Reduced adiponectin:leptin ratio associated with inhalation exposure to vinyl chloride monomer.

The hepatic toxicity of vinyl chloride monomer (VCM) has often been reported, but few studies have assessed insulin resistance or adipose tissue dysfunction. We analyzed the chronic health effects of moderate exposure to VCM on factory workers in Taiwan. Data were collected from personal air samples, urine samples, and immunohistochemical (IHC) examinations of 122 recruited voluntary participants. Air samples were analyzed to assess personal levels of exposure to VCM and ethylene dichloride (EDC). Urine samples were collected from each worker before they started and after they finished their daily shift. Urinary thiodiglycolic acid (TDGA) levels were analyzed using high-performance liquid chromatography-tandem mass spectrometry (HPLC/MS/MS). IHC examinations included liver function and serum adipokine level tests for insulin resistance. Consequently, the participants included for the final analysis were 113. After confounders had been adjusted for, the airborne VCM concentration significantly (P = 0.043) correlated with pre-shift urinary TDGA levels (ß = 0.194). A multivariate analysis showed a significant (P = 0.013) inverse correlation between the adiponectin:leptin ratio and the airborne VCM concentration (ß = -0.283), which means that exposure to VCM might increase the risk of insulin resistance and adiponectin abnormalities. We hypothesized that pre-shift urinary TDGA levels can be used as exposure biomarkers for the exposure of workers to VCM.

Relationship between urinary concentrations of di(2-ethylhexyl) phthalate (DEHP) metabolites and reproductive hormones in polyvinyl chloride production workers.

OBJECTIVES: We investigated the relationship between urinary metabolites of di(2-ethylhexyl) phthalate (DEHP) and reproductive hormones in workers of polyvinyl chloride (PVC) production plants. After exposure, most of the DEHP is rapidly metabolised to mono(2-ethylhexyl) phthalate (MEHP), mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), which may be associated with reproductive hormone interruption and testicular toxicity. Some studies report that urinary concentrations of phthalate metabolites for plastics workers are significantly higher than for the general population. However, little is known about the disruption of reproductive hormones for DEHP exposure workers. METHODS: This cross-sectional study of 82 male workers measured the biomarkers for their reproductive hormones and their exposure to DEHP. Relationships between urinary concentrations of DEHP metabolites were estimated using multivariate linear regression and quartile analysis models. RESULTS: The geometric means of urinary creatinine-adjusted (µg/g-Cre) concentrations of MEHP, MEOHP and MEHHP during the post-shift period were 23.9, 66.9 and 84.6, respectively. In multiple regression models adjusted for potential confounders, there were significant positive associations between urinary concentrations of DEHP metabolites and estradiol (E2) (p<0.01), and in the ratio of E2 to testosterone (p<0.05). Moreover, quartile analysis showed significant positive relationships between the total urinary concentration of DEHP metabolites and E2 (ptrend=0.024), and in the ratio of E2 to testosterone (ptrend=0.031). CONCLUSIONS: Relationships between reproductive hormones and the total urinary concentration of DEHP metabolites in male PVC production workers were significantly positive. This indicated that aromatase activity had increased in male workers exposed to DEHP, which is consistent with animal studies.

Estimating the contribution of inhalation exposure to di-2-ethylhexyl phthalate (DEHP) for PVC production workers, using personal air sampling and urinary metabolite monitoring.

Because of troubling reports of high urinary metabolite levels and adverse reproductive health effects in workers exposed to di(2-ethylhexyl)phthalate (DEHP) in occupational settings, concern about exposure to DEHP in occupational settings is increasing. However, the contributions of different routes of exposure to DEHP are unclear. We used personal air sampling and biomonitoring to determine the contribution of inhalation exposure to the body burden of DEHP in the workplace. Eighty-nine workers (high-exposure group: 66 raw-materials workers; low-exposure group: 23 administrative workers) were recruited from three polyvinyl chloride (PVC) factories. Urinary levels of mono(2-ethylhexyl) phthalate (MEHP), (mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) were measured in pre-shift and post-shift samples. The geometric means of airborne concentrations of DEHP were 5.3 µg/m3 (low-exposure group) and 32.7 µg/m3 (high-exposure group) (P<0.01). Correlation analysis showed a consistently significant association between airborne DEHP concentration and urinary DEHP metabolite levels in the high-exposure group. Calculating daily DEHP intake based on total urinary metabolite levels showed that the geometric means of total daily urinary metabolite levels of DEHP were 9.2 µg/kg/day (low-exposure group) and 15.5 µg/kg/day (high-exposure group) (P<0.01). A quartile analysis of all workers showed a significant trend toward an association between the individual contribution of inhalation exposure to DEHP and urinary DEHP metabolite levels, for which the mean inhalation contribution was 46.7% in the highest quartile. We conclude that inhalation-absorbed airborne DEHP significantly increased the total body burden of DEHP in these occupationally exposed workers.