Exposure to environmental tobacco smoke in the household and urinary cotinine excretion, heavy metals retention, and lung function.

The relationship between urinary levels of cotinine (U-cotinine) and arsenic (U-As), blood levels of cadmium (B-Cd), blood levels of lead (B-Pb), lung function, and questionnaire data on smoking habits were studied in 107 parents and their 46 children (7-10 y of age). There was a statistically significant relationship between the reported amount of tobacco smoked and U-cotinine levels. Nonsmokers who were married to persons who smoked had three times higher U-cotinine levels than nonsmokers whose spouses did not smoke. There was a significant association between the number of parents who smoked in the family and the U-cotinine levels of children. If only one parent smoked, maternal smoking was of greater importance than paternal smoking. There was also an association between U-cotinine and B-Cd. A study of lung function in the children revealed that vital capacity and functional residual capacity (corrected for sex, age, and height) increased as the number of parents who smoked increased. Therefore, the present study showed that (1) U-cotinine was a useful index of active smoking and environmental tobacco smoke exposure in adults and children, (2) U-cotinine was associated with the blood concentration of cadmium, and (3) environmental tobacco smoke exposure was associated with changes in lung function of children.     

Measures of maternal tobacco exposure and infant birth weight at term

This study was undertaken to determine the relation between self-reported number of cigarettes smoked per day and urine cotinine concentration during pregnancy and to examine the relations between these two measures of tobacco exposure and birth weight. Data were obtained from the Smoking Cessation in Pregnancy project, conducted between 1987 and 1991. Cigarette smoking information and urine cotinine concentration were collected for 3,395 self-reported smokers who were receiving prenatal care at public clinics in three US states (Colorado, Maryland, and Missouri) and who delivered term infants. General linear models were used to quantify urine cotinine variability explained by the number of cigarettes smoked per day and to generate mean adjusted birth weights for women with different levels of tobacco exposure. Self-reported number of cigarettes smoked per day explained only 13.9% of the variability in urine cotinine concentration. Birth weight declined as tobacco exposure increased; however, the relation was not linear. The sharpest declines in birth weight occurred at low levels of exposure. Furthermore, urine cotinine concentration did not explain more variability in birth weight than did number of cigarettes smoked. These findings should be considered by researchers studying the effects of smoking reduction on birth outcomes.     

Questionnaire or objective assessment for studying exposure to tobacco smoke among asthmatic and healthy children: The French VESTA Study

BACKGROUND: The underreporting of environmental tobacco smoke (ETS) exposure by parents of study children may depend on the instrument used and population studied, underlining the need for questionnaire validation in specific study settings. This study explores the validity of parent-reported ETS exposure in a French multicenter study on asthma. METHODS: The study population was composed of 313 children ages 4 to 14 years. Exposure to ETS was evaluated both by questionnaires on recent ETS exposure and by assessment of urinary cotinine by an enzyme immunoassay. RESULTS: According to parents' reports, about one-third of children were exposed to ETS within the past 2 days before cotinine measurement, and on average 14.9 +/- 15.4 cigarette-equivalent were smoked in their homes. The mean urinary cotinine was 435 +/- 530 nmol/mol creatinine and increased with the reported number of cigarette-equivalents smoked at home but it did not differ between children registered as being exposed to 1-10 cigarettes and children registered as unexposed. Agreement between questionnaire and urinary cotinine was moderate to poor according to our correlation coefficient (0.22) and kappa coefficient (0.09). CONCLUSION: These results show that our questionnaire is not discriminating enough to distinguish between nonexposure and mild exposure, but reveals gradients of higher exposure.     

A passive smoking screening program for children

BACKGROUND: There has been no report to date on mass screening of passive smoking in children using biomarkers. METHOD: To identify children exposed to actual environmental tobacco smoke (ETS), 261 children were divided into the following 3 groups: (A) both parents smoke; (B) one parent smokes; and (C) no parent smokes. Child urinary cotinine measurement and a parent questionnaire were obtained. RESULTS: Urinary cotinine was positive (>10 ng/ml) in 92 (35.2%) of the 261 children. Of the 92 children, 29 were classified into group A, 47 into group B, and 16 into group C. The percentages of children who tested positive for urinary cotinine in groups A, B, and C were 56.9%, 31.1%, and 27.1%, respectively. However, in group B, the percentage of children who tested positive for urinary cotinine was significantly higher if only the mother smoked (47.1%) than if only the father smoked (29.1%) (P<0.05). The mean+SD urinary cotinine level in group A was 12.9+/-6.5 ng/ml, and that in group B was 10.4+/-3.8 ng/ml if the mother smoked and 5.4+/-2.6 ng/ml if the father smoked. CONCLUSIONS: This smoking screening program may be useful in identifying children with actual ETS exposure and motivating their parents to either quit smoking or modify their smoking behavior around children.     

Environmental tobacco smoke exposure during infancy.

We collected information about household smoking habits from 518 mothers when they made their first well child visit with a 6 to 8-week old infant. A urine sample was also collected from the infant, the cotinine concentration measured, and the measurement correlated with data provided by the mother. Eight percent of the infant urine cotinine values fell at or above 10 micrograms/L in the 305 households where no smoking was reported. Corresponding rates were 44 percent in the 96 households where a member other than the mother smoked, 91 percent in the 43 households where only the mother smoked, and 96 percent in the 74 households where both the mother and another household member smoked. In households where the mother smoked, infant urine cotinine levels were lower in the summer, and higher when the infant was breast-fed. A screening question about family smoking habits in conjunction with well child care could effectively define a group of infants exposed to environmental tobacco smoke and thus be at greater risk for respiratory diseases.     

Saliva cotinine levels in smokers and nonsmokers

The authors collected by mail self-reported data on smoking habits and saliva samples that were analyzed for cotinine concentration in 222 smokers and 97 nonsmokers. Participants were members of the University of Geneva (Switzerland) in 1995. The 207 cigarette-only smokers smoked on average 10.7 cigarettes/day and had a median concentration of cotinine of 113 ng/ml. The cotinine concentration was moderately associated with the number of cigarettes smoked per day (+14 ng/ml per additional cigarette, p < 0.001, R2 = 0.45) and was 54 ng/ml higher in men than in women after adjustment for cigarettes per day and for the Fagerstr?m Test for Nicotine Dependence. The cotinine level was not associated with the nicotine yield of cigarettes (r= 0.08). In nonsmokers, the median concentration of cotinine was 2.4 ng/ml. The cotinine concentration was 1.5 times higher in nonsmokers whose close friends/spouses were smokers than in nonsmokers whose close friends/spouses were nonsmokers (p = 0.05). A cutoff of 7 ng/ml of cotinine distinguished smokers from nonsmokers with a sensitivity of 92.3% and a specificity of 89.7%; a cutoff of 13 ng/ml provided equally satisfactory results (sensitivity, 86.5%; specificity, 95.9%). This study provides evidence for the construct validity of both questionnaires and saliva cotinine for the assessment of active and passive exposure to tobacco smoke.     

Is the hair nicotine level a more accurate biomarker of environmental tobacco smoke exposure than urine cotinine?

STUDY OBJECTIVE: The aim of this study was to compare the two biomarkers of exposure to environmental tobacco smoke (ETS); urine cotinine and hair nicotine, using questionnaires as the standard. DESIGN: A cross sectional study of children consecutively admitted to hospital for lower respiratory illnesses during the period of the study. SETTINGS: Three regional hospitals in the larger Wellington area, New Zealand. PARTICIPANTS: Children aged 3-27 months and admitted to the above hospitals during August 1997 to October 1998. A total of 322 children provided 297 hair samples and 158 urine samples. MAIN RESULTS: Hair nicotine levels were better able to discriminate the groups of children according to their household's smoking habits at home (no smokers, smoke only outside the home, smoke inside the house) than urine cotinine (Kruskall-Wallis; chi(2)=142.14, and chi(2)=49.5, respectively (p<0.0001)). Furthermore, hair nicotine levels were more strongly correlated with number of smokers in the house, and the number of cigarettes smoked by parents and other members of the child's households. Hair nicotine was better related to the questionnaire variables of smoking in a multivariate regression model (r(2)=0.55) than urine cotinine (r(2)=0.31). CONCLUSIONS: In this group of young children, hair nicotine was a more precise biomarker of exposure to ETS than urine cotinine levels, using questionnaire reports as the reference. Both biomarkers indicate that smoking outside the house limits ETS exposure of children but does not eliminate it.     

Exposure of young infants to environmental tobacco smoke: breast-feeding among smoking mothers.

OBJECTIVES: This study examined the degree to which breast-feeding and cigarette smoking by mothers and smoking by other household members contribute to the exposure of infants to the products of tobacco smoke. METHODS: The subjects were 330 mother-infant pairs derived from a cohort of 1000 pairs enrolled in a longitudinal study of the pulmonary effects of prenatal and postnatal smoking. The main outcome measure was corrected urinary cotinine levels. RESULTS: Urinary cotinine levels were 10-fold higher in breast-fed infants of smoking mothers than among bottle-fed infants of smoking mothers. Among infants of nonsmoking mothers, urine cotinine levels were significantly increased in infants living in homes with other smokers; in this group there was no significant difference between bottle-fed and breast-fed infants. Infants whose mothers smoked in the same room as the infant had only nonsignificant increases in cotinine levels compared with infants whose mothers restricted their smoking to other rooms. CONCLUSIONS: Breast-fed infants of smoking mothers have urine cotinine levels 10-fold higher than bottle-fed infants whose mothers smoke, suggesting that breast-feeding, rather than direct inhalation of environmental tobacco smoke, is the primary determinant of cotinine levels in infants whose mothers smoke.     

接触二硫化碳对子代神经行为及尿5-HIAA水平的影响

目的研究怀孕前父、母亲有不同浓度二硫化碳(CS2)接触史的儿童神经行为功能和尿中5-羟吲哚乙酸(5-HIAA)改变。方法选择怀孕前父亲或母亲有CS2接触史者所生育的子女61名为接触组,按父母接触水平分为高浓度组和低浓度组。同时选取同一地区父母无任何毒物接触史的39名儿童为对照组,进行神经行为功能和尿中5-HIAA水平测试。结果父亲或母亲接触高浓度组儿童注意力、反应速度、心理运动能力、运动协调能力都受到影响,低浓度组仅在视感知和运动协调能力方面有所影响。分成母亲接触组、父亲接触组与对照组比较,除心理运动能力外未见到其他指标测试结果的差异有显著性。尿中5-HIAA水平,接触组与对照组儿童间差异未见有显著性。结论接触CS2对子代可产生一定的神经行为改变,且有一定的剂量-反应关系。     

上海市10~11岁学生贫血现状分析

【目的】 了解上海市10～11岁小学生的贫血状况及其影响因素,提出改进措施。 【方法】 采用分级整群随机抽样,按照“区-学校-年级”的抽样技术路线,在上海市逐级抽取样本。共10个区,每个区1所小学,每所学校抽取5年级全部学生进行调查。最终对1 675名10～11岁学生进行了问卷调查和贫血筛检。 【结果】 上海市10～11岁小学生贫血患病率为2.7％(男2.5％、女3.0％)。男女之间贫血患病率差异无统计学意义(χ²=1.080,P=0.583),市区和郊区贫血发生率差异有统计学意义(χ²=4.969,P=0.026)。父亲经常吸烟学生贫血患病率高于父亲未经常吸烟学生贫血患病率,差异有统计学意义(χ²=5.359,P=0.021)。多因素Logistic分析其影响因素为食欲差、其父亲经常吸烟、非市区。 【结论】 贫血问题在上海市小学生中依然存在,应在小学及家长中全面开展有关营养与饮食卫生的健康教育,为其创造良好的生活学习环境。     

基于尿液可替宁含量的农村幼儿二手烟暴露干预研究结果分析

目的 通过分析干预前后幼儿二手烟暴露的变化情况,为国内制定降低儿童二手烟暴露的干预措施提供实证依据。方法 纳入临海市和路桥区共414户有5岁以下幼童的吸烟家庭,基线调查后分为干预组和对照组进行持续半年的干预研究。第2个月,第6个月,第12个月都对研究对象进行重复调查和幼儿尿样采集。采用混合效应线性模型对成人每天吸烟量和幼儿尿可替宁含量变化情况进行分析。结果 干预组198人,对照组216人。吸烟者年龄以30~70岁间为主,身份主要为被调查幼童的父亲或爷爷。吸烟者每周吸烟支数与幼儿高尿可替宁呈现线性剂量-反应关系;干预组和对照组在基线、2月、6月和12月的每日吸烟支数存在差异(F=10.520, P时间=0.001);基线、2月、6月和12月的幼儿尿可替宁含量存在差异(F=5.010, P时间=0.026)。结论 台州农村地区家庭成员吸烟支数越多,幼儿出现高尿可替宁的危险越大,对家庭内吸烟者进行持续性宣传或提供干预可有效降低幼儿的二手烟暴露水平。     

Passive smoking in children: effect of avoidance strategies, at home as measured by hair nicotine levels

Hair nicotine levels were studied among children, relative to their caregivers' reported exposure to environmental tobacco smoke. A total of 117 children, aged 3 months to 10 years, were recruited consecutively from hospital inpatients, and their respective parents or caregivers were interviewed. Degree of exposure to environmental tobacco smoke was assessed via questionnaire. Scalp hair samples were collected from children and were assayed for nicotine. Levels of nicotine in hair among children reportedly exposed to smokers were higher than levels among unexposed children (chi2 = 26.46, p < .0001). In addition, hair nicotine levels were higher among children with mothers who smoked, compared with those whose mothers did not smoke. Whether household members smoked outside or inside the house had no significant effect on hair nicotine levels of children. Hair nicotine levels differed between children who were reportedly unexposed to environmental tobacco smoke at home and those who were exposed. Smoking outside the home, as reported by parents, did not cause a reduction in nicotine levels in the hair of children.     

Passive Smoking in Children: Effect of Avoidance Strategies at Home as Measured by Hair Nicotine Levels

Hair nicotine levels were studied among children, relative to their caregivers' reported exposure to environmental tobacco smoke. A total of 117 children, aged 3 months to 10 years, were recruited consecutively from hospital inpatients, and their respective parents or caregivers were interviewed. Degree of exposure to environmental tobacco smoke was assessed via questionnaire. Scalp hair samples were collected from children and were assayed for nicotine. Levels of nicotine in hair among children reportedly exposed to smokers were higher than levels among unexposed children (χ² = 26.46, p < .0001). In addition, hair nicotine levels were higher among children with mothers who smoked, compared with those whose mothers did not smoke. Whether household members smoked outside or inside the house had no significant effect on hair nicotine levels of children. Hair nicotine levels differed between children who were reportedly unexposed to environmental tobacco smoke at home and those who were exposed. Smoking outside the home, as reported by parents, did not cause a reduction in nicotine levels in the hair of children.     

Breast feeding and smoking hygiene: major influences on cotinine in urine of smokers'' infants.

The determinants of urine cotinine levels were studied in a group of 101 infants aged 3 months, including 79 infants whose mothers were current smokers. At a pre-arranged home visit the infants' mothers completed an interviewer-administered questionnaire, and samples of maternal urine and breast milk and infants' urine were collected. Cotinine and nicotine levels were determined by gas-liquid chromatography. Infant urine cotinine levels ranged from 0 to 140 micrograms/l (0-1120 ng cotinine/mg creatinine). A linear dose response relation between mother's smoking rate and infant urine cotinine level was observed among breast-fed infants (r = 0.79, p less than 0.001). The relation was weaker among infants fed by both breast and bottle (r = 0.56, p = 0.01) and was not apparent among bottle-fed infants (r = 0.15, p = 0.16). In addition to mode of feeding and mother's smoking rate, mother's smoking "hygiene" (assessed by the reported frequency of smoking while feeding and with infant in same room) was independently associated with infant urine cotinine level. Father's smoking pattern and exposure to smoke outside the household did not relate significantly to infant cotinine levels. We conclude that when mothers smoke, breast feeding is the principal determinant of cotinine in infants' urine. It is likely that most of this cotinine comes from cotinine in mothers' breast milk, but further research is needed to establish how much nicotine is ingested by breast-fed infants of mothers who smoke, and to investigate possible health effects.     

Saliva cotinine and recent smoking--evidence for a nonlinear relationship.

Cotinine concentration in various body fluids is considered to be among the most useful markers of nicotine exposure currently available. Despite the prevailing consensus concerning cotinine''s usefulness, cotinine''s large intrasubject variability has led some to question the value of a single-point measurement. Several individual differences (for example, age, race, sex, and so forth) may affect cotinine excretion, and a peculiar nonlinearity between the number of cigarettes smoked and cotinine concentration has been reported previously in the literature. The purpose of this investigation was to examine the nature of the association between cotinine and reported number of cigarettes smoked after adjustment for the relationship between cotinine and age, a key individual difference known to affect drug absorption, distribution, metabolism, excretion, and tissue sensitivity. The authors examined the relationship between saliva cotinine and daily cigarette consumption in 116 smokers (mean age = 37.4 years; average number of cigarettes smoked daily = 20.1) who logged each cigarette into a hand-held computer as part of a study on the accuracy of recall. The Pearson correlation between saliva cotinine and the logged number of cigarettes smoked in the previous 17 hours (the time window corresponding to the half-life of cotinine) accounted for significantly more of the variance in cotinine than did the average logged number of cigarettes smoked daily during 5 days. Age was also significantly associated with cotinine levels. Further examination of the relationship between cotinine and amount smoked in the previous 17 hours revealed evidence for a significant nonlinear component.(ABSTRACT TRUNCATED AT 250 WORDS)     

Environmental tobacco smoke and canine urinary cotinine level

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.     

Tobacco smoke and formation of N-(2-hydroxyethyl)valine in human hemoglobin

Human exposure to ethylene oxide (EtO) occurs mainly through inhalation of polluted air in occupational workplaces and/or via tobacco smoke. A significant biochemical reaction of EtO converts the terminal valine of hemoglobin into N-(2-hydroxyethyl)valine (HOEtVal). In the present study, the extent of HOEtVal formation in 360 healthy adults who were not occupationally exposed to EtO was measured with a gas chromatograph/mass spectrometer in the electron-capture negative chemical ionization mode. This parameter was correlated with smoking habits and urinary cotinine concentration, exhibiting a positive relationship between HOEtVal and the number of cigarettes smoked (r2 = .4416). Urinary cotinine measurements also correlated with HOEtVal and the number of cigarettes smoked. This positive correlation between urinary cotinine and HOEtVal (r2 = .3893) provides a new perspective on the early stages of carcinogenic processes.     

Relation between lead and cadmium in blood and the involuntary smoking of children

The blood lead (PbB) and blood cadmium (CdB) levels, as well as the parental smoking habits, of 133 children aged 4 to 11 years were studied. The children were from a town with a lead smeltery and a surrounding rural area. There was a significant association between the higher PbB levels of the children and involuntary (parental) smoking in the home. The CdB levels of the children were not affected by parental smoking habits. The children whose parents did not smoke at home had lower PbB values than those with one smoking parent. These children, in turn, had lower levels than children with two smoking parents. Mothers who smoked had a greater impact than fathers who smoked. There was also a dose-response relationship between the amount of tobacco smoked by the mother and the PbB level of the child. The PbB value was higher for the children living near industrial lead emissions than for children from the rural area. The association between PbB level and involuntary smoking is probably not due to inhalation of lead originating from tobacco smoke. A small airways disease affecting the absorption of inhaled lead particles is proposed as an explanation.     

Determinants of children's exposure to environmental tobacco smoke (ETS): a study in Southern Germany

Maternal smoking has been repeatedly found to be the most important determinant of children's exposure to environmental tobacco smoke (ETS). Here, we further investigated predictors for the urinary cotinine/creatinine ratio (CCR, ng/mg) in 1220 preschool children for the year 1996. Children from smoking homes (35.1%) had significantly higher CCR than children from nonsmoking homes (mean: 55.5 vs. 14.9 ng/mg). The level of education of the parents was a strong predictor for CCRs even after adjusting for number of cigarettes smoked, maternal smoking and dwelling space. Additionally, dwelling space was inversely related to children's urinary cotinine level. The CCR- levels in children investigated in 1996 and 1998 were significantly correlated (Pearson's r=0.67). The parents of 806 children agreed for a visit to their homes. In 79 of the 536 (14.7%) of the self-reported, nonsmoking households, smoking was admitted during the visit. The mean urinary CCR of these children was 25.2 ng/mg. We conclude that in addition to parental smoking behaviour, other variables such as dwelling space and social and educational status predict the children's exposure to ETS. Our data also revealed that a considerable percentage of parents denied the ETS exposure of their children at home.     

The effect of passive smoking on the development of respiratory syncytial virus bronchiolitis

In spite of the increasing evidence that passive smoking increases the incidence of respiratory infections and bronchial hyper-responsiveness, the information about whether exposure to sudden heavy smoke enhances the development of acute respiratory infections in children remains inadequate. In this study, to quantitate the level of exposure to environmental tobacco smoke, in 28 children (age ranging 2–18 months) with respiratory syncytial virus (RSV) bronchiolitis and in 30 children (age ranging between 2–15 months) with non-respiratory symptoms, the serum levels of cotinine, the major metabolite of nicotine, were measured at admission to the emergency department. Parents were asked to fill in a questionnaire about the housing conditions and their smoking habits. Serum samples were taken again from the children with RSV bronchiolitis at their second visit at 1 month after discharge from the hospital. The children with RSV bronchiolitis had higher levels of serum cotinine (mean of 10.8 ng/ml) in the acute stage, compared with post-bronchiolitis stage (mean of 7.4 ng/ml). Moreover, patients admitted with non-respiratory symptoms had significantly lower levels of serum cotinine (mean of 3.9 ng/ml) than both phases of patients with RSV bronchiolitis. Children with RSV bronchiolitis were found to have higher levels of cotinine when either the mother or both of the parents smoked, than the children with non-smoker parents. In conclusion, children admitted to the hospital with RSV bronchiolitis were shown to be acutely exposed to more cigarette smoke after 1 month and much more than the children admitted for non-respiratory diseases. These findings may imply that sudden heavy cigarette smoke exposure may predispose to an acute respiratory infection.