Spectrofluorometric method for measuring tobacco smoke particulate matter on cigarette filters and Cambridge pads

Paszkiewicz, Geraldine; Pauly, John L.

doi:10.1136/tc.2007.024109

Cited by 8 publications

(6 citation statements)

References 26 publications

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“…After the fifth day, the animals were exposed to five cigarettes/day from day 25 to day 49. We chose Marlboro cigarette for smoke exposure because total particulate matter (TPM, 56.7 ± 5.0 × 10 -3 /ml acridine orange units) of Marlboro cigarette is similar to TPM values of Kentucky Reference 2R4F (63.1 ± 4.6 × 10 -3 /ml acridine orange units) [30]. …”

Section: Methodsmentioning

confidence: 99%

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

et al. 2011

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BackgroundMany studies have found that smoking reduces lung function, but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated, particularly the role of mast cells. This study aimed to investigate the effects of smoke exposure on allergic asthma and its association with mast cells.MethodsBALB/c mice were sensitized and challenged by OVA to induce asthma, and bone marrow-derived mast cells (BMMCs) were stimulated with antigen/antibody reaction. Mice or BMMCs were exposed to cigarette smoke or CSE solution for 1 mo or 6 h, respectively. The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H&E staining, collagen deposition by Sircol assay, penh values by a whole-body plethysmography, co-localization of tryptase and Smad3 by immunohistochemistry, IgE and TGF-β level by ELISA, expressions of Smads proteins, activities of signaling molecules, or TGF-β mRNA by immunoblotting and RT-PCR.ResultsCigarette smoke enhanced OVA-specific IgE levels, penh values, recruitment of inflammatory cells including mast cells, expressions of smad family, TGF-β mRNA and proteins, and cytokines, phosphorylations of Smad2 and 3, and MAP kinases, co-localization of tryptase and Smad3, and collagen deposition more than those of BAL cells and lung tissues of OVA-induced allergic mice. CSE solution pretreatment enhanced expressions of TGF-β, Smad3, activities of MAP kinases, NF-κB/AP-1 or PAI-1 more than those of activated-BMMCs.ConclusionsThe data suggest that smoke exposure enhances antigen-induced mast cell activation via TGF-β/Smad signaling pathways in mouse allergic asthma, and that it exacerbates airway inflammation and remodeling.

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Section: Methodsmentioning

confidence: 99%

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

et al. 2011

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“…This dose was calculated by manually drawing puffs from the same type of cigarettes (using a syringe), with the same average puff volume and inter-puff intervals that had been measured in an ad lib smoking baseline session. The smoke particulate matter was trapped in Cambridge filters (Paszkiewicz and Pauly 2008), and after extraction with ethanol, a spectrophotometer was used to measure the absorbance of the solution at a wavelength of 400 nm, a measure of “tar” concentration (Hinds, First et al 1983). Using published values for the nicotine/tar ratio for each brand of cigarette (Federal Trade Commission 2000), the estimated nicotine delivery per puff was calculated.…”

Section: Methodsmentioning

confidence: 99%

Reinforcing effects of nicotine and non-nicotine components of cigarette smoke

et al. 2010

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We assessed the reinforcing effects of nicotine and non-nicotine components of cigarette smoke, by presenting a concurrent choice paradigm in which participants had access to intravenous (IV) nicotine infusions vs. saline (placebo) infusions and puffs from denicotinized (“denic”) cigarettes vs. air (sham puffs). We also measured the effects on self-administration of prior satiation with each component. Sixteen smokers participated in 7 sessions, consisting of: 1) a baseline smoking assessment, which was used to tailor the nicotine dose per infusion to that of puffs from subjects’ preferred brands of cigarettes; 2) two sessions in which participants were trained to discriminate IV nicotine vs. saline infusions and denic smoke vs. sham (air) puffs; and 3) four sessions assessing choice behavior after different satiation conditions. Results showed that subjects self-administered more puffs of denic smoke than any other alternative, including IV nicotine. IV nicotine, however, was preferred over IV saline and sham puffs. Preference for denic smoke vs. IV nicotine was highly correlated with subjective ratings of “comfort” associated with the two alternatives. Satiation with smoke diminished the number of denic puffs taken during choice periods, while prior administration of nicotine did not affect the number of puffs taken. Smoking withdrawal symptoms were alleviated both by nicotine administration and by denic smoke. These results show that in established smokers, non-nicotine aspects of cigarette smoking have potent reinforcing effects. While current smoking cessation pharmacotherapies primarily address the nicotine component of cigarette addiction, future cessation strategies should also be designed to target non-nicotine factors.

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“…Paszkiewicz and Pauly (86) have devised a scheme for measuring TPM on cigarette filters using a procedure in which the filters from smoked Marlboro, Marlboro Ultralight, and 2R4F Reference Standard Cigarettes were dissolved rapidly with 10 ml of anhydrous dimethlysulfoxide (DMSO), manual inversion, then three hours of shaking. Contaminants such as titanium dioxide were removed by centrifuging for 5 minutes.…”

Section: Resultsmentioning

confidence: 99%

Cigarette Filter–based Assays as Proxies for Toxicant Exposure and Smoking Behavior—A Literature Review

Pauly

O’Connor

Paszkiewicz

et al. 2009

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Cigarettes are being marketed with filters that differ in composition and design. The filters have different toxicant trapping efficiencies, and smoking stains reflect variations in smoking behavior. Presented herein are the results of a structured literature review that was done to identify cigarette filter-based assays that may serve as proxies for mouth-level exposure and assessing smoking methods. Methods: A search of the published scientific literature and internal tobacco company documents from 1954 to 2009 was carried out. Results: The literature search identified diverse schemes for assessing cigarette filters, including visual inspection and digital imaging of smoked-stained spent filters, and quantitative determinations for total particulate matter (TPM), nicotine, and solanesol. The results also showed that: (a) there are sufficient data to link filter-based chemical measures to stan-

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Spectrofluorometric method for measuring tobacco smoke particulate matter on cigarette filters and Cambridge pads

Cited by 8 publications

References 26 publications

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

Reinforcing effects of nicotine and non-nicotine components of cigarette smoke

Cigarette Filter–based Assays as Proxies for Toxicant Exposure and Smoking Behavior—A Literature Review

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