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KNOWN TO BE A HUMAN CARC7NOGEN for worker exposure. The National Occupational Hazard Survey, conducted by NIOSH from 1972 to 1974, estimated that 1,300 workers were possibly exposed to Direct Blue 6 (NIOSH, 1976). In 1980, NIOSH estimated that about 500 workers were potentially exposed to the dye in the workplace (NIOSH Review, 1980). Occupational exposure to Direct Blue 6 may occur for workers in a variety of industries identified by NIOSH, including paper and allied products, petroleum and related industries, rubber and plastic products, leather and leather products, instrumentation and measuring devices, and banking. In addition, the textile industry accounts for substantial risk for occupational exposure. Direct Blue 6 has been detected in the workplace air of a textile dyeing operation, at total airborne particulate concentrations of 1.20-3.94 mg/m3. It has been estimated that 25% of the benzidine-derived aw dyes are applied to textiles, 40% to paper, 15% to leather, and the remainder to other diverse applications (NIOSH 24, 1978; IARC V.29,1982). The general population may possibly be exposed to Direct Blue 6 through the use of retail packaged dyes containing the benzidine- based dye. Potential consumer exposure to Direct Blue 6 depends upon the ability of the dye to migrate our of the consumer product and either penetrate the skin or break down prior to penetrating the skin. A risk of potential exposure to Direct Blue 6 may have existed for people using hair dyes which contained the compound. In addition, ingestion of Direct Blue 6 may occur if food is eaten which contained residues from packaging in which the dye was used. Regulations In late 1980, CPSC collected scientific and economic data to propose a ban on the use of all benzidine congener dyes in consumer products. CPSC also completed studies on the dermal penetration of two of these dyes, and noted no dermal penetration. The use of benzidine congener dyes in retail packaged dyes for home and school use has been voluntarily decreased. Therefore, CPSC voted to deny the petition that requested a ban of these consumer dye products. Educational materials have been developed and are available to warn artists of the potential danger of benudine congener dyes. EPA regulates Direct Blue 6 under the Superfund Amendments and Reauthorization Act (SARA), and the Toxic Substances Control Act (TSCA), subjecting it to reporting requirements. FDA does not regulate the cosmetic use of Direct Blue 6, but was petitioned to approve the chemical for use as an indirect food additive (e.g., as a dye for paper and paperboard products). In 1979, the petition was withdrawn. OSHA regulates Direct Blue 6 under the Hazard Communication Standard and as a chemical hazard in laboratories. Reguladons are summarized in Volume II, Table A-24. Environmental Tobacco Smoke* First Listed in dte Ninth RePortoaCarrbmgenr Carcinogenicity Environmental tobacco smoke (ETS) is known to be a human rarclnogen based on sufficienr evidence from studies in humans that indicate a causal relationship between passive exposure to tobacco smoke and human lung cancer (reviewed in fARC V. 38 1986; USEPA 1992, CEPA 1997). Studies also support an association of ETS with cancers of the nasal sinus (CEPA 1997). Evidence for an increased cancer risk from ETS is from studies examining nonsmoking spouses living with individuals who smoke cigarettes, exposures of nonsmokers to ETS in occupational settings, and exposurt to parents' smoking during childhood. Many studies, including recent large population-based case control studies, have demonstrated increased risks of about 20% for developing lung tancer ~ IlEPORT ON C.ARLINO6EN5, N/NTH EDmON ENVIftONMENTAL 7OBACCO SMOKE following prolonged exposure to ETS, with some studies suggesting higher risks with higher exposures. Exposure to ETS from spouses smoking or exposure in an occupational setting appears most strongly related to increased risk. Additional Information Relevant to Carcinogenesis or Possible Mechanisms of Carcinogenesis ETS is a complex mixture of gases and particles comprising smoke from the burning cigarette, cigar or pipe tip (sidesrream smoke), mainstream smoke which is not inhaled by the smoker, and exhaled smoke. Sidestream smoke and mainstream smoke contain many of the same chemical constiments induding at least 250 chemicals known to be toxic or carcinogenic. There is evidence from animal studies that the condensate of sidesneam smoke is more carcinogenic to the skin of mice than equivalent weight amounts of mainstream smoke. Exposure to primarily mainstream smoke through active tobacco smoking has been determined to cause cancer of the lung, urinary bladder and renal pelvis, oral cavity, pharynx, larynx, esophagus, lip, and pancreas in humans. Between 80 to 90% of all human lung cancers are attributed to tobacco smoking. Exposure of nonsmokers to ETS has been demonstrated by detecting nicotine, respirable smoke particulates, tobacco specific nicrosanrines and other smoke constituents in the breathing zone, and by measurements of a nicotine metabolite (corinine) in the urine. However, there is no good biomarker of aunuladve past exposure to tobacco smoke, and all of the information collected in epidemiology studies determining past exposure to ETS relies on estimates which may vary in their accuracy (recall bias). Other suggestions of systematic bias have been made concerning the epidemiological information published on the association of ETS with cancer. These include misdassification of smokets as nonsmokers, facrors related to lifestyle, diet, and other exposures that may be common to couples living together and that may influence lung cancer incidence, misdiagnosis of metastatic cancers from other organs in the lung, and the possibility that epidemiology studies examining small populations and showing no effeccs of ETS would not be published (publication bias). Three recent population-based (Stockwdl et aL 1992; Brownson et aL 1992; Fontharn et aL 1994) and one hospital-based (Kahat tt al. 1995) case control studies have addressed potential systematic biases. The three population-based studies each showed an increased risk from prolonged ETS exposure of a magnimde consistent with prior estimates. The hospiral-based study gave similarly increased risk estimates, bur the results were not statistically significant. The potential for publication bias has been examined and dismissed (CEPA 1997), and the reported absence of increued risk for lung cancer for nonsmokers exposed only in occupational settings has been found not to be the case when the analysis is restricted to highor quality studies (Wells 1998). Thus, factors related to chance, bias, and/or confounding have been adequately excluded, and exposure to ETS is established as causally related m human lung cancer. Properties Environmental tobacco smoke (ETS) is the sum of sidestream smoke (SS) (interval between puffs), mainstream smoke (MS) emitted at the cigarette mothpiece during inhalation, compounds diffused through the wrapper, and MS that the smoker exhales (NRC 1986; U.S. EPA 1992; CEPA 1997). Tobacco pyrolysis products are formed both during smoke inhalation and during the interval between inhalations (NRC 1986). A number of chemicals present in ETS are known or suspected roxicants/irritants with various acute health effects. Prominent among them are the respiratory irritants: ammonia, formaldehyde, and sulfur dioxide. Acrolein, hydrogen cyanide, and formaldehyde affect mucociliaty function and at higher concenQations can inhibit smoke rlruance from lungs (Batosra 1976). Nicotine is I

T I I I I I I I ' I I I I I ENVIRONMENTAL TOBACCO SMOKE addictive and has several pharmacrological and toxicological actions. Nitrogen oxides and phenol are some other toxicants present in ETS. Over 50 compounds in ETS have been identified as known or reasonably anticipated human catcinogens. Most of these compounds are present in the particulate phase (IARC 1986). Use There are no known uses of environmental tobacco smoke. Production Environmental tobacco smoke is a direct result From lighting a cigarette and its production cannor be quantitatively measured. Exposure Exposure to environmental tobacco smoke mainly results from inhalation of sidestream and exhaled mainstream smoke. The National Research Council (NRC) estimated that nonsmokers exposed to ETS averaged urinary concentrations of 25 ng/mL cotinine (active smokers had levels of 1,825 nglmL). The cotinine Level varies depending upon occupations, with higher cotitdne concentrations for those occupations where workers are exposed to higher levels of tobacco smoke; such as in restaurants, bars and bowling alleys (Millar 1991). It should also be noted that many people who reported no exposure to ETS do have low levels of systemic cotinine, possibly from exposure to nicotine from the diec Mean nicotine levels varied from 0.120 µg/m3 to 21.5µg1m3 depending upon various environmental exposure m ETS. ETS exposure levels were also estimated by measuring respirable suspended particles (RSP) (<2.5 pm). Millar (1991) cited that Repace and Lowrey (1980, 1982) found RSP concentrations in public access buildings averaging 0.242 µg/m3. In later studies, they estimated a 62% probability of nonsmoker exposure in the workplace. The mean RSP exposare levels varied from 18.5gg1m3 to 45.4µg/m3 depending upon the work environment (Repace and Lowrey 1980, 1982). Levels of ETS in restaurants were found to be approximately 1.6-2.0 times higher than other office workplaces and 1.5 times higher than residences of, at least, one smoker. Isolating smokers to a specific section of restaurants was found to affford some protection for nonsmokers, but the best protection resulted fmm seating arrangements that segtrgared smokers by a wall or partition. Nonsmokers are still exposed to nicotine and respirable particles. Food-servers, who spend more time in restaurants, are exposed even more to ETS, though they may work in nonsmoking sections (Lautbert eta11993). Levels of ETS in bars were found to be- approximately 3.9-6.1 times higher than in office workplaces and:4.4-4.5 times higher than in residences. Bars are not always compelled to provide smoking and nonsmoking sections and this may account focthe higher lere{ of E£S exposure in bzrs versuss restaurants (Siege11993f: Mattson et aL (1989) studied personal E£5 saposure in airplanes Levels of nicorine:fdundin cabins seem to vary widely owing to unstandardized methods of collection and measurement. Oldaker and Conrad (1987) measured nicotine levels in the passenger cabins of cnmmerdal airliners...Usingaltidden suitpse pump, they found that the average nicotine concentration in nonsmoking areas wu_ 5.5 µglm3 (0.03-40.2 µglm3 [range; n=49]); while in the smoking sections it was 9.2 p.gW (0-08-112.4. Jiglm3 [range: n=26]). Using these data, calculated "cigarette equivaknta°, for the smoking section ranged from 0.00008-0.15 cigarettes per 55 minute flight. Comparisons of rhe results, however, have shown some consistendes Studies have shown that nonsmoking seats near the smoking section have levelsas high as those seatsin smoking sections; The type of ventilation system a plane used seemed m be the most important fector in ETS exposure. Planes with 100% freslt air had lower levels of ET$ compared to 50% fresh and 5096 recirculating'air. Recirculating m-a4 KNOWN TO BE A HUMAN CARqNOGEN air systems, however, have been used in more new planes berause they improve fuel economy. Since attendants are nor confined to the nonsmoking section, they had higher ETS exposures than passengers in nonsmoking sections (Mattson et aL 1989). Regulations ETS is regulated by Environmental Protection Agency (EPA), food and Drug Administration (FDA), and Occupational Safety and Health Administration (OSHA). Regulations are summarized in Volume II, Table A-25. *There is no separate CAS registry number assigned to environ- mental tobacco smoke. Erionite CAS No. 66733-21-9 First Listed in the Seventh AnnualReport on Carcinogrnr Carcinogenicity Erionite is kuaum to be a human carcinogen baud on su4fieient evidence of carcinogenicity in humans (IARC V.42. 1987; U1RC 5.7, 1987). Descriptive studies have demonstrated very high mortality from malignant mesothelioma, mainly of the pleura, in three Turkish villages where there was contamination from erionite and where the population had been exposed from birth. Erionice fibers were identified in lung rissue samples in cases of pleural mesothefioma; ktruginous bodies were found in a much higher proportion of inhabitants in contaminated villages than ofthose in two control villages. An IARC Working Group reported that there is sufficient evidence of carcinogenicity of erionite in experimenatl animals (IARC V.42, 1987; IARC 5.7, 1987). When administered by inhalation, erionite induced plural mesodteliomas in rats of both sexes. When administered by intraperitoneal injection, erionite induced peritoneal mesotheliomas in male mice. When administered by intrapleural injection, erionite induced pleural tnrsotheliomas in male and female rats. Properties Erionire is a naturally occurring fibrous zeolite. Its basic structure is aluminosilicate tetrahedra. The oxygen is shared between two tetrahedra. The structure of etionite is chainlike, with six tetrahedra '' n on each edge of the unit forming part of a chain of indefinite length. Erionite consists of white prismatic crystals in radiating gmups. It is nor known to occur in other than fibrous fnrm, in single needles or in clusters. Erionire fibers, with a maximum length of approximately 50 pm, are generally shorter than asbestos fibers. Erionire particles (ground ta powder) resemble amphibok asbeseas flhers. It absorbs water up to 20% of its weighl Its gas absotpaon, ion exchange, and catalytic properties are highlyselecri.va.Zeolites, in general, have good i thermal stability, rehydrarion kinetics, and water vapor adsorption capacity (Clifton, 1985). - Use Natural zeolites have many commercial uses; these molecules selectively adsorb molecules from water or air. A former use of erion'tte -wass as a noble metal-impregnared catalyst in a hydrocarbon-cracking process (IARC V.42: 1987; USEPA, 1988). A minor and probably unintentional use of erionite is for housebuilding materials-of etionite- rich blacla (lARC V.42, 1987). Its use m irtaeasc soil fertility and to control odors in. livestock produstion has been studied. Natural erionite has been replaced by-syndtetie non5brotrs zeolires (USEPA, 1988). Etionite is not known m be currently mined or marketed for commercial purposes (fARC V.42,1987). - 2073777276