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BACKGROUND: Acrolein is a highly reactive α,β unsaturated aldehyde and respiratory irritant. Acrolein is formed during combustion (e.g., burning tobacco or biomass), during high-temperature cooking of foods, and in vivo as a product of oxidative stress and polyamine metabolism. No biomonitoring reference data have been reported to characterize acrolein exposure for the U.S. population. OBJECTIVES: Our goals were to a) evaluate two acrolein metabolites in urine--N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3HPMA) and N-acetyl-S-(2-carboxyethyl)-L-cysteine (CEMA)--as biomarkers of exposure to acrolein for the U.S. population by age, sex, race, and smoking status; and b) assess tobacco smoke as a predictor of acrolein exposure. METHODS: We analyzed urine from National Health and Nutrition Examination Survey (NHANES 2005-2006) participants [greater than or equal to]12 years old (n = 2,866) for 3HPMA and CEMA using ultra-high-performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry (UPLC/ESI-MSMS). Sample-weighted linear regression models stratified for nontobacco users versus tobacco smokers (as defined by serum cotinine and self-report) characterized the association of urinary 3HPMA and CEMA with tobacco smoke exposure, adjusting for urinary creatinine, sex, age, and race/ethnicity. RESULTS: 3HPMA and CEMA levels were higher among tobacco smokers (cigarettes, cigars, and pipe users) than among non-tobacco users. The median 3HPMA levels for tobacco smokers and non-tobacco users were 1,089 and 219 µg/g creatinine, respectively. Similarly, median CEMA levels were 203 µg/g creatinine for tobacco smokers and 78.8 µg/g creatinine for non-tobacco users. Regression analysis showed that serum cotinine was a significant positive predictor (p < 0.0001) of both 3HPMA and CEMA among tobacco smokers. CONCLUSIONS: Tobacco smoke was a significant predictor of acrolein exposure in the U.S. population. Environ Health Perspect 123:1302-1308; http://dx.doi.org/10.1289/ehp.1409251, Introduction Acrolein is a chemical contaminant that is ubiquitous in the environment. It is formed from carbohydrates, vegetable oils, animal fats, and amino acids during heating of foods and by [...]

Background Marijuana is seeing increased therapeutic use, and is the world's third most-popular recreational drug following alcohol and tobacco. This widening use poses increased exposure to potentially toxic combustion by-products from marijuana smoke and the potential for public health concerns. Objectives To compare urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs) among self-reported recent marijuana users and nonusers, while accounting for tobacco smoke exposure. Methods Measurements of PAH and VOC metabolites in urine samples were combined with questionnaire data collected from participants in the National Health and Nutrition Examination Surveys (NHANES) from 2005 to 2012 in order to categorize participants (≥ 18 years) into exclusive recent marijuana users and nonusers. Adjusted geometric means (GMs) of urinary concentrations were computed for these groups using multiple regression analyses to adjust for potential confounders. Results Adjusted GMs of many individual monohydroxy PAHs (OH-PAHs) were significantly higher in recent marijuana users than in nonusers ( p < 0.05). Urinary thiocyanate ( p < 0.001) and urinary concentrations of many VOC metabolites, including metabolites of acrylonitrile ( p < 0.001) and acrylamide ( p < 0.001), were significantly higher in recent marijuana users than in nonusers. Conclusions We found elevated levels of biomarkers for potentially harmful chemicals among self-identified, recent marijuana users compared with nonusers. These findings suggest that further studies are needed to evaluate the potential health risks to humans from the exposure to these agents when smoking marijuana. [ABSTRACT FROM AUTHOR]

Background Health risks of using styrene to manufacture windblades for the green energy sector are unknown. Methods Using data collected from 355 (73%) current windblade workers and regression analysis, we investigated associations between health outcomes and styrene exposure estimates derived from urinary styrene metabolites. Results The median current styrene exposure was 53.6 mg/g creatinine (interquartile range: 19.5-94.4). Color blindness in men and women (standardized morbidity ratios 2.3 and 16.6, respectively) was not associated with exposure estimates, but was the type previously reported with styrene. Visual contrast sensitivity decreased and chest tightness increased (odds ratio 2.9) with increasing current exposure. Decreases in spirometric parameters and FeNO, and increases in the odds of wheeze and asthma-like symptoms (odds ratios 1.3 and 1.2, respectively) occurred with increasing cumulative exposure. Conclusions Despite styrene exposures below the recommended 400 mg/g creatinine, visual and respiratory effects indicate the need for additional preventative measures in this industry. Am. J. Ind. Med. 58:1150-1159, 2015. © 2015 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Measurement of environmental endotoxin exposures is complicated by variability encountered using current biological assay methods arising in part from lot-to-lot variability of the Limulus-amebocyte lysate (LAL) reagents. Therefore, we investigated the lot-to-lot repeatability of commercially available recombinant Factor C (rFC) kits as an alternative to LAL. Specifically, we compared endotoxin estimates obtained from rFC assay of twenty indoor dust samples, using four different extraction and assay media, to endotoxin estimates previously obtained by Limulus amebocyte lysate (LAL) assay and amounts of 3-hydroxy fatty acids (3-OHFA) in lipopolysaccharide (LPS) using gas-chromatography mass spectroscopy (GC-MS). We found that lot-to-lot variability of the rFC assay kits does not significantly alter endotoxin estimates in house dust samples when performed using three of the four assay media tested and that choice of assay media significantly altered endotoxin estimates obtained by rFC assay of house dust samples. Our findings demonstrate lot-to-lot reproducibility of rFC assay of environmental samples and suggest that use of rFC assay performed with Tris buffer or water as the extraction and assay medium for measurement of endotoxin in dust samples may be a suitable choice for developing a standardized methodology. [ABSTRACT FROM AUTHOR]

Perchlorate is ubiquitous in the environment, leading to human exposure and potential impact on thyroid function. Nitrate can also competitive^ inhibit iodide upake at the sodium-iodide symporter and thus reduce thyroid hormone production. This study investigates the intake of Perchlorate, nitrate, and iodide attributable to direct and indirect tap water consumption. The National Health and Nutrition Examination Survey collected tap water samples and consumption data from 3262 U.S. residents during the years 2005-2006. The median perchlorate, nitrate, and iodide levels measured in tap water were 1.16,758, and 4.55 μg/L, respectively. Measured Perchlorate levels were below the United States Environmental Protection Agency (U.S. EPA) drinking water equivalent level for Perchlorate (24.5 μg/L). Significant correlations were found between iodide and nitrate levels (r = 0.17, p < 0.0001) and Perchlorate and nitrate levels (r = 0.25, p < 0.0001). On the basis of 24 h recall, 47% of the study participants reported drinking tap water; 89% reported either direct or indirect consumption of tap water. For the adult population (age ≥ 20 yrs) the median tap water consumption rate was 11.6 mL/kg-day. Using individual tap water consumption data and body weight we estimated the median Perchlorate, nitrate, and iodide dose attributable to tap water as 9.11, 11300, and 43.3 ng/kg-day, respectively, for U.S. adults. This Perchlorate exposure dose from tap water is relatively small compared to the total Perchlorate exposure dose previously characterized for die U.S. adults (median 64 ng/kg-day) and the U.S. EPA reference dose (700 ng/kg-day). [ABSTRACT FROM AUTHOR]

The cytotoxicity and genotoxicity of nitromethane and its halogenated analogues in mammals raise concerns about potential toxicity to humans. This study shows that halonitromethanes are not stable in human blood and undergo dehalogenation to form nitromethane. We quantified nitromethane in human blood using solid-phase microextraction (SPME) headspace sampling coupled with gas chromatography (GC) and high resolution mass spectrometry (HAMS). The limit of detection was 0.01 μg/L with a linear calibration curve spanning 3 orders of magnitude. This method employs isotope dilution to precisely quantify trace amounts of nitromethane (coefficient of variation <6%). At three spiked concentrations of nitromethane, method accuracy ranged from 88 to 99%. We applied this method to blood samples collected from 632 people with no known occupational exposure to nitromethane or halonitromethanes. Nitromethane was detected in all blood samples tested (range: 0.28-3.79 μg/L, median: 0.66 μg/L). Time-course experiments with trichloronitromethane- and tribromonitromethane-spiked blood showed that nitromethane was the major product formed (1 nmole tribromonitromethane formed 0.59 nmole of nitromethane, whereas 1 nmole trichloromtromethane formed 0.77 nmole nitromethane). Nitromethane may form endogenously from peroxynitrite: nitromethane concentrations increased proportionately in blood samples spiked with peroxynitrite. Blood nitromethane can be a biomarker of exposure to both nitromethane and halonitromethanes. This sensitive, accurate, and precise analytical method can be used to determine baseline blood nitromethane level in the general population. It can also be used to study the health impact from exposure to nitromethane and halonitromethanes in occupational environments and to assess trichloronitromethane (chloropicrin) exposure in chemical terrorism investigations. [ABSTRACT FROM AUTHOR]

Describes the use of an enzyme-linked immunosorbent assay to assay (1->3)-beta-D-glucans in house dust samples, some mold cultures and metal working fluid samples. Basis of the assay on the use of a high-affinity receptor (galactosyl ceramide); Insensitivity of the assay to interference caused by agents which affect the Limulus assay.

Three green mills and two dry mills were studied for personal exposure to wood dust and biohazards associated with wood dust and their correlation to lung function and work-related symptoms among sawmill workers. The levels of exposure to endotoxin, (1→3)-β-D-glucan, bacteria and fungi were high in green mills compared with dry mills. Compared with dry mill workers, green mill workers had significantly high prevalence of regular cough, chronic bronchitis, regular blocked nose, regular sneezing, sinus problems, flu-like symptoms, and eye and throat irritation. Significant positive correlations were found among endotoxin and Gram (−)ve bacteria, (1→3)-β-D-glucan and fungi, and endotoxin and (1→3)-β-D-glucan exposure levels. Significant dose–response relationships were found for personal exposures and lung function, and lung function and work-related respiratory symptoms. The significant correlations found for respirable fractions show that not only inhalable but also respirable fractions are important in determining potential health effects of exposure to wood dust. The management and employees of the sawmilling industry should be educated on the potential health effects of wood dust. Wood dust should be controlled at the source. [ABSTRACT FROM PUBLISHER]

Personal exposure to fungi, bacteria, endotoxin, and (1 3)-beta-D-glucan was determined at different woodworking sites-logging sites, sawmills, woodchipping sites, and joineries. Exposure levels to fungi at logging sites and sawmills were in the range of 10[sup 3]-10[sup 4] cfu/m[sup 3], at the woodchipping mill, 10[sup 3]-10[sup 5] cfu/m[sup 3], and at joineries, 10[sup 2]-10[sup 4] cfu/m[sup 3]. Although mean endotoxin levels were lower than the suggested threshold value of 20 ng/m[sup 3], some personal exposures at sawmills and a joinery exceeded the standard. The geometric mean personal (1 3)-beta-D-glucan exposure level at the woodchipping mill was 2.32 ng/m[sup 3], at sawmills, 1.37 ng/m[sup 3], at logging sites, 2.02 ng/m[sup 3], and at joineries, 0.43 ng/m[sup 3]. Highly significant associations were found between mean personal inhalable endotoxin exposures and Gramnegative bacteria levels (p < 0.0001), and mean personal inhalable (1 3)-beta-D-glucan exposures and fungi levels (p = 0.0003). The prevalence of cough, phlegm, chronic bronchitis, nasal symptoms, frequent headaches, and eye and throat irritations was significantly higher among woodworkers than controls. Dose-response relationships were found between personal exposures and work-related symptoms among joinery workers and sawmill and chip mill workers. [ABSTRACT FROM AUTHOR]

Perchlorate is an inhibitor of iodide uptake that is found widely in the environment. Given the potential for perchlorate accumulation during egg formation and the widespread consumption of eggs, it is important to examine eggs as a source of exposure to perchlorate and other potential inhibitors of iodide uptake (nitrate and thiocyanate). This study was conducted to determine potential human exposure to perchlorate from eggs produced by chicken flocks consuming differing amounts of perchlorate. The mean concentrations of perchlorate (7.16 ( 1.99 microg/kg of dry weight), nitrate (2820 ( 2100 microg/kg of dry weight), thiocyanate (574 +/- 433 microg/kg of dry weight), and iodide (2980 ( 1490 microg/kg of dry weight) in eggs (n = 180) from 15 chicken houses on 3 U.S. farms were determined. Chickens secreted into eggs an average of 23% of the perchlorate ingested from feed and water. Perchlorate levels in eggs were positively correlated with perchlorate intake (p < 0.001). Increased intake of perchlorate, nitrate, and thiocyanate was associated with decreased iodide levels in eggs, possibly indicating a competitive transport mechanism, such as sodium-iodide symporter. It was estimated that egg consumption contributes minimal perchlorate (approximately 0.040 microg) compared to the average total intake of approximately 10.5 microg for U.S. adults. Additionally, it was found that egg consumption was not associated with increased perchlorate exposure in 2820 individuals from the National Health and Nutrition Examination Survey (p value for the difference of least-squares means, pDiff = 0.225). From these findings it was concluded that, although chickens secrete perchlorate in eggs, eggs do not appear to be a significant source of perchlorate exposure for adults in the United States.

Background: 3-Hydroxy fatty acids (3-OHFAs), components of lipid A of gram-negative bacteria are useful chemical markers of endotoxin., Methods: We analyzed 3-OHFAs in house dust as trimethylsilyl (TMS) methyl ester derivatives in the electron impact ionization mode using gas chromatography ion-trap mass spectrometry. Linear calibrations with r > 0.995 were observed for all the 3-OHFA methyl ester external standards., Results: Recovery efficiency experiments with house dust demonstrated that accurate quantification requires calibration curves to be subjected to phase separation and solid phase extraction (SPE) because of differing clean-up losses according to chain length of 3-OHFAs. Recovery experiments also demonstrated interference with detection of C16:0 by the ion trap, which may be due to suppression of ionization by a constituent in house dust. Interference was overcome by injecting 1:4 dilutions of derivatized samples. The range of recoveries was 89.3%-111.5% for 3-OHFAs added to house dust. The reproducibility of injections was high (CV for C14:0 = 2.36%). The limit of detection (LOD) was 0.15 ng/mg for each 3-OHFA., Conclusions: The modifications we made included: use of 3-hydroxy C11:0 and C13:0 methyl esters as internal standards, subjecting calibration standards to phase separation and SPE; addition of water to phase separation; addition of 1-pentadecanol as a carrier; injecting 1:4 diluted TMS derivatives of 3-OHFAs; and monitoring both m/z 131 and 133 ions to improve stability of area measurements for product ions. This method of optimization establishes an appropriate technique for quantification of 3-OHFAs in house dust., (Copyright 2006 Wiley-Liss, Inc.)

Background: Measurement of exposure to environmental endotoxin is frequently performed using a Limulus amebocyte lysate (LAL) based assay. Recently, a new method has become available with similar sensitivity and potentially greater specificity using recombinant Factor C (rFC) from the horseshoe crab Carcinoscorpius rotundicauda. A preliminary study was carried out to determine the comparability of LAL and rFC in measuring endotoxins in house dust for large scale epidemiologic studies., Methods: House dust samples were collected from family rooms by vacuuming 1 m2 of the center of the room. Sixty sieved house dust samples were assayed for endotoxin by LAL (Cambrex, KQCL lysate) and rFC (Pyrogene, Cambrex) and for (1 --> 3)-beta-D-glucans by ELISA. The resistant parallel line estimation was used for data analysis of LAL and rFC. A four-parameter logistic fit with inverse prediction was used to calculate (1 --> 3)-beta-D-glucan levels of the samples., Results: The spike recovery was 113.63% (95% CI = 101.69, 125.57%) for LAL and 99.69% (95% CI = 90.14, 109.24%) for rFC assays. The LAL assay gave higher endotoxin estimates compared with rFC. The LAL and rFC estimates were highly correlated (r = 0.86, P < 0.0001). The difference between LAL and rFC endotoxin estimates correlated with the LAL estimates (r = 0.51, P < 0.0001). However, the difference was not correlated with (1 --> 3)-beta-D-glucans., Conclusion: LAL and rFC gave comparable results, hence either assay can be used for studies of endotoxin exposure. The current study shows that (1 --> 3)-beta-D-glucan is not a major factor interfering with endotoxin measurements in house dust using a Cambrex KQCL LAL preparation., (Copyright 2006 Wiley-Liss, Inc.)