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Title: Environmental tobacco smoke and canine urinary cotinine level

Abstract

Epidemiologic studies of companion animals such as dogs have been established as models for the relationship between exposure to environmental tobacco smoke (ETS) and cancer risk in humans. While results from these studies are provocative, pet owner report of a dog's ETS exposure has not yet been validated. We have evaluated the relationship between dog owner's report of household smoking by questionnaire and dog's urinary cotinine level. Between January and October 2005, dog owners presenting their pet for non-emergency veterinary care at the Foster Hospital for Small Animals at Cummings School of Veterinary Medicine, Tufts University, were asked to complete a 10-page questionnaire measuring exposure to household ETS in the previous 24 h and other factors. A free-catch urine sample was also collected from dogs. Urinary cotinine level was assayed for 63 dogs, including 30 whose owners reported household smoking and 33 unexposed dogs matched on age and month of enrollment. Urinary cotinine level was significantly higher in dogs exposed to household smoking in the 24 h before urine collection compared to unexposed dogs (14.6 ng/ml vs. 7.4 ng/ml; P=0.02). After adjustment for other factors, cotinine level increased linearly with number of cigarettes smoked by all household members (P=0.004). Othermore » canine characteristics including age, body composition and nose length were also associated with cotinine level. Findings from our study suggest that household smoking levels as assessed by questionnaire are significantly associated with canine cotinine levels.« less

Authors:
 [1];  [2]; ;  [1];  [1];  [3];  [4]
  1. Department of Public Health, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA (United States)
  2. (United States), E-mail: ebertone@schoolph.umass.edu
  3. (United States)
  4. Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA (United States)
Publication Date:
OSTI Identifier:
21077752
Resource Type:
Journal Article
Resource Relation:
Journal Name: Environmental Research; Journal Volume: 106; Journal Issue: 3; Conference: 8. international conference on the protection and restoration of the environment, Mykonos (Greece), 28 Jun - 1 Jul 2004; Other Information: DOI: 10.1016/j.envres.2007.09.007; PII: S0013-9351(07)00194-6; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ACCIDENTS; BODY COMPOSITION; DOGS; HAZARDS; HOSPITALS; HOUSEHOLDS; NEOPLASMS; POLLUTION; TOBACCO SMOKES; URINE; VALIDATION; VETERINARY MEDICINE

Citation Formats

Bertone-Johnson, Elizabeth R., Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA, Procter-Gray, Elizabeth, Gollenberg, Audra L., Ryan, Michele B., Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, and Barber, Lisa G. Environmental tobacco smoke and canine urinary cotinine level. United States: N. p., 2008. Web. doi:10.1016/j.envres.2007.09.007.
Bertone-Johnson, Elizabeth R., Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA, Procter-Gray, Elizabeth, Gollenberg, Audra L., Ryan, Michele B., Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, & Barber, Lisa G. Environmental tobacco smoke and canine urinary cotinine level. United States. doi:10.1016/j.envres.2007.09.007.
Bertone-Johnson, Elizabeth R., Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA, Procter-Gray, Elizabeth, Gollenberg, Audra L., Ryan, Michele B., Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, and Barber, Lisa G. 2008. "Environmental tobacco smoke and canine urinary cotinine level". United States. doi:10.1016/j.envres.2007.09.007.
@article{osti_21077752,
title = {Environmental tobacco smoke and canine urinary cotinine level},
author = {Bertone-Johnson, Elizabeth R. and Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, MA and Procter-Gray, Elizabeth and Gollenberg, Audra L. and Ryan, Michele B. and Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA and Barber, Lisa G.},
abstractNote = {Epidemiologic studies of companion animals such as dogs have been established as models for the relationship between exposure to environmental tobacco smoke (ETS) and cancer risk in humans. While results from these studies are provocative, pet owner report of a dog's ETS exposure has not yet been validated. We have evaluated the relationship between dog owner's report of household smoking by questionnaire and dog's urinary cotinine level. Between January and October 2005, dog owners presenting their pet for non-emergency veterinary care at the Foster Hospital for Small Animals at Cummings School of Veterinary Medicine, Tufts University, were asked to complete a 10-page questionnaire measuring exposure to household ETS in the previous 24 h and other factors. A free-catch urine sample was also collected from dogs. Urinary cotinine level was assayed for 63 dogs, including 30 whose owners reported household smoking and 33 unexposed dogs matched on age and month of enrollment. Urinary cotinine level was significantly higher in dogs exposed to household smoking in the 24 h before urine collection compared to unexposed dogs (14.6 ng/ml vs. 7.4 ng/ml; P=0.02). After adjustment for other factors, cotinine level increased linearly with number of cigarettes smoked by all household members (P=0.004). Other canine characteristics including age, body composition and nose length were also associated with cotinine level. Findings from our study suggest that household smoking levels as assessed by questionnaire are significantly associated with canine cotinine levels.},
doi = {10.1016/j.envres.2007.09.007},
journal = {Environmental Research},
number = 3,
volume = 106,
place = {United States},
year = 2008,
month = 3
}
  • We describe a polyclonal-antiserum-based {sup 125}I-radioimmunoassay for cotinine that is suitable for measuring nonsmokers' passive exposure to tobacco smoke in the environment. The standard curve ranged from 0.25 to 12.0 micrograms/L, with an estimated lower limit of sensitivity of 0.2 microgram/L (95% B/Bo = 0.2 microgram/L; 50% B/Bo = 4.0 micrograms/L). The median within-assay CVs for patients' samples with cotinine values from 0.4 to 1.3, 1.4 to 2.4, 2.5 to 4.6, and 4.7 to 15.6 micrograms/L were 13.9%, 7.2%, 5.1%, and 5.7%, respectively. Between-assay CVs for two quality-control sera with average values of 1.53 and 3.68 micrograms/L were 14.3% andmore » 7.8%, respectively. Analytical recoveries of cotinine from smokers' sera diluted in zero calibrant ranged from 91% to 116%. Cotinine values determined on 79 paired sera and urines from nonsmokers showed significant correlation with self-reported exposure to environmental tobacco smoke (r = 0.49, P less than 0.001 for sera; r = 0.57, P less than 0.001 for urine). The log of the values for serum and urine cotinine were also significantly correlated (r = 0.85, P less than 0.001). Evidently, polyclonal antiserum can be used to develop a cotinine assay for measuring exposure to environmental tobacco smoke that compares well with that described for monoclonal-based assays.« less
  • To document passive smoke exposure, the authors measured concentrations of serum cotinine, a major metabolite of nicotine, in 38 young children and compared the results with the smoking histories of home residents. Cotinine was detected in 26 children (68%), of which ten had no household exposure according to a questionnaire. The serum cotinine concentration was significantly elevated in blacks compared with whites after controlling for the number of smokers in the home. After stratifying by race, there was a significant direct correlation between the serum cotinine concentration and the number of smokers in the home, the amount smoked by themore » mother, and the amount smoked by others in the home. We conclude that the serum cotinine concentration is a useful indicator of the actual exposure of young children to tobacco smoke and that unexplained racial differences in cotinine levels exist.« less
  • To investigate the extent to which personal values and experiences among scientists might affect their assessment of risks from dioxin, radon, and environmental tobacco smoke (ETS), we conducted an experiment through a telephone survey of 1461 epidemiologists, toxicologists, physicians, and general scientists. Each participant was read a vignette designed to reflect the mainstream scientific thinking on one of the three substances. For half of the participants (group A) the substance was named. For the other half (group B), the substance was not named but was identified only as Substance X, Y, or Z. Knowing the name of the substance hadmore » little effect on the scientists` evaluation of dioxin, although those who knew the substance to be dioxin were more likely to rate the substance as a serious environmental health hazard (51% vs. 42%, p = 0.062). For radon, those who knew they were being asked about ETS rather than substance X were significantly more likely to consider the substance an environmental health hazard (88% vs. 66%, p < 0.001), to consider the substance a serious environmental health hazard (70% vs. 33%, p < 0.001), to believe that background exposure required public health intervention (85% vs. 41%, p < 0.001), and to believe that above-background exposure required public health intervention (90% vs. 74%, p < 0.001). These findings suggest that values and experiences may be influencing health risk assessments for these substances, and indicate the need for more study of this phenomenon. 20 refs., 6 tabs.« less
  • Studies of phase distributions and emission factors for polycyclic aromatic hydrocarbons (PAH) in environmental tobacco smoke (ETS) require collection and analysis of very small samples. To achieve the necessary selectivity and sensitivity, a method has been devised and tested for extraction and cleanup of gas- and particulate-phase ETS samples. Gas-phase species were trapped by polymeric sorbents, and particles were trapped on filters. The samples were extracted with hot cyclohexane, concentrated, and passed through silica solid-phase extraction columns for cleanup. After solvent change, the PAH were determined by high-performance liquid chromatography with two programmed fluorescence detectors. PAH concentrations in 15-mg aliquotsmore » of National Institute of Standards and Technology Standard Reference Material (SRM) 1649 (urban dust/organics) agreed well with published values. Relative precision at the 95% confidence level was 8% for SRM 1649 and 20% for replicate samples (5-mg) of ETS particles. Emission factors have been measured for a range of gas- and particulate-phase polycyclic aromatic hydrocarbons in ETS. The emission factors per cigarette were 13.0 {+-} 0.5 mg of particulate matter, 11.2 + 0.9 {mu}g for gas-phase napthalene, and 74 {+-} 10 ng for particulate benzo[a]pyrene. 21 refs., 5 figs., 7 tabs.« less
  • Inhalation exposure of environmental tobacco smoke (ETS) particles may increase health risks, but only to the extent that the particles deposit in the respiratory tract. We describe a technique to predict regional lung deposition of environmental tobacco smoke particles. Interpretation of particle size distribution measurements after cigarette combustion by a smoking machine in a test room yields an effective emissions profile. An aerosol dynamics model is used to predict indoor particle concentrations resulting from a specified combination of smoking frequency and building factors. By utilizing a lung deposition model, the rate of ETS mass accumulation in human lungs is thenmore » determined as a function of particle size and lung airway generation. Considering emissions of sidestream smoke only, residential exposures of nonsmokers to ETS are predicted to cause rates of total respiratory tract particle deposition in the range of 0.4-0.7 {mu}g/day per kg of body weight for light smoking in a well-ventilated residence and 8-13 {mu}g/day per kg for moderately heavy smoking in a poorly ventilated residence. Emissions of sidestream plus mainstream smoke lead to predicted deposition rates about a factor of 4 higher. This technique should be useful for evaluating health risks and control techniques associated with exposure to ETS particles. 36 refs., 6 figs., 3 tabs.« less