Polychlorinated dibenzo-p-dioxins, dibenzofurans, biphenyls, and naphthalenes in plasma of workers deployed at the World Trade Center after the collapse.

Blood plasma samples (n = 43) collected retrospectively from New York State employees and National Guard personnel who had been assigned to work in the vicinity of the World Trade Center (WTC) during the week after the collapse of the buildings were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and polychlorinated naphthalenes (PCNs). On the basis of algorithms developed to rank individual exposures to dust and debris and to smoke, we categorized the samples as: more smoke exposure (MSE), more dust exposure (MDE), less smoke exposure (LSE), and less dust exposure (LDE). Mean concentrations of PCDDs were 1070, 223, 3690, and 732 pg/g lipid wt, and mean concentrations of PCDFs were 910, 1520, 230, and 117 pg/g lipid wt, for the MSE, MDE, LSE, and LDE groups, respectively. The concentrations of PCDFs were higher in the two "more exposure" groups than in the two "less exposure" groups. Calculated TEQ concentrations of coplanar PCBs and PCDD/Fs in plasma samples were, on average, 1.12 and 41.2 pg WHO-TEQ/g lipid wt, respectively. TEQ concentrations of PCDFs were higher than those of PCDDs in both "more exposure" groups but lower than those of PCDDs in "less exposure" groups. This result is suggestive of exposure of the WTC responders to PCDFs after the WTC collapse. PCDFs contributed the majority of TEQs and are therefore the critical dioxin-like compounds in MSE/MDE groups, whereas PCDDs are the critical compounds in the LSE/LDE groups.

Use of newborn screening program blood spots for exposure assessment: declining levels of perluorinated compounds in New York State infants.

Temporal biomonitoring studies can assess changes in population exposures to contaminants, but collection of biological specimens with adequate representation and sufficient temporal resolution can be resource-intensive. Newborn Screening Programs (NSPs) collect blood as dried spots on filter paper from nearly all infants born in the United States (U.S.). In this study, we investigated the use of NSP blood spots for temporal biomonitoring by analyzing perfluorooctane sulfonate (PFOS), perfluorooctane sulfonamide (PFOSA), perfluorohexane sulfonate (PFHxS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) in 110 New York State (NYS) NSP blood spot composite specimens collected between 1997 and 2007, representing a total of 2640 infants. All analytes were detected in > or =90% of the specimens. Concentrations of PFOS, PFOSA, PFHxS, and PFOA exhibited significant exponential declines after the year 2000, coinciding with the phase-out in PFOS production in the U.S. Calculated disappearance half-lives for PFOS, PFHxS, and PFOA (4.4, 8.2, and 4.1 years, respectively) were similar to biological half-lives reported for retired fluorochemical workers. Our results suggest sharp decreases in perinatal exposure of NYS infants to PFOS, PFOSA, PFHxS, and PFOA and demonstrate, for the first time, the utility of NSP blood spots for assessment of temporal trends in exposure.

Biomonitoring of perfluorochemicals in plasma of New York State personnel responding to the World Trade Center disaster.

The collapse of the World Trade Center (WTC) on September 11, 2001 resulted in the release of several airborne pollutants in and around the site. Perfluorochemicals including perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA), which are used in soil- and stain-resistant coatings on upholstery, carpets, leather, floor waxes, polishes, and in fire-fighting foams were potentially released during the collapse of the WTC. In this pilot study, we analyzed 458 plasma samples of New York State (NYS) employees and National Guard personnel assigned to work in the vicinity of the WTC between September 11 and December 23, 2001, to assess exposure to perfluorochemicals released in dust and smoke. The plasma samples collected from NYS WTC responders were grouped based on estimated levels of exposure to dust and smoke, as follows: more dust exposure (MDE), less dust exposure (LDE), more smoke exposure (MSE), and less smoke exposure (LSE). Furthermore, samples were grouped, based on self-reported symptoms at the time of sampling, as symptomatic and asymptomatic. Eight perfluorochemicals were measured in 458 plasma samples. PFOS, PFOA, perfluorohexanesulfonate (PFHxS), and perfluorononanoic acid (PFNA), were consistently detected in almost all samples. PFOA and PFHxS concentrations were approximately 2-fold higher in WTC responders than the concentrations reported for the U.S. general population. No significant difference was observed in the concentrations of perfluorochemicals between symptomatic and asymptomatic groups. Concentrations of PFHxS were significantly (p < or = 0.05) higher in the MDE group than in the LDE group. Concentrations of PFNA were significantly higher in the MSE group than in the LSE group. Significantly higher concentrations of PFOA and PFHxS were found in individuals exposed to smoke than in individuals exposed to dust. A significant negative correlation existed between plasma lipid content and concentrations of certain perfluorochemicals. Our initial findings suggest that WTC responders were exposed to perfluorochemicals, especially PFOA, PFNA, and PFHxS, through inhalation of dust and smoke released during and after the collapse of the WTC. The potential health implications of these results are unknown at this time. Expansion of testing to include all archived samples will be critical to help confirm these findings. In doing so, it may be possible to identify biological markers of WTC exposure and to improve our understanding of the health impacts of these compounds.

Cyanide adducts with human plasma proteins: albumin as a potential exposure surrogate.

Cyanide (CN) is a ubiquitous environmental toxicant. The measurement of CN in whole blood is a common exposure assay, but values are error prone because of CN's rapid metabolism and clearance (t1/2 < 1 h) from this compartment. This study was undertaken to determine whether CN forms covalent adduct(s) with plasma proteins that could serve as stable biomarker(s) and potential surrogate(s) of exposure. When added to human blood, plasma, or serum, CN formed covalent adducts with immunoglobulin G (IgG) and serum albumin (HSA) in the plasma fraction. Covalent adducts were not detected in the cellular, primarily erythrocyte, fraction. With human, mouse, and rabbit IgGs, the reaction with CN occurred at intra- and/or interchain disulfide linkages in the heavy and light chains. Digestion of CN-treated HSA with trypsin or the endoproteinase Lys-C at basic pH produced tautomeric 2-iminothiazoline-4-carboxylyl/2-aminothiazolidine-4-carboxylyl (itcCys) N-terminal peptides exclusively, consistent with prior model peptide/protein studies showing that under basic conditions internal S-cyanylated-Cys residues cyclize with concomitant release of the upstream peptide. The most readily detectable reaction of CN with purified HSA was at Cys34, the only Cys of the 35 present not connected as internal cystines. Because CN does not react with free sulfhydryl groups, it is probable that S-cyanylation at Cys34 occurs at those residues that carry GSH, Cys, or other small molecules as mixed disulfides. Relatively less detectable, modified Cys residues were also identified at positions 53, 124, 392, 477, and 487. When 14CN was added to human serum or whole blood at concentrations spanning a putative nontoxic to lethal range, stable adduct formation with HSA occurred in a linear, concentration-dependent reaction that was complete within 2 h. These attributes of the reaction, coupled with a plasma compartment location, suggest that quantitation of CN bound to HSA would provide a much more reliable assessment of exposure than does measurement of CN in blood.