研究顯示化妝品及香水中鄰苯二甲酸酯類(Phthalates, PAEs)的檢出率高達70％以上，而化妝品及香水銷售員在銷售產品過程中是否暴露PAEs及其暴露程度如何？過去並無任何研究進行適當之評估。因此，本研究選定台南市某百貨公司之女性化妝品、香水及服飾專櫃銷售員進行工作前、後之尿液及銷售環境空氣之定點採樣，並以問卷進行飲食習慣、個人化妝品使用量、飲水量及包裝材使用量調查，以評估該族群於銷售環境中PAEs之暴露程度。本研究完成化妝品專櫃銷售員(n=23)、香水專櫃銷售員(n=4)及服飾專櫃銷售員(n=9)四次工作前後尿液及銷售環境空氣樣品採樣，共採集32個環境空氣樣本及121個尿液樣本。尿液樣本以預洗之燒杯收集約30mL後貯存於棕色玻璃瓶，再以固相萃取匣萃取、淨化，最後使用LC-ESI/MS/MS分析；環境空氣樣本使用Gillian個人空氣採樣器搭配聚氨酯泡綿(PUF)及玻璃纖維濾紙(GFF)，以3L/min流量進行4-8小時採集，以hexane及acetone (1:1)進行索氏萃取，濃縮後以GC/MS分析。
研究結果顯示，化妝品、香水及服飾專櫃銷售員尿液中PAEs代謝物中位數濃度在mono-methyl phthalate (MMP)依序為服飾銷售員(27.8μg/g-creatinine)、化妝品銷售員(25.7μg/g-creatinine)及香水銷售員(16.1μg/g-creatinine)；mono-ethyl phthalate (MEP)濃度依序為化妝品銷售員(94.0μg/g-creatinine)、香水銷售員(89.8μg/g-creatinine)及服飾銷售員(51.6μg/g-creatinine)；mono-butyl phthalate (MBP)濃度依序為化妝品銷售員(218.4μg/g-creatinine)、香水銷售員(189.0μg/g-creatinine)及服飾銷售員(148.2μg/g-creatinine)；mono-benzyl phthalate (MBzP)濃度依序為化妝品銷售員(15.7μg/g-creatinine)、香水銷售員(14.3μg/g-creatinine)及服飾銷售員(12.4μg/g-creatinine)；MEHP濃度依序為香水銷售員(47.0μg/g-creatinine)、化妝品銷售員(37.1μg/g-creatinine)及服飾銷售員(32.7μg/g-creatinine)。五種PAEs代謝物檢出濃度以MBP最高、MEP次之，其次是MEHP，顯示DBP、DEP及DEHP等三種PAEs的暴露量佔總PAEs暴露量85％以上。
化妝品(n=16)、香水(n=8)及服飾(n=8)銷售環境空氣中DMP中位數濃度在香水銷售員較高 (0.11 μg/m3)，化妝品及服飾銷售員較低 (0.09 μg/m3及0.09 μg/m3)；在DEP以化妝品銷售員最高(1.77 μg/m3)，香水銷售員次之 (1.75 μg/m3)，服飾銷售員最低 (0.89 μg/m3)；在DBP以服飾銷售員最高(0.84 μg/m3)，香水銷售員次之 (0.72 μg/m3)，化妝品銷售員最低 (0.70 μg/m3)；在BBP亦以服飾銷售員最高 (0.29 μg/m3)，化妝品及香水銷售員較低 (0.19 μg/m3及0.19 μg/m3)；在DEHP以香水銷售員較高 (6.89 μg/m3)，化妝品銷售員次之 (2.41 μg/m3)，服飾銷售員最低 (2.16 μg/m3)，此結果與過去文獻顯示DEHP在香水中之含量較高可能有關。DEHP在各個採樣點之空氣樣本中皆為濃度最高之PAEs，其次依序為DEP、DBP、BBP及DMP。
三組銷售員之飲食習慣、飲水情形、外食量及包裝材使用量僅在豬內臟、雞鴨鵝內臟之攝食量及市售瓶裝礦泉水之飲水量有差異，但因內臟攝食量不高，且瓶裝礦泉水包裝材質常溫下較不易滲出PAEs，因此不至於對三組尿液中PAEs濃度造成差異。以尿液中PAEs代謝物含量推估暴露劑量，並依空氣中PAEs含量推估空氣吸入之暴露劑量，結果顯示空氣PAEs暴露劑量頗低約佔每日暴露劑量之7％以下，顯示其它暴露來源（如：食物、個人化妝品使用）仍為三組銷售員PAEs暴露之主要來源。由工作前、後尿液中濃度觀察，化妝品及香水銷售員於工作中較服飾銷售員易暴露DMP、DBP、BBP及DEHP。DMP及BBP為化妝品及香水中較少添加之成分，因此對三組暴露劑量不至造成差異，雖然高脂肪食物及塑膠包裝材的使用會增加DEHP及DBP的暴露，但此三組銷售員之飲食習慣對三組PAEs暴露濃度不至於造成差異，因此推測化妝品及香水銷售原可能由職場暴露較多DEHP及DBP。
以尿液中PAEs代謝物含量推估每日暴露劑量，並與美國環保署之容許暴露劑量計算危害指標，結果顯示三組銷售員在DEP、BBP及DBP之危害指標(Hazard Index)均小於1，顯示目前此三種PAEs暴露劑量尚未超過每日可接受攝入量。但50%以上之化妝品及香水銷售員以及約25%服飾銷售員DEHP之危害指標已大於1，顯示部分銷售員體內DEHP暴露量可能對健康上造成潛在之影響。

Some reports have showed that over 70% of name-brand cosmetics contained phthalate (PAEs). However, few exposure assessments of PAEs in cosmetic sales clerks were conducted to evaluate their occupational exposure of PAEs. The aims of this study are as 1) to measure the concentrations of five PAEs in ambient air of their working environment and those of five urinary phthalalte monoesters from cosmetic, perfume and clothing sales clerks by collecting their urine samples pre-shift and after shift; 2) to evaluate the contribution of air PAEs to the total exposure of PAEs in subjects; 3) to assess the occupational exposure of PAEs in cosmetic sales clerks and non-cosmetic sales clerks by integrating profiles of PAEs exposure from questionnaire, which included dietary habits, food consumption, usage of cosmetic products, and exposure levels of PAEs.The demographic characteristics and exposure scenario were obtained from an interviewed questionnaire.
A total of 32 air samples from 8 sampling sites and 121 urine samples were collected from cosmetic (n=23), perfume (n=4) and clothing (n=9) sales clerks. Urine samples collected by glass bottles were extracted by solid phase extraction (SPE) and analyzed by LC-ESI/MS/MS. Gillian pumps equipped with glass fiber filter (GFF) and polyurethane foam (PUF) were used to collect gaseous and particle phase PAEs at a flow rate of 3 L/min. Air samples were extracted with hexane and acetone (1:1) by Soxhlet extraction, and analyzed by GC-MS.
Median levels of five PAEs metabolites measured from three groups were list in order as followed: 27.8μg/g-creatinine in clothing sales clerk, 25.7μg/g-creatinine in cosmetic sales clerk and 16.1μg/g-creatinine in perfume sales clerk for mono-methyl phthalate (MMP); 94.0μg/g-creatinine in cosmetic sales clerk, 89.8μg/g-creatinine in perfume sales clerk and 51.6μg/g-creatinine in clothing sales clerk for mono-ethyl phthalate (MEP);214.8 μg/g-creatinine in cosmetic sales clerk,189.0μg/g-creatinine in perfume sales clerk and 148.2 μg/g-creatinine in clothing sales clerk for mono-butyl phthalate (MBP);15.7μg/g-creatinine in cosmetic sales clerk, 14.3μg/g-creatinine in perfume sales clerk, 12.4μg/g-creatinine in perfume sales clerk for mono-benzyl phthalate (MBzP); 47.0μg/g-creatinine in perfume sales clerk, 37.1μg/g-creatinine in cosmetic sales clerk and 32.7μg/g-creatinine in clothing sales clerk for mono-ethylhexyl phthalate (MEHP). Our results showed that over 85％ of PAEs exposure in sales clerks were contributed by di-n-butyl phthalate (DBP), diethyl phthalate (DEP) and di-(2-ethylhexyl) phthalate (DEHP).
Median levels (μg/m3) of PAEs in air samples from cosmetic (n=16), perfume (n=8) and clothing(n=8) counters were 0.09 (ND~0.22), 0.11 (ND~0.17) and 0.09 (ND~0.21)μg/m3 for dimethyl phthalate (DMP); 1.77 (0.72~6.58), 1.75 (0.16~3.96) and 0.89 (0.25~1.87) μg/m3 for DEP; 0.70 (0.06~1.09), 0.72 (0.02~1.45) and 0.84 (0.56~1.41)μg/m3 for DBP; 0.19 (0.04~0.41), 0.19 (0.04~0.46) and 0.29 (ND~1.33) μg/m3 for butyl benzyl phthalate (BBP); 2.41 (0.09~6.32), 6.98(0.09~29.40) and 2.16 (1.01~7.21) μg/m3 for DEHP, respectively. Our results showed that DEHP and DEP were predominant PAEs in workplace of cosmetic sales clerks.
Dietary habits in the comsumption of pig viscera, chicken viscera and bottom water were significant different among three groups. But, comsuptions of pig viscera, chicken viscera and bottom water were few different, PAEs exposure from diatery were too few to make the difference of PAEs exposure. Airborne PAEs exposure from working environment contributes lower exposure dose of PAEs, and the main exposure sources of PAEs for three groups were usage of personal cosmetic and food. Cosmetic and perfume sales clerks were exposed more DMP, DBP, BBP and DEHP than clothing sales clerks.
Due to less DMP and BBP were added in cosmetics and perfume, there is no difference of using MEP and MBzP were observed between three groups. It is revealed that cosmetics and perfume sales clerks may be exposed to DEHP and DBP occupationally.
The hazard index (HI) of DEP, BBP and DBP in three groups were all smaller than one. It is indicated that exposure dose of DEP, BBP and DBP in cosmetic, perfume and clothing sales clerks were under acceptable daily intake. The HI of DEHP in 50％ of cosmetic and perfume sales clerks and 25％ of clothing were higher than 1, which revealed that exposure dose of DEHP in parts of sales clerks may cause pose potential treated to their health.

Adibi JJ, Perera FP, Jedrychowski W, Camann DE, Barr DB, Jacek R, Whyatt RM. 2003. Prenatal exposures to phthalates among women in New York City and Krakow, Poland. Environ Health Perspect 111:1719–1722.

Akingbemi BT, Ge R, Klinefelter GR, Zirkin BR, Hardy MP. 2004. Phthalate-induced Leydig cell hyperplasia is associated with multiple endocrine disturbances. Cell biology 101:775-780.

Andrade AJM, Grande SW, Talsness CE, Grote K, Golombiewski A, Sterner-Kock A, Chahoud I. 2006. A dose–response study following in utero and lactational exposure to di-(2-ethylhexyl) phthalate (DEHP): Effects on androgenic status, developmental landmarks and testicular histology in male offspring rats. Toxicology 225:64–74.

Anzion C, 1984. Het voorkomen van ftalaten in het milieu, Free University,
Amsterdam.

ATSDR. 2002. Toxicological profile for di-(2-ethylhexyl)phthalate (DEHP). Atlanta, GA: Agency for Toxic Substances and Disease Registry

ATSDR. 1995. Toxicological profile for diethyl phthalate (DEP). Atlanta, GA:
Agency for Toxic Substances and Disease Registry

ATSDR. 2001. Toxicological profile for di-n-butyl phthalate (DBP). Atlanta, GA:
Agency for Toxic Substances and Disease Registry

BASF. 1992. Study on the oral toxicity of dibutyl phthalate in Wistar rats. Administration via the diet over 3 months. Eastman–Kodak Company, 31S0449//89020

Blount BC, Milgram KE, Silva MJ. 2000. Quantitative detection of eight phthalate metabolites in human urine using HPLC-APCI-MS/MS. Anal Chem 72:4127-4134.

Blount BC, Milgram KE, Silva MJ, Malek NA, Reidy JA, Needham LL, Brock JW, 2000a.Quantitative detection of eight phthalate metabolites in human urine using HPLC-APCI-MS/MS. Anal. Chem. 72(17):4127–413
Blount BC, Silva MJ, Caudill SP, Needham LL, Pirkle JL, Sampson EJ, Lucier GW, Jackson RJ, Brock JW. 2000 a. Levels of seven urinary phthalate metabolites in a human reference population. Environ Health Perspect 108:979–982.

CMA. 1999. Comments of the Chemical Manufacturers Association phthalate esters
panel in response to request for public input on seven phthalate esters. FR Doc.
99-9484. Washington, DC: Chemical Manufacturers Association.

Corton JC and Lapinskas PJ, 2005. Peroxisome Proliferator-Activated Receptors:
Mediators of Phthalate Ester-Induced Effects in the Male Reproductive Tract?
Toxicological Sciences 83: 4-17.

David RM, 2000.Exposure to pshthalate esters. Environmental Health Perspectives 108:A440.

Davis BJ, Maronpot RR, Heindel JJ. 1994. Di-(2-ethylhexyl)phthalate suppresses estradiol and ovulation in cycling rats. Toxicol. Appl. Pharmacol 128:216-223.

DeLeon IR, Byrne CJ, Peuler EA, Antoine SR, Schaeffer J, Murphy RC, 1986. Trace
organic and heavy metal pollutants in the Mississippi river. Chemosphere 15:795-805.

Duty SM, Ackerman RM, Calafat AM, Hauser R. 2005. Personal care product use predicts urinary concentrations of some phthalate monoesters. Environ Health Perspect 113:1530–1535.

Ema M, Miyawaki E, Kawashima K. 2000. Effects of dibutyl phthalate on reproductive function in pregnant and pseudopregnant rats. Reproductive Toxicology 14:13–19.

Ema M, Murai T, Itami R, Kawasaki H. 1990. Evaluation of the teratogenic potential of the plasticizer butyl benzyl phthalate in rats. Journal Apply Toxicology 10:339–343.

EU Commission Decision 1999/815/EC:OJ L 314,9.12.1999.

EU Ecientific Committee on Toxicity, Ecotoxicity and the Environment (SCTEE), 1998. Phthalate migration from soft PVC toys and child-care articles. Opinion expressed at the SCTEE third plenary meeting; Brussels.

Fatoki OS, Vernon F. DiGangi J, Norin H. 2002. TNO report. Phthalates in European Cosmetic Products. 1-26.

Field EA, Price CJ, Sleet RB, George JD, Marr MC, Myers CB, Schwetz BA, Morrissey RE. 1993. Developmental toxicity evaluation of dimethyl phthalate in rats. Teratology 48:33-44. Research Triangle Park: National Toxicology Program.

Field EA, Price CJ, Marr MC, Myers CB. 1989. Developmental toxicity evaluation of butyl benzyl phthalate (CAS No. 85-68-7) administered in feed to CD rats on gestational days 6 to 15. NTP-89-246. Research Triangle Park: National Toxicology Program.

Fisher JS, Macpherson S, Marchetti N, Sharpe RM, 2003. Human testicular
dysgenesis syndrome: a possible model using in-utero exposure of the rat to
dibutyl phthalate. Human Reproduction 18:1383-1394.

Fromme H, Küchler T, Otto T, Pilz K, Müller J, Wenel A, 2002. Occurrence of
phthalates and bisphenol A and F in the environment. Water Research 36(6):
1429-1438.

Furmann K. 1994. Phthalate in surface water- a method for routine trace level analysis. Fresenius J. Anal. Chem. 248:291-296.

Heindel JJ, Powell CJ. 1992. Phthalate ester effects on rat Sertoli cell function in vitro: effects of phthalate side chain and age of animal. Toxicol Appl Pharmacol 115(1):116-23.

Houlihan J, Brody C, Schwan B. 2002. Phthalates, Beauty Products& the FDA. 1-20.

Huntingdon HLS-A, 1996. Phthalic acid, di(2-ethylhexyl) ester (DEHP): study of
embryo-foetal toxicity in the CD-1 mouse by oral gavage administration. Report
no.: 95/EHM007/0705 IARC.

Itoh H, Yoshida K, Masunaga S. 2005. Evaluation of the effect of governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Int. J. Hyg. Environ.-Health 208:237–245.

Jones HB, Garside DA, Liu R, Roberts JC. 1993. The influence of phthalate etrers on Leydig cell structure and function in vitro and in vivo. Experimental and Molecular Pathology 58:197-193.

Joseph DG, Helena N., 2002. Pretty Nasty– Phthalates in European Cosmetic Products. Health Care Without Harm.

Kato K, Silva MJ, Needham LL, Calafat AM. 2005. Determination of 16 phthalate metabolites in urine using automated sample preparation and on-line preconcentration-high performance liquid chromatography-tandem mass spectrometry. Anal. Chem. 77:2985-2991.

Kavlock R, Boekelheide K, Chapin R, Cunningham M, Faustman E, Foster P, Golub M, Henderson R, Hinberg I, Little R, Seed J, Shea K, Tabacova S, Tyl R, Williams P, Zacharewski T. 2002. NTP center for the evaluation of risks to human reproduction:
phthalates expert panel report on the reproductive and developmental toxicity of di-n-butyl phthalate. Reproductive Toxicology 16:489–527.

Kavlock R, Boekelheide K, Chapin R, Cunningham M, Faustman E, Foster P, Golub M, Henderson R, Hinberg I, Little R, Seed J, Shea K, Tabacova S, Tyl R, Williams P, Zacharewski T. 2002. NTP center for the evaluation of risks to human reproduction:
phthalates expert panel report on the reproductive and developmental toxicity of di(2-ethylhexyl) phthalate. Reproductive Toxicology 16:529–653.

Kavlock R, Boekelheide K, Chapin R, Cunningham M, Faustman E, Foster P, Golub M, Henderson R, Hinberg I, Little R, Seed J, Shea K, Tabacova S, Tyl R, Williams P, Zacharewski T. 2002. NTP center for the evaluation of risks to human reproduction:
phthalates expert panel report on the reproductive and developmental toxicity of butyl benzyl phthalate. Reproductive Toxicology 16:453–487.

Koch HM, Drexler H, Angerer J. 2003a. An estimation of the daily intake of di(2-ethylhexyl)phthalate (DEHP) and other phthalates in the general population. Int. J. Hyg. Environ. Health 206(2):77-83.

Koch HM, Rossbach B, Drexler H, Angerer J. 2003b. Internal exposure of the general population to DEHP and other phthalates-determination of secondary and primary phthalate monoester metabolites in urine. Environ. Res. 93(2):177-185.

Koch HM, Gonzalez-Reche LM, Angerer Ju¨rgen. 2003. On-line clean-up by multidimensional liquid chromatography–electrospray ionization tandem mass spectrometry for high throughput quantification of primary and secondary phthalate
metabolites in human urine. Journal of Chromatography B, 784:169-182.

Koo HJ, Lee BM. 2004. Estimated exposure to phthlates in cosmetics and risk assessment. Journal of Toxicology and Environmental Health Part A 67:1901–1914.

Koo HJ, Lee BM. 2005. Human monitoring of phthalates and risk assessment.
Journal of Toxicology and Environmental Health Part A 68:1379-1392.

Lamb IV, 1987. Reproductive effects of four phthalic acid esters in the mouse.
Toxicol Appl Pharmacol 88:255–269.

Latini G, Felice CD, Presta G, Del Vecchio A, Paris I, Ruggieri F, Mazzeo P. 2003b. In utero exposure to di-(2-ethylhexyl) phthalate and duration of human pregnancy. Environmental Health Perspectives 111:1783-1785.

Lovekamp-Swan T, Davis BJ. 2003. Mechanisms of phthalate ester toxicity in the female reproductive system. Environ Health Perspect 111:139–145.

Marsman DS. 1995. NTP technical report on toxicity studies of dibutyl phthalate (CAS no. 84-74-2) administered in feed to F344 rats and B6C3F1 mice NIH Publication 95-3353. Research Triangle Park: National Toxicology Program

Morrissey, R.E., Lamb IV, J.C., Morris, R.W., Chapin, R.E., Gulati, D.K., Heindel,
J.J., 1989. Results and evaluations of 48 continuous breeding reproduction studies
conducted in mice. Fundamental and Applied Toxicology 13:747-777.

NTP, 1988. Developmental toxicity evaluation of diethyl phthalate(CAS No. 84-66-2)
administered to CD rats on gestational days 6 through 15. NTP-88-336. National
Toxicology Program, National Institute of Environmental Health Sciences,
Research Triangle Park, NC 27709, USA.

Page BD, Lacroix GM. 1995. The occurrence of phthalate ester and di-2-ethylhexyl adipate plasticizers in Canadian packaging and food sampled in 1985-1989: a survey. Food Additives and Contaminants 12(1):129-151.

Peakall DB. 1975. Phthalate esters: occurrence and biological effects. Residue Rev 54:1-41.

Piersma A.H., Verhoef A., Dortant P.M., 1995. Evaluation of the OECD 421
reproductive toxicity screening test protocol using butyl benzyl phthalate.
Toxicology 99:191–197.

Pereira C, Mapuskar K, Rao CV. 2006. Chronic toxicity of diethyl phthalate in male Wistar rats—A dose–response study. Regulatory Toxicology and Pharmacology 45:169–177.

Poon R, Lecavalier P, Mueller R, Valli VE, Procter BG, Chu I, 1997. Subchronic oral
toxicity of di-n-octyl phthalate and di (2-ethylhexyl) phthalate in the rat. Food
Chem Toxicol 35: 225–239.

Preuss R, Koch HM, Angerer J. 2005. Biological monitoring of the five major metabolites of di-(2-ethylhexyl)phthalate (DEHP) in human urine using column-switching liquid chromatography–tandem mass spectrometry. Journal of Chromatography B 816:269–280.

Price CJ, Tyl RW, Marr MC, Myers CB, Sadler BM, Kimmel CA, 1988. Reproduction and fertility evaluation of diethylhexyl phthalate (CAS No. 117-81-7) in CD-1 mice exposed during gestation. Research Triangle Park, NC: National Toxicology Program.

Reel JR, Lawton AD, Feldman DB, Lamb JC. 1984. Di(N-butyl) phthalate: reproduction and fertility assessment in CD-1 mice when administered in the feed. NTP-84-411: National Toxicology Program, National Institute of Environmental Health Sciences

Ruud JB Peters. 2005. phthalates and artificial musk in perfumes. TNO report 1-27.

Schilling K, Deckardt K, Gembardt C, Hildebrand B. 1999. Di-2-ethylhexyl phthalate – two-generation reproduction toxicity range-finding study in Wistar rats,
continuous dietary administration Laboratory Project ID: 15R0491/997096: BASF
Aktiengesellschaft.

Silva MJ, Slakman AR, Reidy JA, PreauJr JL, Herbert AR, Samandar E, Needham LL, Calafat AM. 2004b. Analysis of human urine for fifteen phthalate metabolites using automated solid-phase extraction. J. Chromatogr. B Analyt. Technol. Biomed. Life Sci. 805(1):161-167.

Sharman M, Read WA, Castle L, Gilbert J. 1994. Levels of di-(2- ethylhexyl) phthalate and total phthalate esters in milk, cream, butter and cheese. Food Addition Contamination 11:375–385.

Staples CA, Peterson DR, Parkerton TF, Adams WJ. 1997. The environmental fate of phthalate esters-A literature review. Chemosphere 35:667-749.

Tan GH, 1995. Residue levels of phthalate esters in water and sediment samples from
Klang river basin. Bull Environmental Contaminant of Toxicology. 3654:
171-17633-40.

Tickner JA, Schettler T, Guidotti T, McCally M, Rossi M. 2001. Health risks posed by use of di-2-ethylhexyl phthalate (DEHP) in pvc medical devices: a critical review. Am J Ind Med 39:100-111.

Thuren A. 1986. Determination of Phthalates in Aquatic Environments. Bull Environ Contam Toxicol 36:33-40.

Tienpont B, David F, Sandra P, Vanwalleghem F. 2002. Evaluation of Sorptive Enrichment for the Analysis of Phthalates in Air Samples. J. Microcolumn Separations 12(4):194-203.

Tsumura Y, Ishimitsu S, Saito I, Sakai H, Kobayash Y, Tonogai Y, 2001. Eleven
phthalate esters and di (2-ethylhexyl) adipate in oneweek duplicate diet samples
obtained from hospitals and their estimated daily intake. Food Additives and
Contaminants 18(5): 449-460.

Yuan SY, Liu C, Liao CS, Chang BV. 2002. Occurrence and microbial degradation of phthalate esters in Taiwan river sediments. Chemosphere 49:1295–1299.

Zacharewski T. 1998. Identification and assessment of endocrine disruptors: limitations of in vivo and in vitro assays. Environ Health Perspect 106: 577–582

張碧芬，2000，河川環境鄰苯二甲酸酯類化合物之調查及生物降解之研究。環境荷爾蒙研討會論文集。

陳佳飛、陳美蓮、毛義方, 2002 食品容器及包裝用塑膠材質之塑化劑溶出研究

陳美蓮、毛義方、陳靖雄、蔡欣倢, 2004. 食物中常見六種酞酸鹽類同時測定法及國人暴露生物偵測研究

行政院環保署，2001，毒性化學物質環境流布暴露調查分析。

行政院環保署，2002，毒性化學物質污染排放調查與模式之建立-一般環境中。

行政院環保署，2004，毒性化學物質環境流布調查分析。

行政院環保署，2005，河川及海洋水質維護改善計畫與斯德哥爾摩公約計畫─毒性化學物質環境流布調查。