Search PubMed⌕ Search

Biomedical subjects

C Eliopoulos

Publications and source records attributed to C Eliopoulos.

At least 19 recordsLinked to original sources
PubMed1999

Homeopathy.

Explore the source record for details and available documents.

Holistic Nursing↗
PubMed1999

Magnet therapy.

Explore the source record for details and available documents.

Complementary Therapies↗
PubMed1999

Aromatherapy.

Explore the source record for details and available documents.

Aromatherapy↗
PubMed1998

Pharmacokinetic predisposition to nicotine from environmental tobacco smoke: a risk factor for pediatric asthma.

During the last decade several studies have shown that children whose parents smoke have higher rates of asthma. Recently, hair concentrations of cotinine have been shown to reflect systemic exposure to this constituent of smoke in both children and adults. At the present time it is not known, however, why some children exposed to passive smoking have asthma while others, similarly exposed, do not. The present study aimed at verifying whether asthmatic children are different from nonasthmatic children exposed to similar degrees of passive smoking in the way their bodies handle nicotine, a constituent of cigarette smoke. Seventy-eight asthmatic children were compared to 86 control children, all attending a consulting pediatric clinic in Toronto. A questionnaire completed by the parents and children detailed the daily number of cigarettes the child was exposed to and the identity of the smokers. Clinical data were extracted from the patients' charts. Urinary (corrected for creatinine) and hair concentrations of cotinine were measured by radioimmunoassays. The asthmatic and control children were of similar age, gender, and ethnic distribution, parental education, and socioeconomic status. Parents of asthmatic children tended to report a lower daily number of cigarettes (7.4 +/- 1.3/day vs. 11.2 +/- 2.3/day, p = 0.14), and this report agreed with the trend of urinary cotinine (47.1 +/- 9.1 ng/mg vs. 62.6 +/- 11.5 ng/mg, respectively). Conversely, children with asthma had on average twofold higher concentrations of cotinine in their hair (0.696 +/- 0.742 ng/mg) than control children (0.386 +/- 0.383) (p = 0.0001). In a similar manner, the hair:urine concentration ratio was significantly higher in children with asthma (0.028 +/- 0.002) than in their controls (0.18 +/- 0.003) (p = 0.0001). These results suggest that under exposure to similar amounts of nicotine, children with asthma have on average twofold higher systemic exposure to this constituent of cigarette smoke. These data suggest that out of all children passively exposed to environmental tobacco smoke, those who exhibit asthma have a higher systemic exposure to nicotine, possibly due to lower clearance rate. This is the first evidence of pharmacokinetic predisposition to environmental tobacco smoke as an etiological factor in pediatric asthma.

Adult↗
PubMed1996

Validation of self-reported smoking by analysis of hair for nicotine and cotinine.

Evidence suggesting the use of self-reports as an index of systemic exposure to cigarette smoke in selected study populations is highly inaccurate. In order to assess the use of hair analysis as a biochemical marker of cigarette smoking, we compared measurements of nicotine and cotinine in the hair and plasma of 36 volunteers whose reports of smoking were deemed to be reliable. A significant correlation was observed between the number of cigarettes smoked and hair measurements of nicotine (r = 0.48, p = 0.004) and cotinine (r = 0.57, p = 0.0008). In addition, a good correlation was found between the reported number of cigarettes smoked and plasma nicotine, plasma cotinine, and carboxyhemoglobin levels. These results suggest that hair analysis is a reliable noninvasive method of determining human exposure to cigarette smoke and is comparable to blood analysis.

Adult↗
PubMed1996

Passive smoking in children. Racial differences in systemic exposure to cotinine by hair and urine analysis.

Passive smoking has been shown to adversely affect the health of infants and children. Black children and adults appear to be more susceptible to a variety of tobacco smoke health hazards for unknown reason. The objectives of this study were as follows: (1) to correlate the number of cigarettes reported to have been smoked by parents with urine and hair concentrations of cotinine in children; and (2) to identify race differences in systemic exposure to cotinine in children. This was an observational study in a consulting pediatric office on 169 nonsmoking children between 2 and 18 years of age, not actively smoking. The outcome measures of interest were urinary cotinine concentrations corrected for milligram of creatinine and hair concentration of cotinine (per milligram of hair). There were significant correlations between the number of cigarettes the child was exposed to and urinary cotinine (r = 0.68, p = 0.0001) or hair cotinine concentrations (r = 0.19, p = 0.02), and between urinary and hair cotinine (r = 0.3, p = 0.0005). In this cohort, parents of black children (n = 21) tended to smoke less (6.6 +/- 3/d, mean +/- SEM) than white parents (n = 97) (12 +/- 1.8, mean +/- SEM) (p = 0.2). Despite being exposed to less cigarettes, black children had higher hair concentrations of cotinine than white children (0.89 +/- 0.25 ng/mg vs 0.48 +/- 0.05 ng/mg; p = 0.05). The ratio hair/urine concentrations of cotinine was twofold higher in black children (0.035 +/- 0.01 vs 0.019 +/- 0.002; p = 0.004). White children with dark hair did not differ significantly from white children with fair hair in any of these indexes. The amount of urinary cotinine per milligram of creatinine caused by 1 cigarette per day was twofold higher in black children (14.7 +/- 5.2 ng/mg of creatinine) than in white children (6.3 +/- 1.2 ng/mg of creatinine) (p = 0.02). These data suggest that black children handle cigarette smoke differently from white children and that black children have higher systemic exposure to this constituent of cigarette smoke.

Adolescent↗