Dale A. Chatfield

Residual tobacco smoke pollution in used cars for sale: air, dust, and surfaces.

Regular tobacco use in the enclosed environment of a car raises concerns about longer-term contamination of a cars microenvironment with residual secondhand smoke pollutants. This study (a) developed and compared methods to measure residual contamination of cars with secondhand smoke, (b) examined whether cars of smokers and nonsmokers were contaminated by secondhand smoke, and (c) how smoking behavior and restrictions affected contamination levels. Surface wipe, dust, and air samples were collected in used cars sold by nonsmokers (n = 20) and smokers (n = 87) and analyzed for nicotine. Sellers were interviewed about smoking behavior and restrictions, and car interiors were inspected for signs of tobacco use. Cars of smokers who smoked in their vehicles showed significantly elevated levels of nicotine (p < .001) in dust, on surfaces, and in the air compared with nonsmoker cars with smoking ban. When smokers imposed car smoking bans, air nicotine levels were significantly lower (p < .01), but dust and surface contamination levels remained at similar levels. Smoking more cigarettes in the car and overall higher smoking rate of the seller were significantly associated with higher secondhand smoke contamination of the car (p < .001). Use of a cutpoint for nicotine levels from surface wipe samples correctly identified 82% of smoker cars without smoking bans, 75% of smoker cars with bans, and 100% of nonsmoker cars. Surface nicotine levels provide a relatively inexpensive and accurate method to identify cars and other indoor environments contaminated with residual secondhand smoke. Disclosure requirements and smoke-free certifications could help protect nonsmoking buyers of used cars.

Altered Bile Acid Metabolism in Childhood Functional Constipation: Inactivation of Secretory Bile Acids by Sulfation in a Subset of Patients

Objective: An elevated concentration in the colon of the primary bile acid chenodeoxycholic acid (CDCA) or the secondary bile acid deoxycholic acid (DCA) is known to induce water secretion, causing diarrhea. We hypothesized that of the many fecal bile acids, only CDCA and DCA function as endogenous laxatives; therefore, a decrease in their proportion may be a cause of childhood functional constipation. To test this possibility, fecal bile acid composition was determined in children with functional constipation and in nonconstipated control children. Patients and Methods: Fecal samples were obtained from 207 children, 103 with functional constipation and 104 with normal bowel habits. Bile acid classes were determined by use of electrospray ionization—single ion monitoring—mass spectrometry (ESI-SIM-MS), and individual bile acids were measured by gas chromatography (GC)-MS (GC-MS). The structure of individual sulfated bile acids was obtained by use of liquid chromatography (LC)-MS (LC-MS). Results: By ESI-SIM-MS, the proportions of DCA did not differ in constipated children (n = 73) from that in control children (n = 92), but monosulfated dihydroxy bile acids were greater (P < 0.05). The difference was attributable to 6 patients in the constipated group whose major fecal bile acid by LC-MS was the 3-sulfate of CDCA. Sulfation of CDCA is known to abolish its secretory activity. By GC-MS, the bile acid profile was identical in the 2 groups. Conclusions: In most children with functional constipation, the fecal bile acid profile seems to be normal. There is a small subset of children, however, whose dominant fecal bile acid is the 3-sulfate of CDCA, indicating a novel disturbance in bile acid metabolism. Such sulfation abolishes the secretory activity of CDCA and may contribute to constipation.

Thirdhand smoke and exposure in California hotels: non-smoking rooms fail to protect non-smoking hotel guests from tobacco smoke exposure

Introduction This study examined tobacco smoke pollution (also known as thirdhand smoke, THS) in hotels with and without complete smoking bans and investigated whether non-smoking guests staying overnight in these hotels were exposed to tobacco smoke pollutants. Methods A stratified random sample of hotels with (n=10) and without (n=30) complete smoking bans was examined. Surfaces and air were analysed for tobacco smoke pollutants (ie, nicotine and 3-ethynylpyridine, 3EP). Non-smoking confederates who stayed overnight in guestrooms provided urine and finger wipe samples to determine exposure to nicotine and the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone as measured by their metabolites cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), respectively. Findings Compared with hotels with complete smoking bans, surface nicotine and air 3EP were elevated in non-smoking and smoking rooms of hotels that allowed smoking. Air nicotine levels in smoking rooms were significantly higher than those in non-smoking rooms of hotels with and without complete smoking bans. Hallway surfaces outside of smoking rooms also showed higher levels of nicotine than those outside of non-smoking rooms. Non-smoking confederates staying in hotels without complete smoking bans showed higher levels of finger nicotine and urine cotinine than those staying in hotels with complete smoking bans. Confederates showed significant elevations in urinary NNAL after staying in the 10 most polluted rooms. Conclusions Partial smoking bans in hotels do not protect non-smoking guests from exposure to tobacco smoke and tobacco-specific carcinogens. Non-smokers are advised to stay in hotels with complete smoking bans. Existing policies exempting hotels from complete smoking bans are ineffective.

Wipe Sampling for Nicotine as a Marker of Thirdhand Tobacco Smoke Contamination on Surfaces in Homes, Cars, and Hotels

INTRODUCTION Secondhand smoke contains a mixture of pollutants that can persist in air, dust, and on surfaces for months or longer. This persistent residue is known as thirdhand smoke (THS). Here, we detail a simple method of wipe sampling for nicotine as a marker of accumulated THS on surfaces. METHODS We analyzed findings from 5 real-world studies to investigate the performance of wipe sampling for nicotine on surfaces in homes, cars, and hotels in relation to smoking behavior and smoking restrictions. RESULTS The intraclass correlation coefficient for side-by-side samples was 0.91 (95% CI: 0.87-0.94). Wipe sampling for nicotine reliably distinguished between private homes, private cars, rental cars, and hotels with and without smoking bans and was significantly positively correlated with other measures of tobacco smoke contamination such as air and dust nicotine. The sensitivity and specificity of possible threshold values (0.1, 1, and 10 μg/m(2)) were evaluated for distinguishing between nonsmoking and smoking environments. Sensitivity was highest at a threshold of 0.1 μg/m(2), with 74%-100% of smoker environments showing nicotine levels above threshold. Specificity was highest at a threshold of 10 μg/m(2), with 81%-100% of nonsmoker environments showing nicotine levels below threshold. The optimal threshold will depend on the desired balance of sensitivity and specificity and on the types of smoking and nonsmoking environments. CONCLUSIONS Surface wipe sampling for nicotine is a reliable, valid, and relatively simple collection method to quantify THS contamination on surfaces across a wide range of field settings and to distinguish between nonsmoking and smoking environments.

Children’s Exposure to Secondhand and Thirdhand Smoke Carcinogens and Toxicants in Homes of Hookah Smokers

INTRODUCTION We examined homes of hookah-only smokers and nonsmokers for levels of indoor air nicotine (a marker of secondhand smoke) and indoor surface nicotine (a marker of thirdhand smoke), child uptake of nicotine, the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and the toxicant acrolein by analyzing their corresponding metabolites cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and NNAL-glucuronides (total NNAL) and 3-hydroxypropylmercapturic acid. METHODS Data were collected at 3 home visits during a 7-day study period from a convenience sample of 24 households with a child 5 years or younger. Three child urine samples and 2 air and surface samples from the living room and the child bedroom were taken in homes of nonsmokers (n = 5) and hookah-only smokers (n = 19) comprised of daily hookah smokers (n = 8) and weekly/monthly hookah smokers (n = 11). RESULTS Nicotine levels in indoor air and on surfaces in the child bedrooms in homes of daily hookah smokers were significantly higher than in homes of nonsmokers. Uptake of nicotine, NNK, and acrolein in children living in daily hookah smoker homes was significantly higher than in children living in nonsmoker homes. Uptake of nicotine and NNK in children living in weekly/monthly hookah smoker homes was significantly higher than in children living in nonsmoker homes. CONCLUSIONS Our data provide the first evidence for uptake of nicotine, the tobacco-specific lung carcinogen NNK, and the ciliatoxic and cardiotoxic agent acrolein in children living in homes of hookah smokers. Our findings suggest that daily and occasional hookah use in homes present a serious, emerging threat to childrens long-term health.

Towards smoke-free rental cars: an evaluation of voluntary smoking restrictions in California

Introduction Some car rental companies in California and other states in the USA have established non-smoking policies for their vehicles. This study examined the effectiveness of these policies in maintaining smoke-free rental cars. Methods A stratified random sample of 250 cars (non-smoker, smoker and unknown designation) was examined in San Diego County, California, USA. Dust, surfaces and the air of each vehicle cabin were sampled and analysed for residual tobacco smoke pollutants (also known as thirdhand smoke (THS)), and each car was inspected for visual and olfactory signs of tobacco use. Customer service representatives were informally interviewed about smoking policies. Findings A majority of putative non-smoker cars had nicotine in dust, on surfaces, in air and other signs of tobacco use. Independent of a cars smoking status, older and higher mileage cars had higher levels of THS pollution in dust and on surfaces (p<0.05), indicating that pollutants accumulated over time. Compared with smoker cars, non-smoker cars had lower levels of nicotine on surfaces (p<0.01) and in dust (p<0.05) and lower levels of nicotine (p<0.05) and 3-ethynylpyridine (p<0.05) in the air. Non-smoking signage in cars was associated with lower levels of THS pollutants in dust and air (p<0.05). Conclusions Existing policies and practices were successful in lowering THS pollution levels in non-smoker cars compared with smoker cars. However, policies failed in providing smoke-free rental cars; THS levels were not as low as those found in private cars of non-smokers with in-car smoking bans. Major obstacles include inconsistent communication with customers and the lack of routine monitoring and enforcement strategies. Strengthening policies and their implementation would allow car rental companies to reduce costs, better serve their customers and make a constructive contribution to tobacco control efforts.

Providing Coaching and Cotinine Results to Preteens to Reduce Their Secondhand Smoke Exposure: A Randomized Trial

BACKGROUND Secondhand smoke exposure (SHSe) poses health risks to children living with smokers. Most interventions to protect children from SHSe have coached adult smokers. This trial determined whether coaching and cotinine feedback provided to preteens can reduce their SHSe. METHODS Two hundred one predominantly low-income families with a resident smoker and a child aged 8 to 13 years who was exposed to two or more cigarettes per day or had a urine cotinine concentration ≥ 2.0 ng/mL were randomized to control or SHSe reduction coaching groups. During eight in-home sessions over 5 months, coaches presented to the child graphic charts of cotinine assay results as performance feedback and provided differential praise and incentives for cotinine reductions. Generalized estimating equations were used to determine the differential change in SHSe over time by group. RESULTS For the baseline to posttest period, the coaching group had a greater decrease in both urine cotinine concentration (P = .039) and reported child SHSe in the number of cigarettes exposed per day (child report, P = .003; parent report, P = .078). For posttest to month 12 follow-up, no group or group by time differences were obtained, and both groups returned toward baseline. CONCLUSIONS Coaching preteens can reduce their SHSe, although reductions may not be sustained without ongoing counseling, feedback, and incentives. Unlike interventions that coach adults to reduce child SHSe, programs that increase child avoidance of SHSe have the potential to reduce SHSe in all settings in which the child is exposed, without requiring a change in adult smoking behavior.

Tobacco use and asking prices of used cars: prevalence, costs, and new opportunities for changing smoking behavior

Secondhand smoke (SHS) causes premature death and disease in children and adults, and the scientific evidence indicates that there is no risk-free level of exposure to SHS. Smoking tobacco in a car can pollute the microenvironment of the car with residual SHS, leaving telltale signs to potential buyers (e.g., odor, used ash tray). This study examined (a) the proportion of used cars sold in the private party market that may be polluted with tobacco smoke and (b) whether asking prices of smoker and nonsmoker cars differed for cars of otherwise equivalent value. A random sample of 1,642 private party sellers were interviewed by telephone, and content analyses of print advertisements were conducted. Findings indicate that 22% of used cars were advertised by smokers or had been smoked in during the previous year. Among nonsmokers, 94% did not allow smoking in their car during the past year. Only 33% of smokers had the same restrictions. The smoking status of the seller and tobacco use in the car were significantly (p < .01) associated with the asking price independent of a cars Kelley Blue Book value (KBB). Used nonsmoker cars were offered at a considerable premium above their KBB value (>11%) and above comparable smoker cars (7–9%). These findings suggest that community preferences are affecting the value of smoke-free cars. New directions for research, tobacco control policies, and health education are discussed to further reduce smoking behavior, to help consumers make informed purchasing decisions, and to protect nonsmokers from SHS exposure.

When smokers quit: exposure to nicotine and carcinogens persists from thirdhand smoke pollution

Background Over a 6-month period, we examined tobacco smoke pollutants (also known as thirdhand smoke, THS) that remained in the homes of former smokers and the exposure to these pollutants. Methods 90 smokers completed study measures at baseline (BL). Measures were repeated among verified quitters 1 week (W1), 1 month (M1), 3 months (M3) and 6 months (M6) following cessation. Measures were analysed for THS pollutants on household surfaces, fingers and in dust (ie, nicotine, tobacco-specific nitrosamines) and for urinary markers of exposure (ie, cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)). Results We observed significant short-term reduction of nicotine on surfaces (BL: 22.2 μg/m2, W1: 10.8 μg/m2) and on fingers of non-smoking residents (BL: 29.1 ng/wipe, W1: 9.1 ng/wipe) without further significant changes. Concentrations of nicotine and nicotine-derived nitrosamine ketone (NNK) in dust did not change and remained near BL levels after cessation. Dust nicotine and NNK loadings significantly increased immediately following cessation (nicotine BL: 5.0 μg/m2, W1: 9.3 μg/m2; NNK BL: 11.6 ng/m2, W1: 36.3 ng/m2) before returning to and remaining at near BL levels. Cotinine and NNAL showed significant initial declines (cotinine BL: 4.6 ng/mL, W1: 1.3 ng/mL; NNAL BL: 10.0 pg/mL, W1: 4.2 pg/mL) without further significant changes. Conclusions Homes of smokers remained polluted with THS for up to 6 months after cessation. Residents continued to be exposed to THS toxicants that accumulated in settled house dust and on surfaces before smoking cessation. Further research is needed to better understand the consequences of continued THS exposure after cessation and the efforts necessary to remove THS.

Identification of Sphingolipid Metabolites That Induce Obesity via Misregulation of Appetite, Caloric Intake and Fat Storage in Drosophila

Obesity is defined by excessive lipid accumulation. However, the active mechanistic roles that lipids play in its progression are not understood. Accumulation of ceramide, the metabolic hub of sphingolipid metabolism, has been associated with metabolic syndrome and obesity in humans and model systems. Here, we use Drosophila genetic manipulations to cause accumulation or depletion of ceramide and sphingosine-1-phosphate (S1P) intermediates. Sphingolipidomic profiles were characterized across mutants for various sphingolipid metabolic genes using liquid chromatography electrospray ionization tandem mass spectroscopy. Biochemical assays and microscopy were used to assess classic hallmarks of obesity including elevated fat stores, increased body weight, resistance to starvation induced death, increased adiposity, and fat cell hypertrophy. Multiple behavioral assays were used to assess appetite, caloric intake, meal size and meal frequency. Additionally, we utilized DNA microarrays to profile differential gene expression between these flies, which mapped to changes in lipid metabolic pathways. Our results show that accumulation of ceramides is sufficient to induce obesity phenotypes by two distinct mechanisms: 1) Dihydroceramide (C14:0) and ceramide diene (C14:2) accumulation lowered fat store mobilization by reducing adipokinetic hormone- producing cell functionality and 2) Modulating the S1P: ceramide (C14:1) ratio suppressed postprandial satiety via the hindgut-specific neuropeptide like receptor dNepYr, resulting in caloric intake-dependent obesity.