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Acrolein and 1,3-butadiene in cigarette smoke generally are measured using two separate analytical methods, a carbonyl derivative HPLC method for acrolein and a volatile organic compound (VOC) GC/MS method for 1,3-butadiene.
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It is shown that the selectivity for acrolein increases strongly with time on stream for the bismuth molybdate catalyst.
1,3-Butadiene is one of the precursors for acrolein.
Both acrolein and nicotine should be considered toxic substances to cell cultures, and particularly so for acrolein.
Using an antibody against the cleaved fragment of caspase 3 (17–19 kDa), we demonstrated by Western blotting that treatment with both acrolein and nicotine for 1 h increased levels of active caspase 3, which was most pronounced for acrolein.
The distribution of 1999 annual ambient acrolein concentrations is presented in Table 2. Annual ambient acrolein concentrations exceeded the current RfC for acrolein in > 75%, 90%, and 50% of all U.S. census tracts, census tracts within urban counties, and census tracts within rural counties, respectively.
Since OYEs are involved in detoxification of acrolein, a high-throughput method for selecting yeasts expressing high enoate reductase activity, based on their acrolein resistance, was developed.
Although the RfC for acrolein is based on respiratory system impairment, conventional risk assessment methods applied to animal data do not provide estimates of potential incidence or severity of adverse effects.
There are some data suggesting that glycerol, a material sometimes added to tobacco as a humectant, is an additional precursor for acrolein [18].
The annual normalized mean error (NME) was in the range of 36 70% normalized mean error for all HAPs except for acrolein (>70%).
Except for acrolein and formaldehyde, all CC showed a clear trend of reduction in the emissions from B2 to B100 (40% reduction, on average).
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