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Ftalan dibutylu – frakcja wdychana

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Ftalan dibutylu (DBP) jest przezroczystą, oleistą cieczą o charakterystycznym dla estrów zapachu, którą stosuje się przede wszystkim jako dodatek zmiękczający do takich żywic i polimerów, jak: PCV (76% produkcji), uszczelniaczy, klejów i spoiw (14% produkcji) oraz tuszów drukarskich (7% produkcji). Pozostałe 3% produkcji ftalanu dibutylu stosuje się przy wytwarzaniu: farb nitrocelulozowych, włókien szklanych oraz kosmetyków. Ze względu na niską prężność par w temperaturze pokojowej podwyższone stężenia ftalanu di butylu mogą wystąpić jedynie w procesach technologicznych przebiegających w podwyższonej temperaturze mlub w procesach związanych z występowaniem aerozoli ftalanu dibutylu w powietrzu środowiska pracy. Na podstawie wyników pomiarów z lat 90. udostępnionych przez jeden z europejskich zakładów, wykazano, że w procesie produkcji ftalany dibutylu średnie stężenie na większości stanowisk pracy nie przekraczało 0,5 mg/m3, a w przypadku kilku stanowisk wynosiło 1,1 lub 5 mg/m3. W innym zakładzie średnie stężenie ftalanu dibutylu wynosiło 0,04 mg/m3 w 1992 r. oraz 0,7 mg/m3 w 1995 r. Pomiary stężeń wykonane w 1996 r. przy wytwarzaniu produktów zawierających ftalan di butylu wskazują, że stężenia tego związku wynosiły 0,19 - 0,75 mg/m3 (produkcja kabli), < 0,008 mg/m3 (produkcja polimerów) oraz < 0,03 (produkcja polimerów dla przemysłu dekarskiego). Według danych GIS, zarówno w 2007 r., jak i w 2010 r. nie było pracowników narażonych na stężenia ftalany dibutylu przekraczające obowiązujące normatywy (NDS – 5 mg/m3 i NDSCh – 10 mg/m3). W wykazie chorób zawodowych obejmującym lata 2001-2010, opracowanym na podstawie danych Centralnego Rejestru Chorób Zawodowych w Instytucie Medycyny Pracy, odnotowano tylko jeden przypadek choroby skóry u osoby narażonej na ftalan dibutylu w zakładzie przetwórstwa przemysłowego. Ftalan dibutylu wchłania się do organizmu przez układ oddechowy oraz pokarmowy, nie ulega kumulacji i jest wydalany głównie z moczem. Na podstawie mediany dawek lub stężeń śmiertelnych ftalanu dibutylu, które uzyskano na podstawie wyników badań doświadczalnych na gryzoniach, wykazano, że ftalan dibutylu jest substancją o stosunkowo małej toksyczności ostrej. W większości badań związek nie wykazywał działania drażniącego ani uczulającego ludzi i zwierząt doświadczalnych. Jak wynika z dostępnego piśmiennictwa, skutki działania toksycznego ftalanu dibutylu w warunkach narażenia podprzewlekłego i przewlekłego oceniano prawie wyłącznie na podstawie wyników badań na szczurach narażanych dożołądkowo. Wartości NOAEL dla działania toksycznego wyznaczano na poziomie 176 - 353 mg/kg m.c./dzień, a najczęściej obserwowanymi skutkami narażenia było: zmniejszenie masy ciała, zmiany parametrów krwi, zwiększenie masy wątroby i nerek. Jeśli chodzi o szkodliwe działanie ftalanu dibutylu, to jest to przede wszystkim związek o potwierdzonym szkodliwym działaniu na rozrodczość i dziecko w łonie matki. Zgodnie z rozporządzeniem Parlamentu Europejskiego i Rady (WE) nr 1272/2008 ftalan di butylu jest zaklasyfikowany jako substancja działająca szkodliwie na rozrodczość, kategoria zagrożeń 1B, z przypisanym zwrotem wskazującym rodzaj zagrożenia H360Df – może działać szkodliwie na dziecko w łonie matki; podejrzewa się, że działa szkodliwie na płodność. W dostępnych wynikach badań szkodliwego działania ftalanu dibutylu na rozrodczość, najmniejsze wyznaczone wartości NOAEL wynosiły: 50 mg/kg m.c./dzień dla zaburzeń płodności oraz 30 mg/kg m.c./dzień dla szkodliwego działania na płód. W Polsce, podobnie jak w większości państw Europy, wartości najwyższego dopuszczalnego stężenia (NDS) ftalanu dibutylu ustalono na poziomie 5 mg/m3. Stężenie to zabezpiecza przed uciążliwymi warunkami pracy związanymi z narażeniem na aerozole, którego należy oczekiwać w przypadku ftalanu dibutylu ze względu na jego małą prężność par. Biorąc pod uwagę dużą wartość NOAEL, oszacowano, że dotychczasowa wartość NDS ftalanu dibutylu powinna również zabezpieczać zarówno przed skutkami jego działania toksycznego, jak i jego szkodliwym wpływem na rozrodczość i płód. Zaproponowano więc pozostawienie wartości NDS ftalanu dibutylu na dotychczasowym poziomie wynoszącym 5 mg/m3. Jednocześnie proponuje się zrezygnowanie z dotychczas obowiązującej wartości najwyższego dopuszczalnego stężenia chwilowego (NDSCh – 10 mg/m3) ftalany dibutylu, dlatego że wyniki dostępnych badań nie wskazują na działanie drażniące związku. Obecnie brak jest podstaw do zaproponowania wartości dopuszczalnego stężenia ftalanu dibutylu w materiale biologicznym (DSB). Zaleca się oznakowanie substancji w wykazie literami „Ft” oznaczającymi substancję działającą toksycznie na płód.
EN
Dibutyl phthalate (DBP) is a clear, oily liquid with ester-like odour. It is used mostly as a plasticizer for resins and polymers such as polyvinyl chloride (76% production), sealants and adhesives (14% production) and inks (7% production). The rest 3% of DBP production is used for nitrocellulose lacquers, safety glass and cosmetic products. As far as occupational exposure is concerned, the inhalation route of exposure is important and, to a lesser extent, dermal contact. Because of low vapour pressure at room temperature, the high concentration of DBP may only occur during technological processes where the temperature is elevated or DBP aerosols are generated. Measurements done by a European company in the 1990s showed that during DBP production the mean concentration of this substance in the workplace was below 0.5 mg/m3, and only in a few workplaces 1.1 or 5 mg/m3. In a different plant, the mean DBP concentration was 0.04 mg/m3 in 1992 and 0.7 mg/m3 in 1995. The measurements of DBP concentration carried out in 1996 at production processes of different products containing DBP showed that the concentration of this chemical was 0.19 – 0.75 mg/m3 (cables), < 0.008 mg/m3 (polymers) and < 0.03 (polymers for the tiling industry). In 2007 and 2010, according to data of Polandʼs Chief Sanitary Inspectorate, no workers were occupationally exposed to DBP in concentrations in excess of Polish OEL values. According to the Polish inventory of occupational diseases of the Nofer Institute of Occupational Medicine (Lodz, Poland), in 2001-2010 there was only one case of skin disorder in a worker occupationally exposed to DBP. DBP is absorbed in the respiratory and gastrointestinal tract, no significant accumulation has been recorded and it is excreted mainly in urine. LD50 values derived from experiments with rodents revealed that DBP was a substance of relatively low acute toxicity. In most studies, the substance caused no irritation or sensitisation in human or in laboratory animals. According to available data, subchronic and chronic toxicity of DBP was evaluated almost exclusively on the basis of studies on rats exposed orally. NOAEL values were equal to 176 – 353 mg/kg bw/d; the most often observed effects of exposure were decrease in body weight, changes in blood parameters and a relative increase in the weight of the liver and kidneys. DBP is a compound of a confirmed reprotoxic activity. According to Regulation (EC) No. 1272/2008 of the European Parliament and of the Council, DBP is classified as Reprotoxic, category 1B with hazard statement H360Df (may damage the unborn child, suspected of damaging fertility). In the available studies on DBP reprotoxocity, the lowest described NOAELs were 50 mg/kg bw/d for fertility and 30 mg/kg bw/d for foetus effects. In Poland, like in most European countries, the OEL value was set at the level equal to 5 mg/m3. This value is supposed to protect from burdensome working conditions connected with exposure to DBP aerosols expected due to its low vapour pressure. Taking into account the NOAEL values cited in the available literature, it was agreed that this level should also protect from toxic and reprotoxic DBP activity. It was agreed that the previous DBP OEL value of 5 mg/m3 should remain unchanged. Simultaneously, it was proposed that the previous STEL value of 10 mg/m3 should be removed from the Polish inventory of OELs as inaccurate due to no irritation activity of DBP confirmed in available studies. It is also recommended to label DBP, in the Polish inventory of OELs, with the letters ‘Ft’ – a substance toxic to the foetus.
Rocznik
Tom
Strony
37--70
Opis fizyczny
Bibliogr. 137 poz., rys., tab.
Twórcy
  • Instytut Medycyny Pracy im. prof. dr med. Jerzego Nofera 91-348 Łódź ul. św. Teresy od Dzieciątka Jezus 8
autor
  • Instytut Medycyny Pracy im. prof. dr med. Jerzego Nofera 91-348 Łódź ul. św. Teresy od Dzieciątka Jezus 8
Bibliografia
  • 1.Abe S. i in. (1977) Chromosome aberrations and sister chromatid exchanges in Chinese hamster cells exposed to various chemicals. J. Natl. Cancer Inst. 58(6), 1635–1640.
  • 2.ACGIH (2000) Dibutyl phthalate. Documentation of the TLVs and BEIs with other worldwide occupational exposure values.
  • 3.ACGIH (2011) TLVs and BEIs threshold limit values for chemical substances and physical agents and biological exposure indices.
  • 4.Albro P.W. i in. (1974) Identification of the metabolites of simple phthalate diesters in rat urine. J. Chromatogr. 94, 209–218.
  • 5.Agarwal D.K. i in. (1985). Mutagenicity evaluation of phthalic acid esters and metabolites in Salmonella typhimurium cultures. J. Toxicol. Environ. Health 16, 61–69.
  • 6.Aldyreva M.V. i in (1975) Effect of plasticizers on reproductive function. Gig. Tr. Prof. Zabol. 12, 25–29 [cyt. Za IPCS 1997].
  • 7.Anderson W.A.R. i in. (2000) A biomarker approach to quantify human dietary exposure to phthalates, risk assessment and communication for food safety [Abstract]. Presented at the first joint CSL/JIFSAN symposium on food safety and nutrition 20-22 June 2000, Central Science Laboratory, Sand Hutton, York, UK. [cyt za RAR 2004].
  • 8.ATSDR, Agency for Toxic Substances and Disease Registry (2001) Toxicological profile for di-nbutylphthalate. Update, US Department of Health & Human Services, Public Health Service, Atlanta, GA, USA.
  • 9.Barber E.D. i in. (1987) Peroxisome induction on seven phthalate esters. Toxico. Indust. Health 2, 7–22.
  • 10.Barlow N.J. i in. (2003) Pathogenesis of male reproductive tract lesions from gestationthrough adulthood following in utero exposure to di(n-butyl) phthalate. Toxicol. Pathol. 31, 397–410.
  • 11.BASF (1957) Confidential report. Abteilung Toxikologie, unveroeffentlichte Untersuchung, V/282. Dated 11.04.1957 [cyt. za RAR 2004].
  • 12.BASF (1958) Confidential data. Palatinol C (flüssig) = Phthalsäure-di-butylester uns. Vers. Nummern VIII/117 und VIII/332. Dated 1-12-1958 [cyt. za RAR 2004].
  • 13.BASF (1961) Confidential data. Bericht über die toxikologische Prüfung von Palatinol C, IC, AH, DN und VII/3- 6. IX/418. Dated 10-1-1961 [cyt. za RAR 2004].
  • 14.BASF (1990a) Confidential report. Report on the acute dermal irritation/corrositivity to the intact dorsal skin of dibutylphthalate in white rabbits. Project No.: 18H0449/892113. Dated 12-2-1990 [cyt. za RAR 2004].
  • 15.BASF (1990b) Confidential report. Report on the acute irritation to the eye of dibutylphthalate in white rabbits. Project No.: 11H0449/892114. Dated 12-2-1990 [cyt. Za RAR 2004].
  • 16.BASF (1990c) Confidential report. Report on the Maximization Test for sensitizing potential of dibutylphthalate in guinea pigs. Project No. 30H0449/892115. Dated 1 March 1990 [cyt. za RAR 2004].
  • 17.BASF (1990d) Confidential report. Department Toxicology. Cytogenetic study in vivo of dibutylphthalate in mice micronucleus test. Single oral administration. Project No.: 26M0449/894382. Dated 3 April 1990 [cyt. za RAR 2004].
  • 18.BIBRA (1986) Confidential report to chemical manufacturers association. Project No. 3.0495/3/85. Report No. 0495/3/85. CMA Ref. PE 28.0-BT-BIB. A 21-day feeding study of di-n-butylphthalate to rats: Effects on the liver and liver lipids. Dated February 1986 [cyt. za RAR 2004].
  • 19.BIBRA (1987) Toxicity profile on dibutyl phthalate (DBP). Dated March 1987 [cyt. za RAR 2004]. 20.
  • 20.BIBRA (1990) Confidential report. BIBRA project No. 3.0826. BIBRA Report No. 826/2/90. An investigation of the effect of dibutyl phthalate (DBP) on rat hepatic peroxisomes. Dated January 1990 [cyt. za RAR 2004].
  • 21.Bronaugh R.L. i in. (1982) Methods for in vitro percutaneous absorption studies. I. Comparison with in Vivo results. Toxicol. Appl. Pharmacol. 62, 476–480.
  • 22.BUA (1987) German Chemical Society. GDCh-Advisory Committee on Existing Chemicals of Environmental Relevance. Dibutylphthalate, BUA-Report 22, December 1987 [cyt. za RAR 2004].
  • 23.Cagianut B. (1954) Keratitis erosiva und Nephritis toxica nach Einnahme von Dibutylphthalat. Schweiz. Med. Wochenschr. 84, 1243–1244 [cyt. za RAR 2004].
  • 24.Calnan C.D. (1975) Dibutyl phthalate. Dermatitis 11, 388.
  • 25.Cater B.R. i in. (1977). Studies on dibutylphthalateinduced testicular atrophy in the rat: effect on zinc metabolism. Toxicol. Appl. Pharmacol. 41(3), 609–618.
  • 26.Chen C.Y. i in. (2011) The combined toxicity of dibutyl phthalate and benzo(a)pyrene on the reproductive system of male Sprague Dawley rats in vivo. J. Hazard Mater. 186(1), 835–41.
  • 27.Cummings A.M. i in. (1987) Dibutyl phthalate: maternal effects versus fetotoxicity. Toxicol Lett 39, 43–50.
  • 28.Drake A.J. i in. (2009) Glucocorticoids amplify dibutyl phthalate-induced disruption of testosterone production and male reproductive development. Endocrinology vol. 150 no. 11, 5055–5064.
  • 29.Duty S.M. i in. (2003) Phthalate exposure and human semen parameters. Epidemiology 14, 4 i 3, 269–277.
  • 30.Duty S.M. i in. (2005) Phthalate exposure and reproductive hormones in adult men. Hum Reprod 20, 604–610.
  • 31.Elsisi A.E. i in. (1989) Dermal absorption of diesters in rats. Fund. Appl. Toxico. 12, 70–77.
  • 32.Ema M. i in. (1993) Teratogenic evaluation of di-nbutylphthalate in rats. Toxicol. Lett. 69, 197–203.
  • 33.Ema M. i in. (1994) Characterization of the developmental toxicity of di-n-butyl phthalate in rats. Toxicology 86, 163–174.
  • 34.Ema M. i in. (1997) Developmental effects of di-n-butyl phthalate after a single administration in rats. J. Appl. Toxicol. 17(4), 223-229.
  • 35.Ema M. i in. (1998) Further evaluation of developmental toxicity of di-n-butyl phthalate following administration during late pregenancy of rats. Toxicol. Lett. 98, 87–93.
  • 36.Ema M. i in. (2000a) Critical period for adverse effects on development of reproductive system in male offspring of rats given di-n-butyl phthalate during late pregnancy. Toxicol. Lett. 111, 271–278.
  • 37.Ema M. i in. (2000b) Effects of dibutyl phthalate on reproductive function in pregnant and pseudopregnant rats. Reprod. Toxicol. 14, 13–19.
  • 38.Ema M. (2002) Antiandrogenic effects of dibutyl phthalate and is metabolite, monobutyl phthalate, in rats. Congenital Anomalies 42, 297–308.
  • 39.Farombi E.O. i in. (2007) Curcumin and kolaviron ameliorate di-n-butylphthalate-induced testicular damage in rats. Basic Clin. Pharmacol. Toxicol. 100, 43–48.
  • 40.Fisher J.S. i in. (2003) Human ‘testicular dysgenesis syndrome’: a possible model using in-utero exposure of the rat to dibutyl phthalate. Hum. Reprod. 18, 1383–1394.
  • 41.Foster P.M.D. i in. (1982). Differences in urinary metabolic profile from di-n-butylphthalate-treated rats and hamsters. A Possible Explanation for Species Differences in Susceptibility to Testicular Atrophy. Drug Metabol. Disp. 11(1), 59–61.
  • 42.Foster P.M. (2005) Mode of action: impaired fetal Leydig cell function – effects on male reproductive development produced by certain phthalate esters. Crit. Rev. in Toxicol. 35, 713–719.
  • 43.Foster P.M. (2006) Disruption of reproductive development in male rat offspring following in utero exposure to phthalate esters. Int. J. Androl. 29, 140–147.
  • 44.Fukuoka M. i in. (1989) Mechanism of testicular atrophy induced by di-n- butyl phthalate in rats. Part 1. J. Appl. Toxicol. 9(4), 277–283.
  • 45.Fukuoka M. i in. (1990) Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 2. The effects on some testicular enzymes. J. Appl. Toxicol. 10(4), 285–293.
  • 46.Fukuoka M. i in. (1993) Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 4. Changes in the activity of succinate dehydrogenase and the levels of transferring and ferritin in the sertoli and germ cells. J. Appl. Toxicol. 13(4), 241–246.
  • 47.Fukuoka M. i in. (1994) Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. VI. A possible origin of testicular iron depletion. Biol. Pharm. Bull. 17(12), 1609– 1612.
  • 48.Fukuoka M. i in. (1995) Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 5. Testicular iron depletion and levels of ferritin, hemoglobin and transferrin in the bone marrow, liver and spleen. J. Appl. Toxicol. 15(5), 379–386.
  • 49.Gamer A.O. i in. (2000) Di-n-butyl Phthalate – subacute inhalation study in Wistar rats. 20 Exposures as a liquid aerosol. Confidential report from BASF Aktiengesellschaft, Experimental Toxicology and Ecology, Ludwigshafen/Rhein, Germany. Project No. 4010486/98063, dated February 09, 2000 [cyt. za RAR 2004].
  • 50.GESTIS (2011) [komputerowa baza danych].
  • 51.Gilioli R. i in. (1978) Horizontal and longitudinal study of a population employed in the production of phthalates. Med. Lav. 69, 620–631.
  • 52.Gray T.J. i in. (1982) Species difference in the testicular toxicity of phthalate esters. Toxicol. Lett. 11, 141–147.
  • 53.Gray L.E. i in. (1983) The effects of dibutylphthalate on the reproductive tract of the male and female rat and hamster. Toxicologist 3, 22.
  • 54.Gray L.E. Jr i in. (1999) Administration of potentially antiandrogenic pesticides (procymidone, linuron, chlozolinate, p,p'-DDE, and ketoconazole) and toxic substances (dibutyland diethylhexylphthalate, PCB 169, and ethane dimethane sulphonate) during sexual differentiation produces diverse profiles of reproductive malformations in the male rat. Toxicol. Ind. Health 15(1-2), 94–118.
  • 55.Gray L.E. Jr i in. (2006) Chronic di-n-butyl phthalate exposure in rats reduces fertilityand alters ovarian function during pregnancy in female Long Evans hooded rats. Toxicol. Sci. 9, 189–195.
  • 56.Greenough R.J. i in. (1981) Confidential Report from Inveresk Research International to Hüls AG. Report No. 1956. Safety tests of Vestinol C Dibutylphthalate. IRI Project No. 416746. Dated February 1981 [cyt. za RAR 2004].
  • 57.Harris C.A. i in. (1997) The estrogenic activity of phthalate esters in vitro. Environ Health Perspect 105(8), 802–811.
  • 58.Hauser R. (2006) Altered semen quality in relation to urinary concentrations of phthalate monoester and oxidative metabolites. Epidemiology. 2006 Nov, 17(6), 682–91.
  • 59.Hazleton (1986). Confidential Report from Hazleton Biotechnologies Comp. to Chemical Manufacturers Association. Mutagenicity of 1C in a mouse lymphoma mutation assay. Final Report HB Project No. 20989. Report Date September 1986 [cyt. za: IPCS 1997].
  • 60.HSDB (2011) [komputerowa baza danych].
  • 61.Husain S.L. (1975) Dibutyl phthalate sensitivity. Contact Dermatitis 1, 395 [cyt. za: IPCS 1997].
  • 62.IRDC (1984) International research and development corporation. Confidential report to Monsanto Chemical Company provided by Hüls AG. Test article: dibutyl phthalate. Subject: Study of fertility and general reproductive performance in rats (IR-83-145). Dated: December 3, 1984 [cyt. za RAR 2004].
  • 63.Ishidate M. Jr i in. (1977) Chromosome tests with 134 compounds on Chinese hamster cells in vitro – a screening for chemical carcinogens. Mutat. Res. 48, 337–354.
  • 64.Izmerov N.F. i in. (1982) Toxicometric parameters of industrial toxic chemicals under single exposure UNEP/IRPTC. Centre of Intern. Proj. Moscow 44.[ In:] Mulder D.E. i in. (1986) Review of literature on diethylphthalate, dibutylphthalate and benzylbutylphthlate [cyt. za RAR 2004].
  • 65.Jackson E.M. (2007) Subungual penetration of dibutyl phthalate in human fingernails skin pharmacol physiol 2008, 21, 10–14.
  • 66.Janjua N.R. i in. (2007) Systemic uptake of diethyl phthalate, dibutyl phthalate, and butyl paraben following whole-body topical application and reproductive and thyroid hormone levels in humans. Environ. Sci. Technol. 41, 5564–5570.
  • 67.Jansen E.H.J.M. i in. (1993) Confidential Report from the National Institute of Public Health and Environmental Protection (RIVM), the Netherlands to the Dutch Chief Inspectorate of Health Protection. Report nr. 618902013 [cyt. za RAR 2004].
  • 68.Jobling S. i in. (1995) A variety of environmentally persistent chemicals, including some phthalate plasticizers, are weakly estrogenic. Environ Health Perspect 103(6), 582–587.
  • 69.Kaaber S. i in. (1979) Skin sensitivity to denture base materials in the burning mouth syndrome. Contact Dermatitis, 5(2), 90–96.
  • 70.Kawano M. i in. (1980) Toxicological studies on phthalate esters. 2. Metabolism, accumulation and excretion of phthalate esters in rats. Jap. J. Hyg. 35(4), 693–701.
  • 71.Kim T. i in. (2004) Effects of in utero exposure of diethylstilbestrol and dibutyl phthalate on the testis descent in rat offspring. Toxicologist 78,118.
  • 72.Kleymenova E. i in. (2005) Exposure in utero to di(nbutyl) phthalate alters the vimentin cytoskeleton of fetal rat Sertoli cells and disrupts Sertoli Cell-gonocyte contact. Biol. Reprod. 73, 482–490.
  • 73.Kurata H. (1975). Studies on the mutagenic effects of phthalates. Report to Ministry of Health and Welfare (Japan), Scientific Research on Food Hygiene Program. [In:] Omori Y. (1976) Recent progress in safety evaluation studies on plasticizers and plastics and their controlled use in Japan. Environ. Health Perspect. 17, 203–209 [cyt. Za RAR 2004].
  • 74.Lake B.G. i in. (1977). The in vitro hydrolysis of some phthalate diesters by hepatic and intestinal preparations from various species. Toxicol. Appl. Pharmacol. 39, 239– 248.
  • 75.Lamb IV J.C. i in. (1987) Reproductive effects of four phthalic acid esters in the mouse. Toxicol. Appl. Pharmacol. 88, 255–269.
  • 76.Latini G. i in. (2006) Phthalate exposure and male infertility. Toxicology 21, 226(2-3), 90–8.
  • 77.Lehmann K.P. i in. (2004) Dose-dependent alterations in gene expression and testosterone synthesis in the fetal testes of male rats exposed to di (n-butyl) phthalate. Toxicol. Sci. 81, 60–68.
  • 78.Litton Bionetics (1985) Confidential Report to Chemical Manufacturers Association. Evaluation of 1C in the in vitro transformation of Balb/3T3 cells assay. Final Report. LBI Project No.: 20922. Report Date: April l985 [cyt. Za RAR 2004].
  • 79.Liu K. i in. (2005) Gene expression profiling following in utero exposure to phthalate esters reveals new gene targets in the etiology of testicular dysgenesis. Biol. Reprod. 73, 180–192.
  • 80.Main K.M. i in. (2006) Human breast milk contamination with phthalates and alterations of endogenous reproductive hormones in infants three months of age. Environ Health Perspect 114, 270–276.
  • 81.MAK-Di-n-butylphthalat (2010).
  • 82.Marsee K. i in. (2006) Estimated daily phthalate exposures in a population of mothers of male infants exhibiting reduced anogenital distance. Environ Health Perspect. 114(6), 805–9.
  • 83.Men'shikova T.A. (1971) Hygienic evaluation of dibutylphthalate in relation to the use of polymer finishes in shipboard living quarters. Hyg. Sanit. 36, 349–353.
  • 84.Milkov L.E. i in. (1973) Health status of workers exposed to phthalate plasticizers in the manufacture of artificial leather and films based on PVC resins. Environ. Health Perspect. 3, 175–178.
  • 85.Morissey R.E. i in. (1989) Results and evaluation of 48 continuous breeding reproduction studies conducted in mice. Fundam. Appl. Toxicol. 13, 747–777.
  • 86.Mylchreest E. i in., (1998) Male reproductive tract malformations in rats following gestational and lactational exposure to di(n-butyl) phthalate: an antiandrogenic mechanism? Toxicol. Sci. 43, 47–60.
  • 87.Mylchreest E. i in. (1999). Disruption of androgenregulated male reproductive development by di(n-Butyl) phthalate during late gestation in rats is different from flutamide. Toxicol. Appl. Pharmacol. 156, 81–95.
  • 88.Mylchreest E. i in. (2002) Fetal testosterone insufficiency and abnormal proliferation of Leydig cells and gonocytes in rats exposed to di(n-butyl) phthalate. Repro. Toxicol. 16, 19–28.
  • 89. NIOSH (2011) Pocket Guide.
  • 90.NTP (1995) National Toxicology Program. Toxicity Report Series Number 30. by DS Marsman. NTP Technical Report on toxicity studies of dibutyl phthalate (CAS No. 84-74-2). Administered in feed to F344/N rats and B6C3F1 mice. NIH Publication 95-3353. US Department of Health and Human Services. Public Health Service. National Institutes of Health. Dated April 1995.
  • 91.NTP (2000) NTP-CERHR expert panel report on dinbutyl phthalate. Alexandria, VA: Center for the Evaluation of Risks to Human Reproduction, U.S. Department of Health and Human Services, National Toxicology Program. NTP-CERHR-DBP-00 [cyt za Tox. Prof. 2001].
  • 92.NTP (2002) Dibutyl phthalate (CAS No. 84-74-2): Multigenerational reproductive assessment by continuous breeding when administered to Sprague-Dawley rats in the diet. NTP Report # RACB97003, US Department of Health and Human Services. Public Health Service. National Institutes of Health, Bethesda, MD, USA [abstract].
  • 93.Oishi S. i in. (1980) Testicular atrophy induced by phthalic acid esters: effect on testosterone and zinc concentrations. Toxicol. Appl. Pharmacol. 53, 35–41.
  • 94.Oliwiecki S. i in. (1991) Contact dermatitis from spectacle frames and hearing aid containing diethylphthalate. Contact Dermatitis 25, 264–265.
  • 95.Plummer S. i in. (2005) Identification of gene clusters and signaling pathways affected by dibutyl phthalate – nuclear receptor interactions in foetal rat testes. Toxicologist 79, 463.
  • 96.Pugh G.J. i in. (2000) Effects of di-isononyl phthalate, di- 2-ethylhexyl phthalate, and clofibrate in cynomolgus monkeys. Toxicol. Sci. 2000, 181–188.
  • 97.Queiroz E.K. i in. (2006) Occupational exposure and effects on the male reproductive system. Cad Saude Publica 22(3), 485–93 [abstrakt].
  • 98.RAR, Risk Assessment Report (2004) Dibutyl phthalate, 1st Priority List Vol. 29 [ http://ecb.jrc.it/].
  • 99.Rhodes C. i in. (1986) Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl) phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 65, 299–308.
  • 100.Rolecki R. i in. (1995) Dwubutylu ftalan. Dokumentacja proponowanych wartości dopuszczalnych poziomów narażenia zawodowego. PiMOŚP 1995, 13, 169–192.
  • 101.Rowland I.R. i in. (1977) Hydrolysis of phthalate esters by the gastro-intestinal contents of the rat. Food Cosm. Toxicol. 15, 17–21.
  • 102.Rozporządzenie Parlamentu Europejskiego i Rady (WE) nr 1272/2008 z dnia 16.12.2008 r. w sprawie klasyfikacji, oznakowania i pakowania substancji i mieszanin, zmieniające i uchylające dyrektywy 67/648/EWG i 1999/45/WE oraz zmieniające rozporządzenie WE nr 1907/2006. Dz. Urz. UE L 353 z dnia 31.12.2008 r., 1. z 1 ATP. Dz.Urz. UE L 235 z dnia 5.09.2009 r.
  • 103.Rozporządzenie (WE) nr 1907/2006 z dnia 18.12. 2006 r. w sprawie rejestracji, oceny, udzielania zezwoleń i stosowanych ograniczeń w zakresie chemikaliów (REACH) i utworzenia Europejskiej Agencji Chemikaliów, zmieniające dyrektywę 1999/45/WE oraz uchylające rozporządzenie Rady (EWG) nr 793/93 i rozporządzenie Komisji (WE) nr 1488/94, jak również dyrektywę Rady 76/769/EWG i dyrektywy Komisji 91/155/EWG, 93/67/EWG, 93/105/WE i 2000/21/WE (ze zmianami). Dz.Urz. UE L 396 z dnia 30.12.2006 r.
  • 104.Rozporządzenie Komisji (UE) nr 143/2011 z dnia 17.02. 2011 r. zmieniające załącznik XIV do rozporządzenia (WE) nr 1907/2006 Parlamentu Europejskiego i Rady REACH. DzU L 44 z dnia 18.2.2011 r.
  • 105.RTECS, Registry of Toxic Effects of Chemical Substances (2010) National Institute for Occupational Safety and Health [komputerowa baza danych].
  • 106.Saillenfait A.M. i in. (1998) Assessment of the developmental toxicity, metabolism and placental transfer of Dinbutyl phthalate administered to pregnant rats. Toxicol. Sci. 45(2), 212–224.
  • 107.Schilling K. i in. (1992) Confidential report from BASF, Department of Toxicology. Study of the oral toxicity of dibutyl phthalate in Wistar rats. Administration via the diet over 3 months. Project No. 31S0449/89020. Dated 23.03.1992 [cyt. za RAR 2004].
  • 108.Schulsinger C. i in. (1980) Polyvinyl chloride dermatitis not caused by phthalates. Contact Dermatitis 6, 477–480.
  • 109.Seed J.L. (1982) Mutagenic activity of phthalate esters in bacterial liquid suspension assays. Environ. Health Perspect. 45, 111–114.
  • 110.Shahin M.M. i in. (1977) Mutagenic and lethal effects of α-benzene hexachloride, dibutyl phthalate and trichloro ethylene in Saccharomyces cerevisiae. Mutat. Res. 48, 173–180.
  • 111.Shiota K. i in. (1980) Embryotoxic effects of di-2- ethylhexyl phthlate (DEHP) and di-n-butyl phthlalate (DBP) in Mice. Environ. Res. 22, 245–253.
  • 112.Short R.D. i in. (1987) Metabolic and peroxisome proliferation studies with di(2-ethylhexel)phthalate in rats and monkeys. Toxicol. Ind. Health 3(1), 185–195.
  • 113.Shultz V.D. i in. (2001) Altered gene profiles in fetal rat testes after in utero exposure to di(n butyl) phthalate. Toxicol. Sci. 64, 233–242,
  • 114.Silva M.J. i in. (2003) Glucuronidation patterns of common urinary and serum monoester phthalate metabolites. Arch. Toxicol. 77, 561–567. Erratum in: Arch. Toxicol. 2005, 79, 302.
  • 115.Silva M.J. i in. (2004a) Urinary levels of seven phthalate metabolites in the U. S. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000. Environ Health Perspect 112, 331–338.
  • 116.Silva M.J. i in. (2004b) Detection of phthalate metabolites in human amniotic fluid. Bull. Environ Contam. Toxicol. 72, 1226–1231.
  • 117.Silva M.J. i in. (2005) Detection of phthalate metabolites in human saliva. Arch. Toxicol. 11, 647–652.
  • 118.Sneddon I.B. (1972) Dermatitis from dibutyl phthalate in an aerosol antiperspirant and deodorant. Contact Dermatitis Newsletter 12, 308.
  • 119.Srivastava S.P. i in. (1990) Testicular effects of di-n-butyl phthalate (DBP): biochemical and histopathological alterations. Arch. Toxicol. 64, 148–152.
  • 120.Swan S.H. (2006) Prenatal phthalate exposure and anogenital distance in male infants. Environ Heath Perspect 114, A88–89.
  • 121.Takahashi T. i in. (1989) Biochemical studies on phthalic esters. V. Comparative studies on In vitro hydrolysis of di-n-butyl phthalate isomers in rats. Arch. Toxicol. 63, 72–74.
  • 122.Tanaka A. i in. (1978) Biochemical studies on phthalic esters. III. Metabolism of dibutyl phthalate (DBP) in animals. Toxicology 9, 109–123.
  • 123.Thompson C.J. i in. (2004) Di(n-butyl) phthalate impairs cholesterol transport and steroidogenesis in the fetal rat testis through a rapid and reversible mechanism. Endocrinology 145,1227–1237.
  • 124.Thompson C.J. i in. (2005) Differential steroidogenic gene expression in the fetal adrenal versus the testis and rapid and dynamic response of the fetal testis to di(n-butyl) phthalate. Biol. Reprod. 73, 908–917,
  • 125.Tomita I. i in. (1977) Phthalic acid esters in various foodstuffs and biological materials. Ecotoxicol. Environ. Safety 1, 275–278.
  • 126.Tsutsimi T. i in. (2004) Renal toxicity induced by folic acid is associated with the enhancement of male reproductive toxicity of di(nbutyl) phthalate in rats. Reprod. Toxicol. 18, 35–42.
  • 127.Vidovic R. i in. (1985) Contact dermatitis in workers processing polyvinyl chloride plastics. Dermatosen 33(3), 104–105.
  • 128.Voronin A.P. (1975) Toxicological and hygienic characteristics of the plastifier dibutyl phthalate. [In:] Toxicology and Hygiene of the Petrochemical and Oil-Refining Products (The Second All-Union Conference), Yaroslav, 1972, 83–88 [cyt. za RAR 2004].
  • 129.Walseth F. i in. (1984) Phthalate esters. II. Effects of inhaled dibutylphthalate on cytochrome P-450 mediated metabolism in rat liver and lung. Arch. Toxicol. 55, 132–136.
  • 130.Weuve J. i in. (2006) Exposure to phthalates in neonatal intensive care unit infants. Urinary concentrations of monoesters and oxidative metabolites. Environmental Health Perspectives 114, 9, 1424.
  • 131.White R.D. i in. (1980) Absorption and metabolism of three phthalate diesters by the rat small intestine. Food Cosm. Toxicol. 18, 383–386.
  • 132.Williams D.F. i in. (1975) The retention, distribution, excretion and metabolism of dibutyl phthalate-7-14C in the rat. J. Agric. Food Chem. 23(5), 854–858.
  • 133.Wine R.N. i in. (1997) Reproductive toxicity of di-nbutylphthalate in a continuous breeding protocol in Sprague- Dawley Rats. Environ. Health Perspect. 105(1), 102– 107.
  • 134.Zacharewski T.R. i in. (1998) Examination of the in Vitro and in Vivo estrogenic activities of eight commercial phthalate esters. Toxicol. Sci. 46, 282–293.
  • 135.Zeiger E. i in. (1985) Mutagenicity testing of di(2- ethylhexyl)phthalate and related chemicals in Salmonella. Environ. Mutagen. 7, 213–232.
  • 136.Zhou Y. i in. (1990) Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 3. Changes in the activity of some enzymes in the Sertoli and germ cells, and in the levels of metal ions. J. Appl. Toxicol. 10 (6), 447–453.
  • 137.Zimmermann F.K. i in. (1984) Testing of chemicals for genetic activity with Saccharomyces cerevisiae: a report of the US Environmental Protection Agency. Gene-Tox Program. Mutat. Res. 133, 199–244.
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