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A level III fugacity model was applied to characterize the fate of gamma-HCH in Tianjin, China, before the 1990s when the contamination reached its maximum at steady state. Geometric means were used as model inputs. The concentrations of gamma-HCH in air, surface water, soil, sediment, crops, and fish as well as transfer fluxes across the interface between the compartments were derived under the assumption of steady state. The calculated concentrations were validated by independent data collected from the literature. There was generally good agreement between the estimated and the observed concentrations, and the differences were all less than 0.6 log units for air, water, soil, sediment, and fish and approximately 1 order of magnitude for crops. Around 97% of gamma-HCH accumulated in soil and sediment. Wastewater irrigation was not an important pathway for delivering gamma-HCH to soil as compared to the dominant source of agricultural application. Degradation and advective airflow carried much gamma-HCH out of the system. Sensitivities of the model estimates to input parameters were tested, and a coefficient of variation normalized sensitivity coefficient was defined for the test. The most influential parameters were degradation rates in sediment and soil, application rates, concentrations in wastewater, and adsorption coefficients. Monte Carlo simulation was conducted for model uncertainty analysis. The model was run 20 000 times using randomly generated data from predefined log-normal distribution density functions. All calculated concentrations and fluxes were log-normally distributed. The dispersions of the calculated and observed concentrations were compared in terms of coefficients of variation to distinguish between true variability and model uncertainty.

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This paper provides the results of an investigation on dietary intakes and internal doses of polycyclic aromatic hydrocarbons (PAHs) for nonsmoking women from Beijing, China. Concentrations of PAHs were measured by gas chromatography/mass spectrometry (GC/MS) for human milk, placenta, and umbilical cord blood samples from 40 nonsmoking women and for 144 composite food samples covering major food categories. Information on food consumption and estimated ingestion doses of PAHs by the cohort was also collected individually. Relationship among the studied human samples and relative importance of breastfeeding to the total exposure dose of infants were addressed. The median (mean and standard deviation) total concentrations of 15 PAHs in human milk, placenta, and umbilical cord blood with (or without) fat normalization were 278 (9.30 ± 5.75), 819 (35.9 ± 15.4), and 1370 (5.521 ± 3.71) ng/g of fat, respectively, and the corresponding levels of benzo[a]pyrene equivalent (B[a]P(equiv)) were 11.2 (0.473 ± 0.605), 16.2 (0.717 ± 0.318), and 13.1 (0.140 ± 0.225) ng/g of fat, respectively. The calculated intake of B[a]P(equiv) by Beijing cohort varied from 0.609 to 4.69 ng·kg(-1)·day(-1) with a median value of 1.93 (2.09 ± 0.921 mean ± standard deviation) ng·kg(-1)·day(-1). Significant correlations were found among human milk, placenta, and umbilical cord blood (p < 0.05) for low-molecular-weight PAHs, indicating selective transfer potential of individual PAHs from mother to fetus. Internal dose of PAHs was not in proportion to amounts of food ingestion, daily dietary intake, lifestyle, and social-demographic characteristics of the participants (p > 0.05). Ingested doses of PAHs (3.00-102 ng·kg(-1)·day(-1)), which were much higher than the inhaled doses (0.152-8.50 ng·kg(-1)·day(-1)), were 3-4 orders of magnitude lower than the recommended reference doses, unlikely to impose any obvious risk based on current knowledge.