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Philip Morris

Clean Your Room A Compendium on Air Pollution

Date: Feb 1982
Length: 19 pages
2025684279-2025684297
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Author
Brown, E.G., J.R.
Lytle, A.A.
Spohn, R.B.
Area
SLAVITT,JOSHUA/OFFICE
Type
SCRT, REPORT, SCIENTIFIC
BIBL, BIBLIOGRAPHY
CHAR, CHART, GRAPH, TABLE, MAPS
Site
N340
Request
Stmn/R1-037
Stmn/R1-102
Named Organization
Bureau of Home Furnishings
Ca Legislature
Comm on Indoor Pollution
Dow Chemical
Epa, Environmental Protection Agency
Merle Norman Cosmetics
Natl Research Council
Paarc
Task Force
Who, World Health Org
Ashrae, American Society of Heating, Refrigerating + Air-Conditioning Engineers
British Medical Journal
Named Person
Aranow
Ayres
Barad
Bland
Bonham
Cameron
Colley
Davies
Froeb
Garfinkel
Glantz
Hagod
Harlap
Hirayama
Lowrey
Luguette
Repace
Schilling
Speer
Spengler
Tager
Trichopoulos
Weber
White
Wilson
Document File
2025684071/2025684856/Americans for Non Smokers
2025684072/2025684855/Americans for Non Smokers
Litigation
Stmn/Produced
Author (Organization)
Ca Dept of Consumer Affairs
Ca State + Consumer Services Agency
Master ID
2025684073/4854
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EXTR, EXTRA
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23 May 1999
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I A COMP'E N DI U'M ON IN'~DOOR POLLUTION' DEPARTMENT OF CONSUMER AFFADRS H'-1
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I CLEAN YO'lJ R ROOM ! I A Compendiiam Describing a Wide Variety of Indoor Pollutants and!Their Health Effects, andi,Containing Sage Advice tolBot!h Housetioldiers and! Statespersons in the Matter of Cleaning,Up,, C C AND INCLUDING I A List of Experts Who Know What They're Talking About I AS WELL AS A Consurner Clean-Up Kit REPLETE WITH A Body Chart EDMUND G. BROWN JR. Governor ALICE A. LYTLE, Secretary Sta~te~ and'lConsume~~r'S~erwices ~ Algency RICHARD B. SPOHN, Director Department of Cornsumer Affairs j!V ~. ~ ~ ~ ~~ €nsumer ~ " ~ Fsa?~r.~arv TQ07 ~, a H-2
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0 E.~ Tb'EACCp'SMO~KE ," Smoke was probably the first "indoor pollutant." Smoke from tobacco poses a majlor health hazard, but also a fundamental issue of individual "choi'ce." It starkly presents a political challenge, to our ability to, protect our health and to, controll our indoor environment. Exposure of non-smokers to ambient (sidlestream)' smo,ke is defined as "involuntary"' or "passive" smoking. Numerous studies have shown involuntarysmoki'ngtobe a si~gnificanthealth, hazard, for several populations incl'udingi infants, children,, pregnant women, elderly people, individuals with cardiovascular disease,, and individuals with impaired pulmonary (respiratory) function, including asthmatics and those with obstructive airway disease. In addition, documentation, is appearing which shows that pro- longed'exposure to sidestream tobacco smoke significantly increases the risk of dilsease in otherwise healthy individuals. Health hazards induced' by involuntary smoking include lung cancer, respiratory infection, anginal (chest pain), decreasedi blood oxygen levels, decreased exercise tolerance, decreased pulmonary function, broncho-constriction and broncho-spasm. Research also shows that tobacco smoke is a major irritant for both smokers and non-smokers, causing symptomswhich include burning eyes, nasal congestion and draina~ge (rhinitis), sore throat, cough, headache and~nauseai. The establishment of separate smoking and no-smoking sections in restaurants, offices, and other public places can be an effective means of'protecting non-smakers. Another alter- native is to require self-extinguishing, cigarettes: this would reduce deaths caused by cigarette-relatedifires and'would. protect bystanders from the fumes of partially-extinguished cigarettes. Adequate ventilation of smoking-areas should be ass!ured',. Research and public information activities are needed to improve public knowledge and awareness.
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......,....~.,.~.,_.,,.....,...Y...,.~ C Chapter III.E TOBACCO SMOKE; A MAJOR SOURCE OF GASEOUS AND PAFtTZCULATE INDOOR AIR POLLUTION 1. SUMMARY Tobacco smoke is a major contributor to indoor air pollution. Exposure of non-smokers to ambient (sidiestream) smoke is defined as "involuntary" or "passive" smoking. Numerous studies have shown involuntary7 smoking to be a significant health hazard for several populations including infants, ch~ildren, elderly people, individuals with cardiovascular disease, and individuals with impaired pulmonary(respi~ratory) function, including asthmatics andi those with obstructive airway disease. In addition, documentation is appearing which, shows that prolongeid exposure to sidestream tobacco smoke significantly increases the risk of disease in otherwise healthy, individuals. Health hazards induced by involuntary smoking include: increased risk of respiratory infection, lung cancer,, decreased blood oxygen levels, decreasedizxercise tolerance, increased episodes of angina in those with heart d'isease, decreased pulmonary function, broncho- constriction, and broncho-spasm. Research also shows that tobacco smoke is a major irritant for both smokers and non-smokers, causing symptoms which include burni'ng eyes, nasal congestion and drainage (rhinitis), sore throat, cough, headache and, nausea. There follows a discussion of some of the hazardous components-of tobacco smoke and' their effects on the body, threshold for harm levels, a review of current literature on health effects of involuntary smoking and suggestions for controlling involuntary inmalation of tobacco smoke. 2. BACKGRO'UND 2.A. COMPONENTS OF'TOSACCO SMOKE It is estimated that one-third of the adult populationin the Uni~ted States smokes tobacco (19). Virtually everyone is exposed to tobacco smoke in varying degrees depending on the concentratiom of smoke and the effectiveness of ventilation found in the indoor envixonment (21):. Two types of smoke are discussed in the literature. Mainstream smoke is defined as smoke drawn through the tobacco~during inhalation, resulting in higher temperatures, more complete combustion and a greater degree of absorption by the -tobacco, the filter if present, andi the smoker himself. Mainstream smoke~ H-4
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n accounts for approximately 4% of the total smoke prodluced. (Exhaled smoke is included in this 4$) Sidestream smoke is defined as smoke arising,f'rom thee smoldering tobacco and accounts for'ttre majority (96$) of' gases and particulates produced (79) . The National Res'edxch Council Committee on Indoor Pollution, provides an in-depth, analysis of the compos'i- tion, of sidestream and mainstream amoke._ Sidestreamsmoke contains higher concentrations (greater than 2:1 in most cases) of.bot'h gaseous and particulate components (19). , 2'. B'. EXPOSURE LEVELSI OF S'ID'ESTAtEAM SMIOM Federal regulations establishing; standards zor' outdoor air pollution levels have been enacted in response to demonstrable adverse health etfects found when the concentration of respirable suspended , particulates (RSP) exceeds threshold for ttiarm~ l!e'vels.. The Environmental Protection Agency has set the 24 hour outdoor RSP level at 75 micrograms per cubic meter (,pg;/m3 ). This is referredl to as the National Ambient Air Quality' Standard or NAAQS. The maximum level, which cannot be exceeded more than once a year, is 260 -(Wgi/m3). Ftepace and Lowrey sampled a number of restaurants, bars, lodge halls, etc. and tound ipdoor RS'P' levels ranging from 30-5'5 ~ug/m3 in non-smoking areas, to.86-697 ug;/m3 in smoking areas. Outdoor samples taken, at the same time ranged from 24-60, pg/m3.(21) All values where tobacco smoke was present exceed the NAAQS for outdoor air ot 75 yg,/m3, and many exceed the very dangerous level of 260 Ag,/m3'. These data become highly significant when we consider that Americans spend over 90% of their time indoors (20). The potential hazard to health appears to be even greater for indoor pollution tharn for outdoor pollution. Standards for safe indoor levels of RS'P have not been established. The American Society ot Heating, Ftefrigeration, and! Air Conditioning Engineers (ASHRAE) has established minimum ventilation standards for ~ acceptable indoor air qvallilty. However,, these standards are not enforceable by any government agency. As energy conservation has become a major priority in this country, there has Deen a significant decrease in, indoor ventilation rates. Air is recirculated (at lower cost) instead of exchang,ed for outdoor (fresh) air, resulting in a higher concentration of respirable particles and greater exposure to tobacco smoke. III.E. 2 H-5
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C. Repace and Lowrey have stiown that a major portion of indoor RSP comes from tobacco smoke. They have established that concentration of tobacco smoke, is directly proportional to smoker density (# of smokers x # cigarettes smoked)! and inversely proportional to effective ventilation rates. They studied RSP'levels for nonsmokers exposed to involuntary smokingiand found them to be in excess of the NAAQS level by tactors of 1.2, 2.0:and 10.0. Another way to look at the data is to gi~ve equivalents in terms of cigarettes smoked. Repace and.Lowrey found their subjec'ts.involuntarily smoked' the equivalents of' 5, 27' and 50 cigarettes per day (21). - Epidiemiological studies have established "threshold f or harm" levels on which the NAAQS level of 75 ug,/m3 is based (29). Some ot these, levels with respect to certain populations are listed below. THRESHOLD FOR HARM LEVELS OF RSP R5P level Cug,/m3) per 24 hrs. ~, ~, Population ( ~ ~ 100 ug/m3 ~ children / ~ ~ ~ 102 ,ug,/m3 ch ilidren ( ~ (I ~ ~ 100 ,ug,/m3 adults ~ (CQP'D)* ~. ~ 80-1010 pig/m3 elderly ( ~ ~ 1170 Pg,/m3 asthmatics (I I I Eft ect I ~ decreasedllung. ~. function ~ increased! ~I respiratory disease ~I . ~. increasedd chronic (, bronchitis J. increased cardio- ( pulmonary symptoms ~, ; increased broncho- J constr'iction andi 11 broncho-spasm *COPD - chronic obstructive pulmonary disease The following graph from the National Research Council sh©ws the monthl~y mean respirable particle concentraitions resulting from differing smoker density in 8,0 homes across six cities. Respirable particulate concentrations may reach 10Orug/m3 with two-smokers in the home (;which exceedLs the NAA;QE level for outdoor air of 75,ug/m3 over 2'4 hour period). III.E. 3 c t H'-6'
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FIGURE I ' -f a s 120 100 80 60 20 . . ~........s ~ Q a0 . ~, .__ ` % ~ ~ ~ . ~ .~ . I •. No. Jan Mar Miv Jul Seo tNmr Jan ANSr 1976 1977 1978 Sample represents 80 homes across six cities (approximately 10-15, homes per city),. Ft'eprintedw.ithperrnissionfr:om S~peing,le~retr al. Source: 2aational'Research Council. Indoor Pollutants. Committee on Indoor Pollution. Washington D.C.: National Academy Press, 19:81. p. IV.109. III-.S. 4 a-T
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The National Research Council reports that over 2,000 compounds have been identif ied ini tobacco smoke. Some of the more hazardous compounds and their mechanisms for action ont~he bodyare described, below. A few, definitions are in order here. PPM, or pp m denotes a quantification in parts per millon Threshoidilevel is the concentration of a compound (in ppm): atwhich, it•becomeshazardious to humain, heal'th . NAA,QS level is the NationalAmbie~ntAir QualityStandiard. (in micrograms per cubic meter Lug/m3). It has been established by the Environmental Protection, Agency as the allowable concentration (on a daily basis) of respirable particles in outdoor air. 2. C. GASES AND y1iPORS FOUND IN SIDESTREAM SMOKE 1. Carbon, monoxide has 210 times greater affinity for hemoglobin (the oxygen carrying component ot the blood) than oxygen. The presence of carbon monoxide permanently prevents the binding, transport, and release of oxygen by the hemoglobin of each affected' cell, therebyrediuci.ng oxygienievels in, blood and tissues. The body mu~st, produce new red blood cells to compensate. The lack ofsuffic~ient oxygen can'increa~se stress int~he heart,, impair reflexes, and worsen respiratory symptoms ior those with pre-existingi lung~ disease. Symptoms, of carbon monoxide toxicity in healthy individuals include headache, dizziness, fatigue, and.nausea. The NAAQS level for carbon monoxide is 9 ppm. Carbon monoxide concentrations in rooms and vehicles wherecig~aretteswere being; smoked ranged from 12; ppmto 90~ ,ppm(7) . Z. Formaldehyde,caluses respiratory irritation. It is, detectable at relatively low, levels (,'0.S ppm) by most people. Formaldehyde causes headache, fatigue, eye, nose and throat irritation, coughing, wraeezing, nausea and skin, reactions (19). Laboratory studies have shown that formaldehyde~ has long term carcinogieni~c, mutagenic, and teratogenic properties. The NAAQS level for formaldehyde is 0.5 ppm. 3'. Nitrogen dioxide causes inflamination of the air passages (bronchioles) in,tne lung,. It is known to N destroy cellular and subcel'lular structures and induces Q emphysema in- lataoratory animals. Symptoms may include . ~ L11 ~ ~ III.E. 5 N ~ c f H-8 0I
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"tightness" in the chest, coughing, and wheezing. The NAAQS level is 5 ppm. Sidiestream, smoke levels nave ueen recorded at 1lesstha~n 1ppm, (,19)1. 4. Acetaldehyde causes irritation and damage (paralysis) to the cilia (hair like pcojections), which liine the upper respiratory tract (29). Respiratory symptoms of coughingiand wheezing may occur. Damage to the cilia results in, a lessening of the body's ability to protect itself agai~nst infectioni, due to an inability to remove particulates and'toxins from the respiratory tract. 2. D. PARTICULATES IN SIDESTREAM SMOKE 1. Nicotine is a poisonous alkaloid used as an insecticide. It constricts blood vessels, increases the likelihood of ventricular arrhythmias, increases blood pressure, increases pulse rate, may cause blood clotti~ng in the.arteries, (thereby increasing risk of artheros- clerotic heart disease) and aggravates respiratory disease. It acts as both a, stimulant and depressant on the nervous systemi(7 )~. 2. Benzoi(a)pyrene and dimethylnitrosamine are known to be carcinogenic to: laboratory animals and to tnumans (29). They are measurable in small amounts in, sidestream smoke. Threshold levels have not been established. 3. Phenols destroy the action of' respiratory tractt cilia. Phenols have also been shown to, potentiate the carcinogenic action of benzo('a)pyrene (29!). 4. Cadmium, lead, arsenic, and fluoride are also potentially tox:ic to humans at relatively low, concentrations and are present in measurable levels in s idestreamismoke . (,'219 ) 3. HEALTH EFFECTS! OF INVOLUNTARY SMO'EING' 3.A. E'FFECTS' OF INVOLUNTARY SMOKING ONI INFANTS AN'D CHILDREN There have been several studies on the effects of parental smoking on thelhealth of their children. The studies show that, children of smoking parents have an increased incidence of upper respiratory infecti~ans, bronchitis, asthma:andl pneumonia, as well as a significant decrease in pulmonary function. It is theorized that children may be more susceptible to air pollutants than adults due to (,1) a greater rate of III.E. 61 HI-9
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C breathing per unit of body 'weight arr4 (12) because they breathe air in the lower levels which have higher concentrations of particulates (26). Cameron, et al. (11969) found that in 727 Detroit households with children under the age of sixteen the presence of tobacco smoke increased the incidence of acute illness (6). Colley (1974) also found a relationship between parental smoking habits (including cough, arnd, ph~leg~mproduction) and the prevalence of respiratory illness in British children (18). In a later study, Colley, et. al. (1974) found the incidence of pneumonia and bronchitis in the first year of life was highest when both parents smoked, intermediate when one parent smoked and lowest when neither parent srnoked.(91) Harlap and Davies (1974) found similar results in a study of hospital admissions for bronclaitis and pneumonia, among 10, 67'2 inf ants in West Jerusalem (14). Schilling;, et al. (,'1977') failed! to detect any relation- ship between parental smoking and'childrens' symptoms and lung function ('23). Bland, et al. (1978) found that. British secondary school students wgo--se parents smoked wexe more likely to report symptoms of cough andi breathlessness (4). Tager, et. al. (1979) found that parental smoking measurably degraded the children's pulmonary function. Tager also found that children of two smoking parents showed a greater, deterioration of lung function than children of a single smoking parent (,27),. Bonham a!nd, Wilson (1981)i examined illness among 39,7191 children f rom birth to, 16 years of age. . They considered the number of smokers per household and ther number of cigarettes smoked. In families with one smoker, they found 7% more days in which the child's activity was restricted and 1418 more days during which, the child was bedriddien, compared to households with noo smokers. ('The children had predominantly respiratory illnes~ses,. ); Children firomhouseholdswith two smokers showed 29% more restricted activity days. For children in families where 45 or more cigarettes were smoked pez day, restricted activity days were 46% higher than for children in families where no cigarettes were smoked (5')'. In sium, children exposedl to involuntary smoking, are sick more frequently and experience measurable deterioration of lung function. This exposure leads to more days of restricted activity, days in.bed', and III.E. 7 H-10 < t

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