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-9 I I I I I I I I f I I I I I I I I I SlLICA, CRYSTALLINESILICA (RESPIRABLE SIZE) airborne samples contained more than 0.10 mg silica/m3. Several mining industries involvcd respirable silica concentrations of greater than 0.05 mg/m3. Of all the samples analyzed, only 175 (<0.4010) were reported to contain cristobalite or tridymite in concentration greater than 1%. Workers in sandstone, clay, and shale and miscellaneous nonmetallic mineral mills had the highest exposures to silica dust (2.2%-40.9% of the samples exceeded the applicable exposure limit) (IARC 1987). Within the mills the workers with the highest exposures were the baggers, general laborers, and personnel involved in the crushing, grinding, and sizing operations. Cristobalite was found in 168 samples and tridymite, in 3. Personnel grinding and milling quartz or quartzite rock to produce silica flours are also potentially exposed to high levels of silica dust. The particle size of over 98% (by weight) of silica flours is <5 pm. Personal samples of respirable dust were collected at two U.S. silica flour mills. Eighty-five percent of 91 samples from planr employees contained > 0.05 mglm3 dust made up of 95-98% crystalline silica. Cleaning personnel and bagging machine operators were exposed to average respirable concentrations of 0.65 and 1.0 mg/m3, respectively (13 and 20 times greater than the recommended limit). Fifty-four percent of dust samples from 27 U.S. silica flour mills collected between 1974 and 1979 contained more than 0.10 mg/m3 respirable silica. In 1984, approximately 2,400 work sites for 15,000-20,000 coal miners exceeded the level of 5% silica. Major sources of silica exposure in these mines were continuous mining operations; roof, floor, and rock band cutting; and roof bolting operations. Floor and roof samples were found to contain 18%-82% quartz, whereas the coal itself contained only 1%-4%. Granite and stone industry and construction personnel are potentially exposed to respirable silica. Sculptors and carvers, stencil cutters, polishers, and sandblasters had the highest potential exposures; the silica content of respirable dust ranged from 4.8-12.2%. In 1972- 1982, 29% of 45 samples collected at building construction sites in the United Stares exceeded the permissible silica exposure limit by a factor of two or more. Findings were similar for construction work other than buildings; potential exposure of twice the silica permissible exposure limit was found in 27% of 270 samples collected in cut stone and stone products industries. Respirable silica exposures in clay pipe factories ranged from 0.01-0.20 mg/m''; 10% of 348 samples collected from glass manufacturing industries had silica concentrations at least two times the permissible exposure standards; 23-26% of samples from day products and pottery industries had concentrarions more than twice the exposure limits; one-third of dust samples from fibrous glass plants had concentrations of respirable silica dust in excess of 0.10 mg/m3; levels of respirable crystalline silica in a ceramic electronic equipment parts plant ranged from 0 to 0.18 mg/m3; and 23% of samples collected in iron and steel foundries had concentrations in excess of 0.20 mgJm3 respirable silica. Respirable silica exposures have been measured for personnel involved with other miscellaneous silica uses and processes. Silica concentrations in the breathing zone averaged 4.8 mgfm3 for sandblasters (averages inside and outside protective hoods-not actual worker exposure) and 0.7 mg/m3 for helpers. Silica concentrations inside hoods with no air supply ranged from 0.4-7.7 mg/m3. Respirable dust from an abrasive chip factory was found to comain 0.4- 5.896 silica. NIOSH has compiled a list (with percentage of noncompliance) of industries for which respirable silica samples were found to be at least two times the permissible exposure limit; these include agriculture, 63%; mining, 57%; building construction, 29%; construction other rhan buildings, 30%; food and food products manufacturing, 52%; textile manufacturing, 27%; paper and paper products, 13%; chemicals and chemical products, 13%; petroleum refrning, 11%; glassware and glass products, 11%; structured clay products, 26%; pottery and pottery products, 23%; concrete, gypsum, and plaster products, 12%; cur srone and stone products, 27%; abrasive products, KNOWN TO BE A HUMAN CARClNOGEN 16%; blast furnace, steel works, and rolling and finishing mills, 32%; iron and steel foundries, 23%; rolling and extruding nonferrous metals, 22%; miscellaneous metal products, 46%; fabricated metal except machinery, 22%; machinery except electrical, 13%; electrical machinery and supplies, 23%; transportation equipment, 20%; and measuring, analyzing, and controlling instmments and photographic and medical instruments, 3.6%; miscellaneous manufacturing, 9%; and all other industries, 15% (IARC 1987). Nonoccupational exposure to respirable crystalline silica results from natural processes and anthropogenic sources; silica is a common air contaminanc Quartz is the most stable mineral on the earth's surface and is the most common mineral in waterborne sediments (IARC 1987). Residents near quarries and sand and gravel operations arc potentially exposed to respirable crystalline silica. A major source of cristobalite and tridymite in the United States is volcanic rock in California and Colorado (NIOSH 198fi). Local conditions, especially in deserts and areas around recent volcanic eruptions and mine dumps, can give rise to silica-containing dust. Silica and its common forms are found in a large number of consumer products. Talc is derived from crushed rock; spackling, patching, and taping compounds for dry-wall construction are formulated from a blend of minerals including crystalline silica (IARC 1987). Silica flour is added to toothpaste, scouring powders, wood fillers soaps, paints, and porcelain (NIOSH 1986). Consumers may be exposed to respirable crystalline silica from abrasives, sand paper, detergent, cement, and grouts. Crystalline silica also may be an unintentional contaminant; e.g., diatomaccous earth, used as a filler in reconstituted tobacco sheets, may be converted to cristobalite as it passes through the burning rip of tobacco products (IARC 1987). Cristobalite and tridymire are used in insulation, filters, and furnace linings (NIOSH 1986). Regulations Respirable Crystalline Silica is federally regulated by EPA, FDA and OSHA. NIOSH proposed a recommended exposure limit (REL) for all forms of crystalline silica of 50 pg/m3 to protect workers from silicosis as well as potential carcinogenicity. The NIOSH recommendation included that silica, crystalline quaru (respirable) be labeled a potential occupational carcinogen. OSHA has established permissible exposure limits (PEL) for an 8-hr time-weighted average (TWA) forerystalline quartz (a 0.1 mg/m3) and crystalline crisrobalire and crystalline tridymite (< 0.05 mglm3). OSHA also regulates silica, crystalline (respirable) under the Hazard Communication Standard and as a chemical hazard in laboratories. Regulations are summarized in Volume Il, Table A-33. *There is no separate CAS registry number assigned to silica, crystalline silica (respirable size). Smokeless Tobacco* First Listed in the Ninth Report on Carcinogens Carcinogenicity The oral use of Smokeless Tobacco is known to be a human catcinogen based on sufficient evidence of carcinogeniciry from studies in humans which indicate a causal relationship between exposure to smokeless tobacco and human cancer (reviewed in IARC V.37, 1985; Gross et al., 1995). Smokeless tobacco has been determined to cause cancers of the oral cavity. Cancers of the oral cavity have been associated with the use of chewing tobacco as well as snuff which are the two main forms of smokeless tobacco used in the United States. Tumors often azise at the site of placement of the tobacco. REPOAT ON CAflC/NOGENS, NINTH EO/nON

i[,yOWN TO 9E A HUMAN CARCINOGEN Additional Information Relevant to Carcinogenesis or possible Mechanisms of Carcinogenesis (n 1985, IARC determined there was inadequate evidence to indicate that smokeless tobacco is carcinogenic to experimental anima(s. Most reported studies had deficiencies in design. Subsequent studies have provided some evidence that snuff or extracts of snuffproduce tumors of the oral cavity in rats. Smokeless robacco products contain a variety of nitrosamines which have been shown to be carcinogenic to animals. The oral use of smokeless robacco is estimated to be the greatest exogenous source of human exposure m these compounds. Nirrosamines are metabolically hydroxyiated to form unstable compounds that bind to DNA. Exnacts of smokeless tobacco have been shown to induce mutations in bacteria and mutations and chromosomal aberrations in mammalian cells. The oral cavity tissue cells of smokeless tobacco users have been shown to contain more chromosomal damage than those from nonusers (IARC V.37, 1985). Properties Chewing tobacco and snuff are the two main forms of smokeless tobacco used in the United States. Chewing tobacco consists of the robacco leaf with the stem removed and various sweeteners and flavorings such as honey, licorice, and mm. Snuff consists of the entire tobacco leaf, dried and powdered or finely cut, menthol, peppermint oil, camphor, and/or aromatic additives such as attar of roses and oil of cloves (IARC V.37, 1985). Chewing tobacco and snuff contain known carcinogens such as volatile and nonvolatile nitrosamines, tobacco-specific N- nitrosamines (TSNAs), polynuclear aromatic hydrocarbons, and polonium-210 (Z[nPo). These carcinogenic TSNAs are present in vwice or more the concentration found in other consumer products (l3runnemann er al., 1986). TSNAs, including 4-(methylnitrosamino)-1-(3-pyridyl)-1- hutanone (NNK) and N-nitrosonornicotine (NNN), present in tobacco and tobacco smoke are formed from nicotine and tobacco alkaloids. They are known carcinogens in laboratory animals. The concentrations of NNK and NNN, the most carcinogenic of the TSNAs, are high enough in tobacco and tobacco smoke that their total estimated doses to long-term snuffusers and smokers are similar in magnitude to the total doses required to produce cancer in laboratory animals (Hecht and Hoffman, 1989). Snuff stored at ambient room temperature (37 °C) for 4 weeks has shown a significant increase in TSNA levels. The TSNA levels rose from 6.24 to 18.7 ppm, nittosamino acid (NAA) rose from 3.13 to 16.3 Ppm, and volatile N-nitrosamines (VNA) rose from 0.02 to 0.2 ppm (Djordjevic er a1.,1993), Use The use of smokeless tobacco probably dates back 7000 years and is found rhroughout the world. Snuff also had early beginnings. It was u+ed in many of the European and Asian countries and in many cases tite way ir was carried, e.g. snuff boxes, was a sign of wealth and rank. Nvrth America accepted chewing tobacco in favor of snuff around the 1850s (IARC V.37, 1985). After the USDA reclassified some chewing tobacco products as snuff in 1982, rhe male per-capita consumption ofchewing tobacco in ncc United States was estimated to be 1.06 lb in 1983 (U.S. Department ofAgriculmre, I984b; cited by IARC V.37, 1985). Snuff is the only smokeless tobacco product that has had ncreasing sales in the United States (Djordjevic er al., 1993). In the rhree leading brands of snuff that account for 92o/n of the U.S. marker, concentrations of nicotine and TSNAs were significantly higher than in the fourth and fifth most popular brands (Hoffman et sl., 1995). SMOKELESS TOBACCO Production Chewing tobacco production in 1983 was reported to be 39,300 Mg or metric rons. This included plug, moist plug, twist/toll, and loose leaf. Snuff production increased between 1880 and 1930 from 4 million lb (1800 Mg) to more than 40 million lb (18,000 Mg) per year (Garner, 1951; cited by IARC V.37, 1985). FTC (1997), in its sixth biennial report m Congress mandated by the Comprehensive Smokeless Tobacco Health Education Act of 1986, compiled U.S. sales figures for smokeless tobacco collected from the five largest manufacturers (99% of the market). Annual U.S. sales between 1985 and 1995 fluctuared between 114.4 million lb (51,900 Mg [metric tons]) in 1988 and 121.4 million Ib (55,100 Mg) in 1985. The total 116.4 million lb (52,800 Mg) sold in 1995 comprised 54.6 million lb (24,800 Mg) loose leaf/chewing tobacco, 4.2 million lb (1900 Mg) plug/twist chewing tobacco, 4.5 million lb (2000 Mg) Scotch snuff/dry snuff, and 53.1 million 111 (24,100 Mg) moist sauff. Moist snuff has shown the strongest increase in sales-nearly 50% since 1986; it has been advertised the most heavily among the smokeless tobacco products. Regulations Applicable regulations are given in detail in the Regulations table. Federal regulations related to tobacco products that concern taxation, customs duties, and the potential for hand-to-mouth tranafer of toxic substances when using tobacco in the workplace are not addressed in thissection. The U.S. Food and Dmg Administration (FDA) regulates nicotine- containing cigarettes and smokeless tobacco products as nicotine- delivery medical devices under 21 CFR Part 897 "to reduce the number of children and adolescents who use these products and to reduce the life-threatening consequences associated with tobacco use." Measures to reduce the appeal of and access to cigarettes and smokeless tobacco products include numerous restrictions on advertising, including promotional items and event sponsorship. Tobacco-product-dispensing vending machines and self-service displays are prohibited except in adult establishments that do not allow children on the premises at any time. Retailers must request thar persons up to the age of 27 present photographic identification bearing their birth date. Free distribution of tobacco products is prohibited. Each package and advertisement must bear the label `Nicotine-Delivery Device for Persons 18 or Older." Cigarettes may not be sold in packages of fewer than 20. Analyses of FDA jurisdiction over tobacco products (cigaretres and smokeless tobacco products) have been published in the Federal Regirter, including 60 FR 41453-41787, August 11, 1995, with a correction at 60 FR 65349-65350; 61 FR 44615 ff., August 28, 1996; and 61 FR 45219-45222, August 28, 1996. FDA published Children and Tobacco Executive Summaries (U.S. FDA, 1996 a,b), which are available free on the Internet and by mail. The Federal Trade Commission (FTC) of the Department of Commerce administers and enforces the Comprehensive Smokeless Tobacco Health Education Act of 1986, Public Law 99-252 (FTC, 1998). Regulations published in 16 CFR Part 307 include the requiremenr that one of three warning messages in regcrlar rotation and distribution throughout the United States on packages of smokeless robacrn products and in their advertisements. One of the messages is "WARAIING: THIS PRODUCT MAY CAUSE MOUTH CANCER" The requirements are given in derail in the Regulations cable. The Federal Communications Commission (FCC) shares responsibility wirh FTC for the ban of advertisements of cigarettes and smokeless tobacco on radio and television (FTC, 1998). A CFR citation was not located for 15 U.S.C. Sec. 4402(0, which banned, effective August 1986, advertising for smokeless tobacco products on any electronic communication medium subject to FCC jurisdiction. The Centers for Disease Control and Prevention's (CDC) Office on Smoking and Healrh (OSH) is the delegated authoriryto implement RFPOR7ON CARCINOGENS, NINTH EDITION 2073777278 111-47

SMax;;LESS TOBACCO I I I I I I I I I I I I I I I I I major components of the DHHS's tobacco and health program, which comprises programs of information, education, and research. CDC's authority includes collection of tobacco ingredients information to facilirare HHS's overall goal of reducing death and disabiliry from use of tobacco products (CDC, 1997). Manufacturers, packagers, and importers of smokeless tobacco products are required by the Comprehensive Smokeless Tobacco Health Education Act of 1986 (Public Law 99-252) to report to The Secretary of HHS the ingredients, including nicorine, in smokeless tobacco products. HHS is authorized to undertake research on the health effects of ingredients. CDC has published requests for comments in the Federal Register on its proposed darm mllection in 61 FR 49145-49147, September 18, 1996, and 62 CFR 24115-24116, May 2, 1997. CDC has also requested comments on an analytical protocol proposed for measuring the quantity of nicotine in smokeless tobacco products (62 FR 24116-24119, May 2, 1997, and 62 FR 29729, June 2, 1997). (These regulations were not final as of Januaty 31, 1999.) HHS, under 45 CFR Part 96-Subpart L-Subsrance Abuse Prevention and Treatment Block Grant, requires that to be eligible for Block Grants to support substance abuse prevention and rreatment services, each State must have in effect and strictly enforce a law that prohibits sale or distribution of robacco products to persons under age 18 by manufacturers, distributors, or retailers. Federal agendes have issued regulations to implement Public Law 104-52, the Prohibition of Cigarette Sales to Minors in Federal Buildings and Lands. Some agencies have nor rescricted their corresponding regulations to cigarettes. For example, the General Services Administration (41 CFR) and the Treasury Department (31 CFR) prohibit the vending and free distribution of tobacco products on property under their jurisdictions. Under 32 CFR 85.6, health promotion efforts in each military service should include smoking prevention and cessation programs. Health care providers are encouraged to take the opportunity at routine medical and dental examinations to apprise service personnel of tobacco use risks (including smokeless tobacco) and how to ger help to quir_ Regulations are summarized in Volume II, Table A-34. *There is no separate CAS registry number assigned to smokeless tobacco. Solar Radiation and Exposure to Sunlamps or Sunbeds* First listed in the Ninrh Report on Carrinogenr Carcinogenicity Solar radiation is known to be a human carcinogen, based on sufficient evidence of carcinogenicity from studies in humans, which indicate a causal relationship between exposure to solar radiation and cutaneous malignant melanoma and non-melanocyde skin cancer. Some studies suggest that solar radiation may also be associated with melanoma of the eye and non-Hodgkin's lymphoma (reviewed in IARC V.55, 1992). Exposure to sunlamps or sunbeds is known to be a human carcinogen, based on sufficient evidence ofcarcinogenicity from studies in humans, which indicate a causal relationship between exposure to sunlamps or sunbeds and human cancer. Epidemiological studies have shown that exposure to sunlamps or sunbeds is associated with cutaneous malignant melanoma (Swerdlow er al., 1988; Walter et al., 1990; Autier et al., 1994; \vJesterdahl et al., 1994). Exposure-response relationships were observed for increasing duration of exposure, and effects were especially pronounced in individuals under 30 and those who experienced sunburn. Malignant melanoma of the eye is also associated with use of sunlamps. In contrast, there is little support for KNOWN'TO BEA HUMAN CARCf :'Ou: an association of exposure to sunlamps or sunbeds with nori melanocytic skin cancer (IARC V.55, 1992). The evidence that solar radiation and exposure to sunlamps , sunbeds are human carcinogens is supported by experimental studi, in laboratory animals, and studies demonstrating UV-induced D\ damage in human and animal cells. Sunlamps and sunbeds em. radiation primarily in the ultraviolet A (UVA) and ultraviolet . (UVB) portion of the spectrum. Numerous studies have shown th:, simulated solar radiation, broad spectrum UV radiation, UN". radiation, UVB radiation, and UVC radiation are carcinogenic i. experimental animals. There is evidence for benign and malignar. skin tumors and for tumors of the cornea and conjunctiva in mia rats, and hamsters. UV radiation also causes a wide spectrum of DN.damage resulting in mutations and other genetic alterations in variety of in vitrn and in vivo assays for genotoxicity, including assay using human skin cells (LARC V.55, 1992). Properties Solar radiation from the sun includes most of the electromagneti spectrum (IARC V.55, 1992). Of The bands within the optic: radiation spectrum, UV light is the most energetic and biologicall damaging. UV light is divided into UVA, UVB, and UVC. UVA i the most abundant of the three, representing 95% of the solar L1 energy to hit the equator, and UVB represents The other 5%. Th:t short wavelength UVC rays are absorbed by ozone, molecular oxygen and water vapor in the upper atmosphere so that measurable amount from solar radiation do not reach the earth's surface (Farmer zn, Naylor, 1996). Molecules that absorb UV and visible light contain moieties rallec chromophoric groups in which electrons are excited from the grounc stare to higher energy states. In returning to lower energy or grounc states, the molecules generally re-emit tight (Dyer, 1965). Molecule sensitive to UV light absorb and emir UV light at characteristi. maximum wavelengths (k), often expressed as 2.ms. Photochemical and photobiological interactions occur wher photons of optical radiation react with a photoreactive molecule resulting in either a photochemically altered molecule or twc dissociated molecules (Phillips, 1983; Smith, 1989; both cited bc IARC V.55, 1992). To alter molecules, a sufficient amount of energi' is required to alter a photoreacrive chemical bond (breaking the original bond and/or forming new bonds). UVB is considered to be the major cause of skin cancer despite its not penetrating the skin as deeply as UVA or reacting with the epidermis as vigorously as UVC. UVB's reactivity with macromolecules combined with depth of penetration make it the biologically most potent portion of the UV spectrum, with respect tc short-term and long-term effects. UVA, while possibly not as dangerous, also induces biological damage (Farmer and Naylor. 1996). Photobiological reactions of concern for skin cancer risk due to UV light exposure are the reacrions with the main chromophores of the epidermis-urocanic acid, DNA, rryprophan, tyrosine and the melanins. DNA photoproducts include pyrimidine dimers. pyrimidine-pyrimidone (6-4) photoproduas, thymine glycols, and DNA exhibiting cytosine and purine damage and other damage such as DNA strand breaks and cross-links and DNA-protein cross-links. The different DNA photoproducts have varying mutagenic potential (IARC V-55, 1992). . UV-induced DNA photoproducts produce a variety of cellular responses that contribute to skin cancer. Unrepaired DNA photoproducts may result in the release of qRokines that contribute to mmor promotion, tumor progression, immunosuppression, and The induction of latent viruses (Yarosh and Kripke, 1996; L`1RC V.55, 1992). REPORT ON CARClNOGENS, NINTH EDITION ' 111-0a 2073777279