The skin of 20 human participants was exposed to ∼110 ppb O 3 and volatile products of the resulting chemistry were quantified in real time. Yields (ppb product emitted/ppb ozone consumed) for 40 products were quantified. Major products of the primary reaction of ozone-squalene included 6-methyl 5-hepten-2one (6-MHO) and geranyl acetone (GA) with average yields of 0.22 and 0.16, respectively. Other major products included decanal, methacrolein (or methyl vinyl ketone), nonanal, and butanal. Yields varied widely among participants; summed yields ranged from 0.33 to 0.93. The dynamic increase in emission rates during ozone exposure also varied among participants, possibly indicative of differences in the thickness of the skin lipid layer. Factor analysis indicates that much of the variability among participants is due to factors associated with the relative abundance of (1) "fresh" skin lipid constituents (such as squalene and fatty acids), (2) oxidized skin lipids, and (3) exogenous compounds. This last factor appears to be associated with the presence of oleic and linoleic acids and could be accounted for by uptake of cooking oils or personal care products to skin lipids.

This study aims to elucidate in greater detail the dermal uptake of nicotine from air or from nicotine-exposed clothes, which was demonstrated recently in a preliminary study. Six non-smoking participants were exposed to gaseous nicotine (between 236 and 304 μg/m ) over 5 hours while breathing clean air through a hood. Four of the participants wore only shorts and 2 wore a set of clean clothes. One week later, 2 of the bare-skinned participants were again exposed in the chamber, but they showered immediately after exposure instead of the following morning. The 2 participants who wore clean clothes on week 1 were now exposed wearing a set of clothes that had been exposed to nicotine. All urine was collected for 84 hours after exposure and analyzed for nicotine and its metabolites, cotinine and 3OH-cotinine. All participants except those wearing fresh clothes excreted substantial amounts of biomarkers, comparable to levels expected from inhalation intake. Uptake for 1 participant wearing exposed clothes exceeded estimated intake via inhalation by >50%. Biomarker excretion continued during the entire urine collection period, indicating that nicotine accumulates in the skin and is released over several days. Absorbed nicotine was significantly lower after showering in 1 subject but not the other. Differences in the normalized uptakes and in the excretion patterns were observed among the participants. The observed cotinine half-lives suggest that non-smokers exposed to airborne nicotine may receive a substantial fraction through the dermal pathway. Washing skin and clothes exposed to nicotine may meaningfully decrease exposure.

Detailed offline speciation of gas- and particle-phase organic compounds was conducted using gas/liquid chromatography with traditional and high-resolution mass spectrometers in a hybrid targeted/nontargeted analysis. Observations were focused on an unoccupied home and were compared to two other indoor sites. Observed gas-phase organic compounds span the volatile to semivolatile range, while functionalized organic aerosols extend from intermediate volatility to ultra-low volatility, including a mix of oxygen, nitrogen, and sulfur-containing species. Total gas-phase abundances of hydrocarbon and oxygenated gas-phase complex mixtures were elevated indoors and strongly correlated in the unoccupied home. While gas-phase concentrations of individual compounds generally decreased slightly with greater ventilation, their elevated ratios relative to controlled emissions of tracer species suggest that the dilution of gas-phase concentrations increases off-gassing from surfaces and other indoor reservoirs, with volatility-dependent responses to dynamically changing environmental factors. Indoor–outdoor emissions of gas-phase intermediate-volatility/semivolatile organic hydrocarbons from the unoccupied home averaged 6–11 mg h–1, doubling with ventilation. While the largest single-compound emissions observed were furfural (61–275 mg h–1) and acetic acid, observations spanned a wide range of individual volatile chemical products (e.g., terpenoids, glycol ethers, phthalates, other oxygenates), highlighting the abundance of long-lived reservoirs resulting from prior indoor use or materials, and their gradual transport outdoors.

Many studies have reported consistent associations between exposure to particulate matter (PM) and cardiovascular and respiratory diseases, neurodegenerative disorders, cancer, premature mortality, and morbidity. [1][2][3][4][5][6][7][8][9][10] Since even low levels of ambient PM can cause detrimental health effects, investigators have attempted to identify the primary cause of PM toxicity. Chemical composition and biologically active chemical species of PM are considered to be more important contributors to the health effects than particle mass concentration by itself. [11][12][13] Levels of reactive oxygen species (ROS) may be a major factor in the health effects associated with PM exposure. [14][15][16][17][18][19][20][21] Reactive oxygen species (ROS) are relatively unstable oxygen-containing radicals and non-radicals. Biologically relevant ROS include superoxide (O 2 •−), hydroxyl (HO • ), hydroperoxyl (HOO • ), and alkylperoxyl (ROO • ) radicals as well as non-radicals such as hydrogen peroxide (H 2 O 2 ), organic peroxides (ROOR), hypochlorite (OCl − ), and peroxynitrite (ONOO − ). 22,23 Reactive oxygen species can be generated in human cells (endogenously) through aerobic metabolism and other biochemical reactions. [24][25][26][27][28][29][30][31][32][33] In addition to endogenous formation of ROS, there are several exogenous sources such as air pollution, food, drugs, heavy metals, organic solvents, and pesticides which have the potential to

Reactive oxygen species (ROS) are among the species thought to be responsible for the adverse health effects of particulate matter (PM) inhalation. Field studies suggest that indoor sources of ROS...