Tobacco Documents Online

, Indoor Po,~utants Committee oni Indpor Pollutants Board on Toxicology andi Environmental Health Hazards Assembly of Life Sciences National Research Council NATIONAL ACADEMY PRESS Washington, D.C. 1981 r (

7 or deliberate disruption of asbestos-containing surfaces can result in increased fiber concentrations in the indoor environment. There have been a small number of studies in which fiber counts have been documented in association with normal building use. FSctrapol!ation from what we currently undesstand about the exposure-response relationships for asbestos fibers to the very low concentrations reported in indbor spaces, such as school!s, suggests a small health risk under conditions of'normal use. However, deliberate modification of surfaces to remove asbestos from buildings may create a risk of exposure of'occupants and workers. Buildings in wbich asbestos exposure is likely to occur can be identified'. The risk of'exposure from dislodged fibers can be reduced by containment. The occurrence of inesothelloma (a specific form oflcancer believed to result only from the inhalation of asbestos fibers) may provide a very sensitive indicator of'the exposure of'tbe general population. Home~exposure to asbestos due~to aging, cracking,, or physical disruption of insulated pipes or, asbestos-containing ceiling tiles and spackling compounds may be g!reater, than public exposures in schools, which have received the most attention. Homes built before 195A in, northern climates are more likely to have pipes insulated with asbestos plaster., Given the very' common use of'aasbestos ini homes, schools,and other buildings, there is a need for further assessment to identify structures where actual asbestos exposure constitutes substantial risk to humans. The extent of exposure of'tbe general public to asbestos fibers has not been assessed; however, the occurrence of inesothelioma should be carefully monitored in the general population. Manr-made fibers have produced skin irritation, but have not otherwise been demonstrated convincingly as hazardous to health. Epidemiologic and toxicologic investigation of synthetic fibers should continue. On the basis ofl present knowledge, synthetic! fibers in the indoor environment should not cause undue concern. TOBACCO SMOKE Virtually every member of'our society is exposed'to tobacco smoke r 33% of the population smokes, and'the rest are exposed to the smoke released by others. The constituents of tobacco smoke are well documented as hazardous, the prevalence of'population exposures is very high, and there is ani increased incidence of~respiratory tract symptoms and functional, decrements in children residing in homes with smokers, compared with those in homes without smokers. These comsiderations and recent evidence of increased!l'ung-cancez rates among nonsmoking women living with smoking husbands have led us to conclude that indoor, exposure to tobacco smoke has adiverse effects. Coughing, headache, nausea, and irritation of eyes, nose, and! throat are among the reported!symptoms. Although many studies have measured various components of tobacco smoke indoors, total exposure has nott been determdned. Passive exposure to tobacco smoke may constitute an i'mportant exposure to respirable particl'es, such, gaseous compoundsas H-21

l acro,lein and formaldehyde, benzo{alpyrene, andlvazious trace metals. Reduced ventilation increases concentrations of tobacco smoke. As an energy-conserving compromise, smokingl could be restricted: to zones that are well ventilated. Public policy should clearly articulate that involuntary exposure to tobacco smoke has adverse health effects and ought to be minimized or avoided where possible. Under this framework, the prohibition or restriction, of smoking in public buildings, offices, etc., is a control option to be considered!with ventilation and ailr-cleaning,. INDOOR CfJMBUSTI0Ni When fuel combustion occurs indoors--e.g., for heating,, cooking, and power machinery, including automobiles-it gives rise to increased concentrations of gases and particles. Unvented gas cooking is probably responsible for a large portion of nitrogen dioxide exposures in our population. In many homes, chronic exposures to nitrogen dioxide indoors may exceed established natiional ambient-air quality standards. Shorter-term 1-h average concentrations indoors often exceed'the highest hourly concentrations measured!outdoors. The concentrations of nitrogen dioxide and carbon monoxide in residencesi have not been fully documented. However, some studies have shown an, association between gas cooking and the impa3rment of lung function in! children. Gas cooking appliances are also sources of carbon monoxide, carbon dlioxide, formaldehyde,, hydrogen cyanide, sulfate particles, organic particulate matter, and organi'c vapors. The probl'em of' chronic or even peak exposures to combusti'on products indbors will be accentuated with decreased ventilation and the increased!use of portable space-heaters, wood- and coal-burning stoves, and indoor venting of gas dryers.. Carbon monoxide, nitrogen oxides, and particles from automobile exhaust can produce increased concentrations, in office buildi'ngs and public! areas. Concentrations exceeding: 1-h carbon monoxide national ambient-air quality standards (NAAQS) by a factor of'2-4 have beenireported io several ice-skating rinks that usee gasoli'ne-powered ice resurfacing,machinery. Office buildings andi apartment buildings with attached or underground garages can also havee sustained high concentrations of carbon monoxide indoors. Because both carbon monoxide and, nitrogen dioxide are odorless at typical concentrations, the presence of increased and possibly hazardous concentrations may go undetected'6 Although confirmation is necessary, the available evidence suggests that important population exposures to nitrogen dioxide and carbon monoxide can occur indoors and may constitute a, suffici'ent threat to the general public health,to justify remedlial action. Reducing exposure to those gases is.relatively straightforward. Source removal or direct venting,of'combustion sources.should be considered., Efforts to conserve energy present other potential problems indoors. Effective enerqy-conservation measures can result in an overcapac,ity otexisting heating equipment. Operation of'such Hi-22 G l (

50 (} Some of this emission occurs over long periods. Thus, longrterm, effects in humans continuously exposed to formaldehyde at low, concentrations needito be studied. There is a particular need to assess the carcinogenic potential in the concentration, ranges of human exposures, inasmuch,as one study in one strain each of'rats and micee has shown that long-term exposure (lasting 24 mo) caused nasal cancer. Humans have been and are now being exposed to formaldehyde in several' types of occupations and in a variety of structures. Epidemiolocgic investigations are needed to assess the human healthh effects of'formaldiehyde, the magnitude and duration of exposure, and the influence of cigarette-smoking habits and the presence of other contaminants. The mutagenic, embryotoxic, and teratogenic effects must be included in the epidemiologic and animal studies. In humans exposed to formaldehyde, the mechanisms of airway and target cell responses must be evaluated and'characterized as to sensitization and adverse effects in susceptible populationgroups, such as asthmatics and persons with chronic obstructive lung disease. Exposure-effect relations and the mechanisms involved in the biologic effects require further animal toxicologic research. Formaldehyde should be restricted to the extent that household! consumer products and building, products in normal use will not release potentially hazardous or irritating amounts of formaldehyde into indbor air. TOBACCOSMaKE Tobacco smoke has s,hown some evidence of being a major contaminantt in many indoor environments. Involuntary exposure to tobacco smoke should' be assessed to identi'fy locations and populations with high exposure and to determine the factors that contribute to high exposures indoors. Physical and biologic evaluation of'tobacco-smoke constituents should be continued. Tobacco-smoke constituents should be tested for their toxic effects, thei'r ability to act as mutagens or, promoters of carcinogenesis, and their effects in combination with other indoor pollutants. In addi~tion, such properties of tobacco smoke as mass and age, chemical'compositi'on, irritation factors, and odor components should'be examined to learn how, they are affected by ventilation rate, occupancy, extent of smoking, air-cleaning, and other control strategies. The extent to which passive exposure to sidestream tobacco smoke produces respiratory tract symptoms and functional decrements in nonsmokers, especially children, needs further documentation and measurement. Prospective studies of chilldreni in homes with smokerss would be especially desi'rable to determine rates of lung maturation andiillness frequency duringichildhood and adolescence. Information on the potential health effects of exposure of nonsmokers to tobacco smoke,should be widely disseminated. The "energy-cost penalty" of providing adequate ventilation in, indoor environments that permit smokingi should be analyzed in a variety of public buildings. Increasedlciga€ette taxation as a mechanism of H~-23'

51 reimbursement for the cost of the additional air-conditioning needledl to remove tobacco smoke should be explored by governments at all levels. ASBESTOS AND ASBESTIFOAIM FIBERS ii A systematic survey is needed for the evaluation of the distribution, integrity, and concentrations of asbestos in buildings that contain or are thought to contain asbestos ma'terial. However, before this survey can be conducted, there is a need!to: develop; new instruments to record!fi~ber counts continuously, with si'ze determination and possibly asbestiforn-fiber ident'ification, because current sampling andlanalytic techniques: inadequate. Synergistic and interactive toxic effects of asbestos fibers in combinatiom with other air pollutants, particularly organic vapors, should be examined in animal toxicologic! and'mutageni'city studies. Although some asbestiform fibers themselves do not appear, to constitute an immediate health concern~, their role as initiators or promoters in various disease processes should be studied. The incidence.of inesothelioma in humans should be monitored via a registry and.appropriate surveillance methods, to detect cases associated with substantial nonindustrial exposure to asbesti:form fibers. Guidelines should be dieveloped for the control of exposure to airborne asbestos fibers during maintenance, renovation, and reconstruction in bui'ldingGs'that contain, asbestos and asbestos-be'ar'ing shingles, tiles, plaster, etc. COMBUSTICN Indoor combustion produces a number of contaminants. Among the contaminants.that deserve special attention are ni'trogen, dioxide, carbon monoxide, respirable particles, nitrosamines, and! polynuclear aromatilc hydtocarbons. The rates of'their emission from sources of indoor combustion have not been adequately evaluated., The.Committee recommends that contr©lled chamber experiments be condlocted to determine the products and their rates, of emission from various types of combustionlunder various conditions. These experiments should focus pzincipally'on ga&and electric cooking appl!iances~and supplemental heating systems, such as natural-gas, propane, and kerosene~heaters and coal- and wood-burning stoves. Air-venting and air-clieaning systems.should be studied as means of reducing indoor concentrations of contaminants. Indoor concentrations of combustion products have only recently been surveyed. Combustion products are present in many indbor locations, such, as restaurants, cafeterias, homes, hotels, buildings with attached garages, and recreational facili~ties that use gasoline- powered'.equipment. More comprehensive and systematic surveys are needied to identify the range of combustion-product concentratioms encountered indoors and the numbers, of people expasedlto~them. These (I H-24

377 i.. l I with the decline increasing with number of'cigarettes smoked. This effect was independent of the smoking habits of the children.. Pulmonary infection, early in life has been shown to affect pulmonary function in children and adults adversely, and the decline in flow rates reported by Tager et al. may be secondary to the excess risk of .pneumonia in infants whose parents smoke. They attempted to examine this by retrospectively asking the parents about childhood illness, but did not show an association between parental smoking and childhood infection, in contrast with the results of' Rantakallio and' Harlap. It is not clear whether this represents a true difference in the populations. In a further studly of 5- to 9-yr-old children in the same population, Weiss e al.67 reported that parental cigarette-smoking was linearly rel'ated to the occurrence of persistent wheeze (P - 0.012) and lower degrees of'mean forced midiexpiratory flow, Currentt persistent wheeze occurred in one of 57 children (1.8%)' from households where both parents had never smoked= in 10 of 146 children (6.8i) with one parent currently smoking; and in 20 of'169 children (112!8) with both parents currently smoking. When the analysis was repeated with the exclusion of mothers with wheeze, the results were simi'lar--0, 1.8, and 7'.78 wheeze in children with no smoking parents, one smoking parent, and two smoking parents, respectively. Exclusion of'fathers with wheeze gaNe 0, 6I.7, and 14% wheeze, respectively. In summary, children of'smoking parents have an i'ncreased, incidence of persistent wheeze and may be at excess risk of repiratory infection at least for the first year of life. They may also have reduced pulmonary function as adults. The exact interplay amongithe effects of maternal smoking during pregnancy, involuntary smoking by children, and actual occurrence of infection has not been established. CONCLUSIONS • Tobacco smoke is a major source oflpollution in the indoar environment. • The nonsmoker absorbs measurable amounts of carbon monoxidiee and nicotine and may absorb small amounts of other constituents, owing to involuntary smoking. • The amount of carbon monoxidle absorbed owing to exposure to tobacco smoke in the environment varies from negligible amounts in well-ventilated office buildings to enough to raise carboxyhemoglobin contents by 2-3% in a l- to 2-h exposure. • The carboxyhemoglobin produced by the most severe involuntary smoking exposures likely to occur, in everyday living can reduce thee maximali exercise capacity in normal, healthy adulits, but does not effect submaximal exercise to any measurable degree. • Involuntary smoking has not been shown to prodluce acute change in lung volumes, expiratory flow rates, closing volumes, or the slope of phase III of the single-breath nitrogen washout in normal, healthy adults; but longrterm exposure to cigarette smoke i's related to small-ai'rway dysfunction and an increased! incidence of lung cancer in healthy nonsmoking adiusts. H -25

378 • Small changes in visual and auditory vigilance have been. demonstrated at carboxyhemoglobin contents capable of being prodhced by involuntary smoking, but no change initests of complex functionhas been dem~onstrated. The interaction o'flfatigue, alcohol, and carbon monoxide exposure on complex functions, such as automobile driving, has not been investigated for CDHb contents capable of'being prodl:ced under normal conditions of involuntary smoking. • Patients with angina pectoris have reduced'exercise tolerance af'terintvol'untarysmoking thatmaybe~a combi'na~tion, of psychologic stress and a reduction in oxygen delivery to the myocardium induced by carbon monoxide. Carbon monoxide clearly reduces the amount.of exercise possible until the onset of angina in, patients with angina pectoris at COHb contents that may be reached as a result of invol'untary' smoking. .• Carbon monoxide has been shown in one study to reduce the amount of exercise that patients with hypoxic chronic obstructive lung disease can perfmrm.until.the onset of'dyspnea.. • l4ost.nonsmokers find it annoying to be exposedlto cigarette smoke. This annoyance is probably due to substances in the gas phase of't'he smoke. • Cigarette-smoke exposure results in eye,.nose, throat, and respiratory irritation. The eyes~are most sensitive, followe&by the nose and!throat. The particulate phase of ci'garette sanoke seems to be predominantly responsible for this irritation. • Persons with al'lerg,ies are more sensit'ive!to the irritant effects of' ciga'rette smoke. However, there is no p'roof of tobacco allergy. • Children.whose parents smoke may be more likely to have respi'ratory symptoms, bronchitis, and pneumonia as infants and may have poorer pulmonary function as advlts, compared withchildten of nonsmoking parents.Thi'~s relationship is not.indiependent of parental symptoms, socioeconomic class, an6the smokingihabits of'the chdl'dren; and it i~s associatedh with the number of cigarettes s:noked' per day, by the parents. REFERENCES 1. Anderson, E. W.,R. J'. Andelman, J'. M-Strauch, NI. J. Fortuin, and'. J. J. Knelson. Effect of low-level carbon monoxide exposure on, onset and duration of'angina.pectori's. A study in ten patients with. ischemic heart disease. Ann. Intern. Med. 79:46-50, 1973.. 2. Anderson, G., and T. Dalhamn. The risks to healthof passive smoking. Lakartidningen 70:2833-283i61, 19'T3'.. 3. Aronow, W. S. Effects o.f passive smoking on angina pectori!s. D]i. Engl. J. l+ied. 299 :21-24 , 19'7'8'.. 4'. Aronow, W. S., and J. Cassidy. Effect of carbon monoxide on maximal treadmtlli exercise. A study in n'or:aall persons. Ann. Intern. Med. 83:496-499, 1975. 5. Aronow, W. S., J'. Cassidy, J. S. Vangrow, Hi. March, J. C. Kern, J. R. Goldsmith, M. Khemka, J. Pagano, and M. Vawter. Effect of . M C C C H-2b

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3'80, 23. Gliner, J. A., P. B. Raven, S. M. Horvath, B. L. Drinkwatez, and J'. C', Sutton. Man's physiologic response to long-term work during thermal pollutant stress. J. Appl. Physiol. 39.62'8-632, 1975. 24. Harke, H.-P. The problem of' 'passive smoking.' MUnch. Med. Wochenschr. 11Z:23'Z8-2334, 1970. (dn G+erman; English aummary) 25. Harke, H.-P., and A. Bleichert. On the problem of passive smoking. Int. Arch. Arbeitsmed. 29:312-322, 1972. (lin German; Ernglish~ summary) 26. Harlap, S., and A. M4 Davies. Infant admissions to:hospital andd maternal smoking. Lancet 1:529-532, 1974. 27. Hirayama, T. Non-smoking,wives of heavy smokers.have a;higher risk ofllung cancer: A s!tudy from Japan. Br. Med. J'. 2!82A83-185, 1981. 28. Hugodi, C., L. H. &awkins, and P. Astrup. Exposure of passive smokers to tobacco smoke constituents. Int.,Arch. Occup. Environ. Health 4Z:21-29, 1978- 29. Johansson, C. R. Tobacco smoke,imroom air-an experimental investigation of odour perception and irritating effects. Build.. Services Eng. 41:254-262I, 19'76. 30. Johansson, C. R., and 8'. Ronge. Akuta irritationseffekter av tobaksrSk i rumslutt. (Acute irritation effects of tobacco smoke in the room atmosphere). blcrd. Hyg. Tidskr. 4i61:45-50, 1965.. 31. Laties, V. G., andiii'. H. Mtrigan. Behavioral effects of'carbonf monoxide on animals and'man. Ann. Rev. Pharmacol. Toxicol. 19:357-392', 1979. 3Z. Lebowitz, M. D., and B. Burrows. Respiratory symptoms relatedito smoking habits of family adults. Chest 69:48!-50r 1976. 31. beeder, S. R., R. Cbrkhill, L. M. Irwig, W. W. Holland, and J. R. T. Colley. Influence of family factors on the incidence of lower respiratory illness during, the first year, of life. Br. J.. Prevent. Social Med. 30:203-212, 1976. 34. Luquette, A. J., C. W. Landiss, and D: J. Merki. Some immediate effects of a smoking environment on children of elementary school age. J. School Health 40:533-53&, 19'710. 35. National Clearinghouse for Smoking and 8eaith,. Adult Use of Tobacco, 1975. U.S. Department of Health, Education, and Welfare, National Cleariinghouse~for Smoking and'Health, June 1976. 23 pp. 36. National ResearchiCouncil, Committee on Medical and Biologic Effects of Environmental Pollutants. Carbon Mono:cide. Washingtom, D.C.: National Academy of Sciences, 1977. 239 pp. 3'7.,0'Connell, E. J., and'G. B. Logan. Parental smoking,in childhood asthma. Ann. Allergy 32':L42-145, 1974. 38. Pimca, P. E., F. Silverman, and1R. Ji. Shephard. Physiological effects of acute passive~exposure to cigarette smoke. Arch. Environ. Health 33:201-213, 1978. 39. Rantakallio, P. Relationship of maternal smoking to morbidity and mortality of the, child'up to the age of'five. Acta Paediatr. Scandi. 67:621-631, 19718'. 401. Rantakallio, P. The effect of maternal smoking on birth1weight and the subsequent health of the child. Earliy Human Dev. 2:371-382, 1978. H-z8 t

381 41. Raven, P. B., B. L. Drinkwater, S. M. Horvath, R. 0. Ruhling, J. A. Gliner, J. C. Sutton, and N. W. Bolduan. Age, smoking habits, heat stress, and their iriteracti've effects with carbon monoxide andd peroxyacetylnitrate on man's aerobic power. Int. J. Biometeorol. 18:222-232', 1974. 42. Repace, J. L., and A. H. Lowzey. Indoor air pollution, tobacco~ smoke, and public health. Science 20'8:464-472, 19,80. 43. Rummel, R. M., M. Crawford, and P. B'ruce. The physiological effects of inhaling exhaled cigarette smoke in relation to attitudie~of thee nonsmcker. J. School Health 45:524-52'9, 1975. 44. Russell, M. A. H., P. V. Cole, and E.. Brown. Absorption by non-smokers of cacbon.monoxiide from room air polluted by tobacco smoke. Lancet 1:576-579, 1973. 45. Russell, M. A. H., and C. Feyerabend. Blood and'urinary nicotine in non-smokers. Lancet 1:179-181, 1975.. 46. Rylander, R., Ed. Environmental Tobacco Smoke Effects on the Nonsmoker. Report from a Workshop. Scandi. J. Respir. Di~s. ($uppl. 91) :1'-90, 1974.. 47. Rylander, R. Perspectives on environmental tobacco smoke effects.. Scand. J. Respdlr. D'is. ('Suppl. 91)':79-8'7, 1974'. 48. Said, G., and J. Zalokar. Incidence of upper respiratory tract disorders in ch,iildrem of smokers. Ann, d'Otorlaryngol. Chi'!r. Cervico-Fac. 95I:236-240, 19'78. 49:. Schilling, R. S. F., A. D. Letai', S. L. Hui, G. J. Beck:, J. B. Schoenberg, and A. Bouhuys. Lung function, respiratory disease, and smoking in families. Amr J. Epidemiol. 10i61:274-283, 1977. 50. Seppanen, A. Smoking in closed space and its effect on carboxyhaemoglobb'n saturation of smoking andinonsmoking subjiects. Ann. C1in. Res. 9:281-283, 1977. • 51. Seppinen, A., and A. J. Liusitalo. Carboxyhaemoglobin saturation i'n, relation to smoking and various occupational conditions. Ann. C1in4 Res. 9:2'61-268, 1977. 52. Shephara, R. J., R. Collins, and F. Silverman. Responses of' exercising subjects to acute "passive" cigarette smoke exposure. Enwiron. Res. 19:279-291, 1979.. 53. Speet, F. Tobacco and the nonsmoker. A study of subjective symptoms. Arch6 Environ. Health 16':443-446, 1968. 54. Srch, Mi. Uber die Bedeutungides Rohlenoxyds beim,2'igarettenrauchen im Perspnenkraftwageninneren. Dtsch. Z. Gesamte Gerichtl. Med. 60(3):80-89, 1967. (in German) 55. Stezli~ng,, T: D., and D. M. Kobayashi. Exposure to: pollutants in enclosedi"living spaces." En!virc,n. Res. 13:1-35, 1977. 56. Szac!kows!ki, D., H.-P. Harke, and'J. Angerer. Body, burden of carbon monoxide from passive smoking in offices. Innere Med. 3':310-313, 1976. 57. Tager, I. B., B. Rosner, P. V. Tishler, F. E. Speizer, and E. H. Kass. Household aggregation of' pulmonary functioniand chronic bronchitils. Am. Rev. Respir. Dis. 114:485-492, 1916. 58. Tager, I. B., S. T. Weiss.,, B. Rosner, and F. E. Speizer. Effect of parental' cigarette smoking on the pulmonary functiora of chi'ldzen. Am. J. Epidemiol. 110:15-26, 197'9'. H-29