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Introduction Environmental-tobacco smoke exposure conditions. DRAFT SESSION 4 CRITERIA FOR EfJVIRONt•tENTAL TOBACCO SMOKE EXPOSURE-~_ 3.1 Effects of different substances Particulate matter 3.1.1 General 3.1.2 Nicotine 3.2 Carbon monoxide 3.3 Irritant gases 3.4 Odorous compounds --~=f~rrr~ci~les for control

CRITERIA FOR ENVIRONNENTAL TOBACCO SP"OKE EXPOSURE --0- 1a health criteria for environmental tobacco smoke have to be defined against the background of knowledge con- cerning the concentration of the agent under various-conditions, the etfect that can be suspected and the combination of the two = the dose-response relationship. In the following a review is given of each of the three aspects against the background of the discussions during the workshop. both during working and at home. Major other pollutants are air .pollutants caused by combustion of fuels for heating or transport ,_._b_o.rne.-po_1J.u,tants to -wh1 ch man i,s exposed to under ~normal ronditi o-ns Exposure conditons Environmental tobacco smoke is one of the many air- systems, indoor pollutants created by man himself in terms of skin scales and bacteria, dust which becomes airborne during normalJactivities in enclosed spaces and compounds produced by man`himself such as carbon monoxide, carbon dioxide'and odorous Typical values for indoor particulates without tobacco.smoke are xx mg/m3 or yy particles/m3 air.. The presence of odorous substances is usually detected when .ventilation decreases below z air changes/hour/person. exact data are present concerning the the p N No ~ ~ N importance of various ~ N . amounts of airborne bacteria but heavy concentrations are OD i known to occur if coughing or sneezing persorrs are present.

I -2- To define the exact exposure conditions for environmental tobacco smoke under various circumstances the -following technical parameters must be known : Number of cigarettes smoked Ventilation characteristisc (air changes/unit time) The number of cigarettes smoked by an individual s probably determined by the nicotine requirements of the smoker and to a certain extent upon his environmental situation. The number of cigarettes smoked is regulated to the personal optimal dose of nicotine. The generating source - the smoker - thus has built-in regulatory mechanism of the generation of smoke. The critical factor for the concentration of the agent will thus be a . ~~the number of smokers present in a particular group of people. Concerning the volume of the room, certain data on ' ,minimum vol'ume per occupant have been suggested. A review of volumes required for different types of rooms is given in Table 1. Table 1 :.'Suggested minimal volumes/occupant for' various .types of rooms : m3/occupant Office X Workshop Y .Meeting room z O N Sleeping XX V N N N CD

S -3- Concerning the size of the ventilation figures for minimal air changes/time unit have bee.n recommended . These are ~ often based on the odor threshold from human pollutants. A list of such ventilation criteria is given in Table 2. Table 2 Air Changes Required Per Person and Hour Type of room Ventilation required Living rooms x m3/h y m3/h z m3/h For rooms where tobacco smoke is being generated a ventilation requirement of 80 m3/p/m has been suggested. Against available data on smoke generation and the existing ventilation, it is possible to define certain levels for the concentration of tobacco smoke compounds. These will be representative for average conditions and for uniform mixing of the tobacco smoke in the room. Higher concentrations might be present ;for_;.short time periods in smoke trails or in very specific atmospheres. Air flows around the head are influenced by body ._,. . eat,'air velocity and body movement and might cause variations .0 - around the average vaiue. Table 3 reports a summary of environmental tobacco smoke compounds in relation to various average environments. The values in the tables are partially based upon extrapolation from measured data,The equation used to calculate the doses has however 01252230

-4- been shown to be accurate (ref. McNall's paper) and should therefore be looked upon as realistic for the different 3.1.1 General 3. 3. Effects of Different Substances . 3.1 Particulate matter ' The particulate matter as such in tobacco smoke is badly defined and the term has originated from physical methods to separate various components of tobacco smoke.. The portion of tobacco smoke which is collected on a high efficiency filter has been termed as the particulate phase whereas the portion which passes thorugh the filter has'been called the. vapor phase. From physical and chemical point of view, this vapor phase in the tobacco smoke at any given time represent distinction is not always correct. The particulates and the an equilibrium and compounds may exist in either of the two phases. <,.During the filtration through an absolute filter certain when the concentration on the filter increases or the air-flow substances can initially deposit on the filte•r and later evaporate the temperature changes. In this respect new analytical metho,ds such as fluorence detection might provide a useful tool for a better definition of the particulate compounds. From biological point of view the definition particulate matter is neither very appropriate. In the same way as one cannot O N N include nitric dioxide, ozone and acrolein and i.n other cases N N ~..~ N talk abouty toxicity of gases in generak which would sometimes

carbon dioxide, the composition of the particulate matter can vary widely. Until the development of more data concerntng the biological effect of various compounds in t-he particulate phase the term will have to be used especially in biological experiments. not possible to establish the desired dose-res-ponse ConcE.•ning environmental tobacco smoke the biological effects not been studied with an adequate dose control. It is relationship for environmental tobacco smoke. pol l uti on ._.s..u.bs.ta.nces i.n .t-he communi ty. An expert gro-u-p -w-orki ng wit-hi n information and formulate recommendations concerning air Extensive work has been performed to collect available An alternative approach would be to evaluate the situation using experience from studies of other particulates where dose-response relationships have been established. the World Health Organisation presented the report "Air Quality Criteria and Guides for Urban Air Pollutants" in 1972. The report contains a review of various air pollution substances, data concerning exposure effects and a presentation.~of criteria and maximum concdntrations. The expert groups points out that . :pol•lutants is both complicated and to a large extent unknown. ,~n....`: .. ~ the connection b etweeen human disease and exposure to air from a respiratory disease. A review of the criteria presented by such as very young people, old people or persons who already suffer Certain groups in the population might be more sensitive than others Y WHO for parti cul ate matter i s gi ven i n Tabl e 4. 01252232

,-1: Mortality & Admission to lospitals smaJ 1. The data reported in.the talbe are not directly applicable A certain value referring to a given effect does not mean that all persons exposed to that value will develop the effect. Usually smoke it is probably prudent not to consider the environmental O 6 Table 4 Patients with Symptoms from upper Lung disease - respiratory airways Se` worse Annoyance reactions 250 MG/m3 100 MG/m3 80 ,ft/m3 (Daily mean) (Arithmetic (Geometric yearly yearly mean) - mean) aerosol which is administere 24 hours a day. It is pointed out in the WHO report that the data given above criteria cannot be applied without certain reservation's. .Even if the above criteria for particular air pollutant represent a difference dose-response pattern as compared to tobacco N tobacco smoke as less toxic until this is proven and in acute M exposures expect reactions at the level which are stated in the N C.~ WHO criteria. w As the data in the WHO.criteria were derived from epidemiological observations on various populations it would be realistic to assure to the tobacco smoke exposure situation. The WHO criteria on particulates are evaluated in,connection with the simultaneous presence of sulphur dioxide. The type of pollution is further "~= different from chemical point of view in as that it represents A# e_nubmer of people in the population which 'develop an effect il

z that they in addition to the environmental air pollution also were exposed to environmental tobacco smoke. For particularly sensitive individuals this exposure might have been low as these persons would probably avoid prolonged staying in environments with concentration above 100 MG/m3. Referring back to concentrations in different environments reported in Table 3, the effects, therefore, probably occur along a minority of persons in smoky atmospheres. It is expected that the effects would be more common among the people who have already developed upper respiratory disease such"as bronchitic patients or patients with asthma. These can then be taken to constitue index groups in the population or the acute effects. Concerning chronic lung ef~fects less information is available concerning at which doses this might appear. Considerable information is available concerning mechanisms behind the carcinogenesis effect but as these experiments are mainly performed on animal or cellular models they cannot be used to establish dose-response relationship, but rather represent situations where the mechanism behind carcinogenesis can be evaluated. ~In comparison to the dose received during direct smoking the environmental tobacco smoke dose exposure can be considered low. Barious estimates have shown that it might be equivalent to a tenth of a cigarette under heavy exposure conditions which .would not be expected to prevail more than a few hours. 01252234 Judging from a epidemiological data chronic lung effects develop among persons actively smoking a low number of cigarettes in the region of 1 to 2 per day. Most data for these 'groups are based on

8 extra polations with the assumption that dose-reponse relationship is a straight one and that no threshold effect occurs. In view of the important defence mechanisms of the body this could well be disputed. As the environmental tobacco it is doubtful if smoke represents a further decrease of that dose it is no-t likely that the exposure will cause widespread chronic lung effects in the exposed population. Support is also given to this theory from the fact that people exposed to high amounts of environmental tobacco smoke, such as pipe and cigar smokers, a.lmost are comparable to nonsmokers in terms of the incidence of chronic lung disease. If an effect should be present in a small percentage ,.-of..•especially -sensitive individuals it would probably be masked by the higher incidents of disease-caused by other pollutants or factors in the environment such as u.rban air or industrial Experience from acute exposre to high amounts of environmental tobacco smoke demonstrates that an increased excretion of nicotine is found in nonsmokers. The amount excreted is in the order of magnitudes below that found in smokers. No data concerning dose-response relationships is available for this low exposure and experience based upon injection ~ N N or mouth intake of nicotine would not be applicable as the N environmental tobacco smoke exposure represent inhalation W ~ challenge where the effects.are known to occur much more rapidly and with smaller doses.

i 9 headache. The effect would probably is difficult to under heavily polluted environments might in susceptible individuz.'s cause light symptoms such as nausea and In spite of the absence of data, it cannot be ruleP- out that the small nicotine exposure which takes place distinguish from that caused by irritant gases and-other odorous substances in the smoke. 3.2 Carbon Monoxide Concentrations that are present under realistic environ- or,long time periods. mental conditions also in rooms polluted with relatively high concentrations'of environmental tobacco smoke range in the order of 5-10 ppm. At levels of around 6 ppm most exposed subjects report-tye or upper respiratory irritation which under normal circumstances will induce action to decrease the exposure also in smokers. Higher levels are unlikely to occur at least levels no evidence has yet been produced which would indicate ris wel-l below the suggested WHO standard of 4% . At these Corresponding carbon monoxide haemoglob.i- n levels under such circumstances would reach a maximum of around 2% which that any biological effects occur. O N N Tobacco smoke contains a multitude of irritant gases u i . N such as formaldehyde, acrolein, ammonia and others. From a biological point of view many of these N W . ~ exert a strong biological effect in terms of protein combining, effects on enzymes and on other molecular structures. .