Nitromethane is a known toxicant and suspected human carcinogen. Exposure to nitromethane in a representative sample of the civilian, noninstitutionalized population in the United States >/=12 years old was assessed using 2007-2012 National Health and Nutritional Examination Survey (NHANES) data. Nitromethane was detected in all 8000 human blood samples collected, of which 6730 were used for analyses reported here. Sample-weighted median blood nitromethane was higher among exclusive combusted tobacco users (exclusive smokers; 774 ng/L) than nonusers of tobacco products (625 ng/L). In stratified sample-weighted regression analysis, smoking 0.5 pack of cigarettes per day was associated with a statistically significant increase in blood nitromethane by 150 ng/L, and secondhand smoke exposure (serum cotinine >0.05 ng/mL and <10 ng/mL) was statistically significant with a 31.1 ng/L increase in blood nitromethane. Certain dietary sources were associated with small but statistically significant increases in blood nitromethane. At median consumption levels, blood nitromethane was associated with an increase of 7.55 ng/L (meat/poultry), 9.32 ng/L (grain products), and 14.5 ng/L (vegetables). This is the first assessment of the magnitude and relative source apportionment of nitromethane exposure in the U.S. population.

Ethylbenzene and styrene are air toxicants with widespread nonoccupational exposure sources, including tobacco smoke and diet. Ethylbenzene and styrene (EB/S) exposure was quantified from their common metabolites measured in spot urine samples obtained from participants (>/=6 years old) in the 2005-2006 and 2011-2012 cycles of the National Health and Nutrition Examination Survey (NHANES; N = 4690). EB/S metabolites mandelic acid (MA) and phenylglyoxylic acid (PGA) were measured using ultra-high performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry (UPLC-ESI-MS/MS). MA and PGA were detected in 98.9% and 90.6% of tested urine specimens, respectively. Exclusive smokers had 2-fold and 1.6-fold higher median urinary MA and PGA, respectively, compared with non-users. Sampleweighted regression analysis among exclusive smokers showed that smoking 0.5 pack cigarettes per day significantly increased MA (+97.9mug/L) and PGA (+69.3mug/L), controlling for potential confounders. In comparison, exposure from the median daily dietary intake of grain products increased MA by 1.95mug/L and was not associated with statistically significant changes in urinary PGA levels. Conversely, consuming vegetables and fruit was associated with decreased MA and PGA. These results confirm tobacco smoke as a major source of ethylbenzene and styrene exposure for the general U.S. population.

Sources of human aldehyde exposure include food additives, combustion of organic matter (tobacco smoke), water disinfection byproducts via ozonation, and endogenous processes. Aldehydes are potentially carcinogenic and mutagenic, and chronic human aldehyde exposure has raised concerns about potential deleterious health effects. To aid investigations of human aldehyde exposure, we developed a novel method to measure 19 aldehydes released from Schiff base protein adducts in serum using controlled acid hydrolysis, solid-phase microextraction (SPME), gas chromatography (GC), and high-resolution mass spectrometry (HRMS). Aldehydes are released from Schiff base protein adducts through acid hydrolysis, and are quantified in trace amounts (mug/L) using stable isotope dilution. Detection limits range from 0.1 to 50 mug/L, with calibration curves spanning 3 orders of magnitude. The analysis of fortified quality control material over a three-month period showed excellent precision and long-term stability (3-22% CV) for samples stored at -70 degrees C. The intraday precision is also excellent (CV, 1-10%). The method accuracy ranges from 89 to 108% for all measured aldehydes, except acrolein and crotonaldehyde, two aldehydes present in tobacco smoke; their analysis by this method is not considered robust due in part to their reactivity in vivo. However, results strongly suggest that propanal, butanal, isobutanal, and isopentanal levels in smokers are higher than levels in nonsmokers, and thus may be useful as biomarkers of tobacco smoke exposure. This method will facilitate large epidemiological studies involving aldehyde biomonitoring to examine nonoccupational environmental exposures.