pfizer Hospital Products Group Award for Innovation Pfizer lbapital Products Group 73S E. 42nd 8t. New York. NY 10017 CMAJ. VOL 135. AUGUST 15, 1986 323

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