Chemistry of the Conversion of Nitrate Nitrogen to Smoke Products

Johnson, William R.; Hale, R. W.; Clough, Stuart C.; Chen, P. H.

doi:10.1038/243223a0

Cited by 45 publications

(16 citation statements)

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“…When a-amino nitrogen, total polyphenols, and leaf positions are used, estimated catechol (!lg/cigarette) = This observation supports the concept that nitrate in tobacco is a main precursor for ammonia in the smoke (8) and, thus, for smoke pH (2,8 …”

Section: 'Dsupporting

confidence: 76%

Simple Correlation and Multiple Regression among Leaf and Smoke Characteristics of Burley Tobaccos

Tso¹,

Chaplin²,

Adams³

et al. 1982

Beiträge Zur Tabakforschung / Contributions to Tobacco Research

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Leaves from 8 stalk positions from four Burley tobaccos, the cultivars Burley 21, Ky 14 and Ky 12 and one breeding line of low-alkaloid Burley 21 (LA Burley 21), were tested in this study. A total of 116 variables, including leaf and smoke characteristics, were determined by collaborating scientists using established methods. Simple correlations and multiple regressions among selected variables were determined to examine the relationship among these variables. Generally, Burley tobaccos do not differ from bright tobaccos, in that the nitrogenous fractions and combustibility appear to be the major factors affecting nicotine and dry TPM (total particulate matter) delivery as well as other major smoke constituents. Stalk position and varieties also demonstrated significant differences in nicotine and dry TPM delivery. Benzo[a]pyrene content, however, did not show significant differences among these experimental Burley tobaccos or stalk positions.

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Section: 'Dsupporting

confidence: 76%

Simple Correlation and Multiple Regression among Leaf and Smoke Characteristics of Burley Tobaccos

Tso¹,

Chaplin²,

Adams³

et al. 1982

Beiträge Zur Tabakforschung / Contributions to Tobacco Research

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show abstract

“…Of these, around 400 have been quantified, at least 200 are toxic to humans and/or experimental animals, and over 50 have been identified as known, probable, or possible human carcinogens (Kirsti, 2004). Studies indicate that compared with mainstream smoke collected under standard FTC/ISO smoking parameters, sidestream smoke has higher levels of PAHs (Grimmer et al, 1987; Evans et al, 1993), nitrosamines (Brunnemann et al, 1977, 1980; Hoffmann et al, 1979a; Ruhl et al, 1980), aza-arenes (Dong et al, 1978; Grimmer et al, 1987), aromatic amines (Patrianakos and Hoffmann, 1979), carbon monoxide (Hoffmann et al, 1979b; Rickert et al, 1984), nicotine (Rickert et al, 1984; Pakhale and Maru, 1998), ammonia (Brunnemann and Hoffmann, 1975), pyridine (Johnson et al, 1973; Brunnemann and Hoffmann, 1978), and the gas phase components 1,3-butadiene, acrolein, isoprene, benzene, and toluene (Brunnemann et al, 1990). In addition to these deleterious compounds, other factors such as the type of tobacco, the chemicals added to the tobacco, the way the tobacco product is smoked, and, for cigarettes and cigars, the material in which the tobacco is wrapped can also affect second-hand smoke chemical composition (International Agency for Research on Cancer, 2002; National Toxicology Program, 2005; US Department of Health and Human Services, 2006).…”

Section: Constituents Of Tobacco Smokementioning

confidence: 99%

RAGE and tobacco smoke: insights into modeling chronic obstructive pulmonary disease

et al. 2012

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Chronic obstructive pulmonary disease (COPD) is a progressive condition characterized by chronic airway inflammation and airspace remodeling, leading to airflow limitation that is not completely reversible. Smoking is the leading risk factor for compromised lung function stemming from COPD pathogenesis. First- and second-hand cigarette smoke contain thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic lung inflammation and destructive alveolar remodeling. Receptors for advanced glycation end-products (RAGE) are multi-ligand cell surface receptors primarily expressed by diverse lung cells. RAGE expression increases following cigarette smoke exposure and expression is elevated in the lungs of patients with COPD. RAGE is responsible in part for inducing pro-inflammatory signaling pathways that culminate in expression and secretion of several cytokines, chemokines, enzymes, and other mediators. In the current review, new transgenic mouse models that conditionally over-express RAGE in pulmonary epithelium are discussed. When RAGE is over-expressed throughout embryogenesis, apoptosis in the peripheral lung causes severe lung hypoplasia. Interestingly, apoptosis in RAGE transgenic mice occurs via conserved apoptotic pathways also known to function in advanced stages of COPD. RAGE over-expression in the adult lung models features of COPD including pronounced inflammation and loss of parenchymal tissue. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of COPD.

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“…Ammonia present in cigarette smoke is formed though the reduction of nitrates and pyrolysis of glycine [19] . It is to a large extent released to the sidestream smoke.…”

Section: Chemical Constituents In Cigarette Smokementioning

confidence: 99%

Smoke Chemistry

Zemann¹

2011

Cigarette Smoke Toxicity

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Chemistry of the Conversion of Nitrate Nitrogen to Smoke Products

Cited by 45 publications

References 0 publications

Simple Correlation and Multiple Regression among Leaf and Smoke Characteristics of Burley Tobaccos

Simple Correlation and Multiple Regression among Leaf and Smoke Characteristics of Burley Tobaccos

RAGE and tobacco smoke: insights into modeling chronic obstructive pulmonary disease

Smoke Chemistry

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