Fetal exposure to tobacco smoke products: A comparison between self‐reported maternal smoking and concentrations of cotinine and thiocyanate in cord serum

Nafstad, Per; Kongerud, Johny; Botten, Grete; Urdal, Petter; Silsand, Terje; Pedersen, Babill Stray; Jaakkola, Jouni J. K.

doi:10.3109/00016349609055025

Cited by 67 publications

(61 citation statements)

References 20 publications

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“…We evaluated the validity of questionnaire information by using the levels of cotinine and thiocyanate in umbilical cord serum in 202 randomly selected mothers. There was an excellent agreement between high and low levels of biomarkers and daily and nonsmoking mothers (25).…”

Section: Methodsmentioning

confidence: 75%

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Environmental tobacco smoke, parental atopy, and childhood asthma.

Jaakkola

Nafstad

Magnus

2001

Environ Health Perspect

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We hypothesized that the joint effect of genetic propensity to asthma and exposure to environmental tobacco smoke on the risk of childhood asthma is greater than expected on the basis of their independent effects. We performed a population-based 4-year cohort study of 2,531 children born in Oslo, Norway. We collected information on the child's health and environmental exposures at birth and when the child was 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma at the age of 4 years. Parental atopy was defined as a history of maternal or paternal asthma or hay fever. Exposure to environmental tobacco smoke was defined on the basis of questionnaire information on household smokers at birth. In logistic regression analysis adjusting for confounding, parental atopy alone increased the risk of bronchial obstruction [odds ratio 1.62; 95% confidence interval (CI) 1.10-2.40] and asthma (1.66; 95% CI, 1.08-2.54). In children without parental atopy, there was little effect of exposure to environmental tobacco smoke on bronchial obstruction (1.29; 95% CI, 0.88-1.89) and asthma (0.84; 95% CI, 0.53-1.34). The presence of parental atopy and exposure had a substantial effect both on bronchial obstruction (2.88; 95% CI, 1.91-4.32) and asthma (2.68; 95% CI, 1.70-4.22). The results are consistent with the hypothesized joint effect of parental atopy and exposure to environmental tobacco smoke. This phenomenon--denoted as effect modification of environmental exposure by genetic constitution, or gene by environment interaction--suggests that some genetic markers could indicate susceptibility to environmental factors.

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Section: Methodsmentioning

confidence: 75%

“…The exposure information was collected before the onset of the outcome of interest, so any bias due to awareness of the disease of interest was avoided. We evaluated the questionnaire information on maternal smoking by biomarker concentrations in cord serum and found that smoking habits were reported accurately (25).…”

Section: Discussionmentioning

confidence: 99%

Environmental tobacco smoke, parental atopy, and childhood asthma.

Jaakkola

Nafstad

Magnus

2001

Environ Health Perspect

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“…Questionnaire information on maternal smoking at the end of pregnancy was compared with biomarkers in umbilical cord serum taken at birth for 202 randomly selected mothers [35]. An excellent agreement was shown, which indicated that the mothers reported their smoking habits correctly.…”

Section: Discussionmentioning

confidence: 99%

Breastfeeding, maternal smoking and lower respiratory tract infections

Nafstad¹,

Jaakkola²,

Hagen³

et al. 1996

Eur Respir J

152

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B Br re ea as st tf fe ee ed di in ng g, , m ma at te er rn na al l s sm mo ok ki in ng g a an nd d P. Nafstad*, J.J.K. Jaakkola* + , J.A. Hagen*, G. Botten*, J. Kongerud** Breastfeeding, maternal smoking and lower respiratory tract infections. P. Nafstad, J.J.K. Jaakkola, J.A. Hagen, G. Botten, J. Kongerud. ERS Journals Ltd 1996. ABSTRACT: The objective of the study was to assess the relationship between breastfeeding and lower respiratory tract infections (LRTIs) during the first year of life, with special reference to maternal smoking.A cohort of 3,754 children born in 1992-1993 in the City of Oslo, Norway was recruited and data were collected at birth, 6 and 12 months of age. Complete information was obtained from 3,238 children (follow-up rate 86%). The main outcome was an episode of a LRTI, such as pneumonia, bronchitis or bronchiolitis, based on a self-administered questionnaire addressed to parents when the child was 6 and 12 months old. The outcome was specified as physician-diagnosed.In logistic regression analysis adjusting for confounding, maternal smoking increased the risk of LRTIs in children breastfed for 0-6 months (odds ratio (AOR) 1.7; 95% confidence interval (95% CI) 1.2-2.4), but not essentially when the child was breastfed for more than 6 months (AOR 1.1; 95% CI 0.7-1.6). Short-term breastfeeding (0-6 months) and no maternal smoking was related to an adjusted AOR of LRTIs of 1.3 (95% CI 1.0-1.7), and short-term breastfeeding combined with maternal smoking was related to an adjusted AOR of 2.2 (95% CI 1.6-3.1), as compared with long-term breastfeeding and no maternal smoking.The present study indicates a protective effect of long-term breastfeeding on the risk of lower respiratory tract infection during the first year of life. The results suggest that the protective effect is strongest in children exposed to environmental tobacco smoke.

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“…Among children, salivary and urinary cotinine levels have been shown to rise with the number of smoking parents in the home [31,38], and in infants, urinary cotinine levels increased with the number of cigarettes smoked by the mother during the previous 24 h [67]. Among 202 newborns, the cord serum level of cotinine was significantly linearly related to the average daily number of cigarettes smoked by the mother during pregnancy [68]. The cotinine levels measured in nonsmokers exposed to ETS have ranged from less than 1% to about 8% of the levels measured in active smokers [5,69].…”

Section: Biomarkersmentioning

confidence: 99%

Assessment of exposure to environmental tobacco smoke

Jaakkola¹,

Jaakkola²

1997

Eur Respir J

237

221

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Since the early 1980s, there has been growing concern about potential adverse health effects related to exposure to environmental tobacco smoke (ETS). Evidence has accumulated on ill-health associated with ETS, and such exposure has now been documented among children and adults in many countries [1][2][3][4][5][6][7][8]. A major difficulty in studying the ill-health effects of ETS has been assessing exposure, since this may occur in multiple settings with highly variable concentrations and exposure profiles may vary considerably during different age periods. Accurate and precise exposure assessment is crucial, since health effects of ETS are likely to be relatively small in magnitude. Appropriate exposure assessment is also needed for inferring causality and for risk assessment. In addition, exposure assessment is obviously necessary for development of preventive strategies.The purpose of this paper is to present a theoretical framework for assessment of exposure to ETS, and to review current methods of exposure assessment in order to provide guidelines for choice of appropriate methods for different types of study. General definitions and concepts of exposure and its assessment will be presented, followed by definitions and components of ETS. The principles for assessment of ETS exposure will then be presented. Current methods of assessment will be reviewed in terms of their advantages and disadvantages, followed by a very brief summary of the ill-health effects of ETS. This allows the criteria for selection of the appropriate method of assessing ETS exposure to be set in context, and to be formulated as user guidelines. Definitions of concentration, exposure and dose ConcentrationConcentration is the amount of a contaminant at a particular location in a particular medium [9]. For example, for an air pollutant it is the amount of the material contained in a specified volume of air. Air pollutant concentrations are usually expressed as mass per unit volume, e.g. µg·m -3 , and gaseous pollutants may also be expressed as a mixing ratio with air, e.g. parts per million (ppm) by volume. Air pollutant concentrations vary in time and space. ExposureExposure is defined as the contact of pollutant with a susceptible surface of the human body [9][10][11]. For ETS, this means contact with the eyes, the epithelium of the nose, mouth and throat, and the lining of the airways and alveoli. With respect to time, there are a number of possible formulations, including instantaneous exposure, peak exposure, average exposure over a specified time period, and cumulative exposure [11]. The best approach to assess ETS exposure will depend on the aim of the study, the health outcome, and the resources. Personal monitoring of nicotine or RSPs is the best method in studies of short-term health effects with small study samples. Stationary measurements of indoor air nicotine or RSPs are suitable for overall monitoring of ETS in different microenvironments over time. Questionnaires and interviews are suitable when studying health outcomes ...

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Fetal exposure to tobacco smoke products: A comparison between self‐reported maternal smoking and concentrations of cotinine and thiocyanate in cord serum

Cited by 67 publications

References 20 publications

Environmental tobacco smoke, parental atopy, and childhood asthma.

Environmental tobacco smoke, parental atopy, and childhood asthma.

Breastfeeding, maternal smoking and lower respiratory tract infections

Assessment of exposure to environmental tobacco smoke

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