Monograph on the Potential Human Reproductive and ... - OEHHA

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BISPHENOL A 179 Table 16 TWA Measurements of Bisphenol A in the Workplace 8-hr TWA (mg/m 3 ) Industry or activity Location/year No. of samples Sample type mean (range) b Bisphenol A manufacture Various U.S./not specified Not specified Bisphenol A NS (Not detected to 2.6) Filling big bags Europe/1998 3 Inhalable bisphenol A 0.81 (0.21-1.79) Filling silo tankers Europe/1998 3 Inhalable bisphenol A 0.89 (o0.5-1.61) Various tasks Europe/1998 8 Inhalable bisphenol A 0.3 (0.13-0.62) Plant operator Europe/not specified 7 Inhalable bisphenol A NS (0.021-1.04) Maintenance Europe/not specified 3 Inhalable bisphenol A NS (0.52-1.35) Maintenance Europe/1998–2000 8 Bisphenol A NS (o0.05–0.62) Charging big bags Europe/1996–1997 5 Inhalable bisphenol A 0.35 (0.02–0.93) Plant operator Europe/not specified 13 Bisphenol A 0.61 (0.02–2.13) Maintenance Europe/not specified 2 Bisphenol A 1.06 (0.4–2.08) operator Epoxy resin manufacture Loading/unloading U.S./1970-mid 1990s 26 Bisphenol A 0.18 (o0.1-0.99) Bagging/palletizing U.S./1970-mid 1990s 37 Bisphenol A 0.25 (o0.1-2.8) Process operators U.S./1970-mid 1990s 25 Bisphenol A 0.26 (o0.1-1.1) Equipment U.S./1970-mid 1990s 6 Bisphenol A o0.1 technician Maintenance U.S./1970-mid 1990s 2 Bisphenol A 0.8 (0.37-1.2) Bisphenol A Use Powder paint use a U.S./B1979 7 (3 personal and 4 area Bisphenol A (plant 1) 0.005 (0.004–0.006) samples) 21 (15 personal and 6 Bisphenol A (plant 2) 0.175 (0.001–1.063) area samples) a NIOSH (1979). Other data are from the European Union (2003). b Range given representing different occupational activities. NS, not specified. (NIOSH, 1984) or in a plant where an epoxy resin coating was applied to steam turbine generators (NIOSH, 1985). Rudel et al. (2001) used a GC/MS technique to measure bisphenol A concentrations at one United States workplace where plastics were melted and glued; a concentration of 0.208 mg/m 3 was reported. [Bisphenol A exposures in U.S. powder paint workers were estimated at B0.1–100 lg/kg bw/day based on TWA exposures of 0.001–1.063 mg/m 3 , an inhalation factor of 0.29 m 3 /kg day (USEPA, 1988), 100% absorption from the respiratory system, and 8 hr worked per day.] No information was located for dermal exposure to bisphenol A in occupational settings. Using their Estimation and Assessment of Substance Exposure model, the European Union (2003) estimated that dermal exposure of workers to bisphenol A was unlikely to exceed 5 mg/cm 2 /day. It was noted that the highest potential exposure to bisphenol A would occur during bag filling and maintenance work. One study provided information on biological monitoring of bisphenol A in workers exposed to an epoxy compound. In 3 Japanese plants, exposed workers included 42 men who sprayed an epoxy hardening agent consisting of a mixture of bisphenol A diglycidyl ether (10–30%), toluene (0–30%), xylene (0–20%), 2-ethoxyethanol (0–20%), 2-butoxyethanol (0–20%), and methyl isobutyl ketone (0–30%) (Hanaoka et al., 2002). The workers wore ‘‘protection devices’’ during spraying. Controls consisted of 42 male assembly workers from the same plants who Birth Defects Research (Part B) 83:157–395, 2008 did not use bisphenol A diglycidyl ether. In 1999, urine samples were collected periodically, treated with bglucuronidase, and examined for bisphenol A by HPLC. Urinary bisphenol A concentrations were significantly higher in exposed workers (median: 1.06 mmol/mol creatinine [2.14 lg/g creatinine]; range: o0.05 pmol to 11.2 mmol/mol creatinine [o0.1 pgto22.6 lg/g creatinine]) compared to controls (median: 0.52 mmol/mol creatinine [1.05 lg/g creatinine];range: o0.05 pmol to 11.0 mmol/mol creatinine [o0.1 pg to 22.2 lg/g creatinine]). The difference of the averages was reported as 2.5 mmol/mol creatinine [5.05 lg/g creatinine] (95% confidence interval [CI] 1.4–4.7 mmol/mol creatinine [2.8–9.5]). Bisphenol A was not detected in three exposed workers and one control. [Assuming excretion of 1200 mg/day creatinine (Ouchi and Watanabe, 2002), mean (ranges) of bisphenol excretion in urine were 2.57 lg/day (o0.12 pg to 27.1 lg/ day) in exposed workers and 1.26 lg/day (o0.12 pg to 26.6 lg/day) in unexposed workers. With an assumed body weight of 60 kg, bisphenol A occupational intake was estimated at 0.043 lg/kg bw/day (o0.002 pg to 0.45 lg/kg bw/day) in exposed workers and 0.021 lg/kg bw/day (o0.002 pg to 0.44 lg/kg bw/day) in unexposed workers.] 1.3 Utility of Data Numerous studies reported bisphenol A concentrations in canned foods and infant formula. Experiments examined potential concentrations of bisphenol A
180 CHAPIN ET AL. Table 17 Maximum Reported Bisphenol A Concentrations in U.S. Ambient Air and Dust Samples Sample Bisphenol A concentration Reference Outdoor air o52 ng/m 3 Monthly average 0.12–1.2 ng/m 3 Wilson et al. (2003, 2006); Matsumoto et al. (2005) Indoor air r193 ng/m 3 Wilson et al. (2003, 2006); Rudel et al. (2001, 2003) Indoor dust r17.6 mg/g Wilson et al. (2003, 2006); Rudel et al. (2001, 2003) Drinking water o0.1 (MDL) o0.005 Boyd et al. (2003); Kuch and Ballschmiter (2001) Table 18 Maximum Reported Bisphenol A Concentrations Measured in Foods or Food Simulants Exposure source Bisphenol A concentration Table reference Polycarbonate infant bottles r55 mg/L (o5 mg/L in U.S. study) Table 4 Polycarbonate tableware r5 mg/kg Table 4 Canned infant formulas r113 mg/L (o6.6 mg mg/kg in U.S. study of water mixed Table 5 formula; o13 mg/kg in U.S. formula concentrate) Canned infant foods r77.3 mg/kg Canned foods r842 mg/kg (r39 mg/kg in U.S. studies) Table 6 resulting from leaching of bisphenol A from polycarbonate bottles under a variety of conditions. There minimal data available for bisphenol A concentrations in drinking water but these show concentrations below the limit of detection. Bisphenol A has been detected in surface waters and solid waste landfill leachates. Bisphenol A has been detected in indoor dust samples and indoor and outdoor air samples. Data for occupational exposure to bisphenol A in the U.S. are very limited. Only 2 studies reported TWA exposures to bisphenol A in U.S. workers. Several estimates of human bisphenol A exposure were developed using bisphenol A concentrations measured in food and the environment. Although very limited for U.S. populations, there are data reporting bisphenol A concentrations in urine, breast milk, and amniotic fluid, but none for blood or fetal blood. Exposure estimates have been derived from urinary bisphenol A concentrations in multiple studies. 1.4 Summary of Human Exposure In 1999 and 2003, it was reported that most bisphenol A produced in the U.S. was used in the manufacture of polycarbonate and epoxy resins and other products [reviewed in (Staples et al., 1998; SRI, 2004)]. Polycarbonate plastics are used in various consumer products and the products most likely to contribute to human exposure are polycarbonate food containers (e.g., milk, water, and infant bottles). Epoxy resins are used in protective coatings. Food cans lined with epoxy resin are a potential source of human exposure. Some polymers manufactured with bisphenol A are FDA-approved for use in direct and indirect food additives and in dental materials (FDA, 2006). Resins, polycarbonate plastics, and other products manufactured from bisphenol A can contain trace amounts of residual monomer and additional monomer may be generated during breakdown of the polymer (European-Union, 2003). Bisphenol A may be present in the environment as a result of direct releases from manufacturing or processing facilities, fugitive emissions during processing and handling, or release of unreacted monomer from products (European-Union, 2003). Because of its low volatility and relatively short half-life in the atmosphere, bisphenol A is unlikely to be present in the atmosphere in high concentrations (European- Union, 2003). A study of 222 homes and 29 day care centers found bisphenol A in 31–44% of outdoor air samples with concentrations of oLOD (0.9) to 51.5 ng/ m 3 (Wilson et al., 2006). Rapid biodegradation of bisphenol A in water was reported in the majority of studies reviewed by the European Union (2003) and Staples et al. (1998). Drinking water concentrations of bisphenol A at Louisiana and Detroit Michigan water treatment plants were below the limit of detection (o0.1 ng/L). Chlorinated congeners of bisphenol A resulting from chlorination of water may be degraded less rapidly (Gallard et al., 2004). Bisphenol A is not expected to be stable, mobile, or bioavailable from soils (Fent et al., 2003). A study of 222 homes and 29 day care centers found bisphenol A in 25–70% of indoor dust samples with concentrations of oLOD (20) to 707 ng/g (Wilson et al., 2006). The potential for bioconcentration of bisphenol A in fish is low (Staples et al., 1998; European- Union, 2003). Table 17 summarizes concentrations of bisphenol A detected in environmental samples and drinking water. The highest potential for human exposure to bisphenol A is through products that directly contact food such as food and beverage containers with internal epoxy resin coatings and polycarbonate tableware and bottles, such as those used to feed infants (European-Union, 2003). Studies examining the extraction of bisphenol A from polycarbonate bottles or tableware into food simulants are summarized in Table 4. Studies measuring bisphenol A concentrations in canned infant foods are summarized in Table 5 and studies measuring bisphenol A concentrations in canned food are summarized in Table 6. Table 18 summarizes the general findings from all the food contact–material studies. Bisphenol A concentrations were measured in canned foods produced and purchased from various countries. Table 19 summarizes BPA concentrations reported in human body fluids. Measurement of bisphenol A concentrations are affected by measurement technique, Birth Defects Research (Part B) 83:157–395, 2008
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National Toxicology Program U.S. De
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NTP.will.transmit.the.NTP-CERHR.<st
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National Toxicology Program U.S. De
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nTp brief tainers.with.internal.epo
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Population Adult General. Populatio
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Table 3. Blood and Breast Milk Biom
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Figure 2b. The weight of evidence t
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in.considering.the.biological.plaus
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isphenol.A.as.efficiently.as.adult.
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isphenol.A..For.example,.this.raise
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laboRaToRy aNImal STudIeS In.contra
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of.normal.sex-based.differences.bet
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death.(168),.synaptic.plasticity.(1
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gland.carcinogen.or.that.bisphenol.
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understand.the.possible.long-term.c
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strategies.to.improve.the.sensitivi
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• • Howdeshell.et.al. (55).repo
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and.cystic.endometrial.hyperplasia.
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cutaneous. injection. 20 . vom. Saa
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are CurrenT exposures To bisphenol
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w/day;.95th.percentiles.0.289.-.0.2
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Page 59 and 60: 12.. Padmanabhan. V,. Siefert. K,.
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Page 67 and 68: Thyroid.Function.in.Juvenile.Female
Page 69 and 70: droxylase.immunoreactivity..76:423.
Page 71 and 72: stanceschimiques.gc.ca/challenge-de
Page 73 and 74: Watanabe.H,.Ohta.Y,.Iguchi.T.(2006)
Page 75 and 76: 226..vom. Saal. FS,. Cooke. PS,. Bu
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Page 79 and 80: appendix i. nTp-Cerhr bisphenol a e
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Page 91 and 92: 168 CHAPIN ET AL. comparison of the
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Page 107 and 108: 184 CHAPIN ET AL. fetuses (3.572.7
Page 109 and 110: 186 CHAPIN ET AL. Secondary sources
Page 111 and 112: 188 CHAPIN ET AL. Table 25 Maternal
Page 113 and 114: 190 CHAPIN ET AL. Table 27 Bispheno
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Page 119 and 120: 196 CHAPIN ET AL. Table 36 Toxicoki
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Page 137 and 138: 214 CHAPIN ET AL. Model and exposur
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Page 141 and 142: 218 Model and exposure Husbandry a
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Page 147 and 148: 224 Table 57 In Vitro Genetic Toxic
Page 149 and 150: 226 CHAPIN ET AL. Table 58 In Vivo
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230 CHAPIN ET AL. Table 62 Toxicoki
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232 CHAPIN ET AL. Table 64 Tissue R
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234 CHAPIN ET AL. Table 68 Toxicoki
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236 CHAPIN ET AL. treatment conditi
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238 CHAPIN ET AL. clinical signs, b
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240 CHAPIN ET AL. Table 71 Benchmar
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242 CHAPIN ET AL. group, 5 from 1 l
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244 CHAPIN ET AL. least significant
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246 CHAPIN ET AL. group was a reduc
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248 CHAPIN ET AL. 100-151 g for fem
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250 CHAPIN ET AL. 3.2.3.2 Developme
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252 CHAPIN ET AL. weights, bispheno
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254 CHAPIN ET AL. 120 mg/kg bw/day
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256 CHAPIN ET AL. comparisons condu
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258 CHAPIN ET AL. the findings of t
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260 CHAPIN ET AL. analyzed.] Anogen
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262 CHAPIN ET AL. purposeful confou
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264 CHAPIN ET AL. increased lordosi
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266 CHAPIN ET AL. that there was a
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268 CHAPIN ET AL. duration of adver
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270 CHAPIN ET AL. doses of potent e
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272 CHAPIN ET AL. Table 74 Effects
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274 CHAPIN ET AL. reproductive orga
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276 CHAPIN ET AL. tyrosine-hydroxly
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278 CHAPIN ET AL. include small sam
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280 CHAPIN ET AL. males/group. [It
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282 CHAPIN ET AL. termination, whic
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284 CHAPIN ET AL. provided a reliab
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286 CHAPIN ET AL. grooming, and out
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288 CHAPIN ET AL. method of oral do
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290 CHAPIN ET AL. reared by their d
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292 CHAPIN ET AL. has been informed
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294 CHAPIN ET AL. buffered paraform
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296 CHAPIN ET AL. unit. Further, th
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298 CHAPIN ET AL. PND 21 and housed
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300 CHAPIN ET AL. Tando et al. (200
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302 CHAPIN ET AL. Purina Certified
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304 CHAPIN ET AL. high-doses of bis
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306 CHAPIN ET AL. born to those dam
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308 CHAPIN ET AL. average weight we
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310 CHAPIN ET AL. study authors con
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312 CHAPIN ET AL. used for extracti
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314 CHAPIN ET AL. jar, and there we
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316 CHAPIN ET AL. of testes and com
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318 CHAPIN ET AL. differentiation o
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320 CHAPIN ET AL. Table 81 Summary
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322 CHAPIN ET AL. Table 82 Continue
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328 CHAPIN ET AL. 600 mg/kg bw/day)
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330 CHAPIN ET AL. (Nagao et al., 19
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332 CHAPIN ET AL. antinuclear antib
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334 CHAPIN ET AL. least 6 animals.
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336 CHAPIN ET AL. Utility (Adequacy
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338 CHAPIN ET AL. stomach weight wa
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340 CHAPIN ET AL. Schirling et al.
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342 CHAPIN ET AL. Endpoint Table 88
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344 CHAPIN ET AL. different diets b
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346 CHAPIN ET AL. with 40 mg vitami
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348 CHAPIN ET AL. the bisphenol A v
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350 CHAPIN ET AL. and determining t
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352 CHAPIN ET AL. expression [to B6
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354 CHAPIN ET AL. indicated] at 0 (
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356 CHAPIN ET AL. concentrations us
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358 CHAPIN ET AL. animals were non-
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360 CHAPIN ET AL. following adjustm
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362 CHAPIN ET AL. Table 94 Treatmen
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364 CHAPIN ET AL. Table 97 Effects
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366 CHAPIN ET AL. Table 99 Treatmen
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368 CHAPIN ET AL. Therefore the NTP
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370 CHAPIN ET AL. weeks before mati
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374 Table 101 Summary of High Utili
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376 Table 102 Summary of Limited Ut
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380 CHAPIN ET AL. from other suppli
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382 CHAPIN ET AL. U.S. populations.
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384 CHAPIN ET AL. 10. Critical desi
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386 CHAPIN ET AL. Engel SM, Levy B,
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388 CHAPIN ET AL. alpha and beta ex
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390 CHAPIN ET AL. Murray TJ, Maffin
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392 CHAPIN ET AL. Ryan BC, Vandenbe
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394 CHAPIN ET AL. Thomas P, Dong J.
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appendix iii. publiC CommenTs and p
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