Andrew Bryant

Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement

Abstract Objective To examine the associations between a biomarker of overall passive exposure to tobacco smoke (serum cotinine concentration) and risk of coronary heart disease and stroke. Design Prospective population based study in general practice (the British regional heart study). Participants 4729 men in 18 towns who provided baseline blood samples (for cotinine assay) and a detailed smoking history in 1978-80. Main outcome measure Major coronary heart disease and stroke events (fatal and non-fatal) during 20 years of follow up. Results 2105 men who said they did not smoke and who had cotinine concentrations < 14.1 ng/ml were divided into four equal sized groups on the basis of cotinine concentrations. Relative hazards (95% confidence intervals) for coronary heart disease in the second (0.8-1.4 ng/ml), third (1.5-2.7 ng/ml), and fourth (2.8-14.0 ng/ml) quarters of cotinine concentration compared with the first (≥ 0.7 ng/ml) were 1.45 (1.01 to 2.08), 1.49 (1.03 to 2.14), and 1.57 (1.08 to 2.28), respectively, after adjustment for established risk factors for coronary heart disease. Hazard ratios (for cotinine 0.8-14.0 ν ≥ 0.7 ng/ml) were particularly increased during the first (3.73, 1.32 to 10.58) and second five year follow up periods (1.95, 1.09 to 3.48) compared with later periods. There was no consistent association between cotinine concentration and risk of stroke. Conclusion Studies based on reports of smoking in a partner alone seem to underestimate the risks of exposure to passive smoking. Further prospective studies relating biomarkers of passive smoking to risk of coronary heart disease are needed.

Cigarette withdrawal symptoms in adolescent smokers

One hundred and sixteen female adolescent smokers were asked about withdrawal symptoms experienced during past attempts to give up smoking for good. Sixty-three percent reported difficulties during abstinence of the kind experienced by adult smokers. Daily smokers were more likely to report withdrawal effects than non-daily smokers (74% versus 47%, P<0.005). Reported experience of withdrawal symptoms was positively related to self-reports of cigarette consumption and depth of inhalation and nicotine intake as indexed by salivary cotinine concentrations. Reported occurrence of at least one withdrawal effect correlated positively with nicotine intake after controlling for behavioural variables. Our results indicate that teenage smokers are likely to suffer withdrawal symptoms when they try to give up. Behavioural factors and expectations based on observations of adults may have played a part in their experience of withdrawal, but it is also likely that pharmacological factors are implicated even at this early stage.

Measuring nicotine intake in population surveys: comparability of saliva cotinine and plasma cotinine estimates.

Both plasma and saliva cotinine levels have been reported in surveys of smoking behavior, and it is of interest to know how closely these two measures correspond. Plasma and saliva specimens were gathered from a sample of 605 respondents in the 1998 Health Survey for England and assayed for cotinine by a well-proven gas chromatographic method. Plasma and saliva cotinine concentrations were highly correlated (r=.99). On average, concentrations in saliva were 25% higher than in plasma, and this ratio applied both at the low levels attributable to passive smoking and across the range of active smoking values. The ratio was somewhat lower in younger people than in older people and also varied significantly by body mass index but did not differ by gender. Calculation of the limits of agreement revealed substantial uncertainty in the predicted plasma value corresponding to a given saliva cotinine, and vice versa. For comparisons across subjects, the mean plasma cotinine level corresponding to a mean saliva cotinine level can be estimated with confidence, but at the level of the individual, considerable predictive uncertainty remains.

NICOTINE INTAKE IN YOUNG SMOKERS - LONGITUDINAL-STUDY OF SALIVA COTININE CONCENTRATIONS

Smoking habits and smoke intake were studied over three consecutive years in 197 girls, initially aged 11 to 14 years. Saliva cotinine concentrations in girls who were smokers throughout the three years increased over each year of the study, the greatest increase occurring during movement from occasional to daily smoking. Cigarette consumption also increased over the two years. For a group of continuing daily smokers (n = 23), inhalation of smoke per cigarette as indexed by the ratio of cotinine concentration to average daily cigarette consumption did not change over time. Cotinine concentrations in 16 girls who were smoking on a daily basis within a year of starting to smoke suggested the early development of inhalation. Our findings suggest that young smokers learn to inhale cigarette smoke very early in their smoking careers, that further increases in smoke intake mainly reflect increased cigarette consumption, and that the pharmacological effects of nicotine are already important in reinforcing their smoking.

Determination of cotinine in biological fluids of non-smokers by packed column gas-liquid chromatography

A method is described for the analysis of cotinine in plasma, saliva and urine using packed‐column gas‐liquid chromatography, which is sufficiently sensitive and reproducible for quantitative study of the low levels resulting from exposure of non‐smokers to other peoples smoke. The lower limit of detection of cotinine in these fluids was 100 pg ml−1. The coefficient of variation over the range 0.25 to 2.0 ng ml−1 averaged 7.7%. In a sample of 85 non‐smokers the concentrations of cotinine in plasma correlated 0.82 with those in urine and saliva, while the correlation between the saliva and urine concentrations was 0.91. Saliva cotinine concentrations were quantitatively related to passive exposure to parental smoking in a population study of 569 non‐smoking schoolchildren.