Tobacco smoke formaldehyde

Compounds that induce bronchoconstriction include tobacco smoke, formaldehyde, and diethyl ether. Several other compounds, such as acidic fumes (e.g., sulfuric acid) and gases, such as ozone and nitrogen dioxide, as well as isocyanates, can cause bronchoconstriction. Also, cellular damage in the airways induces bronchoconstriction because of the release of vasoactive compounds. Frequently, different mechanisms work at the same time, provoking bronchoconstriction and increased secretion of mucus, both of which interfere with respiration. 

Air quality in homes and workplaces is affected by human activities, construction material, underground minerals, and outside pollution. The most common indoor pollutants are radon, carbon oxides, nitrogen oxides, tobacco smoke, formaldehyde, and a large variety of organic compounds. Indoor atmospheres can also be contaminated with fine particles such as dust, aerosols (from spray cans), fungal spores, and other microorganisms. 

Formaldehyde is an important industrial chemical for the production of synthetic resins. These resins are applied primarily as adhesives in the production of a large number of consumer products and construction materials that end up in homes. Other sources of indoor formaldehyde include urea-formaldehyde foam insulation, textile additives, as well as combustion and tobacco smoke. Formaldehyde is one of the many VOCs present indoors and it is considered the most abundant among them. It has important toxic effects in the 0.1-5 ppm concentration range. 

Tobacco smoke contains a variety of air pollutants. In a survey of 80 homes ia an area where the outdoor TSP varied between 10—30 lg/m, the iadoor TSP was the same, or less, ia homes having ao smokers. la homes having oae smoker, the TSP levels were betweea 30—60 lg/m, while ia homes having two or more smokers, the levels were betweea 60—120 lg/m (64). la other studies, iadoor TSP levels exceeding 1000 lg/m have beea fouad ia homes with aumerous smokers. la additioa to TSP, burning tobacco emits CO, NO formaldehyde [50-00-0] bea2opyreaes, nicotine [54-11-5] pheaols, and some metals such as cadmium [7440-43-9] and arsenic [7440-38-2] (65). 

Sources of human exposure to formaldehyde are engine exhaust, tobacco smoke, natural gas, fossil fuels, waste incineration, and oil refineries (129). It is found as a natural component in fmits, vegetables, meats, and fish and is a normal body metaboHte (130,131). FaciUties that manufacture or consume formaldehyde must control workers exposure in accordance with the following workplace exposure limits in ppm action level, 0.5 TWA, 0.75 STEL, 2 (132). In other environments such as residences, offices, and schools, levels may reach 0.1 ppm HCHO due to use of particle board and urea—formaldehyde foam insulation in constmction. 

Dinitrophenyl-hydrazine has been successfully employed in the analysis of simple aldehydes, substituted aldehydes, glyoxal and gluteraldehyde (43-45), all the isomers of the C3 to C7 aliphatic ketones (44,45) and in the determination of formaldehyde in tobacco smoke (46). 

Formaldehyde is a harmful compound released from walls and furnitures in new houses because adhesives containing HCHO are often used in constmction materials. In addition, H CHO is emitted by tobacco smoke and combustion exhaust gases. Long exposure to HCHO causes serious health problems called sick house diseases. In Japan, the concentration of HCHO in indoor air is regulated [54] to under 0.08 ppm based on the recommendation of the World Health Organization (WHO). 

Formaldehyde (HCHO) is a colorless gas with a pungent odor. Formaldehyde has found wide industrial usage as a fungicide and germicide, and in disinfectants and embalming fluids. The serious sources of indoor airborne formaldehyde are furnimre, floor underlayment insulation, and environmental tobacco smoke. Urea formaldehyde (UF) is mixed with adhesives to bond veneers, particles, and fibers. It has been identified as a potential hazardous source. 

If the insult persists, hyperplasia (cell proliferation) proceeds and leads to an abnormal epithelium. Injury produced by chronic exposure to irritants such as SO2, NO2, O3, formaldehyde, and tobacco smoke includes undifferentiated basal cells (hyperplasia), squamous metaplasia, and goblet cell metaplasia. In practice, many irritants produce responses between mild and severe, and various combinations of degeneration, inflammation, and proliferation may be observed. 

The California Air Resources Board has prepared risk assessments for a number of toxic airborne compounds and mixtures, designated as toxic air contaminants, TACs (Table 16.15). For example, risk assessments for individual compounds such as benzene, benzo[a]pyrene (see Chapter 10), formaldehyde, and vinyl chloride have been carried out, in addition to complex mixtures such as diesel exhaust (California Air Resources Board, 1997a) and environmental tobacco smoke (California Environmental Protection Agency, 1997). These risk assessment documents form the basis for controls imposed as part of the risk management process (e.g., see Seiber, 1996). 

Formaldehyde is found in construction materials such as particle board and triplex, textiles, floor covering, furniture, soft plastic, paper, paint, glues, household products, ink, and tobacco smoke, and can cause serious problems for MCS patients. For information about formaldehyde, see www.allergybuyerscl ub.com/leaming/ montanaformaldehyde. html. 

Methyl glyoxal has been found in many foods, such as bread ( 3 ), boiled potatoes (4 ), roast turkey (5 ), and tobacco smoke (6 ). It is a well known fact that sugar caramelization produces numerous carbonyls including formaldehyde and methyl glyoxal ( 7). Among... 

Tobacco smoke contains both particulate matter (see Chapter 4) and a large number of gaseous and vapor components. These components include CO, CO2, NO, NO2, acrolein, pyridine, methyl chloride, acetaldehyde, formaldehyde, and dimethylnitrosamine. Particulate matter comprises, for example, nicotine, pyrene, benzo( )pyrene, naphthalene, methyl naphthalene, aniline, and ni-trosonomicotine. 

Significant quantities for formaldehyde are consumed in the production of other resins or polymers such as polyacetyls, melamine resins, and alkyl resins. Formaldehyde is also used in rubber/latex manufacture, textile treatment other than permanent-press fabrics, dye manufacture and use, photoprocessing chemicals, laboratory fixatives, embalming fluids, disinfectants, and preservatives. Formaldehyde can also be emitted by combustion appliances, wood fires, tobacco smoke, and in indoor chemistry. 

Beryllium, chromium, isocyanates, mercury, phthalic anhydride, trimellitic anhydride Asbestos, silica, metals, toluene, oxidant gases, tobacco smoke, benzene, toluene Formaldehyde, isocyanates, ethylenediamine... 

In Fig. 4, the relative contribution of individual airborne hazardous pollutants to lung cancer rates are presented. The results presented in Fig. 4 were obtained after removing cancer incidents that are directly attributable to tobacco smoke which primarily is an indoor pollutant. As seen from this figure the PIC (which includes PAH), 1,3-butadiene, benzene, and formaldehyde, which are produced by all combus-tion/incineration processes, were the largest contributors to lung cancer, representing in excess of 50% of the risk, far more than dioxins. However, because different chemicals target different parts of the body. 

Removing formaldehyde sources from the house will also reduce the risk of exposure. Since formaldehyde is found in tobacco smoke, not smoking or smoking outside will reduce exposure to formaldehyde. Unvented heaters, such as portable kerosene heaters, also produce formaldehyde. If you do not use these heaters in your home or shop, you help to prevent the build up of formaldehyde indoors. 

Although formaldehyde is widely recognized as a dermal irritant that can sensitize the skin in humans, the evidence for immunologically-mcdiatcd sensitization of the respiratory tract is weak. Despite the widespread use of formaldehyde in several occupational exposure scenarios (and the widespread occurrence of formaldehyde in tobacco smoke), there are only a few available case reports of formaldehyde-exposed workers who display marked changes in pulmonary function variables (e g.,... 

A major route of formaldehyde exposure for the general population is inhalation of indoor air releases of formaldehyde from new or recently installed building materials and furnishings may account for most of the exposure. Environmental tobacco smoke may contribute 10-25% of the exposure. Since formaldehyde in food is not available in free form, it is not included in estimated exposures (Fishbein... 

Smokers and persons who live in a home with a cigarette smoker also may be exposed to higher levels of formaldehyde. Environmental tobacco smoke, which is a combination of diluted sidestream smoke released from a cigarette s burning end and mainstream smoke exhaled by an active smoker, can contribute 10-25% (0.1-1 mg/day) of the total average indoor exposure to formaldehyde (Fishbein 1992). 

Carraro et al. (1997) developed an indirect competitive immunoenzyme assay to detect serum IgG antibodies against formaldehyde conjugated to human serum albumin. This technique was used to compare the presence or absence of the antibodies in 219 healthy subjects who differed in smoking habits (tobacco smoke is a significant source of fonnaldehyde exposure) and occupational exposure to formaldehyde. The indirect competitive immunoenzyme assay was developed and applied as a qualitative method. Additional research is needed to detennine if the method can be modified to provide a reliable and precise measure to quantify exposure level or exposure duration. 

Godish T. 1989. Formaldehyde exposures from tobacco smoke A review. Am J Public Health 79 1044-1045. 

Mansfield CT, Hodge BT, Hege RB, et al. 1977. Analysis of formaldehyde in tobacco smoke by high performance liquid chromatography. J Chromatogr Sci 15 301-302. 

Quackenboss JJ, Bronnimann D, Camilli AE, et al. 1988. Bronchial responsiveness in children and adults in association with formaldehyde, particulate matter, and environmental tobacco smoke exposures [Abstract]. Am Rev Respir Dis 137 253. 

Formaldehyde and other aldehydes are receiving increasing attention both as toxic substances and as promoters in the photochemical formation of ozone in the atmosphere. They are released into residential buildings from plywood and particle board, insulation, combustion appliances, tobacco smoke, and various consumer products. Aldehydes are released into the atmosphere in the exhaust of motor vehicles and other equipment in which hydrocarbon fuels are incompletely burned. A sensitive method for analyzing aldehydes and ketones is based on the sorption of these compounds to an SPE sorbent and their subsequent reaction with 2,4-dinitrophenylhydrazine (DNPH) on the sorbent. They are then analyzed as their hydrazones by HPLC (Fig. 7.9). A gradient analysis by HPLC may separate as many as 17 components with detection by ultraviolet (UV) light. 

In 1954, Kosak (2170) pnblished a list of components reported to be present in tobacco smoke. His list is shown in Table 111-1. The aldehydes listed included formaldehyde, acetaldehyde, acrolein (2-propenal), butyraldehyde (bntanal), benzaldehyde, and 2-fnraldehyde. In several instances, Kosak qnestioned whether the analytical data reported were snffi-cient to define nneqnivocally the identity of the smoke component. The ketones listed by Kosak included 3-pentanone (diethyl ketone), 4-heptanone (di-n-propyl ketone), 17-tritri-acontanone (dipalmityl ketone), 2,3-butanedione (biacetyl), and higher ketones. 

The major ciliastatic components in tobacco smoke are water soluble. These include formaldehyde, acetaldehyde, crotonaldehyde, ethyl carbamate, and hydrazine all are water-soluble tobacco smoke components that appear as tumorigens... 

This raises the question as to how much formaldehyde or acetaldehyde or crotonaldehyde in ETS, an already extremely dilute system, will reach the lung whether inhaled orally or nasally Are the levels of these tobacco smoke components in ETS sufficient for these compounds to be included on the Hoffmann and Hecht list (1727), the Occupational Safety and Health Administration (OSHA) list (2825), the Hoffmann and Hoffmann lists (1740, 1741, 1743), or the Hoffmann et al. list (1744) ... 

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